life stress unrelated to either social support (Hopkins et al., 1987) or infant stressors (O’Hara et
al., 1984) did not distinguish depressed from nondepressed groups.
If the defection hypothesis can elucidate PPD at the level of function, then perhaps it can
elucidate depression in general. Whenever a social strategy has failed, be it a job, marriage, or
other important endeavor involving the cooperation of others, individuals should be aware that
they have suffered a fitness cost, and they should lose interest and reduce or eliminate their
investment in this activity. They should defect. When individuals find that the social costs of
defecting are high, that is, when they have little power to renegotiate social contracts, they may
stop investing in themselves until these social costs are reduced or investment by others in the
venture is increased. This view is consistent with that of Wenegrat (1995), who argues that the
high rates of depression among women are a consequence of their relative lack of power in
society.
Because PPD occurs predictably among approximately 10% of a readily identifiable
population (i.e., pregnant women), it represents an ideal opportunity to study depression. If
PPD is to serve as a model for depression, however, then it should share fundamental
similarities with depressive episodes in general. Whiffen (1992) carefully reviewed 24 studies
on PPD published between 1964 and 1991 specifically to determine whether PPD differed from
depression in any important aspects. It did not. She concluded that research and practice
would benefit from abandoning PPD as a distinct diagnosis. In a study specifically designed to
determine whether PPD is fundamentally different from general depression, Whiffen and Gotlib
(1993) conclude that the primary difference between women with PPD versus women with
non-PPD is that PPD woman are less depressed, and that the data collected in their study do not
support the hypothesis that PPD is separate diagnostically from non-PPD. PPD thus appears to
be a good model for depression in general. Nevertheless, they concede that other factors like
family psychiatric history, treatment response, and biological variables must be considered
before a firm conclusion can be reached.
Self-report methodologies
Most of the evidence in favor of the defection hypothesis cannot be explained as an artifact
of biased reporting by depressed mothers. With the exception of maternal perceptions of
paternal investment, all important correlates of PPD are supported, at least in part, by objective
measures, including hospital charts, researcher ratings of mother-infant interactions, face-to-face
interviews and observations, income levels, and unemployment status (Campbell & Cohn, 1991;
Campbell et al., 1992; Hopkins et al., 1987; Kumar & Robson, 1984; O’Hara et al., 1984; Paykel
et al., 1980; Warner et al., 1996; Whiffen & Gotlib, 1989). The validity of the paternal
investment data is supported by longitudinal studies where the maternal perception of paternal
support was collected prepartum when the mothers were not depressed (e.g., Gotlib et al., 1991),
and where the father’s mood (assessed by the father’s self-report) predicted the mother’s future
mood.
Further testing of the defection hypothesis
Proof of the defection hypothesis will require substantially more data than is currently
available. This includes stronger evidence that PPD occurs cross-culturally when conditions
warrant, that, in its major forms, it actually does increase the investment of others, and that, in
addition to the support and infant variables, low levels of resources, maternal health, and mate
quality are etiological factors. Conversely, mothers should NOT suffer a loss of interest in the
infant when the infant is of high viability, when there is sufficient social support and
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