A pilot study measuring thiamine diphosphate (TDP), erythrocyte transketolase activity (TKT), and activity coefficients (ETKAC) in adults with and without type 2 diabetes (T2D) found that these three measures frequently disagree. Whole-blood TDP did not differ between T2D and control groups, yet absolute TKT activities varied sixfold across participants. Critically, ETKAC-defined deficiency appeared in individuals whose TDP fell within the reference range. Magnesium supplementation of erythrocyte lysates raised TKT activity, implicating cofactor availability beyond TDP as a functional determinant. In UK National Diet and Nutrition Survey data, higher thiamine intake strongly predicted lower ETKAC-defined non-sufficiency, yet substantial insufficiency persisted even with adequate reported intake.
This finding challenges the clinical assumption that a normal blood TDP level rules out functionally significant thiamine insufficiency — a particularly important point given that thiamine deficiency underpins serious conditions including Wernicke encephalopathy and beriberi. The TDP-glucose association observed exclusively in T2D participants adds an intriguing metabolic thread, though causality cannot be established here. The magnesium interaction deserves attention: magnesium deficiency, itself common in T2D, may silently impair thiamine-dependent metabolism even when TDP appears adequate. Limitations are substantial — this is a small pilot cohort with no sample-size disclosure in the abstract, and observational design precludes causal conclusions. As a preprint posted to medRxiv and not yet peer-reviewed, these findings must be treated as preliminary. Still, the evidence that single-marker thiamine assessment may systematically misclassify status is clinically meaningful and warrants larger, prospective validation.
