AUTISM PREVENTION FATHER BABIES 24-34 PATERNAL AGE IS KEY IN NON-FAMILIAL AUTISMVaccines

"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.

Friday, July 06, 2007

Beverly Sills Two Children With Her Older Husband Peter Jr. who is autistic and mentally retarded and Meredith who has MS and who is deaf

She met Greenough in Cleveland while on a 1955 tour with City Opera. "He winked, which I thought was pretty corny," Ms. Sills told The Christian Science Monitor in 1985, "but it worked." Greenough died last year.

Ms. Sills had three stepchildren from Greenough's previous marriage and two children with her husband: a son, Peter Jr., who is autistic and mentally retarded, and a daughter, Meredith, who suffers from multiple sclerosis and who is deaf.

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Friday, May 25, 2007

Children Born to Couples who have IVF are more likely to be autistic, have cancers, cerebral palsy and mental retardation

THE ARTICLE DOESN'T POINT OUT THAT THIS IS DUE TO THE AGE OF THE FATHER IN MOST CASES


Children born
after IVF treatment 'face higher health risks'


Ian Sample in New Orleans
Thursday October 26, 2006
The Guardian



Children born to couples who have undergone fertility treatment are more likely to be diagnosed with autism, cancer and other disorders such as cerebral palsy and mental retardation, researchers claimed yesterday.
The higher risk to child health is believed to be caused by medical problems in the parents, such as diabetes and hypertension, damaging the child in the womb, but doctors conducting the study said IVF and other fertility treatments may also play a role. Medical records of children born after their parents sought fertility treatment showed they were four times more likely to have autism than those born to fertile parents. Childhood cancers including leukaemia and brain tumours also rose.

The risk of more minor problems, such as attention deficit hyperactivity disorder, rose by 40%, and other medical conditions affecting hearing and sight nearly doubled. Children had a 30% higher chance of being admitted to neonatal intensive care units and to stay in hospital for more than three days if they were born following fertility treatment, the study found.

The researchers stressed the figures represent relative risks. In July researchers at Guy's and St Thomas' hospital in London reported the prevalence of autism to be 0.39% in the general population, a figure that will include some children born to parents aided by fertility treatment. A fourfold rise in the risk of autism would see a child's chances of having the condition increase to 1.56%.

Mary Croughan at the University of California in San Francisco studied 2,000 women who either gave birth naturally after a long period of infertility, or conceived after a variety of fertility treatments, and compared them with 2,000 fertile mothers who gave birth between 1994 and 1998. More than 19,000 medical records were used to build up a picture of the women's pregnancies and deliveries and the health of their children up to six years of age.

The researchers found infertile women had more complications such as pre-term labour and pre-eclampsia, more delivery difficulties and caesarean sections. Children born to infertile women were 20% more likely to have low birth weights and were twice as likely to show evidence of poor growth in the womb. Speaking at the American Association for Reproductive Medicine (ASRM) conference in New Orleans, Dr Croughan said that medical conditions more common in infertile couples may be to blame for the rise in childhood health problems. She said: "The vast majority of children born to infertile couples are healthy, but if a couple has any risk factors that could lead to a child not being born healthy, then those should of course be taken into consideration."

Clare Brown, chief executive of Infertility Network UK, said "continual research" was needed to ensure "treatment is safe for couples and potential children".

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Tuesday, May 15, 2007

Mental Retardation and Cancer CNVs Polymorphisms Germ-line Mutations/ Paternal Age?



Researchers Determine Genetic Causes of Mental Retardation
Marco Marra of the University of British Columbia and Lisa Lit of the University of California, Davis, discuss chromosome copy number in mental retardation.

VANCOUVER, Canada, December 11, 2006 — University of British Columbia scientists, led by Marco Marra and Jan Friedman, have identified chromosomal abnormalities—genetic duplications and deletions as small as 37.6 kb—that are responsible for the development of mental retardation in children. Using whole-genome sampling analysis (WGSA) with Affymetrix Mapping 100K Arrays, the researchers pinpointed the probable genetic causes of mental retardation in at least twice as many children as conventional cytogenetic analysis, and were able to detect smaller abnormalities than can be detected using BAC-tiling-path arrays.

The researchers examined 100 children and their unaffected parents; each of the children had been assessed by clinical geneticists who were unable to identify the cause of the child’s mental retardation. The team found that 11 children harbored genetic alterations, including eight deletions, two duplications and one with additional copies of chromosome nine in approximately 20 percent of cells. Some deletions were not unique—they appeared in more than one individual
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deletions and you’ll see associations of haplotypes of amplifications. In other words, we will begin to see how germ-line polymorphic alleles might be contributing to the cancer that develops. I think that’s one very exciting area which can really only be looked at using the SNP array platform.
Maris: Yes, I agree with that completely. The 500K especially is going to open up a whole new world in terms of doing classic genetic association studies as well as pretty novel cancer-specific genomics. So we’re excited about that as well.

For mainly technological reasons, we have had a very, uni-focal, looking-under-the-lamppost type of approach, and prognostic biomarkers have been assessed one at a time, a deletion here, or an amplification there by itself and correlated with corollary measures, clinical
factors. And it is very clear that it’s the pattern of DNA aberrations across the genome that really gives you a much more refined picture of the phenotype. There are cooperating loci and associations that if you can consider those together, may be more powerful than the uni-focal approach that we have now. So that’s one of the big areas of interest in our lab, what is the pattern of aberrations and can you learn more from the entire profile than you can from the region-by-region approach, considering things one at a time.

The only downside I see is as we’ve gotten higher and higher resolution, we’ve really run into this problem of how complex the human genome is in terms of copy number polymorphisms, and separating out the real signal from the noise is still a bit of a challenge.

Sellers: Some of that will be offset by the scale of
some of the germ-line studies that are planned by the medical population geneticists using the 500K. With researchers running 10,000 normal germ-line DNAs on the 500K, you’re going to have a pretty good map of polymorphisms pretty soon. It’ll never find the ones that are less than one in a thousand, but I think we can count on our medical population genetics colleagues to identify many of these, and that will help us just simply subtract these by database searches.

Maris: I agree. In the meantime, we are going to be scratching our heads until there is a big database of these copy number polymorphisms

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