WEIGHT GAIN AND HIGHER BLOOD PRESSURE: IS IT JUST FAT?

We read the article by Cseh et al with interest.¹ The authors present intriguing findings from their pilot study of overfeeding on blood pressure changes among young normal body weight subjects that increased their mean Body Mass Index (BMI) from 23.1 kg/m² to 25.0 kg/m². We suggest consideration of two additional explanations that warrant exploration in a fully powered study: meal content and overfeeding itself. Aside from the excess 800–1,000 kcal/day intake, the paper does not allow an evaluation of the total calories consumed and complete meal composition per day of the intervention including sodium. Larger meals are associated with greater cardiac output.² High-fat meals result in post-prandial endothelial dysfunction.³ The effects of repeated larger and higher fat meals on cardiac output and blood pressure over time could plausibly have cumulative effects on endothelial function and potentially blood pressure in the presence of increased cardiac output. Notably, the process of over-feeding itself may be deleterious. Previous work suggests that gains in visceral fat while significantly associated with increases in blood pressure (R=0.45), explain less than 25% of the variance (0.45²) in a rise in blood pressure with overfeeding.⁴ Surgical removal of large fat volume has a modest (3.5 mm Hg) and temporary impact on blood pressure with a nadir 50 days post-surgery.⁵ In contrast, blood pressure reduction following bariatric surgery often occurs within 1–2 weeks.⁶ These findings suggest the possibility that overeating itself may increase sympathetic nervous system activity and blood pressure (in addition to increasing visceral fat).⁷ Quantifying the relative contributions of overeating, meal size, and fat gains to increases in cardiac output and blood pressure may benefit from repeated measures of changes in blood pressure using ambulatory blood pressure monitoring cardiac and assessments of visceral fat and statistical methods such as crossed-lagged panel models to assess the primary directionality of effects.