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54 Factors that May Increase Dopamine

Written by Biljana Novkovic, PhD | Last updated:
Puya Yazdi
Medically reviewed by
Puya Yazdi, MD | Written by Biljana Novkovic, PhD | Last updated:

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Dopamine is the compound that fuels our drive and motivation. It increases attention, improves cognitive function, and stimulates our creativity. It makes us more social and extroverted and helps us form romantic and parental bonds. However, dopamine, when too high, can also have detrimental effects.

What Is Dopamine?

Dopamine is a neurotransmitter, which is a chemical released by neurons (nerve cells) to send signals to other nerve cells [1].

Many areas of the brain produce dopamine. It is produced in the ventral tegmental area (VTA in the image above) of the midbrain, the substantia nigra pars compacta, and the arcuate nucleus of the hypothalamus [2].


The most important dopamine pathway in the brain controls reward-motivated behavior [1].

Most types of rewards, such as new experiences or accomplishments can increase dopamine levels in the brain, according to some scientists. In addition, most addictive drugs and behavioral addictions increase dopamine in certain parts of the brain [3].

Dopamine has many other important roles in humans, including movement, memory, attention, learning, sleep, and mood [2].

Scientists believe that dysfunctions of the dopamine system contribute to Parkinson’s disease, schizophrenia, restless legs syndrome, and attention-deficit hyperactivity disorder (ADHD) [1].

Read more about the benefits and drawbacks of dopamine here.

Ways to Increase Dopamine



Exercise increases dopamine release, as seen in multiple animal studies [4, 5, 6].

A systematic review of 15 studies found robust effects of physical activity on dopamine release [7].

For example, one study has reported that exercise decreases the activity of COMT — the enzyme that breaks down dopamine — thereby increasing dopamine levels in women (especially in the prefrontal cortex) [8].

In 2 trials of 39 Parkinson’s disease patients, exercise increased dopaminergic neurotransmission and dopamine release [9, 10].

Relaxation Techniques

Acute stress increases dopaminergic activity according to 2 systematic reviews. However, one of them noted that chronic stress during adolescence leads to blunted prefrontal dopamine transmission in adulthood [11, 12].

Meditation has been associated with increased release of dopamine (and serotonin) in the brain, thus increasing the feelings of pleasure and well-being [13, 14, 15].

However, the effects seem to be only temporary unless meditation is practiced regularly and consistently. For example, one study reported that long-term meditation practice is needed to induce stable changes in the baseline levels of dopamine (in the striatum) [16].

3 months of practicing yoga was reported to increase the circulating blood levels of dopamine in men. The authors of this study also suggested that yoga practices may help in the long-term prevention of age-related health issues in healthy males (such as reduced cardiovascular, metabolic, and cognitive functions) [17].


According to one study, people who received a massage showed a 31% increase in the levels of dopamine in their urine, which may suggest increased levels of dopamine throughout the rest of the body and brain [18].

Massage has also been reported to increase dopamine levels in pregnant women suffering from depression [19, 20], adolescents with bulimia [21], women with breast cancer [22, 23], and patients with chronic lower back pain [24].

Sunlight Exposure

Bright, natural sunlight can improve our mood. Scientists hypothesize that this may partially be due to dopamine. For example, one study has reported that light may increase dopamine, and thereby improve mood in women with mild seasonal mood disorders [25].

In a placebo-controlled trial of 32 women with seasonal affective disorder, the ingestion of a phenylalanine/tyrosine-deficient mixture caused impaired dopamine neurotransmission (reflected as greater processing of sad emotional stimuli), except in those exposed to bright light [26]. 

A case series of 12 patients with Parkinson’s disease found that bright light exposure decreased the need for dopamine replacement therapy [27].

Light also stimulates the release of dopamine in the retina, which may be beneficial for maintaining good vision [28].


Several major parts of the brain involved in mood, motivation, and reward — such as the striatum and nucleus accumbens — have been reported to release dopamine when people listen to pleasurable music [29, 30, 31, 32].

A placebo-controlled trial of 29 participants found that music enhances memory consolidation through dopamine-dependent reward. The greater the reward experienced while listening to music, the better the memory recollection performance. Dopaminergic disruption with an antagonist drug impaired this effect [33]

Additionally, not just listening to music — but also creating and / or performing it — has also been linked to increased levels and activity of dopamine in the brain [34].

Vagus Nerve Stimulation

In rats, vagus nerve stimulation activates dopaminergic neurons and increases extracellular dopamine levels in the prefrontal cortex and nucleus accumbens while its impairment inhibits the dopamine system [35, 36, 37]. However, it didn’t increase dopamine levels in dogs [38]. Moreover, chronic vagus nerve stimulation causes biochemical changes in dopaminergic neurons that may cause their gradual degeneration [39].

Vagus nerve stimulation also preserved dopaminergic neurons and improved locomotion in rat models of Parkinson’s disease [40, 41].

In a clinical trial of 107 patients with major depressive disorder, vagus nerve stimulation was comparably effective to citalopram at improving the symptoms. Both treatments increased dopamine levels [42].

Touch & Close Physical Contact

Pleasurable physical contact can increase dopamine. In rats, it was shown that stroking stimulates the release of dopamine in the nucleus accumbens (a critical part of the brain’s reward system) [43].

Tickling, as a form of play behavior in adolescent rats, has also been reported to stimulate dopamine release (once again in the nucleus accumbens) [44].

Finally, another study reported that rats who received more physical contact at an early age showed improved spatial working memory (compared to other rats with less physical contact), as well as increased dopamine activity [45].


Tyrosine- and Phenylalanine-rich Food

Our bodies produce dopamine from the amino acid tyrosine. In turn, tyrosine can be produced from phenylalanine [46].

Both tyrosine and phenylalanine are commonly found in protein-rich foods such as [47]:

  • Chicken and Turkey
  • Fish
  • Almonds
  • Avocados
  • Bananas
  • Pumpkin and Sesame seeds
  • Dairy: Milk, Cheese, Yogurt, Cottage cheese
  • Legumes: Soy, Lima beans, Peanuts

Bananas contain especially high levels of dopamine and L-Dopa [48, 49]. Bananas had antidepressant effects in mice, in part by activating D2 dopaminergic receptors [50]. In diabetic rats, it increased brain dopamine levels and improved cognitive impairment [51]. In an old study on healthy volunteers, eating bananas alone only slightly increased dopamine levels in some subjects but significantly increased sulfate-conjugated dopamine. When combined with ascorbic acid, conjugated dopamine further increased. Similarly, a study of 12 healthy volunteers identified dopamine sulfate as one of the best predictive biomarkers of banana intake [52, 53]. In a non-placebo-controlled trial of 14 trained cyclists who completed two 75-km cycling time trials, dopamine was the only metabolite differentially increased when comparing those who ate bananas with those who ate carbohydrates [54].

Chicken hydrolysate delayed age-related cognitive impairment, in part by increasing dopamine levels, in mice [55].

Cadmium-treated rats exhibited reduced levels of dopamine and other neurotransmitters in the brain. Dietary supplementation with almonds and walnuts normalized these neurochemical aberrations and reduced depression, anxiety, and memory impairments [56].

Both sesame oil and its active component sesamin prevented brain damage caused by 6-hydroxydopamine toxicity in rats, resulting in increased levels of dopamine and its metabolite DOPAC and reducing damage to dopaminergic neurons [57, 58]. Similarly, sesamin increased dopamine levels to 133% and enhanced the dopamine-raising effects of L-DOPA in cells [59].

The whey-derived lacto-tetrapeptide β-lactolin improved memory in 3 placebo-controlled trials of healthy older adults [60]. In mice, β-lactolin improved memory and depression in part by increasing both dopaminergic activity and dopamine levels [61, 62, 63]. Another lactopeptide had similar effects in mice and showed inhibitory effects on MAO-B, resulting in higher dopamine levels [64].

In rats with iron deficiency anemia, supplementation with fermented goat milk increased dopamine levels while decreasing the levels of MAO-A and MAO-B [65]. Similarly, camel milk counteracted the neurotoxic effects of fenpropathrin (including decrease in dopamine levels) in rats [66]. Human milk fat globule-EGF factor 8 protein protected dopaminergic neurons in a rat model of Parkinson’s disease [67]. Supplementation with complex milk lipids enhanced neuroplasticity and improved memory in rats, in part by increasing dopamine output [68, 69].

Choosing Healthy Fats

Saturated fats may suppress dopamine. Equivalent intake of monounsaturated fats (from olive oil) protects against dopamine decreasing. However, you still want to consume cholesterol-rich foods in moderation (unless directed otherwise by a doctor) because cholesterol is a precursor to pregnenolone, which has been reported to increase dopamine in animals [70, 71, 72].

Fish, fish oil, and other types of seafood are some of the richest dietary sources of docosahexaenoic acid (DHA), a compound that has been reported to increase dopamine levels in the brains of rats [73].

A meta-analysis of 10 trials and 699 children with ADHD found treatment with omega-3 fatty acids, particularly EPA, effective at improving the symptoms. Omega-3 fatty acids may alter cell membrane fluidity, thus modulating dopamine and serotonin neurotransmission [74].

According to one study, DHA supplementation increased the levels of dopamine in the frontal cortex, striatum, and hippocampus of rats by as much as 40%. This may be due to the inhibition of monoamine oxidase, the enzyme that normally “breaks down” (metabolizes) dopamine and other neurotransmitters throughout the brain [75].

Additionally, according to another animal study (in mice), DHA may also boost dopamine levels by significantly increasing the brain’s levels of tyrosine hydroxylase (by as much as 89%). Tyrosine hydroxylase is one of the main enzymes responsible for producing (synthesizing) dopamine in the brain [76].

In contrast, 2 reviews of animal studies concluded that omega-3 fatty acid deficiency impairs dopamine neurotransmission and increases the risk of disease involving this system [77, 78].

Green Tea

Green tea has been reported to increase dopamine levels and activity in rats [79, 80], including its constituents theanine and caffeine.

For example, according to a few animal studies in rats, increasing amounts of stress were associated with reduced levels of dopamine and norepinephrine. However, supplementing these rats with green tea extracts (which contained important natural compounds such as polyphenols) was reported to reverse some of these stress-induced reductions in neurotransmitter levels. There were also some mild cognitive and anti-anxiety effects observed in the treated rats, which the study’s authors suggest may be due to increased levels of dopamine and serotonin. Additionally, these green tea-based supplements were also reported to show significant antioxidant effects, suggesting that it may also help promote overall brain health by combating oxidative stress [81, 82, 83].

Theanine, one of the major amino acid compounds naturally found in green tea, has also been associated with increased dopamine levels in several other animal studies [84, 85, 86, 87].

Theanine has also been linked with a variety of improvements in mood and cognitive function in a number of studies in both humans and animals, which has led some researchers to propose that this compound may have future potential as a treatment for several major neurological diseases and psychiatric disorders, such as Parkinson’s disease and anxiety disorders [88].

Caffeine’s stimulating effects are believed to arise due to its effects on the brain’s dopamine system. For example, caffeine has been reported to help maintain a higher dopamine concentration — especially in those brain areas linked with attention [89].

According to some human studies, caffeine may help promote increased levels of dopamine throughout the brain — especially in brain regions involved in attention, alertness, and motivation [89, 90].

In a placebo-controlled trial of 30 male volunteers, caffeine ingestion before treadmill running stimulated dopamine release [91]


A cell-based study identified the following coffee components as stimulators of dopamine release: caffeine, trigonelline, N-methylpyridinium, chlorogenic acid, catechol, pyrogallol and 5-hydroxytryptamides [92].

In a non-placebo-controlled trial of 10 healthy volunteers, both caffeinated and decaffeinated coffee rapidly increased blood dopamine levels [93].

In a rat model of Parkinson’s disease, coffee consumption preserved dopaminergic neurons [94]. Its component kahweol also preserved dopaminergic neurons in a cell-based study [95]

In animal models of brain damage, green coffee extract stimulated dopamine neurotransmission and restored dopamine levels [96, 97].

Vitamin D

Brain cells have vitamin D receptors. Several animal and cell-based studies show that vitamin D deficiency during fetal brain development alters the growth of dopaminergic neurons, potentially causing behavioral abnormalities during adulthood and increasing the risk of conditions such as schizophrenia and autism. Maternal supplementation helped prevent these defects [98, 99, 100, 101, 102, 103, 104].

Interestingly, the ff genotype of the VDR FokI polymorphism reduces the expression of the dopamine D1 receptor, possibly explaining its association with bipolar disorder [105].   

In rat models of Parkinson’s disease, supplementation with vitamin D protects dopaminergic neurons from damage [106, 107].

Vitamin D supplementation improved ‘anhedonia-like symptoms’ in rats with depression caused by chronic stress, possibly by stimulating dopamine transmission [108].

Two studies of 266 participants associated vitamin D deficiency with restless leg syndrome, a condition related to abnormalities in central dopamine pathways [109, 110].


Choline, especially in the form of CDP-choline, increases dopamine levels and dopamine receptor density in the brain [111, 112, 113]. In a cell-based study, CDP-choline had neuroprotective effects on dopaminergic neurons [114].

In 2 old placebo-controlled trials, CDP-choline improved rigidity and bradykinesia and increased blood dopamine levels [115, 116].

In a placebo-controlled trial of subjects with cocaine dependence, which is associated with dopamine depletion, CDP-choline improved mood states associated with cocaine craving [117].

Vitamin A

Vitamin A is required for the expression of the dopamine D2 receptor [118]. In line with this, high vitamin A intake increased D2 receptor levels in two studies in rats [119, 120].

A review of 82 studies found that children with ADHD, characterized by a dysfunction in the dopamine system, had lower vitamin A levels [121].

Vitamin C

Vitamin C is a cofactor for dopamine β-hydroxylase, the enzyme that converts dopamine into norepinephrine [122, 123, 124].

Moreover, studies in rats and brain slices found that vitamin C increases the differentiation of dopaminergic neurons [125, 126, 127].

In a study of 52 patients with a first psychotic episode, those with the lowest vitamin C levels showed the worst response to antipsychotic treatment, possibly through its effects on the dopaminergic system [128].

Interestingly, a study in mice found dual effects for vitamin C depending on the dose. While low doses potentiate its dopaminergic action, higher doses block it [129].

Vitamin B6

Pyridoxal-5-phosphate, the active form of vitamin B6, is a cofactor for the enzyme that converts levodopa to dopamine. Interestingly, low COMT activity has been associated with improved response to pyridoxine in patients with Parkinson’s disease [130]. 

Moreover, vitamin B6 may help with neurodegenerative diseases by protecting dopaminergic neurons from damage, as seen in a study in mice [131]. In line with this, both vitamin B6 and vitamin B2 restored normal dopamine levels and reduced oxidative stress in rats treated with the oxidant 3-nitropropionic acid [132].

In a study in diabetic rats, treatment with pyridoxine restored alterations in dopamine D1 and D2 receptors [133].

Vitamin B1

Vitamin B1 deficiency reduces dopamine synthesis and promotes its breakdown according to 2 studies in rats [134, 135].

Its derivative thiamine tetrahydrofurfuryl disulfide enhances locomotor activity in rodents by enhancing dopamine release in the medial prefrontal cortex [136].


Folate is needed for the synthesis of dopamine and other neurotransmitters [137, 138].

In a mouse model of Parkinson’s disease, folate deficiency increased dopaminergic neuron death by increasing homocysteine levels [139]

Vitamin B2

Both vitamin B2 and vitamin B6 restored normal dopamine levels and reduced oxidative stress in rats treated with the oxidant 3-nitropropionic acid [132].



Supplementation with tyrosine has been associated with increased dopamine levels in animals [140, 141, 142].

One study in particular has reported that tyrosine supplementation may effectively enhance cognitive performance — particularly in short-term stressful and/or cognitively-demanding situations, when dopamine is temporarily depleted [143, 140].

A systematic review of 15 studies found that tyrosine supplementation counteracts decrements in working memory and information processing induced by demanding situational conditions such as extreme weather or cognitive load in healthy humans. The authors suggested it does so by preventing the depletion of dopamine and other catecholamine neurotransmitters. Tyrosine depletion has the opposite effects [144].

Interestingly, carriers of a variant of the gene encoding the dopamine receptor DRD2 associated with lower dopamine levels (T at rs6277) benefit more from tyrosine supplementation than C/C homozygotes [145].


According to some early studies in animals, extracts of compounds naturally found in the herb Gingko biloba have been reported to increase dopamine levels and activity throughout several key regions of the brain (including the paraventricular nucleus (PVN), ventral tegmental area (VTA), and the striatum) [146, 147].

Some of the authors of these studies have speculated that this increase in dopamine may partially explain some of the cognitive benefits that have been associated with Gingko supplementation (such as improved memory). Additionally, based on these findings, some researchers have suggested that Ginkgo may have future potential for preventing or treating age-related cognitive decline and other neurodegenerative disorders (such as Alzheimer’s disease) [147, 148].

Ginkgo extract improved cognitive flexibility and response inhibition in a placebo-controlled trial of 61 elderly volunteers. The authors speculated these effects were due to enhanced prefrontal dopamine [149].


Vitamin B9 — commonly known as folate — is a vitamin naturally found in leafy green vegetables. It is needed for the production (synthesis) of several important monoamine neurotransmitters, including dopamine, epinephrine, and serotonin [150].

Without adequate folate, the body may not be able to produce enough of these neurotransmitters. Folate deficiencies have been associated with the development of depression and other mental health conditions. Therefore, ensuring that you get adequate folate in your diet (or through supplementation) can be an important step to ensure proper dopamine levels [150, 151].

St. John’s Wort

A number of studies have reported that St. John’s Wort, an herbal supplement commonly used for its anti-depressant effects, may increase dopamine levels throughout the reward systems of the brain (including regions such as the nucleus accumbens and striatum) [152, 153, 154, 155, 156].

A placebo-controlled trial of 16 healthy volunteers found that St. John’s wort may increase dopamine levels by inhibiting dopamine beta-hydroxylase (based on increased blood levels of its metabolite dopamine beta-hydroxylase) [157]. St John’s wort also increased the levels of growth hormone while decreasing prolactin in 2 clinical trials, suggesting increased dopaminergic function [158, 159].

Mucuna pruriens

Extracts from the plant Mucuna pruriens have been associated with a variety of potential benefits, such as protecting the brain against the harmful effects of oxidative stress and inflammation [160, 161].

Some researchers have proposed that these effects may be due to Mucuna’s high concentration of L-Dopa, one of the main natural “building blocks” (metabolic precursors) of dopamine. Some extracts of mucuna have concentrations of L-Dopa as high as 4-7%, which could theoretically help boost the brain’s natural levels of dopamine [160, 162, 161].

In a trial of 150 men, those with infertility had lower dopamine levels that were improved with Mucuna pruriens supplementation [163].

Lactobacillus plantarum

The probiotic Lactobacillus plantarum has been reported to increase dopamine levels in the brains of mice (especially within the striatum). Some researchers have even suggested that these mechanisms could potentially be used to treat anxiety-like behaviors and other psychiatric disorders [164, 165].

In a placebo-controlled trial of 111 stressed adults, supplementation with this probiotic reduced symptoms of stress, anxiety, and psychological scores while improving cognitive function. L. plantarum sustained dopamine function by stabilizing the expressions of TH and DBH [166].


Pregnenolone is a hormone that the body uses as one of the main “ingredients” (metabolic precursors) for producing a number of other important hormones such as testosterone, progesterone, cortisol, and estrogen [167, 168, 169].

According to a handful of animal studies in rats, one of the effects of pregnenolone may be to stimulate the release of dopamine throughout the reward system of the brain (including areas such as the nucleus accumbens and the striatum). These effects, in turn, have been associated with potential improvements in dopamine-related brain functions such as mood and motivation [71, 70, 71, 170].


Some components of the natural herb Ginseng have been reported to increase levels of dopamine in the brain in multiple animal studies [171, 172, 173].

These effects have, in turn, been associated with beneficial effects on attention, cognitive processing, sensorimotor function and auditory reaction time in both healthy human subjects as well as patients with neurological diseases [171, 174, 175].

However, some studies have reported that ginseng may also inhibit the release of dopamine in response to other stimulants, such as nicotine and cocaine [176, 177]. Findings such as these suggest that there may be some important interactions between ginseng and other common compounds and substances which could make its exact effects and mechanisms hard to predict.


A systematic review found that saffron administration increases brain dopamine levels in a dose-dependent manner [178].

In a placebo-controlled trial of 28 healthy men, supplementation with saffron improved happiness, in part by increasing dopamine levels [179] Saffron also improved depression, probably by increasing dopamine and serotonin secretion in the brain, in a placebo-controlled trial of 57 recovered consumers of methamphetamine [180]. The metabolites derived from the intake of saffron extract stimulated both dopamine and serotonin release in a study of 10 healthy men and a study in mice [181, 182]

Components of saffron such as crocin and crocetin increased dopamine levels and preserved dopaminergic neurons in several animal models of Parkinson’s disease, as well as in chronically stressed mice [183, 184, 185, 186, 187, 188]


Curcumin, found in the spice turmeric, has also been reported to increase dopamine concentrations in the brain [189, 190, 191] — specifically, by inhibiting the breakdown (metabolism) of dopamine by the enzyme monoamine oxidase (MAO) [192].

A handful of animal studies suggest that at least some of curcumin’s effects stem from its ability to increase the levels and activity of dopamine throughout the brain. Several different mechanisms may be involved in its dopamine-related effects: for example, it may “directly” stimulate the release of dopamine from neurons; additionally, it may also “indirectly” increase dopamine levels, such as by inhibiting monoamine oxidase, the enzyme that is responsible for breaking down and removing (metabolizing) dopamine throughout the brain [189, 190, 191].

According to several animal studies, curcumin has been reported to have some “antidepressant” effects in mice and rats — possibly due to some of its effects on stimulating the brain’s dopamine system (although curcumin’s effects also target several other major neurotransmitter systems, including serotonin, norepinephrine, and acetylcholine, which also likely play a role in its effects) [189, 193, 190].

Curcumin’s effects on dopamine may also be responsible for some of its cognitive effects. For example, curcumin was reported to reverse some of the memory impairments observed in rats with experimentally-induced Parkinson’s disease (a neurodegenerative disorder that primarily involves the loss of dopamine neurons in the basal ganglia). However, some of curcumin’s cognitive effects may also stem from increased levels of important natural anti-oxidants (such as superoxide dismutase, or SOD) and important brain growth compounds (such as nerve growth factor, or NGF) — and so more research will be needed to determine which of these mechanisms are the most directly responsible for these effects [191].

Finally, one animal study found that the potential “antidepressant” effects of curcumin in mice became much stronger when curcumin was supplemented along with piperine (a natural compound found in black pepper and other common dietary sources). This is believed to be because piperine significantly enhances the ability of the body to absorb curcumin effectively (also known as “bioavailability”) [190].


S-adenosyl-l-methionine — commonly referred to as “SAM-e” — is an over-the-counter dietary supplement commonly used to balance mood. Although its mechanisms are still being discovered, several studies have reported that SAMe may act in part by stimulating the production of dopamine and other important monoamine neurotransmitters [194, 195, 196, 197, 198].


In a study in mice, creatine supplementation exerted its antidepressant effects by activating dopamine D1 and D2 receptors [199].

Creatine has neuroprotective effects, resulting in a reduced loss of dopamine and dopaminergic neurons, as seen in several animal and cell-based studies [200, 201, 202, 203, 204, 205, 206, 207].

In a placebo-controlled trial of 60 patients with Parkinson’s disease, supplementation with creatine improved mood and slightly reduced the required dose of dopaminergic therapy [208].

Huperzine A

Huperzine A is a “cholinergic” substance, meaning that it increases the levels and activity of the neurotransmitter acetylcholine. However, some evidence suggests that it may also influence the levels of other important neurotransmitters, including dopamine.

For example, a preliminary animal study in rats has reported that huperzine A injections significantly increased the levels of dopamine and norepinephrine throughout the prefrontal cortex (by as much as 129%) [209].

Additionally, the influence that huperzine A appears to have on acetylcholine and dopamine levels has led some researchers to investigate its potential to treat addiction to drugs like cocaine, which heavily involve the brain’s dopamine system [210].


According to some early evidence from animal studies in mice, magnesium has been reported to have some potential antidepressant effects, which may involve increased levels of important monoamine neurotransmitters including dopamine and serotonin [211].

Magnesium is believed to have antidepressant effects, which may partially be tied to increased dopamine activity throughout the brain [211].

Oregano / Carvacrol

According to some preliminary research in animals, oregano extract has been reported to increase dopamine levels (possibly by inhibiting the breakdown and reuptake of dopamine throughout the brain). While the authors of this study have proposed that these effects may translate to healthy human users, more research will still be needed to fully confirm this [212].

A wide variety of substances are present in oregano essential oil, with some of the most common and medicinally-active ones being polyphenols, carvacrol, and thymol [213, 214].

Some evidence from early animal studies suggests that carvacrol, in particular, may have antidepressant-like effects in mice, which have been associated with this compound’s ability to stimulate the brain’s dopamine system [215].

However, the effects of carvacrol on dopamine activity may be quite different at different dosages (i.e. “dose-dependent”). For example, one study in rats reported that low doses of carvacrol increased dopamine levels in the prefrontal cortex and hippocampus, but that high doses actually reduced dopamine activity. Therefore, much more research will still be needed to understand the effects of this compound on dopamine — especially in healthy human users [216].

Butyrate/Resistant Starch

Butyrate is a short-chain fatty acid that has many functions in the body. 

Butyrate stimulates the activity of the gene responsible for creating tyrosine hydroxylase, one of the main enzymes involved in the production (synthesis) of dopamine.

  • Butyrate has been reported to increase dopamine levels in rats with experimentally-induced Parkinson’s disease (supplemented daily for 14 days). It reversed reduced dopamine levels in the striatum, as well as increased levels of BDNF and counteracted increased oxidative stress and inflammation [217].
  • Similar results (increased dopamine levels / activity) have also been reported in another animal study (in fruit flies) [218].

You can get butyrate in the diet by consuming soluble fibers found in fruits and vegetables or ghee.

Resistant starch is a type of soluble fiber that the body naturally converts into butyrate.

Uridine/Brewer’s Yeast

According to some early animal research, uridine-5′-monophosphate has been reported to increase dopamine levels and activity in the brains of rat — especially in key areas of the reward system, such as the striatum [219].

Some common dietary sources of uridine include [220, 221, 222]:

  • Nutritional and brewer’s yeast
  • Several types of vegetables, such as mushrooms and broccoli
  • Oats
  • Organ meat (e.g. liver, pancreas) and fish
  • Beer

Uridine can also be taken as a supplement — however, some researchers have raised safety concerns about long-term supplementation with uridine, so caution is advised [223, 224, 225, 226].


According to some early animal studies, the anti-oxidant compound resveratrol may act in part by increasing dopamine levels.

For example, one animal study reported that resveratrol treatment led to increased levels of dopamine, serotonin, and norepinephrine in the brains of rats subjected to chronic stress. These effects are believed to have been due to the inhibition of monoamine oxidase A, one of the main enzymes responsible for the “breakdown and removal” (metabolism) of these neurotransmitters in the brain [227].

Additionally, another animal study has reported that resveratrol treatment increased dopamine levels in the striatum of older rats by as much as 53% [228].


Zinc is an inhibitor of dopamine reuptake, which may explain its potential to improve ADHD [229, 230, 231, 232].

High doses of zinc improved spatial reference memory in rats by increasing the binding affinity of the dopamine D1 receptor for dopamine [233]. In contrast, it may reduce the affinity fo D2 receptors for antagonists [234].

In a study in rats, treatment with insulin plus zinc increased dopamine levels in the cerebellum/medulla oblongata [235].


Three old studies found that forskolin injection in the brain increases dopamine levels by inducing tyrosine hydroxylase in rats and human fetuses [236, 237, 238, 239].

Moreover, forskolin increased the levels of dopamine D2long receptors in several animal and cell-based studies [240, 241, 242].


High doses of kava (Piper methysticum) have been reported to increase dopamine levels in the brains of rats (specifically, in the nucleus accumbens) [243, 244, 245].

However, kava contains many different individual compounds, and some of these may have contrasting effects on dopamine. For example, some of kava’s components (such as yangonin) appear to increase dopamine levels, whereas other components (such as desmethoxyyangonin) have been reported to decrease dopamine [243].

Therefore, the specific extract or formulation of kava could potentially have a significant impact on its ultimate effects on the brain — and more research will be needed to understand these more subtle nuances.


According to one large-scale review of data from multiple cell-based and animal studies, the common herb rosemary (Rosmarinus officinalis) has been reported to increase brain dopamine levels, as well as stimulate certain dopamine receptors (such as D1 and D2 receptors) [246].


A review speculated that hops may improve cognitive function in part by activating dopamine neurotransmission [247]. Similarly, hops bitter acids enhanced stress resilience-related hippocampal dopaminergic activity in a mouse model of social defeat stress [248].

Hops also prevented the death of dopaminergic neurons in a cell-based study [249].


The Brazilian traditional medicinal plant catuaba (Trichilia catigua), has been reported to increase dopamine release, and may have dopamine-mediated antidepressant effects in both mice and rats [250].

An herbal product containing this plant called Catuama was reported to have similar effects in another animal study in mice [251].


Shilajit is a naturally-occurring biomass found in the Himalaya mountains. It has a long history of use in traditional Indian medicine, where it is often used to alleviate anxiety and stress.

Although the precise biological mechanisms of Shilajit are not fully known, some preliminary research suggests that its ability to influence the levels of dopamine throughout the cortex and hippocampus might be central to some of its cognitive and psychological effects [252].


According to two animal studies, extracts from the plant Bacopa monnieri have been reported to counteract the reductions in dopamine levels observed in chronically-stressed rats. Bacopa treatment was also associated with some improvements in cognitive performance (such as learning and memory) [253, 254].

However, these effects were only seen in response to stress, and whether bacopa would have similar effects in non-stressed animals — or healthy human users — remains unclear, and more research will be needed.

Fresh Cut Grass / Essential Oils

Hexanal is a compound found in plants that is responsible for the “green” odor that many people associate with natural smells, such as fresh-cut grass.

According to two preliminary studies in cells, hexanal was reported to stimulate the release of dopamine from neurons taken from the striatum of rat brains. Some researchers have proposed that this mechanism may be why people who are exposed to the smells of nature often report increased mood and attention — however, much more research would be needed to confirm this [255, 256].


In a rat model of depression, exposure to the odor of vanilla (vanillin) increased dopamine and serotonin levels in the brain [257].

Oral or injected vanillin preserved dopamine levels in a rat model of Parkinson’s disease [258]


Dietary myo-inositol increased dopamine and serotonin levels in broiler chicken [259].

In guinea pigs, chronic treatment with inositol increased the levels of dopamine D2 receptors in the brain [260].

Tongkat Ali

In a study in male rats, treatment with Tongkat ali extract (50-800 mg/kg) had aphrodisiac activity, in part by increasing brain cortical and hippocampal dopamine [261]

Clary sage

According to one preliminary animal study, essential oil from the plant Salvia sclarea — also commonly known as “clary sage” — was reported to have some potential “antidepressant” effects in rats, which may be due to its interactions with the brain’s dopamine system [262].


According to a single preliminary study in cells, the plant Salvia miltiorrhiza — also known as “red sage” or “danshen” — has been reported to stimulate the release of dopamine from neurons in the striatum [263].

Other Factors that Increase Dopamine

This section summarizes the research behind hormonal and drug-related factors that may increase dopamine levels.

Do not take any of the below-mentioned substances without talking to your doctor.

Some of the substances listed here can have detrimental health effects by acting on dopamine pathways, potentially increasing the risk of addiction or dependence.

Many addictive substances increase dopamine and should be strictly avoided. Others have addictive potential and should only be used with a doctor’s prescription for approved indications. Be sure to discuss your medications and lab results with your doctor.



Estrogen may increase dopamine. Women act more impulsively in the early as opposed to the late phase of the menstrual cycle [264].

In rats, estrogen-induced improvements in recognition memory were shown to be due, in part, to increased dopamine [265].

However, dopamine’s relationship to cognitive performance is not linear – dopamine function follows an ‘inverted U-shaped’ curve, where optimal dopamine results in maximal function and both insufficient or excessive levels lead to dysfunction [266]. That is why too much estrogen is not beneficial.


Ghrelin stimulates dopamine release in rats (amygdala, nucleus accumbens, VTA, prefrontal cortex) [267, 268].

Dopamine Drugs


Nicotine “hi-jacks” the reward circuitry in the brain by increasing dopamine release (striatum, VTA, amygdala, nucleus accumbens, prefrontal cortex). We highly advise against taking nicotine in any form, as it is an addictive substance [269, 270, 267].


L-dopa is made from tyrosine and then converted into dopamine. Basically, it is the precursor of dopamine [271].


Bromantane increases the amount of dopamine in the brain by increasing its synthesis from tyrosine (increases Tyrosine Hydroxylase, AAAD) [272, 273].

Enhancement of dopamine is observed in the hypothalamus, striatum, ventral tegmental area, nucleus accumbens, and other regions [274, 275, 276].

By increasing dopamine, Bromantane increases alertness and wakefulness [277] and improves short-term memory, motivation, planning abilities, and attention [273].


Tianeptine increases the release of dopamine in rats (nucleus accumbens > striatum) [278].


Phenibut is a nootropic drug that stimulates dopamine receptors [279].


Dopamine release may contribute to the rewarding effects of alcohol and may thereby play a role in promoting alcohol addiction (nucleus accumbens) [280].


Amphetamine exerts rewarding and reinforcing effects by elevating dopamine and prolonging dopamine receptor signaling [281].

Methylphenidate works in the treatment of ADHD by increasing levels of dopamine in children’s brains.

Previous research has shown that some people with attention deficit hyperactivity disorder may have too many dopamine transporters, which results in low levels of dopamine in the brain.

The drug seems to raise levels of dopamine by blocking the activity of dopamine transporters, which remove dopamine once it has been released [282].


Modafinil seems to inhibit the reuptake of dopamine by dopamine transporter, thereby increasing the concentration in humans [283, 284].

Supplements that May Decrease Dopamine

Supplements have not been approved by the FDA for medical use. In general, dietary supplements lack solid clinical research. Regulations set manufacturing standards for supplements but don’t guarantee that they’re safe or effective. Speak with your doctor before supplementing.


Melatonin suppresses dopamine activity [285].


Lithium impairs dopamine release [286, 287].


Long-term manganese decreases dopamine release in the brain [288, 289].

A study showed that manganese exposure, even within the safety limit, decreased dopamine production in primates [290].


Serotonin shares the same conversion and breakdown enzymes with dopamine.

Long-term supplementation with 5-HTP, the immediate precursor of serotonin, can cause dopamine depletion, which may worsen certain neurological and psychiatric diseases [291].


CBD partially blocks the dopamine D2 receptor (partial agonist), which has antipsychotic effects [292].

Conditions Linked with Low Dopamine


Inflammation decreases dopamine [293]. That’s why we feel less motivated and more sluggish when we are sick [293].

Maternal Deprivation

Maternal deprivation of rat pups leads lower dopamine levels. However, these pups reared in isolation have higher levels in response to stress [294].

Diet High in Saturated Fats

Saturated fats can suppress dopamine [72, 295].

Chronic Sugar Intake

Sugar acutely increases dopamine, which, over time, leads to a reduced number of D2 receptors and possibly a reduction in dopamine itself, leading to desensitization. These effects would not be due to the acute effects of sugar, but rather would occur over weeks to months with chronically elevated and intermittent sugar ingestion [296].

Iron Deficiency

Iron is a cofactor for tyrosine hydroxylase, a key enzyme in dopamine production [297]. Iron-deficient rats have reduced brain dopamine levels [297].

Low brain iron stores may contribute to ADHD symptoms because low iron levels in the brain can alter the activity of dopamine [298].

Weaning rats fed an iron-deficient diet showed decreased physical activity and increased anxiety-like behavior with a reduction of brain dopamine receptors [299].

However, some studies indicate iron deficiency has the exact opposite effect [300].

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3967083/figure/Fig3/ increase dopamine

About the Author

Biljana Novkovic

Biljana Novkovic

Biljana received her PhD from Hokkaido University.
Before joining SelfHacked, she was a research scientist with extensive field and laboratory experience. She spent 4 years reviewing the scientific literature on supplements, lab tests and other areas of health sciences. She is passionate about releasing the most accurate science and health information available on topics, and she's meticulous when writing and reviewing articles to make sure the science is sound. She believes that SelfHacked has the best science that is also layperson-friendly on the web.

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