Tier 4 — mechanistic

Genetic Determinants of Circulating Glycine Levels and Risk of Coronary Artery Disease

Jia Q, Han Y, Huang P, Woodward NC, Gukasyan J, Kettunen J, Ala-Korpela M, Anufrieva O, Wang Q, Perola M, Raitakari O, Lehtimäki T, Viikari J, Järvelin MR, Boehnke M, Laakso M, Mohlke KL, Fiehn O, Wang Z, Tang WHW, Hazen SL, Hartiala JA, Allayee H
Journal of the American Heart Association 2019 8(10):e011922

Bibliography

PubMed
PMID 31070104
PubMed Central
PMC6585317
DOI
10.1161/jaha.119.011922
Funding
Support included NIH, Fondation Leducq, Academy of Finland, Novo Nordisk Foundation, NHMRC and UK MRC sources.
Competing interests
Some investigators disclosed cardiovascular-diagnostic patents, royalties, industry research/consulting relationships or Nightingale Health stock options.

Study snapshot

DesignHuman genetic association and Mendelian-randomization analyses
ModelAdult humans
SampleUp to 30,118 European-ancestry participants in the glycine GWAS meta-analysis
InterventionGenetic analyses separating glycine-associated variants by pleiotropic effects
DurationGenetic epidemiology; no dosing period
EndpointsGlycine loci; Coronary artery disease; Traditional cardiovascular risk factors

What the study showed, in plain terms

This study found additional genetic determinants of glycine, but its more selective genetic models did not provide conclusive evidence that glycine itself prevents coronary disease.

Key findings

  • Several glycine-raising variants also related to other cardiovascular traits.
  • Models restricted to two glycine-degradation variants did not associate with coronary disease.

What this study can and cannot tell us

Instrument choice and pleiotropy materially affected interpretation.

Results cannot establish either clinical benefit or harm from oral glycine.

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Editorial review

Reviewed by the Biohack Blueprint research team

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Dr. Khaled Mahmoud, MBBChCritical Care Medicine, Longevity Science & Editorial Direction