Evaluating CMR

Is the whole greater than the sum of its parts?

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Several prospective studies have shown that all metabolic syndrome criteria enhance CVD and type 2 diabetes risk (7, 11, 12). However, given the fact that each individual component of the metabolic syndrome increases risk, these observations are not very surprising. When the individual components are combined, the risk is likely greater. This raises the question whether the metabolic syndrome as a whole is more closely linked to CVD and type 2 diabetes risk than its individual components. Many specialists hold opposing views on the issue, which is being debated in the literature. In the Hoorn Study, investigators described a linear relationship between metabolic syndrome components and CVD risk and stated that the number of components provided more information in assessing CVD risk than diagnosis of the metabolic syndrome itself (7). With the findings of the Framingham Offspring Study, Wilson et al. (9) stated that diagnosing the metabolic syndrome is clinically relevant, especially for patients with modestly elevated risk factors who are not necessarily insulin resistant. In the Strong Heart Study, de Simone et al. (13) concluded that both NCEP-ATP III and WHO screening tools predicted CVD independent of their individual components, while this was not the case for IDF criteria. These authors therefore suggested that diagnosis of the metabolic syndrome is clinically relevant, especially for non-diabetic individuals at increased CVD risk.

Another important question is whether diagnosis of the metabolic syndrome influences treatment: is treating the metabolic syndrome really different than treating each underlying abnormality? There seems to be a consensus surrounding both the treatment of the metabolic syndrome and the treatment of its components. Lifestyle interventions aimed at increasing physical activity/exercise and improving nutritional habits have been shown to reduce waist girth and underlying metabolic markers of dyslipidemia, namely insulin resistance and blood pressure (14, 15). However, lifestyle modification as a treatment of obesity has been shown to be unsuccessful and disappointing in clinical practice (16). In light of this, the pharmaceutical industry is now keenly interested in pharmacotherapies targeting abdominal obesity as the underlying cause of the metabolic syndrome.

Reference

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7. Dekker JM, Girman C, Rhodes T, et al. Metabolic syndrome and 10-year cardiovascular disease risk in the Hoorn Study. Circulation 2005; 112: 666-73.

9. Wilson PW, D'Agostino RB, Parise H, et al. Metabolic syndrome as a precursor of cardiovascular disease and type 2 diabetes mellitus. Circulation 2005; 112: 3066-72.

11. Wang JJ, Qiao Q, Miettinen ME, et al. The metabolic syndrome defined by factor analysis and incident type 2 diabetes in a chinese population with high postprandial glucose. Diabetes Care 2004; 27: 2429-37.

12. Lorenzo C, Okoloise M, Williams K, et al. The metabolic syndrome as predictor of type 2 diabetes: the San Antonio heart study. Diabetes Care 2003; 26: 3153-9.

13. de Simone G, Devereux RB, Chinali M, et al. Prognostic impact of metabolic syndrome by different definitions in a population with high prevalence of obesity and diabetes: the Strong Heart Study. Diabetes Care 2007; 30: 1851-6.

14. Orchard TJ, Temprosa M, Goldberg R, et al. The effect of metformin and intensive lifestyle intervention on the metabolic syndrome: the Diabetes Prevention Program randomized trial. Ann Intern Med 2005; 142: 611-9.

15. Knowler WC, Barrett-Connor E, Fowler SE, et al. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med 2002; 346: 393-403.

16. Wooley SC and Garner DM. Obesity treatment: the high cost of false hope. J Am Diet Assoc 1991; 91: 1248-51.

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