Lower Diet Quality Associated with Subclinical Gastrointestinal Inflammation in Healthy United States Adults

Abstract

Background: Higher diet quality has been associated with lower risk of developing inflammatory bowel disease, but associations between diet and gastrointestinal (GI) inflammation in healthy adults prior to disease onset are understudied.

Objectives: The purpose of this project was to examine associations between reported dietary intake and markers of GI inflammation in a healthy adult human cohort.

Methods: In a cross-sectional observational trial of 358 healthy adults, participants completed ≤3 unannounced 24-h dietary recalls using the Automated Self-Administered Dietary Assessment Tool and a Block 2014 Food Frequency Questionnaire to assess recent and habitual intake, respectively. Those who provided a stool sample were included in this analysis. Inflammation markers from stool, including calprotectin, neopterin, and myeloperoxidase, were measured by ELISA along with LPS-binding protein from plasma.

Results: Recent and habitual fiber intake was negatively correlated with fecal calprotectin concentrations (n = 295, P = 0.011, 0.009). Habitual soluble fiber intake was also negatively correlated with calprotectin (P = 0.01). Recent and habitual legume and vegetable intake was negatively correlated with calprotectin (P = 0.013, 0.026, 0.01, 0.009). We observed an inverse correlation between recent Healthy Eating Index (HEI) scores and calprotectin concentrations (n = 295, P = 0.026). Dietary Inflammatory Index scores were calculated and positively correlated with neopterin for recent intake (n = 289, P = 0.015). When participants with clinically elevated calprotectin were excluded, recent and habitual fiber, legume, vegetable, and fruit intake were negatively correlated with calprotectin (n = 253, P = 0.00001, 0.0002, 0.045, 0.001, 0.009, 0.001, 0.004, 0.014). Recent total HEI score was inversely correlated with subclinical calprotectin (P = 0.003).

Conclusions: Higher diet quality may be protective against GI inflammation even in healthy adults. This trial was registered at clinicaltrials.gov as NCT02367287.

Keywords: diet; humans; inflammation; inflammatory bowel disease; vegetables.

FIGURE 1

CONSORT of distributions included in this analysis based on completion of dietary data and availability of plasma and stool samples.

FIGURE 2

Density distributions of GI inflammation markers (A) calprotectin, (B) myeloperoxidase, (C) neopterin, and (D) LBP. Red dotted lines indicate threshold for clinical inflammation for calprotectin (100 μg/g) and myeloperoxidase (2000 ng/g). GI, gastrointestinal.

FIGURE 3

Partial regressions of (A) transformed fecal calprotectin and (B) transformed neopterin with significant predictors. (A) The y-axis is the residuals of transformed fecal calprotectin given covariates—sex, age, BMI–(holding them constant) and x-axis is the residuals of total Healthy Eating Index score (holding covariates constant). (B) The y-axis is the residuals of transformed fecal neopterin given covariates—sex, age, BMI–(holding them constant) and x-axis is the residuals of total Dietary Inflammatory Index score (holding covariates constant). Blue line shows best fit and gray shading shows standard error (95% confidence interval). BMI, body mass index; DII, Dietary Inflammatory Index; HEI, Healthy Eating Index.

FIGURE 4

Partial regression plots of the residuals of transformed fecal “subclinical” calprotectin given covariates—sex, age, BMI (holding them constant)—and the residuals of reported dietary intake (holding covariates constant) where the reported dietary intake is (A) habitual fiber intake, (B) habitual legume intake, (C) habitual total vegetable intake, or (D) recent total HEI score. Only participants with subclinical fecal calprotectin (n = 253) are included in this analysis. Blue line shows best fit and gray shading shows standard error (95% confidence interval). BMI, body mass index; HEI, Healthy Eating Index.