In a recent review published in nutrientsIn , researchers identified 45 drug-nutrient interactions (DNI) that alter micronutrient status, focusing specifically on how acetylsalicylic acid (ASA) and warfarin affect patients through various mechanisms. ) was discussed.
These comprehensively address the complexity of DNI, highlight the influence of factors such as polymorphisms, gut microbiota, and dietary components, and provide practical recommendations for effectively managing DNI in vulnerable populations. information to clinicians.
study: Potential drug and nutrient interactions of 45 vitamins, minerals, trace elements, and related dietary compounds with acetylsalicylic acid and warfarin – a review of the literature. Image credit: AleksSafronov/Shutterstock.com
background
Although DNIs are less studied than drug-drug interactions, they are still clinically relevant. Drug therapy can directly or indirectly affect micronutrient status through physicochemical, physiological, or pathophysiological mechanisms.
These interactions include bioinactivation, changes in absorption, efficacy, or excretion. Medications can compete with micronutrients, induce physiological changes, and indirectly affect health.
Although DNI can be beneficial or harmful, it is often underreported and large-scale comprehensive studies in this area are lacking.
Researchers in this article review the DNI of ASA (an antiplatelet drug) and warfarin (an anticoagulant), drugs widely used in cardiology, which can affect patients through various mechanisms. May affect micronutrient status.
Micronutrient “hidden hunger”
“Hidden hunger” refers to micronutrient deficiencies. Micronutrients are essential for basic physiological functions, such as vitamins (water-soluble and fat-soluble), minerals, and trace elements.
The Institute of Medicine recommends dietary reference intakes for these nutrients and additional compounds such as taurine and ergothioneine, which are essential for the proper functioning of longevity proteins.
ASA and DNI
The interactions between ASA and various micronutrients are complex and multifaceted, with both reported and suspected interactions. Although some interactions between ASA and micronutrients are well established, others remain uncertain and require further research.
Reported ASA interactions include increased urinary excretion of thiamine, modulation of niacin flush, changes in renal excretion and serum concentrations of folate, potential effects on cobalamin absorption, and effects on vitamin C absorption and excretion. It has been.
Fat-soluble vitamins such as tocopherols/tocotrienols may potentiate the antiplatelet effects of ASA and protect the stomach, whereas minerals such as sodium show decreased excretion at high doses of ASA and may be less effective in blood pressure regulation. may have an impact.
Trace elements such as iron may be affected and increase the risk of anemia, while related dietary compounds such as taurine may enhance the antiplatelet effects of ASA and protect the stomach.
However, some interactions remain questionable, such as interactions with riboflavin, pantothenic acid, and retinol. Niacin exhibits antiplatelet effects, but the clinical significance remains unclear.
Similarly, minerals such as phosphorus, calcium, magnesium, potassium, copper, zinc, selenium, and chromium have uncertain interactions with ASA. Related dietary compounds such as lycopene, α-carotene, β-carotene, β-cryptoxanthin, and astaxanthin do not show definitive interactions.
Additionally, some micronutrients such as biotin, chloride, sulfur, iodine, manganese, molybdenum, fluoride, arsenic, boron, nickel, silicon, and vanadium have not been reported to interact with ASA.
The effects of ASA on mitochondrial oxidative phosphorylation raise concerns about potential metabolic misuse of micronutrients, but clinical relevance in humans requires further evaluation.
Warfarin and DNI
Although some interactions between warfarin and certain nutrients have been reported, other interactions remain questionable or unstudied. Niacin is associated with synergistic effects of water-soluble vitamins, in some cases significantly increasing the international normalized ratio (INR).
Folate deficiency can occur by avoiding foods rich in vitamin K and can affect the health of patients. There is conflicting evidence regarding the interaction of high doses of vitamin C with warfarin, so careful monitoring is required.
Among the fat-soluble vitamins, retinol and tocopherols/tocotrienols interact with warfarin, causing adverse events such as bleeding and arterial calcification. Vitamin D status may influence the anticoagulant effect of warfarin and the risk of arterial calcification.
Additionally, magnesium is associated with stabilization of INR levels and may influence the outcome of warfarin treatment. Low-vitamin K foods that are high in potassium may pose a risk for patients with chronic kidney disease due to hyperkalemia.
Astaxanthin has been reported to interact with warfarin, but the exact mechanism remains unclear. Several nutrients, such as riboflavin, cobalamin, and calcium, and trace elements, such as iron, lutein, zeaxanthin, lycopene, β-carotene, and β-cryptoxanthin, have a clinically significant relationship with warfarin, based on available evidence. Does not show any interaction.
Further research is needed to fully understand the potential interactions of warfarin with other elements such as thiamine, pantothenic acid, sulfur, manganese, and molybdenum, but data are currently lacking.
conclusion
By moving towards predictive, preventive, and personalized care models, clinicians can leverage omics technologies to detect early signs of disease and stratify risk for DNI.
These findings highlight the importance of considering dietary factors and nutrient intake in patients receiving ASA or warfarin treatment to optimize treatment outcomes and minimize adverse events.
However, this review is limited by the lack of a uniform methodology, small scale of human cohort studies, reliance on animal models, and lack of data on specific micronutrient interactions.
In conclusion, due to the interaction between nutrient intake, individual physiology, and drug use, DNI should be considered in clinical practice, especially in vulnerable populations. It highlights the need for an individualized approach to nutritional assessment and management.
