“Love is merely a madness; and, I tell you, deserves as well a dark house and a whip as madmen do; and the reason why they are not so punish’d and cured is that the lunacy is soordinary that the whippers are in love too.”
— Shakespeare, As You Like It, Act III, Scene 2, line 286
“To turn Karl [Popper]’s view on its head, it is precisely the abandonment of critical discourse that marks the transition of science. Once a field has made the transition, critical discourse recurs only at moments of crisis when the bases of the field are again in jeopardy. Only when they must choose between competing theories do scientists behave like philosophers.”
— Thomas S. Kuhn
If You Think The Diagnosis Of Depression Is Scientific, Think Again:
Why did the American Psychiatric Association select five criteria as the magic figure? What is the difference between a person who meets six criteria — and is therefore diagnosed as having a Major Depressive Episode and needing antidepressant treatment — and one who meets four criteria, and therefore receives no psychiatric diagnosis or treatment? Why five criteria? Why not three? Or seven? How valid are these criteria?
Carlat: How did you decide on five criteria as being your minimum threshold for depression?
Spitzer: It was just consensus. We would ask clinicians and researchers, “How many symptoms do you think patients ought to have before you would give them a diagnosis of depression?” And we came up with the arbitrary number of five.
Carlat: But why did you choose five and not four? Or why didn’t you choose six?
Spitzer: Because four just seemed like not enough. And six seemed like too much.Carlat commented that ‘Spitzer smiles mischievously’ as he uttered the last sentence above. This is the quality of the “science” upon which the diagnosis of depression is based.
The Americanization of Mental Illness:
In short, Shorter was convinced that medicine did not just “reveal” disorders that had previously escaped medical attention, but that one could actually increase their prevalence by simply putting the disorder on the cultural map.
To explain how this could happen, Shorter made use of an interesting metaphor — that of the “symptom pool.” Each culture, he argued, possessed a metaphorical pool of culturally legitimate symptoms through which members of a given society would choose, mostly unconsciously, to express their distress. It was almost as if a particular symptom would not be expressed by a given cultural group until the symptom had been culturally recognized as a legitimate alternative — that is, until it had entered that culture’s “symptom pool.” This idea could help explain, among other things, why symptoms that were very common in one culture would not be in another.
Why, for example, could men in Southeast Asia but not men in Wales or Alaska experience what’s called Koro (the terrifying certainty that their genitals are retracting into their body)? Or why could menopausal women in Korea but not women in New Zealand or Scandinavia experience Hwabyeong (intense fits of sighing, a heavy feeling in the chest, blurred vision, and sleeplessness)? For Shorter, the answer was simple: symptom pools were fluid, changeable, and culturally specific, therefore differing from place to place.
This idea implied that certain disorders we take for granted are actually caused less by biological than cultural factors — like crazes or fads, they can grip or release a population as they enter or fade from popular awareness. This was not because people consciously chose to display symptoms that were fashionable members of the symptom pool, but just that people seem to gravitate unconsciously to expressing those symptoms high on the cultural scale of symptom possibilities. And this of course makes sense, as it is crucial that we express our discontent in ways that make sense to the people around us (otherwise we will end up not just ill but ostracized).
As Anne Harrington, professor of history of science at Harvard, puts it, “Our bodies are physiologically primed to be able to do this, and for good reason: if we couldn’t, we would risk not being taken seriously or not being cared for. Human beings seem to be invested with a developed capacity to mold their bodily experiences to the norms of their cultures; they learn the scripts about what kinds of things should be happening to them as they fall ill and about the things they should do to feel better, and then they literally embody them.” Contagions do not spread through conscious emulation, then, but because we are unconsciously configured to embody species of distress deemed legitimate by the communities in which we live.
And this is why the historian Edward And this is why the historian Edward Shorter believed that when it came to the spread of symptoms, the same “bandwagon effect” could be observed too. If enough people begin to talk about a symptom as though it exists, and if this symptom is given legitimacy by an accepted authority, then sure enough more and more people will begin to manifest that symptom.
This idea explained for Shorter why symptoms can dramatically come and go within a population — why anorexia can reach epidemic proportions and then suddenly die away, or why self-harm can suddenly proliferate. As our symptom pool alters, we are given new ways to embody our distress, and as these catch on, they proliferate.
After reading Shorter’s work, Dr. Lee began to understand what had happened in Hong Kong. Anorexia had escalated after Charlene’s death because the ensuing publicity and medical recognition introduced into Hong Kong’s symptom pool a hitherto foreign and unknown condition, allowing more and more women to unconsciously select the disorder as a way of expressing their distress.
This theory was also consistent with another strange change Dr. Lee had noticed. After Charlene’s death it wasn’t just the rates of anorexia that increased but the actual form anorexia took. The few cases of self-starving Lee treated before Charlene’s death weren’t characterized by the classic symptoms of anorexia customarily found in the West, where sufferers believe they are grossly overweight and experience intense hunger when they don’t eat. No, this particular set of Western symptoms did not match the experiences of anorexics that Lee encountered before the mid-1990s, where anorexics had no fear of being overweight, did not experience hunger, but were simply strongly repulsed by food.
This all changed as Western conceptions of anorexia flooded Hong Kong’s symptom pool in the mid-1990s. Young women now began to conform to the list of anorexic symptoms drawn up in the West. Like Western anorexics, those in Hong Kong now felt grossly overweight and desperately hungry. In short, as part of the Western symptom drained eastward, the very characteristics of anorexia in Hong Kong altered too.
Does Psychiatry Need Science? The Strange Case of Melancholia and the Brain:
A detailed understanding of the brain, with its hundred billion neurons and trillions of synapses, remains elusive, leaving psychiatry dependent on outward manifestations for its taxonomy of mental illnesses. Indeed, it has been doubling down on appearances since 1980, which is when the American Psychiatric Association created a Diagnostic and Statistical Manual of Mental Disorders (D.S.M.) that intentionally did not strive to go beyond the symptom. In place of biochemistry, the D.S.M. offers expert consensus about which clusters of symptoms constitute particular mental illnesses, and about which mental illnesses are real, or at least real enough to warrant a name and a place in the medical lexicon. But this approach hasn’t really worked to establish the profession’s credibility. In the four revisions of the D.S.M. since 1980, diagnoses have appeared and disappeared, and symptom lists have been tweaked and rejiggered with troubling regularity, generally after debate that seems more suited to the floors of Congress than the halls of science. The inevitable and public chaos — diagnostic epidemics, prescription-drug fads, patients labelled and relabelled — has only deepened psychiatry’s inferiority complex.
Not only did the DSM become the bible of psychiatry, but like the real Bible, it depended a lot on something akin to revelation. There are no citations of scientific studies to support its decisions. That is an astonishing omission, because in all medical publications, whether journal articles or textbooks, statements of fact are supposed to be supported by citations of published scientific studies. (There are four separate “sourcebooks” for the current edition of the DSM that present the rationale for some decisions, along with references, but that is not the same thing as specific references.) It may be of much interest for a group of experts to get together and offer their opinions, but unless these opinions can be buttressed by evidence, they do not warrant the extraordinary deference shown to the DSM.
The drug industry, of course, supports other specialists and professional societies, too, but Carlat asks, “Why do psychiatrists consistently lead the pack of specialties when it comes to taking money from drug companies?” His answer: “Our diagnoses are subjective and expandable, and we have few rational reasons for choosing one treatment over another.” Unlike the conditions treated in most other branches of medicine, there are no objective signs or tests for mental illness — no lab data or MRI findings — and the boundaries between normal and abnormal are often unclear. That makes it possible to expand diagnostic boundaries or even create new diagnoses, in ways that would be impossible, say, in a field like cardiology. And drug companies have every interest in inducing psychiatrists to do just that.
The Loss of Sadness amounts to a relentless dismantling of the DSM — one that seems confined at first to a single inadequacy, only to blossom into an exposure of the manual’s top-to-bottom arbitrariness. I am not sure, in fact, that the authors themselves understand the full gravity of the challenge they have posed for American psychiatry.
At the core of their book lies a demonstration that episodic sadness has always been a socially approved means of adjusting to misfortune and that much is lost, both medically and culturally, when it is misread as a depressive disorder. Yet as Robert L. Spitzer, the chief architect of DSM-III and Christopher Lane’s bête noire, concedes in a generous foreword, the manual has propagated that very blunder by failing to clarify the difference between environmentally prompted moods — those responding to stress or hardship — and dysfunctional states persisting long after the causes of stress have abated. In no sense, however, can that indictment be confined to just one disorder. The Loss of Sadness implies that nearly every nonpsychotic complaint is subject to overdiagnosis unless contextual factors — familial, cultural, relational, financial — are weighed in the balance.
As might be expected, then, Horwitz and Wakefield end by begging the compilers of DSM-V (now projected for 2012) to teach their colleagues the need for inquiry into each patient’s circumstances before concluding that they are faced with a bona fide disorder. The bar for authentic pathology must be set higher. If this is done, the authors declare, the DSM will be more scientifically respectable; its users, instead of regarding disadvantaged classes as infested with mental illness, will gain an appreciation of socioeconomic reasons for unhappiness; and a brake will be placed on the expensive middle-class hypochondria that the drug companies have so assiduously encouraged and exploited.
As for psychiatry’s inability to settle on a discrete list of disorders that can remain impervious to fads and fashions, that is an embarrassment only to clear academic thinkers like these two authors. For bureaucratized psychological treatment, and for the pharmaceutical industry that is now deeply enmeshed in it, confusion has its uses and is likely to persist.
Later that year, gay activists, including some psychiatrists, after years of increasingly public and contentious debate, finally persuaded the APA to remove homosexuality from the DSM — a good move, no doubt, but one that, especially after what had happened to the graduate students, couldn’t help but reveal that even when psychiatrists did agree on a diagnosis, they might have been diagnosing something that wasn’t an illness. Or, to put it another way, psychiatrists didn’t seem to know the difference between sickness and health.
Forty years, two full rewrites, and two interim revisions of the DSM later, they still don’t. Psychiatrists have gotten better at agreeing on which scattered particulars they will gather under a single disease label, but they haven’t gotten any closer to determining whether those labels carve nature at its joints, or even how to answer that question. They have yet to figure out just exactly what a mental illness is, or how to decide if a particular kind of suffering qualifies. The DSM instructs users to determine not only that a patient has the symptoms listed in the book (or, as psychiatrists like to put it, that they meet the criteria), but that the symptoms are “clinically significant.” But the book doesn’t define that term, and most psychiatrists have decided to stop fighting about it in favor of an I-know-it-when-I-see-it definition (or saying that the mere fact that someone makes an appointment is evidence of clinical significance). Instead, they argue over which mental illnesses should be admitted to the DSM and which symptoms define them, as if reconfiguring the map will somehow answer the question of whether the territory is theirs to carve up.
This kind of argument leads to all sorts of interesting drama, but none of it can answer the question I posed about Sandy: Is disease really the best way to understand his craziness? How much of our suffering should we turn over to our doctors — especially our psychiatrists?
I don’t know the answer to that question. But neither do psychiatrists. Even in a case as florid as Sandy’s, they cannot say exactly how they know he has a mental illness, let alone what disorder he has or what treatment it warrants or why the treatment works (if it does), which means that they cannot say why his problem belongs to them. That’s no secret. Any psychiatrist worth his or her salt will freely acknowledge (and frequently bemoan) the absence of blood tests or brain scans or any other technology that can anchor diagnosis in a reality beyond the symptoms. What they are more circumspect about is the disquieting implication of this ignorance: that if a physician wants to claim that drapetomania and homosexuality and, as the DSM-5 has proposed, at one time or another, Hypersexuality and Internet Use Disorder and Binge Eating Disorder are medical illnesses, there is nothing to stop him from doing so and if he is shrewd and lucky and smart enough to persuade his colleagues to follow him, the insurers, the drug companies, the regulators, the lawyers, the judges, and, eventually, the rest of us will have no choice but to go along.
Why You’re Crazy: The DSM Story
In their rush to create the most comprehensive listing of mental disorders possible, diagnosticians regularly conflated mental illness with a range of social and political concerns, professional consensus, and cultural, racial, and gender biases to arrive at a dizzying array of hybrid disorders. Homosexuality, for example, had been a largely controversial category since it was included in the first edition of the manual.1 The Freudian interpretation of homosexuality as a deviation in sexual development, and therefore a “disease state,” was largely accepted in this early edition. Effectively, a practicing homosexual in the late 1950s onward could be “officially” labeled as having a psychiatric disorder and thus burdened with all the opprobrium and, often, the punitive constraints associated with these types of disorders. Throughout the 1960s, however, gay men and lesbians, support groups, and enlightened analysts and clinicians fought the DSM’s designation, but they were unable to have the disorder removed from subsequent manuals. In later editions, the language changed but the disordered character of homosexual activity remained. Retaining the disorder was a direct result of the strictly unscientific institutional power plays that had become common to the formation of the newly issued editions of the DSM. The Nomenclature Committee, the most powerful arm of the APA’s so-called Task Force, had skillfully maneuvered the other small committees to create a new designation, Ego-Dystonic Homosexuality (302.00). In this rearranged substitute illness, the homosexual was still sick, but now he was sick because of the immense guilt he felt at being a homosexual, and the overwhelming need to change his tormented ways. In a homophobic society, this resulted in little more than blaming the victim.
Women do not fare much better in the history of the DSM. Early editions of the DSM tended to translate common biases against women into full-fledged disorders, and later editions maintain the subtle nomenclature of sexism, developed by the all-male committees first convened by the APA, that are still widely used within psychiatry and medicine. A good example of this is the designation and subsequent re-designation of Masochistic Personality Disorder. In earlier editions of the DSM, women’s supposed passivity and dependence on men fit nicely with the psycho-sexual dynamics of Freudian construed masochism. In short, mistreated women got what they begged for, psychologically speaking. This designation, however, ran into some trouble in subsequent editions, particularly when it became linked with a DSM-III-R invention: Paraphilic Rapism, a disorder in which certain males cannot help themselves from raping females. If a female Masochistic personality type comes in contact with a male victim of Paraphilic Rapism, she might give him exactly the kind of signals that would turn him on. Then, if apprehended, the poor devil could make either an insanity plea or to elicit extreme sympathy on the part of judge or jury. Feminists who fought hard to exclude this unfortunate confluence from the DSM-IV were able to have the Paraphilic Rapism category completely altered and retro-fitted, but Masochistic Personality Disorder remained.2 It appears in the form of the cleansed emendation, Self-Defeating Personality Disorder. Rapism is dispensable; sexism is not.
SSRIs, Minimal Effectiveness and High Risk:
If psychiatry were a bona fide medical field, a meta-analysis of this quality yielding these results would send Richter 9 shock waves through the profession. The prescription of SSRIs for depression is probably the single most frequent activity performed by psychiatrists in their day-to-day work. The unambiguous revelation that this activity is doing more harm than good should be generating enormous concern for psychiatry’s leadership and for the rank and file.
But the publication of this study on February 8 generated no discernible concern within the profession. This is because psychiatry has very little interest in the scientific assessment of its “treatments.” Psychiatry is drug-pushing, pure and simple. The primary criteria of success are customer retention, and volume of product sold. As long as the “patients” keep coming back for more, psychiatrists can convince themselves that they are doing good.
The fact that the “patients” have been duped by unsubstantiated assertions of chemical imbalances, and are, in many cases, addicted to the pills, are inconvenient truths that can readily be eclipsed by self-deception and in-group mutual reassurance.
There was just one problem with this utopian vision of better psychiatry through science: the “science” hadn’t yet been done. “There was very little systematic research, and much of the research that existed was really a hodgepodge — scattered, inconsistent, and ambiguous,” Theodore Millon, one of the members of the DSM-III task force, says. “I think the majority of us recognized that the amount of good, solid science upon which we were making our decisions was pretty modest.” Members of the various committees would regularly meet and attempt to come up with more specific and comprehensive descriptions of mental disorders. David Shaffer, a British psychiatrist who worked on the DSM-III and the DSM-IIIR, told me that the sessions were often chaotic. “There would be these meetings of the so-called experts or advisers, and people would be standing and sitting and moving around,” he said. “People would talk on top of each other. But Bob would be too busy typing notes to chair the meeting in an orderly way.” One participant said that the haphazardness of the meetings he attended could be “disquieting.”
He went on, “Suddenly, these things would happen and there didn’t seem to be much basis for it except that someone just decided all of a sudden to run with it.” Allen Frances agrees that the loudest voices usually won out. Both he and Shaffer say, however, that the process designed by Spitzer was generally sound. “There was not another way of doing it, no extensive literature that one could turn to,” Frances says. According to him, after the meetings Spitzer would retreat to his office to make sense of the information he’d collected. “The way it worked was that after a period of erosion, with different opinions being condensed in his mind, a list of criteria would come up,” Frances says. “It would usually be some combination of the accepted wisdom of the group, as interpreted by Bob, with a little added weight to the people he respected most, and a little bit to whoever got there last.”
Because there are very few records of the process, it’s hard to pin down exactly how Spitzer and his staff determined which mental disorders to include in the new manual and which to reject. Spitzer seems to have made many of the final decisions with minimal consultation. “He must have had some internal criteria,” Shaffer says. “But I don’t always know what they were.” One afternoon in his office at Columbia, I asked Spitzer what factors would lead him to add a new disease. “How logical it was,” he said, vaguely. “Whether it fit in. The main thing was that it had to make sense. It had to be logical.” He went on, “For most of the categories, it was just the best thinking of people who seemed to have expertise in the area.
So Dr. Freud, the causes are all in the brain? Isn’t there some explanation in my childhood?” It was a good-natured tease.
“I specialize in prescribing medications,” I said with a smile. I was a psychopharmacologist and specialized in medication rather than psychotherapy. “I can refer you to a good therapist in the area if you’d like.”After J.J. left my office, I realized, uncomfortably, that somehow, over the course of the decade following my residency, my way of thinking about patients had veered away from psychological curiosity. Instead, I had come to focus on symptoms, as if they were objective medical findings, much the way internists view blood-pressure readings or potassium levels. Psychiatry, for me and many of my colleagues, had become a process of corralling patients’ symptoms into labels and finding a drug to match.
Leon Eisenberg, an early pioneer in psychopharmacology at Harvard, once made the notable historical observation that “in the first half of the 20th century, American psychiatry was virtually ‘brainless.’ . . . In the second half of the 20th century, psychiatry became virtually ‘mindless.’ ” The brainless period was a reference to psychiatry’s early infatuation with psychoanalysis; the mindless period, to our current love affair with pills. J.J., I saw, had inadvertently highlighted a glaring deficiency in much of modern psychiatry.
A Psychiatrist’s Prescription For His Profession:
So, like most of my patients, Carol saw me for medications, and saw a social worker colleague for therapy. Her symptoms gradually improved, but whether this was due to the medications or the therapy, or simply the passage of time, I cannot say.
Carol’s treatment was not particularly dramatic, but her story illustrates both the triumphs and the failures of modern psychiatry. Over the last thirty years, we have constructed a reliable system for diagnosing mental disorders, and we have created medications that work well to treat a range of psychological symptoms. But these very successes have had unpredictable consequences. As psychiatrists have become enthralled with diagnosis and medication, we have given up the essence of our profession — understanding the mind. We have become obsessed with psychopharmacology and its endless process of tinkering with medications, adjusting dosages, and piling on more medications to treat the side effects of the drugs we started with. We have convinced ourselves that we have developed cures for mental illnesses like Carol’s, when in fact we know so little about the underlying neurobiology of their causes that our treatments are often a series of trials and errors.
Theories of the neurobiology of PTSD, depression, and the range of other mental illnesses have come and gone over the years, but we are still far away from a true understanding of the biological causes of these diseases. Clearly, thoughts and emotions arise from the activity of neurons, and it makes sense that when emotions are distorted severely, the neurons must in some way be “broken.”
Theories about depression over the years have included different versions of the “chemical imbalance” idea. The 2009 version of the American Psychiatric Association’s Textbook of Psychopharmacology reviews these candidate chemicals in depth.2 Researchers have found evidence of abnormalities in serotonin, norepinephrine, dopamine, cortisol, thyroid, growth hormone, glutamate, and brain-derived neurotrophic factor — yet no specific defect has been identified. Straying outside the world of chemistry, other researchers have tried to find the causes of depression through neuroimaging scans. But this research has been just as inconclusive.
Naïve as I was, I found myself astonished at the level of detail that drug companies were able to acquire about doctors’ prescribing habits. I asked my reps about it; they told me that they received printouts tracking local doctors’ prescriptions every week. The process is called “prescription data-mining,” in which specialized pharmacy-information companies (like IMS Health and Verispan) buy prescription data from local pharmacies, repackage it, then sell it to pharmaceutical companies. This information is then passed on to the drug reps, who use it to tailor their drug-detailing strategies. This may include deciding which physicians to aim for, as my Wyeth reps did, but it can help sales in other ways. For example, Shahram Ahari, a former drug rep for Eli Lilly (the maker of Prozac) who is now a researcher at the University of California at San Francisco’s School of Pharmacy, said in an article in The Washington Post that as a drug rep he would use this data to find out which doctors were prescribing Prozac’s competitors, like Effexor. Then he would play up specific features of Prozac that contrasted favorably with the other drug, like the ease with which patients can get off Prozac, as compared with the hard time they can have withdrawing from Effexor.
The American Medical Association is also a key player in prescription data-mining. Pharmacies typically will not release doctors’ names to the data-mining companies, but they will release their Drug Enforcement Agency numbers. The A.M.A. licenses its file of U.S. physicians, allowing the data-mining companies to match up D.E.A. numbers to specific physicians. The A.M.A. makes millions in information-leasing money.
Once drug companies have identified the doctors, they must woo them. In the April 2007 issue of the journal PLoS Medicine, Dr. Adriane Fugh-Berman of Georgetown teamed up with Ahari (the former drug rep) to describe the myriad techniques drug reps use to establish relationships with physicians, including inviting them to a speaker’s meeting. These can serve to cement a positive a relationship between the rep and the doctor. This relationship is crucial, they say, since ‘drug reps increase drug sales by influencing physicians, and they do so with finely titrated doses of friendship.’
Drug Companies and Doctors: A Story of Corruption
In recent years, drug companies have perfected a new and highly effective method to expand their markets. Instead of promoting drugs to treat diseases, they have begun to promote diseases to fit their drugs. The strategy is to convince as many people as possible (along with their doctors, of course) that they have medical conditions that require long-term drug treatment. Sometimes called “disease-mongering,” this is a focus of two new books: Melody Petersen’s Our Daily Meds: How the Pharmaceutical Companies Transformed Themselves into Slick Marketing Machines and Hooked the Nation on Prescription Drugs and Christopher Lane’s Shyness: How Normal Behavior Became a Sickness.
To promote new or exaggerated conditions, companies give them serious-sounding names along with abbreviations. Thus, heartburn is now “gastro-esophageal reflux disease” or GERD; impotence is “erectile dysfunction” or ED; premenstrual tension is “premenstrual dysphoric disorder” or PMMD; and shyness is “social anxiety disorder” (no abbreviation yet). Note that these are ill-defined chronic conditions that affect essentially normal people, so the market is huge and easily expanded. For example, a senior marketing executive advised sales representatives on how to expand the use of Neurontin: “Neurontin for pain, Neurontin for monotherapy, Neurontin for bipolar, Neurontin for everything.”15 It seems that the strategy of the drug marketers — and it has been remarkably successful — is to convince Americans that there are only two kinds of people: those with medical conditions that require drug treatment and those who don’t know it yet. While the strategy originated in the industry, it could not be implemented without the complicity of the medical profession.
Inside the Battle To Define Mental Illness:
This is hardly the first time that defining mental illness has led to rancor within the profession. It happened in 1993, when feminists denounced Frances for considering the inclusion of “late luteal phase dysphoric disorder” (formerly known as premenstrual syndrome) as a possible diagnosis for DSM-IV. It happened in 1980, when psychoanalysts objected to the removal of the word neurosis — their bread and butter — from the DSM-III. It happened in 1973, when gay psychiatrists, after years of loud protest, finally forced a reluctant APA to acknowledge that homosexuality was not and never had been an illness. Indeed, it’s been happening since at least 1922, when two prominent psychiatrists warned that a planned change to the nomenclature would be tantamount to declaring that “the whole world is, or has been, insane.”
Some of this disputatiousness is the hazard of any professional specialty. But when psychiatrists say, as they have during each of these fights, that the success or failure of their efforts could sink the whole profession, they aren’t just scoring rhetorical points. The authority of any doctor depends on their ability to name a patient’s suffering. For patients to accept a diagnosis, they must believe that doctors know — in the same way that physicists know about gravity or biologists about mitosis — that their disease exists and that they have it. But this kind of certainty has eluded psychiatry, and every fight over nomenclature threatens to undermine the legitimacy of the profession by revealing its dirty secret: that for all their confident pronouncements, psychiatrists can’t rigorously differentiate illness from everyday suffering. This is why, as one psychiatrist wrote after the APA voted homosexuality out of the DSM, “there is a terrible sense of shame among psychiatrists, always wanting to show that our diagnoses are as good as the scientific ones used in real medicine.
Why Are There No Biological Tests in Psychiatry?
When the third edition of psychiatry’s manual of mental illness, the DSM-III, was published 30 years ago, there was great optimism it would soon be the willing victim of its own success, achieving a kind of planned obsolescence. Surely, the combining of a reasonably reliable system of descriptive diagnosis with the revolutionary new tools of neuroscience would quickly yield a deep and broad understanding of psychopathology. And just as surely this would translate into standardized biological tests that would replace the cookbook listing of subjective symptoms and subjectively evaluated behaviors that comprised the DSM-III criteria sets.
Sadly, progress has been much slower than anyone expected, with many exciting findings turning out to be no more than dead ends. The vast research funding has indeed provided a basic science revolution, but so far its discoveries have had no impact whatever on clinical diagnosis. Even the most promising candidates — biological tests for the accurate diagnosis of dementia — are several years away. And, for the rest of psychiatry, there is no immediate prospect that our rich basic science knowledge base and powerful investigative tools will contribute to clinical practice any time soon.
We have learned a great deal in the past 30 years, but perhaps the most important lesson is that the brain is ineluctably complex and reveals its secrets only slowly and in very small packages. There has been no low hanging fruit. The expectation that there would be simple gene or neurotransmitter or circuitry explanations for schizophrenia or bipolar or obsessive-compulsive disorder has turned out to be naïve and illusory. The problem of teasing out heterogeneous clinical presentations in psychiatry is compounded by the fact that they also have heterogeneous underlying mechanisms. There will not be one pathway to schizophrenia; there may be dozens, perhaps hundreds. Biological tests that appear to be associated with schizophrenia are never useful for making the diagnosis because they always show more variability within the category than between categories. And seemingly intriguing findings usually don’t replicate.
Brain Scans Cannot Differentiate Between Mental Health Conditions:
A new study analyzing over 21,000 participants found that differences in activation of brain regions in different psychological “disorders” may have been overestimated, and confirms that there is still no brain scan capable of diagnosing a mental health concern.
A new study, published in the journal Human Brain Mapping, questions previous findings that specific brain regions are implicated in particular mental health conditions. Instead, according to the researchers, biased study design and the difficulty of publishing negative findings may have led to inaccurate results. While the researchers did find some differences in brain activation between people with mental health conditions and people without mental health conditions, they were not able to discriminate between specific diagnoses. The current study suggests that there are few, if any, differences in brain regions activated by specific mental health conditions. That is, there is still no brain scan that can tell whether a person has depression, social anxiety, or schizophrenia, for example.
Researchers have theorized that the different symptom clusters that form mental health diagnoses are linked to specific regions of the brain. If confirmed, such a finding would suggest that mental health diagnoses have biological components that could be targeted medically. However, the finding of the current study undermines this theory. Instead, the results indicate that while there is a general tendency for large parts of the brain (such as the amygdala and the hypothalamus) to be activated in a number of mental health conditions (as well as when humans are under stress in a number of ways), there is little difference between the varying diagnoses — even for diagnoses as seemingly different as social anxiety, depression, and schizophrenia.
I explained to them that I had learned that psychiatric categories are not, as was widely believed due to false advertising, solidly based in high-quality science. That statement had credibility because I told them that I had served for two years on two committees that were creating the fourth edition of the DSM and had seen with my own eyes that the manual’s authors often ignored, distorted, even lied about good scientific research if it failed to support what they chose to include or exclude, as well as that they often presented junk science as though it were good science if that could be used to support their decisions.
I said that the hundreds of categories of DSM disorders had been constructed by a small number of mostly white, male, American psychiatrists who shared many beliefs about what should and should not be called mental disorders and that their choices were akin to decisions about which celestial stars to “connect” in order to form constellations. I explained that it had been proven that two therapists seeing the same patient had a high probability of given that patient different DSM labels and that one patient seen over time often got very different labels at different points.
I said that human behavior is so multiply determined and complex that it is often impossible to know what caused a particular problem or difference and that the labels had not been helpful at identifying causes or effective interventions. In other words, I explained, it was a myth that if they just got the right diagnosis, it would be clear what courses of action might be helpful.
Why Can’t We Treat Mental Illness by Fixing The Brain?
Ask any psychiatrist what happens in the brain to make people depressed, and she will probably mention serotonin. Serotonin is one of the many chemicals that neurons release. The psychiatrist singles out this one because most of the drugs used to treat depression seem to work by altering its levels in the brain. Altering noradrenaline (a related neurotransmitter) is also effective.
At a psychiatrists’ clinic, there are no machines or blood tests that aid diagnosis. How different from the cardiologist next door!
And yet, there is no evidence at all that the levels of serotonin or noradrenaline in the brains of depressed people are any different from normal. The logic is flawed: you cover a cut on your finger by a sticking plaster, which helps recovery; but the cut was not caused by a lack of sticking plasters. So altering serotonin can speed recovery in some people — and there are those who question even this — without telling us anything about what depression is or how it occurred in the first place.
At present, a pathologist looking at the brain of a depressed person could not distinguish it from the brain of someone who was mentally well. (Given the brain of someone who’d had multiple sclerosis, he could see the scars that the disease makes.) And if you visit a psychiatrists’ clinic, you will find no machines or blood tests that aid diagnosis. How different from the cardiologist next door!
Things are a little better for neurologists. Modern imaging techniques can often reveal what has gone wrong in the brain, because these illnesses are commonly caused by observable changes in its structure. Here, the problem is knowing what to do about it, unless it’s something removable like a tumour. Actually, this is a little unfair to the state of neurological medicine. There are circumstances in which treatments can be at least partially effective, and this is an active area of research. The treatment of multiple sclerosis, for example, has improved a good deal during the past decade, and there are promising signs that we might be able to help the damaged spinal cord to repair itself before too long. But for now, neurologists have very limited treatments, and this also reflects our ignorance of how the brain works or how to fix it.
In his book The Death of Psychiatry, psychiatrist E. Fuller Torrey, M.D., wrote “None of the conditions that we now call mental ‘diseases’ have any known structural or functional changes in the brain which have been verified as causal.” In his book The New Psychiatry, Columbia University psychiatry professor, Jerrold S. Maxmen, M.D., says “It is generally unrecognized that psychiatrists are the only medical specialists who treat disorders that, by definition, have no definitively known causes or cures. … A diagnosis should indicate the cause of a mental disorder, but as discussed later, since the etiologies of most mental disorders are unknown, current diagnostic systems can’t reflect them” (Mentor 1985, pp. 19 & 36, italics in original). In 1988, Seymour S. Kety, M.D., Professor Emeritus of Neuroscience in Psychiatry, and Steven Matthysse, Ph.D., Associate Professor of Psychobiology, both of Harvard Medical School, said “an impartial reading of the recent literature does not provide the hoped-for clarification of the catecholamine hypotheses, nor does compelling evidence emerge for other biological differences that may characterize the brains of patients with mental disease” (The New Harvard Guide to Psychiatry, Harvard University Press, p. 148). In 1992 a panel of experts assembled by the U.S. Congress Office of Technology Assessment concluded: “Many questions remain about the biology of mental disorders. In fact, research has yet to identify specific biological causes for any of these disorders. … Mental disorders are classified on the basis of symptoms because there are as yet no biological markers or laboratory tests for them” (The Biology of Mental Disorders, U.S. Gov’t Printing Office 1992, pp. 13–14, 46–47). In a December 1996 Psychiatric Times article, “Commentary: Against Biologic Psychiatry”, psychiatrist David Kaiser, M.D., says “modern psychiatry has yet to convincingly prove the genetic/biologic cause of any single mental illness.” In his book The Essential Guide to Psychiatric Drugs, Columbia University psychiatry professor Jack M. Gorman, M.D., says “We really do not know what causes any psychiatric illness” (St. Martin’s Press 1997, p. 314).
In his book Saving Normal: An Insider’s Revolt Against Out-of-Control Psychiatric Diagnosis, DSM-5, Big Pharma, and the Medicalization of Ordinary Life, HarperCollins 2013, pp. 10, 11, 244), Dr. Frances says “The powerful new tools of molecular biology, genetics, and imaging have not yet led to laboratory tests for dementia or depression or schizophrenia or bipolar or obsessive-compulsive disorder or for any other mental disorders … We still do not have a single laboratory test in psychiatry. …thousands of studies on hundreds of putative biological markers [for mental illness] have so far come up empty.”
In 2011, Hagop Akiskal, M.D., Professor of Psychiatry at the University of California at San Diego, acknowledged that “Despite the diligent search for biomarkers for the so-called functional mental disorders during the past 100 years, nothing specific has emerged” (“Biomarkers for Mental Disorders: A Field Whose Time Has Come”, psychiatrictimes.com, November 18, 2011). In 2012, Connecticut psychiatrist Simon Sobo, M.D., acknowledged “We haven’t yet discovered the etiology of any DSM-IV diagnosis” (“Does Evidence-Based Medicine Discourage Richer Assessment of Psychopathology and Treatment?” psychiatrictimes.com, April 5, 2012). In a lecture at the University of New England on February 25, 2013, British psychiatrist Joanna Moncrieff, M.B.B.S., M.Sc., MRCPsych, M.D., said “There is just absolutely no evidence that anyone with any mental disorder has a chemical imbalance of any sort…absolutely none” (“Joanna Moncrieff — The Myth of the Chemical Cure; The Politics of Psychiatric Drug Treatment”, YouTube.com, at 53:52).
In 1991 in his book Toxic Psychiatry, psychiatrist Peter Breggin, M.D., said “there is no evidence that any of the common psychological or psychiatric disorders have a genetic or biological component” (St. Martin’s Press, p. 291). 24 years later, on the Coast-to-Coast AM radio show on February 9, 2015, Dr. Breggin said “There is no known physical connection to any psychiatric disorder. There is no genetically determined cause. It’s all drug company propaganda, because the pharmaceutical industry with its billions of [advertising] dollars, and the medical industry, thinks you’re more likely to take drugs if you think you have a genetic or biological disease.” In 2015 in his book Deadly Psychiatry and Organized Denial, Dr. Peter C. Gøtzsche, a physician specializing in internal medicine, and professor of Clinical Research Design and Analysis at the University of Copenhagen, said “it hasn’t been possible to demonstrate that people suffering from common mental disorders have brains that are different from healthy people’s brains” (People’s Press, p. 26).
So if mental illnesses, mental diseases, or mental disorders or syndromes must have a biological etiology or cause to qualify as illness, disease, disorder, or syndrome, none have been proved to exist.
The problem, though, is that the efficacy of such treatments, and the mechanisms by which they work, tend to be oversold and presented as long-term solutions. We are right to be cautious about the overprescription of antidepressants, to take one example. These tend to be prescribed along with a scientifically dodgy idea that the pills are rejigging an imbalance in serotonin, a chemical messenger in the brain. Similarly, emerging evidence suggests that the long-term prescription of antipsychotics may actually hinder recovery for many.
Psychological and social factors are at least as significant and, for many, the main cause of suffering. Poverty, relative inequality, being subject to racism, sexism, displacement and a competitive culture all increase the likelihood of mental suffering — as the survivor-led collective Recovery in the Bin brilliantly illuminates. Add into the mix individual experiences such as childhood sexual abuse, early separation, emotional neglect, chronic invalidation and bullying, and we get a clearer picture of why some people suffer more than others.
Crucially, all of these experiences affect our psychological and physiological makeup. For example, the Adverse Childhood Experiences studies show that childhood trauma, neglect and structural oppressions manifest later not just in mental distress but in chronically inflamed bodies stuck on hyper-alert (this we can pick up through blood tests).
Governments and pharmaceutical companies are not as interested in these results, throwing funding at studies looking at genetics and physical biomarkers as opposed to the environmental causes of distress. Sociologists argue that this is because citizens who consider themselves ill are easier to manage than people who consider themselves maddened by toxic families and injustice.
Head Case: Can Psychiatry be a Science?
Kirsch’s conclusion is that antidepressants are just fancy placebos. Obviously, this is not what the individual tests showed. If they had, then none of the drugs tested would have received approval. Drug trials normally test medications against placebos — sugar pills — which are given to a control group. What a successful test typically shows is a small but statistically significant superiority (that is, greater than could be due to chance) of the drug to the placebo. So how can Kirsch claim that the drugs have zero medicinal value?
His answer is that the statistical edge, when it turns up, is a placebo effect. Drug trials are double-blind: neither the patients (paid volunteers) nor the doctors (also paid) are told which group is getting the drug and which is getting the placebo. But antidepressants have side effects, and sugar pills don’t. Commonly, side effects of antidepressants are tolerable things like nausea, restlessness, dry mouth, and so on. (Uncommonly, there is, for example, hepatitis; but patients who develop hepatitis don’t complete the trial.) This means that a patient who experiences minor side effects can conclude that he is taking the drug, and start to feel better, and a patient who doesn’t experience side effects can conclude that she’s taking the placebo, and feel worse. On Kirsch’s calculation, the placebo effect — you believe that you are taking a pill that will make you feel better; therefore, you feel better — wipes out the statistical difference.
Part 2 of this series will cover the main relevant books of the anti-psychiatry and critical psychiatry movements, as well as books from the Philosophy of Psychiatry that engage with many of the conceptual (as opposed to the merely empirical) problems at the heart of many of the criticisms raised against Psychiatry.
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