Across many nations, cultures, and ethnicities, women are about twice as likely as men to develop depression (Nolen-Hoeksema, 1995). By late adolescence, girls are twice as likely as boys to be depressed, and this gender ratio remains more or less the same throughout adulthood. The absolute rates of depression in women and men vary substantially across the life span, however. Because women have less power and status than men in most societies, they tend to experience certain traumas, particularly sexual abuse, more often than men. They also experience more chronic strains, such as poverty, harassment, lack of respect, and constrained choices. Moreover, even when women and men experience the same stressors, women may be more likely than men to develop depression because of gender differences in biological responses to stressors, self-concepts, or coping styles (Nolen-Hoeksema, 2001).
It is these differences in biological responses to stress between females and males that capture my imagination as they might relate to our class discussions. In a brief section in the depression chapter, Higgins and George (2013) refer to the notion of gene expression in which genes for depression, in this case, are expressed when some individuals encounter stressful events. This theory seeks to explain why some individuals are more likely to lapse into depression when faced with difficult life situations while others who face the same or similar life situations do not. The authors refer to two versions of the gene that produces the serotonin transporter – a short allele and a long allele. According to one study the authors cite, individuals with copies of the short allele who encountered a stressful event were predisposed to develop major depression while individuals with copies of the long allele were not. Unfortunately, a meta-analysis combining 14 studies did not yield evidence that the gene that produces the serotonin transporter was alone responsible for elevated risk of depression. Higgins and George (2013) sagely point out that the disappointing results are likely due to the narrow focus on one gene when depression is likely the result of several genes. Fair enough, but I was still intrigued that at least one gene has been identified that is surely implicated in depression and that that gene might account for some of the gender differences one finds in major depression. I looked further.
I found a team of Swedish researchers who in a 2006 article explored sex differences in the prediction of depression when there was interaction of the serotonin transporter gene and adverse social conditions (Sjöberg et al.). From a randomized sample of 81 boys and 119 girls ages 16 to 19 years old, 61% of the males and 74% of the females had the short allele. The study yielded two very intriguing results. First, males and females with the short allele respond to different environmental factors. Based on a psychosocial interview protocol, the male students were negatively affected, on a significant level, by living in public housing rather than in a home their family owned, and they were negatively affected by living with separated parents. The female students, on the other hand, were negatively affected by traumatic events within the family unit. Although we cannot draw any definitive conclusions from one study with a small sample size, these findings can help point us in the right direction as we try to understand differences in triggers for depression in males and females. This first finding suggests that triggers for male depression might be variables that are closely associated with social status. In this example, living in public housing may stigmatize the males in a way that makes it difficult for them to save face with their peers. While males with the long allele may be able to recover from such a stigma, males with the short allele are vulnerable to depressive episodes. The female triggers for depression appear to be closely associated with variables for interpersonal relationships. Females with the short allele may have difficulty recovering from disruptions in their primary relationships, which can then lead to depressive episodes.
The second important finding is that females and males carrying the short allele had responses to environmental stress that went in opposite directions. Females tended to develop depressive symptoms in response to environmental stress, whereas their male counterparts appeared to be “protected” from depressive symptoms, according to the depression scale used in the study. One possibility is that adolescent males develop other pathological behaviors, which might be a variant of male depression but that produces inverted scores on the depression scale. This finding has important implications for the diagnosis of depression in males.
Gene expression as the result of interactions with environmental stressors is an exciting new field that promises to expand our understanding of the etiology of mental illness. With a better understanding of the etiology of mental illness will come better ways to not only treat the symptoms of mental illness, which we are already fairly good at, but also in pre-empting mental illness from occurring at all.
Higgins, E. S., George, M. S. The Neuroscience of Clinical Psychiatry: The Pathophysiology of Behavior and Mental Illness, 2nd edition. Philadelphia, PA: Lippincott Williams & Wilkins; 2013.
Nolen-Hoeksema, S. Gender differences in coping with depression across the lifespan. Depression. 1995; 3: 81.
Nolen-Hoeksema, S. Gender differences in depression. Current Directions in Psychological Science. 2001; 10: 173.
Sjöberg, R. L., Nilsson, K. W., Nordquist, N., Öhrvik, J., Leppert, J., Lindstrom, L., and Oreland, L. Development of depression: Sex and the interaction between environment and a promoter polymorphism of the serotonin transporter gene. International Journal of Neuropsychopharmacology 2006; 9: 443.