5-HTP (5-Hydroxytryptophan) vs. Prozac (SSRIs)

5-HTP (5-Hydroxytryptophan) vs. Prozac (SSRIs)
by Ward Dean, MD, James South, MA, and Jim English
Neurotransmitters are specialized biochemicals that nerve
cells use to 'talk' to each other. Serotonin is one of some
ten major brain neurotransmitters. Deficiencies of
serotonin in the brain have been linked to a number of
disparate conditions, including: depression (especially the
agitated, anxious, irritable type), (1-6) anxiety, (7) suicide,
(8) alcoholism, (9) violent behavior, (8) PMS, (10) obesity,
(10,11) compulsive gambling, (12) insomnia, (13)
carbohydrate craving, (10) SAD (seasonal affective
disorder), (10) and migraine headaches. (14)
Serotonin nerve circuits promote feelings of well-being,
calmness, personal security, relaxation, confidence and concentration. (15) Serotonin
circuits also help counterbalance the tendency of two other major neurotransmitters in
the brain — dopamine and noradrenaline — to encourage overarousal, fear, anger,
tension, aggression, violence, obsessive-compulsive actions, overeating, anxiety and
sleep disturbances. (15) Many people suffer from various degrees of brain serotonin
deficiency, leading to a host of mental, emotional and behavioral problems. To
understand why brain serotonin deficiency is becoming more common in modern
society, it is necessary to look at how the brain makes serotonin.
Serotonin Function
Serotonin (5HT), dopamine, and noradrenaline are the three main 'monoamine'
neurotransmitters — 'mono' because each one is made from a single, specific amino
acid. Serotonin is made from tryptophan, while dopamine and noradrenaline are made
from tyrosine and phenylalanine. Since the blood-brain barrier prevents serotonin from
being 'imported' from outside the brain, all serotonin used by our brain cells must be
made within the neurons. Normally the blood-brain barrier serves as a protective device
to prevent toxins from entering the brain. But this protection comes at a price — even
'friendly' molecules, such as amino acids needed by the brain, are limited by this barrier.
When nutrients are allowed to cross the blood-brain barrier they must be 'ferried' by
specialized transport molecules, much as passengers being transported on a bus. This
process creates a special 'bottleneck' for serotonin. Serotonin itself cannot pass through
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the blood-brain barrier, while its precursor, tryptophan, must share its transport 'bus' with
five other amino acids — leucine, isoleucine, valine, tyrosine and phenylalanine.
In any normal diet, animal protein-based or vegetarian, tryptophan is the least plentiful of
all 20 food amino acids. Thus, tryptophan is typically outnumbered as much as 9:1 in its
competition to secure its transport through the blood-brain barrier into the brain. Eating a
high-protein diet in an attempt to increase dietary tryptophan (a typical diet provides only
1-1.5 grams/day) only increases its competition even more. Ironically, the only dietary
strategy that increases brain tryptophan supply is a high-carbohydrate, low-protein diet.
When large amounts of carbohydrates are eaten, the body secretes large amounts of
the hormone insulin to lower the resulting high blood sugar. In addition to lowering blood
sugar levels, insulin also clears most of the five amino acids that compete with
tryptophan for a 'ride' to the brain. The result is that tryptophan has the 'bus' to itself,
allowing plenty of tryptophan to reach the brain. (10)
Carbohydrates for Stress
This dietary strategy is instinctively known and practiced
by many Americans who eat large amounts of
carbohydrates, including candy, cake, pie, bread, chips,
ice cream, etc., when they are feeling stressed,
depressed or anxious. The resulting increase in brain
serotonin levels suppresses arousal and anxiety, and
promotes a (temporary) sense of well-being and security.
Unfortunately, this strategy comes at a high price. The
same insulin which enhances brain serotonin levels also
increases the conversion of the fats, carbohydrates and
amino acids cleared from the blood into stored body fat!
Hence the carbohydrate addiction/ obesity/serotonin
connection. (10)
Tryptophan vs. 5-HTP
In the 1970s, the American health food industry began to provide an alternative method
of getting more tryptophan to the brain -- tryptophan supplements. Many people found
that 500 to 3,000 mg of supplementary tryptophan daily provided practical relief from
depression, PMS, insomnia and obsessive-compulsive disorders. In 1989, the FDA
removed tryptophan from the American health food market due to a mysterious outbreak
of a rare but serious ailment -- eosinophilia myalgia (EMS). This EMS 'epidemic' was
later traced to a single batch of contaminated tryptophan from a Japanese producer.
Thirteen years later, although tryptophan has been proven to be safe (and is currently
available in baby food formulas, intravenous feeding solutions, and veterinary products)
the FDA still shows no signs of allowing tryptophan back onto the market as a dietary
supplement.
Fortunately, a safe, natural and effective alternative to tryptophan has been researched
for over 30 years. This substance is L-5-Hydroxytryptophan (5-HTP). 5-HTP is not
produced by bacterial fermentation (as was the tainted tryptophan) nor chemical
synthesis, but is extracted from the seeds of the Griffonia plant.
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Tryptophan to Serotonin Conversion
When neurons convert tryptophan into serotonin, they must first use a vitamin B3-
dependent enzyme to convert tryptophan into 5-HTP. A vitamin B6-dependent enzyme is
then used to convert 5-HTP into serotonin. One researcher noted, 'There are several
advantages of considering L-5-HTP, as opposed to L-tryptophan, as being the major
determinant in elevating brain serotonin levels: L-5-HTP is not degraded by tryptophan
pyrrolase to kynurenine, the major pathway for peripheral degradation of L-tryptophan
(about 98 percent).
Furthermore, L-5-HTP easily crosses the blood-brain barrier ...' (1) Additionally, it should
be noted that 5-HTP is not incorporated into proteins, as is tryptophan; nor is 5-HTP
used to make vitamin B3, as is tryptophan. Thus, in comparison to tryptophan, 5-HTP is
virtually a 'guided missile' that is directly targeted to increasing brain serotonin levels.
Strikingly, some studies have shown better results using 200 to 300 mg of 5-HTP per
day as an antidepressant than other studies using 2000 to 3,000 mg or more of
tryptophan per day. (17)
A placebo-controlled, double-blind study reported in 1992 found excellent results treating
obesity using doses of 5-HTP as high as 900 mg daily, with minimal side effects (the
greatest side effect being diarrhea or upset stomach)! (11) In one study, the
antidepressant effects of 5-HTP was compared with fluvoxamine, a prescription Prozaclike
drug used in Europe. The 5-HTP patients showed slightly better treatment response
than the fluvoxamine group, yet had significantly fewer and less severe side effects. The
researchers note: 'Regarding tolerance and safety, however, oxitriptan [5-HTP] proved
superior to fluvoxamine as was apparent from a marked difference in severity of
untoward side effects between the two compounds. The study presented here ...strongly
confirm[s] the efficacy of 5-HTP as an antidepressant.' (4)
Prozac
In a society that has made the book Listening to Prozac a
mega-bestseller, some may still consider serotonin-selective
re-uptake inhibitor (SSRI) drugs such as Prozac the 'gold
standard' of managing the serotonin-deficiency syndrome,
even though the Poeldinger study showed 5-HTP to be
superior to a major SSRI, fluvoxamine. A study reported by
Risch and Nemeroff demonstrates, however, that even those
'successfully' treated with SSRIs (ignoring their frequent and sometimes serious side
effects) are dependent upon their brains’ producing adequate serotonin from either
tryptophan or 5-HTP.
SSRIs work by conserving existing brain serotonin supplies by keeping more serotonin
in the synaptic gap between neurons. They achieve this through preventing enzymatic
degradation of synaptic serotonin. SSRIs do not enhance serotonin production. Risch
and Nemeroff state: "...depressed patients were treated with low-tryptophan diets that
were supplemented with high doses of neutral amino acids [which compete with
tryptophan for transport through the blood-brain barrier]... Remitted depressed subjects
receiving serotonergic antidepressants (e.g. fluoxetine [Prozac], fluvoxamine) who were
challenged with low-tryptophan diet supplemented with neutral amino acids promptly
relapsed into severe clinical depression. When the tryptophan supplementation was
provided, the patients promptly recovered..." (3)
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The many successful published studies using 5-HTP show that 5-HTP, by naturally
elevating brain serotonin, can alleviate the serotonin-deficiency syndrome without any
help from SSRI drugs. Yet the study related by Risch and Nemeroff eloquently shows
that the success of SSRI drugs is crucially dependent upon the brain producing
adequate serotonin (from either tryptophan or 5-HTP), and that brain serotonin
production is the controlling or rate-limiting variable underlying the apparent success of
SSRIs. It appears that the more logical and economically sound choice to alleviate
conditions that result from the serotonin deficiency syndrome is 5-HTP, the immediate
precursor of the deficient substance.
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References
1. K. Zmilacher, et al. L-5-Hydroxytryptophan Alone and in Combination with a Peripheral Decarboxylase Inhibitor in the
Treatment of Depression. Neuropsychobiology. 1988; 20: 28-35.
2. W. Byerley, et al. 5-Hydroxytryptophan: A Review of Its Antidepressant Efficacy and Adverse Effects. J Clin
Psychopharmacol 1987; 7: 127-37.
3. S. Risch and C. Nemeroff. Neurochemical Alterations of Serotonergic Neuronal Systems in Depression. J Clin
Psychiatry. 1992; 53: 3-7.
4. W. Poeldinger, et al. 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.
5. H. van Praag. Management of Depression with Serotonin Precursors. Biol Psychiatry. 1981; 16: 291-310.
6. S Takahashi, et al. Effect of L-5-Hydroxytryptophan on Brain Monoamine Metabolism and Evaluation of Its Clinical
Effect in Depressed Patients. Psychiat Res 1975; 12: 177-87.
7. R. Kahn and H. Westenberg. L-5-Hydroxytryptophan in the Treatment of Anxiety Disorders. J Affect Disord, 1985; 8:
197-200.
8. V. Linnoila and M. Virkkunen. Aggression, Suicidality, and Serotonin. J Clin Psychiatry. 1992; 53: 46-51.
9. L. Buydens-Branchey, et al. Age of Alcoholism Onset. II. Relationship to Susceptibility to Serotonin Precursor
Availability. Arch Gen Psychiatry. 1989; 46: 231-36.
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