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Tyrosine for ADHD

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Tyrosine for ADHD

Tyrosine is a precursor in the synthesis of dopamine. Although the rate-limiting enzyme of catecholamine synthesis is not tyrosine but tyrosine hydroxylase, an increase in tyrosine levels in the brain stimulates catecholamine production, but only in actively firing neurons 12

More on this under Tyrosine In the article Dopamine formation and storage

1. Tyrosine increases dopamine and noradrenaline

Tyrosine administration increased extracellular dopamine in the striatum and nucleus accumbens in rats.3 Another source also reported this for the striatum, but only if the animals had previously received a dopamine receptor antagonist (halperidol).4 Tyrosine administration also significantly increased (in light only) the conversion of tyrosine to L-dopa (part of the dopamine synthesis pathway) in the retina of rats5 and subsequently increased dopamine in the retina.6 Since dopamine suppresses melatonin, this pathway could influence the circadian rhythm. More on this at Melatonin and dopamine and the circadian rhythm in the article Melatonin in ADHD
In rats, the tyrosine level in the hypothalamus varies linearly with a range of protein content in the diet between 2 and 10 %. At 20 %, the tyrosine level in the hypothalamus barely increased further.1

A type input in humans

  • improved impulse control in a stop signal task one hour after ingestion.7
  • increased cognitive flexibility / facilitated task switching8
  • in DRD2 gene C957T (rs6277) T/T homozygous carriers (associated with lower striatal DA levels) produced greater improvements in a stop signal task and working memory updating in an N-back task than C/C homozygous carriers (associated with higher striatal DA levels). Thus, tyrosine worked better at low striatal dopamine than at higher levels.9
  • improved cognitive performance in stressful or demanding situations with reduced dopamine / noradrenaline levels10111213
  • reduced temporal discounting and reduced arousal, shorter response times with the same response qualityl14
  • deteriorated task switching under high cognitive load15
    • in our opinion, this could possibly be explained if the high cognitive load already caused stress-related increased dopamine and noradrenline levels, which were then further increased by tyrosine administration and thus moved even further away from the optimal level (inverted-U effect for catecholamines).

Rats given glutamate in the striatum showed increased dopamine synthesis from tyrosine and only moderate changes in dopamine release.1617

2. Protein-rich food increases tyrosine

Protein-rich food increases the tyrosine level in the brain. Theoretically, a protein-rich diet could therefore improve a dopamine deficiency and improve ADHD symptoms if these arise due to dopamine synthesis problems caused by tyrosine deficiency. Although this is probably only rarely the case, we believe it is conceivable that this could be one of the many pathways leading to ADHD and could therefore help people with ADHD.
A few people with ADHD reported an improvement in ADHD symptoms with a ketogenic diet or tyrosine intake. More on this under Ketogenic diet In the article Nutrition and diet for ADHD
In SHR, the most widely used animal model for ADHD, which also serves as an animal model for hypertension, tyrosine caused a reduction in blood pressure and an increase in extracellular noradrenaline levels.18 Like the inhibition of prolactin release caused by tyrosine in rats pre-treated with reserpine, this is thought to be due to a stimulation of dopamine and noradrenaline synthesis1
Tyrosine is also said to improve working memory in humans under cold stress conditions.19
Administration of L-tyrosine to rats increased extracellular dopamine in the mPFC and striatum2021 and norepinephrine release in the hippocampus.22

3. Competing amino acids reduce tyrosine and thus dopamine

The amount of tyrosine available in the brain is also influenced by other large neutral amino acids that compete with tyrosine for the same transporter across the blood-brain barrier, e.g:123

  • Tryptophan
  • Phenylalanine
  • L-methionine
  • Histidine
  • Threonine
  • L-glycine
    • different24
  • L-lysine
  • L-arginine
  • L-leucine
  • L-isoleucine
  • L-valine
  • DOPA24
  • Cysteine24
  • Histidine24
  • Glutamine24
  • Asparagine24
  • Serine24
  • but not

Therefore, administration of a combination of these large neutral amino acids (without tyrosine and without phenylalanine, as phenylalanine is immediately metabolized to tyrosine in the liver) can reduce brain tyrosine levels in the hypothalamus and retina within 2 hours.23 Consequences are that the dopamine level in the brain also decreases, but not in the PFC.125
In other brain regions, only the tyrosine level decreased within 2 hours after administration of the competing amino acids, but not the dopamine or noradrenaline level26

  • Cortex (tyrosine reduced by 50 %, dopa reduced by 20 to 24 %)
  • Hippocampus (tyrosine reduced by 50 %)
  • Striatum (tyrosine reduced by 50 %, dopa reduced by 44 %)
  • Nucleus accumbens (dopa reduced by 34 %)

The tyrosine level recovered completely after 6 hours26

Insofar as the studies were carried out on people without ADHD, an even more significant effect can be expected in people with ADHD due to the ADHD-related dopamine and noradrenaline deficits. Non-affected persons showed a few hours after taking the competing amino acids:

  • neurophysiological changes
    • Dopamine levels
      • in the striatum
        • reduces27 by 6 %28
        • unchanged26
      • in the hypothalamus is reduced (indicated by an increase in prolactin)293031
      • cerebral reduced32
    • Reduced activity in the putamen33
      • Putamen and SMA mediate the storage of temporal information in working memory
    • Reduced activity in the supplementary motor area (SMA)33
      • Putamen and SMA mediate the storage of temporal information in working memory
  • frontostriatal connectivity impaired34
  • reduced deactivation in areas that are suppressed during attention-demanding tasks, including:34
    • mPFC
    • posterior cingulate cortex
    • Hippocampus
  • Behavioral changes
    • spatial working memory
      • deteriorated293536
      • worsens in women only on low-fat/low-sugar diets, not on high-fat/high-sugar diets37
      • unchanged38 but associated ERP showed neurophysiological deterioration39
    • episodic memory unchanged, but associated ERP showed neurophysiological deterioration39
    • State of mind / mood
      • deteriorates2940 , at least slightly3141
      • worsened pain assessment32
      • deteriorated mood after stress42
      • unchanged354344
    • Pain and temperature sensation unchanged4132
    • other planning and memory skills
      • unchanged38
      • Go/no-go task: increased number of errors in healthy adults31
      • Simon Task: Results unchanged, but N-40 changed45
      • Timing impaired33
      • Time perception changes depending on the tyrosine base value46
      • Reward response (delay discounting and working memory)
        • Effect only dependent on COMT gene type; increased elective impulsivity with COMT val/val (which causes increased dopamine degradation in the PFC)47
      • Habitual control (only in women) stronger than goal-directed control when goal-directed and habitual systems competed for control in the slips-of-action test48, also for tryptophan depletion49
    • Learning from positive and negative reinforcement (probabilistic selection task) improved in women with low-fat/low-sugar diets as with high-fat/high-sugar diets37
    • directed attention deteriorates with simultaneous serotonin depletion50
    • Reaction time unchanged with divided attention51

For comparison: tryptophan depletion, executive functions and impulsivity

Similarly, depletion of tryptophan, which is a precursor in the formation of serotonin, results in a reduction of serotonin in the brain and effects on executive functions and impulsivity:

  • Go/NoGo task52
    • unchanged (3 studies)
    • improved accuracy and response times (1 study)
    • increased number of errors (1 study)
  • Continuous Performance Test52
    • Increased impulsivity (4 studies)
    • unchanged (1 study)
  • Four-choice Serial reaction time task52
    • Increased impulsivity (1 study)
  • Wisconsin card sorting test52
    • unchanged (2 studies)
  • Tower of London52
    • increased response time (1 study)
    • unchanged (2 studies)
  • Stroop Test52
    • improved (focused) attention (3 studies)
    • unchanged (1 study)
  • Probabilistic reversal learning52
    • unchanged (2 studies)

The reduction of tryptophan by a tryptophan-free amino acid mix could be prevented by blocking protein formation. Apparently, the tryptophan reduction is mediated by the formation of proteins (from tryptophan).53 It is possible that this prevents tryptophan degradation54

We think it is worth considering whether tyrosine depletion (at the appropriate dosage) could be a helpful or even supportive treatment for disorders based on elevated dopamine levels (such as autism or schizophrenia and the rare cases of ADHD, which (according to the DAT-KO model) are based on elevated dopamine levels) or elevated noradrenaline levels, such as PTSD.
One study reports an improvement in manic symptoms in people with ADHD.55 A case study reports a cure (!) of a person with ADHD through a gluten- and casein-free diet.56 However, studies that systematically compared gluten-free and casein-free diets in relation to autism found no relevant influence.5758
Products that contain a lot of casein also contain a lot of tyrosine. A study on children with ASD found reduced tyrosine blood levels.59 In our view, it is at least theoretically conceivable that reduced tyrosine blood levels may not be a contributory cause of ASD, but the consequence of a diet that people with ADHD have unconsciously perceived as helpful in reducing their symptoms.
Even if the background is interesting, it would be completely illusory to regard a diet low in tyrosine and phenylalanine as a cure for autism. An individual case is not proof of treatment for an entire disorder.
The major risk is that there are other (possibly previously unknown) amino acids or other substances that are absorbed into the brain via the same transporters through the blood-brain barrier. Long-term intake of an amino acid mixture that occupies the blood-brain barrier transporters would cause deficiency states of these amino acids/substances, which could cause considerable damage.
In view of the possibility of significant side effects, we therefore strongly advise against experiments that are not supported by a doctor.

Theoretically, we also thought it was conceivable that taking tyrosine-depleting amino acids 2 hours before going to bed could help with sleep.
This option has not yet been discussed medically and should therefore be considered with particular caution. Even if these substances are available over the counter, they should never be taken without consulting a doctor.

As shown above, tyrosine intake can increase dopamine and noradrenaline and tyrosine depletion can decrease dopamine and noradrenaline.
However, a lower noradrenaline level is helpful to calm down.
A combined intake of the amino acids that compete with tyrosine for the same transporters across the blood-brain barrier may help to reduce dopamine and noradrenaline.
Taking a combination of the amino acids mentioned (without tyrosine and phenylalanine) could therefore possibly help people with ADHD with increased arousal to calm down.
To avoid disadvantages during the day, this should be combined with a morning intake of tyrosine and phenylalanine.

Conversely, the administration of tyrosine to reduce sleep problems caused by certain forms of stress, which are associated with reduced noradrenaline levels, has been discussed.60 Similarly, a study of unaffected individuals found that tyrosine reduced arousal.14


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