<unk>  mood symptoms are only present in menstruating women. Thus, symptoms do not occur during pregnancy, after menopause, or in women who have anovulatory cycles. Other mood disorders typically persist across all reproductive life events and are independent of a woman's menstrual cycle. The current consensus on the cause of<unk>  is a combination of heightened sensitivity to fluctuating levels of certain hormones (i.e. the reproductive hormones), environmental stress, and genetic predisposition. The sex steroids—estrogen and progesterone—are neuroactive; they have been noted in rat models to be involved in serotonin pathways. Serotonin is involved in mood regulation alongside estrogen, whose receptors are found in the prefrontal cortex and hippocampus—the regions most known for their involvement in regulating one's mood and cognition overall. While the timing of symptoms suggests hormonal fluctuations as the cause of<unk> , a demonstrable hormonal imbalance in women with<unk>  has not been identified. In fact, levels of reproductive hormones and their metabolites in women with and without<unk>  are indistinguishable. It is instead hypothesized that women with<unk>  are more sensitive to normal levels of hormone fluctuations, predominantly estrogen and progesterone, which produces biochemical events in the nervous system that cause the premenstrual symptoms. These symptoms are more predominant in women who have a predisposition to the disorder. It is apparent that the premenstrual disorders are biologically driven and are not only psychological or cultural phenomena.<unk>  has been reported by menstruating women worldwide, indicating a biological basis that is not geographically selective. Most psychologists infer that this disorder is caused by both a reaction to hormone flux and also genetic components. There is evidence of heritability of (retrospectively-reported) premenstrual symptoms from several twin and family studies done in the 1990s, with the heritability of<unk>  proving to be about 56%. Genetic factors While whether or not this disorder has a specific genetic basis is still being discussed in the academic community and the possible genetic factors contributing to<unk>  have yet to be thoroughly researched, there has recently been multiple genetic factors identified that contribute to the moodiness, depression, irritability, increased appetite, trouble sleeping, acne, fluid retention, headaches, nausea, and other symptoms that are all associated with this disorder. Many studies have noted that a polymorphism of the brain-derived neurotrophic factor gene (BDNF), a gene that helps support neurons in their function and survival in the brain by creating a protein that helps in the growth, maturation, and maintenance of these cells, may play a role in causing<unk>  symptoms. This is because the result of this polymorphism mimics the hallmarks of<unk> : volatile moods, depression and irritability centered around the menstrual cycle. This gene has been studied extensively in its association with depression and, promisingly for<unk>  research, mice homozygous for the BDNF polymorphism exhibited anxiety-like traits that fluctuated and changed around the mice’s estrus, analogous to the human’s menstruation, therefore mimicking some of the symptoms of<unk> . Risk Factors Environmental stressors have also been found to prospectively increase risk for<unk>  symptoms. Environmental components such as stress, hormonal fluctuation, and epigenetics play a key role in the pathology and onset of the disorder. Some studies have noted evidence of interpersonal trauma (domestic violence, physical or emotional trauma, or substance abuse) or seasonal changes (making<unk>  potentially comorbid with Seasonal Affective Disorder) having an impact on<unk>  risk. But the most common pre-existing disorder found in those diagnosed with<unk>  is major depression, wherein they either actually had it or were misdiagnosed when they should have only been diagnosed with<unk> . Finally, an easily modifiable risk factor for<unk>  is cigarette smoking. One meta-analysis found dramatically increased risk of developing<unk>  in menstruating women who smoke. Relationship to pregnancy and menopause Women with<unk>  usually see their symptoms disappear while they are pregnant.<unk>  is primarily a mood disorder that is associated with onset of menstruation; pregnancy, menopause, and hysterectomies all cause menstruation to cease, thereby stopping the proposed sex steroid-/serotonin-caused symptoms from occurring. Although one might expect a higher rate of postpartum depression among those with<unk> , a large study of women with prospectively-confirmed<unk>  did not find a higher prevalence of postpartum depression than in controls. If a woman had experienced PPD beforehand, there was found to be a less-than 12% chance of<unk>  pathology emerging—hardly any differentiation from the regular population of those who have never experienced postpartum depression. However,<unk>  symptoms can get worse following pregnancy, or other associated events such as birth and miscarriage. Mental Health Comorbidities in<unk>  The lifetime incidence of other psychiatric disorders is high among women with<unk> . An older review article (2002) utilizing the previous edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) used studies from 1966 to 2002 on PMS and mental health disorders and selected for patients who retrospectively met the diagnostic criteria for<unk>  and found that Major Depressive Disorder, Seasonal affective disorder, and generalized anxiety disorder often co-occur in<unk> . Another systematic review study suggests that patients with bipolar disorder, type I or II, have a higher incidence of<unk> . While the diagnosis of<unk>  requires a mental health provider to determine that the symptoms a woman is facing is not due to an underlying mental or physical health condition, it is important to note that other conditions often co-occur and impact the quality of life and treatment plan for people with<unk> . Suicidality in<unk>  Previous links to suicidality and PMS have been made, but women with<unk>  are more likely still to consider and attempt suicide even when controlling for mental health comorbidities. Despite the increase in suicidal ideation and attempts in this population, the data currently suggests that suicidal ideation or action is not more likely to occur during the late luteal phase when<unk>  symptoms would occur. It is difficult to study whether treatment reduces suicidality because of the multifaceted reasons provided for suicidal ideation. However, treatment has been well documented to reduce physical and emotional symptoms of<unk> .
Premenstrual dysphoric disorder
Major depressive disorder
Premenstrual syndrome
Anxiety disorder
Menstrual disorder
Postpartum depression
Postpartum psychosis
Minor depressive disorder