Tier 4 — mechanistic

Betaine excretion correlates with plasma homocysteine when plasma lipids are elevated

Michael Lever, Sandy Slow, Peter M George, Stephen T Chambers
Clinical biochemistry 2012 45(1-2):154-156

Bibliography

PubMed
PMID 22093969
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

DesignComparative observational analysis
ModelHuman participants
SampleClinical subgroups with differing lipid profiles
InterventionMeasured betaine status and related metabolites; no randomized TMG treatment
DurationCross-sectional clinical sampling
EndpointsBetaine excretion; Homocysteine; Lipids

What the study showed, in plain terms

Published in 2012, this source examined human observational and biomarker research. Design: Comparative observational analysis. Sample/model: Clinical subgroups with differing lipid profiles. 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 correlation between urinary betaine loss and homocysteine was stronger in groups with elevated plasma lipids.

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 correlation between urinary betaine loss and homocysteine was stronger in groups with elevated plasma lipids.
  • The recorded outcome domains were Betaine excretion; 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: Indexed abstract and bibliographic data. Missing method details, funding information or participant denominators are not inferred.

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