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Dopamine – what is it and what does it do?

Dopamine – the ‘feel-good’ neurotransmitter, the reward chemical – highly sort after through many means by humans. So, what is it why does it make us feel so good?

Dopamine is an organic chemical that belongs to the Catecholamines family – catecholamines are hormones like many, made by the adrenal glands that sit upon our kidneys. When directed by the brain in response to signaling, catecholamines are released into the bloodstream. These three catecholamines include:

  • Dopamine.
  • Norepinephrine.
  • Epinephrine.

Location of Dopaminergic Neurons

Today, we are observing the function of Dopamine. Dopaminergic signaling as we know is mediated when we feel good, it’s a reward-motivated driven behavior response. Dopamine is produced by dopaminergic neurons in the brain, and for the neural nerds; these are located in the following sections of the midbrain:

  • Substantia Nigra.
  • Ventral Tegmental.
  • Arcuate Nucleus of the hypothalamus.

Dopamine roles

Dopamine serves as an integral neurotransmitter that signals to produce an effect on the central nervous system. From here we see the effects on our:

  • Motor control. [1]
  • Motivation/reward. [1]
  • Arousal/reproductive mechanisms. [1]
  • Maternal Drive. [1]
  • Reinforcement and pattern development. [1]
  • Spatial Memory Function. [1]
  • [1]

Dopamine Synthesis

Dopamine is synthesized through enzymatic conversion of dietary/systemic Tyrosine (conditionally essential), however, if this is not in abundance, then tyrosine can be converted from another amino acid – l-phenylalanine, and l-phenylalanine being an essential amino acid found in protein sources, yogurt, milk, eggs, soybean flours, tofu, and some nuts and seeds – is easy enough to find! Regardless of where the Tyrosine is sourced, Tyrosine Hydroxylase the active enzyme in the production of levodopa through several co-factors such as Tetrahydrodrobiopterin, Oxygen, and iron (fe2+) forms part one of two metabolic actions for the development of dopamine. From here L-Dopa or levodopa is converted to dopamine.

One other way that dopamine can be made is through a trace amine derived from tyrosine, which from here can be converted through means of the cytochrome p450 pathway activity in the Substantia Nigra of the midbrain, however, this is a less likely pathway involvement in the production of dopamine.

Top 10 food sources of Tyrosine/phenylalanine for the production of Dopamine

[2][3]

  • Beef.
  • Pork.
  • Fish.
  • Chicken.
  • Tofu.
  • Beans.
  • Seeds.
  • Nuts.
  • Whole grains.
  • Dairy.

Keep in mind: A diet high in the whole intake of tyrosine will require less demand for phenylalanine. However, a diet low in whole consumption of Tyrosine will use up as much as 50% of your Phenylalanine intake to convert for the purpose of Tyrosine use and catecholamine production of dopamine. Phenylalanine has been used in the medical model for approaching depression states in humans, however, more is not always better and excessive Phenylalanine intake as well as sufficient tyrosine where the conversion is not required, can lead to side effects. [3]

(Consult with your health care professional for optimal level inquiries.)

What happens when we don’t have enough Dopamine?

Low levels have now been associated with the development of schizophrenia [6] and neurogenesis of Parkinson’s Disease, which is a disease that affects the nervous system, affecting movement function and includes tremors, poor mobility, loss of balance.[6]

Dopamine deficiency can occur from a poor diet of essential elements to help produce dopamine like that of phenylalanine/tyrosine and the necessary cofactors of which include iron. Poor receptor health from substance abuse which blocks the re-uptake of dopamine and accumulates dopamine in the synapse leading to poor response and higher demand from the brain to produce dopamine leading to addiction and seeking pleasure reward systems. [7]

Stress can also deplete dopamine and aid in dopamine deficient bourne depressive states, this is through the mechanism of the adrenals making these catecholamines we mentioned earlier. Alcohol, obesity, and high intake of caffeine all exhibit taxing effects on the capacity for the adrenals to produce necessary Catecholamines.  [8]

What happens when we have TOO MUCH Dopamine?

When we have too much of a good thing there is usually a subsequent consequence to this. Yin and Yang, balance, homeostasis – all aspects our body is aiming to be in a constant state of. So, what happens to us, and how does excess accumulation/expression of dopamine occur?

Accumulation of dopamine in the cytosol/cytoplasm (liquid found within our cells) through poor methylation and metabolism pathway function of Catechol-o-methyltransferase and Monoamine oxidase have been linked with the on flowing trigger of oxidative stress and neurotoxicity.

Symptoms of the high accumulation of Dopamine include:

  • Exceedingly high libido.
  • Higher instances of anxiety and panic states.
  • Mania.
  • Poor sleep patterns.
  • Increased energy states.
  • Poor ability to perceive and recover from stress.
  • Higher focus and attention to detail.

Prolonged exposure of dopamine has been linked with Schizophrenic, manic states as well as hallucinations. [9]

How do you look after your Dopamine?

Undoubtedly you want to feel good, but don’t want to be throwing yourself out of balance. The best ways to look after dopamine levels is through adequate intake of aspects like Tyrosine or Phenylalanine, Iron, and take care of avoidable stressors, sleep, and recovery which in turn will nurture your adrenal response allowing resources to be used for healthy Catecholamine production. Moderate intake and not excessive intake of caffeine and avoid the obvious ones like alcohol and illicit substances like cocaine and amphetamines that block the reuptake of dopamine and affect the status of dopamine in the brain. [9]

 

References:

  1. Dopamine: Functions, Signaling, and Association with Neurological Diseases.Marianne O. Klein1, Daniella S. Battagello1 Et Al. Cellular and Molecular Neurobiology (2019) 39:31–59 doi.org/10.1007/s10571-018-0632-3
  2. Table of Phenylalanine Content of Foods: Comparative Analysis of Data Compiled in Food Composition Tables. Ana Claudia Marquim F. Araújo,13Wilma M. C. Araújo,Et Al. JIMD Rep. 2017; 34: 87–96. Published online 2016 Oct 8. doi: 10.1007/8904_2016_12
  3. Kühn, S., Düzel, S., Colzato, L. et al.Food for thought: association between dietary tyrosine and cognitive performance in younger and older adults. Psychological Research 83, 1097–1106 (2019). https://doi.org/10.1007/s00426-017-0957-4
  4. Litwack, G. (2018). Metabolism of Amino Acids. Human Biochemistry, 359–394.doi:10.1016/b978-0-12-383864-3.00013-2
  5. Nutritional Management of Phenylketonuria Erin L. MacLeod and Denise M. Ney* Ann Nestle Eng. 2010 Jun; 68(2): 58–69. doi: 10.1159/000312813NMDANMDA receptor function, memory, and brain agingNMDA receptor function, memory, and brain aging
  6. NMDA receptor function, memory, and brain aging. John W Newcomer MD, Nuri B. Farber MD Et Al. Dialogues Clin Neurosci. 2000 Sep; 2(3): 219–232
  7. What If We Don’t Have Enough Dopamine?
  8. Dopamine Primer – How dopamine makes us human.
  9. Increased expression of the dopamine transporter leads to loss of dopamine neurons, oxidative stress and L-DOPA reversible motor deficits. ST Masoud,1LM Vecchio,1 Y Bergeron, Et Al. Neurobiol Dis. Author manuscript; available in PMC 2016 Feb 1.Published in final edited form as: Neurobiol Dis. 2015 Feb; 74: 66–75. doi: 1016/j.nbd.2014.10.016
  10. The Role of Dopamine as a Neurotransmitter in the Human Brain
  11. Recommendations for the nutrition management of phenylalanine hydroxylase deficiency. Rani H. Singh, PhD, RD1 , Fran Rohr, MS, RD2 , Dianne Frazier Et Al. advance online publication 2 January 2014. doi:10.1038/gim.2013.179
  12. Dopamine: Functions, Signaling, and Association with Neurological Diseases. Marianne O Klein1, Daniella S Battagello Et Al. Cell Mol Neurobiol 2019 Jan;39(1):31-59. doi: 10.1007/s10571-018-0632-3.
  13. Dopamine and Glutamate Interaction Mediates Reinstatement of Drug-Seeking Behavior by Stimulation of the Ventral Subiculum. Int J Neuropsychopharmacol. 2015 Jan; 18(1): pyu008. Published online 2014 Dec 22. doi: 10.1093/ijnp/pyu008
  14. The Role of Dopamine in Schizophrenia from a Neurobiological and Evolutionary Perspective: Old Fashioned, but Still in Vogue. Et Al. Ralf Brisch,1,*Arthur Saniotis,2,3 Rainer Wolf,4 Front Psychiatry. 2014; 5: 47. 2014 May 19. doi: 10.3389/fpsyt.2014.00047
  15. Single-Cell Analysis Reveals a Close Relationship between Differentiating Dopamine and Subthalamic Nucleus Neuronal Lineages. Kee et al., 2017, Cell Stem Cell 20, 29–40 January 5, 2017 ª 2017 Elsevier Inc. http://dx.doi.org/10.1016/j.stem.2016.10.003
  16. Addiction and the brain: the role of neurotransmitters in the cause and treatment of drug dependence. Denise M. Tomkinsand Edward M. Sellers CMAJ March 20, 2001 164 (6) 817-821;