Charting the Depths

Depression is depression

Jonathan Rottenberg, Ph.D. — Wed, 17 Mar 2010 14:33:15 +0000

I recently read Allen Frances thoughtful post questioning the possible change in DSM-V to allow the diagnosis of depression in the context of a recent bereavement. He is concerned about the medicalization of ordinary grief and the overdiagnosis and overtreatment of depression in people who are grieving.

Here I would like to briefly discuss the premise of the bereavement exemption. The premise is that the exact environmental precipitant for depression matters.

Should our diagnostic manuals make a sharp distinction between depression that is due to bereavement (normal) and depression due to other losses (a sign of a mental illness)? This makes little sense from the perspective of what we know about mood. Isn't our mood system configured to respond in similar ways to any major loss—be it of a job, relationship, or reputation. Whether it comes from the loss of a spouse or one’s life savings, depression is depression. I don't see how we (myself, a psychiatrist, the DSM-V panel) can sit in judgment concerning the reasons why a person is depressed. A man loses his job at the factory after 25 years of loyal service and we consider his depression a sign of a mental illness. If another man becomes depressed after the death of a distant relative we consider his depression to be normal variation.

By my mind, it is awkward and arbitrary to judge whether a person's depression is "normal" for a given environmental precipitant. If we are concerned about the overdiagnosis and overtreatment of depression in people who are experiencing a loss, it would make more sense to re-examine the threshold for diagnosis.

Frances argues that the threshold for diagnosis in the context of grief is too murky, "There is no bright line separating those who are experiencing loss in their own necessary and particular way from those who will stay stuck in a depression unless they receive specialized psychiatric help." I agree, but can't the same point be made for depression as a whole? Right now 5 symptoms are the diagnostic cutoff for a major depressive episode but are 5 symptoms really a bright line where depression begins? Should people who have 3 or 4 symptoms of depression be turned away from treatment? Of course not. Indeed, a recent research article found that in practice small changes to the diagnostic threshold for even one symptom of depression led to drastically different rates of diagnosis.

Frances worries that medicating grief may be inappropriate because it will interfere with the process of coping and sensemaking that operate around this loss situation. I don't disagree at all with the worry; in fact I have a bigger version of the same worry: Aren't we too quick to medicate people who are faced with other sorts of loss situations? The bereavement exclusion has, for some time, allowed us to dodge this important question.

The social environment shapes whether depression treatments work

Jonathan Rottenberg, Ph.D. — Thu, 11 Mar 2010 20:44:12 +0000

Depression has certainly been in the popular press of late. You may or may not agree with the idea summarized in the NY Times Magazine that low mood states are adaptations that help with social problem solving. For reaction and commentary see here here here and here. My major concern about the debate about the "upside" of depression, both pro and con, is that it has become disconnected from any actual data.

Regardless of whether you think that depressed mood invariably helps solve social problems, there is clear and growing evidence that garden-variety depressed mood (and significant case-level depression) is often aroused by social adversity.

Case in point is the March 2010 issue of Journal of Affective Disorders, which contains a powerful and novel demonstration led by George Brown and Tirril Harris that the success of treatments is intimately connected to the social environment.

Brown and Harris have, in their previous work, found that significant depression is often preceded by very specific kinds of social contexts, particularly negative events that involve a theme of humiliation or entrapment.

The new study shows that these same social contexts also shape whether depression treatments will work. Shockingly, there had been virtually no research on whether the social environment influences the impact of antidepressant medications.

In their study, 220 patients with significant depression symptoms were randomly assigned to either supportive care or to SSRIs plus supportive care (SSRIs are the class of medications most commonly used to treat depression such as Prozac and Paxil).

The investigators undertook a detailed assessment of each person's social environment (both events that were negative and positive in nature) at the beginning of the study and 12 weeks later, after the treatments had begun.

What they found was that those patients who faced significant environmental adversity at any point were only half as likely to respond to the treatments and remit from depression than patients who were in more benign environments. It did not matter what kind of treatment the patients received. Remission rates among patients in aversive social contexts were much lower irrespective of treatment type. In fact, only 1/5th (!) of those in aversive social contexts remitted after 12 weeks of treatment.

One interesting question that is unresolved by the JAD study is exactly why ongoing adversity undermines treatment. Brown and Harris focus on the idea of entrapment -- the idea that an ongoing adversity will bring about cognitive changes, such as seeing the situation as hopeless, that might interfere with treatment, but this is just one idea.

Examples of aversive social environments that the authors mentioned (and were presumably reported by study participants) included (a) a father caring alone for three children one of whom is hyperactive and a constant concern, and (b) a woman with crippling arthritis living with a highly critical and at times violent partner.

These, certainly, are difficult life problems. And it seems our current mainline treatments for depression, whether antidepressants, or cogintive behavioral therapy are not all that well suited to addressing them. Whether or not depression itself is nature's solution to these life problems (and a single blog post is inadequate to address such a complex issue), clinical science and clinical practice needs to more fully engage the social environment if we are to understand and treat depression. Brown and Harris are pointing the way....

Listening to Prozac, but Hearing Placebo

Jonathan Rottenberg, Ph.D. — Sat, 20 Feb 2010 17:52:46 +0000

Irving Kirsch is an expert in statistics and in clinical trial methodology. In The Emperor's New Drugs, he absolutely dismantles the case for antidepressants as a pharmacologically effective treatment.

The cornerstone of the book is a careful analysis of a vast database of drug company data. Using the Freedom of Information Act, Kirsch managed to get the data that the drug companies had sent to the FDA in the process of getting their medications approved.

Some of the key points include:

1) Nearly all the benefit of antidepressant medications can be attributed to the placebo effect. When all of the data are arrayed, Kirsch finds that common antidepressants barely beat dummy pills. More than half of the clinical trials sponsored by the pharmaceutical companies showed no significant difference at all between drug and placebo. As important, the benefit of the medication over the placebo is not clinically meaningful. The overall advantage amounts to 1.8 points on the 54-point scale used to gauge severity of depression (through questions about mood, sleep habits, and the like). For example, your mood could be just as rotten and you could be just as bothered by insomnia, poor concentration and all of the other symptoms of a depression, but if you're little less fidgety during the assessment, that's 1.8 points right there.

(2) When antidepressants do beat placebos in clinical trials, it is actually another version of the placebo effect. While the clinical trials are supposed to be double blind (neither patient nor evaluator knows who is getting drug and who is gettting placebo), patients in clinical trials can often correctly guess that they are receiving the investigational drug because they experience pronounced side effects. Knowledge that you may be receiving a potential cure enhances the placebo effect.

(3) Pharmaceutical companies and the FDA are not being intellectually honest. The pharmaceutical companies are given wide latitude concerning which clinical trials they want to publish and which data they want to include in the publications. This is important because many of the clinical trials yield negative findings (i.e., no differences between drug and the dummy pills). If a drug company does 10 studies and only 2 support the efficacy of the drug, they can elect to publish only the two. There is no law against cherry picking the data. The FDA does not compel disclosure of all of the unsuccessful trials. This leads to inflated perceptions about the drugs' efficacy from both doctors and the wider public.

Kirsch has written a book for grown-ups. He writes clearly and bends over backward to explain technical language. He refrains from heated rhetoric even when discussing the most controversial findings. Kirsch is a lover of data. If he ever goes beyond the data, he labels his statements as such. The data leads him to conclude that psychotherapies provide treatments for depression that are just as effective in the short-run and more cost-effective in the long run than antidepressants. I expect many readers will be convinced. The measured tone and laser-like focus of Kirsch's compact book are in some sense the exact opposite of Gary Greenberg's Manufacturing Depression, which I described as "a rambling, blistering, entertaining, attack on the biomedical disease model of depression." Kirsch is as sober as Greenberg is lyrical, but the net effect is not all that different. Read together, these new books are a powerful one-two punch against psychiatric and pharmaceutical orthodoxy.

Ironically, Kirsch's matter-of-fact argument for the power of the placebo effect may ultimately undermine the clinical effect of antidepressants. If we lose faith that they work, they won't work.

A blistering, rambling, entertaining attack on the biomedical disease model of depression

Jonathan Rottenberg, Ph.D. — Fri, 05 Feb 2010 00:24:13 +0000

How did we get to this point, this point in our history where it is common, if not mandatory, to think of our unhappiness as a disease?

That's the big question in Manufacturing Depression: The Secret History of a Modern Disease. Gary Greenberg has written a blistering, rambling and entertaining attack on the biomedical disease model of depression. It's the story of how advertising, pharmaceutical companies, and psychiatrists packaged unhappiness as a medical disease to be treated with antidepressants.With nearly thirty million Americans taking antidepressants at an annual cost of 10 billion dollars, Greenberg is David armed with a slingshot, careful research, and clever one-liners.

Greenberg wants to shake us up. What genre is this? His book mixes together personal memoir, case histories (he's a practicing therapist), intellectual and business history, and guerilla journalism (he shows up as a mischievous patient in a clinical trial).

He shakes us up by jumping around in his narrative His lyrical history includes detours into germ theory, the transformation of German synthetic dye companies into pharmaceutical industry titans, and the numerous turf wars between psychiatrists, psychologists, and neurologists over what is mental illness and who gets to diagnose and treat it.

Greenberg also keeps the reader busy. We have to track that he is making several different cases against the biomedical disease model.

There's the historical case. The disease model was not foreordained or inevitable, but represents the coming together of big pharma and the cultural needs of the late 20th century. He delights in the irony that discredited treatments in the early 20th century such as insulin coma therapy and lobotomy set the stage for the magic pharmaceutical bullets.

There's the scientific case. Greenberg hammers home the differences between depression and bona fide diseases cancer, diabetes, or flu. Unlike the latter, there remains no reliable biological marker of depression, or a validated theory of the biology that produces its symptoms. He covers the sad history of failed attempts to establish a biological basis of depression, from black bile to serotonin.

There's the clinical case. Greenberg points out that medications don't work well enough to be considered magic bullets. For example, the antidepressants beat placebo in only about half of clinical trials.

Finally, and probably dearest to Greenberg, there's the humanist case. He objects to DSM's one-size-fits-all checklist - how the diagnoses rendered with this system stunt the experience and expression of psychological suffering. Where is the place for experience in the biomedical model that treats consciousness as "merely the steam rising off the amino-acid-rich neurochemical soup that roils in dumb silence in your head?" As a practicing psychotherapist, he objects to how the disease model preempts the potentially redemptive power of self-exploration. He worries that if we call our misery a disease, we won't bother to try to fashion our past and present troubles into a coherent narrative. He worries that calling pessimism the symptom of an illness leads us to turn over our discontents to the medical industry and to surrender perhaps the most important portion of our autonomy, especially if our feelings of pessimism are "an ally at a time of crisis?"

This isn't your father's antipsychiatry. This isn't Peter Breggin railing against drugs that are rotting your brain, the chemical straightjacket. Greenberg has nothing against using psychiatric drugs to change feeling or perception, just as long as you don't call it treating a disease.

Greenberg is temperamentally a skeptic, and he is satisfied if he can help us understand what depression is not, not a disease. Given the history of muddled thinking on this topic, that is enough, for now. We must tear down before we can build. In the end, his book is more than a dizzying, dazzling critique of the biomedical disease model of depression. It is probably the most thoughtful book on depression ever written for a lay audience.

Botox Treatment Slows Perception of Negative Emotions

Jonathan Rottenberg, Ph.D. — Sun, 31 Jan 2010 19:31:28 +0000

Our smiles broadcast, hey world, I am pleased. Our frowns say, don't mess with me.

What about the other way around? Do we use our facial muscles to read emotion in the world?

Our default assumption is that our eyes and our brains are the organs dedicated to processing emotional information. New work led by David Havas of the University of Wisconsin, to be published in the journal Psychological Science, provides a fascinating demonstration that our facial muscles share in this job.

The new study reported on 40 people who were treated with Botox. Tiny applications of the nerve poison were used to deactivate muscles in the forehead that cause frowning (the corrugator muscles).

Before and after the Botox treatment, patients were asked to read written statements that carried an emotional tenor, including statements that were angry ("The pushy telemarketer won't let you return to your dinner"); sad ("You open your email in-box on your birthday to find no new emails"); or happy ("The water park is refreshing on the hot summer day.")

The authors used reading time as a proxy for processing speed.

The results showed no change in the time needed to understand the happy sentences. But in a fascinating result, after Botox treatment, the subjects needed more time to read the angry and sad sentences.

The size of the effect was small, but if others replicate it, the implications are large.

Milions of people undergo this cosmetic procedure every year; it's a profound idea that its effects go beyond smoother surface skin to influence the treated person's perception of the outside world. Study results imply that immobilizing muscles that produce angry or sad expressions may take some of the sting out of an insult, some of the tears out of a tear jerker.

Botox treatment is already controversial. Some look askance at the idea of poisoning the face to look younger. Especially when the treatments must be performed repeatedly. If it is confirmed that the procedure dulls emotion perception, critics will surely seize on this as further evidence of the treatment's unwholesomeness.

Perhaps the most interesting implication of the study is scientific. It shows yet again that our systems for communicating and perceiving emotion are interconnected, often in surprising ways.

Wii and Ennui: Media Use and Child Mental Health

Jonathan Rottenberg, Ph.D. — Fri, 22 Jan 2010 19:08:08 +0000

US kids spend almost eight hours a day surfing the web, watching TV, playing video games or using their mobile devices, according to a new report issued Wednesday by the Kaiser Family Foundation. The report, Generation M2: Media in the Lives of 8- to 18-Year- Olds, was a nationally representative survey of media use in 2,000 children.

The raw numbers are just staggering: The average American child consumes media 53 hours a week. This was, not surprisingly, a sharp increase over what Kaiser found in similar surveys 5 and 10 years ago. The New York Times coverage captured the gist of the results: If your kids are awake, they're probably online.

There are many sides to the issue of how our children spend their time. It speaks to the society we already are, the society we are likely to become, as well as the society we want to become.

I just want to speak to one issue that is important to me as a researcher, parent, and citizen -- whether this heavy media use has negative implications for the mental health of our children.

A sidelight of the Kaiser study considered the connection between the "dose" of media use and the well-being of the child. The researchers contrasted heavy media users (children using media 16hrs a day; believe it or not, there was an appreciable subsample of such children) with other children. Importantly, heavy users were less likely to report feeling happy in school during the last year than lighter media users. Moreover, these heavy users were also more likely to report often feeling sad or unhappy.

The researchers were quick to point out that we don't know from their data if heavy media use is the cause or the effect of a child's discontent. They are correct. However, I submit that other data do suggest that Wii may indeed precede and possibly cause ennui. For example an earlier study in the Archives of General Psychiatry found children who were initially heavier users of media (including more hours of television watching) were more depressed seven years later.

It is tempting to see the cell phone, the Wii, the computer, and the iPod as relatively benign, or at worst mildly annoying. These devices are now part of life's constant backdrop, like wallpaper we don't notice. At the same time, evidence is beginning to mount that heavy media use may be detrimental to the mental health of our children.

Yes, we need more research. The scientist in me would love gold-standard studies that better establish causation. All it would require is randomly assignnig different groups of children to different media lifestyles and looking for sustained impacts on well-being. Obviously don't hold your breath for those data because of the ethical and practical barriers to carrying out that kind of research with real children. Like it or not, citizens, parents, and researchers will have to draw conclusions and form a plan of action based on an imperfect database. In my view what we know already is sufficient cause for concern.

Depression treatment: We need better not simply more

Jonathan Rottenberg, Ph.D. — Wed, 06 Jan 2010 02:01:41 +0000

According to a study published today in the Archives of General Psychiatry only half of all people with depression received treatment. And among those who did receive treatment, only 21% were getting care that is consistent with American Psychiatric Association guidelines.

Naturally, the media ran with the depression-is-undertreated theme. See here here and here for examples. In a sense, that's a feel-good story, a reassuring spin. Figuring out depression is just a technical matter of routing more sufferers into an effective treatment. We can all go home happy, or at least no longer depressed.

One could quarrel about the actual trends. In point of fact, the public increasingly seeks treatment for depression. For example, just between 1977 and 1987, the rate of outpatient treatment for depression tripled from 0.73 per 100 persons to 2.33 per 100 persons. (Olfson et al., 2002). Moreover, the public has also become more accepting of treatment seeking (Motjabi, 2007).

But the just-get-people-into-treatment message misses something more fundamental. Our supposedly effective treatments for depression are not all that effective.

Make no mistake, our pharmacological and psychologically-based treatments are better than nothing. But it's time to be candid: these approaches have taken us to a state of diminishing returns.

Existing treatments leave the majority of patients (even patients who respond) with residual symptoms. For discussion purposes, let's consider antidepressants, in many ways the dominant treatment of our time. In one of the largest treatment studies ever of serious clinical depression, the Star*D treatment trial, which was based on 2,876 patients who were tested across the United States at 41 different sites, 72 percent of the patients still had significant residual symptoms even after 14 weeks of antidepressant treatment. These residual symptoms are more than just a nuisance: they include a nagging low mood, concentration difficulties, continuing insomnia, and feeling that the self is worthless. Even those patients who respond well to a treatment initially are not in the clear. Sadly, their depression will, more likely than not, recur.

As if to hammer home the point, today another major study came out in the Journal of the American Medical Association, reported in the New York Times, with even more chilling results. In a reanalysis of six large clinical trials, Fournier and colleagues found that for people who have mild to moderate depression, common antidepressants worked little better than inert placebo pills. The benefits of antidepressants, when they worked, were confined to people who had severe depression. This is a very important analysis because the majority of depressed people have the mild to moderate variety and not the severe variety.

Undertreatment of depression is not the real story; the real story is the recalcitrance of depression, even to state-of-the-art treatments. That's the hard truth we should be telling the public.

We need better treatments, not simply more of the same. If we are to start to contain depression, the public needs to demand them and to agree to fund the research that will bring them into being. Once we have more effective treatments, then, yes, we can put all of our energy into making sure that sufferers are routed into them. But for now, the very first step should be on research, research that will help us understand why depression is such a tough nut to crack.

References

Fournier et al. (2010). Antidepressant Drug Effects and Depression Severity: A Patient-Level Meta-analysis JAMA, 303: 47-53.

Hector et al. (2010). Depression Care in the United States: Too Little for Too Few. Archives of General Psychiatry, 67, 37-

Olfson, M., Marcus, S.C., Druss, B., Elinson, L., Tanielian, T., & Pincus, H.A. (2002). National trends in the outpatient treatment of depression. JAMA. 287, 203-209.

Motjabi, R. (2007). Americans' attitudes towards mental health treatment seeking: 1990-2003. Psychiatric Services, 58, 642-651.

The Women's Health Initiative Study: A Firebell in the Night?

Jonathan Rottenberg, Ph.D. — Mon, 04 Jan 2010 15:23:06 +0000

Antidepressant medications are among the most commonly prescribed. Are these drugs medically riskier than we think? A new study published in the Archives of Internal Medicine found that women who reported taking an antidepressant drug had increased risk for stroke and increased risk for death relative to women not taking antidepressants.The Women's Health Initiative (WHI) of the National Institutes of Health followed postmenopausal U.S. women for up to 15 years. The current report focused on 136,000 women who were not taking antidepressant drugs when they entered the study. The critical comparison was between the subsequent health history of 5,550 women who started to take antidepressants after study entry (1 or 3 years in) and the rest of the women who did not start taking antidepressants. The study did not find any relationship between antidepressant use and heart disease. However, antidepressants were associated with increased risk of death from any cause and of hemorrhagic stroke among those taking SSRIs.

Here are five reasons why we should pay attention:

(1) The large sample size in and of itself makes this study highly credible. The larger the sample, the more statistical power you have to test your hypothesis in a conclusive way. This study was a more powerful test than previous studies, which used smaller samples. Many health events, such as stroke death, will not be common in an otherwise healthy sample over a short follow up, so large samples and long follow up periods are critical if you want to be able to detect an effect. For example, in this sample, there were 2357 strokes, 445 of which were fatal, over the follow up period. This pool of events is sufficiently large to enable good tests of whether antidepressants were associated with elevated risk for stroke or stroke death.

(2) Health risks were observed across different categories of antidepressants and were not confined to the older tricyclic antidepressants, One reason newer selective serotonin reuptake inhibitor (SSRI) antidepressants (such as Prozac) are prescribed so widely is that they are viewed to be medically benign. However, when SSRIs were examined separately, they also had increased risk for stroke and death.

(3) The size of the effects, though not whopping, are certainly attention-getting. For example, SSRIs were associated with double the risk for fatal hemorrhagic stroke and one-third higher risk of mortality from all causes.

(4) The authors appear to have no axe to grind against antidepressants. This was a multi-site study funded by the National Institute of Health. In fact, I find it interesting that the study authors, in the accompanying press material, are somewhat muted in their alarms, "Depression is a serious illness with its own health risks, and we know that antidepressants can be life-saving for some patients. No one should stop taking their prescribed medication based on this one study, but women who have concerns should discuss them with their physicians," said lead author Jordan W. Smoller, MD, ScD.

(5) An accompanying commentary found little to fault with the study. When a particularly impactful or potentially controversial study is published in the health sciences, it is not uncommon for the journal to publish a critical commentary alongside the original report. In this case, the comment agreed that this was a potentially important study. The main caution in the comment was that we cannot be absolutely certain whether observed health risks were truly attributable to the drugs and not to the depression, or to some other unseen characteristic that goes along with starting antidepressant treatment (i.e., women who take antidepressants take worse care of themselves). Smoller and colleagues did the best they could to control for these other factors statistically. While the caution stands, we have to realize that these may be the best data we will ever have --a study that randomly assigned women to antidepressants and controlled the treatment over 15 years would be impossible to perform, for both ethical and logistical reasons.

Let me end with the clinical language of the commentary, "The findings, in the largest cohort of women yet studied, provide additional warning that antidepressant therapy may in fact be detrimental with respect to stroke and total mortality in this demographic population."

Time will tell whether this study is a firebell in the night.

Why Justin Duchscherer is a Hero

Jonathan Rottenberg, Ph.D. — Sat, 26 Dec 2009 20:41:59 +0000

In a post last month, I wrote about the sad death of Robert Enke, who was a 32 year old goalkeeper on Germany's national soccer team, who committed suicide by stepping in front of a train in Hanover, Germany. Enke battled serious depression for years. So great were his shame and embarrassment about depression that he felt compelled to hide it until it was too late. For me, this was a tragic illustration of the stigma of depression, and of how powerful that stigma continues to be for young men.

Today I read news that the Oakland A's decided to re-sign pitcher Justin Duchscherer. I don't root for the A's, or even like baseball, but boy did this story made me feel hopeful. Duchscherer did not pitch at all last season. It turns out that in addition to an elbow injury, he suffered from serious clinical depression. Like Enke, Duchscherer is 32 years old. Unlike Enke, this athlete took the risk of making his depression public, announcing it earlier this year when he was put on the disabled list. His agent Damon Lapa said that Duchscherer decided to come forward to aid in his recovery and to serve as an example to others suffering from depression, "he been battling this for quite some time, and it's kind of reached the apex where he made a really tough decision and owned up to the problem..."

Coming forward could not have been easy. In A League of Their Own, Tom Hanks famously said there is no crying in baseball. Although Hanks played this line for laughs, the underlying sentiment is serious business, and reflects our very real and, very inhuman, expectations for professional athletes. No crying in baseball means never admitting you are overwhelmed or distressed--or need help--no matter what. In this spirit, I applaud Justin Duchscherer for his candor. I hope that he will continue to speak out about his depression as he returns to ace form.

And I applaud his team for sticking with him.

I truly consider this an A of hope.

Physical Pain and Emotional Pain: More Similar Than You Think

Jonathan Rottenberg, Ph.D. — Thu, 24 Dec 2009 00:30:02 +0000

New research led by psychologist C. Nathan DeWall of the University of Kentucky and reported in the journal Psychological Science suggests that physical pain and emotional pain may be more similar than you think.

In a first experiment, volunteers were randomized either to take 1,000 mg/day of acetaminophen (the equivalent of 2 extra strength Tylenol) or a placebo (inert tablets). Participants completed measures of hurt feelings. The researchers found that particants who were taking acetaminophen tended to report less hurt feelings over time relative to participants who were taking placebo.

A second experiment brought these ideas into an fMRI scanner. Here the researchers had the volunteers take a larger daily dose of acetaminophen (2,000mg) for three weeks. To allow the researchers to examine neural responses to social rejection, participants went into a scanner and played a computer game in which they were rejected. Brain regions associated (in other studies) with both social pain and physical pain were more active in the placebo subjects when they were rejected than in the acetaminophen group. In other words, acetaminophen dulled the brain's reponse to rejection.

Early media reports have naturally seized on the consumer implications of this study. Those implications are timely! Should you take a prophylactic Tylenol before your overbearing relatives arrive for Christmas dinner? Your Uncle Lou is in particularly rare form, perhaps a double dose is needed?

I am more intrigued by the scientific implications.

From the patient's perspective, the pain caused by rejection is as every bit as real as the pain caused by a stiff joint. In interviewing depressed people, I've often been struck by the tremendous blurring between physical and emotional pain. In depression, everything hurts. Now we have a demonstration that our bodily systems for registering social and physical pain overlap in their response to a common household drug.

We usually talk about emotional and physical pain in different terms. And we conventionally take a different drug for a wounded ego than for a wounded arm. But emotional and physical pain may be more similar than you think. This observation makes good sense if we assume that evolution is a conservative force.