麻豆传媒

The Obesity Medicine Association and the National Lipid Association have issued a comprehensive review of the pathological effects of obesity on blood lipids and the resulting elevation in risk of cardiovascular disease (CVD).

Writing in , Harold E. Bays, MD, medical director of the Louisville Metabolic and Atherosclerosis Research Center in Kentucky, and colleagues explained that adipose tissue may store more than 50% of the total free cholesterol in the body and that associated atherogenic triglycerides may account for as much as 99% of the lipid species in adipose tissue. Furthermore, the potential for adipose tissue expansion is responsible for the greatest weight variance among most individuals, with percent body fat ranging from less than 5% to more than 60%.

While population studies suggest a modest increase in blood low-density lipoprotein cholesterol (LDL-C) levels with excess adiposity, the adiposopathic dyslipidemia pattern most often described includes elevated triglycerides, reduced high-density lipoprotein cholesterol (HDL-C), increased non-HDL-C, elevated apolipoprotein B (ApoB), increased LDL particle concentration, and increased small, dense LDL particles.

Bays, who is also editor-in-chief of Obesity Pillars, elaborates on the review in the following interview.

What was the impetus for the review?

Bays: This joint expert review intended to better inform clinicians about the intersection of obesity and dyslipidemia in CVD prevention. Especially among patients with obesity at high CVD risk, a reduction in body fat and improvement in lipid levels may reduce the risk of future CVD events.

How does adipose tissue function differently from other tissues and how is it metabolically harmful?

Bays: Just as with other body tissues, enlargement of fat cells, or adipocytes, and enlargement of the fat organ -- i.e., the body's adipose tissue -- can cause fat tissue to become "sick" and result in pathogenic immune and endocrine responses that are harmful to patients.

Does adiposity impact blood pressure apart from increasing weight and perhaps reducing physical activity?

Bays: Yes. An increase in body fat can result in "sick fat disease" such as high blood pressure, high blood sugar, and fatty liver. It also increases the risk for "fat mass diseases" such as sleep apnea and osteoarthritis. The review focused on the worsening of blood lipids that also occurs among patients with obesity.

Obesity has the potential to increase triglyceride blood levels as well as increase the concentration of atherogenic small low-density lipoprotein particles.

Do medical school curricula sufficiently emphasize the diverse physiological effects of adiposity?

Bays: Medical school curricula often do not include a thorough examination of the pathogenic potential of increased adipose tissue or the wide degree of current treatments, including nutritional and physical activity intervention. Nor do they teach trainees critical skills needed to foster patient behavior modification and provide psychological support in the context of obesity as a disease.

Did any of the findings surprise you?

Bays: Many of the authors of this joint expert review were surprised at how challenging it was to find citations necessary to support some of the most fundamental science applicable to obesity and dyslipidemia. Much of the most basic science was published 50 or more years ago and has since rarely been revisited.

What is essential for treating physicians to understand?

Bays: Obesity increases CVD risk, at least partially by promotion of an adiposopathic, atherogenic lipid profile. Obesity also worsens other cardiometabolic risk factors such as type 2 diabetes mellitus.

Among patients with obesity, interventions that reduce body weight and improve CVD outcomes are generally associated with improved lipid levels. Given the modest improvement in blood LDL-C with weight reduction in patients with overweight or obesity, early interventions to treat both excess adiposity and elevated atherogenic LDL-C and/or levels of other non-HDL-C, such as very LDL-C and intermediate LDL-C, represent priorities for reducing the risk of CVD.

What is your bottom line message for clinicians?

Bays: In addressing management of patients with obesity and dyslipidemia, the optimal approach to reduce CVD risk includes therapies targeted at treating the obesity as well as concomitant treatments targeted at reducing levels of atherogenic lipids such as LDL-C, other non-HDL-C, and ApoB.

Read the review here and expert commentary about it here.