Thanks so much to all of you who participated in this UNC Grand Rounds Discussion Forum. There is still much to learn about the Autism Spectrum Disorders and this can only be accomplished with the work of many people and agencies. While this Forum ends today, we at CDC still welcome your questions and information. To contact us concerning research on the prevalence of the ASDs or risk factors, please see http://www.cdc.gov/ncbddd/dd/ddautism.htm or email DDBinfo@cdc.gov. For questions or information on immunizations and autism, please see http://www.cdc.gov/nip/vacsafe/concerns/autism/autism.htm or email NIPinfo@cdc.gov. Thank you.
There are two different concerns related to autism and vaccines. The first concerns the MMR vaccine and autism. Several large studies have shown no increased risk of being diagnosed with autism following the MMR vaccination. Overall, the MMR vaccine appears to be a safe mechanism for preventing highly contagious diseases of childhood for most people. However, it is still unclear whether there are some individuals who have a unique susceptibility to the MMR vaccine. Studies looking at individual differences are needed and some are underway. For example, the CDC is in the process of completing a study looking at the distribution of the ages of first MMR vaccination among children with autism as compared to children without autism. This study will be looking at clinical subgroups of children with autism including those that showed evidence of regression in development. The results of the study are expected to be published by the end of the year. Other studies are also being designed and conducted to look at the risk for autism among clinical subgroups. For more information on this and other CDC research, please see the NIP page on CDC Autism Research Efforts at:
http://www.cdc.gov/nip/vacsafe/concerns/autism/autism-res-cdc.htm
Studies have also been conducted to look at the potential relationship between thimerosal in vaccines and autism. (It should be noted that the MMR vaccine does not and never has contained the mercury containing preservative). Most recent studies have found no association between thimerosal and autism. While the findings in studies looking at thimerosal and autism have been negative, the FDA has withdrawn vaccines containing thimerosal due to the fact that children were potentially receiving an amount that exceeded the FDAÿffff92s standards for mercury exposure. Vaccines which previously contained thimerosal, such as DTP, Hepatitis B, and Hib, no longer contain the preservative.
See also the response below from the National Immunization Program (NIP).
Did the preliminary Vaccine Safety Datalink (VSD) study find that exposure to thimerosal within the first three months of life increases a child's risk of developing autism?
A statistically significant relationship between autism and thimerosal was not found in either the preliminary VSD study or the later, larger analysis. While a graph in the preliminary report does show an apparent elevation in risk for autism among children exposed to a certain level of thimerosal (> 62.5ug) by the third month of life, this risk was not statistically significant and was likely a chance fluctuation. In fact, later analyses of additional cases showed that a childÿffff92s exposure to thimerosal, either by three months of life or by seven months of life, did not increase his or her risk for developing autism. There was no suggestion of an increased risk for autism even among those children who were exposed to the highest levels of thimerosal by seven months of age (i.e., those receiving 162.5 ug, 175 ug, or more than 175 ug thimerosal by 7 months of age). These preliminary negative results from the VSD project, however, cannot be considered definitive since the study was not specifically designed to evaluate a complex condition such as autism. CDC is planning a more thorough investigation of thimerosal exposure through infant vaccines and risk of autism.
For more information, including contact information, the web address for the NIP autism and vaccines page is: http://www.cdc.gov/nip/vacsafe/concerns/autism/default.htm#thimerosal
Vaccines may fuel autism epidemic
" One reason this isn't getting the attention it needs is that the Food and Drug Administration has very close ties
to the pharmaceutical companies, as does the Department of Health and Human Services [HHS] and the Centers for Disease Control. . . In some cases it appears that it's a revolving door and people leave government health agencies and go to
work for the pharmaceuticals, which I think have undue influence on our health agencies." - Rep Dan Burton
" Neither the Wyeth nor Merck pharmaceutical companies, nor HHS or FDA, returned INSIGHT's calls about this matter."
[Readers might recognize that this news has been reported here weeks ago. While the new research has been extensively covered in the UK, it has been ignored by the US media -- until only just now. Source: Insight on the News.]
http://infobrix.yellowbrix.com/pages/infobrix/Story.nsp?story_id=39906075& ID=infobrix& scategory=Healthcare&
A new study indicates childhood vaccines containing a mercury- based
preservative may be the culprits behind the surge in autism cases sweeping
the United States. The mother of an autistic child wonders aloud when health
officials will wake up to the epidemic that has claimed not only her son but
hundreds of thousands of other children in the United States, with no end in
sight. She muses, " Maybe someday this will be as important as SARS and we'll
get the same attention. God knows we need it."
Autism is a severely incapacitating developmental disability for
which there is no known cure. According to a recently released report by the
California Department of Developmental Services (DDS) entitled Autistic
Spectrum Disorders, Changes in the California Caseload: 1999-2002, the rate
of children diagnosed with full- syndrome autism in the Golden State between
1999 and 2002 nearly doubled from 10,360 to 20,377. The report further
revealed that " between Dec. 31, 1987, and Dec. 31, 2002, the population of
persons with full-syndrome autism has increased by 634 percent." That is a
doubling of autism cases every four years, and the staggering increases are
not limited to California.
Shots in the dark? Infants are being inoculated with vaccines
containing toxic ingredients that can be harmful - or fatal.
According to data provided by the U.S. Department of Education, the
increased autism rate in California is in line with the increases other
states are experiencing. For example, in 1992 Ohio reported 22 cases. A
decade later the number had increased by 13,895 percent to 3,057. In
Illinois the rate of autism cases climbed from just five in 1992 to 3,802 -
an increase of 76,040 percent. Mississippi, New Hampshire and the District
of Columbia reported no cases of autism in 1992, but by 2002 the number of
cases reported were 461, 404 and 144, respectively. Only Puerto Rico can
claim to have an increase of less than 100 percent, with the remaining
states reporting increases of at least 500 percent during the same period.
Although once considered rare, during the last two decades the chance
of a child being diagnosed with autism has skyrocketed from one in 10,000 to
one in 150. In California, full-syndrome autism now is the No. 1 disability
among children and more prevalent than childhood cancer, diabetes and Down's
syndrome. It is estimated that within the next four years autism cases in
the Golden State will exceed the total number of cases of both cerebral
palsy and epilepsy. To get a better idea of how quickly the epidemic is
spreading one need only consider that in 1987 there were 2,778 persons with
autism in California. By 2002 the number had increased to 20,377, and in
2002 3,575 new cases had been added to the rolls, far exceeding the total
number of cases in the state 15 years earlier.
For years there has been a debate about the cause or causes of
autism, but the vast majority of finger-pointing has been directed at
childhood vaccines as the culprit. And considering what is put into the
vaccines injected into hours-old infants, it is easy to understand why they
are at the top of the list of suspects: formaldehyde (used in embalming),
thimerosal (nearly 50 percent mercury), aluminum phosphate (toxic and
carcinogenic), antibiotics, phenols (corrosive to skin and toxic), aluminum
salts (corrosive to tissue and neuro-toxic), methanol (toxic), isopropyl
(toxic), 2- pheoxyethanol (toxic), live viruses and a host of unknown
components considered off-limits as trade secrets. These are just part of
the vaccine mixture.
For those who believe there are elements in vaccines that may be
responsible for the increased number of autism cases and other neurological
disorders, thimerosal currently is at the top of the list of possible
culprits being investigated.
Despite official insistence that the evidence linking injected
thimerosal to autism is inconclusive, the data suggest otherwise. In 1999
the National Academy of Sciences Institute of Medicine (IOM) must have
thought there was something seriously wrong when it supported removal of
thimerosal from vaccines, stating that it was " a prudent measure in support
of the public goal to reduce mercury exposure of infants and children as
much as possible." The IOM further urged that " full consideration be given
to removing thimerosal from any biological product to which infants,
children and pregnant women are exposed."
A recently published study in the Journal of American Physicians and
Surgeons by Mark Geier, M.D., Ph.D., and president of the Genetic Centers of
America and his son, David Geier, president of Medcon Inc. and a consultant
on vaccine cases, was titled " Thimerosal in Childhood Vaccines,
Neurodevelopment Disorders and Heart Disease in the United States." It
presents strong epidemiological evidence for a link between
neurodevelopmental disorders and mercury exposure from thimerosal-containing
childhood vaccines.
Specifically, the authors evaluated the doses of mercury that
children received as part of their immunization schedule, then compared
these doses with federal safety guidelines. Furthermore, to compare the
effects of thimerosal in vaccine recipients, the incident rates of
neurodevelopmental disorders and heart disease reported to the government's
Vaccine Adverse Events Reporting System were analyzed. The results were
dramatic. The report revealed that " U.S. infants are exposed to mercury
levels from their childhood- immunization schedule that far exceed the EPA
[Environmental Protection Agency] and FDA [Food and Drug Administration]-
established maximum permissible levels for the daily oral ingestion of
methyl mercury."
The authors concluded that " in light of voluminous literature
supporting the biologic mechanisms for mercury-induced adverse reactions,
the presence of amounts of mercury in thimerosal- containing childhood
vaccines exceeding federal safety guidelines for the oral ingestion of
mercury and previous epidemiological studies showing adverse reactions to
such vaccines, a causal relationship between thimerosal-containing childhood
vaccines and neurodevelopment disorders and heart disease appears to be
confirmed."
Smoking gun: The Geiers' research presents evidence for a link
between neurodevelopmental disorders and vaccines containing thimerosal.
It is no secret among government and health officials that mercury is
toxic and causes serious adverse reactions. In July 1999 the American
Academy of Pediatrics and the U.S. Public Health Service issued a joint
statement calling for the removal of thimerosal from vaccines. Five years
after the joint statement, however, it still is difficult for parents and
physicians to be sure that the pharmaceutical companies have indeed removed
the toxic substance from their vaccines.
According to Mark Geier, " The 2003 Physicians' Desk Reference [PDR]
still shows childhood vaccines containing thimerosal, including diphtheria,
tetanus and acellular pertussis. DTaP, manufactured by Aventis Pasteur,
contains 25[mu]g [25 micrograms] of mercury, Hemophilus influenzae b (Hib)
vaccine manufactured by Wyeth contains 25[mu]g of mercury and pediatric
Hepatitis B vaccine, manufactured by Merck, contains 12.5[mu]g of mercury."
Geier continues, " In addition, the influenza vaccine that is
recommended for an increasing segment of the pediatric population in the
U.S. also contains 25[mu]g of mercury. Assuming that the labeling is
correct, it is possible that children in the U.S. in 2003 may be exposed to
levels of mercury from thimerosal contained in childhood vaccines that are
at higher levels than at any time in the past. Possible total childhood
mercury in 2003 is more than 300[mu]g."
Whether the " labeling is correct" is the question du jour. According
to Len Lavenda, a spokesman for Avenus Pasteur, the maker of DTaP, " Avenus
only sells the DTaP vaccine in the preservative- free formulation. The PDR
references both the single and multidose. However, when we received the
license for the preservative-free we ceased sales of the multidose vial. For
some reason, the package insert takes much longer to revise than one would
expect. I believe it is at the FDA waiting for approval, but the fact is we
do not sell or market that product. In March 2001 we stopped all sales of
that product in the preservative formulation. We did not recall the product
at that time because it was our belief that if we did children may go
unimmunized. It's been two years since anyone has been able to purchase the
preservative formulation from us."
Lavenda continues: " The package insert talks about both the single
and multidose vials and it says that the single-dose vial is
preservative-free, and that is all that is sold. The PDR is out- dated, but
parents don't have to worry about their children being administered 25[mu]g
of thimerosal. It just takes time to get the paperwork caught up. The
current package insert does not accurately reflect what is being marketed."
Geier is astounded by Lavenda's admission. " If this is true, they
should be in jail. They can't have an insert on a drug that is totally
wrong. It is against all regulations. If I'm a doctor and I'm giving you a
shot and the insert says such and such is in the shot, it had better be in
it. If doctors can't rely on the instructions that come with what we're
injecting then all bets a\re off. This is a far worse admission than
admitting that thimerosal is still in the vaccine. There are at least 15
laws that say the insert has to match what is in the product. This is
absolutely horrendous. In my entire career in medicine I have never heard of
a drug company claiming that what's in the insert and the accompanying
product don't match. This is total mislabeling and fraud by their own
admission. Legally they should be forced to close down because our clinical
decisions are based on their labeling."
Assuming that the package inserts are correct, Geier tells insight,
" The EPA limit is 0.1 micrograms of mercury per kilogram body weight per
day. It doesn't take a genius to do the calculations when on their day of
birth children are given the hepatitis B vaccine, which is 12.5 micrograms
of mercury. The average newborn weighs between 6 and 7 pounds, so they would
be allowed 0.3 micrograms of mercury but in this one shot they are getting
12.5 micrograms. That's 39 times more than allowed by law. And it gets worse
when you consider that children are getting multiple vaccinations at 2
months. And this limit is for oral ingestion and not injection, which is
much worse."
Recommended Childhood and Adolescent Immunization Schedule for The
United States According to the 2003 Physicians' Desk Reference Rhonda
Smith, a spokeswoman for the federal Centers for Disease Control and
Prevention (CDC), tells INSIGHT that, except for mere traces, thimerosal has
been removed. " All routinely recommended licensed vaccines," says Smith,
" that are currently being manufactured for children in the U.S., except
influenza, contain no thimerosal or only trace amounts - a concentration of
less than 0.0002 percent." But according to the 2003 immunization schedule
and the package inserts, there appear to be a number of childhood vaccines
that still contain mercury, including those for tetanus and diphtheria.
This scenario becomes even more bizarre when one further considers
that thimerosal is not a necessary component in vaccines. It first was
introduced by pharmaceutical giant Eli Lilly and Co. in the 1930s and is
added to vaccines only as a preservative - the theory being that multiple
doses are taken from the same bottle and that thimerosal will protect
against contamination. However, according to Geier, " the solution to any
such problem is to make vaccines available in a single dose, which will cost
the pharmaceuticals about one penny more. What is interesting is that if you
look up the mumps, measles, rubella [MMR] vaccines in the PDR you'll see
that they do not contain thimerosal because it would kill the live virus.
The MMR is available in multi-dose packaging and, yet, there is no
preservative nothing. What they did was put a label on it that says 'This
product does not contain preservatives. Handle with care.' It's that
simple."
Geier insists, " I'm pro-vaccines, but the bottom line is that our
kids are getting massive amounts of mercury. Mercury has been withdrawn from
everything, including animal vaccines, yet we keep injecting it into our
children. Everyone should absolutely refuse to take a vaccine shot that has
thimerosal in it, and they should insist on reading the vaccine package
insert. Our data showed that the more mercury children received in their
childhood vaccines the more neurodevelopment disorders there are. We've
looked at this every possible way and every time there's massive evidence to
support it."
Personal story: Rep. Burton, standing second from left, became an
advocate for victims of autism when his grandson became autistic after
receiving nine vaccines in one day.
So, if everyone acknowledges the toxicity of mercury and top U.S.
health officials have called for its removal, why is thimerosal still in
vaccines? " Maybe," concludes Geier, " the mercury isn't being taken out all
at once because if the pharmaceutical companies did that you would see an
unbelievable change in the rate of autism and there would be massive
lawsuits. If you look at the graphs now they go up and up. If you stop the
thimerosal all at once you'd see the numbers fall dramatically."
Rep. Dan Burton (R-Ind.), a longtime advocate for victims of autism,
has a grandson who became autistic after receiving nine vaccines in one day.
Burton recently sent his second request in as many years to the White House
asking for a conference of scientists, researchers and parents to look into
the causes of autism. The Indiana lawmaker tells INSIGHT, " There is no doubt
in my mind that the mercury in vaccines is a major contributing factor to a
growing number of neurological disorders among children, but in particular
autism."
Burton explains that " thimerosal is a toxic substance - mercury - and
should not be put in close proximity of people, should not be injected into
people, especially children who have a newly formed immune system that may
not be able to handle it. To my knowledge there never have been long-term
tests on thimerosal and we never should have used mercury in vaccines,
period. Now what we've got is an epidemic that is absolutely out of
control."
The Indiana congressman continues, " One reason this isn't getting the
attention it needs is that the Food and Drug Administration has very close
ties to the pharmaceutical companies, as does the Department of Health and
Human Services [HHS] and the Centers for Disease Control. I've said in the
past that in some cases it appears that it's a revolving door and people
leave government health agencies and go to work for the pharmaceuticals,
which I think have undue influence on our health agencies. Of course, they
may not want to look at this because there's a possibility that large claims
would be filed and the pharmaceutical companies would have to cough up the
money to take care of these kids who have been damaged."
Burton means business. He insists, " The FDA, CDC and HHS should put
out in a very public way the dangers of mercury, but as soon as they do it w
ill amount to an admission that their mercury is causing these problems. So
the reports that come out of the FDA, CDC and HHS use ambiguous terms. Well,
if they're not sure, and there's the remotest possibility that mercury in
vaccines could cause autism, they ought to get thimerosal off the market.
Too many kids are being ruined for life because of this stuff."
Barbara Loe Fisher is founder of the National Vaccine Information
Center, a charitable organization dedicated to the prevention of vaccine
injuries and deaths through public education. Fisher tells INSIGHT, " There
are many things in vaccines that could be causing these disorders, and
thimerosal is only part of the problem. In the last 20 years, we've gone
from giving children 23 doses of seven vaccines to 38 doses of 12 vaccines.
I think the mercury is part of it for some kids, though I'm not sure it's
the answer for all." But this is a no-brainer, says Fisher. " Mercury
shouldn't be in vaccines. They've taken it out of everything else so why not
the vaccines? The one thing that people really need to look at is the
dramatic rise in chronic disease and disabilities in our kids in just the
last two decades. You have to admit that there is something occurring that a
growing number of children cannot get through without being immune-system
and brain-system damaged. And what is the one thing that we expose every
child to? Those vaccines."
Fisher concludes, " I've always argued that public health is not
measured only by an absence of infectious disease. It also is measured by
the absence of chronic disease. By that score we get a big fat 'F.' So we
don't have measles and mumps, but look what we have now. It's just really
simple: Take the mercury out and let's see what happens."
Even so, based on the Aventis admission that the package insert does
not reflect what is in the vaccine, it will be difficult to know when, if
ever, the thimerosal actually has been removed. This skews the data about
the relationship between thimerosal and autism. More important, it means
parents cannot be sure the vaccinations their children receive are free of
mercury.
Neither the Wyeth nor Merck pharmaceutical companies, nor HHS or FDA,
returned INSIGHT's calls about this matter.
" The [vaccine] package insert does not accurately reflect what is
being marketed."
[Kelly Patricia O'meara Is An Investigative Reporter For Insight
Magazine.] Copyright Washington Times Corporation
Vaccine damaged children
are called the " acceptable risk"
by industry leaders.
As parents there is nothing ABSOLUTELY
NOTHING acceptable about the risk!
It's time to tell these leaders that we will
no longer allow this to continue
IT'S TIME TO ACT!
P.S. Has anyone studied why autism rise in Puerto Rico seems lower than in the states? What is the vaccination protocol in Puerto Rico? What is the parental rate of vaccination compliance there?
Subject: Re: This is not just about autism
Posted by: Mary Hirzel on 06/27/03
In Reply to: Re: Re: Re: This is not just about posted by CDC DDBInfo on 06/27/03:
Thanks you for your response. I'm sure it is difficult to field such passionate questions with the amount of poise and courtesy that you are attempting.
HOWEVER, and with all due respect, if one of these was YOUR child, I'm sure you would view this in a different light.
Valuable years have been lost, and still the government is dragging it's feet, hoping we will just go away. Credible research has been buried or scoffed at. Professional reputations have been attacked. Date proving a statistically significant link between Thimerasol and neurological damage has been hidden even from the NIH. Ridiculous " reviews" of (selected) literature gets touted in the media as reason to " put parents' minds at ease" about suspected connections between vaccines and the adjuvants and neurological damage.
When two children suddenly died this past winter here in Ann Arbor, the CDC was all over the place, trying to solve the question of just what had happened to these INDIVIDUAL children.
Why do we not see the same response to our plight? Why are we told to look with hope to the National Children's Study, when, by your own description those results will come in about 21 years?????
Our INDIVIDUAL children deserve attention RIGHT NOW! I believe that, despite the CDC/NIH's assertions that there currently is " no evidence" linking this holocaust to vaccine damage, individual scientists and physicians in these agencies are aware that there is more than enough " anecdotal evidence" to be looking at the medical condition of these children more seriously.
This IS an epidemic, and genetics play about the same role in the disaster as a red-headed child's propensity to get sunburned.
I call on you all to recognize that you have a role to play in helping us and yourselves. The stakes are much higher than anyone's career or reputation.
Do the right thing; demand some answers youselves,
Mary
BL Fisher Note: At least someone is finally admitting that the federal government policy of recommending that babies get their first hepatitis B shot in the newborn nursery is to make up for deficiencies in the public health system they operate
Vaccination Graduates to an Older Crowd
By DONALD G. McNEIL Jr.
http://www.nytimes.com/2003/07/01/health/01VACC.html
The future of vaccines, infectious disease experts say, is teenagers.
Parents are used to the idea of their babies getting up to 20 vaccinations by
age 2 to prevent polio, measles, chickenpox and other diseases transmitted by
coughing.
But pharmaceutical companies are inventing new vaccines against diseases usually
transmitted by sex, drug use, foreign travel or living in dormitories or
barracks. Half a dozen are now in the long and tangled medico-regulatory
pipeline between the petri dish and the pediatrician's syringe.
" Adolescent vaccines are the next wave," Dr. Michael D. Decker, vice president
for scientific affairs at the vaccine subsidiary of the Aventis pharmaceutical
giant said recently at a conference on immunization policy. " All the
manufacturers have them in the works."
[rest of article at]
http://www.nytimes.com/2003/07/01/health/01VACC.html
[comment: Infant vaccinations are not safe for every child. Many people believe
that vaccinations are implicated in many cases of Gulf War Syndrome. Thus the
next step is to create a new wave of vaccinations. Dare we suspect that the
really big money is not in the vaccinations themselves but in the ongoing
treatments for chronic problems caused by excessive vaccinations? Are overly
vaccinated people more politically compliant?]
My son who is autistic, was a premie and has had severe respiratory problems since infancy (respiratory distress syndrome, BPD, croup, reactive airway disease). On one chest Xray at approx age 18 months, the pulmonologist pointed out that he had an enlarged thymus gland. A CT confirmed it. He said that was unusual at his age, but that it was probably enlarged due to immune system being worked so hard with respiratory problems.
Looking back, could it have been related to any other taxing of the immune system (i.e. vaccines)?
If so, could a simple chest Xray showing an enlarged thymus
be another early sign that the immune system has been insulted? If nothing else, it could allow for even earlier intervention.
I have not jumped on the bandwagon blaming vaccines for autism, but with SO much exposure/ingestion of chemicals and metals in our society, it sure makes one wonder.
I'll have to be content allowing others to fight this one; I'm too busy working daily with my son!
Thanks so much for this forum.
Hi Cynthia,
You raise an interesting point related to whether an enlarged thymus gland could be an indication of a stressed immune system and might be used to identify children early for intervention. I am a pediatrician, but not an immunologist or pulmonoligist, however, but it is my understanding that the finding of an enlarged thymus is very non-specific; it may not be a good marker for autism. On the other hand, we can find out more about it and if it looks promising as a marker that could be related to autism, we can consider collecting data as part of our autism etiologic study that we are planning. We are very interested in examining immune functioning. Thanks so much for the thought.
Dear CDC representative:
I am delighted to read that you are very interested in examining the immune system connection to autism! PLEASE pursue this! There are too many studies indicating a connection, yet doctors tend to dismiss parental concerns in this area.
Thank you!
A major function of genomic methylation is that of silencing expression of
retroviral and parasitic genes that have become integrated into the human genome
(1-2). Bestor's reviews mention only several of the known genes whereby humans
can have impaired methylation on a genomic level. Vaccines that contain
retroviruses would seem a guaranteed way for iatrogenic illnesses among
individuals with suboptimal methylation status whether as a result of acquired
and/or genetic etiologies.
1: Hum Mol Genet. 2000 Oct;9(16):2395-402.
The DNA methyltransferases of mammals.
Bestor TH.
Department of Genetics and Development, College of Physicians and Surgeons of
Columbia University, 701 West 168th Street, New York, NY 10032, USA.
thb12@columbia.edu
The biological significance of 5-methylcytosine was in doubt for many years, but
is no longer. Through targeted mutagenesis in mice it has been learnt that every
protein shown by biochemical tests to be involved in the establishment,
maintenance or interpretation of genomic methylation patterns is encoded by an
essential gene. A human genetic disorder (ICF syndrome) has recently been shown
to be caused by mutations in the DNA methyltransferase 3B (DNMT3B) gene. A
second human disorder (Rett syndrome) has been found to result from mutations in
the MECP2 gene, which encodes a protein that binds to methylated DNA. Global
genome demethylation caused by targeted mutations in the DNA methyltransferase-1
(Dnmt1) gene has shown that cytosine methylation plays essential roles in
X-inactivation, genomic imprinting and genome stabilization. The majority of
genomic 5-methylcytosine is now known to enforce the transcriptional silence of
the enormous burden of transposons and retroviruses that have accumulated in the
mammalian genome. It has also become clear that programmed changes in
methylation patterns are less important in the regulation of mammalian
development than was previously believed. Although a number of outstanding
questions have yet to be answered (one of these questions involves the nature of
the cues that designate sites for methylation at particular stages of
gametogenesis and early development), studies of DNA methyltransferases are
likely to provide further insights into the biological functions of genomic
methylation patterns.
Publication Types:
Review
Review, Tutorial
PMID: 11005794 [PubMed - indexed for MEDLINE]
2: Novartis Found Symp. 1998;214:187-95; discussion 195-9, 228-32.
The host defence function of genomic methylation patterns.
Bestor TH.
Department of Genetics and Development, College of Physicians and Surgeons,
Columbia University, New York, NY 10032, USA.
It has long been held that reversible promoter methylation allows genes to be
expressed in the appropriate cell types during development. However, no
endogenous gene has been proven to be regulated in this way, and it does not
appear that significant numbers of promoters are methylated in non-expressing
tissues. It has recently become clear that the large majority of genomic
5-methylcytosine is actually in parasitic sequence elements (transposons and
endogenous retroviruses), and the primary function of DNA methylation now
appears to be defence against the large burden of parasitic sequence elements,
which constitute more than 35% of the human genome. Direct transcriptional
repression provides short-term control, and the tendency of 5-methylcytosine to
deaminate to thymidine drives irreversible inactivation. It is suggested that
intragenomic parasites are recognized by virtue of their high copy number, and
that the disturbances of methylation patterns commonly seen in human cancer
cells activate a host of parasitic sequence elements, which destabilize the
genome and tip the cell towards the transformed state.
3: J Rheumatol. 2002 Aug;29(8):1678-82.
Role of DNA methylation in transcription of human endogenous retrovirus in the
pathogenesis of systemic lupus erythematosus.
Okada M et al.
OBJECTIVE: We recently reported that transcription of human endogenous
retrovirus (HERV) clone 4-1-like sequences is increased in patients with
systemic lupus erythematosus (SLE). We therefore investigated the role of DNA
methylation in the transcription of this HERV. METHODS: The effect of a
demethylating agent, 5-aza-deoxycytidine (5-aza C), on the transcription of HERV
clone 4-1 in healthy individuals and patients with SLE was examined using
reverse transcriptase-PCR and real-time quantitative PCR. RESULTS: 5-aza C
increased clone 4-1-like messenger RNA in healthy controls, but not in patients
with SLE. CONCLUSION: Defects of methylation may contribute to the transcription
of HERV in patients with SLE and this may be related to the pathogenesis of SLE.
PMID: 12180729 [PubMed - indexed for MEDLINE]
4: EXS. 1993;64:300-29.
DNA methylation and retrovirus expression.
Bednarik DP.
Child and Adolescent Psychiatry, May 2003 Journal Scan
From
Archives of General Psychiatry
May 2003 (Volume 60, Number 5)
Parent-Child Conflict and the Comorbidity Among Childhood Externalizing Disorders
Burt SA, Krueger RF, McGue M, Iacono W
Archives of General Psychiatry. 2003;60(5):505-513
The authors of this study used data from the Minnesota Twin Family Study (MTFS) to determine genetic and environmental factors associated with the development of externalizing disorders in youth exposed to parent-child conflicts. They entered parent-child conflict, attention-deficit/hyperactivity disorder (ADHD), oppositional defiant disorder (ODD), and conduct disorder (CD) into a multivariate biometrics model to define the role of conflict as part of a shared environmental factor common to ADHD, ODD, and CD.
Average age during the intake visit was 11 years. The cohort included 753 same sex, reared-together monozygotic and dizygotic twins (373 male pairs and 380 female pairs). The authors augmented the sample with twins born between 1989 and 1991 to bring in 55 additional 11-year cohort pairs of twins. The total sample involved 1616 participants. They assessed parent-child relationships as well as lifetime ADHD, ODD, and CD incidence.
Results were as follows. First, parent-child conflict appeared to act as a common vulnerability that increased the risk for multiple childhood disorders. The authors looked at other correlations between psychosocial measures and ADHD, ODD, and CD in male and female children. Conflict was the most highly correlated for all 3 externalizing disorders in both male and females. Low parental involvement, low twin regard for parent, and low parent regard for twin were separate variables associated with this factor. Second, the genes common to ADHD, CD, and ODD may be the same genes that influence conflict. The models showed that the genetic and nonshared environmental disorder-specific paths were all significant. Third, the shared environmental factor that influences conflicts accounted for roughly a quarter of the shared environmental effects common to ADHD, CD, and ODD. Although the study and its design have limitations, the results have important implications. These results include the probability that the source of psychiatric comorbidity may lie in broad latent factors such as parent-child conflict and family environment.
Abstract
--------------------------------------------------------------------------------
Autistic Traits in the General Population: A Twin Study
Constantino JN, Todd RD
Archives of General Psychiatry. 2003;60(5):524-530
The authors of this study sought to examine the prevalence of autistic traits in the general population using a newly established quantitative measure, the Social Responsiveness Scale (SRS). Given the evidence for a broad range of severity of autistic traits, they sought to further define a population at risk for social impairments who may fail to meet full criteria for autistic disorders (Autism, Asperger's, pervasive development disorder-not otherwise specified [PDD-NOS]).
The authors used a population of 788 twin pairs, 7 to 15 years of age, randomly selected from participants in the Missouri Twin Study. The SRS is 65-item parent and/or teacher report questionnaire that inquires about reciprocal social behavior, social use of language, and restricted/stereotypic behaviors or interests, that had previously been shown to distinguish PDDs from other psychiatric conditions and normal controls. The reports included 219 male-male pairs, 319 female-female pairs, and 250 opposite-sex pairs. Mean age was 11 to 12 years. Zygosity was assessed by parent interview. Data were analyzed by use of path models to ascertain sex-specific genetic influences.
Results were plotted separately for boys and girls and showed a continuous distribution. The mean scores were 33% higher in boys vs girls with no significant age effects. Severity of traits for PDD-NOS diagnosis was found in 1.4% of boys and 0.3% of girls. The traits seemed to be moderately to highly heritable, influenced by the same additive genetic factors in both boys and girls. There was no evidence for nonadditive genetic factors. Further analysis revealed no evidence for sex-specific genetic influences. The lower incidence in girl twins suggests a female protection from vulnerability to autistic traits. This protection may arise from environmental factors that may improve development of reciprocal social behaviors in females, who may be more sensitive than boys to environmental influence. Alternatively, girls may have an elevated threshold for phenotypic expression of a trait that is expressed on paternally transmitted X-chromosome. Future genetic linkage studies may further elucidate these mechanisms.
Abstract
--------------------------------------------------------------------------------
--------------------------------------------------------------------------------
Section 2 of 3
Medscape Psychiatry & Mental Health 8(1), 2003. ÿffffa9 2003 Medscape
I will exhibit OCD, repetitive, posting behavior or whatever it takes until our children are medically treated.This psychiatric diagnosis and subsequent studies represent a waste of money that should be be used to test
and biologically treat our sick children.God help our newborns at the pace we are going! Ada
Clinical articles on this topic
Join a Discussion with your colleagues
Advanced Search
Medscape DrugInfo
MEDLINE
About Medscape Privacy & Ethics Terms of Use Help WebMD Health
All material on this website is protected by copyright, Copyright ÿffffa9 1994-2003 by Medscape. This website also contains material copyrighted by 3rd parties. Medscape requires 4.x browsers or better from Netscape or Microsoft.
Warning: New Hepatitis Vaccine Recs Can Devastate Newborn's Health
The newly released 2002 immunization schedule encourages the routine use of hepatitis B vaccine for all infants before hospital discharge to
Safeguard against maternal hepatitis B testing errors and test reporting failures
Protect neonates discharged to households in which hepatitis B chronic carriers other than the mother may reside
Enhance the completion of the childhood immunization series
The annual " Recommended Childhood Immunization Schedule" of the American Academy of Pediatrics (AAP), the Advisory Committee on Immunization Practices (ACIP) of the Centers for Disease Control and Prevention (CDC), and the American Academy of Family Physicians (AAFP) is issued in January of each year.
Pediatrics Vol. 109 No. 1 January 2002, pp. 162
--------------------------------------------------------------------------------
DR. MERCOLA'S COMMENT:
Folks I am outraged. We need to take action now. These recommendations are inexcusable.
There is no possible logical recommendation for this action. All of these arguments are fatally flawed.
If you are new to the site these may sound like lunatic ramblings of some quack, but before you come to that, or a similar conclusion, I challenge you to examine the facts.
The central fact, and the one that helps to explain these insane recommendations, is that the maker of the hepatitis B vaccine, Merck, makes about $1 billion a year from vaccine sales.
A billion dollars a year goes a long way toward influencing public policy.
Who is Behind This?
The group that is pushing this through is called The Hepatitis B coalition. Part of the Immunization Action Coalition, this group was started by a $750,000 grant from the CDC. It is supported by the World Health Organization, World Bank, Rockefeller Foundation and ongoing funding from Smith-Kline, Merck, Aventis and Johnson & Johnson.
Let us not forget that it has been less than three years since the federal government asked the drug companies to take mercury out of this vaccine, and they still haven't complied.
I have seen many dozens of children who were given this vaccine on the first day of life and subsequently developed autism. Others, like Michael Belkin's daughter, weren't as lucky and died immediately after the vaccine.
Michael is a successful Wall Street Financial analyst with his own company, and has testified to Congress on this issue and regularly forwards news health stories to me.
Well in the single dose hepatitis B vials, the drug companies have replaced the mercury with aluminum, which is another potent neurotoxin that has been associated with Alzheimer's. But who knows what damage it will do to the immature central nervous system of a one-day old infant.
The multi dose hepatitis B vials still contain mercury.
Folks, hepatitis B is about as difficult to catch as AIDS. Namely, you nearly always need to have blood or sexual contact of some sort. That is why the main risk factors are IV drug abusers and those who engage in sex with multiple partners.
Is Hepatitis Vaccine Safe?
The Vaccine Adverse Event Reporting System (VAERS) was developed by the government to report vaccine reactions. Many experts believe that only 10% of the adverse reactions are reported though as reporting is not mandated by law.
Even with only 10% of the problems being reported there were nearly 25,000 VAERS hepatitis B reports from July 1990 to October 31, 1998, showing 439 deaths and 9673 serious reactions involving emergency room visits, hospitalization, disablement or death.
The presence of findings such as brain edema in healthy infants who die very soon after receiving hepatitis B vaccine is profoundly disturbing, especially in view of the frequency of neurologic symptoms in the VAERS.
Does this make any sense?
Is Hepatitis B Vaccine Effective in Newborns?
Vaccine derived immunity is thought to be short lived. Between 30-50% of vaccinated individuals lose their antibiodies within 7 years.
Up to 60% of persons who initially respond will lose detectable antibodies within 12 years.. So that means that these vaccines will provide little to no protection to the real risks of acquiring hepatitis B, promiscuous sexual behavior and IV drug abuse.
Does this make any sense?
How Many Children Are Hurt or Helped By Hepatitis B Vaccine?
Hepatitis B is a rare, mainly blood-transmitted disease. In 1996 only 54 cases of the disease were reported to the CDC in the 0-1 age group. There were 3.9 million births that year, so the observed incidence of hepatitis B in the 0-1 age group was just 0.001%. In the Vaccine Adverse Event Reporting System (VAERS), there were 1,080 total reports of adverse reactions from hepatitis B vaccine in 1996 in the 0-1 age group, with 47 deaths reported.
Let us put this in simpler terms. For every child with hepatitis B there were 20 that were reported to have severe complications. Let us also remember that only 10% of the reactions are reported to VAERS, so this means:
Traditional medicine is harming 200 children to protect one from hepatitis B.
Does this make any sense?
How Serious Is a Hepatitis B Infection?
The numbers speak for themselves.
Approximately 50% of patients who contract Hepatitis B develop no symptoms after exposure.
However, the exposure ensures that they will have life-time immunity. An additional 30% develop only flu-like symptoms, and again, this group will acquire life-time immunity.
Of the remaining 20% exposed to Hepatitis B will develop the symptoms of the disease. 95% of this 20% will fully recover, with life-time immunity.
Therefore, less than 5% of people who contract Hepatitis B will become chronic carriers of the infection.
The numbers get even smaller: of that 5%, nearly 75% (or 3.75% of the total exposed) will live with an asymptomatic infection and only 25%, (or only 1.25% of the total number of people exposed) will develop chronic liver disease or liver cancer, 10-30 years after the acute infection. (Hyams, K.C. (1995) Risks of chronicity following acute hepatitis B virus infection: A review. Clin. Infect. Dis. 20, 992-1000.)
Think of that in terms of probability: the possibility of contracting the disease is exceedingly difficult for children and only 1.25% of those that are exposed will actually develop the most serious complication!
This type of a " protecting the needle in the haystack" medicine is absurd at best, dangerous at worst.
Does this make any sense?
How Many Safety Studies Have Been Done On Hepatitis B Vaccine?
None.
A manufacturer's representative was asked in a 1997 Illinois Board of Health hearing to show evidence that the hepatitis B vaccine is safe for a 1-day old infant. The representative stated:
" We have none. Our studies were done on 5- and 10-year-olds."
-- The Congressional Quarterly, August 25, 2000, pg. 647
One would think that these would be mandatory, but they are not. All that is required is to show efficacy, (i.e. that the vaccine stimulates an antibody response after it is give), not safety.
In most other industries the fraud represented here would lead to criminal charges.
Does this make any sense?
What Can You Do?
Please tell every pregnant woman you know who about this issue. They need to know the facts BEFORE they are in the hospital and have time to make an informed objective decision. If they are still convinced their child needs hepatitis B vaccine, beg them to make sure their child does not receive the vaccine as a newborn. Delay the vaccine until they really are at a possible risk, like late adolescence.
I am not asking much here. Only some compassion for the helpless. If you have ever seen the agony of families who are struggling with caring for brain injured children you will know what I mean.
I have shown dozens of times in this newsletter, drugs that are thought to be safe are pulled from the market after they have killed dozens or hundreds of people. I am hopeful that hepatitis B vaccinations in newborns will be stopped. Medical science will have to recognize the truth sooner or later.
Folks, drug deaths pale in comparison to the devastation in lost lives that is resulting from implementation of this hepatitis B recommendation.
You can play a large role here. Most of all us did not have a chance to make a difference in the 9/11 tragedy, but nearly everyone of us can help protect the precious brain cells of a newborn.
Don't Delay.
Contact every pregnant woman you know immediately. Save a life.
God Bless you in your efforts to protect the future of our civilization.
--------------------------------------------------------------------------------
Note To Physicians:
I am a member of the Association of American Physicians and Surgeons (AAPS). This is a group of over 10,000 US medical doctors, and most of us have reached the conclusion that the head of the organization, Dr. Jane Orient, has about this issue.
To the extent that the physician simply complies without making an independent evaluation of the appropriateness of the vaccine for each patient, he is abdicating his responsibility under the Oath of Hippocrates to:
" prescribe regimen for the good of my patients according to my ability and my judgment and never do harm to anyone."
My thanks to Dr. Sherri Tenpenny for her editing assistance on this important topic.
--------------------------------------------------------------------------------
Related Articles:
Beware the FDA Approves Combined Hepatitis Vaccine
The Fallacy of the Hepatitis A Vaccine
Hepatitis B Vaccinations: Michael Belkin Testimony to Congress Tuesday May 18, 1999
Hepatitis B Vaccine
Mercury in Vaccines
Autism 'Linked to Mercury Vaccine'
Follow the Money on Vaccines
--------------------------------------------------------------------------------
Return to Table of Contents #292
Print this Page E-mail to a Friend
Privacy/Security Current Newsletter Contact Info
ÿffffa9Copyright 2003 Dr. Joseph Mercola. All Rights Reserved. This content may be copied in full, with copyright, contact, creation and information intact, without specific permission, when used only in a not-for-profit format. If any other use is desired, permission in writing from Dr. Mercola is required.
Disclaimer - The entire contents of this website are based upon the opinions of Dr. Mercola. They are not intended to replace a one-on-one relationship with a qualified health care professional and they are not intended as medical advice. They are intended as a sharing of knowledge and information from the research and experience of Dr. Mercola and his community. Dr. Mercola encourages you to make your own health care decisions based upon your research and in partnership with a qualified health care professional.
--------------------------------------------------------------------------------
--------------------------------------------------------------------------------
Vaccines fueling autism epidemic?
Report: U.S. infants exposed to mercury beyond EPA, FDA limits
--------------------------------------------------------------------------------
Posted: June 9, 2003
5:00 p.m. Eastern
Editor's note: WorldNetDaily is pleased to have a content-sharing agreement with Insight magazine, the bold Washington publication not afraid to ruffle establishment feathers. Subscribe to Insight at WorldNetDaily's online store and save 71 percent off the cover price.
By Kelly Patricia O Meara
ÿffffa9 2003 News World Communications Inc.
The mother of an autistic child wonders aloud when health officials will wake up to the epidemic that has claimed not only her son but hundreds of thousands of other children in the United States, with no end in sight. She muses, " Maybe someday this will be as important as SARS and we'll get the same attention. God knows we need it."
Autism is a severely incapacitating developmental disability for which there is no known cure. According to a recently released report by the California Department of Developmental Services, or DDS, entitled Autistic Spectrum Disorders, Changes in the California Caseload: 1999-2002, the rate of children diagnosed with full-syndrome autism in the Golden State between 1999 and 2002 nearly doubled from 10,360 to 20,377. The report further revealed that " between Dec. 31, 1987, and Dec. 31, 2002, the population of persons with full-syndrome autism has increased by 634 percent." That is a doubling of autism cases every four years, and the staggering increases are not limited to California.
Infants are being inoculated with vaccines containing toxic ingredients that can be harmful ÿffff97 or fatal.
According to data provided by the U.S. Department of Education, the increased autism rate in California is in line with the increases other states are experiencing. For example, in 1992 Ohio reported 22 cases. A decade later the number had increased by 13,895 percent to 3,057. In Illinois the rate of autism cases climbed from just five in 1992 to 3,802 - an increase of 76,040 percent.
Mississippi, New Hampshire and the District of Columbia reported no cases of autism in 1992, but by 2002 the number of cases reported were 461, 404 and 144, respectively.
Only Puerto Rico can claim to have an increase of less than 100 percent, with the remaining states reporting increases of at least 500 percent during the same period.
Although once considered rare, during the last two decades the chance of a child being diagnosed with autism has skyrocketed from one in 10,000 to one in 150. In California, full-syndrome autism now is the No. 1 disability among children and more prevalent than childhood cancer, diabetes and Down's syndrome. It is estimated that within the next four years autism cases in the Golden State will exceed the total number of cases of both cerebral palsy and epilepsy. To get a better idea of how quickly the epidemic is spreading one need only consider that in 1987 there were 2,778 persons with autism in California. By 2002 the number had increased to 20,377, and in 2002 3,575 new cases had been added to the rolls, far exceeding the total number of cases in the state 15 years earlier.
For years there has been a debate about the cause or causes of autism, but the vast majority of finger-pointing has been directed at childhood vaccines as the culprit. And considering what is put into the vaccines injected into hours-old infants, it is easy to understand why they are at the top of the list of suspects: formaldehyde (used in embalming), thimerosal (nearly 50 percent mercury), aluminum phosphate (toxic and carcinogenic), antibiotics, phenols (corrosive to skin and toxic), aluminum salts (corrosive to tissue and neurotoxic), methanol (toxic), isopropyl (toxic), 2-pheoxyethanol (toxic), live viruses and a host of unknown components considered off-limits as trade secrets. These are just part of the vaccine mixture.
For those who believe there are elements in vaccines that may be responsible for the increased number of autism cases and other neurological disorders, thimerosal currently is at the top of the list of possible culprits being investigated.
Despite official insistence that the evidence linking injected thimerosal to autism is inconclusive, the data suggest otherwise. In 1999 the National Academy of Sciences Institute of Medicine, or IOM, must have thought there was something seriously wrong when it supported removal of thimerosal from vaccines, stating that it was " a prudent measure in support of the public goal to reduce mercury exposure of infants and children as much as possible." The IOM further urged that " full consideration be given to removing thimerosal from any biological product to which infants, children and pregnant women are exposed."
A recently published study in the Journal of American Physicians and Surgeons by Mark Geier, M.D., Ph.D., and president of the Genetic Centers of America and his son, David Geier, president of Medcon Inc. and a consultant on vaccine cases, was titled " Thimerosal in Childhood Vaccines, Neurodevelopment Disorders and Heart Disease in the United States." It presents strong epidemiological evidence for a link between neurodevelopmental disorders and mercury exposure from thimerosal-containing childhood vaccines.
Specifically, the authors evaluated the doses of mercury that children received as part of their immunization schedule, then compared these doses with federal safety guidelines. Furthermore, to compare the effects of thimerosal in vaccine recipients, the incident rates of neurodevelopmental disorders and heart disease reported to the government's Vaccine Adverse Events Reporting System were analyzed. The results were dramatic. The report revealed that " U.S. infants are exposed to mercury levels from their childhood-immunization schedule that far exceed the EPA [Environmental Protection Agency] and FDA [Food and Drug Administration]-established maximum permissible levels for the daily oral ingestion of methyl mercury."
The authors concluded that " in light of voluminous literature supporting the biologic mechanisms for mercury-induced adverse reactions, the presence of amounts of mercury in thimerosal-containing childhood vaccines exceeding federal safety guidelines for the oral ingestion of mercury and previous epidemiological studies showing adverse reactions to such vaccines, a causal relationship between thimerosal-containing childhood vaccines and neurodevelopment disorders and heart disease appears to be confirmed."
It is no secret among government and health officials that mercury is toxic and causes serious adverse reactions. In July 1999 the American Academy of Pediatrics and the U.S. Public Health Service issued a joint statement calling for the removal of thimerosal from vaccines. Five years after the joint statement, however, it still is difficult for parents and physicians to be sure that the pharmaceutical companies have indeed removed the toxic substance from their vaccines.
According to Mark Geier, " The 2003 Physicians' Desk Reference, or PDR, still shows childhood vaccines containing thimerosal, including diphtheria, tetanus and acellular pertussis. DTaP, manufactured by Aventis Pasteur, contains 25ÿffffb5g [25 micrograms] of mercury, Hemophilus influenzae b (Hib) vaccine manufactured by Wyeth contains 25ÿffffb5g of mercury and pediatric Hepatitis B vaccine, manufactured by Merck, contains 12.5ÿffffb5g of mercury."
Geier continues, " In addition, the influenza vaccine that is recommended for an increasing segment of the pediatric population in the U.S. also contains 25ÿffffb5g of mercury. Assuming that the labeling is correct, it is possible that children in the U.S. in 2003 may be exposed to levels of mercury from thimerosal contained in childhood vaccines that are at higher levels than at any time in the past. Possible total childhood mercury in 2003 is more than 300ÿffffb5g."
Whether the " labeling is correct" is the question du jour. According to Len Lavenda, a spokesman for Aventis Pasteur, the maker of DTaP, " Aventis only sells the DTaP vaccine in the preservative-free formulation. The PDR references both the single and multidose. However, when we received the license for the preservative-free we ceased sales of the multidose vial. For some reason, the package insert takes much longer to revise than one would expect. I believe it is at the FDA waiting for approval, but the fact is we do not sell or market that product. In March 2001 we stopped all sales of that product in the preservative formulation. We did not recall the product at that time because it was our belief that if we did children may go unimmunized. It's been two years since anyone has been able to purchase the preservative formulation from us."
Lavenda continues: " The package insert talks about both the single and multidose vials and it says that the single-dose vial is preservative-free, and that is all that is sold. The PDR is outdated, but parents don't have to worry about their children being administered 25ÿffffb5g of thimerosal. It just takes time to get the paperwork caught up. The current package insert does not accurately reflect what is being marketed."
Geier is astounded by Lavenda's admission. " If this is true, they should be in jail. They can't have an insert on a drug that is totally wrong. It is against all regulations. If I'm a doctor and I'm giving you a shot and the insert says such and such is in the shot, it had better be in it. If doctors can't rely on the instructions that come with what we're injecting then all bets are off. This is a far worse admission than admitting that thimerosal is still in the vaccine. There are at least 15 laws that say the insert has to match what is in the product. This is absolutely horrendous. In my entire career in medicine I have never heard of a drug company claiming that what's in the insert and the accompanying product don't match. This is total mislabeling and fraud by their own admission. Legally they should be forced to close down because our clinical decisions are based on their labeling."
Assuming that the package inserts are correct, Geier tells Insight, " The EPA limit is 0.1 micrograms of mercury per kilogram body weight per day. It doesn't take a genius to do the calculations when on their day of birth children are given the hepatitis B vaccine, which is 12.5 micrograms of mercury. The average newborn weighs between 6 and 7 pounds, so they would be allowed 0.3 micrograms of mercury ÿffff96 but in this one shot they are getting 12.5 micrograms. That's 39 times more than allowed by law. And it gets worse when you consider that children are getting multiple vaccinations at 2 months. And this limit is for oral ingestion and not injection, which is much worse."
Rhonda Smith, a spokeswoman for the federal Centers for Disease Control and Prevention, tells Insight that, except for mere traces, thimerosal has been removed. " All routinely recommended licensed vaccines," says Smith, " that are currently being manufactured for children in the U.S., except influenza, contain no thimerosal or only trace amounts - a concentration of less than 0.0002 percent." But according to the 2003 immunization schedule and the package inserts, there appear to be a number of childhood vaccines that still contain mercury, including those for tetanus and diphtheria.
This scenario becomes even more bizarre when one further considers that thimerosal is not a necessary component in vaccines. It first was introduced by pharmaceutical giant Eli Lilly and Co. in the 1930s and is added to vaccines only as a preservative ÿffff96 the theory being that multiple doses are taken from the same bottle and that thimerosal will protect against contamination. However, according to Geier, " the solution to any such problem is to make vaccines available in a single dose, which will cost the pharmaceuticals about one penny more. What is interesting is that if you look up the mumps, measles, rubella [MMR] vaccines in the PDR you'll see that they do not contain thimerosal because it would kill the live virus. The MMR is available in multidose packaging and, yet, there is no preservative ÿffff96 nothing. What they did was put a label on it that says 'This product does not contain preservatives. Handle with care.' It's that simple."
Geier insists, " I'm pro-vaccines, but the bottom line is that our kids are getting massive amounts of mercury. Mercury has been withdrawn from everything, including animal vaccines, yet we keep injecting it into our children. Everyone should absolutely refuse to take a vaccine shot that has thimerosal in it, and they should insist on reading the vaccine package insert. Our data showed that the more mercury children received in their childhood vaccines the more neurodevelopment disorders there are. We've looked at this every possible way and every time there's massive evidence to support it."
So, if everyone acknowledges the toxicity of mercury and top U.S. health officials have called for its removal, why is thimerosal still in vaccines?
" Maybe," concludes Geier, " the mercury isn't being taken out all at once because if the pharmaceutical companies did that you would see an unbelievable change in the rate of autism and there would be massive lawsuits. If you look at the graphs now they go up and up. If you stop the thimerosal all at once you'd see the numbers fall dramatically."
Rep. Dan Burton, R-Ind., a longtime advocate for victims of autism, has a grandson who became autistic after receiving nine vaccines in one day. Burton recently sent his second request in as many years to the White House asking for a conference of scientists, researchers and parents to look into the causes of autism.
The Indiana lawmaker tells Insight, " There is no doubt in my mind that the mercury in vaccines is a major contributing factor to a growing number of neurological disorders among children, but in particular autism."
Burton explains that " thimerosal is a toxic substance ÿffff96 mercury ÿffff96 and should not be put in close proximity of people, should not be injected into people, especially children who have a newly formed immune system that may not be able to handle it. To my knowledge there never have been long-term tests on thimerosal and we never should have used mercury in vaccines, period. Now what we've got is an epidemic that is absolutely out of control."
The Indiana congressman continues, " One reason this isn't getting the attention it needs is that the Food and Drug Administration has very close ties to the pharmaceutical companies, as does the Department of Health and Human Services [HHS] and the Centers for Disease Control. I've said in the past that in some cases it appears that it's a revolving door and people leave government health agencies and go to work for the pharmaceuticals, which I think have undue influence on our health agencies. Of course, they may not want to look at this because there's a possibility that large claims would be filed and the pharmaceutical companies would have to cough up the money to take care of these kids who have been damaged."
Burton means business. He insists, " The FDA, CDC and HHS should put out in a very public way the dangers of mercury, but as soon as they do it will amount to an admission that their mercury is causing these problems. So the reports that come out of the FDA, CDC and HHS use ambiguous terms. Well, if they're not sure, and there's the remotest possibility that mercury in vaccines could cause autism, they ought to get thimerosal off the market. Too many kids are being ruined for life because of this stuff."
Barbara Loe Fisher is founder of the National Vaccine Information Center, a charitable organization dedicated to the prevention of vaccine injuries and deaths through public education. Fisher tells Insight, " There are many things in vaccines that could be causing these disorders, and thimerosal is only part of the problem. In the last 20 years, we've gone from giving children 23 doses of seven vaccines to 38 doses of 12 vaccines. I think the mercury is part of it for some kids, though I'm not sure it's the answer for all." But this is a no-brainer, says Fisher. " Mercury shouldn't be in vaccines. They've taken it out of everything else so why not the vaccines? The one thing that people really need to look at is the dramatic rise in chronic disease and disabilities in our kids in just the last two decades. You have to admit that there is something occurring that a growing number of children cannot get through without being immune-system and brain-system damaged. And what is the one thing that we expose every child to? Those vaccines."
Fisher concludes, " I've always argued that public health is not measured only by an absence of infectious disease. It also is measured by the absence of chronic disease. By that score we get a big fat 'F.' So we don't have measles and mumps, but look what we have now. It's just really simple: Take the mercury out and let's see what happens."
Even so, based on the Aventis admission that the package insert does not reflect what is in the vaccine, it will be difficult to know when, if ever, the thimerosal actually has been removed. This skews the data about the relationship between thimerosal and autism. More important, it means parents cannot be sure the vaccinations their children receive are free of mercury.
Neither the Wyeth nor Merck pharmaceutical companies, nor HHS or FDA, returned Insight's calls about this matter.
--------------------------------------------------------------------------------
Subscribe to Insight
Kelly Patricia O'Meara is an investigative reporter for Insight magazine.
--------------------------------------------------------------------------------
--------------------------------------------------------------------------------
Maybe someday this will be as important as SARS and we'll get the same attention. God knows we need it.
-- Mother of autistic child
I'm pro-vaccines, but the bottom line is that our kids are getting massive amounts of mercury. Mercury has been withdrawn from everything, including animal vaccines, yet we keep injecting it into our children.
-- Dr. Mark Geier, president of the Genetic Centers of America
--------------------------------------------------------------------------------
1: Med Hypotheses. 2003 May;60(5):650-3. Related Articles, Links
Does the MMR vaccine and secretin or its receptor share an antigenic epitope?
Mehta BK, Munir KM.
Memorial University of Newfoundland, Newfoundland, Canada
In a subgroup of children with autism-spectrum like conditions symptoms seem to appear as a 'regression' (in normal development). It has been postulated that the onset of such autistic symptoms may involve an autoimmune response against the central nervous system and that the antigenic determinant could possibly be gastrointestinal in origin. It has been suggested that the presence of the measles virus and 'autistic enterocolitis' demonstrates the possibility that the MMR triple vaccine may be mediating the inflammation with possible production of antibodies against the virus containing vaccine. Such an antibody may share antigenic determinant to molecules found in the gut. We propose that this may be secretin or its receptor, found in the gut as well as in the central nervous system. The antibody response to the gut may also conceivably occur in the brain at a critical time in development. The modulation of development by secretin may be a static event possibly occurring at a specific time in early childhood development and if it involves an autoimmune response then a disruption in development may result. These hypothesized events can only occur if the MMR vaccine shares antigenic determinants that resemble secretin or any of its receptor types and remains to be studied.
PMID: 12710897 [PubMed - in process]
--------------------------------------------------------------------------------
Summary Brief Abstract Citation ASN.1 MEDLINE XML UI List LinkOut Related Articles Domain Links 3D Domain Links GEO DataSet Links Genome Links GEO Links Nucleotide Links OMIM Links PMC Links Cited in PMC PopSet Links Protein Links SNP Links Structure Links Show: 5 10 20 50 100 200 500 Sort Author Journal Pub Date Text File Clipboard E-mail Order
: Gut. 2002 Dec;51(6):816-7. Related Articles, Links
Effect of Pentavac and measles-mumps-rubella (MMR) vaccination on the intestine.
Thjodleifsson B, Davidsdottir K, Agnarsson U, Sigthorsson G, Kjeld M, Bjarnason I.
Department of Medicine, University Hospital, Hringbraut, Reykjavik, Iceland.
BACKGROUND: The safety of infant vaccination has been questioned in recent years. In particular it has been suggested that the measles, mumps, and rubella (MMR) vaccination leads to brain damage manifesting as autism consequent to the development of an " enterocolitis" in the immediate post-vaccination period. AIM: To assess if MMR vaccination is associated with subclinical intestinal inflammation, which is central to the autistic " enterocolitis" theory. METHODS: We studied 109/58 infants, before and two and four weeks after immunisation with Pentavac and MMR vaccines, for the presence of intestinal inflammation (faecal calprotectin). RESULTS: Neither vaccination was associated with any significant increase in faecal calprotectin concentrations. CONCLUSIONS: The failure of the MMR vaccination to cause an intestinal inflammatory response provides evidence against the proposed gut-brain interaction that is central to the autistic " enterocolitis" hypothesis.
PMID: 12427783 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
Summary Brief Abstract Citation ASN.1 MEDLINE XML UI List LinkOut Related Articles Domain Links 3D Domain Links GEO DataSet Links Genome Links GEO Links Nucleotide Links OMIM Links PMC Links Cited in PMC PopSet Links Protein Links SNP Links Structure Links Show: 5 10 20 50 100 200 500 Sort Author Journal Pub Date Text File Clipboard E-mail Order
Write to the Help Desk
NCBI | NLM | NIH
Department of Health & Human Services
Freedom of Information Act | Disclaimer
Jun 12 2003 10:19:17
Dr. Deth's (Deeth's) finding that thimerosal shuts off
methionine synthase as effectively as does ethanol and does so at levels
Pichichero et al described in well babies!
AND
2: Neuropediatrics 2000 Dec;31(6):314-7
Comment in: Neuropediatrics. 2001 Dec;32(6):335-6.
Hydrocephalus internus in two patients with 5,10-methylenetetrahydrofolate
reductase deficiency.
Baethmann M, Wendel U, Hoffmann GF, Gohlich-Ratmann G, Kleinlein B, Seiffert P,
Blom H, Voit T.
Department of Pediatrics, University Hospital, Essen, Germany.
Hydrocephalus internus (HCI) of all four ventricles in association with early
neurological abnormalities is described as the presenting symptom in two
patients with 5,10-methylenetetrahydrofolate reductase (MTHFR) deficiency.
Decreased activity of MTHFR leads to reduction of 5-methyltetrahydrofolate, the
main methyl donor for methionine synthesis necessary for synthesis of
S-adenosyl-methionine (SAM). Demyelination in MTHFR deficiency has been
attributed to low SAM levels in the brain. The biochemical hallmarks of the
disorder are hyperhomocystinemia, homocystinuria and low levels of plasma
methionine. Hydrocephalus internus requiring neurosurgical intervention has to
our knowledge not been reported as a presenting feature of homocystinuria due to
deficiency of MTHFR so far. The surprising finding of HCI of all four ventricles
in MTHFR deficiency must be kept in mind when evaluating patients with
hydrocephalus of unknown origin.
PMID: 11508552 [PubMed - indexed for MEDLINE]
3: AJNR Am J Neuroradiol 2001 Mar;22(3):554-63
Early-onset combined methylmalonic aciduria and homocystinuria: neuroradiologic
findings.
Rossi A, Cerone R, Biancheri R, Gatti R, Schiaffino MC, Fonda C, Zammarchi E,
Tortori-Donati P.
Department of Pediatric Neuroradiology , G. Gaslini Children's Research
Hospital, Genoa, Italy.
BACKGROUND AND PURPOSE: Combined methylmalonic aciduria and homocystinuria
(MMA-HC) is caused by impaired hepatic conversion of dietary cobalamin to
methylcobalamin and adenosylcobalamin, resulting in decreased activity of
methylmalonyl-CoA mutase and methionine synthase. Patients with the early-onset
variety present within 12 months of age with severe neurologic, hematologic, and
gastrointestinal abnormalities. We describe the neuroradiologic features of
early-onset MMA-HC and discuss related pathophysiological mechanisms. METHODS:
Twelve infants with hypotonia, failure to thrive, poor feeding, and hematologic
abnormalities were diagnosed with MMA-HC on the basis of a typical plasmatic and
urinary metabolic profile and enzyme activity in fibroblastic cultures.
Complementation studies were performed in two cases, and yielded a CblC result.
MR imaging was performed at presentation in four cases and later in the others.
All patients showed prompt biochemical improvement with intramuscular
hydroxocobalamin administration, and most had moderate neurologic improvement.
RESULTS: Diffuse supratentorial white matter edema and dysmyelination was the
typical MR picture at presentation, whereas white matter bulk loss characterized
later stages of the disease. Nucleocapsular areas of gliosis were an additional
finding in one case. One patient had tetraventricular hydrocephalus at
presentation. CONCLUSION: White matter damage is probably caused by reduced
methyl group availability and nonphysiological fatty acids toxicity, whereas
focal gliosis results from homocysteine-induced toxicity to the endothelium.
Hydrocephalus may result from diffuse intracranial extracerebral arterial
stiffness, known as reduced arterial pulsation hydrocephalus. MR imaging
features at presentation and at follow-up are nonspecific.
PMID: 11237984 [PubMed - indexed for MEDLINE]
4: Eur J Pediatr 2000 Oct;159 Suppl 2:S109-13
The neurochemistry of phenylketonuria.
Surtees R, Blau N.
Institute of Child Health (UCLMS), London, UK. r.surtees@ich.ucl.ac.uk
The mechanisms by which deficiency of hepatic phenylalanine hydroxylase causes
central nervous system disease are reviewed. The neurological disease appears to
be secondary to increased concentrations of phenylalanine and a decrease in the
concentrations of other large neutral amino acids, especially methionine and
tyrosine, within the central nervous system. This causes a deficiency of the
neurotransmitter dopamine, reduced protein synthesis and demyelination. Similar
mechanisms appear to be operating when blood phenylalanine concentrations are in
the range expected for early continuously treated phenylketonuria. CONCLUSION:
The severe brain disease found in phenylketonuria is caused by a raised blood
phenylalanine content which increases the brain free phenylalanine and decreases
the concentration of other large neutral amino acids. Brain protein synthesis is
decreased, myelin turnover is increased and there are abnormalities in amine
neurotransmitter systems.
Publication Types:
Review
Review, Tutorial
PMID: 11043156 [PubMed - indexed for MEDLINE]
5: http://www.journals.uchicago.edu/AJHG/journal/issues/v66n2/990553/990553.web.pdf
Am J Hum Genet 2000 Feb;66(2):347-55
Methionine adenosyltransferase I/III deficiency: novel mutations and clinical
variations.
Chamberlin ME, Ubagai T, Mudd SH, Thomas J, Pao VY, Nguyen TK, Levy HL, Greene
C, Freehauf C, Chou JY.
Heritable Disorders Branch, National Institute of Child Health and Human
Development (NICHD), National Institutes of Health, Bethesda, MD 20892, USA.
Methionine adenosyltransferase (MAT) I/III deficiency, caused by mutations in
the MAT1A gene, is characterized by persistent hypermethioninemia without
elevated homocysteine or tyrosine. Clinical manifestations are variable and
poorly understood, although a number of individuals with homozygous null
mutations in MAT1A have neurological problems, including brain demyelination. We
analyzed MAT1A in seven hypermethioninemic individuals, to provide insight into
the relationship between genotype and phenotype. We identified six novel
mutations and demonstrated that mutations resulting in high plasma methionines
may signal clinical difficulties. Two patients-a compound heterozygote for
truncating and severely inactivating missense mutations and a homozygote for an
aberrant splicing MAT1A mutation-have plasma methionine in the 1,226-1,870
microM range (normal 5-35 microM) and manifest abnormalities of the brain gray
matter or signs of brain demyelination. Another compound heterozygote for
truncating and inactivating missense mutations has 770-1,240 microM plasma
methionine and mild cognitive impairment. Four individuals carrying either two
inactivating missense mutations or the single-allelic R264H mutation have
105-467 microM plasma methionine and are clinically unaffected. Our data
underscore the necessity of further studies to firmly establish the relationship
between genotypes in MAT I/III deficiency and clinical phenotypes, to elucidate
the molecular bases of variability in manifestations of MAT1A mutations.
PMID: 10677294 [PubMed - indexed for MEDLINE]
6: Pharmacol Ther 2000 Jan;85(1):1-9
Molecular genetics of hepatic methionine adenosyltransferase deficiency.
Chou JY.
Heritable Disorders Branch, National Institute of Child Health and Human
Development, National Institutes of Health, Bethesda, MD 20892-1830, USA.
chou@helix.nih.gov
Hepatic methionine adenosyltransferase (MAT) deficiency is caused by mutations
in the human MAT1A gene that abolish or reduce hepatic MAT activity that
catalyzes the synthesis of S-adenosylmethionine from methionine and ATP. This
genetic disorder is characterized by isolated persistent hypermethioninemia in
the absence of cystathionine beta-synthase deficiency, tyrosinemia, or liver
disease. Depending on the nature of the genetic defect, hepatic MAT deficiency
can be transmitted either as an autosomal recessive or dominant trait. Genetic
analyses have revealed that mutations identified in the MAT1A gene only
partially inactivate enzymatic activity, which is consistent with the fact that
most hepatic MAT-deficient individuals are clinically well. Two
hypermethioninemic individuals with null MAT1A mutations have developed
neurological problems, including brain demyelination, although this correlation
is by no means absolute. Presently, it is recommended that a DNA-based diagnosis
should be performed for isolated hypermethioninemic individuals with unusually
high plasma methionine levels to assess if therapy aimed at the prevention of
neurological manifestations is warranted.
Publication Types:
Review
Review, Tutorial
PMID: 10674710 [PubMed - indexed for MEDLINE]
7: Eur J Pediatr 1998 Apr;157 Suppl 2:S122-6
Relevance of vitamins, homocysteine and other metabolites in neuropsychiatric
disorders.
Allen RH, Stabler SP, Lindenbaum J.
Department of Medicine, University of Colorado Health Sciences Center, Denver
80220, USA.
Indistinguishable hematologic abnormalities are seen in most patients with
cobalamin (Cbl, vitamin B12) or folate deficiency. Approximately one third of
Cbl-deficient patients develop a wide variety of non-focal neuropsychiatric
abnormalities that are not seen in folate deficiency. Serum levels of
homocysteine are elevated to a similar degree in Cbl-deficient patients with and
without neuropsychiatric abnormalities, and in folate-deficient patients. Serum
levels of eight other metabolites including methylmalonic acid also fail to
elucidate the biochemical basis for the neuropsychiatric abnormalities. Levels
of homocysteine and methylmalonic acid are often only slightly elevated in
Cbl-deficient patients who have significant neuropsychiatric defects. Moderate
elevations of homocysteine and methylmalonic acid occur in 20%-30% of various
elderly populations (mean age 80) and may play a role in the similar
neuropsychiatric abnormalities that occur increasingly with aging. Taken
together, these studies suggest that an important unknown Cbl-dependent enzyme,
metabolic abnormality, environmental factor, or genetic factor may play a major
role in the pathophysiology of the neuropsychiatric abnormalities caused by Cbl
deficiency.
Publication Types:
Review
Review, Tutorial
PMID: 9587039 [PubMed - indexed for MEDLINE]
8: Eur J Pediatr 1998 Apr;157 Suppl 2:S118-21
Demyelination and inborn errors of the single carbon transfer pathway.
Surtees R.
Institute of Child Health (UCLMS), London, UK.
Inborn errors of the single-carbon transfer pathway are rare disorders of folate
and cobalamin metabolism. They may be complicated by demyelination resembling
subacute combined degeneration of the cord and brain. The study of CSF
metabolites in children with serial errors affecting the single-carbon transfer
pathway has suggested that S-adenosylmethionine deficiency is a cause of the
demyelination. This deficiency is corrected by treatment that causes clinical
improvement and remyelination. Some treatments can only have an indirect effect
on the brain and this is discussed with other evidence that the liver may
produce factors that are necessary for the maintenance of central myelin.
Publication Types:
Review
Review, Tutorial
PMID: 9587038 [PubMed - indexed for MEDLINE]
9: Nutr Rev 1996 Dec;54(12):382-90
Folate, vitamin B12, and neuropsychiatric disorders.
Bottiglieri T.
Kimberly H. Courtwright and Joseph W. Summers Institute of Metabolic Disease,
Baylor University Medical Center, Dallas, Texas, USA.
Folate and vitamin B12 are required both in the methylation of homocysteine to
methionine and in the synthesis of S-adenosylmethionine. S-adenosylmethionine is
involved in numerous methylation reactions involving proteins, phospholipids,
DNA, and neurotransmitter metabolism. Both folate and vitamin B12 deficiency may
cause similar neurologic and psychiatric disturbances including depression,
dementia, and a demyelinating myelopathy. A current theory proposes that a
defect in methylation processes is central to the biochemical basis of the
neuropsychiatry of these vitamin deficiencies. Folate deficiency may
specifically affect central monoamine metabolism and aggravate depressive
disorders. In addition, the neurotoxic effects of homocysteine may also play a
role in the neurologic and psychiatric disturbances that are associated with
folate and vitamin B12 deficiency.
Publication Types:
Review
Review, Tutorial
PMID: 9155210 [PubMed - indexed for MEDLINE]
10: http://www.jci.org/cgi/reprint/98/4/1021.pdf
J Clin Invest 1996 Aug 15;98(4):1021-7
Demyelination of the brain is associated with methionine adenosyltransferase
I/III deficiency.
Chamberlin ME, Ubagai T, Mudd SH, Wilson WG, Leonard JV, Chou JY.
Heritable Disorders Branch, National Institute of Child Health and Human
Development, National Institutes of Health, Bethesda, Maryland 20892, USA.
Individuals deficient in hepatic methionine adenosyltransferase (MAT) activity
(MAT I/III deficiency) have been demonstrated to contain mutations in the gene
(MATA1) that encodes the major hepatic forms, MAT I and III. MAT I/III
deficiency is characterized by isolated persistent hypermethioninemia and, in
some cases, unusual breath odor. Most individuals with isolated
hypermethioninemia have been free of major clinical difficulties. Therefore a
definitive diagnosis of MAT I/III deficiency, which requires hepatic biopsy, is
not routinely made. However, two individuals with isolated hypermethioninemia
have developed abnormal neurological problems, including brain demyelination,
suggesting that MAT I/III deficiency can be deleterious. In the present study we
have examined the MATA1 gene of eight hypermethioninemic individuals, including
the two with demyelination of the brain. Mutations that abolish or reduce the
MAT activity were detected in the MATA1 gene of all eight individuals. Both
patients with demyelination are homozygous for mutations that alter the reading
frame of the encoded protein such that the predicted MATalpha1 subunits are
truncated and enzymatically inactive. The product of MAT, S-adenosylmethionine
(AdoMet), is the major methyl donor for a large number of biologically important
compounds including the two major myelin phospholipids, phosphatidylcholine and
sphingomyelin. Both are synthesized primarily in the liver. Our findings
demonstrate that isolated persistent hypermethioninemia is a marker of MAT I/III
deficiency, and that complete lack of MAT I/III activity can lead to
neurological abnormalities. Therefore, a DNA-based diagnosis should be performed
for individuals with isolated hypermethioninemia to assess if therapy aimed at
the prevention of neurological manifestations is warranted.
PMID: 8770875 [PubMed - indexed for MEDLINE]
11: Drugs 1994 Aug;48(2):137-52
The clinical potential of ademetionine (S-adenosylmethionine) in neurological
disorders.
Bottiglieri T, Hyland K, Reynolds EH.
Metabolic Disease Center, Baylor Research Institute, Dallas, Texas.
This review focuses on the biochemical and clinical aspects of methylation in
neuropsychiatric disorders and the clinical potential of their treatment with
ademetionine (S-adenosylmethionine; SAMe). SAMe is required in numerous
transmethylation reactions involving nucleic acids, proteins, phospholipids,
amines and other neurotransmitters. The synthesis of SAMe is intimately linked
with folate and vitamin B12 (cyanocobalamin) metabolism, and deficiencies of
both these vitamins have been found to reduce CNS SAMe concentrations. Both
folate and vitamin B12 deficiency may cause similar neurological and psychiatric
disturbances including depression, dementia, myelopathy and peripheral
neuropathy. SAMe has a variety of pharmacological effects in the CNS, especially
on monoamine neurotransmitter metabolism and receptor systems. SAMe has
antidepressant properties, and preliminary studies indicate that it may improve
cognitive function in patients with dementia. Treatment with methyl donors
(betaine, methionine and SAMe) is associated with remyelination in patients with
inborn errors of folate and C-1 (one-carbon) metabolism. These studies support a
current theory that impaired methylation may occur by different mechanisms in
several neurological and psychiatric disorders.
Publication Types:
Review
Review, Academic
PMID: 7527320 [PubMed - indexed for MEDLINE]
12: Annu Rev Nutr 1992;12:59-79
Cobalamin deficiency and the pathogenesis of nervous system disease.
Metz J.
Department of Hematology, South African Institute for Medical Research,
Johannesburg.
Neuropathy commonly complicates cobalamin (Cb1) deficiency in humans, monkeys,
fruit bats, and pigs. The neuropathy is characterized by demyelination of the
posterolateral columns of the spinal cord (subacute combined degeneration). The
lesion was thought to arise primarily from impairment of the
adenosylcobalamin-dependent methylmalonyl CoA mutase reaction, leading to the
formation of abnormal odd-chain and branched-chain fatty acids and their
incorporation into myelin with resultant demyelination. Data from recently
developed animal models of the Cb1 neuropathy induced by exposure to nitrous
oxide do not substantiate this hypothesis, but rather identify impairment of the
methylcobalamin-dependent methionine synthetase reaction as the more important
basic defect. The key evidence for this hypothesis is the ability of methionine
to delay the onset of Cb1 neuropathy in experimental Cb1 deficiency. In the
Cb1-deficient pig, adenosylhomocysteine accumulates in neural tissue, presumably
owing to the inability to recycle homocysteine via the defective methionine
synthetase reaction. Accumulation of adenosylhomocysteine results in a fall in
the adenosylmethionine:adenosylhomocysteine methylation ratio, and this change
is believed to cause defective methylation and demyelination in the nervous
system. However, in the Cb1 neuropathy in the fruit bat, adenosylhomocysteine
does not accumulate in the nervous system, the methylation ratio does not
change, and no defect can be demonstrated in the methylation of myelin lipid or
basic protein. Although a central role for methionine in the pathogenesis of the
Cb1 neuropathy has been established, defective methylation attendant upon
impairment of the methionine synthetase reaction may not be the universal defect
underlying the Cb1 neuropathy. This would suggest that the methionine effect
could be mediated via its role in formate metabolism or polyamine synthesis, or
by some as yet unidentified pathway.
Publication Types:
Review
Review, Tutorial
PMID: 1354465 [PubMed - indexed for MEDLINE]
13: Lancet 1991 Dec 21-28;338(8782-8783):1550-4
Association of demyelination with deficiency of cerebrospinal-fluid
S-adenosylmethionine in inborn errors of methyl-transfer pathway.
Surtees R, Leonard J, Austin S.
Department of Child Health, Institute of Child Health, London, UK.
Long-term deficiency of cobalamin or folate causes a demyelinating disease of
the brain and spinal cord. A reduced supply of methyl groups has been implicated
as its cause. To examine the mechanisms of demyelination in human beings, we
have studied three children with sequential inborn errors of the methyl-transfer
pathway. One child had abnormal methylfolate metabolism, one abnormal
methylcobalamin metabolism, and one hypermethioninaemia probably caused by
methionine adenosyltransferase deficiency. Magnetic resonance imaging of the
brain and measurement of cerebrospinal-fluid concentrations of
5-methyltetrahydrofolate, methionine, and S-adenosylmethionine were carried out
before and after 6-12 months of appropriate treatment. Each patient had abnormal
myelination before treatment; the scans suggested demyelination. The only
consistent biochemical abnormality in the cerebrospinal fluid was a low
concentration of S-adenosylmethionine. Treatment led to substantial clinical
improvement, apparent remyelination, and increases in cerebrospinal-fluid
S-adenosylmethionine concentration into the normal range. Cerebrospinal-fluid
concentrations of S-adenosylmethionine and methionine were significantly lower
in eight other children with errors of the methyl-transfer pathway than in an
age-matched reference population (mean [95% confidence interval] standard
deviation score -1.81 [0.57], p less than 0.001 for S-adenosyl methionine and
-1.82 [0.19], p less than 0.001 for methionine). The concentrations of these
metabolites increased to within the reference range on treatment. We have shown
that demyelination is associated with cerebrospinal-fluid S-adenosylmethionine
deficiency and that restoration of S-adenosylmethionine is associated with
remyelination.
PMID: 1683972 [PubMed - indexed for MEDLINE]
14: Neurology 1988 Mar;38(3):459-62
Demyelination and decreased S-adenosylmethionine in
5,10-methylenetetrahydrofolate reductase deficiency.
Hyland K, Smith I, Bottiglieri T, Perry J, Wendel U, Clayton PT, Leonard JV.
Institute of Child Health, London, United Kingdom.
We previously described demyelination in the brain and subacute combined
degeneration of the spinal cord in a patient with 5,10-methylenetetrahydrofolate
reductase deficiency. To assess the role of methionine, S-adenosylmethionine,
folate, and neurotransmitter amine metabolism in the demyelination process, we
measured these metabolites in CSF from this patient; the findings are compared
with those obtained from three patients in whom neurologic deterioration had
been halted by the administration of betaine. Folate concentrations were low,
and amine and biopterin metabolism were abnormal in all patients. Methionine and
S-adenosylmethionine concentrations were undetectable in the first patient. In
those receiving betaine, methionine concentrations were proportional to the dose
administered and S-adenosylmethionine concentrations were near normal. The
results provide the first evidence for an association between defective
S-adenosylmethionine metabolism and demyelination in humans.
PMID: 3347350 [PubMed - indexed for MEDLINE]
15: Biochim Biophys Acta 1996 Nov 15;1317(2):101-4
Thiamine (vitamin B1) supplementation does not reduce fasting blood homocysteine
concentration in most homozygotes for homocystinuria.
Franken DG, Blom HJ, Boers GH, Tangerman A, Thomas CM, Trijbels FJ.
Department of Radiology, University Hospital Nijmegen, The Netherlands.
Homozygotes for homocystinuria due to cystathionine synthase (CS) deficiency
accumulate homocysteine and methionine in their blood and tissues. High-dose
pyridoxin, folic acid, vitamin B12, or betaine are therapeutical options to
lower the elevated homocysteine concentration. These compounds stimulate the
transsulfuration or remethylation of homocysteine. Despite such treatment,
elevated blood homocysteine concentrations may persist in many homocystinurics.
Therefore, it is warranted to study alternative regimen to reduce the blood
homocysteine concentration in homocystinurics. Apart from entering the
transsulfuration pathway, methionine can be catabolized via the transamination
pathway, by conversion into 4-methylthio-2-oxobutyrate (MTOB), followed by
oxidative decarboxylation of MTOB to 3-methylthiopropionate. Thiamine
pyrophosphate, the active form of thiamine, is a cofactor of the supposed
rate-limiting oxidative decarboxylation in the transamination of methionine. The
effect of thiamine administered in 2 or 3 daily doses of 25 mg orally, was
studied in nine homozygote CS deficient patients. Methionine levels decreased in
6 out of 9 patients. In 8 out of 9 patients, however, the levels of plasma
homocysteine remained virtually unchanged, as did the serum transamination
metabolites in all patients. We conclude that vitamin B1 cannot be used as an
additional homocysteine-lowering treatment in most homozygotes for
homocystinuria.
Publication Types:
Clinical Trial
PMID: 8950194 [PubMed - indexed for MEDLINE]
16: Appl Environ Microbiol 1994 Sep;60(9):3450-3
Nutritional requirements for growth of Helicobacter pylori.
Nedenskov P.
Department of Microbiology, University Hospital of Tromso, Norway.
A chemically defined medium consisting of a buffered mineral base supplemented
with amino acids, a purine, and thiamine supported growth of 23 clinical
isolates and the type strain of Helicobacter pylori. The growth of four strains
was inhibited by the presence of certain amino acids. All but one strain
required alanine for growth. The amino acids leucine, valine, phenylalanine,
methionine, arginine, and histidine were generally required. Isoleucine either
was required or stimulated growth. Strains could be differentiated into groups
on the basis of a requirement for one or more of the amino acids cysteine,
serine, and proline. Only one strain however, demonstrated a requirement for all
three of these amino acids.
PMID: 7944377 [PubMed - indexed for MEDLINE]
Will this board be left up for reading????????
We are waiting for clarification from the web coordinator and will post as soon as possible.
A previous citation reported that hypermethioninemia can be acquired (2). We
note here that genetic examples demonstrate that hypermethioninemia can induce
demyelination (1). These two cites suggest that, akin to genetic
hypermethioninemia, prolonged acquired-hypermethioninemia might also contribute
to demyelination, especially if additional etiologic factors occurred during the
acquired hypermethioninemia. Such factors would include but not be limited to
thimerosal injections, roseola (HHV-6), other brain-inflammatory processes (eg,
as often follow vaccinations).
1. Am J Hum Genet 2000 Feb;66(2):347-55
Methionine adenosyltransferase I/III deficiency: novel mutations and clinical
variations.
Chamberlin ME, Ubagai T, Mudd SH, Thomas J, Pao VY, Nguyen TK, Levy HL, Greene
C, Freehauf C, Chou JY.
Heritable Disorders Branch, National Institute of Child Health and Human
Development (NICHD), National Institutes of Health, Bethesda, MD 20892, USA.
Methionine adenosyltransferase (MAT) I/III deficiency, caused by mutations in
the MAT1A gene, is characterized by persistent hypermethioninemia without
elevated homocysteine or tyrosine. Clinical manifestations are variable and
poorly understood, although a number of individuals with homozygous null
mutations in MAT1A have neurological problems, including brain demyelination. We
analyzed MAT1A in seven hypermethioninemic individuals, to provide insight into
the relationship between genotype and phenotype. We identified six novel
mutations and demonstrated that mutations resulting in high plasma methionines
may signal clinical difficulties. Two patients-a compound heterozygote for
truncating and severely inactivating missense mutations and a homozygote for an
aberrant splicing MAT1A mutation-have plasma methionine in the 1,226-1,870
microM range (normal 5-35 microM) and manifest abnormalities of the brain gray
matter or signs of brain demyelination. Another compound heterozygote for
truncating and inactivating missense mutations has 770-1,240 microM plasma
methionine and mild cognitive impairment. Four individuals carrying either two
inactivating missense mutations or the single-allelic R264H mutation have
105-467 microM plasma methionine and are clinically unaffected. Our data
underscore the necessity of further studies to firmly establish the relationship
between genotypes in MAT I/III deficiency and clinical phenotypes, to elucidate
the molecular bases of variability in manifestations of MAT1A mutations.
2. Mol Genet Metab 2003 May;79(1):6-16
Infantile hypermethioninemia and hyperhomocysteinemia due to high methionine
intake: a diagnostic trap.
Harvey Mudd S et al.
" Retrospective data on dietary methionine intakes and plasma
concentrations of methionine and related metabolites established that the
hypermethioninemia in nine of the 10 babies was related to ingestion of an
infant protein hydrolysate formula, the methionine content of which had been
increased from May 1998 to February 2001. The formula in question has now been
reformulated and is no longer available."
---------------------------------------------------------------------
While researching methionine adenosyltransferase [MAT] (an enzyme which
contributes to pathways affected by B6, methylcobalamin, SAMe, etc), I
encountered the word " hypermethioninemia" . A search for title words via
hypermethionin*[ti] generated 40 citations. Not only are some individuals marked
by elevated methionine, that condition can be acquired (eg, 1).
A fine review (2) offers an important clinical distinction:
" These individuals with persistent hypermethioninemia due to hepatic MAT
deficiency are free from homocysteinemia, tyrosinemia or serious liver disease,
[traits which are] signs of conditions where hypermethioninemia is a secondary
effect..." (p274).
Thus, depending upon cause, an individual with hypermethioninemia will or won't
have traits such as " homocysteinemia, tyrosinemia or serious liver disease" .
1: Mol Genet Metab 2003 May;79(1):6-16
Infantile hypermethioninemia and hyperhomocysteinemia due to high methionine
intake: a diagnostic trap.
Harvey Mudd S et al.
Studies were carried out to identify the cause of combined severe
hypermethioninemia and moderate hyperhomocysteinemia in a cluster of 10 infants
ascertained between 1999 and early 2001. Although several were thought initially
to have cystathionine beta-synthase (CBS) deficiency and treated accordingly,
CBS deficiency and other known genetic causes of hypermethioninemia were ruled
out by assay of CBS activity in fibroblasts of four patients and by assays of
plasma cystathionine and S-adenosylmethionine. Retrospective data on dietary
methionine intakes and plasma concentrations of methionine and related
metabolites established that the hypermethioninemia in nine of the 10 babies was
related to ingestion of an infant protein hydrolysate formula, the methionine
content of which had been increased from May 1998 to February 2001. The formula
in question has now been reformulated and is no longer available. The 10th
infant manifested similar metabolic abnormalities while receiving TPN containing
excessive methionine. Brain MRI abnormalities indicative of cerebral edema, most
marked in the cerebral cortex and posterior brainstem, occurred in two patients
near times of extreme hypermethioninemia. Metabolic and MRI abnormalities
resolved when the methionine intake decreased. A third infant had a normal MRI 1
day after the formula was changed. The possible relationship between extreme
hypermethioninemia and cerebral edema is discussed and a working hypothesis
offered to explain the relative sensitivity of the inferior colliculi, based
upon the facts that this is the region most active in glucose utilization and
that Na(+),K(+)-ATPase is inhibited by methionine and related metabolites.
2: Pharmacol Ther 1997;73(3):265-80
S-adenosylmethionine synthesis: molecular mechanisms and clinical implications.
Mato JM, Alvarez L, Ortiz P, Pajares MA.
Instituto de Investigaciones Biomedicas, CSIC, Madrid, Spain.
Methionine adenosyltransferase (MAT) is an ubiquitous enzyme that catalyzes the
synthesis of S-adenosylmethionine from methionine and ATP. In mammals, there are
two genes coding for MAT, one expressed exclusively in the liver and a second
enzyme present in all tissues. Molecular studies indicate that liver MAT exists
in two forms: as a homodimer and as a homotetramer of the same oligomeric
subunit...
Ms. Sepulvada,
You have a lot of information and resources to share. It might be helpful if you posted the general topic of each in the " Subject" line so readers can sort through the materials in reference to the topic.
Thank you,
CDC DDBinfo
CDC:I can go on posting so much information that I cannot do it all today beating the deadline. So please consider my simple study proposal. Enroll ADS children in a medical clinical setting and conduct a thorough clinical and laboratory evaluation(immunology, gastroenterology, endocrinology, neurology, genetic, psychological, etc...). Make sure they have daily access to ABA, OT, PT, Speech therapy. Make sure that there is no cost involved to the parent for we have already paid a price too great. I am certain you will find many answers to this puzzle. Let me know where and when so that I can enroll my 4-year-old autistic son. He cannot wait for the CDC, NIH, etc... to find the so called " responsible genes" . He needs accessible treatment for his medical disease NOW! Thank you!
Sincerely,
Ada Sepulveda
(718)-438-7280
Dear Dr.Cordero et. al:
PLEASE respond and help our children!
CDC:I can go on posting so much information that I cannot do it all today beating the deadline. So please consider my simple study proposal. Enroll ADS children in a medical clinical setting and conduct a thorough clinical and laboratory evaluation(immunology, gastroenterology, endocrinology, neurology, genetic, psychological, etc...). Make sure they have daily access to ABA, OT, PT, Speech therapy. Make sure that there is no cost involved to the parent for we have already paid a price too great. I am certain you will find many answers to this puzzle. Let me know where and when so that I can enroll my 4-year-old autistic son. He cannot wait for the CDC, NIH, etc... to find the so called " responsible genes" . He needs accessible treatment for his medical disease NOW! Thank you!
Sincerely,
Ada Sepulveda
(718)-438-7280
Lancet 6th June: Vaccination and autoimmune disease
Vaccination and autoimmune disease: what is the evidence?
David C Wraith, Michel Goldman, Paul-Henri Lambert
As many as one in 20 people in Europe and North America have some form of autoimmune disease. These diseases arise in genetically predisposed individuals but require an environmental trigger. Of the many potential environmental factors, infections are the most likely cause. Microbial antigens can induce cross-reactive immune responses against self-antigens, whereas infections can non-specifically enhance their presentation to the immune system. The immune system uses fail-safe mechanisms to suppress infection-associated tissue damage and thus limits autoimmune responses. The association between infection and autoimmune disease has, however, stimulated a debate as to whether such diseases might also be triggered by vaccines. Indeed there are numerous claims and counter claims relating to such a risk. Here we review the mechanisms involved in the induction of autoimmunity and assess the implications for vaccination in human beings.
Published online June 3, 2003
To review Full Article " Vaccinations and autoimmune disease: what is the evidence?" click for PDF http://image.thelancet.com/extras/02art9340web.pdf (398 KB)
New Study Shows MMR/Autism Link
[From Autism Research Campaign For Health 23 June 2003. See referenced
abstract below " Elevated levels of measles antibodies in children with
autism" by Vijendra K. Singh PhD*, and Ryan L. Jensen BS.]
A new study, published in Pediatric Neurology, Vol. 28, No. 4, is
expected to show that MMR and autism are linked, despite the denials of the
UK Department of Health and the recent court judgement that ordered two
girls to receive the controversial MMR vaccine.
World-renowned autism researcher Dr. Vijendra Singh, at the Utah State
University, and fellow-researcher Ryan Jensen have announced that their
latest study," Elevated Levels of Measles Antibodies in Children with
Autism" , points directly to an MMR/autism link.
Singh and Jensen analysed samples from 52 autistic children, all of
whom had had the MMR vaccination, and 30 normal children, plus a further 15
siblings of autistic children.
They showed that measles antibody levels, a sign of an immune reaction
to measles virus, were significantly greater in children with autism
compared with the non-autistic children. Levels of mumps and rubella
antibodies were not different from the non-autistic children.
Strikingly, they found that 43 out of the 52 (83%) of the autistic
children had antibodies to the measles vaccine virus. None of the 30 normal
children, and none of the 15 siblings, had these antibodies.
Singh and Jensen have concluded that the antibody results show that
many autistic children have suffered an abnormal response to the measles
element of the MMR vaccine, causing them to develop " inappropriate"
antibodies.
Singh and Jensen were testing a hypothesis that, as viruses are common
trigger agents for autoimmune diseases, where the human body attacks itself,
then autism could involve a virus-induced autoimmune response, in turn
leading to autism.
The study looked at 88 autistic children, all of whom had a firm
diagnosis of autism. Not all children were tested for all the three viruses,
of measles, mumps or rubella. In those children tested, the level of mumps
or rubella antibodies did not attain statistical significance, leaving the
researchers to focus upon the measles element of MMR. None of the autistic
children had any history of measles rash or wild-type natural measles
infection.
This points to the source of the measles antibody as being vaccine
strain. The researchers are undertaking further study work on this crucial
aspect.
If the new research by Singh and Jensen is correct, then it backs up
the claims of many families who have reported that their children became
autistic after MMR. It also confirms the validity of the1998 study by Dr.
Andrew Wakefield and other researchers in the UK, and a number of other
studies published since that time.
Over 1,000 cases of autism following MMR are being brought before the
High Court in London in April 2004. If the claims are upheld, it will have
dramatic implications for vaccine policy worldwide, and will throw a
spotlight on the way vaccines are licensed and regulated.
Background
ARCH - Autism Research Campaign for Health - is a group of parents
campaigning for more research into the causes and treatment of autism. It
was set up in response to the departure of Dr Andrew Wakefield from the
Royal Free Hospital - which ARCH viewed as a sign that medical scientists
were no longer free to follow their own lines of enquiry. We are profoundly
worried that medical science is now dictated by government, the medical
establishment and the pharmaceutical industry who between them control the
vast sums of research money and determine which topics are legitimate
research and which are not. This state of affairs is unacceptable to the
growing number of children and parents who must live with the painful
consequences of autism, and with the lack of research into the alarming
increase in the prevalence of autism in many countries across the world.
ARCH believes that there is mounting evidence that suggests MMR is
unsafe. It calls on the UK Government to fund clinical research into the
effects of MMR vaccine on the immune system of autistic children and its
role in the onset of regressive autism, epilepsy and bowel disease.
Visit ARCH on http://www.autism-arch.org
The Institute of Science in Society
Science Society Sustainability http://www.i-sis.org.uk
General Enquiries sam@i-sis.org.uk Website/Mailing List
press-release@i-sis.orguk ISIS Director m.w.ho@i-sis.org.uk
UNSUBSCRIPTION INSTRUCTIONS ARE AT THE FOOT OF THIS MESSAGE
SARS Virus Genetically Engineered?
The mystery surrounding the SARS virus deepens. Dr. Mae-Wan Ho
raises further questions on whether genetic engineering could have
contributed to creating it.
Sources for this article are posted on ISIS' members website.Details here.
The SARS epidemic
The SARS epidemic started in the weeks that the 'allied forces' were
waging war on Iraq to hunt down Saddam Hussein and his still elusive
'weapons of mass destruction'.
SARS - Severe Acute Respiratory Syndrome - is a completely new
infectious disease spread by human contact. By 20 June 2003, World Health
Organisation figures registered 8461 cases in 31 countries worldwide, and
804 deaths. The overall death rate is nearly 10% and could be 20% or
higher.
Although there are signs that the disease is under control, there
are also fears that it may return.
Mystery of the SARS virus
The World Health Organisation, which played the key role in
coordinating the research of a dozen laboratories, formally
announced on 16 April that a new pathogen, a member of the
coronavirus family never before seen in humans, is the cause of
SARS, though lingering doubt has remained. The virus cannot be
identified all patients diagnosed with SARS, and it can only be isolated
from cultured green monkey kidney cells.
Known coronaviruses are placed in three groups based on similarities
in their genomes. Group 1 contains the porcine epidemic diarrhoea
virus (PEDV), porcine transmissible gastroenteritis virus (TGEV),
canine coronavirus (CCV), feline infectious peritonitis virus (FIPV)
and human coronovirus 229E (HuCV229E); Group 2 contains the avian
infectious bronchitis virus (AIBV) and turkey coronavirus; while Group 3
contains the murine hepatitis virus (MHV) bovine coronavirus (BCV), human
coronavirus (HuOC43) and others.
The molecular phylogenies published 10 April in the New England
Journal of Medicine, based on small fragments of the polymerase gene,
have placed the SARS virus in a separate group somewhere between groups 2
and 3.
More detailed analysis, subsequently published in the New England
Journal of Medicine, Science and the Lancet indicate that the new
virus is not closely related to any known virus at all, human,
mouse, bovine, cat, pig, bird, notwithstanding. It is neither a
mutant that switched host, nor a recombinant from existing
coronaviruses. It is more complicated than that.
SARS virus - a product of genetic engineering?
Two scientists who have genetic engineered coronaviruses in their
laboratories, Holmes and Enjuanes, suggested in a commentary in the
journal Science that the SARS virus probably " evolved separately
from an ancestor of the known coronavirus, and infected an unidentified
animal, bird, or reptile host for a very long time before infecting humans
and starting the SARS epidemic." (p.1377)
Following soon afterwards, there was a claim that the SARS virus
came from the masked civet cat in south China. But that claim could
not be substantiated. An alternative hypothesis entertained in the
mainstream journals was that the virus came from outerspace.
There are very unusual features to the SARS virus. Its sequence most
closely matches that of mouse hepatitis virus (MHV) and Bovine corona
virus (BCV), both in group 3. The match is quite good in the middle third
of the genome that's nearly 30 000nt long, and not good at all for the
first third or last third of the sequence.
But, antibodies to the SARS virus cross react with FIPV, HuCV229E
and TGEV, all in Group 1. And the SARS virus can grow in Vero green monkey
kidney cells, which no other coronavirus can, with the exception of PEDV,
another virus in Group 1.
Could the SARS virus have come from genetic engineering? This is a
question that Ho and Cummins have put to the scientific community.
So far, we have not had a proper reply.
Holmes and Enjuanes stated in their commentary, " SARS-CoV is also
unlikely to have been created from known coronaviruses by genetic
engineering, because at present it would be impossible to modify 50% of a
coronavirus genome without abrogating viral infectivity." (p.1377)
This is a quite a feeble response. The whole point to genetic
engineering is that it greatly increases the scope of recombination, and
provides selective tools to find the most unlikely recombinants that are
still infectious.
Coronaviruses have been subjected to increasing genetic manipulation
since the latter half of the 1990s, when P.S. Masters in Wadworth
Center, New York State Department of Health and New York State
University at Albany, used RNA recombination to introduce extensive
changes into the genome of mouse hepatitis virus (MHV). In a review
published in 1999, he wrote, " targeted recombination could be used to
create extensive substitutions to the cornavirus genome, generating
recombinants that could not be made otherwise between two viruses
separated by a species barrier." (p.254)
'Defective interfering RNAs' - sequences of the viral genome with
large deletions as well as mutations and substitutions or insertions -
were used as donor sequences to introduce major substitutions and point
mutations into the genome of the viruses by RNA recombination.
In the course of such work, researchers have even isolated a
recombinant of cororanvirus with the green fluorescent protein (GFP) gene,
presumably from cells in which coronaviruses have been cultured, which has
become inserted into the spike protein gene. The GFP gene, originally from
a jelly-fish, is extensively used in genetic engineering as a marker gene
because it makes the cells that have taken up the foreign genes give off a
green glow under uv light. The GFP-coronavirus recombinant could
only have come about as an unintended by-product of genetic
engineering.
In the same review, P.S. Masters showed that both point mutations
and large substitutions can readily be transferred to the last third of
the genome of MHV and other coronaviruses. He further indicated that
similar strategies could be used to mutate and substitute the first third
of the genome, though not for the middle third. " A comprehensive genetic
study of the highly complex gene for the RNA polymerase and all of its
associated activities [encoded by the middle third of the genome] will
likely await either the construction of an infectious full-length clone or
the development of an innovative scheme for mutant selection." (p.259)
Is that why the middle third of SARS virus genome has retained good
homology to MHV and BCV, which were the first coronaviruses to be
engineered in this manner, while the other parts are much more
different?
Another feature of the SARS virus is that the spike protein, which
determines host range, is unlike the spike protein of any known
coronavirus. Instead, it appears to have homologies to segments of the
human chromosome 7, according to sequence analysis performed by Howard
Urnovitz.
Urnovitz believes that the spike protein of the SARS virus is the
result of genetic rearrangements provoked by environmental genotoxic
agents, much like those he and his colleagues have detected in Gulf War I
veterans suffering from Gulf War Syndrome.
But how did the virus get to south China? A possible answer was
provided by Urnovitz: Migratory birds that frequent gene-swapping
hot spots like southeast China could have carried the SARS virus
there.
Urnovitz himself doesn't think the SARS virus is the real cause of
SARS. Instead, it is the piece of reshuffled human chromosome 7 that
others are referring to as the spike protein gene of the SARS virus.
That alone is sufficient to trigger serious autoimmune responses in
people.
Hence, to create vaccines against that 'spike' protein is also
tantamount to vaccinating people against their own genes (see " Dynamic
genomics" , this series).
This article can be found on the I-SIS website at
http://www.i-sis.org.uk/ >
* If you would prefer to receive future mailings as plain
text please let us know. * If you would like to be removed from
our mailing list - please reply to press-release@i-sis.orguk
with the word unsubscribe in the subject field *
The Institute of Science in Society, PO Box 32097, London NW1 OXR
telephone: [44 20 8731 7714] [44 20 7383 3376] [44 20 7272 5636]
General Enquiries sam@i-sis.org.uk - Website/Mailing List
< mailto:press-release@i-sis.org.uk> press-release@i-sis.orguk - ISIS
Director m.w.ho@i-sis.org.uk
MATERIAL IN THIS EMAIL MAY BE REPRODUCED IN ANY FORM WITHOUT
PERMISSION, ON CONDITION THAT IT IS ACCREDITED ACCORDINGLY AND
CONTAINS A LINK TO http://www.i-sis.org.uk/
[Thnx to DB for sharing the item]
Yahoo! Groups Sponsor
ADVERTISEMENT
The Honorable Dan Burton
Chairman of the House Government Reform
Subcommittee on Human Rights and Wellness
U.S. House of Representatives
2157 Rayburn House Office Building
Washington, DC 20515
By Facsimile
Letter to Demand a Congressional Investigation and Hearing on the
Introduction of Simian Virus 40 (SV40), a Cancer-Causing Monkey Virus, into
the American Population From Contaminated Polio Vaccines
Dear Representative Burton:
I am writing this letter on June 7, 2003. Exactly seven years ago, on June
7, 1996, my son Alexander was born. He would die in my arms 30 months
later in a little motel room in Houston, Texas as we, his parents, tried
desperately to safe his life. This letter is written in commemoration of
Alexanderÿffff92s short life and the injustice that befell him and the cause of
the brain tumor (medulloblastoma) that killed him.
This letter is also the result of four long years of struggle by myself and
my husband to find out why our beautiful healthy young son would be
stricken by cancer. Now, our lawsuit against the manufacturer of the oral
polio vaccine, American Home Products, (i.e. Lederle), has come to a close.
As a result, much of the information that has been under a protective
order for over three years has been entered into the public record through
our legal documents filed with the Federal Court for the Central District
of California in Los Angeles. What happened to Alexander is not an
isolated event. We contend that his death was caused by a Public Health
Disaster that has befallen others and will continue to kill children until
it is addressed.
On August 12, 1999, we wrote you when you where Chairman of the Committee
on House Government Reform in support of your investigations into pediatric
vaccines - Vaccines; Finding the Balance Between Public Safety and Personal
Choice. In this letter we described how various childhood vaccines contain
known carcinogens and yet not a single vaccine is tested for
carcinogenicity. While shampoos and cosmetics are tested to see if they
cause cancer, incredibly, biological substances that are squirted or
injected into healthy infants and children have never been tested.
On June 7, 2000, My husband and I also appeared before your Committee to
discuss the FDAÿffff92s control of effective non-toxic pediatric cancer therapies
in Cancer Care for The New Millenium - Integrative Oncology. During our
sworn testimony we described how Alexander suffered enormously and
unnecessarily as a result of the administration of four toxic but
ineffective chemotherapy drugs (vincristine, cytoxan, etoposide, and
cisplatin - Protocol CCG 9921). We described how the FDA would not allow
our son to have access to a non-toxic cancer therapy that offered him the
best chance of saving his life. We presented photographs to your Committee
that demonstrated how Alexander struggled to stay alive and then suffered a
horrific death.
From your own considerable effort in investigating vaccine production,
testing, and safety you know that childhood vaccines contain formaldehyde
(i.e. formalin), mercury (i.e. thimerosal), aluminum, and other toxic
substances. In addition, vaccines can also contain animal viruses -
contaminants from the animal substrates upon which the vaccines are
manufactured. One of these viruses, a monkey virus called Simian Virus 40
is carcinogenic and found its way into the oral polio vaccine (OPV) and the
inactivated polio vaccine (IPV) in the late 1950's and early 1960's. Such
an event was not surprising because monkey kidneys contain a multitude of
simian viruses and the polio vaccine is grown on monkey kidney cells.
The oral polio vaccine is a " live" trivalent vaccine which means that it
contains three strains of poliovirus - Types I, II, and III, and each
strain is attenuated (i.e. weakened). Dr. Albert Sabin, who was
responsible for the creation of the licensed OPV, had to passage his
poliovirus strains through a myriad of animals and animal host cells in
order to attain the right virulence-strong enough to illicit an immune
response, but sufficiently attenuated so as to not cause polio in the
recipient. For example, Type I has the following lineage:
In 1941, Drs. Francis and Mack isolated the Mahoney poliovirus " from the
pooled feces of three healthy children in Cleveland." Dr. Salk then
passed this strain through fourteen living monkeys and two cultures of
monkey testicular cultures. In 1954, the strain (now called Monk14 T2) was
given to Drs. Li and Schaeffer who subjected the virus to nine more
passages through monkey testicular cultures. Next, the strain (now called
Monk14 T11) underwent fifteen more passages in monkey testicular cultures,
eighteen passages in monkey kidney cells, two passages through living
rhesus monkeys skin, and additional passages through African Green monkey
skin and monkey kidney cell cultures. This strain was now called MS10 T43
and LS-c. In 1956, Dr. Sabin took this virus and passaged it through seven
cultures of African Green Monkey kidney cells. That same year, the
pharmaceutical company, Merck, Sharp & Dohme, passed the strain (now called
LS-c, 2ab/KP2) through a rhesus monkey kidney cell culture. The resulting
material was called Sabin Original Merck (SOM) and was provided to Lederle
in 1960 as the seed material to manufacture its polio vaccine.
Types II and III were created in a similar fashion.
Once the strains were isolated, the pharmaceutical companies needed a
method to propagate the viruses in order to produce the vast quantities of
vaccine needed for nation-wide immunization campaigns. This required a
substrate upon which the poliovirus could be efficiently grown and
harvested. Kidney cells from rhesus monkeys were chosen because they were
found to be an effective growth medium. A small quantity of poliovirus
could be added to the minced kidneys removed from these monkeys and within
a few days, large quantities of poliovirus could then be harvested from
these same monkey cells.
Between 1959 and 1960, Bernice Eddy, Ph.D., of the National Institute of
Health (NIH) examined minced rhesus monkey kidney cells under a microscope.
These were the cells of the same species of monkeys used to create and
produce the oral polio vaccine. Dr. Eddy discovered that the cells would
die without any apparent cause. She then took suspensions of the cellular
material from these kidney cell cultures and injected them into hamsters.
Cancers grew in the hamsters. Within a few months, the virus responsible
for creating these cancers would be isolated and identified by Dr. Eddy and
other scientists. Because it was the 40th simian virus found it was named
simian virus 40 (SV40).
According to the FDA:
The discovery in 1960 that a DNA tumor virus, designated simian virus 40
(SV40), was an inadvertent contaminant of rhesus monkey cells, and
consequently the poliovirus and adenovirus vaccines that were made in these
cells, was a watershed event in vaccine developmentÿffff85"
By 1960, the Salk injectable polio vaccine (IPV) had been administered to
about 98 million American children and adults, and Sabinÿffff92s oral polio
vaccine (OPV) had been administered to about 10,000 Americans and millions
in the USSR where the clinical trials had been conducted. It was estimated
that 10% to 30% of the vaccines contained live SV40. The federal agency in
charge of vaccine licensing and safety at the time was the Division of
Biologics Standards (DBS) of the National Institute of Health (NIH).
Incredibly, this agency did not order a recall of any of the
SV40-contaminated vaccines. The tainted vaccines continued to be
administered until 1963 when they were all used and replaced by allegedly
SV40-free vaccines as required by the new federal regulations promulgated
in 1961.
In 1961, federal regulations were implemented to ensure that SV40 would no
longer contaminate the polio vaccine. Despite these regulations, we
contend that the OPV has been sporadically contaminated with SV40 for the
last four decades. As a result, we allege that some of the children who
have been administered the contaminated vaccines have been stricken with
cancer and others are at risk. The main points are summarized below:
1) SV40 (Simian Virus Number 40) is a cancer causing monkey virus found in
the kidney cells of Rhesus and African Green Monkeys. The kidney cells of
these two species of monkeys comprise the substrate that has been used to
create poliovirus strains and manufacture the oral polio vaccine for four
decades.
2) SV40 is a human carcinogen for brain cancer and mesothelioma and it is a
suspected carcinogen in osteosarcomas (bone cancers) and Non-Hodgkinÿffff92s
Lymphomas.
3) Alexander was administered the OPV in November 1997. He was diagnosed
with a brain tumor in August 1998. Alexander died on January 31, 1999.
4) Four independent laboratories using DNA testing and laser
micro-dissection found SV40 in Alexanderÿffff92s brain tumor.
5) SV40 has been found in the cancers of many other children. Pediatric
brain tumors and other childhood cancers including osteosarcomas (bone
cancer) and Non-Hodgkins Lymphomas have been found to contain SV40.
6) When Alexander was born on June 7th, 1996, I had his cord blood saved
and stored by a private laboratory. The cord blood was the blood shared by
Alexander and myself at the time of Alexander's birth. We had this blood
tested for SV40. This marked the very first time the cord blood of a child
with an SV40 positive brain tumor would be tested for SV40. To the
astonishment of the scientists it was negative for SV40. This suggested
that at the time Alexander was born he had not been exposed to SV40.
7) It is known that SV40 can be spread through contaminated blood so my
husband and myself underwent a battery of tests from 2000 to 2001. Using a
variety of sophisticated DNA tests to isolate the genetic fingerprint of
the SV40 virus including Polymerase Chain Reaction (PCR), the scientists
checked blood, urine and semen multiple times looking for any trace of SV40
(even antibodies). The scientists were once again surprised. Despite the
repeated tests by leading SV40 laboratories both in the United States and
Europe, we had absolutely no trace of SV40.
8) The scientists concluded that Alexander did not get SV40 from his
parents, nor did he give SV40 to us.
9) The original oral polio vaccine (OPV) seed stocks created by Dr. Albert
Sabin and used to make OPV since 1961 were known to be contaminated with
SV40. In fact, SV40 was isolated from Sabin's OPV seeds - the original
material used to make OPV for four decades.
10) Dr. Sabin had admitted that OPV seeds were contaminated with SV40 in a
peer-reviewed scientific publication. Dr. Sabin wrote, " The three types
of the large lots produced by Merck, Sharp and Dohme in rhesus monkey
kidney cell cultures contained SV40."
11) Lederle, the sole American manufacturer of OPV for many years, received
their OPV seeds from Merck, Sharp and Dohme. There is no evidence that
Lederle ever tested their seeds for SV40 nor discarded their presumably
contaminated seed stocks.
12) There are Lederle documents (not under a protective order) that
demonstrate that their early OPV vaccines were contaminated with SV40.
13) Lederle did not use the SV40-neutralization procedures recommended by
Dr. Sabin.
14) Monkeys used to produce OPV were not tested for SV40 by Lederle because
of economic considerations.
15) After reviewing all of the Lederle records and the Lederle systems in
place, our expert concluded that the contamination detected in the OPV
material ultimately administered to Alexander was SV40.
16) The medical literature is unequivocal - the pediatric brain cancer rate
in the U.S. has been climbing at a rate of approximately 3% for the last
four decades.
17) A recent study has demonstrated that 11% of Americans are currently
infected or have been infected with SV40.
SV40 is not only responsible for causing the cancer, but also for making
these particular cancers incurable. Orthodox cancer therapies such as
chemotherapy and radiation can not cure an SV40 positive cancer. Pediatric
brain cancers and other solid cancers have been found to contain SV40.
SV40 binds with the tumor suppressor genes p53 and RB and stops tumor cells
from undergoing apoptosis (programmed cell death). Apoptosis is what
radiation and chemo depend on to work in order to trigger the cancer cell
to die. Exposing SV40 positive cancer cells to chemo and radiation does not
kill the cells but simply creates more genetic mutations - making the
cancer more aggressive. The bottom-line is that SV40 causes human cancer,
stops orthodox cancer therapies (i.e. chemo and radiation) from providing
any benefit, and can make the cancer even more aggressive.
Despite these facts, children diagnosed with cancer are not given a choice
of whether they should undergo debilitating and toxic chemo and radiation.
Alexander should have been tested for SV40 upon his diagnosis, not after he
died. He should not have been administered ineffective and unnecessary
chemotherapy which provided no benefit and only made him suffer. Children
with SV40 positive cancers (or p53 mutations) should not be used as guinea
pigs and profit centers for pediatric oncologists, hospitals, and
pharmaceutical companies.
A Congressional Hearing should be immediately convened to examine how a
federally policed vaccine program has introduced a deadly monkey virus into
countless American men, women and children for the past 45 years and what
the public health consequences have been of this tragedy.
This government investigation should demand to know:
Why a vaccine manufacturer was allowed to use vaccine seed stocks for four
decades that came from a source contaminated with SV40?
Why did this manufacturer violate federal regulations and allowed
contaminated vaccines to be released?
Why weren't sophisticated tests to detect SV40 during OPV production and to
eliminate the virus ever required by the federal government?
Why aren't children with cancer tested for SV40 when they are diagnosed,
not when they are dead, because an SV40 positive cancer means that chemo
and radiation will be ineffective?
Why is there a significant percentage of Americans (children and adults)
walking around with evidence of having had an SV40 infection and what does
that mean for their risk of cancer and chances for a successful treatment?
Like our son, many children are already dead, victims of this virus, and
many adults will be stricken later. Time is of the essence, not for our
beloved Alexander anymore, but for other children who are infected with
this cancer causing virus.
Sincerely,
Raphaele Moreau-Horwin M.A., M.F.S. Michael
Horwin, M.A., J.D.
http://www.ouralexander.org
cc: Barbara Loe Fisher, Co-Founder & President of the National Vaccine
Information Center
Yahoo! Groups Sponsor
THE NIDS MEDICAL ADVISORY BOARD PRESENTS:
A DRAFT PROPOSAL OF ITS NEURO-IMMUNOLOGY HYPOTHESIS STATEMENT CONCERNING AUTISM
Clinical Hypothesis - Immune " Dysfunction / Dysregulation" - A Reason for Childhood Neuro-Cognitive Dysfunction:
Autism, as classically defined, is a devastating disorder that often robs children of their ability to communicate and thrive in society. It is characterized by primary alterations in social interactions and receptive/expressive language, and is often accompanied by symptoms including ritualistic behaviors and a lack of imaginative play. Additionally, many " autistic" children exhibit a craving for sensory (vestibular) stimulation that often manifests itself in self-stimulatory behaviors (e.g., spinning and hand-flapping).
By definition, autism has an early onset before 30 months of age (which has now been extended to 36 months under the DSM-IV guidelines), while disorders appearing later in life have been thought to be symptomatically and medically different from " autistic" conditions. However, publications over the last 13 years have cast some doubt on this assumption, and it has been noted in the literature that there is no firm evidence that similar or identical syndromes might not develop in older children.
From an epidemiological standpoint, autism has migrated from a rare disorder to one that is now ten (10) to twenty (20) times more likely to be diagnosed. Ten years ago, " autism" occurred in 1-3 per 10,000 births. Now, current estimates suggest an incidence rate of 20 ÿfffff1 40 per 10,000 births. In fact, " cluster groups" throughout the world are currently being analyzed due to even higher incidence rates. It is also worth noting that other neuro-cognitive conditions such as " quiet" ADHD and " mixed" ADHD have received a renewed focus and attention among children and adolescents due to their perceived increase in incidence rates. Although a portion of these increases can likely be attributed to better and earlier recognition by the medical community and parents, the NIDS Board believes that this increase must prompt a change in how we approach these children. Specifically, we must begin to consider that these are not congenital, brain-damaged conditions but instead are medical disease processes acquired early in life.
In accordance with this premise, recent discussions have focused on the differentiation between " congenital autism" (including " classic" Kanner autism) and another form related to neurologic and medical disorders such as tuberous sclerosis, phenylketonuria, congenital rubella, and Downÿffffeds syndrome. However, a third form has emerged which is being referred to as " acquired or regressive autism" (perhaps the largest sub-group of these children). For purposes of this hypothesis statement, " acquired autism" is a condition in which the child develops normally for the first 12 to 18 months of life and then regresses into the increasingly wide spectrum of " autistic" disorders.
These children challenge the previous belief that 70% to 80% of autistic children are mentally retarded. They crawl, sit up, walk, and usually attain " normal" motor milestones on schedule. Until the age of symptom onset, they are affectionate and appear to have above average intelligence. Children with acquired autism may begin to develop some speech but then, without warning, cease to progress, and begin to regress. Suddenly, these children become withdrawn. They vacillate between being quiet and hyperactive. Often self-stimulatory behaviors (i.e. arm flapping, rocking, spinning, or head banging) may develop. Over time, some manifest symptoms that are both similar and atypical of children previously diagnosed as having congenital autism. The authors propose that many of these children with acquired autism fall into the medical category of N.I.D.S. (Neuro-Immune Dysfunction Syndromes), and need to be viewed as suffering from an auto-immune medical illness that is potentially treatable.
The Past:
Unfortunately, without the tools or the technology to accurately investigate the human brain, the label of " autism" evolved as a set of symptoms in a young, dysfunctional child. In its most severe form (" classic autism" ), effective speech was absent and clinicians often saw symptoms of repetitive, highly unusual, aggressive and sometimes self-injurious behavior. Those afflicted had extremely abnormal ways of relating to people, objects, or events. Parents noticed that something was " not right," often within the first three to six months of life. These children typically did not smile and often resisted affection.
Most researchers and clinicians did not look for " medical" answers to autism because they believed it was a disorder that was medically untreatable. Without the technology to understand these children, pediatricians and pediatric psychologists accepted the concepts of poor parenting, childhood psychosis/schizophrenia and classified " autism" as a psychological and/or developmental disorder. Treatment was typically delivered by psychologists and psychiatrists.
Eventually, it became well documented that known medical disorders such as tuberous sclerosis, PKU, congenital rubella, and others could cause autism. However, to date, these remain rare disorders and a small sub-group of autism. Given that researchers are just now beginning to understand the medical origins and implications of the potential therapies for these children, autism is still treated primarily by psychologists and educators (with mixed results).
Past Medical Research:
A review of the existing medical literature relative to autism research reveals evidence of an emerging medical disease process in these children. For instance, research indicates that autism can follow infectious disorders affecting the central nervous system including encephalitis.,,, Multiple studies have focused on various anatomic locations of suspected dysfunction.,,, It is important to note that emphasis is often put on the medial temporal lobe. Pertinent to this new " model" of dysfunction, are the multiple published reports of autistic symptoms developing in association with encephalitis in children. (Ref: 1981 DeLong, 1986, Gillberg, 1989,) Most of these reports site injury to the temporal lobes as part of their findings. This is consistent with the areas of decreased function identified on NeuroSPECT scans initially by Dr. Ismael Mena from the NIDS Board and now by Dr. Bruce Miller and Dr. Fred Mishkin, both of who have clinical research in progress.
New research techniques are increasing the rates at which Herpes Simplex Virus (HSV) sequences are being identified in temporal lobe tissues, (i.e., locales likely to be substrates for various aspects of autism). In 1975, an article was published in Cortex describing a syndrome similar to autism in adult psychiatry. The condition involves the loss of emotional significance of objects, the inability to adapt in social settings, the loss of recognition of the significance of persons, and the absence of sustained purposeful activity after temporal lobe damage.
The literature also comments on the cognitive and behavioral deficits caused by temporal lobe damage in Herpes encephalitis. There are many reports, particularly in the British literature, suggesting a connection to coxsackie/enteroviruses, while in the United States it has been suggested that many cases may be linked to the Herpes family of viruses (i.e., EBV, HHV6, HHV7, CMV, etc.).,,,, Neither theory has been conclusively proven, nor has the evidence for a contagious disorder been conclusive (although some have inferred it based upon incidents related to epidemic outbreaks,) However, HSV in humans has long been known to prefer temporal lobe and limbic sites. One theory focuses on the olfactory nerves as a possible route for infection, but oral cavities may also provide entry. In 1996, OÿffffedMeara et al postulated that: " Inoculation of murine tooth pulp with HSV selectively infected the mandibular division of the trigeminal nerve and caused encephalitis predominantly affecting the temporal cortex and limbic system, a pattern of disease similar to human HSE [herpes simplex encephalitis]...."
While other studies have also implicated the temporal lobes in the pathogenesis of autism,, a direct association between temporal lobe pathology and autism has not yet been proven conclusively. In fact, research has found a variety of lesions in the " autistic" brain, particularly in the cerebellum. These variable findings may be due to the heterogeneity (differences) in the possible etiologies or time/duration effects within this syndrome.
Although Herpes virus has a predilection for the temporal lobes, the course of autism does not suggest an acute infection with traditional Herpes viruses. However, delayed temporal lobe development early in life may produce different symptoms from those arising from deterioration or destruction of previously normal lobes.
In summary, although not conclusive, past research further strengthens the linkage of the temporal lobe and " autistic" symptoms. Boucher and Warrington noted similarities between behavioral deficits reported in animals with hippocampal lesions and autistic behavior. Medial temporal lobe damage on pneumoencephalograms was reported in a subset of autistic children. Damasio and Mauer proposed that " the syndrome results from dysfunction in a system of bilateral neural structures that includes the ring of mesolimbic cortex located in the mesial frontal and temporal lobes, the neostriatum, and the anterior and medial nuclear groups of the thalamus. At least two other studies have also implicated the temporal lobes in the pathogenesis of autism.,
The Present:
With new and more precise tools and technology available to us now, the medical anatomy of " autism" is gaining definition after years of conflicting findings. Currently, EEG abnormalities, immune markers, and NeuroSPECT findings support the concept of a medical disease process occurring in these childrenÿffffeds brains. For example, it is generally recognized that an EEG finding of " slow" waves or " abnormal" brain wave activity is often consistent with the idea of an underlying and unknown " encephalopathy/encephalitis."
In addition, recent work with the NeuroSPECT strengthens the connection of blood flow abnormalities and neuro-dysfunctional states, particularly in situations in which patients appear to have immune and/or possible viral etiologies. NeuroSPECT scans capture blood flow through specific areas of the brain. Blood flow correlates with function/activity., As noted, NeuroSPECT scans on children with autism have shown a decrease in blood flow in the temporal and parietal areas, which is consistent with past reports of temporal lobe dysfunction in such children. Neurological models of the brain correlate right temporal lobe areas with social skills and left temporal lobe areas with speech and auditory dysfunction, all of which are compromised in autistic children. It should also be noted that there is no good explanation for our finding of increased blood flow in the frontal lobes of a group of these children, which is more consistent with ADD and Hyperactivity. Further research is required relative to this finding.
Also, the Board has been monitoring the emerging body of evidence related to the immune system and its interactive messengers: interleukins and cytokines. It appears that a dysregulated immune system state, whether triggered by a virus, genetic disposition, intrauterine, prenatal, neonatal stress or trauma, may account for the cognitive processing and other deficits seen in some children with autism. This concept is supported by the lack of consistent neurological/anatomical abnormalities and metabolic abnormalities in these children. We now know that neuro-polypeptides called cytokines can and do restrict brain blood flow under certain conditions. In these children, we may be looking at an immune system continually sending out signals to restrict brain blood flow. Whether this continues as an " auto-immune" reaction (whereby the immune system continues this pathway with no active reason to do so) or is due to the presence of a retro-viral or other viral process is open to further research. However, the concept of an immune-related disease process in a large number of these children appears unquestionable at this point in time.
Futhermore, many autistic children have major allergies or intolerances to many chemicals and foods. While occasionally these reactions may turn into urticaria or asthma, the effect in the majority of these children is the worsening of autistic-like behavior. Family history often reveals eczema, migraines (especially in mothers) hay fever, asthma, and histories of other disorders, which are often immune-mediated. These external symptoms may well prove to be signs of a " hyper-reactive" / stressed / dysfunctional immune system underlying the biochemistry of these children. Many anecdotal reports of successful therapies for autistic children (e.g., gammaglobulin, allergy-free diets) can most likely be explained through the concept of regulating a dysfunctional immune system and/or altering metabolic sensitivities and dysfunction.
Examples of autismÿffffeds probable connection to immune dysfunctional states are:
Extensive clinical work over the last four to five years further supports the Boardÿffffeds hypothesis that we are facing an immune-mediated disease state affecting the central nervous system (CNS) in these children. The literature is replete with articles connecting immune system abnormalities to autism, ADD, ADHD, CFS and CFIDS. Among the main examples are:
Multiple researchers have found evidence that autoimmunity is a possible mechanism to explain autistic symptoms.,,,,
An increased incidence of two or more miscarriages and infertility as well as pre-eclampsia and bleeding during pregnancy have been shown to occur in mothers of autistic children. There are also multiple studies in the obstetrical literature connecting these events to immune autoantibody production.
Studies have been done comparing the maternal antibodies of mothers with their autistic children, suggesting an association of abnormal maternal immunity with autism. Antibodies reactive with lymphocytes of fathers of autistic children have also been found.
Multiple researchers have shown an interaction of maternal antibodies with trophoblast or embryonic tissue antigens, and a cross-reaction with antigens found on lymphocytes.,,,
Researchers have also shown a significant depression of CD4+ T helper cells and their suppresser-inducer subset, with an increased frequency of the null allele at the complement C4B locus in children with autism. As similar changes have been known to occur in other autoimmune diseases,, these researchers have postulated that immune activation of a T-cell subpopulation may be important in the etiology of the disorder in some children with autism. (Note: Many of the autistic children evaluated by the Board have shown very high CD4 and CD8 counts, low natural killer (NK) cells, or other " markers" consistent with immune dysfunction/ dysregulation).
Abnormalities of Cell Adhesion Molecules (NCAM) have been reported.
Antibodies to neurofilament axonal proteins (NFAP) have been noted in autistic children 56a and have been reported in neurotropic slow virus diseases (Kuru and Creutzfeld-Jacob disease) in adults. Other studies, have suggested an association of an infectious agent (slow virus) in the etiology of these diseases. This is considered indirect evidence that some cases of autism may also be associated with the concept of a " slow virus."
Anti-central nervous system serum immunoglobin reactivity has been reported that was specifically directed against the cerebellum. 56a
A small percentage of autistic children with demonstrable immunologic abnormalities have normalized their autistic symptoms with intravenous immunoglobulin treatment. 59a 59b This result shows that immune abnormalities can cause autism in a subset of children and that " acquired autism" can be effectively treated.
Singh et al. hypothesized that autoimmunity secondary to a virus infection may best explain autism in some children. Congenital rubella virus and congenital cytomegalovirus have been indirectly involved as causative factors in autism.
Given this support from the medical research literature, the concept of immune dysregulation as a medical disease process in childhood neuro-cognitive dysfunction is an emerging reality. This concept could easily account for a portion of the increase of neuro-cognitive diagnoses over the last ten years. Whether the etiology of this dysfunction is related to environmental factors (e.g., ozone layer depletion, local toxins, etc.), new retro-viruses, stealth, spongiform or other viruses (or altered viral responses), we now have a medical hypothesis that can facilitate the definition of clinical sub-groups and lead to the treatment of these patients without first determining the origin or etiology.
If an infectious etiology indeed exists, it may be as ordinary as the common cold, or so rare that we have not yet developed the tools to either identify or study it. Whether an ongoing agent is present, or the body simply remains in a dysfunctional state, it seems likely we are confronted with a phenomenon/illness that has multiple etiologies, multiple origins, and various clinical manifestations. At this point, they appear linked by an immune dysfunction or possible viral-mediated state. Genetic predisposition to this syndrome may have a great deal to do with why certain individuals suffer with these symptoms. However, we must begin to consider these apparently heterogeneous expressions as linked and potentially treatable through the common pathway of an immune dysfunctional/CNS dysregulated state. For example, in a recent study on Chronic Fatigue Syndrome (CFS), two NIDS Board members reported a significant diminution of blood flow in both the temporal and, to a lesser degree, the parietal lobes in children suffering from CFS and Chronic Fatigue Immune Dysfunction Syndrome (CFIDS). These findings are similar to those previously noted in children with acquired autism.
Based on the evidence presented herein, the NIDS Board believes that developing a focus on the inter-relationship of autism, ADD, ADHD, CFS, CFIDS and other immune-modulated conditions is a key to helping groups of these children in ways never before possible. If we can address the physiologic part of the dysfunction in these children (irrespective of its specific etiology), educational therapy, counseling, study techniques and most/all other current therapies have a far greater probability of success. In addition, research focused on developing and initiating new therapies for autism are likely to be useful in treating these other inter-related childhood disorders.
The Future:
As outlined, we have witnessed the evolution of what is now being recognized and accepted at the National Institutes of Health (NIH), the Centers for Disease Control (CDC), and academic institutions world-wide as a " neuro-immune" epiphenomena. Studies are now confirming the concept of physiologic immune-mediated diseases underlying an abnormal physiologic state for these patients. This, in turn, creates both physical and neuro-cognitive deficits and dysfunction, usually of long-term duration.
The NIDS Board believes that many of the characteristics ascribed to autistic (and " quiet" ADHD) children overlap with the multiple complaints of adults afflicted with components of CFS/CFIDS and adult " ADHD" . As previously noted, all of these groups have reports of various immune abnormalities including T-cell changes reflected, for example, by increased or decreased CD4/CD8 cells, increased / decreased NK and B cells, and altered viral titers. It is this common denominator of immune alterations that gives hope for potential new therapies in the near future for these children.
However, while this hypothesis now has support in the literature, there are many important questions to be answered. How many " autistic" children have evidence of or are linked to an immune-dysfunctional state or a conclusive viral etiology? Can these children be viewed and treated differently than the " classic autistic" child of 20 to 30 years ago? Is their prognosis for recovery significantly better than the " classic autistic" children from the past?
It is time to recognize that these children are likely suffering from a medical disease process and need our clinical and research efforts now! Current treatments need to be modified and adjusted to account for this finding. The symptoms of the " quiet" ADD child (who is likely connected to this phenomenon) is not consistent with the past training or processes used to " explain" and address the " hyper" ADD child. It seems likely that the cognitive defects described in adults and children with CFIDS may be thought of as milder, later-onset form of " autism" , as they are similar in symptomatology and possible etiologies. The continued exploration of an immune-dysfunctional epiphenomena, and the potential etiologies linked to it, is a door we must walk through if we expect to change the future of this generation of children!
It is the proposed mission of this Board to accelerate the integration of the above clinical and research findings to facilitate the employment of new (and perhaps some older) immune-modulating therapies in the treatment of " acquired autism" , ADD/ADHD and CFS/CFIDS. We believe that by helping to " regulate" or " normalize" the immune system, we can restore health to these children. Through our unique acceleration of clinical knowledge and academic research, there is a chance to recognize and treat this disease process while these children are still young and while there is still time to effectively help their cognitive development.
NIDS Medical Board Members
Questions #1
(This one is straight-forward, then I'll get on my soapbox for the other questions)
Does the CDC collect data for cause of death of individuals with ASD? I've heard that the life expectancy is basically the same as the general population; however, many ASD people have common coexisting medical problems, are somewhat clumsy, and may face safety concerns throughout their lives. Do these factors occasionally lead to accidental death?
Question #2
Are you involved in, or do you know of any research being done on the relationshop between ASD children and their parent(s) having thyroid disorders?
I have a history of thryoidectomies (partial, then total),MANY adjustments to Synthroid levels, infertility, miscarriages, and premature birth resulting in our autistic son. I know of friends and aquaintances (parents of ASD children) who also have thyroid or other endocrine-related disorders.
Question #3
What studies/research, if any, have been done on a possible relationship between ASD individuals and fluoride? What research was done on the safety and efficacy of fluoride prior to adding it to toothpastes, oral rinses and public water systems?
Similarly, there are concerns related to high concentrations of metals in ASD individuals (also, high concentrations of aluminum in post-mortem brains of Alzheimer's victims).
Is it coincidence that we are the generation who grew up with daily uses of fluoride, and aluminum in our anti-perspirants -- not to mention soda cans and other food storage containers-- and now we are having a baby-boom of autistic kids? What about insect repellant, sunscreen, makeup and other lotions we apply to our skin (our largest organ)? Certainly these products have made our lives " better" , but I'm beginning to wonder if we, the parents, have toxic levels of substances that are affecting our unborn babies, and could WE be tested for these before planning a family?
[Other concerns were noted by other listmates regarding insecticides and pesticides.]
Question #4
The food pyramid. What is up with that? (I know that's the FDA not you fine folks at the CDC.)
Six to eleven servings of grains each day??? Even for typically-developing, healthy people that seems a bit extreme.
I'll admit, I was caught up in giving " cereals-for-snacks"
to my kids, as were/are most other moms I know. After all, they are " healthy" . No wonder we have a childhood obesity problem -- don't starches store as sugars??
And the problem is, we start offering those kinds of snacks often before we see the symptoms of autism, and are perhaps " feeding" the celiac problems so many of our kids have.
And now I'm on the top step of my soapbox:
Milk. This is a huge industry! It's a way of life for us, and I'm not suggesting that we shut down all dairy operations. However, some of us choose not to give our kids dairy products, or at least to limit them. We are looked upon as if we have three eyes, or as if we are terrible parents depriving our children of life-sustaining substances. Humans wean their babies from breastmilk. All mammals do the same. So many ASD kids have caseine problems. Certainly milk is a very " convenient" source of much-needed calcium, and it's fat-content makes it taste good. But other foods contain calcium, too, as long as we get enough sunshine (natural vit D) to work with our calcium intake. That is unless you are using suncreen, or are taking prescriptions that cause you to limit your time in the sun.
Food for thought(pardon the pun), but here's my question:
Do you have some official information from respected sources that you could make available to pediatricians and other providers in the ASD community, stating that it's OK to try GFCF diets, and also with suggestions for replacing the nutrients within the dairy and grains food groups?
Thank you for providing this discussion forum. It is always interesting to read the concerns of others regarding autism. I have found some useful resources from some of the other postings.
What is available for young adults who has never been diagnosed with ASD and are over 18yrs? It has only been in the last few years that ASD has become an issue. I beleive that some of these children have learning disabilities that are related to this condition. Since diagnosis is usually done at a early age, it would seem that we may have a whole generation that also need special assistance and not just be labeled as mentally retarded.
It is not uncommon for people to be diagnosed with an ASD for the first time as an adult. This is more common for people on the higher end of the spectrum and people with Asperger's, but late diagnosis can happen for people at all levels.
The National Information Center for Children and Youth with Disabilities (NICHCY) may be helpful in finding resources for someone in this situation http://www.nichcy.org
as may be the Autism Society of America
http://www.autism-society.org/site/PageServer?pagename=homepage
For information on vocational services you can see the
Department of Education Office of Special Education and Rehabilitative Services
http://www.ed.gov/offices/OSERS/RSA/
I am extremely disturbed by the continuing revelations that indicate a white washing of data surrounding the threat that Thimerosal poses to our children and their Autism. Here is the link to a current interview which illustrates my frustration and the frustration of many others. Http://www.bbc.co.uk/radio4/news/ram/fileon4.ram
I am particularly upset about the section of the interview with Kathleen Straton (about 16 minutes in) of the IOM who clearly stated that the report made to the IOM on the Thomas Verstraeten " Thimerosal VSD study Phase I 2/29/00 did not include the very stricking data on Autism. A 2.48 Relative Risk is defined in the Phase I study but only data on stammering and ADD was reported to IOM according to Kathleen Straton. Even with just the stammering and ADD data the IOM was able to state that a biologically plausable link to Thimerosal was possible! If complete disclosure had been made perhaps a full recall of the Hg containing vaccines would have been made at the time - sparing thousands and thousands of children from injury. As a researcher I need to know what happened here. As the grandparent of an affected child I demand to know what happened here!!! These reports are being read by hundreds of thousands of parents with afflicted children, this PR " problem" will not go away. I believe in immunization but the damage that this fiasco has done and will continue to do to the credibility of the nations immunization program is going to have catastrophic effects on the health of children everywhere.
Respectfully,
Leslie Davidson
Attachment: Http://www.bbc.co.uk/radio4/news/ram/fileon4.ram
Thank you for your participation in this forum and for responding to one another. While Friday, June 27th is the last date to submit questions and comments, CDC's National Center on Birth Defects and Developmental Disabilities will respond to as many postings as possible up through next Wednesday, July 2nd.
Thank you again for working together to understand the ASDs and help each person reach their full potential.
Will this board be left up for viewing, or knocked down?
Scientists claim direct link between MMR and autism
Jun 24 2003
by Madeleine Brindley, The Western Mail
THE row over the safety of the controversial MMR vaccine intensified last
night as new scientific evidence emerged of a direct link between the jab
and autism.
US researchers say they can prove that a significant number of children
suffered an abnormal response to the measles component of MMR, triggering
autism.
Their findings back up those published five years ago by Dr Andrew Wakefield
that started widespread concerns about a link between the triple combined
jab, autism and bowel disease.
Parents of autistic children allegedly damaged by the vaccine have welcomed
the findings. Welsh mother Julie Loch, who lives near Newport, believes her
six-year-old son Oliver developed autism after the MMR jab. She told The
Western Mail, " This study proves that our children have followed the same
normal development pattern but have regressed after having MMR and it seems
as though the key is the children's immune systems.
" These findings reinforce what parents have been saying for so many years -
something is happening to this group of children as they are reacting
abnormally, with devastating effects. Our children cannot be ignored any
longer."
The research, by Dr Vijendra Singh and Ryan Jensen, of the Utah State
University, into samples from 52 autistic children who had been vaccinated
with MMR, found that measles antibodies - a sign of an immune reaction to
the measles virus - were significantly greater in this group than among the
non-autistic children studied.
More than 80% of the autistic children had these antibodies compared with
none of the 30 normal children and none of the 15 siblings involved in the
research.
Singh and Jensen believe the presence of antibodies show that many autistic
children have suffered an abnormal response to the measles element of the
MMR vaccine, causing them to develop these " inappropriate" antibodies.
The findings, which are published in the journal Paedi-atric Neurology, are
the result of the pair's theory that as viruses are common trigger agents
for auto-immune diseases, where the human body attacks itself, autism could
involve a virus-induced auto-immune response, which in turn leads to autism.
Crucially, none of the autistic children involved had any history of measles
rash or wild-type natural measles infection, which implies that the source
of the measles antibody is the strain of measles virus used in the MMR
vaccine.
This new research comes 10 days after the High Court ruled that two girls,
aged four and 10, had to have the MMR jab, on their absent fathers'
insistence, despite their mother's concerns about its safety.
Public confidence and take-up rates of MMR have plummeted since Dr
Wakefield's controversial study in 1998 linking it to autism and bowel
disease.
In Wales the MMR take-up rate has fallen again over the last quarter to just
78.1%, compared with a year ago when 82.5% of children were vaccinated with
MMR.
Chief Medical Officer for Wales Dr Ruth Hall said,
" I realise that parents are concerned about the MMR vaccine and the unproved
allegation that the vaccine can harm some children, but it is the safest way
to protect children from measles, mumps and rubella.
" The vaccine is used successfully in over 30 countries around the world and
is the vaccine recommended by the World Health Organisation. " Measles is one
of the world's biggest killers and the recent outbreaks in the Cardiff area
demonstrate the importance of the MMR vaccine.
I would like to see a group formed that takes a " big-picture" approach to minimizing the long-term financial impact of ASD.
This group should be chartered with trying to pull individual service providers, i.e., early intervention programs, public schools, and social service departments, out of the silos in which they operate. To do this, training and funding should be provided so these groups can provide interventions BASED ON EMPIRICAL EVIDENCE OF EFFICACY.
If, for example, a study shows that an intervention has a 50% rate of " recovery," and this is the best result of any intervention studied to date, service providers should be able (if not mandated) to provide this intervention. By recovery, I mean ASD children are mainstreamed into regular classrooms by 5 or 6 years old, and a classroom observer wouldn't be able to distinguish the ASD child from the typical developing kids.
Think about the financial savings over the course of an individuals liketime. If we can " recover" 50% of ASD children, that's a huge savings over having to provide lifetime support for all of them.
With the near epidimic rise in the rate of autism, we have to look at the big picture. Fundamental changes must take place in the way school districts and ECI programs are funded and operate.
I look forward to comments on this.
Thank You,
Sean McFerren
Attachment: C:\Cost-benefit Estimates of EIBI.doc
A good way to begin may be to support Senator Clinton and Senator Collins in their new bipartisan legislation.
June 10, 2003 Clinton and Collins Announce Bipartisan
Legislation to Prevent Developmental Disabilities
Washington, DC - Today, Senator Hillary Clinton (NY) and Senator Susan M. Collins (ME) introduced the 2003 Act to Prevent Developmental Disabilities in Education. With more than 12 million children suffering from a developmental, learning, or behavioral disability, this legislation is designed to identify preventable causes and stop this growing epidemic.
" How can we expect our children to learn in the classroom if their homes are making them sick? In New York State, more than 12,000 children suffered from lead poisoning, and 9,533 of those children live in New York City. It is time for us to stand up and protect our children from threats that exist in their environment," Senator Clinton said. " In order to succeed in life, every child needs a healthy start: loving parents, quality health care and nutrition, a strong education and an environment that is free from hazards that impede their ability to reach their full potential. This legislation would help us identify links between environmental hazards and disabilities so that our children can lead healthy lives."
" Childhood lead poisoning remains the number one public health threat to children," Senator Collins said. " Despite the fact that childhood lead poisoning is entirely preventable, Maine children are at particularly high risk for lead poisoning because more than 60 percent of our state's homes were built before lead-based paint was banned in 1978. I will work with my Senate colleagues to urge passage of this legislation to ensure that every child can live in an environment free of hazards such as lead."
This legislation would require the Department of Education to coordinate with the Centers for Disease Control and Prevention to improve data collection on developmental disabilities and study possible causes of high disability rates and environmental causes. At this time, the Department of Education collects information on the prevalence of disabilities among children in schools and the Centers for Disease Control collects information on environmental toxins, but the two data systems are not coordinated. With the National Academy of Science releasing a study that says 28 percent of developmental disabilities are due to environmental cause, a strong partnership between the DCD and the Department of Education is needed to better understand the correlation between a child's ability to learn and his or her environment.
The federal and state education departments spend a staggering $43 billion each year on special education programs for individuals with developmental disabilities between three and twenty-one years of age. By coordinating these data systems, policymakers and researchers could better identify where environmental hazards may be causing developmental disabilities and target these areas for abatement. If 1% of developmental disabilities can be prevented by coordinating current efforts, then $926 million can be saved in health and special education services.
Senator Clinton and Senator Collins will fight to include this provision in the Individuals with Disabilities Education Act, which is being reauthorized by the Health, Education, Labor and Pensions Committee.
We have so much more to understand about the Autism Spectrum Disorders (ASDs), but one thing we do know is that intensive, early intervention can be very beneficial. There is no doubt that the needs of people with ASDs are complex and are often unmet and it will take coordination between many organizations and groups of people to accomplish all that we need to help each person reach their full potential. In addition to legislation that enables agencies to provide intervention services, adequate financial support is needed to implement these programs. The way our governmental agencies are set up now, particular agencies specialize in specific needs. For example, the Office of Special Education and Rehabilitative Services (http://www.ed.gov/offices/OSERS/index.html) oversees educational services for people with developmental disabilities, but state and local variations are great. In addition, programs like Early Intervention are administered by different agencies in each state (http://nectas.unc.edu/contact/ptccoord.asp). These are just examples of important programs working to address the needs of people with an ASD, but when we are looking at the needs across the lifespan, many agencies, both public and private, are involved.
At present, some significant progress has been made to increase the collaboration between different government and research organizations concerning the ASDs. In 2001, the Department of Health and Human Services (HHS) established the Interagency Autism Coordinating Committee (IACC), which is organized by the National Institutes of Health (NIH). Please see http://www.nimh.nih.gov/autismiacc/index.cfm for more information. The IACC serves as a forum to provide a more coordinated effort in addressing the needs of people with an ASD. Representatives from health, education, social services and other government agencies work together with private advocacy and research groups, such as the Autism Society of America (ASA) and Cure Autism Now (CAN), to identify the needs of people with an ASD. IACC meetings are open to the public and you can contact them directly to express your concerns.
Also, concerning research on the effectiveness of intervention for the ASDs, the National Institutes of Mental Health (NIMH) held a research meeting to evaluate the ÿffff93state of the scienceÿffff94 and has since formed working groups to make recommendations for future studies evaluating intervention. Please see http://www.nimh.nih.gov/events/autismconference.cfm for more information.
CDC Response to Postings:
I have been notified that some submissions to this online discussion platform were deleted by the UNC webmaster due to what was perceived to be inflammatory language. CDC staff were not made aware that this action had been taken, and have not seen the original remarks that were deleted from the site.
I would like to express my sincerest apologies that this was perceived as an attempt by CDC to limit discussion. I invite participants to repost any comments that may have been deleted. In the spirit of generating useful and productive dialogue, we are open to viewers expressing their questions and ideas. CDC does not have all the answers and we realize there is much more work to be done. We are committed to working with others to increase our collective understanding of the autism spectrum disorders.
I look forward to viewing questions, comments, and respectful dialogue between all participants.
Josÿffffe9 F. Cordero, MD, MPH
National Center on Birth Defects and Developmental Disabilities
Centers for Disease Control and Prevention
Food for thought:
" And we have made of ourselves living cesspools, and driven doctors to invent names for our diseases" Plato
" The significant problems we have cannot be solved at the same level of thinking with which we created them" Einstein
" Great spirits have always found violent opposition from mediocrities. The latter cannot understand it when a man does not thoughtlessly submit to hereditary prejudices but honestly and courageously uses his intelligence" Einstein
Thank You
Sincerely,
Ada Sepulveda
Dear Dr. Cordero:
Thank you for encouraging a sincere and open discussion.As a former healthcare provider (pharmacist/MPA)and mother of an autistic 4 year old, I urge you and your colleages to read our posts and take ethical action. Our children need medical treatment NOW and not just psychotropics to placate their physical and emotional pain. Our newborns need screening before there is an ASD child in every American household.WE have too many specialists, we also need generalists. It is time to revise our vaccination chemical constituents; immunization protocol; and benefit vs. risk ratio.It is time to give ASD a diagnosis code out of the psychiatric umbrella. It is time to provide accessible treatment to ALL these children regardless of genetics or socio-economic status (nutritional supplements, secretin, immune-modulators, laboratory and clinical evaluations, whatever it takes within our medical light. Only in this scenario can ABA or other educational be effective. Who knows, maybe then the children would excel in mainstream school, and we can take our time looking for the many complicated genes involved. Sometimes we are so close to the forest, we don't see the trees! (or might not want to see them). Thank You. I look forward to you being one of the strong voices speaking on behalf of our silent children.
Sincerely,
Ada Sepulveda
I am the Public Health Grand Rounds project director. Our broadcast series is supported by a partnership between the CDC and the UNC School of Public Health and strives to give communities a forum in which to discuss timely issues related to the public's health. It is my responsibility to make sure this forum is conducted in the appropriate manner. I am not a content expert on the subject of autism spectrum disorders, but I am an educator. I have removed a few entries, not for their content, but for their hostile tone, which has no educational value. As you may have noticed, others have discussed the same issues in this forum, but in a much different manner. Please be objective in your postings and remember that this is an academic based discussion.
Thank you
Thanks for your clarification. Many of us have seen a lot of important information kept from view surrounding this grave national issue. The CDC has not been above suspicion in this and this naturally makes many people more than a little frustrated.
I hope you can understand that those of us in science take offense to the practice of altering data to suit political climate and subsequently screening what is permitted to be known by the public.
Much of what we heard during the Grand Rounds presentation seemed over-rehearsed and frankly contrived. It was offensive to be listening to how we are fortunate that the level of funding has come so far, when in fact it has been and remains pitiful. The tone was almost condescending, as if we had no information and we should be somehow wowed by the insights of the participants. Many who listened were hoping for some novel information from current research or at least insight as to how to implement what we do know in concert with others to maximize successful outcomes in concrete ways.
Personally, I truly had hoped that the CDC's research would have been discussed and other research acknowledged so that some meaningful interpretation could have been explored and shared with the developmental professionals for whom the program was made available. I do hope that you might consider having " Grand Rounds" in the future that does just that. I think the idea is a good one and with more current and comprehensive content The Grand Rounds format could be a powerful tool to educate the frontline professional as well as to heal some of the growing distrust that the CDC has earned for itself.
I was interested in the discussion but cannot say that I learned anything new. However perhaps there were mentioned some resources that will be helpful. One is this discussion follow up. I coordinate a support group for parents of children with special needs. Autism and sensory integration disorder are the most common problems. THere seems to be few resources to the parents. We had a psychologist come to speak to us once who spoke about TEACH materials. WE have tried to get those, maybe get training etc. We have been unable to get the speaker back. We would like to get materials that would help parents AND our childcare team learn how to work with an autistic child. Strategies, techniques etc-specifics. Are there educational toys that would help? What training (that does not take years) is there for us to help parents?
We would like to train babysitters how to work with these children so the parents can get breaks.
Hi,
I think I would need to know a little more about your location to direct you to the most appropriate resources. I will email you and if we find something, we'll post them on the discussion forum.
Thank you
I continue to be amazed if not appalled at the editorial license some agencies take with information in this country today. I don't know why the Shapiro posts were removed but it certainly reminds me of the recent Scientific EPA report that was sequestered by the white house and edited by politicians before release in an abridged form some 9 month later. When it was released the vast majority of the Mercury discussion was missing! Hmmm.
Or the never released (until the freedom of information act was invoked) CDC Phase I VSD study on Thimerosal that showed a 2.4 Relative Risk for Autism! Or the Simpsonwood meeting documents which discussed the findings on Thimerosal in vaccines and directed the committee members to consider the information " embargoed" until a determination was made on how to 'handle' the problematic results.
My personal feeling about this " Grand Rounds" was that it was a back stroking for the good old boys. A real feel good event for them, but was totally out of touch with the realities of the families dealing with Autism at home and the concrete problems they face with their school systems and medical environments. It failed to even acknowledge the biological underpinnings of many of the symptoms developmental specialists deal with and therefore failed to encourage the development of synergistic relationships between these groups of committed professionals. Quite frankly, with very few exception, pediatricians are reluctant to make the early diagnosis and when they do they ship these kids off to psychiatrists for drugs, never to have their issues of malnutrition and basic health etc addressed. This is a travesty and I am sickened by the part that the CDC and this conference has played in promoting this negligence. I would like to suggest that someone from your " Group" attend one of the Scientific Research Conferences on the biology of ASD - Autism One leaps to mind. Professionals, clinicians and researchers alike gather to share and discuss recent discoveries, and there have been many of late. Perhaps a look at what is becoming known in the research arena would give your Grand Rounds a more comprehensive scope and promote synergistic efforts from a broader base of professioanls.
Yes, I agree with you 100%! The Shapiro posts must immediately be restored!!!
Wanda Brown
http://www.latitudes.org/forums/index.php?act=ST& f=11& t=124& s=80e336ed2cb096dae52d8db9831f7eb8
Approximately 17% of our children under the age of 18 have a developmental disability with about 2% of these being severe impairments (http://www.cdc.gov/ncbddd/dd/default.htm). In most cases, the origin of the disability is unknown and parents and providers, such as educators, physicians, etc. must painstakingly determine the needs and best course of intervention for each child. While there are some basic principles that we now about providing effective behavioral intervention for people with an ASD and specific developmental delays, we have a long way to go before we really understand the complex issues associated with the range of developmental problems that children may develop.
Continued research and intervention is needed and more groups and agencies have become focused on addressing the needs of children with an ASD. For example, there is now a Congressional Autism Caucus http://www.autismcoalition.org/ consisting of members of Congress concerned about issues related to ASDs. Private support and research organizations have made great progress in providing information and support for research to better understand causes and intervention, (see the Autism Coalition http://www.autismcoalition.org/).
A promising project that will provide a great deal of information about the health and development of a large number of children in the US is the National Childrenÿffff92s Study. This study will follow 100,000 US children from birth to age 21 looking at a wide range of exposure, developmental, and outcome measures. Please see the website for more information:
http://www.nationalchildrensstudy.gov/about/overview.cfm
Thank you for your post. However, I don't think you either did not understand my point, or wish to dance around it.
My point is that there are many children who do NOT have a diagnosis of autism whose lab work is matching up right along side that of children with " regressive autism." These children include those with various labels: learning disabled, OCD, ODD, ADHD, ADD, seizure disorder, you name it. Many of these children (my son included) are testing positive for mercury toxicity, antibodies to myelin basic protein, sky high titers to rubeola, subclinical vaccine strain measles in the gastro tract (identified in O'Leary's Dublin clinic by Taqman PCR), disordered mineral transport, dysfunctional immune responses, autoimmunity, demyelination, impaired sulfation, and more.
YOU and the majority of the pediatricians may not know where these problems are coming from, but WE most sincerely believe we do.
I do not ask you to believe me, but ask you to make a sincere effort to look into these issues for yourself, in spite of what your trade union/public relations organizations (AAP, AMA, etc.) tell you is fact. (Isn't this a little like only listening to the fox when the hen house had been raided?) The worst that can happen to you is that you'll feel you " wasted" a little time. The best is that you'll be able to sleep at night, knowing that you took the ethical route over job security.
If I can be of any help to you, please feel free to contact me.
Thank you for the clarification and for offering your assistance. Your point about not understanding the issues affecting a wide range of people is why we need more research, such as the National Children's Study and other studies on specific environmental components on children's health and development.
Before a biomedical diagnostic and intervention system becomes standard of care, it would need to be well-research to understand both the positive and negative effects for a wide range of individuals. Each individual family needs to weigh the risks and benefits of any particular treatment, and what helps one childÿffff92s symptoms may not help anotherÿffff92s. Progress in finding appropriate interventions is made by good ideas being evaluated and holding up as effectively resulting in meaningful outcomes with reasonable costs (safety, emotional, personal, financial, etc.). There are currently many possible treatments for autism that still need further evaluation and practitioners are encouraged to seek out ways to provide carefully implemented research with well-defined populations that can help build the evidence base for these interventions. There are a variety of resources available for funding, both private and public (see below).
Studies like the CADDRE and CHARGE studies are part of the process of getting to the root of the causes of ASDs by looking at environmental exposures, history of immune disorders, chronic conditions, and genetic factors, but they are only part of the base of research that is needed to more fully understand the ASDs.
Some possible resources are:
NIHÿffff92s National Center for Complementary and Alternative Medicine
http://www.nccam.nih.gov/
Department of Health and Human Services
http://www.hhs.gov/grants/index.shtml
National Alliance for Autism Research
http://www.naar.org/
Cure Autism Now
http://www.canfoundation.org/
Organization for Autism Research
http://www.researchautism.org/
Thanks you for your response. I'm sure it is difficult to field such passionate questions with the amount of poise and courtesy that you are attempting.
HOWEVER, and with all due respect, if one of these was YOUR child, I'm sure you would view this in a different light.
Valuable years have been lost, and still the government is dragging it's feet, hoping we will just go away. Credible research has been buried or scoffed at. Professional reputations have been attacked. Date proving a statistically significant link between Thimerasol and neurological damage has been hidden even from the NIH. Ridiculous " reviews" of (selected) literature gets touted in the media as reason to " put parents' minds at ease" about suspected connections between vaccines and the adjuvants and neurological damage.
When two children suddenly died this past winter here in Ann Arbor, the CDC was all over the place, trying to solve the question of just what had happened to these INDIVIDUAL children.
Why do we not see the same response to our plight? Why are we told to look with hope to the National Children's Study, when, by your own description those results will come in about 21 years?????
Our INDIVIDUAL children deserve attention RIGHT NOW! I believe that, despite the CDC/NIH's assertions that there currently is " no evidence" linking this holocaust to vaccine damage, individual scientists and physicians in these agencies are aware that there is more than enough " anecdotal evidence" to be looking at the medical condition of these children more seriously.
This IS an epidemic, and genetics play about the same role in the disaster as a red-headed child's propensity to get sunburned.
I call on you all to recognize that you have a role to play in helping us and yourselves. The stakes are much higher than anyone's career or reputation.
Do the right thing; demand some answers youselves,
Mary
As yet another citizen who pays your salaries, I want you to immediately restore the posts of Paul Shapiro that you deleted.
I intend to take this up with my congressional representatives.
Sincerely,
Mary Hirzel
The CDC NAZIS, Open Discussion My Eye
The nerve of you removing my posts because my position is not in agreement with yours. My posts brought another point of view to this discussion. You call this an opened forum.
You are all salaried with my taxes, and my positions should be respected.
Can't understand why you just didn't respond with your position and we would have an honest debate?
Paul Shapiro
Mr. Shapiro,
As a follow-up to my personal email to you, I encourage you to repost your views in a manner consistent with the academic and objective nature of this forum.
Thank you
Thimerosal in Childhood Vaccines Neurodevelopment Disorders and Heart Disease in the United States
MarkR. Geier, M.D., Ph.D. David A. Geier
http://www.jpands.org/vol8no1/geier.pdf
Abstract
In this study, we evaluated doses of mercury from thimerosal-containing childhood immunizations in comparison to US Federal Safety Guidelines and the effects of increasing doses of mercury on the incidence of neurodevelopment disorders and heart disease. This study showed that children received mercury from this source in excess of the Federal Safety Guidelines for the oral ingestion of methylmercury. Our analyses showed increasing relative risks for neurodevelopment disorders and heart
disease with increasing doses of mercury. This study provides strong epidemiological evidence for a link between mercury exposure from thimerosal-containing childhood vaccines and neurodevelopment disorders.
Introduction
Many sources now confirm an autism epidemic in the United States. The prevalence of autism has risen from one in about 2,500 children in the mid-1980s to one in about 300 children in 1996.1,2,3 Several studies report that there is an association between mercury exposure and an increased risk of heart disease.4 '5Many in the scientific/medical community have, initially, been highly skeptical that thimerosal, an ethylmercury preservative, in childhood vaccines could be associated with neurodevelopment disorders.
Thimerosal is an organic mercury compound. It is metabolized to ethylmercury and thiosalicylate and has been present since the 1930s as a preservative in many vaccines and pharmaceutical products to prevent bacterial and fungal contamination.
In 2001, the Institute of Medicine (TOM) of the US National Academy of Sciences concluded that the hypothesis that exposure to thimerosal-containing vaccines could be associated with neurodevelopment disorders is not established and rests on indirect and incomplete information, primarily from analogies with methylmercury and levels of maximum mercury exposure from vaccines given in children. They concluded that the hypothesis is biologically possible, but the possible relationship between thimerosal from vaccines and neurodevelopment disorders of autism, attention deficit/hyperactivity disorder (ADHD), and speech or language delay remained seriously suspect.7 Since the publication of the TOM report, we published the first epidemiological evidence showing a direct association between thimerosal-containing childhood vaccines and neurodevelopment disorders in children.8 We showed that there was from a 2 to 6-fold
increased incidence of neurodevelopment disorders following an additional 75-100 jig dosage of mercury from thimerosal-containing childhood vaccines in comparison to thimerosal-free childhood vaccines.
As the first part of this study, we evaluated the doses of mercury that children received from thimerosal containing vaccines, as part of the routine US childhood immunization schedule, in comparison to the US Federal Safety Guidelines for the oral ingestion of methylmercury. In 1999, the US Food and Drug Administration (FDA) determined that under the recommended childhood immunization schedule infants might be exposed to cumulative doses of ethylmercury that exceed some federal safety guidelines established for the oral ingestion ofmethylmercury.9 Secondly, in order to analyze the effects of thimerosal in vaccine recipients, we analyzed the incidence rates of neurodevelopment disorders and heart disease reported following thimerosal containing vaccines in comparison to thimerosal-free vaccines based upon analysis of the Vaccine Adverse Events Reporting System (VAERS) database. We analyzed thimerosal-containing Diphtheria-Tetanus-whole-cell-Pertussis (DTwcP) and Diphtheria-Tetanusacellular-Pertussis (DTaP) vaccines in comparison to thimerosal-free DTaP vaccines.
Finally, we analyzed data from the US Department of Education on the number of children of various ages in US schools who were reported with various types of disabilities in comparison to the mercury dose that children received from thimerosal in their childhood vaccines.
Methods EPA/FDA Exposure Limits
In this study, the amount of mercury children received as part of their routine childhood immunization schedule and the EPA and FDA maximum permissible doses for the oral ingestion of methylmercury were determined from the TOM report.7 The maximum permissible doses for the oral ingestion of methylmercury by the EPA and FDA are 0.1 jig /kg body weight/day and 0.4 jig /kg body weight/day, respectively. The average size of infants at various ages was determined from Geigy Scientific Tables.1
The VAERS Database
The incidence of neurodevelopment disorders and heart disease following thimerosal-containing DTaP and DTwcP vaccines in comparison to thimerosal-free DTaP vaccines was based upon analysis of the VAERS database, using Microsoft Access. The VAERS database is an epidemiologic database maintained by the Centers for Disease Control and Prevention (CDC) since 1990. All adverse reactions are to be reported to the VAERS database as required by US law. The CDC requires written and telephonic confirmation of serious adverse reactions and follows up these patients one year later. The FDA inquires into deaths reported to the VAERS database by contacting the patient's healthcare provider and physician. The FDA also continually monitors reports to the VAERS database to determine whether any vaccine or vaccine lot has a higher than expected incidence rate of events. The VAERS Working Group of the CDC, the FDA, and we analyze and publish epidemiologic studies based upon analysis of the VAERS database.
+ Paper continues: http://www.jpands.org/vol8no1/geier.pdf
Thank you for bringing this artical to our attention. Dr Greier is not listed in the American Board of medical specialists. And this is not one of the top journals . I will admit that makes me skeptical. How ever I have printed the artical to study in depth. We all need to keep an open mind. I am old enough that I remember the horrors of polio from my child hood. As ayoung doc I worked through a measles epidemic of 3-5000 cases . There were children with permant brain damage from measles encephalitus. Pertusis is still with us and I have had babies die from it . My hospital had a case of diptheria last year. So I also see the importance of immunizations. I personaly don't think we have the answer but will continue to study with intrest articale such as this
The argument that vaccines must be given to all children at the same age in massive doses is pure Utilitarianism (sacrifice some for the good of the majority). The United States has a strong history of protecting small groups from the dominant will of the majority (The Bill of Rights comes to mind).
If a time-spaced vaccine schedule for children genetically predisposed to adverse reactions could prevent even one case of autism and would still provide the same " herd" protection you are so quick to defend, why isn't it explored? My son went into a COMA following his two-month DTP shot, yet I was still pressured into allowing further vaccines--in those horrendous triples you all defend as necessary.
I am not opposed to vaccines. I have encouraged family members to vaccinate their children despite what happened to my son. However, the injection of a neurotoxin like mercury is COMPLETELY UNNECESSARY and should be stopped at once. The current " recommendation" to remove Thimerosal has not gone far enough. Our local pediatrician recently checked his batch of vaccines and discovered (to his surprise) that the vaccines contained mercury. It's still out there and its only purpose is to save money and its possible effect is...well, we don't know the effect. That's terrible!
A member of my family has fought for this country in every war (and " undeclared war" ) in our nation's history. I have close relatives who have earned every medal possible--in every branch of the service--except the Congressional Medal of Honor. They went in believing that our way of life is the best in the world and should be defended at all costs. I still believe that, but I'm becoming more and more suspicious of the attitude exhibited by an administration that apparently seeks to hide information from the parents of disabled children (not to mention take away their rights to public education). This is NOT a side issue. This is IMPORTANT! LISTEN TO US!!!
Dr. Noble and listmates:
I truly appreciate your emphasis on keeping on open mind. As a pharmacist and mother of an autistic 4 year old boy, I admit to relying on conventional journals for all medical information. Lately, I see medicine in a different light. It cannot be denied that immunizations have saved many lives, but we must begin to question if the benefits outweigh the price. I always read statitics on acute vaccine reactions (when reported),and never questioned their worth. But what about chronic, delayed vaccine reactions? What about measles vaccine induced encephalopathy? What about chronic mercury poisoning? What about playing with the immune system to such a degree
creating autoimmunity, overimmunity, underimmunity-immune dysfunction? What about the mutations of viruses? Look at what happened with antibiotic overuse! Look how we treated ulcers before H. pyloris! Look what happened with the Rotovirus vaccine! Look at the problems with Prevnar! etc. We need a new paradigm in medicine. We might have replaced the acute epidemic morbidity and mortality with silent, insidious, chronic diseases such as autism, ADHD, diabetes,cancer...particularly in children.
Autistic children,particularly those who suffered regression mustleave the psychiatric diagnostic umbrella and be examined biologically, biochemically, just like any patient with a disease. My son, for example, deteriorated physically before mentally: Weight loss, jaundiced, tremors,rashes, drooling, cataract-like eyes,abdominal pain and distention, constipation alternating with diarrhea etc.
Then he stopped looking, playing, answering to his name, talking etc. He became a statue in my house!!!Diagnosis: Autism by a psychologist! The neurologists have not even bothered with a routine neurological exam. My pediatrician looks at me like I have two heads!
I am convinced that this form of autism is a neuro-immune dysfuction syndrome and should be treated by a medical doctor, not a psychiatrist, under medical insurance.It is also urgent that we screen for genetic susceptibilty in all newborns before we hit them with 52 vaccines.Take out all mercury, aluminum etc. etc. We must research the gut-brain connection now. Soon we will only need special education teachers and disability checks for all our children.This is truly a national crisis that must be addressed immediately. Let's examine our affected children NOW; they will present plenty of laboratory and clinical data to begin treatment NOW. Let's focus less on epidimiological studies and examine our sick, NOT crazy children WE ARE SO CLOSE TO THE FOREST WE DON'T SEE THE TREES.Thanks.
Ada
That does NOT sound like Autism to me. He needs another neurologist to look at inborn errors of metabolism and storage disorders. Another group of profesinels who look for these metabolic diseases are genetisits. Keep looking for a diagnosis and good luck.
Dear Dr. Noble:
Thank you for your prompt response. I had an amnio, ultra high level sonograms, and fetal EKG during my pregnancy since I was 41. Everything was normal except for an inversion at chromosome 1 p11-q22. I have the same inversion. When my son was diagnosed, I went back the geneticist who said this was a normal variant in the population and had nothing to do with his autism. My son was negative for Fragile X and PKU.After the process leading to the autism abyss, I enrolled him in an ABA program. I also started the dairy-gluten free diet, and vitamin supplementation. His eye contact and reponding has improved, but he is apraxic and predominantly non-verbal. He also engages in behaviors such as hand-flapping,jumping, running if not actively engaged with someone at all times. Some testing revealed
IGG mediated food allergies and the presence of high levels of candida,clostridium,Klebsiella, and parasite (intestines). He often breaks out in rashes and gets runny nose and wheezing.He stools range from extreme constipation to foul smelling diarrhea. He suffers from excrutiating abdominal pain. My son was disqualified from a secretin study due to elevated markers for intestinal inflammation and pancreatic insufficiency! I think my son has Autistic Regressive enterocolitis.Why are we not treating this?
What triggers this and what is its connection to the brain pathology? Can you please give me ideas as to what metabolic/genetic testing I should pursue. Thank You and please keep reading our posts.
Ada,
Your post is very familiar to me. My son with ASD has many of the medical conditions you describe for your child, including the chronic gastrointestinal symptoms and significant weight loss. The good news is these medical conditions are treatable. There is more and more research findings being published on children with ASD. Too bad it isn't more readily available so all parents and physicians of children with autism are aware of it. I recommend you contact the Autism Research Insitute, 4182 Adams Avenue,
San Diego, CA 92116 Fax: (619) 563-6840. Visit ARI website at http://www.autism.com/ari/index.html to learn more about the Defeat Autism Now! (DAN!) protocol and how to seek physicians across the country who have attended many DAN! conferences, workshops and trainings. These physicians have treated many, many children with ASD. Medical treatment for ASD is not a " one size fits all" approach. Rather, an individualized treatment plan based on early, periodic screening, diagnostic and treatment services.
To help us in our quest to find proper medical care from physicians experienced in treating common medical problems found in children with ASD, I read " Children with Starving Brains A Medical Treatment Guide for Autism Spectrum Disorder - 2nd Edition by Jaquelyn McCandless, MD ISBN 188364710X at http://www.autism-rxguidebook.com/forums/. I highly recommend it!
Please feel free to email me privately should you wish to discuss this further.
Best wishes for continued healing,
Wanda
Dear Wanda,
Thank you for your willingness to help. I have a DAN doctor; I have attended several DAN conferences; and I am familiar with Dr. McCandless' book and work. I also thank you for providing crucial references to this group. I have seen great improvement in my 4 year old son since I started the DAN protocol. Unfortunately, I often fall behind with labwork and therapies due to lack of money. This is an emotional, physical, and financial stress that should not be taking place today. Many parents are not aware of treatment alternatives, since conventional medicine only offers ABA(if lucky)and psychotropic medications. They feel doomed and guilty about their genetic makeup.Others have the money, but not the knowledge. My child and many other children are suffering from a medical neuro-immune-gastrointestinal disease and require a team of neurologists,immunologists, gastroenterologist,psychologists, and educators. This cannot be delegated to teachers and psychiatrists. This form of regressive autism is permeating our neighborhoods and is a MEDICAL not a PSYCHIATRIC disorder. It should be treated by doctors via medical insurances as SUCH. After all,we treat every disease without their complete genetic understanding based on laboratory data and clinical symptomology: lupus, diabetes,cancer etc. Research money should be deducted from genetic research and epidemialogical studies and devoted to an intense medical checkup of these ASD children. Then, will get more knowledge of this medical condition than we might want to know. It is a moral obligation within the light of present information:Sighn, Wakefield,Goldberg,McCandless and many others. There are too many affected children that will need institutional settings and disability checks. This is immoral and NOT cost-effective.Medical practice should be dynamic, open-minded, and above all Ethical.Are we not overdoing it with vaccines? Are we not playing a Supreme Being role by claiming to prevent all diseases? What happened with the overuse of antibiotis? What is happening with Prevnar? What happened to Rotavirus vaccine? Where is common sense with our current vaccine protocol? Why trivalent vaccines? Why neurotoxins and contaminants being injected? Is this wise and cost-effective preventative medicine or are we creating a monster here with our " big brains," and profit-present oriented society.We are so close to the forest we don't see the trees! Thank you Wanda and other listmates. I urge the CDC to take prompt ethical action and save our children from not only autism but diabetes, cancer, etc.It's time for a new medical paradigm.
Sincerely,
Ada
Ada,
Your post is very familiar to me. My son with ASD has many of the medical conditions you describe for your child, including the chronic gastrointestinal symptoms and significant weight loss. The good news is these medical conditions are treatable. There is more and more research findings being published on children with ASD. Too bad it isn't more readily available so all parents and physicians of children with autism are aware of it. I recommend you contact the Autism Research Insitute, 4182 Adams Avenue,
San Diego, CA 92116 Fax: (619) 563-6840. Visit ARI website at http://www.autism.com/ari/index.html to learn more about the Defeat Autism Now! (DAN!) protocol and how to seek physicians across the country who have attended many DAN! conferences, workshops and trainings. These physicians have treated many, many children with ASD. Medical treatment for ASD is not a " one size fits all" approach. Rather, an individualized treatment plan based on early, periodic screening, diagnostic and treatment services.
To help us in our quest to find proper medical care from physicians experienced in treating common medical problems found in children with ASD, I read " Children with Starving Brains A Medical Treatment Guide for Autism Spectrum Disorder - 2nd Edition by Jaquelyn McCandless, MD ISBN 188364710X at http://www.autism-rxguidebook.com/forums/. I highly recommend it!
Please feel free to email me privately should you wish to discuss this further.
Best wishes for continued healing,
Wanda
I need to leave for a lecture and will only be in briefy tomorrow. I won't be back in town until Monday. If you want to e-mail me at cnoble@nomc.org We can chat at greater length
Colleen Noble
That does NOT sound like Autism to me. He needs another neurologist to look at inborn errors of metabolism and storage disorders. Another group of profesinels who look for these metabolic diseases are genetisits. Keep looking for a diagnosis and good luck.
Here is the newest paper by Dr. Mark Geier and David Geier on thimerosal and neurodevelopmental disorders... it is the lead article in the very prestigious peer-reviewed scientific/medical journal of Experimental Biology
& Medicine.
Full text article available at:
http://home.earthlink.net/~talulahbelle/Geier1.pdf or www.ebmonline.org
1: Exp Biol Med (Maywood). 2003 Jun;228(6):660-4.
Neurodevelopmental disorders after thimerosal-containing vaccines: a brief communication.
Geier MR, Geier DA.
The Genetic Centers of America, Silver Spring, Maryland 20905.
We were initially highly skeptical that differences in the concentrations of thimerosal in vaccines would have any effect on the incidence rate of neurodevelopmental disorders after childhood immunization. This study presents the first epidemiologic evidence, based upon tens of millions of doses of vaccine administered in the United States, that associates increasing thimerosal from vaccines with neurodevelopmental disorders. Specifically, an analysis of the Vaccine Adverse Events Reporting System (VAERS) database showed statistical increases in the incidence rate of autism (relative risk [RR] = 6.0), mental retardation (RR = 6.1), and speech disorders (RR = 2.2) after thimerosal-containing diphtheria, tetanus, and acellular pertussis (DTaP) vaccines in comparison with thimerosal-free DTaP vaccines. The male/female ratio indicated that autism (17) and speech disorders (2.3) were reported more in males than females after thimerosal-containing DTaP vaccines, whereas mental retardation (1.2) was more evenly reported among male and female vaccine recipients. Controls were employed to determine if biases were present in the data, but none were found. It was determined that overall adverse reactions were reported in similar-aged populations after thimerosal-containing DTaP (2.4 +/- 3.2 years old) and thimerosal-free DTaP (2.1 +/- 2.8 years old) vaccinations. Acute control adverse reactions such as deaths (RR = 1.0), vasculitis (RR = 1.2), seizures (RR = 1.6), ED visits (RR = 1.4), total adverse reactions (RR = 1.4), and gastroenteritis (RR = 1.1) were reported similarly after thimerosal-containing and thimerosal-free DTaP vaccines. An association between neurodevelopmental disorders and thimerosal-containing DTaP vaccines was found, but additional studies should be conducted to confirm and extend this study.
PMID: 12773696 [PubMed - in process]
Here is the newest paper by Dr. Mark Geier and David Geier on thimerosal and neurodevelopmental disorders... it is the lead article in the very prestigious peer-reviewed scientific/medical journal of Experimental Biology
& Medicine.
Full text article available at:
http://home.earthlink.net/~talulahbelle/Geier1.pdf or www.ebmonline.org
1: Exp Biol Med (Maywood). 2003 Jun;228(6):660-4.
Neurodevelopmental disorders after thimerosal-containing vaccines: a brief communication.
Geier MR, Geier DA.
The Genetic Centers of America, Silver Spring, Maryland 20905.
We were initially highly skeptical that differences in the concentrations of thimerosal in vaccines would have any effect on the incidence rate of neurodevelopmental disorders after childhood immunization. This study presents the first epidemiologic evidence, based upon tens of millions of doses of vaccine administered in the United States, that associates increasing thimerosal from vaccines with neurodevelopmental disorders. Specifically, an analysis of the Vaccine Adverse Events Reporting System (VAERS) database showed statistical increases in the incidence rate of autism (relative risk [RR] = 6.0), mental retardation (RR = 6.1), and speech disorders (RR = 2.2) after thimerosal-containing diphtheria, tetanus, and acellular pertussis (DTaP) vaccines in comparison with thimerosal-free DTaP vaccines. The male/female ratio indicated that autism (17) and speech disorders (2.3) were reported more in males than females after thimerosal-containing DTaP vaccines, whereas mental retardation (1.2) was more evenly reported among male and female vaccine recipients. Controls were employed to determine if biases were present in the data, but none were found. It was determined that overall adverse reactions were reported in similar-aged populations after thimerosal-containing DTaP (2.4 +/- 3.2 years old) and thimerosal-free DTaP (2.1 +/- 2.8 years old) vaccinations. Acute control adverse reactions such as deaths (RR = 1.0), vasculitis (RR = 1.2), seizures (RR = 1.6), ED visits (RR = 1.4), total adverse reactions (RR = 1.4), and gastroenteritis (RR = 1.1) were reported similarly after thimerosal-containing and thimerosal-free DTaP vaccines. An association between neurodevelopmental disorders and thimerosal-containing DTaP vaccines was found, but additional studies should be conducted to confirm and extend this study.
PMID: 12773696 [PubMed - in process]
Conservative estimates for the current incidence of autism at about 1 in 500 births make autism at least 10 times more common than cystic fibrosis and childhood cancer, yet research funding for autism is a tiny fraction of these other well publicized diseases. Why does the NIH and CDC still consider autism a low priority?
Federal agencies, such as CDC and NIH receive money as appropriated by Congress. As part of our governmental system, Congress is charged with using the taxpayerÿffff92s money in ways that reflect the needs and concerns of the people they represent. In the case of CDC, the National Center on Birth Defects and Developmental Disabilities was established in 2001 by the Childrenÿffff92s Health Act of 2000. The creation of a specific center to address the public health concerns of people with disabilities represented major progress in building our national capacity to understand these conditions and respond to promote the health of all individuals. CDCÿffff92s autism funding has grown from just over $1 million in 2000 to almost $11 million in FY2003. As a result of this, CDC has been able to support more comprehensive efforts in the areas of monitoring and research into early risk factors. CDC currently supports 5 Centers of Excellence in Autism and Developmental Disabilities Research and Epidemiology, 7 states to participate in the Autism and Developmental Disabilities Monitoring Network, and conducts its own model tracking and research program in Atlanta. The programmatic and funding history of autism demonstrates an increase in these activities, largely a reflection of the growing public awareness about this condition and concerns over the fact that more people in the autism spectrum are being identified today.
While it would be ideal to have a well-funded, already-established monitoring and research system for disabilities and child health, in general, that could quickly respond to questions about the ASDs, building this system in the US will take the support and interest of many people and agencies. CDC is concerned with the health of the public, and our country and world are currently in an era where globalization and preventing the spread of new infectious diseases, such as SARS, monkeypox, and others, as well as concerns about bioterrorism, make the distribution of funding a challenge.
While the response and results have not always been satisfactory to everyone, CDC is committed to working with others to address the public health issues related to the ASDs. For example, it is important to understand the true magnitude of the number of people with an ASD, so that service providers can plan appropriately. Given current estimates of 2-6 people per 1,000 having an ASD, it is important to plan accordingly. Continued research and intervention is needed and more groups and agencies have become focused on addressing the needs of children with an ASD. For example, the Interagency Autism Coordinating Committee (IACC), which is organized by the National Institutes of Health (NIH) has been established to improve coordination of autism research efforts (please see http://www.nimh.nih.gov/autismiacc/index.cfm for more information). In addition,
there is now a Congressional Autism Caucus (http://www.autismcoalition.org/caucus.asp) consisting of members of Congress concerned about issues related to ASDs. Private support and research organizations have made great progress in providing information and support for research to better understand causes and intervention, (see the Autism Coalition http://www.autismcoalition.org/).
Prevalence rates are much lower than 1 in 500 -- its more like 1 in 150 (or lower)!
Dr. Eric Fombonne, Epidemiologist, AMA The Journal Editorial 1/1/03
[This is an editorial in THE JOURNAL By Eric Fombonne, MD. Dr. Fombonne is a well known epidemiologist. The Jounal is published by the American Medical Association. This article and the next is about the Altanta Study on the prevalence of autism. The report, Prevalence of Autism in a US
Metropolitan Area, by Marshalyn Yeargin-Allsopp, MD, Catherine Rice, PhD, Tanya Karapurkar, MPH, Nancy Doernberg, Coleen Boyle, PhD, Catherine Murphy, MPH
~2OO3 American Medical Association. All rights reserved. (Reprinted) JAMA, January 1, 2003-Vol 289, No. 1 49, can be downloaded at http://www.freewebz.com/schafer/autismatlanta.pdf.
Thanks to Beth Clay and the Schafer Autism Newsletter.]
The number of epidemiological studies of autism has increased in recent years, including in the United States, where investigators are now catching up in what has traditionally been a weak area of child psychiatric
research in North America. In this issue of THE JOURNAL, Yeargin-Allsopp et al1 report the findings of a survey, which was funded by the Centers for Disease Control and Prevention, that found a rate of 34 per 10,000 for
autism spectrum disorders (ASDs) among 3- to 10-year-old children in metropolitan Atlanta. The strengths of the survey include use of multiple ascertainment sources and large sample size (ie, 987 confirmed ASD cases compared with a median sample size of 50 in 32 previous studies),2 thereby allowing the authors to have good precision in the estimates and to conduct meaningful subgroup analyses. In addition, this study is the first to derive a robust
population-based estimate for the rate of ASD in black children, which is comparable to other racial groups.
Other findings are typical of those found in previous surveys with ASD cases, with a strong overrepresentation of boys, cognitive impairments in more than two thirds of cases, and a relatively high rate (8%) of epilepsy.
Approximately 18% of the sample did not have a previous diagnosis or were not suspected of having ASD, and children from black, younger, or less educated mothers were more often identified through schools as the only source of case finding. These findings highlight the need to rely on
multiple ascertainment sources in epidemiological studies of ASD and caution against findings that are based on single service provider databases. The prevalence rate of 34 per 10,000 is, however, likely to be an underestimate. First, as the authors point out, children with milder or
high-functioning (ie, normal IQ) ASD subtypes are likely to have been missed. Second, the lower prevalence in 3- and 4-year-olds may reflect lower sensitivity of case identification among younger children for developmental
disorders that often are diagnosed later. Third, there was an unexpected decrease in prevalence among 9- and 10-year-olds. Although it would be tempting to interpret this age trend as indicative of a secular increase in the rate of ASD (ie, the younger the birth cohort, the higher the
prevalence), such an explanation is both unlikely and biologically implausible because rates plateaued for birth cohorts aged 5 through 8. Rather, the authors suggest that these differences might reflect new diagnostic criteria for autism and increased availability of developmental
disability services for children with autism in the 1990s. What this means, however, is that the rate of 41 to 45 in 10,000 obtained for the 5- to 8-year-olds might be more accurate. This rate also is more in line with those of 3 recent surveys that yielded prevalence estimates in the range of 60 per 10 000.3-5 High prevalence rates from more recent epidemiological surveys have fueled the debate about a possible epidemic of autism. However, 4 separate
issues need to be addressed. The first issue concerns the best current estimate for the prevalence of autism and related disorders. Increasing and consistent evidence from recent surveys shows that the prevalence rate for
ASDs (including not only autism disorder but also Asperger disorder and pervasive developmental disorder-not otherwise specified) is approximately 60 per 10 0003-5; the study results from Yeargin-Allsopp et al concur with this conclusion. This estimate translates to approximately 425,000 children younger than age 18 years with ASDs in the United States, including 114,000 children younger than 5 years.
The second issue is whether the prevalence of ASD has increased over time. Surveys conducted in the 1960s and 1970s only dealt with autism disorder (as opposed to ASD) and with a rather narrow definition of autism, as per Kanner's descriptions,6 and not accounting for autism occurring in subjects who are not mentally retarded. Thus, comparisons of rates over time generally deal with studies that have used different case definitions, making interpretation of time trends difficult. The closest estimate of ASD prevalence available in the late 1970s was 20 per 10 000 in a survey from the United Kingdom that was limited to the severely impaired children with ASD.7 Comparing rates for subtypes of ASD provide another avenue for estimation over time especially for autism disorder, but as shown by Yeargin-Allsopp et al1 and other surveys,3-5 the breakdown in ASD subtypes is not always reliable. Nevertheless, rates of autism disorder in recent surveys have consistently been more than 10 per 10 000 whereas previous prevalence estimates ranged from 4 to 5 in 10 000.2 Therefore, from the available evidence it can be concluded that recent rates for both ASD and autism disorder are 3 to 4 times higher than 30 years ago.
The third issue addresses possible interpretations of this increase in prevalence. That is, does this increase reflect a broadening of the concept of ASD with more inclusive diagnostic criteria and improved methods of case finding in population surveys? It is generally agreed that the definition of autism has been broadened over the last decades, particularly at the less severe end of the spectrum. These major changes occurred in nosology from
the Diagnostic and Statistical Manual of Mental Disorders, Third Edition (DSM-III)8 in 1980 to the DSM-Revised Third Edition9 in 1987 and the DSM, Fourth Edition10 in 1994. Kanner's infantile autism6 was replaced in 1980 by
the concept of pervasive developmental disorder. Among the pervasive developmental disorders, pervasive developmental disorder-not otherwise specified (or atypical autism) has now become the most widely used ASD diagnosis, and Asperger disorder emerged as a new diagnostic category in the 1990s. Unless comparisons also control rigorously for changing case
definitions, interpretation of differences in prevalence rates over time and across surveys will be virtually impossible. Moreover, there is strong evidence that differences in methods for case finding can account for a huge proportion of the variability of prevalence estimates between surveys. For example, in 4 US and 4 UK studies
published recently, 14- and 6-fold variations in prevalence rates were found, respectively.2 Although these 2 sets of studies were conducted at the same time, in similar age groups, and in the same countries, the lack of
consistency in estimates is striking and demonstrates how unique design features within each study can affect the prevalence estimation. In both countries, studies relying on single administrative sources for identifying cases yielded low estimates, whereas investigations using proactive methods for case finding, that is, multiple sources of ascertainment and direct diagnostic procedures, yielded much higher rates. Needless to say, comparisons of population surveys over time are bound to be even more
confounded by factors difficult to control. Referral statistics also have been used to evaluate trends over time,
but these data are confounded by changes over time in factors such as referral patterns, availability of services, public and professional awareness, age at diagnosis, and diagnostic concepts and practices. For
example, the report from the Department of Developmental Services, Sacramento, Calif,11 showed an increase in the number of children receiving public services, but it failed to adjust for key factors, such as changes in population size, diagnostic practices, or differential migration.12 Another widely publicized report on children enrolled in this public service system concluded that " some, if not all, of the observed increase represents a true increase in cases of autism in California." 13(p42) Yet, the authors stated earlier in this report that " Improved case finding could result in an apparent increase in the number of cases. . . . This study does not examine the extent to which differences in case finding over time have resulted in
any changes in the number of autistic children who present to the Regional Centers." 13(p13) By contrast, a recent reanalysis of this dataset indicated that during 1987 to 1994, diagnostic substitution occurred; thus, while the prevalence of autism increased from 5.8 to 14.9 per 10 000, the prevalence for mental retardation decreased from 28.8 to 19.5 per 10 000. These trends then cancel each other.14 According to the authors, new federal legislation (Individuals with Disabilities Education Act15) mandating that states provide early intervention programs for toddlers with developmental delays played a role in the increasing use of the diagnosis of autism. Moreover, in the last 15 years evidence has accumulated for the effectiveness of early intensive behavioral interventions for autism,16 and most families could not support their high costs outside the public service delivery system. Thus, there is good evidence to support that higher prevalence rates reflect changes in diagnostic practices, improved identification and availability of services,
and other similar factors. The fourth issue involves the hypothesis of an increasing trend in the incidence of ASD. Whereas evidence exists that a substantial part of the
increase in prevalence is due to methodological factors, the additional possibility of a secular increase in the incidence of autism cannot be ruled out. Unfortunately, most available epidemiological data are derived from
prevalence surveys, and the few studies that provide incidence rate estimates have not been adequate to test this hypothesis. In addition, no strong candidate environmental exposures have been identified. Claims of an
association with measles-mumps-rubella immunization have not been borne out by recent studies,17-19 and evidence for causal association with other exposures, such as mercury-containing vaccines, is weak.20, 21 Extending the already substantial research effort, the Centers for Disease Control and Prevention has recently funded a surveillance network across several states.22 This and other initiatives should help address more directly hypotheses about secular changes in the incidence of ASDs. Finally, the current social context seems to exert a stronger influence on the debate than the scientific arguments. Although claims about
an epidemic of autism and about its putative causes have the most weak empirical support, the subsequent controversy has put autism on the public agenda. In recent years, children with autism, their families, and professionals involved in their care and in research have seen welcome and
legitimate increases in public funding. Yet, ironically, what has triggered substantial social policy changes in autism appears to have little connection with the state of the science. Whether this will continue to be the case in the future remains to be seen, but further consideration should be given to how and to why the least evidence-based claims have achieved such impressive changes in funding policy.
Author/Article Information
Author Affiliation: McGill University and Montreal Children's Hospital, Montreal, Quebec.
Corresponding Author and Reprints: Eric Fombonne, Montreal Children's Hospital, 4018 St Catherine W, Montreal, Quebec, Canada (e-mail: eric.fombonne@mcgill.ca). Editorials represent the opinions of the authors and THE JOURNAL and not those of the American Medical Association.
References
1. Yeargin-Allsopp M, Rice C, Karapurkan T, Doernberg N, Boyle C, Murphy C. Prevalence of autism in a US metropolitan area. JAMA. 2003;289:49-55.
2. Fombonne E. Epidemiological trends in rates of autism.
Mol Psychiatry. 2002;7(suppl 2): S4-S6.
3. Baird G, Chairman T, Baron-Cohen S, et al.
A screening instrument for autism at 18 months of age: a 6 year follow-up study. J Am Acad Child Adolesc Psychiatry. 2000;39:694-702.
4. Chakrabarti S, Fombonne E. Pervasive developmental disorders in preschool children. JAMA. 2001;285:3093-3099.
5. Bertrand J, Mars A, Boyle C, Bove F, Yeargin-Allsopp M, Decoufle P. Prevalence of autism in a United States population: the Brick Township, New Jersey, investigation.
Pediatrics. 2001;108:1155-1161. MEDLINE
6. Kanner L. Autistic disturbances of affective contact.
Nervous Child. 1943;2:217-250.
7. Wing L, Gould J.
Severe impairments of social interactions and associated abnormalities in children: epidemiology and classification. J Autism Dev Disord. March 9, 1979:11-29.
8. American Psychiatric Association.
Diagnostic and Statistical Manual of Mental Disorders, Third Edition. Washington, DC: American Psychiatric Association; 1980.
9. American Psychiatric Association.
Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition. Washington, DC: American Psychiatric Association; 1987.
10. American Psychiatric Association.
Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. Washington, DC: American Psychiatric Association; 1994.
11. Department of Developmental Services.
Changes in the population of persons with autism and pervasive developmental disorders in California's Developmental Services System: 1987 through 1998.
Report to the Legislature March 1, 1999:1-19. Available at:
http://www.dds.ca.gov:1999. Accessed December 11, 2003.
12. Fombonne E. Is there an epidemic of autism?
Pediatrics. 2001;107:411-413.
13. Report to the Legislature on the Principal Findings from the Epidemiology of Autism in California.
A Comprehensive Pilot Study.
Davis, Ca: M.I.N.D. Institute, University of California, Davis; October 17, 2002.
14. Croen LA, Grether JK, Hoogstrate J, Selvin S.
The changing prevalence of autism in California.
J Autism Dev Disord. 2002;32:207-215.
15. The Education for All Handicapped Children Act of 1975.
Pub L No. 94-145, 20 USC 1401 et seq. Federal Register. August 23, 1977; 42(163):42474-42518.
16. Rogers S.
Empirically supported comprehensive treatments for young children with autism. J Clin Child Psychol. 1998;27:168-179.
17. Fombonne E, Chakrabarti S.
No evidence for a new variant of measles-mumps-rubella-induced autism. Pediatrics. 2001;108:E58.
18. Madsen KM, Hviid A, Vestergaard M, et al.
A population-based study of measles, mumps, and rubella vaccination and autism.
N Engl J Med. 2002;347:1477-1482.
19. Taylor B, Miller E, Lingam R, Andrews N, Simmons A, Stowe J. Measles, mumps, and rubella vaccination and bowel problems or developmental regression in children with autism: population study. BMJ. 2002;324:393-396.
20. Stratton K, ed, Gable A, ed, McCormick MC, ed.
Immunization Safety Review Committee: Thimerosal-Containing Vaccines and Neurodevelopmental Disorders. Washington, DC: National Academies, Institute of Medicine; 2001.
21. Pichichero ME, Cernichiari E, Lopreiato J, Treanor J.
Mercury concentrations and metabolism in infants receiving vaccines containing thiomersal: a descriptive study. Lancet.
2002;360:1737-1741.
22. Centers for Disease Control and Prevention, National Center on Birth Defects and Developmental Disabilities, Autism and Developmental Disabilities Monitoring Network.
Available at: http://www.cdc.gov/ncbddd/dd/aic/states/default.htm#addm.
Accessed December 10, 2002.
Sadly, the research dollars spent to examine the efficacy of different treatment approaches for autism is even lower. As a parent, I am, of course, interested in the cause of autism. But, as the parent of a young child with autism who responded very well to intensive ABA, I am appalled at the lack of funding for studies regarding variations of ABA, SSRIs, etc. We have an epidemic on our hands and we're spending almost all of the precious little research money we have trying to identify the genes alone. We definitely need a LOT more research money and we need to earmark a certain percentage to help determine the parameters and efficacy of treatment approaches.
What about detoxing, and healing leaky gut? Necessary Nutrients cannot get to the brain if the food is not digested properly...heavy metals affect every system in hte body including digestion.
I believe these help more than most...then re-training with ABA, sensory training, etc.
Most people would be amazed to know that the autistic child hears, understands, and remembers most of what is being said to them, even though they may look totally oblivious.
Brick Township, N.J. has a rate of 7 autistic children per 1000 .There is also a high rate of childhood leukemia in girls in that area, so I've been told. Has anyone researched a possible connection ? What is the rate of autism found in families who have been vacationing close to the Atlantic Ocean in New Jersey for generations ? I know of three cases,three different families, within one block , one block from the ocean in Ocean County.
In 1998, CDC partnered with the Agency for Toxic Substances and Disease Registries (ATSDR) to investigate the prevalence of the ASDs in Brick Townhsip, NJ in Ocean County. While CDC found the rate of ASDs to be higher than previous studies in the US, the rates were similar to recent studies in other countries looking at the entire spectrum of autism conditions. ATSDRÿffff92s environmental analysis did not identify any connections between the exposures studied in the community as impacting the rates of ASDs. You can read more about the findings at: http://www.cdc.gov/ncbddd/dd/aic/cdc/default.htm#brick
In an effort to get additional data on the rates of ASDs in Ocean County, CDC has partnered with researchers at the University of Medicine and Dentistry in Newark to examine the prevalence of ASDs. The project is currently collecting data in 4 NJ counties, including Ocean County. You can get more information about the status of this project at the website and by contacting the Principal Investigator listed below:
http://www.cdc.gov/ncbddd/dd/aic/states/nj.htm
Walter M. Zahorodny, Ph.D.
New Jersey Medical School
185 South Orange Avenue, Room F 511
Newark, NJ
Phone: 888-699-8038.
Email: autism@umdnj.edu
I work at a preschool for children with special needs in Southern California, and as a part of our program for children with autism, we use a " sensory diet" . The Occupational Therapist designs programs for the children based on their sensory needs... sensory integration. We find that many of the children respond well to using deep pressure (proprioceptive), tactile stimulation, and vestibular motions such as swinging. Does anyone else use such programs for helping to regulate behaviors in children with autism?
Sensory integration is a common technique used by many occupational therapists as part of an intervention program for people with an ASD. There are many variations on how sensory integration is used. Although it is commonly used, there is not a great deal of research on this topic. You can find out more about using occupational therapy techniques, including sensory integration, by contacting the following organizations or research institutions:
The American Occupational Therapy Association
http://www.aota.org/
National Board for Certification in Occupational Therapy
http://www.nbcot.org/nbcot/scripts/state_reg/reg_entities.asp
UNC-Chapel Hill ÿffff96 Division of Occupational Science
http://www.alliedhealth.unc.edu/ocsci/
I am not a teacher, but a parent of a 12 yo non-verbal autistic boy. We are in West-Central FL He gained alot from the sensory diet, as a matter of fact his therapist was able to get a couple of words out of him while swinging, bouncing, etc. Unfortunately for us,this therapist has become full-time Mommy. The therapist that has him now says he stimms too much on it. ... I use deep pressure, joint compression, etc. which calms him. He thoroughly enjoys it and signs for more. KEEP using it!
I have a niece that's autistic and is having a hard time in public school. The school district disagrees that she should be placed in a non-public school. My niece is high functioning and in a regular classroom with an assistant. She will now be starting Jr. High School. The problem is that she has a hard time with changes and adapting to her new environment and people. We feel the school has failed her because she is not being taught any social skills and she comes home crying because she can't understand why the other kids don't want to be her friend. During recess and lunch time she just hangs out by herself or following her assitant around the yard. She isn't being encouraged to socialize and therefore, continues to have some inappropriate skills. The other problem is that my sister hasn't explained to her that she is autistic. How can we explain. Please help.
Explaining to a child that he or she has an ASD is a hard decision each family has to make. Some children will understand the concept better than others. It can be helpful for parents to consult the childÿffff92s intervention team or others who know the child well. For parentsÿffff92 comments on telling a child he or she has an ASD, try the following website:
http://www.bbbautism.com/pros_and_cons_plaintext.htm
For information concerning the Individualized Education Program (IEP), which is the document written jointly between parents and school personnel detailing goals, placement, etc. for children receiving Special Education Services, the following websites may be helpful.
Office of Special Education and Rehabilitative Services
U.S. Department of Education
http://www.ed.gov/offices/OSERS/OSEP/Products/IEP_Guide/
National Information Center for Children and Youth with Disabilities
http://www.nichcy.org/
Books for parents and educators of children with ASDs on many subjects ÿffff96 including teaching social skills, Middle School, and teaching strategies - can be found at many sites, including the Autism Asperger Publishing Company website: http://www.asperger.net/bookstore_aapc.htm
Any child with a disability is entitled to a free and APPROPRIATE education. I just had a 4 month battle with the public school system to get my non-verbal autistic son into a private school where he is doing much better. The school is required to pay for this private school because the public school could not provide an appropriate education.
My state(FL) has scholarships to help pay for private schools if the public schools are not appropriate. He is eligible for this next year. The public school system does not want anyone to take their child out of the system because the school get government money$$$$$$ for each child...just like everything else...it's all about $$$$$!
I have a niece that's autistic and is having a hard time in public school. The school district disagrees that she should be placed in a non-public school. My niece is high functioning and in a regular classroom with an assistant. She will now be starting Jr. High School. The problem is that she has a hard time with changes and adapting to her new environment and people. We feel the school has failed her because she is not being taught any social skills and she comes home crying because she can't understand why the other kids don't want to be her friend. During recess and lunch time she just hangs out by herself or following her assitant around the yard. She isn't being encouraged to socialize and therefore, continues to have some inappropriate skills. The other problem is that my sister hasn't explained to her that she is autistic. How can we explain. Please help.
Two things come to mind as I read your message. Our 10 year old has a program at school called " Circle of Friends" which was established by the school social worker. Initially she discussed with the class our daughter's disabilities in a manner which was understandable to the grade level and with an emphasis on kindness and understanding. Then she took volunteers for the " Circle" in which this rotating group of participants would gather in her office and do things that friends do - look at family photos, listen to a cd, talk about pets, whatever was of general interest.
Our daughter's in-class aide is overwhelmed with the response and the change, in not only our daughter, but in the maturation and kindness of her classmates. There are still strides to be made, but this seems to have gone a long way in reaching out to the class mates and easing a pathway to friendships.
Secondly, regarding discussions with the child regarding their condition, I attended a seminar at which Temple Grandin spoke. One of the questions posed to her was the manner and timing of this type of conversation with the child. It is important for self awareness for the child to understand what is happening to them and to give them a means for helping themselves. I observe many instances of my daughter taking in situations, where she is obviously trying to understand the social dynamic. I think that you would be doing a child a favor to discuss these instances in a manner which is suited to their level of understanding and with the goal of giving them a way to interpret and grow past these diffulties.
I would be happy to discuss any of this further if you wish. You may contact my email if you or your family think it would be of value to you.
Kind regards-
Despite the fact that Autism has risen in direct correlation to the increase in thimerasol in vaccines and the MMR shot, the CDC and pharmacuetical companies continue to play this down and try to discredit this theory as crackpot.
If a tire manafacturer had introduced a new ingredient in it's manufacturing process and tire failures had increased at the same rate as Autism has, resulting in accidents and injuries, but there was no proof it was the new ingredient. Would the NTSB sit on the fence or launch an investigation and recall all suspect products. Would the press be covering it on the front pages. Would consumer groups be calling for blood and revenge.
food for thought.
Ok then how come not all the children who has recieved MMR shots between a certian time period been dx with ASD? I wonder this because I have two children and one is PDD/NOS (atypical autism) and the other is " typical" ?? Please enlighten me ?
certain children have a predisposition and can't tolerate the mercury or have a weakened immune system that is not able to excrete it as a typical child does. The mercury builds up in the organs and brain and does the damage. The MMR shot just pushes them over the edge (live measles virus has been found in the gut of Autistic children).
Our son developed totaly normal until the MMR shot two days after his first birthday. Two weeks after the MMR he had regressed into Autism. We have video of him on his bithday and two weeks after which shows two completely different children.
Just a coincidence?
See that is what bothers me .. some kids start showing signs of autism at that age. My daughter I knew at 6mths old that she was different from every other child I saw. But she never was sick, never had a fever with her shots. Including the MMR shots. She didn't even have an ear infection until she was 5. Now granted by age two when she wasnt talking I was yelling at her Ped. for help. But I can't it was her shots that cause the problems. I think there are more things we have to discover about Autism before we can point the finger at one certain thing.
Once again I agree with Joyce. Although there was a change in my son's personality around age 2, all the signs of asperger's (unfortunately this is in hindsight) were there from the very beginning.
That is what makes autism such an enigma. My son developed totally normal with ALL milestones reached and we have video that clearly demonstrates this. Yet within two weeks of the MMR shot he has clearly regressed into autism.
Contrary to the panel's statement about no credible autism/vaccine research link, read this article and the abstract below. Thanks to the wonderful Schafer Autism Newsletter (Delivered Fresh Daily to Your Emailbox). To Subscribe http://home.sprynet.com/~schafer/ Or mailto: subs@doitnow.com. No Cost! Every parent loving and living with autism(and professionals) should subscribe!
Wanda Brown
New Study Shows MMR/Autism Link
[From Autism Research Campaign For Health 23 June 2003. See referenced abstract below " Elevated levels of measles antibodies in children with autism" by Vijendra K. Singh PhD*, and Ryan L. Jensen BS.]
A new study, published in Pediatric Neurology, Vol. 28, No. 4, is expected to show that MMR and autism are linked, despite the denials of the UK Department of Health and the recent court judgement that ordered two
girls to receive the controversial MMR vaccine.
World-renowned autism researcher Dr. Vijendra Singh, at the Utah State University, and fellow-researcher Ryan Jensen have announced that their latest study," Elevated Levels of Measles Antibodies in Children with Autism" , points directly to an MMR/autism link.
Singh and Jensen analysed samples from 52 autistic children, all of whom had had the MMR vaccination, and 30 normal children, plus a further 15 siblings of autistic children.
They showed that measles antibody levels, a sign of an immune reaction to measles virus, were significantly greater in children with autism compared with the non-autistic children. Levels of mumps and rubella antibodies were not different from the non-autistic children.
Strikingly, they found that 43 out of the 52 (83%) of the autistic children had antibodies to the measles vaccine virus. None of the 30 normal children, and none of the 15 siblings, had these antibodies.
Singh and Jensen have concluded that the antibody results show that many autistic children have suffered an abnormal response to the measles element of the MMR vaccine, causing them to develop " inappropriate"
antibodies.
Singh and Jensen were testing a hypothesis that, as viruses are common trigger agents for autoimmune diseases, where the human body attacks itself, then autism could involve a virus-induced autoimmune response, in turn
leading to autism.
The study looked at 88 autistic children, all of whom had a firm diagnosis of autism. Not all children were tested for all the three viruses, of measles, mumps or rubella. In those children tested, the level of mumps
or rubella antibodies did not attain statistical significance, leaving the researchers to focus upon the measles element of MMR. None of the autistic children had any history of measles rash or wild-type natural measles
infection.
This points to the source of the measles antibody as being vaccine strain. The researchers are undertaking further study work on this crucial aspect.
If the new research by Singh and Jensen is correct, then it backs up the claims of many families who have reported that their children became autistic after MMR. It also confirms the validity of the1998 study by Dr.
Andrew Wakefield and other researchers in the UK, and a number of other studies published since that time.
Over 1,000 cases of autism following MMR are being brought before the High Court in London in April 2004. If the claims are upheld, it will have dramatic implications for vaccine policy worldwide, and will throw a spotlight on the way vaccines are licensed and regulated.
Background
ARCH - Autism Research Campaign for Health - is a group of parents campaigning for more research into the causes and treatment of autism. It was set up in response to the departure of Dr Andrew Wakefield from the
Royal Free Hospital - which ARCH viewed as a sign that medical scientists were no longer free to follow their own lines of enquiry. We are profoundly worried that medical science is now dictated by government, the medical
establishment and the pharmaceutical industry who between them control the vast sums of research money and determine which topics are legitimate research and which are not. This state of affairs is unacceptable to the growing number of children and parents who must live with the painful
consequences of autism, and with the lack of research into the alarming increase in the prevalence of autism in many countries across the world.
ARCH believes that there is mounting evidence that suggests MMR is unsafe. It calls on the UK Government to fund clinical research into the effects of MMR vaccine on the immune system of autistic children and its role in the onset of regressive autism, epilepsy and bowel disease.
Visit ARCH on http://www.autism-arch.org
Elevated Levels Of Measles Antibodies In Children With Autism
Abstract
http://www.sciencedirect.com/science?_ob=ArticleURL& _udi=B6TBD-481FFJP-3& _us
er=1940244& _handle=W-WA-A-A-DW-MsSAYVA-UUA-AUCZVVWUWA-AAWEDVBCU-DW-U& _fmt=su
mmary& _coverDate=02%2F27%2F2003& _rdoc=51& _orig=browse& _srch=%23toc%235140%23
9999%23999999999%2399999!& _cdi=5140& view=c& _acct=C000050221& _version=1& _urlV
ersion=0& _userid=1940244& md5=f765897a42a589a5efa9d1a803d03145
Vijendra K. Singh PhD*, and Ryan L. Jensen BS Department of Biology & Biotechnology Center, Utah State University, Logan, Utah, USA
Virus-induced autoimmunity may play a causal role in autism. To examine the etiological link of viruses in this brain disorder, we conducted a serological study of measles virus, mumps virus, and rubella virus. Viral antibodies were measured by enzyme-linked immunosorbent assay in the serum of autistic children, normal children, and siblings of autistic children.
The level of measles antibody, but not mumps or rubella antibodies, was significantly higher in autistic children as compared to normal children (p = .003) or siblings of autistic children (p [less than or equal to]
.0001). Furthermore, immunoblotting of measles vaccine virus showed that the antibody was directed against a protein of approximately 74 kd molecular weight.
The antibody to this antigen was found in 83% of autistic children but not in normal children or siblings of autistic children. Thus autistic children have a hyper-immune response to measles virus, which in the absence
of a wild-type measles infection might be a sign of an abnormal immune reaction to the vaccine strain or virus reactivation.
Author Keywords: Autism; measles virus; vaccine; viral antibodies; mumps virus; rubella virus
Corresponding author. Correspondence should be addressed to: Dr. Singh; Biotechnology Center; Utah State University; 4700 Old Main Hill, Logan, Utah, 84322, USA.
Having heard similiar stories from other people, what I'm wondering is autism too much of a catch-all.
Should we be looking at the kids born with autistic-type behavior differently than the kids who suffered some trauma that led to autistic-type behavior?
I also was treated like a moron when I was addressing my daughters Developments and Concerns, but not After MMR, after her DTAP shot when she had extremly high fever of 105.5 and had to be taken to the hospital and treated. I had not idea about thimersal in the Vaccines. But I do know that after that my daughter lost eye contact, started thrashing her body during feeding, her head stopped growing for 10 months, started Toe walking and hand flapping. My pediatrician kept telling me dont worry. Well I did and Im doing something about it as should everyone else. I dont believe that its one particular vaccination that would cause autism, but the bodies tollerance to a certain amount of Mercury. Some people can tollerate it and others cant. Hense people coming down with ALZHEIMERS later in life. CONNECTION CONNECTION CONNECTION
I had to reply to this. My son went into a COMA and was hospitalized for 3 days following the DTP (didn't have the a-cellular version back then). He developed PDD, then overcame his autistic traits through intensive ABA therapy. I don't think vaccines are the only answer, but I think the mercury issue warrants further investigation. Thankfully, Congressman Dan Burton is committed to this issue.
No not at all. We should all be attempting the same goal, that is to find the cause and cure for autism and support all of those affected by it.
Whether or not the autism is regressive or was not, makes no difference in my eyes. We all have a role to play and suffer in exactly the same manner.
Are there any surveillance systems or population-based studies that are collecting data on the use of major antipsychotics such as risperdone among adults with autism? Any estimates of the prevalence of the use of these medications among adults with autism? Any systems for collecting data on undesirable or harmful effects of these drugs? Any data measuring the efficacy of these medications for decreasing aggressive or self-injurious behavior?
The use of medications to treat the ASDs is used to treat particular symptoms under the guidance of a physician, and does not represent a complete intervention program.
The Food and Drug Administration (FDA) regulates and licenses the use of drugs and other biologic therapeutic supplements and there is a reporting system for adverse reactions. Information on the FDA reporting system for adverse events related to approved drugs can be found at:
http://www.fda.gov/cder/aers/default.htm
There is not an ongoing monitoring system set up to track the use of specific drugs in adults with an ASD; however, some studies have been done. You can find them by searching under ÿffff93autism and antipsychoticsÿffff94 at www.pubmed.org. Please see the abstract below for a summary of one study of medication use in adults with an ASD. Managed care companies or HMOs may have data on both diagnoses and treatments used by patients.
The Metropolitan Atlanta Developmental Disabilities Surveillance Program (MADDSP) is an ongoing monitoring system for multiple developmental disabilities and data currently being collected includes the prevalence of the ASDs and reported use of stimulant medications in 8 year olds in metropolitan Atlanta (http://www.cdc.gov/ncbddd/dd/ddsurv.htm).
Prevalence and patterns of use of psychoactive medicines in individuals with autism in the Autism Society of North Carolina.
J Child Adolesc Psychopharmacol. 2002 Winter;12(4):311-21.
PMID: 12625991 [PubMed - indexed for MEDLINE
Langworthy-Lam KS, Aman MG, Van Bourgondien ME.
The Nisonger Center for Mental Retardation and Developmental Disabilities, The Ohio State University, Columus, Ohio 43210, USA.
The aim of this study was to assess the prevalence and patterns of psychoactive and over-the-counter medicines in a large cohort of individuals with autism. We conducted a mail survey of 3,228 families that are members of the Autism Society of North Carolina. This is one of the largest chapters of the Autism Society of America. The survey form addressed current medicines used, side effects, demographic characteristics, and medical conditions. Some 1,538 member families within the society (48%) responded to the survey. In all, 703 (45.7%) individuals with autism were taking psychotropic drugs, 191 (12.4%) antiepileptic drugs (AEDs), and 86 (5.7%) supplements for autism. The total number taking psychotropic, antiepileptic, or vitamin treatments was 816 (53.1%). Antidepressants (taken by 21.7% of the sample), antipsychotics (16.8%), and stimulants (13.9%) were the most commonly prescribed agents. Univariate and multivariate analyses were conducted to examine factors associated with treatment. Greater age, more severe autism and mental retardation, and more restricted housing were often associated with greater use of psychoactive agents. These findings suggest that individuals with autism are a frequently medicated group, although the empirical research support for most agents being used is still very limited.
PMID: 12625991 [PubMed - indexed for MEDLINE]
Why not get to the true ROOT of the problem...Mercury poisoning, and DETOX? IMO more drugs make more problems. My son has never improved on drugs, but has made great strides since avoiding them and going to natural, alternative remedies.
What is the best developmental screening tool to use for age 0-3yrs?
My personal opinion: Mother of Autistic 3 yr old.
I feel the the best screening tool is yourself. Forget the standardized test although they can help somewhat. Go with your gut at all times, and always get second and third opinions. You know your child and what is normal and not normal. If you feel something is wrong; such as if your child is not looking at you in your eyes, or responding to his/her name. Possilbe displaying some " Quirky" Behaviors. ei:toe walking hand flapping sniffing mouthing things at a later age, rocking, spinning, not speaking or babbling. Always keep in mind that a Dr. Spends minimal amount of time with your child you spend the most and see whats going on. Speak out
The following screening tools are validated, brief, easy to use and score:
Ages and Stages Questionnaire (ASQ) by Jane Squires, Ph.D. & Diane Bricker, Ph.D. et al.
Child Development Review by Harold Ireton, Ph.D. et al.
Infant/Toddler Checklist for Language and Communication by Amy Wetherby, Ph.D. & Barry Prizant, Ph.D.
Parents Evaluation of Developmental Status (PEDS) by Frances Page Glascoe, Ph.D.
http://www.firstsigns.org/pages/physician_resources/tools_dev.html
The CHAT which is from the U.K. and the M-CHAT is the american version that is specific to autism can also be found at
www.firstsigns.org
Thank you, Elaine, for the excellent information.
In addition, you can find a parentÿffff92s guide on working with your pediatrician at:
http://www.medicalhomeinfo.org/screening/Autism%20downloads/Johnson_6-FPGParentHandoutSPA8.doc
http://www.medicalhomeinfo.org/screening/cdc_rev1.htm#Autism
Other early screening initiatives include Bright Futures (http://www.brightfutures.org/) and Healthy Steps (http://www.healthysteps.org/)
Are there differences in the rates of ASD for those who were breastfed as infants for at least 6mos vs. those who were not?
My son was breastfed with his twin sister until age 4 months....He was diagnosed w/autism @22 months , and has not spoken since age 3, immediately after a tetanus shot.
They are 12.
Well I am a mother of two. I nursed both. My daughter is dx as PDD/NOS (atypical autism)and a string of other things. And my son is typical. So I don't think there is a connection between nursing and not nursing children.
I agree with Joyce. I breastfed both my sons for a year each. The older one has aspergers and the younger is typical. I was much more careful about my diet (soda's etc) while nursing the first than with the second.
There are not many studies on breastfeeding and the ASDs, but all indications are that there are no associations (see abstract below).
CDCÿffff92s CADDRE study of early risk factors for the ASDs will be collecting additional information on the breastfeeding patterns in children who later did and did not have an ASD. http://www.cdc.gov/ncbddd/dd/aic/states/default.htm#caddre
J Dev Behav Pediatr. 1988 Oct;9(5):247-51.
A comparison of breastfeeding rates among children with pervasive developmental disorder, and controls.
Burd L, Fisher W, Kerbeshian J, Vesely B, Durgin B, Reep P.
Child Evaluation and Treatment Program, Medical Center Rehabilitation Hospital, Grand Forks, ND 58202.
The breastfeeding rates for 50 children with pervasive developmental disorder (PDD) from North Dakota's roster of PDD patients were compared with the national average and with the rates for a control group matched for age, sex, and IQ. In addition, the breastfeeding rates for the normal siblings of the PDD and control groups were compared with the national average to help determine whether the lower breastfeeding rate among PDD patients was a function of parenting practices. The breastfeeding rates for the PDD and control groups were not significantly different from each other, but both were significantly lower than the national average. The breastfeeding rate for the normal siblings of PDD children was almost identical to the national average, but the rate for the siblings of the matched control group was significantly lower than the national average. These results are discussed in terms of hypotheses regarding the early parent-child interactions and characteristics in the families of PDD children.
PMID: 3225319 [PubMed - indexed for MEDLINE]
This is great that everyone whats early dx. But what happens to the child if they can't be intergrated into a regular ed. classroom by age 5? And what about the children and young adults that are out there now that aren't getting these so call services ? Where can parents in other states besides Florida find these services ? How do we access them?
Other responders to this question have given some good suggestions. Also, the Department of Education website includes the Education Organizations Resource Directory (EROD) which lists resources from each state. The home page for EROD is
http://bcol02.ed.gov/Programs/EROD/index.cfm
There are wide range of outcomes of children with an ASD. This book follows 10 children with autism into adulthood.
Fragile Success: Ten Autistic Children, Childhood to Adulthood, Second Edition
by Virginia Walker Sperry, Sally Provence, Sally A., M.D. Provence, Fred R., M.D. Volkmar, Virginia Sperry
I am in FL, and I would like to know where all the wonderful services are that are supposed to be here...? My son is 12, and it had been a complete BATTLE...I HAD to homeschool him in 3rd grade. I would do it every year if I could, financially. It is strange that the pub. school get$$$ for our kids schooling, but we get ZILCH when we homeschool!
Joyce call your local Mental Health office and also look into the Autism Society in your area. Best help will come from those two places..
SSI may also be available for anyone in a low income family.
The previously listed places can assist you in reading material and encourage you to get involved in Legislation and contact your Senators, as we all need to do. They may also be able to assist you in getting on a waiver waiting list for services, however; they won't be able to provide assisted living services. My child is 17 years old, he is still on the waiver waiting list. To date no services have been available. MRDD has informed parents, he will be lucky to recieve waiver services before he reaches age 26, that is, if state waiver rules haven't changed before, which has already occured with one waiting list he was placed on.
Many parents/guardians (I'm guessing 1 in every 150 in the U.S.), including myself, would be interested in which states actually have waiver services, assisted living, medicaid or any services available with no family income limits. The cost of an unqualified, parent trained caregiver runs $12.00 per hour and up. Therapy and Medical coverage is seldom provided by Insurance. We've made every available contact, no services are available in our state.
NY has a medicaid waiver based only on the income of the child. My child is now 10 y/o and was not diagnosed until age 5 1/2 (although actively sought one). He has only improved after the age of 5 with biomedical interventions and our hard work and efforts supplementing his inadequate and inappropriate educational program at home. My son began to speak late between ages 5 1/2 and 6 y/o and is now highly verbal, although still needs add'l pragmatic skills. Recent research has shown brain plasticity continues throughout young adulthood, yet professionals still drill into our heads about this " window of opportunity" which will drop at age 7-7 1/2. This is not true. ABA, behavioral interventions and appropriate educational programs, and biomedical intervention may benefit ALL and EVERY individual with ASD. So what if it should take awhile longer to confer benefit. There is no reason to terminate education, training or services because a child is no longer considered for early intervention. Today, instead of dreading every birthday, we look forward to our child's future with hope and optimism. Keep looking and preparing for ways to fulfill your child's goals, needs and dreams!
Best wishes,
Wanda
Thanks Terssa for the info.
I connected those agentcies 6 years ago and they didn't have services available at the time to help my daughter. So I took it upon my self to sit at the school every day and talk to the teacher everyday. Was the biggest pain in the hinny as I could to get my daughter the stuff she needed to become the best Autistic child in the school. But the question that really is on my mind is what about the children that parents can't sit at the school everyday and be a pain for all around the district to help improve their child's future?
I am in a combined residency program leading to board elgibility in pediatrics and child & adolescent psychiatry. We have a 28 month old son with ASD.
We consider ourselves fortunate that we were able to identify and get services for our son before age 2, and happy to report we've seen some remarkable improvement!
It appears that prematurity and the in-utero enviroment that often leads to premature delivery may be risk factors for the development of ASD.
One barrier we noted to early detection of ASD is the practice of " adjusting" the routine Denver developmental screen for the degree of prematurity (ie. a former 34 week gestational age infant is adjusted 6 weeks on each screen until age 2). This gave us and our peditrican a false sense that our son " would catch up" .
This made early identification more difficult in our son's case and in other children I have interacted with. I would question whetehr this practice is warrented at all and urge that if an infant shows significant delays or cautions at any age, referal for multi-disiplinary service should be initiated immediately, regardeless of " adjusted age" .
I have an 8 year old son who is autistic. He was also a
32 week premie. I have always had a " gut" feeling that the two are connected. I had two miscarriages within the 20 months prior to his birth and all three pregnancies were exactly alike -- only he made it to 32 weeks. I think if anything, the autism caused the miscarriages/premature birth, not the other way around.
Do you, or does anyone out there, know of any research concerning premature birth and autism?
I agree with your concern about the age adjustment in developmental screening. I first saw the stereotypical signs of classic autism when our son was about 14 months old; however, the early intervention " specialist" pooh-poohed the idea, reminding me (as if I had forgotten) that he was a premie and premies often have odd behaviours in their quest to " catch-up" . Fortunately, I followed my instincts and was able to find appropriate help for him.
Too much emphasis is put on " catching up" , and I believe parents and providers let their guard down thinking the child can do this on his or her own.
Too many specialists are afraid to suggest, let alone dx an ASD at an early age. I would think that if it is even a remote possibility, EARLY AND INTENSIVE intervention should be started. It certainly can't hurt, and would in fact be helpful to any child.
I am a pediatrician in neurodevelopmental pediatrics. I have been doing premie follow up for 25 years. It is important to adjust the screening in ex-premies. If you want the long explanation e-mail me . The problem is that the Denver is just not a good test. It misses a lot of children with problems.
Yes, I can see some instances where adjusting developmental screening tools for prematurity is warrented and appropriate.
But given the strong evidence in support of early intervention for ASD and a wide array of other developmenttal disorders (speech, motor, ect...)I think screening tools can be mis-interpreted leading to delayed recognition and early intervention.
If the Denver Screen is a sub-optimal screening tool, what should pediatricians and family physicans be using as a screening tool for routine check ups?
The following developmental screening tools are validated, brief, and easy to use and score:
Ages and Stages Questionnaire (ASQ) by Jane Squires, Ph.D. & Diane Bricker, Ph.D. et al.
Infant/Toddler Checklist for Language and Communication by Amy Wetherby, Ph.D. & Barry Prizant, Ph.D.
Parents Evaluation of Developmental Status (PEDS) by Frances Page Glascoe, Ph.D.
http://www.firstsigns.org/pages/physician_resources/tools_dev.html
For more information about healthy developmental milestones, red flags, the screening process, developmental and autism screening tools for use in practice and other links to helpful information for practitioners and parents, visit:
www.firstsigns.org
I agree that those are much better tools. Ages and stages is also available in Spanish and you can score it without knowing the language. When in doubt or always if there is parental concern referr to a speech and language therapist for a full evaluation.
I live in Hickory North Carolina, and I am trying to find a counselor specializing or at least having extensive experience in Self-Injurious behavior. I currently am unable to locate a counselor who can give consistent weekly counseling in regards to self-injurious behavior.
If you know of someone or know how I can get in touch with someone, please let me know.
The National Information Center for Children and Youth with Disabilities (NICHCY)may be able to give guidance or direct you to resources in your area. Their web address is http://www.nichcy.org/
I am not sure of the persons name however I do believe that UNCG was doing something with thier students regarding this. Look into using the college there for help.
Out of five close high school girlfriends from Granada Hills, CA,: 3 have autistic daughters, 1 has typical children and 1 had a hysterectomy in her 30s. Is this something the CDC/NIH should know about?
Dear Laurie and listmates:
I live in Brooklyn, New York. I personally know 5 ASD children on my street within a distance of 9 blocks. The other day I walked into a Dunkin Donut, at random, for a cup of coffee and I met 2 sets of parents with their autistic children (mine made a total of 3). This donut place is as big as my living room. Maybe autism is contagious? Maybe it's caused by donuts? After all, the new theory on increased incidence of childhood diabetes is being blamed on the 39 cents hamburger! Unfortunately, there are may babies and toddlers with diabetes now that do not yet eat McDonald's! I think if this is genetic we should start reviewing Darwin' theories on evolution. I certainly do not think it is due to better and more inclusive diagnosis. It is very difficult to hide a non-verbal child who hand-flaps, stims,toe-walks,sniffs,etc; or a verbal one who repeats everything like a tape-recorder without any comprehension of conversation. Where they kept locked in a closet for al these years? Their behavior and clinical presentation is quite distinct from other disorders. What is going on?
Sincerely,
Ada
Yes many children were hidden away. I remember with horror touring the state facility for the disabled during med school in the mid 70's it was like something out of a bad Dickens novel. I worked in one in another state as part of my pediatric residency. It was a required rotation. Ther were kids and adults who flapped and grunted and screamed . many were nonverbal. Some came as babies and were never seen by their familys again. Some came as adults who had spent their entire life at home, with no edcation or therapy, not even a trip to the donut shop, when their elderly parents could no longer care for them. It was still up and running when I graduated and left the state in 1977. For those of us who have or care for disabled children We know how much remains to be done, but we have come a remakable way in the last 25 years
The CDC is funding Centers for Excellence for Autism and Developmental Disabilities Research and Epidemiology (CADDRE) in several states, including California. The California Department of Health Services conducts this program within 6 counties. The California Center will conduct 4 major projects, including monitoring the incidence rate of ASDs and working with other states to find the cause or causes of ASD. For more information on CADDRE in California, please see http://www.cdc.gov/ncbddd/dd/aic/states/ca.htm
In order to report concerns about autism prevalence rates or other health issues, contact the California Department of Health Services.
California Department of Health Services
Environmental Health Investigations Branch
1515 Clay Street, Suite 1700 Oakland, Ca 94612
Phone: 510-622-4600 Fax: 510-622-4505
Email: autism@dhs.ca.gov
For other states, please contact your state Department of Health
http://www.fda.gov/oca/sthealth.htm.
Would someone please post the ASD Communication and Other Indicators that were presented in the PowerPoint slides? I couldn't write quite fast enough. Much thanks.
Beth ~ Look under " resources" and click on " acronym guide." The information you're looking for is contained there.
As a parent of a PDD/autistic child, I suspect some indoor plant spray chemicals that I was using in my job up through 6/7 months pregnancy may be linked to some of the damage seen in my PDD/autistic son. Does the CDC or some other source have any documentation on different sprays and plant chemicals and their relation to Pdd/autism spectrum?
While there are many hypotheses about what causes autism, we do not yet have a definitive answer and there are no studies specifically showing a link between insecticides and autism.
In an effort to gain a better understanding of the characteristics of and causes of the Autism Spectrum Disorders (ASDs), the CDC, through the Childrenÿffff92s Health Act of 2000, established the Centers for Autism and Developmental Disabilities Research and Epidemiology (CADDRE). Please see http://www.cdc.gov/ncbddd/dd/aic/states/default.htm for more information.
CADDRE is comprised of 6 states in the United States whose goals are to conduct surveillance and participate in a collaborative case-control study. The case-control study will be studying the behavioral characteristics of children with autism and will examine prenatal, perinatal, and postnatal risk factors for autism including maternal exposures to infection, toxic elements, and medications- to name a few. While this study will capture some information on exposure to toxic elements another study entitled the Childhood Autism Risks from Genetics and the Environment (CHARGE) Study is being conducted to look at specific environmental exposures and autism. This study is sponsored by NIH and is being conducted by the MIND Institute at the University of California. Similar to the study being conducted by CADDRE, Researchers at the MIND Institute/UC Davis are attempting to determine the underlying causes of autism and developmental delay by looking at children's medical history, environmental exposure to toxins, diet, genetic background, and many other aspects of their lives, both before and after birth. To find out more about programs on autism funded through the National Institute of Environmental Health Sciences of NIH, go to http://www.niehs.nih.gov/oc/news/nucehr.htm.
The National Center on Environmental Health (NCEH) at CDC has been working since 2001 to establish state-based programs to track environmental health hazards in relation to diseases and disabilities. The long-term goal of these programs is to have a system ready to respond to and investigate concerns about particular conditions and their relationship to environmental exposures. You can find out more about these programs at http://www.cdc.gov/nceh/tracking/.
Also, the Agency for Toxic Substances and Disease Registries has compiled a research review of environmental exposures and autism. To get more information, please contact:
ATSDR Information Center
Mail Stop E-57
1600 Clifton Road
Atlanta, GA 30333
Fax: (404) 639-6359
http://www.atsdr.cdc.gov/press/ma981216.html
My 4 year-old son was diagnosed with PDD a few months ago. We live 0.5 miles from a toxic dump that produced insecticides. I also grew up in this neighborhood. I am also an RN who works in a major pediatric oncology hospital. I gave a lot of chemotherapy to children during my pregnancy with my son who is affected with ASD. Could there be a connection with either one of these factors?
Please see the response to Sheri Moore about environmental exposures and autism. There is currently no known association between chemotherapy and autism, but the CADDRE studies will be investigating the medical and birth histories of children with and without autism and other disabilities and their parents. These results will give us an idea of whether exposure to agents, such as chemotherapy, warrant further exploration.
I am sure other areas are having a budget crunch as those of us living here in Minnesota, we have a good early childhood program in this state but in the last round of budget cuts I believe that their budgets were cut by nearly 40%. How are we to deal with all of these cuts and still keep improving the services that are needed to be provided for autistic individuals and their families?
As you know, there is no easy answer to this one! Federal agencies, such as CDC and NIH receive money as appropriated by Congress. As part of our governmental system, federal, state, and local governments are charged with using the taxpayerÿffff92s money in ways that reflect the needs and concerns of the people they represent. In an era where globalization and preventing the spread of new infectious diseases, such as SARS, monkeypox, and others, as well as concerns about bioterrorism, the distribution of funding is a particular challenge.
We can continue to work together to show that the issues of people affected with ASDs are important. Continued research and intervention is needed and more groups and agencies have become focused on addressing the needs of children with an ASD. For example, the Interagency Autism Coordinating Committee (IACC), which is organized by the National Institutes of Health (NIH) has been established to improve coordination of autism research efforts (please see http://www.nimh.nih.gov/autismiacc/index.cfm for more information). In addition,
there is now a Congressional Autism Caucus (http://www.autismcoalition.org/caucus.asp) consisting of members of Congress concerned about issues related to ASDs. Private support and research organizations have made great progress in providing information and support for research to better understand causes and intervention, (see the Autism Coalition http://www.autismcoalition.org/).
I cannot stress enough the importance of pediatricians listening seriously to parents concerns regarding their toddler's development. Most exams are too short for a doctor to see signs of delay without a critical history from the parents. Our pediatrician was aware of one of our twins' speech delay and failure to respond to her name for one year. We were told not to compare her to her twin sister. Our daughter was not diagnosed until she was 3 3/4 years old.
I too, cannot STRESS the importance of listening to parents. We KNOW our kids and know when something is wrong.
When my son was having screaming attacks in the middle of the night,he would hyper-extend with pain to the point where only his head and heels touched the floor, and throw himself around the floor. I had to put big pillows all over so he would not injure himself. These lasted anywhere from 20 minutes to 2 hours. His Ped. said they were night terrors. I knew it was more...My son was in excrutiating pain! and I could do NOTHING because no one believed me. Then came the Autism. He was diagnose at 22 months...the episodes finally subsided around 3 years
The same thing happened to me...My son developed Autism...his twin sister was originally thought to have Down's Syndrome...but she is fine today except for some sensory issues and declining eyesight. They are 12.
My son lost all words at age 3, and has not spoken since.
Dear Lindy and listmates:
I had the same so-called night terror episodes with my son. He was in excrutiating pain exactly as you described. After,he would kneel on the floor and rest his stomach against the side of the toddler bed and actually sleep in this position! I guess it is simple to discard all this physical symptomology as autistic stimming,aggression etc.
Where are our medical doctors? Immunologists,pediatricians, gastroenterologists,etc. This is NOT a psychiatric issue!
Ada
It is critical for pediatric physicians and parents to establish an abiding partnership where concerns are acted upon whenever they arise. Routine developmental screening at well-visits facilitates this partnership. Accurate detection is heightened when practitioners systematically elicit parentsÿffff92 concerns through the routine use of screening tools. Parents have been shown to be accurate reporters and predictors of behavioral and developmental concerns, due to their constancy in their childrenÿffff92s lives and to their tendency to compare their children to others (Glascoe, 1999). Additionally, pediatric physiciansÿffff92 observations enhance and strengthen the accuracy of screening tool measures. By listening carefully to parental concerns and by exercising a heightened index of suspicion in practice, pediatric physicians can use the developmental surveillance and screening processes to increase the chance of detection during very early development and to provide a clear compass for referral and treatment if a concern is flagged.
Our non-profit organization, First Signs, is dedicated to informing physicians and parents about the early warning signs of ASD and other developmental disorders and the efficacy of early intervention. We have heard similar concerns from countless parents and have experienced this situation ourselves as parents of young children with ASD. So instead of saying " Don't worry, wait and see," we say " Don't worry, take action." There is so much that can be done to help children at risk if we start early. Please visit our web site for more information about typical developmental milestones, red flags, the screening process, validated screening tools for use in practice and links to other helpful information for parents and professionals.
www.firstsigns.org
You know because of the short time Peds get with children it makes it hard for them to listen and see what is going on. I know my Ped kept telling me with my daughter that she will talk when she gets read. Until I got mad and started yelling " THERE IS SOMETHING WRONG WITH MY DAUGHTER AND I WANT YOU TO TELL ME WHAT IT IS!!!!!!!!!!!!!!!" and that got his attention and the referral we needed for her to be tested.
I had a similar problem with my family practitioner pretty much stifling my concerens about my 2-3 year old not really speaking or interacting. " Boys can just be slower and wait 3, 4, 6 months to see how he does" ended up putting us further behind when we could have gotten a jump start with Early Infant Child Services. We had to research on our own to learn of the preschool services available in our school district, and had to call around town for a pediatrician that knew something of this. I think I prefer a pediatrician instead of family practice generalities for a child now.
Not to be cynical, but I know of several children who were not diagnosed until they were in their teens and halfway through junior high school (granted with more high-functioning ASD). Given this, diagnosis at anything under age 4 is a tremendous head start.
I would be interested in hearing about resources for teenagers and adults with ASD, particularly Asperger's and high-functioning Autism, and their parents. In my experience, the majority of resources are directed to younger children and their parents. Parents face different issues as their children mature, and support and resources intended for preschoolers and children in elementary school are not adequate to meet the needs of these parents, families, and ASD adults.
Anyone?
For more information on resources and intervention across the ages and spectrum, please see:
National Organizations / Resources
Asperger Syndrome Coalition of the U.S. (ASC-U.S.)
P.O. Box 351268
Jacksonville, FL 32235-1268
(866) 4-ASPRGR
Website: http://www.asperger.org/index_asc.html
Asperger Syndrome Education Network, Inc. (ASPEN)
E-mail: info@AspenNJ.org
Website: http://www.aspennj.org/
Autism Services Center
National Autism Hotline
P.O. Box 507
605 9th Street
Huntington, WV 25710
(304) 525-8014
Autism Society of America (ASA)
7910 Woodmont Avenue, Suite 300
Silver Spring, MD 20814
(301) 657-0881
(800) 3-AUTISM
FAX: (301) 657-0869
Website: http://www.autism-society.org
MAAP Services
http://www.maapservices.org/index.html
National Alliance for Autism Research (NAAR)
414 Wall Street
Research Park
Princeton, NJ 08540
(888) 777-NAAR
Website: http://www.naar.org
Online Asperger Syndrome Information and Support (OASIS)
Website: http://www.udel.edu/bkirby/asperger/
Yale University Child Study Center Developmental Disabilities Clinic & Research
Main Website: http://info.med.yale.edu/chldstdy/autism/
PDD Resources: http://www.med.yale.edu/chldstdy/autism/pdd.html
You may be able to find additional national organizations by searching the National Information Center for Child and Youth with Disabilities (NICHCY)
database of organizations at http://www.nich
What I beleive is needed is a cradle to grave solution for autism. At the moment their are so many seperate agencies involved and they change as the child gets older, meaning difficult transitions for the child and family involved. Then at age 21, nothing. As soon as an individual with autism reaches 21 years of age, the authorities act as if he dissapeared or somehow got cured.
Try the many links to this information at:
http://www.firstsigns.org/pages/parent_resources/related_sites_websites_asd.html
The American Academy of Pediatrics (AAP) issued guidelines for pediatricians concerned with the ASDs and a key point is to listen to the parents. Please see http://www.aap.org/policy/autism.html
No surprise that parents are the ones that know about their children and there are now some very quick and easy tools that parents can complete and bring to their primary caregiver when they suspect a problem. Please see http://www.pedstest.com/test/peds_manual.html
I would like to see a group formed that takes a " big-picture" approach to minimizing the long-term financial impact of ASD.
This group should be chartered with trying to pull individual service providers, i.e., early intervention programs, public schools, and social service departments, out of the silos in which they operate. To do this, training and funding should be provided so these groups can provide interventions based on empirical evidence of efficacy.
If, for example, a study shows that an intervention has a 50% rate of " recovery," and this is the best result of any intervention studied to date, service providers should be able (if not mandated) to provide this intervention. By recovery, I mean ASD children are mainstreamed into regular classrooms by 5 or 6 years old, and a classroom observer wouldn't be able to distinguish the ASD child from the typical developing kids.
Think about the financial savings over the course of an individuals liketime. If we can " recover" 50% of ASD children, that's a huge savings over having to provide lifetime support for all of them.
With the near epidimic rise in the rate of autism, we have to look at the big picture. Fundamental changes must take place in the way school districts and ECI programs are funded and operate.
I look forward to comments on this.
Thank You,
Sean McFerren
My child's school gets nearly $20,000/year to provide an education for him. As usual...It's all about money...sad but true. I fought a 4 month battle to get him into a private school, which will now get my son's funding. The sad thing is that My son made more progress when I homeschooled him in 3rd grade than he did all previous years in public school.(I used ABA and sensory integration)
The school determined that he made progress in 3 years time, therefore they were " adequate." I strongly disagreed, hence the homeschooling.
Another point....The school system gets my son's money, but do I get any when I homeschool him? Of course not! All the materials came out of my pocket.
Something is drastically WRONG with this picture!
Lindy
The attachment is a copy of a study showing early intensive behavioural intervention can save up to $2.5MM. Despite this fact parents have to battle with the authorities on a daily basis to get anywhere near the 40 hours per week that is required if EIBI is to be effective
Attachment: G:\Documents and Settings\John\Desktop\EIBI Saves Up to.doc
John,
Thanks for that very informative article. It's clear to me what needs to happen.
Can anyone here identify drawbacks to funding treatment now that has the potential to save in the range of $1,686,061 to $2,816,535, per child?
Might some of the " content experts" who are facilitating these discussions be able to comment? Is there any type of effort to act on this?
Thank,
Sean McFerren
We have so much more to understand about the Autism Spectrum Disorders (ASDs), but one thing we do know is that intensive, early intervention can be very beneficial. There is no doubt that the needs of people with ASDs are complex and are often unmet and it will take coordination between many organizations and groups of people to accomplish all that we need to help each person reach their full potential. In addition to legislation that enables agencies to provide intervention services, adequate financial support is needed to implement these programs. The way our governmental agencies are set up now, particular agencies specialize in specific needs. For example, the Office of Special Education and Rehabilitative Services (http://www.ed.gov/offices/OSERS/index.html) oversees educational services for people with developmental disabilities, but state and local variations are great. In addition, programs like Early Intervention are administered by different agencies in each state (http://nectas.unc.edu/contact/ptccoord.asp). These are just examples of important programs working to address the needs of people with an ASD, but when we are looking at the needs across the lifespan, many agencies, both public and private, are involved.
At present, some significant progress has been made to increase the collaboration between different government and research organizations concerning the ASDs. In 2001, the Department of Health and Human Services (HHS) established the Interagency Autism Coordinating Committee (IACC), which is organized by the National Institutes of Health (NIH). Please see http://www.nimh.nih.gov/autismiacc/index.cfm for more information. The IACC serves as a forum to provide a more coordinated effort in addressing the needs of people with an ASD. Representatives from health, education, social services and other government agencies work together with private advocacy and research groups, such as the Autism Society of America (ASA) and Cure Autism Now (CAN), to identify the needs of people with an ASD. IACC meetings are open to the public and you can contact them directly to express your concerns.
Also, concerning research on the effectiveness of intervention for the ASDs, the National Institutes of Mental Health (NIMH) held a research meeting to evaluate the ÿffff93state of the scienceÿffff94 and has since formed working groups to make recommendations for future studies evaluating intervention. Please see http://www.nimh.nih.gov/events/autismconference.cfm for more information.
Excellent broadcast--but I'm still unclear about one of the objectives of the broadcast, which was to identify three reasons for a rise in numbers if individuals diagnosed. Can you offer further explanation?
However, the MIND Instutute (Autism research facility associated with UC Davis in California) did a study and found that even if you take into consideration the factors of better understanding, awaresness and diagnostic techniques as well as other factors, there is still a huge rise in numbers that cannot be explained by those reasons.
http://www.ucdmc.ucdavis.edu/mindinstitute/
Thank you, Teresa. I am aware of the most recent " partnership" between California Department of Developmental Services and the M.I.N.D. Institute. So. . . I think I'm back to where I was earlier . . . We know there is an increase but we don't know why (other than a broader definition of the autism spectrum, more complete diagnoses, better awareness on the part of parents)?
Let me suggest that there is another reason for the increased prevalence of autism. This increase was addressed in a Wired Magazine article:
< http://www.wired.com/wired/archive/9.12/aspergers.html>
A similar view was put forward by Bernard Rimland in his 1964 book on autism. Dr. Rimland felt that autism was high intelligence gone awry from the beginning. Very bright parents are the sort of people who beget autistic children. Kanner made the same point in his original paper on autism.
To get to the Wired Magazine article delete just the " greater than" character at the end of the address.
Or maybe this link will work:
http://www.wired.com/wired/archive/9.12/aspergers.html
Ken Fabian
Reasons for an increase in the prevalence include the following:
1. Better diagnostic practices that identify more people with ASD
2. Inclusion of the entire spectrum of ASD and milder forms in the diagnosis of autism, thereby increasing the number of people with the diagnosis
3. Greater awareness among parents who bring the signs and symptoms to the attention of children's health care providers
All recent studies have concluded that the reasons you state are NOT responsible for the rise in Autism. Autism has increased in direct proportion to the increase in the use of thimerasol in childhood vaccines and the MMR shot.
Our local pediatrician explains it this way: The MMR shot is given around 15 to 18 months of age. This is also the time when most parents start noticing the childs development or lack of. He stated this is the same shot we all received when we were children and WE do not have high episodes of autism. This is his defense against blaming the MMR vacine on autism. Who knows? Maybe it is in the food we eat or water we drink? No one has the answer yet. But something has definitely got to be done soon. Many states need to get on the ball and train teachers to help these children. I live in Alabama and we have nothing but money problems regarding everything in this state. So we will not get any extras as far as helping with autism is concerned. When I ask about having speech therapy more than just 2 times a week for 20 min, It was suggested at the IEP I could pay to get more from a private therapist and insurance does not cover it. So there is no extra help in our state. But of course we are used to being at the " bottom" of the list in many areas.
There is evidence that individuals with autism have a problem with the production of metallothionein proteins, which are responsible for binding to heavy metals. It could be a factor that those with autism cannot detoxicate, and begin accumulating toxins the day of conception. This would explain why the symptoms of autism so closely (often identically) match those of heavy metal toxicity. This also explains why individuals with autism, upon testing, are found to have a toxic accumulation of heavy metals. Further, upon treatment for problems with mattallothionein proteins and metal toxicity, these individuals (in all age groups) are found to improve; often beyond expectations, enabling them to become contributing members of society.
In regards to the previous post and possible reasons for the rise in autism: IF those with autism cannot efficiently detoxicate and have been accumulating toxins from the day of conception. The rise in autism numbers would than correlate with 1.) The rise in environmental toxins i.e. contaminated seafood. 2.) The rise in the amount of toxins contained in mandated vaccines. 3.) The rise in risk of possible unknown neurological warfare. 4.) The rise in risk related to pesticide spraying.
I believe the rise in actual diagnosis has nothing to do with the rise in autism amoung us, with or without diagnosis; we are experiencing an epidemic number of individuals with neurologically related impairments. Often too many aren't being provided a timely diagnosis, denying diagnosis doesn't make these epidemic numbers disappear. Every school and neighborhood is overwhelmed with cases of neurologically disabling impairments. The latest word is...we have a new endangered species - OUR CHILDREN. WHY? Because these patients are medically neglected. Families, parents and schools (with no training) are being abandoned to cope alone with this epidemic number of devastating neurological impairments.
Those with autism have more than medical behavioral issues. We must get to the cause of the behavioral problems: Those with autism also have known medical: neurological, gastrointestinal, fungal, visual, sensory, motor, speech, detoxification and many more health related problems. The medical establishment must begin medically treating the physical symptoms in these patients. Insurance must also be required to cover these patients. The behavioral issues are a direct result of their need for medical attention and intervention. Treatment is often not prescribed and when it is prescribed; Insurance won't cover it. Most families(including upper middle class)are struggling to cover the cost of assisted care, not to mention the extreme cost of medical treatment that Insurance refuses to cover.
Dear Lisa,
I agree wih you 100%!
Ada
Besides the Miami project that was illustrated in the Broadcast, are there any other County/City Health Departments that have developed exemplary programs to deal with the issues of Autism?
Where did Miami receive their funding for this project?
You can find out more about the partnerships between the various agencies in Miami-Dade County, Florida by contacting the programs directly at:
University of Miami ÿffff96 CARD Center
http://inetsrv.psy.miami.edu/CARD/
Florida Diagnostic and Learning Resources System (FDLRS)
http://fdlrs-south.dade.k12.fl.us/web/default.html
North Carolina has a statewide, legislatively-mandated diagnostic and intervention for people with ASDs known as TEACHH (http://www.teacch.com/teacch.htm).
Also, contact your state health departments to inquire about programs specific to your state at:
http://www.fda.gov/oca/sthealth.htm.
Dr. Martinez ÿffff96 thank you for being the contact for the MA Department of Health.
I have the same question. I live and work in the Western part of Massachusetts, Amherst to be precise. I work with children diagnosed within the Spectrum, as a behavior specialist and find that we work isolated and that makes the job harder.
I see the Dade County project as an excellent model of collaboration betweeen agencies and the University of Miami.
Where can I get more information about how to start a coallition and funding. I'm ready to move on with a project. We are based in the Five College Area. I think this will be a great movement in this area, where we have a high incidence of cases diagnosed within the spectrum. I would like to know if there is a way to contact DPH and find out more. I am very active in the community, but feel that we are working isolated, and the rad is hard.
I coordinate the system of Specialty Service Providers for children with ASD in the early intervention system in MA, which are funded by the Department of Public Health. Would be glad to talk with you about this system.
I have the same question. I live and work in the Western part of Massachusetts, Amherst to be precise. I work with children diagnosed within the Spectrum, as a behavior specialist and find that we work isolated and that makes the job harder.
I see the Dade County project as an excellent model of collaboration betweeen agencies and the University of Miami.
Where can I get more information about how to start a coallition and funding. I'm ready to move on with a project. We are based in the Five College Area. I think this will be a great movement in this area, where we have a high incidence of cases diagnosed within the spectrum. I would like to know if there is a way to contact DPH and find out more. I am very active in the community, but feel that we are working isolated, and the rad is hard.
Has there been any progress in the development of new born screening to detect autism or in utero tests to determine an inborn metobolic error?
Thanks
The finding of possible biomarkers for autism identified in newborn bloodspots was reported by Dr. Karin Nelson and others in 2001 (see below). These results have yet to be replicated and no other clear biomarkers to identify infants with an Autism Spectrum Disorder (ASD) have been found yet. However, it might be helpful to contact Dr. Nelson at the National Institute of Neurological Disorders and Stroke (http://www.ninds.nih.gov/) or her colleagues directly to find out any updates on their research.
CDC has a partnership with a group of researchers in Denmark to develop the technology and screen newborn bloodspots for biomarkers for the ASDs and Cerebral Palsy. You can contact the Danish research directly at:
North Atlantic Neuro-Epidemiology Alliances,
Department of Epidemiology and Social Medicine,
University of Aarhus, Paludan Møllersvej 17,
DK-8000 Aarhus C, Denmark
Phone +45-8942-2350
Fax +45-8942-2365
E-mail nanea@nanea.dk
Team leader & Head: Poul Thorsen, MD, PhD
The identification of an early biomarker for the ASDs would be extremely helpful for starting intervention as early as possible, and the hope is that we will one day be able to screen for these conditions like already known newborn metabolic disorders. For information on the newborn screening programs currently available in the US, please see the following website: http://www.cdc.gov/nceh/dls/newborn_screening.htm#Links.
At present, we do know that some of the earliest behavioral signs of autism can be identified in the 2nd year of life. Close attention to early social and communication signs and the use of developmental screening tools can be very helpful in identifying children in need of intervention as soon as possible. For more on developmental screening and the early signs of autism, please see the websites for First Signs (www.firstsigns.org) and the American Academy of Pediatrics (http://www.aap.org/policy/autism.html).
Nelson KB. Grether JK. Croen LA. Dambrosia JM. Dickens BF. Jelliffe LL. Hansen RL. Phillips TM. Neuropeptides and neurotrophins in neonatal blood
of children with autism or mental retardation. [Journal Article] Annals of Neurology. 49(5):597-606, 2001 May.
There has been little exploration of major biologic regulators of cerebral development in autism. In archived neonatal blood of children with autistic spectrum disorders (n = 69), mental retardation without autism (n = 60), or cerebral palsy (CP, n = 63) and of control children (n = 54), we used recycling immunoaffinity chromatography to measure the neuropeptides substance P (SP), vasoactive intestinal peptide (VIP), pituitary adenylate cyclase-activating polypeptide (PACAP), calcitonin gene-related peptide (CGRP), and the neurotrophins nerve growth factor (NGF), brain-derived
neurotrophic factor (BDNF), neurotrophin 3 (NT3), and neurotrophin 4/5 (NT4/5). Neonatal concentrations of VIP, CGRP, BDNF, and NT4/5 were
higher (ANOVA, all p values < 0.0001 by Scheffe test for pairwise differences) in children in the autistic spectrum and in those with mental retardation
without autism than in control children. In 99% of children with autism and 97% with mental retardation, levels of at least one of these substances
exceeded those of all control children. Concentrations were similar in subgroups of the autistic spectrum (core syndrome with or without mental retardation,
other autistic spectrum disorders with or without mental retardation) and in the presence or absence of a history of regression. Among children with mental
retardation, concentrations did not differ by severity or known cause (n = 11, including 4 with Down syndrome). Concentrations of measured substances
were similar in children with CP as compared with control subjects. SP, PACAP, NGF, and NT3 were not different by diagnostic group. No measured
analyte distinguished children with autism from children with mental retardation alone. In autism and in a heterogeneous group of disorders of cognitive
function, overexpression of certain neuropeptides and neurotrophins was observed in peripheral blood drawn in the first days of life.
There is a vocal population in my area bolstering the dietary interventions for treatment and vaccine avoidance for prevention of autism. How do I as a Pediatrician combat these issues?
Perhaps these parents like me have read the abstracts below.
Journal articles regarding autism food allergy gastrointestinal abnormalities gluten dairy and the effects of the opiate properties of milk and wheat-derived peptides on neurological function
http://www.autismndi.com/studies.htm
Summary: Based on reports from caregivers, case studies and observation of patients with schizophrenia and children with severe behavioral disorders, Dr. FC Dohan hypothesized in 1960s and 70s that gluten and dairy seemed to worsen these behaviors, and that in many cases, a restricted diet could lead to significant improvement or recovery from these disorders. The biochemical explanation for this phenomenon remained unclear, however, several other studies seemed to bear out this observation, and in 1981, using more advanced laboratory technology, Dr. Karl Reichelt, Director of Clinical Chemistry for the Department of Pediatric Research at the Rikshospitalet (National Hospital) in Oslo, Norway, found and reported abnormal peptides in the urine of schizophrenics and autistics. Peptides are pieces of proteins that are not completely broken down into individual amino acids. Dr. Reichelt has observed that these peptides, which are 4 or 5 or 6 amino acids long, have sequences that match those of opioid peptides (casomorphin and gliadomorphin). The known dietary sources of these opiate peptides are casein (from milk) and gliadin or gluten (from cereal grains). He has since conducted several studies examining this finding, as have several other researchers, including Paul Shattock at the University of Sunderland in England, Dr. Robert Cade at the University of Florida, Gainesville, and Dr. Alan Friedman, of Johnson and Johnson Ortho Clinical Diagnostics. The best evidence for this correlation lies in the thousands of case reports of improvement or recovery of children with autism on this diet. However, responsible physicians who have taken the time to review these studies must agree that there is, indeed, significant scientific evidence to support a trial period of careful elimination of these proteins from the diet of children on the autistic spectrum.
.
Whiteley P, Shattock P: Biochemical aspects in autism spectrum disorders: updating the opioid-excess theory and presenting new opportunities for biomedical intervention. Expert Opin Ther Targets. 2002 Apr;6(2):175-83.
Abstract:
Autism Research Unit, School of Sciences (Health), University of Sunderland , Sunderland , SR2 7EE , UK . aru@sunderland.ac.uk
Autism is a lifelong condition usually described as affecting social, cognitive and imaginative abilities. For many years, parents and some professionals have observed that in concordance with the behavioural and psychological symptoms of the condition, there are a number of physiological and biochemical correlates which may also be of relevance to the syndrome. One area of interest that encompasses many of these observations is the opioid-excess theory of autism. The main premise of this theory is that autism is the result of a metabolic disorder. Peptides with opioid activity derived from dietary sources, in particular foods that contain gluten and casein, pass through an abnormally permeable intestinal membrane and enter the central nervous system (CNS) to exert an effect on neurotransmission, as well as producing other physiologically-based symptoms. Numerous parents and professionals worldwide have found that removal of these exogenously derived compounds through exclusion diets can produce some amelioration in autistic and related behaviours. There is a surprisingly long history of research accompanying these ideas. The aim of this paper is to review the accompanying evidence in support of this theory and present new directions of intervention as a result of it.
Vojdani A, Campbell AW, Anyanwu E, Kashanian A, Bock K, Vojdani E: Antibodies to neuron-specific antigens in children with autism: possible cross-reaction with encephalitogenic proteins from milk, Chlamydia pneumoniae and Streptococcus group A. J Neuroimmunol 2002 Aug;129(1-2):168-77.
Abstract:
Section of Neuroimmunology, Immunosciences Laboratory, Inc., 8693 Wilshire Boulevard, Suite 200 , Beverly Hills , CA 90211 , USA . immunsci@ix.netcom.com
We measured autoantibodies against nine different neuron-specific antigens and three cross-reactive peptides in the sera of autistic subjects and healthy controls by means of enzyme-linked immunosorbent assay (ELISA) testing. The antigens were myelin basic protein (MBP), myelin-associated glycoprotein (MAG), ganglioside (GM1), sulfatide (SULF), chondroitin sulfate (CONSO4), myelin oligodendrocyte glycoprotein (MOG), alpha,beta-crystallin (alpha,beta-CRYS), neurofilament proteins (NAFP), tubulin and three cross-reactive peptides, Chlamydia pneumoniae (CPP), streptococcal M protein (STM6P) and milk butyrophilin (BTN). Autistic children showed the highest levels of IgG, IgM and IgA antibodies against all neurologic antigens as well as the three cross-reactive peptides. These antibodies are specific because immune absorption demonstrated that only neuron-specific antigens or their cross-reactive epitopes could significantly reduce antibody levels. These antibodies may have been synthesized as a result of an alteration in the blood-brain barrier. This barrier promotes access of preexisting T-cells and central nervous system antigens to immunocompetent cells, which may start a vicious cycle. These results suggest a mechanism by which bacterial infections and milk antigens may modulate autoimmune responses in autism.
Knivsberg AM, Reichelt KL, Hoien T, Nodland M: A randomised, controlled study of dietary intervention in autistic syndromes. Nutr Neurosci 2002 Sep;5(4):251-61.
Center for Reading Research, Stavanger University College, Norway. ann-mari.knivsberg@slf.his.no
Abstract:
Impaired social interaction, communication and imaginative skills characterize autistic syndromes. In these syndromes urinary peptide abnormalities, derived from gluten, gliadin, and casein, are reported. They reflect processes with opioid effect. The aim of this single blind study was to evaluate effect of gluten and casein-free diet for children with autistic syndromes and urinary peptide abnormalities. A randomly selected diet and control group with 10 children in each group participated. Observations and tests were done before and after a period of 1 year. The development for the group of children on diet was significantly better than for the controls.
Hadjivassiliou M, Grunewald RA, Davies-Jones GA : Gluten sensitivity as a neurological illness. J Neurol Neurosurg Psychiatry. 2002 May;72(5):560-3. [No abstract available]
Hadjivassiliou M, Boscolo S, Davies-Jones GA, Grunewald RA, Not T, Sanders DS, Simpson JE, Tongiorgi E, Williamson CA, Woodroofe NM: The humoral response in the pathogenesis of gluten ataxia. Neurology 2002 Apr 23;58(8):1221-6.
Abstract:
Department of Clinical Neurology, The Royal Hallamshire Hospital , Sheffield , UK . m.hadjivassiliou@sheffield.ac.uk
OBJECTIVE: To characterize humoral response to cerebellum in patients with gluten ataxia. BACKGROUND: Gluten ataxia is a common neurologic manifestation of gluten sensitivity. METHODS: The authors assessed the reactivity of sera from patients with gluten ataxia (13), newly diagnosed patients with celiac disease without neurologic dysfunction (24), patients with other causes of cerebellar degeneration (11), and healthy control subjects (17) using indirect immunocytochemistry on human cerebellar and rat CNS tissue. Cross-reactivity of a commercial IgG antigliadin antibody with human cerebellar tissue also was studied. RESULTS: Sera from 12 of 13 patients with gluten ataxia stained Purkinje cells strongly. Less intense staining was seen in some but not all sera from patients with newly diagnosed celiac disease without neurologic dysfunction. At high dilutions (1:800) staining was seen only with sera from patients with gluten ataxia but not in control subjects. Sera from patients with gluten ataxia also stained some brainstem and cortical neurons in rat CNS tissue. Commercial anti-gliadin antibody stained human Purkinje cells in a similar manner. Adsorption of the antigliadin antibodies using crude gliadin abolished the staining in patients with celiac disease without neurologic dysfunction, but not in those with gluten ataxia. CONCLUSIONS: Patients with gluten ataxia have antibodies against Purkinje cells. Antigliadin antibodies cross-react with epitopes on Purkinje cells.
Garvey J: Diet in autism and associated disorders. J Fam Health Care 2002;12(2):34-8.
Abstract:
Royal Free Hospital, London .
A dietitian discusses the theory that peptides with opioid activity may cause or trigger autism. The use of an exclusion diet to treat autism is explained, weighing the potential benefits against some of the practical difficulties of keeping to a strict exclusion diet. The use of nutritional supplements is described. An abnormal gut flora has also been implicated in autism and the use of probiotics and prebiotics in improving the integrity of the gut mucosa is also discussed.
Cornish E: Gluten and casein free diets in autism: a study of the effects on food choice and nutrition. J Hum Nutr Diet 2002 Aug;15(4):261-9.
Abstract:
Senior Community Dietitian, Community Nutrition Service, South Derbyshire Community Health NHS Trust, Dar es Salaam , Tanzania .
BACKGROUND: There is growing interest in possible dietary involvement in the aetiology and treatment of Autistic Spectrum Disorders (ASD). Research has focused on the physiological and behavioural effects of dietary change but has not examined the effect of exclusion diets on nutritional intake. AIMS: The aim of this study was to examine whether the removal of major dietary staples placed children with autism at risk of nutrient deficiency and compares their food choice with ASD children not following gluten and/or casein free diets. METHODS: A postal questionnaire was sent to parents of children aged 3-16 years, diagnosed with ASD belonging to the National Autistic Society in Leicestershire and southern Derbyshire. Detailed dietary information and a 3-day food diary were collected. The sample size was small: those using gluten/casein free diets (n = 8) and those not following diet (n = 29). RESULTS: Nutrient intakes fell below the Lower Reference Nutrient Intake (LRNI) in 12 children (32%) for zinc, calcium, iron, vitamin A, vitamin B12 and riboflavin in the nondiet group and four children (50%) for zinc and calcium in the diet group. Fruit and vegetable intakes were higher and cereal, bread and potato consumption were lower in those children using gluten and/or casein free diets. CONCLUSION: No significant differences in the energy, protein and micronutrient intakes were found between the two groups of children. A longitudinal prospective study is suggested to examine whether differences in food choice are the result of dietary intervention or the prerequisite for the successful application of diet in this special group of children.
Knivsberg AM, Reichelt KL, Nodland M: Reports on dietary intervention in autistic disorders. Nutr Neurosci 2001;4(1):25-37.
Center for Reading Research, Stavanger College , Norway . ann-mari.knivsberg@slf.his.no
Abstract:
Autism is a developmental disorder for which no cure currently exists. Gluten and/or casein free diet has been implemented to reduce autistic behaviour, in addition to special education, since early in the eighties. Over the last twelve years various studies on this dietary intervention have been published in addition to anecdotal, parental reports. The scientific studies include both groups of participants as well as single cases, and beneficial results are reported in all, but one study. While some studies are based on urinary peptide abnormalities, others are not. The reported results are, however, more or less identical; reduction of autistic behaviour, increased social and communicative skills, and reappearance of autistic traits after the diet has been broken.
Jyonouchi H, Sun S, Le H.: Proinflammatory and regulatory cytokine production associated with innate and adaptive immune responses in children with autism spectrum disorders and developmental regression. J Neuroimmunol 2001 Nov 1;120(1-2):170-9
Abstract:
Department of Pediatrics, University of Minnesota , MMC 610 FUMC, 420 Delaware Street SE , Minneapolis , MN 55455 , USA . jyono001@tc.umn.edu
We determined innate and adaptive immune responses in children with developmental regression and autism spectrum disorders (ASD, N=71), developmentally normal siblings (N=23), and controls (N=17). With lipopolysaccharide (LPS), a stimulant for innate immunity, peripheral blood mononuclear cells (PBMCs) from 59/71 (83.1%) ASD patients produced > 2 SD above the control mean (CM) values of TNF-alpha, IL-1beta, and/or IL-6 produced by control PBMCs. ASD PBMCs produced higher levels of proinflammatory/counter-regulatory cytokines without stimuli than controls. With stimulants of phytohemagglutinin (PHA), tetanus, IL-12p70, and IL-18, PBMCs from 47.9% to 60% of ASD patients produced > 2 SD above the CM values of TNF-alpha depending on stimulants. Our results indicate excessive innate immune responses in a number of ASD children that may be most evident in TNF-alpha production.
Hadjivassiliou M, Grunewald RA, Lawden M, Davies-Jones GA , Powell T, Smith CM: Headache and CNS white matter abnormalities associated with gluten sensitivity. Neurology 2001 Feb 13;56(3):385-8.
Abstract:
Department of Clinical Neurology, The Royal Hallamshire Hospital , Sheffield , UK . m.hadjivassiliou@sheffield.ac.uk
The authors describe 10 patients with gluten sensitivity and abnormal MRI. All experienced episodic headache, six had unsteadiness, and four had gait ataxia. MRI abnormalities varied from confluent areas of high signal throughout the white matter to foci of high signal scattered in both hemispheres. Symptomatic response to gluten-free diet was seen in nine patients.
Dubynin VA , Ivleva IuA, Malinovskaia IV, Kamenskii AA, Andreeva LA, Alfeeva LIu, Miasoedov NF Changes in beta-casomorphine-7 effect on behavior of albino rat pups in postnatal development [Article in Russian]. Zh Vyssh Nerv Deiat Im I P Pavlova 2001 May-Jun;51(3):386-9.
Abstract:
Lomonosov State University , Institute of Molecular Genetics , Russian Academy of Sciences, Moscow .
The analgetic effect of heptapeptide beta-casomorphine-7 in newborn albino rats (20 mg/kg, i.p.) was recorded already 14 days after birth in the " hot plate" test. The first signs of a possible influence of the peptide on motor activity were observed only at the age of 28 days. They are expressed in impairment of motor coordination and change in locomotion level (" Opto-Varimex" test). The obtained evidence probably reflect the processes of discrete maturation of different components of the opioid system of the rat brain.
Cavataio F, Carroccio A, Iacono G.: Milk-induced reflux in infants less than one year of age. J Pediatr Gastroenterol Nutr 2000;30 Suppl:S36-44
Abstract:
1st Divisione Pediatria, Gastroenterologia, Ospedale dei Bambini G. Di Cristina, Palermo , Italy .
Cow's milk allergy (CMA) and gastroesophageal reflux are considered to be among the most common disturbances in infants less than 1 year of age. In recent years, the relationship existing between these two entities has been investigated and some important conclusions have been reached: In just under half the cases of GER in infants less than 1 year of age there is an association with CMA; in a high proportion of cases, GER is not only CMA-associated but also CMA-induced; the frequency of this association should induce pediatricians to screen for possible concomitant CMA in all infants with GER less than 1 year old; with the exception of some patients with mild typical CMA manifestations (diarrhea, dermatitis, or rhinitis), the symptoms of GER associated with CMA are the same as those observed in primary GER; immunologic tests are useful in a suspected association between GER and CMA; and subjects with GER secondary to CMA show a typical pH-monitoring tracing pattern, characterized by a progressive, slow decrease in esophageal pH between feedings. This article reviews the main features of the two diseases, stressing the aspects in common between them and comments on all the listed points.
NOTE: Reflux appears to be common in autistic infants.
Carroccio A, Montalto G, Custro N, Notarbartolo A, Cavataio F, D'Amico D, Alabrese D, Iacono G: Evidence of very delayed clinical reactions to cow's milk in cow's milk-intolerant patients. Allergy 2000 Jun;55(6):574-9.
Abstract:
Internal Medicine, University Hospital of Palermo , Italy .
BACKGROUND: In patients with cow's milk protein intolerance (CMPI), delayed clinical reactions to cow's milk (CM) ingestion may be misdiagnosed if the clinical symptoms are not " classical" and there is a long time lapse between ingestion of CM and the clinical reaction. The aim was to evaluate the clinical outcome of CMPI in a cohort of CM-intolerant children, with particular attention to the occurrence of clinical manifestations beyond 72 h after CM challenge. METHODS: Eighty-six consecutive patients (44 boys, 42 girls) with new CMPI diagnoses were enrolled; median age at diagnosis was 4 months. Patients were followed up for a mean period of 40 months. In all patients, CMPI diagnosis was made on the observation of symptoms, their disappearance after elimination diet, and their reappearance on double-blind CM challenge. At CMPI diagnosis, immunologic tests to demonstrate IgE-mediated hypersensitivity were performed. After 12 months of CM-free diet, CM tolerance was re-evaluated with a CM challenge continued at home for up to 30 days, according to a double-blind, placebo-controlled method. Patients who did not achieve CM tolerance continued a CM-free diet and subsequently underwent yearly CM challenge. RESULTS: The percentages of CMPI patients who became CM-tolerant after 1, 2, and 3 years of CM-free diet were 30%, 54.5%, and 70%, respectively. At the end of the follow-up period, 26/86 subjects showed persistent CMPI; these patients had a higher percentage of positivity of total serum IgE (P< 0.05), RAST (P< 0.01), and cutaneous prick tests for CM antigens (P< 0.001) than all the others. At CMPI diagnosis, all patients had a clinical reaction within 72 h from the beginning of the CM challenge; at the subsequent " cure" challenges, we observed patients who first reacted to CM more than 72 h after ingestion. In total, 10 out of 86 patients showed " very delayed reactions" ; in these patients, the mean time between the beginning of CM challenge and the onset of a clinical symptom was 13.3 days (range 4-26 days). The number of " very late reactors" increased from the first to the third of the " cure" CM challenges, performed at yearly intervals. The " very delayed" CMPI manifestations in these subjects were constipation (five cases), wheezing (two cases), dermatitis plus constipation (two cases), and dermatitis alone (one case); in 6/10 patients, the symptoms observed at the " cure challenge" were different from those at CMPI onset. CONCLUSIONS: Very delayed clinical reactions to reintroduction of CM in the diet can occur in CMPI patients; thus, accurate follow-up and frequent outpatient observation in patients with a long history of CMPI are probably more useful and safer than prolonged CM challenge.
Cade R, Privette M, Fregly M, Rowland N, Sun Z, Zele V, Wagemaker H, Edlestein C: Autism and schizophrenia: intestinal disorders. Nutritional Neuroscience 3: 57-72, 2000. [No abstract available]
Pedersen OS, Liu Y, Reichelt KL. Serotonin uptake stimulating peptide found in plasma of normal individuals and in some autistic urines. J Pept Res 1999 Jun;53(6):641-6
Abstract:
Research Institute, University of Oslo , Rikshospitalet , Norway .
We have isolated a tripeptide from normal plasma and autistic urines which stimulates the uptake of serotonin (5-HT) into platelets. This peptide was purified by high-performance liquid chromatography (HPLC) and characterized by sequenation and mass-spectrometry. Synthetic peptide showed co-chromatography with the biological sample in the HPLC systems used. Close to 60% of the autistic children diagnosed using the Diagnostic Statistical Manual III-R had an increased HPLC peak eluting like this peptide in their urines compared with controls.
Ek J, Stensrud M, Reichelt KL. Gluten-free diet decreases urinary peptide levels in children with celiac disease. J Pediatr Gastroenterol Nutr 1999 Sep;29(3):282-5.
Abstract:
Department of Pediatrics, Buskerud Central Hospital , Drammen , Norway .
BACKGROUND: Increased urine secretion of peptides has been found in celiac disease, probably resulting from increased intestinal uptake of peptides caused by damage to the small gut mucosa. METHODS: High-performance liquid chromatography of low-molecular-weight peptides in the urine was performed over 6 months, before and after a gluten-free diet was instituted in children who clinically improved while consuming the diet. RESULTS: A significant decrease of peptide levels was observed in children consuming the gluten-free diet. Certain peptide peaks thought to be gluten related decreased the most after the patients began the diet. CONCLUSIONS: Because the peptides decrease in patients consuming a gluten-free diet, it is reasonable to conclude that such peptides have a mostly dietary origin.
Cade JR et al: Autism and schizophrenia linked to malfunctioning enzyme for milk protein digestion. Autism, Mar 1999.
Cade JR, Privette RM, Fregly M, Rowland N, Sun Z, Zele V, Wagemaker H Edelstein C: Autism and schizophrenia: Intestinal disorders. Nutritional Neuroscience 1999, 2, 57-72.
Alberti A, Pirrone P, Elia M, Waring RH, Romano C. Sulphation deficit in " low-functioning" autistic children: a pilot study. Biol Psychiatry 1999 Aug 1;46(3):420-4.
Abstract:
Department of Pediatrics, Oasi Institute for Research on Mental Retardation and Brain Aging (IRCCS), Troina , Italy .
BACKGROUND: Parents of autistic children and autism support groups often report that autistic episodes are exacerbated when the children eat certain foodstuffs such as dairy products, chocolates, wheat, corn sugar, apples, and bananas. The hypothesis that autistic behavior might be related to metabolic dysfunctions has led us to investigate in a group of " low functioning" autistic children and in an age-matched control group each made up of 20 subjects, the sulphation capacity available. METHODS: Utilizing the biochemical characteristics of paracetamol we evaluated by high performance liquid chromatography, the urine paracetamol-sulfate/paracetamol-glucuronide (PS/PG) ratio in all subjects following administration of this drug. RESULTS: The PS/PG ratio in the group of autistic subjects gave a significantly lower results than the control group with p < .00002. CONCLUSIONS: The inability to effectively metabolize certain compounds particularly phenolic amines, toxic for the CNS, could exacerbate the wide spectrum of autistic behavior.
Iacono G, Cavataio F, Montalto G, Florena A, Tumminello M, Soresi M, Notarbartolo A, Carroccio A: Intolerance of cow's milk and chronic constipation in children. New England Journal of Medicine 1998 / 339 (16) / 1100-1104.
Abstract:
Divisione di Pediatria, Ospedale G. Di Cristina, Palermo , Italy .
BACKGROUND: Chronic diarrhea is the most common gastrointestinal symptom of intolerance of cow's milk among children. On the basis of a prior open study, we hypothesized that intolerance of cow's milk can also cause severe perianal lesions with pain on defecation and consequent constipation in young children. METHODS: We performed a double-blind, crossover study comparing cow's milk with soy milk in 65 children (age range, 11 to 72 months) with chronic constipation (defined as having one bowel movement every 3 to 15 days). All had been referred to a pediatric gastroenterology clinic and had previously been treated with laxatives without success; 49 had anal fissures and perianal erythema or edema. After 15 days of observation, the patients received cow's milk or soy milk for two weeks. After a one-week washout period, the feedings were reversed. A response was defined as eight or more bowel movements during a treatment period. RESULTS: Forty-four of the 65 children (68 percent) had a response while receiving soy milk. Anal fissures and pain with defecation resolved. None of the children who received cow's milk had a response. In all 44 children with a response, the response was confirmed with a double-blind challenge with cow's milk. Children with a response had a higher frequency of coexistent rhinitis, dermatitis, or bronchospasm than those with no response (11 of 44 children vs. 1 of 21, P=0.05); they were also more likely to have anal fissures and erythema or edema at base line (40 of 44 vs. 9 of 21, P< 0.001), evidence of inflammation of the rectal mucosa on biopsy (26 of 44 vs. 5 of 21, P=0.008), and signs of hypersensitivity, such as specific IgE antibodies to cow's-milk antigens (31 of 44 vs. 4 of 21, P< 0.001). CONCLUSIONS: In young children, chronic constipation can be a manifestation of intolerance of cow's milk.
Iacono G, Cavataio F, Montalto G, Soresi M, Notarbartolo A, Carroccio A: Persistent cow's milk protein intolerance in infants: the changing faces of the same disease. Clin Exp Allergy 1998 Jul;28(7):817-23.
Abstract:
II Divisione di Pediatria, Ospedale Di Cristina, Universita di Palermo, Italy.
BACKGROUND: Recent research has shown that cow's milk protein intolerance (CMPI) often persists beyond 4 years of age. AIMS: To evaluate the clinical and immunological characteristics of a group of infants with persistent CMPI. PATIENTS AND METHODS: Twelve infants (6 m, 6f) with persistent CMPI were followed up from birth until a median age of 5 years. The patients underwent CMP challenge each year to evaluate CMP-tolerance. As controls we followed 26 infants (12 m, 14 f) with CMPI that resolved within 1-2 years. RESULTS: A family history of atopic disease was found in 10/12 patients with persistent CMPI and in 10/26 controls (P< 0.01). Clinical presentation changed over time: at onset symptoms were prevalently gastrointestinal, while at the end of the study there was an increased frequency of wheezing and constipation and a higher frequency of delayed reactions to CMP-challenge than at study commencement (9/12 vs 2/12; P< 0.007). 11/12 infants with persistent CMPI and 3/26 controls (P< 0.0001) presented multiple food intolerance. During the observation period 9/12 infants with persistent CMPI and 2/26 controls showed atopic disease: asthma, rhinitis, eczema (P < 0.0001). CONCLUSIONS: Persistent CMPI forms are characterized by: (a) considerable importance of familial atopic disease; (b) change in CMPI manifestations over time and more prolonged delay between CMP consumption and manifestation of symptoms; (c) very high frequency of multiple food intolerance and allergic diseases.
Teschemacher, H. et al, Milk protein-derived opioid receptor ligands. Biopolymers. 1997 / 43 (2) / 99-117.
Abstract:
Rudolf-Buchheim-Institut fur Pharmakologie, Justus-Liebig-Universitat, Giessen , Germany .
Milk is mammalian characteristic and is of particular importance for humans: Mother's milk or its substitutes from cows' milk are absolutely essential nutriments for the neonate and cows' milk also represents a basic foodstuff for adults. However, in addition to their well-known nutritive role, milk constituents apparently are also able to carry specific information from the milk producer's to the milk receiver's organism: Thus, a number of milk protein fragments has been shown to behave like opioid receptor ligands able to address opioidergic systems in the adult's or in the neonate's organism. With respect to the proteins, which they are derived off these peptides have been named alpha-casein exorphins or casoxin D (alpha-casein), beta-casomorphins or beta-casorphin (beta-casein), casoxin or casoxin A, B, or C (k-casein), alpha-lactorphins (alpha-lactalbumin), beta-lactorphin (beta-lactoglobulin) or lactoferroxins (lactoferrin). Only casoxins and lactoferroxins display antagonistic properties; the other peptides behave like opioid receptor agonists. Most of the information available so far has been collected about beta-casomorphins. These peptides obviously can be released from beta-casein in the adult's or in the neonate's organism, where they might elicit opioid effects in the frame of a regulatory role as " food hormones" . Several synthetic beta-casomorphin derivatives have been shown to be highly specific and potent mu-type opioid receptor ligands which frequently have been used as standard tools in opioid research.
Fukudome, S. et al, Release of opioid peptides, gluten exorphins by the action of pancreatic elastase. FEBS Lett. 1997 / 412 (3) / 475-479.
Abstract:
Food Research Laboratory, Nisshin Flour Milling Co. Ltd., Saitama , Japan .
The release of opioid peptides, gluten exorphins A, which have been isolated from the pepsin-thermolysin digest of wheat gluten, with gastrointestinal proteases was examined. High levels of gluten exorphin A5 (Gly-Tyr-Tyr-Pro-Thr) immunoreactive materials were detected in the pepsin-pancreatic elastase digest by a competitive ELISA. From this digest, gluten exorphin A5, B5 and B4 were isolated. This means that these peptides are released in the gastrointestinal tracts after ingestion of wheat gluten. The yield of gluten exorphin A5 in the pepsin-elastase digest was larger than that in the pepsin-thermolysin digest. The gluten exorphin A5 sequence is found 15 times in the primary structure of the high molecular weight glutenin. The region from which gluten exorphin A5 was released by the action of pancreatic elastase was identified using synthetic fragment peptides.
Scifo R, Cioni M, Nicolosi A, Batticane N, Tirolo C, Testa N, Quattropani MC, Morale MC, Gallo F, Marchetti B: Opioid-immune interactions in autism: behavioural and immunological assessment during a double-blind treatment with naltrexone. Ann Ist Super Sanita 1996;32(3):351-9.
Abstract:
Servizio di Psichiatria, Istituto OASI per lo Studio del Ritardo Mentale e l'Involuzione Cerebrale, Troina (Enna), Italy .
The emerging concept of opioid peptides as a new class of chemical messengers of the neuroimmune axis and the presence of a number of immunological abnormalities in infantile autism prompted us to correlate biological (hormonal and immunological) determinations and behavioural performances during treatment with the potent opiate antagonist, naltrexone (NAL). Twelve autistic patients ranging from 7 to 15 years, diagnosed according to DSM-III-R, entered a double-blind crossover study with NAL at the doses of 0.5, 1.0 and 1.5 mg/kg every 48 hours. The behavioural evaluation was conducted using the specific BSE and CARS rating scales NAL treatment produced a significant reduction of the autistic symptomatology in seven (" responders" ) out of 12 children. The behavioural improvement was accompanied by alterations in the distribution of the major lymphocyte subsets, with a significant increase of the T-helper-inducers (CD4+CD8-) and a significant reduction of the T-cytotoxic-suppressor (CD4-CD8+) resulting in a normalization of the CD4/CD8 ratio. Changes in natural killer cells and activity were inversely related to plasma beta-endorphin levels. It is suggested that the mechanisms underlying opioid-immune interactions are altered in this population of autistic children and that an immunological screening may have prognostic value for the pharmacological therapy with opiate antagonists.
Hadjivassiliou M, Gibson A, Davies- Jones GA , Lobo AJ, Stephenson TJ, Milford-Ward A: Does cryptic gluten sensitivity play a part in neurological illness? Lancet 1996 Feb 10;347(8998):369-71.
Abstract:
Department of Neurology, Royal Hallamshire Hospital , Sheffield , UK .
BACKGROUND: Antigliadin antibodies are a marker of untreated coeliac disease but can also be found in individuals with normal small-bowel mucosa. Because neurological dysfunction is a known complication of coeliac disease we have investigated the frequency of antigliadin antibodies, as a measure of cryptic gluten sensitivity, and coeliac disease in neurological patients. METHODS: Using ELISA, we estimated serum IgG and IgA antigliadin antibodies in 147 neurological patients who were divided into two groups. There were 53 patients with neurological dysfunction of unknown cause despite full investigation (25 ataxia, 20 peripheral neuropathy, 5 mononeuritis multiplex, 4 myopathy, 3 motor neuropathy, 2 myelopathy). The remaining 94 patients were found to have a specific neurological diagnosis (16 stroke, 12 multiple sclerosis, 10 Parkinson's disease, 56 other diagnoses) and formed the neurological control group. 50 healthy blood donors formed a third group. FINDINGS: The proportions of individuals with positive titres for antigliadin antibodies in the three groups were 30/53, 5/94, and 6/50 respectively (57, 5, and 12%). The difference in proportion between group 1 and the combined control groups was 0.49 (95% CI 0.35-0.63). Distal duodenal biopsies in 26 out of 30 antigliadin-positive patients from group 1 revealed histological evidence of coeliac disease in nine (35%), non-specific duodenitis in ten (38%), and no lesion in seven (26%) individuals. INTERPRETATION: Our data suggest that gluten sensitivity is common in patients with neurological disease of unknown cause and may have aetiological significance.
D'Eufemia P., Celli M., Finocchiaro R., Pacifico L., Viozzi L., Zaccagnini M., Cardi E., Giardini O: Abnormal Intestinal Permeability in Children with Autism. Acta Paediatrica,1996; 85: 1076-1079.
Abstract:
Institute of Pediatrics , La Sapienza University of Rome , Italy .
We determined the occurrence of gut mucosal damage using the intestinal permeability test in 21 autistic children who had no clinical and laboratory findings consistent with known intestinal disorders. An altered intestinal permeability was found in 9 of the 21 (43%) autistic patients, but in none of the 40 controls. Compared to the controls, these nine patients showed a similar mean mannitol recovery, but a significantly higher mean lactulose recovery (1.64% +/- 1.43 vs 0.38% +/- 0.14; P < 0.001). We speculate that an altered intestinal permeability could represent a possible mechanism for the increased passage through the gut mucosa of peptides derived from foods with subsequent behavioural abnormalities.
Lucarelli, S., Frediani, T., Zingoni, A.M., Ferruzzi, F., Giardini, O., Quintieri, F., Barbato, M., D'Eufemia, P., Cardi, E.: Food allergy and infantile autism, Panminerva Med., 1995 Sep; 37(3): 137-41.
Abstract:
Department of Paediatrics, University of Rome La Sapienza , Italy .
The etiopathogenesis of infantile autism is still unknown. Recently some authors have suggested that food peptides might be able to determine toxic effects at the level of the central nervous system by interacting with neurotransmitters. In fact a worsening of neurological symptoms has been reported in autistic patients after the consumption of milk and wheat. The aim of the present study has been to verify the efficacy of a cow's milk free diet (or other foods which gave a positive result after a skin test) in 36 autistic patients. We also looked for immunological signs of food allergy in autistic patients on a free choice diet. We noticed a marked improvement in the behavioural symptoms of patients after a period of 8 weeks on an elimination diet and we found high levels of IgA antigen specific antibodies for casein, lactalbumin and beta-lactoglobulin and IgG and IgM for casein. The levels of these antibodies were significantly higher than those of a control group which consisted of 20 healthy children. Our results lead us to hypothesise a relationship between food allergy and infantile autism as has already been suggested for other disturbances of the central nervous system.
Lensing P, Schimke H, Klimesch W, Pap V, Szemes G, Klingler D, Panksepp J: Clinical case report: opiate antagonist and event-related desynchronization in 2 autistic boys. Neuropsychobiology 1995;31(1):16-23.
Abstract:
Department of Physiological Psychology, University of Salzburg , Austria .
Event-related desynchronization and visual orientational behavior were examined in 2 autistic boys to determine if blockade of endogenous opioid activity facilitates cognitive processing at a cortical level. Before naltrexone, the boys showed no selective alpha blocking during exposure to either mother's pictures or white light. Unlike normals, they exhibited strong alpha band enhancement at temporocentral recording sites. Two hours after administering 0.5 mg/kg naltrexone, mother-as well as light-related alpha blocking appeared at occipital, occipitotemporal, and prefrontal sites. These effects were gone 24 h after dosing in one child, but persisted in the other. A parallel increase in visual pursuit in a social context was observed. These results affirm that autistic gaze aversion can be caused by excessive opioid activity interfering with corticothalamocortical processing of visual stimuli.
Kurek M, Czerwionka-Szaflarska M, Doroszewska G.Pseudoallergic
skin reactions to opiate sequences of bovine casein in healthy
children. Rocz Akad Med Bialymst 1995;40(3):480-5.
Abstract:
Department of Gastroenterology, Academy of Medicine , Gdansk .
Skin tests with opioid peptides naturally occurring in cow's milk: beta-casomorphin-7 and alpha-casein (90-95), were performed in 25 healthy children. Wheal and flare reactions, similiar to histamine and codeine were observed in all children. The area of these reactions was concentration dependent. Pretreatment with H1 antagonist--cetirizine significantly inhibited the skin response to both peptides. Beta-casomorphin-7 and alpha-casein (90-95) are noncytotoxic histamine releasers in humans.
Knivbserg A.M., Reichelt K.L., Nodland M., Hoien T.: Autistic syndromes and diet. A four year follow-up study. Scand J Educat. Res. 1995, 39: 223-236. [No abstract available]
Bouvard MP, Leboyer M, Launay JM, Recasens C, Plumet MH, Waller-Perotte D, Tabuteau F, Bondoux D, Dugas M, Lensing P, et al: Low-dose naltrexone effects on plasma chemistries and clinical symptoms in autism: a double-blind, placebo-controlled study. Psychiatry Res 1995 Oct 16;58(3):191-201.
Abstract:
Service de Psychopathologie de l'Enfant et de l'Adolescent, Hopital Robert Debre, Paris, France.
The effect of month-long naltrexone (NTX) treatment at a daily oral dose of 0.5 mg/kg/day was contrasted with placebo (PLC) in a double-blind study with conjoint clinical and biochemical evaluations of therapeutic effects. Modest clinical benefits were achieved with both PLC and NTX, with marginally better overall results following NTX, and degree of improvement appeared to be related to plasma chemical profiles. Massively elevated levels of beta-endorphin were observed in all children with assays using C-terminal antibody but not with an N-terminal antibody assay. In addition, 70% of the children exhibited abnormally low levels of adrenocorticotropic hormone, and smaller subsets exhibited elevated norepinephrine (60%), arginine-vasopressin (50%), and serotonin (20%). The best clinical responders exhibited the clearest normalization of the elevated plasma chemistries, especially in C-terminal-beta-endorphin and serotonin. There was some evidence of therapeutic carry-over effects in both clinical and biochemical measures in those children who received NTX before PLC. The results suggest that NTX only benefits a subgroup of autistic children, who may be identified by the presence of certain plasma abnormalities. These results suggest a possible linkage between abnormal plasma chemistries, especially those related to the pro-opiomelanocortin system, and autistic symptoms.
Reichelt K.L. Knivsberg AM, Nodland M, Lind G: Nature and consequences of hyperpeptiduria and bovine casomorphin found in autistic syndromes. Develop Brain Dysfunct. 1994, 7: 71-85. [No abstract available]
Gardner M.L.G.: Absorption of intact proteins and peptides. Physiol of gastrointestinal Tract 3rd edit (edit: LR Johnson) Raven press, New York 1994: 1795-1820.
Leboyer M, Bouvard MP, Launay JM, Recasens C, Plumet MH, Waller-Perotte D, Tabuteau F, Bondoux D, Dugas M: Opiate hypothesis in infantile autism? Therapeutic trials with naltrexone [Article in French]. Encephale 1993 Mar-Apr;19(2):95-102.
Abstract:
Service de Psychiatrie Adulte, Hopital Pitie-Salpetriere, Paris.
The opioid hypothesis suggests that childhood autism may result from excessive brain opioid activity during neonatal period which may constitutionally inhibit social motivation, yielding autistic isolation and aloofness (Panksepp, 1979). This hypothesis has now received strong support and is currently based on three types of arguments: (1) similarity between autistic symptomatology and abnormal behaviors induced in young animals by injections of exogenous opioids, such as increasing social aloofness and decreasing social vocalization; (2) direct biochemical evidence of abnormalities of peripheral endogenous opioids being reported in autism and (3) therapeutic effects of the long lasting opioid receptor blocking agent naltrexone in autism. In this article, we give description of open and double-blind studies of naltrexone in autism. Naltrexone has been tested in several open studies. We performed an open trial with naltrexone in 2 autistic girls, displaying serious self-injurious behavior, reduced crying and a marked preference for salty and spicy foods, symptoms that could be related to a dysfunction of the opioid system. With dosages of 1 mg/kg/day, we observed an immediate reduction of hyperactivity, self-injurious behavior and aggressiveness, while attention improved. In addition, social behaviors, smiling, social seeking behaviors and play interactions increased (Leboyer, Bouvard et Dugas, 1988). Campbell et al. (1988) has also reported a tranquilizing and a stimulating effect in 6 out of 8 children with autism. We did confirm these preliminary results in a double-blind study performed on 4 children with autism. In a cross-over double-blind study, three dosages of naltrexone (0.5, 1 and 2 mg/kg/day) and placebo were compared. (ABSTRACT TRUNCATED AT 250 WORDS)
Fukudome S, Yoshikawa M: Gluten exorphin C , A novel opioid peptide derived from wheat gluten. FEBS 1993; 316: 17-19.
Abstract:
Research Control Department, Nisshin Flour Milling Co., Ltd., Nihonbashi, Tokyo , Japan .
A novel opioid peptide, Tyr-Pro-Ile-Ser-Leu, was isolated from the pepsin-trypsin-chymotrypsin digest of wheat gluten. Its IC50 values were 40 microM and 13.5 microM in the GPI and MVD assays, respectively. This peptide was named gluten exorphin C. Gluten exorphin C had a structure quite different from any of the endogenous and exogenous opioid peptides ever reported in that the N terminal Tyr was the only aromatic amino acid. The analogs containing Tyr-Pro-X-Ser-Leu were synthesized to study its structure-activity relationship. Peptides in which X was an aromatic amino acid or an aliphatic hydrophobic amino acid had opioid activity.
Bidet B, Leboyer M, Descours B, Bouvard MP, Benveniste J. Allergic sensitization in infantile autism. J Autism Dev Disord 1993 Jun;23(2):419-20. [No abstract available.]
McLaughlin P.J., Zagon I.S.: Endogenous opiod systems and clinical implications for infantile autism. Proceedings of the International Symposium on Neurobiology of Infantile Autism, Tokyo , 1990, Neurobiology of Infantile Autism, Excerpta Medica 1992.
Lensing P, Klingler D, Lampl C, Leboyer M, Bouvard M, Plumet MH, Panksepp J: Naltrexone open trial with a 5-year-old-boy. A social rebound reaction. Acta Paedopsychiatr 1992;55(3):169-73.
Abstract:
School Psychology of Upper Austria , Linz .
The neurobiological rationale for an opiate antagonist pharmacotherapy of autism is presented. Naltrexone efficacy in decreasing autistic behaviour and in increasing social-affiliative behaviour was explored in a 5-year-old autistic boy. Naltrexone (0.5 mg/kg 3 times peer week) was effective in immediately decreasing gross motor activity and stereotyped behaviour and caused a delayed increase of crying, smiling and rough-and-tumble play. This single case presents preliminary evidence that a therapeutically valuable rebound reaction is possible and that the human opioid system modulates social-affective processes. The possibility of psychological factors being instrumental in achieving this effect is discussed as being suitable for future clinical trials.
Kurek M, Przybilla B, Hermann K, Ring J: A naturally occurring opioid peptide from cow's milk, beta-casomorphine-7, is a direct histamine releaser in man.Int Arch Allergy Immunol 1992;97(2):115-20.
Abstract:
Department of Dermatology, Ludwig-Maximilian-University, Munich .
beta-Casomorphine-7, a naturally occurring product of cow's milk with opiate-like activity, was studied for possible direct histamine liberation activities in humans. It was found to cause concentration-dependent in vitro histamine release from peripheral leukocytes of healthy adult volunteers. Intradermal injection of beta-casomorphine-7 induced a wheal and flare reaction in the skin similar to histamine or codeine. Oral pretreatment with the H1 antagonist terfenadine significantly inhibited the skin responses to beta-casomorphine-7. The intradermal injection of an opiate receptor antagonist, naloxone, inhibited in vitro histamine release and skin reactions only in a 100-fold excess over beta-casomorphine-7. These findings suggest that beta-casomorphine-7 can be regarded as a noncytotoxic, direct histamine releaser in humans. The clinical relevance of these findings deserves further studies.
Fukudome S, Yoshikawa M : Opioid peptides derived from wheat gluten: their isolation and characterization. Federation of European Biochemical Societies (FEBS) 1992; 296: 107-111.
Abstract:
Research Control Department, Nisshin Flour Milling Co., Ltd., Tokyo , Japan .
Four opioid peptides were isolated from the enzymatic digest of wheat gluten. Their structures were Gly-Tyr-Tyr-Pro-Thr, Gly-Tyr-Tyr-Pro,Tyr-Gly-Gly-Trp-Leu and Tyr-Gly-Gly-Trp, which were named gluten exorphins A5, A4, B5 and B4, respectively. The gluten exorphin A5 sequence was found at 15 sites in the primary structure of the high molecular weight glutenin and was highly specific for delta-receptors. The structure-activity relationships of gluten exorphins A were unique in that the presence of Gly at their N-termini increased their activities. Gluten exorphin B5, which corresponds to [Trp4,Leu5]enkephalin, showed the most potent activity among these peptides. Its IC50 values were 0.05 microM and 0.017 microM, respectively, on the GPI and the MVD assays.
Dubynin VA , Maklakova AS , Nezavibat'ko VN, Alfeeva LA, Kamenskii AA, Ashmarin IP: Effects of systemically-administered beta-casomorphin-7 on nociception in rats. [Article in Russian] Biull Eksp Biol Med 1992 Sep;114(9):284-6.
Abstract:
The influence of food-derived heptapeptide beta-casomorphin-7 (beta-CM-7) on pain sensibility of white rats was studied by tail flick test. As shown for doses 10 and 20 mg/kg intraperitoneally, injected beta-CM-7 induced significant analgesia; lower peptide concentration (5 mg/kg) was ineffective. As a whole, there is a significant positive correlation between the intensity of analgesia and the quantity of administered exorphine. These changes of pain sensibility were observed for one hour after injection of heptapeptide; further measurements showed no significant difference of time reaction between control and experimental groups of rats. It was found out that animals with high native level of pain sensibility (4-8 sec) made the main contribution to manifestation of analgesia.
Bouvard M.P., Leboyer M., Launay J.M., Kerdelhue B., Dugas M.: The opiod excess hypothesis of autism: A double-blind study of naltrexone. Proc. of the Intern. Symp. on Neurob. of Inf. Autism , 1990, Neurobiology of Infantile Autism , Exerpta Medica 1992.
Teschemacher H, Koch G: Opioids in the milk. Endocr Regul 1991 Sep;25(3):147-50.
Abstract:
Rudolf-Buchheim-Institut fur Pharmakologie, Justus-Liebig-Universitat Giessen, Germany.
In various studies, the milk has been screened for the presence of free or precursor-bound opioids. In fact, various opioid receptor ligands with agonistic or even antagonistic activity were found. Besides the alkaloid morphine, peptides derived from alpha-casein (alpha-casein exorphins), beta-casein (beta-casomorphins; beta-casorphin), alpha-lactalbumin (alpha-lactorphins) and beta-lactoglobulin (beta-lactorphin) were among the agonists. In addition, certain peptides derived from k-casein (casoxins) or from lactoferrin (lactoferroxins) were found to behave like opioid antagonists. Although a functional role in the mammalian organism for all of these compounds appears to be well possible, evidence has only been presented for the functional significance of beta-casomorphins, so far. These peptides might play a role in reproduction or nutrition in the female, in the newborn's or in a milk consumer's organism, respectively. Thus, opioids related to milk might represent essential exogenous extensions of the endogenous opiodergic systems.
Risebro, B.: Gluten-free diet in infantile autism. Tidsskr Nor Laegeforen 1991 Jun 10;111(15):1885-6 [Article in Norwegian]
Reichelt K.L., Knivsberg A.M., Lind G., Nodland M.: The probable etiology and possible treatment of childhood autism. Brain Dysfunct. 1991, 4: 308-319. [No abstract available]
Longoni R, Spina L, Mulas A, Carboni E, Garau L, Melchiorri P, Di Chiara G: (D-Ala2)deltorphin II: D1-dependent stereotypies and stimulation of dopamine release in the nucleus accumbens. J Neurosci 1991 Jun;11(6):1565-76.
Abstract:
Institute of Experimental Pharmacology and Toxicology, University of Cagliari , Italy .
In order to investigate the relative role of central delta- and mu-opioid receptors in behavior, the effects of (D-Ala2)deltorphin II, a natural delta-opioid peptide, and PL017, a beta-casomorphin derivative specific for mu receptors, were compared after local intracerebral and intraventricular administration. Intracerebral infusion of the two peptides was done bilaterally in the limbic nucleus accumbens and in the ventral and dorsal caudate putamen of freely moving rats through chronic intracerebral cannulas. After intra-accumbens infusion, the two peptides elicited marked but opposite behavioral effects: while (D-Ala2)deltorphin II evoked dose-dependent motor stimulation characterized by locomotion, sniffing, and oral stereotypies, PL017 elicited motor inhibition with rigidity and catalepsy. These effects were site specific because they could not be evoked from the ventral or from the dorsal caudate. Low doses of naloxone (0.1 mg/kg, s.c. ) blocked the effects of PL017 but not those of (D-Ala2)deltorphin II, which instead were reduced by high doses of naloxone (1.0 mg/kg) and by the putative delta-antagonist naltrindole; this drug failed to affect the catalepsy induced by PL017. Therefore, while (D-Ala2)deltorphin II effects were delta-mediated, PL017 effects were mu-mediated. Blockade of dopamine D1 receptors by SCH 23390 abolished (D-Ala2)deltorphin II effects, while blockade of dopamine D2 receptors by raclopride or by haloperidol was without effect. Local application by reverse dialysis of (D-Ala2)deltorphin II (5 microM) to the accumbens resulted in a naloxone-sensitive increase of extracellular dopamine concentrations; these effects could not be evoked from the caudate, nor by PL017 in the accumbens. Intracerebroventricular administration of (D-Ala2)deltorphin II or of PL017 elicited behavioral effects qualitatively similar to those obtained from the accumbens.
If deltorphin II is indeed present in the urine, this may explain why low doses of naloxone are often only moderately effective at reducing autistic behaviors.
Fukudome S.-I. and Yoshikawa M.: Opioid peptides derived from wheat gluten: Their isolation and characterization. FEBS Letters 1991, 296: 107-111.
Abstract:
Four opioid peptides were isolated from the enzymatic digest of wheat gluten. Their structures were Gly-Tyr-Tyr-Pro-Thr, Gly-Tyr-Tyr-Pro,Tyr-Gly-Gly-Trp-Leu and Tyr-Gly-Gly-Trp, which were named gluten exorphins A5, A4, B5 and B4, respectively. The gluten exorphin A5 sequence was found at 15 sites in the primary structure of the high molecular weight glutenin and was highly specific for delta-receptors. The structure-activity relationships of gluten exorphins A were unique in that the presence of Gly at their N-termini increased their activities. Gluten exorphin B5, which corresponds to [Trp4,Leu5]enkephalin, showed the most potent activity among these peptides. Its IC50 values were 0.05 microM and 0.017 microM, respectively, on the GPI and the MVD assays.
Shattock P. Kennedy A, Rowell F, Berney T: Role of neuropeptides in autism and their relationships with classical neurotransmitters. Brain Dysfunct 1990, 3: 328-346. [No abstract available]
Reichelt K.L., Ekrem J., Scott H.: Gluten, milk proteins and autism: Dietary interventions effects on behavior and peptide secretion. J Appl Nutrition 1990, 42: 1-11. [No abstract available]
Marchetti B, Scifo R, Batticane N, Scapagnini U: Immunological Significance of Opioid Peptide Dysfunction in Infantile Autism. Brain Dysfunction ,3: 346-354,1990. [No abstract available]
Leboyer M, Bouvard MP, Lensing P, Launay JM, Tabuteau F, Arnaud P, Waller D, Plumet MH, Recasens C, Kerdelhue B, Dugas M, Panksepp J: Opioid Excess Hypothesis of Autism. Brain Dysfunction 1990; 3: 285-298. [No abstract available]
Knivsberg A.M., Wiig K., Lind G., Nodland M., Reichelt K.L.: Dietary intervention in autistic syndromes. Brain Dysfunc. 1990, 3: 315-327. [No abstract available]
Cade R. et al.: The effects of dialysis and diet in schizophrenia. Psychiatry: A World perspective 1990, 3: 494-500. [No abstract available]
Barthelemy C, Bruneau N, Adrien J, Roux S, Lelord G:Clinical, Biological and Therapeutic Applications of the Functional Analysis of Autistic Disorders. Brain Dysfunction, 3: 271-284, 1990. [No abstract available]
Herrera-Marschitz M, Terenius L, Grehn L, Ungerstedt U: Rotational behaviour produced by intranigral injections of bovine and human beta-casomorphins in rats. Psychopharmacology (Berl) 1989;99(3):357-61.
Abstract:
Department of Pharmacology, Karolinska Institutet, Stockholm , Sweden .
The biological activity of beta-casein derived beta-casomorphin peptides was evaluated by injecting bovine beta-casomorphin-5 (Tyr-Pro-Phe-Pro-Gly), the homologous sequence in human beta-casein (Tyr-Pro-Phe-Val-Glu) and the corresponding N-terminal tetrapeptides into the left substantia nigra of rats. Their ability to produce rotational behaviour was compared to that produced by three reference compounds, morphine, D-ala2D-leu5 enkephalin and U50,488H, ligands for mu, delta and kappa types of opioid receptors, respectively. The relative potencies of beta-casomorphins and morphine were compared to those tested in two in vitro assays for opioid activity: (1) inhibition of the electrically induced contraction of the isolated myenteric plexus-longitudinal muscle of the guinea-pig ileum and (2) displacement of 3H-dihydromorphine binding to brain membranes. The same ranking order of potency was found in all three assays, the peptides from human beta-casein being about 10-fold less potent than those from bovine beta-casein. The effects of both morphine and bovine beta-casomorphin-5 in producing rotational behaviour were antagonized by naloxone; however, approximately 10-fold more naloxone was required to antagonize the beta-casomorphin-5 effect than that of morphine. The present data are discussed in the light of the recent observation that high concentrations of beta-casomorphin-like peptides are found in the cerebrospinal fluid and plasma of women with postpartum psychosis.
Ramabadran K, Bansinath M. Opioid peptides from milk as a possible cause of sudden infant death syndrome. Med Hypotheses 1988 Nov;27(3):181-7.
Abstract:
Department of Anesthesiology, New York University Medical Center , NY 10016 .
Milk from breast or baby formula is the exclusive source of nutrition for newborn infants. Short chain opioid peptides such as beta-casomorphins have been isolated from breast milk as well as baby formula. These biologically active peptides are absorbed from the gastrointestinal tract. In infants predisposed to respiratory apnea because of abnormal autonomic nervous system development and respiratory control mechanisms, opioid peptides derived from milk might be one of the etiological factors for sudden infant death syndrome and near miss sudden infant death syndrome.
Paroli E : Opioid Peptides from Food (the Exorphins). World Review of Nutrition and Dietetics 1988; 55: 58-97. [No abstract available]
Hole K. et al.: Attention deficit disorders: A study of peptide-containing urinary complexes. J Develop Behav Pediatrics 1988, 9: 205-212.
Abstract:
Department of Physiology, University of Bergen , Norway .
In several behavioral disorders, we have observed that abnormal amounts of peptides and protein-associated peptide complexes are excreted in the urine. The gel filtration patterns of these excreted substances have some specificity for the different disorders. The urinary excretion of peptide-containing complexes was studied in 91 boys and 13 girls (mean age 9.4 years, range 1-23) with the clinical diagnosis of attention deficit disorder (ADD), with or without hyperactivity. The gel filtration of urine precipitate showed patterns in all patients that were different from those seen in 36 normal controls. Sixty-four patients had increased benzoic acid-glycoprotein-peptide complexes in the late peaks. The symptoms of all these patients fit the criteria for diagnosis of attention deficit disorder with hyperactivity (ADDH). Thirty-five patients showed reduced amounts of uric acid complexes in the late peaks. Clinically, this group, with the exception of three patients, fit the criteria for diagnosis of attention deficit disorder without hyperactivity. Five patients showed reduced amounts of all urinary complexes; four of these were hyperactive. Moderate exercise in control children did not change the urinary pattern. One urinary peptide fraction from hyperactive patients, purified to homogeneity, increased the uptake of 14C[5-HT] in platelets. Strict clinical, neuropsychological, and psychophysiological selection of the patients reduced the heterogeneity of the patterns. Although more studies are needed, the findings seem promising for the possibility of developing biochemical tests that may be helpful diagnostically.
Dohan, FC: Genetic hypothesis of idiopathic schizophrenia : its exorphin connection. Schizophr. Bull. 1988 / 14 (4) / 489-494.
Abstract:
Medical College of Pennsylvania , Eastern Pennsylvania , Psychiatric Institute, Philadelphia 19129.
This brief overview proposes a testable oligogenic model of the inheritance of susceptibility to idiopathic schizophrenia: " abnormal" genes at each of a few complementary loci. The model is based on my assumptions as to the likely genetic abnormalities at possibly four or five interacting loci that would permit exorphins, the opioid peptides from some food proteins, especially glutens and possibly caseins, to go from gut to brain and cause symptoms of schizophrenia. Exorphins may reach the brain cerebrospinal fluid (CSF) in harmful amounts because of their genetically increased, receptor-mediated transcellular passage across the gut epithelial barrier plus decreased catabolism by genetically defective enzymes. A schizophrenia-specific, genetically enhanced affinity for exorphins by opioid receptors influencing dopaminergic and other neurons would permit sustained dysfunction at low CSF exorphin concentrations. Tests of each postulated genetic abnormality are suggested. This model is supported by a variety of evidence, including a significant effect of gluten or its absence on relapsed schizophrenic patients, the high correlation of changes in first admission rates for schizophrenia with changes in grain consumption rates, and the rarity of cases of schizophrenia where grains and milk are rare.
Sahley TL, Panksepp J: Brain opioids and autism: an updated analysis of possible linkages. J Autism Dev Disord 1987 Jun;17(2):201-16.
Abstract:
Considerable clinical evidence suggests that autistic children lack the normal ability or desire to engage others socially, as indicated by their poor social skills and inappropriate use of language for communicative purposes. Specifically, these children seem to lack normal amounts of social-emotional interest in other people, leading perhaps to a decreased initiative to communicate. This paper summarizes experimental evidence supporting a neurological theory, which posits that autism, at least partially, represents in the brain, such as brain opioids. These substances modulate social-emotional processes, and the possibility that blockade of opioid activity in the brain may be therapeutic for early childhood autism is discussed.
Kahn A, Rebuffat E, Blum D, Casimir G, Duchateau J, Mozin MJ, Jost R: Difficulty in initiating and maintaining sleep associated with cow's milk allergy in infants. Sleep 1987 Apr;10(2):116-21.
Abstract:
To confirm that sleeplessness in infants can be related to an undiagnosed allergy to cow's milk proteins, 71 infants were studied. Group I consisted of 20 infants referred for chronic insomnia that had appeared in the early days of life. Group II was made up of 31 infants admitted for skin or digestive symptoms attributed to cow's milk intolerance; 13 of these infants were shown to sleep as poorly as the infants of group I. Group III consisted of 20 infants with no history of sleep disturbance or milk allergy. The three groups of infants were comparable for sex and age. Laboratory tests revealed immunologic reactions to milk in all the infants in groups I and II. The sleep of the insomniac infants (group I, and the 13 " poor sleepers" in group II) became normal after cow's milk was eliminated from the diet. Insomnia reappeared when the infants in group I were challenged with milk. We conclude that infants with clinically evident milk allergy may suffer from sleeplessness and that when no evident cause for a chronic insomnia can be found in an infant the possibility of milk allergy should be given serious consideration.
Meisel, H: Chemical characterization and opioid activity of an exorphin isolated from in vivo digests of casein. FEBS Lett. 1986 / 196 (2) / 223-227.
Abstract:
The in vivo formation of an opioid peptide (exorphin) derived from beta-casein has been proved for the first time. It was isolated from duodenal chyme of minipigs after feeding with the milk protein casein. The exorphin has been identified as a beta-casein fragment by end-group determinations and qualitative amino acid analysis of the purified peptide. This peptide, named beta-casomorphin-11, displayed substantial opioid activity in an opiate receptor-binding assay.
Alpers DH: Uptake and fate of absorbed amino acids and peptides in the mammalian intestine. Federation Proc. 1986; 45:2261-2267.
Abstract:
Intraluminal and brush-border digestion of proteins results in a mixture of amino acids and small peptides. Thirteen brush-border peptidases have been described. Despite all of these enzymes, some peptides escape digestion and are absorbed intact. The assimilated products of protein digestion can follow multiple paths: absorption into the blood as amino acids or small peptides, metabolism within the enterocyte, incorporation into proteins of the enterocyte, and incorporation into proteins to be secreted into plasma. Unlike other tissues, the intestinal mucosa is not very responsive to metabolic regulation as regards amino acid uptake or regulation of protein synthesis. Most effects after dietary manipulation or drug or hormonal stimulation are modes (two-to fivefold increases). This constitutive metabolism of amino acids in the intestinal mucosa is consistent with its essential role in absorption. The mucosa also is a major contributor to apolipoproteins, which are probably the quantitatively most important proteins secreted from the intestine. Alterations in apoprotein secretion have been noted after fat feeding, and are both transcriptionally and translationally regulated. Although the fractional renewal rate of protein in the intestine is the highest of any tissue in the body, the quantitative importance of alterations in protein synthesis or secretion to the fate of intracellular amino acids is not known.
Svedberg, J.et al, Demonstration of beta-casomorphin immunoreactive materials in in vitro digests of bovine milk and in small intestine contents after bovine milk ingestion in adult humans. Peptides 1985 / 6 / pag.825-830.
Abstract:
Healthy young volunteers ingested one liter of cows' milk; then the contents of the small intestine were aspirated through an intestinal tube at various times and assayed for the presence of bovine beta-casomorphin immunoreactive materials. Considerable amounts of beta-casomorphin-7, but no beta-casomorphin-5 and only small amounts of beta-casomorphin-4 or -6 immunoreactive materials were found. Chromatographical characterization showed that most of the beta-casomorphin-7 immunoreactive material was not identical with beta-casomorphin-7, whereas the major part of the beta-casomorphin-4 or -6 immunoreactive materials might be identical with their corresponding beta-casomorphins. Analogous results were obtained for in vitro digestion of bovine milk which had been designed as a rough imitation of the gastrointestinal digestion process. A regulatory influence of beta-casomorphins as " food hormones" on intestinal functions is suggested.
Saelid G, et. al.: Peptide-Containing Fractions in Depression. Biol Psychiatry 1985, 20: 245-256.
Abstract:
A mixture of peptides and glycoproteins has been found in benzoic acid-precipitable material from urines of psychomotorically agitated and retarded endogenous depressive patients. This complex mixture of compounds is fractionated on a Sephadex G-25 gel, from which the different peaks are further separated on Biogel P2. The G-25 elution profiles ultraviolet absorbance, 280 nm) from depressive patients deviated from the normal pattern. The increase in hydrolyzable ninhydrin-colorable material of the P2 fractionation step encountered in psychotic depression was several-fold that of the normal population. Neurochemically active peptide-containing fractions were found. As explanation of these findings, it is probable that a genetically determined peptidase insufficiency is present, causing a peptide overflow when the secretion outstrips the breakdown. This model could easily combine more psychodynamic models with the genetic-biological models. The variability of the peptide patterns could possibly reflect the considerable clinical variability of the syndrome. Furthermore, the presence of a group of active compounds with different neuropharmacological activities might reflect the composite nature of the depressive syndrome.
Rix KJ, Ditchfield J, Freed DL, Goldberg DP, Hillier VF: Food antibodies in acute psychoses. Psychol Med 1985 May;15(2):347-54.
Abstract:
Antibodies to a variety of foods, and in particular cereals, were measured in serum from 100 patients with acute psychoses and 100 elective surgical patients. For 13 out of 14 foods to which non-IgE antibodies were detected the schizophrenics had slightly more antibodies than the controls. There was an association between a possible secondary mania and the presence of IgE antibodies to wheat or rye. However, neither the schizophrenia nor the mania findings can be regarded as evidence for food allergy causing psychiatric disorder, since the immunological findings in both cases may represent consequences of the illnesses or their treatment, rather than causes of the illness.
Chang, KJ, Su YF, Brent DA, Chang JK: Isolation of a specific mu-opiate receptor peptide, morphiceptin, from an enzymatic digest of milk proteins. J. Biol. Chem. 1985 / 260 (17) / pag. 9706-9712.
Abstract:
Specific radioimmunoassays have been developed for the measurement of naturally occurring morphiceptin and beta-casomorphin. These peptides and related exorphins were isolated from an enzymatic digest of caseins by chromatographic techniques including gel filtration, hydrophobic column and multiple-step high pressure liquid chromatography. Three exorphins were purified and characterized in their radioimmunological, biological, and chemical properties. They were identified as morphiceptin, beta-casomorphin, and 8-prolyl-beta-casomorphin. Since morphiceptin is a highly specific mu-agonist and can be derived from a milk protein, it is possible that morphiceptin is an exogenous opioid ligand specific for mu-receptors in the brain and gastrointestinal tract.
Takahashi M, Fukunaga H, Kaneto H, Fukudome S, Yoshikawa M: Behavioral and pharmacological studies on gluten exorphin A5, a newly isolated bioactive food protein fragment, in mice. Jpn J Pharmacol 2000 Nov;1984(3):259-65.
Abstract:
Department of Pharmacoinformatics, School of Pharmaceutical Sciences, Nagasaki University , Japan . takahashi@net.nagasaki-u.ac.jp
Central effects of gluten exorphin A5 (Gly-Tyr-Tyr-Pro-Thr), a fragment from wheat gluten, were studied on the pain-inhibitory system, emotionality and learning/memory processes in mice. Orally administered gluten exorphin A5 produced neither an antinociceptive effect nor an effect on morphine analgesia. Intracerebroventricularly (i.c.v.) administered gluten exorphin A5 produced mild but significant antinociception in a dose-depepndent manner, while not affecting the morphine analgesia. On the other hand, oral gluten exorphin A5 suppressed the endogenous pain-inhibitory system, i.e., antinociception induced by socio-psychological- (PSY-) stress (SIA) using a communication box; intraperitoneal gluten exorphin A5 abolished both footshock- (FS-) stress-induced antinociception (SIA) and PSY-SIA; and i.c.v. gluten exorphin A5 suppressed FS-SIA, but rather potentiated PSY-SIA. This peptide given by these routes was without effect on forced swim-SIA. In addition, oral gluten exorphin A5 tended to prolong the retention time on open arms in the elevated plus-maze test. Finally, oral gluten exorphin A5 when given during the post-training period of learning/memory processes significantly increased the latency into the dark compartment in the one-trail step-though type passive avoidance test, indicating that the peptide also facilitates the acquire/consolidation process of learning/memory. Thus, gluten exorphin A5 has been found to produce various effects not only in the peripheral nervous systems but also in the central nervous system.
Pfeiffer CC: Schizophrenia and wheat gluten enteropathy. Biol Psychiatry 1984 Mar;19(3):279-80. [No abstract available]
Lindstrom LH, Nyberg F, Terenius L, Bauer K, Besev G, Gunne LM, Lyrenas S, Willdeck-Lund G, Lindberg B: (1984) CSF and plasma beta-casomorphin-like opioid peptides in post-partum psychosis. Amer. J. Psychiat. 1984, 141: 1059-1066.
Abstract:
The authors measured opioid receptor-active components in the CSF of 11 women with postpartum psychosis, 11 healthy lactating women, and 16 healthy women who were not lactating. Activity that eluted with 0.2 M acetic acid 0.7-0.9 times the total volume of the column (fraction II activity) was significantly higher in the CSF of both healthy and psychotic women in the puerperium than in that of the lactating women. Very high levels of fraction II activity were seen in four psychotic patients. Material from these patients was further characterized by electrophoresis and high-performance liquid chromatography: The material migrated as bovine beta-casomorphin. Receptor-active material with the same characteristics was also found in the plasma of these four patients. The authors conclude that certain cases of postpartum psychosis are associated with the occurrence in plasma and CSF of unique opioid peptides probably related to bovine beta-casomorphin.
Huebner FR, Lieberman KW, Rubino RP, Wall JS: Demonstration of high opioid-like activity in isolated peptides from wheat gluten hydrolysates. Peptides 1984 Nov-Dec;5(6):1139-47.
Abstract:
Because of a possible relationship between schizophrenia and celiac disease, a condition in some individuals who are sensitive to wheat gluten proteins in the diet, there has been interest in observations that peptides derived from wheat gluten proteins exhibit opioid-like activity in in vitro tests. To determine the origin of the peptides exhibiting opioid activity, wheat proteins were fractionated by size (gel filtration), by charge differences (ion exchange chromatography) and by differences in hydrophobicity (reversed-phase HPLC). These fractions were hydrolyzed by pepsin or pepsin and trypsin and the resulting peptides separated by gel filtration chromatography. The separated peptides were tested for opioid-like activity by competitive binding to opioid receptor sites in rat brain tissue in the presence of tritium-labeled dihydromorphine. The peptides showed considerable differences in activity; while some peptides exhibited no activity, 0.5 mg of the most active peptides were equivalent to 1 nM of morphine in the binding assay. The most active peptides were derived from the gliadin fraction of the gluten complex.
Dohan et. al. " Is Schizophrenia Rare if Grain is Rare?" Biol Psychiat 1984; 19(3): 385-399.
Abstract:
If, as hypothesized, neuroactive peptides from grain glutens are the major agents evoking schizophrenia in those with the genotype(s), it should be rare if grain is rare. To test this, we analyzed the results of our clinical examinations (e.g., kuru) and observations of anthropologists on peoples consuming little or no grain. Only two overtly insane chronic schizophrenics were found among over 65,000 examined or closely observed adults in remote regions of Papua New Guinea (PNG, 1950-1967) and Malaita , Solomon Islands (1980-1981), and on Yap , Micronesia (1947-1948). In preneuroleptic Europe over 130 would have been expected. When these peoples became partially westernized and consumed wheat, barley beer, and rice, the prevalence reached European levels. Our findings agree with previous epidemiologic and experimental results indicating that grain glutens are harmful to schizophrenics.
Loukas, S. et al, Opioid activities and structures of alpha-casein-derived exorphins. Biochemistry 1983 / 22 (19) / 4567-4573.
Gardner MLG: Evidence for, and implications of, passage of intact peptides across the intestinal mucosa. Biochemical Society Transactions 1983; 11: 810-812. [no abstract available]
Morley, J.E., Food peptides. A new class of hormones ? J. Am. Med. Assoc. 1982 / 247 (17) / 2379-2380. [No abstract available]
Reichelt KL, Hole K, Hamberger A, Saelid G, Edminson PD, Braestrup CB, Lingjaerde O, Ledaal P, Orbeck H: Biologically active peptide-containing fractions in schizophrenia and childhood autism. Adv Biochem Psychopharmacol 1981; 28: 627-643.
Abstract:
It is well documented that peptides have a major role in the effective functioning of higher animals at all levels from enzyme stabilization to homeostatic mechanisms governing essential functions such as eating, sexual behavior, and temperature regulation. The effects of exogenously administered peptides on neurotransmitter release, uptake, metabolism and behavioral consequences are also well established. We have attempted to extend these findings by postulating peptidergic neurons as transducers of multisignal inputs, and that development of pathological states may be due to genetically-determined reduced levels of activity of key peptidases, leading to excretion of regulatory peptides into the circulation. We have been able to demonstrate that, in schizophrenia and autism (in well defined clinical cases), the patterns of peptides and associated proteins from urinary samples differ considerably from each other and from normal controls. In addition to this, further purification of the material obtained has led to the discovery of a number of factors capable of modulating the function of major neurotransmitters. Some of these are in the final stages of characterization as peptides, while the remainder are also probably peptides, as purification has been followed by both biological testing and chemical analysis for peptidic material. We have outlined a number of parameters which we consider relevant in any attempt to put psychiatric disorders on a biological foundation. Any new advances in the neurochemical understanding of such disorders must take into consideration the observations of several different disciplines including genetics and psychology. However, at this stage of research it is far too early to speculate on the relevance of the various biological activities to the etiology and symptomatology of schizophrenia and childhood autism.
Trygstad OE, et al: Patterns of peptides and protein-associated-peptide complexes in psychiatric disorders. Br J Psychiatry 1980 Jan;136:59-72.
Abstract:
Peptidic neurones may be considered as multisignal intergrators and transducers. When formation or release of peptide outstrips genetically determined breakdown capacity, overflow of peptides to the body fluids and urine may be expected. In this paper, pathological urinary chromatographic patterns of peptides are shown for genetic, functional and mixed disorders. Part symptoms of the disorders may be induced with the biologically isolated and purified peptides as well as with chemically synthesized peptides.
Ross-Smith, P, Jenner FA: Diet (gluten) and Schizophrenia. J. Hum. Nutr. 1980 / 34 (2) / 107-112.
Four aspects of clinical evidence for an association between gluten and schizophrenia are examined. The scientific evidence for the role of gluten is set out. Finally, reference is made to other dietary approaches.
Zioudrou C, Streaty RA , Klee WA : Opioid peptides derived from food proteins. The exorphins. J. Biol. Chem.1979 / 254 (7) / 2446-2449.
Abstract:
Peptides with opioid activity are found in pepsin hydrolysates of wheat gluten and alpha-casein. The opioid activity of these peptides was demonstrated by use of the following bioassays: 1) naloxone-reversible inhibition of adenylate cyclase in homogenates of neuroblastoma X-glioma hybrid cells; 2) naloxone-reversible inhibition of electrically stimulated contractions of the mouse vas deferens; 3) displacement of [3H]dihydromorphine and [3H-Tyr, dAla2]met-enkephalin amide from rat brain membranes. Substances which stimulate adenylate cyclase and increase the contractions of the mouse vas deferens but do not bind to opiate receptors are also isolated from gluten hydrolysates. It is suggested that peptides derived from some food proteins may be of physiological importance.
Panksepp J: A neurochemical theory of autism. Point of View, North-Holland Biomedical Press, Jul 1979.
Hole K, Bergslien AA, Jørgensen H, Berge O-G, Reichelt KL & Trygstad OE.(1979) A peptide containing fraction from schizophrenia which stimulates opiate receptors and inhibits dopamine uptake. Neuroscience, 4, 1139-1147. [No abstract available]
Dohan: Schizophrenia and neuroactive peptides from food. Lancet 1979 May 12;1(8124):1031. [No abstract available]
Brantl V, Teschemacher H: Naunyn Schmiedebergs Arch Pharmacol 1979 Apr 30;306(3):301-4. A material with opioid activity in bovine milk and milk products.
Abstract:
Chloroform-methanol extracts of lyophilized milk, of commercially available dried milk or baby food and of casein digests were tested for opioid activity on the guinea-pig ileum longitudinal muscle-myenteric plexus preparation. Compounds with opioid activity--which proved to be resistant to peptidases--were detected in certain batches of baby food, casein digest, and cow milk in considerably varying amounts.
Ashkenazi et. al. " Immunologic reaction of psychotic patients to fractions of gluten" Am J Psychiat 1979; 136: 1306-1309.
Abstract:
Production of a leukocyte migration inhibition factor by peripheral blood lymphocytes in response to challenge with gluten fractions was studied in hospitalized patients with schizophrenia and other psychoses compared with normal individuals and with children and adolescents with celiac disease. The schizophrenic and other psychotic patients could be subdivided into two groups, one that responded in the leukocyte migration inhibition factor test as the celiac patients did and one that responded as the normal control subjects did. The psychotic and schizophrenic patients did not show any evidence of malabsorption. The authors speculate that gluten may be involved in biological processes in the brain in certain psychotic individuals.
O'Banion D, Armstrong B, Cummings RA, Stange J.: Disruptive behavior: a dietary approach. J Autism Child Schizophr 1978 Sep;8(3):325-37.
Abstract: The effect of particular foods on levels of hyperactivity, uncontrolled laughter, and disruptive behaviors was studied in an 8-year-old autistic boy. The floor of the child's room was taped off into six equal-sized rectangles to measure general activity level. Frequency data were recorded on screaming, biting, scratching, and object throwing. A time-sample technique was used to record data on laughing. Data were gathered during four phases. During an initial 4-day period the child was fed a normal American diet. A 6-day fasting period followed, during which time only spring water was allowed. The third phase lasted 18 days and involved the presentation of individual foods. During the final phase of the study the child was given only foods that had not provoked a reaction in the third phase. Results showed that foods such as wheat, corn, tomatoes, sugar, mushrooms, and dairy products were instrumental in producing behavioral disorders with this child.
Singh MM, Kay SR: Wheat gluten as a pathogenic factor in schizophrenia. Science 1976 Jan 30;191(4225):401-2.
Abstract:
Schizophrenics maintained on a cereal grain-free and milk-free diet and receiving optimal treatment with neuropleptics showed an interruption or reversal of their therapeutic progress during a period of " blind" wheat gluten challenge. The exacerbation of the disease process was not due to variations in neuroleptic doses. After termination of the gluten challenge, the course of improvement was reinstated. The observed effects seemed to be due to a primary schizophrenia-promoting effect of wheat gluten.
Dohan FC, Grasberger JC: Relapsed schizophrenics: earlier discharge from the hospital after cereal-free, milk-free diet. Am J Psychiatry. 1973 Jun;130(6):685-8. [No abstract available]
Goodwin MS, Cowen MA, Goodwin TC: Malabsorption and cerebral dysfunction: a multivariate and comparative study of autistic children. J Autism Child Schizophr 1971 Jan-Mar;1(1):48-62. [No abstract available]
Dohan " Is celiac disease a clue to pathogenesis of schizophrenia?" Mental Hyg 1969; 53: 525-529. [No abstract available]
Dohan FC: Wheat " consumption" and hospital admissions for schizophrenia during World War II. A preliminary report. Am J Clin Nutr. 1966 Jan;18(1):7-10. [No abstract available]
Cooke WT, Smith WT: Neurological disorders associated with adult celiac disease. Brain 1966, 89: 683-722. [No abstract available]
Dohan FC: Cereals and schizophrenia: data and hypothesis. Acta Psychiat Scand 1966; 42: 125-152. [No abstract available]
Studies regarding gastrointestinal abnormalities in autism
Studies regarding immune system dysfunction in autism
Perhaps these parents like me have read the abstracts below.
Journal articles regarding autism food allergy gastrointestinal abnormalities gluten dairy and the effects of the opiate properties of milk and wheat-derived peptides on neurological function
http://www.autismndi.com/studies.htm
Summary: Based on reports from caregivers, case studies and observation of patients with schizophrenia and children with severe behavioral disorders, Dr. FC Dohan hypothesized in 1960s and 70s that gluten and dairy seemed to worsen these behaviors, and that in many cases, a restricted diet could lead to significant improvement or recovery from these disorders. The biochemical explanation for this phenomenon remained unclear, however, several other studies seemed to bear out this observation, and in 1981, using more advanced laboratory technology, Dr. Karl Reichelt, Director of Clinical Chemistry for the Department of Pediatric Research at the Rikshospitalet (National Hospital) in Oslo, Norway, found and reported abnormal peptides in the urine of schizophrenics and autistics. Peptides are pieces of proteins that are not completely broken down into individual amino acids. Dr. Reichelt has observed that these peptides, which are 4 or 5 or 6 amino acids long, have sequences that match those of opioid peptides (casomorphin and gliadomorphin). The known dietary sources of these opiate peptides are casein (from milk) and gliadin or gluten (from cereal grains). He has since conducted several studies examining this finding, as have several other researchers, including Paul Shattock at the University of Sunderland in England, Dr. Robert Cade at the University of Florida, Gainesville, and Dr. Alan Friedman, of Johnson and Johnson Ortho Clinical Diagnostics. The best evidence for this correlation lies in the thousands of case reports of improvement or recovery of children with autism on this diet. However, responsible physicians who have taken the time to review these studies must agree that there is, indeed, significant scientific evidence to support a trial period of careful elimination of these proteins from the diet of children on the autistic spectrum.
.
Whiteley P, Shattock P: Biochemical aspects in autism spectrum disorders: updating the opioid-excess theory and presenting new opportunities for biomedical intervention. Expert Opin Ther Targets. 2002 Apr;6(2):175-83.
Abstract:
Autism Research Unit, School of Sciences (Health), University of Sunderland , Sunderland , SR2 7EE , UK . aru@sunderland.ac.uk
Autism is a lifelong condition usually described as affecting social, cognitive and imaginative abilities. For many years, parents and some professionals have observed that in concordance with the behavioural and psychological symptoms of the condition, there are a number of physiological and biochemical correlates which may also be of relevance to the syndrome. One area of interest that encompasses many of these observations is the opioid-excess theory of autism. The main premise of this theory is that autism is the result of a metabolic disorder. Peptides with opioid activity derived from dietary sources, in particular foods that contain gluten and casein, pass through an abnormally permeable intestinal membrane and enter the central nervous system (CNS) to exert an effect on neurotransmission, as well as producing other physiologically-based symptoms. Numerous parents and professionals worldwide have found that removal of these exogenously derived compounds through exclusion diets can produce some amelioration in autistic and related behaviours. There is a surprisingly long history of research accompanying these ideas. The aim of this paper is to review the accompanying evidence in support of this theory and present new directions of intervention as a result of it.
Vojdani A, Campbell AW, Anyanwu E, Kashanian A, Bock K, Vojdani E: Antibodies to neuron-specific antigens in children with autism: possible cross-reaction with encephalitogenic proteins from milk, Chlamydia pneumoniae and Streptococcus group A. J Neuroimmunol 2002 Aug;129(1-2):168-77.
Abstract:
Section of Neuroimmunology, Immunosciences Laboratory, Inc., 8693 Wilshire Boulevard, Suite 200 , Beverly Hills , CA 90211 , USA . immunsci@ix.netcom.com
We measured autoantibodies against nine different neuron-specific antigens and three cross-reactive peptides in the sera of autistic subjects and healthy controls by means of enzyme-linked immunosorbent assay (ELISA) testing. The antigens were myelin basic protein (MBP), myelin-associated glycoprotein (MAG), ganglioside (GM1), sulfatide (SULF), chondroitin sulfate (CONSO4), myelin oligodendrocyte glycoprotein (MOG), alpha,beta-crystallin (alpha,beta-CRYS), neurofilament proteins (NAFP), tubulin and three cross-reactive peptides, Chlamydia pneumoniae (CPP), streptococcal M protein (STM6P) and milk butyrophilin (BTN). Autistic children showed the highest levels of IgG, IgM and IgA antibodies against all neurologic antigens as well as the three cross-reactive peptides. These antibodies are specific because immune absorption demonstrated that only neuron-specific antigens or their cross-reactive epitopes could significantly reduce antibody levels. These antibodies may have been synthesized as a result of an alteration in the blood-brain barrier. This barrier promotes access of preexisting T-cells and central nervous system antigens to immunocompetent cells, which may start a vicious cycle. These results suggest a mechanism by which bacterial infections and milk antigens may modulate