Low-Dose Creatine Supplementation Lowers Plasma Guanidinoacetate, but Not Plasma Homocysteine, in a Double-Blind, Randomized, Placebo-Controlled Trial
Peters BA, Hall MN, Liu X, Parvez F, Siddique AB, Shahriar H, Uddin MN, Islam T, Ilievski V, Graziano JH, Gamble MV
The Journal of nutrition · 18 citas
Cómo se estudió
- Diseño
- Ensayo controlado aleatorizado (indexado por PubMed)
- Estudiado en
- Personas
- Resultado principal
- Marcadores de salud y funcionamiento
Quién lo pagó
- Financiación
- Financiación independiente
- Gobierno
- National Institutes of Health
- Gobierno
- National Cancer Institute
- Gobierno
- National Institute of Environmental Health Sciences
- Gobierno
- NIH
- Gobierno
- NIEHS NIH HHS
- Gobierno
- NCI NIH HHS
- Subvenciones
- National Cancer Institute (R01 CA133595); National Institute of Environmental Health Sciences (R01 ES017875); National Institute of Environmental Health Sciences (P42ES010349); National Institute of Environmental Health Sciences (R00ES018890); National Institutes of Health (R01CA133595); National Institutes of Health (R01ES017875); National Institutes of Health (P42 ES010349); National Institute of Environmental Health Sciences (P30ES009089)
Según 6 financiadores declarados.
Publicación
- Publicado
- 2015-08-26 · J Nutr · vol. 145 · número 10 · págs. 2245–2252
- Editorial
- Elsevier BV
- Citado
- 23 citas · más que el 90% de estudios similares · 2.9× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 48 trabajos
- Acceso
- Lectura gratuita
- Áreas de investigación
- Folate and B Vitamins Research · Muscle metabolism and nutrition · Metabolism and Genetic Disorders
- Palabras clave
- creatine supplementation, guanidinoacetic acid, homocysteine, S-adenosylmethionine, S-adenosylhomocysteine, folic acid, methyl group metabolism, creatine synthesis, plasma biomarkers, Bangladeshi adults, dietary creatine, methionine metabolism, folic acid supplementation
- MeSH
- humans, hyperhomocysteinemia, creatine, folic acid, homocysteine, s-adenosylhomocysteine, s-adenosylmethionine, glycine, cohort studies, double-blind method, down-regulation, dietary supplements, adult, middle aged, patient dropouts, bangladesh, female, male, intention to treat analysis, biomarkers
11 autores
- Brandilyn A. Peters
- Megan N. Hall
- Xinhua Liu🇺🇸Columbia University
- Faruque Parvez
- Abu B Siddique🇺🇸Columbia University
- Hasan Shahriar🇺🇸Columbia University
- Mohammad Nasir Uddin🇺🇸Columbia University
- Tariqul Islam🇺🇸Columbia University
- Vesna Ilievski
- Joseph H. Graziano
- Mary V. Gamble · autor de correspondencia
Resumen
El texto original del estudio, en el idioma en que se publicó.
Background
Creatine synthesis from guanidinoacetate consumes ~50% of s-adenosylmethionine (SAM)-derived methyl groups, accounting for an equivalent proportion of s-adenosylhomocysteine (SAH) and total homocysteine (tHcys) synthesis. Dietary creatine inhibits the synthesis of guanidinoacetate, thereby lowering plasma tHcys in rats.
Objective
We tested the hypotheses that creatine supplementation lowers plasma guanidinoacetate, increases blood SAM, lowers blood SAH, and lowers plasma tHcys.
Methods
Bangladeshi adults were randomly assigned to receive 1 of 4 treatments for 12 wk: placebo (n = 101), 3 g/d creatine (Cr; n = 101), 400 μg/d folic acid (FA; n = 153), or 3 g/d creatine plus 400 μg/d folic acid (Cr+FA; n = 103). The outcomes of plasma guanidinoacetate and tHcys, as well as whole blood SAM and SAH, were analyzed at baseline and week 12 by HPLC. Treatment effects of creatine supplementation were examined with the use of the group comparisons of Cr vs. placebo and Cr+FA vs. FA.
Results
Plasma guanidinoacetate declined by 10.6% (95% CI: 4.9, 15.9) in the Cr group while increasing nonsignificantly in the placebo group (3.7%; 95% CI: -0.8, 8.5) (Pgroup difference = 0.0002). Similarly, plasma guanidinoacetate declined by 9.0% (95% CI: 3.4, 14.2) in the Cr+FA group while increasing in the FA group (7.0%; 95% CI: 2.0, 12.2) (Pgroup difference < 0.0001). Plasma tHcys declined by 23.4% (95% CI: 19.5, 27.1) and 21.0% (95% CI: 16.4, 25.2) in the FA and Cr+FA groups, respectively (Pgroup difference = 0.41), with no significant changes in the placebo or Cr groups (Pgroup difference = 0.35). A decrease in guanidinoacetate over time was associated with a decrease in tHcys over time in the Cr+FA group (β = 0.30; 95% CI: 0.17, 0.43; P < 0.0001).
Conclusions
Our findings indicate that whereas creatine supplementation downregulates endogenous creatine synthesis, this may not on average lower plasma tHcys in humans. However, tHcys did decrease in those participants who experienced a decline in plasma guanidinoacetate while receiving creatine plus folic acid supplementation. This trial was registered at clinicaltrials.gov as NCT01050556.
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