Community Acquired Pneumonia - and How To Avoid it

 

 

This a strategic post about pneumonia.  By strategic I mean I hope to clarify what it is and how to prevent it.  This is not about diagnosing and treating it.  Most people reading this blog either don’t need to know that or know a lot more than me about it. Instead, I hope to address three things – misinformation about it, barriers in the modern healthcare system to acute care, and how to prevent it.

My focus will be on community acquired pneumonia (CAP).  It is a term I am very familiar with dating back 40 years to med school and my medical internship. As an intern I carried around my copy of Sanford’s antimicrobial therapy and the relevant section of Phantom Notes which was basically an outline of the leading Internal Medicine text at the time.  Thirty percent of the people I admitted to the hospital had some kind of pulmonary problem.  Depending on who you read chronic obstructive pulmonary disease (COPD) is as high as the third leading cause of death worldwide.  Exacerbations of COPD were very common reasons for hospital and ICU admission. 

CAP by definition is acquired in the community and not in a hospital setting.  It can be cause by a range of microorganisms and host factors.  It can also develop in people with no known risk factors. Conventional wisdom used to be that the lung was sterile territory but now we know that it contains a low biomass microbiome consisting of bacterial, viral, and fungal elements that are there via microaspiration of mouth contents.  Local physiological changes can occur to change the microbiome, or pathogens can be inhaled that establish primary infections (1).   Certain lung diseases like COPD and asthma can also lead to selective proliferation of elements of the microbiome. 

The ability of the lung to repair itself after injury or infection is controversial. Some research suggested that the lung was permanently changed by infection.  One example would be the association of asthma with previous rhinovirus infection. More recent work suggests there is room for optimism if the regenerative capacity of the lung can be activated (2).  

My motivation for this post was a clinical trial I read in the New England Journal of Medicine.  It was about treating CAP in East Africa.  The research question was whether adding glucocorticoids to antibiotic treatment as usual would improve outcomes.  That study quotes the mortality of CAP as 25-30%. The study was conducted in Kenya.  2,180 study patients were randomized to standard care versus glucocorticoids.  All patients were admitted to a hospital and CAP was defined as “the presence of at least two of the following signs and symptoms for less than 14 days: cough, fever, dyspnea, hemoptysis, chest pain, or crackles on chest examination.”  Imaging was not a criterion for study entrance because it was not available in many settings.  They were started on the protocol within 48 hours of admission. Glucocorticoids were provided for free as one of five glucocorticoids in bioequivalent doses for a total of 10 days (including after discharge) in addition to standard care (6 mg of dexamethasone, 160 mg of hydrocortisone, 30 mg of methylprednisolone, 50 mg of prednisolone, or 50 mg of prednisone).  Standard care was antibiotic therapy per World Health Organization (WHO) guidelines (beta lactam and macrolide antibiotics). Exclusion criteria are available in the paper.

30-day mortality was the primary endpoint in an intent-to-treat analysis.  To get to the treatment population a total of 46,224 patients were screened.  Of the 2,180 patients mortality was 530 (24.3%) at 30 days.  246 of 1089 (22.6%) were in the glucocorticoid group and 284 of 1091 (26.0%) in the glucocorticoid group.  That translates to a hazard ratio of 0.84.  The authors explain the limitations (comorbid illnesses – HIV, hypertension) and advantages (large N, lower media age) of their study.  That seems like a slight reduction in mortality for the intervention, but the authors point out that several other studies had better results up to a 50% reduction in mortality with glucocorticoids and it is a low tech readily available intervention.

In looking at the side effects of glucocorticoids   Pulmonary tuberculosis and hyperglycemia were the most common adverse effects in the glucocorticoid treated group.  Pulmonary tuberculosis and acute kidney injury were the most common adverse effects in the standard care group. 

The striking part of this study for me are the mortality figures. Although the researchers emphasized throughout their study that this was a pragmatic trial in a healthcare system with fewer resources – the estimated mortality for community acquired pneumonia in the United States is 6% at 30 days for hospitalized patients but that increases to 34% at 30 days for patients who do not initially improve initially (4).  There are treatment guidelines for primary care physicians about who can or cannot be treated on an ambulatory basis.  Age is a risk factor for increased incidence of pneumonia with the rate increasing from 248 (all adults) to 634 (ages 65 to 79) to 16,430 per 100,000 after the age of 80 (5).  Pre-existing COPD increases the risk of hospitalization 9-fold.

There are characteristic patterns of pneumonia by pathogen based on the immune response.  Bacterial infections elicit an infiltration of neutrophils into the alveolar space in a pattern of lobar or bronchopneumonia that results in an exudate of dead cells and phagocytes in the alveolar space.  Viral infections cause an interstitial pattern of inflammation with lymphocytic cell infiltrates.  Identification of the pathogen is largely done on a clinical basis due to difficulty identifying the pathogens.  Indirect methods can be used like determining acute and convalescent phase antibodies to specific viruses. Both types of infection compromise normal physiology and can lead to hypoxia and in the case of bacteria secondary infections - like meningitis.      

Recent sporadic and annual viral pandemics have created a confluence of factors at the hospital that are best avoided.  The first is the use of broad-spectrum antibiotics.  Since a significant portion of people admitted with viral pneumonia develop hospital acquired secondary bacterial infections – antibiotics are given prophylactically to prevent that complication.  Increasing exposure to increasingly potent antibiotics leads to multiple drug-resistant bacteria.  The best pathway is to avoid getting the respiratory infection in the first place. 

The absolute best way to avoid is vaccinations.  Vaccinations are currently available for influenza, COVID-19 (Sars-CoV-2), respiratory syncytial virus (RSV), and Streptococcus pneumoniae (pneumococcal pneumonia and meningitis).  They have all been tested and offer relative protection (rather than absolute) against serious illness, hospitalization, and death, especially for adults 65+ years of age.  Vaccinations have become a mixed bag of accessibility.  On the one hand you can get them from pharmacies and that is a recent development.  On the other hand we have an elected government that has appointed a well known antivaccination promoter as the head of Health and Human Services – Robert F. Kennedy, Jr.  So far there have been restrictions on the COVID vaccination to people who are 65+ or have an underlying health condition.  Since the administration is apparently making health decision based on politics and ideology many states and professional organizations are publishing their own guidelines.  As an example here is a list of respiratory virus vaccination guidelines from the American Academy of Family Practice (AAFP).  The CDC still has pneumococcal vaccination recommendations for children less than the age of 5 and adults over the age of 50.

The University of Minnesota Center for Infectious Disease Research and Policy (CIDRAP) program has a good brief on the vaccine controversy and chaos introduced by the Trump administration and the lack of scientific origins at this link.

Apart from vaccinations risk factor modification should be considered.  If you were born and raised in American culture – it is important to realize that you have been socialized to expect to get sick in the wintertime.  I did not realize that until I was getting sick 2-3 times a year on the inpatient unit where I worked.  They were viral illnesses that took 2-3 weeks to recover from.  The building was made in an era where preservation of heat was the primary design goal.  There was minimal circulation of clean air or filtration.  My suggestions to improve the air quality were ignored.  The mini-epidemics were made worse by admitting people who were ill with respiratory viruses and not using any precautions to prevent the spread of those viruses.  The new personal time off (PTO) policies that make no distinction between vacation and sick days also lead to increased exposure to sick employees who would rather work sick than use PTO days for sick time.  Since the COVID pandemic even outpatient clinics ask questions every time they see you to minimize staff exposure to respiratory viruses.

Masks work.  They must be N95 masks and fit correctly but there is no doubt that they work.  These days it is common to see political arguments and in the extreme ridicule heaped on people who use them. Large scale uncontrolled studies are often cited as evidence that they are a weak intervention.  These studies are almost all self report with no measures of actual adherence to masking.  The best studies are done in a lab that look at filtering virus sized particles and there is no doubt they are equal to that test.  

Risk factor modification is probably important.  Cardiopulmonary diseases are significant risk factors for pneumonia – so maintaining the best possible treatment for those conditions is important.  Weight control and activity level are also important.  There is at least one study showing that 65+ year olds who maintain high activity levels have better immunity than those who do not.  The specific dose of exercise for that effect is unknown currently. 

Expert advice on vaccine allergies is an important point.  I have personal history of an anaphylactic reaction to anti-rabies duck embryo vaccine in 1975.  For the next 30 years I did not get a single vaccine against influenza because it was egg based.  I had innumerable episodes of viral illness that was probably influenza and decided to see an immunologist to see if I could be desensitized to eggs so I could get the flu vaccine.  When he confirmed that I could eat eggs without a problem he said that I would probably not have any problems with the vaccine.  He was correct and I have not missed an annual dose since.

Look for respiratory infection season onset and peaks.  They are typically available through your state public health department and the CDC. When I notice it – I change my routine to shop at nonpeak hours and wear a mask in stores.  In addition to protection from the airborne transmission route hand washing is also important.  Shopping carts, door handles, and other high traffic areas are unavoidable areas for direct contact transmission. That may include being in a public bathroom any time somebody flushes a toilet.  Keep in mind that there are number of circulating common cold viruses that include 4 coronaviruses that can make you very ill.

What about barriers to care in the current healthcare non-system in the US?  There are many since businesses have taken over health care in the past 40 years.  Healthcare is rationed by both businesses and governments with only a very grudging nod to quality. The most obvious example is avoidance of the emergency department if you need it.  Anyone with previous experience knows about waits in emergency departments and delays in care.  People avoid paramedics and ambulances out of fear they will be billed for that service.  If you expect that you are ill beyond a typical cold and have additional warning signs like shortness of breath – seek help immediately.  I have given that advice to many people and it is included in the final paragraph of this AMA information sheet.   Keep in mind that pneumococcal infection can also cause meningitis which is even a more significant emergency and those symptoms can include a severe headache and neck stiffness.  Maintain a low threshold for checking these symptoms out with your primary care physician’s office during working hours and their call line after hours. But if that is not available or able to give you an answer call 911 and get a paramedic there in person to advise you and advocate for you getting timely care.  Even in our fragmented healthcare system you do not have to go it alone.  

Finally – you must realize that the infectious disease space has been infiltrated by many people who do not belong there.  They have mixed agendas involving politics and health and wellness profits.  In some cases, they are just promoting themselves.  This varies from a kernel of truth rhetoric (eg. “most people who get this virus do not die”) to outright lies (eg. “this vaccine has never been adequately tested”).  There are many points in between such as “He died of pneumonia not COVID”.  In outrageous cases they have attacked and threatened public health officials.  It is important to recognize who these people are and why they must be ignored to preserve your interest and that is your personal health.             

That is my overall strategy to avoid pneumonia.  It is most important as you age into categories where your risk doubles (65+ yrs old) and increases 25-fold (80+ yrs old).  I use these strategies myself and have found them to be very effective.  And remember the overall strategy is to avoid the physical virus or bacteria if at all possible and failing that make sure your immune system is activated by a vaccination to attack it if you are infected.

 

George Dawson, MD, DFAPA

 

References:

1: Li, R., Li, J. & Zhou, X. Lung microbiome: new insights into the pathogenesis of respiratory diseases. Sig Transduct Target Ther 9, 19 (2024). https://doi.org/10.1038/s41392-023-01722-y 

2:  Ainsworth C. Lung, heal thyself. Nature. 2026 Jan 29;649:S9 – S11.

3:  Lucinde RK, Gathuri H, Mwaniki P, et al. A Pragmatic Trial of Glucocorticoids for Community-Acquired Pneumonia. N Engl J Med. 2025 Dec 4;393(22):2187-2197. doi: 10.1056/NEJMoa2507100. Epub 2025 Oct 29. PMID: 41159889; PMCID: PMC12659994.

4:  Peyrani P, Arnold FW, Bordon J, et al. Incidence and mortality of adults hospitalized with community-acquired pneumonia according to clinical course. Chest. 2020;157(1):34-41.    

5:  Jain S, Self WH, Wunderink RG, et al.; CDC EPIC Study Team. Community-acquired pneumonia requiring hospitalization among U.S. adults. N Engl J Med. 2015;373(5):415-427.

Graphic:

Pages from my trusty copy of Phantom Notes that I used on wards as a medical student.  I went back to check to see if community acquired pneumonia was a thing back then and it was not.  If you can read it they do discuss where it was acquired under Classification (D3).   According to PubMed that term was used just twice in 1981 - but became progressively more popular in the 1990s.

Note also that we have an expanded list of viral pathogens compared with 1981.

Phantom Notes Medicine 79-80 edition copyright Joe D. Glickman, Jr, MD All Rights Reserved.  

A Shocking Anecdote about Pneumococcus:

When I was an intern on neurology (1983) I was called down to the emergency department to assess a 70 year old woman for "agitation".   That was all they could tell me aside from the fact that her labs and exam were normal.  She was unresponsive, groaning softly and rolling from side to side on the bed.  I proceeded with my examination and found that she had a stiff neck and pus draining out of her left ear.  I called my two senior neurology residents and they came sprinting to the ED.  A quick gram stain of the pus showed gram positive cocci and we gave her 1 gram of IV chloramphenicol, did a lumbar puncture and transferred her to the Neurology ICU.  She subsequently developed ARDS and required transfer to the medical ICU for ventilatory support.  She was discharged a month later and was completely deaf as a result of pneumococcal meningitis.

 

Grandparents....

 

I was driving through my favorite coffee shop the other day.  The barista told me that I owed her a little over $10 so I gave her a ten and several ones.  I told her to “keep the change”.  She looked nervous as she collected the change from the cash register and put it in the tip jar.  She said: “Do you want your ones back?”  Of course I did not, but I knew what was going on.  It was the same thing that happened to me 60 years ago.

I was 14 years old and told that I could help my grandfather for the first time on a furniture moving job.  He had a hauling business and moved just about anything using a 1933 Diamond-T stake truck.  The job was only 3 blocks away, so I walked over there, but about ½ block away I froze.  I was nervous and even though I knew everyone at that job – I turned around until I heard: “Chorge!”  That was the way my grandfather pronounced my name.  He saw me turn and from a half block away encouraged me to keep moving in his direction.  Everything went well on the job, and it was the first time I got paid for doing real adult work.

Just a few nights ago I dreamed I was sleeping in the snow behind my grandparents’ home.  The ground was covered in about 4 inches of snow.  The exposed areas looked more like weeds than grass. As I slowly got off the ground – I realized I was on the property line of my grandparent’s neighbor Oliver.  Oliver was a machinist.  I remember being in his garage and seeing all kinds of machinist tools and lathes.  It was dark except for a single hanging light bulb.  There was a strong odor of oil in the air.  He did machinist work in his garage for a while after he retired – but then he and my grandfather just sat on a bench next to his garage and talked.  They were both old Scandinavians, but I never saw them drink coffee in the afternoon. I knew my grandfather always had plenty on board by that time of the day.

The years went by and I did more work for my grandfather.  At one time or another I was joined by four different uncles (Bill, Jim, Carl, Tom), my father (George, Sr), and another man (Elwood) who was there most of the time.  My grandmother kept the books.  Things seemed to be going well, but I know my grandparents were concerned about me at times.  When I was a freshman in college, I got very ill with appendicitis and sepsis.  After recovering from that illness – I did not feel like doing much.  I was laying in bed one morning and woke up to see my grandfather standing there.  His spine was bent two different directions from decades of heavy lifting. When he walked, he led with his hips, and his shoulders were never square over his lower body.  I could tell from that outline it was him even before I saw his face.

He started an awkward dialogue intended to motivate me.  He wanted to make sure that I was not taking his criticism of colleges and professors too seriously.  He wanted to make sure I kept going to college.  I thought my grandmother might have put him up to it but it was not her advice.  She would tell me to avoid roadhouses – usually when I stopped in to say hello on my way to a roadhouse.  The only reason he was there was that he heard I was not doing well – and he thought he could motivate me like that first day working with him.

The years went by quickly after that.  I completed college and was in the Peace Corps half the world away when I got the letter from my grandmother.  “Your grandfather died – he always loved you and worried about you.” – it read.  That was back in the 1970s and he was about the same age that I am right now.  My grandmother lived another 20 years, and I saw her whenever I could.  Work and geography create quite a barrier.  When my grandmother died, my aunt gave me a bundle of all the letters that I sent her from East Africa.  I have not been able to reread them.  

I woke up earlier this week with the thought: “I wish I could go back to the 1970s and see my grandparents to let them know I did all right.”  The only thing my grandfather knew was that he had a neurotic grandson who was hesitant, cautious, and reluctant in life.  My grandfather seemed like a nervous guy, but when he was college age, he was hanging off the side of an oredock on a swing – bolting together the top deck with an air powered wrench while he sat 90 feet above Lake Superior.  He told me a few horror stories from the industrial accidents that occurred on that site while I was on the mend in the hospital.  He told me a lot of stories about his friends that were mostly about fishing but also what we used to call power stories. Power stories in the North Country were tales of supernatural ability.  It was implicit that there could be some embellishment.  One of his favorites was telling me about a man who ran a hauling business with a team of dray horses.  From handling reins all day long he developed extremely callused hands to the point that anyone who shook hands with him would “just shiver.”

My grandfather had tattoos.  They were probably from sometime in the late 1920s or 1930s.  If you looked close enough you could tell they were women wearing grass skirts and dancing.  My grandfather never talked about the tattoos, and it was before the time they were popular again. I don’t have any and he never spoke to me about the subject and whether he recommended them or regretted his decision.

In my grandfather’s dining room, there was a picture of him and his younger brother when they were children about 5 and 7 years old.  The picture looked nothing like him as an adult.  He was bald and both children in the picture had abundant long wavy hair.  I have a post about a shocking event that occurred on the paternal side of the family.   On the maternal side, the shocking event was that my grandfather’s brother left town one day and was never seen or heard from again.  Nobody has any idea about what happened to him.  Like the event of my paternal uncle being killed as a child, the disappearance of my maternal grandfather’s brother was never mentioned over the 20 years that I knew him.

My grandparents talked about the Great Depression and how it affected them.  They were frugal even though my grandfather ran a business and had a payroll.  They had a woodburning stove in the kitchen and used that to heat bath water.  They used a large, galvanized steel tub to bathe in and did not replace it with a modern bath tub until late in life.    

When I saw that young barista, anxious about my tip – I imagined for a minute that I was a grandparent.  When I say imagined - I mean in retrospect.  In real time, I knew I had to reassure her that things were OK and that there were no problems.  I could see she was relieved and happy. And for a minute – I realized that I was living both my life and my grandfather’s - like on that day back in 1960 when he kept me on track.  I also realized why it was important to help young people through generosity – even if it helped for only a few minutes. 

I did a lot of research about grandparents for this post – but it turns out that the research says almost exactly what you expect it to say.   A good relationship with your grandparents especially on an emotional level is good for children, adolescents, and even adult grandchildren.  The relationship needs to be balanced.  Social media contains all kinds of stories about grandparents not having good experiences.  Complaining seems to be what social media is designed for.  There is also the standing joke about why grandparents have a more fun relationship with their grandchildren than the parents do - they do not have to set as many limits as the parents and can overindulge them.  My grandparents were generous with their time, energy, and finances when our family needed support.  They had a great sense of humor.  They taught us how to be kind and resilient.  There is some literature on how the grandparents benefit as well.  But I don’t think that they considered anything beyond doing the right thing for their family and the fact that they really liked us. 

And getting back to my coffee shop drive through – my grandparents taught me the importance of supporting younger struggling generations – whether you are their real grandparent or not.   

 

George Dawson, MD, DFAPA

 

Note on the Grandfather Transference:  Transference is an important concept and feature of psychiatric treatment.  Physicians and psychiatrists in particular notice that the way patients interact with them varies over the course of their career.  Early on it is common to hear statements like:  "You look too young to be a doctor."  That might reflect concerns about adequacy of training or experience that could affect the treatment relationship.  As mid-career years approach there are fewer comments about age, but potential concerns about being more career and revenue focused to the exclusion of individualized care and knowing the relevant details about the patient. In the years approaching retirement, I think people realize that you have seen a thing or two and are probably competent, caring, and looking out for their best interest. People seem less likely to challenge formulations or treatment recommendations.  They are less likely to become confrontational.  I have termed this last phase as a period of grandfather (or grandmother) transference.  I don't think it has been studied but it seems like it does enhance the therapeutic relationship. 

 Additional Note on Furniture Moving:  Over the years many people found out that I was a professional furniture mover and requested help with moves.  Requesting help and taking advice are two different things.  Invariably something was done against my advice that resulted in damaged furniture.  My grandfather and the men working for him were proud of the fact that there was never an insurance claim against them for damaged furniture.  If you think about it furniture is fragile - mirrors, finishes, pianos, TVs, dishes and other breakable items, spindly legs, and moved in the same truck with heavy appliances.  Just a slight shift in the load can result in massive damage. 

So if a professional furniture mover tells you that covering your very expensive piano with a bed sheet and baling twine is not a good idea - believe them.

That seems like another parallel to psychiatry.  It seems like a job so easy anybody could do it.  It is just common sense - right?

Supplementary:  Could not work it in above but many years ago I heard a very positive review of a book about Grandmothers on public radio.  I have never been able to locate that book.  If anyone has that reference please let me know.

 

Graphics Credit:  Peachyeung316, CC BY-SA 4.0 <https://creativecommons.org/licenses/by-sa/4.0>, via Wikimedia Commons.

Combinatorics Summary....

 

 

I realized that I have a combinatorics thread running through my blog across several subjects.  I have been interested in combinatorics since I sent an email to Robert Spitzer on the various combinations of diagnostic criteria.  His only comment was “Interesting”.  Since then, I have commented on a post that purported to discredit psychiatric diagnoses based on combination of diagnostic criteria (too many), a study of the real combinations of major depression diagnoses, and character and word phrase combinations for encryption and password protection.  I went as far as getting dice and using them to construct passphrases of varying length using the Electronic Frontier Foundation (EFF) word list for that purpose.

If you have no experience with combinations or it has been a long time since your college statistics course – dice are a good place to start.  Each die has 6 sides with corresponding numbers. The total combinations possible are 6ⁿ, where n = the number of dice rolled at once.  The EFF world list is 6,667 word long and that happens to be 6^5.  So, to generate passphrases – 5 dice are rolled and the corresponding number is looked up on the word list and recorded.  The process is repeated until the desired phrase length is generated.  The only downside to this method is that some sites still insist on additional numbers and special characters.  They can still be inserted in the passphrase, but other systems like hexadecimal may be more convenient.  The advantage to passphrases is that they are theoretically easier to memorize and type without error.  That breaks down with very long phrases.

In biology and medicine, combinatorics can be applied at several levels. Some have more meaning than others.  On this blog, I responded to a paper suggesting that the possible combinations of diagnostic criteria meant that psychiatric diagnoses were meaningless and unscientific.  The lesson from this post is to have an idea of what you are counting and what it means. The total combinations of verbal criteria depend a lot on the phrasing and the total number of criteria whether large or small is not necessarily disqualifying as illustrated in this post.  The combinatorial upper limit can be unrealistically large based on how it is defined and just running the numbers does not mean that all possible combinations will be found.  There also seems to be some magical thinking involved – just because you count something does not say anything about what that means.  It is quite literally an exercise in the map is not the territory. 

I looked at a second paper where the authors looked at a lower number of combinations based on the DSM diagnostic criteria for major depression.  In that case the total number of diagnoses was much lower at 227 combinations.  The authors of that second paper did standardized interviews on 3,800 people and of the 1,566 with major depression – just 10 of those combinations accounted for 50% of the cases.  About ¼ of the possible combinations (57/227) did not occur in any group.  This paper is a stark reminder that just counting things in biology or medicine doesn’t necessarily mean anything.

That brings me to the concept of how we make sense out of the most valid combinatorial explosions in medicine. For me validity is baked into the biology and not a verbal description of things.  The backing for that comes from biological taxonomy and the fact that molecular biology and genomics is solving problems that could not be solved by the verbal description of direct observations in the Linnean tradition.  To that end I am reproducing a table below that is all about the polygenic risk for bipolar disorder. 

Note that in this table the authors are estimating the total possible combinations of 803 polygenes. The theoretical number of possible combinations can be calculated using the formula n! / r!((nr)!,where n represents the number of genetic variants analyzed in a study, and r represents the number of genetic variants per combination. In the case of  SNP genotypes,3^r.the formula is n! / r!(n-r)! ×3^r.  The authors point out that the lowest value for r is 2 but the upper limit is unknown.  They also show how the number of combinations can be limited experimentally.  Of the 57,911,211 combinations found only in patients and not controls they could all be random but there were a significant number of SNPs associated with different groupings in bipolar disorder.    

Using the equations from above in a more readable graphic form:

 

 

Substitution yields the following:

- from the top equation, for 100 variants the theoretical 10-variant combinations would be 1.73 x 10¹³

- from the bottom equation, for 500,000 SNPs analyzed there would be 2.3 × 10¹² two-variant combinations and 3.4 × 10¹⁸ three variant combinations.

The application of practical measure includes scanning SNPs for varying combination lengths in the population of interest relative to controls. At lower numbers those combinations can be taken out scanning for longer combinations. A further simplification is to scan only for combinations found in patient populations.  An example of that study is included in the tables below for 803 SNPs in 607 bipolar disorder patients and  1,354 controls. 

Cluster and subgroup analysis is required in very heterogeneous conditions to analyze clusters containing a specific SNP, the distribution of SNP genotypes relative to controls, and cluster selection that contains an SNP for a specific biological function.  Using this kind of analysis 73/609 bipolar disorder patients had these clusters compared to none in the control population. 

While the SNP and variant analysis in 2017 is a good example of combinatoric applications – it did not address the problem of missing heritability.  Missing heritability is the difference between what is observed in familial heritability studies and what is predicted with genetic analysis.  Looking at the predictions from SNP based analysis only a low percentage of familial inheritance was predicted.  That improved with more sensitive analytical techniques that considered additional genetic mechanisms.  The additional mechanisms included SNV (single nucleotide variation), insertions or deletions (indels), SVs (structural variations), CNV (copy number variations), and STR (short tandem repeat (3-5).  Applications that identify all these variations are much more likely to predict the heritability of the pedigree than earlier techniques.  I hope to revisit some of these genetic innovations in an upcoming post about the DSM-6 proposals.

 

George Dawson, MD, DFAPA 

 

References:

1:  Mellerup E, Møller GL. Combinations of Genetic Variants Occurring Exclusively in Patients. Comput Struct Biotechnol J. 2017 Mar 10;15:286-289. doi: 10.1016/j.csbj.2017.03.001. PMID: 28377798; PMCID: PMC5367802.

2:  Koefoed P, Andreassen OA, Bennike B, Dam H, Djurovic S, Hansen T, Jorgensen MB, Kessing LV, Melle I, Møller GL, Mors O, Werge T, Mellerup E. Combinations of SNPs related to signal transduction in bipolar disorder. PLoS One. 2011;6(8):e23812. doi: 10.1371/journal.pone.0023812. Epub 2011 Aug 29. PMID: 21897858; PMCID: PMC3163586.

3:  Behera S, Catreux S, Rossi M, Truong S, Huang Z, Ruehle M, Visvanath A, Parnaby G, Roddey C, Onuchic V, Finocchio A, Cameron DL, English A, Mehtalia S, Han J, Mehio R, Sedlazeck FJ. Comprehensive genome analysis and variant detection at scale using DRAGEN. Nat Biotechnol. 2025 Jul;43(7):1177-1191. doi: 10.1038/s41587-024-02382-1. Epub 2024 Oct 25. PMID: 39455800; PMCID: PMC12022141.

4:  Wainschtein P, Zhang Y, Schwartzentruber J, Kassam I, Sidorenko J, Fiziev PP, Wang H, McRae J, Border R, Zaitlen N, Sankararaman S, Goddard ME, Zeng J, Visscher PM, Farh KK, Yengo L. Estimation and mapping of the missing heritability of human phenotypes. Nature. 2026 Jan;649(8099):1219-1227. doi: 10.1038/s41586-025-09720-6. Epub 2025 Nov 12. PMID: 41225014; PMCID: PMC12851931.

5:  Grotzinger AD, Werme J, Peyrot WJ, Frei O, de Leeuw C, Bicks LK, Guo Q, Margolis MP, Coombes BJ, Batzler A, Pazdernik V, Biernacka JM, Andreassen OA, Anttila V, Børglum AD, Breen G, Cai N, Demontis D, Edenberg HJ, Faraone SV, Franke B, Gandal MJ, Gelernter J, Hatoum AS, Hettema JM, Johnson EC, Jonas KG, Knowles JA, Koenen KC, Maihofer AX, Mallard TT, Mattheisen M, Mitchell KS, Neale BM, Nievergelt CM, Nurnberger JI, O'Connell KS, Peterson RE, Robinson EB, Sanchez-Roige SS, Santangelo SL, Scharf JM, Stefansson H, Stefansson K, Stein MB, Strom NI, Thornton LM, Tucker-Drob EM, Verhulst B, Waldman ID, Walters GB, Wray NR, Yu D; Anxiety Disorders Working Group of the Psychiatric Genomics Consortium; Attention-Deficit/Hyperactivity Disorder (ADHD) Working Group of the Psychiatric Genomics Consortium; Autism Spectrum Disorders Working Group of the Psychiatric Genomics Consortium; Bipolar Disorder Working Group of the Psychiatric Genomics Consortium; Eating Disorders Working Group of the Psychiatric Genomics Consortium; Major Depressive Disorder Working Group of the Psychiatric Genomics Consortium; Nicotine Dependence GenOmics (iNDiGO) Consortium; Obsessive-Compulsive Disorder and Tourette Syndrome Working Group of the Psychiatric Genomics Consortium; Post-Traumatic Stress Disorder Working Group of the Psychiatric Genomics Consortium; Schizophrenia Working Group of the Psychiatric Genomics Consortium; Substance Use Disorders Working Group of the Psychiatric Genomics Consortium; Lee PH, Kendler KS, Smoller JW. Mapping the genetic landscape across 14 psychiatric disorders. Nature. 2026 Jan;649(8096):406-415. doi: 10.1038/s41586-025-09820-3. Epub 2025 Dec 10. PMID: 41372416; PMCID: PMC12779569.

 

Graphics Credit:

Table 1 is reused from open access reference 1 above per  CC BY license (http://creativecommons.org/licenses/by/4.0/). 

 

The 12 Word Note...

 

I had one of my typical work-related nightmares last night.  Three years into retirement and I am still anxious about work. I think it is an interesting exercise in how human consciousness works and how it led to the above graphic so here goes.

As usual it starts out in a medical center, in this case what appears to me a medical unit in a large hospital.  I have never been in this specific setting before, but it has a similar arrangement to many units where I have worked.  There is a walled off central square nurses’ station surrounded by a ten-foot-wide walking area leading to the patient rooms.  Judging by the equipment and floor coverings it is from about 1980 to 2000.  I am seated in the nurses’ station and looking at a chart.  I have been consulted to see someone on that floor and review the chart.  There are no computers, everything is written on paper, and the chart clips it all together at the top.  As a result, the notes must be flipped on the short edge to maintain the same reading orientation. The setting is drab but in color.  There is a lot of activity but nothing overly hectic that would indicate an emergency.

I look at a note from the pervious consultant.  It is in outline form with headings only and spaces to be filled in later.  The chart notes are all lined in a typical tablet format.  There is about a page and a half and then there is about a ½ page narrative written like a paragraph by a different staff person.  I stare at the space between the two notes.  That space is about 1 ½ pages in length.  I start thinking about how I can squeeze my typically micrographic consult note into 1 ½ pages. 

I start to get anxious.  I realize I am just staring at the chart and not doing anything.  I look at the doorway to the room containing the patient I am supposed to see.  I feel like I am frozen and I will never get out of there if I don’t get in there and figure out how to record my note.  I start to panic.  I wake up anxious with an elevated heart rate.

After laying in bed for a while and thinking about the dream, I associate to the Milwaukee VA and my first Internal Medicine rotation. The charts in the dream seem like old VA charts.  I remember writing in those charts – very long histories and physicals and consult notes and progress notes that were considerably shorter.  I remembered a neurosurgery rotation where a handful of us covered an entire floor of very ill patients, a neurosurgery ICU, and all the emergency room and general consults from two large hospitals.  The only possible way we could do that was by completing all the rounding and documentation in 2-3 hours because we were also expected to be in the OR for many hours per day.  The typical rounding note was less than 20 words – “Afebrile; VSS; (brief description of neuro status and surgical wound).” 

That led me to think about the shortest Internal Medicine note by a resident.  Internal Medicine residents were some of the smartest and most industrious people I have ever met.  But in the 1980s they (and me their intern) were seriously abused.  A typical call schedule was on call every third night.  On a call night 10 admissions all night long of very ill patients while cross covering the entire hospital was typical. That usually meant no sleep – but you were expected to do the usual work until 5PM on your sleep deprived day until you could go home and sleep. This resulted in some embarrassing moments like falling asleep while writing notes or in one case – not putting the note in the chart until my resident reminded me, I was still carrying it around on my clipboard.     

One day in that VA hospital a friend of mine said “I want show you something”.  He showed me a note written by his resident that was written in 48-point font.  The only reason I know that is because of the experiment at the top of this page (that is my standard 12 point at the top and 48 point at the bottom).  It was the largest cursive I had ever seen and there were only 3 or 4 words per line.  We both laughed about it.  My friend told me all his notes were like that, and they were signed off by attendings. He was basically writing down 12-15 words per page to my 300-400.  We did not take the time to analyze the content of the notes – we were just amazed by the form. 

This morning, I thought about whether it was possible to write all your notes like that – even in 1982.  It certainly would not pass muster in the modern era of excessive and often useless documentation required by governments and insurance companies. He would get audited for “bullet points” and would never get reimbursed.  In the modern world every note needs to contain bullet points of specific documentation whether it is relevant to the medical care or not.   I was in a mandatory seminar in the late 1990s when an FBI agent claimed that any physician not completing the bullet points could be charged with mail fraud and sentenced to federal prison on a RICO violation. That was before 911 and the FBI discovered they could probably be doing better things than threatening physicians.

At times, I get the mental image of hard drives spinning in large storage arrays containing all this worthless medical documentation that will never be read again.  I used to think it was a high environmental burden until large language model AI came on the scene.  Now these AI companies are building their own power plants just so the AI can scan vast amounts of worthwhile and worthless documents to synthesize an answer that may contain some accurate data or it may be an AI hallucination/confabulation - like a medical reference that does not exist.

All those thoughts sprang from a bad dream of an old, retired guy who at times wishes he was still working.  But at other times realizes that retirement is a good idea.

 

George Dawson, MD, DFAPA

 

Supplementary:

Maybe Hospital Dreams could be a sequel to Train Dreams.  I tried to work it in, but it did not fit. 

 

References:

1.  Arvikar SL, Schaefer PW, Lemieux JE, Steere AC. Case 3-2026: A 58-Year-Old Woman with Diplopia and Fever. N Engl J Med. 2026 Jan 22;394(4):383-391. doi: 10.1056/NEJMcpc2412529. PMID: 41564400.

My test sentence above is the first line in this week’s Case records of the MGH.  One sentence is fair use. 

Dermatology Informs the Rhetoric About Psychiatry

 

I have posted in the past about the similarities between rheumatology and psychiatry.  The classification systems are the same, there is a lot of diagnostic flexibility, all of the conditions are very heterogenous, the underlying pathophysiology is not clear, and the mechanisms of action of most of the treatments used are unknown.  I thought I would do a similar comparison with Dermatology.  As an acute care psychiatrist I noticed that dermatology problems are frequently ignored by both patients and physicians or treated incorrectly with over-the-counter preparations.  There is some overlap with both psychiatric and neurological conditions, but most of the skin conditions I detected were not in that category.  I was always grateful I had specialists available who could see my patients quickly.  In some cases, the treatment was lifesaving.

Dermatology is a classic example of pattern-matching in diagnoses and if you missed it I will post my favorite case here.  It happened in medical school on an infectious disease rotation. We were asked to see a patient for spontaneous bacterial peritonitis, an infection of ascitic fluid in the abdomen.  After reviewing all the preliminaries, we came into the patient’s room with the attending.  From across the room the attending said: “What am I seeing from here that needs to be addressed?”   We all looked puzzled.  He came across the room and pointed out a large confluent pink rash on the man’s left ankle. He aspirated a small sample from the edge of the rash and sent it to his lab for further analysis. He was an expert in streptococcal infections and guessed what type of strep it would be.  He picked an antibiotic that he thought would work for both conditions.    

The prevalence and comorbidly of dermatology diseases is high.  At any given moment 25-33% of the world’s population has one of these diseases (1).  That may be as high as one in three Americans in the US (2).  Some studies have suggested the point prevalence may be much higher (up to 64% in some studies) because people are unaware of the fact that they have the diseases (like rosacea and actinic keratoses). Studies also have variable inclusion criteria for the 5 most common diseases to all possible diseases.  Variability also exists within the same category like atopic dermatitis that can range from  2.6 – 9.6% and in some cases those authors point to variable diagnostic criteria.  To illustrate some of this variability consider the following case:

66 YO man with a history of asthma and anaphylactic reactions.  No history of atopic dermatitis as a child but newly diagnosed in his 60s when it presented with intense pruritic and patchy crusty lesions that were not associated with scratching. He also had a recent 24 hr. cardiac monitor and had similar crusting lesions at the electrode sites for two weeks after they were removed. He has also been seeing a dry eye specialist for a severe dry eye problem that interferes with his work.  The dry eye specialist has diagnosed Meibomian Gland Dysfunction. He uses artificial tears 6-8 times a day, eyelid scrubs, and occasional ocular glucocorticoids for relief.  On exam he is noted to have patchy lesions on his shoulders, an erythematous rash on his right medial thigh, and an erythematous rash with skin peeling on his right palm.  Examination of the scalp shows flaky dandruff with oily inflamed patches.  He has areas of facial induration with some facial acne with redness and indurated subcutaneous patches not associated with the acne. Some of of those areas of induration are tender. 

The final dermatology diagnoses based on exam and clinical picture are:  atopic dermatitis, contact dermatitis, rosacea, seborrheic dermatitis of the scalp, and probable ocular rosacea. The recommended treatment includes a topical facial medication containing azelaic acid, metronidazole, and ivermectin, topical glucocorticoids for the seborrhea and atopic dermatitis, prescription strength (5%) ketoconazole shampoo twice a week, and CeraVe applied to all areas of the body with active rash or pruritic from atopic dermatitis. None of the medications are curative and are to be used on a maintenance basis as needed with annual follow up visits.  Dry eye follow up is separate per that specialist.  Despite 3 diagnoses, this patient has 5 distinct lesions for atopic dermatitis, 4 distinct lesions for rosacea, and 2 for seborrhea.

How does all this aid in understanding the typical social media criticisms of psychiatry?  Here are a few:

1:  Number of diagnoses:  I have looked at this issue in detail and counted the diagnoses in the DSM-5 several ways. According to the American Board of Dermatology, dermatologists are trained to recognize and treat over 3,000 diagnoses of skin disease. Does it seem reasonable that the most complex organ in the human body might have at least 281?

2:  High prevalence:  typical social media criticisms of psychiatry focus on the high prevalence of disorders and the treatment of those disorders.  Many wellness industry influencers use this as a basis for suggest that lifestyle changes and whatever products they are hawking are the real solution and the problem is excessive medical care. Some point prevalence studies suggest that dermatology conditions may be as high as 68% of the population and that there are always millions with the most common conditions like atopic dermatitis (2-10%), seborrheic dermatitis (4%), and psoriasis (2-3%).  There are also single syndromes that have very high reported prevalence in the literature like Sensitive Skin Syndrome that is reported to have a prevalence of 60-70% in women and 50-60% in men.  Self-reported skin sensitivity decreased with age and reported severity.  11% of men and 19% of women 25 years of age or less reported their skin was sensitive or very sensitive compared to 7% and 12% respectively at or greater than age 55. (20)

3:  Heterogeneity: Social media criticism and some research go to absurd lengths to show that psychiatric conditions are heterogeneous.  When that is studied in dermatology the heterogeneity is just as significant. The reality is that biology produces heterogeneous individuals and diseases and heterogeneous diseases in the same individual.   

As an illustration, consider the following simple calculation the flows from polygenes or a disorder determined by multiple genes.  A recent study of major depression (23) found 697 associations across 636 loci.  Since each locus has the 3 possible states (homozygous dominant - AA, heterozygous - Aa, and homozygous recessive - aa) a first approximation of the total number of gene combinations is 3^636 = 2.812 x 10^303.  This is an impossibly large number, but it does indicate the massive amount of information that relatively simple biological configurations can carry.  On this blog I have examined attempts to look at the combinations of diagnostic criteria and their real-life shortcomings.  The best contrast was a group who suggested that large number of diagnostic feature combinations meant that psychiatric diagnoses were “unscientific” and a group who actually examined the features in clinical practice and determined they were manageable.  The latter group showed that there were 225 possible combinations for major depression and about ¼ of them did not appear in a single patient.

The above approximation based on polygenes is problematic at a couple of levels – foremost is that not all polygenes are as likely to be associated with the disorder.  That analysis requires more advanced statistical methods (24).  But even considering modest number of contributing genes explains heterogeneity, severity differences, and treatment resistance.  I will take it a step further and suggest that anyone who does not appreciate that heterogeneity is a feature of biology and not a problem for diagnosis lacks a basic understanding of biology and medicine.  

4: Comorbidity:  A 2022 study showed that (after excluding cancer screening) 43.35% reported having had at least one dermatological condition or disease in the past 12 months with 35.38% had one skin disease, 24.32% had two skin diseases, 14.06% had three skin diseases, and 26.34% had four skin diseases or more.  Critics seem to think that comorbidity is a weakness of psychiatric diagnosis when every other specialty recognizes equivalent or greater amounts of comorbidity.

5:  Diagnostic certainty:  In the past I taught a course in diagnostic thinking to medical students.  One of my cited references was a paper comparing the diagnostic expertise of dermatologists to primary care physicians on a standard set of photos about dermatology diagnoses (13).  The evidence on evaluating clear cut cases of dermatological disease and equivocal cases the dermatologists are much better than non-specialist physicians.  The diagnostic process in dermatology also suggests that pattern-matching is probably a more significant factor than rules-based processes for experienced physicians. By rules based processes – I mean written diagnostic criteria. There is no reason to think that pattern matching does not apply in psychiatry at several levels.

Pattern matching also speaks to different phenotypes in the same individual. In the case example, this man has several different equivalents of the same underlying disease – 5 variants of atopic dermatitis and 2 for rosacea all on his body at the same time.    

6:  Underlying pathophysiology:  The standard social media caricature of psychiatry is that it is a poorly defined morass of conditions with no known specific etiologies or pathophysiology.  In fact, 67% of DSM listed diagnoses have either a known pathophysiology or a specific medical test.  Every psychiatric diagnosis has a medical differential diagnosis.  It is why psychiatrists are medical specialists. The same is true for dermatological disorders and there are many cutaneous manifestations of underlying medical conditions. In addition to medical causes of both psychiatric and dermatological conditions there are two addition important areas of overlap.

The first are conditions where there is no known clear unitary pathophysiology.  On the dermatology side there are many common and rare conditions like atopic dermatitis, seborrheic dermatitis, acne vulgaris, rosacea, psoriasis, granuloma annulare, vitiligo, lichen planus, erythema multiforme, bullous pemphigoid, and pemphigus vulgaris. Many have one or more hypotheses about the pathophysiology, and these hypotheses guide treatment attempts. The case report above is a clear example of multiple treatments contained in the same topical medication for rosacea. The major psychiatric disorders when underlying medical causes have been ruled out are in a similar situation.  Over the past 30 years there have been over 100 hypotheses about the pathophysiology of depression and recently (21) some of these hypotheses have been combined.

The second are conditions where there is overlap between psychiatry and dermatology sometimes called psychodermatology.  A study by Balieva, et al (19) examined the bidirectional relationship between skin disorders and psychiatric disorders.  It was a large registry study from Norway that selected patients based on their seeing dermatologists and being treated for common disorders with psychiatric disorders being the outcome variable.  That population was compared to a non-dermatology diagnosis groups and odds rations were calculated. The authors demonstrated that patients were 2-3 times as likely to develop depression given the dermatology diagnoses with elevated risks for anxiety, somatoform disorders, and obsessive-compulsive disorder but not eating disorders. The authors reconciled this with several previous studies with similar findings, but they broadened the number of psychiatric diagnoses.

Psychodermatology classifies the combination of psychiatric and dermatological disorders based on which disease is primary and whether the skin pathology is a manifestation of psychopathology (delusional parasitosis, trichotillomania, pathological skin picking, and psychogenic pruritis.).  In a recent study (17), the latter group had a very high risk of neuropsychiatric disorders – depression, anxiety disorders, and personality disorders.  Dermatology conditions exacerbated by stress including atopic dermatitis, psoriasis, acne vulgaris, and vulvodynia – were all associated with depressive disorders, sleep disorders, and neurodevelopmental disorders.

7:  Mild-moderate-severe designations:  Another common criticism of psychiatric diagnoses is that it seems like the following qualifier in most diagnostic criteria is arbitrary:

The disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.  

Since there are no formal diagnostic criteria for dermatology there is no threshold for diagnosis.  That is not necessarily problematic since the many intermediate phenotypes for any major psychiatric disorder may also not meet this threshold but nonetheless seem like a good idea to treat.  In dermatology practice there is a significant cosmetic component that can be purely subjective.  Many studies have mild-moderate-severe categorizations based on the judgment of clinicians.  In dermatology, the disappearance of the cutaneous manifestations often leads to the patient stopping treatment when the treatment needs to be continued.  An example is the use of emollients in atopic dermatitis and avoiding skin irritants.  

8: Medications with clearly defined mechanism of action: Glucocorticoids (prednisone, triamcinolone, betamethasone) have potent effects on inflammatory and immune responses that are not disease specific.  Biologics for dermatology conditions can be pathway specific for inflammatory pathways, but they are not technically disease specific.

I reviewed 11 monoclonal antibodies used for dermatology diseases and found that they are characterized as pathway specific but not disease specific.  In other words, they shut down specific inflammatory pathways that can be involved in more than one dermatological disease and there is overlap with other allergic, rheumatic, and inflammatory diseases as well as cancer.  

On  larger scale,  the overlap between immune medicated conditions obviously cuts across the turf of multiple specialties.  That includes several CNS diseases that produce neuropsychiatric syndromes and may soon include purely psychiatric disorders with no other identifiable causes (22).

9: Transdiagnostic considerations:  there has been and explosion of the use of the term “transdiagnostic” in psychiatry – typically as a criticism to suggest that diagnostic categories are cruder than in the rest of medicine. The term is just being extended to other commentaries.  In the case of dermatology – rash is considered one of the leading symptoms that leads to medical evaluations. Here is a list of 71 causes of a rash.  But the transdiagnostic concept does not stop there it also applies to treatments across several categories that are non-specific but effective. 

Transdiagnostic was initially considered based on the assumptions that disorders had similar etiological and maintenance factors and responded to non-specific therapies like cognitive behavioral therapy (16).  One of the associated criticisms was that categorical diagnosis was less specific due to high comorbidity.  In a systematic review of 116 studies only 3% met standardized criteria (Mansell) for a study of transdiagnostic approaches in psychiatry (16). That same study reviewed all the commonly used approaches.  The authors conclude that transdiagnostic approaches have overpromised and undelivered.  The authors present an extensive discussion of the problems some of which are evident in a typical network diagram they include in their paper.  I want to focus on just one – and that is: “transdiagnostic approaches are largely based on an epistemological error, which triggers an illusion of continuity”.  When classification systems like the DSM and ICD use simplified language – psychopathology is ignored and it collapses reality into unitary disorders.  Suddenly all depression is equivalent to a handful of criteria.  A depression checklist like the PHQ-9 suddenly becomes a phenotype for large epidemiological studies and a basis for transdiagnostic treatments.

What happened to the endophenotypes of the recent past?  If there is any variance in clinical practice it all seems to be swept into a spectrum or a continuum like electromagnetic radiation. The real patterns that physicians have diagnosed and treated with success over the years are collapsed into a number on rating scale and there are as many rating scales as you want.

The dermatology diagnoses discussed so far are clear reasons why we need to keep the patterns real. Recognizing the importance of those patterns is why there is no PHQ-9 for atopic dermatitis.  This process has often been oversimplified as prototypical diagnoses in the past – but there are no protypes when you are recognizing hundreds of different microphenotypes rather than one large oversimplified one.               

10:  Polypharmacy, cure, and discontinuation:  Deprescribing has become the latest buzzword used to criticize psychiatry as if psychiatrists have never discontinued medications in the past and do not know how to do it.  As far as I know this has not be a problem focused on dermatology, but many papers say that patients frequently stop their medications prematurely because they are worried about using them on a long-term basis.  With all complex polygenic illnesses – being followed by a physician familiar with your problem who can monitor the course of the illness and make the appropriate adjustments is the best course.  That is necessary because most of these diseases are genetically complex and not predictable. Detrimental genotypes may never be expressed or in the case presented occur in old age rather than youth.  Environmental factors are also important.  Physicians are all generally trained to do that monitoring and decide when the medications can be stopped or held.  In the case where a maintenance medication is needed, they also have a goal of minimizing side effects from it.

I am hoping that the above comparisons make sense. Much of the hyperbole focused on psychiatry is not based in how psychiatry is taught or practiced.  Psychiatry is often isolated from the rest of medicine when it uses the same diagnostic and treatment approach.  It has the same genetic architecture as other polygenic diseases.  Even though the DSM has criteria listed for diagnoses – a diagnosis by a psychiatrist is much more than that.  Just like a dermatologist can see several diagnostic equivalents rashes, a psychiatrist is able to recognize many phenotypes of illness that are equivalent to the classification.  Those phenotypes include both validity markers and psychosocial characteristics that are not listed in the DSM but are important for individualized care.  And contrary to what you might read – it does not take an extensive battery of testing to get results.  

 

George Dawson, MD, DFAPA

 

Supplementary 1:

In human embryology the skin and the brain both originate form the same germ layer - the ectoderm.  The ectoderm differentiates into the neuroectoderm  and surface ectoderm that eventually becomes the epidermis and the surface appendages (hair and nails)  

Supplementary 2:

A typical polygenic risk analysis is available at the top of this post:  https://real-psychiatry.blogspot.com/2024/04/what-economist-doesnt-know-about.html

Note that this patient is at risk for 9 dermatology and 9 psychiatric conditions according to this graph.

Graphics Credit:

 Lead graphic is from:  

Boguniewicz, M, Fonacier L, Leung DYM. Atopic and contact dermatitis. In: Rich, Robert R., Fleisher, Thomas A, Shearer, William T., Schroeder, Harry, Frew, Anthony J., Weyand, Cornelia M.  Clinical Immunology : Principles and Practice, 5th ed. London: Elsevier; 2018  : p. 614

License number:  1693945-1

Graphics 2 and 3 were generated by me from FDA package inserts in Graphic 2 and the Table of Contents of the leadg graphics text (Rich R, Shearer TA, et al) and several research papers in the case of Graphic 3.  

References:

 1:  World Health Organization.  WHO’s first global meeting on skin NTDs calls for greater efforts to address their burden.  March 31, 2023:  https://www.who.int/news/item/31-03-2023-who-first-global-meeting-on-skin-ntds-calls-for-greater-efforts-to-address-their-burden

2:  Grada A, Muddasani S, Fleischer AB Jr, Feldman SR, Peck GM. Trends in Office Visits for the Five Most Common Skin Diseases in the United States. J Clin Aesthet Dermatol. 2022 May;15(5):E82-E86. PMID: 35642232; PMCID: PMC9122273.

3:  Schaefer I, Rustenbach SJ, Zimmer L, Augustin M. Prevalence of skin diseases in a cohort of 48,665 employees in Germany. Dermatology. 2008;217(2):169-72. doi: 10.1159/000136656. Epub 2008 Jun 5. PMID: 18525204.

4:  Schäfer T. Epidemiology of psoriasis. Review and the German perspective. Dermatology. 2006;212(4):327-37. doi: 10.1159/000092283. PMID: 16707882.

5:  Tian J, Zhang D, Yang Y, Huang Y, Wang L, Yao X, Lu Q. Global epidemiology of atopic dermatitis: a comprehensive systematic analysis and modelling study. Br J Dermatol. 2023 Dec 20;190(1):55-61. doi: 10.1093/bjd/ljad339. PMID: 37705227.

6:  Laughter MR, Maymone MBC, Mashayekhi S, Arents BWM, Karimkhani C, Langan SM, Dellavalle RP, Flohr C. The global burden of atopic dermatitis: lessons from the Global Burden of Disease Study 1990-2017. Br J Dermatol. 2021 Feb;184(2):304-309. doi: 10.1111/bjd.19580. Epub 2020 Nov 29. PMID: 33006135.

7:  Gether L, Overgaard LK, Egeberg A, Thyssen JP. Incidence and prevalence of rosacea: a systematic review and meta-analysis. Br J Dermatol. 2018 Aug;179(2):282-289. doi: 10.1111/bjd.16481. Epub 2018 May 31. PMID: 29478264

8:  Polaskey MT, Chang CH, Daftary K, Fakhraie S, Miller CH, Chovatiya R. The Global Prevalence of Seborrheic Dermatitis: A Systematic Review and Meta-Analysis. JAMA Dermatol. 2024 Aug 1;160(8):846-855. doi: 10.1001/jamadermatol.2024.1987. PMID: 38958996; PMCID: PMC11223058.

9:  Skayem C, Richard MA, Saint Aroman M, Merhand S, Ben Hayoun Y, Baissac C, Halioua B, Taieb C, Staumont-Sallé D. Epidemiology of atopic dermatitis: a global worldwide study. Clin Exp Dermatol. 2025 Sep 25;50(10):2054-2056. doi: 10.1093/ced/llaf233. PMID: 40448692.

10:  Urban K, Chu S, Scheufele C, Giesey RL, Mehrmal S, Uppal P, Delost GR. The global, regional, and national burden of fungal skin diseases in 195 countries and territories: A cross-sectional analysis from the Global Burden of Disease Study 2017. JAAD Int. 2020 Nov 30;2:22-27. doi: 10.1016/j.jdin.2020.10.003. PMID: 34409349

11:  Lazanas P, Antonatos C, Tsoumani KT, Sgourou A, Vasilopoulos Y. Shared Genetic Architecture Between Atopic Dermatitis and Autoimmune Diseases. Int J Mol Sci. 2025 Sep 18;26(18):9124. doi: 10.3390/ijms26189124. PMID: 41009683; PMCID: PMC12470386.

12:  Richard MA, Paul C, Nijsten T, Gisondi P, Salavastru C, Taieb C, Trakatelli M, Puig L, Stratigos A; EADV burden of skin diseases project team. Prevalence of most common skin diseases in Europe: a population-based study. J Eur Acad Dermatol Venereol. 2022 Jul;36(7):1088-1096. doi: 10.1111/jdv.18050. Epub 2022 Mar 22. PMID: 35274366; PMCID: PMC9415115.

13:  Norman GR, Rosenthal D, Brooks LR, Allen SW, Muzzin LJ. The Development of Expertise in Dermatology. Arch Dermatol. 1989;125(8):1063–1068. doi:10.1001/archderm.1989.01670200039005

14:  Tran H, Chen K, Lim AC, Jabbour J, Shumack S. Assessing diagnostic skill in dermatology: a comparison between general practitioners and dermatologists. Australas J Dermatol. 2005 Nov;46(4):230-4. doi: 10.1111/j.1440-0960.2005.00189.x. PMID: 16197420.

15:  Aljohani AG, Abduljabbar MH, Hariri J, Zimmo BS, Magboul MA, Aleissa SM, Baabdullah A, Alqutub A, Alafif K, Faidah H. Assessing the Ability of Non-dermatology Physicians to Recognize Urgent Skin Diseases. Cureus. 2023 Apr 19;15(4):e37823. doi: 10.7759/cureus.37823. PMID: 37214029; PMCID: PMC10197985.

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17:  Abdi P, Turk T, Haq Z, Diaz MJ, Dytoc M. Epidemiology and Comorbidities of Psychodermatologic Conditions. J Cutan Med Surg. 2025 Jun 24:12034754251347569. doi: 10.1177/12034754251347569. Epub ahead of print. PMID: 40552522.

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