Tuesday, October 22, 2019

Comments by Morias Enkomion

Showing 100 of 104 comments. Show all.

  • Jonah,

    You drag me back from the dead! Luckily I still remember the random sequence of numbers I had changed my password to in order to lock myself out of my MIA account.

    I would hate for you to think that my leaving MIA had anything to do with our last exchange or with anything you or anyone else has said. I’ve never been offended by anyone here, but I see how you could have gotten that idea and I’m sorry. I shouldn’t have made quite as dramatic an exit, I wanted to say goodbye rather than just disappear.

    I have good reasons to kill off “Morias Enkomion”; I’ve been enjoying anonymity a bit too much and I think the time is coming for me to come out in the open in my own field and under my own name and see what I can do. Can’t let Robert do all the work.

    All the best,

    Morias no more

  • Messenger is good, Robert; just don’t let your guard down.

    And if I may, one last word of advice, (and for a number of reasons this will also be my last word on MIA): you know how they say that it helps to imagine your audience naked if you have to do public speaking? In your case I think it might help you more to imagine your audience recording what you say with the intention to take it out of context and use it against you. Paranoid? Maybe, but as Joseph Heller said, just because you are paranoid it doesn’t mean they aren’t after you.

    Choose your battles wisely, stay safe and keep up the good work.

    It has been great being able to exchange comments with the people here in MIA; I’ll keep reading it with great interest as I keep doing what I can to get the truth out there.

    Thank you and goodbye,

    Morias Enkomion

  • Hi Jonah and Cannotsay,

    Brief reply as I’m beginning to feel foolish talking about what Robert should or shouldn’t do – he’s a cleverer man than me and I’m sure he knows what to do.

    I’m certainly not defending appeasement, but saying that Robert needs to choose his battles carefully and choose which critics to answer and which are not worth his time (e.g. Marvin Ross). And also that he should be quite careful about his speaking engagements in potentially “hostile” environments such as NAMI (I’ll say more about this later).

    I do think it is definitely true that the better known an investigative journalist (emphasis on “investigative”) becomes, the less effective he or she becomes. Celebrity status closes more doors than it opens.

    As for having opinions, I think you are all forgetting how crazy what Robert has to say sounds to the average person out there, to the kind of people who make up “public opinion”. It would not be very hard to destroy Robert’s reputation by presenting him as an “anti-psychiatry zealot with no scientific training who got some sick people killed”. You and I and a minority of people would know that’s not true but that would be small consolation. Robert’s only defence, the armour that keeps him safe, is the fact that he only reports on facts; he is the messenger, and everybody knows you can’t shoot the messenger. The moment he strays from that role, the moment he gives his opinion, he opens himself up to attack and “they” have a lot more money and resources and don’t mind playing dirty.

    By suggesting that Robert might need to distance himself from MIA I did not mean disappear from it completely, only, I don’t know, be very careful, perhaps more careful that he has been of late. To give a concrete example I think Robert’s last post in MIA, “Harrow+Wunderkin+…” was a very dangerous thing for him to write. Not because I don’t agree with everything he says there, I do agree, but as I say his only armour is that he is only the messenger, and a messenger cannot express his opinions, which Robert openly did at the end of that post.

    About NAMI and hostile environments, I think perhaps Robert does not quite realize what he is dealing with there. Robert is very knowledgeable about what is wrong with psychiatry, about the drugs, the conflicts of interest and about what mental illness isn’t, but I don’t think he has given the same thought to what mental illness actually is, to the aetiology of this thing called “mental illness”. Why am I saying this in connection with NAMI? Because I think Robert might not be prepared for the fact that the people he might logically expect to be his greatest allies, the families of people diagnosed as mentally ill, will be in many cases his most virulent enemies; this seems inexplicable until one accepts certain things about the aetiology of “mental illness”.

    Anyway, I’ve said more that I meant to and I’m sure I’ll regret it later (I always do). I’ll just add that Robert consistently makes it into my list of “the 10 people I respect the most” so I hope he’s really watching his step, because it’s a minefield out there.

  • Hi Jonah,

    Very briefly regarding low profiles (which is not the same as hiding) and journalism: a journalist needs to be able to approach lots of different people and access lots of different environments, something which might become difficult the better known one becomes. How many members of APA you think will be willing to speak with Robert now? Of course this is to some extent unavoidable, but it is a matter of balance, and the more you can make people wonder what your own opinion is, the better.

    I think Robert combines unique qualities which have made his books stand out in a crowded field: he is a journalist who understands the science, a very rare combination. This is however a very dirty war and his position is not unassailable, he has not got the backing (or funding) of a organization behind him and so he has to be very careful to remain (and be seen to remain) a journalist who objectively reports on facts which can be independently corroborated, and not leave himself open to the accusation of having a personal agenda.

    What if the son of Angry Mum had jumped off a bridge and died and Angry Mum decided to sue Robert after all? It doesn’t matter that she would not have had a chance to win, I’m sure generous donors would have come forward to fund her legal expenses and make Robert’s life a misery and perhaps even compromise his ability to find a decent publisher in the future.

    I think Robert would be more effective providing the ammunition for other people to fire than firing it himself. It’s a basic rule: keep your ammunition factory as far away from the front lines as possible.

  • Yes, but this watching Robert’s back might involve understanding that Robert needs to distance himself from MIA and choose very carefully (i.e. reduce the number of) his public speaking engagements.

    Of course I could be completely wrong in this, but I do think that the guiding criteria for Robert should be to preserve his reputation as an independent impartial journalist at all costs, and not become associated or identified with any one group or movement.

    I’m not sure if I’m correct in saying this but my impression is that Robert’s greatest impact has been through his book writing, and I think he should protect that more than anything else. Otherwise his activities as an investigative journalist could be seriously compromised even though he has done nothing wrong. Reputations are very fragile things and can be destroyed with lies and unfair accusations just as easily as with the truth, perhaps more so.

    I do think that Robert maintaining a relatively low-profile might be much more useful in the long term than to engage with critics who are likely to be “agents provocateurs”.

    Anyway, I’m repeating myself now, so I’ll just shut up about this.

  • This Marvin Ross blog is precisely the kind of drivel I think Robert should not waste his time with. I am not however all that busy, so:

    Mr Ross’s actual writing we can put aside, it really is beneath comment, but this quote from Dr Torrey is interesting:

    “Whitaker clearly believes that schizophrenia should be treated without medication if at all possible. However he fails to focus any attention on the fact that on any given day in the United States half of all individuals with schizophrenia, or about one million people, are not being treated. This is a huge natural experiment to test his thesis.”

    Mmmmm, let’s look at Dr Torrey’s beautiful deductive argument:

    Premise 1: “Whitaker clearly believes that schizophrenia should be treated without medication if at all possible.” Correct.

    Premise 2: “on any given day in the United States half of all individuals with schizophrenia are not being treated.” Correct (give or take)

    Inference: “This is a huge natural experiment to test his thesis”… er… no, please refer back to 1) “should be TREATED without medication”, which is not the same as “not being treated”, so I’m afraid premise 2 is not a “huge natural experiment to test his thesis”. A modestly sized man-made experiment to test his thesis, on the other hand, might easily be found in the Open Dialogue project in Finland, for example.

    Poor Dr Torrey, I’m afraid he gets and F in logic.

  • I don’t think we are going to agree on this Seth, and you could very well be right. But as Chrys says “wind-up merchants” can be a very effective way of silencing critics, even when you manage to beat them, because no-one has infinite stores of time and energy. I’m not sure these people are so much interested in stopping Robert from speaking as they might be in getting him involved into some ugly spat with an expendable goon so that they can tarnish his reputation as a credible objective journalist and make it impossible for him to write more books that hit them where it really hurts.

    Karl Marx might have said that education itself is insufficient to produce change, but all Marx ever did was write books, and those books changed the world. Not that I’m comparing Robert to Marx, obviously Robert’s books are much better researched.

  • Robert, I think your greatest strength is that you always stick to the facts and never get personal or speculative; in other words, that you are a journalist and a very good one. If I can offer a word of probably controversial advice: don’t become too much of an activist. Not because the cause is not worthy or you would not make a great activist, but because you’ll be far more effective as a “whiter than white” independent journalist, unearthing the inconvenient truths and presenting them to the public in ways that make people stop and pay attention. Don’t let the goons take up too much of your time and energy.

    They want to stop you from speaking here or there? I don’t know, maybe you should let them and use your time to write them off the face of the Earth – I think you have it in you to drive into their lies the wedge of truth that will bring the whole thing crumbling down (yes, this is a convoluted way to humbly request “Anatomy of an Epidemic Part II”).

  • I agree, Marian; I don’t think the infantilization of labelled people is the consequence of the labelling but rather its cause, or at least part of the process which in many cases leads to the superconcentrated anger, pain and fear which goes by the name of “mental illness”.

    Children who must always be wrong so that their parents can always be right. Adult men and women forced to remain childlike so that they can continue to be wrong while the “adults” around them can continue to be right. Unfortunate scapegoats into which dysfunctional families can pour their dysfunction so they can continue with their functional pretense.

    People will say that this is not true of every case, and it probably isn’t, but it is true of many, many cases, and for as long as it is not acknowledged—in each family, in society at large—the chain of darkness and misery passing from one generation to the next will remain unbroken.

  • I personally think it is THE biggest issue. Big Pharma/psychiatry would not have the power that it has today if it had not been given to them by families all too eager to avoid having to look at themselves too closely.
    If this is not addressed it doesn’t matter whether we defeat the DSM or the biological model, something just as bad will come to fill in the vacuum (see the “vulnerability” model) and nothing will really change.

  • Thank you, Chaya. Thank you so much for daring to tell the truth. It can’t have been easy, but I think it is more important that any number of research papers or academic discussions. Without people like you daring to speak out in the open of these painful and uncomfortable truths there can be no meaningful discussion of “mental illness” and no real progress.

    I cannot really convey in words how important I think your post and your story is, and how desperately the world needs to stop and listen to it. So please, keep telling it. And thank you again.

  • I’m glad to read in the update that this man is all right. “All right” is, of course, a relative term here since he has been hospitalized. What will happen to him while he is hospitalized? What kind of help will he receive?

    If one puts aside the manipulative use Pete Earley makes of the letter (David’s “Assassination of Marat”? Oh, please), the letter itself is worth reading. My first reaction is to wonder why this man’s “voice was telling him we [his parents] were devils, our house was haunted by evil spirits and we were  trying to poison him. He said God was commanding him to not live with us anymore”. I know very well that this will be dismissed as the meaningless delusions of a diseased brain, random neuronal misfiring. And indeed the mother tellingly describes his son’s words, his desperate attempt at communication, as “nonsense”. What a sad, heartbreaking story indeed.

    I wish this man the very best, I really do. And precisely because I do, I hope Robert Whitaker never stops doing what he is doing, but that he does more of it, and that more people do it. I also hope that this anonymous “schizophrenic” eventually finds someone who listens to what he has to say.

    With that in mind, I would invite anyone reading this (Mr Earley? Broken Hearted and Angry Mum?) to read Chaya Grossberg’s recent post in MIA, “Many Ears Make Light Listening” and to really think about what she says there.

    https://www.madinamerica.com/2013/07/many-ears-make-light-listening/

  • Thank you abbot (Philip K. Dick is one of my favorite writers; personal favorite: “Now Wait for Last Year”)

    I was just trying to be realistic (and coherent which, believe me, does not come easily or quickly) in my comment above. I think we often get carried away into thinking that this is all a question of getting “them” to see the light. And to some extent it is, but what happens after they see the light? In the end I don’t think you can change “the profession” any more than you change “society”; real change happens one person at a time or not at all. This real individual change might take the shape of a psychiatrist realizing the DSM5 has fatally poisoned the golden egg goose and retraining to become a neurologist or psychologist while there’s still time, or it might take the shape of a religious conversion in which a psychiatrist realizes the sinfulness of his or her actions and gives up the profession to spend the rest of his or her days in penance and contrition, or it might take the shape of a psychiatrist losing his or her job when it becomes clear he or she doesn’t know what he or she is talking about (and this is an important point: this decision will be made one person at a time by the public or private organizations which employ them; don’t expect big sweeping mass deportations of psychiatrists or a UN resolution banning psychiatry), or it might take the shape of lawsuits against individual psychiatrists. One person at a time.

    But having said that, I think you really have something there with this Canadian/American border patrol idea. Not as an enforced deportation, of course (as I just said, that’s just wishful thinking), but as a generous offer to relocate into a different job with better long-term prospects. I see a lot of promise in this plan, particularly if you are referring to the Yukon/Alaska border. Maybe they could even be offered a field research job in a big study on human/bear interaction.

  • This article illustrates something which I think is crucial but easily forgotten: although we are used to speak of “psychiatry” and of how psychiatry must change, psychiatry is of course an abstract concept and we should be careful not to reify it. Psychiatry cannot change any more than it can stay the same or eat a hamburger, it is psychiatrists who need to change.

    Psychiatrists who, like Craddock, cannot change because that would mean throwing away the careers they have build for themselves or who, like Burns, do not mind to change provided they are allowed to stay on top, regardless of how ill-suited they might be to be on top of anything other than a scrap-heap.

    And that is really the problem, isn’t it? I mean, put yourself in their shoes. What is the one quality most practicing professional psychiatrists must develop in the course of their professional careers in order to be good psychiatrists? An utter lack of empathy for their patients and an astonishing capacity to treat them as objects and ignore anything they say. And now, what do you want them to do? Enter into a human relationship with their patients? Retrain? Go back to school? Is that realistic? I don’t know, to me it sounds like giving a copy of the Tao Te Ching to Vladimir Putin and expect him to give up everything and become a Zen monk. It’s just not going to happen.

    The gap between what psychiatrists know how to do and what actually needs to be done to help people is just too big, and most of them will not be able to close that gap in their actual professional practices. So the question is, what do you do with these thousands of highly-trained well-paid professionals who are good for nothing? If only we could offer them something equally well-paid that they could do with their skills in some other field, then I’m certain we would see real change in the field of mental health, real fast. I just can’t think of anything.

  • Yes, there’s so much of this out there, and the BBC is second to none when it comes to promoting the wonders of psychiatry. A few months ago they had a program about the daughter of the new Archbishop of Canterbury and her depression, how she has come to accept she has an illness. It was heartbreaking to watch – you could tell she wasn’t really buying any of it but she had nowhere else to turn.

  • Thank you for the review, it does sound good. And by the way, thank you for your post on publication bias, which was excellent.

    I had been thinking lately that it would be a great thing if MIA was to start a regular book review section. Speaking of which, I’ve just heard some good things about this book:

    “Is Science Compatible with Free Will?” Edited by Antoine Suarez and Peter Adams

    http://www.amazon.com/Science-Compatible-Free-Will-Consciousness/dp/1461452112/ref=sr_1_1?s=books&ie=UTF8&qid=1363960961&sr=1-1&keywords=is+science+compatible+with+free+will#reader_1461452112

    As far as I know it does not touch directly on psychiatry but it deals with fundamental questions which are key to neurological research into mental processes. It is not however a cheap book, so I invite anyone out there who can buy it using someone else’s money to get it and post a review here in MIA.

  • I’m glad to hear that Kathy, and I’m very interested in your book which I have added to my reading list after looking through it in Amazon (although I must confess my reading list is quite long at the moment, but I’ll get there eventually).

    I find very interesting your last phrase “to show the face behind the illness” – when I read it just now it struck me what a powerful metaphor this is.

    The face behind the illness… and indeed, the illness is something that covers the face, the real face of the person. Or is it? I mean, is there really something there, this “illness”, covering like a mask the true and real face of the person underneath? And if there is such a thing, this mask, this “illness”, where does it come from? From inside the “ill” person, perhaps? From a “broken brain”, as the say? But then, if it comes from inside the person, from their brains, in what sense can we say that it is like a mask that covers the real face of the person, rather than part of that face? Or is it rather that this mask is something that other people put over the face of the “ill” person? Something we put on them precisely so that we don’t have to look at their real faces, so that we don’t have to look at faces which are sometimes full of pain, and full of anger, and suffering, faces which makes us very uncomfortable? Uncomfortable because to a greater a lesser extent we are responsible for that pain, anger and suffering, so that their faces are also an accusation, and accusation we would rather cover up with the mask of “illness” so we don’t have to look at it any more?

    I don’t know, but like all good metaphors I think this one invites many reflections – thank you so much for bringing it up.

  • I think I draw the line at violence – if MIA was a physical space and someone started beating the living daylights out of someone else I think the organizers (and not only them) would need to intervene to “moderate” the situation. Of course MIA is not a physical space but you can still get verbal violence and abuse.

    For example, I think it is ok to tell another commentator (these are only hypothetical examples! Please, no moderation needed): “perhaps you should go away and do some research rather than saying stupid things”. I think that’s ok; borderline, but ok. But if someone says: “perhaps the problem here is that you are a f*****g r****d”, then that is the verbal equivalent of punching someone in the face, and not acceptable. It it those kinds of comments that I think need moderation; anything else, I’d rather err on the side of immoderation. But I think there is a non-violence line that should not be crossed, I don’t know if you’ll agree with this (I’ve watched some Canadian hockey…)

  • Thank you Matthew, chiming in – which will of course require 100 times more effort on your part (effort which I’m sure will not go unappreciated) – would make a whole world of difference. It would be a dialogue rather than the cold impersonal slap on the face of “this comment has been moderated”.

    Like abbot says above, this lack of dialogue, this incontestable: “the form in which you have expressed yourself is unacceptable and so the content of what you have expressed -and by implication you yourself- must be suppressed and erased from existence” parallels exactly the way in which psychiatry operates. Perhaps also the way in which many “mental illnesses” originate, because few things are more maddening than being consistently ignored and suppressed for telling the truth – or at least your truth.

    Personally I think it is amazing how civil and reasonable MIA commentators are in their exchanges – even the more “extreme” ones – compared to usual blog standards. And when you consider what some of them have been through in their lives I think they deserve a medal for self-restrain and emotional control. Also, on the whole I’d say a lot of “self-moderation” takes place where commentators moderate each other and defuse potentially nasty exchanges.

    I myself would even like for “mainstream” professionals to be invited (and have the guts) to blog in MIA (although if “mainstream” blogs were posted in MIA they should be posted alongside a response form a regular MIA blogger – not an unusual practice). And I’m also trilled when people with mainstream views comment in MIA, but I don’t see why MIA needs to change in order for this to happen. Nothing wrong with people with mainstream views getting a taste of what is like to be the minority opinion for a change, and if some exchanges are sometimes a bit “robust”, well… I’m always amused by the fact than more often than not it is the psychiatrists and other professionals who seem to be far more emotionally fragile than survivors, ex-users or just plain crazy people. Perhaps they are not as used to being contradicted.

    I do think some moderation is necessary, but only of the most outright personally abusive comments. Off-topic moderation for example I think is very counterproductive (if it had been applied throughout history it would have killed most scientific and philosophical discoveries).
    In my very limited view of this website I’d say that it isn’t broken, so it doesn’t need fixing, and it would be a terrible mistake to try to “normalize” it; the last thing the world needs is yet another forum where people feel they have to talk like lawyers or politicians to be allowed to speak.

    And finally, if these new moderation efforts are completely unconnected with NAMI’s approaches, I’m afraid Bob’s comment on this thread was unfortunate in that it seemed to link the two things, and for obvious reasons Bob’s comments carry an enormous weight here. I (for once) don’t want to stray from topic, so I won’t say what I think of these “advances”. Only this, Bob, if you are reading this, may I recommend to you an excellent book called “Anatomy of an Epidemic”? It shows that the biggest problem in psychiatry is not so much lack of knowledge but corruption and conflicts of interests – please remember than one thing is dealing with the rank and file of an organization and a very different one dealing with those who have the power to change things from within that organization.

  • As someone who has just been moderated for the first time (for objecting to someone else’s comment being moderated) and who started his MIA’s commenting life with a bit of a spat with another commentator (which was luckily allowed to resolve itself without moderation), I have to say that while I understand the need to keep standards and make the website welcoming, I do think there’s some confusion here between the “moderation” of the posts (posted by the bloggers), which is the editor’s job, and the actual moderation of comments to those posts.
    The new standards of moderation which seem to be taking shape in MIA are, I think, a bit too “editorial”. All the more so in a website which is precisely trying to give a platform to people who have had their voices ignored and denied for a long time. Other than the most obvious personal attacks I think the comments section should be left to thrive as a wild and somewhat dangerous jungle; an “enter at your own peril” sort of place where people can scream and shout if that’s all they can do at that point in time. If it is going to turn into a safe and pleasant park with waste bins and “keep off the grass” signs, it will lose -for me at least- that which makes it a place worth visiting.

    And the fact that all this has come up because of NAMI’s overtures is the most worrying thing of all – an organization which is positioning itself to switch masters from the sinking APA to the more profitable biomarker industry…

    (Bob, please make sure they don’t change you faster than you can change them; it’s just so easy to not notice what’s happening until it is too late, the rewards so big, the compromises so seemingly small.

  • Good point about the South African Truth and Reconciliation process – in many respects I think both processes are analogous. If TaR worked (when it worked, which was by no means always) it was because the abusers had a chance to understand and admit the harm they had done and ask the forgiveness of those they had abused – obviously for the process to work there has to be an admission of guilt or responsibility; it does not work if those responsible for the abuse turn around and say to the victim: “we didn’t do anything wrong – we just did what was best for you”

    I think all too often people forget the greatest difficulty of the theory of trauma as the cause of “mental illness” (which is also the greatest strength of the biological model): 9 times out of 10 it places responsibility (I think correctly) on the family environment. So I think Cannotsay is just basically stating a minimum requirement for any “family therapy” to work: family members must be open to the fact that they might have been part of the problem to begin with. Ironically this was much better understood in the 50’s (right before Big Pharma came to the rescue of families with guilty consciences) when people like Gregory Bateson were talking about “schizophrenic families” rather than individuals.

    I think the kind of work Jennifer is doing is the way forward, but this uncomfortable aspect of it must be clearly understood or else it won’t really work.

  • Thank you so much for posting this, Kathy; there’s so much to comment on what you say. I would just encourage you to keep on doing your own research and questioning what you’re told – be it by a doctor, be it by Robert W. (I’m sure he wouldn’t want it any other way!)
    Doing your own research might feel overwhelming at first but remember that the only thing that separates you from an expert is a few years’ worth of reading – through your son you already have access to first-hand information most experts don’t have. So keep reading and, more importantly, keep talking to your son, keep listening to him.

    And one more thing: perhaps it would help you to stop calling drugs currently prescribed for psychosis “antipsychotics” (as in “And how on earth do we treat people who are psychotic if not with antipsychotics?”). In doing that you are already assuming that they work in the way they say they do, but that is precisely the question, isn’t it? Are these drugs really “antipsychotics”, or are they just drugs, as Copy_cat says above? Yes, they seem of work, but do they work like antihistamines work or do they work like alcohol or heroine works? Perhaps we should start calling them “the drugs formerly known as antipsychotics” as a first step to question what they really do.

  • Many Thanks, Robert. I hope your experience at the Vatican did not discourage you to count them as promising interlocutors. It sounds to me that it went as well as it could be expected: you got to say your (far too short) piece at a place where you never know who’s listening. Of course the reception must have been chilly to say the least; do not underestimate how outlandish what you are saying is, even if it is completely true. For all that the evidence is beginning to accumulate, critics of mainstream psychiatry are still a voice crying out in the wilderness.

    I hope Marcia and Barry will persevere with plans to bring first-hand personal accounts of psychiatry survivors to the Vatican. If there’s an institution that should be attuned to the value of personal accounts, it should be the Catholic Church.

  • I don’t think one can overestimate the potential importance of this event, particularly if, as Marcia Barbacki says, it leads to the Catholic Church looking at the wider issue of psychiatry as a whole.

    I am convinced that it is only lack of truthful information, together with an understandable reluctance to interfere in the world of “science”, that has led to the Catholic Church’s silence in this critical area. I have no doubt however that if this information is made available and genuinely understood by the Church’s hierarchy, the Catholic Church will act with the same determination that it is evident in other areas where very harmful ideologies and interests masquerade as science.

    From a purely Catholic perspective I’d add something else: a reassessment of psychiatry and psychology, and of the Church’s care for those people who are now diagnosed as being “mentally ill” must be a fundamental aspect of the New Evangelization. For as long as the Church puts her trust in psychiatry (and in this the sex-abuse scandal is a tragic lesson that must not be forgotten) and fails to care for those whom society now calls “mentally ill”, for as long as it does that, the Church will fail in its evangelical mission in the developed world. The “mentally ill” need the Church, but equally the Church, if it is to fulfil its mission as the Church of Christ, needs the “mentally ill”. I am reminded of Ezekiel 34:4-6, which begins “You have failed to make the weak sheep strong” and ends “no one bothers about them and no one looks for them”.

    I hope and pray that this conference will be the first of many; it would be only fitting that this long-awaited awakening began in the Year of Faith.

  • I know it is unwise to say this but I AM anti-psychiatry. Not anti-psychology or anti-therapy or anti-neurology or anti-biology or anti-pharmacology, I am not even anti-animal-testing. I am just anti-psychiatry. Someone should tell Dr. Lieberman (what an ironic name for such a nasty piece of work to have) that it is not all the same; actually, I’m sure he already knows that very well.

  • Sandra,

    Of course it is an hypothesis, wouldn’t dream of claiming anything else – and in fact I’m sure it is incomplete and parts of it are probably just plain wrong. In order to be more than a hypothesis it will need confirmation from research – and I will also admit that this presents its own challenges since it is a hypothesis that bleeds into philosophy and so not all aspects of it are subject to falsification, but some certainly are.

    My problem with the other hypotheses I’m so critical about (let’s call it the “biological model” for short) is precisely that the research that supports this hypothesis is for the most part flawed or just plain fraudulent. In other words, that the biological model is treated as a validated theory when it is nothing more than a hypothesis, and one that it is full of holes and “mysteries”. I don’t have a problem with genuine research into hypotheses I think are wrong, but I do have a problem with bad research into any hypothesis being passed off as good. And when it comes to psychiatry bad research is not the exception but the rule.

    And let’s not be disingenuous here, this is not just an academic discussion. We’ve had 40 years of therapies based on the “biological” hypothesis, with immense resources thrown into it and the result is the situation described in Anatomy of an Epidemic. On the other hand you have very small initiatives like the Hearing Voices movement based on the “non-biological” hypothesis (which admittedly is still to be formulated in a rigorous way) and which despite the difficulties they face are producing great results. When you have two competing hypotheses the proof is, as they say, in the pudding.

    As for genome as “unchangeable biological essence” I think it is correct to say this in the context of the current practice of psychiatry. Whether it is or it isn’t in actual fact is not so much the question; the question is whether it is assumed to be so by mainstream psychiatry and whether this is the narrative that is presented to patients: or are you going to say that psychiatry does not operate from the assumption that these “genetic” conditions are life-long conditions which require life-long treatment of one kind of another? How many of your colleges have you seen taking an interest in neuroplasticity? Also, bear in mind that neuroplasticity is not magic – it does have its limits, so it does not render irrelevant the question of genetic determination.

    But of course in the end the question is whether conditions such as “schizophrenia” -or better, voice hearing-have a genetic etiology or not. And they don’t; and they cannot have it – to explain why we would need to get into evolutionary theory: the evolution of genetic traits which reduce survival is a tricky thing, and as far as I know no-one has even proposed a theoretical model of how something with the complex genetic architecture which voice hearing would need to have (or else we would have found those elusive genes already) could possibly have evolved. I’ve tried before to get into this subjects in other comments and things get too long, so I won’t go into it here; I will only say that if indeed there’s a genetic component to voice hearing it will need to have been positively selected, so it is likely to be a different variant of intelligence. Of course this is only a hypothesis, but at least it tries to account for all the facts rather than cherry-picking them.

    About genes that turn on and off and all this epigenetic stuff that seems to have become so fashionable lately, like neuroplasticty, it is not magic. You can’t use epigenetics to cover up all the holes in the biological model. Epigenetics won’t turn an environmental etiology into a genetic one.

    But to get back to basics: my greatest objection to psychiatry is that the vast majority of research which appears to validate its “biological model” is deeply flawed. The only reason it is not exposed as flawed is that it is backed by very powerful economic interests. And the drug therapies which have been developed based on this flawed research are extremely harmful. And the proof is in the pudding. So I invite you to take a good hard look at your pudding.

    Psychiatry is like a mythical land which is supposed to exist between the kingdoms of neurology, psychology and pharmacology, but it just isn’t there. There’s nothing between those three kingdoms, only foetid hot air.

    It’s been a pleasure exchanging ideas with you, Sandra, I hope I have not given too much offence. Unfortunately I won’t be able to comment any longer as I am pressed for time with work, and try as I may, I just don’t seem to be able to keep my comments brief. I hope some of this will make you reflect on the state of affairs in your profession.

  • Marian and Steve,

    I apologize for using the word “symptom” above – I never meant it in a biological or even psychological sense. I’m afraid that because I often use (in my own head) the terms “disease” and “symptoms” to mean the “social disease” and “social symptoms” of groups rather than individuals, I used the word very carelessly.

    I could not agree more with what you both say. For me one of the most important aspects of “mental health” is precisely the recognition that all these behaviours, the “symptoms” of “mental illnesses”, are in fact RATIONAL behaviours – as Steve says “all behaviours meet a need”. Similarly, the “delusions” of “psychotics” are not in any way irrational but convey a rational meaning in symbolic form; they make perfect sense and are always true, even if that truth requires careful interpretation (but then again, all communication is symbolic – the difference is only in that in “psychotic” communication the symbols are not as shared as in other forms of communication).

    To me, classifying a behaviour as “irrational” necessarily denies the humanity of that behaviour. If you then spuriously link that “irrational” behaviour with a person’s genes, with their unchangeable biological “essence”, you are denying their very humanity. This is not to say that there are no genuine irrational behaviours: it is precisely the abusive behaviours which cause amongst other things the distress of “mental illness” that can be described as irrational – that is to say, inhuman behaviours.

    This might sound extreme, but I think it is correct to say that, just like by denying the humanity of the Jews the Nazis became themselves inhuman, psychiatry, by denying the rationality of the “mentally ill” has become itself irrational. There can be no progress until psychiatry recognizes the rationality of the “mentally ill”, but in order to do this psychiatry needs to deny its basic premises – it needs to deny its own validity. Psychiatry, quite simply, needs to disappear.

  • Hi Sandra,

    If I am still to answer this question it is only because you have never asked it before. You asked me “What AREA of research do you find to be of value?” And so I answered that: life-long neuroplasticity

    I don’t like to make personal comments but I have to say that from our short exchange you seem to have a bad habit of “changing the past”. If I mention philosophy of science you turn it into philosophy of mind; if I talk about dishonesty in a research paper you turn it into a question of DSM categories. If I answer one question you slightly change the question I just answered. I’ll put it down to carelessness and not a conscious or unconscious attempt to change the meaning of your interlocutor’s statements so that you don’t have to engage with them while appearing to do so. But please do watch out for it; it’s enough to drive anyone crazy (pun intended – in fact Gregory Bateson referred to a pattern of communication not dissimilar from this when he formulated his double-bind theory for schizophrenia).

    Steve above expands a bit on neuroplasticity, Bruce Perry, etc. Needless to say I agree with everything he says. Neuroplasticity is not just “another thing” that you can take or leave – it’s a game changer; it is, to use Kuhn’s terminology, a paradigm shift. The failure of psychiatry to engage with this shift is nothing short of scandalous, and inexplicable if you don’t factor in very powerful commercial interests and a great dearth of professional ethics.

    So how would I approach it? Very simply by factoring in neuroplasticity and making sure the design of these studies takes neuroplasticity into account. I don’t want to repeat myself, but in the sample study I linked in my first comment it is obvious that -given neuroplasticity- the 4 members of the control group who developed MDD should have been given a second set of fMRIs, and those results compared with the baseline fMRIs of those members of the study group who went on to develop MDD. Particularly since “There were however significant differences between the groups for baseline clinical measures of depression from the HAM-D (p = 0.004). There were also significant differences at baseline between the groups for measures of cyclothymia (p = 0.001). For both these measures the HR who developed MDD scored the highest.” [HR = high risk; the study group]. I don’t think I need to spell it out.

    In a recent comment on a different post I said half-jokingly that I’m waiting for the longitudinal study on a random sample of 100,000 subjects who are given a complete battery of fMRIs every 5 years from birth to death. Actually, make that a 500,000 random sample and add complete genome sequencing and a detailed assessment of environmental factors at each 5 year interval. Does this sound absurdly far-fetched? I don’t know, look at the Large Hadron Collider; if the will was there on the side of the psychiatric profession, funding for meaningful large-scale studies would be found.

    Meanwhile, back in the real world, if you want to see studies that I “condone” (not a word I would use; makes it sound like a crime) you can check some of the studies in “Human Neuroplasticity and Education” (2011) edited by the Pontifical Academy of Sciences (again this is something I just referenced on another comment so I have it fresh in my memory) you can access it for free here:
    http://www.casinapioiv.va/content/accademia/en/publications/scriptavaria/neuroplasticity.html

    You’ll see that it is a mixed bag of many different studies (or presentation papers), and I don’t think everything in them is correct, but I think they are all honest, methodologically correct approaches. In other words: these people are at least trying, something that cannot be said for most of what passes for research in psychiatry these days.

    And one last thing since you ask me how I would approach things; I would certainly like to see the end of researchers treating the “Conclusions” section as the section in which they speculate freely about the data. I’m sick to death of results that “suggest”, “point in the direction of”, “seem to”… It’d be much better for everybody if researches confined themselves to what the data does or does not say. Research papers should not be works of speculative fiction.

  • But what I am saying Duane, is that those psychiatric labels are not based on nothing as you say, they are actually based on lies (when I am feeling diplomatic I call them “mistakes”, but to call things by their name, they are lies)

    So if you concentrate only on the label and leave the lies behind the label untouched, you are only replacing one labelling system with another. What we need to challenge is the lies in the science.

    Anyway, I am not defending DSM labels, in a alternative world, without the lies that have gone into them to give them concrete shape, they might not have been a bad thing in themselves, but in this real world we live in of course they are bad. So yes, off with the DSM, but don’t buy into the RDoC or anything along those lines either. It’s just switching one label with another.

  • I’ll add here something to my last comment above. Perhaps a lot of people will disagree with this, but in a way there’s nothing wrong with DSM categories themselves. The problem is what psychiatry and Big Pharma have done with them. To give a collection of symptoms a name is nothing particularly bad. On the other hand, to carry out a skewed research study which incorrectly claims to show that a particular DSM category has a genetic etiology is very bad. To claim that a research paper shows that a drug is effective in the treatment of a DSM category when in fact the data shows the drug to be completely ineffective and dangerous, is very bad indeed.

    The problem is not in the DSM or its categories but in the scientific studies themselves. And this will not change with RDoC. On the contrary it seems to be getting worse.

    Dropping the DSM is a smoke-screen to try to silence mounting doubts over psychiatry as a profession and its biological model. A scapegoat; a bone thrown to the dogs to quieten them. Like Tomasi di Lampedusa says in The Leopard: “everything needs to change, so everything can stay the same”.

    Don’t get me wrong, it isn’t as though I want to keep the DSM, but to have it replaced with something worse is not good news. The problem is Big Pharma, dishonest research scientists, psychiatrists (honest and dishonest, since the foundations of their profession are just plain wrong).

    Getting rid of the DSM would be a victory, but still a small victory. Only a battle in a much greater war.

  • Neuroplasticity. As in life-long neuroplasticity. But bear in mind I’m not a scientist.

    I said philosophy of science (to better understand why that study is a parody of a farce), not philosophy of mind. Not that philosophy of mind is not extremely relevant to all this, although I’m afraid that field is a bit of a mess in itself – still, you might find interesting reading up on the problems associated with epiphenomenalism: http://plato.stanford.edu/entries/epiphenomenalism/#ArgAgeMat

    The flaws I point out in the study have absolutely nothing whatever to do with DSM categories, please do not try to explain them away with that easy argument. They do however have EVERYTHING to do with what Insel is trying to do. The card-castle of bad studies I mentioned is precisely this RDoC of his; it is already half-built (I realize this study still uses DSM categories, but actually what it shows is how you can transition from DSM to RDoC). This study is, so to speak, a building block of the RDoC; one brick of many. The RDoC is not an improvement on the DSM, it is something far far more damaging and pernicious. And it is more damaging and pernicious because these research papers are simply not honest. There is not way these “flaws” are accidental – this is flagrant, intentional dishonesty. And it is getting through. And professionals like yourself are looking the other way while this monstrosity is taking shape.

    Please forgive me if I sound harsh, but I cannot emphasize enough how damaging this could be if it is not questioned and nipped in the bud. The RDoC is a wolf in sheep’s clothing, and potentially a much bigger and hungrier wolf than the DSM: it is not only after people with symptoms of emotional distress but after their children too.

    From wht you say I get a sense that your heart is in the right place (unless you are a very cynical person, but I’ll chose not to believe that). You need to start asking some difficult questions or before you know it you could unwittingly be part of something very bad indeed.

  • Of course the study focuses on individuals with a family history of mood disorder, that’s the first problem: the study assumes the genetic origin of mood disorders and simply discards any data that might have contradicted their starting hypothesis. And then tries to justify this by saying “yes, but we did not set out to study those other things in the first place”. I’m sorry Sandra, but I do hope you realize that this is just not the way scientific research works; if you don’t you may have to go to more talks on philosophy of science.

    There is actually a funny side to this study if you can be bothered to read it:

    Notice that it studies close relatives of people with Bipolar Disorder, not MDD, who go on to develop MDD, not BD. The authors justify this peculiarity with the sweeping statement that BD and MDD have an “overlapping genetic architecture”. But if you look at the figures you will see that despite their own claim that first-degree relatives of individuals affected by BD: “have a more than a ten-fold increased risk of developing bipolar disorder (BD), and a three-fold risk of developing major depressive disorder (MDD)”, in their study group of close relatives of people with BD only 2 people actually developed BD! So: “Since only 2 individuals had developed a mood disorder with a manic component, the main analysis focussed on individuals who had developed MDD only.” In other words, they had to shift the focus of their study because otherwise they would have had no study… thank heavens for overlapping genetic architectures!

    As for the conspiracy side of things, I agree not much in the world is well-orchestrated, perhaps I should have said badly-orchestrated, but orchestrated nonetheless. Look at this study, follow the studies referenced in it, look at the funding, the competing interests. Do you not see a card-castle of bad studies building up, one bad study propping the next? Is it not clear which companies and organizations support this whole “research industry”? Or the influence they have on professional organizations? If you want to write “in the spirit of Robert Whitaker’s work” you have to start following things up to see where they take you. To a large extent we are talking about your colleagues and your profession, so you share a portion of responsibility in this. It is not enough to look the other way and say, “oh, I just didn’t know”. Remember that bad things happen because good people allow them to happen.

    This reminds me of something a French philosopher whose name escapes me just now said: “I don’t believe in conspiracies of men, but I believe in conspiracies of devils”. By which he meant, greed, arrogance, incompetence and fear of losing one’s well-respected career – or one’s well-respected profession, for that matter.

    (I notice in my previous comment I wrote MMD instead of MDD a couple of times, sorry about that)

  • Hi Sandra,

    I’ll start by saying that I believe in the identity between mental processes and brain physiology/morphology, so in theory I’m very keen on neuroscience. But as other commentators have pointed out, we do not live in an ideal world and research into this field is not driven by scientific curiosity but by a ruthless industry seeking to increase their profits by any means.

    Rather than speak in generalities I’d ask you to please take the time to look at this study by way of an example:

    http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0057357

    It is not a particularly substantial study but it is recent and freely available (and I had it handy from a previous comment in MIA)

    In particular I’d draw your attention to this: “Controls who developed a mood disorder were also excluded (n = 4, all MDD)”

    Now, you tell me: in a study that claims to have found a hereditary difference of brain morphology linked to MDD, is it not imperative that the 4 members of the control group who develop MMD are given a second round of fMRIs to see if they also exhibit said brain morphology – thereby showing that it is the result of neuroplasticity and not genetics? Particularly since those members of the study group who did develop MMD and show atypical morphology already had signs of incipient depression at baseline?

    Notice how carefully the authors word their conclusions to divert attention from those 4 controls: “These findings offer the potential of future risk stratification in individuals at risk of mood disorder for FAMILIAL reasons.” (capitals mine). You might also want to pay close attention to the Competing Interests section, and wonder why the study has 10 different authors.

    I’ll tell you what I make of it: this is a dishonest study (one of many), part of a well-orchestrated push to advance an agenda of “preventive interventions”, “early detection” and “screenings of at-risk groups” (see this recent item of news from the UK, for example: http://www.bbc.co.uk/news/health-22478706 ). This is something very dark and very dangerous, and neuroscience – or rather bad neuroscience – plays a big role in this push. You cannot just pretend it isn’t happening or “it’s not as bad as all that”. It’s worse.

    No offence, but if you really think you are playing with nice guys on a level playing field you are very naive. And I don’t think the people you are trying to help can afford that naivete.

  • Hi Scott,

    I never thought you were a psychiatrist because you are too interested in psychiatry, and on the whole I find psychiatrists just don’t give a **** about their own subject.

    Do you sound a bit angry in your last reply to me? That might be a good thing… believe me, I share your frustration re. ships in the night.

    I myself am not an empirical scientist and I don’t work with data; the last data I handled was my income tax return. I’m more of an abstract theory type of person; that’s the kind of thing I do and what I can offer, for whatever’s worth. There is some of this data you ask for in AoE and Emperor’s New Drugs, (and I’m sure many other books I haven’t read), which is why I keep recommending them to you; I honestly think you will appreciate them. Of course their case is not 100%; they don’t offer proof in a strict sense, but they do present a lot of evidence in a fairly rigorous way – more evidence than the other side, I’d say. They’re worth the money.

    But you do have to give them some time, you have to allow yourself to think for a moment, could this possibly be right? Can we interpret the available evidence in this way? This is what I meant when I said I don’t think you are being honest with yourself. You have to play devil’s advocate with yourself, not just with MIA. Isn’t this one of those basic rules of philosophy of science (which much to the world’s regret no research scientist actually follows)? Never set out to prove your hypothesis right, set out to prove it wrong; and if you can’t maybe it is right, but you must always be on the outlook for new ways to prove it wrong.

    I do believe all minds are equally resilient to “immaterial” pathogens such as trauma. Do I have proof ? No, I have arguments and I think it fits better the available data (that I know of). In any case, to really talk about this kind of thing in detail we would have to first get into the relationship brain-mind, the organ and the mental processes, and I’m not going to go there here (I have to save something for the book I want to write when I retire, don’t I?)

    I’ll sort of leave it here… I’m a bit washed out after my analogy of colours; I was so pleased with myself when I was writing it and I don’t think anybody got it…

    I’m interested to hear that you do agree with the idea of life-long neuroplasticity. Where does that leave all these brain-imaging studies that look for differences in brain morphology in adults in order to stablish a “genetic component”? Isn’t it a bit too obviously absurd?

    Me, I’m waiting for the longitudinal study on a random sample of 100.000 people who are given a battery of fMRIs at 5 year intervals from birth to their natural deaths. Maybe then we would have some data worth talking about.

    Till next time.

  • Hi Joanna (I hope this comment ends in the right place)

    I’m afraid I cannot say anything of help when it comes to specific therapies for autism, but I just wanted to thank you for posting your experience of catatonia which I think is incredibly valuable – I hope I’m not trivializing it by saying this.

    I really just cannot understand how psychiatrists can ignore accounts such as yours and refuse to take them as their starting point. How can their minds be so closed? At one level I understand why, but I still find it hard to believe; it is so profoundly irrational, this inability to see what’s right in front of their faces. To me this irrationality of psychiatrists is something that rightly deserves the name “mental illness”.

    Anyway, I’m sure you don’t need another rant; I’m sorry I cannot be of help and thanks again

  • I’d say we disagree 100%, but at least we’re getting closer to understanding how we disagree. The colours thing is an attempt to explain in a simple way how a phenotype variant can be associated with a particular type of “disease” without this implying in any way that that phenotype predisposes for that disease. It answers, if you like, the “mystery” of adoption studies (a mystery that is not resolved by saying “there must be something genetic in schizophrenia, we just haven’t found what yet”). I know it all sounds a bit convoluted but it is extremely important in practical terms, particularly in connection with ‘preventive psychiatric interventions’ and the combined use of neuroimaging and genetics. If these “finer points” are not clearly understood we might be heading towards a very bad place (I’ll avoid mentioning the nazis).

    Precisely my point is that I do not think some brains are more resilient than others, or rather: yes, brains as organs can (like the rest of the body) be more or less resilient to “material” pathogens (virus, etc), but MINDS are not. All minds are equally resilient or vulnerable to trauma. We are dealing with “mental” disorders, not brain disorders (that is the whole basic debate, isn’t it?) and the mind, the active brain, is not a brain-in-a-jar, but a system of interactions. Trauma or abuse is not a material pathogen but a relational -“immaterial”- pathogen, and psychosis is not a “disease” of the brain, but one of the ways in which the mind defends itself from this relational pathogen. If you are looking for a disease, a mental disease, you are looking for a relational disease -a disease of the system- and so you must look at the whole system of complex interactions around the ‘schizophrenic’ individual. To put it another way: one ‘schizophrenic’ individual is not a diseased individual but a symptom of a disease affecting the social group of that individual.

    All minds (in your terms, all brains) are equally resilient and given the same trauma they all experience the same harm, but this harm is expressed in different ways – some more damaging for the group than others. And I’d say that “schizophrenia” is actually at the lower end in terms of harm to the group: “schizophrenia” is -for society- one of the least harmful responses to trauma. ‘Schizophrenics’, so to speak, ‘trap’ the harm done to them inside themselves and only pass on small amounts of it; they suffer so conspicuously because they don’t pass on the harm, they wrestle with it in their minds. Other responses to harm involve passing it on, such as in the extreme case of the sexually-abused who becomes a sexual abuser (just one example of many); these responses are far more harmful to the group. I don’t think anybody can be exposed to trauma and be “fine”, it is just that some ways of not being fine are less obvious or more socially accepted than others. And by the way, although this is too large a subject: the more socially accepted a way of not being fine is, the more harm it causes to a society; societies which accept too many ways of not being fine as ways of being fine collapse and “die”.

    Of course all this is in many ways a very uncomfortable hypothesis; for one thing it implies that if ‘schizophrenics’ do not develop ‘schizophrenia’ because they have an innate vulnerability which makes them unable to deal with ordinary levels of stress, but on the contrary only abuse of one type or another can bring about ‘schizophrenia’ (as a defence mechanism against abuse), then for every ‘schizophrenic’ there must be one or more abusers. This hypothesis shifts the responsibility from the ‘schizophrenic’ to the surrounding group, and of course the group does not particularly like that.

    About autism: the greatest problem with autism is that if ‘schizophrenia’ is a near meaningless term because it is just an umbrella term for some vaguely defined traits, ‘autism’ is ten times worse in that respect. If fact there’s no doubt that the term ‘autism’ applies to several disorders (and some non-disorders) with completely different etiologies, which is why it’s really called ‘autism spectrum disorder’, the ‘spectrum’ meaning: this is not just one thing but many. So it is impossible to discuss autism in general.

    Some forms of ‘autism’ are in fact genetic disorders (or rather, behaviours associated with genetic disorders) but here is the catch: in these cases we have already identified the genes responsible for the disorder – there are no complicated mysteries, no elusive genetic ‘vulnerabilities’. A very different story from ‘disorders’ such a schizophrenia where the genes have not been found and the only evidence that there is a genetic component comes from those ridiculously limited and flawed twin and adoption studies. Studies which even if they were not flawed yield results which can be interpreted in different ways (I showed you one, there’s probably others I haven’t thought of). The situation could not be more absurd (and tragic).

    But since you bring autism up, check this out:

    http://www.casinapioiv.va/content/dam/accademia/pdf/sv117/sv117-bear.pdf

    It isn’t a research paper but a presentation given at the Pontifical Academy of Sciences (which has a lot of very interesting material available for free – a little-known treasure-trove of references).

    You’ll like this paper, it describes research into a drug to reduce cognitive dysfunction (‘autism’) in people with fragile X syndrome. It is 100% biological psychiatry – this is in fact how it starts:

    “We have entered the era of ‘molecular medicine’ in which it is anticipated that the knowledge of the human genome will reveal causes and treatments for mental illnesses. This process begins with careful clinical identification of patients who can be distinguished by a common set of phenotypic traits, thus defining a syndrome. Molecular genetic studies are then undertaken to test the hypothesis that the syndrome has a shared genetic cause.”

    Needless to say I think the author is working within the wrong conceptual framework but he is nonetheless an honest scientist going about things the right way; the paper shows good science at work. If drugs currently in use in psychiatry had been developed like this I can assure you not a single one of them would have ever reached the market or be in use.

    I don’t think you are being quite honest with yourself, Scott… a good starting point would be reading AoE.

    One last thing, this paper I link ends with this paragraph:

    “It is important to add, however, that while drug therapies might correct disruptions in synaptic biochemistry, they will never substitute for quality sensory experience and education. We imagine the drug treatment will unlock the potential for substantial gains in cognitive and social behaviors. But this potential will only be realized when pharmacotherapy is combined with appropriate cognitive and behavioral therapies that exploit life-long neuroplasticity.”

    ‘Life-long neuroplasticity’, now that’s something worth talking about and of immense importance for all “mental illnesses” whatever their etiology; but we don’t hear a lot about it, in fact almost nothing, I wonder why?

  • I break my self-imposed silence to briefly clarify something from my comment above:

    In my analogy of colours, just like yellow (trauma) goes in, it can also go out – it is not a one-way process. If you end up of a colour that is a “disease” (very bright green, or very bright orange) in the sense that it impairs your functioning in the world or in the sense that you are a nasty piece of work knowingly or unknowingly destroying the world, it does not mean that you cannot change and get rid of enough yellow (probably not all, true) to be a much better shade. Depending on the amount of yellow presents some will be able to do it on their own, some will need help (that is, real help and not abuse masquerading as help), but I am sure it is always possible.

    Just wanted to clarify this because if you imagine the analogy with paints it might read like I’m describing an irreversible process. Imagine it with light rays and the analogy works better…

  • Hi Faith, Hi ScottW,

    First of all, Faith, to clarify, I agree with you, not with ScottW (no offence, Scott). I don’t know if my arguments sometimes sound like I’m rooting for “the other camp”, but unless I misunderstand myself (and I don’t think I do) I am definitely not.

    What I am saying is that if you are going to call “schizophrenia” (and I don’t think that word means anything, but it’s shorter than discussing separate symptoms which is what we should really be doing), if you are going to call “schizophrenia” a “mental illness” then everybody in the world without exception is “mentally ill”. There is no essential difference between a schizophrenic and a non-schizophrenic – the difference is one of quantity, not of quality, and nobody gets a completely free ride. Do I believe in “mental illness”? No, not unless you are happy calling something that is present in every single person’s personal make-up an “illness”.

    Perhaps another analogy might be helpful to explain what I mean:

    If you mix yellow and blue you get green, if you mix yellow and red you get orange, right? If you have a gradation from red to blue (a long row of boxes with different mixes of red and blue, with pure red at one end and pure blue at the other) and you mix yellow into that gradation you’ll get a different gradation from orange to green. A given amount of yellow will change the whole red-blue gradation. It won’t change one box more than another; the change throughout all the boxes will be uniform. If you add more yellow the whole gradation will change more, if you add less yellow it will change less.
    Now, say yellow is “trauma” and the red-blue gradation represents all possible human phenotypes (expressed genomes). If you apply the same amount of trauma you’ll get the same amount of change in all different phenotypes, but of course this change will look different for each phenotype; even though the yellow is the same, each box has a different colour to begin with, so obviously each resultant colour will also be different. But the rate of change will be the same. Given the same amount of trauma, the magnitude of effect on each phenotype will be the same. Since the amount of trauma (yellow) depends on the environment and each individual’s environment is in some respects different from any other individual’s, no two individuals actually receive the exact same amount of trauma (of yellow) so their actual rates of change are different, but this is because the input of trauma is different, not because they respond differently to the same input.
    Now imagine an observer -“society”- labels the shades that are more obviously green as “mental illnesses”; a particular cluster of shades of green is labelled “schizophrenia”. There is however no reason to say that the original shades of blue had a “propensity” or “vulnerability” for “mental illness”. For this to be true, blue would have to change more than red when it is mixed with the same amount of yellow; the rate of change would have to be different, and it isn’t (or that’s what I think and how I interpret adoption studies).

    I know Scott will be thinking, OK, maybe, but green would still be a “disease” because it makes the “green people” less able to cope with their environment; it decreases their capacity to adapt and “survive” whereas orange people do fine, so “oranges” are not ill. But what I’m saying is that orange people don’t do fine either, and here is where we have to question a bit what a disease actually is.

    A disease is something which lowers survival, yes, but when it comes to “mental illnesses” we have to take into account that the human mind is in constant interaction with the environment and very particularly with the social group, with “society”. In this context survival cannot just mean survival of the individual, but must also mean survival of the group as a group. What I am suggesting is that the disease of the “oranges” who seem to be doing fine is a “social disease”; a disease which affects the survival of their social group rather than their own individual biological survival.
    So for example: an “orange” might be a very successful executive of a pharmaceutical company, and the lack of empathy and obsession with personal success which are the result of the “trauma” he’s received in his upbringing does not have a negative impact on his life as far as anyone can see. But this lack of empathy and obsession with personal success makes him cover up the fact that one drug his company manufactures has very bad unreported side-effects and 0 effect on the condition it’s supposed to treat (let’s call this hypothetical drug “Proxac”). What he is doing might no even be illegal and it has no negative effect in his life: his employers love him, he makes more money; life’s good. But in the meantime “Proxac” is causing havoc in his social group, his country, culture, by disabling an increasingly large number of people, putting stress on resources, damaging the economy, etc. His actions are having a detrimental effect on the survival of his group: they are a “social disease”. Like the body is made up of cells, the social body is made up of individuals, and you can (you must) apply the concept of disease to both bodies to get the full picture.

    That’s more or less it in a nutshell, although obviously this is a gross oversimplification and there are other fundamental aspects to this I’m not touching on, such as Free Will (yes, it exists). The only other thing I’d mention is that I think we are all exposed to certain amount of trauma, so everyone has a certain amount of “yellow” in them. As you can see, this hypothesis crosses over from science into philosophy and so I’m not sure to what extent it is falsifiable in a strict sense, although certainly parts of it are.

    Also, Scott, although I don’t want to go into it in detail I’ll just mention because I think it might interest you that in other comments I have written about psychosis being a defence mechanism, not a symptom of the disease but part of the healing process; much like fever which is part of the body’s immune response to a pathogen and not just a symptom of a “disease”. Of course, just like fever can in extreme cases be harmful in itself and an intervention is needed to stabilize the patient, the same is true of psychosis, but the emphasis is on the fact that this is only justified in extreme cases and, crucially, the intervention must actually stabilize the patient and not just appear to do so while in fact adding wood to the fire, so to speak. In this I’d say that current psychiatric interventions are catastrophic; the only good thing you can say about them is that they are better than a bullet to the head, which is not really something to be proud of. To follow the fever analogy, they are like trying to lower a fever by blood-letting (actually, blood-letting for fever has a sounder scientific rationale).

    By the way, in case I cause confusion: the 50%-10% figure in my previous comment was completely made up as a hypothetical example; it does not come from an actual study.

    And Faith, I never got around congratulating you for your article, I thought it was very good. But your responses to ScottW are even better; I think it’s good of ScottW to pop up from the underground from time to time.

    Thank you ScottW for being the “devil’s advocate” here (and please do read AoE; it’s not the bible, but it condenses a lot of information in a clear format – and don’t forget “The Emperor’s New Drugs” either).

    Now I really have to get back to work; might not be able to comment/answer for a while (collective sigh of relief?)

  • Hi ScottW,

    As I’m sure you realize now my first reply to your first comment referred to “exactly the SAME rate of…” Anyway, I don’t think I need to comment on that anymore…

    Regarding twin-adoption studies, I think their two greatest flaws are a) the absolutely ridiculously tiny sample size (nobody’s fault, there just aren’t that many identical twins separated at birth into different adoptive families who go on to develop “schizophrenia”), and b) the fact that, given the problems associated with such small samples, the studies do not control for the possibility that higher rate of schizophrenia in the twin group is simply due to chance – I know this might sound ridiculous to you if you are used to studies with much larger samples where this kind of thing simply does not happen, but when you are dealing with sample sizes so small the possibility of simple chance cannot be ignored; a seemingly impressive higher rate of concordance might come down to two or three extra twin pairs. Perhaps I remember this incorrectly, but I think that in some Finnish study where a database exists which allows to look at the adoptive family environments of the study’s subjects (which had not been looked at when the studies where published) this chance difference in family environments could account for a lot of the difference between twins and non-twins: by chance more twins than non-twins had ended up in “dysfunctional” families.
    The point is that these studies should look at the adoptive family environments as part of the study, and they do not.

    But all that aside, let’s say that in the end you do find a higher rate of concordance in twins than in non-twins (adopted non-twins, you cannot compare with rates in general population since the adoption itself could play a part in schizophrenia). I get your point that this seems to point to a “genetic component” and to some extent I agree, but only to some extent, since to me that genetic component is of no importance whatsoever from a therapeutic perspective and cannot be said to form part of the “disease”. I know this all sounds a bit convoluted; perhaps a good way to explain it is this:

    Let’s say for the sake of argument that you do find that 50% of adopted monozygotic twins develop “schizophrenia” and only 10% of adopted non-twins develop it. I say you can still interpret that as evidence of a 100% environmental disorder. But what could this possibly mean other than I’m a sore loser? It means that the 40% non-twins who are not developing schizophrenia but who, for the disease to be environmental should develop it, are in fact developing something else – another “disorder” which goes under the radar of the study because it does not fall within the conceptual framework of a “medical disease”. And it is not one single disorder either, but many, and just as “bad” if not worse that schizophrenia. The pathogen is in the environment, and it causes damage to all who are exposed to it (to 50% of both twins and non-twins) but depending on very complex genetic differences (what in the good old days of common-sense used to be called “temperament”) this damage expresses itself as “schizophrenia” in some cases and as other “non-medical disorders” in other cases.

    What could these “non-medical disorders” be? Let’s use an example: imagine a person “S” with temperament “s” (coded by many genes spread throughout their chromosomes) suffers repeated sexual abuse as a child and as a consequence develops “schizophrenia”. A different person “P” with temperament “p” suffers the same sexual abuse and does not develop “schizophrenia” Aha! “S” has a vulnerability for schizophrenia! No, not quite; here is the catch: “P” becomes a paedophile and a violent sexual predator. Furthermore, “P” is quite clever and escapes detection so his disorder is never noticed. This is a very crude example but I think you’ll get the idea of what I mean. One environmental “pathogen”, 2 genetically-determined temperaments and two different disorders, one “medical” the other not quite (a lot of debate about that). One, schizophrenia, will be very visible whereas the other can go unnoticed for a long time and continue “infecting” other people. Which one would you say is “worse”? Is there any point other than academic curiosity in finding out what the genetic variations which code for temperament “s” (or “p”) are? Particularly if it turns out that temperament “s”, in the absence of abuse, results in particularly intelligent well-adjusted people? Are you going to “correct” their genes in case they are sexually abused later on in life? Your target, obviously, should not be “s” or “p”, but sexual abuse.

    But does this hypothesis obtain in the real world? The great difficulty is to know what these “non-medical disorders” are, and also what “abuse” or “trauma” is, because of course it is not always going to be something as obvious as paedophilia and sexual abuse. I’ll just say this: take a look at the world. Do you see poverty, crime, random violence, war, pettiness, anxiety, insecurity, substance addiction, human trafficking, selfishness of all kinds and shapes? I walk past the same homeless man everyday and sometimes he catches my eye and smiles, and you know what I do? I look somewhere else. Is that the response of a “healthy” human being?

    I know, this is not the nice, clean and simple science where “diseases” are simple discrete entities; it sounds too much like philosophy and too much like politics and almost like religion, but I’m afraid reality is not nice, clean and simple but very, very complex (and in its complexity very beautiful too). The “mind” sciences are not going to go anywhere if they continue to think within the little boxes of XIX century scientific disciplines… whatever happened to the interdisciplinary revolution?

    Oh! And next time you “see someone with severe psychosis, disheveled, unable to speak, unable to take care of their basic human needs” please try to find out what medications he or she is on and for how long he or she has been on it; that might have something to do with it… (did you get around to reading “Anatomy of an Epidemic” yet?)

  • The article has a nice North Korean touch about it: “Citizens rejoice! Government and Industry are working together for your safety!”

    Faith R. makes an interesting point, though: Big Food is just as big and bad, if not bigger and badder, than Big Pharma. So that makes me think that this caffeinated gum was probably not selling and they were going to pull it anyway, but that’d be a commercial failure which makes company executives look bad. Much better to throw a bone at the FDA, who gets to pretend they are actually doing something for public health; Mars gets to look all caring and enlightened and can continue with the business of selling beautifully packed blends of salt, fat, sugar and possibly carcinogenic chemicals without any objections from the FDA. I know, it’s paranoia, but at least it keeps me entertained.

    By the way, they forgot to mention in the article: anyone getting jittery from sudden caffeine withdrawal must contact their doctor for a safe prescription of benzodiazepines.

  • Ron, I’m glad you bring up humility since what spurred me to comment on this post was what to me seemed a remarkable lack of humility in Alison Brabban’s intervention (true that the video only shows small fragments out of context). I wonder how it struck you. I could not help thinking that given the relative successes of the HV movement and conventional therapies -when you adjust for differences in funding, access, etc.- conventional therapists such as Alison should be approaching the HV movement with a lot of humility and a learning, rather than a teaching, attitude.

    Regarding the other points you make I fear we are misunderstanding each other, which is not surprising since we are dealing with subjects that cannot be discussed in a few short phrases. I won’t press the point of “vulnerability” although I’d ask you to consider the impact that kind of terminology has at a policy-making level on issues such as enforced medication, etc.

    I will make however on last attempt to clarify the question of whether “voice hearing is a cause of stress or a way to deal with deep-seated underlying stress caused by a history of trauma.” I can see from your comment that the way I phrased it was too confusing.

    Of course the experience of hearing voices will often be stressful (to say the least), that is in fact the whole point: the voices act as a channel through which the voice hearer can access emotional trauma (as well as other aspects of him or herself, but let’s leave that aside) and deal with it through symbols at a conscious level. Without the voices the trauma would still be there, but would be harder to “reach” and come to terms with, and would potentially cause more damage: self-harming, aggression, suicide, etc.

    The voices are, so to speak, tunnels which give access to the trauma buried deep within the person. If through them you can reach the trauma and heal it (as far as that is possible) the voices should cease to be a source of distress; in some cases they’ll disappear, in others become part of an harmonious self. Of course facing trauma and making sense of it, although necessary for the healing process (CBT might disagree with that), is in itself an stressful experience and the voices might be frightening and hurtful even if they are part of a positive healing process.

    Needless to say this is an extremely crude oversimplification of something very complex, but that’s the general idea. And of course, where the trauma is severe the voice hearer might be overwhelmed by emotional distress, overwhelmed “by” the voices, and be in need of help, therapy (for the underlying trauma, not for the voices themselves) or in extreme cases emergency interventions to guarantee his/her safety or that of others (the damaging abuse that takes place in those emergency interventions as carried out in current practice is a different story, but it needn’t be like that). A therapist trained to heal trauma might indeed have a lot to offer (whether CBT is best suited for this, that’s also a different story) and his or her job as a therapist should be in fact facilitated by the voices, if he or she knows how to listen to them. But that’s one of the difficulties, without first-hand experience or at least a “native guide” he or she might get lost navigating the voices and miss the unique opportunity for healing that the voices represent.

    Anyway, I’m getting tangled up in my own rhetoric and this comment is already far too long so I’ll leave it at that.

  • Then we agree to some extent, but I’d suggest “vulnerability” is the wrong term, as it does imply a degree of irreversibility. At least I think you’ll agree that most people who talk in terms of vulnerability use the term in that way. I don’t think the concept of vulnerability includes the possibility of its being derived from a “positive quality” but on the contrary it is often associated with the need for life-long treatment of one kind or another – almost inevitably it leads to people perceiving themselves as “ill”. I think perhaps what you describe could be better called a Hypersensitivity-stress model, where early exposure to high levels of stress (trauma) leads to a stress hypersensitivity – a better model than the vulnerability one but still, I think, incorrect.

    In previous comments I have used the analogy of “the gene that codes for better food absorption and the contaminated food”. I won’t repeat it again because it gets quite long, but the point of it is precisely to emphasize the difference between a vulnerability (or predisposition for a disease) and a positive trait which in the presence of a deleterious environmental agent (trauma) can become disadvantageous for the individual that possesses that trait. The two things might be difficult to tell apart but they are fundamentally different.

    This difference is very important for lots of reasons, but I’ll mention only what I think is key in connection to the relationship between the HV movement and something like CBT (and I admit I don’t know much about CBT… or the HV movement). The key question is: how do you view “psychosis”? Or to narrow it down, voice hearing; how do you view voice hearing? As a positive or a negative trait? Is voice hearing an expression of health or of disease? My own reply is that it is an expression of health – and I don’t say this to make voice hearers feel good about themselves.

    What do I mean then, that voice hearing is an expression of health? To put it very briefly, I’d say that voice hearing is a defence mechanism is the presence of extreme trauma. In other words, it is the healthy “normal” response of a healthy “normal” human organism when it is exposed to certain deleterious environmental agents. But if voice hearing (or other forms of “psychosis”) is the healthy response, what is then the unhealthy response? Isn’t the healthy response worse than the disease? Not when you put things in context; the unhealthy response is mainly death or extreme forms of withdrawal. Psychosis is what a healthy brain does when the only other logical response is jumping out the window.

    Of course the objection to this idea is that not all psychotic people, not all voice hearers, appear to have been exposed to what we might call “extreme trauma”, and there are also people exposed to trauma who do not become voice hearers. And “psychotic episodes” are usually not brought on by traumatic incidents but by everyday-type stress. Hence this idea of vulnerability: the voice hearer as someone less able to cope with trauma or stress… it really is too complex a subject to go into it in a blog’s comment, I have to cut it short here. But I hope this might make you look more closely at the Vulnerability-stress model and ask yourself this question: is hearing voices a “natural therapy” with which the healthy body tries to combat a “relational disease” (traumatic relations created by one type or another of abuse)? Or, on the contrary, is voice hearing a symptom of a disease (psychological, physiological; same difference)? Is voice hearing to be carefully encouraged because it gives the voice hearer the best possible tool to deal with underlying emotional distress? Or is it to be discouraged, the aim of therapy being to minimize voice hearing and seek other avenues of dealing with emotional distress? Is voice hearing a cause of stress or a way to deal with deep-seated underlying stress caused by a history of trauma?

    And one last thing: if we are talking of encouraging voice hearing, can anyone other than someone with first-hand experience of voice hearing take on that responsibility, no matter how highly trained a therapist they may be? I’m not so sure.

  • Neural activity yes, but brain morphology? Can it be changed by experience? I think so, and plenty of evidence, but psychiatrists on the whole don’t – they operate within an ephiphenomenalistic framework (Philip has written about this on previous posts).

    If you believe experience cannot change brain morphology, and a brain scan shows your brain’s morphology to be different… then the way to the extermination camp does open up, or at least that’s what history teaches us; the belief that there are unchangeable physical traits which determine our behaviour in a way that cannot be altered by experience can take us to very bad places indeed.

  • But is it not the point that the HV movement is NOT a therapy? A therapy by its very nature has a structure therapist-patient, and no matter how much to try to disguise that structure it is always there defining and conditioning the relationships of the people involved. On the other hand HV, not being a therapy, has a completely different underlying relationship between people who take part – between its members (not “patients”).

    Clearly CBT is a therapy, so while dialogue -exchange of information- is of course possible and welcome, I don’t see how you can mix HV and CBT; they can be good neighbours, but not bedfellows. If you try to turn HV into a therapy you will alter its structure and completely destroy it – it will lose that which makes it work in the first place.

    Also, I don’t think the vulnerability-stress model issue is a small detail; it’s like saying that it’s OK for a group of people who work for the emancipation of black slaves to think black people belong to an inferior race, because slaves should be happy for any help they can get. As for a non-genetic vulnerability, I’m afraid I’m not sure I understand what you mean. The whole point of a vulnerability is that it is innate (maybe not genetic, but innate and “biological”); if it is the result of trauma then it is not a vulnerability but simply damage caused by trauma, which accumulates up to the point where it becomes symptomatic (“psychosis”). The vulnerability in the “vulnerability-stress” model is always innate, and once “triggered” by trauma there is no point trying to treat the “trigger”, which is why neither conventional psychiatrists nor CBT therapists give genuine importance to life histories and to making sense of past experiences and their relation with present experiences as part of the healing process. I think the only dialogue possible between HV and any group that believes in the vulnerability-stress model is to show that group that the model is wrong. That should be the basic starting point.

  • Very interesting video, thank you. Alison Brabban made me laugh (bitterly) at around 18:24. It seems that if you give a scientific-sounding name to what you do at Hearing Voices you’ll be greatly rewarded by the Powers That Be. Make sure it’s a name with a catchy acronym though, that’s the most important part. I’d suggest: Altered Perception Endogenous Intertransactional Therapy, or APEIT for short (get it? Ape it… I’m sorry)

    I think professionals get very nervous when they are left out of the loop. If you don’t classify what you do and give it a nice acronym, they cannot teach it at university and make money from it themselves, and they can’t eventually tell you how in fact you are doing it wrong because you are not a qualified practitioner of APEIT. If you classify it and give it a good acronym you can then stop looking at the people and concentrate on following the manual; you don’t need empathy, sensitivity, intelligence or (God forbid!) first-hand experience; it is enough that you follow your manual accurately en efficiently. And of course politicians and bureaucrats love that, that’s all they really understand.

    This has nothing to do with science; nothing stops researchers from approaching Hearing Voices groups and doing a longitudinal study of outcomes of people in those group so they can compare them with outcomes of people receiving drug therapy or CBT. I would love to see that study, but it is certainly not HV’s job to do that study, their job is to help people heal. You do what you do because it works – I think clinging to that is the best way to avoid colonization. It is not about big social changes in the future (those never quite work out the way we want), but helping real people in the here and now.

  • Thank you for this article, Philip.

    I confess my heart sank when I read Thomas Insel’s post. First thoughts: “the biggest rats are jumping off the sinking ship”. The good news is that the ship is sinking, the bad news is that the biggest rats are getting away and they are building themselves a new, bigger and better ship, provisionally named “RDoC”. Partial good news is that the new ship is not yet quite finished and operational; it’s still in dry dock.

    If these rats that are getting away from the DSM manage to complete and launch RDoC we’ll enter a new era which will make what has gone on until now in psychiatry look like a picnic in the sunshine. At least with symptom-based diagnostics you need to have some symptoms, however vague; something like the RDoC will do away with that minor inconvenience. And as for it being open to falsification, on the evidence of what passes for acceptable evidence in mental healthcare, don’t hold your breath for falsification. At least not until unimaginable harm has already been done. The phrase “jumping out of the frying pan into the fire” comes to mind.

    I hope I’m crazy and these clouds I see gathering are only in my mind.

    PS – I’m a great fan of neuroimaging and I think it offers great potential, but not like this. Not like this.

  • In case it is not very clear:

    The study is a very limited study which looks at just one particular type of anti-depressant. As far as I can understand it – which I admit is not very far at all – it is not badly conducted, although of course it looks at suicide ideation rather than actual suicide, and makes no claims as to the link between those two things. As the authors of the study themselves conclude: “Until functional alleles are demonstrated or replication is shown in an independent sample, these findings should be viewed as preliminary.” Let me emphasize that: preliminary.

    And yet NeuroMark Genomics – a company whose CEO was Kim Bechtold and where Wayne Bechthold was listed as Vice President of Administration and which, like Sundance DX, is or was located at Boulder, Colorado – made this announcement on September 27, 2007, that is to say, on the very same day the research paper was published online:

    “NeuroMark, a Boulder, Colorado company, announced today the immediate availability of a genetic test to identify people at risk of suicidal ideation – thoughts of committing suicide – when prescribed an antidepressant drug. The test, called the Mark-C™ test, is expected to help restore public confidence in antidepressant medication and help to reduce a recently announced spike in suicide rates among U.S. youth. “This is an exciting example of the power of genetics to address a critical need and make important drugs safer for patients worldwide,” stated Kim Bechthold, NeuroMark’s CEO.”

    So Kim’s company already had a test developed and ready to go based on a study which describes its own findings as “preliminary” and in need of further confirmation before any conclusion can be drawn from them. In spite of which Kim had no trouble saying that a test based on that preliminary study “is expected to help restore public confidence in antidepressant medication.”

    Perhaps it’s just me, but I just cannot see these as the actions of people genuinely concerned with saving lives. To me these are the actions of opportunistic individuals whose only concern is making money, no matter what the consequences might be for others. I repeat my question: what happened to the Mark-C test which Kim Bechthold was marketing with such enthusiasm only a few years ago?

    I will not continue posting on this subject; I will resist the temptation to list all the details which give “Sam” away as Sundance’s plant (just a hint, Kim: no CEO would ever say when posting in her professional capacity, no matter how jokingly, “we would like to hire Sam”)

    I will just say this to Maria:

    Maria, if you are still considering giving some kind of endorsement to Sundance DX, please, please at the very least wait not only until they have published the results of their research but until their test has been in use for some time and they can provide you with reliable statistics on the accuracy and usefulness of that test – statistics that can be independently verified. Please do not rush into an association which could so easily destroy everything you have worked so hard to build when there are still so many questions unanswered.

  • It’s true that Sundance’s research is not available yet. Anyone interested can however check out the research on which NeuroMark Genomics, Kim and Wayne Bechthold’s previous company (Wayne being now the president of Sundance dx), based their Mark-C test, also designed to identify suicide risk linked to anti-depressants.

    Research here:

    http://ajp.psychiatryonline.org/data/Journals/AJP/3834/07aj1530.PDF

    A very informative and unbiased article about Mark-C here:

    http://www.dreamfigure.org/entry/mark-c-test-reduces-antidepressants-related-suicide-rate/

    And an interesting side-story here with links worth checking:

    http://neurocritic.blogspot.co.uk/2007/09/on-your-neuromark-get-set.html

    I have to say that from all this literature the Mark-C test sounds very impressive, I wonder what happened to it or to the “Mark-C Outcomes Database”?
    Or to NeuroMark Genomics (their website seems to be down at the moment).

  • Kim, Sam,

    Please stop it, you are embarrassing yourselves.

    Maria,

    I hope this exchange helps you see what you are dealing with. If you still have any doubts please consult with any independent person who knows anything about genuine genetic research.

  • Karl Popper was the man who came up with the notion of falsification as a way to distinguish between what is a scientific statement and what isn’t. He developed this concept in his 1934 book “The Logic of Scientific Discovery” (well, the original is of course in German, “Logik der Forschung”). Popper himself, being a philosopher and not a scientist, was not dismissive of all unscientific statements, he was simply interested in finding a criterion of demarcation for scientific statements.

    By the way, Sam, I have to say I really admire your quick thinking. Considering that at 5:16, when I posted my mention of Kirsch’s book, you had “never read anything about Irving Kirsch” it is very impressive that by 6:05 you had managed to find so many arguments against Kirsch research, and that you were able to read through all that material and make up your mind about it, let alone write the actual post. Truly impressive – I must say I’m humbled.

    Oh! And of course I never said you were a troll, I hope you didn’t get the idea that I resented any of what you said. I said you might be plant, but of course you know I’m only joking.

    Give my best to your son. I hope he is doing well.

  • Kim, I just realized I misread your post. I didn’t notice the “known” when you wrote “invest in very expensive whole genome sequencing so that we could find every KNOWN marker for genetic high risk rather than just a few”.

    So of course you are not engaged in GWAS research, which would’ve been very odd, that was stupid of me.

    I think the reason I was confused by your statement is because I’m not sure why you need to sequence the whole genome in order to look for already known markers for “genetic high risk”. I can see how it might be a good marketing ploy since “whole genome sequencing” sounds impressive but I don’t see the scientific rationale behind it, since whole genome sequencing is not going to give you any more accurate predictions that only looking at the specific known markers. But of course I don’t know exactly which specific markers you refer to – may I suggest that you should perhaps include this information in your website, as well as links to the relevant studies that claim to have established an association between those markers and higher suicide risk? Because of course the efficacy of your test in predicting suicide risk will only be as good (or as bad) as those studies.

  • Hi Sam,

    First of all let me tell you how sorry I am to hear about your son.

    I’m more or less familiar with those criticisms of Kirsch’s work and I don’t think they have much weight. Kirsch’s work consists mainly of analysing clinical trials conducted by the anti-depressant manufactures themselves (mostly the clinical trials used to get the drugs approved) so criticism like: “His study looked at research with durations from 1 to 20 weeks, but it is well known that the full therapeutic effect of SSRIs requires 6 weeks, so why would he include studies from 1 to 5 weeks?” can hardly apply. Whatever the shortcomings of the studies, they are in fact the shortcomings of the manufactures’ clinical trials which, if anything, raises even more questions about the efficacy of anti-depressants.

    I’m afraid I don’t have the time to go through the criticisms one by one, so I’ll just say please read the book, or if you are used to reading research papers (as it sounds you might be), then I would encourage you to look at Kirsch’s actual research – the book comes with a very complete bibliography. At the very least I can assure you that it is all pretty mainstream scientific analysis; no “chiropractic adjustment”s anywhere in sight.

    Also, since Maria Bradshaw mentions that “I understand sundance have been in contact with David Healy and are hoping to engage him in reviewing the data” (March 16, 2013, at 5:16pm), it might interest you to read David Healy’s praise for “The Emperor’s New Drugs” (printed on the inside of the front cover of the edition I have). He writes:

    “Irving Kirsch brilliantly documents a grim scandal of regulatory and clinical failures concerning antidepressants but also holds out hope in one of the most profound meditations for 50 years on the nature and role of the placebo effect in clinical care.”

    I’m glad to hear you use the word “falsified”; not a lot of people seem to be aware of Popper’s criterion of demarcation these days. I know some people still question de validity of falsifiability, but in this I’m a staunch Popperian – and I certainly feel psychiatry would benefit enormously from applying falsifiability a bit more strictly (such as for example to “genetic safety testing”).

    As for your question: “If […] depression is not a matter of brain chemistry imbalance, then what is it?” I wish I could go into it but as I said I’m afraid I don’t have the time at the moment, and in any case this is not really the ideal format to go into such a big question in detail. I’ll just say that it isn’t so much whether depression is a “brain chemistry imbalance” or not , but what the etiology of that “imbalance” is, and how it can be best corrected (“imbalance” is not a very helpful term, it would be better to speak of “atypical physiology” or “atypical morphology”). Without getting into it I can only point you in the direction of neuroplasticity and activity-dependent plasticity, which explains how environmental experiences (such as trauma or psychotherapy) can lead to changes in “brain chemistry” and even brain morphology. It is really a question of which is the cause and what the effect; a chicken and egg sort of thing. The field of neuroplasticity is still in its infancy but it is already ringing the death-knell of biologically-determined psychiatry.

    By the way, and please don’t take this the wrong way, but isn’t it funny how if you look at your first post and the timing of Kim Bechthold’s reply to it, and now your reply to my reply to Kim’s reply to your post, it almost looks like you could be Sundance’s “plant” in this thread? Like you could almost be working for them… you aren’t, are you? (Just kidding!)

  • Hi Maria,

    I hope you read my reply to Kim Bechthold above. Please forgive me if I’m blunt, and of course this is only my personal opinion, but I feel this is too important an issue to not speak clearly: it seems to me that Sundance Diagnostics are taking you for a ride in the most unprincipled way imaginable.

    I hope I’m wrong, and I’m sorry to be so blunt; if I speak like this is only out of genuine concern for you and the great work you are doing through CASPER.

  • Hi Kim,

    Thank you for taking the time to write here and share with us some of the challenges a company such as yours face.

    If I understand it correctly Sundance Diagnostics is carrying out its own GWAS (or Whole-Exome?) studies into anti-depressant suicide risk? I looked through Sundance’s website but could not find any information on this.

    I did however find these texts on Sundance’s website:

    “The labels on all antidepressant drugs warn of the risk of suicide, causing a parent to worry about whether to seek treatment for a child who is depressed, a partner to worry whether to seek treatment for his loved one, a son to worry whether to seek treatment for his parent.
    This worry can cause delay while the depressed person’s life may be hanging in the balance. The genetic safety testing we are developing should give the patient and the family more confidence in proceeding quickly with treatment.”

    “When a drug makes a patient feel worse rather than better, he is likely to discontinue treatment. Untreated depression results in higher medical costs, hospitalizations and loss of job productivity, and can affect the ability of a mother or father to care for the family.”

    I wonder if you are familiar with research that shows that the effectiveness of all anti-depressants can be accounted for by their placebo effect, and that their active ingredients (which will be likely to play a significant role in the increase of suicide risk in children and adolescents) play little or no part in their anti-depressant effect. For an accessible review and explanation of this research I would refer you to Irving Kirsch’s excellent “The Emperor’s New Drugs” (ISBN 9781847920836).

    In light of this it would seem clear that the most effective way to prevent child suicide would be NOT to administer anti-depressants to children, and yet that does not seem to be the aim of your company, which does not seem to focus on preventing at-risk children from being prescribed anti-depressants but rather on “giv(ing) the patient and the family more confidence in proceeding quickly with treatment.” Which I presume refers to treatment with anti-depressants.

    This comments column is not the right format to go into a lengthy discussion as to why I think “genetic safety testing” for anti-depressant induced suicide is misguided, but I will go as far as to say that if you see this testing as a way to make people who would otherwise have had reservations about putting their children on anti-depressants “proceed quickly with treatment”, then your test will without a doubt contribute to an increase, rather than a decrease, in child suicide.

  • Great quote (Szasz’s – I should read him; I confess I haven’t); I think I know what he means. To me it is clear that psychosis can be interpreted as a defence mechanism: what a healthy organism does to defend itself from harmful stimuli. Psychosis is what the brain does to endure the unendurable.

  • Although these findings are good (did we really need a study to tell us?)I think studies like this do more harm than good in that they perpetuate the use of the concept of “resilience”.

    I don’t think resilience is a useful concept, certainly not as it is applied to human psychology. It makes people get stuck into thinking in terms of “lack of resilience”, and of “predispositions” to mental disorders; in terms of “deficits”, which I is neither correct nor useful.

  • Donna, I agree with most of what you say (I won’t say with all, because I haven’t read everything you’ve written!). My interest in the mental death profession is by way of my own profession, although in a very roundabout way. Not that I’m completely untouched by it at a personal level (who is these days?) but not too closely. Without going into a lot of detail I’ll just say that it has become progressively clear to me that a lot of people are lying about psychiatry and I don’t like that at all. I used to think that it was ignorance or lack of knowledge, but not any more. Of course, I won’t say that every single person in the field is lying, but far too many are, and certainly all those “at the top of the food-chain” are.

    Someone has written here that you are angry; well, I guess I’m angry too. Perhaps not enough people are angry or they are not as angry as they should be. I know it might be hard for a practising psychiatrist to give up everything he or she knows (and maybe a lot of what they own), but just like people affected as “users” have to rebuild their lives, any honest person practising psychiatry should face the fact that, like their patients, they have also been the victims of a lie and they need to walk away from it and rebuild their lives. I don’t think there’s any room to sit on the fence in this. To narrow it down to something specific: if in your profession you are using the DSM (or the equivalent sections of the ICD) you are part of the problem, not the solution.

    Getting back to the book thing, I mentioned it because I think one of the things that is really missing in terms of letting people know what is going on are more voices in “popular culture”. We can have a scientific debate about it, and it is happening whether pharmaceuticals want it or not because advances in areas of research that are not under their control, like for example neuroplasticity, are in clear contradiction to the model of biologically-determined psychiatric disorders; but science progresses very slowly and it’s going to be a while before that body of evidence is so overwhelming that they cannot bury it with money. We can have scientific journalism like “Anatomy of an Epidemic”, and without a doubt it does a lot of good and we need more of it; but a lot of people won’t read that kind of book (and they are not getting translated into other languages either). But I think we also need people telling their own experiences in a way that reaches a wide audience, we need “page-turners”, books that Hollywood will want to buy the rights of. Books that simply tell people “this is what happened to me”, no theories, no speculation, just letting the facts speak for themselves. Of course not everybody can write a book like that, but everybody can try, and out of 10,000 who try one might succeed, and sometimes one book is all it takes to tip the balance.

    Anyway, I just thought that if I saw a book called “The Mental Death Profession”, I’d buy it.

  • Hi Donna. This is completely off-topic and I don’t want to be a pest since I already said before how much I like your expression “mental death profession”. But now that you mention in passing your own personal experiences I cannot help feeling that that expression might be just the perfect title for a book, written by you.

    Of course other that having read a few of your posts I don’t know anything about you so this could be a ridiculous suggestion, but have you ever considered writting a personal book about your own experiences? I have a feeling you could do it very well, and books can be very powerful.

  • Hi ScottW!

    First, I owe you an apology. I was pressed for time in my reply yesterday and I’m afraid I was way too dismissive, particularly about diabetes II, something which has been niggling at me all day yesterday. I’m afraid I’m also pressed for time today, so again I’ll have to try to be brief, although I can honestly say that I would rather continue this conversation that do what I have on my desk… but I can only say a couple of things in reply to your thoughtful comments:

    About diabetes II, I think you might be right, although not necessarily in the way you think – diabetes II might not be a multifactorial disorder either, but a 100% environmental (I’ll return to this is a moment – I assure you it isn’t just a difference in semantics).
    Initially I just thought “diabetes II – probably autoimmune”, but if I’m honest with myself I was just avoiding the subject because, what do I know about the evolution of the immune system, autoimmune conditions or allergies? Not much, and I have to wonder why because it is a extraordinarily interesting area, so actually a big thank you for “forcing” me to think of this. One thing, though, about any possible analogy between diabetes II and psychiatric disorders (from a “clinical” rather than an etiological perspective, which I know is what we were discussing): insulin is not the “cure” but a very effective treatment for a symptom, hyperglycemia. The cure involves loss of weight, change of diet, etc. that in some cases can lead to complete recovery from diabetes II; you are cured when you don’t have diabetes II anymore, not when your sugar levels are under control. The cure is then to stop new “toxins” or “trauma” from entering the organism (change of diet) and give the organism a chance to heal (loss of weight) if damage has not yet become permanent. Of course insulin is a very effective treatment for hyperglycemia and the balance of benefit for the patient is as near perfect as you can hope for since it is not really a drug but you are redressing an imbalance (and I know that word immediately brings to mind SSRIs – for brevity I won’t touch on them other than to say please also read Kirsch’s “The Emperor’s New Drugs”).

    Now, when it comes to schizophrenia the drugs in use are, as insulin for diabetes II, not a “cure” but a way to manage the symptoms. Well, so far so good, but we are not just talking about an abstract model, so we would need to look at those specific drugs and their balance of benefit for the patient. And that balance is a catastrophe – to be blunt, they do far more harm than good. Practically the only way in which they manage the symptoms of schizophrenia is in a “social” way, by making the schizophrenic “less of a problem” (a bit like methadone prescription – an analogous case in this sense). And in the meantime what of the cure? Or at the very least what of other strategies which might be far, far more successful at managing the symptoms to the point that the patient can remain medication free and far healthier than on any medication? Would you make no effort whatsoever to look at the role of diet and exercise in diabetes II and just be happy handing out insulin to an ever-increasing number of people? Except of course the “insulin” given to schizophrenics doesn’t really “rebalance their glucose” but just keeps them from complaining about it while in the process giving them half a dozen serious conditions as a side effect. I really encourage you to read some of the recovery (or even non-recovery) stories in this website and familiarize yourself with the “voice hearer” movement. What can I say? To me it is a source of unabated horror how the psychiatric profession (clinicians as well as researchers) simply dismiss recovery stories; how they simply refuse to look in that direction and refuse to even consider for example the connection between the content of a schizophrenic’s “delusions” with their life histories. If nothing else it represents a lack of scientific curiosity that shames the entire field.

    Going back to multifactorial – 100% environmental: the question goes back to how a disorder evolves and is transmitted (although those two things are really just one) and how that sits with natural selection. Of course I’m not saying that “no gene variant can exist which is not fundamentally healthy for the organism” but I am saying that there is a threshold of complexity of genetic architecture beyond which a condition cannot possibly be seen as a disorder but must be considered as a trait – beneficial or at least neutral for the organism. You mention Huntington’s but of course Huntington’s has en extremely simple genetic architecture: autosomal dominant with bog-standard mendelian inheritance. And that is precisely the point, you can easily model how such a genetic disorder evolves and is transmitted and how natural selection lets it “slip through”. But schizophrenia has no simple genetic architecture (or we would have found it already) – in fact it must be so complex that we are not just talking about different genes at different loci but different loci on different chromosomes (again, if it wasn’t like this I think we would have found it already) . How would this complex architecture first develop and then be transmitted if it is a disorder – that is, it if it reduces survival/reproduction rates? And not only that, then we have to look at the incidence and distribution of schizophrenia across the globe – what kind of model would account for that pattern? There are also other considerations such as the fact that schizophrenia tends to develop relatively early in life (unlike for example Alzheimer’s) so that it would have a big impact on reproductive success “in the wild”. The only option which makes sense is that whatever genes might be associated with schizophrenia (if any, and I have my doubts that there really are any) the association is between a trait (a perfectly healthy type of human, if you like) and a deleterious environmental factor. If, as I said before, the “bad part” is wholly on the environment you cannot call that disorder multifactorial rather than environmental, even if there is an association to some genes – it would be like saying that my height is part of a multifactorial disorder because I keep hitting my head on a low door-frame to the point that I eventually develop brain damage; you don’t need to find ways of making me shorter or even find out what makes me tall or absent-minded (it might be interesting theoretically, but pretty useless from a clinical perspective), you just need to make a taller door-frame, put a cushion on the lintel or shout when you see me heading for the door. Or maybe you might find away to “cure” my absent-mindedness, but then that may be a fundamental part of my thinking process and by doing that you remove my ability to concentrate and find the solution to world hunger (I flatter myself a bit here). So, all in all, does it not make a lot more sense to concentrate on the environment?

    What I am saying is that if (big if) any genes are associated with schizophrenia those genes are a valuable healthy variation – an asset to the individual and its group (in this case humankind); they will likely code for a slightly “different type of intelligence”, more attuned to certain stimuli (for example non-verbal communication, although this is only based on anecdotal evidence and probably completely off the mark).

    A strategy on diabetes II should focus on avoiding overeating certain foods and exercising; similarly a strategy on schizophrenia should focus on finding the root causes (which are not the genes, in the same way that the root cause of diabetes II is not genetic since no matter what your genes are you won’t develop diabetes II if you have a healthy diet, etc). Where schizophrenia has already developed – or rather “voice hearing”, since we should really be talking in terms of specific symptoms rather than a dubious syndrome – then we should look at ways in which this symptom can be managed. And in this the evidence will show you that a combination of psychotherapy (the “talking” type) to treat underlying trauma coupled with learning strategies to accept and manage the voices (rather than suppress them) actually works, and very well. It makes people able to live fulfilling productive “normal” lives. Drug therapies on the other hand do not only not work but make things much much worse; they only work by making the patient “less of a problem”.

    In closing I’ll say that of course I never suggested you yourself ever said “if you have whatever gene variant then you should get a medicine even if you don’t have symptoms”. Sorry if it read that way. But a lot of people are really suggesting this. “They” are Pzifer, Janssen… and a lot of researchers with a very keen interest in pushing an agenda of “preventive intervention” or “early detection”. I posted in this thread a link to one recent study pointing in that direction – just one of many. I could be wrong but I bet you (let’s say a one trillion dollar coin) that you are going to hear a lot more about psychiatric preventive interventions and about medicating people who have nothing wrong with them other than a particular combination of genes (or brain morphology or whatever) which some exceedingly questionable studies have associated to a higher risk of psychiatric disorders.

    I hope you’ll stick around MIA – even if I might not always have the time to answer it doesn’t mean I’m not reading and taking things on board.

    Oh! One more thing: sickle cell anemia – malaria. Yes, I am saying that in the absence of malaria in the US sickle cell anemia would eventually disappear. But only if you close down all hospitals (modern medicine messes up natural selection – not that I’m complaining, being rather “weak” myself ), revert to a hunter-gatherer culture and then wait, I don’t know, 50,000 years? Having said that, one thing is how a genetic disorder first develops and another whether it can remain in a population after the environmental conditions that made it possible disappear; that is an important point to keep in mind. The question still is, what is the etiology of schizophrenia (or PPD, or MDD, or BD, or OCD, or ADHD…)

  • Oh, and of course people without gene G (or g1, g2,..) who have been exposed to very high levels of contaminated food will develop disorder D “for no apparent (genetic) reason”, whereas people with gene G who are not exposed to contaminated food will not develop disorder D or any other disorders – and people with gene G who are only exposed to small amounts of contaminated food might develop d1 or d2 instead of D.

    You get the idea. Basically you have two variables, one genetic (toxin absorption), one environmental (toxin consumption), giving rise to a wide range of “disorders”

    Toxin consumption/Toxin absorption = disorder type

    If you try to look at the disorders as discrete entities things will get more and more complex until they become absurd – which is where I’d say psychiatry is at the moment. If, on the other hand, you look at the disorders as part of a continuum of various degrees of “intoxication”, everything falls into place.

    What the “toxin” in question is in the case of psychiatric disorders is a more complex subject. I use “trauma” as a shorthand with a very inclusive (and so imprecise) meaning.

  • Ok, then, you need to read “Anatomy of an Epidemic”.

    Just joking, although, yes, you should read “Anatomy of an Epidemic” as well (perhaps more so than “Mad In America”). Also, if I can recommend another book, try “The Emperor’s New Drugs” by Irving Kirsch, it’s a very good and clear book and it gives a good sense of what is wrong with scientific research in psychiatry.

    About twin studies, we are in luck! Jay Joseph has just posted a very good article about them on this site. I think it will answer a lot of your questions. He doesn’t go into adoption studies (the studies on identical twins separated at birth you refer to) but I hope he will write another article about those soon (yes, this is a humble request).

    Regarding the point I was trying to make about the difference between a multifactorial genetic disorder and a disorder that is 100% environmental even though it is the result of the interaction between a genetic trait and the environment, perhaps I did not explain myself clearly. It isn’t easy to go into it in this format – it’s hard to be both clear and brief. Bear in mind that we are talking about evolution; about the development and transmission of a trait (or disorder) over thousands of generations – the time-scale is very “slow”.

    Perhaps the easiest way to understand it is by looking at the practical consequences of what might otherwise sound like a mere play on words. For that I return to the “gene for food absortion” analogy which I used before. Imagine people with this gene, “G”, develop a disorder “D” because of their higher rate of absortion of nutrients also means they absorb more of the toxins in contaminated food. Imagine that scientists, who are convinced that disorder D is a multifactorial genetic disorder, identify gene G and say “this gene gives you a propensity to develop disorder D”, so they start giving everybody with gene G (whether they have been exposed to contaminated food or not) medication which somehow ameliorates the symptoms of intoxication but does not prevent intoxication if exposed to contaminated food.
    The problem is that, on the one hand the medication itself is toxic and has brutal side-effects, often worse than disorder D itself, and, on the other hand, no effort is made to identify the toxin that is making people with gene G develop disorder D. Also, bear in mind that people without gene G who are exposed to the toxin in the food might not develop disorder D but will develop other less obvious disorders, disorder d1, d2…- the toxin affects everybody which comes into contact with it (scientists note this but erroneously conclude that D, d1, d2… have “overlaping genetic architectures”). Since no attention is given to the toxins in the contaminated food, and no attempt is made to remove them from the food supply, their concentration continues to increase so that now even people without gene G (people with a variant that gives them slightly lesser good nutrient absortion, “g1” and who up to now were developing disorder d1) begin to develop disorder D too. Of course, I forgot to mention that disorder D is actually a syndrome – a collection of symptoms of diverse severity depending on the amount of toxin consummed/amount of toxin absorbed… (at this point, if you are still thinking in terms of genetic disorders things get very complicated and nothing makes any sense anymore)

    Now, would you say that gene G codes for a disorder? No, it doesn’t, in fact in normal circumstances it actually makes you healthier since you get more nutrition from the same food. Gene G is a good thing, it does not need to be medicated. Disorder D is an interaction between genes and environment but cannot be said to be a multifactorial genetic disorder; the toxins in the food are real toxins, they poison everybody, they affect everybody negatively – we are not talking about an allergy but a genuine intoxication.

    I don’t know if this helps you understand how a disorder might be the result of the interaction between genes and environment and yet have a 100% environmental etiology. The “bad part” is wholly on the side of the environment, not on the side of the genes. I think this also holds for schizophrenia and other psychiatric disorders and that only this model is really consistent with evolutionary theory.

    About kin selection and diabetes II, I won’t go into that, just to say that they don’t really apply. Diabetes II is not really analogous to psychiatric disorders and psychiatric disorders do not give any advantage to the group so kin selection is not a factor.

    Enjoy “Mad in America” and “Anatomy of an Epidemic” and “The Emperor’s New Drugs”…

  • Yes, this is the kind of article that gets my blood pressure up. On my very long post above (which by the way is riddled with typos, sorry) I talk about something similar, although I speak of genes or “genetic markers” and not of biomarkers which is a more general concept. But basically a similar idea applies, when it comes to biomarkers there’s such a thing as too many biomarkers. More is not better.
    But to be honest that is not even the question with that article, which is a good example of the rubbish that gets published every day. When it says that “365 biomarkers for schizophrenia have been discovered” it means that studies which claim to have found an association between those biomarker and schizophrenia have been published in peer-reviewed journals. That doesn’t mean that anything has been “discovered”. These days people seem to think that getting your study published is a validation of your conclusions; well, it isn’t (and let’s not even talk about the integrity of some journals). We would have to look at all those studies which claim to have found a biomarker for schizophrenia (even the ones that have been “replicated at least 5 times”) and see what they really say – I’m pretty sure that after doing that we would go down from 365 biomarkers to somewhere around 0.
    But what really makes me angry is that the article mixes markers for schizoprenia with “markers of drug response”, which half the time are markers of years of (enforced) drug abuse. Like for example prolactin, which is mentioned in the article: high prolactin is observed in “schizophrenics” so it becomes a biomarker for schizophrenia. No, actually hyperprolactinemia (high polactin) is CAUSED by antipsychotic drugs and so of course it is associated with people who have been given antipsychotics on a regular basis (i.e. “schizophrenics”).
    The scary thing is that the article seems to be advocating blood tests to diagnose schizophrenia (probably in the absence of any clear symptoms). Are we approaching the days of “asymptomatic schizophrenia”?
    Frankly, I think the best explanation for that article is probably to be found in Dr. Henry A. Nasrallah’s bank account.

  • A small precision I wanted to make further into my reply before it grew too big. When I said I agree 100% with you that “everything has a physiological etiology, unless it is magic” I wasn’t being completely honest. I agree that everything has a physical etiology; physical, yes, but not necessarily physiological. The functioning brain is not a “brain in a jar”, it is part of a system of complex interactions which involves not just the body but, (at the very least) the entire material universe. The brain might be a “thing”, but the mind is a system, and when you are looking at “mental disorders” you have to think in terms of systems and interactions, not isolated “things”. But I don’t want to end up writing another monstrously long comment, so that’ll have to do.

  • Hi ScottW. First of all I’ll say that I agree 100% with you when you say that “everything has a physiological etiology, unless it is magic”, but I think you draw the wrong conclusions from that premise.

    I’ll try to be brief in this reply and only raise a couple of points rather than answering all your comments. I’ll also not take on your challenge to “tell me why Alzheimer’s disease is fundamentally different than a psychiatric illness”, even though I’m itching to do so, but that would make for an extremely long reply. I’ll tell you however in what way they are not different: in that we don’t know much about the etiology of either and in that we have effective treatments for neither.

    I also agree very much with you that one thing is aetiology and another is treatment, so let’s looks at those two things separately. I will focus on schizophrenia as a case study because it is normally thought of as the most clear-cut case of a psychiatric condition with a strong genetic component in its etiology:

    The question of whether schizophrenia’s etiology is genetic, environmental, epigenetic or multifactorial is important because, above all, it would not just sift the focus of treatment research but also open (or close) the door to prevention research. You cannot prevent a genetic condition (other than through eugenic practices) but you may be able to prevent an environmental condition. I see that you yourself are not a supporter of a crude genetic etiology of schizophrenia so I’ll skip that. I’ll also skip epigenetics for the sake of brevity and because I don’t think anything will come out of that – in any case you could say that it is a sub-type of multifactorial inheritance. So let’s look at multifactorial: shizophrenia as an inheritable disorder which results from the interaction between genes and environment. Of course at one level schizophrenia is an interaction between genes and the environment (what isn’t?) but in what sense would it be an inheritable disorder? The very notion of disorder, like disease, implies that it reduces the chances of survival of the organism, or in the case of a social organism such as ourselves, the chances of survival of the individual organism and/or its social group. That of course has very important implications from an evolutionary perspective, and particularly when it comes to the evolution and inheritance of genetic disorders or, most importantly for the case of schizophrenia, the evolution and inheritance of a “propensitiy” for a disorder – a genetically-determined “weaknesses”. We know already that whatever the genetic influence on schizophrenia might be, it hasn’t got a simple genetic architecture – there is no “single” gene coding for either the condition or the “propensity” – in fact, its architecture must be very complex or we would have identified it already. Now, when a disorder has such complex genetic architecture as schizophrenia should have (since we have more or less discarded all the simple options) it becomes increasingly difficult to consider it a disorder, since it is not possible to account for how such a complex genetic architecture could evolve in the face of negative natural selection (and all disorders are negatively selected unless they confer an advantage in certain environments, like sickle cell anemia-malaria). So what option do we have left? That the genetic component of schizophrenia is not a “propensity” or a “weakness” but a neutral or quite possibly advantageous trait which only becomes deleterious when exposed to particular environmental factors. I have used elsewhere the analogy of a gene that codes for better absorption of food: this gene would be advantageous and under normal conditions it is positively selected, but if the organism is exposed contaminated food the organism might develop a “disorder” while organisms who do not have this gene remain healthy. In the case of schizophrenia you might be looking for individuals who are more “sensitive”, who process certain signals like non-verbal language better than average, etc. But you are not looking for a “weakness” and there is not evidence at present to suggest that schizophrenia is multifactorial rather than 100% environmental – of course genes play a part in it, but not in the sense of there being a genetic “weakness”.
    Now, I’m not saying that it is impossible that schizophrenia would turn out to be a multifactorial genetic disorder, that is still within the realm of possibility, but it would be a big surprise, it would go against everything we think we know about evolution and inheritance and against all the evidence (the real evidence) that we have so far. So why, one might ask, the insistence that it is a genetic disorder in one way or another? Because of a few twin-adoption studies that, quite frankly, are not worth the paper they are written on? Explain to me why all the research is directed towards the least likely etiological hypothesis of schizophrenia instead of into much more likely hypothesis. It is a big mystery to me unless you take into account very powerful commercial interests, a certain degree of ideological pressure (by which I mean mainly gay activism – since they have their own vested interests on the heritability of traits which reduce reproductive success), and the fact that it is a lot easier to obtain funding for neat genetic research that for more complex research into environmental factors.
    Environmental factor are notoriously hard to pin-point, even when your common sense tells you that you are looking at it. Take trauma in connection to schizophrenia for example. A lot of “schizophrenics” have histories of childhood trauma, but not all. Or is it that they just don’t remember the trauma? And what is trauma exactly? Sexual abuse? Or simple a “double-bind” pattern of communication? A lot of people suffer childhood trauma and do not develop symptoms of “schizophrenia”, but how can you compare trauma with trauma? Even if you narrow it down to, say, sexual abuse, can you really compare two cases? Can you account for all the factors? Maybe the whole difference between two seemingly identical cases might be that in one the child had a dog that came to sit with him after the abuse took place whereas the other didn’t have a dog, or had a dog that didn’t come to sit with him. Research into environmental factors is notoriously difficult, but that doesn’t mean we shouldn’t even try it.

    And I meant to be brief… I’m afraid I’ll have to cut it short without going into “treatment”. I’ll only say this about it: the question is not whether medication could help people with psychiatric “disorders”, but whether the actual medication that is currently in use does help or not. Or whether in fact it makes things worse. And I’d say that there’s enough evidence out there to say quite definitively that it does not work and that it does makes things worse. If you want to look at this evidence “Anatomy of an Epidemic” is indeed a good place to start. I’m not saying that people with schizophrenia or depression do not have a problem and that they don’t need “treatment” (I personally would prefer the word “help”), but I would very much question the treatment they are getting at the moment and the network of interests which support those treatments.

    I will also add one last thing: if you look at enough studies into mental disorders you will begin to notice what cannot be describe as anything other than lies. Conclusions not supported by their own data, data excluded for no conceivable reason other than manipulating results, etc. Not one case or two, but many – I just posted one recent example in, “Preventing Depression: SSRIs for At-Risk Populations?”, nothing too dramatic, just the last one I have noticed myself. This is not a level playing field, and you should maybe ask yourself why isn’t it? If the “biological model” (and I agree that the word is very misleading, but you know what I mean) is right, why can’t they just let the data speak for itself?

    There is a lot more I’d like to say, since you do raise some very interesting points, but I’m afraid I’ll have to stop here for now. Thanks for your comments – it is always good to hear a dissenting voice.

  • I agree with what you say, there’s a much larger cultural issue and, frankly, I think a lot of the great ‘social triumphs’ of the modern world need to be questioned and re-examined; I suppose that makes me retrograde. I think however that there’s a stark difference of responsibility between those who don’t know any better, those who should know better but don’t, and those who do know but don’t care. It’s the ones who know and don’t care that worry me the most; there’s no line they will not cross because, well, they just don’t care.

  • I don’t know much about the difficulties of doctors and psychiatrists, I know a bit more about the difficulties of research scientists and most are lucky if they can maintain the standard of living of a graduate student; research does not pay (unless you are in the private sector, of course). Is that a justification for bending the truth in their research? For lying? No. I understand why some do it, yes, but that doesn’t make it any better; it does not exculpate them; it doesn’t attenuate their guilt. A lie is a lie even if it is only a half truth.
    Is it better to be unemployed and sidelined then? Well, if the only two options are collaborating with a harmful lie or be sidelined, then you bet being sidelined is better. Infinitely better.

    Alicia, don’t take away from your own achievement. Even if everything you had achieved was simply not collaborating with a harmful lie, that would already be an awful lot.

  • “mental death profession”

    That is simply brilliant, Donna! It is both catchy and painfully accurate. It isn’t just a witty play on words but a very deep reflexion on the nature of the problem. Simply brilliant.

  • I have already posted a link to this study on Chrys Muirhead’s “Brain Surgery For Mental Illness In Scotland: Going Under The Knife When Treatment Resistant”, but I think I should re-post it here since it is closely connected to the subject of this article and perhaps Leo & Lacasse will find it interesting if they are not already aware of it. The study in question is: Whalley HC, Sussmann JE, Romaniuk L, Stewart T, Papmeyer M, et al. (2013) Prediction of Depression in Individuals at High Familial Risk of Mood Disorders Using Functional Magnetic Resonance Imaging. PLoS ONE 8(3): e57357. doi:10.1371/journal.pone.0057357

    It can be accessed online at:

    http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0057357

    I think there is little doubt that this study is part of a drive to push for preventive intervention in psychiatry, and in fact claims to have found an effective predictor for MDD (major depressive disorder). Their own conclusion is: “These results suggest that increased activation of the insula can differentiate individuals at high-risk of bipolar disorder who later develop MDD from healthy controls and those at familial risk who remain well. These findings offer the potential of future risk stratification in individuals at risk of mood disorder for familial reasons.”

    I confess I have not read the study in detail and in any case I cannot really comment on the data from the fMRIs, but even a cursory look at the study sets off alarm bells. I’ll just mention one issue by way of an example:

    Of a control group of 70 (which, interestingly, was almost 40% smaller than the experimental group), 4 people developed MDD. These 4 were simply excluded from the study. This might at first glance seem logical since the control group was supposed to provide the mean values of “healthy” brain functioning with which to compare “high-risk pre-MDD” brains (my terms, not theirs). But in a study which is precisely attempting to identify predictors for MDD one cannot simply exclude 4 members of the study which have in fact developed MDD. To do so is to intentionally exclude relevant data from the study. The fMRI data for those 4 individuals had already been collected, and although they should certainly not be included in the HC (healthy control) group, the HRW (high risk group who remain well at two year follow-up) or the HR-MDD (high risk group who has developed MDD at two year follow-up), they should have been assigned to a group of their own: C-MDD (Control group who has developed MDD at two year follow-up).
    A great deal is made in the study of the fact that differences of insula activation have been observed in ALL subjects in the HR group who had MDD two years after being scanned but, leaving aside the reliability of that claim, how about the 4 subjects in the C-MDD group? Did they show differences in insula activation two years prior to MDD diagnostic (or rather, two years prior to follow-up assessment)? If they did, this significantly strengthens the researchers’ claim that atypical insula activation is a predictor of MDD and so it would be absurd to leave that data out of their study. On the other hand, if they did not show differences in activation, this clearly undermines their case for insula activation being a good predictor for MDD, and to leave that data out would call into question their integrity. It is interesting at this point to note the exact wording of their conclusion: “increased activation of the insula can differentiate individuals at high-risk of bipolar disorder who later develop MDD from healthy controls and those at familial risk who remain well.” But not, it would seem, differentiate between healthy controls and controls who later develop MDD…

    There is also something else to note about these 4 individuals in the control group who developed MDD, a great missed opportunity: had they been subjected to the same fMRI scanning at the two year follow-up (none of the subjects were, since the study is only concerned with prediction, and apparently only in -potentially lucrative- “high-risk” groups), they could’ve compared brain functioning and/or morphology in those individuals before and after MDD diagnostic. I suspect the findings of this comparison could have been extremely valuable (even if it was in a small number of people) and possibly challenged the assumption that all differences in brain functioning and/or morphology observed in subjects with mood disorders must be in one way or another hereditary and degenerative. But that of course would not sit well in a study that starts: “Mood disorders […] are known to be heritable, with overlapping genetic architecture.”

    A lot more (and nothing good) could be said about this study, and this without even touching on the FMRIs themselves. I hope whatever its authors are getting in exchange for their scientific integrity is worth it (as usual, the “Competing Interests” section makes informative if somewhat predictable reading).

  • The most astonishing thing about these psychiatric preventive interventions is that according to the model of the very people who propose them they would prevent genetically-determined conditions which should not affect most people regardless of their circumstances. I know that in general psychiatrists are not too bothered about being consistent with their own models of mental illness aetiology but this takes it to new heights of absurdity. You really couldn’t make it up.

  • I wish I could believe that – it would be a relief to think that at least they know what they’re doing. But my fear is that it might be more a case of the blind leading the blind, all following the tinkling of coins in each other’s pockets.
    But whatever the reason or unreason behind the idea of preventive psychiatric interventions I can think of fewer things that could unravel a society faster and more efficiently than this. It is just pure madness – the bad kind of madness.

  • I think the mention of the eugenics movement in the first half of the XX century is particularly apt. The combination of bad science, ideology and economic interests that drove the eugenics movement are very comparable to what drives psychiatry nowadays.

    But this comparison also offers some hope; I’m thinking of G.K. Chesterton, the writer who in the UK managed to almost single-handedly deflate the support for eugenic policies (Churchill was very keen on them) by continuously exposing the absurdity of eugenics with great humour and common-sense. He was not a scientist or a politician or someone in a position of power, just a man with a brain, courage and, admittedly, a degree of access to the media. He showed that it can be done.

    His articles against eugenics make very educational reading; you might want to check out for example “Eugenics and Other Evils” edited by Michael W. Perry. Inkling Books, Seattle, 2000. (ISBN 1-58742-002-3)

  • It really is hard to know whether to laugh or cry. Even accounting for rampant stupidity and corruption it becomes increasingly hard not to give in to paranoid tendencies and start believing there’s a Dr. No-style villain pulling the strings from some secret base in an uncharted tropical island and trying to bring about the collapse of civilization. Where’s 007 when you really need him?

    Coincidentally I was just reading this on the BBC:

    http://www.bbc.co.uk/news/magazine-21636723

    An out-of-work single mother of two living in a motel and relying on a food bank to (more or less) feed her children says: “I seen a doctor… for depression. She put me on some anti depressants and Xanax for my panic attacks.”

    Well, there you have it, forget stroke patients, think big – unemployment carries a big risk of depression, so does poverty, what better group for carrying out government-funded campaigns of mass prevention of depression? Think about it, what a gold mine!

  • Lowry, while I agree with you that this thread has gone off-topic, and that isn’t very fair on Daniel Fisher (or you), I also notice that the title of his article is “We are Whole People, Not Broken Brains”. And shouldn’t ‘whole people’ be able to -occasionally- go off-topic to talk about what’s on their minds?
    I don’t think it’s so bad to go off-topic from time to time, provided, I agree, it does not become the norm. It’s a way of getting to know each other, even if it means getting angry with each other, and apologizing, and accepting apologies; it’s part of the ‘community’ part of this site. These things might be as important for recovery as challenging the biological model of psychiatry; I don’t think we should be so quick to dismiss them.

    But yes, it is true that we have strayed from topic; perhaps we can get back to it via Saint Augustine himself (I know, I know, I’m sorry):

    “How stupid man is to be unable to restrain feelings in suffering the human lot! That was my state at the time. So I boiled with anger, sighed, wept, and was at my wits’ end. I found no calmness, no capacity for deliberation. I carried my lacerated and bloody soul when it was unwilling to be carried by me. I found no place where I could put it down. There was no rest in pleasant groves, nor in games and songs, nor in sweet-scented places, nor in exquisite feasts, nor in the pleasures of the bedroom and bed, nor, finally, in books and poetry. Everything was an object of horror, even light itself; all that was not he made me feel sick and was repulsive – except for groaning and tears. In them alone was there some relief. But when my weeping stopped, my soul felt burdened by a vast load of misery. I should have lifted myself to you, Lord, to find a cure. I knew that, but I did not wish it or have the strength for it. When I thought of you, my mental image was not of anything solid and firm; it was not you but a vain phantom. My error was my god.”
    Confessions. IV. vii (12)

    What chances would Augustine have to not end up on a life-long course of medication if he was living in the US or Europe today? What chances of making anything of himself -let alone of writing books which would change the course of history- after being diagnosed with, say, bipolar psychosis?
    Now, I don’t know if being told you have a broken brain reduces stigma or doesn’t, but I’m pretty sure it does not make you feel great about your chances of making some contribution to the world around you, and if you take that away from people you don’t leave them much, do you?

  • We all have a long way to go. In a way, I think the worst thing that can happen to us is that we forget that.

    Your poem -that’s what it is to me- really struck me. You can tell there’s anger in it but at the same time it has genuine honesty, and that is very powerful (and I say this as someone who reads a lot). It’s a very good reminder that it isn’t just psychiatrists who label people.

    All this talk of Saint Augustin, and then thinking of Benedict XVI, has made me think of Benedict’s encyclical “Spe Salvi” where he comments extensively on some of Augustin’s ideas. It’s a great piece of writing regardless of what your beliefs or disbeliefs might be:

    http://www.vatican.va/holy_father/benedict_xvi/encyclicals/documents/hf_ben-xvi_enc_20071130_spe-salvi_en.html

  • Thank you for this comment, Duane; I really mean that.

    A lot of people here will have been to hell and back because at some point in their lives someone who didn’t really know anything about them and had no interest whatsoever in learning anything about them thought that they knew everything there was to know about them.

    This made me think of something Pope Benedict XVI -a man for whom I have nothing but the greatest respect- wrote some time ago; I think it’s only fitting to quote it on the day he retires:

    “At times one gets the impression that our society needs to have at least one group to which no tolerance may be shown; which one can easily attack and hate. And should someone dare to approach them – in this case the Pope – he too loses any right to tolerance; he too can be treated hatefully, without misgiving or restraint.
    Dear Brothers, during the days when I first had the idea of writing this letter, by chance, during a visit to the Roman Seminary, I had to interpret and comment on Galatians 5:13-15. I was surprised at the directness with which that passage speaks to us about the present moment: “Do not use your freedom as an opportunity for the flesh, but through love be servants of one another. For the whole law is fulfilled in one word: ‘You shall love your neighbour as yourself’. But if you bite and devour one another, take heed that you are not consumed by one another.” I am always tempted to see these words as another of the rhetorical excesses which we occasionally find in Saint Paul. To some extent that may also be the case. But sad to say, this “biting and devouring” also exists in the Church today, as expression of a poorly understood freedom. Should we be surprised that we too are no better than the Galatians? That at the very least we are threatened by the same temptations? That we must always learn anew the proper use of freedom? And that we must always learn anew the supreme priority, which is love?”

  • An interesting article but’ at the risk of sounding petty, there’s a glaring typo in the text.

    where it says:

    “One of the big secrets of psychiatry is that we don’t know exactly how the drugs work,”

    Should say:

    “One of the big secrets of psychiatry is that we know exactly how the drugs don’t work,”

    They just switched a couple of words around – could happen to anyone.

  • Thanks Steve. I agree with you on the basics and disagree on the details – but we have indeed strayed onto philosophy and it is too big a topic!

    Still, anyone interested on epiphenomenalism please follow this link to what I think is a good, concise introduction (maybe I should be posting this on “Pinball Wizards”):

    http://plato.stanford.edu/entries/epiphenomenalism/#ArgAgeMat

    Just one last thing: just as I think the division between psychology and physiology is spurious, I also think the division between morphology and physiology is to a large extent spurious, particularly when it comes to the brain. The division morphology/physiology comes from mechanistic analogies that do not hold true for biological systems and do not take into account basic things like ‘self-repair’: the fact that in any biological system a fundamental aspect of its physiology is to repair its own morphology. Again, the causation is not just morphology>physiology but also physiology>morphology. There’s constant ‘feedback’ in the system.

    I think this is important because neurologists in particular (sorry, Irene) tend to make a sharp distinction between the two when it comes to ‘mental illness’. They tend to see normal functioning as physiology and consider atypical morphology as evidence of a disorder, whereas in fact atypical morphology can also be explained as the result of atypical experiences. The brain is an organ whose physiology is precisely to continuously alter its own morphology in response to stimuli from the ‘environment’ (the environment being any information which reaches the brain either from the body or from the ‘outside world’ through the senses). This idea is, if you like, the translation into scientific terms of the philosophical question of epiphenomenalism.

    By the way, this just reminded me of something I read some time ago: neuroscientists had studied people who had practised martial arts for a long time and found differences in the morphology of their brain areas controlling motor skills, compared to a control group. So… maybe people born with brains that give them superior motor skills naturally gravitate towards martial arts? But then the differences only showed on those who had been practising for a long time (the ‘black belts’)…

  • Irene, when you say that you knew spinocerebellar atrophy was an autosomal disease, I imagine this was so because you had strong evidence from family studies. Now, where does the evidence that schizophrenia has a genetic aetiology come from? Also from family studies, mainly adopted twin studies. I’d suggest you look at those studies and honestly ask yourself whether they are in any way convincing and whether they aren’t riddled with methodological flaws (most notably not assessing whether some form of abuse or trauma had taken place in the adoptive families). You might find this of interest:
    http://www.plosmedicine.org/article/info%3Adoi%2F10.1371%2Fjournal.pmed.0030366

    You ask “what empirical evidence is there that the cause [of schizophrenia] is not disordered brain function?”, but I’m afraid that is the wrong question. I’m certain that schizophrenia -or rather the symptoms gathered under that name- are cause by ‘disordered’ brain function (which is not the same as a brain disorder). The question however is not that, the question is what is the aetiology of that disordered brain function.

    In the first reply to your comment Steve raises something that I think is crucial here: “It is possible that a person’s thoughts lead to feelings of depression which are accompanied by certain changes in brain chemistry. The thought could cause the change, but the change and the depressed feelings occur together. The chemistry difference doesn’t cause the depression, they just happen to be associated. ” I don’t agree that they just happen to be associated, but where I think Steve is correct is in suggesting that direction of causality is not only brain>thoughts, but also thoughts>brain. In fact, although I know many will find this controversial, I would suggest that the relationship between thoughts (mind) and brain is not one of causality at all, but one of identity – this is however too complex a subject to discuss here.

    I think it is clear from your comment that you subscribe to a epiphenomenalistic view of the relationship brain-mind and I think it is something you should question. Coincidentally Philip Thomas has just published a very interesting article here in MIA touching on this: “Pinball Wizards and the Doomed Project of Psychiatric Diagnosis” which you might find interesting.

    I know absence of evidence is not evidence of absence, but I think there is by now plenty of evidence to suggest that schizophrenia (to say nothing of depression or bipolar disorder) is not a genetic disorder – and this is not just because the genes have not been identified, but there are also serious questions from an evolutionary perspective.
    So if it is not genetic, what then? Because it certainly is something. How about a pathogen? How about a pathogen called “abuse”, or “trauma”? Does this seem far-fetched? I confess I’m always surprised when I hear psychiatrists talk about conditions with a physiological cause vs conditions with a psychological cause. What exactly is a psychological cause? In what sense is psychology not physical?

    Take this example: a child is continuously subjected to verbal abuse and develops low self-esteem. The abuse is never ‘physical’ in a conventional sense, but it is of course a physical process in the sense that the abusive words are soundwaves that reach the child’s ear, stimulate nerves, produce biochemical reactions in the brain, and cause a ‘disordered brain function’: low self-esteem. Similarly, if the child is then consistently praised this might ‘re-order’ brain functioning – or not, if the abuse was too prolonged, or at a crucial stage of brain development, etc. Call it psychological if you will but you are referring to a process which is as physical as a virus infection. The identity between psychology and physiology (the identity mind-brain) raises of course important questions and many people immediately jump to the erroneous conclusion that it precludes free-will or genuine decision-making. This is not so but as I said before the issue is too complex and this comment is already far too long!

  • Outstanding article; thank you Philip. I’m so glad that you bring up ephiphenomenalism which, as you say, underlies much of what is wrong with psychiatry. I remember talking to a psychiatrist (and a university professor to boot) and being shocked by the extent to which he was not aware of this basic problem in the conception of the relationship mind-brain; “we don’t really used the word ‘mind’ in our profession” was his response.
    I think the problem is compounded by an almost superstitious belief that brain morphology does not change throughout adult life, or that if it does this change is controlled by genes rather than caused by experience. I suppose the alternative makes people nervous because they misinterpret it as advocating ‘mind over matter’. I hope research into neuroplasticity is moving things in the right direction but, again, many people seem to regard neuroplasticity as a dirty word.

    Thank you again for this article. I think it is fundamental to raise awareness of the philosophical assumptions underpinning psychiatry.

  • Although the first natural reaction to this study might be ‘you’ve got to be kidding me’, there is a very interesting side to this.

    From the abstract (the punctuation makes it a bit more confusing than it needs to – you can tell it’s been written by Japanese): “The animal models should be developed through the method which is consistently associated with the theory of the mental disorders while many of conventional models had been developed by genetic manipulations or surgical operations on nerve system. We considered that a novel animal model could be developed by stress exposure using a small mobile robot. We then implemented this method to the experimental system which had been developed in our past study. An experiment was conducted using the system, and the method was then verified. Therefore, we conclude that the animal model of depression developed by proposed method, exposing continuous attack by the robot in immature period and interactive attack in mature period, can be a novel animal model of depression.”

    In other words (and leaving the robot aside, which is the least important part of it): this experiment shows that ‘depression’ is caused in rats not by genetic or surgical manipulation but by exposure to stress, or rather, trauma. If you punish a young rat continuously so that there is no right option for it to take, the rat becomes ‘depressed’ (and I bet that if rats had a more complex brain -or if we could measure their responses more accurately- they would not simply become ‘depressed’ but also ‘psychotic’)

    The evidence is everywhere you look, when is the penny finally going to drop?

  • I think that’s an extremely important point you make, Peter, and entirely correct. As behavioral geneticists become more desperate they seem to be retreating into this idea of a ‘genetic predisposition’ which is then ‘triggered’ by environmental factors; some sort of hereditary weakness which, needless to say, needs to be medicated (ideally, I presume, before symptoms start and it is “too late”). But nothing seems to point to that kind of hereditary weakness and I think that model makes very little sense from an evolutionary point of view.

    To use yet another analogy after football and horses: if an individual has some genes that make his gut better at absorbing nutrients that is not in any way a genetic weakness – in normal circumstances it should in fact be beneficial and positively selected. But if that individual is exposed to contaminated food, his greater ability to absorb nutrients might in fact work against him, and make him ill while individuals without this gene which eat the same food remain healthy, or at least asymptomatic. Clearly the genes coding for better absorption are not the cause of the disease, the contaminated food is. Efforts should be directed at identifying the contaminated food as well as ways to remove the toxins from the already affected individual – and, if permanent damage has occurred, then to devising coping strategies to help the individual live with the damage. But the one thing you don’t need to do is ‘treat’ the gene, or even find out which gene it is because there is absolutely nothing wrong with it (although I suppose that identifying the gene might help identify the toxin – but that’s a long roundabout way of going about it).

    Having said all that (and it went on for a bit longer that I intended, sorry) I personally don’t think there is any strong association between any of the symptoms of ‘mental illnesses’ and any genes or even any epigenetic processes.

  • Yes, there’s no use pretending the situation is not dire. But hopeless though the situation seems at times (most of the time, in fact) I genuinely think no effort is ever useless, however small, however seemingly wasted. The seeds of change are really taking root even if nothing is poking out above the surface yet, but change is a very slow-growing plant and it needs constant attention.

  • This could be a godsend; it might help research into loss of inhibition and paradoxical stimulant reactions to benzodiazepines and other anxiolytic drugs.
    I’m usually suspicious of extrapolations of animal behaviour to humans, but this sounds promising.

  • That’s the greatest fear, isn’t it David? That bad science gives politicians free rein to justify almost anything in the name of the common good. And once scientists get used to lying there’s nothing they will not put their name to for some funding and a paid holiday.
    My pet fear at the moment is ‘early detection’. I’m just reminded of Philip K. Dick’s ‘Minority Report’ -the novella, not the awful film adaptation. The very efforts to prevent the crime before it happens actually cause the crime in the first place. The situation right now has all the makings of a Greek tragedy’s self-fulfilling prophecy on a nationwide scale.

    Still, I remain pessimistically optimistic.

  • I’m still not sure what Sebelius means. What are these ‘physicians’ supposed to tell their patients about guns and gun safety? That guns are dangerous? Not to shoot people with them? I don’t think lack of awareness is the problem here. ‘Gun safety’? I’d have thought people who carry out mass shootings are in general very well informed as to how to handle a gun safely – I don’t remember any of then shooting themselves or anyone else accidentally.

    I could understand if she was saying that physicians should be able to talk to (or even with) their patients about the patients’ feelings of anger, homicidal ideation, etc. Or even is she was saying that physicians should talk to law enforcement officers about their patients’ record (I might disagree with that, but at least I would understand what she means). But physicians talking to their patients about guns and gun safety? I really don’t know what she could possibly meant by that. It is the strangest mishmash of gun control and mental health I have ever heard from the mouth of a politician – and that is saying something.

    It isn’t a very encouraging beginning and I don’t think it bodes well for this ‘Mental Health Dialogue’. Having said that, I agree with Kermit that if Sebelius and the Obama administration have opened a door for alternative viewpoints and recovery stories, that offer should be taken up and made the most of. Even if there are good reasons to believe that this will have little impact right now, I think it is important to take the long-term view. I am sorry to say but it is almost certain this is not the last mass shooting we’ll see, and eventually politicians will have to question their expert advice and look elsewhere – be sure you are there waiting and ready when they do.

    Every story of recovery out there is a small grain of sand adding up to the plate until the balance finally tips. Personally, I’m afraid things will have to get worse before they begin to get better, but I have no doubt they will get better eventually. How does the quote go? You can fool some of the people all of the time, and all of the people some of the time, but you cannot fool all of the people all of the time. It’s really not a question of if but rather of when and of how much suffering and broken lives it’s going to cost.

  • “We know there is no single solution to the problem of gun violence,” Sebelius said. “But physicians should be able to talk to their patients about guns and gun safety.”

    Talk to their patients about guns and gun safety? I’m sorry, I’m not being cynical, just trying really hard to interpret that phrase in a way that makes some sense but I just can’t do it. Is it taken out of context? I honestly don’t get it.

  • John, I’m sorry, I should have written mental illness in quotation marks: “mental illness”.

    In my first comment I was just trying to draw attention to the fact that the exact same bad science that supports the current consensus on schizophrenia (or bipolar disorder, or ADHD, etc.) as a genetic “chemical imbalance of the brain” also supports the consensus that sexual orientation is an unchangeable inborn trait. But it is not easy to discuss this fact – and it is a fact – when it is instantly countered with accusations of homophobia (incidentally, some people within the APA have for a while now been trying to include homophobia as a mental disorder; no doubt that if they succeed they’ll quickly find out it responds very well to psychoactive drugs.)

    Anyway, I’m sorry if I don’t explain myself very well; I’m sure Jay Joseph, who clearly has a good understanding of the science on this issue could explain it much better than me.