Tier 4 — mechanistic

Extreme urinary betaine losses in type 2 diabetes combined with bezafibrate treatment are associated with losses of dimethylglycine and choline but not with increased losses of other osmolytes

Michael Lever, Christopher J McEntyre, Peter M George, Sandy Slow, Jane L Elmslie, Helen Lunt, Stephen T Chambers, Amber Parry-Strong, Jeremy D Krebs
Cardiovascular drugs and therapy 2014 28(5):459-468

Bibliography

PubMed
PMID 25060556
DOI
10.1007/s10557-014-6542-9
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

DesignMatched observational drug comparison
ModelHuman participants
Sample32 bezafibrate-treated diabetic patients and 64 comparators
InterventionMeasured betaine status and related metabolites; no randomized TMG treatment
DurationCross-sectional samples from an earlier study
EndpointsFibrate exposure; Betaine loss

What the study showed, in plain terms

Published in 2014, this source examined human observational and biomarker research. Design: Matched observational drug comparison. Sample/model: 32 bezafibrate-treated diabetic patients and 64 comparators. The exposure or intervention was Measured betaine status and related metabolites; no randomized TMG treatment. Follow-up or treatment period: Cross-sectional samples from an earlier study.

Urinary betaine and dimethylglycine losses were substantially higher during bezafibrate treatment; supplementation benefit was proposed but not tested.

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

Continue with TMG Data Center

Continue with TMG for Weight Loss: Body-Fat Findings and Their Limits

Key findings

  • Urinary betaine and dimethylglycine losses were substantially higher during bezafibrate treatment; supplementation benefit was proposed but not tested.
  • The recorded outcome domains were Fibrate exposure; Betaine loss.
  • 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.

Related papers in the corpus

Tier 4
Dietary Choline and Betaine Are Not Associated With the Risk of Type 2 Diabetes. A Systematic Review and Meta-Analysis of Observational Studies
Elham Sharifi-Zahabi et al. · Journal of diabetes research · 2026
Tier 2
Metabolic Effects of Betaine: A Randomized Clinical Trial of Betaine Supplementation in Prediabetes
Ana Maria Grizales et al. · The Journal of clinical endocrinology and metabolism · 2018
Tier 4
High Betaine, a Trimethylamine N-Oxide Related Metabolite, Is Prospectively Associated with Low Future Risk of Type 2 Diabetes Mellitus in the PREVEND Study
Erwin Garcia et al. · Journal of clinical medicine · 2019
Tier 4
Associations between Serum Betaine, Methyl-Metabolizing Genetic Polymorphisms and Risk of Incident Type 2 Diabetes: A Prospective Cohort Study in Community-Dwelling Chinese Adults
Xiaoting Lu et al. · Nutrients · 2022
Tier 4
Dietary Choline and Betaine and Risk of CVD: A Systematic Review and Meta-Analysis of Prospective Studies
Katie A Meyer et al. · Nutrients · 2017
Tier 4
Association of choline and betaine with the risk of cardiovascular disease and all-cause mortality: Meta-analysis
Qinglin Yang et al. · European journal of clinical investigation · 2023

Editorial review

Reviewed by the Biohack Blueprint research team

Last verified

Dr. Khaled Mahmoud, MBBChCritical Care Medicine, Longevity Science & Editorial Direction Dr. Amr Yasser, PhDCardiometabolic, Musculoskeletal, Gut & Bioavailability Dr. Abdulla Mostafa, PhDCellular Senescence, Neurological, Mitochondrial & Brain-Ageing Biology