Doctor's Best 5HTP Enhanced with Vitamins B6 and C 120 vegi caps
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5-HTP (5-hydroxytryptophan) is a
naturally-occurring metabolite of the essential amino acid tryptophan.
5-HTP for use in dietary supplements is derived from the seeds of the
Griffonia simplicifolia plant.
Metabolism and
absorption of 5-HTP
5-HTP (5-hydroxytryptophan) is formed by the
addition of a hydroxyl group (-OH) to the 5 carbon of the indole ring
of tryptophan. Conversion of tryptophan to 5-hydroxytryptophan is
catalyzed by the enzyme tryptophan hydroxylase.1
5-HTP functions as the precursor for serotonin, and is converted to
serotonin in a pyridoxal phosphate (vitamin B6) dependent reaction
catalyzed by the enzyme L-amino acid decarboxylase.2
Synthesis of serotonin in the
brain requires an adequate supply of either tryptophan or 5-HTP as
precursors. The supply of tryptophan available for conversion to 5-HTP
depends on a number of factors, including nutritional status and
competition between tryptophan and other amino acids for transport
across the blood brain barrier.
Disturbances in the serotonin
metabolic pathway may disrupt central nervous system functions which
utilize serotonin as a neurotransmitter.2
Administration of 5-HTP bypasses the conversion of tryptophan to 5-HTP.
5-HTP readily crosses the blood brain barrier and becomes available for
serotonin synthesis. Serotonergic neurons (nerve cells stimulated by
serotonin) regulate sleep, appetite, nociception (the perception of
pain), and aggressive behavior.2
Serotonin is metabolized to 5-HIAA
(5-hydroxyindolacetic acid) which is its primary breakdown product.3
The concentration of 5-HIAA in cerebrospinal fluid is used as an
indicator of serotonin turnover in the CNS serotonin level. Psychiatric
patients have been found to have low levels of 5-HIAA in the CNS fluid,
suggesting serotonin deficiency.3
5-HTP is readily absorbed by the
mucosal cells of the gastrointestinal tract. In one study using five
subjects, systemic absorption of 5-HTP in combination with carbidopa
averaged 69.2 percent.4 Another absorption study
found that carbidopa enhanced the increase in serum 5-HTP concentration
5 to 15 fold.5 In this study, a single dose of
5-HTP increased the plasma level of 5-HTP only slightly, whereas 5-HIAA
increased 9-20 fold. This suggests that the gut mucosa has a storage
capacity for 5-HTP, and that plasma increases occur after maximum
capacity is reached.5
Serotonin in the central nervous system is
recognized as a causative factor in some depressed persons.6,7 A
comprehensive review of seven open and seven controlled clinical
studies found that oral consumption of 5-HTP improved mental and
emotional status in 60 to 70 percent of depressed people. The results
varied from "modest" to "marked."8 Dosages ranged from 50 to 300 mg
daily.
The accumulated evidence is
inconclusive as to whether 5-HTP is more effective combined with
decarboxylase inhibitors than when taken alone. Many of the early trials
used the combination, and this has been a frequently used therapeutic
strategy for reducing conversion of 5-HTP to serotonin outside the CNS.
It is generally accepted that a large portion of absorbed 5-HTP is
metabolized to serotonin in peripheral tissues before it can enter the
brain.8
Peripheral conversion of 5-HTP to
serotonin would theoretically limit the usefulness of oral 5-HTP for
improving CNS functions and mental health. However, trials in which
5-HTP was given alone do show benefits. A small open trial in which 25
people were given 5-HTP either alone or with a decarboxylase inhibitor
found no difference in effectiveness.9 Thirteen of
the patients had "very good" or "good" improvement, 8 had "moderate,"
and in 4 out of the twenty-five the results were judged to be "poor."
A more recent randomized
double-blind study compared the efficacy of oral 5-HTP (100 mg T.I.D.,
without a decarboxylase inhibitor) to that of fluvoxamine, a selective
serotonin reuptake inhibitor.10 (SSRIs block the
reabsorption of serotonin by postsynaptic receptors, thus increasing the
available supply of serotonin in the synaptic cleft.) The two were found
to be equally effective, and 5-HTP was better tolerated. It should be
noted that 5-HTP was given in the form of enteric-coated pH-sensitive
capsules which dissolve in the small intestine, thus preventing
conversion of 5-HTP to serotonin in the stomach.
In contrast to MAO inhibitors and
SSRIs, medications which act by blocking normal physiologic functions,
5-HTP supports normal function in its role as a serotonin precursor.
Correcting serotonin deficiency has been called a
"functional-dimensional approach" in the treatment of depression.10
Improves Sleep
Quality
Studies have shown that 5-HTP influences the
quality of sleep by increasing REM (rapid eye movement) sleep.
Administration of 5-HTP in the evening prior to bedtime has been shown
to increase the duration of REM sleep and decrease the amount of
non-REM sleep.11,12
5-HTP–A Free-radical
Scavenger
The OH group which is added to tryptophan in the
formation of 5-HTP gives 5-HTP antioxidant properties.13
(Compounds such as vitamin E and flavonoids derive their free-radical
quenching ability from OH groups, which donate electrons to oxidants.)
5-HTP quenches a variety of free-radicals. This is in contrast to
tryptophan, which is sensitive to oxidation.
Adverse effects of
5-HTP
Oral administration of 5-HTP in clinical studies
has resulted in gastrointestinal disturbances such as nausea, vomiting
and diarrhea. According to a review by Byerley, et. al. these effects
are tolerated by most patients and tend to lessen over time.8
Side effects are more marked with higher doses, and may be reduced by
the use of enteric-coated, pH sensitive capsules or tablets.8,10.
Notice: Not to be used concurrently
with MAO inhibitors, selective serotonin reuptake inhibitors (SSRIs) or
other anti-depressant medications. It should also not be used by
individuals taking any of the category of medications known as "triptans"*.
2. Peters, J.C. Tryptophan nutrition and metabolism: An overview.
Advances in Experimental Medicine and Biology 1991;294:345-349.
3. van Pragg, H.M. Central monoamine metabolism in depressions. I.
Serotonin and related compounds. Comprehensive Psychiatry
1980;21(1):30-43.
4. Magnussen, I., Neilsen-Kudsk, F. Bioavailability and related
pharmacokinetics in man of orally administered L-5-hydroxytryptophan in
steady state. Acta pharmacol. et toxicol. 1980;46:257-62.
5. Magnussen, I., Jensen, T.S., Rand, J.H., Van Woert, M.H. Plasma
accumulation and metabolism of orally administered single dose
L-5-hydroxytryptophan in man. Acta pharmacol. et toxicol.
1981;49:184-89.
6. van Pragg, H.M. Korf, J. 5-hydroxytryptophan as an antidepressant.
Journal of Nervous and Mental Disease 1974;158(5):331-37.
7. van Pragg, H.M. Management of depression with serotonin precursors.
Biological Psychiatry 1981;16(3):291-310.
8. Byerley, W.F. et. al. 5-Hydroxytryptophan: A review of its
antidepressant efficacy and adverse effects. Journal of Clinical
Psychopharmacology 1987;7(3):127-37.
9. Zmilacher, K. Battegay, R., Gastpar, M. L-5-hydroxytryptophan alone
and in combination with a peripheral decarboxylase inhibitor in the
treatment of depression. Neuropsychobiology 1988;20:28-35.
10. Pöldinger, W., Calanchini, B., Schwarz, W. A functional-dimensional
approach to depression: Serotonin deficiency as a target syndrome in a
comparison of 5-hydroxytryptophan and fluvoxamine. Psychopathology
1991;24:53-81.
11. Zarcone, V.P. Hoddes, E., Smythe, H. Oral 5-hydroxytryptophan
effects on sleep. in Serotonin and Behavior, edited by Barchas, J.,
Usidin, E., NY: Academic Press; 1973:499-505.
12. Wyatt, R.J., et. al. Effects of 5-hydroxytryptophan on the sleep of
normal human subjects. Electroencephalography and Clinical
Neurophysiology 1971;30:505-09.
13. Simic, M.G. Al-Sheikhly, M. Jovanovic, S.V. Inhibition of free
radical processes by antioxidants-tryptophan and 5-hydroxytrytophan.
Bibl Nutra Dieta 1989;43:288-96
*Above statements have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat, cure or prevent any disease.
