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Neurobiological cause of intergroup conflict: 'Bonding hormone' drives aggression towards competing out-groups

Date:
June 15, 2010
Source:
Universiteit van Amsterdam (UVA)
Summary:
Researchers in the Netherlands provide first-time evidence for a neurobiological cause of intergroup conflict. They show that oxytocin, a neuropeptide produced in the brain that functions as hormone and neurotransmitter, leads humans to self-sacrifice to benefit their own group and to show aggression against threatening out-groups. This finding qualifies the wide-spread belief that oxytocin promotes general trust and benevolence.

New evidence suggests there is a neurobiological cause of intergroup conflict.
Credit: iStockphoto/Anja Hild

Researchers at the University of Amsterdam provide first-time evidence for a neurobiological cause of intergroup conflict. They show that oxytocin, a neuropeptide produced in the brain that functions as hormone and neurotransmitter, leads humans to self-sacrifice to benefit their own group and to show aggression against threatening out-groups. This finding qualifies the wide-spread belief that oxytocin promotes general trust and benevolence.

Results were published in the journal Science.

An important qualification of this research is that oxytocin, commonly referred to as the "bonding hormone," functions as a cause of defensive aggression -- aggression oriented towards neutralizing a threatening out-group. When the competing out-group was not considered a threat, oxytocin only triggered altruism towards one's own group. This finding provides a neurobiological explanation for the fact that conflicts between groups escalates when other groups are seen as threatening. When such threat is low, for example because there are (physical) barriers between the group territories, conflict escalation is less likely.

The evolution of altruism in intergroup conflict

The research team at the University of Amsterdam, directed by Dr. Carsten de Dreu, wondered why oxytocin would promote altruistic behavior. Whereas classic economic theory has difficulty accounting for altruism, an evolutionary perspective suggests that altruism functions to strengthen one's own group, from which the individual benefits in the long run. Because aggression towards competing out-groups helps one's own group to become relatively stronger, aggression is an indirect form of altruistic, loyal behavior towards one's own group.

Charles Darwin already observed that groups whose members are altruistic towards the own group have a greater likelihood to prosper, to survive, and spread. The researchers reasoned that if this is true, neurobiological mechanisms should have evolved that sustain altruism towards the own group, and aggression towards competing other groups. The discovery that oxytocin promotes altruism towards the own group, and aggression towards threatening out-groups, supports this evolutionary perspective.


Story Source:

The above story is based on materials provided by Universiteit van Amsterdam (UVA). Note: Materials may be edited for content and length.


Journal Reference:

  1. C. K. W. De Dreu, L. L. Greer, M. J. J. Handgraaf, S. Shalvi, G. A. Van Kleef, M. Baas, F. S. Ten Velden, E. Van Dijk, S. W. W. Feith. The Neuropeptide Oxytocin Regulates Parochial Altruism in Intergroup Conflict Among Humans. Science, 2010; 328 (5984): 1408 DOI: 10.1126/science.1189047

Cite This Page:

Universiteit van Amsterdam (UVA). "Neurobiological cause of intergroup conflict: 'Bonding hormone' drives aggression towards competing out-groups." ScienceDaily. ScienceDaily, 15 June 2010. <www.sciencedaily.com/releases/2010/06/100614114445.htm>.
Universiteit van Amsterdam (UVA). (2010, June 15). Neurobiological cause of intergroup conflict: 'Bonding hormone' drives aggression towards competing out-groups. ScienceDaily. Retrieved July 23, 2014 from www.sciencedaily.com/releases/2010/06/100614114445.htm
Universiteit van Amsterdam (UVA). "Neurobiological cause of intergroup conflict: 'Bonding hormone' drives aggression towards competing out-groups." ScienceDaily. www.sciencedaily.com/releases/2010/06/100614114445.htm (accessed July 23, 2014).

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