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The Myth of Mental Illness: Thomas Szasz on Freedom and Psychotherapy

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Thomas Szasz on Freedom and Psychotherapy

by Randall C. Wyatt

The foremost psychiatric critic of our times, Thomas Szasz, engages in an in-depth dialogue of his life’s work including freedom and liberty, the myth of mental illness, drug laws, the fragile state of psychotherapy, and his passion for humanistic values and social justice.
Randall C. Wyatt: I am going to ask you a wide variety of questions, given the diversity of your interests, and I want to make sure to also focus on your work as a psychotherapist. A little background first. You’ve been well-known for the phrase, “the myth of mental illness.” In less than 1000 words, what does it mean?
Thomas Szasz: The phrase “the myth of mental illness” means that mental illness qua illness does not exist. The scientific concept of illness refers to a bodily lesion, that is, to a material — structural or functional — abnormality of the body, as a machine. This is the classic, Virchowian, pathological definition of disease and it is still the definition of disease used by pathologists and physicians as scientific healers.

The brain is an organ — like the bones, liver, kidney, and so on — and of course can be diseased. That’s the domain of neurology. Since a mind is not a bodily organ, it cannot be diseased, except in a metaphorical sense — in the sense in which we also say that a joke is sick or the economy is sick. Those are metaphorical ways of saying that some behavior or condition is bad, disapproved, causing unhappiness, etc.

In other words, talking about “sick minds” is analogous to talking about “sick jokes” or “sick economies.”

In other words, talking about “sick minds” is analogous to talking about “sick jokes” or “sick economies.” In the case of mental illness, we are dealing with a metaphorical way of expressing the view that the speaker thinks there is something wrong about the behavior of the person to whom he attributes the “illness.”

In short, just as there were no witches, only women disapproved and called “witches,” so there are no mental diseases, only behaviors of which psychiatrists disapprove and call them “mental illnesses.” Let’s say a person has a fear of going out into the open. Psychiatrists call that “agoraphobia” and claim it is an illness. Or if a person has odd ideas or perceptions, psychiatrists say he has “delusions” or “hallucinations.” Or he uses illegal drugs or commits mass murder. These are all instances of behaviors, not diseases. Nearly everything I say about psychiatry follows from that.

RW: Let’s say that modern science, with all the advances in genetics and biochemistry, finds out that there are some behavioral correlates of biological deficits or imbalances, or genetic defects. Let’s say people who have hallucinations or are delusional have some biological deficits. What does that make of your ideas?
TS: Such a development would validate my views, not invalidate them, as my critics think. Obviously, I don’t deny the existence of brain diseases; on the contrary, my point is that if mental illnesses are brain diseases, we ought to call them brain diseases and treat them as brain diseases — and not call them mental illnesses and treat them as such. In the 19th century, madhouses were full of people who were “crazy”; more than half of them, as it turned out, had brain diseases — mainly neurosyphilis, or brain injuries, intoxications, or infections. Once that was understood, neurosyphilis ceased to be a mental illness and became a brain disease. The same thing happened with epilepsy.
RW: It’s interesting, because a lot of students of mine, and colleagues, who have read your work or heard of your ideas, think that when condition previously thought to be mental is to be a brain disease, as noted, your ideas become moot.
TS: That’s because they are not familiar with the history of psychiatry, don’t really understand what a metaphor is, and don’t want to see how and why psychiatric diagnoses are attached to people. Ted Kaczynski, the so-called Unabomber, was diagnosed as schizophrenic by government psychiatrists. If people want to believe that a “genetic defect” causes a person to commit such a series of brilliantly conceived crimes — but that when a person composes a great symphony, that’s due to his talent and free will — so be it.

Objective, medical diagnostic tests measure chemical and physical changes in tissues; they do not evaluate or judge ideas or behaviors. Before there were sophisticated diagnostic tests, physicians had a hard time distinguishing between real epilepsy — that is to say, neurological seizures — and what we call “hysterical seizures,” which is simply faking epilepsy, pretending to have a seizure. When epilepsy became understood as due to an increased excitability of some area of the brain, then it ceased to be psychopathology or mental illness, and became neuropathology or brain disease. It then becomes a part of neurology. Epilepsy still exists. Neurosyphilis, though very rare, still exists, and is not treated by psychiatrists; it is treated by specialists in infectious diseases, because it’s an infection of the brain.

The discovery that all mental diseases are brain diseases would mean the disappearance of psychiatry into neurology. But that would mean that a condition would be a “mental disease” only if it could be demonstrated, by objective tests, that a person has got it, or has not got it. You can prove — objectively, not by making a “clinical diagnosis” — that X has neurosyphilis or does not have it; but you cannot prove, objectively, that X has or does not have schizophrenia or “clinical depression” or post traumatic stress disorder. Like most nouns and verbs, the word “disease” will always be used both literally and metaphorically. As long as psychiatrists are unwilling to fix the literal meaning of mental illness to an objective standard, there will remain no way of distinguishing between literal and metaphorical “mental diseases.”

RW: Psychiatrists, of course, don’t want to be pushed out of the picture. They want to hold on to schizophrenia as long as they can, and now depression and gambling, and drug abuse, and so on, are proposed as biological or genetically determined. Everything is thought to have a genetic marker, perhaps even normality. What do you make of this?
TS: I hardly know what to say about this silliness. Unless a person understands the history of psychiatry and something about semantics, it’s very difficult to deal with this. Diagnoses are NOT diseases. Period.

Psychiatrists have had some very famous diseases for which they have never apologized, the two most obvious ones being masturbation and homosexuality.

Psychiatrists have had some very famous diseases for which they have never apologized, the two most obvious ones being masturbation and homosexuality. People with these so-called “diseases” were tortured by psychiatrists — for hundreds of years. Children were tortured by antimasturbation treatments. Homosexuals were incarcerated and tortured by psychiatrists. Now all that is conveniently forgotten, while psychiatrists — prostitutes of the dominant ethic — invent new diseases, like the ones you mentioned. The war on drugs is the current psychiatric-judicial pogrom. And so is the war on children called “hyperactive,” poisoned in schools with the illegal street drug called “speed,” which, when called “Ritalin,” is a miracle cure for them.

Let me mention another, closely related characteristic of psychiatry, as distinct from the rest of medicine. Only in psychiatry are there “patients” who don’t want to be patients. This is crucial because my critique of psychiatry is two-pronged. One of my criticisms is conceptual: that is, that mental illness is not a real illness. The other one is political: that is, that mental illness is a piece of justificatory rhetoric, legitimizing civil commitment and the insanity defense.

Dermatologists, ophthalmologists, gynecologists, don’t have any patients who don’t want to be their patients. But the psychiatrists’ patients are paradigmatically involuntarily.

Dermatologists, ophthalmologists, gynecologists, don’t have any patients who don’t want to be their patients. But the psychiatrists’ patients are paradigmatically involuntarily.

Originally, all mental patients were involuntary, state hospital patients. That concept, that phenomenon, still forms the nucleus of psychiatry. And that is what is basically wrong with psychiatry. In my view, involuntary hospitalization and the insanity defense ought to be abolished, exactly as slavery was abolished, or the disfranchisement of women was abolished, or the persecution of homosexuals was abolished. Only then could we begin to examine so-called “mental illnesses” as forms of behavior, like other behaviors.

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Survivors of Psychiatry

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Image credit: Alex Widdowson ©2012


Belgium, 1992. I completed my psychiatric residency. Five years of training gives me, among other things, a good psychodynamic foundation and an exposure to a range of psychiatric medications, including the newest ones being touted as, ironically, both scientific and miraculous. In my heart there is an eagerness to learn more, a penchant towards borderline pathology and a desire to relieve souls in suffering.

Since then I have journeyed through very different places: from hospitals and private practice in the European system of universal healthcare (albeit only for its citizens), to the streets, prisons, outpatient services and psychiatric emergency rooms of Los Angeles, a multicultural jungle, and a place where extremes either collide or else ignore each other completely.

Although I was a young psychiatrist convinced of the effectiveness of psychotherapy, there was definitely something thrilling in the ‘Decade of the Brain’ and its ’intelligent molecules’, which were presented as having no serious side effects. Not only would they be a cure for debilitating chronic illnesses but the molecules themselves (or the imbalance thereof) would be the long-awaited scientific explanation of mental illness itself. Suddenly, my new profession, whose ethics were so often questioned (remember the Gulag and lobotomies) and challenged as to its ‘real’ scientific value (Popper and psychoanalysis), acquires the seal of scientific respectability.

Almost overnight, the psychiatrist-prescriber becomes the expert of the new sciences of chemical imbalance, methodical classifications of illnesses and evidence-based treatment. The new science of human consciousness has arrived, a modern discipline where pesky existential questions seem obsolete. In the euphoria of the late twentieth century, pharmaceutical companies and psychiatrists discover one another and embark on a risky love affair. Lavish international conferences are organized during which prestigious panels of experts attempt to give concrete meaning to the inexplicable and in doing so propel the exponential expansion of the market base of the drug industry.

Clinicians (of which I am one) and academics, in a surprising moment of “méconnaissance intéressée”  in the words of Derrida, do not seem (or want) to be aware of the potential conflicts of interest in this thrilling adventure. Very quickly, both international psychiatric research and physician’s education become more and more dependent on money from pharmaceutical lobbies.

In medical school, psychotherapy starts to look outmoded. Young doctors are amazed (and perhaps reassured) by the molecular and genetic versions of human passions, and build themselves a new identity, that of the psycho-pharmacologist. The psychosocial model in force in the mental health community no longer seems to apply to a ‘modern’ psychiatry. In libraries, Freud and Frankl are taken off the medicine shelves and end up in the literature department with Albert Camus and Jean Paul Sartre.

At the same time, other voices are speaking up – those of the mental health patients themselves and their families. As part of the wave of civil rights movements that were rushing through America in the 1960s and ‘70s, patients and former patients, some calling themselves “Survivors of Psychiatry”, demand an active role in their own care. “Nothing about us without us”, is their war chant. Under their influence, terminology changes, too. The word ‘patient’, with its implication of suffering and passivity gives way to ‘users’, ‘clients’, and ’consumers’ in keeping with the more active participation of a patient in his or her own treatment. Importantly, this new terminology is also more in sync with a capitalist world where ‘care’ becomes more than ever an object of consumption with profit its underlying goal.

It is into these turbulent waters that I dove when, in 1999, I came to the United States to continue my interest in borderline personality disorders (BPD). Curiously, in these times of medical exhilaration, this group of patients seems to balk at any reductionist classification. BPD doesn’t respond to the “pill-to-heal-everything” approach. BPD patients’ long resistance to both psychiatric and psychoanalytic treatment has earned them a history of rejection and disqualification, the alleged reason being that these patients are difficult, manipulative, or worse, not really sick. It appeared as if only a categorical diagnosis or a treatment validated by modern science could bestow on these sufferers the seal of authenticity.

In my new American reality, I am on the frontlines observing how theoretical, political and social contexts can affect the expression or the occurrence of a symptom, its recognition and what we choose to do (or not do) about it. With BPD patients in particular, the fact that there is no pill to treat them encourages some ER staff members to discharge them swiftly without really addressing their issues. Verbal complaints and “scratches” that may lead to necessary treatment in my previous home of Belgium will generally bring disdain in a US emergency room, where much deeper self-mutilations is required in order to hold the patient long enough to initiate therapeutic engagement . So, the self-inflicted wounds of Otto Kernberg’s and Marsha Linehan’s patients in the US somehow appear more threatening and bloodier than the ones I observed in my small European country. It seems necessary to shout louder in the US in order to have our healthcare system decide finally to take care of you.

Social and political contexts also influence the writing of a prescription. An antipsychotic medication identified as “very safe” in Belgium, might suddenly bring a lawsuit in the United States, due to the fact that a rare side-effect is emphasized in a ‘Black Book’, a tome sold primarily to lawyers.

During my second residency, I was lucky enough to be trained in cognitive and behavioral therapies (CBT). Contrary to the naïve and/or arrogant belief of the psychoanalytical circles in which I did my original training, I realized how well these techniques can work and how easily teachable they are. I have been impressed by the willingness of practitioners of cognitive therapy to prove the effectiveness of their methods, thus gaining ‘scientific’ legitimacy and resulting financial reimbursement.

Forced to question my theories and techniques, I discovered research that suggests that, for a majority of conditions treated in psychotherapy, all the major modes of psychological treatment produce similar outcomes . In fact, this research suggests that only 8% of the variance is due to the type of therapeutic technique, while 70% is due to the overall effect of treatment itself, such as the factors of empathy, a good working relationship between the therapist and his or her client etc. The residual 22% of the variance remains unexplained.

Fascinated by these oddly un-‘modern’ results, I felt reassured in my belief that the individual caregiver’s role is central to the therapeutic process. After all, isn’t modern psychiatry but a new iteration of the age-old combination of witches and wardens?

While the paths of neuroscience and psychology may seem to diverge, an expert interested in both disciplines, Eric Kandel, is trying to force a dialogue between them. In the early 2000s, armed with his recent Nobel Prize for research in neuroplasticity, he proposed a “biological” legitimacy to psychotherapeutic techniques . He has helped us to understand how environment affects the development of our brains as much or more than a chemical molecule does.

If only something biological gives legitimacy to a ‘modern’ treatment, then we must recognize that the interaction between two human beings is also a biological treatment , because it affects our brain’s function and development. For example, the environment may affect the way our genome is translated into proteins, building blocks of cellular receptors essential to our learning mechanisms .

Along this line, researchers have started studying the interactions between the modalities of attachment and molecular genetics , and a new Society of Neuro-psychoanalysis has been created. In borderline patients, neuro-imaging studies have discovered abnormalities specific to their struggles . This is apparently what is needed for science to finally recognize them as real patients.


50 shades of normality

Breaking news from a mental institution

This post was from the site Rethinking psychiatry. Read more for inspiration!

Image credit: Alex Widdowson ©2012

The sound of not being there

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reblogged from: brokenbutbeingrepaired

**Trigger Warning-Descriptions of Self injury**

Why is D.I.D a controversial diagnosis???

we/me do not exist in the eyes of many and it hurts

Why aren’t diabetes or asthma controversial?

In the area of the UK I live in, it is impossible to find an NHS psychiatrist who believes in D.I.D or other Dissociative Disorders. Eh? Believes in? It is not a doctors job to believe in a symptom / illness, surely?
Isn’t it their job to asses symptoms and use their findings to make a diagnosis before offering appropriate treatment?

I mean, imagine your Dr doesn’t believe in diabetes, or asthma. Then, imagine you are hypoglycaemic or in the midst of an asthma attack and the medical professionals there to help tell you they don’t believe in the symptoms you are displaying.
Is a diabetic or asthmatic meant to just curl up and die in the corner?

This pi**es us off so much.

To have had to pay privately to be assessed and diagnosed, to be unable to rely on services our taxes pay for in order to be supported, to look online for information and find “controversy” and D.I.D intertwined amongst the “D.I.D does not exist” in all search engines.

Yes, there are people who are wrongly diagnosed with D.I.D. In my view, many with D.I.D are incorrectly diagnosed with various other disorders and made to endure ‘help’ that is damaging.

When diagnosed with D.I.D, it is down to the individual (you know what I mean, hopefully) to research terms like attachment theory, structural dissociation, and so much more.
It is down to that individual to track down a therapist who is willing to a)believe in D.I.D b)be prepared to work with a D.I.D client for years.

I don’t know of anywhere that is available in the UK on the NHS. I know that where I live there is absolutely no such support available.

Why should I have to spell ‘d i s s o c i a t i v e i d e n t i t y d i s o r d e r ‘ before giving the ICD10 codes and DSMIV codes to health professionals?
Why should I then be told that “I’ve never heard of it” and “Oh, we don’t believe in that”.
When looking through my local NHS trusts website, I put Dissociative Disorders into their search box and came up with nothing, except a leaflet on personality disorders which mentioned D.I.D being a personality disorder.I emailed them regarding this and apparently it will be changed when they update their leaflet. Who knows if/when the leaflet will be updated.

I cannot access support from the agencies we’re supposed to rely on.

Yes, I am very fortunate to have a fantastic therapist and really good back up from the Dr who asessed and diagnosed me (privately) . What if K was no longer able to work with me? There is no plan B since I asked all the right places and the only recommendation I got was K which on one hand is reassuring but it fills me with fear over what we’d do without her.

Why should going past the buildings where I accessed the CMHT (community mental health team) trigger panic attacks? Why should I have the fear that if one time, the self injury goes too far, I can’t go to A+E (which would result in either admittance to the Psych ward or referral to the CMHT). Wounds that need sutures don’t get sutured since my local A+E is such a frightening place where dignity, respect and care have been forgotten about. The last time I was there, requiring treatment for selfinjury wounds, the curtains around the bay were open at all times so other patients and their visitors saw and heard things that every part of me works so hard in hiding. What if a wound were arterial, though? let’s not think about that


The sound of breathing in and out

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Can Mindfulness Meditation Really Reduce Pain and Suffering by 90 percent?

by danny on Tuesday, November 19, 2013

Claire stared at the computer screen before cocking her head slightly to one side. She winced as a sharp pain angled its way through her neck and down her left arm. Her fingers went numb and then began to throb. Claire’s youthful good looks dissolved and she suddenly looked twenty years older. She stretched her arm and slowly began rubbing her neck to loosen the muscles. Her shoulders and neck had cramped up, making her whole upper body look tense and contorted. She reached for a glass of water and gulped down two more painkillers.

Why won’t this pain just stop? Why won’t these blasted painkillers work any more? They’re useless. I’m so sick and tired of this.

Three years previously Claire had been injured in a car crash and suffered two broken ribs, a fractured wrist and whiplash. Her ribs and wrist had healed completely within three months, but the after-effects of her whiplash refused to go away. The doctors were puzzled by her pain. Several scans had shown that her neck had completely healed, but the pain stubbornly remained. It was worse if she stayed in one place for too long. After twenty minutes, sharp jagged pains would arc up and down her neck. When she finally did move, she would feel stiff and achy all over.

Claire felt increasingly trapped and broken. Her doctor had prescribed several courses of physiotherapy without any long-term success. Now she was forced to continually take painkillers and anti-inflammatory drugs. They worked, more or less, but often left her feeling washed out and jaded. They were OK for stubborn ‘achiness’, but did nothing for the frequent sharp twinges of pain. Lately, her doctor had begun suggesting antide- pressants to lift her mood. Her response was always the same: ‘I’m not depressed,’ she’d snap. ‘I’m angry because that man who drove into me has taken my life away. I used to dance all night. Now I can barely walk!’

Experiences like Claire’s are not confined to injuries such as whiplash, but are common across a range of diseases. Conditions such as ‘bad back’, migraine, chronic fatigue syndrome and fibromyalgia can all cause pain long after the original injuries have healed or without any obvious cause that shows up on scans or tests. And even when there is a clear physical cause, as with illnesses like arthritis, heart disease or cancer, the pain often comes and goes without any apparent rhyme or reason. Doctors then feel forced to prescribe long-term courses of painkillers, but these can have side effects such as memory loss, lethargy and even addiction.

Claire and millions of others exist in a world of suffering; a place where even the simplest of tasks can amplify their pain. This often leads to anxiety, stress, depression and exhaustion, each of which serves to further enhance suffering in a downward spiral. Such vicious cycles are driven by newly discovered psychological forces that underlie the perception of pain. And crucially, this discovery offers a wholly new approach to the management of pain and illness that has the potential to transform suffering.



The commonsense view of pain is that it arises from damage to the body. This attitude was formalised in the seventeenth century by the French philosopher René Descartes with his ‘rope-pull’ model of pain: just as pulling a rope in a church steeple rings a bell, Descartes thought that damage to the body is a tug that causes the awareness of pain in the brain. For centuries after Descartes, doctors regarded pain in a similar light. The intensity of pain was thought to be directly proportional to the degree of damage to the body, which would mean that if different people had the same injury they would experience the same amount of pain. If no obvious physical cause was found, the patient would be regarded as malingering or making it up.

Since the 1960s, science has come to accept another model of pain known as the ‘Gate Theory’ developed by Ronald Melzack and Patrick Wall.1 They suggest that there are ‘gates’ in the brain and nervous system that, when open, allow you to experience pain. In a sense, the body sends a continuous low-level ‘chatter’ of pain signals to the brain, but it is only when the gates are opened that the signals reach your conscious mind. These gates can also close, which is what happens when your pain lessens or fades away. Opening and closing these pain gates is a phenomenally complex process. Although the details are still being worked out, it is clear that pain is far more subtle and complex than the traditional idea of damage signals being sent to the brain which are then passively felt. Pain is a sensation, which means that it is an interpretation made by the brain before it is consciously felt. To make this interpretation, the brain fuses together information from the mind as well as the body. In practice, this means that the thoughts and emotions flowing through your mind, both conscious and unconscious, have a dramatic effect on the intensity of your suffering. Not without reason did the ancient Greek philosophers consider pain to be an emotion.



Suffering occurs on two levels. Firstly, there are the actual unpleasant sensations felt in the body – this is known as ‘Primary Suffering’. This can be seen as the ‘raw data’ that is sent to the brain from, say, an injury, an ongoing illness or changes to the nervous system itself (this is believed to lie, at least partly, behind such conditions as chronic pain syndrome and phantom limb syndrome). Overlaid on top of this is ‘Secondary Suffering’, which is made up of all the thoughts, feelings, emotions and memories associated with the pain. These might include anxiety, stress, worry, depression and feelings of hopelessness and exhaustion. The pain and distress that you actually feel is a fusion of both Primary and Secondary Suffering.

This insight is crucial because it reveals a path away from suffering. For if you can learn to tease apart the two flavours of suffering, you can greatly reduce – or even eliminate – your pain and distress. This is because Secondary Suffering tends to dissolve when you observe it with the mind’s compassionate eye. Mindfulness allows you to see the different elements of pain laid out in front of you. And when you see this vista, something remarkable begins to happen: your suffering gradually begins to subside and evaporate like the mist on a summer’s morning.

It’s important to understand that although the sensation of pain is created by the mind, your suffering is still real. You really do feel it. It exists and it can be genuinely overwhelming. But once you understand the underlying mechanisms of pain, you can begin to temper its power and the hold it has over you.

To go back to Claire, had she been asked to look inside herself a little more closely she would have realised that there was not one single ‘thing’ that she could label as an ‘ache’ or as a ‘pain’. Both were ‘bundles’ of different feelings that were constantly changing; becoming either more or less intense. There was the underlying unpleasant ‘tightness’ of the muscles and tendons in her neck, which were twisting her vertebrae slightly out of alignment and creating the most pronounced of her painful feelings. There were also twinges of outright pain – which felt like sharp spikes of electricity running through her muscles and down into her arm. And then there were patches of ‘numbness’ in her left arm and hand. These would alternate with pins and needles. Those were the obvious sensations of pain. This was her Primary Suffering.

But there were other feelings too – powerful emotions and disturbing thoughts that would frequently sweep across her mind, often with no apparent rhyme or reason. Stress, worry and exhaustion had become a way of life. Troubling thoughts constantly nagged at her soul: Why won’t this just stop? The doctors must have missed something, surely? Maybe I’m going to end up a cripple, or even dead. Are they too afraid to tell me? Such thoughts and emotions were constantly bubbling away in the background. And while they were often less obvious than the nagging feelings of pain, ultimately they were far more significant because they were central to the way that her mind interpreted and felt the raw feelings of pain. In a sense, they controlled the intensity or ‘volume’ of her pain. This was Secondary Suffering; and Claire had it in spades.

Claire’s Secondary Suffering had its roots in the five days she spent in hospital after her accident. They were the worst of her life. She was in considerable pain and on a morphine drip for the first twenty-four hours. She could cope with the physical pain – just. Far worse, however, were her turbulent emotions: her fears and worries for herself and the future. Neither she nor the doctors could predict the outcome of her neck injuries. Would she be partially paralysed? Would she be in pain for the rest of her life? There was also a sense of anger mixed with bitterness. The man who crashed into her didn’t appear to care. He just walked away from the accident with no cuts or bruises at all. He’d been drinking, but was just inside the legal drink–drive limit. Was he insured? It turned out he wasn’t. Every time she thought about it, Claire’s anger boiled over. Such thoughts and overwhelming emotions constantly washed across her mind. It was mental pain and just as real and tormenting as her physical injuries.

She lay in her hospital bed at night crying quietly to herself. She was wracked with fears and worries for the future, and ‘what ifs’ filled her mind. If only she had left home a minute or two later, then none of it would have happened. She’d had a feeling something was wrong before she had left home. Why hadn’t she waited just a few minutes longer?

After the accident and the subsequent months of physiotherapy, a new emotion was added to the list: depression. Claire refused to believe that she was depressed, but it was there none the less, gnawing away at her in the background. It wasn’t an all- consuming depression. It simply drained her of all energy and enthusiasm for life. Such powerful emotions as anxiety, fear, anger, worry and depression can feed into the mind’s perception of pain. Other feelings, too, can have an incredibly strong effect. Feeling tired and overwhelmed, fragile and broken, stressed and anxious, can all magnify suffering and tip you into a downward spiral. How often has the intensity of your suffering increased when you felt anxious, stressed, exhausted or sad? These emotions act like amplifiers in the mind’s pain circuits. They can open the floodgates of suffering.

The effect of such emotions can be observed with a brain scanner. Work at Oxford University,7 for example, shows the significant impact that even mild levels of anxiety can have on pain. Scientists at the university’s Department of Clinical Neurology induced low-level anxiety in a group of volunteers before burning the back of their left hand with a hot probe. As anxiety built, you could see the waves of emotion sweeping through the volunteers’ brains. This primed areas of the brain that collectively make up the ‘pain matrix’. It was almost as if the volunteers’ minds were turning up the volume on their pain amplifiers ready to ‘hear’ its first ‘notes’, so that they could take action to protect themselves. This meant that when the skin of the anxious volunteers was actually burned, they experienced far more pain and suffering than the ‘non-anxious’ volunteers. You could see this extra pain represented in the brain scans too. As the Oxford neuroscientists noted, anxiety primes the ‘behavioural responses that are adaptive to the worst possible outcome’. In other words, anxiety and other powerful ‘negative’ emotions prepare the body to sense pain quickly and with great intensity.

The reverse is also true. Reducing anxiety, stress, depression and exhaustion can lower the perception of pain and even eliminate it completely. This is one of the main routes by which mindfulness helps reduce suffering. Mindfulness soothes the mind’s perception of pain – essentially Secondary Suffering – by replacing it with a sense of peace and wholeness.

Neuroscientist Fadel Zeidan and his team at Wake Forest University School of Medicine in America decided to investigate this effect using scanners to map activity in different parts of the brain.8 They did this by exploiting a curious quirk of brain anatomy. Every part of the body is reflected in a specific part of the brain known as the primary somatosensory cortex. So if the sole of your left foot is brushed with a feather, an area of the primary somatosensory cortex lights up; if you feel a pain in your lower back, a different part becomes active. Neurosurgeon Wilder Penfield charted this brain region and produced a ‘map’ that reflects the human body overlaid on the brain (see illustration below). It was termed the cortical ‘homunculus’.

Homunculus Graphic from Chap 2 v2

Fadel Zeidan and his team reasoned that if mindfulness affected the perception of pain, then this should be visibly reflected in the level of activity in the corresponding regions of the primary somatosensory cortex. To test this, Zeidan studied the perception of pain in a group of students. The students first had the back of their right calf burned with a piece of hot metal while their brain was scanned with the latest functional Magnetic Resonance Imaging (fMRI) scanner. Each was then asked to rate both the intensity and unpleasantness of the pain. If pain was music, ‘intensity’ would be the volume and ‘unpleasantness’ would be the level of emotion it aroused. As expected, when the students’ legs were burned the ‘right calf’ region of their primary somatosensory cortex lit up as the pain swept over them.

The students were then taught mindfulness meditation and the experiment was repeated. The results could not have been more different second time around. Activity in the ‘right calf’ region of the primary somatosensory cortex had diminished to such a degree that it had become undetectable. But not only that. Meditation increased activity in regions of the brain related to the processing of emotion and of cognitive control – areas where the sensations of pain are actually interpreted and ‘built’. These brain areas modulate the sensations of pain and give it ‘meaning’ before it is consciously felt. What’s more, experienced meditators (those who scored higher on a standard scale of mindfulness) tended to have enhanced activity in these regions and to experience less pain. That is, they tended to devote more brain power in this region to moderating the pain-related information – and to, in effect, turning down its ‘volume’.

Zeidan’s co-worker Dr Robert C. Coghill explains:

These areas all shape how the brain builds an experience of pain from nerve signals that are coming in from the body. Consistent with this function, the more that these areas were activated by meditation, the more that pain was reduced. One of the reasons that meditation may have been so effective in blocking pain was that it did not work at just one place in the brain, but instead reduced pain at multiple levels of processing.

And what of the students’ conscious experience of pain? On average they experienced a 40 per cent reduction in pain intensity and a 57 per cent lessening of pain ‘unpleasantness’. Perhaps the most surprising thing was the amount of practice required to achieve this level of pain relief: just four training sessions of twenty minutes each. Remarkable though these results were, they masked something even more intriguing. The more accomplished meditators suffered far less than these averages might suggest. They experienced a reduction in pain intensity of 70 per cent and its unpleasantness was reduced by 93 per cent. This meant that it could barely be felt and hardly bothered them at all. Overall, said Zeidan, mindfulness produced a greater reduction in pain than standard doses of morphine and other pain-relieving drugs.


Loosening the bonds of pain

Secondary Suffering can be seen as resistance to pain. It is entirely natural to struggle against and resist pain with all of your might. You want to eliminate it. Stamp on it. Do anything at all to get rid of it. This is absolutely understandable. But what if this was also precisely the wrong approach? What if, in your bid to eliminate pain, you were actually creating far more of it instead? This is the lesson from Zeidan’s research and from many other studies too. And this holds true not just for pain, but for many other disease symptoms as well. Stress, exhaustion and depression can all be made far worse through resistance.

But if the act of resisting pain can make it worse, the converse is also true. Acceptance of your pain can actually diminish it – and might even get rid of it completely. Allow us to explain this seemingly outrageous idea. Neuroscientists have a saying: ‘What we resist persists.’ In other words, if you resist the messages that your mind and body are sending you, those messages will keep on being dispatched (and felt) until you accept them. This holds true not only for messages of pain, but also for thoughts, feelings, emotions, memories and judgements. If you mindfully accept (or feel) these messages, they will have done their job and will tend to melt away of their own accord.

Mindfulness meditation creates a sense of safety, of space, in which you can begin to tentatively explore the raw sensations of pain and, as such, it is the vehicle through which you can begin to accept these messages. And when you do so, you will often find that pain waxes and wanes quite dramatically. There can be long moments of normality followed by flickers or spikes of pain. There are often different sensations too. Some are hot. Others cold. Some feel ‘tight’, others throb, while still others feel sharp or stabbing. Not all are completely unpleasant. The different sensations often rise and fall like the waves on the sea. They constantly change in character and intensity. By exploring each of these different sensations, moment by moment, you come to accept that they are like black clouds in the sky: you can watch as the sensations arise, drift past and disappear again. Your mind is like the sky and individual thoughts, feelings, emotions and sensations are like different types of cloud. So in a sense, mindfulness teaches you to observe the weather without becoming embroiled in it. And no matter what happens, the sky – your mind – remains untouched by it.

It is important to realise that mindful acceptance is not resignation to your fate. It is not the acceptance of the unacceptable. It is simply the acceptance of the situation as it is, for now, at least. It is a period of allowing, of letting be, of non-resistance, so that you cease to struggle. And when this struggle ceases, a sense of peace takes its place. Secondary Suffering then progressively diminishes. Often as not, Primary Suffering will begin to do so too.

We can explain this to you in minute detail. We can cite numerous scientific trials that prove the point. We could even show you scans of your own brain as it ‘builds’ the sensations of pain from all of your thoughts, feelings and emotions – but only when you have experienced the power of mindfulness for yourself will you truly believe it.

This is why it is called a practice. Accepting pain can be difficult. It’s just better than the alternative, which is to live in a state of perpetual suffering.

Countless participants on our Breathworks courses have discovered this for themselves. Claire was one. She found that when her neck began to hurt she was also assailed by fear, anger, stress, sorrow, hopelessness, despair and exhaustion. So not only did she feel the initial unpleasant sensations in her neck, but she was also swamped with yet more suffering. It was almost as if she was struck with an arrow, and when she reacted to it she was then hit by a second one. Now she had to bear the pain of two arrows – that from the second being caused by resistance to the first. It is an entirely natural response. In fact, in cases of acute, rather than chronic, pain, it might even be the best response because it’s a powerful driving force to take yourself out of danger. When it comes to chronic pain and illness, however, it is often precisely the wrong solution because it simply compounds your suffering. And, of course, it can then seem as if you’re pierced not by two arrows, but by many, many more.

Accepting the sensations of Primary Suffering allows the Secondary Suffering to take care of itself – and to progressively diminish. Claire discovered that she could resist pain for days or even weeks. She could distract herself with alcohol, cigarettes and food. She could squash the pain with powerful drugs. If those failed, she could ignore the pain – for a while, at least. But all this came at a cost: the rest of her life. She discovered that in ignoring and walling off the pain she had also isolated herself from all that is wonderful and precious about life. The world became increasingly wan and grey. Food lost its flavour and texture. She no longer laughed or cried. Her love life declined into irrelevance. All this meant that when she could no longer maintain the struggle, she simply crashed and burned. So not only did the pain return, but, with all of the things that normally sustained her love of life having evaporated, she was left feeling fragile and broken. No wonder her doctor wanted to prescribe her antidepressants.

After three years of struggling, Claire embraced mindfulness – not because she believed that it would work, but because she was desperate. And when she began to mindfully explore the sensations of pain, something remarkable and counter-intuitive began to happen. Not only did the pain begin to subside, but she began to experience all of the good things that had been squeezed out of her life too. It opened the door to a wealth of emotions such as happiness, love, compassion and empathy, as well as sadness. Claire realised that life is bittersweet, and when she let go of expecting it to be either wholly wonderful or truly distressing and to hold in an honest heart a delicate mixture of the two, she felt increasingly relaxed and open. Through facing up to and becoming sensitive to her own predicament, she became a happier and more centred person with greater empathy for others. She also began to heal.


Taken from our new book Mindfulness for Health: A Practical Guide to Relieving Pain, Reducing Stress and Restoring Wellbeing by Dr Danny Penman and Vidyamala Burch

Buy from Amazon UK


‘A beautiful and compassionate book, Mindfulness for Health will put you back in touch with the extraordinary person you already are’ Professor Mark Williams, University of Oxford

‘This book provides an extremely effective and elegant mind-body approach to healing . . . Highly recommended’ Jon Kabat-Zinn, PhD, author of Full Catastrophe Living and Coming to Our Senses

‘In a world of much suffering this book is a gift of wisdom and practical help’ Professor Paul Gilbert, PhD, OBE, author of The Compassionate Mind



1. Wall, Patrick D. & Ronald Melzack, The Challenge of Pain (Penguin Books, 1982), p. 98; Melzack, R. Wall, p. D. (1965), ‘Pain Mechan- isms: a new theory, Science, 150(3699), pp. 371–9.

2. Cole, Frances, Macdonald, Helen, Carus, Catherine & Howden-Leach, Hazel, Overcoming Chronic Pain (Constable & Robinson, 2005), p. 37; Bond, M., Simpson, K., Pain: Its Nature and Treatment (Elsevier, 2006), p. 16, offers an alternative definition from the International Association for the Study of Pain as acute pain (lasting less than one month), sub-acute pain (lasting one to six months) and chronic pain (lasting six months or more).

3. ‘Health Survey for England 2011’, Health, social care and lifestyles, Chapter 9 Chronic Pain, The Health and Social Care Information Centre (NHS) 20 December 2012,

4. Gaskin, Darrell J. & Richard, Patrick (2012), ‘The Economic Costs of Pain in the United States’, Journal of Pain, 13(8), p. 715.

5. ‘Health Survey for England 2011’, Health, social care and lifestyles, Chapter 9 Chronic Pain, The Health and Social Care Information Centre (NHS) 20 December 2012,

6. NOP Pain Survey (2005), 23–25 September, on behalf of the British Pain Society.

7. Ploghaus, Alexander, Narain, Charvy, Beckmann, Christian F., Clare, Stuart, Bantick, Susanna, Wise, Richard, Matthews, Paul M., Nicholas, J., Rawlins, P. & Tracey, Irene (2001), ‘Exacerbation of Pain by Anxiety Is Associated with Activity in a Hippocampal Network’, Journal of Neuroscience, 21(24), pp. 9896–903.

8. Zeidan, Fadel, Martucci, Katherine T., Kraft, Robert A., Gordon, Nakia S., McHaffie, John G. & Coghill, Robert C. (2011), ‘Brain Mechanisms Supporting the Modulation of Pain by Mindfulness Meditation’, Journal of Neuroscience, 31(14), pp. 5540–48. See also the accompanying comments regarding morphine effectiveness by Fadel Zeidan of the Wake Forest University School of Medicine at


The sound of swan song

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How much do you know about the brain? consisting of 100 billion neurons that each can connect to from 1000-10000 others, it hides the secrets of our being, and the path to enlightenment. The most fascinating feat of this grey-wrapped supercomputer, is how it can be influenced by the world around us. Lately, I have read an amazing book about dissociation where I found information about near-death experience. The author explained how”near-death” sound like certain experiences people have when they dissociate. And now I found even more information about the subject, on another blog. Enjoy!  

More information:

(The stranger in the mirror)

 The New York Times
  • The Washington Post
    A Flight of Mind, The Act of Dissociation Can Protect Children Emotionally From Trauma, but Repeated Use May Cause Lasting Harm

  • Yale Scientific
    The Shattered Self: Understanding Dissociative Disorders

  • Clinical Psychology News
    Are Dissociative Disorders Unusual or Ubiquitous?

  • Science News
    Interviews Unmask Multiple Personalities

  • Psychiatric Times
    Advances in Diagnosis and Treatment of Dissociation: The SCID-D in Clinical Practice
  • Many Voices
    Dissociation and Trauma: A Professor’s Perspective

The brain’s swan song: hyperactivity near death

TL;DR: Near-death experiences are ‘electrical surge in the dying brain? …But dude, what does it all mean?

Swan-Song-detail-2 copy

We often think of death as flipping a switch: one minute you’re there, next all lights go out. But this is a simple caricature of the dying process: sparks of activity still linger in the brains of those undergoing cardiac arrest, in whom both breath and heartbeat flutter and abruptly halt. Researchers have long thought that these sad, sparse bouts of activity characterize the brain’s descent into permanent unconsciousness. However, a new study suggests that the complete opposite – a surge of heightened connectivity – paradoxically marks the final step towards death. Although a long (and I mean LOOOONG!) stretch, the authors propose that the observation may partially underlie the enigmatic near-death experience(NDE).

Reports of NDE are nothing new. The luckily revived few often re-emerge from “the other side” with realer-than-real stories of long tunnels, intensely vivid visions and meetings with those bygone. NDEs are treated by some as proof of an afterlife, or by others, the existence of a “mind” beyond the brain and body. Spiritual connotations aside, the biological underpinnings remain mysterious, although abnormal dopamine and glutamate transmission may be involved (and probably everything else – the brain IS dying!). Here, the authors turned the focus away from individual neurotransmitters, and instead asked: after the heart stops, what happens to the oscillating waves of neural activity in the brain?

Jimo Borjigin et al. 2013. Surge of neurophysiological coherence and connectivity in the dying brain. PNAS. doi: 10.1073/pnas.1308285110 

Researchers fitted 9 rats with electrodes to measure their brain waves – rhythmic brain activity generated by feedback connections between large numbers of neurons that differ in frequency. Alpha activity, for example, is often detected during relaxed wakefulness, while the faster theta activity is linked to cognitive processing. Gamma waves – the most recently discovered component – are particularly interesting to cognitive neuroscientists (and pseudo-science marketers) studying consciousness.

Why? The low gamma band, oscillating at 25-55Hz, has long been linked to visual consciousness, or the perception and awareness of visual stimulation. It seems to promote associative learning, and is also present during REM sleep (and slow wave sleep/deep sleep as well), which involves dreaming and complex visuals. Gamma bands also appear during transcendental mental states, as measured in Tibetan monks told to generate feelings of compassion as they meditated. Some even propose that gamma bands are behind the heightened sense of consciousness and bliss following a meditative bout. Sounds pretty magical, eh? As things goes, it’s also a tough band to measure with EEG – in fact,there are even skeptics who doubt its existence.

Screen Shot 2013-08-14 at 11.28.24 AM

Back to the study. After fitting rats with electrodes, researchers monitored changes in each brain wave component as the rats passed through three states: awake, under ketamine-induced anesthesia and after cardiac arrest. Unsurprisingly, after the loss of heartbeat and oxygen flow, the strength (“power”) of all brain wave frequencies measured tanked – except for low gamma bands, which spiked in power and became the dominant frequency in the spectrum as you can see above.

After cardiac arrest, gamma waves also showed higher levels of synchrony – that is, the neural activity in various brain regions became more “in tune”, even compared to an awake state. This high level of coherence between different brain regions is often associated with a highly “aroused” brain – that is, a state in which high levels of information processing may occur. Thus the authors concluded that the brain might exist in a hyper-conscious state for tens of seconds after the heart stops.

Sounds a bit too philosophical? I feel you. Where to start? First, the data really doesn’t tell us much. We already know that for a brief time following clinical death (which will most likely be redefined in the future), the brain remains active – so that’s nothing new. The increase in gamma wave power and synchrony is intriguing, especially since it appeared in all 9 rats (but really, just 9?), and the magnitude of the changes were large. But to link those changes to hyper-consciousness (what does that even mean?) and near-death experiences (NDEs) is going a step too far.

For one, there is absolutely no direct proof that gamma waves reflect NDEs. It has never been recorded in people there-and-back-again. While it’s true that high power gamma activity is often measured during conscious brain activity (and dreaming), its presence does not “lead to” conscious perception. Hence we can’t conclude, for example, that the rats were experiencing heightened awareness like NDEs – if they even have the ability to – because they show increased gamma oscillation. Along the same lines, higher gamma activity in the visual cortex does not necessarily mean there is more visual awareness and sensation. It may let you watch your life flash before your eyes, or it might just be a random quirk in the brain before all lights go out.

I’m not bashing research on consciousness. I just dislike interpretations that take data completely out of the realm of scientific discussion. I’d perk up if the authors repeated this experiment on people who have undergone cardiac arrest and experienced NDEs, and found the same pattern of changes in gamma waves. But even then it wouldn’t really tell us much. Now if only we had the ability to experimentally manipulate gamma (or any other) bands and “implant” an NDE in those still alive…

Note: I’d love for the EEG experts out there pitch in. How hard is it to measure and isolate gamma band from noise? What conclusions (if any) would you make out of this study?
Borjigin J, Lee U, Liu T, Pal D, Huff S, Klarr D, Sloboda J, Hernandez J, Wang MM, & Mashour GA (2013). Surge of neurophysiological coherence and connectivity in the dying brain. Proceedings of the National Academy of Sciences of the United States of America PMID:23940340

Antipsychotics and brain shrinkage

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Antipsychotics and Brain Shrinkage:
An Update

Joanna Moncrieff

June 19, 2013

Evidence that antipsychotics cause brain shrinkage has been accumulating over the last few years, but the psychiatric research establishment is finding its own results difficult to swallow. A new paper by a group of American researchers once again tries to ‘blame the disease,’ a time-honoured tactic for diverting attention from the nasty and dangerous effects of some psychiatric treatments.

In 2011, these researchers, led by the former editor of the American Journal of Psychiatry, Nancy Andreasen, reported follow-up data for their study of 211 patients diagnosed for the first time with an episode of ‘schizophrenia’. They found a strong correlation between the level of antipsychotic treatment someone had taken over the course of the follow-up period, and the amount of shrinkage of brain matter as measured by repeated MRI scans. The group concluded that “antipsychotics have a subtle but measurable influence on brain tissue loss” (1).

This study confirmed other evidence that antipsychotics shrink the brain. When MRI scans became available in the 1990s, they were able to detect subtle levels of brain volume reduction in people diagnosed with schizophrenia or psychosis. This lead to the idea that psychosis is a toxic brain state, and was used to justify the claim that early treatment with antipsychotics was necessary to prevent brain damage. People even started to refer to these drugs as having “neuroprotective” properties, and schizophrenia was increasingly described in neo-Kraeplinian terms as a neurodegenerative condition(2).

The trouble with this interpretation was that all the people in these studies were taking antipsychotic drugs. Peter Breggin suggested that the smaller brains and larger brain cavities observed in people diagnosed with schizophrenia in these and older studies using the less sensitive CT scans, were a consequence of antipsychotic drugs(3), but no one took him seriously. It was assumed that these findings revealed the brain abnormalities that were thought to constitute schizophrenia, and for a long time no one paid much attention to the effects of treatment. Where the effects of antipsychotics were explored, however, there were some indications that the drugs might have a negative impact on brain volume(4).

In 2005, another American group, led by Jeffrey Lieberman who headed up the CATIE study, published the largest scanning study up to that point of people with a first episode of psychosis or schizophrenia(5). The study was funded by Eli Lilly, and consisted of a randomised comparison of Lilly’s drug olanzapine (Zyprexa) and the older drug haloperidol. Patients were scanned at the start of the study, 12 weeks and one year later and patients’ scans were compared with those of a control group of ‘healthy’ volunteers.

imageAt 12 weeks haloperidol-treated subjects showed a statistically significant reduction of the brain’s grey matter (the nerve cell bodies) compared with controls, and at one year both olanzapine- and haloperidol-treated subjects had lost more grey matter than controls. The comparative degree of shrinkage in the olanzapine group was smaller than that in the haloperidol group, and the authors declared the olanzapine-related change not to be statistically significant because, although the result reached the conventional level of statistical significance (p=0.03) they said they had done so many tests that the result might have occurred by chance. In both haloperidol and olanzapine treated patients,however, there was a consistent effect that was diffuse and visible in most parts of the brain hemispheres.

The idea that schizophrenia or psychosis represent degenerative brain diseases was so influential at this point, that the authors first explanation for these results was that olanzapine, but not haloperidol, can halt the underlying process of brain shrinkage caused by the mental condition. They did concede, however, that an alternative explanation might be that haloperidol causes brain shrinkage. They never admitted that olanzapine might do this.

It seems as if Eli Lilly and its collaborators were so confident about their preferred explanation, that they set up a study to investigate the effects of olanzapine and haloperidol in macaque monkeys. This study proved beyond reasonable doubt that both antipsychotics cause brain shrinkage. After 18 months of treatment monkeys treated with olanzapine or haloperidol, at doses equivalent to those used in humans, had approximately 10% lighter brains than those treated with a placebo preparation.(6)

Still psychiatrists went on behaving as if antipsychotics were essentially benign and arguing that they were necessary to prevent an underlying toxic brain disease (Jarskoget al 07 Annual review). Andreasen’s 2011 paper was widely publicised however, and it started to be increasingly acknowledged that antipsychotics can cause brain shrinkage. Almost as soon as the cat was out of the bag, however, attention was diverted back to the idea that the real problem is the mental condition.

Later in 2011 Andreasen’s group published a paper that reasserted the idea that schizophrenia is responsible for brain shrinkage, in which there is barely a mention of the effects of antipsychotics that were revealed in the group’s earlier paper(7). In this second paper, what the authors did was to assume that any brain shrinkage that could not be accounted for by the method of analysis used to explore the effects of antipsychotic treatment must be attributable to the underlying disease.
The way they had analysed drug treatment in the first paper only looked for a linear association between antipsychotic exposure and changes in brain volume, however. A linear analysis only detects an association that is smooth and consistent- in other words an association in which brain volume shrinks by a consistent amount with each increment in antipsychotic exposure. The total effect of drug treatment may not follow this pattern however. It seems from other evidence that there is a threshold effect whereby being on any amount of an antipsychotic has the greatest relative effect, with a levelling out of the impact as duration of exposure reaches a certain level.(8) In any case, without a comparison group which has not been medicated, a virtual impossibility in this day and age, it is simply not possible to conclude that the whole effect is not drug-induced.

The latest paper by this research group replicates the findings on antipsychotic-induced brain shrinkage, but also claims that brain volume reduction is related to relapse of the psychotic disorder(9). Relapse was defined retrospectively by the research team for the purposes of this particular analysis, however, and not at the time the study data were collected. Moreover, the definition used does not refer to any significant change in functioning, but only to a deterioration in the severity of symptoms. But the group’s previous analysis of severity of symptoms, using data collected at the time, found that severity had only a weak association with brain volume changes, and moreover that symptom severity was correlated with antipsychotic exposure.(1)

The most recent analysis ignores the probable association between antipsychotic treatment intensity and relapse, but it seems likely that people undergoing periods of ‘relapse,’ or more accurately deterioration of symptoms, would be treated with higher doses of antipsychotics. If this is so, and the two variables ‘relapse’ and ‘treatment intensity’ are correlated with each other, then the analysis is questionable since the statistical methods used assume that the variables are independent of each other.

So Andreasen’s group have found strong evidence of an antipsychotic-induced effect, which they have replicated in two analyses now. The predictive value of the severity of symptoms, on the other hand (which is essentially what relapse appears to define) is weak in the initial analysis, and in neither analysis was it clearly differentiated from drug-induced effects.

These researchers seem determined to prove that ‘schizophrenia’ causes brain shrinkage, although their data simply cannot establish this, as none of their subjects seem to have gone without drug treatment for any significant length of time. So even though their recent analysis once again confirms the damaging effects of antipsychotics, they conclude that the results demonstrate the need to make sure patients take, and do not stop, their antipsychotic medication. The only concession made to the antipsychotic-induced changes revealed is the suggestion that low doses of antipsychotics should be used where possible.

Yet other prominent psychiatric researchers have now abandoned the idea that schizophrenia is a progressive, neurodegenerative condition, and do not consider that Andreasen’s study provides evidence of this.(10) Bizarrely, Nancy Andreasen is a co-author of a recently published meta-analysis which combines results of 30 studies of brain volume over time, which clearly confirms the association between antipsychotic treatment and brain shrinkage (specifically the grey matter) and finds no relationship with severity of symptoms or duration of the underlying condition.(11)

What should antipsychotic users and their families and carers make of this research? Obviously it sounds frightening and worrying, but the first thing to stress is that the reductions in brain volume that are detected in these MRI studies are small, and it is not certain that changes of this sort have any functional implications. We do not yet know whether these changes are reversible or not. Of course the value of antipsychotics has been much debated on this site and elsewhere, and their utility almost certainly depends on the particular circumstances of each individual user, so it is impossible to issue any blanket advice. If people are worried, they need to discuss the pros and cons of continuing to take antipsychotic treatment with their prescriber, bearing in mind the difficulties that are associated with coming off these drugs.(12) People should not stop drug treatment suddenly, especially if they have been taking it for a long time.

People need to know about this research because it indicates that antipsychotics are not the innocuous substances that they have frequently been portrayed as. We still have no conclusive evidence that the disorders labeled as schizophrenia or psychosis are associated with any underlying abnormalities of the brain, but we do have strong evidence that the drugs we use to treat these conditions cause brain changes. This does not mean that taking antipsychotics is not sometimes useful and worthwhile, despite these effects, but it does mean we have to be very cautious indeed about using them.

Reference List

(1) Ho BC, Andreasen NC, Ziebell S, Pierson R, Magnotta V. Long-term Antipsychotic Treatment and Brain Volumes: A Longitudinal Study of First-Episode Schizophrenia. Arch Gen Psychiatry 2011 Feb;68(2):128-37.

(2) Lieberman JA. Is schizophrenia a neurodegenerative disorder? A clinical and neurobiological perspective. Biol Psychiatry 1999 Sep 15;46(6):729-39.

(3) Breggin PR. Toxic Psychiatry. London: Fontana; 1993.

(4) Moncrieff J, Leo J. A systematic review of the effects of antipsychotic drugs on brain volume. Psychol Med 2010 Jan 20;1-14.

(5) Lieberman JA, Tollefson GD, Charles C, Zipursky R, Sharma T, Kahn RS, et al. Antipsychotic drug effects on brain morphology in first-episode psychosis. Arch Gen Psychiatry 2005 Apr;62(4):361-70.

(6) Dorph-Petersen KA, Pierri JN, Perel JM, Sun Z, Sampson AR, Lewis DA. The influence of chronic exposure to antipsychotic medications on brain size before and after tissue fixation: a comparison of haloperidol and olanzapine in macaque monkeys. Neuropsychopharmacology 2005 Sep;30(9):1649-61.

(7) Andreasen NC, Nopoulos P, Magnotta V, Pierson R, Ziebell S, Ho BC. Progressive brain change in schizophrenia: a prospective longitudinal study of first-episode schizophrenia. Biol Psychiatry 2011 Oct 1;70(7):672-9.

(8) Molina V, Sanz J, Benito C, Palomo T. Direct association between orbitofrontal atrophy and the response of psychotic symptoms to olanzapine in schizophrenia. Int Clin Psychopharmacol 2004 Jul;19(4):221-8.

(9) Andreasen NC, Liu D, Ziebell S, Vora A, Ho BC. Relapse duration, treatment intensity, and brain tissue loss in schizophrenia: a prospective longitudinal MRI study. Am J Psychiatry 2013 Jun 1;170(6):609-15.

(10) Zipursky RB, Reilly TJ, Murray RM. The Myth of Schizophrenia as a Progressive Brain Disease. Schizophr Bull 2012 Dec 7.

(11) Fusar-Poli P, Smieskova R, Kempton MJ, Ho BC, Andreasen NC, Borgwardt S. Progressive brain changes in schizophrenia related to antipsychotic treatment? A meta-analysis of longitudinal mri studies. Neurosci Biobehav Rev 2013 Jun 13.

(12) Moncrieff J. Why is it so difficult to stop psychiatric drug treatment? It may be nothing to do with the original problem. Med Hypotheses 2006;67(3):517-23.

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