Breastfeeding is the best way to provide newborns with crucial nutrients and produce a unique bond between mother and child. Breast milk is rich in nutritious and non-nutritive bioactive components, such as immune cells, cytokines, chemokines, immunoglobulins, hormones, fatty acids, and other constituents. Maternal effects during gestation and lactation can alter these components, influencing offspring outcomes. Chronic inflammatory maternal conditions, such as obesity, diabetes, and hypertension, impact breast milk composition. Breast milk from obese mothers exhibits changes in fat content, cytokine levels, and hormonal concentrations, potentially affecting infant growth and health. Similarly, diabetes alters the composition of breast milk, impacting immune factors and metabolic markers. Other pro-inflammatory conditions, such as dyslipidemia and metabolic syndrome, have been barely studied. Thus, maternal obesity, diabetes, and altered tension parameters have been described as modifying the composition of breast milk in its macronutrients and other important biomolecules, likely affecting the offspring’s weight. This review emphasizes the impact of chronic inflammatory conditions on breast milk composition and its potential implications for offspring development through the revision of full-access original articles.

Human breast milk (BM) is an essential fluid for infant development, with a dynamic composition adapted to the infant's needs. It contains bioactive lipids like cholesterol, typically transported by lactosomes, extracellular vesicles, and milk fat globules. However, classic cholesterol‐carrying lipoproteins have not been described in BM. This study included BM from 22 healthy women attending paediatric follow‐up. BM lipoproteins were isolated by ultracentrifugation, and their density was determined by refractometry. Cholesterol and triglyceride levels in whole milk and from BM‐lipoproteins were quantified using commercial kits. The main lipoproteins were quantified by western blot and Luminex assays. Native gel electrophoresis was used to identify lipoprotein migration patterns. BM lipoproteins exhibited densities between 0.999 and 1.043 g/mL, consistent with very low‐density lipoproteins, intermediate‐density lipoproteins, and low‐density lipoproteins (LDLs). No classic high‐density lipoproteins (HDLs) were detected by density, but apolipoproteins AI and B, markers of HDL and LDL, respectively, were detected. BM lipoproteins contained significantly less cholesterol and triglycerides than whole milk and showed migration patterns similar to adult serum HDL and LDL. This study provides the first evidence of classical BM lipoprotein classes, expanding knowledge of lipid transport in BM and suggesting a potential role in neonatal lipid metabolism and cholesterol homeostasis.

Increased albuminuria represents a risk factor for chronic kidney disease (CKD), and it is associated with the development and progression of kidney inflammation and fibrosis. The expression of neutrophil gelatinase-associated lipocalin (NGAL), a biomarker for kidney damage, is increased in CKD patients and experimental animal models of kidney damage. However, it is unknown whether NGAL is necessary for the promotion of kidney inflammation and fibrosis associated with the albumin exposition. Male C57BL6/J wild-type (WT) and NGAL (knockout) KO mice (8-12 weeks, n = 5-6) were subjected to the albumin overload (AO) model (10 mg/g/day i.p.) or Vehicle (0.9% NaCl i.p.) for 7 days. Kidney function and inflammatory and fibrotic status in the kidney were assessed. In WT and NGAL-KO mice, AO significantly increased plasma protein (1.3-fold, p < 0.001) and albuminuria (5.6-fold, p < 0.01). In WT mice, AO induced a significant increase in F4/80-positive kidney macrophages, which was prevented in NGAL-KO mice (p < 0.01). This effect was in accordance with the prevention of kidney increases in TNF-α and iNOS mRNA levels after AO (p < 0.05). Finally, AO significantly increased collagen deposition in the kidneys of WT mice (p < 0.05) and the expression of collagen-1, which was prevented in NGAL-KO mice (p < 0.01). Our results suggest that NGAL is required for albumin-induced kidney inflammation and fibrosis in mice in the AO model, which appears to be independent of changes in kidney function.

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.