This compound is NOT likely to build up to cytotoxic levels because you have methionine transmethylation reactions that results in natural creatine synthesis.
Only GAMT gene deficient individuals would have neurotoxic effects from using this compound.
But wait, our author presupposes that because you aren't getting your full fucking 10 grams of betaine anhydrous, your aren't getting your fill of methylation power.
He then *misses* the only salient ingredient that you might want to think twice about in this product: CLA.
Its a mixture of isomers, one is exaggerates and other controls insulin response. Most of us do no recommend its use. The company really should reconsider its use, along with the dose of MCT (which this author correctly points to being on the high side).
Creatine is formed by the transmethylation of guanidine-acetic acid ransmethylation with methionine. The methionine is the endproduct of the folate/homocysteine pathway in liver.
The rest of the story:
Activation of GABA(A) receptors by guanidinoacetate: a novel pathophysiological mechanism. Neu A, Neuhoff H, Trube G, Fehr S, Ullrich K, Roeper J, Isbrandt D. Zentrum fur Molekulare Neurobiologie Hamburg, Universitat Hamburg, Germany. Neurobiol Dis. 2002 11(2):298-307.
Guanidinoacetate methyltransferase (GAMT) deficiency is an autosomal recessively inherited disorder of creatine biosynthesis. The disease occurs in early life with developmental delay or arrest and several neurological symptoms, e.g., seizures and dyskinesia. Both the deficiency of high-energy phosphates in neurons and the neurotoxic action of the accumulated metabolite guanidinoacetate (GAA) are candidate mechanisms for the pathophysiology of this disease. To examine a potential role of GAA accumulation, we analyzed the electrophysiological responses of neurons induced by GAA application in primary culture and acute murine brain slices. GAA evoked picrotoxin- and bicuculline-sensitive GABA(A) receptor-mediated chloride currents with an EC(50) of 167 microM in cortical neurons. Pathophysiologically relevant GAA concentrations hyperpolarized globus pallidus neurons and reduced their spontaneous spike frequency with an EC(50) of 15.1 microM. Furthermore, GAA acted as a partial agonist at heterologously expressed GABA(A) but not GABA(B) receptors. The interaction of GAA with neuronal GABA(A) receptors represents a candidate mechanism explaining neurological dysfunction in GAMT deficiency.