Choice, Pathology, and the Disease Model of Addiction
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.
Clinical Supervisor for two psychiatry floors in a community hospital in WV. Currently pursuing a MSN to become a PMHNP.
Joined Jul '16; Posts: 46; Likes: 86.May 18, '17I kinda like calling it a disorder which is how most mental health conditions and "behavioral addictions" are termed. Disease implies we already understand the pathology behind addiction which we don't.May 18, '17We understand the pathology fairly well. Like all things in medical science, we do not have the full picture. There are very few disorders that are not also diseases, since the terms are not mutually exclusive.May 19, '17The disease model for addiction has been around for more than 30 years. The real question is: Has adopting the disease model improved outcomes? It seems to me that the number of addictions and people chronically in treatment keeps going up. One guy told me last week, "I'm on six antidepressants and I'm still not happy." Do you see the migration to the disease model improving outcomes on a large scale?Last edit by RobbiRN on May 19, '17 : Reason: clarityMay 19, '17The disease model has been around, largely in the medical community. The general public and more importantly (perhaps as a consequence of public consensus) policy-makers have been much slower in adoption. So, despite many healthcare providers understanding this...we have not, as a society, practiced it.
Fortunately, however, this is not an unknowable question. When wondering if outcomes can be improved through this understanding, we can examine data and see that countries that use this model to guide policy tend to have much better outcomes. Harm reduction, greater access to treatment (with a welcoming of medication-assisted treatment), and destigmatization are all effective strategy.May 19, '17Lol. Win some. Lose some. Check out the NEJM reference for a less 'ostentatious,' satisfyingly denser article. Don't let my writing style turn you off to soaking up the exciting research that continues to come out.Last edit by Issaiah1332 on May 19, '17 : Reason: AddingMay 19, '17Quote from Issaiah1332If you are suggesting that the US is lagging behind the rest of the world in passing out pills to treat addiction, or anything else, I don't buy it. The US already uses the disease model to treat every problem imaginable. We lead the world in passing out prescriptions to create addiction. There is a well-documented opiate abuse epidemic ("disease") in our country with 33,000 OD deaths in 2015. 80% of the opiates consumed on the planet are downed by Americans. And the answer is more pills? Based on the consumption stats alone, in general, other countries start their better outcomes by creating fewer addicts. No one gets addicted to pills he or she has never taken.The disease model has been around, largely in the medical community. The general public and more importantly (perhaps as a consequence of public consensus) policy-makers have been much slower in adoption. So, despite many healthcare providers understanding this...we have not, as a society, practiced it.
Fortunately, however, this is not an unknowable question. When wondering if outcomes can be improved through this understanding, we can examine data and see that countries that use this model to guide policy tend to have much better outcomes. Harm reduction, greater access to treatment (with a welcoming of medication-assisted treatment), and destigmatization are all effective strategy.May 19, '17Interesting...there comes that anger again.
"No one gets addicted to pills he or she has never taken"
I think I address that argument. You'd have to discount the fact that people begin using for a legitimate reason, genetic predisposition, and the whole fact that the choice doesn't negate the disease. That is to say, regardless of the genesis, people need treatment.
Of course, medication-assisted treatment doesn't HAVE to rely on pills at all. There are monthly antagonist injections.
"And the answer is more pills?"
Well, assuming you're referring to something like suboxone, then the answer would be: "yes, for some people." Especially considering the fact that overdose rates are cut in half with its usage, fatal adult overdoses are extremely rare in the US and, by the way, other countries have used this strategy. Let's stop pretending all drugs are created equal.
Yeah, we use the disease model to treat many things; but largely public policy has not adapted to do so for addiction. This is evident in much of the data and the differences in that data as differentiates countries. Sure, countries start at differing points in severity; but their policies still show positive outcomes.Last edit by Issaiah1332 on May 19, '17 : Reason: Adding "adult"May 20, '17Isn't is intersting that the addiction rate has skyrocketed ever since we started calling addiction disease? I think it's a grave error to give addicts this to hang their hats on. I know so many addicts now that "I can't help myself...after all, I have a real disease." It's an addiction. The insurance companies love this and so do the addicts. It vindicates the addiction. I know I'm in the minority here but as I watch the bodies pile up in the name of disease; it just proves my point.
When are we going to start calling smoking ciggarettes a disease, or shopping? Compulsive behavior has it's place in the mental health field. If I change my diet my brain and function change. I can mentally alter my brain processes with no outside sources...do I have a disease?
Now that society is more accepting of addiction we need to make a new model that fits addiciton more precisely. We are doing no one any favors keeping this on the disease model. When addicts start taking responsibility for their actions again; that will be the day addiction rates go back down.
Disorder v disease...May 20, '17You can correlate the rise of addiction with a variety of things, but the disease model isn't one of them. Unless you have some data to support it. The research grew out of the explosion of addiction, not the other way around.
No one is giving addicted people an excuse but understanding the etiology/pathology of addiction. Per definition, it is a disease. This is a categorical determination provided by the community of experts studying the phenomenon. Frankly, whether something can be an excuse or not and regardless of whether it's a contributing factor to its increase...neither matters in the determination.
Type II diabetes is a condition riddled with choice. There are instances in which it can be entirely prevented and entirely controlled with little more than choice. That doesn't change the words nor the disease state.
Also- you can't THINK your brain into changing. The ability to think a certain way and the degree of will one has is laid out in the physiologic and genetic cards one draws at birth. This is the Cartesian dualism I address. Your mind isn't separate and it surely isn't a small being sitting in your skull and pulling levers based on its current whim.
People love to state that "things haven't gotten better since we called it a disease!" Well, surely one can call anything any word they want...unless one actually DOES something about it, then things don't change. I'm not sure why so many of these comments presume that we've suddenly become so exceptionally compassionate and evidence-based, as a society, when it comes to treating addiction. We haven't.
We have very little treatment centers. We largely incarcerate the addicted. We have incorporated no, large-scale harm reduction techniques. We drastically limit the ability of providers to prescribe agonist-antagonist opioid treatment, whilst not instituting any limitations on the amount of patients a provider can hand out oxycodone to. We continue to stigmatize an entire subset of the mental health community and somehow take pride in the gross ignorance of scientific fact and research (the only medical condition we do this with and that it's acceptable).
Yes, a cigarette smoker is addicted and they have a disease. Just as dumping tons of sugar into your body can produce a disordered, diseases pathology...so can tobacco. Considering the profound epigenetic changes, which can actually predispose one to additional addictions (such as cocaine), and the same, general feedback loop malfunction...this applies. I say this with hours of training, a certification, and as one that teaches tobacco cessation (an area where we have no problem providing agonist treatment with, by the way). My article was never meant to solely rest on opioid addiction. It just so happens that people have chosen to ignore the other addictions. I'd imagine this is because it's easier to point the finger at this group.
"We are not doing any favors keeping the disease model"
Science doesn't merely 'do favors,' it allows evidence to navigate categorical determination and treatment. So, considering that we've actually seen evidence that indicates positive outcome in the utilization of this model...then it certainly appears your anecdotal account is wrong and that we may very well be doing sufferers, as well as society (especially as crime rates lower with these interventions), a "favor."Last edit by Issaiah1332 on May 20, '17May 20, '17Issaiah1332
1. You stated "You can't think your brain into changing."
But you can indeed think your brain into changing. We have really good evidence for that.
Biologic effects of mindfulness meditation: growing insights into neurobiologic aspects of the prevention of depression
2. When we talk about "disease model" we are really talking about at least 3 different models.
The disease model for scientific understanding of addiction.
The disease model for treating addiction.
The disease model for social understanding of addiction.
The "model" may work for one or two of these but not all. It might be better as a metaphor. Your article clumps these all together.
You argue that the disease model is not responsible for recent increase in addiction. Maybe.
But the adaptation of the disease model has not brought down rates of addiction. So it is fair to question its usefulness.
You are relating stigma to questioning of the disease model. But we can acknowledge that stigma is harmful while still questioning the disease model. Put another way, just because stigma is wrong doesn't mean that the disease model is right.
Your discussion of cartesian dualism and thus on the existence of free will, separation of mind and matter, are clouding and clogging the issue.
We should be able to have a discussion about healthcare delivery for addicts without going all the way back to "I think, therefore I am." Shouldn't we?May 20, '171. I concede the notion of neural plasticity IN the article. The idea, however, that one can simply change their brain into whatever structure one believes is simply not the case (I realize this isn’t necessarily what you’re saying). You have only a certain range of adaptation within your biology's set of possibilities, nothing more. Take psychopathy, for example, through empathy training...many psychopaths can be trained to develop a higher degree of cognitive empathy and, to a much lesser degree, some affective empathy. The notion, however, that someone with a genetic predisposition to violence (a certain allele, for instance, on the MAO gene) and tons of other deficits in the empathy circuit, is suddenly going to become an empath paralyzed by their own good will is profoundly unlikely. Your will is simply not separate from your biology. The degree to which you are even capable of thinking about thinking about some of these changes is dependent on biologic structure.
Yes, meditation and mindfulness (something I am a huge proponent of and incorporate into every, single group I facilitate) can get you so far. SO FAR. You're not going to meditate or otherwise will your way out of something like schizophrenia or autism. Even if one concedes that there are some diseases of the brain/mind in which one can will their way out of, this provides nothing in negating the disease model.
2. You're playing semantics. I absolutely mean to "clump them all together." When I say "disease model" I am referring to the scientific understanding and applications. The social understanding should follow. Unless, that is, there is evidence to the contrary. It seems, however, that the evidence largely favors the disease model and how it relates to public policy.
Perhaps, there are ways to apply the same interventions that have been shown to work and not agree with the disease model…that is certainly possible. It could be that some of the interventions people, like myself, advocate for get it right just by happenstance and that this could be accomplished via a different model. If the evidence eventually goes that way, then we will have to adapt accordingly. This is what science, especially medicine, has done for centuries. Right now, however, this isn’t happening.
"But the adaptation of the disease model has not brought down rates of addiction. So it is fair to question its usefulness."
That would be fair, IF IT HAS BEEN APPLIED. I have addressed this. Unless you can reference public policy or the ways that this has been effectively applied...then this objection holds no water. It simply hasn't found application. The fact that medical professionals continue to debate scientific evidence is, alone, a premise in support of my point. I listed some holes in the treatment model we are currently applying. Actually, the interventions that one would expect to be a consequence of this model are showing to be VERY effective.
But let us assume some things, hypothetically. Assume that we, as a society, largely go the direction I am advocating for; but the rates of addiction seem to remain stagnate. Does this mean that we are completely wrong about the model and we should scrap it? Of course not. The disease model could be the perfect model and the interventions not be right route. It would certainly depend on measurement, too. It could be that the incidence of addiction is equal to or greater than the rate of improvement in those already addicted. Possibly addiction, as a disease, is more treatment resistant than anticipated. Many of the archaic ways we’ve used to treat other diseases were mostly ineffective throughout history, but this doesn’t mean they were wrong to assume a given condition was a disease and needed medical treatment. It could be due to an entirely different variable. A recent example is adolescent smoking. We’ve seen this as a public health issue for decades and have sought to educate against it. This has mostly been successful. Recently, however, adolescent smoking has increased for the first time in years in the US. This doesn’t mean we throw away everything we’ve been doing. There is simply another variable, electronic cigarettes, that is shaping this phenomenon.
3. "You are relating stigma to questioning of the disease model. But we can acknowledge that stigma is harmful while still questioning the disease model. Put another way, just because stigma is wrong doesn't mean that the disease model is right."
I apologize if this is how it came off, but this is not my point at all. I don’t mean to say that there is an inverse relationship between the two in the way you describe. My point was that the stigma that this is a moral failing is preventing the disease model from effectively being applied.
"Your discussion of cartesian dualism and thus on the existence of free will, separation of mind and matter, are clouding and clogging the issue."
The discussion on existence of libertarian free will (mostly debunked by science) is a direct consequence in the notion of biology and the manifestation of disease. I don't mean to clog the issue. I think this is getting into an area that is too philosophically dense (which I actually enjoy, but don't mean to conflate here). So long as one thinks that one can merely will themselves out of addiction, as if waking up one day and making a choice magically erases the pathologic changes, then the thinking will be wrong. MOST addicted people WANT to be free of their addiction. MOST will make the choice to be clean and do so over and over, but MOST will relapse. This isn’t testament to poor willpower. It’s testament to the changes of the brain. I'll try to sum up how I see this as relevant:
-As far as the causal chain: I am not sure where free will falls. I simply don't know, which is something I don't mind saying. We know that genetics play a big role, but we also are gaining broader understanding of epigenetic changes too (the classic nature/nurture issue). Whether that necessarily predestines one to addiction...I'm not sure. Part of me wants to say that this is probably not the case, at least not in a linear, simplistic way. I think there is a choice at the start: "Do I take this drug or not" and then it is likely the case that genetics and environment start doing their work. Of course, the other side of that is that if this is the case...then odds are one will come in contact with an addictive behavior or substance at some point. So...how "free" is it? We know environment is a HUGE factor (we see this in the Rat Park experiments), how much choice does one really have over environment? Not much, at least in the beginning of one's life, which happens to be the most formative years in neural development.
-The ability to think is not separate from the brain, was what I was meaning. Certainly the power of thought is important, but there are occasions where the full spectrum of thought is not available to a person. We see this when depressed people feel helpless and are unable to see beyond their depression. They can adapt through therapy. I would never advocate that therapy, largely dependent on the power of thinking, is fruitless. If, however, one is completely constricted (perhaps neurochemically)…then therapy will not be effective. A depressed person may need to do nothing more than some lifestyle changes, get away from a spouse, get a job, etc; but they may very well be unable to see beyond their depression to make those changes or to be receptive to therapy. This is why antidepressants can be so effective. We tweak the chemicals, provide the molecular foundation necessary for one to be receptive to therapy so they can make changes and then possibly we taper the medication away. Until then, however, there may be an entire degree of thought unavailable to them.
"We should be able to have a discussion about healthcare delivery for addicts without going all the way back to "I think, therefore I am." Shouldn't we?"
I love that and I don't mean that sarcastically. I think it’s a really eloquently put and important question. My immediate response is: yes and no. I'm not sure we need to go back to that point, because we know that "choice" and free will (as it relates to the start of a pathology) is irrelevant in the definition of disease. But I still think it is important to understanding and treating disease, for some reasons you may agree with. I see the brain as malleable within the confines of one’s specific possibility. CBT can help one shape their perspective, gain insight, take responsibility, and make the changes necessary for remaining sober. Medication, in many forms (not just Suboxone), may be able to tweak the chemistry enough to provide one with the clarity necessary for these changes to be effective. Clearly, if I saw addiction as a stagnate fate, then I wouldn’t argue for the importance of treatment. One’s biology can shape predispositions and the changes undergone in addiction can absolutely affect the decision-making capacity of the sufferer. This doesn’t mean they are helpless. We can help reverse those changes, but it takes time. We can seek to alleviate some of the risk factors and predispositions, while developing strategies to help the sufferer live with those things we cannot change. We do this with many diseases.
I think that there is a misunderstanding, judging by several comments here, of my position. I don't mean to overemphasize free will. I was actually wanting to do the opposite. Whether one chooses to first act or not says nothing as to the disease state after the fact. My intent of this article was to argue for the disease model and why it applies via elaborating on the physiologic justifications for why we call addiction a disease. It wasn’t intended to be comprehensive. I just noticed that many people seem to oversimplify this as all having to do with choice and willpower. I wanted to shed light on the physiologic changes and why it isn’t this simple.
So...there's a novel in response. My apologies for length and any typos.Last edit by Issaiah1332 on May 20, '17
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