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5-Hydroxytryptophan: Difference between revisions
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5-HTP is also used by users of [[MDMA]] to reduce the negative [[MDMA#After_effects|after effects]] that occur during the drug's [[duration|come down]] period, including [[anxiety]], [[depression]], and [[cognitive fatigue]].<ref>http://www.sciencedirect.com/science/article/pii/S0306452207006732 | Wang, X.; Baumann, M. H.; Dersch, C. M.; Rothman, R. B. (2007-08-10). "Restoration of 3,4-methylenedioxymethamphetamine-induced 5-HT depletion by the administration of l-5-hydroxytryptophan". Neuroscience. 148 (1): 212–220. doi:10.1016/j.neuroscience.2007.05.024. PMID 17629409.</ref> Since 5-HTP is a precursor for the neurotransmitter [[serotonin]] and MDMA depletes serotonin levels in the brain, it is believed that taking 5-HTP after coming down will speed the production of serotonin. 5-HTP should not be taken until 12 hours after the MDMA was last dosed because combining the two drugs could result in a potentially life-threatening condition called [[serotonin syndrome]]. | 5-HTP is also used by users of [[MDMA]] to reduce the negative [[MDMA#After_effects|after effects]] that occur during the drug's [[duration|come down]] period, including [[anxiety]], [[depression]], and [[cognitive fatigue]].<ref>http://www.sciencedirect.com/science/article/pii/S0306452207006732 | Wang, X.; Baumann, M. H.; Dersch, C. M.; Rothman, R. B. (2007-08-10). "Restoration of 3,4-methylenedioxymethamphetamine-induced 5-HT depletion by the administration of l-5-hydroxytryptophan". Neuroscience. 148 (1): 212–220. doi:10.1016/j.neuroscience.2007.05.024. PMID 17629409.</ref> Since 5-HTP is a precursor for the neurotransmitter [[serotonin]] and MDMA depletes serotonin levels in the brain, it is believed that taking 5-HTP after coming down will speed the production of serotonin. 5-HTP should not be taken until 12 hours after the MDMA was last dosed because combining the two drugs could result in a potentially life-threatening condition called [[serotonin syndrome]]. | ||
==Pharmacology== | ==Pharmacology== | ||
[[File:5htp.png|300px|thumbnail|right]] | |||
The psychoactive action of 5-HTP is derived from its increase in production of serotonin in central nervous system tissue. 5-HTP is decarboxylated to serotonin (5-hydroxytryptamine or 5-HT) by the enzyme aromatic-L-amino-acid decarboxylase with the help of vitamin B6.<ref>https://www.ncbi.nlm.nih.gov/pubmed/6983619 | Effect of pyridoxal phosphate deficiency on aromatic L-amino acid decarboxylase activity with L-DOPA and L-5-hydroxytryptophan as substrates in rats.</ref> This reaction occurs both in nervous tissue and in the liver.<ref>https://www.ncbi.nlm.nih.gov/pubmed/6974228 | Characteristics of dihydroxyphenylalanine/5-hydroxytryptophan decarboxylase activity in brain and liver of cat.</ref> 5-HTP crosses the blood–brain barrier,<ref>https://www.ncbi.nlm.nih.gov/pubmed/18445233 | Augmented brain 5-HT crosses the blood-brain barrier through the 5-HT transporter in rat.</ref> while 5-HT does not. | The psychoactive action of 5-HTP is derived from its increase in production of serotonin in central nervous system tissue. 5-HTP is decarboxylated to serotonin (5-hydroxytryptamine or 5-HT) by the enzyme aromatic-L-amino-acid decarboxylase with the help of vitamin B6.<ref>https://www.ncbi.nlm.nih.gov/pubmed/6983619 | Effect of pyridoxal phosphate deficiency on aromatic L-amino acid decarboxylase activity with L-DOPA and L-5-hydroxytryptophan as substrates in rats.</ref> This reaction occurs both in nervous tissue and in the liver.<ref>https://www.ncbi.nlm.nih.gov/pubmed/6974228 | Characteristics of dihydroxyphenylalanine/5-hydroxytryptophan decarboxylase activity in brain and liver of cat.</ref> 5-HTP crosses the blood–brain barrier,<ref>https://www.ncbi.nlm.nih.gov/pubmed/18445233 | Augmented brain 5-HT crosses the blood-brain barrier through the 5-HT transporter in rat.</ref> while 5-HT does not. | ||
==Toxicity and harm potential== | ==Toxicity and harm potential== | ||
Due to the conversion of 5-HTP into serotonin by the liver, there may be a significant risk of heart valve disease from serotonin's effect on the heart.<ref>https://www.ncbi.nlm.nih.gov/pubmed/15781732 | Long-term serotonin administration induces heart valve disease in rats.</ref><ref>https://www.ncbi.nlm.nih.gov/pubmed/12466135 | Serotonin mechanisms in heart valve disease II: the 5-HT2 receptor and its signaling pathway in aortic valve interstitial cells.</ref> | Due to the conversion of 5-HTP into serotonin by the liver, there may be a significant risk of heart valve disease from serotonin's effect on the heart.<ref>https://www.ncbi.nlm.nih.gov/pubmed/15781732 | Long-term serotonin administration induces heart valve disease in rats.</ref><ref>https://www.ncbi.nlm.nih.gov/pubmed/12466135 | Serotonin mechanisms in heart valve disease II: the 5-HT2 receptor and its signaling pathway in aortic valve interstitial cells.</ref> | ||