Impact of Obesity on Cardiovascular Disease

Abstract

Obesity is associated with increased risk of cardiovascular disease (CVD), heart failure, diabetes, cancer, and ultimately all-cause mortality. Obesity is causally related to dyslipidemia, hypertension, and diabetes, all strong CVD risk factors, and so causally related to CVD risk. In fact, a substantial part of the risk imparted by obesity on CVD outcomes operates via traditional risk factors. Obese men are almost twice as likely and women almost two and half times as likely to develop hypertension. Obese individuals are around 50% more likely to have a stroke and have around 6–12 times higher risks of developing type 2 diabetes compared to those with a normal BMI.

Obesity is also linked to greater risk for development of heart failure. Yet, there appears to be an obesity paradox in established heart failure such that the risk of death is lower in overweight and mildly obese individuals than in those with normal weight. Such observations are likely partially driven by reverse causality whereby disease-specific issues drive weight loss rather than higher weight per se being protective.

While obesity is most commonly defined by BMI, the importance of body fat distribution and markers such as waist circumference, waist: hip ratio, visceral and ectopic fat volumes are becoming better appreciated. The concept of harmful fat distribution is therefore topical and recent evidence suggest those who can store more fat subcutaneously (and so delay their ectopic depot expansions until much heavier) have lesser diabetes and cardiovascular risks. This paradigm may also largely explain men’s greater risks for both chronic conditions at similar BMI’s to women.

Trials of weight loss add strong support for causal links between adiposity and CVD; for example, the best evidence suggests that losing around 1 kg reduces SBP by around 1 mmHg. Weight loss also improves lipid profiles with reduced total cholesterol, LDL-cholesterol, and in particular triglyceride levels. Weight loss of around 5 kg reduces the risk of obese individuals progressing to impaired glucose tolerance and type 2 diabetes. In those with type 2 diabetes, 5 to <10% intentional weight loss is associated with 3.5 times increased odds of obtaining a 0.5% reduction in HbA1c. Not surprisingly, substantial weight loss has been associated with significantly lower mortality from several causes.

This chapter will show how the best epidemiological evidence, using methods to lessen the impact of reverse causality, supports strong graded links between adiposity and CVD. It will also examine and explain the apparent obesity paradox of heart failure. The chapter will then describe the effect on CVD outcomes of robust lifestyle and surgical intervention studies and trials. Finally, we will also explain how genetics data have helped support causal associations between increasing BMI and CVD, including understanding better the causal links between regional adiposity and CVD.

In conclusion, several lines of evidence, including observational, trial, and genetic, collectively support causal links between obesity, cardiovascular morbidity and mortality, and all-cause mortality.