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  Tryptophan / Serotonin
Alcoholism alters Tryptophan / Serotonin

Altered tryptophan and serotonin levels occur in alcoholics. Serotonin neurotransmitter deficiency can produce depression. Tryptophan is an essential amino acid, which means the human body cannot produce it, although it is needed, to produce other amino acids. Tryptophan is available by prescription, as L-tryptophan or as an over the counter non-prescription supplement, 5-Hydroxytryptophan. ( 5-HTP ). In the body, tryptophan is transformed to niacin ( Vitamin B3 ) or the neurotransmitter serotonin. If inadequate niacin is present, tryptophan will be converted to niacin, before conversion to serotonin. Conversion of tryptophan to serotonin requires Vitamin B6 ( pyrodoxal 5 phosphate ) and magnesium, as cofactors. Alcohol depletes magnesium and Vitamin B6. 

Research by Borg, S, et. al., (1985) indicates alcohol temporarily increases serotonin levels during intoxication, but can decrease serotonin levels for months after the alcoholic becomes sober. Borg measured the serotonin metabolic product, 5-Hydroxyindoleacetic acid ( 5-HIAA ), in cerebrospinal fluid of male alcoholics and controls. 5-HIAA levels increased with blood alcohol levels and gradually decreased with increased abstinence. Subnormal levels occurred in alcoholics abstinent for three months. 

Branchey L., et. al., (1985) observed lower plasma tryptophan levels in male patients who had experienced blackouts, compared to patients who had not experienced blackouts. There was no significant difference between proportions of other amino acids which share the tryptophan blood-brain barrier transport carrier. Although increasing serotonin levels can benefit many recovering alcoholics, Bankole, A., et al., (2000) found Odansetron, a 5-HT3 antagonist (which blocks serotonin 3 receptors) reduced drinks per day, approximately 53 percent, in early age onset alcoholics. 

Serotonin levels can be increased with l-tryptophan or 5-hydroxytryptophan supplementation, in addition to pharmaceuticals. ( P?nger, W. et. al.,1991) compared 5-hydroxytryptophan ( 5-HTP ) to fluvoxamine ( Luvox ), a selective serotonin reuptake inhibitor antidepressant, in a 6 week double blind study, with 69 depressed participants. Both treatments produced highly significant reductions in Hamilton Rating Scale for Depression, at 2, 4 and 6 weeks. 5-HTP produced greater reductions in insomnia, 61.7 to 55.9 percent, physical symptoms, 47.6 to 37.8, anxiety, 58.2 to 48.3, and depressed mood, 65.7 to 61.8, than fluvoxamine. 5-HTP was better tolerated, with four fluvoxamine patients dropping out of study, compared to one in the 5-HTP group, with 38.9 percent of 5-HTP group reporting side effects, while 54.5 percent of fluvoxamine group reported side effects. Side effects in the 5-HTP group were milder and the sole 5-HTP dropout lasted 5 weeks, while the 4 fluvoxamine dropouts lasted 2 weeks. Dosage was 100 mg 5-HTP three times per day or 50 mg fluvoxamine 3 times per day. 

Amen, D and Routh, L. (2003) report brain uptake of 5-HTP is 70 percent, while brain uptake of l-tryptophan is only 3 percent. Additional information concerning depression treatment with amino acids is available, at Amen's website, amenclinics.com. 

 


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