What Does Dopamine Do? 26 Surprising Health Effects

Can’t Get Enough of That Dopamine

What Does Dopamine Do? 26 Surprising Health Effects

For decades it has been rare to pick up a psychiatry or neuroscience journal and not see several articles on aspects of the dopamine neurotransmitter system. Although the number of neurons using dopamine as a neurotransmitter is modest, its importance in brain function is great.

Dopamine neurons with cell bodies in the midbrain, in particular, extend their axons and ramify to many sites in the brain, including the basal ganglia, prefrontal cortex, and, with a lesser density of innervation, the amygdala, hippocampus, insula, and thalamus.

Dopamine signaling is thought to set a tone for neural activity in these areas (for example, see West et al. [1] ) and, by so doing, be involved in numerous and diverse brain functions.

Of relevance to neurology, dopamine innervation of the basal ganglia participates in the coordination of movement, and the loss of dopamine neurons leads to Parkinson’s disease.

Of relevance to psychiatry, dopamine blockade by antipsychotic drugs can produce many of the symptoms of Parkinson’s disease (the so-called extrapyramidal side effects of the drugs). Even more important, through their many connections, dopamine neurons participate in the modulation of expectation, reward, memory, activity, attention, drives, and mood—the very substrates of psychiatric illness.

Evidence for altered dopamine system activity exists for schizophrenia, bipolar disorder, depression, and attention deficit disorder. Also, related to its role in reward, most if not all substances of abuse appear to have important direct or indirect effects on dopaminergic neurotransmission.

Drugs and medications with effects mediated through dopamine have an ancient and remarkable history. Cocaine, one of the earliest known recreational drugs, increases dopamine signaling, which is believed to underlie its euphorigenic effects.

The earliest known drug therapy for psychosis, reserpine, mentioned in Vedic texts of India, depletes dopamine.

Many current psychiatric medications still target dopamine, prominently including the stimulant drugs and direct dopamine agonists, which enhance dopaminergic signaling, and the antipsychotic drugs, which to varying degrees are antagonists of dopamine, especially at dopamine type 2 (D 2 )- receptors.

Some of the original studies on the role of dopamine in reward and motivation were based upon experiments in which laboratory animals were treated with dopamine-blocking antipsychotic drugs. This work led to the seminal theory that dopamine antagonists block motivational arousal and reward (2) .

The report of Mizrahi and colleagues in this issue of the Journal advances our understanding of the relationship between dopamine receptor blockade by antipsychotic drugs and the dysphoric or anhedonic subjective feelings that often develop during drug treatment.

The authors studied patients 2 weeks after they were randomly assigned to low or high doses of olanzapine or risperidone. Overall, higher drug occupancy (blockade) of dopamine receptors in the brain, as measured by PET, was strongly associated with higher ratings of negative subjective states on a self-report scale.

In particular, blockade of dopamine receptors in the striatum was strongly correlated with a sense of impaired mental function and blockade of dopamine receptors in the temporal lobe with altered emotional regulation.

Lesser blockade in the striatum, insular cortex, and parts of frontal and temporal lobe were associated with greater feelings of well-being.

The authors speculate that negative subjective states, consequent to dopamine receptor blockade by antipsychotic drugs, may be responsible for the high rates of drug discontinuation observed in clinical practice and documented in treatment studies (3) .

While this innovative study was small (12 subjects), it provides important data regarding the associations between the molecular and regional effects of antipsychotic drugs and their therapeutic and side effects.

In time, further research will reveal the precise relationships of dose and dopamine blockade by region to components of drug effects, including beneficial effects and the various elements of negative subjective effects, from dysphoria to agitation to impaired cognition.

In the meantime it is notable that the Patient Perspectives suggest that many of the patients on low doses of drug showed substantial clinical improvement. Thus, one practical lesson of the study may be to confirm an older literature suggesting that beneficial effects can be achieved at doses that spare side effects (4) . High doses rarely lead to greater therapeutic effects, but they almost always lead to greater side effects. Until brain monitoring of dopamine receptor blockade to optimize antipsychotic effects is routinely available, the low-tech solution of using lower doses, allowing time for the drug to work before raising doses, and monitoring side effects is strongly suggested by the results of this and past studies.

Cocaine and related stimulants are known to directly affect dopamine release and reuptake, and with repeated use they lead to compensatory changes in dopamine neurotransmission that alter drive and reward and may underlie the development of addiction and the frequent tendency of those who abuse drugs to relapse.

In the report by Martinez and colleagues in this issue, the authors, again using PET, tested whether they could document dysfunction in the dopamine system of the brain in 24 cocaine-dependent subjects compared with 24 healthy volunteers.

Using techniques they developed, the authors observed a modest decrease in dopamine receptors but a substantial reduction in dopamine release in response to amphetamine in subjects with a history of cocaine dependence. This reduction was especially notable in parts of the basal ganglia related to the limbic system, which mediates emotion and choice.

It is perhaps not surprising that the euphoric effect of amphetamine was blunted in subjects with reductions in dopamine release. In addition, a blunted dopamine response was associated with decisions of subjects to receive cocaine instead of a financial reward with a street value of more than the cocaine offered.

A large animal study literature consistently documents marked degrees of change in dopamine systems, including blunting and supersensitivity, with repeated cocaine administration. This is one of the first studies to show changes in human drug users and advances the details of the findings to a level of regional analysis beyond those previously reported.

It is interesting that, on the basis of animal models, it has been hypothesized that drug-induced increases (rather than decreases) in dopamine system function are the substrate of sensitized drug “wanting” in addicts (5) . The opposite state described in the Martinez et al. report highlights the complexity of dopamine systems and their actions in the brain.

Elements of supersensitivity and blunting may coexist, and the evidence presented in this study confirms clinical observations that stimulant users are in an abnormal physiologic state and locked in a cycle of needing to keep taking stimulants to enhance (or normalize) their brain dopamine systems. It is not clear how reversible dopamine abnormalities will be after years of drug use.

It is ly that they cannot be reversed by the very drugs that cause them. Rather, resetting the dopamine system will require agents that work to restore responsivity and connections. As with the report by Mizrahi and colleagues, the novel technology developed and reported here may someday play a role in documenting and monitoring the effects of both damaging drugs and restorative treatments.

A shared feature of these new reports is their pointing to a particular role of dopamine, i.e., its role in emotional tone. Without adequate dopamine signaling, our patients do not feel “well.” When dopamine systems are dysfunctional, patients seek a change.

This may involve stopping a medication, such as antipsychotic drugs that block dopamine. Alternatively, it may be manifest as taking a drug, such as cocaine, that enhances dopamine activity.

Either way patients are probably seeking to restore dopamine function, and it is not surprising that our patients, who often have illness-related or drug-induced dysphoria, are frequent users of dopamine-enhancing drugs.

Despite all of the past research on dopamine, many details are missing on how dopamine acts to produce its effects in the brain. Equally important, as illustrated by this month’s reports, there is much more to be learned about modifying dopamine in the brain to produce desirable—and avoid undesirable—effects.

Most current medications that modify dopamine function, from antipsychotic drugs to stimulants, do so directly, following mechanisms that, as cited, go back to antiquity. As emphasized in both of the new reports, this may be a strategy that has been adequately played out.

Although new theories touting the importance of ventral striatal D 2 receptors in the antidepressant response (6) may contribute to a renaissance for dopamine-based therapies for depression, it may be more productive to seek ways to modify or restore dopamine systems through alternative or indirect means.

One such approach involves drugs that target dynorphin and its receptor, the kappa receptor (7) . Dynorphinergic neurons are in a feedback relationship with dopaminergic systems. Dynorphin-containing neurons appear responsive to changes in dopamine, and dynorphin levels appear altered in addiction.

Changing dynorphin signaling has been shown to modify dopaminergic neurotransmission, and kappa antagonists have been suggested as having possible antidepressant effects. Conversely, kappa agonists may have antimanic effects.

Many other means to modulate dopamine systems in particular or the functions they subserve will be revealed with continued research. One possibility is that feeling good or feeling bad is not actually dependent upon dopamine per se but rather the intracellular consequences of dopamine receptor stimulation.

Various treatments that cause aversive- states in rats have common effects on dopamine-linked intracellular signaling pathways in the ventral striatum (8) .

An improved understanding of whether reduced D 2 receptor function is necessary–or merely sufficient–to cause dysphoria will have critical implications for the development of improved treatments for mood disorders.

Studies of the genetics of psychiatric and substance abuse disorders are already yielding new targets for drugs to modulate mood, cognition, and attention.

Only time will tell if any of these new approaches will lead to success anything that of studying dopamine and developing agents that directly modify its effects.

In the meantime, the more we can learn about the dopaminergic effects of existing agents, the better we will be in serving our patients who expose themselves or whom we expose to dopaminergic drugs.

Address correspondence and reprint requests to Dr. Cohen, Department of Psychiatry, Harvard Medical School, McLean Hospital, 115 Mill St., Belmont, MA 02478.

The authors report no competing interests.

References

1. West AR, Floresco SB, Charara A, Rosenkranz JA, Grace AA: Electrophysiological interactions between striatal glutamatergic and dopaminergic systems. Ann NY Acad Sci 2003; 1003:53–74Google Scholar

2. Wise RA: Neuroleptics and operant behavior: the anhedonia hypothesis. Behav Brain Sci 1982; 5:39–87Google Scholar

3. Lieberman JA, Stroup TS, McEvoy JP, Swartz MS, Rosenheck RA, Perkins DA, Keefe RSE, Davis SM, Davis CE, Lebowitz BD, Severe J, Hsiao JK: Effectiveness of antipsychotic drugs in patients with chronic schizophrenia. N Engl J Med 2005; 353:1209–1223Google Scholar

4. Baldessarini RJ, Cohen BM, Teicher MH: Significance of neuroleptic dose and plasma level in the pharmacologic treatment of psychoses. Arch Gen Psychiatry 1988; 45:79–91Google Scholar

5. Robinson TE, Berridge KC: Incentive-sensitization and addiction. Addiction 2001; 96:103–114Google Scholar

6. Gershon AA, Vishne T, Grunhaus L: Dopamine D2- receptors and the antidepressant response. Biol Psychiatry 2007; 61:145–153Google Scholar

7. Carlezon WA Jr, Cohen BM: Potential utility of kappa ligands in the treatment of mood disorders, in Opioid Receptors and Antagonists: From Bench to Clinic. Edited by Dean RL III, Bilsky EJ, Negus SS III. Totowa, NJ, Humana Press (in press)Google Scholar

8. Chartoff EH, Mague SD, Barhight MF, Smith AM, Carlezon WA Jr: Behavioral and molecular effects of dopamine D1 receptor stimulation during naloxone-precipitated morphine withdrawal. J Neuroscience 2006; 26:6450–6457Google Scholar

Source: https://ajp.psychiatryonline.org/doi/full/10.1176/ajp.2007.164.4.543

Top Hacks to Increase Dopamine and Success

What Does Dopamine Do? 26 Surprising Health Effects

Do you want to be happier, smarter, wealthier, better with people, or get more stuff done? How about more creative and focused? Join the club. You might need some more dopamine for that.

Here you’ll find out all about how dopamine can make you more successful, and what you can do to increase your levels of it. Welcome to the field of personality hacking through biohacks!

The Birth of Personality Hacking

Have you ever gotten into trying to change your personality with mental hacks? By willing it enough? Been there. Done that. The result was a marked increase in neurosis, and then anxiety.

I’m a strong believer that the self-help movement has only helped increase anxiety and neurosis.

I make it my business to not attempt to change anything about myself, even not interfering with my attempts to change myself. Self-help is poison for me. It’s my kryptonite.

I believe you have to change your natural biological state and let nature take its course. This Zen attitude resonates with me and I am most comfortable with it.

Therefore, I’ve been engaged in an attempt to modulate my personality through biological manipulation.

I am naturally very introverted, but as a CEO of 2 companies, I have been forced to increase my extroverted self.

Once upon a time, I was able to lock myself in a room and speak to no one. But now I am forced to speak to various people most of the day, multi-task, put out fires, and get distracted by various things that come up. These situations have forced me to become extroverted.

Also, in the past 4 months, I’ve been dating quite a bit, speaking with investors, and interviewing potential employees, so it’s been critical to ‘turn on’ my extroverted side for months at a time, or even permanently.

Dopamine and Personality – Joe’s Experience

Overall, the data supports that dopamine and its pathways increase social status and make you more social [1].

In general, it seems increasing dopamine is a good idea before social situations.

I’ve subjectively noticed that increasing my dopamine makes me more social, funnier, confident – and attractive to women, as nerdy as that sounds.

You can say that dopamine is the “success” neurotransmitter.

My Top Dopamine Hacks

The main methods I use to increase dopamine are:

I also use various supplements that can be found here.

Read these great posts:

Can Decrease Inflammation (By Reducing Th1 and Th17 Dominance)

Dopamine may interact with the immune system, being its action dependent on the receptor type. Animal and cell research has found that the dopamine D3 and D5 receptors are pro-inflammatory, while the D1, D2, and D4 receptors reduce inflammation [2].

Although the immune effects are quite complex dopamine decreases inflammation overall because it reduces Th1 and Th17 dominance [2].

Low levels of dopamine mainly stimulate the D3 receptor in T cells, thus favoring Th1- responses and T cell activity. Moderate dopamine levels stimulate the D5 receptor as well, thus inhibiting T cell function but favoring inflammation. At higher levels, dopamine reduces both T cell response and inflammation [2].

DRD1 signaling inhibited the NLRP3 inflammasome (an immune system receptor that induces inflammation in response to infections) in mice and cells, suggesting that its activation can help treat NLRP3-driven inflammation and diseases [3].

Observations in animals suggest that high dopamine levels may help alleviate autoimmune diseases such as rheumatoid arthritis, IBD, and lupus [4].

Q&A

Q: What’s the connection between telling people to increase dopamine but then telling people the study associations are with more receptors?

A: It’s just easier to understand. When I say increasing dopamine, it just means to increase some part of the pathway, including increasing receptors.

It can get complex because if you have more D2 receptors, it can reduce the dopamine you have, but it functions better in specific ways.

The idea is the dopamine system, in general, is very important for success.

For example, light doesn’t increase dopamine, it increases the D2 receptor.

Q: These seem weak dopamine increasers. Why not dl-phenylalanine, green tea, Rhodiola, etc..?

They don’t seem to have as good of an effect for me. Green tea/EGCG is not bad. My top hacks are simply a subjective list of what works for me. The dopamine system is quite complex, so it requires more of a systems or big-picture thinking.

Source: https://selfhack.com/blog/top-hacks-increase-dopamine/

What Is Dopamine & Is It Bad In Excess?

What Does Dopamine Do? 26 Surprising Health Effects

Without dopamine, we wouldn’t feel driven and motivated.

But what happens when dopamine stops being a means to an end and turns into an end in itself? Dopamine has been blamed for many destructive behaviors of our modern lifestyle, making “dopamine fasting” the newest Silicon Valley craze. Is an excess of this neurotransmitter turning us into insensitive pleasure junkies or is the science a bit more complicated? Read on!

Definition

Dopamine is a neurotransmitter, 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. In addition, most addictive drugs and behavioral addictions can increase dopamine [3].

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

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

Schizophrenia is characterized by high striatum dopamine, but abnormally low prefrontal dopamine activity [4].

Genetics Behind Dopamine

See this post for a more comprehensive guide on the genetics of dopamine.

Cons of Excessive Dopamine

Dopamine levels are a marker of mental health. Low or high dopamine levels don’t necessarily indicate a problem if there are no symptoms or if your doctor tells you not to worry about it.

1) Plays a Role in Schizophrenia

Schizophrenia is characterized by negative symptoms such as apathy and poor social functioning, and positive symptoms, such as hallucinations and delusions [4].

The dopamine hypothesis proposes that schizophrenia is caused by excessive production of dopamine in the brain [7].

Studies support the idea that an overactive dopamine system may result in schizophrenia. Medications that block dopamine receptors, specifically D2 receptors, reduce schizophrenia symptoms [8].

Additionally, some evidence suggests that the negative symptoms and some of the cognitive deficits in schizophrenia may be related to lower prefrontal cortex function. This, in turn, may be associated with decreased dopamine activity. However, there is only indirect evidence to support this [9].

Thus, some features of negative schizophrenia (social withdrawal, apathy, and the inability to feel pleasure) are thought to be related to low dopamine levels in certain areas of the brain [2].

2) Can Drive Drug Addiction

Drugs such as cocaine, nicotine, and amphetamines act to increase dopamine in the striatum. This can lead to drug addiction [10].

The reinforcing effects of these drugs don’t only come about because of increased dopamine, but also because of the fast rate that dopamine increases. The faster the increase, the more intense the reinforcing effects [11]. This can reduce (“down-regulate”) the dopamine receptors over a period of time, causing increased need (“cravings”) for the drugs, as well as many other chronic problems.

Long-term drug use seems to be associated with decreased dopamine function. The reductions in D2 dopamine receptors and dopamine release in the striatum in addicted subjects supports this hypothesis [11].

3) Involved in Porn Addiction (and Other Behavioral Addictions)

Dopamine may contribute to compulsive sexual behaviors [12].

Both sexual experience and drugs act through dopamine D1 receptors (nucleus accumbens) [13].

Sexual novelty is compelling because it triggers bursts of dopamine in regions of the brain strongly associated with reward and goal-directed behavior. However, compulsive internet pornography users show a stronger preference for novel sexual images. Also, they get used to them more rapidly, which fuels the search for more novel sexual images [13].

In Parkinson’s disease, dopamine replacement therapies (levodopa, dopamine agonists) have been associated with compulsive sexual behavior and other impulse-control disorders [12]. Some patients reported uncharacteristic compulsive pornography use and had greater brain activity in response to sexual pictures, correlating with enhanced sexual desire [13].

Is porn addiction a problem? Some link porn to the increase in sexual performance problems and low sexual desire in men under 40. When a porn user has linked his sexual arousal to internet pornography, sex with desired real partners may register as “not meeting expectations”, resulting in a corresponding decline in dopamine, and erectile problems [13].

It is important to consider this question: are we, as a society, becoming “dopamine junkies”?

A lot of people today may succumb to “pleasure-maximizing choice behavior”. Some argue that we may be turning ourselves into mindless pleasure junkies, looking for the next dopamine shoot [14].

Basically, our choice behavior becomes biased towards short-term pleasure-maximizing goals, just as in the addicted brain and away from long-term prosperity and general well-being maximizing objectives [14].

4) Affects Weight

Dopamine, along with serotonin, opioids, cannabinoids, orexin, leptin, and ghrelin, mediates the rewarding effects of food [15].

It is associated with the desire to eat the food and with the conditioning of food cues. It is also involved with the motivation to perform the behaviors necessary to buy, prepare, and consume the food [15].

So, dopamine will cause you to desire food when you simply smell it. It causes you to ‘want’ food as opposed to just ‘liking’ the food [15].

Because dopamine is released when someone eats food, this could contribute to overeating. They will seek to increase their dopamine levels with food consumption which can cause weight gain and obesity [16], especially in people with low dopamine levels.

Dopamine is also associated with the motivation to alleviate negative emotions through eating. In both normal-weight and obese participants, emotional eating was associated with higher dopamine receptor D2R binding [17].

5) May Cause Aggression

High levels of dopamine can cause aggression. Blocking dopamine receptors decreases aggression in some people [18].

6) Decreases Empathy and Cooperation

Some observe that our modern society is a dopaminergic society. It is an extremely goal-oriented, fast-paced, and even manic society. Dopamine is known to increase activity levels, speed up our internal clocks, and create a preference for novel environments over unchanging ones [19].

On the other hand, high-dopamine individuals lack empathy and exhibit a more masculine behavioral style: conquest, competition, and aggression over nurturance and communality [19].

Increasing dopamine decreases empathy. In some human subjects, dopamine precursor levodopa increased the decisions to inflict pain on oneself and others for financial gain [20].

In a different study, people with the COMT 158Val variant, resulting in lower dopamine levels, showed higher cooperation compared to 158Met people with higher dopamine. Carriers of two 158Val variants (lower dopamine) are considered to be more helpful and empathic [21].

7) Can Cause Constipation

While dopamine can help with gut function, it can also cause constipation in some patients [22].

Dopaminergic medications in Parkinson’s disease can increase constipation risk [23].

8) May Cause Vitamin B6 Deficiency

Dopamine has been found to alter the requirements and storage mechanisms of vitamin B6, suggesting that excess dopamine can lead to vitamin B6 deficiency in certain individuals [24].

Source: https://selfhacked.com/blog/dopamine-definition-excess/

What Is Dopamine?

What Does Dopamine Do? 26 Surprising Health Effects

Dopamine is a type of neurotransmitter. Your body makes it, and your nervous system uses it to send messages between nerve cells. That's why it's sometimes called a chemical messenger.

Dopamine plays a role in how we feel pleasure. It's a big part of our unique human ability to think and plan. It helps us strive, focus, and find things interesting.

Your body spreads it along four major pathways in the brain. most other systems in the body, you don’t notice it (or maybe even know about it) until there’s a problem.

Too much or too little of it can lead to a vast range of health issues. Some are serious, Parkinson’s disease. Others are much less dire.

It’s made in the brain through a two-step process. First, it changes the amino acid tyrosine to a substance called dopa, and then into dopamine.

It affects many parts of your behavior and physical functions, such as:

It’s hard to pinpoint a single cause of most mental health disorders and challenges. But they're often linked to too much or too little dopamine in different parts of the brain. Examples include:

Schizophrenia. Decades ago, researchers believed that symptoms stemmed from a hyperactive dopamine system. Now we know that some are due to too much of this chemical in certain parts of the brain. This includes hallucinations and delusions. A lack of it in other parts can cause different signs, such as lack of motivation and desire.

ADHD. No one knows for sure what causes attention deficit hyperactivity disorder (ADHD). Some research shows it may be due to a shortage of dopamine. This problem may be due to your genes. The ADHD drug methylphenidate (Ritalin) works by boosting dopamine.

Drug misuse and addiction. Drugs such as cocaine can cause a big, fast increase of dopamine in your brain. That satisfies your natural reward system in a big way.

But repeated drug use also raises the threshold for this kind of pleasure. This means you need to take more to get the same high. Meanwhile, drugs make your body less able to produce dopamine naturally.

This leads to emotional lows when you’re sober.

It also plays a role in diseases that aren’t related to mental health. One of these is Parkinson’s disease. Another is obesity, which the American Medical Association classified as a disease in 2013.

Parkinson’s disease. Dopamine enables neurons in your brain to communicate and control movement. In Parkinson’s, one type of neuron steadily degenerates.

It doesn’t have a signal to send anymore, so your body makes less dopamine. The chemical imbalance causes physical symptoms. These include tremor, stiffness, slowness of spontaneous movement, poor balance, and poor coordination.

Doctors treat these symptoms with medications that raise levels of this chemical.

Obesity. Most of the time, if you take in more calories than you burn, you’ll gain weight. So why can’t obese people simply eat less and slim down? The answer isn’t that simple. They may face obstacles that others don't.

They could have problems with their natural reward systems. This can affect the amount of food they eat before they feel satisfied.

Imaging studies suggest that in people with this condition, the body may not release enough dopamine and another feel-good hormone, serotonin.

This chemical usually plays a secondary role in the body, but in certain medical situations, it’s literally a lifesaver. Doctors use prescription dopamine (Inotropin) to treat:

There are possible complications with any drug, even if taken under close supervision. The main ones associated with dopamine include:

Because many drugs interact with it, it’s important that your doctor knows all the medications you take.

SOURCES:

Translational Psychiatry: “Effects of dopamine D2/D3 receptor antagonism on human planning and spatial working memory.”

Journal of Mental Disorders and Treatment: “Dopamine: Receptors, Functions, Synthesis, Pathways, Locations and Mental Disorders: Review of Literatures.”

Merck Manual: “Neurotransmission.”

Nature Neuroscience: “What does dopamine mean?”

U.S. National Library of Medicine (PubChem): “Dopamine.”

Frontiers in Psychiatry: “The Role of Dopamine in Schizophrenia from a Neurobiological and Evolutionary Perspective: Old Fashioned, But Still in Vogue.”

Neuropsychiatric Disease and Treatment: “Attention-deficit-hyperactivity disorder and reward deficiency syndrome.”

BMJ: “Methylphenidate works by increasing dopamine levels.”

Neuropharmacology: “Imaging dopamine's role in drug abuse and addiction.”

Medscape: “AMA Declares Obesity a Disease,” “Dopamine (Rx).”

Madame Curie Bioscience Database: “Dopamine and Parkinson's Disease.”

Metabolism: “The role of central dopamine and serotonin in human obesity.”

© 2019 WebMD, LLC. All rights reserved.

Source: https://www.webmd.com/mental-health/what-is-dopamine

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