ReviewJournal of inherited metabolic disease1997
The role of vitamins in the pathogenesis and treatment of hyperhomocyst(e)inaemia.
Review in Journal of inherited metabolic disease, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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4 citing papers in PubMed, 51 citations in OpenAlex.
- Cognitive capacity in amyotrophic lateral sclerosis: the value of diagnostic markers in cerebrospinal fluid and the influence of nutrition and pulmonary function.Brain communications · 2025Article
- Scientific Opinion on Dietary Reference Values for cobalamin (vitamin B12).EFSA journal. European Food Safety Authority · 2015Article
- Influence of the consumption of fruits and vegetables on the nutritional status of a group of institutionalized elderly persons in the Madrid region.The journal of nutrition, health & aging · 2010Article
- The C677T mutation of the 5,10-methylenetetrahydrofolate reductase gene is a moderate risk factor for spina bifida in Italy.Journal of medical genetics · 1998Article
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1 author at 1 institution in 1 country.
Funding
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Abstract
The relation between vitamin nutritional status and circulating plasma homocyst(e)ine concentrations is reviewed. Several studies have shown that plasma concentrations of folate, vitamin B12 and pyridoxal 5'-phosphate are inversely associated with plasma total homocyst(e)ine concentrations. Of the three vitamins mentioned above, folate is the most powerful homocyst(e)ine lowering agent and a daily supplement of 0.65 mg/day is sufficient to normalize moderate hyperhomocyst(e)inaemia in most individuals with normal renal function. In patients with severe renal failure, high doses of folate are required to treat hyperhomocyst(e)inaemia. Folic acid is ineffective in reducing plasma total homocyst(e)ine concentrations in patients with a vitamin B12 deficiency. Vitamin B6 supplementation has no effect on fasting plasma total homocyst(e)ine concentrations, but attenuates the post-methionine load plasma homocyst(e)ine peak. At least one report has shown that some individuals appear to be unable to maintain plasma total homocyst(e)ine concentrations in the normal reference range by a dietary intake of folic acid only. Long-term vitamin supplementation may be indicated in these individuals. However, the clinical benefit of vitamin supplementation has not yet been demonstrated and controlled trials are urgently required.
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