I never imagined that 40 years later, as a psychiatrist, I’d be reading about this incident in connection with one of the most mysterious mass outbreaks of neurological symptoms in recent memory. And yet, this past January, the environmental-activist-cum-movie-star, Erin Brockovich, began investigating a possible connection between that chemical spill and the bizarre outbreak among a group of LeRoy Junior-Senior High School students.

I truly don’t know what explains the strange constellation of signs and symptoms seen in this group of young people. I’m not sure anybody does. Most of the expert opinion has settled on the description of “mass psychogenic illness.”

Some clinicians have used the term “conversion disorder,” which, in the older psychiatric classification (DSM-II), was considered a type of “hysterical neurosis.” (Subsequent DSMs expunged the terms “hysteria” and “neurosis” for a variety of reasons.) From the reports I have read, the teenagers involved have had a thorough medical and neurological evaluation. Dr. Gregory Young of the N.Y. Department of Health told NBC News, “We have conclusively ruled out any form of infection or communicable disease and there’s no evidence of any environmental factor.’’

My colleague and CNN mental health expert, Dr. Charles Raison, recently reviewed this story in a thoughtful commentary. He concluded—quite reasonably—that “conversion disorder is a plausible explanation” for the tics, verbal outbursts, and apparent seizures afflicting this group of 12 or more adolescent females. (It seems that one male and a 36-year-old female are also among those now showing tic-like symptoms).

But as Dr. Raison rightly observed, “No one likes conversion disorder as an explanation for the tic epidemic. Patients feel insulted, stigmatized and dismissed. Their parents feel dismissed and terrified that something medical has been missed… And what doctor worth his or her salt would be truly satisfied with an explanation that tells us nothing about the cause of the disease or how to specifically treat it?”

Indeed, there are many difficulties with both the concept of conversion disorder and the secondary explanation of “mass contagion.” When I was in residency, one of my revered teachers used to say, “Beware of diagnosing hysteria. It’s usually the last diagnosis the patient will ever receive.” She meant that once a patient had been labeled with “conversion disorder” or “hysteria,” no doctor would ever again take the patient’s symptoms seriously. The patient could end up in the emergency room with crushing, substernal chest pain radiating to her jaw—classic symptoms of a heart attack—and still be labeled “a hysteric!”

But the problems with “conversion disorder” go much deeper. First of all, what exactly is being “converted” in this disorder? This particular diagnosis—listed among the so-called somatoform disorders– is actually an anomaly in the modern-day classification scheme. As even many non-psychiatrists know, the current DSM-IV normally uses a combination of personal history, behavioral observations, and reports from the patient as the basis for diagnosing a given disorder. The premise behind the post-DSM-II classification schemes is that the diagnostic criteria should not speculate on “hidden” or internal causes, such as the “unconscious defense mechanisms” so dear to psychoanalysts.

Indeed, with a few exceptions—for example, Adjustment Disorders, Post-traumatic Stress Disorder, and certain disorders due to medical or neurological causes—the DSM-IV steers clear of “explaining” much of anything. So again: what is being “converted” in conversion disorder? In truth, nobody knows. In psychoanalytic theory—not necessarily synonymous with the truth—it was hypothesized that a repressed idea or unconscious conflict was “converted” into a bodily (somatic) symptom, such as a paralyzed limb. In effect, the psychoanalysts argued that the body would “speak” for the mind’s dark, submerged impulses—particularly in young females. For example, a wife’s unconscious, “forbidden wish” to strike her husband might lead to sudden paralysis of her arm.
But no scientific study or experiment has ever proved this theory—nor is such proof likely, given the obvious difficulties in spotting those repressed ideas as they are mysteriously transformed into bodily impairments.

But even if the psychoanalytic theory were somehow proved, we would then have the further difficulty of explaining the “contagion” effect—how the “hysterical neurosis” leaps from the initial sufferer to other nearby individuals, as has been theorized in LeRoy. Does the original unconscious conflict get converted into some sort of electromagnetic wave that travels to the brains of susceptible victims? Or, more plausibly, do we need to invoke sociological theories, involving empathic “identification” of suggestible subjects with the initial sufferer? Perhaps so—but here, too, we are more in the realm of speculation than of science. And yet, there is no denying that history records many outbreaks of what, for lack of a better term, we call “mass psychogenic illness” –often, but not always, among young females.

In recent years, advances in neuroimaging have fostered more “brain-based” studies of so-called conversion phenomena. For example, Dr. Jon Stone and colleagues in Edinburgh, Scotland, studied patients diagnosed with conversion-related ankle weakness, and compared them with control subjects instructed to simulate the same symptom—that is, control subjects were told to “fake” ankle weakness. Using a technique called functional magnetic resonance imaging (fMRI), these researchers found a distinctive pattern of regional brain activation in the conversion subjects. The pattern overlapped with, but differed from, that seen in the “simulators.”

But it’s not yet clear whether the pattern in the conversion subjects represents a cause or a consequence of the underlying problem. And, thus far, there is still no consensus on the underlying neurobiology of conversion symptoms. Some evidence suggests that individuals (mainly females) with conversion symptoms have higher-than-expected rates of childhood trauma, including physical or sexual abuse. While this could point to “psychological” explanations of conversion, it may also suggest that early childhood trauma has long-lasting effects on brain structure or function. Indeed, the more we examine conversion phenomena, the less useful the “mind vs. brain” dichotomy appears. Calling conversion symptoms “psychogenic” – suggesting that they are mere phantasms of the mind — may greatly oversimplify their underlying nature. Many cases of apparent “hysteria” eventually prove to have underlying medical or neurological causes. Furthermore, there are documented cases in which “hysterical” symptoms have been found to co-exist with bona fide neurological disease.

Whatever the ultimate cause or causes of conversion, it seems clear that this condition does not represent “malingering” or an attempt to deceive others. Unfortunately, individuals diagnosed with conversion symptoms are often written off as “crocks” or “fakers” and denied a thorough medical evaluation. For some patients with apparent conversion symptoms, “hysteria” is indeed the last diagnosis they are likely to receive. In time, we may discover a number of distinct causes for the symptoms experienced by the LeRoy students, varying from person to person. For now, we need to keep an open mind about whatever is afflicting these young people, and treat them with respect, understanding, and patience.

Thanks to Dr. Charles Raison for his helpful comments on this piece.

Image courtesy of Wikimedia Commons.

Most psychiatrists, and many patients, sense that psychiatry is in trouble these days. The reasons are complex, but boil down to a crisis of confidence: many in the general public — if they ever had faith in psychiatry — have begun to lose it.

Many psychiatrists who, like me, began their careers with hopeful idealism are now expressing pessimism or cynicism. Here, too, the reasons are complex, and have much to do with the sense that psychiatry has drifted away from its core values and central mission: the relief of human suffering and incapacity. Of course, the corrosive influence of “Big Pharma” and the gradual decline in the use of psychotherapy have contributed to this down-beat attitude.

And the highly-publicized dust-up over revision of psychiatry’s diagnostic classification — the DSM-5 (what the media love to call, “Psychiatry’s Bible”) — has certainly not filled psychiatrists with joy.

A number of prominent psychiatrists have criticized both the process and content of the still-developing DSM-5. Some have alleged that the DSM work groups have been too insulated from outside review, and that their proposed revisions will lead to an unwarranted “medicalization” of life’s normal stresses and strains. For example, critics worry that conditions like ADHD or major depressive disorder will be “over-diagnosed” using the proposed new criteria, and that this will lead, in turn, to excessive use of psychotropic medication. There are arguments to be made on both sides of these issues — but in my view, the critics are merely nibbling around the edges of the real problem.

In truth, the entire premise underlying the DSMs is severely flawed—and many psychiatrists routinely ignore the DSM in their clinical practices. Indeed, if the DSM is psychiatry’s “Bible,” it is fair to say that a great many psychiatrists are heretics. In my view, psychiatry needs to scrap the present diagnostic system and begin afresh, with its core ethical and clinical mission firmly in mind. This means getting rid of the “One from column A, one from column B”, research-oriented, diagnostic criteria, and providing clinicians with a manual that is practical and useful.

The present model of psychiatric diagnosis is useful primarily for researchers. It suits their needs for uniformity in diagnosis, by providing a set of “necessary and sufficient” signs and symptoms that define a particular disorder. These cut-and-dried criteria help ensure what researchers call “inter-rater reliability.” But this well-intentioned attempt to “carve Nature at its joints” doesn’t capture the diverse ways psychiatric illnesses actually appear in clinical settings; nor does the DSM’s penchant for pigeon-holing comport with how most psychiatrists actually “diagnose” their patients.

Most experienced clinicians listen carefully to the patient’s personal and family history; weigh this narrative in light of some general diagnostic categories, and arrive a “gestalt” understanding of their patient’s condition. Sure, psychiatrists — like other mental health professionals — are required to “play ball” with third-party payers, and provide the official DSM code for a given patient’s disorder. But this doesn’t mean that psychiatrists place much stock in the DSM’s categorical approach to understanding so-called “mental disorders”. This term is itself highly problematic, as it perpetuates the Cartesian “mind-body” split. Indeed, the original DSM-IV (1994) acknowledged this problem. No term is perfect, but I’d rather see a “Manual of Neurobehavioral Disease” — or simply, “Manual of Psychiatric Disorders”–than one of “mental disorders.”

Titles aside, here is the core problem: the DSM framework does very little to enlighten the clinician regarding the “inner world” of the suffering patient.

Let me be clear: I have great respect for my friends and colleagues who have spent many years developing the DSMs. And, I do not mean to disparage the assiduous efforts of the DSM-5 workgroups to refine the present set of diagnostic criteria. Clinical research is crucial for psychiatry, and there is a need for very specific diagnostic criteria in order to assure that subjects in a research study actually warrant a particular diagnosis.

Indeed, I believe the present (DSM-IV) criteria could serve as a launching point for a more refined set, based on the latest scientific studies, which could then be used by psychiatric researchers. Whether to publish these research-oriented criteria as a separate manual, or to include them in an appendix to the main document, is not critical. The real issue is that, from the work-a-day clinician’s standpoint, the DSMs that have appeared in the last thirty years (DSM-III and IV) have managed to embody “the worst of both worlds”, despite the good intentions of their authors.

Why is this so? Well, on the one hand, none of the major DSM psychiatric disorders, such as schizophrenia and bipolar disorder, is linked to any specific biological abnormality or “biomarker” — the proverbial “lab test” so many in my profession have been seeking. This is nobody’s fault: it simply reflects our limited (though growing) biological knowledge in what is still a relatively young science.

On the other hand, the observation-based, symptomatic criteria of the DSMs shed little light on the inner workings of psychiatric illnesses — how the patient suffering from, say, schizophrenia actually experiences the world. It is one thing to list a few symptoms of schizophrenia, such as auditory hallucinations or paranoid delusions. It is quite another to understand the illness from the patient’s perspective — an approach known as phenomenology. I would argue that many recently-trained psychiatrists have had little exposure to the phenomenology of the major mental illnesses. Most have been steeped in the culture of symptom check lists — not in the sorrows of the soul.

The present DSM categories convey the impression that diseases have “necessary and sufficient” features that define them—akin to the Platonic concept of ideal “forms.” A contrasting view is that of the philosopher Ludwig Wittgenstein, who argued that such “essential” definitions do not represent how language actually works. Wittgenstein wrote, instead, of “family resemblances” that help characterize a particular word or category, in a particular context. By analogy, no single feature or features characterize all five members of, say, the Jones family; however, four of the Joneses have blond hair, three of those four have blue eyes, and four are very tall. We can see the “resemblances” when the Joneses stand together for the family photo. Wittgenstein compared family resemblances to the overlapping fibers of a rope—no single fiber is present throughout the rope, but a large number of fibers overlap so as to create a continuous and recognizable object. The same may be posited with respect to any given psychiatric disease category. There may be no single set of “necessary and sufficient conditions” that define schizophrenia or bipolar disorder; but patients who suffer with either illness resemble one another in very characteristic ways.

Almost contemporaneously with Wittgenstein, philosophers such as Edmund Husserl—and later, existentialists like Jean-Paul Sartre—began to emphasize the unique structure and contents of the individual’s experience: her way of “being in the world.” It is this phenomenological perspective that would inform what I call “disease prototypes” in psychiatry. Essentially, these are narrative accounts of illness that try to capture the most salient and typical features of the condition, emphasizing the typical patient’s subjective experiences. Such prototypes would compose the core of the diagnostic system I am proposing.

What might a narrative prototype of a psychiatric illness sound like? In the case of schizophrenia, perhaps something like this:

Sal is a 30-year-old single male whose chief complaint is, “I can’t find pieces of me, and the pieces I do have are fading, fading, fading, into inter-dimensional space.” Sal’s problems began when he was about 14. According to his parents, Sal began to withdraw from friends and schoolmates and “seemed to enter a world of his own.” He became increasingly unable to maintain his hygiene, school performance, or social relations, often spending days at a time secluded in his room and refusing to shower or speak. He would eat only foods that had been “de-contaminated from radiation”, which he believed was being “beamed” into the house. By age 18, Sal complained of “gamma rays eating away at my brain”, and described hearing several persons discussing him in derogatory terms while alone in his room. Sal sometimes feels that “my thoughts are leaking out of my head” and that others “can read my mind.” At times, Sal will laugh or giggle inappropriately, as when attending the funeral of a family member, and his family reports difficulty in understanding Sal when he does speak…

An actual disease prototype would be much more detailed, of course, and would incorporate most of the signs and symptoms now listed in the DSM criteria. For disease entities that have highly variable presentations, more than one prototype would be provided. Each prototype would be accompanied by the latest data on any known biological abnormalities associated with the particular condition; detailed demographic correlates; and common findings on the mental status exam. (Ideally, this would be followed by information on the best-validated treatment strategies for a given condition, but that might well require a separate treatment manual). Each prototype would be compatible with its corresponding “research diagnostic criteria” (RDC), but would be framed in very different terms. (The proposed DSM-5 criteria for schizophrenia may be viewed here).

In short, it is not enough for psychiatrists simply to peck away at the proposed DSM-5. True, we will be stuck with the DSM-5 for the next decade or two, and we should strive to improve it while we still can. But in the longer term, psychiatrists and other mental health professionals owe it to themselves and their patients to think more boldly — and more philosophically — about their diagnostic system.

For further reading:

Frances A: DSM-5 Will Not Be Credible Without An Independent Scientific Review. Psychiatric Times, Nov. 2, 2011. http://www.psychiatrictimes.com/blog/dsm-5/content/article/10168/1982079

Phillips J: The missing person in the DSM. Psychiatric Times, Dec, 21, 2010. http://www.psychiatrictimes.com/blog/dsm-5/content/article/10168/1766260

Mishara A, Schwartz MA: Who’s on First? Mental Disorders by Any Other Name? (Word document). Association for the Advancement of Philosophy and Psychiatry (AAPP) Bulletin 2010;17:60-63

Paris J: Commentary in : The Six Most Essential Questions In Psychiatric Diagnosis: A Pluralogue: Edited by James Phillips, M.D., & Allen Frances, M.D. Philosophy, Ethics, and Humanities in Medicine (PEHM) in press.

Pierre J: Commentary in The Six Most Essential Questions In Psychiatric Diagnosis: A Pluralogue: Edited by James Phillips,M.D., & Allen Frances, M.D. Philosophy, Ethics, and Humanities in Medicine (PEHM), in press.

Kecmanovic D. Conceptual discord in psychiatry: origin, implications and failed attempts to resolve it. Psychiatr Danub. 2011 Sep;23(3):210-22. Review.

Pies R: Reclaiming our role as healers: a response to Prof. Kecmanovic.
Psychiatr Danub. 2011; 23:229-31.

Pies R, Geppert CM. Psychiatry encompasses much more than clinical neuroscience. Acad Med. 2009; 84:1322.

Wittgenstein L: The Blue and Brown Books, New York, Harper Torchbooks,
1958.

Knoll JL IV: Psychiatry: Awaken and return to the path. Psychiatric Times, March 21, 2011. www.psychiatrictimes.com/display/article/10168/1826785

You have asked me about the cause of your mood disorder, and whether it is due to a “chemical imbalance”. The only honest answer I can give you is, “I don’t know”—but I’ll try to explain what psychiatrists do and don’t know about the causes of so-called mental illness, and why the term “chemical imbalance” is simplistic and a bit misleading.

By the way, I don’t like the term “mental disorder”, because it makes it seem as if there’s a huge distinction between the mind and the body—and most psychiatrists don’t see it that way. I wrote about this recently, and used the term “brain-mind” to describe the unity of mind and body.¹ So, for lack of a better term, I’ll just refer to “psychiatric illnesses.”

Now, this notion of the “chemical imbalance” has been much in the news lately, and a lot of misinformation has been written about it—including by some doctors who ought to know better ². In the article I referenced, I argued that “…the “chemical imbalance” notion was always a kind of urban legend—never a theory seriously propounded by well-informed psychiatrists.”¹ Some readers felt I was trying to “re-write history”, and I can understand their reaction—but I stand by my statement.

Of course, there certainly are psychiatrists, and other physicians, who have used the term “chemical imbalance” when explaining psychiatric illness to a patient, or when prescribing a medication for depression or anxiety. Why? Many patients who suffer from severe depression or anxiety or psychosis tend to blame themselves for the problem. They have often been told by family members that they are “weak-willed” or “just making excuses” when they get sick, and that they would be fine if they just picked themselves up by those proverbial bootstraps. They are often made to feel guilty for using a medication to help with their mood swings or depressive bouts.

… most psychiatrists who use this expression feel uncomfortable and a little embarrassed…

So, some doctors believe that they will help the patient feel less blameworthy by telling them, “You have a chemical imbalance causing your problem.” It’s easy to think you are doing the patient a favor by providing this kind of “explanation”, but often, this isn’t the case. Most of the time, the doctor knows that the “chemical balance” business is a vast oversimplification.

My impression is that most psychiatrists who use this expression feel uncomfortable and a little embarrassed when they do so. It’s a kind of bumper-sticker phrase that saves time, and allows the physician to write out that prescription while feeling that the patient has been “educated.” If you are thinking that this is a little lazy on the doctor’s part, you are right. But to be fair, remember that the doctor is often scrambling to see those other twenty depressed patients in her waiting room. I’m not offering this as an excuse–just an observation.

Ironically, the attempt to reduce the patient’s self-blame by blaming his brain chemistry can sometimes backfire. Some patients hear “chemical imbalance” and think, “That means I have no control over this disease!” Other patients may panic and think, “Oh, no—that means I have passed my illness on to my kids!” Both of these reactions are based on misunderstanding, but it’s often hard to undo these fears. On the other hand, there are certainly some patients who take comfort in this “chemical imbalance” slogan, and feel more hopeful that their condition can be controlled with the right kind of medication.

They are not wrong in thinking that, either, since we can get most psychiatric illnesses under better control, using medication—but this should never be the whole story. Every patient who receives medication for a psychiatric illness should be offered some form of “talk therapy”, counseling, or other kinds of support. Often, though not always, these non-medication approaches should be tried first, before medication is prescribed. But that’s another story—and I want to get back to this “chemical imbalance” albatross, and how it got hung around the neck of psychiatry. Then I’d like to explain some of our more modern ideas of what causes serious psychiatric illnesses.

Back in the mid-60s, some brilliant psychiatric researchers—notably, Joseph Schildkraut, Seymour Kety, and Arvid Carlsson– developed what became known as the “biogenic amine hypothesis” of mood disorders. Biogenic amines are brain chemicals like norepinephrine and serotonin. In simplest terms, Schildkraut, Kety, and other researchers posited that too much, or too little, of these brain chemicals was associated with abnormal mood states—for example, with mania or depression, respectively. But note two important terms here: “hypothesis” and “associated”. A hypothesis is just a stepping-stone along the path to a fully-developed theory—it’s not a full-blown conception of how something works. And an “association” is not a “cause”. In fact, the initial formulation of Schildkraut and Kety ³ allowed for the possibility that the arrow of causality might travel the other way; that is, that depression itself might lead to changes in biogenic amines, and not the other way around. Here is what these two researchers actually had to say back in 1967. It’s pretty dense biology-speak, but please do read on:

“Although there does appear to be a fairly consistent relationship between the effects of pharmacological agents on norepinephrine metabolism and on affective state, a rigorous extrapolation from pharmacological studies to pathophysiology cannot be made. Confirmation of this [biogenic amine] hypothesis must ultimately depend upon direct demonstration of the biochemical abnormality in the naturally occurring illness. It should be emphasized, however, that the demonstration of such a biochemical abnormality would not necessarily imply a genetic or constitutional, rather than an environmental or psychological, etiology of depression.

Whereas specific genetic factors may be of importance in the etiology of some, and possibly all, depressions, it is equally conceivable that early experiences of the infant or child may cause enduring biochemical changes and that these may predispose some individuals to depressions in adulthood. It is not likely that changes in the metabolism of the biogenic amines alone will account for the complex phenomena of normal or pathological affect. Whereas the effects of these amines at particular sites in the brain may be of crucial importance in the regulation of affect, any comprehensive formulation of the physiology of affective state will have to include many other concomitant biochemical, physiological, and psychological factors.”^{3 (italics added)}

Now remember, Mrs. ——, these are the pioneers whose work helped lead to our modern-day medications, such as the “SSRIs” (Prozac, Paxil, Zoloft and others). And they certainly did not claim that all psychiatric illnesses—or even all mood disorders—are caused by a chemical imbalance! Even after four decades, the “holistic” understanding that Schildkraut and Kety described remains the most accurate model of psychiatric illness. In my experience over the past 30 years, the best-trained and most scientifically-informed psychiatrists have always believed this, despite claims to the contrary by some anti-psychiatry groups.⁴

Unfortunately, the biogenic amine hypothesis got twisted into the “chemical imbalance theory” by some pharmaceutical marketers,⁵ and even by some misinformed doctors. And, yes, this marketing was sometimes aided by doctors who—even if with good intentions–didn’t take the time to give their patients a more holistic understanding of psychiatric illness. To be sure, those of us in academia should have done more to correct these beliefs and practices. For example, the vast majority of antidepressants are prescribed not by psychiatrists, but by primary care physicians, and we psychiatrists have not always been the best communicators with our colleagues in primary care.

Neuroscience research has moved beyond any simple notion of a “chemical imbalance”…

All that said, what have we learned about the causes of serious psychiatric illness in the past 40 years? My answer is, “More than many in the general public, and even in the medical profession, realize.”  First, though: what we don’t know, and shouldn’t claim to know, is what the proper “balance” is for any given individual’s brain chemistry. Since the late 1960s, we have discovered more than a dozen different brain chemicals that may affect thinking, mood, and behavior. While a few seem particularly important—such as norepineprhine, serotonin,  dopamine, GABA, and glutamate—we have no quantitative idea of what the optimal “balance” is for any particular patient. The most we can say is that, in general, certain psychiatric illnesses probably involve abnormalities in specific brain chemicals; and that by using medications that affect these chemicals, we often find that patients are significantly improved. (It is also true that a minority of patients have adverse reactions to psychiatric medications, and we need further study of their long-term effects).⁶

But neuroscience research has moved beyond any simple notion of a “chemical imbalance” as the cause of psychiatric illnesses. The most sophisticated, modern theories posit that psychiatric illness is caused by a complex, often cyclical interaction of genetics, biology, psychology, environment, and social factors. ⁷ Neuroscience has also moved beyond the notion that psychiatric medications work simply by “revving up” or toning down a couple of brain chemicals. For example, we have evidence that several antidepressants foster the growth of connections between brain cells, and we believe this is related to the beneficial effects of these medications.⁸ Lithium—a naturally occurring element, not really a “drug”—may help in bipolar disorder by protecting damaged brain cells and promoting their ability to communicate with each other. ⁹

Let’s take bipolar disorder as an example of how psychiatry views “causation” these days (and we could have a similar discussion of schizophrenia or major depressive disorder). We know that a person’s genetic make-up plays a major role in bipolar disorder (BPD). So, if one of two identical twins has BPD, there is better than a 40% chance that the other twin will develop the illness, even if the twins are reared in different homes. ¹⁰ But note that the figure is not 100%–so there must be other factors involved in the development of BPD, besides your genes.

Modern theories of BPD hold that abnormal genes lead to abnormal communication between various inter-linked regions of the brain—so-called “neurocircuits”—which in turn increases the likelihood of profound mood swings.  There’s growing evidence that BPD may involve a sort of top-down, “failure to communicate” within the brain.  Specifically, the frontal regions of the brain may not adequately dampen over-activity in the “emotional” (limbic) parts of the brain, perhaps contributing to mood swings. ¹¹

So, you ask—is it still all a matter of “biology”? Not at all—the person’s environment certainly matters. A major stressor may sometimes trigger a depressive or manic episode. And, if a child with early-onset BPD is raised in an abusive or unloving home, or is exposed to many traumas, this is likely to increase the risk of mood swings in later life¹²—though there is no evidence that “bad parenting” causes BPD. (At the same time, abuse or trauma in childhood may change the “wiring” of the brain permanently, and this in turn may lead to more mood swings—truly, a vicious circle).¹³ On the other hand, in my experience, a supportive social and family environment can improve the outcome of a family member’s BPD.

Finally—while the individual’s approach to “problem-solving” is not a likely cause of BPD—there is evidence that how the person thinks and reasons makes a difference.  For example, cognitive-behavioral therapy and family-focused therapy may reduce the risk of relapse, in BPD.¹⁴ And so, with appropriate support, the person with bipolar disorder can take some control of her illness–and maybe even improve its course– by learning more adaptive ways of thinking.

So, boiling it all down, Mrs.——–, I certainly can’t tell you the exact cause of your or anybody’s psychiatric illness, but it’s a lot more complicated than a “chemical imbalance”.  You are a whole person–with hopes, fears, wishes, and dreams—not a brain filled with chemicals! The originators of the “biogenic amine” hypothesis understood this over forty years ago—and the best-informed psychiatrists understand it today.

Sincerely,

Ronald Pies MD

Note: The above “letter” was addressed to a hypothetical patient. A full disclosure statement for Dr. Pies may be found at: http://www.psychiatrictimes.com/editorial-board

References

1. Pies R: Psychiatry’s new brain-mind and the legend of the chemical imbalance. Psychiatric Times, July 11, 2011. http://www.psychiatrictimes.com/blog/couchincrisis/content/article/10168/1902106
2. See, for example, M. Angell MD, in the New York Review of Books: “The shift from “talk therapy” to drugs as the dominant mode of treatment coincides with the emergence over the past four decades of the theory that mental illness is caused primarily by chemical imbalances in the brain that can be corrected by specific drugs…”  http://www.nybooks.com/articles/archives/2011/jun/23/epidemic-mental-illness-why/
3. Schildkraut JJ, Kety SS. Biogenic amines and emotion. Science. 1967; 156:21-37.
4. See, eg, “The cornerstone of psychiatry’s disease model today is the theory that a brain-based, chemical imbalance causes mental illness.” http://www.cchr.org/sites/default/files/Blaming_The_Brain_The_Chemical Imbalance_Fraud.pdf (PDF)
5. Lacasse JR, Leo J. Serotonin and Depression: A Disconnect between the Advertisements and the Scientific Literature. PLoS Med. 2005; 2(12): e392. doi:10.1371/journal.pmed.0020392
6. El-Mallakh RS, Gao Y, Jeannie Roberts R. Tardive dysphoria: the role of long term antidepressant use in-inducing chronic depression. Med Hypotheses. 2011; 76:769-73.
7. Moran M: Brain, Gene Discoveries Drive New Concept of Mental Illness. Psychiatric News, June 17, 2011.
8. Castrén E, Rantamäki T. The role of BDNF and its receptors in depression and antidepressant drug action: Reactivation of developmental plasticity. Dev Neurobiol. 2010;70:289-97.
9. Machado-Vieira R, Manji HK, Zarate CA Jr. The role of lithium in the treatment of bipolar disorder: convergent evidence for neurotrophic effects as a unifying hypothesis. Bipolar Disord. 2009;11 (Suppl 2):92-109.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2800957/?tool=pubmed

10. Kieseppä T, Partonen T, Haukka J et al. High concordance of bipolar I disorder in a nationwide sample of twins. Am J Psychiatry. 2004 161; 1814-21.
11. Lagopoulos J, Malhi G. Impairments in “top-down” processing in bipolar disorder: a simultaneous fMRI-GSR study. Psychiatry Res. 2011; 192:100-8.
12. MacKinnon D, Pies R. Affective instability as rapid cycling: Theoretical and clinical implications for borderline personality and bipolar spectrum disorders. Bipolar Disord. 2006;8:1–14.
13. Heim C, Newport DJ, Bonsall R, et al: Altered pituitary-adrenal axis responses to provocative challenge tests in adult survivors of childhood abuse. Am J Psychiatry. 2001;158:575-81.
14. Zaretsky AE, Rizvi S, Parikh SV. How well do psychosocial interventions work in bipolar disorder? Can J Psychiatry. 2007;52:14-21.

Recommended reading:

Kramer P: In defense of antidepressants. New York Times Sunday Review, July 9, 2011. http://www.nytimes.com/2011/07/10/opinion/sunday/10antidepressants.html?pagewanted=all

You needn’t use much imagination. In Florida, Gov. Rick Scott is expected to sign a bill (SB-432) that will prohibit doctors from asking patients if they own guns, except when “…the information is relevant to the patient’s medical care or safety or the safety of others…”

The Florida bill was written with the help of — no surprise here — the National Rifle Association, which insists that this legislation is designed to prevent doctors from intruding on a patient’s privacy; “harassing” gun owners; and interfering with the patient’s second amendment “right to bear arms.” Similar bills are being considered in North Carolina and Alabama.

Now, the “relevance exception” clause may sound quite reasonable, at first blush. Evidently, it persuaded the Florida Medical Association, who ultimately went along with the bill. But the exception clause has not persuaded many Florida pediatricians, who believe such a law would have a chilling effect on the doctor’s evaluation. According to a report on National Public Radio², one specialist in adolescent medicine recently told a Florida Senate committee, “What if I have an adolescent who’s been bullied, [but] who’s not suicidal? I don’t think, under the current bill, I’m entitled to ask him if there’s a gun in the home, or if he’s carried a gun to school, or if he’s thinking of harming someone else with a gun.”

Indeed, the newly-added “relevance” clause may actually put the physician — and perhaps other clinicians — in a medico-legal “double bind”. If he or she fails to inquire about gun possession because it is not deemed “relevant”, and the patient goes on to commit some act of gun-related violence, the physician may be held liable for failing to ask the “relevant” questions. On the other hand, if the physician decides that a query about gun possession is relevant; but the patient believes otherwise, and becomes angry about the “invasion of privacy”, he or she could initiate a suit against the doctor, on the grounds that the gun possession query was not clinically “relevant” as per state law.

There are, of course, important constitutional issues raised by bills of this sort, not least of which is the physician’s right to freedom of speech, under the first amendment. Since when is it the role of government to control what may or may not be said, in the supposedly confidential relationship between physician and patient? Since when are such communications subject to monitoring and muzzling by a state government? And, by the way — how, exactly, is the second amendment’s right to bear arms infringed upon by a doctor’s mere inquiry, regarding guns in the home? Is the idea that the doctor is going to lead a group of left-wing, anti-gun zealots out to the patient’s house, and confiscate legally-owned firearms?

But these are questions best left in the hands of constitutional scholars and jurists. As a psychiatrist, I have a more direct interest in protecting the safety of patients, their families, and society. In fact, I am professionally obligated to inquire about firearms (and many other risk factors) whenever I believe there is a potential danger to the patient or others. As a therapist, in many jurisdictions, I am legally obligated by either case law or state statutes to consider notifying police or a third party who may be the target of violence on the part of a patient I have evaluated; for example, a distraught, angry patient in psychotherapy who reveals his intent to shoot a particular individual. What effect would a Florida-style law have on assessing the risk of gun-related violence, if the physician fears legal sanctions for stepping across the line of “relevance” specified in the exception clause?

These are hardly academic issues. Recently, a three-year-old South Carolina girl fatally shot herself in the head, using a pistol that was left loaded on a windowsill in her parent’s bedroom. In another case from California, reported in the May 11, 2011 New York Times, a 10-year-old boy shot his father to death, at home, using a handgun. Of course, lax firearms regulations in the U.S. contribute to such tragedies. Indeed, according to data from UCLA and Harvard researchers, the U.S. firearm-related suicide rate is almost six times higher than in comparison countries, and unintentional firearm-related deaths are about five times higher in this country.¹

Some proponents of the Florida bill respond to critics with a classic reductio ad absurdum argument. They ask, “If doctors need to inquire about guns in the home, why don’t they ask about poisonous snakes or dangerous dogs in the neighborhood? Why don’t they ask about tall buildings with unprotected balconies, open sewers, etc?” The emptiness of this argument should be evident to any clinician with a modicum of forensic experience. Obviously, there are infinite risks a physician, psychologist, or social worker could inquire about, but our time with the patient is finite — and few domestic dangers pack the lethality of a loaded gun in the house. Moreover, the possession of firearms in the home is a professionally-recognized risk factor for both gun-related homicide and suicide. As noted by Garen J. Wintemute, M.D., M.P.H. (Professor of Emergency Medicine and director of the Violence Prevention Research Program at the University of California, Davis, School of Medicine):

“Gun violence is often an unintended consequence of gun ownership. Americans have purchased millions of guns, predominantly handguns, believing that having a gun at home makes them safer. In fact, handgun purchasers substantially increase their risk of a violent death. This increase begins the moment the gun is acquired — suicide is the leading cause of death among handgun owners in the first year after purchase — and lasts for years. The risks associated with household exposure to guns apply not only to the people who buy them; epidemiologically, there can be said to be “passive” gun owners who are analogous to passive smokers. Living in a home where there are guns increases the risk of homicide by 40 to 170% and the risk of suicide by 90 to 460%.¹

These facts confer a very high degree of responsibility on the part of the physician. As Norris and Price have pointed out:

“Access to firearms is an important factor for clinicians to consider in any risk assessment of suicidal patients. Miller and Hemenway report that “in 2005, an average of 46 Americans a day committed suicide with a firearm, accounting for 53% of all completed suicides.”… All discussions with the patient and his or her family regarding firearms should be documented. When clinicians are doing a psychiatric examination of suicidal patients, they should inquire about the availability of firearms in the household. If a firearm is available, concerns about safety should be raised with the family and police. This is particularly true when children and adolescents reside in the household.”²

Obviously, the “gun possession” question will rarely be raised when a patient goes to the ER with a sore throat — any more than an astute physician would do a rectal exam under such circumstances. Furthermore, patients who decline to answer a physician’s questions about gun possession should never be harassed, disparaged or denied care — but doctors do not need a law to instruct them in such basic medical ethics. More important: the physician should not be looking over his or her shoulder at the question of how much legal risk is entailed in asking clinically-indicated questions about firearms.

These judgments should be guided by the physician’s medical training and clinical evaluation — not by misbegotten legislation that intrudes on the physician’s freedom of speech, and on the privacy of the doctor-patient relationship.

Acknowledgments: The author wishes to thank Michael P. Hirsh, MD, FACS, FAAP; and James L. Knoll IV, MD, for their helpful comments on earlier drafts of this piece.

References

1. Wintemute GJ. Guns, fear, the Constitution, and the public’s health. N Engl J Med. 2008 Apr 3;358(14):1421-4. Epub 2008 Mar 19.

2. Allen G: Florida Bill Could Muzzle Doctors On Gun Safety. National Public Radio, May 7, 2011. Accessed at: http://www.npr.org/2011/05/07/136063523/florida-bill-could-muzzle-doctors-on-gun-safety

3. Norris D, Price M: “Firearms and Mental Illness” Psychiatric Times, Oct. 30, 2009

You got other problems? Talk to your therapist!

If the front-page article in the March 6 New York Times¹ can be believed — and who wouldn’t believe America’s “Paper of Record”? — this is essentially what the practice of American psychiatry has become. But how accurate was the Times’ portrait of outpatient psychiatry? How grounded was it in the best available research? And given the roughly 30,000 psychiatrists in the U.S., how clear a picture can we get by peering through the eyes of one beleaguered practitioner who believes that psychotherapy is no longer “economically viable”?

As an occasional contributor to the Times who has great respect for its journalistic integrity, I’m sorry to say that this story was a disservice both to the Times readership, and to the profession of psychiatry. Although the article may have been a well-intended expose of malign insurance company practices, it amounted to a jaundiced caricature of psychiatric care — accurate in some respects, but distorted in many others. Furthermore, by disparaging the role of psychiatric medications, the Times article reinforced the “mind-body” split that has bedeviled psychiatry for the past 50 years, as Tanya Luhrmann showed in her classic study, Of Two Minds: The Growing Disorder in American Psychiatry.

But before critiquing the Times article, let’s own up to some real problems associated with current psychiatric practice.

It’s true that some psychiatrists have become more comfortable with molecules than with motives.  And, alas, as James Knoll MD has recently argued, some psychiatrists have gotten caught up in the “business” of psychiatry and strayed from the path of insightful and compassionate listening.² The beleaguered psychiatrist profiled in the New York Times piece certainly seems to have lost his way, despite his good intentions.

Let’s also acknowledge that the general trend reported by the Times — the diminishing use of psychotherapy by psychiatrists — is quite real. Over the past decade or so, the percentage of psychiatrists offering psychotherapy to all or most of their patients appears to have dropped. One study — very selectively cited in the Times article — found that “just 11 percent of psychiatrists provide talk therapy to all patients…”¹ This was based on a study by Mojtabai and Olfson,³ which found a decline in the number of psychiatrists who provided psychotherapy to all of their patients — from 19.1% in 1996-1997 to 10.8% in 2004-2005. The study also found that the percentage of visits involving psychotherapy declined from 44.4% in 1996-1997 to 28.9% in 2004-2005, which “…coincided with changes in reimbursement, increases in managed care, and growth in the prescription of medications.”²

But the very same study found that almost 60% of psychiatrists were providing psychotherapy to at least some of their patients. Also, the threshold for considering a session “psychotherapy” was set quite high in the Mojtabai-Olfson study: the meeting had to last 30 minutes or longer. But as my colleague Paul Summergrad MD has pointed out, common practice and standard CPT billing codes (e.g., 90805) specifically include 20-30 minute visits for psychotherapy, with or without pharmacotherapy.⁴ Furthermore, Mojtabai and Olfson acknowledged that

“Some visits likely involved use of psychotherapeutic techniques but were not classified as psychotherapy in the current analysis. Psychotherapeutic techniques can be effectively taught and used in brief medication management visits by psychiatrists and other health care providers.”³ (p.968)

This last point was totally lost in the New York Times report. When I used to see patients for “medication checks” in my private practice, I would sometimes spend more time providing supportive psychotherapy than dealing with the medication issues, if the patient’s emotional needs warranted it. (If the patient was seeing another therapist in formal psychotherapy, I would try to remain an empathic listener, while encouraging the patient to raise the issue with the therapist).  Furthermore, in providing medication for some severely personality-disordered patients, it is often impossible to maintain the therapeutic alliance without understanding the patient’s self-sabotaging defenses. As Glen Gabbard MD has observed, “…psychotherapeutic skills are needed in every context in psychiatry” — including during the much-maligned 15-20 minute “med check.”⁵

Moreover, other data, omitted from the Times article, contradict the impression that psychiatrists have given up on psychotherapy, or that most meetings with psychiatric patients are just 15 minutes long.   For example, Reif et al (2010) found that, in a managed care psychiatric practice setting, two-thirds of claims involved medication management, and two-thirds involved psychotherapy — with an overlap of about 30%.⁶ The authors concluded that

“Despite potential financial disincentives for psychiatrists to conduct psychotherapy,  our findings show that billed claims for psychotherapy by psychiatrists were common… [and] it appears that the broader skill set of psychiatrists is still being tapped, with provision of both medication management and psychotherapy.”⁶

Furthermore, according to Dr. Mark Olfson, there has been a decline of about 9% in the mean visit duration for psychiatric appointments, in the past 11 years. That may sound like a lot, but it amounts to only a modest change: from 36.8 minutes (1995-1996) to 33.3 minutes (2006-2008) (M. Olfson, personal communication, 3/31/11).  This finding also contradicts the impression — strongly reinforced by the New York Times article — that 15-minute “med checks” are now the most common pattern of interaction with psychiatrists.

Although the Times article did not deal specifically with psychiatric residency training, there is a perception in some quarters that psychiatric residency no longer provides adequate training in psychotherapy.  A corollary of this view is that younger psychiatrists no longer regard psychotherapy as important; and hence, are at a disadvantage with respect to other mental health professionals, such as psychologists and social workers.  In fact, there are sound reasons for being skeptical of this downbeat assessment — or at least for tempering it with more hopeful information.

It is true, on the one hand, that many academic psychiatrists have expressed concern for the diminishing role of psychodynamic psychotherapy in residency training. There are also indications that while over half of psychiatry residents believe their programs provide high-quality psychotherapy training, about 28% express concerns about the adequacy of time and resources in their programs.⁷

You probably lost sleep, and didn’t feel much like eating. You may have felt this way for a few weeks, a few months, or even longer. All this belongs to the world of ordinary bereavement — not of clinical depression.

Yet the two constructs of “normal grief” and major depression are a source of continued controversy and confusion — and not just among the general public.

Many clinicians still find it hard to disentangle grief and depression, inspiring countless debates over “where to draw the line” between normality and psychopathology.

But the problem is not one of “fuzzy boundaries.” Grief and depression occupy two quite different psychological territories, and have vastly different implications with regard to outcome and treatment.

For example, ordinary grief is not a “disorder” and doesn’t require treatment; major depression is, and does. Unfortunately, the inner worlds of grief and depression are hardly glimpsed in the symptom check lists of our present diagnostic classification, the DSM-IV. And, alas, it’s not clear that the DSM-5 will bring great improvement in this regard.

What is Grief Anyway?

The classic studies of bereavement, performed by Dr. Paula Clayton in the 1970s, made it clear that some depressive symptoms were often present early in the course of grieving, sometimes lasting several months after the death of a loved one. Indeed, sadness, tearfulness, sleep disturbance, decreased socialization, and decreased appetite are features seen in both normal, adaptive grief and in major depression — sometimes confusing the diagnostic picture.

Clinicians therefore look at other “objective” features of the patient’s presentation to help make the diagnosis. For example, in ordinary bereavement, the grieving person is generally able to carry out most activities and obligations of daily living, after the first two or three weeks of grieving. This is not usually the case in episodes of severe major depression, in which social and vocational functioning is markedly impaired for many weeks or months. Moreover, early morning awakening and pronounced weight loss are more common in major depression than in n uncomplicated bereavement.

But by themselves, observational data do not always distinguish ordinary grief from clinical depression, especially during the first few weeks of bereavement. Accordingly, my colleague, Dr. Sidney Zisook, and I have tried to describe the phenomenology or “inner world” of grief, as distinct from that of clinical depression. We believe that these experiential differences provide important diagnostic clues.

Thus, in major depression, the predominant mood is sadness tinged with hopelessness and despair. The depressed person often feels that this dark mood will never end—that the future is bleak, and life, a kind of prison-house. Typically, the depressed person’s thoughts are almost uniformly gloomy. If an optimist sees life through rose-colored glasses, the depressed person sees the world “through a glass darkly.”

The writer William Styron, in his book, Darkness Visible, describes depressed individuals as having “their minds turned agonizingly inward.” Their thoughts are almost always focused on themselves — usually in a self-negating way. The severely depressed person thinks, “I am nothing. I am nobody. I am rotting away. I am the worst sinner that ever walked the face of the earth. Not even God could love me!”

At times, these nihilistic thoughts reach delusional proportions — so-called psychotic depression. And, despite the best efforts of friends and family to “cheer up” their depressed loved one, the sufferer is often inconsolable. Neither love, nor riches, nor the blessings of art and music can penetrate the core of despair. Suicide becomes an ever more tempting option—and often, the only option the sufferer can imagine.

The Inner World of the Bereaved

The inner world of the bereaved is unquestionably one of loss and sadness, but it differs in crucial ways from that of the depressed. In depression, sadness is constant and intractable; in bereavement, it is intermittent and malleable. The bereaved individual typically experiences sadness in “waves”, often in response to some reminder of the deceased. Usually, painful recollections of the loved one are interspersed with positive thoughts and memories. Unlike the seriously depressed person, the grieving individual usually feels that life will someday get back to “normal”, and that she will once again feel like her “old self.” Suicidal intentions are rarely present, though the bereaved may fantasize about “joining” or “reuniting” with the deceased.

Unlike the severely depressed person — alone on an island of self-loathing — the bereaved person usually maintains her self-esteem, as well as an emotional connection with friends and family. Perhaps the hallmark of ordinary grief, as psychologist Kay Jamison has noted, is the ability to be consoled. Indeed, in her book, Nothing Was the Same, Jamison astutely distinguishes between the grief she felt after the death of her husband, and her frequent periods of severe depression.

“The capacity to be consoled,” she writes, “is a consequential distinction between grief and depression.” Thus, during her bouts of major depression, poetry was of no consolation to Jamison; whereas during her grief, reading poetry was a source of comfort and solace. Jamison writes: “It has been said that grief is a kind of madness. I disagree. There is a sanity to grief… given to all, [grief] is a generative and human thing…it acts to preserve the self.”

Since they are distinct conditions, grief and major depression can occur together, and there is clinical evidence that concurrent depression may delay or impair the resolution of grief. Contrary to widespread claims in the media, the DSM-5 framers do not want to limit “normal grief” to a two-week period — which would be foolish, indeed. The duration and intensity of grief is extremely variable, depending on a variety of personal and interpersonal factors. Research by Dr. George Bonnano has found that after the death of a spouse, chronic grief was associated with pre-loss “dependency” upon the deceased spouse. In contrast, more resilient subjects showed less interpersonal dependency, and greater acceptance of death. Resiliency was by far the most common pattern observed, with most of the bereaved showing a return to relatively normal functioning within 6 months of the loss.

What are the implications of all this for the DSM-5? I believe that symptom check lists alone provide only a narrow window into the patient’s inner world. The DSM-5 should provide clinicians with a richer picture of how grief and bereavement differ from major depression — not just from the observer’s perspective, but from that of the grieving or depressed person. Otherwise, clinicians will continue to have difficulty distinguishing depression from what Thomas a Kempis called, “the proper sorrows of the soul.”

Acknowledgments: Thanks to Dr. Sid Zisook for his comments on this piece, and to Drs. Charles Reynolds and Katherine Shear for their important research contributions.

For Further Reading:

Bonanno, G. A., Wortman, C. B., Lehman, D. R. et al: Resilience to loss and chronic grief: A prospective study from pre-loss to 18 months post-loss. Journal of Personality and Social Psychology, 2002;83: 1150-1164.

Jamison KR: Nothing Was the Same. Vintage Books, 2011.

Pies R, Zisook S: Grief and Depression Redux: Response to Dr. Frances’s “Compromise” Psychiatric Times Sept. 28, 2010. Accessed at: http://www.psychiatrictimes.com/dsm-5/content/article/10168/1679026

Pies R. The anatomy of sorrow: a spiritual, phenomenological, and neurological perspective. Philos Ethics Humanit Med. 2008; 3: 17. Accessed at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2442112/

Zisook S, Shear K: Grief and bereavement: what psychiatrists need to know.

Zisook S, Simon N, Reynolds C, Pies R, Lebowitz, B, Tal-Young, I, Madowitz, J, Shear, MK. Bereavement, Complicated Grief, and DSM, Part 2: Complicated Grief. J Clin Psychiatry. 2010;71(8): 1097-8.

While the facts are still unfolding, and the accused shooter’s motivations — Jared Lee Loughner — still unclear, the murders in Arizona have once again raised a number of troubling questions: what if any link is there between violence and mental illness? Which problems in our health care system may contribute to untreated or inadequately treated mental illness? How should we balance civil liberties — including legitimate second amendment rights — against society’s very real safety concerns, when deciding whether guns should be sold to those with a history of severe mental illness? And would the answers to these questions have made any substantial difference in the case of the Arizona shootings?

In dealing with these complex questions, I don’t claim to “represent” psychiatrists, physicians, or any particular interest group. I am writing as a concerned citizen who happens to be a psychiatrist and bioethicist. I do not propose to offer any armchair “diagnoses” of the person now charged with murder in the Arizona shooting. Nor do I want to pre-empt a determination of the shooter’s degree of responsibility and culpability — those will be determined, one hopes, through due process of law and appropriate expert testimony. (Mental illness, so-called, is sometimes a partial explanation of someone’s behavior — is not an “excuse” for carrying out evil acts, nor does it rule out personal or political motives for a given action). Finally, by way of personal disclosure, I am a supporter of both single-payer, national health insurance; as well as more stringent controls over the sale and possession of lethal firearms.

Let’s start with the supposed link between mental illness and violence. Though the data are complicated, the overall conclusion from recent research is that violence is not closely linked to the major psychiatric disorders (major depression, bipolar disorder, and schizophrenia) per se. For example, the 1998 MacArthur Violence Risk Assessment Study, led by John Monahan and Henry Steadman, evaluated psychiatric patients recently discharged from the hospital. Unlike some studies that relied solely on self‐reports of violence, the MacArthur study used a combination of self‐reports, collateral informants, and police and hospital records.

The study found that the prevalence of violence among discharged psychiatric patients without a substance abuse disorder was similar to that among community‐dwellers who did not abuse substances. Furthermore, violence by these discharged patients rarely involved vicious attacks on strangers or clinicians. Usually, it resembled violence committed by other community‐dwellers, such as hitting a family member inside the home. The study revealed 6 homicides committed by 3 of the 951 discharged patients — thus, approximately 0.3% (3 in 951) of the released population were homicidal or committed acts of lethal violence. This rate is indeed higher than that in the general population, and is certainly not to be dismissed lightly. Still, in my view, the findings suggest that lethal violence among discharged psychiatric patients is quite rare.

To be sure, the MacArthur study has been criticized on various methodological grounds (see Torrey et al, 2008). Furthermore, mental disorders do increase susceptibility to substance abuse, and thus, indirectly increase risk of violence.

Nevertheless, a recent study by Eric Elbogen and colleagues at the University of North Carolina Chapel Hill School of Medicine tends to confirm the MacArthur findings.  Based on face-to-face surveys conducted by the National Institute on Alcohol Abuse and Alcoholism, and involving nearly 35,000 subjects, Elbogen and his team found that when psychiatric diagnosis was examined, severe mental illness alone was not associated with increased risk of violence — but severe mental illness plus substance abuse/dependence was significantly associated. Indeed, severe mental illness per se did not independently predict future violent behavior; rather, other factors — such as a history of physical abuse, environmental stressors, or parental arrest record — predicted violent acts.

The image of the violent mentally ill person must also be tempered by research from Linda A. Teplin and colleagues, of Northwestern University. Teplin et al have found that those with mental illness are much more likely to be victims than perpetrators of a violent crime. They discovered in their work that among psychiatric outpatients, about 8 percent reported committing a violent act, whereas about 27 percent reported being the victim of a violent crime.

Aside from being poor and dealing with some physical limitations, Patrice had no discernible cause for her chronic depression. Her marriage was good, and despite her straitened
circumstances, Patrice lived in a modest but comfortable home. Unlike many depressed patients, Patrice herself had no “narrative”— no internalized account of how she came to be depressed. Her mood disorder was as much a puzzle to her as to me — the kind of illness that, in the 1960s, would have been called “endogenous depression”— arising, rather mysteriously, from within.

Patrice had the usual symptoms of major depression — lack of energy, poor concentration, inability to experience pleasure, suicidal thoughts, etc.— but there was another layer to her pathology. She had a quality textbooks describe as “importuning,” and which most people would call “clingy” and “demanding.” When I listened to Patrice ’s complaints, it was as if my pant leg were being tugged by someone groveling piteously on the ground. When I examined my emotional reaction to Patrice, I could see that on some level, her “neediness” angered me—perhaps because it left me feeling helpless. This, generally, is not a feeling those in the medical field handle well.

Patrice had been on several of the most robust antidepressant regimens I knew of, to little avail. She was too uncomfortable to sit through an “exploratory” or psychoanalytically-oriented therapy, so I used a supportive approach. Contrary to popular belief, “supportive psychotherapy” does not consist of patting the patient on the shoulder and saying, “There, there!;” rather, it is aimed at shoring up the patient’s more mature coping mechanisms and helping him acquire new problem-solving skills.

But after many months, Patrice was no better. I began to conclude that underneath her depression, Patrice suffered from a personality disorder—what the textbooks describe as “a lifelong pattern of maladaptive behavior.”  Indeed, Patrice fit quite nicely into what was once termed “Passive-Dependent Personality Disorder” and what later became “Dependent Personality Disorder” in the current DSM-IV classification. Individuals with DPD are described as having a long-standing need to be “taken care of;” “clinging” behavior; a fear of being abandoned and difficulty making everyday decisions without excessive reassurance from others. Patrice fit the bill, all right. And yet, she had apparently functioned adequately in her life, marriage, and career, until about ten years prior to my seeing her, when her mood inexplicably began to plummet.

One day, I received a call from the emergency room. Patrice had been admitted after a “moderate overdose” on the medications I had prescribed. After speaking with the inpatient service, which quickly agreed to admit her, I felt myself foundering in the waters of guilt, anger and denial. Rather than admit to myself how badly my treatment had failed, I felt that Patrice had failed me—by “acting out” in this “passive-aggressive” manner. After discussing my patient’s voluminous treatment history with the inpatient unit director, I was surprised to hear her say, “Maybe it’s time for electricity.” This, of course, was “shop talk” for electroconvulsive therapy, or ECT—one of the most controversial treatments in psychiatry, and the stuff of innumerable myths and misunderstandings. “She’s been tried on everything,” the unit director pointed out, “and I think we owe her our best treatment.”

Indeed, there is no question that ECT is the most effective treatment available for severe, intractable major depression. Remission rates with ECT are in the range of 60-90%—much higher than rates with initial antidepressant treatment, which hover around 25%. ECT is also known to decrease suicidal ideation during the course of treatment. Yet this valuable intervention is often used as a “last resort,” even by experienced psychiatrists, frequently as a result of misconceptions on the part of clinician, patient, or both.

I recently heard a talk by Mrs. Kitty Dukakis—whose own ECT treatment was clearly lifesaving—in which she implored the audience of psychiatrists to use ECT earlier in treatment. Contrary to the myth fostered by Ken Kesey’s movie, “One Flew Over the Cuckoo’s Nest”—in which Jack Nicholson’s character, McMurphy, receives punitive ECT without a muscle relaxant –modern ECT methods do not cause convulsions. Neither does ECT cause detectable damage to brain tissue, based on several biological measures. (Many viewers of “Cuckoo’s Nest” seem to confuse ECT with lobotomy, which is no surprise, since McMurphy is later forced to undergo this barbaric neurosurgical procedure!). In fact, some preliminary evidence suggests that ECT actually increases certain “nerve growth factors” that enhance connections between brain cells. The beneficial effects of ECT treatment may last for many months, but some patients require occasional “maintenance” treatments, once a month or so, in order to stay in remission.

The biggest concern — memory loss — is usually mild, transient, and circumscribed, using the latest technical modifications of ECT technique. Recent data suggest that ECT’s effects on memory are comparable to those associated with long-term pharmacotherapy. While a small percentage of patients may report significant and enduring memory problems after ECT*, the vast majority do not, when the most advanced and “conservative” ECT methods are used. Most studies find that, six months after a course of ECT, neuropsychological testing reveals no substantial mental impairment in patients whose depression is in remission. Furthermore, cognitive risks must be weighed against the enormous degree of suffering, incapacity, and mortality—i.e., at least a 4% rate of suicide—associated with severe major depressive disorder. Nonetheless, candidates for ECT must receive detailed “risk-benefit” information as part of the informed consent process, and consultation with family members is often an important part of that process. It should go without saying—but I will say it!—that nobody should be coerced into accepting ECT, or undergo the procedure without having provided informed consent.

Somewhat to my surprise, Patrice did consent to the ECT, and I fully concurred. When I saw her a month later, as an outpatient, she had undergone a routine course of unilateral ECT, in which the electrical stimulus was administered to the “non-dominant” side of her brain. This method is known to minimize cognitive side effects, all other factors being equal. I was impressed, but not entirely surprised, that Patrice’s depression had been knocked back on its heels—she was clearly in remission. Her mood, energy, and zest for life had returned. She did not complain of any significant memory problems. What I found absolutely jaw-dropping was Patrice’s profound change in personality: she seemed, in every meaningful sense, a “new woman.”

The piteous and needy demeanor that I had attributed to a personality disorder had been completely transformed. The radiant woman who now sat before me wore the confident, beaming and assertive face of her youth. Patrice began spouting off on plans, projects, and long-postponed pleasures—without a hint of dependency or neediness.

The “real Patrice” had emerged, butterfly-like, from the cocoon of inadequately-treated depression. And I had learned two valuable lessons: first, patients don’t fail treatments; treatments fail patients. And second: what appears to be etched in the hard stone of personality is sometimes merely scratched in the shifting sand of treatable illness.

Note: “Patrice” is not the patient’s actual name.

Sources for Further Reading:

An Overview of Electroconvulsive Therapy (ECT) – Psych Central

Electroconvulsive therapy (ECT) – Mayo Clinic

Electroconvulsive therapy (ECT) – McLean Hospital

Smith GE, Rasmussen KG Jr, Cullum CM et al: A randomized controlled trial comparing the memory effects of continuation electroconvulsive therapy versus continuation pharmacotherapy: results from the Consortium for Research in ECT (CORE) study. J Clin Psychiatry. 2010 Feb;71(2):185-93.

Bocchio-Chiavetto L, Zanardini R, Bortolomasi M et al: Electroconvulsive Therapy (ECT) increases serum Brain Derived Neurotrophic Factor (BDNF) in drug resistant depressed patients. Eur Neuropsychopharmacol. 2006 Dec;16(8):620-4.

Shock: The Healing Power of Electroconvulsive Therapy, by Kitty Dukakis and Larry Tye; New York, Avery, 2006.

*For one patient’s personal perspective on her memory loss associated with ECT, see:

Donahue AB: Electroconvulsive therapy and memory loss: a personal journey. J ECT. 2000 Jun;16(2):133-43. [The PDF is available on line. This patient reported substantial and enduring problems with her memory, yet says she probably owes her life to her ECT treatment—RP]

Acknowledgment: I wish to thank Psychcentral’s Sandy Naiman for her careful reading of this article; however, the opinions expressed herein are solely mine.

But the other day, amidst all the commentary on Shirley Sherrod, a short article buried inside the Sunday New York Times caught my eye. Innocuously entitled, “No Air-Conditioning, and Happy,”¹ the article concerned a certain agricultural scientist and his wife who “…do not use air-conditioning as a matter of personal preference and principle — even on the most hostile days.” The scientist, Stan Cox, recently wrote an op-ed piece for the Washington Post, in which he questioned the excessive use of air conditioning in modern society.

And what does this have to do with the Sherrod debacle?

Well, according to the Times report, Mr. Cox has “faced death threats” since publishing his op-ed, which was followed by “…sixty-seven pages of cringe-inducing email messages”, one of which “threatened to shoot Mr. Cox.” Shoot someone? Over an opinion piece questioning the use of air conditioners? Mr. Cox’s response was a blandly good-natured shrug: “Maybe enjoyment of thermal variety isn’t for everybody,” he opined. But Mr. Cox may not have appreciated that, like Shirley Sherrod, he had been the target of what I call our “Gotcha-Pounce Culture”.

The gotcha-pounce ritual begins when a particular individual is “caught” in some alleged crime, scandal, or indiscretion (“Gotcha!”). Then, long before the facts are fully known, the unfortunate person is pounced upon by various bloggers and pundits, often to the lasting detriment of his or her reputation. And whereas most commentaries on Ms. Sherrod depicted such character assassination as an “inside the Beltway” blood-sport, I believe the problem is far more pervasive in this country. The gotcha-pounce maneuver has become the default mode for much of our internet and broadcast communication, and for what nowadays passes as journalism.

The anonymity of the internet is no doubt a major catalyst for our growing tendency to “flame first, ask questions later.” What could be easier–and more satisfying–than hurling a blazing, nameless email out into the blogosphere, verbally incinerating one’s enemy? I suspect (but can’t prove) that this anonymous, gotcha-pounce messaging is accompanied by a massive flood of dopamine in the “reward circuits” of the sender’s brain—the same circuits that are activated by cocaine, alcohol, and other substances of abuse. A recent article by Neil Swidey in the Boston Globe Magazine² highlighted the problem of “…people who are allowed to name-call without any obligation to reveal their own names.” To be sure, there are pros and cons to such anonymity, as Swidey points out: “On one side, anonymous comments give users the freedom to be completely candid in a public forum. On the other, that freedom can be abused and manipulated to spread lies or mask hidden agendas.”²

But the underlying problem can’t be reduced to one of internet anonymity. After all, the “attack video” that caused so much pain for Ms. Sherrod was released by a well-known blogger, Andrew Breitbart, who did nothing to conceal his identity. Rather, in my view, there are forces at work in our culture that go well beyond the internet, and have to do with fundamental shifts in the way Americans relate to one another in the past few decades.

By now, it is a truism to claim that there has been a “breakdown in civility” in this country — my Google search using that phrase turned up 44,800 results. Much of the commentary on this trend has focused on the abysmal level of political “discourse” in recent years, particularly since the beginning of the Obama administration — for example, the infamous “You lie!” outburst by Rep. Joe Wilson. But “civility” has to do mainly with courteous and considerate social behavior. The profusion of venomous personal attacks — and the “gotcha-pounce” phenomenon I have described — goes well beyond incivility. We need an explanation of why decency itself seems to be in decline.

But is this impression well-founded? To be sure, there are still millions of decent and caring people out there. And, in casting stones against our own times, we risk sounding a bit like Miniver Cheevy, the embittered character in the E. A. Robinson poem who longs for “the days of old/when swords were bright and steeds were prancing.” True: there has always been hatred, libel and slander—but there is evidence that certain kinds of hateful behavior have been on the increase in recent years.

For example, between 2002 and 2008, reports of “cyber-bullying” — defined as the “willfull and repeated harm inflicted through the use of computers, cell phones, and other electronic devices” — have increased from about 15% to more than 30% of respondents, according to research by criminologists Sameer Hinduja and Justin W. Patchin.3 Even more disturbing, Human Rights First (HRF) — a non-profit, nonpartisan international human rights organization — reports that in the U.S. and in many other countries, violent “hate crimes” are on the rise. In a recent survey of 56 European and North American countries, HRF found that “…violent hate crime — individuals or property targeted with violence on account of race, religion, ethnicity, sexual orientation, disability or similar status — is occurring at historically high levels in many [surveyed] countries.”⁴ More specifically,

People of African origin, regardless of their citizenship status, were subjected to some of the most persistent and serious attacks, and were among the principal victims of racist and xenophobic violence in Europe and North America…African Americans continue to be the largest group targeted for hate crime violence in the United States… In the United States, recent debates on immigration have polarized society and provided the backdrop for a surge in reported violent assaults against people of Hispanic origin, both citizens and immigrants, in the last several years…⁴

Perhaps there is no unifying theory that can explain why hate crimes world-wide are on the increase, or why people as diverse as Shirley Sherrod and Stan Cox should be subjected to vilification and abuse. As a psychiatrist, I am trained to look primarily at individuals, not whole cultures and societies. So it is merely informed speculation when I suggest that, in the U.S., the decline of decency may be driven by at least three confluent forces:

1. Increased rates of cultural narcissism, with an accompanying sense of overweening personal entitlement⁵;
2. Increased strain and fragmentation within the American family, with a consequent loss of basic trust in other people; and
3. Increased religious, political and economic upheaval, with its attendant pitting of one interest group or extremist faction against another, all competing for scarce resources.

These factors are certainly not meant to be exhaustive. But we as a people must begin our self-examination somewhere, lest we wind up in a Hobbesian society where life is “solitary, poor, nasty, brutish and short.” Indeed, as Franklin D. Roosevelt reminded us, “If civilization is to survive, we must cultivate the science of human relationships — the ability of all peoples, of all kinds, to live together, in the same world at peace.”

References

1. Saulnay S: No air conditioning and happy.
2. Swidey, N: Inside the mind of the anonymous online poster
3. Hinduja S, Patchin JW: Bullying Beyond the Schoolyard: Preventing and Responding to Cyberbullying. Corwin Press, 2008.
4. Hate Crime Survey: Overview.
5. Pies R: Have we become a nation of narcissists?

Now, thankfully, nobody has seriously proposed including loneliness in the DSM-5. Indeed, loneliness is usually thought of as simply an unpleasant part of life — one of the “slings and arrows” that pierce almost all of us from time to time. Loneliness, in some ways, remains enmeshed in a web of literary and cultural clichés, born of such works as Nathaniel West’s darkly comic novel, Miss Lonelyhearts, and the Beatles’ whimsical anthem, “Sgt. Pepper’s Lonely Hearts Club Band.”

But loneliness turns out to be a serious matter. And as psychiatry debates the diagnostic minutiae of DSM-5, all of us may need to remind ourselves that millions in this country struggle against the downward tug of loneliness. Yet even among health care professionals, few seem aware that loneliness is closely linked with numerous emotional and physical ills, particular among the elderly and infirm.

It’s easy to assume that loneliness is simply a matter of mind and mood. Yet recent evidence suggests that loneliness may injure the body in surprising ways. Researchers at the University of Pittsburgh School of Medicine studied the risk of coronary heart disease over a 19-year period, in a community sample of men and women. The study found that among women, high degrees of loneliness were associated with increased risk of heart disease, even after controlling for age, race, marital status, depression and several other confounding variables. (In an email message to me, the lead author, Dr. Rebecca C. Thurston, PhD, speculated that the male subjects might have been more reluctant to acknowledge their feelings of loneliness).

Similarly, Dr. Dara Sorkin and her colleagues at the University of California, Irvine, found that for every increase in the level of loneliness in a sample of 180 older adults, there was a threefold increase in the odds of having heart disease. Conversely, among individuals who felt they had companionship or social support, the likelihood of having heart disease decreased.

The young, of course, are far from immune to loneliness. Researchers at Aarhus University in Denmark studied loneliness in a population of adolescent boys with autism spectrum disorders (an area of great controversy in the proposed DSM-5 criteria). More than a fifth of the sample described themselves as “often or always” feeling lonely—a finding that seems to run counter to the notion that those with autism are emotionally disconnected from other people. Furthermore, the study found that the more social support these boys received, the lower their degree of loneliness. We have no cure for autism in adolescents — but the remedy for loneliness in these kids may be as close as the nearest friend.

And lest there be any doubt that loneliness has far ranging effects on the health of the body, consider the intriguing findings from Dr. S.W. Cole and colleagues, at the UCLA School of Medicine. These researchers looked at levels of gene activity in the white blood cells of individuals with either high or low levels of loneliness. Subjects with high levels of subjective social isolation — basically, loneliness — showed evidence of an over-active inflammatory response. These same lonely subjects showed reduced activity in genes that normally suppress inflammation. Such gene effects could explain reports of higher rates of inflammatory disease in those experiencing loneliness.

Could inflammatory changes, in turn, explain the correlation between loneliness and heart disease? Inflammation is known to play an important role in coronary artery disease. But loneliness by itself may be just one domino in the chain of causation. According to Dr. Heather S. Lett and colleagues at Duke University Medical Center, the perception of poor social support — in effect, loneliness — is a risk factor for development, or worsening, of clinical depression. Depression may in turn bring about inflammatory changes in the heart that lead to frank heart disease. This complicated pathway is still speculative, but plausible.

Loneliness, of course, is not synonymous with “being alone.” Many individuals who live alone do not feel “lonely.” Indeed, some seem to revel in their aloneness. Perhaps this is what theologian Paul Tillich had in mind when he observed that language “… has created the word “loneliness” to express the pain of being alone. And it has created the word “solitude” to express the glory of being alone.” Conversely, some people feel “alone” or disconnected from others, even when surrounded with people.

Let’s admit that not everybody is capable of experiencing the “glory of being alone” or of transforming loneliness into “solitude.” So what can a socially-isolated person do to avoid loneliness and its associated health problems? Joining a local support group can help decrease isolation; allow friendships to form; and give the lonely person an opportunity both to receive and to provide help. This reciprocity can bolster the lonely person’s ego and improve overall well-being.

Support groups geared to particular medical conditions can also help reduce disease-related complications. Although there are always risks in going “on line” to find support, Daily Strength appears to be a legitimate and helpful website for locating support groups of all types, including those for loneliness. Psych Central also provides opportunities to exchange ideas and “connect” with many individuals who feel isolated or alone. For those who feel lonely even in the midst of friends, individual psychotherapy may be helpful, since this paradoxical feeling often stems from a fear of “getting close” to others.

No, loneliness is not a disease or disorder. It certainly shouldn’t appear in the DSM-5 — but it should be on our minds, as a serious public health problem. Fortunately, the “treatment” may be as simple as reaching out to another human being, with compassion and understanding.

But first, let’s be clear: a “myth” is not the same thing as a lie. A myth is a transgenerational story we tell ourselves, which often has a grain of truth to it, and which usually serves some unifying function in our culture. It is a myth that George Washington threw a silver dollar across the Potomac River — there were no silver dollars at the time — but the story usefully reminds us, across many generations, that our first President was a powerful man capable of great accomplishments. No lie in that!

So, too, we have the myth of depression as a “clarifying force,” or as an “adaptive response to affliction” — notions being advanced by a number of psychologists, psychiatrists, and sociologists. Thus, Lehrer quotes psychiatrist Andy Thomson as saying, “…even if you are depressed for a few months, the depression might be worth it if it helps you better understand social relationships… Maybe you realize you need to be less rigid or more loving. Those are insights that can come out of depression, and they can be very valuable.”

Now, with all due respect to Dr. Thomson, I am inclined to ask, “Worth it to whom?” Perhaps the patients Dr. Thomson has treated emerge from their three-month bouts of depression saying, “Ya know what, Doc? It’s been a bad three months—lost my job, almost killed myself, and couldn’t get a damn thing done—but overall, it was worth it!” The depressed patients I evaluated over the past nearly 30 years almost never reported that their major depressive episodes had a “net mental benefit,” to quote Lehrer’s article. Most felt that their lives and souls had been stolen from them for the duration of their depressive episode. Many would have understood and endorsed Willam Styron’s description of his own depression, in his book Darkness Visible:

“Death was now a daily presence, blowing over me in cold gusts. Mysteriously and in ways that are totally remote from normal experience, the gray drizzle of horror induced by depression takes on the quality of physical pain… [the] despair, owing to some evil trick played upon the sick brain by the inhabiting psyche, comes to resemble the diabolical discomfort of being imprisoned in a fiercely overheated room.”

The notion that severe depression may bring forth good things reminds me of a lecture I once attended on “fire safety” in the hospital setting. We were shown a movie of a house that had burned down in such ferocious heat that a package of frozen muffin dough had been completely baked. “So, the house wasn’t a total loss!” quipped one of the world-weary attendees. Yes, of course—people can learn from their severe depressive episodes, but often at the cost of emotional and spiritual conflagration.

Similarly, Lehrer trots out the old war-horse claim that there is a “…striking correlation between creative production and depressive disorders.” But such a correlation hardly proves that depression itself heightens creativity. Psychiatrist Richard Berlin, M.D., editor of Poets on Prozac: Mental Illness, Treatment, and the Creative Process, has summarized his experience as follows:

“The idea that depression might enhance creativity is a myth, often based on the life stories and statements of deceased artists and writers… Contemporary poets who are alive and can tell us about their experience with depression are consistent in reporting that it was only after effective psychiatric treatment that they were able to create at their highest levels.” (R.M. Berlin M.D., personal communication, 1/27/08).

One of the other notions put forward in Lehrer’s article is that depressive “rumination” may actually help us analyze our way out of difficult dilemmas — the so called “analytic-rumination” hypotheses. To support this claim, Lehrer cites several studies showing that depression leads to increased activity in the “problem-solving” part of the brain, the prefrontal cortex.

But there are also numerous studies showing the precise opposite, which Lehrer fails to note. For example, Hosokawa and colleagues in Japan found that, compared with healthy controls, subjects with major depression showed decreased metabolic activity in frontal brain regions. Furthermore, there are innumerable studies showing that major depression impairs higher-level thought processes. Dr. Charles DeBattista, in a recent review, concluded that, “The types of executive deficits seen in depression include problems with planning, initiating and completing goal-directed activities” and that such “executive dysfunction” tends to worsen in direct proportion to the severity of depression.

Lehrer is a thoughtful writer, but in this article, his conflation of terms like “depression,” “sadness,” “melancholy,” and “low mood” produces a kind of conceptual tossed salad. Some of the studies he cites, in which subjects are tested under transient, experimentally-induced states of low mood, have evidently befuddled Lehrer, who assumes that these brief, artificial states are somehow comparable to clinical depression. For example, Lehrer cites the work of social psychologist J.P. Forgas, who “…has repeatedly demonstrated in experiments that negative moods lead to better decisions in complex situations.” But Forgas’s research induces “negative mood” by giving his subjects bad feedback on a bogus test of their verbal abilities. It is simply ludicrous to extrapolate from a few minutes of bruised feelings to a few weeks of severe, major depression.

Lehrer also perpetuates the fiction that antidepressant treatment “interferes” with recovery from depression, by posing the issue as a classic false-choice. Citing psychiatrist Andy Thomson and psychologist Steven Hollon, Lehrer suggests that depressed patients prescribed medication will be “discouraged from dealing with their problems” — as if prescribing a medication slams the door shut on providing concomitant psychotherapy! Most studies find that, for severe depression, medication and “talk therapy” complement and enhance one another. There is no credible, controlled evidence that antidepressants “interfere” with the development of problem-solving skills.

That said, I fully agree that effective psychotherapy may have a greater “protective” effect than medication alone in preventing depressive relapse. Indeed, I advocate psychotherapy as the “first line” treatment for most mild-to-moderate depressive states.

Finally, it is time to challenge the dubious notion that if a condition, such as depression, is highly prevalent in the general population, this must mean that the condition confers some kind of evolutionary advantage, or represents a useful “adaptation.” (Following that line of logic, ignorance and superstition must also have some adaptive advantages, since they are both so widespread throughout the world!). It is more likely that the tendency to develop depression remains “conserved” in the human genome as a spandrel — a kind of genetic hitchhiker that does nothing to improve the ride.

In architecture, a spandrel is simply the space between two arches. Molecular evolutionist Richard Lewontin and paleontologist Steven Jay Gould argued that many traits in nature are nonadaptive, and—like spandrels—are simply byproducts of other, presumably adaptive traits. For example, Gould notes that bones are made of calcite and apatite for adaptive reasons, but they are white simply because that’s the color dictated by those minerals—not because “whiteness” confers an adaptive advantage.

In her upcoming book, The Pocket Therapist, Therese J. Borchard candidly observes that, “…the sensitivity that produces so much of my [emotional] pain is precisely what makes me the compassionate person I am.” [Disclosure: I wrote the forward to Borchard’s book]. I believe that Borchard may be gesturing toward one possible mechanism by which depression is genetically conserved: not by virtue of its adaptive value, but by virtue of depression’s ability to “hitchhike” along — as a spandrel — with a sensitive, altruistic, and compassionate nature: traits that are indeed adaptive, in many social contexts.

As Borchard wisely counsels, we should not renounce or disown the part of us that produces depression — it is a piece of our messy, complex, and wondrous humanity. And, to be sure: ordinary sadness or grief may indeed be a good teacher. We should not rush to suppress or “medicate” what Thomas à Kempis called “the proper sorrows of the soul.” At the same time, we should be under no illusion that severe clinical depression is a “clarifying force” that helps us navigate life’s complex problems. That, in my view, is a well-intentioned but destructive myth.

References

Lehrer, J: Depression’s Upside. New York Times Magazine, Feb. 28, 2010.

Forgas, JP: On being happy and mistaken. Journal of Personality and Social Psychology 1998;75:318-31.

Hosokawa T, Momose T, Kasai K. Brain glucose metabolism difference between bipolar and unipolar mood disorders in depressed and euthymic states. Prog Neuropsychopharmacol Biol Psychiatry. 2009 Mar 17;33(2):243-50

DeBattista, C. Executive dysfunction in major depressive disorder. Expert Rev Neurother. 2005 Jan;5(1):79-83.

Borchard, TJ. The Pocket Therapist. New York, Center Street, 2010 (April).

Gould, SJ: The Structure of Evolutionary Theory. Belknap Press of Harvard University Press, 2002.

Pies, R: The anatomy of sorrow: a spiritual, phenomenological, and neurological perspective. Philos Ethics Humanit Med. 2008 Jun 17;3:17. Accessed at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2442112/?tool=pubmed

In the past few days, Meagan had found it increasingly hard to fall asleep, and noticed that her appetite was poor. From time to time, she found herself weeping or sighing, but not knowing what to do. She wondered if “maybe having a few drinks” might do her some good.

Meagan (a composite character) has a number of risk factors for feeling down or depressed. First, women have rates of serious depression about twice those of men, and are also at higher risk for a particular type of major depression called Seasonal Affective Disorder (SAD). In addition, the combined stresses of holiday chores, child care, and financial woes put Megan at risk for what is popularly known as “the holiday blues.” So does Meagan’s “anniversary reaction” over the death of her mother. But what do we really know about the “holiday blues,” beyond hundreds of anecdotes and Internet postings? How do the “blues” differ from SAD and other forms of major depression? And is the commonly-held notion that suicide rates soar during the Christmas and winter holiday season really valid? Some recent research sheds light on these questions, while also highlighting many “grey areas” in our knowledge.

Let’s deal with the “Christmas suicide” story first. From all the data we have gathered in the U.S. and parts of Europe, we can say confidently that this is a myth. In fact, we have evidence going back to the 19th century that suicide rates generally decline in the late fall and winter months, and spike upward in late spring and summer. The precise reasons for this pattern are not known, but the finding is consistent across many studies. In fact, data from Zurich, Switzerland, show that suicide rates begin to fall as early as late November, and remain lower until just after New Year’s Eve. That’s the good news, and ought to allay fears that Christmas, Chanukkah, Kwanzaa or other winter celebrations are times of high suicide risk. The not-so-good news, however, is that suicide rates appear to spike upward after New Year’s Eve — largely among men. Rates for women seem to return to baseline, without a major spike.

There are two main hypotheses to explain these patterns. The “broken promises” hypothesis holds that, during the holiday season, people have very high expectations. Like Meagan, many view the holidays as a time to put things right, experience the joy of family and friends, and perhaps to experience some kind of spiritual renewal. Unfortunately, many are disappointed when these hopes are dashed — and some who become very despondent may take their lives. In contrast, the “withdrawn support” hypothesis begins with the observation that the winter holidays are usually a time of increased contact with family and friends. Social contact and support are known to protect against the risk of suicide. But after New Year’s Day, social supports usually diminish rapidly. This is what I call the “picking up the wrapping paper phase,” and it may be the time some very vulnerable individuals decide to take their own lives. Why does the post-holiday increase in suicides affect men more than women, at least in Switzerland? It may be partly because women are better than men at maintaining post-holiday social support networks, but this remains speculative.

With all the annual hoopla over the “holiday blues,” it is surprising that so little solid research has been done on it. There seems to be no specific definition of the term, and — so far as I can tell — there are no well-designed epidemiological studies of the phenomenon in the U.S. That said, Dr. Jennifer Wider reports that nearly two-thirds of women surveyed by the National Women’s Health Research Center reported feeling depressed during the previous year’s winter holidays. I’m not aware of comparable data for men. However, Dr. Wider observes that often, during the holidays, the burdens of family caretaking fall mainly on the shoulders of women. Increased alcohol use during the holidays, combined with family stressors, may set many women up for the holiday blues. Of course, men are hardly immune to this condition, and are at higher risk for completed suicide.

Psychologist Dr. Herbert Rappaport believes that those he calls “fixers” — individuals intent on “making everything right” during the holidays — are especially prone to grief reactions after Christmas and Chanukkah. Fortunately, the “holiday blues” are usually short-lived, lasting a few days or perhaps a week or two in most cases. This differs from SAD, which tends to last weeks or months, and reappears winter after winter, regardless of social stressors. SAD, which affects perhaps 10 percent of the population, may be related to decreased daylight in the winter months, which in turn may reduce mood-boosting brain chemicals like serotonin. SAD is often characterized by excessive daytime sleep, substantial weight gain, inability to function, and persistent thoughts of suicide. Unlike the “blues,” SAD and other types of major depression require professional intervention.

Preventing the holiday blues involves four main strategies: keeping expectations realistic; delegating responsibilities; shoring up social supports; and avoiding excessive alcohol consumption. More detailed advice is found in several of the articles listed below. Finally, another good strategy, according to Dr. Hinda Dubin of the University of Maryland Medical Center, is to find ways of helping those less fortunate than oneself. Taking the focus off your own problems and aiding somebody truly in need may be the best gift you’ll ever get during the holiday season!

For more information on coping with the “holiday blues,” see the following websites:

• Beating the Holiday Blues
• Managing the holiday blues
• Beating the Holiday Blues
• Nine Ways to Beat the Bah Humbugs
• Wrung-Out by Ringing-In the Holidays: Dealing with Post-Holiday Blues

As Dr. John Grohol has cogently argued, there are many reasons to be skeptical of “Internet Addiction” as a discrete and specific “disorder” or diagnosis. Yet I am impressed, and a bit dismayed, by all the attention this issue seems to garner in the popular media. I don’t intend any disrespect to the reporters and journalists who are trying to cover the topic, several of whom have graciously interviewed me. Some reporters are as skeptical as many of us in the mental health field, and a number have asked pertinent questions as to how real so-called Internet addiction is. I simply wish that devastating illnesses like schizophrenia, major depression, and bipolar disorder created such a buzz in the media and in the awareness of the general public. Over the last 30 years as a psychiatrist, I’m guessing I have been contacted by the media perhaps four or five times, to discuss these serious disorders. I have had nearly that number of requests to discuss “Internet addiction” in the past three months.

Some of the interest probably stems from a professional article I did on the subject, but I suspect other factors are driving the media frenzy. For example, the pervasive influence of the Internet in our society; the hot button issues of online pornography, gambling, and gaming; and perhaps the perverse pleasure of skewering the psychiatric profession for even considering Internet addiction as a new diagnosis in the upcoming DSM-V. There also is a great deal of confusion around terms such as “addiction” (which is not even used in the DSM-IV), “disorder,” “disease,” and related terms of art. And so, after several interviews with inquiring reporters, here is my take on where the controversy stands.

In theory, we can distinguish harmful or self-defeating behaviors and bad habits from “disease.” But if the behavior goes on long enough and dramatically alters the individual’s brain chemistry, the central nervous system may be changed in enduring ways. There is not always a bright line between self-defeating habits–which, at first, may be relatively conscious, controlled, and deliberate–and pathological changes in the brain’s structure and function. These brain changes may lead to behaviors that become harder and harder for the individual to control. Over time, what started as a mere “bad habit” may become a self-sustaining impulse control disorder.

Nicotine dependence is a good example. A person may, at first, simply choose to smoke for pleasure or relaxation. Eventually, however, nicotine alters the reward centers of the brain in ways that may be hard to reverse. For example, nicotine is known to activate brain circuits using the chemical dopamine, and perhaps also circuits involving the body’s own natural opioid compounds, called endorphins. Over time, these circuits become more and more entrained — ready to reverberate at the first whiff of secondhand smoke, and impel the person to “light up.” I believe a similar continuum — from “bad habit” to disease — may also apply to excessive Internet use. Over long periods of time, the brain may become rewired in enduring ways by excessive Internet-mediated stimulation.

In an already susceptible individual — let’s say, someone with underlying chronic depression or an aversion to social contact — the person may eventually wind up in a state of such suffering and incapacity that the term “disease” (dis-ease) actually applies. A vicious circle is soon set up: the more the “Internet-addicted” person withdraws from the outside world, the less competent he or she becomes in carrying out the social and vocational functions the world requires. This in turn leads to more avoidance and isolation, which worsens the person’s depression, intensifies the Internet use, and round and round we go.

But does this unfortunate individual have a specific disease, one that is discrete and biologically identifiable (e.g., H1N1 flu or Parkinson’s disease)? Or should we consider it one of a family of related diseases or disorders which may have similar genetic origins, brain chemistry, course, outcome and response to treatment?

Let’s take obesity as an analogy. It would seem odd and a little silly if we started creating specific diseases called Twinkie-induced obesity, nachos-induced obesity, French fries-induced obesity, etc. We presume that these are not discrete diseases, like swine flu, but different pathways to a common disorder (obesity). Similarly, it may not make sense to elevate Internet addiction to the status of a discrete disorder if the same brain chemistry is involved in pathological gambling, nicotine and cocaine dependence. As mental health professionals, we surely want to avoid adding dozens of new disease entities as new electronic media are invented.

If we picture aberrant reward system disorders (ARSDs) as a large, multi-room house, it may be that there are many different doorways into that structure. It seems counterproductive to give each door a name and a status as a unique disorder, just as it would to speak of Twinkie-induced obesity in contrast to nachos-induced obesity. On the other hand — and this is a matter of empirical investigation — if it should turn out that pathological Internet use is very different from, say, nicotine dependence or pathological gambling in certain key respects, then perhaps separate disease status will need to be accorded each of these doorways.

For example, suppose we studied thousands of subjects with various ARSDs. If Internet addiction were shown to have a unique pattern of abnormal brain chemistry, associated genetic factors, co-occurring psychiatric disorders, course of illness, and response to treatment, we might then have to grant it status as a discrete disorder. But in my view, the data are simply not there to justify such a conclusion. We sorely need large-scale, comparative studies of these conditions to know how they relate to one another.

Yes, there are some individuals who are both suffering and incapacitated by their pathological
Internet use, and they deserve our compassionate care and attention. But let’s keep their problem in perspective, and hope that the media begin to focus on the many serious psychiatric disorders and diseases that afflict our friends, family, and loved ones.

It doesn’t take a psychiatrist to conclude that all three individuals placed their momentary emotional needs over the feelings and wishes of others — and that they failed to play by the proverbial rules of the game. Though their intrusive behavior may be rationalized as “off the cuff” or “from the heart,” the fact remains that each of these individuals performed a calculation over a period of seconds, minutes, or perhaps hours: they calculated that their anger or resentment was more important than the decorum others expected of them.

Sure, we all “lose it” from time to time, and impolite outbursts have probably been with us since our Neanderthal forebears first learned to growl. Furthermore, the impression that manners have gotten worse and worse over the years may not be supported by historical data. John F. Kasson, in his book, Rudeness and Civility, points out that people in medieval times behaved far more boorishly than our modern-day, “It’s all about me!” crowd. Citing the work of sociologist Norbert Elias, Kasson writes that, compared to more recent times, “…people in the late Middle Ages expressed their emotions—joy, rage, piety, fear, even the pleasure of torturing and killing enemies—with astonishing directness and intensity.”

Maybe so — but the recent tripleheader of West, Williams and Wilson made many of us wonder if we are turning into a nation of self-absorbed boors. (A Boston Globe editorial on 9/15/09 proclaimed, “Shouting is the New Opining.”) This thesis is hardly new. Thirty years ago, Christopher Lasch put forward essentially the same argument, in his book The Culture of Narcissism. But Lasch’s claims were mainly impressionistic. Now, however, a number of researchers and mental health professionals point to studies showing that, indeed, excessive self-absorption is on the increase.

For example, in their book, The Narcissism Epidemic: Living in the Age of Entitlement, Jean M. Twenge, Ph.D and W. Keith Campbell, Ph.D. provide ample evidence for what they term “the relentless rise of narcissism in our culture.” Twenge and Campbell identify several social trends that have contributed to this problem, including what they term “the movement toward self-esteem” that began in the late 1960s; and the movement away from “community-oriented thinking” that began in the 1970s. But the root causes go far deeper. For example, in a chapter entitled “Raising Royalty,” Twenge and Campbell point to “…the new parenting culture that has fueled the narcissism epidemic.” In effect, the authors argue, there has been a shift away from limit-setting toward letting the child get whatever he or she wants.

Twenge and her colleagues have empirical data to back up their claims. For example, in a paper published in the August 2008 Journal of Personality, the authors report on 85 samples of American college students, studied between 1979 and 2006. The subjects were evaluated using an instrument called the Narcissistic Personality Inventory (NPI). Compared with their peers in the 1979-85 period, college students in 2006 showed a 30 percent increase in their NPI score. That’s “the bad news.”. If there is some good news, it might be this: Twenge and her colleagues Sara Konrath, Joshua D. Foster, W. Keith Campbell, and Brad J. Bushman point to a rise in several “positive traits” correlated with narcissism, such as self-esteem, extraversion, and assertiveness. Of course, a cynic might reply that these traits are “positive” only up to a point: When someone’s idea of “assertiveness” involves jumping up on stage and grabbing the microphone from an award-winning singer, assertiveness has arguably crossed the line into loutishness.

Twenge and Campbell take pains to knock down the myth that all narcissists are basically insecure folks with very low self-esteem. Their research suggests otherwise — most narcissists seem to have a heaping helping of self-esteem! But Twenge and Campbell focus mainly on individuals they call the “socially savvy narcissists who have the most influence on the culture.” These high-fliers may be the sort one of my colleagues had in mind when he defined a narcissist as “somebody who, at the moment of peak sexual bliss, cries out his own name!”

These celebrity narcissists are not, for the most part, the kind of individuals I have treated in my own psychiatric practice. My patients tended to fall into the group Twenge and Campbell call “vulnerable narcissists.” These unfortunate souls seem to cloak themselves in a mantle of gold, while feeling that, on the inside, they are nothing but rags. They suffer, to be sure — but they also induce suffering in others, by acting out their insecurities in a thousand provocative ways. And, like some of their celebrity counterparts, these vulnerable narcissists are prone to outbursts of anger, verbal abuse, or just plain rudeness — usually when they feel rejected, thwarted, or frustrated. They remind one of philosopher Eric Hoffer’s observation that “rudeness is the weak man’s imitation of strength.”

If we are indeed producing increasingly self-obsessed individuals in our society, what can we do about it? There is clearly no simple prescription for what are evidently deep-seated cultural and familial ills. There is almost certainly no “Prozac for Narcissists” anywhere on the pharmacy shelves. As Twenge and Campbell argue, there is much in the way that we raise our children that may need to change. In my view, it is not simply a matter of refusing to spoil or over-indulge our children. Rather, we must also instill positive values that will help inoculate our children against narcissism.

In my book, Everything Has Two Handles: The Stoic’s Guide to the Art of Living, I argue that the values of the ancient Stoics can help us achieve personal happiness. I believe that these same values can help our children grow into strong, responsible, and resilient citizens. And what are Stoic values? It’s not just a matter of keeping a stiff upper lip, nor does Stoicism hold that you should tamp down all your feelings. Rather, Stoics believed that the good life is one characterized by virtuous beliefs and actions—in brief, a life based on duty, discipline, and moderation. The Stoics also believed in the importance of taking life on its own terms–what they would have described as “living in harmony with nature.”

Stoics did not whine when they were passed over for an award, nor did they throw a hissy fit when they didn’t get their way. As the Stoic philosopher, Seneca (106-43 BCE) put it, “All ferocity is born of weakness.” Perhaps most important, Stoics understood the tremendous value of gratitude — not only for the gifts we have received, but also for the grief we have been spared. Maybe if more children were inculcated with these teachings, we would find our celebrities showing more gratitude and less “attitude.”

We found out about the lost movies a day after Continental flight 3407 went down, just a few miles from the small town in western New York where I grew up. And as the magnitude of the disaster became clear—as the stories of so many bright lives snuffed out unfolded — I began to feel slightly ashamed and foolish. The people on that plane would never again have to worry about lost home movies, or paying taxes, or where their next meal would come from. They would never again have the opportunity to burn a piece of toast, wreck a relationship, or be on the receiving end of a pink slip. The passengers who lost their lives on flight 3407 would now have no problems at all – and would never have problems again. Having problems means you are alive. It is a great gift that we often mistake for an insufferable burden.

As a psychiatrist, I am usually focused on helping people overcome their emotional problems. So are most of my colleagues in the mental health profession, and that is as it should be. People come to us with various crises and in various states of suffering and incapacity. We do what we can to help them get back on their feet. But with the exception of some who practice an existential form of psychotherapy, we rarely teach our patients the spiritual value of having problems — which is to say, the value of the ineffably precious and fleeting gift of life.

In the Jewish tradition, there is a folk saying: “When a Jew breaks his leg, he thanks God he did not break both legs. When he breaks both, he thanks God he did not break his neck.” This is not quite the same as being thankful for one’s problems, but it does acknowledge, with gratitude, that one’s problems could be much worse.

In Islam, the well-known declaration usually translated as, “God is great!” — the takbir — is spoken both at times of joy and on occasions of mourning. And the German Christian monk, Thomas a Kempis, taught that, “…it is good to encounter troubles and adversities, from time to time; for trouble often compels a man to search his own heart.”

Let me be clear: I am in no way endorsing the misguided notion that clinical depression is somehow “good for the soul”, or that it is represents a state of heightened spiritual or artistic awareness. This myth has been thoroughly debunked by my colleague, Dr. Peter Kramer, in his book Against Depression. But I am saying that when we find ourselves dealing with everyday problems, we can find a measure of consolation in the fact that we are troubled only because we are alive — and life is something we must never take for granted. Just as the philosopher Martin Heidegger argued that the awareness of death allows us to live a more intense and “authentic” life, I believe that the embrace of our problems leads us to a deeper appreciation of our pleasures.

The medieval philosopher Boethius observed that, “Good fortune deceives; adverse fortune teaches.” I believe he meant something like this. We are often lulled into a false sense of complacency by the good things that happen to us. We win the lottery or make a killing in the stock market, and we imagine that good fortune will always be ours. The present financial crisis befalling the nation has shown us the emptiness of such ersatz optimism. On the other hand, adversity points us toward a hard truth: we are all just flesh and blood; we are all mortal. It is silly to fuss and fume over a few lost reels of film. The tragic end of flight 3407 has deprived fifty of our fellow human beings the rich pleasure of having problems. We can honor their memory by living our lives more authentically, and rejoicing in the sweetness of our adversities.