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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Two days later, your son complains that his knee hurts a lot and that he “feels crummy.” He didn’t sleep well the night before, and his face seems a little flushed. You remove the gauze pad and notice that his knee is red and swollen, and there is a foul-looking, greenish liquid oozing out of the wound. You get that sinking, “Uh-oh!” feeling, and decide you had better have your family doctor take a look at the knee.

As you are about to drive off, your friendly neighbor buttonholes you and asks where you are going. You explain the whole situation to him. He looks at you like you are from Mars, and says, “Are you nuts? You want this kid to grow up to be a wimp? He is supposed to be in pain! Pain is a normal part of life! We all have to learn how to live with pain. Redness and swelling are normal, after you bang up your knee! Let the kid heal up naturally! The doctor is just going to put him on some damn antibiotic, and you know the kind of side effects those drugs have. Those doctors, you know, they just make money on all those prescriptions!”

Would you feel that your well-intentioned neighbor was giving you good advice? I very much doubt it. Well, it’s the kind of advice some well-meaning but misinformed individuals give, when dealing with the issue of severe grief and depression. In part, this attitude is a remnant of our Puritan roots—the idea that suffering is God’s will, that it ennobles the soul, or that it is just plain good for us!

Now, it is certainly true that life is full of bumps, bruises, and falls. It is also full of disappointment, sorrow, and loss. Not all of these are occasions for a medical diagnosis or professional treatment — most are not. But there are times when a simple cut can become infected, and there are also times when so-called “normal” grief can become a very nasty beast called clinical depression. Learning how to deal with disappointment and loss is part of becoming a mature human being. Coping with loss may indeed be a “growth-promoting” experience, under the right circumstances. But “hanging tough” and refusing to seek help in the face of overwhelming pain — physical or emotional — is an affront to our humanity. It is also potentially dangerous.

The Case of Jim

I recently had an essay published in the New York Times (9/16/08), in which I argued that the line between profound grief and clinical depression is sometimes very faint. I also argued against a popular thesis that says, in effect, “If we can identify a very recent loss that explains the person’s depressive symptoms — even if they are very severe — it’s not really depression. It’s just normal sadness.”

In my essay, I presented a hypothetical patient — let’s call him Jim — who was based on many patients I’ve seen in my psychiatric practice. Jim comes to me complaining of “feeling down” for the past three weeks. A month ago, his fiancée left him for another man, and Jim feels that “There’s no point in going on” with life. He has not been sleeping well, his appetite is poor and he has lost interest in nearly all of his usual activities.

I deliberately withheld a lot of important information that any well-trained psychiatrist, psychologist, or psychiatric social worker would obtain. For example: in the past three weeks, had Jim lost a great deal of weight? Was he awakening regularly in the wee hours of the morning? Was he unable to concentrate? Was he extremely slowed down in his thinking and movement (so-called “psychomotor retardation”). Did he lack energy? Did he see himself as a worthless person? Did he feel completely hopeless? Was he filled with guilt or self-loathing? Had he been unable to go to work or function well at home, over the past three weeks? Did he have any actual plans to end his life?

I wanted to make the case ambiguous enough to be suggestive of clinical depression without “clinching” the diagnosis by providing answers to all these questions. (A “yes” answer to most of these questions would point to a serious bout of major depression).

But even given the limited information in my scenario, I concluded that people like Jim were probably better understood as “clinically depressed” than as “normally sad.” I argued that individuals with Jim’s history merited professional treatment. I even had the temerity to suggest that some grieving or bereaved individuals who also show features of a major depression may benefit from antidepressant medication, citing the research of Dr. Sidney Zisook. (If I had to write the piece all over again, I would have added, “Brief, supportive psychotherapy alone may do the job for many people with Jim’s symptoms”).

Well, my goodness! The blogosphere lit up like a swarm of fireflies. You would think that I had advocated the killing of the first-born! I should not have been surprised by the reaction from the “Hate Psychiatry First” crowd, who get their information about psychiatry from Tom Cruise. They wrote me off as either a shill for the drug companies [see disclosure], or someone who was “declaring grief to be a disease.” One of the most irate bloggers opined that my medical license should be revoked!

Nearly all of my colleagues were very supportive and felt that I had made some good points. But a few responses from mental health professionals really surprised me. One PhD-level “bereavement specialist” scolded me for failing to let my hypothetical patient “heal naturally” from his “normal grief”. Never mind that my patient had lost interest in nearly all his usual activities, and sounded vaguely suicidal—to this critic, feeling suicidal was all par for the course and nothing to get too upset about. She spoke of her ten years of experience, and how many people with “normal grief” feel like “not going on” with life. Well, after 26 years of practice, I guess I just lack confidence!

One thing I do know: nobody inside or outside my profession is very good at predicting who will attempt suicide. There is also good research from Dr. Lars V. Kessing showing that suicide rates are not markedly different for those whose depression is apparently a “reaction” to some stressor or loss, versus those with no apparent cause for their depression. And, as I note in my NY Times article, it is not always clear whether a depressed person is “reacting” to some life event, or whether the depression preceded and precipitated the event. For example, the person who insists, “I got depressed after I lost my job” may actually have been depressed while still employed, and may not have been working at her usual efficiency.

But now consider Gina, a patient described by psychologists Barbara and Gregory Markway, in their book, Painfully Shy. In school, Gina not only dreaded being called on by the teacher, she would also “freeze up” and literally be unable to speak — a condition termed “selective mutism.”

Now, in her adult years, Gina never dates and is so anxious about how her co-workers will judge her, she won’t eat lunch with them. Gina tells Dr. Markway that, “I feel like I’m always under the spotlight, as if people are evaluating every word I say, every move I make. Sometimes I feel paralyzed by it. I just know I’m going to do or say something to make other disapprove of me.” She adds, tearfully, “I feel like there’s something terribly wrong… the way I am is not normal.”

Does Gina have a psychiatric disorder? Probably so, and it goes by the name of Social Anxiety Disorder (SAD). Some clinicians refer to this as “Social Phobia,” but others reject this term. They point out that the generalized form of SAD often pervades the sufferer’s life in ways that so-called simple phobias, such as an intense fear of spiders, do not.

A recent national survey known as the NESARC (1) assessed more than 43,000 adults in the U.S. and found that 5% suffered from SAD at some period in their lives. This would make SAD one of the most common psychiatric disorders, with a higher lifetime prevalence than bipolar disorder. SAD usually begins between 11 and 19 years of age, and affects slightly more females than males. Some evidence indicates that SAD may run in families. In my own practice, I found that many patients with intense social anxiety also had problems with depression, substance abuse, or both. This was confirmed in the NESARC study: nearly half of those with SAD also suffered from an alcohol use disorder; and more than half, from a mood disorder. The NESARC study also found that SAD usually ran a chronic course with marked impairment in social and vocational function.

Yet SAD remains controversial, both outside and within the mental health profession. Writing in the Sept. 21, 2007, New York Times, English professor Christopher Lane found it “baffling” that “…ordinary shyness could assume the dimension of a mental disease…if a youngster is reserved, the odds are high that a psychiatrist will diagnose social anxiety disorder and recommend treatment.”

Well, not really — not if the psychiatrist is well-trained and has a lick of common sense. What pushes a condition into the realm of illness is marked and persistent suffering and incapacity. Indeed, the current diagnostic criteria for SAD (in the Diagnostic and Statistical Manual of Mental Disorders, 4th edition) require the presence of “marked and persistent fear” of social or performance situations; avoidance of these situations; and the person’s recognition that the fear is “excessive or unreasonable”. In those under age 18, symptoms must be present for at least six months. Most critically, the social anxiety “interferes significantly with the person’s normal routine, occupational (academic) functioning, or social activities.” DSM-IV is not talking “butterflies” in the stomach!

Yet even some mental health professionals have raised questions about SAD. Writing in the April 13, 2002 British Medical Journal, psychiatrist Dr. Duncan Double argues that, “…although definitions of the syndromes of shyness and social phobia may differ, the distinction is difficult to make…Furthermore, we should be skeptical about the potency and benefits of drugs for this condition.” Even psychiatrist Dr. Bruce Black, one of the most prominent early researchers of SAD, wrote me to say that, “Everybody has some social anxiety…So even though I see individuals of all ages with severe impairment, I can understand some of the criticism of social anxiety as a categorical disorder.”

Similarly, as psychologist Dr. John Grohol recently wrote me, “Social anxiety disorder is a real disorder in a small set of the population. …On the other hand, because there are some medications now available for this disorder, I believe it is being over-diagnosed and that doctors do not rigorously [or] reliably apply the diagnostic criteria we do have.”

Perhaps so, in clinical settings where a thorough evaluation isn’t performed. Yet the NESARC study found that over 80% of SAD sufferers received no treatment, and that the number of treated cases hasn’t changed in the last 20 years. This hardly supports the notion that “Big Pharma” has steam-rolled doctors into over-diagnosing and over-medicating SAD. Furthermore, we have good evidence from countries as diverse as Australia, Brazil, China, and Japan that SAD is “real”, common, debilitating, and often under-treated.

In the U.S., the NESARC study found a one-year SAD prevalence of 2.8%. An Australian study by Lampe and colleagues (2) found a similar yearly SAD prevalence of 2.3% in Australia—despite the comparatively limited “marketing” influence of the Australian pharmaceutical industry. In Brazil, Rocha and colleagues (3) found one-year SAD prevalence rates of 5-9%, depending on the diagnostic criteria. And in the first such study of Chinese patients by Dr. Sing Lee and colleagues, the one-year prevalence of SAD was 3.2% — similar to that in the U.S. These multi-cultural data simply don’t support the notion that American psychiatrists are pulling this diagnosis out of thin air.

To be sure: clinicians must adhere to strict criteria for SAD, so that everyday “shyness” is not pulled into the net of psychopathology. We must also continue our search for the genetic, biochemical, and psychosocial factors that lead to SAD. But first, we need to take care of those, like Gina, who suffer greatly with this condition.

The writer is Professor of Psychiatry, SUNY Upstate Medical Center, Syracuse, N.Y.; and Clinical Professor of Psychiatry at Tufts University School of Medicine in Boston. His most recent book is, Everything Has Two Handles: The Stoic’s Guide to the Art of Living. (Hamilton Books).

Notes:

1. National Epidemiologic Survey on Alcohol and Related Conditions, reported by Dr. Bridget Grant and colleagues in the November 2005, Journal of Clinical Psychiatry.
2. Reported in the May 2003 issue of Psychological Medicine
3. Writing in Rev Bras Psiquiatr. 2005 Sep;27(3):222-4. Epub 2005 Oct 4.)

“…who came to believe he was a turkey. He took off all his clothes and got under the table and lived there on scraps and crumbs and bones. The King called in many doctors, but none of them could cure him. Finally, he called in a certain wise man, who took off his own clothes and sat down under the table with him. I am a Turkey, the prince told him. ‘I am a turkey too,’ the wise man said. The two of them sat there together for a very long time and then the wise man said, ‘Do you think a turkey can’t wear a shirt? You can wear a shirt and still be a turkey.’ So the prince put on a shirt. ‘Do you think you can’t be a turkey and wear trousers?’ So the prince put on his trousers too, and in this way, the wise man coaxed the prince to put on all his clothes, to eat real food, and finally to come up from under the table and to sit at the table, and in the end, the prince was completely cured.”

Rabbi Lew goes on to cite Avraham Greenbaum, a contemporary Bratslaver teacher, who elaborates on Nachman’s tale:

“The wise man went under the table, and the very first thing he did, his first lesson, was just to sit there. You might have thought he would have been anxious to get started and take the first steps in his plan to cure the prince, In fact, sitting was the first step. Indeed, if you think about the story as a whole, you notice that most of the time the wise man took to cure the prince was spent just sitting with him. This is because the ability to sit calmly is one of the most important prerequisites of clear-headedness.” (Lew, 2008, italics added).

Now, I have never actually gotten under the table with any of my patients, and I suspect my supervisors would have frowned on the practice. Nor do I believe it is generally wise to enter directly into the delusional world of psychotic patients. (Most of them, very quickly, would sense a certain insincerity in this, or else feel vaguely patronized). But there is a lesson in Rabbi Nachman’s tale that I applied, in a very attenuated way, when I was working with an extremely provocative and hate-filled psychotic patient. This was a man I described in a piece for the New York Times (January 31, 2006) as a “brilliant and tortured” individual with chronic paranoid schizophrenia — and a virulent form of anti-Semitism. One of the quirks of his delusional system was the idea that, if he increased his dose of antipsychotic medication by even a single milligram, it would injure or kill him. As a result, he insisted that he would take only 30 milligrams of Thorazine, a “first generation” antipsychotic that is almost never used anymore. Now, thirty milligrams is about one-tenth of a therapeutic dose. It might have been better than nothing for this patient’s schizophrenia, but just barely so. I spent hours, during our first sessions, trying to persuade Mr. A. to increase his medication, even by a few milligrams. The answer was always the same — any increase would kill him. What else could I do but — in a sense — get “under the table” with Mr. A.?

No, I didn’t affirm his delusions in the way the “wise man” of Rabbi Nachman’s tale did. I judged that to be too risky. But I did sit with Mr. A. — a lot. I also talked to him about the things he most cared about: theology, philosophy, and the “hidden meanings” of words. Sometimes he would send me letters in which he would subject my comments to a kind of mystical, Kabbalistic analysis, along the lines of,

“You use the term “paranoia”, Doctor. Paranoia is derived from the Greek, para- “beyond” + noos “mind.” Note the similarity between “noos” and “noose”. The mind is what hangs you, doctor! So I must go beyond the mind.” (This is just a re-creation of Mr. A’s mode of thought, not an actual quotation).

Getting “under the table” with Mr. A. meant, in part, giving him the freedom and safety to explore these preoccupations—and the respect of a civilized debate. Indeed, I often gently sparred with him on his interpretations of my words, and he seemed to relish this. This, after all, was a man whose forensic skills had been honed by the Jesuits, in the years before his calamitous illness struck.

As for his medication, I continued to prescribe the feeble dose of chlorpromazine. I decided that struggling with Mr. A. over this would lead only to his leaving treatment. At least, with our regularly scheduled meetings, I could monitor his general state of health. In fact, he actually agreed to get some routine laboratory tests done, which allowed me to rule out any serious metabolic disturbance.

Sometimes, “getting under the table” with psychotic patients means taking their words very seriously, but not literally. This means being willing to meet the patient’s language “half way”, rather than responding too concretely. For example, if John, who has paranoid schizophrenia, says, “My mother is poisoning my coffee,” the therapist might be tempted to take the orthodox approach and say, “Well, based on your lab results, and what I know of your mother, I think that’s very unlikely.” There is nothing necessarily wrong with this approach, and sometimes it helps. But more often than not, the psychiatrist’s attempt to be the “Ambassador of Reality” tends to alienate the psychotic patient. It is better, at times, to get part-way “under the table” with the patient. So I might say, in response, “John, it sounds like you and your mother have a very bitter relationship.” I am deliberately picking up on — almost punning on — the image of the poisoned coffee. I am also using a highly-charged sensory term to characterize the patient’s relationship with his mother: bitter. In my experience, this is often a more promising approach to resonating with the patient’s emotive world than meeting it with the full force of Western logic and reason.

The writer Anatole Broyard once commented that, “Inside every patient, there is a poet trying to get out.” Sometimes, in order to hear the patient’s inner poem, the therapist needs to take advantage of unusual acoustics: those found only “under the table.”

Ron Pies, M.D. is a Professor of Psychiatry and Lecturer on Bioethics & Humanities at SUNY Upstate Medical University in Syracuse, NY; and Clinical Professor of Psychiatry at Tufts University School of Medicine in Boston. He is the author of several textbooks in psychiatry, as well as the new book, Everything Has Two Handles: The Stoic’s Guide to the Art of Living.

Resources:

Broyard, Anatole. “Doctor, Talk to Me.” In On Doctoring: stories, poems, essays, edited by Richard Reynolds and John Stone, with Louis LaCivita Nixon and Delese Wear, 166-172. New York: Simon & Schuster, 2001.

Lew A: Choose This Life, Rosh Hashanah II 5758. Accessed 5/14/08 at: http://www.bethsholomsf.org/CBS/pages/page.phtml?page_id=240

Steinsaltz A: The Tales of Rabbi Nachman of Bratslav. Northvale, Jason Aronson, 1993.

Wield the Pen, Yield the Soul: Examining the role of literature in medicine: Essay by “Linda”.

And this is truly a shame. The “Angel or Devil” dichotomy does nobody any favors, and certainly does not help patients with serious emotional disturbances. In truth, the human brain is the crucible in which all the elements of our experience and sensation are transformed into thought, feeling, and action. We can affect the function and structure of the brain directly, by altering its chemical constituents; or we can affect its function and structure indirectly, by pouring helpful words into the ear of the patient. Speech, music, poetry, art, and a myriad of other “inputs” are all transduced into neuronal connections and electrochemical processes in the brain.

This does not mean that we ought to greet our patients by asking, “How are your serotonin molecules this morning, Mrs. Jones?” Part of our shared behavior as human beings is the use of language that speaks to our felt experience, not our neurons. But this does not mean that our experience is ultimately something over and above the workings of our brains. Moreover, far from being “cosmetic” in nature, many psychotropic medications work at the most fundamental level of the gene, actually increasing the production of nerve growth factors.

These are all reasons why we should not dismiss psychotropic medications out of hand. They are neither agents of the devil, as some extremist factions argue; nor are they angels of redemption, as one might conclude from the “rainbow and butterfly” ads put out by some pharmaceutical companies. Psychotropic medications, as I tell my patients, are neither a crutch nor a magic wand; they are a bridge between feeling bad and feeling better. The patient must still walk — sometimes painfully — across that bridge. This means doing the hard work of changing thoughts, feelings, and behaviors. Medications can often aid that process, and are sometimes needed to get the patient’s work in therapy moving. For example, some patients with very severe depression are so lethargic and cognitively impaired that they can’t fully engage in psychotherapy. After three or four weeks of antidepressant treatment, many of them are able to benefit from “talk therapy”, which then may provide long-term protection against depressive relapse. Some evidence suggests that initial antidepressant treatment can help “set up” the patient for subsequent long-term psychotherapy. As a recent review by Dr. Timothy J. Petersen [1] concluded,

“…sequential use of psychotherapy after induction of remission with acute antidepressant drug therapy may confer a better long-term prognosis in terms of preventing relapse or recurrence and, for some patients, may be a viable alternative to maintenance medication therapy.”

Other evidence indicates that talk therapy and medication work synergistically — one reinforcing the other. Medications may help more with “somatic” aspects of depression, such as impaired sleep and appetite; psychotherapy, more with cognitive aspects, such as guilt or hopelessness. Evidence from brain imaging studies suggest that each intervention may work through overlapping but somewhat different mechanisms: antidepressant medication seems to work “from the bottom up”, arousing lower brain centers associated with emotion. Psychotherapy appears to work from “the top down” by changing neural patterns in higher brain centers, such as the prefrontal cortex.

Given the huge literature on psychotropic medications, I am focusing on antidepressants in this essay — a diverse group of agents that has been the focus of tremendous controversy. In recent years, for example, questions have been raised regarding both the efficacy and safety of antidepressants. There is a voluminous literature on these topics, but here is my best professional synopsis. Antidepressants seem to “show their stuff” more robustly in cases of severe depression, but this may be partly an artifact of how most studies are designed and analyzed. For example, the most recent review from Kirsch and colleagues [2] suggests that in mild-to-moderate depression, antidepressants do not work better than a sugar pill (placebo). In very severe depression, Kirsch et al found, the newer antidepressants outperform placebo, though their benefits are not as robust as in earlier studies (1960s-70s) of the “old” tricyclic antidepressants.

However, we need to put these recent findings in perspective. Numerous posts on the internet have declared, based on the Kirsch et al study, that “Antidepressants Don’t Work!” But this is not what the study showed. Rather, it lumped together results from 47 antidepressant trials and found that the active drug showed a clinically significant “separation” from placebo only in the most severe cases of depression. This is actually much better than finding that antidepressants work only for very mild depression! That said, the Kirsch study attributed the apparent benefit of antidepressants in the most severely ill patients to reduced responsiveness to placebo rather than to increased effectiveness of the drug.

There are a number of problems with the Kirsch study, many of which are nicely discussed in Dr. Grohol’s recent blog (2/26/08) on this website. For one thing, the entire Kirsch study turns on whether a 2-point improvement in a single depression rating scale (the Hamilton Rating Scale for Depression, or HAM-D) amounts to a “clinically significant” (not just statistically significant) change. That is, of course, a matter of judgment. Second, the Kirsch study looked only at antidepressant trials in the FDA data base done prior to 1999; an analysis of more recent trials might have produced different results. Third, the kind of “number crunching” that goes on in any meta-analysis (basically, a study of studies) can obscure not only individual differences, but also subgroup differences. That is, a given patient with certain depressive symptoms—or a subgroup with certain features—may do quite well on an antidepressant, but the results are “submerged” in the overall mediocre success rate in the study as a whole.

There are many other reasons why studies of antidepressants may be yielding less than spectacular results in more recent decades, and the interested reader can find details in an editorial by Kobak and colleagues, in the February 2007 Journal of Clinical Psychopharmacology. These authors point out, among other things, that if the interviews producing HAM-D depression scores are not performed skillfully, the results of the study may be distorted. Kobak and colleagues pointed to several instances in which poor interviewing technique led to outcomes showing little difference between the antidepressant and placebo; conversely, good interviewing technique led to a more robust improvement rate (“effect size”) for the antidepressant. It is not clear how many such “junk interview” studies were included in the Kirsch et al meta-analysis.

Part of the relatively weak showing of antidepressants in recent studies (compared with those done in the 1960s and 70s) may be due to the increasingly “good show” put on by the placebos. What might account for this? My colleague David Osser MD, Associate Professor of Psychiatry at Harvard Medical School, observes that placebo response rates have actually been rising in recent years, as confirmed by Dr. B. Timothy Walsh and colleagues (JAMA Vol. 287 No. 14, April 10, 2002 ). Dr. Osser thinks it likely that this “placebo inflation” is due, in part, to recruitment of less severely ill subjects for study. The less ill the subjects, the more likely a “sugar pill” is going to work for them. Dr. Osser points out (as suggested by Walsh et al) that subjects in modern studies are often recruited from ads in magazines, rather than from samples of “real” patients, who are often much sicker.

There is a larger point to be made about the kind of analysis Kirsch et al have done. Basically, it involved crunching numbers on trials in which, usually, a single antidepressant was tested over a period of a few weeks. But when psychiatrists use a “full court press” and treat depressed patients over many months, using various combination and augmentation strategies, we often see better results with medication. For example, a recent series of carefully-controlled, multi-stage studies known as STAR*D, sponsored by the National Institute of Mental Health, looked at remission rates in patients with resistant major depression. These patients had gone through several levels of intensive antidepressant treatment, without full recovery. After the fourth and final “hoop” was jumped through, the cumulative rate of remission (few or no symptoms) was about 67% [3]. The nature of the STAR-D study precluded use of a placebo group. However, the cumulative remission rate of 67% is certainly much higher than generally reported rates of remission with placebo, which average around 30%.

To be sure, non-specific interventions, such as talking to a friend, taking up a hobby, joining a club, etc. might work as well as an antidepressant for many patients with mild depressive symptoms. (Many individuals with “normal sadness”, of course, will feel better simply by waiting a few weeks). But for those with the most severe types of depression — and certainly for those with psychotic depression — medication is often required, at least in the early stages of treatment. Patients with depression due to bipolar disorder (“manic-depressive illness”) will require special treatment using a “mood stabilizer”, and may actually become agitated or manic if treated with an antidepressant. It is critically important that the patient with depression is carefully evaluated to rule out a bipolar disorder [4].

With regard to safety, there is probably a very small subgroup of depressed patients who will worsen with an antidepressant. Data from the U.S. Food & Drug Administration (FDA) suggest that a small minority of children and adolescents may develop suicidal thoughts or behaviors (“suicidality”) when treated in the short-term with an antidepressant. About 4 in 100 taking an antidepressant may develop these thoughts or behaviors, versus about 2 in 100 taking a placebo [5]. No actual suicides occurred, in the studies reviewed by the FDA.

Indeed, other lines of evidence from other countries call into question the association between antidepressants and suicidal behavior. For example, several studies from the Netherlands and other European countries suggest that as prescriptions for serotonergic antidpressants (“SSRIs”, such as Prozac and Zoloft) declined from 1998-2005, suicide rates actually rose in children and adolescents. Conversely, increased prescription of SSRIs is associated with decreased suicide rates in several European countries [6]. Moreover, results of a comprehensive review of pediatric trials conducted between 1988 and 2006 suggest that the benefits of antidepressant medications greatly outweigh their risks to children and adolescents with major depression and anxiety disorders [7]. Another study of over 226,000 depressed veterans found that SSRIs actually had a protective effect against suicide attempts, in all adult age groups [8].

In my own experience over the past 25 years, antidepressant treatment — usually in combination with talk therapy — may literally be life-saving for seriously depressed adult patients. I have also found that in many cases of “paradoxical” or adverse reactions to antidepressants, the patient actually suffers from an undiagnosed bipolar disorder. Although the use of antidepressants in bipolar disorder is controversial, I try to avoid it whenever possible.

So– “devil or angel”? Asking this of psychotropic medication is a bit like asking, “Will fire burn down my house, or will it warm it in the winter?” In this piece, I have focused almost entirely on antidepressant medication. If I were to go on at even greater length — discussing mood stabilizers, antipsychotics, and anti-anxiety agents — we would see that pharmacotherapy is neither devil nor angel. It is merely one instrument in service of helping the patient. As such, it may do good or ill, depending on the skill of the physician, the constitution of the patient, and the nature of the illness. Medication may be over-sold and “hyped”, as it is by many in the pharmaceutical industry; or it may be vilified and disparaged, as it has been by some vociferous anti-psychiatry groups in this country. In the end, as physician and educator Alfred Stille (1813-1900) observed: “It is quite as necessary for the physician to know when to abstain from the use of medicine as it is…[to know] when medication is necessary…”

Acknowledgment: I would like to thank Dr. John Grohol for inviting this piece, and Dr. Dave Osser for his helpful comments.

The author is Professor of Psychiatry and Lecturer on Bioethics & Humanities at SUNY Upstate Medical University in Syracuse, NY; and Clinical Professor of Psychiatry at Tufts University School of Medicine in Boston. He is the author of several textbooks in psychiatry, as well as the forthcoming book, Everything Has Two Handles: The Stoic’s Guide to the Art of Living. Dr. Pies reports no conflicts of interest with respect to the material in this piece.

References

1. Petersen TJ: Enhancing the efficacy of antidepressants with psychotherapy Journal of Psychopharmacology, Vol. 20, No. 3 suppl, 19-28 (2006)

2. Kirsch I, Deacon BJ, Huedo-Medina TB et al: Initial Severity and Antidepressant Benefits: A Meta-Analysis of Data Submitted to the Food and Drug Administration. PLoS Medicine. Accessed at:

3. Rush AJ, Trivedi MH, Wisniewski SR et al: Acute and longer-term outcomes in depressed outpatients requiring one or several treatment setps: a STAR*D report. Am J Psychiatry 2006;163:1905-17.

4. Ghaemi, SN, Miller CJ, Berv DA, Klugman J, Rosenquist KJ, Pies R: Sensitivity and Specificity of a New Bipolar Spectrum Diagnostic Scale. Journal of Affective Disorders 2005; 84:273-77.

5. URL

6. Gibbons RD, Brown CH, Hur K et al: Early Evidence on the Effects of Regulators’ Suicidality Warnings on SSRI Prescriptions and Suicide in Children and Adolescents. Am J Psychiatry 2007; 164:1356-1363.

7. Bridge JA, Iyengar S, Salary CB et al: Clinical response and risk for reported suicidal ideation and suicide attempts in pediatric antidepressant treatment: a meta-analysis of randomized controlled trials. JAMA. 2007; 297:1683-96.

8. Gibbons RD, Brown CH, Hur K et al: Relationship between antidepressants and suicide attempts: an analysis of the Veterans Health Administration Data Sets. Am J Psychiatry 2007;164:1044-49.