Saturday, October 20, 2018

The NEJM "Addiction As Learning And Not Disease" Article

The latest installment of what appears to be an endless debate about whether addiction is a disease or not hit this weeks New England Journal of Medicine in an article entitled "Brain Change in Addiction as Learning and Not Disease." I have looked at a few of the previous articles along the same line that purport to show why addiction is not a disease and it is fairly easy to show that disease or not a disease generally depends on the author's definition and pointing out why the other definitions do not seem to fit. It is basically an exercise in rhetoric.  Those approaches invariably end up at quite a distance from opinion polls that illustrate that most of the public and even more medical professionals consider addiction and severe mental illnesses to be diseases.  I will come back to the philosophical underpinnings of those polls at the end of this article.

In this case the author is essentially making three arguments.  Two of the arguments are in side panel graphics and the third argument is in the main text.  The first side panel argument (p. 1552) concerns the Brain Disease Model and Stigma. In it the points out that the disease model can be destigmatizing but it also can be stigmatizing to some people.  Although I do not agree with some of his premises let us accept that his argument is basically a wash and the people who feel stigmatized and recoil from the prospect of the addiction illness perfectly cancel out those that accept the model are are consoled by it. I recognize that a substantial part of the recovery community base their recovery work on the disease concept of addiction although it is not strictly similar to the biomedical disease that is typically described.  This entire panel described a sociocultural model of disease (2).  This concept is basically that different societies and the physicians in that society may have diverse views of diseases that vary from other cultures.  A secondary factor is that medical recognition may change how that disease has come to be viewed by the society at large.  For example, an illness that was once thought be be caused by moral deficiency is seen differently after it is recognized as a process that may be beyond the control of the afflicted person.  Mental illness, alcoholism, and addiction are common examples.  An associated feature of this model is that this concept cannot be used by the medical field that must concentrate on understanding the biological mechanisms that underlie the disease.  That makes this panel irrelevant to a medical disease concept.

The second side panel (p 1553) looks at Learning Models and Empowerment.  It can also be understood as a sociocultural model.  In this panel the author develops a number of arguments to suggest that if people were free of thinking they had a disease they would be more prone to self examination and less dependent on professionals and the need to adhere to what professionals tell them.  He suggests that disease mechanisms would lead to pessimism on the part of the person with the problem that would not exist if they were engaged in any number of learning programs to help them recover.  He uses the familiar quote that most people recover spontaneously without any help from professionals.  This argument depends on a couple of premises that are clearly flawed.  The first is the group that is described as having an addiction.  The convention I use for that is Volkow's definition of being equivalent to severe DSM-5 substance use disorder in any category.  That category has a high level or mortality, comorbidity, and chronicity. In this case the author seems to minimize the interventions used by addiction professionals to "making life-style choices to improve their prognosis."  That minimization serves his purpose to suggest that learning is an entirely novel approach to addiction when it has been used for decades.  Spontaneous recovery is an often quoted argument against a disease model, when it happens all the time in other conditions (obesity, metabolic syndrome, diabetes mellitus Type II, hypertension).  The fact is, spontaneous recovery by any number of conscious interventions does not preclude a disease process.

The bulk of the author's argument in the main text is based on illustrating how learning in addiction and normal learning are similar if not identical processes and therefore disease is a learning problem rather than a disease.  The most logical way to analyze this argument is to examine the conclusions first.  Looking at the conclusion highlights the seriously flawed premises in the author's argument that addiction is not a disease but is just learning.  I did not see any qualifiers that addiction is a special case of learning or not.

The author's believes that he has developed a "balanced model of addiction" that incorporates various learning mechanisms into what he calls and "embodied cognition model" of addiction.  In this model he sees baseline and adaptive biology interacting with the environment to produce the addiction.  It is interesting that the key environmental feature of drug use disorders - exposure to the drug is way down his list of other social, cultural and familial factors.  Some of his examples illustrate this point.

He discusses the socially disadvantaged youth raised in an adverse environment: "These persons tend to find increased meaning in drugs that reduce stress or promote feelings of security and well being especially because these effects can be attained without medication by other people." That does not explain the flood of advantaged white middle class youths who became addicted to heroin and represent a substantial number of overdose deaths.  It also does not explain the difference between two inner city youths who have to walk past 3 drug dealers on their way to school each day and one of them becomes addicted and the other does not.  One of the important lessons of the current  opioid epidemic should be that exposure to a highly addicting drug in biologically predisposed people is one of the central mechanisms of addiction.     

The authors "addiction spiral" is also problematic.  It begins with "early adversity and trauma" as the first step effectively limiting any explanatory power to that population. In step 2, he discusses development changes in the autonomic nervous system that may occur in response to childhood trauma that can lead to hypercortisolemia as an adult. That makes this model appropriate only for adults who have been traumatized as children and even then - only those children with this pathophysiology.  There can be a broad range of factors that lead to behavioral inhibition and anxious temperament (3). In step 3, he discusses early childhood adversity as a cause of epigenetic changes that can predispose to addiction.  He omits the concept that exposure to compounds like nicotine and other addictive substances are much more potent causes of an array of epigenetic changes and correlate highly with addiction. Kandel and Kandel (4) among others have shown that DNA hyperacetylation from nicotine is associated with cocaine use.  Epigenetic changes from drugs of abuse are widespread .  A recent study of the impact of smoking on the human genome concluded that as many as one third of genes in the human genome can be affected (5) by methylation of 18,760 statistically significant cytosine-phosphate-guanine sites. In order to claim a more potent learning effect at least an equivalent neurobiology of learning with equivalent impact that it applies across the entire population of people with addictions should be presented.  I don't think this paper reaches that threshold.   

That brings me to the point of whether it is relevant to use the disease concept at all.  I am sure that students have heard me say from time to time that it is not. That statement is usually accompanied by the statement that it still has to be recognized as a severe problem that is a significant cause of mortality and morbidity.  There is a little used philosophical approach to the disease concept that I have rarely heard about outside of reference 2.  That concept is disease as a departure from normal functioning (p 160).  In this discussion the authors develop the concept that organisms are a special case of programmed systems.  Normal homeostasis in humans is a result of that programming.  Biomedical research is focused on being able to discover that program and how it is coded, uncoded, and expressed as disease.  One of the authors' conclusions is:

"There is reason to believe that as research progresses, more and more biological processes at all levels of organization will come to be understood as programmed processes."

They refer to closed programming that are those resulting from direct decoding of the genome with inborn errors of metabolism being a key example.  Other phenomenon require an interaction with the environment to result in the full development of the programmed process.  They go on to suggest the existence of "open" programming where some form of learning or conditioning is required to complete the process.  Some of the programs may be "closed" at a certain point and not amenable to further decoding.  All of these programs are shaped by the evolutionary process.  Viewing organisms as biologically programmed systems (p 163) takes social values and norms out of the equation and provides a definition of normal functioning and it also defines the acceptable evidence necessary to delineate abnormal functioning.  The authors' straightforward definition of disease is given below:

"Disease is a failure of normal functioning."

Consider the following vignettes to illustrate that definition. None of the subjects noted had any adverse childhood experiences or pre-existing psychiatric disorders.  They all had positive family histories of addiction.

Patient 1: 22 year old woman who received hydrocodone after her wisdom teeth were removed at age 20.  She received a 14 day prescription and continued to take it even when her pain was gone.  At this point she started to acquire opioids from nonmedical sources and eventually switched to heroin for economic reasons and was injecting herself 4-6 times per day.  She went to treatment and was placed on buprenorphine-naloxone 16 mg/day.  On that dose she had no cravings for opioids and no withdrawal symptoms.  Her family has decided to withdrawal support based on considerable expenditures for various therapies that have been ineffective. She goes to a sober house but after a week there learns that there are fentanyl based products available.  She leaves the sober house in search of these products.

Patient 2:  45 year old man who is an IT professional.  His father and grandfather were alcoholics.  His grandfather died of cirrhosis. He decided at an early age that he needed to avoid alcohol in order to avoid alcoholism and did well with that strategy until about age 40.  At that point professional pressures to socialize with clients lead to some drinking that he escalated at home.  He can work from home and his drinking escalated significantly to the point he was drinking a liter a day of vodka that he consumed between 7PM and midnight.  This pattern continued for several years until he started to get episodes of alcoholic pancreatitis that required longer and more complex hospitalizations. He tried to stop drinking on his own.  He tried online courses that used cognitive behavioral therapy.  He went to Rational Recovery and eventually AA. Nothing worked and he knew that every episode of pancreatitis at this point was life threatening.       

Patient 3: 30 year old carpenter with no previous history of substance use. He was working in a new construction area and found one of his coworkers inhaling paint out of a plastic bag.  He tried it and experienced an intense episode of euphoria.  That night he went home and found Internet sites where solvent-inhalant users compare their experiences and give tips on usage. He picked up a popular computer duster product and was soon inhaling many cans a day. He eventually crashed his truck while inhaling the solvents and as the police pulled him out of the vehicle - he was still inhaling the solvent. When he was seen in the emergency department he told the physician there that he could not stop using inhalants because: "It felt like pure dopamine was coursing through my veins!"

The previous examples are not extreme cases in addiction medicine and addiction psychiatry. They illustrate a failure of normal functioning by compulsive use of a substance despite knowing that this use is irrational and repeated failures to stop.  One of the common comments about the majority of people with addiction stopping on their own totally ignores the people being seen in addiction settings.  It is this combination of severity, inability to stop despite severe consequences, and chronicity that leads physicians and lay persons alike to consider addiction as a disease.

What about the evidence of failure?  It can come in various forms.  In a standard medical format there is a signature clinical course or phenomenology of the illness.  Symptoms can be obvious in a physical or mental status exam. Laboratory testing including chemical and microbiological analyses, electrophysiological studies, imaging studies of various regions and tissues can be undertaken.  In all of these determinations the evidence can always be equivocal, false positive, false negative, or truly positive.  It often takes a level of expertise to interpret the evidence and a good example is electrocardiography.   

From a philosophical standpoint the authors in reference 2 point out the initial value of a functional-failure model of disease.  It has obvious implications for basic science research of disease mechanisms.  That research should be focused on discovering the programming errors in the human organism that results in failure of normal functioning with the hope of understanding the underlying pathophysiology and correcting it.  The model clarifies a role for statistics in the disease model specifically the strength of association of certain variables with normal and abnormal functioning as well as ways to analyze tests for those variables.  And finally, the concept makes it very clear that the disease in question is real and exists independently of societal biases.  I don't think for example that any of the above vignettes could be considered anything less than a failure of normal functioning. In the people addiction specialists treat, there is generally a trajectory of progressive isolation, multiple psychosocial losses, loss of relationships, poverty associated with addiction, and in too many cases - premature death due to the direct or indirect results of addiction.

That is the reality and it is captured by disease as a loss of normal functioning.

I am going to bring this post to a close at this point, but look for a more extensive look at the specific types of learning listed in this article compared with the biological impact on plasticity when people are exposed to addictive drugs.  I started out thinking that I was just going to continue my opinion about the disease concept being irrelevant but instead find that I have been invigorated by a view from a book I read over 20 years ago that is still relevant today.  I will end with a communication I received from one of the authors that I hope sums up this post and illustrates why physicians should probably not cloud the disease concept with popular notions like stigma or  empowerment:

"Most people would think epistemology is always irrelevant to ordinary life, but clearly it isn’t."

George Dawson, MD, DFAPA


1: Lewis M. Brain Change in Addiction as Learning, Not Disease. N Engl J Med.2018 Oct 18;379(16):1551-1560. doi: 10.1056/NEJMra1602872. PubMed PMID: 30332573

2:  Albert DA, Munson R, Resnik MD.  Reasoning in Medicine: An Introduction to Clinical Inference.  Baltimore, Maryland: The Johns Hopkins University Press, 1988: 150-180.

3: Fox AS, Kalin NH. A translational neuroscience approach to understanding the development of social anxiety disorder and its pathophysiology. Am J Psychiatry. 2014 Nov 1;171(11):1162-73. doi: 10.1176/appi.ajp.2014.14040449. Review. PubMed PMID: 25157566.

4:  Kandel ER, Kandel DB. A Molecular Basis for Nicotine as a Gateway Drug. The New England journal of medicine. 2014;371(10):932-943. doi:10.1056/NEJMsa1405092.

5: Vaillancourt K, Ernst C, Mash D, Turecki G. DNA Methylation Dynamics and Cocaine in the Brain: Progress and Prospects. Genes (Basel). 2017 May 12;8(5). pii: E138. doi: 10.3390/genes8050138. Review. PubMed PMID: 28498318.

5:  Joehanes R, Just AC, Marioni RE, et al. Epigenetic Signatures of Cigarette Smoking. 2016. Circulation: Cardiovascular Genetics. 2016;9: 436–447. Full text

Supplementary 1:

My thanks to both Ron Munson and Mike Resnik two of the authors of Reasoning in Medicine - reference 2 above.  Further thanks for Ron Munson for the quote at the end of this post and encouragement to explore his ideas about the disease concept.  It means a lot to hear from both of these authors at a point when they could have easily ignored me.  It is a sign that there are many kind and thoughtful scholars out there. 

As I type this at 2AM that thought about scholars gives me a warm feeling.

Supplementary 2:

The quote used for patient 3 is found on the Internet and used for this hypothetical patient.  I have feedback from at least one addiction psychiatrist that the vignettes provided above are realistic and typical of addiction psychiatry practice.

Supplementary 3:

I added this on 12/22/2018 when I encountered an excellent example of Wittgenstein's work in Existential Comics.  In this case consider the parallel argument about disease or non-disease based on the hot dog versus sandwich argument.  What do you think Wittgenstein would say?

Existential Comics: Is a Hotdog a Sandwich? A Definitive Study.  December 2018.

Sunday, October 14, 2018

What Do Surgeons and Psychiatrists Have In Common? - Dread

I have had two surgeries this summer that have really impacted my work and daily life.  I only consent to surgery if it is a problem severe enough that I can't function or will kill me and the first one was for that.  I found a highly skilled surgeon who had done more of the procedures than occur in most countries in the world.  The procedure itself seemed to go surprisingly well. He gave me a prescription for oxycodone but the only treatment I needed for post op pain was acetaminophen.

I went in to see him a month later and everything was still going very well. No surgical complications and the target symptoms were in good remission. I did well for another 2 weeks and then got symptomatic again.  I was reexamined and the original surgery had scarred over requiring a second surgery to remove the scar tissue. He explained that is was very rare in his practice for that to happen, but that he did need to fix is as soon as possible.  The second surgery as done and I was functioning as good as new again.  He advised me to come back in 6 months for follow up.

There were post operative complications.  Despite antibiotic prophylaxis given during surgery I developed an infection with a fever and tachycardia.  He prescribed antibiotics but it got worse. I eventually went into the emergency department at midnight and was given intravenous Rocephin and told to continue the oral antibiotics until they were gone.  The infection cleared up in about 5 days.

I did very well and then at the 6 week mark again, I got progressively symptomatic and called the surgeon again:

Me:  "The symptoms are back, at about the same time frame and course of onset as they were in the past. Do I need surgery again?"

Surgeon: "Well probably.  It is highly unusual that it happened the first time and even more unusual if this has happened again.  I will just schedule the OR so we can take care of it early next week.  Can you do it then."

Me: "Well yes - I will do whatever I need to do to take care of this problem. I can't really go on like this."

Surgeon:  "I was just talking with my partner here and we need to alter the procedure to really remove more tissue when we take out the scar tissue this time. We really need to open that area up"

He sounded a little shaken. He is a top surgeon in his field and this is not just one complication but a second complication of the same initial surgery.  He was consulting his colleague and in this group all of the surgeons are very experienced and highly regarded. I wondered if he was concerned about what I was thinking?  He was safe there - even though it is practically an American standard to blame surgeons for sub-optimal outcomes that was never going to happen. I have seen surgeons with less skill than others and I picked him because of his record. There was no way that I was not going to let him do his job or suggest that I was in any way dissatisfied with his work.

I started to think about all of my years in acute care and how common it was to walk in the door in the morning and get blamed for everything by people who I have never seen before.  People who were there because they were in an alcohol or drug induced state and ended up under my care because there were unsafe and needed to be detoxified and in some cases treated for the psychiatric complications of substance use. People who were admitted for severe psychiatric disorders and associated aggressive or suicidal behavior.  Once they learned I was their psychiatrist - it was my fault that they were there - even though it was my job to get them out of there as soon as possible. My failure to do that resulted in a second tier of blame.  This time by hospital administrators who were often quite aggressive in encouraging me to get patients out of the hospital whether I though they were stable or not.  Shortly before I left the job, one of them actually told me that if I did not get the patient out - he would come down and discharge the patient himself.

I smiled to myself at that point and realized it was a very good thing that I was not blaming my surgeon for anything.

And then I thought about being in the same situation. Most people who have not practiced in acute care have not seen some of the problems that have no solutions.  Aggressive behavior that does not respond to medications.  Catatonic behavior that rapidly leads to life threatening dehydration or starvation.  Bipolar patients on dialysis who are delirious for months waiting for kidney transplants.  Patients with multiple medical complications who are agitated and can't sleep.  On some days an endless list of problems that would keep me up all night long trying to figure out solutions.  I would call and email one of three colleagues who I knew I could count on. They had been working acute care as long as me and I always appreciate their input. We only consulted one another in situations where we had no obvious solutions and we also had a sense of dread. Dread in the sense that you start to ask yourself: "Is there really no solution here? What am I missing? Have I lost it? Do I need to take a break and work somewhere else for awhile?"

There were a lot of nights where I would just lay in bed, thinking about the situation - sensing the blood pulsate throughout my body and feeling a light sweat on my skin. I would get out of bed in the morning amped up on adrenaline and feeling like I had slept for 8 hours when it was probably closer to 1 or 2.

Luckily in my case, there was resolution.  It could happen after a couple of sleepless nights. On many of those nights I would have contact with the nursing staff to see if any modifications could be done while I was away.  I would finally get a break and things would be all right for 2-4 weeks before another crisis hit. It would usually be a surprise. I walk into the unit in the morning and hear "Mr/Mrs Smith is up out of bed eating this morning.  They made a big turnaround last night."

Hoping for that break is the only thing that kept me going. You can only tell yourself that you have done everything right for so long. I never got to the point where I expected that break. It always struck me as very lonely and bleak. My senses seem dulled and everything slowed down around that problem. When the break happened - life was finally good again.

I was able to step back from these associations and realize that my surgeon was likely experiencing some of the dread I typically encountered in acute care.  Despite extended and best efforts - things are not going well and you don't really know why. There are no easy or apparent solutions.

Surgeon: "I should probably see you tomorrow before the surgery. I am sorry this happened. Can you be there are 7:30?"

Me: "Thanks. Yeah I can be there at 7:30.  See you then."

I was very calm and I slept well that night.

George Dawson, MD, DFAPA

Image Credit:

1.  Above image as my second preop identification and allergy band.

2.  Image for Twitter post was from Shutterstock per their standard agreement by Francey Scary Foggy Road downloaded on 10/14/2018. 

Saturday, October 13, 2018

Biomedical or Biopsychosocial or Psychopharmacologist?

Elements of a psychiatric evaluation

Apparently these are desperate times for some professionals.  So desperate that they have nothing better to do than argue about proven psychiatric methods that include the clinical methods that includes data gathering and diagnosis. Some would prefer to move psychiatry away from the rest of medicine based on fallacious arguments that there are no clear connections between biology and clinical phenomenon and no apparent connection between psychiatry and the rest of medicine. These arguments are so extreme that they lack clinical utility and yet there is a small by vocal group of people who try to gain political favor with what is essential reworked antipsychiatry rhetoric. As a reminder I use that term as a philosophical definition that has been used to characterize the work of Szasz and Foucault. It is agnostic in terms of the proponents. In other words, as far as I can tell you don't need to be a cult member to be a proponent of antipsychiatry. You can be a psychiatrist like Szasz.

I posted a good example of this position a few years ago.  In the post I looked at a special interest group using medical model pejoratively and applying it to psychiatry.  I illustrated how the authors account of medical model on 2 1/2 of 3 dimensions that they were using as a basis for their argument.  The eventually develop a trauma based model of psychosis and state that is all that you need to know in terms of etiology and treatment. That is their refutation of the comprehensive psychiatric model for information gathering and analysis.

Another incredible critique of the field came from the journal Health Affairs and it suggested (like most critiques of the field) that the authors really had no knowledge of psychiatry or what psychiatrists do. Specifically they seemed to have no knowledge of the biopsychosocial model of psychiatry, specific psychiatric research in that field, and how all of that information is used in day to day psychiatric practice.

The obvious point that I am making here is that psychiatrists are trained and interested in multiple factors that may be important in both the etiology and treatment of psychiatric disorders.  That includes many biological factors like toxin exposure, endocrine conditions, infectious diseases, and brain injuries as well as more subtle biologically determined factors like temperament and developmental history.  It includes the status of interpersonal relationships and psychological factors. It includes the status of other organ systems in the body and chronic medical conditions.  There are specific posts on this blog about cardiac status, sleep apnea, cirrhosis and liver disease and pancreatitis. All of these illnesses and more are encountered in routine psychiatric practice.  Psychiatrists must in some cases make the diagnosis and in other case modify therapy to account for these illnesses and not provide treatment that is contraindicated.

That leads me to the figure at the top of the page.  All of the elements are contained in the assessment of the patient. It is not unique to psychiatry, and most physicians who directly assess patients have been using one form or another of it since they were first or second year medical students learning how to examine patients.  The main difference for psychiatrists from other physicians is the formulation section. This is not the list of diagnoses, but a synthesis of all of the data gathered during the interview process and at times from collateral sources.  Consider the following hypothetical example:



The patient is a 48 year old married woman with a history of insomnia and depression dating back to middle school.  She also had nightmares and night terrors during childhood but they resolved by the time she was in her late teens. Her current sleep problem is initial and intermittent insomnia.  She has been on various antidepressant medications about 90% of the time since she was 18 years old and has not found any of them to be very effective, but she does think that she gets some partial relief from fluoxetine.  She has been married for 18 years.  Her husband is supportive and they have a solid relationship.  The couple has 3 sons who are 10, 12, and 17 years old.  she had no episodes of postpartum depression.  She took fluoxetine during the last pregnancy.  There is a family history of depression in her mother and maternal grandmother. Her maternal grandmother was institutionalized and received electroconvulsive therapy.  Father and paternal grandfather had alcohol use problems. She is an electrical engineer and works in the tech industry in chip design.  She was previously active in a group that encouraged girls and young women to focus on STEM subjects in school and as a career choice but she has fallen away from that lately.  Over the past three years her alcohol consumption has increased from 2-3 standard drinks per day to 8-10 drinks per day. When she is drinking on  daily basis her mood is significantly more depressed.  During a recent episode of intoxication she sustained an intracerebral hemorrhage that was noted on an MRI scan of the brain in the left frontal cortex. She reports no cognitive or personality changes with that lesion but has had frequent headaches. She denies any history of abuse or psychological trauma, but said that her parents spent less time with her than her older brothers and that left her with a feeling of being less valued at times and questioning her self worth. She identifies strongly with her father who was also an engineer and encouraged her interest in math and science.


1.  Persistent depressive disorder
2.  Primary insomnia
3.  Intracerebral hemorrhage - assessed and treated by Neurosurgery trauma service. Serial scans show resolution with no evident abnormality.
4.  Headaches secondary to 3.


A typical medical surgical evaluation using the same general outline will not put all of the data together to explain the patients psychiatric diagnoses or symptomatology.  Medical or surgical evaluations typically end with a list of diagnoses that typically focus on an organ system or the brain idendependent of any psychiatric factors.  The diagnostic formulation is a psychiatric innovation that has utility as a way to study diverse etiologies of mental illnesses and in this case to try to understand the unique biological, social, and psychological variables for each person who is being treated.  It is in contrast to the diagnoses which are supposed to be atheoretical (but are not really) in the DSM. The formulation allows us to develop unique theories about what might be contributing to the person's distress.

I have been a longstanding critic of the lack of a psychiatric focus on the conscious state.  Only recently did I have the thought that this biopsychosocial (BPS) formulation is an approach to the study of a unique conscious state. The broadest definition of consciousness is experience.  If you develop a good technique and confirm the observations and theory about how all of the dimensions impact on them - it is basically a study of a unique conscious state.  An elaboration of the elements contained in either outline - would lead to a discussion of the person's experience of any number of life events including growing up in her family of origin, going to school, working, her leisure time experience, and her experiences as a wife and mother.  That is probably a very liberal interpretation of the BPS model.  Interested readers can find original papers written by George Engel in the references below.  The BPS model generally looks at multiple systems relevant to biological organisms and the philosophy of general systems theory.  The reader can get a good overview of Engel's theory by looking at the articles and the accompanying diagrams. Ghaemi has written an excellent book on BPS (6), it shortcomings and what he considers a more appropriate model for psychiatry - method-based psychiatry.  In his book he goes so far to outline how it can be taught to residents. 

The problem with all of the terminology is that I know very few psychiatrists who practice or prefer to practice in a restricted biomedical mode. A few examples that come to mind were some of the psychoanalysts who were my teachers 35 years ago who "prescribed a little amitriptyline for sleep." I suppose there may be some psychiatrists out there prescribing fluoxetine and not attending to their patients medical disorders - but happy to report that I don't know any.

That brings me back to the central point of this post. Do you really need to distinguish yourself as a biomedical or biopsychosocial psychiatrist if every other psychiatrist is doing what you do? Do you need to call yourself a psychopharmacologist?  Do you need to call yourself a medical psychiatrist?

I would say that you do not. Psychiatric training exposes trainees to the same content and clinical contexts where they an observe and treat severe problems. In many of those situations they are responsible for the total medical care of the patient.  They accumulate medical knowledge on a consistent basis as they accumulate knowledge about diagnosis and treating medical conditions. It is an inescapable part of the practice of medicine. Where do all of these titles come from?

I see a couple of origins.  The first is political and that is people who are using the terms in a pejorative way. There are apparently psychiatrists in the UK who use the term biomedical psychiatrist in a pejorative way because they don't believe in any diagnosis or they adhere to the old Szaszian concept of disease and do not want to see psychiatry practiced as a medical specialty. Many would go as far as not using diagnoses at all. They often equate diagnosis with the pejorative term labeling. When I think about that movement and its origins and how psychiatry got to where it currently is today - I ask myself about the development of both paths of thought. Without going into too much detail - there are no geniuses on the antipsychiatry path. Many of the early proponents on that path failed because they really had nothing to offer people with serious mental illnesses. If anyone wants to refer to me as a biomedical psychiatrist - I embrace it because it certainly does not deter me from doing  thorough psychiatric assessment that includes a formulation that contains social, cultural, and biological factors unique to the person I have assessed and trying to appreciate their conscious experience in each one of those domains.

The second application of the various descriptors is to differentiate oneself from the rest of the pack. That also seems to be a dubious distinction. The best example I can think of is psychopharmacologist.  If I have studied the subject, attended the seminars and courses, but spent most of my career discontinuing medications and treating complications in polypharmacy situations - am I psychopharmacologist?  Or do I need to be the person prescribing all of the polypharmacy? As far as I can tell - all psychiatrists are (or should be) psychopharmacologists.  They should also be aware of the limitation and be able to practice specificity in the prescription of psychiatric medications. 

 Psychiatrists are psychiatrists.  They are the same, but different like any other discipline.  Apart from what they know or should know their conscious state is certainly a factor in how they practice and there are always potential differences in skill levels.

I continue to be impressed by the high level of skill of my colleagues and think that we can all be psychiatrists and be confident that we don't have to be defined by anyone else.  Anyone who suggests that they have a better approach or that they can treat patients without a diagnosis should be confident enough to proceed and compete directly.  That said we do need to refine the technical skills in the field.  A primary consideration is realizing that we have come as far as we can go with the DSM approach.  Ghaemi's suggested methods based approach presents some good ideas on a philosophical basis - but the personalized medicine and omics approaches also hold a lot of promise.

George Dawson, MD, DFAPA


1:  Engel G. The need for a new medical model: a challenge for biomedicine. Science 1977; 196:129-136.

2:  George L. Engel, MD. JAMA.2000;283(21):2857. doi:10.1001/jama.283.21.2857

3: Engel GL. The clinical application of the biopsychosocial model. Am J Psychiatry. 1980 May;137(5):535-44. PubMed PMID: 7369396.

4:  Campbell WH, Rohrbaugh RM. The Biopsychosocial Formulation Manual. New York, Routledge Taylor & Francis Group, 2006, 164 pages.

5:  Chisholm MS, Lyketsos CG. Systemic Psychiatric Evaluation. Baltimore, The John Hopkins University Press, 2012, 243 pages.

6:  Ghaemi SN. The Rise and Fall of the Biopsychosocial Model.  The John Hopkins University  Press, 2010, 253 pages.  


Some useful books for those interested in this topic (all referenced above):

Tuesday, October 9, 2018

Moderation Policy - Reposted

With a recent post from Scotland to a blog post from 4 years ago as well as an high frequency of advertising related posts - I decided to repost the moderation policy from October 2016.  Please consider these points carefully in posting responses on this blog and consider these points if your post does not appear.

This is just a reminder and to establish an anchor point about moderation on this blog.  If you attempted to post a response on the blog and it did not show up it is most likely due to one of these reasons.  It is always possible that I made a mistake or that your response ended up in my spam file.  In fact, several posters clued me in about that happening and I did find and post their responses.  It should be pretty clear that you do not have to agree with me but there are some limits that are fairly basic to a small barely read blog like this one.  These limits follow:

1.  No trolls - I am not fascinated by trolls or the troll culture.  One of the reasons that I started this blog was that I used to post in what I thought was a professional forum that was dominated by a troll.  There was no moderation and eventually all of the interesting posters left and went elsewhere.  So spare me the First Amendment arguments - that kind of rhetoric just doesn't fly here.  My reasonable test is what would happen to a troll in any medical staff meeting?  Consider this a similar atmosphere.

2.  No advertising - This is a strictly non-commercial enterprise.  I type it up on my own and there is no sponsor or source of revenue.  As I have pointed out to people who want to advertise here, I have many copyright permissions at this point that are all contingent upon the non-commercial status of this blog so at no point is it possible for me to accept advertising.  The Creative Commons license allows anyone to repost the contents of this blog with the proper attribution.  If you like the content - just repost it or link to it.  No advertising also includes posts with hyperlinks to product advertising and that kind of link results in a rejected post.  It also includes posts with no content and apparent compliments that are hyperlinked to advertising through the name of the poster.

3.  No anti-psychiatry rhetoric - There can be discussions of anti-psychiatry from a philosophical standpoint, but if the main point of the post is to bash psychiatry or psychiatrists this is not the place and you probably already know that.  There are many anti-psychiatry blogs that you can flock to.  Some of them are even contain active posts by psychiatrists.  Psychiatry attracts a lot of haters and my original analyses of the problem in 2012 still stands as well as a clear anti-psychiatry bias in the media.  At least part of that media bias is that they are just being provocative to draw a crowd and of course they have no responsibility to people with clear problems.

4.  No personal attacks - ad hominem is the poorest form of criticism.  If the argument cannot be addressed, attacking the person is not a substitute - at least here.  There are many other blogs and media sites where that is acceptable.  The standard I use for physicians is the expected behavior in professional settings with colleagues.  If a post does not meet that standard it is on shaky ground.

5.  No medical advice - this blog is not the place to seek personal medical advice.  Nothing here should be construed as medical advice or a discussion of an actual patient.  My opinion stated here in many places is that only your personal physician or physicians knows enough about you to make suitable recommendations.

6.  No interminable arguments - I don't have to have the last word on anything and frequently just stop posting.  I will not post repeated posts making the same argument or with very slight modifications.  One of the most interminable arguments has to do with the link between psychiatrists and pharmaceutical companies.  I have debunked that argument on this blog many times.  I would refer you to blogs where they have interminable arguments about how bad psychiatric medications are and how corrupt psychiatrists are for their connections to Big Pharma.  Neither argument is accurate but this is the place to read about how medications are actually used.

7.  Stay on topic - It is a reasonable requirement to address the topic.  Newspaper web sites are good examples of what can happen when this simple rule is not followed.  A corollary is to address the topic in a timely manner.  I have had people notice posts from 3 years ago and write a response.  Blogger does not allow me to terminate discussions like some web sites.  My only option is to not post untimely responses.  Six months is a reasonable time frame.

That is what I have so far.  I reserve the right to add more as they come to me.  The goal is to maintain coherence and rational discussion.  Any inspection of the blog posts shows that there is not a lot of discussion and stimulating discussion is not one of my primary objectives. I appreciate the people who have taken the time to read this blog and post their comments - many of which make excellent points and do stimulate further discussion.

My goal all along has been to produce opinion and analysis consistent with the way that real psychiatrists train, work, and practice.  I do not see myself as unique in any way.  I routinely have contact with excellent psychiatrists who I have trained with and who are colleagues.  They approach problems in psychiatry and think about those problems in very similar if not identical ways that I do.    I see this blog as a creative outlet as well as one of the few places on the Internet where this kind of content is available.

George Dawson, MD, DFAPA


The photo:  John Schneider.  RCA 40A Ribbon Microphone. August 19, 2007.
Attribution-NonCommercial 2.0 Generic (CC BY-NC 2.0)

Sunday, October 7, 2018

Drug Overdoses As A Proxy For Drug Epidemics

Figure 1 - Mortality rates from unintentional drug overdoses.
(A and B) Mortality rates for (A) individual drugs and (B) all drugs. Detailed data for individual drugs are only available from 1999 to 2016, although additional data for all drugs are available since 1979 (this area is grayed out). The exponential equation and fit are shown for all drugs. (Synth Opioids OTM: synthetic opioids other than methadone. This category includes fentanyl and its analogs.) from reference 1 with permission.

A recurrent topic on this blog is drug overdoses due to street drugs and the epidemiology of these overdoses.  As an addiction psychiatrist it is obvious that access to drugs and alcohol is a critical feature of epidemics and the broad exposure has resulted in increased accidental overdoses. The clearest example I can think of is the spread of heroin overdoses to rural America.  That phenomenon did not exist 20 years ago.  The implicit aspect of the access argument is that other commonly held reasons for addiction and overdose deaths like poverty, race, culture, etc are really not reasons that people get addicted to drugs and alcohol.  That happens because they have a biological predisposition and they have access. There is a lot of resistance to this basic idea because it runs counter to the idea of broad legalization of cannabis and other drugs like psychedelics. It runs counter to the idea that the war on drugs is the real problem here and the situation would improve without it.  It also runs counter to the alternate theories about substance use that some people see are identifying remediable problems like poverty and disparity.  I see those theories as being equally stigmatizing and inaccurate.

For all of these reason I was very interested in the recent paper in Science (1) that looks at accidental drug overdoses as a chronic problem rather than a discrete series of events.  The authors analyzed a total of 599,255 deaths from 1979 through 2016 from the National Vital Statistics System, specifically the Mortality Multiple Cause Micro-data Files.  Their main finding is illustrated in Figure 1 above and that is the aggregate overdose mortality rate increases exponentially for a period of 38 years (panel B).  The individual drugs are broken out in panel A. Only accidental deaths due to drugs were included and that determination adds some element of uncertainty to the numbers.

This is probably the best place to comment on the methodology of this research and further visualizations of the data.  Inspection of the individual drug shows that there are a total of 7 drugs.  Common drugs of concern in overdose situations like benzodiazepines and z-drugs are not mentioned specifically but there is a category of unspecified drugs and unspecified options.  The supplementary material lists accidental poisoning due to antiepileptic, sedative-hypnotic, antiparkinsonism and psychotropic drugs - not elsewhere classified, hallucinogens - not elsewhere classified, other drugs acting on the autonomic nervous system, and unspecified drugs, medicaments and biological substances.  By that description benzodiazepines, z-drugs, and other neurological and psychiatric medications are probably in that category. Poisoning by solvents or intentional use was not included. Intentional drug poisoning - both suicide and homicide was not included.  The coding of the cause of death changed substantially in 1999 providing more detail and allowing for the separation of synthetic and semi-synthetic opioids after that time. Mortality rates were calculated by drug type, age, sex, and urbanicity.

A few points from the initial graphs. Mortality curves have generally increased for all of the drugs of interest since 2010 except methadone and the unspecific drugs. By the authors definition the range of the unspecified drugs is so broad that it may conceal clear trends within subcategories like benzodiazepines and z-drugs - both important in polydrug overdoses.  The authors suggest that the variability in some of these lines like the dip in the prescription opioid line after 2010 may have been related to attempts to reduce the number of prescriptions, laws making mandatory checking for prescriptions for controlled substances prior to prescribing, and the production of a long acting and less abusable form of oxycodone in 2010.  It seems as likely that that a lot of prescription opioid users switched to heroin at that point reflected by the rapid increase in heroin death rates from 2010 to the end of the study period.  There is a time lag to 2013 and at that point the fentanyl death rates begin an even steeper curve to the end of the study period.  There is no associated decrement in the heroin or prescription opioid curve at that point suggesting that the fentanyl rates reflects a different problem from the baseline opioid death rates. Those problems could include the fact that fentanyl is much more toxic, it could be an adulterant, it could be sold as heroin by diluting it, and it could be sought out as a way to pursue a high when tolerance has developed to the original opioid being used. The authors points out that increased access to fentanyl was documented by increased seizures by law enforcement. The decrease in methadone deaths may have been due to its removal from pain formularies and  CDC initiative on discouraging use for pain medication due to excessive toxicity.

In panel B, the authors shade the area up to 1998 to show when the opioid epidemic begins.  They make the point "of particular interest is the observation that the first half of this long smooth exponential growth curve predates the opioid epidemic."  While that may be true, it is obvious graphically that the 1979-1998 curve could also be extended without the inflection point in 1998 without the superimposed opioid epidemic and significantly higher mortality rates.

The authors also examined what they referred to as drug specific subepidemics, building on their assumptions that the exponential mortality curve that they describe is due to subepidemics. Their methods of analysis included heat mapping and geospatial hotpot analysis.  I elected to license the latter image and include it below.

Figure 2 - Geospatial hotspot analysis by drug and period.

The Gi* statistics are standardized using pooled statistics across all drugs and periods. The various shades of red and blue indicate pooled standard deviations above and below the pooled mean, respectively, as shown in the legend. The small black circles indicate major cities with populations greater than 300,000 people. None of the regions were less than 2 pooled standard deviations below the pooled average. (Synth Opioids OTM: synthetic opioids other than methadone. This category includes fentanyl and its analogs.) From reference 1 with permission.

For the above geospatial hotspot analysis. the authors looked at 8 drug categories, during 4 times frames and all of the time frames are from the opioid epidemic. The only drug that showed a peak intensity and spatial distribution followed by a decline was methadone. All of the prescription and nonprescription opioids show a progressive increase during this time frame.  That patterns are also remarkable for a spread from metro areas to non-metro areas. There are some interesting geographic observations including a relatively cold spot of overdose mortality in the north central states.

Heatmap analysis (not shown) showed a bimodal distribution of mortality in 20-40 yr olds and 40 to 60 yr olds.  Heroin, synthetics, white race, male gender, and urban counties were over represented in the younger group. The older group deaths were predominately white women in rural counties using prescription opioids.  Prescription drug mortality rates four times higher in younger men than women were attributable largely to synthetic opioids.

The authors main point in the paper is that the combination of epidemics came together to compose the exponential curve after the inflection point and that there is not clear way to figure out how that happened. They emphasize the importance of understanding these forces and cite a number of possibilities including supply side components of more efficient manufacturing of drugs, better supply chains, high purities and lower prices.  These are all well known factors in why people stop using prescription opioids and fentanyl from illegal sources.  They discuss sociological factors like fragmentation of communities, despair and a lack of purpose. They discuss public health interventions like community surveillance for patterns of drug use and availability addiction treatment for secondary and tertiary prevention.

As I read the article, I thought about my model of addiction and that is biological vulnerability + access leads to addiction.  Certainly there are people who will say that the sociological concerns described by these authors can lead to the biological vulnerability, but the protective factors in some of those communities are generally ignored. The authors seem to have at least some of the data here to show that socioeconomic status and race do not determine drug epidemics. Availability determines drug epidemics and there is no better example than some of the data they present here. In addiction to race, urbanization is also an example of vulnerability + access with the spread of overdose mortality out into the country side. There is an addition dimension of data here that could be used to look at these mortality rates and that is US Census data provided tract-level measures of poverty, education, crowding, and race/ethnicity. In other words how does the mortality correlate with these factors. A recent study of alcohol retail density showed a high correlation with these factors.  In other words, urban minority populations face a higher level of retail alcohol outlet density and exposure than white populations in urban or rural zip codes. The only difference from the study in reference 2 is that there are no clear measures of opioid exposure. 

This is an important study with a unique approach to the problem of progressive drug epidemics.  Mortality rate from overdoses is not the same as measuring the total drug exposure and resulting addiction but there is no clear way to determine that.  I would also not consider the heroin and fentanyl mortality rates to be independent of the original increase due to prescription opioids. My rationale is that there are very few people that start using either compound. Once an addiction to opioids starts there are progressively larger number of people each year competing for the pool of illicit opioids. They are looking for less expensive alternatives. Many are not risk averse and are consciously looking for more potent opioids. Although there is no data to support the progression from prescription opioids to fentanyl and heroin - clinical experience suggests it is the likely explanation and it could account for the mortality curve in Figure 1 as a single rather than multiple epidemics. 

These authors have come up with a unique contribution to the literature and I encourage anyone interested in the epidemiology of drug epidemics to read the full text of this paper.

George Dawson, MD, DFAPA 


1:  Jalal H, Buchanich JM, Roberts MS, Balmert LC, Zhang K, Burke DS. Changing dynamics of the drug overdose epidemic in the United States from 1979 through 2016. Science. 2018 Sep 21;361(6408). pii: eaau1184. doi: 10.1126/science.aau1184. PubMed PMID: 30237320.

2: Berke EM, Tanski SE, Demidenko E, Alford-Teaster J, Shi X, Sargent JD. Alcohol retail density and demographic predictors of health disparities: a geographic analysis. Am J Public Health. 2010 Oct;100(10):1967-71. doi: 10.2105/AJPH.2009.170464. Epub 2010 Aug 19. PubMed PMID: 20724696.


Both Figure 1 and Figure 2 above are used with permission from the American Academy for the Advancement of Science (AAAS) the copyright holders.  The figures are both from reference 1 above used with permission per the following license number  4441420359702  obtained on October 3, 2018.  The AAAS also requires the following notice based on this content:

"Readers may view, browse, and/or download material for temporary copying purposes only, provided these uses are for noncommercial personal purposes. Except as provided by law, this material may not be further reproduced, distributed, transmitted, modified, adapted, performed, displayed, published, or sold in whole or in part, without prior written permission from the publisher."

Tuesday, October 2, 2018

Components of Patient Outcome

It is a good idea to go back and take a look at some basic components that predict patient outcome in medical (including surgical) treatment. There is a  skewed representation of practically all medical information that is portrayed in the press.  A big part of that misrepresentation comes back to missing what the real components are that determine the outcome.  I have listed a few of what I consider to be the major components in the above diagram and will take a look at each one in order.

Technical expertise of the physician is obvious in surgical and other invasive procedures.  Henry Marsh covered it in a book on his career as a neurosurgeon (1).  He discussed the process of surgery but also the unpredictable results.  An operation may have seemed flawless but the patient ends up with a postoperative complication that had to be due to the surgery and dies or is permanently disabled.  I have discussed the issue with neurosurgeons myself and directly observed them in action.  There are clear differences in skill level and operative outcomes that appear to be based strictly on manual dexterity and coordination. There are differences based on the number of procedures that are done.  Expertise is easy to conceptualize at a manual level.

Psychiatrists on the other had usually balk when I refer to the technical expertise required in the field.  The clearest example in training is learning about inpatient psychiatry before proceeding to outpatient clinics.  Most psychiatric trainees just don't know enough as first year residents to proceed to an outpatient clinic and start to treat anyone who walks through the door.  The inpatient setting provides the training necessary to address emergencies first.  Outpatient skills can be built on that foundation. An associated issue is how much you need to know. If you are immersed in medical settings like hospitals, you probably need to know about a broad range of medical and surgical conditions and how they can lead to or complicate treatment of psychiatric disorders. That knowledge base includes a broad range of basic sciences and the updates relevant for the field. Expertise in psychiatry also encompases the interpersonal dimension. Psychiatrists should be the medical specialists that have the highest level of competency in the interpersonal dimension and how their personal feelings toward patients can complicate care.  That requires a significant level of training and expertise.

Biological variability is poorly understood by nonphysicians.  The best examples are allergic reactions to medications and severe idiosyncratic reactions like liver failure or kidney failure in response to a medication.  But they can also be more common on a population wide basis and mediated though a number of mechanisms.  The variability has to do with both the way the medication is absorbed and metabolized and also specific effects that occur at the tissue level.  In some cases this leads to clinical trials where the results do not seem that impressive (antidepressants, radiofrequency ablation for atrial fibrillation) but where there is a clear consensus that the intervention works.

 Every procedure in medicine whether it is a prescription, a surgical procedure or a medical device is characterized by a study.  The quality of those studies varies in terms of design and statistical analysis.  The usual goals of early studies is to gain FDA approval for release into the market in the US and elsewhere.  In the process of the safety and efficacy studies, quire a lot is learned about the drug characteristics applied over a larger population.  That data is applied toward describing that population based effect to the physicians who will eventually be prescribing the medical or procedure.  In some cases there are considerable political cross currents that can affect the straightforward statistical data as in the case of coronary artery bypass grafting or the use of beta blockers for hypertension or preventatively post acute MI.  There is currently an active debate about prostate screening and the burdens and harm done by screening, but at the same time there are clinical trials that show prostate cancer survival is improved by radical prostatectomy (RP) - but that there is no difference between standard RP versus robotic surgery.  It is  doubtful that the statistical facts of the procedure will ever be far from the expertise domain.

The final critical outcome parameter is the patient's ability to consent. It is not an easy task to hear about current medications or interventions with imperfect results and decide what the best course of action is.  Apart from the cognitive analysis, there is an emotional component of having a significant illness.  There is also the requisite ability to tolerate risk. Practically no medical interventions are risk free but some have much higher risks that others. The risk ranges from death or disability to an allergic reaction or long list of possible side effects.  The risk of not taking the medication or having the procedure done can also be significant including death.         

One of the best examples in the literature about the importance of the patient related component of these outcome variables was Kurt Gödel.  He was a renowned mathematician and logician who suffered from severe medical problems including gastric ulcers, prostatic hypertrophy with severe lower urinary tract obstruction who either postponed or refused treatment to the point where he was near death or in severe distress. He had a severe urinary tract obstruction and refused surgery to correct the obstruction. He elected to remain catheterized for a period of 4 years until the time of his death.  He eventually died of starvation in a hospital refusing to eat because he believed his food had been poisoned and at the time of his death weighed 65 pounds (he was 5'6" in height). Gödel was one of the geniuses of the 20th century who experienced problems that consistently and adversely affected his health.  Shortly before his own death and Gödel's death his friend economist Oskar Morgenstern made this observation in his diary (from reference 2; p 251) after a phone call from Gödel:

"It is hard to describe what such a conversation means for me; here is one of the most brilliant men of our century, greatly attached to me ..... [who] is clearly mentally disturbed, suffering from some kind of paranoia, expecting help from me, and I am unable to extend it to him. Even when I was mobile and tried to help him I was unable to accomplish anything. [Now,] by clinging to me - and he has nobody else, that is quite clear - he adds to the burden I am carrying." - July 10, 1977.

Morgenstern died 16 days later of metastatic prostate cancer.

 The main takeaway message from this brief commentary of variables affecting patient outcome is that it is a complicated process. There needs to be open communication about the uncertainty at every step of the way. In the informed consent discussion (that should always occur) there should be enough information exchanged so that the patient/decision maker has a clear idea of the risk involved.

Even then, the most intelligent decision makers can fail.

George Dawson, MD, DFAPA


1:  Henry Marsh.  Do No Harm. Thomas Dunne Books, St. Martin's Press; 2014.

2:  John W. Dawson.  Logical Dilemmas: The Life and Work of Kurt Gödel. Natick, MA: AK Peters, LTD; 1997: 229-253.