Niyati Parekh
Niyati Parekh
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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
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. (n.d.).Publication year
2016Journal title
Ethnicity and DiseaseVolume
26Issue
4Page(s)
529-536AbstractObjective: 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.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. (n.d.).Publication year
2016Journal title
BMC GastroenterologyVolume
16Issue
1AbstractBackground: 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. (n.d.).Publication year
2015Journal title
Journal of HypertensionVolume
33Issue
11Page(s)
2223-2230AbstractBackground: 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. (n.d.).Publication year
2015Journal title
Cancer Causes and ControlVolume
26Issue
2Page(s)
277-286AbstractPurpose: 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. (n.d.).Publication year
2015Journal title
Journal of NutritionVolume
145Issue
3Page(s)
555-563AbstractBackground: 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. (n.d.).Publication year
2015Journal title
American Journal of Preventive MedicineVolume
49Issue
6Page(s)
974-979Greater 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. (n.d.).Publication year
2015Journal title
Journal of NutritionVolume
145Issue
3Page(s)
564-571Insulin 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. (n.d.).Publication year
2015Journal title
Cancer Causes and ControlVolume
26Issue
8Page(s)
1189-1195AbstractPurpose: 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. (n.d.).Publication year
2015Journal title
Topics in Clinical NutritionVolume
30Issue
4Page(s)
289-301AbstractAdult 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. (n.d.).Publication year
2014Journal title
British Journal of NutritionVolume
112Issue
9Page(s)
1562-1574AbstractVaried 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. (n.d.).Publication year
2014Journal title
Cancer Causes and ControlVolume
25Issue
2Page(s)
161-170AbstractPurpose: 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. (n.d.).Publication year
2014Journal title
Breast Cancer Research and TreatmentVolume
143Issue
3Page(s)
551-570AbstractEffective 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. (n.d.).Publication year
2014Journal title
British Journal of NutritionVolume
111Issue
11Page(s)
2010-2023AbstractThe 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. (n.d.).Publication year
2014Journal title
British Journal of NutritionVolume
111Issue
4Page(s)
724-734AbstractFew 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. (n.d.).Publication year
2013Journal title
Unknown JournalVolume
109Issue
9Page(s)
1557-1572AbstractDietary 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. (n.d.).Publication year
2013Journal title
Cancer Causes and ControlVolume
24Issue
7Page(s)
1427-1436AbstractConsumption 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. (n.d.).Publication year
2013Journal title
Cancer Causes and ControlVolume
24Issue
3Page(s)
577-585AbstractObjectives: 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.Dietary fat in breast cancer survival
AbstractMakarem, N., Chandran, U., Bandera, E. V., & Parekh, N. (n.d.).Publication year
2013Journal title
Annual Review of NutritionVolume
33Page(s)
319-348AbstractLaboratory evidence suggests a plausible role for dietary fat in breast cancer pathophysiology. We conducted a systematic literature review to assess the epidemiological evidence on the impact of total dietary fat and fat subtypes, measured pre- and/or postcancer diagnosis, in relation to breast cancer-specific and all-cause mortality among breast cancer survivors. Studies were included if they were in English, had a sample size ≥200, and presented the hazard ratio/rate ratio for recurrence, disease-specific mortality, or all-cause mortality (n = 18). Although the results are mixed, most studies suggested that higher saturated fat intake prediagnosis was associated with increased risk of breast cancer-specific and all-cause mortality. Postdiagnostic trans fat intake was associated with a 45% and 78% increased risk of all-cause mortality. Higher monounsaturated fat intake before and after diagnosis was generally associated with increased risk of all-cause and breast cancer-specific mortality, albeit the majority of the studies were statistically nonsignificant. Two studies evaluating omega-3 fat intake suggested an inverse association with all-cause mortality. Although there were too few studies on fat subtypes to draw definitive conclusions, high consumption of saturated fat may exert a detrimental effect on breast cancer-specific and all-cause mortality, whereas omega-3 fat may be beneficial. The inconsistent and limited evidence warrants research to assess the impact of consumption of fat subtypes on breast cancer recurrence and mortality.Life course epidemiology in nutrition and chronic disease research: A timely discussion
AbstractParekh, N., & Zizza, C. (n.d.).Publication year
2013Journal title
Advances in NutritionVolume
4Issue
5Page(s)
551-553AbstractHumans are exposed to a complex and changing combination of nutritional factors during the life course, necessitating their investigation over time to capture "critical periods of sensitivity." A life course approach provides a framework to examine trajectories and long-term effects of nutritional and other risk factors, particularly the role of timing, accumulation, and temporal relationships of these exposures in relation to chronic disease development. Currently, most epidemiologic research does not sufficiently address this issue in relation to disease etiology. Although applying a life course approach would augment our knowledge about disease development, this approach presents major challenges in designing, conducting, and analyzing studies. A scientific symposium was held that reviewed emerging research and discussed methodological concerns in applying the life course approach. The research presented at this session focused on the role of timing, with the pre- and postnatal and pubertal periods as critical windows of exposure for chronic conditions. Methodological issues and complexities in analyzing and selecting datasets were highlighted. This symposium elucidated unique study designs and statistical strategies to demonstrate the strengths of this methodology, and served as a catalyst for new research in the area of nutrition and chronic disease epidemiology.Metabolic dysregulation of the insulin-glucose axis and risk of obesity-related cancers in the Framingham heart study-offspring cohort (1971-2008)
AbstractParekh, N., Lin, Y., Vadiveloo, M., Hayes, R. B., & Lu-Yao, G. L. (n.d.).Publication year
2013Journal title
Cancer Epidemiology Biomarkers and PreventionVolume
22Issue
10Page(s)
1825-1836AbstractBackground: Obesity-related dysregulation of the insulin-glucose axis is hypothesized in carcinogenesis. We studied impaired fasting glucose (IFG) and other markers of insulin-glucose metabolism in the Framingham Heart Study-Offspring Cohort, which uniquely tracks these markers and cancer>37 years. Methods: Participants were recruited between 1971 and 1975 and followed until 2008 (n = 4,615; mean age 66.8 years in 2008). Serum glucose, insulin, and hemoglobin A1c were determined from fasting blood in quartannual exams. Lifestyle and demographic information was self-reported. HRs and 95% confidence intervals (CI) of cancer risk were computed using time-dependent survival analysis (SASv9.3), while accounting for temporal changes for relevant variables. Results: We identified 787 obesity-related cancers, including 136 colorectal, 217 breast, and 219 prostate cancers. Absence versus presence of IFG 10 to 20 years and 20-years before the event or last follow-up was associated with 44% (95% CI, 1.15-1.79) and 57% (95% CI, 1.17-2.11) increased risk of obesity-related cancers, respectively. When time-dependent variables were used, after adjusting for age, sex, smoking, alcohol, and body mass index, IFG was associated with a 27% increased risk of obesity-related cancer (HR = 1.27; CI, 1.1- 1.5). Associations were stronger in smokers (HR=1.41; CI, 1.13-1.76). Increased risk was noted among persons with higher insulin (HR = 1.47; CI, 1.15-1.88) and hemoglobin A1c (HR = 1.54; CI, 1.13-2.10) for the highest (≤5.73%) versus lowest (≤5.25%) category. A>2-fold increase in colorectal cancer risk was observed for all blood biomarkers of insulin-glucose metabolism, particularly with earlier IFG exposure. Nonsignificant increased risk of breast and prostate cancer was observed for blood biomarkers. Conclusions: Earlier IFG exposure (>10 years before) increased obesity-related cancer risk, particularly for colorectal cancer. Impact: Our study explicitly recognizes the importance of prolonged IFG exposure in identifying links between glucose dysregulation and obesity-related cancers.Sugary food and beverage consumption and epithelial ovarian cancer risk: A population-based case-control study
AbstractKing, M. G., Olson, S. H., Paddock, L., Chandran, U., Demissie, K., Lu, S. E., Parekh, N., Rodriguez-Rodriguez, L., & Bandera, E. V. (n.d.).Publication year
2013Journal title
BMC CancerVolume
13AbstractBackground: Ovarian cancer is the deadliest gynecologic cancer in the US. The consumption of refined sugars has increased dramatically over the past few decades, accounting for almost 15% of total energy intake. Yet, there is limited evidence on how sugar consumption affects ovarian cancer risk.Methods: We evaluated ovarian cancer risk in relation to sugary foods and beverages, and total and added sugar intakes in a population-based case-control study. Cases were women with newly diagnosed epithelial ovarian cancer, older than 21 years, able to speak English or Spanish, and residents of six counties in New Jersey. Controls met same criteria as cases, but were ineligible if they had both ovaries removed. A total of 205 cases and 390 controls completed a phone interview, food frequency questionnaire, and self-recorded waist and hip measurements. Based on dietary data, we computed the number of servings of dessert foods, non-dessert foods, sugary drinks and total sugary foods and drinks for each participant. Total and added sugar intakes (grams/day) were also calculated. Multiple logistic regression models were used to estimate odds ratios and 95% confidence intervals for food and drink groups and total and added sugar intakes, while adjusting for major risk factors.Results: We did not find evidence of an association between consumption of sugary foods and beverages and risk, although there was a suggestion of increased risk associated with sugary drink intake (servings per 1,000 kcal; OR=1.63, 95% CI: 0.94-2.83).Conclusions: Overall, we found little indication that sugar intake played a major role on ovarian cancer development.The "sweet" truth about cancer.
Parekh, N. (n.d.).Publication year
2013Journal title
Oncology Nutrition ConnectionVolume
21Issue
2Page(s)
13-17Dietary fiber intake and colorectal cancer risk: Weighing the evidence from epidemiologic studies
AbstractRomaneiro, S., & Parekh, N. (n.d.).Publication year
2012Journal title
Topics in Clinical NutritionVolume
27Issue
1Page(s)
41-47AbstractThe 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. (n.d.).Publication year
2012Journal title
Journal of ObesityVolume
2012AbstractLongitudinal 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. (n.d.).Publication year
2012Journal title
Annual Review of NutritionVolume
32Page(s)
311-342AbstractAlthough 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.