Summary of L-Tyrosine
Primary Information, Benefits, Effects, and Important Facts
L-Tyrosine is an amino acid found in the diet that is metabolized to produce catecholamines such as dopamine and adrenaline. It is also used in the production of thyroid hormones. For these reasons, weight loss supplements often include it.
When it comes to the topic of actually increasing dopamine and adrenaline outright, L-tyrosine does not seem to hold much promise. The synthesis of catecholamines is highly regulated in the body, so simply increasing the amount of L-tyrosine in your body does not necessarily increase catecholamine production.
However, some studies have noted that in stressful situations where noradrenaline exerts a protective effect, supplying L-tyrosine seems to provide a 'safety buffer' of building blocks that can prolong the anti-stress effect of catecholamines by delaying their depletion. This has been noted in situations of cold stress and sleep deprivation in humans but at a relatively high dose of 150mg/kg. Improvements in memory during stressful situations have also been found. However, more research is needed to confirm this. What little research we have doesn't suggest an effect on depression.
Tired of all the misinformation spread by supplement companies?
Learn what works, what's a waste, and how to achieve your health goals with our free supplement mini-course.
Things To Know & Note
L-tyrosine is stimulatory. It may thus theoretically interact with other stimulatory pharmaceuticals or supplements.
L-tyrosine can theoretically interact with the absorption of some drugs that look like certain amino acids (e.g. levodopa). It can also theoretically interact with MAOIs and exacerbate hyperthyroid conditions.
How to Take L-Tyrosine
Recommended dosage, active amounts, other details
Anecdotally, L-Tyrosine tends to be taken in doses of 500-2000mg approximately 30-60 minutes before any acute stressor (this tends to be exercise)
Studies in humans showing most anti-stress promise for acute supplemental L-Tyrosine use a dosage range of 100-150mg/kg bodyweight which can be taken 60 minutes before exercise; this is a dosage range of 9-13.5g for a 200lb person and 7-10g for a 150lb person.
If using higher doses and finding digestive issues, this may be split into two doses separated by half an hour (30 and 60 minutes prior to acute stress).
Human Effect Matrix
The Human Effect Matrix looks at human studies (it excludes animal and in vitro studies) to tell you what effects l-tyrosine 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.
|Minor||Very High See all 3 studies|
|-||High See all 3 studies|
|Minor||Very High See 2 studies|
|Minor||Moderate See 2 studies|
|Minor||Moderate See 2 studies|
|-||- See study|
|-||- See study|
|-||- See study|
|-||- See study|
Scientific Research on L-Tyrosine
Click on any below to expand the corresponding section. Click on to collapse it.
The catecholamine metabolic pathway in vivo starts with the amino acid L-phenylalanine, which gets converted into L-tyrosine by the enzyme phenylalanine hydroxylase. L-tyrosine then gets converted into the compound L-DOPA via tyrosine hydroxylase. L-DOPA is then decarboxylated via aromatic L-amino acid decarboxylase into Dopamine, which later turns into noradrenaline via oxidation from the enzyme dopamine-beta-hydroxylase and then finally converted to adrenaline via Phenylethanolamine-N-methyl-transferase. The last three compounds (Dopamine, NA, Adrenaline) are collectively referred to as 'Catecholamines'; the rate limiting step in this formula is the enzyme tyrosine hydroxylase. 
Supplementing with any of the prior substrates has the ability to increase adrenaline levels, given that the enzyme between said substrate and adrenalines are not maxed out.
Supplemental L-Tyrosine is converted into L-DOPA and then into active catecholamines (adrenaline/epinephdrine, noradrenaline/norepinephrine, and dopamine). L-Tyrosine forms a pool of substrate that this group of catecholamine neurotransmitters can get substrate from when their production is needed.
Phenylketonuria (PKA) is a genetic disease in which the body fails to properly metabolize the amino acid Phenylalanine, and said amino acid can build up to toxic levels.
Tyrosine has been looked at for possibly alleviating symptoms of PKA (as a reduction of phenylalanine may reduce catecholamines, but this can be attenuated with L-Tyrosine which is what Phenylalanine turns into in order to create catecholamines). Results, however, are preliminary.  
L-tyrosine can go through three types of metabolisms: the amino acid can be taken up in the tissues and incorporated into peptides and proteins, small amounts can be converted into thyroxine, melanin and catecholamines, or it can be deaminated to form p-hydroxy phenylpyruvic acid (a substrate for gluconeogenesis). The enzyme that catalyzes tyrosine to form the substrate for gluconeogenesis is most active in the day in in vivo rat livers with lower tyrosine concentrations; in humans, tyrosine concentration in plasma is the lowest between 1:30- 2:30 am and rises to a peak at 10:30 am. 
Tyrosine is usually metabolized into L-dopa via hydroxylation, but another pathway involving its decarboxylation can lead to build-up of trace amines such as tyramine.  The hydroxylation of tyrosine by the enzyme tyrosine hydroxylase is the rate-limiting step in the synthesis of catecholamines like norepinephrine and epinephrine. 
There is some concern that tyrosine may decrease the effectiveness of L-dopa. Tyrosine and levodopa compete for absorption in the proximal duodenum by the large neutral amino acid (LNAA) transport system. Doses of tyrosine and L-dopa should be separated by at least 2 hours. Additionally, tyrosine is a precursor to thyroid hormones and might boost levels of thyroid hormone medication like levothyroxine and liothyronine.   Tyrosine is also contraindicated with MAOI like isocarboxazid, phenelzine, tranylcypromine, and selegiline. Monoamine oxidase is the enzyme responsible for the breakdown and inactivation of the catecholamines. A buildup of the catecholamines, including tyramine, which can be found in certain foods and formed from exogenous tyrosine in the gut by certain bacteria in some foods, can result in dangerous increases in blood pressure.
There are drug interactions between L-tyrosine and MAOI medications, thyroid medications, and levodopa.
150mg/kg L-Tyrosine taken in a vessel of apple sauce can elevated plasma Tyrosine concentrations from 56.3nmol/L (baseline and similar to control values) to the range of 140-168nmol/L within 90 minutes, which remained within that concentration until measurements stopped at 150 minutes; a significant difference from placebo existed within 30 minutes and was measured at approximately 80nmol/L.  These changes in plasma tyrosine concentrations were not matched with increases in plasma noradrenaline, which were similar between groups.  Plasma tyrosine concentrations increased to a mean of 203 mmol/L in response to large doses (about 10 g) of extra tyrosine in healthy individuals.  Reference values of tyrosine concentrations in plasma vary between 35-102 mmol/L for different age groups and sexes (including children and adults) after an overnight fast.  In nonfasting healthy young adults, plasma tyrosine concentrations vary between 61-99 mmol/L.  
A similar spike in serum Tyrosine levels is noted in rats (serum norepinephrine untested) and the increase in serum Tyrosine appears to return to baseline 4 hours after oral administration. 
Fairly rapidly absorbed from the intestines into the blood, and remains peaked for approximately 2-4 hours after ingestion
L-Tyrosine (200-400mg/kg) can acutely increase noradrenaline (aka. norepinephrine or NE) concentrations in the hippocampus and prevent an acute stress-induced reduction of NE concentrations in rats subject to cold stress.  This may precede the ability of L-Tyrosine administration to reverse losses of memory induced by cold stress in humans.  This study (n=8) noted that 150mg/kg L-Tyrosine (dissolved in apple sauce that placebo ingested solely) taken before cognitive testing in a room where the temperature was reduced from 22°C to 4°C was able to reduce the time taken to answer a delayed Matching-to-Sample test and increase the amount of correct answers relative to cold placebo, but was unable to fully preserve performance seen in warm control periods (where L-Tyrosine did not appear to further improve performance). 
Currently no evidence that L-Tyrosine supplementation can improve memory function from baseline, but may be able to attenuate a decrease in memory formation associated with acute stressors
One study in children with diagnosed ADHD given a combination supplement of Tyrosine and 5-HTP (doses being titrated, with the lowest reported dose being 1,500mg tyrosine and 150mg 5-HTP and the highest being 3,750mg and 425mg respectively) noted that supplementation was associated with a greater reduction in symptoms as assessed by ADHD-RS; this study is also confounded with the inclusion of other nutrients (1,000mg of vitamin C, 220mg of calcium citrate, 75mg of vitamin B6 and 400μg of folate, 500mg of L-Lysine and 2,500-4,500mg L-cysteine, and 200-400μg of selenium).
Although L-Tyrosine may have a contribution in promoting attention, it has not been tested in isolation at this moment in time and thus it is unsure what role it plays
One study has combined supplemental L-Tyrosine and 'extended wakefulness' and noted that 150mg/kg of L-Tyrosine was able to attenuate the decrease in cognitive performance that was associated with sleep deprivation. 
May improve cognitive performance during sleep deprivation without significantly affecting sleep function
Acute uncontrollable stress is a phenomena that is able to deplete norepinephrine (NE) concentrations in neural tissue, particularly the hypothalamus and brainstem (containing the locus coeruleus)  and behavioural alterations associated with NE depletion in research animals have been shown to be avoidance/escape,  spontaneous motor activity,  aggressive behaviors,  and swimming. Ingestion of L-Tyrosine can attenuate the development of behavioural abnormalities associated with acute uncontrollable stressors in research animals in the range of 200-400mg/kg (oral or intravenous) 30-60 minutes prior to the acute stressor.   
Appears to mitigate some overt symptoms of acute and uncontrollable stress (this is in contrast to the adaptogen class of molecules, which may be effective against chronic and manageable stress); the two stress respones being mediated by different mechanisms
Some studies have been conducted specifically as it applies to cold stress (the goal of cold exposure therapy) have noted decrease immobility time in a dose-dependent manner in mice given 200-400mg/kg L-Tyrosine injections to a similar magnitude of 5-20mg/kg Phenylpropanolamine; Tyrosine appeared to synergistically reduce immobility time when paired with either Phenylpropanolamine or Amphetamines.  These effects correlated with hippocampal noradrenaline concentrations, which were preserved with L-Tyrosine.  These protective effects have been noted in human subjects, albeit a small sample size. 
May reduce the adverse effects of cold stress, has some human evidence of doing so (as it pertains to memory function)
One study in humans subjected to high altitudes has noted protective effects against acute stress due to lessened symptoms of acute stress, where 100mg/kg L-tyrosine (divided into two doses taken an hour apart) was associated with less headaches, stress, fatigue, distress, sleepiness, muscular soreness, and coldness due to the acute stressor as assessed by the Environmental Symptoms Questionnaire.  This study also noted improvements (relative to placebo) on global ratings of mood and happiness (assessed by Clyde Mood Scale and Profile of Mood states) and cognitive function (various cognitive tests).  Similar results are noted with the same oral dose after acute noise stressor  and some of these effects are noted after acute physical lower body stressors. 
Protection against acute stress has also been noted during a week-long combat training session, where 42g of protein (of which 2g were Tyrosine) was compared to placebo and associated with a preservation of cognitive performance, although this study failed to find significant improvements in mood between groups. 
Increasing levels of L-tyrosine in the brain is being looked at as a pharmaceutical method of alleviating neurological decline as catecholamines are typically decreased in states of dementia.
Surprisingly, catecholamines may act as anti-oxidants in the brain and be neuroprotective. 
150mg/kg L-Tyrosine taken prior to a cognitive test (with acute stressor) failed to significnatly influence blood pressure inherently or the spike in blood pressure induced by the acute stressor (which L-Tyrosine did not modify, spiking in both control and L-Tyrosine condition). 
One study conducted in cadets undergoing combat training who consumed 42g protein (2g tyrosine, confounded with other amino acids) noted that supplementation was associated with a decrease in systolic blood pressure by 10.4% from baseline, with placebo experiencing a lesser and nonsignificant decrease in blood pressure; no significant change noted in diastolic in this study although a trend towards reduction was noted  and another study under acute noise stress noted that L-Tyrosine ingestion was associated with a reduction in diastolic blood pressure within 15 minutes of ingestion of 100mg/kg.  This reduction in diastolic blood pressure has been noted previously in research animals.  
Although there isn't much reliability in the evidence currently, supplemental L-Tyrosine appears to either be ineffective or slightly reduce blood pressure; studies are confounded with the inclusion of stressors (which increase blood pressure) and effects of L-Tyrosine per se cannot be easily separated from the effects of an L-Tyrosine and stress interactions
L-tyrosine is typically supplemented with to alleviate the decline in neurological performance associated with moderate to long term mental exertion (which can be through study or exercise).
It is suspected in increasing performance from neurally intensive activites, as it does not appear to enhance performance systemically. 
N-Acetyl-L-Tyrosine appears to be able to contribute free L-Tyrosine in vivo after administration IV administration, but only able to increase L-Tyrosine concentrated 20% despite much larger increases in serum NALT.  56% of the adminstered dose of NALT is excreted in 4 hours  and another study suggests that, overall, 35% of the total NALT dose (administered parentally) is excreted via the urine as NALT and not L-Tyrosine. 
Limited practical evidence on NALT as an alternative to L-Tyrosine
Rats were given doses of 0, 200, 600, or 2000 mg/kg a day to examine toxicity of L-tyrosine. Edema of the cornified layer of the forestomach was seen in 600 mg/kg supplementation in female rats and in both sexes at 2000 mg/kg day. There was increased weight and hypertrophy of hepatocytes in the liver associated with an increase in ALT and AST in both sexes when given 2000mg/kg/day of L-tyrosine. An increase of kidney weight and urinary protein was also seen at 2000 mg/kg/day. Lastly, an increase in triglycerides, total cholesterol, phospholipids, potassium ions, calcium, total protein, and alpha one globulin were seen in both sexes at 2000 mg/kg/day. 
While the etiology of chronic migraine headaches is not well-understood, one hypothesis for its genesis involves abnormal metabolism of tyrosine.  Tyrosine is usually metabolized into L-dopa via hydroxylation, but another pathway involving its decarboxylation can lead to build-up of trace amines such as tyramine. It is this abnormal build-up of trace amines which is suspected by some researchers to play a role in migraines.  Some research has found that chronic migraine sufferers have elevated plasma levels of major products of tyrosine, including the neurotransmitters dopamine and norepinephrine, along with the trace amine tyramine.  This is consistent with the hypothesis that abnormal tyrosine metabolism favoring trace amine synthesis leads to high release of these neurotransmitters, which contributes to migraines.  It is possible that increased intake of L-tyrosine in migraine sufferers may fuel this process and make migraines worse, although there is currently no direct evidence substantiating this claim.
L-tyrosine is Generally Recognized as Safe (GRAS) in the USA.  When L-tyrosine is used orally and short term at a dose of ≤150 mg/kg or ≤12 g per day for up to three months is generally safe.    
Mothers with PKU could be taking tyrosine supplementation due to the hypothesis that low fetal tyrosine concentration in blood can cause mental retardation. However, this hypothesis has not been proven in any trial with a treatment based on tyrosine supplementation without phenylalanine restriction. 
A toxic effect of a combination of mildly increased phenylalanine and tyrosine was shown in offsprings of rats after taking tyrosine supplementation. The offsprings of the rats showed difficulties in learning. However, there have been no studies showing this toxic effects in humans. 
There has been hypotheses that tyrosine may be bad to the fetus. However, no human studies can prove this hypothesis.
Patients with hereditary tyrosinemia or persistent hypertyrosinemia may develop skin and eye lesions when the plasma level is 10 times of that found in clinical trials administering a tyrosine dose of 150 mg/kg to humans. 
In patients with hereditary tyrosinemia, it may cause skin and eye lesions at doses above the recommended intake.
When 100 mg/kg of tyrosine is administered to humans, tyrosine decreased diastolic blood pressure.   However, in another human study, tyrosine increased heart rate and blood pressure after 150 mg/kg tyrosine supplementation. 
Following tyrosine supplementation of 12 g in 113 g of applesauce in adults with normal thyroid function in Antarctica during the summer, thyroid-stimulating hormone decreased by 30%. In the winter, there was a 47% improvement in mood and TSH decreased by 28% along with an increase of 6% in serum-free triiodothyronine.  Additionally, 10g/day of L-tyrosine was given to patients with schizophrenia and resulted in increased saccadic intrusions. 
In children with nemaline myopathy (a condition which causes chewing and swallowing difficulties, recurrent aspiration, and poor control of oral secretions), 250-3000 mg/day L-tyrosine supplementation caused an initial decrease in sialorrhea and an increase in energy levels.  Patients with severe dementia due to Alzheimer’s disease received a combination treatment of 5-hydroxy-tryptophan, carbidopa, and tyrosine (4 g) which caused diarrhea, drowsiness, nausea, vomiting, and agitation. However, it is not clear if these side effects were due to tyrosine alone. 
L-tyrosine can have an effect on blood pressure, heart rate, and mood. It may cause gastrointestinal upset, drowsiness, and agitation.
- Nakashima A, et al. Role of N-terminus of tyrosine hydroxylase in the biosynthesis of catecholamines. J Neural Transm. (2009)
- Webster D, Wildgoose J. Tyrosine supplementation for phenylketonuria. Cochrane Database Syst Rev. (2010)
- Poustie VJ, Rutherford P. Tyrosine supplementation for phenylketonuria. Cochrane Database Syst Rev. (2000)
- Wurtman RJ, Chou C, Rose CM. Daily rhythm in tyrosine concentration in human plasma: persistence on low-protein diets. Science. (1967)
- D'Andrea G, et al. Pathogenesis of migraine: role of neuromodulators. Headache. (2012)
- Daubner SC, Le T, Wang S. Tyrosine hydroxylase and regulation of dopamine synthesis. Arch Biochem Biophys. (2011)
- DiPiro JT, et al. Pharmacotherapy: A pathophysiologic approach. 4th ed.. Stamford, CT: Appleton & Lange. (1999)
- van Spronsen FJ, et al. Phenylketonuria: tyrosine supplementation in phenylalanine-restricted diets. Am J Clin Nutr. (2001)
- Melmed, S, Williams RH. Williams Textbook of Endocrinology. Saunders Elsevier. (2011)
- DiPiro JT, et al. Pharmacotherapy: A pathophysiologic approach. 4th ed.. Stamford, CT: Appleton & Lange. (1999)
- Shurtleff D, et al. Tyrosine reverses a cold-induced working memory deficit in humans. Pharmacol Biochem Behav. (1994)
- Glaeser BS, et al. Elevation of plasma tyrosine after a single oral dose of L-tyrosine. Life Sci. (1979)
- Armstrong MD, Stave U. A study of plasma free amino acid levels. II. Normal values for children and adults. Metabolism. (1973)
- Ashley DV, et al. Plasma amino acid responses in humans to evening meals of differing nutritional composition. Am J Clin Nutr. (1982)
- Elia M, et al. Amino acid metabolism in muscle and in the whole body of man before and after ingestion of a single mixed meal. Am J Clin Nutr. (1989)
- Topall G, Laborit H. Brain tyrosine increases after treating with prodrugs: comparison with tyrosine. J Pharm Pharmacol. (1989)
- Fernstrom JD, Fernstrom MH. Tyrosine, phenylalanine, and catecholamine synthesis and function in the brain. J Nutr. (2007)
- Lehnert H, Wurtman RJ. Amino acid control of neurotransmitter synthesis and release: physiological and clinical implications. Psychother Psychosom. (1993)
- Yeghiayan SK, et al. Tyrosine improves behavioral and neurochemical deficits caused by cold exposure. Physiol Behav. (2001)
- Treatment of attention deficit hyperactivity disorder with monoamine amino acid precursors and organic cation transporter assay interpretation.
- Neri DF, et al. The effects of tyrosine on cognitive performance during extended wakefulness. Aviat Space Environ Med. (1995)
- Lehnert H, et al. Neurochemical and behavioral consequences of acute, uncontrollable stress: effects of dietary tyrosine. Brain Res. (1984)
- Irwin J, Suissa A, Anisman H. Differential effects of inescapable shock on escape performance and discrimination learning in a water escape task. J Exp Psychol Anim Behav Process. (1980)
- Weiss JM. Effects of coping behavior in different warning signal conditions on stress pathology in rats. J Comp Physiol Psychol. (1971)
- Brady K, Brown JW, Thurmond JB. Behavioral and neurochemical effects of dietary tyrosine in young and aged mice following cold-swim stress. Pharmacol Biochem Behav. (1980)
- Behavioral Depression Produced by An Uncontrollable Stressor: Relationship to Norepinephrine, Dopamine, and Serotonin Levels in Various Regions of Rat Brain.
- Tyrosine Pretreatment Reverses HypothermiaInduced Behavioral Depression.
- Tyrosine and Stress: Human and Animal Studies.
- Banderet LE, Lieberman HR. Treatment with tyrosine, a neurotransmitter precursor, reduces environmental stress in humans. Brain Res Bull. (1989)
- Deijen JB, Orlebeke JF. Effect of tyrosine on cognitive function and blood pressure under stress. Brain Res Bull. (1994)
- Dollins AB, et al. L-tyrosine ameliorates some effects of lower body negative pressure stress. Physiol Behav. (1995)
- Deijen JB, et al. Tyrosine improves cognitive performance and reduces blood pressure in cadets after one week of a combat training course. Brain Res Bull. (1999)
- Jodko K, Litwinienko G. Oxidative stress in the neurodegenerative diseases--potential antioxidant activity of catecholamines. Postepy Biochem. (2010)
- Yamori Y, et al. The hypotensive effect of centrally administered tyrosine. Eur J Pharmacol. (1980)
- Tyrosine administration reduces blood pressure and enhances brain norepinephrine release in spontaneously hypertensive rats.
- Meeusen R, Watson P, Dvorak J. The brain and fatigue: new opportunities for nutritional interventions. J Sports Sci. (2006)
- Magnusson I, et al. N-acetyl-L-tyrosine and N-acetyl-L-cysteine as tyrosine and cysteine precursors during intravenous infusion in humans. Metabolism. (1989)
- Hoffer LJ, et al. N-acetyl-L-tyrosine as a tyrosine source in adult parenteral nutrition. JPEN J Parenter Enteral Nutr. (2003)
- Shibui Y, et al. 13-week repeated dose toxicity study of l-tyrosine in rats by daily oral administration. Food Chem Toxicol. (2016)
- D'Andrea G, et al. The role of tyrosine metabolism in the pathogenesis of chronic migraine. Cephalalgia. (2013)
- CFR-Code of Federal Regulations Title 21.
- Wood DR, Reimherr FW, Wender PH. Amino acid precursors for the treatment of attention deficit disorder, residual type. Psychopharmacol Bull. (1985)
- Reimherr FW, et al. An open trial of L-tyrosine in the treatment of attention deficit disorder, residual type. Am J Psychiatry. (1987)
- Jongkees BJ, et al. Effect of tyrosine supplementation on clinical and healthy populations under stress or cognitive demands--A review. J Psychiatr Res. (2015)
- Lewis SA , Lyon ICT, Elliott RB. Outcome of pregnancy in the rat with mild hyperphenylalaninaemia and hypertyrosinaemia: Implications for the management of “human maternal PKU. J Inherit Metab Dis. (1985)
- Thomas JR, et al. Tyrosine improves working memory in a multitasking environment. Pharmacol Biochem Behav. (1999)
- Palinkas LA, et al. Psychoneuroendocrine effects of combined thyroxine and triiodothyronine versus tyrosine during prolonged Antarctic residence. Int J Circumpolar Health. (2007)
- Deutsch SI, et al. L-tyrosine pharmacotherapy of schizophrenia: preliminary data. Clin Neuropharmacol. (1994)
- Ryan MM, et al. Dietary L-tyrosine supplementation in nemaline myopathy. J Child Neurol. (2008)
- Meyer JS, et al. Neurotransmitter precursor amino acids in the treatment of multi-infarct dementia and Alzheimer's disease. J Am Geriatr Soc. (1977)