I have often heard these distressing words: "I eat right, exercise, don't smoke and take good care of myself. How come my ovaries are failing prematurely." My answer has been, "The ovaries don't care how you take care of yourself, they age based on genetics." According to a new article, they age independantly of the rest of the body. Of course, one can engage in habits, like smoking, which will make them age faster.
Reproductive and somatic aging use different molecular mechanisms that show little overlap between the types of genes required to keep oocytes healthy and the genes that generally extend life span, according to Coleen Murphy, Ph.D., of Princeton University, who described her new findings on oocyte aging at the American Society for Cell Biology Annual Meeting in Denver.
The different genetic pathways help explain why a woman's fertility begins to decline after she is 35 years old, while her other cells do not show significant signs of aging until decades later, Murphy explained. To compare the molecular mechanisms that are switched on or off with the aging of oocytes and somatic cells, Murphy's lab turned to the model organism, Caenorhabditis elegans (C. elegans), the worm-like nematode that set off the whole field of longevity research with the discovery in the 1990s that gene mutations affecting insulin regulation doubled the worm's life span. Insulin/insulin-like growth factor (insulin/IGF) signaling pathways also have been identified in humans. These pathways also seem to regulate longevity in humans.
Using DNA microarrays to measure the expression levels of genes, Dr. Murphy and her colleagues noted a distinctive DNA signature for aging eggs. They also found that the eggs of aging insulin and transforming growth factor-beta (TGF-beta) mutant mice had the same DNA profile that characterized young females.
Finding ways to delay oocyte aging would reduce an older woman's risk of giving birth to a child with birth defects, Murphy said.