Illiterate, vulgar and irresponsible

His Holiness the Dalai Lama some years ago was addressing a group of young people in America. One of them asked him, ‘What’s the quickest way to enlightenment?’ His Holiness, for whom compassion is a way of life, responded by bursting into tears at the spectacle of  someone being so very far from enlightenment as to ask such a stupid question.

There is, of course, no shortcut to enlightenment. Yet this does not stop people trying to bypass the sustained and devoted efforts required to achieve it with drugs.

Taking drugs for this purpose, or merely to ‘get high’, is inherently dangerous. It can bring about an altered state of consciousness through causing a chemical imbalance in the brain, or to put it bluntly, by poisoning the brain.

The dangers are spelled out in a BBC online news article (26 June 2017):

Man dies after taking potent MDMA drug in Oldham. MDMA is better known as Ecstasy.

A man has died and four others are in a critical condition after taking a ‘particularly potent’ form of the drug MDMA, Greater Manchester Police said.

Ten people were admitted to hospital after taking the drug over the weekend, with four remaining in intensive care.

Det Insp Jim Faulkner said the situation was ‘incredibly worrying [and] we are doing all that we can to warn people against taking the drug and help those who may have taken it.’

There is a link, ‘This is what happens if you take too much MDMA’, where we find the following:

So what happens to your body when you take too much MDMA? We asked an addiction psychiatrist, Dr Adam Winstock, to explain….And although Dr Winstock says the number of deaths in the UK where MDMA is implicated is on the rise, overall he describes it as a ‘remarkably safe’ drug.

This struck me as a surprising. I looked up Dr Winstock – and then the penny dropped. He is associated with the well-named Professor David Nutt whose antics I have written about previously:

Dr Winstock wrote an illiterate, vulgar and irresponsible post, ‘Let clubs be honest about drug use so they can educate people and save lives’ on ‘Mixmag’ (24 November 2016), an ‘electronic dance and clubbing magazine’. He believes it is a good idea to advise people how to take Ecstasy:

Safer drug use at venues means less use of emergency services; safer drug use at venues means less (sic) people leaving early and spending less at the bar; safer drug use at venues means happier, healthier punters (sic) who are more likely to be repeat visitors.

The relationship between MDMA dose and the risk of death is inconsistent and unpredictable. [That’s the trouble!]

People need to know how to dose with MDMA (start low go slow, tell your mates so they know). They need to know when they will come up (15min – to over an hour), how they will feel (they might feel nauseous) and when to re-dose (not when you are peaking). They need to know that twice the dose is not twice the high – even small increases in dose can lead to very big increases in actual blood levels and can tip you into feel sick and unwell. They need to know not to take MDMA from different batches. And then there’s all the basic stuff: not drinking too much water, not getting p****d on alcohol on a pill, not mixing with other stimulants and leaving a month or more between doses. If you are reading this and nodding in agreement, then you are in the majority. But with so many people out there a minority of people is still a s**t load of people who could be so much safer if they knew a few basic rules.

He may say he is being realistic, since people are going to take this drug anyway, so they might as well be advised how to take it safely. But there is no guarantee that anyone can take MDMA safely – it is a hit and miss affair. You cannot know in advance how it will affect you. That is why one man died and ten were in hospital. And what to do if someone is adversely affected? Go to A&E – unload it on the health service. Wonderful. People should be advised not to take these drugs. There is no need for it. The use of mind-altering drugs should be strongly discouraged.

Where Dr Winstock also goes wrong is that he thinks people take these drugs for pleasure. They may find it pleasurable the first time, unless they have a bad trip or it kills them, but then what? Take it regularly and get hooked on it?

The Guardian (3 December 2012) carries a headline: ‘Drugs are taken for pleasure – realise this and we can start to reduce harm.’  Professor David Nutt dilates:

One of the most important motivations for taking drugs, which cannot easily be acknowledged by the authorities, is personal pleasure.

How does he know? Do people in clubs and parties find their lives so boring and bland that they need an artificial source of pleasure by taking mind-altering drugs? Something that is intended to cause a chemical imbalance in the brain? He goes on:

The fact that there are so many users of ‘illicit’ drugs such as cannabis, MDMA and ketamine means that the pleasures must often be seen to outweigh the pain, just as they do for alcohol and tobacco. Until we properly understand the personal value of all drugs (including alcohol and tobacco), harm- and use-reduction policies are bound to fail.

Does Professor Nutt understand nothing about drug addiction? You cannot lump alcohol with illicit drugs, and my views on tobacco are well known ( As for harm- and use-reduction policies for illicit drugs, Professor Nutt is right – they will fail.

These drugs should be banned.

Text © Gabriel Symonds

Depression, Busy Doctors and Winnie-the-Pooh

Whenever I hear of busy doctors, I am reminded of the Bisy Backson.

If you haven’t left your childhood too far behind, you will probably know this comes from the Winnie-the-Pooh stories, specifically from the delightful book, The Tao of Pooh by Benjamin Hoff. When Rabbit went to visit Christopher Robin he found a note saying: ‘GON OUT. BACKSON. BISY. BACKSON. C.R’

Benjamin Hoff comments, ‘The Bisy Backson has practically no time at all, because he’s too busy wasting it by trying to save it.’

Now here’s an item I saw on the BBC online news (19 October 2016), so it must be true. It’s about antidepressants.

A woman is shown in a film who says:

I was an absolute mess – wanting to take my life, like continually. I read the leaflet and I was getting exactly what it said I was getting – seizure-like symptoms where my muscles were kind of jolting around of their own accord and I felt disorientated and sick and had digestive problems and infections. I mean it’s really really extreme.

Subtitle: One in 11 British adults take antidepressants. But these pills can come with some serious side-effects.

Then we have a quote by Professor David Healy, who knows a thing or two about antidepressants – he wrote a book called Let Them Eat Prozac – and he says these pills can make many people’s problems worse:

One in four people become more anxious, rather than less. And they can become extraordinarily anxious, so that some people become very agitated and some go on from that to become suicidal.

After that, another patient, Darren, is shown. We are told he developed muscle spasms and a stammer when the dosage of his antidepressants was increased. The film shows him with violent shaking of his right arm. He says ‘I can stop it but if I do somewhere else goes’ and we can see his head and upper body start shaking.

On the other hand, Dr Sarah Jarvis, a GP in west London, says people can benefit from the right kind of antidepressant:

I think with people with severe depression, you may well need to try two or possibly three before you find one that does work. But for most people with severe depression we can find a medicine which will help them, and where the benefits will outweigh the risks.

The point of this news item is that ‘People who say their lives have been ruined by commonly prescribed antidepressants, known as SSRIs, are taking their case to Parliament on Wednesday.’

So we have opposing views from two experts on the value of antidepressants.

I think what underlies this difficult problem – do antidepressants do more harm than good? – is the concept of depression as a disease, like pneumonia or arthritis. As I have said in previous posts, depression is a symptom, not a diagnosis. What is going on with patients who are labelled as suffering from depression? It seems the common approach to mental distress is the same as with purely physical illnesses: take a history, do a physical examination if appropriate, possibly do some blood tests or an X-ray; then you can make a diagnosis and the treatment follows. For example, a patient comes with pain in the abdomen, it hurts more if the doctor presses at the lower right part, a blood test shows a raised white blood cell count, and a diagnosis of appendicitis is made; the treatment is to remove the appendix. Of course it may not be so simple as this and appendicitis can be difficult to diagnose. But how much more difficult it is with mental symptoms! The trouble, it seems to me, is that once a diagnostic label is attached the treatment that follows is often a pill of one sort or another. This is a gross oversimplification.

What is going on in the mind of the patient who is diagnosed with depression? If given the opportunity in a supportive and non-judgemental setting, such patients almost invariably have plenty to say. The origin of the problem may go back to childhood, or be related to family, work or financial difficulties. A sympathetic ear can do much to ease such patients’ distress. The prescription of a so-called antidepressant can feel like a rejection: the ‘busy’ doctor – and why are doctors always busy? – doesn’t have time to go into all the patient’s troubles and issuing a script for a pill is often the quickest way to ‘dispose’ of the patient. Dispose is actually a medical term – rather unfortunate I think – for dealing with the problem that the patient brings to the doctor.

It reminds me of when I first started to work in general practice in London in the 1960s. Computers hadn’t been invented and records were kept in what were called Lloyd-George envelopes, named after the Liberal politician who was instrumental in introducing socialised medicine into Britain. They contained cards about 5 x 7 inches where one could write the clinical notes: often the entry consisted of only two words, apart from the date: a symptom and a drug. For example: ‘Tonsillitis – penicillin’, or ‘Cough – Gee’s linctus’.

In some ways this approach hasn’t changed much, except these days we use computers: Depression – Prozac.

Text © Gabriel Symonds

This entry was posted in Depression, Psychiatry and tagged antidepressants, Professor David Healy, Prozac on November 8, 2016 by Gabriel Symonds. Edit

Medicine and manners

I believe that in medical practice, courtesy between colleagues is of the highest importance. If it is not observed it may have unfortunate consequences for the patient as well as for the professionals involved. ‘Unfortunate’ is putting it mildly – it could have been fatal in the case I shall relate.

Some years ago a patient came to see me with massive bruising all down one side of his body. He had also been suffering from symptoms of depression. In those days I was very busy with my general practice and didn’t have time to take on another patient for regular hour-long psychotherapy sessions. Therefore I referred him to a colleague, a woman lay therapist whom I knew and who had, I thought, quite a good reputation among the foreign population of Tokyo.

I heard nothing further until this patient turned up three weeks later with the bruising. The story was as follows: the psychotherapist to whom I had referred him turned out not to have confidence enough to treat him herself; she referred him on to another practitioner, a Japanese psychiatrist. The psychiatrist, in the way that psychiatrists do, prescribed him an antidepressant. Unfortunately he omitted to take a work history, that is, to ask the patient what he did for a living. Or maybe he did ask but failed to take this information into account in his prescribing.

The patient was a professional racing driver. I have known several racing drivers in my career; they were all rather interesting, introverted people. The job requires athletic physical fitness and intense concentration; you need the ability to make split-second decisions. Yet it is quite a lonely sport – you are most of the time strapped into the cockpit of the car with little direct human interaction. The 1966 film Grand Prix shows this rather well, I think.

What is absolutely clear is that when you are driving at speeds which may exceed 300kph (186mh) there is zero margin for error. Your mind must be unclouded – or the result could be fatal to yourself or to other people on the track.

Under the circumstance the antidepressant was ill-advised. Such drugs all have side effects that can include drowsiness. This may not matter too much in ordinary life but they are absolutely contraindicated (must not be used) in a racing driver! Before this treatment he was fine in the car even though he was depressed; it is in a way a meditation; when racing you cannot think of anything else but the job in hand.

The patient had been in a crash and nothing worse had happened than the severe bruising. He was lucky.

Why, oh why, did the psychotherapist take it upon herself to refer the patient on to someone else without conferring with me? Did she think, because of my well-known reluctance to use mind-drugs, so-called antidepressants, the patient was not safe in my hands? Apart from the potentially fatal outcome indirectly due to her failure to refer back to me, this was a lapse of common courtesy. Needless to say I never referred her another patient.

This incident highlights another problem that is especially evident in Japan: the lack of a general practitioner who is recognised as being in overall charge of the patient’s medical situation. What often happens is that a person independently consults specialists at different hospitals; there may be little or no communication between them. This fragmentation of care can result in reduplication of tests and treatment or inappropriate prescribing. Also, hospital doctors often work in rotating training schemes and the patient may not see the same doctor twice. If there is a query, whom should the patient approach? If there is no general practitioner, who will provide continuity of care?

Text © Gabriel Symonds

This entry was posted in Depression, Psychiatry and tagged antidepressants, professional courtesy, racing driver on November 16, 2016 by Gabriel Symonds. Edit

Mental illnesses are brain diseases – or are they?

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: she suffered hallucinations, paranoid delusions and ended up in a catatonic state. On a brain biopsy and lumbar puncture evidence of  inflammation was found. Thus 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 that about 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 what are called 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 antidepressants 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

This entry was posted in C G Jung, Depression, Psychiatry and tagged antidepressants, autoimmune brain disease on November 23, 2016 by Gabriel Symonds

Mental Illness Doesn’t Happen in a Vacuum

The fifth edition of the so-called bible of psychiatry, usually referred to as DSM-5, which means the Diagnostic and Statistical Manual of Mental Disorders, was published by the American Psychiatric Association in 2013. It contains an expanded list of diagnoses of mental illnesses compared with the 4th edition. I do not intend to enter into the controversy of whether many of the latest inclusions are real illnesses, or ‘disorders’ – as they are invariably called in this book.

Incidentally, it would read better, in my view, as well as making the book a lot shorter, if the word ‘disorder’ were dropped. For example, instead of shyness – yes, this is actually regarded as a mental illness – being called social anxiety disorder, why not just call it social anxiety? Schizophrenia is now schizoaffective disorder and drug abuse is labelled substance use disorder, etc. Well, no doubt psychiatry has moved on a bit since I did my psychiatric residency in the 1970s, but how much is due to real progress in understanding the causes of mental illness and how much is just a difference in nomenclature? It is true that many more drugs are now available, and very helpful they can be – particularly in the more severe forms of depression and in psychoses (such as schizophrenia). However, it should be kept in mind that these are empirical treatments: they may work but how they work is speculative. The oft-quoted fond idea that such drugs adjust a chemical imbalance in the brain that is the cause of the disorder is unproven. There is no way at present to measure levels of serotonin, dopamine or other neurotransmitters in the living human brain, and anyway the alleged chemical imbalance may well be the result of the mental disturbance rather than the cause.

These thoughts came to mind recently after I read an autobiographical account of severe depression suffered by the late American author William Styron: Darkness Visible: A Memoir of Madness (1989). He is probably best known for his controversial novel, Sophie’s Choice. The experiences he describes are harrowing, but he eventually recovered after being admitted to a mental hospital. It seems the secure environment and empathy of the staff were the major factors in his recovery. He was not given ECT (electro-convulsive therapy) and there is little mention of drugs. But why did he become depressed? Brain disease? Probably, but what was the cause of that? Mr Styron tells us: he abused alcohol for forty years and was addicted to a sleeping tablet called Halcion which was unwisely prescribed long term and in high dose. Under these circumstances it is hardly surprising he became depressed. In addition, there was likely a psychological cause in that he lost his mother to cancer when he was only thirteen.

I regard the use of drugs in mental problems, not as a cure, but as a means of helping patients cope with a difficult time in their lives, and I do prescribe them when necessary. However, I believe it is just as important, if not more so, to try to help patients work through the underlying problems and repressed conflicts which are often involved in the cause of their distress.

This entry was posted in Medical on May 1, 2016 by Gabriel Symonds. Edit

Messing up your brain

It has long been suspected that regular use of cannabis (marijuana), especially the high potency variant called ‘skunk’, can increase the risk of psychosis in vulnerable people.

And now Sir Robin Murray, professor of psychiatric research at King’s College London, rightly says, ‘It’s not sensible to wait for absolute proof that cannabis is a component cause of psychosis.’ He adds, ‘There’s already ample evidence to warrant public education around the risks of heavy use of cannabis, particularly the high-potency varieties. For many reasons, we should have public warnings.’

This view is echoed by a government spokesperson: ‘We must prevent drug use in our communities and help people who are dependent to recover, while ensuring our drugs laws are enforced. There is clear scientific and medical evidence that cannabis is a harmful drug which can damage people’s mental and physical health, and harms communities.’ (The Guardian, 15 April 2016.)

With this preamble, let me get to my theme: the treatment of depression.

There is no doubt that in extreme cases the illness called major depressive disorder can be devastating. I have seen patients reduced to a state of complete immobility, unable to work or even get out of bed because of overwhelming unhappiness. These, however, are a minority. The vast majority of people who have been labelled as suffering from a depressive ‘disorder’ have what might better be called normal human misery.

There are no blood tests or other objective criteria for making the diagnosis; it is made entirely on symptoms or observations such as these:

Depressed mood most of the day, nearly every day…Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day…Significant weight loss when not dieting or weight gain…Insomnia or hypersomnia (excessive sleepiness) nearly every day…agitation…Feelings of worthlessness or excessive or inappropriate guilt…Diminished ability to think or concentrate…Recurrent thoughts of death…recurrent suicidal ideation…or a suicide attempt or a specific plan for committing suicide…(Diagnostic and Statistical Manual of Mental Disorders, 5th edition, 2013, American Psychiatric Association.)

These are pretty serious symptoms, but they are all subjective and need to be interpreted. How do you decide when a symptom is ‘marked’ or ‘significant’? There is a risk that people suffering from normal extreme sadness, such as after a bereavement, may be misdiagnosed as having a depressive disorder because the symptoms have lasted longer than the American Psychiatric Association deems appropriate. (There is a whole book dealing with this very problem: The Loss of Sadness: How Psychiatry Transformed Normal Sorrow into Depressive Disorder, by A V Horwitz and J C Wakefield,  OUP 2007.)

Such a view is echoed in an article on this same problem in The British Medical Journal (9 December 2013) on medicalising unhappiness which noted:

Over recent decades there has been an increasing tendency, especially in primary care, to diagnose depression (commonly major depressive disorder) in patients presenting with sadness or distress and offer them antidepressant medication.

Many patients report sadness or distress during consultations with primary care doctors. Such emotions may be related to grief and other life stresses, including the stress of physical illness. Sometimes sadness appears out of the blue, without obvious relation to external causes.

Without a doubt, depression is real and horrible and deserving of the highest standards of medical care.

What to do about it? Rather than reaching for the prescription pad, it might be better to listen to the patient. He or she, if given the chance in a supportive,  non-judgemental environment, nearly always has got plenty to say – attesting to the importance of the psychological causes of depression.

If the doctor does decide a prescription is warranted, it should be understood by both parties that this is empirical treatment. The fond idea that antidepressant correct a chemical imbalance in the brain is purely hypothetical. Such imbalances, if they exist, could well be the result rather than the cause of the depression. Antidepressants, nonetheless, can be helpful to tide a patient over a difficult patch, but they are not a cure. Do they work? They appear to work in some people, but it is unpredictable. Some patients, especially those with more severe degrees of depression, may find it preferable to be in the drugged state which antidepressants induce than to suffer their unmedicated distressing feelings; the same applies to people with severe anxiety and agitation.

Further, psychiatrists, although their skills may be helpful in choosing a drug for those patients whose unhappiness is deemed serious enough to give it a try, should not be under any illusions about what they are doing. Antidepressants do not cure depression. At best they can help to reduce symptoms and thereby make life easier to bear.

This is all the more relevant in the light of a recent study on depression reported in The Lancet Psychiatry ( that there is a drug which is consistently effective in 35-40% of patients: it is called placebo.

Text © Gabriel Symonds

This entry was posted in Depression, Psychiatry and tagged antidepressants, cannabis, marijuana, placebo, psychosis, Sir Robin Murray, The Loss of Sadness on November 27, 2016 by Gabriel Symonds. Edit

The Tragic Death of Edward Mallen

I only know what I heard and read on the BBC, so it may not be the whole story, but it’s so sad and upsetting that I’m going to stick my neck out.

Edward Mallen, who was only 18, had been battling with depression and, tragically, took his own life in February 2015.

He had seen a GP two weeks before his death and had given consent for his parents to be told of his suicidal thoughts, but they were not told.

Why did the GP seek, and obtain, permission to inform his parents, but then fail to inform them?

The GP did, however, contact the local NHS Foundation Trust crisis intervention team and recommended, rightly under these circumstances, that Edward should be seen within twenty-four hours. But, unfortunately, ‘a triage mental health nurse who spoke to Mr Mallen on the phone said a five day wait was appropriate as he did not think there was a significant risk.’

How can it be that a nurse, merely as a result of a phone conversation, has the authority to over-ride the GP’s recommendation?

(It’s unclear from the BBC report whether it was the GP or the mental health service, or both, who didn’t inform the parents.)

The Assistant Coroner said ‘Edward Mullen had fallen through cracks in the system and there had been no continuity of care.’

That’s the problem. Why had there been no continuity of care, and who should have provided it? Presumably the GP.

The bereaved father said: ‘The hearing today confirmed what I suspected was the case, that there are deep structural inadequacies across the health system with regard to mental health.’

He very decently blamed only ‘the system’ saying it was ‘not really fit for purpose.’ But a system such a health service is only as good as the people who work in it. Being faced with a suicidal youngster who had consented for his parents to be told, of course they should have been told, and straightaway. Then close follow-up should have been arranged – whether the doctor was officially on duty or not – until this poor boy was safely in the hands of specialists.

It may not have made a difference but, as a Trust spokeswoman said, ‘The Trust didn’t do everything that could possibly be done…we must therefore accept some responsibility.’

In similar vein is the account, also reported by the BBC, of the case of Julie Bignell who had a three month wait to see a psychiatrist.

 … I took an overdose, because I felt that nobody understood the way that I felt. It wasn’t…that I wanted to die…I just couldn’t cope with what was going on in my mind. Nobody could understand me, and I couldn’t understand me, and I wanted somebody to help me. Well, the waiting time to see somebody…just increased the anxiety, the depression.

It’s unacceptable to have to wait so long to see a psychiatrist, and there’s a call to set a twenty-eight day target for access to mental health services. But what about the GP in the meantime? Could not he or she have offered to see this patient – and I apologise if I’m mistaken – once a week for an hour’s session to listen to her problems and, if necessary, start empirical treatment with an antidepressant or anti-psychotic drug? Any GP worthy of the name should be capable of doing this. And surely, in case of doubt it’s possible for the GP to confer with a specialist on the phone for advice on drug treatment in the meantime?

Why doesn’t it happen? It is because many GPs are part-timers? Or is it because they feel they’re not up to the job? Or have guidelines and the Quality and Outcomes Framework (QOF) hamstrung doctors so that they can’t take responsibility for their owns decisions?

By the way, what is the QOF? It’s a voluntary system started in 2004 which rewards GPs for carrying out work which any self-respecting GP would do anyway, in my view.

Let’s see what the current QOF has to say about mental health problems. To start with it says this:

It is recommended that patients receive health promotion and prevention advice appropriate to their age, gender and health status.

How condescending. Do they think GPs are lazy or stupid? It gets worse. This is what the QOF says about depression:

10 points will apply if 45-80% of patients aged 18 or over with a new diagnosis of depression in the preceding 1 April to 31 March have been reviewed not earlier than 10 days after and not later than 56 days after the date of diagnosis. (Slightly paraphrased.)

Are we playing a computer game? Suppose the GP decides the patient needs to be followed up in a week rather than ten days? Then he misses the 10 points and an extra fee! No wonder there have been calls for the QOF to be scrapped.

One of the great satisfactions of being a general practitioner used to be that you treated the patients to the best of your ability as you saw fit. You didn’t have or need anyone looking over your shoulder in effect telling you what to do or withholding pay if you didn’t do it. No wonder British general practice is in a crisis and failings in the system lead to tragedies such as those mentioned in this post.

© Gabriel Symonds

This entry was posted in Medical on June 18, 2016 by Gabriel Symonds. Edit

The Disappearing Jung

Can you imagine a history of Europe without mention of Napoleon? Well, the learned editors of the highly esteemed New Oxford Textbook of Psychiatry have done something similar in the second edition (2009) compared with the first edition (2000).

In the Preface, from which I quoted in a previous post, it says ‘textbooks are still needed to provide the comprehensive account of established knowledge’. Indeed.

But right here we have a difficulty. To talk of ‘established knowledge’ in relation to psychiatry is an assumption bordering on hubris. Psychiatry essentially involves the mind observing itself, so how is one to decide what is established knowledge and what isn’t? Even in physics, for example when considering Newton’s laws of motion or the periodic table of the elements, such knowledge is only established until disproved by later developments. In fact, throughout the Textbook a much more modest approach is evident in the various sections where the provisional and speculative nature of many psychiatric diagnoses and treatments and their theoretical underpinnings are acknowledged.

In the current edition there is a whole section on Sigmund Freud, but while there was a  chapter by Anthony Storr on the famous Swiss psychiatrist, C G Jung, in the first edition, there is barely a word about him in the second, and he does not appear in the index.

I wrote to each of the four editors of the Textbook about this surprising omission and received replies from two of them. One said: ‘We thought long and hard about Jung: Anthony Storr’s chapter in the first edition was excellent but he died before we prepared the second. We therefore took – and followed – expert advice.’ Of course he wouldn’t tell me who these experts were nor their reasons for advising that Jung be excluded.

Anthony Storr died in 2001, so there should have been plenty of time to find someone else to write a new chapter on Jung if that was what they wanted to do. For one, there is Dr Anthony Stevens, an eminent psychiatrist who has written extensively on Jung. Or they could have simply reprinted Storr’s chapter – after all, the chapter on Freud is reproduced virtually unaltered.

I also wrote to the publisher, Oxford University Press, and was told they wanted to keep the book to a reasonable size. Since the new edition is 110 pages shorter than the old (2021 v 2131 pages), I found this unconvincing.

Why then, when Freud and others in the psychoanalytical movement are mentioned, with Freud rightly having a chapter to himself, is Jung all but expunged? (Jung is mentioned twice, but only very briefly in footnotes.) Even if the editors disagreed with Jung, why didn’t they say so in a section offering a critical assessment of his work?

The contribution of Freud to psychoanalysis can hardly be over-estimated, but Jung built upon Freud’s theories and developed them much further. The two men met in 1907 and until 1912 enjoyed a close and fruitful relationship. Jung was nineteen years younger than Freud who at first looked to him as his heir. But Jung’s independent spirit and need to stick to his own path led to their inevitable falling out – a breach which took a heavy toll on both of them. The main reason for this was that Jung could not accept Freud’s theories that the unconscious is merely the repository of repressed and forgotten  memories, and that the sex drive is at the root of virtually all human motivation. Jung’s concepts, based on empirical data, of the collective unconscious and the archetypes are two of his main contributions to psychiatry, and the idea of the psychological types called introversion and extraversion (note the spelling) derive from his work.

An example of the importance of Jung today can be seen in the congress of the International Association for Analytical Psychology, held in Kyoto in 2016, where I was one of nearly seven hundred participants from all over the world.

I am, therefore, left to speculate as to the reasons for this glaring omission from the Textbook, and can only conclude it is because Jung was perceived as not being ‘scientific’ enough. This criticism he often had to deal with in his lifetime, especially, as he ruefully observed, when it was made by people who had not read his books, let alone understood them.

Jung was at pains to emphasize that he was an empiricist, not a metaphysician; he dealt with observable facts. For example, if someone believed in God, that was a psychological fact; whether God actually exists he was not in a position to say. Jung was even accused of being a mystic, but it will be obvious to anyone who takes the trouble to study his works that he was nothing of the kind.

Jung said: ‘People sometimes call me a religious leader. I am not that. I have no message, no mission; I attempt only to understand.’

Text © Gabriel Symonds

This entry was posted in C G Jung, Medical, Psychiatry and tagged Anthony Stevens, Anthony Storr, Freud, IAAP on October 25, 2016 by Gabriel Symonds

Smoking and Schizophrenia

According to an article in the British Medical Journal (10 July 2015), smoking may increase the risk of developing schizophrenia, a severe type of mental illness called psychosis.

An association between cigarettes and psychotic symptoms has been noted before, but is this because patients take up smoking as a way to try to counteract symptoms or help reduce the side effects of drugs used to treat them?

Although not proven, the researchers at the Institute of Psychiatry, Psychology and Neuroscience at King’s College, London, concluded that ‘smoking should be taken seriously as a possible risk factor for developing psychosis’.

The cause(s) of schizophrenia and other mental illnesses are unknown, but there is a theory that they are due to chemical imbalances in the brain. Or maybe chemical changes in the brain, if such exist, could be the result of mental illnesses.

People who smoke cigarettes inhale into their lungs nicotine and thousands of other chemicals, many of which are poisonous. These include cadmium, polonium, arsenic, lead, carbon monoxide, cyanide, ammonia and benzene.

Inhaling tobacco smoke, therefore, results in a drugged state.

It’s hardly surprising that if you’re suffering from a mental illness, you aren’t going to do yourself any good by putting numerous chemical poisons into your bloodstream in addition.

This is doubtless connected with the fact that when smokers stop smoking they often feel much better with less anxiety and depression.

©Gabriel Symonds

This entry was posted in Smoking on August 16, 2015 by Gabriel Symonds. Edit

Scientific Psychiatry

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

This entry was posted in Medical, Psychiatry and tagged PET scan, phrenology, psychiatry on October 23, 2016 by Gabriel Symonds. Edit