Why Test Alcoholics for Drugs in Treatment?

August 27th, 2014

If you’ve been reading what I write you probably read the title and said, “Wait a minute. Howard doesn’t think there’s any difference between addicts just because of the drug they use. Why would he ask this question?” And you’d be right. It doesn’t make sense. People with addiction can use anything and often switch; monitoring for this illness should be broad and frequent. In addition, people in treatment are thrown together with others who have experience with drugs they’ve never tried. Unless monitoring is comprehensive, people can start taking something they’ve never taken before that you’ll never think to look for if you limit your monitoring to their usual suspects.

So why would I bring this up? Well, there are two groups of people who have a problem with the policy of comprehensive testing for addicts who have only used alcohol in the past: insurance companies and alcoholics. The insurance companies don’t want to pay to test alcoholics for cocaine, “They’d never use cocaine; they’re alcoholics.” Alcoholics don’t want to be tested for drugs, “What do you think I am, an addict?” Why yes I do.

Recently an offended alcoholic complained to his insurance company that we wasted their money testing him for drugs he’d never use. They showed us his case and told us it did not meet their medical necessity criteria to test alcoholics for drugs. I don’t know who makes up these rules, but they don’t seem to have any data.

Well, you know me. I went for the data.

In our EHR we have 340 patients from this insurance company. 117 or 34.4% have a primary alcohol dependence diagnosis and the other 223 (65.6%) have a primary dependence dx with another drug. We also have the results of all the Medical Monitoring for Adherence tests we’ve done. Here’s what we’ve learned.

It is indeed more common for a person with a non-alcohol primary drug than alcohol as a primary drug to have at least one positive for a non-alcohol drug. 136 or 61% of the non-alcoholics had at least one positive for a drug other than alcohol. Of the 117 “alcoholics” 41 or 35% had at least one positive for a drug other than alcohol. So it’s a little more than half as common as with those “drug addicts.” More than one in three “alcoholics” had confirmed positives indicating new use of some drug other than alcohol at some point in treatment.

We also looked at it the other way; who drank during treatment. Of the 117 “alcoholics,” 46 (39.3%) were positive for alcohol at some point while “only” 22.4% of the “non-alcoholics” were positive for alcohol at some point during treatment. Maybe we should stop testing “drug addicts” for alcohol; they might get insulted.

So 35% of the primary alcohol dependent patients used a non-alcohol drug at some point and 39% used alcohol at some point. I feel an odds ratio coming on. (39/35 = 1.11) So it’s 1.11 times more likely that a primary alcohol patient will be positive for alcohol than positive for another drug. That’s a pretty wimpy odds ratio; not the kind of thing I’d drop important monitoring for. I think if I was 11% less likely to get malaria if I went to the tropics I’d still take the prophylactic medicine.

What’s key to understand here is that addiction is deadly, just like malaria, diabetes, and heart disease. We don’t do drug screens on substance abusers. We are treating ill people for the biological illness of addiction and we are using medical testing to monitor their progress in treatment. So who would want to save 10% even if it meant some cases weren’t found and treatment correctly? I don’t know, but I bet they don’t believe addiction is an illness.

Now Here’s a Crazy Idea

August 23rd, 2014

“It might sound crazy what I’m ’bout to say…”
– “Happy” by Pharrell Williams

I’m a big fan of always questioning the received wisdom. For instance, while it’s true that heavy early use of drugs and alcohol is correlated with later diagnoses of “substance abuse,” it does not necessarily follow that it was the early use that caused the later abuse. It could have been the primary symptoms of addiction that caused both the early use and the later attachment seen to the drug that relieved the symptoms.

Another example is the growing prison population in America. I’ve heard lot’s of reasons for it and many of them seem to have face validity: the war on drugs, more effective prosecutorial tools to force pleas, increased mandatory sentences, etc. I came across another correlation that is interesting. Remember, I’m about to tell you about a correlation, not a causation. The two things seem to go together, but that doesn’t mean that one causes the other. But maybe we can figure out a test to see if one does.

Here’s the correlation. The green line is prison population per capita, that is, the prison population divided by the number of people in the country. You could also consider it the percent of Americans in prison or jail. The orange line is the pounds of high fructose corn syrup (HFCS) consumed per person in the US. Notice that the prison population is fairly stable to declining until right after the invention of HFCS and its first report here in 1966. Also notice that shortly after the consumption of HFCS starts to decline there begins a slight decline in the prison population.

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For those of you who are statistically inclined. The variance in prison population explained by the amount of HFCS consumed is 79% and p<.0001. For those of you not statistically inclined, just enjoy that I put green and orange on the same graph.

Am I saying that the introduction of HFCS caused the increase in the prison population? No, I'm not.

This is just correlation, mind you, not causation, but one thing we can do in time-series like this is instead of matching one year's prison population to the same year's HFCS intake we can vary the year to find if HFCS for a certain time before the prison population is a better correlation. We could also use later dates compared to the prison population. It turns out that the best correlation is the prison population to the HFCS 6 years prior. I picked six years because the prison population peaked 6 years after HFCS peaked. Here's that picture:

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And for those of you who are statistically inclined, the variance explained is 97% and p<.0001. But does this show causation?

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No, correlation is still only correlation, but even if there was causation here, we’d need some theory to test. Can you think of some way that HFCS could increase the prison population? Well, oddly, I can. I know, it’s going to be odd, but in my defense, I first heard the idea from an NIH researcher. Here’s the issue: corn and all its components are high in omega 6 fatty acids and very low in omega 3 fatty acids.

Not only that, the researcher pointed to his work and that of others at NIH and in England that showed that the higher the omega6/omega3 ratio was, the more inflammation, and the greater the manifestation of several problems including violence, anhedonia, and substance use. Now that last one I’m not so sure of because of the negative correlation I see in alcohol and nicotine intake with HFCS, but he was talking about his tests of inflammation in individuals who changed their diets and noted changes in drug intake.

But there aren’t any fatty acids in HFCS you say, and you’d be right! I’m not saying that there’s a direct causation. It could be that a diet high in HFCS is also one likely to be low in omega3 fatty acids. It might be that because we are making a lot of HFCS we have a lot of the rest of the corn left over and getting more of it as filler in other foods and getting the omega6 that way. It could be there’s no connection with omega6 and this is completely wrong. So here’s the test.

We could take a look at two groups of people. Those who use a lot of HFCS and have their own diet and those that use a lot of HFCS but have a diet supplemented with a lot of omega3 fatty acids. The second group will have a lower 6/3 ration and we can compare the differences. It’s an expensive study with a very large N to be able to look at incarceration rates. I didn’t say it’s an easy study. I just said I could think of a way to test the hypothesis.

Maybe someone else can come up with a better way. I just wanted you to see the pretty picture. I have to go now – I have to go get some more fish oil so I can get “Happy.”

A New Paradigm?

August 15th, 2014

I was recently told about a report of the Institute of Behavior and Health Inc. titled “A New Paradigm for Recovery” that purported to be a road map for making recovery and not relapse the expected outcome of addiction treatment. So I took a look at the report and found an old paradigm in a new wrapper.

The big point of the report is to trumpet the success of professional monitoring programs and propose an expansion to the general population. These programs place the professional’s license in jeopardy of loss if there is a positive drug test and then impose a long term (at least 5 year) random urine monitoring program to ensure abstinence. They are successful as has been shown in many reports, but the success is always abstinence from identified drugs that are impairing. There has not been a study of such programs that encompass addiction symptom suppression as an end point, or, for that matter, the cessation of all use of compulsive rewards. Specifically, such professionals may still be overeating, gambling, compulsively working or engaging in compulsive sexual activity and the studies would have shown the same outcome.

Here are some of old paradigm idea celebrated in this report:
1. Stigma: “Unhealthy patterns of drug and alcohol use warrant “stigma”, to warn others to avoid such behaviors and to help persons engaged in such behaviors identify the need for help. In itself, illegal drug use merits stigma.” The report goes on to say that we should limit stigma to the bad behavior and not encompass the person. Good luck with that.
2. Focus on substances only: “The disease of addiction results from use of alcohol and other drugs. In many ways addiction is a disease of youth; the earlier the initiation of substance use, the more likely an individual will have later substance use problems, including addiction.” This is after listing the ASAM definition that the report’s writer clearly doesn’t subscribe to. There is no recognition in this report that addiction is a primary disease that may involve other rewards besides drugs and alcohol.
3. Sees the illness as non-progressive biologically: “This is because drugs hijack the brain’s thinking and change the brain over time in persons with substance use disorders.” They completely miss that the brain with addiction continues to get worse even if it’s not using drugs to feel better. That leads me to the next old idea.
4. Focus on behavior and not symptoms: “All substance use disorder treatment programs, whether abstinence-based or medication-assisted, need to focus during treatment on the use of alcohol and other drugs, and all treatment programs need to extend their focus beyond discharge to what happens to patients after they leave formal episodes of treatment.” Couched in the laudatory sentiment of seeing addiction as a chronic illness is the idea that the chronicity is only about behavior. There is not one mention in this report about the individual pain of the untreated addict, the mental anguish caused by the primary symptoms. That mental anguish is described by newcomers in the same language in an Overeaters Anonymous meeting as in a meeting of Alcoholics Anonymous. The symptoms of the illness are no different regardless of reward used to feel better.

Four’s enough for now, but there are more, like the legalistic approach and the use of urine monitoring to “catch” people as opposed to medical monitoring. We desperately need a new paradigm for the treatment of addiction in this country, but this report isn’t the answer. It is, in fact, highly unlikely that the same minds that created or participated in the “War on Drugs” is going to come up with the new answer after 40 years of failure. As Thomas Kuhn related in his book on scientific revolutions, the new paradigm has been there all along. What was necessary was for the people invested in the old paradigm to go out of power. We’re still waiting, I guess.

Suicide and Addiction

August 12th, 2014

I don’t know Robin Williams. I’ve never met Robin Williams. This blog entry isn’t about Robin Williams. But since he was found dead yesterday, someone will think it might be, and I must admit that his death at his own hand inspired me to write this. I’ve been treating addiction for a long time and I’ve seen more people with addiction commit suicide than I’d like. I’ve searched my memory and there seem to be three main classes of such people.

First is the group that has never been able to get sober. Nothing they’ve tried has ever worked. They can’t see a way out and a way forward has become impossible. There seems to hope and they are completely isolated.

Second is the group that have made some progress. They’ve felt sobriety; they’ve had success. But the disease is progressive and active again. Because this is a progressive disease the way they got sober the first time doesn’t work as well now. They think it’s because they are doing something wrong, that they can’t recover. They know that success is possible but not for them any longer. They see other recovering people and have just a sense of isolation that they cannot reasonably expect to rejoin and stay in that group. They are completely isolated.

Third is the group that have long term success in recovery. They have never, in the common usage, “relapsed.” Their disease and the primary symptoms have continued to progress, and while abstinent, they no longer enjoy life. They know they should feel better and imagine that the reason is because of something they are doing wrong. Not enough meetings, not enough service, not enough or the right kind of something that works to make others in their situation happy. They wonder is this all there is to sobriety and they feel the desperate pointlessness of going on with everyone else. They are completely isolated.

By now you’ve figured out what the three groups have in common; they are alone. It may not look that way to you, but that’s how it feels to them. It’s not the fault of their family or friends. It’s nothing that anyone is doing wrong. The disease does that.

And the great and terrible shame of all this is that most of these deaths could be prevented. Another thing that all three of these groups have in common is the unsuppressed primary symptoms of addiction: relative anhedonia, poor motivation, poor memory, poor attention, inability to attach to others, etc. These are symptoms of low midbrain dopamine and not, in these people, symptoms of depression. But so many talk shows use the word depression today, and it’s so much more socially acceptable to have that than be struggling with addiction, that depression is how these symptoms are labeled. The problem is that most treatments for depression can actually make these symptoms worse, and I’ve met dozens of people who have told me of the seemingly endless cycle of feeling better on SSRIs only to feel worse and the resulting thoughts that it could work if only they were better. I think this is why SSRIs are associated with suicide; I think further research, if anyone ever does any, will show that it’s primarily people with low midbrain dopamine that have this effect.

But even if you’re not a psychopharmacologist you can do something for the people in these three groups. Name the problem. Be willing to look at it in the face. Don’t shrink from it or acknowledge stigma. It’s diabetes; it’s a broken leg; it’s addiction; it’s just an illness. Tell them you love them not just in spite of addiction but for entirely who they are including addiction, and that you’ll walk with them to go get help. Because there is help. There is primary medical treatment for addiction, and it has nothing to do with how long ago someone’s last drink was.

Is High Fructose Corn Syrup a Drug?

August 11th, 2014

Anyone following this blog or who has read my book knows the graph I use all the time to show that we’ve started to eat more as a country when we stopped using as much alcohol and tobacco. Here it is just as a reminder:

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As you can see, the data ends in 2005 which was the last federal data available before the first printing of the book. I’ve been working on a revision so I went to get the latest data. It’s not easy to do, because the USDA doesn’t report the alcohol figure anymore in a direct way, but that’s another story. Anyway, I got the data and took a look. I found something interesting.

I found some new historical data on caloric intake that was broken down into sugars and fat, so I had some new data on the pounds of caloric sweetener we consume per person by year. I thought I’d do a statistical comparison of that with the Nicotine-Alcohol Dopamine Load.

Screen Shot 2014-08-11 at 10.02.47 AM

The first thing I noticed was that the statistical test told me that the relationship was not statistically significant. Then I looked at the picture. You can clearly see there are two curves instead of one. The top curve which does seem to vary by dopamine load and the bottom curve that is more flat. Well I took a look and it turns out that every dot in the bottom curve was before 1966. That was curious. What happened in 1966 that all of a sudden changed the relationship between caloric sweeteners and intake of nicotine and alcohol. You guessed, I’m sure. It’s high fructose corn syrup (HFCS), first reported in 1966 by the USDA as having zero pounds per person in that year. Before then, in the report, it didn’t exist.

So I went back and got the data specifically on HFCS. Different picture.

Screen Shot 2014-08-11 at 10.09.50 AM

This relationship is highly significant. The variance in dopamine load that’s explained by HFCS intake is 79% and p<0.0001. It doesn't get much better than that. You'll notice those three little dots in the lower right that seem to be out of sync with the rest. Those are the first 3 years that HFCS were reported in this series, before the "drug" became widely used.

In short the more we smoke and drink, the less we eat HFCS. The more HFCS we eat, the less we smoke and drink. Addiction is still the same; we're just switching drugs. And now we're switching again.

There's been a lot of controversy over HFCS and obesity in the past several years and concerted educational efforts to get us to use less of it. In fact those efforts have succeeded to some part. Notice below that HFCS rises to about the year 2000 and then starts to fall. Also notice that after a 20 year fall in the percentage of the population that has used illicit drugs in the last month there was a plateau at 5% until the year 2000 and a start to increase again.

Screen Shot 2014-08-11 at 11.42.07 AM

We don’t have any good government statistics on the amount of drugs used, only this SAMHSA data on percent of the population that used. Could we be seeing a return to drugs with a decrease in cigarettes, tobacco and HFCS? Another possibility is the rise of “vaping” nicotine which doesn’t show up in government cigarette statistics.

In any case, these relationships just further highlight the need to see addiction as an illness. We have to stop focusing on a drug, or the drugs, or this or that substance and start looking at the underlying illness. Otherwise we’ll just continue this shift, and we’ll never see the next one coming.

Did Prohibition Work?

July 30th, 2014

In the last week, and in the context the New York Times coming out in favor of repeal cannabis prohibition, two of my colleagues have used a graph that I showed them from my book to make the point that prohibition worked. Here’s the graph:

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So yes, in the year after prohibition, this country consumed half as much alcohol for every man, woman, and child as it did in the year before prohibition. Both of these colleagues used this data to argue for prohibition of a drug, in this case cannabis. They missed the larger point of the graphs that follow in my book.

First look at the graph of alcohol use. It was pretty steady at around 25 gallons before prohibition, but then started to fall off even before the law was passed. While the end of prohibition shows that the per capita intake was only 10 gallons, half of the 20 gallons per capita before prohibition, notice how fast the number rises. The slope was much higher than seen before prohibition. We see the same increase in craving when someone with addiction stops using but doesn’t get treatment. Periods of “stopping” often end with use escalated to levels above those seen before the stop.

Yes alcohol use dropped, so will use of any drug when we make it more costly, either socially or economically, to use. And normal people who don’t need or generally use drugs will probably not use it at all once we make it illegal. However people with addiction will still look for something to calm the symptoms of the biological brain illness they suffer from. So, what, I asked myself, might addicts who used alcohol have moved to when alcohol became illegal. Here’s the graph of cigarettes.

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In that last year before prohibition, 1919, America drank 19.6 gallons per 10 people, or 1.96 gallons per capita and smoked 727 cigarettes per person. Let’s just assume that we’re getting dopamine from both and multiply them together to get what you might term a “dopamine load.” 1.96 X 727 = 1424. Now let’s look after prohibition. In 1934, America drank only .97 gallons of alcohol per capita and smoked 1483 cigarettes per person. .97 X 1483 = 1438. No decrease; those who needed dopamine and couldn’t get alcohol just smoked more. Here’s a graph of the combined product for each year:

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One colleague answered the New York Times in a letter to the editor and said that while prohibition may have been a political failure, it was a public health success. Really? Before prohibition, alcohol use was falling. After prohibition it rose faster. Before prohibition tobacco use was rising slowly. During and after prohibition tobacco use rose far faster. Before prohibition we did not have powerful organized crime syndicates with access to large amounts of money. Prohibition gave us this, and when the crime bosses saw the money about to go away with the end of prohibition, they used their organizations to start pushing a new drug, heroin, into the same markets they ran. An increase in smoking, an increase in heroin, and an increase in violent crime. A public health success? We don’t need many more of those.

Is smoking pot a good idea? No, even if you don’t have addiction. It’s not a good idea to smoke anything. How about not smoking, but taking another way if you don’t have addiction? I don’t know. There’s no evidence that’s yet good enough to say. Healthy? doubtful. Harmless in moderation? don’t know. We live in a free society and if you want to take a chance I can’t stop you.

This is our opportunity to stop worrying about the drug and start looking at the real cause of the problem. Normal people actually don’t like drugs that much, and their use of them tends to be moderate and temporary. People with addiction however aren’t safe using anything. Unless we treat the illness they’ll most likely switch back and forth between sources of dopamine spikes depending on the social and economic costs at the moment. Can we make them use less of something? Sure, but they’ll just use something else. Here’s what happened when we got people to drink less and smoke less in the 80′s:

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We stopped drinking and smoking as much and started eating more. Are we healthier? Not if you use our healthcare expenditures as a measure of success.

Goodhart’s law says that once a measure becomes the object of policy it stops being an accurate measure. I’m all for people smoking less pot, but let’s not target the pot. The real low hanging fruit is the disease of addiction. Treat that, and a lot of things will get better.

Can We Still Treat Addiction if Cannabis is Legalized?

July 27th, 2014

There’s probably two issues being talked about in addiction today more than any other. The first is the epidemic of opioid overdose deaths and the second is the legalization of marijuana by some states. I haven’t heard of anyone in favor of opioid overdoses so that has little controversy. The same cannot be said for legal pot.

One of the reasons for the controversy in this issue is that it’s really the amalgamation of more than one issue. The arguments I’ve heard both for and against have all been the conflation of arguments for and against four separate proposals. They are: legalizing marijuana for medical use (medical marijuana), local and state decriminalization of marijuana (decriminalization), state legalization of personal use marijuana (personal use legalization), and full federal legalization of marijuana (repeal of prohibition). The mixing and matching of these arguments adds to confusion. It isn’t uncommon, for example, for a person arguing for repeal of prohibition to use arguments for medical marijuana and be answered by the arguments against personal use legalization. In this case neither debater is actually debating the question they think they’re talking about.

Please understand, I actually am quite neutral on this issue. All I do is treat addiction and it’s just as easy for me to treat a patient using a legal drug as an illegal drug. I really don’t care one way or the other.

This was going to be a large opus listing all the pros and cons of the various proposals above, and it has sat in draft form for over a month, but time has gotten ahead of me. Two things have prompted me to wrap this up and put it out in a smaller form: the increasing negative health affects of synthetic cannabinoids and the recent editorial in the New York Times supporting repeal of prohibition.

Anyone who’s read my book or has followed my blog knows that I see addiction as a single illness. The effect of prohibiting a drug is to increase the cost (both economic and social) of using that drug. People with and without addiction will be incentivized to not use it, however people with addiction will just switch to another drug – unless we treat the illness. And make no mistake, cessation of drug use is not treating the illness; neither is putting people in jail. So prohibiting a drug, any drug, is not helpful to addicted patients.

But then I hear the arguments from colleagues “Repealing prohibition of cannabis will make it harder to treat addiction because people will claim they should still be able to smoke it like cigarettes.” I think that’s ridiculous. If you have to threaten your patients with legal consequences you probably don’t know how to treat addiction. If you aren’t addressing smoking as part of the illness, you probably don’t know how to treat addiction. Okay, I say to patients everywhere, “Maybe it is just like smoking cigarettes, and there’s good evidence that if you continue to pop your dopamine with cigarettes you’re more likely to restart the use of the thing you just went to treatment for. We’re not asking you to stop smoking and be miserable; we’re asking you to let us help you with medication and other treatments to improve the state of your illness so that your brain no longer wants to smoke.” I really don’t care that tobacco is legal; it’s not a good idea for someone with addiction to smoke. I don’t care that sugar is legal; it’s not a good idea for someone with diabetes to eat it.

So really, purely as an addiction doctor, I can’t say that repeal of prohibition would make my job any harder. Are there going to be social consequences? Quite likely. But I think society gets to make that choice, and does so, with all sorts of things. What society is doing when it says one drug is legal and another isn’t, is choosing the social consequences. All drugs have them, and democratic society has a right to pick which ones it will tolerate and which it won’t. I’ll never live in a society free from social consequences of drug use, so I’ll get used to whatever you guys choose. The real choice society hasn’t faced yet is whether we’re going to continue on this prohibition marry-go-round regulating one drug or the other while the disease goes undressed or if we’re tired of 50 years of a drug war and want to start actually addressing the illness.

And speaking on consequences, there’s one we should ask ourselves about concerning cannabis prohibition. THC is a partial agonist at the Cannabinoid Receptor Type I (CB1), that means that it turns on the receptor part of the way. Cannabis has been grown so that it’s more potent per gram than it was 30 years ago but THC is still a partial agonist, and cannabis still has more than THC in it. There are many cannabinoids in cannabis, and some may counter the effects of THC. It’s not completely known. But one thing is certain, it’s not like pot is a pure agonist at CB1, but the synthetic cannabinoids being marketed in convenience stores are.

With the rise of an internationalized world, chemists in the eastern hemisphere were able to synthesize an increasing number of pure full agonists at CB1 that are far more powerful than even the most potent cannabis out there. The first synthetic cannabinoids were the JWH compounds and after a couple of years they were made illegal. Before they even were, the chemists had the next set ready, and the next. We will never be able to make new chemicals illegal faster than scientists in another country can make new ones we’ve never heard of. On top of that, we can’t create confirmatory tests to use for these things at anywhere near the pace of their invention so we’ll always have people in treatment who are negative for existing tests even though they are using. That’s new, and that does make treating addiction harder. Now we aren’t dealing with a readily available partial agonist with known effects and a good way to track its use, but a range of unknown full agonists that are causing an increasing number of catastrophic health effects (this will be the next epidemic after opioids calm down).

So the question society needs to ask is this, “Would there be as much use of synthetic cannabinoids with the attendant psychosis, suicides, and homicides we’ve been seeing lately if cannabis itself were legal and regulated?” I won’t pretend for a minute that if we repealed prohibition that synthetic cannabinoids would go away; that genie is out of the bottle, but would there have been as much economic incentive to create these things if cannabis had been legal? We need to take a look at the second order costs of our decisions, and so far, we only look at the first order savings. We see there are problems with pot and we make it illegal to save those problems. Now we have bigger problems that we didn’t see coming.

The real problem is how we look at costs and benefits. We keep thinking that the choices for people are between using this bad thing and not using anything. That’s never been the choice. The overwhelming amount of drugs used are used by the few people who use a lot and those people, mostly, have addiction. For them not using isn’t an option without treatment and recovery, so the choice we are really making with prohibition is this, take legal risks and keep using this or go find something else. We might even like what they find (smoking cigarettes, over work, eating too much), but the disease, without treatment, just gets worse regardless of the social acceptability of the drug used. Whether pot is legal or not, the real question before is whether we’re ready to look at this disease the way it exists in nature and deal with it, or if we want to continue our half-century of delusion and continue to complain.

The Most Important Problem in Addiction

July 24th, 2014

A tweet I read led me to watch a video of chemists giving career advice. I don’t particularly need career advice from chemists, but clicked the link anyway. The tweeter, David Collum (@DavidBCollum), said in the video that he had been in a job interview and the interviewer had asked two questions. The first was, “What is the most important problem in organic chemistry.” Being young and wanting to impress, Dr Collum replied with something about genetics and biology. The questioner’s next question was this: “Then why aren’t you working on it?”

The interview gave me pause. What is the most important problem in addiction and am I working on it? I’ll tell you want I think.

I think the most important problem in addiction today is our society’s conceptualization of it as a behavioral diagnosis rather than a medical one. Because the diagnosis is behavioral, we assume everyone is normal before they use the first drug. That allows us to blame the formation of the illness on stupid behavior. That allows us to believe that we can prevent the illness by preventing drug use. That allows us to underfund treatment, aim at the wrong place for efforts at prevention, focus on punishment as deterrence, and fight the war on drugs. That’s another war we’ve spent billions losing.

If we didn’t have this conceptualization, we’d see the biology of midbrain dopamine and understand its genetic origins. Instead of focusing on prevention of drugs or drug use, we’d be doing early identification of people at risk. We’d be intervening early with kids who had lowered dopamine tone and improve their function so that, if they took a drug, it wouldn’t do anything. We’d save billions if not trillions, not to mention the lives that would go un-ruined and un-lost.

I’m glad to say, if anyone asked me the questions they asked Dave, I’d be able to say, “I have been.” But I can’t claim to have been very successful. I’m in contact with colleagues every day and even in those I respect a great deal I hear bits of the old thinking. I’m inpatient, I guess. On the other hand I meet young people in my field who get it.

Thomas Kuhn popularized the term “paradigm shift” in his book called The Structure of Scientific Revolutions. He didn’t say that paradigms shift because new information comes out or because everybody thinks it’s a good idea. He basically said that paradigms finally shift when the old guard retires or dies and the new guard takes over. Maybe if people with addiction would stand up a bit more, advocate for themselves a bit more, some of the old guard would retire faster.

Opioid Substitution Therapy: Measuring Impairment in a Clinically Relevant Population

July 23rd, 2014

Opioid Substitution Therapy: Measuring Impairment in a Clinically Relevant Population
J. Cameron Davis and Howard Wetsman MD FASAM

Background: The CDC has labeled opioid overdoses an epidemic while treatment is readily available to those suffering. Current research indicates that the best treatment outcomes are in opioid maintenance therapies, yet such therapies carry a significant stigma; opioid maintenance therapy is impairing to patients. Methods: Measures of cognitive ability, the Iowa Gambling task (IGT) and the continuous performance task (CPT), were used to determine cognitive impairment in opioid maintenance patients before and after prescription buprenorphine use. Data was collected from a retrospective chart review of patients enrolled in a medically managed intensive outpatient program that uses frequent neurocognitive testing. Participants were 38 sequential opioid dependent admissions from August to December 2012 who both received buprenorphine and had both before and after testing. Results: A significant difference in IGT scores between the pre and posttest conditions was found with buprenorphine medicated patients having higher average scores than in the pre medication condition, F (74) = 10.74, p=.0016. Target accuracy on the CPT did not differ significantly in any of the time blocks between pre and posttests. A significant difference in foil accuracy was found between the pre and posttests in both the two second block, F (74) = 10.81, p=.0015, and the four second block, F (74) = 5.41, p=.0228 with medicated patients showing improvement over their pre-medicated condition. Conclusion: Evidence from this study does not support the currently prevalent idea that introduction of buprenorphine opioid maintenance treatment will impair patients. This has tremendous implications for buprenorphine maintenance therapy demonstrating that reward overvaluation and impulsivity both decreased after the introduction of prescription buprenorphine in a clinically relevant population. The research also supports the subjective report of opioid dependent maintenance patients that they actually function better when prescribed buprenorphine.

Opioid substitution therapy: Impairment
Opioid dependence is a fast rising cause of death, with opioid overdoses reaching epidemic status(1). In spite of this, treatment is readily available and can help opioid dependent individuals. Risk of relapse following opioid withdrawal is common, and “detox” alone does not count as satisfactory treatment for opioid dependence(2). Best treatment outcomes are in opioid maintenance therapies(3). Unfortunately opioid substitute therapy still carries a significant stigma.
Opioid maintenance therapy in the form of methadone has been available since the 1960’s, but requires a large infrastructure under current law. Recently, maintenance has also become available in the forms of buprenorphine, which specially licensed physicians can prescribe in an office based setting. While this increase in treatment options is welcomed, buprenorphine is a largely underutilized treatment. In contrast, there has been an overall increase in full opioid agonist pain treatment. This has been accompanied by a 63 percent increase in opioid deaths from 1999 to 2004 according to a 2007 national survey on drug use and health(4). This calls for a reevaluation of the stigma surrounding opioid maintenance therapy and a need to use the best therapy available.

In spite of its good record as treatment, there are other problems with methadone. Pud et al. (2012) reported that methadone maintenance patients experience pain, depression, and sleep disorders, which disrupts their general state of health and well-being(5). Methadone has also been found to be impairing. Mintzer et al. (2002) researched psychomotor and cognitive performance among methadone maintenance patients(6). Assessed on a broad range of performance tasks; methadone patients exhibited impairment relative to controls in five out of eight tasks. Methadone maintenance patients are also significantly more likely to make risky decisions when they had been unsuccessful on the previous trial(7). Such disruptions further hinder the success of rehabilitation.

Buprenorphine has been approved because of the need for a new maintenance treatment with fewer drawbacks. Buprenorphine is a semi-synthetic opioid approved by the Food & Drug Administration in 2002 in the forms of ‘Subutex’ and ‘Suboxone’ for treatment of opioid addiction. Buprenorphine is a partial mu opioid agonist and kappa antagonist utilized as an effective treatment of opioid dependence (8,9,10,11,12,13). There are many additional benefits such as effectiveness in treating neuropathic pain, having a ceiling effect on respiratory depression, mild withdrawal symptoms, less physical dependence, and less cognitive impairment compared to other forms of treatment(14). Buprenorphine has been increasingly replacing methadone maintenance because of its lower risk of abuse, side effects, and its ceiling effects for respiratory depression.
While numerous studies have compared the impairment of buprenorphine to methadone, with most research finding buprenorphine less impairing than methadone (15-25) there is an ongoing perception among those who treat addiction that buprenorphine is an impairing opioid. Soyka et al. (2005) compared both treatments in a randomized study of drug dependent patients and found that buprenorphine was less impairing on cognitive functions than methadone in a driving-related battery(26).
Unfortunately, a cursory perusal of the literature tends to confirm the perception of buprenorphine as impairing, because most confirming studies used strictly healthy volunteers. MacDonald et al. (1989) examined the psychomotor effects of buprenorphine in 12 healthy male volunteers and found it caused significant psychomotor impairment on seven out of eight psychomotor tests(27). Effects peaked at four hours post-dose and were still apparent eight hours later. Similarly, Zacny et al. (1997) cited buprenorphine as increasing impairment on subjective and psychomotor performance measures compared to equianalgesic morphine. The impairment was found in a study examining 16 subjects without history of opiate dependence(28). This evidence supports what is known about the opiate buprenorphine. As opioid dependent persons generally find opioids stimulating rather than sedating, these two studies are not applicable to a clinical population.
To further the understanding of buprenorphine impairment Mintzer et al. (2004) evaluated dose-related effects of repeated administration of buprenorphine/naloxone sublingual tablets in opioid dependent patients. Results revealed minimal impairment in performance as dosage increased. The only significant effect was impairment in episodic/long-term memory at the highest level of buprenorphine (32/8mg) (29).
Additionally, research indicates that long term buprenorphine maintenance does not cause impairment to those undergoing treatment. Shmygalev et al. (2011) studied the impact of long-term maintenance treatment by comparing 30 patients utilizing sublingual buprenorphine treatment with 90 matched controls. Three control subjects were used on each buprenorphine patient with subjects matched for age and sex. They were tested for driving ability using the Vienna Test System and showed no significant cognitive deterioration. Patients receiving a stable dose of sublingual buprenorphine showed no significant impairment of complex psychomotor or cognitive performance compared to healthy controls (30).
Stable doses are only present in laboratory studies, whereas in a clinical atmosphere a patients prescription will change or they may forget to medicate. Singhal et al. (2008) cited that buprenorphine maintenance patients often abuse the drug by taking additional doses over and above the maintenance dose. To examine the impact this might have on psychomotor performance, they studied 19 subjects maintained on buprenorphine and administered the maintenance dose followed by three additional doses at two-hour intervals. Subjects completed a psychomotor performance battery following each administration. Performance on Digit Symbol Substitution Test and Trail Making Test-A and B improved significantly with each assessment, while other tests remained unaffected (31). Buprenorphine dose increase has no effect on impairment. Other possibilities could explain the presumption of buprenorphine “abuse.” For example, patients could be under-dosed because of the sedating stereotype of the opiate and therefore perform better once closer to their effect dosage.

Another popular treatment method for opioid dependence is naltrexone maintenance; approved by the Food and Drug Administration in 1984. Naltrexone, unlike methadone and buprenorphine, is an opioid antagonist or blocker and cannot induce any euphoric drug-like effects. Messinis et al (2009) compared the neurophyshological functioning of 18 buprenorphine maintenance patients, 32 naltrexone maintenance patients, and 34 healthy controls. The results indicate that there were no significant difference in any of the cognitive measures between the buprenorphine and naltrexone groups or between the naltrexone group and controls. Yet, the study cites buprenorphine to have performed more poorly than controls on conceptual flexibility, executive functions, encoding and delayed recall of verbal and visual information(32). This study’s conclusions are questionable because the authors find no difference in impairment between buprenorphine maintenance and naltrexone, while they also claim that naltrexone is less impairing. Moreover, Minozzi et al. (2011) reviewed 13 studies of naltrexone versus placebo or other treatments. The analysis inferred the studies conducted have not been all-encompassing enough to adequately evaluate naltrexone for treatment of opioid dependence (33). In spite of the lack of evidence there are still advocates for naltrexone maintenance therapy as a less impairing alternative to buprenorphine.

Missing from the literature is a clinically relevant comparison of buprenorphine maintenance patients versus those treated with naltrexone or with those not treated at all. Extended evaluation of this comparison may indicate which treatment leads to lesser degree of impairing effects. Choosing a treatment plan that is both effective and does not sacrifice cognitive abilities could lead to more people completing treatment and more people seeking treatment because of a higher success rate. Many clinical and laboratory observations have hypothesized that the primary neural substrates of persistent compulsive drug use are long-term associative memory processes involving multiple neural circuits that receive input from midbrain dopamine (34). In a naturalistic clinical setting, we examined the outcomes from two common cognitive testing measures associated with dopamine tone yet to be used to measure function of buprenorphine maintenance, the continuous performance task (CPT) and the Iowa Gambling task (IGT). If the common presumption of buprenorphine as impairing is correct, this should be evident in before and after measures of these tests.


Data was collected from a retrospective chart review of patients enrolled in a medically managed intensive outpatient program that uses frequent neurocognitive testing. As an anonymous retrospective chart review, the research was granted exempted status by Crescent city IRB. The participants were 38 sequential opioid dependent admissions from August to December 2012 who both received buprenorphine and had both before and after testing. There were 21 males and 17 females. To evaluate the effects of buprenorphine and not other medications or other aspects of the program, only the tests directly before and after being prescribed buprenorphine were examined.

Cog Testing: Iowa Gambling Task & Continuous Performance Task
Measures of cognitive ability: the Iowa Gambling task (IGT) and the continuous performance task (CPT) were used to determine cognitive impairment. The testing occurred on a desktop computer in an undisturbed room at the treatment center using the freeware PEBL.
The IGT is a card task that measures reward overvaluation (35). The goal of the task is to win as much money as possible in 100 trials picking from four possible decks. Each participant starts with a $2000 loan. After each card selection, a reward and a penalty are given to the participant. The reward depends on the deck you choose, while the penalty is different for different cards in the deck. Graphics at the bottom of the screen display the earnings or losses acquired. The IGT is a measure of reward overvaluation, a hardwired symptom of low dopamine tone (36). Those with reward overvaluation also initially sample all of the decks, but then go on to lose money. Reward overvaluation caused by low midbrain dopamine tone occurs when rewards are overvalued and risks unrecognized.
The CPT is a go/no-go task measure of attention and impulsivity. Using the letter “X” as the non-target stimuli and all other letters as target stimuli; responses were recorded using the spacebar. Over a 14 minute period the letters cycle through three distinct intervals between letters: one, two, and four seconds. The goal of the test is for the participant to respond as quickly and accurately to target stimuli, while not responding to non-target stimuli. The major variables the CPT produces are target accuracy, foil accuracy, and reaction time means for correct & error responses. Target accuracy accounts for the rate at which the participant correctly responds to the target stimuli. Foil accuracy accounts for the rate at which the participant correctly did not respond to non-target stimuli. Mean reaction time measures the average amount of time between presentation of the stimuli and the participants’ response at that interval. These measures are calculated for each block (1, 2, & 4 seconds) of stimuli.

The IGT and CPT were given together by an administrator. The administrator led each participant into an undisturbed room and seated them at a desk with a computer monitor. The administrator then opened the testing program PEBL, explained the gambling and impulsivity testing about to take place, and exited the room as the participant began. The testing lasted about 25 minutes on average. After each testing session the administrator recorded the results. Participants were tested at the very beginning of the treatment program, after symptom scores stabilize and/or change in medication, and upon discharge from the program.

A one-way within subjects ANOVA was conducted using the software JMP to compare the effects of buprenorphine on IGT and CPT scores. A significant difference in IGT scores between the pre and posttest conditions was found with buprenorphine medicated patients having higher average scores than in the pre medication condition, F (74) = 10.74, p=.0016.

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Target accuracy on the CPT did not differ significantly in any of the time blocks between pre- and post-tests.

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A significant difference in foil accuracy was found between the pre and posttests in both the two second block, F (74) = 10.81, p=.0015, and the four second block, F (74) = 5.41, p=.0228 with medicated patients showing improvement over their pre-medicated condition. No statistically significant difference was found for the one second block.

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Using tests close together allows examination of the impact of the drug while minimizing the benefits of the additional addiction therapy. The practice effect was not a factor because the pre drug test was not the first time all of the participants were tested.
The IGT is a measure of reward overvaluation, a hardwired symptom of low dopamine tone. Reward overvaluation occurs when rewards are overvalued and risks unrecognized. The magnitude of motivation positively correlates with the incentive salience of reward-related cues and the reward itself (37), thus allowing the behavioral mechanisms to be carried out to fruition without regard for any impediments or distractions. If reward overvaluation can be decreased even an impulsive patient will at least not be impulsive with the same dangerous behaviors as before. The data support that buprenorphine maintenance treatment does not worsen reward overvaluation. This has tremendous implications for buprenorphine maintenance therapy demonstrating that buprenorphine in a clinical population does not impair this executive function.
Similarly, low foil accuracy on the CPT is related to decision-making impairments: impulsivity and inattention (38). A normal brain, when given more time, will take more time to notice the “X” and increase accuracy. A brain with low midbrain dopamine will, instead, speed up in an attempt to speed up the computer. The data are supportive of the thesis that impulsivity and attention are not worsened with buprenorphine treatment.
Generally, target accuracy is used as a proxy for attention, but it has been noted by us that only severely impaired patient or patients who do not understand the directions score less than 90% accuracy; rendering this statistic of questionable use to the study question. Target accuracy was examined only to confirm the integrity of the testing.
In summary, reward overvaluation and impulsivity did not worsen after the introduction of prescription buprenorphine in a clinically relevant population. Evidence from the current research does not support the currently prevalent idea that introduction of buprenorphine opioid maintenance treatment will impair patients. The research may also lend support to the subjective report of opioid dependent maintenance patients that they actually function better when prescribed buprenorphine.
Limitations of the current study include the small sample size and the geographical constraints of using an outpatient facility. Both of which are factors that deserve attention in future replication of this research.
Anecdotally other addiction patients, outside of this study, at the same facility indicated feelings of frustration intolerance during the CPT and during the long (4sec.) block. They began to answer rapidly to try and “speed up the test” to no avail. Future research would benefit by looking at the implications the CPT may have on frustration intolerance in clinical populations. Also future studies could further investigate the relationship between genetics, testing, and dopamine and serotonin levels on reward overvaluation to better pinpoint at risk genotypes.

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Addiction and Economic Decision Making

July 14th, 2014

I just had the opportunity to listen to a podcast with Dr Colin Camerer that I thought was very interesting. If you click the link there are two interviews. The first is with James Rickards and worth the listen (it’s the reason I listened to the podcast in the first place), but it’s the last one, with Dr Camerer, that I want to write about today. It has implications for people with addiction who want to invest in financial markets to fulfill their responsibilities to others to maintain the wealth they create.

What he said was so interesting to me that I started to look up his other work. I didn’t realize anyone had done these studies or confirmed conjectures I’d been using to treat addiction. To find someone outside of the addiction field doing it is amazing.

So the upshot is that using fMRI to study people who are trading an imaginary stock for real money in a situation where the actual value of the stock is known, bubbles still happen. The group still runs the price up above where they all know it belongs and they do it knowingly. They know that, for instance, the fair market price is 14 and when the project ends the price will be 14 and yet they still run the price up to 15,16,17 and higher.

He noted there were three groups of people. The first group, see the bubble and don’t participate. They weren’t very interesting to him, but I bet they were pretty good value investors. The second group he noted were those that rode the price up and sold too slow to get out in time, and the third group were those that bought on the way up and dumped quickly. The last group were the most successful. Something to note though is that everyone went through this only one time, so you really can’t tell if people were “smart” or lucky. It may very well be that people switch groups after they learned from mistakes, but he’ll have to look at that in future studies.

With that background, let me tell you what he found on fMRI. The first group, the ones that stayed out. Their Insula lit up while watching the price feed. The group that lost money, their Nucleus Accumbens lit up while trading. So why is that important?

The Inusla is a sort of internal perception engine. It tells you if you have a fever, if you’re eating something disgusting, if someone is making a bad face at you, if your dopamine level is too low, or any other “bad” internal signal. The Inusla is the part of your brain that says, “Look, something is wrong here. I don’t know what it is, but figure it out, because it could be a saber tooth tiger.” There’s another part called the Cingulate that is designed to tell you how urgently you need to fix this and get you motivated, sort of like “Wow, that is a tiger. Run!!!!” or “No, you just have a fever. Lay down.” So that group that stayed out of the bubble, took a look at the prices rising and knew there was something wrong. They didn’t feel the need to ride it up. They could take a look at the prices, see they were irrational, and sit there doing nothing. Wow, how many people can do that? But that’s what a normal brain does.

Now the people who lost the most had the Nucleus Accumbens light up when they traded. That tells me they were getting reward. There’s a funny thing about people with normal reward levels, that is, normal levels of dopamine at the Nucleus Accumbens. They don’t get reward from stuff like trading and their Insula works fine. But if you are low in dopamine, your insula isn’t fine and stuff like being right on a stock gives you a big lift. That doesn’t sound like a problem, but the other part of that dopamine hit in an otherwise low dopamine Nucleus Accumbens is that it sets up an association to the reward. If you get reward from trading stocks, you’ll want to trade stocks. If you get reward from watching porn, you’ll want to watch porn. If you get reward from shooting heroin, you’ll want to shoot heroin. Or maybe you’ll want to shoot heroin while watching porn while trading on your Schwab account. Good luck with that.
If you trade for reward, you aren’t trading for profit, and you’ll lose money. Investing should be boring, not exciting. If you have addiction and someone gives you a reward, you’ll form an attachment and do that thing more than is good for you. See the connection?

So what about the other people, the ones Camerer calls the smart money. They bought even though they knew it was a bubble, but they got out in time. How do I explain those people? Well, until Camerer does this again, I’m going with “they were just lucky.” I know investors who can look at a rising market and say, “Wow, that’s a bubble. There are some really stupid people that are going to run this thing up past it’s fair value. I can get on board and be ready to get off early before they all figure out they’re stupid,” but I don’t know many of them. Most people I know who participate in bubbles have an almost religious devotion to the belief in whatever is bubbly and instead of seeing an impending top they just see a new buying opportunity. The normal people among them learn after a few times and just avoid bubbles. I believe it is those people with addiction, low dopamine at the Nucleus Accumbens, that are getting a perceptible dopamine spike and reward from trading who can’t get out in time. They get attached because of the dopamine spike and can’t relate rationally to the rewarding event. They don’t get the signal from their Insula that something is wrong for two big reasons: the Insula is already saying something is wrong because of the low dopamine state, and the event precipitates brief normalization of dopamine and a relief of anything that’s wrong. So where a person without addiction is seeing more risk, a person with addiction sees, not risk, but something wonderful that there should be more of.

So if you have addiction, should you not invest? No, that’s not what I’m saying. I will say you shouldn’t day trade or even trade much at all, but investment is great. In fact, value investing is a wonderful long term way for addicted people to gain wealth, and like all functions in recovery, it’s best done in groups. You can’t go very far wrong with a group conscious. I may like IBM and think it’s undervalued but if 4 other sane sober minds who have read they same thing I have think it isn’t, it probably isn’t, especially when I’m sure it is. In fact the more sure I am that everyone else is wrong, the greater the probability that I’m not thinking right.

Another important recovery tool in successful sober investing is inventory. “We bought IBM at 115 because we thought it was undervalued and we said we’d be wrong if it fell to 100. It did; we were wrong.” If you can’t say you’re wrong when you’re wrong, don’t invest.

So until we all have fMRI headsets at home, we’ll have to use recovery principles in this field of endeavor, just like any other field of endeavor, in order to stay on track.