AddictionDoctor.Org

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.”

I wonder why people use leverage in the financial world. Why do they borrow to make investments they couldn’t normally make? While other ethical, legal and business systems in the world may disagree, it’s not abnormal to borrow money for business here. So why do I say it’s the root of a loss of integrity?

I’m not saying borrowing is bad all together. There’s good borrowing too. In any economy that’s big enough to create things that  person couldn’t create by himself in a brief period of time, someone will need to borrow someone else’s excess capital in order to complete the project. We can tell the difference between good borrowing and bad borrowing by looking at the goal of the borrowing. Are we borrowing to consume or to create. Borrowing to consume may be an emergency necessity, but as a way of life it’s unsustainable.

Handled correctly, borrowing and leverage are tools to create something. They are powerful tools as they let people have the time and resources to create what they could not otherwise have done. As with any tool, handled well, leverage can be a force for creation; handled poorly, it can be a force of destruction. A backhoe is an amazing tool for clearing land and used skillfully by a trained operator, can greatly aid in construction. Can you imagine the havoc if everyone drove a backhoe, even the people who weren’t trained to? That’s what’s happened with leverage. Our society has taken a tool that is supposed to be handled by a few expert tool handlers in order to construct bigger things, and, instead, has given everyone the ability to borrow other people’s money to consume more without constructing anything.

With a few people using leverage to construct projects in their area of expertise (building factories, starting companies, etc) the risk was manageable. A few of these experts would make mistakes and fail. They would go bankrupt and the lenders would not get all their money back. That’s the nature of risk. Some people lose and end up stressed, but others don’t. But with everyone using leverage the risk has become systemic. It’s all over and there’s nowhere safe.

I want to be clear that I’m not blaming people who borrowed money to buy a house. When I’m talking about excess leverage I’m talking about Wall Street brokers creating 40 to one or 100 to one leverage. And since they all did it, they all borrowed money to lend to each other. Instead of the normal person’s 5 to one leverage when they buy a house, these firms have leverage that’s so high that they have to get out at the first sign of something being wrong.

So what’s this got to do with addiction and the brain? Our brain is designed handles acute stress differently than chronic stress. Acute stress is not problem. Chronic stress, on the other hand, is a big problem. Our brain interprets all chronic stress as famine. That makes sense because it’s the only source of chronic stress that our ancient ancestors faced. So when bankers are living on a knife’s edge, and they know that if the brokers they lent money to lose even a little they’ll go bankrupt and if they do the bank won’t be able to pay the people it borrowed the money from in the first place, everyone in the system is living in chronic stress. I know several people who work in and around Wall Street and it’s been this way for a long time.

What happens in chronic stress is that the stress response blunts the brain’s ability to feel the dopamine release of reward. To feel good it needs more and more dopamine signal. The midbrain reward system doesn’t work right and the pre-frontal judgement area doesn’t get enough signal to work right. We become more motivated by hunger and less by rational thought. We become selfish and unthoughtful. It’s how we’re designed to act in a famine to protect our own lives. 

So to bring these two posts to a conclusion, over use of leverage creates situations of chronic stress. In chronic stress, the very thing we need to act rationally becomes less powerful and baser needs gain in strength. We feel hungry and become greedy. We worry that what we’ll have will never be enough and we need to get more and more. Integrity goes into the background to some degree and people will increase leverage more and more, to get more and more in an unsustainable cycle. I’m not just making this up, the cycle has repeated itself again and again in history. Hopefully, if we understand that this is not a problem of “bad” people, but of humans under stress, we’ll make the systemic changes we need to prevent it from happening again.

It’s pretty obvious to everyone that the country is going through some tough times, and not just economically. A pretty close second is the tough time we’re having ethically. Whether it’s a large Ponzi scheme, banks borrowing billions to pay bonuses to the executives that ran them into trouble in the first place, or someone trying to sell a Senate seat, it seems that there’s a lot of public behavior that you wouldn’t want to admit to your grandmother.

You may wonder how this interests an addiction doctor. This may seem like a round about explanation but it’s the only one I’ve got. Integrity is the basis of a good healthy life as well as a good healthy recovery whether you have addiction or not. In addition, the survival drive of an ill reward system is so powerful that the necessity for integrity seems to be the first victim.

People are very found of saying a lot about how much addicts lie. The old saw, “How do you know when an addict’s lying? His lips are moving,” pretty much sums it up. I don’t know how many, if any, of the people behind the behaviors above have the chronic illness of addiction, but it’s not that important to know. Addicts, that is people with this incurable disease, aren’t the only ones who have a reward system that can go haywire.

The reward system is a survival mechanism. It’s what gets us to find food in a famine. When I lecture about the reward system to people without the disease I often refer to hunger. When I ask how many people in the audience steal on a regular basis, no one raises their hand. When I ask how many people would steal to eat if they hadn’t eaten in four days, everyone raises their hands. Can you imagine how many of us would still be here if our ancestors had been able to say something like, “Well, I know I’m starving, but to go steal food is an antisocial act that might cause the death of others, so it would be better if I died of starvation?” That may be a fine sentiment that we’d like to think we were capable of but the human race wouldn’t be around for long if we were.

When people are under stress, the reward system is supposed to not work the way it does when we’re not under stress. That’s one of it’s values; it senses what’s critically important to survival, and under stress, what’s critically important to survival is different.

I can just hear someone out there saying, “Hey wait a minute. Scientists have show that cooperation rather than competition actually increases survival. You’re full of poop.” Actually I don’t think they said, “Poop.” But the point’s the same. Why do we ask, “What’s in it for me,” when it would be more effective to ask, “How can I help others so they can help me?” I can’t say I know the absolute answer, but I have a an idea.

The reward system is the essentially the same in all mammals. Ours, the rat’s, it doesn’t matter. This thing is in us for the survival of the organism itself and it’s been serving that role evolutionarily a lot longer than whatever got us to produce civilization. It’s just older and stronger than the new parts of the brain. In fact, the newer parts seem to be wired in such a way as to turn off when the reward system isn’t acting normal. So that would mean that all these people out there acting selfishly were under some stress that got their  reward system to act in a non-normal way.

I think that is probably the case, and it begs the question of what kind of stress and how’d they all end up under stress. I think the answer lies in one word, leverage. Leverage is when you use a tool to enable something of small power to move something that takes a larger power. In financial terms it means borrowing somebody else’s money so you can act as if you had that much money. It may or may not be normal in evolutionary terms for humans to use leverage, I can’t argue that point. But it seems that leverage is necessary precursor to going off the rails of integrity, and I right more about that later.

Why “Why” is important

Correlational studies are the first step in examining the relationship between disease and genetics. These studies tell us “what” but cannot tell us “why” these things are correlated. The correlations found can only be applied in the context of the understanding of the disease process. An example is the relationship between Major Depressive Disorder, Serotonin (5HT), and a Serotonin Transporter (5HTT) polymorphism (HTTLPR).

The HTTLPR polymorphism of the serotonin transporter was discovered to have short (s) and long (l) variants. It was noticed early on that transporters from individuals bearing the s allele had less activity at the transporter, that is, took less serotonin up from the synapse. Selective Serotonin Reuptake Inhibitors (SSRIs) were used in treating depression and it had been hypothesized that “low 5HT” was the cause of depression. To account for how a low activity reuptake pump could cause low levels of neurotransmission a hypothesis was developed that the s allele caused dysfunction by increasing synaptic serotonin, thereby causing a reactive loss of responsiveness at the serotonin receptor, and leading to decreased serotonin tone.  It didn’t seem to occur to anyone to ask why increasing serotonin by blocking reuptake further with an SSRI would help in such a situation. The medications were useful in depression and someone had found the polymorphism and its function so the two had to be reconciled. Unfortunately, a lot of money and literature has been expended to expand on and enlarge the hypothesis.

What no one seemed to consider was evidence that such “low serotonin tone” causes of depression didn’t make much sense. SSRI anti-depressants work much better in people with the l allele as they have too much function at the 5HTT. But people with the s allele seemed to have more depression, more violence, more reactivity to angry faces, and more neuroticism on personality testing.

There is an explanation for this seeming contradictory information. The higher serotonin is, the lower is dopamine release. So for those with the s allele who have less expression of the serotonin transporter, and therefore higher synaptic serotonin levels, there will be a lower dopamine tone. Low dopamine tone has been associated with aggression, inability to feel reward or pleasure, irritability, poor sleep and several other things seen in “depression.” Here’s why this difference is very important.

SSRIs have been implicated in causing suicidal ideation and suicides. Actually the warning extended to all the new non-tricyclic antidepressants, all but one of which is an SSRI. If depression was caused by low 5HT tone, this wouldn’t make sense, and, in  fact, psychiatry has responded with derision towards the idea. However, if SSRIs increase 5HT and thereby decrease DA tone, it would be expected that we would see some of the things we see with the s allele at the HTTLPR site. Interestingly, of all the anti-depressants that were lumped in the suicide warning, the one not actually associated with any suicides was buproprion, the lone dopamine raising agent.

So correlation is not enough, we have to understand such relationships in the clinical context of modern medicine. Unfortunately, such context can get stuck in a rut with no one doing much thinking, even when things don’t go right.

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.