No grounds for alleged link between stress and premature ovarian failure.
Contrary to what a Bangalore Mirror article suggests, there is little reason for young women to fear that job-related stress or everyday chemical exposures will lead to premature menopause.
In her July 23rd article in the Bangalore Mirror, reporter Sahana Charan discusses a possible rise in premature ovarian failure among young Indian women, suggesting that job-related lifestyle, pollution and pesticides are contributing to menopause as early as the mid-20s.
Unfortunately, the misleading conclusions drawn in the article are based on anecdote and misinterpretation of scientific research and may cause readers unnecessary alarm. In particular, Charan mistakenly equates premature ovarian failure – essentially menopause occurring before age 40 – with other less serious reproductive disorders, such as irregular menstrual periods.
Although stress and toxic substances may contribute to the latter, there is virtually no evidence to suggest they may cause irreversible ovarian failure in young women.
The premise of the article rests on the claim that rates of premature ovarian failure are increasing in Indian women. No studies are cited to support that claim. The reporter quotes several physicians who imply that stressful jobs, irregular work shifts, pesticides in food and pollution are causing this alleged rise in premature ovarian failure. Had she probed a little deeper or consulted scientists working in the field, Charan would have learned that none of those factors are proven contributors to premature ovarian failure.
In reality, very little is known about what causes the disorder that strikes one percent of women, although it has been linked to certain genetic conditions, autoimmune disorders and chemotherapy.
Part of the confusion lies in the fact that Charan and the experts quoted in the article fail to distinguish between the two very different health conditions: the unusual and serious premature ovarian failure and the more common, minor reductions in fertility. Even catastrophic environmental exposures, such as the extreme levels of dioxin encountered in women who lived through the Italian Seveso disaster, tend to be associated with only reductions in measures of fertility – such as an increased time until conception – rather than the extreme decline in fertility characterized by premature ovarian failure. Although common environmental exposures such as air pollution or bisphenol A may have effects on various aspects of fertility and pregnancy – miscarriage rates or success during in vitro fertilization, respectively – there is currently no evidence to suggest that they cause premature ovarian failure.
The Bangalore Mirror article risks unnecessarily alarming readers and causing young women to fear that stressful jobs and unavoidable environmental exposures may make them infertile, when in reality, such claims are ungrounded in scientific fact.
