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  University of Idaho
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  Psychology Dept.
  University of Idaho
  Design - P&D

As we see in slide two, this is really one side of the nature/nurture debate. Genetic models are one of the primary players in this debate. When we talk about these models in relation to substance abuse, the early debates focused on alcoholism. That is, what caused alcoholism? Nature, has the biology side, the genetics, etc., while the nurture side proposes it is your environment that caused the addiction to occur. There are also many proponents on both sides.

As we can see in slide three, this discussion goes way, way, way back. Aristotle talked about it in his writings and Hippocrates observed that diseases ran in families. Ultimately, these and later theorists contended that substance abuse such as alcoholism worked the same. This debate continued up through the twentieth century (and into the present)

There are a variety of different models to explain addiction from the genetics standpoint and these are listed in slide four. What I would like to do is walk through each of these and give you a little bit of an idea about them. But, before I do, I want to talk about a concept that is called a Concordance Rate (shown in slide five). Basically concordance rates are defined as the number of people who develop a disease when comparing two different groups. For example; Families with alcoholic members have a higher number of offspring who develop alcoholism than families who do not have an alcoholic member. This also occurs with other disorders including mental disorders.

So, how does that relate to genetics? Well, let's talk primarily about the pure genetics model (shown in slide six).  Pure genetics models have primarily focused on alcoholism and have been around a long time. Basically these models contend one particular thing. That a specific gene (whatever that is) causes alcoholism. Many of the early theorists used markers such as hair color or eye color. We talked about those last time. They looked then at the concordance rates. The problem was that when one examines these rates in the more recent studies, there is no real evidence to support the model.

What about evidence before Jellinek? Well, there is lots of discussion, and again, all this was tied to the disease model.  But again, there is no real evidence to support the genetics model prior to Jellinek.

So, what did Jellinek do? As we can see in slide eight, Jellinek in his analysis found that many alcoholics went through different stages, and there were a lot of different types of alcoholics. What Jellinek contended was that there was something inside the alcoholic's that made them different than all the other individuals who drank alcohol. Jellinek called this variable the "X" factor. As we can see in slide nine, Jellinek did not identify what the "X" factor was. He really did not have enough evidence to say what it was so he stopped there.  However, that didn't stop others (primarily in AA and the other addiction's agencies and advocates) from saying the "X" factor was a genetic difference. As a consequence, the "X" factor and all the genetics associating it with alcoholism became dogma.  Further, you either bought into the model or you suffered the consequences. The problem was, there was no real evidence to support the model.

So, what is the evidence people are using today to help support this particular model? These are primarily what we call the Twin Studies. The classic example of the twin studies is shown in slide ten and developed by Goodwin. Goodwin had observed that for century’s, offspring of alcoholics had higher concordance rates for becoming alcoholics. So, what he did was examine rates of alcoholism among twins.

The first of these studies began looking at fraternal twins (and is shown in slide eleven). Basically, what Goodwin did was compare concordance rates of alcoholism between fraternal twins and offspring who were not twins.  And, low and behold, what he found was that fraternal twins had higher concordance rates of alcoholism than offspring that were not twins. His conclusion was that this was evidence which supported that alcoholism was genetic.

However, there was a problem, (and this is shown in slide twelve). Frankly, these were correlational designs, and while the rates were statistically significant, they were not that large practically. So, consequently you had a face validity issue.  In addition, fraternal twins interact differently than non-twins because they are raised in the same environment. So, here what we have a nurture issue that creates confounds with this particular type of twin study.

To resolve the problem of the fraternal twin studies, Goodwin decided to use a different approach. He then moved on to what we call the Monozygotic Twin Studies (shown in slide thirteen). Basically, monozygotic twins are twins who share the same genetic information at birth. What he found was that monozygotic twins had higher concordance rates for alcoholism than fraternal twins and non-twin offspring. That is, when one twin developed alcoholism the other twin also had a higher probability of developing alcoholism. So, what is the problem with this?

As we see in slide fourteen, monozygotic twins are not like other twins. They do similar things. They often wear the same clothes. They also share the same environment. And so, as a consequence, monozygotic twin studies basically have the same problems as the fraternal twin studies. Finally, they are also correlational in nature.

To again try to resolve the nurture part of the problem, Goodwin decided to take a different approach (shown in slide fifteen) with what are called the Adoption Studies. Basically, what Goodwin did was look for monozygotic twins that had been physically separated at birth (usually due to some type of parental fatality). What he found is that some European countries kept records of these twin groups. And so, he compared monozygotic,  fraternal, and non-twin groups.  Low and behold (as we see in slide sixteen), he found that when one monozygotic twin was an alcoholic, sixty percent of the time the other twin became an alcoholic. This was held as the definitive study that genetics causes alcoholism. This evidence has since been reported by other the proponents for the model. Well, what's the problem?

As we see in slide seventeen, if sixty percent of the time the person becomes an alcoholic, what about the other forty percent that do not become alcoholics?  In addition, even despite the controls it is still a correlational design. The third major problem is that Goodwin's studies, (while well designed and from a variety of different standpoints) only apply to alcoholism. So, if there is one gene for alcoholism, is cocaine or heroin addiction also genetic as well? If so, what particular gene causes them?  So, if one gene does not cause the problem what genetic part does?

As we can see in slide eighteen, there is a variety of different alternatives. The first alternative is that there must be multiple genes that cause alcoholism. This gets around the problem that Goodwin described, that is, you must have all the genes. The problem is monozygotic genes, by definition, have the same genetics. So, when one person is an alcoholic their twin should be an alcoholic. But, this does not occur. Also, what about the other drugs?

A second alternative explanation is shown in slide nineteen. The reason all the monozygotic twins did not become alcoholic must be some recessive gene that is expressed in some, but not all, of monozygotic genes, and this results in alcoholism. The problem was which one was it? Also, how does it explain other types of substance abuse?

To resolve this problem a third alternative was developed and is shown in slide twenty. This is what we call the Diathesis - Stress Model.  Basically, what these models contend is that you have a genetic predisposition toward alcoholism, but you must have the right environment before you become an alcoholic. This would then explain the Goodwin problem with his twin studies.

The problem is (as we can see in slide twenty-one), which is the right environment? Some people live with alcoholics but never develop it. Other people do not live with it but do become alcoholics.  And again, what about other substances? In addition, which is the right gene?

So again, another alternative explanation is shown in slide twenty-two. That is, one gene does not cause a substance abuse disorder, what it does is change the brain biochemistry, some neurotransmitter, or some reward pathway. Again, as we have talked about in the past, all of this research is correlational despite the techniques that are used, including (PET) etc. In addition, the data is inconsistent.

So, what about the final alternative? Well, let's look at the human genome project say some proponents (shown on slide twenty-three). Since the human genome study has been developed, we have been looking for identifying genes that cause alcoholism. We have identified some that might have a role in that. However, none has been specifically identified to cause alcoholism.

So, what are the conclusions to all of this? Well, as we see in slide twenty-four, there are a lot of different genetic models but each has a problem. So, is alcoholism genetic? As we see in slide twenty-four, the answer is....The evidence does not support it. Further, it definitely does not support that other substance abuse disorders are genetic either. For example, we have not been able to find genes responsible for cocaine(ism), or methamphetamine(ism), or heroin(ism), or whatever it may be.

What are the implications for all this? As we see in slide twenty-five, what does it really mean to clients if the substance abuse is not genetic? Or, if it is genetic?  Well, in relation to therapeutic techniques and working with your clients, the answer is...Nothing!  The person still has a problem with alcoholism, or methamphetamine abuse, or heroin dependence, or whatever it may be, and the therapeutic techniques used in counseling remains the same.

What does it mean for academics then? Well, as we can see in slide twenty-six, it means a lot! It goes directly at the heart of why the person becomes an alcoholic.  Further, if alcoholism is actually a learned behavior, with appropriate behavior it should be able to be unlearned. That is, you could become social drinkers, etc.  Currently, there is even evidence to support this contention. The problem is that while some individuals can become social drinkers; remember I told you about that thirty percent; others revert to out of control drinking.   So, how do you determine which treatment you are going to use? Currently, that we cannot do that with high regularity or reliability. So, again, what one might want to do is focus on an abstinence-based model or some other particular type of model depending upon where the client is in relation to the addiction process.

Slide 27. So, what are some other explanations for substance abuse and specifically alcoholism? Well, one explanation is that alcoholism is a learned behavior. And that results in of some kind of brain biochemical changes. These changes cause the out of control drinking.  Further, as the changes take a long time to occur, they also take a long time to recover.

As we also see in slide twenty-eight we have lots of different types of alcoholics and for this we may need different types of treatment. For example, we might just need to educate some people about substance abuse or retraining a person to drink, or abstinence. And again, this model does not work with other particular types of drugs due to high tolerance and addiction potential.

So, what about all the political implications of all this in relation to genetics? Well, as we can see in slide twenty-nine, the general population does not think it's genetic either!  If it is genetic, basically what it allows the person to do is not take responsibility for their behavior.  We also have court issues, as well.  Can you get off because you are an alcoholic or substance abuser?  The court could monitor your behavior.  These are also the same issues for mental health issues. You could basically be institutionalized for a mental condition prior to even having the condition. There are also insurance issues as well. Let's take a genetic test, and if it is genetic, you could then be identified as having a substance abuse problem and then no one would insure you.

So, in relation to all this, what is it we should all remember? As we can see in slide thirty, it does not matter where one stands academically.  When a person is working with a client who is having out of control drinking or has alcohol or substance abuse issues, or if they are having health issues as well.  For people such as this, abstinence is probably only the best approach. On the contrary, if one has tried multiple abstinence models and still has not controlled the problem, then you may want to try some other types of solutions (including medications, controlled drinking, harm reduction, etc)..

Again, this is all dependent on the client’s condition. As you see in slide thirty-one, many clients that we see need abstinence, they should not be drinking any more, and they should not be using substances. Some, on the contrary, do not. A teen caught drinking at a party probably does not need inpatient treatment for substance abuse unless they are experiencing tolerance or some kind of withdrawal problems.  Thus, again, what we need to be doing when working with these clients is have a thorough assessment about the clients condition.

So, in conclusion, as we see in slide thirty-two, the genetics model has lots of issues and they have lots of controversy, as well. We need a lot more and significantly greater and better experimental research to make a conclusion regarding this issue.  We also do not need any more correlational research. We really need to develop the experimental models to really test if substance abuse is genetic or whether it is not.

In the next section we will begin talking about the alternative models to the biological models. The first of these will really be related to psychological models and specifically to the classical and operant conditioning.

So, until then we hope you are enjoying your day and we look forward to talking to you soon.