This result argues for the development of an effective male contraceptive that would shut off spermatogenesis until a man is ready to father children. Note that as sperm progenitor cells go thru each cell division there is a risk of error during the duplication process. So a way to shut down the process until real functioning sperm are needed could greatly reduce the rate at which harmful mutations accumulate:
Importantly, disorders linked to advancing paternal age begin to increase rapidly at about the same time as maternal risks increase -- age 33 to 35. Until now, the only evidence for paternal age effects has come from determining how many children with these diseases are born to fathers of various ages.
To obtain the first genetic explanation for these effects, the scientists studied sperm from about 60 men of various ages and looked for two genetic changes responsible for 99 percent of the cases of Apert syndrome. They found that men over 50 were, on average, three times as likely as men under 30 to have sperm with at least one of these changes. The mutations were not more common in blood samples as men aged.
The scientists say it's likely that the number of cell divisions that go into making a sperm plays a large role in the link between Apert syndrome and paternal age, and represents a fundamental difference between how aging egg and sperm can impact the health of a child.
|Share |||Randall Parker, 2002 October 18 05:55 PM Biotech Reproduction|