Niyati Parekh's additional information
-
-
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.
-
-
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
-
-
Faculty Honors Awards
-
-
Publications
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.Treatment and outcomes in diabetic breast cancer patients
AbstractGold, H. T., Makarem, N., Nicholson, J. M., & Parekh, N. (2014). Breast Cancer Research and Treatment, 143(3), 551-570. 10.1007/s10549-014-2833-xAbstractEffective breast cancer management is more complex with diabetes present and may contribute to poor outcomes. Therefore, we conducted two simultaneous systematic reviews to address the association of diabetes with (1) treatment patterns in breast cancer patients and (2) breast cancer recurrence rates or breast cancer-specific and all-cause mortality. We searched major databases for English language peer-reviewed studies through November 2013, which addressed either of the above research questions, following the preferred reporting items for systematic reviews and meta-analyses (PRISMA) method. Analyses compared treatment patterns or health outcomes for breast cancer subjects with and without diabetes. We used STROBE quality criteria and conducted a random-effects meta-analysis of all-cause mortality. The review yielded 11 publications for question 1 and 26 for question 2, with nine overlapping. Treatment studies showed chemotherapy was less likely in patients with diabetes. Of 22 studies, 21 assessing all-cause mortality indicated a statistically significant increased overall mortality for patients with diabetes (hazard ratios: 0.33-5.40), with meta-analysis of eligible studies indicating a 52 % increased risk. Nine studies assessing breast cancer-specific mortality had inconsistent results, with five showing significantly increased risk for diabetes patients. Results were inconsistent for recurrence and metastases. The majority of studies reported detrimental associations between diabetes and optimal treatment or all-cause mortality among women with breast cancer. Divergence in variable and outcomes inclusion and definitions, potential participation bias in individual studies, and differing analytic methods make inferences difficult. This review illuminates the importance of the impact of diabetes on breast cancer patients and explicitly recognizes that co-management of conditions is necessary to prevent excess morbidity and mortality.Trends in dietary carbohydrate consumption from 1991 to 2008 in the Framingham Heart Study Offspring Cohort
AbstractMakarem, N., Scott, M., Quatromoni, P., Jacques, P., & Parekh, N. (2014). British Journal of Nutrition, 111(11), 2010-2023. 10.1017/S0007114513004443AbstractThe intake of carbohydrates has been evaluated cross-sectionally, but not longitudinally in an ageing American adult population. The aim of the present study was to examine trends in the intake of dietary carbohydrates and their major food sources among the Framingham Heart Study Offspring (FOS) cohort, which had been uniquely tracked for 17 years in the study. The FOS cohort was recruited in 1971-1975. Follow-up examinations were conducted, on average, every 4 years. Dietary data collection began in 1991 (examination 5) using a validated semi-quantitative FFQ. The study included 2894 adults aged ≥ 25 years with complete dietary data in at least three examinations from 1991 to 2008. Descriptive statistics were generated using SAS version 9.3, and a repeated-measures model was used to examine trends in the intake of carbohydrates and their food sources in the whole sample, and by sex and BMI category. Over 17 years of follow-up, the percentage of energy from total carbohydrates (51·0-46·8 %; P for trend < 0·001) and total sugars (18·2-16·6 %; P for trend < 0·001) decreased. There was a decrease in the percentage of energy from fructose (5·4-4·7 %; P for trend < 0·001) and sucrose (9·8-8·8 %; P for trend < 0·001). Dietary fibre intake increased (18·0-19·2 g/d; P for trend < 0·001). The number of weekly servings of yeast bread, soft drinks/soda, cakes/cookies/quick breads/doughnuts, potatoes, milk, pasta, rice and cooked grains, fruit juice/drinks, potato chips/maize chips/popcorn, and lunch foods (e.g. pizzas and burgers) decreased significantly (P for trend < 0·001), while the intake of ready-to-eat cereals, legumes, fruits, dairy products, candy and ice cream/sherbet/frozen yogurt increased significantly (P for trend<0·04) . Similar trends were observed when the analyses were stratified by sex and BMI. The present results suggest favourable trends in dietary carbohydrate consumption, but dietary guidelines for fruits, vegetables and fibre were not met in this cohort.Trends in dietary fat and high-fat food intakes from 1991 to 2008 in the framingham heart study participants
AbstractVadiveloo, M., Scott, M., Quatromoni, P., Jacques, P., & Parekh, N. (2014). British Journal of Nutrition, 111(4), 724-734. 10.1017/S0007114513002924AbstractFew longitudinal studies carried out in US adults have evaluated long-term dietary fat intakes and compared them with the national recommendations during the two-decade period when the prevalence of obesity and insulin resistance increased substantively. In the present study, we examined trends in the intakes of dietary fats and rich dietary sources of fats in the Framingham Heart Study Offspring Cohort over a 17-year period. The cohort was established in 1971-75 with follow-up examinations being conducted approximately every 4 years. Dietary data were collected using a semi-quantitative FFQ beginning in 1991 (exam 5). We included 2732 adults aged ≥A 25 years with complete dietary data in at least three examinations from 1991 to 2008. Descriptive statistics were generated using SAS version 9.3, and a repeated-measures model was used to examine trends in macronutrient and food intakes using R. Over the 17 years of follow-up, the percentage of energy derived from total fat and protein increased (27·3-29·8A % of energy and 16·8-18·0A % of energy, respectively) and that derived from carbohydrate decreased (51·0- 46·8A % of energy; P-trend <A 0·001). Increases in the percentage of energy derived from all fat subtypes were observed, except for that derived from trans-fats, which decreased over time (P-trend <A 0·001). Trends were similar between the sexes, although women exhibited a greater increase in the percentage of energy derived from saturated fat and less reduction in the percentage of energy derived from trans-fats (P interaction <A 0·05). Trends in fat intake were similar across the BMI categories. The number of weekly servings of cheese, eggs, ice cream desserts, nuts, butter and sausages/processed meats increased, whereas the intake of milk, margarine, poultry, confectioneries, chips and breads decreased (P-trend <A 0·001). In this cohort of predominantly Caucasian older adults, the percentage of energy derived from dietary fats increased over time, but it remained within the national recommendations of less than 35A % of total energy, on average.Associations between dietary variety and measures of body adiposity: a systematic review of epidemiological studies.
AbstractVadiveloo, M., Dixon, L. B., & Parekh, N. (2013). Unknown Journal, 109(9), 1557-1572. 10.1017/S0007114512006150AbstractDietary variety is positively correlated with energy intake in most studies. However, the associations between dietary variety and measures of body adiposity are inconsistent in the literature, which limits the development of clear national nutrition recommendations regarding dietary variety. In the present systematic review, we critically evaluate the associations between dietary variety and measures of body adiposity among healthy adults within the existing literature. We conducted a systematic search of the MEDLINE and Web of Science databases in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses statement to examine these associations. We identified twenty-six studies in total that investigated the associations between dietary variety and body adiposity measures. Total variety was non-significantly associated with body adiposity in most studies, while variety in recommended foods was either inversely associated (six out of ten studies) or non-significantly associated (three out of ten studies) with body adiposity. Conversely, variety in non-recommended foods (i.e. sources of added sugars and solid fats) increased the likelihood of excess adiposity in most studies (six out of nine studies). Definitions and measurement of dietary variety were inconsistent across studies and contributed to some of the discrepancies noted in the literature. In conclusion, among the studies that met the inclusion criteria for the present review, dietary variety was inconsistently associated with body adiposity in diverse populations. Using consistent and specific definitions of dietary variety may help provide further insight into the associations between dietary variety and excess adiposity before definitive public health messages are maConsumption of sugary foods and drinks and risk of endometrial cancer
AbstractKing, M. G., Chandran, U., Olson, S. H., Demissie, K., Lu, S. E., Parekh, N., & Bandera, E. V. (2013). Cancer Causes and Control, 24(7), 1427-1436. 10.1007/s10552-013-0222-0AbstractConsumption of foods high in sugar promotes insulin production, which has been linked to endometrial carcinogenesis. We evaluated the impact of dietary intake of sugary foods and beverages, as well as added sugar and total sugar on endometrial cancer risk in a population-based case-control study, including 424 cases and 398 controls. Participants completed an interview and food frequency questionnaire, and provided self-recorded waist and hip measurements. Women in the highest quartile of added sugar intake had significantly increased endometrial cancer risk (OR = 1.84, 95 % CI 1.16-2.92). Among women with waist-to-hip ratio ≥0.85, risk was significantly higher for the highest versus lowest tertile of added sugar intakes (OR = 2.50, 95 % CI 1.38-4.52). The association with added sugar also became stronger when analyses were restricted to never users of hormone replacement therapy (OR = 2.03; 95 % CI 1.27-3.26, for highest versus lowest tertile). There was little evidence of effect modification by body mass index or physical activity. Given the high prevalence of intake of sugary foods and drinks in Western populations, additional research is warranted to confirm our findings on endometrial cancer.Diabetes mellitus as a risk factor for gastrointestinal cancers among postmenopausal women
AbstractLuo, J., Chlebowski, R., Liu, S., McGlynn, K. A., Parekh, N., White, D. L., & Margolis, K. L. (2013). Cancer Causes and Control, 24(3), 577-585. 10.1007/s10552-012-9996-8AbstractObjectives: While diabetes has been linked to several cancers in the gastrointestinal (GI) tract, findings have been mixed for sites other than colorectal and liver cancer. We used the Women's Health Initiative (WHI) data and conducted a comprehensive assessment of associations between diabetes and GI malignancy (esophagus, stomach, liver, biliary, pancreas, colon, and rectal). Methods: A total of 145,765 postmenopausal women aged 50-79 enrolled in the WHI were followed for a mean 10.3 years. Cox proportional hazard regression models were used to estimate hazard ratios (HRs) and 95 % confidence intervals (CIs) for the association between GI cancers and diagnosed diabetes, including its duration and treatment. Results: Diabetes at enrollment was associated with increased risk of liver (HR = 2.97; 95 % CI, 1.66-5.32), pancreatic (HR = 1.62; 95 % CI, 1.15-2.30), colon (HR = 1.38; 95 % CI, 1.14-1.66), and rectal (HR = 1.87, 95 % CI: 1.22-2.85) cancer. Diabetes severity, assessed by duration or need for pharmacotherapy, appeared to have stronger links to risk of liver, pancreatic, and rectal cancer, but not colon cancer. There was no statistically significant association of diabetes with biliary, esophageal, and stomach cancers. Conclusion: Type 2 diabetes is associated with a significantly increased risk of cancers of the liver, pancreas, colon, and rectum in postmenopausal women. The suggestion that diabetes severity further increases these cancer risks requires future studies.