Obesity represents one of the greatest public health crises of the 21st century. Its rising prevalence is associated with a broad spectrum of cardiovascular comorbidities, including cardiac remodeling, diastolic dysfunction, and, in more advanced stages, heart failure. In this setting, the search for non-pharmacological weight-control strategies has driven increased consumption of dietary supplements, often without robust scientific support. Among these compounds, capsinoids (Cap) stand out as non-pungent capsaicin analogs extracted from sweet peppers of the genus Capsicum, proposed as potential thermogenic and anti-obesity agents.
The biological plausibility rests on activation of transient receptor potential vanilloid type 1 (TRPV1), a mechanism shared with capsaicin. Meta-analyses in humans have shown that capsaicin and Cap increase energy expenditure and lipid oxidation, particularly in overweight individuals, and may modestly reduce total cholesterol and triglycerides, although effects on LDL, HDL, and glycemic parameters remain inconsistent and supported by low-certainty evidence.– In the cardiovascular system, capsaicin has exerted favorable effects in models of hypertension, improving cardiac mechanical function via nitric oxide bioavailability. In this context, the study published in this issue of Arquivos Brasileiros de Cardiologia offers an original contribution. The authors evaluated the effects of chronic Cap administration (10 mg/kg/day for 8 weeks, by gavage) on metabolic parameters and the contractility of isolated cardiomyocytes in obese Wistar rats. The results challenge expectations: treatment did not reduce adiposity, did not improve glycemic, lipid, or hormonal profiles, and impaired cellular contractile function, with reduced fractional shortening and increased time to 50% peak shortening in the obese group treated with Cap compared with untreated obese animals.
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