Familial Factors Associated with Early versus Late Onset Depression

According to the National Institute of Aging, depressive symptoms in older adults peak around age 50 and then again after age 80. Research suggests that early onset depression (EOD) differs from late onset depression (LOD) in... [ view full abstract ]

According to the National Institute of Aging, depressive symptoms in older adults peak around age 50 and then again after age 80. Research suggests that early onset depression (EOD) differs from late onset depression (LOD) in associated personality characteristics, childhood events, family psychiatric history, and neuroimaging characteristics.  However, it is unclear whether observed differences represent genetically different manifestations of depression or the influence of environmental factors.  This study examined 288 male twins from the Vietnam Era Twin Study of Aging who reported any lifetime depression to examine familial and genetic contributions to EOD and LOD.  LOD was defined as onset occurring at 40 years of age and older.  GEE analyses indicated that a history of alcohol misuse in father (OR=1.89, p =.016), cotwin (OR=2.68, p < .001), and closest sibling (OR = 2.00, p =.036) increased the odds of developing EOD relative to LOD.  A history of depression in mother (OR = 2.35, p < .001), cotwin (OR = 2.13, p =.002), and closest sibling (OR = 1.91, p =.019) increased the odds of developing EOD relative to LOD.  A history in any family member of drug misuse or trouble with the law did not increase the odds of developing either EOD or LOD.  Neither comparisons of concordance rates by zygosity or analyses of polygenic risk scores for depression provided clear-cut evidence for genetic influences on EOD versus LOD.  However, given the relatively small number of individuals with depression, these methods were underpowered.  Our results indicate that there are significant familial influences on whether an individual experiences EOD versus LOD.  However, we were unable to distinguish family environmental influences from genetic influences responsible for this effect.  There are two plausible reasons for the pattern we observed.  First-degree relatives may share a genetic risk for depression and genetic influences on depression may also impart a risk for alcohol abuse, particularly in males.  It is also plausible that the family environment in which a parent or sibling has depression or alcohol abuse may be depressogenic. It is likely that our results reflect both genetic and environmental factors.