Dopamine Optimization Claims Check: What the Evidence Says

On 2 November 2026 the X account @theriac33 posted a graphic titled “What your dopamine loves / hates”, with the caption “i did what’s required to OPTIMIZE my dopamine” [1]. It lists 12 “loves” and 9 “hates”. This article takes each item as a claim and checks it against the best evidence we could open, focusing on dopamine itself rather than mood, sleep or general health.

Key points

• Few of the 21 items have been measured against dopamine in humans. The best-supported “love” is modafinil, whose effect on dopamine was imaged by PET in 10 men [5]. Cabergoline acts directly on dopamine D2 receptors [24].
• The “Prolactin” entry is an error. Prolactin is a protein hormone, and dopamine suppresses its release, not the reverse in any study we found [21][22].
• Some “hates” are backwards or untested. A single intravenous SSRI dose in 12 healthy volunteers slightly lowered D2 availability on PET, which suggests more dopamine, not less [10].
• “Optimizing dopamine” has no agreed meaning, because dopamine does different jobs at different timescales and receptors adapt [2][3][4].

Why “dopamine optimisation” is loosely defined

Dopamine is not a pleasure chemical. Reviews describe it as a modulator of both learning and motivation, and one argues that it provides “a dynamic estimate” of whether spending effort, attention or time is worthwhile [2]. Another notes that it is “an overgeneralization” to label dopamine neurons as reward neurons, and that accumbens dopamine is involved in effort, approach and sustained task engagement more than in appetite or pleasure itself [3].

The old split between slow “tonic” dopamine for motivation and fast “phasic” bursts for learning is also contested. Berke argues that motivation-related dopamine changes occur on subsecond timescales and are shaped locally at the nerve terminal [2]. A single “level” to maximise therefore does not exist. A PET scan with raclopride also measures only one thing, the change in D2/D3 receptor availability, which is read as a proxy for extracellular dopamine in the striatum.

Finally, the system adapts. In 15 alcohol-dependent adults versus 15 controls, PET found 17 to 21% lower D2 receptor availability across striatal regions and a blunted dopamine response to amphetamine in the limbic striatum [4]. More dopamine in the short run can coexist with less responsiveness later. A graphic that ranks substances as “loved” or “hated” ignores dose, duration, brain region and who was studied.

Claim table: the “loves”

Verdicts use our four labels: supported, partly supported, not supported, could not be verified. “PET” means human positron emission tomography.

Claim	Verdict	What the evidence shows about dopamine
9-ME-BC	Could not be verified	Cell work only: in midbrain astrocyte cultures 9-methyl-beta-carboline inhibited monoamine oxidase and raised neurotrophic factor expression [16]. We found no human dopamine measurement.
Bromantane	Could not be verified	Rat studies from a Russian group; one authors’ abstract calls its effect on sexual behaviour “dopamine-positive” [17]. We found no human dopamine data. See /articles/bromantane-evidence-and-status/.
Vitamin B6 (P-5-P)	Could not be verified	We could not open the NIH fact sheet (HTTP 403) and found no dopamine study in healthy people. Left unrated rather than guessed.
L-tyrosine	Partly supported	Tyrosine is the dopamine precursor. A 2015 review concluded it helps cognition mainly in stressful or demanding situations when dopamine or noradrenaline is temporarily depleted, with minimal benefit for exercise [9]. It did not measure brain dopamine.
Exercise	Not supported by PET we read	In 12 regular exercisers, [11C]raclopride binding was unchanged 5 to 10 minutes after 30 minutes of treadmill running (4.22 vs 4.17), so no change in synaptic dopamine was detected [7]. Exercise may help other outcomes; this is not evidence for dopamine.
Circadian rhythm / sunlight	Could not be verified	We found no human study of circadian timing or sunlight and dopamine. In 86 healthy adults, each scanned once, 18F-DOPA PET showed higher putamen dopamine synthesis in fall-winter than in spring-summer [8]. That is a seasonal, between-person difference, not a test of light exposure.
Cabergoline	Supported (receptor action)	The US label describes it as a dopamine receptor agonist with high D2 affinity, approved for hyperprolactinemic disorders in adults [24]. It stimulates receptors; it does not raise dopamine.
Uridine	Could not be verified	Mouse studies only. Uridine reduced morphine-induced dorsal striatal dopamine release in one [20]; in another it altered dopamine release and receptor expression in a seizure model [20]. Direction is context-dependent.
Phenylpiracetam	Partly supported (animal)	Mouse studies report that its R and S isomers bind the dopamine transporter [18]. No human PET data found. See /articles/phenylpiracetam-status-and-evidence/.
Modafinil	Supported	In 10 healthy men, PET showed lower raclopride binding (6.1% in caudate, 6.7% putamen, 19.4% nucleus accumbens) and high dopamine transporter occupancy; the authors read this as increased extracellular dopamine [5]. See /articles/modafinil-complete-guide/.
Sabroxy / oroxylin A	Could not be verified	Rat and in-vitro work: oroxylin A inhibited dopamine uptake in vitro and its effect on impulsivity in spontaneously hypertensive rats was blunted by haloperidol [19]. No human data found.
Liver	Could not be verified	We found no study linking eating liver to brain dopamine.

Claim table: the “hates”

Claim	Verdict	What the evidence shows about dopamine
“Prolactin”	Not supported (error)	See the next section.
Cannabis	Partly supported	Acute: in 7 healthy people, inhaled THC lowered raclopride binding in the ventral striatum, consistent with dopamine release [11]. Chronic: 19 regular users showed lower striatal dopamine synthesis capacity than 19 controls, driven by users meeting abuse or dependence criteria [12]. Both studies are small.
Alcohol	Partly supported	In alcohol dependence (15 vs 15), lower D2 availability and blunted amphetamine-induced dopamine release in the limbic striatum [4]. Findings come from dependent people; acute effects in light drinkers were not reviewed here.
High estrogen	Could not be verified	We found no human dopamine study on estrogen. An in-vitro study on cultured human pituitary cells showed estradiol raised prolactin release and blunted dopamine’s inhibition in tumour cells [21].
Canola oil	Could not be verified	We found no study of canola oil and dopamine in humans.
Phone use in bed	Sleep link supported; dopamine untested	A meta-analysis of 21 cohort studies (548,338 participants) linked each extra hour of screen time with 3 to 5 minutes less sleep and later bedtimes [15]. These are associations, and none measured dopamine.
SSRIs (fluvoxamine, paroxetine)	Not supported (acute)	One intravenous citalopram infusion in 12 healthy volunteers reduced D2 availability by about 5%, “presumably” from more dopamine [10]. Long-term dopamine effects: not verified.
Pornography	Could not be verified	A 2014 MRI study of 64 men found less right caudate gray matter and putamen activation with more weekly hours, but it did not measure dopamine, and the authors note that the direction of cause is unknown [14].
Screen time	Not supported (acute)	In an early PET study, playing a video game released dopamine in the human striatum, in proportion to performance [13]. The sleep association above is separate. The ~14-hour phone screenshot in the post is an anecdote.

The prolactin error

The graphic’s “Prolactin” item shows a drawn chemical structure. By our transcription, it is a methoxylated flavone, a small plant-type molecule [1]. Prolactin is not that. Human prolactin (UniProt P01236) is a protein: a 227-residue precursor whose mature chain spans residues 29 to 227, or 199 amino acids [22]. MedlinePlus describes it as a hormone produced by the pituitary gland, mainly signalling breast tissue to grow in pregnancy and make milk [23].

The relationship runs the other way from the graphic’s implication. Dopamine inhibits prolactin release. Dopamine suppressed prolactin release by 24% in cultured normal human pituitary cells [21], and cabergoline lowers prolactin by acting on D2 receptors of pituitary lactotrophs [24]. We found no human study showing that high prolactin lowers brain dopamine.

Regulatory status

Checked for the US only, against current DailyMed labels:

• Cabergoline: indicated for hyperprolactinemic disorders in adults, either idiopathic or from pituitary adenomas; the label advises against its use to suppress postpartum lactation (label revised 06/2026) [24].
• Paroxetine (SSRI): indicated in adults for major depressive disorder, OCD, panic disorder, social anxiety disorder, generalized anxiety disorder and PTSD [25].
• Fluvoxamine (SSRI): indicated for obsessive-compulsive disorder [26].
• Modafinil (Provigil): indicated to improve wakefulness in adults with excessive sleepiness from narcolepsy, obstructive sleep apnea or shift work disorder; a Schedule IV controlled substance (label revised February 2025) [6].

We did not check the UK, Germany or the EU in this article. We did not check regulator registers for 9-ME-BC, bromantane, phenylpiracetam, oroxylin A or uridine; see the linked articles. “Research use only” products are not approved medicines.

Risks and unknowns

Prescription drugs belong with a prescriber. The cabergoline label warns of valvular heart disease and of new gambling, sexual or spending urges, and asks that valves be evaluated before starting [24]. The modafinil label lists its own warnings [6].

For the other items, what is missing is human data. The cell, rat and mouse results above do not show that the same effect occurs in people, or that it is wanted. PET studies of this kind are small (7 to 19 per group here), mostly men, and measure short windows. Receptor binding changes do not tell us how someone feels or functions.

Frequently asked questions

Can you measure dopamine in a living person? Not directly in routine practice. Researchers use PET tracers such as raclopride, where lower binding is read as more extracellular dopamine, or 18F-DOPA, which estimates synthesis capacity [5][8]. Blood or urine tests do not reflect brain dopamine.

Is prolactin a hormone or a chemical like the one drawn? It is a protein hormone made mainly by the pituitary gland, with a mature chain of 199 amino acids [22][23].

Does exercise raise dopamine? One PET study of 12 regular exercisers found no change in striatal dopamine signal after 30 minutes of running [7]. That does not rule out effects in other regions or with other protocols, which we did not review.

Do SSRIs lower dopamine? An acute PET study in 12 healthy volunteers suggested a small rise [10]. Long-term effects and effects in people with depression were not covered by the sources we read.

Sources

1. @theriac33 on X, “What your dopamine loves / hates” graphic and caption (2026-11-02); graphic transcribed from the image, text read through the fxtwitter mirror. https://x.com/theriac33/status/2117361887457505469 (claims, not evidence)
2. Berke JD, “What does dopamine mean?” (2018-05-14). https://pubmed.ncbi.nlm.nih.gov/29760524/
3. Salamone JD, Correa M, “The mysterious motivational functions of mesolimbic dopamine” (2012). https://pubmed.ncbi.nlm.nih.gov/23141060/
4. Martinez D et al., “Alcohol dependence is associated with blunted dopamine transmission in the ventral striatum”, Biol Psychiatry (2005-07-14). https://pubmed.ncbi.nlm.nih.gov/16018986/
5. Volkow ND et al., “Effects of modafinil on dopamine and dopamine transporters in the male human brain”, JAMA (2009). https://pubmed.ncbi.nlm.nih.gov/19293415/
6. Apotex Corp., “PROVIGIL (modafinil) tablets, prescribing information”, DailyMed (revised February 2025). https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=0391f182-1958-9fef-a944-53b229ce99e7
7. Wang GJ et al., “PET studies of the effects of aerobic exercise on human striatal dopamine release” (2000). https://pubmed.ncbi.nlm.nih.gov/10945526/
8. Eisenberg DP et al., “Seasonal effects on human striatal presynaptic dopamine synthesis” (2010). https://pubmed.ncbi.nlm.nih.gov/21048126/
9. Jongkees BJ et al., “Effect of tyrosine supplementation on clinical and healthy populations under stress or cognitive demands: a review” (2015). https://pubmed.ncbi.nlm.nih.gov/26424423/
10. Smith GS et al., “SSRI modulation of striatal dopamine measured with [11C]-raclopride and PET” (2009). https://pubmed.ncbi.nlm.nih.gov/18925655/
11. Bossong MG et al., “Delta 9-tetrahydrocannabinol induces dopamine release in the human striatum” (2008). https://pubmed.ncbi.nlm.nih.gov/18754005/
12. Bloomfield MA et al., “Dopaminergic function in cannabis users and its relationship to cannabis-induced psychotic symptoms”, Biol Psychiatry (2013). https://pubmed.ncbi.nlm.nih.gov/23820822/
13. Koepp MJ et al., “Evidence for striatal dopamine release during a video game” (1998). https://pubmed.ncbi.nlm.nih.gov/9607763/
14. Kühn S, Gallinat J, “Brain structure and functional connectivity associated with pornography consumption” (2014). https://pubmed.ncbi.nlm.nih.gov/24871202/
15. He X et al., “The association of screen time and the risk of sleep outcomes: a systematic review and meta-analysis” (2025-12-17). https://pubmed.ncbi.nlm.nih.gov/41480345/
16. Keller S et al., “9-Methyl-beta-carboline inhibits monoamine oxidase activity and stimulates the expression of neurotrophic factors by astrocytes” (2020). https://pubmed.ncbi.nlm.nih.gov/32285253/
17. Kuzubova EA et al., “The effect of bromantan on the sexual behavior and conception in rats” (2004). https://pubmed.ncbi.nlm.nih.gov/15341065/
18. Zvejniece L et al., “S-phenylpiracetam, a selective DAT inhibitor, reduces body weight gain without influencing locomotor activity” (2017); and “Neuroprotective and anti-inflammatory activity of DAT inhibitor R-phenylpiracetam in experimental models of inflammation in male mice” (2020). https://pubmed.ncbi.nlm.nih.gov/28743458/ ; https://pubmed.ncbi.nlm.nih.gov/32279140/
19. Yoon SY et al., “Oroxylin A improves ADHD-like behaviors in the spontaneously hypertensive rat and inhibits reuptake of dopamine in vitro” (2013). https://pubmed.ncbi.nlm.nih.gov/23371806/
20. Liu P et al., “Uridine decreases morphine-induced behavioral sensitization by decreasing dorsal striatal dopamine release” (2014); Wang T et al., “Antiepileptic effect of uridine may be caused by regulating dopamine release and receptor expression in corpus striatum” (2018). https://pubmed.ncbi.nlm.nih.gov/25088943/ ; https://pubmed.ncbi.nlm.nih.gov/29555238/
21. Lamberts SW et al., “Differences in the interaction between dopamine and estradiol on prolactin release by cultured normal and tumorous human pituitary cells” (1986). https://pubmed.ncbi.nlm.nih.gov/3782422/
22. UniProt, “P01236 (PRL_HUMAN), Prolactin” (accessed 2026-11-08). https://rest.uniprot.org/uniprotkb/P01236.json
23. MedlinePlus, “Prolactin levels” (updated 2024-01-03). https://medlineplus.gov/lab-tests/prolactin-levels/
24. Mylan Pharmaceuticals, “Cabergoline tablets, prescribing information”, DailyMed (revised 06/2026). https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=e497366b-a124-4d7f-bd45-a883c392d4bb
25. PD-Rx Pharmaceuticals, “Paroxetine tablets, prescribing information”, DailyMed (label listed 2026-11-05). https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=65c81817-34d3-4c57-a4bf-fb10be98386d
26. PD-Rx Pharmaceuticals, “Fluvoxamine maleate tablets, prescribing information”, DailyMed (label listed 2026-10-29). https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=9972efbb-46cd-45b7-b71c-35032311b70c

Studies 2 to 5 and 7 to 21 were read as abstracts through Europe PMC; PubMed itself blocked automated access, so full texts were not read.

This article is information, not medical advice.