Parental Obesity and Offspring Risk for Cardiorenal Diseases

Obesity rates have increased dramatically during the past four decades, and these increases have occurred in children and adolescents, as well as in adults at reproductive age. Currently, 40.3% of men and 39.7% of women 20-39 years of age in the United States are classified as obese, leading to a substantial rise in parental obesity. Obesity is a major risk factor for cardiovascular, metabolic and renal diseases, including hypertension, type 2 diabetes, and chronic kidney diseases. This review examines current evidence of how parental obesity programs offspring susceptibility to cardiorenal and metabolic dysfunction and discusses the potential underlying mechanisms that contribute to the long-term health consequences in the offspring.

Increasing evidence indicates that parental obesity, particularly maternal obesity, predisposes offspring to cardiovascular, metabolic, and renal dysfunction that can emerge early in life and persist into adulthood, even when controlled for lifestyle factors. Although alterations in the intrauterine and early postnatal environments are believed to underlie developmental programming, the mechanisms by which parental obesity influences long-term offspring health remain poorly understood. Emerging evidence suggests that dysregulation of neurohumoral pathways, chronic inflammation, mitochondrial dysfunction, and intercellular signaling may be transmitted across generations and contribute to increased risk of cardiorenal and metabolic diseases. Elucidating these mechanisms is essential for identifying novel therapeutic targets and determining whether interventions implemented before conception, during pregnancy, or during early life can mitigate adverse health outcomes and improve long-term offspring health.