Are there common familial influences for major depressive disorder and an overeating-binge eating dimension in both European American and African American Female twins?

ABSTRACT Objective Although prior studies have demonstrated that depression is associated with an overeating–binge eating dimension (OE‐BE) phenotypically, little research has investigated whether familial factors contribute to the co‐occurrence of these phenotypes, especially in community samples w...

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Veröffentlicht in:The International journal of eating disorders 2015-05, Vol.48 (4), p.375-382
Hauptverfasser: Munn-Chernoff, Melissa A., Grant, Julia D., Agrawal, Arpana, Koren, Rachel, Glowinski, Anne L., Bucholz, Kathleen K., Madden, Pamela A.F., Heath, Andrew C., Duncan, Alexis E.
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Sprache:eng
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Zusammenfassung:ABSTRACT Objective Although prior studies have demonstrated that depression is associated with an overeating–binge eating dimension (OE‐BE) phenotypically, little research has investigated whether familial factors contribute to the co‐occurrence of these phenotypes, especially in community samples with multiple racial/ethnic groups. We examined the extent to which familial (i.e., genetic and shared environmental) influences overlapped between Major Depressive Disorder (MDD) and OE‐BE in a population‐based sample and whether these influences were similar across racial/ethnic groups. Method Participants included 3,226 European American (EA) and 550 African American (AA) young adult women from the Missouri Adolescent Female Twin Study. An adaptation of the Semi‐Structured Assessment for the Genetics of Alcoholism (SSAGA) was administered to assess lifetime DSM‐IV MDD and OE‐BE. Quantitative genetic modeling was used to estimate familial influences between both phenotypes; all models controlled for age. Results The best‐fitting model, which combined racial/ethnic groups, found that additive genetic influences accounted for 44% (95% CI: 34%, 53%) of the MDD variance and 40% (25%, 54%) for OE‐BE, with the remaining variances due to non‐shared environmental influences. Genetic overlap was substantial (rg = .61 [.39, .85]); non‐shared environmental influences on MDD and OE‐BE overlapped weakly (re = .26 [.09, .42]). Discussion Results suggest that common familial influences underlie MDD and OE‐BE, and the magnitude of familial influences contributing to the comorbidity between MDD and OE‐BE is similar between EA and AA women. If racial/ethnic differences truly exist, then larger sample sizes may be needed to fully elucidate familial risk for comorbid MDD and OE‐BE across these groups. © 2014 Wiley Periodicals, Inc. (Int J Eat Disord 2015; 48:375–382)
ISSN:0276-3478
1098-108X
DOI:10.1002/eat.22280