Association Between Dietary Patterns and Subgingival Microbiota: Results From the Oral Infections, Glucose Intolerance, and Insulin Resistance Study (ORIGINS)

ObjectiveTo study the association between dietary patterns and subgingival microbiota.MethodsParticipants (n = 651) who were enrolled in the Oral Infections, Glucose Intolerance, and Insulin Resistance Study (ORIGINS) with subgingival plaque sampling (n = 890 plaques) and a dietary assessment were included. 16S rRNA gene amplicon sequences of subgingival plaque from sites with either probing depth <4 or ≥4 mm were processed separately and used to obtain α‐diversity metrics (Faith, Shannon, Simpson, Observed) and taxa ratios (Red Complex to Corynebacterium [RCLR], Treponema to Corynebacterium [TCLR], and Treponema to Neisseria [TNLR]). Food frequency questionnaires (FFQs) were processed to calculate Alternate Healthy Eating Index (AHEI) and A Priori Diet Quality Score (APDQS) scores. Mixed regression models examined the mean levels of microbial metrics across quartiles of diet quality. Means ± standard errors are reported along with p‐values.ResultsIn multivariable models assessing the association between diet scores and α‐diversity metrics, higher AHEI values were significantly associated with lower Faith (p‐value = 0.01) and Observed (p‐value = 0.04) diversity values; similar findings were observed for APDQS (p‐value = 0.01, p‐value = 0.04). In multivariable models assessing the association between diet scores (AHEI and APDQS) and taxa ratios (RCLR, TCLR and TNLR), as the AHEI quartile increased, all taxa ratios decreased significantly as follows: −1.06 ± 0.093 in Q1 to −1.34 ± 0.099 in Q4 (RCLR), −0.43 ± 0.077 in Q1 to −0.64 ± 0.083 in Q4 (TCLR) and −0.09 ± 0.083 in Q1 to −0.38 ± 0.089 in Q4 (TNLR), respectively. In contrast, as the APDQS quartiles increased, only TNLR decreased significantly from −0.08 ± 0.085 in Q1 to −0.34 ± 0.091 in Q4.ConclusionDiets rich in fruits, vegetables, whole grains and other nutritionally rich plant foods are associated with lower oral microbial diversity and favourable ratios of pathogenic to commensal microbiota.