Sunday, April 23, 2017

Is Diet Soda A Biohazard?

I woke up to a scary story about diet soda several days ago.  At least I thought it was scary.  It was clear at some point the the reporter had lost track of what the story was all about and was talking about regular and diet soda as being interchangeably toxic.  I can see how that might happen, since most of the recent soda scares have focused on regular soda or as it is referred to "sugary" soda.  Sugar in the current hysteria and it must be eliminated.  The media routinely informs us that for years cholesterol and fat were vilified and now we have that all wrong.  Fat and cholesterol are now acceptable and sugar is the villain.  To complicate matters, the message is to consume large quantities of colorful fruits and vegetables - 6 - 8 servings a day.  The problem is those colorful fruits on a serving per serving basis generally contain as much sugar as "sugary" soda.

The latest story was presented as they all are - a news headline rather than a work in progress. News flash - drink diet soda and you will get Alzheimer's Disease or a stroke.  In fact - drink as little as 1 can per day and get a stroke.  A few news outlets, talked about the other part of the story - consuming those sugary drinks in the same study did not increase the risk for dementia or stroke.  But even then it was presented in way to keep the hysteria going: "That does not mean you should start drinking those sugary soft drinks?"  Really - why not?  You just told me they don't cause strokes or Alzheimer's Disease.  Oh that's right - they contain that well known toxin - sugar.

Time for some self-disclosure in the interest of transparency before I get to the real story.  I eat a lot of sugary foods.  I like just about every imaginable kind of desert.  I am generally averse to vegetables unless they have a starchy consistency. I have consumed massive amounts of soda and diet soda in my life time.  I realize that everybody has a story of the outlier who beat the food and health odds.  "Grandpa smoked two packs of cigarettes a day and died at 95 of old age" or "Grandpa ate raw bacon every day and lived to 95 of old age."  That is not my point here.  As a physician, more than anybody I know better than to challenge medical common sense and hope to survive it.  I happen to be a health nut who consumes junk food.  I don't eat meat, fat. or cholesterol and I exercise a lot.  If I had to guess where the proclivity for sweet consumption comes in - I would attribute it to the Scandinavian side of my genome - cookies, pies, cakes, donuts with coffee of course.  So I am not here to defend or vilify sugar or artificial sweeteners.  In fact, I would definitely try my hardest to stop consuming this stuff if it was really a biohazard.

With that self disclosure, the real story in this case is easy to find and publicly accessible.  There is not only the original research article but an editorial.  To keep myself honest, I wrote about the article without reading the editorial first. but did read it.  The original article and the editorial are references 1 and 2 respectively and full text is available.  One of the associations I automatically have when dealing with food headlines is the Framingham Study.  This study was big when I was in medical school.  It offered the first exposure to epidemiology and risk factor analysis in cardiovascular pathology.  That was built on in the epidemiology course where several of the professors were experts.  There were board exam questions based on a knowledge of this study.  Generations of physicians have studied papers based on this study and probably react to the cardiovascular risk factor headlines the same way that I do.  I was mildly surprised to see that this study of diet soda and sugar sweetened drinks was based on the Framingham Study.

In this case the researchers looked at the Framingham Heart Study Offspring cohort.  That study began in 1971 with 5124 volunteers.  The participants are studied in examination cycles about every 4 years.  To date that means there have been 9 cycles so far with the last one occurring in 2014.  For the purpose of this study, they looked at the 10 year risk of stroke and dementia beginning with the 7th cycle (1998-2001).  A total of 3539 subjects were available at exam 7 and 3029 completed the Food Frequency Questionnaire (FFQ).  That population was split based on age and other criteria to an arm that was to be analyzed for 10 year risk of of incident stroke (N=2888) and another arm that was to be sampled for 10 year risk of incident dementia.  The FFQ was used to determine total sugary beverage consumption, sugary sweetened soft drink, and artificially sweetened soft drink in various rates of consumption where one can or bottle equaled one drink.  Answers at exam cycle 7 were used to measure recent intake and averaged responses over exams 5,6, and 7 were used to calculate cumulative intake over 7 years.  This was a prospective study, so time to stroke or dementia (using standard definitions) was done over the next ten years (from examination cycle 7).  The total number of events form the article are listed below.  The article contains tables detailing all of the demographic details by cohort and by consumption of sugary or artificially sweetened drinks.  The authors also present 10 year survival curves for both the stroke and dementia cohorts.  About 53% of the sample drank at least 1 artificially sweetened drink per week with 18% drinking more than one per day.

Stroke Cohort
Total Events (all strokes)
Ischemic Stroke
Recent Intake
Cumulative Intake

Dementia Cohort
Total Events (all cause dementia)
Alzheimer’s Disease
Recent Intake
Cumulative Intake

The main finding was that consumption of any amount of artificially sweetened soft drinks was associated with risk of stroke in both the case of recent (HR 1.88-2.17) and cumulative intake (HR 1.75-2.20).  Drinking greater than or equal to 1 artificially sweetened soft drink was associated with increased risk of all-cause (HR 2.28) and Alzheimer's dementia (HR 2.48) but only in the cumulative intake mode.

 They controlled for two major variables - hypertension and diabetes mellitus are immediately relevant for both strokes and dementia.  Controlling for diabetes mellitus, intake of artificially sweetened beverages remained a significant predictor of stroke, all cause dementia and Alzheimer's dementia but diabetes was found to be a partial mediator of the effect.  Excluding people with hypertension decreased the effect of artificially sweetened drinks on all strokes.

This was a very well done prospective study.  The HRs for artificially sweetened soda and stroke risk appear to be robust nearly doubling the rate across the board.  There is also a dose related effect with the HRs for subjects drinking ≥ 1/day artificially sweetened drink being a greater rate than those drinking > 0-6 drinks/week.  For dementia, significant HRs were noted only for cumulative intake of ≥ 1/day.  The authors do a good job of listing the limitations of the study. They point out that there were no ethnic minorities and that limits generalizability to populations of non-European decent.  While that is true, it may also be true that the study is not generalizable to other white populations.  They provide the usual disclaimer about causality from observational studies.  They discuss recall bias on the FFQ, but they previously discussed validity of recall of Coke/Pepsi product in the range of 0.81-0.85.  They mentioned undetermined confounding variables.  They also did not adjust for multiple comparisons which is surprising in a study with this many variables.  That seemed to be the weakest methodological link

When I thought a bit more about the study, there was no clear mechanism of why strokes and dementia would be produced by artificial sweeteners.  They discuss theories about how these compounds have been implicated as increasing cardiometabolic risk factors.  The other factor is that several of these compounds have been consumed by the public for over 50 years.  The FDA provides information that some of the compounds have been extensively studied for safety in both animals and humans.  Is it possible that the FDA missed some excessive cardiovascular, cerebrovascular or dementia mortality due to high-intensity sweeteners?  Their approach seems to be to suggest an average daily intake (ADI) of these compounds and suggest that consuming that amount over the course of a lifetime is safe.

The other main factor that affects how physicians think about these studies is whether or not there is supporting or contradictory data.  This paper lists the  Nurses Professional and Health Professionals Follow-Up Study that showed that both artificially sweetened and sugar sweetened soft drinks were both associated with a higher risk of stroke over 28 years of follow up for women and 22 years of follow up for men.  The sample size was large (women N=84085 and men N=43371).  The pooled Relative Risk of stroke was 1.16 and the authors suggest drinking decaffeinated coffee reduced risk.  The authors also listed the Northern Manhattan Study (N=2564) that showed that artificially sweetened soda increased the combined risk of vascular events but not stroke.  In the editorial, the authors list two negative studies.  In the first, there was an association between coronary heart disease and biomarkers of coronary heart disease for sugar sweetened beverages but not artificially sweetened beverages (6).  The second study (7) showed the identical result with risk for sugar sweetened but not artificially sweetened beverages.  

I am always skeptical of the results of studies with many variables and clear-cut effects - at least until they are replicated.  This is a good study that will be quoted for years.  You can't believe what you hear in the media about it - but to physicians and researchers it raises significant questions.  I think that it is useful to known this literature in order to discuss it with people who need to take specific medications that increase their cardiometabolic risk like atypical antipsychotics.

At a personal level, the question is what if anything should be done?  It is clear that although the study points to increased risk, the majority of the research subjects who ingested diet soda did not experience an adverse outcome during the test period.  Doing a basic literature search shows that there are many epidemiological studies looking for various adverse outcomes from artificial sweetener exposure and few positive findings.  I will take it as a sign that I need to get more disciplined in terms of my intake of high intensity sweeteners as well as sugar.  Why take something toxic if there is even a theoretical risk?  The answer of course is preferences over time and those preferences die hard.

Wish me luck.

George Dawson, MD, DFAPA


1: Pase MP, Himali JJ, Beiser AS, Aparicio HJ, Satizabal CL, Vasan RS, SeshadriS, Jacques PF. Sugar- and Artificially Sweetened Beverages and the Risks of Incident Stroke and Dementia: A Prospective Cohort Study. Stroke. 2017 Apr 20. pii: STROKEAHA.116.016027. doi: 10.1161/STROKEAHA.116.016027. [Epub ahead of print] PubMed PMID: 28428346

2: Wersching H, Gardener H, Sacco RL. Sugar-Sweetened and Artificially Sweetened Beverages in Relation to Stroke and Dementia: Are Soft Drinks Hard on the Brain? Stroke. 2017 Apr 20. pii: STROKEAHA.117.017198. doi: 10.1161/STROKEAHA.117.017198. [Epub ahead of print] PubMed PMID: 28428347.

3: Kissela BM, Khoury JC, Alwell K, et al. Age at stroke: Temporal trends in stroke incidence in a large, biracial population . Neurology. 2012;79(17):1781-1787. doi:10.1212/WNL.0b013e318270401d.

4: Barraclough H, Simms L, Govindan R. Biostatistics primer: what a clinician ought to know: hazard ratios. J Thorac Oncol. 2011 Jun;6(6):978-82. doi: 10.1097/JTO.0b013e31821b10ab. Erratum in: J Thorac Oncol. 2011 Aug;6(8):1454. PubMed PMID: 21623277.

5: Bernstein AM, de Koning L, Flint AJ, Rexrode KM, Willett WC. Soda consumption and the risk of stroke in men and women. Am J Clin Nutr. 2012 May;95(5):1190-9. doi: 10.3945/ajcn.111.030205. Epub 2012 Apr 4. PubMed PMID: 22492378.

6: de Koning L, Malik VS, Kellogg MD, Rimm EB, Willett WC, Hu FB. Sweetenedbeverage consumption, incident coronary heart disease, and biomarkers of risk in men. Circulation. 2012 Apr 10;125(14):1735-41, S1. doi: 10.1161/CIRCULATIONAHA.111.067017. Epub 2012 Mar 12. PubMed PMID: 22412070.

7: Fung TT, Malik V, Rexrode KM, Manson JE, Willett WC, Hu FB. Sweetened beverage consumption and risk of coronary heart disease in women. Am J Clin Nutr. 2009 Apr;89(4):1037-42. doi: 10.3945/ajcn.2008.27140. Epub 2009 Feb 11. PubMed PMID: 19211821.


Image at the top is from Shutterstock per their standard license agreement.  Title is:
"Yellow tin for drinks with a symbol of biological danger" by Liusa.


Thursday, April 20, 2017

'Tis The Season - Seasonality and Suicide

From reference 1 - see for details. 

My first job as a staff psychiatrist was in a clinic in Superior, Wisconsin just across the harbor from Duluth, Minnesota where I lived.  For two of the years I worked there, a local television station would interview me about depression, suicide, and Christmas - at least that was their take on the story.  What would be better drama than a tumultuous family gathering, heated arguments, disappointment, and increasing depression?  That would be a great dramatic story if it was true, but it is not.  For two years, I battled with the reporters to tell the real story about seasonality and suicide, but in the end I lost.  Prior to the last interview, I went as far as saying: "Look - don't make the connection between Christmas and depression or suicide.  It really does not exist."  The first question I was asked: "Isn't it true that depression peaks at Christmas time?  Can you suggest a few reasons why that occurs?"   I fumbled along trying my best to explain what really happens.  All of these interviews are heavily edited down to a couple of sound bites.  The final version really did not have much to say about anything.

In the intervening 30 years, I have had a lot of time to think about the problem.  To a clinical psychiatrist the main problem is suicide prevention.  Seasonality and suicide is never really mentioned in modern day suicide assessment or treatment.  The popular screening checklists don't have anything to say about seasons.  I have no doubt that clinically - suicidal thinking and suicide attempts correlate well with what is written in the literature.  The literature says that late spring is the peak season for suicides and that is what I have observed directly over 30 years of experience.  The main question is how this is relevant to the treatment and prevention of suicidal thinking and behavior.

In the referenced review, the authors do a reasonable job of summarizing what is known about the association of various environmental factors and suicide.  Studies of rare events are always affected by the ecological fallacy of inferring the behavior of individuals from membership in large groups.  We end up with extremely small numerators of people who have completed suicide relative to their membership in rather massive groups - like all Spring allergy suffers or in the case of biological psychiatrists the even larger group of everyone with seasonally low tryptophan levels.  The authors description of the effect of seasons on tryptophan levels and serotonin turnover is interesting but I disagree with their conclusion.  I do not think that much higher levels of serotonin turnover in bright sunlight negate tryptophan levels as an arbiter of suicidal behavior in the late spring.  We are currently approaching the end of April in southern Minnesota.  That last two days have been bitterly cold and wet.  Everybody is talking about how gloomy and depressing the weather is.  At this point in time, practically every friend, family member, and patient I have seen has had at least two upper respiratory tract infections (URI) of varying severity.  These viruses are generally flu-like illnesses (FLI) in that they produce all of the same symptoms except high fevers and can last up to 2 1/2 weeks.  In April and May, the population is in survival mode and we are looking for a break.  It doesn't necessarily have to be better weather, but that is the only practical way to be rid of the pestilence that is associated with winter.  The authors in the review look at cytokine and immune modulated mechanisms but they are highly speculative.  Not enough is known about the specific environment that suicidal people have experienced.  In the USA for example, not everybody at a certain latitude will see reduced sunlight and epidemic exposure to URIs.  At some point technology may allow widespread sampling and reconstruction of the true environment.  In the mean time studying specific work or school environments may be a more productive research approach.  

Seeing patients who tell me that they are getting more depressed and experiencing suicidal thoughts this time of the year makes me more vigilant.  After seeing most patients with these problems, I run the conversation back in my head a few more times than usual.  I am trying to see if I may have missed anything.  It is my version of the preemptive psychological autopsy - to prevent the necessity of a real one.  Psychotic depression can be very subtle and  people with that particular problem can be difficult to establish a working alliance with.  They may also have suicide attempts by highly lethal means.  The most important part of the conversation is giving them hope and having a plan to access emergency services.  But even before that I caution them that the progression to a state where they consider suicide is a sequence of events that needs to be recognized and interrupted at the earliest possible point.  All of that is the talking necessary in addition to any pharmacotherapy.  One of the most important aspects of any mental health crisis is recognizing that you will be coming through on the other side.

That is as true about Spring as it is for anything else.

George Dawson, MD, DFAPA


1:  Woo J-M, Okusaga O, Postolache TT. Seasonality of Suicidal Behavior. International Journal of Environmental Research and Public Health. 2012;9(2):531-547. doi:10.3390/ijerph9020531.

Figure at the top of this page is from reference 1 - an open access article. Reprinted here per
Creative Commons Attribution 3.0 Unported (CC BY 3.0) license. Original graph is unaltered.

2:  Hankoff LD. Suicide and attempted suicide. in Handbook of Affective of Disorders. Eugene S. Paykel (ed). The Guilford Press. New York. 1982 pages 417-428.

"Durkheim's study of the seasonality of suicide helped to confrim his impression of social factors on suicide.  ..... From the months of January through June there was a progressive increase in the rate of suicide and from June onward a progressive decrease."  p. 418

Monday, April 17, 2017

When and Where Does Depression End?

For the past 7 years I have been seeing patients who have been carefully selected for having an alcohol or other substance use disorder.  My task is to determine if there is an associated psychiatric disorder, whether or not it can be treated, initiate treatment, and follow up.  Most of the people I see have anxiety and/or mood disorders and determining adequacy of treatment and the actual diagnosis can be a challenge.  I have highlighted a couple of the problems in the past including a high prevalence of primary sleep disorders and the issue of people with disorders of temperament that might seem like a primary disorder but that are fundamentally different.  These distinctions are critically important in terms of when the disorder ends if it is treated.  I don't think the problem have been adequately addressed in the literature.  In many ways it is a failure to recognize that conscious states exist out there that are not easily captured by a handful of descriptors or the derivative checklists.  Checklists are frequently seen are the endpoints in clinical research.  They are used to determine if treatments are effective.

A couple of texts (1,2) describe typical endpoints for depression.  In the first reference the authors discuss the concept and how it has evolved since the 1970s from broad terms like treatment resistant to more specific antidepressant resistant or refractory.  They discuss staging methods including the Thase and Rush staging method (TRSM), the European Staging Method (ESM), the Massachusetts General Staging Method (MGH-S) and the Maudsley Staging Method (MSM).  The ratings vary in how they rate the treatment resistant dimension (antidepressant resistant,  electroconvulsive resistant, duration of trials).  The MSM is the only scale that rates multiple dimension including symptoms severity at baseline, duration and specific number of treatment failures.  Treatment resistance is a biological psychiatry based term that is not applied to psychotherapy.

Looking at what is available, there should be concerns about people being able to recall that level of detail.  I prompt people with a list of all known medications.  A substantial number of people cannot recall medication names, even when prompted.  Unless the medication regimen has been uncomplicated like: "I took fluoxetine for 10 years and then changed to venlafaxine" specific duration will not be recalled (the ESM has 5 specific intervals of treatments demarcated in weeks). Unless medical records are available for review by researchers, I would be skeptical of a large population of research subjects being able to provide the information necessary to make these classifications.

I generally try to reconstruct the history from late childhood and adolescence through adulthood.  That allows for the determination of global subtypes of depression from persistent depressive disorder or what used to be called dysthymia to discrete episodes of major depression.  When I was trained we had an entity of double depression or episodes of major depression superimposed on dysthymia.  In DSM-5 parlance that would be called persistent depressive disorder with intermittent major depressive episodes with or without current episode.  Since the diagnostic criteria for persistent depressive disorder involves having at least two of six symptoms that results in a total of 15 combinations of two symptoms.

In focusing on how to determine if the depression is gone most clinicians like myself are looking at binary outcomes.  We are treating depression until the symptoms are gone.  Research studies depend more on metrics like rating scales that are done directly by the research subjects or researchers.  Remission or partial remission is based on the scores of those rating scales.  For example, a typical psychopharmacological study would look at either the amount of decrease on a depression rating scale or where the rating scale score is relative to the established cutoff.  For example, treatment resistance could be defined as less than a 50% reduction in depression rating scale scores after a course of treatment.  It could also be defined as a failure to attain the require responder score or remission score after an adequate course of antidepressant therapy.  In primary care these days, a lot of people are diagnosed and treated with a depression rating scale - the PHQ-9.  Their PHQ-9 scores are tracked and their depression is classified as remitted if their score is 5 or less (the total score ranges from 0-27).

For the purpose of this post consider the following scenario.  I see a person back after they have been treated with an antidepressant.  In reviewing whether the medication has been working the patient reports his sleep has normalized, he is eating and exercising well, he has gone back to enjoying his previous activities, and most of his depressogenic thinking has resolved.  He no longer has any hopelessness or suicidal thinking - the original reason for the referral.  For further clarification, the discussion proceeds to the issue of dysthymia:

MD:  "Do you remember the first time we talked and you told me that you had been depressed since middle school and it had never gone away?  With the improvement you are noticing right now - do you feel like it has gone away?"
Pt:  " I am a lot better but I still feel depressed.  I would say that I am about 60-70% better."
MD:  "We have covered pretty much all of the critical symptoms for depression.  Let me ask you - what else would need to clear up right now in order for the depression to be completely gone?"
Pt:  "I guess my wife and family would need to treat me better.  I know that you can't do much about that - but that is a big problem.  If that happened I would be feeling a lot better?"

What to do about what seems to be an external factor affecting our neat little conceptualization of depression?  A typical formulation considers this to be an external factor.  A factor amenable to environmental engineering or adaptation.  Either way, the patient is still depressed despite what appears to have been a significant treatment effect.  On dichotomous analysis of depressive symptoms appear to have resolved for the most part.  He could be handed a rating scale and score in the mild to moderate range.  But the most important part of the assessment is that he still feels subjectively depressed.  In the 1970s or 1980s general systems theorists proposed that the brain is able to develop models of the environment so well that becomes an important part of any central nervous modulated process.  Motor activity provides the most obvious models.  A person walking with a cane has a much different cortical representation of what walking with a cane is than before they walked with a cane.  The cane is an actual extension of the CNS process.  You can easily demonstrate this by going through the motions of brushing your teeth without the tooth brush.  Within seconds it is obvious that you are not engaged in the same process and the parts are much more than the weight and feel of the toothbrush.  Can this exist in depression?  Can there be brain representations of relationships that are disturbed and lead to chronic depression?

I don't see why not.  Many psychiatrists would see this as a bad thing.  Many critics of psychiatry would see this as a good thing.  I see it as a brain thing.  A person would have to be fairly naive to believe that the most complex object in the universe could be parsed into a couple hundred diagnoses based on verbal criteria.  That is why psychiatrists are extensively trained.  Trained psychiatrists should be able to do much more than read the DSM-5.  I think that this is where Kendler's idea about indexing is valuable.  These are ballpark estimates of problems that need further refinement both over the course of treatment and by active research.  Formulations of these estimates can allow for successful medical treatment as well as successful psychotherapy.

These formulations can also suggest when active treatment can stop and a person can pick up the ball and start to make a lot of discoveries on their own - whether they consider themselves to be chronically depressed or not.

There is more to life than a score on a rating scale.


George Dawson, MD, DFAPA


1: Carvalho ACCF, McIntyre RS. Treatment-resistant mood disorders. Oxford: Oxford University Press; 2015.

2: Greden JF, Riba MB, McInnis MG. Treatment Resistant Depression, A Roadmap for Effective Care. American Psychiatric Pub; 2011.

Saturday, April 15, 2017

Does Learned Helplessness Explain The Suicidal Thoughts Of Medical Students?

The headlines are everywhere.  Medical students have a significant prevalence of suicidal thoughts and suicides.  The typical explanations are burnout and depression associated with the rigors of medical training.  Considering that medical training has always been rigorous the obvious questions include - is depression and suicidal thinking more prevalent now and if that is true - why?

The research offers little hard data.  There are no consistent longitudinal studies that use the same methodology to look at the issue of suicidal thoughts or suicide attempts in medical students.  The studies are generally cross sectional using diverse methodologies and involving different cultures (1).  The prevalence of suicidal thoughts varied from 11.2 to 14% for a given year.  The prevalence of lifetime suicide attempts ranged from 1.4 to 6.2%.  Some studies have determined suicide rates for male (15.6/100,000) and female medical students (18.9/100,000).  This studied showed no difference between suicide rates in men compared with the general population but higher rates for women.  Most studies do not look at comparison with rates  in the general population.

There is no evidence that I am aware of that medical training has become more rigorous or stressful than it used to be.  In my early training days, I saw residents in particular subjected to training schedules that I am guessing can no longer occur due to limitations on work hours.  Some of the best examples were surgical specialty rotations where second and third year residents hardly ever left the hospital.  Even as an intern in those days it was common to work 24 hours straight and then the next day until 5 PM or (total of 36 hours) every three or four days. Those schedules were exhausting but they were widely accepted until recent changes were made in the allowable hours for trainees.

The volume of material covered in medical school combined with the poorly defined guidelines about what needed to be known to be a proficient physician is not the most efficient approach to study.  Comparing medicine to a rigorous undergraduate course of training illustrates the problem.  If I was taking Physical Chemistry as a chemistry undergraduate, I knew I had to read specifics sections of the text, know the lecture notes, and take the tests on the lecture notes and text.  In medical school, the connections are less clear.  You can read one (or more) texts and know the lecture notes, but the testing was often guess work and typically on a body of knowledge that was more fluid - it might not hold up from year to year.  That level of inefficiency keeps people studying far too long in order to take tests that in the long run mean a lot less.  

The typical way that depression and suicidal behavior in physicians and trainees is studied is to look at the prevalence of depression, suicidal ideation and suicide in these populations.  Those studies generally suggest that suicide as a preventable cause of death is one that physicians as a group are not good at self correcting (2).   The typical comparison is that physicians as a group are better than the public at large when it comes to smoking cessation and reduced risk for cardiovascular and pulmonary disease.  That has led some experts to hypothesize that unlike smoking, getting treatment for depression and suicidal thinking involves many barriers relative to other health care interventions. Physicians may be more concerned about confidentiality, stigma, and the potential impact on career than with standard health measures.  In some cases the issue of reporting and disciplinary action has been mentioned.  Expert opinion generally recommends education about depression and suicidal thinking in physicians and facilitating access to mental health care.  Screening trainees for depression has also been suggested.  Burnout has become a popular theory lately and efforts to put a number on burnout suggest very high rates in most medical specialties.  The relationship of burnout to depression and suicidal thinking is less clear.

As I looked at the problem over time, the most striking factor in medical practice has been the total loss of control by physicians.  Thirty years ago, all of the medical students and residents in training programs were exposed to strenuous training schedules, but they also saw physician models who could provide the latest scientific care and have a direct impact on the patient and the treatment environment in general.  Most medical students start out valuing direct patient contact time.  The ones who don't end up in fields where there is minimal patient contact.  The contrast today is striking.  Today students and residents as exposed to training environments that are under the strict control of business managers.  This management is frequently a direct obstacle to scientifically based care and a frequent obstacle to routine care.  What rational person is going to subject themselves to intensive and stressful training only to see that their professional futures are under the control of people who routinely interfere with care and who can waste physicians time to an incredible degree based on a whim?  To me this seems like a textbook example of the learned helplessness paradigm and observing it.

Learned helplessness is a research paradigm for depression.  In laboratory animals, it is observed when the animal is subjected to an inescapable aversive stimulus.  At some point the animal just stops responding (trying to escape).  That response deficit is associated with biological markers consistent with depression and it can be treated with some of the same pharmacological agents used to treat depression.  Rodent models of learned helplessness are considered screens for molecules that have potential antidepressant effects.  An  interesting variation of this effect is learned helplessness by proxy.  Animal studies show that fear conditioning can be learned by proxy (3,4).  There is a research literature on the intergenerational transmission of anxiety and depression (6).  These studies suggest that the learning effects, especially in environments where there is a significant amount of emotion, can be significant.  Less studied phenomena like identification with mentors are also in effect in these environments.  There are several linear crisis model of suicide that are generally based on a progression of risk factors.  In my experience suicide is a non-linear process that involves subtle changes in the conscious state.  Stressful and emotional environments are more likely to be associated with these altered conscious states.

With physicians at all levels of training there are several factors that make it very difficult to escape a real or imagined failure in pursuing a career in medicine.  The debt factor is significant (7). One of the ongoing justifications of physician salaries in the US is the high cost of medical training.  Walking away from that is an anxiety producing scenario and yet one study showed that 40-46% of medical students considered that due to excessive workload and exam stress (1).  The expectations of mentors, friends, and family is a variable consideration that can increase the thoughts of failure for men and women at this life stage.  Most physicians in training have some idea of what real medical practice will be like when they are finally ready to make that transition.  There used to be clear models in the form of the attending physicians encountered on rotations.  My recollection of these attendings were that they appeared to have normal and full lives, especially in the time they were not active in clinical rotations.

Today medical students and residents don't see practicing physicians with normal lives.  They don't see physicians coming in for one or two month rotations.  Now they see practicing physicians who rotate one week on and one week off all year long for the rest of their lives.  They see primary care fragmented between clinic staff and hospitalists.  In the case of psychiatric rotations, they generally see people hospitalized in settings where nobody wants to stay, nobody really gets much better, and readmission rates are very high.  Ruling all of this are case managers with no medical training - telling the attending physicians what to do.  That has got to be a shock that puts many medical students off of the idea of a career in medicine even before they get started.  It gives them the message that they did not really need to go to medical school when their decision making is dictated by business managers.  It also gives them the message that they are a cog in business-of-medicine machine and cannot expect much personal contact with patients or medical treatment based on that relationship.  Finally - they notice the science of medicine that they were immersed in has suddenly become relative to the next great idea of the head administrator.  Whatever that business idea is - suddenly all of the physicians in the organization are doing it whether it is scientific or relevant.

Concerns about suicide prevention are always a legitimate endeavor, irrespective of the quality of the epidemiological evidence.  As physicians we have an obligation to recognize when our colleagues are in crisis and try to help them.  There do appear to be significant barriers to medical trainees and physicians getting help and that should be widely recognized.  I fear that the deteriorated practice environment is not being given sufficient weight as an etiological factor.  What sense does it make to go through what is widely acknowledged as very stressful training, when in the end physicians are no longer allowed to practice as professionals?  What impact occurs when trainees observe that many physicians are  currently practicing like they did when they were residents - with no end in sight?  Learned helplessness has always been there - but now instead of  being limited to training it is a permanent dimension of medical practice.    

That sounds like a recipe for desperation to me.   It is time for the profession to acknowledge that professional control of the practice environment is necessary not only for the good of our patients but for our own well being as well.

And there is nothing wrong with that.

George Dawson, MD, DFAPA


1: Rau T, Plener P, Kliemann A, Fegert JM, Allroggen M. Suicidality among medical students - a practical guide for staff members in medical schools. GMS Z Med Ausbild. 2013 Nov 15;30(4):Doc48. eCollection 2013. Review. PubMed PMID:24282451, (figures cited above are from numerous references in this paper).

2: Center C, Davis M, Detre T, Ford DE, Hansbrough W, Hendin H, Laszlo J, Litts DA, Mann J, Mansky PA, Michels R, Miles SH, Proujansky R, Reynolds CF 3rd, Silverman MM. Confronting depression and suicide in physicians: a consensus Statement. JAMA. 2003 Jun 18; 289 (23): 3161-6. Review. PubMed PMID: 12813122.

3: Ramaker MJ, Dulawa SC. Identifying fast-onset antidepressants using rodent models. Mol Psychiatry. 2017 Mar 21. doi: 10.1038/mp.2017.36. [Epub ahead of print] PubMed PMID: 28322276.

4: Bruchey AK, Jones CE, Monfils MH. Fear conditioning by-proxy: social transmission of fear during memory retrieval. Behav Brain Res. 2010 Dec 6;214(1):80-4. doi: 10.1016/j.bbr.2010.04.047. Epub 2010 May 2. PubMed PMID: 20441779.

5: Jones CE, Riha PD, Gore AC, Monfils MH. Social transmission of Pavlovian fear: fear-conditioning by-proxy in related female rats. Anim Cogn. 2014 May;17(3):827-34. doi: 10.1007/s10071-013-0711-2. Epub 2013 Dec 6. PubMed PMID: 24310150; PubMed Central PMCID: PMC3984423.

6: Nauta MH, Festen H, Reichart CG, Nolen WA, Stant AD, Bockting CL, van der Wee NJ, Beekman A, Doreleijers TA, Hartman CA, de Jong PJ, de Vries SO. Preventing mood and anxiety disorders in youth: a multi-centre RCT in the high risk offspring of depressed and anxious patients. BMC Psychiatry. 2012 Apr 17;12:31. doi: 10.1186/1471-244X-12-31. PubMed PMID: 22510426.

7: Priceonomics.  Which Graduate Degree Gets You Out of Debt the Fastest?  April 13, 2017.


Quotation of the song lyrics posted here for academic illustration only.  Song was released in 1994 and copyrighted by Virgin Records.  Use here does not imply endorsement by or affiliation with the artists or label and is strictly for non-commercial educational purposes.

Saturday, April 8, 2017

Physician Generational Effects of Oppression By The Managerial Class

One of the dynamics that I consider to be essential to the survival of the profession is whether there is any way to resist the manipulations of the managerial class.  Since the profession has been almost completely subordinated to the managerial class, the question may not seem very relevant.  Too much depends on physician independence to give it up that easily.  Without physicians independence there is really nobody advocating for our patients.  Do we really want to be cogs in a government sanctioned business empire that decides when people live and people die or who gets medication or who gets reasonable medical care?  There is no physician I know who is willing to give those decisions up to administrators.  Those decisions are happening by manipulation and default every day.  Administrative representatives sitting in on medical teams with the full blessing of the CEO or department head.  Cross them and you may be out of a job either directly or pressured out by becoming person non grata or a handy "disruptive physician" label.  That is a high price to pay for disagreeing with management, especially when they are making decisions that only a physician is trained to make.

I have had the opportunity to work with residents and early career physicians for about the past 15 years and I noticed that they had a tendency to get a lot less riled up about these scenarios than I did.  It is paradoxical in a way.  Even though older physicians tend to be much more bothered by the managerial class than our younger colleagues, all of the burden of these managers is falling directly on them.  Electronic health record (EHR) mandates, EHR software that is essentially junk, arbitrary maintenance of certification (MOC) requirements, billing and coding requirements to avoid financial penalties, and on and on and on.  The burden of the managerial class on physicians gets worse every year and there is no end in sight.  There has been very little resistance to this burden.  The only exception that comes to mind in the National Board of Physicians and Surgeons - an alternate route to maintenance of certification through standard life-long learning approaches rather than the methods recommended by the American Board of Medical Specialties (ABMS).  The NBPS was founded by Cardiologist Paul Teirstein, MD who graduated from medical school in 1980.

As far as I can tell there is very little research on the generational effects of changing physician demographics.  By that I mean - how are the specific groups of physicians impacted by excessive management, do they react to it, and do they have any success in changing it in a positive way for physicians.  The raw data on physicians based on Census data is fairly interesting.  Looking at the graph below the population of physicians is fairly stable between the current age range of 34-59 with a more even distribution of men to women starting with 32 year olds.  That distribution has been more even in psychiatry than more other specialties for much longer - at least the departments that I have worked in.

Using standard generational nomenclatures that means that there are still physicians practicing who were born in 1945 or earlier (72 yo and greater).  The Baby Boomers are in the 53-71 yo range.  Gen X are the 41 - 52 year olds.  The Millennials are 22-40.  It looks like there are also a total of 34 Gen Y physicians who are currently 21 years of age.  All of the named generations seem to be represented.  I don't put much stock in generational characteristics being applied across standardized age ranges.  Certainly younger physicians are more likely to text and use more Smartphone apps, but it really is impossible for physicians practice these days and not have more than a passing command of basic technology.  If they don't know it and the implications, they will probably have to be trained in it.  

The demographics are available but outside of the burnout literature, there is very little written about the generational effects of management.  These are important questions because non-medical business management has unprecedented influence on medical care in this country.  Business managers determine how long people get to stay in the hospital, how much time physicians have to spend on documentation and record keeping, how many patients physicians need to see each day, and the entire structure of outpatient medical care.  A great example is how psychiatric practice has changed from seeing patients fairly frequently and discussing many aspects of a persons care to isolated brief appointments to discuss a medication that may be only moderately effective.  If you see a medical specialist - you might be limited to one appointment per year.  Business managers have widely implemented team approaches and sold this idea to the public.  What the public does not know is that there are management representatives on these teams who lack medical credentials and given that fact have a disproportionate amount of input into patient care.  Physicians are micromanaged at every decision point.

My real question boils down to what happens when that case manager on your "team" tells you that the patient needs to go and as a physician you know they are not stable and can benefit from continued care?  How does a 53 - 71 year old physician react to that dilemma compared with a 22-40 year old physician?  Are there intergenerational conflicts based on those reactions or the perceptions of those reactions?  What are the reality factors involved?  I know that there are plenty of anecdotes.  It is common to hear that Boomer generation physicians are retiring as soon as possible to avoid oppression by managers.  It is also common to hear that Millennial generation physicians are laboring under unprecedented levels of medical school debt.  That plus a mortgage and a family gives them limited options in responding to oppressive management practices.  That is especially true when short staffed hospitals offer signing bonuses to early career physicians.  There is some intergenerational conflict on the maintenance of certification (MOC) issue.  The Boomer generation is more likely to be incensed and point out that there is really no "evidence" that the requirements made up by the ABMS are necessary.  Some of the younger generation is critical of the Boomers, especially about the fact that many are "grandfathered in" based on age.  There is no more critical issue for all physician generations and the political forces that have the most to gain from MOC are just waiting for a generational split to give them the advantage they need to continue their agenda.

The other movement is an exodus of physicians into private practice and in some cases cash only practices or some variation.  That is a definitive way to escape oppressive management practices, but the managers and their friends in government have a long reach.  The electronic health record (EHR) is one example.  Even though the EHR remains not ready for prime time for a number of reasons, it is mandated for use by physicians and pharmacies.  It is a relatively new cost for any physician or group who wants to try to make it outside of the systems of government payers, managed care organizations, and pharmacy benefit managers.  Finding an EHR that has more value than problems is a daunting task.  It is probably the most imperfect software that you can find anywhere.

Those are a few thoughts on this is this Saturday morning.  Make no mistake about it all physicians are targeted for oppression by managers at some level.  On a daily basis it is not difficult to find some business entity that has made a bad decision about the care of one of your patients or one that is not actively trying to interfere with your care of a patient.  In some cases, the physician is just an afterthought.  They are swept into the battle between pharmaceutical benefit managers and pharmaceutical manufacturers over medication pricing structure and how it is reflected in the written prescription.  But all of that still comes back to the physician when they are ordered to make what amount to trivial but time consuming changes.

The goal of examining these issues would be to get rid of micromanagement initially.  There is no reason why prescriptions for inexpensive generic medications should be micromanaged.  It amounts to harassment.  It seems more complicated if we are talking about teams where a manager is sitting in a team meeting and dictating care, but it is not.  Most of medicine these days is still based on subjective decisions and experience.  That may not seem to fit into the rhetoric of evidence based medicine, but it is the property that currently gives physician the advantage over computers.  Recognizing experienced based patterns in patient diagnosis and care is the reason that medical training is necessary.

Business managers don't have it.  Looking at the generational effects may give physicians some ideas of how get rid of some of these practices and present a more united front to the people adversely affecting our care of patients.                

George Dawson, MD, DFAPA  


1:  Carol A. Bernstein.  The Changing Face of Medicine: The Next Generation of Psychiatrists.  Keynote address.  Minnesota Psychiatric Society October 8, 2010.

Tuesday, April 4, 2017

The Loose Connection Between Disease Definition, Addiction, and Neuroscience

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

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

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

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

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

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

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

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

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

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

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

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

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

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

George Dawson, MD, DFAPA

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

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

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

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

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