Spousal concordance for alcohol dependence: evidence for assortative mating or spousal interaction effects?

BACKGROUND

Alcohol dependence (AD) is among the most common psychiatric disorders, and impacts the health and well-being of problem drinkers, their family members, and society as a whole. Although previous research has consistently indicated that genetic factors contribute to variance in risk for AD, little attention has been paid to nonrandom mating for AD. When assortative mating occurs for a heritable trait, spouses are genetically correlated and offspring are at increased risk of receiving high-risk genes from both parents. The primary goal of the present analyses is to test hypotheses about the source(s) and magnitude of spousal associations for AD using a twin-spouse design.

METHODS

DSM-IV AD (without the clustering criterion) was assessed via telephone interview for 5,974 twin members of an older cohort of the Australian Twin Register (born 1902-1964) and 3,814 spouses of the twins. Quantitative genetic modeling was used to determine the extent to which variability in risk for AD was influenced by genetic factors, the extent of spousal association for AD, and whether the association was attributable to assortative mating, reciprocal spousal interaction, or both processes.

RESULTS

Genetic factors explained 49% of the variance in risk for AD. There was no evidence of gender differences in the spousal interaction effect, the degree of rater bias, or the association between the twin's report of spouse AD and the spouse's AD phenotype. Either the assortative mating parameter or the spousal interaction parameter could be removed from the model without a significant decrement in fit, but both could not be dropped simultaneously, suggesting a lack of power to differentiate between these 2 causes of spousal correlation. When both effects were included in the model, the spousal correlation was 0.29, the assortative mating coefficient was 0.45 (i.e., "like marries like"), and the reciprocal spousal interaction coefficient was -0.10 (i.e., after controlling for assortative mating, the additional impact of spousal interactions is slightly protective).

CONCLUSIONS

These analyses provide evidence of significant spousal associations for AD, with assortative mating increasing spouse similarity and spousal interaction effects decreasing it after controlling for assortative mating. Although the genetic impact is modest, assortative mating results in an increased proportion of offspring exposed to 2 alcoholic parents and the associated detrimental environmental sequelae, and increases the likelihood of offspring inheriting high-risk genes from both parents.