Old Mike said...
Why do the neurotransmitters get out of balance, what in modern lifestyle is the cause or multiple causes.
According to this paper
"In recent years, a genetic defect of the OCTN1 and OCTN2 of the colon has been identified in patients with Crohn’s disease. The OCTN1 and OCTN2 are responsible for transport of cations, including the monoamines of the serotonin–dopamine system and their precursors. It is known with Crohn’s disease patients that there is a marked increased in serotonin levels of the proximal and distal colon associated with a defect in serotonin synthesis. It remains to be proven whether a transport problem exists in the serotonin–dopamine system induced by the OCTN1 and OCTN2 genetic defect found in Crohn’s disease."
Though, I've also found a lot of similarities between this approach and the mutations related to the methylation genes.From mthfr.net
http://mthfr.net/mthfr-a1298c-mutation-some-information-on-a1298c-mthfr-mutations/2011/11/30/ said...From Wikipedia
The MTHFR enzyme appears to contribute function in both two major pathways: BH4 and Methylation.
The area which the A1298C MTHFR mutation works appears to disrupt function in the BH4 cycle.
The BH4 cycle is absolutely critical for these various functions:
assists the breakdown of phenylalanine
helps form these neurotransmitters:
- Norepinephrine (noradrenaline)
- Epinephrine (adrenaline)
cofactor to produce Nitric Oxide (NO)
assists breakdown of ammonia
Methylenetetrahydrofolate reductase (MTHFR) is the rate-limiting enzyme in the methyl cycle, and it is encoded by the MTHFR gene. Methylenetetrahydrofolate reductase catalyzes the conversion of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, a cosubstrate for homocysteine remethylation to methionine. Genetic variation in this gene may influence susceptibility to occlusive vascular disease, neural tube defects, colon cancer and acute leukemia, and mutations in this gene are associated with methylenetetrahydrofolate reductase deficiency.
So, those of you that have seen positive results by this therapy (or those who don't) might also want to get yourself tested for mutations of the methylation genes. From my understanding the amino-acid therapy's approach tries to surpass the limited production of neurotransmitters by providing great amounts of their precursors. However the root of the problem might be the incorrect function of methylenetetrahydrofolate reductase.