Neuroticism and depression

Farmer et al (2002) draw conclusions that we believe are not supported by the results of their study. The study compared probands with depression and their siblings, with healthy probands with no history of depression and their siblings. Between two-thirds and three-quarters of the participants were women. The groups did not differ in age that varied from 36.2 to 39.1 years.

The absence of a difference in mean scores for neuroticism for the never-depressed siblings of both the healthy probands and those with depression was interpreted to suggest that this scale does not measure a genetically influenced trait for depression. This finding, however, can be interpreted otherwise. As the siblings of the probands with depression were in their mid-thirties and had not, as yet, experienced a depression, it is reasonable to assume that they have passed the age of risk for a first episode (Burke et al, 1990) and therefore may not have inherited a vulnerability for the disorder. The finding that the siblings of the probands with depression obtained scores for the trait of neuroticism similar to those obtained by siblings of the healthy probands, who presumably are not genetically vulnerable to depression, could be interpreted to suggest that neuroticism is necessary for depression. As long as there is no way to determine whether an individual carries the genes associated with depression, a cross-sectional study of adults cannot ascertain whether neuroticism reflects a part of the genetic vulnerability for depression. A prospective, longitudinal investigation in which the trait, or an age-appropriate proxy for the trait, is measured before the onset of symptoms could untangle the relationship between neuroticism and depression. Studies comparing monozygotic and dizygotic twins could also address the issue, as did Kendler and colleagues (Kendler et al, 1993) who reported that the genetic liability for major depression largely overlapped with that for neuroticism. The finding that neuroticism scores are positively correlated with symptoms of depression and with severe life events does not address the aetiological question.

It is important to determine whether the trait of neuroticism reflects a part of the genetic vulnerability for depression. It is also important to identify the factors that exacerbate the inherited vulnerability and lead to depression, in order to design prevention programmes for children at risk for depressive disorders. Among parents with a major affective disorder, neuroticism may have more influence on the development of their offspring than does the severity of their disorder. In a prospective study of the children of parents with bipolar disorder, we have found that neuroticism is associated with high levels of negative life events, low levels of psychosocial functioning and with poor parenting, which in turn are associated with the children's level of psychosocial functioning and symptoms (Hodgins et al, 2002; further details available from the author upon request). By contrast, none of the indices of the severity of the parents' disorder is associated with psychosocial functioning or symptoms of the offspring. These findings suggest that neuroticism, rather than the disorder, influences parental behaviours that impact on the mental health of the offspring.

In light of the above considerations, we believe that Farmer et al's ‘Clinical implication’ that ‘Neuroticism reflects subclinical or residual symptoms of depression’ is misleading. Among adult patients, symptoms of depression do appear to be associated with scores for neuroticism, as has been reported previously (Sauer et al, 1997). Whether or not the trait of neuroticism also represents a risk factor for depression, however, is not known. The cross-sectional study reported by Farmer et al (2002) does not address this important question. Available data suggest that the trait of neuroticism may play a critical role in the development of depressive disorders, conferring an inherited vulnerability and leading to parental behaviours associated with impaired functioning among the offspring.