Affective responses to the menstrual cycle vary widely. Some individuals experience severe symptoms like those with premenstrual dysphoric disorder, while others have minimal changes. The reasons for these differences are unclear, but prior studies suggest stressor exposure may play a role. However, research in at-risk psychiatric samples is lacking.

In a large clinical sample, we conducted a prospective study of how lifetime stressors relate to degree of affective change across the cycle. 114 outpatients with past-month suicidal ideation (SI) provided daily ratings (n = 6187) of negative affect and SI across 1–3 menstrual cycles. Participants completed the Stress and Adversity Inventory (STRAIN), which measures different stressor exposures (i.e. interpersonal loss, physical danger) throughout the life course, including before and after menarche. Multilevel polynomial growth models tested the relationship between menstrual cycle time and symptoms, moderated by stressor exposure.

Greater lifetime stressor exposure predicted a more pronounced perimenstrual increase in active SI, along with marginally significant similar patterns for negative affect and passive SI. Additionally, pre-menarche stressors significantly increased the cyclicity of active SI compared to post-menarche stressors. Exposure to more interpersonal loss stressors predicted greater perimenstrual symptom change of negative affect, passive SI and active SI. Exploratory item-level analyses showed that lifetime stressors moderated a more severe perimenstrual symptom trajectory for mood swings, anger/irritability, rejection sensitivity, and interpersonal conflict.

These findings suggest that greater lifetime stressor exposure may lead to heightened emotional reactivity to ovarian hormone fluctuations, elevating the risk of psychopathology.

We aimed to describe the clinical characteristics of female patients presenting with premenstrual disorders to a tertiary service in the UK. We conducted a retrospective case-note review of referrals to the National Female Hormone Clinic from April 2014 to August 2020. Based on clinical assessment, we determined whether the patient met criteria for premenstrual dysphoric disorder or premenstrual exacerbation of an underlying psychiatric disorder.

Of 146 patients seen in clinic for premenstrual disorders, an ICD-10 psychiatric diagnosis was made in 130 (89.0%); a minority 16 (11.0%) did not have a psychiatric diagnosis. Following assessment, 94 patients (64.4%) met criteria for premenstrual dysphoric disorder and 67 (45.6%) had exacerbation of a psychiatric disorder.

Patients presenting to this specialist service had complex psychiatric comorbidity; almost half presented with exacerbation of a psychiatric disorder.

The psychological risk factors of premenstrual dysphoric disorder (PMDD) are not fully understood, but initial evidence points to a potential role of unfavorable cognitive emotion regulation (ER-) strategies. Given the symptom cyclicity of PMDD, ambulatory assessment is ideally suited to capture psychological and physiological processes across the menstrual cycle. Our study examines habitual ER-strategies in women with PMDD and their predictive value for the course of mood and basal cortisol across the cycle in affected women.

Women with and without PMDD (n = 61 each) were compared regarding habitual mindfulness, reappraisal, and repetitive negative thinking (RNT). Momentary affect and cortisol output were assessed over two consecutive days per cycle phase (menstrual, follicular, ovulatory, late luteal).

Women with PMDD reported lower mindfulness, less use of reappraisal and stronger RNT than controls (ps < 0.035). In women with PMDD, higher mindfulness and reappraisal and lower RNT predicted decreased negative and increased positive affect across the menstrual cycle (ps < 0.027). However, women using more favorable ER-strategies displayed stronger mood cyclicity, resulting in stronger mood deterioration in the late luteal phase, thereby resembling women with more unfavorable ER-strategies toward the end of the cycle. Lower mindfulness predicted lower cortisol in the menstrual phase.

Protective ER-strategies seem to be generally linked to better momentary mood in women with PMDD, but do not appear to protect affected women from premenstrual mood deterioration. Habitual mindfulness, in turn, seems to buffer blunted cortisol activity in women with PMDD, especially in the menstrual phase.

Premenstrual dysphoric disorder (PMDD) is a new Diagnostic and Statistical Manual of Mental Disorders (DSM)-5 diagnosis characterized by the cyclical emergence of emotional and physical symptoms in the luteal phase of the menstrual cycle, with symptom remission in the follicular phase. Converging evidence highlights the possibility of distinct subtypes of PMDD with unique pathophysiologies, but temporal subgroups have yet to be explored in a systematic way.

In the current work, we use group-based trajectory modeling to identify unique trajectory subgroups of core emotional and total PMDD symptoms across the perimenstrual frame (days −14 to +9, where day 0 is menstrual onset) in a sample of 74 individuals prospectively diagnosed with DSM-5 PMDD.

For the total daily symptom score, the best-fitting model was comprised of three groups: a group demonstrating moderate symptoms only in the premenstrual week (65%), a group demonstrating severe symptoms across the full 2 weeks of the luteal phase (17.5%), and a group demonstrating severe symptoms in the premenstrual week that were slow to resolve in the follicular phase (17.5%).

These trajectory groups are discussed in the context of the latest work on the pathophysiology of PMDD. Experimental work is needed to test for the presence of possible pathophysiologic differences in trajectory groups, and whether unique treatment approaches are needed.

Individuals with a borderline personality disorder (BPD) suffer from a constellation of rapidly shifting emotional, interpersonal, and behavioral symptoms. The menstrual cycle may contribute to symptom instability among females with this disorder.

Fifteen healthy, unmedicated females with BPD and without dysmenorrhea reported daily symptoms across 35 days. Urine luteinizing hormone and salivary progesterone (P4) were used to confirm ovulation and cycle phase. Cyclical worsening of symptoms was evaluated using (1) phase contrasts in multilevel models and (2) the Carolina Premenstrual Assessment Scoring System (C-PASS), a protocol for evaluating clinically significant cycle effects on symptoms.

Most symptoms demonstrated midluteal worsening, a perimenstrual peak, and resolution of symptoms in the follicular or ovulatory phase. Post-hoc correlations with person-centered progesterone revealed negative correlations with most symptoms. Depressive symptoms showed an unexpected delayed pattern in which baseline levels of symptoms were observed in the ovulatory and midluteal phases, and exacerbations were observed during both the perimenstrual and follicular phases. The majority of participants met C-PASS criteria for clinically significant (⩾30%) symptom exacerbation. All participants met the emotional instability criterion of BPD, and no participant met DSM-5 criteria for premenstrual dysphoric disorder (PMDD).

Females with BPD may be at elevated risk for perimenstrual worsening of emotional symptoms. Longitudinal studies with fine-grained hormonal measurement as well as hormonal experiments are needed to determine the pathophysiology of perimenstrual exacerbation in BPD.

Difficulties in regulating emotions are linked to the core symptoms of premenstrual dysphoric disorder (PMDD). We therefore investigated the neural substrates of emotion-regulation problems in women with PMDD.

On the basis of self-evaluations over 2 months on the Daily Record of Severity of Problems, eligible participants were assigned to two groups: PMDD and control (18 per group). Functional magnetic resonance imaging (fMRI) and a well-validated task were used to assess brain function during emotion regulation. Participants were tested twice, once during the follicular (asymptomatic) and once in the late luteal (symptomatic) phase of the menstrual cycle.

Women with PMDD gave higher ratings of negative affect in the luteal phase than in the follicular phase, and compared with healthy control participants during the luteal phase. A region-of-interest fMRI analysis indicated that during the late luteal phase, women with PMDD had hypoactivation in right dorsolateral prefrontal cortex (dlPFC) during all conditions of the emotion-regulation task, not only in the contrast that isolated emotion regulation. An exploratory whole-brain, voxel-wise analysis showed that women with PMDD had less activation in the precentral gyrus during the luteal phase than the follicular phase, and less activation in the postcentral gyrus compared with control participants.

During the luteal phase of the menstrual cycle, women with PMDD experience difficulty regulating emotions. Hypoactivation in the right dlPFC may contribute to this problem, but may be related more generally to other affective symptoms of PMDD. Hypofunction in the right pre- and postcentral gyri warrants additional study.

Women who experience significant premenstrual symptoms differ in the extent to which these symptoms cause cyclical impairment. This study clarifies the type and number of symptoms that best predict premenstrual impairment in a sample of women undergoing prospective assessment for premenstrual dysphoric disorder (PMDD) in a research setting. Central research goals were to determine (1) which emotional, psychological, and physical symptoms of PMDD are uniquely associated with premenstrual impairment, and (2) how many cyclical symptoms optimally predict the presence of a clinically significant premenstrual elevation of impairment.

A total of 267 naturally cycling women recruited for retrospective report of premenstrual emotional symptoms completed daily symptom reports using the Daily Record of Severity of Problems (DRSP) and occupational, recreational, and relational impairment for 1–4 menstrual cycles (N = 563 cycles).

Multilevel regression revealed that emotional, psychological, and physical symptoms differ in their associations with impairment. The core emotional symptoms of PMDD were predictors of impairment, but not after accounting for secondary psychological symptoms, which were the most robust predictors. The optimal number of premenstrual symptoms for predicting clinically significant premenstrual impairment was four.

Results enhance our understanding of the type and number of premenstrual symptoms associated with premenstrual impairment among women being evaluated for PMDD in research contexts. Additional work is needed to determine whether cognitive symptoms should receive greater attention in the study of PMDD, and to revisit the usefulness of the five-symptom diagnostic threshold.

Previous studies have shown significant within-person changes in binge eating and emotional eating across the menstrual cycle, with substantial increases in both phenotypes during post-ovulation. Increases in both estradiol and progesterone levels appear to account for these changes in phenotypic risk, possibly via increases in genetic effects. However, to date, no study has examined changes in genetic risk for binge phenotypes (or any other phenotype) across the menstrual cycle. The goal of the present study was to examine within-person changes in genetic risk for emotional eating scores across the menstrual cycle.

Participants were 230 female twin pairs (460 twins) from the Michigan State University Twin Registry who completed daily measures of emotional eating for 45 consecutive days. Menstrual cycle phase was coded based on dates of menstrual bleeding and daily ovarian hormone levels.

Findings revealed important shifts in genetic and environmental influences, where estimates of genetic influences were two times higher in post- as compared with pre-ovulation. Surprisingly, pre-ovulation was marked by a predominance of environmental influences, including shared environmental effects which have not been previously detected for binge eating phenotypes in adulthood.

Our study was the first to examine within-person shifts in genetic and environmental influences on a behavioral phenotype across the menstrual cycle. Results highlight a potentially critical role for these shifts in risk for emotional eating across the menstrual cycle and underscore the need for additional, large-scale studies to identify the genetic and environmental factors contributing to menstrual cycle effects.

Significant associations between changes in ovarian hormones and binge eating are present across the menstrual cycle in women with bulimia nervosa. However, no study has examined these relationships in a non-clinical sample, despite the need for these data for designing risk-factor studies.

In study 1, we modified several continuous measures of binge eating and identified those that were most sensitive to menstrual-cycle fluctuations in a non-clinical sample of 10 women who completed measures for 35 days. In study 2, we explored associations between ovarian hormones and binge-eating scores in nine women who completed these same measures for 65 days and provided daily saliva samples for assays of estradiol and progesterone concentrations.

In study 1, the Emotional Eating subscale of the Dutch Eating Behavior Questionnaire exhibited superior reliability and was most sensitive to predicted menstrual-cycle changes in binge eating (i.e. increased scores in the mid-luteal/premenstrual compared with follicular/ovulatory phases). In study 2, this scale showed predicted inverse associations with estradiol and positive associations with progesterone across the menstrual cycle that could not be accounted for by changes in negative affect.

Associations between ovarian hormones and binge eating are robust and present in clinical and non-clinical samples. Findings support the ability to examine the role of ovarian hormones as risk factors for binge eating in large-scale prospective studies and twin studies.

The objective of the study was to correlate quantitative changes in the lipid composition of human cerumen with changes in age, sex and menstrual cycle stage.

Cerumen samples were collected from the external ear canal and analysed using sequential, one dimensional, high performance thin layer chromatography.

The following age groups of both sexes were investigated: one to 10 years; 11–18 years; 19–40 years; and 40 years and over. Additionally, cerumen samples from subjects in three stages of the menstrual cycle were compared.

In the cerumen samples, the peak values for wax ester and cholesterol occured between the ages of one and 10 years for both sexes. However, squalene and triglyceride content reached maximum levels at puberty. Men aged 19–40 years had a significantly greater percentage of cerumen lipid squalene content than women from the same age group; however, their cholesterol content was found to be lower. Regarding the various menstrual cycle stages, cerumen samples taken at the follicular stage from women aged 19–40 years had a significantly lower free fatty acids content, and higher cholesterol and squalene levels, compared with samples taken in the luteal or menstrual stages.

The proportions of the lipid constituents of cerumen varied with age, sex and menstrual stage. In cerumen, the main lipid constituent stimulated at puberty appears to be squalene, not wax esters as reported for sebum. The relevance of lipid constituents to cerumen's protective role is discussed.