The Genetics of Trust


Estimates of the genetic influence on trust from twin studies range from 10% to 66%. The estimates vary because of differences in the measurement of trust and differences in sample characteristics. Twin studies only inform us about the relative importance of genetic factors, whereas molecular genetic approaches can identify the specific DNA variants that influence a trait. The oxytocin receptor gene has previously been associated with trust, but the results are inconsistent and no effect is observed in larger samples. No other genetic variants have been identified so far using genome‐wide association studies. Estimates of heritability using genetic variants suggest that 7% of the variance in trust is explained by common DNA variants. This is much lower than the 66% estimated from twin studies and the difference is known as missing heritability. Future research should increase sample sizes and continue to try and understand the complex pathways from genes to trust.

Key Concepts

  • Twin heritability estimates of trust range from 10% to 66% with large variability because of different measurements of trust and sample characteristics.
  • SNP heritability estimates of trust range from 6% to 7% explaining around 12% of the twin heritability estimates.
  • Candidate gene studies have suggested a role of the oxytocin receptor gene in explaining the underlying heritability. However, this is not found to be associated consistently across studies.
  • Genome‐wide association studies of trust are currently too small to detect any genome‐wide significant SNPs because trust is a polygenic complex trait with many SNPs having small effects.
  • Therefore, much larger samples are required for future GWAS, emphasising the importance of GWAS consortia bringing together smaller cohorts with measures of trust.

Keywords: genetics; heritability; trust; behaviour genetics; quantitative genetics; molecular genetics

Figure 1. Illustration of the trust game. Arrows indicate possible decisions and matrices indicate possible monetary reward.
Figure 2. The twin design. A = additive genetic effects, C = shared environmental effects and E = nonshared environmental effects. rMZ = the correlation between monozygotic twins and rDZ is the correlation between dizygotic twins.


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Further Reading

For a review of the genetics of all prosocial behaviour see:

Conway CC and Slavich GM (2017) Behavior genetics of prosocial behavior. In: Compassion: Concepts, Research and Applications, pp. 151–170. London: Routledge.

For more information on the methods reviewed here see:

Rana BK and Schork NJ (2007) Genetic Epidemiology of Complex Traits. In: eLS. Chichester: John Wiley & Sons, Ltd. DOI: 10.1002/9780470015902.a0005412.pub2.

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For more information on gene‐envrionment interplay:

McGue M, Skytthe A and Christensen K (2014) The nature of behavioural correlates of healthy ageing: a twin study of lifestyle in mid to late life. International journal of epidemiology 43 (3): 775–782.

Vinkhuyzen AAE, Van Der Sluis S, De Geus EJC, Boomsma DI and Posthuma D (2010) Genetic influences on ‘environmental’ factors. Genes, Brain and Behavior 9 (3): 276–287.

For further reading on oxytocin:

Bakermans‐Kranenburg MJ and Van IJzendoorn MH (2014) A sociability gene? Meta‐analysis of oxytocin receptor genotype effects in humans. Psychiatric genetics 24 (2): 45–51.

Di Simplicio M, Massey‐Chase R, Cowen PJ and Harmer CJ (2009) Oxytocin enhances processing of positive versus negative emotional information in healthy male volunteers. Journal of Psychopharmacology 23 (3): 241–248.

Feldman R (2012) Oxytocin and social affiliation in humans. Hormones and behavior 61 (3): 380–391.

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Wootton, Robyn E(Jan 2018) The Genetics of Trust. In: eLS. John Wiley & Sons Ltd, Chichester. [doi: 10.1002/9780470015902.a0027868]