Fred H. Previc (2002) An Appealing but Unproven and Incomplete Theory: Evolutionary. Psycoloquy: 13(003) Evolution Bipolar Disorder (2)

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PSYCOLOQUY (ISSN 1055-0143) is sponsored by the American Psychological Association (APA).
Psycoloquy 13(003): An Appealing but Unproven and Incomplete Theory: Evolutionary

Commentary on Sherman on Evolution-Bipolar-Disorder

Fred H. Previc
Northrup Grumman Information Technology
4241 Woodcock Dr. Ste B100
San Antonio TX 78228


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.


Biological clock; Bipolar Disorder; depression; cold adaptation; environment; evolution; Kretschmer; mania; physique; seasonal.
1. I find J.A. Sherman's article (2001) on the evolutionary origin of bipolar disorder (BD) quite appealing. As one who has emphasized the role of environmental factors in the evolution of human intelligence (Previc, 1999) and is pursuing the role of thermoregulatory factors in schizophrenia (Previc, in preparation), I am favorably inclined to viewing brain evolution within an ecological context. Sherman's theory makes intuitive sense in that the need to balance energy expenditure with seasonal fluctuations in food availability would seem essential to human existence prior to the emergence of agricultural societies. Sherman presents a collection of physiological evidence (e.g., physique, fat stores), behavioral evidence (weight gain, sexual desire, sleep, etc.), and seasonal psychiatric incidence data to support her theory. I find the seasonal fluctuation in clinical symptoms (especially mania) to be the most convincing evidence for her theory, although the behavioral and physiological findings also tend to be supportive of the concept that BD is an adaptation to the seasonal climatic cycles at latitudes of 30 degrees and higher. However, Sherman's theory must still be considered unproven and incomplete for two reasons: 1) its epidemiological foundation remains weak, and 2) the neurochemical basis for the evolutionary adaptation has not been established.

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.


Arbisi, P. A., Depue, R. A., Krauss, S., Spoont, M. R., Leon, A., Ainsworth, B., & Muir, R. (1994). Heat-loss response to a thermal challenge in seasonal affective disorder. Psychiatry Research, 52, 199-214.

Berrettini, W. H. (2000). Are schizophrenic and bipolar disorders related? A review of family and molecular studies. Biological Psychiatry, 48, 531-538.

Blackburn, J. R., Pfaus, J. G., & Phillips, A. G. (1992). Dopamine fluctuations in appetitive and defensive behaviours. Progress in Neurobiology, 39, 247-279.

Jain, S., Kaliaperumal, V. G., Chatterji, S., Rao, S., & Murthy, R.S. (1992). Climate and admissions for mania in tropics. Journal of Affective Disorders, 26, 247-250.

Lee, T. F., Mora, F., & Myers, R. D. (1985). Dopamine and thermoregulation: An evaluation with special reference to dopaminergic pathways. Neuroscience and Biobehavioral Reviews, 9, 589-598.

Magnusson, A. (2001). An overview of epidemiological studies on seasonal affective disorder. Acta Psychiatrica Scandinavica, 101, 176-184.

Morral, N., Bertranpetit, J., Estivill, X., Nunes, V., Casals, T., Giminez, J., et al. (1994). The origin of the major cystic fibrosis mutation (@F508) in European populations. Nature Genetics, 7, 169-175.

Myers, D. H., & Davies, P. (1978). The seasonal incidence of mania and its relationships to climatic variables. Psychological Medicine, 8, 433-440.

Previc, F. H. (1999). Dopamine and the origins of human intelligence. Brain and Cognition, 41, 299-350.

Previc, F. H. (in preparation). The role of thermoregulation in the origins and manifestation of schizophrenia.

Sherman, J. A. (2001). Evolutionary origin of bipolar disorder (EOBD), Psycoloquy, 12(028).

Swerdlow, N. R., & Koob, G. F. (1987). Dopamine, schizophrenia, mania, and depression: Toward a unified hypothesis of cortico-striato-pallido-thalamic function. Behavioral and Brain Sciences, 10, 197-245.

Wehr, T. A. (1998). Effect of seasonal changes in daylength on human neuroendocrine function. Hormone Research, 49, 118-124.

Weissman, M. M., Bland, R. C., Canino, G. L., Faravelli, C., Greenwald, S., Hwu, H.-G., et al. (1996). Cross-national epidemiology of major depression and bipolar disorder. Journal of the American Medical Association, 276, 293-299.

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