Chris: So, you have been researching the effects of alcohol addiction for many years now. How did you get started with this?

David: As people can probably tell from the accent, I am an American originally. I’ve been in Finland since 1972, but I started in alcohol research long before that as an undergraduate at the University of Cincinnati. I was working with the professor R J Center, and he had a grant to study alcohol. I was one of the students that he hired, and I was very lucky. I made a discovery that turned out to be very important in the field. At the time, people believed that alcohol drinking – we already knew it wasn’t for the pleasure, but most people thought it was in order to avoid the withdrawal that alcohol dependence was caused by physiological dependence. Hold on to that thought for a second. I wanted to do a study with rats that had been drinking alcohol there. So, Dr. Center said there were some left over control rats from a previous study, and they had a choice between water and alcohol solution. Very happy rats, but they really didn’t like the alcohol very much. They drank seventy percent from the water bottle, and only thirty percent from the alcohol bottle. So, it looked like water in both, and it was fifty-fifty. It looked like they were avoiding the alcohol. So, I went down in the middle of the afternoon to the rats that hadn’t had any alcohol for two weeks. Rats are nighttime creatures. So, they do all their drinking when I’m not there. I’d never actually seen a rat drink alcohol. I’m not sure if anyone had. I put the first alcohol bottle on the cage, and the rat sort of shook his head and came up the front, and started drinking. I got to see my first rat drinking alcohol. I put the second bottle on, and the rat was there and grabbed the bottle and pulled it inside the cage. Every single rat in the whole rack of cages started drinking immediately. It was obviously very powerful motivation for alcohol. They didn’t stop to drink the water at all. These were the same rats that two weeks earlier hadn’t like the alcohol. One of the questions the whole field was, why bother studying rats because they don’t like alcohol? Only people are crazy enough to drink. Here I was seeing the rats drinking. What was causing it? We went back and did all kinds of control studies, and found there was one extremely powerful factor. We called it the alcohol deprivation effect. It’s like with hunger that if you wan to see hunger, you have to take the food away for a while. If you want to see hunger for alcohol, you have to take the alcohol away. This has been replicated over and over again, it’s found to be true for other things. For instance, they just found that the same thing works for cocaine, morphine, but it’s particular powerful for addictive drugs. Now, there are two reasons why this is important. One is Chris, what is the major treatment that people do for alcoholism in America today?

Chris: Well, of course, for any addiction, they tell you not to do it.

David: Yes, they put through detox, and then they’ll put you in rehab where you’re not able to get any of the stuff. So, they dry you out. They deprive you of alcohol for three weeks or so, and if indeed the hunger for alcohol was caused by the physiological dependence, you are done with that pretty much. You go through withdrawal during the first day or two. In fact, the people come out of the dependence still craving alcohol. It does not get rid of the craving. If anything, it makes it worse. It’s like trying to cure the desire for food by starving a person for a couple of days. It doesn’t work.

Chris: What are the traditional success rates for the abstinence type programs?

David: Roy puts numbers around five to ten percent. You will also get the same type of numbers just by talking to people. The detox itself does not get rid of the craving. The other thing that this did, discovering the alcohol deprivation effect was to get me an animal model. I had rats that would show motivation for it, and they would drink whenever I wanted them to. All I needed to do was to take the alcohol away. We could give them a happy hour. Once a day, they would have alcohol presented for them, and they would be waiting for them. I’d put them up on the tray, and they could run away. They’re not going to. They’re happy rats. They jump back in the cage, and sit there waiting for the alcohol to come. Then, I could do things of testing medicines if they affected the alcohol drinking. So, it was a beautiful animal model, plus it told me that we needed to look for another theory of what causes addiction to alcohol. It is not physiological dependence. It’s not the pleasure. It’s something else.

Chris: How many years ago was this when you first noticed this?

David: I think it was 1965. It became my Master’s Thesis in ’67. I know that, and then I came out to Oregon, and continued doing alcohol research. I think probably the most important thing we found in Oregon was a link between alcohol drinking and morphine. The idea wasn’t mine. In fact, I was completely against the idea. There had been a paper that was published, and it was suggesting that there’s something from alcohol that is a bit like morphine or opiates. Other people came in and immediately said, “Ah, that’s not true because the withdrawal symptoms are completely different, and if you’re going through morphine withdrawal, giving alcohol doesn’t cure it. You don’t have cross dependence.” But, it had just found that the dependence part was not the reason for drinking. I knew there was something that was causing the motivation. So, I was going to do a proper test to show that there was no similarity between the alcohol drinking that we do, and the opium taking that they do. Of course, they’re different. Everybody knows they are. So, I did one experiment in which I gave morphine to rats during the period that they were deprived of alcohol. Guess what? It blocked the alcohol deprivation effect. The morphine satisfied them. I did study after study, and in every one of them, it turned out that morphine was a substitution drug for alcohol. Finally, I gave them, and said the idea was right. There is this link between the two, and published it in Nature a little bit later. So, I was doing all the work in alcohol, and that became my doctoral thesis in Oregon in 1972. After that, I came over to Finland. I should tell about the laboratory here in Finland. I had mentioned that I was one of the few people who had seen motivation for alcohol in rats. Most people didn’t think that rats alcohol. One exception was here in Finland, where a Dr. Huvero Ericksen had bread a special line of rats, the AA line that loved alcohol. It was a very strong genetic component. In fact, we didn’t know when I started in alcohol research, and now it is quite accepted that there is a strong genetic component to the risk of alcoholism, and how much people like alcohol. This started out with rats while in Chile, and then here in Finland. Then, it went on to twin studies showing it in humans. So, Oley (S?) had the heavy drinking rats. We had been exchanging reprints, and I really liked what they were doing in Finland. They were putting this story together, not just one little study, but trying to make sense of things. I might mention one reason for this. Alcohol research isn’t taught as a field of study in the universities. You can not major in alcohol research. Most researchers at that time in America who wanted to do something on alcohol were coming from some other field, and nothing about alcohol. They do a grant. Spend two years learning about alcohol, one year doing the research, and not get the grant the next year. You need to be dedicated working on it year after year after year. So, in Finland there was this laboratory, Alcos Laboratory, that was a full time thing. All it did was alcohol research, and it became a career. Then, you could have the background and the time in the area to try to put things together. So, on April 28, 1972, at six a.m. in the morning, I handed in my dissertation, caught an airplane from Portland, Oregon, and arrived in Finland for the national drinking holiday of Valco (SP?). It was a good introduction to drinking. This is Chris Costello interviewing for Michael Senoff’s

Chris: How do the rates of alcoholism compare to the US?

David: Actually, the numbers at that time in America was drinking much more in the total amounts of alcohol that was consumed. Now, Finland is higher, but it was more obvious here because of the style of drinking. Remember the alcohol deprivation effect I was talking about? Well, in Finland, people don’t drink on Sunday or Monday or Tuesday or Wednesday or Thursday, and at that time on Friday. But, when Saturday night came around, they drank the entire week’s worth for a lot of public intoxication. It’s different from what you see in France, for instance, the Mediterranean style. I don’t know whether you can say one is better than the other. There are disadvantages to both, and special problems with both. I think that Roy’s title for his book is The Cure for Alcoholism. People do question the word “cure,” but I think that can be backed up. I might make it a little bit softer. I think I would say, “The cure for one type of alcoholism, or for the main type of alcoholism,” because what we found when we first started the clinic here in Finland, and we found that the treatment we were using was effective in 78 percent of the patients. They were doing quite well, most of them beautifully, and that was fantastic to see them, but there were ten percent who didn’t comply. They didn’t take the medicine, so we don’t know. There were twelve percent who were taking the medicine and following the instructions, and it wasn’t working for them. So, there is another type of alcoholism that we still don’t know how to treat. The main thing we know is the one we can treat is opiatedergic (SP?). It is being affected by the same system in the brain as morphine. So, that’s how we can treat it. The other one, people are calling it the dark side of alcoholism. Probably it is similar to barbiturates and benzoasphaphenes (S?), but we’re still speculating.

Chris: A different area of the brain is being affected?

David: Different chemicals in the brain. Alcohol is a very messy medicine. It affects all kinds of things, and one of the things it does is to release endorphins. These are the chemicals that your brain releases that are like opiates like morphine, and that is one way to becoming addicted to alcohol through these endorphins, from their reinforcement from the endorphins. I’ll go back to that in a little bit. There are other people who are affected by other things that alcohol does. When you’re falling down and lack of motor coordination, that is caused not by the endorphins, but by the effect of alcohol on – it’s called gava, these little tiny neurons all over the brain, and the most common neuron you have. Alcohol disturbs them, and you lose your balance. This is the same way that barbiturates and benzoasphaphenes work. So, this is probably the other way of becoming addicted, but that we don’t know. But, let me go back to the thing that we do know. I mentioned a long time ago in Oregon, we had found there this was link between the opiate system and alcohol. The other key is that alcohol drinking is learned. No one is born an alcoholic. You may be born with genetics like our AA rats making it a higher risk, but if you never drink alcohol, you’re never going to become an alcoholic. That’s sure. Somehow, in the process of drinking, your brain changes, so you end up being wired. So, it’s almost a reflex to think about alcohol all the time and end up drinking it. It’s important to know what your own family history is, and to consider it in what you’re telling your kids, and for the kids to consider it and what their behavior is. This is an entire other field of alcohol education, and there is also the possibility of prevent alcohol with the same medicine. Let’s consider a little bit more what exactly is happening. When a person drinks alcohol, the alcohol is absorbed and it comes up into the brain and one of the things it does is to release these endorphins. The endorphins are sort of floating around the brain like a hormone almost, and the pathways in the brain if they’ve just been used, the neurons that made you think about alcohol, made you lift the glass, made you go to the pub, all these ones that just were used become a little bit stronger and easier to use tomorrow. So, tomorrow, you’re walking by the pub, and you’re more likely to think about alcohol, more likely to go in, more likely to order another drink, and endorphins again are flowing down and making the pathway still stronger. It’s a learning process. It’s very slow. Alcohol is not a good reinforcer, but over ten years or something like that, in some people, these pathways become so strong they can’t be controlled. It’s almost like a knee jerk reflex. If someone taps you on the knee and your foot lifts up, you don’t have much choice about it. Maybe you can hold it for a little bit, but pretty soon, your foot is going to go up. It becomes the same way for an alcoholic. Again, there’s this genetic factor. Some people can do the drinking, and then forget about it soon afterwards, but some people get a lot more endorphins released when they drink, are much more susceptible, and eventually when they get too much reinforcement too many times, these pathways are so strong, they can’t control them. After the thing has been learned very, very well, there is no choice anymore. This is a very important thing for people to accept that there are some behaviors that they can not control. There’s the statement that you hear over and over again, “Just say no.” To a teenager, that is something that is possible. To an alcoholic, it’s a meaningless statement. Consider holding your breath. Now, you have a little bit of control over it to begin with. If I told you Chris to hold your breath, you could do it for twenty seconds here. At thirty seconds, I’ll say, “I’ll give you ten dollars Chris if you hold it another ten seconds,” and you might make it up so far, and there comes a point when it doesn’t matter how much I offer you, whether the gun is pointed at your head, you can’t do it anymore. You can not control it. That is the key issue with alcohol drinking and alcoholism. An alcoholic is someone who can not control the alcohol drinking in some situations. The behavior has become so reflexive that they don’t have control.

Chris: What do people do about this?

David: Well, what we had concluded was that alcoholism is simply a behavior that had been learned so well, that you couldn’t control it anymore in some circumstances. Now, if you ask any psychologist, you have a learned behavior, and you want to weaken it, what can you do? Pavlov, many, many years ago, would have said to extinguish it. Most people have heard of Pavlov’s dogs that learned to salivate when he rang the bell and then gave some food, and pretty soon the bell alone would make them salivate. Then, he discovered that was the process of learning, but there’s something the opposite of learning that takes away the learned behavior. If he rang the bell and the dogs salivated, but he didn’t give the food reinforcement, then the behavior got weaker. Eventually, the dogs were no longer salivating much at all to the bell. There’s been tens of thousands of experiments on extinction. It seems to be a basic mechanism in the brain. It’s sort of the brain’s way of erasing mistakes. You’ve learned something that gives you something you need – food or water or whatever, and if it no longer does it, your brain needs to have a way to erase that behavior so you don’t continue doing the wrong thing. So, theoretically, if a person were to drink alcohol, but not receive the endorphin reinforcement from it, then the brain should weaken. These reflexes should break down the pathways gradually, and so eventually you have control over it. It was a good idea. You need to have some how to block the effect of the endorphins. Back at the time when we were thinking this, they just discovered chemicals like Naltrexone that block the effect of opiates. If you have a heroine addict, and you give them Naltrexone, if they take heroine, they don’t feel anything, no effect at all. The Naltrexone fits into the receptor where heroine or morphine goes, and blocks it like having the wrong key in the lock. Imagine that morphine or endorphin is a key, and it normally fits into a lock and causes effects, but Naltrexone is the wrong key. It is fitting in that lock, and as long as it’s in there, the morphine or the endorphins just bounce off and don’t do anything. We tried this in rats. We gave them Naltrexone, and then some alcohol to drink, and indeed what we found was that to begin with the first day there’s no effect at all. They come up running happy to drink after the Naltrexone. They start drinking, and it looks normal, but the next day they’re not so fast at running up to get it, and by the third day, they’re very slow about it. By the fifth day, most of the rats didn’t care at all about it. They weren’t thinking about alcohol anymore. It looked exactly like extinction. In science, you don’t prove anything. You just eliminate everything else. So, the next two year were experiments to eliminate every other conclusion, and we ended up deciding that you could remove the overly strong desire for alcohol by extinction with Naltrexone. All of the pieces for understanding we should be able to use Naltrexone really were present within two years after the time I got to Finland. If anybody bothered sitting down and thinking about it for a minute, we would have seen it then. In fact, we got side-tracked and ten years went here, and five years went there. In the meantime, I wrote a book called The Rest Principle, A Neurophysiological Theory of Behavior. In this, it is explaining how learning occurs in neurons, and how extinction occurs in neurons, and when I’d written the book and could see how learning is happening, not by some little person choosing to do something from a monkey list, but rather by neurons changing their synapses, the strength of the wiring of the brain changing. Then, it was obvious that all you need to do is use Naltrexone or similar type of medicines, Nalmafed or Nalaxon (SP?), and you should be able to extinguish it. However, who cares whether rats drink or not? The important thing is does it work on humans. There were other people who tried it on monkeys later, and it did work on them, but the critical thing was would it work with human beings. We needed to have clinical trials done. I went over to the hospital just in back of me here now, and asked them if they would do it, and they thought it was a good idea. Let me just jump ahead here. We had the ideas for doing it, but we didn’t get the money in order to do that. I won’t cry over the lack of money. We did get the support eventually, and we did our clinical trial, but the first clinical trials were done in America, and the first one was by Chuck O’Brien’s group at the University of Pennsylvania. Almost at the same time, Stephanie O’Malley’s group at Yale did the studies. I heard a preliminary announcement at a conference in ’89. It was this short publication in ‘90s, but the main papers came out in ’92. Things move slowly, three times as slow as they should if you really want to help people, but they have very good results. Moreover, it happened that they noticed some things that in the Chuck O’Brien study that the main effects were in those patients who actually drank alcohol while they were on the Naltrexone, and that’s exactly what you need for extinction. That has been the main problem ever since, and still is what Roy’s book is trying to illustrate the main thing that I had been doing. Our own clinical trial here in Finland had compared two different methods of using Naltrexone. One idea for how Naltrexone should work, I should preface this as the wrong idea, is that it’s sort of like a diet pill that you take the medicine, and it immediately takes away your desire for alcohol, and you can use it in order to remain sober and abstinent. So, if it works like this, the doctor says you go through the detox and rehabilitation, and the doctor says, “Don’t drink anything,” and here’s your Naltrexone pill. Take it all the time, but particularly if you’re having any craving to block the craving. If it worked that way, then they should find that people getting the Naltrexone pill are slower to relapse to taking the first drink than people on the placebo, but they’re not. In fact, there’s been 39 trials. We just had another one reported here in Helsinki two weeks ago, and none of them have found that the Naltrexone slows up your starting to drink alcohol again. It doesn’t work like a diet pill. You have to use the Naltrexone at the same time as drinking because that changes the brain. First, let me describe the way that we’ve been doing it here in Finland, which is being called the Sinclair Method. You start with patients who are drinking. They haven’t gone through detoxification, haven’t gone through rehab. They were drinking yesterday, and you tell them, “If you’re going to drink tomorrow, take a Naltrexone an hour before you start drinking.” You don’t force them to drink. You tell them, “Don’t drink and drive, and don’t drink more, but just drink what you want to.” What we find is in the very beginning during the first couple of days, there’s hardly any change at all. They’re drinking about the same amount. We’re asking them what their craving is, and it’s about the same, but then gradually week after week, month after month both the craving and the drinking go down. It’d go down further and further until the people start to be able to control it, and then start to be able to have days off. With the 78 percent that are successful, we get on the average a 75 percent reduction in alcohol drinking. So, they’re going down on the average to less than two drinks a day, about nine drinks a day. Many of them have quit completely. We asked them what their goals are in the beginning, and most of them did not want abstinence. About two percent said they wanted to become abstinent. Most wanted to be like everybody else when drinks are being served that they can take one drink along with it, and that’s the way they end up. Now, let me just caution. This works, social drinking for alcoholics, if they’re on Naltrexon. Our clinical trial that we did here in Finland, when we had placebo and controlled drinking, it was an utter failure. If you’re not on the Naltrexon, don’t try social drinking. It just does not work, but with Naltrexon, it is possible. In fact, it is the way to go.

Chris: Is this basically just a normal treatment in Finland?

David: It is becoming the standard treatment. It wasn’t an obvious one here either. We found that the first clinic that started doing it, was doing the abstinence way. It’s sort of the intuitive thing to give it during abstinence. People have been using and abused that way, and also what the doctors want to do is say, “Don’t drink.” So, it’s difficult for them to change their way of giving. So, we started our own clinic here, Contral Clinics that we’re doing it the right way so that extinction could occur, and then it’s spread around Finland and through many other countries. It still is not as popular as I would like. It was not given to everybody, but in America, it’s something like two percent. In Hazleton, only four percent of the alcoholics have ever been giving Naltrexon. It’s really a shame because it does work, but it’s not being used. The message hasn’t gotten to doctors. Scientifically, there have been 79 clinical trials now showing that Naltrexon can work, if you allow the distinction to occur. It is one of the most solidly confirmed conclusions you can have. In the conference we just finished having two weeks ago, the major conclusion was Naltrexon is a success story scientifically. It definitely works, but the rest of the world couldn’t care less. The largest clinical trial ever conducted and alcohol research project combined was completed a few years ago, and one of the findings that they made was that Naltrexon worked without intensive counseling. When it was originally approved by the FDA in 1995, it was approved for use with incomprehensive programs like Betty Ford or Hazleton. So, regular doctors didn’t feel up to using it. That wasn’t the way it was supposed to be use. But, they found now that it worked with just medical maintenance, and therefore, it can be used just a general care giver, a general practitioner could give Naltrexon, and it should be working.

Chris: So, you didn’t include counseling in your research with your rats?

David: Yeah, right, that was exactly what I said at the meeting in Chicago when they announced this. They were pointing out that you didn’t need all the counseling, and I said, “I’m not surprised about that. The rats never listened to anything I said to them. I didn’t speak Finnish properly.” But, Wellingrain is saying that he expects to have a Prozac moment in the near future for Naltrexon. When general practitioners start prescribing Naltrexon for functional alcoholics, the ones who can walk into his office, maybe then the usage will start going up. But, there’s also the question you should know what you’re doing with it. I think this is one reason to read Roy’s book because we have a lot of experience that Roy has used for putting up this book, and also the alcoholics are helped with this. There’s a whole chapter in there for doctors to read on how to use the Naltrexon with the patients that are coming in to them. I think that there is a possibility, a very strong possibility that we’ll see a major change in the usage in the near future. Also, the people who are the experts are beginning to see the light, to understand. One of the main German researchers was here, and he came up to me and said, “It’s all becoming clear now because you have to use it with the extinction. You have to use it in the right ways. The things that had been puzzling are now beginning to make sense.” There are people who said that put together, the results from the study, they use it the wrong way and the right way, and when you average them out, you don’t get much of anything. So, you have to split the studies up into the ones that use it with extinction and those who didn’t, if you want to evaluate them properly. Okay, let me go back just a second to the point that only four percent are using it. This suggests that the real problem has been in the promotion, and maybe there’s been complaints that I’ve been pushing too hard. I see something that I help put together, and it should be used, and I want to go around and tell people the right way to do it. So, after one study did it the wrong way, I flew over to NIAA and gave a lecture there. I flew to Yale, and gave a lecture there. I knew the right way to use it. I knew the results we were getting in Finland, and if you use it the right way, it’s not perfect, but it’s better than anything else we have right now. The treatment that we’re doing doesn’t require any detoxification or any rehab. Here in Finland and in America, we have invested fortunes in building these rehab hospitals and detoxification centers and training all the people, a lot of investment in this. Many countries don’t have this. For instance, most of the developing world does not have an infrastructure for treating alcoholism, but they still have a problem. This treatment with Naltrexon provides a way that they can start treating without putting in all that investment. Roy went to Northern Indian along with a non-profit organization and taught them how to use Naltrexon the way we’ve been using it in Finland, and they didn’t have to build a hospital first or build a resort for people to stay in. They could just start taking a pill before drinking. With some counseling as far as to improve your life and what to do with your time now, the results that they got were almost exactly the same that we got in Finland. They had a 75 percent success rate. I think this is important. It’s a little bit like the story here in Finland about cell phones. Finland is the home of Nokia for people who don’t know and think it’s Japanese, and Fins are very proud of Nokia. They say that cell phones were very nice in the developing world, but sort of in competition to begin with with the land lines. Where they really are great is in places like Africa where they haven’t put down the investment already and the copper wires between cities has allowed leapfrogging technology. So, the people were able to jump up to the level of technology of the rest of the world, with the use of cell phones. Naltrexon provides the same thing. They can find places like Indian and many other parts of the world. You can start treating alcoholism without having all this investment. I think it’s also important with indigenous people. My niece was working in Australia, and there is a horrible problem among the indigenous people with alcoholism, and very little they can do. They’ve instituted prohibition again. Well, they can give them Naltrexon. One of our workers here is at the World Health Organization’s headquarters in Geneva giving out copies of Roy’s books particularly to their Australian representative. I hope that we can get some type of an international program going, in which we would try to train the people in other countries – developing countries how to use Naltrexon. It is just economically, it is so much cheaper. Only scratching the surface, Roy has done it in one little spot in Northern India, and there’s an entire world out there that needs help. This is the type of thing for the World Health Organization to come in on, and maybe some philanthropic organizations that particular want to help indigenous people or developing countries. This would be an excellent project for them to work on. Just mentioning the economics in America, I understand you’re having a little bit of debate in America about the cost of healthcare. When you look at alcoholism treatment, the main thing that insurance companies pay for is detoxification, and that, we already showed in 1965, doesn’t work. If you wanted to have a much cheaper and more effective system, you can eliminate all these steps that are expensive. They’re also dangerous. Detoxification is dangerous. It has a risk of addiction to other medicines. Rethink the health system, particularly in the case of alcohol, and put it together again in a rational less expensive way that helps more people. My mother and father lived in Florida, and my father was sick, turned out terminally ill. He had gone to the hospital. When I found out it was serious, I flew over to see him. I might mention that my father was a salesman. When I got there, his surgeon came up to me and said, “I have bad news. Your father is going to need another operation, but about this alcoholism treatment your father has been telling us all about.” My father had managed to sell the Naltrexone treatment to all the nurses and all the doctors who were in ear shot of him. So, the surgeon had a friend who was a psychiatrist, and said, “Could you come out with us at lunch, and tell us about this?” Then, the psychiatrist wanted me to see his manager, and she said she wanted to start a clinic there, just like you said. So, this was sort of my father’s memorial. He didn’t make it through the second operation, but he was one heck of a salesman, but we started the clinic there, and they’re still operating. They haven’t found out how to make a fortune out of it, and therefore to spread all over the place. One point that I should mention on this, and this is probably the hottest topic right now in the Naltrexone field. In the same area in Southern Florida, there was a researcher Mike Mullins at the Roskamp Institute who had discovered a particular genetic mutation that changed the receptor where endorphins go into, made them work a little bit better. He found that people with this mutation were more likely to be alcoholics. He happened to be this change in the opiate system. So, it occurred to me that these would be people that you could treat particularly well with the Naltrexone. So, I went down there and had a meeting with Mike Mullins’ group, and it was all set up trying to get the international finances going, and we never got the research going – a great idea. Ten years later, it was found that this mutation makes a tremendous difference in how successful Naltrexone is. The project combined that I mentioned, the patients who have this mutation, the C Carriers of the 118A. Among them, Naltrexone was effective in 87.1 percent of the patients. That’s phenomenal in the alcoholism field, 87 almost 90 percent of success rate in a double blind placebo controlled study. The thing that many people are talking about now is looking for this marker, and if you can find the patients in which it’s probably 90 percent effective, it’s immoral for a doctor not to be giving Naltrexone to them because it works so well. It’s a rather simple test. I’m not sure whether it’s available regularly. It is here in our laboratory. We’re setting it up, and we’re hoping to have even simpler ways of doing it in the future, but this is not expensive to do. It’s relatively quick, and you can look to treat the patients with Naltrexone where you’re almost certain to be successful. This should be a way of helping the reputation of the treatment. Now, I have to mention, this was in the patients who didn’t get the counseling. The same thing did not show up in the group that had a lot of counseling about not drinking and abstaining. So, if you’re going to insist upon using the abstinence way of, “Don’t drink, and here’s your pill,” then it’s not going to help having the marker. You have to use it so they drink at the same time that they’re on the Naltrexon, and then the marker should give you very good results.

Chris: I jut don’t understand why this wouldn’t be phenomenally successful if you were a doctor and you wanted to treat people with this.

David: It’s the same question everywhere. The publisher asks the same question of Roy and insists he put a chapter in there, but let’s go back to the Stephanie O’Malley study. She had two different ways of doing it. One of them was coping, in which essentially, they were allowed to drink and it worked beautifully. She had the second group in which was with abstinence, and it didn’t work, but she tried it and got beautiful results. As I said, there’s 77 or 79 clinical trials telling you it does work. So, people haven’t done it, but the PR is certainly the problem. What you have to overcome with the PR is this idea that it works as a diet pill. Even some of the ones that did the basic animal studies thought it was working that way. It’s such a strong feeling that you can take a medicine and it changes the way that you feel that they sort of accept that automatically. I just finished a review that’s going to be coming out this fall, which I go through all of the research, the lab with rats and in the clinics and in the clinical trials, and not a single bit of evidence showing anything of a diet pill effect. I have cases in which people have gotten doctors, but there are many people writing in from England and America talking about how they can’t get a doctor to give it to them. One thing I am hoping for here – have you heard of the campaign to make Nalexon over the counter?

Chris: No.

David: Nalexon works the same way in the brain as Naltrexon, but you use only a little tiny dose, and they are giving it out to friends of opiate addicts. In Chicago, there’s a group that has given out 11,000 kits of a syringe with one dose of Nalexon in it. If they see a friend who is going into an overdose, then they stab them with this in the hip, and they’ve had over a thousand reversed overdoses. It would be even nicer if this stuff were available without a prescription. The medicine of Nalexon, and Naltrexon too, but Nalexon is even safer, and it’s so safe that it doesn’t have to be a doctor choosing when to give it, it can be an addict or a friend of an addict choosing when to give it, and it’s saving lives. So, it’d be nice if it were available in drug stores, and if you can start getting the antagonist available over the counter, then you’re going to see lots of people start using it. You don’t need to overcome biases. They can read the book and find out how to use it. Doctors would have used anything they could before, but this does give a new possibility, and I would like to see it more in this direction.

Chris: If you’d like to know more about what Dr. Sinclair is doing, you can email him, or if you have questions for him, you can email him at David.Sinclair@THL.Fi. Thank you so much for joining us.

David: Thank you for having me on the show.

Chris: That’s the end of our interview, and I hope you’ve enjoyed it.