Adverse Effects of Medications on Micronutrient Status: From Evidence to Guidelines.

Recent dietary reference intake workshops focusing on nutrient requirements in chronic disease populations have called attention to the potential adverse effects of chronic medication use on micronutrient status. Although this topic is mostly ill defined in the literature, several noteworthy drug-nutrient interactions (DNIs) are of clinical and public health significance. The purpose of this narrative review is to showcase classic examples of DNIs and their impact on micronutrient status, including those related to antidiabetic, anticoagulant, antihypertensive, antirheumatic, and gastric acid-suppressing medications. Purported DNIs related to other drug families, while relevant and worthy of discussion, are not included. Unlike previous publications, this review is primarily focused on DNIs that have sufficient evidence supporting their inclusion in US Food and Drug Administration labeling materials and/or professional guidelines. While the evidence is compelling, more high-quality research is needed to establish clear and quantitative relationships between chronic medication use and micronutrient status.

The Impacts of Slc19a3 Deletion and Intestinal SLC19A3 Insertion on Thiamine Distribution and Brain Metabolism in the Mouse.

The Thiamine Transporter 2 (THTR2) encoded by SLC19A3 plays an ill-defined role in the maintenance of tissue thiamine, thiamine monophosphate, and thiamine diphosphate (TDP) levels. To evaluate the impact of THTR2 on tissue thiamine status and metabolism, we expressed the human SLC19A3 transgene in the intestine of total body Slc19a3 knockout (KO) mice. Male and female wildtype (WT) and transgenic (TG) mice were fed either 17 mg/kg (1×) or 85 mg/kg (5×) thiamine hydrochloride diet, while KOs were only fed the 5× diet. Thiamine vitamers in plasma, red blood cells, duodenum, brain, liver, kidney, heart, and adipose tissue were measured. Untargeted metabolomics were performed on the brain tissues of groups with equivalent plasma thiamine. KO mice had ~two- and ~three-fold lower plasma and brain thiamine levels than WT on the 5× diet. Circulating vitamers were sensitive to diet and equivalent in TG and WT mice. However, TG had 60% lower thiamine but normal brain TDP levels regardless of diet, with subtle differences in the heart and liver. The loss of THTR2 reduced levels of nucleic acid and amino acid derivatives in the brain. Therefore, mutation or inhibition of THTR2 may alter the brain metabolome and reduce the thiamine reservoir for TDP biosynthesis.