From Reward to Slavery, the Stages of Addiction
The word “addiction” is derived from a Latin term for “enslaved by” or “bound to.” Anyone who has struggled to overcome an addiction — or has tried to help someone else to do so — understands why. In the first chapter, addiction was presented as a continuum, as there are degrees of severity, it’s not an on-or-off condition. In chapter 2, we saw that the criteria become more severe as the disorder progresses. In this section, we are going to look at addiction from a new direction — from the standpoint of neuroplasticity. If a substantial part of addiction is learned behavior, how and why does it happen, and most importantly, how can we go about reversing or countermanding the learned part of the process.
Earlier, we learned that there are three phases, or stages of normal learning. the acquisition phase, where we gather sensory data and decide what to do with it; the declarative phase, or memory we use in conscious decision-making; and finally, working or habit memory, which governs actions we take without the intervention or collaboration of our conscious mind. Although behavioral characteristics vary with the particular drug, the process of addiction can also be divided into three distinct stages, which correspond to the three memory phases.[i]
All drugs of abuse trigger the limbic system by stimulating the release of dopamine in the neurons.[ii],[iii] This stimulation focuses our attention, gives us pleasure, and causes our brain circuitry to record the entire experience, so it can be repeated in the future. Because it’s the limbic system that’s involved, the message is powerful, and even the early experiences are encoded quite strongly.[iv] The dopamine release triggered by drug use is two to ten times stronger and of much longer duration than that of any normal biological rewards.[v] For such rewards, (eating, sex, etc.) once the person has learned the most efficient behavior to obtain a reward, dopamine release to facilitate further learning is not necessary and does not occur.[vi] Drug use, on the other hand, always produces a dopamine release if a sufficient amount is taken, even in chronic users.[vii]
During this initial phase, which corresponds to the acquisition stage of memory development, we are simply storing cues, triggers, and everything relevant about the experiences we are having. To a non-smoker, the ringing of a telephone, a cup of coffee, or ordering a drink, are not triggers that bring a cigarette to mind. They were to me when I was a smoker. A line of white powder on a table-top, a syringe, or the sight of a crack pipe, are not triggers or cues for me. I didn’t use those particular drugs, so I have no memories associated with the drugs themselves, the acts necessary to use them, or the environment in which they’re used. However, a friendly pub, a glass of scotch, or the sight of a cold beer on a hot day, would have been a different story for me, twenty-five years ago.
While we’re socially using, we’re driven by the positive feedback we receive from the drug. The world seems better to us, and many of us believe we fit in to it more easily then we did before. We are more comfortable with ourselves, and those we are around. We notice that the drug mitigates many of the everyday stresses we normally face — at least for a while. As long as the experience remains pleasant overall, we tend to repeat it, putting up with occasional hangovers, bad experiences, and minor negative occurrences. In the meantime, we’re learning that drug-seeking behavior is more important then seeking normal rewards — like sex or a good meal. Each time a drug is used, the pathways that record the surrounding events get stronger and more ingrained.
The limbic system didn’t evolve to addict us to cocaine or alcohol, it evolved to provide a powerful incentive to perform behaviors that benefit ourselves and our species. After we learn a pleasurable behavior, such as sex, for instance, certain cues will cause a release of dopamine when there appears to be any chance of the pleasurable activity taking place. A glimpse of an attractive person at a cocktail party, for instance, can immediately trigger the limbic system. Your pulse quickens, your attention is focused, and your brain is engaged. It’s no different with addiction. Once the patterns are well-established, the slightest cue or trigger is enough to release dopamine and begin drug-seeking behavior.[viii]
The second stage of addiction, referred to as regulated relapse, corresponds to the use of declarative memory in conscious decision making. A cue or trigger activates the reward system, and first we consider if using is currently appropriate. If it is, we go ahead and do it, if not, we put it off. If we choose not to use, the chance of impending reward disappears, so dopamine levels will slowly return to normal, until the next cue or trigger. There’s no hard-and-fast rule governing the beginning (or for that matter the end) of this stage. It varies from person-to-person and from drug-to-drug.
One defining characteristic of regulated relapse is tolerance — it takes more of the drug to achieve the same effects as before. Tolerance occurs when the brain reacts to repeated drug exposure by changing itself physically and chemically to offset the effect of the drug. If the drug causes the release of great amounts of a particular neurotransmitter, for instance, the brain will decrease the number of receptors for that neurotransmitter, so larger amounts of the drug are necessary to achieve the same effects. Withdrawing the drug leaves the brain with an imbalance, because it is now dependent upon the drug.[ix]
If the pattern is repeated often enough for a long-enough time, the addict moves-on to the third stage of addiction, called Compulsive relapse, which corresponds to the formation of working, or habit memory. There is little conscious thought involved in the decision to use or not, because it’s very difficult for the executive decision-making capacity to intrude upon the drug seeking behavior.[x] FMRI imaging of people addicted to various drugs shows very little involvement of areas of the brain which are used in decision-making, when the addicts are presented with various cues.[xi]
There is an additional force that drives compulsive using in this stage — negative reinforcement, or the “gotta have its.” It we don’t eat for a long time, it’s our limbic system that makes us feel uncomfortable, causes that pain in the belly, and focuses our attention on obtaining that next meal. The longer we go without eating, the higher our anxiety level, and the more focused we become. The urge to use becomes exactly like that — an overwhelming force screaming that it simply has to have the drug, that using is a life-and-death situation, and cannot be ignored. With most drugs, there are also withdrawal symptoms that help drive us to use. At this point, the addict puts the drug ahead of everything — wife, family, job, goals, none of which will be allowed to interfere with the overwhelming need for the drug. The addict will continue to use in spite of severe negative consequences.
The journey to addiction begins with our receiving positive reinforcement from use of the drug — it makes us feel good, and ends with the “gotta have its” screaming in our ear. For some, it seems like a hopeless situation, but the vast majority of us find a solution to the problem
[i] Kalivas, P.W., and O’Brien, C. 2008. Drug Addiction as a Pathology of Staged Neuroplasticity. Neuropsychopharmacology Reviews, 33, pg. 167
[ii] Kelley, A.E. 2004. Memory and addiction: shared neural circuitry and molecular mechanisms. Neuron 44: pps 161-179
[iii] Nestler, E.J. 2005. Is there a common molecular pathway for addiction? National Neuroscience 8: 1445-1449
[iv] Berridge, K., Robinson, T. 1998. What is the role of dopamine in reward: hedonic impact, reward learning, or incentive salience? Brain Research Reviews 28: pps 309-369
[v] How Addiction Higacks the Brain. Harvard Helpguide: http://www.helpguide.org/harvard/addiction_hijacks_brain.htm
[vi] Deutch, A.Y., Roth, R.H. 1990. The determinants of stress-induced activation of the prefrontal cortical dopamine system. Progressive Brain Research 85: pps 357-393
[vii] Kalivas, P.W., and O’Brien, C. 2008. Drug Addiction as a Pathology of Staged Neuroplasticity. Neuropsychopharmacology Reviews, 33, pg. 168
[viii] Schultz, W. 2004. Neural coding of basic reward terms of animal learning theory, game theory, microeconomics and behavioural ecology. Current Opinion in Neurobiology 14: 139-147
[ix] Wilson, W.A., & Kuhn, C.M. 2005. How addiction hijacks our reward system. Cerebrum: The Dana Forum on Brain Science Vol. 7, No. 2, pps 53-66
[x] Everitt, B.J., & Robbins, T.W. 2005. Neural systems of reinforcement for drug addiction: from actions to habits to compulsion. Nature Neuroscience: 8: 1481-1489
[xi] Kolb, B. et al. 2004. Plasticity and functions of the orbital frontal cortex. Brain and Cognitive Sciences 55: pps 104-115