Maternal obesity during lactation as a hypertensive cardiovascular risk factor in the offspring.

Maternal obesity is a major public health concern, with growing evidence supporting its role in the developmental programming of cardiometabolic disease. Although prenatal mechanisms have been investigated extensively, the contribution of lactation as a postnatal window of cardiovascular (CV) programming remains insufficiently understood. Breast milk is a complex and dynamic biofluid that contains immune mediators, hormones, lipids and extracellular vesicles, which actively shape early-life immune maturation, metabolic regulation and vascular development. Emerging data indicate that maternal obesity is associated with alterations in breast milk immune mediators, adipokines and lipid composition, particularly an increased omega-6 to omega-3 polyunsaturated fatty acid ratio, and extracellular vesicle-associated microRNAs. These changes might influence endothelial function, oxidative stress balance, inflammatory signalling pathways, neurohumoral regulation and adipose tissue development in the offspring during a critical postnatal window of CV maturation. This review synthesizes current evidence on how maternal obesity reshapes the immunological, microbiological, hormonal, lipidic and epigenetic landscape of breast milk and discusses the potential implications for offspring hypertensive CV programming. We highlight key knowledge gaps, including the need for comprehensive characterization of maternal metabolic status, longitudinal vascular assessment in offspring and mechanistic studies that distinguish between pre- and postnatal influences. Understanding how lactation-mediated signals contribute to early vascular priming might offer new opportunities for preventive strategies to reduce intergenerational transmission of CV risk.