There was a recent programme on the BBC consisting of sound bites about the latest so-called breakthrough in trying to understand mental illness – a field of medicine in which understanding is sorely lacking:
It’s pretty radical – that we can develop new treatment options that work through the immune system…It is ground-breaking…demonstrating that depression is a disorder of the whole body…really exciting advance…a challenge to the idea that mental illness is all in the mind
One patient describes the development of her psychosis: hallucinations, paranoid delusions and ending up in a catatonic state. She had a brain biopsy and lumbar puncture and they found evidence of inflammation; she was diagnosed with auto-immune encephalitis. We are told that some doctors believe many more cases of mental illness could be due to an immune disease.
Caution is in order here. In some patients with extreme mental symptoms, inflammation of the brain was found and they had physical symptoms as well. This is not surprising. Many physical disorders can cause mental symptoms, for example delirium associated with high fever from infections with bacteria, viruses, malaria or syphilis; poisoning with many substances and drugs; physical degeneration of the brain in dementia, and so on. But just because an inflammatory cause has been found in these cases it doesn’t necessarily mean patients without physical symptoms will also turn out to have an identifiable disease of the brain.
In support of the ‘mental illness = brain disease’ hypothesis, we’re told it’s estimated that one in ten people with psychoses have antibodies indicating inflammation. Then what about the other nine of the ten?
In these particular patients with inflammation they used plasma exchange to remove the antibodies, gave intravenous immunoglobulin or prescribed steroids (cortisone). But it should be remembered that these are entirely non-specific treatments. Steroids themselves can even cause psychosis in some people. Steroid treatment, though it can be life-saving, has been likened to ‘kicking the telly when it’s on the blink’ – in the days of cathode-ray tube television sets.
Then the programme turns to depression. One sufferer gives this account:
My depression gets so bad that I can’t leave the bed, I can’t leave the bedroom, I can’t go downstairs and be with my partner and his two children. I can’t have the television on. I can’t have any noise, light. I have suicidal thoughts. I have self-harmed. I can’t leave the house and everything else just feels too much.
This is obviously a severe case, but of her history we are told nothing. Antidepressant drugs and psychological treatments like cognitive behavioural therapy may help some of these patients, but because so many don’t respond, researchers are now looking into ‘whether the immune system could be causing depression’ and whether ‘inflammation is actually the cause of the disease.’ They even wheel out a professor of ‘biological psychiatry’ (whatever that is) who says: ‘Maybe 30-40% of depressed patients have high levels of inflammation.’ This is pure speculation.
In any case, as I’ve asked before, how do you decide when normal human misery becomes a disease? Furthermore, some people without any symptoms may have ‘inflammatory markers’ in their bloodstream. Now they want to go on and ‘measure in the saliva stress hormones like cortisone and inflammation markers and look at the correlation with depression.’
Some of these scientists, in their efforts to develop an overarching biological theory of the cause of depression, almost get into contortions:
[In] individuals who have a history of early life trauma, even if they’ve never been depressed, there’s an activated immune system so they [are] at risk which then will lead to an increased risk of depression if the individual meets another [adverse] advent later in life.
This circular reasoning seems to be saying that if you suffer adverse events in early life you may be at increased risk of being depressed if you meet another adverse event later on.
An actual patient with depression appears in the film who says:
I had sertraline, Prozac, citalopram, duloxetine and metazoline , so I was on three at one point – it’s totally trial and error. (That’s the problem!)
To this, another scientist comments:
We’re not able to predict at the beginning whether someone will respond to one of the antidepressant’s that’s routinely prescribed. But we think by measuring inflammation in the blood we’ll be able to identify individuals who do require more complex, more intense antidepressant treatment, perhaps a combination of more than one antidepressant or antidepressant and anti-inflammatory or go straight into more complex treatments.
It’s all assumption and theory patched together.
Let’s consider depression a bit further.
Is depression a symptom or a disease? If it’s a disease how do you define it? The fact that some people with physical disorders become depressed is no reason for supposing that all or most cases of depression are also due to physical causes. Maybe it’s the depression itself which causes the immune disorder.
I think the pendulum has swung too far. In efforts to make psychiatry a discipline comparable with other medical specialties, a number of assumptions are being made that are extremely difficult to explain with the present state of our knowledge. Unlike, say, heart disease where there is a physical organ which can be investigated, in psychiatry the mind of the doctor is observing the mind of the patient. But what is the mind? Is it the same as consciousness? What is the source of the unconscious (in the Jungian sense)? How does the brain give rise to the perceived experiences of sensations and thoughts?
Let’s start – if it should be possible – with a provable definition of the mind and see where we go from there. Then, perhaps, we might begin to understand mental disorders.
Text © Gabriel Symonds