"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.

Tuesday, April 29, 2008

Autism and Schizophrenia Identical-- My Words

Autism and Schizophrenia Have Same Molecular Basis
Copyright © 2008 Cell Press. All rights reserved.
Neuron, Vol 58, 165-167, 24 April 2008
Schizophrenia: Genome, Interrupted
Rita M. Cantor1,2, and Daniel H. Geschwind1,2,3,

1 Department of Human Genetics, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA
2 Center for Neurobehavioral Genetics, Semel Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA
3 Program in Neurogenetics, Department of Neurology, University of California, Los Angeles, Los Angeles, CA 90095, USA

Corresponding author
Rita M. Cantor

Corresponding author
Daniel H. Geschwind

"The specificity of the identified variants
for schizophrenia remains unknown. For
example, CNVs in Neurexin 1 and recurrent
CNV on chromosome 16p11 previously
reported in ASD and other neurodevelopmental
disorders were also
observed in this study. This is not problematic,
but rather it presents a significant
opportunity to understand the relationship
of these disorders at a molecular
level. If the same genes carry mutations
for the development of schizophrenia or
autism, it suggests genetic pleiotropy,
where multiple disorders derive from mutations
in the same gene, and the disorder
is conditional upon the presence of other
modifying alleles, environment factors, or
chance. It also should be recognized that
childhood schizophrenia shares some
clinical features with ASD and has been
considered part of the ASD spectrum in
the past. Thus, from a neurobiological perspective,
these genetic data support the
notion of a link between disorders involving
neurodevelopmental processes that
are currently considered to be clinically
This work makes significant inroads
in breaking down the somewhat
artificial clinical distinctions between neuropsychiatric
diseases and provides support
for defining core phenotypes related
to the common genetic mechanisms"

Labels: ,

Sunday, April 27, 2008

establishing an association with rare copy number variants (CNV), which are over-represented in neurodevelopmental genes.

Copyright © 2008 Cell Press. All rights reserved.
Neuron, Vol 58, 165-167, 24 April 2008

Schizophrenia: Genome, Interrupted
Rita M. Cantor1,2, and Daniel H. Geschwind1,2,3,

1 Department of Human Genetics, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA
2 Center for Neurobehavioral Genetics, Semel Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA
3 Program in Neurogenetics, Department of Neurology, University of California, Los Angeles, Los Angeles, CA 90095, USA

Corresponding author
Rita M. Cantor

Corresponding author
Daniel H. Geschwind


Structural chromosomal variation is increasingly recognized as an important contributor to human diseases, particularly those of neurodevelopment, such as autism. A current paper makes a significant advance to schizophrenia genetics by establishing an association with rare copy number variants (CNV), which are over-represented in neurodevelopmental genes.

Labels: ,


Miley Cyrus makes the headlines but rising paternal age as a major cause of autism etc Does Not

A Topless Photo Threatens a Major Disney Franchise

Published: April 28, 2008
LOS ANGELES — Fifteen years old, topless and wrapped in what appears to be a satin bedsheet in the June issue of Vanity Fair. Did Miley Cyrus, with the help of a controversy-courting magazine, just deliver a blow to the Walt Disney Company’s billion-dollar “Hannah Montana” franchise?

Labels: ,

North doc calls for probe into jab claims

North doc calls for probe into jab claims
Apr 27 2008 by Phil Doherty, Sunday Sun

THE Government has been slammed by a North expert for refusing to fund research into possible links between autism and vaccines when it is top of the agenda for US presidential candidates.

Democratic hopefuls Hillary Clinton and Barack Obama as well as Republican nominee John McCain last week pledged to provide cash following the case of Hannah Poling, aged nine, from Georgia in the US, if they won the race to the White House.

The Sunday Sun revealed a court ruled that Hannah developed autism after receiving a cocktail of jabs.

Experts fear her condition might have been triggered by two of the vaccinations which contained thiomerosal, a mercury-based preservative, which reacted with a DNA defect in Hannah’s body.

It comes at a time when Dr Andrew Wakefield is before the UK’s General Medical Council facing a charge of misconduct originating from his claims of a possible link between autism and the MMR jab.

Paul Shattock, head of Sunderland University’s Autism Research Unit, said: “It is time the British Government investigated this issue properly.

“We are not saying this is the cause — or the full cause — of the problem but it should be researched correctly.

“But this means the Government will have talk to other experts and not just their friends in the drug companies who have a vested interest.

“The problem is that when research is controlled by people who have a vested interest in the subject the study could be seriously flawed.”

A US court ruled Hannah should receive compensation. Her five inoculations included Measles Mumps and Rubella — MMR — whooping cough, polio and diphtheria.

According to research, only 0.2 per cent of the general population have the DNA defect compared to 38pc of autism sufferers.

Mercury has now been removed from child UK vaccines. However, it has long been the suspicion of some that before its removal it contributed to autism levels here.

It was in 1998 Dr Wakefield, then working at London’s Royal Free Hospital, first suggested a link between the MMR triple jab and an increased risk of developing autism.

The British Government has always denied any link, pointing to a series of studies backing its claims, the latest published recently by a team of researchers from London’s Guy’s and St Thomas’s Hospital.

A Department of Health spokeswoman, said: “The evidence is clear, there is no link between vaccines and autism.

“The childhood immunisation programme continues to be a cornerstone of public health protection in this country.”

Defence in tatters

HEALTH bosses have been left red-faced after it emerged an autistic boy they put forward as a "guinea pig" to see if vaccines cause the condition has the same DNA damage as a previous case they dismissed as "extremely rare".

When the US Vaccine Court ruled Hannah Poling’s autism had been caused by vaccines aggravating an underlying DNA condition, health officials tried to play it down saying she was a one off case.

She was withdrawn as one of three test cases from the huge class action involving 4900 autistic children and replaced with the boy.

But now claims that Hannah is an "isolated, unusual case" have been left in tatters after it emerged the boy has the same DNA markers as she has, suggesting he too has DNA damaged by the inoculations.

According to research mitochondria DNA dysfunction in autistic children who have the regressive form of the condition could be as high as 38 per cent.

In the general population it is 0.2pc.

The crisis has forced the US Government to examine whether they are vaccinating children too early.


Saturday, April 26, 2008

Asperger’s syndrome may not lead to lack of empathy

Asperger’s syndrome may not lead to lack of empathy
By Tina Hesman SaeyApril 24th, 2008Web edition Text Size People with autism can feel others’ pain, two new studies show.Autism robs people of social and language skills and locks people in their own worlds. Scientists thought that the social defects were due in part to an autistic person’s inability to determine what other people think and feel and adjust behavior accordingly. But new research from scientists in Switzerland and the Netherlands shows that the brains of people with Asperger’s syndrome or other high-functioning autism spectrum disorders do respond with empathy to others’ pain or emotion.

Tania Singer of the University of Zurich in Switzerland and her colleagues studied people who have trouble identifying their own emotions, a condition known as alexithymia. “You need to understand your own feelings to understand the feeling of other people,” Singer says.

The disorder isn’t well known and often doesn’t interfere with people’s lives, Singer said April 14 in San Francisco at a meeting of the Cognitive Neuroscience Society. About 10 percent of people in the general population may have alexithymia. But people with Asperger's syndrome are far more likely to have alexithymia, with 60 to 80 percent of this group having the condition.

The researchers first tested couples to find out how empathy works in the brain normally. One partner was in a brain scanner known as an functional MRI, which uses magnetic fields to measure blood flow in the brain, an indicator of brain activity. Researchers made the person feel pain in a hand. A part of the brain called the insula, involved in linking body responses and emotion, lit up in response to the pain. When the partner of the person in the scanner experienced pain, the insula of the partner in the scanner lit up in sympathy.

But in people who have alexithymia, their insulas didn’t activate when they saw their partners in pain. The insulas of people with Asperger's syndrome also lit up when they saw others in pain, but only when they were in touch with their own emotions.

The result may mean that researchers and clinicians should rethink the deficit in empathy associated with Asperger’s syndrome. “I would just claim not all Asperger's [patients] will have an empathy deficit,” Singer says. It’s the degree to which people have alexithymia that determines whether they have an empathy deficit.

Another study seems to back up Singer’s claim. Researchers at the University Medical Center Groningen in the Netherlands showed short videos of people tasting a drink to healthy controls and high-functioning people with autism spectrum disorders. The video showed a person making a disgusted face after tasting the drink, showing no reaction or showing pleasure. When healthy people viewed the videos, the parts of their brain that control emotion and face movement responded just as they would if they had tasted a disgusting or pleasant drink. The brains didn’t respond much to the neutral face, as expected. On average, people responded more to the disgusted face than to the pleased face. That is not unusual. Many studies have shown more of a reaction to negative emotions and images than to positive ones.

Previous studies showed that when viewing pictures of people making emotional faces, children with autism fail to turn on “mirror” neurons responsible for helping people mimic others’ actions and to empathize.

The researchers expected that the brains of people with autism would not respond to the videos as much as those of healthy people did, says Jojanneke Bastiaansen, one of the Dutch researchers, who presented the results April 15 at neuroscience society meeting.

“It was a nice hypothesis,” she says.

But people with autism actually showed more activity in emotion-control areas and in the parts of the brain associated with controlling facial motion. The result indicates that the mirror neuron system is not broken, Bastiaansen says.

Still, the reaction is far from normal, says Marina Pavlova of the University of Tübingen in Germany. The overactivation could be a sign that people with autism have to expend more effort to empathize or could be an indicator of overstimulation, she says.

“You can have so much empathy that it’s painful for you, so you have to disengage,” Pavlova says. “Sometimes autistic people are not insensitive; they’re too sensitive.”


More Evidence of the Harm of the Ageing Dads to Offspring

Eur J Epidemiol. 2008 Apr 25 [Epub ahead of print]Paternal age and mortality in children.Zhu JL, Vestergaard M, Madsen KM, Olsen J.
The Danish Epidemiology Science Centre, University of Aarhus, Vennelyst Boulevard 6, 8000, Aarhus C, Denmark,

Background Since paternal age correlates with some diseases that have a high case-fatality, a paternal age effect on offspring's survival is expected but unsettled. We examined the association between paternal age and mortality in children in a large population-based cohort taking maternal age and socioeconomic factors into account. Methods From the Danish Fertility Database (1980-1996), we identified 102,879 couples and their firstborn singleton children. Information on childhood death (N = 831) was obtained by linking the cohort to the nationwide register on cause of death (1980-1998). Results We observed a U-shaped association between paternal age and the overall mortality rate in children up to 18 years of age. Adjustment for maternal age and other confounders reduced the mortality rate ratio (MRR) for children of younger fathers but not for children of older fathers. Compared with children of fathers aged between 25 and 29 years, the adjusted MRR was 1.77 (95% confidence interval 1.28-2.45) for children of fathers aged between 45 and 49 years and 1.59 (1.03-2.46) for children of fathers aged 50 years or more. The cause-specific MRRs were highest for congenital malformations [2.35 (1.42-3.88)] and injury or poisoning [3.43 (1.49-7.92)] for children of fathers aged 45 years or more. Conclusion Our data revealed a higher mortality in offspring of fathers aged 45 years or more that lasted into adulthood. This adds to the cumulating evidence on adverse effects of advanced paternal age in procreation.

PMID: 18437509 [PubMed - as supplied by publisher]


Friday, April 25, 2008

"I don't want there to be a panic, but I think it's safe to say that the father's age should be one of many factors couples should put into the

equation when planning a family.

Thursday, April 24, 2008

The biological clock may no longer be ticking on just the woman's side of the bed.

If current research is correct, a man's baby-making alarm may start to ring not too long after a woman's chimes its final warning toll -- around age 40.

"I don't want there to be a panic, but I think it's safe to say that the father's age should be one of many factors couples should put into the equation when planning a family," says Karine Kleinhaus, MD, PhD, a researcher at Columbia University who recently spearheaded a study on paternal age and miscarriage.

Over the past decade -- and particularly during the last five years -- studies have been mounting indicating that the age of the father may affect the health of the offspring in more ways than one.

Risk of Birth Defects
Associations have been made between paternal age and the risk of birth defects and developmental disorders such as autism and Apert's syndrome, as well as mental illnesses like schizophrenia. Moreover, studies conducted by Kleinhaus and colleagues at Columbia University looked at some 90,000 births and concluded the older a man is when he conceives a child, the more likely his partner is to miscarry -- even when she is young, healthy, and has no other risk factors.

Many believe this is just the beginning of what there is to learn.

"What we know now may be just the tip of the iceberg, particularly regarding birth issues we don't fully understand. We are just beginning to look at the role of a father's age. And as time goes by it's likely we are going to learn a lot more," says Jeremy Silverman, PhD, a professor of psychiatry at Mt. Sinai Medical Center in New York City, and the researcher of a study that associated paternal age with risks of autism.

Aging Dads: What Goes Wrong
Like every system in the body, experts say the male reproductive organs have not been spared the ravages of time.

"First there seems to be some clear changes that happen on a purely chemical level as a man ages. He has lower testosterone levels, lower DHEA, lower estrogen, plus higher levels of FSH and LH, which signal pretty much the same thing in men as in women -- reproductive failure," says Hackensack University embryologist Dave McCulloh, PhD, director of laboratory services at University Reproductive Associates in Hasbrouck Heights, N.J.

In a French study of nearly 2,000 men published in 2005 in the journal Fertility and Sterility, doctors concluded that even in couples undergoing IVF an aging father could figure into the pattern of pregnancy failure, more than previously thought.

But it's not just the idea of making fewer babies that is of concern. The new research is also tampering with conventional fertility wisdom, which has long asserted that because new sperm is made daily, male fertility remains untouchable.

And while the notion of unending sperm production hasn't changed, some researchers now believe that as a man ages, the task of churning out that daily supply is a little like trying to make a fresh batch of macaroni in a worn-out pasta machine.

In short, while the ingredients may be fresh, the mechanism that puts it all together gets slower and works less efficiently with age. And that means far fewer perfect macaroni -- and sperm -- to show for it.


Thursday, April 24, 2008

The Next Hannah Poling

Green our Vaccines
The Next Hannah Poling
by David Kirby - The Next Hannah Poling

In February, I leaked news of the Federal government’s admission that vaccines had triggered autism in a little girl named Hannah Poling. The stunning revelation, though still reverberating around the world, was roundly downplayed by US officials, who insisted that Hannah had an extremely rare, genetic case of “aggravated” mitochondrial disorder, with zero bearing on other autism cases.

Dr. Julie Gerberding, Director of the US Centers for Disease Control and Prevention (CDC), rushed to the airwaves, exhorting parents to adhere the nation’s intensive and virtually mandatory immunization schedule, and brushing off their legitimate anxieties by saying: “We've got to set aside this very isolated, unusual situation.”

Well, the days of setting aside are over: Hannah Poling is neither isolated nor unusual.

In fact, the boy who was selected to replace Hannah Poling as the first-ever thimerosal “test case” in so-called Vaccine Court, has just been found with many of the same unusual metabolic markers as… you guessed it, Hannah Poling.

Hannah’s case was scheduled to be heard in Federal Claims Court on May 12 -- as one of three “test cases” of the theory that thimerosal (a mercury-based vaccine preservative) can cause autism.

Test cases will help address general causation issues in all 4,900 autism claims now pending in Vaccine Court. But following the government concession, Hannah was withdrawn as the first test case of the thimerosal theory, and attorneys scrambled to find a replacement: a young boy from New York.

Last week, however, the court announced that the replacement thimerosal test case was also being withdrawn, in order to “proceed to an individual hearing on a different theory of causation.”

That theory, which applies to Hannah as well, maintains that children with dysfunctional mitochondria (the little batteries within each cell that convert food into energy) are susceptible to autistic regression, triggered by a vaccine-induced overtaxing of the immune system.

“We want to pursue an additional theory, not a different theory,” the boy’s father told me. “We are by no means abandoning the thimerosal theory of causation but, in the context of the test case, the thimerosal theory would have eclipsed our other evidence, including evidence of metabolic dysfunction,” such as impaired mitchondria and low cellular energy.

Following the Poling concession, he said, “I saw right away that we needed to pursue the mitochondrial theory,”but the lead attorneys did not see it that way. “Perhaps they did not properly understand the concession, and believed the finding was of a rare, genetically caused mitochondrial disorder,” as the government contends. “I think they rightly want to keep clear focus on thimerosal in the test case, and not muddy the presentation with other theories.”

The court’s test case process is unusual and unwieldy. “They limit the cases to one theory at a time, when the theories are not mutually exclusive,” the father said. “For example, thimerosal could cause, contribute to, or aggravate mitochondrial dysfunction. These cases can't be wrapped into neat little packages.”

The unexpected withdrawal of two test cases in a row – both because of their apparent mitochondrial underpinnings – is sure to have larger ramifications in the Court of Federal Claims, as well as the much larger court of public opinion.

A new, additional theory of causation is about to be introduced in Vaccine Court: Vaccines can trigger a chain of events in children with mitochondrial dysfunction that causes autism.

But the US Government now has a major quandary to deal with. Federal officials already conceded that, far from being “theoretical,” this chain of events already happened to Hannah Poling. This will make it exceeding difficult, if not impossible, to argue against compensating the boy from New York, when compensating a nearly identical case – Hannah Poling – was already deemed appropriate.

Some estimates of mitochondrial dysfunction in children with autism range as high as 20%-30%. But among the regressive subset of cases (comprising 100% of the claims in Vaccine Court) up to half of the children might show signs of it.

No one knows how many of those families will pursue a similar strategy of individual hearings on causation, based on the mitochondrial concession in the Poling case. But my guess is that there could be hundreds of them, following in the precedent of this case’s footsteps. The legal ramifications, inside Vaccine Court and throughout the judicial system, remain incalculable at this point.

Still, when the American public finds out that the exceedingly “rare” Poling case was replaced by what is shaping up to be yet another exceedingly rare case – they will follow the lead of all three presidential candidates and finally reject the tired mantra that, “there is no link” between vaccines and autism.

Then perhaps will end, “One of the most vitriolic debates in medical history,” as it is called by Dr. Bernadine Healy, former head of the NIH and the Red Cross. “At some level,” she said, the Poling case “was a vindication for families,” adding that, “vaccines as a trigger carry a ring of both historical and biological plausibility.”

The government is currently examining the national vaccine schedule to see if we are, perhaps, immunizing children too early and too often (and with too much thimerosal from the flu shot).

I personally thought that one Hannah Poling emerging out of Vaccine Court would be enough to change the way we vaccinate in this country. But now we have two. And there are many more Hannah’s out there, waiting to be counted.


Nassau County To Hold Vaccine Autism Hearings

Adventures in Autism: Nassau County NY First Municipality to Hold Vaccine Autism Hearings#links#links


Autism controversy clouds immunization decisions

Last modified 4/24/2008 - 6:52 am
Originally created 042408

Autism controversy clouds immunization decisions

The potential link has parents questioning the safety of the shot series.

By Jake Armstrong, The Times-Union

ATLANTA - Childhood vaccinations have helped stamp out a number of debilitating infectious diseases.

For most parents, protecting children from polio or measles is as easy as a few trips to the doctor's office.

But as the federal and state governments press to improve vaccination rates, especially this week during National Infant Immunization Week, the cloud of controversy hovering over a potential link between vaccines and autism in children may have some parents questioning whether the doctor's needle is a double-edged sword.

While statistics show the prevalence of autism is higher than previously thought - one in 150 children had some form of the developmental disorder in 2007, according to the Centers for Disease Control and Prevention - research has yet to definitively prove or disprove a tie between routine child vaccinations and the rise in autism rates.

A healthy dose of questions for doctors should accompany more research, suggests Terry Poling, an Athens mother who believes her daughter Hannah's autism developed after multiple vaccinations administered during a single doctor's visit in 2000 aggravated a latent disorder in her mitochondria, the powerhouse of cells.

Poling said she is concerned the salvo of shots most children receive at an early age may be too much too soon for developing immune systems.

"We might be bombarding their bodies," Poling said.

A child can receive about 20 shots by age 1, according to CDC vaccination schedules. CDC officials did not respond to a request for comment on altering vaccination schedules.

Hannah Poling, now 9, is among the first people compensated from a federal vaccine injury fund due to her development of autism. The federal government maintains vaccines are safe.

Poling said parents should talk with their child's doctor about altering the vaccination schedule if the parent is concerned.

Much more research into the cause of autism is needed, Poling said.

Until it is determined, parents may be left skeptical about the safety of vaccinations for their children, she said....


Wednesday, April 23, 2008

Flea a Pediatrician Wrote

Flea: Old Fathers

There are many studies with data on conditions that are associated with increasing paternal age. To not take seriously, the Reichenberg study of more than 318,000 offspring, born in the 1980s, showing that men over 40 were almost six times more likely to father an autistic child as those under 30, is a mistake. The risk goes up to nine times with fathers over 50.

There's a 5-year old I know from our neighborhood playground. I know only two things about her: Her father was 84 when she was born, and she is profoundly autistic.

I know that anectdotes are meaningless and data are everything, but I couldn't help think of this precious little girl when I read of this study in the Archives in General Psychiatry

Data are everything, but I can't help wondering what this study will do to the conversation about autism.

My guess is it will do nothing. Could delayed parenthood be partly responsible for the "autism epidemic"? Americans don't want to hear that their lifestyle choices may have deleterious effects on their children. My guess is that some folks will shun this data as vigorously they shun the data that demonstrate, convincingly, that vaccines do not cause autism
Labels: American Lifestyle, autism epidemic, Flea at his most brilliant, old fathers


Tuesday, April 22, 2008

Obama Climbs On The Vaccine Bandwagon

Get Email Alerts Similar Bloggers
Obama Climbs On The Vaccine Bandwagon
Posted April 22, 2008 | 11:29 AM (EST)


Breaking Home News

Barring some big Clinton blowout in Pennsylvania today, the next President of the United States will unequivocally support research into the growing evidence of some link between vaccines and autism.

Republican John McCain has already expressed his belief that vaccines and the mercury containing preservative thimerosal could be implicated in what he has rightly termed an "autism epidemic."

Yesterday, at a rally in Pennsylvania, Barack Obama had this rather surprising thing to say:
"We've seen just a skyrocketing autism rate. Some people are suspicious that it's connected to the vaccines. This person included. The science right now is inconclusive, but we have to research it


I think the public has the right to know that Higher Paternal Age is a Cause of Non-familial Autism

In general science does not usually inform the public of the research that will save lives, prevent disease, prevent vaccine and drug related injuries, or in general help people have healthier babies or lead healthier lives.

Scientific Misconduct Blog: Whistleblowing 101


Sunday, April 20, 2008

Dad's Hidden Influence A father's legacy to a child's health may start before conception and last generations

Dad's Hidden Influence
A father's legacy to a child's health may start before conception and last generations
Tina Hesman Saey

Pregnant women know the drill. Don't drink. Don't smoke. Don't eat too much fish. Take vitamins. Mothers have long shouldered the responsibility, and the blame, for their children's health. Fathers don't usually face the same scrutiny.

How a man lives, where he works, or how old he is when his children are conceived doesn't affect their long-term health, scientists used to think. But growing evidence suggests that a father's age and his exposure to chemicals can leave a medical legacy that lasts generations.

Animal studies demonstrate that drugs, alcohol, radiation, pesticides, solvents, and other chemicals can lead to effects that are handed from father to son. Human studies are less clear, but some show that fathers play a role in fetal development and the health of their children.

Teenage dads face increased risk that their babies will be born prematurely, have low birth weight, or die at birth or shortly afterward, a new study in Human Reproduction shows.

Babies of firefighters, painters, woodworkers, janitors, and men exposed to solvents and other chemicals in the workplace are more likely to be miscarried, stillborn, or to develop cancer later in life, according to a review in the February Basic & Clinical Pharmacology & Toxicology.

Fathers who smoke or are exposed at work to chemicals called polycyclic aromatic hydrocarbons put their children at risk of developing brain tumors.

And, older fathers are more likely to have children with autism, schizophrenia, and Down syndrome and to have daughters who go on to develop breast cancer.

Though some of these observations are decades old, attitudes lag even further behind, says Cynthia Daniels, a political scientist at Rutgers University–New Brunswick in New Jersey. Dads aren't held accountable if something goes wrong during fetal development.

Matter of math
Since men make new sperm every 74 days, people used to reason, the genetic slate is wiped clean every couple of months. And even if a man makes defective sperm, the "all-or-nothing" view of reproduction holds that damaged sperm don't fertilize eggs. No harm. No foul.

So no one bothers to remind men to protect themselves against environmental toxins. There are no images of "crack dads" and "crack babies" in the media like those of women who harm developing fetuses with drug and alcohol use, Daniels said in February at a meeting of the American Association for the Advancement of Science held in Boston.

When someone does study fathers-to-be, the focus is usually on fertility, not on the consequences for children's health, she says.

Yet even fertility messages meet resistance from many men.

Harry Fisch, director of the Male Reproductive Center and a urologist at Columbia University Medical Center, found that out when he suggested that men, like women, have ticking biological clocks.

Men can produce sperm throughout life, but that doesn't mean their cells are forever young.

"Every cell in the body ages," says Fisch. "Every cell. The older you get, the more chance of an abnormality. The same thing goes for sperm."

Men younger than 20 and older than 30 make more abnormal sperm than men in their 20s. These damaged sperm could create an unhealthy embryo or pass on damage that could lead to birth defects or illness in offspring.

It is not a popular message.

"Men do not want to hear this," Fisch says. "When my book came out, I got e-mails. I got faxes saying, 'How dare you say this? How can you say this? We know that there are men in their 70s having healthy children.'"

Despite these anecdotal accounts of elderly dads, studies demonstrate that older men are at increased risk of passing on genetic abnormalities. It's a matter of math.

Women are born with all the eggs they will produce in their lifetime. The cells that give rise to eggs divide 24 times, all before birth. But the cells that produce sperm continue to divide throughout a man's lifetime. Each year after puberty, a man's sperm-producing cells replicate about 23 times. Every time the cells divide is another chance for error.

As a result, the sperm produced by a 40-year-old man have gone through about 610 rounds of replication. That's 610 chances of introducing a mutation in the DNA, or improperly divvying up genetic material.

Parents over age 40 are six times more likely to have children with Down syndrome than 25-year-old parents, Fisch and colleagues showed in a 2003 study in the Journal of Urology. An extra copy of chromosome 21 causes Down syndrome. This extra chromosome is just as likely to come from dad as mom in the older couples.

Older dads also have a higher risk of fathering children with rare mutations that cause dwarfism or a premature aging disease called Hutchinson-Gilford progeria syndrome.

But sometimes aging fathers pass along traits that can't be traced to only a single mutation. Fathers 40 and older have an increased chance that their children will develop complex disorders such as autism or schizophrenia. There is growing evidence that those disorders are caused by defects in many genes and the way genes are turned off and on.

Scientists don't yet understand the changes that age induces in sperm-making germ cells, and environmental exposure presents an even bigger mystery. People come in contact with a plethora of chemicals every day. But it is no easy task to sort out exactly which ones, or which combinations, cause heritable problems. The effects chemicals and radiation may have on offspring don't always follow predictable patterns either.

And when researchers do find a clear link between a father's lifestyle and his children's health, it's not always clear what the data mean.

"What we can say is that we identified a group of fathers with adverse outcomes for their fetuses, but we don't have an idea of the mechanism," says Shi Wu Wen of the University of Ottawa in Canada and one of the lead authors of the study showing that babies of teenage fathers have a greater risk of birth problems.

Wen and his colleagues examined birth records for more than 2.6 million babies born between 1995 and 2000 to married, first-time, 20-something mothers in the United States. Looking at the husbands' ages, the team found that babies of teenage fathers, but not middle-age men, had an elevated risk of still birth, low birth weight, and other birth problems. The study was published online Feb. 6 in Human Reproduction.

'Preposterous' inheritance
Some animal studies showing paternal effects emerged years ago but were roundly dismissed, says Gladys Friedler, professor emeritus at Boston University.

OLDER AGE, HIGHER RISK. As men age, they stand a greater chance of fathering children who will develop schizophrenia by age 34. Paternal age is only one of many factors linked to schizophrenia.
E. Roell, (Source: D. Malaspina, et al., Arch. of Gen. Psychiatry, 2001)

Four decades ago, Friedler was studying tolerance to narcotics, one of the first steps of addiction. To find out if a mother rat could pass tolerance on to her offspring along with antibodies and other immune factors, as some scientists theorized, Friedler exposed female rats to morphine before pregnancy. Babies of exposed mothers were born much smaller than average. And those babies also went on to give birth to tiny babies, even though the offspring had never encountered the drug.

Friedler also gave male rats morphine before they bred. "To my total disbelief and bewilderment, paternal exposure also affected progeny," Friedler said at the AAAS meeting.

Her adviser dismissed the result. Morphine doesn't cause mutations, so the idea that males could hand down a trait without passing along a mutation seemed preposterous. The whole thing smacked of Lamarckism, the long-rejected idea that environmental influences can change an animal or plant's structure and offspring can inherit that change.

But in recent decades, scientists have discovered that chemical modifications to DNA and proteins can change the way genes are packaged and regulated without changing the genes themselves. Such modifications are known as epigenetic changes.

"What was Lamarckian is now epigenetic," Friedler says.

Epigenetic modifications act as a molecular scrapbook, preserving memories of events in parents' lives and handing them down to the next generation and beyond.

"There's a chromosomal memory," says Anne Ferguson-Smith, a developmental geneticist at Cambridge University in England. "The chromosomes remember whether they came from the mother or the father."

That memory is established in the form of a chemical mark called methylation. Methylation usually turns a gene off. At least 100 genes in humans are turned off only on the chromosome contributed by the mother or only on the chromosome that came from the father. Such genes are called imprinted genes because of the indelible impression parents leave on their offspring's DNA.

Several imprinted genes help build the placenta or encode growth factors that need to be tightly controlled so an embryo will develop correctly. "There's a contribution from both parents that is essential," Ferguson-Smith says. "One can't do without the other. They must work together to have a healthy offspring."

Imprints and other methylation marks are not encoded in the DNA. Instead the epigenetic modifications decorate chromosomes like ornaments on a Christmas tree. But these ornaments are heirlooms of a different type. It's as if a seedling grows straight from the ground already gussied up with tinsel and lights in the same places its parents were decorated. If a chemical or aging alters the epigenetic pattern on a man's chromosomes, his heirs could bequeath mismarked DNA to their children, too. Some mistakes may be as benign as exchanging a red bulb for a blue one. Other alterations, akin to placing the star on the lowest branch instead of the treetop, are likely to have more profound consequences.

Male mice exposed to cocaine, for example, pass memory problems on to their pups, a 2006 study in Neurotoxicology and Teratology shows. The male mice inhaled cocaine in long daily sessions akin to crack binges. When they mated with females never given coke, they had pups that had trouble learning and remembering where to find food in simple mazes. The problem was especially severe for female offspring. The researchers couldn't find any obvious DNA damage in coke-smoking males' sperm, but did find altered levels of two enzymes involved in the methylation of DNA in sperm-producing tissue in the father mice. The result suggests that epigenetic changes may be responsible for the offspring's behavior problems.

Fungicide legacy
Matthew Anway doesn't know whether the rats in his lab at the University of Idaho in Moscow have methylation problems. Some studies suggest they do, but Anway doesn't yet have definitive proof.

He can prove that male rats exposed to a fungicide in the womb can pass tumors and diseases of the prostate and kidney down for at least three generations. The rats could provide the first model for how prostate disease is inherited, he says.

Male babies born to mothers that had been injected with fungicide had prostate problems that mimic those seen during human aging. The second-generation rats also had more tumors, kidney defects, and higher rates of abscesses, cysts, and other infections than unexposed control rats. Germ cells in the testes of exposed rats also died more quickly than those in the control rats.

Subsequent generations of male rats also had the prostate and testes defects, and both male and female offspring developed kidney problems and tumors.

But only male rats could pass along the defects. The exposed rats bequeathed their fungicide legacy to their sons, grandsons, and great-grandsons even though none of the later generations were exposed to the chemical.

Exposed animals decrease production of enzymes that methylate DNA, Anway says. But he hasn't yet found consistent changes in the methylation patterns in exposed rats.

It's not clear whether Anway's results have any implication for human health. The rats were exposed to extremely high doses of fungicide through the completely unnatural route of injection.

What's important is that the male shares experiences with descendants for years to come. Further research could give new insights, Anway says, into how alterations in early development could lead to adult disease in humans.


If you have a comment on this article that you would like considered for publication in Science News, send it to Please include your name and location.


Why call Paternal Age Childhood Schizophrenia Autism? Why 36 required Vaccinations? Why obfuscate?

Scientific Misconduct Blog: Telling it like it is (Procter and Gamble)


Chandler's Progress

Adventures in Autism: Pervasive Developmental Disorder – Almost Specified#links#links Biomed


Saturday, April 19, 2008

Autism is a Heterogeneous Syndrome

Nature Reviews Genetics 9, 341-355 (May 2008) | doi:10.1038/nrg2346

Advances in autism genetics: on the threshold of a new neurobiology
Brett S. Abrahams1 & Daniel H. Geschwind1

Autism is a heterogeneous syndrome defined by impairments in three core domains: social interaction, language and range of interests. Recent work has led to the identification of several autism susceptibility genes and an increased appreciation of the contribution of de novo and inherited copy number variation. Promising strategies are also being applied to identify common genetic risk variants. Systems biology approaches, including array-based expression profiling, are poised to provide additional insights into this group of disorders, in which heterogeneity, both genetic and phenotypic, is emerging as a dominant theme.

Author affiliations
Programs in Neurogenetics and Neurobehavioural Genetics, Neurology Department, and Semel Institute for Neuroscience and Behaviour, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California 90095-1769 USA.
Correspondence to: Brett S. Abrahams1Daniel H. Geschwind1 Email:; Email:


Thursday, April 17, 2008

The Sad Truth About Scientific Research --Autism Too

Scientific Misconduct Blog: Money and accountability (Procter and Gamble)


Dr. Jon Pauling ( Hannah's father) On Mitochondrial Disorders and Autism-PODCAST

Jon Pauling's advice on vaccinations and autism

Mitochondrial autism a distinct sub population of autism. How common?

The Associated Press and Mitochondrial DNA
Posted on April 25, 2008 by Laz
Caught the following piece on the AP,
“Study says near extinction threatened people 70,000 years ago”
Interesting findings to be sure, but one thing in the article caught my attention,
Previous studies using mitochondrial DNA — which is passed down through mothers — have traced modern humans to a single “mitochondrial Eve,” who lived in Africa about 200,000 years ago.
Which is passed down through the mothers? Yes that is true but is not exclusively true. It has been long believed that mtDNA is only passed down through the mother, it’s in biology books and it is what was taught to me during college. The problem is that there is a couple of papers in the literature that say otherwise, there is paternal transmission of mtDNA.
This from a paper in the journal Science 286:2524 (1999),
The assumption that human mitochondrial DNA is inherited from one parent only and therefore does not recombine is questionable…
This assumption has been used extensively to date events in human prehistory, including the age of our last common female ancestor, “Eve”, and the spread of Homo Sapiens in Asia and Europe
In fact one of the paper’s authors, respected biologist John Maynard Smith, “is frustrated but not surprised that the establishment chooses to ignore these findings.” New Scientist 178:48 (2000).
Ok, that’s just one paper, well then there was this one in the New England Journal of Medicine 347:576-579 (2002) titled “Paternal Inheritance of Mitochondrial DNA” which states,
We determined that the mtDNA harboring the mutation was paternal in origin and accounted for 90 percent of the patient’s male mtDNA
It seems that Maynard Smith was correct in his frustration, and one has to wonder why the establishment has not really accepted mt DNA recombination?
Could it be because of the impact it might have on the models (i.e. mitochondrial Eve) which are based in large part on the ASSUMPTION that mtDNA is only inherited from the mother? Or what about the industry (genealogical DNA testing) that is built on this assumption?
Things that make you go hmmm…


Wednesday, April 16, 2008

Byron Richards on How to Prevent Vaccine Injury-Wakefield Gains A Well Known Ally

Adventures in Autism: Andrew Wakefield Gains a Well Known Supporter#links#links

How To Prevent Vaccine Injury
By: Byron J. Richards, CCNSource: http://www.newswithviews.comApril 11, 2008

It is a colossal failure on the part of our government to not warn parents of the actual risks associated with vaccines. The blind insistence that vaccines are safe and effective is not supported by science, at least for a significant number of our children. There are now 25,000 children per year developing autism (1 in 150), a problem that has expanded in direct proportion to the increase in vaccinations. How do you know if your child is at risk?

The government’s primary goal appears to be to prevent parents, en masse, from refusing to vaccinate their children. To prevent such a “run on the public health bank” all caution is being recklessly thrown to the wind. American children are now the most vaccinated people in the world. What are we actually doing? The vaccination problem needs to be objectively solved so that public health is maintained, yet needless vaccine injury is avoided.

It should not be of any great comfort to parents that scientists hardly understand how the immune system works. The simplistic idea that vaccines offer protection against disease has an element of truth and a significant element of risk. This article explores the risk in greater depth. I will first explain what is known about the nature of the risk and follow with some natural options that can really help out.

Vaccine Adjuvants – A Double-Edged Sword

Giving a fully active virus as a vaccine would obviously cause the disease. On the other hand, a weakened or deadened form of the virus may not produce much of an immune response thereby making the vaccine worthless. This problem has been “solved” by combining the weakened disease with an immune activator called an adjuvant.

An adjuvant does not contain the disease; rather it is intended to initiate the first step in fighting an infection – the inflammatory response. This is like giving a general wake up call to the immune system. This can be done with an irritant or a more specific toxin the immune system is likely to recognize based on eons of exposure.

In the irritant category the most common adjuvants used in vaccines your child will get are salts of aluminum (aluminum phosphate and aluminum hydroxide). The safety of aluminum salts has been called into question following the poor health of many Gulf War Veterans who received multiple aluminum adjuvant vaccinations. Many scientists consider that their poor health was caused by the adjuvants in the vaccines they were given. In 2003 French researchers identified aluminum hydroxide vaccine adjuvants as the cause of a new disease consisting of pain and chronic fatigue; noting similarities to problems in Gulf War soldiers.

In a recent study mice were given aluminum hydroxide at doses comparable to Gulf War soldiers. Extensive testing was done of their cognitive ability as well as analysis of the nervous system upon sacrifice. The results showed that aluminum hydroxide caused nerve-related motor defects. Analysis of brain tissue showed 255% increase in inflammatory markers along with 35% loss of motor neurons.

It has been over a year since this study was published. Why isn’t the CDC doing the same experiment with the adjuvant load from their recommended vaccine schedule? Any substance that is adversely neurotoxic in an adult is likely to be more neurotoxic in the evolving nervous system of a baby. Not following up on this is gross negligence on the part of the CDC.

Another common adjuvant is bacterial endotoxin (the outer membrane of the cell wall of Gram-negative bacteria), also known as lipopolysaccharide or LPS. Since we have been battling bacteria since the beginning of our evolution, our immune systems recognize LPS as an invasion – setting off a powerful inflammatory immune system reaction. The toxicity of any bacterial infection relates to LPS.

Scientists at the National Institutes of Health freely acknowledge that the proinflammatory effects of adjuvants in vaccines “underlie many of the observed toxic effects.” What the new science shows very clearly is that all the inflammation that is generated by adjuvants is actually not necessary for activating the immune response.

This means that our government is sticking by a vaccine program that relies on firing a toxic shotgun at the immune system even though they know a laser-guided approach would have much less risk of vaccine injury from direct toxicity. The problem for our government is that they don’t currently have the ability to make safer vaccines; thus they blindly defend the safety of a very crude approach and refuse to conduct tests that would easily show the current vaccine program is not safe. It is quite clear that an inflamed nervous system is an undeniable feature in autism.

What Does NF-kappaB Have to Do With It?

Nuclear Factor kappa-B is the “brain” residing within every cell of your body, including cells of your nervous system. It is a gene transcription factor, meaning that it tells your cells how to behave depending on what is happening. When everything is running smoothly, NF-kappaB has its feet up on the lawn chair in a relaxed mode of operation. Under stress NF-kappaB initiates survival strategies. NF-kappaB is the main regulator of all inflammatory and immune responses, and is intimately involved with the healthy function of your nervous system. NF-kappaB is an active intelligence within your cells. The last thing you would ever want to do is mess up NF-kappaB.

Adjuvants, due to their intentionally inflammatory mode of operation, activate NF-kappaB. This is done to ramp up the immune system so it can “see” the weakened virus in the vaccine. The million dollar question is: “How much NF-kappaB activation can a child take before their NF-kappaB system overheats and sets a fire in their brain called autism?” When NF-kappaB overheats it generates large amounts of inflammatory immune system messengers (like TNFa and IL6) and massive numbers of free radicals that damage nerve cells.

If a child is already acutely inflamed then the NF-kappaB pump has already been primed and the risk for vaccine injury is greater. Acute inflammation is caused by illness, injury, surgery, poor diet, and stress at home. This problem is magnified if the child had a history of inflammation while in the womb, was born prematurely, or had health struggles during the first few years of life. Even a previous round of vaccines can prime the inflammatory NF-kappaB pump. Environmental toxicity is another factor that cannot be ignored, as is the health of the mother prior to and during pregnancy. A mother’s obesity and eating habits have a significant effect on the nerve health of her child.

The main point to understand is that if the NF-kappaB system is already on the edge of overheating due to other factors, then the intentional pushing of this system with vaccines poses a serious risk to the child. Multiple vaccines given at one time, with multiple pro-inflammatory adjuvants, obviously increase the risk. Any person objectively reviewing the science on this issue could reach no other conclusion.

The issue of NF-kappaB is so important that the next generation of vaccines will utilize it in an attempt to make less toxic vaccines (the laser-guided approach rather than the shotgun). While NF-kappaB-targeted vaccines will be less blatantly toxic, making them free of adverse side effects is another story altogether. Manipulating NF-kappaB is playing with the essence of the life force of a cell. At any given time there are numerous ons and offs relating to how NF-kappaB is naturally working to maintain health. The new vaccines will turn on the inflammatory aspect of NF-kappaB – which could easily upset the applecart in some other needed aspect of health.

No matter how good research scientists are at developing new vaccines, there will always be a percentage of at-risk-already-inflamed children who are likely to respond in a poor manner. Vaccine safety is not just about better vaccines; it’s also about protecting those who are most likely to poorly react to them. It is not possible to have a good public health policy for disease prevention that fails to take this fact into account.



Thank you Professor Yasser Metwally How About Also Studying Advancing Paternal Age Autism

Mitochondrial Dysfunction May Play a Role in Autism Spectrum Disorders EtiologyApril 16, 2008 at 10:08 am · Filed under Neurological section

The author: Professor Yasser Metwally


April 15, 2008 — New research suggests mitochondrial dysfunction may play a role in the etiology of autism spectrum disorders (ASD) in a subset of this patient population.

Here at the American Academy of Neurology 60th Annual Meeting, a retrospective analysis of 41 children with ASD who were being evaluated for suspected mitochondrial disease showed that 32 (78%) had defects in skeletal muscle oxidative phosphorylation (OXPHOS) enzyme function and 29 of 39 (74%) harbored abnormalities in the OXPHOS proteins.

“We’re very excited by these findings, and, based on these results, we will continue to pursue this [mitochondrial dysfunction] as a potential cause in a segment of the autistic population,” principal investigator John Shoffner, MD, said owner of Medical Neurogenetics, in Atlanta, Georgia.

While it is common for patients with mitochondrial disorders to have autistic features, Dr. Shoffner said his team investigated whether the opposite was true, that patients with ASD had indicators of underlying mitochondrial disease.

Study subjects were children aged 2 to 16 years who had a confirmed diagnosis of ASD and were referred for investigation of possible mitochondrial dysfunction due to the presence of markers for mitochondrial dysfunction, including increased lactate, pyruvate, and/or alanine.

Significant Numbers of Affected Individuals?

According to Dr. Shoffner, previous recent research has reported that up to 20% of children with autism have hyperlactacidemia and increased ratios of lactate/pyruvate.

“When you consider the frequency of autism in the general population, and you take 20% of that as a rough estimate of the proportion of children that may have these biomarkers [of mitochondrial dysfunction], it begins to raise some interesting questions about how to approach diagnosis, mechanism of disease, and patient management in what could turn out to be significant numbers of individuals,” said Dr. Shoffner.

To find a possible explanation for elevated lactate levels, the investigators conducted a more detailed investigation that included analysis of mitochondrial enzyme activity in skeletal muscle biopsies.

They found defects in a series of selected representative proteins from each of the 5 enzyme complexes, which are responsible for producing and synthesizing energy in the muscles.

“Not only did we find enzyme defects in these patients, but we also took the investigation a step further and isolated and examined selected proteins involved in oxidative phosphorylation and found many of the proteins were also abnormal,” said Dr. Shoffer.

The researchers found defects in all 5 enzyme complexes, often described as the body’s “power plants.” Complex 1 abnormalities were the most common, with 41% of patients affected by OXPHOS enzyme and protein chemistry criteria. In addition to enzyme-function abnormalities, the investigators also found evidence of degradation of their proteins.

The muscle mitochondrial DNA (mtDNA) was sequenced in 40 of the patients. Of these, 75% (30/40) had normal mtDNA. Two subjects had heteroplasmic mtDNA mutations, which are often a marker for pathogenicity. The remainder had changes in the mtDNA that are still under investigation.

According to Dr. Shoffner, these data indicate that nuclear DNA mutations are the most likely causes of the mitochondrial defects. However, mtDNA mutations do occur.

“Obviously, autism is not a single condition but a true spectrum of disorders. There are many ways in which the genes can go awry, and our hope is that this study will open the door to a greater understanding of at least 1 subset of this patient population with metabolic and enzymologist changes,” he said.

However, he added, further research in unselected populations of autistic patients is needed to confirm these findings.



American Academy of Neurology 60th Annual Meeting: Presented April 13, 2008.


Labels: ,

Monday, April 14, 2008

Ginger is a Great Lady and an Excellent Blogger

Adventures in Autism: AAP Takes Two Steps Forward, One Step Back#links#links Adventures in Autism, Ginger Taylor


ASD CARC Had An Old Dads Survey in September of 2006 They Never Reported the Result THE SMOKING GUN

Jeanette J.A. Holden, PhD (Molecular Genetics; Clinical & Behavioural Phenotyping; Prospective Study; Research Registry) Ask Dr. Holden about the smoking gun. Was she paid off not to publish the results? Would the results have shown that fathers of most de novo autistic children are older men?


Autism Schizophrenia and Older Fathers

Autism and Childhood Development By Cindy Rich

For 18 months, William and Elizabeth seemed like typical babies. Then the twins parents started noticing problems. Now, at age five, the children have autism.

Something Happened and We Don’t Know Why

There’s a light breeze over Rehoboth Beach as five-year-old Elizabeth Polanin takes her dad’s hand and walks toward the ocean. “That is one big pool, isn’t it, baby?” her father says.

The water comes close, so Elizabeth steps back. She smiles and shakes a hand in the air, a sign she’s excited, then covers her ears as a wave crashes—like many children with autism, she’s sensitive to sounds.

When the water recedes, Elizabeth walks toward it again, making high-pitched sounds and rubbing her hand against the back of her head. “You’re getting brave now!” her father says.

Water is one of Elizabeth’s favorite things. She once took ten baths in a day. She’ll happily sit in her inflatable pool at home in Greenbelt and watch a toy spin in the water.

Her twin brother, William, likes water too. He used to leave the faucet on for hours and watch it flow.

When Elizabeth comes back from the ocean, she jumps into her mother’s lap, accidentally hitting her.

“Don’t hit people,” William tells his sister. “Don’t hurt your William. Don’t hurt your peoples. Don’t hit your peoples.”

Elizabeth doesn’t respond to her brother. She used to when they were babies, but now she hardly talks at all.

“These children were normal that first year and a half, as normal as two babies could be,” says Joe, her father. “Something happened to them, and we don’t know why.”

Autism is a spectrum disorder—children who have it exhibit a wide range of behaviors. William talks; Elizabeth rarely does. He sleeps in a bed; she sleeps in a crib. He’s learning to write letters and numbers; she’s learning “come here” and “stop.”

The National Institute of Mental Health defines autism as a developmental disorder characterized by an impairment in thinking, feeling, language, and the ability to relate to others. William and Elizabeth fall on ends of the spectrum. He’s “high-functioning,” and she’s “low-functioning.”

According to the Autism Society of America, autism is the nation’s fastest-growing developmental disability. One in 166 children has an autism-spectrum disorder—four times as many boys as girls—and about 40 percent don’t speak.

In Prince George’s County, where William and Elizabeth attend school, more than 800 students fall on the autism spectrum; about 250 did in 1999. Montgomery County has 943 students with an autism-spectrum disorder, and 28 classes exclusively for children with autism. Fairfax County has 1,188 students receiving autism services, up nearly 50 percent from five years ago. Arlington had 87 students on the spectrum in 2001 and has almost twice that now. Loudoun has 450. Alexandria has 63. (DC Public Schools did not provide figures.)

Researchers don’t know what causes the brain abnormalities that lead to autism. Evidence supports both genetic and environmental factors. Nobody knows why the numbers seem to be rising. Some think the high rates have always been there but children now are more accurately diagnosed. Others argue there’s an epidemic.

Neurodevelopmental pediatrician Chuck Conlon, who treats William and Elizabeth, says: “I know very few people, if anybody, who don’t have some connection to someone with autism.”

When Julie Polanin gave birth to two healthy babies in June 2001, she and Joe didn’t give autism a thought.

Julie tried for three years to have children. She was 35 when she found out she had a benign fibroid tumor in her uterus. If she had it removed, doctors told her, the procedure would turn into a hysterectomy, and she wouldn’t be able to have a child.

Julie had finally found the man she wanted to have children with. She’d met Joe Polanin in 1989 while they were working at a Silver Spring nursing home. He was office manager; she coordinated social services. He had custody of his two older sons. Joe and Julie both loved music. She fell for his quirky sense of humor. They married in 1995.

Joe knew it was late to become a father again—he’s now 60—but he knew how much fun kids could be and how much a child meant to Julie.

They found a doctor who could perform the surgery without removing Julie’s uterus. She miscarried two years later in 1999, but doctors were still optimistic.

Julie stayed away from alcohol and caffeine. She avoided fish because she worried about the effects of mercury. She drank bottled water.

In October 2000, she was pregnant again. A sonogram showed twins. Julie was ecstatic.

Six months into her pregnancy, Julie went into preterm labor. Doctors put her on bed rest for three months. Every day, she read about how the babies were growing inside her.

At 38, Julie knew she was at higher risk for Down syndrome. She and Joe agreed to have amniocentesis.

A nurse called soon after and told her, “Your babies are perfect.”

It’s June 2006, and the twins are turning five. A photo on their birthday cake shows them as infants, sitting in the green felt pouches they were in at Halloween. “Two peas in a pod,” their parents called them. The icing on the cake reads my how you’ve grown.

William sits in a hammock, wearing a Spider-Man T-shirt, playing with a toy that churns out bubbles. Elizabeth wanders in and out of the house, unaware she’s turning five today.

The Polanins’ backyard is a private playground. William makes racetracks from sticks and mulch for his toy cars. He rides a tricycle into a small tree, repeatedly saying, “Oops—he crashed.” He looks for trolls hiding among the trees.

Elizabeth often sits in the pool chewing on a toy, or swings so fast that the swing set shakes. She stands on her tire swing and twirls around.

There’s one other child at the party; most guests are Julie and Joe’s friends. William and Elizabeth usually play alone. Neighborhood kids don’t come over—Julie thinks their parents aren’t comfortable letting them play at her house.

“It’s time to cut the cake!” Joe yells.

“Not yet,” William says. He walks to the back door, his hands over his ears. “Let’s go in the house.” He watches from inside the doorway while the others stand near the cake in the backyard and his mom blows out the candles.

Julie and Joe hoped William and Elizabeth would be starting kindergarten soon. Joe would be retiring in a few years from his job as accounts specialist at Adventist Healthcare, so he would be there to greet them after school.

He looked forward to age five as a turning point, as it had been with his older sons. That’s when a parent’s job got easier.

When Dr. Chuck Conlon started his pediatric training at Bethesda’s National Naval Medical Center in 1979, the medical community was just beginning to understand autism. A young patient at the center, who exhibited repetitive behaviors and language that was unclear and disconnected, was diagnosed with “childhood schizophrenia.” Doctors didn’t know what they were seeing.

Autism had been identified in the 1940s by Leo Kanner, a physician at Johns Hopkins Hospital. He studied 11 children who showed signs of social isolation, limited speech, and lack of emotional attachment, and he introduced the label “early infantile autism.” But the term wasn’t widely accepted until the 1980s.

Around the same time Kanner identified autism, an Austrian named Hans Asperger observed a behavior pattern in boys that included normal intelligence and language development, and difficulty adapting to a social environment. It was named Asperger’s syndrome. Both autism and Asperger’s fall under the category of pervasive developmental disorder.

People with Asperger’s also exhibit a range of behaviors, including fixation with a single topic, difficulty understanding abstract concepts, repetitive rituals, socially inappropriate behavior, and lack of coordination. Many such children have a high level of vocabulary. They’re often described as “eccentric.”

In some children with autism, the behavioral signs are subtle; in others, they’re easy to see. “People think about the worst-case scenario,” Dr. Conlon says. “No language, doesn’t interact, never makes eye contact. That’s the rarity these days.”

As babies, William and Elizabeth liked to steal each other’s bottles and toys. Elizabeth laughed at her brother when he rubbed food all over his face. They sat next to each other and played. When Elizabeth was sad, William cried.

Both crawled by six months—earlier than many. Elizabeth liked looking at tags on pillows. She’s going to be a reader, Julie thought.

Julie and Joe took the kids on a winter trip to Rehoboth Beach, where William and Elizabeth enjoyed the hotel’s indoor pool and Elizabeth tasted her first Krispy Kreme doughnut.

By ten months, Elizabeth had started saying “Daddy.” William knew “Mama,” then “cool” and “hot.” Elizabeth walked at a year, a month later than her brother. Around that time her eyes changed from blue to gray.

Fifty people came to celebrate their first birthday. Elizabeth and William scooted around in carts. William said “ooh” and “aah” after every gift was opened.

Elizabeth fell asleep eating cake, and Julie took pictures of her covered in chocolate.

When Julie saw a Washington Post article this September about a study linking autism in children to the age of the father, she sent Joe an instant message.

The study showed that the chances of having a child with autism are five times greater for a father in his forties than for a father in his twenties, and nine times higher for a father in his fifties.

“Did you read it?” she asked.

“Yup, I read it,” he said.

She dropped the subject. She didn’t want Joe to think she was blaming him.

Julie had always thought it was unfair that older women had to worry about having children but older men didn’t. She’d never considered Joe’s age an issue, and doctors hadn’t mentioned it.

“You want children so badly, and time clicks away,” Julie says. “You don’t really sit down and think that these things can happen.”

Joe didn’t get upset when he heard about the age study. He’d heard lots of explanations for autism: The mercury once contained in the measles, mumps, and rubella (MMR) vaccination; lead levels in the air from the cars driven while he was growing up; mercury exposure from coal-burning power plants.

“When people look at the Strom Thurmond and Hugh Hefner types having healthy children, they think it must be okay for guys,” Joe says. “That may not be true.”

Autism researchers continue to focus on brain structure. A study by the University of California at Davis’s MIND Institute—the acronym stands for Medical Investigation of Neurodevelopmental Disorders—showed that males with autism have fewer neurons in the amygdala, a part of the brain associated with emotion and memory. Autism has also been linked to rapid brain growth during infancy.

A study released in June by the Yale University School of Medicine found differences in the placentas of children who fall on the autism spectrum, prompting the headline test could spot autism at birth.

Julie still believes her kids’ problems are connected to the MMR vaccine they had when they were a year old. Even if genetics are a factor, she says, the mercury in that vaccine and others since probably triggered the autism: “Why would anyone put a known neurotoxin in someone’s body?”

Thimerosal, the mercury-based preservative used in the vaccine, has been the subject of debate for a decade. Many large-scale studies have disproved a link between Thimerosal and autism. Last April, nearly 1,000 people gathered in DC for the Mercury Generation March, lobbying for more research. The FDA reports that Thimerosal has been virtually removed from almost all vaccines for kids under seven.

Joe isn’t sure why his children have autism. Early on, he blamed the vaccine. Now he wonders if it’s a combination of factors, including genes. He has no regrets.

“There’s no undoing something you did yesterday,” he says. “You can’t stop living because of all the risks involved.”

In December 2002, when she was 18 months old, Elizabeth stopped responding when Julie called her name. Elizabeth liked looking out the window. She liked watching wheels spin.

Julie didn’t know much about autism: She thought children who had it banged their heads against walls and bit people.

Soon after Christmas, Elizabeth stopped coming to her parents for hugs. She was more interested in watching things in motion than she was in people. She seemed confused, like the Alzheimer’s patients Julie helped in the nursing home. William was playing with wooden trains and putting puzzles together.

That May, the family took a two-week trip to Illinois for the wedding of one of Joe’s sons. In the months before they left, Elizabeth could sing along with “Wheels on the Bus.” She could dance like a ballerina.

On the trip, she cried a lot. She stopped eating with a spoon. She clenched her hands together and rolled her eyes. She stopped saying the words she’d learned, like “ball” and “good girl.”

Julie asked other parents if their children had ever lost their language. “Yes,” one mother told her, “my son just decided he wasn’t going to talk for a while, then started again.”

“All right!” Julie said. “Did you hear that, Joe?”

She sang “The Ants Go Marching,” hoping Elizabeth would sing the “boom, boom, boom” in the refrain as she always did. Her daughter stared at her.

When Julie looks back at photographs of William and Elizabeth, the professional shots where they’re sitting together, she can see their transformation.

“The first year, they looked right at the camera,” she says. “The second year, she’s looking over to the side, and he’s looking straight on. The third year, we couldn’t get either one of them to look.”

About 30 percent of children with autism go through a regression, losing some of the skills they’ve developed.

“In some children with autism, development looks relatively okay but then begins to derail,” says Dr. Rebecca Landa, director of the Center for Autism and Related Disorders at Baltimore’s Kennedy Krieger Institute. “For some children there are telltale clues at 14 months that help us predict whether the child will have an autism outcome. But it’s hard to predict the kids who are going to have a regression.”

Until recently, some members of the medical community weren’t convinced that children regressed. They argued that parents must have missed the signs.

University of Washington researchers studied 56 home videos of children’s first- and second-birthday parties. Among the findings: They saw two-year-olds with symptoms that hadn’t been visible a year earlier. At 12 months, children diagnosed with regressive autism used complex babbling and words more often than did those with early-onset autism.

“We can screen for autism early, but we have to screen at least until the child is three,” says Dr. Landa. “We don’t want to just screen a child one time around their first birthday and say to a parent, ‘You have a clean slate. Your child will never have autism.’ We’re just not there yet.”

Julie looked for reasons why Elizabeth couldn’t have autism: Speech comes more slowly for twins. Maybe she and William had their own language. Elizabeth had been born with torticollis: Her head was turned in the womb, causing the muscle on one side of her neck to be shorter than the other—and one side of her head was flatter than the other. Maybe that was the problem.

Julie called friends and relatives: “You don’t think this could be autism, do you?”

Elizabeth continued to stand in place and roll her eyes, making Julie wonder if she was having seizures. Julie and Joe took Elizabeth to a neurologist at Children’s Hospital in July 2003, when she was two. Joe waited in the hallway with William.

“Is it okay if I let her run?” Julie asked. Elizabeth ran toward the opposite end of the room, where the doctor was sitting, but didn’t look at him. She stopped and stood still, excitedly clenching her fists, then holding them in place.

The doctor asked Julie, “What’s your take on this?”

“I think it could be autism,” she said, “and I’m hoping it’s not.”

“You’re right,” he said. “It is. I don’t have to do any real tests with her.”

Julie felt sick.

The doctor explained that a typical child would acknowledge he was in the room, and what Elizabeth was doing was a form of self-stimulatory behavior. More behaviors would follow, he said. Elizabeth might walk on her toes or flap her hands.

“She is so beautiful,” the doctor told Julie. “She will bring you so many years of joy.”

Elizabeth is fussy, and Julie can’t figure out why. The swings and pool usually keep her happy in the summer, but she wants something else and can’t tell her mom what it is.

She rubs her hands on her Strawberry Shortcake outfit, meaning she doesn’t want to wear it. The weight and texture of clothing are uncomfortable for Elizabeth, so she likes to walk around naked; sometimes she takes off her diaper. Her dad calls her Miss August.

Julie sewed this outfit herself—as well as four others—with lightweight cotton material. She put the zippers in back so Elizabeth couldn’t take them off.

Elizabeth leads her mom upstairs. Julie pulls a box of Pop-Tarts from the cabinet, but Elizabeth pushes it away. She stands in front of the refrigerator and starts to cry.

“What do you want, baby?” Julie asks. “What can I get for you? A graham cracker?”

She doesn’t want that. Julie picks her up to comfort her, and Elizabeth presses her face against her mom’s, wrapping her mouth around Julie’s chin. Some people who have autism crave deep pressure, the feeling they get from touching or holding. The pressure calms Elizabeth.

“I used to get really upset and frustrated when she’d get this way,” Julie says. “Then I realized it wasn’t helping her any to have two of us crying.”

Elizabeth gives up on the food and walks upstairs to William’s room. She lies on his bed and wraps herself in a sheet, then puts a toy in her mouth and stares at the ceiling fan.

Joe thought the neurologist at Children’s Hospital was wrong about Elizabeth. Some kids are late bloomers or just slow. He didn’t talk to Julie about the diagnosis.

“After a while, there is no denying it, and you have to take a second look at what you’ve been thinking,” Joe says. “It doesn’t happen overnight.”

Julie cried to a woman from her church for two hours. “At least she’s happy,” the woman said of Elizabeth.

What does that mean? Julie thought. At least she’s happy? She may never be able to talk.

Julie had always thought her kids would go to college. She’d pictured Elizabeth in the Little Miss Greenbelt Pageant singing “Somewhere Over the Rainbow.”

Now nobody could tell her what her daughter would be like in five years. There was no prognosis.

How could she have tried so hard to get pregnant and then have this happen?

“I’d be really mad at Joe because he wasn’t as sad as I was,” she says.

Joe lost his mother in his twenties; his father died of a heart attack soon after. Joe had a heart attack at 45, 15 years ago, and overheard a doctor say he had five to ten years to live. He’d learned to cope—turning to religion helped.

Soon after the diagnosis, Julie’s minister asked if she could come over. One day as Elizabeth slept, the minister laid her hands on the girl and prayed.

Julie thought William would be her little Einstein. He could recite the alphabet and count to 25 before he was two.

The plan was for William to start kindergarten at St. Hugh’s, a Catholic school connected to the parish Joe belongs to. William would go to DeMatha High School in Hyattsville, as one of his older half brothers had, then he’d study music or technology.

As Elizabeth was losing her language, William was learning hundreds of new words, like hippopotamus and umbrella. He knew train types: steam engine, diesel engine, gondola, boxcar.

But Julie started noticing oddities in his speech. Sometimes he sounded like a parrot: She’d ask, “Do you want a drink?” He’d respond, “Do you want a drink?” He’d use the same inflections as television characters­—even a British accent. His speech seemed scripted, and he couldn’t hold a conversation.

Julie knew there was a chance William had autism. Studies show that a sibling of someone with autism—including a fraternal twin like William—has an 8-to-10-percent chance of having it. Identical twins have concordance rates as high as 90 percent, one reason researchers are confident that genetics play a role in autism.

Julie started writing down all of William’s words: How could he have a developmental disorder when he knew so much? She thought children with autism couldn’t speak—like Elizabeth.

She worked on flashcards with William as he lay in bed. She taught him the planets’ names and had him count coins until he fell asleep.

Sometimes Julie watched William as he slept. She had read that autistic children were diagnosed before they were three, so every morning she was eager to mark another day off the calendar.

We’ll make it through, she told herself. She felt as if she were sitting with a time bomb.

Most children show signs of autism by the time they’re 18 months old: A child might not gaze into a parent’s eyes, or might not smile back at someone.

“Typically developing babies are very engaged and interested in what you do,” says Dr. Rebecca Landa, who is researching autism in infancy. “Even at six to nine months, babies make an effort to get people’s attention.”

The National Institute of Child Health and Human Development publishes a list of possible “red flags” for autism. Among them: The child has poor eye contact, doesn’t respond to his or her name, doesn’t point or wave “bye-bye,” gets “stuck” doing the same things over and over.

A child doesn’t have to meet all the criteria. Someone can exhibit physical mannerisms and not have autism. Someone can have autism and make good eye contact.

Some parents hesitate to take their children to be screened because they aren’t seeing the “autistic” behaviors they expect. Others don’t want to believe their instincts.

“I wish people would get beyond thinking their child has to be 100-percent perfect,” says Julie. “I think they’re afraid, like I was afraid, to bring it up. If Elizabeth had cut her leg, I would have called a doctor immediately, but instead I see her crying and acting a little off and maybe staring into space—and those things I don’t do anything about.”

Although symptoms of autism typically appear before a child is three, many are diagnosed later. Researchers agree that children benefit from early detection. “We can actually teach two-year-olds with autism,” says Dr. Landa, who authored a study on development of infants with autism, recently published in the Journal of Child Psychology and Psychiatry . If children are diagnosed at 18 or 24 months instead of three or four years old, Landa says, they’re likely to have better outcomes.

Detecting autism in a child like William can be especially hard.

“Some may talk on time and show abilities like learning the alphabet, numbers, and how to match things, and understand cause/effect relationships,” Landa says. “They learn these things at an earlier age than expected, so parents think they’re really gifted.”

As the twins’ third birthday approached, William was still repeating himself and imitating his parents. Sometimes when he was excited, he’d scratch his fingertips on the floor. He didn’t know what to say when other kids talked to him.

Julie knew something was wrong, but she didn’t think it fit the classic description of autism. Neither did Joe.

She asked Joe to take William to a doctor—her husband hadn’t been in the room when Elizabeth was diagnosed.

“I wanted him to feel the same thing I’d felt,” says Julie. “I wanted him to grasp what was going on, because I felt like he was in such denial.”

Joe made an appointment with Dr. Conlon from Children’s Hospital. Julie asked Joe not to tell the doctor about Elizabeth—she didn’t want him making any assumptions.

Conlon said he suspected that William was on the high end of the autism spectrum. With an autism diagnosis, Julie realized, he’d get better services at school. He could be in an autism kindergarten instead of a regular special-education class.

“Part of me never wanted the diagnosis because I thought he just seemed a little quirky,” Julie says. “But if he didn’t get the diagnosis, he’d fall behind.”

Julie knew a mother and father who were fighting their son’s diagnosis and sending him to an expensive private school where he wouldn’t be called autistic. The father had said, “That label will follow him around for the rest of his life.”

After her autism diagnosis, Elizabeth was tested for Fragile X, a genetic disorder resulting from a gene mutation that can cause autism. She had an MRI of her brain, an EEG to rule out epilepsy, and a hearing evaluation. Every test came back negative.

When she was two, Elizabeth spent a year in the infant-and-toddler program at Beltsville’s Frances Fuchs Early Childhood Center before starting an all-day autism program with five other children. Her speech wasn’t improving. She had bladder infections, then kidney problems that went undetected for months because she couldn’t tell her parents what was hurting. She had started running from people—children who do this are often called “elopers”—a habit that scared Julie. Joe cried when he had to put a canopy over Elizabeth’s crib to keep her from getting out.

At school, Elizabeth learned to sort items into piles. She sat in her chair when she was supposed to. She starting using the Picture Exchange Communication System: A teacher showed her cards with pictures of food on them, such as Cheerios, and she was able to pick the one she wanted and hand that card to the teacher. Then the teacher gave her the food she’d asked for. Teachers at school called her “the smiling child.”

Elizabeth’s teacher recommended Floortime, a developmental therapy focused on child-directed interactions, introduced by Bethesda psychiatrist Stanley Greenspan, author of The Child With Special Needs . Greenspan believes that the therapy helps children learn to relate, communicate, and think. A parent or therapist spends 20 to 30 minutes interacting with a child on the floor in a play setting, following the child’s lead.

If Elizabeth wanted to communicate something, she’d have to get Julie’s attention. Floortime would create a back-and-forth.

Julie wants to find a buddy for William, someone he can talk to and learn from. When she sees a friendly child in the grocery store, she’s tempted to ask his parent, “Can he come over?”

William tries to play with Elizabeth, but she ignores him. If he puts his arms around her, she usually walks away.

In July, Julie took them on their first Metro ride, which William enjoyed, but Elizabeth plugged her ears and cried. A fear of sirens used to keep William from going outside; Elizabeth has trouble with loud mechanical noises. Sometimes it’s not the noise that bothers them; it’s the pitch.

Like many children with autism, they don’t like how certain foods look and feel. William likes potato chips, bread, cereal, and cheese and crackers, but the cheese has to be yellow. He stopped eating meat and peanut butter last year, so Julie puts a protein supplement in his milk. He won’t eat bananas, yogurt, or ice cream.

“It’s a texture thing,” Julie says. “He’ll put it in his mouth and start to chew it, and he can’t deal with it. If he watches someone else eating those things, he’ll get sick.”

His favorite meal is McDonald’s fries. Elizabeth won’t keep food on a plate and doesn’t use utensils. She’ll take a handful of William’s fries, eat a few, and throw the rest on the floor.

William occasionally takes his sister’s wrists and pulls her around. “Come on, Liz, come on,” he’ll say. “Ring around the rosie.”

“Joe and I have thought, ‘Should we stop him or shouldn’t we?’ ” Julie says. “We usually let it go until she tries to make him stop. I think it’s important that at least he try, and at least she try.”

When Elizabeth fell in the living room, William started crying: “What happened? What happened?” At school the next day, he said, “Her head. She hit her head. She hit her head. She hurts. She’s crying.”

If Elizabeth sounds as if she’s speaking, William praises her the same way her parents do. “Good talking!” he’ll say.

People tell Julie she’s lucky her kids don’t fight. Sometimes she’d rather they did.

After William was diagnosed in January 2005, he went through a screening and evaluation process called Child Find, which helps identify and refer children who need early intervention or special education.

The Child Find evaluators weren’t convinced William had autism. They placed him in a half-day special-education class at Francis Fuchs, Elizabeth’s school, with students who didn’t have autism. They wanted to see how he’d do.

William clung to Julie for the first week. He dropped to the ground and yelled, “Mommy, Mommy, don’t leave me!”

When Julie took him to Columbia Mall that summer, he couldn’t stop crying because of the noises and lights. A girl who worked there asked, “Does he have autism?”

Julie liked to think it wasn’t that obvious.

“Yes, he does,” she said.

“I could tell,” the girl said. “He doesn’t like those loud noises. Well, he’s still really cute.”

Julie couldn’t understand why people seemed surprised that a child with autism was cute.

At the end of the school year, William was still anxious when his mom dropped him off. He was doing more of his mannerisms—turning his hands inward and rubbing them against his stomach. Julie and Joe asked Dr. Conlon if medication or a change in diet might calm him. Conlon said yes but that medications came with side effects.

They decided they’d wait to see how William did in school that fall in an autism class with Timi Gray, his new teacher.

In the spring of 2005, Julie called Easter Seals to inquire about a program called Family Friends, which pairs older volunteers with families who have children with special needs.

That June, Julie met Ginny Jones, their “family friend.” Ginny, 59, had moved to Bowie and remarried. She didn’t know much about autism but wanted to work with kids.

As soon as they met, Elizabeth held Ginny’s hand and gave her hugs. William was scared—he kept saying “goodbye”—but Ginny assured him she wouldn’t touch him. The following week, William was showing her caterpillars. A week later, he told Julie, “She’s a fun lady.”

Ginny visits once a week. She pushes Elizabeth on the swings. William gets her to play “Sidney the Spider,” a tickling game. He takes pictures on her digital camera—she says he captures things she doesn’t see.

Ginny goes to the kids’ medical appointments with Julie and helps distract them. When Julie was nervous that William was bothering people in a waiting room—she often notices people staring—Ginny said, “Who cares what they think?”

Two summers ago, Julie took William and Elizabeth to Ginny’s house to go swimming. Ginny’s five-year-old granddaughter, Valerie, wanted to play with William.

“Grandma, he won’t talk to me,” she said. “I tried to get him to play, but he won’t.”

“William’s just very shy,” Ginny said. “When he’s ready, he’ll talk to you.”

Valerie walked over and said, “William, it’s okay—you can talk to me. Don’t be shy.” He didn’t say anything.

The next day, William was playing with two Little People toys, pretending they were talking to each other.

He made one say, “Don’t be shy. You can talk to me. Don’t be shy.”

The other responded, “I’m not shy.”

In 1999, Timi Gray was teaching children with disabilities in Prince George’s County when she was selected for a seven-week autism training. The county was creating autism programs and planning to start one at her school. They’d need a teacher.

Gray’s students had speech and language delays as well as learning disabilities. She had never met a child with autism. “They just came out of nowhere,” she says.

Once Gray started teaching kids with autism, she didn’t want to stop: “I would have six kids in the class all going their different ways, all in their own little world. That’s what made it challenging—I wanted to reach them.”

When Gray met William in the summer of 2005, he was shy and anxious. He followed along but rarely took part. He sat quietly. He’d say “fire truck” if he wanted one, but he was too nervous to get it himself.

“There was something about him that I had to get to the bottom of,” Gray says. “I knew he could do things, but I knew he was scared. So if I could just get him to feel comfortable, he’d be fine.”

Julie and Joe each came to the classroom to show William that school was a cool place. During one-on-one drills, Gray noticed that William wasn’t performing simple skills, such as putting beads together.

Julie videotaped William doing those tasks at home.

“He was talking to Julie and doing everything she said and answering her questions,” Gray says.

She started using the same language Julie did, and William recognized it. Gray realized that the tasks on William’s Individualized Education Program, a learning plan given to special-education students, were too easy for him.

“I didn’t push him,” she says. “I just took my time, and slowly he came out.”

Julie often thinks she hears Elizabeth say something, but because the words aren’t clear and her voice is soft, it’s hard to be sure. Elizabeth’s teacher said she talks when she’s frustrated—when a classmate had a ball she wanted, Elizabeth said “ball.” She yelled, “Daddy! Daddy!” during a blood test.

She was sitting at the dining table a year ago when Joe heard her say the first seven letters of the alphabet.

“It was out of the clear blue,” he says. “That’s the way her speech comes. You wonder: What the hell triggered that?”

Doctors tell Julie that the sounds are a good sign. “If she’s able to say it, it’s in there,” Dr. Conlon says, “but why aren’t we able to get it out?”

Julie used to look for the magic bullet. She was inundated by Internet claims: This therapy works! Try this diet!

She researched everything from Applied Behavior Analysis, a widely used set of principles that involves repetition and rewards, to nutritional therapies such as a gluten-and-casein-free diet, which eliminates proteins found in wheat, rye, oats, barley, and dairy products.

She read about “crystal children,” said to be highly sensitive children with penetrating eyes and delayed speech patterns who communicate telepathically.

“I think it’s parents grasping for anything to feel better,” says Julie. “I worry that it’s just a slippery slope away from tarot cards and paying people to come to your home and light candles.”

She saw a story on the Today show in 2003 about a little girl with autism who had starting talking at age three. The girl, Ashley, had been treated at Bethesda’s Spectrum Center, where she participated in the Tomatis Method of Auditory Training. The therapy, introduced in the 1950s by French physician Alfred Tomatis, is designed to reawaken the ear’s ability to listen. Using headphones, Ashley listened to music by Mozart as well as recordings of her mother’s voice, meant to simulate what she had heard in the womb. After two days of therapy, Ashley told her parents, “I want a cookie.”

Julie called the Spectrum Center that morning. She thought: This is my answer.

She signed Elizabeth up for Tomatis, but the $7,000 fee was steep, and insurance wouldn’t cover it. In the end, she and Joe decided against it. The same therapy wouldn’t work for everyone. And what if they found a way to pay for it and nothing changed?

They’re still not sure they made the right decision.

Timi Gray kept a poster on the chalkboard with a picture of every activity William and his four classmates would do that day and a time slot for each: circle time at 10:15, story time at 10:30, bathroom and walk at 11.

“The routine gives them security and stability,” Gray says. “When they come in here, they know what to expect.”

The structure helped William relax at school, but he still threw tantrums with his parents. His life wasn’t as regimented at home as it was at school.

Early in the school year, Gray suggested that Julie try a “first and then” board: Julie drove to places she typically takes the kids—the grocery store, the gas station, McDonald’s, and Target, William’s favorite. She took photographs of each place. She wrote the words “first” and “then” in big letters. She clipped them to the appropriate card.

“First we’re going to go to the gas station, then we’re going to go to the Target,” she told William.

“The anxiety and tantrums went out the window,” Julie says. “That was a wonderful day.”

Soon William didn’t need the cards. Gray encouraged Julie and Joe not to put him on medication—she said a drug might take his personality away.

It wasn’t long until William was waking up in the morning excited for school. “Let’s go see Miss Gray,” he’d say.

He started walking to the playground with a boy in his class. Sometimes he’d pretend he didn’t know an answer, just to see Gray’s reaction.

He picked words up quickly. Gray saw William point to the bottom of the doorway and ask his mother, “What’s that? What’s that?”

The next day at school, he picked up a truck, carried it to the doorway, and rolled it.

“Look, Ms. Gray,” he said. “Garbage truck over the threshold.”

Sometimes Julie has to ask William to stop playing on the Hot Wheels Web site so his sister can use the computer.

Elizabeth likes Reader Rabbit touch-screen games. She puts her face to the monitor and uses Julie’s finger to drag shapes into the spaces where they belong. She gets excited and clenches her fists.

One day last summer, Elizabeth didn’t ask for her mom’s hand. She put her own finger up to the screen and moved the shapes. “So good, Lizzie,” Julie said, tears in her eyes. “So good!”

Julie and Joe are relieved that Elizabeth is making progress again. Last year her teacher didn’t use touch-screen computer programs. She was stern with the kids—behavior Elizabeth wasn’t used to. Julie noticed her daughter changing: She would come home from school with her fingers in her ears and pull away from people.

Julie spent much of the summer doing Floortime with Elizabeth while William went to school with Gray. Every few weeks Julie and Elizabeth went to see Jake Greenspan—Dr. Greenspan’s son—for Floortime therapy sessions and parent coaching. Elizabeth liked having her mom to herself. She started showing Julie what she wanted to play with.

They listened to music and danced. Julie turned song lyrics into rhythms as they jumped up and down on the bed, and Elizabeth bounced to the beat.

Elizabeth started to laugh again as she had before. One morning in September, Julie and Joe awoke at 5 am to a little voice coming from down the hall.

“Twinkle, little, little star,” Elizabeth sang. “Dooka, dooka, dooka doo.”

There is no cure for autism or standard medication to treat it. Medications that treat other disorders—including anxiety, depression, and hyperactivity—can sometimes help alleviate symptoms and behaviors associated with autism. These include Prozac, Zoloft, and Ritalin. Risperdal, an antipsychotic medication, recently became the first drug approved by the FDA for the treatment of behaviors associated with autism in children and teens, including agitation and aggression.

Dr. Stephen Mott, chief of Georgetown University Hospital’s pediatric neurology division, credits the synthetic steriod Prednisone—not commonly used in patients who have autism—with helping nonverbal children start to talk.

Over the past seven years, Mott has prescribed the drug—often used to treat asthma, allergic reactions, and autoimmune diseases—to about 100 patients. Seventy percent showed improvement within eight weeks: Nonverbal children spoke. Patients who couldn’t put words together started using complex sentences. Some made better eye contact. A few bounced back from regressions.

Prednisone can cause serious side effects, including suppression of the immune system. A simple infection could become life-threatening.

Mott mentions Prednisone to patients in his list of treatment options, but he doesn’t push it. “It hasn’t undergone scientific scrutiny,” says Mott, who has treated patients with autism since the early 1990s. “I make that clear to families.”

Do the changes last?

“That’s the big question,” he says. Most patients continued with a lower dose, then the drug was tapered off. Of the 70 percent who improved early on, half later regressed to some degree. The other half kept getting better.

Julie used to wake up in the middle of the night with her heart pounding. She takes over-the-counter medication to help her sleep.

She misses going to church. She stopped because she didn’t feel William and Elizabeth were welcome at the Sunday service, and the church didn’t offer babysitting for special-needs children. Two women changed seats to get away from William.

Still, Julie considers herself fortunate. Some parents of children with autism don’t get to cuddle with them because their children don’t like to interact. Some kids hit people or try to injure themselves. Julie’s kids give her hugs. She’s trying to teach William what it means to say, “I love Daddy.”

The same thing that made her mad at Joe after Elizabeth’s diagnosis is what helps her now—his strength.

“He had a wonderful thing his father once told him,” Julie says. “ ‘You have to take care of your family—that’s just the way it is. You just do it.’ ”

The divorce rate among couples who have a child with a disability is higher than the average; there are estimates as high 80 percent. The stress is sometimes too much. Some spouses disagree on medical treatments.

“It’s hard enough for two people to take care of one disabled child,” Joe says. “Imagine one person taking care of two.”

He and Julie don’t agree on everything. She wanted to buy a harness for Elizabeth—William once ran away, and Julie caught him just before he reached a busy street—but Joe refused.

“He says it makes her look like a child on a leash,” Julie says. “My point is safety.”

Money is tight. Elizabeth and William are on a long waiting list for the Maryland Autism Waiver, which would make them eligible for respite care, medical coverage, and other services. Julie and Joe are hoping the waiver will help cover diaper costs, bars for the windows, and augmentative communication—a method that would allow Elizabeth to arrange pictures on a board to form sentences. They also want a new bedroom door with a Plexiglas window for Elizabeth, so they can close the door at night and let her sleep in a regular bed.

Julie and Joe have had five date-type nights out in five years. Elizabeth needs to be watched carefully: She once took a bite out of a wine glass. She likes banging pictures that have black in the frames.

The Arc of Prince George’s County, an organization that helps people with developmental disabilities, will provide assistance such as reimbursing families for a babysitter, but Julie and Joe say it’s hard to find someone they can trust. Two of William and Elizabeth’s godparents—a couple with whom Julie and Joe hoped to leave the children if something happened to them—stopped calling soon after Elizabeth’s diagnosis.

“Let’s play movies,” William says. It’s a summer afternoon, and he’s eager to sit inside the makeshift theater his mom created—a small tent covered with a bedsheet.

Julie is getting William ready to go see the animated movie Cars with his dad in a real movie theater. The last time William went to a movie, he got scared, and they had to leave. This time Julie wants him to know what to expect.

She crawls around the living-room floor gathering toy cars. “I hope we have all our characters here,” she says. “Nope—we’re missing Porscha.”

“You comfortable?” she asks.

“Comfortable,” William says. “Com­fortable.”

She sets the scene: “William is at the movies. He’s with his daddy. He’s got his popcorn and his soda, and it’s going to get dark.”

She puts her hands under the sheet, as if at a puppet show. She gives each car a different voice and makes up dialogue.

William claps at the end and says, “Let’s watch it again! Let’s watch it again!”

A few weeks later, when Joe opens the door to the theater, William won’t go in. He wants to stay in the hallway. He doesn’t want popcorn.

Joe props the door open and sits in a spot where he and William can see each other. William comes in for previews, then leaves when Cars starts. It’s too loud.

Joe waves to him and checks on him, but he doesn’t want to move.

“Is he okay?” an employee asks

“He’s just a little shy,” Joe says.

William watches from the hallway for an hour before he says, “Let’s go home. I wanna go home.”

Joe’s happy. That’s longer than he’d expected.

At the end of last school year, Julie and Joe gave Ms. Gray a ring with a blue sapphire, the color of William’s eyes.

They’re thrilled with how far William has come since he started working with her and her support staff. He rarely throws tantrums. He went to a birthday party for the first time. He lets someone cut his hair.

When the family vacationed in Wisconsin in August, he went on a carousel and rode with Joe in a go-cart—things that used to terrify him. He won a second-place ribbon in Greenbelt’s Labor Day festival for a photograph he’d taken of a gazebo’s patterned-wood floor.

William made it through three innings of an Orioles game with Joe in September but wanted to leave after a player cracked his bat. He thought the batter would be upset.

“He broke the bat, he broke the bat,” William repeated. The cheering overwhelmed him. Sometimes William confuses his emotions: He’ll cry when good things happen—like when Jeff Gordon, his favorite NASCAR driver, wins a race.

He used to refer to himself as William, but he’s starting to use pronouns. He came home from school in the summer and showed Julie a piece of paper he was supposed to read. It had the words i see my written on it four times, with different pictures to end each sentence. Then he sounded out the words: “I see my backpack.”

When William broke a plastic racecar in September, he told his mom that Elizabeth had done it. He was nervously shifting his weight around.

Julie knew the truth­. She told William it wasn’t right to blame someone else for something he had done. She didn’t let him see how excited she was: He’d fibbed for the first time.

Julie drove William to see his new school, Beltsville Elementary, so he wouldn’t be surprised on the first day.

He talked himself through the change, the same way he’d seen Elmo do it on a back-to-school episode of Sesame Street: “Give Mommy a hug, say goodbye, and she’ll pick me up in the green van,” he said.

Gray told Julie that “self-talking” helps William figure things out. He verbalizes what other people do in their heads.

The first day, Julie put William’s backpack on him and he said goodbye. I can’t believe that just happened, she thought.

Julie came home to an empty house and didn’t know what to do. Elizabeth had taken the bus to her new school—Margaret Brent Regional in New Carrollton, a special-needs school where she can go until she’s 21.

William’s teacher sent home a note that day saying she thought he belonged in a regular kindergarten. He could do the same things other five-year-olds were doing except use the bathroom. William likes to sit, wipe, and flush, but he won’t actually go. His parents and his teachers are working on that.

Julie had hoped to have William in a mainstream class in a year or two, but she didn’t think it would happen so fast. He’d never been around typical kids. “It’s exciting but scary because he’s gone from this little quiet kid throwing up to just being so normal overnight,” says Julie. “It’s a shock. I want to just grab him and say, ‘Are you really sure you’re okay?’ ”

The teacher said the transition would be slow. He would have a classroom aide.

That night Julie told Joe, “We may actually have to think about saving for college.”

Julie has read that many adults with autism don’t marry. Why wouldn’t William get married? she thinks. He’s good-looking, smart, and funny: One morning he got out of bed and told her, “I’m not the Jedi I should be.”

She wonders whether William will live on his own or get a good job. She worries that people will take advantage of Elizabeth because she’s pretty and vulnerable. She and Joe are hopeful that if something happens to them, William can help care for his sister.

There’s no typical path for a teenager with autism. A low-functioning teen, with mild retardation, may continue to exhibit behaviors of a young child. A teen who is high-functioning might do well academically but struggle socially.

“I remember one child who had straight A’s and was an excellent brass player, but he did not have one friend,” Dr. Mott says. “He was fine with that. Some want to know why they don’t have friends and what a friend is, but there are others that are content with solitary behaviors.”

Some teens are teased and bullied. They don’t understand jokes or sarcasm and have trouble processing more than one thing at a time. Others blend in.

“Middle school is particularly hard because kids are getting to be so social,” says Roy Richard Grinker, author of Unstrange Minds: Remapping the World of Autism, out in January. “Kids with the social deficits of autism have a hard time functioning.”

Grinker, a George Washington University professor, has a 15-year-old daughter with autism who attends school in Montgomery County. “High school is much better,” he says. “The kids are more mature. They understand what autism is. The rise of autism awareness isn’t just some sign of crisis—it’s a sign that we’re finally understanding what all these people are like.”

Julie has heard that you can “test out” of autism—which she hopes might happen to William—though she realizes he’ll never actually be cured.

“In our clinic, in a small minority of cases, we will say to people, ‘Your child really no longer meets the criteria for this disorder,’ ” says Dr. Lauren Kenworthy, director of the Center for Autism Spectrum Disorders at Children’s Hospital. “We’re not saying they are perfectly normal right now, but we’re saying they’ve made so much progress.”

Julie recorded the 2006 ESPY Awards, for the best performances in sports, because the award for best moment of the year went to a teenager with autism.

Jason McElwain, a high-school senior who managed the basketball team, made six three-pointers in the last four minutes of a game. His team had a big lead, and the coach asked if he wanted to play. Teammates carried him off the court.

Julie didn’t like the way the media referred to McElwain as an “autistic basketball player.”

“Would you call a child with cancer ‘the cancer child’?” she says.

She watches the show over and over: “Every time I see him, I think he looks like Will, and he has the same enthusiasm.”

She and Joe have met only one adult with autism—a man named Dennis who came to their house to look at a train collection Joe had listed in the paper.

Julie introduced herself, and Dennis averted his eyes. He looked like a college professor. He worked at NASA.

Sometimes Dennis spoke Latin. He talked to Joe about Poland, where Joe’s ancestors are from, and about God.

“He spoke like you could jump into his world and know what he knew,” Julie says. “That’s what William does.”

Julie had an uneasy feeling around him, which made her mad at herself.

Dennis was fascinated when Julie said her kids had autism.

“William, did you ever do this?” he asked, patting his head. “When I was your age, my thing was patting men’s heads. I was told it wasn’t socially acceptable.”

Julie had mixed emotions about the visit. Here was an intelligent man making it in the world. But he was a landscaper.

“When he said he worked at NASA,” Julie says, “I thought he was an engineer.”

The water in Ginny’s pool is cold, but William and Elizabeth don’t mind. William helps blow up his Cars floaties for his arms, gets in, and does his scary shark voice.

“Washing machine!” he says. Ginny lifts him up and down as she sings, “Washing machine, washing machine, we have to make the clothes all clean.”

Elizabeth splashes in the water like any little girl who’s big enough to stand but doesn’t know how to swim. She jumps off a low ledge just as William does. She opens her mouth and keeps swallowing water.

“De-licious!” William says.

When Elizabeth takes her floaties off, William brings them to her. “She needs to have them on,” he says. “Put them on, Lizzie.” Ginny tells Julie to let Elizabeth swim without them: She’ll be fine.

Julie looks around and sees Elizabeth playing without her floaties and William wearing goggles that make his nose look funny.

She can’t stop laughing. It’s the first time she’s felt this relaxed in a while. Her kids are having fun in a swimming pool, doing what kids do.


Cindy Rich
Cindy Rich came to The Washingtonian in 2001 from NBC News. A 1998 graduate of the University of Virginia, her recent stories have included “Something Happened and We Don’t Know Why” (November 2006), “I Never Even Saw Him” (June 2006), “Two Hearts Beating as One” February 2006), “How I Saved My Life” (November 2005), “How Many People Did You Kill?” (August 2005), and “A Warrior in Two Worlds” (September 2004). She is the editor of Washingtonian's wedding guides.Rich has received numerous Dateline Awards from the Washington Society of Professional Journalists, including an award for investigate reporting for her November 2004 story “How Teens are Getting High.” Her January 2003 story “When Jared Stopped Smiling,” about a friend’s suicide, was named a notable essay in The Best American Essays 2004.Rich, who grew up in Montgomery County and went to Walter Johnson High School, lives with her husband in Silver Spring.
13. Dec 2006
Recently Published

Articles: (Show Last 20)
March 2004 Bambu
February, 2005 Dirt Cheap Eats: Black Market Bistro
March 2004 Tastee Diner
Two Hearts Beating As One
Secret Life of Teens: Facebook - Cops + Facebook= Busted
Secret Life of Teens: Facebook - The Trouble with Facebook
Secret Life of Teens: Facebook - What's in a Profile?
Happy Hours
February 2005 Dirt Cheap Eats
March 2004 Dirt Cheap Eats
Growing Up Marriott
The Comeback Kid
Secret Life of Teens: Facebook - 5 Groups Explained
Secret Life of Teens: Facebook - Prom Dates and "Poking"
Secret Life of Teens: “Coolest Thing Ever”
Secret Life of Teens: Beyond High School
Secret Life of Teens: Youth Culture
Secret Life of Teens: Voices
Secret Life of Teens: School Daze
Autism and Childhood Development
Secret Life of Teens: Meet Marcus
Secret Life of Teens: Boy Meets Girl
Secret Life of Teens: Meet Caroline
Secret Life of Teens: Teens on Family
Word Magic
Secret Life of Teens: Kids Gone Wild
The Babies of 9/11: “I Don’t Want It to Define Him”
The Babies of 9/11: “We Have to Be Thankful”
"Marriage is Not for Sissies"
The Babies of 9/11: “That Boy Is Going to Be Special”
Feel Good Look Good: Best and Worst DC, VA, and MD Health Clubs
Great Places to Work: The List
The Babies of 9/11: “Wise Beyond Her Years”
The Babies of 9/11: “You Think the World’s Coming to an End”
The Babies of 9/11: “Do You Know What a Miracle Is?”
Bailey and Me
Babies: Popular Baby Names
Breast Cancer Survivor Given More then One Chance
2006 Great Places to Live: Alexandria
2006 Great Places to Live: Arlington
Waiting For A Miracle
Deadly Triangle
A Warrior In Two Worlds
Getting High
Going Up
Buying an Engagement Ring
A Leader in Giving: “How Much Are the Marriotts Giving?”
Apprentice's Kwame Jackson Turns Fame into Success
Fatal Accident: I Never Even Saw Him
Flying High
Easy Living
Local Television News Stars
"How Many People Did You Kill?"
Twins Born Attached Now Living Separately
This Side of Rockville
Secret Life of Teens: Meet Tim
Miracle Girl
When Jared Stopped Smiling
Believe in Magic
Children's Comedy in Silver Spring
Secret Life of Teens: Facebook - Can Yale see my Profile?
Articles: (Show All)
March 2004 Bambu
February, 2005 Dirt Cheap Eats: Black Market Bistro
March 2004 Tastee Diner
Two Hearts Beating As One
Secret Life of Teens: Facebook - Cops + Facebook= Busted
Secret Life of Teens: Facebook - The Trouble with Facebook
Secret Life of Teens: Facebook - What's in a Profile?
Happy Hours
February 2005 Dirt Cheap Eats
March 2004 Dirt Cheap Eats
Growing Up Marriott
The Comeback Kid
Secret Life of Teens: Facebook - 5 Groups Explained
Secret Life of Teens: Facebook - Prom Dates and "Poking"
Secret Life of Teens: “Coolest Thing Ever”
Secret Life of Teens: Beyond High School
Secret Life of Teens: Youth Culture
Secret Life of Teens: Voices
Secret Life of Teens: School Daze
Autism and Childhood Development


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