Mol Nutr Food Res. 2025 Sep 7:e70252. doi: 10.1002/mnfr.70252. Online ahead of print.
ABSTRACT
The relationship between dietary biotin intake and cognitive function remains unclear. This study explores the association between biotin and dementia, and the mediating role of inflammation indicators. Dietary biotin intake was assessed via the 24-h recall questionnaire. Dementia outcomes were identified through “algorithmically defined outcomes,” identified through an algorithm integrating self-reports, hospital admissions, and death certificate records. Participants aged 40-69 with complete biotin and baseline data were included. During a 11.25-year median follow-up, 1256 incident dementia cases occurred among 122 959 participants. Cox proportional hazards models showed that compared to the lowest biotin intake (Q1), biotin reduced the risk of all-cause dementia (HR: 0.75[0.64,0.88] p < 0.001 for Q2; HR: 0.68[0.58,0.81] p < 0.001 for Q3; HR: 0.67[0.56,0.81] p < 0.001 for Q4) and Alzheimer’s disease (AD) (HR: 0.74[0.58,0.96] p = 0.026 for Q2; HR: 0.65[0.49,0.85] p = 0.002 for Q3). Restricted cubic splines (RCSs) revealed an “L-shaped” nonlinear relationship between biotin and all-cause dementia (p nonlinear < 0.001) and Alzheimer’s dementia (p nonlinear = 0.004) and exhibited the saturation effect. Multicategorical mediation analysis suggested that systemic immune-inflammation index (SII), a composite inflammatory marker calculated from platelet, neutrophil, and lymphocyte counts, mediated the association partially. Subgroup and sensitivity analyses confirmed stable results. Higher dietary biotin intake may reduce the risk of dementia.
PMID:40914826 | DOI:10.1002/mnfr.70252
