I found this article of interest...I know there have been several others over time who wanted to know what supplements were required to make serotonin, and I thought I'd post this info pointing to one supplement I was unaware affects serotonin and dopamine levels. The paper is accessible at the link should you care to read it: (Note: I read PLP as P5P, which is active B6) http://discovery.ucl.ac.uk/1310134/ The neurochemical consequences of aromatic L-amino acid decarboxylase deficiency Allen, G.F.G. (2011) The neurochemical consequences of aromatic L-amino acid decarboxylase deficiency. Doctoral thesis, UCL (University College London). Aromatic L-amino acid decarboxylase (AADC) catalyses the conversion of 5-hydroxytryptophan (5-HTP) and L-3,4-dihydroxyphenylalanine (L-dopa) to the neurotransmitters serotonin and dopamine respectively. The inherited disorder AADC deficiency leads to a severe deficit of serotonin and dopamine as well as an accumulation of 5-HTP and L-dopa. This thesis investigated the potential role of 5-HTP/L-dopa accumulation in the pathogenesis of AADC deficiency. Treatment of human neuroblastoma cells with L-dopa or dopamine was found to increase intracellular levels of the antioxidant reduced glutathione (GSH). However inhibiting AADC prevented the GSH increase induced by L-dopa. Furthermore dopamine but not L-dopa, increased GSH release from human astrocytoma cells, which do not express AADC activity. GSH release is the first stage of GSH trafficking from astrocytes to neurons. This data indicates dopamine may play a role in controlling brain GSH levels and consequently antioxidant status. The inability of L-dopa to influence GSH concentrations in the absence of AADC or with AADC inhibited indicates GSH trafficking/metabolism may be compromised in AADC deficiency. 5-HTP was demonstrated to potentially be mildly toxic to human neuroblastoma cells but not astrocytoma cells; however the concentrations required for this response are likely to be higher than pathophysiological levels in AADC deficiency. These results indicate the need for investigations addressing the effects of chronic 5-HTP exposure as only acute effects were investigated in the current study. This thesis also investigated the effect of altered availability of the AADC coenzyme pyridoxal 5‟-phosphate (PLP) on AADC activity, protein and expression. In two patients with inherited disorders of PLP metabolism reductions in plasma AADC activity were observed. Furthermore PLP-deficient human neuroblastoma cells were found to exhibit reduced levels of AADC activity and protein but not altered expression. These findings suggest maintaining adequate PLP availability may be important for optimal treatment of AADC deficiency.