What The Economist doesn’t know about Psychiatry

It is always good to take an in depth look at articles in the popular press about psychiatry – because of the clear antipsychiatry bias. An article from the Economist was posted recently that seemed to get a positive reception in some areas.  In my estimation that reception was not warranted.  Interestingly the same principles of analyzing rhetoric can be applied to this article as the last post on this blog about “doing your own research.”  I will use the same concept by concept approach to examine this article that I used for that video.  At the time the article was posted I read it for free online and I hope it is still available so that any reader here can appreciate the full text.  The author was not listed.

1:  “But her local hospital, in Durham, England, was dismissive, suggesting she had anxiety, a mental-health condition, and that she was probably spending too much time watching videos on TikTok. Her mother describes the experience as “belittling”:

The author begins with a story about an autoimmune condition with many neuropsychiatric manifestations Pediatric Autoimmune-Neuropsychiatric Disorders Associated with Streptococcus (PANDAS).  This is a condition that is known within psychiatry for at least 25 years and is covered in major psychiatric textbooks.  The author proceeds to conflate the lack of a definitive diagnosis with deficiencies in psychiatry as if it is totally unknown in the field. It is not and the pathophysiology and neuropsychiatric manifestations are known and taught within the field.  Secondarily if I had to speculate on the medical specialists who are most likely to see people who are told by a physician or family member that “it’s all in your head” – they would be psychiatrists.  We tend to see more of these people than anybody else.  

2: And infections are one small piece of the puzzle. It is increasingly clear that inflammatory disorders and metabolic conditions can also have sizeable effects on mental health, though psychiatrists rarely look for them. All this is symptomatic of large problems in psychiatry.

Psychiatrists have always been more interested in inflammatory and infectious conditions affecting the brain than most other specialists.  Griesinger mentions inflammation as a mechanism affecting brain function in his 1845 text on psychiatry (2). It is highly likely that in any community - psychiatrists are making more of these diagnoses than primary care physicians because they know the manifestations and they need to rule out physical causes of mental illnesses to make a psychiatric diagnosis.  All psychiatrists are trained in making these diagnoses and not mistaking them for a mental illness occurring in a healthy person or a person with chronic illnesses not affecting brain function.  The only large problem here is the lack of knowledge about how psychiatrists are really trained.

Inflammatory disorders were used as treatments in the early 20^th century.  In the pre-antibiotic era, 5-10% of asylum admissions were due to neurosyphilis and the associated psychiatric manifestations. Some of the early treatments were based on inducing fevers.  Austrian psychiatrist Julius Wagner-Jauregg was awarded the Nobel Prize in Medicine in 1927 for successful treatment of neurosyphilis by inoculating patients with malaria (2).  This work was replicated and additional agents were used to induce fevers by other investigators with similar results. In addition to the experimental results, this represented a sea change in the general attitude of treating psychosis in asylums where a previous biological treatment did not exist.  Subsequent innovations occurred when neuromodulation techniques were introduced in 1932 (5) and psychopharmacology in 1952 (6).

The early focus on gross neuropathology and transition to microanatomy led to the discovery of Alzheimer's Disease in 1906 and Binswanger's Disease a form of vascular dementia in 1894.  Both Alzheimer and Binswanger were considered psychiatrists - Alzheimer by his own designation and training and Binswanger was eventually appointed to head an asylum by age 30.  

As far as "rarely looking for them" goes the top 4 medical conditions I diagnosed in newly seen patients were probably Type 2 diabetes mellitus, hypothyroidism, hypertension, and atrial fibrillation. Any psychiatrist practicing in the last 30 years is aware that psychiatric disorders and pharmacological treatment can be associated with metabolic syndrome and the need to monitor for and prevent that condition. 

3:  Chronic conditions are poorly treated – apparently because they are not cured (paraphrased):

This is always an interesting rhetorical sleight-of-hand. In what other specialty is the expectation that chronic conditions will be cured? It does not take a lot of research to show that nobody is curing most diabetics, hypertensives, asthmatics, arthritics, or patients with a multitude of other chronic conditions. In fact most of these patients remain symptomatic even when they are treated. These are all conditions with clear cut laboratory tests and other disease markers.  These are all conditions where there is at least a speculative biological hypothesis of pathophysiology.  And yet – there is no expectation of cure and in fact much more expected mortality in other specialties. Why is psychiatry different?  It is not.

4:  Some people in the profession believe that biological psychiatry will lead to better characterizations of psychiatric problems including pathophysiology, drug treatment, and pharmacological targets/precision psychiatry (paraphrased):

It is obvious that biological psychiatrists have been at it for decades and much longer.  The journal Biological Psychiatry was founded in 1969 but biology has been a focus of psychiatric research dating back to mid-19^th century when attempts were made to observe brain dissection correlates with behavior.  Griesinger (2) documents efforts by both Pinel and Esquirol to document brain abnormalities in severe mental illnesses. In his text he documents brain diseases leading to psychiatric care and associated organ dysfunction at autopsy in patients identified as having severe mental illness.

In the days of asylum care before biological psychiatry, delirious mania had a mortality rate of 75% (7).  That has essentially been reduced to zero with advances in modern biological psychiatry including electroconvulsive therapy and psychopharmacology.  There is probably no better example of advances due to biological psychiatry occurring over decades.

Like all other medical specialties, biological psychiatry is an active area of research with new journals like Molecular Psychiatry (1997) and Translational Psychiatry (2011) that are focused on the latest innovations in biological psychiatry and potential treatment applications.

5:  The DSM or the Bible of Psychiatry does not specify pathophysiology

Any time you see that the DSM is the “Bible of psychiatry” that is a red flag that indicates the author either lacks knowledge about the Bible or the DSM.  Here is a brief primer on the DSM to correct some misconceptions.  That primer emphasizes that the person using it (typically for diagnostic codes used for administrative purposes) is a trained professional and understands its limitations. Chief among those limitations includes ruling out medical causes of psychiatric symptomatology and understanding that it is not a guide for everyman to use for diagnosis and treatment.  Kendler (8) and others have taken it a step further to point out that it is an index of disorders and therefore a starting point – rather than an actual diagnostic guide.  In other words, meeting criteria for a diagnosis is not that same as having the diagnosis.  This is generally true of all codified systems of medical diagnosis.  An example would be the American College of Rheumatology classification criteria.  There is an extensive discussion of these classification criteria compared with diagnostic criteria and why the ACR currently endorses only the former (9).  It is basically the same discussion that Kendler uses in describing the indexing system – that there is sufficient heterogeneity in clinical presentations over time and geographical areas that every case needs to be individually considered. Here is the rationale from the leading text on systemic lupus erythematosus (SLE) (10):  

“The classification criteria do not contain a complete list of all the possible manifestations of lupus.  The manifestations of SLE often develop over a period of time, sometimes years, making the diagnosis more difficult at initial presentation. The diagnosis of lupus is made on clinical grounds, supported by laboratory data and depends highly on the physician’s knowledge and experience. (author’s emphasis)”

Despite the title, the DSM is not a guide to diagnosis or treatment. People who do not “meet criteria” are not automatically excluded from treatment consideration. Separate knowledge about psychopathology and diagnostic formulation is necessary. Speaking to the author’s concern about the lack of specific etiologies – even the skeletal classification and indexing framework of the DSM has chapters on clear medical, toxicological, and neurological causes of mental disorders.

The Economist dates psychiatry’s “Bible” back to 1952.  That would have been the DSM-I.  I encourage anyone who is interested to read the 6 page Forward to that document.  It started initially to standardize nomenclature. Each training program was using their own version of nomenclature as well as the military.  When trained psychiatrists went out to practice in the community – there was no standard nomenclature being used to described similar phenomenon and the requirements of military and civilian nomenclature were different. The secondary goal was to use this nomenclature to collect statistics that could be used to improve the necessary infrastructure and resources to treat these disorders.  All of this can be done without any specific reference to pathophysiology in both psychiatry and the rest of medicine.    

And here is a news flash from the DSM-5,  my estimate is that 69% of all of the diagnoses listed have a clear pathophysiology or medical test equivalent to any other branch of medicine.  Given the classification problems with all medical diagnoses that overall figure probably compares well with any other branch of medicine.   

Whatever your take away from this post, The Economist knows very little about psychiatry and medicine. But that should not be too surprising.  The tone and factual content clearly resemble much of what you see on the Internet and in the press about psychiatry. That does not make it any less wrong.  If you are really interested in what is going on in the field – I would recommend reading the general literature in the field or summaries about it. The popular press – newspapers and magazines – is clearly not up to the task.

6:  Attempts to find causal mechanisms for mental illnesses have failed (paraphrased):

News flash – that is true of every other complex disease as well as the medication used to treat them.  This post illustrates that fact with medication used to treat multiple sclerosis.  The table lists 18 FDA approved drugs – many of which modify the course of the illness but in every case the specific mechanism of action of the drug is unknown.

7:  Genetics has been a clinical “flop” (paraphrased):

It would probably be a good idea to get the opinion of an expert in psychiatric genetics.  The article seems to focus on the issue of polygenic risk analysis (PRA) and those studies generally have low effect sizes due to the number of genes studied.  Any commercial assessment of a genome will result in hundreds of these profiles – most of them for non-psychiatric illnesses. The example given above illustrates polygenic risk scores (PRS) when the small risk factors (both protective and potentially causative) are summed and compared to a standard sample so that 100% is highest percentile risk in the sample and 0% is the lowest. This is only one approach and there are major psychiatric initiatives in this space doing ongoing research. PRA/PRS is accepted science at this point but the widespread clinical utility is not known for practically all polygenic disorders.

Recent examples given by Kendler (11) in his commentary on whether psychiatric disorders are brain diseases points to the importance of genetics in psychiatry.  To this day there are endless debates, typically by people who are not trained to be psychiatrists that psychiatric disorders are somehow independent of brain substrate. In other words, even though it is widely acknowledged that a brain is required for mental life – there is no evidence at the molecular level that an alteration in brain function causes mental illness. Contrary to The Economist, Kendler states: “I use the most robust empirical findings in all of psychiatry—that genetic risk factors impact causally and substantially on liability to all major psychiatric disorders.”  He quotes the recent literature illustrating that risk variants for schizophrenia are located only in brain tissue.  Similar evidence is accumulating for bipolar disorder and major depression. This correlation of strongest known risk factors and brain substrate location is good evidence of specific genetic effects in the brain. Similar work is being done to identify signaling systems, proteins, and physiological processes underlying the DSM classifiers.  Once again, this is similar to the approaches being taken with all complex non-psychiatric diseases. 

8:  Biology is coming, whether psychiatry is ready or not:

When I saw this caption – it seemed like a joke.  Over the 40 years of my career there has been a constant battle based on the false dichotomy of biological psychiatrists and psychotherapy focused psychiatrists. That left out important additional identities including medical psychiatrists, neuropsychiatrists, and community psychiatrists. Practically all the criticism in the press has been that psychiatrists are too biological. I could probably write a book about this – but in this case suffice it to say that The Economist has not done much homework. The smattering of research projects listed in the last several paragraphs about immunology and metabolism ignores that this type of research has been going on for decades and gradually making progress. 

Every psychiatrist is trained in the biology of medicine and psychiatry - just like me.  We are willing to incorporate the latest research innovations and look forward to them. Biology comes as no surprise.

 

George Dawson, MD, DFAPA

 

 

 

References:

1:  “Many mental-health conditions have bodily triggers: Psychiatrists are at long last starting to connect the dots.:  April 24, 2024.  In the print edition this story is under the general heading "Psychiatry’s blind spots".  No author was listed for the online version that I read.

2:  Griesinger W: Die Pathologie und Therapie der Psychischen Krankheiten: für Aerzte und Studirende. (The pathology and therapy of mental illnesses, for doctors and students). Stuttgart, Germany, Verlagvon Adolph Krabbe, 1845  https://www.deutschestextarchiv.de/book/view/griesinger_psychische_1845?p=47

3:  Wagner-Jauregg J. The treatment of general paresis by inoculation of malaria. J Nerv Ment Dis. 1922;55:369–375. [Google Scholar] [Ref list]

4:  Tsay CJ. Julius Wagner-Jauregg and the legacy of malarial therapy for the treatment of general paresis of the insane. Yale J Biol Med. 2013 Jun 13;86(2):245-54. PMID: 23766744; PMCID: PMC3670443.

5:  Gazdag G, Ungvari GS. Electroconvulsive therapy: 80 years old and still going strong. World J Psychiatry. 2019 Jan 4;9(1):1-6. doi: 10.5498/wjp.v9.i1.1. PMID: 30631748; PMCID: PMC6323557.

6:  Ban TA. Fifty years chlorpromazine: a historical perspective. Neuropsychiatr Dis Treat. 2007 Aug;3(4):495-500. PMID: 19300578; PMCID: PMC2655089.

7:  Bell, L., 1849. On a form of disease resembling some advanced stage of mania and fever.  Am. J. Insanity 6, 97–127. 

8:  Kendler KS. The Phenomenology of Major Depression and the Representativeness and Nature of DSM Criteria. Am J Psychiatry. 2016 Aug 1;173(8):771-80. doi: 10.1176/appi.ajp.2016.15121509. Epub 2016 May 3. PMID: 27138588.

9:  Aggarwal R, Ringold S, Khanna D, Neogi T, Johnson SR, Miller A, Brunner HI, Ogawa R, Felson D, Ogdie A, Aletaha D, Feldman BM. Distinctions between diagnostic and classification criteria? Arthritis Care Res (Hoboken). 2015 Jul;67(7):891-7. doi: 10.1002/acr.22583. PMID: 25776731; PMCID: PMC4482786.

10:  Rudinskaya A, Reyes-Thomas J, Lahita R.  The clinical presentation of systemic lupus erythematosus and laboratory diagnosis. In: Lahita RG, Costenbader KH, Bucala R, Mani S, Khamashta MA.  Lahita’s Systemic Lupus Erythematosus. 6^th ed.  London, England:  Elsevier, 2021: 316.

11:  Kendler KS. Are Psychiatric Disorders Brain Diseases?-A New Look at an Old Question. JAMA Psychiatry. 2024 Apr 1;81(4):325-326. doi: 10.1001/jamapsychiatry.2024.0036. PMID: 38416478.

Addictions Neuroclinical Assessment

I was quite excited when I heard about this paper in Biological Psychiatry a few days ago.  It was hyped as a way to forgo the usual DSM approach and others and make an addiction assessment based more on the neuroscience of addiction.  The basic dimensions for assessment are highlighted in the above diagram.  The authors make a compelling argument in terms of what is needed in addition to the clinical criteria "that has provided a reliable foundation for the practice of addiction medicine."  The clinical criteria that they are referring to are DSM criteria or basically problems and symptoms that are used to classify disorders from non-addictive use of the same substances.  Even the most biologically based of these symptoms - craving, tolerance, and withdrawal vary widely across all individuals in the same diagnostic group.  That variation is most likely due to biological complexity.  The authors contend that there should be a way to examine that heterogeneity among the larger clinical divisions to get at pathophysiologically based subtypes.  They suggest that the focus should be more on process than outcomes.  

They use cancer as an example of the importance of specific etiology in the diagnosis and treatment of disease.  In the case of the diagnosis and treatment of breast cancer, the BRCA1 gene is used to predict increased risk for breast cancer for a subpopulation of women with this diagnosis.  Detection of HER2 protein overexpression can predict response to a monoclonal antibody  (trastuzumab) that  interferes with the HER2/neu receptor.  All of this information is used within the existing clinical context and even then addition information about breast cancer would probably be useful.  The review several similar initiatives in psychiatry and addiction and compares the ANA (Addictions Neuroclinical Assessment).   The other examples include the Research Domain Criteria (RDoC), the Cognitive Neuroscience Treatment Research to Improve Cognition in Schizophrenia (CNTRICS), and the Impaired Response Inhibition and Salience Attribution (iRISA).  Clinicians will note that none of these initiatives has gained a foothold in routine clinical practice.  Only the CNTRICS has assessments across all 5 of the domains addressed by the ANA.

Looking at the major domain for assessment, the authors provide definitions and the rationale for their inclusion.  They define executive function as "processes related to organizing behavior toward future goals".  The reality is that executive function is really defined by convention, typically measures that are thought to reflect to reflect frontal lobe function like mental flexibility and set shifting.  Addiction significantly limits the repertoire of these frontal mechanisms to maintain rather than critically assess the addiction.  Impaired glutamatergic signalling to the stratum and extended amygdala and loss of top-down control are listed as the putative neuroscientific mechanisms.  Incentive salience is described as "psychological processes that transform the perception of stimuli, imbuing them with salience and making them attractive."  The underlying mechanism is given as "activation of mesocortical dopamine system".  Familiarity with the reward and motivational system that is focused on the ventral tegmental area and its dopaminergic projections to the nucleus accumbens is at the heart of this system but it alson includes projections to the frontal cortex.  During the initial phases of exposure to rewarding stimuli, the dopaminergic neurons will fire.  As that process continues, anticipation of reward causes them to fire.  That phasic dopaminergic activation leads to altered response to cue and noncue targets, craving, and heightened relapse risk.  Negative emotionality is defined dysphoria and negative emotional responses to stimuli associated with addictive states.  These states are often mistaken for an treated as depression.  The ANA has instruments to assess hypohedonia.  Brain stress and antistress systems are thought ot be involved with the latter contributing to negative emotionality.

When I look at the table of measures that comprise the ANA a couple of scenarios come to mind.  The first is the omnipresent Attention Deficit-Hyperactivity Disorder (ADHD) diagnosis encountered in psychiatric practice.  Most of these diagnoses are not made by psychiatrists.  In the people who I reassess because they may have an addiction, when I ask them about the diagnosis, I am likely to hear: "My primary care doctor sent me to a psychologist and I had two hours of paper and pencil and computer testing."  The problem is that there are no neuropsychological tests for ADHD, no matter how extensive.  Most of the test battery would be for executive function - right out of the ANA and those tests are not necessary for the diagnosis.  That led Barkley to come up with his own version of checklist symptoms that he thought matched the executive function deficits of the disorder better than the neuropsychological tests did.  The second diagnosis is Alzheimer's dementia.  Cortical dementias are based on higher cortical deficits, memory problems and the characteristic progression.  An extensive test battery for the disorder is not indicated.  I would argue that medical testing to rule out other causes is the single most important biomedical approach and that an extensive test battery would not add much.

In summary, there are several questions about the ANA.  The first is whether it can ever be widely implemented in its current form.  The total length of the test is 205 minutes on paper and three of the tests are based on neuroimaging.  The authors estimate that it would take about 10 hours to complete and cost anywhere from $3000 to $5000 per individual.  That alone restricts the ANA to urban areas where psychiatric clinics are well staffed and have access to neuroimaging and staff with the time and interest in complex diagnoses.  That runs counter to a 30 year trend to ration detox and addiction services and largely move them off of medical campuses.  It also runs counter to the collaborative care idea that suggests psychiatric staff can be marginally involved in primary care clinics that equate psychiatric diagnosis and treatment to a metric that can be completed in 5 minutes or less.  Following that logic, the ANA might fly in these settings if it was 5 to 10 minutes long and would reliably lead to a prescription.  A managed care organization (and they all are these days) will not be applying this kind of test to people with addictions.  It is hard to determine how many people with addictions are seen and assessed by these organizations.  The second question involves the cost-effectiveness argument applied to medicine.  I am certainly averse to this argument, but all of the bean-counters seeing this will ask: "If we do all of these tests will it change anything?  Current treatment of addiction is a crude proposition, but are there specific treatments based on the testing that will improve the process and outcomes of treatment?

From the pure egghead side of the equation, does the ANA go far enough in exploring the conscious state of the person with addiction?  I find that very few assessments examine the cycle of euphoria and positive reinforcement and dysphoria and negative reinforcement best described in a statement by one of the coauthors of this paper:

"Addiction is a chronic relapsing syndrome that moves from an impulse control disorder involving positive reinforcement to a compulsive disorder involving negative reinforcement." - George Koob

As far as I know there are no more accurate statements about addiction that capture course, clinical phenomenology, and implicit neuroscience in one sentence.  If that sentence was all that you knew about addiction, you could diagnose and treat most disorders by deriving your clinical interview from these first principles.  The problem in the DSM world is that the interview ends up being a collection of impersonal markers that may of may not uniquely apply to the person being assessed.  The ANA seems to take the encyclopedic approach to this problem.  The intense euphoric state of early addiction is rarely explored.  A lot of what constitutes a clinical evaluation is the tabulation of various adverse outcomes rather than the ongoing process.

Just adhering to the basic science of the situation are there easier and more straightforward approaches to executive function, negative emotionality, and incentive salience.  I think that there might be.  I am  familiar with most of the measures suggested by the authors but the proper analysis requires a much closer look at all of the suggested metrics and how well they will discriminate between thousands of people with the same clinical diagnosis.  Although I dislike using it in the same context, the PHQ-9 is a good example of a purported measure of depression that really does not discriminate and the authors include several similar measures in their list including the Beck Depression Inventory, the Beck Anxiety Inventory, the Fawcett-Clark Pleasure Scale, and the Toronto Alexithymia Scale.  Degrees of freedom are important in thinking about the total number of items available to characterize the population versus large binary discrimination.  A lot of these measures don't seem up to the task, but i am the first to admit that it would be useful to see research that focuses on that issue.

In the meantime, the take home message for any interested clinician is that the ANA is not ready for prime time - for a number of reasons - but stay tuned.   There also seems to be an opportunity to come up with new assessments of the systems in question that are more efficient and a better complement to clinical practice.

  

George Dawson, MD, DFAPA

References:

1: Kwako LE, Momenan R, Litten RZ, Koob GF, Goldman D. Addictions NeuroclinicalAssessment: A Neuroscience-Based Framework for Addictive Disorders. Biol Psychiatry. 2016 Aug 1;80(3):179-89. doi: 10.1016/j.biopsych.2015.10.024. Review. PubMed PMID: 26772405; PubMed Central PMCID: PMC4870153.

National Neuroscience Curriculum Initiative - a brighter future for psychiatry

As any reader of this blog probably knows, I am a big proponent of neuroscience education for psychiatrists and always have been.  I have suggested in the past that it would take broad collaboration.  I posted some examples of an NIMH initiative on neuroscience  education.  I teach neuroscience (also known as neurobiology) myself and that has led me to be acutely aware of the lack of educational resources on the field.  That background is what has made this the happiest day at a CME conference that I have ever spent.  I am currently at the University of Wisconsin 4th Annual Update and Advances In Psychiatry - a conference that has really been in place for the past 41 years.  After watching a comprehensive update on eating disorders I settled in to listen to Melissa Arbuckle, MD, PhD; Professor of Clinical Psychiatry, Director of Residency Training; Department of Psychiatry, Columbia University Medical Center.  The title of her presentation was Discussing the Neuroscience of Mental Illness with Your Patients.  I turned to the section in the syllabus and there was one page with a case report on the front and a crude drawing of the brain (two views) on the back.  Being a traditional conference guy who likes a ton of technical information, no audience participation, and no role playing - I was prepared to be disappointed.

I was not prepared for what would transpire in the next 90 minutes.  I have posted here many times why I thought that every psychiatrist should know neuroscience and ways to do it, specifically the need for widespread collaboration due to a lack pf neuroscience manpower in most departments.  Dr.  Arbuckle started out explaining what the National Neuroscience Curriculum Initiative was.  It was started by a collaboration of like minded residency directors  to come up with a program to teach neuroscience to psychiatry residents.  She showed the explosion in neuroscience papers in psychiatry just over the past decade.  She referred to an article in JAMA Psychiatry (1) with her collaborators on why neuroscience needs to be integrated into psychiatry right now.  She discussed the New York Times editorial that showed up three weeks later with the criticism of their viewpoint (2).  Although she did not mention it, like a lot of articles it as written from the perspective of a psychiatric identity crisis.  Whenever I see that term it seems like the authors are firmly behind the curve and don't seem to understand what neuroscience encompasses.  Dr. Arbuckle said that the article was critical of the criticism that the brain was the basis of human behavior.  Quoting the article:

"Indeed an article in May in one of the most respected journals in our field JAMA Psychiatry echoed this view: "The diseases we treat are diseases of the brain."........ Even if this premise were true - and many would consider it reductionist and simplistic - an undertaking as ambitious as unraveling the function of the brain would likely take many years."  The author is a psychiatrist and goes on to say that he is all for neuroscience and even talks about some recent research techniques he (implicitly) just doesn't think psychiatrists should study it?  He also seems to conflate psychotherapy as being independent of neuroscience when in fact we have known just the opposite since since Kandel's 1979 seminal lecture Psychotherapy And The Single Synapse.  

I am equally incredulous when people seem to argue about the importance of neuroscience in psychiatry.  I find reductionism and reductionist approaches to be perfectly understandable and acceptable.  It is an interesting form of rhetoric to use these terms pejoratively.  Most people go into medicine because they want to know how things work.  If they did not enter with that goal, it soon becomes apparent that knowing mechanisms whether they are theoretical or not is an important aspect of studying medicine.  Some of the first mechanisms I studied in medical school involved cholera and diphtheria toxin. How is it possible to determine these mechanisms and recent significant epigenetic mechanisms without taking a reductionist approach?

The exercise that Dr. Arbuckle introduced to the audience was the diagnosis and treatment of complex cases.  The case vignette involved a young woman with borderline personality disorder.  The task for the audience was to pair up and role play discussing the relevant neuroscience concepts of treatment with the patient using the brain diagram as an aid.  Eliciting responses from 300 people in a room slows things down.  After the audience was done, she showed a film of an expert presenting this information to a patient and what presentation materials might be available.  It went very well and it presented the rationale for dialectical behavior therapy and not a medication.  It was a clear example of a neuroscience based discussion that provides a rationale for psychotherapy.  There are numerous materials on the web site (9 modules, 56 sessions, 40 authors) and wide scale participation is encouraged.

The information up to that point was quite exciting.  Dr Arbuckle had plenty of enthusiasm in her closing remarks.  In those remarks she pointed out the goal of "getting the entire field up to speed" in neuroscience.  She pointed out that everything on the site is free but at some point they may ask physicians to pay for CME.  She said that she realizes that this is literally "changing the world and that is what we are going to do."        

This was the most exciting commentary from a psychiatrist about teaching the entire field and the future of psychiatry that I have ever heard.  I have never been this impressed by any development in the field during my career.  And I am a psychiatrist who is as pro-neuroscience as anybody.  How is it that I am just hearing about this initiative right now and only because I am attending a conference?  That is why I am posting my experience here and a link to the NNCI web site and materials.

Dr. Arbuckle and her collaborators are one of the few bright spots for the future of psychiatry.

But they are very bright.


George Dawson, MD, DFAPA


References:


1:  Ross DA, Travis MJ, Arbuckle MR. The future of psychiatry as clinical neuroscience: why not now? JAMA Psychiatry. 2015 May;72(5):413-4. doi: 10.1001/jamapsychiatry.2014.3199. PubMed PMID: 25760896.

2: Friedman RA.  Psychiatry's Identity Crisis.  New York Times July 17, 2015. p SR5.


Attribution: 

The graphics at the top are two slides from one of my lectures.  I like to present data on the unique aspects of every individual brain and why that can happen.  The slides are not from the NNCI program and I am not affiliated with that program.  Click on each slide to enlarge.

E. Fuller Torrey on the New Anti-biological Antipsychiatry

This post by E. Fuller Torrey was noted on another blog especially the phrase "the new anti-biological antipsychiatry".  Torrey explains anosognosia both as a biological phenomenon and why it may be "deeply disturbing" to the new antipsychiatrists.  Basically it represents the difference between social behavior based on choice versus social behavior based on brain damage.  The former  might be a civil rights issue but the latter is a medical problem that benefits from identification, study, and treatment.  Torrey is also clear about the consequences of no treatment, facts that the antipsychiatrists conveniently often leave out of their arguments or more conveniently blame on treatment.

There is a lot of technical information apart from the data on anosognosia that is ignored by the new anti-biological antipsychiatry.  There are studies on the prefrontal cortex that go back for decades and the implications for social behavior and the neurobiology of everything from addiction to dementia.

Here is a link to the original blog post by Duncan Double entitled: "E. Fuller Torrey attacks 'The new antipsychiatry.'"  Defending against attacks by the new antipsychiatry is more like it.  Dr. Double laments the fact that at times he is seen as an antipsychiatrist, even though he essentially maintains many of the positions of mainstream antipsychiatry.   He includes a variation of the old antipsychiatry argument that if you don't have a specific test for a disease - the disease does not exist.  That opinion fails to take into account studies about what is or is not a disease as well as a massive literature of biological psychiatry.  It also fails to take into account the fact that these arguments are political in nature and have very little to do with science.

A good example is the chemical imbalance red herring.  Any psychiatrist trained since the 1970s is aware of the complex neurobiology of human behavior.  I can recall reading Axelrod's paper in Science over 30 years ago.  Since then there have been eight editions of The Biochemical Basis of Neuropharmacology and five editions of the ACNP text Neuropsychopharmacology.  Since then a psychiatrist has won the Noble Prize for contributions in neuroplasticity and wrote a seminal article on neuroplasticity and learning in psychotherapy.  That is apparently ignored by the anti-biological antipsychiatry crowd and those who would characterize the field as prescribers versus therapists.  The Internet is currently full of diagrams of cell signalling pathways with the associated proteins and genetics.  The idea that chemical imbalance reflects some central central theory of biological psychiatry or represents anything beyond pharmaceutical company marketing hype reflects a gross misunderstanding of the field.

Any psychiatrist who tries to respond to these crude arguments is at a disadvantage for a couple of reasons.  It is certainly seems true that the antipsychiatrists political stance is really not conducive to scientific discourse.  Suggesting that the appearance of conflict of interest invalidates psychiatry is an obvious example.  Discounting the amassed research on the neurobiology of mental illness is another.  A political argument is well outside the scope of hypothesis generation and testing.  Dismissing the science by attributing it to the "worldview" of a single person is consistent with that political approach.