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Increasing BMI raises risks for type 2 diabetes, CAD
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Among adults with obesity, each 1-standard deviation increase in BMI increases the odds for type 2 diabetes by 67% and for coronary artery disease by 20%, according to a meta-analysis of Mendelian randomization studies published in JAMA Network Open.
“For a long time, it was debatable whether obesity causes CAD or not,” Haitham Ahmed, MD, MPH, FACC, a preventive cardiologist with Cleveland Clinic, told Endocrine Today. “Many researchers felt there was an ‘obesity paradox’ in clinical studies and wondered whether it was confounders (such as hyperlipidemia or hypertension) that were causing the CAD rather than the obesity itself. We could not do randomized controlled trials to answer the question because it is unethical and unfeasible to randomize one group to become obese and another to stay lean. The next best thing is to do Mendelian randomization, which is nature’s randomized trial.”
Ahmed and colleagues analyzed data from five studies conducted through January 2018 with 881,692 participants that used Mendelian randomization methods to examine the association between measures of obesity (BMI and waist-to-hip ratio adjusted for BMI) and incidence of type 2 diabetes, CAD or stroke.
All included studies used BMI as a measure of obesity and mean age of participants in the pooled sample was 60 years. The included studies adjusted for a mean of 47 single nucleotide polymorphisms (range, 9-97).
In four studies reporting on type 2 diabetes (n = 461,871), researchers observed an association between it and obesity (OR = 1.67; 95% CI, 1.3-2.14). Obesity was also associated with CAD (OR = 1.2; 95% CI, 1.02-1.41).
In three studies assessing all-cause stroke, researchers found no association between stroke and obesity. An analysis restricted to 180,795 patients with ischemic stroke did not change the findings, according to researchers.
“This is the largest meta-analysis of Mendelian randomization to date and was able to answer the question as definitively as we’ve ever been able to before — that obesity is likely to be causal of coronary artery disease,” Ahmed said. “Obesity is not benign. When patients say they are ‘fat but fit,’ that is no longer an acceptable excuse to ignore weight gain. Health care practitioners, and especially cardiologists, should continue to emphasize weight reduction in order to prevent coronary events because doing so may be just as important as controlling the LDL cholesterol and systolic blood pressure.”
He said the discovery of single nucleotide polymorphisms associated with obesity was a first step in showing that much of obesity development can be genetic.
“However, we don’t know how that impacts treatment,” Ahmed said. “Do some patients respond to some therapies or strategies better than others based on their genes? We need additional studies that can aid in identifying therapeutic insights based on genetic data in the field of obesity research.”
In commentary accompanying the study, Kaitlin H. Wade, BSc, and George Davey Smith, MD, DSc, FFPH, both of the Integrative Epidemiology Unit at the University of Bristol, United Kingdom, wrote that future considerations of studies using Mendelian randomization methodology should include low- to middle-income countries, testing linearity of associations and identifying risk factors for disease progression other than solely disease onset.
“These results support a global effort to lower the increasing population trends for excess weight and suggest that, in most cases, any reduction in BMI is likely beneficial,” Wade and Smith wrote. – by Regina Schaffer
For more information:
Haitham Ahmed, MD, MPH, FACC, can be reached at Cleveland Clinic, Department of Cardiovascular Medicine, 1955 E. 85th St., Cleveland, OH 44106; email: riazh@ccf.org.
Disclosure: Ahmed reports he has received grants from Akcea Therapeutics.
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