Environmental Drivers of Obesity and Leptin Dysregulation in Hormone-related Cancer

Abstract

With over 650 million adults affected globally, obesity has become a major epidemic that contributes to several chronic illnesses, including cancer. Although it has historically been linked to dietary excess and sedentary lifestyles, mounting data make clear how important environmental exposures are in modifying metabolic processes. Adipokine produced by adipose tissue, leptin, is a critical player in the obesity-cancer axis, controlling hormone signaling, hunger, and energy expenditure. In obesity, leptin resistance and chronic hyperleptinemia disturb normal metabolic balance and stimulate proliferative and inflammatory signaling cascades linked to carcinogenesis. The impact of environmental factors, including air pollutants, dietary contaminants, endocrine-disrupting chemicals (EDCs), and urban lifestyle habits, on the development of obesity and leptin signaling dysregulation was examined. This review examines the mechanisms that increase susceptibility to metabolic imbalance, including oxidative stress, hormonal mimicry, epigenetic reprogramming, and hypothalamic dysfunction. We also outline the function of leptin in cancer biology, with particular attention to hormone-related cancers such as ovarian, breast, prostate, and endometrial cancers, where leptin promotes immunological evasion, angiogenesis, and epithelial–mesenchymal transition. By combining knowledge from epidemiology, molecular biology, and environmental health, this review emphasizes the necessity of a paradigm change in the prevention of obesity and cancer from lifestyle-based strategies to all-encompassing ecological treatments. Precision medicine, early-life exposure regulation, and public health policy are all significantly impacted by the findings, especially when it comes to high-risk and vulnerable populations.