Prolonged Grief Disorder - A Few Comments

The New York Times came out with an article on prolonged grief disorder.  I thought I would write about it because in some ways it is a continuation of the criticism that started with the DSM-5 release in 2015.  The response to that piece is one of the most read articles on thisblog. As I pointed out in that article and several since, the release of the DSM-5 has been a predicted non-event. There were no scandalous developments based on releasing a document that hardly anyone reads and is not even owned by most of the people who prescribe medications for psychiatric indications – primary care physicians.

The new piece based on the release of DSM5-TR is much more balanced.  A well-known psychiatric researcher Katherine Shear, MD is quoted as well as an epidemiologist Holly Prigerson, PhD who discovered data supportive of the diagnosis and studied the reliability and validity.  Paul Appelbaum, MD is the head of the committee to include new diagnoses in the manual and he also explains the rationale.

What did I not like about the article?  It starts out with the old saw about how the DSM 5 is sometimes known as psychiatry’s bible. I appreciate the qualifier but let’s lose the term bible in any reference to the DSM.  That descriptor is wrong at several levels – the most important one being that it is a classification system.  Please refer to it as psychiatry’s phone book or catalogue from now on, even though it is nowhere near as accurate as a phone book or any commercial catalogue.

The author goes on to describe the inclusion of prolonged grief disorder into the latest revision of DSM as controversial and then collects opinions on either side of what I consider to be an imaginary controversy. Why am I so bold to call this controversy imaginary?  Maybe it is not entirely imaginary, but it certainly is not as big a deal as it is portrayed in the article and here is why.

The first argument is that including it in the DSM means that professionals can now bill for it. In fact, all hospitals, clinics, public payers, and insurance companies require ICD-11 codes and not DSM codes.  Granted, the DSM codes are typically coordinated to match ICD-11 codes but there is not a perfect match.  ICD-11 codes are available for free and do not require a copy of the DSM 5 TR. The diagnosis of prolonged grief disorder was included in the ICD-11 in 2020 (2) and it is easier to make the diagnosis.  Quoting from reference 2:

“To meet PGD_ICD-11 criteria one needs to experience persistent and pervasive longing for the deceased and/or persistent and pervasive cognitive preoccupation with the deceased, combined with any of 10 additional grief reactions assumed indicative of intense emotional pain for at least six months after bereavement. Contrary to the 5th revision of the Diagnostical and Statistical Manual of Mental Disorders [DSM-5; (11)] and the 10th revision of the International Classification of Diseases [ICD-10; (12)], the ICD-11 only uses a typological approach, implying that diagnosis descriptions are simple and there is no strict requirement for the number of symptoms one needs to experience to meet the diagnostic threshold.”

The insurance company billing is further complicated by the fact that there are many other current diagnoses that can be used to treat a person severely incapacitated over a prolonged or severe course of grief.  Per my original blog Paula Clayton, MD explained this 45 years ago based on her research that also showed a small percentage of people become depressed during grief and require treatment. A prolonged grief disorder (PGD) diagnoses is not necessary and, in some cases, may lead to problems with insurance companies. It is well known that some insurance companies will not reimburse for some diagnoses that they think do not require treatment by a mental health provider. What they think of a PGD diagnosis is unknown at this time.

The second argument is that it may lead to biological treatments for the disorder. They cite a naltrexone trial for this disorder. Let me be the first to predict that the naltrexone will probably not work but I will also point out it is a medication that could be prescribed right now without putting PGD in the DSM 5 TR. The author states this may set off a competition among pharmaceutical companies for effective medications. That may be true – but what will the likely outcome be?  We already know that many people with PGD actually have treatable depression and respond to conventional treatments. We also know that those medications are all generics, very inexpensive, and the pharmaceutical benefit managers control most prescriptions for expensive drugs. These factors combined with the low prevalence of this disorder and well as the responsiveness to psychotherapy and supportive measure will not produce a windfall for Big Pharma.

There is an inherent bias by some against medical interventions for any disorder that seems to start out as a phenomenon seemingly explained by social or psychological factors. Grief was listed as one of the four major causal factors for depression in Interpersonal Psychotherapy (IPT) and there were no complaints.  IPT has been around for 40 years. Is that because the treatment emphasized was psychotherapy?  Throughout my career I have always had resources available for people who were grieving. Clergy are a professional resource but with the continued secularization of the country it is common to find that most people do not have an identifiable clergy person. Grief support groups are very common – both as self-help groups and groups run by professionals. The question is what if those resources are not enough to assist the grieving person? 

The third argument is that there will be “false positives” or people given the diagnosis when they are emerging from the symptoms. That supposes that the doctor has no discussion with the patient about what might be helpful including non-medical supportive measures and watchful waiting. It also supposes that the patient’s interest in what is happening with them specifically how it is affecting their life and whether they want to do anything about it is never discussed.  I don’t think most doctors – even if they are in a hurry operate that way.

The fourth argument is the danger of making a diagnosis and how that impacts the person. Grief is a universal phenomenon that everyone experiences many times in their life. Everyone knows that through experience. Empathically discussing with a person that this episode of grief is affecting them differently than others does not seem to be discounting or minimizing their emotions or experience to me. The very definition of empathy is that the patient agrees with the empathic statements as adequately explaining their experience.

A fifth argument buried in there is that clinician want to rapidly classify people so that they can get reimbursement. I have already addressed each half of that argument about but let me add – does naming a disorder mean that it did not exist before? There are thousands of examples in medicine and psychiatry of new diagnoses that basically classify earlier conditions where the diagnosis was never made before. A striking example from psychiatry is autoimmune encephalitis.  It was previously misdiagnosed as either a psychosis or bipolar disorder until the actual diagnosis was discovered. Rapid classification leads to many paths other than reimbursement. In the case of autoimmune encephalitis – life saving treatment.

The fundamental problem in writing articles about human biology from a political perspective is that it fails to address the biology. The biology I am referring to here are unique human conscious states and all of the associated back up mechanisms that make them more or less resilient, intelligent, and creative. Is the general classification “grief” likely to capture a large enough number of possibilities to qualify as a rigorous definition? We have known for some time that is not supported by the empirical evidence and that evidence has become more robust over the past 20 years. A small number of people experiencing grief will have a much more difficult time recovering and, in some case, will not recover without assistance. In spite of that, there remain biases against studies that focus on elucidating biological mechanisms or treatments.  It is easier to invoke emotional rhetoric like medicalization or psychiatrization and try to avoid the issue.  To the author’s credit none of those terms were used.

There is also the issue of what this new diagnosis suggests in terms of the science of psychopathology. Does this mean we are closer to classifying all of the possible problems of the human psyche and developing treatments? It reminds me of what one of my psychoanalyst supervisors used to say about the state of the art.  In those days there were basically biological psychiatrists and psychotherapists. He referred to anyone without a comprehensive formulation of the patient’s problem as a dial twister. Are we closer to becoming dial twisters?  I have some concerns about the checklist approach associated with the diagnosis and its understudied phenomenology. That is compounded by the limited time clinicians have to see patients these days and the predictable electronic health record templates with minimal typing of formulations.

Practical considerations aside only time will tell if the new research leads to better identification and treatment of people with clear complications of grief. That does not mean that science has all of the answers. It should be clear that the science of prolonged grief disorder like most of psychiatry only deals with the severe aspects of human experience.  There are clearly other ways to conceptualize grief and learn about it without science. The science is useful for mental health practitioners charged with providing treatments to the severely distressed and with grief the vast majority of people (90+%) will never see a practitioner and even fewer than that will ever see a psychiatrist.

 

George Dawson, MD, DFAPA

 

1:  Ellen Berry.  How Long Should It Take to Grieve? Psychiatry Has Come Up With an Answer. NY Times March 18,2022.

2:  Eisma MC, Rosner R, Comtesse H. ICD-11 Prolonged Grief Disorder Criteria: Turning Challenges Into Opportunities With Multiverse Analyses. Front Psychiatry. 2020;11:752. Published 2020 Aug 7. doi:10.3389/fpsyt.2020.00752

Excerpted per open-access article distributed under the terms of the Creative Commons Attribution License (CC BY).

3:  Prigerson HG, Horowitz MJ, Jacobs SC, Parkes CM, Aslan M, et al. (2013) Correction: Prolonged Grief Disorder: Psychometric Validation of Criteria Proposed for DSM-V and ICD-11. PLOS Medicine 10(12): 10.1371/annotation/a1d91e0d-981f-4674-926c-0fbd2463b5ea.

4:  Lenferink LIM, Eisma MC, Smid GE, de Keijser J, Boelen PA. Valid measurement of DSM-5 persistent complex bereavement disorder and DSM-5-TR and ICD-11 prolonged grief disorder: The Traumatic Grief Inventory-Self Report Plus (TGI-SR+). Compr Psychiatry. 2022 Jan;112:152281. doi: 10.1016/j.comppsych.2021.152281. Epub 2021 Oct 21. PMID: 34700189.

5:  Shear MK, Reynolds CF, Simon NM, Zisook S. Prolonged grief disorder in adults: Epidemiology, clinical features, assessment, and diagnosis. In Peter P Roy-Byrne and D Solomon (eds) UpToDate https://www.uptodate.com/contents/prolonged-grief-disorder-in-adults-epidemiology-clinical-features-assessment-and-diagnosis#H210445955 accessed on 03/21/2022

6:  Klerman GL, Weissman MM, Rounsaville BJ, Chevron ES.  Interpersonal Therapy of Depression.  Basic Books, New York, 1984.

7:  Ratcliffe M. Towards a phenomenology of grief: Insights from Merleau-Ponty.  European Journal of Philosophy 2019; 28: 657-669  DOI: 10.1111/ejop.12513

8:  Clayton PJ. Bereavement in Handbook of Affective of Disorders.  Eugene S. Paykel (ed). The Guilford Press. New York. 1982  pages 413-414

Supplementary 1:

Quote from an initial post on this subject 9 years ago as written by Paula Clayton, MD:

"There are many publications that deal with treating psychiatric patients who report recent and remote bereavement. It is possible to find a real or imagined loss in every patient's past. However, for the most part, because there is little evidence from reviewing normal bereavement that there is a strong correlation between bereavement and first entry into psychiatric care, those bereaved who are seen by psychiatrists should be treated for their primary symptoms. This is not to say that the death should not be discussed, but because these people represent a very small subset of all recently bereaved, they should be treated like other patients with similar symptoms but no precipitating cause. A physician seeing a recently bereaved with newly discovered hypertension might delay treatment one or two visits to confirm its continued existence, but treat it if it persists. So the psychiatrist should treat the patient with affective symptoms with somatic therapy but only if the symptoms are major and persist unduly. A careful history of past and present drug and alcohol intake is indicated. Then, the safest and most appropriate drugs to use are the antidepressants. Electroconvulsive therapy is indicated in the suicidal depressed." (Paykel p413-414)

Abortion, Women's Mental Health, and Politics...

Let me preface this post by saying that I am not a member of a political party and I do not endorse any political views about abortion.  The only interest that I have in abortion is what women tell me about it in the context of a psychiatric evaluation and treatment.  I also do not want to see women's mental health become a surrogate end point for the political debate on abortion.  In the state where I practice the Minnesota Department of Health mails a report on the number of abortions in the state with a number of warnings about the legal requirements of reporting abortions (p 51-57 of this report) despite that fact that 99+% of all physicians and 100% of psychiatrists do not perform abortions.  I bristle when I get that politically motivated report each year.

I am writing this post to examine whether or not any objective research on the mental health effects of abortion can be done.  This examination was precipitated by a post on a forum of the Time story "Abortion Doesn’t Negatively Affect Women’s Mental Health: Study".  Whenever I see an article like that I think of two things - the life experiences that women have told me over the years and where abortion fits in.   I also try to think about how I would do a study of this issue.  What would constitute mental health?  Most large studies don't depend on interviews anymore and that typically means a checklist or some sort of psychometric instrument.  There are typically cutoff scores and comparisons of cutoff scores between the research subjects and a control group.  Correlations are made with come psychiatric diagnosis or psychological construct to determine mental health.  With that kind of technology the underlying assumption is that these are good measures of mental health and that it covers all of the possibilities.  Human consciousness covers a lot of ground and there are generally subtle problems that don't get covered by these gross measures.

The study in question (1) is based on telephone interviews semiannually over a period of 5 years of a cohort of women selected for having an abortion, having a first trimester abortion, being turned away from access to an abortion and giving birth and being turned away from access to abortion and not giving birth.  In their results section, the authors plot the results of 11 interviews, but they point out that the subjects participated in an average of 8 over the 5 year period.  The women who received an abortion presented within 2 weeks of the clinics gestational limit for abortions (N=452).  Women with pregnancies up to 3 weeks past the gestational limit were turned away.  The turnaway group either gave birth (N=161) or had an abortion or miscarried (N=70) as possible outcomes.  Based on those outcomes they were identified as the turnaway-birth and turnaway-no-birth groups.   The first trimester group (N=273) was included to study whether or not the psychological outcomes differed if a woman had an abortion early or late during the pregnancy.

The test metrics were all Likert scales.  The depression and anxiety ratings came from the Brief Symptom Inventory (BSI) a 53 item rating scale of various psychological symptoms.  There are grouped ratings for 9 different symptom constellations including anxiety and depression.  All subjects are asked to rate their level of distress due to a symptom on a severity score ranging from 0 (not at all) to 4 (extremely).  For anxiety and depression their are 6 items each and subjects were identified as a "case" of anxiety or depression if their aggregate score were 9 of the total possible score of 24.  

Life satisfaction was determined by one item from the Satisfaction with Life Scale: "I am satisfied with my life."  One item was also included for self esteem.  Both were rated on a 5 - point scale from 1 (not at all) to 5 (extremely high life satisfaction/self esteem).

Using these variables, the trends were best illustrated in graphics of depressive cases versus time and depressive symptoms versus time (figure 1 above) and similar graphics for anxiety, self esteem, and life satisfaction.  The general trend was for less anxiety and depression slightly higher self esteem and life satisfaction over the 5 year course of the study.  I think analysis of the latter two elements was limited by the the single items 5 point scale and a regression toward the midpoint of the rating.  There is the usual extensive statistical analysis of what I would see as fairly limited data.  The turnaway groups and the near limit group generally had more depressive and anxiety symptoms and cases and lower self esteem and life satisfaction that the first trimester abortion group.  Their statistical analysis is consistent with those observations.

The authors conclude:  "Our findings add to the body of evidence rejecting the notion that abortion increases women’s risk of experiencing adverse psychological outcomes. Women who had an abortion demonstrated more positive outcomes initially compared with women who were denied an abortion."  In their secondary analysis they show that a history of previous mental health problems or psychological trauma correlated with adverse outcomes and may have worse outcomes if they are denied an abortion.  They discuss the importance of individualized care and recognizing the response to an abortion or in this case denial of abortion.  One trend that I did not see any specific comments on was the turnaway-no-birth group and the fact that it seemed to have the best outcome at 5 years in terms of depressive symptoms/syndromes and higher self esteem and life satisfaction.  In their overall conclusion the authors believe that their study shows that there is no necessity for laws warning women about the adverse psychological consequences of abortion and that being denied an abortion is potentially more detrimental.  

In their own discussion of the limitations of the study, loss of subjects over time was significant - 43% over 5 years.  They discuss the methods they used to limit bias due to loss (potentially of subjects with mental illnesses).  They discuss their alteration of the BSI and point out that it is really a screening instrument so that the identified cases in their study would require additional screening for an actual diagnosis of an anxiety disorder or depressive disorder.  

I had several thoughts when I read this study.  Women don't generally come in to psychiatrists and say they are depressed or anxious as the result of an abortion or a denied abortion.  That might be different in psychiatric clinics that specialize in women's health issues.  They often don't discuss the issue at all in the initial diagnostic evaluation.  They disclose these details along with other sensitive issues after a relationship has been established with a psychiatrist.  In that context there can be discussions about thoughts, images,  and feeling states related to abortion into other forms of psychopathology.  An example would be intense guilt, rumination, and self criticism about the abortion during an episode of depression.  When any person gets depressed it is a common experience to scan past personal history for stressful events from the past that lead to the same emotion.  There can be daydreams and fantasies of what the child would have been like.  There can be brief episodes of depression or anxiety related to self criticism, doubt, shame, or interpersonal conflict about having had an abortion.  Many of these thoughts can occur at a future date when the history of an abortion can take on new meaning such as a new committed relationship.   Any life event that impacts person's conscious state and causes them distress is significant to me, whether it is picked up by rating scales or not.  I would see these reactions as being part of normal emotional life rather than anything pathological.

Equating the mental health of women to a DSM diagnosis  or psychometric construct is a mistake.  The DSM is a product of looking at the 5% of people who are outliers and trying to characterize their problems with with categories or continua.  That approach removes human consciousness from the equation and that should no longer be acceptable to psychiatry or anyone interested in the conscious life of real people.  An event with as much potential meaning as abortion can never be adequately characterized as a psychiatric diagnosis or a psychometric scale.  The reactions are too diverse and nuanced.  Suggesting that abortions or the lack of abortions does or does not affect women is more of a political statement than a statement that takes into account the most important aspect of the human psyche - the unique conscious state of every person.  That conscious state is unique because what happens over the course of your lifetime matters and some events matter more than others.

My conclusion from practice is that abortion is one of many events that has the potential to significantly impact the conscious state of a woman.  That should be the consideration in the case of contraception, pregnancy prevention, and abortion and not whether or not it causes mental illness or symptoms.  A woman's unique conscious state should also be considered in the case of unplanned pregnancies and why that decision is much more complex than a list of social variables or whether or not contraception is used.  A more appropriate focus on conscious state rather than mental illness or symptoms would yield a more realistic idea about the effect of life events like abortion.  That result will be anything but simple and that is why simplistic political solutions or response to those solutions do not apply here.

I have a secondary conclusion about the place of politics in both the research and clinical care of women.  It has no place at  all.

It is as obvious as an annual vaguely threatening letter about abortion reporting to a psychiatrist from the state government.  When politicians practice medicine nothing good happens, but this letter goes way beyond that.


George Dawson, MD, DFAPA


References:

1:  Biggs MA, Upadhyay UD, McCulloch CE, Foster DG. Women's Mental Health and Well-being 5 Years After Receiving or Being Denied an Abortion: A Prospective, Longitudinal Cohort Study. JAMA Psychiatry. 2016 Dec 14. doi: 10.1001/jamapsychiatry.2016.3478. [Epub ahead of print] PubMed PMID: 27973641.

Attributions:

1:  Graphic at the top is from Reference 1 with permission from the American Medical Association - Order Number 4024950066424

2:  Thanks  to Pearson Assessments for sending me a sample copy of the Brief Symptom Inventory.  www.pearsonassessments.com

Is The FDA Contraindication On Bupropion Wrong?

Since moving to a strictly outpatient consulting practice, I have been amazed at the number of women who are taking bupropion despite the above contraindication.  I have probable seen 50 women who were under my care in this situation.  In other words, I did not prescribe the bupropion and before seeing this would not have considered prescribing against an FDA contraindication.  The patients I see often have additional contraindications including a history of seizures, sedative hypnotic drug withdrawal, or alcohol withdrawal.  Seizures are the final common pathway for this subset of contraindications.  I have never really observed a seizure from bupropion and the vast majority of the patients with the contraindications have never had a seizure.  I have certainly observed and treated seizures in inpatient settings and understand that there is a low but significant risk of mortality with seizures.  I have also not observed a significant complication of seizures, but at the time I worked in an inpatient hospital environment with rapid access to nursing staff, medications, and experts.  None of the patients that I have initiated treatment on with bupropion have reported seizures, but I was strictly following the contraindication as listed in the FDA package insert.

My dilemma in this situation is always whether or not to continue the bupropion, especially when the patient tells me that it is the only medication that has been effective for them.  Patients who are seen in their late thirties or later generally have been tried on numerous antidepressants from several classes and that complicates the clinical picture.  Most of them have never seen a  psychiatrist and all of the medication trials have been done by primary care physicians.  It is common to see SSRI and bupropion combinations initiated by nonpsychiatrists.   In my current capacity, I am not treating any of these patients long term.  I see them anywhere from 1 to 3 months and at that time they return to see their personal physician or psychiatrist.  I try to contact their personal psychiatrist about the issue but communication among physicians is often difficult to complete.

As I began to see more and more of these patients my first question was a scientific one.  I was aware of the the trials that lead to the decision about eating disorders.  There were all based on immediate release preparations rather than the sustained release (SR) or extended release (XL) versions.  It certainly is possible that I am only seeing the success stories and that the patients with seizure related complications never come to my attention, but the practice of prescribing bupropion to a population that the FDA considers high risk seemed to be on the rise rather than decreasing.  Is it possible that all of the other prescribers had also not heard of this complication.  I knew that most of the patients were never apprised of the contraindication.  I know that because I had them read the contraindication section of the package insert for themselves.  Most would say that nobody have ever told them about this especially the part about any prior diagnosis of anorexia nervosa or bulimia.  It is difficult to tell a 45 year old woman who had bulimia nervosa in college and recovered that the bupropion that she has been taking for the last 10 years without any side effects needs to be stopped because of this contraindication.  The psychiatrists I talked with all minimized the wording in the warning.  They ignored the part about "prior diagnosis".  In fact some initiated treatment as the patient was completing treatment in a specialized eating disorders program.

I turned to the FDA web site for additional guidance on the agencies definition of contraindication.  Was it as relative as these psychiatrists were telling me?  It turns out the definitions used by the FDA in package inserts are defined in the Code of Federal Regulations (CFR).  The section defining contraindications follows (p. 6 of 18):

(5) 4 Contraindications. This section must describe any situations in which the drug should not be used because the risk of use (e.g., certain potentially fatal adverse reactions) clearly outweighs any possible therapeutic benefit. Those situations include use of the drug in patients who, because of their particular age, sex, concomitant therapy, disease state, or other condition, have a substantial risk of being harmed by the drug and for whom no potential benefit makes the risk acceptable. Known hazards and not theoretical possibilities must be listed (e.g., if severe hypersensitivity to the drug has not been demonstrated, it should not be listed as a contraindication). If no contraindications are known, this section must state "None."

People seem to think that there is room for interpreting this definition of contraindication and it does beyond the APA Ethics Committee.  I got the same opinion from an attorney.  I also consulted a national expert on eating disorders.  That expert opined that the contraindication was relative in both  a history of eating disorders and acute eating disorders.  The expert also had inside knowledge of why the FDA might have issued the contraindication in the context of scant evidence.

I have previously posted that the FDA seems to exhibit some biases when it comes to psychiatric disorders.  In some cases they seem to not consider the severity of the the disorder in considering contraindications.  There should be no question that eating disorders and depression are very serious conditions, serious enough that therapeutic options may include some risk.

In the meantime, I have decided to take some action.  The FDA web site is a wall with no way in for people like me with a legitimate problem.  I sent letters out to the US Senators from my state to try to find a way in.  My goal is to get this contraindication taken out so it reflects current clinical practice and the experience of depressed patients with both a past history of an eating disorder or an eating disorder.

If you are a person with that history or a psychiatrist who prescribes bupropion in the face of this contraindication, please join me in advocating for this change.    


George Dawson, MD, DFAPA


References:

1: Dunner DL, Zisook S, Billow AA, Batey SR, Johnston JA, Ascher JA. A prospective safety surveillance study for bupropion sustained-release in the treatment of depression. J Clin Psychiatry. 1998 Jul;59(7):366-73. PubMed PMID: 9714265.

2: Horne RL, Ferguson JM, Pope HG Jr, Hudson JI, Lineberry CG, Ascher J, Cato A. Treatment of bulimia with bupropion: a multicenter controlled trial. J Clin Psychiatry. 1988 Jul;49(7):262-6. PubMed PMID: 3134343.

The Real Solution To Burnout

One of my favorite things these days is the concept (or is it diagnosis?) of burnout.  It seems to be a popular topic in medical and psychiatric news these days.  In the Psychiatric Times January 2016 edition, Editor in Chief Allan Tasman, MD published a column on burnout entitled My New Years Prescription for You.  He goes on to detail the syndrome and what can be done about it.  He points out the high prevalence of burnout in physicians including house staff, physicians in general and psychiatrists.  These studies generally depend on checklist surveys of symptoms suggestive of "burnout."  Dr. Tasman points out that they are relatively nonspecific and people may not see psychiatrists about burnout until there are more recognizable syndromes of anxiety or depression.

My problem with the concept of burnout is that it doesn't accurately describe the problem.  As I think back on some of my most engaging clinical rotations in training - the teams frequently worked to the point of exhaustion.  The attending came in the next day.  There was an air of collegiality and a lot of learning occurred.  There was a lot of dark humor on the part of house staff.  There was an understanding that all of this exhausting work would end some day when you made the transition to a staff or attending physicians and could work more normal hours.  That was the late 1980s and early 1990s.  As politicians and business people wrested control away from physicians, suddenly most physicians continue to work like they are house staff.  Senior physicians in their 60s are suddenly taking all night call and working 60-70 hours per week.  Hospitalist services were invented requiring physicians to work 7 days on and 7 days off - another exhausting schedule.  I have observed to many of these physicians that they are working like they did when they were house staff - interns and residents.  They numbly shake their heads in the affirmative when I ask them that question.  They also acknowledge the fact that by day 6, their cognitive capacity is markedly diminished.  Suddenly it takes them twice as long to do tasks especially all of the documentation.

The reference to Studer in the Tasman article is interesting.  I don't know if any other physicians have had to suffer through a business consultant-based inservice on how to improve "customer satisfaction scores".  There are discussions on how to introduce yourself to the "customer".  There are the usual business based mnemonics.  Physicians may actually have to demonstrate that they know how to introduce themselves to "customers"!  Think about that for a second, especially if you are a psychiatrist who was trained for years in how to interact with patients rather than customers.  If you are a psychiatrist who passed the oral boards,  you know that failing to make the appropriate introduction led to an immediate failure on that exam.  Now flash forward to the bizarre world where patients are "customers" and now there is a formula designed by business people who know relatively nothing about interacting with patients in a therapeutic manner.   You are expected to demonstrate competency in this shallow business paradigm that is setup to optimize results on customer satisfaction surveys.  This is a great example of how physicians are stressed on a regular basis in health care organizations and their time is wasted.  It is also a great example of how public relations, rather than the latest medical knowledge is the dominant performance metric for healthcare organizations.  If there is a recipe for burnout - this is it.

The dynamics of burnout are the dynamics of many clinical situations that psychiatrists try to address.  The referrals are people with chronic depression or depression that seems to have occurred as a result of a sudden change in their life circumstances.  A common scenario is an unreasonable employer or work supervisor.  I will understand it if the employers jump in here and say that they are entitled to tell people how they want them to work for their salary or that their employees are free to find another job.  Those are political arguments that I don't really care about.  Those arguments are also improbable ways of addressing burnout.

When I am faced with person who is chronically anxious and depressed, chronically sleep deprived due to forced swing shifts or double shifts, is dealing with an obnoxious demanding boss, and is not able to change jobs for economic or insurance reasons - I know the patient and I are up against a wall.  I speculate that there are millions of people in this situation who are diagnosed with one anxiety or depressive disorder or another or chronic insomnia and who are trying to get some kind of treatment to alleviate this stress.  There is no evidence that I am aware of that treatment that targets what is basically a chronic stress response is effective.  There may be some small incremental changes if people feel supported and are getting active feedback in therapy about how to deal with the stress in realistic ways, how the dynamics may have personal meaning, and how to reframe the stressful relationships but many people are likely to stay in treatment for the diagnosis for months or years and have little to show for it.  Many people have the expectation that there is a medication that will restore their ability to function in this situation and not require any significant changes on their part.  That is completely false.

That brings me to the issue of physician burnout.  Burnout is more than the clinical diagnoses that are used to describe people who are experiencing chronic workplace stress.  The current work environment for physicians is designed to produce burnout, anxiety, depression, and all of the associated comorbidity.  One of the central dynamics is administrators with no medical knowledge creating an environment that moves physicians away from patients and creates an onerous clerical and administrative burden.  The large increase in managers has created an environment that is both hostile and full of busy work.  The idea that this is something that can be overcome with medications, meditation, exercise, lifestyle management or psychotherapy leaves a lot to be desired.  It is time that psychiatrists focus on an optimized environment for mental and physical well being rather than than trying to treat the fallout from some of those horrific scenarios.

Addressing burnout in physicians is more than a health and wellness consult.  It is more than a weekend retreat to a local resort.  It is more than "lifestyle changes" when you don't have enough time to have a life.  It is a lot more than going on vacation and realizing that on the day you come back - it is like you never left.  Optimizing the work environment for physicians rather than treating burnout is a good place to start.  Recognizing this when it happens in our patients is also more useful than treating it like depression.



George Dawson, MD, DFAPA





  

Depression and the Genetics Of Large Combinations

from:  CONVERGE consortium.  Nature. 2015 Jul 15. doi: 10.1038/nature14659. [Epub ahead of print] - see complete reference 1 below.         

This is an interesting effort from a large number of researchers looking at candidate genes in major depression. The authors studied major depressive disorder (MDD) in 5,303 Han Chinese women selected for recurrent major depression compared with 5,337 Han Chinese women screened to rule out MDD. The depressed subjects were all recruited from provincial mental health centers and psychiatric departments of general hospitals in China. The controls were recruited from patients undergoing minor surgical procedures in general hospitals or from local community centers. All of the subjects were Han Chinese women between the ages of 30 and 60 with four Han Chinese grandparents. The MDD sample had two episodes of MDD by DSM-IV criteria. The diagnoses were established by computerized assessments conducted by postgrad medical students, junior psychiatrists, or senior nurses trained by the CONVERGE team. The interview was translated into Mandarin. Exclusion criteria included other serious medical of psychiatric morbidity (see details in ref 1). 

Whole genome sequences were acquired from the subjects and 32,781, 340 SNPs were identified, 6,242,619 were included in genome-wide association studies (GWAS). Figure 1 above is the quantile-quantile plot for the GWAS analysis resulting from "a linear mixed model with genetic relatedness matrix (GRM) as a random effect and principle components from eigen-decomposition of the GRM as fixed effect covariates." I won't pretend to know what that methodology is, even after reading the Methods, Supplementary Notes section. I expect that it would take a more detailed explanation and in the era of essentially unlimited online storage capacity, I would like to see somebody post it with examples. Without it, unless you are an expert in this type of analysis you are forced to accept it at face value. I am skeptical of manipulations of data points that provide a hoped for result and can cite any number of problems related to this approach. On the other hand information of this magnitude probably requires a specialized approach. 

In this case the authors found two loci on chromosome 10 that contributed to the risk of MDD. They replicated the findings in an independent sample. 

One of the features that I liked about this paper was the focus on patients with severe depression. I have lost count of the number of papers I have read where the depression rating scores were what I consider to be low to trivial. Many rating systems used in clinics seem to use these same systems for determining who gets an antidepressant and who does not.  Whenever I see that, I am always reminded of the "biological psychiatry versus psychotherapy" debates that existed when I was in training in the 1980s.  Once of my favorite authors at the time was Julien Mendlewicz and anything he would publish in the Journal of Clinical Endocrinology and Metabolism (4-6).  There is a table in one of his studies with the HAM-D scores of the patients with unipolar depression he was seeing that ranged from 30-57 with a mean of 41+/- 10.  For bipolar patients in the same study the range was 30-43 with a mean of 36 +/- 5.  One of those patients could not be rated initially because of severe psychomotor retardation.  These are levels of depression that are not typically seen in depression research from either the standpoint of basic science and probably never for psychopharmacological research.  Much of the research that I am aware of allows for the recruitment of patients with HAM-D scores in the high teens and low 20s.  I don't think that is the best way to run experiments on biologically based depressions or antidepressant medications, but there is rarely any commentary on it.  The CONSORT group in this paper finally comments on this factor as being a useful experimental approach even though Mendlewicz was using it in the 1980s.

The second issue that crops up in the paper is replication.  The authors validate their original work by running a second sample for validation.  That is the approach we would use in analytic chemistry.  If we were using a new technique we would run samples in triplicate or in extreme cases in sets of 5 to make sure we could replicate the analysis.  It reminded of one of the first great genetic marker papers in the field that was published in the New England Journal of Medicine by Elliot Gershon's lab in 1984 (2).  It was an exciting proposition to consider that fibroblasts could be grown from a skin biopsy and the muscarinic cholinergic receptor in those fibroblasts would be a marker for familial affective disorder.   The general observation in this pilot study of 18 patients was that they had an increased muscarinic receptor density in fibroblasts compared to controls and that the relatives with histories of minor depression had receptor densities that were more similar to the subjects with mood disorders than normal controls.  The subjects with familial affective disorder were defined as subjects with bipolar I, bipolar II, or major depression according to Research Diagnostic Criteria (RDC).  No rating of depression severity was made acutely or on a historical basis.  These findings could not be replicated, in the end even by the original lab.  That process played out in the pages of the New England Journal of Medicine (3) and the original findings were withdrawn.  It would be interesting to look at how often a similar debate occurs in a prestigious journal these days.  Estimates of non-replicable findings by the pharmaceutical industry suggests that it should happen a lot more often.   

In terms of the original paper, the sheer amount of information involved in the genetic code is staggering.  Just looking at the 130 millions base pairs on Chromosome 10 and thinking about combinations of 2, 3, 4, 5, or 6 base pairs yields the numbers in the table below entitled "Combinations of 130 million base pairs."  The exponential notation ranges from 10¹⁵ to 10⁴⁵ or a quadrillion  to a quattuordecillion combinations.  Figuring out the best way to determine which combinations are relevant in illnesses with polygenic inheritance will be an interesting process.

  

George Dawson, MD, DFAPA

References:

1:  CONVERGE consortium. Sparse whole-genome sequencing identifies two loci for major depressive disorder. Nature. 2015 Jul 15. doi: 10.1038/nature14659. [Epub ahead of print] PubMed PMID: 26176920.

2:  Nadi NS, Nurnberger JI Jr, Gershon ES. Muscarinic cholinergic receptors on skin fibroblasts in familial affective disorder. N Engl J Med. 1984 Jul 26;311(4):225-30. PubMed PMID: 6738616.

3:  Failure to Confirm Muscarinic Receptors on Skin Fibroblasts.  N Engl J Med 1985 Mar 28; 312: 861-862  PubMed PMID: 3974670.

4:  Linkowski P, Mendlewicz J, Kerkhofs M, Leclercq R, Golstein J, Brasseur M,Copinschi G, Van Cauter E. 24-hour profiles of adrenocorticotropin, cortisol, and growth hormone in major depressive illness: effect of antidepressant treatment. J Clin Endocrinol Metab. 1987 Jul;65(1):141-52. PubMed PMID: 3034952.

5:  Linkowski P, Mendlewicz J, Leclercq R, Brasseur M, Hubain P, Golstein J, Copinschi G, Van Cauter E. The 24-hour profile of adrenocorticotropin and cortisol in major depressive illness. J Clin Endocrinol Metab. 1985 Sep;61(3):429-38. PubMed PMID: 2991318.

6:  Mendlewicz J, Linkowski P, Kerkhofs M, Desmedt D, Golstein J, Copinschi G, Van Cauter E. Diurnal hypersecretion of growth hormone in depression. J Clin Endocrinol Metab. 1985 Mar;60(3):505-12. PubMed PMID: 4038712.


Attribution:

Extended Data Figure 1 is from: CONVERGE consortium. Sparse whole-genome sequencing identifies two loci for major depressive disorder. Nature. 2015 Jul 15.  With Permission from Nature Publishing Group  © 2015.  License number 3672900044284.

Supplementary 1:

The Spine In Psychiatric Practice

I am not talking about the spine as a metaphor, I am talking about the real spine.  I am also not going to discuss some alternate therapies affecting the spine, I am going to refer to it only in the context of actual medical practice.  Maybe it was my interest in chronic pain and neurosurgery that led me to the observations, but many years ago I started to notice the high number of patients who were seeing me and had associated spine problems either associated with their psychiatric disorder or making it worse. As far as I can tell, this problem is really not well addressed in the psychiatric literature.

The spectrum of spinal disorder presentations varied from undiagnosed, to incorrectly diagnosed, to diagnosed and treated many times.  There is also the issue of how normal imaging studies vary greatly with age and eventually produce radiology reports that sound pathological but do not necessarily explain the observed pain or disability.  The usual psychiatric diagnoses included depression, anxiety, insomnia, and chronic pain.  The correct diagnoses were most often only possible by a detailed discussion of the problem.  In many cases the patients I was seeing had never actually seen a physician for back pain.  Let me illustrate with a couple of examples (none of these vignettes represent actual patients).

Patient A is a 35 year old woman being seen for depression.  She is in a stressful work situation because she is expected to be physically vigorous and move many 40 pound boxes of paper per day, but she is limited by neck pain and muscle atrophy in the left arm.  She injured her neck at a different job 5 years earlier lifting a heavy piece of equipment down from a shelf.  She felt immediate neck pain and over the next several weeks had muscle twitching in her left arm.  She did not have health insurance from her employer and was never assessed for the injury.  She has had daily pain since the injury and on days where she has more physical activity, she has more pain and more depression.  She is interested in treating the depression.

Patient B is a 50 year old man being seen for depression and insomnia.  He has a 5 year history of taking zolpidem for insomnia.  He is referred by his primary care physician because he has had to increase the dose of zolpidem to 20 mg/day because of worsening insomnia.  The patient gives a history of no longer being able to sleep on his right side because he has neck pain with radiation to the shoulder that resolves when he changes his sleeping position.  He has seen the Silenor and Lunesta commercials and is interested in changing his sleep medication.

Patient C is a 60 year old woman with a history of multiple upper and lower back procedures including fusions, discectomies, and foraminotomies.  She has also had surgical complications including infections and a cerebrospinal fluid leak.  She is taking oxycodone 40 mg QID with addition 5-10 mg prn doses of oxycodone.  She is also taking lorazepam 1 mg TID for anxiety and drinks wine on a daily basis.  She is referred for treatment of depression and chronic pain.

These three descriptions of patients highlight a number of problems unique to psychiatric practice.  Psychiatrists often see people with degenerative or traumatic changes to their spine that have never been assessed by a physician.  We also see patients who have had intensive surgical treatment and who have been treated in pain clinics for a long time before anyone thought to refer them to a psychiatrist.  In both cases an antidepressant seems to be a proxy for a psychiatric evaluation or an interview that seeks to determine if the spinal problem is a cause of depression, insomnia, or anxiety.  That type of evaluation is fairly straightforward but it does require time and the ability to do a medical and neurological review of systems and recognize common patterns of spinal syndromes.  The risks are minimal and the potential rewards are great for the patient.  I have had people ask me why I was asking them so many "medical" questions or report that their primary care physician wanted to know the same thing.   But I have also had people tell me that they were glad to know that they really had chronic pain from a fixable spinal problem rather than chronic insomnia and a need to take sleep medication forever.

This issue also highlights the issue of a physical exam in psychiatric practice.  When is it necessary and in what context can it be done?  In my first job I recall asking the clinic administrator whether she would provide a room and basic equipment for a physical exam.  She said that she would but in the three years I worked there it never happened.  If there is no adequate place to examine a patient I don't think an examination should be done.  There is also the question of the emotional relationship with the patient.  Many people seeing psychiatrists consider them to be their primary physician and have had many intense discussions with them over the years.  Psychiatrists should be aware of this emotional context and the meaning of any physical touch that occurs in that context and keep the assessment at the verbal level.  Referral to a physician who you know does a thorough neurological and spine exam is indicated for most cases, but in many cases you are seeing people referred from these physicians and it has already been done.  What about imaging studies?  My rule of thumb is to do them only if the patient has been physically examined.  I have physically examined people only in acute care settings and ordered imaging studies (CT and MRI) in that context.

On the positive side a lot can be done within the constraints outlined above, first and foremost is a detailed evaluation of the problem.  How is it that insomnia from neck pain can be treated for years as primary insomnia without any attention being paid to the cervical spine pain as being the likely source of that insomnia?  The only explanation I can come up with is a cursory evaluation of the pain.  Borrowing a page from Engel any psychiatric evaluation of a person with depression or anxiety, insomnia, and pain needs to be as comprehensive as possible.  The evolution of those problems since childhood and the relationship to physical and psychological trauma as well as other major life events needs to be detailed.  Assessing the patient for any possible addictions is another requirement.  A description of the pain and associated neurological symptoms is critical.  I like to review old records, imaging reports and the images themselves if possible.  There are a few of the highlights of what is necessary to come up with a psychiatric plan of care for people with spinal problems.  In many cases, a psychiatrist is the only person addressing their pain, even though they have a known diagnosis of degenerative disk disease and chronic back pain.  It is very useful to have referral patterns and treatment plans established to be able to offer treatment of the pain or associated spinal problem in addition to addressing the identified psychiatric syndrome.

The ability to help this group of patients also has training implications.  You don't learn about the spine, neurosurgery or neurology doing psychiatry rotations in medical school.  I was fortunate enough to have intensive exposure to these areas and to excellent clinicians.  I was also fortunate to work in a multispecialty clinic for 23 years where I had the benefit of discussing these cases with specialists from all fields.  I was also able to walk down to Radiology and discuss films with an excellent neuroradiologist.  The training suggested by Insel with a clinical neuroscience in psychiatry, neurology, and neurosurgery would enhance the evaluation of these problems. 

It pays to focus on both the central and peripheral nervous system when indicated.

George Dawson, MD, DFAPA

"Low T Syndrome" and the Fountain of Youth

Psychiatrists are seeing increasing numbers of male patients who are being treated for low testosterone.  The symptoms of "Low T" are being promoted as a reason to get assessed and treated with testosterone.  Not surprisingly, "Low T" is a highly successful pharmaceutical company promotion.  So successful that testosterone seems to have disappeared from the vernacular, replaced by "T".  I have had the opportunity to follow this controversy for the last 30 years.  Back in the days when there were a subgroup of psychiatrists who considered themselves to be "microendocrinologists" testosterone, LH, FSH, and GnRH were studied along with the components of the hypothalamic-pituitary-adrenal and hypothalamic-pituitary-thyroid axes,  particularly in depressives.  Despite a lengthy but low intensity research effort on gonadal steroids in both men and women the data on baseline neuroendocrine correlates and results of supplemental treatments are equivocal.  That said, most psychiatrists have encountered women who have often had a significant response to treatment with gonadal steroids.  Seeing a consistent treatment effect is difficult.

As a clinical psychiatrist, I have found that the clearest information on drugs is available in the FDA approved package insert.  In the case of the product being marketed by the "Low T" ads is a form of testosterone gel that is available in two different strengths.  The only indication for the the product according to that package insert is primary hypogonadism (congenital or acquired) or hypogonadotropic hypogonadism (congential or acquired).  Any use for treating depression or augmenting antidepressants is off label use.  If testosterone was effective as an augmenting agent it would join the ranks of most antidepressant augmenting agents as being an off label prescription.  There are three related issues.

The first is the diagnosis of primary or hypogonadotropic hypogonadism.  In most cases, my speculation would be that a middle aged man sees or hears about the "Low T" ad and goes in to see their primary care physician and a testosterone level is ordered.  Most authoritative sources like UpToDate state that testosterone replacement should only occur in men who are hypogonadal.  Making that determination generally requires two low testosterone levels or in the indeterminant cases some expertise in the hypothalamic-pituitary-gonadal axis (HPG), as well as access to a laboratory with some specialized endocrine capabilities.  This is the level where most assessments seem to break down.  The range I am used to seeing is total testosterone levels ranging from about 300-1,000 ng/ml.  Scattergrams of testosterone versus behavioral parameters of interest like libido, aggression, and energy usually show low levels of correlation.  Many men are getting treated for (like the commercial suggests) low testosterone, or a level in the low normal range but not in the deficient range.  That takes treatment into the realm of off label indications because they do not have a diagnosis of hypogonadism.  A definitive algorithm (1) from endocrinologists is available including when to refer to an endocrinologist.

The second issue is whether there is any evidence testosterone either treats depression or is an effective agent to augment the effects of antidepressants.  That would conceivably move testosterone to the level of the augmenting agents used in the STAR*D study of depression.  The best guidance in the literature comes from Pope, et al (2) article on testosterone replacement in men 65 years of age or younger taking serotonergic antidepressants, a total testosterone level of less than or equal to 350 ng/ml, a PSA less than 4.0 ng/ml and an incomplete response to the antidepressant.  The author's conclude that there were no significant differences in response to testosterone or placebo gel.  Their conclusion is that the current practice of testosterone supplementation of antidepressants is not supported, but that there may be identifiable subgroups in larger studies.

Pope's observations are also critical in that he is an expert in anabolic androgenic steroid (AAS) abuse and has observed a euphorigenic hypomanic response to both AAS and prescription testosterone.  In his article he cites this response occurring in about 4.8% of 105 volunteers taking the equivalent of 500 mg/week of testosterone or an equivalent.  These observations are critical because they factor in addictive behaviors associated with substance use and Pope's group has proposed criteria for anabolic-androgenic steroid dependence.  The criteria highlight that fact that there are a number of associated mood symptoms including depression during the withdrawal phase.  Screening for an AAS use disorder and associated comorbidity like muscle dysmorphia

The third issue is the risk benefit analysis and that makes testosterone as an augmenting agent more unique than the other STAR*D agents.  Testosterone has unique medical risks beyond any risk of an additive effect with an antidepressant.  The main risk with other augmenting agents is usually rare cases of serotonin syndrome or side effects specific to the agent.  They are essentially being prescribed for the same indication.  With testosterone, there is no professional body advocating for supplementation in men with a eugonadal state and the risks may be significant starting with the contraindications (breast cancer, known or suspected prostate cancer) and warnings (benign prostatic hypertrophy, exposure to women and children, edema, sleep apnea, and the need to monitor a number of biochemical parameters).  There have also been recent articles showing a possible correlation with a number concerns about increased myocardial infarction, ischemic stroke, and other mortality (3,4,5).

So for all of you psychiatrists out there who are being referred men who are being treated for "Low T" or being sent to you with a question about testosterone there are a couple of necessary steps at this point.  Make sure that a diagnosis of hypogonadism has been established.  Let your patient know that testosterone supplementation of antidepressants in eugonadal men at this time is experimental and carries risks.  I would also inquire about a past history of anabolic androgenic steroid use, their conscious experience of that use ranging from mood changes to body image concerns and any prior psychiatric history including a history of addictions or using performance enhancing drugs.  For men considering an evaluation and treatment for "Low T" it is much more complex than filling out an online questionnaire on pharmaceutical company website.  Have realistic expectations about what you can expect, especially if someone is suggesting that testosterone supplementation is a treatment for depression.  Take a good look at the risk and consider that there will probably never be a major study that takes a good look at this issue with a large population of men.  The prospective studies will probably be similar to Pope, et al of about 100 men followed for a short period of time and the retrospective studies will have some innovative designs but they will also be limited by selection factors and significant stratification factors.  That generally means that additional information about risk may only be available in the form of FDA warnings from post marketing surveillance or their own analysis of data that may not be publicly available.

George Dawson, MD, DFAPA

References:

1.  Dandona P, Rosenberg MT. A practical guide to male hypogonadism in the primary care setting. Int J Clin Pract. 2010 May;64(6):682-96. doi: 10.1111/j.1742-1241.2010.02355.x. Review. PubMed PMID: 20518947; PubMed Central PMCID: PMC2948422

2.  Pope HG Jr, Amiaz R, Brennan BP, Orr G, Weiser M, Kelly JF, Kanayama G, Siegel A, Hudson JI, Seidman SN. Parallel-group placebo-controlled trial of testosterone gel in men with major depressive disorder displaying an incomplete response to standard antidepressant treatment. J Clin Psychopharmacol. 2010 Apr;30(2):126-34. doi: 10.1097/JCP.0b013e3181d207ca. PubMed PMID: 20520285

3.  Vigen R, O’Donnell CI, Barón AE, et al. (2013) Association of testosterone therapy with mortality, myocardial infarction, and stroke in men with low testosterone levels. JAMA 310:1829-1836.

4.  Basaria S, Coviello AD, Travison TG, et al.  Adverse events associated with testosterone administration. N Engl J Med. 2010 Jul 8;363(2):109-22. doi: 10.1056/NEJMoa1000485. Epub 2010 Jun 30. PubMed PMID: 20592293; PubMed Central PMCID: PMC3440621.

5. Cappola AR. Testosterone therapy and risk of cardiovascular disease in men.  JAMA. 2013 Nov 6;310(17):1805-6. doi: 10.1001/jama.2013.280387. PubMed PMID: 24193077.

Tip:  Follow the lead authors of these references on Medline and you will have a comprehensive look at the literature in this area.

Hyperbole and a Half blogger on NPR

It's Tuesday night and I just finished a lecture at about 7:40 and headed home.  That involves about a 45 minute drive down Minnesota Highway 8.  The last two days in Minnesota have been bitterly cold.  That first bitter cold that feels like it is 35 below, but it is really only there to steel you against 35 below.  It was actually 19 above.  The only consolation to driving down one of the most dangerous roads in Minnesota in the dark and bitter cold is that I get to listen to Terry Gross on NPR.  To make things even more interesting she was interviewing a depressed blogger with huge appeal on the internet.  She writes the popular blog Hyperbole and A Half.  

Terry Gross started out with a lot of questions about the quirky cartoon character that blogger Allie Brosh uses to represent herself on the blog.  The interview proceeds through some introductory excerpts but comes to the author's depression at about the 13:38 mark and goes for about 20 minutes.  As I am listening to her talk about depression, I am thinking of the hundreds of people I have talked with about their depressions.  I am always trying to find out if I missed anything or if there is a different way to view all of these unique presentations of depression.

Ms. Brosh's description of depression and its personal and interpersonal toll is unique among descriptions of depression I have seen in the media.  She talks about the transition from an emotional depression with excessive emotion and self loathing to a state that is totally devoid of emotion.  The "emotional deadening" in some ways is a relief and she later says that it has lead to reduced anxiety.   She has thought of herself as too emotional and thought it was interesting that she no longer had that weakness.  She blogs about it as Adventures in Depression and Depression Part Two and we have already learned that these were very popular posts on her blog.

In one example, she describes an interaction with a friend telling her that her cat has died and she states she is not able to generate enough "organic emotion" that she needs to be concerned about showing an appropriate facial expression to her friend.  Her concern is that she is doomed to live an emotionless state and that rapidly equates to meaninglessness and eventual suicidal thinking.  She talks about needing to manage this information to protect people and also protect herself from their emotional reaction.  She is eventually able to tell her husband and mother, but even during this interview she discloses that her husband may have heard details of her plan that he had never heard before.  This disclosure is clearly painful and she pauses - overcome with emotion.

The emotion in the interview is familiar to me.  It is how people really describe severe depressions.  They don't recite symptoms in a diagnostic manual, they talk about what the depression means to them and how it affects them and their relationships.  They talk about how it affects their inner life.  They talk about what seems to help and what strategies are useful and not useful.  In the moment, it can be painful to be around a person with depression.  Any empathic person resonates with the emotion in this interview.  At one point Terry Gross apologizes for putting her through it.  Things are tense.

Ms. Brosh talks about the type of interpersonal interaction that was most useful.  She cautions against advice giving like "try yoga" or be thankful for everything that you have and you will come out of your depression.  What was helpful was somebody taking her seriously and listening to her experience especially her thoughts about suicide.  As you listen to the interview she is clearly changed by the depression and has adapted to it.  Her main deterrent to suicide was the impact it would have on the people she loved, but we also hear how tenuous that connection can be during severe depression.  We learn that one of the thoughts that would keep her going if she got depressed again would be the idea that she knows she will come out the other side.  Terry Gross asks her about treatment and whether "any kind of therapy or medication that alleviates some of it?"  She clarifies that she is about 60% recovered.  Despite some initial concerns about medication she found that it (bupropion) was "very helpful".

I found this to be a powerful piece  about depression.  It describes the feeling and thinking state of the depressed person and the associated problems with relatedness.  At one point Terry Gross comments on the artistic aspects of creativity that flows from the depression and Ms. Brosh appreciates than comment.  With all of the abstract discussion of depression in the popular press and the assembly line treatment approach in health care systems, this interview is a more genuine discussion and rich source of information about what it is really like for the person and the struggle to recover.  I highly recommend listening to the audio file and reading the blog.

George Dawson, MD, DFAPA

Collaborative Care Model - Even Worse Than I Imagined

I wrote a previous post about the APA backing the so-called collaborative care model and provided a link to the actual diagram about how that was supposed to work.  I noted a more elaborate model with specific descriptions of roles in the model in this week's JAMA.  The actual roles described on this diagram are even more depressing and more predictive of why this model is doomed to fail in terms of clinical care.  It does succeed in the decades long trend in marginalizing psychiatry to practically nothing and providing the fastest route to antidepressant prescriptions.

Wait a minute - I thought psychiatrists were the Big Pharma stooges who wanted to over prescribe antidepressants and get everyone on them?  Well no - it turns out that there are many government and insurance company incentives to assure that you have ultra rapid access to antidepressants even when psychiatry is out of the loop.  You don't need a DSM-5 diagnosis.  You don't need to see a psychiatrist.  If you pulled up the diagram in JAMA, you would discover that the consulting psychiatrist here has no direct contact with the patient.  In fact, about all that you need to do is complete a checklist.

Copyright restrictions prevent me from posting the diagram here even though I am a long time member of both organizations publishing them.  I do think that listing the specific roles of the psychiatrist, the care manager and the primary care physician in this model is fair and that is contained in the table below:

Roles in Collaborative Care Model

Care Manager	Monitors all patients in the practice Provides education Tracks treatment response May offer brief psychotherapy Describes patient symptoms and response to treatment to psychiatrist. Informs Primary care Physician of treatment recommendations from the psychiatrist
Primary Care Physician	Makes initial diagnosis and prescribes medication Modifies treatment based on recommendations from psychiatrist
Psychiatrist	Makes treatment (medication) recommendations. Provides regular psychiatric supervision. Has no direct contact with the patient.

  

see JAMA, June 19, 2013-Vol 309, No. 23, p2426.

As predicted in my original post, the psychiatrist here is so marginalized they are close to falling off the page.  And let's talk about what is really happening here.  This is all about a patient coming in and being given a PHQ-9 depression screening inventory.  For those of you not familiar with this instrument you can click on it here.  It generally takes most patients anywhere from 1 - 3 minutes to check off the boxes.  Conceivably that could lead to a diagnosis of depression in a few more minutes in the primary care clinic.  At that point the patient enters the antidepressant algorithm and they are they are officially being treated.  The care manager reports the PHQ-9 scores of those who do not improve to the "supervising" psychiatrist and gets a recommendation to modify treatment.

This is the model that the APA has apparently signed off on and of course it is ideal for the Affordable Care Act.  It is the ultimate in affordability.  The psychiatrist doesn't even see the patient - so in whatever grand billing scheme the ACA comes up with - they won't even submit a billing statement.  The government and the insurance industry have finally achieved what they could only come close to in the past - psychiatrists working for free.  Of course we will probably have to endure a decade or so of rhetoric on cost effectiveness and efficiency, etc. before anyone will admit that.

Keep in mind what the original government backed model for treating depression was over 20 years ago and you will end up shaking your head like I do every day.  Quality has left the building.

George Dawson, MD, DFAPA

"Is once a week regular?"

"I never knew what depression was.  I knew that 'I'm kind of sad today...I'm kind of blue today,... the Reds lost.'  I knew that.  This I'm telling you you get on an elevator and the bottom drops out.  You can't stand looking at the sunlight.  You can't wait to get back in bed at night. You're shaking.  You're shivering.  I went through this for about 6 months..."  David Letterman as interviewed by Oprah Winfrey on 1/3/2013


I was out of the country for a couple of years back in the 1970s.  When I got back my younger brothers were watching David Letterman's day time TV show.  Since then I have watched him on a fairly regular basis.  Late night TV watchers often have their favorites and I there are clearly preferences based on personality differences and interview style among the various late night talk show hosts.  Letterman's reputation includes a the fact that he has a fairly quiet life style and few people seem to know the details of his private life.  This year he became a Kennedy Center honoree for his lifetime of achievement in the entertainment industry.

He was interviewed recently, first by Alec Baldwin for his public radio show Here's the Thing and earlier this evening by Oprah Winfrey for her interview series Next Chapter.  In both cases, he discusses his depression, how it affected him and even describes his understanding of why the neurotransmitters dopamine and serotonin  may be important:

" I was amazed by it. I was amazed by the chemical mechanism in your brain that can just drop you like that. And then somebody told me that, "You know what, we’re given these chemicals, these serotonins and dopamine and so forth, because if we didn’t have them, the world would scare the crap out of us." I don’t know if that’s true or not, but when I was depressed it made sense."

In the interview with Baldwin he acknowledges taking an antidepressant ("small dose of an SSRI").  In the interview with Oprah, she asks if he is seeing a psychiatrist "regularly".  He replies" "Is once a week regular?" and after that initial joke goes on to describe weekly sessions that have as the goal personal self improvement or bringing his behavior in line with the person he always thought that he was.

I liked these interviews for several reasons.  Dave's matter of fact presentation of depression, how severe it was and the way it impacted his life was striking.  In a few sentences he was able to contrast it with sadness related to disappointments in life and explain how it allowed him to empathize with people.  Prior to experiencing depression himself he was likely to consider depression something that you should just get over on your own: "Go do some push-ups and you’ll feel better." .  He describes both medical treatment of depression and psychotherapeutic treatment.  His primary care physician was instrumental in referring him for treatment.  He also discussed the overall goal of his current psychological therapy.

I am sure that in the days that follow, the networks will have their medical consultants out there with some talking points on depression.  A discussion of depression as a risk factor for coronary artery disease might be one example.  For the sake of this post, he communicated the problems at several levels very well in just a few sentences and I hope that people get to see and listen to these interviews.

George Dawson, MD, DFAPA

Alec Baldwin.  Here's the Thing Transcript of David Letterman Interview June 18,2012.  (depression segment starts 2/3 of the page down).

Oprah Winfrey.  Next Chapter Transcript of David Letterman Interview January 6, 2013. (depression segment starts 2/3 of the second page down).

Revolutionizing the Treatment of Anxiety and Depression

In a word - computers.

I had the good fortune of training with John Greist, MD  at the University of Wisconsin in the 1980s.  Interestingly, many people have the opinion that Dr. Greist is firmly in the camp of biomedical psychiatry.  He and his long time colleague James Jefferson, MD regularly give Door County symposia on the medical treatment of mood and anxiety disorders.  They are highly regarded for their scholarship and teaching ability.  If you haven't listened closely enough over the years, you might miss the fact that Dr. Greist has consistently pointed out the superiority of psychotherapy for various conditions and that  computerized versions of the same psychotherapy perform as well as seeing a therapist.

At a recent MPS meeting, Dr. Greist gave a presentation on computerized therapy.  He made a compelling argument for computerized psychotherapy based on a recent meta-analysis of effectiveness and a comparison of the cost effectiveness of developing moderately effective drugs compared to very cost effective and potentially more effective computerized psychotherapies.  He was an innovator in the field publishing some of the original research and designing some of the original software.  At this meeting he made a strong argument that the software is inexpensive, potentially as effective and more consistent than human therapists and for many conditions more effective than medication.

If there was any market value in the existing mental health field, Dr. Greist's concept would be disruptive.  It would potentially change the way that treatment is provided, especially treatment of anxiety and mood disorders.   Think about the way that treatment of these disorders is currently delivered.  Twenty percent of the adult population is at annual risk.  About 40 percent of that group seeks treatment primarily through primary care clinics.  Very few people see psychiatrists and very few people need to.  The standard of care for almost everyone else is taking a medication prescribed by a primary care clinic.  Many people are treated with benzodiazepines and sedative hypnotic medications that have no efficacy in anxiety or depression and they continue these medications on a chronic basis.  If psychotherapy is available it is two or three sessions of crisis intervention or supportive psychotherapy rather than research proven therapy for a specific disorder.

The lack of availability of psychotherapy in the health care system is another direct result of managed care and rationing.  Managing most of the anxiety and depression with medications and brief visits is ideal for the bean counters.  Outpatient clinics become an assembly line of 15 minute "med checks".   The only reality is a medication and whether that medication works and is tolerated.   An occasional manager may insist that the clinic double book patients to compensate for missed appointments or extra appointments to generate more revenue.

I noticed  today in an effort to send an e-mail to my internist that his primary care clinic offers e-mail consults on treating anxiety and depression for $40.  That is about what most psychiatrists get paid for a face-to face consultation.  I wonder if the $40 fee includes a description of the psychotherapies that might work better than medication?

Enter computerized psychotherapy.  Instead of waiting to get into a clinic that is based solely on medications, a person with anxiety and or depression accesses an Internet Clinic and proceeds through a number of self-guided and computerized cognitive behavioral therapy options.  There are options for preferences, combination therapies, and inadequate response to computerized therapy.  There is no need to travel to a clinic and there is no waiting.  The therapy is available on demand and for free. The cost of treating thousands of patients is trivial, basically limited to staff to maintain the web site, collect treatment data, analyze outcomes, and modify the software as necessary.

All of this has been a known possibility for about two decades.   Why isn't it happening?  Why is mental health treatment limited to medications when psychotherapy, even by a machine is superior in many cases?  Over those two decades we have seen unprecedented rationing of mental health services.  We have seen what used to be clinical decisions turned into business decisions.  The end result has not only been lower quality clinical care but a complete lack of innovation.  It is time for the pendulum to swing back in the right direction.    

George Dawson, MD, DFAPA

Andrews G, Cuijpers P, Craske MG, McEvoy P, Titov N (2010) Computer Therapy for the Anxiety and Depressive Disorders Is Effective, Acceptable and Practical Health Care: A Meta-Analysis. PLoS ONE 5(10): e13196. doi:10.1371/journal.pone.0013196