Updated 07/05/03. First presented 29/09/2001,
Local School – Community Drug Summit
JOHN XX111 COLLEGE, Mr. Claremont Western Australia
BIOMEDICAL RESEARCH: ADDICTION IS A DISEASE
By Charles Slack*
INTRODUCTION: marinated handshakes of impostor transmitters blow your mind
When Susan Greenfield visited Australia last year to deliver the Andrew Olle Memorial Trust Lecture and appear on the ABC’s Science Show, she also took time to explain the latest scientific view of how drugs affect our brains. Professor Greenfield is the first woman director of the prestigious 200-year-old Royal Institution of Great Britain and Fullerton Professor of Physiology at Oxford.
Professor Greenfield says morphine and the opiates are imposters. “They pretend to be natural occurring transmitters, and therefore can zoom in and shake hands with…receptors. But because they are not removed so rapidly, because they are marinating the whole brain, because they are not introduced into the tiny little connections, they are very heavy handed. And it’s like shaking hands in such a way that you make the hand numb. So you need more and more in order to get a sensitive handshake. And that’s one of the bases of addiction.” She concluded, “our minds are configurations of different connections. Drugs and transmitters work at the connections. Then if you change those transmitters, phrases like ‘blowing your mind’ or ‘losing your mind’ might be horribly accurate.”[1]
When someone of the stature of Professor Greenfield, CBE, Life Peerage (non-political), and the recipient of eighteen honorary degrees, describes neuroscience with words like “impostor”, “marinate”, “hand shake”, “blowing your mind” and “losing your mind”, one can be sure it is not done frivolously, superciliously or condescendingly. Baroness Greenfield knows full well that a mountain of solid scientific research stands behind every metaphor she chooses. This research is best classed as “biomedical” implying “hard data” and meaning extremely multi-disciplinary, consisting of repeated, reliable, valid studies done at recognized laboratories in the US, UK, Europe and elsewhere. It is often said to have revolutionized understanding of the nature of drug abuse and addiction. And one conclusion is “addiction may well be the quintessential biobehavioral disorder”.[2]
THE CLINICAL VIEWPOINT: one man, one paper (among hundreds)
At an opposite pole in terms of geography and international prestige, in Des Moines, Iowa, in 1998, shortly before his untimely death, a family doctor named Michael E. Abrams wrote a paper titled “Brain Addiction Disorders”[3]. Abrams, board certified in both Family Medicine and Addiction Medicine was a dedicated practitioner who fought continuously for the medical rights of the homeless, prisoners, alcoholics, drug addicts, the poor, the depressed, the Satanic cult victims and those with chronic pain.[4]
A good doctor and a saintly man, Abrams published little and was unlikely to win honors other than the respect of colleagues and the love of his patients. His reasons for writing were a) his extensive clinical experience with addicted persons in a clinical setting and b) his need to update staff with regard to the latest research. Yet, in its own way, Abrams’ paper is a scientific paper, a summary of hard-earned clinical results. Far from unique – scores like it were published at about the same time – it was written with the specific intent of teaching medical staff, nursing staff and caregivers. Abrams states, “Through over twenty years of managing and treating patients with acute brain disorders, I cannot differentiate the primary brain disease in the emergency department or emergency setting. They all have similar abnormal signs, symptoms/behaviors and disordered thoughts.” The brain disease research had exploded so rapidly in the nineties that professional and paraprofessional staff needed upgrading. The unique thing about papers like Abrams is the confidence with which they reach their nearly identical conclusions and the incredible amount of reliable research available to them, identical research to that alluded to by Professor Greenfield from Oxford University. In other words, Abrams was saying in his humble clinical way that addiction is a brain disease like any other and needs to be treated as such. In this, of course, he was in perfect agreement with Professor Greenfield.
Such unanimity was not always the case. Until the mid-nineteen eighties, “Addiction Studies” was a field more characterized by diversity of belief than consensus of hard fact, a kind of no-man’s-land of social-science jargon, philosophical diversity, clinical inference, self-help group anecdote, religious creed, moral injunction and political opinion. The field appeared to have been abandoned (or at least neglected) by the hard sciences. Thus it remained for drug counselors, fringe practitioners, volunteer helpers, evangelists, emergency staff, detox centres, rehabs, family doctors, and even the addicted patients themselves to devise their own diagnoses and invent their own treatments at the most local level with little or no help from the scientific mainstream.
In other words, family doctors like Abrams were receiving no input from professors like Greenfield. And they needed it badly!
BIOMEDICAL RESEARCH: hope and inspiration
Not so in 1998: all had changed by the time Dr. Abrams wrote his paper. By that time, for at least two decades, the hard sciences and the behavioral sciences had miraculously found a way to combine their efforts, millions of research dollars had been spent, fantastic new equipment purchased, powerful software written, and extensive communication networks had evolved. Laboratories in the US and elsewhere had become beehives of biomedical research on addictions of all kinds, producing multiple-authorship papers with an array of disciplines involved. It all added up to a vast literature of relevant studies, a kind of great pyramid of research results, leading upward to one consummate conclusion: addiction is a disease of the brain.
In his opening paragraph, Abrams was moved to report:
Brain Addictive Drug Disorder (BADO) has captivated the world’s best scholars and scientists in ascertaining the mechanisms of the neuronal-molecular process, initiated by placing a brain-addictive drug into the brain. The 1990s, the ‘decade of the brain’ in around-the-world research, as produced a gusher of scientific, objective discoveries and databases to insatiable professional palates, allowing an intelligent, medical-management approach to once indefinable brain disorders.
Then in his last paragraph, Abrams concludes:
It is important to recognize that neuronal research discoveries and reproducible objective data have given brain-addiction medicine renewed hope, scientific attitude and non-controversial space to discuss and teach, legislate, treat and adequately fund brain research and disease prevention. A public forum about brain addictive disorders from a scientific neuronal biobehavioral foundation should stimulate our brain circuits to say, ‘This is a highly significant stimulus, please repeat the stimulus, so I can learn.’ So be it!
No less impressive than the certainty of Abrams’ conclusions is the depth and variety of research to which he refers in drawing them. And remember – Abrams is not a researcher but a clinician. His paper, intended as a stimulus to upgrade staff, lists twenty-one sources including several solid, peer-reviewed journals:
1. “A Man with Alcoholism and HIV Infection.” JAMA, vol. 274, 10, pgs. 837-843, (September 13, 1995).
2. “Addicted.” Time Magazine, pgs. 67-76, (May 5, 1997).
3. “Addiction and the Brain.” The Harvard Mental Health Letter, Part I, vol.14, 12, (June 1998) and Part II, vol. 14, 1 (July 1998).
4. “Addiction as a Brain Disease.” The American Journal of Psychiatry, vol. 155, 6, editorial and 3 other articles, (June 1998).
5. “Alcohol Health & Research.” World/NIAAA Neuro Science, vol. 21, 2, (1997).
6. “Emerging Approaches to Alcohol Research.” World/NIAAA Neuro Science, vol. 21, 4, (1997).
7. “Management of Alcohol Withdrawal: Two Viewpoints.” Physician Assistant, pgs. 110-116, (May 1996).
8. “New Understanding of Drug Addiction.” Hospital Practice, McGraw-Hill Companies, Inc., (April 1997).
9. “Probing the Biology of Emotion.” Science, vol. 280, pgs. 1005-1007, (May 15, 1998).
10. “Teaching the Brain to Take Drugs.” Science, vol. 280, pgs. 2045-2047, (June 26, 1998).
11. Abrams, M., M.D. and Parham, William, PA-C, D.O. “The Management of Delirium Tremens in Acute Alcoholism.” Physician Assistant, pgs. 69-78, (September 1995).
12. Andreasen, Nancy C. “Linking Mind and Brain, Study of Mental Illness.” Science, vol. 275, 14, pgs. 1586-1592, (March 1997).
13. Gold, Mark S., M.D. “Neurobiology of Addiction and Recovery.” Journal of Substance Abuse Treatment, vol. 11, 2, pgs. 93-97, (1994).
14. Johnson, B.A., M.D., Ph.D. and Roache, J.D., Ph.D. Drug Addiction and Its Treatment, Lippincott-Raven Publishers, (1997).
15. Karch, Steven B., M.D. (Ed.). Drug Abuse Handbook, CRC Press, (1998).
16. Nemeroff, Charles B., M.D. “The Neurobiology of Depression.” Scientific American, pgs. 42-49, (June 1998).
17. Nihart, Mary Ann, R.N., C.S., M.A. “The Neurobiology of Schizophrenia.” Journal of the American Psych Nurses Association, vol. 2, 5, pgs. 174-180, (October 1996).
18. Roob, George, Ph.D., Nesther, Eric J., M.D., Ph.D. “The Neurobiology of Drug Addiction.” Journal of Neuropsychiatry, vol. 9, 3, pgs. 482-496, (Summer 1997).
19. Salloway, Malloy and Cumming. The Neuropsychiatry of Limbic and Subcortical Disorders, American Psychiatric Press, Inc, (1997).
20. Science, 8 articles. Vol. 278, 3, pgs. 35-69, www.sciencemag.org. [On-line]. (October 1997).
21. Sollowagin, Stephen, M.D., M.S. “Addictive Disorders: Brain and Behavior.” Psychiatric Times, (April 1998).
The diversity of titles is striking, as is the range of media, from the Journal of Substance Abuse Treatment to the Psychiatric Times, through the popular Time Magazine, the prestigious Science and the solid professional Journal of the American Medical Association. Some of Abrams’ references, themselves, contain reviews of the literature, hence my pyramid analogy. One can easily access a dozen recent papers similar to Abrams with reference lists at least as long. To clinicians like Abrams, the brain-disease model of addiction in the late twentieth century appears to be a milestone in the historiography of science.
VERDICT: the jury is in
Alan I. Leshner is director of the National Institute on Drug Abuse at the National Institutes of Health, USA and as such has become a spokesperson for the brain disease concept. Leshner says, “It is as if drugs have highjacked the brain’s natural motivational control circuits, resulting in drug use becoming the sole, or at least the top, motivational priority for the individual. Thus, the majority of the biomedical community now considers addiction in its essence, to be a brain disease: a condition caused by persistent changes in brain structure and function.” [5]
After reading Leshner, one arrives at the opinion that “brain disease” has graduated from the “model” stage and into nearly paradigmatic status.
We now know in great detail the brain mechanisms through which drugs acutely modify mood, memory, perception, and emotional states. Using drugs repeatedly over time changes brain structure and function in fundamental and long-lasting ways that can persist long after the individual stops using them. Addiction comes about through an array of neuroadaptive changes and the laying down and strengthening of new memory connections in various circuits in the brain. We do not yet know all the relevant mechanisms, but the evidence suggests that those long-lasting brain changes are responsible for the distortions of cognitive and emotional functioning that characterize addicts, particularly including the compulsion to use drugs that is the essence of addiction.[6]
Leshner then advises us to read nine other recent papers.
Recommended reading (Leshner)
1. J. D. Berke and S. E. Hyman, "Addiction, Dopamine, and the Molecular Mechanisms of Memory," Neuron 25 (2000): 515532 (http://www.neuron.org/cgi/content/full/25/3/515/).
2. H. Garavan, J. Pankiewicz, A. Bloom, J. K. Cho, L. Sperry, T. J. Ross, B. J. Salmeron, R. Risinger, D. Kelley, and E. A. Stein, "Cue-Induced Cocaine Craving: Neuroanatomical Specificity for Drug Users and Drug Stimuli," American Journal of Psychiatry 157 (2000): 17891798 (http://ajp.psychiatryonline.org/cgi/content/full/157/11/1789).
3. A. I. Leshner, "Science-Based Views of Drug Addiction and Its Treatment," Journal of the American Medical Association 282 (1999): 13141316 (http://jama.ama-assn.org/issues/v282n14/rfull/jct90020.html).
4. A. T. McLellan, D. C. Lewis, C. P. O'Brien, and H. D. Kleber, "Drug Dependence, a Chronic Medical Illness," Journal of the American Medical Association 284 (2000): 16891695 (http://jama.ama-assn.org/issues/v284n13/rfull/jsc00024.html).
5. National Institute on Drug Abuse, Principles of Drug Addiction Treatment: A Research-Based Guide (National Institutes of Health, Bethesda, MD, July 2000) (http://165.112.78.61/PODAT/PODATindex.html).
6. National Institute on Drug Abuse, Preventing Drug Use Among Children and Adolescents: A Research-Based Guide (National Institutes of Health, Bethesda, MD, March 1997) (http://165.112.78.61/Prevention/Prevopen.html).
7. E. J. Nestler, "Genes and Addiction," Nature Genetics 26 (2000): 277281 (http://www.nature.com/cgi-taf/DynaPage.taf?file=/ng/journal/v26/n3/full/ng1100_277.html).
8. Physician Leadership on National Drug Policy, position paper on drug policy (PLNDP Program Office, Brown University, Center for Alcohol and Addiction Studies, Providence, R.I.: January 2000) (http://center.butler.brown.edu/plndp/Resources/resources.html).
9. F. S. Taxman and J. A. Bouffard, "The Importance of Systems in Improving Offender Outcomes: New Frontiers in Treatment Integrity," Justice Research and Policy 2 (2000): 3758
One of these (2. Garavan, et al) exemplifies the kind of experimental research now coming out under the brain-disease banner. It is a team effort that, judging from methodology and instrumentation, must have involved specialists in psychiatry, clinical and experimental psychology, functional Magnetic Resonance Imaging, computer systems, experimental design, statistical inference, and pharmacology. The bibliography for this paper contains forty-five references including one about “A volume optimized quadrature elliptical endcap birdcage brain coil (abstract 4015) in Proceedings of the 11th Annual Scientific Congress. Vienna, European Society for Magnetic Resonance in Medicine and Biology, 1992.” Just reading this reference, let alone implementing it, appears to be a specialty.
Yet the results and conclusion of the study are relatively easy to grasp. When cocaine users look at a video of a man smoking cocaine, their brain patterns are similar to those of (otherwise similar) non-users watching a pornographic film. Of course, the experiment is well controlled with neutral (nature) stimuli and a comparison group of non-users: the results are probably quite reliable. I have discussed these results with former cocaine users in Narcotics Anonymous all of whom said the results confirmed their experience. One told me, “They could have asked us and saved their money.”
Indeed, the experiment must have been costly. I imagine we could operate a Perth rehab for several years on the funding for that one study. Nevertheless, now that the data are available, we must give them some attention. One interesting finding: in contrast to the effects of the cocaine film (which really aroused the cocaine users but left the non-users “unactivated”), cocaine users showed a smaller neuroanitomical response than the comparison subjects to the sex film. This suggests that cocaine use has “hijacked” neural processes normally associated with sex and focused them on cocaine paraphernalia, cocaine procurement and cocaine use.
Another finding, true for all such experiments, is that a certain place in the brain and the chemicals associated with this spot are always involved in drug (and perhaps non-drug) addictions. Abrams and nearly every brain-addictions researcher also mention this region (in the middle of the bottom of the brain down near the brain stem). In the conservative manner of scientists writing in the American Journal of Psychiatry, Garavan et al say, “It has been suggested that cocaine’s potency may stem from its ability to directly activate the mesocorticolimbic dopamine system[7].” Actually it is much more than suggested: nearly all say it’s a proven fact that this part of the brain is involved in all addictions.
As a matter of fact, the whole recent explosion of biomedical brain-disease research can be said to have begun with the discovery of this brain zone. And the discovery was not made by a US neurologist, neurosurgeon or any other medical specialist but by a Canadian experimental psychologist working with rats in a learning lab.
At McGill University in Montreal in the 1950s’s, as at many US psychology labs, the reigning scientific philosophy was behaviorism. The extreme form of behaviorism said that the mind didn’t exist because you couldn’t observe it: scientists could actually only observe overt behavior and therefore overt behavior was all that scientists were allowed to talk about.
Of course everybody knew there must be “brain activity” but good behaviorists were simply not allowed to hypothesize it unless they could identify, qualify and quantify it in some way.
One psychologist who thought different was Professor D. O. Hebb at McGill, Hebb believed in “intervening variables” going on inside the skull between the “stimulus” and the “response.”
For this reason, one of Professor Hebb’s brightest students, James Olds, began inserting electrodes through the skulls of rats to give them mild electric shocks at various places in the cerebral cortex. The hope was these shocks might alter “intervening variables” so as to provide proof they really existed. It turned out their speculations were correct - beyond their wildest dreams.
The first experiments were crude but even so, Olds found a place where an electric shock seemed to make his rats happy. He called it the “pleasure zone”. It was in fact the now-famous mesocorticolimbic system. “Pleasure” turned out to be too mild a word for this particular “intervening variable”: Olds’ rats would rather press a lever that delivered a tiny shock to the mesocorticolimbus than eat! In one experiment he rigged up an electric grid on the floor of his rats’ cage. If the brain electrode was placed just right[8], it achieved an astounding result: when current to the floor grid was turned up so high that rats would starve to death rather than cross it, he found they would still cross in order to press the lever for a tiny current to their mesocorticolimbus.
So there you have it: rats with post-traumatic stress and burned feet happily pressing away to get their mesocorticolimbic shock fix – and, by the way, ignoring lady rats and anything else Olds could think of as comparison activities.[9] Small wonder these experiments eventually attracted researchers seeking answers the drug dilemma.
In the Howard Hughes Memorial Institute Bulletin, science writer, Gary Taub[10] gives some more historical details:
While Olds was at work with electrical stimulation, psychologists and pharmacologists were using similar systems to characterize the pharmacology and phenomenology of drug abuse. In their laboratories, rats and monkeys pushed levers to get intravenous amphetamines, cocaine or opiates. These researchers wanted to know which brain chemicals these drugs affected, so they simultaneously gave the animals other drugs to interfere with some of the brain chemicals to see what would happen. In particular, the researchers suspected that a class of neurotransmitters known as catecholamines—which includes norepinephrine, dopamine and serotonin—might be involved. Sure enough, "what we found was that selective blockade of the dopamine system made it so rats wouldn't work for cocaine or amphetamines anymore," says National Institute of Drug Abuse psychologist Roy Wise, who pioneered research in this area in the 1960s and 1970s. "And blocking the dopamine system made animals lose interest in the electrical brain stimulation as well."
By the late 1980s, researchers had demonstrated that activation of this dopamine system in the reward pathways of the nucleus accumbens is the common denominator in all drugs of abuse—whether "downers" such as heroin, morphine and alcohol, or "uppers" such as cocaine and amphetamines…
Having identified which neurotransmitter was mediating the effect of addictive drugs, and where in the brain this was happening, researchers have spent the past decade dissecting the mechanism and its various interactions with both the drugs and other systems in the brain. Normally, when dopaminergic neurons are given the signal to fire, dopamine is released into the extracellular space. There, in the gap between synapses, it binds to dopamine receptors on downstream cells, thus transmitting messages from neuron to neuron. It's a communication process controlled as much by the firing signal as by the amount of dopamine available, which in turn depends on the cells' ability to recapture the dopamine after it has been dispatched. A molecule known as a dopamine transporter has the responsibility of recapturing the dopamine and returning it inside the nerve terminals where it is then repackaged into vesicles for the next firing. "The transporter is often thought of as a pump that pumps neurotransmitters into the cell against their concentration gradients," says Susan Amara, an HHMI investigator at the Vollum Institute in Oregon.
Thus biomedical research begins to provide a foundation for a scientific understanding of the age-old question “why do people use drugs?”
Before drawing conclusions, I would like to refer to another rather separate body of research known as “longitudinal studies”.
So far I have focused on brain-disease experiments. Although treatment recommendations[11] stem from these studies, the studies themselves must be classified as diagnosis research. Treatment research per se involves the comparative study of various treatment methods. All treatment research is limited by its time-lines. Experiments commonly take the form: pretest, treatment, time interval, posttest where the interval between treatment and posttest is less than a year or two. Such studies tend to be biased in favour of false recovery conclusions (addicts appear to have recovered when they are actually only in temporary remission). Those who still have the problem (use drugs symptomatically) may, in the short run, get labeled as improved, recovered or even cured. Only when such cases are followed up closely for many years does the truth emerge: they eventually relapse, they eventually become totally abstinent through some means outside the bounds of the original study or, in some cases, they die prematurely.
Likewise, short-term total-abstinence studies tend to be biased in favour of false relapse conclusions.[12] When addicts initially abstain from drugs, they often appear to get worse rather than better, reporting a variety of discomforts, symptomatoid complaints and disturbing behaviors. In the long term, however, if these same addicts happen to remain totally drug-free, complaints disappear and behavior normalizes. The time required for signs of improvement may be months or years. Hence the need for longitudinal research.
An adequate review of longitudinal research is beyond the scope of my paper. Rather I refer the reader to Vaillant[13] whose book contains thorough reviews of much research and thorough reports of continuing longitudinal studies. Although his work is limited to alcoholism, Vaillant is generally regarded as a summa corona of addiction researchers.
1. Though most of the extensive body of brain-disease research was conducted in the USA, acceptance by scientists and professionals is worldwide. “The majority of the biomedical community now considers addiction, in its essence to be a brain disease: a condition caused by persistent changes in brain structure and function”[14]
.
2. The research was and is largely inspired by neurological discoveries (Olds[15]) and technological developments[16], rather than by social observations, political policies, or ethical beliefs. It was not done to “prove a point” but to “discover more facts”.
3. The research, as a whole, supports the conclusion “that drug addiction is a brain disease that develops over time as a result of the initial voluntary behavior of using drugs.” Thus the first response (and a variable number of subsequent responses) are voluntary but eventually drug use produces “a virtually uncontrollable compulsive drug craving, seeking, and use that interferes with, if not destroys, an individual’s functioning in the family and in society.”[17] With complete abstinence, the compulsions eventually subside (extinguish) but, without complete abstinence, they can last for life.
4. Once addiction has set in, recovery (abstinence) is very difficult to achieve requiring, in addition to treatment, extensive follow-up and long-term accountability. Longitudinal research supports the efficacy of continuing “fellowships” such as Alcoholics Anonymous and Narcotics Anonymous.
5. Addiction is no longer defined in terms of withdrawals but rather in terms of the persistent cravings that result from long-lasting changes in brain structure and function.
6. All drugs of addiction involve certain common regions, networks and chemicals in the brain. Thus it becomes difficult to abstain from one drug without abstaining from all drugs.
7. Since admitting that one is addicted implies that one should abstain, the disease itself, having captured motivational control circuits, prompts addicts to deny the truth of their compulsion. Before addiction sets in, users continue voluntarily because of pleasure. After addiction, users continue because they must but deny they are addicted.
8. To quote Leshner again[18] “It is also important to correct the common misimpression that drug use, abuse, and addiction are points on a single continuum along which one slides back and forth over time, moving from user to addict, then back to occasional user, then back to addict. Clinical observation and more formal research studies support the view that, once addicted, the individual has moved into a different state of being. It is as if a threshold has been crossed. Very few people appear able to successfully return to occasional use after having been truly addicted. Unfortunately, we do not yet have a clear biological or behavioral marker of that transition from voluntary drug use to addiction. However, a body of scientific evidence is rapidly developing that points to an array of cellular and molecular changes in specific brain circuits. Moreover, many of these brain changes are common to all chemical addictions, and some also are typical of other compulsive behaviors such as pathological overeating.”
1. This research generally supports abstinence-based treatments and preventative measures. The ultimate aim of successful treatment is complete avoidance of the addicting drug and other drugs with similar neural networkings. The aim of prevention is also total abstinence. Nevertheless, how the aim of abstinence is to be achieved may differ among persons and between groups.
1. If you have never used drugs of addiction, do not start. If you are currently using but not addicted, quit. If you are addicted, get treatment. If you have had treatment, avoid relapse through lifestyle changes. Reduce “cue-induced” and other craving experiences by associating with non-users and ex-users. “Fellowship” with ex-users and non-users.
2. The research is surprisingly consonant with the “disease concept” of programs like Alcoholics Anonymous and Narcotics Anonymous. To them, “the disease of addiction” is an active agent that takes over one’s life. The disease is sometimes phenomenologically described as “telling us to do things that lead to relapse”. Likewise it is not a great conceptual stretch to relate brain-disease findings to the “demon rum” concepts of the nineteenth century temperance movement. (One might, for example, define “demon”, as a “brain disease with a will of its own” - analogous to a computer virus that takes over your computer and eventually wipes its hard disk.)
3. “Addiction should be understood as a chronic recurring illness. Although some addicts do gain full control over their drug use after a single treatment episode, many have relapses. Repeated treatments become necessary to increase the intervals between and diminish the intensity of relapses, until the individual achieves abstinence.”[19]
.
Most informed clinicians and researchers accept brain-based research in addiction. Nevertheless some who believe biology and psychology to be competing explanations have ignored or opposed the disease concept.
A final quote from Leshner[20], “Many people also erroneously still believe that drug addiction is simply a failure of will or of strength of character. Research contradicts that position. However, the recognition that addiction is a brain disease does not mean that the addict is simply a hapless victim. Addiction begins with the voluntary behavior of using drugs, and addicts must participate in and take some significant responsibility for their recovery. Thus, having this brain disease does not absolve the addict of responsibility for his or her behavior, but it does explain why an addict cannot simply stop using drugs by sheer force of will alone. It also dictates a much more sophisticated approach to dealing with the array of problems surrounding drug abuse and addiction in our society.”
Still another group of (largely social) scientists made an early commitment to be opposed to all “disease models” They opposed the “disease notion” in part because it was associated with total abstinence. Both the disease concept and total abstinence were felt to be holdovers from temperance movements and religious moralisms of nineteenth century Victorian society.
My primary purpose in writing this paper is to correct a serious error of omission in the recently held W. A. Drug Summit[21]. This Summit failed to mention, let alone emphasize, the major brain-disease research findings. Reports in the West Australian media of brain-disease research are rare or non-existent. The public is uninformed. The local biomedical scientific community is failing in its duty. West Australia is behind times.
I fear that other programs and curricula in this state may be ignorant of, or deficient in referring to, this important body of data.
To matriculate students in “addictions studies” who are unfamiliar with this research is propaedeutically unsound.
Finally, to formulate drug policy in the midst of an epidemic without recourse to this literature and the conclusion flowing from it is to court unnecessary disaster.