Is The Next Zoonosis Lurking In Your Back Yard?

 

I just had a recent adventure with rabbits.  Like the experience of many suburbanites, rabbits like to eat all our ornamental vegetation. My wife oversees that department, and she does not like to see that vegetation depleted. She has tried all the repellants and the rabbits keep coming.  She has talked about shooting them like her father used to, but I convinced her that was not a good idea.  She settled on the idea of live trapping the animals and releasing them in an area far away from the house – like a park or wildlife reserve.

I researched the legality of it all.  I was surprised to find out that rabbits are considered a nuisance animal in the state of Minnesota.  As such you can kill them by various means other than poisoning without a license and at any time. There are obstacles to both relocating rabbits or how to dispose of them. I contacted both the county and city natural resource departments. They told me it was illegal to relocate rabbits onto city, county, or state lands including parks and wildlife areas.  The officials confirmed that I did not need a hunting license to kill them, but that if I did kill a rabbit, I needed to report it to the DNR.  I did not let anyone know I thought that killing a rabbit was bad karma and I had no intention of killing them.

I was advised that if I did kill a rabbit, I needed to handle it with nitrile gloves and double bag it in plastic.  Even then I must contact my garbage hauler to make sure that I could dispose of it in the trash. There were no further instructions from officials on the next step if the garbage hauler refuses to take it – but based on how the conversations were going I thought it was probably digging a deep hole in the yard.

Minnesota is populated by one true rabbit species – the Eastern Cottontail (Sylvilagus floridanus) and two hare species – the Snowshoe Hare (Lepus americanus) and the White-tailed Jack Rabbit (Lepus townsendii).  The hares are probably more common in the north.  The defining characteristics of rabbits versus hares include fewer chromosomes (44 versus 48), altricial birth state versus precocial, shorter gestation (30-31 days versus 42 days), smaller bodies and shorter ears, highly social versus solitary, and softer food preference (grass and leafy vegetables opposed to bark, twigs, and buds).  An altricial birth state means offspring are born in a state where they are unable to feed or regulate body temperature and as a result need a prolonged period of close parenting. In the past 10 years there have also been cladistic analyses based on nuclear and mitochondrial DNA.  Like all taxonomy there is some mismatch of classification.  Jackrabbits are hares and Rock hares are rabbits.     

Even before I heard those biosecurity measures from public officials, I researched the issue of rabbit to human disease transmission (1).  Domestic pet rabbits were noted to spread the expected pathogens like E. coli, Salmonella spp, Yersinia pseudotuberculosis, and Cryptosporidium.  They can also be a source of Hepatitis E.   Pasteurella multocida and Bordetella bronchiseptica can be spread as respiratory infections in humans.  Rabies was detected in one group of rabbits thought to have been infected by a wild animal.  Dermatophytes and rabbit fur mites can cause localized infections in humans.

Wild rabbits harbor Francisella tularensis the infectious bacteria causing tularemia. Tularemia is a systemic multisystem disease that can be difficult to diagnose and treat. In the worst case it can cause shock and death.  It has also been implicated as an agent that could be used for bioterrorism.   Rabbits can also have Babesia spp and Anaplasma phagocytophilum the infectious agents that cause babesiosis and human granulocytic anaplasmosis.  

Babesiosis is caused by the obligate intraerythrocytic protozoan parasite Babesia microti (2).  Severity of the illness is related to degree of parasitemia (concentration of parasites in the bloodstream) and host factors that lead to compromised immune response including age. In the extreme cases it can lead to life threatening complications that require acute care like acute renal failure, disseminated intravascular coagulation (DIC), congestive heart failure, acute respiratory distress syndrome (ARDS), and others.

Human granulocytic anaplasmosis is caused by intracellular bacteria from the Anaplasmataceae family – in this case Anaplasma phagocytophilum (3).  It is a tick-borne disease meaning that the major reservoir for the agent is small mammals who transmit it to humans via a tick vector.  Most people who are infected present with an acute flu-like illness that can progress to involved multiple systems (rash, pneumonitis, myocarditis, meningoencephalitis, secondary infections, coma).

Most of the infections identified from rabbits come from direct contact, contact with infected surfaces, and contact with blood, feces, or other bodily fluids. People raising rabbits as pets, as a food source, or hunters would appear to be at highest risk and the suggested biosecurity measures would be protective.  In talking with the local wildlife officials their concern was that rabbit relocation could be a significant source of disease spread – specifically Rabbit Hemorrhagic Fever – a viral illness that results in most rabbits dying of hepatic necrosis 48-72 hours post infection. 

Rabbit Hemorrhagic Disease Virus (RHDV) was first described in China in 1984 and has spread worldwide (4).  It is a small non-enveloped RNA virus about 40 nm in diameter.  The genome is about 8 kilodaltons is size. It is taxonomically classified in the Calciviridae family.  That family has 11 genera (Norovirus, Nebovirus, Sapovirus, Lagovirus, Vesivirus, Nacovirus, Bavovirus, Recovirus, Salovirus, Minovirus, and Valovirus) (5).  Of the major genera Norovirus and Sapovirus cause acute gastroenteritis in humans.  The etiological agent can only be distinguished by laboratory testing. The Lagovirus genus also includes European brown hare syndrome virus (EBHSV) (6).  While the original RHDV virus was species specific – there is a newer strain (RHDV2 (GI.2) that infects both rabbits and hares and is lethal to both.

All these details build a compelling story far beyond suburban landscapers wanting to protect their plants.  The recent pandemic and likely crossover of a bat coronavirus into the human population as well as past crossovers like human immunodeficiency virus and avian influenza highlight the dangers of proximity to animals with high levels of infection. There have been two recent worldwide epidemics of rabbit hemorrhagic disease virus (RHDV) initially from 1984 to the 1990s and more recently from 2010 to present.  At no point in my medical career was I made aware of this viral spread despite hearing about viral spread in other species like elk wasting disease. Evolutionary biologists have suggested the RHDV virus has been in existence for 150 years (7-10). 

The pathogenesis of the virus is known at this point. It causes apoptosis of hepatic cells and hepatic necrosis.  One of the main protective mechanisms’ antioxidant suppression of oxidative stress is overwhelmed.  Apoptosis of endothelial cells leads to procoagulant activity and disseminated intravascular coagulopathy (DIC) and resulting hemorrhage and shock. RHDV2 has enhanced virulence factors and previous infection with RHDV does not confer immunity.     

The risk of RHDV crossover to human is estimated to be low based on several factors.  First, in a large study of human exposure of 269 people exposed to infected rabbits there were no episodes of disease or antibody formation to the virus in any of those people.  Second, there is continued host specificity to lagomorphs with limited documented crossovers to other species (Alpine musk deer, Eurasian badgers).  Third, there is limited ability for viral replication in other mammalian models including mice with immune deficits (interferon 1 receptor deficits). Fourth, high specificity for histo-blood group antigens (HBGAs) (11-12) – that is the virus binds to rabbits specific HBGAs and cell receptor specificities.  Fifth, the molecular biology of the rabbit versus human HBGAs are such that there are no functional binding sites for RHDV virus.

In my efforts to understand why rabbits are considered a nuisance animal and a biohazard, I uncovered an interesting set of factors. Given the rabbit exclusive pandemics that have occurred I can understand why wildlife officials are concerned about the spread of disease from transported rabbits.  The concern about disease transfer to humans from feces, saliva, other bodily fluids, and rabbits carcasses also makes sense. One of my colleagues pointed out that there is a tularemia vaccination for dogs.  Other rabbit predators may be as susceptible as humans to many of these diseases and they are probably relatively protected from RHDV because of the aforementioned factors.  This post also highlights the need for veterinary virologists and epidemiologists to track the evolution and crossover potential of these viruses.   That used to happen in an organized way for Influenza viruses through the World Health Organization (WHO) but the current anti-science and anti-medicine administration has pulled the US out of that organization and had probably negatively impacted the viral surveillance necessary to prevent zoonoses.

At the practical level, if you are a suburbanite interested in protecting your hastes from rabbits, barriers like wire cages are recommended by the public officials I talked with.  Be sure to check with them about live trapping and relocation or other means of controlling rabbits. The literature I reviewed on live trapping recommended always using gloves when handling the trap to avoid contaminants and prevent the transfer of human scent to the trap.  Rabbit waste and carcasses should also be avoided by homeowners and pets.  Some of the pathogens in the table are transmitted by ticks – so the same precautions to prevent Lyme Disease apply.   In terms of surveillance, your state department of natural resources is probably the best resource.   They directed me to the problem of RHDV that is not listed in the human literature but is an ongoing global problem for rabbits at the epizootic level.

The lesson from rabbits so far is that non-humans also have epidemics or epizootics. The only epizootics that humans seem to pay attention to affect domesticated animals or potential high risk crossover situations like avian influenza. Those contacts of humans and animals in suburbia bear watching both for the immediate threats and implications for handling biological materials – but also the potential long term consequences. (13-16).    

 

George Dawson, MD, DFAPA

Supplementary 1:  I thought this was an excellent graphic but could not figure out where to put it in the above essay. It is an estimate of worldwide mortality due to infectious diseases. Zoonotic origins are on the left of the diagram and non-zoonotic on the right.  The authors point out that boundary is not as clear cut as it seems since common causes of crossover like bats, rats, and mice occupy the same biosphere.  In the case of rabbits I would say the backyard is the same biosphere.  

60% of human diseases have animal origins.  Based on the lab origins rhetoric of the past few years Mother Nature is by far the most significant bioterrorist.  It also speaks to why any reasonable approach to prevent these outbreaks requires infectious disease and epidemiology expertise in both human and veterinary medicine.

The graph also contains the implicit information on the non-zoonotic side.  The increasing candida auris infections are thought to be due to man-made climate change.  Warm blooded animals were thought to have natural resistance to fungal infections based on higher body temperature where fungi could not survive. That evolutionary advantage is vanishing due to increasing ambient temperatures and fungal adaptation.  There are also 5 vaccine preventable diseases. There is an active anti-vaccination campaign that has reduced access to some of these vaccinations.         

Graphic is reproduced here via Copyright: © 2022 Weiss RA et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, CC BY 4.0 which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.  Original work is cited as reference 14.

Supplementary 2:  Map of outbreak of RHDV2 a variant that was first detected in France in 2015.  Top map is form the USDA and the bottom map is from reference 17 per Creative Commons Attribution 4.0 (CC BY 4.0) International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format.

Photo Credit:  Photo of an Eastern Cottontail rabbit that I took in my back yard.  I was 5 feet away and the rabbit did not move it just continued to stare at me.  This is highly unusual behavior for wild rabbits who are generally programmed to run explosively in circles to avoid predators.  Similar behavioral changes are often signs of illness in wild animals but this rabbit eventually started moving and hopped away.  

References:

1:  Cotton CN.  Zoonoses: Animals other than dogs and cats.  UpToDate.  Accessed March 31, 2026.  https://www.uptodate.com/contents/zoonoses-animals-other-than-dogs-and-cats

2:  Krause PJ.  Babesiosis: Clinical manifestations and diagnosis.  UpToDate.  Accessed March 31, 2026.  https://www.uptodate.com/contents/babesiosis-clinical-manifestations-and-diagnosis

 3:  Dumler JS.  Biology of Anaplasmataceae.  UpToDate.  Accessed March 31, 2026.  https://www.uptodate.com/contents/biology-of-anaplasmataceae

4:  Abrantes J, van der Loo W, Le Pendu J, Esteves PJ. Rabbit haemorrhagic disease (RHD) and rabbit haemorrhagic disease virus (RHDV): a review. Vet Res. 2012 Feb 10;43(1):12. doi: 10.1186/1297-9716-43-12. PMID: 22325049; PMCID: PMC3331820.

5:  Smertina E, Hall RN, Urakova N, Strive T, Frese M. Calicivirus Non-structural Proteins: Potential Functions in Replication and Host Cell Manipulation. Front Microbiol. 2021 Jul 14;12:712710. doi: 10.3389/fmicb.2021.712710. PMID: 34335548; PMCID: PMC8318036.

6:  Fitzner A, Niedbalski W, Kęsy A, Rataj B, Flis M. European Brown Hare Syndrome in Poland: Current Epidemiological Situation. Viruses. 2022 Oct 31;14(11):2423. doi: 10.3390/v14112423. PMID: 36366520; PMCID: PMC9698305.

EBHSV can infect Sylvilagus spp but not European rabbits Oryctolagus cuniculus. 

7:  Fitzner A, Niedbalski W, Hukowska-Szematowicz B. Simultaneous Occurrence of Field Epidemics of Rabbit Hemorrhagic Disease (RHD) in Poland Due to the Co-8:  8: 

8:  Presence of Lagovirus europaeus GI.1 (RHDV)/GI.1a (RHDVa) and GI.2 (RHDV2) Genotypes. Viruses. 2025 Sep 26;17(10):1305. doi: 10.3390/v17101305. PMID: 41157577; PMCID: PMC12568209.

9:  Abrantes J, van der Loo W, Le Pendu J, Esteves PJ. Rabbit haemorrhagic disease (RHD) and rabbit haemorrhagic disease virus (RHDV): a review. Vet Res. 2012 Feb 10;43(1):12. doi: 10.1186/1297-9716-43-12. PMID: 22325049; PMCID: PMC3331820.

10:  Kerr PJ, Kitchen A, Holmes EC. Origin and phylodynamics of rabbit hemorrhagic disease virus. J Virol. 2009 Dec;83(23):12129-38. doi: 10.1128/JVI.01523-09. Epub 2009 Sep 16. PMID: 19759153; PMCID: PMC2786765.

11:  Stowell CP, Stowell SR. Biologic roles of the ABH and Lewis histo-blood group antigens Part I: infection and immunity. Vox Sang. 2019 Jul;114(5):426-442. doi: 10.1111/vox.12787. Epub 2019 May 9. PMID: 31070258.

12:  Stowell SR, Stowell CP. Biologic roles of the ABH and Lewis histo-blood group antigens part II: thrombosis, cardiovascular disease and metabolism. Vox Sang. 2019 Aug;114(6):535-552. doi: 10.1111/vox.12786. Epub 2019 May 14. PMID: 31090093.

13:  Carman JA, Garner MG, Catton MG, Thomas S, Westbury HA, Cannon RM, Collins BJ, Tribe IG. Viral haemorrhagic disease of rabbits and human health. Epidemiol Infect. 1998 Oct;121(2):409-18. doi: 10.1017/s0950268898001356. PMID: 9825794; PMCID: PMC2809540.

14:  Weiss RA, Sankaran N. Emergence of epidemic diseases: zoonoses and other origins. Fac Rev. 2022 Jan 18;11:2. doi: 10.12703/r/11-2. PMID: 35156099; PMCID: PMC8808746. (open access)

15:  Galindo-González J. Avoiding novel, unwanted interactions among species to decrease risk of zoonoses. Conserv Biol. 2024 Jun;38(3):e14232. doi: 10.1111/cobi.14232. Epub 2024 Jan 3. PMID: 38111356.

16:  Bengis RG, Leighton FA, Fischer JR, Artois M, Mörner T, Tate CM. The role of wildlife in emerging and re-emerging zoonoses. Rev Sci Tech. 2004 Aug;23(2):497-511. PMID: 15702716.

17:  Sun Z, An Q, Li Y, Gao X, Wang H. Epidemiological characterization and risk assessment of rabbit haemorrhagic disease virus 2 (RHDV2/b/GI.2) in the world. Vet Res. 2024 Mar 26;55(1):38. doi: 10.1186/s13567-024-01286-x. PMID: 38532494; PMCID: PMC10967181.

Update on Kratom

 

 

I started writing about kratom on this blog 7 years ago after I noticed more people having problems with it.  One of the main themes of this blog is that any substance that reinforces its own use is a most important property that cannot be denied at the individual, societal, or medical level.  The most successful approaches to limiting the consequence of excessive use are cultural change, limiting access, and criminal penalties.  Without those deterrents the progression from increased use to commoditization and use on a much larger scale is predictable.  It turns out that this extends beyond addictive compounds to behavioral addictions as well. Examples include gambling, sex and pornography addiction, and social media addiction. Rather than acknowledging this reality – the typical way these problems are approached in the US is rationalization, denial, and inadequate remedies.

The examples available just in the past 2 decades are striking. We entered the 21^st century on the cusp of an opioid epidemic.  That was based initially on more liberal prescribing by physicians of compounds that were highly addictive – but those properties were denied using this medication for maintenance treatment.  They were also sold based on the idea that chronic pain was better treated with opioids and that it was possible to eliminate pain.  From there cannabis was sold as the next great universal cure – even though its medicinal use has been in existence for about 2,500 years.  That led to a confusing decade of state-by-state regulations for so called medical cannabis.  Some of those states considered non-medical use illegal.  Some states took that a step farther by decriminalizing cannabis typically based on personal use.  Other states eventually legalized recreational cannabis.  It is currently legal in 40 of 50 states for medical use, in 24 of 50 for recreational use, and decriminalized in 6 states.

Over the past decade the evidence for medical applications of cannabis have been increasingly sparse.  It appears that the initial hype about it being a miraculous medicinal have not played out and it looks like that approach was established to facilitate a path to legalization. Now that medical applications are vanishing, we see it being sold as an industry and even a source of equity for oppressed minorities.

The next frontier seems to be convenience stores.  About 50 years ago, gas stations in the Midwest began selling bread and milk in addition to gasoline.  In those days they were open longer than most grocery stores and people got accustomed to picking up these necessities at odd hours.  As more people used them the stock expanded to the point where today you can get prepared hot food 24 hours a day at some of these stores.

Some but not all these stores are selling compounds like kratom and other potentially problematic compounds.  Many of these drugs being sold fall into loopholes in state statutes and despite warnings from federal agencies are still available for over-the-counter purchase.  They are not FDA approved prescription drugs, so they are not available though pharmacies.  In the case of kratom 30 of 50 states regulate it to some extent, it is illegal as a Schedule 1 drug and banned in 6 states, and in 20 states it is neither controlled or regulated.  I live in one of the states where it is regulated to some extent and it is available for purchase at gas stations. It is only illegal to sell to a person less than the age of 18 years or possess kratom if you are less than age 18.  Both are considered misdemeanor crimes. 

That brings me to the current update (3) from the Mortality Morbidity Weekly Report (MMWR).  The authors analyze data from the National Poison Data System (NPDS) from 2015 to 2025 and have several outcomes and demographics available from that system.  The system depends on self report so mild cases may be minimized, the type of formulation (leaf versus other formulations) was not available, multiple exposures can be reported so causality may be undetermined and repeat calls and misclassification can occur. 

A further analysis problem is that in many cases there are more drugs present than just kratom.  The authors analyze the data about whether there is single substance or multiple substance exposure leading to the morbidity or mortality event.  The case selection and outcomes of interest are illustrated in the top graphic for this post.  The NPDS database tracks deaths and other outcome categories. Hospital admissions are tracked including psychiatric admissions.  Major, moderate, and minor effects.  Major effects are considered life-threatening or resulting in permanent disability or disfigurement.  Moderate effects are systemic, prolonged and require some treatment but are not life threatening. The authors define serious as lethal, major, or moderate for the purpose of their outcomes.

Kratom exposure rates were calculated per million drug exposures in the NPDS database.  They document a 1200% increase in kratom exposures from 2015 (n=258) to 2025 (n=3434).  Multiple substance exposures exceeded single exposures over the same period.  Males had consistently higher rates of kratom only and multiple drug exposures.  Hospitalizations had similar increases of 1200% increase over the study interval.  There were 233 deaths over the period with 49 (21%) due to kratom exposure alone and 184 (79%) due to multiple exposures including opioids, benzodiazepines, and stimulants.  That last mortality statistic is important because many users believe that kratom is a benign substance.  That belief hinges on the amount of raw material (as leaves) that can be used for effect. Any concentrated form should be viewed as potentially as toxic as any other opioid receptor agonist and easily complicated by the use of any other opioids.

The authors attribute the significant increase in 2025 reports to the availability of concentrated semi-synthetic forms like 7-hydroxymitragynine.  It is important to note that persons with substance abuse disorders are not necessarily risk averse. The progression of any addictive process generally involves using more concentrated or bioavailable forms. That process is not rational – so if you have that kind of problem and know this data – you will not necessarily avoid more potent forms of kratom or avoid mixing them with other intoxicants like opioids or benzodiazepines.  The authors also point out that persons with multiple exposures are more likely to require hospitalizations and have more serious outcomes. 

Total lifetime use of kratom increased from 4 million to 5 million persons between 2019 and 2023 and that increase was across all demographic groups.

The overall impact of increased exposure to a drug that reinforcers it own use is expected.  Over time in every case there will be increasing morbidity and where possible mortality.  The exposure to multiple substances is expected, since people using substances for their reinforcing effects tend to use more, make substitutions, and use by routes that lead to increased bioavailability and impact.  No matter who you are this needs to be remembered at every policy debate.  The ideas about raising more revenue form these kinds of compounds and reducing taxes is a pipe dream.  The societal costs of these compounds are always high.  The more widely available they are – the higher the costs.              

 

 

George Dawson, MD, DFAPA

 

References:

1:  Crocq MA. History of cannabis and the endocannabinoid system
. Dialogues Clin Neurosci. 2020 Sep;22(3):223-228. doi: 10.31887/DCNS.2020.22.3/mcrocq. PMID: 33162765; PMCID: PMC7605027.

2:  Legislative Analysis and Public Policy Association.  Kratom: Summary of State Laws.  January 2026.  https://legislativeanalysis.org/wp-content/uploads/2026/02/Kratom-Summary-of-State-Laws.pdf

3:  Towers EB, Thomas YT, Holstege CP, Farah R. Increases in Kratom-Related Reports to Poison Centers - National Poison Data System, United States, 2015-2025. MMWR Morb Mortal Wkly Rep. 2026 Mar 26;75(11):139-145. doi: 10.15585/mmwr.mm7511a1. PMID: 41886310.

4:  US Food and Drug Administration. Import Alert 54–15: detention without physical examination of dietary supplements and bulk dietary ingredients that are or contain kratom (Mitragyna speciosa). Silver Spring, MD: US Department of Health and Human Services, Food and Drug Administration; 2026.  https://www.accessdata.fda.gov/cms_ia/importalert_1137.html

“FDA has seen an increase in the number of shipments of dietary supplements and bulk dietary ingredients that are, or contain kratom, also known as Mitragyna speciosa, mitragynine extract, biak-biak, cratom, gratom, ithang, kakuam, katawn, kedemba, ketum, krathom, krton, mambog, madat, Maeng da leaf, nauclea, Nauclea speciosa, or thang. These shipments of kratom have come in a variety of forms, including capsules, whole leaves, processed leaves, leaf resins, leaf extracts, powdered leaves, and bulk liquids made of leaf extracts. Importers' websites have sometimes contained information about how their products are used.”

5: Substance Abuse and Mental Health Services Administration. National Survey on Drug Use and Health (NSDUH): key resources and tools for NSDUH. Rockville, MD: Substance Abuse and Mental Health Services Administration; 2025. Accessed July 27, 2025. https://www.samhsa.gov/data/data-we-collect/nsduh-national-survey-drug-use-and-health

This reference says nothing about the prevalence of kratom use.

Graphics Credit:

Lead summary graphic was done by me.  Bar graphs of annual outcomes is from reference 3 and open access as an official government publication. 

DSM-6? Don't Get Your Hopes up.....

 

I just spent a while reading all the papers in the American Journal of Psychiatry about the future DSM (1-5).  As you might expect many people have many things to say and that is as true inside as outside the field.  We are on the cusp of another epoch of DSM articles in the popular press that will predictably vary from inadequate to horrific. Those articles will claim that the DSM is published as a source of revenue for the American Psychiatric Association (APA), as a way for pharmaceutical companies to make money, and as a “Bible” for psychiatrists.  There will be philosophical musings tangentially related to the field but extremely critical.  There will be the usual antipsychiatry screeds about how it is unscientific, how there are better systems out there, and how the diagnoses are mere labels that mean nothing. Most of those opinions will be written by people who have never practiced psychiatry or been treated for a mental illness.  It seems that just about anybody believes that they are an expert in psychiatry.

For those of us familiar with the field - our backgrounds are more uniform. A significant number of people are like me – undergrad science majors who are always interested in biological science and medicine. We practiced in acute care settings and saw people with significant medical comorbidity.  We made plenty of medical and neurological diagnoses that nobody else made and were a resource for that kind of referral.  We knew early on that many of the diagnoses listed in the DSM were questionable and we never used them. It turns out we are the last people the DSM is designed for and after reviewing recent opinion pieces I will tell you why and how it can be corrected.

The lead paper by Oquendo, et al (1) briefly reviews common cited problems with the DSM and possible remedies.  The first criticism is that it is atheoretical. That is less of a problem than described.  Any reader of the DSM sees immediately that despite the stated atheoretical stance there are clear stated etiologies for DSM listed diagnoses. To keep it simple, I refer any reader to the table Diagnoses associated with substance class (p. 482).  That table contains 127 diagnoses associated with specific substances.  There are similarly many diagnoses that identify a psychosocial factor as being involved in the etiology.  Categories versus spectrums are listed as problem 2, despite the fact there probably are no spectrums (from the genetic side) and all polygenic medical conditions (hypertension and diabetes mellitus for example) have the same limitations. There are 4 additional uninteresting points and proposed solutions.  One of the subcommittees is focused on the Dahlgren-Whitehead framework for social determinants of health.  At the same time another committee is looking at instruments to assure a more comprehensive sociocultural assessment.  It made me wonder whether anyone on the committee had ever read a current comprehensive psychiatric assessment.  Every psychiatrist should have concerns about more checklists.

The second paper by Cuthbert, et al (2) was about biomarkers and biological factors. The discussion was long on biomarkers and short on biology.  To neuropsychiatrists this section of the DSM has always been a disappointment. As an example, the section with the most biology – neurocognitive disorders has surprisingly little discussion of associated medical features (like a gross characterization of EEG in delirium) or a discussion of neuropathology without any additional discussion of what that looks like clinically.   The Oquendo committee (1) has proposed changing the name of the DSM to the Diagnostic and Scientific Manual because it is no longer used to collect statistics.  If that occurs, they need to put a lot more science into it, and this is the area for it. 

I have proposed a separate DSM for psychiatrists in the past but a separate volume on the current science of psychiatry would be as useful. I am talking about more than just a review of unproven research, but how the science-based psychiatrist translates what we know so far into clinical practice.  I would start with a rewrite of the section on Neurocognitive Disorders and all the important variations before worrying about plasma biomarkers and whether they are FDA approved. There are volumes written on this subject that have been lost on the DSM.  To cite a few examples – should a psychiatrist be able to recognize presentations of encephalitis, meningitis, and the various presentations of vascular dementia from their own assessment and available imaging and lab studies?  Should a psychiatrist be able to diagnose various forms of aphasia and do the indicated evaluation? Of course, they should – and it is all part of the rule out criteria for psychiatric disorders. It is not enough to leave the medicine and neurology of psychiatry to somebody else.  But very little is mentioned in the DSM except the rule out conditions: “the disturbance is (or is not) attributable to the physiological effects of a substance or another medical condition (or mental disorder).”  That is too vague for psychiatrists.  

The Structure and Dimensions Committee (3) is charged with coming up with the most clinically useful structure of the future DSM.  That involves incorporating recent research.  They have produced a lengthy table summarizing the total categories, named categories and prevailing frameworks and theories used for all the DSM starting with the first one. That number goes from 4 to 22 categories in the DSM 5-TR.  There is usually criticism about diagnostic proliferation – but not much about category proliferation.  When I encounter these numbers – I remind myself that we started with a unitary psychosis model in the 19^th century.  By 1918 (6) the situation not much better with the major diagnostic categories being psychosis or not psychosis. It could be argued that early diagnostic and classification efforts failed to recognize or include mental disorders that had been observed since ancient times rather than lower numbers being more ideal.

The fourth paper (4) is focused on Quality of Life (QOL) as an essential part of psychiatric diagnoses. They establish premises based on the often-quoted literature on disability associated with psychiatric diagnoses.  They describe a bidirectional relationship:  “… symptoms of a mental illness can impair the individual’s functioning in daily life, and poor functioning can in turn lead to or exacerbate the symptoms of a mental illness.”  The paper has two definitions of QOL.  The author’s definition is “a person’s subjective perception of their emotional, psychological, and social well-being.”  The paper also contains the World Health Organization (WHO) definition of QOL “incorporates how an individual feels about their emotional, social, and physical well-being, which can affect and be affected by their mental health condition(s).”  WHO further defines QOL as “one’s perceptions of their position in life, contextualized by the culture and value systems in which they live, in relation to their expectations, goals, and standards.”  There is a related discussion on the Global Assessment of Functioning (GAF) from previous DSMs.  QOL metrics were decided to be subjective rather than clinical ranking like the GAF.  The GAF was also thought to conflate symptoms of mental illness with functioning even though there is a clear relationship. 

The authors discuss the World Health Organization Disability Assessment Schedule 2.0) (WHODAS-2.0) and it’s use to rate psychiatric disability. It is a 36-item, 100-point self-administered, 6-dimension rating scale.  Administration and scoring in full clinical schedules was considered a limiting factor, but clinically the question is what happens with more identified problems?  Does the treatment plan expand proportionally?  Will psychiatrists be expected to either treat directly or develop referral sources for all the disabilities identified as communication, mobility, self-care, interpersonal, life and societal activities. Additional briefer QOL instruments are discussed as well as brief interventions.

A critical concept that was not mentioned was the patient’s baseline function. With every patient I saw, I had a subjective (and often other informant) description of their baseline level occupational, academic, and interpersonal functioning.  In some case it involved activities of daily living (ADLs) and instrumental activities of daily living (IADLS).  On inpatient units those ADLs were often documented by occupational therapists.  In my outpatient Alzheimer’s Disease and Memory Disorder clinic – every new patient had their ADLs documented by the RN staffing the clinic.  It required hours of work per day that were not reimbursed.  My clinic was eventually shut down because of that unreimbursed work and my refusal to do the work myself for free. The additional cost and time for these assessments is a reality factor in the modern rationed health care system.

The fifth paper is entitled: “The Future of DSM: A Strategic Vision for Incorporating Socioeconomic, Cultural, and Environmental Determinants and Intersectionality.”  The definition of intersectionality is “a framework for understanding how various social and political identities—such as race, gender, class, sexuality, and ability—overlap and intersect to create unique combinations of privilege and systemic discrimination.”  I have a problem with the use of a vague term that is used rhetorically being implemented in a DSM.  The DSM is a target of rhetoric and putting rhetoric in the manual is likely to amplify its role as a target.  I have also reviewed ample evidence that the major journal of the APA – was unable to separate rhetoric from reality in the case of clear historical evidence about racial discrimination.  This highlights the need for clear definitions and avoiding political rhetoric in any rethinking of this manual.  It also highlights the need for clear evidence rather than rhetoric and that commentaries – even in the flagship journal of the American Psychiatric Association cannot be depended upon for that evidence.

Intersectionality is unnecessary to get at what the authors hope to accomplish.  Cross cultural psychiatric evaluations are the case in point. They involve an assessment of cultural differences and how the culture affects disease definitions and presentations, the sick role in that culture, and how demographic factors affect how a person is advantaged or disadvantaged in their original or adopted culture. The authors suggest it is necessary to promote various public health prevention strategies and promote health care equity.  As far as I can tell, health care equity in the US is strictly in the purview of politics and in one year a massive amount has been destroyed by the Trump administration.  Political features should be avoided as much as rhetorical features in a DSM, especially given the abysmal track record of physician medical organizations in politics.

The authors define socioeconomic, cultural, and environmental determinants of health (SCE-DoH) as the key focus (along with intersectionality). These determinants are all well known to any psychiatrist who has recorded a social history for a detailed assessment and that should include all of us.  They conceptualize them as modifiable or non-modifiable risk factors and how they may be relevant for prevention strategies.  Much of the prevention is outside the scope of psychiatric practice and advocacy by professional organizations has questionable impacts.  They also use the Dahlgren-Whitehead model of main health determinants and cover suggestions of screening patient populations for these variables.  They conclude that the next DSM should include recommendations to use multiple “vetted instruments” to make these SCE-DoH assessments.  They give an example of how this assessment can be built into routine clinical care.  Interestingly, the psychiatric assessment is not included in the “routine diagnostic workflow” (see figure 2).  Looking at the strategy 2 where the SCE-DoH is used to determine “management as usual” versus “enhanced case management” – I made that determination myself for 40 years. For the last 25 years that “enhanced case management” was not available for most people needing it. That tells me that the suggested assessment is already being done by some people and the necessary resources are not there.  I found myself documenting that fact in too many cases.

The Committee realizes that they cannot create an additional burden on clinicians who already have unrealistic demands and provide far too much work for free in rationed environments.  That translates to less time to do comprehensive assessments – not more.  

Even though these are very preliminary statements about the future DSM – I am not very hopeful at this point.  The commentaries so far seem directed at criticisms from outside of the field rather than what psychiatrists need.  Apart from the criticism I have offered so far what is noticeable:

1:  The lack of commentary on medical and neurological diagnoses – in any psychiatric classification it is either explicit (or implicit) that what are considered the current psychiatric diagnoses are not caused by a substance or another medical diagnosis.  The non-DSM diagnostic systems are generally just focused on the listed symptoms of these disorders and there is no provision for other medical conditions.  It is also not explicit enough in medical training. At some level this is explained away and needing to utilize whatever resources are available.  That is not enough.  The DSM should have a section of diseases by system that need to be diagnosed if they are present and at least a reference to how that should be done.  There is not nearly enough information on what medical diagnoses psychiatrists make.  This is also an important feature for resident education since it would suggest how much clinical medicine and neurology residents need to be exposed to and whether they are seeing relevant cases.

2:   Philosophical criticisms while minimizing biology and history –  in several of the papers the authors talk about “natural kinds” and “carving nature at the joints”.  This is philosophy speak that has been used to obfuscate the field. The first time I encountered these arguments they struck me as obvious nonsense.  That was first suggested by Thomas Sydenham when he made this statement in about 1640:

“In writing the history of a disease, every philosophical hypothesis whatsoever, that has previously occupied the mind of the author, should lie in abeyance. This being done, the clear and natural phenomena of the disease should be noted — these, and these only…” (7) 

DeGowin and DeGowin (8) summed up the process over the next three centuries:

"For several thousand years physicians have recorded observations and studies about their patients.  In the accumulating facts they have recognized patterns of disordered bodily functions and structures as well as forms of mental aberration.  When such categories were sufficiently distinctive, they were termed diseases and given specific names.”

It seems that the conceptual clarity here requires no reference to naturalism or essentialism.  It only requires empiricism and a determination of sufficiently distinctive.  In my long and intensive career – the only place I have encountered these philosophical arguments was in a literature that was generally critical of psychiatry.  In the process it also requires psychiatrists to suspend the idea that empirical adequacy is not all that is required, but also all that we were taught. 

Conceptual expansionism or semantic drift has been used to criticize the DSM and psychiatry and that needs to be called out wherever it happens.  By that I mean a concept that is developed within one academic silo that is suddenly applied without precedent or a clear basis to psychiatry.  On this blog I have criticized several of these applications including epistemic and hermeneutical injustice.  Although none of the Am J Psychiatry papers used the term, I did encounter folk psychology now being applied to criticize the DSM (9) in a mailing.  That is a concept I was familiar with from Andy Clark’s work (10).  If you are not familiar with the concept a generally accepted definition would be:  “The everyday ability to predict and explain the behavior of ourselves and others by attributing mental states—such as beliefs, desires, intentions, and fears.”  In other words – you see somebody doing something and come up with a theory of why they are doing it.  I have written about it on this blog as a reason why many people seem confident in their knowledge of psychiatry and psychology even though they have never been trained in either. There are several theories of how a folk psychology theory can apply, but the original debate centered on how the ascribed beliefs, desires, intentions, etc. had no neural equivalent and therefore that at some point these mental states would be replaced by more scientific terms. In other word suggesting that the DSM is folk psychology is basically saying the signs and symptoms used as descriptors have no brain equivalent and therefore it is an invalid classification. This argument is essentially the same argument that there is an explanatory gap between what most people consider consciousness to be and the neural substrates that causes it.  Consciousness is approximately represented in neural substrate and the same thing can be said for mental disorder symptoms.      

3:  The continued lack of focus on what might be useful to psychiatrists - 

When I think about a DSM that might be useful to psychiatrists or at least the kind of psychiatrists I am used to working with – there needs to be more than the usual slicing and dicing of diagnostic criteria.  Adding more work with more rating scales is also a disappointment.  A manual breaking down the current work with examples and a suggestion of the potential exhaustive data points might be. For example, pointing out that the typical phenomenology of a disorder should be adequately represented in the history of the present illness.  That obviously includes any precipitating factors irrespective of what they might be – biological or sociocultural. The next section should include a discussion of the past psychiatric and medical histories as well as comorbid conditions.  Psychiatrists should be expected to know relevant medical diagnoses, how medical comorbidity affects psychiatric treatment, and medical causes of psychiatric presentations.  The usual disclaimer about medical conditions is as inadequate as a disclaimer about sociocultural aspects of care.  The new DSM should not be a mere collection of psychosocial determinants completely devoid of medicine.

A more formal formulation section should be there.  In the DSM-5 for example it is referred to as a “concise summery of the social, psychological, and biological factors that may have contributed to developing a given mental disorder.”  (p. 19).  There are multiple ways to write a formulation (behavioral, psychodynamic, neuropsychiatric, and others) and they should all be discussed in the DSM.

4:  A theory section on the biology of psychiatric diagnoses – why they are complex and how that complexity should be approached.  There are experts in the field who can comment on how polygenes produce quantitative diagnoses that can blend imperceptibility into the normative states.  Some of those same experts can discuss the statistical methods used to try to improve classifications and how that works clinically.  There should be a comparison with other commonly described quantitative disorders like hypertension and diabetes mellitus Type 2.  The classification system of rheumatology could be discussed as a direct comparison to the DSM.

I have written about the problem with the term transdiagnostic. I do not think it adds any specificity to interventions.  In psychiatry what is considered a transdiagnostic symptom can also conceal a potential primary problem. One of the most common scenarios I encountered in practice was longstanding insomnia prior to the onset of depression. In the transdiagnostic scenario, insomnia could be considered just that or a symptom of another disorder rather than a primary sleep disorder. All these issues including categorical versus dimensional diagnoses should be covered in this theory section written by our experts.  There are plenty of reasons not to blindly accept the transdiagnostic jargon as being that relevant.    

Psychometrics can be discussed in the theory section.  We have all heard and read about reliability of diagnoses for decades and a lack of validity. Reliability statistics are available for a range of DSM categories and that could be included as a single graphic with a brief discussion.  The discussion of validity needs to be more extensive and nuanced rather than just dismissed.  Study groups from DSM-5 were working on 11 validity indicators.  It is time to see them on graphics like what can be constructed for reliability. The data should be included where it exists.

5:  A genetics section:  Genetics and the associated molecular biology is the future of medicine and psychiatry. A summary of that data should be available in the DSM as well as the clear importance of this information.  At the biological level, the discussion should be clearly focused on changes in brain systems associated with disorders and the problem of many genes affecting these systems.   

6:  Definition/Threshold of a disorder:

There is always criticism about the dysfunction threshold for making a diagnostic assessment.  There is never much discussion about why it is necessary or why there are consensus diagnoses.  Even a superficial look at other specialties that treat polygenic heterogeneous entities invites comparison.  Rheumatology is a case in point:   

“Rheumatologists face unique challenges in discriminating between rheumatologic and non-rheumatologic disorders with similar manifestations, and in discriminating among rheumatologic disorders with shared features.  The majority of rheumatic diseases are multisystem disorders with poorly understood etiology; they tend to be heterogeneous in their presentation, course, and outcome, and do not have a single clinical, laboratory, pathological, or radiological feature that could serve as a “gold standard” in support of diagnosis and/or classification.”

A recent review of polymyalgia rheumatica (PMR) in the NEJM (11) looked at diagnostic algorithms for both acute PMR and treatment.  The introduction involved the statement:  “The diagnosis of polymyalgia rheumatica is made on the basis of clinical grounds by combining characteristic signs and symptoms with laboratory findings and ruling out common mimickers such as late-onset gout and pseudogout and others.”  (p. 1099).  I counted 23 conditions in the differential diagnosis.  One of the criteria for the diagnosis is “functional impairment”.  The implication is that it is due to morning stiffness or possible pain but that is not specific.  There are limited reviews of how to establish diagnostic criteria for diseases and disorders that lack objective tests (12).  I think the degree of dysfunction is obviously relevant when assessing disorders that are based on purely subjective signs and symptoms.  It factors into routine clinical care of both known and unknown diagnoses. On this blog I have documented examples from numerous medical and surgical specialties.

That is my criticism after reading 5 current papers on the direction of the DSM.  I really do not want the next volume to look like what has been described so far. When I think about my final 1500-2500 word assessments that contain just about everything the authors of these papers discuss and much more – I do not want to see all that good work sacrificed because somebody wants to include more checklists or dimensions of questionable value. I have had people tell me years and in some cases decades later, that they found those assessments to be valuable and useful for future evaluation and treatment of that same person.  

If I had to capture three elements that the future DSM planning seems to miss it is that phenomenological assessments can easily contain as much or more data than checklists, that psychiatry is a medical specialty, and that like all medical specialties the field has boundaries. The current suggestions from these papers stretch those boundaries into activism, politics, and importing criticism from other academic silos rather than a restatement of what is relevant for psychiatric assessment and classification. 

That should be the priority…    

 

George Dawson, MD, DFAPA

 

 

 

References:

1:  Oquendo MA, Abi-Dargham A, Alpert JE, Benton TD, Clarke DE, Compton WM, Drexler K, Fung KP, Kas MJH, Malaspina D, O'Keefe VM, Öngür D, Wainberg ML, Yonkers KA, Yousif L, Gogtay N. Initial Strategy for the Future of DSM. Am J Psychiatry. 2026 Jan 28:appiajp20250878. doi: 10.1176/appi.ajp.20250878. Epub ahead of print. PMID: 41593833

2:   Cuthbert B, Ajilore O, Alpert JE, Clarke DE, Compton WM, Drexler K, Fung KP, Gogtay N, Kas MJH, Kumar A, Malaspina D, O'Keefe VM, Öngür D, Tamminga C, Wainberg ML, Yonkers KA, Yousif L, Abi-Dargham A, Oquendo MA. The Future of DSM: Role of Candidate Biomarkers and Biological Factors. Am J Psychiatry. 2026 Jan 28:appiajp20250877. doi: 10.1176/appi.ajp.20250877. Epub ahead of print. PMID: 41593830.

3:  Öngür D, Abi-Dargham A, Clarke DE, Compton WM, Cuthbert B, Fung KP, Gogtay N, Kas MJH, Kumar A, Malaspina D, O'Keefe VM, Oquendo MA, Wainberg ML, Yonkers KA, Yousif L, Alpert JE. The Future of DSM: A Report From the Structure and Dimensions Subcommittee. Am J Psychiatry. 2026 Jan 28:appiajp20250876. doi: 10.1176/appi.ajp.20250876. Epub ahead of print. PMID: 41593835.

4:  Drexler K, Alpert JE, Benton TD, Fung KP, Gogtay N, Malaspina D, O'Keefe VM, Oquendo MA, Wainberg ML, Yonkers KA, Yousif L, Clarke DE. The Future of DSM: Are Functioning and Quality of Life Essential Elements of a Complete Psychiatric Diagnosis? Am J Psychiatry. 2026 Jan 28:appiajp20250874. doi: 10.1176/appi.ajp.20250874. Epub ahead of print. PMID: 41593851.

5:  Wainberg ML, Alpert JE, Benton TD, Clarke DE, Drexler K, Fung KP, Gogtay N, Malaspina D, O'Keefe VM, Oquendo MA, Yonkers KA, Yousif L. The Future of DSM: A Strategic Vision for Incorporating Socioeconomic, Cultural, and Environmental Determinants and Intersectionality. Am J Psychiatry. 2026 Jan 28:appiajp20250875. doi: 10.1176/appi.ajp.20250875. Epub ahead of print. PMID: 41593836.

6: American Medico-Psychological Association. Statistical Manual for the Use of Institutions for the Insane.  1918:  https://dn790008.ca.archive.org/0/items/statisticalmanu00assogoog/statisticalmanu00assogoog.pdf

7:  Sydenham, Thomas, 1624-1689; Greenhill, William Alexander, 1814-1894; Latham, R. G. (Robert Gordon), 1812-1888.  The works of Thomas Sydenham, M.D.  Volume 1, London. Sydenham Society.  1848-1850. P. 14  https://archive.org/details/worksofthomassyd01sydeiala/page/lv/mode/1up?q=abeyance

Translation of Medical Observations by Thomas Sydenham, London, 1669. The Preface.  Original was in Latin.

8:  DeGowin EL, DeGowin RL.  Bedside Diagnostic Examination, 3^rd ed.  New York.  Macmillan Publishing Company, Inc.  1976. P. 1.

9:  Aftab A. The Future DSM: Bold redesign, lingering blind spots.  Psychiatric Times. March 2026: 12-16.

10:  Clark A.  Microcognition: Philosophy, cognitive science, and parallel distributed processing.  Cambridge, MA.  The MIT press. 1989.   

11:  Dejaco C, Matteson EL. Polymyalgia Rheumatica. N Engl J Med. 2026 Mar 12;394(11):1097-1109. doi: 10.1056/NEJMcp2506817. PMID: 41812194.

12:  White SJ, Barker TH, Merlin T, Holland G, Sanders S, O'Mahony A, Pathirana T, Theiss R, Pollock D, Reid N, Munn Z. Methods for developing diagnostic criteria for conditions without objective tests, biomarkers, or reference standards: a scoping review. J Clin Epidemiol. 2026 Feb;190:112052. doi: 10.1016/j.jclinepi.2025.112052. Epub 2025 Nov 18. PMID: 41265667.

Troll Free Zone is Needed

 

Like many psychiatrists who watched Twitter implode under current management – I decided to try more time on LinkedIN.  I can recall a few years ago hearing that it was supposed to be a more “professional” site.  I tried the paid version to see if that might be true.  After giving it an adequate trial – I can say unequivocally it is not.  There are the usual social media maladies and more. 

For psychiatrists looking for collegial discussion that basically involves being trolled. The trolling comes in various forms, but it typically involves some absurd remarks about psychiatric practice or psychiatrists.  The usual absurdities still apply (see graphic).  There are people who will be repeating them until the end of time.  That strategy works for some politicians.  But there are a couple of variations.  I recently saw the claim that because psychiatrists only prescribe medication they never cure anyone and that it takes a psychotherapist to cure people.  One of the premises of that post was that psychiatrists get the first chance to treat people and that makes it even worse because they will not see a therapist and get cured.

That scenario is both statistically and clinically improbable.  There will never be enough psychiatrists to see everyone who needs to be seen. And psychiatrists are generally tertiary providers of all types of treatment.  As I have written about on this blog in several places – the average person I saw in practice had already seen 2-3 therapists and 1-2 non-psychiatrist medication providers before they saw me.  Prior care had often occurred over a period of many years or decades before they got in to see me.  Psychiatrists are not pulling people in off the street.  Despite the fact we are tertiary care providers – our schedules are generally full of all those people who have seen somebody else and not found that treatment satisfactory. 

Some might say that I am speaking about just a biased group of patients and have left out the group that may have improved with other treatments.  That is called selection bias and it applies in a couple of ways here.  First, all the treatment failures of other providers is a select group.  I don’t know how many improved and did not need to see psychiatrists. On the other hand – the people who did not improve are the people I want to see.  The reason I went into psychiatry was to see people with the most severe forms of mental illness.  Second, the people who are saying they are the only people who can cure mental illness with psychotherapy are only seeing the people who respond to their specific psychotherapy and most importantly who keep showing up.  Drops outs don’t count as cures.

There is also the discussion of cure.  The idea of cure depends a lot more on the nature of the illness than the treatment provider and the modality they are using.  Doing couples therapy about frequent arguments and decreasing the frequency of arguments is not the same as diagnosing dementia or depression due to hypothyroidism and treating that successfully with thyroid hormone.  In general, the treatment of severe mental illness is more complicated than that and there are mutually agreed upon goals for treatment. People return to psychiatrists for ongoing treatment because those goals are being met.    

The attitude also presents a false dichotomy of medical treatment versus therapy.   I don’t know of many psychiatrists who you can see and the conversation is like seeing your internist or family physician.  Whether they make it explicit or not – psychiatrists are trained in psychotherapy, they know how to talk with people in a psychotherapeutic manner, and they can often accomplish psychotherapy interventions in a short period of time.  I have seen people in weekly, biweekly, and monthly sessions for psychotherapeutic interventions in addition to medical treatment.  It is also the nature of psychiatric practice that long term patients will be seen in crises that occur to most of us over the course of our lifespan and that will need to be discussed.  The skillset necessary to do that requires training and exposure to the relevant resources.  As an example, I coteach a 2-hour seminar each week on psychodynamic psychotherapy and case formulation for psychiatric residents.  My colleagues in that seminar are all skilled psychodynamic and psychoanalytical psychiatrists and clinicians.  This week I am presenting on the psychodynamics of prescribing – a much more detailed discussion than the headlines or trolling remarks about psychiatric medications.     

If none of that sounds like the psychiatric practice, you read about on social media – it is not.   I have rarely seen an adequate description of how real psychiatrists practice psychiatry in social media.  It is usually a fleeting collegial discussion among experts.

Beyond the overt trolls there is also subtext.  How many times have you seen the same criticism of the DSM?  Repeatedly - even though it is a marginally significant document.  By that I mean – it is indexed to ICD codes that are the only relevant codes for diagnostic and billing purposes. The only advantage is that the DSM does elaborate more on criteria for codes, but it is very doubtful that the people using the codes are looking them up in a DSM.  Most of the diagnoses are not used.  Most of the physicians using the codes don’t own a DSM or even refer to it.  If I had to speculate, I would say that trainees in mental health fields probably purchase it as an obligatory item thinking they will learn about psychopathology.  But it is not a book about psychopathology.  It is basically a crude attempt to classify patterns of mental illness observed over the centuries of mental illnesses and refine those patterns. 

That brings up another common criticism of the DSM that can rise to troll levels. And that is - the DSM is deficient philosophically or as a diagnostic or classification system.  More pointedly psychiatry is deficient because they make, use, endorse, and sell the DSM.  The obvious problem is that psychiatry is much more than the DSM.  In all my years in acute care settings – the biggest part of my job was not deciding what page of the DSM applied to my work. My job was making sure that nobody died. Making sure they did not have a critical illness because it is hard for anyone to diagnose it in those settings.  Making sure they did not die from suicide or kill or injure somebody else.  Making sure my medical interventions did not adversely affect their medical conditions and making sure I knew what that comorbidity was.  Making sure that those catatonic and severely depressed patients were not getting dehydrated, starved, or a pulmonary embolism.  Making sure that patient with chest pain was not really having a heart attack.  Making sure that everybody on the treatment team was on the same page and not experiencing any countertherapeutic attitudes or emotions.   It is no accident that you don’t hear about that job on social media – the people criticizing psychiatrists have no idea what we do.

The DSM and psychiatry bashing can be accompanied by self-promotion.  Many people cannot promote their ideas without coupling it to criticism of psychiatry.  There is a better system.  Let’s use all the DSM symptoms and count them and rearrange them in different ways and say we have a superior system that will allow us to have superior models of mental illnesses. It reminds me of the debates of clinical versus actuarial judgment from 40-60 years ago (1).  In that reference, actuarial methods specifically the Minnesota Multiphasic Inventory (MMPI) were considered superior to clinical judgment.  But over that same period – that test was adopted to predict DSM diagnoses, was noted to be invalid for sociocultural subgroups and had to be restandardized, went from being a general psychopathology screen for law enforcement and professional schools to being used much less, and is used far less clinically. 

In the 1980s, I was interested in quantitative EEG (QEEG) research.  There were manufacturers that marketed machines with proprietary algorithms that they claimed were correlated with psychiatric diagnoses.  The analysis involved statistical probability mapping of EEG frequency bands and then cluster analysis using non-Euclidean geometry. Even more than that - it required adding clinical data to the algorithm – like whether the person was drinking alcohol, using other drugs, and what medication they were taking.  The resulting reports were not only inaccurate, but they also restricted the application to very few patients.  I have no more confidence that newer systems of phenotyping with old metrics and symptoms will get better results.

The reality for every psychiatrist is that they are face-to-face with a person that needs some degree of help.  Depending on the setting that person will recognize it to varying degrees. It takes a lot of discussion, relationship building, and analysis.  It involves talking with and building relationships with some people that most people would actively avoid.  Those kinds of relationships are critical. It takes a lot of attention to detail at the medical, social, familial, and cultural levels. It takes pattern recognition involving experience in training and in practice to determine what is the best intervention. It is a serious job that very few people want to do.

A realistic social media setting where psychiatrists can aggregate would be a plus for exchanging information, posting research and relevant papers, and discussing relevant treatment modalities.  A setting that is free of the cartoons and slogans designed to ridicule psychiatrists written by people who have no idea of what the experience of a psychiatrist is like. So far – I have not found that site.  Like I started out saying in this essay LinkedIn is like all the rest.  There are certainly many valued colleagues and references over there, but the trolls are building.

Let me know when there is a troll free site with standards and moderation and I will be there.  Let me know if you are interested in making that site and I will give you my ideas of how it can be done.  Until then this blog is my troll-free zone.                      

 

 

George Dawson, MD, DFAPA

 

References:

1:  Dawes RM, Faust D, Meehl PE. Clinical versus actuarial judgment. Science. 1989 Mar 31;243(4899):1668-74. doi: 10.1126/science.2648573. PMID: 2648573.

2:  John ER, Karmel BZ, Corning WC, Easton P, Brown D, Ahn H, John M, Harmony T, Prichep L, Toro A, Gerson I, Bartlett F, Thatcher F, Kaye H, Valdes P, Schwartz E. Neurometrics. Science. 1977 Jun 24;196(4297):1393-410. doi: 10.1126/science.867036. PMID: 867036.

3:  John ER. The role of quantitative EEG topographic mapping or 'neurometrics' in the diagnosis of psychiatric and neurological disorders: the pros. Electroencephalogr Clin Neurophysiol. 1989 Jul;73(1):2-4. doi: 10.1016/0013-4694(89)90013-8. PMID: 2472947.

4:  Fisch BJ, Pedley TA. The role of quantitative topographic mapping or 'neurometrics' in the diagnosis of psychiatric and neurological disorders: the cons. Electroencephalogr Clin Neurophysiol. 1989 Jul;73(1):5-9. doi: 10.1016/0013-4694(89)90014-x. PMID: 2472951.