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.

Wednesday, May 23, 2007

$15,000,000 NARSAD WHY DON'T YOU ANNOUNCE TO THE PUBLIC THAT AT LEAST 33% OF AUTISM AND SCHIZOPHRENIA IS CAUSED BY OLDER FATHERS HAVING BABIES??


Interviewed by Norman Sussman Primary Psychiatry
"The most irrefutable finding is our demonstration that a father’s age is a major risk factor for schizophrenia. We were the first group to show that schizophrenia is linearly related to paternal age and that the risk is tripled for the offspring of the oldest groups of fathers.7 This finding has been born out in every single cohort study that has looked at paternal age and the risk for schizophrenia. The only other finding that has been as consistently replicated in schizophrenia research is that there is an increased risk associated with a family history of schizophrenia. Since only 10% to 15% of schizophrenia cases have a family history, family history does not explain much of the population risk for schizophrenia. However, we think that approximately one third or one quarter of all schizophrenia cases may be attributable to paternal age. Paternal age is the major source of de novo genetic diseases in the human population, which was first described by Penrose8 in the 1950s. He hypothesized that this was due to copy errors that arose in the male germ line over the many cycles of sperm cell replications. These mutations accumulate as paternal age advances. After the Penrose report, medical researchers identified scores of sporadic diseases in the offspring of older fathers, suggesting that these could occur from gene mutations. Particular attention was paid to conditions in last-born children...."
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NARSAD: The Mental Health Research Association Announces 245 New Research Grants To Established And Early-Career Investigators

23 May 2007 - 12:00 PDT



NARSAD: The Mental Health Research Association announces the awarding of 23 Distinguished Investigator grants and 222 Young Investigator grants for 2007. The awards, which represent more than 15 million dollars in new grantmaking, will be used to support brain and behavioral research that offers the potential of breakthrough findings on serious mental illnesses.
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Dolores M. Malaspina, M.D. 2001 Independent Investigator 2001



Dolores Malaspina, M.D., M.S.P.H. (Independent Investigator 2001) of New York State Psychiatric Institute, will examine the novel hypothesis that new genetic mutations can cause schizophrenia, and will attempt to define the clinical profile (phenotype) of this type of schizophrenia, known as sporadic schizophrenia (the birth of an affected individual into an unaffected family). This type of schizophrenia has previously been thought to originate from environmental factors that either act independently or interact with latent genes. Dr. Malaspina has conducted two preliminary studies which support the new mutations hypothesis. As a major influence on new mutations in the human gene pool is related to the advancing age of fathers, Dr. Malaspina first examined the relationship of schizophrenia and paternal age. Data showed a strong escalation in schizophrenia risk as the age of the father increased, accounting for over a quarter of the schizophrenia cases. Another of her studies found that fathers of sporadic schizophrenia cases were 5 years older than familial case fathers. If sporadic schizophrenia can originate from new mutations, then neurodevelopmental genes are reasonable candidates. Her study will examine if patients with sporadic schizophrenia, particularly those with fathers older than 35 at birth, show features found in other neurodevelopmental diseases that correlate with paternal age, such as craniofacial abnormalities, nonspecific cognitive deficits and delayed developmental milestones. However, if genes that arise from mutations are inherited by later generations, then some familial cases with a similar illness would not have a paternal age effect. Dr. Malaspina plans to define the clinical profile in sporadic patients associated with paternal age through group comparisons and cluster analysis.

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