Tier 4 — mechanistic

The contrasting relationships between betaine and homocysteine in two clinical cohorts are associated with plasma lipids and drug treatments

Michael Lever, Peter M George, Wendy Atkinson, Jane L Elmslie, Sandy Slow, Sarah L Molyneux, Richard W Troughton, A Mark Richards, Christopher M Frampton, Stephen T Chambers
PloS one 2012 7(3):e32460

Bibliography

PubMed
PMID 22396767
PubMed Central
PMC3292573
Funding
Funding was not specified in the indexed record or accessible funding metadata.
Competing interests
Reported disclosure: Competing Interests: The authors have declared that no competing interests exist.

Study snapshot

DesignComparative observational cohorts
ModelHuman participants
Sample415 post-coronary urine samples and 158 lipid-clinic patients
InterventionMeasured betaine status and related metabolites; no randomized TMG treatment
DurationCross-sectional clinical sampling
EndpointsUrinary betaine; Homocysteine; Lipids

What the study showed, in plain terms

Published in 2012, this source examined human observational and biomarker research. Design: Comparative observational cohorts. Sample/model: 415 post-coronary urine samples and 158 lipid-clinic patients. The exposure or intervention was Measured betaine status and related metabolites; no randomized TMG treatment. Follow-up or treatment period: Cross-sectional clinical sampling.

The relationship between urinary betaine loss and homocysteine differed with lipid levels and medication context.

Observational exposure analysis: residual confounding and reverse causation remain possible. Associations do not establish that betaine supplementation causes the same outcome.

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Key findings

  • The relationship between urinary betaine loss and homocysteine differed with lipid levels and medication context.
  • The recorded outcome domains were Urinary betaine; Homocysteine; Lipids.
  • The exposure was observed rather than assigned as an isolated supplement treatment.

What this study can and cannot tell us

  • Observational exposure analysis: residual confounding and reverse causation remain possible. Associations do not establish that betaine supplementation causes the same outcome.
  • Confounding, dietary patterns, illness, medication use and reverse causation can influence an association. Blood or dietary concentrations do not identify the effect of starting a capsule.
  • Source basis: Accessible full-text extract plus indexed bibliographic data. Missing method details, funding information or participant denominators are not inferred.

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