In the previous blog post I've told you everything you need to know about dopamine. The current blog post gives you 50+ strategies to both increase and decrease dopamine.
But let's quickly recap what makes dopamine so important:
Again, if you're interested in learning more about what makes dopamine so special then read my previous blog post on the topic. Let's now consider how you can boost your dopamine levels naturally and through other means:
This blog post divides strategies to increase dopamine in several categories:
Want my quick and easy top-10 laws for managing dopamine instead - including strategies not listed in this blog post?
In this section, I'll give you several means to increase your dopamine levels naturally. I hope you're already implementing most of these strategies.
For the best results, implementing more of the strategies listed below is better. Keep in mind that many of these strategies overlap with having a healthy lifestyle. So if you're pursuing a healthy lifestyle you're likely to have higher dopamine levels as well.
Without further ado:
By exiting the jungle, your human ancestors dramatically increased their daily sunlight exposure. The loss of hair on their skin exacerbated that process.
Sunlight, in part, drove that dopaminergic development of human beings.
Sure: higher levels of sunlight exposure are associated with greater dopamine D2 and D3 receptor availability. Increased receptor availability entails that dopamine pathways can be more easily recruited in your brain.
In animal studies, light exposure also increases "TH brain cells". These cells are responsible for increasing dopamine levels in the striatum. Recall that the striatum is located below the cerebral cortex, and responsible for goal-directed behavior and motivation.
How does sunlight achieve that effect?
Easy: ultraviolet light.
Let me explain:
You may know that ultraviolet light is one of the sunlight types that reach the earth's surface. Ultraviolet light gives you sunburns if you stay in the sun or under a tanning bed for too long.
Through skin exposure that ultraviolet light exposure releases several feel-good chemicals, but also affects dopamine levels.
In fact, dopamine is the mechanism by which some people get addicted to sunlight in the first place. Nature has thus programmed your body to get addicted that way, as long as you'll sensibly use the sun to feel good.[65; 66]
That specific dopaminergic mechanism also makes people flock outside once the sun is out in the spring and summertime.
Even disease risk, specifically disorders with excessive dopamine levels, are linked to sunlight exposure. Higher levels of mania occur in the summertime--as opposed to the depressive phase of the winter months.[452; 453]
Vitamin D also protects dopamine in the brain - and you traditionally needed sunlight for creating higher quantities of vitamin D in the past.[455; 456; 457] High-quality animal foods are reasonable vitamin D options too.
Avoid wearing sunglasses or sunscreen when exposing yourself, but also avoid getting sunburned also. Cover up once you've had enough sun. And read my blog on sunlight exposure for the full perspective.
Beware that nothing replaces the sun though. Red light therapy thus remains a "sunlight supplement" - never a replacement. It's always best to restructure your life over time so that you can get sunlight, as it's that important for health.
Let's now meet the second strategy:
The circadian rhythm is the ~24-hour day and night cycle found in all human beings. The light in your environment is key to regulating that rhythm.
Animal studies suggest that an inability to expose yourself to sufficient light in your environment lowers overall dopamine levels. Insufficient light exposure also throws off the circadian rhythm.
Break your rhythm and you'll break dopamine formation as well.
Dopamine itself, on the contrary, also influences that rhythm.[69; 73] The "central clock" in your body, the suprachiasmatic nucleus, is directly affected by dopamine. Boost your dopamine during the day and you'll thus tell your body it's daytime.
Light exposure through the eye is also central to programming that clock. The light signal entering your eye eventually affects the suprachiasmatic nucleus, telling your body it's daytime. Light exposure - specifically ultraviolet light - builds dopamine in the eye. If you don't build that dopamine with bright light, your circadian rhythm will be off.[69; 70]
Lenses and eyeglasses can give problems in that regard, so ditch them if you're standing in the morning sun.
Let's now consider the other part of the equation:
For the circadian rhythm to work properly, you additionally need darkness at night.
At nighttime, your melatonin levels need to be high. You need melatonin to sleep quickly, deeply, and to stay asleep. Melatonin is normally only produced after several hours of darkness. If you're exposed to artificial light at night, you're lowering your melatonin levels and cannot get the best quality sleep.
For the full perspective, read my guide on artificial light at night the blue-blocking glasses solution.
The more your circadian is disrupted, the harder emotional regulation becomes.[68; 72] Several diseases are also associated with emotional dysregulation, including Parkinson's, also show problems in the dopamine system of the brain.
Thus: mind your circadian rhythm!
Over time, sleep deprivation lowers the receptor availability of dopamine in the brain - although some conflicting evidence exists.[77; 78; 79] The end result, in plain English, is lowered dopamine function.
Different receptors are influenced in different ways. Fortunately, short-term sleep deprivation is not yet detrimental. And even if you're consistently kept from the dream stage of sleep for four nights in a row, receptor function does not go down yet either.
In the long-run, however, that pattern is almost certainly reversed. Animal studies confirm that picture.[85; 86] The longer the sleep deprivation persists, the greater the risk to the dopamine system becomes.
The worse your sleep quality, the higher the risk for getting dopaminergic disorders also get. Sleep and dopamine function are thus related.
Activation of several dopamine receptors actually decreases both deep sleep and REM sleep (the period in which you're dreaming).[82; 83] Dopamine and sleepiness are thus inversely related. If you thus engage in high-dopamine activities such as thrill before bedtime, your sleep quality becomes poorer.
The flipside is that long term sleep deprivation at night destroys dopamine function during the day.
Want help improving your sleep? Read Alex' blog on deep sleep to take charge of your sleep quality tonight.
When your ancestors started living in the plains and around water instead of the jungle, they had to travel long distances. Remember that dopamine is not associated with nearby vision, but focuses on what lies further ahead instead.
Animals for hunting or scavenging could perhaps only be spotted 1,000 yards away. Looking for fruit in the tree next to you requires a different focus and visual pattern than hunting animals.
Modern goal achievement may be analogous to that process of seeking out "distant" prey. Dopamine does, in fact, regulate that function. "Reward" is the key phrase for understanding dopamine, or better yet: the "pursuit of reward".
Quick detour to explain that concept:
Three different brain processes are central to the act of achievement in the brain: "liking", "wanting", and "learning".[89; 90] Liking signifies the pleasure you gain from after completing a goal. Wanting is your drive to pursue a goal. Learning is the process by which you're more likely to pursue that goal again.
Of course, that learning process can become erratic. You can become addicted to junk food, for example, or drugs. In such cases, the wanting and learning processes have gone haywire.
By taking addictive substances you're basically learning your brain to release dopamine to want them in the future.
The wanting and learning process, however, can also be conditioned towards productive ends. Learning to love sunlight and healthy food are examples. Through a concept called "neuroplasticity", brain cells can be created or updated to reflect your new behavior.[98; 99; 100; 101]
Achieve goals - the right goals - and your dopamine levels will increase. I'll thus get a dopamine hit when I click "publish" on this blog post, which makes me want to do it again in the future...
Risk-taking improves dopamine levels.
When you get older, you'll generally take fewer risks. Decreasing dopamine explains that change in risky behavior.
Start a business. Approach the man or woman you like. Invest money wisely.
You may think: "but goal achievement comes with stress"
You need to manage stress:
With childhood trauma, for example, your dopaminergic system often takes a hit. The subcortical parts (below the cerebral cortex) - the places in which dopamine is created - are hit hardest.
The best way to build dopamine is to reach for goals that are challenging but not impossible. Expand your comfort zone.
Temporary stress even increases dopamine levels.[110; 112] It's extremely likely that only short-term stress has that effect, its disease-causing "cousin" called "chronic stress" has the opposite effect.[400; 401]
Unfortunately, most of the effect of testosterone on dopamine is currently only proven in animal studies.
A huge overlap between strategies that increase dopamine and strategies increasing testosterone exist as well. Sleeping better, getting some sunlight, achieving goals, all raise both testosterone and dopamine levels.
Additional science-backed strategies to increase testosterone are avoiding non-native electromagnetic fields (e.g. WiFi or "smart" meters) and consuming organic food. The latter instances have not been investigated in relation to dopamine yet.
(For boosting testosterone, read Alex' perfect blog on that topic!)
And let's move to a strategy almost everyone likes:
Did you know male and female sexual behavior are associated with different neurotransmitters (brain signalling substances)?
A rat study demonstrated that testosterone levels affect dopamine's stimulation of sexual behavior in males.
Interestingly enough, dopamine is more important in sexual function and desire than the eventual reward. Erectile dysfunction in men may be a result of having an inadequate dopamine response, for example.
Skip the (internet) porn.
During the last few years, more and more evidence has emerged that watching internet porn may be addictive.[122; 123] Critics who deny that porn is harmful, on the contrary, claim that porn use simply overlaps with sex addiction.
Animal studies demonstrate that traditional female receptivity, on the other hand, is guided by "epinephrine" - that behavior is actually decreased by higher dopamine levels. This strategy may thus be less applicable to females.
Solutions for both sexes exist though:
Massages, secondly, have similar effects.
Getting a massage increases both dopamine and serotonin while lowering stress hormones.
Keep in mind that physical contact, in general, has very positive effects on health. Only get physical contact with people you like of course...
Let's consider yet another exciting strategy:
This strategy is absolutely free too.
Meditation is most exciting for me, in part because it can both increase dopamine as well as helping you deal with curbing negative hyperdopaminergic consequences.
"Hyperdopaminergic consequences" - or "effects of high dopamine levels" include always thinking about your next achievement while never being present in the moment.
Mindfulness meditation specifically trains the skill of being present, mainly through conditioning the lateral prefrontal cortex (the more logical function). That brain area is trained in its capacity to focus on the here and now.
The "insula" is another affected brain area, active in self-awareness and the "story" you and me tell ourselves all day long. Phrased differently, the insula is responsible for self-talk, regardless whether that self-talk is positive or negative.
Through mindfulness meditation, you can (temporarily) learn to deactivate that self-talk, so that you'll be present.
Of course, many of the stories you and I tell ourselves such as "getting closer to achievement X" or "make sure I do Y" are dopaminergic in nature. Stopping that story for a second helps you detach from excessive dopaminergic thinking.
Other studies confirm that finding for mindfulness, while also showing an increase in prefrontal cortex activity.[128; 129] Of course, you already know that the prefrontal cortex activation and dopamine levels are interrelated.
Mindfulness thus allows your brain to re-charge so that it later performs better - it's thus a break from hyperdopaminergic thinking that boosts dopamine function in the long run. The biggest benefit is that you'll increase your conscious control of how dopamine influences your mindset.
The overall health benefits of mindfulness upon your brain are considerable. Mindfulness can help with many areas of cognition, such as maintaining white matter which help connect brain cells. Aging of your brain may also be slowed down.
Check my guide on mindfulness meditation if you'd like to learn more. Free and no sign up required.
Another meditation form, Transcendental Meditation, does not show an increase in dopaminergic levels.
Music is a highly pleasurable human experience. You're probably aware of the strong emotions music can evoke, and dopamine is central to that effect. The lower parts of your brain, not the cerebral cortex, are most responsible for that outcome.
Interestingly enough, music also stimulates the same brain areas as those involved with motor control. The link between music and movement (dance) is thus not coincidental.
Another brain signaling substance called serotonin increases in availability while listening to music. Serotonin tells your brain that "all is well", allowing you to zone out and relax. Even though serotonin generally counters dopamine function, in this case it does not.
Blood flow to the brain increases with music exposure. For that reason, music becomes a highly favorable tool for increasing (cognitive) performance. Many of these brain areas affected by music are intertwined with the dopaminergic system.
For the best results, you'll probably have to listen to music that you find pleasurable. Indications also exist that rhythmic music allows you to "let go" and follow the flow. That zoning-out effect is, again, mediated by dopaminergic brain centers.
The stimulation of cravings, however, can be a side effect there. You may relate to that effect: with good music in the background, you're more prone to grab a good glass of wine to enjoy the moment.
Let's now move to a more daring subject:
Cold exposure is one of the more creative dopamine boosting methods.
Cold baths increase dopamine levels by a whopping 250%. To be rewarded with that benefit you need to stay in 15 degree Celsius water (~60F) water for an hour though. With colder temperatures, the effect will occur sooner.
Cold exposure is one of my favorite ways to boost dopamine. In fact, I've written a guide on cold thermogenesis before. You'll learn how to use cold both effectively and safely in these guides.
Always start light with cold exposure. Cold showers are a great beginning - never commence with ice baths.
The downside of cold exposure is that epinephrine (adrenaline) levels also shoot up by more than 500%. Make sure not to overdo cold: chronic stress reduces dopaminergic activity.
The right intensity of cold exposure will keep building your energy levels and dopamine over time...
Bottom line: stress should be sporadic, never chronic.
What's also interesting is that directly increasing dopamine in animal studies decreases cold tolerance. The reason is that dopamine is generally associated with lower body temperatures. In other studies, dopamine function is correlated with cold tolerance again.
Time will teach the truth I guess...
Let's look at another reason why many people have sub-optimal dopamine levels today:
Gut health has a strong effect on your body's dopamine levels. Recall that dopamine is not just found in the brain, but also throughout the human body.
If you're taking antibiotics, for example, dopamine creation in the gut can suffer. Your immune system may take a hit as well.
And it's not just what goes through your mouth that affects gut function. The light in your environment - such as sunlight - is enormously important too.[147; 148] That link between circadian rhythms and gut health has only been established in the last few years.
Probiotic supplements have been proven to increase dopamine levels, but in general, I'm not a fan of such supplements. Supplementing with probiotics should be one of your later resorts. Many positive effects of probiotic supplements have been established in animal studies though.[152; 153]
Nonetheless, it's better to start with minding your day and night cycles as a precursor for good gut health.
If you're staying up until 2 or 4 AM at night, your gut function will always be impaired. It's thus no coincidence that so many people have gut problems today.
The next step should be fixing your diet. If you're eating at Burger King three times a week, then there's no need to buy probiotics. Fix the low hanging fruits first.
Many compounds in food can alter gut function. Butyrate, for example, improves dopamine levels.[157; 158; 159] Butyrate is found in grass-fed butter. However, your gut should also be producing butyrate naturally when your body digests fiber.
Other foods contain other compounds that influence your gut.
Once again, diet trumps supplements. The relationship between diet and gut function is highly personal though -I cannot prescribe a one-size-fits-all approach.
Are you a couch potato? If so, you'll tank your dopamine levels. Standing or moving once in a while achieves the opposite effect, although the study to draw that conclusion has poor quality.
Exercise is studied in more detail, fortunately.
A very specific benefit of exercise is that it increases "neuroplasticity". Neuroplasticity signifies the brains' ability to adapt to change. Contrary to scientific belief before the 2000s, your brain is continually restructured even well into old age.
The dopamine system, which is traditionally tied to movement as well as abstract thinking potential, is indirectly trained through exercise. Part of the fatigue you experience after a training session may be caused by dopamine depletion.[161; 164; 165]
Fortunately, dopamine receptor function is upgraded over time through exercise. Receptor function enhancement means that you'll become more susceptible to dopamine increases.
Don't spend 5 days a week, 2 hours a day in the gym though--a couple of quick weekly workouts are more than sufficient.
The wanting and learning processes I've discussed before are also activated with exercise - through dopamine. In plain language, that means that engaging in exercise fuels dopamine function in the long run, and dopamine function increases your propensity to exercise in turn.
A virtuous circle is born...
The close tie between dopamine levels and exercise is no coincidence. Parkinson's disease, which is characterized by deterioration of the dopamine system, also results in enormous problems with intentional movement (reflexes are not inhibited).
Animal studies further demonstrate that engaging in movement anyway improves your health if you've got Parkinson's.[166; 167; 168] Animal studies also show that increased exercise capacity allows your brain to better use neuroplasticity to affect the dopamine system.[169; 170; 171]
In humans, exercise can reverse some of the damage to the dopamine system in the brain occur as a result of drug use. Lots of circumstantial evidence thus exists that exercise supports dopamine function - that result is also logical from an evolutionary standpoint.
Want even higher dopamine levels? Consider this strategy:
Evidence exists that if the second trimester of pregnancy occurs during the summertime so that you'll be born during fall, your dopamine levels may be permanently higher.
Epigenetic changes - the process of how your environment activates or deactivates certain genes - is responsible for that dynamic. What environmental factor? Simple: long light cycles and more sunlight exposure during the second trimester.
During evolution, most babies were probably born in spring, due to peaking human fertility in late summer. Remember that pregnancy lasts 9 months on average.
Today women are no longer getting pregnant on the basis of seasons but do so year-round. Circumstantial evidence exists that light exposure to the eye of the mother affects dopamine levels of her offspring.
Other influences around pregnancy can also affect dopamine (negatively) levels later in life, such as drug use, a troublesome birth in with low oxygen levels on the mother's part, and (heavy) immune responses in general.
With women entering the workforce since the 1970s and entering more high-dopamine jobs that require abstract and strategic thinking, offspring's dopamine levels may also have been influenced.
Specifically: high dopamine mothers may pass on that trait to their children.
Women holding more jobs that require the development of dopaminergic pathways have cemented that trait.
Overeating has been linked with lower dopamine functionality. If you're frequently eating junk food or fast food, your brain adapts and experiences less reward from that same food.
Most junk and fast foods combine fat, sugar, protein, and artificial flavors to make them really rewarding to the human brain, driving addiction in the process.
How addictive food is depends on you as an individual.
Also, make sure not to choose a crash diet with very few calories.
The vagal nerve, or nervus vagus, moves from your brain to your heart, lungs, and digestive system.
With relaxed breathing, your body can enter a more calm state. That process is mediated by the vagus nerve. Vagal tone can affect dopamine levels in turn, at least in animal studies.
You should be breathing through your nose 24-7. If you're a mouth breather then you need to correct the problem.
Additional (unmentioned) strategies may exist as well.
Electroconvulsive therapy is one example that is controversial - which entails exposing yourself to electroshocks. The therapy is used to counter depression when other options have been exhausted, for example.
So now that I've considered all lifestyle strategies, let's move on to managing your nutrient intake to control your dopamine levels even further...
Want my top-10 laws for managing dopamine - including strategies not listed in this blog post?
In this section, I'll consider natural dopamine foods--while in the next sections looks at the relationship between supplements, medication, and dopamine.
The list of compounds in foods listed below should give you a good indication of what foods are supportive of high dopamine function. You'll notice below that including foods that have high micronutrient (vitamin and mineral) content is most important.
So without further delay:
Many sources on the internet tell you to "cut out sugar" to increase dopamine levels. The opposite effect is true, in fact.
Contrary to popular opinion (once again), withdrawals are not always bad. If you stop getting good sunlight you'll also experience withdrawal symptoms for example. That presence of withdrawal symptoms is not a sign that sunlight is bad for you.
The same is true for cutting out most of your protein.
Please keep in mind that I'm not advocating for limitless white sugar consumption. I consider white sugar a terrible food that's unhealthy almost independent of context. The same is true for soda.
The reason for my opposition is the absence of vitamins and minerals in processed sugar.
(Organic) fruits, however, contain high levels of vitamins and minerals and are the preferred choice if you're going to consume sugar. Honey is a great source too and contains many beneficial compounds for health as well.
(I'll remain agnostic whether carbohydrates are a superior fuel source to fat, or not. Even if you're following a seasonal diet, you have to consume fruits late summer and early fall)
Iodine is a mineral that's essential for the functioning of your thyroid, a gland in front of your neck. Thyroid hormone, in turn, is essential for dopamine levels.
Remember the amino acid called "tyrosine"? With insufficient thyroid hormone, that amino acid cannot be converted into L-dopa. Tyrosine hydroxylase (TH) is the enzyme responsible for that conversion.
Food sources such as shellfish or sea vegetables are best for getting your iodine needs met. Supplementation with iodine is also an option but quickly leads to overdoses. I'm not convinced that very high doses of iodine are benign. Such high doses are often advocated on the internet.
Dopamine levels do become lower with an iodine deficiency, and the body attempts to compensate by upregulating the number of dopamine receptors.[336; 337] Unfortunately most of these conclusions are based on animal studies.
The few human studies confirm that pattern though.
When it's summer thyroid are generally the highest, which is reflected in increased dopaminergic functioning. Dopamine also has a negative feedback loop with high thyroid hormone levels.[339; 340; 341; 342] That feedback loop entails that you cannot stimulate dopamine without limit by boosting thyroid hormone levels.
Thyroid levels are also higher in human beings than chimpanzees. That observation is interesting because humans have higher metabolisms. That higher metabolism is probably driven by higher thyroid hormones, which enhance dopamine levels in turn.
Higher thyroid hormones are like a furnace for fat burning and boosting dopamine. Iodine is co-responsible for that process.
Zinc frequently returns on this blog, and its role is somewhat underappreciated as a mineral.
In animal studies, optimal zinc status increases the excitability of dopaminergic brain cells. Several brain areas are affected. The end result is cognitive improvement such as enhanced memory function. Zinc also works as an antidepressant.
Moreover, zinc additionally counteracts drugs that negatively influence dopamine functioning.
A zinc deficiency forces more dopamine to be converted into adrenaline, which increases (perception of) stress. Sufficient zinc levels have the opposite effect.
Oysters are the best zinc-rich foods. Other kinds of seafood, organ meats, beef, lamb, eggs, and dairy come in second place.
I've often talked about managing your iron status. The difficulty with iron is that it's stored in your body. Both storing too much iron (an iron overload) and too little iron (an iron deficiency anemia) are dangerous to your overall health.
And it's not just food that affects how much iron you store--sunlight exposure affects your iron status as well.
Shellfish and red meats are foods richest in iron. Plant foods contain a form of iron that's less well absorbed by the human body called "non-heme iron".
With iron deficiency, the receptor sites for dopamine function less well.
What's interesting is that iron is located in many dopaminergic regions, leading to the hypothesis that iron may have been (partially) necessary for the development of increased dopamine levels in Homo sapiens.
Primates don't have much highly absorbable iron in their diets. Meat and shellfish consumption can explain the increase in available iron for humans.
With an iron deficiency, the body even compensates to increase iron stores in the brain while other parts of the body are depleted.[348; 349] Low iron levels may literally be responsible for the degeneration of dopamine-associated brain cells.[350; 351]
Well, iron is required in the process of producing dopamine.[352; 353; 357] Without sufficient iron, both your behavior and emotional regulation will be impaired.[355; 356] Recall that your brain or movement cannot function without dopamine, so low iron levels are very dangerous.
Keep in mind that too much iron is just as dangerous as low iron status though.
Caveat: Unfortunately, most (but not all) of the effects described above are only demonstrated in animal studies.
(These conclusions are based on animal studies, once again.)
How to get selenium?
Brazil nuts (depending on the variety) are also a great selenium source. Mushrooms, (organ) meat, cheese, and eggs are other great sources.
Shellfish are even better...
I hope you're beginning to see a pattern here: all four previous minerals can be found in high quantities in shellfish and crustaceans (e.g. lobster, crab):
Shellfish are extremely good iodine, zinc, iron, and selenium sources.
Remember I talked about shellfish in relation to human development in an earlier section? Now you know why.
Let's consider even more minerals:
As many as 80% of people in modern societies are slightly magnesium deficient, while 40-60% have a severe deficiency.
That statistic is tragic because magnesium is required for almost 1,000 processes in the human body. The cure is also cheap, adding insult to injury.
Brain cells related to dopamine function, moreover, are sensitized by magnesium. Existing dopamine will thus do a better job with adequate magnesium status.
Magnesium also counteracts losses of dopamine functioning if you've got Parkinson's - a condition associated with dopamine dysfunction.
Most people shouldn't rely on getting their magnesium through food though. Farming soils are depleted of magnesium so that many people are magnesium deficient if they're not supplementing. Read my guide on magnesium to learn more.
Dopamine stored in the synapses can thus not even be used without the mineral. Synapses are the connections between nervous system cells.
How to get calcium then?
While milk is the best calcium source in existence, bone meal is a useful second if you're lactose intolerant. Calculate your calcium intake to make sure you're getting enough. Bones from fish are also great.
While counter-intuitive, bone broth is not a great calcium source.
Both plant and animal foods contain proteins. Proteins are built up with "amino acids". Only animal products contain high quantities of specific amino acids such as "tyrosine" and "phenylalanine", however.
Phenylalanine not only increases the amount of dopamine that's created but also allows that dopamine to stay active for longer (for nerds: by preventing re-uptake)
Studies show that without sufficient levels of these aforementioned amino acids the light in your environment (such as sunlight) cannot adequately increase your dopamine levels. The energy of the sun may thus not be usable by your body without the right foods.
Animal foods such as fish, meats, eggs, and cheese are great phenylalanine sources. Soy and seeds are plant phenylalanine sources. I do not recommend eating soy though.
Soy, beans, and seeds (such as pumpkin) are also great tyrosine sources, even though animal foods are superior in general.
And while some plant foods such as beans and seeds contain higher levels of tyrosine, their numbers are still 5-fold lower than the best animal foods such as beef.
Higher stress levels can increase tyrosine demand. Stress and low dopamine can thus enter a vicious cycle: more stress requires more tyrosine, but when unavailable dopamine is lowered, which makes you less able to cope with stress.
The end result is even more stress...
Note: tyrosine can be made from phenylalanine, but not the other way around. Phenylalanine is thus more essential to get from dietary sources.
Want an even greater boost?
Glycine, yet another amino acid, is only found in great quantities in bone broth, gelatin, and collagen. These foods are made from the connective tissue of animals - eating muscle meats won't confer their unique benefits upon you.
Make sure to include at least 1 tablespoon of collagen or gelatin in your diet every day, or a few cups of bone broth.
Bottom line: include animal foods in your diet. Without animal foods, you won't get the right amino acids for dopamine creation.
Three B vitamins...
Let's start with vitamin B6, or "pyridoxal phosphate".
Even during pregnancy, vitamin B6 is necessary for normal brain development, and specifically the dopamine system. The more dopamine you have, the higher your vitamin B6 requirements become.
Food processing depletes vitamin B6. The more you heat foods, the more vitamin B6 is lost. A combination of plant and animal foods is your best bet to get this vitamin.
Vitamin B9 - also known as "folate"
Most people know that vitamin B9 is necessary for proper nervous system development. You may not know that several neurotransmitters are directly dependent on the vitamin for their creation.[373; 375]
An amino acid called "homocysteine", has negative health consequences when it floats around in your bloodstream. Homocysteine is a byproduct of dietary protein breakdown.
Homocysteine also damages brain cells associated with dopamine. You'll thus want to keep homocysteine levels low.
Vitamin B9 recycles homocysteine in a less damaging amino acid called "methionine".
Green vegetables, beans, seeds, nuts, orange, and papaya are great vitamin B9 sources.
Organ meats are a great option too. If you're on a carnivore diet, you need to consume organ meats once in a while.
Lastly, there's vitamin B12.
Contrary to the previous B vitamins, B12 is only found in animal food sources. A vitamin B12 deficiency leads to lower dopamine levels in animal studies.
In childhood, B12 deficiency also leads to an inhibition of "myelination". Myelin is a sheet around nerves that allow for faster conductivity. Myelination is also a process that's highly evolved in human beings.
That loss of myelination negatively affects dopamine function in turn.
A deficiency in all of the aforementioned vitamins increases Parkinson's disease risk. The link between B vitamins and dopamine function is thus not coincidental.
Choline is often considered yet another B-vitamin - B8 to be exact. That choline is also responsible for the "acetylcholine" system in your brain which I've mentioned before. Acetylcholine is related to the "choline" neurotransmitter.
Very high choline levels actually inhibit dopamine synthesis, but optimal levels achieve the opposite effect.
Liver and eggs are the best choline sources in existence. So be inspired by one of nature's own multivitamins and multi-minerals:
In general, I don't recommend supplementing with choline, as it's easy to get the nutrient from food.
If you're not eating eggs or weekly liver, then high-quality choline supplements such as citicoline and alpha GPC can boost your intake. Huperzine A is another choline supplement proven to have the same effect.
Most people consume too few omega-3 fatty acids. The reason for that limited consumption is that most modern junk and fast foods contain lots of omega 6.
Seed and vegetable oils contain exceptionally high levels of omega 6. Those oils are often added to processed foods. Through that mechanism processed foods end up with a 1:10 to 1:20 ratio of omega 3 : omega 6.
Your ancestors consumed fats in a 1:2 to 1:4 ratio.
An unsaturated fatty acid called "DHA" - found in fish - almost certainly supports dopamine function as well.[459; 460; 461; 462] Again, the result is only supported by animal studies, although very consistent.
Takeaway? Cut vegetable oils and junk food from your diet, eat whole healthy foods, and the ratio between omega 3 and 6 should automatically correct itself.
Result of this section: animal proteins, especially shellfish and organ meats are important to consume for dopamine function. Healthy fats and a wide array of plants further that outcome.
In this section I'll consider natural dopamine supplements--while in the next section I'll look at the relationship between medication and dopamine.
I only recommend using supplements to push your dopamine levels higher once you've exhausted most of the lifestyle and food strategies described in previous sections.
Why? In general, if your dopamine system doesn't work properly, there's usually a lifestyle choice causing that defect. Unfortunately, you cannot out supplement poor lifestyle choices.
Note: some of my descriptions below have also been oversimplified.
In animal studies, for example, dopamine-enhancing effects are often measured in different brain areas, such as the hypothalamus, basal ganglia, or the cortex. I've not distinguished between such brain areas in my explanations below.
So without further delay:
Coffee is the ultimate dopamine shortcut but also one of the most dangerous ones. One specific compound in coffee, caffeine, is best studied for its dopaminergic effects.
Caffeine specifically increases dopamine levels, but at the cost of also increasing your cortisol and adrenaline as well. Recall that cortisol and adrenaline are stress hormones.
Consuming calories with your coffee decreases the number of stress hormones released and often leads to much better results.
By consuming caffeine, moreover, you'll lower the uptake of "adenosine" in your brain.[179; 181] Adenosine is a compound that makes you tired, and preventing its reuptake thus increases your energy levels.
Adenosine nonetheless also counters dopamine function. Dopamine may thus affect wakefulness through its (negative) interaction with adenosine.
Coffee is not a free lunch that only gives benefits though. Blood flow in the brain may be reduced with caffeine consumption. Some people also experience poor sleep with coffee.
The simple rule is that coffee is not for everyone. Some people do fantastic on coffee, even later in the day, because they metabolize the substance quickly. In that case, the drink won't affect your sleep.
Lots of people are addicted to coffee though - and the stuff is addictive. Merely expecting your next cup of coffee already induces a dopamine surge.
Additionally, I do think the quality of coffee matters a lot. While studies are less clear about the subject (unlike what Bulletproof proponents claim), low quality coffee dramatically lowers my brain's performance.
I do thus think that Bulletproof has a point in their advocacy for high-quality coffee.
Many people need to cycle their caffeine, and some need to avoid caffeine for the best health results. I fall in the latter category, although coffee remains a guilty pleasure sometimes.
The only way to know for sure how you react to coffee is to test. Skip the coffee for 6 weeks and observe how you feel and sleep. Cycle back and forth a couple of 6-week periods to know for sure.
Time-consuming? Yes. Life-changing? Possibly! Alternatively, get your genes tested and you'll know how you react to coffee.
Get some high-quality Bulletproof coffee here.
(I don't like most of Bulletproof's health recommendations but their coffee is great.)
Irresistible? I hope not...
Curcumin may be especially useful with aging, as increased iron stores in the brain can wreak havoc on dopamine function. Curcumin may prevent that storage. Unfortunately, that effect has only been demonstrated in animal studies (once again).
You can either include curcumin in your diet or buy a curcumin extract. I take curcumin through a spice shot in the morning, which includes a tablespoon of turmeric powder and black pepper (for enhanced absorption). I buy turmeric powder in bulk.
Finally, the king. Mucuna pruriens is also called "velvet bean".
Mucuna may be the ultimate dopamine booster. The reason is that mucuna contains the dopamine precursor L-dopa. Normally amino acids such as tyrosine and phenylalanine need to be converted before L-dopa is formed, but mucuna contains the compound naturally.
Mucuna also counters serotonin, and can thus be dangerous if you're naturally hyperdopaminergic. I still need to test this compound, but I'm pretty sure I'll get anxious, unfocused, and restless from it.
If you're naturally carefree and laid back, mucuna can be great to get yourself into action though.
Excessively boosting your dopamine levels can also bring on the side effects I've discussed earlier.
Tea is a very complex and interesting compound.
First of all, tea contains far less caffeine than coffee. Additionally, that caffeine is buffered by a compound called "theanine". I'll focus on theanine in this subsection.
Theanine increases levels of a brain signaling substance called "GABA", which improves relaxation.
GABA thus counters the stress hormones cortisol and adrenaline which can be increased through coffee consumption. What's even more interesting is that theanine counteracts the decrease in brain blood flow that results because of caffeine.
Theanine is an amazing compound because its beneficial effects are not caused by increasing but by inhibiting stress. Cold exposure, for example, increases dopamine levels through stress, while theanine has the opposite effect.
Tip: lemon and ginger make your tea more potent
Another compound that starts with "thea"?
Surprise, surprise: theacrine is tea-related.
Theacrine is structurally very similar to caffeine. Animal studies show theacrine counteracts adenosine, just as caffeine does - increasing your wakefulness.
Try theacrine, especially if caffeine overstimulates you.
One of my favorite plants.
Dirt cheap and highly effective.
In animal studies, Rhodiola Rosea increases dopamine levels. Low dosages seem to work better. Unfortunately, very few studies have been carried out on the compound right now.
My perception of Rhodiola is very good though. I get really relaxed while taking an extract of this plant, perhaps in part because it also increases serotonin.
Evidence, once again, runs thin in these instances.
Sage, or Salvia sclarea, may increase dopamine levels as established in animal studies. Oregano, or Origanum vulgare, is similar.[203; 204; 205] Rosemary, or Rosmarinus officinalis, likewise.[206; 207; 208]
Just add some herbs to your food. Herbs and spices are not just for taste, as they contain more concentrated nutrient levels than vegetables.
You 'll even make your meals taste better.
Shilajit is truly unique. This black compound is found in the Himalayan mountains, and helpful to combat fatigue, improve your immune system, aiding heart health, decreasing inflammation, and...
Boosting dopamine levels--but proven in just one animal study.
Shilajit contains a compound called "fulvic acid", which is responsible for most of its claimed health benefits. Shijalit capsules are your easiest option.
I've not tried this compound, but many people are raving about it.
Finally, a compound that's very well studied: "acetyl-l-carnitine". The downside is that mostly animal studies exist (once again).
"Carnitine" sounds like "carnivore", and that similarity is no coincidence. Unsurprisingly, meat contains the highest carnitine levels.
Due to the neuroprotective effects, the compound may be especially useful in aging. Alzheimer's disease (a degenerative disease of the brain) and depression may also be countered by acetyl-l-carnitine.
Unfortunately, adrenaline and serotonin levels may also be increased with carnitine consumption. If boosting dopamine is your goal, testing carnitine and observing how you react is your best bet.
If you eat meat, especially raw, you don't need carnitine. Beware: raw meat is not recommended for everyone - do your research first.
Yet another herb...
Hypericum perforatum, or St. John's Wort.
You'd almost assume that you're reading Harry Potter, and in part, you'd be correct: you need high dopamine levels for such a strong imagination.
But instead of just affecting dopamine, serotonin and epinephrine (adrenaline) levels may also be increased the brain through this compound.[226; 228; 229; 231] St. John's Wort thus non-selectively increases all neurotransmitter levels.
Long term treatment gives the best results.
I don't recommend using St. John's Wort before trying many of the other options in this section.
Sam-e, or more complexly written "S-adenosyl-L-methionine", is a natural compound that is found and used in the liver.
Sam-e boosts dopamine levels, but should not be your first choice.
The following two "supplements" are actually steroid hormones - pregnenolone and DHEA. DHEA is even placed on most doping lists. Always consult your physician before trying them.
Pregnenolone is a precursor hormone that is used to form other hormones. Pregnenolone is created out of cholesterol and can be turned into cortisol or testosterone for example.
Of course, the compound also boosts dopamine, otherwise, it would not be included in this list.[241; 242; 243] That effect has only been demonstrated in animal studies. Pregnenolone supplementation is most applicable if you're getting older.
Moving on to the second hormone:
DHEA is a precursor to many neurotransmitters, just as the aforementioned pregnenolone. Your body thus produces hormones such as testosterone and cortisol from DHEA.
DHEA levels generally go down once you age, and maybe one explanatory reason why dopamine levels also drop over time as well.
I do not recommend supplementing with DHEA unless you've done a lot of research. The upside of DHEA is that it's a great supplement for if you're getting older, helping you return your youthful vibe.
Moving on to less risky adventures:
Uridine is produced by the human body - you thus technically don't need to supplement with it.
Uridine increases synapse formation. Synapses are connections between brain cells. Uridine can be bought as a supplement, and also increases dopamine.[250; 251] The substance also works as an antidepressant.
Uridine should not be your first option when trying to increase dopamine. Evidence does exist that taking supplements works better than getting uridine through food.
Many people are aware of the existence of Ginko Biloba nowadays - I've even heard commercials about it.
(I do feel sorry for the researchers who had to study erections in rats.)
Forskolin is often used for enhancing brain function nowadays. The substance can be found in many brain supplements - called "nootropics" - for example.
The dopamine receptors are specifically sensitized through forskolin consumption.[259; 260; 261] More dopamine is also created because the aforementioned "tyrosine" amino acid is increasingly used so that you'll end up with higher levels of the neurotransmitter.
If you want a forskolin-based supplement, try CILTEP - which has been geared towards cognitive performance. The CILTEP formulation contains compounds that make more efficient use of forskolin.
Tri-methylglicine is commonly found in beetroot, and abbreviated by "TMG". TMG is a form of "betaine", a compound in beetroot that's used for performance enhancement nowadays.
The benefit of TMG is mainly the protection of brain cells. When a medicine called L-dopa is administered, for example, TMG is neuroprotective. TMG also works as an antidepressant, which is unsurprising if it affects dopamine function.
You can also eat beetroot to ingest TMG.
While I'm not going to discuss whether drinking alcohol for health is favorable or not, small amounts of alcohol do boost dopamine function.
Nobody should be advocating for continuous or large-dose alcohol consumption, as those behaviors will end up in negative health effects.
Remember that the prefrontal cortex is the brain part that deals with abstraction and imagination, but also impulse inhibition. Alcoholism thus inhibits high-level thinking and self-regulation.
The best way to drink?
Booze in the sun during the day.
That way your body has plenty of time to recover. Avoid drinking at night which inhibits sleep quality. Yes, society has it completely wrong once again.
Let's now consider an underappreciated substance:
Almost done. Let's end with some of the best options - creatine - which is also somewhat underestimated.
The effectiveness of creatine has only been demonstrated in animal studies. Creatine specifically protects the brain cells that are responsible for dopamine production.
Creatine is normally found in large quantities in raw meat and raw fatty fish. If you cook fish or meat, the creatine content dramatically declines.
So if you're not eating raw animal foods regularly, I'd highly recommend increasing your creatine intake.
Unfortunately, dopamine supplementation alone has not demonstrated to prevent dopaminergic disorders such as Parkinson's disease. Creatine is protective of nerve cells associated with the dopaminergic system, nonetheless.[272; 274; 277]
Creatine also has antidepressant effects. The compound is thus not only great for physical performance, but also brain function.
Ginseng is yet another adaptogen, a compound that normalizes stress levels.
Ginseng contains compounds called "saponins", which are responsible for the effect. Ginseng also protects nerve cells associated with dopamine. Dopamine is additionally conserved so that you won't get a "down" that you may get after drinking too much coffee.
If you're experiencing withdrawal symptoms from cocaine or amphetamine, ginseng can help. Cocaine and amphetamine are dopaminergic drugs I'll get to in a second. And if you're "high" on excessive dopamine, lastly, ginseng may be an easy solution:
You can buy high-quality ginseng inexpensively in bulk
The isolated compound can be used as a "nootropic", also known as a cognitive performance enhancer.
Hordenine should not be your first choice when trying to affect your dopamine levels though.
And... that's it for this section.
Section summary: at least 20 different natural dopamine agonists exists. If you're using most of my lifestyle suggestions and still want to boost dopamine, pick 2-6 supplements listed above and cycle them.
Supplements do not and will never replace making the lifestyle changes. Let's now take a peek at medication:
In this section I'll consider eight different dopamine medications. Never use these medications without consulting your physician.
These medications are more likely to have adverse side effects than the plant compounds in the previous section.
Without further ado:
According to the research, cyproheptadine or "cypro" is by far your safest bet in this category.
Many of the substances in the medication category are often unhealthy long-term, such as modafinil or Adderall - I'll consider these in a sec.
Cyproheptadine is a different ballpark though. The reason is that cyproheptadine lowers your overall stress levels, contrary to modafinil or Adderall or even coffee, which often increase it.[281; 282; 283]
I consider the pro-dopaminergic cyproheptadine a superior choice compared to many other antidepressants that are commonly prescribed. Due to boosting serotonin antidepressants such as SSRIs can make you complacent and unmotivated.
Of course, context is key there.
Cyproheptadine lowers serotonin levels. Through inhibiting serotonin - commonly misunderstood as the "happiness" brain signaling substance - dopamine levels are raised.
If you're already a hard-pushing individual, higher dopamine levels may be detrimental though. Cypro is not for everyone, but may be a great replacement if coffee overstimulates you...
Update: I no longer think cypro is pro dopamine because it seems to lower levels in some studies, either directly or indirectly.
L-dopa is commonly used as medication for diseases such as Parkinson's. That condition the brain no longer produces adequate amounts of dopamine, leading to movement disorders and depression, among others.
The full name of L-dopa is " L-3,4-dihydroxyphenylalanine" - a name you can immediately forget.
L-dopa may also have other long-term side effects:
Nerve cells associated with the production of both dopamine and serotonin may be damaged, for instance.
L-dopa is thus only a last resort, and should never be considered without consulting your physician.
Two even more dangerous substances, that are used mostly as a (party) drug (or to improve performance).
Cocaine prevents re-uptake of dopamine, which means that the neurotransmitter keeps affecting synapses. In other words, dopamine stays in your system longer and therefore has more of an effect.
Working 16 hour days in the confinement of an office? If you take some cocaine you'll be able to go on forever.
Cocaine also gives you the typical dopaminergic "internal locus of control". You'll feel you can accomplish everything, even if in reality such events are outside your control.
A resounding "no"...
In fact, chronically using cocaine lowers your brain's ability to make dopamine.[292; 297] Tolerance also builds up, meaning you need more and more cocaine to get the job done. That tolerance remains high even if you've abstained for a long period of time.
One problem with cocaine is also that it's taken up very quickly by the brain, meaning that you get a very strong high. That high leads to upregulation of the "wanting" and "learning" processes I've talked about before. You'll thus start to crave cocaine with more frequent exposure.
Cocaine is made from the coca plant, and isolated so that a very strong stimulatory compound is created.
Amphetamines are another category of drugs affecting your dopamine levels.
Different amphetamines exist.
Methamphetamine is an example thereof - another drug you should steer clear from. Many amphetamines affect your brain's dopamine levels but have long-term negative side effects.
You'll also build tolerance with amphetamines and become addicted.
Ritalin is the brand name of what commonly is called "methylphenidate".
Ritalin is often taken orally in pill form and used as a medication against ADHD (Attention Deficit Hyperactivity Disorder). Lisdexamfetamine is another example of such a drug.
Taken in the right context, if you've got a condition, the effect is calming instead of stimulatory. That outcome should demonstrate how complex the dopaminergic system of the human body is - no universal prescriptions for "hacking your dopamine" exist.
Students also use Ritalin for increasing brain performance. That approach is dangerous because the dopaminergic system can decrease in potential long-term.
"Dextroamphetamine" is sold under the name "Adderall". Adderall is essentially a legalized form of amphetamine sale. The effect of Adderall is generally perceived to be stronger than the aforementioned Ritalin.
When I was in college, some students I knew used Ritalin or Adderall to improve their cognitive performance. The choice for these drugs is a little bit crazy, to be honest, especially when you regularly rely on them.
Prescriptions for these drugs have increased many-fold in the last decades, and hence, it's relatively easy to receive some of these drugs from friends or family.
I'd be sitting in my cold tub and using sunlight for improving my cognitive performance, and other students would sit inside all day and use Adderall for the same effect.
Of course, I've used smart drugs to improve cognitive performance myself. But Adderall is a crude means to accomplish that goal.
Steer clear. And try a safer alternative:
You may think: "So I'll have to smoke cigarettes?"
Not at all. In fact, never use cigarettes as a nicotine delivery method. Far safer methods are available, such as nicotine gum or drops.
Contrary to popular expectation, nicotine alone is not as harmful as expected. Medical ethical commissions regularly often allow research with nicotine to be carried out on human participants--a choice that would be impossible to justify if the compound was additive all by itself.
In fact, the many compounds that are added to cigarettes explain the addictive nature of smoking--not nicotine alone.
If you use nicotine irregularly, the compound can have amazing effects for your ability to be motivated, think outside the box, and focus.[308; 309] Using the compound more regularly will build up a tolerance and is ill-advised.[310; 311]
Nicotine is a great dopamine booster if you're intolerant to coffee. Why? Well, nicotine stays in your system for a much shorter period of time.
Don't use nicotine if you're prone to substance addictions.
Another sign of a hyperdopaminergic society?
Another dangerous compound that should only be used very strategically. Phenibut affects both the GABA (relaxation) and dopamine neurotransmitters.
Phenibut makes you really calm and relaxed, while motivated at the same time. For that reason, phenibut is often used for peak performance moments, such as an important presentation.
Just like cyproheptadine, phenibut thus lowers stress. The substance also works extremely long, having an effect up to 24 hours. Never take this substance more than once per two weeks.
Beware: overuse of phenibut is extremely dangerous, as the withdrawal symptoms are potentially lethal.
One danger is that phenibut is freely sold over the internet. While I'm not in favor of banning substances you don't like, you should be aware that unregulated drugs like phenibut can have negative consequences on your life.
You can buy lithium orotate online. Lithium is much safer than many of the previous options I've described.
Last but not least: modafinil.
Modafinil is traditionally sold as a wakefulness-promoting drug, developed for if you have a condition called "narcolepsy". With narcolepsy, you'll fall asleep during the day.
Many people use modafinil off label though, mostly for performance-enhancing effects. I've tried the substance and I don't get anything out of it--modafinil lowers my productivity because of overstimulation.
That's it, the most common dopamine boosting medications. Moving on to lowering dopamine now:
Psychosis can be caused by excessive dopamine levels.
In fact, I think that many religious experiences are precisely created because of high dopamine activity in the ventromedial prefrontal cortex (the imaginative part that deals with abstractions), combined with a relative inhibition of the lateral prefrontal cortex (that is more logical).
Haloperidol is a prescription medicine that counters psychotic events. In psychosis, you're having trouble distinguishing between imagination and reality (hyperdopaminergic, anyone?)
Dopamine receptors are blocked with haloperidol, and the activation of dopamine-related genes is lowered. Haloperidol is also sedative - and thus increases relaxation.
Recall that serotonin lowers dopamine levels. Several supplements exist that increase serotonin, such as 5-HTP.
5-HTP is a building block compound for serotonin. Using 5-HTP increases serotonin availability in the brain, leading to a decrease in dopamine.[329; 330; 331] 5-HTP is best taken by bedtime when higher serotonin levels are more beneficial.
As a comparison, a category of drugs called "SSRIs" also boosts serotonin while lowering dopamine. You can buy 5 HTP online.
By the way:
Congratulations. You've read the entire blog post. You now know all you need to know about boosting dopamine, either through lifestyle changes, supplements, and medication. Let's finally consider the 30,000-foot view.
Want my top-10 laws for managing dopamine - including strategies not listed in this blog post? Sign up below:
I get it...
You don't want to buy 15 different supplements to boost your dopamine levels. Instead, you want an easy solution, right?
Fortunately, we've reviewed many different supplements at Alexfergus.com which can be used to boost your dopamine levels through the roof.
Here are some examples:
Why Qualia Mind? Well, the supplement contains many of the dopamine-boosting ingredients I've covered above, such as:
And many more compounds that affect dopamine levels indirectly. Hence, Qualia Mind is a perfect supplement if you want to boost your dopamine levels.
You can buy Qualia Mind HERE (use code FERGUS for a discount). Also read Alex' review of Qualia Mind: Qualia Mind Review - Extraordinary Deep Sleep & Cognitive Benefits.
Just like Qualia Mind, Awaken Gold also contains several ingredients that boost dopamine function:
You can get Awaken Gold HERE (code FERGUS gives you a discount of up to 15%)
Be sure to read my review, Awaken Gold Nootropic Review: Awesome Well-Being And Quantifiable Cognitive Performance Benefits as well.
many different ways exist to increase or decrease your dopamine levels, ranging from supplements to natural lifestyle adjustments to prescription medication and supplement stacks...
Hopefully you already know that your dopamine levels are a key piece of understanding health.
Simply put, almost any area of your life can improve by optimizing your dopamine levels, ranging from cognition, your outgoingness, imagination and creativity, and much more.
Hence, optimize your dopamine levels today and you're ready to conquer the 21st century! Why? Well, abstract thinking skills are in higher demand than ever and probably continue increasing. You deserve the best and deserve to be the best version of you!
This is a post by Bart Wolbers. Bart finished degrees in Physical Therapy (B), Philosophy (BA and MA), Philosophy of Science and Technology (MS - Cum Laude), and Clinical Health Science (MS), and is currently a health consultant.
 Krummenacher P, Mohr C, Haker H, Brugger P. Dopamine, paranormal belief, and the detection of meaningful stimuli. J Cogn Neurosci. 2010 Aug;22(8):1670-81. doi: 10.1162/jocn.2009.21313.
 Pavăl D. A Dopamine Hypothesis of Autism Spectrum Disorder. Dev Neurosci. 2017;39(5):355-360. doi: 10.1159/000478725. Epub 2017 Jul 28.
 Hellings JA, Arnold LE, Han JC. Dopamine antagonists for treatment resistance in autism spectrum disorders: review and focus on BDNF stimulators loxapine and amitriptyline. Expert Opin Pharmacother. 2017 Apr;18(6):581-588. doi: 10.1080/14656566.2017.1308483.
 Kriete T, Noelle DC. Dopamine and the development of executive dysfunction in autism spectrum disorders. PLoS One. 2015 Mar 26;10(3):e0121605. doi: 10.1371/journal.pone.0121605. eCollection 2015.
 Denys D, Zohar J, Westenberg HG. The role of dopamine in obsessive-compulsive disorder: preclinical and clinical evidence. J Clin Psychiatry. 2004;65 Suppl 14:11-7.
 Kelsby JP, McGrath JJ, Scott JG. Dopamine, psychosis and schizophrenia: the widening gap between basic and clinical neuroscience. Translational Psychiatryvolume 8, 2018.
 Diamond A. Executive functions. Annu Rev Psychol. 2013;64:135-68. doi: 10.1146/annurev-psych-113011-143750. Epub 2012 Sep 27.
 Rabinovici GD, Stephens ML, Possin KL. Executive dysfunction. Continuum (Minneap Minn). 2015 Jun;21(3 Behavioral Neurology and Neuropsychiatry):646-59. doi: 10.1212/01.CON.0000466658.05156.54.
 Nieoullon A. Dopamine and the regulation of cognition and attention. Prog Neurobiol. 2002 May;67(1):53-83.
 Mehta MA, Riedel WJ. Dopaminergic enhancement of cognitive function. Curr Pharm Des. 2006;12(20):2487-500.
 Gepshtein S, Li X, Snider J, Plank M, Lee D, Poizner H. Dopamine function and the efficiency of human movement. J Cogn Neurosci. 2014 Mar;26(3):645-57. doi: 10.1162/jocn_a_00503. Epub 2013 Oct 21.
 Takakusaki K. Functional Neuroanatomy for Posture and Gait Control. J Mov Disord. 2017 Jan;10(1):1-17. doi: 10.14802/jmd.16062. Epub 2017 Jan 18.
 Takakusaki K, Habaguchi T, ... Sakamoto T. Basal ganglia efferents to the brainstem centers controlling postural muscle tone and locomotion: a new concept for understanding motor disorders in basal ganglia dysfunction. Neuroscience. 2003;119(1):293-308.
 Takakusaki K, Saitoh K, Harada H, Kashiwayanagi M. Role of basal ganglia-brainstem pathways in the control of motor behaviors. Neurosci Res. 2004 Oct;50(2):137-51.
 Meder D, Herz DM, ... Siebner HR. The role of dopamine in the brain - lessons learned from Parkinson's disease. Neuroimage. 2019 Apr 15;190:79-93. doi: 10.1016/j.neuroimage.2018.11.021. Epub 2018 Nov 20.
 Hisahara S, Shimohama S. Dopamine receptors and Parkinson's disease. Int J Med Chem. 2011;2011:403039. doi: 10.1155/2011/403039. Epub 2011 Jun 13.
 Mann NJ. A brief history of meat in the human diet and current health implications. Meat Sci. 2018 Oct;144:169-179. doi: 10.1016/j.meatsci.2018.06.008. Epub 2018 Jun 13.
 Williams AC, Hill LJ. Meat and Nicotinamide: A Causal Role in Human Evolution, History, and Demographics. Int J Tryptophan Res. 2017 May 2;10:1178646917704661. doi: 10.1177/1178646917704661. eCollection 2017.
 Helm CW, McCrea RT, ... Hattingh S. A New Pleistocene Hominin Tracksite from the Cape South Coast, South Africa. Sci Rep. 2018 Feb 28;8(1):3772. doi: 10.1038/s41598-018-22059-5.
 Braun DR, Harris JW, ... Kibunjia M. Early hominin diet included diverse terrestrial and aquatic animals 1.95 Ma in East Turkana, Kenya. Proc Natl Acad Sci U S A. 2010 Jun 1;107(22):10002-7. doi: 10.1073/pnas.1002181107. Epub 2010 Jun 1.
 Steele TE. A unique hominin menu dated to 1.95 million years ago. Proc Natl Acad Sci U S A. 2010 Jun 15;107(24):10771-2. doi: 10.1073/pnas.1005992107. Epub 2010 Jun 7.
 Marean CW. The transition to foraging for dense and predictable resources and its impact on the evolution of modern humans. Philos Trans R Soc Lond B Biol Sci. 2016 Jul 5;371(1698). pii: 20150239. doi: 10.1098/rstb.2015.0239.
 Lou HC. Dopamine precursors and brain function in phenylalanine hydroxylase deficiency. Acta Paediatr Suppl. 1994 Dec;407:86-8.
 Montgomery AJ, McTavish SF, Cowen PJ, Grasby PM. Reduction of brain dopamine concentration with dietary tyrosine plus phenylalanine depletion: an [11C]raclopride PET study. Am J Psychiatry. 2003 Oct;160(10):1887-9.
 Ramdani C, Vidal F, ... Hasbroucq T. Dopamine and response selection: an Acute Phenylalanine/Tyrosine Depletion study. Psychopharmacology (Berl). 2018 Apr;235(4):1307-1316. doi: 10.1007/s00213-018-4846-3. Epub 2018 Feb 9.
 Marlowe FW, Berbesque JC. Tubers as fallback foods and their impact on Hadza hunter-gatherers. Am J Phys Anthropol. 2009 Dec;140(4):751-8. doi: 10.1002/ajpa.21040.
 Lewin R. Man the Scavenger: Hominids of 2 million years ago ate meat: but were they hunters or scavengers? A scavenging hypothesis has now been fully articulated. Science. 1984 May 25;224(4651):861-2.
 Ben-Dor M, Gopher A, Hershkovitz I, Barkai R. Man the fat hunter: the demise of Homo erectus and the emergence of a new hominin lineage in the Middle Pleistocene (ca. 400 kyr) Levant. PLoS One. 2011;6(12):e28689. doi: 10.1371/journal.pone.0028689. Epub 2011 Dec 9.
 Agam A, Barkai R. Elephant and Mammoth Hunting during the Paleolithic: A Review of the Relevant Archaeological, Ethnographic and Ethno-Historical Records. Quaternary 2018, 1(1)
 Nogués-Bravo D, Rodríguez J, ... Araújo MB. Climate change, humans, and the extinction of the woolly mammoth. PLoS Biol. 2008 Apr 1;6(4):e79. doi: 10.1371/journal.pbio.0060079.
 Green AC, Kimlin M, Siskind V, Whiteman DC. Hypothesis: hair cover can protect against invasive melanoma on the head and neck (Australia). Cancer Causes Control. 2006 Dec;17(10):1263-6.
 van Schaik CP, Deaner RO, Merrill MY. The conditions for tool use in primates: implications for the evolution of material culture. J Hum Evol. 1999 Jun;36(6):719-41.
 McGrew WC. Is primate tool use special? Chimpanzee and New Caledonian crow compared. Philos Trans R Soc Lond B Biol Sci. 2013 Oct 7;368(1630):20120422. doi: 10.1098/rstb.2012.0422. Print 2013 Nov 19.
 la Cour LT, Stone BW, ... Fragaszy DM. What limits tool use in nonhuman primates? Insights from tufted capuchin monkeys (Sapajus spp.) and chimpanzees (Pan troglodytes) aligning three-dimensional objects to a surface. Anim Cogn. 2014 Jan;17(1):113-25. doi: 10.1007/s10071-013-0643-x. Epub 2013 Jul 3.
 Dávid-Barrett T, Dunbar RI. Bipedality and hair loss in human evolution revisited: The impact of altitude and activity scheduling. J Hum Evol. 2016 May;94:72-82. doi: 10.1016/j.jhevol.2016.02.006. Epub 2016 Mar 22.
 Lequin M. Paleoanthropology's uses of the bipedal criterion. Hist Philos Life Sci. 2017 Nov 22;40(1):7. doi: 10.1007/s40656-017-0172-z.
 Bratsberg B, Rogeberg O. Flynn effect and its reversal are both environmentally caused. Proc Natl Acad Sci U S A. 2018 Jun 26;115(26):6674-6678. doi: 10.1073/pnas.1718793115. Epub 2018 Jun 11.
 Trahan LH, Stuebing KK, Fletcher JM, Hiscock M. The Flynn effect: a meta-analysis. Psychol Bull. 2014 Sep;140(5):1332-60. doi: 10.1037/a0037173. Epub 2014 Jun 30.
 Bratsberg B, Rogeberg O. Flynn effect and its reversal are both environmentally caused. Proc Natl Acad Sci U S A. 2018 Jun 26;115(26):6674-6678. doi: 10.1073/pnas.1718793115. Epub 2018 Jun 11.
 Shenk D. What is the Flynn Effect, and how does it change our understanding of IQ? Wiley Interdiscip Rev Cogn Sci. 2017 Jan;8(1-2). doi: 10.1002/wcs.1366. Epub 2016 Dec 1.
 Fuertinger S, Zinn JC, ... Simonyan K. Dopamine drives left-hemispheric lateralization of neural networks during human speech. J Comp Neurol. 2018 Apr 1;526(5):920-931. doi: 10.1002/cne.24375. Epub 2017 Dec 21.
 Simonyan K, Herscovitch P, Horwitz B. Speech-induced striatal dopamine release is left lateralized and coupled to functional striatal circuits in healthy humans: a combined PET, fMRI and DTI study. Neuroimage. 2013 Apr 15;70:21-32. doi: 10.1016/j.neuroimage.2012.12.042. Epub 2012 Dec 28.
 Molochnikov I, Cohen D. Hemispheric differences in the mesostriatal dopaminergic system. Front Syst Neurosci. 2014 Jun 11;8:110. doi: 10.3389/fnsys.2014.00110. eCollection 2014.
 Oleksiak A, Postma A, ... van Wezel RJ. A review of lateralization of spatial functioning in nonhuman primates. Brain Res Rev. 2011 Jun 24;67(1-2):56-72. doi: 10.1016/j.brainresrev.2010.11.002. Epub 2010 Nov 6.
 Fitzgerald PJ. Whose side are you on: does serotonin preferentially activate the right hemisphere and norepinephrine the left? Med Hypotheses. 2012 Aug;79(2):250-4. doi: 10.1016/j.mehy.2012.05.001. Epub 2012 May 28.
 Corballis MC. Left brain, right brain: facts and fantasies. PLoS Biol. 2014 Jan;12(1):e1001767. doi: 10.1371/journal.pbio.1001767. Epub 2014 Jan 21.
 Henneberg M. Evolution of the human brain: is bigger better? Clin Exp Pharmacol Physiol. 1998 Sep;25(9):745-9.
 Herculano-Houzel S. The remarkable, yet not extraordinary, human brain as a scaled-up primate brain and its associated cost. Proc Natl Acad Sci U S A. 2012 Jun 26;109 Suppl 1:10661-8. doi: 10.1073/pnas.1201895109. Epub 2012 Jun 20.
 Neubauer S, Hublin JJ, Gunz P. The evolution of modern human brain shape. Sci Adv. 2018 Jan 24;4(1):eaao5961. doi: 10.1126/sciadv.aao5961. eCollection 2018 Jan.
 Cairό O. External measures of cognition. Front Hum Neurosci. 2011 Oct 4;5:108. doi: 10.3389/fnhum.2011.00108. eCollection 2011.
 Sousa AMM, Zhu Y, ... Sestan N. Molecular and cellular reorganization of neural circuits in the human lineage. Science. 2017 Nov 24;358(6366):1027-1032. doi: 10.1126/science.aan3456.
 Raghanti MA, Edler MK,... Lovejoy CO. A neurochemical hypothesis for the origin of hominids. Proc Natl Acad Sci U S A. 2018 Feb 6;115(6):E1108-E1116. doi: 10.1073/pnas.1719666115. Epub 2018 Jan 22.
 Smaers JB, Steele J, ... Zilles K. Primate prefrontal cortex evolution: human brains are the extreme of a lateralized ape trend. Brain Behav Evol. 2011;77(2):67-78. doi: 10.1159/000323671. Epub 2011 Feb 17.
 Williams RA, Mamotte CD, Burnett JR. Phenylketonuria: an inborn error of phenylalanine metabolism. Clin Biochem Rev. 2008 Feb;29(1):31-41.
 Herculano-Houzel S. Numbers of neurons as biological correlates of cognitive capability. Current Opinion in Behavioral Sciences 15 2017: 1-7.
 Rapoport SI. Integrated phylogeny of the primate brain, with special reference to humans and their diseases. Brain Res Brain Res Rev. 1990 Sep-Dec;15(3):267-94.
 Henshilwood CS, d'Errico F, ... Wintle AG. Emergence of modern human behavior: Middle Stone Age engravings from South Africa. Science. 2002 Feb 15;295(5558):1278-80. Epub 2002 Jan 10.
 Pagel M. Q&A: What is human language, when did it evolve and why should we care? BMC Biol. 2017 Jul 24;15(1):64. doi: 10.1186/s12915-017-0405-3.
 Tsai HY, Chen KC, ... Lee IH. Sunshine-exposure variation of human striatal dopamine D(2)/D(3) receptor availability in healthy volunteers. Prog Neuropsychopharmacol Biol Psychiatry. 2011 Jan 15;35(1):107-10. doi: 10.1016/j.pnpbp.2010.09.014. Epub 2010 Sep 26.
 Romeo S, Viaggi C, ... Maggio R. Bright light exposure reduces TH-positive dopamine neurons: implications of light pollution in Parkinson's disease epidemiology. Sci Rep. 2013;3:1395. doi: 10.1038/srep01395.
 Cawley EI, Park S, ... Leyton M. Dopamine and light: dissecting effects on mood and motivational states in women with subsyndromal seasonal affective disorder. J Psychiatry Neurosci. 2013 Nov;38(6):388-97. doi: 10.1503/jpn.120181.
 Castañeda TR, de Prado BM, Prieto D, Mora F. Circadian rhythms of dopamine, glutamate and GABA in the striatum and nucleus accumbens of the awake rat: modulation by light. J Pineal Res. 2004 Apr;36(3):177-85.
 Shieh KR, Chu YS, Pan JT. Circadian change of dopaminergic neuron activity: effects of constant light and melatonin. Neuroreport. 1997 Jul 7;8(9-10):2283-7.
 Khaldy H, León J, ... Acuña-Castroviejo D. Circadian rhythms of dopamine and dihydroxyphenyl acetic acid in the mouse striatum: effects of pinealectomy and of melatonin treatment. Neuroendocrinology. 2002 Mar;75(3):201-8.
 Fell GL, Robinson KC, Mao J, Woolf CJ, Fisher DE. Skin β-endorphin mediates addiction to UV light. Cell. 2014 Jun 19;157(7):1527-34. doi: 10.1016/j.cell.2014.04.032.
 Rosiak J, Zawilska JB. Near-ultraviolet light perceived by the retina generates the signal suppressing melatonin synthesis in the chick pineal gland-an involvement of NMDA glutamate receptors. Neurosci Lett. 2005 May 13;379(3):214-7. Epub 2005 Jan 22.
 Frank MJ, O'Reilly RC. A mechanistic account of striatal dopamine function in human cognition: psychopharmacological studies with cabergoline and haloperidol. Behav Neurosci. 2006 Jun;120(3):497-517.
 Kim J, Jang S, ...Kim K. Implications of Circadian Rhythm in Dopamine and Mood Regulation. Mol Cells. 2017 Jul 31;40(7):450-456. doi: 10.14348/molcells.2017.0065. Epub 2017 Jul 31.
 Korshunov K, Blakemore LJ, Trombley PQ. Dopamine: A Modulator of Circadian Rhythms in the Central Nervous System. Front Cell Neurosci. 2017 Apr 3;11:91. doi: 10.3389/fncel.2017.00091. eCollection 2017.
 Verwey M, Dhir S, Amir S. Circadian influences on dopamine circuits of the brain: regulation of striatal rhythms of clock gene expression and implications for psychopathology and disease.`F1000Res. 2016 Aug 24;5. pii: F1000 Faculty Rev-2062. doi: 10.12688/f1000research.9180.1. eCollection 2016.
 Freyberg Z, McCarthy MJ. Dopamine D2 receptors and the circadian clock reciprocally mediate antipsychotic drug-induced metabolic disturbances. NPJ Schizophr. 2017 Apr 10;3:17. doi: 10.1038/s41537-017-0018-4. eCollection 2017.
 Huang J, Zhong Z, ... Wang H. Circadian modulation of dopamine levels and dopaminergic neuron development contributes to attention deficiency and hyperactive behavior. J Neurosci. 2015 Feb 11;35(6):2572-87. doi: 10.1523/JNEUROSCI.2551-14.2015.
 Baba K, DeBruyne JP, Tosini G. Dopamine 2 Receptor Activation Entrains Circadian Clocks in Mouse Retinal Pigment Epithelium. Sci Rep. 2017 Jul 11;7(1):5103. doi: 10.1038/s41598-017-05394-x.
 Blum ID, Zhu L, ... Storch KF. A highly tunable dopaminergic oscillator generates ultradian rhythms of behavioral arousal. Elife. 2014 Dec 29;3. doi: 10.7554/eLife.05105.
 Jackson CR, Capozzi M, Dai H, McMahon DG. Circadian perinatal photoperiod has enduring effects on retinal dopamine and visual function. J Neurosci. 2014 Mar 26;34(13):4627-33. doi: 10.1523/JNEUROSCI.4887-13.2014.
 Grippo RM, Purohit AM, ... Güler AD. Direct Midbrain Dopamine Input to the Suprachiasmatic Nucleus Accelerates Circadian Entrainment. Curr Biol. 2017 Aug 21;27(16):2465-2475.e3. doi: 10.1016/j.cub.2017.06.084. Epub 2017 Aug 3.
 Volkow ND, Tomasi D,... Ferré S. Evidence that sleep deprivation downregulates dopamine D2R in ventral striatum in the human brain. J Neurosci. 2012 May 9;32(19):6711-7. doi: 10.1523/JNEUROSCI.0045-12.2012.
 Volkow ND, Tomasi D, ... Swanson JM. Hyperstimulation of striatal D2 receptors with sleep deprivation: Implications for cognitive impairment. Neuroimage. 2009 May 1;45(4):1232-40. doi: 10.1016/j.neuroimage.2009.01.003. Epub 2009 Jan 20.
 Volkow ND, Wang GJ, ... Jayne M. Sleep deprivation decreases binding of [11C]raclopride to dopamine D2/D3 receptors in the human brain. J Neurosci. 2008 Aug 20;28(34):8454-61. doi: 10.1523/JNEUROSCI.1443-08.2008.
 Lim MM, Xu J, Holtzman DM, Mach RH. Sleep deprivation differentially affects dopamine receptor subtypes in mouse striatum. Neuroreport. 2011 Jul 13;22(10):489-93. doi: 10.1097/WNR.0b013e32834846a0.
 Volkow ND, Wang GJ, ... Pradhan K. Low dopamine striatal D2 receptors are associated with prefrontal metabolism in obese subjects: possible contributing factors. Neuroimage. 2008 Oct 1;42(4):1537-43. doi: 10.1016/j.neuroimage.2008.06.002. Epub 2008 Jun 13.
 Monti JM, Monti D. The involvement of dopamine in the modulation of sleep and waking. Sleep Med Rev. 2007 Apr;11(2):113-33. Epub 2007 Feb 1.
 Oishi Y, Lazarus M. The control of sleep and wakefulness by mesolimbic dopamine systems. Neurosci Res. 2017 May;118:66-73. doi: 10.1016/j.neures.2017.04.008. Epub 2017 Apr 20.
 Martins RC1, Andersen ML, ... Tufik S. Dopamine transporter regulation during four nights of REM sleep deprivation followed by recovery--an in vivo molecular imaging study in humans. Sleep. 2010 Feb;33(2):243-51.
 Volkow ND, Tomasi D, ... Ferré S. Evidence that sleep deprivation downregulates dopamine D2R in ventral striatum in the human brain. J Neurosci. 2012 May 9;32(19):6711-7. doi: 10.1523/JNEUROSCI.0045-12.2012.
 Tufik S. Changes of response to dopaminergic drugs in rats submitted to REM-sleep deprivation. Psychopharmacology (Berl). 1981;72(3):257-60.
 Perogamvros L, Schwartz S. The roles of the reward system in sleep and dreaming. Neurosci Biobehav Rev. 2012 Sep;36(8):1934-51. doi: 10.1016/j.neubiorev.2012.05.010. Epub 2012 Jun 2.
 Herrera-Solis A, Herrera-Morales W, ... Arias-Carrion O. Dopaminergic Modulation of Sleep-Wake States. CNS Neurol Disord Drug Targets. 2017;16(4):380-386. doi: 10.2174/1871527316666170320145429.
 Berridge KC. The debate over dopamine's role in reward: the case for incentive salience. Psychopharmacology (Berl). 2007 Apr;191(3):391-431. Epub 2006 Oct 27.
 Berridge KC, Robinson TE, Aldridge JW. Dissecting components of reward: 'liking', 'wanting', and learning. Curr Opin Pharmacol. 2009 Feb;9(1):65-73. doi: 10.1016/j.coph.2008.12.014. Epub 2009 Jan 21.
 Zabelina DL, Colzato L, Beeman M, Hommel B. Dopamine and the Creative Mind: Individual Differences in Creativity Are Predicted by Interactions between Dopamine Genes DAT and COMT. PLoS One. 2016 Jan 19;11(1):e0146768. doi: 10.1371/journal.pone.0146768. eCollection 2016.
 Wise RA. Role of brain dopamine in food reward and reinforcement. Philos Trans R Soc Lond B Biol Sci. 2006 Jul 29;361(1471):1149-58.
 Bratcher NA, Farmer-Dougan V, ... Garris PA. The role of dopamine in reinforcement: changes in reinforcement sensitivity induced by D1-type, D2-type, and nonselective dopamine receptor agonists. J Exp Anal Behav. 2005 Nov;84(3):371-99.
 Morita K, Morishima M, Sakai K, Kawaguchi Y. Dopaminergic control of motivation and reinforcement learning: a closed-circuit account for reward-oriented behavior. J Neurosci. 2013 May 15;33(20):8866-90. doi: 10.1523/JNEUROSCI.4614-12.2013.
 Glimcher PW. Understanding dopamine and reinforcement learning: the dopamine reward prediction error hypothesis. Proc Natl Acad Sci U S A. 2011 Sep 13;108 Suppl 3:15647-54. doi: 10.1073/pnas.1014269108. Epub 2011 Mar 9.
 Steinberg EE, Boivin JR, ... Janak PH. Positive reinforcement mediated by midbrain dopamine neurons requires D1 and D2 receptor activation in the nucleus accumbens. PLoS One. 2014 Apr 14;9(4):e94771. doi: 10.1371/journal.pone.0094771. eCollection 2014.
 Gonzales RA, Job MO, Doyon WM. The role of mesolimbic dopamine in the development and maintenance of ethanol reinforcement. Pharmacol Ther. 2004 Aug;103(2):121-46.
 Bao S, Chan VT, Merzenich MM. Cortical remodelling induced by activity of ventral tegmental dopamine neurons. Nature. 2001 Jul 5;412(6842):79-83.
 Green CS, Bavelier D. Exercising your brain: a review of human brain plasticity and training-induced learning. Psychol Aging. 2008 Dec;23(4):692-701. doi: 10.1037/a0014345.
 Thomas MJ, Kalivas PW, Shaham Y. Neuroplasticity in the mesolimbic dopamine system and cocaine addiction. Br J Pharmacol. 2008 May;154(2):327-42. doi: 10.1038/bjp.2008.77. Epub 2008 Mar 17.
 Foley TE, Fleshner M. Neuroplasticity of dopamine circuits after exercise: implications for central fatigue. Neuromolecular Med. 2008;10(2):67-80. doi: 10.1007/s12017-008-8032-3. Epub 2008 Feb 15.
[102[ Matthews RT, Ferrante RJ, ... Beal MF. Creatine and cyclocreatine attenuate MPTP neurotoxicity. Exp Neurol. 1999 May;157(1):142-9.
 Writing Group for the NINDS Exploratory Trials in Parkinson Disease (NET-PD) Investigators, Kieburtz K, ... Wills AM. Effect of creatine monohydrate on clinical progression in patients with Parkinson disease: a randomized clinical trial. JAMA. 2015 Feb 10;313(6):584-93. doi: 10.1001/jama.2015.120.
 Jardí F, Laurent MR, ... Vanderschueren D. Testosterone boosts physical activity in male mice via dopaminergic pathways. Sci Rep. 2018 Jan 17;8(1):957. doi: 10.1038/s41598-017-19104-0.
 Simpkins JW, Kalra SP, Kalra PS. Variable effects of testosterone on dopamine activity in several microdissected regions in the preoptic area and medial basal hypothalamus. Endocrinology. 1983 Feb;112(2):665-9.
 Purves-Tyson TD, Owens SJ, ... Weickert CS. Testosterone induces molecular changes in dopamine signaling pathway molecules in the adolescent male rat nigrostriatal pathway. PLoS One. 2014 Mar 11;9(3):e91151. doi: 10.1371/journal.pone.0091151. eCollection 2014.
 Triemstra JL, Sato SM, Wood RI. Testosterone and nucleus accumbens dopamine in the male Syrian hamster. Psychoneuroendocrinology. 2008 Apr;33(3):386-94. doi: 10.1016/j.psyneuen.2007.12.006. Epub 2008 Jan 30.
 Sinclair D, Purves-Tyson TD, Allen KM, Weickert CS. Impacts of stress and sex hormones on dopamine neurotransmission in the adolescent brain. Psychopharmacology (Berl). 2014 Apr;231(8):1581-99. doi: 10.1007/s00213-013-3415-z. Epub 2014 Jan 31.
 Majcher-Maślanka I, Solarz A, Wędzony K, Chocyk A. The effects of early-life stress on dopamine system function in adolescent female rats. Int J Dev Neurosci. 2017 Apr;57:24-33. doi: 10.1016/j.ijdevneu.2017.01.001. Epub 2017 Jan 5.
 Cabib S, Giardino L, ... Puglisi-Allegra S. Stress promotes major changes in dopamine receptor densities within the mesoaccumbens and nigrostriatal systems. Neuroscience. 1998 May;84(1):193-200.
 Moriam S, Sobhani ME. Epigenetic effect of chronic stress on dopamine signaling and depression. Genet Epigenet. 2013 Feb 10;5:11-6. doi: 10.4137/GEG.S11016. eCollection 2013.
 Isovich E, Mijnster MJ, Flügge G, Fuchs E. Chronic psychosocial stress reduces the density of dopamine transporters. Eur J Neurosci. 2000 Mar;12(3):1071-8.
 Horger BA, Roth RH. The role of mesoprefrontal dopamine neurons in stress. Crit Rev Neurobiol. 1996;10(3-4):395-418.
 Finlay JM, Zigmond MJ. The effects of stress on central dopaminergic neurons: possible clinical implications. Neurochem Res. 1997 Nov;22(11):1387-94.
 Szczypka MS, Zhou QY, Palmiter RD. Dopamine-stimulated sexual behavior is testosterone dependent in mice. Behav Neurosci. 1998 Oct;112(5):1229-35.
 Siris SG, Siris ES, ... Bunney WE Jr. Effects of dopamine blockade on gonadotropins and testosterone in men. Am J Psychiatry. 1980 Feb;137(2):211-4.
 Campbell BC, Dreber A, ... Lum JK. Testosterone exposure, dopaminergic reward, and sensation-seeking in young men. Physiol Behav. 2010 Mar 30;99(4):451-6. doi: 10.1016/j.physbeh.2009.12.011. Epub 2009 Dec 21.
 Morris RW, Purves-Tyson TD, ... Weickert TW. Testosterone and reward prediction-errors in healthy men and men with schizophrenia. Schizophr Res. 2015 Nov;168(3):649-60. doi: 10.1016/j.schres.2015.06.030. Epub 2015 Jul 29.
 Foreman MM, Hall JL. Effects of D2-dopaminergic receptor stimulation on the lordotic response of female rats. Psychopharmacology (Berl). 1987;91(1):96-100.
 Giuliano F, Allard J. Dopamine and male sexual function. Eur Urol. 2001 Dec;40(6):601-8.
 Melis MR, Argiolas A. Dopamine and sexual behavior. Neurosci Biobehav Rev. 1995 Spring;19(1):19-38.
 Hilton DL, Watts C. Pornography addiction: A neuroscience perspective. Surg Neurol Int. 2011 Feb 21;2:19. doi: 10.4103/2152-7806.76977.
 de Alarcón R, de la Iglesia JI, Casado NM, Montejo AL. Online Porn Addiction: What We Know and What We Don't-A Systematic Review. J Clin Med. 2019 Jan 15;8(1). pii: E91. doi: 10.3390/jcm8010091.
 Laneri D, Schuster V, ... Sommer J. Effects of Long-Term Mindfulness Meditation on Brain's White Matter Microstructure and its Aging. Front Aging Neurosci. 2016 Jan 14;7:254. doi: 10.3389/fnagi.2015.00254. eCollection 2015.
 Kjaer TW, Bertelsen C, ... Lou HC. Increased dopamine tone during meditation-induced change of consciousness. Brain Res Cogn Brain Res. 2002 Apr;13(2):255-9.
 Newberg AB, Iversen J. The neural basis of the complex mental task of meditation: neurotransmitter and neurochemical considerations. Med Hypotheses. 2003 Aug;61(2):282-91.
 Bujatti M, Riederer P. Serotonin, noradrenaline, dopamine metabolites in transcendental meditation-technique. J Neural Transm. 1976;39(3):257-67.
 Rubia K. The neurobiology of Meditation and its clinical effectiveness in psychiatric disorders. Biol Psychol. 2009 Sep;82(1):1-11. doi: 10.1016/j.biopsycho.2009.04.003. Epub 2009 Apr 23.
 Chiesa A, Serretti A. A systematic review of neurobiological and clinical features of mindfulness meditations. Psychol Med. 2010 Aug;40(8):1239-52. doi: 10.1017/S0033291709991747. Epub 2009 Nov 27.
 Arnsten AF, Rubia K. Neurobiological circuits regulating attention, cognitive control, motivation, and emotion: disruptions in neurodevelopmental psychiatric disorders. J Am Acad Child Adolesc Psychiatry. 2012 Apr;51(4):356-67. doi: 10.1016/j.jaac.2012.01.008. Epub 2012 Mar 3.
 Zou L, Yeung A, ... Wang H. A Systematic Review and Meta-Analysis of Mindfulness-Based (Baduanjin) Exercise for Alleviating Musculoskeletal Pain and Improving Sleep Quality in People with Chronic Diseases. Int J Environ Res Public Health. 2018 Jan 25;15(2). pii: E206. doi: 10.3390/ijerph15020206.
 Amutio A, Franco C, ... Molero-Jurado MDM. Effects of Mindfulness Training on Sleep Problems in Patients With Fibromyalgia. Front Psychol. 2018 Aug 3;9:1365. doi: 10.3389/fpsyg.2018.01365. eCollection 2018.
 Rusch HL, Rosario M, ... Gill JM. The effect of mindfulness meditation on sleep quality: a systematic review and meta-analysis of randomized controlled trials. Ann N Y Acad Sci. 2018 Dec 21. doi: 10.1111/nyas.13996.
 Black DS, O'Reilly GA, ... Irwin MR. Mindfulness meditation and improvement in sleep quality and daytime impairment among older adults with sleep disturbances: a randomized clinical trial. JAMA Intern Med. 2015 Apr;175(4):494-501. doi: 10.1001/jamainternmed.2014.8081.
 Neuendorf R, Wahbeh H, ... Oken BS. The Effects of Mind-Body Interventions on Sleep Quality: A Systematic Review. Evid Based Complement Alternat Med. 2015;2015:902708. doi: 10.1155/2015/902708. Epub 2015 Jun 16.
 Mavridis IN. Music and the nucleus accumbens. Surg Radiol Anat. 2015 Mar;37(2):121-5. doi: 10.1007/s00276-014-1360-0. Epub 2014 Aug 8.
 Moraes MM, Rabelo PCR, ... Soares DD. Auditory stimulation by exposure to melodic music increases dopamine and serotonin activities in rat forebrain areas linked to reward and motor control. Neurosci Lett. 2018 Apr 23;673:73-78. doi: 10.1016/j.neulet.2018.02.058. Epub 2018 Feb 27.
 Blood AJ, Zatorre RJ. Intensely pleasurable responses to music correlate with activity in brain regions implicated in reward and emotion. Proc Natl Acad Sci U S A. 2001 Sep 25;98(20):11818-23.
 Salimpoor VN, Benovoy M, Larcher K, Dagher A, Zatorre RJ. Anatomically distinct dopamine release during anticipation and experience of peak emotion to music. Nat Neurosci. 2011 Feb;14(2):257-62. doi: 10.1038/nn.2726. Epub 2011 Jan 9.
 Brodal HP, Osnes B, Specht K. Listening to Rhythmic Music Reduces Connectivity within the Basal Ganglia and the Reward System. Front Neurosci. 2017 Mar 28;11:153. doi: 10.3389/fnins.2017.00153. eCollection 2017.
 Moore H, Rose HJ, Grace AA. Chronic cold stress reduces the spontaneous activity of ventral tegmental dopamine neurons. Neuropsychopharmacology. 2001 Apr;24(4):410-9.
 Srámek P, Simecková M, Janský L, Savlíková J, Vybíral S. Human physiological responses to immersion into water of different temperatures. Eur J Appl Physiol. 2000 Mar;81(5):436-42.
 Ootsuka Y, Heidbreder CA, Hagan JJ, Blessing WW. Dopamine D2 receptor stimulation inhibits cold-initiated thermogenesis in brown adipose tissue in conscious rats. Neuroscience. 2007 Jun 15;147(1):127-35. Epub 2007 May 21.
 Hagelberg N, Martikainen IK, ... Pertovaara A. Dopamine D2 receptor binding in the human brain is associated with the response to painful stimulation and pain modulatory capacity. Pain. 2002 Sep;99(1-2):273-9.
 Eisenhofer G, Aneman A, ... Mezey E. Substantial production of dopamine in the human gastrointestinal tract. J Clin Endocrinol Metab. 1997 Nov;82(11):3864-71.
 Xue R, Zhang H, ... Bai L. Peripheral Dopamine Controlled by Gut Microbes Inhibits Invariant Natural Killer T Cell-Mediated Hepatitis. Front Immunol. 2018 Oct 17;9:2398. doi: 10.3389/fimmu.2018.02398. eCollection 2018.
 Smits SA, Leach J, ... Sonnenburg JL. Seasonal cycling in the gut microbiome of the Hadza hunter-gatherers of Tanzania. Science. 2017 Aug 25;357(6353):802-806. doi: 10.1126/science.aan4834.
 Fragiadakis GK, Smits SA, ... Sonnenburg JL. Links between environment, diet, and the hunter-gatherer microbiome. Gut Microbes. 2019;10(2):216-227. doi: 10.1080/19490976.2018.1494103. Epub 2018 Aug 17.
 Jadhav KS, Peterson VL, ... Boutrel B. Gut microbiome correlates with altered striatal dopamine receptor expression in a model of compulsive alcohol seeking. Neuropharmacology. 2018 Oct;141:249-259. doi: 10.1016/j.neuropharm.2018.08.026. Epub 2018 Aug 31.
 Strandwitz P. Neurotransmitter modulation by the gut microbiota. Brain Res. 2018 Aug 15;1693(Pt B):128-133. doi: 10.1016/j.brainres.2018.03.015.
 Mittal R, Debs LH,... Liu XZ. Neurotransmitters: The Critical Modulators Regulating Gut-Brain Axis. J Cell Physiol. 2017 Sep;232(9):2359-2372. doi: 10.1002/jcp.25518. Epub 2017 Apr 10.
 Tillmann S, Awwad HM, ... Obeid R. Probiotics Affect One-Carbon Metabolites and Catecholamines in a Genetic Rat Model of Depression. Mol Nutr Food Res. 2018 Apr;62(7):e1701070. doi: 10.1002/mnfr.201701070. Epub 2018 Mar 13.
 Sarkar A, Lehto SM, ... Burnet PWJ. Psychobiotics and the Manipulation of Bacteria-Gut-Brain Signals. Trends Neurosci. 2016 Nov;39(11):763-781. doi: 10.1016/j.tins.2016.09.002. Epub 2016 Oct 25.
 Deaver JA, Eum SY, Toborek M. Circadian Disruption Changes Gut Microbiome Taxa and Functional Gene Composition. Front Microbiol. 2018 Apr 13;9:737. doi: 10.3389/fmicb.2018.00737. eCollection 2018.
 Liang X, FitzGerald GA. Timing the Microbes: The Circadian Rhythm of the Gut Microbiome. J Biol Rhythms. 2017 Dec;32(6):505-515. doi: 10.1177/0748730417729066. Epub 2017 Sep 1.
 Voigt RM, Forsyth CB, ... Keshavarzian A. Circadian Rhythm and the Gut Microbiome. Int Rev Neurobiol. 2016;131:193-205. doi: 10.1016/bs.irn.2016.07.002. Epub 2016 Sep 6.
 Paiva I, Pinho R, ... Outeiro TF. Sodium butyrate rescues dopaminergic cells from alpha-synuclein-induced transcriptional deregulation and DNA damage. Hum Mol Genet. 2017 Jun 15;26(12):2231-2246. doi: 10.1093/hmg/ddx114.
 Sharma S, Taliyan R, Singh S. Beneficial effects of sodium butyrate in 6-OHDA induced neurotoxicity and behavioral abnormalities: Modulation of histone deacetylase activity. Behav Brain Res. 2015 Sep 15;291:306-314. doi: 10.1016/j.bbr.2015.05.052. Epub 2015 Jun 3.
 St Laurent R, O'Brien LM, Ahmad ST. Sodium butyrate improves locomotor impairment and early mortality in a rotenone-induced Drosophila model of Parkinson's disease. Neuroscience. 2013 Aug 29;246:382-90. doi: 10.1016/j.neuroscience.2013.04.037. Epub 2013 Apr 25.
 Wennberg P, Boraxbekk CJ, ... Dunstan DW. Acute effects of breaking up prolonged sitting on fatigue and cognition: a pilot study. BMJ Open. 2016 Feb 26;6(2):e009630. doi: 10.1136/bmjopen-2015-009630.
 Foley TE, Fleshner M. Neuroplasticity of dopamine circuits after exercise: implications for central fatigue. Neuromolecular Med. 2008;10(2):67-80. doi: 10.1007/s12017-008-8032-3. Epub 2008 Feb 15.
 Petzinger GM, Holschneider DP... Jakowec MW. The Effects of Exercise on Dopamine Neurotransmission in Parkinson's Disease: Targeting Neuroplasticity to Modulate Basal Ganglia Circuitry. Brain Plast. 2015;1(1):29-39.
 Greenwood BN. The role of dopamine in overcoming aversion with exercise. Brain Res. 2018 Aug 29. pii: S0006-8993(18)30452-9. doi: 10.1016/j.brainres.2018.08.030.
 Kintz N, Petzinger GM, Jakowec MW. Treadmill exercise modifies dopamine receptor expression in the prefrontal cortex of the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned mouse model of Parkinson's disease. Neuroreport. 2017 Oct 18;28(15):987-995. doi: 10.1097/WNR.0000000000000865.
 Cordeiro LMS, Rabelo PCR, ... Soares DD. Physical exercise-induced fatigue: the role of serotonergic and dopaminergic systems. Braz J Med Biol Res. 2017 Oct 19;50(12):e6432. doi: 10.1590/1414-431X20176432.
 Vučković MG, Li Q, Fisher ... Petzinger GM. Exercise elevates dopamine D2 receptor in a mouse model of Parkinson's disease: in vivo imaging with [¹⁸F]fallypride. Mov Disord. 2010 Dec 15;25(16):2777-84. doi: 10.1002/mds.23407.
 Tajiri N, Yasuhara T, Shingo ... Date I. Exercise exerts neuroprotective effects on Parkinson's disease model of rats. Brain Res. 2010 Jan 15;1310:200-7. doi: 10.1016/j.brainres.2009.10.075. Epub 2009 Nov 10.
 Mabandla M, Kellaway L, St Clair Gibson A, Russell VA. Voluntary running provides neuroprotection in rats after 6-hydroxydopamine injection into the medial forebrain bundle. Metab Brain Dis. 2004 Jun;19(1-2):43-50.
 Rabelo PCR, Horta NAC, ... Soares DD. Intrinsic exercise capacity in rats influences dopamine neuroplasticity induced by physical training. J Appl Physiol (1985). 2017 Dec 1;123(6):1721-1729. doi: 10.1152/japplphysiol.00506.2017. Epub 2017 Sep 7.
 Gerecke KM, Jiao Y, Pani A, Pagala V, Smeyne RJ. Exercise protects against MPTP-induced neurotoxicity in mice. Brain Res. 2010 Jun 23;1341:72-83. doi: 10.1016/j.brainres.2010.01.053. Epub 2010 Jan 29.
 Wu SY, Wang TF, ... Kuo YM. Running exercise protects the substantia nigra dopaminergic neurons against inflammation-induced degeneration via the activation of BDNF signaling pathway. Brain Behav Immun. 2011 Jan;25(1):135-46. doi: 10.1016/j.bbi.2010.09.006. Epub 2010 Sep 17.
 Robertson CL, Ishibashi K, ... London ED. Effect of Exercise Training on Striatal Dopamine D2/D3 Receptors in Methamphetamine Users during Behavioral Treatment. Neuropsychopharmacology. 2016 May;41(6):1629-36. doi: 10.1038/npp.2015.331. Epub 2015 Oct 27.
 Mahapatra A. Overeating, obesity, and dopamine receptors. ACS Chem Neurosci. 2010 May 19;1(5):346-7. doi: 10.1021/cn100044y.
 Sevgi M, Rigoux L,... Tittgemeyer M. An Obesity-Predisposing Variant of the FTO Gene Regulates D2R-Dependent Reward Learning. J Neurosci. 2015 Sep 9;35(36):12584-92. doi: 10.1523/JNEUROSCI.1589-15.2015.
 Rutledge RB, Smittenaar P, ... Dolan RJ. Risk Taking for Potential Reward Decreases across the Lifespan. Curr Biol. 2016 Jun 20;26(12):1634-1639. doi: 10.1016/j.cub.2016.05.017. Epub 2016 Jun 2.
 Norbury A, Manohar S, Rogers RD, Husain M. Dopamine modulates risk-taking as a function of baseline sensation-seeking trait. J Neurosci. 2013 Aug 7;33(32):12982-6. doi: 10.1523/JNEUROSCI.5587-12.2013.
 Norbury A, Husain M. Sensation-seeking: Dopaminergic modulation and risk for psychopathology. Behav Brain Res. 2015 Jul 15;288:79-93. doi: 10.1016/j.bbr.2015.04.015. Epub 2015 Apr 20.
 Kaasinen V, Aalto S, Någren K, Rinne JO. Expectation of caffeine induces dopaminergic responses in humans. Eur J Neurosci. 2004 Apr;19(8):2352-6.
 Volkow ND, Wang GJ, ... Tomasi D. Caffeine increases striatal dopamine D2/D3 receptor availability in the human brain. Transl Psychiatry. 2015 Apr 14;5:e549. doi: 10.1038/tp.2015.46.
 Manalo RVM, Medina PMB. Caffeine Protects Dopaminergic Neurons From Dopamine-Induced Neurodegeneration via Synergistic Adenosine-Dopamine D2-Like Receptor Interactions in Transgenic Caenorhabditis elegans. Front Neurosci. 2018 Mar 7;12:137. doi: 10.3389/fnins.2018.00137. eCollection 2018.
 Nehlig A, Daval JL, Debry G. Caffeine and the central nervous system: mechanisms of action, biochemical, metabolic and psychostimulant effects. Brain Res Brain Res Rev. 1992 May-Aug;17(2):139-70.
 Ferré S. Mechanisms of the psychostimulant effects of caffeine: implications for substance use disorders. Psychopharmacology (Berl). 2016 May;233(10):1963-79. doi: 10.1007/s00213-016-4212-2. Epub 2016 Jan 20.
 Kulkarni SK, Bhutani MK, Bishnoi M. Antidepressant activity of curcumin: involvement of serotonin and dopamine system. Psychopharmacology (Berl). 2008 Dec;201(3):435-42. doi: 10.1007/s00213-008-1300-y. Epub 2008 Sep 3.
 Kulkarni SK, Dhir A. An overview of curcumin in neurological disorders. Indian J Pharm Sci. 2010 Mar;72(2):149-54. doi: 10.4103/0250-474X.65012.
 Mythri RB, Bharath MM. Curcumin: a potential neuroprotective agent in Parkinson's disease. Curr Pharm Des. 2012;18(1):91-9.
 Du XX, Xu HM, Jiang H, Song N, Wang J, Xie JX. Curcumin protects nigral dopaminergic neurons by iron-chelation in the 6-hydroxydopamine rat model of Parkinson's disease. Neurosci Bull. 2012 Jun;28(3):253-8. doi: 10.1007/s12264-012-1238-2.
 Rana DG, Galani VJ. Dopamine mediated antidepressant effect of Mucuna pruriens seeds in various experimental models of depression. Ayu. 2014 Jan;35(1):90-7. doi: 10.4103/0974-8520.141949.
 Lampariello LR, Cortelazzo A, Guerranti R, Sticozzi C, Valacchi G. The Magic Velvet Bean of Mucuna pruriens. J Tradit Complement Med. 2012 Oct;2(4):331-9.
 Cilia R, Laguna J, ... Pezzoli G. Mucuna pruriens in Parkinson disease: A double-blind, randomized, controlled, crossover study. Neurology. 2017 Aug 1;89(5):432-438. doi: 10.1212/WNL.0000000000004175. Epub 2017 Jul 5.
 Manyam BV, Dhanasekaran M, Hare TA. Neuroprotective effects of the antiparkinson drug Mucuna pruriens. Phytother Res. 2004 Sep;18(9):706-12.
 Stansley BJ, Yamamoto BK. L-Dopa and Brain Serotonin System Dysfunction. Toxics. 2015 Mar 5;3(1):75-88. doi: 10.3390/toxics3010075.
 Dodd FL, Kennedy DO, Riby LM, Haskell-Ramsay CF. A double-blind, placebo-controlled study evaluating the effects of caffeine and L-theanine both alone and in combination on cerebral blood flow, cognition and mood. Psychopharmacology (Berl). 2015 Jul;232(14):2563-76. doi: 10.1007/s00213-015-3895-0. Epub 2015 Mar 13.
 Yamada T, Terashima T, ... Yokogoshi H. Effects of theanine, r-glutamylethylamide, on neurotransmitter release and its relationship with glutamic acid neurotransmission. Nutr Neurosci. 2005 Aug;8(4):219-26.
 Mirza B, Ikram H, Bilgrami S, Haleem DJ, Haleem MA. Neurochemical and behavioral effects of green tea (Camellia sinensis): a model study. Pak J Pharm Sci. 2013 May;26(3):511-6.
 Zhu G, Yang S, Xie Z, Wan X. Synaptic modification by L-theanine, a natural constituent in green tea, rescues the impairment of hippocampal long-term potentiation and memory in AD mice. Neuropharmacology. 2018 Aug;138:331-340. doi: 10.1016/j.neuropharm.2018.06.030. Epub 2018 Jun 23.
 Lardner AL. Neurobiological effects of the green tea constituent theanine and its potential role in the treatment of psychiatric and neurodegenerative disorders. Nutr Neurosci. 2014 Jul;17(4):145-55. doi: 10.1179/1476830513Y.0000000079. Epub 2013 Nov 26.
 Yamada T, Terashima T, ... Yokogoshi H. Theanine, gamma-glutamylethylamide, a unique amino acid in tea leaves, modulates neurotransmitter concentrations in the brain striatum interstitium in conscious rats. Amino Acids. 2009 Jan;36(1):21-7. doi: 10.1007/s00726-007-0020-7. Epub 2008 Jan 15.
 Feduccia AA, Wang Y, ... Bartlett SE. Locomotor activation by theacrine, a purine alkaloid structurally similar to caffeine: involvement of adenosine and dopamine receptors. Pharmacol Biochem Behav. 2012 Aug;102(2):241-8. doi: 10.1016/j.pbb.2012.04.014. Epub 2012 May 9.
 Taylor L, Mumford P, ... Wilborn C. Safety of TeaCrine®, a non-habituating, naturally-occurring purine alkaloid over eight weeks of continuous use. J Int Soc Sports Nutr. 2016 Jan 13;13:2. doi: 10.1186/s12970-016-0113-3. eCollection 2016.
 Chen QG, Zeng YS, ... Hägg U. The effects of Rhodiola rosea extract on 5-HT level, cell proliferation and quantity of neurons at cerebral hippocampus of depressive rats. Phytomedicine. 2009 Sep;16(9):830-8. doi: 10.1016/j.phymed.2009.03.011. Epub 2009 Apr 28.
 Seol GH, Shim HS, ... Min SS. Antidepressant-like effect of Salvia sclarea is explained by modulation of dopamine activities in rats. J Ethnopharmacol. 2010 Jul 6;130(1):187-90. doi: 10.1016/j.jep.2010.04.035. Epub 2010 May 2.
 Mechan AO, Fowler A, ... Mohajeri MH. Monoamine reuptake inhibition and mood-enhancing potential of a specified oregano extract. Br J Nutr. 2011 Apr;105(8):1150-63. doi: 10.1017/S0007114510004940. Epub 2010 Dec 21.
 Mechan AO, Fowler A, ... Mohajeri MH. Monoamine reuptake inhibition and mood-enhancing potential of a specified oregano extract. Br J Nutr. 2011 Apr;105(8):1150-63. doi: 10.1017/S0007114510004940. Epub 2010 Dec 21.
 Zotti M1, Colaianna M, ... Trabace L. Carvacrol: from ancient flavoring to neuromodulatory agent. Molecules. 2013 May 24;18(6):6161-72. doi: 10.3390/molecules18066161.
 Kolling GJ, Panazzolo DM, ... Fischer V. Oregano Extract Added into the Diet of Dairy Heifers Changes Feeding Behavior and Concentrate Intake. ScientificWorldJournal. 2016;2016:8917817. doi: 10.1155/2016/8917817. Epub 2016 Dec 27.
 Noori Ahmad Abadi M, Mortazavi M, ... Ali-Akbari S. Effect of Hydroalcoholic Extract of Rosmarinus officinalis L. Leaf on Anxiety in Mice. J Evid Based Complementary Altern Med. 2016 Oct;21(4):NP85-90. doi: 10.1177/2156587216642101. Epub 2016 Apr 6.
 Kim SJ, Kim JS, ... Chun HS. Carnosol, a component of rosemary (Rosmarinus officinalis L.) protects nigral dopaminergic neuronal cells. Neuroreport. 2006 Nov 6;17(16):1729-33.
 Habtemariam S. The Therapeutic Potential of Rosemary (Rosmarinus officinalis) Diterpenes for Alzheimer's Disease. Evid Based Complement Alternat Med. 2016;2016:2680409. doi: 10.1155/2016/2680409. Epub 2016 Jan 28.
 Bansal P, Banerjee S. Effect of Withinia Somnifera and Shilajit on Alcohol Addiction in Mice. Pharmacogn Mag. 2016 May;12(Suppl 2):S121-8. doi: 10.4103/0973-1296.182170. Epub 2016 May 11.
 Jun YL, Bae CH, Kim D, Koo S, Kim S. Korean Red Ginseng protects dopaminergic neurons by suppressing the cleavage of p35 to p25 in a Parkinson's disease mouse model. J Ginseng Res. 2015 Apr;39(2):148-54. doi: 10.1016/j.jgr.2014.10.003. Epub 2014 Nov 1.
 Halladay AK, Yu YL, Palmer J, Oh KW, Wagner GC. Acute and chronic effects of ginseng total saponin and amphetamine on fixed-interval performance in rats. Planta Med. 1999 Mar;65(2):162-4.
 Oh KW, Kim HS, Wagner GC. Ginseng total saponin inhibits the dopaminergic depletions induced by methamphetamine. Planta Med. 1997 Feb;63(1):80-1.
 Nah SY, Bhatia KS, Lyles J, Ellinwood EH, Lee TH. Effects of ginseng saponin on acute cocaine-induced alterations in evoked dopamine release and uptake in rat brain nucleus accumbens. Brain Res. 2009 Jan 12;1248:184-90. doi: 10.1016/j.brainres.2008.10.064. Epub 2008 Nov 8.
 Shim IS, Won JS, ... Suh HW. Modulatory effect of ginseng total saponin on dopamine release and tyrosine hydroxylase gene expression induced by nicotine in the rat. ] J Ethnopharmacol. 2000 May;70(2):161-9.
 Kim SE, Shim I, Chung JK, Lee MC. Effect of ginseng saponins on enhanced dopaminergic transmission and locomotor hyperactivity induced by nicotine. Neuropsychopharmacology. 2006 Aug;31(8):1714-21. Epub 2005 Oct 26.
 Sershen H, Harsing LG Jr ... Lajtha A. Effect of acetyl-L-carnitine on the dopaminergic system in aging brain. J Neurosci Res. 1991 Nov;30(3):555-9.
 Singh S, Mishra A, ... Shukla S. Acetyl-L-Carnitine via Upegulating Dopamine D1 Receptor and Attenuating Microglial Activation Prevents Neuronal Loss and Improves Memory Functions in Parkinsonian Rats. Mol Neurobiol. 2018 Jan;55(1):583-602. doi: 10.1007/s12035-016-0293-5. Epub 2016 Dec 14.
 Tolu P, Masi F, ... Gambarana C. Effects of long-term acetyl-L-carnitine administration in rats: I. increased dopamine output in mesocorticolimbic areas and protection toward acute stress exposure. Neuropsychopharmacology. 2002 Sep;27(3):410-20.
 Robinson BL, Dumas M,... Kanungo J. Distinct effects of ketamine and acetyl L-carnitine on the dopamine system in zebrafish. Neurotoxicol Teratol. 2016 Mar-Apr;54:52-60. doi: 10.1016/j.ntt.2016.02.004. Epub 2016 Feb 16.
 Smeland OB, Meisingset TW, Borges K, Sonnewald U. Chronic acetyl-L-carnitine alters brain energy metabolism and increases noradrenaline and serotonin content in healthy mice. Neurochem Int. 2012 Jul;61(1):100-7. doi: 10.1016/j.neuint.2012.04.008. Epub 2012 Apr 23.
 Virmani A, Gaetani F, Imam S, Binienda Z, Ali S. Possible mechanism for the neuroprotective effects of L-carnitine on methamphetamine-evoked neurotoxicity. Ann N Y Acad Sci. 2003 May;993:197-207; discussion 287-8.
 Afshin-Majd S, Bashiri K, ... Roghani M. Acetyl-l-carnitine protects dopaminergic nigrostriatal pathway in 6-hydroxydopamine-induced model of Parkinson's disease in the rat. Biomed Pharmacother. 2017 May;89:1-9. doi: 10.1016/j.biopha.2017.02.007. Epub 2017 Feb 12.
 Chiechio S, Canonico PL, Grilli M. l-Acetylcarnitine: A Mechanistically Distinctive and Potentially Rapid-Acting Antidepressant Drug. Int J Mol Sci. 2017 Dec 21;19(1). pii: E11. doi: 10.3390/ijms19010011.
 Masi F, Leggio B, ... Gambarana C. Effects of long-term acetyl-L-carnitine administration in rats--II: Protection against the disrupting effect of stress on the acquisition of appetitive behavior. Neuropsychopharmacology. 2003 Apr;28(4):683-93. Epub 2002 Oct 1.
 Evcimen H, Mania I, Mathews M, Basil B. Psychosis Precipitated by Acetyl-l-Carnitine in a Patient With Bipolar Disorder. Prim Care Companion J Clin Psychiatry. 2007;9(1):71-2.
 Vance KM, Ribnicky DM, Hermann GE, Rogers RC. St. John's Wort enhances the synaptic activity of the nucleus of the solitary tract. Nutrition. 2014 Jul-Aug;30(7-8 Suppl):S37-42. doi: 10.1016/j.nut.2014.02.008. Epub 2014 Feb 28.
 Butterweck V, Böckers T, ... Winterhoff H. Long-term effects of St. John's wort and hypericin on monoamine levels in rat hypothalamus and hippocampus. Brain Res. 2002 Mar 15;930(1-2):21-9.
 Ben-Eliezer D, Yechiam E. Hypericum perforatum as a cognitive enhancer in rodents: A meta-analysis. Sci Rep. 2016 Oct 20;6:35700. doi: 10.1038/srep35700.
 Butterweck V, Böckers T, Korte B, Wittkowski W, Winterhoff H. Long-term effects of St. John's wort and hypericin on monoamine levels in rat hypothalamus and hippocampus. Brain Res. 2002 Mar 15;930(1-2):21-9.
 Nathan PJ. Hypericum perforatum (St John's Wort): a non-selective reuptake inhibitor? A review of the recent advances in its pharmacology. J Psychopharmacol. 2001 Mar;15(1):47-54.
 Yoshitake T, Iizuka R,... Kehr J. Hypericum perforatum L (St John's wort) preferentially increases extracellular dopamine levels in the rat prefrontal cortex. Br J Pharmacol. 2004 Jun;142(3):414-8. Epub 2004 May 17.
 Sarris J, Price LH, ... Mischoulon D. Is S-Adenosyl Methionine (SAMe) for Depression Only Effective in Males? A Re-Analysis of Data from a Randomized Clinical Trial. Pharmacopsychiatry. 2015 Jul;48(4-5):141-4. doi: 10.1055/s-0035-1549928. Epub 2015 May 26.
 Lee ES, Chen H, ... Charlton CG. The inhibitory role of methylation on the binding characteristics of dopamine receptors and transporter. Neurosci Res. 2004 Mar;48(3):335-44.
 Fava M, Rosenbaum JF, ... Pill L. Neuroendocrine effects of S-adenosyl-L-methionine, a novel putative antidepressant. J Psychiatr Res. 1990;24(2):177-84.
 Mellon SH. Neurosteroid regulation of central nervous system development. Pharmacol Ther. 2007 Oct;116(1):107-24. Epub 2007 Jun 16.
 Marx CE, Keefe RS, ... Shampine LJ. Proof-of-concept trial with the neurosteroid pregnenolone targeting cognitive and negative symptoms in schizophrenia. Neuropsychopharmacology. 2009 Jul;34(8):1885-903. doi: 10.1038/npp.2009.26. Epub 2009 Apr 1.
 Turkmen S, Backstrom T, ... Johansson IM. Tolerance to allopregnanolone with focus on the GABA-A receptor. Br J Pharmacol. 2011 Jan;162(2):311-27. doi: 10.1111/j.1476-5381.2010.01059.x.
 Sripada RK, Marx CE, ... Liberzon I. Allopregnanolone elevations following pregnenolone administration are associated with enhanced activation of emotion regulation neurocircuits. Biol Psychiatry. 2013 Jun 1;73(11):1045-53. doi: 10.1016/j.biopsych.2012.12.008. Epub 2013 Jan 21.
 Veiga S, Garcia-Segura LM, Azcoitia I. Neuroprotection by the steroids pregnenolone and dehydroepiandrosterone is mediated by the enzyme aromatase. J Neurobiol. 2003 Sep 15;56(4):398-406.
 Steiger A, Trachsel L, ... Holsboer F. Neurosteroid pregnenolone induces sleep-EEG changes in man compatible with inverse agonistic GABAA-receptor modulation. Brain Res. 1993 Jul 2;615(2):267-74.
 Muneoka KT, Takigawa M. A neuroactive steroid, pregnenolone, alters the striatal dopaminergic tone before and after puberty. Neuroendocrinology. 2002 May;75(5):288-95.
 Barrot M1, Vallée M, ...Piazza PV. The neurosteroid pregnenolone sulphate increases dopamine release and the dopaminergic response to morphine in the rat nucleus accumbens. Eur J Neurosci. 1999 Oct;11(10):3757-60.
 Wong P, Sze Y, Chang CC, Lee J, Zhang X. Pregnenolone sulfate normalizes schizophrenia-like behaviors in dopamine transporter knockout mice through the AKT/GSK3β pathway. Transl Psychiatry. 2015 Mar 17;5:e528. doi: 10.1038/tp.2015.21.
 Labrie F. DHEA, important source of sex steroids in men and even more in women. Prog Brain Res. 2010;182:97-148. doi: 10.1016/S0079-6123(10)82004-7.
 Catalina F, Milewich L, Frawley W, Kumar V, Bennett M. Decrease of core body temperature in mice by dehydroepiandrosterone. Exp Biol Med (Maywood). 2002 Jun;227(6):382-8.
 D'Astous M, Morissette M, ... Di Paolo T. Dehydroepiandrosterone (DHEA) such as 17beta-estradiol prevents MPTP-induced dopamine depletion in mice. Synapse. 2003 Jan;47(1):10-4.
 Wang L, Pooler AM, Albrecht MA, Wurtman RJ. Dietary uridine-5'-monophosphate supplementation increases potassium-evoked dopamine release and promotes neurite outgrowth in aged rats. J Mol Neurosci. 2005;27(1):137-45.
 Yamamoto T, Moriwaki Y, ... Hada T. Effect of beer on the plasma concentrations of uridine and purine bases. Metabolism: Clinical and Experimental 2002, 51 (10): 1317–23.
 Carver JD. Advances in nutritional modifications of infant formulas. The American Journal of Clinical Nutrition 2003 77 (6): 1550S–1554S.
 Wang L, Pooler AM, Albrecht MA, Wurtman RJ. Dietary uridine-5'-monophosphate supplementation increases potassium-evoked dopamine release and promotes neurite outgrowth in aged rats. J Mol Neurosci. 2005;27(1):137-45.
 Agarwal N, Sung YH, ... Renshaw PF. Short-term administration of uridine increases brain membrane phospholipid precursors in healthy adults: a 31-phosphorus magnetic resonance spectroscopy study at 4T. Bipolar Disord. 2010 Dec;12(8):825-33. doi: 10.1111/j.1399-5618.2010.00884.x.
 Yeh KY, Wu CH, Tai MY, Tsai YF. Ginkgo biloba extract enhances noncontact erection in rats: the role of dopamine in the paraventricular nucleus and the mesolimbic system. Neuroscience. 2011 Aug 25;189:199-206. doi: 10.1016/j.neuroscience.2011.05.025. Epub 2011 May 30.
 Yoshitake T, Yoshitake S, Kehr J. The Ginkgo biloba extract EGb 761(R) and its main constituent flavonoids and ginkgolides increase extracellular dopamine levels in the rat prefrontal cortex. Br J Pharmacol. 2010 Feb 1;159(3):659-68. doi: 10.1111/j.1476-5381.2009.00580.x. Epub 2010 Jan 25.
 Kehr J, Yoshitake S, Ijiri S, Koch E, Nöldner M, Yoshitake T. Ginkgo biloba leaf extract (EGb 761®) and its specific acylated flavonol constituents increase dopamine and acetylcholine levels in the rat medial prefrontal cortex: possible implications for the cognitive enhancing properties of EGb 761®. Int Psychogeriatr. 2012 Aug;24 Suppl 1:S25-34. doi: 10.1017/S1041610212000567.
 Beck SM, Ruge H, ... Goschke T. Effects of Ginkgo biloba extract EGb 761® on cognitive control functions, mental activity of the prefrontal cortex and stress reactivity in elderly adults with subjective memory impairment - a randomized double-blind placebo-controlled trial. Hum Psychopharmacol. 2016 May;31(3):227-42. doi: 10.1002/hup.2534.
 Fehske CJ, Leuner K, Müller WE. Ginkgo biloba extract (EGb761) influences monoaminergic neurotransmission via inhibition of NE uptake, but not MAO activity after chronic treatment. Pharmacol Res. 2009 Jul;60(1):68-73. doi: 10.1016/j.phrs.2009.02.012. Epub 2009 Mar 21.
 Mix JA, Crews WD Jr. A double-blind, placebo-controlled, randomized trial of Ginkgo biloba extract EGb 761 in a sample of cognitively intact older adults: neuropsychological findings. Hum Psychopharmacol. 2002 Aug;17(6):267-77.
 Cieza A, Maier P, Pöppel E. Effects of Ginkgo biloba on mental functioning in healthy volunteers. Arch Med Res. 2003 Sep-Oct;34(5):373-81.
 .Johansson MH, Westlind-Danielsson A. Forskolin-induced up-regulation and functional supersensitivity of dopamine D2long receptors expressed by Ltk- cells. Eur J Pharmacol. 1994 Oct 14;269(2):149-55
 Wanderoy MH, Westlind-Danielsson A. Molecular mechanisms underlying forskolin-mediated up-regulation of human dopamine D2L receptors. Cell Mol Neurobiol. 1997 Oct;17(5):547-55.
 Wanderoy MH, Westlind-Danielsson A, Ahlenius S. Dopamine D2 receptor upregulation in rat neostriatum following in vivo infusion of forskolin. Neuroreport. 1997 Sep 8;8(13):2971-6.
 Katz IR, Smith D, Makman MH. Forskolin stimulates the conversion of tyrosine to dopamine in catecholaminergic neural tissue. Brain Res. 1983 Mar 28;264(1):173-7.
 Alirezaei M. Betaine protects cerebellum from oxidative stress following levodopa and benserazide administration in rats. Iran J Basic Med Sci. 2015 Oct;18(10):950-7.
 Di Pierro F, Orsi R, Settembre R. Role of betaine in improving the antidepressant effect of S-adenosyl-methionine in patients with mild-to-moderate depression. J Multidiscip Healthc. 2015 Jan 16;8:39-45. doi: 10.2147/JMDH.S77766. eCollection 2015.
 Di Chiara G. Alcohol and dopamine. Alcohol Health Res World. 1997;21(2):108-14.
 Ma H, Zhu G. The dopamine system and alcohol dependence. Shanghai Arch Psychiatry. 2014 Apr;26(2):61-8. doi: 10.3969/j.issn.1002-0829.2014.02.002.
 Melis M, Diana M, Enrico P, Marinelli M, Brodie MS. Ethanol and acetaldehyde action on central dopamine systems: mechanisms, modulation, and relationship to stress. Alcohol. 2009 Nov;43(7):531-9. doi: 10.1016/j.alcohol.2009.05.004.
 Trantham-Davidson H, Chandler LJ. Alcohol-induced alterations in dopamine modulation of prefrontal activity. Alcohol. 2015 Dec;49(8):773-9. doi: 10.1016/j.alcohol.2015.09.001. Epub 2015 Oct 23.
 Ding ZM, Ingraham CM, Rodd ZA, McBride WJ. Alcohol drinking increases the dopamine-stimulating effects of ethanol and reduces D2 auto-receptor and group II metabotropic glutamate receptor function within the posterior ventral tegmental area of alcohol preferring (P) rats. Neuropharmacology. 2016 Oct;109:41-48. doi: 10.1016/j.neuropharm.2016.05.023. Epub 2016 May 31.
 Trantham-Davidson H, Burnett EJ, ... Chandler LJ. Chronic alcohol disrupts dopamine receptor activity and the cognitive function of the medial prefrontal cortex. J Neurosci. 2014 Mar 5;34(10):3706-18. doi: 10.1523/JNEUROSCI.0623-13.2014.
 Bustamante D, Quintanilla ME, ... Herrera-Marschitz M. Ethanol induces stronger dopamine release in nucleus accumbens (shell) of alcohol-preferring (bibulous) than in alcohol-avoiding (abstainer) rats. Eur J Pharmacol. 2008 Sep 4;591(1-3):153-8. doi: 10.1016/j.ejphar.2008.06.069. Epub 2008 Jun 24.
 Andres RH1, Huber AW, ... Widmer HR. Effects of creatine treatment on the survival of dopaminergic neurons in cultured fetal ventral mesencephalic tissue. Neuroscience. 2005;133(3):701-13.
 Cunha MP, Machado DG, ... Rodrigues AL. Antidepressant-like effect of creatine in mice involves dopaminergic activation. J Psychopharmacol. 2012 Nov;26(11):1489-501. doi: 10.1177/0269881112447989. Epub 2012 Jun 6.
 Riesberg LA, Weed SA, McDonald TL, Eckerson JM, Drescher KM. Beyond muscles: The untapped potential of creatine. Int Immunopharmacol. 2016 Aug;37:31-42. doi: 10.1016/j.intimp.2015.12.034. Epub 2016 Jan 8.
 Andres RH, Ducray AD, Pérez... Widmer HR. Creatine supplementation improves dopaminergic cell survival and protects against MPP+ toxicity in an organotypic tissue culture system. Cell Transplant. 2005;14(8):537-50.
 Beal MF. Neuroprotective effects of creatine. Amino Acids. 2011 May;40(5):1305-13. doi: 10.1007/s00726-011-0851-0. Epub 2011 Mar 30.
 Cunha MP, Martín-de-Saavedra MD, ... López MG. Both creatine and its product phosphocreatine reduce oxidative stress and afford neuroprotection in an in vitro Parkinson's model. ASN Neuro. 2014 Nov 24;6(6). pii: 1759091414554945. doi: 10.1177/1759091414554945. Print 2014.
 Greenway SE, Pack AT, Greenway FL. Treatment of depression with cyproheptadine. Pharmacotherapy. 1995 May-Jun;15(3):357-60.
 Dabaghzadeh F1, Ghaeli P, ... Khazaeipour Z. Cyproheptadine for prevention of neuropsychiatric adverse effects of efavirenz: a randomized clinical trial. AIDS Patient Care STDS. 2013 Mar;27(3):146-54. doi: 10.1089/apc.2012.0410. Epub 2013 Feb 26.
 Konstandi M, Kolijianni A, Sfikakis AD. Effect of cyproheptadine treatment on conditioned avoidance response in female rats. Gen Pharmacol. 1996 Dec;27(8):1401-3.
 Plonk J, Feldman J. Modification of adrenal function by the anti-serotonin agent cyproheptadine. J Clin Endocrinol Metab. 1976 Feb;42(2):291-5.
 Delitala G, Masala A, Alagna S, Devilla L. Effect of cyproheptadine on the spontaneous diurnal variations of plasma ACTH-cortisol and ACTH-GH secretion induced by l-dopa. Biomedicine. 1975 Dec 20;23(10):406-9.
 Krieger DT, Amorosa L, Linick F. Cyproheptadine-induced remission of Cushing's disease. N Engl J Med. 1975 Oct 30;293(18):893-6.
 Mogilnicka E, Scheel-Krüger J, Klimek V, Golembiowska-Nikitin K. The influence of antiserotonergic agents on the action of dopaminergic drugs. Pol J Pharmacol Pharm. 1977 Jan-Feb;29(1):31-8.
 Opacka-Juffry J, Ashworth S, Ahier RG, Hume SP. Modulatory effects of L-DOPA on D2 dopamine receptors in rat striatum, measured using in vivo microdialysis and PET. J Neural Transm (Vienna). 1998;105(4-5):349-64.
 Murata M, Kanazawa I. Repeated L-dopa administration reduces the ability of dopamine storage and abolishes the supersensitivity of dopamine receptors in the striatum of intact rat. Neurosci Res. 1993 Jan;16(1):15-23.
 Snyder GL, Zigmond MJ. The effects of L-dopa on in vitro dopamine release from striatum. Brain Res. 1990 Feb 5;508(2):181-7.
 Schneider MB, Murrin LC, Pfeiffer RF, Deupree JD. Dopamine receptors: effects of chronic L-dopa and bromocriptine treatment in an animal model of Parkinson's disease. Clin Neuropharmacol. 1984;7(3):247-57.
 Guatteo E, Yee A, ... Lipski J. Dual effects of L-DOPA on nigral dopaminergic neurons. Exp Neurol. 2013 Sep;247:582-94. doi: 10.1016/j.expneurol.2013.02.009. Epub 2013 Feb 26.
 Borah A, Mohanakumar KP. Long-term L-DOPA treatment causes indiscriminate increase in dopamine levels at the cost of serotonin synthesis in discrete brain regions of rats. Cell Mol Neurobiol. 2007 Dec;27(8):985-96. Epub 2007 Oct 13.
 García NH, Berndt TJ, Tyce GM, Knox FG. Chronic oral L-DOPA increases dopamine and decreases serotonin excretions. Am J Physiol. 1999 Nov;277(5):R1476-80. doi: 10.1152/ajpregu.1999.277.5.R1476.
 Siciliano CA, Fordahl SC, Jones SR. Cocaine Self-Administration Produces Long-Lasting Alterations in Dopamine Transporter Responses to Cocaine. J Neurosci. 2016 Jul 27;36(30):7807-16. doi: 10.1523/JNEUROSCI.4652-15.2016.
 Verma V. Classic Studies on the Interaction of Cocaine and the Dopamine Transporter. Clin Psychopharmacol Neurosci. 2015 Dec 31;13(3):227-38. doi: 10.9758/cpn.2015.13.3.227
 Kiyatkin EA. Dopamine mechanisms of cocaine addiction. Int J Neurosci. 1994 Sep;78(1-2):75-101.
 Venton BJ, Seipel AT, ... Wightman RM. Cocaine increases dopamine release by mobilization of a synapsin-dependent reserve pool. J Neurosci. 2006 Mar 22;26(12):3206-9.
 Hummel M, Unterwald EM. D1 dopamine receptor: a putative neurochemical and behavioral link to cocaine action. J Cell Physiol. 2002 Apr;191(1):17-27.
 Volkow ND, Fowler JS, Wang GJ. Imaging studies on the role of dopamine in cocaine reinforcement and addiction in humans. J Psychopharmacol. 1999 Dec;13(4):337-45.
 Wang GJ, Volkow ND, ... Swanson JM. Long-term stimulant treatment affects brain dopamine transporter level in patients with attention deficit hyperactive disorder. PLoS One. 2013 May 15;8(5):e63023. doi: 10.1371/journal.pone.0063023. Print 2013.
 Sadasivan S, Pond BB, Pani AK, Qu C, Jiao Y, Smeyne RJ. Methylphenidate exposure induces dopamine neuron loss and activation of microglia in the basal ganglia of mice. PLoS One. 2012;7(3):e33693. doi: 10.1371/journal.pone.0033693. Epub 2012 Mar 21.
 Engert V, Pruessner JC. Dopaminergic and noradrenergic contributions to functionality in ADHD: the role of methylphenidate. Curr Neuropharmacol. 2008 Dec;6(4):322-8. doi: 10.2174/157015908787386069.
 Calipari ES, Ferris MJ, ... Jones SR. Methylphenidate amplifies the potency and reinforcing effects of amphetamines by increasing dopamine transporter expression. Nat Commun. 2013;4:2720. doi: 10.1038/ncomms3720.
 Kodama T, Kojima T, ... Watanabe M. Oral Administration of Methylphenidate (Ritalin) Affects Dopamine Release Differentially Between the Prefrontal Cortex and Striatum: A Microdialysis Study in the Monkey. J Neurosci. 2017 Mar 1;37(9):2387-2394. doi: 10.1523/JNEUROSCI.2155-16.2017. Epub 2017 Feb 2.
 Morton WA, Stockton GG. Methylphenidate Abuse and Psychiatric Side Effects. Prim Care Companion J Clin Psychiatry. 2000 Oct;2(5):159-164.
 Yanofski J. The Dopamine Dilemma-Part II: Could Stimulants Cause Tolerance, Dependence, and Paradoxical Decompensation? Innov Clin Neurosci. 2011 Jan;8(1):47-53.
 Joyce BM, Glaser PE, Gerhardt GA. Adderall produces increased striatal dopamine release and a prolonged time course compared to amphetamine isomers. Psychopharmacology (Berl). 2007 Apr;191(3):669-77. Epub 2006 Oct 10.
 Berman SM, Kuczenski R, McCracken JT, London ED. Potential adverse effects of amphetamine treatment on brain and behavior: a review. Mol Psychiatry. 2009 Feb;14(2):123-42. doi: 10.1038/mp.2008.90. Epub 2008 Aug 12.
 Lakhan SE, Kirchgessner A. Prescription stimulants in individuals with and without attention deficit hyperactivity disorder: misuse, cognitive impact, and adverse effects. Brain Behav. 2012 Sep;2(5):661-77. doi: 10.1002/brb3.78. Epub 2012 Jul 23.
 Novak G, Seeman P, Le Foll B. Exposure to nicotine produces an increase in dopamine D2(High) receptors: a possible mechanism for dopamine hypersensitivity. Int J Neurosci. 2010 Nov;120(11):691-7. doi: 10.3109/00207454.2010.513462.
 Herman AI, DeVito EE, Jensen KP, Sofuoglu M. Pharmacogenetics of nicotine addiction: role of dopamine. Pharmacogenomics. 2014 Feb;15(2):221-34. doi: 10.2217/pgs.13.246.
 Pidoplichko VI, DeBiasi M, Williams JT, Dani JA. Nicotine activates and desensitizes midbrain dopamine neurons. Nature. 1997 Nov 27;390(6658):401-4.
 Perez XA, Ly J, McIntosh JM, Quik M. Long-term nicotine exposure depresses dopamine release in nonhuman primate nucleus accumbens. J Pharmacol Exp Ther. 2012 Aug;342(2):335-44. doi: 10.1124/jpet.112.194084. Epub 2012 May 4.
 Joshi YB, Friend SF, Jimenez B, Steiger LR. Dissociative Intoxication and Prolonged Withdrawal Associated With Phenibut: A Case Report. J Clin Psychopharmacol. 2017 Aug;37(4):478-480. doi: 10.1097/JCP.0000000000000731.
 Lapin I. Phenibut (beta-phenyl-GABA): a tranquilizer and nootropic drug. CNS Drug Rev. 2001 Winter;7(4):471-81.
 Loland CJ, Mereu M, ... Newman AH. R-modafinil (armodafinil): a unique dopamine uptake inhibitor and potential medication for psychostimulant abuse. Biol Psychiatry. 2012 Sep 1;72(5):405-13. doi: 10.1016/j.biopsych.2012.03.022. Epub 2012 Apr 25.
 Andersen ML, Kessler E, ... Howell LL. Dopamine transporter-related effects of modafinil in rhesus monkeys. Psychopharmacology (Berl). 2010 Jun;210(3):439-48. doi: 10.1007/s00213-010-1839-2. Epub 2010 Apr 13.
 Mereu M, Bonci A, Newman AH, Tanda G. The neurobiology of modafinil as an enhancer of cognitive performance and a potential treatment for substance use disorders. Psychopharmacology (Berl). 2013 Oct;229(3):415-34. doi: 10.1007/s00213-013-3232-4. Epub 2013 Aug 10.
 Young JW, Geyer MA. Action of modafinil--increased motivation via the dopamine transporter inhibition and D1 receptors? Biol Psychiatry. 2010 Apr 15;67(8):784-7. doi: 10.1016/j.biopsych.2009.12.015. Epub 2010 Feb 4.
 Volkow ND, Fowler JS,... Apelskog-Torres K. Effects of modafinil on dopamine and dopamine transporters in the male human brain: clinical implications. JAMA. 2009 Mar 18;301(11):1148-54. doi: 10.1001/jama.2009.351.
 Moe RO, Nordgreen J, ... Bakken M. Effects of haloperidol, a dopamine D2-like receptor antagonist, on reward-related behaviors in laying hens. Physiol Behav. 2011 Mar 1;102(3-4):400-5. doi: 10.1016/j.physbeh.2010.12.008. Epub 2010 Dec 14.
 Fox CA, Mansour A, Watson SJ Jr. The effects of haloperidol on dopamine receptor gene expression. Exp Neurol. 1994 Dec;130(2):288-303.
 Lidsky TI, Banerjee SP. Acute administration of haloperidol enhances dopaminergic transmission. J Pharmacol Exp Ther. 1993 Jun;265(3):1193-8.
 Zanatta G, Nunes G, ... Gottfried C. Antipsychotic haloperidol binding to the human dopamine D3 receptor: beyond docking through QM/MM refinement toward the design of improved schizophrenia medicines. ACS Chem Neurosci. 2014 Oct 15;5(10):1041-54. doi: 10.1021/cn500111e. Epub 2014 Sep 18.
 Saeedi H, Remington G, Christensen BK. Impact of haloperidol, a dopamine D2 antagonist, on cognition and mood. Schizophr Res. 2006 Jul;85(1-3):222-31. Epub 2006 May 6.
 Carlson SW, Dixon CE. Lithium Improves Dopamine Neurotransmission and Increases Dopaminergic Protein Abundance in the Striatum after Traumatic Brain Injury. J Neurotrauma. 2018 Dec 1;35(23):2827-2836. doi: 10.1089/neu.2017.5509. Epub 2018 Aug 13.
 Staunton DA, Magistretti PJ, Shoemaker WJ, Deyo SN, Bloom FE. Effects of chronic lithium treatment on dopamine receptors in the rat corpus striatum. II. No effect on denervation or neuroleptic-induced supersensitivity. Brain Res. 1982 Jan 28;232(2):401-12.
 Alevizos B, Alevizos E, Leonardou A, Zervas I. Low dosage lithium augmentation in venlafaxine resistant depression: an open-label study. Psychiatriki. 2012 Apr-Jun;23(2):143-8.
 Blier P, de Montigny C, Tardif D. Short-term lithium treatment enhances responsiveness of postsynaptic 5-HT1A receptors without altering 5-HT autoreceptor sensitivity: an electrophysiological study in the rat brain. Synapse. 1987;1(3):225-32.
 Kameda K, Miura J, ... Koyama T. Effects of lithium on dopamine D2 receptor expression in the rat brain striatum. J Neural Transm (Vienna). 2001;108(3):321-34.
 Stamford JA, Kruk ZL, Millar J. Striatal dopamine terminals release serotonin after 5-HTP pretreatment: in vivo voltammetric data. Brain Res. 1990 May 7;515(1-2):173-80.
 Trachte GJ, Uncini T, Hinz M. Both stimulatory and inhibitory effects of dietary 5-hydroxytryptophan and tyrosine are found on urinary excretion of serotonin and dopamine in a large human population. Neuropsychiatr Dis Treat. 2009;5:227-35. Epub 2009 May 20.
 Molina-Holgado E, Dewar KM, Descarries L, Reader TA. Altered dopamine and serotonin metabolism in the dopamine-denervated and serotonin-hyperinnervated neostriatum of adult rat after neonatal 6-hydroxydopamine. J Pharmacol Exp Ther. 1994 Aug;270(2):713-21.
 Rada P, Avena NM, Hoebel BG. Daily bingeing on sugar repeatedly releases dopamine in the accumbens shell. Neuroscience. 2005;134(3):737-44.
 Murray S, Tulloch A, Criscitelli K, Avena NM. Recent studies of the effects of sugars on brain systems involved in energy balance and reward: Relevance to low calorie sweeteners. Physiol Behav. 2016 Oct 1;164(Pt B):504-508. doi: 10.1016/j.physbeh.2016.04.004. Epub 2016 Apr 9.
 Miranda MI, Rangel-Hernández JA, ... Núñez-Jaramillo L. The role of dopamine D2 receptors in the nucleus accumbens during taste-aversive learning and memory extinction after long-term sugar consumption. Neuroscience. 2017 Sep 17;359:142-150. doi: 10.1016/j.neuroscience.2017.07.009. Epub 2017 Jul 14.
 Naneix F, Darlot F, ... Cador M. Protracted motivational dopamine-related deficits following adolescence sugar overconsumption. Neuropharmacology. 2018 Feb;129:16-25. doi: 10.1016/j.neuropharm.2017.11.021. Epub 2017 Nov 13.
 Overstreet DH, Crocker AD, ... Crocker JM. Alterations in the dopaminergic system and behaviour in rats reared on iodine-deficient diets. Pharmacol Biochem Behav. 1984 Oct;21(4):561-5.
 Crocker AD, Overstreet DH, Crocker JM. Hypothyroidism leads to increased dopamine receptor sensitivity and concentration. Pharmacol Biochem Behav. 1986 Jun;24(6):1593-7.
 Eskildsen PC, Kirkegaard CB. The influence of thyroid disorders on the dopaminergic regulation of prolactin, thyrotropin and growth hormone. J Endocrinol Invest. 1985 Oct;8(5):427-31.
 Feek CM, Sawers JS, ... Toft AD. Influence of thyroid status on dopaminergic inhibition of thyrotropin and prolactin secretion: evidence for an additional feedback mechanism in the control of thyroid hormone secretion. J Clin Endocrinol Metab. 1980 Sep;51(3):585-9.
 Oh-Nishi A , Saji M, Furudate SI, Suzuki N. Dopamine D(2)-like receptor function is converted from excitatory to inhibitory by thyroxine in the developmental hippocampus. J Neuroendocrinol. 2005 Dec;17(12):836-45.
 Dieguez C, Peters JR, ... Scanlon MF. Thyroid function in patients with hyperprolactinaemia: relationship to dopaminergic inhibition of TSH release. Clin Endocrinol (Oxf). 1986 Oct;25(4):435-40.
 Sasaki A, Hanew K, Sato S, Yoshinaga K. Evidence for endogenous dopaminergic regulation of thyrotropin (TSH) secretion in man. Tohoku J Exp Med. 1983 Jan;139(1):1-7.
 Chung J, Chang S, Kim Y, Shin H. Zinc increases the excitability of dopaminergic neurons in rat substantia nigra. Neurosci Lett. 2000 Jun 9;286(3):183-6.
 Turner TY, Soliman MR. Effects of zinc on spatial reference memory and brain dopamine (D1) receptor binding kinetics in rats. Prog Neuropsychopharmacol Biol Psychiatry. 2000 Oct;24(7):1203-17.
 Schetz JA, Chu A, Sibley DR. Zinc modulates antagonist interactions with D2-like dopamine receptors through distinct molecular mechanisms. J Pharmacol Exp Ther. 1999 May;289(2):956-64.
 Doboszewska U, Wlaź P, ... Młyniec K. Zinc in the Monoaminergic Theory of Depression: Its Relationship to Neural Plasticity. Neural Plast. 2017;2017:3682752. doi: 10.1155/2017/3682752. Epub 2017 Feb 19.
 Youdim MB, Ben-Shachar D, Ashkenazi R, Yehuda S. Brain iron and dopamine receptor function. Adv Biochem Psychopharmacol. 1983;37:309-21.
 Pino JMV, da Luz MHM, ... Lee KS. Iron-Restricted Diet Affects Brain Ferritin Levels, Dopamine Metabolism and Cellular Prion Protein in a Region-Specific Manner. Front Mol Neurosci. 2017 May 17;10:145. doi: 10.3389/fnmol.2017.00145. eCollection 2017.
 Jellen LC, Lu L, ... Jones BC. Iron deficiency alters expression of dopamine-related genes in the ventral midbrain in mice. Neuroscience. 2013 Nov 12;252:13-23. doi: 10.1016/j.neuroscience.2013.07.058. Epub 2013 Aug 1.
 Yien YY, Paw BH. A role for iron deficiency in dopaminergic neurodegeneration. Proc Natl Acad Sci U S A. 2016 Mar 29;113(13):3417-8. doi: 10.1073/pnas.1601976113. Epub 2016 Mar 16.
 Matak P, Matak A, ... Andrews NC. Disrupted iron homeostasis causes dopaminergic neurodegeneration in mice. Proc Natl Acad Sci U S A. 2016 Mar 29;113(13):3428-35. doi: 10.1073/pnas.1519473113. Epub 2016 Feb 29.
 Symes AL, Sourkes TL ... Birnbaum H. Decreased monoamine oxidase activity in liver of iron-deficient rats. Can J Biochem. 1969 Nov;47(11):999-1002.
 Youdim MB, Green AR. Iron deficiency and neurotransmitter synthesis and function. Proc Nutr Soc. 1978 Sep;37(2):173-9.
 Hare DJ, Double KL. Iron and dopamine: a toxic couple. Brain. 2016 Apr;139(Pt 4):1026-35.
 Li Y, Kim J, ... Wessling-Resnick M. Severe postnatal iron deficiency alters emotional behavior and dopamine levels in the prefrontal cortex of young male rats. Nutr. 2011 Dec;141(12):2133-8. doi: 10.3945/jn.111.145946. Epub 2011 Oct 19.
 Lozoff B, Corapci F, ... Black M. Preschool-aged children with iron deficiency anemia show altered affect and behavior. J Nutr. 2007 Mar;137(3):683-9.
 Yehuda S, Youdim MB. Brain iron: a lesson from animal models. Am J Clin Nutr. 1989 Sep;50(3 Suppl):618-25; discussion 625-9. doi: 10.1093/ajcn/50.3.618.
 Rasekh HR1, Davis MD, ... Soliman KF. The effect of selenium on the central dopaminergic system: a microdialysis study. Life Sci. 1997;61(11):1029-35.
 Castaño A, Ayala A, ..., Machado A. Low selenium diet increases the dopamine turnover in prefrontal cortex of the rat. Neurochem Int. 1997 Jun;30(6):549-55.
 Solovyev ND. Importance of selenium and selenoprotein for brain function: From antioxidant protection to neuronal signalling. J Inorg Biochem. 2015 Dec;153:1-12. doi: 10.1016/j.jinorgbio.2015.09.003. Epub 2015 Sep 15.
 Naderi M, Ferrari MCO, ... Niyogi S. Maternal Exposure to Dietary Selenium Causes Dopaminergic Hyperfunction and Cognitive Impairment in Zebrafish Offspring. Environ Sci Technol. 2018 Nov 20;52(22):13574-13583. doi: 10.1021/acs.est.8b04768. Epub 2018 Oct 30.
 Khan HA. Selenium partially reverses the depletion of striatal dopamine and its metabolites in MPTP-treated C57BL mice. Neurochem Int. 2010 Nov;57(5):489-91. doi: 10.1016/j.neuint.2010.06.020. Epub 2010 Jul 7.
 Watanabe M, George SR, Seeman P. Regulation of anterior pituitary D2 dopamine receptors by magnesium and sodium ions. J Neurochem. 1985 Dec;45(6):1842-9.
 Vink R. Magnesium in the Central Nervous System. Magnesium in Parkinson’s disease: an update in clinical and basic aspects. University of Adelaide Press; 2011.
 Mena MA, Garcia de Yébenes MJ, ... Garcia de Yébenes J. Effects of calcium antagonists on the dopamine system. Clin Neuropharmacol. 1995 Oct;18(5):410-26.
 Leviel V, Valérie O, Guibert B. The Role of Calcium Ions in Dopamine Synthesis and Dopamine Release. The Basal Ganglia IV: 403-409
 Zhou WL, Antic SD. Rapid dopaminergic and GABAergic modulation of calcium and voltage transients in dendrites of prefrontal cortex pyramidal neurons. J Physiol. 2012 Aug 15;590(16):3891-911. doi: 10.1113/jphysiol.2011.227157. Epub 2012 May 28.
 Ericson M, Molander A, Stomberg R, Söderpalm B. Taurine elevates dopamine levels in the rat nucleus accumbens; antagonism by strychnine. Eur J Neurosci. 2006 Jun;23(12):3225-9.
 Chen VC, Chiu CC, ... Tzang BS. Effects of taurine on striatal dopamine transporter expression and dopamine uptake in SHR rats. Behav Brain Res. 2018 Aug 1;348:219-226. doi: 10.1016/j.bbr.2018.04.031. Epub 2018 Apr 22.
 Guilarte TR. Effect of vitamin B-6 nutrition on the levels of dopamine, dopamine metabolites, dopa decarboxylase activity, tyrosine, and GABA in the developing rat corpus striatum. Neurochem Res. 1989 Jun;14(6):571-8.
 Weir MR, Keniston RC, Enriquez JI Sr, McNamee GA. Depression of vitamin B6 levels due to dopamine. Vet Hum Toxicol. 1991 Apr;33(2):118-21.
 Stahl SM. L-methylfolate: a vitamin for your monoamines. J Clin Psychiatry. 2008 Sep;69(9):1352-3.
 Duan W, Ladenheim B, ... Mattson MP. Dietary folate deficiency and elevated homocysteine levels endanger dopaminergic neurons in models of Parkinson's disease. J Neurochem. 2002 Jan;80(1):101-10.
 Miller AL. The methylation, neurotransmitter, and antioxidant connections between folate and depression. Altern Med Rev. 2008 Sep;13(3):216-26.
 Deana R, Vincenti E, Deana AD. Levels of neurotransmitters in brain of vitamin B12 deficient rats. Int J Vitam Nutr Res. 1977;47(2):119-22.
 de Lau LM, Koudstaal PJ, ... Breteler MM. Dietary folate, vitamin B12, and vitamin B6 and the risk of Parkinson disease. Neurology. 2006 Jul 25;67(2):315-8.
 Lövblad K, Ramelli G, Remonda L, ... Schroth G. Retardation of myelination due to dietary vitamin B12 deficiency: cranial MRI findings. Pediatr Radiol. 1997 Feb;27(2):155-8.
 Giménez R, Raïch J, Aguilar J. Changes in brain striatum dopamine and acetylcholine receptors induced by chronic CDP-choline treatment of aging mice. Br J Pharmacol. 1991 Nov;104(3):575-8.
 Shibuya M, Kageyama N, ... Fujiwara M. Effects of CDP-choline on striatal dopamine level and behavior in rats. Jpn J Pharmacol. 1981 Feb;31(1):47-52.
 Secades JJ, Frontera G. CDP-choline: pharmacological and clinical review. Methods Find Exp Clin Pharmacol. 1995 Oct;17 Suppl B:1-54.
 Hryhorczuk C, Florea M, ... Fulton S. Dampened Mesolimbic Dopamine Function and Signaling by Saturated but not Monounsaturated Dietary Lipids. Neuropsychopharmacology. 2016 Feb;41(3):811-21. doi: 10.1038/npp.2015.207. Epub 2015 Jul 14.
 Dumas JA, Bunn JY,... Kien CL. Dietary saturated fat and monounsaturated fat have reversible effects on brain function and the secretion of pro-inflammatory cytokines in young women. Metabolism. 2016 Oct;65(10):1582-8. doi: 10.1016/j.metabol.2016.08.003. Epub 2016 Aug 9.
 Brenneman DE, Rutledge CO. Alteration of catecholamine uptake in cerebral cortex from rats fed a saturated fat diet. Brain Res. 1979 Dec 28;179(2):295-304.
 Goldberg LI. The role of dopamine receptors in the treatment of congestive heart failure. J Cardiovasc Pharmacol. 1989;14 Suppl 5:S19-27.
 Olsen NV. Effects of dopamine on renal haemodynamics tubular function and sodium excretion in normal humans. Dan Med Bull. 1998 Jun;45(3):282-97.
 Harris RC, Zhang MZ. Dopamine, the kidney, and hypertension. Curr Hypertens Rep. 2012 Apr;14(2):138-43. doi: 10.1007/s11906-012-0253-z.
 Choi MR, Kouyoumdzian NM, ... Fernández BE. Renal dopaminergic system: Pathophysiological implications and clinical perspectives. World J Nephrol. 2015 May 6;4(2):196-212. doi: 10.5527/wjn.v4.i2.196.
 Shnitko TA, Taylor SC,... Robinson DL. Acute phenylalanine/tyrosine depletion of phasic dopamine in the rat brain. Psychopharmacology (Berl). 2016 Jun;233(11):2045-2054. doi: 10.1007/s00213-016-4259-0. Epub 2016 Mar 5.
 Fernstrom JD, Fernstrom MH. Tyrosine, phenylalanine, and catecholamine synthesis and function in the brain. J Nutr. 2007 Jun;137(6 Suppl 1):1539S-1547S; discussion 1548S. doi: 10.1093/jn/137.6.1539S.
 Montioli R, Cellini B, Dindo M, Oppici E, Voltattorni CB. Interaction of human Dopa decarboxylase with L-Dopa: spectroscopic and kinetic studies as a function of pH. Biomed Res Int. 2013;2013:161456. doi: 10.1155/2013/161456. Epub 2013 May 26.
 Treseder SA, Jackson M, Jenner P. The effects of central aromatic amino acid DOPA decarboxylase inhibition on the motor actions of L-DOPA and dopamine agonists in MPTP-treated primates. Br J Pharmacol. 2000 Apr;129(7):1355-64.
 Olson CA, Thornton JA, Adam GE, Lieberman HR. Effects of 2 adenosine antagonists, quercetin and caffeine, on vigilance and mood. J Clin Psychopharmacol. 2010 Oct;30(5):573-8. doi: 10.1097/JCP.0b013e3181ee0f79.
 Alexander SP. Flavonoids as antagonists at A1 adenosine receptors. Phytother Res. 2006 Nov;20(11):1009-12.
 Sommer T, Hübner H, ... Clark T. Identification of the Beer Component Hordenine as Food-Derived Dopamine D2 Receptor Agonist by Virtual Screening a 3D Compound Database. Sci Rep. 2017 Mar 10;7:44201. doi: 10.1038/srep44201.
 Field T, Hernandez-Reif M, ... Kuhn C. Cortisol decreases and serotonin and dopamine increase following massage therapy. Int J Neurosci. 2005 Oct;115(10):1397-413.
 Landau AM, Chakravarty MM, Clark CM, Zis AP, Doudet DJ. Electroconvulsive therapy alters dopamine signaling in the striatum of non-human primates. Neuropsychopharmacology. 2011 Jan;36(2):511-8. doi: 10.1038/npp.2010.182. Epub 2010 Oct 13.
 Baldinger P, Lotan A, Frey R, Kasper S, Lerer B, Lanzenberger R. Neurotransmitters and electroconvulsive therapy. J ECT. 2014 Jun;30(2):116-21. doi: 10.1097/YCT.0000000000000138.
 Singh A, Kar SK. How Electroconvulsive Therapy Works?: Understanding the Neurobiological Mechanisms. Clin Psychopharmacol Neurosci. 2017 Aug 31;15(3):210-221. doi: 10.9758/cpn.2017.15.3.210.
 Arnsten AF. Stress signalling pathways that impair prefrontal cortex structure and function. Nat Rev Neurosci. 2009 Jun;10(6):410-22. doi: 10.1038/nrn2648.
 Isovich E, Mijnster MJ, Flügge G, Fuchs E. Chronic psychosocial stress reduces the density of dopamine transporters. Eur J Neurosci. 2000 Mar;12(3):1071-8.
 Yadid G, Pacak K, ... Goldstein DS. Glycine stimulates striatal dopamine release in conscious rats. Br J Pharmacol. 1993 Sep;110(1):50-3.
 Molander A, Söderpalm B. Glycine receptors regulate dopamine release in the rat nucleus accumbens. Alcohol Clin Exp Res. 2005 Jan;29(1):17-26.
 Previc FH. Dopamine and the origins of human intelligence. Brain Cogn. 1999 Dec;41(3):299-350.
 Verendeev A, Sherwood CC. Human Brain Evolution. Curr Opin Behav Sci. 2017 Aug;16:41-45. doi: 10.1016/j.cobeha.2017.02.003. Epub 2017 Mar 31.
 Previc FH. Thyroid hormone production in chimpanzees and humans: implications for the origins of human intelligence. Am J Phys Anthropol. 2002 Aug;118(4):402-3; discussion 404-5.
 Previc FH. A general theory concerning the prenatal origins of cerebral lateralization in humans. Psychol Rev. 1991 Jul;98(3):299-334.
 Previc FH, Declerck C, de Brabander B. Why your "head is in the clouds" during thinking: the relationship between cognition and upper space. Acta Psychol (Amst). 2005 Jan-Feb;118(1-2):7-24. Epub 2004 Nov 23.
 Previc FH. Prenatal influences on brain dopamine and their relevance to the rising incidence of autism. Med Hypotheses. 2007;68(1):46-60. Epub 2006 Sep 7.
 Beaulieu JM, Espinoza S, Gainetdinov RR. Dopamine receptors - IUPHAR Review 13. Br J Pharmacol. 2015 Jan;172(1):1-23.
 Mishra A, Singh S, Shukla S. Physiological and Functional Basis of Dopamine Receptors and Their Role in Neurogenesis: Possible Implication for Parkinson's disease. J Exp Neurosci. 2018 May 31;12:1179069518779829. doi: 10.1177/1179069518779829. eCollection 2018.
 Rangel-Barajas C, Coronel I, Florán B. Dopamine Receptors and Neurodegeneration. Aging Dis. 2015 Oct 1;6(5):349-68. doi: 10.14336/AD.2015.0330. eCollection 2015 Sep.
 Solinas M, Belujon P, Fernagut PO, Jaber M, Thiriet N. Dopamine and addiction: what have we learned from 40 years of research. J Neural Transm (Vienna). 2019 Apr;126(4):481-516. doi: 10.1007/s00702-018-1957-2. Epub 2018 Dec 19.
 Nutt DJ, Lingford-Hughes A, Erritzoe D, Stokes PR. The dopamine theory of addiction: 40 years of highs and lows. Nat Rev Neurosci. 2015 May;16(5):305-12. doi: 10.1038/nrn3939. Epub 2015 Apr 15.
 Chen W, Nong Z, Li Y, Huang J, Chen C, Huang L. Role of Dopamine Signaling in Drug Addiction. Curr Top Med Chem. 2017;17(21):2440-2455. doi: 10.2174/1568026617666170504100642.
 Schretlen DJ, van der Hulst EJ, Pearlson GD, Gordon B. A neuropsychological study of personality: trait openness in relation to intelligence, fluency, and executive functioning. J Clin Exp Neuropsychol. 2010 Dec;32(10):1068-73. doi: 10.1080/13803391003689770. Epub 2010 Apr 19.
 Deyoung CG. The neuromodulator of exploration: A unifying theory of the role of dopamine in personality. Front Hum Neurosci. 2013 Nov 14;7:762. doi: 10.3389/fnhum.2013.00762. eCollection 2013.
 Previc FH. The role of the extrapersonal brain systems in religious activity. Conscious Cogn. 2006 Sep;15(3):500-39. Epub 2006 Jan 24.
 Meiser J, Weindl D, Hiller K. Complexity of dopamine metabolism. Cell Commun Signal. 2013 May 17;11(1):34. doi: 10.1186/1478-811X-11-34.
 Juárez Olguín H, Calderón Guzmán D, ... Barragán Mejía G. The Role of Dopamine and Its Dysfunction as a Consequence of Oxidative Stress. Oxid Med Cell Longev. 2016;2016:9730467. doi: 10.1155/2016/9730467. Epub 2015 Dec 6.
 Ko JH, Strafella AP. Dopaminergic neurotransmission in the human brain: new lessons from perturbation and imaging. Neuroscientist. 2012 Apr;18(2):149-68. doi: 10.1177/1073858411401413. Epub 2011 May 2.
 Iyengar B. The melanocyte photosensory system in the human skin. Springerplus. 2013 Apr 12;2(1):158. doi: 10.1186/2193-1801-2-158. Print 2013 Dec.
 Ono K, Viet CT, ... Schmidt BL. Cutaneous pigmentation modulates skin sensitivity via tyrosinase-dependent dopaminergic signalling. Sci Rep. 2017 Aug 23;7(1):9181. doi: 10.1038/s41598-017-09682-4.
 Jerardino A, Marean CW. Shellfish gathering, marine paleoecology and modern human behavior: perspectives from cave PP13B, Pinnacle Point, South Africa. J Hum Evol. 2010 Sep-Oct;59(3-4):412-24. doi: 10.1016/j.jhevol.2010.07.003.
 Klein RG, Steele TE. Archaeological shellfish size and later human evolution in Africa. Proc Natl Acad Sci U S A. 2013 Jul 2;110(27):10910-5. doi: 10.1073/pnas.1304750110. Epub 2013 Jun 17.
 Loftus E, Lee-Thorp J, ... Sealy J. Seasonal scheduling of shellfish collection in the Middle and Later Stone Ages of southern Africa. J Hum Evol. 2019 Mar;128:1-16. doi: 10.1016/j.jhevol.2018.12.009. Epub 2019 Jan 10.
 Banday AA, Lokhandwala MF. Dopamine receptors and hypertension. Curr Hypertens Rep. 2008 Aug;10(4):268-75.
 Jose PA, Eisner GM, Felder RA. Regulation of blood pressure by dopamine receptors. Nephron Physiol. 2003;95(2):p19-27.
 Westbrook A, Braver TS. Dopamine Does Double Duty in Motivating Cognitive Effort. Neuron. 2016 Feb 17;89(4):695-710. doi: 10.1016/j.neuron.2015.12.029.
 Yoest KE, Cummings JA, Becker JB. Estradiol, dopamine and motivation. Cent Nerv Syst Agents Med Chem. 2014;14(2):83-9.
 Salamone JD, Pardo M, ... Correa M. Mesolimbic Dopamine and the Regulation of Motivated Behavior. Curr Top Behav Neurosci. 2016;27:231-57. doi: 10.1007/7854_2015_383.
 Castrellon JJ, Seaman KL, ... Samanez-Larkin GR. Individual Differences in Dopamine Are Associated with Reward Discounting in Clinical Groups But Not in Healthy Adults. J Neurosci. 2019 Jan 9;39(2):321-332. doi: 10.1523/JNEUROSCI.1984-18.2018. Epub 2018 Nov 16.
 Oberlin BG , Albrecht DS, ... Yoder KK. Monetary discounting and ventral striatal dopamine receptor availability in nontreatment-seeking alcoholics and social drinkers. Psychopharmacology (Berl). 2015 Jun;232(12):2207-16. doi: 10.1007/s00213-014-3850-5. Epub 2015 Jan 7.
 Kurniawan IT, Guitart-Masip M, Dolan RJ. Dopamine and effort-based decision making. Front Neurosci. 2011 Jun 21;5:81. doi: 10.3389/fnins.2011.00081. eCollection 2011.
 Di Domenico SI, Ryan RM. The Emerging Neuroscience of Intrinsic Motivation: A New Frontier in Self-Determination Research. Front Hum Neurosci. 2017 Mar 24;11:145. doi: 10.3389/fnhum.2017.00145. eCollection 2017.
 Kayser AS, Mitchell JM, Weinstein D, Frank MJ. Dopamine, locus of control, and the exploration-exploitation tradeoff. Neuropsychopharmacology. 2015 Jan;40(2):454-62. doi: 10.1038/npp.2014.193. Epub 2014 Jul 30.
 Ly V, Wang KS, Bhanji J, Delgado MR. A Reward-Based Framework of Perceived Control. Front Neurosci. 2019 Feb 12;13:65. doi: 10.3389/fnins.2019.00065. eCollection 2019.
 Kohno M, Ghahremani DG,... London ED. Risk-taking behavior: dopamine D2/D3 receptors, feedback, and frontolimbic activity. Cereb Cortex. 2015 Jan;25(1):236-45. doi: 10.1093/cercor/bht218. Epub 2013 Aug 21.
 Oswald LM, Wand GS, ... Brašić JR. Risky decision-making and ventral striatal dopamine responses to amphetamine: a positron emission tomography [(11)C]raclopride study in healthy adults. Neuroimage. 2015 Jun;113:26-36. doi: 10.1016/j.neuroimage.2015.03.022. Epub 2015 Mar 18.
 Costa VD, Tran VL, Turchi J, Averbeck BB. Dopamine modulates novelty seeking behavior during decision making. Behav Neurosci. 2014 Oct;128(5):556-66. doi: 10.1037/a0037128. Epub 2014 Jun 9.
 Zald DH, Cowan RL, ... Kessler RM. Midbrain dopamine receptor availability is inversely associated with novelty-seeking traits in humans. J Neurosci. 2008 Dec 31;28(53):14372-8. doi: 10.1523/JNEUROSCI.2423-08.2008.
 Ciarka A, Vincent JL, van de Borne P. The effects of dopamine on the respiratory system: friend or foe? Pulm Pharmacol Ther. 2007;20(6):607-15. Epub 2006 Oct 27.
 Cabezas GA, Israili ZH, Velasco M. The actions of dopamine on the airways. Am J Ther. 2003 Nov-Dec;10(6):477-86.
 Chester DS, DeWall CN, ... Jiang Y. Looking for reward in all the wrong places: dopamine receptor gene polymorphisms indirectly affect aggression through sensation-seeking. Soc Neurosci. 2016 Oct;11(5):487-94. doi: 10.1080/17470919.2015.1119191. Epub 2015 Dec 7.
 Crockett MJ, Siegel JZ, ... Dolan RJ. Dissociable Effects of Serotonin and Dopamine on the Valuation of Harm in Moral Decision Making. Curr Biol. 2015 Jul 20;25(14):1852-9. doi: 10.1016/j.cub.2015.05.021. Epub 2015 Jul 2.
 Aberg KC, Doell KC, Schwartz S. The "Creative Right Brain" Revisited: Individual Creativity and Associative Priming in the Right Hemisphere Relate to Hemispheric Asymmetries in Reward Brain Function. Cereb Cortex. 2017 Oct 1;27(10):4946-4959. doi: 10.1093/cercor/bhw288.
 Lhommée E, Batir A, ..., Krack P. Dopamine and the biology of creativity: lessons from Parkinson's disease. Front Neurol. 2014 Apr 22;5:55. doi: 10.3389/fneur.2014.00055. eCollection 2014.
 Boot N, Baas M, ... De Dreu CKW. Creative cognition and dopaminergic modulation of fronto-striatal networks: Integrative review and research agenda. Neurosci Biobehav Rev. 2017 Jul;78:13-23. doi: 10.1016/j.neubiorev.2017.04.007. Epub 2017 Apr 15.
 Smillie LD, Wacker J. Dopaminergic foundations of personality and individual differences. Front Hum Neurosci. 2014 Oct 30;8:874. doi: 10.3389/fnhum.2014.00874. eCollection 2014.
 Fischer R, Lee A, Verzijden MN. Dopamine genes are linked to Extraversion and Neuroticism personality traits, but only in demanding climates. Sci Rep. 2018 Jan 29;8(1):1733. doi: 10.1038/s41598-017-18784-y.
 Cohen MX, Young J, ... Ranganath C. Individual differences in extraversion and dopamine genetics predict neural reward responses. Brain Res Cogn Brain Res. 2005 Dec;25(3):851-61. Epub 2005 Nov 11.
 Ashok AH, Marques TR, ... Howes OD. The dopamine hypothesis of bipolar affective disorder: the state of the art and implications for treatment. Mol Psychiatry. 2017 May;22(5):666-679. doi: 10.1038/mp.2017.16. Epub 2017 Mar 14.
 Maier F, Merkl J, ... Timmermann L. Hypomania and mania related to dopamine replacement therapy in Parkinson's disease. Parkinsonism Relat Disord. 2014 Apr;20(4):421-7. doi: 10.1016/j.parkreldis.2014.01.001. Epub 2014 Jan 12.
 Kuo JR, Lin SS, .... Liu JM. Deep brain light stimulation effects on glutamate and dopamine concentration. Biomed Opt Express. 2014 Dec 3;6(1):23-31. doi: 10.1364/BOE.6.000023. eCollection 2015 Jan 1.
 Lima LAR, Lopes MJP,... Viana GSB. Vitamin D protects dopaminergic neurons against neuroinflammation and oxidative stress in hemiparkinsonian rats. J Neuroinflammation. 2018 Aug 31;15(1):249. doi: 10.1186/s12974-018-1266-6.
 Sedaghat K, Yousefian Z, ... Choobdar S. Mesolimbic dopamine system and its modulation by vitamin D in a chronic mild stress model of depression in the rat. Behav Brain Res. 2019 Jan 1;356:156-169. doi: 10.1016/j.bbr.2018.08.020. Epub 2018 Aug 23.
 Kesby JP, Turner KM, ... Burne THJ. Developmental vitamin D deficiency alters multiple neurotransmitter systems in the neonatal rat brain. Int J Dev Neurosci. 2017 Nov;62:1-7. doi: 10.1016/j.ijdevneu.2017.07.002. Epub 2017 Jul 14.
 Ziomber A, Thor P, ... Antkiewicz-Michaluk L. Chronic impairment of the vagus nerve function leads to inhibition of dopamine but not serotonin neurons in rat brain structures. Pharmacol Rep. 2012;64(6):1359-67.
 de la Presa Owens S, Innis SM. Docosahexaenoic and arachidonic acid prevent a decrease in dopaminergic and serotoninergic neurotransmitters in frontal cortex caused by a linoleic and alpha-linolenic acid deficient diet in formula-fed piglets. Nutr. 1999 Nov;129(11):2088-93.
 Zimmer L, Hembert S, ... Chalon S. Chronic n-3 polyunsaturated fatty acid diet-deficiency acts on dopamine metabolism in the rat frontal cortex: a microdialysis study. Neurosci Lett. 1998 Jan 16;240(3):177-81.
 Ahmad SO, Park JH, Radel JD, Levant B. Reduced numbers of dopamine neurons in the substantia nigra pars compacta and ventral tegmental area of rats fed an n-3 polyunsaturated fatty acid-deficient diet: a stereological study. Neurosci Lett. 2008 Jun 27;438(3):303-7. doi: 10.1016/j.neulet.2008.04.073. Epub 2008 Apr 25.
 Kuperstein F, Yakubov E, ... Yavin E. Overexpression of dopamine receptor genes and their products in the postnatal rat brain following maternal n-3 fatty acid dietary deficiency. J Neurochem. 2005 Dec;95(6):1550-62. Epub 2005 Nov 23.
Join Over 30,000+ Subscribers!