Premenstrual Dysphoric Disorder (PMDD): A Literature Review of Etiology, Suicidality, and Treatment

Written by: Olivia Mickles

Edited by: Keoni Andrews

ABSTRACT

Premenstrual dysphoric disorder (PMDD) is a severe disorder associated with significant psychological and functional impairment. This literature review examines current research which discusses possible biological and environmental factors of PMDD, its relationship with suicidal ideation and behavior, and available treatment approaches. Research suggests that abnormal sensitivity to seemingly normal hormonal fluctuations, neurological processes, and genetic factors may contribute to PMDD, while also highlighting a concerning association between PMDD and suicidal ideation, plans, and attempts. Of the current treatments available, selective serotonin reuptake inhibitors (SSRIs) are particularly effective in reducing symptoms, while hormonal, psychological, and other nonmedical interventions have more varied results. Overall, the literature supports PMDD as a clinically significant condition and emphasizes the existing gaps in understanding surrounding its causes, identifying suicide risk, and developing effective long-term treatments.

INTRODUCTION

Premenstrual dysphoric disorder is a severe and debilitating condition characterized by recurring emotional, cognitive, behavioral, and physical symptoms that onset during the luteal phase of the menstrual cycle. Though premenstrual symptoms are common, PMDD is a distinguishable disorder due to the severity of its symptoms and how they interfere with daily activity and functioning. PMDD was officially identified as a psychiatric disorder in 2013 in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), signifying an important step toward recognizing severe premenstrual symptoms as a legitimate mental health concern. This diagnosis, however, remains controversial, with some researchers arguing that PMDD pathologizes “normal” female experiences of menstruation and distress (Browne, 2014). This debate has contributed to the uncertainty surrounding the disorder and may have limited the awareness, research, and clinical attention that would be otherwise possible if the disorder was given complete recognition.

Despite these controversies, growing literature suggests that PMDD is associated with clinically significant psychological distress and may be associated with elevated risk for suicidal thoughts and behaviors. This concern is especially important because the DSM-5-TR provides a quite brief discussion of suicidality in relation to PMDD, despite research suggesting significantly high rates of suicidal ideation, suicide planning, and suicide attempts among individuals with the disorder (Wikman et al., 2022; Pilver et al., 2012, & Roy et al., 2025). Understanding this relationship is imperative because PMDD symptoms occur cyclically, meaning that periods of increased psychological distress and suicide risk may correspond with specific phases of the menstrual cycle. The potential relationship between PMDD and suicidality therefore represents an important area for further clinical research and screening.

The purpose of this literature review is to examine the current research surrounding PMDD, with focuses on its possible causes, relationship with suicidal ideation and  behavior, and available treatment options. First, research on the etiology of PMDD is examined, including evidence concerning sensitivity to ovarian hormone fluctuations, neurological and genetic factors, and the interaction between the hypothalamic-pituitary-gonadal and hypothalamic-pituitary-adrenal axes. Second, research is reviewed which examines the relationship between PMDD and suicidal ideation, plans, and attempts, with attention to methodological strengths and limitations across studies. Finally, current treatment approaches are evaluated, including selective serotonin reuptake inhibitors (SSRIs), hormonal interventions, cognitive-behavioral therapy, and non-medical interventions. Overall, this review aims to evaluate the current understanding of PMDD and identify important gaps that may contribute to improved diagnosis, suicide-risk screening, and treatment for individuals affected by the disorder.

ETIOLOGY

Since the Classical Period of Ancient Greece, physicians, philosophers, and scientists have noticed a link between menstruation, behavior, and the brain. In around 450 BC, the Greek physician Hippocrates described a condition he named “agitated blood” where excess blood travelled from women’s brains to be expelled by the uterus. Then, in the 16th century, descriptions of depression, melancholia, and nervous excitement were linked to menstruation; and in the 1930s gynecologist Robert Tilden Frank wrote the first modern description of “premenstrual tension” that recognized that “normal” women experience premenstrual symptoms, but for some women those symptoms are debilitating physically and/or psychologically. Finally, in the late 20th century, late luteal phase dysphoric disorder was included in the DSM-III-R under “Proposed Diagnostic Categories in Need of Further Research”, and was later officially added to the DSM-V in 2013 under the title premenstrual dysphoric disorder (PMDD) (Epperson, 2013). This addition to the diagnostic manual is quite controversial for various reasons that will be discussed later in this review, but it is the result of centuries of documentation of a significant change in women’s behavior and emotionality before menstruation. 

Baller et al. (2013) used positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) scans on women with and without PMDD diagnoses while they completed the n-back task. There were three hormone conditions which include ovarian suppression by leuprolide acetate, a gonadotropin-releasing hormone (Gnrh) agonist, suppression by leuprolide and estradiol, and suppression by leuprolide progesterone. A main effect was observed in both the PET and fMRI studies where women with PMDD, under controlled hormone conditions, had higher prefrontal and dorsolateral prefrontal cortex activation than controls who underwent the same hormone changes. As a whole, this suggests that in PMDD there is abnormal working memory activation in the dorsolateral prefrontal cortex which is related to the disorder’s severity, symptoms, lower Global Assessment of Functioning scores, and early age at onset. Therefore, dysfunction in the dorsolateral prefrontal cortex could be an underlying foundation for risk of developing PMDD rather than hormone differences alone. Other studies, however, have found that estrogen still does have a significant effect on the development of PMDD. Huo et al. (2009) performed haplotype analyses of estrogen receptors alpha and beta in women with and without PMDD to examine the possible genetic sources of affective dysregulation. The findings suggest a link between a genetic variation in the estrogen receptor alpha gene (ESR1) and a higher risk for PMDD due to ESR1 impacting numerous elements of Central Nervous System (CNS) development and function, playing a large role in arousal (Garey et al., 2003), being involved in serotonin function and subsequent mood regulation (Rubinow et al., 1998), and being a hormone which individuals with the disorder display an abnormal behavioral response to even at normal levels (Schmidt et al., 1998). According to the authors, this is the first positive genetic finding surrounding PMDD. 

Another potential contributor to the disorder could be CNS sensitivity to reproductive hormones and genetic and psychosocial factors (i.e. stress). As previously mentioned, women with PMDD do not differ from asymptomatic women regarding ovarian hormone levels, so they may be simply experiencing an abnormal response to normal hormone levels. Hantsoo and Epperson (2015) suggest this response could be due to CNS sensitivity to fluctuations in estrogen and progesterone. Estradiol has strong effects on neurotransmitter systems involved in mood regulation, cognition, eating, sleep, and other behaviors, so the effects of it on serotonin are important to understand when studying the pathophysiology of PMDD. Symptoms of PMDD include depressed mood, food cravings, and impaired cognitive performance during the luteal phase, and all of which are cognitive-affective features that may be influenced by serotonin levels. If considering the CNS sensitivity model, it could then be suggested that women with the disorder are more specifically sensitive to the effects of estrogen on serotonin, which therefore explains the serotonin-related abnormalities in cognition and behavior during the luteal phase that dissipate when estrogen levels rise again after the luteal phase ends. Another hormone, progesterone, has levels rise during the luteal phase and then rapidly drop during menses, creating a whiplash of exposure that could also be a critical factor in the etiology of PMDD. A recent animal model found that rats in withdrawal from doses of progesterone presented with anhedonia, social withdrawal, and an increase in anxious behavior, all of which are common symptoms of PMDD. It was suggested that this fluctuation can alter GABA-A receptor function, leading to progesterone not being blocked from converting to allopregnanolone (ALLO), a neurosteroid derived from progesterone, and negative effects of progesterone surfacing (Smith et al., 2006 & Li et al., 2012). Based on this research, PMDD may therefore be better conceptualized as a disorder of CNS sensitivity to hormonal fluctuations rather than abnormal hormone production. 

The hypothalamic-pituitary-adrenal (HPA) axis is a communication system between the hypothalamus and pituitary and adrenal glands that is responsible for releasing hormones into the blood in response to a stress reaction in the body. The hypothalamic-pituitary-gonadal (HPG) axis, on the other hand, regulates reproductive function by releasing GnRH which leads to the production of estrogen and progesterone in females. Multiple studies have found results that suggest dysregulation of the HPA axis in women with PMDD where their baseline cortisol levels are significantly lower compared to healthy controls. Low basal cortisol can lead to symptoms such as fatigue, mood disturbances, difficulty concentrating, and an inability to tolerate minor stressors (Girdler et al., 1998), all of which are recognized as possible symptoms of PMDD. Hantsoo et al. (2023) highlighted the main finding of multiple animal studies that suggests that a relationship exists between the HPA and HPG axes and changes in progesterone and estradiol. One hypothesis of how that interaction affects those with PMDD is that lower cortisol during the luteal phase can lead to decreased inhibition of the HPA axis, further increasing cortisol levels during stress, leading to symptoms of the disorder such as impaired concentration and mood imbalances like anxiety, depression, and irritability. Hormonal contraception, a common medication taken by women for various reasons, including the treatment of PMDD, is another possible explanation for PMDD regarding changes in the HPA axis due to the combination of progestin and estrogen increasing baseline cortisol levels and subsequently decreasing one’s capacity for increases in cortisol following a stressor (Hertel et al., 2017). This concept, however, requires further research to become a confident claim. Finally, incorporating multiple aforementioned theories together, Crowley and Girdler (2014) suggested that dysregulated ovarian neuroactive steroid control of the HPA axis could be a key contributor to PMDD as neuroactive steroids regulate CNS activity and include ovarian hormones, such as allopregnanolone, as metabolites. Allopregnanolone is active at the GABA-A receptor and regulates the HPA axis in response to stress. Their results showed that individuals with PMDD had both lower basal cortisol levels and higher allopregnanolone levels than control subjects, highlighting the possibility that the interaction of the HPA and HPG axes is a key factor in PMDD pathophysiology.

Aside from hormonal and neurological paths to understanding the etiology of PMDD, it is also necessary to consider environmental and genetic factors. According to Johns Hopkins Medicine (2026), PMDD is a “much more severe” form of premenstrual syndrome (PMS), and, while anyone can develop the disorder, those with a family history of PMS, PMDD, depression, postpartum depression, or other mood disorders are at higher risk, possibly due to higher genetic risk for abnormal reactions to normal hormonal changes or serotonin deficiencies. Those also suggested to be at risk are individuals with less access to education about the management and treatment of PMDD, or less access to healthcare in general, and cigarette smokers. In addition, the DSM-5-TR identifies possible environmental factors, such as stress, history of interpersonal trauma, and sociocultural beliefs regarding female sexual behavior and female gender roles, and genetic factors like the most stable premenstrual symptoms being an estimated 50% heritable. Considering family genetics, uncontrollable environmental disparities, and cultural differences can put young women at risk for developing more severe PMS symptoms and even PMDD, there is a need for a call to action to educate all people, and medical professionals, about the risk factors that can lead to the development and exacerbation of PMDD. 

Despite its inclusion in the DSM-5-TR, PMDD remains a heavily debated disorder within the literature. Some researchers believe in its severity as an understudied, unrepresented mental health condition, while others, like Browne (2014), see it as a socially constructed display of female distress. Browne argues that PMDD pathologizes a normal monthly biological response to the menstrual cycle, yet changes in “normal” functioning do not immediately signal a pathological concern. Even though that statement is not untrue, within the already scarce pre-existing literature on the subject, there is a troubling amount of research with significant findings that demonstrates how PMDD can lead to suicidal ideation and suicide attempts. Even within the DSM-5-TR includes a one sentence warning under the section Association With Suicidal Thoughts or Behavior that reads, “The premenstrual phase has been considered by some to be a risk period for suicide”. Browne makes a point when stating that distress can be significant without having to be pathologized and that the premenstrual phase can come with a “normal” amount of anger and distress that does not fit the criteria for a mental disorder; however, advocates of the diagnosis argue that PMDD is distinguished from average premenstrual experiences by the severity of symptoms, degree of functional impairment, and evidence suggesting changes in sensitivity to normal hormonal fluctuations. Another critique presented is that trauma and the social environment can cause biological changes that lead to monthly distress, so therefore a psychiatrist diagnosis is unreasonable. Although this point does not directly contradict the idea that trauma is a risk factor for PMDD, it reframes trauma-induced biological changes as evidence against PMDD being a discrete disorder, which reflects an alternative interpretation of the relationship between environmental influences and biological mechanisms. However, contemporary models of psychopathology recognize that environmental experiences and biological mechanisms interact, so past trauma originating the path to distress does not invalidate PMDD as a legitimate, significant condition.

RELATION TO SUICIDAL IDEATION

Regardless of ongoing debate surrounding how to classify PMDD, there is a growing amount of empirical literature suggesting that the disorder is associated with a significant relation to suicidal ideation, planning, and attempts. The research demonstrates that the severity and functional impairment that comes with PMDD extends beyond standard premenstrual experiences and warrants serious clinical attention. 

Wikman et al. (2022) aimed to gather more information on the prevalence of PMDD and to examine the correlate of suicidal ideation in the late luteal phase in women with expected and confirmed PMDD. 110 women participated in the study and, utilizing the Montgomery–Åsberg Depression Rating Scale self-rated version (MADRS-S), 75.5% reported previous drug treatment for the disorder, 31.8% reported a history of depression, and 41.8% and 18.2% reported moderate and severe luteal phase depressive symptoms. Suicidal ideation was reported by 39.1%, or 43, of the women, and higher depressive symptoms and previous psychological treatment for the disorder were positively associated with current suicidal ideation, while high ratings of self-rated health were associated with decreased risk of suicidal ideation. Regarding depressive symptoms, according to ratings on the Daily Record of Severity of Problems (DRSP) over the past two menstrual cycles, feelings of hopelessness, worthlessness, guilt, and feeling easily hurt were all significantly higher for women with PMDD and suicidal ideation than women with PMDD without suicidal ideation. A strength of this study is the real-time monitoring of women’s symptoms throughout the menstrual cycle to confirm their PMDD, which reinforces the validity of the diagnosis, and a weakness of is the limited sample size which limits generalizability and increases the chance for sampling errors to occur (Wikman et al., 2022). As a whole, these are concerning findings that suggest that, given a random population of women with PMDD, a significant proportion of them would be experiencing suicidal ideation during the late luteal phase. Though some women in this population sought psychological treatment for PMDD, there is still a lot of misunderstanding and stigma surrounding the condition that can be contributing to the lack of research and implementation of interventions in clinical settings. Meanwhile, many women are feeling extreme levels of depression and anxiety during their luteal phase that has lead some individuals to suicidal behavior.

Pilver et al. (2012) examined whether PMDD status was associated with suicidal ideation, plans, and attempts, unrelated to sociodemographic factors or other comorbid psychiatric disorders. 3,965 women from the United States were assessed using the Collaborative Psychiatric Epidemiology Survey, with the dependent variables measured being suicidal ideation, suicide plans, and suicide attempt(s) and the independent variable being PMDD status (PMDD, moderate/severe PMS, no premenstrual symptoms). The results of the questioning show the prevalence of non-fatal suicidal behaviors increasing in a graded fashion according to individual PMDD status, where women with diagnosed PMDD were at the highest risk for experiencing suicidal ideation (37.4%), plans (19.1%), and attempts (16.2%) compared to women with only PMS or who were asymptomatic. Regarding psychiatric comorbidity, 22% of women with PMDD met the criteria for Substance Use Disorder, 40% met the criteria for Major Depressive Disorder, and 70% met the criteria for Anxiety Disorder. Although a substantial proportion of women with PMDD also met the criteria for Major Depressive Disorder (40%), Pilver et al. found that PMDD remained independently associated with suicidal ideation, plans, and attempts even after controlling for MDD and other psychiatric disorders. This finding supports the argument that PMDD is not simply a premenstrual manifestation of depression, but rather a distinct disorder with its own contribution to suicide risk. The authors further suggest that abnormalities in serotonin functioning may partially explain this relationship, as both PMDD and suicidal behavior have been linked to reduced serotonin activity during the luteal phase. A strength of this study is its use of a nationally representative sample while controlling for numerous demographic and psychiatric confounds, allowing for the isolation of the effect of PMDD on suicidal behavior. However, because PMDD diagnoses were based on retrospective survey data rather than prospective daily symptom ratings, the findings should be interpreted with some caution.

An additional team of researchers conducted a cross-sectional study among Bangladeshi university students with the goal to assess the association between PMDD and depression, anxiety, stress, suicidal ideation, and suicidal attempts. Roy et al. (2025) utilized a questionnaire comprising demographic information, the Depression, Anxiety, and Stress Scale (DASS-21), and the Premenstrual Symptoms Screening Tool (PSST), which is a screening tool for premenstrual symptoms, were administered to measure the aforementioned variables. Consistent with Pilver et al. (2012), women with PMDD reported a significantly higher prevalence of past-year suicidal ideation (38.8%) and suicide attempts (28.6%) than participants with no premenstrual symptoms, along with a significant relationship between moderate/severe PMS and PMDD and a higher probability that suicidal ideation will be reported. After controlling for other variables, such as age at menarche, family history of PMS, presence of chronic disease, and physical exercise, participants with PMDD still remained more than five times as likely to report suicidal ideation than students without premenstrual symptoms, exhibiting that the relationship between PMDD and suicidality existed even after accounting for additional risk factors. Furthermore, depression, anxiety, and stress were all significant predictors of suicidal ideation, and the relationship between PMDD and suicidality became even stronger when these symptoms were present. These findings, consistent with the aforementioned studies, suggest that while PMDD itself is an important risk factor for suicidal ideation, comorbid psychological distress may increase the likelihood of suicidal thoughts and behaviors. The results also highlight the importance of implicating mental and menstrual health therapy for women with PMDD, severe PMS, and those with PMDD or severe PMS with comorbid depression, anxiety, and stress to regularly screen for signs of suicidal thoughts or behaviors. A limitation of this study is once again the retrospective data as well as a lack of clinician interviews which cannot ensure accurate diagnoses of PMDD, PMS, depression, anxiety, and stress. Future studies should use more precise diagnostic measurements and instruments to accurately assess participants. A major strength of this study, however, was its account of demographic and psychiatric variables as possible mediating factors which which was helpful in determining the impact of PMDD on suicidal thoughts and behaviors. Never before was such a diverse array of mediators assessed in this context. 

Key patterns are arising across the literature regarding the relationship between PMDD and suicidal ideation, with PMDD leading to significant increases in suicidal ideation, suicide planning, and suicide attempts among women in the luteal phase. It should also be noted that this pattern was seen among domestic and international samples. With such a large percentage of women struggling with this, it is necessary that proper intervention measures are implemented in medical and psychiatric settings. These measures could include screening tools like the DRSP, DASS-21, and PSST; and new cycle based risk assessments could be developed for even greater accuracy in screening someone with PMDD for suicide risk. Wikman et al. (2022) found that the relationship between women who sought prior psychological treatment for the disorder and suicidal ideation was positively associated, so, if some women with the disorder are seeking help for it, it would therefore be useful to have the proper diagnostic tools to give them the support they need. Also, with more visibility of the disorder curated by medical and psychiatric professionals, women can be made more aware of the disorder, its symptoms and effects, and how to get proper treatment, which in turn can help mitigate the effects of suicidal thoughts and behaviors put on by PMDD.  

TREATMENTS

Though research has identified various promising biological mechanisms underlying PMDD, its exact pathophysiology still remains unknown. Therefore, treatment interventions tend to focus on symptom management rather than resolving the disorder. Current treatments fall into the categories of SSRIs, psychotherapy, hormone therapies, and lifestyle interventions. 

Current literature generally agrees that SSRIs are the most effective first-line treatment for decreasing PMDD symptoms (Hantsoo & Epperson, 2015; Rapkin et al., 2013; Johns Hopkins Medicine, 2026), yet there is less of a consensus regarding alternative approaches. Using SSRIs for PMDD is unusual because the medication can become effective hours to days after the first dose, meanwhile taking SSRIs for depression could take weeks for noticeable effects. The rapid onset is suggested to be because SSRIs convert 5α-dihydroprogesterone to allopregnanolone (ALLO) in minutes, rather than solely affecting serotonin transfer, boosting GABA-A receptors that induce mood regulating effects. This also allows intermittent dosing from ovulation to menstruation to be easily administered to reduce symptoms such as irritability and unpredictable mood swings; however, long term use of SSRIs would be necessary to reduce depressive and somatic symptoms (Hantsoo & Epperson, 2015 & Rapkin et al., 2013). Another positive of this treatment is that previous studies have shown that only a low dose (ex. 25-50 mg of sertraline) is needed to lower symptom severity, and the results were found in populations using fluoxetine (Steinberg et al., 2012), paroxetine (Yonkers et al,. 2006), citalopram (Ravindran et al., 2007), and escitalopram (Freeman et al,. 2005). Despite their effectiveness, SSRIs are not a perfect treatment and are associated with several limitations. They could cause adverse effects such as insomnia, nausea, headache, and possible sexual dysfunction, which may lead to medication discontinuation or prevent patients from using it in the first place. Further, treatment response rates are quite varied among individuals across studies, suggesting that SSRIs may not work for all women with PMDD (Hantsoo & Epperson, 2015 & Rapkin et al., 2013). Collectively, these findings not only support SSRIs as an effective initial therapy for women with PMDD, but also reinforce the theory that PMDD is a distinct neurobiological condition that differs from a form of major depressive disorder.

Since PMDD symptom etiology appears to be linked to ovarian hormone fluctuations, researchers have also examined treatments that aim to stabilize hormone changes by suppressing the HPG axis or inhibit ovulation by controlling sex steroid fluctuations (Rapkin et al., 2013). Oral contraceptives (OCs) are commonly prescribed to treat PMS symptoms, but the evidence supporting their effectiveness for PMDD is weak. Although the number of large-scale studies on the effect of OCs on PMDD is minimal, there is a consensus among the research that OCs only produce mild symptom improvement, with the majority of the benefits deriving from a placebo effect (Hantsoo & Epperson, 2015, Rapkin et al., 2008, & Bäckström et al., 1992). Some research, however, has shown positive effects. For one, Bäckström et al. (1992) found evidence that OCs containing desogestrel, a synthetic progestin hormone, improved mood somewhat more effectively than levonorgestrel, commonly found in emergency contraception. Yet, the majority of findings still do not support OCs as a successful treatment. Joffe et al., (2003) reported that out of a group of women taking different forms of OCs, only 12.3% of participants reported improved mood; and Lopez et al. (2012) suggested that while certain OCs containing drospirenone and ethinyl estradiol slightly reduced PMDD symptoms, there was too large of a placebo effect to attribute the symptom reduction entirely to the hormonal treatment. Similarly, randomized, double-blind, placebo-controlled trials conducted by Freeman et al. (2012) and Halbreich et al. (2012) found that continuous dosing with levonorgestrel (90mcg) and ethinyl estradiol (20mcg) only slightly improved PMDD and PMS symptoms, also with a high placebo effect. 

A second form of hormonal treatment is GnRH agonists, which suppress ovulation by blocking reproductive hormone signals and generating postmenopausal levels of estradiol, progesterone, and ALLO. Using this intervention is usually only recommended to women with PMDD who find SSRI treatment ineffective, and it doubles as a “test” for how a woman would respond to an oophorectomy, or surgical menopause (Hantsoo & Epperson, 2015 & Rapkin et al., 2013). Common forms of GnRH agonists include goserelin, triptorelin, leuprolide, and histrelin. Some studies show that leuprolide acetate has been found to be successful in improving physical, emotional, and behavioral symptoms of PMDD (Pincus et al., 2011), while other research has found GnRH analogs to be successful in improving severe PMS symptoms and have adverse effects for those with premenstrual depression (Brown et al., 1994). Also, with GnRH agonists, there is an elevated risk for coronary artery disease and osteoporosis due to low estrogen levels. To counteract this side effect, estradiol add-back therapy, specifically with tibolone, has been found to improve PMDD and PMS symptoms and prevent bone loss (Wyatt et al., 2004 & Mitwally et al., 2002). Overall, GnRH agonists are seen as a “third-line therapy” that can be useful to confirm whether an individual's symptoms are due to PMDD or an affect disorder and to determine a possible outcome of an oophorectomy, yet their evidence of effectiveness is less extensive and less consistent than evidence for SSRIs. Further, considering hormonal treatment research findings as a whole still contain a significant amount of placebo effects, and not every woman responds to hormonal treatments, therefore other non-medical treatments must be implemented and improved to better treat PMDD. 

Though PMDD has a biological foundation, research has grown to recognize the value of psychological interventions in helping those affected cope with its symptoms. Kleinstäuber et al. (2012) found evidence suggesting that cognitive-behavioral therapy (CBT) improved premenstrual symptoms more effectively than SSRIs, which were found to be more beneficial in improving only the anxiety symptoms of PMDD, as it taught individuals how to cope with the disorder and shift their attribution of their symptoms. The same study also found that CBT produced longer treatment effects at follow-up than SSRIs like fluoxetine, and suggested that recommending SSRIs alone as a first-line treatment should be reexamined. Hunter et al. (2002) found that while fluoxetine reduced severe PMS, including PMDD, symptoms effectively, the use of CBT was associated with long-term improvement; and, multiple other researchers concur that PMDD treatment should advance beyond a medicinal approach toward an individualized, psychological and pharmacological therapy. Finally, an internet-based CBT intervention, a form of which has been reported to be promising for conditions such as postpartum depression, is proposed to be in development for PMDD as well (Kues et al., 2014).     

In comparison to pharmacological and hormonal treatments, non-medical interventions have significantly less empirical support regarding PMDD treatment. Nutritional supplements, dietary modifications, exercise, herbal treatments, and lifestyle interventions have all been studied, yet evidence of their effectiveness remains limited and is often based on PMS studies rather than PMDD studies. Dietary modification and calcium supplementation have been shown to have some minor benefits, particularly for treating PMS, with calcium supplements (1200 mg/day) having the strongest support due to randomized controlled trials that show it can improve both physical and mood symptoms (Thys-Jacobs et al., 1998 & Ghanbari et al., 2009). Vitamin B6, exercise, and other lifestyle modifications all have inconsistent findings with no clear positive effect. However, again, these studies are primarily focused on PMS than PMDD, which limits the generalizability of the aforementioned findings (Rapkin et al., 2013; Hantsoo & Epperson, 2015). 

Many herbal therapies have also shown some promise. A randomized control trial using chasteberry, or agnus castus, found significant positive effects on emotional and somatic symptoms of PMDD compared to a placebo (Schellenberg, R., 2001), and another study’s findings suggest that the response rate to chasteberry is equal to that of fluoxetine (Atmaca et al., 2003). St. John’s Wort was also shown to have a small beneficial effect in comparison with a placebo (Stevinson & Ernst, 2000; Dante & Faccinetti, 2011), but it should be used with caution given its known adverse effects when combined with SSRIs (risk of serotonin excess) and other forms of medication (i.e. interference with efficacy of oral contraceptives). 

Interventions focused on circadian rhythm regulation, such as bright-light therapy and sleep deprivation, have also been explored based on evidence that women with PMDD have similar decreased melatonin secretion as major depressive disorder (Schechter et al., 2010). Sleep deprivation was suggested to correct dysregulated circadian rhythms by influencing the sleep-wake cycle, increasing the total time the individual sleeps at night, inducing more rapid eye movement sleep, and improving mood in women with PMDD. Further, Parry et al. (1989) and Lam et al. (1999) demonstrated that bright-light therapy can alleviate PMDD symptoms if administered early in the morning and/or in the evening. Overall, more research is required to determine the true effects of circadian rhythm therapies on PMDD. 

Unlike SSRIs and CBT, these non-medical treatments lack strong empirical support as the majority of evidence originates from PMS studies and studies that result in mild, adverse, or no effects. Consequently, researchers recommended these strategies only as alternatives to pharmacological and psychological interventions for women seeking additional reliefs for their PMDD, not as the main course of treatment. 

CONCLUSION

The literature reviewed in this paper suggests that PMDD is a clinically significant disorder with symptoms that surpass the typical emotional and physical changes associated with the premenstrual phase. Although its exact pathophysiology remains unclear, research points toward a complex interaction between sensitivity to normal ovarian hormone fluctuations, neurological and genetic factors, and environmental influences such as stress and trauma. Results involving the CNS, estrogen and progesterone sensitivity, and interactions between the HPG and HPA axes suggest that PMDD cannot be explained by abnormal hormone levels alone. Rather, the disorder may involve an abnormal biological response to otherwise normal hormonal changes (Hantsoo & Epperson, 2015).  

The strongest concern identified across the literature is the relationship between PMDD and suicidal ideation and behavior. Studies using both nationally representative samples and clinical populations have found higher rates of suicidal ideation, suicide planning, and suicide attempts among individuals with PMDD, and this association has remained significant even after accounting for comorbidities such as depression and anxiety (Wikman et al., 2022; Pilver et al., 2012, & Roy et al., 2025). This suggests that PMDD may be an independent contributor to suicide risk. Future research may strengthen the evidence regarding this relationship by demonstrating high rates of suicidal ideation during the late luteal phase among women with confirmed PMDD. However, the majority of the existing research is limited by retrospective diagnoses, cross-sectional designs, small samples, and reliance on self-report measures. Future research should therefore prioritize cycle-based assessments of PMDD and suicidality using valid diagnostic and suicide-risk measures.

Treatment research similarly contains both progress and limitations. SSRIs currently have the strongest evidence and remain the primarily recommended treatment, with the ability to produce therapeutic effects within days and to be taken intermittently during the luteal phase. However, adverse effects, varied response rates, and uncertainty regarding the long-term effectiveness of SSRIs suggest that they are not the best treatment for every individual (Hantsoo & Epperson, 2015 & Rapkin et al., 2013). Hormonal treatments, such as oral contraceptives and GnRH agonists, have also produced inconsistent results and demonstrate placebo effects  (Hantsoo & Epperson, 2015, Rapkin et al., 2008, & Bäckström et al., 1992). Psychological interventions, particularly CBT, may provide lasting improvements and could be used alongside pharmacological treatment, while dietary, herbal, exercise, and circadian interventions currently have considerably less empirical support (Kleinstäuber et al., 2012; Hunter et al., 2002). Together, these findings suggest that treatment should be individualized according to symptom profile, response to treatment, and patient preferences to be most effective rather than relying solely on one intervention.

In conclusion, the literature supports the need to take PMDD more seriously as a potential cause of significant psychological distress and suicidal behavior. The debate over whether PMDD is a distinct psychiatric disorder should not prevent researchers and clinicians from investigating individuals who experience severe psychological symptoms. Instead, future research should work toward clarifying the biological and psychosocial mechanisms underlying PMDD, developing more reliable cycle-based diagnostic and suicide-risk screening methods, and identifying treatments that provide sustained improvement. Increased awareness among healthcare and mental health professionals may also improve recognition and treatment of PMDD, particularly for individuals experiencing suicidal thoughts or behaviors during the luteal phase. Addressing these gaps in research and knowledge could lead to earlier identification of PMDD, more effective interventions, and a better understanding of a disorder that remains understudied despite its severity.

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