Niyati Parekh
Professor of Public Health Nutrition
Associate Vice Provost for Faculty Initiatives and Global Engagement, Office of the Provost
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Professional overview
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Dr. Niyati Parekh’s research and teaching are motivated by a deep commitment to reduce nutrition-related disease outcomes in at-risk groups. In pursuit of this goal, as a nutritional epidemiologist, she has developed a robust research portfolio that examines the intersection of biological and behavioral factors of non-communicable diseases in US populations. The overarching theme of her research program is to examine the role of nutrition and diet-related factors in the etiology of non-communicable diseases, with a particular focus on obesity, metabolic dysregulation and cancer. Her multidisciplinary research integrates the intricacies from four distinct areas of expertise: disease biology, nutritional biochemistry, epidemiology and biostatistics. She has developed a research program with three interconnected areas that are unified under the theme of investigating diet and non-communicable diseases in populations, using epidemiologic methods. The first arm consists of leveraging existing data to identify dietary patterns, dietary quality and food consumption patterns in populations of interest. The second is to identify dietary determinants and biomarkers that predict disease outcomes including obesity, diabetes, cardiovascular disease and cancer. The third arm is to measure diets using novel dietary assessment methods that will contribute to more accurate and multi-dimensional measurement of diet. The three areas of her work complement each other and reveal preventive measures for populations, inform health policy and guide clinical practice. She has 75 peer-reviewed publications and her work has been supported by awards from the American Cancer Society and NIH.
Dr. Parekh holds an MS in Clinical Nutrition from Mumbai University and a PhD in Nutritional Sciences with a minor in Population Health Sciences from the University of Wisconsin-Madison (2005). After completing a 2-year postdoctoral fellowship in Cancer Epidemiology at the Cancer Institute of New Jersey-Rutgers, she joined New York University Steinhardt’s Department of Nutrition, Food Studies and Public Health in January 2008. With doctoral and postdoctoral training in epidemiological methods, she cross-pollinated the fields of nutrition and public health. In 2015, as Associate Professor of Public Health Nutrition, she transitioned to NYU’s newly launched School of Global Public Health (GPH), as Director of the Public Health Nutrition program (until 2019). She also has an affiliated appointment at the Department of Population Health-Grossman School of Medicine.
Her recent honors include being inducted as a New York Academy of Medicine Fellow, and her appointment as Independent Consultant at UNICEF. She has served the American Society for Nutrition as Chair of the Nutritional Epidemiology Research Group. She teaches graduate courses in the New York Campus and at study abroad sites (Mexico, Abu Dhabi and Florence). Graduate courses taught include Global Nutrition, Nutritional Epidemiology, Perspectives in Public Health and Global Cancer Epidemiology for which she has received awards. Dr. Parekh has served as the Executive Director of Doctoral Programs at GPH since 2017. In this role, she supports about 30 PhD students, and promotes all aspects of their rigorous research and professional development towards impactful careers.
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Education
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BS, Life Sciences and Biotechnology, Mumbai University, IndiaMS, Foods, Nutrition, and Clinical Dietetics, Mumbai University, IndiaPhD, Nutritional Sciences (minor Population Health Sciences), University of Wisconsin-Madison, Madison, WI
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Areas of research and study
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CancerChronic DiseasesEpidemiologyNutritionObesityPopulation HealthPublic Health Nutrition
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Publications
Publications
Obesity, metabolic syndrome and esophageal adenocarcinoma: Epidemiology, etiology and new targets
Ryan, A. M., Duong, M., Healy, L., Ryan, S. A., Parekh, N., Reynolds, J. V., & Power, D. G. (n.d.).Publication year
2011Journal title
Cancer EpidemiologyVolume
35Issue
4Page(s)
309-319AbstractBackground: Rates of distal and junctional adenocarcinomas are increasing in Western countries. Methods: Systematic review of epidemiological evidence linking obesity to esophageal adenocarcinoma (EA) was performed for studies published from 2005 to 2010. The current understanding of obesity's role in the etiology and potential dysplastic progression of Barrett's esophagus (BE) to EA is reviewed. Results: Accumulating epidemiological studies provide evidence of obesity's role as a driving force behind the increasing rates of EA. The simplest construct is that obesity promotes reflux, causing chronic inflammation and BE, predisposing to adenocarcinoma. However, as obesity is positively associated with the prevalence of many cancers, other mechanisms are important. A link may exist between fat distribution patterns and the risk of BE and EA. Altered metabolic profiles in the metabolic syndrome (MetS) may be a key factor in cell cycle/genetic abnormalities that mark the progression of BE towards cancer. Research highlighting a unique role of MetS in the length of BE, and its association with systemic inflammation and insulin resistance is discussed, as well as adipokine receptor expression in both BE and esophageal epithelium, and how MetS and the systemic response impacts on key regulators of inflammation and tumorigenesis. Conclusions/impact: Obesity is positively associated with EA. The systemic inflammatory state consequent on the altered metabolism of obese patients, and the associated impact of adipocytokines and pro-coagulant factors released by adipocytes in central fat, may underlie obesity's relationship to this cancer. Novel therapeutic agents that may antagonize adipo-cytokines and potentially offer a promising role in cancer therapy are discussed.Vitamin D status and early age-related macular degeneration in postmenopausal women
Millen, A. E., Voland, R., Sondel, S. A., Parekh, N., Horst, R. L., Wallace, R. B., Hageman, G. S., Chappell, R., Blodi, B. A., Klein, M. L., Gehrs, K. M., Sarto, G. E., & Mares, J. A. (n.d.).Publication year
2011Journal title
Archives of OphthalmologyVolume
129Issue
4Page(s)
481-489AbstractObjective: The relationship between serum 25-hydroxyvitamin D (25[OH]D) concentrations (nmol/L) and the prevalence of early age-related macular degeneration (AMD) was investigated in participants of the Carotenoids in Age-Related Eye Disease Study. Methods: Stereoscopic fundus photographs, taken from 2001 to 2004, assessed AMD status. Baseline (1994-1998) serum samples were available for 25(OH)D assays in 1313 women with complete ocular and risk factor data. Odds ratios (ORs) and 95% confidence intervals (CIs) for early AMD (n=241) of 1287 without advanced disease were estimated with logistic regression and adjusted for age, smoking, iris pigmentation, family history of AMD, cardiovascular disease, diabetes, and hormone therapy use. Results: In multivariate models, no significant relationship was observed between earlyAMDand 25(OH)D (OR for quintile 5 vs 1, 0.79; 95% CI, 0.50-1.24; P for trend=.47). A significant age interaction (P=.002) suggested selective mortality bias in women aged 75 years and older: serum 25(OH)D was associated with decreased odds of early AMD in women younger than 75 years (n=968) and increased odds in women aged 75 years or older (n=319) (OR for quintile 5 vs 1, 0.52; 95% CI, 0.29-0.91; P for trend=.02 and OR, 1.76; 95% CI, 0.77-4.13; P for trend=.05, respectively). Further adjustment for body mass index and recreational physical activity, predictors of 25(OH)D, attenuated the observed association in women younger than 75 years. Additionally, among women younger than 75 years, intake of vitamin D from foods and supplements was related to decreased odds of early AMD in multivariate models; no relationship was observed with self-reported time spent in direct sunlight. Conclusions: High serum 25(OH)D concentrations may protect against early AMD in women younger than 75 years.Healthy diets and the subsequent prevalence of nuclear cataract in women.
Mares, J., Voland, R., Adler, R., Tinker, L., Millen, A., Moeller, S., Blodi, B., Gehrs, K. M., Wallace, R., Parekh, N., Chappell, R., Neuhouser, M., & Sarto, G. E. (n.d.).Publication year
2010Journal title
JAMA OpthalmologyVolume
128Issue
6Page(s)
738-749Lifestyle, Anthropometric, and Obesity-Related Physiologic Determinants of Insulin-like Growth Factor-1 in the Third National Health and Nutrition Examination Survey (1988-1994)
Parekh, N., Roberts, C. B., Vadiveloo, M., Puvananayagam, T., Albu, J. B., & Lu-Yao, G. L. (n.d.).Publication year
2010Journal title
Annals of EpidemiologyVolume
20Issue
3Page(s)
182-193AbstractPurpose: Epidemiologic studies suggest that insulin-like growth factor-1 (IGF-1) is associated with obesity and, more recently, cancer. This study investigates multiple lifestyle, physiologic, and anthropometric determinants of circulating IGF-1 concentrations. Methods: Nationally representative data were used from the cross-sectional Third National Health and Nutrition Examination (NHANES III, 1988-1994) survey, which measured IGF-1 concentrations in blood, from a subsample of participants who were examined in the morning. After exclusion of persons with missing data, 6,058 men and women 20 years of age or older were included in the study. Results: The mean IGF-1 concentrations were 260 ng/mL in the entire population and were higher among men as compared with women (278.8 vs. 241.3 ng/mL; p < 0.0001). IGF-1 decreased with increasing age (p < 0.0001), body mass index (p < 0.0001), and waist circumference (p < 0.0001). Individuals with metabolic syndrome had lower IGF-1 concentrations after adjustment for covariates (p = 0.0008). IGF-1 was inversely associated with increasing number of metabolic syndrome abnormalities (p = 0.0008). All associations were stronger among women compared with men except across concentrations of glucose. IGF-1 concentrations did not vary by any other lifestyle or physiologic factors. Conclusions: Age, adiposity, hyperglycemia, and metabolic syndrome influenced circulating IGF-1 concentrations. Diet and physical activity had no impact on IGF-1 in this nationally representative population.Longitudinal associations of blood markers of insulin and glucose metabolism and cancer mortality in the third National Health and Nutrition Examination Survey
Parekh, N., Lin, Y., Hayes, R. B., Albu, J. B., & Lu-Yao, G. L. (n.d.).Publication year
2010Journal title
Cancer Causes and ControlVolume
21Issue
4Page(s)
631-642AbstractInsulin and glucose may influence cancer mortality via their proliferative and anti-apoptotic properties. Using longitudinal data from the nationally representative Third National Health and Nutrition Examination Survey (NHANES III; 1988-1994), with an average follow-up of 8.5 years to death, we evaluated markers of glucose and insulin metabolism, with cancer mortality, ascertained using death certificates or the National Death Index. Plasma glucose, insulin, C-peptide, and lipid concentrations were measured. Anthropometrics, lifestyle, medical, and demographic information was obtained during in-person interviews. After adjusting for age, race, sex, smoking status, physical activity, and body mass index, for every 50 mg/dl increase in plasma glucose, there was a 22% increased risk of overall cancer mortality. Insulin resistance was associated with a 41% (95% confidence interval (CI) (1.07-1.87; p = 0.01) increased risk of overall cancer mortality. These associations were stronger after excluding lung cancer deaths for insulin-resistant individuals (HR: 1.67; 95% CI: 1.15-2.42; p = 0.01), specifically among those with lower levels of physical activity (HR: 2.06; 95% CI: 1.4-3.0; p = 0.0001). Similar associations were observed for other blood markers of glucose and insulin, albeit not statistically significant. In conclusion, hyperglycemia and insulin resistance may be 'high-risk' conditions for cancer mortality. Managing these conditions may be effective cancer control tools.Obesity and prostate cancer detection: Insights from three national surveys
Parekh, N., Lin, Y., Dipaola, R. S., Marcella, S., & Lu-Yao, G. (n.d.).Publication year
2010Journal title
American Journal of MedicineVolume
123Issue
9Page(s)
829-835AbstractBackground: Previous studies suggest that obesity is associated with higher prostate cancer progression and mortality despite an association with lower prostate cancer incidence. This study aims to better understand these apparently inconsistent relationships among obese men by combining evidence from 3 nationally representative cross-sectional surveys. Methods: We evaluated relationships between obesity and 1) testosterone concentrations in the Third National Health and Nutrition Examination Survey (NHANES III; n = 845); 2) prostate-specific antigen (PSA) in NHANES 2001-2004 (n = 2458); and 3) prostate biopsy rates in the National Health Interview Survey (NHIS 2000; n = 4789) population. Mean testosterone, PSA concentrations, and biopsy rates were computed for Body Mass Index (BMI) categories. Results: Testosterone concentrations were inversely associated with obesity (P-trend <.0001) in NHANES III. In NHANES 2001-2004, obese (BMI >35) versus lean (BMI <25) men were less likely to have PSA concentrations that reached the biopsy threshold of >4 ng/mL (3% vs 8%; P <.0001). Among NHIS participants, all BMI groups had similar rates of PSA testing (P = .24). However, among men who had PSA tests, 11% of men with BMI >30 versus 16% with BMI <25, achieved a PSA threshold of 4 ng/mL; P = .01. Furthermore, biopsy rates were lower among men with BMI >30 versus BMI <25 in NHIS participants (4.6% vs 5.8%; P = .05). Conclusions: Obesity was associated with lower PSA-driven biopsy rates. These data support further studies to test the hypothesis that obesity affects prostate cancer detection independent of prostate cancer risk by decreasing the PSA-driven biopsy rates.Protective role of vitamin D against age-related macular degeneration: A hypothesis
Parekh, N. (n.d.).Publication year
2010Journal title
Topics in Clinical NutritionVolume
25Issue
4Page(s)
290-301AbstractAge-related macular degeneration (AMD) is the leading cause of blindness among Americans. Local inflammation is implied in the pathophysiology of AMD that may cause photoreceptor destruction and blindness. Vitamin D may prevent AMD progression via its anti-inflammatory and antiangiogenic properties. Scientific evidence is discussed for the associations of vitamin D (serum, diet, and sunlight) and AMD. Evidence suggests inverse associations between serum vitamin D and its sources (specifically fish), and AMD. Associations with sunlight, hypothesized to increase risk for AMD, have been inconsistent possibly due to protection from vitamin D. Vitamin D may be a new protective factor against AMD.Suspected nonalcoholic fatty liver disease is not associated with vitamin D status in adolescents after adjustment for obesity
Katz, K., Brar, P. C., Parekh, N., Liu, Y. H., & Weitzman, M. (n.d.).Publication year
2010Journal title
Journal of ObesityVolume
2010AbstractThis study investigated a potential independent association between hypovitaminosis D and suspected nonalcoholic fatty liver disease (NAFLD) in a nationally representative sample of the US adolescents. Data from 1630 subjects 12-19 years of age were examined using the National Health and Nutrition Examination Survey, 2001-2004. The vitamin D status of subjects was categorized into quartiles of serum 25-hydroxyvitamin D. Subjects with serum ALT>30 U/L were classified as having suspected NAFLD. Data regarding age, sex, race, BMI, and poverty level were also analyzed in bivariate and multivariate analyses using SAS and SUDAAN software. Suspected NAFLD was identified in 12.1% of adolescents in the lowest quartile compared to 6.9% of adolescents in the second quartile, 8.0% in the third quartile, and 13.17% in the highest quartile of serum 25(OH)D concentrations (P=.05). In analyses utilizing vitamin D as a continuous variable, no independent association was found between Vitamin D levels and rates of elevated ALT levels. In multivariate analyses, higher risks for suspected NAFLD were observed in males and overweight adolescents; however, vitamin D status was not found to be independently associated with suspected NAFLD after adjusting for obesity.Association between dietary fat intake and age-related macular degeneration in the Carotenoids in Age-Related Eye Disease Study (CAREDS): An ancillary study of the women's health initiative
Parekh, N., Voland, R. P., Moeller, S. M., Blodi, B. A., Ritenbaugh, C., Chappell, R. J., Wallace, R. B., & Mares, J. A. (n.d.).Publication year
2009Journal title
Archives of OphthalmologyVolume
127Issue
11Page(s)
1483-1493AbstractObjective: To evaluate the relationships between the amount and type of dietary fat and intermediate age-related macular degeneration (AMD). Design: Women aged 50 to 79 years with high and low lutein intake from 3 sites of the Women's Health Initiative Observational Study were recruited into the Carotenoids in Age-Related Eye Disease Study. Fat intake from 1994 through 1998 was estimated using food frequency questionnaires, and AMD was assessed photographically from 2001 through 2004. Results: Intakes of ω-6 and ω-3 polyunsaturated fatty acids, which were highly correlated (r=0.8), were associated with approximately 2-fold higher prevalence of intermediate AMD in high vs low quintiles. However, monounsaturated fatty acid intake was associated with lower prevalence. Age interactions were often observed. In women younger than 75 years (n=1325), total fat and saturated fatty acid intakes were associated with increased prevalence of AMD (multivariate adjusted odds ratios [95% confidence interval] for intermediate AMD, 1.7 [1.0-2.7] for quintile 5 vs quintile 1 for total fat [P=.10 for trend] and 1.6 [0.7-3.6] for saturated fatty acids [P=.23 for trend]). The associations were reversed in older women. Conclusions: These results support a growing body of evidence suggesting that diets high in several types of fat may contribute to the risk of intermediate AMD and that diets high in monounsaturated fatty acids may be protective.Obesity, Insulin Resistance, and Cancer Prognosis: Implications for Practice for Providing Care among Cancer Survivors
Parekh, N., Okada, T., & Lu-Yao, G. L. (n.d.).Publication year
2009Journal title
Journal of the American Dietetic AssociationVolume
109Issue
8Page(s)
1346-1353Vegetables intake as a preventative measure against type-2 diabetes and cancer
Parekh, N., & Fitzgerald, N. (n.d.). In Fruit and vegetable consumption and health (1–).Publication year
2009Page(s)
81-99Zinc and cognitive development in children: Perspectives from international studies
Black, J. L., Piñero, D. J., & Parekh, N. (n.d.).Publication year
2009Journal title
Topics in Clinical NutritionVolume
24Issue
2Page(s)
130-138AbstractSince 1980, at least 9 studies have assessed the potential associations between zinc supplementation and cognitive development in human infants and children. This article provides a brief review of the literature on the roles of zinc and its proposed associations with cognition. At present, the body of evidence is insufficient to warrant recommending routine zinc supplementation to enhance cognitive performance among children. In the United States and internationally, there are few available data on zinc status or deficiency rates in children and further study is necessary to assess the efficacy of zinc supplementation, alone or in combination with other nutrients, for improving cognitive outcomes.Associations between age-related nuclear cataract and lutein and zeaxanthin in the diet and serum in the carotenoids in the age-related eye disease study (CAREDS), an ancillary study of the Women's Health Initiative
Moeller, S. M., Voland, R., Tinker, L., Blodi, B. A., Klein, M. L., Gehrs, K. M., Johnson, E. J., Snodderly, D. M., Wallace, R. B., Chappell, R. J., Parekh, N., Ritenbaugh, C., & Mares, J. A. (n.d.).Publication year
2008Journal title
Archives of OphthalmologyVolume
126Issue
3Page(s)
354-364AbstractObjective: To evaluate associations between nuclear cataract (determined from slitlamp photographs between May 2001 and January 2004) and lutein and zeaxanthin in the diet and serum in patients between 1994 and 1998 and macula between 2001 and 2004. Design: A total of 1802 women aged 50 to 79 years in Iowa, Wisconsin, and Oregon with intakes of lutein and zeaxanthin above the 78th (high) and below the 28th (low) percentiles in the Women's Health Initiative Observational Study (1994-1998) were recruited 4 to 7 years later (2001-2004) into the Carotenoids in Age-Related Eye Disease Study. Results: Women in the group with high dietary levels of lutein and zeaxanthin had a 23% lower prevalence of nuclear cataract (age-adjusted odds ratio, 0.77; 95% confidence interval, 0.62-0.96) compared with those with low levels. Multivariable adjustment slightly attenuated the association (odds ratio, 0.81; 95% confidence interval, 0.65-1.01). Women in the highest quintile category of diet or serum levels of lutein and zeaxanthin as compared with those in the lowest quintile category were 32% less likely to have nuclear cataract (multivariable-adjusted odds ratio, 0.68; 95% confidence interval, 0.48-0.97; P for trend=.04; and multivariable-adjusted odds ratio, 0.68; 95% confidence interval, 0.47-0.98; P for trend=.01, respectively). Cross-sectional associations with macular pigment density were inverse but not statistically significant. Conclusions: Diets rich in lutein and zeaxanthin are moderately associated with decreased prevalence of nuclear cataract in older women. However, other protective aspects of such diets may in part explain these relationships.Associations of lifestyle and physiologic factors with prostate-specific antigen concentrations: Evidence from the National Health and Nutrition Examination Survey (2001-2004)
Parekh, N., Lin, Y., Marcella, S., Kant, A. K., & Lu-Yao, G. (n.d.).Publication year
2008Journal title
Cancer Epidemiology Biomarkers and PreventionVolume
17Issue
9Page(s)
2467-2472AbstractStudies suggest inverse associations between obesity and prostate-specific antigen (PSA). However, there is little evidence whether factors related to obesity, including lifestyle (diet and physical activity) and physiologic factors (insulin resistance and metabolic syndrome), influence PSA. We used dietary, physical activity, and serum PSA, insulin, glucose, and lipid data for men >40 years from the National Health and Nutrition Examination Survey (2001-2004; N = 2,548). Energy, fat, and carbohydrate intakes were estimated from a 24-hour dietary recall. Men were considered as having metabolic syndrome based on the Adult Treatment Panel III criteria. Leisure-time physical activity and doctor-diagnosed hypertension were self-reported. Body mass index was calculated from measured weight and height. We computed the geometric mean PSA (ng/mL), adjusted for age, race, and body mass index, by tertile of energy, fat, and carbohydrate intake and level of physical activity, and among men with and without insulin resistance and metabolic syndrome in the whole population and by race. The geometric mean PSA (95% confidence interval) among men in the lowest tertile of energy was 1.05 (0.97-1.1) relative to 0.85 (0.8-0.9) in the highest tertile (P = 0.0002) in the whole population. The PSA concentrations were lower among overweight men with higher versus lower energy intake (P = 0.001). The PSA concentrations in men with insulin resistance was lower [0.87 (0.8-0.9)] relative to men without insulin resistance [0.98 (0.9-1.1)] at P = 0.04. All associations were in similar directions within racial subgroups. No associations were observed between the other lifestyle and physiologic factors. Additional studies are required to confirm these results and to investigate the potential mechanisms that may explain these relationships.Dietary fats and age-related macular degeneration
Parekh, N. (n.d.).Publication year
2008Journal title
Topics in Clinical NutritionVolume
23Issue
4Page(s)
347-356AbstractAmount and type of dietary fat may play a role in the pathogenesis of age-related macular degeneration (AMD) via 4 potential mechanisms: (1) atherosclerosis, (2) altering retinal integrity, (3) oxidative damage, and (4) inflammation. In this report, 11 epidemiologic studies are evaluated for evidence of associations between dietary fats and AMD. Taken together, the studies suggest a protective association of higher omega-3 polyunsaturated fats and fish intake with AMD. The relations of AMD with total and types of fat varied across populations and may reflect different patterns of fat intake. Practitioners should advise a low-fat, "heart-healthy" diet and encourage consumption of diets high in omega-3 polyunsaturated fats.Association between Vitamin D and age-related macular degeneration in the third National Health and Nutrition Examination Survey, 1988 through 1994
Parekh, N., Chappell, R. J., Millen, A. E., Albert, D. M., & Mares, J. A. (n.d.).Publication year
2007Journal title
Archives of OphthalmologyVolume
125Issue
5Page(s)
661-669AbstractObjective: To evaluate the associations between levels of vitamin D (25-hydroxyvitamin D) in serum and prevalent age-related macular degeneration (AMD). Methods and Design: Cross-sectional associations of serum vitamin D and early and advanced AMD, assessed from nonmydriatic fundus photographs, were evaluated in the third National Health and Nutrition Examination Survey, a multistage nationally representative probability sample of noninstitutionalized individuals (N=7752; 11% with AMD). Results: Levels of serum vitamin D were inversely associated with early AMD but not advanced AMD. The odds ratio (OR) and 95% confidence interval (CI) for early AMD among participants in the highest vs lowest quintile of serum vitamin D was 0.64 (95% CI, 0.5-0.8; P trend <.001). Exploratory analyses were conducted to evaluate associations with important food and supplemental sources of vitamin D. Milk intake was inversely associated with early AMD (OR, 0.75; 95% CI, 0.6-0.9). Fish intake was inversely associated with advanced AMD(OR, 0.41; 95% CI, 0.2-0.9). Consistent use vs nonuse of vitamin D from supplements was inversely associated with earlyAMDonly in individuals who did not consume milk daily (early AMD: OR, 0.67; 95% CI, 0.5-0.9). Conclusion: This study provides evidence that vitamin Dmay protect against AMD. Additional studies are needed to confirm these findings.Associations between intermediate age-related macular degeneration and lutein and zeaxanthin in the Carotenoids in Age-Related Eye Disease Study (CAREDS): Ancillary study of the Women's Health Initiative
Moeller, S. M., Parekh, N., Tinker, L., Ritenbaugh, C., Blodi, B., Wallace, R. B., & Mares, J. A. (n.d.).Publication year
2006Journal title
Archives of OphthalmologyVolume
124Issue
8Page(s)
1151-1162AbstractObjective: To evaluate the relationship between dietary lutein plus zeaxanthin and intermediate age-related macular degeneration (AMD). Design: Women aged 50 to 79 years in Iowa, Wisconsin, and Oregon with intake of lutein plus zeaxanthin above the 78th (high) and below the 28th (low) percentiles at baseline in the Women's Health Initiative Observational Study were recruited 4 to 7 years later into the Carotenoids in Age-Related Eye Disease Study (CAREDS), when the presence of AMD was determined by fundus photographs. Logistic regression analyses examined the prevalence of AMD in 1787 CAREDS participants, after accounting for potential covariates. Results: The prevalence of intermediate AMD was not statistically different between the high and low lutein plus zeaxanthin intake recruitment groups after adjusting for age (odds ratio, 0.96; 95% confidence interval, 0.75-1.23). Limiting analyses to women younger than 75 years with stable intake of lutein plus zeaxanthin, without a history of chronic diseases that are often associated with diet changes, substantially lowered odds ratios (0.57; 95% confidence interval, 0.34-0.95). Exploratory analyses of advanced AMD in 34 participants resulted in protective, but statistically nonsignificant, associations in the overall sample and in women younger than 75 years. Conclusion: Diets rich in lutein plus zeaxanthin may protect against intermediate AMD in healthy women younger than 75 years.