Abstract Title:

Antioxidant intake from diet and supplements and elevated serum C-reactive protein and plasma homocysteine concentrations in US adults: a cross-sectional study.

Abstract Source:

Public Health Nutr. 2011 Mar 18:1-10. Epub 2011 Mar 18. PMID: 21414247

Abstract Author(s):

Anna Floegel, Sang-Jin Chung, Anne von Ruesten, Meng Yang, Chin E Chung, Won O Song, Sung I Koo, Tobias Pischon, Ock K Chun

Article Affiliation:

1Department of Nutritional Sciences, University of Connecticut, 3624 Horsebarn Road Extension Unit 4017, Storrs, CT 06269-4017, USA.


OBJECTIVE: To investigate the association of antioxidant intakes from diet and supplements with elevated blood C-reactive protein (CRP) and homocysteine (Hcy) concentrations. DESIGN: A cross-sectional study. The main exposures were vitamins C and E, carotene, flavonoid and Se intakes from diet and supplements. Elevated blood CRP and Hcy concentrations were the outcome measures. SETTING: The US population and its subgroups. SUBJECTS: We included 8335 US adults aged≥19 years from the National Health and Nutrition Examination Survey 1999-2002. RESULTS: In this US population, the mean serum CRP concentration was 4·14 (95 % CI 3·91, 4·37) mg/l. Intakes of vitamins C and E and carotene were inversely associated with the probability of having serum CRP concentrations>3 mg/l in multivariate logistic regression models. Flavonoid and Se intakes were not associated with the odds of elevated serum CRP concentrations. The mean plasma Hcy concentration was 8·61 (95 % CI 8·48, 8·74) μmol/l. Intakes of vitamins C, E, carotenes and Se were inversely associated with the odds of plasma Hcy concentrations>13μmol/l after adjusting for covariates. Flavonoid intake was not associated with the chance of elevated plasma Hcy concentrations. CONCLUSIONS: These results suggest that high antioxidant intake is associated with lower blood concentrations of CRP and Hcy. These inverse associations may be among thepotential mechanisms for the beneficial effect of antioxidant intake on CVD risk mediators in observational studies.

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