l-Theanine (γ-glutamylethylamide), a component of green tea, is considered to have regulatory and neuroprotective roles in the brain. The present study was designed to determine the effect of l-theanine on excess dopamine-induced neurotoxicity in both cell culture and animal experiments. The primary cultured mesencephalic neurons or co-cultures of mesencephalic neurons and striatal astrocytes were pretreated with l-theanine for 72 h, and then treated with excess dopamine for further 24 h. The cell viability of dopamine neurons and levels of glutathione were evaluated. Excess dopamine-induced neurotoxicity was significantly attenuated by 72 h preincubation with l-theanine in neuron-astrocyte co-cultures but not in neuron-rich cultures. Exposure to l-theanine increased the levels of glutathione in both astrocytes and glial conditioned medium. The glial conditioned medium from l-theanine-pretreated striatal astrocytes attenuated dopamine-induced neurotoxicity and quinoprotein formation in mesencephalic neurons. In addition, replacement of l-glutamate with l-theanine in an in vitro cell-free glutathione-synthesis system produced glutathione-like thiol compounds. Furthermore, l-theanine administration (4 mg/kg, p.o.) for 14 days significantly increased glutathione levels in the striatum of mice. The results suggest that l-theanine provides neuroprotection against oxidative stress-induced neuronal damage by humoral molecules released from astrocytes, probably including glutathione.
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Dopamine (DA) quinone formation as a dopaminergic neuron-specific oxidative stress plays an important role in dopaminergic neurodegeneration. ( 11 , 12 ) In damaged dopaminergic neurons, free excess DA in the cytosol outside synaptic vesicles is spontaneously oxidized to produce reactive oxygen species (ROS) and DA quinone. DA quinone covalently conjugates with the sulfhydryl group of cysteine on functional protein including tyrosine hydroxylase (TH), DA transporter, parkin protein in dopaminergic neurons, resulting in inhibition of their function. ( 13 &#; 15 ) Our previous studies demonstrated the importance of DA quinone formation in dopaminergic neuronal dysfunction using animal model of Parkinson&#;s disease ( 16 ) and methamphetamine-injected mice. ( 17 ) DA-induced formation of DA quinones and the consequent dopaminergic cell damage in both in vitro and in vivo experiments can be prevented by treatment with superoxide dismutase, glutathione (GSH), and certain thiol reagents based on their quinone-quenching activity. ( 18 , 19 ) We recently showed that astrocytes can protect dopaminergic neurons against DA quinone toxicity, ( 20 ) and that zonisamide, a novel antiparkinsonian agent, increases GSH levels in astrocytes and provides neuroprotection against dopaminergic neurodegeneration in the model of Parkinson&#;s disease. ( 21 ) The present study is an extension to the above studies and was designed to determine whether l-theanine increases GSH synthesis in astrocytes to act as a neuroprotectant against DA quinone toxicity.
l-Theanine (γ-glutamylethylamide) is a major free amino acid component of green tea, and has a suppressive effect against the excitatory action of caffeine, ( 1 ) reducing effect on systemic blood pressure, ( 2 ) and anti-oxidative properties. ( 3 , 4 ) Because l-theanine has a chemical structure similar to glutamate (Fig. ) and can cross the blood-brain barrier, ( 5 ) its effects on the central nervous system have received attention. Kakuda et al. ( 6 ) reported that l-theanine has neuroprotective effects against ischemic brain damage and glutamate-induced cell death in cortical neurons. However, l-theanine is a poor inhibitor of ligand binding to three different ionotropic receptor subtypes of l-glutamate in rat cortical neurons compared with that of glutamate itself. ( 7 ) Other studies confirmed that l-theanine inhibits the incorporation of extracellular glutamine into neurons, resulting in the suppression of exocytotic release of glutamate. ( 8 ) In addition, several studies have also demonstrated the neuroprotective effects of l-theanine against β-amyloid-induced cognitive dysfunction and neuronal cell death, ( 9 ) and against neurotoxicity induced by Parkinson&#;s disease-related environmental toxins, such as rotenone and dieldrin in cultured neuronal SH-SY5Y cells. ( 10 ) However, the mechanism(s) of the neuroprotective effects of l-theanine against dopaminergic neurotoxicity remains obscure.
Western blot analysis was performed as described previously. ( 24 ) Briefly, cytoplasmic lysate (10 µg) was loaded on 10% SDS-polyacrylamide gels and blotted onto polyvinylidene difluoride membranes (Hybond P; GE Healthcare UK, Buckinghamshire, UK). The blots were incubated at room temperature for 1 h with the following antibodies: rabbit polyclonal anti-GCL (dilution, 1:200, Lab Vision, Fremont, CA) and mouse monoclonal anti-α-tubulin (dilution, 1:500, Sigma-Aldrich, St. Louis, MO). After incubation with the corresponding peroxidase-conjugated secondary antibody, blots were washed with 20 mM Tris-buffered saline containing 0.1% Tween 20. Protein-specific signals were visualized by chemiluminescence using the ECL western blotting detection system (GE Healthcare UK). Images were obtained and quantified using a FUJIFILM Luminescent Image Analyzer LAS- (FUJIFILM, Tokyo, Japan) and MultiGauge (ver. 3.0) software. For quantitative analysis, the ratio for specific signals of protein (relative chemiluminescence unit) to that of constitutively expressed α-tubulin protein was calculated to normalize for loading and transfer artifacts introduced in western blotting.
Cytoplasmic lysate from cell cultures were extracted and prepared by using the PARIS protein and RNA isolation system (Ambion, Austin, TX) according to the protocol provided with the kit. Cells from the 6-well culture plates were lysed by incubation in ice-cold Cell Fractionation Buffer with 0.1 mg/ml PMSF for 10 min. The homogenates were centrifuged (500 × g for 3 min at 4°C), and the supernatant was collected as cytoplasmic protein lysate. The protein concentration in the lysate was determined by the DC protein assay kit (Bio-Rad, Richmond, CA), using bovine serum albumin as a standard.
The levels of protein-bound quinones (quinoprotein) were determined by the nitrobluetetrazolium (NBT)/glycinate colorimetric assay, as described previously. ( 19 ) Total cell lysates were prepared by homogenization in ice cold-RIPA buffer [PBS (pH 7.4), 1% nonidet P-40, 0.5% sodium deoxycholate and 0.1% sodium dodecyl sulfate (SDS)] with 10 µg/ml phenylmethylsulfonyl fluoride (PMSF). The cell lysate was added to 100 µl of NBT reagent (0.24 mM NBT in 2 M potassium glycinate, pH 10.0) followed by incubation in the dark for 3 h under constant shaking. The absorbance of blue-purple color developed by the reaction mixture was measured at 530 nm.
The GSH level was determined using the enzymatic recycling method of Tietze ( 23 ) with some modifications. ( 18 ) For preparation of the sample, the cells were homogenized in 0.1 M phosphate buffer (PB; pH 7.4) and then treated with equivalent volumes of 10% trochloroacetic acid. The extracts were mixed with 0.01 M PB (pH 7.4, 174 µl), NADPH (4 mM, 15 µl) and GSH reductase (6 U/ml, 30 µl) and 5,5'-dithiobis-2-nitrobenzoic acid (10 mM, 15 µl), and incubated at 37°C. The formation of 2-nitro-5-thiobenzoic acid was measured at 412 nm. The amount of total GSH was determined from a standard curve constructed using known amounts of GSH. The GSH level in GCM from l-theanine-treated striatal astrocytes was also determined as described above.
All slides were analyzed under a fluorescence microscope (Olympus BX50-FLA, Tokyo, Japan) using a mercury lamp through a 470&#;490 nm or 360&#;370 nm band-pass filter to excite Alexa Fluor 488 or Hoechst dye, respectively. The light emitted from Alexa Fluor 488 or Hoechst was collected through 515&#;550 nm band-pass filter or 420 nm long-pass filter, respectively. TH-immunopositive cells were counted under the microscope in all areas of each chamber slide. Counting was performed by an investigator blinded to the experiments.
The cells were fixed with 4% paraformaldehyde for 20 min at room temperature and washed in 10 mM phosphate-buffered saline (PBS, pH 7.4). After blocking with 2.5% normal goat serum for 20 min at room temperature, the cells were reacted with the primary antibodies for 18 h at 4°C: rabbit anti-TH (dilution, 1:1,000; Protos Biotech Corporation, New York, NY) diluted in 10 mM PBS containing 0.1% Triton X-100 (0.1% PBST). After washing in 10 mM PBS (pH 7.4) three times 10 min each, the cells were reacted for 2 h with goat anti-rabbit IgG conjugated to Alexa Fluor 488 (dilution, 1:1,000; Molecular Probes, Eugene, OR). The cells were counterstained with Hoechst nuclear stain (10 µg/ml) for 2 min and washed before mounting with Fluoromounting medium (Dako Cytomation, Glostrup, Denmark).
The striatal astrocytes were plated onto 6-well plates (Becton Dickinson) and grown in DMEM containing 10% FBS at density of 3.6 × 10 4 cells/cm 2 for 7 days. To prepare glia conditioned medium (GCM), astrocytes were treated with l-theanine (50, 500 µM) diluted in medium (l-theanine-GCM) or vehicle (control-GCM) for 72 h. The conditioned media were collected, centrifuged at 3,000 × g for 3 min to remove cellular debris, and the supernatants were stored at &#;80°C until use. For experiments, the thawed conditioned media were mixed with an equal volume of fresh culture medium (50% GCM of total medium).
Cultures of primary astrocytes were prepared from the striata of Sprague-Dawley rat embryos at 15 days gestation using the method described previously. ( 22 ) The tissue was treated with 0.125% trypsin and then 0.004% DNase I in the same way as the mesencephalic neurons. After centrifugation (1,500 × g, 5 min), the cells were gently resuspended in DMEM containing 10% FBS and plated at a density of 2.0 × 10 5 cells/cm 2 in 6-well plates coated with poly-d-lysine. The cells were cultured for 5 to 7 days in the same medium, and then subcultured to obtain astrocyte-rich cultures. Over 95% of these cultured glial cells showed immunoreactivity to glial fibrillary acidic protein (GFAP).
Primary neuronal cell cultures were prepared as described previously. ( 22 ) The mesencephalic area was dissected in Sprague&#;Dawley rat embryos at 15 days gestation. The tissue was incubated for 15 min in 0.125% trypsin at 37°C and then centrifuged (1,500 × g, 5 min). The cell pellet was treated with 0.004% DNase I for 7 min at 37°C, and recentrifuged at 1,500 × g for 5 min. The cell pellet was then gently resuspended in a small volume of Dulbecco&#;s modified Eagle&#;s medium (DMEM) containing 10% fetal bovine serum (FBS) and plated in the same medium at a density of 2.0 × 10 5 cells/cm 2 in four-chamber culture slides or in 6-well plates coated with poly-d-lysine (Becton Dickinson, Franklin Lakes, NJ). The cells were maintained in this growth medium at 37°C under 5% CO 2 /95% air environment. Within 24 h of initial plating, the medium was replaced with fresh medium supplemented with 2 µM cytosine-β-d-arabinofuranoside to inhibit the replication of non-neuronal cells, and incubated for a further 5 days. In neuron-rich cultures, 95% of the cells were immunoreactive for the neuronal marker microtubule-associated protein 2. Furthermore, approximately half of the neurons were TH-positive dopaminergic neurons.
Finally, we examined the effects of l-theanine on GSH contents in the striatum and midbrain of normal mice (n = 5). Administration of l-theanine (4 mg/kg, p.o.) for 14 days (by mixing it in drinking water) significantly increased GSH content in the striatum (Fig. ), but not in the midbrain (data not shown). The same treatment had no effect on body weight or water intake (data not shown).
To further evaluate the role of astrocytes in the neuroprotective effects of l-theanine, mesencephalic neuron-rich cultures were incubated in conditioned media from striatal astrocytes treated with/without l-theanine. Preincubation with l-theanine-GCM attenuated the DA (75 or 100 µM)-induced cytotoxicity (Fig. A). Moreover, the marked increase in quinoprotein formation in mesencephalic neurons following DA exposure (100 µM) in NM-pretreated group was significantly prevented by the pretreatment with l-theanine-GCM (50 or 500 µM) (Fig. B). Furthermore, the pretreatment with l-theanine-GCM (50 µM) also tended to inhibit, but not significantly (p = 0.), DA-induced elevation of quinoprotein in control-GCM-pretreated neurons. These results suggest that secreted molecules from l-theanine-treated astrocytes exert neuroprotective effects against dopaminergic neurons by suppressing DA quinone formation.
We first examined the neuroprotective effects of l-theanine against DA neurotoxicity using primary cultured cells. Pretreatment of mesencephalic neuron-rich cultures with l-theanine (500 µM) did not protect dopaminergic neurons against DA (50&#;150 µM)-induced neurotoxicity (Fig. ). However, the addition of 500 µM l-theanine to cocultures of mesencephalic neurons and striatal astrocytes significantly lessened the percentage of TH-positive neurons damaged by 50&#;150 µM of DA (Fig. ). These results indicate that the neuroprotective effects of l-theanine against DA neurotoxicity are mediated by astrocytes.
The present study showed that l-theanine increased GSH supply in striatal astrocytes and exerted neuroprotective effects against excess DA-induced neurotoxicity.
First, we examined whether l-theanine protected dopaminergic neurons against DA-induced neurotoxicity using neuron-astrocyte cocultures. Because DA quinones are predominantly generated from excess cytosolic DA outside the synaptic vesicles in damaged DA neurons, we used astrocytes in the striatum in the present study. Although neuron-rich cultures were sensitive to excess DA-induced toxicity, the presence of astrocytes reduced dopaminergic neuronal loss (Fig. ). These results indicate that astrocytes protect dopaminergic neurons against DA toxicity, consistent with our previous report.(20) Moreover, pretreatment with l-theanine for 72 h significantly attenuated DA-induced neuronal cell death in neuron-astrocyte cocultures, but not in cultures of neurons alone (Fig. ). Cho et al.(10) reported that l-theanine (500 µM) attenuated neuronal cell death induced by neurotoxins such as rotenone and dieldrin, which are considered as potential environmental pathogens of Parkinson&#;s disease, in human dopaminergic SH-SY5Y cells, suggesting its direct detoxicating effects on neuronal cells. However, the present results indicate that l-theanine is able to indirectly protect dopaminergic neurons against excess DA-induced neurotoxicity through affecting astrocytes.
Second, we examined the effects of l-theanine on GSH synthesis in astrocytes. Astrocytes are abundant neuron-supporting glial cells that harbor a powerful arsenal of neurotrophic factors and antioxidants. Previous studies indicated that astrocyte-derived antioxidants, such as GSH and metallothionein, are important to the survival of neighboring neurons.(20,22) GSH is a major antioxidant and protects neurons against oxidative stress. Astrocytes but not neurons express cystine/glutamate exchange transporter (xCT), which takes up cystine, reduce it to cysteine, and release GSH and GSH disulfide through the multidrug resistance protein 1 (Mrp1) of ATP-driven exporters to consequently supply cysteine, the substrate for GSH synthesis in neurons.(25&#;29) We recently reported similar increases in GSH production in astrocytes and increase in GSH release to GCM from astrocytes by the treatment with an antiepileptic drug levetiracetum which exerts neuroprotective effects against dopaminergic neurotoxin 6-hydroxydopamine-induced mesencephalic neurodegeneration.(30) Therefore, GSH synthesis in neurons is dependent on astrocytes. Thus, GSH and its synthesis-related molecules in astrocytes seem to provide protection against dopaminergic neurodegeneration. In this study, we examined the effects of l-theanine on GSH levels in cultured neurons or astrocytes. The basal GSH level in astrocytes was greater than that in neurons. Treatment with l-theanine for 72 h significantly increased GSH levels in astrocytes, but not in neurons (Fig. A). Furthermore, treatment of cultured astrocytes with l-theanine also significantly increased GSH levels in the conditioned medium at dose-dependent manner (Fig. B). These results suggest that l-theanine up-regulates not only GSH synthesis in astrocytes but also GSH supply from astrocytes. In addition, GCM from l-theanine-treated astrocytes prevented excess DA-induced neuronal cell death (Fig. A) and quinoprotein formation (Fig. B). With regard to DA quinone neurotoxicity, DA quinones covalently conjugate with the sulfhydryl group of cysteine on various functional proteins including several key molecules involved in the pathogenesis of PD (e.g., TH, DA transporter and parkin) to form quinoproteins, and inhibit the protein function to cause DA neuron-specific cytotoxicity.(11,13&#;15,31) GSH prevents DA quinone from binding to the sulfhydryl groups of cysteine on functional proteins by their conjugation with DA quinone. Several reports indicated that DA quinone-induced dopaminergic neuronal cell damage can be prevented by GSH based on its quinone-quenching activity.(11,13,18,32) Taken together, the resulting data indicate that humoral factor(s) released from l-theanine-treated astrocytes is involved in the neuroprotective effects of l-theanine, and that GSH secreted from astrocytes is probably one of the neuroprotective humoral molecules against DA quinone neurotoxicity. In the present study, the increment of GSH content in GCM from the l-theanine (500 µM)-treated astrocytes was approx. 0.5 µM (Fig. B). In our recent study, the small increment of GSH content (0.5 µM) in GCM from astrocytes after the levetiracetam treatment, which is equivalent to the increment of GSH in l-theanine-GCM in the present study, exerted neuroprotective effects against 6-hydroxydopamine-induced dopaminergic neuronal death.(30) We also revealed that the pretreatment with the exogenous addition of reduced GSH (0.5 µM) in control-GCM significantly prevented 6-hydroxydopamine-induced dopaminergic neurodegeneration.(30) Therefore, even low increment of GSH (0.5 µM) in l-theanine-GCM would be enough to protect excess DA-induced neurotoxicity.
Recent studies reported that other food chemicals, such as flavonoids, protect against dopaminergic neuron-specific toxicity caused by psychostimulants or neurotoxins,(33,34) and increase GSH synthesis through the activation of nuclear factor erythroid-related factor-2 (Nrf2) transcription factor.(35,36) Therefore, we examined the effects of l-theanine on protein levels of GCL, a GSH-synthesizing enzyme regulated by Nrf2, in astrocytes. However, treatment with l-theanine had no effects on the protein levels of GCL in astrocyte cultures (Fig. C). GSH is a tripeptide of glutamate, cysteine and glycine. l-Theanine is also a derivative of glutamate (Fig. ) and is metabolized to glutamate and ethylamine in the intestine and liver.(37) Kurihara et al.(38) reported the effects of oral administration of l-cysteine and/or l-theanine on GSH levels and immune responses, and reported that co-administration of l-cysteine and l-theanine for 11 days before immunization significantly increased the levels of total GSH in the liver 6 h after immunization compared with the levels in control mice. Considering together the above findings and the present results, we postulate that l-theanine is a substrate instead of glutamate in GSH synthesis in astrocytes. To examine this hypothesis, we constructed in vitro GSH-synthesis system by incubation with glutamate or l-theanine, cysteine and GCL followed by incubation with glycine and GSH synthase. Replacement of l-glutamate with l-theanine in the GSH-synthesis system could also generate GSH-like thiol compounds (Fig. ). This suggests that l-theanine can be a substrate in GSH or related thiol compound synthesis instead of l-glutamate. Further experiments, that are mass spectrometry and tracing experiments testing incorporation of l-theanine compound labeled at alpha-carboxyl group or ethylamine group, would identify the resulting GSH-like thiol compound and clarify underlying detailed mechanism how l-theanine reacts with cysteine by GCL.
Finally, we confirmed the effects of l-theanine treatment on GSH levels in vivo. Administration of l-theanine for 14 days significantly increased striatal GSH levels in mice (Fig. ). In general, DA-induced neurotoxicity with severe neuronal damage is observed in the striatum due to abundant dopaminergic neurons and high DA contents. l-Theanine is thought to cross the blood-brain barrier.(5) l-Theanine makes up 1&#;2% of the dry weight of tea leaves. Drinking two to four cups of green tea every day is equivalent to taking approximate 50&#;200 mg of l-theanine. It has been reported that oral administration of 50&#;200 mg of l-theanine in humans induces alpha-brain wave activity, which correlates with relaxation.(39,40) Taken together with these findings, our results suggest that l-theanine could be a useful and safe compound and it exerts neuroprotective effects against DA quinone-induced neuronal damage by released humoral molecules, in part, by glutathione from astrocytes.
Some supplements and natural ingredients, including probiotics and curcumin, may help improve your dopamine levels and mood.
Dopamine is a chemical in your brain that plays a role in the regulation of cognition, memory, motivation, mood, attention, and learning.
It also aids in decision making and sleep regulation (1, 2).
Under normal circumstances, dopamine production is managed effectively by your body&#;s nervous system. However, there are various lifestyle factors and medical conditions that can cause dopamine levels to plummet.
Symptoms of low dopamine levels include loss of pleasure in things that you once found enjoyable, lack of motivation and apathy (3).
Here are 12 dopamine supplements to boost your mood.
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Probiotics are live microorganisms that line your digestive tract. They help your body function properly.
Also known as the good gut bacteria, probiotics not only benefit gut health but may also prevent or treat various health problems, including mood disorders (4).
In fact, while harmful gut bacteria have been shown to decrease dopamine production, probiotics have the ability to increase it, which may boost mood (4, 5, 6).
Several rat studies have shown increased dopamine production and improved mood and anxiety with probiotic supplements (7, 8, 9).
Additionally, one study in people with irritable bowel syndrome (IBS) found that those who received probiotic supplements had a reduction in depressive symptoms, compared to those who received a placebo (10).
While probiotic research is rapidly evolving, further studies are needed to fully understand the effect of probiotics on mood and dopamine production.
You can add probiotics to your diet by consuming fermented food products, such as yogurt or kefir, or taking a dietary supplement.
Summary Probiotics
are important not only for digestive health but also for many functions in your
body. They&#;ve been shown to increase dopamine production and improve mood in
both animal and human studies.
Mucuna pruriens is a type of tropical bean native to parts of Africa, India and Southern China (11).
These beans are often processed into a dried powder and sold as dietary supplements.
The most significant compound found in Mucuna pruriens is an amino acid called levodopa (L-dopa). L-dopa is needed for your brain to produce dopamine (12).
Research has shown that Mucuna pruriens helps boost dopamine levels in humans, particularly those with Parkinson&#;s disease, a nervous system disorder that affects movement and is caused by a dopamine deficiency (13).
In fact, studies have indicated that Mucuna pruriens supplements may be just as effective as certain Parkinson&#;s medications at increasing dopamine levels (14, 15).
Mucuna pruriens may also be effective in boosting dopamine levels in those without Parkinson&#;s disease.
For example, one study found that taking 5 grams of Mucuna pruriens powder for three months increased dopamine levels in infertile men (16).
Another study found that Mucuna pruriens had an antidepressant effect in mice due to an increase in dopamine production (17).
Summary Mucuna
pruriens has been shown to be effective in increasing dopamine levels in
both humans and animals and may have an antidepressant effect.
Ginkgo biloba is a plant native to China that has been used for hundreds of years as a remedy for various health conditions.
Although research is inconsistent, ginkgo supplements may improve mental performance, brain function and mood in certain people.
Some studies have found that supplementing with Ginkgo biloba in the long term increased dopamine levels in rats, which helped improve cognitive function, memory and motivation (18, 19, 20).
One test-tube study showed that Ginkgo biloba extract appeared to increase dopamine secretion by reducing oxidative stress (21).
These preliminary animal and test-tube studies are promising. However, further research is needed before scientists can determine if Ginkgo biloba also increases dopamine levels in humans.
Summary Ginkgo
biloba supplements have been shown to increase dopamine levels in
animal and test-tube studies. However, further research is needed to conclude
whether ginkgo is successful in increasing levels in humans.
Curcumin is the active ingredient in turmeric. Curcumin comes in capsule, tea, extract and powdered forms.
It&#;s thought to have antidepressant effects, as it increases the release of dopamine (22).
One small, controlled study found that taking 1 gram of curcumin had similar effects as that of Prozac on improving mood in people with major depressive disorder (MDD) (23).
There is also evidence that curcumin increases dopamine levels in mice (24, 25).
However, more research is needed to understand curcumin&#;s role in increasing dopamine levels in humans and its use in the management of depression.
Summary Curcumin
is the active ingredient in turmeric. It has been shown to increase dopamine
levels in mice and may have antidepressant effects.
Oregano oil has various antioxidant and antibacterial properties that are likely due to its active ingredient, carvacrol (26).
One study showed that ingesting carvacrol promoted dopamine production and provided antidepressant effects in mice as a result (27).
Another study in mice found that oregano extract supplements inhibited the deterioration of dopamine and induced positive behavioral effects (28).
While these animal studies are encouraging, more human studies are warranted to determine whether oregano oil provides similar effects in people.
Summary Oregano
oil supplements have been proven to increase levels of dopamine and produce
antidepressant effects in mice. Human-based research is lacking.
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Magnesium plays a vital role in keeping your body and mind healthy.
Magnesium and its antidepressant qualities are still not fully understood, but there is evidence that magnesium deficiency may contribute to decreased dopamine levels and an increased risk of depression (29, 30).
What&#;s more, one study showed that supplementing with magnesium boosted dopamine levels and produced antidepressant effects in mice (31).
Currently, research on the effects of magnesium supplements on dopamine levels is limited to animal studies.
However, if you&#;re unable to get enough magnesium from your diet alone, taking a supplement may be a good idea to ensure you&#;re meeting your requirements.
Summary Most research
is limited to animal studies, but magnesium deficiency may contribute to low
dopamine levels. Taking a magnesium supplement can help.
Green tea has long been touted for its antioxidant properties and nutrient content.
It also contains the amino acid L-theanine, which directly affects your brain (32).
L-theanine can increase certain neurotransmitters in your brain, including dopamine.
Multiple studies have shown that L-theanine increases dopamine production, thus causing an antidepressant effect and enhancing cognitive function (32, 33, 34).
Additionally, studies suggest that both green tea extract and frequent consumption of green tea as a beverage can increase dopamine production and are associated with lower rates of depressive symptoms (35, 36).
Summary Green
tea contains the amino acid L-theanine, which has been shown to increase
dopamine levels.
Vitamin D has many roles in your body, including the regulation of certain neurotransmitters like dopamine (37).
One study showed decreased dopamine levels in vitamin-D-deprived mice and improved levels when supplementing with vitamin D3 (38).
Since research is limited, it&#;s difficult to say whether vitamin D supplements would have any effect on dopamine levels without an existing vitamin D deficiency.
Preliminary animal studies show promise, but human studies are needed to better understand the relationship between vitamin D and dopamine in people.
Summary While
animal studies show promise, human studies are needed to see if vitamin D
supplements increase dopamine levels in those with vitamin D deficiency.
Fish oil supplements primarily contain two types of omega-3 fatty acids: eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).
Many studies have discovered that fish oil supplements have antidepressant effects and are linked to improved mental health when taken regularly (39, 40, 41).
These benefits may be attributed in part to fish oil&#;s influence on dopamine regulation.
For instance, one rat study observed that a fish-oil-enriched diet increased dopamine levels in the frontal cortex of the brain by 40% and enhanced dopamine binding capabilities (42).
However, more human-based research is needed to make a definitive recommendation.
Summary Fish
oil supplements may increase dopamine levels in the brain and prevent and treat
depressive symptoms.
Studies have found that caffeine can boost cognitive performance, including by enhancing the release of neurotransmitters, such as dopamine (43, 44, 45).
It&#;s thought that caffeine improves brain function by increasing dopamine receptor levels in your brain (45).
However, your body can develop a tolerance to caffeine, meaning it learns how to process increased amounts.
Therefore, you may need to consume more caffeine than you did before to experience the same effects (46).
Summary Caffeine
is linked to increased dopamine levels by enhancing dopamine receptors in your
brain. Over time, you may develop a greater tolerance for caffeine and may need
to increase your consumption to have the same effects.
Ginseng has been used in traditional Chinese medicine since ancient times.
Its root can be eaten raw or steamed, but it&#;s also available in other forms, such as tea, capsules or pills.
Studies have shown that ginseng may enhance brain skills, including mood, behavior and memory (47, 48).
Many animal and test-tube studies indicate that these benefits may be due to ginseng&#;s ability to increase dopamine levels (49, 50, 51).
It has also been suggested that certain components in ginseng, such as ginsenosides, are responsible for the increase of dopamine in the brain and for beneficial effects on mental health, including cognitive function and attention (52).
One study on the effects of Korean red ginseng on attention deficit hyperactivity disorder (ADHD) in children observed that lower levels of dopamine were associated with symptoms of ADHD.
The children involved in the study received 2,000 mg of Korean red ginseng daily for eight weeks. At the end of the study, the results showed that ginseng improved attention in children with ADHD (53).
However, further studies are needed to draw definite conclusions about the extent to which ginseng enhances dopamine production and brain function in humans.
Summary Many
animal and test-tube studies have shown an increase in dopamine levels after
supplementing with ginseng. Ginseng may increase dopamine levels in humans,
especially those with ADHD, but more research is needed.
Berberine is an active component present in and extracted from certain plants and herbs.
It has been used in traditional Chinese medicine for years and has recently gained popularity as a natural supplement.
Several animal studies show that berberine increases dopamine levels and may help fight depression and anxiety (54, 55, 56, 57).
Currently, there is no research on the effects of berberine supplements on dopamine in humans. Therefore, more research is needed before recommendations can be made.
Summary Many
studies show that berberine increases dopamine levels in the brains of mice.
However, further research is needed to fully understand the effects of
berberine and dopamine levels in humans.
It&#;s best to consult with your healthcare provider before adding any supplement to your daily routine.
This is especially true if you have a medical condition or if you&#;re on any medications.
Generally, the risk associated with taking the above supplements is relatively low. They all have good safety profiles and low toxicity levels in low-to-moderate dosages.
The primary possible side effects of some of these supplements are related to digestive symptoms, such as gas, diarrhea, nausea or stomach pain.
Headaches, dizziness and heart palpitations have also been reported with certain supplements, including ginkgo, ginseng and caffeine (58, 59, 60).
Summary It&#;s
important to talk to your doctor before taking dietary supplements and stop
using them if negative side effects or medication interactions occur.
Dopamine is an important chemical in your body that influences many brain-related functions, such as mood, motivation and memory.
Generally, your body regulates dopamine levels well on its own, but some medical conditions and diet and lifestyle choices can lower your levels.
Along with eating a balanced diet, many possible supplements may help boost dopamine levels, including probiotics, fish oil, vitamin D, magnesium, ginkgo and ginseng.
This, in turn, could help improve brain function and mental health.
Each of the supplements on this list has a good safety profile when used properly. However, some supplements may interfere with certain prescription or over-the-counter medications.
It&#;s always best to talk to your healthcare provider or registered dietitian to determine if certain supplements are right for you.
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