TY - JOUR
T1 - The heritability of life events
T2 - An adolescent twin and adoption study
AU - Bemmels, Heather R.
AU - Burt, Alexandra
AU - Legrand, Lisa N.
AU - Iacono, William G.
AU - McGue, Matt
N1 - Funding Information:
Supported in part by USPHS grants # AA09367, AA11886, DA05147,and MH066140.
PY - 2008/6
Y1 - 2008/6
N2 - Although life events are often conceptualized as reflecting exogenous risk factors for psychopathology, twin studies have suggested they are heritable. We undertook a mixed twin/adoption study to further explore genetic and environmental contributions to individual differences in the experience of life events. Specifically, a sample of 618 pairs of like-sex adolescent twins, 244 pairs of like-sex adopted adolescent and young adult siblings, and 128 pairs of like-sex biological siblings completed a life events interview. Events were classified as independent (not likely to have been influenced by respondent's behavior), dependent (likely to have been influenced by respondent's behavior), or familial (experienced by a family member), and then summed to form three life event scales. Variance on the scales was assumed to be a function of four factors: additive genetic effects (a2), shared environmental effects (c2), twin-specific effects (t2), and nonshared environmental effects (e2). Data were analyzed using standard biometrical models. Shared environmental effects were found to be the largest contributor to variance in familial events (c2 = .71; 95% confidence interval of .65, .76); additive genetic effects were the largest contributor to dependent events (a2 = .45; Cl = .31, .58); and nonshared environmental effects were found to be the largest contributor independent events (e2 = .57; Cl = .51, .64). A significant twin-specific effect was also found for independent life events, indicating that twins are more likely to be exposed to such events than non-twin biological siblings. Findings are discussed in terms of their implication for understanding the nature of psychosocial risk.
AB - Although life events are often conceptualized as reflecting exogenous risk factors for psychopathology, twin studies have suggested they are heritable. We undertook a mixed twin/adoption study to further explore genetic and environmental contributions to individual differences in the experience of life events. Specifically, a sample of 618 pairs of like-sex adolescent twins, 244 pairs of like-sex adopted adolescent and young adult siblings, and 128 pairs of like-sex biological siblings completed a life events interview. Events were classified as independent (not likely to have been influenced by respondent's behavior), dependent (likely to have been influenced by respondent's behavior), or familial (experienced by a family member), and then summed to form three life event scales. Variance on the scales was assumed to be a function of four factors: additive genetic effects (a2), shared environmental effects (c2), twin-specific effects (t2), and nonshared environmental effects (e2). Data were analyzed using standard biometrical models. Shared environmental effects were found to be the largest contributor to variance in familial events (c2 = .71; 95% confidence interval of .65, .76); additive genetic effects were the largest contributor to dependent events (a2 = .45; Cl = .31, .58); and nonshared environmental effects were found to be the largest contributor independent events (e2 = .57; Cl = .51, .64). A significant twin-specific effect was also found for independent life events, indicating that twins are more likely to be exposed to such events than non-twin biological siblings. Findings are discussed in terms of their implication for understanding the nature of psychosocial risk.
UR - http://www.scopus.com/inward/record.url?scp=45249109376&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=45249109376&partnerID=8YFLogxK
U2 - 10.1375/twin.11.3.257
DO - 10.1375/twin.11.3.257
M3 - Article
C2 - 18498204
AN - SCOPUS:45249109376
SN - 1832-4274
VL - 11
SP - 257
EP - 265
JO - Twin Research and Human Genetics
JF - Twin Research and Human Genetics
IS - 3
ER -