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.

Sunday, June 17, 2007

Thomas Wassink and Joseph Piven Know Very Well That the Rise In Cases of Autism is Due To Older Guys Fathering Babies, But Will They Focus On That, No

Of course there are many other causes of autism. Some is familial, some due to a mother having had an older father at her birth. A family history of autoimmune disorders is a strong risk factor for having an autistic child in the next generation.



Thomas H. Wassink1 and Joseph Piven2

(1) Psychiatry Research, MEB, Department of Psychiatry, University of Iowa Hospitals and Clinics, 52242 Iowa City, IA, USA
(2) Department of Psychiatry, University of North Carolina, Chapel Hill, CB 7160, 27599-7160 Chapel Hill, NC, USA


Abstract Autism is a severe neurodevelopmental disorder characterized by communication and social deficits and by stereotyped, repetitive behaviors. The syndrome of autism is highly heritable, is considered to be etiologically heterogeneous and is thought to be the result of multiple, interacting genes. It is more common than previously thought, and has a complex pattern of genetic transmission. From four recently completed genome-wide linkage screens of autism, distal 7q has emerged as the most prominent chromosomal region of interest. Additional support for 7q comes from autistic individuals with gross 7q cytologic abnormalities, and from linkage and association data in families with language and speech disorders. Chromosome 15q11-13 is also of interest because of numerous reports of macroscopic and molecular abnormalities in the region associated with Prader-Willi and Angelman syndromes. In this review, molecular aspects of these data, as well as future avenues of investigation, are discussed.

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