Diana J. Bigelow and colleagues point out that active smoking doubles the risk of heart disease, while second-hand smoke exposure increases this risk by about one-third. They set out to gain more information on why the risks are especially high among people with obesity, using specially fed laboratory mice that are stand-ins for humans in such experiments.

The report describes how mainstream smoke and to a greater extent, sidestream smoke, inhibit the activity of genes that protect the heart and lungs, and activate genes associated with an increased risk of heart disease. Those changes were more profound in obese mice than normal-weight mice. "The present study is the first, to our knowledge, that addresses the in vivo transcriptional response of the heart to cigarette smoke exposure in the setting of high fat diet and obesity, and thus takes a first step toward identifying the molecular basis of adaptive responses that may lead to an increased risk of heart disease in obese smokers," the report states.

The authors acknowledge funding from the Exposure Biology Program in the National Institute of Environmental Health Sciences, part of the National Institutes of Health.