AddictionDoctor.Org

It’s everybody’s dream. Don’t just treat the illness, or even find a cure for the illness; prevent the illness. It’s a wonderful dream, and with regard to addictions it seems easy to fulfill. Don’t ever drink and you won’t get addicted to alcohol. Don’t allow cocaine in the country and no one will ever get addicted to cocaine. To quote Hemingway, “Isn’t it pretty to think so.”

We’ve got to ask ourselves, “How long have we been at this? And when is it going to work?” Surely, if this were true prohibition in the twenties would have gotten rid of much of Addiction if Addiction could be prevented by preventing use of the drug. However, as I show in Questions and Answers on Addiction, while prohibition temporarily decreased the amount of alcohol used in the US it just caused a switch to another drug. Drinking went down but not Addiction.

I keep asking my Addiction Medicine colleagues to show me one study that shows that any preventive measures aimed at Addiction as a whole have ever worked. I’ve put this challenge out numerous times to the leadership of Addiction Medicine and have yet to get a single response. I get lots of responses about preventing alcoholism or cocaine abuse, but nothing that shows prevention of Addiction as a whole.

Of course, no one has to worry about my thesis on this if they don’t believe Addiction is an illness. If they believe that alcoholism or cocaine dependence is an illness, but that they are different illnesses, then I can be safely shunted aside. It’s probably more convenient for a lot of people treating Addiction to not see the single disease. It’s hard to see your own overeating as a form of the illness while telling someone else to stop drinking.

It also helps when you’re making drug policy not to have to look at Addiction as an illness. It’s hard to get an illness to change by making a policy; it’s so much easier to have a policy about a drug. We’ve had “drug policy” for a long time in this country and spent billions of dollars to implement it. At this point one would have to conclude that either the original thesis of the policy was incorrect or that the implementation was completely botched. Generation after generation of administrations have been able to point to their predecessor and claim a botched implementation, thereby preventing anyone from having to critically look at the original premise.

So if I’m right, can Addiction be prevented? Sure, about as well as Diabetes is prevented or Hypertension. These are largely genetic, chronic illnesses with lifestyle and behavioral components just like Addiction. We can have tertiary prevention and secondary prevention, but primary prevention of a largely genetic illness is going to be hard.

What would we have to prevent to have primary prevention of the Addiction that isn’t genetically derived? We’d have to prevent anyone feeling less than anyone else. We’d have to prevent anyone from feeling isolated from others. In short we’d have to prevent bigotry, prejudice, poverty, inequality, and the list goes on. Really, it’s much easier to just shoot down drug smugglers.

But we have a lot we can do about secondary and tertiary prevention whether something is genetic or not. We can find it quickly and intervene before it gets worse. We can treat it as an illness rather than as a social problem that we hope goes away. We can make sure that people who don’t get better get more treatment, not less. But in order to do any of these things that can be good secondary and tertiary prevention of Addiction, we have to recognize that we can’t do primary Addiction prevention by getting rid of drugs and alcohol. Unless of course you can show me that study, but I’m still waiting.

Growing up, I was taught that Jewish people couldn’t be alcoholics. That was a bit of wishful thinking. The people who taught me this rationalized it by saying that the Sabbath Kiddush socialized us in such a way as alcohol became something used only in a religious way. This never made sense to me as several Christian religions have sacramental use of wine and they didn’t report lower frequencies of alcoholism. So I just passed the whole thing off as a cultural myth and went about my business.

It turns out that Jews do have a lower frequency of alcoholism, but it has nothing to do with the religion or the culture. It’s in the genes.

As alcohol is processed in the body it is first turned from ethanol to ethylaldehyde on it’s way to becoming acetic acid. Ethylaldehyde, like formaldehyde, is not something the body likes, but it isn’t there long or in great quantities when the average person takes a drink. However a point mutation in the enzyme that turns ethanol into ethylaldehyde makes the enzyme run very fast and makes more ethylaldehyde than the body can process. It also gets rid of the ethanol more quickly. So someone with that mutation gets less enjoyment from alcohol and more of the aldehyde with its negative effects, it would sort of be like taking antabuse.

This point mutation is very rare in Europeans, occuring in less than 5%. In east Asians it is very common with more than 90% of Japanese and Chinese having at least one copy of the mutated gene. In Jews the prevalence is greater than 20% or more than 4 times higher than a European population. In fact more and more genetic studies are coming out showing Jews of European ancestry to be genetically more like a Middle Eastern population than a European one. (A professor from Jerusalem is hoping to ignite a grassroots peace process by showing that the Palestinian population are actually the Jews left by the Romans to man the farms in the area. It’s a fascinating topic with a lot of evidence but too much to get into here.)

So as Europeans go, a greater percentage of Ashkenazi Jews than normal “get no kick from Champagne.” This really would lower the prevelence of alcoholism in the Jewish population. However it doesn’t say much about Addiction in general.

If you look at Addiction as the addictions, depending on what drug the person uses, all you need to do is avoid the drug and you can’t get the addiction. But what if Addiction is one disease with multiple drugs? What if compulsive overeating and heroin addiction have the same common cause in the brain? That would mean that being protected from over drinking doesn’t protect someone from the illness called Addiction. This has become an important idea because recent findings at the National Institute of Drug Abuse show the same PET scan results in obese compulsive overeaters, alcoholics, cocaine addicts and heroin addicts.

There is no evidence that the disease of Addiction, taken together in all it forms, varies from population to population. The drug used does and some of that is genetic, but the genetic causes of Addiction seem to be old enough and strong enough to span across all human populations equally.

I had always intended to write more frequently here about what was happening with addiction medicine and addiction treatment. The last several months have been very hectic, and my attention has gone elsewhere. Most of the time has been spent with my business, Townsend.

My business partner and I bought 5 clinics in south Louisiana from our former employer when that company closed. The first several months were spent just keeping it going and handling the usual start up problems that any company faces. Recently though, my energies have gone to completing a new book for patients to be used to guide our treatment program. Because our model of treatment is so different from that taught to most students of counseling, I also wrote a book for the counselors. Both books are finished now. I was also invited to speak at the 4th Annual Neuroscience Meets Recovery conference in Las Vegas next month and it took a good bit of time to create three 90-minute talks.

So the upshot is that I haven’t done much reading and have a large stack of journals to go through. Consequently, I haven’t had much to write about here. I’ll now have time to get both of those done.

Therapy fixes things. Something’s wrong, you go to therapy, you get it fixed, you graduate. Congratulations, you’re well. It works great for neurotics.

The problem is that addicts aren’t neurotics and Addiction isn’t neurosis. You can go to therapy, figure out why you’re an addict, change the thing that caused you to be an addict, graduate, and go out and get drunk that day. Addiction doesn’t go away, and you can’t fix it; you have to learn to live with it. Trying to fix Addiction with therapy is like trying to treat blindness with therapy. You may know why you’re blind, but you’ll still be blind.

Since Addiction can’t be fixed, what’s the goal of treatment? The goal of treatment is to learn to live with the condition and still be happy without using. I read a study recently that tells us exactly why therapy won’t work and teaching someone to live with the condition will.

Loran Nordgren at Northwestern University Kellogg School of Management and his colleagues included 4 studies in a paper entitled “Restraint Bias: how the illusion of self-restraint promotes impulsive behavior.” I really like papers like this. Their idea, restraint bias, is that people’s inflated sense of self-restraint will actually put them at greater risk of impulsive behavior because they’ll be more likely to go into risky situations.

What I like about this paper is that it presents a simple central idea and then tests it, not with one experiment, but a robust suite of studies that look at it from different angles. They base the idea of restraint bias on earlier work on something called the “empathy gap.”

The empathy gap is not about empathy towards others; it’s the difference in feeling someone has in a “hot” state such as craving and a “cold” state when they can no longer remember how it felt to be in the hot state. It’s basically a lack of empathy with yourself in a former state. As old as this idea is (1996), Alcoholics Anonymous discussed it even earlier, “We are unable at certain times to bring into our consciousness with sufficient force the memory of the suffering and humiliation of even a week or a month ago. We are without defense against the first drink.”

From the idea of the empathy gap, Nordgren and his colleagues supposed that in a “cold” state people will take more risks and be more likely to be impulsive because they don’t have an empathy with the “hot” state and overestimate their ability to refrain from action. You may wonder why business school researchers are interested in this, but think of the fact that mechanical stock traders who follow rules generally do better than those that go by their “gut.” The most successful stock traders I have heard of are the ones that know that their own brain is their worst enemy. So Nordgren’s work isn’t just applicable to addicts, the restraint bias is a universal human phenomenon. But for addicts, it’s particularly dangerous, because to take the first drink or drug or bite or bet can be catastrophic.

Their first study had to do with students and their study habits when tired. The second had to do with snack choices when hungry. The third and fourth studies looked at smokers, so lets concentrate there.

In their third study, the split the group into those who believed they had high self control and those with a belief that they had low self control. They then asked both groups to watch a movie that would cue them to smoke without having a cigarette. The kicker is that people would get a monetary reward for not smoking during the film and they got to choose the reward in advance. If they left their cigarettes in another room during the film, they could win 2 Euros. If they left their cigarettes on the desk in the cubicle they could win 4 Euros. Holding it throughout the film got them 6 Euros, or holding it unlit in their mouth could get them 8 Euros. As predicted smokers in the high control group exposed themselves to more risk than did the low control group. In the high control group, which took greater risks, 33% of the subjects smoked, while in the low control group taking less risk, it was only 11%.

The fourth study also had to do with smokers, in this case, smokers who had quit and were past nicotine withdrawal. Again they self divided into those that believed they had good control and those who thought they had a lower level of control. Four months later when they were followed up. As expected, smokers who felt they had high control reported less avoidance of cigarettes, and a greater percentage of those that had less avoidance of cigarettes relapsed.

In their discussion they refer to a recent study of heroin addicts who are asked what price they would pay for a buprenorphine pill. The study found that addicts in withdrawal would value it more highly than those not in withdrawal. While that might seem like common sense, the authors point out that all of the addicts not in withdrawal had been in withdrawal before and knew it was likely that they’d be in withdrawal again, but because they were in a “cold” state, they just couldn’t remember how bad that would be.

So why did I start this off about therapy? It has to do with what therapists are taught. We are taught that self-efficacy is critical to self-control. We are taught that people should be empowered to achieve what they want to achieve. This has always been at odds with AA’s insistence on powerlessness as the path to recovery. What Nordgren’s work shows is that, for addiction anyway, those that embrace the fact of their powerlessness will be more likely to not use and more likely to stay in recovery. It’s always been my experience and it’s always a point of contention when I’m discussing patients with colleagues who treat a more general population than addicts.

Now we have behavioral scientists agreeing with what AA and other 12-step programs have said for 70 years. Perhaps this is why there is no psychological treatment for addiction that has been shown to work any better than 12-step facilitation treatment where the patient is encouraged to get into 12-step recovery. Perhaps going to meetings reminds us of that “hot” state without getting into it because while we can’t empathize with our former selves, we can perhaps empathize with the person sitting next to us now.

Just swing a cat these days and you’ll hit a new paper on genetics in Addiction. This is how they usually go: “We got together a big group of people with addiction to a chemical and another group that doesn’t have addiction to that chemical. We measured single nucleotide polymorphisms (SNPs) of genes that we think may have to do with addiction to the drug and this is what we found.” The results are either positive or negative for a correlation between the group with addiction and a particular SNP. These studies are very interesting and usually end up in a lot of press response that “the gene for (fill in the blank) addiction has been found.” The problem is that there are a lot of problems with this common methodology and the studies don’t mean what everyone thinks they mean.

The first problem is selection of the subjects. Currently DSM IV divides Addiction (which it calls Substance Dependence) into different diagnoses based on the drug used. So when scientists go to select subjects they select for those with a particular DSM diagnosis. The problem is that a lot of things other than the illness go into what drug the person comes to treatment with. Culture, availability and family upbringing all have to do with what drug is used and confound the genetic biology of the illness. For instance, a good percentage of people that come to treatment for “opioid dependence” have a strong history of cocaine use. Many of these will say that they didn’t like cocaine much and didn’t use it much, but other’s will say that cocaine worked well to relieve the symptoms of Addiction, in fact it worked better than opioids, however the cocaine crash was horrible and opioids last longer. So biologically what’s the difference between someone who is using opioids because that’s the best drug and someone who is using opioids because it’s their second best drug and they don’t like the first because of a pharmacokinetic rather than reward phenomenon? We’ll never know if they both get stuck in the same group of opioid addicts for a study.

Another problem is the reporting of the SNPs that are associated with the addicted group without any knowledge of what the SNP does to the active protein. That, in itself, isn’t bad but most of these studies never hold out the possibility of the effect going both ways. It’s pretty easy to assume that if a receptor is mutated it doesn’t work as well as the normal, but that’s not a good assumption. There are many examples of polymorphisms where the mutation causes over activity rather than underactivity of the protein. For instance there is a commonly studied mutation of the COMT enzyme that breaks down dopamine. The people who did the original work didn’t say this but many people assumed that this meant that the mutation kept COMT from working and therefore there was too much dopamine causing enhanced reward and leading to drug use and abuse. However, it turned out that the COMT enzyme actually works better with this polymorphism and so one would suppose a lower dopamine level leading to underactivation and craving. The difference here may seem small but it leads to two entirely different world views of addiction: that drugs cause reward via dopamine and we should block the effect to stop drug use or that people who are addicted have a generally lower dopamine tone and need dopamine increasing treatments to stop using.

The third problem is that of using a SNP by itself. Increasingly, and I’m glad, studies are dropping associations with single SNPs for associations with haplotypes. A haplotype is a grouping of SNPs. For instance lets say that Gene A has 4 SNPs (1,2,3, and 4) each can be either A or G. The haplotypes would be groups of these combinations such as AAGA or AGGA. This is important because one SNP may change the way the protein works and another change it back or cause some other effect. So if we only look at the first one we’ll see an association that may not be there or fail to see one that is.

So, simply, these three problems stand in our way. Of course, there are more problems, but I’m keeping this simple. We don’t know the function of the SNPs we’re measuring and without that we don’t know what to do with the information. We don’t have biological divisions that make sense when testing subjects so we aren’t going to find out the biologically important information. And lastly we should focus on the thing that actually works, the whole protein, not a single amino acid in the protein and therefore we should study hapoltypes more so than single SNPs.

When these three problems get more attention it will become much more common that genetic studies inform treatment for illnesses, including Addiction. People like me who spend all day treating addicts will be much happier when this day comes. So all you genetic researchers out there, get too it. I need a whole lot more informing.

I recently had the opportunity to listen to some thoughts by the leaders of Addiction Medicine about policies of prevention. They all seemed very learned and several quoted important studies, but what seemed missing was an answer to a basic question, “Prevent what?”

Were they talking of preventing illegal substance abuse in order to decrease lawlessness? Or did they have a public health interest in decreasing the use of alcohol, tobacco and other drugs because it’s not healthy to drink an industrial solvent or take neurotoxins? Did they want to decrease the overuse of substances on special occasions by normal people that leads to so much difficulty at British soccer games and on American roads at New Year? Was it Substance Abuse, the chronic maladaptive use of substances in spite of social difficulty, that they wanted to prevent? Could it have been Substance Dependence, an illness characterized by repetitive, compulsive maladaptive use in spite of physical or psychological consequences? Or, finally, were they wanting to prevent Addiction, a largely genetic brain illness with symptoms that occur both with and without drug use or compulsive use of rewarding behaviors?

The answer is, “Yes.”

They wanted to do prevention for all of that, which is laudable, but doomed to failure. It is doomed because they do not sufficiently see the difference between the multiple conditions listed above. It’s all of a piece to our society, and we want to prevent all of it with one prevention program. We use the terms Addiction, Substance Dependence, and Substance Abuse interchangeably with “the drug problem,” “drunk driving” and “drug related crime.” A single effort cannot work against a complex set of social, medical, and societal problems.

For instance let’s prevent diabetes. Do we want to prevent insulin dependent diabetes? Juvenile diabetes? How about diabetes caused by genetic malformations of prancreatic cells? Or diabetes caused by 30 years of too much rich food and no exercise? This is without taking into account preventing the effects of diabetes such as loss of eyesight and heart disease. Would you ever imagine you could prevent all of these with a single effort? The medical people behind prevention in most other chronic illnesses seem to find it of extreme importance to understand the multiple causes of the illness. They differentiate between primary prevention (prevention of the illness), secondary prevention (prevention of illness progression) and tertiary prevention (prevention of complications of the illness). Further, most people working in prevention of medical illness think it’s important to understand first what the core phenomenon of the disease is and what are the epiphenomena that seem to be associated with it. That’s important because if you don’t figure out this difference you end up trying to prevent the epiphenomena instead of the illness. It’s like preventing frequency of urination through a bladder medicine when the person is making more urine because of the diabetes. It might keep them from needing a bathroom as frequently, but it’s not prevention of the illness.

Almost all of these things that are true of people working to prevent medical diseases aren’t true in our field. In addition we have the added twist of having legality caught up in the mix; it’s like what the diabetes prevention people would have to deal with if the government made sugar illegal. Before we get serious about prevention (and we should) we need to understand what we’re trying to prevent.

 We’ve long tried to prevent illegal drug use by punishing those who are caught and attempting to control access to the drugs. This would be the right approach if demand were elastic; that is, if people chose to use and could chose not to if the expected cost was too high. What we have instead is a long history of “drug epidemics” rotating through the various drugs. It’s like the game at the arcade where you try to hit all the gophers coming out of holes. As you hit one another pops up. Make alcohol illegal and smoking goes up. Get people to stop smoking and drinking so much and overeating becomes a problem.

I’m an Addiction Medicine physician, and other than a general public health interest in people not taking poisons or killing themselves and others in cars, my interest in this area is limited to primary, secondary, and tertiary prevention of Addiction. Notice I’m not saying prevention of drug use by addicts; that’s not sufficient. I want to prevent the disease along with all the symptoms and all the suffering, much of which is independent of drug use.

It has been widely supposed that preventing drug use can prevent addiction. I’ve seen no evidence of that. I’ve had a longstanding challenge to my colleagues for someone to show me even one research paper that shows you can prevent a large percentage of addiction by preventing drug use. If I were rich, I’d offer prize money for it. As it is, no one has come forward to show me one to shut me up. Before you get excited and send me a paper, please note I’m not interested in preventing alcoholism or any other ism related to a specific drug or behavior. You need to show me that the primary symptoms of addiction, the things my patients complain of, can be prevented by preventing drug use.

While I’m waiting for the research to prove me wrong, it would probably be a good idea to focus on defining what it is we’re trying to prevent so we will know how. Throwing money down the same hole we’ve been using for 50 years doesn’t sound like a plan for success.

I am often faced with the self-centeredness of people with addiction, as are most people who deal with addicts. It immediately grates on one’s sense of what the interaction should be and often creates a defensiveness in us that keeps us from hearing what the person with addiction is actually saying. Society looks at this self-centeredness and sees willful selfish behavior, not illness.

So the question is, is the self-centeredness of an addict a mark of unconscionable behavior, a personality trait that predisposes to addiction or a result of the biology of addiction. The first two have been long debated as they are the only two that were seen as possibilities without understanding the underlying biology of the illness. Without modern scientific understanding (that is, left with only society’s observations or the observational definitions created by psychiatry) there is no way to understand an original biology that causes addiction and that could account for behaviors that are often seen with the illness but have not been seen to have the same cause. So, any biological model of addiction must explain self-centeredness. I think it does.

If we accept that the biology of addiction is often created genetically or environmentally early in life, and we accept that this biology is best characterized by the effects of a lowered dopamine tone in the reward center, we can begin to understand that the illness begins before the first drug and has a descrete set of symptoms other than drug use. The train of effects of not having enough dopamine tone in the reward center is that there is not a signal of wellbeing to a part of the brain’s cortex (insula) that is set up to calculate the self of “wellness.” It is related to another part of the cortex (cingulate)  that seems to calculate the need for behavioral reaction to the lack of “wellness.” This circuit seems to function in its natural state, not for determining when we need more cocaine, but to tell us when we should act to protect ourselves. It is, in short, a survival mechanism.

As all survival mechanisms, it is unconscious and automatic. It drives behavior at a deep level regardless of what we “think” we ought to do. It should be noted that this circuit doesn’t drive us to ask for help, it drives us to act in our own self interest. Survival mechanisms wouldn’t do much good for the organism if they required help from other organisms.

In most people this circuit only drives behavior in dire circumstances such as famine, war, natural disaster, etc. But in some who have a lowered dopamine tone, this circuit will be active all the time. If the lowered dopamine tone starts early and is lifelong, this drive to act to protect oneself will become ingrained in the person’s repitoire of behaviors. They will act, most of the time, as if their wellbeing depended on their own ability to solve the situation or problem. They will, by necessity, center their behavior and attention on their own needs as those needs are signalled as paramount by their biology.

This hypothesis is testable, I believe. If I am correct we will see more self-centeredness in people who develop the symptoms of addiction early than in those who develop it late in life. Nora Volkow’s work with dopamine receptor density shows that aging lowers dopamine signalling in the reward circuits and suggests that the risk of addiction rises, not declines, with age. While the biology would be the same, the lifelong character on which that biology is superimposed will be different. This is true to the point that we might not even recognize that the elderly lady alcoholic has the same disease as the man who has been drinking since he was 10. In my practice it has become relatively easy to identify those who have had lifelong symptoms and those whose symptoms started late in life. Additionally, genetic testing is coming available that could give an objective measure of genetic causes of low dopamine symptoms though I think this will be less correlated with self-centeredness than early symptom production in general because the symptoms are largely monolithic while the genetics is quite varied.

I look forward to someone proving me wrong. That’s how science works, and it will mean that we now have a better idea than mine.

In an inspired choice, President Obama has named Dr Thomas McLellan as the Deputy Drug Czar (there’s a more official title, but saying this is easier) in charge of decreasing drug demand. Dr McLellan has become known for being a pioneer in quantifying outcomes in treatment and has aided this work with several innovations that allow all in our field to measure our progress. He’s brought up some pretty controversial ideas including compensation by outcome which would really stand our industry on its head.

As Dr McLellan’s brief is to decrease demand, he is the most important person in the office. Decreasing demand for drugs by treating Addiction is key to this effort and treatment must result in more than employment for the treaters. Dr McLellan’s tenure will be sure to shake things up and get us all thinking about what we do and why. I can’t wait.

Perhaps while he’s at it he’ll take a swing at the idea that an Addiction Medicine Specialist should be limited in the number of patients he or she treats with a certain medication. Would we ever tell an endocrinologist that he can only have 100 patients on insulin?

Best of luck, Tom. I’m glad you’re there.

[From the hopefully soon upcoming book Recovering Wealthy - a guide to money management for people with addiction (and everyone else)] 

Rarely have we seen a person fail who has thoroughly followed our path –AA

I could publish the directions in the newspaper and people would still not follow them – Richard Dennis, famous commodity trader

Addicts as a group are not fond of following directions even when those directions are manifestly safer or wiser than their own plan. In recovery and in dealing with money we want success our way. When our way leads to misery or poverty we wonder what went wrong with the world.

We look out at other people who seem to be handling things their own way with success and we wonder why the world is treating them better. Why do they get the breaks? Why are they lucky? And finally, why are we being treated so badly? It couldn’t possibly have anything to do with our decisions, could it?

Like with a drug, dealing with money inspires dreams in us. We look forward to the day when we are financially independent and the sooner the better. The pot at the end of the rainbow glows with a brightness beyond gold. It’s that brightness that blinds us to a reality of money management: risk. Under the influence of expectation of getting our heart’s desire, we are not likely to fully appreciate the pitfalls along the way.

This is not news to anyone in recovery. Your sponsor has told you all this (and if you don’t have a sponsor, close this blog, go to a meeting and get one now). You’ve heard all the 12 step slogans that derive from this reality. What is new is this: scientists agree with you.

In a recent experiment scientists studied methamphetamine dependent people and non-addicted controls and asked them all to play a special game of cards in which they flipped over cards in the order they were in the deck. The game had four decks. The first deck was set up in such a way that the rewarding cards were big rewards, the losing cards were big losses and by the end of the deck the player was in a deep hole. The second deck was the same as the first. The third and forth deck were set up so that the gains were small, the losses small, and by the end of the deck the player was a little ahead.

It probably won’t surprise you when I say the addicted subjects played more of the first two decks and lost more money while the non-addicted subjects stopped playing the first two decks when they got scared and tended to end up a little ahead.

What’s really amazing is that they measured the subjects’ brain metabolism while they were playing, basically making a colored map of each subject’s brain to show which areas were turned on and which were turned off. They found the non-addicted subjects used their more advanced, more uniquely human, frontal cortex while the addicts made their decisions with their evolutionarily older emotional centers.

So does this mean that addicts can’t make reasoned decisions? Should everyone with the disease of addiction just turn over all their money to a custodian and be dependent for the rest of their lives? I don’t think so.

What the study tells me is that in the absence of sufficient midbrain dopamine tone, the more advanced frontal centers don’t work right. One might be tempted to ask why that is, or better yet, why such a response would still be in the gene pool. The answer may be in what low midbrain dopamine means when it’s not found in an addicted person. Low dopamine is a famine or starvation signal. When we’re starving, risk is meaningless. We’ll die anyway, so when we see food, we go for it. The problem for the addict is that their brain is in this state all the time.

That means that the person with addiction needs to have a plan, a map if you will. We know that our brains will respond to sudden views of reward as if we’re starving and will never get another chance. It’s like walking through a dark forest. If we stick to the route we’ll be okay. If we’re lured away from the path by a light in the trees, we’re done for. When we make last minute changes we risk leaving the trail with our eyes closed.

So when you hear about a great business deal, remember that your brain, if you’re addicted, will likely respond as if it’s the last opportunity you’ll ever have. That’s why I put that Richard Dennis quote at the top of the page. He made a better with his business partner. Dennis said that he could teach anyone to trade and become rich. He advertised for some people who wanted to participate and trained the ones he picked. The did quite well. His partner told him that his trading rules wouldn’t work if he taught them to other people. Dennis replied with the quote above. He knew that the problem most people have with money is not the plan, but leaving the plan. He knew that he could print the plan like a map and people would still leave it when they saw something they thought looked better. But rarely have we seen anyone fail who has thoroughly followed our path. Staying on the path is paramount. 

When we think we have it made, when we think that we can judge risk on the fly, when we think we can just change our investment plan because we see what we think is a better one, we’re leaving the path. We’re likely also leaving our best chance for success, in recovery and in investing.

An excellent question.

Yesterday a saw an email exchange between the head of a group of addiction treatment providers and two prominent leaders in addiction medicine. They were expressing fear that people outside themselves would define addiction treatment now that parity legislation has passed. Their fear is, I assume, that people at federal agencies will define addiction treatment to mean or at least allow it to include, treatment with medication only. I wonder if we should call it addiction treatment when the treatment is focused on keeping medication for addiction out.

One of the participants in this email exchange also stated he wants to define what “recovery” is. Maybe I can’t tell him what it is, but the recovery I’m aware of is associated with enough humility to know that we cannot define what recovery is for other people. If I did define it, would I include this patient I saw yesterday.

Adam is a 45 year old artist who I met about three years ago. He was alienated from his family, suffering in his work and not happy in his life. He was using heroin daily. I started him on suboxone and followed him for about a year in a practice where I did not have access to drug screens on site, so I didn’t have a chance to apply my view of abstinence to his care. His life with his family improved immediately, his work stabilized and he began to enjoy his life. I saw him every month for over a year and watched him quickly return to what anyone would call a normal life. He began to be active in raising his son, became reattached to the religious practices of his childhood, and enlarged his spiritual life as well as his relationships with others. All the while I urged him to join a twelve step program but he refused consistently.

My practice pattern changed and he began to be followed by a colleague who continued to see him. Adam remained stable and maintained the improvements in his life in spite of never having entered a 12 step program. Evidently my colleage didn’t have access to drug screens either or didn’t use them regularly because Adam wasn’t drug sceened during this time either. Yesterday Adam came back to see me because my colleague is no longer available. In my current practice we use drug screens frequently to support patients’ abstinence and I usually get the results by computer about half way through a patient’s visit. When I saw Adam he appeared to me just as he did before, calm, happy, energetic and living a fulfilled life. I saw the message come up for the drug screen results but didn’t pay immediate attention because Adam wsa doing so well I assumed it would be clean. As I was about to end the session, I looked at the result to document it and saw that in addition to bupreorphine, it was positive for THC.

I said to Adam, “So what’s with the pot? When did you start smoking?” He replied that he really had never stopped but had answered no when I asked because i asked “Have you been using anything to alter your mood or mind?” and he never had considered pot mind altering as he had never had a problem with it. I was pretty shocked. My first reaction was to want to get him to stop. He asked me why and my the usual reasons failed me. Here was a man who had manifestly maintained a normal life better than his previous life, with a happy family, full employment, and a large circle of friends all the while smoking pot in social situations when his friends did.

I was really concerned and pretty sure I had to do something, but this had taken me by suprise at the end of the visit and I decided to revisit it when I saw him next time. I thought about it a couple of times later that day. What should I do?

Then I saw the email exchange, and, as it happens so often, I saw in someone else the end result of the path I was on. That gave me a chance to decide that it isn’t the path I want to take. Would I say that Adam has not had treatment for his addiction? Can I say he is not in recovery? He’s certainly not in my kind of recovery, but his treatment goals have been met. If I imposed a “no pot rule” on my treatment of him, that’s one goal of his that would not be met.

Who am I to define someone else’s recovery? Who am I to decide to what extent someone should allow me to treat their illness? Isn’t it their illness? Their life? I’m usually so quick with the advice. Here I was brought up short by a guy who didn’t feel he needed my advice. Everything was going along fine for him just the way it was.

In looking at it I’ve met a lot of people like Adam; he’s just the first one I’ve met who used pot. Most of the other ones have been smoking cigarettes. I try to get them to let me help them stop and some just don’t want the help. Like Adam, it’s not a goal for them. All I end up doing is giving them the information behind my reasons to thinking it would be better if they stopped: that studies show that use of any drug or compulsive behavior makes relapse more likely on the drug they came to get abstinent from.

It’s funny. Writing this I’m remembering I saw a woman yesterday with the same story as Adam except that she smoke a few cigarettes a day with her husband who is a heavy smoker. She doesn’t want to stop. Cigarttes have never been “a problem” for her, and she feels that when she smokes with her husband it enhances their relationship. When she’s not with him she doesn’t smoke. She reminded me of another woman I once treated who continued to smoke cigarettes on Suboxone. She smoked two a day because she felt if she didn’t she wouldn’t be able to stand her husband’s smoking and didn’t want to divorce him. She taught me that it is possible even for addicts in recovery to use something for some reason other than their addiction. I just never considered it could be pot. Why not? Is there a difference, besides legality, between sharing a joint once a week with a friend and sharing two cigarettes a day with your husband?

Deciding what’s right for other people is a slippery slope that I really don’t want to start down. That’s why I think the true measures of the success of treatment should be functional and objective. Where I work now we have a set of symptoms we ask about every week with patients in treatment. They self score these symptoms from 1 to 10. We also ask them a number of questions about the functioning of their life. When we’ve looked at our patients over time these scores improve with treatment. I’ve noticed that not many therapists or people who treat addiction like that kind of measure. Like the person in the email exchange I referenced, we all have our own definition of “doing well” that we apply to our patients. I’m reminded of the famous quote of Oliver Cromwell, “I pray thee, brother, think that you might be wrong.”