"It is very possible that PATERNAL AGE is the major predictor of(non-familial) autism." Harry Fisch, M.D., author "The Male Biological Clock". Sperm DNA mutates and autism, schizophrenia bipolar etc. results. What is the connection with autoimmune disorders? Having Type 1 diabetes, SLE,etc. in the family, also if mother had older father. NW Cryobank will not accept a sperm donor past 35th BD to minimize genetic abnormalities.VACCINATIONS also cause autism.

Monday, March 31, 2008

People with schizophrenia may have the disease because they are unlucky enough to end up with an extremely rare combination of genes,

Rare gene
defects might add up to schizophrenia
18:03 27 March 2008 news service
Ewen Callaway

Related Articles
Schizophrenia dooms victims to repeat mistakes
22 January 2008
Childhood brain infections risk of schizophrenia
21 July 2007
Brain growth link to schizophrenia
12 August 2006
Search New Scientist

Contact us
Web Links
Jack McClellan, University of Washington
Daniel Weinberger, National Institute of Mental Health
Schizophrenia, Royal College of Physiatrists
People with schizophrenia may have the disease because they are unlucky enough to end up with an extremely rare combination of genes, according to a genetic study of the devastating illness.

The comparison of schizophrenics and healthy people reveals that the former are far likelier to possess extremely rare gene mutations. It is these mutations, the researchers hypothesise, that underlie many cases of schizophrenia.

About 1% of people suffer from the disease, which typically hits people in their twenties.

"It may well be that some substantial portion of cases comes by rare events – each one is unique. If you collectively add them together, it can explain a large percentage of the disorder," says Jack McClellan, a psychiatrist at the University of Washington in Seattle, who led the study.

Many of the schizophrenia-linked mutations occurred in genes linked to brain development. These might provide the best targets for drug therapies to aim at, he says.

Genetic glitches
Like most mental illnesses, no single genetic mutation sparks schizophrenia, but studies of families hint that genes play a large part. For instance, if one identical twin has the disease, the other has about a 50/50 chance of also developing schizophrenia.

Most researchers think that schizophrenia is caused by lots of gene mutations that are relatively common among humans. By itself, a single mutation plays a bit part in the disease. Together, many of these mutations add up to schizophrenia.

As an alternative explanation, McClellan's team tested whether extremely rare mutations might cause the illness. His team looked at genetic changes called duplications and deletions, where large swaths of DNA are either missing or repeated in the genome of a single person or family.

Among the 150 schizophrenics and 268 healthy people McClellan's team studied, schizophrenics were three times likelier than healthy people to have such genetic glitches.

Five percent of healthy people had very rare deletions or duplications in their DNA, while 15% of schizophrenia patients had such mutations. The difference was even more striking among a second group of patients, who developed schizophrenia as children – a full 20% possessed rare gene deletions or duplications.

'Crossword puzzle'
Many of the mutations occurred in genes linked to brain development, a likely culprit for the disease. "A lot of them help regulate how neurons get from point A to point B over time," McClellan says.

Individual mutations might contribute to schizophrenia and other mental illness, but proving a cause-effect relationship in a single patient is nearly impossible, says Daniel Weinberger, a schizophrenia expert at the National Institute of Mental Health in Bethesda, Maryland.

"Changes in the genome found in only a single individual, are difficult to establish as pathogenic factors," he says.

However, Ben Packard, a geneticist at the University of Edinburgh, says the study agrees with recent findings that rare gene deletions and duplications might cause autism.

Homing in on such mutations in schizophrenia patients should offer quick insights into more general causes of the disease, McClellan says. The mutations could hit many of the same genes, he says. "It's like solving a crossword puzzle. You have to get one letter first."

Journal reference: Science (DOI: 10.1126/science.1155174


Should Every Infant Be Screened For A Mitochondrial Disorder Before Any Vaccination is Given

Adventures in Autism: Julie Gerberding Admits on CNN that Vaccines can Trigger Autism#links#links


I Disagree, Non-Familial Autism is Expected to Rise When Men Father at 34 and Above, also with Mitochondrial Disorders

updated 11:14 a.m. EDT, Mon March 31, 2008Feedback

Autism's mysteries remain as numbers grow

By Val Willingham

ELLICOTT CITY, Maryland (CNN) -- It remains one of the greatest mysteries of medicine. Although autism will be diagnosed in more than 25,000 U.S. children this year, more than new pediatric cases of AIDS, diabetes and cancer combined, scientists and doctors still know very little about the neurological disorder.

Until they were 18 months old, the Gaston triplets seemed like normal, healthy babies.

Unlike childhood diabetes or pediatric leukemia

Labels: ,

Sunday, March 30, 2008

End Childbearing By the Man's 34th Birthday And You Will Prevent Much Paternal Age Autism

By Andrea Anderson
a GenomeWeb staff reporter

NEW YORK (GenomeWeb News) – Individuals with schizophrenia are more likely to carry rare genetic variants than unaffected individuals — particularly in genes involved in brain development and function, new research indicates.

Research led by teams at the University of Washington, Cold Spring Harbor Laboratory, and the National Institute of Mental Health compared the rate of genetic duplications and deletions in schizophrenic and non-schizophrenic individuals. What they found flies in the face of the once accepted “common disease-common allele” model for schizophrenia. Instead the results, published online today in Science Express, hint that many mutations in many genes could contribute to schizophrenia.

“From that perspective, if nothing else, I’m sure we’ll get some discussion going,” co-lead author Jon McClellan, a child and adolescent psychiatrist at the University of Washington, told GenomeWeb Daily News.

About one percent of the population has schizophrenia, a psychiatric condition characterized by hallucinations, delusions, and disordered thinking that usually manifests itself in during late adolescence or early adulthood. Although environmental factors influence it, there is strong evidence that complex genetics contribute to schizophrenia.

As with many common diseases, researchers once viewed schizophrenia as a condition that was caused by a set of shared mutations: the common disease-common allele idea. But recent research suggests that there may be hundreds or even thousands of different mutations that cause this and other complex genetic diseases, McClellan explained.

Similarly, work published in Science last year — by many of the same investigators involved in this study — indicated that autism spectrum disorders are often associated with a variety of new deletions and duplications.

For the latest paper, the team compared genomic DNA from 150 schizophrenic adults with 268 ancestry-matched controls, looking for structural variants larger than 100 kilobases using ROMA 85K probe microarrays. They then validated and refined these results using Illumina 550K microarrays and NimbleGen 2.1M-feature HD2 microarrays.

Though there were not differences in the rate of common mutations, rare or novel mutations were more than three times as common in those with schizophrenia than in non-schizophrenic subjects. Roughly 15 percent of schizophrenic adults had duplications or deletions, compared to about five percent of control individuals. Among those who developed schizophrenia when they were 18-years-old or younger, that number was even higher — up to 20 percent.

In an independent experiment, NIMH researchers compared those with childhood onset schizophrenia — diagnosed before 12 years of age — with their parents. Using genome-wide scans done with Affymetrix 500K SNP Arrays, Agilent 185K or 244K ArrayCGH, and custom BAC arrays, they found that 28 percent of individuals with childhood onset schizophrenia had rare mutations, compared to 13 percent of controls. Most of these appear to have been inherited from unaffected parents.

“If severe mutations leading to schizophrenia are individually rare, then each individual mutation will explain only a small number of patients, or even only one patient,” the authors wrote. “Virtually every rare structural mutation detected in our original series was different.”

This suggests that researchers need to focus on genes within commonly affected pathways rather than on specific alleles, McClellan said.

Intriguingly, many of the mutations detected in both arms of the study affected genes involved in neurobiological pathways — particularly those involved in brain development and communication. Others were in genes previously linked to schizophrenia or autism.

Still, it’s too early to say which of genes, if any, are involved in schizophrenia. To get to the bottom of that, McClellan suggested, the best bet is selecting a suspect gene and sequencing it in a group of schizophrenic individuals to see if they also have distinct mutations in that gene. “If you find lots of other mutations in that gene then it suddenly gets a lot more interesting,” he said.

Not everyone is optimistic about the way schizophrenia genetics are shaking out. Some clinicians are discouraged by the idea that so many unique mutations might be behind one condition, McClellan said: “Sometimes this demoralizes people.” But complex genetics don’t necessarily mean it will be more difficult to develop new therapeutics, he added, especially if researchers start to piece together affected genetic pathways.


Objective To examine the relationship between advancing paternal age at birth of offspring and their risk of autism spectrum

Vol. 63 No. 9, September 2006 Archives

Advancing Paternal Age and Autism
Abraham Reichenberg, PhD; Raz Gross, MD, MPH; Mark Weiser, MD; Michealine Bresnahan, PhD; Jeremy Silverman, PhD; Susan Harlap, MBBS; Jonathan Rabinowitz, PhD; Cory Shulman, PhD; Dolores Malaspina, MD; Gad Lubin, MD; Haim Y. Knobler, MD; Michael Davidson, MD; Ezra Susser, MD, DrPH

Arch Gen Psychiatry. 2006;63:1026-1032.

Context Maternal and paternal ages are associated with neurodevelopmental disorders.

Objective To examine the relationship between advancing paternal age at birth of offspring and their risk of autism spectrum disorder (ASD).

Design Historical population-based cohort study.

Setting Identification of ASD cases from the Israeli draft board medical registry.

Participants We conducted a study of Jewish persons born in Israel during 6 consecutive years. Virtually all men and about three quarters of women in this cohort underwent draft board assessment at age 17 years. Paternal age at birth was obtained for most of the cohort; maternal age was obtained for a smaller subset. We used the smaller subset (n = 132 271) with data on both paternal and maternal age for the primary analysis and the larger subset (n = 318 506) with data on paternal but not maternal age for sensitivity analyses.

Main Outcome Measures Information on persons coded as having International Classification of Diseases, 10th Revision ASD was obtained from the registry. The registry identified 110 cases of ASD (incidence, 8.3 cases per 10 000 persons), mainly autism, in the smaller subset with complete parental age data.

Results There was a significant monotonic association between advancing paternal age and risk of ASD. Offspring of men 40 years or older were 5.75 times (95% confidence interval, 2.65-12.46; P<.001) more likely to have ASD compared with offspring of men younger than 30 years, after controlling for year of birth, socioeconomic status, and maternal age. Advancing maternal age showed no association with ASD after adjusting for paternal age. Sensitivity analyses indicated that these findings were not the result of bias due to missing data on maternal age.

Conclusions Advanced paternal age was associated with increased risk of ASD. Possible biological mechanisms include de novo mutations associated with advancing age or alterations in genetic imprinting.

Author Affiliations: Department of Psychiatry (Drs Reichenberg, Silverman, and Davidson) and Seaver Center for Autism Research (Dr Silverman), Mount Sinai School of Medicine; Department of Epidemiology, Mailman School of Public Health, Columbia University (Drs Gross, Bresnahan, Harlap, Malaspina, and Susser); New York State Psychiatric Institute (Drs Gross, Bresnahan, Malaspina, and Susser), New York; Institute of Psychiatry, King's College, London, England (Dr Reichenberg); and Department of Psychiatry, Chaim Sheba Medical Center, Tel Hashomer (Drs Weiser and Davidson); School of Social Work, Bar Ilan University, Ramat-Gan (Dr Rabinowitz); School of Social Work, Hebrew University, Jerusalem (Dr Shulman); and Medical Corps, Israel Defense Forces, Tel Aviv (Drs Lubin and Knobler), Israel.


This Month in Archives of General Psychiatry
Arch Gen Psychiatry. 2006;63(9):954.


Is Schizophrenia a Syndrome of Accelerated Aging?
Kirkpatrick et al.
Schizophr Bull 2007;0:sbm140v1-sbm140.

Matched follow-up study of 5 8-year-old ICSI singletons: child behaviour, parenting stress and child (health-related) quality of life
Knoester et al.
Hum Reprod 2007;22:3098-3107.

Aberrant Epigenetic Regulation Could Explain the Relationship of Paternal Age to Schizophrenia
Perrin et al.
Schizophr Bull 2007;33:1270-1273.

Identification and Evaluation of Children With Autism Spectrum Disorders
Johnson et al.
Pediatrics 2007;120:1183-1215.

A unified genetic theory for sporadic and inherited autism
Zhao et al.
Proc. Natl. Acad. Sci. USA 2007;104:12831-12836.

Prenatal and Perinatal Risk Factors for Autism: A Review and Integration of Findings
Kolevzon et al.
Arch Pediatr Adolesc Med 2007;161:326-333.

Maternal and Paternal Age and Risk of Autism Spectrum Disorders
Croen et al.
Arch Pediatr Adolesc Med 2007;161:334-340.

Medical Implications of the Male Biological Clock.
Lewis et al.
JAMA 2006;296:2369-2371.

Improving Men's Health: Evidence and Opportunity.
Fontanarosa and Cole
JAMA 2006;296:2373-2375.

The neuropathology, medical management and dental implications of autism.
Friedlander et al.
Journal of the American Dental Association 2006;137:1517-1527.

Is Autism Associated with Advanced Parental Age?
JWatch Pediatrics 2006;2006:2-2.


Father's Age and Autism Risk Paper EBD Blog

Here is the last paragraph of Feldman's paper:

What might be the mechanism that produces higher rates of disorders among children of older fathers? The DNA in a 20 year-old male has been copied approximately100 times but in a 50 year-old father it has been copied over 800 times. Singh and colleagues (2003) studied differences in the sperm of older and younger men. Men over age 35 have sperm with lower motility and more highly damaged DNA in the form of double-strand breaks. The older group also had fewer apoptotic cells, an important discovery. (Apoptosis is form of cell death that protects the parent organism from problems or that permits differentiation, as in resorption of a tadpole’s tail.) A really key factor that differentiates sperm from other cells in the body is that they do not repair their DNA damage, as most other cells do. As a result, the only way to avoid passing DNA damage to a child is for the damaged cells to undergo apoptosis, a process that the study indicates declines with age. Singh is quoted in Science Blog (Sullivan, 2002) as explaining that, “In older men, the sperm are accumulating more damage, and those severely damaged sperm are not being eliminated.”


Elephant Paints a Self Portrait




Adventures in Autism: Ken Stoller Files Complaint Against Anne Schuchat



"Paternal age is consistently associated with increased risk of schizophrenia (Brown et al, 2002; Dalman & Allebeck, 2002; Malaspina et al, 2002; Byrne et al, 2003; El-Saadi et al, 2004; Sipos et al, 2004; Tsuchiya et al, 2005). Paternal age is also associated with increased rates of several types of de novo germ-line mutations (Crow, 2003)."

Br J Psychiatry. 2007 Mar ;190 :194-9 17329737 (P,S,E,B,D) Schizophrenia: a common disease caused by multiple rare alleles.

[My paper] Jon M McClellan, Ezra Susser, Mary-Claire King
Department of Psychiatry, Box 356560, University of Washington, Seattle, WA 98195, USA.
Schizophrenia is widely held to stem from the combined effects of multiple common polymorphisms, each with a small impact on disease risk. We suggest an alternative view: that schizophrenia is highly heterogeneous genetically and that many predisposing mutations are highly penetrant and individually rare, even specific to single cases or families. This ;common disease - rare alleles' hypothesis is supported by recent findings in human genomics and by allelic and locus heterogeneity for other complex traits. We review the implications of this model for gene discovery research in schizophrenia.


Saturday, March 29, 2008


"Take away schizophrenia's hallucinations and delusions," said Jon McClellan, a child psychiatrist at the University of Washington and a leader of the study, published in yesterday's online issue of the journal Science, "and the symptoms that remain, the lack of social interest and withdrawal, are what we call autism. There is clearly an intersection of the brain systems involved." ..........


What Did Julie Gerberding Say About Vaccines and Autism?

Adventures in Autism: Wait! Did Julie Gerberding Just Admit that Vaccines Trigger Autism!?


Fluoride is a Poison It Should Not Be Added to the Water Supply

fluoride a poison


Ginger "Adventures in Autism" Has the Best Blog on Non Paternal Age Autism

Adventures in Autism: More on Mitochondrical Disorders from the Clevland Clinic#links


Did You Ever Notice the Paternal Age Effect in Non-Familial Non-Vaccine Induced Autism?

Thursday, February 28, 2008
an affected first-born is seen most dramatically in the group of AGRE fathers who are 30–39 years

The paternal age distribution of the AGRE fathers, whose first child is autistic differs significantly from that of the 'control' sample (P=0.005). A 2 goodness-of-fit test with 2 degrees of freedom was conducted using percents in the 'control' group age categories to calculate the expected values in the AGRE sample. The shift toward higher paternal ages in those with an affected first-born is seen most dramatically in the group of AGRE fathers who are 30–39 years inclusive, which is 54.7% of the distribution compared with the 41.9 % that is expected. We interpret this shifted age distribution to provide support for the recently reported finding by Reichenberg and co-workers that autism risk is associated with advancing paternal age.

1: Mol Psychiatry. 2007 May;12(5):419-21. Links
Paternal age and autism are associated in a family-based sample.Cantor RM, Yoon JL, Furr J, Lajonchere CM.
PMID: 17453057 [PubMed - indexed for MEDLINE]


A Letter From Dan Burton to the Special Masters at Vaccine Court

Labels: ,

Friday, March 28, 2008




NIXA, Mo., March 28 /PRNewswire-USNewswire/ -- Parents of children who
regressed into autism after receiving vaccines are expressing cautious
optimism that government health officials may at last be catching on to the
link between vaccines and autism.

An article published on Huffington Post by investigative journalist
David Kirby reported details of a conference call held earlier in March,
bringing together federal vaccine safety officials to discuss concerns
surrounding mitochondrial dysfunction, autism and vaccines.

The call came on the heels of a concession by the federal government
that vaccines lead to regressive autism in nine-year-old Hannah Poling of
Atlanta. The ruling is raising many questions, especially in the area of
mitochondrial dysfunction, which the government conceded was exacerbated by
Hannah's vaccines.

In the article, Kirby stated, "The hot topic of the day was
mitochondria - the little powerhouses within each cell that convert food
and oxygen into energy." And that, "Some researchers on the call reported
that mitochondrial dysfunction is probably much more common than the
current estimate of 1-in-4,000 people, making the potential implications
for autism staggering."

Of utmost significance are the following points:

-- Up to 1 in 50 children (2%) may be at risk for mitochondrial

-- Thimerosal, mercury, aluminum, pollution, pesticides, medicines and
prenatal alcohol exposure have all been shown to damage mitochondria.

-- Up to 20% of all children with autism may have underlying
mitochondrial dysfunction.

-- The CDC is aware of this situation and is immediately taking
measures to address the current national vaccine schedule.

-- The genetic susceptibility for mitochondrial dysfunction is not

-- This DNA mutation alone may not be enough to confer cellular
dysfunction; doctors believe there is an environmental trigger as well.

-- Children with mitochondrial dysfunction are more likely to regress
into autism following a fever and illness from viral infections or a
vaccine reaction.

-- Some changes in the vaccine schedule will almost surely be made. The
most difficult decision is how and when to vaccinate children with proven
mitochondrial dysfunction.

The National Autism Association (NAA), a parent-led non-profit
organization, believes that vaccines have contributed to regressive autism
in most children, and that the rise in autism correlates with the increase
in vaccinations. "It's apparent that those in a position to bring the truth
to light about the vaccine-autism connection might finally be listening to
the parents who have witnessed it first-hand," said NAA board chair Scott

A meeting of the HHS National Vaccine Advisory Committee's Vaccine
Safety Working Group will be held in Washington, DC on April 11th. This
meeting will be open to the public.

To read Mr. Kirby's article, please visit:

To learn more about autism, visit:


Wendy Fournier (Portsmouth, RI) 401.835.5828

Rita Shreffler (Nixa, MO) 401.632.6452

SOURCE National Autism Association


Link to this page:

back to top


Andrew Wakefield and Colleagues Should Applauded and Supported

Adventures in Autism: Wakefield and Colleagues Should Be Knighted, Not Persecuted


"Autism the Musical" You Can Watch for Free Through March 30th

Adventures in Autism: Autism: The Musical#links HBO


What’s perfectly clear, however, is that monozygotic twins aren’t perfectly identical.

From the Simons Foundation blog

Un-identical twins
28 Mar 2008 2:33 PM The first indication that autism has genetic origins came from twin studies. Ditto for schizophrenia and many other diseases.

The idea that monozygotic twins – born after a single zygote divides into two embryos – are genetically identical has been the defining feature of thousands of studies, including ones that have tried to tease out the different influences of genes and environment.

Apparently, they were all a bit off.

According to a study in this month’s issue of the American Journal of Human Genetics, monozygotic twins aren’t exactly identical.

It turns out that these twins have different copy number variations – in which large pieces of DNA are either missing or are present in multiple copies. As we’ve been learning with increasing frequency over the past two years, these copy number variations may be important in diseases such as autism and schizophrenia. Of the 19 pairs in this study, for example, only one twin in each of nine pairs showed signs of Parkinson’s disease or dementia.

We already knew that identical twins become gradually less identical as they age and are exposed to different environments, accumulating epigenetic modifications. These are changes in which the genetic sequence itself remains the same, but chemicals that attach to the genes turn them on or off, and in that way alter each twin’s risk of developing, say, cancer or diabetes.

It’s not yet clear whether copy number variations are similarly accumulated over time, or whether they are present at birth or before. And it’s much too soon to conclude that the variations may be the reason for the dementia seen in one twin but not the other.

What’s perfectly clear, however, is that monozygotic twins aren’t perfectly identical.
posted by ApoorvaMandavilli
Add Comment

Labels: ,

Another person involved in controversial research linking the MMR vaccine with autism has defended his work at a medical tribunal.

WOODFORD GREEN: Doctor defends MMR jab research
By Daniel Binns

A DOCTOR involved in controversial research linking the MMR vaccine with autism has defended his work at a medical tribunal.

Professor John Walker-Smith, of Monkhams Drive in Woodford Green, along with colleagues Prof Simon Murch of Tooting and Dr Andrew Wakefield, who now lives in the USA, all deny serious professional misconduct.

The General Medical Council tribunal heard how the men carried out "invasive" procedures on young children - spinal taps' and colonoscopy procedures - while investigating their theory that the measles, mumps and rubella vaccine (MMR) could be linked with a rise in cases of autism in the UK.

The hearing was told of previous cases when some doctors had rejected such painful methods as unnecessary.

Taking the stand, Prof Walker-Smith said: "None of the tests would have been conducted if they were not considered necessary.

"I was fascinated by the possibility that something might be done to unearth what was going on, and in the future down the line to help the children in their plight."

He added: "But that was secondary to the primary concern of getting care for them."

"None of the tests would have been conducted if they were not considered necessary."
Prof John Walker-Smith

The doctors' original research attracted huge controversy when it was first published in medical journal The Lancet back in 1998.

Their influential claims led to a drop in the number of parents putting their children forward for the vaccine nationwide, and in Redbridge the numbers receiving the MMR jab dropped from 90 per cent in 1998 to a low of 72 per cent in 2005, coinciding with a steep rise in the number of cases.

The men's findings have since been emphatically rejected by bodies such as the British Medical Journal, the Medical Research Council and the Department for Health.

Co-defendant Dr Wakefield also stands accused of paying children at his son's birthday party £5 each for blood samples while he was conducting his research and "joking" about it afterwards at a medical conference.

Outside, dozens of protestors fiercely defended the doctor and his research, claiming he was the victim of a "witch hunt".

The men face being struck off the medical register in the UK if found guilty.

The hearing continues


Thursday, March 27, 2008

"This certainly shows why we should treat patients as individuals,"

UW study finds surprising genetic causes of schizophrenia
Errors in DNA don't seem to follow pattern

As if the science of how genetics leads to disease isn't already complex enough, researchers in Seattle and Long Island, N.Y., say individuals appear to develop schizophrenia from a varying smorgasbord of bad genes rather than common genetic flaws.

Scientists at the University of Washington and Cold Spring Harbor Laboratory report in Friday's edition of the magazine Science that multiple errors or deletions in a person's genetic code, or DNA, can lead to schizophrenia -- a psychiatric illness characterized by delusions and disordered thinking that today affects one of every 100 people.

The finding that multiple genes are involved is, by itself, not surprising, since other diseases or disorders are, or strongly appear to be, the result of many flaws rather than just a single bad gene. That fits nicely within the standard dogma of genetics.

What is surprising, challenging to the dogma and perhaps confusing to many experts who study the interplay between genetics and neuroscience, is that the UW-Cold Spring Harbor team found strong evidence that it's usually not the same set of genes going bad in people who develop schizophrenia.

"It's different genes in different people," said Dr. Jon "Jack" McClellan, a UW psychiatrist and a co-author of the report. This is a big challenge to the conventional wisdom, McClellan said, adding that he believes this could turn out to be the same for most other complex psychiatric diseases -- if not for all diseases that arise without a simple genetic flaw.

"The standard dogma is that any complex trait (such as mental illness) is going to be caused by the cumulative effect of multiple, common defects," said Dr. Mary-Claire King, a world-renowned geneticist and also one of the UW co-authors on the report.

"But that's not what we found."

It's long been clear, she said, that there had to be some sort of genetic contribution to this debilitating illness, since schizophrenia tends to run in families.

But the familial tendency still seemed kind of sporadic, King said, and there is the mystery of why such a self-defeating genetic disorder should exist at all. Considering the evolutionary process of natural selection, she said, schizophrenia genes should not persist because most of those who are afflicted tend to not produce children.

"The genes should have been selected out," King said. "There have been a lot of these paradoxes with schizophrenia."

King and McClellan worked with geneticist Jonathan Sebat and his Cold Spring Harbor colleague Shane McCarthy, along with the UW's Dr. Tom Walsh, Evan Eichler and others.

They employed some powerful, relatively new techniques of computerized genetic analysis to resolve these mysteries.

The goal was to examine the genome (an individual's entire genetic code, in humans more than 3 billion units of DNA) for patterns that might reveal some answers. The scientists examined the DNA of 150 people with schizophrenia (most of them patients at Western State Hospital) and compared what they found with the genetics of 268 people without the illness.

Assuming that the genes of most interest would be those involved in neural development and brain function, they looked for any differences. All individuals have some level of genetic errors or mutations in their genome. The researchers found that people with schizophrenia had flaws in brain-related genes 15 percent of the time compared with 5 percent in healthy people.

But it was never the same set of genes going bad.

"They were all different," King said. "The only way we could have found this was to look at the overall (genetic) profile."

While this certainly complicates the exploration of the genetics of schizophrenia, McClellan said it does reveal some common "neurological pathways" that may lead to better treatments for those with this mental illness. The many different malfunctioning genes in schizophrenics, he said, all play their parts within a limited number of brain-related functions.

Instead of chasing after individual genes to identify and develop new drugs for schizophrenia, McClellan said, this research suggests the focus should be on fixing the problems that arise -- owing to the widely varying genetic flaws -- on the biochemical pathways that govern brain development and function.

"This certainly shows why we should treat patients as individuals," he said. This shouldn't just be a marketing mantra followed by some generic, uniform therapeutic approach to illness, McClellan said, especially if -- as this study indicates -- individual variation occurs even at the most basic, genetic level of illness.

King said she recognizes that not everyone will be happy with, or even accept, the conclusions that they've drawn from this peculiar finding (even though the study was replicated by a team at the National Institutes of Health). It's not just about challenging dogma, she noted; it's also a challenge to a lot of established, funded studies already well under way.

"A lot of those approaches, based on the assumption that they are looking for common or shared genetic mutations, aren't going to work," King said.

Labels: ,

A diversity of associated medical conditions was documented in 20%, with an unexpectedly high rate of mitochondrial respiratory chain disorders.

Thursday, March 27, 2008

Last night we learned from David Kirby that the CDC is actually waking up to the vaccine/autism connection because of the recent revelation of previously missing middle man Mr. Mitochondria.

Here is the study that was the slap in the fact that has been so badly needed for so long:

Epidemiology of autism spectrum disorder in Portugal: prevalence, clinical characterization, and medical conditions

Adventures in Autism: The Study That FINALLY Got The CDC to Pay Attention#links

Labels: ,

Restless sleep marks autism disorders

Restless sleep marks autism disorders
Virginia Gewin 27 Mar 2008 2:46 PM
Clock wise: There may be molecular links
between circadian rhythms and synaptic activity.
For parents of children with autism, bedtime can be a boondoggle.

Some children with autism replay cartoons in their head or talk incessantly during the three to five hours it can take them to wind down and go to sleep1. In fact, up to 83% of parents report some type of sleep disruption among their autistic children — notably difficulty falling asleep or frequently waking in the middle of the night2.

Although the biological underpinnings of these sleep disorders are unknown, some studies — including ones on the growing number of animal models — indicate that the disruptions may hold molecular clues to the interconnected pathways involved in autism.

The best evidence for a biological link between sleep disruptions and autism comes from animal models of fragile X syndrome, a related disorder resulting from a single mutation in the FMR1 gene. The disorder accounts for between two and six percent of all autism cases.

In one model of the syndrome, for example, fruit flies lacking FMR1 are restless sleepers. “The first thing we found was a robust circadian defect,” says Thomas Jongens, a geneticist at the University of Pennsylvania.....................


It’s possible that different combinations of these alterations produce different diseases, such as schizophrenia or the autism spectrum disorders,

From the Simons Foundation blog editor:

Cumulative effects
27 Mar 2008 4:33 PM It’s been clear for decades that there is no one gene that causes schizophrenia. Rather than being result of any one mutation, it turns out that schizophrenia is the unfortunate outcome of many different deletions and duplications that cause the developing brain to go awry.

This is most likely what’s going on in autism as well. In fact, as I wrote here a few weeks ago, the same deletions have been seen in both schizophrenia and autism.

As they are in people with autism, copy number variations — in which chunks of DNA are deleted or duplicated — are generally more common in those with schizophrenia, according to the report, published today in Science.

And variations that disrupt brain development are even more common: they’re seen in 15 percent of adult-onset schizophrenia and 20 percent of child- and adolescent-onset, compared with 5 percent of controls.

These variations are individually rare, and few of the mutations seen in the sample of 150 adults with schizoprehnia is repeated in more than one person or family. But together, their modest effects coalesce into a much larger syndrome.

Cumulative effects
27 Mar 2008 4:33 PM It’s been clear for decades that there is no one gene that causes schizophrenia. Rather than being result of any one mutation, it turns out that schizophrenia is the unfortunate outcome of many different deletions and duplications that cause the developing brain to go awry.

This is most likely what’s going on in autism as well. In fact, as I wrote here a few weeks ago, the same deletions have been seen in both schizophrenia and autism.

As they are in people with autism, copy number variations — in which chunks of DNA are deleted or duplicated — are generally more common in those with schizophrenia, according to the report, published today in Science.

And variations that disrupt brain development are even more common: they’re seen in 15 percent of adult-onset schizophrenia and 20 percent of child- and adolescent-onset, compared with 5 percent of controls.

These variations are individually rare, and few of the mutations seen in the sample of 150 adults with schizoprehnia is repeated in more than one person or family. But together, their modest effects coalesce into a much larger syndrome.

It’s possible that different combinations of these alterations produce different diseases, such as schizophrenia or the autism spectrum disorders, explaining why many of these diseases have so many features in common.

In this study, the researchers found copy number variations in genes important for the growth, survival and death of neurons. Glutamate and neuregulin, both of which have been implicated in schizophrenia and autism, are also in the list.
posted by ApoorvaMandavilli
Add Commentexplaining why many of these diseases have so many features in common.

In this study, the researchers found copy number variations in genes important for the growth, survival and death of neurons. Glutamate and neuregulin, both of which have been implicated in schizophrenia and autism, are also in the list.
posted by ApoorvaMandavilli
Add Comment

Labels: ,

The work also offers evidence that autism shares some genetic roots with schizophrenia.

Schizophrenia Linked to Rare, Often Unique Genetic Glitches

By Rick Weiss
Washington Post Staff Writer
Friday, March 28, 2008; Page A05

Friday, March 28, 2008; Page A05

Patients with schizophrenia are three to four times as likely as healthy people to harbor large mutations in genes that control brain development, and many of those glitches are unique to each patient, researchers reported yesterday.

The findings are forcing scientists to rethink the reigning model of how genes and environment conspire to cause the debilitating disease, which affects about 1 percent of the population worldwide.

In part, scientists said, the new view is daunting because it suggests that many people with schizophrenia have their own particular genetic underpinnings.

At the same time, the study shows that new screening techniques can find and differentiate among those various mutations. In the long run that could help doctors choose the best medications for individual schizophrenics and speed the development of drugs tailored to certain patients' needs.

"If the genetics tells us that schizophrenia is really 10 different disorders, then let's have 10 treatments that optimize the outcomes for everyone and not just use the same drugs for everybody," said Thomas Insel, director of the National Institute of Mental Health, which helped fund and conduct the study.

The work also offers evidence that autism shares some genetic roots with schizophrenia.

"Take away schizophrenia's hallucinations and delusions," said Jon McClellan, a child psychiatrist at the University of Washington and a leader of the study, published in yesterday's online issue of the journal Science, "and the symptoms that remain, the lack of social interest and withdrawal, are what we call autism. There is clearly an intersection of the brain systems involved." ..........


Childhood Schizophrenia is Now Called Autism There is no longer a diagnosis called childhood schizophrenia ---Older Father's Offspring

"If anything, our findings may indicate that it's even more complex than what we suspected because there may be literally thousands and thousands of different mutations in many different number of genes," McClellan said.

Contact: Jules Asher
NIH/National Institute of Mental Health

Rates of rare mutations soar 3 to 4 times higher in schizophrenia
Multiple genetic glitches disrupt pathways critical for brain development
People with schizophrenia have high rates of rare genetic deletions and duplications that likely disrupt the developing brain, according to studies funded in part by the National Institutes of Health.

These tiny anomalies were found in 15 percent of adult onset schizophrenia patients and 20 percent of child and adolescent onset patients, compared with only 5 percent of healthy participants. Collectively, the mutations carried by patients were significantly more likely than those in healthy participants to disrupt genes involved in brain development -- potentially implicating hundreds of genes in the illness, which affects about 1 percent of adults.

“This is an important new finding in the genetics of schizophrenia,” said NIMH Director Thomas R. Insel, M.D. “Identifying genes prone to harboring these mutations in brain development pathways holds promise for treatment and prevention of schizophrenia, as well as a wide range of other neurodevelopmental brain disorders.”

Two independent teams of researchers report on their combined findings in an article published online in Science Express, March 27, 2008. One team was led by Judith Rapoport, M.D., and Anjene Addington, Ph.D., National Institute of Mental Health (NIMH), Intramural Research Program. The other team was led by Jonathan Sebat, Ph.D., and Shane McCarthy, Ph.D., Cold Spring Harbor Laboratory, and by Jon McClellan, Ph.D., Tom Walsh, Ph.D., and Mary-Claire King, Ph.D., University of Washington. Their research was supported in part by the NIMH, National Institute of Child Health and Human Development, National Institute of Neurological Disorders and Stroke, National Center for Research Resources, and the National Institute on Aging.

The prevailing genetic model of schizophrenia implicates common variants of certain suspect candidate genes, each exerting modest effects, in interaction with each other and environmental factors. This hypothesis holds that risk stems from common variations in the sequence of the genetic code that result in altered protein products.

About a year ago, Sebat, King and colleagues reported evidence strengthening the case for a different kind of genetic risk. Many people with autism were found to have different, spontaneous and individually rare structural variations -- variations in the number of copies of genes. These copy number variations were scattered throughout the genome, suggesting that many different genes could be involved in autism spectrum disorders.

The new findings in schizophrenia echo those in autism, but also broaden their implications. The results suggest a new approach for discovering genes for schizophrenia and other mental disorders, say the researchers. Any mutation in the hundreds of genes involved in brain development could lead to a different set of neurodevelopmental consequences – schizophrenia, autism, mental retardation, or no illness at all. Each person with one of the illnesses could have a different genetic cause for the disorder.

The functional consequences of these structural genetic variations may differ, depending on interactions with other genes or environmental events, say the researchers, making any gene harboring a deleterious structural mutation a “candidate gene.” Any gene harboring one mutation likely contains others. Although each might be individually rare, together such disease-causing variations in one gene could explain a substantial number of illness cases, they suggest.

Among key study findings:

* Genes disrupted in patients, as opposed to healthy participants, were significantly over-represented in pathways critical for brain development. These included genes involved in creating the infrastructure by which neurons communicate -- and for neuronal growth, migration, proliferation, differentiation, and cell death. Among these were genes important for neuronal communications via glutamate and neuregulin, both of which have previously been implicated in schizophrenia.

* The mutations were often specific to single cases or families. Virtually every mutation detected by King, Sebat and colleagues was different in a sample of 150 adults with schizophrenia and 268 healthy controls.

* In families affected by childhood onset schizophrenia, Rapoport and colleagues found that 28 percent (23) of 83 patients harbored mutations, compared with 13 percent (10) of 77 controls. By using the non-transmitted chromosomes of the patients’ parents as controls, the researchers were able to determine if the mutations in their children were likely inherited or spontaneous. The majority turned out to be inherited rather than spontaneous, some from parents unaffected by the illness. Childhood onset schizophrenia is thought to be a more severe and more genetically influenced form of the illness.


The research was also funded by the Forrest C. and Frances H. Lattner Foundation, NARSAD, the Simons Foundation, the Stanley Medical Research Foundation, the Howard Hughes Medical Institute.

Rare Structural Variants Distrupt Multiple Genes in Neurodevelopmental Pathways in Schizophrenia

Tom Walsh1*, Jon M. McClellan2*#, Shane E. McCarthy3*, Anjene M. Addington4*, Sarah B. Pierce1, Greg M. Cooper5, Alex S. Nord5, Mary Kusenda3, Dheeraj Malhotra3, Abishek Bhandari3, Sunday M. Stray1, Caitlin F. Rippey5, Patricia Roccanova3, Vlad Makarov3, B. Lakshmi3, Robert L. Findling6, Linmarie Sikich7, Thomas Stromberg4, Barry Merriman8, Nitin Gogtay4, Philip Butler4, Kristen Eckstrand4, Laila Noory4, Peter Gochman4, Robert Long4, Amalia Dutra9, Zugen Chen8, Sean Davis10, Carl Baker5, Evan E. Eichler5, Paul S. Meltzer10, Stanley Nelson8, Andrew B. Singleton11, Ming K. Lee1, Judith L. Rapoport4, Mary-Claire King1, 5, Jonathan Sebat3.

1 Department of Medicine, University of Washington, Seattle, WA 98195, USA
2 Department of Psychiatry, University of Washington, Seattle, WA 98195, USA
3 Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA
4 Child Psychiatry Branch, National Institute of Mental Health, NIH, Bethesda, MD 20892, USA
5 Department of Genome Sciences, University of Washington, Seattle, WA 98195, USA
6 Department of Psychiatry, Case Medical Center, Cleveland, OH 44106, USA
7 Department of Psychiatry, University of North Carolina, Chapel Hill, NC 27599, USA
8 Department of Human Genetics, University of California, Los Angeles, CA 90095, USA
9 Genetic Disease Research Branch, National Human Genome Research Institute, NIH, Bethesda, MD 20892, USA
10 Cancer Genetics Branch, National Cancer Institute, NIH, Bethesda, MD 20892, USA
11 Neurogenetics Laboratory, National Institute on Aging, NIH, Bethesda, MD 20892, USA

*These authors contributed equally to this work.
#To whom correspondence should be addressed. E-mail:

The NINDS ( is the nation’s primary supporter of biomedical research on the brain and nervous system.

The NICHD sponsors research on development, before and after birth; maternal, child, and family health; reproductive biology and population issues; and medical rehabilitation. For more information, visit the Institute's Web site at

The National Center for Research Resources (NCRR) provides laboratory scientists and clinical researchers with the environments and tools they need to understand, detect, treat, and prevent a wide range of diseases. Through the CTSA consortium and other collaborations, NCRR supports all aspects of translational and clinical research, connecting researchers with one another, and with patients and communities across the nation. For more information, visit

The NIA leads the federal government effort conducting and supporting research on the biomedical and social and behavioral aspects of aging and the problems of older people. For more information on aging-related research and the NIA, please visit the NIA website at

The National Institute of Mental Health (NIMH) mission is to reduce the burden of mental and behavioral disorders through research on mind, brain, and behavior. More information is available at the NIMH website,

The National Institutes of Health (NIH) - The Nation's Medical Research Agency - includes 27 Institutes and Centers and is a component of the U. S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical, and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit


MMR-autism link doctor Andrew Wakefield defends conduct at GMC hearing

MMR-autism link doctor Andrew Wakefield defends conduct at GMC hearing
By Nick Allen
Last Updated: 7:48pm GMT 27/03/2008

The doctor at the centre of the controversy over the MMR vaccine has denied committing serious professional misconduct, saying it had been his "duty as a physician and a human being" to investigate potential links between the jab and autism in children.

Dr Andrew Wakefield, the doctor at the heart of the MMR controversy

In a passionate defence of his research Dr Andrew Wakefield told a disciplinary hearing at the General Medical Council in London that he had responded to the "plight" of mothers with sick children.

Dr Wakefield faces being struck off the medical register after he and two colleagues published findings in the respected medical journal The Lancet in 1998 suggesting a link between the triple jab for measles, mumps and rubella and inflammatory bowel disease and autism.

It led to a dramatic fall in the number of children being given the MMR jab.

The scientific community and the Government have since tried to reassure parents that the vaccine is safe.

As Dr Wakefield arrived to give evidence he was greeted by several dozen supporters holding placards declaring he was the victim of a "witch hunt".


More Info on CDC and Their Foisting of Vaccines From Adventures in Autism

Adventures in Autism: CDC Offers Another Non Response on Autism and Vaccines in the AJC This is what science is. No wavering from the CDC's point of view.


Wednesday, March 26, 2008

Another surprise came when one researcher announced an "inheritance pattern" that linked each case through the genetics of the father:

The Next Big Autism Bomb: Are 1 in 50 Kids Potentially At Risk?
Posted March 26, 2008 09:30 PM (EST)
David Kirby The Huffington Post

Adventures in Autism: David Kirby Drops Another Bomb: Autism Risk May Be 1 in 50
The Next Big Autism Bomb!
Submitted by SadInAmerica on 2008, March 30 - 11:17am.
Alarming stats! Will 1 in every 50 children now be diagnoised with some form of autism?

On Tuesday, March 11, a conference call was held between vaccine safety officials at the US Centers for Disease Control and Prevention, several leading experts in vaccine safety research, and executives from America's Health Insurance Plans, (the HMO trade association) to discuss childhood mitochondrial dysfunction and its potential link to autism and vaccines.

It was a sobering event for all concerned, and it could soon become known as the Conference Call heard 'round the world.

The teleconference was scheduled by a little known CDC agency called the Clinical Immunization Safety Assessment (CISA) Network, a consortium of six research centers working on "immunization-associated health risks," in conjunction with the CDC's Immunization Safety Office and the health insurance lobby -- whose companies cover some 200 million Americans.

The hot topic of the day was mitochondria - the little powerhouses within each cell that convert food and oxygen into energy for use by the body. Recent news events have implicated mitochondria in at least one case of regressive autism, following normal development.

Some researchers on the call reported that mitochondrial dysfunction is probably much more common than the current estimate of 1-in-4,000 people. The potential implications for autism, then, are staggering.

"We need to find out if there is credible evidence, theoretically, to support the idea that childhood mitochondrial dysfunction might regress into autism," one of the callers reportedly told participants.


One person on the call (those interviewed for this article asked to remain anonymous) told me that, "the CDC people were informed, in no uncertain terms, that they need to look into this issue immediately, and do something about it." The clock is ticking, they were told, and if they don't respond, the information will be made public.

Still, the doctor said, he was enormously impressed by the "seriousness" with which CDC officials treated the possibility of a link between mitochondria, autism and possibly vaccines as well.

In the recent landmark Hannah Poling case, filed in Federal "Vaccine Court," officials conceded that Hannah's underlying mitochondrial dysfunction was aggravated by her vaccines, leading to fever and an "immune stimulation that exceeded metabolic reserves."

But on March 6, CDC Director Dr. Julie Gerberding claimed that Hannah's case was a rare, virtually one-of-a-kind incident with little, if any relevance to the other 4,900 autism claims currently pending in the court -- or to any other case of autism for that matter.(There were conflicting accounts about whether Gerberding was on the call or not).

Since then, however, Dr. Gerberding and other CDC officials were made aware of a Portuguese study, published last October, which reported that 7.2% of children with autism had confirmed mitochondrial disorders. The authors also noted that, "a diversity of associated medical conditions was documented in 20%, with an unexpectedly high rate of mitochondrial respiratory chain disorders."

"Apparently, the Portuguese study really got their attention," one of the participants said. "It's a highly significant finding. And it's worrisome enough to definitely look into. I think the CDC people know that."

They also know that some reports estimate the rate of mitochondrial dysfunction in autism to be 20% or more. And the rate among children with the regressive sub-type of autism is likely higher still.

Vaccine safety officials on the March 11 call may have been open to discussing mitochondria and autism, but they were probably highly unprepared for what was to come next.

One doctor reported his findings from a five-year study of children with autism, who also showed clinical markers for impaired cellular energy, due to mild dysfunction of their mitochondria.

The biochemistry of 30 children was studied intensively, and in each case, the results showed the same abnormalities as those found in Hannah Poling, participants said. Each child had moderate elevations or imbalances in the exact same amino acids and liver enzymes as Hannah Poling.

All thirty children also displayed normal, healthy development until about 18-24 months of age, when they quickly regressed into clinically diagnosed autism (and not merely "features of autism"), following some type of unusual trigger, or stress, placed on their immune system.

Researchers explained on the call that some data show that mitochondrial dysfunction can convert into autism "in numbers that make it not a rare occurrence," one participant told me. They explained this as "a distinct syndrome; not a mixed bag at all. Every kid had mild mitochondria dysfunction and autistic regression."

Another surprise came when one researcher announced an "inheritance pattern" that linked each case through the genetics of the father: In families where two cousins had autism, the genetic link was always through the father.

This unexpected discovery would clearly implicate nuclear DNA inheritance, and not mitochondrial DNA, which is inherited only through the mother.

Gerberding and others had previously insisted that Hannah and her mother, Teri Poling, both had the same single point mutation in their mitochondrial DNA. CDC officials asserted that Hannah had a pre-existing disease, a rare genetic glitch in her mitochondria, that may well have manifested as "features of autism" on its own, perhaps even without an environmental trigger.

"It's not in the mitochondrial DNA, and it's not rare," one participant confirmed. In fact, he said, many people probably carry the nuclear DNA mutation that confers susceptibility to mitochondrial dysfunction, they just don't know it.


On the call, speculation on the prevalence of a genetic mutation that could confer mild mitochondrial dysfunction in the general population ranged from about 1-in-400, to a staggering 1-in-50, or 2% of all Americans.

There was talk about the urgent need to do mapping studies, and find the locus of this gene. Some of the researchers said they want to test all 30 children for the actual DNA mutation. There was some expectation that they might discover that the mutation goes back generations, so parents and grandparents might be tested as well.

One belief is that a particular mutated gene may have become prevalent over the centuries, because of selective advantage. Mild mitochondrial dysfunction reportedly has been associated with intelligence, because it can increase activity of the brain's NMDA receptors. A large number of receptors can produce increased intelligence, but it can also increase risk of brain disease, one doctor explained to me. It's possible that increased receptor activity acts in same way.

But not everyone agrees that mitochondrial dysfunction is a purely inherited affair. Some researchers believe that, while a susceptibility gene for mitochondrial problems certainly exists, some type of environmental trigger, or "adversity," as one doctor put it, is needed to turn the mutation into a dysfunction.

The medical literature is replete with studies on mitochondrial health and the adverse impact of mercury, aluminum and other toxins. Even AIDS drugs like AZT and prenatal alcohol consumption can damage mitochondria and impact cellular energy.

The mercury-containing vaccine preservative, thimerosal, for example, "can definitely kill cells in vitro through the mitochondria," one teleconference participant told me. "And some people are beginning to suspect that the dose of hepatitis B vaccine given at birth might be interfering with proper mitochondrial function in certain children."

While the cause of mitochondrial dysfunction is up for the debate, so too is its potential effect on regressive autism.

All the researchers I spoke with agreed that, in many cases, there was an underlying, asymptomatic mitochondrial dysfunction, aggravated by some other stressful event imposed on the child's immune system, resulting in autism.

Such "metabolic decomposition" occurs when a child's system simply "cannot meet the energy demand needed to fight the stress of illness," one doctor explained.

But what causes the stress? That is a very big question.

Apparently, in only two of the 30 cases, or 6%, could the regression be traced directly and temporally to immunizations, and one of them was Hannah Poling. In the other cases, there was reportedly some type of documented, fever-inducing viral infection that occurred within seven days of the onset of brain injury symptoms.

All 30 of the regressions occurred between one and two years of age, at a time when the still-developing brain is particularly vulnerable to injury.

But if a significant minority of autism cases was caused by mitochondrial dysfunction aggravated by common childhood illnesses, then shouldn't we see fewer cases today than, say, at the beginning of the 20th Century? And wouldn't developing countries likewise show far more prevalence of autism than the United States?

Not necessarily, some experts said. They noted that many viral infections are still quite prevalent in modern-day America, and many children still get these types of viral infections about once a month, on average.

If that is the case, then why doesn't every child with "mito" dysfunction regress into autism? Surely, they must encounter viral infections during their yearlong window of neurological peril.

Again, not necessarily: Some doctors said it would depend on the severity of the dysfunction, the type of virus encountered, and perhaps other factors that are still not understood.

But at least two of the 30 kids with mito deficiencies were pushed over the edge into autism by their vaccines, and some researchers feel the number is probably much higher than that in the larger population.

"Vaccines, in some cases, can cause an unusually heightened immune reaction, fever, and even mild illness," one participant said. "A normal vaccine reaction in most kids would be very different in a kid with a metabolic disorder. We know it happened to at least two kids in this study, and I'm certain there are many more Hannahs out there."

One theory currently in circulation about what happened to Hannah and other children like her, is an apparent "triple domino effect." According to this hypothesis, it takes three steps and two triggers to get to some types of autism, and it goes like this:

STEP ONE: Child is conceived and born healthy, but with an underlying nuclear DNA genetic susceptibility to mitochondrial dysfunction, inherited from dad.

TRIGGER ONE: An early environmental "adversity" occurs in the womb or during the neonatal period, perhaps caused by prenatal exposure to heavy metals, pollutants, pesticides and medicines. Or, it occurs in early infancy, through environmental toxins, thimerosal exposure, or even the Hepatitis B vaccine "birth dose." This trigger results in:

STEP TWO: Child develops mild, usually asymptomatic mitochondrial dysfunction (though I wonder if the ear infections and eczema so common in these cases might also be symptoms of mito problems).

TRIGGER TWO: Child, now with an underlying mitochondrial dysfunction, suffers over-stimulation of the immune system beyond the capacity of his or her metabolic reserves. This stress is either via a viral febrile infection, or from multiple vaccinations, as in the Poling case. This trigger results in:

STEP THREE: Acute illness, seizures, encephalopathy, developmental regression, autism.

Such a scenario might help explain why autism has increased right along with the addition of more vaccines to the national schedule.

And it might help explain why autism rates are not plummeting now that thimerosal levels have been significantly reduced in most childhood vaccines.

It's possible that exposures from the flu shot, and residual mercury left over in other vaccines -- perhaps in synergistic effect with aluminum used as an "adjuvant" to boost the immune response - might "contribute to the toxic mix that causes childhood mitochondrial dysfunction in the first place," one of the doctors said.

But like many hypotheses, this one has competition. Some researchers believe that the modern American diet is largely to blame for an increase in the number of children whose underlying mitochondrial dysfunction is "triggered" into autism by febrile infections.

The answer, they hypothesize, is corn.

The American diet has become extraordinarily dependent on corn oil and corn syrup used in processing, these experts contend. They say that corn oil and syrup are inflammatory, whereas fish oil is anti-inflammatory. Could our diet be a factor in making this mutated gene become more pathogenic? It's a biochemical defect that leads to biochemical disease, supporters of this theory say: The gene itself becomes more of a problem.


This information raises so many questions it makes your head swim.

First and foremost among them: What to do about vaccinating children with known mitochondrial dysfunction?

In many respects, these kids should be first in line for vaccination, to prevent some illnesses that might trigger an autistic regression during the window of vulnerability. On the other hand, with multiple vaccinations, such as the case with Hannah, there is also a risk of overtaxing the immune system, and likewise triggering regression into autism.

What's needed most urgently, if possible, is a quick, affordable and efficient method of testing children for low cellular energy, perhaps before vaccination even begins.

There was some discussion on the conference call about altering the vaccine schedule in some way, to lower the risk of immune over-stimulation in susceptible children. Certainly, pressure will grow for a change in the schedule - the question is how, when, and if such changes will be made.

Some of the suggestions may not be popular among public health officials. They include:

1) Establishing a maximum number of vaccine antigens to which any child could be exposed on any given day.

2) Permitting the option of separating out the measles-mumps-rubella (MMR) live virus combination vaccines into three distinct "monovalent" shots.

3) Not giving the varicella vaccine (chicken pox) on the same day as the MMR injection - the CDC recently withdrew is recommendation for the Pro-Quad MMR+Varicella vaccine because it doubled the risk of seizures.

Another option is to create new "recommendations for administering multiple vaccines to children who have fallen behind in the recommended childhood immunization schedule," according to the website of the Institute for Vaccine Safety at Johns Hopkins Bloomberg School of Public Health.

Hannah had missed some shots and her doctor decided to "catch up" with the schedule by administering five shots, containing nine vaccine antigens, at once. But some autism activists have pointed out that giving five shots in one day is not that uncommon.

Moreover, they claim, many children regressed into autism following normal vaccination, when the parents religiously adhered to the official schedule.

According to the Johns Hopkins site, "Additional research is needed to determine if other children with autism, especially those with 'the regressive form' of autism, have the same or similar underlying mitochondrial dysfunction disorders."

It adds that, "the advisory groups who make recommendations regarding vaccines will undoubtedly examine this case carefully and make decisions regarding the potential need for changes."

That day may come sooner than you think. It was just announced that, on April 11 in Washington, DC, the National Vaccine Program Office at HHS will convene a meeting of the National Vaccine Advisory Committee's Vaccine Safety Working Group. The Working Group was established to go over the CDC's Immunization Safety Office draft research agenda, and to, "review the current vaccine safety system."

The meeting is open to the public, and I have my seat reserved. But I honestly don't envy the Working Group's very tricky task at hand.

It remains to be seen how all this plays out. And many important questions still lie ahead.

For example, if mitochondrial dysfunction turns out to be as common as 200-per-10,000, and autism is now at 66 per 10,000, did anything bad happen to any of the other 134-per-10,000 children, apart from autism (i.e., ADD, ADHD, speech delay, etc.)?

Moreover, if 10-20% of autism cases can actually be traced to an underlying mitochondrial dysfunction, then what about the majority of autism cases where this did not come into play?

And, if 20% of autism cases are mito related, and 6% of those cases regressed because of vaccines, that would mean that at least 1% of all autism cases were vaccine related. Some estimates of autism go as high as a million Americans - that would mean 10,000 people with vaccine-triggered autism, and billions of dollars in the cost of lifetime care.

(While we are on the subject, isn't it time to fund a study of vaccinated and unvaccinated children, to settle this debate once and for all?)

Finally, the goals of the CISA Network, (which convened the teleconference) are rather progressive and far reaching. It remains to be seen how well the Network fulfills its stated mission, which includes:

Conduct research into "the role of individual variation" on vaccine injury;

"Empower individuals to make informed immunization decisions;"

Help policy makers "in the recommendation of exclusion criteria for at-risk individuals," and;

"Enhance public confidence in sustaining immunization benefits for all populations"

Let's see how long it takes before Network members hang out the proverbial banner: "Mission Accomplished."

David Kirby - March 26, 2008 -

Tag this page!

On Tuesday, March 11, a conference call was held between vaccine safety officials at the US Centers for Disease Control and Prevention, several leading experts in vaccine safety research, and executives from America's Health Insurance Plans, (the HMO trade association) to discuss childhood mitochondrial dysfunction and its potential link to autism and vaccines.

It was a sobering event for all concerned, and it could soon become known as the Conference Call heard 'round the world.

Researchers explained on the call that some data show that mitochondrial dysfunction can convert into autism "in numbers that make it not a rare occurrence," one participant told me. They explained this as "a distinct syndrome; not a mixed bag at all. Every kid had mild mitochondria dysfunction and autistic regression."

Another surprise came when one researcher announced an "inheritance pattern" that linked each case through the genetics of the father: In families where two cousins had autism, the genetic link was always through the father.

This unexpected discovery would clearly implicate nuclear DNA inheritance, and not mitochondrial DNA, which is inherited only through the mother.


Paxil, Birth Defects and Autism

Paxil, Birth Defects and Autism
May 11, 2007. By Jane Mundy RSS Seed Newsvine Facebook

Over the past few years, has interviewed dozens of women who took Paxil during their pregnancy and whose babies were born with birth defects. During these interviews, many women told us that their children -- usually about age three and upwards -- were also diagnosed with autism.

Mothers reported that some children are high-functioning with mild autism (HFA), while others have been diagnosed with Asperger's syndrome (AS, also known as Asperger Disorder), which is very similar to HFA. AS can exhibit a variety of characteristics and the disorder can range from mild to severe.

Haltom City, Texas: In the case of Sue Brown's daughter Alice, AS is severe. Sue took Paxil throughout her entire pregnancy; Alice was also born with a hole in her heart.

"My daughter had two heart surgeries and I thought we were out of the woods. But around three months of age she started to get developmentally weak. She started to curl up her hands, wobbled her head, and couldn't hold it up. Her head fell straight back as if there was no strength in her neck," says Sue.

"The doctor thought Alice had neurological problems. The neurologist said she had spinal muscular atrophy but blood tests didn't bear out the diagnosis. She appeared to be developing everything else normally but by two years old, she seemed depressed and had panic attacks. She got so upset that I would almost have to smother her with my body to calm her down. She got so worked up at little things like me telling her 'No'. And if I scolded her about anything it was devastating.

She would go outside and sing a sad song -- very dramatic -- and cry at the drop of a hat. By the time she reached kindergarten, behavior problems interfered with school and learning. I felt like it was my fault, that I wasn't a good mother. By grade one she was finally diagnosed with Asperger Syndrome.

She is now 10 and academically, she is at 1st grade level. She has to be in a special class (we can't afford a special school) and she had to repeat 2nd grade. She has friends but it is hard to keep them. When she loses a friend, she is completely devastated. She loves everybody and is very artistic -- I say God gave her this gift. Unfortunately, her siblings don't understand so it is hard for her to get along with her brothers and sisters... It has been a real hardship and I just want to wrap her in bubble wrap and protect her from the world...

Lindsay Ontario: Sherry S. only took Paxil for the first two months of her pregnancy. Her doctor told her to stop taking Paxil when Sherry told him she was pregnant. Still, the damage was done. Her daughter Melanie was born three weeks premature, and not breathing. She had two holes in her heart and suffered a stroke. At seven, she is just now learning to form words.

"She has these little ticks," says Sherry. "Before she tries to say anything, she will turn in circles and she clears her throat, over and over. Melanie is so different from my other three kids; she throws temper tantrums that can blow the roof off the house -- in seconds." And just like Sue Brown, Sherry didn't take Paxil when she was pregnant with her other four kids -- only with Alice.

Metuchen, NJ: Arlene's four-year-old son Wesley was diagnosed with high-functioning autism. "I took Paxil throughout my entire pregnancy with him," says Arlene. "He has sensory problems, speech delay and hypotonia but we are luckier than others because he will most likely be able to function normally in society, even though his way of seeing things will always be different from you and me. Wesley goes to a special school and he gets excellent speech and physical therapy; we are also lucky to be able to afford treatment."

Wisconsin: "I took Paxil from the second trimester on but it was a low dose," says Tammy F. "Everything seemed fine when Owen was born but around age three, he started having social difficulties. We took him to a psychiatrist and he was diagnosed with AS. Owen is now six and he is in special education. I also have a two-year-old son and he is fine; I didn't take Paxil during my pregnancy with him.

"I was reading about the relationship between Paxil and heart defects on the Internet and it occurred to me that there might be a relationship with other disorders and Paxil. It didn't come as any surprise to me that there might be a link between this drug and autism.

When I took Paxil, it was a fairly new drug and I don't think anybody really knew the risks. Since then, we know a lot more about it.

It seems likely that Paxil could cause autism and it does seem so pervasive; maybe biological factors such as AS can be triggered by a chemical.

One thing I want to add is this: a lot of people are dealing with autism and we are all here to help each other -- mainly thanks to the Internet and an online community. We are not alone -- and it will be more than interesting to find out how many women who took Paxil during their pregnancy have autistic children..."

The Centers for Disease Control and Prevention released a study February 8, 2007 confirming that about one in 160 children -- higher than the one-in-200 estimate from the 1980s -- develops autism or a related disorder like Asperger's Syndrome by the age of 8. Diagnosis is typically around the age of three.

This study infers that approximately 560,000 Americans age 21 or under suffer with some degree of autism.

Researchers say that both genetic variation and developmental factors combine to cause the disorders, but little more is known than that. One thing is known for sure: these disorders are affecting way too many children.

Labels: ,

Yup Can't Find the Article but he or she is Right!

Enough about vaccines; more about fathers
Arizona Daily Star, AZ - Mar 5, 2008
Interestingly, the children with autism who were born to these older fathers were evenly split by gender. In others words, while there are generally three ...


Tuesday, March 25, 2008

Virginia Tech Offering Settlement of $100,000

Was father's Age a Factor in Va. Tech Shootings? Fathers After 40

Daddy G

Wednesday, April 25, 2007
Was father's age a factor in Va. Tech shootings?
I've struggled this week about just how to write this. Several news outlets have reported that the father of Virginia Tech gunman Cho Seung-Hui is 61. The shooter was 23, which would mean the father was in his late 30s when his son was born. Not old by the standards around here, but it does bring home the seriousness of what the decision to delay childbearing can mean. It's unclear to me what exactly Cho was diagnosed with in the past, but two things I have seen have been schizophrenia and autism.

The link between advanced paternal age and schizophrenia has been recognized for a long time now. And just what is advanced paternal age in this case? Late last year, a French researcher concluded that while "no threshold can be precisely defined," there did seem to be a difference in risks for those younger than 35 and those older than 35. There also studies that show an association between both maternal and paternal age in autism. In fathers, there may be an increased risk with each advanced decade of the father's age. Without knowing anything more than the father's age and the son's reported behaviors and ultimate violent act, it's impossible to say here if the father's age had any effect whatsoever. But I think we can conclude it was one, and only ONE, of the potential risk factors involved in this tragic case.

That said, it's important to note that Cho's actions could not be explained away by either a diagnosis of schizophrenia or autism. Obviously, most people with those disorders never do anything like he did. I don't think we'll ever know what got in him to do what he did. To say "he did this because he was autistic" - or whatever - does more to stigmatize those with disorders than it does to satisfy the need to explain why it happened.

It also doesn't mean that older dads are destined to have violent, angry kids. As I've stated many times before, the vast majority of our kids will turn out to be just as quote-unquote normal as our younger-parenting counterparts, though there are some increased risks. Those risks are real and should be taken seriously when making family-planning decisions................ Posted by Daddy G.
Labels: Daddy G. Journal Now Father's After 40, father's age and risk of autism/schizophrenia

Labels: ,

Monday, March 24, 2008

From the Simons Foundation Blog on Autism Unraveling mitochondria’s mysterious link to autism

Unraveling mitochondria’s mysterious link to autism
Virginia Hughes 24 Mar 2008 9:00 AM
Unexplained origins: Some researchers say there is a real
association between autism and mitochondria.
In the past two weeks, autism researchers and advocacy groups have been agog with news that autism could be linked to an extremely rare group of metabolic diseases.

The controversy began when leaked court documents suggested that the U.S. Court of Federal Claims had ruled that when triggered by a vaccination, defects of the mitochondria — the ‘power plants’ of every cell that turn food into energy — could cause autism.

In November 2007, the court heard a case alleging that routine vaccinations caused severe neurological damage to a nine-year-old girl named Hannah Poling. Poling’s doctors testified that the five vaccinations she received at age 19 months aggravated a preexisting ‘mitochondrial respiratory chain disorder’ and led to degenerative brain disease with “features consistent with autistic spectrum disorder.” For these injuries, the court ruled that the Polings are entitled to government compensation.

For most autism researchers, the mention of a link to mitochondria came as a complete surprise. “We’re all wondering where the science is to back this up,” says pediatrician and vaccine expert Paul Offit.

Only a handful of case studies have been published addressing the link between autism and mitochondrial disease, but they all indicate that there is a real association. The debate is focused on just how large the association is, and whether vaccinations have any impact on the underlying biological mechanism.

“Autism is probably caused by many, many things, most of them genetic, and this is one of them,” says mitochondrial expert Salvatore DiMauro of Columbia University, who published one study1 of five autistic individuals with mitochondrial disease.

The only way to know for sure, DiMauro says, is to perform a thorough epidemiological study looking for mitochondrial defects in a few hundred autistic patients. “I don’t think we’ll find a lot of them. But that would be worthwhile,” he says.

Others insist the link is more common. A small group of scientists originally affiliated with the Poling case is drafting a report of about 30 children under age five with both mitochondrial disease and regressive autism. One of the authors, Richard Kelley, a biochemical geneticist a Johns Hopkins University who first diagnosed Poling with mitochondrial disorder, estimates that “at least 10 percent” of children with autism have an underlying mitochondrial disorder.

“We’ve moved very slowly and carefully in gathering data because we knew it would be extremely difficult to convince people that this is a real phenomenon,” Kelley says. “It takes something big to wake everyone up to something that's been staring them in the face for years.”

Rare cases:
Genetic mitochondrial diseases are as varied as they are rare. Hundreds of types exist. Depending on the country, prevalence estimates range from 1 in 3,000 to 1 in 5,000 adults, according to molecular neurologist Anu Suomalainen-Wartiovaara, whose lab at the University of Helsinki specializes in mitochondrial dysfunction. “Maybe 5 or 10 percent of all our genes are making mitochondrial proteins,” she says. “So it's a huge group of diseases.”

Some people with the disease get sick just after birth, and may die after an especially violent epileptic attack. Others develop normally for several years before seeing any symptoms. In these cases, the disease is usually triggered by stresses to the immune system, such as a minor respiratory infection or, some claim, a vaccination.

Because mitochondria are vital to producing energy in most of the body’s cells, many organ systems can be affected by their dysfunction. The most common symptoms include muscle weakness, epilepsy, diabetes, liver failure and — as in Poling’s case — encephalopathy or regressive brain disease.

“Psychiatric symptoms are quite common in these patients,” says Suomalainen-Wartiovaara. With severe encephalopathy, she adds, “it’s hard to make the diagnosis of autism because so many different structural changes are happening and causing psychiatric symptoms.”

This means that autism could either be over- or under-diagnosed in these patients. Unlike certain types of diabetes, which have been definitively shown to be associated with specific point mutations in mitochondrial DNA, “there’s just no hard data on autism,” she says.

A handful of case studies and small population studies have explored how genetic mitochondrial disorders might be associated with autism. The largest2, published in 2005, was led by pediatrician Guiomar Oliveira of Portugal’s Centro de Desenvolvimento da Criança. Oliveira found that 5 out of 69 autistic children (or 7.2 percent) had an underlying mitochondrial respiratory chain disorder — the same type as Poling.

Though this is a much higher prevalence than in the general population, “we don't know if it is a primary cause of autism,” Oliveira wrote in an email. The autism could be caused by another metabolic or genetic defect that is also controlled by the mitochondria, she explained.

Cause and effect:
According to the leaked court documents, within hours of vaccination, 19-month-old Hannah Poling showed a host of physical and behavioral deficits, including loss of language skills, eye contact and the ability to relate to other people — all of which are also common features of autism spectrum disorders.

Kelley says mitochondrial disease has a significant link to this kind of regressive autism, in which a child develops normally until about 18 months. “Most kids I’ve assessed with regressive autism have an underlying mitochondrial problem,” he says.

In 2003, he presented an abstract at the Current Trends in Autism Conference in Boston, stating that for kids diagnosed at the Kennedy Krieger Institute with developmental disabilities, mitochondrial disease was the most common diagnosis, accounting for as many as 20 percent of autistic children.

“It’s a very distinctive biochemical fingerprint of abnormalities that we see, and it’s very consistent from patient to patient,” he says.

During brain development, timing is everything. Kelley theorizes that if children with specific types of mitochondrial disease are exposed to a “stressful event” — which might include an immune reaction — between the age of one and two years, “they’ll often develop the phenotype of autism.”

If that stress comes during a different period of brain development, the disease might manifest into other symptoms.

He bases this theory partly on work done in mice by his colleague Michael Johnston, who found that the density of a certain brain cell protein, called the NMDA receptor, peaks around 18 months of development.

NMDA receptors are important for chemical communication between brain synapses and require energy to function. A higher density of receptors, Kelley reasons, requires more energy — which is difficult to produce without fully functional mitochondria. This could have a huge impact on brain maturation and the pruning of neurons, the developmental processes occurring at that time.

“Overstressing that system might create a massive pruning at a time when you’re only supposed to have a little bit of pruning,” Kelley says, possibly leading to regressive autism.

Bolstering this hypothesis, he says, is that many children with regressive autism also have an “inflammatory phenotype,” meaning they have ear infections or multiple allergies. “Their immune systems might be especially tuned up, causing them to overreact to stress,” he says.

A scientific study testing this theoretical mechanism in humans has not yet been published.

Kelley says his biochemical approach to studying the mitochondrial origins of autism has delivered insights missed by most autism experts. “Most people dealing with autism don’t understand metabolic [science], so I understand why they’re skeptical,” he says.

The vaccination trigger is the most controversial part of the theory, and of Poling’s court case. “I reject that part of [the Poling case] completely,” says DiMauro. “Mitochondrial diseases are caused by mutations in genes,” he explains. “There is no way a vaccination can cause a mitochondrial disease.”



Pons R. et al. J Pediatr. 144, 81-85 (2004) PubMed ↩

Oliveira G. et al. Dev. Med. Child Neurol. 47, 185-189 (2005) PubMed ↩


What DOES the CDC and Julie Gerberding Really KNOW about "AUTISM" and Paternal Age and Vaccinations?

From on is the CDC acting in the interest of US citizens or the pharmaceutical industry? Paul Offit,etc.

Labels: , , ,

Sunday, March 23, 2008

Is There Hanky-Panky Behind Mandatory Vaccines? by: Phyllis Schlafly

Is There Hanky-Panky Behind Mandatory Vaccines? by: Phyllis Schlafly

August 25, 1999

After parents whose children had been severely damaged from
vaccines attended a couple of congressional hearings, we might have
thought Bill Clinton's response would have been, "I feel your pain."
Not on your life. The Clinton Administration instead floated plans to
gut the federal trust fund that compensates the families of children
who are injured or killed by reactions to vaccines.

Surgeon General David Satcher told a House committee this month
that Health and Human Services Secretary Donna Shalala might
recommend that a large portion of the National Vaccine Injury
Compensation Program's $1.4 billion trust be turned over to vaccine
research. That would be a cruel betrayal of the parents who financed
this trust fund by a 75 cents per dose assessment on vaccines and
were promised compensation from it in exchange for virtually
eliminating the pharmaceutical companies' financial liability for
injuries caused by their products.

The Vaccine Adverse Event Reporting System (VAERS) received
11,000 complaints last year from doctors or parents. In presenting
their claims of vaccine damages, parents must face a battery of 17
full-time, veteran Justice Department lawyers assigned to argue
against them.

These lawyers have been successful in denying compensation to all
but 1,300 of 5,300- plus families. The Clinton Administration has
tightened the screws to make it become more and more difficult for
parents to get any compensation.

Since most children today get up to 33 immunizations before they
can be admitted to public school, parents are starting to ask a
fundamental question. Which is the greater risk: getting and being
injured by the disease, or being injured from the vaccine that purports
to protect us from it?

For example, serious adverse events after receiving the hepatitis B
vaccine, including 48 deaths, are reported three times as frequently
as cases of hepatitis B in children under the age of 14. And, the only
polio cases in the United States since 1991 have been those caused
by the oral polio vaccine, whose use was discouraged only a few
weeks ago!

Adults are free to assume risk for reasons of their choice: health,
safety, protection of family or property, entertainment, or even
excitement. But risk is not something that government, in a free
society, should ordinarily force people to accept.

The Association of American Physicians and Surgeons (AAPS) has
just written Secretary Shalala a letter charging that "federal vaccine
policy results in the violation of informed consent, and is based on
incomplete studies of efficacy and potential adverse effects of the
vaccines." The AAPS letter points out that federal vaccine
"recommendations" are transformed into "mandates by state health
departments," and that schools often require many vaccines "as a
condition of attendance."

These adverse events include not only immediate reactions to the
vaccines, such as seizures and even death, but also possible
long-term effects from damage to a child's immune system. We
urgently need an independent study to discover if there is a
relationship between vaccines, especially when so many are given to
infants in multiple doses, and the dramatic recent increases in
autism and asthma.

The peremptory demand that all infants be immunized, regardless of
whether they are at risk, is now being imitated by the U.S. Armed
Forces. In May 1998, the Department of Defense mandated anthrax
vaccination -- requiring six shots in the first 18 months followed by
annual booster shots -- for all 2.4 million service personnel.

Serious questions have been raised about the vaccine's safety. The
vaccine was approved by the Food and Drug Administration (FDA)
back in 1970 after being tested on only 26 human recipients, and the
long-term effects are unknown.

Israel does not force its military to take this vaccine. Neither does
France. Neither does England. No country in Europe or Asia forces
this vaccine on its soldiers.

There is so much opposition to the anthrax vaccination among the
military that morale and combat readiness are suffering. This vaccine
policy has caused an ominous exodus of some of our most
experienced pilots from the reserves and the Air National Guard.

There is something drastically amiss when hundreds of servicemen
with exemplary records are accepting court martial, dishonorable
discharge, pay reduction, and time in the brig rather than obey an
order to be vaccinated.

So who is profiting from this gigantic vaccine mandate? The
Pentagon contracted with a single supplier, BioPort Corp., and
recently agreed to pay $10.64 per dose even though the contractual
obligation was only $4.36 per dose.

ABC News reported that Admiral William J. Crowe Jr. owns 22.5
percent of Intervac, which gives him a 13 percent share of BioPort,
even though he hasn't "invested a penny" in the venture. Crowe was
Chairman of the Joint Chiefs of Staff under President Bush, but made
big news in 1992 when he gave Clinton cover for his draft dodging.
Clinton rewarded Crowe with the prize plum of appointment as
Ambassador to England.

The Pentagon badly needs Congressional supervision, and Rep.
Benjamin Gilman (R- NY) and Rep. Walter Jones (R-NC) have
introduced separate bills to halt the mandatory anthrax vaccinations.

Phyllis Schlafly column 8-25-99
This column may also be found at:

Eagle Forum
PO Box 618
Alton, IL 62002 Phone: 618-462-5415
Fax: 618-462-8909


Top Autism Sites Health Blogs -  Blog Catalog Blog Directory StumbleUpon Toolbar Stumble It! blog directory PageRank Button Add to Technorati Favorites Health Blogs
Directory of Health Blogs Blogarama - The Blog Directory