deficiency
17 interactions related to deficiency
prednisone + vitamin d
Glucocorticoids such as prednisone speed up the breakdown of vitamin D and blunt vitamin D-driven calcium absorption at the gut, which contributes to bone loss. Population data link oral steroid use to a higher rate of severe vitamin D deficiency, so vitamin D plus adequate calcium is a standard part of long-term steroid care.
carbamazepine + biotin
Carbamazepine gradually lowers biotin (vitamin B7) status by reducing intestinal absorption, increasing urinary loss, and accelerating breakdown of the vitamin. The effect is biomarker-level and well documented over decades; frank deficiency and serious adult harm are uncommon.
phenobarbital + vitamin d
Phenobarbital is a strong inducer of liver enzymes that speed the breakdown of vitamin D, so long-term use can lower 25-hydroxyvitamin D and, over months to years, contribute to softened bones (osteomalacia in adults, rickets in children) and higher fracture risk. Children and older or housebound adults are most vulnerable. The drop in vitamin D is well documented; some experimental work also suggests phenobarbital may slow vitamin D activation, though that mechanism rests on animal and cell studies. Have vitamin D and bone-related labs reviewed and discuss ongoing vitamin D with your doctor or pharmacist.
famotidine + vitamin b12
Long-term daily famotidine lowers stomach acid, which can modestly reduce absorption of vitamin B12 bound to food. Supplemental and fortified-food B12 are unaffected because they do not require stomach acid for absorption.
esomeprazole + vitamin b12
Esomeprazole and other PPIs suppress stomach acid, which can reduce absorption of food-bound vitamin B12 over long-term use; crystalline B12 in supplements is unaffected.
vitamin a + zinc
Zinc is required for the liver to synthesize retinol-binding protein, the carrier that moves vitamin A from liver stores into the bloodstream. When zinc is low, circulating vitamin A can stay low even though liver stores are adequate, and in deficient populations supplementing the two together corrects vitamin A status more reliably than vitamin A alone.
alcohol + folate
Chronic alcohol use causes folate deficiency through several mechanisms: it inhibits the reduced folate carrier in the intestine (blocking absorption), reduces the liver's uptake and storage of folate, and increases urinary folate loss. Folate depletion in turn accelerates alcohol-induced liver injury and disrupts one-carbon metabolism and DNA methylation.
alcohol + zinc
Chronic alcohol use lowers the body's zinc through reduced intake, impaired intestinal absorption, increased urinary loss, and altered zinc transporters (notably ZIP14). The relationship is bidirectional: zinc deficiency in turn worsens alcohol-related liver injury by weakening the intestinal barrier, allowing more bacterial endotoxin to leak into the portal blood, and reducing the liver's antioxidant defenses.
phenytoin + folate
Phenytoin and folate interact in both directions: long-term phenytoin lowers folate through enzyme induction and reduced absorption, while supplemental folate can speed phenytoin clearance and lower its blood level enough to allow seizures to return in some people. The interaction is real but monitorable, so changes should be coordinated with your neurologist rather than avoided.
phenytoin + vitamin d
Phenytoin induces the liver enzymes that break down vitamin D, accelerating clearance of 25-hydroxyvitamin D and lowering circulating levels over time. The downstream result can be reduced calcium absorption, a compensatory rise in parathyroid hormone, and an increased risk of softened bones (osteomalacia) and fractures with long-term use.
omeprazole + vitamin b12
Omeprazole suppresses gastric acid, which is needed to release vitamin B12 from dietary proteins before it can bind intrinsic factor and be absorbed. With long-term use this can lower serum B12 and, over time, contribute to deficiency. Supplemental (crystalline) B12 is not affected because it does not depend on stomach acid.
coffee + vitamin b1
Coffee and tea were historically labeled antithiamine beverages, but later biochemistry walked the claim back: chlorogenic and caffeic acids do not destroy thiamine under physiological conditions, and the real activity comes from polyphenol oxidation products and tannins, which are lower in coffee than tea. The net effect on thiamine status is modest and unlikely to matter for well-nourished people; it becomes relevant only on a marginal diet or in groups already prone to deficiency.
valproate + biotin
Valproate appears to lower biotinidase activity and may impair mitochondrial biotin handling, contributing to subnormal biotin status that has been linked to the drug's characteristic hair thinning and brittle nails. Case reports describe biotin supplementation reversing valproate-related hair loss, though the underlying biotin-status studies are mixed.
carbamazepine + vitamin d
Carbamazepine activates the pregnane X receptor and induces the liver enzymes (including CYP3A4 and CYP24A1) that break down vitamin D, accelerating the clearance of 25-hydroxyvitamin D into inactive metabolites. A meta-analysis and observational studies consistently show lower 25(OH)D in long-term carbamazepine users, along with a secondary-hyperparathyroidism pattern and reduced bone density that raises fracture risk over years of therapy.
smoking + vitamin b12
Cigarette smoke can lower usable vitamin B12 by converting active coenzyme forms to inactive cyanocobalamin and by impairing gastric absorption, creating a low-grade nutritional draw rather than a dangerous reaction.
alcohol + thiamine
Alcohol depletes thiamine (vitamin B1) at multiple levels — reducing its absorption from the gut, impairing the liver's ability to convert it to its active form, and increasing how much is lost in urine. In heavy drinkers this can lead to Wernicke encephalopathy, a neurologic emergency, which if untreated may progress to Korsakoff syndrome, a chronic and often irreversible memory disorder.
alcohol + magnesium
Alcohol acts as an acute magnesium diuretic, increasing urinary magnesium excretion within hours of intake. Regular and heavy drinking can deplete body magnesium stores through renal wasting combined with reduced intestinal absorption and poor diet, and low magnesium is common in chronic alcohol-use disorder.