What About Biological Factors?


It has been suggested that biological factors are responsible for the gender differences found in depression. First, there is the possibility that women may be at a greater risk because of the biological consequences of pregnancy andchildbirth. There has been a failure to specify what these biological consequences might be, however, and evidence to support biological explanations has been inconsistent.

In some contexts, having had children appears to be a risk factor for depression (Brown and Harris, 1978), while it appears to have no effect in others (Gaminde et al., 1993). It is possible that parity may operate through culturally influenced psychosocial pathways, rather than biological ones.

We found that parity among women was unrelated to risk (Nazroo et al., 1997, 1998). Thirty-eight percent of women with children had an episode of depression, compared to 33% of women without children.

While this suggests that biological changes related to parity are not important, the role-determined nature of the difference in risk between men and women (described earlier) suggests that the social changes that follow childbirth are of some importance. The implication is that any difference related to having had children is a consequence of increased exposure to life events rather than biological changes.

Another possibility is that sex hormones are responsible for gender differences in depression. Despite the fact that gender differences in the experience of depression appear to emerge around puberty (Bebbington, 1996), there is no clear evidence that hormonal changes associated with the menstrual cycle, resulting in perimenstrual mood changes, are involved (Harris et al., 1991; Popay et al., 1993).

We found that only certain crises were associated with a greater risk of depression for women but only when there were clear role differences between the men and women in associated domains (Nazroo et al., 1997, 1998). The fact that the gender difference turned out to have such a specific relationship with the nature of the stress suggests that such a general biological difference was not involved.

It thus seems that the gender difference in depression reported here was unlikely to be the result of biological differences related either to sex hormones or to parity.

In summary, there was no evidence to support the possibility that the higher risk was the consequence of a measurement artifact. The higher rate of depression among women was not a consequence of gender-typed responses to crises. The very specific context in which gender differences for risk of depression occurred suggested that they were not the consequence of a general difference in biological risk either.

Rather, the higher risk of depression among women was the consequence of gender differences in roles, with women only having a higher risk following crises involving children, housing and reproduction, rather than those involving finances, work and the marital relationship. Following such crises, there was only a gender difference in risk if there was a clear difference in the role salience of the crisis to the man and woman. Where the crisis had a similar role salience for both, the man had a similar risk of depression to the woman.
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