Psychology Today Blogs - Peter D. Kramer

Psychosis Up Close

Peter D. Kramer — Mon, 08 Sep 2008 07:33:36 -0700

What is the experience of psychosis? What does mania look like up close?

In an overview essay that the New York Review of Books has generously posted on line, the neurologist Oliver Sacks explores the phenomenology of bipolar disorder in its extreme phase. The occasion for the essay is the publication of Hurry Down Sunshine, by Michael Greenberg, a father’s account of his daughter’s illness. But Sacks takes the opportunity to remind readers of descriptions by patients, notably John Custance, who wrote in the 1950s, and Kay Jamison.

From the viewpoint of psychiatry, the unbalancing and inflammation of a mind is so common a misfortune that doctors may forget how extraordinary and unfamiliar the state is the person who experiences it and, then, those around her. In the passages quoted by Sacks, Greenberg, a contributor to the Times Literary Supplement, approaches psychosis with a writer’s art, using a close third person to evoke his 15-year-old daughter Sally’s deranged ecstasy: “[S]he walked out onto Bleecker Street and discovered her life had changed. The flowers in front of the Korean deli in their green plastic vases, the magazine covers in the news shop window, the buildings, cars — all took on a sharpness beyond anything she had imagined.”

Lately I have been dipping into James Wood’s elegant primer How Fiction Works. Despite the rare clunker, the book, which has been savaged in the press, strikes me as quite fine, especially in its emphasis on what Wood calls “free indirect style.” Wood is referring to that same close third person — Chekhov is its master — in which a single adjective may serve to switch the viewpoint from the author’s to the character’s. We use this technique in psychotherapy. Here, Leston Havens is the great practitioner, offering observations whose provenance is ambiguous, so that the patient may wonder whose thoughts are being exposed, hers or Havens’s. In that uncertainty lie other possibilities, reassurance and perturbation, each stimulating further exploration and discovery.

Sally Greenberg’s doctor employed the first and second persons to advance this sort of speculation: “’I bet you feel as if there's a lion inside you’ are her first words . . .” What a fine example of the skillful use of language in psychotherapy! The speculation, enlivened by metaphor, at once averts resistance to the encounter (through disrupting expectations of how doctors speak) and promises the patient that she will be understood.

Anyway — for me, the Sacks essay led to thoughts about this commonalty between writing and therapy, the need for effective rhetoric. Of course, the review serves a more — I am tempted to say “another” — down-to-earth function. At a moment when the scope of bipolar disorder is, quite properly, in dispute, Sacks (and, evidently, Michael Greenberg) provides a reminder that the core disorder is prevalent, grave, and very real — and that effective treatment, pharmacologic and psychologic, can be of enormous help.

More Harsh Reality: Aging Fathers and Bipolar Children

Peter D. Kramer — Thu, 04 Sep 2008 06:11:27 -0700

Like depression, bipolar disorder has been romanticized as an affliction that confers hidden benefits. It may, but evidence is accumulating that suggests manic-depression results from the sorts of genetic disruption that contribute to other severe afflictions, such as schizophrenia and autism.

Readers of this blog may recall that schizophrenia and autism have been linked to “de novo” mutations, new abnormal genes that develop in the parent’s sperm line and have not passed a Darwinian, evolutionary test of fitness. The amino acid sequences are simply disrupted. Readers who have looked at yet earlier columns will recall that problems in gene regulation — epigenetic “scarring” — can also give rise to mental illness. Scientists are now suggesting that both of these mechanisms, new mutations and gene dysregulation, may be implicated in bipolar disorder.

Emma Frans and other researchers at the Karolinska Institute in Stockholm looked at a sample of over seven million Swedes and identified over 13,000 patients who had been hospitalized at least twice for bipolar disorder. The epidemiologists compared these subjects to over 70,000 matched controls. The investigators found that older fathers are more likely (the increase is on the order of 37%) to have offspring with manic depression. Older mothers had more bipolar children, too, but the association was less marked.

More, when the investigators looked at subjects with early-onset bipolarity, the association was very high. Compared with men in their early twenties, men over 55 were more than two-and-a-half times as likely to father a child who would go on be hospitalized for manic depression before age 20.

As with schizophrenia, some manic depression is familial and hereditary, caused in part by genes that have been passed down for generations. Conceivably, as well as doing harm, those genes may confer some adaptive fitness in sufferers or their relatives. Theorists have suggested that high energy and decisiveness, if not frank mania, may be the traits selected for over time. But the association between paternal age and mental illness points in a different direction.

Part of what distinguishes older fathers from older mothers is the nature of the gene line. Women’s eggs go through 23 replications and then are held in the uterus (or expelled) throughout life; the eggs’ genes may deteriorate, but they are much less vulnerable to “gene copy errors.” In contrast, the cells that make sperm have gone through 200 divisions by age 20; by age 40, the number of divisions is up to 660. The sperm of older men is much more likely to have acquired mistakes through faulty replication. On a separate basis, altered genetic regulation in offspring has been related to paternal age. The Karolinska researchers speculate that these two mechanisms may explain why older fathers have more bipolar offspring. Either way, the influence is via “one-off” events, new abnormalities that changes the offsprings’ brain development.

Other interpretations of the data are possible. Perhaps older fathers simply do a worse job of parenting. Here is where the question of early onset comes into play. Early-onset bipolar disorder is more heritable and less related to environmental factors. The fact that manic depression in the teenage years was so much more common in the children of older father speaks toward genetic transmission.

Interestingly, very young (teenaged) fathers also have more children who go on to experience early-onset bipolarity. It may be that “immature sperm” also give rise to de novo genetic disorders; or environment may play a role, via drug and alcohol abuse in the fathers, poor prenatal care on the part of young mothers, epigenetic problems in parents who themselves have been stressed, and then the additional disruption in the early lives of children born to parents who are poor and who (studies show) may demonstrate conduct disorders.

Of course, the association with paternal age proves nothing. It is easy to conjure up epigenetic evolutionary mechanisms that might explain the same data. Perhaps nature has arranged for the sperm of aging parents to be reconfigured to favor manic depression in a sort of “Boy Named Sue” strategy. If the parents may well die early, bipolarity could be a sort of double-or-nothing bet, in which low-level mania gives orphaned offspring a better shot at survival.

But the Karolinska researchers read the results differently. For now, bipolarity is another on a list of mental illnesses that seem to arise from random changes in genes or gene expression — which is to say: syndromes that have long been categorized as mental illness look like just that, expressions of frank biological pathology.

Plus ça change department

Peter D. Kramer — Tue, 02 Sep 2008 07:31:40 -0700

Sad, the end of summer, and not just because our serotonin transporter density changes as the days shorten. Prime cycling season’s over.

Summer mornings, I’m out on my bike early, between six and seven so that my outings are invisible, completed before the rest of the family rises. Bicycling is not a religion for me. Swimming is, and writing. Not an otherwise superstitious man, I believe that if I miss a chance to swim — I mean in the open ocean — or to write, then in future, the sun will not shine on me. Cycling is in the more modest category, exercise. The worry is that if I don’t do it today, I’ll find an excuse not to do it tomorrow, a concern that’s odd, since I would say that I love to be out on the road.

Readers of this blog may recall a post or two where I wrote about my use of sports for metaphor in psychotherapy. This season’s lesson is: change is difficult. Or: change is illusory. We kid ourselves.

I’d had a bad cycling year. Since the injunction to ride was not absolute, I’d let all sorts of considerations keep me home so that I entered the crucial month, August, with too few miles behind me. Still, I was ambitious. I’d been getting pointers on gearing and cadence. I thought I’d ratchet up my endurance, and my speed.

I tell myself not to worry about speed. Putting in the time, pushing the body, enjoying the early morning sights, making it home safe, those are enough. Camaraderie, too, when the gang is out there. Still, I’m slower than the guys I sometimes ride with, slower than anyone who rides as much as I do should be. It would be nice to keep up with the big boys.

I’ve come under the tutelage of a friend I’ll call Coach. He’s the one who, a few years back, badgered me into getting the old clunker out of the tool shed. When Coach had got the bug into me, he sat with me in the library and led a search on eBay for a used entry-level racing road bike. The one we chose was never top-of-the-line, and a past owner had detuned it, substituting tires that have more tread and take lower pressure than the ones real speedsters use. But my ride is light and fast enough that, once assembled, it constituted something of a revelation. Perhaps cycling is religion after all.

All August, I pushed myself. First, the goal was to get into last year’s form, then, to move beyond. My usual course is a hilly fifteen miles. If the others are out there, I serve to warm them up — they go on to do a total of forty or fifty. If I’m not taking advice from Coach, I sprint the whole way, and even so I tend to plateau at an average of sixteen to sixteen -and-a-half miles an hour. Recreational bikers go at twelve to fourteen, but the group that’s out there every day commits to eighteen; most days, they’re up above twenty.

As I say, I try to set pace to the side. I focus on the uphills, hoping to hit them fast and stick with the cadence. Most often, I won’t check the average speed on my Cateye odometer until I hit mile fourteen. Then, if I’m near a personal best, I’ll flog myself to the finish.

That happened this Labor Day weekend. Saturday, rain had kept me indoors. Sunday, I had been set for a longer ride, twenty-five miles — but then family obligations caused me to change my route entirely. The difficulty of the hills seemed comparable. I thought I’d push myself, to make speed substitute for distance. A mile before the end, I clicked the Cateye to “average speed.” Up popped a number I’d never seen at any substantial distance: 17.2. The route ahead was all flats and “faux plats” There was no trouble getting the screen to read 17.4 by the ride’s end.

Good, I thought. Back in shape. Perhaps I had put in more miles than I imagined. Or since the odometer belied that fantasy, perhaps I’d pedaled harder, stretched myself more. I’d changed my style, tolerated faster curves and downhills, downshifted less on the uphills, dug harder with my heels, achieved a rounder stroke.

The next day, I was back on the old route. The guys were out, and I took the first five miles with them. No luck. I was barely in the peloton. When I turned off on my own, I lowered my head into the wind, followed the curves tight, refused to listen to protests from my thighs. There I was at the end. Sixteen, sixteen-and-a-half. No improvement at all.

Which makes sense. I’m a year older. I hadn’t put the work in. I hadn’t changed my form. Not enough.

That’s the lesson, as I say, in sport and in therapy. We lie to ourselves about the effort we’ve made. We lie to ourselves about what’s needed. Think how much change you need to make. No, it’s more: more than you think.

Note: This topic provides an excuse for me to plug “Bike4theBrain,” a Kansas City road race meant to raise awareness of mental illness. For those nearby: The event is on September 28. Check the Website for routes.

The Good News Is: You Don’t Have Alzheimer’s. The Bad News Is: You’re Going to Die

Peter D. Kramer — Thu, 28 Aug 2008 08:45:22 -0700

I’ve come across an online “in advance of publication” report that would be funny if it were not so grim.

Let’s say you’re not as young as you once were . . . and your mind starts to slip. You have problems with various cognitive capacities — word finding, calculation, and the like. Are you suffering early Alzheimer’s Disease? You visit your doctor and he or she reassures you. There’s no dementia. But then, that news isn’t all good.

As part of a longer term study, a research team led by Valgeir Thorvaldsson at Göteborg University in Sweden followed 228 individuals without dementia from age 70 until the subjects died. In the final fifteen years of life, these normal men and women suffered substantial cognitive decline. The falloff began with changes in perception, 15 years out, and moved on to spatial ability, about 8 years before death, and then, at 6 to 7 years, problems in verbal performance. The researchers speculated that the relatively sharp increases in impairment might be related to cardiovascular problems.

So: You’re not demented, you’re in what is called "terminal decline."

Normal aging is not so benign as we had been led to believe. Or rather, as neurology progresses, the nature of the normal will change. Doctors will begin attending to the conditions that cause a drop-off in mental functioning and predict worse to come.

A Quick Note: It's Depression That Keeps People Off the Job

Peter D. Kramer — Wed, 27 Aug 2008 07:01:13 -0700

As an addendum to my posting earlier this week on the harm that depressive symptoms cause for patients with bipolar disorder —

Regarding the question of mood and days lost from work: Researchers from the University of Washington in Seattle have just published results from a 2-year-long overview of the employment status of outpatients with bipolar disorder. Depressive symptoms but not mania were significantly associated with time off work. Patients with substantial depressive symptoms missed about a day of work a week more than did patients in remission. That's an enormous difference, representing very substantial impairment. (Patients with manic symptoms missed work, too, but this finding did not meet statistical standards of significance.) The depressed patients were also 15% less likely to be employed. Almost half of the unemployed were experiencing a full depressive episode.

The researchers conclude: "Among patients with bipolar disorder, depression is strongly and consistently associated with decreased probability of employment and more days missed from work due to illness. Symptoms of mania or hypomania have more variable effects on work productivity."

Adding to a large literature on the disabling effects of mood disorders, this study underscores the harm done by depression in particular.

Note: My former Brown colleague Mark Bauer contributed to both this study of employment and the one referenced in my prior post, on subsyndromal symptoms in bipolar disorder.

To Treat or Not to Treat: The Debate Over Residual Symptoms of Depression

Peter D. Kramer — Mon, 25 Aug 2008 06:41:05 -0700

How vigorously should we treat depression?

Research in the last two decades, and here the trend is overwhelming, shows that patients with “residual symptoms,” indicators of depression that persist even when by standard definitions mood disorder is no longer present, are likely to become depressed more rapidly — and then to suffer the consequences of a “career” of chronic disability and disease. This risk extends even to seemingly minor symptoms like insomnia.

On the other hand, depression can be hard to treat. Eradicating every last symptom is a demanding goal, one likely to expose patients to multiple medication trials and, if they can afford it, extended periods of psychotherapy. Thoughtful doctors have suggested that the risk from complex treatment is unknown and that despite the problems of chronicity it may be more helpful, and more realistic, to leave some patients in an intermediate state in which they are “better but not well.”

This argument is certain to persist until we have access to new, more effective treatments. In the meanwhile, an in-advance-of-publication article in the Journal of Affective Disorders weighs in on the “treat to remission” side of the argument.

The authors looked at over 1500 patients with bipolar disorder and found 310 to be in an episode of major depression, while 112 were in a “subsyndromal” state — that is, they had depressive symptoms that were not numerous or severe enough to trigger a diagnosis. These figures are typical. Bipolar patients spend about a third of their adult lives depressed — and it is depressive, not manic symptoms that are the best predictor of poor functioning in manic depression.

The histories of these patients differed in the direction you would expect. Those in remission had fewer past episodes of depression; those with frank depression had the most. The patients with partial depressions often suffered other disorders and symptoms, like anxiety. Oddly, the remitted patients were most likely to have experienced a psychosis in the past; it may be that these patients then received the most vigorous treatment. In terms of measurable personality traits, the three groups were comparable.

It was the measures of impairment in daily living that were surprising. Both partial and full (subsyndromal and syndromal) depression led to bad outcomes, in terms of work, relationships, recreation, and overall life satisfaction — and the two groups looked remarkably similar. The diagnosed depressives lost more days at work, but otherwise, low-level depression, among bipolar patients, looked as harmful as full-blown episodes. The authors observe that “patients with sustained continued symptoms experience essentially the same functional burden as those experiencing a full episode of depression.” In terms of particular residual symptoms, sadness, lassitude, and the inability to experience pleasure were especially harmful.

This study would seem to argue for vigorous interventions for of residual depression in bipolar patients — but there are caveats. Antidepressants can make bipolar patients manic. It may even be that some of the disability in bipolar patients with low-level depression arises from their treatment, if it gives them hypomania, or low-level manic symptoms.

A note on the study and its funding and authorship: These results arise as part of the STEP-BD research, a multi-site investigation (conducted at major universities) fully funded by the National Institute of Mental Health. The lead author of the current article is Lauren Marangell, who during the trials was at the Baylor College of Medicine; she has since been hired by Eli Lilly. That corporate name can make readers leery. But in the world of research, a multi-site NIMH-sponsored study is about as good as it gets.

The take-home message — and many other studies lead to the same conclusion — is that, in bipolar patients, residual depression is not just a risk factor for future illness; it is also a predictor of current misery. It is reasonable to argue that we just don’t know what the tradeoffs may be when doctors press onward, treating symptoms in order to prevent future illness. But doctors are likely to want to make those efforts for another reason: their patients are floundering here and now.

Debunking CBT, Part 2: What's It Good For?

Peter D. Kramer — Mon, 18 Aug 2008 05:30:19 -0700

What is cognitive-behavioral therapy good for? Is it an all-purpose treatment, useful for the “neurotic” states for which patients have traditionally consulted psychotherapists? Or is CBT most like its more mechanical parent, behaviorism, a tailored intervention best suited to afflictions in which disordered actions play a prominent role?

In an earlier posting, I looked at the summary results from an authoritative meta-analysis, or statistical amalgamation, of research on CBT in the treatment of anxiety disorders. My read was that while CBT had been shown to work, the integrated findings exposed the therapy as either untested or fairly disappointing in the treatment of the very conditions it had been designed for.

Today, I propose to return to the meta-analysis and ask: where exactly has CBT been shown to work?

Looking at specific diagnoses, Stefan Hofmann and Jasper Smits, the authors of the overview, found that CBT was most effective for two diagnoses: obsessive-compulsive disorder (or OCD) and acute stress disorder (ASD). But that conclusion is based on meager data.

No study of OCD met Hofmann and Smits’s strictest criteria for scientific merit, and only one study met their second-level, less rigorous standards. That research did not really employ CBT. It tested a behavioral method in which patients were confronted with an anxiety-provoking stimulus (like touching a dirty object) and then prevented from enacting their compulsive response (like hand-washing). "Exposure and response-prevention" is a known, effective treatment for OCD, although to be fair, training patients not to enact their main symptoms and then (as an outcome criterion) measuring symptomatic behaviors is a fairly sure way of achieving statistical significance.

Then, too, because there are few placebo responses in OCD, it is an illness in which many standard treatments, including antidepressant medications, are shown to good effect. And of course, a meta-analysis that is based on only one study does not add much to the scientific literature; there is no data that needs combining. Instead of announcing “meta-analysis confirms that CBT treats OCD,” it would be as well to say that there is still one fairly good study that says a related treatment works for the indication.

Similarly, only one ASD study met the authors’ inclusion criteria.

For those unfamiliar with ASD, the condition is a troubled response to recent stress. Its main importance is as a risk factor for a more substantial affliction, post-traumatic stress disorder or PTSD. ASD is one of those diagnosable conditions that lead to criticism of the Diagnostic and Statistical Manuals. Is it an illness or not?

Only one research group seems to have looked at CBT for ASD. Not surprisingly, the scientists found that focusing on a person’s distorted perceptions of an event diminishes the event’s impact. Still, no one knows whether ASD sufferers resemble traditional candidates for psychotherapy.

It turns out that the only anxiety disorders that have been at all well studied, in terms of response to CBT, are PTSD and panic anxiety. For panic, Hofmann and Smits found two or three top-flight research trials; for PTSD, one or two. Two other studies, one of social anxiety disorder and one of generalized anxiety disorder, met the authors’ second-rank quality criteria. In other words, when it comes to the treatment of anxiety, there is surprisingly little basis for assessing CBT. As for outcomes, the efficacy for these common conditions was mostly at the weaker end of the range, significantly less than what was reported for the behavioral treatment of OCD. For conditions like PTSD, the strongest results came in the less rigorous studies.

To be fair, the problem here is mostly “rigor.” Hofmann and Smits are looking for “intention to treat,” or ITT, analyses: if you enter a study, what are the odds that you will respond to CBT? Most early trials were reported via “completer” analyses: if you follow through with all the sessions and fill out all the questionnaires, what are the odds that you will have improved with treatment?

One reason that both psychotherapy and psychopharmacology have looked good, over most of the past half-century, is that scientists accepted “completer” studies. After all, what you as a consumer want to know is, if I follow my doctor’s recommendation, will I get a good result?

Unfortunately, completer studies do not quite answer that question. People who are floundering are more likely to drop out of the study; perhaps they are especially likely to drop out of the more onerous arm, the one that (in the case of psychotherapy) makes psychological demands or (in the case of medication) causes side effects. You could make the opposite argument, that people who believe they are in active treatment are more likely to see things through. But generally, completer trials are thought to be biased in favor of the intervention under study. If completer studies are looking at a select sample — of people who seem to be making progress throughout the trial — then of course they will show that the treatment works.

So if you are stoical, if you would stick with any treatment right up to the end of an eight- or twelve-week trial, then the result you achieve will likely sit somewhere between the completer and intention-to-treat outcomes. Seen through the lens of ITT trials, CBT is unimpressive. If you believe that completer trials contain some of the truth, then you are likely to think more highly of CBT; but then, you will also think more highly of other psychotherapies and of other approaches to anxiety disorders, like medication.

Politicians Risking it All: the Infuriating Sequel

Peter D. Kramer — Mon, 11 Aug 2008 08:15:16 -0700

Despite the other entries on this topic, I thought today might be a good day to re-link to my prior postings on politicians and risky sex.

I’m off in the boonies, without good Web access, so I don’t know how many others have expressed these sentiments — many I imagine — but I’m angry as can be at the Edwards couple for their blithely endangering the Democratic Party, the country, and the world. That Bill and Monica gave us preemptive war, Abu Ghraib, and the rest is a reasonable thought — and the Edwards-Rielle Hunter affair was a similar disaster in the making.

Both John and Elizabeth Edwards should have known that they stood a good chance of extending Republican rule. What if, as of last week, John were the presumptive nominee — and then this affair had emerged? I know that cancer leads to desperate judgments, but still, why didn’t Elizabeth say what any of us might: John, if you care about the workingman, if you care about liberal values, if you want to avoid a train wreck, then stay out of this race?

A Grand Week for Couch Potatoes

Peter D. Kramer — Wed, 06 Aug 2008 14:47:32 -0700

It's been a grand week for couch potatoes. First, the Chicago Tribune ran a round-up piece that cast doubt on the proposition that physical exertion staves off dementia. Then the Archives of General Psychiatry weighed in with research suggesting that exercise might not lessen anxiety or depression.

Looking at almost 6000 twins from the Netherlands and 2600 near relatives, researchers found that yes, working out correlates with untroubled mood, especially in women — but that this association is probably genetic. People inclined to exercise are also people protected from mood disruption; unknown “common genetic factors” may underly both tendencies.

This breathtaking — and, once proposed, reasonably intuitive — finding casts at least a light shadow on research that has found exercise training to be a (sometimes modestly effective, sometimes powerful) treatment for depression.

In a recent discussion on National Public Radio about alternative approaches to mood disorder, I raised the “intention to treat” issue. Most studies of interventions like exercise are “completer” trials. They look at people who follow through on the regimen and see how many get better. But of course, people disinclined to exercise might drop out of the “active intervention” arm of a trial of say, jogging. If those are the same people who carry a predisposition for low mood, then any positive research outcomes become suspect. Perhaps it’s not the exercise but the pressure for vulnerable subjects to quit the study that makes running look better than placebo. The Archives analysis makes clear why we should hold alternative treatments to the same research standards that apply to psychotherapy and medication.

I recommend at least a trial of exercise for all my depressed patients. But a good number are already working out vigorously — exercise is no panacaea.

The new evidence notwithstanding, I’m back to my summer regimen of swimming and bicycling. I’ll return to the intention-to-treat issue presently, in my promised second posting on cognitive behavior therapy in the treatment in anxiety.

Addendum: Overnight I found an "exercise versus medication for depression" study that uses an "intention to treat"analysis. The two interventions look equally good, but both have low effect sizes. Even so, depending on how exercise interacts with resilience, the bias problem arising from selective dropouts may not be entirly eliminated.

Dear Abby: Is Autism a Mental Illness?

Peter D. Kramer — Thu, 31 Jul 2008 05:46:30 -0700

While we are on the question of disease labels I see that “Dear Abby” has been “corrected” by many readers who find her “way off base” for misclassifying autism. In a prior column, she had called it a “mental-health disorder.” Now she accepts that she was mistaken. Because autism is “genetically predetermined — biologically based” or “neurologically based,” it is not a mental health disorder.

Jeanne Phillips, writing under the pen name Abigail van Buren, quotes a Mayo Clinic doctor to the effect that autism “affects behavior, cognitive ability and social skills” and notes that the syndrome appears as a diagnosis in the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders. That list would seem to argue for the label Dear Abby had applied initially, mental health disorder.

No, Phillips now says. Autism is a “neurodevelopmental disorder.” But aren’t many mental illnesses neurodevelopmental disorders? Conditions that first appear in childhood are especially likely to fit that description. Think of pervasive developmental disorder or early-onset schizophrenia. Those conditions stand at the core of child psychiatry — and they are likely to require the services that, within medicine, the mental health professions provide.

The same is true for autism. The primary treatments are behavioral and psychological; where medications play a role, they tend to be the ones that psychiatrists prescribe. Much of the finest research on autism was performed by psychiatrists, such as my beloved teacher, the late Donald J. Cohen. His work serves as a model of integration, using the research methods of genetics and neuroscience and the therapeutic techniques of psychopharmacology, behaviorism, teacher training, and, yes, psychoanalysis, in a wiser mode.

Some of the impetus for the reclassifying autism is to spare affected families shame, that is, the shame of having raised a child with mental illness. This reaction is understandable, given the history of autism in psychiatry, and particularly in psychoanalysis where the condition was once attributed to bad parenting. Autism can be heartbreaking for parents; certainly it is a neurodevelopmental disorder, and if that's what families prefer to call it, we should probably all join in. But then, the question arises, what is autism being distanced from? What do we make of families whose children suffer obsessive-compulsive disorder, Tourette syndrome, and the rest? We might note that autism overlaps substantially with those very diseases.

So, yes, it is easy to see why families whose members are afflicted by autism might hope to recategorize the condition. But, Dear Abby, might you have replied that today an alternative and arguably yet more humane response would consist in embracing the “mental illness” label — and insisting that that isn’t shameful?

Note to readers: Following the tradition established by Sigmund Freud — to many psychiatrists it is among the greatest of his contributions — I will be abandoning my office for much of August, to enjoy vacation time and to work on longer writing projects. As a result,I expect to post here less frequently. Enjoy the summer!//pdk