Depression is common in the United States, affecting about one in eight people sometime during their lifetime, according to the National Epidemiologic Survey of Alcoholism and Related Conditions. However, only 60 percent of depressed individuals are treated for their condition, and up to two-thirds of treated patients do not respond to the first medication prescribed by their physicians. Alternative remedies, such as 5-HTP, are frequently used by depressed patients in an attempt to control their symptoms, but such treatments are largely untested, and there is no evidence they are more effective than prescription agents. Ask your doctor if 5-HTP is appropriate for you.
Neurotransmitter Imbalance
It is generally accepted that depression is caused by abnormalities in the synthesis or activity of neurotransmitters in your brain. Neurotransmitters convey impulses that regulate your emotions and moods as well as the myriad other functions that allow you to function as a living organism. Among the many neurotransmitters that modulate mood, serotonin stands out as a principal player. Insufficient serotonin production or inadequate serotonin receptor activity has been implicated as a common cause of depression, and many prescription drugs and alternative therapies – trazodone and 5-HTP included – target the serotonin system.
Trazodone
Trazodone is a prescription drug that has been used to treat depressed patients in the U.S. for three decades, but its exact mechanism of action is still not completely understood. It is believed that trazodone works in two ways. First, it inhibits the removal of serotonin from your synapses – the microscopic spaces between your nerves – thereby increasing serotonin concentrations and enhancing serotonin activity at receptors that decrease depressive symptoms. A more prominent property of trazodone is its blockade of specific serotonin receptors that actually contribute to depression. Thus, trazodone is classified as a serotonin antagonist and reuptake inhibitor, or SARI.
5-HTP
L-tryptophan, an essential amino acid obtained from your diet, is converted to serotonin in your brain in a two-step enzymatic pathway. In the first step, L-tryptophan is converted to 5-HTP by tryptophan hydroxylase. The second step involves the conversion of 5-HTP to serotonin by a decarboxylase enzyme. Many depressed patients take 5-HTP, the immediate precursor of serotonin, to increase serotonin levels in their central nervous system. However, most clinical studies supporting the practice of 5-HTP supplementation for depression are 20 years old, so its effectiveness when compared to prescription drugs, such as trazodone, is not well documented.
A Counterproductive Combination?
The chemistry of depression is quite complex. When serotonin stimulates some receptors, it improves depression; when it stimulates others, it worsens depressive symptoms. A study published in the May 1984 issue of “Neuropharmacology” showed that trazodone blunted some of 5-HTP’s metabolic effects in the bloodstream of laboratory animals by blocking certain serotonin receptors. Whether this effect is seen in humans or whether it has any relevance in your brain’s biochemistry is still unclear, but combining 5-HTP with trazodone could conceivably reduce the effectiveness of both agents. If you are considering using 5-HTP for depression -- and particularly if you plan to combine 5-HTP with trazodone -- consult a medical professional first.
References
- “American Family Physician”; Treatment-Resistant Depression; A. Little; July 2009
- “Drugs and Aging”; Trazodone: A Review of Its Pharmacology, Therapeutic Use in Depression and Therapeutic Potential in Other Disorders; M. Haria, et al.; April 1994
- “Psychosomatics”; Novel Treatment Strategies for Depression in Patients With Hepatitis C; J.M. Loftis, et al.; Jul-Aug 2010
- “Neuropharmacology”; Interactions of Trazodone With Serotonin Neurons and Receptors; R.W. Fuller, et al.; May 1984
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