Stress and sex hormones
Stress hormones influence, and are influenced by, male and female sex hormones. Stress hormones have been shown to inhibit or interfere with regular reproductive hormone levels, particularly in females. The influence doesn’t just go in one direction. Sex hormones, think estrogen and testosterone, can also alter the amount of stress hormones released during the stress response. However, whether males or females benefit depends on various factors, including whether animal or human subjects are being tested and age. For instance, there is evidence that the class of male sex hormones, called androgens, can reduce the stress hormone response. This is a strong, replicated effect in the animal literature. In humans, the pattern appears reversed, with women showing blunted stress hormone responses compared with men, but only during certain times of the menstrual cycle.
Understanding the pathways that govern sex hormones and stress hormones is helpful in understanding how and why these hormone systems might interact. In line with the research discussed on this website, here we will stick to the female sex hormone system with additional focus on the estrogen system. The pathway regulating the stress hormone response system is called the hypothalamic-pituitary-adrenal (HPA) axis and the pathway regulating sex hormones is called the hypothalamic-pituitary-gonadal (HPG) axis. As indicated in the pathway names, both the stress and sex hormone systems start in the hypothalamus, a small brain region involved in regulating most hormone systems in the body. They also share the next stop in the pathway, the pituitary gland, which sit below the hypothalamus and essentially helps the hypothalamus send signals for the production and release of hormones elsewhere in the body. Next, depending on the system, the adrenal gland, located on top on each kidney, will release stress hormones, while the gonads, or ovaries in women, will produce and release estrogens. It is the shared stops along the way that allow the systems interact with one another, and the effects in these higher up regions that allow for effects to take place in the adrenal glands and ovaries.
That HPA-HPG interactions are bidirectional, it is important to understand whether, and how, these interactions may change when one system is dramatically altered, such as when women use hormonal contraception or go through the menopause transition. For instance, given the interactions between systems, the dramatic and sustained decrease in estrogens that occur during and after menopause may alter how HPG activation affects HPA function. My work is focused on investigating this type of effect. How do changes in estrogen levels across the female lifespan affect HPA activity in response to stress? Whether these changes are part of the natural menstrual cycle, altered through hormonal contraceptive use, or with the loss of estrogen during and after menopause. I extend this investigation beyond the physiological stress response by investigating how any effects on the stress hormone response alters subsequent effects of stress on learning and memory. For a thorough overview of these systems, their interactions, and implications for women, please see my dissertation.