10/28/15

Positively NOT Psychiatry

© lightwise | 123RF.com

© lightwise | 123RF.com

Positive psychiatry is a growing phenomenon within the profession of psychiatry. And Dr. Dilip Jeste, a former APA President, seems to be the primary “evangelist” for the positive psychiatry movement. The theme for his year as APA President in 2012 was: “Pursuing Wellness Across the Lifespan.” He said positive psychiatry was the future of psychiatry.  In a Psychiatric News article for June of 2012, Jeste said: “I believe that, as the medical field begins to appreciate the value of positive psychosocial factors in the prevention and management of pathology, positive psychiatry will increasingly take a central stage within medicine and health care.”

David Rettew, a child psychiatrist, wrote of his invitation by Dr. Jeste, to speak at a symposium on Positive Psychiatry at the 2015 annual conference of the American Psychiatric Association (APA) held in Toronto. He was excited by the opportunity and sees positive psychiatry as an opportunity for his profession to become “physician experts in mental health,” as opposed to their current emphasis on mental illness. Dr. Rettew noted that for too long, psychiatry has had two primary interventions: psychotherapy and medications. “Expanding our efforts into domains of wellness gives us so many more avenues to help children and families thrive.”

Jeste is also one of the editors of Positive Psychiatry: A Clinical Handbook, which was just released in June of 2015. Dr. Rettew is one of the contributing authors to that work. Jeste, Barton Palmer (co-editor of Positive Psychiatry), Rettnew, and Samantha Boardman (contributor to Positive Psychiatry) coauthored an article in the June 2015 issue of the Journal of Clinical Psychiatry, “Positive Psychiatry: Its Time Has Come.” They noted how psychiatry has traditionally focused on the diagnosis and treatment of mental illnesses. However, trying to find what causes mental illness and developing “safe and effective treatments” has not been enough to fulfill “the enormous potential of psychiatry to promote human welfare.”

The time has come to integrate positive mental health into psychiatric practice, training, and research and to expand psychiatric expertise to encompass the full spectrum of mental functioning.

Instead of an emphasis on managing mental disorders, Jeste et al. said positive psychiatry is a science and clinical practice that seeks to promote well-being through “assessment and interventions aimed at enhancing behavioral and mental wellness.” As a branch of medicine, positive psychiatry is rooted in biology and seeks to decipher the biological underpinnings of positive psychosocial characteristics (PPCs). “And eventually promote health and well-being through psychosocial/behavioral and biological interventions.“

Positive psychiatry traces its immediate influence to the positive psychology movement that was pioneered by Milton Seligman in the later 1990s. In his presidential address to the American Psychological Association in 1998, he called for “a reoriented science that emphasizes the understanding and building of the most positive qualities of an individual.” These qualities include: optimism, courage, work ethic, future-mindedness, interpersonal skills, the capacity for pleasure and insight, and social responsibility. Similarly, Jeste et al. pointed to how a growing body of research shows that higher levels of PPCs, such as resilience, optimism, and social engagement are associated with objectively measured better health outcomes. You can watch a TED talk given by Seligman, “The New Era of Positive Psychology,” where he describes positive psychology.

Possible biomarkers for positive mental health were noted by Jeste et al. They were: allostatic load, telomere length, oxidative stress, neuroinflammation and immune function. The authors then ran through the “association” of several positive psychological characteristics (PPCs) with biological factors. Jeste et al. believed that by strengthening the development of positive traits through psychotherapeutic, behavioral, social and biological interventions, “positive psychiatry has the potential to improve health outcomes and reduce morbidity as well as mortality.”

Instead of being narrowly defined as a medical subspecialty restricted to the management of mental illnesses, psychiatry of the future will develop into a core component of the overall health care system. Psychiatrists will thereby more explicitly reclaim their role as physicians in addition to their roles as mental health professionals. Clearly, much more work is needed to make positive psychiatry a norm in psychiatric practice, but it is time to start that process.

I’m troubled by the rhetoric of the so-called “positive psychiatry” movement. On the one hand, it is encouraging to hear an eminent psychiatrist like Dr. Jeste call for attention and research into positive psychological traits. Psychiatry has concentrated on the prevention and management of pathology, while it largely ignored positive psychological traits like resilience, optimism and self-efficacy and how important they are in preventing and managing pathology. This next quote, taken from the Jeste et al. article, succinctly captures both what encourages me and sends chills up my spine: “The time has come to integrate positive mental health into psychiatric practice, training, and research and to expand psychiatric expertise to encompass the full spectrum of mental functioning.”

The time has come to consider positive mental health in psychiatry. However, the expansion of psychiatric “expertise” and the authority that will accompany such expertise in modern society is not a positive outcome for society. It has disturbing social and political dimensions that were foreseen and noted by psychiatrist Thomas Szasz over fifty years ago. In his 1977 work, The Theology of Medicine, he said:

In the scientific-technological concept of the state, therapy is only a means, not an end: the goal of the therapeutic state is universal health, or a least unfailing relief from suffering. The untroubled condition of man and society is a quintessential feature the medical-therapeutic perspective on politics: conflict among individuals, and especially the individual and the state, is invariably seen as a symptom of illness or psychopathology; and the primary function of the state is accordingly the removal of such conflict through appropriate therapy—imposed by force if necessary. (Thomas Szasz, The Theology of Medicine, p. 128)

If we value personal freedom and dignity, we should, in confronting the moral dilemmas of biology, genetics, and medicine, insist that the expert’s allegiance to the agents and values he serves be made explicit and that power inherent in his specialized knowledge and skill not be accepted as justification for his exercising specific controls over those lacking such knowledge and skill. (Thomas Szasz, The Theology of Medicine, p. 17)

It seems that within “positive psychiatry,” psychiatrists are seeking to not only maintain their hegemony over preventing and managing pathology, but expand it to “encompass the full spectrum of mental functioning.” There has been a growing concern with the failed promises of psychiatry, such as the identification of biological or genetic cause in the “mental illness.” Critiques of DSM diagnosis have come from within psychiatry from individuals such as Allen Frances and Thomas Insel. Frances was the chair for the DSM-IV. Insel is the Director of the National Institute of Mental Health (NIMH). In Saving Normal, Frances’s critique of the DSM-5 and the medicalization of everyday life, he said: “Unfortunately, the DSM approach has been far too influential—dominating the filed in a way we never intended.” Insel announced before the publication of the DSM-5 that the NIMH would be “reorienting its research away from DSM categories” (see “Psychiatry Has No Clothes”).

It was encouraging to hear Dr. Rettew acknowledge how psychiatry has been having an identity crisis. He alluded to the dominance psychiatry had as “skilled therapists” when it was ruled by psychoanalytic thought. But there is another way to see the consequences of the “explosion of neuroscience” and the “promise of medications.” Just as the reliability and validity of psychiatric diagnosis was effectively questioned, and from within and outside psychiatry, and psychiatrists faced losing their social status and power, they reframed diagnosis along purely biological guidelines and aligned themselves with the pharmaceutical industry.

As Rettew said: “Recent research has revealed that many of the risks of medications may have been under appreciated while the benefits somewhat overblown.”  He noted how neuroscience research has been impressive, but lacking immediate clinical applications. Despite the promise that these results may eventually help improve early identification and facilitate effective treatment with a variety of disorders, “in reality there remains a large number of dots to connect before that actually happens.”

Positive psychiatry seems to be about maintaining hegemony in the face of another serious challenge to its authority. It is not humbly admitting the limitations of a purely biochemical explanation for human behavior, it’s just “kicking the can” of research further down the road. The reductionism of the medical model is still at the heart of how positive psychiatry views psychopathology. Biology is still the “root” of positive psychiatry. Jeste et al. said:

As a branch of medicine, positive psychiatry is rooted in biology and seeks to decipher biological underpinnings of PPCs [positive psychosocial characteristics] and eventually promote health and well-being through psychosocial/behavioral and biological interventions.

Jeffery Liebeman, the president of the APA immediately after Dr. Jeste, has published a book, Shrinks, that purports to tell the story of how psychiatry overcame its dubious past. Lieberman seems more willing to acknowledge the still dominant medical model in psychiatric diagnosis and treatment.  With regard to the field of psychiatry, he said: “Ever since the very earliest psychiatrists began conceiving of disturbed behaviors as illnesses (and even long before), they held out hope that direct manipulation of a patient’s brain might one day prove therapeutic” (Shrinks: The Untold Story of Psychiatry, p. 160).  With regard to diagnosis, he said: “The DSM-III turned psychiatry away from the task of curing social ills and refocused it on the medical treatment of severe mental illnesses.” (Shrinks, p. 147)

Research into the impact of positive psychological characteristics on mental functioning and psychopathology is certainly a good thing, but it is positively NOT psychiatry that should have a controlling, leading role in that research. Its seemingly positive and hopeful view of the future is based upon seeing humanity as biological machines. While not I don’t think this would lead to the dystopian future, like that portrayed in the Terminator movies, the rise of the biological machine would be just as apocalyptic.  For an alternative way of doing psychiatry, see “Psychiatry Is Not Neurology.”

10/19/15

Binge Drinking Biomarkers

© Konstantin Kulikov | 123rf.com

© Konstantin Kulikov | 123rf.com

Over two years ago, the Chair of the DSM-5, David Kuyper admitted that despite telling patients for decades that they anticipated finding biomarkers for psychiatric disorders, that discovery continues to be “disappointingly” out of reach. The hope is that at some future time, the promise will become a reality. “In the future, we hope to be able to identify disorders using biological and genetic markers that provide precise diagnoses that can be delivered with complete reliability and validity.”

In “What are Biomarkers?”, Strimbu and Tavel said by definition, biomarkers are objective, quantifiable characteristics of biological processes. The WHO said a biomarker is almost any measurement that reflects the interaction between a biological system and a potential hazard. “The measured response may be functional and physiological, biochemical at the cellular level, or a molecular interaction.” They cautioned that the overreliance on biomarkers “presents a serious and persistent risk of producing misleading, and in some cases dangerous, erroneous conclusions.” And yet, in many areas of research, it appears this warning is ignored.  Keep this in mind as we review here three different studies into biomarkers for—of all things—binge drinking.

A recent press release announced that a biomarker distinguishing binger drinkers from moderate drinkers among young adults has been found by researchers at the University of Illinois at Chicago. The press release suggested the biomarker, “called phosphatidyl ethanol (PEth), could be used to screen young adults for harmful or heavy drinking such as binge drinking.” The lead author for the study, Mariann Piano, said: “Using a biomarker of heavy alcohol consumption such as PEth along with self-reporting could provide an objective measure for use in research, screening and treatment of hazardous alcohol use among young adults.” But I’m not convinced that it would be an appropriate or even helpful screening tool as suggested.

The association of PEth to alcohol consumption has been known for some time, so the suggestion this was a “groundbreaking” research study examining “the relationship between biomarkers and alcohol consumption” by Brent McCluskey in The Fix was a bit misleading. McClusky later clarified that the study was “groundbreaking” because this was the first study to investigate PEth levels in young adults. A search of just the journal Alcohol and Alcoholism, where the Piano et al. study was published, indicated there were 34 total articles meeting the search criteria of “PEth.”

Dr. Lena Gustavsson was the winner of the ESBRA Award in 1994 for her work on phosphatidyl ethanol (PEth). Aradottir et al. reported in 2006 that PEth was a promising new marker for ethanol abuse. They found that blood concentrations of PEth were highly correlated to alcohol intake. “Its diagnostic sensitivity is higher than that for previously established alcohol markers.”

In 2011, Isaksson et al. noted that since the formation of PEth was specifically dependent upon ethanol, “the diagnostic specificity of PEth as an alcohol biomarker is theoretically 100%.” They added that the half-life of PEth in blood is around four days.

Helender et al. (2012) concluded that PEth was the most sensitive biomarker of current alcohol consumption and prior drinking because the PEth test can detect lower consumption levels.

Jain et al. in 2014 found strong associations between PEth and self-reported measures of alcohol consumption among young injection drug users. They suggested PEth may be a useful marker “in settings where alcohol consumption is difficult to assess,” or to confirm or refute self-reported measures of alcohol consumption.

Kechagias et al. (2015) concluded that PEth was the only marker that could discriminate between abstinence and a moderate daily consumption of alcohol.

So the PEth biomarker would help to confirm whether or not someone is honestly reporting their recent consumption of alcohol. It would NOT be a biomarker to identify at risk binge drinkers. And it seems to have little application for treatment other than as an “honesty test” in treatment to affirm or rule out recent alcohol consumption. It may be a more accurate or sensitive test than a breathalyzer, but that doesn’t strike me as groundbreaking news.

Biological Psychiatry had another study in its in June 2015 issue by Warnault et al. that suggested a gene variant, Met68BDNF, reduced the release of brain-derived neurotrophic factor (BDNF) in mice. These mice would consume excessive amounts of alcohol and continue to drink despite negative consequences. An NIH news release said the researchers treated the alcohol with bitter-tasting quinine. “This suggests Met68BDNF carriers compulsively drink alcohol despite aversive consequences.”

The implication is that in humans, this gene variant may put an individual at greater risk of developing an alcohol use disorder. By administering a pharmaceutical compound developed to mimic the action of BDNF, the researchers were able to stop the compulsive drinking behavior in the mice. “This compound (LM22A-4) may have potential as a therapeutic for humans. It appears to reduce compulsive drinking without a generalized effect on motivation.”

BDNF is a protein in humans that is encoded by the BDNF gene. It acts on certain neurons, “helping to support the survival of existing neurons, and encourage the growth and differentiation of new neurons and synapses.” In the brain, it is active in areas vital to memory, learning and higher thinking. The BDNF gene may play a role in the regulation of stress response and in the biology of mood disorders. The expression of BDNF is reduced in Alzheimer’s and Huntingdon disease. Linda Gabriel described BDNF as Miracle-Gro for the brain.” If you’re interested, Alomone Labs is offering a free sample of human BDNF.

Although an interesting finding, it has only been demonstrated within mice at this point in time. If further research were to show that Met68BDNF in humans was associated with a higher risk of alcohol use disorders, compounds like LM22A-4 may help in reducing the neurochemical element in craving or compulsive drinking. But there’s more to compulsive drinking than just biology and neurochemistry.

The most interesting study to me was reported in News & Views for The Scripps Research Institute. Herman et al. reported that the deletion of GIRK3 subunits (G-protein-gated inwardly rectifying potassium) in mice. They compared “knockout” mice, ones missing GIRK3, with normal mice. During a simulated “happy hour” when access to alcohol was limited to two hours a day, GIRK3 knockout mice consumed significantly more alcohol than the control group of normal mice. When mice were given continuous access to alcohol, conditions where mice do not get intoxicated, the effect was not evident.

There was no difference found between the GIRK3 and control mice in how alcohol was metabolized. Both groups also experienced a similar loss of balance, sleepiness and reduced body temperature in response to alcohol. The researchers thought there were two possibilities. Mice without GIRK3 could be drinking more because they felt more pleasure from alcohol, so they wanted to drink more. Or they felt less pleasure and thus needed to drink more to reach the same level of pleasure as normal mice.

In order to answer this question, they looked at the mesocorticolimbic dopaminergic pathway (the reward pathway in the brain) and found that the pathway was completely insensitive to alcohol without GIRK3. Even at high doses, alcohol did not alter the firing of neurons missing GIRK3. Alcohol also failed to trigger the release of dopamine in the ventral striatum of GIRK3 mice. The results suggested that mice drink more alcohol to boost the engagement of other neural pathways mediating alcohol’s rewarding effects.

By reintroducing GIRK3 in the knockout mice, the researchers were able to alter the binge drinking down to normal levels. Normal mice with increased GIRK3 drank even less. “This has led the researchers to believe that a compound selectively targeting GIRK3-containing channels may hold promise for reducing alcohol consumption in heavy binge drinkers.” An abstract for the study published in the Proceedings of the National Academy of Sciences can be found here.

PEth, BDNF, and GIRK3 are all biomarkers of some sort that are being applied to the potential hazard of “binge drinking.” As Strimbu and Tavel observed, the key issue is determining the relationship between any given biomarker and the relevant clinical endpoints, which in this case is binge drinking. In some cases, biomarkers may be shown to measure the process of a key pathway stage in reaching the clinical endpoint of binge drinking. But assuming this relationship risks mistaking correlation for causation. PEth seems to be an example of a correlational biomarker. And caution needs to be exercised at this point with any conclusions drawn from the findings of studies with BDNF and GIRK3.

While there is growing evidence of a genetic connection with alcoholism, the evidence is not conclusive at this time. Following Carleton Erickson, I’d say that while alcohol dependence runs in families, it is not purely a genetic disease. “Rather, the tendency to become alcoholic is inherited. Thus alcoholism can skip generations, or affect only certain individuals in an alcoholic family.” See “The Genetic Connection” for more discussion on genetic research into alcohol dependence.

11/26/14

The Quest for the Holy Grail of Psychiatry

Our brain: the final frontier. This is the unending quest of research into biomarkers. Its continuing mission: to explore strange new theories, to seek out new mental illnesses and new diagnoses, to boldly go where no psychiatric research has gone before.

The quest for biomarkers (measurable indicators of a biological state or condition) of mental disorders has gone on for decades without success. The recently proposed research strategy of the National Institute of Mental Health (NIMH) know as Research Domain Criteria (RDoC), has proposed to set aside the DSM diagnoses used to frame past mental health research and utilize data from neuroscience, genomics and behavioral science to spell out the etiology of mental illness.

Psychiatrist Giovanni Fava views the RDoC model as “the reflection of an intellectual crisis in psychiatry.” While its “blanket” approach aims to see that all possible biological and behavioral measurements are utilized, Fava thinks it will result in conflicting results that may be difficult to interpret. He said it was “misguided” to assume that nothing will be missed with such a strategy and that “innovative classification systems will ensue automatically.” The complexity of the new approach and the potential for interpretive problems it is illustrated by this recently published article in World Psychiatry, “Biomarkers and clinical staging in psychiatry.”

He pointed out that major clinical challenges were left without independent research. Among these challenges was the problem of the loss of clinical effects during long-term antidepressant treatment. And despite a lack of any evidence to support their superiority, antidepressant drugs are increasingly used as a first-line treatment for anxiety disorders. Studies on psychological treatment were also “scandalously under-supported.”

A major problem in the development of the Research Domain Criteria project has been the fact that its strong ideological endorsement by leading figures of the National Institute of Mental Health has resulted in suppression of an adequate debate. How many investigators who are likely to submit funding applications to that agency may afford disclosing that the emperor has no clothes and that the strategy may be a road to nowhere?

Fava et. al thought the exclusive reliance upon diagnostic criteria had impoverished the clinical process and did not reflect “the complex thinking that underlies decisions in psychiatric practice.” Current diagnostic definitions of psychiatric disorders are based on collections of symptoms from very heterogeneous populations and are likely to yield “spurious results when exploring biological correlates of mental disturbances.”

The large studies of biomarkers across diagnostic categories proposed by RDoC are anticipated to yield improved clinical information. But “such a view is based on the concept of assessment as a collection of symptoms devoid of any clinical judgment and interpretation.” There is no evidence to support the research direction taken by RDoC. Fava et al. noted that although Kapur, Phillips and Insel proposed that new biomarker-defined subtypes be identified, they were not able to “provide exemplifications suggesting that this approach was likely to yield meaningful clinical results in psychiatry.” Incidentally, Thomas Insel is the current director of the NIMH.

Using meta-analyses of biomarkers commonly used in cardiovascular medicine as an example, Fava et al. noted the presence of publication bias and selective reporting. They said biomarkers could end up being the result of various mechanisms and not necessarily the result of a specific disease process.

The complexity of the brain and the spurious nature of measurements that can be recorded constitute a major difficulty for psychiatry. Specifically, the neuroplastic properties make the brain a unique organ that essentially has to be studied and understood in a longitudinal, lifetime and transgenerational perspective.

Biological reductionism was said to have resulted in an approach that is far from the “explanatory pluralism” required by clinical practice. The exclusion of the methodological triad of observation (outer viewing), introspection (inner viewing), and dialogue (inter-viewing) makes this approach unscientific. Either the human realm was excluded from scientific inquiry or the scientific approach was conformed to the reductionistic, mechanistic requirements of the biomedical paradigm.

This restrictive ideology characterizes the Research Domain Criteria. It is time to enrich such criteria with clinically relevant dimensions and add clinical validity to the reliability and reductionism-focused mainstream of psychiatry research.

Elsewhere (“We Are But Thinking Reeds”) I’ve spoken of the necessity to see human nature as a psychosomatic unity of body (soma) and soul (psyche). The human mind is more than just a manifestation of brain activity. Any approach to “mental” illness research that fails to acknowledge this will never entirely succeed in its quest to find the holy grail of psychiatry.

10/15/14

Psychiatry’s Mythical Phoenix

Prominent research psychiatrists are beginning to sound like their “antipsychiatric” critics. They are saying the current DSM diagnostic system isn’t valid; that something new, something scientifically sound and useful for treating patients is needed. One of these research psychiatrists is Thomas Insel, the Director of the Director of the National Institute of Mental Health (NIMH). He dropped a bombshell last year when he announced that the NIMH would be “re-orienting its research away from DSM categories.” The New York Times quoted Insel as saying: “As long as the research community takes the D.S.M. to be a bible, we’ll never make progress. . . . People think that everything has to match D.S.M. criteria, but you know what? Biology never read that book.”

So the NIMH has developed a new research strategy to classify mental disorders based upon “dimensions of observable behavior and neurobiological measures.” This strategic plan is known as: Research Domain Criteria (RDoC). The long-term goal is for RDoC to be “a framework to guide classification of patients for research studies.” It was not meant to be a useful clinical tool. “It is hoped that by creating a framework that interfaces directly with genomics, neuroscience, and behavioral science, progress in explicating etiology and suggesting new treatments will be markedly facilitated.”

RDoC is in search of the holy grail of psychiatry: reliable biomarkers (measurable indicators of a biological state or condition) for mental disorders. This search for biomarkers has been going on for decades. David Kupfer, the chair of the DSM-5 Task Force said: “We’ve been telling patients for several decades that we are waiting for biomarkers. We’re still waiting.” Susan Kamens suggested that the imminent discovery of biomarkers has been “the driving expectation of psychiatry since its birth in the 18th century.” But there are some problems with the RDoC quest.

What RDoC proposes is to replace the DSM diagnoses used currently to frame mental health research with broad categories based upon cognitive, behavioral and neural mechanisms. This means that the NIMH will be supporting research projects that look across or sub-divide existing DSM categories. But this very same DSM is what is used to assess the potential of future NIMH-funded research under RDoC.

In an article found in Nature, “Psychiatry Framework Seeks to Reform Diagnostic Doctrine,” Nassir Ghaemi said: “It is very hard for people who have been following the DSM their entire professional lives to suddenly give it up.” Ghaemi has felt shackled by the DSM. He wanted to do some research that cut across DSM categories. But his colleagues warned him against straying too far from the DSM structure when he applied for funding from the NIMH, because peer reviewers tended to insist on research structured by the DSM. So he held off from applying.

Steven Hyman, a former NIMH director, blames the DSM for hampering research into the biological or genetic basis of psychiatric illness. He said it was “a fool’s errand” to use symptom-based DSM diagnosis with little basis in nature to try and find a biomarker. Hyman urged the NIMH to think about how biomarkers identified by RDoC would be incorporated into mental health practice with the DSM. “It would be very problematic for the research and clinical enterprises to wake up in a decade to a yawning gulf.”

But Susan Kamens sees a deeper problem with blaming the DSM for hampering the search for biomarkers—it takes for granted that the biomarkers exist. In other words, it presumes what it seeks to find. According to Kamens:

“The main difference is belief versus doubt in the hypothesis that what we call mental disorder is primarily a disorder of biology. We treat that hypothesis as unfalsifiable, as if the proof [that mental disorder is biological] arrived before the evidence. We don’t test whether the hypothesis holds; we test whether and how to make the data fit it. When critics raise doubts, they’re often accused of ignoring the very same evidence that psychiatric researchers have recently declared to be utterly insufficient.”

Kamens noted that the RDoC “blueprint” is no less theoretical that the DSM-5. While the RDoC constructs are more measurable than the categories listed in the DSM, they are “essentially no more than basic human emotions and behaviors.”  She asked how RDoC would make clinically meaningful determinations into its “domains” and “constructs”? How would the research reveal anything beyond the coordinates of normal psychological processes? “In other words, how is RDoC anything beyond basic (nonclinical) neuroscience?”

RDoC is developing a new research model that will undoubtedly yield unprecedented data, but it focuses on the biogenetic correlates and normative mapping of basic psychological processes like visual perception, language, fear responses, and circadian rhythms. The idea is to create interventions for psychological and physiological processes that deviate from the norm. For this reason, RDoC is less likely to save psychiatry than it is to resurrect eugenics.

The quest for biomarkers in psychiatry can be likened to the legend of the phoenix, a mythological bird that repeatedly rises out of the ashes of its predecessor. The DSM seems to be near end of its life-cycle. Now psychiatry is building an RDoC “nest” that it will eventually ignite, reducing both the DSM and RDoC to ashes. And from these ashes, it is hoped, a new diagnostic system—a new phoenix—will arise.

Also see my blog post, “Psychiatry Has No Clothes.”