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Betaine supplementation decreases post-methionine hyperhomocysteinemia in chronic renal failure

David O McGregor, Warwick J Dellow, Richard A Robson, Michael Lever, Peter M George, Stephen T Chambers
Kidney international 2002 61(3):1040-1046

Bibliography

PubMed
PMID 11849459
Funding
Funding was not specified in the indexed record or accessible funding metadata.
Competing interests
A competing-interest declaration was not available in the indexed record or accessible disclosure metadata.

Study snapshot

DesignRandomized crossover controlled trial
ModelHuman participants
Sample36 patients with chronic renal failure
InterventionBetaine 4 g/day added to folic acid 5 mg and pyridoxine 50 mg/day
Duration3 months per treatment
EndpointsFasting and post-load homocysteine; Lipids

What the study showed, in plain terms

Published in 2002, this source examined homocysteine, methylation and vascular function. Design: Randomized crossover controlled trial. Sample/model: 36 patients with chronic renal failure. The exposure or intervention was Betaine 4 g/day added to folic acid 5 mg and pyridoxine 50 mg/day. Follow-up or treatment period: 3 months per treatment.

Adding betaine reduced post-methionine-load homocysteine by approximately 18% but did not further lower fasting homocysteine. Small lipid increases were observed.

Disease-specific biochemical outcomes; no cardiovascular or renal clinical benefit was demonstrated.

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Continue with TMG and Homocysteine: How Much Can Betaine Lower It?

Key findings

  • Adding betaine reduced post-methionine-load homocysteine by approximately 18% but did not further lower fasting homocysteine.
  • Small lipid increases were observed.
  • The recorded outcome domains were Fasting and post-load homocysteine; Lipids.
  • The result applies to the tested exposure: Betaine 4 g/day added to folic acid 5 mg and pyridoxine 50 mg/day; 3 months per treatment.

What this study can and cannot tell us

  • Disease-specific biochemical outcomes; no cardiovascular or renal clinical benefit was demonstrated.
  • An individual controlled trial must be interpreted alongside its comparator, sample size, endpoint selection and independent replication. It does not validate a different commercial formulation or a general longevity claim.
  • Source basis: Indexed abstract and bibliographic data. Missing method details, funding information or participant denominators are not inferred.

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