# Clustered cardiometabolic risk in pregnancy and dysmenorrhea in offspring: Results from a prospective birth cohort study

## TL;DR

Higher maternal pre-pregnancy BMI increases the risk of dysmenorrhea in daughters, partly due to higher BMI and earlier puberty in the offspring.

## Contribution

Identifies maternal pre-pregnancy BMI as a novel risk factor for dysmenorrhea in offspring, partially mediated by BMI and menarcheal age.

## Key findings

- Higher maternal pre-pregnancy BMI was associated with increased dysmenorrhea risk in offspring.
- The association was partially mediated by offspring's higher BMI and earlier menarche.
- Overall maternal cardiometabolic risk showed no significant link to dysmenorrhea.

## Abstract

Dysmenorrhea, a common gynaecological complaint, is often underdiagnosed, particularly in adolescents. The Developmental Origins of Health and Disease hypothesis suggests that maternal cardiometabolic conditions during pregnancy may influence offspring reproductive health. We investigated whether cardiometabolic risk (CCMR) is associated with dysmenorrhea risk in offspring and whether early‐puberty BMI and menarcheal age mediate these associations.

Data was from the Amsterdam Born Children and their Development cohort. A total of 982 mother‐daughter pairs were included. Maternal CCMR included pre‐pregnancy body mass index (BMI), blood pressure, glucose, triglycerides and Apolipoprotein A1. Dysmenorrhea was defined as menstrual abdominal/back pain requiring analgesics. Inverse probability weighted multivariable logistic regression examined associations between maternal CCMR or its components and dysmenorrhea in offspring. Multiple imputation was used to handle missing data in the sensitivity analysis. Serial multiple mediation analysis tested the mediating role of offspring's BMI and menarcheal age.

Dysmenorrhea was reported in 49.2% of daughters. In the model adjusted for maternal age, socioeconomic status, smoking, alcohol use, anxiety and depressive symptoms, CCMR was not significantly associated with dysmenorrhea (OR: 1.03, 95% CI: .72–1.48). However, higher maternal pre‐pregnancy BMI was associated with increased dysmenorrhea risk in offspring (OR: 1.20, 95% CI: 1.02–1.42). A partial mediation via BMI and menarcheal age was observed (indirect effect: 1.01, 95% CI: 1.00–1.03).

No evidence was found of maternal CCMR and dysmenorrhea in offspring. However, higher maternal pre‐pregnancy BMI increased dysmenorrhea risk, partly mediated by heavier BMI and earlier pubertal timing in offspring. These findings align with the hypothesis of a possible intrauterine origin of menstrual disorders and highlight the importance of early life factors in dysmenorrhea research.

Dysmenorrhea is a leading gynaecological complaint starting from adolescence, yet its developmental origins remain poorly understood. Using data from 982 mother‐daughter pairs in the ABCD cohort, we examined maternal cardiometabolic risk (CCMR) during pregnancy and its association with adolescent dysmenorrhea. While overall CCMR showed no significant link, higher maternal pre‐pregnancy BMI increased dysmenorrhea risk in offspring, partly mediated by higher BMI and earlier menarche. By revealing that dysmenorrhea risk may be influenced before birth, this work highlights the need to consider intergenerational and developmental environments in reproductive research.