Some evidence indicates that other vitamins and minerals, such as folic acid1 and copper,2 require the presence of stomach acid for optimal absorption. Long-term use of H-2 blockers may therefore promote a deficiency of these nutrients. Individuals requiring long-term use of H-2 blockers may therefore benefit from a multiple vitamin/mineral supplement.
Some evidence indicates that other vitamins and minerals, such as folic acid3 and copper,4 require the presence of stomach acid for optimal absorption. Long-term use of H-2 blockers may therefore promote a deficiency of these nutrients. Individuals requiring long-term use of H-2 blockers may therefore benefit from a multiple vitamin/mineral supplement.
NSAIDs cause gastrointestinal (GI) irritation, bleeding, and iron loss.5 Iron supplements can cause GI irritation.6 However, iron supplementation is sometimes needed in people taking NSAIDs if those drugs have caused enough blood loss to lead to iron deficiency. If both iron and ibuprofen are prescribed, they should be taken with food to reduce GI irritation and bleeding risk.
Stomach acid is needed for the vitamin B12 in food to be absorbed. H-2 blocker drugs reduce stomach acid and may therefore inhibit absorption of the vitamin B12 naturally present in food. However, the vitamin B12 found in supplements does not depend on stomach acid for absorption.7 Lab tests can determine vitamin B12 levels in people.
The flavonoids found in the extract of licorice (Glycyrrhiza glabra) known as DGL (deglycyrrhizinated licorice) are helpful for avoiding the irritating actions NSAIDs have on the stomach and intestines. One study found that 350 mg of chewable DGL taken together with each dose of aspirin reduced gastrointestinal bleeding caused by the aspirin.9 DGL has been shown in controlled human research to be as effective as drug therapy (cimetidine) in healing stomach ulcers.10
In healthy people, a magnesium hydroxide/aluminum hydroxide antacid, taken with famotidine, decreased famotidine absorption by 20–25%.11 People can avoid this interaction by taking famotidine two hours before or after any aluminum/magnesium-containing antacids. Some magnesium supplements such as magnesium hydroxide are also antacids.
Ibuprofen may cause sodium and water retention.13 It is healthful to reduce dietary salt intake by eliminating table salt and heavily salted foods.
White willow bark (Salix alba) contains salicin, which is related to aspirin. Both salicin and aspirin produce anti-inflammatory effects after they have been converted to salicylic acid in the body. The administration of salicylates like aspirin to individuals taking oral NSAIDs may result in reduced blood levels of NSAIDs.14 Though no studies have investigated interactions between white willow bark and NSAIDs, people taking NSAIDs should avoid the herb until more information is available.
Ibuprofen has caused kidney dysfunction and increased blood potassium levels, especially in older people.15 People taking ibuprofen should not supplement potassium without consulting with their doctor.
Supplementation may enhance the anti-inflammatory effects of NSAIDs while reducing their ulcerogenic effects. One study found that when various anti-inflammatory drugs were chelated with copper, the anti-inflammatory activity was increased.16 Animal models of inflammation have found that the copper chelate of aspirin was active at one-eighth the effective amount of aspirin. These copper complexes are less toxic than the parent compounds as well.
1. Russell RM, Krasinski SD, Samloff IM. Correction of impaired folic acid (Pte Glu) absorption by orally administered HCl in subjects with gastric atrophy. Am J Clin Nutr 1984;39:656.
2. Tompsett SL. Factors influencing the absorption of iron and copper from the alimentary tract. Biochem J 1940;34:961-9.
3. Russell RM, Krasinski SD, Samloff IM. Correction of impaired folic acid (Pte Glu) absorption by orally administered HCl in subjects with gastric atrophy. Am J Clin Nutr 1984;39:656.
4. Tompsett SL. Factors influencing the absorption of iron and copper from the alimentary tract. Biochem J 1940;34:961-9.
5. Bjarnason I, Macpherson AJ. Intestinal toxicity of non-steroidal anti-inflammatory drugs. Pharmacol Ther 1994;62:145-57.
6. Threlkeld DS, ed. Blood Modifiers, Iron-Containing Products. In Facts and Comparisons Drug Information. St. Louis, MO: Facts and Comparisons, Jun 1998, 62-9a.
7. Aymard JP, Aymard B, Netter P, et al. Haematological adverse effects of histamine H2-receptor antagonists.Med Toxicol Adverse Drug Exp 1988;3:430-48.
8. Aymard JP, Aymard B, Netter P, et al. Haematological adverse effects of histamine H2-receptor antagonists.Med Toxicol Adverse Drug Exp 1988;3:430-48.
9. Rees WDW, Rhodes J, Wright JE, et al. Effect of deglycyrrhizinated liquorice on gastric mucosal damage by aspirin. Scand J Gastroenterol 1979;14:605-7.
10. Morgan AG, McAdam WAF, Pacsoo C, Darnborough A. Comparison between cimetidine and Caved-S in the treatment of gastric ulceration, and subsequent maintenance therapy. Gut 1982;23:545-51.
11. Bachmann KA, Sullivan TJ, Jauregui L, et al. Drug interactions of H2-receptor antagonists. Scand J Gastroenterol Suppl 1994;206:14-9.
12. Kellermann AJ, Kloft C. Is there a risk of bleeding associated with standardized Ginkgo biloba extract therapy? A systematic review and meta-analysis. Pharmacotherapy 2011;31:490-502.
13. Threlkeld DS, ed. Central Nervous System Drugs, Nonsteroidal Anti-Inflammatory Agents. In Facts and Comparisons Drug Information. St. Louis, MO: Facts and Comparisons, Mar 1993, 251j-1l.
14. Olin BR, ed. Central Nervous System Drugs, Analgesics and Anti-inflammatory Drugs, Nonsteroidal Anti-inflammatory Agents, In Drug Facts and Comparisons. St. Louis, MO: Facts and Comparisons, 1993, 1172-90.
15. Bailie GR. Acute renal failure. In Applied Therapeutics: The Clinical Use of Drugs, 6th ed. Vancouver, WA: Applied Therapeutics, 1995, 29-33.
16. Sorenson JRJ. Copper chelates as possible active forms of the antiarthritic agents. J Medicinal Chem 1976;19:135-48.
Last Review: 04-29-2014
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