Derivation and Validation of a Food Inflammatory Index Calibrated to Brazilian Dietary Patterns in Adults After Acute...

The inflammatory potential of the diet modulates immune pathways implicated in residual cardiovascular risk after acute myocardial infarction (AMI). Because dietary patterns differ across populations, culturally calibrated tools are needed to accurately assess the inflammatory properties of habitual intake. We aimed to derive a food group-based Food Inflammatory Index (FII), anchored to a multimarker inflammatory panel, in Brazilian adults undergoing secondary prevention and to evaluate its construct validity.

This cross-sectional analysis included baseline data from 170 adults enrolled two to six months after AMI in a dietary intervention trial. Dietary intake was assessed using a validated food frequency questionnaire and aggregated into 31 food groups. Seven plasma biomarkers (interleukin (IL)-2, IL-4, IL-6, IL-10, tumor necrosis factor alpha (TNF-α), interferon gamma (IFN-γ), and C-reactive protein (CRP)) were standardized and combined into a composite inflammatory gradient. Reduced-rank regression identified dietary patterns that maximized the explained variance in this gradient. Backward stepwise linear regression was then applied to derive food group weights for the FII, with higher scores indicating a more pro-inflammatory dietary profile. Biological coherence was examined using correlation and multivariable regression analyses.

Participants were predominantly male (74.1%, n = 126), with a mean age of 58.6 ± 9 years and a mean body mass index (BMI) of 28.5 ± 4.4 kg/m². The median FII was 1.82 (interquartile range (IQR): 0.74-3.16). Weak but statistically significant correlations were observed between the FII and TNF-α (ρ = 0.16, p = 0.035) and IFN-γ (ρ = 0.15, p = 0.049); however, these associations were no longer significant after adjustment for age, sex, BMI, physical activity, and energy intake.

An empirical FII calibrated to Brazilian dietary patterns in adults after AMI was derived using a multibiomarker inflammatory approach. The index showed modest evidence of biological coherence through weak unadjusted associations with selected inflammatory biomarkers, but these associations were not sustained after multivariable adjustment. Therefore, findings should be interpreted as exploratory and hypothesis-generating. Further longitudinal and external validation studies are necessary to determine the reproducibility, predictive validity, and clinical applicability of the proposed index.