Addiction Narratives Versus Reality.......

I recently posted my take on this issue of race in addiction treatment. The main argument that I was responding to was that the current opioid epidemic is whitewashed so to speak. In other words white opioid addicts are considered to be "victims" of the opioid epidemic and black addicts are considered just to be addicts at best and criminalized at worst.  Part of the way that white people are framed as victims is by calling addiction a disease.  The author who I was critiquing at the time suggested that the opioid epidemic was marketed to white people along with the medication (buprenorphine) that would "cure" them.  Further, that buprenorphine was more easily available to white people by the nature of the prescribing requirements.  The article went on to selectively highlight one segment of the population where "non-Hispanic blacks" had a higher rate of overdose deaths, despite the fact that the majority of people dying in most categories were white.  I consider my counterargument to be a solid one and that is - there is no known difference in the biological predisposition to addiction of any kind that is based on race and if that likelihood is equal - the only consideration is who is exposed to the drug.

The racialization of the opioid epidemic picked up more speed over the weekend.  One of the theories proposed was that there were no previous "epidemics" of opioid use and that this is another way to sanitize the problem and make it more acceptable to white people.  The article was written for a newspaper - the Guardian and the headline says it all:  "Amid the opioid epidemic, white means victim, black means addict."  That is the basic thesis that runs through the entire essay.  You are either a white, Christian, Republican racist, who considers himself to be a victim of prescription opioid tablets or drug dealers or the hypocritical structure of American society insults you for being black and an addict.  It is suggested directly in the article that common rationalizations of addicts - the ones that everybody uses irrespective of race or substance are the exclusively used by whites to deny responsibility for addiction.  Self-loathing of the addict is described as though that never happens with white people.  Guilt, shame, and self loathing happens to everyone with an alcohol or drug misuse problem.
          
A couple of the arguments can be debunked at the outset. The idea that the term epidemics is applied only to white people so that they can rationalize being victims ignores the medical literature of the 1970s.  In those days researchers were using the terms epidemics and microepidemics and applying the terms across racial groups (3-6).  Successful naturalistic studies were conducted in both white and black neighborhoods and the success in a Chicago study (6) was  correlated with use of the term medical management.  Those same authors used what they called an infectious disease model for intervening in heroin epidemics (5).  The Chicago study was so successful that it was suggested as an alternative to involuntary treatment (4):

 "This work suggests that heroin addiction can be prevented in many who are at risk; it further suggests that prevention may be possible by using psychological and social concepts based on humanist principles without the use of coercion. The authors' approach deserves close attention not only because it offers hope in the face of a mounting national tragedy but also because of its relevance in the current high-level and little-publicized debate over the use of compulsory urine testing and compulsory treatment of drug dependent persons."   - p.1156
     
It appears that at least in psychiatry - humanism was emphasized as the critical element in treating drug dependent persons (not addicts) as far back as 46 years ago.  The design of the naturalistic study in question was impressive and methadone maintenance treatment was used in a majority of the patients.

The issue of differences in the story about the self perception of a white versus black addict does not have the equivalent empirical basis.  I can say unequivocally that any attitude in treatment about being a "victim" of substance use of any type  would be vigorously confronted by treatment staff.  It is not possible to actively participate in treatment with that attitude.  The same is true of the self loathing patient.  Guilt, shame, and self loathing need to be actively explored and corrected to allow participation in the recovery process.  Both attitudes can lead to distress or increased cravings to use drugs and alcohol and relapse.

What about the contention that cultural differences and disparities are the primary problem with treatment differences.  I refer any interested reader to an in depth analysis of the issues by Coleman Hughes (2) and what he describes as the disparity fallacy - in other words that the difference in outcomes between blacks and whites (or any two groups) is due to discrimination being the causal factor.  He lists an impressive number of examples, but I see the underlying principle as being one of undeterminism (7) that is there are multiple theories to account for differences, and people tend to have a favorite and ignore all of the other possibilities.  There is probably no better example than the race rhetoric around addiction.  The promotion of these arguments ignores the primary causes of addiction - a biological predisposition and exposure to the addictive substance.  I am not suggesting disparities are irrelevant to exposure or treatment access but focusing on them as casual ignores the major factors.           

The continued stories about racial differences in treatment and self perception are not really conducive to reshaping America's addiction treatment landscape.  It misses the big picture that there are no differences in race when it comes to addiction.  Any reasonable treatment approach would disabuse anybody coming through the door who believed they were either a victim or a self-loathing addict.  Identical treatment modalities should be offered irrespective of race and that includes medication assisted treatment of all types, necessary psychiatric and psychological treatment, medical evaluation and treatment, and drug and alcohol counseling focused on recovery.  One of the reasons why addiction is viewed as a chronic illness is the high likelihood of relapse and need for ongoing recovery services and support.  One of the main tenets of any 12-step recovery program based on the AA model is that nobody is turned away. The only requirement for membership is a desire to get sober.   

The real problem with drug and alcohol treatment is not racial disparity. It would be fairly obvious if racial discrimination was occurring in any comprehensive treatment program.  The real problem with drug and alcohol treatment is the lack of standards and consistency in treatment.  The most clear cut example is the availability of detox services.  Some forms of withdrawal are life threatening and need to be immediately recognized and treated.  I doubt that the majority of treatment programs in any state have that capability.  Hospitals have been defunded from providing detox services from anyone who is not experiencing life threatening withdrawal for about 30 years now. That has led to a proliferation of subpar and non-medical county detox facilities where limited to no medical care is rendered.  These kinds of inconsistencies in care occur across the board and it is common to see patients who have not received even basic addiction care - completing a treatment program and being released back to their home setting.

Racism has no place in medicine.  I have discussed the advantages of therapeutic neutrality on these pages before and certainly any physician who is not able to do that should not be practicing medicine in the 21st century.  The psychiatric standard for neutrality is higher.  Psychiatrists in particular are trained to understand cultural differences, but it is not possible to be an expert on every culture.  It is possible to appreciate the person in the room and proceed cautiously enough to assure that culturally sensitive care is being provided.         

In the end, there are clearly ways to prevent and treat addiction. Suggesting that race and the narratives around race are the primary factors that account for addiction or recovery is unfounded.


George Dawson, MD, DFAPA


References:

1:  Brian Broome.  Amid the opioid epidemic, white means victim, black means addict.  April 28, 2018.

2:  Coleman Hughes.  The Racism Treadmill.  Quillette May 14, 2018.

3: DuPont RL, Greene MH. The dynamics of a heroin addiction epidemic. Science.1973 Aug 24;181(4101):716-22. PubMed PMID: 4724929.

4: Freedman DX, Senay EC. Heroin epidemics. JAMA. 1973 Mar 5;223(10):1155-6. PubMed PMID: 4739378. 

5: Hughes PH, Crawford GA. A contagious disease model for researching and intervening in heroin epidemics. Arch Gen Psychiatry. 1972 Aug;27(2):149-55. PubMed PMID: 5042822.

6: Hughes PH, Senay EC, Parker R. The medical management of a heroin epidemic. Arch Gen Psychiatry. 1972 Nov;27(5):585-91. PubMed PMID: 5080286.

7:  Stanford, Kyle, "Underdetermination of Scientific Theory", The Stanford Encyclopedia of Philosophy (Winter 2017 Edition), Edward N. Zalta (ed.), URL = https://plato.stanford.edu/archives/win2017/entries/scientific-underdetermination/.

The Loose Connection Between Disease Definition, Addiction, and Neuroscience

Carl Hart is a neuroscience professor and department head at Columbia.  He wrote an opinion piece in the first edition of the new journal Nature Human Behavior about the social consequences of calling addiction a brain disease. The original article is reference 1 below with a link.  I encourage anyone interested to read it several times.  I say that because the concepts contained in the article are emotional, confusing, and politicized.  Repeated reading allows a clearer picture of these concepts.

In the introduction he discusses his early hope that by learning neuroscience and curing addiction "through neural manipulations" that he could help rid resource poor communities of crime and poverty.  His main arguments against the notion that addiction is a "disease" is that the majority of people who use a drug do not become addicted and the old argument that is typically used against psychiatric disorders - there is no actual lesion in the brain to differentiate the addicted from the non-addicted.  He uses the example of Huntington's or Parkinson's Disease as brain diseases that nobody would argue with.

The form of those initial premises should not be lost on any student of rhetoric because one does not follow the other. With any disease that occurs as a result of environmental exposure, it is likely that a large percentage of the exposed population will not develop the disease.  A lot of that depends on the toxicity of the exposure and the personal biology of the exposed.  One of the best examples is alcohol exposure.  It takes a certain amount of exposure to cause pancreatitis and cirrhosis both of which cause observable end organ damage and yet the vast majority of people exposed to alcohol develop neither.  The epidemiological estimates are also group averaged effects, so it is possible to observe outliers who ingested well beyond the suggested dose necessary to produce the disease and yet they have no evidence of damage.

The results are even more variable when it comes to Wernicke-Korsakoff syndrome an alcohol related illness caused by thiamine deficiency.  The vast majority of alcoholics never develop the symptoms but a significant number of people do and there are a significant number who are diagnosed at autopsy but not when they are alive (5).  An autopsy diagnosis is possible because of discrete brain lesions caused by the disorder.

The brain lesion argument is inaccurate at a number of levels.  First, equating disease with brain lesion is not accurate.  Medical diagnostic terminology has always been approximate rather than precise when it comes to pathognomonic lesions.  There are very few.  Nobody seems to argue that migraine headaches or cluster headaches are not diseases with significant disability.  Despite the fact that there are no brain lesions like neurodegenerative diseases or "identified biological substrates" that differentiate migraine patients from the rest of the population. Syndenham pointed out that there are disorders are identified based on a consistent pattern of symptoms, family history, a natural history and course and predictable response to treatment.  This general trend led Merskey to say:

There is no royal road to medical diagnosis.  For every condition with a defined lesion there will be several with no lesion at all.  My favorite is cervicalgia or neck pain.  If you follow ICD 10 codes it is M54.2.  It is no small problem because at least half of the population aged 65 or older had significant degenerative arthritis and much of this is in the spine.  To make things even more nonspecific, practically all of these patients will have abnormal imaging studies of the spine.  Unless there is a clear finding on physical exam or by electrophysiological testing the pain cannot be attributed to any specific lesion.  As the pain becomes chronic there is even less connection to any underlying anatomy or physiology.  Connections between "real" diseases and biological substrates are not hard and fast by any means.

In addition to Syndenham's approach to disease definition,  there is a common sense approach.  Even when psychiatric disorders and addictions have no clear laboratory test, polls indicate that they are generally recognized as diseases by physicians and the public in general.  I would argue that all physicians encounter the severest problems in both groups of people.  I speculate that the public realizes that uncontrolled use of an intoxicant to the point that it disrupts your life and leads to steady psychosocial deterioration to the point that all of your significant relationships are lost and you are unable to self correct - is a form of disease very close to severe psychiatric problems.   Severe life-threatening problems that are beyond a person's capacity to self correct are seen as diseases.

Dr. Hart's next argument is one that has been found in the media over the past two years - more research funding should be directed at the psychosocial aspects of addiction rather than the neurobiological and basic science aspects.  We have seen this line of reasoning applied to a Stanley Foundation grant to look at the genetics of psychiatric disorders and the National Institute or Health budget itself.  It is generally a utilitarian argument based on the premise that basic science and brain research produces no useful solutions or that there has been a lack of focus on psychosocial determinants or consequences of drug use or addiction.  If the initial argument is that most people who use drugs do not get addicted - it does not follow that there would be widespread consequences.  In terms of determinants, they have been studied in many cases in detail and in the context of racial disparities in care (2-4).  But studying them and even applying common sense does not produce a solution.  The clearest example is 40 years of research on psychotherapies that are effective and designing a health system designed to ignore that fact.  With addiction the psychosocial research has even more readily been ignored.

The argument about how the diseased brain model leads to unrealistic policies is quite a stretch.  Dr. Hart suggests that such a model only allows for two solutions - focus on the diseased brain or focus on removing the drug from society. He incorrectly concludes that any focus on the brain removes an interest in socioeconomic factors in "maintaining or mediating drug addiction."  Practically any available treatment for addiction whether it involves residential or outpatient treatment - cognitive behavioral therapy or twelve step recovery involves a comprehensive look at the psychosocial factors that may impede recovery or keep the cycle of addiction going.  Do we really need further research to know that psychosocial factors increase the exposure to addictive drugs?  After all the exposure is the first part of the problem.  He has already concluded that the vast number of this exposed do not end up addicted.  What is it about that exposure and that particular person who does end up with the addiction?  How are they different and in any group will psychosocial determinants tell us why these differences exist?

He makes the statement: "The insidious assumption of the diseased brain theory is that any use of a certain drug is considered pathological, even the non-problematic, recreational use that characterizes the experience of the overwhelming majority who ingest these drugs."  That statement is totally incorrect.  People like me are treating people with addictions.  By definition they have uncontrolled use of the drug to the point that they are no longer able to function.  In many cases they have accumulated considerable medical and psychiatric comorbidity because of their inability to stop using drugs.  That is what I am talking about when I consider addiction a brain based disease.  It is a disease that involves the ingestion of an intoxicant with predictable long term consequences.  That is not "recreational use."  The issue of recreational use cannot be taken lightly.  According to the CDC, a person who is addicted to prescription opioids is 40 times more likely to use heroin compared with a person who is not.  Every addicted prescription opioid user who I have talked with started out as a recreational user.  Since I only see people with addictions, the only recreational users of opioids who I see, could not tolerate opioids and moved on to something else.

The crux of Dr. Hart's argument seems to be that focus on neuroscience has led to malignant law enforcement efforts to eliminate drug use from marginalized citizens.  He cites the differences in the legal penalties for crack cocaine as opposed to powdered cocaine a frequent illustration of discrimination against blacks as opposed to suburban whites.  He seems to ignore that fact that drug and alcohol use takes a heavy toll and that toll occurs independent of race.  The leap from neuroscience to politics and law enforcement is quite a leap.  Is it possible for example that the police, the prosecutors and the politicians involved are more likely to discriminate against the marginalized citizens that Hart refers to?  I would say it is highly likely and would offer several of the posts on this blog documenting active discrimination from politicians and insurance companies against addicts and the mentally ill.  None of the people making those discriminatory policies, rationing resources or denying rational treatment care one bit about neuroscience.  Most of them barely know that the brain is located in the head.        

Let me conclude with what is know about addictions and why that knowledge is only peripherally related to politics.  A significant portion of the population is at risk for addiction.  Many of them know it because they notice that there are several generations of addicts and/or alcoholics in their family and in general - most people can see that trend without talking to professional.  Exposure to drugs or alcohol is the other critical variable.  Contrary to the suggestion of recreational use, people predisposed to addictions recognize early on that their pattern of use is distinct from that of their peers.  They recognize at one point that their ability to control it is gone.  They recognize it is taking a heavy toll on their physical health, mental health, finances, and relationships but they can't stop.  They recognize neurobiological features like craving, tolerance, and withdrawal.  More importantly for the purposes of Dr. Hart's argument - addiction is an equal opportunity disease.  Racism has certainly suggested otherwise on a historical basis, but the opioid epidemic and its reach into rural America has illustrated that anyone can become a heroin addict.  Exposure to the drug is the critical factor and not the few genes that determine skin color.

You can call that a disease if you want and most lay people and physicians would agree with you.  My only qualification is that the definition of disease is very imprecise.  People arguing that addiction is not a disease seem to not know that.  Are there demonstrable changes due to addiction in animal models and humans?  Of course there are and most modern addiction medicine text books exhaustively list them in each chapter on a specific addictive drug.  It is much more specific to call an addiction what it is, cite the actual neurobiology and study it - just like modern approaches to any number of difficult biological problems in medicine.

That doesn't rule out psychosocial research on addiction.  That research happens all of the time.  The problem is the same problem that was previously noted in psychiatric research.  We have 30 years of research proven psychosocial therapies in psychiatry.  They have modest effect sizes, but the problem is that nobody will pay for them.  There is a strong overlap with addiction since many of the therapies are similar.  The real cause of discrimination is not at the level of the scientific community.  The real cause of discrimination occurs at the levels of the bureaucrats running the healthcare system and a political system that is clearly set up to favor businesses and the wealthy.


George Dawson, MD, DFAPA




1:  Hart CL.  Viewing addiction as a brain disease promotes social injustice.  Nature Human Behaviour, Published online: 17 February 2017; doi:10.1038/s41562-017-0055

2:  Greene EL, Thomas CR. Minority Health and Disparities-Related Issues: Part I. Med Clin North Am. 2005 Jul;89(4):721-919, PubMed PMID: 16129107.

3:  Greene EL, Thomas CR. Minority Health and Disparities-Related Issues: Part II.  Med Clin North Am. 2005 Sep;89(5):921-1066, PubMed PMID: 16129107.

4:  Ruiz P, Primm A (eds).  Disparities in Psychiatric Care.  Philadelphia, PA: Lippincott Williams & Wilkins, 2010.

5: Sechi G, Serra A. Wernicke's encephalopathy: new clinical settings and recent advances in diagnosis and management. Lancet Neurol. 2007 May;6(5):442-55.  Review. PubMed PMID: 17434099.

The Surgeon General's Report on Addiction

Last week, the current Surgeon General Vivek H. Murthy, MD came out with the first report from that office on addiction.  The full text is available on line at this link.  The document is 428 pages long but it is full of a lot of unnecessary text.  As an example the first 64 pages are essentially an introduction and a listing of personnel who worked on the report as well as references.  The last 85 pages are references and appendices.  I don't know the chain of command but both the US Department of Health and Human Services (DHHS) and the Substance Abuse and Mental Health Services Administration (SAMHSA) have their imprint on it and that is not necessarily a good thing.  The Surgeon General came out with a letter earlier this fall about how to stop the opioid epidemic that I commented on.  That letter was brief, to the point, and could have been expanded into a more concise document than the current report.

There is a lot wrong with this report.  Just from an administrative side, it is clear that the report sends a strong public relations message about what the government is doing to advance the treatment of addiction and a lot of that message is flat out spin.  I am always interested in detoxification from addictive drugs so I naturally searched on that and found this paragraph:

 "Until quite recently, substance misuse problems and substance use disorders were viewed as social problems, best managed at the individual and family levels, and sometimes through the existing social infrastructure—such as schools and places of worship, and, when necessary, through civil and criminal justice interventions. In the 1970s, when rates of substance misuse increased, including by college students and Vietnam War veterans, most families and traditional social services were not prepared to handle this problem. Despite a compelling national need for treatment, the existing health care system was neither trained to care for nor especially eager to accept patients with substance use disorders." (p 1-19).

That is really not what happened.  It is not even close.  Services to treat addiction were rationed just like services to treat mental illnesses.  With the federal and state governments giving carte blanche to managed care companies - hospitalizations that required detoxification could be denied even if the patient had a significant psychiatric disorder.  Trauma surgeons were also affected by this discrimination.  People with serious traumatic injuries who also had positive toxicology for drugs or alcohol were denied payment for a hospitalization that required extensive surgery and prolonged hospital stays.  The very thin system of care for addictions and mental illness were outside of the funding stream of mainstream medicine because that is exactly where the government and the business world placed it.  In the entire document there is one reference to prior-authorization (p. 6-24) and then only to say that it is one of many strategies used by states to ration Medicaid resources used for treating addictions.

On the issue of training, in about 1992 I had accumulated a series of cases that involved inpatient detoxification that were denied payment by a managed care intermediary representing the state government.  All of these denials have appeal processes that are stacked against physicians and patients.  In this case I was told I would need to argue all of them in front of an administrative law judge.  I took a vacation day and was ready to do that.  On the day before the hearing, I was notified that the judge had made a summary decision in favor of the managed care company and I did not have to show up for the hearing.  This is obviously not a training issue when I am doing detoxification, a managed care company is telling me to discharge patients (2/3 of whom also have significant mental illnesses), and the state is backing them up.

In the entire document there are 4 paragraphs on detoxification - referred to as "Acute Stabilization and Withdrawal Management". (p. 4-12 - 4-13).  It really minimizes the medical aspects of detoxification and the potential complexity of the situation to the degree that it seems to have been written by a nonphysician.  The clear intent is to stress that detoxification by itself is not treatment for an addiction but only a necessary first step.  In the process it also minimizes the medical and nursing expertise necessary to get people through the detoxification phase.  After an entire chapter on neurobiology there is no mention of the craving and dysphoria that often prevent people from completing detoxification or cause them to immediately relapse afterwards.  There is no mention of the medical comorbidity that needs to be addressed along with the detoxification process.  There is no mention of the complexity involved in detoxifying people from multiple addictive substances - a common scenario these days.  There is no mention of why allowing people to detoxify themselves at home with addictive substances may or may not be a good idea.  There is no mention of why "social detoxification" in non-medical detox centers run by municipalities may or may not be a good idea.  There is no mention of the psychological aspects of detoxification and why it presents one of the most significant obstacles to care in the treatment of addiction.  In short, detoxification would seem to have a much more prominent role in a report about facing addiction than it does in this report.  The treatment of addiction would have been better served if all of these issues would have been addressed and the minimum medical requirements for detoxification could have been established.  

On the less wrong but not perfect side of things, there is a lot of neurobiology in the report, both in terms of basic science and medication assisted treatment.  The neurobiology is fairly intense for the average reader who is part of the target audience.  Even at the level of physicians who I lecture to and train the concept of the extended amygdala is comprehended by very few people.  I could probably say the same thing about the amygdala.  In fact, I attended a course of brain dissection by one of the pioneers of this concept Lennart Heimer, MD.  At the end of that two day course, in a room of highly motivated and interested people I think that few understood the importance of the concept.  My point in all of this is the old adage - you can know just enough neurobiology to be dangerous.  At some point all of these names just become pseudo-explanations, especially for people with a poor understanding of science.  I have talked with people who knew all of the jargon and started to explain their own addictions with it.  That was not a good scientific or clinical approach and I wonder if the public may have been better served by an approach that focuses on the conscious state of the addict.  We still do not know how that is derived from the underlying neurobiology - even though the neurobiological explanations make it seem like we do.  

Criticism aside, there are some things that the report does well.  It provides a fair outline of the NIDA based continuum of care guidelines for addiction treatment for people with severe addictions.  The specific section can be found starting on  page 4-13 and the section: Principles of Effective Treatment And Treatment Planning.  The average person or family interested in seeking treatment for someone with an addiction is often faced with a staggering array of treatment services and a lot of associated politics.  The news media is often a source of increasing confusion rather than clarity.  A recent example is the rise of certain treatment methods that claim very high rates of success, or that are critical of more traditional treatment approaches like 12-step recovery (AA, NA, TSF (Twelve-Step Facilitation Therapy) and residential treatment.  Managed care companies continue to ration residential treatment 1 or 2 or 5 or 7 days at a time.  From the report:

"A typical progression for someone who has a severe substance use disorder might start with 3 to 7 days in a medically managed withdrawal program, followed by a 1- to 3-month period of intensive rehabilitative care in a residential treatment program, followed by continuing care, first in an intensive outpatient program (2 to 5 days per week for a few months) and later in a traditional outpatient program that meets 1 to 2 times per month. For many patients whose current living situations are not conducive to recovery, outpatient services should be provided in conjunction with recovery-supportive housing."  (p. 4-18).

That recommendation on the continuum of care should be kept in mind by anyone who is seeing an addiction specialist from any discipline in their office on an outpatient basis and finds that they are not able to stop using drugs or alcohol.  That would include physicians or other prescribers who are providing medications and possibly making the situation more dangerous because of the combination of prescribed and addictive drugs.  There is a temptation to say that with new innovations in medication assisted treatments that all that is necessary is seeing a physician and getting medications to treat the addiction.  A close read of any of the FDA approved package inserts on these medications addresses the complexity and points out that psychosocial treatments like the ones in the above paragraph are necessary.  There is no strictly medical cure for addiction.

It is also fairly common these days to see Alcoholics Anonymous and their principles being bashed in various forums like the popular media or web sites that seek to aggregate professionals.  They appeal to people who don't like the model for various reasons, consider it antiquated, or claim more success using some other treatment.  Some of these sources are also confused, often by neurobiology or an ignorance of the treatment literature and claim that there is no evidence that 12-step recovery works.  The report provides solid evidence to the contrary.  TSF is listed as a treatment intervention with a solid evidence basis and results as good as any and it works as a stand-alone intervention or in combination with other treatment modalities (p. 4-28 to 4-30) that are often suggested as competing treatment models.

That's my overall take on the report.  Like most government documents it is a lot of unnecessary reading so I may have missed something and I can't comment on everything.  It is clearly the product of committees, meetings, and bureaucrats.  Documents like these serve a variety of purposes in addition to the stated purposes of educating the public and establishing public health policy.  As a person who lived through it, this is also a serious rewrite of history.  That history is decades of what has been called "health care reform".  In this country that means hiring proxies to ration healthcare.  When that happens the most disenfranchised patients get the most rationing.  Those patients have always been people with addictions and mental illnesses.   The real intervention needed in the addiction treatment landscape is establishing some controls on companies who are set to profit from denying care for addiction treatment and the governments that encourage it.

That is the single-most powerful intervention that we need in the addiction treatment field and it was nowhere in the report.


George Dawson, MD, DFAPA


References:

U.S. Department of Health and Human Services (HHS), Office of the Surgeon General, Facing Addiction in America: The Surgeon General’s Report on Alcohol, Drugs, and Health. Washington, DC: HHS, November 2016.


Disclosure:

I have no connection with any of the parties of agencies who wrote this report.  I am obviously a psychiatrist with a life long commitment to treating mental illness and addiction and extensive personal experience with the rationing of these treatment services.  I am currently employed at a treatment center that uses most of the treatment modalities specified in this report including medication assisted therapies (MAT).

Eric Kandel Comes To Minnesota

Eric Kandel, MD

Nobel Laureates don't come to Minnesota very often but they apparently come at least once a year to Gustavus Adolphus College and the annual Nobel Conference.  This year's conference was particularly interesting to me because it starred the only modern psychiatrist to be a Nobel Laureate - Eric Kandel.  He shared the podium with his wife and research collaborator Denise Kandel.  Eric Kandel is a giant in neuroscience and has continued to extend his research well into the time in life where most people have been retired for years.  In my addiction lectures, I use his well known paper Psychotherapy and the Single Synapse published in 1979 and his recent work on nicotine exposure and the risk of cocaine use entitled A Molecular Basis for Nicotine as a Gateway Drug published in 2014 as lecture references.  Kandel has been a neuroscientist and a psychiatrist longer than I have been a psychiatrist.  The other aspect of Kandel's more accessible work is his ability to integrate basic neuroscience and cognitive neuroscience into a coherent story of possibilities.  The best example is the book The Age of Insight that I briefly reviewed on this blog.  It is clear from reading Kandel that he has a lot on his mind and he is actively seeking answers and organizing his observations.  Another feature that piqued my interest in this case was why he was presenting at an addiction conference in a state where many people believe that addiction treatment was invented.  I did not find out about the conference until it was too late to take time off of work to attend.  I was very pleased to find the presentations and Q&A sessions by Eric Kandel and Denise Kandel available online.  There are a total of 4 videos and they will load and play in succession.  There may be more videos with the Kandels but I only watched these four.

In the first session Kandel discusses some of the early discoveries in brain systems and how the idea of localization of brain function played out.  For most physicians with a passing knowledge of aphasia and strokes it is a bit tedious.  Eventually he gets to a discussion of memory localization and talks about implicit and explicit memory.  That allows him to look at different features, animal models and the molecular biology of these types of memory.  He goes on to look at age-associated memory loss and Alzheimer's Disease and the different brain substrates and mechanisms.  At that point some of his slides illustrate chromatin and transcription sites but he does not get bogged down in the details as he defers the chromatin issue to a later presentation and discusses RbAp48 as a critical transcription factor in the formation of long term memories.  He showed a plausible mechanism for exercise leading to osteocalcin secretion from bones and improvement in memory as one possible humoral factor associated with vigorous exercise.  In terms of style points, he had great graphics especially the diagram of the DNA strand wrapped around histone octamers and how the transcription process is affected by various molecules. He was clearly there to present a lot of information to non-molecular biologists.  He was a little hurried at times.  He makes a few misstatements and gets distracted like all of us do during presentations.   He interjects some humor along the way.  As the presentation continues it is clear that this is important information.

The Q & A session was focused primarily on the question: "Is addiction a brain disease?"  The other panelists and their biographical sketches can be viewed at this page.  I did not realize it until after I had viewed all of the sessions that the lectures were not a good fit in terms of answering that question.  The lectures were focused on the neurobiology of learning and how epigenetic changes due to nicotine exposure lead to other addictions.  They were not lectures on the neurobiology of addiction per se, but there were some partially suggested mechanisms related to Kandel's work on memory.  Addiction being a brain disease was really not the point of the lectures.    It was obvious that the other panelists were at the minimum resistant to the idea but there was also open opposition.  If you read the biographical sketches one of the panelists has written a book on why addiction is not a disease.  If they really wanted to argue that point they could have brought me down for a Neurobiology of Addiction lecture and I could have dissected the arguments about addiction being a disease or not.  A much better idea would be to bring Eric Nestler in for the lecture.

 The panelists seemed of the opinion that plastic changes in the brain were normal and therefore plastic changes in the brain caused by addictive compounds was not a sign of pathology.  Some seemed not to be focused on the brain at all but cultural or social factors that they thought were important.  In at least one case, they seemed to suggest that addiction needs to occur in a certain context - that all addictions are not created equal.  The example given was a wealthy white guy with a cocaine addiction could just jet off to the Caribbean and go swimming as a way to deal with his addiction.  Someone else would not have that opportunity.  Kandel had a singular focus that all human behavior, that everything that we are occurs because of what is happening in the brain.  He kept going back to this idea and pointed out that alterations in brain plasticity certainly occur during addiction but they are negative and not positive changes.  He of course agrees that social and psychological processes are important intervening factors but all of the processing occurs at the level of the brain.  Some of the panelists seemed uncomfortable with this basic idea and he got into it with one of them, but eventually summarized the problem as a lack of a common culture.  He extended that comment to include the idea that the panel is discussing these problems so that younger generations in the audience will not have to start at that contentious point.  To me it came back to the mismatch between the Kandels' lectures on the epidemiology and molecular biology of nicotine as a gateway drug and the other panelists arguing that addiction was not a disease.

Denise Kandel began the third session reviewing the epidemiology of when people start using addictive substances and what the relationship is to nicotine.  In general, nicotine use is a strong predictor of cocaine use and ongoing cocaine use.   She analyzed three databases that are essentially cross sectional surveys of substance use including the NSDUH (National Survey On Drug Use and Health),  MTF (Monitoring the Future) and NESARC (The National Epidemiologic Survey on Alcohol and Related Conditions).  She discussed the concept of Translational Epidemiology or making population wide observations and then looking at models to explain the observations.  She had what I would call a critical observation on the observed drop in cocaine use and cocaine related mortality and cigarette use.  The recent drop in cocaine related mortality seems to correlate with a decrease in smoking.  Eric Kandel stepped in for the basic science section to elaborate on the mechanism of histone acetylation and how that occurs from nicotine exposure.  Denise Kandel returned to talk about the problems with e-cigarettes as potentiating factors for the use of other drugs and also as probably not a good way to stop smoking.  If you had time to watch one of the videos I would recommend this one.

The final Q & A session was an interesting one.  One of the panelists talked about the sociological theories of drug use rather than a gateway involving a biological substance.  For example, the fact that you take a substance that makes you feel good, increases the likelihood that you will take additional compounds that will do the same and that you will associate with people who have common interests and they will encourage further drug use.  Kandel had three comments during this session that I thought were very interesting.  The first involved the scientific rationale of a reductionist approach.  When you hear it explicitly stated rather than being used in a vague and rhetorical manner - it makes a lot more sense.  The second had to do with a painting by Gustav Klimt called Judith beheading Holofernes (Judith I and the head of Holofernes).  He tells the story about this biblical incident and discusses how this is a painting that combines elements of aggression and sensuality and how recent work by Anderson has shown that there is a 20% overlap between areas of the brain that govern aggressive behavior and areas that govern sexuality and reproductive behavior.  At one point Kandel seemed frustrated by some other panel members and made a reference to reproducibility that may have startled a few of them.  Denise Kandel had previously alluded to the bias against reductionism in her discussion with the statement:   "It's a reductionist approach to which some members of this audience are going to object strenuously"

The videos were very affirming for me.  When I think about the lectures I give on Kandel's work and some of the posts on this blog - I am confident that I have come to the same conclusions that he comes to about the brain and about reductionism.  Of course it is easier for me, because he provides the conclusions and I merely teach them.  I don't think that everybody has come to those conclusions either at a scientific or philosophical level.  It is too easy to get hung up on polarizing questions and political debates about science these days, especially using imprecise definitions like the word disease or claiming that reductionism is a fatal flaw rather than a good way to do science.  It is too easy to mistake journalism - in many cases hatchet-job journalism - for science.  The other striking factor is that this is a brain centric view of the world and that seems like the only logical approach to me.  Various critics will attack the brain centric view of neuroscience or psychiatry in ways that seem to miss the point.  Much of the criticism comes down to the definitions of diseases or disorders and the idea that a biomedical approach to the brain means that only biomedical treatments are possible.

I think that it might be easier to reconcile the brain centric view if the ultimate result of that view is considered and that is tremendous computational power that results in billions of people with billions of unique conscious states.  That is the ultimate product of what Dr. Kandel is talking about in terms of human learning - how it affects the conscious state and the associated brain substrate.  That may have something to do with biomedical treatments, but it also applies to every other intervention that can be brought to bear to facilitate recovery.  To make an even more obvious argument - the cure is in your head - not out in the ether somewhere.  The corollary is that it is important to know what those mechanisms are.

If you have time, watch these videos.  It is a rare chance to see one of the brightest guys in psychiatry and neuroscience in action.  I would also encourage reading The Age of Insight.  It left me with the impression that this is a scientist at the top of his game and it is inspirational reading.


George Dawson, MD, DFAPA  


References:

1: Kandel ER. Psychotherapy and the single synapse. The impact of psychiatric thought on neurobiologic research. N Engl J Med. 1979 Nov 8;301(19):1028-37. PubMed PMID: 40128.

2: Kandel DB, Kandel ER. A molecular basis for nicotine as a gateway drug. N Engl J Med. 2014 Nov 20;371(21):2038-9. doi: 10.1056/NEJMc1411785. PubMed PMID: 25409384.

3: Anderson DJ. Optogenetics, sex, and violence in the brain: implications for psychiatry. Biol Psychiatry. 2012 Jun 15;71(12):1081-9. doi: 10.1016/j.biopsych.2011.11.012. Epub 2011 Dec 29. Review. PubMed PMID: 22209636.

Attribution:  The picture of Eric Kandel is By Bengt Oberger (Own work) [CC BY-SA 4.0 (http://creativecommons.org/licenses/by-sa/4.0)], via Wikimedia Commons.  The file URL is:  https://upload.wikimedia.org/wikipedia/commons/c/ca/Eric_Kandel_01.JPG.



Supplementary 1:  I am fully aware of the fact that Denise Kandel and the other participants in the conference were there and are all scholars.  The title of this post reflects that fact that the Nobel Laureate came to the Noble Conference.

Supplementary 2:  This is a blog and it should be obvious that none of the speakers, institutions, or content producers mentioned in this blog post endorse this work or even know about it.  This statement is for anyone who does not think it is that obvious.  I did not attend this meeting and had no input into its content.

"Junk" Neuroscience?

A recent comment on my observation that normal function of human memory could explain what he considered to be obvious lies prompted a reading suggestion.  The author suggested that I should read a book called "Junk Neuroscience" by Satel. The only book I could find with a similar title was  Brainwashed: The Seductive Appeal of Mindless Neuroscience.   I am reluctant to spend good money on a polemics when I can get as much polemic as I want by reading it for free on the internet.  It turns out I am familiar with the author's work from a Frontiers in Psychiatry series that I reviewed last year before presenting a CME course lecture on the neurobiology of addiction.  There are currently 19 papers collected there including Satel and Lilienfeld's.  It is somewhat ironic that the entire series is based on a what I would see as assumptions that have a faulty historical, medical and certainly neurobiological premise and that is:

"For much of the 20th Century, theories of addictive behavior and motivation were polarized between two models. The first model viewed addiction as a moral failure for which addicts are rightly held responsible and judged accordingly. The second model, in contrast, viewed addiction as a specific brain disease caused by neurobiological adaptations occurring in response to chronic drug or alcohol use, and over which addicts have no choice or control....."

The first few lines captures the main problem with debates about any topic but it is particularly pernicious when it comes to addiction and neuroscience.  It leads to a number of false observations that seem to be cropping up in the popular press at an increased frequency.  The observation that most addictions spontaneously remit is taken as evidence that they do not require treatment or that neurobiological factors do not need to be considered.  There is the idea that you can be a "heavy drinker" without being an alcoholic suggesting that "heavy drinking" is protective against the factors leading excessive mortality and morbidity in alcoholism.  Those same arguments lead back to the idea that addiction is either a choice or a bad habit.  Both are gross oversimplifications of how complex decision-making is affected in addictions.  One of the main diagnostic systems for addiction from the American Society of Addiction Medicine (ASAM) describes addiction as:  "Addiction is a primary, chronic disease of brain reward, motivation, memory and related circuitry".  It does not however suggest that addicts "have no choice or control".  In fact, much treatment of addiction depends on a 12-step recovery model that is designed to help learn new controls, improve social affiliation, and re-engineer living environments to remove triggers for relapse.  The learning, affiliation, cravings and relapse triggers all have neurobiological substrates.  Against that backdrop there are 19 papers offered and Satel and Lilienfeld's is one of them.

I happen to be fortunate enough to work at a residential center that specializes in treating addictions.  In addition to the clinical work I present a number of lectures to graduate students, physicians, and residents.  The residents are in primary care and psychiatry.  The two slides that follow are right out of my PowerPoint on the neurobiology of addiction.  The Theories of Addiction slide is intended as a rapid survey of addiction theories.  I put it out there as a warm up and free associate to the theories on the slide.  As an an example, I will look at the nutritional deficiency theory of alcohol or look at alcohol being considered a medicine by itself and how that correlates with per capita alcohol consumption in the US.  I can build on that point by looking at the cultural factors that affect per capita alcohol consumption int he US and the UK.  I might ask groups of physicians if Self Medication is a legitimate theory of addiction.  Practically all physicians have heard: "Listen doc, if you can't do something about my (pain, depression, anxiety, insomnia) - I know what I can do to make it go away for a few hours."  Everybody in the room also knows that in the long run, none of those symptoms/syndromes/disorders can be treated and in fact many become considerably worse as a result of the drug or alcohol use.  Even the example of availability proneness that I typically use only partially accounts for addiction.

Any approach to neurobiology has to account for pathways to recovery as well as pathways to addiction.  In treatment centers most of those pathways are based on learning interventions.  I digress to talk about the how learning occurs both in the addiction process and in the recovery process.  I start out with Kandel's example from his classic New England Journal of Medicine article on plasticity.  His original example talks about two people in a room during a psychotherapy session, and the brain changes that occur in both as a result of that session.  Both people leave the room and their brains have been changed by the discussion.  Experience dependent changes in the brain.  That brief introduction brings me to the four considerations of the neurobiology lecture.  They are listed in the second slide below.  

I think that these are all fairly basic starting points for a lectures on neurobiology and proceed to talk about a number of systems and structures that are thought to be important from a neurobiological standpoint.  I bring in the concept that nobody knows how it all works together by a brief discussion of Chalmers hard problem or the fact that we don't know how anyone's unique conscious state comes about and what that implies.  I am evolving to a new lecture that looks at complex decision making and its roots in the neuroanatomical structures that I discuss in this lecture.  Studying this field is what I consider to be fun.  It brings together a number of concepts from my previous scientific studies.  I would probably be focused on this if I was practicing clinical psychiatry or retired.  I will be the first to admit that I am not a trained neuroscientist, but I have been trained in science and worked in scientific research.

That brings me to Satel and Lilienfeld's paper.  I don't know either author.  If you read the paper it is definitely well written and it has 121 references.  There is a bolded statement before the text begins saying that this paper is excerpted from the book Brainwashed: The Seductive Appeal of Mindless Neuroscience.  As far as I know that is the book that would apparently straighten out my views about neuroscience.  The author's begin with: "The brain-disease model implies erroneously that the brain is necessarily the most important and useful level of analysis for understanding and treating addiction." and build rapidly to a second: "In short, the brain-disease model obscures the dimension of choice in addiction, the capacity to respond to incentives, and also the essential fact people use drugs for reasons (as consistent with a self-medication hypothesis)."

Working at an addiction treatment center and talking with thousands of people in my career with severe addictions leads me to have an explosion of associations whenever I see broad generalizations about the problem.  I don't know that the concept of disease means that an affected organ system is necessarily "the most important and useful level of analysis."  There seem to me to be many diseases where that is not true.  On the issue of "reasons to take drugs" it is seldom as rational as the author's suggest.  A classic example is one that I frequently use when lecturing about the current opioid epidemic.  A significant portion of the population is prone to get a hypomanic euphorigenic effect from taking opioids.  For nonpsychiatrists, that mean the person becomes extremely euphoric, energetic, productive, and socially outgoing.  On the initial night or two, they may engage in work or creative activities at a rate that surprises them.  Many will say: "I thought I had become the person I always wanted to be."  Carefully interviewing that person several months later will get the description that they developed a tolerance to that effect.  Now they were taking the opioid "just to stay well" or prevent withdrawal symptoms.  Koob has described this cycle as  "a chronic relapsing syndrome that moves from an impulse control disorder involving positive reinforcement to a compulsive disorder involving negative reinforcement."  Consistent with this definition is that the drug has both positive (euphoria) and negative (prevents withdrawal) reinforcing effects.  The reason to take the drug is an addiction or the specific match of drug effects on a specific nervous system.  Even in a case when addictive drugs are taken for other reasons (there is a long list) it often is due to the fact that the drug is perceived as having magical qualities or as a rationalization for continuing the addiction.

I could make similar arguments for all of the main points in this paper that I have laid out in the following table.  The authors provide ample details examples to support their contentions.  Part of the problem is that the concept of disease is complex.  When you try to dissect it the problems become apparent.  The other problem is that if this is a disease, it is a disease of complex decision making and very few people focus on that.  

What after all is considered a disease?  Any reader can come up with conditions that they consider diseases for many of the ten points above.  That is easiest for the points involving the clearest comparisons with disease (1, 2, 6, 10).  In other cases (4), their point seems to be somewhat arbitrary.  With any chronic illnesses it is usually possible to function with limited incapacity due to the illness until the late stages.   In some cases the critique has more to do with the unique capacity of the organ than anything else.  For example in point (3), emergent properties that are less obvious can be considered a property an any electrical tissue.  Cardiac tissue can produce electrical patterns of decreasing complexity as a heart ages or is affected by disease.  The brain can produce a very similar pattern (see Supplementary 1).  The only difference is that heart tissue is unable to produce a conscious state.  Two of the points (5, 9) minimize the role of a systems involved in complex decision-making.  This is no trivial matter because it is associated with addictive behaviors that lead most people to classify alcohol and drug use disorders as diseases.  Common examples include people who are unable to stop using drugs and alcohol despite life threatening illnesses, repeated pleas from family members, or repeated problems with relationships, employment or the law.  Deaths due to addiction are common and they impact on a large population.  You are much more likely to see a condition as a disease if you know it has killed somebody.  Point (7) is a curious argument.  In the past several years, I have attended seminars showing for example that in some trials of buprenorphine maintenance for opioid use disorders that the addition of counseling adds nothing to the outcome beyond the medication.   I don't personally believe that, but I am used to seeing people with severe addiction who cannot stop until they are taken out of their using environment.  In every residential treatment center that I am aware of, the main focus is on "personal agency" whether that is 12-step recovery (Alcoholics Anonymous, Narcotics Anonymous) or other methods for psychological change.  As part of that process there is often a focus on neurobiology not as an excuse but as an explanation for how people can become somebody that they never thought they could become and how that process can be reversed.  The other reason for a focus on neurobiology is medication assisted treatment and a discussion of how those medications might work as part of both informed consent and interest on the part of the patients.

I wonder if the best characterization of what is going on here has more to do with philosophy than neuroscience.  As I previously pointed out in a critique of a philosopher's attack on psychiatry - a straw man approach was used.  He suggested that something was true about the field and then proceeded with his attack as if it was true.  When confronted with that single fact and asked about any evidence to support the contention - the people supporting that contention drew an apparent blank.  To this day as far as I know there is no rational way to argue that the APA has an implicit position in the DSM-5 that teaches people how to live their lives.  Even as I write it on the page it is absurd and yet that was the form of the argument.   The current paper is much more sophisticated than that.   It points out the limitations of the disease concept and how that can be used rhetorically but then proceeds to eschew what they refer to as a "neurocentric view" of addiction.  I don't think that argument carries the day largely because there is very little evidence that the people who know neuroscience have the adverse effects that the authors suggest.  There is plenty of evidence that the neuroscientist-clinicians are focused on multiple levels of care.  I have a lot more to say about what is a disease and diseases of complex decision-making but I am going to stop here.  Look for those topics to be addressed in individual posts in the future.  In the meantime, read about the neuroscience of addiction.  The field has added more to brain neuroscience than just about any other discipline in the past three decades.  

I think an additional explanation of my intent in the reply is necessary.  I use the term "political" a lot when referring to editorials, rhetoric, and other polemics.  People who should know better seem to respond to a lot of these articles as though they are either the "truth" or the "facts" that happen to support their viewpoint.  I like my science very dry.  I ascribe to Pigliucci's observation that science is a process and if there is a truth it only occurs at the end of a very long process or a series of approximations.

Seeing it any other way shuts down that process and we are left with something that is ideologically based and no longer science.

George Dawson, MD, DFAPA

1: Satel S, Lilienfeld SO. Addiction and the brain-disease fallacy. Front Psychiatry. 2014 Mar 3;4:141. doi: 10.3389/fpsyt.2013.00141. eCollection 2013.   Review. PubMed PMID: 24624096


Supplementary 1:

I attached these graphics to illustrate that electrically active tissue can have emergent properties that are really unknown by either looking at the tissue or doing other kinds of biological analyses.  That is true for both the brain and the heart.  I don't have the heart graphs but could probably find them.  They are identical.  I do have the graphs of brain activity from a patient with Alzheimer's Disease and a normal control patient.  Recordings are from a single parietal electrode in the delta frequency and show the degree of variability over the same time interval.

Single Electrode EEG - Control

Single Electrode EEG - Alzheimer's Disease

The Denial of Plasticity

For the past couple of months, I have spent a lot of my free time working on a presentation on neurobiology.  The presentation is the lead off in a series of lectures on addiction and the target audience is primary care physicians.  I have a lot of experience with this topic because I give a very similar lecture at least six times a year to physicians and other professionals who take a course on the treatment of addiction at the facility where I work.  I have been preparing and delivering these lectures for 3 1/2 years at this point.  Incorporating some of the most recent data on these topics is always a challenge and I depend a lot on Nature, Science, and Neuron for the latest reviews, research and commentaries.  In order to make it more relevant I ran across a collection of article in Frontiers in Psychiatry on the issue of whether or not addiction is a disease or not and it seems like a lot of that has to do with neurobiology.  Neurobiology has also become en vogue in many ways.  There is a conference posted in my clinic entitled "The Neurobiology of Play Therapy".  I thought I would post my observations of the implications of neurobiology in addiction and psychiatry.

The modern day interest in neurobiology owes a lot to Eric Kandel and his 1979 New England Journal of Medicine article "Psychotherapy and The Single Synapse."  The focus of that article was on the application of his basic science research on plasticity to the psychotherapy situation.  Plasticity was a relatively new concept at the time with the initial description of long-term potentiation (LTP) in 1973.  Kandel's basic argument was that nervous systems of varying complexity are designed to change with the experience of the organism.  The interesting part of his article is that it starts out with his experience as a psychiatric resident and the tension between the psychotherapists and the biological psychiatrists as they were called when I encountered the same dynamic in psychiatric training over twenty years later.  It is an important consideration because people outside of the field often have a skewed perspective of what makes up the training of a psychiatrist and this tension has been present for as long as I can remember - with articulate faculty on both sides.  He discusses this from the perspective of a parent discipline and an "antidiscipline" or one that is narrower in scope than the parent discipline and invigorates but does not displace it.  Neurobiology being the antidiscipline to psychiatry.  Molecular biology being the antidiscipline to cell biology and so on.  At the experimental level Kandel uses habituation and sensitization experiments on the sea snail to illustrate that "dramatic and enduring" changes in neural transmission occur with changes in plasticity.  He develops the theme that the functional-organic pathology based on gross or microscopic brain lesions is a false dichotomy.  Profound changes in networks of neurons can occur with no change in the numbers of neurons involved.  The mind is a function of the brain, but as Kandel later stated we do not have to think that all human behavior can be broken down to a specific biological level.

Getting back to the issue of addiction as a disease as opposed to something else offers a unique look at the plasticity concept and how it applies to brain problems.  I looked at all of the papers in the Frontiers series and briefly describe the details in the table below.  I would encourage reading the actual details in the papers since they are all freely accessible online and my one or two sentence summaries do not capture the complexity of some of these arguments. (click to enlarge)

There was a striking lack of the term "plasticity" in all of these papers.  It only surface in the paper on choice by Heyman in the following sentences: "First, most drug addicts quit.  Thus, drug induced plasticity does not prevent quitting."  That is a restricted view of plasticity.  First, it does not speak to the fact that plastic changes even if they appear to be long term can be reversed.  Second, it treats plasticity as a linear process when it is likely that the brain processes involved in recovery and in all of the other mechanisms cited by these authors as being more important in the recovery process are plasticity based.  The articles in general have the tone of polemics.  There is certainly nothing wrong with that.  As I have written on this blog, science is a dynamic process and part of that is an argument about theories over time.  The argument about the neurobiology of addiction seems to get hung up on both the disease concept and morality.  There can certainly be important neurobiology with or without disease.  That neurobiology is there whether or not medication, social processes, or psychotherapy influences it.  At least two of the authors equate neurobiological disease as the "no fault" condition and suggest that a biology based model is more blameless than one that suggests that addicts do have choices and respond to contingencies.  I think moral interpretations of a mental illness or addiction have less meaning if we are accurately describing the process.  It is much more than biology being no-fault and consciousness capable of decisions implying a moral judgment.  Plasticity mediated mechanisms gets us a lot closer to the science of how the brain works and away from the primitive interpretations of the 19th and 20th centuries.  

Plasticity is the best paradigm for describing addiction and the recovery process. Processes involving plasticity are all testable and the theory is falsifiable.  The most significant obstacle to the application of brain plasticity as a central process is the old functional-organic dichotomy where organic implied a neuroanatomical brain lesion.  It has been known from habituation and sensitization experiments like those described by Kandel in his 1979 paper that "dramatic and enduring" changes in neural transmission, do not require brain lesions or other abnormal anatomical features.  A recent paper (3) proposing that maladaptive NMDA-mediated synaptic plasticity as a unifying theory for tardive dyskinesia is a good example of plasticity mediated illness.  

There is no reason to believe that addiction and recovery may not be mediated by the same mechanisms.

George Dawson, MD, DFAPA


1: Kandel ER. Psychotherapy and the single synapse. The impact of psychiatric thought on neurobiologic research. N Engl J Med. 1979 Nov 8;301(19):1028-37. PubMed PMID: 40128.

" In each case, even in the most socially determined neurotic illness, the end result is biologic. Ultimately, all psychologic disturbances reflect specific alterations in neuronal and synaptic function. And insofar as psychotherapy works, it works by acting on brain functions, not on single synapses, but on synapses nevertheless. Clearly, a shift is needed from a neuropathology also based only on structure to one based on function."

2:  Alternate Models of Addiction.  Frontiers in Psychiatry.

3. Teo JT, Edwards MJ, Bhatia K. Tardive dyskinesia is caused by maladaptive synaptic plasticity: a hypothesis. Mov Disord. 2012 Sep 1;27(10):1205-15. doi: 10.1002/mds.25107. Epub 2012 Aug 1. Review. PubMed PMID: 22865512