Serum 25-Hydroxyvitamin D Concentration and Auditory P300 Characteristics in Healthy Young Adults: A Cross-Sectional...

Vitamin D receptors and metabolizing enzymes are expressed in brain regions involved in attention and memory, but evidence relating serum 25-hydroxyvitamin D (25(OH)D) to objective electrophysiological indices of cognition in healthy young adults is limited. We examined the associations between serum 25(OH)D and auditory P300 latency and amplitude.

This cross-sectional study prospectively enrolled 40 healthy adults aged 18-40 years: 20 with vitamin D nonsufficiency (≤30 ng/mL) and 20 with sufficiency (>30 ng/mL). Total serum 25(OH)D was measured by quantitative delayed one-step competitive chemiluminescent microparticle immunoassay on the ARCHITECT i2000SR platform (Abbott Diagnostics, Abbott Park, IL). Auditory P300 was recorded at Cz using a two-stimulus oddball paradigm. Prespecified primary analyses used independent-samples t-tests. Secondary analysis used analysis of covariance adjusted for age, sex, and body mass index (BMI). Pearson correlation and multivariable linear regression treated serum 25(OH)D as a continuous exposure in exploratory analyses. Holm-Bonferroni correction was applied separately within the primary, secondary, correlation, and regression analysis families.

The groups were comparable in age, sex distribution, height, weight, and BMI. Primary comparisons were not statistically significant. Mean latency was 326.88 ± 9.75 ms in the nonsufficient group and 321.46 ± 8.06 ms in the sufficient group (mean difference: 5.42 ms, 95% confidence interval (CI): -0.31 to 11.14). Mean amplitude was 5.87 ± 0.69 and 6.17 ± 0.53 µV, respectively (mean difference: -0.294 µV, 95% CI: -0.686 to 0.098). The secondary adjusted latency contrast was nominally significant (adjusted mean difference: 5.94 ms, 95% CI: 0.003-11.88; unadjusted p = 0.0499) but did not remain significant after Holm correction (adjusted p = 0.100). In exploratory analyses, serum 25(OH)D correlated inversely with latency (r = -0.450; unadjusted p = 0.004; Holm-adjusted p = 0.007), and its adjusted regression coefficient was -0.437 ms/ng/mL (95% CI: -0.695 to -0.178; unadjusted p = 0.002; Holm-adjusted p = 0.003). The adjusted amplitude coefficient was not significant (Holm-adjusted p = 0.140).

The prespecified group comparisons did not provide statistically conclusive evidence of different P300 latency or amplitude according to the operational vitamin D threshold. The nominal secondary latency contrast did not remain significant after multiplicity correction. The continuous inverse latency association remained statistically significant after Holm correction but was exploratory and does not establish causality, a neurophysiological cutoff, or a rationale for screening or supplementation. Larger prospective studies are needed.