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The interactive theory suggests being female always poses a risk for depression, but the events of adolescence activate that risk factor. For example, imagine females are more concerned than males with their relationships— before and after adolescence—and that unsatisfying relationships are more strongly related to girls’ than boys’ distress. Concern with relationships would be the “female risk factor.” This concern could interact with events likely to occur during adolescence such as interpersonal conflict. Because females are more relationship focused than males, girls will be more likely than boys to react to interpersonal conflict with depression.

In sum, these theories suggest either that the cause of depression is the same for men and women, that there are different causes for male and female depression, or that environmental factors interact with predisposing factors to predict depression. Each of the theories that follow supports one of these perspectives.

Biology Genes. There is undoubtedly a genetic influence on depression (Mosing et al., 2009). The question is whether this genetic risk accounts for the sex difference. If there is a genetic explanation for the sex difference in depression, we would expect the depression risk factor to lie on the X chromosome. That being the case, we would predict that depressed fathers would be more likely to pass on their depressive gene to daughters than sons because fathers give daughters their X chromosome and sons their Y chromosome. However, more father– son pairs are depressed than father–daughter pairs (Nolen-Hoeksema, 1987). It is also the case that females have higher rates of depression than males among other-sex twins (Takkinen et al., 2004). Thus, sex-linked genes alone cannot explain depression.

Because genes are present at birth, a genetic theory of depression has difficulty explaining the emergence of depression in females during adolescence. Genetic theories would have to suggest that women are at risk for depression and the events of adolescence interact with that risk. One study that evaluated 8- to 20-year-old monozygotic and dizygotic twins showed that some genetic effects are activated around the age of puberty, partly supporting this theory (Kendler, Gardner, & Lichtenstein, 2008). However, other genetic effects seemed to wane over time. Genetic factors may interact with psychological variables to increase depression. A five-day study in which female twins were prompted throughout the day to complete measures of stress and negative affect showed that the relation of stress to negative affect was stronger for monozygotic twins than dizygotic twins, especially if there was a history of depression (Wichers et al., 2007). Wichers and colleagues concluded that there was a genetic contribution to reactions to daily Stressors. Hormones. In contrast to genes, hormones change over the life span, and there is a great deal of hormonal fluctuation during adolescence when sex differences in depression emerge. Thus hormones would seem to be an ideal explanation for the sex difference in depression. However, no consistent evidence supports the theory that the changes in hormones during puberty are associated with the onset of depression in adolescent females (Nolen-Hoeksema & Girgus, 1994). Hormones may interact with other environmental factors, supporting the interactive theory of depression. For example, some research suggests that hormonal changes during puberty alter the way the body responds to stress in females (Stroud et al., 2004).

Aside from the hormonal changes that occur during puberty, researchers have attempted to link hormonal changes at other times in women’s lives to depression. Fluctuations in women’s hormones, in particular estrogen, prior to menstruation and after the birth of a child are related to depression, but these effects are not nearly large enough to account for the sex difference in depression. One study observed that depression increased as women transitioned through menopause and then decreased after menopause (Freeman et al., 2006). These changes in hormones were associated with the increase in depression that occurred during menopause. However, another study was unable to link the decline in estrogen in the elderly to depression (Erdincler et al., 2004). In sum, it has been difficult to link increases in female hormones to depression. It seems more likely that a general pattern of hormonal fluctuation is related to depression.

Some research has focused on the protective effects of male hormones, specifically testosterone, in regard to depression. However, even that relation is not a simple one. In one study, testosterone showed a curvilinear relation to depression, such that people with extremely low or extremely high levels of testosterone were depressed (Booth, Johnson, & Granger, 1999). The relation of high testosterone to depression appeared to be accounted for by its relation to antisocial behavior. High-testosterone men were more likely to engage in antisocial behavior, which was linked to depression. This research is consistent with the idea that men and women manifest depression in different ways. In this study, low testosterone levels were associated with the

11/1/2017 Yuzu: Psychology of Gender: Fourth Edition

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more stereotypical female form of depression, whereas high levels were associated with the more stereotypical male form of distress—acting-out behavior.

A more recent theory of hormonal influences on depression has focused on oxytocin. Oxytocin increases during puberty and has been shown to promote affiliative behavior (Campbell, 2010). In experimental research, the administration of intranasal oxytocin increased trust during a game with a stranger (Kosfeld et al., 2005), maintained trust when it was violated (Baumgartner et al., 2008), increased generosity (Zak, Stanton, & Ahmadi, 2007), and improved the recognition of happy faces (Marsh et al., 2010). Likewise, displays of affiliative behavior, such as touch, have been associated with the release of oxytocin (Holt-Lunstad, Birmingham, & Light, 2008).

Affiliative behavior, however, should not lead to depression. But, affiliative behavior could interact with some of the events during adolescence to place women at risk for depression. Specifically, changes in oxytocin regulation during puberty may cause females to be more reactive to interpersonal Stressors (Klein, Corwin, & Ceballos, 2006). Research has linked oxytocin to relationship difficulties (Taylor et al., 2006; Taylor, Saphire- Bernstein, & Seeman, 2010). However, the direction of the relation is not clear. Do high levels of oxytocin cause greater relationship difficulties, or do relationship difficulties lead to elevated levels of oxytocin?

Thus, it appears that interpersonal stress increases oxytocin, which then promotes affiliative behavior and prosocial behavior, both of which could reduce distress. So, how does oxytocin enter into the relation