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How Everyone Became Depressed:

The Rise and Fall of the Nervous Breakdown

Edward Shorter

(London Times)

Blame the economy, blame the weather, blame the zeitgeist or just gloomy human nature, but depression nowadays seems to be everywhere. In the UK, an estimated one in six of us will be given the diagnosis at some time in our lives.

How can so many people be suffering from the same condition? Well, according to the bestselling American medical historian Edward Shorter, they aren’t. The trouble with depression today, says the historian of psychiatry at the University of Toronto, is that the term implies there is a single illness at work.

Instead, he argues in a new book, How Everyone Became Depressed: The Rise and Fall of the Nervous Breakdown, the diagnosis may cover manifold different causes and symptoms. “It’s like trying to lump measles and TB together under one diagnosis on the basis that they are both contagious,” explains Professor Shorter. This has disastrous consequences for millions of people who suffer them. The problem is that medicine, like hemlines and music, frequently falls slave to the fickle whims of fashion.

But very often it is not just diagnostic labels that change. Whole regimens shift, driven by some new big idea or vigorously hyped wonder drug.

That was certainly the case with Prozac. Launched by a big-spending publicity campaign 25 years ago, it quickly won the name “bottled sunshine”. Its promise of an “easy” cure for depression sparked a revolution in treatment. In the process, the green-and-white pill brought the term depression out from the medical shadows.

Oddly, Prozac was originally intended as a blood-pressure pill. Its American developer, the pharma giant Eli Lilly, had found that its active ingredient, fluoxetine, lowered hypertension in some animals. But tests failed in humans. Then it was tried as an anti-obesity therapy. Again it failed. But when the company tested it on five volunteers with mild depression, it lightened their moods. Marketing experts rebranded fluoxetine as a cure for intractable sadness, giving it a name that combined positivity with zap.

To market the pill, Lilly hugely raised the profile of the diagnosis “depression”, which previously had been largely a taboo term because it implied weakness of character. Lilly printed eight million brochures highlighting the symptoms, as well as publicising its new no-hassle panacea. Prozac had advantages over previous drugs, including tranquilisers such as Valium, which carry a serious risk of addiction and side-effects such as confusion, amnesia and aggression.

Prescriptions soared. So did depression diagnoses. Within ten years of its launch, Prozac was generating more than a quarter of Eli Lilly’s annual £6 billion income. Its use is still rising. In the UK between 2010 and 2011, the drug was prescribed 4.2 million times on the NHS at a cost of more than £19 million.

Prozac’s success created a new class of similar antidepressants: SSRIs — selective serotonin re-uptake inhibitors. These are believed to work by blocking the brain’s ability to re-absorb the “feelgood” chemical serotonin, increasing its levels in the brain and lifting a person’s mood. While Prozac is increasingly prescribed, the treatment is actually in crisis. Recent years have brought warnings that SSRIs do not actually work for millions of patients. The real problem, however, is that we don’t seem to have any better drugs to hand. The difficulty, says Professor Shorter, is that “depression is a real illness, but there are different kinds”, and Prozac-type drugs seem only to treat a minority of sufferers of what might best be called deep melancholic depression. The fundamental error, he argues, is that the modern diagnosis of clinical depression does not exist. “It covers both melancholia and non-melancholia.

But they are two different diseases,” Professor Shorter says. “Melancholia is a very distinctive condition. The despairing faces it causes have been known, written about and depicted in paintings throughout history. They were described by the Ancient Greeks and Romans.”

As a rule of thumb, he says, about one in five patients diagnosed with depression has melancholia. “Melancholia patients have a characteristic physical slump. There are biological markers for this. This is the type of depression that can respond to appropriate drug treatments, such as antidepressants and electroconvulsive therapy (ECT). With depression, the sicker you are, the more likely you are to respond to these treatments.”

Authoritative research supports this idea that depression is a cover-all term for different ailments. For example, in 2008, Irving Kirsch, a professor of psychology at the University of Hull, studied drug manufacturers’ trial results for four common SSRI antidepressants. He discovered mildly and moderately depressed patients in the trials who had been given sugar-pill placebos saw their depression scores improve just as much as those on the real drugs.

Professor Kirsch concluded that Prozac and other SSRIs probably have a real clinical benefit only for the 20 per cent of patients who have severe depression, where the cause is physical brain problems, such as chemical imbalances or neurological quirks.

But what of the remaining 80 per cent of patients diagnosed with depression: what is wrong with them, and how can it best be alleviated?

Professor Shorter believes that their problems are caused by a constellation of conditions that feature chronic mood problems. They might best be described accurately if we go back to old, unfashionable, diagnostic labels, he says. “The old-fashioned term is ‘nervous disorder’. The problem is mainly a disorder of sadness, anxiety and tiredness,” he says. “These are not necessarily exclusively mood disorders. Such patients have lots of somatic [or mind-body] symptoms, too, such as vague physical pains. Sufferers agonise and obsess about these things.”

One useful label might be “mixed anxiety depression”. This used to exist, but was removed from the “psychiatrists’ bible”, the Diagnostic and Statistical Manual of Mental Disorders, in 1980. “We have not gone forward with any treatment for these people since,” Professor Shorter says. “For non-melancholic depression, exercise therapy and psychological therapy are important. But drugs are overdone instead. It is a great shame. If you put people with non-melancholic depression on Prozac, they get all of the side-effects and none of the benefits.”

Professor Shorter believes the only way ahead is to scrap pharmaceutically inclined committees that write the Diagnostic and Statistical Manual and to come up with a whole new system of diagnosing psychological illness. “We need to come up with labels for diseases that really do exist. We have to go back to ground zero with our diagnoses. We need to scrap the DSM system and come up with proper psychiatric diseases that correspond to what people really have.”

The broad sweep of his arguments is supported by Dr Trevor Turner, a consultant psychiatrist at the East London NHS Foundation Trust, who studies the history of psychiatric medicine. “There has always been melancholia since time began,” he says. “Then the ‘English Malady’ of depression in the 1700s came along with increased leisure time — people sitting round with not much to do. We began it in this country, by generating spare time and leisure through industrialisation and commerce.”

Twenty five years ago, it was rare to be diagnosed with depression. Millions suffered the symptoms, but the D-word was taboo. It was thought to be evidence of “weak character”. Instead, GPs treated patients for “nerves” or “anxiety”. Before the Second World War, the label used was a “nervous breakdown”; and in the late 1800s, medics favoured scientific-sounding terms such as “neurasthenia” as a term for depressive nervous exhaustion.

Neurasthenia is still cited in some modern medical texts and tests. “Nowadays, it comes under ‘other neurotic disorders’,” Dr Turner says. “Then there was ‘nerves’, which came along with discoveries about the nervous system. Following that came the Freudian analysts, who took over the naming rights with ‘anxiety’ and ‘neuroses’.”

No matter what the label, the outcomes were generally the same, he says. “If you look at the history of depression pre-medication, it was a recurrent illness that tended to go away spontaneously after months or years. The advent of antidepressants in 1959 opened up the era of psychological pharmacology and brought us faster signs of relief, though not cure.”

The first type were called monoamine oxidase inhibitors. They are still used as a last resort, with brand names such as Nardil and Manerix. Like Prozac, they were discovered by accident. “They were tried as a treatment for TB patients. It didn’t help, but doctors noticed that it cheered them up,” Dr Turner says. “Ultimately, the big breakthrough drug was Prozac, not least because you can take it without feeling awful, and you can’t overdose on it.”

To some degree, our understanding of depressive conditions has advanced, believes Dr Turner. “We know a lot more about the depressed brain. The problem is that symptoms of depression are such a broad church.”

He adds: “Melancholia is as physical a condition as you can get, but other depressions are more subtle. Some do turn out to be down to serotonin deficiency, as treatable by SSRI drugs. With the others, we have a problem. Symptoms of depression due to personality, lifestyle or relationships are indistinguishable. We have found, though, that cognitive behavioural therapy (CBT) is quite effective in some people.”

It is all too tempting, however, for us to dismiss CBT as yet another “latest thing” and resignedly expect yet another new big fashion in drugs or therapy to come trundling along soon — with the basic illness remaining intractable. But Dr Turner says we must not become downhearted. “We have to be optimistic about these things, and our chances to find more therapies,” he says. “Otherwise we will all get depressed.” More books on Mind

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