caileesnana

Is Addiction Really a Disease?
By Kevin T. McCauley, M.D.

This year the American Society of Addiction Medicine celebrates its 50th anniversary. Yet even after a half-century of accomplishments, the field of addiction medicine struggles for legitimacy. And while a recent study by Harvard University and the Robert Wood Johnson Foundation demonstrated that most Americans believe that addiction is a medical problem, the debate over whether or not addiction can truly be considered a disease continues.

The argument against calling addiction a disease centers on the nature of free will. This argument, which I will refer to as the “choice argument,” considers addiction to be a choice: the addict had the choice to start using drugs. Real diseases, on the other hand, are not choices: the diabetic did not have the choice to get diabetes. The choice argument posits that the addict can stop using drugs at any time if properly coerced.

In making the argument in favor of calling addiction a disease, it is important to tacitly admit that the behavior of addicts is unpleasant. To be sure, the behavior of addicts can be frustrating, revolting — even criminal. But in medicine, the character of the patient is separated from his or her symptoms, however unpleasant or harmful. Patients are not judged based on the palatability of their symptoms. If that were the case, patients with cholera would receive the harshest sentences.

I would like to think that physicians do this out of a sense of clinical humility for medicine’s past mistakes. Many times, we have thought we were looking at badness when, in fact, we were looking at a disease process. Just because we observe bad behavior in a patient, we cannot always be certain that what is driving that behavior is some kind of intrinsic badness.

The law makes a similar distinction. Except in cases of strict liability, a truly just conviction requires more than the commission of a harmful act. The prosecution must show intent, a state of mind bent on doing harm.

So when we ask the question, “Is addiction really a disease?” we are asking a question about causality: I’m seeing bad behavior, what’s the cause? Are addicts sociopaths? Are they inherently liars, cheats, and thieves? Do they have an addictive personality disorder? Did their parents raise them improperly? Did they learn addictive behavior from a bad crowd? We have bad acts, but do we have bad actors? Or are these symptoms of a disease?

To answer the disease question, we must have a standard. What is disease? What does it take to get into the “disease club” and earn the rights and privileges that accompany that distinction? In medicine, the causal model we use to explain illness is the disease model. This model, which is only 100 years old, emerged from the germ theory described by early microbiologists such as Louis Pasteur and Robert Koch.

Simply put, the disease model says that you have an organ (bone, liver) that gets a physical, cellular defect (cells die, cancer develops, an infection sets in, a bullet whizzes through the organ), and as a result you see symptoms. You see the same symptoms in all patients with that defect in that organ, differing only by severity or stage of illness.

It is easy to see how the disease model works. Let’s take a broken leg. The organ is the femur, the defect is a fracture, and the symptoms are screaming, bleeding, bone deformity, and disability. The beauty of the disease model is that it strips away the nonsense about personality and social environment. There is no “femoral personality disorder.” We don’t have a problem with “femur gangs.” The disease model gets us to the real cause of the problem: the fracture. It tells us how to treat this patient. We do not go after the symptoms, we go after the defect — fix that, and the symptoms go away. In the case of diabetes, the organ is the pancreas, the defect is islet cell death leading to a lack of insulin, and the symptoms are the seemingly unrelated symptoms that go along with diabetes. We can’t cure diabetes, but the model reveals how to treat it — we replace the insulin and the symptoms get better. It may not look like much, but the disease model is so powerful a causal model that it has doubled the human lifespan in less than a century.

One hundred years ago, doctors knew they had a winner. Doctors knew the disease model would boost medicine’s reputation; for the credibility of medicine, they had to decide what was and was not a disease. It was easy to see how a broken leg fit the disease model. They could even fit diabetes to the model. But addiction? What was the organ? The brain? Some doctors thought it might be the liver. What was the defect in addiction? And what about the symptoms? At first glance, the symptoms of addiction don’t look like symptoms at all. They look like badness. And so doctors made a decision that affects every day of every addict’s life: they decided that addiction was no longer a disease.

Almost overnight, treatment innovation for addiction ended, research into the problem of addiction stopped, and advocacy on the part of physicians for their addicted patients ceased. When doctors could not fit addiction to the new disease model, they walked away. That didn’t mean that addiction disappeared. It meant that another group of professionals had to come in and handle the problem. That group is the criminal justice system.

And so today there are more than two million people in prison — many of them nonviolent drug offenders, many more convicted for offenses committed under the influence of drugs or alcohol. Because doctors abdicated their responsibility to addicted patients, the United States deals with addiction punitively. But with numbers like two million, the problem looks less like a criminal justice problem and more like a public health problem. The problem falls back into medicine’s lap.

If we could fit addiction to the disease model — if we could show what part of the brain was involved in addiction, what the nature of the defect was, and link that defect in that organ to the symptoms of addiction, then addiction would be a disease. Everything would change. And for 100 years we’ve been unable to do that.

Until now. In the last few years we have finally learned enough about the brain — we have finally gotten enough pieces of the puzzle — that we know exactly what part of the brain is involved in addiction. We know the nature of the defect. And we can link that defect in the brain to the frustrating, revolting, and criminal symptoms of addiction. For the first time in the history of medicine we have some hard and fast knowledge about what happens in the human brain when it becomes addicted to drugs. There are very good brain chemistry reasons for the things addicts do. We can explain everything about addiction without having to resort to causal variables like “bad choices” or “addict personality.”

That information is very powerful. I believe that in our lifetimes, we will see everything that we do for addiction change. I believe that the people in treatment centers today are among the last generation of Americans who will be faced with the threat of a jail cell if they don’t sober up on somebody else’s timeframe.

Here is a brief summary of what we know in neuroscience about addiction:


Drugs work in the midbrain. This is not the part of the brain that handles morality, personality, parental input, sociality, or conscious choice. That processing takes place in the cerebral cortex. The midbrain is the amoral, limbic, reflexive, unconscious survival brain. As humans, we have a bias in favor of the cortex. We believe that the cortex should be able to overcome the libidinal impulses of the midbrain. Normally that’s exactly what happens. But in addiction, a defect occurs at a level of brain processing far earlier than cortical processing. The midbrain becomes bigger than the cortex.

While predisposing factors are important (especially genetic burden), the primary cause of addiction is stress. We all face stress, but not all of us experience it in the same way. The stress that changes the midbrain is chronic, severe, and unmanaged. When the cortex does not resolve the stress, the midbrain begins to interpret it as a threat to survival.

Persistent severe stress releases hormones such as Corticotripin Releasing Factor (CRF). CRF acts on genes for novelty-seeking and dopamine neurotransmission. People under severe stress increase their risk-taking behavior in the search for relief. At the same time, the brain’s ability to perceive pleasure and reward — mediated through dopamine — becomes deranged. The patient becomes anhedonic. He or she is unable to derive normal pleasure from things that used to be pleasurable. Addiction is a stress-induced defect in the midbrain’s ability to properly perceive pleasure.

Drugs of abuse, whether uppers or downers, b or weak, legal or illegal, have a common property: they cause the rapid release of dopamine in the midbrain. If the stressed and anhedonic patient is exposed to this drug-induced surge of dopamine, the midbrain will recognize a dramatic relief in the stress and tag the drug as a survival coping mechanism. At this point the line is crossed — from the normal, drug-using, or drug-abusing brain to the drug-addicted brain. The drug is no longer just a drug. As far as the midbrain is concerned, it is life itself. This process tagging of the drug is unconscious and reflexive. Conscious cortical processing is not involved.

Increases in stress (and CRF) trigger craving — a tool the midbrain uses to motivate the individual to seek the drug. For non-addicts, craving is simply an unusually b desire. Even though the word is the same, it is critical to remember that craving for the addict is a constant, intrusive, involuntary obsession that will persist until the drug is ingested and the survival threat is relieved. Craving is true suffering. The tendency to underestimate the misery of craving is a major reason for the failure by healthcare professionals to effectively intervene in addictive behavior. Brain imaging is able to demonstrate a difference in the midbrain activity of the addict and non-addict during craving. (These scans also demonstrate a relative inactivity in the cortex.)


In light of this new understanding of addiction in neuroscience, the choice argument takes several hits:


Punishment will not work to coerce addicts into making the right choice because the drug is tagged at the level of survival. Nothing is higher than survival. And so nothing used as leverage — threat of loss of job, prison, loss of child custody — can compete with an existential threat. The midbrain give the addict the message that the way to take care of the children, keep the job, calm the probation officer is to first secure survival (by using the drug). When the craving really kicks in, punishment has no effect and coercion is useless.

Addiction is a disorder of pleasure. I believe all the moral loading of addiction stems from the fact that the patient with a disorder in his or her ability to correctly perceive pleasure is much more likely to be interpreted as being immoral before he or she is seen as being blind or deaf.

Under stress, the addict craves drugs. As far as the midbrain is concerned, the addict’s moral sense is now a hindrance to securing survival. It is not that addicts don’t have values; in the heat of that survival panic, the addict cannot draw upon his or her values to guide behavior. Values and behavior become progressively out of congruence, increasing stress. In order to consummate the craving, the addict’s cortex will shut down. But that’s not the same as badness. The absence of one thing (cortical function) cannot stand for the presence of another (criminal intent).

While it is true that a gun to the head can convince the addict to choose not to use drugs, the addict is still craving. The addict does not have the choice not to crave. If all you do is measure addiction by the behavior of the addict — using, not using — you miss the most important part of addiction: the patient’s suffering. The choice argument falls into the trap of behavioral solipsism.

Just as a defect in the bone can be a fracture and a defect in the pancreas can lead to diabetes, a defect in the brain leads to changes in behavior. In attempting to separate behaviors (which are always choices) from symptoms (the result of a disease process), the choice argument ignores the findings of neurology. Defects in the brain can cause brain processes to falter. Free will is not all-or-nothing; it fluctuates under survival stress.


This information allows us to fit addiction to the disease model: the organ is the midbrain, the defect is a stress-induced hedonic (pleasure) dysregulation, and the symptoms are loss-of-control of drug use, craving, and persistent use of the drug despite negative consequences.

But something very important happened when I filled in the disease model for addiction: addicts became patients! And that means addicts earn the same rights as the patient with diabetes or a broken leg. If I cannot ethically punish the diabetic, I cannot ethically punish the addict. If I cannot effectively treat broken legs with incarceration, I cannot treat addiction with jail time.