BackgroundVitamin D status has been hypothesized to protect against development of diabetic retinopathy via its anti-inflammatory and anti-angiogenic properties. Additionally, in vitro and in vivo studies suggest vitamin D favorably influences blood pressure and blood glucose control, strong risk factors for diabetic retinopathy. We examined the association between vitamin D status and prevalent diabetic retinopathy in participants with diabetes from a population-based cohort.MethodsAmong participants in the Atherosclerosis Risk in Communities (ARIC) study with diabetes at visit 3 (1993–1995), 1339 (906 Caucasians, 433 African Americans) had serum 25-hydroxyvitamin (25[OH]D) concentrations assessed at visit 2 (1989–1992) and nonmydriatic retinal photographs taken at visit 3. Dietary intake of vitamin D was assessed at visit 1 (1987–1989). Logistic regression was used to estimate odds ratios (ORs) and 95 % confidence intervals (CIs) for diabetic retinopathy by categories of season-adjusted 25(OH)D (<30 [referent], 30–<50, 50–<75 and ≥75 nmol/L), by quartile of vitamin D intake (IU/day), and use of vitamin D or fish oil supplements (yes/no). P for trend was estimated using continuous 25(OH)D or vitamin D intake. ORs were adjusted for race, and duration of diabetes. We further adjusted for HBA1c and hypertension to examine if 25(OH)D influenced diabetic retinopathy via its effects on either glycemic control or blood pressure.ResultsORs (95 % CIs) for retinopathy, adjusted for race and duration, were 0.77 (0.45–1.32), 0.64 (0.37–1.10), and 0.39 (0.20–0.75), p for trend = 0.001, for participants with 25(OH)D of 30–<50, 50–<75, and ≥75 nmol/L, respectively. Further adjustment for hypertension minimally influenced results (data not show), but adjustment for HBA1c attenuated the OR among those with 25(OH)D ≥75 (0.47 [0.23–0.96], p for trend = 0.030). No statistically significant association was observed between vitamin D intake from foods or supplements and retinopathy.Conclusions25(OH)D concentrations ≥75 nmol/L were associated with lower odds of any retinopathy assessed 3 years later. We speculate this may be due in part to vitamin D’s influence on blood glucose control.Electronic supplementary materialThe online version of this article (doi:10.1186/s12933-016-0434-1) contains supplementary material, which is available to authorized users.

Purpose We tested the hypothesis that dietary intake of lutein is inversely associated with prevalence of diabetic retinopathy due to its antioxidant and anti-inflammatory properties and its location within the retina. Methods We used logistic regression to examine the association between prevalent DR and energy-adjusted lutein intake [by quartile (Q)] using data collected from 1,430 ARIC study participants with diabetes (n=994 White and n=508 Black). DR was assessed using a 45-degree nonmydriatic retinal photograph from one randomly chosen eye taken at visit 3 (1993–95). Dietary lutein intake was estimated using a 66-item food frequency questionnaire at visit 1(1987–89). Results The median estimated daily lutein intake was 1,370 μg/1000 kcals and the prevalence of DR was ~21%. We found a crude association between lutein and DR [OR (95% CI) for Q4 (high intake) vs. Q1 (low intake) =2.11 (1.45–3.09); p for trend<0.0001] which was attenuated after adjustment for race, duration of diabetes, glycosylated hemoglobin levels, field center and energy intake [1.41 (0.87–2.28); p for trend=0.01]. In analyses limited to persons with a short duration of diabetes (<6 years), the association no longer persisted [0.94 (0.31–2.16); p for trend=0.72] as compared to the association in those with a longer duration of diabetes (≥6 year) [1.58 (0.91–2.75); p for trend=0.01]. Conclusion 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.

Objective Vitamin D status has been hypothesized to protect against development of early age-related macular degeneration (AMD) via its anti-inflammatory properties and its possible beneficial influence on blood pressure control. We investigated the association between vitamin D status and prevalent early AMD in a community-based cohort. Design This was a cross-sectional study. Setting This was a secondary data analysis of already existing data from the Atherosclerosis Risk in Communities Study (ARIC) cohort study collected from 1990 to 1995. Participants There were 9,734 (7,779 Caucasians, 1,955 African American) ARIC participants (aged 46 to 70 at visit 2 [1990-1992]) with 25(OH)D data available at visit 2, AMD assessment at visit 3 (1993-1995), and complete covariate data. Measurements Vitamin D status was assessed with serum 25-hydroxyvitamin D (25(OH)D) concentrations from bloods drawn at visit 2. Prevalent, early AMD (n=511) was assessed at visit 3 (1993-95) with nonmydriatic retinal photographs of one randomly chosen eye. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for early AMD by categories of 25(OH)D in nmol/L (deficient <30, inadequate 30-<50, and two categories of adequate status: 50-<75 and ≥75). Linear trend was estimated using continuous 25(OH)D concentrations. ORs were adjusted for age, race, and smoking status. We further adjusted for hypertension status to examine if vitamin D status influenced early AMD via its effects on blood pressure. Exploratory analyses of effect modification by age, gender, race and high risk genotypes [Y402H complement factor H (CFH) rs1061170 and the A69S age-related maculopathy susceptibility 2 (ARMS2) rs10490924 polymorphisms] were conducted. Results The prevalence of early AMD was 5%, and 5% of participants were vitamin D deficient. The adjusted OR (95% CIs) for early AMD among those with adequate (≥75 nmol/L) compared to deficient (<30 nmol/L) vitamin D status was 0.94 (0.59-1.50), p-trend=0.86. Further adjustment for hypertension status did not influence results (OR [95% CI]=0.95 [0.59-1.52], p-trend=0.84). Results did not vary significantly by age, race, gender, early AMD subtype (soft drusen or retinal pigment epithelium depigmentation), ARMS2 genotype, or CFH genotype in African Americans. Although the p for multiplicative interaction between 25(OH)D and CFH genotype was 0.06 in Caucasians, OR [95% CIs] for AMD in participants with 25(OH)D ≥50 compared to <50 nmol/L were similar in each CFH genotype and not statistically significant. Conclusions Vitamin D status was not associated with early AMD in this cohort sample.

SIGNIFICANCE Lifestyle influences eye health and other chronic diseases. All health care providers, not just primary care physicians, should have the necessary information and training to advise and refer patients on lifestyle to take advantage of opportunities to provide such advice. PURPOSE The extent to which optometrists offer lifestyle advice to their patients is largely unknown. The Optometrists' Practices in Advising about Lifestyle (OPAL) study aimed to examine lifestyle advice that optometrists offer, to whom such advice is offered, and reasons for not offering this advice. METHODS We developed and administered a mail-in survey to 140 optometrists in Western New York. RESULTS Five surveys were returned because of death, retirement, and relocation. Of the 135 remaining eligible participants, 46 of the optometrists contacted responded to our survey; however, only 42 (31%) provided signed consent forms. Of these, more than 93% report offering advice on smoking, dietary supplements, and diet, and >59% reported offering on physical activity and alcohol use. Eighty-three percent offer advice to only those with unhealthy behaviors or certain conditions. Most advice consisted of mentioning the lifestyle factor's influence on eye or overall health. Reasons for not offering advice included lack of knowledge or training or the belief that advice would not change behaviors. CONCLUSIONS Optometrists reported offering advice primarily to those with unhealthy lifestyle behaviors or pre-existing health conditions. Future studies should address low response rates, include nonphysician health care providers in addition to optometrists, and also examine patients' perceptions and understanding of the advice offered to better understand whether this advice is received as the provider envisioned.

PurposeTo investigate the association between serum 25-hydroxyvitamin D (25[OH]D) concentrations at visit 2 (1990–1992) and the 18-year incidence of age-related macular degeneration (AMD) between visit 3 (1993–1995) and visit 5 (2011–2013).MethodsThis prospective analysis was conducted in a subset of participants (n = 1225) from the Atherosclerosis Risk in Communities Study. We evaluated the incidence of any, early, and late AMD from visit 3 to 5. The 25(OH)D concentrations were assessed in 2012–2013 by using stored serum from visit 2. Retinal fundus photographs taken at both visits were graded side by side to determine the incidence of AMD. Logistic regression was used to estimate the odds ratios (ORs) and 95% confidence intervals (CIs) for incident AMD outcomes during 18 years of follow-up (1993–1995 to 2011–2013) by tertile of 25(OH)D adjusted for age, race, and smoking status. P for linear trend was estimated by using continuous 25(OH)D concentrations. Sensitivity analyses applied inverse probability weights to account for selection to have eye photographs, death, and loss to follow-up.ResultsThere was a decreased odds of any incident AMD (n = 139) and large, soft drusen (n = 80) in 25(OH)D tertile 3 versus 1, with OR (95% CI) = 0.57 (0.36–0.90), P trend = 0.11 and with 0.52 (0.28–0.93), P trend = 0.18, respectively. Applying sampling weights attenuated these results to 0.66 (0.38–1.16), P trend = 0.32 (any incident AMD) and 0.54 (0.27–1.09), P trend = 0.36 (large, soft drusen), respectively, suggesting these associations may be biased by loss to follow-up and sampling for retinal photographs at visit 5. No statistically significant results were observed with pigmentary abnormalities (n = 46) or incident late AMD (n = 26).ConclusionsHigh 25(OH)D concentrations, approximately >70 nM, may be associated with decreased odds of incident early AMD.