Selected characteristics of the all person-visits with the potential to contribute to the primary analyses and all person-visits with complete data for the final models.

<p>Selected characteristics of the all person-visits with the potential to contribute to the primary analyses and all person-visits with complete data for the final models.</p

Proportion of potential participants who met inclusion and exclusion criteria, relative to the total number of people seen at each study visit.

<p>Proportion of potential participants who met inclusion and exclusion criteria, relative to the total number of people seen at each study visit.</p

Prevalence of proliferative diabetic retinopathy, gross proteinuria, and peripheral neuropathy by diabetes duration and visit.

<p>(a) Prevalence of proliferative diabetic retinopathy. (b) Prevalence of gross proteinuria. (c) Prevalence of peripheral neuropathy.</p

Comparison between base and final models of proliferative diabetic retinopathy, gross proteinuria and peripheral neuropathy.

<p>Comparison between base and final models of proliferative diabetic retinopathy, gross proteinuria and peripheral neuropathy.</p

Adjusted estimated prevalence of each complication at each study visit.

<p><b>(</b>a) Proliferative diabetic retinopathy–adjusted for duration of diabetes and visit. (b) Proliferative diabetic retinopathy–adjusted for duration of diabetes, visit, glycosylated hemoglobin, and systolic blood pressure. (c) Gross proteinuria—adjusted for duration of diabetes and visit. (d) Gross proteinuria—adjusted for duration of diabetes, visit, glycosylated hemoglobin, mean arterial blood pressure, and sex. (e) Peripheral neuropathy—adjusted for duration of diabetes and visit. (f) Peripheral neuropathy—adjusted for duration of diabetes, visit, glycosylated hemoglobin, sex, and smoking status. Log odds = log [p/(1-p)], i.e. log odds of -0.5 = prevalence of 38%, log odds of -1.0 = prevalence of 27%, log odds of -1.5 = prevalence of 18%, and log odds of -2.0 = prevalence of 12%.</p

Comparison between base and final models of proliferative diabetic retinopathy, gross proteinuria and peripheral neuropathy when participants on dialysis or with kidney, pancreas or islet cell transplants are included.

<p>Comparison between base and final models of proliferative diabetic retinopathy, gross proteinuria and peripheral neuropathy when participants on dialysis or with kidney, pancreas or islet cell transplants are included.</p

Number of person-visits contributing to each model in the primary analyses, based on availability of data on all of the variables included in each model.

<p>Number of person-visits contributing to each model in the primary analyses, based on availability of data on all of the variables included in each model.</p

Dates of the WESDR examinations and numbers of participants with type 1 diabetes.

<p>Dates of the WESDR examinations and numbers of participants with type 1 diabetes.</p

Association between Dietary Xanthophyll (Lutein and Zeaxanthin) Intake and Early Age-Related Macular Degeneration: The Atherosclerosis Risk in Communities Study

<p><i><b>Purpose</b></i>: To examine the association between xanthophyll intake and prevalent early age-related macular degeneration (AMD) using data from the Atherosclerosis Risk in Communities Study (<i>n</i> = 10,295). Potential effect modification by genetic polymorphisms and biomarkers of high-density lipoprotein (HDL) metabolism was explored.</p> <p><i><b>Methods</b></i>: 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 (<i>CFH</i>) rs1061170 and age-related maculopathy susceptibility 2 (<i>ARMS2</i>) rs10490924 genotypes, as well as by median cutpoints of HDL biomarkers.</p> <p><i><b>Results</b></i>: Xanthophyll intake was not associated with AMD in the overall sample, Caucasians (<i>n</i> = 8257), or African-Americans (<i>n</i> = 2038). Exploratory analyses observed that the association between xanthophyll intake and AMD varied statistically significantly by <i>CFH</i> rs1061170 genotype among Caucasians (<i>p</i> for interaction = 0.045) but not African Americans. No interactions were observed between xanthophyll intake and <i>ARMS2</i> 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 (<i>p</i> for interaction = 0.048).</p> <p><i><b>Conclusion</b></i>: Xanthophyll intake was not associated with early AMD. Further studies to investigate this association by genetic susceptibility or variations in HDL metabolism are needed.</p

Dietary Intake of Lutein and Diabetic Retinopathy in the Atherosclerosis Risk in Communities Study (ARIC)

<p><i><b>Purpose</b></i>: We tested the hypothesis that dietary intake of lutein is inversely associated with prevalence of diabetic retinopathy (DR) due to its antioxidant and anti-inflammatory properties and location within the retina.</p> <p><i><b>Methods</b></i>: We used logistic regression to examine the association between prevalent DR and energy-adjusted lutein intake by quartile (Q) using data collected from 1430 Atherosclerosis Risk in Communities Study (ARIC) participants with diabetes (<i>n</i> = 994 white, <i>n</i> = 508 black). DR was assessed from 45° non-mydriatic retinal photographs of one randomly chosen eye taken at visit 3 (1993–1995). Dietary lutein intake was estimated using a 66-item food frequency questionnaire at visit 1 (1987–1989).</p> <p><i><b>Results</b></i>: Median estimated daily lutein intake was 1370 µg/1000 kcals and prevalence of DR was ~21%. We found a crude association between lutein and DR (odds ratio, OR, 2.11, 95% confidence interval, CI, 1.45–3.09 for Q4, high intake, vs. Q1, low intake; <i>p</i> for trend <0.0001), which was attenuated after adjustment for ethnicity, duration of diabetes, glycosylated hemoglobin levels, field center and energy intake (OR 1.41, 95% CI 0.87–2.28; <i>p</i> for trend = 0.01). In analyses limited to persons with short diabetes duration (<6 years), the association no longer persisted (OR 0.94, 95% CI 0.31–2.16; <i>p</i> for trend =0.72) compared to the association in those with longer diabetes duration (≥6 years; OR 1.58, 95% CI 0.91–2.75; <i>p</i> for trend = 0.01).</p> <p><i><b>Conclusion</b></i>: Contrary to our hypothesis, we found that the odds of higher lutein intake were greater among those with DR than those without DR. However, after adjusting for confounders, intake of lutein was not associated with DR.</p