The Biological Reasons for Addiction

THE BIOLOGICAL DISEASE MODEL

The biological disease model has some advantages over the moral viewpoint as it removes the moral stigma and opens up the possibility of treatment.  Instead of moral weakness, biological and genetic factors are thought to cause addiction.  Those who are labeled alcoholic or addict are considered qualitatively different from moderate users.  In this view, alcoholism and drug addiction are progressive, irreversible diseases that ultimately result in death if left untreated. Any usage is believed to result in loss of control.  Abstinence is therefore the primary goal of treatment, and the addicted person is cautioned to maintain vigilance against relapse. Recovery is considered never ending; hence, terms such as recovering alcoholic are favored over recovered alcoholic.  The primary intervention agents are other recovering alcoholics, clergy and treatment professionals.    Several implications of the disease model may be problematic in treating relapse.  First, the belief that one has a disease may wrongly be interpreted as total absolution of responsibility should a relapse occur.  Individuals may then explain relapses as an inevitable result of their disease and loss of control.  This prevents a careful examination of the faulty decision-making processes that often precede relapse.  The addict who hides behind the disease label is a challenge to the chemical dependency professional.  The label offers the addict a potential rationalization that excuses him or her from personal responsibility for his or her behavior.  "Sure I went out and used drugs and alcohol again" the addict and alcoholic often cries, "I have a disease!"   However, and this is the point often overlooked by addicts and alcoholics: with the power to label oneself diseased come certain responsibilities toward the care and treatment of that disease.  When the addict attempts to hide behind the disease label, it is up to the chemical dependency counselor to confront the addict or alcoholic with the fact that the label "disease" does not absolve the individual from responsibility for the treatment of his or her affliction.  Rather, this underscores the issue of personal responsibility in the control and treatment of the disorder. Thus, with the knowledge that one is addicted comes a definite responsibility to work toward sobriety.   Second, the belief in loss of control may result in a self-fulfilling prophecy.  Instead of differentiating between lapses and relapses, relapsers may presume that further substance usage is inevitable.  Some may use the loss of control concept as an excuse to continue using drugs and alcohol.    Third, the disease model focuses primarily on biological factors even though most relapse precipitants are psychological and social.  The excessive focus on physical solutions takes needed attention away from lifestyle changes that promote long-term recovery from any addiction.     Finally, the biological disease approach implies that there is a provider and a patient in an inherently unequal relationship.  This model places the patient in a passive position, waiting for the expected treatment.  Treatment compliance research from a variety of disciplines indicates that patients adhere to treatment more strongly if they are actively involved as participants.  

There is significant evidence to suggest that alcoholism and addiction have a biological basis, although science has not yet fully defined the biological flaw that results in drug and alcohol dependency.  In spite of the evidence drug and alcohol addiction remains a most curious disease because it also requires some measure of active participation by the individual in the disease process.  

The vulnerabilities to drug dependence that are under genetic control are usually discussed as risk factors in developing drug dependency, but they also have a relationship to relapse.  Adoption, twin, and animal studies provide evidence of important genetic factors in alcoholism.  The risk of developing alcoholism is closely associated with the degree of genetic relationship to an alcoholic parent. Offspring of alcoholic parents have an increased risk of developing alcoholism, a relationship which holds even when the children are raised separately from each other and from the biological parents. 

The theory postulates a genetically transmitted biochemical abnormality that predisposes some individuals to drug and alcohol abuse.  The genetic theory explains why not everyone who drinks heavily develops alcoholism and why people who have the abnormality are more likely to relapse if they depart from abstinence.  Genetic theory is used to bolster the disease model of drug dependence.  Vulnerability on a genetic basis is used as a "nonjudgmental" way of explaining to drug abusers why they cannot return to "controlled" drug use. 

The genetic theory has also been proposed for opiate dependence.  Researchers hypothesized that some individuals might be predisposed to develop narcotic dependency.  They hypothesize that a person could inherit an endorphin deficiency.  If people with this deficiency happened to use narcotics, they would discover a euphoric effect in excess of that experienced by people without the abnormality.  This effect would predispose them to a dependency for opiates and make it harder to remain abstinent. 

There is reason to hypothesize that similar genetic influences may be found for compulsive use of other psychoactive substances.  Some have proposed a model of addiction based on changes in enzyme levels, which result from compulsive use of drugs or alcohol. It is these alterations in enzyme levels which cause addicts to react differently from non addicts to the same experience.  This altered response of the individual may be brought about not only by genetic predisposition but also by chronic ingestion of an addictive substance.  This does not negate the concept of addictive disease, since there are many diseases that can be related to a genetic predisposition and also can be caused by environmental and behavioral factors.  Diabetes, for example, can be inherited or can be environmentally induced.

To understand the genetic nature of alcoholism, consider the mechanism by which alcohol is metabolized in the liver.  Alcohol (ethanol) is converted to acetaldehyde utilizing the enzyme alcohol dehydrogenase (ADH).  The conversion requires a coenzyme, nicotinamide adenine dinucleotide (NAD+).  Acetaldehyde is then further oxidized to acetate and finally to carbon dioxide and water.  The conversion of acetaldehyde to acetate requires another enzyme known as aldehyde dehydrogenase (ALDH) and the same coenzyme NAD+ needed to convert alcohol to acetaldehyde.  

Since enzymes (in this case ADH and ALDH) are involved in the metabolism of alcohol, any alteration in the level of these enzymes would change the rate at which alcohol is metabolized.  Therefore the alcoholic's inappropriate response to alcohol could be explained on the bases of an inherited altered level of the enzymes ADH or ALDH or both, which are necessary to metabolize alcohol.  There have been a number of studies which show that certain individuals at genetic risk to alcoholism metabolize alcohol differently than those individuals reportedly not at risk.  For example, the conversion of acetaldehyde into acetate in alcoholics is performed at about half the rate as in the case of non alcoholics.  This explains the well-known fact that in alcoholics there is an accumulation of acetaldehyde. Also the blood acetaldehyde level was higher in those individuals with a positive family history of alcoholism than in those with no family history of alcoholism.  It has also been demonstrated that this metabolic abnormality exists prior to heavy drinking.  That is, the children of alcoholics who before the experiment had never ingested alcohol were unable to convert acetaldehyde to acetate at the normal speed. 

Many other metabolic abnormalities of alcoholics have been observed.  One example is the formation of the substance 2-3 butandiol produced when alcoholics metabolize or break down alcohol during digestion.  This substance is not found in the blood of asymptomatic drinkers.  Some researchers have investigated genetic hypotheses by studying differences in alcohol metabolism between races.  In addition, others have shown that racial differences in sensitivity to alcohol may be related to corresponding differences in levels of the enzyme ALDH.  Some argue that cultures which have biochemically adapted to alcohol after long periods of exposure have fewer problems with drinking than those with relatively recent history of exposure.

In the early 1960's researchers were studying the metabolic kinetics of morphine when they observed improvement in subjects' functioning in response to substituting methadone for morphine.  Long before the discovery of narcotic receptors, or endorphins, they believed that repeated exposure to narcotic drugs might induce metabolic changes in neurons.  Methadone corrected the metabolic change.  Since methadone was meeting a metabolic need of the patient, replacement methadone therapy, perhaps lifelong, was rational and the treatment fit a medical model (i.e., like insulin for a diabetic).

The hypothesis that exposure to narcotics produces metabolic alterations is supported by more recent work with opiate receptors, beta-endorphin, and enkephalins.  After the discovery that some neurons had specialized recognition sites on the cell's membrane for opiates, scientists searched for an endogenous substance with opioid activity that would bind to the receptor.  They hypothesized that the use of heroin would suppress endorphin production, analogous to feedback regulation of other hormones.  Further, persistent opiate withdrawal symptoms would result from endorphin deficiency, and protracted narcotic withdrawal symptoms would help account for the high relapse rate among opiate addicts. 

The metabolic theory of opiate dependence give support for opiate dependency as a biological disease.  Reduced endorphin levels of narcotic addicts provide plausible medical reason for a relapse. Metabolic theories bolster the biological disease model of narcotic drug abuse and provide a medical foundation for narcotic maintenance therapy (e.g., methadone).  The endorphin deficiency model also has an implication about the duration of methadone treatment.  If one supposes that the addict inherited an endorphin deficiency, analogous to insulin deficiency in diabetics, then "replacement" could be lifelong.  Many providers of methadone maintenance do not use this model.  They view the need for methadone maintenance to be temporary and the appropriate use of methadone to be to provide a time-limited period of psychosocial stabilization while rehabilitation occurs.   

THE DISEASE OF ADDICTION

Jellinek is the person who created the comprehensive disease model of alcoholism.  Jellinek advanced the theory that alcoholism was actually a biological disease, with symptoms, and a progressive course, in an era when the predominant school of thought was that alcoholism was a moral weakness.    The key elements to the Jellinek model were:  (a) a loss of control over drinking, and (b) the belief that alcoholism was a progressive disorder.  In other words, Jellinek proposed that the alcoholic was unable to consistently predict in advance how much he would drink at any given time.  Alcoholism, like other disease states, was also viewed as a progressive disorder that would, if not stopped, result in the individual's death.  

Jellinek viewed alcoholism as a disease that might take any of many different forms, or styles, of drinking.  Jellinek classified several subgroups of alcohol-drinking patterns.  The first of these was the Alpha alcoholic.  Jellinek thought that the Alpha alcoholic was psychologically dependent on alcohol but believed that this individual could abstain for periods of time from the use of alcohol, if this were necessary.   Loss of control was part of the Alpha alcoholic's psychological dependence, which might manifest itself in regular drinking.  The Alpha alcoholic was viewed by Jellinek as possibly suffering from the nutritional disorders brought about by alcoholism, as well as family conflict caused by his alcohol use.  But, the Alpha alcoholic was not viewed as being physically dependent on alcohol.    Alpha alcoholism was not thought to be automatically progressive by Jellinek.  Rather, Jellinek thought that the Alpha form of alcoholism was sometimes a stable pattern of drinking.  If the Alpha drinking pattern were to evolve into another form of alcoholism, Jellinek believed that the Alpha alcoholic could evolve into the Gamma form of alcoholism.  However, as previously stated, the Alpha form of alcoholism was thought to be relatively stable.    Jellinek also classified some drinkers a Beta alcoholics.  The Beta alcoholic was described as not being psychologically or physically dependent on alcohol.  But the Beta alcoholic might demonstrate medical symptoms of chronic alcohol use such as gastritis and cirrhosis of the liver. If the Beta alcoholic progressed, it could also turn into the Gamma form of alcoholism.   The Delta alcoholic was physically dependent on alcohol but manifested few or no physical problems from chronic drinking.  In contrast to this, the Gamma alcoholic was seen as demonstrating both physical symptoms from drinking and physical dependence on alcohol.  The Gamma alcoholic also demonstrated a progressive loss of control over alcohol use.  As noted above, both the Alpha, and, less frequently, Beta alcohol use patterns could progress to the Gamma pattern of alcohol use over time.    Finally, the Epsilon alcoholic might best be classified as the binge drinker.    Jellinek's model of alcoholism offered a number of advantages to physicians.  It provided a diagnostic framework within which physicians could classify different patterns of drinking, as opposed to the restrictive dichotomous "is he or isn't he an alcoholic?" view that had previously prevailed.  It also helped to classify alcoholism as a physical disease, worthy of medical treatment.  Prior to this alcoholism was viewed as a moral weakness.    



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