Recovery & The Law
 Part II

"Understanding a Better Way"

By: Daniel V. Lane, JD, CCRC II - MAFC

     The uninitiated often see abstinence or self-control as the primary goal for alcoholics and addicts – the enduring ability to apply the battle cry of our former First Lady, "Just Say No." This perspective ignores, however, the fundamental dynamic of the diseases of addiction. Responsibility for actions requires response ability, the ability to say, "No." This ability is removed from alcoholics and addicts by the very diseases from which they suffer. If we have ears to hear and eyes to see, the headlines tell us this story on a daily basis.

     Less than a month ago, shortly following the submission of the first article in this series, Ignorance is Not Bliss, a dejected and beaten woman entered a plea of guilty in court to two counts of vehicular homicide. After a binge-drinking episode last March, she had driven her pickup truck the wrong way on the interstate near Cle Elum, Washington, and crashed head-on into an oncoming car, killing the 38-year-old driver and his 12-year-old daughter. A half-empty bottle of vodka by the driver’s side, her blood-alcohol level was 0.26, over three times the legal limit. It’s a story that sadly repeats itself daily somewhere in this country, but this time there was added irony. The woman is Audrey Kishline, the founder and former national spokesperson for Moderation Management, a program that advocates the notion that problem drinkers can be taught to drink in moderation – that they can learn to say, "No." Too late, Ms. Kishline realized that she could not drink in moderation. Too late, she understood, as she put it, moderation programs involve a lot of "alcoholics covering up their own alcoholism."1 Too late, she got in touch with her own personal denial of the disease from which she suffers: "I was too full of embarrassment and shame to seek help. In self-pity I gave up and believed my nightly drinking at home could hurt no one but myself."2

     And, thus, we have one more tragic lesson of what the Moral Model’s illusion of control can do; of the pain and suffering wrought by society’s continued embrace of the ignorance of the past. But, there is another answer, and it lies in understanding a better way – one that can be found in learning what medical studies have revealed about the diseases of addiction. Once understood, we will have a clearer perspective of the concepts of responsibility and response ability and, thereby, what the law can do to effectively serve and protect the society of which we are all a part.

     Following the 1970’s Scandavian study of twins and the ensuing statistical studies of ethnic/cultural groups we reviewed last month, additional research followed. Much of the intial efforts focused on the relationship between alcohol consumption and opiate receptors in the brain. In animal research conducted by Drs. Pert and Snyder in 1973, the presence of specific binding sites for opiates were confirmed.3 In 1975, Dr. Charles Lieber, chief of the research program on liver disease and nutrition at the Bronx Veterans Administration Hospital, found that the same amount of alcohol seemed to produce very different blood acetaldehyde levels in alcoholics and non-alcoholics. Much higher levels were reached in alcoholics. Dr. Lieber theorized that this unusual buildup of acetaldehyde was caused in part by a liver malfunction.4

     At the time of Dr. Lieber’s work, Dr. Virginia Davis, was in the midst of a cancer research project in San Antonio, Texas. In her work, Dr. Davis removed brains for study from the cadavers of chronic alcoholics who had died on Skid Row. She confirmed the presence of large quantities of a chemical, tetrahydroisoquinoline (THQ), in the brains of all of the cadavers. Through additional study, Dr. Davis discovered the connection between the alcoholic’s increased levels of acetaldehyde, noted by Dr. Lieber; the presence of THQ she had discovered in the brains of chronic alcoholics; and the binding sites in the brain, noted by Drs. Pert and Snyder.

     Put simply, when a non-alcoholic ingests alcohol, it is absorbed through the lining of the stomach into the bloodstream. In the liver, two biochemical reactions occur by which the alcohol is effectively degenerated and eliminated from the body. In the first, the enzyme alcohol dehydrogenase breaks down the alcohol into acetone and the toxic chemical known as acetaldehyde. The acetone is excreted from the body. In the second biochemical reaction, the enzyme acidaldehyde dehydrogenase breaks down and eliminates the acetaldehyde. In the alcoholic this process operates differently with devastating effects. In the initial biochemical reaction, the alcoholic’s liver produces acetaldehyde at an accelerated rate, so much so that the effect is that the liver is bombarded with twice the amount it is capable of immediately processing. This results from an insufficient supply of the enzyme acidaldehyde dehydrogenase being present to immediately break down and eliminate all of the acetaldehyde from the body. The excess acetaldehyde is dumped into the bloodstream and, traveling to the brain is there condensed with dopamine into THQ. And, this process is repeated each time that an alcoholic takes a drink. Slowly but surely, he or she builds up an ever-larger cache of THQ in the reward centers of the brain.

     Further research was done using rats, bred to refuse the consumption of alcohol, in an effort to determine the effect of THQ. The study began by placing these rats in a cage with a very weak solution of vodka and water. The rats refused to drink; some literally thirsting to death. Having reconfirmed the rats’ non-alcoholic preference, a minute quantity of THQ was injected into the brain of each test subject. Thereafter, the solution of vodka and water was again placed in the cage. The rats scurried across the cage to get to the alcohol mixture, drinking and drinking to the point that they lost consciousness. One, in fact, drowned in the bowl. Next, the concentration of vodka was increased, and the rats drank more and faster. The researchers also noted that the rats suffered withdrawal symptoms when alcohol was withheld, and, when it was again offered, the rats drank as though to avoid the disagreeable and painful withdrawal symptoms. Not only had the researchers created animal behavior that mimicked the alcoholic’s drinking behavior, but also they had demonstrated conclusively that with just one quick injection of THQ into the brain, a teetotalling rat could be transformed into an alcoholic rat. Additional research, utilizing our closest animal relative in medical terms, the monkey, was undertaken to determine how long THQ remains in the brain. A minute, specified quantity of THQ was injected directly into the brain tissue of selected subjects. Over a period of seven years, the monkeys were cared for and provided no alcohol or additional THQ injections. At the end, the subjects were sacrificed and their brain tissue studied to determine the quantity of THQ that remained. The study demonstrated that in each case, there had been no deterioration in the level of THQ over a period of seven years.5

     The conclusions were undeniable. Depending on an individual’s metabolism and other factors not yet fully understood, a human with this genetic liver dysfunction who drinks will eventually accumulate a sufficient quantity of THQ in the brain to create an irresistible craving for alcohol. Once that level is achieved, environmental triggers will cause a craving for alcohol that cannot be ignored. The alcoholic then crosses over the shadowy line into a whole new way of life – a life in which he or she no longer has control over drinking. In A.A. terms – the alcoholic is then and will forever remain powerless over alcohol, and so long as he or she believes drinking can be controlled, the alcoholic will not stop.

     From the outset of this series, I have used the phrase, diseases of addiction. You will now see why. As we have just learned, for many alcoholics, the genetic disease mechanism at work involves a liver dysfunction resulting in the build up of tetrahydroisoquinoline (THQ) in the brain. For other alcoholics and drug addicts, another genetic disease mechanism is present. But to grasp its nature, we must first gain some rudimentary understanding of the brain’s intricate systems which millions of years ago were designed to ensure the survival of our species.6

     At the core of the human brain lies the limbic system, known as the reptilian brain, which still performs functions necessary for survival much as it did for our primal ancestors hundreds of millions of years ago. The three primal survival behaviors – eating, avoiding being eaten, and reproducing – are directed by this system and designed to ensure we stay alive.7 This ancient part of the brain gathers sensory input necessary for survival channeling the information to a cluster of nerve-cell bodies in the brain known as the nucleus accumbens. It is the nucleus accumbens, processing input from various parts of the brain that produces the needed response, "gotta have it," and, it does this through producing the pain of craving. The pain produced, if ignored, grows in intensity, until it cannot be resisted. We learn quickly that in order to stop the pain, we "gotta have it," and so we go get it.8 This power to move us to action is generated in the nucleus accumbens by its release of a neurochemical, dopamine, which sends the signal to act. The amount of dopamine released depends on the intensity of the stress. The greater the stress, the greater the rise in dopamine. The faster and greater the rise in dopamine, the more powerful the craving.9 We cannot easily say "No" to dopamine’s commands.10

     But what is it that makes us feel safe, sated and satisfied? What stops the behavior dopamine starts? It is another primitive neurochemical, serotonin. Serotonin constrains dopamine’s actions. When one of our survival systems brings a need to our attention, it causes pain and thereby produces stress. Dopamine levels rise. We are on alert, ready to act. If we are unable to find food, a safe place, or a mate, the urgency increases. Serotonin levels decrease. At this point, we cannot let the thought go. While the primal survival system drives us to seek food, safety and sex, it is not until the serotonin drops low enough that the idea becomes an obsession. If, then, dopamine is the "gotta have it," serotonin is the "got it." It is the rising dopamine that motivates us to action, and it is the attainment, the full belly, the safe place, the completed sexual act that raises serotonin. The brain is in a high dopamine and high serotonin state. Contentment floods our being. We feel safe, satisfied and secure. The craving is gone. We can stop.11

     What does this have to do with the diseases of addiction? We define addictive behavior as the compulsive use of a substance or activity. "Gotta have it" occurs because the brain produces a craving response for that substance or activity – no craving, no addictive behavior – no addictive behavior, no addiction. Craving is a response that occurs only when survival is at stake. The pain produced by this system is intense, allowing only those thoughts that will remove the pain.12 Ivan Pavlov, the great, Russian scientist, found that salivation in response to the presentation of food could rapidly be transferred to another stimulus. In his classic experiments, Pavlov found that a bell tone repeatedly associated with the presentation of food could, on its own, after a suitable number of trials, elicit the identical physiological reactions to the presentation of food. The animal associated the bell with sight of food and the sight of food with food in the mouth. This association of food in the mouth with the bell produced the physiological response of salivation.13 This type of learning fits into the natural life order. Nature wanted as many possible patterns to motivate survival actions.14  So, in response to pattern recognition, dopamine levels rose in the nucleus accumbens to motivate us to seek those things that can stop the pain of craving. And, to work, once the pattern was recognized, the response had to be unstoppable.

     What makes the response unstoppable in an addict? What directs him or her to alcohol, cocaine, caffeine, heroin, methamphetamine, gambling and other chemicals and activities? In essence, what produces addictive behavior? The first part of the answer lies in the ability of substances and activities to raise dopamine in the nucleus accumbens. Alcohol and drugs do just that. And, as Pavlov’s research showed, this rise in dopamine can be transferred to other patterns. The jingle of ice cubes in a glass can raise dopamine if it has been associated with the ingestion of alcohol. It does not take the alcoholic long to recognize that where he sees a bar, he will find alcohol. This pattern recognition conditionally raises dopamine and motivates behavior.15  The alcoholic cannot stop his feet from walking through the door. And, each pattern recognition and response process is conditioned separately. Seeing a junkie’s syringe will not stimulate a person to think narcotics if the needle has not been previously associated with the delivery of the drug. Once conditioned however, the needle, the wrapper, the plunger, or even a small broken piece of syringe will produce the response of rising dopamine – the "gotta have it"; the "On" switch.

     The second part of the answer lies in a genetically induced low serotonin level in the brain of an addict. With pattern recognition, the "gotta have it" message is sent; the addict responds by using the substance the brain demands he or she must have to survive; the level of dopamine rises further in response to the drug, creating an even stronger "gotta have it." This is the diseased brain of an addict at work – a brain that has no way of telling itself it’s had enough. With its abnormally low serotonin level, there is no automatic regulatory system to produce a sense of satiety – there is no "Off" switch; no "got it" message. The addict uses and uses and uses. Not pain, not sickness, not severe injury, not hospitalization, not divorce, not even prison will stop this proverbial dog as it chases its tail. This is the genetic disease of addiction that no amount of consequences or punishment can cure.16

     The alcoholic or addict suffering from this genetic disease does not possess response ability, the power of choice, any more than the alcoholic suffering from the genetic liver dysfunction. Is either, then, responsible for the behaviors the disease elicits? That’s a tough question at this point. We may have come a long way in our understanding through the first two articles in this series. Certainly, we have learned the history of ignorance that still holds our society and our legal system in its grasp, and we have learned about the diseases of addiction. Yet there is still much more we need to understand to feel comfortable with our answer.

     Next month, in Recovery & The Law, Part III, we will continue to explore addiction and how it removes from the alcoholic and addict response ability. We will also begin to examine 12-Step based treatment and why it works. In so doing we will move toward the answer we seek – how to provide those afflicted with the power of choice and thereby legal responsibility for their actions. It is in this process, a better way will present itself to us – the way to provide healing while still adequately serving and protecting.

  1. Rivera, Elaine, "License to Drink," Time, (New York, NY: Time-Warner, July 31, 2000).
  2. Verhovek, Same Howe, "Moderate-Drinking Advocate Learns Sobering Lesson," The New York Times, (New York, NY: The New York Times, July 6, 2000).
  3. Schuckit, Marc A., and V. Rayses, "Ethanol Ingestion Differences in Blood Acetaldehyde Concentrations in Relatives of Alcoholics and Controls," Science, 203 (1979): p. 54.
  4. Lieber, C. S., Y. Hasumara, R. Teschke, S. Matsuzaki, and M. Korsten, "The Effect of Chronic Ethanol Consumption on Acetaldehyde Metabolism," The Role Of Acetaldehyde in the Actions of Ethanol, ed. K. O. Lindros and C. J. P. Ericksson, (Helsinki: Finnish Foundation for Alcohol Studies), 23 (1975): ps. 83-104.
  5. Ohlms, David L., "The Disease Concept of Alcoholism," (Belleville, IL: Gary Whiteaker Company, 1983); Ohlms, David L., "The Disease of Alcoholism," (Cahokia, IL: Gary Whiteaker Corporation, 1994).
  6. Ruden, Ronald A., M.D., Ph.D., "The Craving Brain," (New York, NY: Harper Collins Publishers, 1997).
  7. McFarland, D., ed. The Oxford Companion to Animal Behavior, (New York: Oxford University Press, 1987).
  8. Phillips, A. G., J. R. Atkinson, J. R. Blackburn, and C. D. Blaha, "Increased Extracellular Dopamine in the Nucleus Accumbens of the Rat Elicited by a Conditional Stimulus for Food: An Electrochemical Study," Canadian Journal of Physiology and Pharmacology,, 71 (1993): ps. 387-93.
  9. Willner, P., and J. Scheel-Kruger, The Mesolimbic Dopamine System: From Motivation to Action, (New York, John Wiley & Sons, 1991).
  10. Wilder, A., "Conditioning Factors in Opiate Addiction and Relapse,"Journal of Substance Abuse Treatment, 1 (1984): ps. 277-85.
  11. McFarland, D., ed. The Oxford Companion to Animal Behavior, (New York: Oxford University Press, 1987).
  12. Ludwig, A. M., "Pavlov’s Bells and Alcohol Craving," Addictive Behaviors, 11 (1986): ps. 87-91.
  13. Jacobs, W. J., and J. R. Blackburn, "A Model of Pavlovian Conditioning Variations in the Representation of the Unconditional Stimulus," Integrative Physiological and Behavioral Science, 30 (1995): ps. 12-33.
  14. Sutherland, N. S., "Outlines of a Theory of Visual Pattern Recognition in Animals and Man," Proceedings of the Royal Society B., 171 (1968): ps. 297-317.
  15. Wilder, A., "Conditioning Factors in Opiate Addiction and Relapse,"Journal of Substance Abuse Treatment, 1 (1984): ps. 277-85.
  16. Spoont, M. R., "Modulatory Role of Serotonin in Neural Information Processing: Implications for Human Psychopathology," Psychological Bulletin, 112 (1992): ps. 330-50.

      Daniel V. Lane is a former attorney with an undergraduate degree from the University of Southern California and a degree of Juris Doctor from Southwestern University School of Law. His experience in the field of chemical dependency includes both correctional and community-based treatment settings. He is SASCA Case Manager for Cornerstone of Southern California and has certifications as a supervisory level Criminal Reformation Clinician and a Master Addictions Forensic Counselor. He is the author of numerous articles in regional and national professional publications in addition to his ongoing series, "Recovery & The Law," currently appearing at www.anonymousone.com. In addition to writing in the field of chemical dependency, he frequently lectures on a variety of recovery topics, including spirituality & the 12-Steps, the diseases of addiction and the use of rational emotive therapeutic techniques in recovery. You can contact Dan at (714) 547-2061 or by e-mail bluephoenix@Adelphia.net  

NOTE: For more information concerning the brain function in relation to the disease of addiction and the dynamics of recovery, the reader is urged to consult the work of Ronald A. Ruden, M.D., Ph.D. Publication of the newly updated and revised edition of his seminal work, The Craving Brain, will be available in the Fall, 2002.

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