New Insight Into Male Infertility: Deviation From Basic Tenets of Life

Abstract

Male reproductive health faces mounting concern as global sperm concentration (SC) has declined markedly, with evidence linking this trend to environmental and lifestyle factors rather than natural variability. In parallel, rising rates of obesity, diabetes, and hypertension point to shared mechanisms with infertility, particularly those rooted in diet. High intake of processed sugars, especially high‐fructose corn syrup (HFCS), contributes to metabolic dysfunction, oxidative stress, hormonal imbalance, and inflammation, all of which can impair sperm function and disrupt the hypothalamic–pituitary–gonadal (HPG) axis. Unlike glucose, fructose undergoes hepatic metabolism, fostering insulin resistance, fat accumulation, and nonalcoholic fatty liver disease (NAFLD), further aggravating reproductive risks. In this review, four models of obesity, the energy balance model (EBM), carbohydrate‐insulin model (CIM), obesogen model, and OBS/REDOX model, are applied to explain how excess fructose and obesogenic exposures drive metabolic dysfunction, oxidative stress, and endocrine disruption. Collectively, these processes reduce testosterone levels, impair spermatogenesis, compromise sperm quality, and may even induce epigenetic alterations transmissible to future generations. With modern diets increasingly dominated by HFCS and ultra‐processed foods (UPFs), understanding fructose’s role in reproductive decline is crucial for developing effective interventions. This review underscores the need for further research to clarify how dietary fructose and environmental obesogens jointly shape metabolic and reproductive health, offering insights into public health strategies aimed at protecting male fertility in the face of modern lifestyle challenges.