Dopamine is the most popular molecule of our time. No matter what your background is, if you have been alive during the 21st century, you have certainly heard a lot of praise on dopamine. People these days want to boost their dopamine because they have been told it is the molecule of pleasure, motivation, focus, and achievement. In this article, we are going to dig a bit deeper to try to understand what we are talking about when we are talking dopamine.

Previous Pop Icons

Before dopamine, the happy molecule was serotonin. During the rise of antidepressants like Prozac and other selective serotonin reuptake inhibitors (SSRIs), we were told serotonin was the solution to our mood problems.

Back then, millions of people used them on a daily basis, and still, we didn’t see waves of blissful citizens walking across the streets with a maniac smile on their faces. And so, we realized serotonin didn’t make you happy, maybe it just made you a bit calmer, less prone to extreme emotions, but for sure nothing similar to pure bliss.

Then dopamine took over.

Suddenly everybody was talking about it. If you weren’t the hyperfocused tech-entrepreneur, the successful businessman, or the competitive athlete you wanted to be, surely it was because you needed to boost your dopamine levels.

You ‘ve been told you should either get a prescription for a stimulant or take one of the many supplements that have been created to “enhance” dopamine. If you insisted to go the chemical-free way then at least you should read a blog about “dopamine fasting” so that you can “dopamine-detox” and “reset” your dopamine levels.

But what’s the truth about all this fuss?

The problem of Associating Neurotransmitters to Feelings

If you ask me what does dopamine do? My answer would be: what it does where? The problem of associating neurotransmitters to emotions is that it is a very simplistic view that doesn’t resemble reality.

When you eat meat, it gets broken into proteins, and proteins get broken into amino acids in your liver. One of these amino acids is tyrosine, and from the liver, it travels through your blood to your brain, where it will be converted into L-Dopa and then into dopamine.

And when I say to your brain, I mean all of it, not only certain parts. This is important because once tyrosine is converted into dopamine in neurons it will do different things depending on where in the brain these neurons are placed.

So dopamine is not only about focus or motivation, dopamine also has a crucial impact on other body functions like movement, memory, learning, sleep, cognition, and prolactin production.

This is the first takeaway: when we talk of boosting dopamine levels through diet or supplements, we cannot talk about enhancing one particular function, like focus or motivation, because tyrosine will be distributed to all parts of the brain where it will impact other functions at the same time.

In fact, the focus shouldn’t be on dopamine at all. Dopamine is just one of many neurotransmitters acting as a key to open the communication between neurons. There are also other chemicals like norepinephrine and epinephrine that act in a similar way, they bind to the receptor of the postsynaptic neuron and voilá, electrical impulses can flow from one neuron to another.

It is well known that many drugs target norepinephrine (NE) or epinephrine (EP) instead of dopamine and have similar effects. Actually, you can’t even have dopamine without NE or EP because dopamine is converted into norepinephrine by enzymes, and then norepinephrine is converted into epinephrine by other enzymes, and all of that happens very fast.

When you feel motivated, it is the electricity flowing in certain areas of your brain that makes you feel that way. As I mentioned in my previous article, you could just put a device zapping the brain in that area with electricity and you would feel the same, without dopamine involved at all.

Feelings and thoughts are not made of chemicals, they are made of just energy flowing from neuron to neuron, that’s all.

So even if dopamine is indeed involved in feelings of reward and motivation, it is not the cause of the positive valence of these emotions.

Therefore we could have fallen in love with neurons in the striatum instead, and it might happen one day. Then we would have “the striatum diet”, “striatum marketing”, and blogs about “how to boost neurons in your striatum”.

Cool, so now that we have clear the idea of different functions in different places, let’s see what we know about dopamine in the areas that interest us, that is the midbrain section called the mesolimbic pathway.

The Reward System Is Not About Rewards

When the media talk about “dopamine” they are generally speaking only about dopamine released from neurons in the midbrain towards the striatum, which is a neural pathway involved in making predictions and learning from them.

Imagine your paycheck comes with an extra bonus next month, that’s something you couldn’t expect, so it is a prediction error and a very positive one.

When something like this happens, a huge spike of dopamine is released in a short period of time in the synapses between neurons of a small part of the brain called the striatum. The function of this dopamine increase is to make neurons fire and signal a prediction error, which is crucial for survival.

This is the reward mechanism that has made dopamine famous.

Only that it is not about reward, it is about novelty.

Bear with me.

Let’s picture now the opposite situation, next month comes payday, and there is no money sent to your account. That’s another surprise, only that now there is no reward, it is indeed a very negative prediction error.

Well, guess what? A dopamine spike is released exactly in the same way as in the example before.

The Brain Prize of 2017 was awarded to scientists Peter Dayan, Ray Dolan, and Wolfram Schultz, for discovering that dopamine increase signals unexpected events, both positive and negative ones.

The implications of this research are huge, including disorders of decision-making in conditions such as gambling, drug addiction, compulsive behavior, and schizophrenia.

Even just normal things, like losing appeal for your favorite meal after eating a lot of it, or the unavoidable decrease in passion between lovers after the years, are better understood because of this mechanism.

Basically, we are programmed to react strongly to novelty, and learn from it. When novelty becomes normality, and we begin to expect something, there is no need to signal that event. Dopamine stops being released.

It is not a reward. Dopamine neurons do not fire when you get something good. They fire when you get something unexpected. And they sulk when you don’t get something you expected.

Pleasure and Motivation Are Not The Same Things

Rewards are both ‘liked’ and ‘wanted’, and those two words seem almost interchangeable. However, the prediction error mechanism that mediates the psychological process of ‘wanting’ a particular reward is dissociable from the circuitry that mediates the degree to which it is ‘liked’.

To put it in other words, one thing is desire, the craving, and another thing is the actual pleasure or enjoyment you obtain. In fact, many addictions and habits stop being pleasurable, or at least not so much as in the beginning, yet people keep craving them.

So the desire, the craving, or ‘wanting’, which is a form of motivation, is generated by this large neural and robust system we have described, mediated by mesolimbic dopamine.

By comparison, the actual pleasure or ‘liking’ that we derive from the things we like, is mediated by other smaller and fragile brain circuits, and they are not even dependent on dopamine.

The hedonic hotspots however have been identified in subcompartments within the nucleus accumbens shell, ventral pallidum, parabrachial nucleus, orbitofrontal cortex (OFC), and insular cortex. Other neurotransmitters and not dopamine, like opioids, endocannabinoids, and orexin are responsible for neurons firing and thus, enhancing liking in these hotspots.

The incentive-sensitization theory posits the essence of drug addiction to be excessive amplification specifically of psychological ‘wanting’, especially triggered by cues, without necessarily an amplification of ‘liking’.

This is due to long-lasting changes in dopamine-related motivation systems of susceptible individuals, called neural sensitization. A quarter-century after its proposal, evidence has continued to grow in support of the incentive-sensitization theory. Further, its scope is now expanding to include diverse behavioral addictions and other psychopathologies.