Risk Factor | Cutpoint |
---|---|
Abdominal obesity | |
Men | Waist circumference ≥ 40 inches |
Women | Waist circumference ≥ 35 inches |
Elevated triglycerides | ≥ 150 mg/dL |
Low HDL cholesterol: | |
Men | < 40 mg /dL |
Women | < 50 mg/dL |
Elevated blood pressure | ≥ 130 / ≥ 85 mm Hg |
Elevated fasting glucose | ≥ 110 mg/dL |
Table 1. ATP III Diagnostic Criteria for Metabolic Syndrome[37]
Risk Factor | Cutpoint |
---|---|
Abdominal obesity | |
Men | Waist circumference ≥ 40 inches |
Women | Waist circumference ≥ 35 inches |
Elevated triglycerides | ≥ 150 mg/dL |
Low HDL cholesterol: | |
Men | < 40 mg /dL |
Women | < 50 mg/dL |
Elevated blood pressure | ≥ 130 / ≥ 85 mm Hg |
Elevated fasting glucose | ≥ 110 mg/dL |
Table 1. ATP III Diagnostic Criteria for Metabolic Syndrome[37]
Risk Factor Component | Cutpoint for Abnormality |
---|---|
Overweight/obesity | BMI ≥ 25 kg/m2 |
Elevated triglycerides | ≥ 150 mg/dL |
Low HDL-C | |
Men | < 40 mg/dL |
Women | < 50 mg/dL |
Elevated blood pressure | ≥ 130/85 mm Hg |
2-hour postglucose challenge | |
Other risk factors | Family history of type 2 diabetes, hypertension, or cardiovascular disease |
Polycystic ovary syndrome | |
Sedentary lifestyle | |
Advancing age | |
Ethnic groups having high risk for type 2 diabetes or cardiovascular disease |
Table 2. AACE Diagnostic Criteria for the Insulin Resistance Syndrome*[37]
AACE = American Association of Clinical Endocrinologists; BMI = body mass index
*Diagnosis depends on clinical judgment, which is based on risk factors.
Parameter | Mean (SD) | |
---|---|---|
Metabolic Syndrome (n = 194) |
No Metabolic Syndrome (n = 382) |
|
LDL-C, mg/dL | ||
Baseline | 187 (20) | 186 (18) |
Week 12 | 99 (31) | 96 (25) |
% change | -47 (15) | -48 (12) |
HDL-C, mg/dL | ||
Baseline | 44 (9) | 54 (13) |
Week 12 | 49 (11) | 58 (14) |
% change | +10 (13) | +9 (12) |
Triglycerides (mg/dL) | ||
Baseline | 216 (60) | 155 (57) |
Week 12 | 167 (64) | 122 (50) |
% change | -23 (20) | -19 (24) |
Non-HDL-C (mg/dL) | ||
Baseline | 230 (23) | 217 (21) |
Week 12 | 132 (35) | 120 (27) |
% change | -43 (14) | -45 (12) |
Non-HDL-C/HDL-C ratio | ||
Baseline | 5.4 (1.2) | 4.2 (1.0) |
Week 12 | 2.8 (1.1) | 2.2 (0.8) |
Δ % | -47 (15) | -48 (13) |
ApoB (mg/dL) | ||
Baseline | 182 (22) | 173 (20) |
Week 12 | 115 (26) | 106 (21) |
% change | -37 (14) | -38 (12) |
ApoA-I (mg/dL) | ||
Baseline | 141 (23) | 155 (25) |
Week 12 | 150 (25) | 164 (27) |
% change | +7 (13) | +6 (12) |
ApoB/ApoA-1 ratio | ||
Baseline | 1.3 (0.3) | 1.1 (0.2) |
Week 12 | 0.8 (0.2) | 0.7 (0.2) |
% change | -40 (15) | -41 (13) |
Table 3. Baseline and Week 12 Lipid Levels and Percent Change From Baseline in Patients With Hypercholesterolemia Treated With Rosuvastatin 10 mg
Reproduced with permission from Ballantyne et al.[57] Copyright 2004. Elsevier Science.
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Metabolic syndrome affects approximately 24% of the US adult population; according to the Third National Health and Nutrition Examination Survey (NHANES III) criteria, about 47 million people have metabolic syndrome,[16] including 44% of those in the ≥ 50-year age group.[17] Metabolic syndrome is present in 10% of women and 15% of men with normal glucose tolerance; 42% and 64% of those with impaired fasting glucose; and 78% and 84% of those with type 2 diabetes.[18] Most patients (> 80%) with type 2 diabetes have metabolic syndrome, but the converse is not necessarily true.
Physician visits for obesity-related disorders rose nearly 90% from 1988 to 1994.[19] The high prevalence of metabolic syndrome in the United States is the story of a population "squeezed from both ends" of the age spectrum: on the one hand, through increasing obesity among young adults and on the other through reduced muscle mass and elevated fat mass (ie, sarcopenic obesity) in elderly persons (a growing population segment).
Given the widespread availability of fast foods in modern industrialized societies, environmental factors are often cited as causes of the American obesity epidemic: in short, "haste makes waist." On the other hand, environmental factors do not play equally causative roles in all racial and ethnic groups. Populations that are genetically or otherwise susceptible include South Asians (Indian subcontinent), Southeast Asians (eg, Polynesian, Japanese), African-Americans (particularly African-American women), Mexicans, and Native Americans (eg, Pima Indians).
Metabolic syndrome (without type 2 diabetes) significantly increases the risk of coronary heart disease (CHD). Recent subanalyses of the Scandinavian Simvastatin Survival Study (4S) and the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS) showed that placebo controls with metabolic syndrome (but not type 2 diabetes) were at ~1.5 times higher risk of coronary events than those without metabolic syndrome.[20] Risk increased strikingly when type 2 diabetes developed. Notably, the presence of metabolic syndrome increased the risk of major coronary events irrespective of 10-year absolute coronary risk above or below 20%, the ATP threshold for initiating treatment to reduce low-density lipoprotein cholesterol (LDL-C) to levels of 100 mg/dL or below.[20]
Among NHANES III participants aged 50 years or older,[17] the age-adjusted prevalence of CHD was highest in patients with both type 2 diabetes and metabolic syndrome (19.2%), followed by patients with metabolic syndrome but not type 2 diabetes (13.9%). Notably, the prevalence of CHD was no higher in patients with type 2 diabetes but without metabolic syndrome than in individuals who had neither type 2 diabetes nor metabolic syndrome (Figure 1).[17]
Increased risks of CHD and/or all-cause mortality have been demonstrated in other "prediabetic" populations, including American women in the Nurses' Health Study[21] and a Scandinavian adult population (Figure 2).[22]
With regard to the increase in cardiovascular risk associated with metabolic syndrome, the whole far exceeds the sum of its parts. For instance, the 4-year risk of incident myocardial infarction (MI) among men ages 40-65 in the Prospective Cardiovascular Münster (PROCAM) study was increased 2.5 times in the presence of either type 2 diabetes or hypertension; 8 times in the presence of both factors; and 19 times in the presence of both factors plus an abnormal lipid profile.[18,23]