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Social defeat: Risk factor for schizophrenia?

  • Jean-Paul Selten (a1) and Elizabeth Cantor-Graae (a2)
Summary

The hypothesis that chronic and long-term experience of ‘social defeat’ may increase the risk for schizophrenia is proposed. This increased risk may result from sensitisation of the mesolimbic dopamine system and/or increased baseline activity of this system. Data supporting the social defeat hypothesis are presented.

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Copyright
Corresponding author
Dr J. P. Selten, Department of Psychiatry, University Hospital, PO Box 85500, 3508 GA Utrecht, The Netherlands. Tel: +31 30 2508 180; fax: +31 302505443; e-mail: j.p.selten@azu.nl
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Declaration of interest

None.

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References
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Arseneault, L., Cannon, M., Witton, J., et al (2004) Causal association between cannabis and psychosis: examination of the evidence. British Journal of Psychiatry, 184, 110117.
Boydell, J., van Os, J., McKenzie, K., et al (2001) Incidence of schizophrenia in ethnic minorities in London: ecological study into interactions with the environment. BMJ, 323, 14.
Cantor-Graae, E. & Selten, J. P. (2005) Schizophrenia and migration: a meta-analysis and review. American Journal of Psychiatry, 162, 1224.
Covington, H. E. & Miczek, K. A. (2001) Repeated social-defeat stress, cocaine or morphine. Effects on behavioral sensitization and intravenous cocaine self-administration “binges”. Psychopharmacology 158, 388398.
David, A. S., Malmberg, A., Brandt, L., et al (1997) IQ and risk for schizophrenia: a population-based cohort study. Psychological Medicine, 27, 13111323.
Isovich, E., Engelmann, M., Landgraf, R., et al (2001) Social isolation after a single defeat reduces striatal dopamine transporter binding in rats. European Journal of Neuroscience, 13, 12541256.
Janssen, I., Hanssen, M., Bak, M., et al (2003) Discrimination and delusional ideation. British Journal of Psychiatry, 182, 7176.
Laruelle, M. (2003) Dopamine transmission in the schizophrenic brain. In Schizophrenia (eds Hirsch, S. R. & Weinberger, D.), pp. 365387. Oxford: Blackwell.
Pedersen, C. B. & Mortensen, P. B. (2001) Evidence of a dose–response relationship between urbanicity during upbringing and schizophrenia risk. Archives of General Psychiatry, 58, 10391046.
Tidey, J.W. & Miczek, K. A. (1996) Social defeat stress selectively alters mesocorticolimbic dopamine release: an in vivo microdialysis study. Brain Research, 721, 140149.
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The British Journal of Psychiatry
  • ISSN: 0007-1250
  • EISSN: 1472-1465
  • URL: /core/journals/the-british-journal-of-psychiatry
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Social defeat: Risk factor for schizophrenia?

  • Jean-Paul Selten (a1) and Elizabeth Cantor-Graae (a2)
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eLetters

The Social Defeat hypothesis: Difficult to refute

Muzaffar Husain, SHO in Learning Disabilities
19 August 2005

Selten and Cantor-Graae(1) have presented a very convincing case for the social defeat hypothesis. They invite readers to dwell on it and ‘carry out empirical experiments to confirm or refute the proposal’. Such sentiments are laudable, but my query is, how easy would it be to falsify such a proposition in the first place?(2)

The authors acknowledge that social defeat is a relatively ubiquitousphenomenon, and something which is so common would indeed be difficult to discount in any model of schizophrenia. Therein lies the risk of all research in this field. Over the past years there has been an explosion ofnew evidence on the possible causation of schizophrenia. However, vague and generalist hypotheses are difficult to refute. That is why it seems that a lot has been proposed but very little actually recanted.

I suppose it is easier to shout out ‘Eureka’, than to say ‘No, I accept, I was wrong’. Advancing a hypothesis is easier than taking it back.

From evidence in molecular genetics, the glutamate hypothesis looks set to overthrow dopamine dysregulation as the central feature of schizophrenia(3). But as with the risk factor of social defeat, glutamate too is ubiquitous. It is found all over the brain. It becomes very difficult to build any model of schizophrenia with the glutamate system unaffected.

Even when results do reveal contradictory findings, how often are researchers obliged to retract their discoveries? Recent linkage and association studies have revealed several loci as markers of schizophrenia. The history of most of these loci is marked by enthusiasticdiscovery, followed by non-replications in other samples (usually by a different research group). How many times have researchers taken back their claims of discovery in the light of conflicting evidence? How much does this add to our knowledge anyway?

Science requires hard work and dedication. But it also requires courage. Schizophrenia research would be better guided were scientists obliged to frame narrower and more falsifiable hypotheses. They ought to also have a greater sense of ownership of these propositions. Any approachotherwise, seems doomed to take us further away from what really matters.

1. Selten, J.,P., and Cantor-Graae, E.(2005) Social Defeat: risk factor for schizophrenia? British Journal of Psychiatry , 187, 101-102

2. Popper, K (2002) Logic of Scientific Discovery

3. McGuffin, P ,Owen M., and Gottesman, I., I., (2004) Psychiatric Genetics and genomics- An update, 449-464
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Conflict of interest: None Declared

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