Whitney L. Do

Ms. Whitney L. Do

Emory University
orcid

Research Focus & Metrics

Academic Career Length

11Years (2016-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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23 February 2016 in Sustainability
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Journal Article
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DGDavid Gustafson
David Gustafson
AGAlona Gutman
Alona Gutman
WDWhitney L. Do
Whitney L. Do
ADAdam Drewnowski
Adam Drewnowski
JFJessica Fanzo
Jessica Fanzo
JIJohn Ingram
John Ingram
Sustainability considerations have been absent from most food security assessments conducted to date, despite the tremendous economic, environmental, and social implications of meeting accelerating food demand in the face of water shortages and climate change. In addition, previous food security work has generally focused only on achieving adequate calories, rather than addressing dietary diversity and micronutrient adequacy, both of which are critical to maintaining a healthy overall nutritional status. In response to the limitations of previous assessments, a new methodology is proposed here based on the concept of “sustainable nutrition security” (SNS). This novel assessment methodology is intended to remedy both kinds of deficiencies in the previous work by defining seven metrics, each based on a combination of multiple indicators, for use in characterizing sustainable nutrition outcomes of food systems: (1) food nutrient adequacy; (2) ecosystem stability; (3) food affordability and availability; (4) sociocultural wellbeing; (5) food safety; (6) resilience; and (7) waste and loss reduction. Each of the metrics comprises multiple indicators that are combined to derive an overall score (0–100). A novel SNS assessment methodology based on these metrics can be deployed by decision-makers and investors to set meaningful goals, track progress, and evaluate the potential impact of food system interventions intended to improve sustainability and human nutrition outcomes.

23 December 2020 in International Journal of Epidemiology
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Journal Article
Open access
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WDWhitney L. Do
Whitney L. Do
EWEric A Whitsel
Eric A Whitsel
RCRicardo Costeira
Ricardo Costeira
OMOlatz M Masachs
Olatz M Masachs
CRCaroline I Le Roy
Caroline I Le Roy
KCKaren N Conneely
Karen N Conneely
Diet quality is a risk factor for chronic disease and mortality. Differential DNA methylation across the epigenome has been associated with chronic disease risk. Whether diet quality is associated with differential methylation is unknown. This study assessed whether diet quality was associated with differential DNA methylation measured across 445 548 loci in the Women’s Health Initiative (WHI) and the TwinsUK cohort. The discovery cohort consisted of 4355 women from the WHI. The replication cohort consisted of 571 mono- and dizygotic twins from the TwinsUK cohort. DNA methylation was measured in whole blood using the Illumina Infinium HumanMethylation450 Beadchip. Diet quality was assessed using the Alternative Healthy Eating Index 2010 (AHEI-2010). A meta-analysis, stratified by study cohort, was performed using generalized linear models that regressed methylation on AHEI-2010, adjusting for cell composition, chip number and location, study characteristics, principal components of genetic relatedness, age, smoking status, race/ethnicity and body mass index (BMI). Statistical significance was defined as a false discovery rate < 0.05. Significant sites were tested for replication in the TwinsUK cohort, with significant replication defined by P < 0.05 and a consistent direction. Diet quality was significantly associated with differential DNA methylation at 428 cytosine-phosphate-guanine (CpG) sites in the discovery cohort. A total of 24 CpG sites were consistent with replication in the TwinsUK cohort, more than would be expected by chance (P = 2.7x10-4), with one site replicated in both the blood and adipose tissue (cg16379999 located in the body of SEL1L). Diet quality was associated with methylation at 24 CpG sites, several of which have been associated with adiposity, inflammation and dysglycaemia. These findings may provide insight into pathways through which diet influences chronic disease.

18 July 2021 in Obesity Reviews
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Journal Article
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WDWhitney L. Do
Whitney L. Do
JGJazib Gohar
Jazib Gohar
LMLauren E. McCullough
Lauren E. McCullough
KGKarla I. Galaviz
Karla I. Galaviz
KCKaren N. Conneely
Karen N. Conneely
KNK. M. Venkat Narayan
K. M. Venkat Narayan

22 December 2021 in Clinical Epigenetics
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Journal Article
Open access
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WDWhitney L. Do
Whitney L. Do
SNSteve Nguyen
Steve Nguyen
JYJie Yao
Jie Yao
XGXiuqing Guo
Xiuqing Guo
EWEric A. Whitsel
Eric A. Whitsel
KNK. M. Venkat Narayan
K. M. Venkat Narayan
Background: Body mass index (BMI), a well-known risk factor for poor cardiovascular outcomes, is associated with differential DNA methylation (DNAm). Similarly, metabolic health has also been associated with changes in DNAm. It is unclear how overall metabolic health outside of BMI may modify the relationship between BMI and methylation profiles, and what consequences this may have on downstream cardiovascular disease. The purpose of this study was to identify cytosine-phosphate-guanine (CpG) sites at which the association between BMI and DNAm could be modified by overall metabolic health. Results: The discovery study population was derived from three Women’s Health Initiative (WHI) ancillary studies (n = 3977) and two Atherosclerosis Risk in Communities (ARIC) ancillary studies (n = 3520). Findings were validated in the Multi-Ethnic Study of Atherosclerosis (MESA) cohort (n = 1200). Generalized linear models regressed methylation β values on the interaction between BMI and metabolic health Z score (BMI × MHZ) adjusted for BMI, MHZ, cell composition, chip number and location, study characteristics, top three ancestry principal components, smoking, age, ethnicity (WHI), and sex (ARIC). Among the 429,566 sites examined, differential associations between BMI × MHZ and DNAm were identified at 22 CpG sites (FDR q < 0.05), with one site replicated in MESA (cg18989722, in the TRAPPC9 gene). Three of the 22 sites were associated with incident coronary heart disease (CHD) in WHI. For each 0.01 unit increase in DNAm β value, the risk of incident CHD increased by 9% in one site and decreased by 6–10% in two sites over 25 years. Conclusions: Differential associations between DNAm and BMI by MHZ were identified at 22 sites, one of which was validated (cg18989722) and three of which were predictive of incident CHD. These sites are located in several genes related to NF-kappa-B signaling, suggesting a potential role for inflammation between DNA methylation and BMI-associated metabolic health.

23 October 2020 in Nutrients
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Journal Article
Open access
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WDWhitney L. Do
Whitney L. Do
KBKai M. Bullard
Kai M. Bullard
ASAryeh D. Stein
Aryeh D. Stein
MAMohammed K. Ali
Mohammed K. Ali
KNK M Venkat Narayan
K M Venkat Narayan
KSKaren R. Siegel
Karen R. Siegel
In this study, we examined the associations between the consumption of foods derived from crops subsidized under the 2008 United States (US) Farm Bill and cardiometabolic risk factors and whether the magnitude of these associations has changed since the 2002 US Farm Bill. Four federal databases were used to estimate daily consumption of the top seven subsidized commodities (corn, soybeans, wheat, rice, sorghum, dairy, and livestock) and to calculate a subsidy score (0–1 scale) for Americans’ daily dietary intake during 2009–2014, with a higher score indicative of a higher proportion of the diet derived from subsidized commodities. The cardiometabolic risk factors included obesity, abdominal adiposity, hypertension, dyslipidemia, and dysglycemia. Linear and logistic regression models were adjusted for age, sex, race/ethnicity, the poverty–income ratio, the smoking status, educational attainment, physical activity, and daily calorie intake. During 2009–2014, adults with the highest subsidy score had higher probabilities of obesity, abdominal adiposity, and dysglycemia compared to the lowest subsidy score. After the 2002 Farm Bill (measured using data from 2001–2006), the subsidy score decreased from 56% to 50% and associations between consuming a highly-subsidized diet and dysglycemia did not change (p = 0.54), whereas associations with obesity (p = 0.004) and abdominal adiposity (p = 0.002) significantly attenuated by more than half. The proportion of calories derived from subsidized food commodities continues to be associated with adverse cardiometabolic risk factors, though the relationship with obesity and abdominal adiposity has weakened in recent years.

31 March 2020 in Breast Cancer Research and Treatment
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Journal Article
Closed access
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WDWhitney L. Do
Whitney L. Do
KCKaren Conneely
Karen Conneely
SGSheryl Gabram-Mendola
Sheryl Gabram-Mendola
UKUma Krishnamurti
Uma Krishnamurti
ODOlivia D’aNgelo
Olivia D’aNgelo
LMLauren E. McCullough
Lauren E. McCullough