Racial and ethnic disparities in predictors of glycemia

a moderated mediation analysis of inflammation-related predictors of diabetes in the NHANES 2007–2010

Sarah Nowlin, Charles M. Cleland, Niyati Parekh, Holly Hagan, Gail D'Eramo Melkus

Research output: Contribution to journalArticle

Abstract

Background/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.

Original languageEnglish (US)
Article number56
JournalNutrition and Diabetes
Volume8
Issue number1
DOIs
StatePublished - Dec 1 2018

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Nutrition Surveys
Type 2 Diabetes Mellitus
Inflammation
Hemoglobins
C-Reactive Protein
Body Mass Index
Diet
Glucose

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

Cite this

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title = "Racial and ethnic disparities in predictors of glycemia: a moderated mediation analysis of inflammation-related predictors of diabetes in the NHANES 2007–2010",
abstract = "Background/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.",
author = "Sarah Nowlin and Cleland, {Charles M.} and Niyati Parekh and Holly Hagan and {D'Eramo Melkus}, Gail",
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T2 - a moderated mediation analysis of inflammation-related predictors of diabetes in the NHANES 2007–2010

AU - Nowlin, Sarah

AU - Cleland, Charles M.

AU - Parekh, Niyati

AU - Hagan, Holly

AU - D'Eramo Melkus, Gail

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N2 - Background/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.

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