The association of race, ethnicity, and socioeconomic status on the severity of menopause symptoms: a study of 68,864 women.

OBJECTIVE: This study aimed to evaluate if and how race, ethnicity, and socioeconomic status (SES) are associated with the severity of menopause symptoms in a large, diverse sample of women. METHODS: For this cross-sectional study conducted between March 24, 2019, and January 13, 2023, a total of 68,864 women were enrolled from the Evernow online telehealth platform. Participants underwent a clinical intake survey, which encompassed demographic information, detailed medical questionnaires, and a modified Menopause Rating Scale. The modified scale was adapted for ease of use online and is available in the supplementary material along with the full intake. Symptom severity was evaluated using a multivariate binomial generalized linear model, accounting for factors such as race, ethnicity, age, body mass index, smoking status, bilateral oophorectomy status, and SES. Odds ratios (OR) and CIs were calculated based on the linear regression coefficients. RESULTS: Of the participants, 67,867 (98.6%) were included in the analysis after excluding outliers and those with unknown oophorectomy status. The majority of respondents identified as White (77.4%), followed by Hispanic (9.0%), Black (6.7%), two or more races/ethnicities (4.4%), Asian (1.2%), Indigenous/First Nations (0.8%), Middle Eastern (0.3%), and South Asian (0.2%). Notably, individuals identifying as Black (hot flashes OR, 1.91; 97.5% CI, 1.75-2.09; P < 0.001), Hispanic (skin/hair changes OR, 1.58; 97.5% CI, 1.45-1.71; P < 0.001), Indigenous/First Nations (painful sex OR, 1.39; 97.5% CI, 1.19-2.75; P = 0.007), Middle Eastern (weight changes OR, 2.22; 97.5% CI, 1.25-4.37; P = 0.01), or with two or more races/ethnicities (skin/hair changes OR, 1.41; 97.5% CI, 1.26-1.58; P < 0.001) reported higher levels of symptom severity compared with their White counterparts. Conversely, Asian and South Asian participants reported lower symptom severity. Even after incorporating SES into the linear model, racial and ethnic groups with lower SES (Black, Hispanic, Indigenous, and multiple ethnicities) exhibited slight shifts in OR while maintaining high statistical significance (Black [hot flashes OR, 1.87; 97.5% CI, 1.72-2.04; P < 0.001], Hispanic [skin/hair changes OR, 1.54; 97.5% CI, 1.42-1.68; P < 0.001], Indigenous/First Nations [painful sex OR, 1.74; 97.5% CI, 1.17-2.70; P = 0.009], multiple ethnicities [skin/hair changes OR, 1.41; 97.5% CI, 1.26-1.58; P < 0.001]). CONCLUSIONS: Our study suggests that the relationship between race and ethnicity and the severity of menopause symptoms is not solely explained by differences in SES but is itself an independent factor. Understanding and addressing social, cultural, and economic factors are crucial to reduce disparities in menopausal symptoms.

Temperature-dependent differences in mouse gut motility are mediated by stress.

Researchers have advocated elevating mouse housing temperatures from the conventional ~22 °C to the mouse thermoneutral point of 30 °C to enhance translational research. However, the impact of environmental temperature on mouse gastrointestinal physiology remains largely unexplored. Here we show that mice raised at 22 °C exhibit whole gut transit speed nearly twice as fast as those raised at 30 °C, primarily driven by a threefold increase in colon transit speed. Furthermore, gut microbiota composition differs between the two temperatures but does not dictate temperature-dependent differences in gut motility. Notably, increased stress signals from the hypothalamic-pituitary-adrenal axis at 22 °C have a pivotal role in mediating temperature-dependent differences in gut motility. Pharmacological and genetic depletion of the stress hormone corticotropin-releasing hormone slows gut motility in stressed 22 °C mice but has no comparable effect in relatively unstressed 30 °C mice. In conclusion, our findings highlight that colder mouse facility temperatures significantly increase gut motility through hormonal stress pathways.