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
Increasing mortality in the United States from cholangiocarcinoma: An analysis of the National Center for Health Statistics Database
AbstractYao, K. J., Jabbour, S., Parekh, N., Lin, Y., & Moss, R. A. (2016). BMC Gastroenterology, 16(1). 10.1186/s12876-016-0527-zAbstractBackground: While mortality in the United States has decreased for most cancers, mortality from combined hepatocellular liver cancer and intrahepatic cholangiocarcinoma (ICC) has increased and ranked 1st in annual percent increase among cancer sites. Because reported statistics combine ICC with other liver cancers, mortality rates of cholangiocarcinoma (CCA) remain unknown. This study is to determine CCA mortality trends and variation based on national data. Methods: This nation-wide study was based on the underlying cause of death data collected by the National Center for Health Statistics (NCHS) between 1999 and 2014. The Center for Disease Control (CDC) Wide-ranging Online Data for Epidemiologic Research (WONDER) system was used to obtain data. ICC and extra-hepatic CCA (ECC) were defined by ICD-10 diagnosis codes. Age-adjusted mortality rate was standardized to the US population in 2000. Results: There were more than 7000 CCA deaths each year in the US after 2013. CCA mortality for those aged 25+ increased 36 % between 1999 and 2014, from 2.2 per 100,000 (95 % confidence interval [CI] 2.1-2.3) to 3.0 per 100,000 (95 % CI, 2.9-3.1). Mortality rates were lower among females compared with males (risk ratio [RR] 0.78, 95 % CI 0.77-0.79). Asians had the highest mortality. Between 2004 and 2014, the increase in CCA mortality was highest among African Americans (45 %) followed by Asians (22 %), and whites (20 %). Conclusion: Based on the most recent national data, CCA mortality rates have increased substantially in the past decade. Among different race/ethnic groups, African Americans have the highest increase in CCA mortality.Concordance with DASH diet and blood pressure change: Results fromthe Framingham Offspring Study (1991-2008)
AbstractJiang, J., Liu, M., Troy, L. M., Bangalore, S., Hayes, R. B., & Parekh, N. (2015). Journal of Hypertension, 33(11), 2223-2230. 10.1097/HJH.0000000000000710AbstractBackground: Concordance with the Dietary Approaches to Stop Hypertension (DASH) diet has been shown to reduce blood pressure (BP) in short-term intervention studies, but the long-term impact is unclear. We evaluated the association of DASH diet concordance with BP trajectories and incidence of hypertension, in 2187 men and women (mean age 52.5 years at baseline) participating in the Framingham Offspring cohort. Method: Diet and BP were assessed from 1991 to 2008, with a median follow-up time of 13.4 years. DASH scores (ranging from 0 for worst to 10 for best concordance with DASH diet) were calculated by summing 10 food components that comprise the DASH diet pattern, including fruits and vegetables, low-fat dairy products, lean meat, and plant-based protein. Mixed-effect and Cox regression models were applied, to assess the association of DASH diet concordance with BP longitudinal change and with incidence of hypertension, respectively. All analyses were adjusted for age, sex, smoking status, history of diabetes, BMI, and physical activity. Result: Overall, SBP increased by 0.34mmHg and DBP by 0.10mmHg annually, in the Framingham Offspring cohort. Every unit increase in the DASH score resulted in a modest increase in SBP of 0.054 mmHg/year (P=0.028). No associations were observed between DASH diet concordance and DBP or incidence of hypertension. Conclusion: Long-term concordance with the DASH diet was not associated with a decreasing BP trajectory over time, or with decreased incidence of hypertension, in this population of middle-aged adults.Concordance with World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) guidelines for cancer prevention and obesity-related cancer risk in the Framingham Offspring cohort (1991–2008)
AbstractMakarem, N., Lin, Y., Bandera, E. V., Jacques, P. F., & Parekh, N. (2015). Cancer Causes and Control, 26(2), 277-286. 10.1007/s10552-014-0509-9AbstractPurpose: This prospective cohort study evaluates associations between healthful behaviors consistent with WCRF/AICR cancer prevention guidelines and obesity-related cancer risk, as a third of cancers are estimated to be preventable. Methods: The study sample consisted of adults from the Framingham Offspring cohort (n = 2,983). From 1991 to 2008, 480 incident doctor-diagnosed obesity-related cancers were identified. Data on diet, measured by a food frequency questionnaire, anthropometric measures, and self-reported physical activity, collected in 1991 was used to construct a 7-component score based on recommendations for body fatness, physical activity, foods that promote weight gain, plant foods, animal foods, alcohol, and food preservation, processing, and preparation. Multivariable Cox regression models were used to estimate associations between the computed score, its components, and subcomponents in relation to obesity-related cancer risk. Results: The overall score was not associated with obesity-related cancer risk after adjusting for age, sex, smoking, energy, and preexisting conditions (HR 0.94, 95 % CI 0.86–1.02). When score components were evaluated separately, for every unit increment in the alcohol score, there was 29 % lower risk of obesity-related cancers (HR 0.71, 95 % CI 0.51–0.99) and 49–71 % reduced risk of breast, prostate, and colorectal cancers. Every unit increment in the subcomponent score for non-starchy plant foods (fruits, vegetables, and legumes) among participants who consume starchy vegetables was associated with 66 % reduced risk of colorectal cancer (HR 0.44, 95 % CI 0.22–0.88). Conclusions: Lower alcohol consumption and a plant-based diet consistent with the cancer prevention guidelines were associated with reduced risk of obesity-related cancers in this population.Dietary variety is inversely associated with body adiposity among us adults using a novel food diversity index
AbstractVadiveloo, M., Beth Dixon, L., Mijanovich, T., Elbel, B., & Parekh, N. (2015). Journal of Nutrition, 145(3), 555-563. 10.3945/jn.114.199067AbstractBackground: Consuming a variety (vs. monotony) of energy-poor, nutrient-dense foods may help individuals adhere to dietary patterns favorably associated with weight control. Objective: The objective of this study was to examine whether greater healthful food variety quantified using the US Healthy Food Diversity (HFD) index favorably influenced body adiposity. Methods: Men and nonpregnant, nonlactating women aged ≥20 y with two 24-h recalls from the cross-sectional NHANES 2003-2006 (n = 7470) were included in this study. Dietary recalls were merged with the MyPyramid Equivalent database to generate the US HFD index, which ranges from 0 to ~1, with higher scores indicative of diets with a higher number and proportion of healthful foods. Multiple indicators of adiposity including BMI, waist-to-height ratio, android-to-gynoid fat ratio, fat mass index (FMI), and percentage body fat were assessed across US HFD index quintiles. ORs and 95% CIs were computed with use of multivariable logistic regression (SAS v. 9.3). Results: The US HFD index was inversely associated with most adiposity indicators in both sexes. After multivariable adjustment, the odds of obesity, android-to-gynoid ratio >1, and high FMI were 31-55% lower (P-trend < 0.01) among women in quintile 5 vs. quintile 1 of the US HFD index. Among men, the odds of obesity, waist-to-height ratio =0.5, and android-to-gynoid ratio >1 were 40-48% lower (P-trend = 0.01) in quintile 5 vs. quintile 1 of the US HFD index. Conclusions: Higher US HFD index values were inversely associated with indicators of body adiposity in both sexes, indicating that greater healthful food variety may protect against excess adiposity. This study explicitly recognizes the potential benefits of dietary variety in obesity management and provides the foundation to support its ongoing evaluation.Dietary Variety: An Overlooked Strategy for Obesity and Chronic Disease Control
Vadiveloo, M. K., & Parekh, N. (2015). American Journal of Preventive Medicine, 49(6), 974-979. 10.1016/j.amepre.2015.06.014Greater healthful food variety as measured by the US healthy food diversity index is associated with lower odds of metabolic syndrome and its components in US adults.
Vadiveloo, M., Parekh, N., & Mattei, J. (2015). Journal of Nutrition, 145(3), 564-571.Insulin receptor variants and obesity-related cancers in the Framingham Heart Study
AbstractParekh, N., Guffanti, G., Lin, Y., Ochs-Balcom, H. M., Makarem, N., & Hayes, R. (2015). Cancer Causes and Control, 26(8), 1189-1195. 10.1007/s10552-015-0613-5AbstractPurpose: The insulin-signaling pathway plays a pivotal role in cancer biology; however, evidence of genetic alterations in human studies is limited. This case–control study nested within the Framingham Heart Study (FHS) examined the association between inherited genetic variation in the insulin receptor (INSR) gene and obesity-related cancer risk. Methods: The study sample consisted of 1,475 controls and 396 cases from the second familial generation of the FHS. Participants who provided consent were genotyped. Nineteen single-nucleotide polymorphisms (SNPs) in the INSR gene were investigated in relation to risk of obesity-related cancers combined and breast, prostate and colorectal cancers. Generalized estimation equation models controlling for familial correlations and include age, sex, smoking and body mass index as covariates, assuming additive models, were used. Results: Three SNPs, rs2059807, s8109559 and rs919275, were significantly associated with obesity-related cancers (p value < 0.02) with the most significantly associated SNP being rs2059807 (p value = 0.008). Carriers of two copies of SNP rs2059807 risk allele T were significantly less prevalent among subjects with obesity-related cancers [f(TT)cases = 14 vs. f(TT)controls = 18 %; OR 1.23]. In exploratory analyses evaluating site-specific cancers, the INSR rs2059807 association with these cancers was consistent with that observed for the main outcome (ORs colorectal cancer = 1.5, breast cancer = 1.29, prostate = 1.06). There was no statistically significant interaction between the INSR–SNP and blood glucose in relation to obesity-related cancer. Conclusions: The INSR gene is implicated in obesity-related cancer risk, as 3 of 19 SNPs were nominally associated, after false discovery rate (FDR) correction, with the main outcome. Risk allele homozygotes (rs2059807) were less prevalent among subjects with obesity-related cancer. These results should be replicated in other populations to confirm the findings.Sensitivity and specificity of malnutrition screening tools used in the adult hospitalized patient setting a systematic review
AbstractPlatek, M. E., Hertroijs, D. F. L., Nicholson, J. M., & Parekh, N. (2015). Topics in Clinical Nutrition, 30(4), 289-301. 10.1097/TIN.0000000000000046AbstractAdult hospitalized patients are at risk for malnutrition. The sensitivity and specificity of screening tools were compared with Subjective Global Assessment. Methods included a systematic review using PubMed, CINAHL Plus, and EMBASE through April 2014. Study quality was assessed using the Quality Assessment of Diagnostic Accuracy Studies method. The results showed that the Malnutrition Universal Screening Tool, Nutrition Risk Screening-2002, and Malnutrition Screening Tool were most frequently tested. The specificity was generally good (>80%), but sensitivity was variable. Malnutrition Universal Screening Tool, Nutrition Risk Screening-2002, and Malnutrition Screening Tool are screening tools that consider population characteristics and risk cut points and are easy to administer. Key words: malnutrition, nutrition assessment, nutrition screening, sensitivity and specificity, subjective global assessment, undernutrition.Development and evaluation of the US Healthy Food Diversity index
AbstractVadiveloo, M., Dixon, L. B., Mijanovich, T., Elbel, B., & Parekh, N. (2014). British Journal of Nutrition, 112(9), 1562-1574. 10.1017/S0007114514002049AbstractVaried diets are diverse with respect to diet quality, and existing dietary variety indices do not capture this heterogeneity. We developed and evaluated the multidimensional US Healthy Food Diversity (HFD) index, which measures dietary variety, dietary quality and proportionality according to the 2010 Dietary Guidelines for Americans (DGA). In the present study, two 24 h dietary recalls from the 2003-6 National Health and Nutrition Examination Survey (NHANES) were used to estimate the intake of twenty-six food groups and health weights for each food group were informed by the 2010 DGA. The US HFD index can range between 0 (poor) and 1 - 1/n, where n is the number of foods; the score is maximised by consuming a variety of foods in proportions recommended by the 2010 DGA. Energy-adjusted Pearson's correlations were computed between the US HFD index and each food group and the probability of adequacy for fifteen nutrients. Linear regression was run to test whether the index differentiated between subpopulations with differences in dietary quality commonly reported in the literature. The observed mean index score was 0·36, indicating that participants did not consume a variety of healthful foods. The index positively correlated with nutrient-dense foods including whole grains, fruits, orange vegetables and low-fat dairy (r 0·12 to 0·64) and negatively correlated with added sugars and lean meats (r - 0·14 to - 0·23). The index also positively correlated with the mean probability of nutrient adequacy (r 0·41; P< 0·0001) and identified non-smokers, women and older adults as subpopulations with better dietary qualities. The US HFD index may be used to inform national dietary guidance and investigate whether healthful dietary variety promotes weight control.Racial differences in the association of insulin-like growth factor pathway and colorectal adenoma risk
AbstractOchs-Balcom, H. M., Vaughn, C. B., Nie, J., Chen, Z., Thompson, C. L., Parekh, N., Tracy, R., & Li, L. (2014). Cancer Causes and Control, 25(2), 161-170. 10.1007/s10552-013-0318-6AbstractPurpose: Insulin resistance is believed to play an important role in the link between energy imbalance and colon carcinogenesis. Emerging evidence suggests that there are substantial racial differences in genetic and anthropometric influences on insulin-like growth factors (IGFs); however, few studies have examined racial differences in the associations of IGFs and colorectal adenoma, precursor lesions of colon cancer. Methods: We examined the association of circulating levels of IGF-1, IGFBP-3 and IGFBP-1, and SNPs in the IGF-1 receptor (IGF1R), IGF-2 receptor (IGF2R), and insulin receptor genes with risk of adenomas in a sample of 410 incident adenoma cases and 1,070 controls from the Case Transdisciplinary Research on Energetics and Cancer (TREC) Colon Adenomas Study. Results: Caucasians have higher IGF-1 levels compared to African Americans; mean IGF-1 levels are 119.0 ng/ml (SD = 40.7) and 109.8 ng/ml (SD = 40.8), respectively, among cases (p = 0.02). Mean IGF-1 levels are also higher in Caucasian controls (122.9 ng/ml, SD = 41.2) versus African American controls (106.9, SD = 41.2), p = 0.001. We observed similar differences in IGFBP3 levels by race. Logistic regression models revealed a statistically significant association of IGF-1 with colorectal adenoma in African Americans only, with adjusted odds ratios (ORs) of 1.68 (95 % CI 1.06-2.68) and 1.68 (95 % CI 1.05-2.71), respectively, for the second and third tertiles as compared to the first tertile. One SNP (rs496601) in IGF1R was associated with adenomas in Caucasians only; the per allele adjusted OR is 0.73 (95 % CI 0.57-0.93). Similarly, one IGF2R SNP (rs3777404) was statistically significant in Caucasians; adjusted per allele OR is 1.53 (95 % CI 1.10-2.14). Conclusion: Our results suggest racial differences in the associations of IGF pathway biomarkers and inherited genetic variance in the IGF pathway with risk of adenomas that warrant further study.