Dopamine is a chemical and neurotransmitter in the brain. The major role dopamine plays is in allowing reward-motivated behavior. It encourages action and perseverance. It is also needed for proper motor control and the release of hormones.

Dysfunction of dopaminergic function causes Parkinson’s Disease and is implicated in schizophrenia, fibromyalgia, attention deficit disorder, restless legs, social phobia, addiction, and depression. Lack of dopamine release or receptor sensitivity causes anhedonia, the inability to experience pleasure. Confident people have better dopaminergic function and social status modulates the dopamine systems so the relationship between the two is mutual (Watanabe and Yamamoto, 2015). Increased risk-taking and sensation-seeking in youths is linked to changes in patterns of dopaminergic activity during puberty (Steinberg, 2008). Decision-making and confidence in those decisions “may be encoded by dopaminergic firing” (Schwartenbeck et al., 2015).

The nootropic, biohacker, and nutrition communities focus on dopamine but I think there is a lack of simplistic, authentic, and aggregated information for enhancing dopaminergic function inexpensively. Many terrible and pathetic clickbait articles exist with names like “5 Foods to Supercharge Dopamine” and “How to Supercharge Dopamine Levels to Never Feel Sad Again”. Sorry pal, you’re not supercharging anything but wasted time. L-tyrosine, the amino acid precursor to dopamine found in foods, doesn’t cross the blood-brain barrier so will not “supercharge” or raise dopamine (“Desensitization: A Numbed Pleasure Response”). Nevertheless, sufficient and abundant nutrition is a prerequisite to this guide since dopamine and other neurotransmitters cannot be synthesized without it. Cognitive therapy, exercisemeditation, and romance all improve dopamine release and dopamine receptor function but I will cover mostly pharmacological and subtle lifestyle methods, organized loosely.

The Vitamin A metabolite, retinoic acid, increases the expression of the dopamine D1 and D2 receptor (Bondioni et al., 2008). Vitamin A-deficient mice exhibit the locomotor symptoms of Parkinson’s Disease (Wolf, 1998) and have blunted responses to cocaine (Krezel et al., 1998). Retinoic acid protects against degeneration of dopaminergic neurons in PD (Lian-Hu et al., 2012). Now Foods Vitamin A is $3 to $9.50 or you can just eat some carrots daily.

Vitamin B1, thiamine, is needed to turn sugar and amino acids into energy. Thiamine deficiency causes neuropathy, degeneration of the nervous and cardiovascular systems, malaise, weight loss, irritability, confusion, and amnesia. Beriberi, a disease caused by thiamine deficiency, translates to “weak, weak” or “I can’t, I can’t”. Thiamine deficiency depletes catecholamines like dopamine and noradrenaline and impairs learning in rats (Mair et al., 1985). If enough calcium is present, thiamine induces dopamine release in the striatum, the brain’s reward system (Yamashita et al., 1993). There is low thiamine in the cerebrospinal fluid of Parkinson’s patients and doses of 100 mg injected daily or twice a week can reverse Parkinsonian symptoms (Jiménez-Jiménez et al., 1999; Constantini and Fancellu, 2016). Doses of 600-1500 mg improve fatigue in multiple sclerosis, fibromyalgia, and chronic fatigue syndrome (Constantini et al., 2013). 6 to 8 grams daily is beneficial for dementia and Alzheimer’s (Meador et al., 1993). There is no known toxicity of excess thiamine. More expensive, apparently more effective “fat soluble” forms of thiamine like benfotiamine and sulbutiamine are potentially toxic and have no studies proving their superiority to traditional thiamine HCl. Now Foods Thiamine HCl is $4.50.

Vitamin B3, niacinamide, protects against energy depletion, dopamine depletion, and dopamine neurotoxicity from amphetamine and methamphetamine. It increases ATP in the striatum, the reward system (Wan et al., 1999; Huang et al., 1997). I like Solaray Niacinamide ($5)

Vitamin B6, pyridoxine, is a dopamine agonist and a prolactin antagonist. In 10 children administered B6, prolactin fell to 42% of baseline levels. This is desirable because prolactin opposes dopamine and vice versa. In a study on B6-deficient rats, one dose of 10 mg/kg B6 normalized neurotransmitter function. B6 reverses neuroleptic (antipsychotic)-induced Parkinsonism and Tardive Dyskinesia while reducing psychosis at 100 mg daily. B6 enhances Parkinson’s drugs like levodopa and protects from their adverse effects (Mims et al., 1975). Long-term B6 treatment “normalizes completely the pattern of ADHD behavior (Dolina et al., 2014). Taking the active B6, P5P, bypasses the liver’s conversion, reducing the risk of B6 toxicity and increasing benefits. A general therapeutic human dose is 100-150 mg daily. Good brands are Country Life ($14) and Now Foods ($10).

Vitamin C, ascorbate, increases the number of dopamine neurons, is neuroprotective against toxic dopaminergic metabolites, maintains dopaminergic homeostasis, and is “essential for dopamine action to inhibit prolactin release” (Bagga et al., 2008; Hansen et al., 2014; Shin et al., 1999). Now Foods Sodium Ascorbate is $10 or you can just eat lots of fruit.

Vitamin D, cholecalciferol, is a neurosteroid needed by the dopaminergic system. It upregulates genes that synthesize dopamine, modulates dopamine circuitry, and enhances amphetamine-induced dopamine release. Vitamin D deficiency promotes addiction, obesity, and decreases locomotion in rats (Trinko et al., 2016). Therapeutic dosages are 5000 IU up to 10,000 IU daily. I use the NOW Foods brand ($11) and sunbathe in spring and summer.

Taurine, an amino acid, increases synthesis of dopamine and noradrenaline and inhibits dopamine depletion while enhancing noradrenaline depletion. Taurine increases testosterone in rats by 200% (Prous et al., 1978). Now Foods Taurine is $6.50.

L-theanine, an amino acid found mainly in green tea, increases dopamine and lowers serotonin, an inflammatory mediator. “A dosage of about 400 mg daily would increase dopamine by about 45% and reduce serotonin by about 44%” (Haidut). Theanine costs $12 to $20 or you can just drink green tea.

Aspirin protects from dopamine depletion, unlike other NSAIDs. Regular aspirin intake is associated with an over 70% reduction in Parkinson’s incidence (Aubin et al., 1998). Used alone, dosages of 5-6 grams are dopaminergic. In combination with 50-60 mg caffeine, 500 mg of aspirin synergizes with it and displays dopaminergic effects that last up to 6 hours (Haidut; Collins et al., 1979). Quality aspirin brands like Bayer and Geri-Care cost $4-$10 depending on pill count.

Caffeine upregulates dopamine receptors and increases striatal dopamine receptor availability (Volkow et al., 2015). Caffeine regulates dopamine transporter density and improves attention and cognition in ADHD patients (Pandolfo et al., 2013). Chronic caffeine consumption in prepubescent children has long-term cognitive benefits which may make caffeine a candidate for the treatment and prevention of ADHD (Pires et al., 2010). Caffeine is neuroprotective and restores lost function in Parkinson’s patients (Prediger, 2010). PureBulk’s and BulkSupplements’ Pure Caffeine Capsules are $14 while additive-containing brands like ProLab are $8. Magnesium glycinate, l-theanine, aspirin, and sugar reduce caffeine’s anxiogenic effect.

Cocoa contains dopamine agonists bromocriptine and caffeine. Bromocriptine stimulates the heart while caffeine stimulates the brain. Rats administered with 24 mg/kg daily of cocoa polyphenolic extract (Acticoa powder) for one year showed improved cognition, increased lifespan and high urinary free dopamine levels (Bisson et al., 2008). Thus, a quality chocolate containing cocoa/cacao can produce this effect. Viva Naturals and Healthworks sell 1 LB of cacao powder for $11.

Stimulants like amphetamine (Adderall), methylphenidate (Ritalin), and modafinil (Provigil) are dopamine reuptake inhibitors, which means they force the brain to increase dopamine concentrations. These drugs powerfully enhance pleasure, motivation, cognition, and sociality. Taken at normal therapeutic doses, they cause the brain to downregulate its dopamine receptors which leads to tolerance, where the drug’s efficacy lessens with time. Some users cycle off the drug, taking “drug weekends” to reduce tolerance. One controversial and possibly more effective method is hormesis, wherein microdoses of the drug are taken which causes the brain to quickly and dramatically upregulate its dopamine receptors, effectively reducing tolerance or completely resetting it. Some users warn against this, as super sensitized dopamine receptors can cause side effects like insomnia and motor tics. Users also report that this effect persists after stopping the drug, permanently increasing features like motivation, pleasure, and paranoia.

Piracetam is a nootropic drug that, at 100 mg/kg, increases dopaminergic activity and locomotion in rats (Budygin et al., 1996). Piracetam protects rat brains from hemorrhagic shocks (Grässler et al., 1987). The nootropic community generally suggests choline replenishment during piracetam use. Previously, I used the Nootropics Depot ($12) brand.

Creatine’s antidepressant effect is “likely” mediated by an activation of dopamine D1 and D2 receptors (Cunha et al., 2012). BulkSupplements‘ Creatine Powder is $8 to $19 while Optimum Nutrition‘s is $15.

Chewing (mastication) relieves stress, significantly raises dopamine and activates the dopaminergic system in rats (Ono et al., 2015). Additionally, chewing during stress reduces gastric ulcer formation, cognitive dysfunction, and bone loss (Kubo, Iinuma and Chen, 2015). Soft diet feeding decreases dopamine release and impairs learning and memory in rats, compared to rats fed a hard diet (Kushida et al., 2008).

Mild tactile stimulation of the skin for at least 5 minutes releases dopamine. So things like massage, exercise, and intimacy will do this in addition to their independent effects (Maruyama et al., 2012).

Infrared and near-infrared light “neuroprotect dopaminergic cells”. Just four 90-second near-infrared exposure cycles spaced over 30 hours achieves this. In the mice experiment, the stress of prolonged bright light exposure increased dopaminergic function and suppressed melatonin, a hibernation hormone, in the short term. However, 90 days of bright light exposure caused a significant decrease in dopamine. Additionally, Parkinson’s is correlated with sky light pollution (Romeo et al., 2013). This is probably because of fluorescent light’s toxicity. Ray Peat, PhD emphasizes the crucial difference between blue (which includes fluorescent) and red light. Red, infrared, and incandescent light are neuroprotective while blue light is neurodegenerative (“Aging Eyes, Infant Eyes, and Excitable Tissues”; “Light is Right”). I use Uvex Blue Light Blocking Glasses ($9) for blue light protection and the Philips R40 Infrared ($11) and PLT PS30 Incandescent ($2.50!) bulbs for indoor red light exposure.


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Works Cited

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Collins, Catherine, R. I. Laird, P. T. Richards, G. A. Starmer, and Solveig Weyrauch. “Aspirin-caffeine Interaction in the Rat.” Journal of Pharmacy and Pharmacology 31.1 (1979): 611-14. Print.

Cunha, M. P., D. G. Machado, J. C. Capra, J. Jacinto, L. E. Bettio, and A. L. S. Rodrigues. “Antidepressant-like Effect of Creatine in Mice Involves Dopaminergic Activation.” Journal of Psychopharmacology 26.11 (2012): 1489-501. Print.

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Dolina, S., D. Margalit, S. Malitsky, and A. Rabinkov. “Attention-deficit Hyperactivity Disorder (ADHD) as a Pyridoxine-dependent Condition: Urinary Diagnostic Biomarkers.” Medical Hypotheses 82.1 (2014): 111-16. Print.

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“Effects of Caffeine in Parkinson’s Disease: From Neuroprotection to the Management of Motor and Non-motor Symptoms.” Journal of Alzheimer’s Disease : JAD. U.S. National Library of Medicine. Web. 10 Dec. 2016.

Hansen, Stine, Pernille Tveden-Nyborg, and Jens Lykkesfeldt. “Does Vitamin C Deficiency Affect Cognitive Development and Function?” Nutrients 6.9 (2014): 3818-846. Print.

Harris, Arthur R. C., M. Susan Smith, S. Alex, H. A. Salhanick, A. G. Vagenakis, and And L. E. Braverman. “Pyridoxine (B6)-Induced Inhibition of Prolactin Release in the Female Rat*.” Endocrinology 102.2 (1978): 362-66. Print.

Huang, Nai-Kuei, Fang-Jung Wan, Ching-Jiunn Tseng, and Che-Se Tung. “Nicotinamide Attenuates Methamphetamine-induced Striatal Dopamine Depletion in Rats.” NeuroReport 8.8 (1997): 1883-885. Print.

“Inhibition of Stimulated Dopamine Release from Striatum Slices after Hemorrhagic Shock in the Rat. Protective Effect of Piracetam.” Methods and Findings in Experimental and Clinical Pharmacology. U.S. National Library of Medicine. Web. 10 Dec. 2016.

Krel, W. “Impaired Locomotion and Dopamine Signaling in Retinoid Receptor Mutant Mice.” Science 279.5352 (1998): 863-67. Print.

Kubo, Kin-Ya, Mitsuo Iinuma, and Huayue Chen. “Mastication as a Stress-Coping Behavior.” BioMed Research International 2015 (2015): 1-11. Print.

Kushida, S., K. Kimoto, N. Hori, M. Toyoda, N. Karasawa, T. Yamamoto, A. Kojo, and M. Onozuka. “Soft-diet Feeding Decreases Dopamine Release and Impairs Aversion Learning in Alzheimer Model Rats.” Neuroscience Letters 439.2 (2008): 208-11. Print.

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Mims, Robert B., Cranford L. Scott, Onyechi Modebe, and John E. Bethune. “Inhibition Ofl-Dopa-Induced Growth Hormone Stimulation by Pyridoxine and Chlorpromazine.” The Journal of Clinical Endocrinology & Metabolism 40.2 (1975): 256-59. Print.

Ono, Yumie, So Koizumi, and Minoru Onozuka. “Chewing Prevents Stress-Induced Hippocampal LTD Formation and Anxiety-Related Behaviors: A Possible Role of the Dopaminergic System.” BioMed Research International 2015 (2015): 1-7. Print.

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“[The Effect of a Low Dose of Piracetam on the Activity of the Dopaminergic System in the Rat Striatum].” Eksperimental’naia I Klinicheskaia Farmakologiia. U.S. National Library of Medicine. Web. 10 Dec. 2016.

3 thoughts on “Dopamine: Restoration, Protection, Expansion

  1. ” “fat soluble” forms of thiamine like benfotiamine and sulbutiamine are potentially toxic and have no studies proving their superiority to traditional thiamine”. What is your evidence that these two forms of thiamine are toxic and would you say the same principal applies to allithiamine?

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    1. TTFD is the form with mechanistic possibility of toxicity (http://onibasu.com/archives/am/116173.html) and the risks with benfotiamine and sulbutiamine seem to be sourcing-contamination and not from the actual -tiamine molecules (https://raypeatforum.com/community/threads/vitamin-b1-dosage.681/#post-32060). Keep in mind that latter link is from 2013 and I haven’t paid attention to if conditions have changed or new evidence found.

      The same risks do seem to apply to allithiamine (http://onibasu.com/archives/amc/57504.html ; http://onibasu.com/archives/am/122625.html). There are people defending against these points (http://onibasu.com/archives/am/122612.html) but the possibility of serious harm makes me prefer caution.

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