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Folate/Nutrient Depletion:- AlcoholAlcohol: Based on secondary sources, excessive use of alcohol may increase the requirement for folic acid.
- Aminosalicylic acidAminosalicylic acid: Based on secondary sources, aminosalicylic acid may reduce dietary folate absorption, worsening the folate deficiency often seen with active tuberculosis, or preventing its reversal during treatment. Megaloblastic anemia occurs rarely and usually when there are other contributing factors, such as concurrent vitamin B12 malabsorption. Patients being treated for tuberculosis may be advised to take folic acid supplements if their dietary folate intake is low.
- AntacidsAntacids: Based on secondary sources, chronic use of large doses of antacids may reduce folic acid absorption, but this is likely only significant if dietary folate intake is very low. Based on secondary sources, folic acid absorption from the small intestine is optimal at pH 5.5 to 6.0.
- AntibioticsAntibiotics: Based on secondary sources, antibiotic therapy may disrupt the normal GI flora, interfering with the absorption of folic acid.
- AntiepilepticsAntiepileptics: In humans, oxcarbazepine did not decrease folic acid levels (276).
- AspirinAspirin: Based on secondary sources, aspirin may decrease serum folate levels, especially with chronic large doses. It is suggested that folate is just being redistributed in the body rather than an actual folate deficiency.
- CholestyramineCholestyramine: Based on secondary sources, cholestyramine may reduce folic acid absorption. It may lower serum and red blood cell folate levels in children taking large doses for several months.
- ColestipolColestipol: Based on secondary sources, colestipol (Colestid®) may interfere with absorption of folic acid, and reduced serum folate levels may occur.
- CycloserineCycloserine: Based on secondary sources, cycloserine may reduce serum folate levels, and rare cases of megaloblastic anemia have occurred.
- DiureticsDiuretics: Based on secondary sources, diuretics may increase excretion of folic acid. Reduced red blood cell folate levels, possibly contributing to increased homocysteine levels, were found in one group of people taking diuretics for six months or longer.
- Conjugated estrogensConjugated estrogens: Based on secondary sources, reduced serum and red blood cell folate levels may occur in some women taking conjugated estrogens (Premarin®), but this is unlikely in women with adequate dietary folate intake.
- Folic acid antagonistsFolic acid antagonists: Folic acid antagonists include capecitabine, trimethoprim, triamterene, carbamazepine, chloramphenicol, phenytoin, phenobarbital, primidone, pyrimethamine, and fosphenytoin. These agents may reduce serum folate levels, but megaloblastic anemia has not been reported. Concerns due to low folate levels may occur in pregnant women.
- H2 BlockersH2 Blockers: Based on secondary sources, chronic use of large doses of antacids may reduce folic acid absorption, but this is likely only significant if dietary folate intake is very low. Based on secondary sources, folic acid absorption from the small intestine is optimal at pH 5.5 to 6.0. The increased pH associated with the use of H2 blockers [such as cimetidine (Tagamet®), famotidine (Pepcid®), nizatidine (Axid®), and ranitidine (Zantac®)] may therefore reduce folic acid absorption.
- HypoglycemicsHypoglycemics: Based on secondary sources, metformin use might reduce folate levels.
- Methylprednisolone sodium succinate (Solu-Medrol®)Methylprednisolone sodium succinate (Solu-Medrol®): Based on secondary sources, reduced serum folate levels have been noted in people with MS after treatment with methylprednisolone sodium succinate (Solu-Medrol®).
- Non-steroidal anti-inflammatory agentsNon-steroidal anti-inflammatory agents: Based on secondary sources, folate-dependent enzymes have been inhibited in laboratory experiments by certain NSAIDs [ibuprofen (Advil®, Motrin®, Nuprin®), naproxen (Anaprox®, Aleve®), indomethacin (Indocin®), and sulindac (Clinoril®)].
- Oral contraceptivesOral contraceptives: Based on secondary sources, severe clinical and hematological manifestations of folate deficiency occurred in a previously healthy, fully breastfed, 10 month-old infant whose mother took oral contraceptives (271). Based on secondary sources, oral contraceptives may impair folate metabolism producing depletion, but the effect is unlikely to cause anemia or megaloblastic changes.
- Pancreatic extractsPancreatic extracts: Based on secondary sources, reduced folate levels may occur in some people taking pancreatic extracts (such as Pancrease®, Cotazym®, Viokase®, Creon®, Ultrase®) possibly due to reduced absorption. Folate levels should be checked in patients taking pancreatic enzymes for prolonged periods.
- Pemetrexed disodiumPemetrexed disodium: Pemetrexed is an anti-folate agent (333). Folic acid is suggested along with pemetrexed disodium (334; 335).
- PentamidinePentamidine: Based on secondary sources, pentamidine may decrease serum folate levels, and megaloblastic bone marrow changes may occur rarely with prolonged intravenous pentamidine.
- Proton pump intihibitorsProton pump intihibitors: Based on secondary sources, chronic use of large doses of antacids may reduce folic acid absorption, but this is likely only significant if dietary folate intake is very low. Based on secondary sources, folic acid absorption from the small intestine is optimal at pH 5.5 to 6.0. Proton pump inhibitors may also affect folic acid.
- SulfasalazineSulfasalazine: Based on secondary sources, sulfasalazine inhibits absorption and metabolism of folic acid. Patients on chronic sulfasalazine therapy may be advised to increase their dietary folate intake and to take a supplement if they have any other condition, which could also contribute to deficiency.
- TobaccoTobacco: Smoking resulted in decreased folic acid levels (340; 341; 342).
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Copyright © 2011 Natural Standard (www.naturalstandard.com)
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The information in this monograph is intended for informational purposes only, and is meant to help users better understand health concerns. Information is based on review of scientific research data, historical practice patterns, and clinical experience. This information should not be interpreted as specific medical advice. Users should consult with a qualified healthcare provider for specific questions regarding therapies, diagnosis and/or health conditions, prior to making therapeutic decisions.
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