Almost 40% of the general public are not aware of the symptoms of depression, the results of a new survey have found. This is despite the fact that around 300,000 Irish people are affected by the illness.

The survey found that among those who could name a symptom, 21% pinpointed feeling down or low most of the time, while 13% said feeling tired all of the time. A further 13% knew that disrupted sleep was a symptom, while 12% said changes in eating patterns. Other symptoms mentioned included being anxious and a having a lack of energy.

Commenting on the high number of people who were unaware of the symptoms, Professor Patricia McKenna, a consultant psychiatrist at the Mater Hospital in Dublin, said that these results further demonstrate the need for public education on this issue.

“Depression continues to be an illness that is under-reported and this can be partly attributed to the lack of understanding among the general public as to what constitutes depression”, Professor McKenna said.

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Today, the central questions at the intersection of psychiatry and culture seem to concern diagnosis. A number of books have appeared on the subject, each claiming that the medical professions have pathologized normality-making illnesses of unhappiness, shyness, and boyish impulsivity. To my mind, the most thoughtful of these efforts is The Loss of Sadness, by Allan V. Horwitz and Jerome C. Wakefield. It relies on a theory of mental disorder elaborated over decades. It is serious and scholarly. But I consider the book’s premises and conclusions to be profoundly, fundamentally wrong.

This week, I had the honor of debating Jerry Wakefield in a lecture-and-discussion session and an academic seminar at Rutgers University. On my website, I have posted the talk I prepared as the opening statement in that dialogue. What follows is a condensed account of key points.

To summarize the issue under debate: Wakefield (along with Horwitz) mistrusts the current standard diagnosis of depression, the one that says that if you have a cluster of symptoms for an interval of time, and if they cause sufficient impairment, then you are in an episode of illness. Wakefield complains that the method fails to take into account causation. He points to an exception recognized in the diagnostic manual: if the trigger for the depressive symptoms is the loss of a loved one, and if the syndrome is brief (less than two months) and only moderately severe, then the sufferer is considered to be bereaved, not depressed. Wakefield asks what is special about bereavement. If you are divorced or laid off from work, and you experience symptoms of moderate duration and severity, aren’t you are exhibiting an expectable response to loss? Shouldn’t you be called sad, and not depressed? Wakefield argues that the standard definition—the one that ignores the issue of cause—leads to over-diagnosis and over-treatment, especially with psychotherapeutic medication. Wakefield says that the definition of depression would be more valid if we extended the “bereavement exclusion” into a “major loss exclusion.”
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Do antidepressants work? They do. New evidence comes from a study of children and adolescents, patients in age groups where the efficacy of antidepressants has been hard to demonstrate. It’s just the sort of research that critics of drug trials ought to find convincing.

Antidepressants seem to do less good in the young. For decades, there were few studies showing that the medications helped at all in patients under age 18. Scientists had even put forth theories – I review some in Against Depression – explaining why antidepressants ought not to have the same effects in children as in adults.

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The antidepressant, Prozac, may help to curb disease activity in a particular form of multiple sclerosis (MS), new research indicates.

A team of researchers followed the progress of 40 patients with the relapsing remitting form of MS.

MS is a condition which affects the brain and spinal cord. It is characterised by a slowly progressing disablement. According to the Multiple Sclerosis Society of Ireland, most people with MS start off with the relapsing remitting type. This means they have attacks followed by remissions. During remissions, they may have fewer or no symptoms. Relapses tend to be unpredictable and their causes are unclear.

The researchers randomly allocated the 40 patients to treatment with either 20mg daily of fluoxetine (Prozac) or a placebo for a period of 24 weeks.

Detailed MRI scans were carried out every four weeks to check for new areas of neurological inflammation, which is a hallmark of active MS.

The brain scans found that those in the placebo group had more new areas of inflammation, compared to those in the Prozac group.

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There’s major news on the antidepressant front, but it comes in an odd form: research on treating “lazy eyes” in rats. A study suggests that, yes, Prozac and similar medicines really do make the brain more flexible.

The report, titled “The Antidepressant Fluoxetine Restores Plasticity in the Adult Visual Cortex,” appears in the current issue of Science. It tests the hypothesis, current for some time now, that drugs like Prozac work through stimulating factors in the brain that allow nerve cells there to grow and make new connections. If that theory holds, then perhaps the medications might allow the adult mammalian brain to take on some of the “plasticity,” or capacity for adaptive change, normally present only early in development.

The researchers, José Fernando Maya Vetencourt of the Scuola Normale Superiore in Pisa, Italy, and colleagues elsewhere in Europe, began by depriving rats of the use of one eye by sewing it shut. Over time, the visually-deprived rats came to rely solely on the working eye and lost the capacity for binocular vision even when both eyes were again open.

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The New York Times science section today features an essay on the long-term use of antidepressants. The lead refers to the sort of question I introduced in Listening to Prozac: how do these medications shape identity? But most of the piece concerns the biological effects of taking the drugs for years.

The author, Richard A. Friedman, quite properly says that we do not know about the effects of extended use and calls for better post-marketing studies. This point cannot be emphasized enough. Since we have vast numbers of people on antidepressants chronically, it is irresponsible for us as a society not to examine the medications through multi-year studies. This kind of research is hard to motivate; few young scientists in need of publications choose to undertake work whose results will emerge far down the road. The Food and Drug Administration, which has taken baby steps in this direction, should be mandating the relevant investigations; the National Institute of Mental Health should be supervising them.

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Over time, how deadly is the combination of depression and heart attacks? A recent study that received attention in the media found no connection, in the long term, between depression and death in heart attack victims. But that study was followed almost immediately by another that found the combination of heart attack and depression to be especially deadly.

We know that cardiovascular disease and mood disorder are intertwined. By middle age, depression is a powerful risk factor for heart disease. In the elderly, depression increases the risk of death from cardiac causes. One way of understanding depression is to see it as a multisystem disease, active in heart and blood vessels as much as brain.

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Antidepressants may be associated with an increased risk of suicidal behaviour, particularly in the early stages of treatment, the results of three new studies indicate.

The studies, which looked at SSRIs (selective serotonin reuptake inhibitors) – the most commonly prescribed class of antidepressant – as well as tricyclic antidepressants, are published in the latest edition of the British Medical Journal.

For the first study, a team of researchers analysed 702 trials involving over 87,000 patients with depression, to establish whether the use of SSRIs was linked to suicide attempts.

That study found that patients taking SSRIs were twice as likely to attempt suicide, compared with patients who were taking a placebo.

However when fatal suicides only were taken into account, i.e. where a person had succeeded in taking their own life, SSRIs did not appear to increase the risk. The researchers said that while the absolute risk of suicide is low, the widespread use of SSRIs makes this a ‘population health concern’.

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What would you say about a remedy for depression that lifted your mood, restored your energy, realigned your brain chemistry, improved your sense of self-and cost nothing?

Then put on your walking shoes or find a workout class. Researchers are finding that physical activity works at least as well against mild to moderate depression as any other treatment. It may be an alternative to current forms of treatment or a complement to them, even in severe cases.

Mental health experts are carefully building a scientific dossier on exercise as therapy for depression. Already, mounting evidence indicates that regular activity combats depression on many fronts:

• Animal studies show that exercise alters neurotransmitters such as norepinephrine in the brain’s frontal cortex and the hippocampus, both involved in circuits of emotion; the changes are similar to those produced by antidepressants.
• It appears to stimulate the vagus nerve, improving function of the brain’s emotion-sensing network as well as of the heart. The vagus nerve is increasingly recognized as an important pathway of depression.
• By acting on neurohormones that govern the stress response, exercise seems to improve the ability of the body to tolerate stress and to meet changing demands. A dysregulated stress response, perhaps stemming from early psychological trauma, is implicated as a cause of depression.
• Exercise has definite cognitive effects; it changes people’s perception of themselves, providing a sense of personal mastery and positive self-regard. It also reduces negative thinking.
• Exercise keeps on working, making it especially promising for preventing depression recurrences. People who continue to exercise have continuing reductions in symptoms.

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Depression is a major mental health issue in America. But it is also, increasingly, a major workplace issue. A landmark 2003 study draws the sobering conclusion that depression costs employers $44 billion a year in lost productivity alone. Those are strictly indirect costs; they don’t even begin to reflect medical costs.

The vast majority of that $44 billion loss in productivity comes not from absenteeism due to the disorder. It’s the product of so-called presenteeism, the many people with depression showing up for work but not functioning at anywhere near full capacity—failing to return phone calls, turning in poor-quality work, missing deadlines altogether, not following up on new business leads, being paralyzed with indecision, inability to face work at all, coming in late, leaving early, or not even returning from lunch, difficulty getting along with coworkers, withdrawing from the social environment at work.

Absenteeism, presenteeism, $44 billion-these are all abstractions. Depression, however, always wears a human face—the face of Mary Jo West, for example. A broadcast journalist, West became the first TV anchorwoman in Phoenix, in 1976. She produced award-winning features. She was a celebrity around town, instantly recognizable to everyone. Within a year, the pressure of breaking barriers along with her perfectionist professionalism collided with a deep vein of vulnerability.

West’s story is perhaps unusual because of the visibility. But in many ways it is business at its most usual. Depression affects 5 million American working women-21 percent of women in the workplace.
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