This is a piece I wrote for the Goteborgs Posten, a Swedish paper for which I write a monthly column (which is translated into Swedish).
I’ve spent a good deal of time lately reading up on the set of historical, medical and philosophical conditions known for centuries as melancholia and more recently as depression. My interest is that I’ve been commissioned to write a book about melancholia, but I’ll be writing it because it’s a subject I’ve lived with and thought around most of my life. I wonder what took me so long — and then again, I don’t. As far as I can understand it, I’ve had bouts of depression since I was a child. When I was little, it was called being ‘in a mood’ or ‘sulking’, and no one, including me, thought to query that definition. Looking back, the sense of hopelessness, despair, of seeing no way out of the dark place in which I suddenly or gradually found myself completely trapped, was just as present when I was ‘in a mood’ at the age of eight or nine, as it was when I was first diagnosed as clinically depressed and hospitalised at the age of fifteen, and then at twenty, and then at thirty-four, with non-hospitalised episodes lasting weeks or months plentifully in-between.
I came to think of myself as chemically prone to depression. Not that I reject the idea that the circumstances of my very messy family had been a perfectly reasonable cause, but undoubtedly, given the many possibilities of psychological responses, depression was how it took me. I’ve never had the slightest tendency towards symptoms that might define a schizophrenic illness (aside from taking drugs). Never heard voices, seen things that were apparently not there, felt impelled to act by something alien, outside or inside myself. I was perhaps tipped into a lifelong depressive illness by my experiences as a child, but never into psychosis.
Life and chemistry makes good sense to me as a pairing, and though chemistry might cause the problem on its own, I doubt that how you respond psychologically to life is unconnected to the balance of your physiology. Chemistry affects how you respond to experience and experience affects the chemistry of mood. That doesn’t mean that one’s psychology is absolutely determined and unalterable: talking therapy and medication can change what might be an impossible life into one that functions quite well. Freud spoke of returning people to ‘ordinary unhappiness’. Sadness and mood variation are not illnesses but part of life unless they become overwhelming. No one sloughs their life experience off like a lizard its skin, but with assistance it’s possible to use experience rather than let it use you. At any rate, up to a point.
Nevertheless, the history of the idea of melancholia and depression is as vivid and fascinating as any other subject that turns out to be so broad that you are unlikely to come to the end of learning about it. The actual writing of my book is still in progress – there is so much to read on such a range of topics that I have forcibly to stop myself reading and making notes, and get to grips with actually writing a book that is intended to take in as many aspects of melancholia (including a whole spectrum of my own experiences) as it’s possible to grasp or speculate about. But then that’s probably true of any book one ever wants to read or write.
I started, of course, with the key text: Robert Burton’s Anatomy of Melancholy, written in the early seventeenth century. In well over 1000 pages, Burton informs, infuriates, amuses, terrifies and delights the reader with everything that was or might be known on the subject of melancholy. Like the French essayist, Montaigne, no possible digression is left unexplored, and also like Montaigne, Burton claims to be writing his vast book in order to keep his own melancholic condition under control. Unlike Montaigne, he isn’t explicitly exploring himself or using his own experience as an example of both the particularities and generalities of humankind. He wants to establish an order for the subject (melancholia as an Elizabethan fashion, as an incredibly varied medical diagnosis, as religious excess, as a love disorder) and show everything that can be known about it, as well as to suggest ways in which afflicted people might be cured. But like many humanist texts at the time of the Renaissance, and maybe all good books, it is even bigger (in more than just its brick-like size) than the subject it claims to be about.
At the same time, I read that watershed text in thinking about mood disorders, Freud’s Mourning and Melancholia, as well as more recent commentaries and reports of neurological findings. What strikes me most at the moment is the language which Burton (and, for example, Hidegard of Bingen, or Saint Theresa of Avila) uses to describe the medical and moral condition. It goes back to the humoural theory of the Greeks: the four ‘humours’ that coursed through the body and in various combinations caused one of four main personality types: phlegmatic, choleric, sanguine and melancholic. Galen, Burton, Hildegard and St Theresa describe a very specific physiology – the places in the body and activity of the humours. They discuss the intricate circulation of the humours that had their source in bodily organs and affected the heart and the brain – when the brain was overheated with the fumes of too much ‘burnt bile’, the eyes spilled out liquid tears to relieve the pressure which were believed to be of a different kind to those tears that were the result of physical hurt. No one was in perfect balance, and medicine’s job was to adjust the proportions. Too much black bile from the spleen was the main cause of melancholia, but it was much more complicated than that. It is a plausible system in its world, but by the time that Burton had finished writing his Anatomy, the new experimentalists, like Francis Bacon, were doing away with humoural theory and insisting on the visible evidence discovered by cutting up bodies and describing what was found.
Jump ahead four hundred years and I am struck by the similarity between the somewhat haphazard theories of depression then and now. For years now, I have taken a maintenance dose of a serotonin-reuptake-inhibitor (SSRI). I decided after sitting through many of my depressions, that it was only a matter of time before the suicidal thoughts beat the natural tendency of depression eventually to lift. I figured I’d been there and done that, and so took and continue to take an anti-depressant which, even if it doesn’t make me giggly and happy-go-lucky, at least seems to stop me becoming immobilised for months by despair. The pill is said to work by increasing the amount of serotonin in my brain, a neurotransmitter thought to be involved in mood disorders. The idea would be that for reasons of physiology or life experience I was not producing enough of it. Anti-depressants are said to work on a monoamine imbalance, though no one I’ve spoken to has explained exactly why. The pills are supposed to be rebalancing my unbalanced brain chemistry.
But recent research in the United States has shown that there is not very much statistical difference between the effectiveness on depression of SSRIs (50% positive) and of placebos (30-35% positive). One serotonin enhancer (tianeptine) has been found to decrease serotonin but it does not induce depression – which makes the theory of monoamine imbalance look doubtful. There is something that professionals call ‘treatment resistant depression’. It means, I suppose, that they don’t know why some depressed people stay depressed, which suggests a less certain understanding of the nature of depression than we might expect with all our medical and technological science. The longer I look into modern theories of mood disorders, the more they start to look strangely similar to the old humoural theories and remedies. Too little of this, increase that. If that doesn’t work, try some hellebore. Neither Robert Burton nor a medical psychiatrist can explain exactly what happens physiologically when a person becomes depressed, nor why precisely this or that remedy does or doesn’t make a difference. And I know even less, for all that I have spent much of my life thinking and reading about the issue. What looks like an airy-fairy made-up description of complicated channels of unknowable humours in Burton’s physiology of melancholia means no less to me than the serotonin I so easily talk about and take a remedy to enhance. I might as well be following Galen’s prescriptions as my doctor’s for all I really know of my brain chemistry. Just as the old physicians had suggested, in the early 20th century a physiologist discovered that tears of grief and sadness were indeed chemically different from tears of pain. Remembering his time living with the Azande people of north central Africa, the anthropologist E. E. Evans-Pritchard said after he returned to England that he thought their habit of studying of chicken entrails was as good a way as any he had come across in his life of making decisions. I have a feeling that Galen’s and Hippocrates’s humoural imbalance theories are in much the same relationship with modern monoamine imbalance depression theory. And perhaps that’s even a bit of a relief.