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Papers In Press, published online ahead of print September 1, 2009
J. Lipid Res., doi:10.1194/jlr.P900039-JLR200

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Journal of Lipid Research, Vol. 50, 1927-1935, September 2009
Copyright © 2009 by American Society for Biochemistry and Molecular Biology

Patient-Oriented and Epidemiological Research

Alterations in cholesterol absorption/synthesis markers characterize Framingham Offspring Study participants with CHD^[S]

Nirupa R. Matthan^1,*, Michael Pencina^**, Jane M. LaRocque^*, Paul F. Jacques, Ralph B. D'Agostino^**, Ernst J. Schaefer and Alice H. Lichtenstein^*

^* Cardiovascular Nutrition, Jean Mayer USDA Human Nutrition Research Center on Aging, Tufts University, Boston MA
Nutritional Epidemiology, Jean Mayer USDA Human Nutrition Research Center on Aging, Tufts University, Boston MA
Lipid Metabolism Laboratories, Jean Mayer USDA Human Nutrition Research Center on Aging, Tufts University, Boston MA
^** Statistics and Consulting Unit, Boston University, Boston MA

¹ To whom correspondence should be addressed. e-mail: nirupa.matthan{at}tufts.edu

Data is limited on measures influencing cholesterol homeostasis in subjects at high risk of developing cardiovascular disease (CVD) relative to established risk factors. To address this, we quantified circulating indicators of cholesterol homeostasis (plasma phytosterols and cholesterol precursor concentrations as surrogate measures of cholesterol absorption and synthesis, respectively) in Framingham Offspring Study Cycle-6 participants diagnosed with established CVD and/or 50% carotid stenosis not taking lipid lowering medication (cases, N = 155) and matched controls (N = 414). Cases and controls had similar plasma LDL-cholesterol; HDL-cholesterol was significantly lower in males, while triglyceride concentrations were significantly higher in female cases relative to their respective controls. Cholesterol absorption markers were significantly higher (229 ± 7 vs. 196 ± 4, 169 ± 6 vs. 149 ± 3 and 144 ± 5 vs. 135 ± 3 for campesterol, sitosterol, and cholestanol, respectively), whereas cholesterol synthesis markers were significantly lower (116 ± 4 vs. 138 ± 3, 73 ± 3 vs. 75 ± 2 for lathosterol and desmosterol, respectively) in cases compared with controls, irrespective of sex. After controlling for standard risk factors, campesterol (2.47 [1.71-3.56]; P < 0.0001), sitosterol (1.86 [1.38-2.50]; P < 0.0001), cholestanol (1.57 [1.09-2.27]; P = 0.02), desmosterol (0.59 [0.42-0.84]; P = 0.003), and lathosterol (0.58 [0.43-0.77]; P = 0.0002) were significantly associated with CVD (odds ratio [95% confidence interval]). These data suggest that impaired cholesterol homeostasis, reflected by lower synthesis and higher absorption marker concentrations, are highly significant independent predictors of prevalent CVD in this study population.

Supplementary key words lipids • lipoproteins • lathosterol • desmosterol • phytosterols • campesterol • sitosterol • coronary heart disease

Abbreviations: ABC, ATP-binding cassette; CAD, coronary artery disease; CI, confidence interval; CVD, cardiovascular disease; E, energy; FFQ, food frequency questionnaire; FOS, Framingham Offspring Study; OR, odds ratio; MI, myocardial infarction

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