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Imagine you walked into your doctor’s office for your annual check-up. Afterwards he asks you into his office to talk about the results (I know the idea of a doctor sitting down to talk to you is weird, but bear with me). He points out that your blood pressure is not in control. “Have you been taking your medicine, watching what you eat?” “Well, no,” you say. He looks at you with a condescending look and says, “Well, I guess your just not ready. Don’t bother me again until you are,” and fires you from his practice.

If that happened to me I’d feel a range of feelings: shame, rage, hurt, fear. All of which would decrease my dopamine receptor levels in my reward center and make it much less likely that I’ll actually feel any motivation to change and do what the doctor wants. In the addiction treatment world, I hear this kind of attitude all the time, and when I do, the practitioners of this schema inevitably say it works. If you only remember your successes, and forget the people who never come back, I’m sure it looks like a good plan. When I ask people who treat patients this way for written retention figures for their practice or program, I get blank stares.

There’s a fantasy that seems to infect addiction treaters; it’s called “The Bottom.” If everyone had a Bottom we could safely let go of them and let them keep falling until they hit it, and, then, they’d come back to us in a more reasonable teachable way. I think the origin of this fantasy is the experience of getting into recovery. So many of us got into the addiction treatment world through our own recovery that we think everyone has the experience we did. Well, the members of the addiction treatment community who got sober are a self selected group that had Bottoms. To assume everyone has one because you had one is like assuming everyone is as tall as you are. It makes no sense on the face of it.

And what if not everyone has a Bottom? If we let them drop assuming they’ll bounce, and there’s no Bottom, they’ll just die of this disease. Since most people with this disease die of it and very few get into and stay in treatment, I’m betting there’s more evidence against the fantasy of The Bottom than for it.

So when we’re faced with a patient who doesn’t want the treatment we offer, or doesn’t want to adhere to the treatment plan, or thinks there’s another way then what we say, we have two choices. One, my way or the highway; and two, okay let’s try it your way, but remember I have another one if this one doesn’t work. It’s pretty obvious to me that if we meet the patient where he is and pick number two we’ll be able to be of more help. However there are some barriers to picking number two, and they’re systemic in addiction treatment.

One is the limited training most people have who treat addiction. This society confuses drug use, drug abuse, and addiction on a daily basis. Because we focus on the drugs, we focus training on stopping the drugs. A great deal of my psychiatry residency was focused on dealing with resistance on the part of patients. Unfortunately it’s not a subject that gets a great deal of interest in the addiction field.

Another problem is the structure of the “programs” that treat addiction. If you’re a hammer, you only look for nails. If someone doesn’t want to be a nail, you’ll try to hammer him anyway. And when it doesn’t work; he just wasn’t ready to be a nail. If all you offer is inpatient treatment or IOP or residential 28 days then you can’t meet the patient where he is unless he’s where you are already. The goal should be to be a tool box, not a tool.

Many people call addiction a chronic disease, but until we in the addiction treatment field start treating our patients as if they are ill, instead of not ready, we’ll never be accepted by society or mainstream medicine as people who treat an illness. When we do start treating them as patients with an illness, I think they won’t feel so much shame, rage, hurt, and fear. Their dopamine tone will actually go up, and they’ll have more motivation to follow our advice. So the best reason to meet people where they are is because it works better.

As addiction is a chronic disease and medicine has been treating chronic diseases for years, we actually have something to look at in this case. We can look at how the rest of the medical world measures their chronic diseases and compare that to what we’re measuring in Addiction.

The first thing measured in any chronic disease is adherence to the care plan. For Diabetics it’s taking medicine, a good diet, and moderate exercise, etc. For addiction it’s don’t use, don’t use anything else, and participate in a recovery program. That’s actually as far as we’ve gotten. What we’ve been measuring isn’t relapse, though we call it that. Relapse is the return of previously suppressed symptoms and we’ll get to that in a minute, but what we’ve been measuring is only the patients adherence to the plan of care. At least we were doing that much.

But adherence isn’t very good in any chronic disease, something like 30-40% is about as good as it gets. People get tired of being sick. They long for a vacation from abnormality. They want to behave and feel like a normal person. They want to forget they’re ill, and to do that, they have to forget the care plan. Are addicts any different? Not in the least. Addicts get tired of having to know they’re different. They just want to feel normal and so, like diabetics, they forget they’re ill and try to live without the care plan from time to time. And it’s important to adhere to the care plan, because, hopefully, it’s what’s keeping those symptoms suppressed.

Has it been a minute yet? We’re ready for the symptoms. For a diabetic the symptoms would be loss of control of blood glucose levels. In addiction the symptoms, are not drug use, but the expression that led to the use of drugs in the first place. Those are largely the low dopamine symptoms I’ve written about elsewhere so I won’t go into a big discussion here. I only want to mention that when we have measured these in our field, since the role of symptom was already being mistakenly taken by drug use, we had nothing to call these symptoms but co-morbid illnesses. We’ll get back to measuring co-morbidity in another minute.

So we have adherence to the care plan and symptom suppression. They actually exist in a kind of circle. If you don’t adhere, you get symptoms. As you suppress symptoms the urgency of adherence goes away and you tend to non-adherence. Any understanding of outcomes of a chronic disease has to take into consideration the non-linear nature of the natural history of a chronic disease. We’ve been trying to measure a donut’s circumference with a yard stick, perhaps possible, but needlessly difficult.

We need to also measure function. Treatment of symptoms doesn’t do the patient or society a whole lot of good unless we restore the patient to full function, or as close as we can get. Here we have things like relationships, work, ability to take care of the normal duties of life. Addiction outcomes have measured some of these, and it’s becoming more popular to do so. One thing we rarely do is ask the patient’s spouse how they are doing. That would be an eye-opener I’ll bet. So, how’s the relationship? How’s work? That’s an outcome of treatment for a chronic disease as well. Has it been another minute already? Time flies when you’re talking about outcomes. So now on to co-morbidities.

With co-morbidities we actually have two subjects: those illnesses that naturally travel with the chronic disease who’s outcome we’re measuring and those illnesses caused by the disease we’re measuring. Of course, we’ll look at the last one first. In diabetes we’d look for changes in vision and any sign of developing heart disease among other things. For addiction we may look for sequelae of drug use or of the use of compulsive behaviors (gaining weight, losing money, etc). Those we’re used to, but are there really illnesses that are naturally co-morbid with addiction? I personally doubt it. When you look deeply at what we’ve called commonly co-morbid illnesses, you find the primary symptoms of Addiction. Sure people have Addiction and Major Depression, but no more often than a population under stress gets Major Depression. Sure you see Bipolar Mood Disorder and Addiction, but no more often than you see Bipolar Mood Disorder in non-addicts, if you understand the bipolar nature of addiction itself. OCD? Schizophrenia? All about in the same amounts you’d see in anyone else. The closest I can come to understanding a true co-traveler with Addiction is PTSD and the only mechanism I can imagine is the consequence of the patient’s parent having Addiction so, it too, is a sequela, not a fellow traveler.

So, what should we measure? Not using? Certainly. But it can’t end there. We need to measure not only adherence but symptoms. And we need to measure them in a way that is informed by the circular nature of their relationship. We also need to measure function, both social and occupational. What Addiction outcomes lack most is the surveillance of sequelae. We can’t measure 6 month outcomes, it’s a chronic disease. We need to measure outcomes for life.

One other thought on outcomes, and here, even the rest of medicine is behind. We need to consider the patient’s goal in their recovery from a chronic disease. We may have the ethic that the patient should function as well as possible for as long as possible and die of something else. That may not be what the patient wants. If we decide to measure things that are not in the direction of the patient’s wishes, we will not likely show success. Our field needs a vigorous discussion about this, as we are particularly resistant to hearing the patient’s goal when we come up with a treatment plan.

Like underwater reefs, hidden barriers can rip the bottom out of a patient’s ship as he tries to sail into safe harbor. And like any harbor manager, treatment programs like to look down and see their port filled with busy and vigorous ships producing lots of commerce. In the case of the treatment centers, it’s lots of healthy recovering patients staying sober. And in both cases, the harder you make it to get into your harbor, the more likely it will be that only the better equipped ships with the least damage will get in.

Of course there’s  a constant tension between profit and outcomes. The harder you make it to get into your treatment program, the fewer people you’ll be able to treat. A good port changes itself to fit its customers by providing berthing and services that are varied and can accommodate a wide range of ship types. That’s what we ought to do as well, let in everyone and make ourselves flexible enough to handle the diversity.

If you ask treatment providers, 90% will tell you they already do that. If you ask drivers, 90% say they are above average drivers, too. So let’s not ask treatment providers, let’s think about this from the patient’s perspective.

What if I don’t want to go to AA? What if I really don’t want to try for full abstinence? What if I don’t believe I’m ill and should stop drinking? Our traditional answer has been, “Well you’re not ready. Go back out and drink some more until you’re ready to do it my way.” How arrogant can we get?

So we only take patients when they’re ready, and we show our outcomes to the world as if they were our creation. It reminds me of a line in a poem by New Orleans poet, Brod Bagert, “Born on third-base and think they hit a triple.” That’s us, working with a selected population and thinking we did all the work. I guess we did do the work; we set up the barriers.

The one thing we most commonly ask is, “Are you ready to stop?” And what’s the one thing we measure? Staying stopped. That’s a little self-serving isn’t it? What if the patient got to pick the outcome? What would he pick? And what’s the point of our treatment?

We’ll start with the last one first. The point of treating any chronic illness is to suppress symptoms and prevent progression. If you’ve been reading this blog you know that I think addiction symptoms start before the first “drug” use and, in fact, lead to the drug use. What most people with addiction will pick as a goal is to feel better, to be able to function normally, and, if given the choice, at the beginning of treatment they would probably not pick spiritual enlightenment as a goal. Does your doctor say things like, “Alright lady, if you don’t lose 100 pounds I’m not treating your diabetes,” or, “Cut out the salt or you and your high blood pressure are out of my practice,” or, “Buddy, get rid of the dog, or I’m not giving you your asthma medicine.” What if Buddy’s goal is to do the best with his asthma that he can while still keeping the dog he loves?

Someone’s out there saying, “That Wetsman guy just wants to give people medicine and let them drink if they want to.” No he doesn’t. Let me tell you about Carlos (obviously, I’m not using his real name), a guy I saw this week. He came in for opiate dependence and has stabilized on Suboxone. He’s been in the IOP but has had trouble making it to sessions and individuals because of work and because he’s not sure he needs treatment. He’s almost finished the IOP portion of the program now and saw me this week for his medication follow up. He asked when he could get off of Suboxone. When I asked Carlos what, if anything he had used to alter his mood or his mind in the last month he said, “Nothing, just a couple of beers but that’s alright, right?” I told him that we have statistical studies showing that people who use any drug will more likely relapse onto the one they’re trying to avoid and since his goal is to not use opioids he would be wise not to use anything, including alcohol. We also talked about meetings outside of treatment which he had not been attending for the last couple of weeks. I told him that recovery changes his brain and if he stopped his medicine now without having a strong recovery program he be most likely to have the brain he had before treatment. He said, “And that’s the brain that used drugs, huh?” Sounds kind of good, like Carlos is making progress. But only if you think Carlos’s goals are important. If my goals of no drug use and working a strong recovery program are the goals, he’s taking his sweet time. Where would Carlos be if I’d said weeks ago, “If you’re not ready to work a program, you’re not ready, so get out.”

Some may fantasize that Carlos would be sitting in a 12-step room listening to a speaker, but, while I’d love to believe I’m that powerful and persuasive, it’s more likely that Carlos would be out of treatment and using again, if not in jail. As addiction treatment has been divorced from medicine for a long time, it will be a difficult reconciliation. The fields have different languages and different ethics. In medicine it would largely be considered unethical to refuse treatment if a patient didn’t follow instructions. What would be required is an intervention aimed at making sure the patient understood the instructions and was competent to make a decision to ignore the advice. So, what does all this have to do with outcomes?

We’re going to have to change how we think of outcomes. Six months of no drug use isn’t going to cut it. We’re going to have to understand that this is a chronic disease and the success of treatment is suppression of symptoms and prevention of progression, and not just for 6 months. The first outcome starts before treatment; how many people who call actually get assessed? Then how many assessed actually enter the program? While low percentages getting in may make for better six month sober rates, they mean less people with the disease get help and that’s a bad outcome. Then, once people are in the progam, do they stay in care. I’m not saying do they stay in inpatient care, or IOP; I’m saying all care. It’s not bad if the patient decides to leave inpatient care after a week. Maybe he’s right and it’s not for him. Are people who make money off of his staying in the best position to decide? But does he stay in care when he leaves? “Yes” is good, “no” is not. So another outcome that starts before treatment is how we design our program. Are we a hammer that only treats nails or are we a toolbox full of solutions for people suffering from this disease?

As we move forward to make sure that we’re comparing apples to apples in outcomes we have to recognize that programs that only take a small percentage of people who call are not better programs because they have higher 6 month sober rates. We should be judged by how many ships that approached our harbor are still safely inside, not the percentage of nice clean vessels that have carried gold to our shores. That’s enough on how barriers effect outcomes. Next time I’m going to write about how we actually need to measure different things after treatment than we’re measuring now.

The field of medicine often speaks in terms of outcomes, that is, how well did the treatment work. When dealing with acute illnesses such as Strep Throat we could measure such things as the incidence of negative strep cultures 5 days after treatment or the incidence of complications such as rheumatic fever. Acute illness is a very clear case. The person was well and got sick. They were treated and got well or not, or well with complications or some residual from the illness.

Chronic conditions are different. Since they can’t be cured and can only be controlled, the outcome of “well” is removed from the equations. Even if the person has a well controlled illness with not complications they are not “well” because they require continuing care. Let’s take the oft used example of Diabetes Mellitus (DM).

A person who has no known history of DM loses consciousness at work and is rushed to the hospital. In the Emergency Department the work up shows a blood glucose of 600 (about 6 times normal) which explains the loss of consciousness. The patient is give the correct treatment for the acute emergency and is stabilized enough to be admitted to a medical floor. Once there, a diagnostic work up is done to determine if there is a curable cause of the elevated blood sugar. If such a thing is found (some medications, infection, pregnancy, etc) then the patient doesn’t have DM, they have another type of diabetes (Diabetes of Pregnancy for instance). If the work-up can find no known cause then the patient likely has DM and the correct treatment for this CHRONIC AND INCURABLE illness is begun. The treatment in the hospital is aimed at medical stabilization of the acute symptoms and some education on how the patient should change his or her life to accommodate the illness. Further treatment on an outpatient basis, while the patient is in their actual life, is done to “fine tune” the necessary medical treatment.

One common outcome watched in DM management is Hemoglobin A1C which is the blood’s hemoglobin molecule changed by a high blood sugar, evidence that the patient had a high blood sugar recently. So as that measure is followed and found to be normal the diabetes is considered in control, but the patient is not well. Additionally, the finding of a high Hemoglobin A1C later is not evidence of failed treatment, but evidence of less controlled disease. A search is then launched to identify possible causes of the loss of control and interventions aimed at re-establishing stabilization are instituted.

Enough about DM, this is an Addiction blog. So let’s look at how our field has looked at the illness we treat and measured our success or failure. We rarely, as a field use medical stabilization. Oh yes, we do medical withdrawal, but that is a very time limited thing much like the emergency treatment for diabetic coma. The longer medical stabilization should be aimed at suppression of the primary symptoms, the things that led to the drug use in the first place. Instead we start talking to the patient about changing their life while their symptoms are still out of control.

Our treatments are quite time limited and often take the patient needlessly out of their lives, returning them after treatment with little or know follow up. People need to live with the chronic illness in their real life and so the treatment should be crafted to fit that life unless there is some compelling reason to take the person out of it for a while.

Finally we measure the success or failure of our treatments much the way physicians do with Strep Throat. We report such things as continuous abstinence at 6 months or 90 days as evidence of failure or success. We rarely mention that the abstinence if “successful and continuous” was accompanied by the use of some other compulsive behavior or drug that was not the focus of the first treatment. We also rarely take into account how engaged the patient is in his recovery even if he has had a slip with the drug or behavior that was the original focus.

One more thing I’d like to point out before I discuss outcomes more specifically. Physicians would never report outcomes of DM patients who evidenced motivation differently than those that did not. If the lack of motivation is found to effect treatment than it becomes inherent on the diagnostic process to monitor for low motivation and to include proper interventions in the treatment. Also an Emergency Department would never have someone at the door measuring motivation or building barriers to evidence motivation when they are overcome. Our field routinely does that. I recently called a treatment program that offered medically assisted “detox” that reports “success rates” of over 85% meaning that 85% complete the “detox” protocol. I told them I was an opiate dependent lawyer seeking treatment and asked how long did the treatment take. I was told it was about 18 days, and so I asked if I’d be able to work during that time. The intake person said it would be unlikely as I’d be pretty sick during the 18 days and heavily medicated. Inherent in this interaction is a barrier that requires people who can afford it and afford to not work for 18 days, have enough social support to be heavily medicated for 18 days, afford the medication, and not have a job that would penalize him or stigmatize him for missing 18 days. When the program states its outcomes it does not tell us about these inherent barriers.

So I’m going to write two articles next on outcomes. The first is going to address the nature of hidden barriers and what we can do to more accurately compare apples to apples, and the second will concern some different, and perhaps more appropriate, outcomes we could measure.

An essay on the subject of “What is Recovery” raises, for me, the question of what is Addiction. Since everyone of us has an idea, our own idea, of what Addiction is, we’ll also have our own answer to “What is Recovery?”

Since we don’t have agreement in our field on what Addiction is, I doubt that we can come up with an easy agreement on what recovery is. I could just tell you my definition of both but my goal is not for us to have a debate over which we can come to a resolution. My goal is that we all look at ourselves and how we got to this question. It may be, that after examining ourselves, we may choose to change the question we ask.

Perhaps it would be instructive to take a look at two of the definitions of Addiction that are out there and the resulting definitions of Recovery which follow. We will, of course, have some agreements and disagreements with each, and you may not agree with my interpretation of them. I don’t propose the following as any kind of universal truth, just my own.

The most generally accepted definition of Addiction, at least the definition accepted by most people, does not even bear that name. I refer to the DSM IV criteria for Substance Dependence. While many of us may find fault with it, there are a lot more people outside of our field than in it, and for them it remains the scientifically accepted gold standard.

The first problem with DSM’s definition is that it is entirely medical. Another is that it is specific to a certain drug (except in the case of Poly-substance Dependence) and is based entirely on behavior. This leads to a peculiar definition of DSM’s version of Recovery, Sustained Full Remission. It is far from what most of us would consider Recovery, or even, for that matter, abstinence.

To be in Sustained Remission we would have to have longer than the first 12 months that characterize Early Remission. To be in Full Remission, we can no longer be suffering from any of the problematic behaviors that can still be there in Partial Remission. No, in fact, in Full Remission our use can’t be causing us to meet any criteria for Substance Dependence at all. Yes, you heard that right. An Alcohol Dependent patient can be in Sustained Full Remission while continuing to drink as long as he has not met any of the criteria for Alcohol Dependence for a full year.

Ah, I can hear what you’re thinking (probably because I haven’t taken my Haldol). You’re thinking, “Howard, so what? How likely is it for that alcoholic to continue to drink for a year and not have any criteria for Alcohol Dependence?” And here DSM IV-TR comes to the rescue having added two qualifiers to explain just how someone can still use and not meet criteria: “On Agonist Therapy” and “In a Controlled Environment.” I’m going to come back to them in a bit because they’re probably more common and more important than we generally realize but first I want to take on a major objection with the DSM definition of Recovery that I think most of you will share.

The objection is that the definition is completely behavioral and tells us nothing about what is going on inside the recovering person. Yes, the person has stopped using, but we can’t tell why. We can’t tell if they’ve switched drugs or are just dry drunk. For a contrasting view, let’s take a look at another set of definitions, this time from AA.

Alcoholics Anonymous has put out a number of “tests” one can take to see if one is likely an alcoholic but for a definitive view we need to turn to a book as authoritative for AA as DSM is for psychiatry, Alcoholics Anonymous. Of course we must note here that consistent with AA’s single purpose their definition is limited to Alcoholism, not Addiction as a whole.

In regards to a strict definition of Alcoholism, AA hasn’t been very definate. The closest the Big Book comes to a clear definition is given at the beginning of page 44. “If, when you honestly want to, you find you cannot quit entirely, or if when drinking, you have little control over the amount you take, you are probably an alcoholic.” However, AA was broadminded enough to include a medical opinion as well. Dr William Silkworth, while not speaking for AA, is included and writes that alcoholics have one symptom in common, “…they cannot start drinking without developing the phenomenon of craving. This phenomenon, as we have suggested, may be the manifestation of an allergy which differentiates these people, and sets them apart as a distinct entity.”

So Alcoholism is an illness which manifests itself in craving after any alcohol whatsoever is taken, but what is AA’s definition of recovery? Also in the beginning of the first paragraph of page 44 of Alcoholics Anonymous we see Alcoholism referred to as “an illness which only a spiritual experience will conquer.” This begs the question of what is a “spiritual experience,” and in an appendix of the Big Book it is referred to as that “personality change sufficient to bring about recovery from alcoholism…,” the essence of which is an “awareness of a Power greater than ourselves.”

So we seem to have two diametrically opposed definitions of addiction and recovery. The DSM provides us with a behavioral approach giving no mention to any inner change the patient may have, while AA gives us a version where the behavioral change is secondary and flows from the paramount inner change. But they have one very important thing in common, the focus on one substance only, and this leads us back to one of DSM IV-TR’s new modifiers.

Science has discovered more about the brain than was known when either the current DSM definition or Alcoholics Anonymous was written, it has become clear that the external substance used is not as important as the common end result of all substances and behaviors used in the disease of addiction, the elevation of dopamine tone in the brain’s reward center. The DSM term “On Agonist Therapy” specifically refers to a chemical which acts to turn on the receptor where the abused drug acts. Agonist is a very specific term and many other chemicals can perform the same function while not being agonists. For instance, a medication might increase the level of dopamine by blocking an enzyme that would normally break it down or another might change the shape of the GABA receptor so that it responds more readily to the brain’s own GABA. So “On Agonist Therapy” might be more appropriately referred to as “On Replacement Therapy,” where the medication replaces in a tonic sustained way the transitory effect of the abused substance or behavior.

Addiction Medicine has used Replacement Therapy for years and I don’t refer only to methadone. As an example I have long used buproprion to raise dopamine levels in the reward center to relieve the restlessness, irritability and discontentedness that some addicts feel when they aren’t using. Another example is a new medication for nicotine addiction, varenicline, which is a partial agonist at its receptor.

Now that buprenorphine is available however, people seem to have noticed this phenomenon much more acutely. Perhaps this is because buprenorphine is specifically a partial agonist for its receptor while buproprion merely affects the receptor by raising the level of the brain’s own chemical. Or perhaps no one noticed that buproprion works the same way as cocaine and was essentially replacement therapy for cocaine use because it’s labeled as an anti-depressant. Of course, addicts knew about Replacement Therapy long before doctors did. Partial Replacement Therapy is a tried and true method of stopping or moderating use of a particular drug. Since the brain gets the dopamine from another source, the offending behavior is lessened or stopped.

So now the secret is out. There are people in Recovery who are taking medications which affect the very receptor affected by the drug they abused, and we’re going to have to answer a few questions. One of those questions is, “What is Recovery?” I really can’t answer the question for anyone but myself and, rather than convince you of some opinion of my own, I’d like to ask you to examine your own beliefs in the light of new science and develop your own opinion.

But as a physician I want to weigh in on something some of my colleagues have said, that medication assisted Recovery is somehow different than recovery itself. I think two points are apropos here. First, that medication assistance need not be directly with a cross tolerant medication to achieve the same final goal of increasing dopamine. The second is that even in the most ardent AA version of Recovery the discovery of a Higher Power does not prejudge the plan of that Higher Power or in any way obligate the Higher Power to follow any quid pro quo. That is, there’s nothing in Recovery that requires that, while saved from a hopeless state of mind and body, the sufferer must now be completely relieved of the illness itself or the need for active treatment.

Finally, there are those I’ve heard say that anyone attempting Recovery in some kind of Replacement Therapy is not capable of finding and accepting such a Power; that is, that such a person could not be in the same kind of regular Recovery as someone not on Replacement Therapy. If you are such a person I’d like to tell you that I think that Chapter Five of the Big Book is perhaps the finest example of spiritual writing that I have ever seen. Thank God no one told Bill he wasn’t in good Recovery unless he didn’t use nicotine as Replacement Therapy.

More will always be revealed, and I just treat Addiction.  I’m no one to judge the quality or type of someone else’s Recovery. Even a certain level of denial is compatible with Recovery as this final quote from Bill’s 1960 address to the NACC shows. When asked to explain what he meant by “mental obsession” Bill replied, “Well, as I understand it, we are all born with a certain amount of freedom of choice. The degree of this varies from person to person, and from area to area in our lives. In the case of neurotic people, our instincts take on certain patterns and directions, sometimes so compulsive they cannot be broken by any ordinary effort of the will. The alcoholic’s compulsion to drink is like that. As a smoker, for example, I have a deeply ingrained habit – I’m almost an addict. But I do not think this habit is an actual obsession. Doubtless it could be broken by an act of my own will. If badly enough hurt, I could in all probability give up tobacco. Should smoking repeatedly land me in Bellevue Hospital, I doubt if I would make the trip many times before quitting. But with my alcoholism, well that was something else again. No amount of desire to stop, no amount of punishment, could enable me to quit. What was once a habit of drinking became an obsession of drinking – a genuine lunacy.”

First, let me say that I’m a big proponent of 12-step recovery. I don’t think my field of psychiatry has come up with a tool as effective as 12-step recovery, certainly not one that has worked for 70 years. That said, there are some things I have to take issue with concerning my care for my patients with certain people now presenting themselves as experts in 12-step recovery. Please understand that I’m not taking issue with AA or NA or any other 12-step fellowship. These fellowships do not take a stand on outside issues, and my care of my patients is definitely an outside issue.

Unfortunately, not all members of such fellowships share that view, even some with considerable experience. Here’s an example. A patient of mine had a difficult time staying sober, even on the medication which usually has a great effect. I asked him what was happening, and he told me that he wasn’t taking the medicine after all, because it made him sleepy. Please understand that in my experience this would be a very rare occurrence. Opioids generally don’t make opioid addicts sleepy; they give them energy. This medicine, buprenorphine, is a partial opioid agonist and as such is unlikely to cause an opioid addict to get sleepy.

Now this particular patient is also a compulsive over-eater and is quite overweight. I asked him when he was taking his last dose of medication: 5 pm. His complaint was that he was falling asleep in evening NA meetings. I suggested that it might be his still uncontrolled eating and the binge he had for dinner that was more responsible for his sedation but he thought it otherwise. I thought that he should take his buprenorphine as it would likely decrease his craving to overeat as well as for opioids and, in time, make things better. See, he had talked to other people in NA who saw that he was falling asleep in meetings and told him that buprenorphine was probably the culprit. I told him that was unlikely, but he was sure they were right. He did agree to an experiment though.

I asked him to take his last dose of buprenorphine, not before the meeting, but after meeting. If he was right he’d get a good sedative effect and go to sleep as he wanted to. He’d also get to stay awake in the meeting. If I was right he’d probably still fall asleep in the meeting. Two days later he called and said the buprenorphine kept him up. Was he still sleepy in the meeting? Yes.

This patient’s story illustrates two problems I see a lot. First is that the old wives tale of “one addiction at a time” is alive and thriving in the 12-step community. The second is that there is, concerning some medications for addiction, a rash of “contempt before investigation.”

I don’t know where the idea comes from that we can only deal with one addiction at a time. The concept of one addiction being different from another is so foreign to me that I have a hard time understanding what the phrase means. Does someone who compulsively gambles, compulsively masturbates, compulsively overeats and is an alcoholic and opiate addict really have 5 diseases? We have very good evidence that if someone starts using one drug to stop using another, or even continues using one drug while trying to stop another, it doesn’t work very well. Why would we think it would be different when one is trying to continue a behavior that acts like a drug in the brain while trying to not use another drug? Because overeating is legal and encouraged by the fast food industry? I don’t think our midbrains are aware of congress, food packaging or even what we’re doing to boost our dopamine levels. It only sees that we are or are not getting the dopamine.

The philosophic reaction, without experience with the medications, of some people in the recovering community to medications for addiction is astounding to me. Especially when it comes to buprenorphine. I’m struck with how this medication somehow got a special place in the minds of some recovering people - like the devil incarnate. I’ve heard, “it’s just like heroin,” “I’ll just be addicted to that now,” “he isn’t clean.” I’ve even had the experience with an addictions counselor who said to me, “If you’d only seen the horror stories I’ve seen, you’d never use the drug.” When I asked he’d seen two people who didn’t do well and couldn’t tell me if they had gotten proper addiction medical care or not, but was unwilling to believe that I had seen scores of people who had never before been able to work a 12-step program who could now function well enough to do so.

The whole issue of buprenorphine is too large for this article, but I’m also struck with the number of people in recovery who think it’s okay for me to give a patient buproprion because it’s “an anti-depressant” but not buprenorphine because it’s “a pain med.” Again, I don’t think our midbrains care what words people made up to describe other uses for these medications. The midbrain reward system truly has singleness of purpose and it is this, “Am I getting the dopamine or not?”

It’s very common to have sleep problems in early recovery, and it is also very common for people with addiction to have had sleep problems all their lives. This has less to do with the past drug use than it does with brain functioning, so I’d like to explain a bit about that and how your doctor can help.

In general, there are two kinds of sleep troubles: trouble falling asleep and trouble staying asleep. Trouble staying asleep is most often a direct result of not having enough dopamine tone in the midbrain. Dopamine is the “I have enough” chemical. Low dopamine is the same signal your body uses to tell you you’re in a famine and in a famine you aren’t supposed to sleep soundly. Someone may come and take your food. So your ability to sleep soundly is a marker your doctor can use to know when the medication prescribed for you has returned your dopamine level to normal. If you take a sleep agent, you’ll mask that marker, and it will be harder for your doctor to know when you’ve reached a good dose of the medication.

Trouble falling asleep in addiction is generally not a night time problem; it’s a problem of the whole day. As we go through the day without vigorous recovery work, we accumulate little things here and there that play on our minds. As we’re busy and keeping ourselves distracted with day to day business, we don’t notice. When our head hits the pillow however, the distraction is gone and all that stuff comes rushing back. So the part of us that is keeping us awake can be thought of as the healthiest part that’s saying, “Hey, don’t go to sleep. We have recovery work left to do.” If you just lie there awake in bed, you’ll be practicing being awake in bed. Remember, you get more of whatever you practice. If you take a sleeping pill, you’re shutting up the healthiest part of you. Sounds like a lose/lose situation. Instead, if you can’t fall asleep in 20 minutes or so, get out of bed, sit in a chair, and read the Big Book, Alcoholics Anonymous. Don’t read in bed, don’t read a novel or a magazine. One of two things will happen. You’ll either get tired and go to sleep – you win. Or you’ll get good recovery work done – you win. You may stay up all night reading the Big Book. I’ve given this advice to hundreds of patients and not one (who didn’t nap the next day) has ever told me he didn’t sleep the next night.

Of course there are other causes of not sleeping besides addiction. Some are medical and associated with the brain and some are medical and not associated with the brain. Also, the normal human trauma response disrupts sleep and will generally pass in a few weeks if there are no reasons for it to become chronic. A chronic trauma response is pretty common in people with addiction so it’s a big one to keep in mind. In general, the key is that not sleeping is a symptom, and the principle is not to treat the symptom but find and resolve the underlying disorder.

I recently received a commentary from the Institute for Behavior and Health, an organization dedicated to developing new ideas to decrease illegal drug use. The subject of this commentary is “Canada Cracks Down on Drugged Drivers with ‘Zero Tolerance’ Per Se Drugged Driving Legislation,” and it’s quite positive about what Canada has done. From the commentary it appears that Canada’s law makes it a punishable offense to drive with any detectable levels of drugs in the driver’s body. Let me say first that people should not drive under the influence of any drug that impairs performance. I also think that people shouldn’t drive while doing things that impair performance (I mean talking on a cell phone, get your mind out of the gutter).

The problem with a law like this is not that it limits the rights of impaired drivers. Impaired drivers don’t have a right to drive. The problem with the law is that it doesn’t address impairment and the commentary from IBH seems to take pride in that fact. The commentary states that under “… the new law suspected impaired drivers will no longer be able to refuse roadside sobriety tests and those testing positive will face stiffer fines and longer jail times.” What used to happen before the law was that the person could refuse the sobriety test and administratively lose the right to drive. So if the goal was to get impaired drivers off the road the old law worked fine and so does the current law in most US states. The difference now isn’t that the roads will be safer but that the punishments will be harsher. I could have missed it but the commentary doesn’t mention assessment or treatment, just fines and jail time.

As we come to understand that addiction is a brain disease and not a social problem, that drug use and drug addiction are not the same thing, we’re going to have to come to grips with the fact that our old simple concepts just don’t work. Here’s another example from the IBH commentary: “….that  police will have the right to take any driver suspected of being high on drugs to a police station to take blood, urine or saliva samples.” What if they didn’t use to get “high” but used to calm obsessiveness? Aren’t they still impaired? As long as we stick to our old ideas that all people use drugs for the same reason and all drugs have the same effect, we’re not going to be able to come up with good public policy.

So what would be good public policy? Well first we have to ask what the public goal is. I’m assuming that the public goal is roads as safe as can be, given the general bell shaped curve of driving ability available in the general public. It would be nice to say that the goal is safe roads, but not all of us are good drivers and no matter what we do there will always be some people who are worse drivers than others, so until we have computers driving for us, we’ll have to accept some risk. But we want to limit that risk to the minimum.

So how can we make the roads as safe as possible given the abilities to drive in our population? There are several factors: environment both in the car and out, factors decreasing driver ability, and driver distractions both internal and external are some of them. The first is the area that highway engineers and car manufacturers concentrate on. Are the signs far enough away from the exit to allow for an orderly change of lanes, are the roads striped and signed well, does each care have seat belts, and the list goes on and on.

The next two are what most of society thinks about when we think of safe roads, and, in the case of drug use, the second takes a paramount role in our thinking. But drugs and alcohol aren’t the only factors that decrease driver effectiveness. Studies have shown that driving having taken cold medicine that is available over the counter can be impairing as can be the cold itself. Sleep deprivation is a common cause of driver impairment as well. So if the goal is roads that are as safe as possible we want to avoid impairment of innate driving ability from all causes. So what’s more common, people using drugs and driving or people driving with colds and not having had enough sleep? But we never want to look at ourselves as part of any problem. We don’t want to say, “You know I’m not feeling well today, I don’t think I ought to drive.” That would be inconvenient. It goes down a lot better to say, “You know those people who do things I don’t do? They shouldn’t drive.”

This leads us to the third factor, distractions. Of course a common one is cell phone usage. Currently in Louisiana where I live it is a new law that young drivers cannot drive while using handheld cellphones but can drive with hands free cell phones. The studies of cell phone use and impairment show that using hands free phones don’t improve performance at all and it’s the mental not physical distraction that causes impairment. The studies also show that driving while talking on a phone is as impairing as having a 0.08 BAL which is the legal level of drunk driving in all US states. I’m not suggesting that we let drunk people drive, but I am suggesting that if our goal is safer roads and not punishing drunks then we need to institute all measures to ensure that safety. Who do you think there are more of, people driving while talking on cell phones or people driving drunk? Just take a look around; it’s not even close.

Then there is a group of people much larger than illegal drug users who are, in good faith, seeking care from their doctors to treat an illness. Many medications, for both brain and non-brain problems, can cause alterations in some of the necessary physical abilities that make us a good driver. Vision changes, cognition changes, balance changes, attention changes are just some of what can go wrong even in the best of care. Most doctors have no training whatsoever in how to evaluate whether someone is impaired as a driver or not, yet it is the doctor who bears the greatest responsibility under the law.

Of course there are people whom medications make better. That is the point of them after all. This is why I have an interest in the whole situation; my addicted patients are often better on, than off, some medications. When you study the symptoms of addiction that precede and cause drug use you will encounter a list of symptoms that will generally impair driving ability. Many people will notice they can pay attention better on nicotine than off. Would we be including smokers in that group of per se impaired drivers with drugs in their systems. In fact patients will say the same thing about most of the drugs they use at first and in small quantities while the same drugs in greater quantities will perhaps then lead to impairment. Is the addict who uses cocaine a worse driver when his dopamine level is normal or when it is falling as the drug is wearing off? Now one knows; we’ve never looked. Of course we would never think about this because we believe addicts are normal people who choose to use. Once we recognize that the vast majority are not normal and actually can be made chemically better the real question becomes what chemical, how much, how often and for how long. I’ll agree that nothing over the counter or on the street is going to act as a good medication for long. If it did, I’d be out of a job. But it’s much easier for us to believe that it’s the ones who are using that are more impaired, rather than that the ones who aren’t and are already on the wrong end of the bell shaped curve. So what can we do to address this problem?

The solution is inherently technical and doesn’t involve drug testing. Remember our social goal, not chemical free roads, safer roads. So we need not look at what someone is taking but rather how good a driver, and do they get better or worse when they are taking it. Driving simulators exist today for that purpose and could be put in police vans or police stations as well as doctor’s offices to address the question. That is, in fact, how we know that alcohol at any blood level is likely impairing. Instead of having to guess if someone was a danger, we could actually measure it. Was this possible 20 years ago? No, not even ten, but it’s possible now. The Supreme Court has occasionally ruled that the State can violate someone’s rights when no better solution exists, and so those who advocate a per se standard (you are guilty of driving having smoked cannabis 72 hours ago even though you aren’t under the influence or impaired anymore at all) do not want to address a technical solution that would make our roads safer and protect the personal liberties Americans hold dear. Under the per se standard, one can be convicted of drugged driving having smoked cannabis 72 hours previously with no active drug in their system but metabolites in their bladder. This isn’t about letting people drive drugged. It’s about making sure that people who are driving are driving safely. Do I want myself or my loved ones to be in an accident with a drugged driver? Of course not, but neither do I want them in a an accident with a driver impaired by high blood pressure medication or by talking on a cell phone. If I thought a per se drugged driving standard would be an improvement in safety, I’d go for it. However, modern technology gives us a better, more robust way to ensure safety, if we’d only use it.

A friend sent me his notes on a lecture he attended at the American Psychiatric Association meeting in May by Dr Thomas Brown of Yale University. The subject was adult ADD. Remember, this is from my friend’s notes so I don’t want anything I say to reflect on Dr Brown if I’m misinterpreting him.

Here are a couple of paragraphs from my friend’s notes: “ADD is an extreme presentation of a continuous variable: like high blood pressure or decreased glucose tolerance, it’s a continuous variable, and cut-offs distinguish ‘normals’ from ‘abnormals’ based on statistics. Cases are thus not discontinuous from controls. However, when someone is in the ‘abnormal range’, they definitely experience a significant alteration of functioning. ”

“Most people with ADD can function well, with good focus, in one or more areas of their lives: if they’re really interested in something, or if they are under extreme pressure to perform (‘they have a gun to their head’), they can perform well. Given that there are times/situations in which they can perform well, and others in which they cannot/do not, it appears to others like their dysfunctions are volitional, are a matter of them simply not invoking adequate willpower or personal responsibility to follow through and perform.”

As I maintain that the neurobiology of ADD and addiction are very similar if not the same then everything said above should be true for addiction. Let’s take the first thing first. Addiction is an extreme presentation of a continuous variable. We’re all on a bell shaped curve for almost every trait we have. The same could be said for dopamine tone in the midbrain and hedonic tone. There are some who have great tone and many more who have okay tone. Of course, there are also some who have very poor tone; they are the extreme end of the curve and comprise about 10-20% of the population. So we’re all put somewhere on this bell shaped curve, and if we move too far to the wrong end for reasons of genetics, stress, aging, or any other reason we’ll start to have symptoms. And how do we know when we’re at that end of the curve? Just like the examples above, we have a alteration in functioning.

The examples that my friend or Dr Brown picked were quite interesting: high blood pressure and blood glucose levels. The beginnings of the alteration of functioning in these cases is very hard to find. After years of high blood pressure or high blood sugar there is clear damage, but in the beginning the patient may feel nothing at all. So it may be at the beginning with low midbrain hedonic tone. At first I just eat a little extra food or go on a rollercoaster, and my dopamine level increases. Perhaps I can change how people feel or finish a hard job and get a boost of dopamine there too. Or, to echo Dr Brown’s talk, perhaps I’m one of the people who can make my brain release dopamine by running around in a hyperactive fashion. As I use any of these methods to increase my midbrain dopamine tone several things are happening. My brain is aging and I’m losing tone more and more all the time. As I use something to raise my hedonic tone it becomes less useful as my brain doesn’t calculate reward itself as much as positive reward disconfirmation; that is, if I expected it I don’t get as much dopamine from it. So over time I need more and more new things to make myself feel good. At some point the “alteration in functioning” becomes obvious when the donut becomes a dozen or I lose a relationship because I can’t stop playing a video game. Eventually I need bigger and bigger things and my altered functioning begins to effect more and more people. One day someone will look at me and say, “That guy’s an addict.” It will usually be when I’ve used more of something to feel better than the other guy needs.

My friend’s second paragraph says something about ADD that people with addiction have long known: time is not a constant. People think that the alterations in behavior in addiction are volitional because they aren’t constant. In fact the example of having a gun to one’s head is often used to say that addiction isn’t an illness. “He wouldn’t use if a policeman was there with a gun to his head. See it’s a choice.” Aside from the comparison of drowning a woman in the middle ages to prove that she wasn’t a witch, threatening to kill an addict to make him prove he’s ill actually changes the experiment. “Well, look at that, Your Honor, he really was sick. A shame he’s dead now; we could get him some help.”

Here’s how the experiment changes. When something novel happens to us (and I hope that having a gun put to your head would not be something you’ve had to experience up to this point) we will get a surge of adrenaline and dopamine released to the midbrain. Think about that rollercoaster and multiply that by 10 or so. Even if an addict is craving and has low dopamine tone, the fact that he doesn’t use because we’re threatening to kill him if he does doesn’t mean anything. By issuing the threat we’ve actually raised, temporarily, the midbrain dopamine tone and actually made the craving better for a while.

I hear the same thing about kids with low dopamine. “He can’t have attention problems. He pays great attention to that video game.” At a visual refresh rate of 30 to 60 times a second, a video game will qualify as a novel visual stimulus and increase dopamine tone. He’s not paying attention to the game, he’s medicating with the game. Usually if someone with low dopamine is interested in something, you can bet he’s getting dopamine from it.

Dr Brown’s comment about motivation is true as well. People with addiction often procrastinate and don’t do things until they are “under the gun.” This does not mean that there are conscious choices involved. When we are working under pressure there is more adrenaline and more dopamine and we actually do function better.

So back to what makes an addict an addict. I guess it’s like beauty and is in the eye of the beholder. If I don’t like your way of getting more dopamine I’ll start calling you names. If I don’t mind how you get more dopamine, I probably won’t even notice much less dissapprove of it. I think if we all had light emitting diodes placed on our foreheads that shone red whenever we were low on dopamine life would be a lot simpler. We’d be able to see when our words were “bringing someone down” and we’d be able to understand why someone wasn’t remembering to do what we told them to. We would notice that when they were engaged in certain activities their biology was changed as well as their behavior. We’d be able to know when we should and shouldn’t bring up that subject we are afraid of discussing. In short, we’d be able to behold the functional alteration of addiction in a much different way than we do now. Until we all get that LED implanted, we’ll just have to keep this information in mind when talking to everyone, remembering that addicts are ill whether they’re making us mad or not.

When I think about it, there are few terms in the addiction treatment field that are more silly than “Drug of Choice.” As if we get to choose which drug makes the brain go BAM. When you talk to an addict and ask, “What’s your drug of choice?,” what you get is the answer to “What drug that is available to you lately at a price you can afford that makes you feel better with the least side effects?” Quite a mouthful, huh?

Would we ask a diabetic if their toxin of choice is sugar? How did they choose sugar? Why didn’t they choose to have an abnormal reaction to arsenic instead of sugar? What a stupid choice! Using the concept of choice, as in which would you choose if they were all lined up, can confuse us and strengthen the stigma and the idea that addicts are normal people who choose to use drugs. If we asked an addict if they chose to have cocaine work the way it works with them or if they chose to have an abnormal reaction to alcohol we’d hear a resounding “no.” “If I had the choice of what my brain reacted to I’d have picked something a lot cheaper and easier to get than cocaine.” Something like wildflowers or dandelions, no doubt.

What is it we really want to know when we ask the question? And why? Well, up to now we really haven’t had a good reason. We just needed a word to write down in the “Drug of Choice” box on the assessment. In many cases it meant something, for instance when the person used only one drug. Most of the time however it doesn’t actually mean much with regard to choosing treatment. However because researchers like things that come in boxes there has been a lot of research on “Drug of Choice.” It’s been used to predict treatment outcomes with regard to which treatment is used. One example of such a research question would be, “Do alcoholics or opioid addicts do better when given naltrexone?” By dividing people up by “Drug of Choice” we manage to make one population (alcoholics) which is heterogeneous sound different from another (opioid addicts) which is heterogeneous in a different and overlapping way with regard to neurobiology. It’s really no wonder most addiction research doesn’t make much sense.

But still insurance companies ask the question and the government asks the question so we ask the question, as if we get to choose. But modern science actually gives us a new reason to ask a question about “Drug of Choice.” It’s just not the question we’ve been asking.

We don’t have lab tests that we can use clinically in addiction medicine. It would be great if we had rapid, inexpensive genetic testing or PET scans that actually could predict something in individual patients instead of groups of subjects. But we don’t and they don’t, yet. In the meantime we get to ask the patient about the drugs he’s used and with the knowledge of how those drugs work in the brain we can make some informed choices about which medications might help the patient. The problem is that people use the drug they use for a lot of different reasons and we need to know those reasons as well for it to mean anything clinically.

For instance, we may ask a person if he likes to use cocaine? He says no, that he hates it. If we take it that far and no further we think that cocaine doesn’t work for him and that a dopamine reuptake blocker such as buproprion wouldn’t work as a medication for him. But if we ask him why he doesn’t like cocaine, we may get more information. He may tell us he doesn’t like the crash or the paranoia, but that he can feel normal for about 10 minutes when he uses cocaine. If it was the only drug that worked for him he’d use it but fortunately alcohol works as well and lasts longer so he drinks. It tells us first that he would likely do better on buproprion and second that he’s not likely to respond to naltrexone as some alcoholics do.

So we do need a question; it’s just not, “What’s your Drug of Choice.” It’s more like “What drug or drugs work to make your brain feel normal at the peak of the experience regardless of what side effects or time course may make you not like the experience in general.” You know, the DODWTMYBFNATPOTEROWSEOTCMMYNLTEIG. We need a shorter acronym; the government wouldn’t even use that one, and they thought up SAMHSA! And while we’re at it we need a term that doesn’t make people think that addicts get to choose what makes them feel better. Cocaine doesn’t have a street value because a lot of people choose it; it has a street value because it works to make a lot of people with addiction feel normal for a brief period of time. When we use the word “choose” society gets the wrong idea and will come up with the wrong solution.