Obesity Paradox and Stroke

Abstract

See related articles, pages 3397 and 3646. Obesity has a well-known association with initial incidence of cardiovascular disease, stroke, cancer, and early death. However, a growing number of studies have found that overweight and frankly obese patients who survive the first event tend to have improved subsequent cardiovascular (CVD)1,2 and cerebrovascular disease burden,3,4 morbidity, and mortality. The idea that a known risk factor somehow transforms into a “protective” agent after an occurrence of a vascular clinical event—the obesity paradox—is both surreal and troubling. Should we conclude that our advice of weight loss as the yellow brick road of secondary stroke prevention (for those with above-normal body mass index [BMI]) causes actual harm? First, the definition and measurement of obesity, techniques of statistical analysis, and the various effects of the initial cerebrovascular event on the patients' weight all deserve a closer look. The article by Ovibagele et al5 is the latest study in assessing the link between obesity and recurrent vascular events in stroke survivors. The data from the PRoFESS (Prevention Regimen for Effectively Avoiding Second Strokes Trial) was reviewed with 20 246 subjects being stratified by their BMI measurements and waist circumference. The groups had some important differences: the obese subjects were younger and had a higher proportion of women but a smaller percentage of smokers. They were also more likely to have a lacunar stroke and a greater likelihood of carrying a diagnosis of diabetes, hyperlipidemia, or hypertension, and of taking antihypertensive drugs. Despite differences in the diagnosis of hypertension, the baseline median blood pressure levels were comparable between obese and nonobese subjects. After adjusting for common confounders, the authors found no statistically significant difference in the recurrence of stroke for lean (9.06%), overweight (8.82%), and obese (8.89%) groups over 2.5-year …