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The failing of the obesity paradox in the failing heart.

The prevalence of obesity is increasing worldwide. Obesityrelated metabolic disorders are at the center stage to the development of heart disease, stroke, type 2 diabetes, and certain types of cancer, leading to a reduced quality of health and economic burden (3). In the United States, 40% of adult men and women are obese. These same patients have additional risk factors such as hyperglycemia and hypertension that are associated with cardiometabolic defects including heart failure (HF) (4, 5). According to the Framingham Heart Study, being overweight and obese remains the primary cause and risk factor for the development of HF, accounting for a 5% increase in men and a 7% increase in women for the risk of developing HF per unit of body mass index (8). As highlighted in previous reports, excessive adipose tissue accumulation impacts hemodynamic function, cardiac morphology, adipocytes, and cytokines, which leads to diastolic and/or systolic dysfunction and hypertrophy (4). However, even less is known about pathophysiological basis of sex-specific and age-related cardiac remodeling in HF. In obesity, fat mass, particularly visceral fat, has subsequent effects including insulin resistance and thereby hyperglycemia and type 2 diabetes. In fact, obesity contributes to the development of low-grade chronic inflammation and inflammatory cytokine production. This low-grade inflammation leads to an impairment in insulin signaling; however, not all forms of fat intake or obesity are equal in insulin resistance (6). Due to the enormous heterogeneity of obesity and HF, contrasting reports have indicated that obesity paradoxically confers a better outcome in HF. Conflicting studies have shown that overweight patients with HF have a better survival rate than underweight patients with HF (9). The reason behind this paradox remains unclear, but there are novel hypotheses and data that partially explains that collider bias is the reason for the confounding factors. One of the potential reasons for the obesity paradox is that the lipid mediators/metabolites that are in reserve in circulatory blood bind to endotoxins/leukocyte receptors and inhibit their harmful effects. The other reason is that progressive HF is a catabolic state; thus, a greater metabolic reserve would be helpful in obese patients with HF (2, 9). AGE-RELATED CARDIAC HEALTH IN OBESITY AND DIABETIC MALE AND FEMALE SUBJECTS