Not for the Sake of Pleasure Alone

bylukeprog7y11th Jun 2011133 comments

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When someone tells me that all human action is motivated by the desire for pleasure, or that we can solve the Friendly AI problem by programming a machine superintelligence to maximize pleasure, I use a two-step argument to persuade them that things are more complicated than that.

First, I present them with a variation on Nozick's experience machine,1 something like this:

Suppose that an advanced team of neuroscientists and computer scientists could hook your brain up to a machine that gave you maximal, beyond-orgasmic pleasure for the rest of an abnormally long life. Then they will blast you and the pleasure machine into deep space at near light-speed so that you could never be interfered with. Would you let them do this for you?

Most people say they wouldn't choose the pleasure machine. They begin to realize that even though they usually experience pleasure when they get what they desired, they want more than just pleasure. They also want to visit Costa Rica and have good sex and help their loved ones succeed.

But we can be mistaken when inferring our desires from such intuitions, so I follow this up with some neuroscience.


Wanting and liking

It turns out that the neural pathways for 'wanting' and 'liking' are separate, but overlap quite a bit. This explains why we usually experience pleasure when we get what we want, and thus are tempted to think that all we desire is pleasure. It also explains why we sometimes don't experience pleasure when we get what we want, and why we wouldn't plug in to the pleasure machine.

How do we know this? We now have objective measures of wanting and liking (desire and pleasure), and these processes do not always occur together.

liking expressionsOne objective measure of liking is 'liking expressions.' Human infants, primates, and rats exhibit homologous facial reactions to pleasant and unpleasant tastes.2 For example, both rats and human infants display rhythmic lip-licking movements when presented with sugary water, and both rats and human infants display a gaping reaction and mouth-wipes when presented with bitter water.3

Moreover, these animal liking expressions change in ways analogous to changes in human subjective pleasure. Food is more pleasurable to us when we are hungry, and sweet tastes elicit more liking expressions in rats when they are hungry than when they are full.4 Similarly, both rats and humans respond to intense doses of salt (more concentrated than in seawater) with mouth gapes and other aversive reactions, and humans report subjective displeasure. But if humans or rats are depleted of salt, both humans and rats react instead with liking expressions (lip-licking), and humans report subjective pleasure.5

Luckily, these liking and disliking expressions share a common evolutionary history, and use the same brain structures in rats, primates, and humans. Thus, fMRI scans have uncovered to some degree the neural correlates of pleasure, giving us another objective measure of pleasure.6

As for wanting, research has revealed that dopamine is necessary for wanting but not for liking, and that dopamine largely causes wanting.7

Now we are ready to explain how we know that we do not desire pleasure alone.

First, one can experience pleasure even if dopamine-generating structures have been destroyed or depleted.8 Chocolate milk still tastes just as pleasurable despite the severe reduction of dopamine neurons in patients suffering from Parkinson's disease,9 and the pleasure of amphetamine and cocaine persists throughout the use of dopamine-blocking drugs or dietary-induced dopamine depletion — even while these same treatments do suppress the wanting of amphetamine and cocaine.10

Second, elevation of dopamine causes an increase in wanting, but does not cause an increase in liking (when the goal is obtained). For example, mice with raised dopamine levels work harder and resist distractions more (compared to mice with normal dopamine levels) to obtain sweet food rewards, but they don't exhibit stronger liking reactions when they obtain the rewards.11 In humans, drug-induced dopamine increases correlate well with subjective ratings of 'wanting' to take more of the drug, but not with ratings of 'liking' that drug.12 In these cases, it becomes clear that we want some things besides the pleasure that usually results when we get what we want.

Indeed, it appears that mammals can come to want something that they have never before experienced pleasure when getting. In one study,13 researchers observed the neural correlates of wanting while feeding rats intense doses of salt during their very first time in a state of salt-depletion. That is, the rats had never before experienced intense doses of salt as pleasurable (because they had never been salt-depleted before), and yet they wanted salt the very first time they encountered it in a salt-depleted state. 

 

Commingled signals

But why are liking and wanting so commingled that we might confuse the two, or think that the only thing we desire is pleasure? It may be because the two different signals are literally commingled on the same neurons. Resarchers explain:

Multiplexed signals commingle in a manner akin to how wire and optical communication systems carry telephone or computer data signals from multiple telephone conversations, email communications, and internet web traffic over a single wire. Just as the different signals can be resolved at their destination by receivers that decode appropriately, we believe that multiple reward signals [liking, wanting, and learning] can be packed into the activity of single ventral pallidal neurons in much the same way, for potential unpacking downstream.

......we have observed a single neuron to encode all three signals... at various moments or in different ways (Smith et al., 2007; Tindell et al., 2005).14

 

Conclusion

In the last decade, neuroscience has confirmed what intuition could only suggest: that we desire more than pleasure. We act not for the sake of pleasure alone. We cannot solve the Friendly AI problem just by programming an AI to maximize pleasure.

 

 

Notes

1 Nozick (1974), pp. 44-45.

2 Steiner (1973); Steiner et al (2001).

3 Grill & Berridge (1985); Grill & Norgren (1978).

4 Berridge (2000).

5 Berridge et al. (1984); Schulkin (1991); Tindell et al. (2006).

6 Berridge (2009).

7 Berridge (2007); Robinson & Berridge (2003).

8 Berridge & Robinson (1998); Berridge et al. (1989); Pecina et al. (1997).

9 Sienkiewicz-Jarosz et al. (2005).

10 Brauer et al. (2001); Brauer & de Wit (1997); Leyton (2009); Leyton et al. (2005).

11 Cagniard et al. (2006); Pecina et al. (2003); Tindell et al. (2005); Wyvell & Berridge (2000).

12 Evans et al. (2006); Leyton et al. (2002).

13 Tindell et al. (2009).

13 Aldridge & Berridge (2009). See Smith et al. (2011) for more recent details on commingling.


References

Aldridge & Berridge (2009). Neural coding of pleasure: 'rose-tinted glasses' of the ventral pallidum. In Kringelbach & Berridge (eds.), Pleasures of the brain (pp. 62-73). Oxford University Press.

Berridge (2000). Measuring hedonic impact in animals and infants: Microstructure of affective taste reactivity patterns. Neuroscience and Biobehavioral Reviews, 24: 173-198.

Berridge (2007). The debate over dopamine's role in reward: the case for incentive saliencePsychopharmacology, 191: 391-431.

Berridge (2009). ‘Liking’ and ‘wanting’ food rewards: Brain substrates and roles in eating disordersPhysiology & Behavior, 97: 537-550.

Berridge, Flynn, Schulkin, & Grill (1984). Sodium depletion enhances salt palatability in rats. Behavioral Neuroscience, 98: 652-660.

Berridge, Venier, & Robinson (1989). Taste reactivity analysis of 6-hydroxydopamine-induced aphagia: Implications for arousal and anhedonia hypotheses of dopamine function. Behavioral Neuroscience, 103: 36-45.

Berridge & Robinson (1998). What is the role of dopamine in reward: Hedonic impact, reward learning, or incentive salience? Brain Research Reviews, 28: 309-369.

Brauer, Cramblett, Paxton, & Rose (2001). Haloperidol reduces smoking of both nicotine-containing and denicotinized cigarettes. Psychopharmacology, 159: 31-37.

Brauer & de Wit (1997). High dose pimozide does not block amphetamine-induced euphoria in normal volunteers. Pharmacology Biochemistry & Behavior, 56: 265-272.

Cagniard, Beeler, Britt, McGehee, Marinelli, & Zhuang (2006). Dopamine scales performance in the absence of new learning. Neuron, 51: 541-547.

Evans, Pavese, Lawrence, Tai, Appel, Doder, Brooks, Lees, & Piccini (2006). Compulsive drug use linked to sensitized ventral striatal dopamine transmission. Annals of Neurology, 59: 852-858.

Grill & Berridge (1985). Taste reactivity as a measure of the neural control of palatability. In Epstein & Sprague (eds.), Progress in Psychobiology and Physiological Psychology, Vol 2 (pp. 1-6). Academic Press.

Grill & Norgren (1978). The taste reactivity test II: Mimetic responses to gustatory stimuli in chronic thalamic and chronic decerebrate rats. Brain Research, 143: 263-279.

Leyton, Boileau, Benkelfat, Diksic, Baker, & Dagher (2002). Amphetamine-induced increases in extracellular dopamine, drug wanting, and novelty seeking: a PET/[11C]raclopride study in healthy men. Neuropsychopharmacology, 27: 1027-1035.

Leyton, Casey, Delaney, Kolivakis, & Benkelfat (2005). Cocaine craving, euphoria, and self-administration: a preliminary study of the effect of catecholamine precursor depletion. Behavioral Neuroscience, 119: 1619-1627.

Leyton (2009). The neurobiology of desire: Dopamine and the regulation of mood and motivational states in humans. In Kringelbach & Berridge (eds.), Pleasures of the brain (pp. 222-243). Oxford University Press.

Nozick (1974). Anarchy, State, and Utopia. Basic Books.

Pecina, Berridge, & Parker (1997). Pimozide does not shift palatibility: Separation of anhedonia from sensorimotor suppression by taste reactivity.Pharmacology Biochemistry and Behavior, 58: 801-811.

Pecina, Cagniard, Berridge, Aldridge, & Zhuang (2003). Hyperdopaminergic mutant mice have higher 'wanting' but not 'liking' for sweet rewardsThe Journal of Neuroscience, 23: 9395-9402.

Robinson & Berridge (2003). Addiction. Annual Review of Psychology, 54: 25-53.

Schulkin (1991). Sodium Hunger: the Search for a Salty Taste. Cambridge University Press.

Sienkiewicz-Jarosz, Scinska, Kuran, Ryglewicz, Rogowski, Wrobel, Korkosz, Kukwa, Kostowski, & Bienkowski (2005). Taste responses in patients with Parkinson's diseaseJournal of Neurology, Neurosurgery, & Psychiatry, 76: 40-46.

Smith, Berridge, & Aldridge (2007). Ventral pallidal neurons distinguish 'liking' and 'wanting' elevations caused by opioids versus dopamine in nucleus acumbens. Program No. 310.5, 2007 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience.

Smith, Berridge, & Aldridge (2011). Disentangling pleasure from incentive salience and learning signals in brain reward circuitryProceedings of the National Academy of Sciences PNAS Plus, 108: 1-10.

Steiner (1973). The gustofacial response: Observation on normal and anecephalic newborn infants. Symposium on Oral Sensation and Perception, 4: 254-278.

Steiner, Glaser, Hawillo, & Berridge (2001). Comparative expression of hedonic impact: affective reactions to taste by human infants and other primates.Neuroscience and Biobehavioral Reviews, 25: 53-74.

Tindell, Berridge, Zhang, Pecina, & Aldridge (2005). Ventral pallidal neurons code incentive motivation: Amplification by mesolimbic sensitization and amphetamineEuropean Journal of Neuroscience, 22: 2617-2634.

Tindell, Smith, Pecina, Berridge, & Aldridge (2006). Ventral pallidum firing codes hedonic reward: When a bad taste turns good. Journal of Neurophysiology, 96: 2399-2409.

Tindell, Smith, Berridge, & Aldridge (2009). Dynamic computation of incentive salience: 'wanting' what was never 'liked'. The Journal of Neuroscience, 29: 12220-12228.

Wyvell & Berridge (2000). Intra-accumbens amphetamine increases the conditioned incentive salience of sucrose reward: Enhancement of reward 'wanting' without enhanced 'liking' or response reinforcement. Journal of Neuroscience, 20: 8122-8130.

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