Most of the genetic covariation between major depressive and alcohol use disorders is explained by trait measures of negative emotionality and behavioral control.
paper
Cited
Public
- Authors
- Ellingson, J M; Richmond-Rakerd, L S; Statham, D J; Martin, N G; Slutske, W S
- Year
- 2016
- Journal
- Psychological medicine
- PMID
- 27460396
- DOI
- 10.1017/S0033291716001525
- PMCID
- PMC9361478
BACKGROUND: Mental health disorders commonly co-occur, even between conceptually distinct syndromes, such as internalizing and externalizing disorders. The current study investigated whether phenotypic, genetic, and environmental variance in negative emotionality and behavioral control account for the covariation between major depressive disorder (MDD) and alcohol use disorder (AUD). METHOD: A total of 3623 members of a national twin registry were administered structured diagnostic telephone interviews that included assessments of lifetime histories of MDD and AUD, and were mailed self-report personality questionnaires that assessed stress reactivity (SR) and behavioral control (CON). A series of biometric models were fitted to partition the proportion of covariance between MDD and AUD into SR and CON. RESULTS: A statistically significant proportion of the correlation between MDD and AUD was due to variance specific to SR (men = 0.31, women = 0.27) and CON (men = 0.20, women = 0.19). Further, genetic factors explained a large proportion of this correlation (0.63), with unique environmental factors explaining the rest. SR explained a significant proportion of the genetic (0.33) and environmental (0.23) overlap between MDD and AUD. In contrast, variance specific to CON accounted for genetic overlap (0.32), but not environmental overlap (0.004). In total, SR and CON accounted for approximately 70% of the genetic and 20% of the environmental covariation between MDD and AUD. CONCLUSIONS: This is the first study to demonstrate that negative emotionality and behavioral control confer risk for the co-occurrence of MDD and AUD via genetic factors. These findings are consistent with the aims of NIMH's RDoC proposal to elucidate how transdiagnostic risk factors drive psychopathology.
A model quantifying the extent to which the genetic and environmental covariation between major depressive disorder (MDD) and alcohol use disorder (AUD) is explained by (1) additive genetic and unique environmental factors that influence stress reaction (SR), (2) additive genetic and unique environmental factors that influence behavioral control (CON), and (3) additive genetic and unique environmental factors that influence both SR and CON. For simplicity, this model is illustrated for only one individual from a twin pair. In this model, SR is entered first; thus, the proportion of genetic covariation between MDD and AUD that is attributable to CON (after accounting for genetic variation shared with SR) is [(a23 × a24)/(a13 × a14 + a23 × a24 + a33 × a34)]. To determine the proportion of genetic covariation attributable to SR (after accounting for genetic variation shared with CON), this model was re-run with CON entered first.
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