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 intoxicatio, but decreases 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 5-Hydroxyindoleacetic Acid 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-HT# 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. (Poldinger, 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 tolorated, 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.

Studies show serotonin levels eventually decrease, during selective serotonin reuptake inhibitor (SSRI) antidepressant therapy. Serotonin breakdown to 5-HIAA continues, and SSRI serotonin recycling does not replace serotonin metabolized to 5-HIAA. Tryptophan supplementation can actually increase neurosynapse serotonin levels for longer periods than SSRI antidepressant therapy. Some of the newest SSRI antidepressants, including Lexapro, can boost serotonin levels, very quickly.

Tryptophan is a relatively large amino acid, which requires the Large Amino Acid Transport Carrier protein, for transport through the blood brain barrier. Arteries supplying the brain contain an extra cell layer, called the blood-brain barrier, which prevents many toxins from entering the brain. The blood-brain barrier also limits transport of many amino acids into the brain. The Large Amino Acid Transport Carrier protein only carries one amino acid across the blood brain barrier at a time. Amino Acids sharing the Large Amino Acid Transport Carrier include Tryptophan, Tyrosine, Phenylalanine, Leucine, Isoleucine and Valine. Unless l-tryptophan is taken away from other amino acids and proteins, very little is absorbed, since the Large Amino Acid Transport Carrier “bus” only transports one amino acid, at a time. Brain uptake of 5-HTP does not require the Large Amino Acid Transport Carrier “bus” and 5-HTP can be taken with other foods, including proteins. 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 Daniel Amen’s website, amenclinics.com.

Phenylalanine

Phenylalanine is one of the eight essential amino acids and a precursor for phenylethylamine (PEA).   PEA deficiency can produce depressions, which are unresponsive to tryptophan, 5-HTP, tyrosine, SAME or prescription antidepressants.   High urinary PEA levels have been found in schizophrenics, while low levels have been found in depressed patients. Phenylalanine also is a   tyrosine precursor, and tyrosine is a precursor to thyronine (thyroid hormone component) and dopamine .   Phenylalanine may cause increased blood pressure, or pulse and   should   not be taken if you use monoamine oxidase inhibitors. (Beckmann, H., et. al., 1979) compared DL-Phenylalanine to imipramine, in a double blind study, of 40 depressed patients, for 30 days.   No statistical difference was   found, between the two treatments, on the Hamilton Depression Scale and the Bf-S self-rating questionnaire.   Dosages used were 150-200 milligrams per day of DL-Phenylalanine or imipramine.   Phenylalanine is available as D, L or DL   Phenylalanine, but more commonly available as DL-Phenylalanine.   D-Phenylalanine   inhibits enkephalinase, which metabolizes enkephalins and endorphins and is used in some proprietary formulas to decrease pain and anxiety.   L-Phenylalanine is the form used by the body to produce neurotransmitters and proteins.   DL Phenylalanine is a mixture of D and L Phenylalanine.

Tyrosine

Tyrosine is a naturally occurring amino acid and a precursor for the neurotransmitter dopamine and thyronine (substrate for thyroid hormone). Daniel Amen, MD, is a psychiatrist who has performed over 28,000 SPECT brain scans.  Amen reports tyrosine is helpful for depressions, with reduced dopamine levels, and reduced prefrontal cortex blood flow.    Reduced dopamine levels often occur in attention deficit disorder, and  depressions where sleep, fatigue, lethargy and weight gain are increased.   Low blood pressure and lower heart rates can also occur, with dopamine deficiency.   Tyrosine   may cause increased blood pressure, or pulse and   should  not be taken if you use monoamine oxidase inhibitors.

S-Adenosyl methionine

S-Adenosyl methionine (SAMe) occurs naturally in the body, crosses the blood-brain barrier and has proven effective treating depression and joint pain.   It increases serotonin and dopamine levels and improves brain and nerve cell membrane fluidity. S-Adenosyl methionine has increased manic and hypomanic episodes, in patients with bipolar disorder and should not be used by manic depressive patients. Bell, K, et. al., (1994) conducted a double blind, placebo controlled study comparing SAMe to desipramine, in a 4 week trial with 26 depressed patients, at University of California, Irvine.   SAMe produced improvement in 62 percent of patients, compared to 50 percent of patients treated with desipramine.   Regardless of treatment, patients exhibiting a decrease of 50 percent or more in Hamilton Depression Scale, showed significant increases in plasma SAMe level.   Salmaggi, P., et. al., (1993) found significantly greater improvement in depressed postmenopausal women treated with 1600 milligrams SAMe, than placebo.   During the 30 day, double blind test of 80 women, between 45 and 59 years old, SAMe evidenced superiority by day 10 and side effects were mild.   Amen, D. and Routh, L., (2003) have found SAMe useful for depression.   Jacob Teitelbaum, MD (2003) recovered from chronic fatigue syndrome, and recommends 200 to 800 milligrams SAMe, twice per day, for depressed chronic fatigue and fibromyalgia sufferers, stating improvement can be expected in 10 days. His website, endfatigue.com, and best selling book, From Fatigued to Fantastic, explain how to successfully treat over 90 percent of the disabling symptoms of chronic fatigue and fibromyalgia.