Tyrosine is a non-essential amino acid, meaning the body can typically produce it from another amino acid, phenylalanine [1.7.4]. It serves as a crucial building block for several vital substances, including key neurotransmitters like dopamine, norepinephrine, and epinephrine, as well as thyroid hormones and the skin pigment melanin [1.7.1, 1.9.3]. While beneficial for many bodily functions, particularly in improving cognitive performance under stress, several significant problems are associated with tyrosine metabolism and supplementation [1.6.4, 1.7.2].
The Genetic Problem: Tyrosinemia
The most severe problem related to tyrosine is tyrosinemia, a group of inherited metabolic disorders [1.2.3]. In these conditions, a deficiency in specific enzymes prevents the body from effectively breaking down tyrosine [1.2.2]. This leads to a buildup of tyrosine and its toxic byproducts in tissues and organs, causing serious health complications [1.2.3, 1.2.4].
There are three main types of tyrosinemia, each with distinct symptoms and genetic causes [1.4.3]:
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Tyrosinemia Type I (HT-1): This is the most severe form, caused by a deficiency of the enzyme fumarylacetoacetate hydrolase (FAH) [1.4.5]. Symptoms usually appear within the first few months of life and include poor weight gain, diarrhea, vomiting, a "cabbage-like" odor, and an enlarged liver [1.2.1, 1.4.1]. If left untreated, it leads to severe liver and kidney failure, rickets, and an increased risk of liver cancer [1.2.3]. Without treatment, children often do not survive past age 10 [1.4.3]. Treatment involves a low-tyrosine/phenylalanine diet and the medication nitisinone [1.2.1, 1.4.5].
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Tyrosinemia Type II (HT-2): Caused by a deficiency of tyrosine aminotransferase, this type primarily affects the eyes, skin, and mental development [1.2.6, 1.4.3]. Symptoms include eye pain, redness, light sensitivity, and painful, thickened skin on the palms and soles [1.4.3]. About half of individuals with this type experience some degree of intellectual disability [1.4.3]. The liver and kidneys are not affected in this type [1.2.4].
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Tyrosinemia Type III (HT-3): This is the rarest form, resulting from a deficiency of the enzyme 4-hydroxyphenylpyruvate dioxygenase [1.2.3]. Symptoms can include mild intellectual disability, seizures, and a periodic loss of balance and coordination (intermittent ataxia) [1.4.2, 1.4.3].
Comparison of Tyrosinemia Types
Feature | Tyrosinemia Type I | Tyrosinemia Type II | Tyrosinemia Type III |
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Affected Enzyme | Fumarylacetoacetate hydrolase (FAH) [1.2.1] | Tyrosine aminotransferase (TAT) [1.2.6] | 4-hydroxyphenylpyruvate dioxygenase (HPD) [1.2.3] |
Primary Symptoms | Severe liver and kidney failure, failure to thrive, "cabbage-like" odor [1.2.2, 1.2.3] | Painful skin lesions on palms/soles, eye pain and redness, light sensitivity [1.2.2, 1.4.3] | Intellectual disability, seizures, intermittent ataxia [1.2.2, 1.4.3] |
Age of Onset | First few months of life [1.2.2] | Early childhood [1.2.2] | Varies, can be detected in childhood [1.4.2] |
Worldwide Prevalence | ~1 in 100,000 individuals [1.8.2] | <1 in 250,000 individuals [1.8.2] | Very rare, only a few cases reported [1.8.2] |
Risks of L-Tyrosine Supplementation
For the general population, tyrosine is obtained from high-protein foods like meat, eggs, and dairy and is considered safe [1.9.4]. However, taking L-tyrosine supplements can introduce a different set of problems, including side effects and dangerous drug interactions.
Common Side Effects
Though generally well-tolerated in the short term, L-tyrosine supplements can cause adverse effects for some individuals [1.6.2]. Common side effects include:
- Nausea and heartburn [1.3.5]
- Headaches [1.3.5]
- Fatigue [1.3.5]
- Joint pain [1.3.5]
- Insomnia and irritability [1.3.1]
These side effects are more likely at higher doses [1.3.6]. People with migraines are sometimes advised to avoid tyrosine supplements as they may trigger headaches [1.3.4].
Serious Drug Interactions
The most significant risk of tyrosine supplementation comes from its interaction with certain medications.
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Monoamine Oxidase Inhibitors (MAOIs): This class of antidepressants blocks an enzyme that breaks down tyramine, a substance produced from the breakdown of tyrosine [1.5.4]. Combining MAOIs (e.g., phenelzine, tranylcypromine) with high-tyramine foods or tyrosine supplements can lead to a dangerous buildup of tyramine, causing a hypertensive crisis—a severe and rapid increase in blood pressure [1.5.1, 1.5.3]. This is a medical emergency.
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Thyroid Hormones: The body uses tyrosine to produce thyroid hormones (T3 and T4) [1.5.4]. Taking tyrosine supplements could potentially increase these hormone levels too much. This is a particular concern for individuals with an overactive thyroid (hyperthyroidism) or Graves' disease, as it could worsen their condition or interfere with thyroid medications like levothyroxine [1.6.2, 1.3.2].
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Levodopa (L-dopa): This medication is used to treat Parkinson's disease. Tyrosine can compete with Levodopa for absorption in the body, potentially reducing the drug's effectiveness [1.6.2]. It is often recommended to take these medications at least two hours apart [1.3.2].
Conclusion
The "problem with tyrosine" is multifaceted. For a small part of the population, the issue lies in genetics, where an inability to metabolize tyrosine leads to the life-threatening conditions of tyrosinemia [1.2.2]. For the broader public, problems arise mainly from the misuse of L-tyrosine supplements. While potentially beneficial for cognitive function under stress, these supplements carry risks of side effects and, more critically, can lead to severe hypertensive crises when combined with MAOI antidepressants and may disrupt hormone levels in those with thyroid conditions [1.5.1, 1.5.4]. Therefore, consultation with a healthcare provider is essential before starting tyrosine supplementation, especially for individuals with pre-existing medical conditions or those taking other medications [1.3.6].
Authoritative Link: For more detailed information on inherited tyrosine metabolism disorders, consult the Merck Manual [1.2.6].