Obesity and Cardiovascular Disease: A Bad Relationship that Needs to Change

Obesity is strongly associated with an increased risk of cardiovascular disease, and conventional wisdom reasons that reducing weight would favorably reduce that risk.1 An abundance of evidence associates excess adipose tissue, particularly in the visceral compartment, with insulin resistance, a risk for developing diabetes, increased blood pressure and lipoprotein disorders (low high-density lipoprotein, cholesterol and high triglycerides). There also is evidence that short-term weight loss can improve insulin sensitivity, reduce blood pressure and improve lipoprotein levels.² Unfortunately, there are no long-term randomized clinical trials that demonstrate a reduction in cardiovascular endpoints with sustained weight loss. An obvious explanation is the lack of effective methods to induce and sustain weight loss over many years in most people.

The complex biologic and genetic relationship of hunger and energy balance is finally receiving much-needed scientific attention, and new research is focusing on lifestyle habits, such as the composition of food intake and exercise, and drugs that modulate hunger/satiety and energy expenditure. Even so, the dramatic global rise in obesity threatens the progress thus far in reducing cardiovascular disease (CVD) risk factors. This article examines the epidemic of obesity, its effect on traditional CVD risk factors and the effect of weight loss on controlling CVD risk.