Tier 4 — mechanistic

Association between plasma betaine levels and dysglycemia in patients with coronary artery disease

Fei Guo, Xueting Qiu, Yuanting Zhu, Zhirong Tan, Zhenyu Li, Dongsheng Ouyang
Bioscience reports 2020 40(8):BSR20200676

Bibliography

PubMed
PMID 32756866
PubMed Central
PMC7432995
DOI
10.1042/BSR20200676
Funding
Reported funding/support: This work was supported by the National Development of Key Novel Drugs for Special Projects of China [grant number 2017ZX09304014]; the Natural Science Foundation of Hunan Province [grant number 2019JJ50966]; and the Hunan Key Laboratory for Bioanalysis of Complex Matrix Samples [grant number 2017TP1037].
Competing interests
Reported disclosure: The authors declare that there are no competing interests associated with the manuscript. The consent to publish was obtained from all participants in the present study.

Study snapshot

DesignCase-control biomarker study
ModelHuman participants
Sample307 adults; 165 coronary-disease patients and 142 controls
InterventionMeasured betaine status and related metabolites; no randomized TMG treatment
DurationCross-sectional assessment
EndpointsDysglycemia; Coronary disease

What the study showed, in plain terms

Published in 2020, this source examined human observational and biomarker research. Design: Case-control biomarker study. Sample/model: 307 adults; 165 coronary-disease patients and 142 controls. The exposure or intervention was Measured betaine status and related metabolites; no randomized TMG treatment. Follow-up or treatment period: Cross-sectional assessment.

Betaine was lower in coronary-disease patients with dysglycemia and inversely associated with several glycemic and metabolic measures.

Observational exposure analysis: residual confounding and reverse causation remain possible. Associations do not establish that betaine supplementation causes the same outcome. Diet recall, case selection or illness-related metabolite changes may introduce bias.

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Key findings

  • Betaine was lower in coronary-disease patients with dysglycemia and inversely associated with several glycemic and metabolic measures.
  • The recorded outcome domains were Dysglycemia; Coronary disease.
  • 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. Diet recall, case selection or illness-related metabolite changes may introduce bias.
  • 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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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