Alternative Interpretation of Swedish Twin Study Findings on Personality and Major Depression

In their article “Personality and Major Depression: A Swedish Longitudinal, Population-Based Twin Study,” Kendler and colleagues reported the results of a study that “examined the association between personality and the lifetime risk for depression. . . . ”^{1 (p1118)} They conducted elegant and sophisticated analyses of genetically determined risk for neuroticism and major depression in the context of a beautifully designed longitudinal study conducted in an ideal sample of twins. They concluded, “Results from both longitudinal and genetic analyses support the hypothesis that neuroticism strongly reflects the liability to MD [major depression]. This association arises largely because neuroticism indexes the genetic risk for depressive illness.”^{1 (p1113)}

I am writing to question the assumption that “neuroticism,” as measured by the Eysenck Personality Inventory (EPI), represents a personality trait and to propose an alternative interpretation of their findings. We have long known that personality measures are highly influenced by affective state.² The results of the EPI Neuroticism Scale in particular may be highly influenced by depression and dysthymia because the content of the items in the scale reflects depressive symptoms. The twins in the Swedish registry completed the EPI at the average age of 29 years, at which point dysthymic disorder would usually become manifest in a vulnerable individual. Chronicity of depression has also been demonstrated to be familial^{3 - 4} and likely has a genetic basis. It is known that about 80% of people with dysthymia go on to develop episodes of major depression in their lifetime.⁵ This has been termed double depression.⁶ I am suggesting that the elevated Neuroticism Scale scores may merely have reflected the presence of dysthymia, which rendered those individuals vulnerable to the development of major depression at a later date. Whether there are personality disorders or traits that render individuals vulnerable to the development of depression remains a matter of controversy.

Correspondence: Dr Kocsis, Weill Cornell Medical College, 525 E 68th St, New York, NY 10021-4870 (jhk2002@med.cornell.edu).

Financial Disclosure: Dr Kocsis has received research funding from Sanofi-Aventis, Forest Laboratories, and AstraZeneca.