Summary of 5-HTP
Primary Information, Benefits, Effects, and Important Facts
5-HTP is a compound which gets converted into serotonin in the brain. Serotonin is one of the principal neurotransmitters involved in happiness and anti-depression.
5-HTP has been used with success to restore serotonin levels in those that may suffer from decreased serotonin levels, such as the depressed and those with high levels of body inflammation (typically seen in metabolic syndrome).
Things To Know & Note
5-HTP is neurally active by increasing serotonin levels and will be felt, but its actions are more 'euphoric' or happiness inducing rather than stimulatory.
How to Take 5-HTP
Recommended dosage, active amounts, other details
A typical dose of 5-HTP is in the range of 300-500 mg, taken either once daily or in divided doses. Lower doses may also be effective, although usually when paired with other substances.
For the purpose of reducing food intake, 5-HTP should be taken with a meal as it increases satiety from food intake (rather than reducing appetite/hunger).
5-HTP should not be taken with any neurological drug that has been prescribed for antidepressant or other cognitive purposes unless cleared by a medical doctor. This is most important for SSRI usage, wherein the combination with 5-HTP is potentially lethal.
Human Effect Matrix
The Human Effect Matrix looks at human studies (it excludes animal and in vitro studies) to tell you what effects 5-htp has on your body, and how strong these effects are.
|Grade||Level of Evidence [show legend]|
|Robust research conducted with repeated double-blind clinical trials|
|Multiple studies where at least two are double-blind and placebo controlled|
|Single double-blind study or multiple cohort studies|
|Uncontrolled or observational studies only|
Level of Evidence
? The amount of high quality evidence. The more evidence, the more we can trust the results.
Magnitude of effect
? The direction and size of the supplement's impact on each outcome. Some supplements can have an increasing effect, others have a decreasing effect, and others have no effect.
Consistency of research results
? Scientific research does not always agree. HIGH or VERY HIGH means that most of the scientific research agrees.
|Notable||Very High See all 3 studies|
|Minor||Very High See all 3 studies|
|Minor||- See study|
|Minor||- See study|
Studies Excluded from Consideration
Scientific Research on 5-HTP
Click on any below to expand the corresponding section. Click on to collapse it.
The neurotransmitter serotonin is synthesized from the amino acid tryptophan through 5-HTP. In which tryptophan gets converted into 5-HTP via the enzyme tryptophan hydroxylase and 5-HTP gets converted into serotonin via the enzyme L-amino acid decarboxylase. Serotonin is later degraded into 5-hydroxyindoleacetic acid (5-HIAA) by monoamine oxidase.
A study using an oral cavity spray of 5-HTP (via the plant source of Griffonia Simplicifolia) has noted that 7.68mg of 5-HTP via 30.72mg of Griffonia Simplicifolia extract taken five times daily (total daily dose of around 40mg) has confirmed an increase in urinary 5-HIAA (from 3.71+/-1.27mg/24 hours to 8.80+/-4.02mg/24 hours; a 137% increase) relative to baseline, confirming that 5-HTP can be absorbed sublingually. Similar results have been noted elsewhere with this spray, although it should be noted that it is confounded with other herbs (detailed in the appetite subsection).
Appears to be able to be absorbed sublingually when a spray is applied to the oral cavity
It is used as a supplement (rather than tryptophan) to increase serotonin levels as tryptophan can be diverted into niacin production or protein construction whereas 5-HTP has the sole fate of serotonin synthesis. 5-HTP also crosses the blood brain barrier easily.
Supplementation of 5-HTP has been shown to be more effective than tryptophan supplementation alone. This additional benefit of 5-HTP supplementation arises because 5-HTP bypasses the cell's L-tryptophan's own self-regulation on the IDO enzyme, in which it upregulates the activity of IDO (discussed in next section) to maintain body homeostasis of tryptophan and it bypasses the tryptophan hydroxylase enzyme, which is the rate limiting step in serotonin biosynthesis.
5-HTP is very reliable in increasing serotonin levels. 5-HTP is actually used as a clinical test to judge the potency of drugs that affect serotonin levels (by pairing an experimental drug with 5-HTP to induce 'serotonin syndrome', or serotonin toxicity, one can see how much that drug exacerbates serotonin biosynthesis or bioavailability by seeing how much of a 5-HTP dose is required to induce the syndrome; the lower dose indicative of higher drug potency). This test is known as the 5-HTP induced syndrome test.
At least one study using an extract of Griffonia simplicifolia (10.24mg giving 2.56mg 5-HTP; confounded with Centella asiatica and Taraxacum officinale at 11.7mg and 4.55mg Paulina cupana and 9.75mg Artichoke extract) taken in three hits, five times a day (40mg 5-HTP total), by 20 overweight or obese females (non-depressive and without eating disorders) for 4 weeks has noted an increase in satiety and reduced binge eating tendencies; the increase in satiety was said to account for the improved weight loss results seen in the experimental group when both were given weight loss advice and diets. This spray has been noted elsewhere to increase satiety (and vicariously through that, body weight) over 2 months in a similar demographic of women.
In 19 obese females given either placebo or 8mg/kg (weight not actually given, only BMI between 30-40 for women) daily for 5 weeks without any concurrent dietary recommendations, 5-HTP treatment was associated with a decrease in appetite and food intake (resulting in weight loss) without significantly affecting mood state. This study noted that food intake was reduced from an average of 2,903kcal to 1,819kcal (62% of baseline) while placebo only reduced calories to 80%, and the 0.5kg weight loss in placebo was outperformed by a near 1.5kg loss in 5-HTP. These weight loss effects have been noted with 750mg 5-HTP over 2 weeks in overweight diabetics and over 12 weeks in obese persons given 900mg 5-HTP daily (58% of baseline intake); this latter study had a 6 week trial without a diet (in which significant weight loss was only noted at week 6) followed up by coadministration with a diet where weight loss proceeded to reach an additional 3.3kg over the subsequent 6 weeks; this latter study is duplicated in Medline.
5-HTP appears to reduce food intake secondary to increasing satiety, although most studies are currently conducted in women (in regards to 5-HTP being related to serotonin, this may be relevant; see our creatine page and the Depression section for more information). At least one study that was mixed gender supports the notion it benefits both genders, however
At least one study has actively differentiated between 'an increase in satiety' (sensation of fullness from food) and a 'decrease in appetite' (less desire to eat) and noted that 5-HTP causes an increase in satiety without a concomitant decrease in appetite. Additionally, most studies are in exclusively females which may have more significance with interventions pertaining to serotonin metabolism; only one study mentioned above was conducted in men as well but appears to suggest that it benefits both genders.
A more correct phrase would be that 5-HTP can increase satiety (sensation of fullness) rather than reducing appetite (preventing the desire to eat), although the end result is less food intake. Currently, this is only investigated in obese persons
It should be noted that, anecdotally, 5-HTP is said to reduce cravings for carbohydrates in particular. The serotonergic (related to serotonin) system plays a role in macronutrient selection particular in obese persons with a craving for carbohydrates and enhancing serotonergic transmission is known to reduce these cravings. Beyond this, depressed serotonergic tranmission (hypothalamus) is also implicated in increased eating and reduced satiety in general.
When looking at studies that investigate carbohydrates per se, one study in overweight women given 8mg/kg 5-HTP for 5 weeks noted that while placebo did not reduce carbohydrate ingested (calories were reduced in placebo, but carbohdyrate remained at 38% of voluntary calorie intake) that 5-HTP also retained 38% of intake as carbohydrates despite consuming less calories and carbohydrates in total. A decrease in both carbohydrate and dietary fat has been noted with 750mg 5-HTP daily for 2 weeks in diabetics (with no dietary guidelines given), but appeared to be reduced to a similar degree as calories overall. Only one study supports these anecdotes, where the reduction in calories seemed to be acounted mostly for by carbohydrates (75% of observed reduction) and then fats (25%).
5-HTP supplementation has been reported to cause a selective reduction in cravings for carbohydrates. Currently this is weakly supported (two studies suggest it just reduces all caloric intake indiscriminately) although at least one study suggests it might selectively reduce carbohydrate intake
It has been reported that deficiencies in the amino acid tryptophan (precursor to 5-HTP) are correlated with depression, as evidence by serum tryptophan in depressed persons. Decreased levels of tryptophan in the body can come from various means but are most likely caused by a diet lacking in the amino acid as substrate, or by upregulation of enzymes (most notably indoleamine 2,3-dioxygenase(IDO) and tryptophan 2,3-dioxygenase(TDO)) that degrade tryptophan or direct it to paths that are not serotonin synthesis causing a relative deficiency. These enzymes can be upregulated in states of chronic inflammation and injection of some pro-inflammatory cytokines has been implicated in depression and increasing the kyurenine:tryptophan ratio, which is indicative of IDO activity being increased. The activity of tryptophan hydroxylase can also be further downregulated in cases of Magnesium or vitamin B6 deficiency, stress, or excessive tryptophan levels.
For those deficient in tryptophan, supplemental tryptophan and 5-HTP could be somewhat effective, although a meta-analysis found barely statistically significant results (Odds Ratio of 1.3-13.2) from a statistically subpar collection of studies, and based on the inclusion criteria it set it had to expand its analysis to both 5-HTP and Tryptophan to get two studies to assess.
5-HTP as monotherapy in depression, despite the theoretical benefit, is not yet proven
In regards to interventions, one study in treatment resistant depressed persons that combination therapy of 5-HTP with Carbidopa noted that 43 out of 99 (43.4%) patients improved with an average 200mg (variable 50-600mg) dosage of 5-HTP. It has been noted that since Cardidopa is a peripheral decarboxylase inhibitor that can prevent metabolism of monoamines including serotonin that these results are unlikely to reflect monotherapy with 5-HTP, despite being within the 30-45% range sometimes seen with the placebo effect.
Interventions showing promise with 5-HTP tend to use other compounds alongside 5-HTP to augment efficacy
One study investigating romantic stress that looked at nondepressed youth who went through a recent breakup and were given 60mg of Griffonica Simplicifonia (12.8mg 5-HTP) twice a day for 6 weeks in an open-label study noted reductions in percieved romantic stress when measured at the 3 week mark with no further improvement at 6 weeks; there was no control nor placebo group in this study.
5-HTP has been investigated for its role in hot flashes as Selective Serotonin Reuptake Inhibitors (SSRIs) have been noted to reduce the occurrence of hot flashes and menopausal symptoms. In a study in menopausal females given 150mg 5-HTP daily (50mg taken thrice a day) for a period of one week failed to quantitivatively reduce the occurrance of hot flashes as assessed by a Flashmark Pro recording device.
In 20 persons undergoing alcohol withdrawal taking 5-HTP (5mg) alongside Glutamine (150mg) and D-Phenylalanine (300mg) and some minerals such as Calcium and Magnesium, it was noted that after 40 days of nutritional therapy (in a hospital setting) that all withdrawal symptoms assessed via SCL-90-R except for anxiety noted a greater reduction with nutritional support relative to placebo.
Serotonin appears to be associated with panic attacks. Although studies that have used tryptophan depletion techniques in humans do not necessarily induce a panic attack it appears it may sensitize the body by an increase in neurovegetative panic symptoms and increased anxiety which suggests that serotonin is protective against panic attacks, at least acutely. A study in 24 unmedicated panic disorder patients and normal participants given 200mg 5-HTP prior to a 35% CO2 test (used to induce a panic attack-like response) noted that the test was able to induce panic attack in both panic disorder patients and normal persons and that 200mg 5-HTP was protective in both conditions but to a greater degree in persons suffering from panic disorders. This has been replicated with cholecystokinin-4 induced panic attack with 200mg 5-HTP in otherwise healthy persons.
Persons who suffer from Panic disorders may be more susceptable to serotonergic imbalances, with tryptophan depletion (thought to be a reliable model to reduce serotonin) causing greater susceptability to panic attacks.
Expanding upon the possible anti-panic effects of 5-HTP, one study using 2mg/kg 5-HTP to children (3.2-10.6 years of age) at bedtime for 20 days noted that 5-HTP was asssociated with beneficial response (more than 50% reduction in night terror frequency) of 93.5% of children relative to 28.6% in placebo. Oddly, 6 months after the initial supplementation period the 5-HTP group still reported less sleep terrors (83.9% reporting improvement).
In persons with Panic Disorders (versus persons without as control) ingesting 200mg of 5-HTP, both groups experienced an increase in salivary cortisol within 3 hours but the persons with Panic Attacks continued to have greater increases after the 3 hour mark; this increased cortisol was independent of any percieved side-effects such as headache, fatigue, perspiration, nausea, etc.
It has been noted that isolated supplementation of 5-HTP may deplete or reduce the bioactivity of catecholamines such as dopamine (which extends to L-Tryptophan) and that this relationship also acts in reverse, with supplemental L-Tyrosine possibly able to deplete 5-HTP and Serotonin itself, which extends to supplemental L-DOPA which may reduce all intermediate of serotonin synthesis although L-DOPA may also deplete L-Tyrosine (as it is merely later in the same metabolic chain). Due to excessive levels of either one depleting the other, some authors have suggested that combination therapy of 5-HTP and L-Tyrosine (the furthest back in the metabolic chain while still passing rate limiting enzymes) is a potentially useful avenue for anti-depressive effects.
Monoamine metabolism appears to be in somewhat of a balance, and supplementing compounds early in the catecholamine synthesis pathway (L-Tyrosine and L-DOPA) may reduce levels of those in the serotonergic pathway (L-Tryptophan and 5-HTP) as well as vice-versa
The enzyme dopamine decarboxylase (aromatic L-amino acid decarboxylase) mediates the conversion of 5-HTP into serotonin, and this enzyme is expressed in stomach tissue. Inhibition of this enzyme in the stomach during 5-HTP ingestion is thought to promote the concentration of 5-HTP that reaches neural tissue, which is supported by a study using 100-200mg Carbidopa (pharmaceutical inhibitor) alongside 5-HTP to increase radioactivity of 5-HTP (indicative of neural accumulation) in humans.
The combination of supplemental 5-HTP and a dopamine decarboxylase inhibitor is also thought to reduce the risk for cardiovascular complications, as excess serum (but not neural) serotonin is associated with heart valve disease in rats. Due to the accumulation of 5-HTP in neural tissue following the combination it is plausible to assume a reduction in systemic serotonin; this has not been demonstrated yet, however.
Pairing supplemental 5-HTP with an inhibitor of dopamine decarboxylase appears to promote accumulation of 5-HTP and subsequently serotonin in the brain, which has been noted in human case studies. This theoretically reduces the risk of heart valve complications (not yet demonstrated)
In some studies that record appetite suppression with 5-HTP supplementation, nausea appears to also be reported at higher freqencies than placebo, although some interventions note this as the only relevant side effect. Short term studies tend to note that nausea persists throughout the study period while those expanding beyond three weeks note that reports of nausea tend to decline at this time point.
No toxicity reports have been noted with doses at or below 50mg/kg bodyweight. However, doses of 100-200mg/kg bodyweight have been associated with Serotonin Syndrome in lab animals when administered in isolation.
With normal dosages of 5-HTP (typically around 300mg a day), however, side effects and the serotonin syndrome have not been observed in humans even with coingestion of anti-depressants such as MAOIs. Due to the limited size of the samples in said studies, however, it is suggested that these results be seen as preliminary.
It should be noted that supplemental 5-HTP can cause an increase in urinary 5-HIAA, which is the major metabolite of serotonin that is excreted in the urine. Increased urinary 5-HIAA is also sometimes a diagonistic marker for carcinoid tumors due to increased conversion of tryptophan to serotonin in these tumors, and in this case serum chromogranin A should be measured (as supplemental 5-HTP does not appear to increase chromogranin A).
- Jukić T, et al. The use of a food supplementation with D-phenylalanine, L-glutamine and L-5-hydroxytriptophan in the alleviation of alcohol withdrawal symptoms. Coll Antropol. (2011)
- Rondanelli M, et al. Satiety and amino-acid profile in overweight women after a new treatment using a natural plant extract sublingual spray formulation. Int J Obes (Lond). (2009)
- Rondanelli M, et al. Relationship between the absorption of 5-hydroxytryptophan from an integrated diet, by means of Griffonia simplicifolia extract, and the effect on satiety in overweight females after oral spray administration. Eat Weight Disord. (2012)
- Turner EH, Loftis JM, Blackwell AD. Serotonin a la carte: supplementation with the serotonin precursor 5-hydroxytryptophan. Pharmacol Ther. (2006)
- Birdsall TC. 5-Hydroxytryptophan: a clinically-effective serotonin precursor. Altern Med Rev. (1998)
- The Metabolism of L-Tryptophan by Isolated Rat Liver Cells.
- Metabolism of an oral tryptophan load. I: Effects of dose and pretreatment with tryptophan.
- O'Neil MF, Moore NA. Animal models of depression: are there any. Hum Psychopharmacol. (2003)
- Ceci F, et al. The effects of oral 5-hydroxytryptophan administration on feeding behavior in obese adult female subjects. J Neural Transm. (1989)
- Cangiano C, et al. Effects of oral 5-hydroxy-tryptophan on energy intake and macronutrient selection in non-insulin dependent diabetic patients. Int J Obes Relat Metab Disord. (1998)
- Cangiano C, et al. Eating behavior and adherence to dietary prescriptions in obese adult subjects treated with 5-hydroxytryptophan. Am J Clin Nutr. (1992)
- Cangiano C, et al. Effects of 5-hydroxytryptophan on eating behavior and adherence to dietary prescriptions in obese adult subjects. Adv Exp Med Biol. (1991)
- Precursor control of Neurotransmitter Synthesis.
- Wurtman RJ, Wurtman JJ. Brain serotonin, carbohydrate-craving, obesity and depression. Obes Res. (1995)
- Routh VH, Stern JS, Horwitz BA. Serotonergic activity is depressed in the ventromedial hypothalamic nucleus of 12-day-old obese Zucker rats. Am J Physiol. (1994)
- Total and Free tryptophan concentration in the plasma of depressive patients.
- Decreased plasma tryptophan levels in major depression.
- Taylor MW, Feng GS. Relationship between interferon-gamma, indoleamine 2,3-dioxygenase, and tryptophan catabolism. FASEB J. (1991)
- Myint AM, Kim YK. Cytokine-serotonin interaction through IDO: a neurodegeneration hypothesis of depression. Med Hypotheses. (2003)
- Transcriptional activation of Indoleamine Dioxygenase by Interleukin 1 and Tumor Necrosis Factor α in Interferon-Treated Epithelial Cells.
- The phenomenology and treatment of interferon-induced depression.
- Bonaccorso S, et al. Increased depressive ratings in patients with hepatitis C receiving interferon-alpha-based immunotherapy are related to interferon-alpha-induced changes in the serotonergic system. J Clin Psychopharmacol. (2002)
- Shaw K, Turner J, Del Mar C. Are tryptophan and 5-hydroxytryptophan effective treatments for depression? A meta-analysis. Aust N Z J Psychiatry. (2002)
- van Hiele LJ. l-5-Hydroxytryptophan in depression: the first substitution therapy in psychiatry? The treatment of 99 out-patients with 'therapy-resistant' depressions. Neuropsychobiology. (1980)
- Hinz M, Stein A, Uncini T. 5-HTP efficacy and contraindications. Neuropsychiatr Dis Treat. (2012)
- Hinz M, Stein A, Uncini T. Amino acid management of Parkinson's disease: a case study. Int J Gen Med. (2011)
- Hinz M, Stein A, Uncini T. Monoamine depletion by reuptake inhibitors. Drug Healthc Patient Saf. (2011)
- Shell W, et al. A randomized, placebo-controlled trial of an amino acid preparation on timing and quality of sleep. Am J Ther. (2010)
- Emanuele E, et al. An open-label trial of L-5-hydroxytryptophan in subjects with romantic stress. Neuro Endocrinol Lett. (2010)
- Speroff L, et al. Efficacy and tolerability of desvenlafaxine succinate treatment for menopausal vasomotor symptoms: a randomized controlled trial. Obstet Gynecol. (2008)
- Stearns V, et al. Paroxetine is an effective treatment for hot flashes: results from a prospective randomized clinical trial. J Clin Oncol. (2005)
- Freedman RR. Treatment of menopausal hot flashes with 5-hydroxytryptophan. Maturitas. (2010)
- Freedman RR, Wasson S. Miniature hygrometric hot flash recorder. Fertil Steril. (2007)
- Park SB, et al. Tryptophan depletion in normal volunteers produces selective impairments in learning and memory. Neuropharmacology. (1994)
- Oldman A, et al. Biochemical and behavioural effects of acute tryptophan depletion in abstinent bulimic subjects: a pilot study. Psychol Med. (1995)
- Cleare AJ, Bond AJ. The effect of tryptophan depletion and enhancement on subjective and behavioural aggression in normal male subjects. Psychopharmacology (Berl). (1995)
- Klaassen T, et al. Effects of tryptophan depletion on anxiety and on panic provoked by carbon dioxide challenge. Psychiatry Res. (1998)
- Miller HE, Deakin JF, Anderson IM. Effect of acute tryptophan depletion on CO2-induced anxiety in patients with panic disorder and normal volunteers. Br J Psychiatry. (2000)
- Schruers K, et al. Effects of tryptophan depletion on carbon dioxide provoked panic in panic disorder patients. Psychiatry Res. (2000)
- Schruers K, et al. Acute L-5-hydroxytryptophan administration inhibits carbon dioxide-induced panic in panic disorder patients. Psychiatry Res. (2002)
- Maron E, et al. The effect of 5-hydroxytryptophan on cholecystokinin-4-induced panic attacks in healthy volunteers. J Psychopharmacol. (2004)
- Bruni O, et al. L -5-Hydroxytryptophan treatment of sleep terrors in children. Eur J Pediatr. (2004)
- Schruers K, et al. L-5-hydroxytryptophan induced increase in salivary cortisol in panic disorder patients and healthy volunteers. Psychopharmacology (Berl). (2002)
- Stamford JA, Kruk ZL, Millar J. Striatal dopamine terminals release serotonin after 5-HTP pretreatment: in vivo voltammetric data. Brain Res. (1990)
- Zhelyaskov DK, Levitt M, Udenfriend S. Tryptophan derivatives as inhibitors of tyrosine hydroxylase in vivo and in vitro. Mol Pharmacol. (1968)
- Awazi N, Guldberg HC. On the interaction of 5-hydroxytryptophan and 5-hydroxytryptamine with dopamine metabolism in the rat striatum. Naunyn Schmiedebergs Arch Pharmacol. (1978)
- Breier JM, Bankson MG, Yamamoto BK. L-tyrosine contributes to (+)-3,4-methylenedioxymethamphetamine-induced serotonin depletions. J Neurosci. (2006)
- Correlation between brain tryptophan and plasma neutral amino acid levels following food consumption in rats.
- Ritvo ER, et al. Effects of L-dopa in autism. J Autism Child Schizophr. (1971)
- Karobath M, Díaz JL, Huttunen MO. The effect of L-dopa on the concentrations of tryptophan, tyrosine and serotonin in rat brain. Eur J Pharmacol. (1971)
- Borah A, Mohanakumar KP. Long-term L-DOPA treatment causes indiscriminate increase in dopamine levels at the cost of serotonin synthesis in discrete brain regions of rats. Cell Mol Neurobiol. (2007)
- van Praag HM. In search of the mode of action of antidepressants. 5-HTP/tyrosine mixtures in depressions. Neuropharmacology. (1983)
- Henman FD. Amino acid decarboxylase enzymes--vital or irrelevant to gastric secretion. Digestion. (1975)
- Orlefors H, et al. Carbidopa pretreatment improves image interpretation and visualisation of carcinoid tumours with 11C-5-hydroxytryptophan positron emission tomography. Eur J Nucl Med Mol Imaging. (2006)
- Bertoldi M, Gonsalvi M, Voltattorni CB. Green tea polyphenols: novel irreversible inhibitors of dopa decarboxylase. Biochem Biophys Res Commun. (2001)
- Gustafsson BI, et al. Long-term serotonin administration induces heart valve disease in rats. Circulation. (2005)
- Aliño JJ, Gutierrez JL, Iglesias ML. 5-Hydroxytryptophan (5-HTP) and a MAOI (nialamide) in the treatment of depressions. A double-blind controlled study. Int Pharmacopsychiatry. (1976)
- Kline N, Sacks W. Treatment of depression with an mao inhibitor followed by 5-HTP--an unfinished research project. Acta Psychiatr Scand Suppl. (1980)
- Nicolodi M, Sicuteri F. Fibromyalgia and migraine, two faces of the same mechanism. Serotonin as the common clue for pathogenesis and therapy. Adv Exp Med Biol. (1996)
- Comparison of the Antidepressant Action of Tryptophan, Tryptophan/5-Hydroxytryptophan Combination and Nomifensine.
- Nardini M, et al. Treatment of depression with L-5-hydroxytryptophan combined with chlorimipramine, a double-blind study. Int J Clin Pharmacol Res. (1983)
- van der Horst-Schrivers AN, et al. Persistent low urinary excretion of 5-HIAA is a marker for favourable survival during follow-up in patients with disseminated midgut carcinoid tumours. Eur J Cancer. (2007)
- Joy T, et al. Increase of urinary 5-hydroxyindoleacetic acid excretion but not serum chromogranin A following over-the-counter 5-hydroxytryptophan intake. Can J Gastroenterol. (2008)