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Whole Blood Serotonin and Family Background Relate to Male Violence

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Part of the book series: Nato ASI Series ((NSSA,volume 292))

Abstract

Clinical and animal studies suggest that brain serotonergic systems may regulate aggressive behavior. However, the serotonin/violence relation has not been assessed at the epidemiological level. For study of an epidemiological sample we examined blood serotonin; certain physiological and behavioral data suggested that it might serve as an analogue marker for brain serotonergic function. Whole blood serotonin was measured in a representative birth cohort of 781 21-year-old women (48%) and men (52%). Violence was measured using cumulative court conviction records and participant’s self-reports. Potential intervening factors addressed were: gender, age, diurnal variation, diet, psychiatric medications, illicit drug history, season of phlebotomy, plasma tryptophan, platelet count, body mass, suicide attempts, psychiatric diagnoses, alcohol and tobacco dependence, socio-economic status, IQ, and overall criminal offending. Whole blood serotonin related to violence among men but not women. Violent men’s mean serotonin level was .56 SD above the mean of nonviolent men. The finding was specific to violence, as opposed to general crime, and it was robust across two different methods of measuring violence. Together, the intervening variables accounted for 25% of the relation between serotonin and violence. Developmental context interacted significantly with serotonin; serotonin was linked to violence primarily among men who grew up in families with little cohesion and much conflict. To our knowledge, this is the first demonstration that altered blood serotonin concentration is related to violence in the general population, and that the relation may depend on family origins.

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Moffitt, T. et al. (1997). Whole Blood Serotonin and Family Background Relate to Male Violence. In: Raine, A., Brennan, P.A., Farrington, D.P., Mednick, S.A. (eds) Biosocial Bases of Violence. Nato ASI Series, vol 292. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-4648-8_14

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