This article seeks to examine the disease model of addiction and rebuttal the skepticism surrounding this topic that has permeated blogs and found a viral (pun intended) mode of transmission via social networks. My goal is to create a concise, easily understood exposé on addiction by discussing some of the principles behind the chronic disease model, the physiologic changes taking place in the presence of addiction and even prior to, and why the argument of “choice” may not be so important.
Let us begin by considering two scenarios. The first is a middle-aged woman who, despite never smoking a single cigarette in her life, has recently struggled with shortness of breath and blood-tinged sputum. Scared, she schedules an appointment with her medical provider and is quickly scheduled for a CT scan. The results show a nodule which, after additional testing, is determined to be malignant. In the second scenario, we imagine the same, exact series of events with a change in a single variable: the woman has smoked two packs a day for more than half her life. Which woman has cancer?
Assuming a certain level of rationality, most of us would think this is a moot discussion and marvel at the coldness that accompanies the question. Nevertheless, this example makes it easy for one to see the irrelevance of choice in determining disease process. That is to say, if the woman chose to smoke or not, we do not alter the categorical determination of whether she is suffering from a disease based on that choice. This makes good sense, after all, since so many (possibly even most) disease processes have etiologies and risk factors that are largely dependent on a person's choice. One can see this pattern in cases of sexually transmitted disease, type II diabetes, hypertension, and, yes, even many cancers. Surely, however, we would not choose (there's that pesky word again) to inaccurately label something like cancer as anything other than a disease simply because a sufferer chose to use tobacco, lie in a tanning bed, or have sex (in the case of HPV-linked cancers). Put simply, when it comes to chronic disease, choice comes in only as it pertains to prevention, treatment (choosing better habits and lifestyle changes), and management but not in the definition of disease itself. We will get back to this argument again shortly. First, however, I owe you readers an introduction to what we're doing here.
You may have gathered, by the title and the opening paragraphs, that this article seeks to examine the disease model of addiction and rebuttal the skepticism surrounding this topic that has permeated blogs and found a viral (pun intended) mode of transmission via social networks. My goal is to create a concise, easily understood exposé on addiction by discussing some of the principles behind the chronic disease model, the physiologic changes taking place in the presence of addiction and even prior to, and why the argument of "choice" may not be so important.
"Fine! Call it whatever you want, but had they never used in the first place...then they wouldn't have the problem to begin with!" This is, by far, the most arrogant response I am faced with. The overall intent of this argument seems to be about grandstanding with the undertone that its speaker has simply chosen to make better choices than an addict. Rarely, if ever, do I stand face-to-face with a saint who has never made a choice to partake in something potentially addicting: sex, gambling, alcohol, marijuana, etc. That person, in order to be immune to critique, must have one or more of the following characteristics: either they have never engaged in an act or used a substance with addictive properties, simply have extraordinary willpower, or they have the unique ability to introspectively view their neurophysiology and/or genome and can definitively say they're not at risk for developing addiction and act accordingly. Most of us will drink alcohol in our lifetime and, unless we have that power of introspection, we will do so without knowing if this act will doom us to a life of alcoholism. The same principle applies to the poor soul undergoing a rotator cuff repair and precisely taking their Vicodin as prescribed. They are not gifted with the knowledge of their biochemistry, unfortunately, and may fall victim to it following apparently innocuous choices. We all make mistakes and decisions we regret. Some may even be cursed with an event that demands the use of pain medication. It becomes all too easy to those of us that pulled the long straw in the genetic lottery to cast stones, despite our falling short of sainthood.
Why do we call addiction a disease? In order to gain insight into this answer, one must first understand the term. A disease, per Merriam-Webster, "is a condition of a living animal that impairs its normal functioning and is typically manifested by distinguishing signs and symptoms." Addiction isn't just any disease, however, it is a chronic disease. That is to say, it cannot easily be cured and may relapse and remit. When we think of disease, most of us think of physical phenomena. I think this would be a good place to start in understanding the disease model.
I generally point to a review of the medical science as it applies to the pathologic changes addiction exerts on the brain. Given that article's length, the relative attention span of most readers, and the guaranteed headache of this writer...this article will not be able to summarize all the science as it pertains to addiction. I will, however, link the article I often refer to in the references. With some exception, this article, published in The New England Journal of Medicine, is my main reference here.
It will be helpful to begin with tearing down the popular concept that the mind and the body are separate entities ("Cartesian Dualism" for all you philosophically adept readers). This cannot be further from the case. Although there is much to learn, let me assure each of you that every mental process that occurs has some basis in the brain. That means one's willpower, for instance, is dependent on the physiology of one's brain. Sure, we are continuing to learn about plasticity and the way the brain can change, but this holds true. There are simply some things that are not in the cards for some people. One cannot simply choose not to have schizophrenia, for instance. This is an important understanding as we go forward.
Addictive substances activate "feel good" or reward circuits of the brain through its primary messenger: dopamine. This means that the brain's receptors (picture receptors as tiny locks and substances like dopamine as the keys) are constantly being tripped by surges in dopamine. Eventually, the brain's cells will stop responding to the reward (such as heroin) itself and, instead, respond to the cues that predict the delivery of the reward. Remember when Pavlov's dog began salivating when the bell rang and not just when the bell accompanied food? This is the same idea. This is a good thing, because it enables learning and memory formation. Unfortunately, in the presence of addiction, environmental triggers can become entangled with drug use. For example, I once had a patient tell me that the smell of urinal cakes made him crave heroin because he spent so much time shooting up in public bathrooms. These stimuli are not only environmental but can also take the form of mental states, such as feeling depressed. If someone was depressed when they used, then they'll want to use when they're depressed. This can be especially problematic, as we will see, since depression is an ultimate consequence of addiction. (Volkow, Koob, & McClellan, 2016)
In the presence of these triggers, an addicted person may receive a surge of dopamine and thusly begin craving the drug. This can occur long after cessation of the addictive substance. The stronger the reward response, the further a person is willing to go to satisfy that craving, despite negative consequences. Normally, however, dopamine cells will cease activation following consumption of the reward (food, sex, etc.) and therefore one will no longer feel driven to pursue it further. Addictive drugs are able to work around this mechanism, increasing dopamine levels and perpetuating compulsive behavior. (Volkow, Koob, & McClellan, 2016)
As time goes on, an addicted brain produces much less dopamine in response to a drug. The reward system becomes less sensitive to these substances, as well as other activities that would be rewarding (such as socialization). This explains why addicts become detached from relationships. These changes, unfortunately, do not quickly return to normal once someone "gets clean." (Volkow, Koob, & McClellan, 2016)
Next, the stress response is altered as negativity causes an exaggerated response. During withdrawal, stress hormones are released in greater number, causing the addict to enter a "fight-or-flight" mode. Just as the reward circuit pulls one toward the drug, there is an equal response by the stress response to push one away from the discomfort of withdrawal. It is this process that changes the pattern from using a substance to "get high" to the addict using a substance to relieve the negative effects of withdrawal. This begets the cycle of binging to relieve suffering, thereby worsening the previously mentioned cycle, leading to more binging and more suffering. (Volkow, Koob, & McClellan, 2016)
Lastly, the addicted person's brain quite literally continues to change and restrict their freewill. The prefrontal cortex plays a large part in "executive decisions" or the ability to critically think, weigh options, and enable one to rationally act. It carries this out in a number of ways, such as delaying reward, assimilating knowledge, and allowing one to check oneself (before one wrickity-wrecks oneself). As dopamine decreases in the reward circuit, there is a corresponding decrease in the prefrontal region, thereby impairing decision-making and an addict's ability to resist urges to use the drug. These regulations are compromised, alongside the reward system and emotional response, impairing the ability of the user to quit. (Volkow, Koob, & McClellan, 2016)
We know that addiction runs in families, likely the result of a complex relationship between environment and heredity. Further exemplifying the disease model, science continues to unearth genetic clues underlying addiction (just as it has with many other diseases). For example, the DRD2 dopamine receptor gene is more common in people addicted to alcohol or cocaine (Genetic Science Learning Center, 2013). This is just one of many genes (Htr1b, Per2, etc.) correlated with addiction with some genes (Mpdz, Creb, etc.) offering protection against addiction (Genetic Science Learning Center, 2013). These genetic predispositions may mean that one's free will may not be so "free" even prior to first use.
"How dare you call it a 'disease' or compare it to cancer!" After cowering to escape the barrage aerosol of spit and venom sprayed at me, I try to reassure people that I am in no way demeaning those suffering from cancer. I am merely employing a rhetorical strategy of finding something we may both agree on and drawing similarities. Actually, I am arguing FOR someone suffering of cancer by saying that their choices do not make their disease any less awful. What I find most troubling about this argument is the notion that one thing cannot have the same determination if it is perceived as less horrible than something else. It would be ridiculous to say that certain skin cancers are not diseases simply because melanoma has a worse fatality rate. Put simply, it is not a contest and the presence of one disease does not lessen the perception of another.
"Okay...okay...but does it really matter what we call it?" Ummm...yes! Without an accurate understanding and insight into the nature of addiction, then we cannot adequately treat it. For instance, by understanding the brain disease model and the maturation of the adolescent brain, then it becomes apparent the priority for intervening and educating adolescents. Understanding the stress response can help in tailoring behavioral and drug therapy to better treat those suffering from addiction. Gene therapy may one day assist in altering genetics to minimize the chances for addiction, whilst utilizing the protective benefits of other genes. None of this is possible as long as we, as a society, continue doing what we are doing: stigmatizing and shaming those suffering from this disease. We have a lot to gain, especially since relapse rates for drug addiction are lower than other chronic diseases, such as hypertension and asthma, even despite our hitherto terrible record on addressing this topic (McLellan, Lewis, O'Brien, & Kleber, 2000). If we have any hope in improving the lives of those suffering from addiction and beating the opioid epidemic, then it lies in the disease model of addiction.
"Disease." Merriam-Webster.com. Merriam-Webster, n.d. Web. 16 May 2017.
Genetic Science Learning Center. (2013, August 30) Genes and Addiction. Retrieved May 12, 2017, from Genes and Addiction
McLellan, A.T., Lewis, D.C., O'Brien, C.P., and Kleber, H.D. Drug dependence, a chronic medical illness: implications for treatment, insurance, and outcomes evaluation. JAMA 2000;284 (13) 1689- 1695
Volkow, N.D., G.F. Koob, and A.T. McLellan. 2016. Neurobiologic advances from the brain disease model of addiction. New England Journal of Medicine 374: 363-371.