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, May 20, 2007

There were four men out of 97 retirees from the Lawrence Berkeley Labs at increased risk of transmitting multiple genetic and chromosomal defects



Advancing age has differential effects on DNA damage, chromatin integrity, gene mutations, and aneuploidies in sperm
A. J. Wyrobek*,,, B. Eskenazi,, S. Young, N. Arnheim¶, I. Tiemann-Boege¶, E. W. Jabs||, R. L. Glaser**, F. S. Pearson*, and D. Evenson

*Biosciences Directorate, Lawrence Livermore National Laboratory, P.O. Box 808, Livermore, CA 94550; School of Public Health, University of California, Berkeley, CA 94720-7380; ¶Molecular and Computational Biology Program, University of Southern California, Los Angeles, CA 90089; ||Institute of Genetic Medicine, Center for Craniofacial Development and Disorders, Departments of Pediatrics, Medicine, and Surgery, Johns Hopkins University, Baltimore, MD 21205; **Department of Biology, Massachusetts College of Liberal Arts, North Adams, MA 01247; and Department of Chemistry and Biochemistry, South Dakota State University, Brookings, SD 57007

Edited by James E. Cleaver, University of California, San Francisco, CA, and approved April 21, 2006 (received for review August 12, 2005)




Implications. Our findings are based on convenience samples of generally healthy nonsmoking workers and retirees in a nonclinical setting and may not be representative of men attending fertility clinics and those with health problems. Furthermore, markers for other gene mutations, translocations, and deletions were not explored. Also, evidence for group-specific age associations raises questions of whether sperm defects were due to age per se or arise from lifestyles or increased opportunities for mutagenic exposures in older men.


Our sperm findings provide further evidence that men choosing to delay fatherhood may have a lower likelihood of a successful pregnancy free of early loss and gene defects. However, unlike women, older men do not appear to be at increased risk for trisomic or triploid pregnancies. The poor correlations among sperm defects suggest that multiple measures of genomic damage are needed to fully assess the reproductive and genetic burden in sperm, and that men with good semen quality may still be at risk for fathering a child with a genomic defect. Our study also identified a small fraction of men who may be at increased risk for transmitting multiple genetic and chromosomal defects, raising further concerns for men who delay fatherhood.

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