Monoamine oxidase inhibitors (MAOIs) currently have a "bad rap" and are thus infrequently used in psychopharmacology, even by experienced clinicians. Misinformation about the dietary and drug interactions of MAOIs is widespread, whereas pragmatic tips for utilizing MAOIs to minimize risks and to maximize therapeutic actions are largely lacking in the contemporary literature. While clearly not first-line treatments, MAOIs, in the hands of experienced and well-informed clinicians, can be a powerful therapeutic intervention for patients with depression, panic disorder, and other anxiety disorders who have failed first-line treatments. This article focuses on the pharmacologic mechanisms of MAOIs, since an understanding of these mechanisms may provide a rationale to empower experts to expand their use of these agents. Discussed here are not only the mechanisms of therapeutic action of MAOIs, but also the mechanisms explaining their side effects, including hypertensive interactions with dietary tyramine (so-called "cheese reactions") and drug interactions that can lead to hypertensive reactions with some drugs and serotonin toxicities with others. This article also provides practical tips on how to use MAOIs, including debunking certain myths and giving specific guidance about which foods and drugs to avoid. Those with no previous interest in MAOIs may discover in this article a new "secret weapon" to add to their therapeutic armamentarium for patients who fail to respond to the better-known agents.

Compared with men, women are at increased risk of depression, especially at several reproductive-related lifecycle points. This may be partially due to changing levels of estrogen, a hormone that can affect levels of neurotransmitters and neural proteins. As estrogen levels vary throughout the lifespan, risk of depression in women also varies, and not all treatments are appropriate or effective at all times. In adolescence, onset of depression may be associated with onset of puberty, but treating underage girls with antidepressants can risk suicidality. In females of childbearing age, mood disturbances associated with menstrual cycles signal a risk for later full-blown major depressive disorder. In depressed pregnant and postpartum women, risks of treatment versus risks of nontreatment are intricate and require case-by-case evaluation. In perimenopause, vasomotor symptoms may be harbingers of oncoming depression and also may signal the presence of dysregulated hormones and neurotransmitters. Relieving vasomotor symptoms may be a necessary dimension of treating depression. In postmenopause, response to selected antidepressants may depend on whether the patient is also taking hormone-replacement therapy. To attain optimal outcomes, modern psychopharmacologists must tailor treatment of depression to a woman's reproductive stage of life. TRIMONOAMINE MODULATORS AND DEPRESSION Clinicians often target the three neurotransmitters most implicated in depression-serotonin (5-HT), norepinephrine (NE), and dopamine (DA)-by using antidepressants to block reuptake at the respective neurotransmitter reuptake transporters. 1 However, other agents can modulate all three neurotransmitters without