What is Alcohol Addiction?
Research on Alcohol and Alcoholism
Each chapter is written by expert(s) in that particular subject area:
page 316 begins the article "What Characterizes Alcohol Addiction?"
and is authored by Roger E Meyer, MD.
He begins with two definitions of alcoholism: physiological and behavioral.
The former is a description of an alcoholic as an individual who has lost control of their alcohol abuse and experiences tolerance and physical dependence. In the latter, the authors of The Pharmacological Basis of Therapeutics describe alcoholism as a behavioral pattern that leads to physical dependence and addiction.
A biochemical basis is described by Dr Bill Boggan, on his website dedicated to information on alcoholism, from the section Alchohol Chemistry and You:
What is the current thinking about biochemical basis of addiction? Two general processes contribute to alcohol addiction.
The first process is a modified reward process where by drinking of alcohol provides a net positive effect, such as feelings of mild euphoria or cessation of feelings of anxiety. When this net positive effect combines with the tendency (in vulnerable individuals) with a pattern minimizing/ignoring the negative impacts of overconsumption (hangovers, loss of memory, fights, violence and arrests), the risk for addiction to alcohol increases.
Conversely, in the less vulnerable individual equates heavy alcohol consumption as overall unpleasant as result of the negative effects outweighing the positive.
Mental Effects of Alcohol Addiction
Rewarding experiences after drinking include:
The rewarding aspects of ethanol use involve the brain's reward system:
- the taste of the alcohol itself
- the increase in rewarding feelings, such as relaxation and euphoria
- the increase in ability to socialize
The VTA and the nucleus accumbens are two structures involved in the reward system for all drugs, including alcohol and tobacco, although other mechanisms might be involved for specific drugs.This system is comprised of brain structures and circuitry (e.g. ventral tegmental area, extended amygdala and the nucleus accumbens within) that appears to be important in the reinforcing (rewarding) properties of a variety of drugs.
- The alcohol reward system includes the ventral tegmental area (VTA) and nucleus accumbens (NA) and affects the structures that use GABA (gamma-aminobutyric acid) as a neurotransmitter. GABA is widely distributed in numerous areas of the brain, including the cortex, cerebellum, hippocampus, superior and inferior colliculi, amygdala, and nucleus accumbens. It acts as one of the major inhibitory (relaxing) neurotransmitters in the brain. (NIDA NOTES, September/October, 1996)
The second process important in addiction has to do with the ability of the brain to adapt to influences, which affect its normal function. The ability is called neuroadaptation.
Neuroadaptation is a mechanism by which the brain changes to accomodate and mitigate the negative impacts of a substance (ethanol) in an effort to maintain normal function.
For example, the drinking of one or two beers or one or two drinks (acute intake of ethanol) activates a variety of processes in the body and in particular impacts the functioning of the brain.
In order to keep the brain functioning normally, the brain attempts to chemically counteract whatever ethanol is doing to disrupt its action, an example of which would be the tolerance that frequent drinkers build up, resulting in a need to drink more to achieve the state of positive affect desired.
Effects of Alcohol in the Brain
Ethanol: mechanism of action
facilitates the action of the major depressant
neurotransmitter in the brain (GABA) and
inhibits the action of the major excitatory
neurotransmitter in the brain (glutamate).
Physical Effects of alcohol addiction
Table 1: Alcohol and Its Effects on Neurotransmitters and Receptors
- Glutamate
- Alcohol inhibits glutamate receptor function
- This causes muscular relaxation, discoordination, slurred speech, staggering, memory disruption, and blackouts
- Ether and chloroform have similar effects on the glutamate system
- GABA (gamma-aminobutyric acid)
- Alcohol enhances GABA receptor function
- This causes feelings of calm, anxiety-reduction and sleep
- Valium has a similar effect on the GABA system
Ethanol acts by binding GABA and glutamate receptors, thus influencing the action of these receptors to create a net depressive effect as described above, by down-regulating glutamatergic activity and up-regulating GABA-ergic activity. This is how ethanol acts as a central nervous system (CNS) depressant.
- Alcohol raises dopamine levels
- This leads to excitement and stimulation
- Cocaine and amphetamine have similar effects on the dopamine system
- Endorphins
- Alcohol raises endorphin levels
- This kills pain and leads to an endorphin "high"
- Morphine and heroin have similar effects on the endorphin system
With neuroadaptation, the brain attempts to counteract this depressant effect by increasing the activity of the glutamate system and decreasing the activity of the GABA system. This in part can be accomplished by altering the number or function of the receptors.
GABA and glutamate receptors are only two of a number of key players in the transmission of information from one cell to the next. When a receptor is bound and 'activated,' meaning it begins a series of intra- and inter-cellular signalling cascades with many downstream chemical reactions and subsequent release of other neurotransmitters. This ability of a receptor to have differential downstream effects based on type of ligand bound is the basis for neuroadaptation occurring at other locations and by varying mechanisms within the cascade of events that take place in the brain.
The Dangers of Alcohol
Neuroadaptation also occurs when a brain/body adapted to the presence of ethanol is suddenly deprived, as when an alcoholic quits 'cold-turkey' and experiences withdrawals. Initially, since the brain has up-regulated the excitatory neurotransmitter glutamate and down-regulated the inhibitory neurotransmitter GABA, the withdrawing alcoholic will experience anxiety, shakiness, and in extreme cases, delirium tremens (the DT's):
Although alcohol withdrawal is common and usually mild, the abrupt cessation of alcohol consumption by a patient with alcohol dependence may lead to delirium tremens (a severe dysautonomic and encephalopathic state) and withdrawal seizures, both of which may be fatal. The effects of alcohol withdrawal can be life-threatening if excitatory activity reaches a critical level and seizing occurs (McKeon et al).
Alcohol Dependence
Social Effects of Alcohol Addiction
The development of alcohol dependence, withdrawals and the role of 'triggers' is described nicely by the National Institutes of Health:
If a person chooses to drink more regularly (chronic intake), the brain attempts to adapt to the increasing amounts of ethanol. Generally, neuroadaptation can take place up to a point. After chronic consumption and ongoing adaptation, it will now take more ethanol to produce the same effect as the first drink. When this is the case, tolerance has developed and substantial adaptation has taken place. If the person now chooses to quit drinking the body tries to return to its original state in doing so causes a number of withdrawal signs including tremors, seizures, nausea, and negative emotional states. Since further drinking will delay, diminish, or prevent withdrawal, the person often chooses to drink again. Even if the person stops drinking, the neuroadaptations that took place in the brain may persist for a period of time well beyond the time when ethanol is no longer present in the body. It has been speculated that these may be the source of the urges to drink again.
For most people, it is relatively easy to modulate ethanol intake. Depending upon the vulnerability of the individual, as drinking progresses regulation of drinking becomes more difficult. Simultaneously, the ability of the brain to adapt is diminished or lost. Systems become increasingly dysregulated, perhaps due to damage, so that in the brain communication and coordination diminishes or fails. This is particularly true after repeated withdrawals from ethanol since the severity of withdrawal increases. Perhaps this is the reason for saying the drink appears to take on a life of its own.
"First, the person takes a drink, then the drink takes a drink, then the drink takes the person".
In general, there appears to be a general loss of control. The individual has lost control over drinking and neuroadaptive mechanisms have been overwhelmed. Thus alcoholism can be characterized as a disease with takes over the body and brain.
The environment associated with drinking is now known to play a crucial role in the addictive process. The environment associated with the drinking becomes associated with the positive attributes of drinking. Thus, it common knowledge that if one always drinks in a particular bar, or with cigarettes in their hand, or with a certain group of friends, then the bar, cigarette, and friends can trigger the urge to drink. This is because the bar, cigarette, and friends have become cues associated with drinking and can trigger the brain reward system in a manner somewhat similar to that seen with the ethanol. Attempts to help alcoholics return to normal functioning must include understanding of the important role of cues in addiction. [7]
Current Medical Diagnosis of Alcoholism
DSM-IV Diagnostic Criteria for Alcohol Dependence
A maladaptive pattern of alcohol use, leading to clinically significant impairment or distress, as manifested by three or more of the following seven criteria, occurring at any time in the same 12-month period:
- Tolerance, as defined by either of the following:
- A need for markedly increased amounts of alcohol to achieve intoxication or desired effect.
- Markedly diminished effect with continued use of the same amount of alcohol.
- Withdrawal, as defined by either of the following:
- The characteristic withdrawal syndrome for alcohol (refer to DSM-IV for further details).
- Alcohol is taken to relieve or avoid withdrawal symptoms.
- Alcohol is often taken in larger amounts or over a longer period than was intended.
- There is a persistent desire or there are unsuccessful efforts to cut down or control alcohol use.
- A great deal of time is spent in activities necessary to obtain alcohol, use alcohol or recover from its effects.
- Important social, occupational, or recreational activities are given up or reduced because of alcohol use.
DSM-IV Diagnostic Criteria for Alcohol Abuse
- Alcohol use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by the alcohol (e.g., continued drinking despite recognition that an ulcer was made worse by alcohol consumption)
- A maladaptive pattern of alcohol abuse leading to clinically significant impairment or distress, as manifested by one or more of the following, occurring within a 12-month period:
- Recurrent alcohol use resulting in failure to fulfill major role obligations at work, school, or home (e.g., repeated absences or poor work performance related to substance use; substance-related absences, suspensions or expulsions from school; or neglect of children or household).
- Recurrent alcohol use in situations in which it is physically hazardous (e.g., driving an automobile or operating a machine).
- Recurrent alcohol-related legal problems (e.g., arrests for alcohol-related disorderly conduct).
- Continued alcohol use despite persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of the alcohol (e.g., arguments with spouse about consequences of intoxication or physical fights).
- These symptoms must never have met the criteria for alcohol dependence.
Models of Addiction
Disease model
Cause: congenital defect/deficit, inherent chemical imbalance
Treatment: lifelong abstinence from any mind-altering substance (except caffeine/nicotine), use of support groups (AA), maintenance (opiates)
Addiction is a physical and/or psychological compulsion over which the addict has no control and which is causing dysfunction in his/her life. organizations like AA center their treatment methods around this model, as described thoroughly by Dickon here.
Social Education model
Climento, Carlo C. Addiction and Change, pp. 14-15
Cause: poor socialization/social anxiety, poor coping skills, poor role model
Treatment: desensitization (by recounting specific experiences) and reconditioning
Using experiences reinforce/reward the actions leading up to and during use, generating sensitivity to environmental, stress, and habit-induced cues and conditioned behavior. the user chooses to use because it is rewarding. behavioral conditioning results in 'habits' that are more rewarding than are daily activities. the user uses because drugs and the environmental and emotional cues leading up to use trigger the reward pathway, often before any substance is ingested. see Pavlov.
Behaviour-Choice Model
Hypothesizes that certain physiological and personality characteristics may increase the reinforcement value of alcohol (Corcoran, 1973)
1. repeated use of an addictive drug decreases its future value and the future value of competing activities.
2. the frequency of an activity is a function of its relative (not absolute) value...an activity that reduces the values of competing behaviors can increase in frequency even if its own value also declines.
3. effective reinforcement contingencies are relative to a frame of reference, and this frame of reference can change so as to favor optimal or sub-optimal choice.
4. if the frame of reference is local, reinforcement contingencies will favor excessive drug use, but if the frame of reference is global, the reinforcement contingencies will favor controlled drug use. The transition from a global to local frame of reference explains relapse and other compulsive features of addiction.
Alcohol Withdrawal
Bayard et al describe alcohol withdrawal as being anywhere from mild (tremors and anxiety) to severe (Delerium tremens and seizures). the DSM-IV criteria for withdrawal are as follows:
TABLE 1
Diagnostic Criteria for Alcohol Withdrawal
A. Cessation of (or reduction in) alcohol use that has been heavy and
prolonged.
B. Two (or more) of the following, developing within several hours to a few
days after
Criterion A:
1. Autonomic hyperactivity (e.g. sweating or pulse rate more than 100 bpm)2. Increased hand tremor
3. Insomnia
4. Nausea or vomiting
5. Transient visual, tactile, or auditory hallucinations or illusions
6. Psychomotor agitation
7. Anxiety
8. Grand mal seizures
C. The symptoms in criterion B cause clinically significant distress or
impairment in social, occupational, or other important areas of
functioning.
D. The symptoms are not due to a general medical condition and are not better accounted for by another mental disorder.
Treatment Options for Alcohol Addiction
"Treatment Programs in the National Drug Abuse Treatment Clinical Trials Network" D. McCarty et al.
This article describes three general treatment philosophies, under which most regimens (in-patient, out-patient , group, etc):
The Institute of Medicine identified three program philosophies or orientations that guide treatment strategies: physiological (addiction is a progressive disease that requires medical intervention including
the use of pharmacotherapy), psychological (addiction is a behavioral and emotional problem that responds to intensive group and individual therapy), and sociocultural (addiction is the result of socialization in environments that promote use of alcohol and other drugs and treatment require environmental restructuring and new social relationships) (Institute of Medicine 1990).
The following treatment strategies fall within the above definitions of the three philosophies:
Alcoholics Anonymous (AA)
According to current addiction treatment dogma in some countries holds that addiction is a chronic disease, the therapy for which is abstinence. however, the relapse rate for those who underwent court-ordered treatment was 90%.
In contrast, data from a study of Vietnam vets addicted to heroin upon their departure from Vietnam was only 12-14% three years after returning to the states (Heyman,1996). obviously, much of the discrepancy is due to environment (availability, legality, cost, etc), but the data clearly do not support the disease model in this specific case. It is supported in many other instances, however, many individuals must abstain from using completely, while others can scale back and use only occasionally. Many cobble together coping strategies by taking ideas from various sources.
The 12 Step Programme
The 12 steps of Alcoholics/Narcotics Anonymous
1. We admitted that we were powerless over our addiction, that our lives had become unmanageable.
2. We came to believe that a power greater than ourselves could restore us to sanity.
3. We made a decision to turn our will and our lives over to the care of God, as we understood Him.
4. We made a searching and fearless moral inventory of ourselves.
5. We admitted to God, to ourselves, and to another human being the exact nature of our wrongs.
6. We were entirely ready to have God remove all these defects of character.
7. We humbly asked Him to remove our shortcomings.
8. We made a list of all persons we had harmed and became willing to make amends to them all.
9. We made direct amends to such people wherever possible, except when to do so would injure them or others.
10. We continued to take personal inventory, and when we were wrong promptly admitted it.
11. We sought through prayer and meditation to improve our conscious contact with God, as we understood Him, praying only for knowledge of His will for us, and the power to carry that out.
12. Having had a spiritual awakening as a result of those steps, we tried to carry this message to addicts and to practice these principles in all our affairs.
Biophysical Therapy
Addresses first the issue of getting a user to a physiologically stable state, and then addressing underlying emotional issues.
Cognitive-Behavioral Therapy Approach to Addiction
A therapist works with a patient to identify the thought and subsequent behavior patterns that are problematic. this often includes implementing changes in behaviors such as socializing: depressed individuals often avoid social situations, which further isolates the individual and perpetuates a vicious cycle. an example of a cognitive exercise would be mentally walking a patient through a fearful situation and rehearsing a new behavior, making it easier for the patient to implement when (perceived) threatening situations actually do arise. other techniques include positive reinforcement of the patient's successful employment of changes in thought and/or behavioral patterns (conditioning), desensitization to perceived threats by repeated exposure and, when possible, direct confrontation of the threat, and teaching the patient to actively evaluate their psychological reactions and trust that they are appropriate.
Pharmacologic Options for the Prevention of Alcohol Abuse
Inhibitory compounds, such as naltrexone and acamprosate, that bind mu- and kappa-opioid receptors effectively block the effects of alcohol, simply by binding and thus blocking the receptor upon which ethanol acts. The mechanism of action isn't fully understood, but since opioid-inhibitory compounds are effective in blocking the effects of ethanol, inhibition of the VTA-nucleus accumbens dopaminergic pathway is likely to mediate inhibition of a significant part of the reward pathway for ethanol in the brain.
The thinking behind this strategy for treating addiction lies in de-conditioning the brain to the reward response elicited by alcohol, instead of the usual scenario: have a drink, start to feel good, have another, and so on, the scenario becomes: have a drink, feel nothing (or feel sick, depending on the type of inhibitory drug used)--each time this latter cycle repeats, and alcohol fails to elicit a reward response, the less the brain associates alcohol with reward.
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References
1. Climento, Carlo C. Addiction and Change, pp. 14-15
2. The Brain's Drug Reward system. NIDA Notes, Sept-Oct. (1996)
3. Corcoran, KJ. Cognitive and Situational Factors Predict
Alcoholic Beverage Selection. Addictive Behaviors, 20:4 (1995).
4. Heyman, Gene M. (1996). Resolving the contradictions of addiction.
Behavioral and Brain Sciences 19 (4): 561-610.
5. Karl Mann, Falk Kiefer, Michael Smolka, Horst Gann, Stefan Wellek,
Andreas Heinz, and the PREDICT Study research team. Searching for
Responders to Acamprosate and Naltrexone in Alcoholism Treatment:
Rationale and Design of the Predict Study. Alcoholism: Clinical and
Experimental Research 33:4 (2009).
6. McKeon A, Frye MA, Delanty N. The Alcohol Withdrawal Syndrome.
Journal of Neurology, Neurosurgery, and Psychiatry 2008;79:854-862
7. NIH/NIDA Tenth Annual Review
[category]Recovery & Addiction[/category]
