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

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

The answer is, “Yes.”

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

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

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

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

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

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

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

© Howard C Wetsman MD FASAM

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

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

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

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

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

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

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

© Howard C Wetsman MD FASAM