The current aging population is paralleled by a surge in obesity rates, forming a vicious cycle that significantly contributes to the growing burden of cardiovascular disease. This concomitant rise in obesity does not seem coincidental but it is most likely mechanistically linked to population aging. In their recent review, Ruperez and colleagues [1] explore the complex interplay between obesity and aging, spanning molecular mechanisms to whole organ function, with a particular focus on cardiovascular aging.

Obesity is associated with an increased cardiovascular risk [2], and it is well established that obesity exacerbates, or even drives, a range of cardiovascular disorders. For instance, obesity has been shown to influence cardiac remodeling and diastolic dysfunction [3], and is the most significant predictor of left atrial remodeling [4].

Both clinical and experimental evidence support a strong connection between obesity and biological aging. Obesity induces metabolic disturbances in the hearts of young individuals, resembling those observed in older non-obese individuals. At the cellular and molecular levels, obesity mimics the biological processes of aging. Many hallmarks of aging [5], such as impaired macroautophagy, loss of proteostasis, epigenetic changes, mitochondrial dysfunction, cellular senescence, disrupted metabolic and nutrient-sensing pathways, dysbiosis, and chronic inflammation, are also common features in obese humans and in animal models.

This interesting review discusses these parallels across molecular, cellular, and organismal scales, particularly within the cardiovascular system. It presents both preclinical and clinical evidence of age-related cardiovascular abnormalities in which obesity serves as a driving factor, supporting the idea that obesity may act as an accelerator of aging or even a form of premature biological aging.

Importantly, several metabolic interventions aimed at reducing obesity have also been shown to exert anti-aging effects on the cardiovascular system. The authors discuss different examples of metabolic and anti-obesity therapies, such as caloric restriction, bariatric surgery, GLP-1 receptor agonists, SGLT2 inhibitors, and NAD+ precursors amongst other, that not only provide cardiovascular benefits but are increasingly recognised as acting as anti-ageing interventions.

The review offers valuable insights into how a deeper understanding of the shared mechanisms between obesity and aging can inform the development of more effective cardiovascular therapies tailored to the growing population of aged and obese individuals. With obesity now affecting more than 40% of adults globally, public health policies must prioritize early prevention. Notably, the duration of obesity independently amplifies cardiovascular risk, regardless of current BMI [6]. Therefore, interventions during adolescence and young adulthood could delay cardiovascular aging and help preserve health span in an increasingly elderly population.
In conclusion, obesity functions as a catalyst for cardiovascular aging, shifting the burden of morbidity into younger populations. This review serves as a call to action to address the dual epidemics of aging and obesity through integrated lifestyle, pharmacological, and public health strategies designed to disrupt their shared pathogenic pathways.