ArticleBiology of sex differences2026
Breastfeeding in infancy confers sex-specific, long-term protection against metabolic dysfunction-associated steatohepatitis and adverse liver outcomes.
Article in Biology of sex differences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundIt remains unclear whether breastfeeding in infancy is associated with risk of metabolic dysfunction-associated steatohepatitis (MASH) and adverse liver outcomes in adulthood.
methodsWe analyzed data from the prospective UK Biobank. Breastfeeding in infancy was ascertained via self-report. In a cross‑sectional analysis involving 26,850 participants with liver MRI data, metabolic dysfunction-associated steatotic liver disease (MASLD) was defined as PDFF > 5.5%, and MASH as PDFF > 5.5% combined with cT1 > 800 ms. Additionally, a longitudinal analysis of 378,702 participants assessed associations with incident cirrhosis, hepatocellular carcinoma (HCC), and liver‑related mortality.
resultsIn MRI-based analysis, breastfeeding in infancy was associated with lower odds of MASLD (OR 0.89, 95% CI 0.80-0.99) and MASH (OR 0.79, 95% CI 0.65-0.97) in females but not males, with a significant sex interaction for MASH (P for interaction = 0.023) but not for MASLD (P for interaction = 0.301). Over a median follow‑up of 14.9 years, breastfeeding was associated with reduced risks of cirrhosis (HR 0.71, 95% CI 0.60-0.83), HCC (HR 0.52, 95% CI 0.33-0.82), and liver‑related mortality (HR 0.63, 95% CI 0.46-0.86) in females. No such associations were observed in males (P for interaction = 0.047, 0.030, and 0.008, respectively). Mediation analysis revealed that circulating insulin-like growth factor-1 (IGF-1) mediated the association specifically in females, with a sex difference in the indirect effect (FDR < 0.001).
conclusionsBreastfeeding in infancy confers a long-term protective effect against MASH and adverse liver outcomes in women, but not in men. This sex-specific protective association was mediated by circulating IGF-1, suggesting a potential underlying mechanism.
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