ANN ARBOR, MI — Obesity did not appear to be associated with better survival in people with incident cardiovascular disease, arguing against the existence of an “obesity paradox” for CVD in such cases, in a large US longitudinal cohort study starting in 1992[1].
On the other hand, there was a “strong and significant” protective effect of obesity in people with established CVD—that is heart failure, ischemic heart disease, or stroke—when they entered the study. That may suggest the appearance of an obesity paradox is limited to prevalent disease, researchers say.
Together the findings suggest that claims of a CVD obesity paradox may largely be the result of statistical bias, according to their report published November 29, 2017 in PLOS One.
“The loss of an obesity paradox when switching from prevalent to incident cases and prediagnosis weight in the same data set suggest that prevalent models are likely biased by factors such as disease-related weight loss and selective survival,” lead author Dr Virginia W Chang (NYU College of Global Public Health, New York, NY) told theheart.org | Medscape Cardiology.
“There is provocative and interesting literature suggesting that obesity might be protective or lower the risk of death compared with being normal weight in people who have cardiovascular disease,” Chang explained, “even though obesity is an important risk factor for getting CVD in the first place.”
The topic is difficult to study “because once you have cardiovascular disease, the people who are sicker tend to lose weight, which can artificially make obesity look protective. The relationship becomes confounded in this scenario,” Chang said.
“You can also have the situation where obese persons with more severe disease die sooner, and you are left with a more select obese population that is healthier. This means that you can observe a survival benefit of being obese, but none of it points to obesity causally offering any sort of protection,” she said.
“Given that many diseases result in wasting at the end of life, the notion that extra catabolic reserve can prolong survival makes intuitive sense. There are also explanations relating to various inflammatory and neurohormonal processes,” she pointed out.
“However, despite the plausibility of these hypotheses, we did not find evidence of an obesity paradox when using methods that are less prone to bias.”
The study looked at the association between obesity and mortality among people with CVD, comparing incident and prevalent disease cases in the same data set.
They used data from the Health and Retirement Study, an ongoing, nationally representative longitudinal survey of adults in the US age 50 years and older. Begun in 1992, the Health and Retirement Study links surveys of more than 30,000 individuals to Medicare claims.
When looking at prevalent CVD, Chang and her team used patients’ current weights; when studying incident disease, they used patients prediagnosis weights.
A strong and significant obesity paradox was observed in patients with existing cardiovascular disease. The risk of death was 18% to 36% lower for people with a body-mass index (BMI) 30 to 34.9 compared with those of normal weight.
However, in incident disease models of the same conditions within the same data set, there was no such indication of a survival benefit for obesity.
“If obesity is protective, and yet we tell patients to lose weight, we might be having an unintended negative effect. But we don’t find evidence to support that,” she said. “Our findings do not support reevaluating guidelines in pursuit of a potential obesity paradox.”
The study was supported by a Clinical Translational Research Award from the American Diabetes Association and the National Institute on Aging. The authors report they have no relevant financial relationships.
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