Medicine (Baltimore). 2026 Aug 14;105(33):e50195. doi: 10.1097/MD.0000000000050195.
ABSTRACT
Stroke remains a leading cause of global morbidity and mortality. While dietary flavonoids are recognized for their antioxidant and anti-inflammatory properties, their specific association with stroke prevalence in the U.S. population is not well-established. This study aimed to investigate the association between the intake of dietary flavonoid subclasses and stroke prevalence using a nationally representative U.S. adult cohort, and to elucidate potential mechanisms through network pharmacology. We analyzed data from 12,424 participants from the National Health and Nutrition Examination Survey (NHANES) 2007-2010 and 2017-2018. Multivariable logistic regression, restricted cubic splines (RCS), and subgroup analyses were employed to assess the associations between flavonoid intake and stroke. A higher intake of anthocyanins was inversely associated with stroke prevalence (Quartile 4 vs 1: OR = 0.69; 95% CI: 0.48, 0.98; p for trend = 0.047), exhibiting a significant nonlinear relationship (p for nonlinearity = 0.018). Subgroup analysis revealed this protective association was particularly evident in non-hypertensive individuals. Furthermore, higher flavanone intake was significantly associated with a lower stroke prevalence in females (Q4 vs 1: OR = 0.49; 95% CI: 0.30, 0.82; p for trend = 0.04). Mechanistically, network pharmacology identified 193 anthocyanin-stroke and 89 flavanone-stroke overlapping targets. Pathway enrichment analysis indicated these targets are significantly involved in key biological processes, including the lipid and atherosclerosis, MAPK, and PI3K-Akt signaling pathways. Anthocyanins were strongly linked to inflammation-modulating pathways (e.g., TNF and IL-17 signaling), while flavanones were associated with pathways related to diabetic complications and cellular stress responses. Higher dietary intake of anthocyanins and flavanones is associated with a lower prevalence of stroke in U.S. adults, with effects potentially moderated by hypertension status and sex. These associations are supported by mechanistic data implicating the modulation of critical inflammation, atherosclerosis, and metabolic signaling pathways.
PMID:42601753 | DOI:10.1097/MD.0000000000050195