Results of Expert Meetings: Obesity and Cardiovascular DiseaseObesity, the metabolic syndrome, and cardiovascular disease☆,☆☆
Section snippets
Metabolic syndrome
A desirable content of body fat for men ranges from 12% to 20% of total body weight. For women it ranges from 20% to 30%. Accordingly, obesity is defined as a body fat content >25% or >33% of total body weight in men and women, respectively.4 This means that obesity is characterized by excess fat weight; body mass index (BMI) is used as an alternative measure of body fat. BMI (calculated as weight in kilograms/height in meters squared) has been used extensively in epidemiologic studies to
Prevalence of risk factors for CHD in overweight and obese subjects
The National Heart, Lung, and Blood Institute and the World Health Organization have introduced a weight classification for BMI. According to their classification, a normal weight range is a BMI of 18.5 to 24.9 kg/m2, overweight ranges from 25.0 to 29.9, and obesity is a BMI ≥30 kg/m2. There are 3 classes of obesity—class 1: 30.0 to 34.9, class 2: 35.0 to 39.9, and class 3 > 40 kg/m2. Recently, Must et al18 used data from the third National Health and Nutrition Examination Survey (NHANES III)
CHD risk imparted by the metabolic syndrome
Algorithms for estimation of CHD risk have been developed from longitudinal trials such as the Framingham Heart Study19 and the PROCAM study.20 The Framingham risk factor assessment includes age, total or LDL cholesterol, HDL cholesterol, BP, and the presence or absence of type 2 diabetes mellitus or smoking. CHD risk estimation is sex specific.19 The PROCAM algorithm includes age, LDL cholesterol, HDL cholesterol, triglycerides, smoking, type 2 diabetes mellitus, and family history of CHD.20
Putative role of nonesterified fatty acids in the metabolic syndrome
An excess fat weight is associated with increased release of nonesterified fatty acids (NEFAs) from the adipose tissue.4 Increased serum levels of NEFAs are likely an integral component of the metabolic syndrome. Still, the association of NEFAs with risk for CHD is not well documented. In recent years more attention has been given to the role of NEFAs in the etiology of type 2 diabetes mellitus. A view has emerged that dysregulation of NEFA release by the adipose tissue, particularly abdominal
Summary of ATP III guidelines for the treatment of the metabolic syndrome
ATP III3 included the metabolic syndrome as a secondary target of risk reduction therapy along with treatment of LDL cholesterol. The goal of treatment for LDL cholesterol varies according to the severity of risk factors for CHD. Table IV summarizes the ATP III recommendations on treatment for the metabolic syndrome. Persons with the metabolic syndrome are considered candidates for intensified therapeutic lifestyle changes. The centerpiece of treatment is LDL cholesterol. The goals of LDL
Prioritizing risk factor management during treatment of the metabolic syndrome
Because persons with the metabolic syndrome have a cluster of risk factors, it is interesting to speculate about how the treatment of these risk factors should be prioritized. For example, for individuals with a 10-year risk of >20%, instituting therapeutic lifestyle modification and pharmacotherapy for dyslipidemia may be the first priority. The target of treatment for dyslipidemia may be non–HDL cholesterol because most persons with the metabolic syndrome have serum triglycerides between 200
Conclusion
This review has summarized typical features of the metabolic syndrome and presented estimates regarding the relative risk for CHD in persons with this syndrome. It is important to note that systematic work is still required to develop algorithms specific for risk assessment with respect to the metabolic syndrome. Wilson et al22 have made a step in this direction by developing an algorithm that includes traditional risk factors and BMI, insulin, and glucose levels, but algorithms specific to the
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Reprint requests: Gloria Lena Vega, PhD, Center for Human Nutrition, UT Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390-9052. E-mail: [email protected]
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Am Heart J 2001;142:1108-16.