Ok, I was asked to write down what to do about dopamine deficiency in this thread.
If the brain is dopamine deficient, of course it won’t work optimally. Motivation, feelings of gratification, the ability to concentrate, and memory are seriously impaired. Extreme dopamine deficiency occurs in Parkinson’s disease where the dopamine deficiency gets so severe that motor functions get impaired, so that the patients have problems with moving. More moderate dopamine deficiency can cause dopamine deficient depression (DDD), which I currently seem to suffer from. I guess dopamine deficiency lies behind anhedonia (both motivational and consummatory anhedoia). It may also have connections with ADD or ADHD.
These are my personal guesses, and they are mostly only founded in personal observations and hypotheses, which can be biased, so take this paragraph with a few grains of salt. I assume that moderate dopamine deficiency and the tendency for getting into periods of DDD, ADD, or ADHD is more pronounced for people with above average intelligence. And I suspect that the reason for that is a lack of adequate positive stimuli and feedback from their environment. The general social environment is normalized for average people with average intelligence, and it’s at least slightly inappropriate for people with blow or above average intelligence, because expectations and interests don’t align and communication is difficult. Lacking an appropriate environment the dopaminergic system becomes activated less, which perhaps causes some kind of neural atrophy that stabilizes the diminished activity of the dopaminergic system. Moving into a better stimulating environment can contribute to fixing that problem, but not immediately, because the neural atrophy needs to be reversed gradually, similar to muscular atrophy.
Dopamine synthesis pathway
It’s helpful to understand the biological dopamine synthesis pathway, which is explained very nicely in the following video:
L-phenylanaline -> L-tyrosine -> L-dopa -> dopamine -> noradrenalin -> adrenalin
So, it can start with L-phenylalanine that is converted into L-tyrosine in the liver. This conversion step is needed when starting with L-phenylalanine, because dopamine cannot be made from L-phenylalanine directly. Therefore, what is really required only is L-tyrosine, which gets converted into L-dopa within the brain. While neurotransmitters like dopamine cannot normally cross the blood brain carrier, L-tyrosine usually can do that, and L-dopa can pass the blood brain barrier, too. Anyway, L-tyrosine is easily available as supplement and is generally very safe to take in doses up to 1 g per day (or possibly more), while its use for DDD might require higher doses of up to 5 g per day. Folate is a required cofactor for the conversion of L-tyrosine into L-dopa, so a folate deficiency would sabotage the dopamine pathway. Finally, the conversion of L-dopa to dopamine requires vitamin B6 in the form of pyrodoxal 5’-phosphate (P5P) as cofactor, which can be deficient especially with conditions like pyroluria.
What I currently take that is
Daily doses:
- 1000 mg L-tyrosine
- 400 mcg folate from the Two-Per-Day tablets by Life Extension
- 75 mg vitamin B6 in a mixed form from the Two-Per-Day tablets by Life Extension
- 50 mg P5P
- 2-10 g vitamin C (for fighting oxidative stress in general)
- 24 mg astaxanthin (for fighting oxidative stress even in the brain)
- 300 mg bupropion, a selective dopamine and noradrenalin reuptake inhibitor (it’s quite effective, but it’s not ideal to take it long-term, because many users – including myself – report (reversible) adaptation/tolerance effects)
This may be a rather extreme supplement and drug stack, so I’ll suggest starting with 500 mg L-tyrosine and the Two-Per-Day tablets from Life Extension (or some even better multimineral and multivitamin supplement, if available). Fighting oxidative stress helps preventing the oxidation of dopamine, which would render it useless.