|Not so fast! Just because it may have shuttled more creatine into the muscle GAA does not have to be able to build more strength or size.|
First things first, we are dealing with a randomized, double-blind, cross-over trial that was financed by a government grant - not non-existing (as of now) supplement companies who are pimping guanidinoacetic acid (GAA) as a "superior new form of creatine".
Now, technically speaking, this claim would be bogus, anyways, GAA is, after all, an intermediate product formed enzymatically in the liver, pancreas, and kidney in the synthesis of creatine and not "a creatine" - "superior", or not.
|Figure 2: Percentage change of tissue creatine levels 0 vs. 4 weeks. GAA denotes guanidinoacetic acid. Values are presented as means, with error bars represent the standard error of the means (SEM). P between trials (Ostojic. 2016b).|
Next to the formation of homocysteine during the conversion process of GAA to creatine, the fact that this process requires additional methyl donors could be another reason why Ostojic et al. (2014) found that Hcy started to pile up in the blood of their GAA study (see Figure 3). Similar neg. effects on Hcy have been reported before; among others by Stead, et al. (2001). And it seems only logical: If the methyl-donors are used for the GAA - creatine conversion they are no longer available to recycle homocysteine so that the latter is increasing progressively. This is bad news, since a high serum HCy concentration is an independent risk for cardiovascular disease and Alzheimer’s disease, dementia and cognitive impairment (Morris. 2003; Ganguly. 2015) - the causal nature of the epidemiologically observed link has yet been put into question, repeatedly, but until GAA receives the label "clinically proven safety" I cannot recommend using it as a replacement for creatine.
- further investigations of the potential (health-)relevance of the subsequent increase in methylation reactions that occur during the formation of creatine from GAA in the human body (more specifically, the question "Is the sign. increase in homocysteine levels a health problem for GAA users?" will have to be answered - esp. in the long-term; after all, Ostojic's 2014 study indicated that these start to raise with time / Figure 3), and
- long(er) term studies and studies comparing different dosages of GAA and creatine; after all, the former is supposed to work, because it offers a greater variety of uptake channels - an advantage that may be easy to compensate by (a) administering more creatine (3.4g is not much) and/or for a longer time (4 weeks is short)
- independent confirmation of the experimental results from another lab to exclude a potential bias of the researchers who have been working on the issue for years, now.
Not a single one of these studies has yet been conducted. So that we are left, for the time being, with this short-term study with a very 'limited' (you could also say 'hardly sufficient') number of subjects.References:
- da Silva, Robin P., et al. "Creatine synthesis: hepatic metabolism of guanidinoacetate and creatine in the rat in vitro and in vivo." American Journal of Physiology-Endocrinology and Metabolism 296.2 (2009): E256-E261.
- Ganguly, Paul, and Sreyoshi Fatima Alam. "Role of homocysteine in the development of cardiovascular disease." Nutrition journal 14.1 (2015): 1.
- Morris, Martha Savaria. "Homocysteine and Alzheimer's disease." The Lancet Neurology 2.7 (2003): 425-428.
- Ostojic, Sergej M., et al. "Dose–response effects of oral guanidinoacetic acid on serum creatine, homocysteine and B vitamins levels." European journal of nutrition 53.8 (2014): 1637-1643.
- Ostojic, Sergej M., Patrik Drid, and Jelena Ostojic. "Guanidinoacetic acid increases skeletal muscle creatine stores in healthy men." Nutrition 32.6 (2016a): 723-724.
- Ostojic, Sergej M., et al. "Guanidinoacetic acid vs. creatine for improved brain and muscle creatine levels: a superiority pilot trial in healthy men." Applied Physiology, Nutrition, and Metabolism (2016).
- Stead, Lori M., et al. "Methylation demand and homocysteine metabolism: effects of dietary provision of creatine and guanidinoacetate." American Journal of Physiology-Endocrinology And Metabolism 281.5 (2001): E1095-E1100.