Longevity & AgingArticle de rechercheAccès libre

Pro-Inflammatory Diet Accelerates Sarcopenia in Older Polish Adults

A new study links high dietary inflammatory index scores to faster muscle loss, weaker grip, and slower walking speed in adults over 60.

mercredi 30 septembre 2026 0 vue
Publié dans Sci Rep
Elderly person's hands gripping a dynamometer beside a colorful plate of vegetables and fish in a clinic setting

Résumé

Researchers studied 121 Polish adults aged 60–96, classifying them as sarcopenic, probably sarcopenic, or healthy using the EWGSOP2 algorithm. They calculated each participant's Energy-adjusted Dietary Inflammatory Index (E-DII) from 24-hour dietary recalls and measured inflammatory biomarkers including IL-1β, IL-6, TNFα, CRP, and cell-free DNA (cfDNA). An E-DII threshold of 2.283 predicted sarcopenia with 70.6% sensitivity and 75.6% specificity. Higher E-DII correlated significantly with slower gait speed and worse 6-minute walk test results. Combining E-DII with cfDNA achieved the best diagnostic discrimination (AUC = 0.805), outperforming conventional cytokine markers alone. The findings suggest that a pro-inflammatory diet compounds age-related muscle decline and that dietary modification could be a meaningful intervention target.

Résumé détaillé

Sarcopenia—the progressive loss of skeletal muscle mass, strength, and function—affects roughly 18.6% of older Polish adults and dramatically shortens survival. Chronic low-grade inflammation driven by poor diet and physical inactivity is increasingly recognized as a key driver of this condition, yet few studies have quantified dietary inflammatory potential alongside both physical performance metrics and a broad panel of inflammatory biomarkers in the same cohort.

This prospective study enrolled 121 community-dwelling adults aged 60–96 from a University of the Third Age program in Poland. Participants were categorized as sarcopenic (n=38), probably sarcopenic (n=38), or non-sarcopenic (n=45) according to the EWGSOP2 clinical algorithm, which incorporates handgrip strength, appendicular skeletal muscle mass index (ASMI), and physical performance via the 6-minute walk test (6MWT). Dietary intake was assessed through two 24-hour dietary recalls (one weekday, one weekend day), and the Energy-adjusted Dietary Inflammatory Index (E-DII) was calculated per 1,000 kcal to correct for total energy intake. Blood biomarkers included IL-1β, IL-6, TNFα, CRP, albumin, and cell-free DNA (cfDNA).

The optimal E-DII cut-off for sarcopenia risk was 2.283, yielding an AUC of 0.734, sensitivity of 70.6%, and specificity of 75.6% (p<0.001). Sarcopenic individuals had significantly higher E-DII scores than non-sarcopenic peers, indicating more pro-inflammatory dietary patterns. Critically, E-DII correlated inversely with gait speed (rs = −0.502, p=0.001) and 6MWT distance (rs = −0.496, p=0.001), linking diet quality directly to functional decline. When E-DII was combined with cfDNA in a diagnostic model, AUC improved to 0.805 with 79.7% classifier accuracy—outperforming models using conventional cytokines (IL-1β, IL-6, TNFα), which achieved acceptable but lower discrimination (AUC 0.7–0.8). CRP and albumin ratio also showed utility as accessible inflammatory markers.

The study highlights cfDNA as a particularly promising emerging biomarker: cellular damage from chronic inflammation releases cfDNA into circulation proportionally to inflammation severity, and its combination with dietary inflammatory scoring provides a novel, higher-accuracy sarcopenia prediction tool. This is among the first studies to directly connect E-DII with cfDNA levels in any population.

Caveats include the cross-sectional dietary assessment relying on a single-day recall per occasion, limiting precision; the predominantly female sample (91 of 121 participants) reduces generalizability to men; and the study's observational design precludes causal inference. Despite these limitations, the results support dietary intervention—specifically shifting toward anti-inflammatory eating patterns—as a plausible strategy to slow sarcopenia progression in aging populations.

Principales conclusions

  • E-DII threshold of 2.283 predicted sarcopenia with AUC 0.734, 70.6% sensitivity, and 75.6% specificity.
  • Higher E-DII scores correlated strongly with slower gait speed (rs = −0.502) and shorter 6-minute walk distance (rs = −0.496).
  • Combining E-DII with cell-free DNA (cfDNA) achieved the best diagnostic accuracy (AUC = 0.805, 79.7% classifier accuracy).
  • cfDNA outperformed conventional cytokines IL-1β, IL-6, and TNFα as a complement to dietary inflammatory scoring.
  • Sarcopenia prevalence in this Polish cohort aligned with national estimates of ~18.6%, with 31% classified as fully sarcopenic.

Méthodologie

Prospective observational study of 121 Polish adults aged 60–96 classified by EWGSOP2 sarcopenia criteria. Dietary intake was assessed via two 24-hour recalls; E-DII was calculated per 1,000 kcal. Inflammatory biomarkers (IL-1β, IL-6, TNFα, CRP, cfDNA) were measured from blood samples; ROC curve analysis determined diagnostic cut-offs.

Limites de l'étude

Dietary assessment relied on only two 24-hour recalls per participant, which may not capture habitual intake. The cohort was predominantly female and drawn from a single community program, limiting broader generalizability. The cross-sectional design cannot establish causality between diet inflammation and sarcopenia progression.

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