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The British Journal of Psychiatry (2006) 188: 393-394. doi: 10.1192/bjp.188.4.393-a
© 2006 The Royal College of Psychiatrists
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Correspondence

Social defeat and schizophrenia

C. Cantor

Department of Psychiatry, University of Queensland 4072, Australia.

Correspondence: E-mail: cantor98{at}powerup.com.au

Selton & Cantor-Graae (2005) proposed that long-term experiences of social defeat may sensitise the mesolimbic dopamine system, increasing the risk for schizophrenia. Regrettably they continued the tradition of ignoring the distal evolutionary perspective. An underemphasised observation is that although neurological illnesses have lifetime prevalence rates in the order of thousands, prevalence rates for psychiatric illness often lie between 1% (as for schizophrenia) and about 20%. When considering highly disabling conditions such as schizophrenia, depression or anxiety, one must consider the survival implications. Over evolutionary time if there were not some adaptive advantage these genes would have been eliminated. The suggestion that these conditions are products of modern culture is untenable, as they are found in all cultures and have been observed back in time as far as history permits. Furthermore, animals certainly have depression and anxiety.

Selton & Cantor-Graae could have referred to the book by Stevens & Price (2000) on the evolutionary adaptiveness of social subordination and schizophrenia. They proposed that schizotypal individuals at times of social crises may come to the fore and lead individuals with similar genes in new directions. Similarly, work by Gilbert (1992) and Sloman (2000) on depression and defeat warrant consideration.

Evolutionary perspectives often suggest obvious but new directions for gene–environment research. For example, I have proposed a model of post-traumatic stress disorder (PTSD) based on mammalian defences (Cantor, 2005). An understanding of these suggests that looking for genes for the entity PTSD is misguided. The six mammalian defences operate under different selection regimes, therefore greater evolution of one will be associated with a decreased need for others. The tortoise, although not a mammal, provides the perfect example: its extraordinary defensive shell reduces the need to flee or fight to virtually zero.

Furthermore, the possibility arises that future gene therapies may have serious untoward consequences (Watson & Andrews, 2002). The genes associated with social defeat may encourage a battered wife to yield to her brutal husband, albeit at the price of chronic depression. Should her relevant genes be deleted by future gene therapy, potential consequences include being killed as a result of not yielding, killing her abuser in retaliation or at least a heightened state of domestic abuse. The potential for such untoward consequences must be considered.

REFERENCES

Cantor, C. (2005) Evolution and Posttraumatic Stress: Disorders of Vigilance and Defence. Hove: Routledge.

Gilbert, P. (1992) Depression: The Evolution of Powerlessness. Hove: Lawrence Erlbaum.

Selton, J. P. & Cantor-Graae, E. (2005) Social defeat: risk factor for schizophrenia? British Journal of Psychiatry, 187, 101 –102.[Abstract/Free Full Text]

Sloman, L. (2000) How the involuntary defeat strategy relates to depression. In Subordination and Defeat: An Evolutionary Approach to Mood Disorders and Their Therapy (eds L. Sloman & P. Gilbert), pp. 47–67. Mahwah, NJ: Lawrence Erlbaum.

Stevens, A. & Price, J. (2000) Prophets, Cults and Madness. London: Duckworth.

Watson, P. J. & Andrews, P. W. (2002) Toward a revised revolutionary adaptationist analysis of depression: the social navigation hypothesis. Journal of Affective Disorders, 72, 1 –14.[CrossRef][Medline]





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