Gov't Examines Link between Autism and Vaccines Mitochondrial Disorders Implicated

Gov't Examines Link between Autism and Vaccines
Mitochondrial Disorders Implicated
By DAN HARRIS, LIZ SINTAY and EMILY YACUS
June 30, 2008
4 comments
health agencies, including the Food and Drug Administration, the Centers for Disease Control and Prevention, and the National Institutes of Health, met in Indianapolis Sunday to discuss whether cellular diseases known as mitochondrial disorders should be considered in research on autism.

Mitochondrial disorder vaccinations could possibly cause autism.At the heart of the issue for many specialists and concerned parents is whether vaccines -- suspected by some people as being a cause of autism -- might trigger mitochondrial disorders, which lead to autism.

One of the people at the meeting in Indianapolis was Jon Poling, father of 9-year old Hannah Poling, who was diagnosed with autism after receiving a series of vaccines.

Poling, who is also a neurologist, said he believes the vaccines may have aggravated a pre-existing condition, called mitochondrial disease, which in turn, led to Hannah's autism.

Some hope that this meeting will generate more research.

"I guess I kind of feel like it's Christmas Eve," Poling said. "Tomorrow is Christmas morning and, hopefully, those presents will be grants in the form of serious federal monies to look into autism and its relationship to mitochondrial disorders."

Related
Link Up With Autism OrganizationsGovt. Group Urges New Vaccines for KidsFamilies Seek $$ for Autism-Vaccine LinkMitochondria are tiny structures inside the cells whose job is to generate energy for metabolism and other body functions. Doctors said perhaps 5 percent to 10 percent of patients with mitochondrial disorders show symptoms of autism.


"Parents have observed a time association between when their child got vaccinated and when they had a worsening of their clinical state," said Dr. Douglas Wallace, director of the Center for Molecular and Mitochondrial Medicine and Genetics at the University of California-Irvine. "But just because two things occur at the same time, it doesn't mean that one caused the other."

While many mitochondria specialists said they are excited to study this potential link, they also said there is no evidence that vaccines play a major role in causing autism, as many parents of autistic children suspect.

Dr. Bruce Cohen, a neurologist at the Cleveland Clinic, has weighed the possible link and said the issue is complicated.

"I think there is some potential of causing undue concern when one hears about situations such as the Hannah Poling case," Cohen said. "But when we look at all the benefits of the vaccine program in preventing horrible diseases and horrible deaths, I think you have to take it all into consideration."


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"It is very possible that PATERNAL AGE is the major predictor of(non-familial) autism." Harry Fisch, M.D., author "The Male Biological Clock".

This statement is a fact. Mitochondrial disease is another cause of autism. Mothers who had older fathers when they were conceived is another cause of autism. Familial autism is very high risk for autism and family history of auto immune disorders is another key risk factor.

The causes of new/non-familial/sporadic autism are NOT UNKNOWN BE INFORMED.

Father babies by 33, do not vaccinate according to the schedule and study all the web sites on vaccinations. Press for tests for mitochondrial disorders before any vaccination.

Read the research and articles on this blog.

Adventures in Autism: Autism Speaks Undercuts the Children of PA

Adventures in Autism: Autism Speaks Undercuts the Children of PA

Mitochondrial Disease and Vaccinations

Experts to Discuss a Puzzling Autism Case, as a Second Case Looms

By GARDINER HARRIS
Published: June 28, 2008
Federal health officials on Sunday will call together some of the world’s leading experts on an obscure disease to discuss the controversial case of a 9-year-old girl from Athens, Ga., who became autistic after receiving numerous vaccinations.


But the government has so far kept quiet a second case that some say is more disturbing and more relevant to the meeting.
On Jan. 11, a 6-year-old girl from Colorado received FluMist, a flu vaccine, and about a week later “became weak with multiple episodes of falling to ground” and “difficulty walking,” according to a case report filed with federal health officials and obtained by The New York Times.
The girl grew increasingly weak and feverish and “became more limp, appears sleepy, acts as if drunk,” the report said. She was hospitalized and underwent surgery and was finally withdrawn from life support. She died on April 5, according to the report.
Both the 9- and 6-year-olds had mitochondrial disorders, a spectrum of genetic diseases that have received almost no attention from federal health officials. The 9-year-old, Hannah Poling, was 19 months old and developing normally in 2000 when she received five shots against nine infectious diseases. Two days later, she developed a fever, cried inconsolably and refused to walk. In the next seven months, she spiraled downward, and in 2001 doctors diagnosed autism.
No one knows whether vaccinations had anything to do with the girls’ health problems, and the scientific significance of individual cases is always difficult to assess. But suggestions that mitochondrial disorders could be set off or worsened by vaccinations, and that the disorders might be linked to autism, prompted the meeting on Sunday and has brought the disorders sudden national attention.
Those scheduled to present at the meeting who were contacted by The Times said they knew nothing of the Colorado case.
“I haven’t heard about this case,” said Dr. Thomas R. Insel, director of the National Institute of Mental Health and the day’s first speaker.
Dr. John Iskander, acting director of the immunization safety office at the Centers for Disease Control and Prevention, said his group had studied the Colorado case closely but did not discuss it with those presenting at the meeting and had no plans to present the case to the conference, although he and members of his group will attend.
“Part of the consideration is, what was the best use of that time?” Dr. Iskander said in an interview. “To a large extent, the judgment of the meeting organizers was to have the experts in these conditions — which are not vaccine safety experts — to have most of the agenda.”
Dr. Iskander said the Clinical Immunization Safety Assessment Network of the disease agency reviewed the medical records related to the Colorado and Georgia cases, searched for similar reports and asked vaccine manufacturers if they knew of similar cases. A spokeswoman for MedImmune, the maker of FluMist, declined to comment.
The team noted that the Colorado child had not experienced any problems with her previous vaccinations and was relatively old at the time of her diagnosis. Dr. Iskander said the group had concluded “that this is another case that points to the need of better data on the risks and benefits of vaccinations in children with these rare disorders.”
Study after study has failed to show any link between vaccines and autism, but many parents of autistic children are convinced that vaccines — usually given around the time autism becomes apparent — are to blame.
Parents and a small group of doctors have offered a variety of scientific explanations in recent years to try to explain why they think vaccines may cause or contribute to autism. Among the first was that the measles vaccine caused a low-level measles infection that affected children’s brains. The science underlying that theory has since been discredited.
The next theory was that a mercury-containing vaccine preservative, thimerosal, poisoned their brains, causing autism. Multiple studies have failed to find any relationship between thimerosal exposure and autism, and nearly seven years after the preservative was removed from childhood vaccines, autism rates seem unaffected.
The Poling case, however, offered advocates a new theory: that vaccines may cause or contribute to an underlying mitochondrial disorder, which in turn causes autism. Although autism is common among children with mitochondrial disorders, several experts in the disorders dismissed the notion that vaccines may cause the disease, which is widely understood to have a genetic origin.
“After caring for hundreds of children with mitochondrial disease, I can’t recall a single one that had a complication from vaccination,” said Dr. Darryl De Vivo, a professor of neurology and pediatrics at Columbia University who will present at the meeting on Sunday and is one of the premier experts in the field.
Mitochondria, which serve as the energy factories of cells, have their own genetic material that is passed directly from mother to child. Flaws in this material are relatively common. As those flaws multiply, they interfere with mitochondrial function.
Dr. De Vivo said as many as 700,000 people in the United States had flawed mitochondria, and in roughly 30,000 of them the genetic flaws were expansive enough to cause disease.
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An Excellent Article in Scientific American Magazine on the Genetic Male Biological Clock

June 26, 2008

Fact or Fiction: Men Have a Biological Clock
Does male fertility have an expiration date?
By Anne Casselman



In other studies, older men were more likely to father children with mental illness or other deficits. Roughly 11 children out of a thousand conceived by men over age 50 developed schizophrenia compared with under three children out of a thousand for fathers under 20 in one study from the Archives of General Psychiatry. And the children of men 40 years or older were nearly six times more likely to have autism spectrum disorders than kids begot by men under 30.

So do men's sperm get staler over time? To maintain sperm levels, cells known as germ cells must continue dividing. After all, men find ways to dispose of sperm—ahem—and once ejaculated they only survive for several days. By the age of 50, these germ cells will have divided 840 times. Each one of those divisions is an opportunity for something to go wrong. "There's more of a chance to have genetic abnormalities the more the cells divide," Fisch says. In sperm these mutations dot the genes with changes in the basic structure of the DNA—and can lead to problems in the resulting offspring.

We also note that schizophrenia and autism share certain risk factors such as advanced paternal age

We also note that schizophrenia and autism share certain risk factors such as advanced paternal age. Apart from genomic imprinting, copy number variants related to advanced paternal age may also contribute to the differential trajectory of brain development associated with autism and schizophrenia


: Behav Brain Sci. 2008 Jun;31(3):264-265.
Animal models may help fractionate shared and discrete pathways underpinning schizophrenia and autism.Burne TH, Eyles DW, McGrath JJ.
Queensland Centre for Mental Health Research, The Queensland Brain Institute, The University of Queensland, St Lucia, Brisbane, 4072, Australia. t.burne@uq.edu.au http://www.qbi.uq.edu.au eyles@uq.edu.au http://www.qbi.uq.edu.au john_mcgrath@qcmhr.uq.edu.au http://www.qbi.uq.edu.au.

Crespi & Badcock (C&B) present an appealing and parsimonious synthesis arguing that schizophrenia and autism are differentially regulated by maternal versus paternal genomic imprinting, respectively. We argue that animal models related to schizophrenia and autism provide a useful platform to explore the mechanisms outlined by C&B. We also note that schizophrenia and autism share certain risk factors such as advanced paternal age. Apart from genomic imprinting, copy number variants related to advanced paternal age may also contribute to the differential trajectory of brain development associated with autism and schizophrenia.

The Fragile X Factor

The Fragile X Factor
Thursday, Jun. 26, 2008 By CLAUDIA WALLIS
Cari Wheeler, center, and her dad Gary Boyer, seated, did not know they carried the fragile X trait until Max, center, was born with fragile X syndrome.
They called him "the singing baby." As a newborn, Maxwell Wheeler would lie in his crib, whistling shrilly as he breathed in and out. For Cari and Andrew Wheeler of Madera Ranchos, Calif., it was one of the first signs that all was not right with their second child--an infant who didn't like to be touched, refused to nurse and struggled to keep down formula. At 10 months, when Max was still spitting up more than sitting up, the Wheelers consulted an occupational therapist, who noticed an extra fold above his eyelids, prominent ears and other features she called "dysmorphic."

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"I said, 'What do you mean dysmorphic?'" Cari recalls. "'I think he's cute!'" But she and Andy agreed to have their baby tested for genetic disorders. And so began a medical odyssey that would engulf three generations of the family.

I met the Wheelers at the MIND (for Medical Investigation of Neurodevelopmental Disorders) Institute at the University of California at Davis, where they arrived with Max, now 7, his brother Brockton, 10, and Cari's parents Mary and Gary Boyer. It was one of many visits for the Wheeler-Boyer clan. Max raced around a visitors' room, occasionally hugging his mom and trying to pull his beloved granddad up from his chair. Mildly autistic and mildly retarded, Max doesn't speak much, and he didn't respond to my overtures. In addition, Max suffers from hyperactivity, low muscle tone, gastrointestinal problems and a tendency to spike scorchingly high fevers. Though he's doing fine in kindergarten--with an aide--he only recently managed to pass potty-training.

Max wasn't the only one in the room struggling with a worrisome condition. His grandfather Gary, 70, sat stiffly in his chair, tuning in to and out of the conversation. An architect with a Ph.D. in urban engineering, he has developed a tremor in his left hand, and he's so unsteady on his feet that he's taken several falls. "My legs are gone," he says. "I'm very numb from the knees down." Perhaps more alarming are the changes in his personality. The first sign was hoarding household items. "Then I started noticing that he became antisocial," says his wife Mary. "He didn't want to go out. And he didn't want to talk when people came over. He would sit on the patio and smoke."

Cari has been just as stunned by the changes in her once outgoing father, but lately she has had some odd symptoms of her own. Though only 35, she has begun to experience hot flashes, and her menstrual periods have become brief and irregular.

Ten years ago, no one would have connected Max's autism and other symptoms with Gary's neurological decline or Cari's premature signs of menopause. Now, however, researchers realize that all three are caused by changes in the same gene, one that's related to a disorder called fragile X syndrome (FXS), perhaps the most complicated genetic condition you've never heard of. Max has full-blown FXS. The disorder, as its name implies, is the result of a defective gene on the X chromosome, one of the pair of chromosomes that determines gender. FXS affects roughly 1 in 2,500 boys, causing autism spectrum disorders in about half of them. That makes FXS the most common known cause of autism, responsible for roughly 5% of all cases. It is also the most common inherited cause of mental retardation. Though the FXS defect occurs just as frequently in girls, they tend to be less severely affected.

Fragile X has been known for decades, but an explosion of new research, prodded along by advocacy groups like the National Fragile X Foundation and FRAXA, is yielding insights that have implications for understanding and treating autism--and perhaps a number of other conditions too. "Fragile X is leading the autism field in terms of new treatments," says pediatrician Randi Hagerman, medical director of the MIND Institute. "We know the gene, we know a lot about the biology, and we know how to fix it. That's pretty exciting!"

In addition, new research has revealed that relatives who carry the fragile X trait, like Max's mother and grandfather, may themselves be affected by it. At the National Institutes of Health (NIH), a new panel has been charged by Congress to direct research into FXS and related conditions. "We hope to learn lessons that may be applicable to helping people with Huntington's disease, Alzheimer's and myotonic dystrophies too," says Tiina Urv, who heads the panel. Research on the FXS family of disorders may also yield clues to some forms of infertility.

Most of us move through our days with only a vague awareness of our genetic endowment, fretting perhaps over a familial tendency toward heart disease or beaky noses. But families affected by fragile X can discuss their genome with startling specificity. Their key concern is a small strip of DNA on the long arm of the X chromosome. Normally, humans have five to 55 repetitions of the nucleotides CGG (cytosine, guanine, guanine) in this region. But for unknown reasons, the number of CGG repeats can expand beyond normal as the DNA is copied from mother to child.

Cari, for instance, has one normal X chromosome (with 24 repeats), inherited from her mother, and another with an abnormal 85 repeats, inherited from her father, who has 89 repeats. Cari's son Max has 363. Any number greater than 200 causes full-blown fragile X syndrome (so named because, under a microscope, the expanded X chromosome may look bent to the point of breaking). The reason boys are more likely than girls to develop major symptoms is that girls carry a pair of X chromosomes, which means that if one is defective, the other can compensate. Boys, however, carry an X and a Y, so the damaged chromosome is on its own.

People like Cari and her father, with 55 to 200 repeats, are considered carriers of a fragile X "premutation." Carriers are relatively common: about 1 in 250 women and 1 in 800 men have the premutation, though some studies suggest the prevalence is higher. Until recently no one worried too much about those numbers, since carriers were thought to be unaffected.

It was pediatrician Hagerman who first noticed in the late 1990s that mothers of kids with FXS often reported that their father was experiencing neurological symptoms. "I thought, This can't be a coincidence," she recalls. At an FXS conference in 2000, Hagerman asked some 100 fragile X family members if an older male relative was having problems with balance, tremors or dementia. About a third of the audience members shot their hands into the air. Within a few years, a newly recognized genetic disorder called FXTAS (fragile X--associated tremor, ataxia syndrome) was part of the literature, though the illness is still often mistaken for Alzheimer's, Parkinson's or Lou Gehrig's disease.

MicroRNAs Provide New Insight in Study of Autism, UC Santa Barbara Scientist Reports (Paternal Age?)

Wed Jun 25 16:36:41 2008 Pacific Time

MicroRNAs Provide New Insight in Study of Autism, UC Santa Barbara Scientist Reports
SANTA BARBARA, Calif., June 25 (AScribe Newswire) -- MicroRNAs may play an important role in the development of autism spectrum disorder, according to a new paper by University of California, Santa Barbara professor Kenneth S. Kosik.

Kosik, co-director of UCSB's Neuroscience Research Institute and the Harriman Professor of Neuroscience, was senior author of the paper, "Heterogeneous Dysregulation of microRNAs across the Autism Spectrum," published this month in the journal Neurogenetics.

"There is such a broad interest in autism," Kosik said. "This is the first work in this area."

Autism is a neurological disorder that impairs social interaction and communication, usually before a child turns three years old.

In addition, Kosik's research discovered that autism may be even more genetically diverse than previously thought. "We can't continue to look at this (autism) as a monolithic entity," Kosik said. "This is not a single disease."

Instead, his paper revealed that microRNAs have a unique type of genetic signature that shows the very broad underlying diversity of autism. While many studies lump together all cases of autism, some recent papers have reported mutations among small numbers of autism patients. Kosik's microRNA research shows that autism does indeed cover a broad spectrum.

Ribonucleic acid, or RNA, is a link between DNA and protein. Some RNAs, according to Kosik, do not make a protein. One such type of RNA is called a microRNA because it's very short. While there are 23,000 genes in the human body, there are about 1,000 different microRNAs.

The short RNA sequences can bind to many different, longer RNAs and inhibit them from making the protein, Kosik's study found. "In this manner, they exert a broad regulatory control over the expression of many different proteins," he said. And many of the genes they control are involved in brain development.

"It was of interest to find that various members of the microRNA family are frequently dysregulated in autism," Kosik said. "This result points to a single control layer in the cell that can change in quite different ways with autism as the end result."

Kosik's study took two years and was funded by the National Alliance for Autism Research and the W. M. Keck Foundation. Working with Kosik on the paper was, among others, Kawther Abu-Elneel, a post-doctoral fellow with the UCSB Neuroscience Research Institute.

- - - -

CONTACT: George Foulsham, UCSB Office of Public Affairs, 805-893-3071, george.foulsham@ia.ucsb.edu

NOTE TO EDITORS: Ken Kosik can be reached at kosik@lifesci.ucsb.edu or 805-893-5222

David Kirby on the Joan Hamburg Show

Adventures in Autism: Kirby on NYC Radio: The Joan Hamburg Show#links

Is Research on Autism a Business or Why Is the Paternal Age Connection to Autism Not Widely Known?

Scientific Misconduct Blog: ORI Research misconduct survey reports the obvious - again

http://www.neighborsgo.com/video/924

This study clearly demonstrates an increase in sperm double-stranded DNA breaks with age.

1: Fertil Steril. 2003 Dec;80(6):1420-30. Links
Effects of age on DNA double-strand breaks and apoptosis in human sperm.Singh NP, Muller CH, Berger RE.
Department of Bioengineering, University of Washington, Seattle, Washington 98195-7962, USA. narendra@u.washington.edu

OBJECTIVE: This study was designed to explore the relationship between men's age and DNA damage and apoptosis in human spermatozoa. DESIGN: Semen samples were collected from men between the ages of 20 and 57 years. Sperm DNA double-strand breaks were assessed using the neutral microgel electrophoresis (comet) assay, and apoptosis was estimated using the DNA diffusion assay. SETTING: Academic medical center. PATIENT(S): Sixty-six men aged 20 to 57 years were recruited from infertility laboratory and general populations and consented to donate a semen sample. Recruitment was determined by time and day of analysis; the only exclusions were for azoospermia, prostatitis, or prior cancer therapy. INTERVENTION(S): None. MAIN OUTCOME MEASURE(S): DNA damage and apoptosis in human sperm. RESULT(S): Age correlated with an increasing percentage of sperm with highly damaged DNA (range: 0-83%) and tended to inversely correlate with percentage of apoptotic sperm (range: 0.3%-23%). For example, percentage of sperm with highly damaged DNA, comet extent, DNA break number, and other comet measures was statistically significantly higher in men aged 36-57 years than in those aged 20-35 years, but percentage apoptosis was statistically significantly lower in the older group. Semen analysis showed percentage motility to be significantly higher in younger age groups. CONCLUSION(S): This study clearly demonstrates an increase in sperm double-stranded DNA breaks with age. Our findings also suggest for the first time an age-related decrease in human sperm apoptosis. These novel findings may indicate deterioration of healthy sperm cell selection process with age.

PMID: 14667878 [PubMed - indexed for MEDLINE]

(i) older men have increased sperm DNA damage associated with alkali-labile sites or single-strand DNA breaks ...

Hum Reprod. 2007 Jan;22(1):180-7. Epub 2006 Oct 19. Links
The effects of male age on sperm DNA damage in healthy non-smokers.Schmid TE, Eskenazi B, Baumgartner A, Marchetti F, Young S, Weldon R, Anderson D, Wyrobek AJ.
Lawrence Livermore National Laboratory, Livermore, CA, USA.

BACKGROUND: The trend for men to have children at older age raises concerns that advancing age may increase the production of genetically defective sperm, increasing the risks of transmitting germ-line mutations. METHODS: We investigated the associations between male age and sperm DNA damage and the influence of several lifestyle factors in a healthy non-clinical group of 80 non-smokers (mean age: 46.4 years, range: 22-80 years) with no known fertility problems using the sperm Comet analyses. RESULTS: The average percentage of DNA that migrated out of the sperm nucleus under alkaline electrophoresis increased with age (0.18% per year, P = 0.006), but there was no age association for damage measured under neutral conditions (P = 0.7). Men who consumed >3 cups coffee per day had approximately 20% higher percentage tail DNA under neutral but not alkaline conditions compared with men who consumed no caffeine (P = 0.005). CONCLUSIONS: Our findings indicate that (i) older men have increased sperm DNA damage associated with alkali-labile sites or single-strand DNA breaks and (ii) independent of age, men with substantial daily caffeine consumption have increased sperm DNA damage associated with double-strand DNA breaks. DNA damage in sperm can be converted to chromosomal aberrations and gene mutations after fertilization, increasing the risks of developmental defects and genetic diseases among offspring.

PMID: 17053003 [PubMed - indexed for MEDLINE]

A link between autism and schizophrenia?

A link between autism and schizophrenia?
Datum nieuwsfeit: 23-06-2008
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A link between autism and schizophrenia?

Patients with Multiple Complex Developmental Disorder (MCDD) have clinical features of both autism (social impairment) and schizophrenia (cognitive impairment).

In addition to social problems and problems regulating their emotions, they also have thinking disorders and in many cases develop a schizophrenia spectrum disorder (more than 60 percent in adults). In her doctoral dissertation, Bertine Lahuis wonders whether a number of neurobiological parameters can be used to differentiate MCDD as a subtype within autistic spectrum disorders. She studied brain structure using structural imaging, psychophysiological parameters (Smooth Pursuit Eye Movement, Prepulse Inhibition, and P50), and neuropsychological aspects.

Bertine Lahuis will receive her PhD from Utrecht University on June 24. The title of her dissertation is "Neurobiological parameters in Multiple Complex Developmental Disorder, a subtype of the Pervasive Developmental Disorder-Not Otherwise Specified." 24 June 2008

'Mitochondrial Disorders of Childhood: Testing, Potential Relationships to Autism Spectrum Disorders, and Triggers for Neurological Deterioration'

Adventures in Autism: Sharyl Attkisson Reports on the Governmnets "See No Evil" Behavior: "Workshop

Mitochondrial Disorders of Childhood: Testing, Potential Relationships to Autism Spectrum Disorders, and Triggers for Neurological Deterioration June 29, 2008

Workshop Goals and Objectives

'Mitochondrial Disorders of Childhood: Testing, Potential Relationships to Autism Spectrum Disorders, and Triggers for Neurological Deterioration' is a workshop to be held on Sunday June 29th after the close of the United Mitochondrial Disease Meeting in Indianapolis at the Hyatt Regency Indianapolis. The workshop will convene 11 experts in mitochondrial disorders or autism to discuss how the neurology of mitochondrial disorders might inform autism research.

The conference is sponsored by a number of Federal agencies including DHHS, CDC, FDA, NINDS and NIMH. Observers are welcome as seating allows.

Location

Hyatt Regency Indianapolis
Posted by Ginger Taylor, M.S. at Monday,"

Perhaps because of our vigorious response, Bill 10942 did not pass and is still in Committee.

Good News on New York's Bad, Bad Bill


New York State Assembly Bill 10942 is among the worst pro-vaccine bills yet. If passed it will make ALL vaccines recommended by the CDC's Advisory Committee on Immunization Practices (ACIP) MANDATORY for every child and health care worker in New York State. True, there is a religious exemption for students but not for health care workers or others. And the State can administer vaccines supposedly against sexually transmitted diseases to minors without parental notification or permission.
The ACIP never met a vaccine it did not like, including for example:
The Rotovirus vaccine which has been found to cause epilepsy, pneumonia and death in children but was approved by the FDA anyway
The HPV vaccine which acts against 4 HPV strains NOT associated with cervical cancer and which increases the chances of a vaccinated woman coming down with cervical cancer by as much as 400% (!) according to the FDA's own pre-approval documents (!)
The same mercury-containing flu vaccine which the CDC said did not confer protection on the majority of people receiving it while they also reccomended that children, adults and the elderly get this shot anyway (!)

Perhaps because of our vigorious response, Bill 10942 did not pass and is still in Committee. Click here (http://salsa.democracyinaction.org/o/568/t/1128/campaign.jsp?campaign_KEY=21833), whether you live in New York State or not, to tell New York Legislators and your own State and Congressional legislators, what a bad idea this bill is and how strongly you oppose compulsory vaccinaton.

Father's Advanced Age Feed Autism Risk

Father's advanced age feeds autism risk

Helen Pearson 25 February 2008 09:00:00 EST
Children of fathers aged 40 or older are nearly six times more
likely to have autism.
Are older fathers more likely to have children with autism? A series of epidemiological studies is giving credence to the idea, suggesting that, with age, sperm may accumulate damage that increases risk in the next generation.

Advancing age of the father is known to be a significant risk factor for schizophrenia1. These studies — along with anecdotal suggestions that fathers of autistic children tend to be older than average — prompted Avi Reichenberg of Mount Sinai School of Medicine, New York, to launch one of the first thorough epidemiological investigations into a link between the two.

Reichenberg and his colleagues had access to a vast database of health information collected from more than 132,000 Israeli adolescents who underwent draft board assessment, including psychiatric screening, before entering the army. The researchers were able to identify those who were diagnosed with autism spectrum disorders (ASD), along with the age of their parents.

Children of fathers in their 30s are about 1.6 times more likely to have ASD than children of fathers below age 30, the study found2. Compared with the youngest group, children of fathers aged 40 or older were nearly six times more likely to have ASD. “It was much stronger than we had thought,” Reichenberg says.

Since then, a handful of other epidemiology studies have backed the autism-paternal age connection. In one of these3, a team led by Lisa Croen of Kaiser Permanente Northern California Division of Research in Oakland, California, mined a health database of more than 130,000 births and found that each decade of paternal or maternal age increased risk of autism spectrum disorder by around 30%.

Paternal age “is still a relatively small contributor,” Croen says, “but when you see something that keeps coming up in different populations and study designs you start thinking there must be something to this.”

The link may be real, but researchers have yet to explain what causes it. Perhaps, says Croen, older parents are simply more attuned to the development of their children and therefore more likely to get a diagnosis. “It could be an artifact,” she says. “We don’t have enough data yet to really rule that out.”

Genetic origins
Another simple explanation is that fathers who themselves have autism or mild social deficits are likely to marry and have children at a later age than other men, and these children inherit factors putting them at high risk of developing the condition themselves.

But Reichenberg says that in his studies he has found no link between traits such as shyness, sensitivity and aloofness in parents and the age at which they have children. “It’s not definitive but the evidence is definitely against such an explanation,” he says.

Many researchers instead favor a genetic origin for the phenomenon. Male germ cells go through multiple rounds of division to manufacture sperm throughout a man’s life and, according to one idea, they may accumulate DNA damage as the molecule is copied again and again.

Sperm produced by older men are more likely to carry genetic defects, and these defects could boost their children’s risk of autism. Female germ cells divide far fewer times.

It is also possible that older sperm are more likely to acquire epigenetic defects: ones that do not change the DNA sequence itself, but that alter the activity of genes due to structural or chemical changes to DNA such as methylation.

These genetic changes arise in the egg or sperm rather than being inherited from the parents. Both concepts fit with the knowledge that the majority of ASD cases have a genetic cause, even though they are also the first in a family.

For precedent, geneticists point to a condition called achondroplasia, a common cause of dwarfism and the textbook example of a genetic condition associated with paternal age. The risk of sperm carrying a single point mutation in the gene for a growth factor receptor is thought to increase with the age of the father.

“It would be overwhelmingly logical,” for something similar to be going on in some cases of autism, says human geneticist Arthur Beaudet at Baylor College of Medicine in Houston, Texas. Perhaps just one or two of the many genes associated with the disorder are susceptible to detrimental point mutations as the germ cells age.

Beaudet says he would like to see genetic and epigenetic analyses of single sperm to see if mutation rates differ in the fathers of autistic children, and between younger and older men. “That would be the approach I’d be enthusiastic about,” he says. Reichenberg says that he is pursuing such studies.

Because there are few clearly defined genes for autism risk, it’s not yet clear where to look for these increased mutation rates. And genome-wide studies looking for differences in the rates of point mutations in many sperm are still too expensive and laborious.

Copy numbers
Last year, molecular studies showed that mutations called copy number variations (CNVs) — genomic chunks that can be deleted or duplicated from one person to the next — appear to be major contributors to sporadic autism.

A group led by Michael Wigler and Jonathan Sebat at the Cold Spring Harbor Laboratory in New York looked for CNVs that were present in autistic individuals, but not in their parents. They found CNVs in 10% of children with sporadic autism, 2% of those with familial autism and 1% of controls4.

This suggests that many more cases of sporadic autism may be attributable to spontaneous mutations — either CNVs or more subtle mutations — than had been realized.

Sebat has not examined whether the frequency of these CNV mutations increases in aging germ cells — but he suspects it might. “We don’t have data one way or the other,” he says, “but it’s a very tantalizing hypothesis.”

Many of the cellular systems that protect DNA from mutation might begin to fail in aging germ cells, so that their mutation rate increases, Sebat suggests. He is planning to test in a larger group of autistic individuals whether the CNV mutations are more common in children of older parents.

Reichenberg and his colleagues are also testing these hypotheses. In one study, they are trying to compare old and young fathers of autistic children, looking for differences in the rate of new mutations and their association to genetic hotspots previously linked to autism.

They are also doing mouse studies to explore whether offspring of older males tend to suffer more behavioral problems that mimic autism.

There remains some debate about whether the mother’s age is as important a risk factor as that of the father, and studies have differed in their findings. A maternal age effect is harder to tease out, partly because women have children within a more limited age range than men: very few over-40 women have children.

In her study, Croen found that maternal age is just as important and says that other studies have lacked the statistical power to tease this out. “Our data show that maternal age is also in the mix,” she says.

The fact that schizophrenia risk also increases with age leads some researchers to wonder whether some of the same genes may contribute to both disorders – and perhaps to other psychiatric conditions as well.

It’s a “feasible hypothesis”, Reichenberg says, “and I believe a worthwhile one to pursue.”

References:

--------------------------------------------------------------------------------

Malaspina D et al. Arch. Gen. Psychiatry 58, 361-367 (2001) PubMed ↩

Reichenberg A. et al. Arch. Gen. Psychiatry 63, 1026-1032 (2006) PubMed ↩

Croen L. et al. Arch. Pediatr. Adolesc. Med. 161, 334-340 (2007) PubMed ↩

Sebat J. et al. Science 316, 445-449 (2007) PubMed ↩
posted by ApoorvaMandavilli

There are those who know very well about Paternal Age and Autism, Most People Don't Know

This increase in risk with paternal age is no surprise to me, but it is a surprise to practically everyone else.

The increase risk for older mothers for Down syndrome is well-known.

As part of my work as a clinical geneticist, I see couples every week who come to ask about the risk of having babies because of the age of the mother.

We talk about this and often, as the male partner is also older, we talk about the risk of his age. Most of the partners are quite surprised and even taken aback with this news.

In today's society, delaying pregnancy until later is often done for career and other purposes but usually only the age of the mother is taken into account in planning when to start a family. Why is the increased risk in relation to a father's age not widely known?

CURE FOR AUTISM?

NO WAY?

PREVENT SOME NON-FAMILIAL AUTISM? YES YOU CAN.

Donor Standards

Our donors are recruited from the school campuses of
western Montana and eastern Washington. Most of our
donors are either currently involved with, or have finished
their higher education at the time of their participation in
our donor program. All donors are between 18 and 35
years of age in order to minimize genetic abnormalities.
All donors are frozen in very limited quantities, in order
to guarantee that the number of pregnancies created
from any one donor are limited. Although all donor
histories are reviewed to provide you with donors that
should give you a great chance of concieving a healthy
and normal baby, there is of course no way to
guarantee such an outcome. As all donor family histories
will present with their own unique positive and negative
attributes, we encourage all clients to review donor
information thoroughly prior to purchase and use of
specimens.

Our donor screening meets or exceeds the standards set
forth by the AATB, ASRM, and CFAS. (American
Association of Tissue Banks, American Society for
Reproductive Medicine, and the Canadian Fertility and Andrology Society)

The 59-year-old Fresno attorney says he appreciates a lot of things about being Colby's father.

Wider perspective on life Lawyer Jim Wagoner learns from his severely disabled son.By Diana Marcum / The Fresno Bee06/15/08 21:57:14



Jim Wagoner says he'll run in Fresno's Father's Day race until his legs fall off.

Every year he pushes his son Colby in a jogger. At 12 years old, Colby weighs 163 pounds. He can't speak because of severe mental retardation and autism, but he flaps his hands in joy and squeals when they run through the tunnels because he seems to like to hear his voice bounce back.

"I take great pride in being able to push my son in the race. I enjoy hearing him yell," says Wagoner.
The 59-year-old Fresno attorney says he appreciates a lot of things about being Colby's father.

"Colby taught me the outside of life," he says. "I work at a law firm where all the families are as close to perfect as they can be. The men and women are good-looking. The kids are going to Harvard. There's an inside groove -- the mainstream freeway. But when you step outside or circumstances put you outside that groove you have a much wider perspective on life.

"Colby gives me the joy of riding on the frontage road of life. Before Colby, I was mostly a freeway guy."

His wife and his friends describe Jim Wagoner as very competitive.

He says he disagrees with that assessment.

"If you're competitive with others, you're shooting too low," he says. "I'm just interested in doing my best."

But he does say that age and Colby have made him slow down and make sure he's "really enjoying the special moments."

When Wendy Wagoner was pregnant with Colby there was no sign of trouble. It wasn't until Colby was 9 months old and not developing as he should that doctors discovered a genetic defect.

Wendy, 45, also an attorney, quit work and stayed home, with the main goal of getting Colby out of diapers. They're still working on that.

When Colby was 6 years old, Jim told Wendy they should have another child.

"I was terrified. I didn't think it was a good idea," she says.

But Jim Wagoner was convinced she should have the experience of raising a healthy child as well as Colby.

"I knew it was going to be OK. We'd talked it over," he says, pointing upward to indicate he is a praying man.

Wendy says his argument for another child was the best closing argument he ever gave.

"She was third in her class in law school. My wife is very, very smart. I knew I had to do well," he says.

Jim Wagoner has nicknamed 6-year-old daughter Nicole -- a healthy, chatty child -- "Breezy." He says some of his best moments are seeing "Wendy and Breezy head off to do girl stuff" while he stays with Colby.

Wendy's home all day with Colby and Jim knows she needs breaks. Colby can be difficult -- he sometimes hits and scratches. But he also hugs and smiles and gives what the Wagoners call "hippo kisses," big open-mouthed smacks of affection. Colby sleeps best when he's curled up against one of them. Jim Wagoner says he doesn't think Wendy ever gets more than three hours of sleep at a time. He says she is his inspiration.

On Sunday morning in downtown Fresno the whole Wagoner family runs the Father's Day race. Jim Wagoner's older, strapping sons from a previous marriage, Daniel, 24, and Joey, 20, are the first of the family at the finish line.

Wendy Wagoner, pushing Nicole in a stroller, comes in later and stands waiting to watch Jim and Colby cross the finish line.

"Here comes Daddy and Colby," she says to Nicole when she spots them.

"He's amazing, just amazing," she says quietly -- seemingly to herself-- as Jim and Colby finish 61 minutes after they began the 6-mile run.

"I can barely walk and push him in that thing and Jim runs the whole six miles every year just because Colby enjoys it," she says. She's teary-eyed.

Wendy Wagoner worries about how long the Father's Day race tradition can be maintained with Jim getting older and Colby getting bigger.

But Jim, his skin showing only a slight sheen of sweat, says it's not that much of a feat.

"It's not that hard," he says. "Just lean forward, don't stop and don't let the family down."
The reporter can be reached at dmarcum@fresnobee.com or (559) 441-6375.

Autism Speaks Rakes in the Money But Never Warns About the Known Risk Factor of Advancing Paternal Age

Attention News Editors:

Dr. Lonnie Zwaigenbaum keynote speaker at Autism Speaks event this Sunday
Local MP, Mike Lake and family to join families, service providers and
other community supporters at Walk Now for Autism Kick-Off Lunch.

EDMONTON, June 20 /CNW/ - On Sunday June 22, Dr. Lonnie Zwaigenbaum,
Associate Professor, Department of Pediatrics (University of Alberta) and
Co-Director of the Autism Research Centre at Glenrose Rehabilitation Hospital
will be the keynote speaker at a free luncheon hosted by Autism Speaks Canada.
Dr. Zwaigenbaum will address families, friends, service providers,
educators and others interested in learning more about current trends in
autism research with emphasis on the exciting discoveries of the global High
Risk Baby Siblings Research Consortium, of which he is a key member. "Lonnie
has an outstanding reputation for his ability to translate science into plain
language and we are so excited that the autism community will have the
opportunity to hear his dynamic and informative presentation," notes Suzanne
Lanthier, Executive Director of Autism Speaks Canada.
Mike and Debi Lake will be in attendance along with their children, Jenae
(age 9) and Jaden (age 12). Jaden is affected by autism. Mr. Lake, who was
instrumental in having the first UN declared World Autism Awareness Day -
April 2, 2008 - recognized in the House of Commons will be joined by Jaden to
talk about his experiences as a parent of a child on the autism spectrum.
Also speaking will be Krista Hauffe, Miss Teen Edmonton International
2008, who has a personal connection to autism. Representatives from community
partner agencies, Children's Autism Services of Edmonton and the Autism
Society of Edmonton and Area will be joining the luncheon, expected to draw
over 120 people.
The luncheon is the official kick-off event for Autism Speaks' Inaugural
Edmonton Capital Region Walk Now for Autism being held on September 7 at
Lion's Park/St. Albert Place in St. Albert. The luncheon is being held at the
Fantasyland Hotel from 11:30 - 1:30 PM. The event is free and lunch will be
provided but pre-registration is required by calling 1-888-362-6227.
Autism affects one in every 150 children. One in 94 boys will be
affected. More children will be diagnosed with autism this year than diabetes,
cancer, and AIDS combined.

Autism Speaks' Walk Now for Autism, North America's largest grassroots
autism walk program, is our signature fundraising and awareness event, taking
place in communities across the Canada, the United States and the United
Kingdom. Powered by volunteers and families with loved ones on the autism
spectrum, this successful grassroots fundraising effort not only generates
vital funds for autism research but also raises awareness about the increasing
prevalence of autism and the need for increased research funding to combat
this complex disorder.
Autism Speaks is dedicated to increasing awareness of autism spectrum
disorders; funding research into the causes, prevention and treatments and
advocates for the needs of individuals with autism. To learn more about Autism
Speaks, please visit www.autismspeaks.org. Since 1998 close to $6 million has
been granted to the Canadian autism research community by Autism Speaks.




For further information: Suzanne Lanthier, Executive Director, Autism
Speaks, Cell: (416) 388-3139 or email: slanthier@autismspeaks.org




AUTISM SPEAKS CANADA - More on this organization

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American Academy of Pediatrics Decides That Insulting Parents Will Increase Vaccination Rates

Adventures in Autism: AAP Decides that Insulting Parents Will Increase Vaccination Rates

From Dr. Aubrey Blumsohn's Blog, 'Scientific Misconduct'

Scientific Misconduct Blog: How a new paradigm is created#links

As men age they do not lose their capacity to generate spermatozoa; however, the quality of these gametes deteriorates. This change can be visualized

What Has Happened With This Bill?

Parents protest NY’s vaccination requirements
June 10 Westchester and Rockland county residents were among dozens of people who rallied in Albany today to protest childhood vaccinations. The activists held signs that said things like “Parents call the shots,” and chanted, “My kids, my choice.”

The families are against legislation that would increase the number of immunizations children have to get. Under the bill, seventh graders and students preparing to enter college would have to get meningitis vaccines, minors could get vaccinated for sexually transmitted infections without parental consent, and future requirements for vaccines would be tied to national standards.

Lisa Rudley of Briarcliff Manor said two of her children have suffered health problems because of vaccines. One has recovered and another is one the way to recovering, she said.

Dr. Lynn Friedman, a chiropractor, said she unsuccessfully sued the Clarkstown School District to allow her son, now 12, to attend school without vaccinations. The state grants exceptions to the mandatory vaccine requirements for medical and religious reasons. Friedman said the district questioned the validity of her religious exemption. Her son goes to private school.

Elisa DiBari of North Salem said her son, now 10, stopped speaking after receiving the measles/mumps/rubella vaccine at 15 months. He has had a lot of treatments over the years but is doing well.

“He’s a very positive kid. Nothing stopped him,” she said, holding a sign with blown-up photo of him.

The families favor separate proposals that would allow families to opt out of the mandated vaccine program for philosphical reasons, and protections for parents who decline to have their children immunized for religious reasons.

From AGE OF AUTISM

BELIEVE | Main

June 17, 2008
SICK HAMSTERS: MORE EVIDENCE THAT THIMEROSAL HARMS INFANTS
By Mark F. Blaxill

In his best-selling book Evidence of Harm, our Age of Autism colleague David Kirby saved his “final note” for a comment on the global legacy of thimerosal exposure in vaccines. In the book’s closing passage, he wrote:

“If thimerosal is one day proven to be a contributing factor to autism, and if U.S. made vaccines containing the preservative are now being supplied the world over, the scope of this potential tragedy becomes unthinkable.

“The United States, at the dawn of the twenty-first century, is not exactly the most beloved nation on earth. What if the profitable export of our vaunted medical technology has led to the poisoning of hundred of thousands of children? What then?”

As Bush Administration officials have moved with surprising determination to defend the safety both of the current flu vaccine program (which targets expectant mothers with injections of ethyl mercury) and past vaccine program recommendations (which permitted the injection of unintentionally excessive amounts of ethyl mercury in infants), one often overlooked implication of the Administration’s policy has been to make Kirby’s nightmare suggestion a reality. U.S. vaccine manufacturers have continued to ship thimerosal containing vaccine formulations all over the world, in effect offering a defiant double standard of mercury risk for infants from rich countries as compared to poor countries.

One of the countries where thimerosal has been retained in vaccines is Peru. This situation is a consequence of a controversial decision by the World Health Organization (WHO) and its Latin American partner the Pan American Health Organization (PAHO) to retain thimerosal as a vaccine preservative because of economic considerations. PAHO buys most of its vaccines from the same vaccine manufacturers who sold thimerosal-containing vaccines (TCVs) in the United State. And like the US in the early 1990s, PAHO countries like Peru have recently adopted the Hib and hepatitis B vaccines as part of their recommended childhood immunization programs. Peru also continues to use the thimerosal-containing whole cell DPT vaccine, instead of the safer but more expensive acellular pertussis variety.

The result of these PAHO decisions is that Peruvian children are now exposed to thimerosal in amounts that would be considered in excess of EPA guideline in the U.S. Not surprisingly, some Peruvian scientists have taken issue with this choice and took it upon themselves to investigate the issue. In their words:

“In Peru, the authorities of the Ministry of Health (MINSA) continue using vaccines with high thimerosal content (whose multidose…form is, to date used in some health establishments), noting that it has no side effects. This generated a serious challenge by the public, part of the medical community and a number of non-governmental organizations. This debate requires that begin (sic) to shed light on the investigations and take concrete steps on this issue.”

So these Peruvian researchers published a study, published in the September 2007 edition of the Peruvian medical journal Anales de la Facultad de Medicina but only recently translated into English (for the on-line version of the September 2007 edition, see HERE) in which they examined the effect of thimerosal exposure on infant hamsters. They exposed 45 baby hamsters to three different series of injections, two of which involved no thimerosal exposure and a third that was designed to mimic the weight-adjusted ethyl mercury content of the U.S. childhood immunization program in the 1990s.

The findings were stark. As the three groups of infants matured, the thimerosal-exposed hamsters showed clear signs of developmental injury due to their ethyl mercury exposure, a weight adjusted concentration that added up to less a total dose of less than 1 microgram (an amount many times less than the 187.5 micrograms human infants received). The mercury exposed hamsters showed dramatic developmental differences in terms of body weight, brain weight and heights, with a statistical certainty that there was a toxic effect that exceeded 99.99%.

When the 45 hamsters were sacrificed, the researchers compared the brain tissue of the three groups and again found dramatic differences in the thimerosal-exposed infant hamster brains. Ethyl mercury produced clear injuries in the three types of brain tissue: hippocampus, cerebellum and cerebral cortex. Furthermore, the exposed hamsters showed clear evidence of many different kinds of tissue damage, such as reduced neuron density, increased cell death, impaired myelin development and increased inflammation. These results were also significant with a certainty of greater than 99.99%.

The Peruvian team didn’t mince words. Taking pains to translate their full paper into English (the journal typically publishes English language abstracts, but provides full text only in Spanish), they summarized their findings in unambiguous terms.

“In conclusion, thimerosal exposure, in quantities equivalent to those of human vaccines, reduced the body weight, encephalon weight and height of postnatal hamsters in a significant way; in this way, it produced a lesser development and growth delay. Also, it produced severe neurotoxic effects at encephalon level expressing histopathological alterations at hippocampus, cerebral cortex and cerebellum levels.”

This hamster model doesn’t simply stand alone. Instead it joins a succession of animal studies all of which demonstrate that exposing infant animals to thimerosal produces developmental brain injury. Mady Hornig’s work in mice provided the template for the Peruvian group and their hamster findings provide confirmation for Hornig’s finding of thimerosal toxicity in mice. In her recent presentation at the International Meeting for Autism Research (IMFAR), Laura Hewitson (see the Age of Autism article HERE ) reported on a primate model that showed clear evidence of developmental injury in rhesus macaque monkeys after exposure to thimerosal and a range of vaccine antigens.

We can’t take human infants and cut up their brains. That’s why scientists use animal models to evaluate the effect of potentially dangerous medical treatments and toxic chemicals. In a consistent set of these models, a wide range of researchers from different labs all over the world, researchers are finding that thimerosal causes injury in infant animals. Despite this dramatic and repeated body of evidence, public health authorities—the CDC, the WHO, the PAHO—persist in exposing the developing human brain to ethyl mercury, one of the most toxic chemicals man has ever invented. These officials consider the interests of their programs—the economics of distribution of vaccines in Peru, the yield of flu vaccine production in the U.S. and the continued targeting of pregnant women and infants for flu shots—to carry greater weight than any countervailing evidence. But by now, the evidence is so indisputable that the question has become a question of moral rather than scientific choices. Why do these officials persist in continuing policies and products that harm children?

The Peruvian researchers are clearly calling their PAHO colleagues to account for their decisions. In the final paragraph of their paper the authors write, in somewhat halting English translation:

“While it is true, it is very difficult to extrapolate these findings to other animal experimentation groups and over human beings, our results, as the multiple scientific evidence recently published about thimerosal, clearly indicates the toxic nature of this substance at the same dose and the same chronology as human immunizations; therefore we suggest the employment of alternative preservatives in vaccines, especially those intended to pregnant women, neonates and small children based in the prevention and precaution principles of all medical interventions.”

Sick mice. Sick hamsters. Sick monkeys. Sick children. The evidence is clear and the policies are devastating a generation of children on a global basis. When will this madness stop?

Mark Blaxill is Editor-at-Large for Age of Autism

As men age the DNA of their sperm gets damaged and this can cause disease in their children later in life

As men age the DNA of their sperm gets damaged and this can cause disease in their children later in life

Calling All Vaccine-Autism Critics by David Kirby

Calling All Vaccine-Autism Critics
stumble digg reddit del.ico.us news trust buzz up
Posted June 15, 2008 06:46 PM (EST)


In the next two weeks, I will give three public lectures and Q&A sessions, free and open to the public, at Brown University in Providence, NYU Law School in Manhattan, and Northeastern University in Boston. (Other events are to be announced soon for New Jersey, Long Island and Southern California).
I sincerely encourage any and all vaccine-autism skeptics, critics, agnostics and cynics living in the northeastern US to please consider attending one of these talks, armed with all of your most pointed, difficult and critical questions.
For my part, I will present slides showing evidence to support and refute the link between autism, vaccines, mercury & heavy metals, air pollution and other environmental factors.
My only arguments will be that the evidence is NOT conclusive against a link, and it is premature to declare that vaccines and their ingredients have been 100% exonerated as environmental contributors to autism.
I hope to have a reasoned and enlightening public discussion with members of the audience. Among the subjects we will tackle are:
1) The Poling Case - in which the government conceded that vaccines induced autism in one little girl, and updates on other court cases.
2) Brand New Evidence - of a link between mitochondrial dysfunction and autistic regression, and evidence of mitochondrial issues in many ASD kids.
3) Research Underway - at top universities on the connection between environmental toxins, oxidative stress, glutathione depletion, neuro-inflammation and autistic encephalopathy.
4) Declarations - By the US Presidential candidates and the former NIH director that autism is epidemic and calling for more research into vaccines and mercury as possible causes.
5) Recent Studies - Linking autism spectrum disorder with heavy metals and contaminants in air pollution.
Here are the times and locations:
PROVIDENCE: Thursday, June 19 - 6:30-9:00PM Brown University, Salomon Center, Room 101On the Campus Green Hosted By Wendy Fournier, President of the National Autism Association
NEW YORK CITY: Thursday, June 26 - 6:30-9:00PMNYU School of Law, 40 Washington Square SouthVanderbilt Hall, Room 204Hosted By Mary Holland, NYU Law SchoolNOTE: RSVP REQUIRED: kirbylecture@gmail.com
BOSTON: Friday, June 27 - 6:30-9:00PMNortheastern UniversityBehrakis Health Science Building (Bldg #26) - Room 10Hosted by Dr. Richard Deth, Northeastern University Professor of Pharmacology
This series was made possible by Generation Rescue, Autism Research Institute, National Autism Association, Coalition for SAFE MINDS, and Talk About Curing Autism. Announcements for each event can be downloaded at www.evidenceofharm.com - please feel free to circulate these electronically and otherwise to all interested parties.
ALL EVENTS ARE FREE AND OPEN TO THE PUBLIC

Whichever way you look at it, aging and reproduction are incompatible bedfellows.

May 2008, Vol. 3, No. 3, Pages 267-271
(doi:10.1586/17474108.3.3.267)



Just how safe is assisted reproductive technology for treating male factor infertility?
R John Aitken


As men age they do not lose their capacity to generate spermatozoa; however, the quality of these gametes deteriorates. This change can be visualized as an age-dependent increase in DNA fragmentation in spermatozoa [13,14]. Paternal age is also widely recognized as a key factor in the etiology of dominant genetic diseases, such as Apert syndrome or achondroplasia [15]. Furthermore, genetic damage to the spermatozoa of aging males is thought to contribute to the etiology of more complex polygenic conditions such as autism, spontaneous schizophrenia and epilepsy [8]. Since older men tend to be married to older women it is significant that as oocytes age in the ovary, they suffer the depletion of several key genes involved in protection against oxidative stress and the maintenance of DNA integrity, including genes with a probable role in DNA repair [16]. Thus, age-related changes to the integrity of DNA in the spermatozoa are compounded by age-related declines in the oocytes’ capacity for DNA stabilization and repair. In combination, these factors could well make a significant contribution to the elevated incidence of birth defects associated with assisted conception therapy. Whichever way you look at it, aging and reproduction are incompatible bedfellows.

dependent on reproductive technologies, an Australian reproductive biologist says we must remain vigilant to avoid the spread of

genetic defects.

Expert calls for vigilance on IVF technology
By Anna Salleh for ABC Science Online
Posted 4 hours 30 minutes ago


As humans become more dependent on reproductive technologies, an Australian reproductive biologist says we must remain vigilant to avoid the spread of genetic defects.

The warning comes in an editorial by Professor John Aitken, of the University of Newcastle, in the current issue of Expert Review of Obstetrics and Gynecology.

"People shouldn't be too confident that just because the baby looks normal there is no damage there that won't appear later in life," he said.

"People underestimate how much genetic damage they're passing onto the embryos."
Professor Aitkin says one in every 35 babies born in Australia are a result of IVF.

"In some countries it's more like one in 20 and there are models that predict it will be one in 10 before too long," he said.

Professor Aitken says because IVF allows infertile men to reproduce, the more we use it the more it will be needed in the future.

"So we better make sure it's safe because a large proportion of the population will be generated in this way," he said.


Ageing sperm

Professor Aitken says a number of factors are known, or suspected, to cause genetic damage to sperm that do not necessarily cause defects obvious at birth.

For example, Professor Aitken says the sperm of ageing males is thought to contribute to conditions such as autism, schizophrenia and epilepsy.

He says there is strong evidence linking sperm DNA damage to smoking, which can lead to the development of childhood cancers.

Epigenetic changes to sperm DNA that can affect fertility through several generations have also been reported.

For example, several recent papers have shown that infertile men have a dramatically altered DNA methylation profile.Screening and monitoring

Professor Aitken says genetic problems mean it is important that reproductive clinics do a good job at screening sperm samples for genetic damage.

He is presenting the latest evidence on one screening technique he is developing with biotech company nuGEN at the Australian Research Council's Graeme Clark Research Outcomes Forum in Canberra next week.

But Professor Aitken says long-term monitoring of children born through IVF and other reproductive technologies is also essential, because such techniques can not pick up epigenetic damage.

"There are all kinds of things that can and could still go wrong," he said.

While he says IVF children are being monitored, he is concerned about complacency among clinics who celebrate their ability to produce normal looking babies from sperm with high levels of DNA damage.

IVF defended

Professor Michael Chapman of the Fertility Society of Australia, who also works for IVF Australia, says genetic damage is considered by IVF clinics.

"They're concerns that are shared within the IVF profession," he said.

Professor Chapman says one rare epigenetic disease has shown up in IVF children, at a rate of one in 1,500 versus one in 5,000 in the general population.

But he says Professor Aitken's "provocative" article overstates the problem since in the 20 years that IVF has been around, few long-term problems have arisen, despite thousands of children being monitored.

"I'm sure that if something starts to turn up, it will jump out at us," he said.

Sandra Hill, chief executive officer of ACCESS Australia, a group led by patients seeking IVF treatment, is confident that IVF is well-monitored, and she agrees this should continue.

But she says many of the concerns raised by Professor Aitken also apply to natural conception and she thinks the use of IVF should not be singled out.

She says it could be useful to educate men in general about the concerns raised by Professor Aitken - especially the need for men to have children before they get too old.

Professor Aitken says this may be so, but IVF still presents a unique challenge.

"With IVF you are facilitating the fertilisation of eggs with sperm that would otherwise be unsuccessful," he said.

Professor Aitken also says the rate of birth defects in IVF children are up to twice that of normally-conceived children, although he expects that to improve as techniques improve.

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Professor R. John Aitken ScD, FRSE
Director, ARC Centre of Excellence in Biotechnology and Development,
Professor of Biological Sciences,
School of Environmental and Life Sciences,
University of Newcastle
Callaghan
NSW 2308.

E mail: jaitken@mail.newcastle.edu.au
Tel: (+61 2) 4921 6143
Mobile: 0414 667 878
Fax: (+61 2) 4921 6308



John Aitken is currently Director of ARC Centre of Excellence in Biotechnology and Development and Professor of Biological Sciences at the University of Newcastle, NSW. His research interests focus on the cell biology of male germ cells, particularly the cell biology of human spermatozoa and the mechanisms regulating the formation and recruitment of primordial follicles within the ovary.





Qualifications: BSc (Special Hons) University of London

MSc University of Wales

PhD University of Cambridge

ScD University of Cambridge

Fellow of the Royal Society of Edinburgh



Positions:

1982-1987 Senior Scientist, Medical Research Council Reproductive Biology Unit, University of Edinburgh.

1987-1998 Special Appointment, Professorial Grade, Medical Research Council Reproductive Biology Unit, University of Edinburgh

1992- Honorary Professorship, Department of Obstetrics and Gynaecology, University of Edinburgh

1998- Professor of Biological Sciences, Faculty of Science and IT, University of Newcastle, NSW.

1998 Director of the Centre for Life Sciences, University of Newcastle, NSW.

2003 Director of the ARC Centre of Excellence in Biotechnology and Development


Honours:

1984 Honorary Fellow of the Faculty of Medicine,University of Edinburgh.

1985 Ayerst Lecturer, Pacific Coast Fertility Society,Caesar's Palace, Las Vegas.

1985 Ortho-McMaster Lecturer, McMaster University Medical Centre, Hamilton, Canada.

1985 Convener, Chairman and Editor, WHO symposium on The Zona-free Hamster Oocyte Penetration test in the Diagnosis of Male Infertility, Boston, Massachusetts, USA.

1986 The Walpole Prize, Society for the Study of Fertility, United Kingdom

1987 The Walpole Prize, Society for the Study of Fertility, United Kingdom

1989 1989 University of Catania Prize, Scientific Committee, Faculty of Medicine.

University of Catania, Italy.

1990 The Puvan Memorial Lecture. Opening Address of the 27th Malaysian Congress of Obstetrics and Gynaecology.

1990 The Jennifer Hallum Memorial Lecture. Royal College of Obstetricians and Gynaecologists,

1992 Honorary Professorship, Department of Obstetrics and Gynaecology, Faculty of Medicine, University of Edinburgh.

1994 Opening Address Thaddeus Mann Symposium. Seventh International Congress of Spermatology, Cairns, Australia.

1994 American Fertility Society State-of-the-Art Lecture. Annual Meeting, San Antonio, Texas,

1995 Elected a Fellow of the Royal Society of Edinburgh

1997 Plenary Lecture European Society of Human Reproduction and Embryology Congress 1997. Edinburgh Conference Centre.

1997 The Bruce Stewart Memorial Lecture 1997 American Urology Society Lecture, American Society for Reproductive Medicine, Cincinnati, OH, USA.

1998 The 1998 Amoroso Lecture. The human spermatozoon-a cell in crisis? Society for the Study of Fertility, Annual Meeting, University of Glasgow, UK

1998 Society for Male Reproduction/Urology Prize Paper. 16th World Congress on Fertility and Sterility/54th Annual Meeting of the American Society for Reproductive Medicine, San Francisco

1999 M.J. Edwards Lecture. Australian Birth Defects Society. University of Sydney.

2000 Best Poster Award. Combined meeting of the Society for Free Radical Research on Oxidants, Antioxidants and Nutrition and ComBio 2000. Wellington, New Zealand.

2002 Plenary Lecture, World Congress on Human Reproduction, Montreal, Canada

2003 Lloyd Cox memorial Lecture, University of Adelaide.

2004 The Founders Lecture, Society for the Study of Reproduction, Annual Meeting, Sydney.





Relevant Employment History:

1987-98 Special Appointment -Professorial Level

MRC Reproductive Biology Unit, University of Edinburgh,



1992-present Honorary Professorship, Faculty of Medicine, University of Edinburgh.



1982-1987 Senior Scientist

MRC Reproductive Biology Unit, University of Edinburgh.



1977-1982 Research Scientist Grade 1

MRC Reproductive Biology Unit, University of Edinburgh.



1976-1977 Chargé de Recherche

Faculte de Medicine, Universitie de Bordeaux.



1975-1976 Consultant Scientist

Human Reproduction Programme, World Health Organisation, Geneva.



1973-1975 MRC Post-Doctoral Fellowship

Department of Genetics, University of Edinburgh.



Publications and Presentations:
More than 350 peer review publications and more than 300 presentations at national and international meetings. Examples:



Angell, R.R., Aitken, R.J., Van Look, P.F.A., Lumsden, M.A. & Templeton, A.A. (1983) Chromosome abnormalities in human embryos after in vitro fertilization. Nature, 303, 336-338.



Aitken, R.J. & Clarkson, J.S. (1987) Cellular basis of defective sperm function and its association with the genesis of reactive oxygen species by human spermatozoa. Journal of Reproduction and Fertility, 83, 459-469.

This article was awarded the Walpole Memorial Prize and Lecture by the Society for the Study of Fertility



Henderson, C.J., Hulme, M.J. & Aitken, R.J. (1988) Contraceptive potential of antibodies to the zona pellucida. Journal of Reproduction and Fertility, 8, 325-343.

This article was awarded the Walpole Memorial Prize and Lecture by the Society for the Study of Fertility



Nasr-Esfahani, M, Aitken, R.J. & Johnson, M.H. (1990) The measurement of H2O2 levels in preimplantation embryos from blocking and non-blocking strains of mice. Development, 109, 501-507.



Aitken, R. J., M. Paterson, H. Fisher, D.W. Buckingham & Van Duin, M. (1995) Redox regulation of tyrosine phosphorylation in human spermatozoa is involved in the control of human sperm function. Journal of Cell Science, 108, 2017-2025.





Aitken, R. J., Buckingham, D.W. & Irvine, D.S. (1996) The extragenomic action of progesterone on human spermatozoa: evidence for a ubiquitous response that is rapidly down-regulated. Endocrinology 137, 3999-4009.



Twigg, J., Fulton, N., Gomez, E, Irvine D. S. & Aitken, R. J. (1998) Analysis of the impact of intracellular reactive oxygen species generation on the structural and functional integrity of human spermatozoa: lipid peroxidation, DNA fragmentation and effectiveness of antioxidants. Human Reproduction 13, 1429-1437. Featured as an ‘Outstanding Article’ by the journal



Aitken, R. J., Harkiss, D., Knox, W., Paterson, M. and Irvine, D. S. (1998) A novel signal transduction cascade in capacitating human spermatozoa characterized by a redox-regulated, cAMP-mediated induction of tyrosine phosphorylation. Journal of Cell Science 111, 645-656.



Aitken, R. J. (1999) The human spermatozoon: a cell in crisis? The Amoroso Lecture. Journal of Reproduction and Fertility 115, 1-7.



Aitken, R.J. & Marshall Graves, J. A. (2002) The Y chromosome, oxidative stress and the future of sex. Nature 415, 963.



Ecroyd, H., Asquith, K., Jones, R.C. & Aitken R.J. (2004) The development of signal transduction pathways during epididymal maturation is calcium dependent. Developmental Biology 268, 53-63.



Baker, M.A., Hetherington, L., Ecroyd, H. & Aitken, R.J. (2004) Analysis of the mechanism by which calcium negatively regulates the tyrosine phosphorylation cascade associated with sperm capacitation. Journal of Cell Science 117, 211-222.



Asquith, K. L., Baleato, R. M. McLaughlin, E. A., Nixon B. & Aitken R.J. (2004) Analysis of the mechanisms by which tyrosine phosphorylation regulates sperm-zona recognition in the mouse, a chaperone-mediated event? Journal of Cell Science 117, 3645-3657.



Aitken, R.J., Koopman, P. & Lewis S. E. (2004). Seeds of concern. Nature. 432, 48-52.

Mandatory Forced Vaccination for NY: The Worst Vaccine Law Yet

June 9, 2008
Mandatory Forced Vaccination for NY: The Worst Vaccine Law Yet

If you are with in driving distance, please attend. This CANNOT be allowed to pass.

From NAA:

Parents Rally in Albany Against Forced Vaccination
Forwarded from our friends at NVIC www.nvic.org

Parents will rally in Albany, NY on Tuesday, June 10, to protest a vaccine bill (AB10942) that would mandate the 69 doses of 16 vaccines the Centers for Disease Control (CDC) recommends for all children through age 18 plus would automatically mandate all new vaccines federal officials recommend in the future. Sponsored by the NY House Rules Committee at the request of NY State Health Commissioner Richard Daines, provisions in the legislation would force all children to get annual influenza shots as well as force child use of vaccines for sexually transmitted diseases, such as hepatitis B and HPV, without obtaining permission from parents.

The legislation would make unelected physicians, who are appointed to the federal Advisory Committee on Immunization Practices (ACIP) by unelected CDC officials, de facto state lawmakers because CDC recommendations for new vaccine use by all children would be automatically turned into state mandates. Duly elected New York state legislators would no longer be accountable to the people who elected them and could look the other way when federal officials recommend every new vaccine produced by industry for "universal use" by every child born in America.

If New York and other states had already passed this kind of legislation before the poorly tested and highly reactive GARDASIL vaccine was recommended by the CDC in 2006 for universal use by all 11 year old girls, Merck would not have had to spend money mounting a national advertising and lobbying campaign in a failed attempt in 2007 to ram GARDASIL vaccine mandates through state legislatures. (Public health laws, including vaccine laws, are enacted by the states and not by the federal government).

Every new vaccine that industry has created and marketed for children in the last quarter century has been recommended by the CDC for universal use by all children, tripling the numbers of doses of vaccines pediatricians give children. During this same time period, the numbers of children suffering with chronic disease and disability has also tripled with no explanation coming from U.S. public health officials about why so many highly vaccinated children are so sick.

In what appears to be a classic act of collective political cowardice, NY Assembly Bill 10942 would force nearly six dozen doses of vaccines on children and many more in the future but there are no publicly named individual sponsors attached to the bill. The only sponsor listed is the "Rules Committee" headed by Assembly Speaker Sheldon Silver (D-Manhattan) . There is a lot of speculation about how much influence Merck and other vaccine manufacturers, as well as medical organizations and government officials pushing the forced vaccination political agenda, are bringing to bear on legislators behind the scenes.

Parents in New York claim that Assembly Speaker Silver is blocking passage of
AB 5468 for philosophical belief exemption to vaccination in the Assembly (there is a companion bill, SB 3031, in the state Senate). Current NY law only allows parents to file a medical or religious exemption to vaccination and both of these exemptions have become increasingly difficult to obtain in New York. Many parents are reporting that their religious exemptions are being denied or revoked after they have been grilled for hours by state attorneys and school officials about their spiritual beliefs. Some doctors practicing in New York are also reporting that they cannot write medical exemptions without being harassed by state health officials.

Parents protesting attempts by the pharmaceutical industry and government to force nearly six dozen vaccines on children or deny them an education, which limits their ability to hold a job and function in society, are also supporting Assembly Bill 3064 (also SB 1563) for religious exemption to vaccination that would prevent state officials from grilling parents about their religious beliefs for the purpose of denying a religious exemption to vaccination. This bill states that "this legislation is intended to protect parents from inappropriate and intrusive inquiry into their beliefs by government authorities" and already has numerous sponsors.

Parents are also supporting Assembly Bill 3180 (also SB 1575) for medical exemptions to vaccination to allow licensed physicians and certified nurse practitioners to write medical exemptions for children if they believe that "such immunization or immunizations may be detrimental to the person's health or is otherwise medically contraindicated for health reasons" without being subject to override by state health officials seeking to deny medical exemptions. This bill also already has numerous sponsors.

New York citizens, who want to attend the 11:30 a.m. June 10 rally and press conference on the steps of the Capitol Building (Swan St. side) in Albany, can get more information about bus transportation from Long Island, Rochester and suburban Albany as well as other details about the event at www.mykidsmychoice.com. After the rally, parents plan to meet with legislators and then attend a Health Committee meeting at 1 p.m. in the Legislative Office Building (Room 823).

For more information on contacting New York state legislators, go to
http://assembly.state.ny.us/. New York voters can type in their zip code and find contact information for their own Assemblyperson and Senator and voice their opinion. To find out more about contacting NY legislators on this issue, go to the website of A-Champ.

Rita Palma, a Bayport mother of three, said "Vaccines are under more scrutiny than ever. Yet some lawmakers pick right now to create a bill that actually increases vaccine mandates. This bill is a slap in the face to worried parents throughout New York. AB 10942 is being pushed by Big Pharma lobbyists. We need to show them that New Yorkers will not stand for this and make our voices heard."

Congratulations to the parents and those principled lawmakers in New York, who are standing up and being counted in support of legislation protecting the human right to informed consent to vaccination. Every American should have the right to hold sincere religious and conscientious belief convictions about whether or not to subject themselves or their children to harm from a pharmaceutical product, such as a vaccine, that carries an uncertain risk of injury or death.

Doctors are not infallible and the products drug companies create for profit are not always safe or effective for everyone. And no child in America should be subjected to vaccination or any other medical procedure without the informed consent of his or her parents. New York AB 10942 backed by Big Pharma and Big Government is a prescription for tyranny.

Stand Up! Be Counted. Your health and your freedom is on the line.

Posted by Ginger Taylor, M.S. at Monday, June 09, 2008 3 comments Links to this post

Labels: NAA, New York, Vaccine Injury

THE BEST ARTICLE ON AUTISM ETC PREVENTION FROM CLINICAL GENTICIST LES SHEFFIELD

Genetic clock ticks for men Les Sheffield

June 12, 2008 12:00am
MOST men would have been surprised to read that overseas researchers had found the death rate of young adults was higher if they had been born to older fathers.

This is no surprise to me. It has been scientifically established that genetic changes occur more often in the sperm of older fathers than younger fathers.

As men age there is a higher chance of changes in the genes in the sperm.

These changes can cause genetic conditions in their offspring, such as birth defects, autism and schizophrenia.

Their partners can also have an increased risk of miscarriages.

The presumed reason for the increase occurrence of all of these conditions is that they are all due to a new genetic change in the sperm of the older father.

Genetic changes are occurring all the time. Sometimes they have a beneficial effect, such as making the individual stronger, taller or smarter.

This is part of the concept of "survival of the fittest".

Sometimes, when the gene change is in a non-coding part of the genome, they have no effect. At other times, they can be harmful.

The problem is that these harmful effects are extremely varied because they can affect any one of the 20,000 or so human genes.

For example, they often change the structure of the body. One example is dwarfism, where the arms and legs are short due to a genetic change. The commonest type of dwarfism is achondroplasia.

An individual with this condition will have a 50 per cent risk of having an affected child themselves.

Indeed, about 20 per cent of the parents of achondroplastic babies have one of the parents with this condition, but the remaining 80 per cent do not.

If you look at the parents of babies with achondroplasia, who do not have the condition themselves, you find their average age is older than other people having babies in the population.

Significantly, statistics show it is the father's age which is important and not the mother's.

Achondroplasia is rare and it is only one of the many genes that can go wrong. Collectively, any of the 20,000 genes can change and this causes an increase in risk from about the age of 40.

The risk in men for any single gene change is one in 200 at age of 40, 20 at age 50 and rises steeply after that.

This increase in risk with paternal age is no surprise to me, but it is a surprise to practically everyone else.

The increase risk for older mothers for Down syndrome is well-known.

As part of my work as a clinical geneticist, I see couples every week who come to ask about the risk of having babies because of the age of the mother.

We talk about this and often, as the male partner is also older, we talk about the risk of his age. Most of the partners are quite surprised and even taken aback with this news.

In today's society, delaying pregnancy until later is often done for career and other purposes but usually only the age of the mother is taken into account in planning when to start a family. Why is the increased risk in relation to a father's age not widely known?

There are many possible reasons. Some of the information - such as increased death rates of adults - is new.

But information about single gene changes, such as achondroplasia, has been around for many years.

I think the real reason for the lack of knowledge is the conditions that can be caused are varied and can't really be prevented by a screening program like the one offered for Down syndrome.

In fact, most of the conditions, such as achondroplasia, can't even be picked up by the normal ultrasound scan for abnormalities done at 18-20 weeks of a pregnancy.

So, if you're a male, the only way not to be exposed to this increased risk of genetic defects in your offspring is to plan your children early and regard the increasing risks of the woman in her late 30s and early 40s as also applying to you.

In other words, stop your child bearing at the same sort of age that women stop child bearing. This may not be what older men want to hear, but they need to seek information about what the risks actually are before making child-bearing decisions.

We hear about the positive sides of parenthood in some older celebrity fathers but the story last week about the increase in death rates of the offspring brings out the hidden risks associated with fathering children at an older age.

Associate Professor Les Sheffield is a clinical geneticist with the Victorian Clinical Genetics Services