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
Associations of Whole and Refined Grain Intakes with Adiposity-Related Cancer Risk in the Framingham Offspring Cohort (1991–2013)
AbstractMakarem, N., Bandera, E. V., Lin, Y., McKeown, N. M., Hayes, R. B., & Parekh, N. (2018). Nutrition and Cancer, 70(5), 776-786. 10.1080/01635581.2018.1470647AbstractCase-control studies suggest that higher whole grain and lower refined grain intakes are associated with reduced cancer risk, but longitudinal evidence is limited. The objective of this prospective cohort study is to evaluate associations between whole and refined grains and their food sources in relation to adiposity-related cancer risk. Participants were adults from the Framingham Offspring cohort (N = 3,184; ≥18 yr). Diet, measured using a food frequency questionnaire, medical and lifestyle data were collected at exam 5 (1991–95). Between 1991 and 2013, 565 adiposity-related cancers were ascertained using pathology reports. Cox proportional hazards models were used to estimate adjusted hazard ratios and 95% confidence intervals for associations of whole and refined grains with risk of adiposity-related cancers combined and with risk of breast and prostate cancers in exploratory site-specific analyses. Null associations between whole and refined grains and combined incidence of adiposity-related cancers were observed in multivariable-adjusted models (HR: 0.94; 95% CI: 0.71–1.23 and HR: 0.98; 95% CI: 0.70–1.38, respectively). In exploratory analyses, higher intakes of whole grains (oz eq/day) and whole grain food sources (servings/day) were associated with 39% and 47% lower breast cancer risk (HR: 0.61; 95% CI: 0.38–0.98 and HR: 0.53; 95% CI: 0.33–0.86, respectively). In conclusion, whole and refined grains were not associated with adiposity-related cancer risk. Whole grains may protect against breast cancer, but findings require confirmation within a larger sample and in other ethnic groups.Consumption of sugars, sugary foods, and sugary beverages in relation to adiposity-related cancer risk in the framingham offspring cohort (1991–2013)
AbstractMakarem, N., Bandera, E. V., Lin, Y., Jacques, P. F., Hayes, R. B., & Parekh, N. (2018). Cancer Prevention Research, 11(6), 347-358. 10.1158/1940-6207.CAPR-17-0218AbstractBackground: Higher sugar consumption may increase cancer risk by promoting insulin-glucose dysregulation, oxidative stress, hormonal imbalances, and excess adiposity. This prospective study investigates the association between dietary sugars (fructose and sucrose) and sugary foods and beverages in relation to combined and site-specific (breast, prostate, colorectal) adiposity-associated cancers. Methods: The analytic sample consisted of 3,184 adults, aged 26–84 years, from the Framingham Offspring cohort. Diet data were first collected between 1991 and 1995 using a food frequency questionnaire. Intakes of fructose, sucrose, sugary foods, and sugary beverages (fruit juice and sugar-sweetened beverages) were derived. Participants were followed up until 2013 to ascertain cancer incidence; 565 doctor-diagnosed adiposity-related cancers, including 124 breast, 157 prostate, and 68 colorectal cancers occurred. Multivariable-adjusted Cox proportional hazards models were used to evaluate associations. Tests for interaction with BMI and waist circumference were conducted. Results: No associations were observed between fructose, sucrose, sugary food consumption, and combined incidence of adiposity-related cancers or the examined site-specific cancers. While total consumption of sugary beverages was not associated with site-specific cancer risk, higher intakes of fruit juice were associated with 58% increased prostate cancer risk (HR: 1.58; 95% CI, 1.04–2.41) in multivariable-adjusted models. In exploratory stratified analyses, higher sugary beverage intakes increased overall adiposity-related cancer risk by 59% in participants with excessive central adiposity (HR: 1.59; 95% CI, 1.01–2.50; P trend ¼ 0.057). Conclusions: In this cohort of American adults, higher sugary beverage consumption was associated with increased cancer risk among participants with central adiposity. Impact: These analyses suggest that avoiding sugary beverages represents a simple dietary modification that may be used as an effective cancer control strategy.Consumption of sugars, sugary foods, and sugary beverages in relation to cancer risk: A systematic review of longitudinal studies
AbstractMakarem, N., Bandera, E. V., Nicholson, J. M., & Parekh, N. (2018). Annual Review of Nutrition, 38, 17-39. 10.1146/annurev-nutr-082117-051805AbstractHigh sugar intake may increase cancer risk by promoting insulin-glucose dysregulation, oxidative stress, inflammation, and body adiposity, but epidemiologic evidence is unclear. Associations between dietary sugars and lifestyle-related cancer risk from longitudinal studies were evaluated. We systematically searched PubMed, Embase, and CINAHL and identified 37 prospective cohort studies (1990-2017) reporting multivariable adjusted risk estimates for dietary sugars in relation to cancer. Of 15 and 14 studies on total sugar and sucrose respectively, 11 reported a null association in relation to cancer. Of 14 studies on fructose, 8 reported null associations, and 2 reported protective and 4 reported detrimental associations. In two of five studies on added sugars, a 60-95% increased cancer risk was observed with higher intakes. In 8 of 15 studies on sugary foods and beverages, a 23-200% higher cancer risk was observed with higher sugary beverage consumption. In conclusion, most studies were indicative of a null association, but suggestive detrimental associations were reported for added sugars and sugary beverages.Nutrition Literacy among Cancer Survivors: Feasibility Results from the Healthy Eating and Living Against Breast Cancer (HEAL-BCa) Study: a Pilot Randomized Controlled Trial
AbstractParekh, N., Jiang, J., Buchan, M., Meyers, M., Gibbs, H., & Krebs, P. (2018). Journal of Cancer Education, 33(6), 1239-1249. 10.1007/s13187-017-1238-zAbstractKnowledge of nutrition among breast cancer patients is insufficient, despite their motivation to seek valid information about healthy food choices. This study examines the feasibility of nutrition education workshops for cancer survivors, to inform the design of a multi-center intervention. Fifty-nine female English-speaking breast cancer patients, who had completed treatment, were enrolled. Participants were randomized to the intervention or control group. The intervention group attended six nutrition education sessions, and the control group received brochures. Measurements were done at baseline and 3-month follow-up and included the Assessment Instrument for Breast Cancer (NLit-BCa), fruit/vegetable and general health literacy screeners. Height and weight were measured. Changes in nutrition literacy, health literacy, and food intake from baseline to follow-up (within-group change) were calculated for both groups (effect sizes were reported as Cohen’s d). Participants were mostly white, with a mean age of 58 years, BMI of 31.6 kg/m2, and had college degrees. Follow-up rates were high (89% = control and 77% = intervention group). At baseline, participants scored high for most NLit-BCa assessment components except food portions in both groups. At the 3-month follow-up, effect sizes (d) on the NLit-BCa ranged from −0.5 to 0.16. The study met its recruitment goals within 6 months. Focus groups indicated that (a) attending six sessions was acceptable, (b) patients found social/emotional support, (c) improvements should include information for special diets and booster sessions. This pilot study suggests that the intervention was acceptable and that scaling up of this intervention is feasible and could provide benefit to breast cancer survivors.Racial and ethnic disparities in predictors of glycemia: a moderated mediation analysis of inflammation-related predictors of diabetes in the NHANES 2007–2010
AbstractNowlin, S., Cleland, C. M., Parekh, N., Hagan, H., & Melkus, G. (2018). Nutrition and Diabetes, 8(1). 10.1038/s41387-018-0064-7AbstractBackground/Objective: Racial/ethnic disparities in type 2 diabetes (T2D) outcomes exist, and could be explained by nutrition- and inflammation-related differences. The objective of this study is to identify associations between race/ethnicity and glucose control among participants from NHANES 2007–2010, as influenced by diet quality, body mass, and inflammation and grouped by T2D status. Subjects/Methods: The following is a cross-sectional, secondary data analysis of two NHANES data cycles spanning 2007–2010. The association between race/ethnicity and hemoglobin A1c (HbA1c) as mediated by dietary intake score, body mass index (BMI), and C-reactive protein (CRP) was assessed, as was the strength of the difference of that association, or moderation, by T2D status. The sample included n = 7850 non-pregnant adult participants ≥ 20 years of age who had two days of reliable dietary recall data, and no missing data on key variables included in the analysis. The primary outcome examined was HbA1c. Results: The model accurately explained the variation in HbA1c measures in participants without T2D, as mediated by diet quality, BMI, and CRP. However, significant variation in HbA1c remained after accounting for aforementioned mediators when contrasting non-Hispanic White to non-Hispanic Black participants without T2D. The model was not a good fit for explaining racial/ethnic disparities in HbA1c in participants with T2D. A test of the index of moderated mediation for this model was not significant for the differences in the effect of race/ethnicity on HbA1c by T2D status (moderator). Conclusions: This study demonstrated that diet quality, BMI, and CRP mediated the effect of race/ethnicity on HbA1c in persons without T2D, but not in persons with T2D. Further research should include additional inflammatory markers, and other inflammation- and T2D-related health outcomes, and their association with racial/ethnic disparities in diabetes.Ultra-processed food consumption and excess weight among US adults
AbstractJuul, F., Martinez-Steele, E., Parekh, N., Monteiro, C. A., & Chang, V. W. (2018). The British Journal of Nutrition, 120(1), 90-100. 10.1017/S0007114518001046AbstractUltra-processed foods provide 58 % of energy intake and 89 % of added sugars in the American diet. Nevertheless, the association between ultra-processed foods and excess weight has not been investigated in a US sample. The present investigation therefore aims to examine the association between ultra-processed foods and excess weight in a nationally representative sample of US adults. We performed a cross-sectional analysis of anthropometric and dietary data from 15 977 adults (20-64 years) participating in the National Health and Nutrition Examination Survey 2005-2014. Dietary data were collected by 24-h recall. Height, weight and waist circumference (WC) were measured. Foods were classified as ultra-processed/non-ultra-processed according to the NOVA classification. Multivariable linear and logistic regression was used to evaluate the association between ultra-processed food consumption (% energy) and BMI, WC and odds of BMI≥25 kg/m2, BMI≥30 kg/m2 and abdominal obesity (men: WC≥102 cm, women: WC≥88 cm). Prevalence of BMI≥25 kg/m2, BMI≥30 kg/m2 and abdominal obesity was 69·2, 36·1 and 53·0 %, respectively. Consuming ≥74·2 v. ≤36·5 % of total energy from ultra-processed foods was associated with 1·61 units higher BMI (95 % CI 1·11, 2·10), 4·07 cm greater WC (95 % CI 2·94, 5·19) and 48, 53 and 62 % higher odds of BMI≥25 kg/m2, BMI≥30 kg/m2 and abdominal obesity, respectively (OR 1·48; 95 % CI 1·25, 1·76; OR 1·53; 95 % CI 1·29, 1·81; OR 1·62; 95 % CI 1·39, 1·89, respectively; P for trend<0·001 for all). A significant interaction between being female and ultra-processed food consumption was found for BMI (F 4,79=4·89, P=0·002), WC (F 4,79=3·71, P=0·008) and BMI≥25 kg/m2 (F 4,79=5·35, P<0·001). As the first study in a US population, our findings support that higher consumption of ultra-processed food is associated with excess weight, and that the association is more pronounced among women.Birth weight, early life weight gain and age at menarche: a systematic review of longitudinal studies
AbstractJuul, F., Chang, V. W., Brar, P., & Parekh, N. (2017). Obesity Reviews, 18(11), 1272-1288. 10.1111/obr.12587AbstractBackground and objective: Adiposity in pre- and postnatal life may influence menarcheal age. Existing evidence is primarily cross-sectional, failing to address temporality, for which the role of adiposity in early life remains unclear. The current study sought to systematically review longitudinal studies evaluating the associations between birth weight and infant/childhood weight status/weight gain in relation to menarcheal age. Methods: PubMed, EMBASE, Web of Science, Global Health (Ovid) and CINAHL were systematically searched. Selected studies were limited to English-language articles presenting multi-variable analyses. Seventeen studies reporting risk estimates for birth weight (n = 3), infant/childhood weight gain/weight status (n = 4) or both (n = 10), in relation to menarcheal age were included. Results: Lower vs. higher birth weight was associated with earlier menarche in nine studies and later menarche in one study, while three studies reported a null association. Greater BMI or weight gain over time and greater childhood weight were significantly associated with earlier menarche in nine of nine and six of seven studies, respectively. Conclusions: Studies suggested that lower birth weight and higher body weight and weight gain in infancy and childhood may increase the risk of early menarche. The pre- and postnatal period may thus be an opportune time for weight control interventions to prevent early menarche, and its subsequent consequences.Carbohydrate nutrition and risk of adiposity-related cancers: Results from the Framingham Offspring cohort (1991-2013)
AbstractMakarem, N., Bandera, E. V., Lin, Y., Jacques, P. F., Hayes, R. B., & Parekh, N. (2017). British Journal of Nutrition, 117(11), 1603-1614. 10.1017/S0007114517001489AbstractHigher carbohydrate intake, glycaemic index (GI), and glycaemic load (GL) are hypothesised to increase cancer risk through metabolic dysregulation of the glucose-insulin axis and adiposity-related mechanisms, but epidemiological evidence is inconsistent. This prospective cohort study investigates carbohydrate quantity and quality in relation to risk of adiposity-related cancers, which represent the most commonly diagnosed preventable cancers in the USA. In exploratory analyses, associations with three site-specific cancers: breast, prostate and colorectal cancers were also examined. The study sample consisted of 3184 adults from the Framingham Offspring cohort. Dietary data were collected in 1991-1995 using a FFQ along with lifestyle and medical information. From 1991 to 2013, 565 incident adiposity-related cancers, including 124 breast, 157 prostate and sixty-eight colorectal cancers, were identified. Cox proportional hazards models were used to evaluate the role of carbohydrate nutrition in cancer risk. GI and GL were not associated with risk of adiposity-related cancers or any of the site-specific cancers. Total carbohydrate intake was not associated with risk of adiposity-related cancers combined or prostate and colorectal cancers. However, carbohydrate consumption in the highest v. lowest quintile was associated with 41 % lower breast cancer risk (hazard ratio (HR) 0·59; 95 % CI 0·36, 0·97). High-, medium- and low-GI foods were not associated with risk of adiposity-related cancers or prostate and colorectal cancers. In exploratory analyses, low-GI foods, were associated with 49 % lower breast cancer risk (HR 0·51; 95 % CI 0·32, 0·83). In this cohort of Caucasian American adults, associations between carbohydrate nutrition and cancer varied by cancer site. Healthier low-GI carbohydrate foods may prevent adiposity-related cancers among women, but these findings require confirmation in a larger sample.Consumption of whole grains and cereal fiber in relation to cancer risk: A systematic review of longitudinal studies
AbstractMakarem, N., Nicholson, J. M., Bandera, E. V., McKeown, N. M., & Parekh, N. (2016). Nutrition Reviews, 74(6), 353-373. 10.1093/nutrit/nuw003AbstractContext: Evidence from previous reviews is supportive of the hypothesis that whole grains may protect against various cancers. However, the reviews did not report risk estimates for both whole grains and cereal fiber and only case-control studies were evaluated. It is unclear whether longitudinal studies support this conclusion. Objective: To evaluate associations between whole grains and cereal fiber in relation to risk of lifestyle-related cancers data from longitudinal studies was evaluated. Data Sources: The following 3 databases were systematically searched: PubMed, EMBASE, and Cochrane CENTRAL. Study Selection: A total of 43 longitudinal studies conducted in Europe and North America that reported multivariable-adjusted risk estimates for whole grains (n=14), cereal fiber (n=23), or both (n=6) in relation to lifestyle-related cancers were included. Data Extraction: Information on study location, cohort name, follow-up duration, sample characteristics, dietary assessment method, risk estimates, and confounders was extracted. Data Synthesis: Of 20 studies examining whole grains and cancer, 6 studies reported a statistically significant 6%-47% reduction in risk, but 14 studies showed no association. Of 29 studies examining cereal fiber intake in relation to cancer, 8 showed a statistically significant 6%-49% reduction in risk, whereas 21 studies reported no association. Conclusions: This systematic review concludes that most studies were suggestive of a null association. Whole grains and cereal fiber may protect against gastrointestinal cancers, but these findings require confirmation in additional studies.Explaining racial/ethnic dietary patter ns in relation to type 2 diabetes: An analysis of NHAN ES 2007-2012
AbstractNowlin, S. Y., Cleland, C. M., Vadiveloo, M., Parekh, N., Melkus, G. D. E., & Hagan, H. (2016). Ethnicity and Disease, 26(4), 529-536. 10.18865/ed.26.4.529AbstractObjective: The purpose of this article is to examine sociodemographic and health behavior factors associated with dietary intake as measured by the healthy eating index (HEI-2010) for persons with and without diabetes (T2D). Design: A secondary data analysis of three NHANES data cycles spanning 2007-2012. Multiple linear regression assessed racial/ ethnic differences in HEI-2010 scores in those without T2D, with T2D, and with undiagnosed T2D. Participants: The sample included nonpregnant adults aged ≥20 years who had two days of reliable dietary recall data. Outcome Measures: Total scores for the HEI-2010. Results: For those without T2D, there was a significant association between race/ ethnicity and HEI score, with non-Hispanic Blacks achieving significantly lower scores than their non-Hispanic White counterparts. Differences in HEI-2010 score were also associated with age, sex, smoking status and time spent in the United States. Racial/ ethnic differences in dietary patterns were present, but not significant in those with undiagnosed or diagnosed T2D. Conclusions: Racial/ethnic disparities in dietary patterns are present in individuals without T2D, but differences are not statistically significant in those with undiagnosed or diagnosed T2D. Non-Hispanic Blacks without T2D received significantly lower HEI-2010 scores than non-Hispanic Whites. Further research is necessary to determine whether or not similarities in dietary intake across racial/ethnic groups with T2D will be reflected in diabetes-related health outcomes in this population.