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Wanting and liking are different systems

By the Myo team

You can want something intensely and enjoy it barely at all. That isn't a character flaw: it's two dissociable brain systems, and only one of them sensitizes.

Here is an experience almost everyone has had and almost nobody has a decent explanation for.

You reach for the thing. You want it, really want it, and the pull is physical. You get it. And it's... fine. Mildly pleasant. Nothing close to the size of the wanting.

Then, twenty minutes later, you want it again.

The intuitive reading is that you're deceiving yourself, or weak, or that the wanting is somehow fake. The actual explanation is that wanting and liking are produced by different systems, and one of them can grow while the other doesn't.

The finding

Terry Robinson and Kent Berridge published the incentive-sensitization theory in 1993. Decades of follow-up work have tested it, and the central split has held up better than most ideas in the field.

The claim: mesolimbic dopamine mediates incentive motivation ("wanting", the pull toward a reward) but not the hedonic impact of that reward when you actually get it. "Liking" runs on different circuitry.

The evidence was awkward for everyone at the time, including its authors. In rats with almost all of their dopamine destroyed, a taste of sugar still produced the normal facial "liking" reactions: the same tongue protrusions and relaxed mouth movements a healthy rat makes. What those rats lost was the drive to go and get it. Push the system the other way and you see the mirror image. Animals with amplified dopamine signalling work harder and pursue more intensely, but their hedonic reactions to the reward itself don't grow. The wanting scales. The liking doesn't.

Berridge has said the result surprised him. He'd assumed, like nearly everyone, that dopamine was the pleasure molecule. It turned out to be closer to the pursuit molecule.

Where liking actually lives

If dopamine isn't making things feel good, something else is. Berridge and Morten Kringelbach's work maps pleasure to small "hedonic hotspots": small patches of tissue in the nucleus accumbens, ventral pallidum and a few other sites. Stimulate opioid or endocannabinoid signalling inside a hotspot and liking reactions increase. Stimulate dopamine in the same place and you get more wanting without more liking.

Two consequences fall out of the anatomy. Liking is a small, fragile system, easy to dampen and hard to inflate. Wanting is a large, sturdy system that can be recruited by almost any cue linked to reward. You would expect the bigger system to win most arguments, and it does.

How a cue earns its pull

Wanting attaches to cues, not just to rewards.

Wolfram Schultz's recordings from monkey dopamine neurons showed how this happens. At first the neurons fire when a reward arrives unexpectedly. After a few pairings, they fire to the cue that predicts the reward instead, and the reward itself barely registers. The cue has become the event.

Robinson and Berridge's term for what the cue acquires is incentive salience: it becomes attractive and attention-grabbing in its own right. A lock screen lighting up, the red badge, the first frame of a feed, the sound of a bag of crisps. The variable-ratio post covers why unpredictable rewards make cues especially sticky; this post is about what happens once they are.

Sensitization: the part that stings

The second half of the theory is where it starts explaining your life. Repeated exposure can sensitize the wanting system, making it more reactive rather than less, in a way that persists long after the exposure stops. And sensitization is selective. It amplifies wanting without amplifying liking.

So the gap doesn't stay constant. It widens. The pull gets stronger while the payoff stays flat or even fades, because tolerance and opponent processes chip away at the pleasure side at the same time.

This is why Robinson and Berridge's theory explains something withdrawal-based accounts struggle with: people relapse long after withdrawal has resolved, and long after the thing has stopped being enjoyable. If pursuit were driven by anticipated pleasure, that wouldn't happen. If pursuit runs on a separately sensitized system, it's exactly what you'd expect.

What the research shows, and where it stops

The core findings are solid. The leap to phones is not, and it's worth keeping those apart.

  • The original theory. Robinson and Berridge 1993 argued that repeated drug use sensitizes the dopamine systems that give cues incentive salience, while liking is not sensitized the same way. Limit: it is a theory of drug addiction. Applying it to apps or scrolling is an extrapolation, and this post is doing exactly that.
  • The dopamine depletion test. Berridge and Robinson 1998 reviewed the taste-reactivity work in rats with near-total dopamine loss and concluded dopamine mediates incentive salience, not hedonic impact or learning itself. Limit: rat taste reactions are a narrow window on pleasure.
  • The hotspots. Berridge and Kringelbach 2015 summarise the evidence that pleasure is generated by opioid and endocannabinoid hotspots, while dopamine supports wanting. Limit: a review, with hotspots mapped mainly in rodents.
  • Effort, not enjoyment. Salamone and Correa 2012 show that depleting accumbens dopamine shifts animals toward low-effort options but leaves food liking intact. Limit: mostly rodent data in a narrative review. The effort post picks up this thread.
  • Cues become the signal. Schultz, Dayan and Montague 1997 recorded the transfer of dopamine firing from reward to cue in monkeys. Limit: simple lab cues and single neurons.
  • A cue study that didn't hold. Ward et al. 2017 reported that the mere presence of your own phone on the desk, even switched off, lowered working-memory scores. It became a popular "cue drains you" story. Then Ruiz Pardo and Minda 2022 replicated the design and found no effect of phone location, and a 2023 meta-analysis found high heterogeneity across studies. So the safe claim is narrower: using and checking a phone costs attention. Whether its silent presence alone does is contested.
  • Cue timing matters in the field. Fitz et al. 2019 randomised 237 people for two weeks. Batching notifications three times a day improved attention, mood and sense of control, while removing notifications entirely raised anxiety and FOMO. Limit: self-report, mid-size sample, and Dan Ariely is a co-author, whose other work has faced integrity scrutiny.

Notice what is missing: nobody has measured dopamine sensitization in people who scroll. The theory gives a strong reason to expect the gap, not proof that it applies to you.

What this changes about self-blame

Most people run an implicit model where wanting something is evidence that it's good, and continuing to want something that isn't good is evidence of a defect in them.

Under the dissociation, that inference just doesn't hold. Wanting is a learned flag on a cue. It doesn't consult the system that evaluates whether the experience was any good.

You are not being irrational when you want something you no longer enjoy. You're reading one system's output and assuming it came from the other.

That reframe matters practically, not just emotionally. "Stop wanting it" is an instruction to a system that doesn't take instructions. "Change what the cues are doing" is an instruction that has somewhere to land.

Cue work you can do this week

The target is the cue, because that's where wanting attaches. Liking you leave alone, since nothing here is aimed at making things less pleasant.

  1. Map three cues. For three days, note what was happening in the ten seconds before you picked up the phone or the snack. A sound, a pause in conversation, a doorway, a feeling of being stuck. You are looking for the trigger.
  2. Remove the visual ones. Move the apps that pull hardest off the home screen and turn off badge counts. A cue you never see has nothing to fire on, and this is the cheapest step on the list.
  3. Batch the audible ones. Following Fitz 2019, route non-urgent notifications into two or three delivery windows a day instead of switching everything off, which in that trial backfired.
  4. Rate the payoff out loud. After the thing, give it a score from one to ten for how good it actually was. You are feeding the liking system's verdict back into awareness, so you can see the gap instead of just feeling the pull.
  5. Give the wanting somewhere else to go. Pair a cue you can't remove (the end of a meeting, the walk home) with a different first action. The how to stop doomscrolling guide has replacement ideas.

Measure success by how often the cue fires and how hard it pulls. If enjoyment itself has gone flat, that's a different problem, covered in how to enjoy things again.

Wanting and liking come apart, and only one of them sensitizes. The useful question isn't "why do I still want this when it isn't even good". It's which cues your wanting system has been trained on, and what happens when you change them.

How Myo uses this

Myo has no "liking" score. That's a design decision, not an omission.

In Myo's model, craving risk rises with a depleted modelled baseline, accumulated chronic load and the opposing process, never with pleasure. There's no term where enjoying something more reduces the pull, because in the literature it doesn't. Sensitization appears as an accumulator that strengthens with each prior peak, so a system trained harder generates more pull from the same input. Everything is computed from what you log; Myo does not measure dopamine or craving directly. The structure follows the published work, the weights are Myo's modelling choices, and both are labelled on the science page. For a quick sense of what self-report can and can't capture, here is why there is no at-home dopamine test.

FAQ

Why do I crave things I don't even enjoy anymore?

Because craving and enjoyment run on separate brain systems. Dopamine-driven "wanting" attaches to cues and can become more reactive with repetition, while "liking" is produced by small opioid and endocannabinoid hotspots that don't grow the same way. Robinson and Berridge's incentive-sensitization theory predicts exactly this gap. It was built on drug research, so treat the everyday version as a well-grounded extrapolation rather than a proven fact about you.

What is incentive salience?

Incentive salience is the quality that makes a cue attractive and attention-grabbing, so you feel pulled toward it. It is the "wanting" part of reward, and Berridge and Robinson argue that dopamine is what assigns it. A cue with high incentive salience, like a notification sound, can trigger the urge to act before you have consciously thought about whether you want the reward at all.

Can you want something without liking it?

Yes. In rat experiments, animals with almost all their dopamine destroyed still showed normal liking reactions to sugar but stopped working to get it. Boosting dopamine produced the reverse: more pursuit without more pleasure. In people, the everyday version is the reach for a phone or snack that ends in "that was fine" and a repeat twenty minutes later.

Why does craving come back after weeks without something?

The incentive-sensitization theory says the wanting system can stay sensitized long after use stops, so old cues can still trigger a strong pull even when withdrawal is over. That is why a familiar place, time of day or sound can set off craving after a long break. Changing or removing the cues tends to help more than waiting for the urge to fade on its own.

If I stop enjoying something, will I stop wanting it?

Not reliably. Because wanting and liking are separate, enjoyment can fall while craving stays the same or grows. Waiting for a habit to become unpleasant enough to quit rarely works on its own. Working on the cues that trigger the wanting tends to do more than trying to dislike the reward.

Sources

Myo models dopaminergic state from behavior; it does not measure dopamine. Not medical advice.

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