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Researchers in the field of aging have posited several theories to explain how and why the body ages. One of these theories, the somatic mutation theory of aging, is based on the idea that DNA damage accumulates over time – the result of day-to-day living and oxidative stress. A variety of mechanisms within cells can repair DNA damage and prevent potentially harmful mutations. These repair mechanisms become less efficient as the body ages, however, promoting age-related disease and decline. A new study suggests that loss of the body’s capacity to repair itself starts during adolescence and could influence fertility among women.

The authors of the study assessed germline mutation rates based on blood samples from 41 three-generation families enrolled in a large, multigenerational study in the United States. Germline mutation rates are typically higher among men can vary considerably among people of the same sex.

The analysis revealed that a faster age-adjusted mutation rate increased all-cause mortality rates in both sexes. The rate of DNA mutations increased considerably during adolescence, but later onset of menstruation appeared to slow the rate. In addition, the mutation rate varied, with some participants acquiring mutations at a rate three-fold faster than others. People with slower mutation rates were more likely to have been born to younger parents.

The authors predicted that a faster mutation rate shortened a person’s life as much as five years – roughly equivalent to the effects of smoking or a sedentary lifestyle. The mutation rate also appeared to influence fertility among women, with a faster rate associated with fewer live births and older age at the time of their last child.

These findings suggest that germline mutation rates serve as markers of reproductive and systemic aging and interventions geared toward reducing mutation rates to those found before puberty could have beneficial effects in terms of reducing the incidence of disease and death.

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