Early life nutrition and redox dysregulation: Implications for lifelong metabolic health

Early-life growth patterns are increasingly recognised as critical determinants of long-term health trajectories. A substantial body of evidence links suboptimal growth during early development with an elevated risk of chronic, age-related disorders in adulthood. In particular, maternal undernutrition leading to foetal growth restriction, especially when followed by rapid postnatal catch-up growth, markedly increases susceptibility to cardiometabolic and other degenerative diseases later in life. Conversely, maternal overnutrition and associated metabolic disturbances also exert lasting effects on offspring physiology, predisposing individuals to conditions such as cardiovascular disease, type-2 diabetes, and metabolic syndrome. Emerging mechanistic insights highlight redox imbalance as central mediator of maternal nutrition-induced developmental programming. Perturbations in oxidative homeostasis during critical windows of development can induce persistent alterations in cellular energetics, metabolic regulation, and tissue function, thereby accelerating biological ageing processes. In parallel, accumulating evidence implicates epigenetic modifications, including changes in DNA methylation, histone modifications, and non-coding RNA expression, as key mechanisms through which maternal nutritional status exerts durable effects on gene expression and disease susceptibility.