Dopamine precursors like L-phenylalanine and L-tyrosine are required for the synthesis of all catecholamine neurotransmitters.
Phenylalanine and tyrosine are both amino acids which constitute the first two preliminary steps in the dopamine biosynthesis pathways. They are then used to make L-DOPA, which is converted into dopamine by the enzyme DOPA decarboxylase with the help of the cofactor Vitamin B6.
Dopamine serves as a precursor for the synthesis of other catecholamines including adrenaline (epinephrine) and noradrenaline (norepinephrine). These catecholamines are excitatory chemicals and influence cognitive functions like learning, movement, emotional state, sleep, sex drive, creativity and more.
In simplest form, the primary catecholamine synthesis pathway looks like this:
Phenylalanine –> Tyrosine –> L-Dopa –> Dopamine –> Norepinephrine –> Epinephrine



- Supports energy & motivation
- Promotes focus & mental clarity
- Improves mood & stress response
Dopamine Precursor: Phenylalanine
Related Topics
To manufacture dopamine and other catecholamine hormones, the brain requires certain raw materials.
Neurotransmitters like dopamine are chemical substances which are made from micronutrients found in the diet – like amino acids, enzymes, vitamins and minerals.
The first dopamine precursor necessary is the essential alpha amino acid: L-phenylalanine (C9H11NO2).
Being “essential” for an amino acid means that the body cannot synthesize it. It must be gained from the diet, or via dietary supplementation.
Phenylalanine then gets converted to tyrosine via the monooxygenase enzyme: phenylalanine hydroxylase.
This reaction causes the attachment of a hydroxyl group to the end of phenylalanine’s 6-carbon aromatic ring. When there is dysfunction in the phenylalanine biosynthesis pathway, tyrosine synthesis is subsequently affected.
If phenylalanine hydroxylase is unavailable for any reason, then tyrosine cannot be metabolized. This deficiency is called PKU (phenylketonuria).
PKU is an autosomal recessive disorder that occurs when the liver lacks phenylalanine hydroxylase. If left untreated, brain and nervous system damage may result.
PKU is a lifelong condition in most cases. If it is detected early, then it can be treated effectively. By adhering to a PKU diet and routinely taking certain supplements, PKU symptoms can be minimized or entirely negated.
Dopamine Precursor: Tyrosine
The second required dopamine precursor is the proteinogenic alpha amino acid: tyrosine (C9H11NO3).
Also known as 4-hydroxyphenylalanine, tyrosine is considered conditionally essential. That means that it becomes essential only in cases where it cannot be biosynthesized; as in cases of PKU. Then it must be gained from foods or supplements.
Tyrosine gets converted to L-DOPA in humans, as well as certain other animals and some plants. This is catalyzed by the enzyme tyrosine hydroxylase (tyrosine 3-monooxygenase).
The conversion also requires cofactors of molecular oxygen, tetrahydrobiopterin and iron (Fe2+). This conversion process is the rate-limiting step in the synthesis of dopamine and of all catecholamines.
Tyrosine hydroxylase is a dopamine precursor enzyme which is found in peripheral sympathetic nerves, the CNS and the adrenal medulla.
Along with phenylalanine hydroxylase and tryptophan hydroxylase, tyrosine hydroxylase comprises the AAAH (aromatic amino acid hydroxylases) family.
Dopamine Precursor: DOPA
There is common confusion concerning the differences between the terms “DOPA”, “L-DOPA” and “levodopa”.
DOPA is an amino acid also called dihydroxyphenylalanine. It is comprised of a molecule of phenylalanine and two hydroxyl groups. DOPA occurs naturally in many animals and plants.
In mammals, DOPA is biosynthesized inside the liver from tyrosine during the production of epinephrine and melanin. Its L isomer then travels across the blood brain barrier to be converted into dopamine inside the brain.
L-DOPA and levodopa are terms used to denote the levorotatory form of DOPA. This can be manufactured in laboratories and is commonly used to treat Parkinson’s disease and other conditions associated with low dopamine symptoms.
As a nootropic, L-DOPA is used to enhance memory, focus and learning capacities. It is also used to prevent and treat depression, anxiety and the effects of chronic stress.
Common trade names for pharmaceutical-grade L-DOPA include Prolopa, Atamet, Madopar, Stalevo and Sinemet.
Certain herbaceous plants contain concentrated amounts of natural L-DOPA. The best known of these in Mucuna pruriens seeds (velvet beans) which are comprised of roughly 5% L-DOPA.
Other good sources are Vicia faba (broad beans, fava beans) – and botanic genera including Canavalia, Cassia, Dalbergia, Phanera and Piliostigma.
DOPA to Dopamine Conversion
The precursor L-DOPA (C9H11NO4) is converted into dopamine (C8H11NO2) via the actions of the enzyme dopa decarboxylase. This lyase enzyme is also called aromatic L-amino acid decarboxylase – or more simply: AAAD.
This same enzyme is responsible for converting 5-HTP into serotonin, L-histidine into histamine, phenylalanine into phenylethylamine, L-tyrosine into tyramine and tryptophan into tryptamine.
In all of these processes, the conversion basically involves the removal of carboxyl groups. Carboxyl groups are comprised on two O2 atoms, one C atom and one H atom.
DOPA decarboxylase also uses the active form of vitamin B6 (pyridoxal phosphate) as a cofactor for this conversion process.
Conclusions
Phenylalanine, tyrosine, oxygen, iron, vitamin B6 and certain other micronutrients and enzymes are required precursors for dopamine biosynthesis.
Dysfunction in any part of the dopamine synthesis pathway can result in serious disruptions of all catecholamine neurotransmitters, which can negatively affect mood, attention span, energy levels and mental drive.
In most healthy individuals, availability of dopamine precursors can be kept stable via a proper diet, regular exercise and effective stress management. Dopamine-boosting supplements can also be used to naturally remedy signs of deficiency.
- Fernstrom JD1, Fernstrom MH Tyrosine, phenylalanine, and catecholamine synthesis and function in the brain. J Nutr. 2007 Jun;137(6 Suppl 1):1539S-1547S; discussion 1548S.
- Lou HC1. Dopamine precursors and brain function in phenylalanine hydroxylase deficiency. Acta Paediatr Suppl. 1994 Dec;407:86-8.
- Lucia Raffaella Lampariello,1 Alessio Cortelazzo,2 Roberto Guerranti,2 Claudia Sticozzi,3 and Giuseppe Valacchi3,4,* The Magic Velvet Bean of Mucuna pruriens Journal ListJ Tradit Complement Medv.2(4); Oct-Dec 2012PMC3942911
- Yokogoshi H1, Kobayashi M, Mochizuki M, Terashima T. Effect of theanine, r-glutamylethylamide, on brain monoamines and striatal dopamine release in conscious rats. Neurochem Res. 1998 May;23(5):667-73.
- Janssen PA1, Leysen JE, Megens AA, Awouters FH. Does phenylethylamine act as an endogenous amphetamine in some patients? Int J Neuropsychopharmacol. 1999 Sep;2(3):229-240.
- Liju, Vijayastelter B., Kottarapat Jeena, and Ramadasan Kuttan. "An Evaluation of Antioxidant, Anti-Inflammatory, and Antinociceptive Activities of Essential Oil from Curcuma Longa. L." Indian Journal of Pharmacology 43.5 (2011): 526–531. PMC. Web. 7 Apr. 2016.
- Wing VC1, Payer DE2, Houle S3, George TP4, Boileau I2. Measuring cigarette smoking-induced cortical dopamine release: A [¹¹C]FLB-457 PET study. Neuropsychopharmacology. 2015 May;40(6):1417-27. doi: 10.1038/npp.2014.327. Epub 2014 Dec 15.
- Kempster PA1, Gibb WR, Stern GM, Lees AJ. Asymmetry of substantia nigra neuronal loss in Parkinson's disease and its relevance to the mechanism of levodopa related motor fluctuations. J Neurol Neurosurg Psychiatry. 1989 Jan;52(1):72-6.
- Jiang H1, Wang J2, Rogers J3, Xie J4. Brain Iron Metabolism Dysfunction in Parkinson's Disease. Mol Neurobiol. 2016 Apr 2. [Epub ahead of print]
- Arnsten AF1, Girgis RR2, Gray DL3, Mailman RB4. Novel Dopamine Therapeutics for Cognitive Deficits in Schizophrenia. Biol Psychiatry. 2016 Jan 18. pii: S0006-3223(16)00044-5. doi: 10.1016/j.biopsych.2015.12.028. [Epub ahead of print]
- Arnsten AF1, Wang M2, Paspalas CD2. Dopamine's Actions in Primate Prefrontal Cortex: Challenges for Treating Cognitive Disorders. Pharmacol Rev. 2015 Jul;67(3):681-96. doi: 10.1124/pr.115.010512.
- Torres-Courchoud I1, Chen HH. Is there still a role for low-dose dopamine use in acute heart failure? Curr Opin Crit Care. 2014 Oct;20(5):467-71. doi: 10.1097/MCC.0000000000000133.
- Salinas AG1, Davis MI2, Lovinger DM2, Mateo Y3. Dopamine dynamics and cocaine sensitivity differ between striosome and matrix compartments of the striatum. Neuropharmacology. 2016 Mar 29. pii: S0028-3908(16)30121-6. doi: 10.1016/j.neuropharm.2016.03.049. [Epub ahead of print]
- Field T1, Hernandez-Reif M, Diego M, Schanberg S, Kuhn C. Cortisol decreases and serotonin and dopamine increase following massage therapy. Int J Neurosci. 2005 Oct;115(10):1397-413.
Article last updated on: July 6th, 2018 by Nootriment
2 Comments
Mi consulta es para pedir una recomendación. Sufro de síndrome de piernas inquietas. Se atribuye a una deficiencia de dopamina. Tomo una dosis baja de un medicamento para Parkinson. ¿Qué suplemento sería conveniente para este problema. Gracias.
HOla. Una mala praxis. Iatrogenia. Un corta y pega de hace 11 años. Me llevó a una psiquiatra de la seguridad social Que lo dicho. Cortó y pegó. Y me dió alonzapina, xeplion. Neurolepticos anuladores de la dopamina…no soy fuerte. Tengo una enfermedad reumatica. Sindrome de hiperlaxitud. Y me quedo rigido despues de un año de tomar tal. Cuadriceps-artrosis…rigidez. No puedo andar más de 50 m sin notar el cuello rigido. TOmo l tirosina, l fenilalanina. Y no me hace. Los neurologos-pasan. Solidaridad entre ellos. ¿Que puedo tomar?. Natural. L dopa. Me da miedo. Solo si me lo manda un medico. Aminoacidos bien. pero no me hacen. ¿Sabes de algun caso asi?. Que la rigidez sea muy fuerte, y tomara l dopa?. Salud.