Niyati Parekh's additional information
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Prof. 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.
Prof. 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. Prof. Parekh served as the Executive Director of Doctoral Programs at GPH from 2017-2021. In this role, she supported PhD students school-wide, and promoted all aspects of their rigorous research and professional development towards impactful careers. Prof. Parekh was appointed as the Associate Vice Provost of Faculty Initiatives in August 2021 and is responsible for mentoring early career tenure track-faculty.
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PhD, Nutritional Sciences (minor Population Health Sciences), University of Wisconsin-Madison, Madison, WIMS, Foods, Nutrition, and Clinical Dietetics, Mumbai University, IndiaBS, Life Sciences and Biotechnology, Mumbai University, India
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Faculty Honors Awards
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Publications
The "sweet" truth about cancer.
Parekh, N. (2013). Oncology Nutrition Connection, 21(2), 13-17.Dietary fiber intake and colorectal cancer risk: Weighing the evidence from epidemiologic studies
AbstractRomaneiro, S., & Parekh, N. (2012). Topics in Clinical Nutrition, 27(1), 41-47. 10.1097/TIN.0b013e3182461dd4AbstractThe hypothesis is that fiber protects against colorectal cancer because of various biologic properties. Although several human studies have examined the relationship between fiber and colorectal carcinogenesis, the association remains unclear. This review evaluates key epidemiologic research in large populations conducted since 2003. With a combined analysis of 9 studies, results are mixed. Four studies show a statistically significant reduced risk of developing colorectal cancer with increased dietary fiber intake, and 5 studies show no association. On the basis of these equivocal findings, it cannot be concluded that a protective association exists between increased dietary fiber intake and reduced colorectal cancer risk.Longitudinal associations of leisure-time physical activity and cancer mortality in the Third National Health and Nutrition Examination Survey (1986-2006)
AbstractParekh, N., Lin, Y., Craft, L. L., Vadiveloo, M., & Lu-Yao, G. L. (2012). Journal of Obesity, 2012. 10.1155/2012/518358AbstractLongitudinal associations between leisure-time physical activity (LTPA) and overall cancer mortality were evaluated within the Third National Health and Nutrition Examination Survey (NHANES III; 1988-2006; n = 15,535). Mortality status was ascertained using the National Death Index. Self-reported LTPA was divided into inactive, regular low-to-moderate and vigorous activity. A frequency-weighted metabolic equivalents (METS/week) variable was also computed. Hazard ratios (HRs) and 95 confidence intervals (CI) were calculated for overall cancer mortality in the whole sample, by body mass index categories and insulin resistance (IR) status. Nonsignificant protective associations were observed for regular low-to-moderate and vigorous activity, and for the highest quartile of METS/week (HRs range: 0.66-0.95). Individuals without IR engaging in regular vigorous activity had a 48 decreased risk of cancer mortality (HR: 0.52; 95 CI: 0.28-0.98) in multivariate analyses. Conversely, nonsignificant positive associations were observed in people with IR. In conclusion, regular vigorous activity may reduce risk of cancer mortality among persons with normal insulin-glucose metabolism in this national sample.Obesity in cancer survival
AbstractParekh, N., Chandran, U., & Bandera, E. V. (2012). Annual Review of Nutrition, 32, 311-342. 10.1146/annurev-nutr-071811-150713AbstractAlthough obesity is a well-known risk factor for several cancers, its role on cancer survival is poorly understood. We conducted a systematic literature review to assess the current evidence evaluating the impact of body adiposity on the prognosis of the three most common obesity-related cancers: prostate, colorectal, and breast. We included 33 studies of breast cancer, six studies of prostate cancer, and eight studies of colo-rectal cancer. We note that the evidence overrepresents breast cancer survivorship research and is sparse for prostate and colorectal cancers. Overall, most studies support a relationship between body adiposity and site-specific mortality or cancer progression. However, most of the research was not specifically designed to study these outcomes and, therefore, several methodological issues should be considered before integrating their results to draw conclusions. Further research is urgently warranted to assess the long-term impact of obesity among the growing population of cancer survivors.Obesity, metabolic syndrome and esophageal adenocarcinoma: Epidemiology, etiology and new targets
AbstractRyan, A. M., Duong, M., Healy, L., Ryan, S. A., Parekh, N., Reynolds, J. V., & Power, D. G. (2011). Cancer Epidemiology, 35(4), 309-319. 10.1016/j.canep.2011.03.001AbstractBackground: 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
AbstractMillen, 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. (2011). Archives of Ophthalmology, 129(4), 481-489. 10.1001/archophthalmol.2011.48AbstractObjective: 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. (2010). JAMA Opthalmology, 128(6), 738-749.Lifestyle, Anthropometric, and Obesity-Related Physiologic Determinants of Insulin-like Growth Factor-1 in the Third National Health and Nutrition Examination Survey (1988-1994)
AbstractParekh, N., Roberts, C. B., Vadiveloo, M., Puvananayagam, T., Albu, J. B., & Lu-Yao, G. L. (2010). Annals of Epidemiology, 20(3), 182-193. 10.1016/j.annepidem.2009.11.008AbstractPurpose: 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
AbstractParekh, N., Lin, Y., Hayes, R. B., Albu, J. B., & Lu-Yao, G. L. (2010). Cancer Causes and Control, 21(4), 631-642. 10.1007/s10552-009-9492-yAbstractInsulin 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
AbstractParekh, N., Lin, Y., Dipaola, R. S., Marcella, S., & Lu-Yao, G. (2010). American Journal of Medicine, 123(9), 829-835. 10.1016/j.amjmed.2010.05.011AbstractBackground: 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.