Harry Fisch- His advice? "If my son or daughter was to ask, I'd tell them to have kids early -- and that's before 30."

Yo, dude, check your bio clock -- now
New studies warn that it isn't just women who become less fertile as they age
Sarah Treleaven , The Ottawa Citizen
Recently, I've had a lot of conversations about baby-making with my male friends.

"I worry that I might be too selfish to ever have children," said my friend Joe, 29, somewhat pensively over gin and cucumber cocktails. Ditto for Colin, who just broke up with a woman he loves because she wants to have kids in the next few years and, at 35, he just doesn't feel ready yet. Kids or no, they both feel like they have all the time in the world to decide.

I, on the other hand, just turned 30 and have been making a lot of jokes about needing an apartment with a second bedroom for my soon-to-be-frozen eggs.



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Font:****Lots of women wring their hands about having a baby. Not only do we have to worry about our plummeting fertility (which begins to tank in our mid-20s), but we also have to worry about job retention and advancement once those kids (come biology, adoption or surrogacy) eventually appear. And it's the physical limitations of the female ability to procreate that have placed such a heavy emphasis on the reproductive biological clock, shaping the way many women live, work and even date.

But evidence is increasingly emerging that men, too, have a reproductive biological clock -- and that it ticks much more loudly than most of us have thought. Even as stories occasionally emerge about septuagenarian and octogenarian men becoming proud papas -- author Saul Bellow, for example, fathered a child at 84 -- several recent studies are challenging the conventional wisdom that men have an invincible ability to procreate.

A French study released in July found that women's pregnancy rates drop and miscarriages increase when the mother is over 35 and the father is over 40. Another study suggests that a man's fertility begins to decrease as early as his 20s. Researchers from the University of California at Berkeley and the Lawrence Livermore National Laboratory tested men between the ages of 22 and 80, and found that semen volume and sperm motility were both significantly compromised by aging.

Additionally, the increased odds for older fathers producing genetic abnormalities have been well documented, and studies have demonstrated that fathers over 40 are six times more likely to produce an autistic child than fathers under 30.

The numbers related to schizophrenia are similarly compelling. A study utilizing health databases in Jerusalem found that fathers over 40 were twice as likely to produce schizophrenic children as fathers who were under 25; for fathers over 50, the odds tripled when compared to fathers who were under 25.

Dr. Harry Fisch, director of the Male Reproductive Center at New York-Presbyterian Hospital/Columbia University Medical Center and the author of The Male Biological Clock, says that he's been ringing the alarm bell for years.

"There's a female biological clock; we all agree on the decline in fertility, more genetic problems and a decline in estrogen.

"The same thing happens in men -- a little bit differently, but essentially the same," Fisch says. "Why is it important? Well, demographically more men and women are waiting until they're over 30 to have a baby."
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Facing Autism in New Brunswick --A Father Who Wants to Know

Facing Autism in New Brunswick
Autism News and Opinion
Sunday, October 26, 2008

Autism, Parental Age and Birth Order
A study in the United States has found a link between higher parental age and the likelihood of first born children of older parents developing autism. The study, Advanced Parental Age and the Risk of Autism Spectrum Disorder, by Maureen S. Durkin, Matthew J. Maenner, Craig J. Newschaffer, Li-Ching Lee, Christopher M. Cunniff, Julie L. Daniels, Russell S. Kirby, Lewis Leavitt, Lisa Miller, Walter Zahorodny, and Laura A. Schieve is published in the advance access section of the online edition of the American Journal of Epidemiology, October 21, 2008.
The study defined "older" parents as mothers aged 35 or older and fathers aged 40 or older (maternal age 35, paternal age 40 years). The risk of developing ASD increased significantly with each 10-year increase in both maternal age and paternal age. Each 10-year increase in maternal age was associated with a 20% increase in ASD risk while each 10-year increase in paternal age was associated with a 30% increase in ASD risk.The study also confirmed earlier studies showing greater risk of ASD development amongst first born children of older parents:"The risk of ASD within each of 3 parental age categories (both parents "younger," 1 parent "older," and both parents "older") was highest among firstborn children and declined with increasing birth order" ....... The results of this study provide the most compelling evidence to date that ASD risk increases with both maternal and paternal age and decreases with birth order."
What I find curious is the greater risk of autism development amongst firstborn children given that the parental age will always be greater amongst the subsequently born children than amongst first born. The authors of the study offer no conclusion on this point but provide several existing hypotheses as possible explanations:The observation in this and at least 2 previous studies (2, 4) that the risk of developing ASD was highest for firstborn children and declined with increasing birth order is a pattern also observed for other childhood disorders, including type I diabetes and atopy, and is cited as support for the "hygiene hypothesis." According to this hypothesis, firstborn children are exposed to fewer infections from other children early in childhood and, because of delayed immunologic challenge, may be more likely to develop autoimmune responses including those that may adversely affect neurodevelopment (29). Another possible factor that could lead to the observed birth-order effect is exposure to potentially neurotoxic, fat-soluble chemicals accumulated in maternal tissue that have been passed to offspring transplacentally or through breast milk (30). Because of accumulation over a lifetime, the load of such neurotoxins transmitted might be expected to be highest for firstborn children, particularly when combined with advanced maternal age. Another possible explanation for the observed birth order effect is "stoppage" or a tendency for parents of 1 child with ASD not to have subsequent children because of the demands of parenting a child with a disability or concerns about genetic susceptibility (31), thus increasing the likelihood in the cohort as a whole that a child with ASD will have a low birth order. Information available for the present study did not allow examination of these hypotheses.
I was 42 when my younger son Conor, subsequently diagnosed with Autistic Disorder, was born. As an older father within the definition of this study I hope that this line of study continues to be explored objectively and professionally and is not derailed or distorted by the anger, from all "sides", that afflicts much public discussion of autism causes and treatments.
Anyone interested in following this issue in the "blogosphere" should check out the blog AUTISM PREVENTION FATHER BABIES 25-33 PATERNAL AGE IS A KEY IN NON-FAMILIAL AUTISMVaccines by concernedheart which is listed on my Autism Blog List in the right side bar of this blog. Concernedheart has been following this area for awhile and updates regularly.
autism
Sphere: Related Content

Terry Poling answers Paul Offit on Hannah's Autism and her Nine Vaccinations in One Day

LETTER TO THE EDITOR, NEW YORK TIMES


Vaccines, Autism and Our Daughter, Hannah


Published: April 5, 2008
To the Editor:

Skip to next paragraph
Related
Op-Ed Contributor: Inoculated Against Facts (March 31, 2008) Re “Inoculated Against Facts,” by Paul A. Offit (Op-Ed, March 31):

Our daughter, Hannah, developed normally until receiving nine vaccines at once. She immediately developed a fever and encephalopathy, deteriorating into what was diagnosed, based on the Diagnostic and Statistical Manual of Mental Disorders, or D.S.M. IV, as autism.

The federal government, not an “unusual court,” made the concession. The decision wasn’t “careless,” as your subheading called it. It was based on a thorough review of Hannah’s records by Health and Human Services doctors.

The National Vaccine Injury Compensation Program does rely on a “preponderance of evidence” standard, which Hannah’s case met. It doesn’t necessarily compensate families “quickly, generously and fairly.” We filed our claim six years ago, pain and suffering are capped at $250,000, and Hannah has yet to receive compensation.

Dr. Offit’s assertion that “even five vaccines at once would not place an unusually high burden on a child’s immune system” is theory and risky practice for a toddler’s developing brain. No one knows if Hannah’s mitochondrial dysfunction existed before receiving vaccines. Dr. Offit’s claim that Hannah had “already weakened cells” is unfounded.

We support a safe vaccination program against critical infectious diseases. We need straight facts, serious science and speedy answers on these important issues. Jon Poling

Terry Poling
Athens, Ga., April 3, 2008

The writers are, respectively, a neurologist and a lawyer and nurse.

signaling pathway involving the D4 subtype of dopamine receptor that is linked to the risk of ADHD, autism, schizophrenia and Alzheimer�s disease.

Thursday, March 20, 2008
Richard Deth, PhD - Methionine Synthase A Methyl B12-Dependent Redox Sensor in Neuronal Cells


There is a connection between autism, schizophrenia and Alzheimer's disease


"Dr. Richard Deth is a molecular neuropharmacologist and Professor of Pharmacology and at Northeastern University in Boston. His research interests are directed toward elucidating the molecular events that cause neuropsychiatric disorders in which impaired attention is a prominent feature.

Dr. Deth�s laboratory has discovered a new signaling pathway involving the D4 subtype of dopamine receptor that is linked to the risk of ADHD, autism, schizophrenia and Alzheimer�s disease. A key aspect of his work is the role of folate-dependent methylation reactions, including their regulation by dopamine and growth factors and their inhibition by neurodevelopmental toxins.

Dr. Deth is the author of a recently published book entitled: "Molecular Origins of Human Attention: The Dopamine-Folate Connection"."

Source: http://www.podcast.azcast.net

Researchers find high rates of copy number mutations in non-heritable forms of autism

http://www.the-scientist.com/news/home/52940/



Most of the mutations seen in the autistic children overall were deletions.


who said that human bodies are "less tolerant" of deletions. "When you're down to only your back-up copy for a gene, you're at greater risk for whatever minor defects may exist in that that gene." said Jonathan Sebat


-------------------------------------------------------------------------------------Increased paternal age and deletions are connected in the area of genetics known as point mutations.
-------------------------------------------------------------------------------------



Copy number linked to autismResearchers find high rates of copy number mutations in non-heritable forms of autism

[Published 15th March 2007 06:02 PM GMT]


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

Copy number variation could be an important factor in autism, according to a new study published in Science today (March 15).

The largest percentage of copy number mutations occurred in families with one autistic child, the so-called sporadic, or spontaneously occurring cases -- not in families with multiple autistic children, indicating genetic inheritance.

An Excellent Post on Vaccinations

Congratulations on your new baby! And Welcome to the War on Disease!
By Julie Obradovic
The Rescue Post


I have been wrong to exclude the influence of mercury and other ingredients of vaccinations in causing autism because I am so interested in the subject of how advancing paternal age is a cause of neurological and immunological disorders. Both increasing paternal age and the ingredients of vaccinations cause neurocognitive developmental disorders and detrimental effects.


http://www.youtube.com/watch?v=hq7FSYYVMEU

Do PR Firms Sell the Glamour of Older Fathering of Babies and For How Long Have They Been Doing This?

Terrific! Don't miss it."
--Molly Ivins
Publisher's Weekly describes Toxic Sludge Is Good For You as "a chilling analysis of the PR business...a cautionary reminder that much of the consumer and political world is created by for-hire mouthpieces in expensive neckties."
Since its publication in late 1995, Toxic Sludge has already gone into its sixth printing amid rave reviews. It's been featured on ABC-TV's Good Morning America, National Public Radio's Marketplace, and in scores of other radio, TV and print stories.


You've read the book, now see the video!WHAT REVIEWERS ARE SAYING
"A chilling expose."
--Tom Vanderbilt, Village Voice Literary Supplement, 11/95

"Toxic Sludge should appear on the short list of anyone serious about the study of public relations in the United States."
--Paul Swift, Public Relations Quarterly, Fall 1996

"An instant classic!"
--Norman Solomon, author

"Written with humor and outrage at the public relations industry's worst excesses."
--Utne Reader, January/February 1996

"A startling portrait of the poisoning of the American democratic process by the nation's professional spin doctors... exposes the bare-knuckled, invisible hand guiding and shaping public opinions."
--Will Fantle, The Progressive, 12/95

"A real eye-opener."
--O'Dwyer's PR Services Report, 10/95

"A font of knowledge on the anti-knowledge biz."
--Leslie Savan, Village Voice, 12/12/95

"A powerful indictment of an industry 'designed to alter perception, reshape reality and manufacture consent.' "
--Laura Castaneda, Dallas Morning News, 12/17/95

"Terrific! Don't miss it."
--Molly Ivins, author

"Revealing and motivating."
--Ralph Nader, consumer advocate

"Important ... unmasks how corporations manipulate our democracy."
--William Greider, author, Who Will Tell The People

"Exposes how far we've tumbled down the dark hole of 'Newspeak' that Orwell warned about ... it could be the flashlight to find our way out."
--Jim Hightower, author and commentator

"A well-written, enlightening look at a war of the powerful against society."
--Edward Herman, co-author, Manufacturing Consent

"Great book - I love it!"
--Bill Lutz, founder, Doublespeak Quarterly

"Helps us see corporate crime and media distortion up close."
--Jeff Cohen, Executive Director, Fairness & Accuracy In Reporting (FAIR)

"Powerful."
--Ben Bagdikian, author, The Media Monopoly

TABLE OF CONTENTS
Acknowledgments

Introduction: Torches of Liberty, by Mark Dowie

CHAPTERS

Burning Books Before They're Printed
The Art of the Hustle and the Science of Propaganda
Smokers' Hacks
Spinning the Atom
Spies For Hire
Divide and Conquer
Poisoning the Grassroots
The Sludge Hits the Fan
Silencing Spring
The Torturers' Lobby
All the News That's Fit to Print
Taking Back Your Own Back Yard
APPENDICES

PR Industry Leaders

The Clorox PR Crisis Plan

Suggested Reading

Notes


hat tip

The CDC Cannot Handle Drug Resistant TB and It Can Not Inform the Citizens of the USA that Advancing Paternal Age is a Robust Risk Factor for Autism

Speaker Contradicts CDC On TB Warnings
Border Patrol Did Not Stop Speaker

POSTED: 7:04 am PDT June 6, 2007


Andrew Speaker told a U.S. Senate panel Wednesday that he always fully cooperated with health officials and told them his travel plans, contradicting testimony from the head of the Centers for Disease Control, who said that he violated a sense of trust.

Speaker, a 31-year-old lawyer from Atlanta, caused an international scare after taking two trans-Atlantic flights to Europe for his wedding and honeymoon while infected with extensively drug-resistant tuberculosis.

He said he was told he was not contagious and was told he was not a threat to his wife or daughter. He also pointed out that he was allowed to continue working and going to court, despite his diagnosis.


Speaker was in Italy when health agencies determined he had XDR-TB, not just multiple drug-resistant TB........


..................................................................................


Family: CDC Said TB Patient Not Contagious
National Jewish Says First Two Sputum Tests Negative

POSTED: 11:38 am MDT June 4, 2007
UPDATED: 6:43 pm MDT June 4, 2007



DENVER -- The family of Andrew Speaker, the 31-year-old Atlanta attorney in isolation at a Denver hospital with a rare and dangerous form of tuberculosis, is speaking out.

In an exclusive interview with ABC's Good Morning America, Cheryl and Ted Speaker and Robert and Betsy Cooksey said they are "in hell" and "we just want to get out of hell."

They said they are frustrated that while on the surface it appears as though Speaker was reckless in his decision to travel to and from Europe, they claim that the Centers for Disease Control and Prevention gave them no indication that Speaker was contagious with his drug-resistant TB
------------------------------------------------------------------------------------Wednesday, June 6, 2007 - Page updated at 02:06 PM




TB-infected traveler tells Congress he wasn't on the run
By DEVLIN BARRETT

The Associated Press

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WASHINGTON — The globe-trotting tuberculosis patient now in quarantine insisted to Congress today that doctors told him he wasn't contagious and didn't order him to stay in the United States for treatment — even as health officials painted a picture of a man on the run.

"I didn't go running off or hide from people. It's a complete fallacy, it's a lie," Andrew Speaker, a 31-year-old Atlanta lawyer, said by telephone from the Denver hospital room where he remains in government-ordered isolation.

But in testimony to a Senate subcommittee, federal and local health officials said Speaker took an international flight two days earlier than planned after he had been told he had a drug-resistant form of TB and should not travel.

Fulton County health officials told Speaker, "No you should not travel," Dr. Steven R. Katkowsky, the health department's director, said. "Was he ordered not to travel? The answer to that was no. The local health department does not have the authority to prohibit or order somebody not to travel."

U.S. border officials told Congress this morning that a lone customs officer undid their efforts to stop a man with a dangerous form of tuberculosis from entering the country — but that explanation was met with skepticism from lawmakers who said the case exposed plenty of holes in the nation's security.

"We dodged a bullet," House Homeland Security Committee chairman Bennie Thompson said as he opened a hearing into the case of Speaker, whose wedding and honeymoon travel caused an international health scare.

State Department policy requires sick U.S. citizens abroad to pay their own way home. But U.S. health officials felt that Speaker was such a danger to others that they wanted to help transport him — only to be unable to find an airplane with the separate air ventilation required to prevent TB's spread before Speaker fled.

TB traveler's trail


The Centers for Disease Control and international health authorities are contacting people who may have been exposed to Andrew Speaker, the U.S. traveler with extensively drug-resistant TB. (For more information on the disease and the controversy surrounding Speaker, see www.cdc.gov/tb/xdrtb/)

Here are some details of his travels:

— He left Atlanta on May 12 on Air France flight 385/codeshare Delta flight DL8517, arriving in Paris on May 13

— He flew from Paris to Athens on May 14 on Air France flight 1232

— On May 16 he flew on Olympic Airlines flight 560 from Athens to Santorini, Greece for his wedding.

— On May 21 he flew from Mykonos, Greece to Athens and then from Athens to Rome

— On May 24, after being told by health authorities not to fly, he flew from Rome to Prague on Czech Air Flight 0727. The same day he flew to Montreal aboard Czech Air Flight 0104

— He drove from Montreal to New York on the same day, crossing the U.S.-Canada border even though his passport triggered an electronic notification after U.S. officials flagged it.

— The CDC says it is very unlikely anyone aboard the shorter flights could have been infected. Only exposure of eight hours or more could have infected anyone, so only those who were on trans-Atlantic flights are being contacted.

Seattle Times staff and news services
"We have a gap there," Dr. Julie Gerberding, director of the Centers for Disease Control and Prevention, told a separate Senate hearing.


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



Prenatal and Perinatal Risk Factors for Autism
A Review and Integration of Findings

Alexander Kolevzon, MD; Raz Gross, MD, MPH; Abraham Reichenberg, PhD


Arch Pediatr Adolesc Med. 2007;161:326-333.

Objective To review the evidence for the presence of prenatal and perinatal factors that affect the risk of autism and autism spectrum disorders.

Data Sources Relevant articles were identified by searching MEDLINE, screening reference lists of original studies, and searching major journals likely to publish epidemiological studies on the topic. ....




The results of this review show that 3 of the 4 population-based studies28-29,32 to examine paternal age reported a significant association with risk of autism and ASDs. The fourth study31 also found that paternal age was older in fathers of case patients with autism compared with fathers of controls, although this relationship was statistically weaker in the adjusted analysis. Thus, advancing paternal age is consistently associated with increased risk of autism and ASDs.
Advanced paternal age has been associated with several congenital disorders, including Apert syndrome,40 craniosynostosis,41 situs inversus,42 syndactyly,43 cleft lip and/or palate,44-45 hydrocephalus,44 neural tube defects,46 and Down syndrome.47 In addition, advanced paternal age has been associated with schizophrenia15 and decreased intellectual capacities in the offspring.48 The most widely proposed mechanism underlying these congenital anomalies is known as the "copy error" hypothesis, first proposed by Penrose.49 After puberty, spermatocytes divide every 16 days, and by the age of 35 years, approximately 540 cell divisions have occurred. As a result, de novo genetic mutations that result from replication errors and defective DNA repair mechanisms are believed to propagate in successive clones of spermatocytes. These mutations accumulate with advancing paternal age and thus help explain how this disorder, which has a large genetic component, can be maintained in the population despite reduced reproduction in affected individuals.-----------------------------------------------------------------------------------


May 2007 PATERNAL AGE AND AUTISM ARE ASSOCIATED IN A FAMILY-BASED SAMPLE

: Mol Psychiatry. 2007 May;12(5):419-421.Paternal age and autism are associated in a family-based sample.Cantor RM, Yoon JL, Furr J, Lajonchere CM.
[1] 1Department of Human Genetics, David Geffen School of Medicine at University of California at Los Angeles, Los Angeles, CA, USA [2] 2Department of Pediatrics, David Geffen School of Medicine at University of California at Los Angeles, Los Angeles, CA, USA [3] 3AGRE Consortium, Los Angeles, CA, USA.

PMID: 17453057 [PubMed - as supplied by publisher]


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

"Autism's Angels" "Inexplicably on the rise"? Give Me A Break

Survey on Advanced Grandpaternal Age and Autism


From the August 2006 Town & Country article "Autisms Angels", And the number of diagnosed cases of autism has leaped alarmingly in recent years." So has average paternal age. "
"Autism is the nation's fastest-growing developmental disorder." Thomas Insel would you perhaps conclude that paternal age is a significant factor? Insel is quoted in this article, ""I'm not convinced that this increase can be explained by differences in diagnosis. "

I guess all the very wealthy older fathers of autistic children can fund all kinds of programs, but it won't change the fact that men over 33 are increasingly at risk for fathering autistic children, period. Hundreds and Hundreds of millions of dollars and you won't admit that you were past the age when it is healthy to father a child and that is why some of your children are very far from normal. The business of autism is vast, but the message for anyone worried about autism/schizophrenia is not to father children past the age of 33 or if the mother to be's father was over 33 when she was born, especially if there is any family history of any autoimmune disorders or of any autism/schizophrenia or other neurocognitive disorders in the family already. One could adopt or use a sperm donor.

Autism is in no way inexplicably on the rise, it is on the rise because so many men, at least 40% more than in 1980, are fathering babies 35-49 and many more at the ages of 50+. Ken Birnbaum, 63, the proud new father of twins, I guess has no idea, of the high risk for sporadic autism, schizophrenia, mental retardation, diabetes, cancers, Alzheimer's, those boys have compared the boys of a father under 30.



The Article From August 2006









We are dedicated to funding global biomedical research into the causes, prevention, treatments, and cure for autism; to raising public awareness about autism and its effects on individuals, families, and society; and to bringing hope to all who deal with the hardships of this disorder. We are committed to raising the funds necessary to support these goals.Autism Speaks aims to bring the autism community together as one strong voice to urge the government and private sector to listen to our concerns and take action to address this urgent global health crisis. It is our firm belief that, working together, we will find the missing pieces of the puzzle.Autism Speaks. It's time to listen.We are dedicated to funding global biomedical research into the causes, prevention, treatments, and cure for autism; to raising public awareness about autism and its effects on individuals, families, and society; and to bringing hope to all who deal with the hardships of this disorder. We are committed to raising the funds necessary to support these goals.Autism Speaks aims to bring the autism community together as one strong voice to urge the government and private sector to listen to our concerns and take action to address this urgent global health crisis. It is our firm belief that, working together, we will find the missing pieces of the puzzle.Autism Speaks. It's time to listen. "













What they don't say is that Andy Shih and others try to minimize all the paternal age data as if it is new or speculative and do all they can to generate funds for genomic research and biomedical research when it is worthless at helping the people who have autistic children already, the autistics children in need themselves. It certainly doesn't help prevent one case of autism.


Autism comes from numerous genetic mutations and is preventable, in some cases by earlier fathering, and wise family planning.


It is preventable through adoption if one might be a carrier of genes due to autism already in the family. One has to realize that autism did not come out of the blue and has a history. One also has to realize that childhood schizophrenia is now called autism and schizophrenia is caused in maybe one third or more cases, depending on the demographics of older fathering of babies, by the mutations in the sperm and sperm making cells of older fathers in non-familial cases.





The cause of the "inexplicable rise" is VERY CLEAR.









THE AGE OF THE FATHER AND THE
HEALTH OF FUTURE GENERATIONS

　
Leslie B. Raschka M.D., Associate Professor (retired),
Department of Psychiatry, University of Toronto
Address: 27 Edgecombe ave, Toronto, Ontario, Canada
M5N 2Xl, Tel. (416) 783-6938
2
Abstract
Purpose: To assess the role of paternal age in the origin of genetic illness in future generations.
Data Sources: All reference data originated in English language international scientific literature and findings of original research conducted by myself.
Study Selection: Original articles published between 1938 and 1998 were selected according to the stated purpose. One article was written by myself.
Data Extraction: The present paper deals with 4 subtopics: andrology, genetics, pathology, and psychiatry.
Results: Nine articles reporting on 1399 patients described the deterioration of the quality of semen related to ageing. Five articles reported an increased mutation rate in the male germ cells as compared to the female germ cell. Twenty-four articles reported on 1230 patients and related studies described paternal age effect on increased mutation rate causing genetic illness. Eight articles reporting on 10,347 patients described increased prevalence of mental illness as related to older paternal age.
Conclusions: The age of the father is an important determinant of the health of future generations. Children conceived by fathers older than 36 years of age are at increased risk for genetic illness due to recent mutation in the male germ cell.
3The genetic illness of a child could originate in a mutation related to the age of the father or to a mutation in the spermatogenesis caused by ageing in previous generations. The ageing process in the male is an important, probably the most important, cause of genetic illness in human populations.
　Key Words: Age of the father, mutation, genetic illness
4 Demographic changes taking place in the 20th Century have directed attention to all possible determinants of the health of future generations. The relationship between maternal age and Down Syndrome is a currently recognized scientific fact. The study of the reproductive efficiency of the male is also relevant to the health of future generations. Most children are born healthy regardless of paternal age; however, the age of the father is a determinant of ill health for a significant minority in future generations.
　
5 Andrology
Ageing in the male is expressed in a progressive decline both in the quality and quantity of the sperm (1). Changes include a decrease in motility (2), decreased vitality and an increased percentage of malformed sperm (3, 4, 5, 6, 7). The deterioration associated with ageing can be noticed first in men between the ages of 35 to 40 years (8, 9).
　
6 Genetics
The mutation rate is higher in the male than in the female germ cell (10, 11, 12, 13, 14). While the ageing male germ cell is especially sensitive to mutation (15) there is a significant difference in mutation, rates among different genes. There is evidence that mutation frequencies for a number of different genes causing illness increase with advancing paternal age. The rate of increase differs among different genes (16); not all genes are subject to the paternal age effect. Almost all new mutations were reported to occur in the male germ cell; however, paternal age effect is not equally pronounced in all mutations (12). It is operant in recent germline mutations. Inherited illnesses such as hemophilia A have their origins in mutations in earlier generations where, for example, increased maternal grandparental age was found and new germline mutation related to increased paternal age transmitted to future generations can result in hereditary illness. In the development of illness, more than one gene can be involved. The phenotypic expression can be influenced by modifying genes. The importance of mutations for the health of future generations was born out by the Bulletin of the World Health Organization 1986 (17), which states that about 1% of children will be born with a serious genetic disease and another 1% will develop a serious genetic illness later in life.
7 Pathology
The relationship between increased paternal age and pathological conditions of known genetic origin was reported for achondroplasia in nineteen publications (15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34); for Apert Syndrome in sixteen publications (15, 19, 20, 22, 23, 24, 25, 26, 27, 28, 30, 31, 32, 33, 34, 35); on Marfan Syndrome in thirteen publications (15, 20, 21, 22, 23, 25, 26, 27, 30, 31, 32, 33, 34); on osteogenesis imperfecta in five publications (16, 19, 24, 25, 29); on basal cell naevus syndrome in three publications (22, 26, 32); in Waardenburg Syndrome in five publications (22, 26, 31, 32, 33); on Crouzon Syndrome in seven publications (22, 26, 28, 31, 32, 33, 35); on oculo-denta; digital syndrome in four publications (22, 26, 31, 32); on thanatophoric dysplasia in three publications (28, 29, 35); on Pfeiffer Syndrome in three publications (28, 32, 35); on tuberous sclerosis in three publications (31, 33, 36); on multiple endocrine neoplasm in three publications (32, 34, 37); on myositis ossificans in nine publications (15, 19, 21, 22, 24, 30, 31, 32, 33); and on Treacher Collins disease, four publications (22, 26, 31, 33). All of these illnesses are transmitted in an autosomal dominant fashion. Increased risk for X-linked conditions associated with increased maternal grand-parental age is known to exist regarding classical hemophilia and was reported in nine publications (15, 17, 23, 25, 26 31, 32, 34, 38). This is also true for Lesch-Nyhan syndrome, reported in five publications (10, 17, 27, 31, 38). The mutation is transmitted to the child through carrier mothers.
8Psychiatry
Mutations occurring in the course of gametogenesis in the male and the association of psychosis was described in one article (39). Older maternal and paternal age in schizophrenia was reported in four articles (39, 40, 41, 42). My own study involving 574 patients has shown that the increased age of the father is a causative factor in a sub-group of the schizophrenic population (43). Two other articles, reporting on 662 and 8000 patients respectively, confirmed my conclusions, as well as indicating that increased maternal age was secondary to increased paternal age (41, 42). Three articles reporting on 1081 patients described increased paternal age in Alzheimer’s disease (44, 45, 46).
　
9 Discussion
All genetic illnesses have their origin in a distant or recent mutation. Paternal age is an important determinant of mutation frequency in new germ cell mutation, causing both autosomal dominant and X-linked recessive illnesses. The role of other mutagenic factors is not the subject of this study. The results of my own research are supported by other information which indicates that the leading cause of genetic illness present in human populations is the ageing process in the male. Conceiving children by men younger than 35 years of age would prevent many genetic illnesses in future generations.
　
10 Bibliography
Johnson L, Nguyen H B, Petty C S, et al. Quantification of Human Spermatogenesis: Germ Cell Degeneration during Spermatocytogenesis and Meiosis in Testes from Younger and Older Adult Men. Biol Reprod 1987; 37: 739.
Nieschlag E, Lammers U, Freischem C W, et al. Reproductive Functions in Young Fathers and Grandfathers. J Clin Endocrinol Metab 1982; 55: 676.
Holstein A F. Spermatid Differentiation In Man During Senescence. In. : Andre J, ed. Proceedings of the Fourth International Symposium on Spermatology; 1982 June; The Hague. Martinus Nijhoff, 1983: 15-18.
Homonnai Z T, Fainman N, David M P, et al. Semen Quality and Sex Hormone Pattern of 39 Middle Aged Men. Andrologia 1982; 14(2): 164.
Bacetti B, Renieri T, Selmi M G, et al. Sperm Structure and Function in 70 Year Old Humans. In: Andre J, ed. Proceedings of the Fourth International Symposium on Spermatology; 1982 June; The Hague. Martinus Nijhoff, 1983: 19-23.
Spira A, Ducot B. Variations physiologiques du spermatogramme. Ann Biol Clin (Paris) 1985; 43: 55.
Sternbach H. Age-Associated Testosterone Decline in Men: Clinical Issues for Psychiatry. Am J Psychiatry 1998; 155: 1310.
11
Bishop M W H. Aging and Reproduction in the Male. J Reprod Fert 1970; (Suppl. 12): 65.
Schwartz D, Mayaux MJ, Spira A, et al. Semen characteristics as a function of age in 833 fertile men. Fertil Steril, 1983; 39: 530.
Vogel F. Editorial. A probable sex difference in some mutation rates. Am J Hum Genet, 1977; 29: 312.
Haldene J B S. The Mutation Rate of the Gene for Haemophilia and it’s Segregation Ratios in Males and Females. Ann Hum Genet 1947; 13: 261.
Vogel F, Motulsky AG. Human Genetics, Problems and Approaches. Berlin: Heidelberg: New York: Springer Verlag, 1979; 282.
Crow J F, Denniston C. Mutation in Human Populations. In: Harris H, Hirschhorn K, eds. Advances in Human Genetics. New York: London: Plenum Press, 1985; 14: 59-123.
Shimmin L C, Chang B H, Li W. Male-driven evolution of DNA sequences. Nature 1993; 362: 745.
Vogel F, Rathenberg R. Spontanious Mutation in Man. In: Harris H, Hirschhorn K, eds. Advances in Human Genetics. New York: London: Plenum Press, 1975; 5: 223-318. 12

Evans HJ. Mutation as a cause of genetic disease. Phil Trans R Soc Lond 1988; 319: 325.
Berg K, Bochkov N P, Coutelle C, et al. Bull WHO 1986; 64(2): 205.
Penrose L S. Parental Age and Mutation. The Lancet 1955; 2: 312.
Modell B, Kuliev A. Changing paternal age distribution and the human mutation rate in Europe. Hum Genet 1990; 86:198.
Murdoch J L, Walker B A, Hall J G, et al. Achondroplasia-a genetic and statistical survey. Ann Hum Genet 1970; 33: 227.
Rogers J G, Danks D M. Birth defects and the father. Med J Austr 1983; 2: 3.
Karp L E. Older Fathers and Genetic Mutations. Am J Med Genet 1980; 7: 405.
Tunte W. Human Mutations and Paternal Age. Hum Genet 1972; 16: 77.
Modell B, Kuliev A. Impact of public health on human genetics. Clin Genet 1989; 36: 286.
　
　
13
Carothers A D, McAllion S J, Paterson C R. Risk of dominant mutation in older fathers: evidence from osteogenesis imperfecta. J Med Genet 1986; 23: 227.
Jones K L, Smith D W, Sedgwick Harvey M A, et al. Older paternal age and fresh gene mutation: Data on additional disorders. J Ped 1975; 86: 84.
Hook EB. Paternal Age and Effects on Chromosomal and Specific Locus Mutations and on Other Genetic Outcomes in Offspring. In: Mastroianni L Jr, Paulsen C A, eds. Aging, Reproduction and the Climacteric. New York and London: Plenum Press, 1986: 117-145.
Wilkin D J, Szabo J K, Cameron R, et. al. Mutations in Fibroblast Growth -Factor Receptor 3 in Sporadic Cases of Achendroplansia Occur Exclusively on the Paternally Derived Chromosome. Am J Hum Genet 1998; 63: 711.
Orioli J M, Castilla E E, Scarano G, et. al. Effect of Paternal Age in Achondroplasia, Thanatophoric Dysplasia and Osteogenesis Imperfecta. Am J Med Genet 1995; 59: 209.
Erickson D, Cohen M M Jr., A Study of parental age effects on the occurrance of fresh mutations for the Apert syndrome. Ann Hum Genet 1974; 38: 89.

14
Bordson B L, Leonardo VS. The appropriate upper age limit for semen donors: a review of the genetic effects of paternal age. Fertil Steril 1991; 56: 397.
Sankaranarayanan K. Ionizing radiation and genetic risks IX. Estimates of the frequencies of mendelian diseases and spontaneous mutation rates in human populations: a 1998 perspective. Mutat Res 1998; 411: 129.
Friedman J M. Genetic Disease in the Offspring of Older Fathers. Obstet Gynecol 1981; 57: 745.
Carlson K M, Bracamontes J, Jackson C E, et al. Parent-of-Origin Effects in Multiple Endocrine Neoplasia Type 2B. Am J Hum Genet 1994; 55: 1076.
Moloney D M, Slaney S F, Oldridge M, et al. Exclusive paternal origin of new mutations in Apert syndrome. Nat Genet 1996; 13: 48.
Osborne J P, Fryer A, Webb D. Epidemiology of Tuberous Sclerosis. Ann NY Acad Sci 1991; 615: 125.
Schuffenecker I, Ginet N, Goldgan D, et al. Prevalence and Parental Origin of De Novo RET Mutations in Multiple Endocrine Neoplasia Type 2A and Familial Medullary Thyroid Carcinoma. Am J Hum Genet 1997; 60: 233.
　
15
Crow J F. How Much Do We Know About Spontaneous Human Mutation Rates? Environ Mol Mutagen 1993; 21: 122.
Crow T J. Editorial. Mutation and psychosis: A suggested explanation of seasonality of birth. Psychol Med 1987; 17: 821.
Gordon A. The Incidence of Psychotic Disorders in Individuals Whose Parents Married at an Advanced Age. Med Records 1938; 148: 109.
Kinnell H G. Parental Age in Schizophrenia. Br J Psychiatry 1983; 142: 204.
Hare E H, Moran PAP. Raised Parental Age in Psychiatric Patients: Evidence for the Constitutional Hypothesis. Br J Psychiatry 1979; 134: 169.
Raschka L B. Parental Age and Schizophrenia. Magyar Andrologia-Hungarian Andrology 1998/2; III: 47.
Bertram L, Busch R, Spiegl M, et al. Paternal age is a risk factor for Alzheimer disease in the absence of a major gene. Neurogenetics 1998; 1: 277.
Whalley L J, Thomas B M, Starr J M. Epidemiology of Presenile Alzheimer’s Disease in Scotland (1974-88). 11. Exposures to Possible Risk Factors. Br J Psychiatry 1995; 167: 732.
16

This is so disturbing and no one mentions that it is the 63 year old father's sperm that are going to give these boys troubles

IN THEIR FAVOR IS THAT THEY WEREN'T DAUGHTERS WHO WOULD BE AT A MUCH INCREASED RATE FOR SCHIZOPHRENIA DUE TO MUTATIONS THAT ACCUMULATE WITH A FATHER'S AGE ON THE VERY VULNERABLE X CHROMOSOME




NO ONE SPEAKS OF THE HIGH CHANCE THESE BOYS HAVE OF TYPE 1 DIABETES, AUTISM OF SOME TYPE, SCHIZOPHRENIA, PROSTATE CANCER, ALZHEIMER'S, AND MANY OTHER PATERNAL AGE DERVIDED GENETIC DISORDERS. WHICH BEGIN TO SHOW UP IN CHILDREN WHEN FATHERS ARE THE RIPE OLD AGE OF 35. MAYBE MR. BIRNBAUM IS SUPERMAN AND HIS SIX YEAR OLD IS FINE, BUT MAYBE NOT.

FOR INFORMATION ON THE DISORDERS THAT INCREASE WITH INCREASING PATERNAL AGE THAT HAVE ACTUALLY BEEN STUDIED AND ARE NOT OBVIOUS AT BIRTH


Single gene disorders that start rising in offspring in ones mid 30s


Doctors at crossroads with birth of US twins

May 25 2007 at 03:35PM

By Di Caelers


...........................................................................


'Immoral as well as dangerous to the health of mother and child'
Wiswedel's partner in the clinic, Dr Paul le Roux, is well known in the US for his expertise in assisted pregnancies among older women, and many comments on different websites attest to the fact.

The Cape Fertility Clinic found itself in hot water three years ago when a US website offered a picture catalogue of South African women wanting to sell their eggs for fertility treatments, which would be performed at the local clinic.

In 2004, when the controversy broke, Wiswedel told the Cape Argus he and Le Roux had nothing to do with choosing the couples or providing the donors advertised on the website.

He said then that he had alerted Robin Newman, head of the US company, to his concern that she was not operating within the South African guidelines.

According to the website of the Cape Fertility Clinic, fertility treatment is legally governed by the National Health Bill, signed into law in 2004. It regulates all egg donations, "and the procedure is legal in this country".

But Dr Paul Dalmeyer, head of the Port Elizabeth Fertility Clinic and an executive member of the International Federation of Fertility Societies, described the birth to the 60-year-old woman as "pushing the envelope".

The New Jersey woman and her husband, Ken Birnbaum, 63, already had three children, including two adult children aged 33 and 29. She was quoted as saying she wanted siblings for her six-year-old son, Ari.

In overseas press reports, it emerged that she had previously had eggs frozen, but declined to say whether these were used for the latest pregnancy.

The birth of the twins made Birnbaum the oldest woman in the US to give birth to twins.

Although many local specialists were loath to enter the age debate, it emerged that it was generally accepted that it was ethical to offer fertility treatment to women only until their early 40s.

In the US there are no federal standards for age limits on in-vitro fertilisation, but the Society for Assisted Reproductive Technology there recommends that women be under 50 if the treatment involves a donor egg, and under 44 if they are using their own eggs.

In France, Wikipedia reports, the country approved a bill in the 1990s which prohibits post-menopausal pregnancy, which the French health minister at the time, Philippe Douste-Blazy, called "immoral as well as dangerous to the health of mother and child".

In Italy, the Association of Medical Practitioners and Dentists prevents its members from giving fertility treatment to women aged 50 and older. In spite of the law, though, in 1994 Italian woman Rosanna Della Corte gave birth to a son at age 62 after intervention by doctor Severino Antinori.

She used a donor egg and her husband's sperm, fell pregnant on the first attempt, but miscarried after 40 days. It took six more attempts before the successful birth.

In 2006, the same doctor helped the United Kingdom's Patricia Rashbrook fall pregnant and she gave birth to a son at the age of 62.

The birth sparked a major debate in the UK over the ethics of late motherhood.

Dalmeyer, who was the local organiser of the recent World Congress on Fertility and Sterility in South Africa, said legislation in South Africa was much more lenient than in other countries.

He questioned whether the treatment here for Birnbaum was exploiting the local legislation.

"When the Italian situation occurred in 1994 I can tell you that the international federation was certainly not impressed.

"The general feeling is definitely that this type of procreation and reproduction is not okay," Dalmeyer said.

WHAT IF PEOPLE KNEW THAT FATHERING BABIES PAST THE AGE OF 34 CAUSES DE NOVO AUTISM, SCHIZOPHRENIA, CANCERS, DIABETES, MS, LUPUS, ALZHEIMER'S, FIBRO

CSHL Trustee David Rubenstein
and Liz Watson




Hedge fund manager Bruce Kovner, Dr. Bruce Stillman, David Koch

Honoree Bob Wright, Lonnie Ali, Muhammad Ali, Suzanne Wright,
Lab President Dr. Bruce Stillman, Dr. James Watson

November 9, 2006
CSHL RAISES $2.5 MILLION AT INAUGURAL DOUBLE HELIX MEDALS EVENT & LAUNCHES $200 MILLION CAPITAL CAMPAIGN


EFFORT CITED AT INAUGURAL DOUBLE HELIX MEDALS DINNER HONORING MUHAMMAD ALI, BOB AND SUZANNE WRIGHT, PHILLIP SHARP


Presenters include Meredith Vieira, Phil Donahue, Deborah Norville, Dr. James D. Watson



Dr. James Watson Cold Spring Harbor Laboratory (CSHL), the renowned institution where Nobel laureate Dr. James D. Watson gave the first public presentation of the discovery he and fellow scientist Dr. Francis Crick made of the structure of DNA, is launching a $200 million capital campaign to fortify and expand its leadership role in making groundbreaking research discoveries and developing innovative technologies to study the fundamental aspects of human health. The campaign will enable CSHL, home to seven Nobel Prize winners and recently ranked #1 in cited research in molecular biology and genetics by Science Watch, to make substantial increases in laboratory space, create endowed research centers to support innovation and growth, and provide funding to recruit talented scientists.





Bruce Stillman, Evening Presenter "Inside Edition's"
Deborah Norville, Jim Watson, Honoree Dr. Phillip A. Sharp

The campaign was cited at CSHL's inaugural Double Helix Medals Dinner tonight at the Mandarin Oriental New York. The black-tie gala honored boxing legend and humanitarian Muhammad Ali; Bob Wright, chairman and CEO of NBC Universal, and his wife Suzanne; and Nobel laureate Dr. Phillip Sharp of MIT. The double helix refers to the unique structure of DNA molecule, which carries all of life's information. It is central to biological research, and is at the heart of the CSHL's work.




Dr. James Watson Cold Spring Harbor Laboratory (CSHL), the renowned institution where Nobel laureate Dr. James D. Watson gave the first public presentation of the discovery he and fellow scientist Dr. Francis Crick made of the structure of DNA, is launching a $200 million capital campaign to fortify and expand its leadership role in making groundbreaking research discoveries and developing innovative technologies to study the fundamental aspects of human health. The campaign will enable CSHL, home to seven Nobel Prize winners and recently ranked #1 in cited research in molecular biology and genetics by Science Watch, to make substantial increases in laboratory space, create endowed research centers to support innovation and growth, and provide funding to recruit talented scientists.



The campaign was cited at CSHL's inaugural Double Helix Medals Dinner tonight at the Mandarin Oriental New York. The black-tie gala honored boxing legend and humanitarian Muhammad Ali; Bob Wright, chairman and CEO of NBC Universal, and his wife Suzanne; and Nobel laureate Dr. Phillip Sharp of MIT. The double helix refers to the unique structure of DNA molecule, which carries all of life's information. It is central to biological research, and is at the heart of the CSHL's work.



dinner was chaired by Jeff Zucker, CEO of NBC Universal Television Group, and his wife Caryn; Thomas Quick, retired vice chairman of Quick & Reilly/Fleet Securities, Inc., and a Trustee of CSHL; David Rubenstein, a CSHL Trustee who is co-founder and managing director of The Carlyle Group, and his wife Alice; and Roy Zuckerberg, a CSHL Trustee and senior director of Goldman Sachs.

Some $2.5 million was raised at the dinner to benefit CSHL's groundbreaking biomedical research, innovative technologies and educational initiatives seeking to understand and identify therapeutic approaches and cures for devastating diseases such as cancer, autism, schizophrenia, Alzheimer's and Parkinson's, among others.


“Cold Spring Harbor Laboratory has long been recognized for its excellence in research in the biological and biomedical sciences,” said Dr. Bruce Stillman, president. “Our $200 million capital campaign will enable us to expand our stellar research and continue to teach the next generation of scientists.”


Added Dr. Watson: “Never before has biology and medicine had the capacity to move so rapidly. I excitingly look forward to keeping Cold Spring Harbor Laboratory in its long valued leadership role.”


CSHL has already raised $130 million in the silent phase of the capital campaign. It is customary for institutions to have about one-third to one-half of the campaign completed before making a public announcement.


Major capital and endowment gifts include: $20 million from New York State for campus construction; $15 million from the Starr Foundation, which will go toward cancer genetics; $10 million from the DeMatteis Family, whose name will appear on a building for human genetics research; $10 million from Donald Everett Axinn for research into cognitive disorders; and $10 million from David H. Koch for biomathematics research.



“Cold Spring Harbor Laboratory's work in determining the causes of diseases like cancer through the study of genetics is second to none,” said David H. Koch, a former trustee of the Laboratory who has been a generous supporter of biomathematics at the Laboratory. “I am proud to have my name affiliated with an institution that has made, and will continue to make, important discoveries in the treatment of genetic diseases through outstanding biomedical research.”


“It gives me a great sense of pride to help Cold Spring Harbor Laboratory expand its facilities for groundbreaking research in Parkinson's, Alzheimer's, autism and schizophrenia,” said Donald Everett Axinn, who has made a contribution toward research on cognitive disorders.

DO COPY NUMBER VARIATIONS FOUND IN SPORADIC AUTISM EXIST IN THE SPERMATAGONIA OF THE FATHERS? WILL ANYONE LOOK FOR THEM?

Jonathan Sebat and colleagues found the key to sporadic autism and it seems they will fail to follow up and look for the same CNVs in the father's sperm and spermatagonia. ESPECIALLY BE WARNED ABOUT AUTISM IF YOU HAVE AUTOIMMUNE DISORDERS OR YOUR CLOSE RELATIVES DO. DISEASE CAUSING MUTATIONS ACCUMULATE IN SPERM MAKING CELLS BETWEEN 33-35. YOUR RISK IS MUCH GREATER IF THERE IS ANY AUTISM OR OTHER BRAIN RELATED DISORDERS IN THE FAMILY. TRY TO FATHER YOUR BABIES BY 35-40 AT THE LATEST. IF YOU ARE ABLE TO AND YOUNGER THAN 35 CRYOPRESERVE YOUR SEMEN FOR ANY LATER FATHERING OF BABIES.

CANCERS, ALZHEIMER'S, AUTOIMMUNE DISEASES/ALL OF THEM, AUTISM, SCHIZOPHRENIA, AND MANY OTHER DISORDERS CAN BE CREATED DE NOVO IN OFFSPRING THROUGH SPONTANEOUS MUTATIONS IN SPERM MAKING CELLS. THESE MUTATIONS INCREASE WITH INCREASING PATERNAL AGE.



Finding the genes responsible for autism is one of the goals that Sebat and his colleagues have set for their next project. "We'll be screening at least 2,000 families over the next three years using a much higher resolution platform," Sebat said. He added that he hopes the data will provide a better estimate of the frequency of CNV in sporadic autism, as well as a view of a larger array of genes involved than when researchers restricted their studies to inherited cases. "I think this will be a study that really tips the balance in the field towards using technologies that can directly detect mutations, [and] focusing on the majority of cases that are sporadic."

Thinking In Pictures By Sadaf Shahid

Thinking in pictures



By Sadaf Shahid

I saw him sitting at the curb. Silent and still. Despite the cold December, what he was wearing, or rather was wrapped up in, could hardly be described as clothes. An unkempt, shabby beard covered his face. His hair, like dry twirled weed. Sometimes he would get up hurriedly and walk aimlessly about — completely oblivious to the mad traffic, the honking cars swarming all around him. Lost in a world of his own. Muttering to himself, echolalic and incoherent. Harming no one, his presence a source of suspicion and disquiet for all. Some may have taken him to be a terrorist or a spy incognito. To some, he was a beggar trying to earn sympathy and eke out a living. To the religiously susceptible, he was a sadhu, a malang, a fakir. Only I knew his secret. I knew who he was. He was none of the above. He was autistic.

A shiver ran down my spine. He was homeless and uncared for. There was nothing any one could do for him, and no one cared. Blaming providence for my knowledge, when ignorance was such bliss, I moved on, just like everyone else.

Autism is one of the most common developmental disabilities in the world, affecting approximately one out of every 166 children. Its prevalence rate makes it the second most common developmental disability — even more common than Down’s Syndrome. It occurs four times more often in boys than in girls. It is a lifelong disability with no known cure. The symptoms of autism tend to appear very early in life, usually within the first three years.

We don’t have estimates of the children diagnosed with autism in Pakistan but, thankfully, awareness is increasing. Children are now being diagnosed and enrolled into different rehab programs. Whether these programs are following a neurological and scientific approach or not, is another question. Nothing was known about autism until a few years back. Children with autism had little or no help. They were either diagnosed as mentally retarded or cases of extreme environmental deprivation. They were admitted into special schools for the emotionally and intellectually challenged. And finally, when they became self-injurious or so aggressive that their behaviour became socially unacceptable and the aging parents could no longer keep them at home, they were sent off to ‘residential facilities’ — or mental asylums.

OPRAH SPENDS AN ENTIRE HOUR ON AUTISM AND SHE DOESN'T MENTION PATERNAL AGE

I WONDER WHY? WHAT IS THE AGENDA OF ANDY SHIH AND AUTISM SPEAKS?

Dr. Dolores Malaspina in her excellent discussion of neural cogntive disorders and the paternal germ line wrote:

Finally, we examined if paternal age was related to the risk for autism in our cohort. We found very strong effects of advancing paternal age on the risk for autism and related pervasive developmental disorders (Reichenberg et al., in press). Compared to the offspring of fathers aged 30 years or younger, the risk was tripled for offspring of fathers in their forties and was increased fivefold when paternal age was >50 years. Together, these studies provide strong and convergent support for the hypothesis that later paternal age can influence neural functioning.


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


Maternal and Paternal Age and Risk of Autism Spectrum Disorders
Lisa A. Croen, PhD; Daniel V. Najjar, MS; Bruce Fireman, MA; Judith K. Grether, PhD
Arch Pediatr Adolesc Med. 2007;161:334-340.

Objective To explore the association between maternal and paternal age and risk of autism spectrum disorders (ASDs) in offspring.






Results Risk of ASDs increased significantly with each 10-year increase in maternal age (adjusted RR, 1.31; 95% confidence interval [CI], 1.07-1.62) and paternal age (RR, 1.28; 95% CI, 1.09-1.51). Adjusted RRs for both maternal and paternal age were elevated for children with autistic disorder (maternal age: RR, 1.18; 95% CI, 0.87-1.60; paternal age: RR, 1.34; 95% CI, 1.06-1.69) and children with Asperger disorder or pervasive developmental disorder not otherwise specified (maternal age: RR, 1.45; 95% CI, 1.09-1.93; paternal age: RR, 1.24; 95% CI, 0.99-1.55). Associations with parental age were somewhat stronger for girls than for boys, although sex differences were not statistically significant.

Conclusion Advanced maternal and paternal ages are independently associated with ASD risk.

Low Birthweight and Advancing Paternal Age

Research and Practice
Paternal Age as a Risk Factor for Low Birthweight
Nancy E. Reichman 1* Julien O. Teitler 2


AJPH First Look, published online ahead of print March 29, 2006


©
American Journal of Public Health, 10.2105/AJPH.2005.066324


1 Robert Wood Johnson Medical School
2 Columbia University


Objectives. We examined associations between paternal age and low birthweight in the US urban population.

Methods. Using a population-based sample of 4621 births, we used multiple logistic regression analysis to estimate associations between paternal age and low birthweight, controlling for maternal age, other demographic factors, and the child's gender.

Results. When the child’s gender and the mother's race/ethnicity, birthplace, parity, marital status, and health insurance type were controlled, teenaged fathers were 20% less likely and fathers older than 34 years were 90% more likely than fathers aged 20 to 34 years to have low-birthweight babies. The associations were significant when maternal age was also controlled. No racial/ethnic differences in associations between paternal age and low birthweight were found.

Conclusions. We identified paternal age as an independent risk factor for low birthweight in the US urban population, suggesting that more attention needs to be paid to paternal influences on birth outcomes and to the interactive effects of urban environments and individual risk factors on health.

Key Words: Birth Outcomes, Socioeconomic Factors

FATHER'S AGE AND DEVASTATING DISORDERS

"Until recently, health care professionals have focused almost exclusively on the mother's age as a risk factor for health problems in the child. But we now know that the father's age also adds to the risk of potentially devastating diseases. And there is no practical way to detect these illnesses during pregnancy. For those weighing the risks, the decision can be wrenching. Adoption and in some instances a sperm donation may be acceptable alternatives to older fathers wanting to build a healthy family."

Michael Craig Miller, M.D. is Editor in Chief of the Harvard Mental Health Letter. He is also associate physician at Beth Israel Deaconess Medical Center and assistant professor at Harvard Medical School. He has been practicing psychiatry for more than 25 years and teaches in the Harvard Longwood Psychiatry Residency Program.

Later Paternal Age Can Influence Neural Functioning

Finally, we examined if paternal age was related to the risk for autism in our cohort. We found very strong effects of advancing paternal age on the risk for autism and related pervasive developmental disorders (Reichenberg et al., in press). Compared to the offspring of fathers aged 30 years or younger, the risk was tripled for offspring of fathers in their forties and was increased fivefold when paternal age was >50 years. Together, these studies provide strong and convergent support for the hypothesis that later paternal age can influence neural functioning. The translational animal model offers the opportunity to identify candidate genes and epigenetic mechanisms that may explain the association of cognitive functioning with advancing paternal age.

One Problem--YOU CAN'T CURE AUTISM

CSHL is pursuing a $200 million capital campaign to fund such ventures as the construction of new research facilities dedicated to the study of autism.



The Simons Foundation is a private family foundation based in New York City. The primary mission is to fund advanced research in science and mathematics. A secondary mission is to help children with learning differences. Bridging these two areas, the Simons Foundation has recently undertaken a major initiative supporting research into autism and its treatment. The Foundation aims to spend $100 million long-term to find a cure for the developmental disorder.

Gerald D. Fischbach, M.D., Scientific Director of the Simons Foundation

Gerald D. Fischbach

Gerald D. Fischbach, M.D., is Executive Vice President for Health and Biomedical Sciences; Dean of the Faculties of Health Sciences and Dean of the Faculty of Medicine at the College of Physicians and Surgeons of Columbia University. Dr. Fischbach received his M.D. degree in 1965 from Cornell University Medical School and interned at the University of Washington Hospital. He began his research career at the National Institutes of Health, serving from 1966-1973. He subsequently served on the faculty of Harvard Medical School, first as Associate Professor of Pharmacology from 1973-1978 and then as Professor until 1981. From 1981-1990, Dr. Fischbach was the Edison Professor of Neurobiology and Head of the Department of Anatomy and Neurobiology at Washington University School of Medicine. In 1990, he returned to Harvard Medical School where he was the Nathan Marsh Pusey Professor of Neurobiology and Chairman of the Neurobiology Departments of Harvard Medical School and Massachusetts General Hospital until 1998. He served as Director of the National Institute of Neurological Disorders and Stroke, National Institutes of Health from 1998-2001.





NIH's Gerald D. Fischbach,Named Columbia's Vice President for Health and Biomedical Sciences






Gerald D. Fischbach

Gerald D. Fischbach, M.D., Director of the National Institute of Neurological Disorders and Stroke at the National Institutes of Health (NIH), has been named Columbia University's Vice President for Health and Biomedical Sciences, Dean of the Faculty of Health Sciences and Dean of the Faculty of Medicine, Columbia President George Rupp announced Tues., Dec. 5. Fischbach will also be the Harold and Margaret Hatch Professor of the University in the Faculties of Health Sciences and of Medicine.

A pioneering researcher Fischbach was the Nathan Marsh Pusey Professor of Neurobiology and Chairman of the Neurobiology Departments at both the Harvard Medical School and Massachusetts General Hospital before assuming his current position at NIH in 1998.

At Columbia he will head a division that includes four health science professional schools with 27 academic departments, 3,000 students and 2,300 full-time faculty; a biotechnology park; some 40 biomedical research and treatment centers; and physician practice affiliations with two dozen hospitals. The Health Sciences Division has an annual operating budget of $815 million and has $230 million in sponsored research grants.

Fischbach replaces Herbert Pardes, M.D., who left Columbia in December 1999

THE CREATION OF A DNA DATABANK WILL ONLY BENEFIT THE POCKETS OF THE INVESTORS AND SCIENTISTS AND COMPANIES INVOLVED AND DO NOTHING FOR AUTISTICS

Grant to Yale from Simons Foundation to explore genetic causes of autism
Researchers at the Yale School of Medicine Child Study Center and 10 other institutions will share a $10 million gift from James and Marilyn Simons of The Simons Foundation to create a databank of DNA samples from autism patients around the country.

The goal is to collect a total of 3,000 samples from autism patients around the country to help identify different variants of autism and develop treatments. The principal investigators at Yale, Ami Klin and Matthew State, M.D., have received $1.2 million for three years to collect DNA samples from patients completing clinical evaluations or research protocols at the Autism Program at the Yale Child Study Center.

Autism is a complex brain disorder that inhibits a person’s ability to communicate and develop social relationships, and it is often accompanied by extreme behavioral challenges. Autism Spectrum Disorders are diagnosed in one in 150 children in the United States and affects four times as many boys as girls. Researchers do not know how many subtypes of autism exist. Klin, the Harris Associate Professor of Child Psychology and Psychiatry at Yale, said the gene data might help identify meaningful subtypes of autism, thus advancing knowledge that is critical for behavioral and brain studies, and promoting treatments that will likely be more specific to an individual’s variant of autism.

Other universities participating in the DNA databank collection include Harvard, Columbia, Emory, McGill, Boston, Washington University, the University of Washington, the University of Illinois-Chicago and the University of California, Los Angeles.

The Simons Consortium represents the most comprehensive and detailed effort to date to relate genotypic and phenotypic data in autism. Subjects completing the protocol will have the most refined genotypic analyses that can then be related to a wealth of data on the affected individuals themselves and on their family members. The Consortium will house the data in a centralized repository that will be accessible to researchers within and outside the institutions involved in this effort.

###
The Simons Foundation is a private family foundation based in New York City. The primary mission is to fund advanced research in science and mathematics. A secondary mission is to help children with learning differences. Bridging these two areas, the Simons Foundation has recently undertaken a major initiative supporting research into autism and its treatment. The Foundation aims to spend $100 million long-term to find a cure for the developmental disorder.


James Simons

Complex mathematical theories are reborn as investment strategies at Renaissance Technologies. The hedge fund manager, which has some $12 billion in assets under management, focuses on using computer technical models to predict the movement of markets; many of the firm's analysts hold Ph.Ds in math or science disciplines (including astrophysics). Renaissance Technologies was founded by Jim Simons, a former MIT and Harvard math professor who, despite his relative anonymity, ranks among the world's highest-paid hedge fund managers. (Simons is known in mathematical circles as co-author of the Chern-Simons Invarients, used in theoretical physics.)




James H. Simons

Simons is President and founder of Renaissance Technologies Corp. Prior to his financial career, Dr. Simons served as chairman of the Mathematics Department at S.U.N.Y. Stony Brook, taught mathematics at M.I.T. and Harvard University, and was a cryptanalyst at the Institute of Defense Analyses in Princeton, N.J. Dr. Simons’ scientific work was in the area of geometry and topology, and his most influential work involved the discovery and application of certain measurements, now called the Chern-Simons Invariants, which have had wide use, particularly in theoretical physics. James Simons holds a B.S. from MIT, a Ph.D. from U.C. Berkeley, and won the American Mathematical Society’s Veblen Prize for his work in geometry in 1975. He is a former Chairman of the Stony Brook Foundation, and is currently a trustee of Rockefeller University, MIT, and the Institute for Advanced Study.