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J.M. Seddon, G. Gensler, M.L. Klein, N. Rifai; Association Between C–Reactive Protein and Lutein/Zeaxanthin, Fish Intake, Body Mass Index and Other Age–Related Macular Degeneration Risk Factors . Invest. Ophthalmol. Vis. Sci. 2005;46(13):2380.
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Purpose: We previously reported the association between C–reactive protein (CRP), a systemic inflammatory marker, and age–related macular degeneration (AMD).1 To further explore potential AMD mechanisms, we evaluated the relationship between CRP and nutritional as well as other risk or protective factors associated with AMD. Methods: Subjects included 930 participants at two Age Related Eye Disease Study sites. Fasting blood specimens were analyzed for high sensitivity CRP, and for one site ( N=465), additional serum specimens were also analyzed for antioxidant vitamins, minerals, and cholesterol levels. All subjects had an ocular examination and fundus photography, height, weight and blood pressure measurements, and also completed a standardized risk factor questionnaire and a food frequency questionnaire. Regression analyses were performed to evaluate the association between CRP and other covariates, with adjustment for age, sex and study treatment. Results: Among those with additional serum specimens, increased serum lutein/zeaxanthin ( p=.02), increased serum beta–carotene (p=.004), and increased serum vitamin C (p= .0005) were associated with lower CRP values, while increased serum vitamin E (adjusted for cholesterol) was associated with higher CRP values (p=.0002). Among all subjects, more frequent fish intake was associated with lower CRP values (p=.04), while higher body mass index (BMI) was associated with higher levels of CRP (p=.0001). Conclusions: Serum lutein/zeaxanthin, serum vitamin C, serum beta–carotene, and dietary fish intake were associated with lower levels of the inflammatory marker, CRP, whereas elevated vitamin E and BMI were associated with increased CRP. Results suggest a connection between nutritional and lifestyle factors associated with AMD and inflammatory pathways. 1. JAMA 2004;291:704–710.
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