AddictionDoctor.Org

On August 15th, ASAM published their new definition of Addiction, and on August 16th Maia Szalavitz, a health writer for Time, published an online critique of it. That was quick, she must be a fast reader.

Her first point is that while the intention of the new definition is, in part, to decrease stigma, calling something a brain disease is a bad way to do it. As evidence she sights a 2010 study in the American Journal of Psychiatry by Pescosolido, et al, entitled, “A Disease Like Any Other?” The study examined the difference in attitudes toward Major Depression, Schizophrenia, and Alcohol Dependence between 1996 and 2006 with regard to the public’s acceptance of these as neurobiological disorders and associated stigma. She points out that:

“While the percentage of people who said they believed alcoholism was a brain disorder increased from 38% to 47%, that shift was not linked with a decrease in stigma. In fact, over the same time period, the percentage of people who said they thought alcoholism was linked with “bad character” also increased significantly, from 49% to 65%.”

Ms Szalavitz misses the internal inconsistency in the data that stems from the “old” definition of addiction. Until ASAM’s new definition, every biological explanation of addiction as a whole or divided up into parts as addictions considered the etiology of the illness to be the drug which was used. Only such a definition could lead us to an increased understanding of something as a disease of bad character. What is missing in her critique is an examination of the real difference in the new definition: the word primary.

What ASAM’s definition says, at least by my reading, is that addiction is a primary change in brain function leading to symptoms which leads to the characteristic behavioral manifestations. This is utterly new. Addiction is not caused by using drugs; there is no mistake made by a weak person of bad character which caused the illness. This concept is so new, so different from what the public has been taught to believe that any past examination of beliefs about addiction would hardly be relevant.

Ms Szalavitz’s second point is that the word “chronic” in the definition is just wrong. As evidence she sites a study by Dawson et al in Addiction in 2005 that examined a natural history of DSM-IV alcohol dependence. Again, what she misses is the essential point. DSM defines alcohol dependence on a set a behaviors rather than as a biological disorder; it assumes no active illness if behavior changes, and does not consider drug switching in the definition. So in DSM, an alcohol dependent person who meets three of the seven criteria in a 12 month period modifies his drinking by increasing his use of pot (or overeating, or cigarettes or any other source of increased midbrain dopamine tone) no longer meets criteria for active alcohol dependence and would have been categorized in Dawson’s study as in non-abstinent recovery. What ASAM says is chronic is not the behavior, but the illness.

What ASAM’s definition gives us is a bottom up biologically based view much more like other illnesses than the behaviorally based view of DSM that has confused the public (and the press) into understanding addiction as a self caused “disease.” What seems to upset Ms Szalavitz is that ASAM is using words in it’s new definition that don’t fit her old definition.

Here’s her final example: the word spiritual. I take her point, “When trying to convince doctors and the general public that a condition is a genuine disease, I would argue that it’s probably best to leave God out of it.” However, as most people associate recovery from addiction with 12-step recovery, some concept of how the neurobiological fits with the spiritual may actually help with the acceptance of the definition. I won’t say more here as I have already written enough on this in a previous blog post in May of 2010.

Ms Svalavitz ends with, “Like depression, addiction is a real medical disorder that affects the brain. But if we want to reduce the stigma associated with it, emphasizing recovery and resilience is probably more useful than focusing on definitions of brain disease. To increase the use of effective and non-stigmatizing care, let’s stick to the empirical evidence, not the ineffable.” ASAM’s definition is based on far more empirical evidence of neurbiology than any previous definition. While I agree that focusing on recovery is important, the mistreatment, misunderstanding, and mis-application of treatment principles that have stood in the way of the recovery of so many is so pervasive in our field that ASAM would have been negligent not to step up and, using the latest scientific findings, give us a new view that offers a great improvement in treatment options.

© Howard C Wetsman MD FASAM

I was amused to hear from the computer support person that my problem was a PICNIC. What’s a PICNIC? “Problem in chair, not in computer.”

Genetic studies have a similar problem. Let call it PIPNIG, Problem in phenotype, not in genotype.

Let’s say that we are going to do a study looking for the genetics of depression. The first problem will be the diagnosis of depression. The American Psychiatric Association has a definition by criteria for the diagnosis in DSM IV, but most people in America use the word to mean something different. Well that’s so obvious that no one would use a question such as “Have you ever had depression?” for a genetic study. Perhaps they’d tighten that up by saying, “Have you ever been treated by a physician for depression?”

That won’t be a whole lot better. Most cases of “depression” are treated by physicians who aren’t psychiatrists and who aren’t fluent in the diagnostic criteria in DSM. In addition to that anti-depressants are used for a variety of symptoms and syndromes and patients aren’t always clear about what they are being treated for. So people taking Prozac for pre-menstrual dysphoric disorder may very well think they are being treated for depression when they learn the medicine is an anti-depressant. I hear this response from patients all the time.

So it’s probably already obvious that it’s going to be a bigger problem to get information on psychiatric illnesses than, let’s say, gall stones. I mean, there either were gall stones or not. I know, there are still some confounders, but it’s a lot clearer than depression.

So we’ll have to move away from single question screening for phenotype. Maybe we should use the criteria themselves? Good idea. Should we use DSM IV? Or the Research Diagnostic Criteria? Or the ICD-10 criteria? Or perhaps some of the other many criteria invented to define the illness. And while we’re on the subject of the illness, should we use the criteria for major depression or dysthymia. reactive depression or atypical depression?

People have developed elaborate researcher given sets of questions to answer who has what. Even then, these are questions that are mostly behavioral or not biologically based, so that what we’ve really got is a group of man-made “phenotypes.” It’s so bad that if someone’s genetic research validated the current constructs, I’d have a tough time believing they didn’t make up the data. A genetic study that showed no association to these man-made constructs would be believable.

The bottom line is that the broken bone of mental illness has been missing all along. If you break your leg, you can take an X ray and see it’s broken. If there’s a problem with your brain, mostly we’ve been relying on seeing evidence in your behavior. So our definitions are behavioral and not, largely, biological. So if genetic studies don’t have great results with psychiatric illness, there’s a good reason: PIPNIG.

So what’s the solution? Stop using psychiatric diagnoses in genetic studies. Instead use actual biological phenotype. It won’t get us the holy grail answers the first time out but it will define and help us segregate the actual biological issues and eventually clarify the core of the problem. What are some of these? There are lab tests, but if we’re going to limit ourselves to self reports in order to get a lot of research done quickly we’re going to have to pass those up.

Here are some examples of what we could ask:

1. If you are a woman, if you have ever been pregnant, if you feel you had chronic problems with low mood before pregnancy, did you notice that your mood was better when pregnant? [this measures for increased dopamine release with increased estrogen of pregnancy]

2. If you have ever been in an automobile accident in which you thought you would be killed or badly hurt, did you have sleep disturbance afterwards, and, if so, for how many days? [this is a proxy for the biological increase in autonomic sensitivity following trauma] [you could substitute any trauma or ask about many and combine for a trauma score - such as the Childhood Trauma Experiences Scale that Bess David and I developed] [you would want to ask about age of the trauma as well]

3. Have you ever been spoken to in such a shaming manner that you felt you’d never be happy again. [this is a proxy for the propensity for dopamine receptors to decrease in density when we are made to feel less than] [this may be a risk factor for early drug use]

I could keep going, but I think you get the point. We can take what we want to study and find in it the biological kernel and ask only about that. Hopefully, then, we won’t have a PIPNIG.

© Howard C Wetsman MD FASAM