The evolutionary origin of bipolar disorder (EOBD) proposed by Dr. J. A. Sherman is intuitively appealing but lacking in two important respects: 1) epidemiological evidence does not provide clear support for it; and 2) it is lacking a neural foundation. The latter problem may be corrected by assuming that seasonal fluctuations in dopamine partly underlie the symptomatology of BD.
2. As regards the first issue, Sherman proposes that BD is an adaptation to a seasonal climate of long winters and short summers. This is consistent with the fact that seasonal fluctuations in mania are more likely to occur at temperate-to-extreme latitudes than tropical ones (Jain, Kaliaperumal, Chatterji, Roa, & Murthy, 1992). However, the effects of latitude on seasonal fluctuations in depression, which may be a more complex and multi-faceted disorder than mania, are much less pronounced (see Magnusson, 2000).
3. Assuming that the evolutionary adaptation proposed by Sherman is largely genetic which Sherman implies, and which is clearly suggested by the high genetic inheritance in BD (Berretini, 2000), then it should be most widely evident among individuals of European and/or Asian descent. If that were the case, the genetic adaptation most likely occurred after the emergence of modern humans in Europe and Northern Asia (e.g., within the past 30,000-50,000 years). Indeed, the major genetic mutation resulting in cystic fibrosis (delta F508) appears to date back around 50,000 years and is predominantly found among European populations (Morral et al., 1994). An even worldwide distribution of BD would be contrary to Sherman's hypothesis, since it would imply that the genetic adaptation occurred at least 100,000 years ago, when humans first emerged from equatorial Africa (where there are little or no seasonal temperature fluctuations). Unfortunately, the evidence concerning the worldwide distribution of most major psychological disorders (including BD) is inconclusive, due to nonstandardized diagnostic, sampling, and other methodological problems. However, one of the largest and best-controlled cross-national studies did not find a greatly increased incidence of BD in persons of European or Asian descent (Weissman et al., 1996). Moreover, there does not appear to be a major difference in the incidence of seasonal depression between individuals of African or non-African origin living at northern latitudes (Magnusson, 2000). To the contrary, there is evidence that recent migrants to northern latitudes are more likely to suffer from seasonal affective disorder than are natives (Magnusson, 2000), which is seemingly counter to Sherman's hypothesis that BD represents an adaptation to a seasonally fluctuating climate.
4. The second issue involves the neural substrate for BD and its relation to environmental fluctuations, which Sherman (2001) does not adequately address. According to a leading theory (Swerdlow & Koob, 1987), the key neurotransmitter involved in both depression and mania is dopamine. Too little dopamine leads to depression (at least in terms of the symptoms that do not involve mood), whereas too much dopamine leads to mania (as well as the related positive symptoms of schizophrenia) (Swerdlow & Koob, 1987). Dopamine has long been considered important in sexual and other "motivational" behaviors as well as motor activity and abstract intellectual thought (Blackburn, Pfaus, & Phiillips, 1992; Previc, 1999), though it may contribute much less to consummatory behavior such as feeding (Blackburn et al., 1992). This conforms to the diagnostic profile of mania, which includes grandiosity, talkativeness, racing thoughts, psychomotor agitation, flight of ideas, increase in goal-directed activities, and heightened sexual activity (Sherman, 2001). In addition, dopaminergic systems help to regulate a number of hormones such as prolactin and thyroid and growth hormones, which also show seasonal fluctuations (Wehr, 1998).
5. Dopamine levels are believed to fluctuate seasonally (Arbisi et al., 1994) and are elevated in response to high ambient temperatures, which is in line with the hypothermic action of dopamine (Lee, Mora, & Myers, 1985). This temperature-sensitivity of CNS dopamine levels is significant in that ambient temperature, even more than day-length, may be the environmental catalyst in manic episodes (Myers & Davies, 1978). Thus, Sherman may well care to expand on the dopaminergic role in BD, as well as that of other neurotransmitter systems that may fluctuate either seasonally or during BD episodes.
6. Sherman is to be commended for having integrated several lines of evidence in support of an ecological basis for BD, and her theory should be the basis for further research in this area. The ultimate triumph of her theory, however, will require more confirmatory evidence concerning the epidemiology of BD as well as a more complete neurochemical account.
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