S. Nassir Ghaemi, MD, MPH

SPECIAL REPORT: OCD AND RELATED DISORDERS

BD-OCD comorbidity’s burden and clinical management is a critical issue in psychiatry.

The evidence so far on BD-OCD nosology, which is mainly based on the course of illness, supports the view that the majority of cases of comorbid BD-OCD are in fact BD cases. Obsessive-compulsive symptoms usually are secondary manifestations of depressive or manic mood episodes.

Mood stabilization should be the primary goal in treating patients with BD-OCD. Because of the risk of worsening BD via serotonin reuptake inhibitors-induced mania/hypomania, antidepressants should only be used in a minority of cases of refractory OCD.

In a classic 1970 publication, the famous epidemiologist Alvan R. Feinstein, MD, defined comorbidity in relation to a specific index condition as “any distinct additional entity that has existed or may occur during the clinical course of a patient who has the index disease under study.”

 In Feinstein’s formulation, the implication was that a completely different and independent disease occurred at the same time as another disease. These two diseases co-occurred, more often than not, randomly.

On the other hand, DSM explicitly offers overlapping clinical criteria for many diagnoses, especially mood and anxiety disorders, guaranteeing comorbidity in quite a different sense than in the medical meaning of the term as co-occurrence of independent diseases. Using the DSM definition, it is unclear whether concomitant diagnoses actually reflect the presence of distinct clinical entities or refer to multiple manifestations of a single clinical entity.

A good example of this problem is the comorbidity of bipolar disorder (BD) and OCD. More than half of patients with BD have an additional diagnosis, one of the most difficult to manage being OCD. More than 150 years ago, French psychiatrist BÃ©nÃ©dict-Augustin Morel first described patients with BD-OCD, which resulted in questions regarding nosology and the clinical meaning of this condition.

In a standard 1969 psychiatry textbook, Mayer-Gross and colleagues,

 who had a significant focus on course of illness, included patients with BD-OCD in the manic-depressive disorders.

In the hierarchical approach to diagnosis, which contradicts the DSM comorbidity approach, anxiety presentations like OCD should not be diagnosed as separate conditions when co-occurring with mood presentations such as BD. In other words, OCD should not be diagnosed unless BD is ruled out. If this non-DSM approach is correct, patients with OCD should be evaluated for family history for mood disorders, course of illness of mood symptoms in relation to OCD symptoms, and other evidence of bipolarity.

BD-OCD comorbidity has importance in nosology as well as therapeutic implications. The question of nosology is whether this common comorbidity represents two separate diseases that co-occur by chance, or a severe subtype of BD or OCD. The therapeutic question is whether and how to treat the comorbidity since the main treatment for OCD serotonin reuptake inhibitors (SRIs) can worsen BD.

Although recent studies have looked at the co-occurrence of anxiety and bipolar disorders, there is insufficient research and the relationship between BD and OCD remains unclear. Given the available scientific evidence, however, some observations can be made (

Apparent BD-OCD comorbidity is a common condition in psychiatry (

from a large cross-continental multiple OCD treatment center study (3711 patients with OCD), showed a lifetime prevalence of comorbidity with BD-I and BD-II of 4.5% and 23.7%, respectively.

In our meta-analysis, the pooled prevalence of OCD in BD was 17.0% (95% CI 12.7-22.4), which was comparable to the results reported by the pooled prevalence of BD in OCD (18.35%, 95% CI 13.2-24.8).

Although limited by retrospective study design, small sample size, different thresholds for BD diagnosis (ie, categorical versus dimensional approach) and a different accuracy in diagnosing OCD (ie, discrimination between true ego-dystonic obsessions and depressive ruminations), these results confirm the relevance of comorbid BD-OCD.

Most patients experience the onset of OCD before the onset of BD. Only in a 

, the onset of OCD is concomitant with the first mood episode, rather than preceding or following it.

As reported by recent studies, OC symptoms in 

 seem to increase the risk of a later BD diagnosis, this being suggestive of partially shared etiopathogenetic mechanisms between these severe psychiatric disorders.

 Moreover, results from our meta-analysis showed higher comorbidity rates in youths (24.2%, 95% CI 10.36-41.60, n = 345, z = -9.5) compared with adults (13.56%, 95% CI 10.4-16.25, n = 539).

 Considering course of illness as a key diagnostic validator, especially among patients with a primary diagnosis of BD, most comorbid OCD cases appeared to be related to mood episodes. Obsessive compulsive symptoms in comorbid patients appeared more often-and sometimes exclusively-during depressive episodes, and comorbid BD and OCD cycled together, with obsessive compulsive symptoms often remitting during manic/hypomanic episodes.

Taken together, the evidence so far on BD-OCD nosology, supports the view that most comorbid OCD appears to be related to mood episodes. Obsessive compulsive symptoms in childhood and adolescence may be expression of vulnerability to BD and an increased risk for BD. Obsessive compulsive symptoms would initially coexist with BD symptoms, even cycling together, and would gradually tend to decrease in the adulthood.

 assessed family history for OCD or BD in comorbid BD-OCD probands using clinical interviews and clinical records. The majority of these studies reported a higher prevalence of family history for mood disorders and lower prevalence for OCD in patients with BD-OCD.

 Moreover, a family history for mood disorders was reported to be more frequent in episodic OCD patients than in continuous/chronic OCD patients.

Investigators from the US analyzed the serotonin-transporter (5-HTT) binding potential using positron-emission tomography (PET) and [

C]DASB, a radioligand with high sensitivity and specificity for 5-HTT. They reported higher 5-HTT binding potential in the insula, the posterior cingular cortex, the subgenual anterior cingulate cortex, and the dorsal cingulate cortex in patients with OCD-BD.

From a neurobiological perspective, BD mostly 

hypoactivity in the orbitofrontal cortex (ie, decision making, impulse control) and in the dorsolateral prefrontal cortex (ie, planning, attentional set shifting) with grey matter volume reduction associated to manic episodes. OCD mainly presented hyperactivity of the orbitofrontal cortex with a deficit in emotional processing.

 The overlap of similar cortical-subcortical circuits may partially explain clinical features of comorbid BD-OCD during the course of illness.

If clinical observations are correct, then many patients who are said to have both BD and OCD in fact only have BD, with OCD symptoms being caused by or secondary to mood symptoms. Therefore, mood stabilization should be the primary goal in treating BD-OCD patients.

 The treatment implication would be that such patients would improve with mood stabilizers alone, for both mood and OCD symptoms.

Serotonin reuptake inhibitors would be unnecessary for OCD symptoms and, in fact, could undermine OCD treatment by worsening the underlying causal mood episodes. This worsening could occur in two ways: either by causing mania, which would trigger a mood cycle leading to later depression; or by causing a long-term worsening rapid-cycling course of illness, with more and more mood episodes, in turn producing more and more OCD symptoms. Adding SRIs may be needed only in a minority of patients who have BD with refractory OCD.

Besides mood stabilizers, neuroleptics may also be effective in both BD and OCD. Aripiprazole augmentation to lithium carbonate, even at low doses (10-15 mg/d), seemed to be the best option in comorbid patients with treatment-resistance.

 Reports of exacerbation of OC symptoms with neuroleptic agents tend to relate to schizophrenia, not BD.

Study findings suggest that most cases of DSM-based BD-OCD comorbidity are not in fact comorbidity as defined by Feinstein.

 Rather these are cases of BD, with OC symptoms as secondary manifestations of mood episodes. This observation does not deny the remaining patients who have two separate disorders, BD and OCD, that occur simultaneously.

 is Researcher and Psychiatrist, Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), Section of Psychiatry, University of Genoa, Genoa, Italy; IRCCS Ospedale Policlinico San Martino, Genoa, Italy; and Mood Disorders Program, Tufts Medical Center, Boston, MA. 

is ChargÃ©e d'einsegment et de Recherche, Psychiatrist and Neurologist, Department of Psychiatry, Faculty of Medicine, University of Geneva (UNIGE), Geneva, Switzerland; Department of Psychiatry, ASO Santi Antonio e Biagio e Cesare Arrigo Hospital, Alessandria, Italy

 is Researcher and Psychiatrist, DINOGMI, Section of Psychiatry, University of Genoa, and IRCCS Ospedale Policlinico San Martino; 

 is Associate Professor, DINOGMI, Section of Psychiatry, University of Genoa, and IRCCS Ospedale Policlinico San Martino. 

 is Conjoint Professor, School of Medicine, Western Sydney University, Blacktown Hospital, Sydney, NSW, Australia. 

 is Professor, DINOGMI, Section of Psychiatry, University of Genoa, and IRCCS Ospedale Policlinico San Martino. 

 is Professor, Mood Disorders Program and Department of Psychiatry, Tufts University Medical School, Boston, MA. 

 report no conflicts of interest concerning the subject matter of this article; 

 reports that he is employed by Novartis Institutes for Biomedical Research and holds equity in Novartis.

1. Maj M. Psychiatric comorbidity: an artefact of current diagnostic systems? 

 ed. London: Elsevier Health Sciences; 1969.

3. Brakoulias V, Starcevic V, Belloch A, et al. Comorbidity, age of onset and suicidality in obsessive-compulsive disorder (OCD): an international collaboration. 

4. Amerio A, Stubbs B, Odone A, et al. The prevalence and predictors of comorbid bipolar disorder and obsessive-compulsive disorder: a systematic review and meta-analysis. 

5. Tonna M, Amerio A, Odone A, et al. Comorbid bipolar disorder and obsessive-compulsive disorder: which came first? 

6. CederlÃ¶f M, Lichtenstein P, Larsson H, et al. Obsessive-compulsive disorder, psychosis, and bipolarity: a longitudinal cohort and multigenerational family study. 

7. Amerio A, Odone A, Liapis CC, et al. Diagnostic validity of comorbid bipolar disorder and obsessive-compulsive disorder: a systematic review. 

8. Amerio A, Tonna M, Odone A, et al. Heredity in comorbid bipolar disorder and obsessive-compulsive disorder patients. 

9. Joshi G, Mick E, Wozniak J, et al. Impact of obsessive-compulsive disorder on the antimanic response to olanzapine therapy in youth with bipolar disorder. 

10. Ekman CJ, Lind J, RydÃ©n E, et al. Manic episodes are associated with grey matter volume reduction - a voxel-based morphometry brain analysis. 

11. Amerio A, Maina G, Ghaemi SN. Updates in treating comorbid bipolar disorder and obsessive-compulsive disorder: a systematic review. 

12. Fonseka TM, Richter MA, MÃ¼ller DJ. Second generation antipsychotic-induced obsessive-compulsive symptoms in schizophrenia: a review of the experimental literature. 

Articles

This review highlights an important diagnostic and therapeutic task: the importance of differentiating true bipolar disorder/obsessive-compulsive disorder comorbidity from BD with secondary OCD.

Differentiating Comorbid Bipolar Disorder and OCD

Early on, psychiatry accepted the idea that unconscious psychology affected the body to cause disease. By the 1970s, the rise of psychiatric drugs pushed the field in a biological direction, and by the 1980s, psychoanalysis was in full retreat, at least in the halls of psychiatric power. S. Nassir Ghaemi, MD, adds to the debate.

Can We Salvage the Biopsychosocial “Model”? 

The Nine Lives of Biopsychosocial Framework

The Postmodern Assumptions of the Biopsychosocial Approach

I appreciate my friend Dr Ron Pies’ thoughtful essay,

Can We Salvage the Biopsychosocial Model? A Reformulated Biopsychosocial Paradigm Can Be Clinically Useful

, where he accepts some of my central criticisms of the biopsychosocial (BPS) model. However, I think the problem goes beyond the issue of whether it was a model in a scientific sense, as opposed to a more general approach to a worldview.

The key problem, if I were to simplify it in one sentence, is that the BPS model for the past half century has served as a postmodernist excuse for eclecticism.

The BPS of the past half century is not the same BPS of George Engel in 1977, or for that matter Roy Grinker of 1954, when the term was first coined. Grinker and Engel were psychoanalysts who specialized in “psychosomatic medicine,” which meant finding unconscious emotional causes for medical diseases. Engel was a gastroenterologist who specialized in ulcerative colitis and worked on a consultation-liaison psychiatry service. In the 1950s and 1960s, their views were mainstream. Psychiatry was highly psychoanalytic so it accepted the idea that unconscious psychology affected the body to cause disease. By the 1970s, the rise of the new psychiatric drugs was pushing the field in a biological direction, and by the 1980,s psychoanalysis was in full retreat, at least in the halls of psychiatric power (chairmen of departments, funding, organizational leaders). Engel and Grinker were nearing the end of their careers, and 

 to turn the clock back to 1957. He was, essentially, seeking to preserve a place for psychoanalytic ideas in medicine.

This history may or may not be relevant to current defenses of the BPS model, such as those of my friend Ronald Pies. One could argue, as Dr Pies does, that the BPS model could be revised and accepted on its own merits, irrespective of what Engel intended or its roots. But this would be like saying Marxism can ignore Marx, or psychoanalysis Freud. In fact, all such ideologies evolve, and one can reject many aspects of the founder’s ideas. But not entirely. Or if one goes so far away from the original concept, then why keep the label? Socialists don’t need to be called Marxists. Psychotherapists who accept the idea of unconscious emotions don’t need to be labeled psychoanalysts. Both Marx and Freud have useful insights; that’s what matters, not their ideologies. I would say the same about Grinker and Engel: they had insights which may be valuable, but that doesn’t mean one has to cling to the BPS label.

Postmodernism (PM), in my usage, is a philosophy, rooted in Schopenhauer and Nietzsche, and expressed most clearly later by Heidegger and Foucault.

 It rejects the Enlightenment heritage in its claim that science can replace religion as the source of independent truths. (There is more to it; but let’s focus on this point). PM in this classic form is relativistic and critical (or cynical) about science in general, and psychiatry in particular (the target of much of Foucault’s ire). If PM is accepted, there are two options: nothing is true-nihilism; or anything can be true-eclecticism.

That is how the BPS model has played out in the past half century. Mental health clinicians do whatever they like, and they claim support for that anarchy in the BPS approach. This attitude leads to over-prescibing of psychiatric drugs (giving drugs for any and all kinds of symptoms); incorrect use of psychotherapies (letting therapists do their favorite therapy for everyone); and unnecessary mixes of both (a common refrain is that both treatments are better than either alone, a statement that is false, or at least unproven, when made generically).

American culture has become highly postmodernist in the last half century (beginning with the 1960s counterculture), and this is why, in my view, so many clinicians are attracted to the postmodernist-influenced PM model.

Postmodernism is not an epithet. I am not sure why so many colleagues are unwilling to accept it. This is a description, not a criticism. There are insights to be had in Nietzsche which are very important. Karl Jaspers, who with Heidegger founded existentialist thought, was able to apply PM insights while not being relativistic about science.

Ideas are unconscious too. Many of the readers of this article will have postmodernist-influenced ideas without knowing so. For instance, any defense of science is commonly criticized as if one does not know of critiques of science based on PM-related concepts like pragmatism and social constructionism (Pierce, Popper, Kuhn). One can accept those critiques and still defend science.

So I defend science qua science, understood non-simplistically with all its limitations. And that is what psychiatry needs-to be more scientific, like all of medicine, not to hang on to a false eclectic theory. The problem is less with phrasing (model versus approach) but rather with content. What benefit does the BPS approach provide? What does it add to a wise science (e. g, Jaspers’ work in philosophy) informed by a general humanism (eg, William Osler’s tradition in medicine)? There are plenty of good ideas beyond this disproven psychosomatic medicine tradition.

 is a psychiatrist and researcher with expertise in depression and bipolar illness, and training in philosophy and public health. He is Lecturer on Psychiatry at Harvard Medical School and Professor of Psychiatry at Tufts University. He also directs early drug discovery at Novartis Institutes for Biomedical Research in Cambridge MA. He is the author of multiple books, most recently 

The Rise and Fall of the Biopsychosocial Model 

(Johns Hopkins University Press, 2009). He has published over 200 scientific articles or book chapters. He is an associate editor of 

, on the editorial board of a number of journals, and active in numerous professional organizations. The views expressed here are solely his own and do not reflect those of his employers or 

Dr Ghaemi reports he is an employee for Novartis Institutes for Biomedical Research, Cambridge, MA.

1. Pies RW. Can We Salvage the Biopsychosocial “Model”? A Reformulated Biopsychosocial Paradigm Can Be Clinically Useful. 

https://www.psychiatrictimes.com/couch-crisis/can-we-salvage-biopsychosocial-model

Rise and Fall of the Biopsychosocial Model: Reconciling Art and Science in Psychiatry.

 Baltimore, MD: Johns Hopkins University Press; 2010.

The need for a new medical model: a model for biomedicine

4. Dennett DC. Postmodernism and truth. 

Way to Wisdom, An Introduction to Philosophy.

 New Haven, CT: Yale University Press; 1951.

Is bipolar disorder overdiagnosed? Underdiagnosed? Neither?

These questions are the focus of a presentation that S. Nassir Ghaemi, MD, MPH, will make at the American Psychiatric Association Annual Meeting, during the symposium “Bipolar Disorder: Update on Diagnosis and Treatment.” In this podcast, Dr Ghaemi offers his perspective on those questions.

Dr Ghaemi is Professor of Psychiatry, and Director of the Mood Disorders Program at Tufts Medical Center, and a member of the 

Is Underdiagnosis the Main Pitfall When Diagnosing Bipolar Disorder? Yes

Is Underdiagnosis the Main Pitfall in Diagnosing Bipolar Disorder? No

The Mistaken Claim of Bipolar ‘Overdiagnosis’: Solving the False Positives Problem for DSM-5/ICD-11

Podcasts

Is bipolar disorder overdiagnosed? Underdiagnosed? Neither? In this podcast, Dr S. Nassir Ghaemi offers his perspective on those questions.

Bipolar Disorder: Update on Diagnosis

Can Validity and Pragmatism Go Hand in Hand?

In my reference to Prof. Decker’s excellent history of DSM-III, I don’t mean to imply that Prof. Decker herself agrees with my interpretation of her exposition. Readers can judge for themselves if the facts she uncovers agree with my interpretations or hers. To adapt an old saying: the facts are the facts; interpretations can differ. Besides her book, readers should also consult the work of the historian Edward Shorter (

The main problem here is not that past DSM leaders were derelict or purely political. The problem is that they now say that they would place science below pragmatism, meaning whatever they think is best, as the core criterion for revising DSM. This is a clear statement that DSM is unscientific; it doesn’t require much interpretation. Furthermore, I maintain that any science, whether physics or psychology, has certain basic standards, the first of which is actually believing that there are right answers, and seeking to get them right. The pragmatic approach of these DSM leaders is to try to reach consensus on what the profession wants, irrespective of whether it is right (meaning proven scientifically whatever extent that might be considered acceptable; I’ve provided numerous examples in my own interactions with the DSM-IV leadership on this point). Prof. Decker shows that DSM-III started with scientific intentions, and she also shows how far away it went from those intentions. The fact that she herself is not willing to draw that conclusion reflects her own interpretation of psychiatry as a profession. My view is that we should try to be as scientific as possible, and not settle for as little science as has been allowed into the DSM process. This doesn’t mean that I’m setting the standard at astrophysics. I just think, as she noted, that if a huge scientific literature supports a concept like personality dimensions, then the APA Board of Trustees should not have the power to veto it.

I would like to clarify a few matters of detail:

(1) Of the 10 personality disorders in DSM-III, there still are basically no studies proving scientific validity (using the 4 Robins/Guze validators) for 7 of them. This is the case now; it was the case in 1980. Hence, MOST personality disorders were included by Spitzer in 1980 without any evidence of scientific validity, and this remains the case. Even for the other 3, borderline PD being one of them, there was hardly any evidence of scientific validity for that condition in 1980. The fact that Spitzer was meticulous in defining it doesn’t mean that he had the scientific evidence that it was a valid diagnosis. Prof. Decker seems to conflate reliability and validity here.

(2) She may be correct that Dr Spitzer did not directly seek to mollify the psychoanalytic community on the issue of personality disorders. Her book makes it clear, though, that the psychoanalytic community was a hugely powerful constituency that needed to be won over before DSM-III could be ratified. Personality disorders were one aspect of that process (as was the axis II concept in general, and other matters: the unscientific broadening of “major depressive disorder” to include concepts of neurosis, as Edward Shorter so well documented from the APA archives.)

(3) The issue of schizoaffective disorder is well-described. I was in communication with some members of the schizoaffective committee for DSM-5. There has been a large amount of research in the past 3 decades on this topic, supporting a major revision in the concept. It seems to have little evidence as a legitimate scientifically valid diagnosis. The schizoaffective researchers I spoke with agreed, but one member of the committee ended further discussion of attempting to influence the DSM-5 task force on this matter, with the comment: “They are clear they will not make any major changes.” No science, of any variety, works this way. If some in our profession are fine with this approach, so well documented by Prof. Decker, they are entitled to that view. But I think we should have a higher standard, as is the case in most other medical disciplines, and give science a higher priority than the pragmatic preferences of a profession from 33 years ago.

"The main problem here is not that past DSM leaders were derelict or purely political. The problem is that they now say that they would place science below pragmatism," according to this clinician.

Science and “Pragmatism” in DSM: A Question of Priorities

A Spirited Exchange about the Biology of Mental Disorders and DSM-5

and Nassir Ghaemi is, I contend, good for the field.  Rather than avoid the sensitive or uncertain issues, both psychiatrists turn to face them with their own thought provoking styles and piercing insight. Would that we had more such collegial exchanges in psychiatry. Drs Pies and Ghaemi model for us how to abandon our defensiveness in an objective, respectful and passionate discourse. 

, our field is highly complex, quite young and "our understanding of the biology of mental disorders has been slow in coming." But it is, in fact, slowly progressing. The question of how long it will take to gain a more precise understanding of the underpinnings of mental illness has no definite answer. Or as Dr Theodore Pearlman has stated - "is any psychiatrist's guess."

And so in this spirit of continued scholarly dialogue, I offer a well-reasoned, trenchant response to Dr Ghaemi by Dr Pearlman, which can be found at the end of Dr Ghaemi’s esssay.

Dr Ron Pies makes many insightful comments 

. My view about why DSM revisions have been unscientific is based on concepts of science that are in agreement with much of what he describes. If science is defined as some kind of systematic study of observed experience applied to hypotheses or theories, and then confirmation or refutation of those hypotheses or theories, followed by new hypotheses or theories that are further tested and refined by new observations – if this is the core of any scientific inquiry, I think that no objective observer can attribute the history of DSM-III, IV, and 5 to anything that approximates this process.

Let’s review this history, so well documented now by historian Hannah Decker with archival, often unpublished evidence for DSM-III.

 In the 1970s, scientific studies that meet the above definitions were collected mainly by researchers centered at the Washington University of St. Louis, and about 2 dozen diagnoses were found to be definable based on such empirical evidence. These were published a few times, lastly in 1978, as the Research Diagnostic Criteria. Within 2 years, Robert Spitzer had taken those scientifically-based diagnoses as the basis for DSM-III, but, through an immense amount of political wheeling-and-dealing (documented in painful detail by Decker), he produces 292 diagnoses. Obviously, in 2 years, a huge amount of scientific research did not suddenly identify 270 new diagnoses. Fourteen years later, with DSM-IV, 365 diagnoses were produced, but the original 270 were little changed. Now, about 20 years later, we still have almost 400 diagnoses, with little change in the original 292 from the Groundhog Year of 1980. 

How were these other 200 to 300 diagnoses developed? Was it through a scientific process? As so well documented by Decker and historian Edward Shorter

and others who observed the process, like Michael Alan Taylor,

 these other diagnoses were based almost entirely on the opinions and beliefs of leaders and interest groups in the psychiatric profession. Why do we have about 10 personality “disorders”? Because psychoanalysts believe in those ideas. Were those ideas tested with observational studies, and then revised based on confirmations and refutations of their content? Not before 1980, and hardly since. As an example, Taylor describes a DSM-IV conference on personality where a huge amount of scientific research was presented on personality traits, and then the DSM-IV leaders stated clearly that they would ignore that scientific evidence and would hardly change the DSM-III personality disorder definitions at all.

 Twenty years later, after literally thousands more studies with some of the best possible scientific evidence possible in experimental psychology, the DSM-5 task force had no choice but to admit the need to add personality dimensions to the nosology. It got all the way to the APA Board of Trustees, and within weeks of publication, was simply rejected tout court.

The original DSM-III personality disorders were almost completely based on psychoanalytic opinion, with hardly any scientific validity literature to support them, as documented well by Hannah in her archival research. In the intervening 30 years, a number of scientific validity studies (using the classic nosology validators of phenomnelogy, course, genetics, and biological markers) have invalidated most DSM-IV personality disorders; in other words, they have been falsified scientifically. In fact, this was the scientific conclusion of the personality disorder research summary provided for DSM-5 by the world’s most prominent personality researchers.

 And yet DSM personality disorders have remained little changed in DSM-5 by fiat. This is another proof of being unscientific: the DSM nosology refuses to accept the falsification of its cherished beliefs. 
 
This is the problem. It’s not complicated, and philosophically difficult. If you have opinion, and nothing else, it’s not science. If you refuse to change your opinions, it’s not science. Most of DSM has been based on opinion, and our profession has refused to change most of that opinion for 2 generations. How can anyone imagine that any profession would ever experience progress, much less scientific progress, if it refuses to change its opinions, themselves based on nothing but prior opinion?

We are much more ignorant than Hippocrates over 2 millennia ago. He knew that opinion breeds ignorance, while science is the father of knowledge. We mistake our opinions for science.

Dr Pies’ attempt to distinguish the terms “scientific” and “validity” is mistaken when applied to DSM, I think, partly because he uses the word “valid” in both English and scientific usage, which is not the same. “Validity” when applied to nosology means that a diagnosis is true; it exists; it is not wrong. Cancer is valid; drapetomania is not. This is different from the English usage, when Dr Pies says [in his footnote] that the steady-state theory of the universe was invalidated by the Big-Bang theory. In the latter example, physicists were testing hypotheses by evidence, and changing their theories based on those experimental results. That’s science.

In the DSM process, psychiatric leaders enforce their opinions, and then they refuse to change them at all based on any experimental research. That’s not science. There are some cases, much less common, where DSM changes have been based on scientific evidence. So my claim here is not absolute, but it does reflect the predominant approach in DSM changes for the 4th revision almost entirely, and for the 3rd and 5th revisions mostly.)  

Worse, the leader of DSM-IV is explicit that science is low in priority and should not be valued as the main method of revising diagnosis.

Instead, he says, we should base revisions mainly on “pragmatism,” meaning what DSM leaders think is good for everyone else. (

: It seems clear to me that pragmatic concerns for patient welfare always trump ‘science,’ especially since the ‘science underpinning psychiatric diagnosis is so thin and subject to alternative interpretations.”)

As usual, the disciples are far inferior to the master. Freud knew better when he wrote in Future of an Illusion: “No, our science is no illusion. But an illusion it would be to suppose that what science cannot give us we can get elsewhere.”

Nosological validity means applying scientific methods of hypothesis and experiment, and – most importantly – changing theories and hypotheses based on observations and experiments. This is not how the original 292 DSM-III diagnoses came about, and it is certainly not how they’ve been handled for the last 3 decades. 

That’s why science and nosological validity (based on the 5 validators described by Dr Pies-see footnote) are synonymous in the field of psychiatric diagnosis. There’s no way to be scientific unless you use examine the evidence, which comes from those 5 areas.  That’s nosological validity; that’s science.

The issue is not whether scientific ideas are later “invalidated”; here Dr Pies is using the word in its English meaning, not in its technical meaning in the science of nosology. Validity in nosology means studies that use the 5 validators (or pathology); that is different from the use of the term in the general English meaning that something is tested and confirmed based on experiment. The KIND of experiment varies from science to science: in histology, validity is based on microscopes; in astrophysics, telescopes; in psychiatric diagnosis, the 5 validators. The use of the word “invalidated” is English, and different from the term “validity” in nosology.

If you divide the 2 dozen somewhat validated psychiatric diagnoses, by the 400 or so claimed by DSM-5, we can precisely state that DSM-5 is about 97% unscientific. We need to change the attitude of 2 generations in our profession: paying lip-service to science, and then ignoring it. 

The Making of DSM-III®: A Diagnostic Manual's Conquest of American Psychiatry.

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As an elder psychiatrist practicing before and after DSM-III became the standard diagnostic handbook for psychiatrists in the 1980s, I take issue with Dr Ghaemi’s position that DSM lacks scientific credibility. Dr Ghaemi wants psychiatry to confine its knowledge to diagnosing and treating only some dozen of the 265 DSM listed disorders-the conditions which he believes are the only true diagnosable psychiatric diseases. The rest Dr Ghaemi asserts, are essentially psychogenic entities, formulated through self-deception and agreed upon falsehoods by members of the DSM task forces in order to seemingly promote reliability but lacking true validity.

I believe that far from deviating from scientific truth, the task forces of DSM were spurred towards seeking a truthful classification of psychiatric illnesses for sound research and treatment purposes. Various criteria influenced this authenticity. Firstly, the DSM represented an atheoretical classification of mental disorders and avoided non-creditable speculation as to causation of psychiatric illness. Nowhere in the manual does the term disease associated with a functional psychiatric disorder appear; which would erroneously imply proven structural brain pathology. Furthermore, in accordance with the concept of true illness, each diagnosis required a level of malfunction causing clinically significant distress or impairment in social, occupational or other important areas of functioning.

Before the advent of DSM-III, clinical psychiatry was bogged down by unproductive emphasis and debate on what appeared biological and genetic, versus psychological reactions to adverse environmental or personality factors. Hence as Dr Ghaemi has inferred, Sir Martin Roth, past doyen of British psychiatry and knighted by Queen Elizabeth for his services to British psychiatry, asserted that endogenous depression [phased in DSM-III into the nomenclature of Major depression] was exclusively a biological disease. Reactive depression termed neurotic depression by Roth was considered exclusively psychogenic in origin and to be managed with psychotherapy alone.

The problem with the Roth concept that endogenous depression is a structural brain disease is that the argument fails to mandate any proof of brain pathology. Instead there is speculation about the existence of innate brain molecular dysfunction which science thus far has failed to elucidate. Despite the unquestionable efficacy of antidepressants and ECT with endogenous depression, its pathology remains largely unknown. Symptom relief with SSRI and SNRI drugs or ECT does not directly imply an innate deficiency of brain amines, much as aspirin relieving fever in cases of strep throat does not imply deficiency of innate anti-fever substances in the body. How long psychiatry will take to discover the structural brain pathology of severe depressive illness, like bacteriology concerning the etiology of strep throat discovered centuries gone by, is any psychiatrist’s guess. In the meantime, while we wait for discovery of brain molecular pathology underlying endogenous depression, the DSM classification of depressive disorders on a continuum of diminishing severity namely from major to dysthymia, and both treatable with integrated biological and psychological treatment, remains psychiatry’s closest alignment to creditable scientific methodology and towards the ongoing search for the whole truth.

Theodore Pearlman, MD
Irvine, California
 

Diagnostic and Statistical Manual of Mental Disorders

, Fourth Edition; American Psychiatric Association, Washington D.C. 1994.
2. Slater E. Roth M. 

, Bailliere Tindall and Cassell: London: 3rd Edition, p. 10-13 1969.

If science is defined as some kind of systematic study of observed experience applied to hypotheses or theories, and then confirmation or refutation of those hypotheses or theories, followed by new hypotheses or theories that are further tested and refined by new observations – if this is the core of any scientific inquiry, I think that no objective observer can attribute the history of DSM-III, IV, and 5 to anything that approximates this process.

Why DSM-III, IV, and 5 are Unscientific

[[{"type":"media","view_mode":"media_crop","fid":"15680","attributes":{"alt":"","class":"media-image media-image-right","id":"media_crop_5094651023296","media_crop_h":"0","media_crop_image_style":"-1","media_crop_instance":"778","media_crop_rotate":"0","media_crop_scale_h":"213","media_crop_scale_w":"160","media_crop_w":"0","media_crop_x":"0","media_crop_y":"0","style":"float: right;","title":" ","typeof":"foaf:Image"}}]]Almost 2 decades ago, when I graduated from psychiatric residency, DSM-IV was published. You will receive this letter along with, I’m sure, the spanking new shiny edition of DSM-5. I have one wish for you. When 20 years and another generation pass, I hope this will be the last of the DSMs. My wish is that in one more generation, our profession will learn to go beyond DSM to the truths of science.

When I graduated a generation ago, I accepted DSM-IV as if it were the truth. I trusted that my elders would put the truth first, and then compromise for practical purposes where they had no truths to follow. It took me 2 decades to realize a painful truth, spoken now frankly by those who gave us DSM-III when Ronald Reagan was elected and DSM-IV when Bill Clinton was president: the leaders of those DSMs don’t believe there are scientific truths in psychiatric diagnosis-only 

It might not have been so bad if, as the framers of DSM-III wished, reliability had been a way station to validity. First, let’s agree on what we call things, then we can study them better and change the definitions to get gradually closer to the truth.

 Robert Spitzer, who headed the DSM-III task force, may have believed this idea, too, when he published the 

 in 1978 with the leaders of the famed Washington University, St Louis, department of psychiatry.

 After about a decade or two of research, they provided their best available research-supported diagnostic criteria for about 2 dozen psychiatric diagnoses.

This was the high-water mark of science in American psychiatry.

But immediately the project went awry. Spitzer used the Research Diagnostic Criteria as the basis for DSM-III. He convened his task force work groups, and a dozen diagnoses became a hundred. He then took the results of the task force to the 

 (APA) assembly (mostly psychoanalysts), which is equivalent to the president sending a bill to Congress. Diagnoses became fruitful and multiplied. The Board of Trustees of the APA had to finalize and approve DSM-III. Somewhere along the line, 2 dozen diagnoses became 265 disorders (not modifiers), without a single piece of new scientific evidence for the other 241.

I suggest you read new historical books that carefully study the 

 You’ll understand why about 90% (241 of 265) of DSM-III diagnoses are unscientific, and you’ll also understand how even the poor 2 dozen that had decent scientific evidence were distorted and deformed.

Take major depressive disorder-a meaningless term. Have you ever wondered why it is “major”? The historian Edward Shorter describes how the initial goal had been to include severe depression as a 

 psychiatric diagnosis, since so many milder depressive presentations (which used to be called “neurotic depression”) can happen solely in relation to the stresses of life or perhaps because of a personality disposition. In either case, these mild chronic depressive/anxiety presentations (which also used to be called “community nervousness”) are quite different from the severe episodes of depression that begin and end, and alternate with long periods with little or no depression.

These severe episodic depressions were seen before DSM-III as part of manic-depressive illness, in contrast to neurotic depression, which was seen either as a personality state or as a reaction to the stresses of life only.

 On the basis of genetic and course studies, the Washington University researchers agreed with Kraepelin’s German critic, Karl Leonhard, that the severe recurrent depressive episodes are different from recurrent mania alternating with depression, so they took the view that the first condition should be called “unipolar” depression and the second “bipolar” disorder.

The term “bipolar disorder” was formalized in DSM-III in 1980 and remains little changed. You will note the term “unipolar” is nowhere to be found in DSM. The DSM-III leadership realized that the APA could not accept the removal of the concept of “neurotic depression,” which was the main insurance coding used to pay psychoanalysts, with nothing to replace it. So they proposed the term “minor” depression instead, and unipolar depression was defined, in contrast, as “major” depression-minor and major: the original proposal.

Eventually the word “minor” got dropped because of concerns among APA psychoanalysts that it would be accompanied by minor insurance reimbursement.

” and “generalized anxiety disorder” were recruited to replace it, and the “major” depression definition was broadened to include not only the severe episodes of depression, as in the original unipolar concept, but all shades of mild to moderate severity and chronicity. The Washington University researchers, led by Eli Robins, were disgusted and withdrew from the DSM-III process, which had replaced science with a host of political compromises. The most erudite European psychopathologists, like Sir Martin Roth, warned that this mangling of neurotic depression into MDD was a major scientific and clinical mistake.

 Such wise warnings went unheeded. The DSM-III task force plowed on.

We have lived with this largely unscientific definition of “major depressive disorder” for almost two generations, and nobody dares change it. It is the same in DSM-5 with 

 as it was when it was gerrymandered into being by DSM-III when Ronald Reagan was elected. Somewhere along the way, the goal of validity was jettisoned, and what we decided in 1980 has become so dear to us that we cannot bear to change a single word of it.

Did you ever wonder why two generations of studies in 

and even pharmacology have mostly failed in psychiatry? Because they were doomed to fail by a diagnostic system that was “pragmatically” made up for professional, not scientific, purposes. Why should nature decide to order genetics in the same way that we want insurance companies to pay us?

Yet strident critics of DSM, often psychologists, are wrong: they want to claim that there is no part of psychiatry, not a single shred, that is medically legitimate: there are no diseases in psychiatry. But there are psychiatric diseases (eg, schizophrenia, manic depression), just not almost 200 of them.

Can anyone accept this notion? That DSM is not 100% false (it is 91.9% false, based on the original 2 dozen RDC criteria divided by 297 DSM-IV diagnoses), and not 100% true either. That there are diseases (in psychiatry as well as in medicine), but most clinical pictures (in medicine as well as in psychiatry) are not diseases.

The whole DSM system leads to this confusion and debate. The system has become ossified, like a Politburo that refuses to change. Reform is no longer an option: DSM-5 could have been that change, but it couldn’t enact even the addition of dimensions to personality traits, one of the most strongly proven scientific facts in psychology. When the APA Board of Trustees rejected personality traits as part of DSM-5, we lost the chance for a Gorbachev to reform the system. Now we can only wait for a wholesale change, a Yeltsin standing on a tank. Or, barring that, we will succumb to professional hibernation for generations more.

Our DSM leaders did not lie; they deceived themselves, which is worse, because then they could honestly mislead the rest of us. Our strident antipsychiatry critics do not lie; they mistake half the truth for the whole, which is worse, because irrationally held truths are more harmful than reasoned errors.

Good intentions abound all around, so respect everyone with whom you disagree; but don’t forget to keep disagreeing. Good intentions aren’t enough.

If we are ever to get to validity, we need to have the courage to start anew. Let 

-who gets paid for what-not just for physical but for mental illnesses. Let researchers use pure research criteria in defining psychiatric diagnoses. And then leave clinicians free to use the best of what they know to diagnose, or not to diagnose, not because they are told to do so in a certain way by DSM, but in their best judgment of the art and science of psychiatry. This works fine for other medical specialties; it can work well for us, and it would be a huge advance over pretending that false DSM “disorders” have some kind of reality.

I trust clinicians; DSM leaders don’t. I don’t trust DSM leaders; I trust you.

Frances A. DSM in philosophyland: curioser and curioser; 2010. 

 Klerman GL, Vaillant GE, Spitzer RL, Michels R. 

Spitzer RL, Endicott J, Robins E. Research diagnostic criteria: rationale and reliability. 

The Making of DSM-III®: A Diagnostic Manual’s Conquest of American Psychiatry.

2nd ed. New York: Oxford University Press; 2007.

 Roth M, Kerr T. The concept of neurotic depression: a plea for reinstatement. In: Pichot P, Rein W, eds. 

The Classification of Endogenous Psychoses. 

This psychiatrist's wish is that in one more generation, our profession will learn to go beyond DSM to the truths of science.

Requiem for DSM

I write to you as an American who was once not an American. Of course, all Americans, at one time, were not Americans, but there is still a prototype: the Christian American of European descent. I’m not in that majority, so I write to you as something of an American, but also as a non-American.

You ask me what I would advise a young psychiatrist beginning a career in another country? I would first bring to your attention what you already know: the world has one great power-America. This country is not just a military power; it is a cultural force. In psychiatry, it has taken over almost every country at least as effectively as its political forces vanquished Soviet communism.

All psychiatry, anywhere in the world, is American psychiatry. This is both bad and good.

All psychiatry, anywhere in the world, is American psychiatry. This is both good and bad.

Author | S. Nassir Ghaemi, MD, MPH

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