My interpretation of the evidence for a specific biological vulnerability to depression in women may be politically driven, since the choice between social and biological theories can be represented at the choice between seeing women either as universally disadvantaged, or as inherently vulnerable with all the associated implications of inferiority.
Direct evidence linking hormone status to depressive disorder has some face validity: oestradiol and progesterone seem to modulate the neurotransmitter and neuroendocrine systems, including those involving monamines, and there are transitions in women's lives characterized by hormonal shifts that may also be associated with mood disturbance (childbirth and the menopause).
The evidence in this area is extremely complicated (Bebbington, 1996). Moreover, there is a more plausible neuroendocrine hypothesis for depression involving glucocorticoids. This offers an explanation for a range of other neurohumoral phenomena, and a mechanism whereby extrinsic stress may result in the features of depressive disorder (Checkley, 1998; Dinan, 1994). It links overactivation of the hypothalamico-pituitary-adrenal (HPA) axis and the associated hypercortisolism with the changes in the central monaminergic pathways thought to underlie depression and the actions of antidepressants. These changes will probably turn out to be the major hormonal concomitants of depressive disorder. Unfortunately for our purpose, they cannot explain the sex difference: specifically, the function of the HPA axis in general does not differ by sex in the required manner (Allen & Pitts, 1984; Ansseau et al., 1987; Hunt et al., 1989; Maes et al., 1989).
The failure to find a convincing sex-related biological mechanism for depression that would account for the sex difference has its parallel in genetic studies. It is extremely unlikely that biological differences between women would be unaffected by intrafamilial (specifically, genetic) factors. The most plausible model is one based on multiple threshold liability. This assumes that the familial liability to a disorder is continuously distributed, comprising both genetic factors and familial-environmental effects. Depression in women can be conceived as a broad form of disorder with a lower threshold than the narrow male form, thus accounting for the higher prevalence rate in women. Under this model, the relatives of male probands will be more frequently affected, because in them the loading of familial factors will be greater (Carter, 1969). In practice, the relatives of male depressives are not at higher risk than the relatives of female depressives (Kupfer et al., 1989; Merikangas et al., 1985). Kendler and Prescott (1999) and Sullivan and colleagues (2002) were led to conclude that the heritability of the liability to depression was similar in men and women, even though the specific genetic factors might not overlap completely. Thus, it seems that the sex ratio must be explained in terms of extra-familial influences. This still allows for genetic effects in the transmission of depression, we merely assert that they do not cause the sex difference.
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