## FAQs About Alcoholism & The Sinclair Method

  
  


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Questions and Answers About the Sinclair Method  
  
The Questions and Answers section recapitulates the major themes presented in the Cure for Alcoholism. People have raised several salient questions in relation to the Sinclair Method. Readers may want answers to the numerous questions about the rationale for extinction treatment and why it is so different and so much more beneficial than other methods. How and why is the method a revolutionary breakthrough in addiction science? What would AA say about the Sinclair Method? Is it really a “cure” for alcohol addiction? Can it help with other compulsive behaviors? How safe is the treatment? What other substances and behaviors release endorphins in the brain? What about the ethics involved? Why do you have drink your way sober according to the formula Naltrexone + Drinking = De-Addiction? How does the Sinclair Method serve as a blue-print for the solution to other addictions? Can it save treatment costs? How could it be used in developing countries?   
  
Q: My husband does not want treatment. He will not hear of it. He denies that he has a problem but has been warned that he is endangering his own life and that of others since he often drives drunk. Could I “spike” his food or drink with the medication? Would it work?  
  
A: Under no circumstance should you or anyone spike anyone’s food or drink with medication. The individual must always give his or her consent if able to do so. It would not only be unethical, but also illegal for you to do this. I must admit, however, that one of my first thoughts when learning of pharmacological extinction was to put naltrexone into alcoholic beverages. So I have been thinking about this question for a long time. Theoretically, it probably should work. When rats secretly have naltrexone or nalmefene added to some chocolate sauce they are allowed to eat before access to alcohol, they show extinction of alcohol drinking. Naltrexone and nalmefene are safe non-abusable medications. They cannot produce a “high” or impair motor function. In theory, if you regularly “spiked” your husband’s food or beverage before he drank alcohol, you would notice that his drinking levels would steadily subside. But this would not happen instantaneously. He would gradually begin to crave and think about alcohol less and less. His drinking would decrease notably over two to three months. Three or four months later, he might be saying things like, “Gee, I’ve gone off alcohol.” Most likely he would not feel anything different. Like the alcoholic AA rats on Naltrexone + Drinking treatment he would not know why he had lost interest in drinking. He would not be aware that the program running the addiction in his opioid-reinforced brain had been removed. The program would simply have stopped running in the background – and that’s all. He might notice, as patients in the clinical trials have, that he no longer thinks about or eagerly anticipates alcohol. It might be a mystery to him, and he might say things like “I wonder why I no longer feel like having a drink. I just don’t miss it.” Drinking just is not that important anymore. A word of caution at this stage. This ploy would not work if you occasionally “spiked” the food or drink. It would only produce extinction if you did this every time he had a drink, at home and away.. And you would have to do this for 3 to 4 months.   
  
This question is included for illustrative purposes only. It is included to show the power of extinction and that drinking is an unconscious, reflexive process which could theoretically be extinguished in humans the same way as in experimental rats. The same way Dr. Schumsky said his behavior had shaped by learning and extinction.   
  
Humans are not rats. Stunts of this kind cannot be condoned and would in general be considered unethical, illegal, and not permissible. One additional word, however. If your husband’s primary reason for not entering treatment is that he denies he is an alcoholic, you might still get him to begin taking naltrexone before he drinks. After all, he does not have to stop drinking or “be an alcoholic” to benefit from this treatment. The Sinclair Method has been shown clinically to help people who drink only slightly over the safety limit find their way back to more acceptable levels. Furthermore, naltrexone can be taken not only to reduce an existing problem but also to prevent the development of alcoholism. So even if your husband denies that he has a problem, he might be willing to take a tablet before drinking to prevent alcoholism. This would work best if he has an alcoholic relative, and you can explain that taking the pill is to prevent your husband becoming like his Uncle Jack “the alcoholic.”   
  
Q: You actually say that the Sinclair Method is a cure for alcoholism. Isn’t it going too far by using the term “cure.” After all, many claims for cures for addictions turned out to be unwarranted – too good to be true. Why and how is the Sinclair Method actually a “cure” for alcoholism?   
  
A: The term “cure” is not used lightly, or without deep consideration. Sinclair’s method is equivalent to a cure because it actually restores the brain to the condition such that the craving and interest in alcohol are similar to the way they were before alcoholism was learned. The fundamental neurological scaffolding - the biological pathways causing craving and drinking, which are slowly yet deeply established by reinforcement from the drinking, are actually dismantled. Even after naltrexone has left the body, the reduction in craving and drinking remains. De-addiction occurs because the neural system that has been super-strengthened by reinforcement from endorphins – the wiring driving the addiction - is dismantled over the course of extinction treatment. In other words, if Bill Wilson, one of the founders of Alcoholics Anonymous in 1934 had been through Naltrexone + Drinking extinction treatment he would have not have found himself experiencing periodic spikes in his craving for alcohol - even after his profound mystical experience which led to the founding of AA.   
  
That was of course 1934. It would be another fifty years until naltrexone was approved by the FDA for alcoholism in 1994. The correct way of administering naltrexone - by prescribing it together with ongoing drinking - is only truly becoming recognized as the treatment-of-choice for heavy drinking and alcoholism since the turn of this century.   
  
A treatment may only counteract the symptoms of an ailment. A cure is distinguished by the fact that it removes the underlying cause of the problem. AA is not a cure and has never pretended to be; it says instead that the people in it remain alcoholics. Antabuse was not a cure: the cause for the craving and drinking were stil present, and Antabuse only tried to establish a barrier against drinking. It is no more a cure than physical barriers when incarcerating an alcoholic provide a cure. In contrast to these and all previous treatment procedures, the Sinclair Method does remove the thing that is causing the alcoholism - the neural pathway that when it fires causes craving and drinking.  
  
To be precise, pharmacological extinction does not remove all of the pathway causing drinking nor even return all of it to the level prior to the learning of alcoholism. In order for drinking to occur, firing must proceed all along the pathway. When alcohol then is drunk and endorphins released, all connections (collections of synapses) in the pathway are made stronger. Similarly, in the beginning of extinction, all of the connections are made weaker each time one drinks while on naltrexone. The pathway is, however, only as strong as its weakest link. Once the state is reached where one of the connections is too weak to fire the next neuron in the pathway, then the drinking stops at least for the time being. Many other parts of the pathway may still be considerably stronger than they were before drinking ever began, but this remnant of previous alcoholic learning is apparently only if you start drinking again without naltrexone. At that point, the remaining strengthened portions help make relearning of alcohol drinking behaviors be faster than the initial learning had been.   
  
Q: What would Alcoholics Anonymous say about the Sinclair Method? Surely AA would object to Naltrexone + Drinking? How would the Sinclair Method respond to AA?   
  
A: From an AA perspective, anything that can save people from the ravages of alcohol addiction must be worthwhile – even if it means patients continue drinking at medically safe levels. Since 80 % of patients regain control over alcohol through the Sinclair Method, and since it is supported by clinical trials proving its efficacy, we can surmise that AA can only approve of naltrexone and Pharmacological Extinction. Sinclair (2000) 1 responds this way: “The question has arisen how Alcoholics Anonymous would react to the Sinclair Method. Interestingly, the people asking the question and suggesting that AA would object, have not been AA members. Perhaps the difference is that AA people tend to see the issue from the alcoholic's point of view. It must be emphasized that to AA members and others who are currently maintaining abstinence, from a Sinclair perspective, we have a very simple message: "Congratulations! Keep it up. You do not need our help, and we have nothing to offer you.”   
  
The message to most individuals who have relapsed and are presently drinking out of control is:   
  
Previously, before the Sinclair Method, you had two choices:   
  
1) to continue drinking without treatment, with high risks to your health and safety   
  
or   
  
2) to undergo traditional detoxification, with:   
  
a) very high financial costs – in some cases up to $30,000 (£18,000) per rehab  
  
b) extremely unpleasant withdrawal symptoms  
  
c) a small but real risk of death from exposure to new additive drugs   
  
(e.g. benzodiazepines)  
  
e) due to relapse, subsequent re-treatment at additional cost  
  
f) no decrease, and a likely increase in your alcohol craving  
  
expectations of having to repeat detoxification   
continued treatment – for instance 90 meetings in 90 days - and regular AA meetings for life   
  
The Sinclair Method offers a new alternative You simply start taking naltrexone (or nalmefene) before drinking alcohol, with:   
  
a) no hospitalization or separate cost for detoxification a gradual reduction in craving  
  
gradual reduction in drinking,   
slowly withdrawing and detoxifying gradually   
d) no exposure to new addictive drugs (naltrexone and nalmefene are completely non-addictive)  
  
e) automatic gradual elimination of physiological dependence  
  
f) a high chance for a permanent elimination of excessive drinking   
  
To people in AA, this is good news. Indeed, people in AA who have understood the Sinclair Method say there is no conflict between it and the ideals and goals of AA. A reporter for the London Times Magazine, after coming to Finland and interview Sinclair and the clinician using pharmacologic extinction wrote that there may be even more in accord between AA and the Sinclair Method than even Sinclair realizes.   
  
Many of the doctors and clinicians first using the Sinclair Method were themselves AA members. They reported that AA had worked for them, and they wanted to help others in return. They had been frustrated because AA or 12 steps did not work for many of their patients. Now with pharmacological extinction they were able to help practically all of their patients, and that was what they had wanted to do all along.  
  
It is true that some people in AA have a prejudice against the use of all medicines in the confrontation with alcoholism. To a large extent those prejudices have been justified by experience with earlier medicines. Many of those prescribed for alcoholics were themselves addictive. People who have already demonstrated that they have a high risk of developing addictions are rightfully leery of a new addictive medicines.   
  
Other medicines impose a threat of pain or even of death if the alcoholic is unable to abstain, underlining the doctor’s inherent assumption that alcohol addiction is merely a matter of choice and strength of character. Prescribing Antabuse announces the belief that alcoholics could stop drinking any time they wanted to, if they really wanted to. The Antabuse solution is simply to increase the stakes for the poor alcoholic. It ignores the changes that have occurred in alcoholics making them wired to consume alcohol and no longer having the luxury of freedom of choice about drinking.   
  
Naltrexone and nalmefene are not like these other medicines. Their use in pharmacological extinction poses no risk of addiction and is built upon an understanding of the addiction process. As such, the opioid antagonists should be welcomed by AA. And that is what they will do - once the AA members know the truth about these medicines and the new way of treatment. There remains the task, however, of communicating this information to the people in AA and similar treatments.   
  
Q: The opioidergic system and endorphins sound fascinating. Can you expand on this?  
  
A: Certain neurons in the brain release substances that are similar to morphine and other opiates. These substances are called endorphins and enkephalins. They fit into the same receptors as morphine and heroin. The release of such substance also occurs in the most primitive organisms. Even some bacteria release opiate-like substance, apparently as a signal to other bacteria that something has disturbed the integrity of the community. In higher organisms, the natural opiates play a role in intestinal contraction. They also can block the transmission of pain, for instance from injury or child birth, and endorphins are naturally rising before women give birth. This is why morphine is effective as a painkiller. In the brain, the endorphins are generally released into the open space between neurons, rather than being confined to a small space within a synapse. Thus, one neuron releasing endorphins is able to affect hundred or thousands of neurons in its vicinity. Endorphins, therefore, do not act like synaptic transmitters such as glutamate or acetylcholine and might instead be called a local hormone. Both external opiates and natural endorphins provide reinforcement. That is, they strengthen the connections within the pathway of neurons that have just recently been used; therefore, whatever behavior was made just before the opiates or endorphins appear is made more likely to be performed again in the future. (Some researchers have speculated that endorphins produce reinforcement by releasing dopamine, but it now seems more likely that the endorphins have a direct reinforcing ability themselves.) In other words, each time you use a pathway that produces a behavior that in turn releases endorphins, the endorphins make that pathway stronger – they reinforce it. As a result, it will take less stimulation to get that pathway activated again in the future, and the harder it will be for some other pathway to inhibit it and prevent the behavior from being made.   
  
The opioid system has evolved the function of reinforcing behaviors particularly on the basis of sensory input. For example, putting a drop of sugar or saccharin on the tongue causes sensory neurons to fire and eventually produces a release of endorphins in the brain. This provides a very useful survival function from an evolutionary perspective. Instead of having to wait until after a food has been digested to reinforce the behavior that produced the food, we have developed an instant chemical dipstick - our tongue. We stick it into a food. It analyses the amount of sugar present. If there is a lot, endorphins are released, and we quickly and efficiently learn to eat ripe fruit with the nutrients we need instead of unripe, unhealthy fruit. The endorphin reinforcement requires only the sensory input, rather than the actual ingestion of the nutritious substances. Consequently, although it is a useful short cut for learning, it can be fooled, for example, with saccharin that produces the sensation but no nutrition.   
  
Q: You say that the aim of the Sinclair Method is either to abstain completely or to reduce drinking to safe levels as defined by the World Health Organization. Isn’t this a contradiction since “Once an Alcoholic, Always an Alcoholic” is a fundamental rule? After I complete the Sinclair Method, can I drink moderately or must I become a complete teetotaler?”   
  
A: It is true that the Sinclair Method really can sound like a contradiction. It is also true that an alcoholic not treated using the Sinclair method is always at risk of relapsing. In this instance, “once an alcoholic, always an alcoholic” is a true statement. Or rather it was a true statement until a way was found for removing the underlying cause of the person’s alcoholism.   
  
Before the discovery of spectacles, it might have been said that once a person had developed bad eyesight, they would always have bad eyesight – and to a large extent the statement would have been true. It no longer was true, however, once corrective lenses were able to counteract the underlying physiological cause of bad eyesight. An even better analogy with pharmacological extinction, however, would be the modern surgical techniques that actually remove the cause of myopia.   
  
In the case of Pharmacological Extinction or the Naltrexone + Drinking formula, patients remain in control of their drinking indefinitely so long as they follow Step 5 - the “Golden Rule” and never drink without the medication. In fact, many patients report that after treatment they are able to abstain altogether and those who do drink on the medication do so moderately. Enjoying fine wines is possible after a successful course of treatment, again as long as patients stick to Step 5 meticulously. In the Finnish follow-up study, about three years after the start of treatment, those patients still taking naltrexone before drinking averaged a maximum of only about 1.5 drinking occasions per week, and on those occasions averaged a maximum of 4 drinks.2 It should be noted, however, that if a patient starts drinking without taking naltrexone first, addictive drinking will be relearned over several months. In the follow-up study, the few patients who did start drinking without naltrexone, averaged a maximum of about 4.5 drinking sessions per week and a maximum of about 14 drinks per occasion – they had reacquired their alcohol addiction. Thus, it is important to continue to use naltrexone whenever drinking.   
  
The Sinclair Method is not a question of taking the cure and then going back to your previous life without naltrexone. It is your choice. You can drink as much as you want so long as you take naltrexone first. If you drink nothing, you take no naltrexone. And since the craving has been extinguished, this is not hard to do. . Or you can continue drinking together with naltrexone to prevent the addictive program from being reinstalled into your nervous system. You can also choose to start drinking without naltrexone and end up re-addicted to alcohol.   
  
Q: How can you distinguish between a patient treated using the Sinclair Method and one treated using other methods?   
  
A: In effect, this is what one sees in a controlled experiment where one group gets naltrexone and the other placebo (a sugar pill), while both receive counseling for their drinking problems. The placebo patients are equivalent to ones being treated with traditional means. Research indicates that if the placebo patient tries drinking any alcohol again, they relapse badly – they do not stop at one drink and return to harmful drinking. The Sinclair patient on naltrexone can, however, take one or two drinks and then stop. This has been the clearest measure for the success of naltrexone in the clinical trials: the reduction in the rate of relapse to heavy drinking. The main reason for this is that there is no extinction until the patients are actively drinking on naltrexone. Most trials started by first detoxifiying the patient.. After that and before the first drink, the naltrexone patients were no better off than the placebo patients. Consequently, in almost all of these trials, naltrexone did not help delay the relapse to drinking. After drinking had started, however, naltrexone became beneficial because it triggered the extinction of craving and drinking. The placebo patients without anything to weaken their craving, went on to relapse. But patients on extinction treatment with naltrexone patients were prevented from relapse. Often there were even larger benefits from naltrexone relative to placebo in the number of patients who, having relapsed once, went on to relapse a second or third time. That first relapse was a powerful extinction session for the naltrexone patients, greatly reducing their subsequent craving and risk of drinking.   
  
One important feature distinguishes the Sinclair patient from ones treated With traditional methods. A group of patients treated with any other method will be best at the beginning of treatment but ever after that they will be getting worse and worse. The typical graph for showing results of traditional treatments is called a “survival curve”. It shows the ever diminishing number of patients who, with time, are still in the program and have dropped out and gone back to alcohol abuse. Patients with the traditional treatments are hanging “on to the wagon” waiting for the almost inevitable time when they too will “fall off the wagon.”  
  
Such graphs are of no use with the Sinclair patients because they are headed in the opposite direction; they are progressively improving with time. During the first week, all of them are drinking – like the alcoholics they are. After that, the craving and drinking decreases. The number of patients who have succeeded in reducing their drinking in half will increase. At a lower level but still progressively increasing will be the number of patients who have stopped drinking completely.   
  
There are exceptions. In the beginning, when the data from the first 20 patients treated with naltrexone in Finland were examined, there were 19 curves going in one the direction of improvement. There was one patient whose curve went in the opposite direction. Despite the instruction, she started out abstaining during the first weeks on naltrexone. A little later she started drinking a little bit, and then more and more. Only when she had started drinking at the level of the other alcoholics did the benefits start developing. Then her curve changed direction and she began getting better.   
  
Q: Why would someone take the medicine? After all, it is a “pleasure blocker” isn’t it? No alcoholic would take it. What about compliance - will the treatment work only if the person “wants” it to?   
  
A: This is a classic error. You should not be concerned if you asked yourself this question. It is also made by some of the most well respected alcohol and addiction researchers in the world. People, even top research scientists, often tend to think in terms of a “homunculus” – as though there were a little person inside the head making the choice to drink, thinking about getting the next drink, and generally in control of the decision making process. In fact, there is no homunculus, and the alcoholic is no more in control over choosing to drink or think about drinking than a computer is of stopping to load a program like Windows XP once the program has been launched. Addictive drinking has little in reality to do with the concept of “pleasure.” Addictive drinking has everything to do with reflexive action. It happens at a non-conscious, automatic level. It takes time and many instances of drinking to strengthen addictive circuitry in the brain. Each time the person who is genetically at risk drinks, there is reinforcement to the opioid system via endorphin release. Eventually there is a broadening of existing opioid pathways into great drinking super-highways. In reality, we find that most people who truly suffer from alcoholism do not claim that they enjoy drinking. They get little pleasure out of it, much like heroin addicts do not gain much pleasure once they have become addicted. Certainly not enough pleasure to balance all the suffering caused by the alcohol or opiates. Alcohol abuse is not rational. That is also why it is a problem and why we should not confuse the terms “pleasure” and “reinforcement.” Finally, we see that in practice that compliance to take naltrexone with alcohol has not been a problem for the majority of the tens of thousands of patients have already treated.3 If a doctor tells an alcoholic, “Don’t drink! You will get sicker”, then there is a major problem with compliance – which is why the person is an alcoholic. But the simple act of taking a pill before drinking is not difficult at all. It is much easier to comply with the direction: “it is better for you health if you abstain, but if you are going to drink, always take your naltrexone before you do.”   
  
Q: Why do most other treatments have such low success rates and how different are the success rates for the Sinclair method? “Evidence Based” methods are the rage now so is there a treatment-of-choice for alcoholism?   
  
A: Other treatments – which include AA and a wide range of psychotherapies, body therapies, self-help and group therapies - are unable to dismantle the neuronal system producing the craving and drinking. These mainly rely on some kind of cognitive control or willpower over the addiction. Until now they have been the best one could offer. However, it is widely accepted that they achieve a 10 to 15 % rate of success in their own terms – usually measured as complete abstinence at one year after treatment. They do not remove the cause of drinking - the addictive wiring in the brain. The Sinclair Method actually produces a physiological restoration of the original neuronal pathways through gradual extinction over the course of treatment. This results in a massive weakening of the addictive wiring in the brain and a resultant reduction in craving levels and number of drinks consumed per week. (Please refer to the Extinction Curves in the Chapter 2 and in the Appendix). The sustained success rates for the Sinclair Method suggest by now that it is the treatment-of-choice for alcohol problems in the 21st century.  
  
The choice of which treatment to use certainly should be based upon scientific evidence. Unfortunately, there is very little solid data about how effective most alcoholism treatments are. This is the case especially with AA. The best researched treatment in the field is the use of naltrexone. There is more solid evidence from placebo-based clinical trials for naltrexone than for any other treatment. The conclusion from this abundant evidence is that use of naltrexone is the most effective treatment.  
  
Q: Why is the Sinclair method not 100 % effective? What about the remaining 20 % who do not seem to benefit from it?   
  
A: No treatment is 100 % effective outside the highly controlled setting oaf the laboratory. The Sinclair method is 100 % effective in the laboratory in the treatment of alcoholic rats. All of these animals have the similar genetic backgrounds and similar life histories. In theory, if humans were kept in a laboratory setting, in a situation where we could be absolutely certain they were given their medication and regularly drank alcohol for 3 to 4 months it is possible we could begin to approach 100 % success rates, but probably there would be some rare individuals who did not respond. In reality though, humans are much more varied, and we really wouldn’t want them to be like laboratory animals…  
  
Some of the treatment failures with the Sinclair Method are caused because the patients stop taking their medication before extinction has had an opportunity to have much effect. It is well known that patients often don’t comply with doctors orders. Some even neglect to take life-saving medications such as insulin or blood pressure medications - despite the risk of fatality. Non-compliance may be a big factor for the 20 % who have not responded by reducing drinking to safe levels. The best estimate is that it accounts for about half of the failures. Having a 10% rate of non-compliance is extremely good especially in the field of alcoholism and drug research. A problem with this kind of research is that it depends on honest patient self-report. Patients may self-report they are taking the medication but in fact – for whatever reason – are not always taking the medication before drinking. However, we do know the treatment will not be effective if you not follow the formula Naltrexone + Drinking = De-Addiction.   
  
Some patients may fail to comply with the second rather than the first part of the equation. They may take the medicine without drinking. This has indeed been found in the drinking diary records of a few patients. As we saw in Chapters 2 and 3, naltrexone is ineffective according to the formula of Naltrexone + No Drinking Allowed.   
  
Theoretically, another possible explanation for non-responsiveness is that naltrexone can block “first-drink” effects – the slight euphoria we experience as we take the first drink. Some patients may confuse this with success and think: “Wow, I’ve just taken it for a week and it works – I’m cured!” And then skip the rest of the treatment. Of course they are nowhere yet de-addicted after a week There are no known cases so far of this having happened.   
  
There have been very rare cases of patients stopping treatment because of idiosyncratic reactions supposedly to naltrexone.   
  
But non-compliance cannot account for everything. Some patients stay in the treatment for weeks, say that they have been taking the medication, and yet report no benefits. How these patients differ from the vast majority that do benefit is a major topic for research today.   
  
It has been found recently that the failures were often patients who did not have a biological marker indicating a strong opioidergic system and did not have a family history of alcoholism.4 Had these patients learned their alcohol drinking as a result of reinforcement through other neurotransmitter systems like dopamine, norepinephrine, or serotonin? What about as yet unidentified neurotransmitters and the role hormones like oxytocin, leptin, cortisol?5 We simply do not yet know the full implications.  
  
Several current research projects are aimed at finding markers for responsiveness to naltrexone therapy. For example, a particular mutation in one type of opioid receptor was found in Project Combine to be related to how effective naltrexone was, according to a report by Dr. Ray Anton at the 2007 meeting of the Research Society on Alcoholism, in agreement with some but not all previous studies. Again, more research is needed.   
  
It is possible that the naltrexone doses used in the clinical trials may have been too low for some patients. Most trials use the standard dose of 50 mg yet toxicology studies show that the medication is safe at up to 300 mg, six times the usual dose. It is certain that variations in drug dosing is a major concern in applied medicine. For instance, some people respond well to 50 mg per day of the beta-blocker, atenalol, for rapid pulse and high blood pressure. Others require doses of up to 200 mg a day to achieve results. The role of drug metabolism is also very important. Some may metabolize naltrexone out of the system far more rapidly than others and this would mean that they are drinking without opioid antagonist blockade – tantamount to drinking without naltrexone coverage.   
  
It may well turn out that nalmefene will improve the success rates when it becomes fully approved for alcoholism. This medication may replace naltrexone as the standard medication used in Pharmacological Extinction because it: 1) stays in the body longer; 2) is less likely to stress the liver; and 3) is an even more potent opioid antagonist (endorphin and opiate blocker).   
  
A word of caution should be added about increasing naltrexone dosage. One of the first responses of most doctors if a patient is not responding is to increase the dosage. The usual 50 mg dose, however, is supposed to be more than enough to block 100% of the relevant opioid receptors. Therefore, increasing the dosage should not improve the benefits. There might be patients who could benefit from a higher dose, but so far there is no clear evidence that higher dose are better.   
  
Q: Is it ethically acceptable to instruct alcoholics to drink? Moreover, is it ethical to conduct clinical trials where alcoholics are instructed to drink? Surely this is unethical as patients should first detox then be given medication?   
  
A: The answer depends primarily upon whether the alcoholic is abstinent or currently drinking. If patients have been able to remain abstinent for a long time, it would be unethical to tell them to start drinking or do anything that encourages them to relapse. If you are already addicted that first drink - as AA correctly points out - might start a binge with dire consequences. Therefore, naltrexone is not a suitable medicine - for abstinent alcoholics who are managing their abstinence well - since it only works when combined with drinking. While some studies indicate that the drug, acamprosate, may be a better medicine for such patients, others such as the huge Combine Project on alcoholism do not (Anton , 2006).6 On the other hand, an alcoholic who is currently drinking, who has had over 20 drinks every day for the past month, is unlikely to suffer from having a few drinks tomorrow. And there is no need to “instruct” the alcoholic to drink; that is bound to happen anyway. The instructions used are both simple and ethical: if you drink alcohol always take naltrexone an hour before you do – remember it is best not to take the medication if you are not going to drink. This allows for extinction automatically lowering both craving and drinking levels. It also makes it much easier for the patient to abstain in the future. There is nothing damaging or unethical about using this procedure to withdraw from alcohol gradually and safely. It is preferable to abrupt, often dangerous withdrawal. In addition, it avoids the need for other addictive medicines such as valium and librium which are often given to prevent fatal seizures caused by withdrawal. Indeed, the ethical question might well be reversed. Is it unethical, short-sighted, and plain cruel to instruct alcoholics to take naltrexone and not to drink. This was done, perhaps unintentionally, by Krystal (2001) and associates in their Yale study of 627 VA hospital alcoholics. Needless to say their study reported abject failure. We might question the ethics of conducting this clinical trial - especially in light of the 19 prior successful clinical trials at the time where Naltrexone + Drinking was allowed or encouraged in contrast to 8 previous unsuccessful trials with Naltrexone + Abstinence since successful treatment is dependent on having alcoholics drink and take the medication at the same time, it could be seen as unethical to use any other clinical trial protocol. 7   
  
Ethics must be based upon the benefits or dangers to which a patient is subjected. There is nothing unethical about giving naltrexone prior to alcohol detoxification because there is no danger or harm to the subject. Perhaps there is confusion here with opiate addiction. Giving naltrexone to a heroin addict without prior detoxification is indeed dangerous and can be fatal because it can precipitate serious withdrawal symptoms. It has, however, long been established that there is little or no cross-dependence between opiates and alcohol. This means that naltrexone does not cause alcohol withdrawal symptoms. Of course, this procedure was first thoroughly tested and shown to be safe in rats. The clinical trials have demonstrated significantly fewer side-effects from naltrexone without prior alcohol detoxification than from naltrexone during abstinence. In general, health professionals using naltrexone in the treatment of alcoholism and other addictions ought to be fully informed about the theory, practice, and outcome data before they even start treatment. They should be aware that if they prescribe opioid antagonists to already detoxified abstaining patients, they are proposing a treatment that has never been found to have a significant benefit over placebo in all of the clinical trials in which it – Naltrexone + No Drinking Allowed - has been attempted. Naltrexone has repeatedly been found to be effective, but only after the patients drinks while on the medication – and only after a period of 3 to 4 months. Of course, one could detoxify the patients first, and then wait for them to relapse and drink while on naltrexone, but this forces the patients to undergo a detoxification program that can be hazardous, painful, and very uncomfortable, if not life-threatening. Detoxification also requires expensive hospitalization. A safer, more acceptable, and less expensive procedure is to eliminate the unnecessary step of prior detoxification. Simply start the patients on naltrexone while they are still drinking. Detoxification then occurs automatically, slowly and safely, as extinction lowers the craving and drinking levels over several weeks.   
  
Q: Are people are born alcoholic?   
  
A: No one is born an alcoholic. Some people are, however, born with a much higher risk of developing alcoholism. For instance, research by Dr Esther van den Wildenberg at the University of Maastricht in the Netherlands investigated the role of a gene mutation involving endorphin receptors known as “mu opioid” which are activated by endorphins.8 The study was reported in the journal Alcoholism: Clinical and Experimental Research. Researchers recruited 108 male, heavy drinkers who were either homozygous for the A allele (n=84) or carrying at least one copy of the G allele (n=24). The subjects were exposed to water and beer in three-minute trials and their subjective craving for alcohol was measured. In short, the research suggests when the gene variant or “G allele” is present there is a higher potential for alcohol craving.   
  
This study represents just one of many supporting the conclusion that some people are born with a genetic predisposition causing them to be more responsive or sensitive to the reinforcement from endorphins released by alcohol than others. The research, starting with breeding of the high drinking AA and low drinking ANA rat lines in Finland, has proven conclusively that genetic plays a very important role in alcohol drinking by animals. Genetics also is important for how intoxicated an individual rat or mouse gets from a given dose of alcohol.   
  
Since then, studies on human twins and adopted children have demonstrated that genetics is also important for our drinking. Nevertheless, even if you are genetically predisposed to alcoholism you still need to start drinking – and do so repeatedly and for many months or years before the addiction becomes embedded in your brain. Only after extended practice does craving for alcohol become so strong that you loose control over alcohol.   
  
Q: What is the difference between an “alcoholic” and a “problem drinker”?   
  
A: In the grand scheme of things, it is not all that useful to distinguish between these terms. There are enormous individual differences between the way people use and respond to alcohol. One psychiatrist who treated many patients using the Sinclair Method said, “One beer for one person can have entirely different effects on another.” Apart from the stigma attached – amoral, weak, bad - in general people tend to think of “alcoholics” are being “very badly addicted” to alcohol. Problem drinkers are also stigmatized, but the connotation is perhaps somewhat less tainting. I use the terms somewhat interchangeably in the book, depending on the situation. In general both terms indicate a “drinking problem” – a problem with alcohol. (See Step 2) The term “alcoholic” implies, for some, a very clear, strong addiction – very well established opioid super-highways in the brain. Others think of “problem drinkers” as being “less addicted” on a continuum of addiction. The more strongly addicted the more likely you will be called “an alcoholic.”   
  
Although it may sound paradoxical, some alcoholics drink less than some problem drinkers. For example, there is a stage in cases of people who have been alcoholics for a long time when metabolic factors reduce their drinking levels. The individuals are still alcoholics and must have the alcohol, but the amount they drink each day may be less than that consumed by a problem drinker. Similarly, many binge drinking alcoholics consume alcohol less frequently than even some Mediterranean-style social drinkers.   
  
Clearly most of the “winos” seen on skid row are perceived as “alcoholics.” But many doctors and judges are “alcoholics.” The American Airlines pilot arrested at London’s Heathrow airport in February, 2006, before he could fly passengers to the US might be an “alcoholic” – or perhaps he was simply a “problem drinker.” 9 The tycoon who owns his own private jet and drinks a bottle of vodka plus wine at lunch every day may also be “an alcoholic.” But because he seems to be functioning well and because of his perceived status, people are likely to simply say “he’s a bit of a boozer” – even though the addiction is powerfully entrenched in his brain. Again, these terms are not all that helpful. The goal of the Sinclair Method is to reduce craving and drinking to safe limits and to give any one wants it, more control over drinking. That “anyone” includes alcoholics, alcohol abusers, problem drinkers, social drinkers, and all other classifications of alcohol consumers .   
  
Q: Are naltrexone and its cousin, nalmefene, “magic pills” like penicillin is for bacterial infections?   
  
A: The answer is emphatically No! Naltrexone and nalmefene are not “magic pills.” The point here is that the medication is used as a tool. Naltrexone or nalmefene are not curative agents in themselves – like penicillin is for a bacterial infection. If a doctor prescribes an anti-biotic for say, a throat infection or a dangerous disease like anthrax, he or she can be fairly sure that if the patient takes the course of medication that the infection will in most cases be cured. In this case, it is reasonable to think of penicillin, anti-hypertensives, anti-depressants, or anti-psychotics as “magic pills.” The doctor’s mind-set – “give these pills for this disease” – is the correct thinking. Correct thinking for an illness involving bacterial infection, hypertension, schizophrenia, or depression. In these cases, the patient can be passive. She has nothing more to do than take the medication and wait for the active ingredient to work all by itself. However, the Sinclair Method does not work this way. The naltrexone or nalmefene tablets in themselves will not automatically cure the addiction. They do not function the way other medicines usually do.   
  
The Sinclair Method requires active participation on the part of the patients. Even if patients do not understand the precise rationale behind extinction, as long as they follow the prescription of Naltrexone + Continued Drinking they will meet with success. They should also be aware not take the medication if they are not going to drink. The tablets are merely curative tools to dismantle the addictive wiring driving craving and addiction.   
  
The benefits are not immediate, as they are with some medications. Other medications, like anti-depressants take time to work – one to two months in the case of Prozac-like drugs, which patients take on an ongoing basis, regardless of whether they feel particularly depressed that day. By contrast, alcoholics only take naltrexone or nalmefene if they are going to drink. Treatment takes time, several months for the neural pathways to be weakened and returned to the state they were in before drinking was learned. We cannot stress enough the importance of thinking about the treatment as a Method. It has been repeatedly demonstrated that simply handing out naltrexone or nalmefene tablets will not cure the addiction. The tablets are not “magic.” But the process of Pharmacological Extinction, that is, Naltrexone + Drinking, at least for 80% of patients, produces “magical results.”   
  
Q: If I am an alcoholic and I do not drink alcohol but take naltrexone, would I worsen my addiction?  
  
A: If you are an alcoholic and you take naltrexone or nalmefene without drinking, you will “upregulate” the number of your opioid receptors, causing you nervous system to be “supersentitive” to endorphins… If you then stop taking the medicine and drink, you will receive extraordinarily high amounts of reinforcement from the endorphins released in the brain. As demonstrated in laboratory rats, at this time, soon after the naltrexone has been cleared from your system, you will show pharmacologically-enhanced learning of behaviors that are reinforced by endorphins. The critical question is what behaviors you make at this time. The Sinclair Method guides patients to practice healthy alternative behaviors at this stage, thus promoting new interests and activities as alcohol-related behaviors are extinguished. In contrast, if you drink alcohol during this period of enhanced learning, this will strengthen the pathways that cause your drinking and craving.   
  
There is nothing directly detrimental about taking naltrexone while abstinent, except you are wasting your money on the medication which is doing nothing for you alcohol problem and may instead be weakening some of your other behaviors such interest in sweets or exercise. Upregulation is detrimental only if you drink alcohol while it provides increased reinforcement. Otherwise, it can be a useful tool.   
  
Q: Why do people relapse so often after disulfiram (Antabuse) therapy?  
  
A: Disulfiram or Antabuse was initially thought to be an excellent and logical way of dealing with alcohol addiction. After all, if patients take the medicine before drinking and then drink they experience aversive symptoms like terrible nausea. If patients knew this was going to happen, they would avoid drinking. And many do, particularly if they are kept under close supervision. And if sufficient medication could be administered through a timed-release implant under the skin, long-term coverage theoretically might be achieved. However, this treatment is equivalent to locking up the patient in prison or mental facility where no alcohol is available. Enforced abstinence , as we have seen throughout, produces an Alcohol Deprivation Effect which increases the craving.10 Indeed, animal studies have shown that disulfiram and similar medicines increase the craving even above that produced by the abstinence alone. Therefore, although most patients cannot drink while on disulfiram, they become very anxious to get rid of the medication and start drinking again. The craving induces people to quit taking Antabuse so they can start drinking again. There are stories of alcoholics, cutting open their arms or abdomens in order to remove slow-releases capsules, in order to be free to start drinking.  
  
If a patient is sufficiently motivated to continue taking disulfiram, then it can be an aid for enforcement of total abstinence, but most patients do not have this level of motivation and, although officially approved for alcohol addiction, it has generally not been shown to be truly effective.   
  
Q: If a medication is used in the Sinclair Method, why is it a “psychological” rather than “medical” treatment? How and why is Sinclair’s discovery revolutionary? Why didn’t psychologists think of using a blocking agent to produce extinction long ago?   
  
A: The Sinclair Method is rooted in psychology. The concept does indeed use a medication, an opioid antagonist, as a tool to bring about extinction of alcoholism and other addictions. Sinclair’s discovery of Pharmacological Extinction is based on learning theory, and is derived from experimental and neuropsychology.. Pavlov and others pioneered conditioning learning theory over a hundred years ago. Learning theory was applied as “behavior therapy” with Arnold Lazarus (1976) being the first to use this term in print, in the early 1960s. Learning theory describes how behaviors are learned with the aid of reinforcement, and how behaviors are removed by the process of extinction when reinforcement is withheld. Experimental psychologists might condition a dog to automatically salivate by giving it food and pairing the food with the sound of a bell. The food is the “reinforcement.” Pretty soon, the dog will salivate just to the sound of the bell. But if reinforcement – the food – is withdrawn, the dog will stop salivating. In other words, the dog’s learned response – salivation – will be extinguished. In this case, reinforcement is prevented simply by not giving the substance producing the reinforcement. In the case of alcohol drinking, however, it is important that the sensations produced by the alcohol are still present. Consequently, the Sinclair Method blocks the reinforcement pharmacologically with opioid antagonists. Abram Wikler (1910-1981)11 had proposed using opioid antagonists to block the reinforcement from opiates, since they block all the effects of opiates, in the treatment of heroin addicts. He proposed, however, using it on an inpatient basis. Sinclair showed that alcohol drinking also is a learned behavior and that it, too, is reinforced by the opioidergic system. Therefore, he proposed using naltrexone or other antagonists to produce extinction of alcohol drinking. He also recognized the importance of extinguishing the drinking behaviors in the same natural environments in which they had been learned, and thus the necessity of having the naltrexone treatment in an outpatient situation. Sinclair’s research indicated that alcohol drinking, saccharin drinking, and various other behaviors were reinforced through the release of endorphins in the brain, and that these behaviors could be extinguished pharmacologically with the help opioid antagonist medications.   
  
Although extinction is a well-established mechanism, studied in thousands of experiments, it has been largely ignored clinically. Perhaps the reason for this is that extinction is not part of our conscious experience. We experience it consciously when we learn something and store the fact in our cerebral cortex. The cerebral cortex and higher nervous areas, however, are usually protected against extinction. Consequently, it is practically impossible to remove that memory from your cerebral cortex. Extinction operates primarily in the more primitive brain areas that operate largely outside of consciousness, producing basic behaviors like salivating, eating, and drinking, where the neural connections are not protected from being weakened. Perhaps this explains why clinicians did not think to use extinction for treating alcoholism earlier. Sinclair himself admits that all the facts necessary for developing the concept of pharmacological extinction were present already in 1975. The concept only occurred to him after he had written a book in 1981 about how learning occurs in the nervous system12. The explanation for learning automatically provided an explanation for how learned behaviors could be removed from the nervous system, that is, for the mechanism of extinction. Only then, with all of the pieces of the puzzle staring him in the face, did he see the possibility for using extinction to remove the detrimental learned behavior of alcohol drinking.   
  
Even that was not sufficient. The idea of pharmacological extinction was set aside without further thought until 1985 when Kalervo Eriksson asked Sinclair to write a Five Year Plan. The goal of the plan was clear already: to come up with a better treatment for alcoholism. That was the goal from when he first moved from America to Finland. Now, however, he systematically started analyzing the various possibilities.   
  
His favorite hypothesis initially was some form of substitution drug therapy, like methadone is used as a substitution drug for heroine. There were several medicines that appeared promising as a substitute for alcohol.   
  
Pharmacological extinction was not examined in detail until about page 60 of the 85 page Five Year Plan. Then and only then did the tremendous potential of this new treatment become evident. Sinclair saw for the first time that pharmacologic extinction, unlike all other treatments, would actually be a cure for alcoholism.   
  
Q: Why do you not suggest that patients receive the Sinclair Method in a hospital? After all, you can ensure that patients take their medication and drink in the controlled setting of a hospital?  
  
A: This too is a good question, and one that has occurred to several clinicians in the field. While conventional alcohol treatments, such as standard 28 day detox inpatient programs are run in controlled settings, the Sinclair Method requires that patients extinguish their drinking in all drinking situations that have been associated with their drinking. Thus, if your special triggers are parties or vacations you should take the medication and drink when you go to parties and go on vacation. If you drink alone, you should take the medication and drink on your own. If you drink on Tuesday mornings, take the medication and drink on Tuesday mornings. This is because we want you to extinguish drinking in all situations in which you have previously found yourself drinking. Therefore, confining the treatment to a hospital setting would extinguish your drinking only in the hospital environment. Later, you might come out of the hospital and find that your craving and drinking levels have not abated when at home, at parties, or whatever situation you previously associated with drinking. Exactly this problem was demonstrated in studies in which heroin addicts took heroin in a hospital setting after getting naltrexone. The treatment extinguished the interest in heroin in the hospital but did not generalize to life on the outside. Nevertheless, in some cases it may be useful to start Naltrexone + Drinking in a controlled clinical environment at the start of treatment – perhaps for 2 to 4 weeks depending on the individual – and then continue de-addiction outside the clinic.  
  
There is another reason why the treatment could not be started in most alcoholism treatment hospitals: they would not allow alcohol on the premises for any reason. Allowing some of the patients to drink would completely demoralize the rest of the patients who cannot, it has been claimed. Naturally, the alternative of starting naltrexone in a hospital but not allowing drinking would not be expected to be effective, and in fact has been shown not to work. 13   
  
Q: Why were rats used in Sinclair’s research?  
  
A: Medical and psychological research has used animal models for years. Of course, ethical questions arise from the use of animals. Rats were used because they reflect human behavior, and because scientists can work with pure genetic pools. Specially bred rats are very useful to work with when searching for answers to diseases. In short, there would be no cure for alcoholism were it not for Sinclair’s Finnish rats. Furthermore, rats happen to be a particularly good model for human behavior related to eating or drinking. The control of consumption in carnivores (meat eaters) or herbivores (plant eaters) tends to be different from that of humans. Rats like humans are omnivores: we eat everything. Therefore, the control of intake in rats tends to be similar to that in humans. Rats tend to have rather similar tastes to humans. We both have a sweet tooth. And both rats and humans that like particularly strong sweet solutions are at high risk of abusing alcohol. Pigs, which also are omnivores, are also good animal models in alcohol studies. By coincidence, in these pig studies the most commonly variety are known as Sinclair miniature pigs – with no relation to David Sinclair!   
  
Q: Why do you call the Sinclair Method a “psychobiosocial” treatment?  
  
A: The Sinclair Method involves psychology, biology, and sociology. The psychology refers to the process of extinction, originally described by psychologists like Pavlov over 100 years ago. The biology refers to the function of the human brain, the secretion of endorphins, the super-strengthening of pathways by endorphins or opiates in a select group of genetically predisposed alcoholics. The method involves sociology since alcoholism is also a social problem, and requires interpersonal intervention and support for patients and families.   
  
Q: Why do you have to be so meticulous and careful for the Sinclair Method to work effectively?   
  
A: The catch phrase today is “evidence-based medicine.” The use of opioid antagonists in alcoholism treatment is definitely evidence-based. There have been dozens of controlled clinical trials, as well as a large number of pre-clinical studies showing the medications are safe and effective. There is solid evidence about having to drink while on the medication. There have not, however, been comparative studies showing that psychosocial therapy is necessary or beneficial. Indeed, many trials with both naltrexone and nalmefene that skipped the additional therapy still found the proper use of the medications had significant effects. Nevertheless, most of the trials with naltrexone have been done with comprehensive programs of alcoholism therapy.   
  
Addictions are deeply rooted in the brain and nervous system and treatment must be meticulous. Patients need to know that it is vital they follow instructions, that they keep a record of their drinking, and that above all, they take their medication whenever they drink and do not take it when they are not drinking. Sometimes, the addiction has become so deeply rooted that the patient cannot recall what it might be like to be sober. In a sense, this is much like the institutionalized inmate, prisoner of psychiatric patient, who is released into the real world after having spent many years locked away. Adjustment can be hard. Many ex-prisoners re-offend just so that they can get back into prison where they feel safe. Patients need to be advised that they can expect a real cure – especially those patients who have been for conventional treatments where relapse is practically expected. The Sinclair Method offers the chance of permanent cure – the first time round!   
  
If patients stick to the plan they will crave less and less, and actually drink less and less. They will then be in a position where they can, should they choose, abstain altogether. Adjustment to social life without alcohol may initially be difficult, and it is paramount that patients be offered supportive psychotherapy. In a sense, this serves as an “anti-future shock” therapy and prepares the patient for potential obstacles that may arise: “Am I going to make it? Am I really worthwhile? Will anyone ever trust me again? I am afraid!” are the kinds of thoughts that might pass through their minds. Some patients feel as though they will never recover, that their lives are hopeless, and need the helping hand of a trained professional. Some patients require more supportive therapy, and encouragement.   
  
Competent therapists are aware of the power they possess to affect patients positively in terms of improving self-esteem, self-efficacy, and creating a renewed life. So the treatment has to be taken seriously by all concerned and carried out by those who have at least a basic understanding of how it works. Fortunately, with the Sinclair Method, de-addiction treatment for alcoholism is no longer as complicated as it once was.  
  
It should be noted that although controlled clinical trials have proven the naltrexone works and that it has to be paired with drinking, there have not been scientific tests proving the meticulous protocol described here is the best possible. What is described is the protocol that has been used extensively and has been shown to produce excellent results. The specific features in it make sense clinically, and we believe they all are useful, but unlike the Naltrexone + Drinking feature, they have not been scientifically proven. And if you follow them you should expect to get results similar to what has been seen with them so far. They are not, however, carved in stone. We already know that some things differ from between cultures. Aspects that work in Finland do not always work in Israel; counseling techniques that are beneficial in New England may not be among senior citizens in Sarasota or the Hispanic community in Miami. It is quite possible that improvements will be discovered in the future. What is offered here is the best at this time, but check out the website for future developments, at http://www.De-Addict.com.   
  
Q: What would happen if a researcher were studying the effects of naltrexone without having alcoholic subjects or patients concurrently drink alcohol?  
  
A: This has been done in several clinical trials and in animal experiments. The results are indisputable: it does not reduce drinking. In fact, it may even worsen the craving for alcohol. Simply taking naltrexone is not sufficient to bring about cure. When naltrexone is given as though it were a treatment – as a curative agent in itself - the result is always negative. Experiments have never shown a significant reduction in craving or actual drinking this way. In fact, it has usually made the situation slightly worse by inducing endorphin or opioid receptor “up-regulation” which provides increased reinforcement of drinking.   
  
Another way of looking at the cooperative, interdependence between taking the medication and actually drinking while it is in the brain actively blocking the opioid receptors is to think of the relationship between putting gasoline into the gas tank of a car to make it operate and get you to your destination. If you do not put gasoline into the tank, you will not get to your destination; similarly if you do not take naltrexone you will not reach you goal of reduced craving. But you also have to make the action of driving the car; if you do not drive it, you will never reach the destination no matter how much gasoline you put in the tank. Similar, you have to make the action of drinking; if you do not drink, you will never reach your goal of reduced craving no matter how much naltrexone you take. The addictive wiring regulating your craving and drinking will not be altered. Your drinking pathways will remain like super-highways. Thus far, the only way to get the drinking highways – so to speak – to return to their original state as weaker, narrower pathways is to drink while on the medication over 3 to 4 months.   
  
Q: Many alcoholics are easily able to stop drinking for a month or two using simple will-power. But they often seem to relapse, binge, go on “benders.” Why is this?  
  
A: It is relatively easy to stop drinking after several days of heavy intake because a form of satiety has reduced the craving, just as it is easier to stop eating after having just eaten a large amount. During the subsequent period of abstinence, however, this satiety goes away and the craving for alcohol increases progressively. As we saw in Chapter 2, this is the alcohol-deprivation effect (ADE) in action. Eventually the craving is likely to become high enough that it is able to overcome will power to abstain, and then the person relapses usually after giving in to a single drink. Little is known about the time course of the ADE in humans, but in rats the craving for alcohol rises rapidly for the first week and only slowly thereafter. Generally the speed of processes in human is roughly 30 times slower in humans than rats, so we might guess that the craving in humans continues rising for about 30 weeks before leveling off. This is just speculation, but it suggests that the risk of relapse continues increasing for over 7 months in humans. Furthermore, in rats the craving stays up at the same high layer month after month with no evidence that it ever goes down. So the high risk of relapse may well continue indefinitely in humans as well, although it is also possible that the craving is reduced after years of abstinence. There is, in addition, the problem of relapse being triggered by annual social events and other drinking triggers.  
  
Q: I come from a family where alcoholism and drug addiction are rife. In my own search, I have read many popular books on alcoholism and addiction. Some authors are themselves recovering addicts or alcoholics, and others are in the helping professions. I have noticed that many are opposed to using ‘drugs to treat drugs’ and say that you can’t cure substance abuse with another substance – a drug or chemical. Are they right?    
  
A: It is true that many authors of popular book are themselves recovering drug addicts or alcoholics. Many are health care professionals – psychologists, doctors, social workers and others who now work with alcoholism and drug addiction. Often these writers subscribe to a doctrine that insists that the patient must become clean and sober on his own. Perhaps the negative attitude about pharmacological treatments comes from the failure of earlier medicines, such as Antabuse (disulfiram). Another reason for rejecting drugs in the treatment of addiction is the frequent use of medicines in the treatment that are themselves addictive. Many alcoholics treated with benzodiazepines (Xanax, Valium, Librium) or barbiturates to reduce alcohol withdrawal symptoms have ended up being addicted not only to the alcohol but also to these drugs. Indeed, the policy of prescribing these addictive medicines to patients with a proven propensity to abuse alcohol would be highly questionable if were not for the fact that they do in fact greatly reduce the risk of fatality during acute withdrawal. But naltrexone and nalmefene are not addictive medicines. They have no abuse potential. In fact, they are not mind altering at all and have no subjective psychoactive effects. Patients normally cannot distinguish them (at least in clinical doses) from placebo (inactive, sugar pill). The only time they have an effect is when endorphins are released in the brain (or opiates taken) – which they block completely. Otherwise, they just sit there in the receptors, doing nothing.   
  
Q: What would the world be like if the Sinclair Method were universally adopted like, say the vaccines against childhood disease or antibiotics for infections bacterial diseases?   
  
A: This is a very interesting possibility to consider. The potentials for the Sinclair Method are much broader than only the effective treatment of excessive drinking. A large part of the problems facing our world today are caused by behaviors that have been learned too well and thus become compulsive. If the reinforcement of these behaviors involved the opioid system, they could be extinguished with the use of naltrexone or nalmefene. The most obvious application is heroin addiction. Naltrexone would certainly work, but one cannot advise heroin addicts to shoot up and we should not give naltrexone to them without prior detoxification – first taking them through the arduous process of withdrawal. The likely solution here is to switch them to a legal opiate, such as methadone or buprenorphine, then after detoxification have them take methadone or buprenorphine after first taking naltrexone. This is effective in rats, and clinical trials are planned in humans. There is growing evidence that the naltrexone induced extinction may also be effective with cocaine and amphetamines. Thus, in some future world we might control these addictions at the demand side effectively and inexpensively, rather than with the supply-side as the War on Drugs costing billions and producing questionable results proves. The treatment may also be effective with compulsive gambling as suggested by one published clinical trial. For instance Grant and associates (2006) concluded in a study of 207 pathological gamblers published by the American Journal of Psychiatry that there was a statistically significant reduction in the severity of pathological gambling those who received low dose nalmefene (25/mg/day) while higher doses (50 mg/day and 100 mg/day) resulted in intolerable side effects.14 Extinction of eating sweets with naltrexone has been well established in rats. It is possible pharmacological extinction may be effective for other maladaptive behaviors mediated through the endorphin-opioid system in the brain. Bulimia – excessive eating followed by purging may cause self-reinforcing endorphin release in the brain thereby lending itself to pharmacological extinction via naltrexone – or in this case it might be better to use the short-acting naloxone. More controlled clinical trials are planned. There is anecdotal evidence that naltrexone can extinguish obsessive sexual behaviors, self-harm, and self-mutilation. Extinction may also help with thrill seeking criminal activities such as kleptomania. Other possibilities range from compulsive shopping, obsessive Internet surfing to voyeurism, self-sacrificial suicidal terrorism. So, imagine a world in which these and similar behaviors no longer get out of control, a world in which one could trim one’s behaviors as simply as we trim our fingernails. Imagine the savings to society. Imagine really having control over your own behavior. Pharmacological extinction – the Sinclair Method could become a new branch of medical science. If it does indeed work as well with these other applications as it does with alcoholism, the world will never be the same again.   
  
Q: What is success in treatment and how is this defined?  
  
A: The best answer here is that success is reaching whatever goal the patient realistically sets. If the patient wants abstinence, then only abstinence meets the criteria for success. If the patient wants controlled drinking, then drinking in moderation is success – and it might be added that total abstinence here would not necessarily be considered a success. When patients treated with the Sinclair Method have been asked after about 4 months if they are satisfied with the results, about 75% have said yes. This happens to coincide rather closely with the 78% success rate seen with external criteria. In this case the criteria were a reduction in drinking to safe non-harmful levels. Of course, one can set more exacting criteria as was done in the first Finnish clinical trial in which success criteria required never having drunk more than 4 units a day or on more than 4 days a week over 8 months.   
  
Q: Can I become re-addicted if I stop taking my medication? If so, how long would it take?   
  
A: If you are not drinking and you stop taking your medication, you will not become re-addicted. In fact, you should not take your medication when you are not drinking. But, you most certainly can become re-addicted if you ignore the Golden Rule and drink without taking your medication. If you are addicted to alcohol, it is because you have inherited the genes for alcoholism and also because you have practiced drinking over many occasions. The Sinclair Method does not alter your genetic code. Thus, you will become addicted again if you drink without taking the medication. This will not happen overnight – much like an eighteen-year-old who does not become an instant alcoholic simply by walking into a pub and having a few drinks. Becoming addicted to alcohol takes time. But since you have already learned to drink excessively, crave alcohol, and drink over the weekly safety limits, you will easily relearn your drinking pattern within 3 to 6 months. It is well established that extinguished behaviors are relearned more rapidly than they were learned the first time round. The three year Finnish follow-up study did in fact show that patients who stopped taking naltrexone before drinking had indeed increased their craving and drinking, and the majority of these were back at the high levels they had been before treatment – the only difference being that their liver function had improves as a result of the pause in drinking.   
  
Q: If my problem is severe and I am drinking vast quantities of alcohol do I have to go through detoxification in a hospital or clinic?  
  
A: There is a limitation with the use of naltrexone. It cannot be prescribed for patients with severe liver damage. Therefore, a small percentage of patients seeking treatment with naltrexone have to be rejected. The usual solution for them is to go into detoxification to first rest their livers. This takes care of the physicians responsibility not to prescribe naltrexone to patients with elevated markers of liver damage. There is, however, some question whether it really is appropriate. It is true that a short period of time without alcohol will lower the marker values because they really are recording what damage has been done to the liver recently, but the liver itself does not recover so quickly. Consequently, the doctor giving a naltrexone prescription to a patient after only a short period of abstinence will still be prescribing naltrexone to a person with liver damage. Experience with the clinics in Finland, however, suggests that it did not matter. Patients who had come to the clinics, hoping to begin treatment without having to go through detox, who nevertheless were sent away for detoxification never came back to the clinics. The newer antagonists, nalmefene, should not have this limitation and would be a better solution, but it has not yet receive official approval yet.   
  
Beyond this, the beauty about the Sinclair Method is that it does not require detoxification and withdrawal in a controlled hospital setting. The process is done on an outpatient basis and with minimal demands on the time of the physician and therapist.. As the weeks pass and you automatically start to drink less and less, you will gradually begin to detoxify. De-addiction occurs without will power or effort. Raised liver enzymes, craving, and actual drinking levels reduce to safer levels. Generally, you will not experience the unpleasant symptoms associated with withdrawal. Naltrexone + Drinking allows you to withdraw very slowly and you will not need the benzodiazepines or barbiturates normally prescribed to help cope with withdrawal. Occasionally, as you may remember from Richard’s story in the Case History chapter, exceedingly heavy drinkers experience withdrawal as naltrexone causes them to reduce their drinking very rapidly or even stop. However, this is an exception to the rule. The best “medicine” for counteracting the effects of alcohol withdrawal has been known at least since the time of Sumeria to be alcohol itself, so the gradual tapering off of drinking usually prevents most symptoms. In any event, you should be given therapeutic support along the way and you work scrupulously with your doctor and therapist. Just because it can be cured so easily with pharmacological extinction, alcohol addiction should not be underestimated. Addiction to alcohol is not a joke – it is a very serious, often life-threatening, ailment. The Sinclair Method is not an overnight cure, but it will cure you if you follow the program meticulously. Keep faith. Incredible as it might now seem to many of you, you have every reason to expect success.   
  
Q: What can I realistically expect from treatment on the Sinclair Method?  
  
A: You can realistically expect to be cured. If you were an alcoholic rat you could expect virtually a 100 % chance of being cured. Human alcoholics can expect about an 80 % chance of being successfully de-addicted over the long-term – about 90% if you comply with instructions – the highest success rates for alcohol addiction ever recorded. Most people notice a reduction in their craving and drinking – as reflected in their drinking diaries – within the first month, but they must not stop then. Good control of drinking can be expected in about three months, but the rule that naltrexone is taken before drinking must be followed indefinitely   
  
Q: How about group therapy?  
  
A: Group therapy can be a powerful adjunct to treatment. Many patients though, prefer private consultations because they have been through the most terrifying emotional experiences as result of their addiction. Many suffer immense guilt and self-recrimination over past hurt caused to others. Sometimes, private psychotherapy sessions are very helpful to help overcome these issues. Patients can see that their past self-destructive behavior was in fact caused by their physiological addiction and not because they are inherently “bad”, “weak”, or “depraved” human beings. However, group therapy enables patients to see that they are not alone, that others have been in similar situations. In addition, group therapy can serve to reinforce the positive outcome as patients see how others further ahead in the treatment have progressed. Group therapy may depend on cultural factors. While it may be more acceptable in the US and UK, in general it was not at all popular in Finland - birthplace of the Sinclair Method - perhaps because of the reclusive, private nature of many Finns. Its popularity may also depend upon the therapist; some are very good at working with groups, while others are better in a one-on-one situation. People, however, tend to be far more open to self-help groups and group therapy in the US and UK, and this is very much in their favor. Group therapy also has the advantage of being cost-effective because several patients can be treated simultaneously, and they can support each other in their common de-addiction goals.   
  
Q: Is there such a thing as an addictive personality and how much truth is there to this concept?   
  
A: The term “addictive personality” is a colloquial term. It is not uncommon to hear people say, “Thankfully I do not have an addictive personality”, or “I dumped him because he had an addictive personality.” The truth is that the personality is not “addictive” – it is the brain and nervous system that are genetically predisposed to addiction. For some people, addiction may take the form of substances like alcohol, cocaine, heroin, or amphetamines. The addiction may involve one or more substances. However, the addiction may also take the form of a behavior. This is currently a subject for ongoing research. It looks as though compulsive behaviors like gambling, certain sexual deviations, kleptomania (shop lifting), and self-destructive behaviors (like self-mutilation) may be mediated through the opioidergic system in the brain. In other words, the addicted gambler’s brain secretes endorphins, which then stimulate the opioid receptors causing the pathways to grow. The gambler seeks further gratification because the opioid pathways associated with gambling become like highways. When he stops gambling more opioid receptors associated with gambling literally pop up in his brain. This is a deprivation effect and the same thing happens with alcohol addiction. The popping up of opioids receptors associated with gambling deprivation causes craving. This is why triggers like passing a sign saying “CASINO” on a highway can be as dangerous for the compulsive gambler as triggers such as being in a bar and seeing a cold beer are for the abstinent alcoholic. Addictive gambling is a very powerful addiction. Like all addictions it is irrational. As with alcohol, knowledge of the dangers do not prevent relapse and the compulsive gambler can easily ‘binge gamble’ away his home and savings just to get the jolt of reinforcement caused by the secretion of endorphins and perhaps other substances in the brain. It may seem as though the gambling were planned. But the thinking about gambling is brought about by the Gambling Deprivation Effect – as the interval between gambling events lengthens, the craving goes up. All of this happens unconsciously and reflexively. The concept of addiction as the result of “character flaws” or “addictive personality” is not sustainable – or for that matter helpful - in scientific terms.  
  
The search for the “alcoholic personality” was one of the major quests of alcohol research half a century ago. Perhaps this was based on the mistaken hypothesis that alcoholism was caused by people trying to correct their personality defects by drinking. Consequently, acommon mistake has been to assume that detrimental personality traits are correlated with a high risk of alcoholism. People expect features such as depression, strong reactions to stress, and maladjusted personalities to be associated with alcoholism, perhaps mistaking characteristics caused by the problems caused by alcohol with characteristics that help cause the addiction. Similarly, visiting researchers and students would come to Sinclair’s laboratory with the preconceived belief that the high drinking AA rats would be found to be very sensitive to stress, shy, and easily frightened. The experiments have shown, however, just the opposite. There are “personality” differences between the lines, but it is the low drinking ANA rats that cannot cope with stress well. The best word for characterizing the AAs is “cool”. They are particularly fond of strong stimulation, strong flavors, novel experiences, and open spaces. They are good mothers. And they are the rats that will bite you if you pick them up the wrong way. One might say they are the Hells Angels of the rat community. There is also a resemblance to the Cloninger type 2 alcoholics who generally have a family history of alcoholism, early onset, and low avoidance of harm. 15 There is, however, also the Cloninger type 1 alcoholics with quite different personalities. They generally do not have a family history of alcoholism, so the rat equivalent would not be produced by selective breeding. The experimental evidence suggests that there is not just one type or even just two types of personality associated with alcoholism but rather several types, and often the characteristics are not detrimental in themselves.  
  
One of the rules Sinclair imposed on clinics working with him was that the alcoholics had to be treated with dignity. It was true that many (but not all) of the patients coming in for treatment did not initially inspire feelings of respect. Once the treatment was well underway and the characteristics caused by drinking had been removed, what emerged often were some of the nicest people you can imagine. It was important that the staff should treat them from the beginning in accord with the personality that potentially come out, rather than on the basis of what alcohol was doing to them. Of course, it was true that some of the patients were bastards when they came in, and bastard after they were cured; nevertheless, they still were treated with dignity.   
  
Q: What is “selective extinction” and why is it an important feature in the Sinclair Method?   
  
A: Other behaviors that are reinforced by endorphins can also be extinguished if they are performed while naltrexone is present. Some of the clinical trials have found that interest in sweets, sex, and vigorous exercise has been reduced by the treatment. We don’t want this. We want to extinguish only alcohol drinking and, if anything, build up the other behaviors. This can be accomplished by selective extinction. Patients list before treatment what activities they enjoy. The therapist checks the list, marks the ones thought to be reinforced by endorphins, and advises the patient to try to avoid doing these things while naltrexone is in their system. Then, after alcohol drinking has been extinguished enough that it can be avoided for a couple days, the patient is told to have a weekend without naltrexone and without alcohol. On Monday they know they can go back to drinking (with naltrexone). Meanwhile, Saturday is a washout day, giving time for the naltrexone to leave the body. On Sunday the patients perform some of those liked behaviors they have been avoiding. Since the opioidergic system is supersensitive after many days on naltrexone, these behaviors will be very gratifying and reinforcing. Thus the other behaviors are strengthened, while alcohol drinking is selectively extinguished. This also tends to improve the general satisfaction with life, whereas some studies have reported mild dysphoria from continual naltrexone – when it is in your system all the time.   
  
Q: Will naltrexone sober me up is I have too much to drink? Will it at least reduce my hangovers?  
  
A: Emphatically no on both counts! Naltrexone will not sober you up if you take it and drink enough to get drunk. It will not cause your blood alcohol levels to drop. Alcohol affects many systems in the brain. You will still loose motor control, be impulsive, and suffer hangovers from too much drinking. Naltrexone blocks the effects from its release of endorphins but not the effects of alcohol on other systems in the body. Apart from causing endorphin release, alcohol itself exerts numerous effects on the brain and virtually every other organ in the body. These other systems are responsible for most of the behavioral impairment from alcohol. In fact, experimental results suggest that certain aspects of intoxication may be even slightly worse with naltrexone and alcohol than with alcohol alone16. For example, the ability to divide you attention and respond to stimuli you were not paying attention to appears to be worse with the combination of naltrexone and alcohol. This skill is important for operating a car. Remember, you could still kill yourself and others if you drive while drunk even if you are on naltrexone. Naltrexone is known to reduce the stimulatory effects of produced by low doses of alcohol. In humans, the stimulatory effects are seen most commonly as increased amounts of talking. So you might find that you are a bit quieter on naltrexone and alcohol than just on alcohol alone.   
  
Q: Why do people start drinking in the first place?  
  
A: Drinking is primarily a social activity, one that has been with us for thousands of years. Records of drinking exist in ancient civilizations in Mesopotamia, Egypt, Greece, Rome, India, and China. Drinking is mentioned throughout the Old Testament, and wine is a regular part of Judeo-Christian religious ritual. Jesus is said to have changed water into wine on one occasion. People start drinking mainly because alcohol forms a basic part of the fabric of society. Consequently the age and manner in which people start drinking will reflect the cultural norms. One culture may sanction giving diluted wine to young children at meals, while another demands abstinence until the age of 21 or for life. “Real men” are said to be able to “hold their liquor” and most societies have folklore based on this belief.. It is part of normal life in most societies, even though about 10 % of most populations are genetically at risk for developing alcoholism if they start drinking. Some religions forbid drinking. We can speculate that, in Islamic culture, this was perhaps because the risk of developing an addiction to alcohol was thought to be too high a price for society to pay. In addition to the larger culture, the particular practices of the family help determine when alcohol drinking begins. People generally start drinking because it is the time and place when their culture and their family considers it appropriate, with role modeling being an important factor. Of course, the standards of the other kids in the community will often be important. Generally people drink alcohol if alcohol is available. Many learn to enjoy the taste of wine, beer, and stronger drinks. It should be stressed that in most societies the majority are not at risk of becoming alcoholic. But remember that 10 % do not protected as a result of inheriting the genetic diathesis enabling them to become very effective drinkers. In the US, this is reflected by the official NIAAA figure of 17 to 18 million problem drinkers in the country. European countries have similar rates for alcoholism and problem drinking.   
  
Q: Why are some groups like North American Indians, Eskimo, and Aboriginal peoples in Australia more prone to alcoholism than other groups? Are the Chinese and Japanese less prone to alcoholism ? Are the Scandinavians more “alcoholic” than say, the French?   
  
A: This is a question that has been dealt with by geneticists and epidemiologists. There now is a general recognition that genes play a crucial role in the development of alcoholism, but cultural factors also are important. Certain groups, like some groups of North American Indians and Aboriginal peoples of Australia appear to be far more at risk of developing alcoholism. There have been various explanations proposed. A widely supported idea is that the risk is caused by alcohol being so new to the culture that it has not developed the cultural traditions for controlling the harm and the genetic characteristics for dealing with alcohol that other cultures have gained as a function of natural selection over many generations of exposure to alcohol. The North American Indians and Aboriginal people in Australia were more or less isolated from alcohol - either because it was not readily available or proscribed. Strong alcohol had only been introduced into their societies within the past few hundred years. Thus, their “genetic resistance” to alcoholism is very low. In contrast, Europeans have been exposed to alcohol for thousands of years. It is thought that natural selection related to alcoholism is further developed among the Europeans - the idea being that their alcoholic offspring died before reproducing and therefore they did not contribute the alcoholic gene pool. By contrast, the gene pool in North American Indians and Aboriginal peoples still carries more of the alcoholic prone gene and places these groups at high risk of developing the addiction.  
  
A minority of Chinese and other Asian people have an inability to rapidly metabolize the acetaldehyde produced in the body from alcohol. This is because they have a different form of the enzyme that normally turns acetaldehyde into harmless vinegar. When they drink the acetaldehyde accumulates in the blood, causing the individual to experience unpleasant symptoms of flushing and palpitations. The unpleasant association of these symptoms and drinking alcohol inadvertently protects these populations from becoming alcoholic because they automatically do not like alcohol and, therefore, avoid it in the first place. Thus many of them do not start drinking in the first place and this prevents them from learning the addiction. Those who get the mutation for a less effective enzyme from both parents may be completely protected from alcoholism. It appears, however, that people who have inherited the mutation from only one parent may be able to “drink through” the initial unpleasant flushing caused by alcohol and may occasionally become addicted. The rest of the population in China and Japan, at least, drink alcohol in quantities similar to that in Europe. In Japan, for instance, binge drinking is a relatively frequent occurrence.  
  
People often assume that there is more alcoholism in Scandinavia than in Southern Europe. This assumption is based on the observation that drunkenness is more often observed in the streets of Helsinki, Oslo, or Stockholm than in Paris, Athens, or Rome. In fact, the populations in Northern European countries consume about the same or less than their counterparts in Southern Europe – in terms of per capita consumption of alcohol.17 What differs is the culture and drinking style. People in Helsinki do all their week’s drinking on one or two occasions; they binge, whereas many Parisians and Romans spread out their drinking virtually every day over the course of the week. The opportunity to drink is another factor. Latest reports from the UK suggest a rise in binge drinking as new laws in 2005 – 2006 removed mandatory closing times and permitted drinking 24 hours . Cheap happy hours have contributed to a rise in binge drinking across the board.   
  
Q: It may sound like a simple question, but why do alcoholics drink? Do they drink for pleasure, to avoid withdrawal effects, to self-medicate against depression, to escape from painful living? Or are they simply “stupid”?   
  
A: This question cannot be answered because the question itself makes a false assumption. It is an assumption that nearly everyone makes, including clinicians. It is built into our language. There was an episode of the television show West Wing that illustrated the point very nicely. One of the characters was an alcoholic struggling to remain abstinent. On the day when the divorce papers came to him, his friends asked if they should come home with him that evening. At first he was puzzled, but then he understood them. “Listen,” he told his friends, “I’m an alcoholic! I don’t need a reason for drinking. I’m wired to drink.” Alcoholics do not drink for pleasure, nor to escape unpleasantness, nor indeed for any purpose – they drink because their brains have become wired to make them drink.   
  
The belief that compulsive drinking is under rational conscious control has led to unsuccessful treatments for the disease and an untold amount of needless suffering and pain. Because of the assumption that abusing alcohol is a rational behavior chosen logically to maximize pleasure and minimize pain, the most common treatment has been to punish drinking.   
  
Just add a bit more pain to the drinking half of the equation and the rational alcoholic will choose not to drink. This is the theoretical basis for subjecting alcoholics to useless punishment. Spouse threaten to divorce them if they do not stop drinking, bosses fire them, relatives disown them, society imprisons them, and traditional treatment centers humiliate them. Their lives have been placed at risk from disulfiram (Antabuse) reactions if they relapse. A treatment used in the Soviet Union had alcoholics being told they had been given “super Antabuse” that would kill them if they drank any alcohol. Then they were given vodka “to taste but not swallow” and at the same time secretly infused with curare, a poison that leaves you completely conscious but paralyzed and unable to breath. It is one of the most frightening of all experiences. The doctors scream at the poor alcoholic, “Oh no! You drank some!” And then run around acting as if they are trying to revive the patient. Eventually the antidote to the curare is infused and the patient regains the ability to breath and move. The doctors warn him to never drink again; they will not be there to rescue him the next time. Interestingly, the report on this treatment then said that subsequently when the patients relapsed, they were incarcerated at a gulag. Punishment does not stop drinking. Theoretically, it should not been expected to succeed, Predictably, punishment makes patients drop out of treatment, escaping from the pain, and going some place else to continue drink. It does not stop drinking or the craving for alcohol. At the same time, this belief continues to blind people to the treatment that has been shown to be effective.   
  
Back in 1994 before we could fully appreciate just how effective pharmacological extinction with naltrexone can be, a personal tragedy related to alcohol struck Senator George McGovern. His daughter Teresa, who began drinking at 13, froze to death while intoxicated after battling her addiction for years through AA and countless rehab programs. In Terry: My Daughter’s Life and Death McGovern (1996) writes, “How I wish that the coming breakthrough in medications, procedures, and other scientific measures to prevent or contain alcoholism had been achieved before this awful disease killed Terry.”18   
  
The desire for pleasure, the need to avoid withdrawal effects, to self-medicate against depression, or escape from painful living did not kill Terry. Nor did stupidity. Terry died because she had become wired to drink, due partly to an inherited brain biology – addiction featured prominently in her family – that made her especially sensitive to endorphins. Today, such tragedies are utterly unacceptable. They are merely an expression of gross negligence in light of the research proving how a once intractable disease such as alcoholism can be cracked with relative ease.   
  
Prior to the Sinclair Method, the strongest factor predicting success in treatment was a religious rebirth or a major change in the patients’ environment. If they drank in the countryside, moving to the city tended to improve their chances. If they drank when married, divorce was good. This makes perfect sense since alcohol drinking is a reflex learned to specific environmental stimuli. If these triggers are not present, or have changed, the craving reflex and drinking are less liable to be triggered.   
  
The best known example of this is with heroin addiction among American servicemen in Vietnam. At first, there were fears there would become a massive problem with addiction when they came home. However, most kicked the habit with little problem.   
  
This does not make sense from the rational view of drinking or drug addiction. Heroin should be as pleasant in San Francisco as in Saigon. Alcohol is as euphoric in the city as it was in the countryside.   
  
Similarly, the ability to understand extinction and to use it properly has been hurt by the common sense view that we only do what will bring us pleasure or reduce our pain. There is no possibility for extinction in a brain controlled by a rational little person inside the brain - a homunculus - choosing to get pleasure and avoid pain. So long as you imagine that all of your behavior is rationally chosen by that homunculus, you will be incapable of imagining that there even is a process of extinction. But if you can instead imagine that a behavior is caused by a pathway of neurons firing – which, of course, is true – then it is easy to imagine that there would be a process that in effect cuts the pathway and thus extinguishes the behavior.   
  
One of the main reasons for this book is to provide people with a different view of their own brains. To see it as a “self-organizing system.” Like a flock of birds or a school of fish, each of the hundred billion neurons only knows what its neighbors are doing. No leader bird decides the flock should land on the tree outside my window. No leader neuron (or homunculus) decides that alcohol should be drunk. In both cases, the results are simply the natural outcome of the self-organizing system in that situation. Extinction is an effective and natural tool for changing the self-organizing nervous system. The alcoholic drinks because that is how he has become wired. Extinction is the brain’s own wire-cutter.   
  
Q: How do the “anti-craving” drugs acamprosate (Campral ®) and topamax (Topiramate) compare with naltrexone? Would the two work better together than either alone?  
  
A: Acamprosate (Campral ®) has received some interest as an “anti-craving drug” for alcoholism. This drug acts on an entirely different mechanism than naltrexone. It does not block endorphins or opiates in the brain the way naltrexone does. Acamprosate affects neurons using glutamate the primary excitatory neurotransmitter in the brain. It had earlier been thought to work on the GABA neurotransmitter system in the brain, the primary source of inhibition and the same system as effected by the benzodiazepines (Valium, Librium, Xanax) and barbiturates but does not have the same ant-ianxiety, hypnotic, or muscle relaxant properties. No one knows exactly how acamprosate functions, but currently the best hypothesis is that it blocks the Alcohol-Deprivation Effect (ADE). Many years ago, Sinclair proposed that ADE is related to the increased desire we have to make any behavior that we haven’t been able to do for a while,19 and that all of them were produced simply by upregulation of glutamate receptors and the resulting supersensitivity of neural pathways that had not been used for a long time.20 If acamprosate somehow prevented the glutamate upregulation or blocked the resulting glutamate supersensitivity, it would suppress deprivation effects including the one caused by not drinking alcohol. Therefore, it might be good to use acamprosate in patients who are abstaining (alcohol deprived) and naltrexone in ones who are still drinking. Another possibility is to use naltrexone first, while patients are still drinking, and then after months of treatment when the patients are abstinent much of the time, or even all of the time, to use acamprosate, switching medicines of course on drinking days. Merely given both naltrexone and acamprosate at the same time was shown in Project Combine, to provide no more benefits that naltrexone alone, but then it also failed to find significant effects if acamprosate alone. Topiramate (Topamax ®) is an anticonvulsant drug used in the treatment epilepsy, bipolar disorder (manic depression), and migraine. It is thought by some to help stabilize mood during withdrawal and abstinence from alcohol. However, neither drug can reverse the damage done to the permanently over-strengthened system maintaining alcohol addiction and driving the craving – as naltrexone does with the Sinclair Method. While these medications may help somewhat with craving reduction, they cannot restore the brain to its original pre-drinking, pre-craving state. While they may be useful clinically to reduce craving and relapse in patients struggling with the normal goal of total abstinence, they are definitely not “curative.” They may be helpful with the goal of abstinence against a permanently entrenched addiction (you remain addicted), but unlike Pharmacological Extinction they do not help to move the addiction from the brain.   
  
Q: I drink too much, that’s for sure. My family and doctor say so, too. The point is that I don’t want to cut down because I think I’m more fun and entertaining when I’ve had one too many. Give me one reason why I should use naltrexone and cut back on my drinking?   
  
A: Of course, it is entirely up to you. We would ask you to think about the effects of excessive drinking on your health and social relations? How is your liver? Your heart? Have you hurt others as a result of your excessive drinking? Have you driven while over the limit? Do you loose your judgment when you’ve had too much to drink? Does drinking make you over impulsive or self-destructive? Do you feel guilty about your drinking but thinks it makes you more fun – the life of the party? Have you tried to limit yourself yet find that as soon as you have had one or two drinks you find yourself going the whole way? We should point out that while people often think they are more entertaining while intoxicated, usually those around them do not agree. The effects of alcohol vary enormously from person to person. Some people loose judgment and say and do things they later regret. Others, of course, do not. Which are you? Remember, the Sinclair Method is not only meant for those with heavy addiction. It is also designed to end less intense drinking problems where “having one too many” has a negative impact on you and others. Remember, as long as you take naltrexone beforehand you can still carry on and enjoy socializing while you drink. Naltrexone does not block alcohol intoxication; you will still stumble and fall; you may still put the lampshade on you head.   
  
Another good reason is the future. Your alcohol drinking today is liable to lead to alcoholism in the future. Taking naltrexone before drinking today will help to prevent that from occurring.   
  
This is similar to the answer often given with regard to what is called the “J-shaped curve.” A great deal of data show that people who consume small amount of alcohol, roughly one or two drinks a day, live longer than people who abstain from drinking completely. The curve relating the amount one drinks to death rates is shaped something like the letter J. The death rate goes down as drinking increases from 0 drinks per day on to 1 or 2 drinks a day. Of course, the death rate then goes back up as drinking increases to 3 or 4 drinks a day, and it then goes on to much higher levels when even more alcohol is consumed. Some people ask, therefore, what is the harm in having a couple drinks a day. The answer is “none” if you can keep your drinking at that level. Unfortunately many people cannot, and because alcohol drinking is learned, the reinforcement one gets from the two drinks may strengthen the behavior progressively and soon you find you are no longer at the bottom of the J but on into the level where you are greatly reducing you life expectance. Unless you take naltrexone before drinking, in which case the endorphin reinforcement is blocked, and the drinking levels will not rise.   
  
Q: Because of that J-shaped curve, if I use the Sinclair Method, am I not better off choosing moderate drinking as my goal rather than becoming a teetotaler?   
  
You may be right. Moderate drinkers do live longer than teetotalers. It is especially clear for middle-aged men with a risk of heart problems. This also could be seen as a further advantage of the Sinclair Method. It is the only treatment for which moderate or social drinking is an acceptable goal. All others must follow the dogma that “One drink is too many (and 100 is not enough)”. This would suggest that only the Sinclair Method allows patients to enjoy the health benefits from moderate drinking. Unfortunately, the data are not good enough to make this conclusion with confidence. The J-shaped curve is for the general population, or for the general population excluding recovering alcoholics. We do not know yet whether the benefits from moderate drinking also are bestowed on former alcoholics.   
  
Q: I never drink alone. Doesn’t this prove I don’t have a drinking problem?  
  
A: There is a popular misconception that if you do not drink alone, you do not have a problem. You can have a problem whether or not you drink alone. If you drink over the accepted safety limits listed in Chapter 4, find that others worry about your drinking, or find yourself drinking to excess too often, you probably have a problem. The CAGE and AUDIT questionnaires mentioned in Section II and reproduced for you in the Appendix are intended to help you assess the problem. One can learn to drink excessively in many different environments, alone or with friends. There is the advantage in doing so with friends that they may care enough for you to point out that you are drinking too much. Sometimes it may be a good idea to listen to what others tell you. But it is also possible that the entire gang may be drinking themselves toward alcoholism. If the group is just a random assortment of people, it is unlikely that all of them would have had the genetic predisposition to develop alcoholism. It is more likely that they all will have the high risk, however, if group membership is based on some characteristic correlated with alcoholism, such as, members of a motorcycle gang, fellow poker players, or simply drinking buddies.  
  
Also listen to what you are saying to yourself internally. Do you find yourself rationalizing why you have a good reason for a serious round of drinking? Do you ever feel guilty about drinking too much? Do you loose your “I’ve had enough” or “switch off button”? Alcoholism has less to do with “how much” someone is drinking, and more to do with what happens when you do drink. Basically, if you have problems when you drink, you have a drinking problem.   
  
Q: Why are so many people afraid of coming forward for treatment?  
  
A: Many people are deterred by the stigma associated with the label alcoholic, lush, or drunk because the association with failure – and who wants to associate with losers? Others dread the detox and the shakes, depression, and anxiety that go along with traditional rehab. The terror of never again being allowed to drink again is another major factor preventing people from coming forward for help.   
  
Despite numerous celebrities who show up at glamorous rehab clinics, the treatment process is still perceived as punishing. You have to get up early, cannot lock your door, confess past sins, and conform to many other strict rules. Past failures with personal will power, abstinence-based treatments such as AA, the harsh reality that submitting to rehab means saying goodbye to your best friend – the bottle – for life. Traditional treatments are also associated with high fees and the threat of future relapse. Many people unconsciously sense that talking about the damage alcohol has caused is no guarantee against relapse and that they will simply have to live with alcohol cravings for the rest of their lives. Another factor is the discrepancy between one’s own drinking behavior and that model of the rational person that we assume is the basis of sanity. Our culture teaches us that a sane person chooses pleasure and avoids pain. A sane person has good rational reasons for their behavior. Alcoholics then look at their own behavior, and it does not match that ideal. One solution for them is to manufacture rational reasons for their drinking: my wife left me, the boss mistreats me, stress and tension, the world situation. Another solution is to deny that one has a drinking problem in the first place. No wonder so many fear coming forward for a month of detention in rehab. This may explain why many go to great lengths to deny they have a drinking problem until they “hit rock-bottom.” But the Sinclair Method offers an entirely new solution. The solution provides a dignified, humane, and effective alternative.   
  
Q: I have heard about once-a-month slow-release naltrexone or nalmefene injections such as Vivitrol® or under-the-skin slow-release implants. Are they a good idea?   
  
A: Time-released naltrexone is available and slow-release nalmefene is planned for release. These formulations ensure that naltrexone or nalmefene are released slowly and continuously into the blood-stream, and are always in your body. When this happens the opioid receptors are blocked continually for a month or more. There are some advantages to this procedure over taking pills orally, but there probably are some disadvantages as well. During the first weeks of treatment, most alcoholics are drinking every day, so they are taking naltrexone every day. During this time there is an advantage to the slow-release procedures, at least from the perspective of many clinicians. They can tell the patients not to drink. If the patient is exceptional and actually able to obey the instruction, the alcohol drinking has been stopped. On the other hand, if the patent does relapse, naltrexone administration cannot be stopped at the same time as drinking starts, as happens with pills. Consequently, the patient is drinking while on naltrexone and thus having the craving and drinking extinguished. And indeed there have been very nice positive results obtained with the sustained release monthly naltrexone injection branded Vivitrol® in the US. 21  
  
There also would be advantages in treating patients who are unable or unwilling to take naltrexone pills. This opens the possibility of forcing individuals to have the treatment.   
  
The likely disadvantages come with regards to alternative behaviors and the long term effects that have not yet been examined with the slow-release preparations. It is impossible to use selective extinction together with the slow-release procedures, since it is impossible to stop administration and be free of naltrexone when practicing other opioidergically-reinforced behaviors. You may weaken other behaviors like eating sweets, enjoying sex, or jogging by doing them at the same time naltrexone is in the body, and it is impossible to take advantage of pharmacologically-enhanced learning to restore and strengthen these alternative behaviors.   
  
As the 5 Steps showed, selective extinction involves only deleting unwanted behaviors such as excessive drinking, but not desirable alternative activities. This means that you should be on opioid antagonist medication only during periods when you are drinking but not when you are abstaining. After all, you do not want to reduce positive behaviors. You want them to be more enjoyable than ever and you want them to be strengthened, easing your way back into a life that is no longer dominated by drinking. Selective extinction represents the state-of-the-art in de-addiction.   
  
The other apparent disadvantage of the slow-release preparations is that there is no clear guide for how to use them on a very long term bais. The Sinclair Method has provided a guide for how to use the pills. The patient starts out using a naltrexone pill and drinking nearly every day, but soon has a weekend off when no pill and no alcohol are taken. The periods off of naltrexone and alcohol then become progressively longer. By the three year follow-up, weeks would go by without taking naltrexone and alcohol. With the slow-release preparations, it may be possible for the patients to continue getting naltrexone injections the rest of their lives, but that of course would be expensive. In addition, the side effects from years of continual naltrexone have not yet been established. If instead, the naltrexone injections are stopped after some period of time, e.g., 6 months or a year, it is predictable that nearly all of the patients will eventually start drinking again and then will relearn the behavior, so that within a few months they will be back to drinking at the same high levels they had before treatment.   
  
An obvious solution would seem to be starting on Vivitrol® and then switch after a month or so to oral naltrexone with selective extinction. So far, however, this solution has never been tested.   
  
Q: I have been for inpatient rehab several times. I have been an outpatient. I have seen several psychiatrists and other therapists over the years. I have enrolled in 12 Step programs - but every time I relapse back to heavy drinking. Why should the Sinclair Method work for me?   
  
A: The research proves that most other treatments are effective in terms of total abstinence at one year at rates of 10 to 15 %. This means that your chances of failure were always about 85 to 90 %. Not only is the Sinclair Method successful in 80 % of cases, but you never have to stop drinking altogether. Total abstinence may be a desirable goal, but drinking normally within World Health Organization safety limits is an equally worthwhile objective. It sounds as if you have a relatively powerful alcohol-deprivation effect. The treatments you have tried are effective for increasing will power but there are limits, and apparently your alcohol-deprivation effect has been so strong that eventually the craving overcame the will power to abstain. None of these treatments reduce craving – and none of them claim to. They only build up your psychological ability to withstand the craving. The Sinclair Method, however, has been shown to extinguish the craving, gradually but progressively weakening the craving, week by week and even year by year. As mentioned before, with all other treatments the outlook for the patients becomes progressively worse the longer the time since the beginning of treatment, and for you and most others, the relapse inevitably happens. With the Sinclair Method, however, the direction is for continual improvement over time.   
  
Q: In terms of relapse, how important are trigger situations?  
  
A: Triggers are very important. Drinking is learned in association with stimuli. All of the stimuli that have been around when you were drinking in the past have the ability of triggering craving and more drinking. Triggers might be passing a pub, being with old drinking buddies, or passing a favorite restaurant where you enjoyed great red wines. Hangover becomes a trigger for people who have used the hair-of-the-dog hangover treatment previously. Particular moods can also be learned asdrinking triggers.   
  
What to do with regard to the triggers is quite different with pharmacological extinction than with earlier treatments. People attempting to stay sober through absolute abstinence programs are told to avoid certain places where they used to drink, lest they be tempted to relapse. They are told to avoid drinking buddies unless the buddies themselves can be brought into the treatment. Many people avoid socializing because they fear temptations to use alcohol are too high. However, with naltrexone as used in the Sinclair Method, trigger situations are nothing to fear. Instead, you can even look forward to your triggers knowing they are being gradually extinguished as you drink on the medication. The recommendations with the Sinclair Method are to practice drinking after taking naltrexone with all of your triggers – all of the places and mood to which you have learned to drink. Thus, going to a party need not be fraught with the fear of relapse. Remember, always take your medication before you do. You will drink there. Perhaps too much to start with at the beginning of your treatment. But within a month or two your drinking will have decreased. By the end of three to four months you have an 80 % chance of being on top of the situation. There have never been such good odds in your favor.   
  
Q: Why do some people seem to survive massive amounts of alcohol over many years while other do not?   
  
A: It is truly incredible how much some people drink and live to a ripe old age. Very heavy drinkers may not always feel physically great, but alcohol does not seem to kill all of them. Some people are more susceptible to the effects of alcohol, and die in their twenties. Yet somehow, others go on rather well, like Winston Churchill who drank diluted whiskey every day from morning to night, and lived into his 90s. Perhaps physiological resistance to the harmful effects of excessive drinking can be explained in terms of natural selection and inheriting certain genes.   
  
Research in Finland helped establish the fact that there are genetic factors controlling sensitivity to alcohol intoxication. Kalervo Eriksson there started not only the AA and ANA rat lines bred for high and low drinking, but also the AT and ANT rat lines bred for high and low innate tolerance to the effects of alcohol on motor coordination. A similar genetic factor in humans would help some individuals avoid alcohol-related accidents. There are indications that genetic factors may also influence the susceptibility to specific medical problems produced by long-term alcohol drinking, such as liver damage.   
  
Q: In AA they say, “Once an alcoholic, always an alcoholic.” So people introduce themselves at a meeting by saying, “My name’s Beth and I’m an alcoholic” even after 30 years of sobriety. Would this also apply to Sinclair Method patients, are they still “alcoholics”?  
  
A: It is true that the 10 to 15 % of patients who manage to stay sober and totally free of alcohol through AA and other methods are still addicted to alcohol. Their brains and nervous systems remain addicted - wired for life - even after years of abstinence. For instance, the alcoholic prisoner who has been locked up for twenty years without a drink can exit prison, and almost immediately end up drinking at his original dangerous levels. As far as his brain is concerned, he is still alcoholic. The years in prison do nothing to remove the addictive wiring in his brain.   
  
However, the wiring of the Sinclair Method patient’s brain is different. He no longer has the addictive circuitry etched into his brain by reinforcement from endorphins. He almost certainly is in better shape than the AA patient or ex-prisoner. He is most unlikely to binge even if he has a drink. Technically, he is no longer “an alcoholic” because the circuits driving his alcoholism have been removed. But he is at risk of relearning the addictive drinking pattern over the course of a few months if he starts drinking without taking his medication. In this sense he could say, “Hi, my name is Bill. I was born with a genetic predisposition to learn addictive drinking. Right now I have been cured of my drinking. But I could easily relearn how to drink and crave alcohol if I ever drink without taking naltrexone. Over time and through practiced drinking, I became an alcoholic. I went through the Sinclair program. Right now I am not an alcoholic. But I could easily become an alcoholic again if I were to start drinking without taking my medication. I have remained abstinent through choice. However, should I ever drink again, may I have the strength, wisdom, and courage never to drink without first taking my medication.” The wise Sinclair patient is aware of this, much like the wise traveler is aware that she should be inoculated against tropical diseases if visiting regions where tropical illnesses are endemic.   
  
Q: In fairness to myself, I think that I drink too much. I have not yet encountered much trouble from my drinking, but I note that when I go out to parties I tend to get drunk. My partner becomes irritated with my behavior. Can extinction help me?   
  
A: Extinction treatment will most certainly help you cut down. You probably have inherited a genetic tendency for alcoholism and although you might not yet be diagnosed with the condition, you may be on the road to a drinking problem. Discuss the option of using naltrexone with your doctor or therapist. You may find that using naltrexone before you drink helps you cut back the amount you drink – for example with typical party binging. However, you must be aware that it will not be effective if you take it sporadically – whenever you feel like it. It only works if you are consistent.   
  
Q: Will I still be able to enjoy a drink if I take naltrexone?   
  
A: The drink will taste the same as ever. Many people who were once only interested in getting as much of any kind of alcoholic beverage into their system find that, after a few months, they drink moderately on naltrexone and are now able to savor the aroma and taste of a fine wine in moderation for the first time in years. You will still be able drink socially and enjoy the company. You will still get intoxicated, although the initial buzz may be reduced and you may not feel any stimulation from the first drink. Once you are into the selective extinction part, you will find many other activities more enjoyable than ever. Almost all patients report a decrease in feelings of depression. The quality of life improves as alcohol problems disappear.   
  
As discussed earlier, drinking to excess is certainly not a rational behavior. The little bit of pleasure, if any, that the alcoholic gets from alcohol is no where close to the amount of pain, humiliation, and suffer produced by high levels of drinking. Using naltrexone to extinguish the addiction, however, is thoroughly rational.   
  
Q: Can you summarize the main discoveries behind the Sinclair Method?   
  
A: David Sinclair’s breakthrough in addiction science can be summarized through six main points. The value of these discoveries is now acknowledged by many senior researchers and is becoming increasingly accepted. We now have a real grip on what drives excessive drinking. We actually know how to treat excessive drinking and craving. In addition, we know how to prevent post-treatment relapses and also how to prevent the problem from happening in the first place. In essence, alcoholism can be solved by understanding the powerful role of these six factors:   
  
The Alcohol Deprivation Effect: Once a strong drinking pattern has been established in the nervous system, craving begins to build up when there is no access to alcohol for periods of time – days, weeks, months or even after twenty years without alcohol, craving can still be a problem. This finding undermined the old hypotheses for alcoholism and provided a powerful animal model for use in searching for a better treatment.   
Alcohol drinking is learned; Alcoholism is learned disorder: Nobody is born an alcoholic. Rather, excessive drinking is learned gradually over many, many practice drinking sessions in which all of the behaviors and feelings related to drinking and craving are reinforced.   
  
The Opioid Connection: Morphine is a substitution drug for alcohol. Therefore, the reinforcement from alcohol, like that from morphine, comes from activation of endorphin receptors.   
  
Pharmacological Extinction: The learned behavior of alcohol drinking can be weakened and removed by the mechanism of extinction. The extinction is produced by drinking while the reinforcement is prevented by a non-addictive medicine that blocks endorphin receptors, such as naltrexone, nalmefene, and naloxone.  
  
Pharmacological enhanced learning of alternative behaviors: Healthy behaviors that one can do instead of drinking can be protected from extinction and instead strengthened at the same time drinking is being extinguished by practicing them only during a pause in the naltrexone treatment when they can get exceptionally large amounts of reinforcement from the supersensitive endorphin receptors.   
  
Prevention: Excessive drinking can be prevented in “at risk” people - even before it has begun.   
  
Q: In a nutshell, what are the essential features of the Sinclair Method? Is psychological therapy an essential component of the therapy?  
  
A: As summarized in Chapter 3 and in the Annotated Bibliography, the evidence from clinical trials around the world confirm the findings over two decades ago from basic research with alcoholic animals. The conclusions are that combining active drinking with naltrexone is the most vital ingredient for success. The other essential features are:  
  
No prior detoxification or withdrawal is required before naltrexone is prescribed.   
  
Naltrexone is taken only when drinking.   
  
Other behaviors reinforced by the opioid system are avoided while on naltrexone and made on days when no naltrexone or alcohol is taken.   
  
Naltrexone is taken before drinking for the rest of the patient’s life. You do not take naltrexone if you are not going to drink.   
  
These features have now been shown in clinical trials to be safe and effective.  
  
These procedures are effective without any need to punish or demoralizing the patient. Consequently, a corollary is:   
  
Patients must be treated with dignity.   
  
Finally, we need to document the progress that is being made, partly for the sake of being able to demonstrate to others how the Method works, but also for your benefit. Therefore data must be collected. Complete, accurate data collection is especially important in the initial clinical trial for testing the Method in a new geographical area.   
  
There have been no clinical trials demonstrating that any one form psychological therapy is itself essential for use along with Pharmacological Extinction. Indeed, not only have there been no studies showing that one form is better than any other, there is no scientific evidence that psychological therapy is needed at all in the program. The results from the largest clinical trial in addiction research, Project Combine published in the Journal of the American Medical Association (2006) led researchers to the conclusion that naltrexone should be widely prescribed in general medical settings - without the need for intensive therapy.   
  
Although counseling is not necessary and the particular form of counseling used in Project Combine did not improve the results with naltrexone, it is likely that the right type of counseling and support are still beneficial.   
  
Perhaps a more important question is whether counseling, even of the right type, is cost-effective. The most expensive item in the treatment often comes from the counseling visits with doctors and therapists. Many more people around the world could be treated if the costs could be slashed without severely reducing the benefits.   
  
Q: What does the World Health Organization say about opioid antagonists for alcohol?   
  
A: Over ten years ago, a joint consultation organized by the Addiction Research Foundation, Toronto, and the WHO Program on Substance Abuse, Geneva and Toronto, Ontario, Canada, 23-26 October 1995 published its findings as follows: “At least one medication, naltrexone, has been identified as a safe and effective treatment for alcohol dependence…In addition, a number of other medications show promise (e.g. serotonergic agents, acamprosate). The demonstration of the efficacy of naltrexone and current studies underway examining related opiate antagonists (e.g. nalmefene) might serve to encourage pharmaceutical companies that medications development in this area is possible. Disulfiram (Antabuse), useful for some patients, might also be effective though its efficacy has been difficult to prove in controlled trials. Alcohol dependence is widespread and cuts across all socio-economic classes… approximately 10 % of the US population either currently or in the past has had an alcohol use disorder. These figures can be even higher is some other countries.”   
  
Q: How do you tell if a substance is addictive?   
  
A: The so-called hallmark of an addictive substance is determined by demonstrating if individuals will work for a particular drug. In August of 2000, the media became particularly excited by reports emanating from the 11th annual World Congress on Tobacco held in Chicago. It was reported that tobacco companies had known for over a decade, but had deliberately kept secret, the fact that nicotine is an addictive drug. A researcher called Victor DeNoble, had determined that nicotine-free cigarettes would not sell and would be a waste of time. DeNoble, who had worked for the Philip Morris company since 1980, discovered that rats would work for nicotine. In order to earn their nicotine reinforcement, the rats would have to press a bar in their cage many times before they could self-administer a dose of nicotine. It was said that Philip Morris forced withdrawal of DeNoble’s research article from being published. DeNoble’s research labs were shut down by Philip Morris in April 1984 as “inconsistent with the company’s positions in pending lawsuits.” 22 In any event, DeNoble had demonstrated that rats readily worked for doses of nicotine, and the media presented this information as though it were somehow ‘new evidence’ that nicotine is an addictive drug. In fact, there was nothing new about this at all. History is replete with examples of how nicotine becomes a powerful currency, a reinforcer, especially in times of deprivation. In situations of unspeakable deprivation, in concentration camps, for instance, people risked their lives for a smoke. Collected cigarette butts are a valuable commodity among the poor and homeless on the streets of any major city. Clearly, nicotine is addictive – all kinds of animals, including humans, would work for nicotine, and one wonders how there could ever have been doubt.23 A similar story occurred in Finland with alcohol research. In 1974, Sinclair published experimental results in the prestigious journal Nature proving that rats would work for alcohol, thus contributing to the literature confirming alcohol as an addictive drug. 24 This was done with full approval of the Finnish government alcohol company, Alko. Alko did not try to cover up the truth. If the litmus test for ascertaining if a drug is addictive is whether people will work for it, then one need go no further than England during the Industrial Revolution, or the introduction of wine-making into South Africa. In England, workers were partly paid in tots of gin quota by factory owners, and in South Africa, farm workers were partially paid, until as recently as 1995, on the dop system – with tots of wine. 25 Just like many modern workers today, the workers would spend their week in alcohol deprivation, and wait for the weekend when they could binge. The difference is that actual payment today cannot legally be made in alcoholic beverages, but a great proportion of weekly wages are nevertheless spent on alcohol with the result that parents, to satisfy their craving, ‘drink their work’, and often cannot provide the basics for their children.   
  
Q: Are heroin and morphine always addictive and how do they relate to alcohol – surely they are not in the same league – after all, alcohol is legal and opiates are illegal or require special prescriptions?   
  
A: There is a pervasive misperception that heroin or morphine and alcohol are so different that only a fool would confuse the two. Morphine and heroin are refined from the opium poppy while alcohol is produced through fermentation – the origins of the drugs were so different. Most people consider heroin and morphine as highly addictive, lethal substances, barely related to alcohol.   
  
Morphine’s status as a dangerously addictive drug has been the cause, ironically, of a great deal of unnecessary pain in patients who are suffering unspeakable pain. In a Scientific American article entitled The Tragedy of Needless Pain, Ronald Melzack (1990) suggests that morphine’s reputation as an addictive drug causes physicians to under prescribe it. Doses administered to children who have had amputations, suffer horrendous burns, or in the midst of cancer are often inadequate to control pain – despite Melzack’s work showing that for those in real pain, the risks of addiction are in fact very low. One wonders why some physicians treating terminally ill cancer patients still worry about causing addiction when the primary concern should be blocking pain.  
  
The first important research indicating that alcohol and morphine are closely related was Sinclair’s work showing that morphine reduced alcohol drinking at the time and morphine given during alcohol deprivation counteracted the increase in alcohol consumption normally seen.26 Sinclair tells, however, that he undertook the research with the expectation of proving just the opposite – that morphine was not related to alcohol consumption. Sinclair says the following about the unexpected connection between alcohol and opiates:   
  
“The story starts in 1970 with a idea published in Science by Davis and Walsh: an extremely unpopular idea! They dared suggest that alcohol drinking might be related to opiate addiction. To most scientists in the field, the idea was outrageous. They quickly pointed out that there is no cross-dependence: alcohol does not block the opiate withdrawal. Therefore, alcohol dependence could not be connected to dependence upon opiates.   
  
That's the objective explanation that was published.  
  
Subjectively, the idea was outrageous because, well, alcohol is the good stuff we take; heroin is the illegal drug they take!  
  
At the time I was a graduate student in psychology at the University of Oregon, working on my doctorate about rats and monkeys voluntarily drinking alcohol. I also suspected that Davis and Walsh were wrong, probably with the same subjective bias. But I did disagree with the critics. The alcohol drinking I saw in my rats and monkeys was not caused by physiological dependence. Indeed, getting rid of dependence made them drink more alcohol. On the other hand, I had one of the few animal models of alcohol drinking, and thus I could test the idea properly. I could show that a morphine injection had no effect on my rats' alcohol drinking and thus prove Davis and Walsh were wrong.  
  
Instead, I was wrong.  
  
Morphine suppressed alcohol drinking, exactly as Davis and Walsh might have predicted. I tried it over and over again in different ways with all sorts of controls, in Oregon and again after coming to Finland. The conclusion was unavoidable: alcohol drinking was affected by opiates. Finally, I gave up, and we published the results in Nature in 1973. Ironically, the one thing the referees made me omit from the paper was all mention of the notorious Davis and Walsh hypothesis.” 27  
  
Q: What is wrong with Antabuse (disulfiram) for alcohol treatment? It makes you throw up if you drink – it’s logical that alcoholics would stop drinking if they felt sick every time they took a sip of alcohol?   
  
A: The drug Antabuse (disulfiram) has been used to treat alcoholism for decades. The problem is that research shows that Antabuse is not effective for the majority of patients. Leading addiction researcher, Joseph Volpicelli (2000) suggests that while disulfiram might sometimes be effective is a select group of very motivated patients, “it has been shown to have limited clinical utility, as seen is several well-controlled clinical trials that failed to show significant differences in treatment outcome between groups of subjects taking disulfiram and placebo.”   
  
What then is the rationale for this medication ?  
  
The idea behind Antabuse is that it acts as a form of logical deterrent. Patients know that if they drink after taking Antabuse they will experience severe nausea, headache, and palpitations,and in severe cases they may die. This is caused by an accumulation of acetaldehyde in the blood-stream if alcohol is consumed while the patient is on Antabuse. There is no aversive or punishing reaction if the patient does not drink. 28 Part of the protocol is that patients must be warned about the potentially dangerous, even fatal consequences of drinking while on Antabuse. It was assumed that any person acting rationally would avoid drinking.   
  
It is true that if they were forced to take Antabuse, most patients would have to stop drinking. Although Antabuse has been administered via a time-released implant surgically inserted under the skin for continual release into the blood-stream, there are doubts as to whether the levels are sufficient to produced a reaction. Patients are usually relied on to take the drug themselves, swallowing it in pill form.   
  
Antabuse does not remove the craving for alcohol. Therefore, the patients become motivated to stop taking the medication, even to the point of cutting open their skin in order to remove their implants. And as soon as the Antabuse is stopped drinking recurs. – usually with a vengeance. Not only is there the increased craving produced by the alcoholdeprivation effect, but animal studies have found an additional long-lasting increase in alcohol drinking caused specifically by the medicine. Dr. Robert Myers, long-time editor of the journal Alcohol, often used this after-effect of Antabuse to make his rats drink so much they would be a model of alcoholism. The same WHO paper endorsing naltrexone cautions that before disulfiram can be recommended, there needs to be research to determine if the temporary administration of disulfiram in human alcoholics also exacerbates their illness.   
  
The use of disulfiram can also be questioned because of the suffering it causes patients. First, there is the suffering from having an overwhelming craving for alcohol, night and day, and not being able to satisfy it. Second, there is the suffering the patients suffer if they do drink and the potential death threat imposed upon them.   
  
Q: Can hallucinogens like LSD and other drugs such as ecstasy (MDMA), ketamine, or the herb ibogaine, herbs be useful? Are there any naturally occurring opioid antagonist-like herbs?   
  
A: Stories about the CIA and renegade researchers using LSD in the 1960s to treat drug addiction have become popular. We cannot be sure if these accounts are urban legends or pure conspiracy theory. Certainly, no serous double-blind placebo controlled studies prove the efficacy of hallucinogens in addiction treatment. The research on Ibogaine, a herbal treatment used in opiate addiction is fascinating and interesting but inconclusive. Ibogaine is claimed to remove the symptoms of drug withdrawal and reduce drug-craving for a period of time after administration. In addition, the “drug's psychoactive properties have been credited with helping users understand and reverse their drug-using behavior.” 29 Ibogaine is said to reduce withdrawal symptoms for addiction to heroin, cocaine, crack cocaine, methadone, and alcohol. It is even claimed to help with nicotine addiction. What is certain, is that in addition to the dangers of “bad trips”, desperate addicts who can afford it try this "one-shot" treatment at considerable cost at private clinics set up in the Caribbean, Central and South America. Ibogaine possession is illegal in many countries and is unlikely to become a mainstream treatment for addiction.   
  
MDMA (ecstasy) is an illegal recreational drug with neurotoxic side-effects. It is used by millions of people around the world. It an abused mood altering drugin contrast to naltrexone which has no mood altering effects and no risk of abuse, Like alcohol MDMA, is ‘addictive’ for some people but not for others. It is not yet know whether naltrexone is effective in treating MDMA addiction. More studies are needed. Finally, as far as we can tell, naturally occurring herbal formulations which have opioid antagonist effects (like naltrexone and nalmefene) have not yet been discovered. 30   
  
Q: The Swiss Heroin Assisted Treatment (HAT) program offers heroin addicts daily pharmaceutical grade heroin (diamorphine), and it seems helpful both for the patients and for society. How about doing the same – giving free alcohol to chronic alcoholics? What difference would naltrexone make to such a trial?   
  
A: “Study Toasts Free Drinks For Homeless Alcoholics” reports the Associated Press in early 2006.31 A study published in the Canadian Medical Association Journal claimed that offering free drinks to homeless alcoholics would reduce their problems with the police.   
  
Seventeen chronic alcoholics who drank upwards of 46 glasses a day over the past 35 years, including cheap substitutes such as mouthwash that often led to unconsciousness, were offered a glass of wine or sherry each hour, from 7:00 am to 10:00 pm at an Ottawa shelter over five to 24 months. Most of the fifteen men and two women, with an average age of 51 years, had tried detox programs and abstention, but were unable to maintain sobriety. "These are people you and I would pass on the street totally inebriated, who had drunk huge amounts," said Jeff Turnbull, one of the authors of the study. Three quit, three died of alcohol-related disease before the end of the study, but 11 others reported "a markedly decreased consumption of beverage and non-beverage alcohol, and most reported improved sleep, hygiene, nutrition and health," according to the authors of the study. More than half of the capital city's 1,000 homeless people abuse alcohol. They typically suffer increased health problems, require emergency services and have frequent contact with police. The likelihood of their rehabilitation is low because of psychiatric illness, poor social support, lack of stable housing, years of addiction or they simply refuse treatment. Participants in this study, however, reported fewer hospital visits, down from an average 13.5 to eight per month, while encounters with police fell from 18.1 to 8.8. The related savings per person for these services was 445 Canadian dollars (387 US) per month. The average cost to administer the program per person was 771 Canadian dollars (670 US) per month. "Once the craziness of their alcoholism is under control, their wasted lives on the street turned around, they're interesting people and all that destructive behavior is behind them," Turnbull said. "They'll never be fully integrated into society, but they'll be less of a drain and even contributors." Critics said the study lacked a comparison group, such as an abstinence program. Others lamented that offering a drunk a drink is contrary to common sense. "We've been accused of facilitating alcohol abuse, but we feel this is a very useful tool in combating a serious societal problem. Just because someone has failed an abstinence-based program doesn't mean they should have to die in the street," Turnbull said. "We agree that abstinence is the best approach to alcohol addiction; however, when abstinence programs have failed, we still have to care for the individuals," he said. "By giving them alcohol in modest and controlled amounts, we've been able to minimize the harm they do to themselves and work on their bad behavior." The program will soon be expanded to 24 beds and healthcare providers in other Canadian provinces and the United States have expressed interest in setting up their own.  
  
A similar program for heroin addicts was launched in Switzerland in the early 1990s. Chronic heroin addicts who qualified for Heroin Assisted Treatment (HAT) were offered pharmaceutical grade heroin (diamorphine) under strict medical supervision.32 An extensive summary of the experimental project was reported with outcome data for 1,035 patients who entered HAT beginning 1994 through mid 2006. On the whole results showed that the HAT program was successful – patients were able to live relatively normal lives – they did not have to resort to crime to support their addiction, they were not at risk of contracting HIV from infected needles, and many could hold down a proper job. “Many patients preferred to combine injectable diamorphine with oral methadone, in order to have more freedom to resume school attendance or employment”, the study reports. In addition, the health of the heroin addicts improved because they reduced their intake of other substances such as benzodiazepines like Valium®, suicidal thoughts reduced, there were fewer seizures, and less paranoia. General nutritional and physical health improved. “Overall, diamorphine (heroin) was found to be more acceptable and effective in terms of retention and compliance than injectable methadone and morphine. Patients doing well on methadone and morphine were allowed to continue, but no new patients were offered this approach.” A follow-up study in 2000, sampling 244 patients over 6 years found that 46% were still in treatment and that 48% of discharged patients had entered a regular addiction treatment program. “A comparison of those still in treatment with those who were discharged found: 1) a significant reduction in illegal heroin, cocaine and Benzodiazepine use in both groups; 2) no reduction in cannabis use in both groups; 3) a significant reduction of homelessness in both groups; 4) no reduction in unemployment in both groups; and 5) a highly significant reduction in living from illegal income and in new court cases.” Overall, HAT proved positive for those addicts who for whom other treatment approaches had failed. Similar studies have been implemented in Germany, Canada, Holland, and Luxemburg.  
  
Clearly giving free heroin (or a legal substitute like methadone) to qualified opiate addicts and alcohol alcoholics produces real benefits to the individuals themselves and to society. It results in harm reduction – they don’t have to resort to crime and live on the streets. Nutrition and health benefit, and it is less costly than warehousing them in prison, which does not stop them from using anyway – inside or upon release.   
  
But is it the best we can do? Clearly, the answer is an emphatic no. It would be far better to offer a real cure in the form of the Sinclair Method. Treating alcoholics with Pharmacological Extinction is far safer and easier. The alcoholics in the Canadian experiment and other similar trials would do far better if they were offered free booze and naltrexone. In this way they would gradually, over the next three to four months, begin to crave and drink less. I am sure many would find the offer acceptable. The damaged opioidergic system governing the addiction in their brains would painlessly and automatically - just like Sinclair’s AA rats - be restored toward pre-drinking, normal levels. Of course, where people have been drinking extensively over decades, other permanent brain damage to the mamillary bodies would not be rectified. Oliver Sacks described this syndrome in his book The Man Who Mistook His Wife for A Hat where a 49-year-old man permanently brain damaged still thought he was nineteen. Offering the Sinclair Method to alcoholics on a national health service basis would help the addicts and society by reducing medical costs and crime. Heroin addicts would benefit as well – however the treatment would have to be very carefully managed and the patients detoxified before treatment because opioid antagonists can precipitate dangerous even fatal withdrawal reactions. The addicts could instead first be switched to methadone - less dangerous and legal – and then after detoxification put on naltrexone. Perhaps they would benefit from long-acting monthly naltrexone injections like Vivitrol. Further study is required.  
  
Q: What is a “Dry Drunk” - is this term fact or fiction?  
  
A: “Dry Drunk” is a pejorative and judgmental term introduced as a colloquial expression by semi-professional addiction counselors to describe “recovering alcoholics” who no longer drink but who are thought to “behave like addicts.” You may not have had a drink for decades but because you are not on a Twelve Step program you are considered a Dry Drunk. The ideology “makes the arbitrary distinction between being sober and abstinent – you can be abstinent but not sober. In AA, sobriety is a state that can only be obtained by both abstaining from alcohol and working the twelve steps of AA, and alcoholism is believed to be a disease state that exists independently of actual alcohol consumption.”33 In other words, even if you can remain abstinent – as 10 -15 % are able to – being a Dry Drunk means you are still considered emotionally unstable. You remain quick to anger, rage, depression, and despair. Being a Dry Drunk means you are especially at risk of bingeing and relapsing more intensely. While the Dry Drunk state is thought by some to be the result of hypoglycemia, it would be more scientifically accurate to view the syndrome in terms of Alcohol Deprivation Effects and the circuitry driving the craving in the already addicted brain. Even though the patient may self-impose abstinence through personal will power, craving continues unabated thus leading to emotional instability and fluctuations in mood. Naltrexone + Drinking treatment removes the highways driving the addiction and the craving. The result is improved mood, less anger, rage, depression, and despair – and therefore in AA terminology the end of the “Dry Drunk” syndrome.   
  
Q: Surely the Sinclair Method missed the point that drug addicts and alcoholics need to express pent-up emotions and resolve deep conflicts from their past which can only be addressed in the warm, safe, and compassionate environment of a formal therapeutic setting?   
  
A: One of my mentors, Prof Arnold Lazarus, a leading clinical psychologist in the United States, once told an audience of two thousand psychologists at the Eastern Psychological Association that in working with patients “nothing moves me more than kindness and compassion.” He went on to say that no amount of compassion could substitute for active ingredients, techniques, or medications that were proven to actually work. Thus, for obsessive-compulsive behavior disorders, the most effective and ethical treatment was a tried-and-tested technique called “response prevention” possibly in combination with medication. Although kindness and compassion are desirable therapist qualities, they are not curative in themselves. Patients suffering from a major affective disorder (manic depression) have a physiological or medical disorder that responds best to medication. No amount of kindness or love can substitute for lithium or one of the newer medications used for bipolar disorders. The most compassionate and kind thing a doctor can do is to first offer the patient the right medication or treatment for the illness – and do so in the right way. In some cases, medication is not the right course of action. Enuresis, or bedwetting, can cause sufferers a great deal of embarrassment and worry. The treatment-of-choice for this condition is not psychotherapy or anti-diuretic medications such as Desmopressin, but the enuresis alarm which teaches bladder control over several weeks with 80 to 90% success rates.  
  
Alcohol addiction is primarily a physiological or medical condition with secondary psychological features by impinging on your life. The data from the NIAAA, the NIDA, and many others prove that 85% relapse back to heavy drinking no matter what kind of therapy is used. All the psychotherapy in the world, all the exploration of inner emptiness, expression of pain, or confession and remorse does nothing to cure the illness. For instance going to an AA meeting and saying, “Hello my name is George, and I am an alcoholic. I killed a mother and child while driving drunk, I hurt my wife and family. I feel like dying…” are useful abreactions but ultimately futile in terms of achieving de-addiction. Grief therapy, cognitive-behavioral therapy, psychodynamic therapy, group therapy, spiritual therapy, yoga, intensive individual therapy can be useful adjuncts to therapy. Indeed a minority of people never abuse alcohol after enrolling in such treatments – but they remain addicted forever. In other words, they can never drink moderately unless they have been through pharmacological de-addiction to remove the physiological addiction. All the theoretical analysis, self-incrimination, blame, insight, and understanding about why you became alcoholic and have done regrettable things are worthless without the proper medical treatment. The Dalai Lama, head of the Tibetan lineage of compassion, would probably agree that the kindest and most compassionate thing one could do for a severe diabetic would be to prescribe insulin. If he were aware of the data on Naltrexone + Drinking, he would be to first to advocate the Sinclair Method first – and then suggest various other forms of palliative or Buddhist therapy for the soul.   
  
Q: How do you know that opioid antagonists like naltrexone and nalmefene work the way Sinclair says it does – through extinction in the brain?    
  
A: The scientific method for establishing how something works is to test every explanation that you can think of or that your colleagues or competitors (yes, there are competitors in the scientific arena) can think of. If one explanation accounts for all the data and has all of its predictions verified, while all of the hypotheses are shown experimentally to be inconsistent with the facts, then that one explanations is tentatively accepted. That is how Sinclair established that opioid antagonists extinguish alcohol drinking. Most of the initial experiments were conducted in rats. The work is reviewed in a chapter he wrote in 1996 (published in 1998).34 At this time, his team had conducted 43 separate experiments on various hypotheses about how naltrexone and other antagonists work. The chapter concludes, “On the basis of all the above evidence, there is little doubt that opioid antagonists can cause extinction of alcohol drinking.”   
  
One example of how this testing process works occurred in 1992. The first controlled clinical trial of naltrexone in the treatment of alcoholism, by a group headed by Dr. Charles O’Brien in Philadelphia at the University of Pennsylvania, had just been published35. Sinclair had met O’Brien at a conference in California – by accident: they both were recording notes on Sinclair Spectra computers – although of course they both knew the other’s research. Sinclair was invited to Philadelphia and presented the results of his work at that time supporting extinction. There was general agreement in the audience that the results from the Finnish rats and also the results from their clinical trial were consistent with extinction. A couple psychiatrists, however, suggested an alternative hypothesis, that the decreased drinking was caused by a mechanism they called “devaluation”. They explained how one could test whether extinction or devaluation was responsible. Sinclair set up the experiment immediately upon returning to Finland. The results were contrary to devaluation but consistent with extinction.36   
  
Scientific testing never stops. The Finnish clinical trial was a test of the extinction hypothesis. The testing also involves seeing the results from trials elsewhere are consistent with the hypothesis. The database of all clinical trials with naltrexone and nalmefene, in the Appendix 1 here, was used in a test published (in Italian) in 200437 and supporting the conclusion that extinction was the mechanism of action responsible for the clinical results.   
  
Is the extinction hypothesis proven? No. Nor is anything is science. It is seldom, however, that one finds such abundant and consistent support for a conclusion, especially in clinical research.   
  
Q: It’s Obvious, You Can’t Cure Addictions with Drugs - Right?  
  
A: Perhaps one the most frustrating misconceptions about treating alcohol and other addictions is the pervasive belief that, by their nature, addictions cannot be treated with drugs. This belief is often held with zealous fervor, and it permeates the politics of addiction treatment.  
  
There are two sides to this belief. The first is that excessive drinking for some reason cannot be reduced by drugs. That idea was disproved long ago with Sinclair’s finding that alcohol drinking can be practically eliminated with high doses of morphine. 38 Siegel then showed the same was true in humans. 39 These findings, however, raise the other half of the objection: that drugs should not be given to alcoholics even if the medicine is beneficial.   
  
In light of all the data, it is tragic how this belief remains cherished by many professionals and lay addiction counselors. At first glance, it appears to be simple common sense: don’t give addicts drugs of any kind. An example can be seen in one New Jersey dentist who had become so addicted to alcohol and cocaine that he lost his home and spent his savings on the drug. He subsequently got into standard inpatient and outpatient recovery, moved to Florida, gave up dentistry, ending up becoming an addiction counselor himself. His stance was fervent if simple: “ I do not allow my patients to take any pills.” “Even vitamins ?” I inquired. “Yes. Vitamins are pills. Pills are the road back to using, and if you think you can use them to deal with addiction you gotta be outa your mind. The only way is to say ‘No to Drugs’, to attend all AA meetings, to trust in a higher power.” The mere mention of the use of naltrexone which, by definition is a non-abusable and non-addictive medication, to treat alcoholism causes many clinicians, including this former dentist, to roll their eyes and say, “not another drug to add to our problems!” 40 Yet these experts agree that over 80 % of their patients relapse within the first year of treatment…  
  
This stubborn, myopic vision can act to suppress the clinical evidence that naltrexone, combined with active drinking, is the most effective treatment to date. Clinical trials, decades of research, and the leading experts in the field concur that the outcome data for alcohol addiction are not good at 10 to 15 % success. 41 Most of these methods are based on getting the patient to cope with craving and deprivation effects; they are to abstain totally, using the mind, will power, numerous forms of psychotherapy, religion, AA, costly 28 day in-patient care programs. The thinking is that we are free to use anything except for other drugs in the battle to go clean. Famous British football star, George Best, tried Will Power and other treatments without success - before and after his liver transplant. Sadly he died of heavy drinking well before his time at a London hospital in 2005.   
  
Q: Why do the pharmaceutical companies which distribute naltrexone not openly explain the Naltrexone + Drinking formula in their prescribing leaflets? How could they possibly get it so wrong?   
  
A: Supplying poor instructions is just one explanation why many have not yet heard much about the positive effects of naltrexone. For instance, the company, DuPont Pharma, initially marketing the medication in the US did not inform doctors, pharmacists, and patients how the drug best works. The research results are clear that the patient has to drink while on the medication. The directions provided by DuPont on the package inserts supplied with naltrexone did not state this. Instead they imply, without directly saying so, that the correct way to use the medicine is according to the formula Naltrexone + No Drinking Allowed, which has been shown repeatedly in the clinical trials not to be effective. An analysis was made of the package inserts in America, Italy, and Israel.42 It concludes:  
  
Theory, preclinical studies, and clinical trials all show that naltrexone is beneficial because primarily it blocks reinforcement when the abused substance is taken, thus causing extinction. Therefore, naltrexone should be used with alcoholics who are actively drinking, and not in detoxified patients while abstinent. None of the inserts provide this critical information. They also omit the significant findings that could have led doctors to a correct usage. Opiate antagonists have great potential for helping in the treatment of alcoholism and drug addiction. They will only be useful, however, when doctors are told how to use them correctly.   
  
The insert from DuPont is actually better than those in the other countries. They included many statements that are completely false. The Israeli insert, for example, states:   
  
You must stop using… alcohol for at least 7-10 days before staring treatment. (False. It is perfectly safe to use naltrexone without prior detox.)   
  
If you start using… alcohol again you must not take ReVia. If you do take ReVia immediately after taking … alcohol you will suffer severe withdrawal symptoms. [emphasis in original] (False. There are no ill effects from taking naltrexone while drinking alcohol.)   
  
Imagine the difficulty in telling a patient in Jerusalem to start taking naltrexone (ReVia) without prior detox while he is still drinking, when the package insert tells him this will cause him to suffer severe withdrawal symptoms.   
  
The American package insert still says that heroin addicts must not use opiates while on naltrexone and if they do, it could kill them, without mentioning that the clinical results showed naltrexone only helped those addicts who disobeyed those instructions.   
  
The package insert in the United States is misleading primarily by omission.  
  
It discusses the 1992 Yale clinical trial, but it fails to mention that there were two types of therapy tested, and that there were no significant benefits from naltrexone with abstinence therapy and that all of the benefits were Naltrexone + Drinking groups. Instead it has the statement “In the clinical studies, treatment with REVIA supported abstinence.” This statement can easily be misunderstood as stating that naltrexone has been effective in programs supporting abstinence. It has not.   
  
The insert fails to mention that the most highly significant findings in the Yale study, that Naltrexone + Drinking was better than Naltrexone + No Drinking Allowed for craving and for the number of drinks per occasion.   
  
The insert states that naltrexone proved superior to placebo on relapse. There are two omissions here. First, it omits saying there was a significant benefit only in the Naltrexone + Drinking groups but none reported with Naltrexone + No Drinking Allowed treatment. Second, the insert does not tell what “relapse” here means more than 4 drinks a day or having more than 4 drinking days in a week. Relapse thus is specifically relapsing to heavy drinking. Many doctors and patients reading the insert might, however, think that a relapse means starting to drink again and thus conclude that naltrexone taken during abstinence helps to delay that first drink. It does not.   
  
The insert mentions the 1992 Volpicelli study but omits the most critical finding: “The primary effect of naltrexone was seen in patients who drank any alcohol while attending outpatient treatment… Perhaps the most dramatic effects of naltrexone were in preventing relapse in patients who reported any drinking.”   
  
Since 1994, the physician prescribing information has not spelled out that the medication is effective only if the patient drinks while the medication is active in the brain. This is a great disservice, because people take the medication without drinking in the false hope that it will somehow magically cure their addiction. Consequently, both doctors and their patients are led to give up after concluding that naltrexone is yet another worthless treatment for alcohol problems. Unfortunately, very few actually know that a vital cure for alcoholism (and other addictions) even exists. But there is some light on the horizon. The situation has slowly begun to change ever since the FDA approved the medication for alcoholism in 1994 and Enoch Gordis former head of the National Institute of Alcohol Abuse and Addiction endorsed the use of naltrexone wholeheartedly. The World Health Organization also agreed that the drug was the first truly effective medication for alcoholism. 43 44   
  
Despite this, doctors and patients generally remained in the dark about how to make naltrexone effective - that it has to be taken together with drinking, and that it has never worked with abstinence. Prescribing Naltrexone + No Drinking Allowed leaves the disease intact – the patient remains primed for relapse.   
  
It in not clear why the pharmaceutical industry has failed to inform doctors how to use naltrexone effectively. It is not a new problem just with the treatment of alcoholism, but rather goes back to the original treatment of opiate addiction.   
  
It is possible that DuPont did not have a financial incentive to find out to use naltrexone properly. The pharmaceutical industry relies on massively expensive advertising and promotional campaigns to inform the nation of new drug discoveries. The reason is that DuPont’s patents on naltrexone had already expired before the FDA gave its approval for its use against alcoholism. DuPont was given only six years of exclusive rights to sell naltrexone in America because it had bought the data from the clinical trials. Furthermore, the agreement with the FDA specified that DuPont could only sell a limited amount of naltrexone (branded as ReVia) without doing more clinical trials. Thus, DuPont may not have been motivated to pay for specific research that would have shown how Naltrexone + Drinking is the correct way to prescribe the medication. Naltrexone has now become a generic drug which means that other drug companies can offer generic copies of the medication at knock-down prices. Without exclusive patent rights there are no real profit incentives. Instead, DuPont sold its interest in naltrexone to Bristol-Myers Squibb and generic copies are now made by several companies around the world.  
  
Perhaps another reason why people do not know about the power of naltrexone is because of the mistaken fear of litigation. When hearing that naltrexone only works when paired together with drinking, many may erroneously jump to the conclusion that doctors would have to tell alcoholics to start drinking again. It is, of course, not only unethical but also dangerous to advise a successfully abstinent alcoholic to fall off the wagon. The litigious climate permeating the US and increasingly in the UK and Europe, might easily be cause for huge legal suits against drug companies. Naltrexone should never be used by alcoholics who are currently abstinent. It should only be prescribed for people who are actively drinking excessively. Doctors can advise them to abstain, but if abstinence is not possible, they should always take naltrexone before drinking. Of course, they should also be warned that the dangers of drinking and driving while on naltrexone. Naltrexone is not a “get sober” pill, and the advice not to use machinery while in treatment applies to many prescribed drugs. So if you drink - don’t drive – even if you are on naltrexone; this not a legal dilemma. Meanwhile, withholding the truth that opioid antagonists like naltrexone work through Sinclair’s extinction formula is clearly unethical.   
  
Q: Why is Addiction Is Not the Same as “Drug Dependence” and “Tolerance”?  
  
A: Addiction = Drug Dependence has been accepted for decades. “Drug Dependence” is taken for granted as an explanation for high relapse rates and consequently seems to have been widely adopted by society through the medical establishment, legal system, and media – as a fundamental truth. Back in the 1960s, cocaine and other stimulants were not expected to be addictive because they did not produce physiological dependence.  
  
The presumption is that if you are an “addict” you are physiologically “dependent” on a substance. Being physically dependent on alcohol means that you experience nasty withdrawal symptoms when you abruptly stop drinking after prolonged abuse. Anyone who has had to endure withdrawal through a traditional “cold turkey” detox at the start of a rehab program will tell you how terribly dysphoric it is: “I felt angry and depressed. I was anxious and paranoid. My heart was palpitating out of my chest. I had the shakes. The seizures almost killed me. I thought I would die. I wanted to kill myself…” are common descriptions of the withdrawal process during standard detox.   
  
But physiological dependence, where alcoholics are thought to drink to avoid nasty withdrawal symptoms and dysphoria, does not explain why they continue drinking once the withdrawal symptoms and dysphoria are long over.   
  
If “alcohol dependence” could explain addiction, patients should not continue to crave and drink excessively after withdrawal is over. But alcoholics do continue to crave alcohol and to relapse to abusive drinking after physiological dependence has been removed by weeks without alcohol - even decades after detox and prolonged abstinence. Why does this happen if they are long past the withdrawal process? Detox should have taken care of “dependence” because it takes care of withdrawal very nicely. After withdrawal is over there are no more symptoms and you are basically ok. According to this line of reasoning, you should no longer be “dependent” on your drug-of-choice. Yet even though withdrawal took place months or years ago doesn’t prevent relapse.   
  
Chapter 2 showed how Sinclair’s Alcohol Deprivation Effect and “alcohol dependence” cannot explain why alcoholics drink. More recent research has demonstrated that there also is a morphine deprivation effect and a cocaine deprivation effect, thus indicating that forced abstinence is not a good treatment for these addictions either. Alcoholics continuing drinking, cocaine addicts still snort, or heroin users go on shooting-up long after recovering from withdrawal. Meanwhile, the concept of Drug and Alcohol Dependence has been used to rationalize some of the most unpleasant, dehumanizing, and perverse forms of treatments imaginable. Apart from the stigma attached to being labeled an addict, it is no wonder why so many don’t come forward for help after hearing what can happen to them if they do.  
  
Q: What role do vested interests play in alcohol treatment?   
  
A: It may sound cynical to suggest that the vested interests in the alcohol and drug rehabilitation industry might not value a one-time cure for addiction. Consider the economics involved. Traditional 28 day inpatient programs cost tens of thousands of dollars – in some cases as much $36,000 for a month’s treatment in the US. In the UK, a well-known private hospital group charges £18,000 ($36,000) for their 28-day inpatient treatment – and there is no shortage of customers. The high incidence of alcohol and drug addiction assures a high occupancy rate. Sometimes there are even waiting-lists. One hundred patients per month works out to £1.8 million ($3 million) – or £18 million ($30 million) income over ten months. No wonder the large European bank, ABN AMRO recently bought such a facility, the Priory Group, for $1.5 billion, in the UK.45 It’s big business. Incidentally, the Priory Group had considered using the Sinclair Method but despite the scientific evidence for its effectiveness, had declined apparently because it would not generate much money itself and might jeopardize their existing treatment business.   
  
In some cases, private health insurance covers the costs for individual treatments. Otherwise costs must come out of the patients own purse. Many patients fail the first time round. If they can afford it, they return for another round of treatment. Profits thus increase for the owners. Of course, traditional programs employ tens of thousands of staff (doctors, psychologists, counselors, catering, cleaning professionals) and, including associated businesses, generate hundreds of millions of dollars annually. Even though the US Census Bureau estimates that over 45 million in the US are without health insurance, treatment is still big business because 245 million people must then covered by health insurance which often covers inpatient substance abuse treatment. 46 Treatment at expensive 28 Day rehab centers are covered for a high percentage of the 17 million with excessive drinking problems in the US – huge potential for huge profit.   
  
By contrast, the Sinclair Method is a highly cost-effective outpatient program. It costs much less that traditional 28 day inpatient programs, even though it takes at least 3 to months to complete. It is true that if the Sinclair Method were to become standard, much of the addiction industry would suffer financially. Many of the public and private companies now thriving on traditional addiction treatment could suffer economically, even go out of business. Part of the problem is that many insurance companies and other agencies only pay for detoxification. Since the Sinclair Method eliminated the need for detoxification, it also eliminates payment.   
  
The side-effects of vested interests and a pervasive “business-as-usual”, blasé attitude simply withholds truly effective treatment and costs valuable lives. We can hope that the health insurance industry will wake up, see the light, and come to the aid of the millions of alcoholics and their families who are not yet getting the effective and cost-effective care they deserve. I would like to predict that in the future, people will have access to the Sinclair Method as standard treatment, because the health insurance industry will see how cost-effective it really is. The savings will accrue not only from lower treatment costs, but more significantly from the billions that would be saved.  
  
The Sinclair Method could save billions in terms of reducing the economic drain caused by excessive drinking and alcoholism. The cost could be saved by preventing millions of lost work-days, high accident rates, heart disease, cancers, diabetes, divorce, and premature deaths, not to mention non-monetary saving in human suffering. There would also be a reduction in crime and costly incarceration rates. It could be this way: physicians, addiction counselors, and others could make a huge impact if Pharmacological Extinction were properly funded and endorsed. And as it becomes apparent that Pharmacological Extinction can be successfully applied to other serious and deadly addictions such as heroin and perhaps even cocaine, we may see a new era in funding and real hope for the future of societies. Certainly this is a proposition tax paying voters would endorse.   
  
Q: I have read on the internet that naltrexone gets rid of craving within 15 minutes. What should I make of this?   
  
A: One clinic in Arizona quotes several of its clients lauding the immediate positive effects of naltrexone.47 For instance, a retired businessman describes how alcohol became the focus of his life and caused marital problems. He had tried “every type of program on earth” and though able to manage short periods of sobriety as most people can anyway, kept relapsing until he found a program using naltrexone. He says that, “Within an hour of taking the naltrexone” he “felt as if a monkey that had been on my back for years, suddenly jumped off. The relief that I experienced was immense and difficult to describe.” While he “completed the recommended 90 days on the naltrexone” he does not say whether he drank alcohol while on naltrexone.   
  
Yet we know it’s impossible for naltrexone on its own to remove the craving within an hour. We can look at the graphs collected scientifically and see that craving drops only gradually, over weeks and months, and only if you drink on it. So, if we are to take this man at his word, we must assume that the “monkey jumping off his back” within an hour was simply an artifact of what psychologists call “expectation effects”, “halo effects”, and “placebo effects.” In other words, he was so hopeful and his therapists were so positive, that his expectations were primed with powerful belief about the magical power of naltrexone. One must always be skeptical of anecdotal reports especially when involving only one person who knows that he has been given an active medicine. There is a reason for the rigid double-blind, placebo-controlled procedure used to test the effects of medicines. One should not have much confidence in a finding until it has been reported by a large number people who did not know whether they had been given the medicine or a placebo. The literature is full of individual case studies that could never be repeated in controlled trials. Perhaps the belief that naltrexone could get the monkey off his back within an hour helped in much the same way as religious rebirth helps some alcoholics remain abstinent – but not physiologically cured of their addiction. Naltrexone is not a magic pill that will take your craving away merely by taking it on its own. As the data show, it is the formula, Naltrexone + Drinking, that is magical - but only you do this for at least 3 to 4 months. If you choose to continue drinking you must take naltrexone for the rest of your life; otherwise you will become re-addicted within a matter of a few months.   
  
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