Anyone reading this magazine has a foundational knowledge of addiction. They know that at the level of true addiction there exists a number of telling symptoms. Arguably a key symptom is a pathological compulsive drug-seeking and drug-taking behavior that seemingly consumes the addict. Another key feature of addiction is that while many individuals wish to change, they continue to use, even though they know that the costs will be very severe. Moreover, many folks in recovery remain vulnerable to relapse sometimes for years after last ingesting a substance. Such behavior befuddles many lay people and even those professionally engaged in this field.
However, there is clarity on the horizon, and it centers in neuroscience research—thus, this strange sounding title. The addiction field is becoming increasingly more scientific in nature. Consider such terms and nomenclature as a means of getting closer to comprehensive understanding of the very essence of addiction. The terms are precise, operationally defined, and yes, a bit technical. Today neuroscience is leading the way, and you are going to be seeing a lot more of this technical terminology.
A Brief Brain Anatomy Lesson
Readers undoubtedly know that drugs alter brain anatomy at the neural level, and those neurological changes have a direct bearing on the addictive process. The identified anatomical brain suspects are located in the mesolimbic area or middle brain. This area includes, among other things, the dopamine-related circuits of nucleus accumbens and the ventral tegmental area that have been the focus of much research in the past few years (Berridge & Robinson, 2011; Di Chiara et al., 2004). While other parts of the brain are certainly involved, these areas have been shown to be particularly important and relevant. In addition, research has also found strong evidence that drugs alter human learning. It has been theorized that drugs promote aberrant learning, which has been seen as a key factor in the addictive process (Hyman, Malenka, & Nester, 2006; Redish, 2004). Aberrant learning is professed as a strong automatic habit that leads to compulsion. However, this general theory has been shown to have some shortcomings. And as we shall shortly see, incentive sensitization offers an upgraded theory for and about addiction.
A Few Definitions
As it applies to this theory, consider “sensitization” to be an increased, amplified, intense effect caused by a drug’s repeated use. An individual abusing substances becomes strongly influenced to a particular drug. Consider “incentive” as inducement, enticement, attraction, or in everyday parlance, temptation.
Now there are elements of learning theory within incentive sensitization theory. But Berridge, the creator of incentive sensitization, has discovered that these theories only focus on the learning component of drug reward. Incentive sensitization points out the limits of such theories that include the notion that habits do not necessarily lead to compulsive behavior. What these learning theories lack is the motivational component (Berridge, 2012).
Like other neuroscience brain theories, incentive sensitization acknowledges that addiction involves changes in brain circuits caused by drugs. The sensitization is especially concentrated in the mesolimbic area of the brain, as we reviewed previously. This area has repeatedly been shown to generate the distinguishing features of addiction. However, the core of this theory is that addiction is a disorder of abnormal incentive (enticement) motivation, due to the neural systems that attach hyper predominance—or influence and power—to specific cues and stimuli.
Yet, incentive sensitization is more than just a theory of abnormal motivation. It maintains that once addiction is established it fundamentally changes the brain by the persistent sensitization or hypersensitivity to the incentive motivational effects of not only drugs themselves, but also drug-associated stimuli (Robinson & Berridge, 2003). Incentive sensitization produces a preference of attention processing toward drug-associated stimuli. This hypersensitization produces a pathological motivation for drugs referred to as intensified wanting or incentive salience (Berridge & Robinson, 2011). The effects of this wanting go way beyond just liking a drug, and “liking” may not be a good explanation for addiction.
Berridge’s research indicates that there are different brain circuits that distinguish liking and wanting. The ingested drugs hijack the wanting circuits and activates the mesolimbic system and other neurobiological events that, according to incentive sensitization, make for an enduring and persistent effect. Simply put, this means that when drug cues are encountered it becomes almost impossible for addicts to ignore. This condition leads to intense cravings and can persist for years, even long after withdrawal. To distinguish liking and wanting, consider liking or pleasure as an outcome that results from drug intake. Wanting, as defined in this theory, is a driver of addiction.
Lastly, incentive sensitization advances the idea that this wanting is mainly an unconscious state in that it takes place in the mesolimbic part of the brain. That part of the brain, for the most part, operates on an unconscious level. So, while the unconscious wanting or motivation has been growing by virtue of the years of abuse, only slowly does this wanting become a conscious state. But by the time all this becomes conscious, the wanting is well established and has been for sometime. This established process is what sets off the wanting drug cues that are sadly entrenched within the addicted individual, and make it difficult for the conscious part of the brain to effectively operate.
The really exciting difference with this and many other emerging theories is that much of this theory is based on neuroscience. These theories are not merely explaining the psychological nature of addiction; they can point to brain mechanisms that are tangible and real.
The theory of incentive sensitization helps illuminate some frequent claims made about the addictive process. For one, it explains the Twelve Step saying, “The man takes the drink, the drink takes the man.” As individuals become hypersensitized to drugs, wanting (not liking) the substance takes over and the drug takes the person.
In addition, it helps explains powerlessness. Hypersensitization, or the formidable wanting, overcomes mere willpower and sincerely meant promises. Not much seems to withstand its onslaught.
It also helps explain how after years of sobriety, even taking so much as a single drink, the addict seems to pick up where he or she left off.
This theory also clarifies the curious sounding DSM-5 substance use disorder symptom “continued use despite consequences.” Knowing that another drink or drug will surely result in more negative costs, the hyper-wanting essentially prevails.
Futhermore, incentive sensitization casts doubt on the theory that there must be some deep underlying psychological problem that continually drives the addiction. If only this subterranean problem could be properly addressed, the addictive use of drugs would cease. Incentive salience is not some deep underlying psychological problem—it is addiction itself.
This takes us to our last illumination, something often found on a profoundly personal level. Listen closely to individuals in recovery as to what it was like to live in active addiction, and you hear phases like, “I had this never-ending craving. It was always there. It never went away. I hungered for the drug. I just wanted it more than my family, my children, and life itself.” Expressions like these make “normies” scratch their heads. That alcohol or a drug could have such power and such dominance is beyond their scope of understanding. Yet, addiction does this and the research is beginning to finally unravel the brain mechanisms of this incessant and relentless hunger.
Sadly, not much has been offered in terms of practical treatment applications at this time. I suspect one day it will.
Berridge, K. C., & Robinson, T. E. (2011). Drug addiction as incentive sensitization. In J. Poland & G. Graham (Eds.), Addiction and responsibility (pp. 21–53). Cambridge, MA: MIT Press.
Berridge, K. C. (2012). From prediction error to incentive salience: Mesolimbic computation of reward motivation. European Journal of Neuroscience, 35(7), 1124–43.
Di Chiara, G., Bassareo, V., Fenu, S., De Luca, M. A., Spina, L., Cadoni, C., . . . Lecca, D. (2004). Dopamine and drug addiction: the nucleus accumbens shell connection. Neuropharmacology, 47(Suppl. 1), 227–41.
Hyman, S. E., Malenka, R. C., & Nester, E. J., (2006). Neural mechanisms of addiction: The role of reward-related learning and memory. Annual Review of Neuroscience, 29, 565–98.
Redish, A. D. (2004). Addiction as a computational process gone awry. Science, 306(5703), 1944–7.
Robinson, T. E., & Berridge, K. C. (2003). Addiction. Annual Review of Psychology, 54(1), 25–53.