**Background:** Obesity affects approximately one in four UK adults and is associated with multiple morbidities including Type 2 diabetes, heart disease, and certain cancers. Previous research has linked early parenthood, high parity, and partnership separation to obesity risk. However, the role of complex family dynamics involving childbearing across multiple partnerships (multi-partner fertility, MPF) has not been adequately studied. This paper examined associations between number of biological children, MPF, and obesity at midlife in a British birth cohort.
**Methods:** Data came from the 1970 British Cohort Study (BCS70), which has followed 17,196 participants born in a single week of 1970 in England, Scotland, and Wales. The analytical sample included 2940 fathers and 3369 mothers with measured obesity at age 46. The exposure was a composite variable combining number of biological children (1, 2, 3+) and MPF status (yes/no) by age 42, with categories: one child, two children with one partner, two children with two partners, three or more children with one partner, and three or more children with two or more partners. The outcome was obesity (BMI ≥ 30) measured by a health professional at age 46. Confounders included parental education, social class, maternal age at birth, maternal smoking (birth); cognitive ability, damp housing, overcrowding, benefits receipt, longstanding illness (age 10); self-esteem, locus of control, malaise, Rutter behaviour scale, parental separation, smoking (age 16). Adult mediators at age 42 included age at first birth, smoking status, alcohol dependency (AUDIT), educational attainment, housing tenure, and malaise. Logistic regression with multiple imputation by chained equations (50 cycles) was used.
**Key Results:** For fathers, no significant associations were found between number of children, MPF, or the composite variable and obesity in any model. For mothers in unadjusted models, MPF was associated with 35% higher odds of obesity (OR 1.35, 95% CI 1.12–1.64). Mothers with three or more children had 26% higher odds (OR 1.26, 95% CI 1.05–1.50). Using the composite variable, mothers with one child (OR 1.24, 95% CI 1.01–1.51), two children with two partners (OR 1.45, 95% CI 1.05–1.99), and three or more children with two or more partners (OR 1.51, 95% CI 1.18–1.93) had higher odds of obesity. After adjusting for parental confounders, the associations for one child (OR 1.21, 95% CI 0.99–1.48) and two children with two partners (OR 1.31, 95% CI 0.95–1.81) were attenuated. The association for three or more children with two or more partners was attenuated after including age 10 confounders (OR 1.28, 95% CI 0.99–1.65). In the fully adjusted model including age at first birth, mothers with one child remained at significantly higher odds of obesity (OR 1.30, 95% CI 1.05–1.60). Mothers with two children with two partners (OR 1.10, 95% CI 0.78–1.56) and three or more children with two or more partners (OR 1.02, 95% CI 0.77–1.35) were no longer significantly different from the reference group.
**Clinical Implications:** The findings suggest that the association between multi-partner fertility and obesity in mothers is largely explained by early-life confounders (parental background, childhood cognitive ability, psychological characteristics) rather than by MPF itself. This supports a selection hypothesis — that childhood circumstances predispose individuals toward both complex family trajectories and poorer health outcomes. The persistent association between having one child only and obesity risk warrants further investigation, potentially related to pre-pregnancy health, pregnancy complications, or gynaecological factors. For clinicians, these results highlight the importance of considering life-course determinants of obesity, particularly early-life socioeconomic and psychological factors. The gender differences observed underscore that biological pathways (pregnancy, breastfeeding, menopause) and social factors (greater childcare responsibility for mothers following separation) may differentially affect obesity risk. The study is limited by potential under-reporting of fertility in men, attrition bias (partnership dissolution predicts loss to follow-up), and inability to account for genetic factors, diet, physical activity, or medication use.