Previc's commentary on the evolutionary origin of Bipolar Disorder (EOBD) brings up the intriguing question: When did the BD adaptation occur? Could BD descend from our most ancient ancestors? More sophisticated epidemiological data are needed to test the EOBD model. Specification of a neurophysiological foundation for the model is appropriately omitted because these events involve proximate causation while the EOBD model concerns ultimate causation, which are two disparate levels of discourse. Discoveries in neurophysiology continue to support the model (new class of light-sensing cells; biological signal of season change in seasonal affective disorder patients).
2. Previc's commentary brings up the question of the timing of the BD adaptation, which involves the controversy between the multiregionalist and out of Africa hypotheses of human evolution (see Templeton 2002). Previc incorrectly attributes to the EOBD model the idea that the BD adaptation took place 30,000-50,000 years ago. This dating is consistent with the extreme form of the out of Africa hypothesis, which suggests that peoples migrating from Africa during the last 100,000 years displaced all other living peoples, and that the latter made no genetic contribution to modern humans. Less extreme versions of the out of Africa hypothesis allow for some genetic contributions from prior groups. The most relevant possibilities for the timing of the BD adaptation are these: 1) The BD adaptation evolved 30,000-50,000 years ago, as Previc suggests. 2) It evolved earlier among peoples of the most recent out of Africa expansion. 3) The BD adaptation evolved in preexisting peoples, and descended to modern humans. (Possibilities relevant to the hypothesis of Gardner[1982] are omitted here.)
3. Previc supports the first option by drawing a parallel between BD and cystic fibrosis. He argues that since the major genetic mutation resulting in cystic fibrosis occurred among Europeans about 50,000 years ago, it is reasonable to suppose that the BD genetic adaptation could have occurred in the same time frame. However, there are important differences between BD and cystic fibrosis. BD probably involves more than one gene (Sherman 2001), while cystic fibrosis is the result of a single mutation. BD is reported to have the genetic epidemiology of an adaptation; cystic fibrosis presumably does not. BD behaviors are hypothesized to be the product of adaptations to climatic conditions, which were shaped over a long period of time, while the cystic fibrosis mutation was presumably an isolated event.
4. General considerations from evolutionary theory also suggest reserve about a recent date for the BD adaptation. Biological adaptations are most likely to occur among small, isolated, homogeneous groups subjected to severe selective pressures, but cultural adaptations reduce the severity of selective pressures. Some paleoanthropologists may argue that peoples of the latest out of Africa expansion were so culturally sophisticated that the necessary conditions for biological evolution were absent or weak. Knowledge of the controlled use of fire, improved shelter, food storage, and clothing, lessened the selective pressures of climate.
5. As implied in the target article, BD or similar behaviors, may have evolved in more than one time and place. Over the passage of time, these behaviors may have been partially or completely subjected to negative selection, more in some places than in others. Contemporary BD could be the product of successive evolutionary contributions that occurred at different times and places. Behaviors acquired at one time and place, even in response to different selective pressures, may have been built upon in other times and places. For example, the substratum of BD behaviors may have evolved as social rank behaviors as Gardner (1982) suggests.
6. Templeton (2002) dates gene flow among Old World human populations back to at least 600,000 years ago, and it seems more likely that the BD adaptation descends from our most ancient ancestors than from our most recent. The ancestral groups that best match maximal conditions for the development of the BD adaptation are Neanderthal and their precursors. They endured the harshest conditions humans have survived; ice barriers served to isolate peoples into small groups, and their culture during the earliest times offered less protection from environmental pressures. Neanderthal had highly derived biological cold adaptations (Sherman 2001), including a cold adapted build, which is correlated with BD. Following the logic of the EOBD model, it would be surprising if a group specialized for cold adaptation did not also manifest the BD adaptation. Could BD be a kind of behavioral fossil? Can we learn about ancient peoples by extrapolating from the characteristics associated with BD? Genetic research has all but ruled out the possibility that Neanderthal genetically contributed to modern peoples, but Neanderthal's predecessors remain a possible source of the BD adaptation.
7. Previc's second major criticism is the lack of a neurochemical basis for the EOBD model. The main issue here is level of discourse. The EOBD model concerns ultimate causation while neurophysiological data concern tiny events of proximate causation. Previc's ideas about dopamine are promising, but neurophysiological theorizing is highly complex and belongs to another level of analysis. A comprehensive theory of the etiology of BD will need to include detailed, integrated knowledge at several levels of discourse. In any case, spelling out a specific neurophysiological foundation for the EOBD model is more appropriately a task for an expert in that field of research. Neurophysiological data consistent with the EOBD model continue to accumulate. Hattar et al. (2002) discovered a new class of light-sensing cells in the retina that appear to reset the body's master biological clock each morning and night. Wehr et al. (2002, 1108) reported, "Patients with seasonal affective disorder generate a biological signal of change of season that is absent in healthy volunteers and that is similar to the signal that mammals use to regulate seasonal change in their behavior." (A large percentage of individuals with seasonal affective disorder are also diagnosed with BD.)
8. Previc's discussion contains misunderstandings of the EOBD model (and questionable points) which will be considered in order of their appearance in his commentary. First, the model is not about the "effects of latitude." There is a danger in reifying operational variables used to test a theory. Data correlating BD behaviors with latitude were cited, but the latitude variable only approximates variations in the environmental conditions (long severe winters and short summers) of the Pleistocene, which are thought to be important in BD's evolution. The EOBD model suggests that genes modified by environmental conditions at particular time(s) and place(s) were subsequently carried all over the world. The interaction of these genes with environmental conditions out of time and place facilitates the unreeling of the inappropriate behaviors we call BD.
9. Previc suggests that the empirical basis for the EOBD model is weakened because data regarding depression fail to demonstrate a seasonality effect so clearly as data concerning Manic Episode, yet this result was anticipated (Sherman 2001). Data regarding the onset of a BD Major Depressive Episode are less reliable than in the case of Manic Episode. Depressed behavior is likely to come to attention only when it is unbearable or life threatening, while manic behavior is intrusive from the start. For these reasons, data based on onset of depressed behaviors are less likely to demonstrate so clear a true effect of seasonality as in the case of mania. However, contrary to Previc's implication, Magnusson (2000) concluded that "depressive symptoms peak in winter."
10. As already indicated, Previc makes a serious misstatement of the EOBD model when he assumes that the BD genetic adaptation most likely occurred in the past 30,000-50,000 years. Therefore, his subsequent conclusion that epidemiological findings do not provide clear support for the EOBD model is inaccurate. Previc asserts that BD, "should be more widely evident among individuals of European and/or Asian descent." The EOBD model doesn't necessarily predict this. The glacial fringes of Europe and Asia were important in BD's evolution, but BD evolutionary processes may have begun much earlier than Previc supposes. Subsequent large migrations and population changes make Previc's prediction moot. Because there is no evidence of massive return migrations to tropical Africa until contemporary times, it is predicted that circular BD will not be found among peoples genetically indigenous to the area (Sherman 2001).
11. Previc suggests that the EOBD model is contradicted by data that find no major difference in the incidence of seasonal depression between individuals of African or non-African origin living at northern latitude (Magnusson 2000). These data (and similar results that could be cited) are inadequate to test the model. They do not concern circular BD, and skin color is a notoriously poor index of genetic descent. A genetic model cannot be tested by data uncontrolled for heredity. In addition, other variables may be involved. For example, what is the general effect of transfer to a vastly different climate than that of childhood? Clearly, new data based on advanced genetic techniques are needed to clarify issues regarding the epidemiology of BD. National, group, and ethnic differences in mental illness are difficult, sensitive issues that require our best scientific methodology.
12. It is hoped that the EOBD model will stimulate other scientists to investigate the etiology of BD. It is a fascinating disorder, and its conquest would alleviate enormous suffering. BD is recommended as a subject for research as the most clearly defined of the severe mental illnesses. An understanding of its etiology promises to enlighten us about less serious affective disorders, and perhaps even our own evolutionary history. The EOBD model may seem crazy, but could it be crazy enough to be true?
Gardner, R. (1982) Mechanisms in manic & depressive disorder: an evolutionary model. Archives of General Psychiatry 39: 1436-41.
Hattar, S., Liao, H.-W., Takao, M., Berson, D. M. & Yau, K.-W. (2002) Melanopsin-containing retinal ganglion cells: architecture, projections, and intrinsic photosensitivity. Science 295: 1065-74.
Magnusson, A. (2000) An overview of epidemiological studies on seasonal affective disorder. Acta Psychiatrica Scandinavica 101: 176-84.
Previc, F. H. (2002) An appealing but unproven and incomplete theory: Evolutionary origin of bipolar disorder. PSYCOLOQUY 13(003) Commentary on Sherman on Evolution-Bipolar-Disorder (2) http://www.cogsci.soton.ac.uk/cgi/psyc/newpsy?13.003
Sherman, J. A. (2001) Evolutionary origin of bipolar disorder (EOBD). PSYCOLOQUY 12(028) Target Article by Sherman on Evolution-Bipolar-Disorder (1) http://www.cogsci.soton.ac.uk/cgi/psyc/newpsy?12.028
Templeton, A. R. (2002) Out of Africa again and again. Nature 41: 45-51.
Wehr, T. A., Duncan, W. C. Jr., Sher, L., Aeschbach, D., Schwartz, P. J., Turner, E. H., Postolache, T. T., & Rosenthal, N.E. (2001) A circadian signal of change of season in patients with seasonal affective disorder. Archives of General Psychiatry 58, 1108-14.