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ABSTRACT
Purpose: To examine the association between xanthophyll intake and prevalent early age-related macular degeneration (AMD) using data from the Atherosclerosis Risk in Communities Study (n = 10,295). Potential effect modification by genetic polymorphisms and biomarkers of high-density lipoprotein (HDL) metabolism was explored.
Methods: Xanthophyll intake was assessed at visit 1 (1987–1989) using food frequency questionnaires. Prevalent early AMD was assessed at visit 3 (1993–1995) via retinal photographs. Logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI) for AMD by quintiles of xanthophyll intake, adjusted for age, sex, race, field center, and pack-years of smoking. To evaluate effect modification, the association between tertiles (T) of xanthophyll intake and AMD was stratified by complement factor H (CFH) rs1061170 and age-related maculopathy susceptibility 2 (ARMS2) rs10490924 genotypes, as well as by median cutpoints of HDL biomarkers.
Results: Xanthophyll intake was not associated with AMD in the overall sample, Caucasians (n = 8257), or African-Americans (n = 2038). Exploratory analyses observed that the association between xanthophyll intake and AMD varied statistically significantly by CFH rs1061170 genotype among Caucasians (p for interaction = 0.045) but not African Americans. No interactions were observed between xanthophyll intake and ARMS2 rs10490924. Moreover, higher xanthophyll intake was associated with decreased odds of AMD among participants with lower HDL (OR = 0.79, 95% CI 0.57–1.09) but not higher HDL (p for interaction = 0.048).
Conclusion: Xanthophyll intake was not associated with early AMD. Further studies to investigate this association by genetic susceptibility or variations in HDL metabolism are needed.
Supplemental data
Supplemental data for this article can be accessed on the publisher’s website.
Declaration of interest
Kristin Meyers’ affiliation was with the University of Wisconsin during her efforts on this manuscript. As of February 2015, she has been an employee of Eli Lilly and Company and her efforts on this manuscript have been limited to critical review. Other co-authors had no conflicts of interest to disclose.
Funding
This research is supported by the NIH National Institute on Aging grant number R01 AG041776, NIH National Heart, Lung, and Blood Institute grant number R01 HL103706, and the NIH Office of Dietary Supplements grant number R01 HL103706-S1 and an unrestricted grant from Research to Prevent Blindness.
The Atherosclerosis Risk in Communities Study is carried out as a collaborative study supported by National Heart, Lung, and Blood Institute contracts (HHSN268201100005C, HHSN268201 100006C, HHSN268201100007C, HHSN268201100008C, HHSN 268201100009C, HHSN268201100010C, HHSN268201100011C, and HHSN268201100012C), R01HL087641, R01HL59367 and R01HL086694; National Human Genome Research Institute contract U01HG004402; and National Institutes of Health contract HHSN268200625226C. Infrastructure was partly supported by Grant Number UL1RR025005, a component of the National Institutes of Health and NIH Roadmap for Medical Research.