A Single Factor Underlies the Metabolic Syndrome: A Confirmatory Factor Analysis

OBJECTIVE Confirmatory factor analysis (CFA) was used to test the hypothesis that the components of the metabolic syndrome are manifestations of a single common factor. RESEARCH DESIGN AND METHODS Three different datasets were used to test and validate the model. The Spanish and Mauritian studies included 207 men and 203 women and 1,411 men and 1,650 women, respectively. A third analytical dataset including 847 men was obtained from a previously published CFA of a U.S. population. The one-factor model included the metabolic syndrome core components (central obesity, insulin resistance, blood pressure, and lipid measurements). We also tested an expanded one-factor model that included uric acid and leptin levels. Finally, we used CFA to compare the goodness of fit of one-factor models with the fit of two previously published four-factor models. RESULTS The simplest one-factor model showed the best goodness-of-fit indexes (comparative fit index 1, root mean-square error of approximation 0.00). Comparisons of one-factor with four-factor models in the three datasets favored the one-factor model structure. The selection of variables to represent the different metabolic syndrome components and model specification explained why previous exploratory and confirmatory factor analysis, respectively, failed to identify a single factor for the metabolic syndrome. CONCLUSIONS These analyses support the current clinical definition of the metabolic syndrome, as well as the existence of a single factor that links all of the core components.

[1]  R. Niaura,et al.  A Single Factor Underlies the Metabolic Syndrome: A Confirmatory Factor Analysis , 2006, Diabetes Care.

[2]  D. Lawlor,et al.  (Mis)use of factor analysis in the study of insulin resistance syndrome. , 2005, American journal of epidemiology.

[3]  R. Kahn,et al.  The metabolic syndrome: time for a critical appraisal , 2005, Diabetologia.

[4]  Laura M. Stapleton,et al.  Re: "(Mis)use of factor analysis in the study of insulin resistance syndrome". , 2005, American journal of epidemiology.

[5]  Peter Arner,et al.  Use of waist circumference to predict insulin resistance: retrospective study , 2005, BMJ : British Medical Journal.

[6]  S. Shoelson,et al.  Local and systemic insulin resistance resulting from hepatic activation of IKK-β and NF-κB , 2005, Nature Medicine.

[7]  Esko Vanninen,et al.  Multiple Abnormalities in Glucose and Energy Metabolism and Coordinated Changes in Levels of Adiponectin, Cytokines, and Adhesion Molecules in Subjects With Metabolic Syndrome , 2004, Circulation.

[8]  A. Aljada,et al.  Circulating Mononuclear Cells in the Obese Are in a Proinflammatory State , 2004, Circulation.

[9]  J. Friedman Modern science versus the stigma of obesity , 2004, Nature Medicine.

[10]  Sonia S Anand,et al.  Vascular viewpoint , 2004 .

[11]  Latha Palaniappan,et al.  Predictors of the incident metabolic syndrome in adults: the Insulin Resistance Atherosclerosis Study. , 2004, Diabetes care.

[12]  K. Petersen,et al.  Impaired mitochondrial activity in the insulin-resistant offspring of patients with type 2 diabetes. , 2004, The New England journal of medicine.

[13]  Jing Chen,et al.  The Metabolic Syndrome and Chronic Kidney Disease in U.S. Adults , 2004, Annals of Internal Medicine.

[14]  L. Chambless,et al.  Risk factors for progression to incident hyperinsulinemia: the Atherosclerosis Risk in Communities Study, 1987-1998. , 2003, American journal of epidemiology.

[15]  Tracey McLaughlin,et al.  Use of Metabolic Markers To Identify Overweight Individuals Who Are Insulin Resistant , 2003, Annals of Internal Medicine.

[16]  K. Lawson,et al.  A confirmatory factor analysis evaluation of the coronary heart disease risk factors of metabolic syndrome with emphasis on the insulin resistance factor , 2003, Diabetes, obesity & metabolism.

[17]  J. Pankow,et al.  Linkage analysis of a composite factor for the multiple metabolic syndrome: the National Heart, Lung, and Blood Institute Family Heart Study. , 2003, Diabetes.

[18]  T. Ogihara,et al.  Serum Uric Acid and Plasma Norepinephrine Concentrations Predict Subsequent Weight Gain and Blood Pressure Elevation , 2003, Hypertension.

[19]  M. Reilly,et al.  The Metabolic Syndrome: More Than the Sum of Its Parts? , 2003, Circulation.

[20]  S. Haffner,et al.  The association between leptin and left ventricular hypertrophy: a population-based cross-sectional study , 2003, Journal of hypertension.

[21]  M. Walters,et al.  Serum Urate as an Independent Predictor of Poor Outcome and Future Vascular Events After Acute Stroke , 2003, Stroke.

[22]  S. Haffner,et al.  The association between leptin and left ventricular hypertrophy: a population-based cross-sectional study. , 2003 .

[23]  P. Vollenweider,et al.  Clustering of cardiovascular risk factors mimicking the human metabolic syndrome X in eNOS null mice. , 2003, Swiss medical weekly.

[24]  Avron Spiro,et al.  Are metabolic risk factors one unified syndrome? Modeling the structure of the metabolic syndrome X. , 2003, American journal of epidemiology.

[25]  Alessandro Pontillo,et al.  Effect of weight loss and lifestyle changes on vascular inflammatory markers in obese women: a randomized trial. , 2003, JAMA.

[26]  L. Niskanen,et al.  Metabolic syndrome and development of diabetes mellitus: application and validation of recently suggested definitions of the metabolic syndrome in a prospective cohort study. , 2002, American journal of epidemiology.

[27]  P. Nilsson,et al.  Frequency of the WHO metabolic syndrome in European cohorts, and an alternative definition of an insulin resistance syndrome. , 2002, Diabetes & metabolism.

[28]  Robert L Hanson,et al.  Components of the "metabolic syndrome" and incidence of type 2 diabetes. , 2002, Diabetes.

[29]  W. Dietz,et al.  Prevalence of the metabolic syndrome among US adults: findings from the third National Health and Nutrition Examination Survey. , 2002, JAMA.

[30]  N. Sattar,et al.  Plasma Leptin and the Risk of Cardiovascular Disease in the West of Scotland Coronary Prevention Study (WOSCOPS) , 2001, Circulation.

[31]  P. Kovacs,et al.  Sex-specific and sex-independent quantitative trait loci for facets of the metabolic syndrome in WOKW rats. , 2001, Biochemical and biophysical research communications.

[32]  P. Poulsen,et al.  Genetic versus environmental aetiology of the metabolic syndrome among male and female twins , 2001, Diabetologia.

[33]  J. Weber,et al.  Quantitative trait loci on chromosomes 3 and 17 influence phenotypes of the metabolic syndrome. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[34]  J. Meigs,et al.  Invited commentary: insulin resistance syndrome? Syndrome X? Multiple metabolic syndrome? A syndrome at all? Factor analysis reveals patterns in the fabric of correlated metabolic risk factors. , 2000, American journal of epidemiology.

[35]  L. Weinehall,et al.  Leptin is a risk marker for first-ever hemorrhagic stroke in a population-based cohort. , 1999, Stroke.

[36]  Rex B. Kline,et al.  Principles and Practice of Structural Equation Modeling , 1998 .

[37]  E. Rimm,et al.  Dietary Fiber, Glycemic Load, and Risk of NIDDM in Men , 1997, Diabetes Care.

[38]  G A Colditz,et al.  Reproducibility and validity of an expanded self-administered semiquantitative food frequency questionnaire among male health professionals. , 1992, American journal of epidemiology.

[39]  R. Turner,et al.  Homeostasis model assessment: insulin resistance and β-cell function from fasting plasma glucose and insulin concentrations in man , 1985, Diabetologia.

[40]  A. Hevener,et al.  IKK-beta links inflammation to obesity-induced insulin resistance. , 2005, Nature medicine.

[41]  H. Minuk,et al.  Metabolic syndrome. , 2005, Journal of insurance medicine.

[42]  S. Shoelson,et al.  Local and systemic insulin resistance resulting from hepatic activation of IKK-beta and NF-kappaB. , 2005, Nature medicine.

[43]  A. Siani,et al.  Plasma leptin and blood pressure in men: graded association independent of body mass and fat pattern. , 2003, Obesity research.

[44]  R. Marfella,et al.  Effect of Weight Loss and Lifestyle Changes on Vascular Inflammatory Markers in Obese Women , 2003 .

[45]  A. von Eckardstein,et al.  The CAG repeat polymorphism in the androgen receptor gene modulates body fat mass and serum concentrations of leptin and insulin in men , 2002, Diabetologia.

[46]  J. Tuomilehto,et al.  Leptin and other components of the Metabolic Syndrome in Mauritius—a factor analysis , 2001, International Journal of Obesity.

[47]  S. Haffner,et al.  Development of the multiple metabolic syndrome: an epidemiologic perspective. , 1998, Epidemiologic reviews.

[48]  I. Godsland,et al.  Hyperleptinemia as a component of a metabolic syndrome of cardiovascular risk. , 1998, Arteriosclerosis, thrombosis, and vascular biology.