By Dr. Theresa MacLean

The following classes of pharmaceutical medications have various effects upon the nutritional status of the user.  Over time, these effects can become very significant as to the comfort level and even the survival of the person taking them.  Compare these effects with those described by your physician and inform him or her of any concerns you might have.

Loop diuretics (furosemide)

• Excretion of sodium, chloride, potassium, hydrogen ions, calcium, magnesium, ammonium bicarbonate, and possibly phosphate is enhanced.

• After 4 weeks of furosemide use, thiamin concentrations and transketolase activity were significantly reduced.

Thiazide diuretics (hydrochlorthiazide)

• Excretion of sodium, chloride, potassium, bicarbonate, magnesium, phosphate, and iodine are enhanced.

• Calcium excretion is decreased.

Triamterene-containing diuretics (Dyazide, Dyrenium, Maxzide)

• Triamterene is potassium-sparing;  supplementation could result in potassium overload.

• Folic acid deficiency is possible.

Histamine H2 antagonists (Tagamet, Zantac, Pepcid, Axid)

• Reduction of gastric acid secretion, resulting in poor digestion of protein.

• Decreased vitamin B12.  Gastric acid is required for B12 absorption.

• Tagamet inhibits cytochrome P-450 pathways.

Biquanides (Metforman)

• Interferes with glucose absorption.

• Decreases absorption of B12.

Potassium Chloride

Interferes with the absorption of B12.

Sulfasalazine

Interferes with folic acid metabolism.

Oral contraceptives

• Oral contraceptives have significantly increased plasma Vitamin A levels.  This is thought to be mediated by steroid-induced alterations in the rate of retinal-binding protein synthesis and release;  depletion of reserves may result.

• Vitamin B6 deficiencies due to alteration in B6 and tryptophan metabolism.

• Interference with folate absorption.

• Reduced serum B12 levels.

• Increased serum copper as a result of increased plasma ceruloplasm;  clinical importance has not been determined.

• Increased serum iron and increased total iron-binding capacity, along with increased incidence of iron deficiency anemia.

• Increased serum magnesium and zinc;  clinical importance has not been determined.

Corticosteroids (hyrocortisone, prednisone, dexamethasone, etc.)

• Corticosteroids increase the rate of Vitamin A transport from the liver, resulting in elevated serum levels and depletion of reserves.

• Negative nitrogen balance due to increased protein catabolism.

• Increased calcium excretion (increased catabolism).

• Sodium retention (mineralocorticoid activity).

• Increased potassium excretion ( sodium is exchanged for potassium).

• May deplete Vitamins B6, B12, and folic acid.

• May deplete Vitamin D3.

Bile acid sequestrants (Questran)

• Interference with absorption of fats and fat-soluble vitamins.

• Enhanced absorption of chloride ions in exchange for bicarbonate ions, which may lead to acidosis.

• Increased urinary calcium excretion.

• Increased urinary magnesium excretion.

• Altered absorption of phosphate and nitrogen.

• Vitamin K deficiency.

• Reduced folic acid absorption.

• Reduced absorption of Vitamin E and iron are possible.

HMG-CoA reductase inhibitors (Zocor, Mevacor, Pravachol)

• Block the biosynthesis of Coenzyme Q-10.

Levodopa

• Pyridoxine reverses the effects of levodopa, although this does not occur when levodopa is given with carbadopa.  (Pyridoxine stimulates decarboxylation of levodopa in the periphery;  carbadopa inhibits decarboxylation.)

Phenytoin (Dilantin)

• Folate deficiency — Increased folate catabolism or utilization as a result of enzyme induction is considered to be the mechanism.  However, supplementation may decrease the effectiveness of the phenytoin.

• Interference with Vitamin D metabolism.

Folic acid analogs (methotrexate, pyrimethamine, trimethoprin)

• These antagonists inhibit the enzyme dihydrofolate reductase, which can lead to a functional folate deficiency.  Supplementation can antagonize the effects of these drugs.

NSAIDS (Motrin, Naprosyn, Tylenol, ASA, etc.)

• Reduce nighttime melatonin secretion (related to prostaglandin inhibition).

Isoniazid

• Increases excretion of pyridoxine into the urine, resulting in deficiency.

• Inhibits the tryptophan-to-niacin pathway, resulting in increased need for niacin and tryptophan.