Tier 2 — strong

Choline supplemented as phosphatidylcholine decreases fasting and postmethionine-loading plasma homocysteine concentrations in healthy men

Margreet R Olthof, Elizabeth J Brink, Martijn B Katan, Petra Verhoef
The American journal of clinical nutrition 2005 82(1):111-117

Bibliography

PubMed
PMID 16002808
DOI
10.1093/ajcn.82.1.111
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

DesignRandomized crossover controlled trial
ModelHuman participants
Sample26 healthy men
InterventionCholine about 2.6 g/day as phosphatidylcholine versus matched oil
Duration2 weeks per treatment
EndpointsHomocysteine; Choline metabolism

What the study showed, in plain terms

Published in 2005, this source examined food sources, absorption and nutrient metabolism. Design: Randomized crossover controlled trial. Sample/model: 26 healthy men. The exposure or intervention was Choline about 2.6 g/day as phosphatidylcholine versus matched oil. Follow-up or treatment period: 2 weeks per treatment.

Fasting and methionine-load homocysteine were lower during high-dose phosphatidylcholine supplementation.

A choline intervention measuring biomarkers; it does not establish clinical cardiovascular prevention or an equivalent TMG dose.

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Continue with Foods High in Betaine: TMG Amounts and Practical Portions

Key findings

  • Fasting and methionine-load homocysteine were lower during high-dose phosphatidylcholine supplementation.
  • The recorded outcome domains were Homocysteine; Choline metabolism.
  • The result applies to the tested exposure: Choline about 2.6 g/day as phosphatidylcholine versus matched oil; 2 weeks per treatment.

What this study can and cannot tell us

  • A choline intervention measuring biomarkers; it does not establish clinical cardiovascular prevention or an equivalent TMG dose.
  • An individual controlled trial must be interpreted alongside its comparator, sample size, endpoint selection and independent replication. It does not validate a different commercial formulation or a general longevity claim.
  • Source basis: Indexed abstract and bibliographic data. Missing method details, funding information or participant denominators are not inferred.

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Editorial review

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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