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Efficacité de l’acide guanidinoacétique pour remplacer la créatine?

28/11/2014 | Etudes Compléments alimentaires et Etudes Perte de poids et Etudes Anti-âge


Je n’ai pas encore compris pourquoi certains prenaient ça mais j’ai renoncé à essayer de tout comprendre

Dose–response effects of oral guanidinoacetic acid on serum creatine, homocysteine and B vitamins levels
European Journal of Nutrition December 2014, Volume 53, Issue 8, pp 1637-1643     Sergej M. Ostojic

Guanidinoacetic acid (GAA) is an intermediate in the biosynthesis of creatine (Cr), yet its use in human nutrition is limited due to a lack of a clear understanding of its’ dose–response effect. Thus, the purpose of this study was to investigate the effect of three different dosages of GAA (1.2, 2.4 and 4.8 g/day) administered for 6 weeks on serum and urinary variables related to GAA metabolism.


Forty-eight healthy volunteers participated in the randomized, placebo-controlled, double-blind, repeated-measure study. At baseline, after 1, 2, 4 and 6 weeks, participants provided both fasting blood samples and 24-h urine.


GAA intervention significantly increased serum and urinary GAA, Cr and creatinine as compared to placebo (P < 0.05). Differences were found for serum GAA and Cr responses between the three GAA dosages, with high-dose GAA resulting in a greater increase (P < 0.05) in the plasma concentration of both variables as compared to other GAA dosages. In GAA groups, fasting plasma total homocysteine (T-Hcy) increased by 3.5 μmol/L on average at post-administration, yet no dose–response differences were found between trials. Serum B vitamins were not affected by either placebo or GAA intervention (P > 0.05).


Results indicate that low-to-high dosages of exogenous GAA can increase serum concentrations of Cr and T-Hcy while not depleting the B vitamins pool available for remethylation of homocysteine.

Creatine metabolism and safety profiles after six-week oral guanidinoacetic acid administration in healthy humans.

Int J Med Sci. 2013;10(2):141-7.      Ostojic SM

Guanidinoacetic acid (GAA) is a natural precursor of creatine, yet the potential use of GAA as a nutritional additive for restoring creatine availability in humans has been limited by unclear efficacy and safety after exogenous GAA administration. The present study evaluated the effects of orally administered GAA on serum and urinary GAA, creatine and creatinine concentration, and on the occurrence of adverse events in healthy humans.
Twenty-four healthy volunteers were randomized in a double-blind design to receive either GAA (2.4 grams daily) or placebo (PLA) by oral administration for 6 weeks.

Exogenous GAA is metabolized to creatine, resulting in a significant increase of fasting serum creatine after intervention. GAA had an acceptable side-effects profile with a low incidence of biochemical abnormalities.

Co-administration of methyl donors along with guanidinoacetic acid reduces the incidence of hyperhomocysteinaemia compared with guanidinoacetic acid administration alone.

Ostojic SM     Br J Nutr. 2013 Sep 14;110(5):865-70.
Guanidinoacetic acid (GAA) is the natural biosynthetic precursor of creatine, in a metabolic reaction that requires only a methyl group transfer. The use of GAA as a food additive for restoring creatine load in human tissues is rather unexplored and data on efficacy and safety are limited. In particular, an increase in serum homocysteine after GAA administration can be regarded as critical and should be prevented. The present study evaluated the effects of orally administered GAA with and without methyl group donors on serum and urine creatine concentrations, and the occurrence of adverse events during an intervention in healthy human subjects. A total of twenty male and female volunteers were randomised in a double-blind design to receive either GAA (2.4 g/d) or GAA with methyl donors (2.4 g/d of GAA and 1.6 g/d of betaine HCl, 5 μg/d of vitamin B12, 10 mg/d of vitamin B6 and 600 μg/d of folic acid) by oral administration for 8 weeks. Serum and urine creatine increased significantly from before to after administration in both groups (P< 0.001). The proportion of participants who reported minor adverse events was 33.3 % in the GAA group, and 10.0 % in the GAA with methyl donors group (P= 0.30). Hyperhomocysteinaemia was found in 55.6 % of participants supplemented with GAA, while no participant experienced hyperhomocysteinaemia in the group supplemented with GAA and methyl donors (P= 0.01). In summary, both interventions strongly influenced creatine metabolism, resulting in a significant increase in fasting serum creatine. The concomitant supplementation of methyl donors along with GAA largely precluded the elevation of serum homocysteine caused by GAA administration alone.

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