Caffeine is the most widely-used mind-altering substance in the world. Although it's not completely clear how caffeine causes the stimulant effects it's well-known for, it's thought most of those effects are traceable back to its action as an antagonist at receptors for the neurotransmitter adenosine. In this video, I discuss how that antagonistic action may lead to arousal and wakefulness.
Since the 1970s, neuroscientists have been confident that dopamine plays an essential role in the brain's processing of rewarding experiences. And many researchers used to be fairly certain they knew exactly what that role was. Dopamine was, as the thinking went, the "pleasure neurotransmitter"---the substance responsible for producing sensations of pleasure in the brain, regardless of whether that pleasure comes from enjoying a good meal, having sex, or snorting cocaine. This understanding, according to a 1997 article in Time magazine, made the answers to questions about what causes addiction, "simpler than anyone has dared imagine." The article goes on to claim that dopamine "is not just a chemical that transmits pleasure signals but may, in fact, be the master molecule of addiction."
The popular press was not completely unjustified in making this assumption, as they took their cues from scientists---many of whom had, to some degree, become advocates for the "pleasure neurotransmitter" perspective. For example, well-known dopamine researcher Roy Wise said in a 1980 article that dopamine was involved in creating experiences of "pleasure, euphoria, or 'yumminess'."
This all, of course, was an oversimplification of dopamine's role in reward. Some time (and more research) allowed everyone to recognize that dopamine's contribution to processing rewarding experiences is much more complex than a simple equation where dopamine = pleasure. This realization is now becoming pervasive, and googling "dopamine and addiction" will return almost as many articles on the first page that emphasize the nuances of dopamine function as those that stick to the simplistic dopamine = pleasure formula. Wise eventually changed his mind as well, asserting in the late 1990s that he no longer believed "that the amount of pleasure felt is proportional to the amount of dopamine floating around in the brain."
Today, even those who are only modestly familiar with current hypotheses in neuroscience would likely be able to tell you that dopamine is not the pleasure molecule. Still, they might have a hard time answering the question, "What, then, is its role in reward?" That's partially because no one knows the answer to that question for sure. There are, however, a few popular competing hypotheses that have been proposed in an attempt to elucidate dopamine's reward-related functions.
First, the basics
The early hypotheses about dopamine's role in reward were formulated based on the evidence that collections of dopamine neurons in the brain tend to be activated in response to the administration of addictive drugs (and other substances generally considered to be rewarding, like sweet foods). Activity in one such collection of neurons in particular, a pathway that stretches from a dopamine-rich area in the midbrain called the ventral tegmental area (VTA) to a nucleus in the forebrain called the nucleus accumbens, has consistently been linked to rewarding events. When someone experiences something rewarding (like snorting a line of cocaine), dopamine neurons in the VTA are activated and send dopamine to the nucleus accumbens, causing dopamine levels in the nucleus accumbens to rise.
This pathway from the VTA to the nucleus accumbens is called the mesolimbic dopamine pathway. It has come to be considered the primary component of what is now known as the reward system, which consists of a group of structures that are activated by rewarding or reinforcing stimuli like addictive drugs. The reward system also includes a number of other structures---as well as other dopamine pathways, such as the mesocortical dopamine pathway, which stretches from the nucleus accumbens to destinations in the cerebral cortex.
The case against dopamine as the "pleasure neurotransmitter"
Although it should be said that there is a great deal of evidence that indicates dopamine release is correlated with pleasure, there is also substantial evidence that suggests dopamine isn't responsible for causing pleasure.
Much of this evidence comes from animal studies. For example, when researchers damaged dopamine neurons in the brains of rats to the point where dopamine in the nucleus accumbens was depleted by up to 99%, rats still exhibited pleasurable reactions to sweet tastes, indicating some component of pleasure was left intact. In monkeys being trained to obtain juice rewards, once they learned the necessary tasks and could predict exactly when they would receive a reward, their dopamine neurons stopped firing in response to such rewards. Yet, they still seemed to enjoy the rewards, suggesting dopamine may be involved in signals about the predictability of rewards, but not the pleasure linked to them.
There is also evidence from humans that suggests that dopamine is not the substance that generates pleasure. In one study, for example, researchers found that dopamine levels in the ventral striatum (a region of the brain that contains the nucleus accumbens) correlated better with craving for amphetamine than with the pleasure experienced from taking the drug. In another study, administration of a dopamine antagonist (which blocks dopamine activity) did not prevent participants from experiencing euphoria after amphetamine administration.
Additionally, studies have found that mesolimbic dopamine neurons also can be be activated during experiences that are aversive---which only further complicates any attempt to consider dopamine the "pleasure neurotransmitter."
These are just a handful of examples that contradict the idea that dopamine is the primary pleasure-causing substance in our brains. The whole body of evidence that is at odds with the perspective is much larger, and it is widely accepted in neuroscience today that dopamine's role in reward is more complicated than the "pleasure neurotransmitter" moniker implies.
Other hypotheses: reward learning, reward prediction, and incentive salience
When it became clear to most researchers that dopamine was not responsible for creating sensations of pleasure, new roles were suggested for dopamine. Many scientists, for example, postulated that the neurotransmitter is involved in some aspect of learning about rewards. Along these lines, it has been suggested that dopamine is involved in the process of linking a pleasurable experience to a stimulus that previously had no value----like associating the pleasure of inebriation with alcohol after drinking it for the first time.
When someone experiences something pleasurable, their brain creates a strong association between that experience and whatever is thought to have caused it. Thus, the brain of someone who drinks alcohol for the first time (and enjoys it) will make a strong connection between alcohol and pleasure (previously alcohol would not have had any value to them because they never would have experienced its effects). Dopamine may be responsible for making that connection.
Similarly, others have proposed that dopamine not only allows for the learning of a new association between some stimulus and pleasure, but that it also is involved in the acquisition of new habits dedicated to obtaining that rewarding stimulus again in the future. In the case of addictive drugs, these habits can become especially persistent, generating patterns of compulsive behavior that persist long after the value of the reward has diminished.
Perhaps the most popular hypothesis that posits a role for dopamine in reward learning is the suggestion that dopamine is involved in identifying potentially rewarding stimuli, predicting how valuable those rewards are likely to be, and then responding strongly whenever something turns out to be more rewarding than was originally expected. This type of signaling is often referred to as reward prediction error signaling.
According to the reward prediction error hypothesis, dopamine neurons are highly active when rewards turn out to be more valuable than predicted and their activity is depressed when a reward is found to be less valuable than expected. This dopamine signaling acts as a mechanism to help us learn what to expect from rewards in the future; in other words, it helps to "train" the brain about what value a potential reward is likely to have. This information can be used to guide behavior, as it can help us determine which rewards are most desirable---and thus which we should pursue.
Additionally, the reward prediction error hypothesis provides us with a way of explaining addiction. According to this hypothesis, addiction can occur when addictive drugs (or other experiences or substances) generate high levels of dopamine release that lead to a reward being overvalued. This causes an individual to develop exceedingly high expectations of the pleasure that will be obtained from the drug reward, which leads to compulsive drug seeking. In essence then, addiction occurs because high levels of dopamine release cause an addict to consistently predict a drug will make them feel better than it really will. This corresponds to anecdotal accounts of drug addiction, where many addicts describe their drug-using experience as a series of failed attempts to recreate the pleasure they felt from their first high.
Another related, but slightly different perspective asserts that it is critically important to separate behavior surrounding a reward into (at least) two responses that are distinctly different but often confused for one another: "wanting" and "liking." "Liking" refers to the pleasurable response to a reward, while "wanting" refers only to the motivation to obtain a reward.
Think, for example, of a time when you were eating at a delicious restaurant but near the end of the main course you were uncomfortably full. Perhaps the waiter, however, left your plate sitting in front of you for some time (maybe while the rest of your party finished). During that time, you may have continued to occasionally take more bites of the food even though your ability to enjoy it was completely diminished due to your fullness. This could be considered an example of the difference between "liking" and "wanting." You still wanted the food and compulsively took bites of it because your brain had identified it as rewarding, but you no longer really liked the food due to your current state of fullness.
Proponents of the incentive salience hypothesis suggest that dopamine plays a critical role in generating "wanting"---a motivated response to attain rewards based on a previous experience with those rewards in which they were deemed to be valuable. Incentive salience involves "wanting" that is associated with some motivational goal (like obtaining a drug).
According to the incentive salience perspective, when we experience something rewarding, our brains (with the help of dopamine) assign incentive salience not only to whatever directly caused the rewarding experience (e.g. a drug), but also to any other stimuli associated with the reward. In the process, our brains become hypersensitive to the rewarding stimulus and anything we have come to associate with it. This hypersensitivity and increased propensity to generate strong feelings of desire can form the basis of an addiction.
For example, someone who has never smoked a cigarette likely would find the smell of cigarette smoke to be unpleasant---or at best neither pleasant nor unpleasant. In the brain of a smoker, on the other hand, an association has been made between the smell of cigarette smoke and reward---incentive salience has been attributed to the smoke because the brain has deemed it an important part of the rewarding experience of cigarette smoking. Thus, upon smelling cigarette smoke, the brain will likely stimulate mechanisms that prompt "wanting" of a cigarette, also known as craving.
These associations between "wanting" and smoking-related stimuli can lead to cravings every time a smoker is exposed to a smoking-related stimulus (e.g. the smell of smoke, seeing someone else smoking, etc.)---which can lead to the type of repetitive smoking that has the propensity to precipitate or intensify addiction to nicotine. According to the incentive salience hypothesis, this increased sensitivity to reward-related stimuli can persist for years, which could help to explain why those who develop an addiction often feel as if they are always susceptible to it---even after years of sobriety.
The broad view
These perspectives are not mutually exclusive, and there is clearly some overlap among them. For example, reward prediction and the attribution of incentive salience are both likely to be important aspects of learning about rewards. Thus, it is not improbable that some elements of each hypothesis accurately explain the role of dopamine in reward.
It's important to remember, too, that there is no contradiction in saying that dopamine may be involved in all of these components of reward processing (as well as with processing aversive experiences). Dopamine, like other neurotransmitters, may exert different actions depending on the subtype of receptors it acts on, the part of the brain its action is occurring in, and even the time course by which it is being released. We must become comfortable giving up our attempts to define neurotransmitters by a short list of actions, as such a simplistic view of neurotransmitter function does not seem to be based in reality.
The consensus, then, is that dopamine is not the substance in our brains that causes pleasure. Instead, it is thought to be involved in some other aspects of reward, but its precise role is still being debated. Regardless, dopamine seems to be more closely associated with reward than most other neurotransmitters, and it is likely to play a paramount role both in processing rewarding experiences and in the pathological states, like addiction, that are linked to faulty reward valuation.
References (in addition to linked text above):
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.
In this video, I discuss the effects of cocaine on the brain. I describe cocaine's primary mechanism of action, which involves inhibition of the reuptake of monoamine neurotransmitters like dopamine, norepinephrine, and serotonin. I also discuss the mesocorticolimbic dopamine pathway, which connects the ventral tegmental area with the nucleus accumbens and is activated when someone uses cocaine.
In Walden, his masterpiece about noncomformity and simple living, Henry David Thoreau wrote, "Every generation laughs at the old fashions, but follows religiously the new." And while Thoreau was specifically talking about society's capriciousness in embracing new styles of clothing, his quote applies just as well to our preference for one shade of skin color over another. For, while many now consider a medium-dark tan to be both healthier-looking and more attractive than pale skin, only 100 years ago a tanned complexion was shunned just like a pale one is today.
Actually, a preference for pale skin has been common throughout much of human history. One reason for this may have been that pale skin used to be an indication of affluence, as it meant that the individual who possessed it didn't have to work outdoors to earn a living. A light complexion was a sign of social status, and people went to great lengths to maintain it. Often these lengths involved applying cosmetic whitening agents that contained dangerous compounds like lead oxide. The effects of such agents could range from skin damage and hair loss to death. Yet, the desire for the pale ideal still pushed many to continue to use them.
Today, however, a tan has come to represent prosperity and the possession of ample time for leisure. It means one does not have to work so much that one cannot relax by the pool or on the beach--or perhaps more likely that one has enough expendable income to pay for regular visits to a tanning salon. But like the lead-based lightening treatments of ages past, tanning exerts a physical cost. Each year over 65,000 people throughout the world die from melanoma-related causes, and it is recognized that frequent sun exposure, a history of sunburns, and frequent use of tanning beds all increase the risk of melanoma. According to one study, ten tanning bed visits in a year nearly doubled melanoma risk in individuals over thirty and increased it almost eight times in individuals under thirty.
Yet these risks don't appear to act as a deterrent for a significant number of individuals who are willing to endure sunburns or regular visits to the tanning salon simply to achieve their goal of sustaining a medium-dark tan. Almost thirty million Americans patronize tanning salons every year, helping to make indoor tanning a $5 billion a year industry in the United States and Northern Europe--an industry that has grown five-fold since the early 1990s. Frequent tanning is especially prevalent among females, teens, and young adults, and even awareness of the risks associated with tanning doesn't seem to dissuade regular tanners from engaging in the behavior. In fact, one study found that 35% individuals who came from families with a history of malignant melanoma had still used a tanning bed in the previous year.
Applying addiction criteria to tanning
The fact that some individuals continue to tan despite the very real health risks associated with it is one reason some have come to consider tanning a potentially addictive behavior, as addiction often involves continuing to do something even when there are adverse consequences linked to it. The attempt to look at tanning in the context of addiction is representative of a generally increased openness to the idea of "behavioral addictions," or addictions that are not associated with the consumption of a particular substance (i.e. a drug). The most recent version of the Diagnostic and Statistical Manual of Mental Disorders (DSM), a comprehensive guide containing diagnostic criteria for psychiatric ailments, included Gambling Disorder in the "Substance-Related and Addictive Disorders"--the first time a behavioral addiction was included in this section. Some believe this represents a shift in how we think about addictive behavior, and that it may pave the way for the diagnosis of disorders involving internet, sex, and video gaming addictions.
To investigate tanning as a behavioral addiction, researchers have modified screening and diagnostic tools for substance abuse and dependence to make them applicable to tanning. The most sophisticated effort along these lines so far has been the development of the Structured Interview for Tanning Abuse and Dependence (SITAD). The SITAD was formulated by Hillhouse et al. (2013) and was adapted from items found in the Structured Clinical Interview for DSM-IV Axis I Disorders (SCID) that deal with opiate abuse and dependence. The SCID is a tool used to guide practitioners in making diagnoses of psychiatric disorders based on a patient interview and DSM criteria. To be classified as tanning dependent according to the SITAD, one has to meet at least 3 criteria modified from the DSM criteria for substance dependence, which include: failed efforts to cut down on the amount of time spent tanning, spending an excessive amount of time tanning or recovering from its effects, and experiencing a form of withdrawal when unable to tan, along with several other criteria.
When testing the SITAD in a sample of 325 college students, Hillhouse et al. found 10.8% met SITAD criteria for tanning abuse and 5.4% met criteria for tanning dependence--rates that are similar to rates for substance abuse and dependence seen in national surveys of substance use. Several other measures supported the validity of the SITAD, such as the fact that those who met criteria for tanning dependence tanned ten times more frequently than those who did not. A separate series of questions about euphoric reactions to tanning also indicated that these reactions were experienced to a much greater degree in those who met criteria for tanning dependence. Also, the participants completed the SITAD at two time points that were six months apart, and the two measures displayed good test-retest reliability for tanning dependence. In other words, participants who were found to be tanning dependent on the first measurement were also likely to be found tanning dependent on the second, which suggests the SITAD is reliable over time--an important quality of a valid measurement tool.
The SITAD is still a relatively untested method for assessing tanning addiction, however. It has only been tested in one population so far (i.e. college students), and despite the favorable results mentioned above there were also some potential issues. For example, although it reliably identified cases of tanning dependence, the SITAD did not appear to be very consistent in its recognition of cases of tanning abuse between the two time points. Much more work with the tool will need to be done before we can be confident in its ability to diagnose tanning addiction. However, what the SITAD and previous attempts to identify tanning addiction in the population seem to suggest is that there are individuals who do display patterns of tanning behavior that are at least somewhat similar to those displayed during addiction to drugs.
Is there a physiological basis for tanning addiction?
Thus, it seems that there are individuals who exhibit tanning behavior that in some ways resembles addiction. But what is the mechanism that could be prompting this compulsive behavior? Addictive drugs have the ability to manipulate neurotransmission in the reward system, causing people to obsessively crave and compulsively seek substances. But exposure to ultraviolet (UV) light is not as overtly rewarding as, for example, cocaine administration. Regardless, some studies have suggested exposure to UV light in frequent tanners is reinforcing, and others have proposed a way UV light exposure could lead to rewarding effects that resemble those of addictive drugs.
When the skin is exposed to damaging (and cancer-causing) UV light for an extended period of time, a defensive mechanism is initiated to protect against UV-induced DNA damage. The mechanism involves the increased production of a precursor protein called proopiomelanocortin (POMC), which is synthesized primarily by the pituitary gland. After it is produced, POMC is cleaved to form several other proteins, one of which is alpha-melanocyte-stimulating hormone (a-MSH). a-MSH stimulates the production of melanin, a pigment molecule that helps to protect the skin by absorbing UV radiation and free radicals generated due to exposure to UV light.
POMC, however, is also the precursor for another peptide: beta-endorphin. Beta-endorphin is an endogenous opioid; its actions in the body are similar to those of opioid drugs like morphine, and it is capable of promoting natural analgesia along with a sense of well-being. Thus, it may not be surprising that a commonly cited reason for enjoying tanning is that it induces a feeling of relaxation and a positive mood.
Although the potential role of endorphins in promoting a positive mood in tanners has not been verified, there is some evidence to support it. In one double-blind study, a small group of regular tanners were given sessions in both a UV tanning bed and a non-UV tanning bed (non-UV rays would not initiate the reaction that leads to increased beta-endorphin production) on Monday and Wednesday every week for six weeks. The participants were not informed of any difference between the two beds, and on the Friday of each week they were asked to choose one of the two beds to tan in. Participants chose to tan in the UV bed 95% of the time--without any knowledge that they were choosing the only bed that provided UV exposure.
A follow-up study conducted by the same research group investigated if administering naltrexone, an opioid antagonist, before tanning would reduce the preference tanners showed for a UV tanning bed. Not only did they see a reduced preference for UV tanning beds in those who had been given naltrexone before tanning, but they also saw what seemed to be withdrawal symptoms in two out of three frequent tanners given the opioid blocker. This study, however, was done with an extremely small sample (eight frequent tanners, eight infrequent tanners--only 1/2 of each group received naltrexone) and will need to be replicated before one can be at all confident in the results. Other studies, in fact, that have tested levels of beta-endorphin in participants' blood after exposure to UV light have not found any increase from baseline levels, casting some doubt on endorphins as the mechanism underlying tanning addiction.
A recent study in rodents, however, supports the endorphin hypothesis of tanning addiction. Fell et al. (2014) exposed partially shaved mice to UV light five days a week for six weeks. After a week, the mice had elevated beta-endorphin levels in their blood. UV-exposed mice also displayed greater pain tolerance, presumably due to higher beta-endorphin levels--an effect that was abolished by pre-treatment with naloxone, an opioid antagonist. Additionally, administration of naloxone caused withdrawal effects to appear in these animals, and mice that had been exposed to UV light also displayed increased tolerance to morphine, suggesting endorphin levels had become high enough to raise tolerance to opioids in general. When Fell et al. attempted these same experiments with mice genetically engineered to be deficient in beta-endorphin production, the mice exposed to UV light did not display elevated pain thresholds, withdrawal upon naloxone administration, or increased morphine tolerance, suggesting beta-endorphin was playing a critical role in these effects in wild-type (i.e. non-genetically engineered) mice.
Is tanning addictive?
Despite the positive findings in rodents, the potential physiological basis of tanning addiction in humans remains unclear. Thus, with tanning we have a behavior that some people seem to go about in a compulsive manner, and which has a plausible--but unverified--mechanism to account for it being reinforcing. The uncertainty about the physiological mechanism underlying tanning addiction should not bear too heavily on deciding if tanning could be considered addictive, however, as the neurobiological mechanism underlying addiction to most drugs was not known before we recognized them as addictive. Regardless, there has been significant controversy surrounding the inclusion of behavioral disorders like tanning addiction in the DSM and other diagnostic manuals.
One of the arguments against considering tanning a behavioral addiction is that compulsive tanning may only be a symptom of some other underlying disorder. For example, compulsive tanners may be trying to compensate for a poor body image and may even suffer from a form of body dysmorphic disorder, which is an obsessive preoccupation with some perceived physical shortcoming (in this case skin color). However, even if compulsive tanners are doing so because of a comorbid disorder, that does not suggest their behavior cannot be classified as addictive. Many alcoholics drink to self-medicate for things like social anxiety disorder, but this doesn't suggest they shouldn't be considered alcoholics.
Another difficulty some have with designating behaviors as addictive may come from our tendency to consider drug-related addictive behavior as potentially more severe than a behavioral addiction. This is understandable, as it is hard to imagine seeing the desperation we sometimes see in severe drug addiction in a compulsive tanner. However, it seems that addictive behavior--like all other behavioral patterns--falls on a spectrum of severity. And, simply because one individual's behavior is not as extreme as another does not mean he or she is not displaying a similar pattern of behavior. The DSM seems to have acknowledged this by replacing the term "substance dependence" with the more general "substance use disorder," and by modifying the diagnosis for this disorder to allow for it to be present on a spectrum that ranges from mild to severe instead of it necessarily being either present or absent.
Similarly, the DSM has begun to dissociate addiction from substances by titling their section that deals with addiction "Substance-related and addictive disorders [emphasis added]" and including a diagnosis for non-substance related disorders. When we don't define addiction as being inextricably linked with a substance, we see that it is simply an impulsive and compulsive pattern of behavior. And it seems that almost anything--not just drugs--can be the target of compulsive behavior, depending on the individual in question. Certain people compulsively use heroin, others compulsively steal (i.e. kleptomaniacs), and others may compulsively have sex, play video games, or tan.
Thus, perhaps we need a more inclusive understanding of addiction. It seems that people can get "addicted" to almost anything; it just requires a combination of the right person and the right behavior or substance. And so maybe attempting to develop diagnostic criteria for each specific focus of addiction--like the DSM does now with alcohol use disorder, opioid use disorder, etc.--is the problem; maybe we should simply be using one general set of criteria for compulsive behavior that can be applied to anything, with no additional restrictions.
Is tanning addictive? Maybe. It really depends on the definition of addiction you are using and the susceptibility of the individual who goes tanning. Perhaps a better question is: do some people display compulsive patterns of tanning behavior that knowingly puts them at risk for serious health consequences later on in life? The answer to that question seems to be yes.
In those who are addicted to drugs (or any other substance or behavior), the desire to re-experience the intoxicating effects they initially felt when they used the drug can be overwhelming. It can lead to compulsive drug-seeking, obsessive thinking, and irrational behavior. In addition to these new thought patterns and behaviors, however, addiction is also associated with a diminished ability to experience pleasure from non-drug rewards. This reduced ability to experience pleasure is termed anhedonia.
Addiction and anhedonia
For example, someone who is addicted to cocaine will obsessively seek cocaine, and consider the procurement and use of it a rewarding experience. However, he may not get much pleasure from other things that many people find rewarding, like going for a walk, watching a favorite movie, or talking to a friend. As you can imagine, an obsession with the rewarding effects of a drug combined with a decreased ability to enjoy other rewarding things in one's life can cause one to pursue drugs even more obsessively, as drugs begin to seem like the only thing that can generate pleasure.
It is not clear if anhedonia is something that predisposes people to use drugs (e.g. people who become drug addicts have trouble experiencing pleasure from everyday rewards and so turn to drugs because they manipulate the reward system more powerfully), or if anhedonia is caused by chronic drug use. Anhedonia does, however, appear to be associated with aberrant brain activity. For example, individuals experiencing anhedonia (whether as part of drug addiction or due to some other disorder like depression) display decreased activity in the ventral striatum, orbitofrontal cortex, and prefrontal cortex, as well as various abnormalities in dopamine signaling.
Reward processing in smokers
A study published recently in Cognitive, Affective, & Behavioral Neuroscience explored altered reward processing (similar to what might be seen in anhedonia) in cigarette smokers, and how it was associated with the ability to refrain from smoking. The researchers, Wilson et al., used functional magnetic resonance imaging (fMRI) to visualize brain activity in a group of smokers while they played a game in which they won small monetary awards ($1 at a time). Then, the participants were given the opportunity to earn an additional $1 for every 5 minutes they were able to put off smoking a cigarette.
The investigators found that the smokers who displayed the least activity in the ventral striatum (an area of the brain thought to be especially important in reward processing) in response to a monetary reward were also least likely to refrain from smoking in the second part of the experiment. The authors suggest this may represent a reduced response to non-drug rewards in those who are addicted to cigarette smoking. Such an attenuated response to rewards other than smoking could be especially problematic when trying to use incentives to help people quit smoking.
For example, if the reduced ability to experience reward outside of smoking cigarettes was applied broadly, it could mean that even the idea of improved health would not be easily appreciated by someone addicted to smoking. And therein lies the rub (or one of them) with addiction: when an individual finds it more difficult to experience pleasure from something other than their preferred substance, what incentive can you give him or her to stop using it? This is one reason why the riddle of addiction has been a difficult one to solve, and why we keep seeking novel treatments (see this article about vaccines to treat addiction) for substance dependence.