Myths about L-tyrosine

A whole mythology has grown up around L-tyrosine: it is called a "natural caffeine," a "dopamine booster," a weight-loss aid and an over-the-counter antidepressant. Some of these ideas grew from real facts of biochemistry but were exaggerated by marketing. The editors checked the most common claims against scientific data.

Myths 1–2: "stimulant" and "more tyrosine means more dopamine"

The most widespread idea is that tyrosine acts as a mild stimulant: it invigorates, increases concentration and mood regardless of circumstances. In reality, at rest and with sufficient sleep, most controlled studies record no noticeable changes in well-being or performance after taking tyrosine. Someone expecting an effect similar to coffee most likely will not feel it.

The reason lies in biochemistry. The rate of catecholamine synthesis is limited not by the amount of tyrosine but by the enzyme tyrosine hydroxylase, which under ordinary conditions is already almost saturated with substrate. In addition, dopamine and noradrenaline inhibit this enzyme via feedback. Additional tyrosine, as Fernstrom and Fernstrom (2007) summarize, noticeably increases synthesis only in neurons that are working intensively.

That is why the effect appears in situations of acute load: cold, hypoxia at altitude, prolonged sleep deprivation, performing several tasks at once. In the study by Banderet and Lieberman (1989) tyrosine reduced the decline in cognitive performance and mood under cold and hypoxia, and in the work by Deijen and colleagues (1999) — in cadets during an exhausting combat-training course.

Another nuance is the "inverted U" concept. Both too low and too high a level of dopamine impair cognitive work. Colzato and colleagues showed that people with an initially "optimal" level may gain no benefit or even worsen their results, whereas those whose resource is depleted gain an advantage.

Myth 3: tyrosine increases endurance

The idea seems logical: during prolonged work the ratio of serotonin to dopamine in the brain rises, which is associated with central fatigue. If you add a dopamine precursor, fatigue should recede. In practice the data are contradictory.

In the study by Chinevere and colleagues (2002) tyrosine, alone or together with carbohydrates, did not improve the results of prolonged cycling under moderate conditions; carbohydrates helped, tyrosine added nothing. Tumilty and colleagues (2011) found an increase in time to exhaustion in the heat, but the subsequent work by Watson and colleagues (2012) under similar conditions did not reproduce this effect.

Thus, as of today there are no grounds to consider tyrosine an ergogenic aid for endurance. A possible effect in the heat needs confirmation, and for ordinary gym workouts there is no convincing data at all.

As for strength performance and muscle mass, tyrosine as a standalone supplement has no advantages over adequate dietary protein: its share in muscle proteins is small, and muscle protein synthesis is limited primarily by leucine and the total intake of essential amino acids.

Myth 4: tyrosine burns fat and "revs up" the thyroid

Tyrosine regularly ends up in "fat burners" with the argument that it is a precursor of noradrenaline, which stimulates lipolysis, and of thyroid hormones, which speed up metabolism. Both chains are real, but it does not follow from them that a tyrosine supplement will increase energy expenditure.

The synthesis of thyroid hormones is regulated by the pituitary thyroid-stimulating hormone and depends on iodine; the body has more than enough free tyrosine for this. A person with a healthy thyroid will not get a metabolic "boost," and in a person with thyroid disease self-medication can only interfere with therapy.

The editors did not find controlled studies that would show a reduction in fat mass thanks to tyrosine. The effect of "fat burners" with tyrosine, if any, is usually explained by caffeine or other stimulants in the composition.

The conclusion is simple: for weight loss tyrosine has no evidential value. A calorie deficit, sufficient protein and training remain the foundation that no amino acid replaces.

Myths 5–6: antidepressant and the "better" NALT form

In the 1980s the catecholamine hypothesis of depression prompted testing tyrosine as a treatment. The double-blind study by Gelenberg and colleagues (1990) found no advantage of tyrosine over placebo in patients with depression. Since then no clinical guideline has recommended it as an antidepressant.

The danger of this myth is that a person with clinical depression may delay seeking help, relying on a supplement. Depression is a disease that requires evaluation by a specialist and treatment of proven effectiveness.

The second popular myth is that N-acetyl-L-tyrosine (NALT) "absorbs many times better." NALT does dissolve better in water, but in humans it is poorly deacetylated: in an intravenous study a significant fraction was excreted in the urine unchanged (Magnusson et al., 1989).

There are no studies that would demonstrate the advantage of oral NALT over ordinary tyrosine for cognitive or physical performance. Almost all positive data were obtained precisely for free L-tyrosine.

Myth 7: safe in any amount

Since tyrosine is a component of food, it is often considered absolutely safe. For healthy adults, at the doses used in studies, no serious side effects have indeed been described, and short courses were well tolerated. However, "well tolerated at the doses studied" is not the same as "safe in any amount."

Large amounts of a single amino acid change the balance of transport of other amino acids into the brain and can cause stomach discomfort, headache, nausea. Data on long-term daily intake of high doses are limited.

There are also groups of people for whom tyrosine is contraindicated or requires coordination with a doctor:

• people with hereditary disorders of tyrosine metabolism (tyrosinemias, alkaptonuria);
• patients taking MAO inhibitors or levodopa;
• people with thyroid diseases;
• pregnant women, breastfeeding women, children.

Thus, the sensible approach is to use tyrosine situationally, in amounts consistent with research, rather than daily "just in case."

Editorial conclusions

L-tyrosine is not a stimulant or a universal "dopamine booster." Its best-documented role is helping to preserve cognitive function under acute stress, when the catecholamine resource is depleted.

The evidence on endurance is contradictory, and on fat burning and treating depression it is absent. NALT has no confirmed advantage over the free form.

Tyrosine is well tolerated by healthy adults but has contraindications that cannot be ignored.

Read more in the editorial articles "Who should not take L-tyrosine," "L-tyrosine: available forms and which to choose" and "What to combine L-tyrosine with."

References

1. Jongkees BJ, Hommel B, Kühn S, Colzato LS. Effect of tyrosine supplementation on clinical and healthy populations under stress or cognitive demands — a review. J Psychiatr Res. 2015;70:50–57.
2. Fernstrom JD, Fernstrom MH. Tyrosine, phenylalanine, and catecholamine synthesis and function in the brain. J Nutr. 2007;137(6 Suppl 1):1539S–1547S.
3. Banderet LE, Lieberman HR. Treatment with tyrosine, a neurotransmitter precursor, reduces environmental stress in humans. Brain Res Bull. 1989;22(4):759–762.
4. Chinevere TD, Sawyer RD, Creer AR, et al. Effects of L-tyrosine and carbohydrate ingestion on endurance exercise performance. J Appl Physiol. 2002;93(5):1590–1597.
5. Tumilty L, Davison G, Beckmann M, Thatcher R. Oral tyrosine supplementation improves exercise capacity in the heat. Eur J Appl Physiol. 2011;111(12):2941–2950.
6. Watson P, Enever S, Page A, et al. Tyrosine supplementation does not influence the capacity to perform prolonged exercise in a warm environment. Int J Sport Nutr Exerc Metab. 2012;22(5):363–373.
7. Gelenberg AJ, Wojcik JD, Falk WE, et al. Tyrosine for depression: a double-blind trial. J Affect Disord. 1990;19(2):125–132.
8. Magnusson I, Ekman L, Wångdahl M, Wahren J. N-acetyl-L-tyrosine and N-acetyl-L-cysteine as tyrosine and cysteine precursors during intravenous infusion in humans. Metabolism. 1989;38(10):957–961.