What is the cause of depression? This sounds like a question a medical student might have to answer in an exam: State the causes of (for example) duodenal ulcer or grand mal epilepsy.
But if we ask, instead, ‘What causes depression?’ the answers are obvious: in most cases it’s adverse life events such as abusive parents, bereavement, financial loss, examination failure, disappointment in love, etc.
The question then becomes, when does ordinary depression, or normal human misery, become a mental illness – assuming there is such a thing? As I have mentioned in a previous post, it’s a matter of degree. But where to draw the line?
The esteemed New Oxford Textbook of Psychiatry, in the current (second) edition, 2009, considers depression under the heading of ‘mood disorders’ and approaches this question cautiously:
Depressive symptoms in the community are common, and defining both the symptom count and duration at which depressive symptoms count as part of a clinical disorder is arbitrary.
(This could have been better written without using the word ‘count’ in two different senses in the same sentence.)
Anyway, this statement is part of a critique of the definition of depression in the DSM-IV (the so-called bible of psychiatry, the Diagnostic and Statistical Manual, 4th edition, of the American Psychiatric Association – now superseded by the 5th edition), in which two American writers are quoted as saying:
…they could find no empirical support for the DSM-IV requirement of duration of two weeks, five symptoms or clinically significant impairment (whatever that means) and that this definition may be no more than a diagnostic convention.
Being unable to define, let alone state the cause(s) of depression, the Textbook then goes on to discuss possible ‘risk factors’. These include genetic factors (though they’re not unique to depression), gender (it’s twice as common in women), childhood experiences (lack of parental care, not surprisingly, is associated with increased rates), personality (it’s associated with neuroticism, however you define that), social environment (for example, depression is commoner in single than in married men) and physical illness (not surprisingly).
The relevance of some of these risk factors is summed up in a reference to another paper which speculates:
…genetic factors influence the risk of onset of depression, in part, by increasing the sensitivity of the individual to the depression-inducing effects of stressful life events.
So, if your genes have made you sensitive to developing depression, then stressful life events may cause you to become depressed. That’s useful to know, I suppose.
Next, we learn that the writer hopes – whether vainly, only time will tell – to integrate psychiatry into clinical medicine:
…success in depression would parallel that seen in moving the management of heart disease from the acute episode of infarction (heart attack) to the treatment of metabolic risk factors.
How can you compare diseases of the heart – a physical organ – with disorders affecting the mind, which by definition are difficult to grasp. What is mind? Where does it reside? In the brain, presumably. But does it? Hearing a symphony apparently coming out of a radio, one might as well look inside the radio to see where the musicians are. It has been said that this is the level of our current understanding of how the mind works.
Then, as would be expected in a scientific textbook, they examine what they call the neurobiology of mood disorders.
Here the writer, a Professor of psychiatry at a prestigious UK University, expounds on ‘key vulnerability factors’, which seem to be more or less the same as some of the previously mentioned risk factors: genetics (‘There has been a terrific (sic) proliferation of possible genetic effects…’), temperament (with reference to animal studies, the relevance of which to human psychiatry eludes me), neuroticism (apparently ‘biologically (sic) founded in negative biases in attention, processing, and memory for emotional material’), early adverse experience (derived from cruel experiments in rats, though with the proviso: ‘Whether separation or stress paradigms in rodents can be taken as precise models of the mechanisms underlying the risk of mood disorder…cannot yet be decided, but their general relevance to the human case seems obvious.’)
Gentle reader, consider the last sentence. Now let me quote from the Preface of this noble two-volume tome:
This new edition, like the first, aims to present a comprehensive account of clinical psychiatry with reference to its scientific basis and to the ill person’s perspective. (Emphasis added.)
So, it cannot be decided whether cruelly induced stress in rats is a model for the risk of mood disorder in humans but its general relevance seems obvious.
In science it’s not good enough that something seems obvious: it must be proved to be so. In any case, if it seems obvious, why bother to do the experiments in the first place? And if it doesn’t seem obvious, what then?
After all that, we come to the bottom line:
It remains true to say that no biological changes have ever been found that distinguish between depressed patients and controls better than does clinical assessment of the patients.
I shall not weary the reader with detail about recent exciting developments in imaging of the brain: PET, SPET and SPECT scans, as they are known. What do they tell us? That certain areas of the brain can be seen to be active in patients with certain symptoms. So what? Of what value are these techniques – no doubt of great interest in themselves and maybe of potential value as research tools – in the practical matters of diagnosis and treatment of psychiatric symptoms? Such techniques have been been likened to a modern form of phrenology, where instead of assessing someone’s personality and mental faculties from the shape of his or her skull, one attempts to assess brain function on a computer screen.
Text © Gabriel Symonds