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The New York Times > Magazine > There’s Nothing Deep About Depression

By PETER D. KRAMER

Shortly after the publication of my book ‘’Listening to Prozac,'’ 12 years ago, I became immersed in depression. Not my own. I was contented enough in the slog through midlife. But mood disorder surrounded me, in my contacts with patients and readers. To my mind, my book was never really about depression. Taking the new antidepressants, some of my patients said they found themselves more confident and decisive. I used these claims as a jumping-off point for speculation: what if future medications had the potential to modify personality traits in people who had never experienced mood disorder? If doctors were given access to such drugs, how should they prescribe them? The inquiry moved from medical ethics to social criticism: what does our culture demand of us, in the way of assertiveness?

It was the medications’ extra effects — on personality, not on the symptoms of depression — that provoked this line of thought. For centuries, doctors have treated depressed patients, using medication and psychological strategies. Those efforts seemed uncontroversial. But authors do not determine the fate of their work. ‘’Listening to Prozac'’ became a ‘’best-selling book about depression.'’ I found myself speaking — sometimes about ethics, more often about mood disorders — with many audiences, in bookstores, at gatherings of the mentally ill and their families and at professional meetings. Invariably, as soon as I had finished my remarks, a hand would shoot up. A hearty, jovial man would rise and ask — always the same question — ‘’What if Prozac had been available in van Gogh’s time?'’

I understood what was intended, a joke about a pill that makes people blandly chipper. The New Yorker had run cartoons along these lines — Edgar Allan Poe, on Prozac, making nice to a raven. Below the surface humor were issues I had raised in my own writing. Might a widened use of medication deprive us of insight about our condition? But with repetition, the van Gogh question came to sound strange. Facing a man in great pain, headed for self-mutilation and death, who would withhold a potentially helpful treatment?

It may be that my response was grounded less in the intent of the question than in my own experience. For 20 years, I’d spent my afternoons working with psychiatric outpatients in Providence, R.I. As I wrote more, I let my clinical hours dwindle. One result was that more of my time was filled with especially challenging cases, with patients who were not yet better. The popularity of ‘’Listening to Prozac'’ meant that the most insistent new inquiries were from families with depressed members who had done poorly elsewhere. In my life as a doctor, unremitting depression became an intimate. It is poor company. Depression destroys families. It ruins careers. It ages patients prematurely.

Recent research has made the fight against depression especially compelling. Depression is associated with brain disorganization and nerve-cell atrophy. Depression appears to be progressive — the longer the episode, the greater the anatomical disorder. To work with depression is to combat a disease that harms patients’ nerve pathways day by day.

Nor is the damage merely to mind and brain. Depression has been linked with harm to the heart, to endocrine glands, to bones. Depressives die young — not only of suicide, but also of heart attacks and strokes. Depression is a multisystem disease, one we would consider dangerous to health even if we lacked the concept ‘’mental illness.'’

As a clinician, I found the what if challenge ever less amusing. And so I began to ask audience members what they had in mind. Most understood van Gogh to have suffered severe depression. His illness, they thought, conferred special vision. In a short story, Poe likens ‘’an utter depression of soul'’ to ‘’the hideous dropping off of the veil.'’ The questioners maintained this 19th-century belief, that depression reveals essence to those brave enough to face it. By this account, depression is more than a disease — it has a sacred aspect.

Other questioners set aside that van Gogh was actually ill. They took mood disorder to be a heavy dose of the artistic temperament, so that any application of antidepressants is finally cosmetic, remolding personality into a more socially acceptable form. For them, depression was less than a disease.

These attributions stood in contrast to my own belief, that depression is neither more nor less than a disease, but disease simply and altogether.

Audiences seemed to be aware of the medical perspective, even to endorse it — but not to have adopted it as a habit of mind. To underscore this inconsistency, I began to pose a test question: We say that depression is a disease. Does that mean that we want to eradicate it as we have eradicated smallpox, so that no human being need ever suffer depression again? I made it clear that mere sadness was not at issue. Take major depression, however you define it. Are you content to be rid of that condition?

Always, the response was hedged: aren’t we meant to be depressed? Are we talking about changing human nature?

I took those protective worries as expressions of what depression is to us. Asked whether we are content to eradicate arthritis, no one says, ‘’Well, the end-stage deformation, yes, but let’s hang on to tennis elbow, housemaid’s knee and the early stages of rheumatoid disease.'’ Multiple sclerosis, acne, schizophrenia, psoriasis, bulimia, malaria — there is no other disease we consider preserving. But eradicating depression calls out the caveats.

To this way of thinking, to oppose depression too completely is to be coarse and reductionist — to miss the inherent tragedy of the human condition. To be depressed, even gravely, is to be in touch with what matters most in life, its finitude and brevity, its absurdity and arbitrariness. To be depressed is to occupy the role of rebel and social critic. Depression, in our culture, is what tuberculosis was 100 years ago: illness that signifies refinement.

Having raised the thought experiment, I should emphasize that in reality, the possibility of eradicating depression is not at hand. If clinicians are better at ameliorating depression than we were 10 years ago — and I think we may be — that is because we are more persistent in our efforts, combining treatments and (when they succeed) sticking with them until they have a marked effect. But in terms of the tools available, progress in the campaign against depression has been plodding.

Still, it is possible to envisage general medical progress that lowers the rate of depression substantially — and then to think of a society that enjoys that result. What is lost, what gained? Which is also to ask: What stands in the way of our embracing the notion that depression is disease, nothing more?

This question has any number of answers. We idealize depression, associating it with perceptiveness, interpersonal sensitivity and other virtues. Like tuberculosis in its day, depression is a form of vulnerability that even contains a measure of erotic appeal. But the aspect of the romanticization of depression that seems to me to call for special attention is the notion that depression spawns creativity.

Objective evidence for that effect is weak. Older inquiries, the first attempts to examine the overlap of madness and genius, made positive claims for schizophrenia. Recent research has looked at mood disorders. These studies suggest that bipolar disorder may be overrepresented in the arts. (Bipolarity, or manic-depression, is another diagnosis proposed for van Gogh.) But then mania and its lesser cousin hypomania may drive productivity in many fields. One classic study hints at a link between alcoholism and literary work. But the benefits of major depression, taken as a single disease, have been hard to demonstrate. If anything, traits eroded by depression — like energy and mental flexibility — show up in contemporary studies of creativity.

How, then, did this link between creativity and depression arise? The belief that mental illness is a form of inspiration extends back beyond written history. Hippocrates was answering some such claim, when, around 400 B.C., he tried to define melancholy — an excess of ‘’black bile'’ — as a disease. To Hippocrates, melancholy was a disorder of the humors that caused epileptic seizures when it affected the body and caused dejection when it affected the mind. Melancholy was blamed for hemorrhoids, ulcers, dysentery, skin rashes and diseases of the lungs.

The most influential expression of the contrasting position — that melancholy confers special virtues — appears in the ‘’Problemata Physica,'’ or ‘’Problems,'’ a discussion, in question-and-answer form, of scientific conundrums. It was long attributed to Aristotle, but the surviving version, from the second century B.C., is now believed to have been written by his followers. In the 30th book of the ‘’Problems,'’ the author asks why it is that outstanding men — philosophers, statesmen, poets, artists, educators and heroes — are so often melancholic. Among the ancients, the strongmen Herakles and Ajax were melancholic; more contemporaneous examples cited in the ‘’Problems'’ include Socrates, Plato and the Spartan general Lysander. The answer given is that too much black bile leads to insanity, while a moderate amount creates men ‘’superior to the rest of the world in many ways. ‘’

The Greeks, and the cultures that succeeded them, faced depression poorly armed. Treatment has always been difficult. Depression is common and spans the life cycle. When you add in (as the Greeks did) mania, schizophrenia and epilepsy, not to mention hemorrhoids, you encompass a good deal of what humankind suffers altogether. Such an impasse calls for the elaboration of myth. Over time, ‘’melancholy ‘’ became a universal metaphor, standing in for sin and innocent suffering, self-indulgence and sacrifice, inferiority and perspicacity.

The great flowering of melancholy occurred during the Renaissance, as humanists rediscovered the ‘’Problems.'’ In the late 15th century, a cult of melancholy flourished in Florence and then was taken back to England by foppish aristocratic travelers who styled themselves artists and scholars and affected the melancholic attitude and dress. Most fashionable of all were ‘’melancholic malcontents,'’ irritable depressives given to political intrigue. One historian, Lawrence Babb, describes them as ‘’black-suited and disheveled . . . morosely meditative, taciturn yet prone to occasional railing.'’

In dozens of stage dramas from the period, the principal character is a discontented melancholic. ‘’Hamlet'’ is the great example. As soon as Hamlet takes the stage, an Elizabethan audience would understand that it is watching a tragedy whose hero’s characteristic flaw will be a melancholic trait, in this case, paralysis of action. By the same token, the audience would quickly accept Hamlet’s spiritual superiority, his suicidal impulses, his hostility to the established order, his protracted grief, solitary wanderings, erudition, impaired reason, murderousness, role-playing, passivity, rashness, antic disposition, ‘’dejected haviour of the visage'’ and truck with graveyards and visions.

‘’Hamlet'’ is arguably the seminal text of our culture, one that cements our admiration for doubt, paralysis and alienation. But seeing ‘’Hamlet'’ in its social setting, in an era rife with melancholy as an affected posture, might make us wonder how much of the historical association between melancholy and its attractive attributes is artistic conceit.

In literature, the cultural effects of depression may be particularly marked. Writing, more than most callings, can coexist with a relapsing and recurring illness. Composition does not require fixed hours; poems or essays can be set aside and returned to on better days. And depression is an attractive subject. Superficially, mental pain resembles passion, strong emotion that stands in opposition to the corrupt world. Depression can have a picaresque quality — think of the journey through the Slough of Despond in John Bunyan’s ‘’Pilgrim’s Progress.'’ Over the centuries, narrative structures were built around the descent into depression and the recovery from it. Lyric poetry, religious memoir, the novel of youthful self-development — depression is an affliction that inspires not just art but art forms. And art colors values. Where the unacknowledged legislators of mankind are depressives, dark views of the human condition will be accorded special worth.

Through the ‘’anxiety of influence,'’ heroic melancholy cast its shadow far forward, onto romanticism and existentialism. At a certain point, the transformation begun in the Renaissance reaches completion. It is no longer that melancholy leads to heroism. Melancholy is heroism. The challenge is not battle but inner strife. The rumination of the depressive, however solipsistic, is deemed admirable. Repeatedly, melancholy returns to fashion.

As I spoke with audiences about mood disorders, I came to believe that part of what stood between depression and its full status as disease was the tradition of heroic melancholy. Surely, I would be asked when I spoke with college students, surely I saw the value in alienation. One medical philosopher asked what it would mean to prescribe Prozac to Sisyphus, condemned to roll his boulder up the hill.

That variant of the what if question sent me to Albert Camus’s essay on Sisyphus, where I confirmed what I thought I had remembered — that in Camus’s reading, Sisyphus, the existential hero, remains upbeat despite the futility of his task. The gods intend for Sisyphus to suffer. His rebellion, his fidelity to self, rests on the refusal to be worn down. Sisyphus exemplifies resilience, in the face of full knowledge of his predicament. Camus says that joy opens our eyes to the absurd — and to our freedom. It is not only in the downhill steps that Sisyphus triumphs over his punishment: ‘’The struggle itself toward the heights is enough to fill a man’s heart. One must imagine Sisyphus happy.'’

I came to suspect that it was the automatic pairing of depth and depression that made the medical philosopher propose Sisyphus as a candidate for mood enhancement. We forget that alienation can be paired with elation, that optimism is a form of awareness. I wanted to reclaim Sisyphus, to set his image on the poster for the campaign against depression.

Once we take seriously the notion that depression is a disease like any other, we will want to begin our discussion of alienation by asking diagnostic questions. Perhaps this sense of dislocation signals an apt response to circumstance, but that one points to an episode of an illness. Aware of the extent and effects of mood disorder, we may still value alienation — and ambivalence and anomie and the other uncomfortable traits that sometimes express perspective and sometimes attach to mental illness. But we are likely to assess them warily, concerned that they may be precursors or residual symptoms of major depression.

How far does our jaundiced view reach? Surely the label ‘’disease'’ does not apply to the melancholic or depressive temperament? And of course, it does not. People can be pessimistic and lethargic, brooding and cautious, without ever falling ill in any way. But still, it seemed to me in my years of immersion that depression casts a long shadow. Though I had never viewed it as pathology, even Woody Allen-style neurosis had now been stripped of some of its charm — of any implicit claim, say, of superiority. The cachet attaching to tuberculosis diminished as science clarified the cause of the illness, and as treatment became first possible and then routine. Depression may follow the same path. As it does, we may find that heroic melancholy is no more.

In time, I came to think of the van Gogh question in a different light, merging it with the eradication question. What sort of art would be meaningful or moving in a society free of depression? Boldness and humor — broad or sly — might gain in status. Or not. A society that could guarantee the resilience of mind and brain might favor operatic art and literature. Freedom from depression would make the world safe for high neurotics, virtuosi of empathy, emotional bungee-jumpers. It would make the world safe for van Gogh.

Depression is not a perspective. It is a disease. Resisting that claim, we may ask: Seeing cruelty, suffering and death — shouldn’t a person be depressed? There are circumstances, like the Holocaust, in which depression might seem justified for every victim or observer. Awareness of the ubiquity of horror is the modern condition, our condition.

But then, depression is not universal, even in terrible times. Though prone to mood disorder, the great Italian writer Primo Levi was not depressed in his months at Auschwitz. I have treated a handful of patients who survived horrors arising from war or political repression. They came to depression years after enduring extreme privation. Typically, such a person will say: ‘’I don’t understand it. I went through — ‘’ and here he will name one of the shameful events of our time. ‘’I lived through that, and in all those months, I never felt this.'’ This refers to the relentless bleakness of depression, the self as hollow shell. To see the worst things a person can see is one experience; to suffer mood disorder is another. It is depression — and not resistance to it or recovery from it — that diminishes the self.

Beset by great evil, a person can be wise, observant and disillusioned and yet not depressed. Resilience confers its own measure of insight. We should have no trouble admiring what we do admire — depth, complexity, aesthetic brilliance — and standing foursquare against depression.

Peter D. Kramer is a clinical professor of psychiatry at Brown University and the author of ‘’Listening to Prozac.'’ This essay is adapted from his book ‘’Against Depression,'’ which Viking will publish next month.

Pessimism Raises Dementia Risk, Study Finds - Yahoo! News

Pessimistic, anxious and depressed people may have a higher risk of dementia, U.S. researchers reported on Thursday.

A study of a group of 3,500 people showed that those who scored high for pessimism on a standardized personality test had a 30 percent increased risk of developing dementia 30 to 40 years later.

Those scoring very high on both anxiety and pessimism scales had a 40 percent higher risk, the study showed.

“There appears to be a dose-response pattern, i.e., the higher the scores, the higher the risk of dementia,” Dr. Yonas Geda, a neuropsychiatrist at the Mayo Clinic in Rochester, Minnesota who led the study, said in a statement.

Geda and colleagues looked at the medical records of 3,500 men and women who lived near the clinic between 1962 and 1965.

They all took the Minnesota Multiphasic Personality Inventory, a standard personality and life experience test, Geda’s team told a meeting of the
American Academy of Neurology in Miami.

In 2004 the team interviewed the participants or family members.

Those who scored higher for anxiety and pessimism on the test were more likely, as a group, to have developed dementia by 2004, including
Alzheimer’s disease and vascular dementia.

This did not mean a person who is pessimistic could assume he or she has a higher risk of developing dementia.

“One has to be cautious in interpreting a study like this,” Geda said.

“One cannot make a leap from group level data to the individual. Certainly the last thing you want to do is to say, ‘Well, I am a pessimist; thus, I am doomed to develop dementia 20 or 30 years later,’ because this may end up becoming a self-fulfilling prophecy.”

And there is not any specific way to prevent dementia, although many studies have shown that a healthy diet, exercise, keeping active in other ways, doing puzzles and other activities lower the risk.

The Seattle Times: Electromagnets provide rays of hope for people with depression

By Nick Perry
Seattle Times staff reporter

Robert Miskimon’s list of treatments for depression reads like a clinician’s almanac.

During his first descent into darkness at age 17, doctors repeatedly injected him with enough insulin to induce a coma, then revived him with glucose, a once-popular treatment called insulin shock therapy. Later came psychotherapy. In the 1990s he tried new wonder drugs such as Prozac and Zoloft.

Each new treatment helped for a while, but then the benefits waned, said Miskimon, 61. The Vashon Island writer remains most enthusiastic about an experimental treatment he first tried two years ago: transcranial magnetic stimulation, or TMS. He said it immediately helped him sleep, eat and feel better.

“It’s the difference between feeling life is hopeless, pointless and futile to, for example, experiencing joy at the sight of an eagle outside my home or the thrill of my daughter doing very well at nursing school,” he said. “To be free from the pervasive gloom and darkness is a wonderful thing. It’s the freedom to have gradations of feelings.”

Transcranial magnetic stimulation uses powerful electromagnets to stimulate electricity inside the brain. What may sound like science fiction has gained respect in the scientific community, with several small studies showing beneficial results.
Now the National Institute of Mental Health has launched the most extensive study yet: a $7 million, four-year federally funded program to track 240 patients. The University of Washington is one of four sites tracking the patients, with the first of 60 due to begin treatment at Harborview Medical Center this month.

Although TMS has not been approved for use in the United States, it is being used in Canada. Should it eventually get the nod of the federal Food and Drug Administration, it would offer hope for thousands of patients who can’t tolerate antidepressant drugs or who don’t respond to them.

The roots of TMS can be traced to the 1930s, when a Hungarian psychiatrist first used electricity to jolt a patient’s brain into a seizure, a controversial procedure that became known as electric shock treatment. Now called electroconvulsive therapy, it remains an effective last resort for many severely depressed patients.

But the problem with inducing a seizure is that it often causes short-term memory loss and confusion. Proponents of TMS believe many patients could benefit from a gentler approach.

TMS typically involves a patient sitting in a chair for 30 to 40 minutes. A doctor rests a coil on the patient’s head, then turns on a powerful electromagnet.

The machinery sends 10 strong, short magnetic pulses every second to a particular point in the brain, stimulating electrical currents. Regular magnets, like those on your fridge, create a constant magnetic pull and won’t stimulate electricity in the same way.

One potential advantage of magnetism is that it effortlessly penetrates the skull, unlike the electrical approach which forces a current through skin and bone. During TMS treatments, patients typically feel little.

“You sit in a nice easy chair with a pad on your scalp and there is a little click and a little buzz and that’s it,” said Jim Kjeldsen, a 56-year-old journalist from near La Conner, Skagit County, who has tried experimental TMS. “It’s a bit of a problem sitting there for half an hour and staying awake.”

The magnet is usually focused on the left prefrontal cortex — a part of the brain thought to play a key role in controlling mood, and which studies show is often less active in people suffering depression.

What happens next is less clear.

According to Dr. Mark George, a pioneer of the treatment, the magnet stimulates or “tickles” the cortex, which in turn sends electric signals to the central limbic system, a more ancient part of the brain also associated with mood control.

George believes this increased electrical activity changes the brain’s chemistry, probably by increasing levels of neurotransmitters such as serotonin and dopamine. That helps elevate mood.

Other people theorize that the mental discord of depression may manifest in a physical way that is comparable to arrhythmia. That theory has TMS acting as a kind of pacemaker to better balance electrical activity, especially between the left and right sides of the brain.

But nobody really knows how TMS may work because scientists have yet to figure out all the intricacies of the brain.

A TMS patient typically gets one treatment per day, five days a week, for three to six weeks. Many proponents believe that an initial course of treatment can lift patients from a depressive episode and that later “maintenance” treatments can keep them from slipping back. That theory will be put to the test in the new study.

George, a psychiatry and neurology professor at the Medical University of South Carolina, began experimenting with TMS in the mid-1990s after finding inspiration while riding an elevator in a London research building. A bubbly man told him that a scientist just made his thumb jerk by putting a magnet against his head.

Noting the man’s animation, George wondered if magnets could be used to directly influence mood control. But the idea wasn’t embraced by the medical community, which had long accepted seizures as a vital part of any direct physical intervention in depression.

“When I began this a decade ago, these ideas were heretical,” George said. “Heretical and anathema.”

Years of failed therapies
Miskimon said he was at boarding school in 1961 when his first bout of depression struck. A good student, he became increasingly agitated and felt he was losing touch with his own body and the world around him. He all but stopped eating, losing 30 pounds and becoming emaciated. He was hospitalized for three months, regularly receiving the insulin-shock treatments.

In the years since, Miskimon tried different therapies and also turned to alcohol, which he hasn’t touched now for 20 years. Nothing worked long term. Miskimon learned to struggle through life with recurring bouts of depression, which seemed, he said, to arrive without warning and in no particular pattern.

Kjeldsen has also lived with depression since he was a teen. Particularly bad bouts seem to strike once every eight or nine years, he said.

“Not knowing if you will ever come out of this black hole is the worst thing about it,” Kjeldsen said. “It’s like a huge weight pressing down on you. You don’t get joy out of anything, and you have to map out every move all day long, because the automatic reflexes that keep you motivated are not there.”

Both Kjeldsen and Miskimon became patients in early TMS clinical trials overseen by Dr. David Avery, a UW professor and the director of inpatient psychiatry at Harborview Medical Center. Avery, another of the treatment’s pioneers, is overseeing the UW part of the new trial.

Kjeldsen said he was skeptical about TMS before the early trials but soon became a believer.

“At the end of the second treatment, I walked out of the building and everything looked a lot brighter, even the sky looked brighter,” he said.

He added that he’s not interested in trying electroconvulsive therapy (ECT), which he believes may cause some brain damage.

“It’s nothing I would like to do. I really like my brain cells, even though they play up,” he joked.

The new TMS trial is not only bigger, it is more nuanced than previous trials, which have administered a single, standard treatment. This time, patients will have their brain structure mapped so doctors can more accurately focus the magnetic pulses in the correct location. And the number of sessions a subject receives will depend on the response to each treatment.

Half the participants will be part of a control group receiving sham treatments — though later they will have the option of getting the real treatment.

Offered in Vancouver, B.C.
While transcranial magnetic stimulation is not approved in the U.S., one TMS device has been approved in Canada since 2002. A group called Mindcare Centres offers the treatment at clinics in Vancouver, B.C., and Toronto.

Iain Glass, Mindcare president and CEO, said the clinics have treated about 170 people. That includes about 60 from the Seattle area who make up a large slice of the Vancouver business.

A course at Mindcare typically involves 20 treatments spread over two weeks at a cost of $4,000 (U.S.). The treatment is not covered by most U.S. health insurers.

“We tend to treat really, really tough cases,” Glass said.

He said the average patient age is 48, and most have lived with depression since they were teenagers. Many have tried medication for years without much success, he said. People who try TMS tend to either respond “profoundly” or not at all, he added.

“It’s wildly exciting,” Glass said. “There are a lot of people for whom the system has failed, and we are giving them their lives back.”

Glass has big ambitions for the U.S. He said he wants to open 50 to 55 clinics here — if and when the FDA gives approval.

Until then, sufferers here will need to find other options. Miskimon said he will continue trying antidepressant drugs along with prayer and meditation.

“I think it would be a tremendous thing to be available,” Miskimon said of TMS. “I think of it as having the benefits of ECT without any of the drawbacks.”

“It’s a kinder, gentler approach to sanity.”

|| DukeMedNews || Exercise, Stress Management Show Physiological Benefits for Heart Patients

DURHAM, N.C. — Behavior modification techniques such as exercise and stress management can not only reduce the levels of depression and distress in heart patients, but can also improve physiological markers of cardiovascular health, according to the results of a randomized controlled trial conducted by Duke University Medical Center researchers.

According to the research team, this may be the first randomized trial to demonstrate that a non-pharmaceutical approach can have positive effects on such physiological determinants of cardiovascular health as blood flow to heart, the responsiveness of the lining of blood vessels and the ability of the cardiovascular system to regulate surges in blood pressure.

“While studies have shown that psychosocial factors such as depression, stress and anxiety place heart patients at a much greater risk of suffering future cardiac events or dying, few have looked at the effects of modifying psychosocial factors,” said Duke medical psychologist James Blumenthal, Ph.D., lead author of a study appearing in the April 6, 2005 issue of the Journal of the American Medical Association. The trial was supported by a $4.3 million grant from the National Institutes of Health.

“Our results suggest that exercise and stress management training offer considerable promise for patients with heart disease by not only improving psychosocial functioning and reactions to mental and physical stressors, but also by modifying important bio-markers of risk that may translate into improved clinical outcomes,” he said.

The Duke trial enrolled 134 patients with stable heart disease and randomized them to one of three groups – exercise, stress management or standard medical therapy. Patients randomized to the exercise group participated in 35 minutes of supervised aerobic exercise training three times a week for 16 weeks. Those in the stress management arm received 16 weekly 1.5-hour classes designed to help patients recognize the sources of stress in their everyday lives and to teach them strategies to respond more adaptively to those stresses.

Patients enrolled had stable heart disease, meaning they did not experience chest pain while at rest, and exhibited evidence of myocardial ischemia, or reduced blood flow to the heart, during exercise. All participants underwent a battery of psychological and physiological testing before randomization, which was repeated four months later.

One of the physiological markers studied was the endothelium, which forms the inner lining of the blood vessels and controls how the vessels reacted to changes in blood flow and pressure. The researchers took ultrasound images of the brachial artery of the arm before and after a tourniquet was applied and released to determine how the vessels responded. Healthy arteries will dilate to accommodate the increased blood flow, while diseased arteries are less responsive, the researchers said.

In these tests of flow-mediated dilation, patients who received the behavioral treatments displayed nearly a 25 percent improvement when compared to those patients who only received usual medical care.

“To our knowledge, this is the first study to show that stress management might reduce cardiovascular risk in part through beneficial effects on vascular endothelial function,” Blumenthal said. “This is a level of improvement is comparable to that achieved in drug trials. For that reason, these findings add additional support for the use of non-pharmaceutical approaches to treating patients with heart disease.”

The researchers also found that patients who received exercise training or stress management had improved baroreflex sensitivity, a phenomenon by which receptors located along the walls of blood vessels respond to changes in blood pressure. These receptors are connected to the heart by nerves, which carry the message to pump faster or slower in response to pressure changes.

“This finding is important because past studies have demonstrated that abnormally low baroreflex sensitivity has been shown to be associated with worse outcomes for patients with heart disease–improvement may produce clinical benefits,” Blumenthal said.

Additionally, the researchers measured changes in the left ventricle — the pumping chamber of the heart — during periods of both mental and physical stress. The research team used radionuclide imaging tests to identify wall motion abnormalities (WMAs). These WMAs, or areas of abnormal contractions of the left ventricle, are known indicators of ischemia.

“While there was no difference in WMA scores between the three groups during mental stress testing, among the subgroup of patients who had mental stress-induced WMAs before treatment, those in the exercise and stress management groups had lower WMA scores after treatment compared to patients in usual care.”

Other findings, which were expected, showed that patients in the exercise group had the largest improvements in such measures as exercise duration and aerobic capacity. For the psychosocial tests, the researchers found that exercise and stress management had reduced general distress and depression compared to usual care controls.

Future studies are planned to determine if stress management and exercise together have an even greater positive effect on these markers of cardiovascular health. The researchers also said further investigation is needed to reveal the biological mechanisms behind the improvements seen.

Valdoxan®: A New Approach to The Treatment of Depression

First Melatonergic Agonist Antidepressant Shows Efficacy and Tolerability Benefits Over Existing Therapies -

Valdoxan® (agomelatine), the first melatonergic (MT1 and MT2 receptor) agonist antidepressant, is an innovation in the treatment of depression with several advantages over existing treatments according to data presented during the 13th Congress of the Association of European Psychiatrists. Besides being an effective antidepressant, Valdoxan has shown particular advantages in improving the often disrupted sleep patterns of depressed patients, without affecting daytime vigilance.

“Agomelatine is an interesting and potentially very valuable antidepressant that is effective in both moderate and severe depression”, says Professor Stuart Montgomery from the Imperial College School of Medicine in London. “The new agent has a unique mode of action, improves sleep without affecting daytime alertness and its efficacy is not compromised by sexual side effects, tolerability problems or discontinuation symptoms.”

Antidepressant efficacy

The antidepressant efficacy of Valdoxan has been shown at a standard dose of 25 mg, once daily in the evening, in a dose-ranging study performed in major depressive disorder (MDD)1. In this multicentre, placebo-controlled, dose-ranging study over eight weeks, Valdoxan was shown to be an effective antidepressant at a dose of 25 mg once daily, by reducing the initial HAMD score to a similar extent to that of the SSRI paroxetine. Further studies versus placebo and comparators have confirmed the efficacy of Valdoxan in adults of all ages, including the severely depressed and elderly depressed. Results from another clinical trial presented here in Munich show that Valdoxan has a similar efficacy to the SNRI venlafaxine.

Improvements of disturbed wake-sleep cycles

“The ability to relieve sleep problems without being sedative is a key advantage for depressed patients who frequently suffer from sleep disturbances associated with their depression”, points out Christian Guilleminault, MD, from Stanford University Sleep Disorders Clinic, California.

Due to its unique pharmacological profile, Valdoxan is the only antidepressant to have a specific action on circadian rhythms, which are often imbalanced in depressed patients. By improving disturbed wake-sleep patterns, according to Dr Guilleminault, Valdoxan is able to relieve sleep complaints of depressed patients with a favourable impact on daytime vigilance.

Tolerability profile

Data presented by Professor Montgomery shows that Valdoxan provides antidepressant efficacy, but lacks typical antidepressant side effects. The new agent does not appear to impair sexual function. A study comparing Valdoxan with venlafaxine showed comparable antidepressant efficacy of both treatments, but significantly less sexual dysfunction of Valdoxan compared to the SNRI. In addition, a placebo-controlled, double-blind study comparing Valdoxan with paroxetine showed that, after one week of treatment discontinuation, no signs of discontinuation symptoms* were seen in the agomelatine group compared to significant discontinuation symptoms in the paroxetine group.2

Valdoxan was discovered and developed by Servier. The drug is currently in Phase III and a registration dossier for an indication in MDD was recently submitted to the European Regulatory Agency (EMEA).

Discontinuation symptoms occur when treatment with certain antidepressants (mainly SSRIs and SNRIs) is stopped. They can include nausea, headache, dizziness, sleep disturbances, anxiety and irritability.

Yahoo! News - Cognitive Therapy Successful Against Depression

TUESDAY, April 4 (HealthDay News) — When provided by experienced psychotherapists, cognitive therapy may be as effective as antidepressant drugs in initial treatment of moderate to severe depression, a new study suggests.

The study, published in the April issue of the journal Archives of General Psychiatry, included 240 people with moderate to severe depression. One group of 60 people received cognitive therapy, another group of 120 received antidepressant medication (usually Paxil), and a third group of 60 received a placebo pill.

According to University of Pennsylvania researchers, patients in the cognitive therapy group attended two 50-minute sessions a week for the first four weeks of the study. They went to one or two sessions a week for the middle eight weeks and to one session a week for the final four weeks of the study.

After eight weeks of treatment, response rates were 50 percent in the medication group, 43 percent in the cognitive therapy group and 25 percent in the placebo group. After 16 weeks of treatment, response rates were 58 percent for patients receiving either medication or cognitive therapy. Remission rates were 46 percent for patients receiving medication and 40 percent for those in the cognitive therapy groups.

“On the whole, these findings do not support the current American Psychiatric Association guideline, based on the TDCRP (the Treatment of Depression Collaborative Research Program) that ‘most (moderately and severely depressed) patients will require medication,’ ” the study authors wrote.

“It appears that cognitive therapy can be as effective as medications, even among more severely depressed outpatients, at least when provided by experienced cognitive therapists,” they wrote.

More information

The U.S. National Institute of Mental Health has more about depression.

Health News Article | Reuters.com

By Michelle Rizzo

NEW YORK (Reuters Health) - Men with a history of depression long before the onset of any memory or other cognitive problems have a substantially higher risk of developing dementia, especially Alzheimer’s disease (AD), later in life, a study indicates. This risk is not observed in women.

Dr. Gloria Dal Forno, of University Campus BioMedico and Associazione Fatebenefratelli per la Ricerca, Rome, Italy, and colleagues examined the association between premorbid symptoms of depression and the development of dementia and AD over a period of 14 years in 1357 subjects enrolled in a study on aging.

Researchers assessed the frequency and severity of depressive symptoms every 2 years using standard instruments.

A total of 49 cases of dementia were diagnosed among women during the study period. Of these, 40 represented AD. A total of 76 men were diagnosed with dementia, of which 67 were AD.

The risk of dementia, especially AD, was significantly increased with premorbid depressive symptoms only in men. The risk was approximately two times greater in those with a history of depression than for those without a history of depression, and was independent of the presence of vascular disease.

“The prevalence and clinical manifestations of both AD and depression differ in men and women,” Dal Forno noted in an interview with Reuters Health.

“We know that male and female brains have anatomical and functional differences and are exposed differently to sex hormones throughout life, hormones known to have effects on both depression and AD,” she noted.

“As a consequence, male and female brains might react to conditions causing or enhancing a disease quite differently, which seems to be precisely what we found in this investigation.”

Given the prevalence of depression and increasing longevity worldwide, “clearly the public health and economic implications are significant,” the researcher added.

Furthermore, “Prevention of depressive disorders and aggressive as well as long-term treatment of depression may impact on the epidemiology of dementia,” she added. “This is particularly relevant in men since they generally are less likely to admit to symptoms of depression and to seek treatment.”

SOURCE: Annals of Neurology March, 2005.