Results of World’s Largest Antidepressant Study Look Dismal

Joanna Moncrieff, MD
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A few months ago I was surprised to receive a request from an obscure journal of consciousness studies to review a paper. I was surprised because, although it was not immediately obvious from the title, the paper contained the first reports of the primary outcome measure of the massive and notorious STAR-D study, 14 years after the study was finished.

What in the world were the main findings of the world’s largest ever antidepressant trial doing being presented now in a little known journal? The answer may lie in the fact that they show how miserably poor the results of standard medical treatment for depression really are!

With 4041 participants, the STAR-D study is by far the largest and most expensive study of antidepressants ever conducted. The intention of the study was to see how antidepressant treatment combined with high quality care performed in usual clinical conditions. It did not involve a placebo or any sort of control. All treatment was provided free for the duration of the study to maximise engagement.

The paper I was asked to review, which is now published in Psychology of Consciousness: Theory, Research and Practice, is written by a group led by Irving Kirsch and based on the original data obtained through the NIMH.1 Shannon Peters describes its findings in detail.

Kirsch’s group point out that the paper that describes the design of the STAR-D trial clearly identifies the Hamilton Rating Scale for Depression (HRSD) as the primary outcome.2 This makes sense since the HRSD is one of the most commonly used rating scales in trials of treatment of depression, especially trials of antidepressants. As the STAR-D authors note in the study protocol “the HAM-D17 (HRSD), the primary outcome, allows comparison to the vast RCT literature” (cited in (1)).

Yet the outcome that was presented in almost all the study papers was the QIDS (Quick Inventory of Depressive Symptomatology), a measure made up especially for the STAR-D study, with no prior or subsequent credentials. In fact, as the authors of the present paper point out, this measure was devised not as an outcome measure, but as a way of tracking symptoms during the course of treatment, and the original study protocol explicitly stated that it should not be used as an outcome measure.

The analysis found that over the first 12 weeks of antidepressant treatment, people in the STAR-D study showed an improvement of 6.6 points on the HRSD. This level of change fails to reach the threshold required to indicate a ‘minimal improvement’ according to the Clinical Global Impressions scale (a global rating scale), which would be 7 points. It is also below average placebo improvement in placebo-controlled trials of antidepressants. A meta-analysis of paroxetine trials, for example, found that the average improvement in placebo-treated patients was 8.4 points on the HRSD.3 A meta-analysis of trials of fluoxetine and venlafaxine reported average levels of improvement on placebo of 9.3 points over just 6 weeks.4 Another meta-analysis found placebo improvement levels of between 6.7 and 8.9 points in placebo groups across trials involving a variety of antidepressants.5

The proportion of people classified as showing a ‘response’ (using the arbitrary but commonly used definition of a 50% decrease in HRSD score as per the original protocol) was 32.5% in the STAR-D study, and the proportion classified as showing remission (HRSD score ≤7) was 25.6%. The meta-analysis of placebo-controlled trials of fluoxetine and venlafaxine reported response rates of 39.9% among people allocated to placebo, and remission rates of 29.3%. In another antidepressant meta-analysis, the response rate on placebo was just above the STAR-D level at 34.7%,6 and in another it was just below at 30.0%.7

The authors of the current paper point out, however, that improvement is lower in placebo-controlled trials, even in the people treated with antidepressants, than it is in trials that compare one antidepressant against another without placebo controls. This is presumably because people in placebo controlled trials are told that there is a chance that they will receive a dummy tablet, while in comparative trials, they know they will receive some sort of active drug. Therefore they compare the results of the STAR-D study to the results of a large meta-analysis of comparative trials (cited in (6)). These find average HRSD improvement levels of 14.8 points; response rates of 65.2% and remission rates of 48.4%. Therefore the STAR-D results are approximately half the magnitude of those obtained in standard comparative drug trials.

The authors propose that the reasons for this poor performance of antidepressants in the STAR-D study is due to the selection of more complex patients. Industry studies in particular exclude people with ‘co-morbid’ conditions and symptoms or history of self-harm, and often recruit people via advertisements. It may also be due to the intensive attention and assessment procedures people undergo in industry-funded studies, and the added placebo effect of being in a trial of a ‘new’ treatment, which most trials involve.

Whatever the reason, STAR-D suggests that in real life situations (which the STAR-D mimicked better than other trials) people taking antidepressants do not do very well. In fact, given that for the vast majority of people depression is a naturally remitting condition, it is difficult to believe that people treated with antidepressants do any better than people who are offered no treatment at all.

It seems this may be the reason why the results of the main outcome of the STAR-D study have remained buried for so long. Instead, a measure was selected that showed results in a slightly better light. Incidentally, even then results were pretty poor, especially over the long-term, as Piggott et al have showed in a previous analysis.8

Whether this was deliberate on the part of the original STAR-D authors or not, it was certainly not made explicit. There should surely be uproar about the withholding of information about one of the world’s most widely prescribed class of drugs. We must be grateful to Kirsch and his co-authors for finally putting this data in the public domain.

Show 8 footnotes

  1. Kirsch I, Huedo-Medina TB, Pigott HE, Johnson BT. Do outcomes of clinical trials resemble those “real world” patients? A reanalysis of the STAR-D antidepressant dataset. Psychology of Consciousness: Theory, Research and Practice 2018;Sept 2018.
  2. Rush AJ, Fava M, Wisniewski SR, Lavori PW, Trivedi MH, Sackeim HA, et al. Sequenced treatment alternatives to relieve depression (STAR*D): rationale and design. Controlled Clinical Trials 2004;25:119-42.
  3. Sugarman MA, Loree AM, Baltes BB, Grekin ER, Kirsch I. The efficacy of paroxetine and placebo in treating anxiety and depression: a meta-analysis of change on the Hamilton Rating Scales. PLoS One 2014;9(8):e106337.
  4. Gibbons RD, Hur K, Brown CH, Davis JM, Mann JJ. Benefits from antidepressants: synthesis of 6-week patient-level outcomes from double-blind placebo-controlled randomized trials of fluoxetine and venlafaxine. Arch Gen Psychiatry 2012 Jun;69(6):572-9.
  5. Kirsch I, Moore TJ, Scoboria A, Nicholls SS. The emperor’s new drugs: an analysis of antidepressant medication data submitted to the US Food and Drug Administration. Prevention and Treatment 2002;5.
  6. Rutherford BR, Sneed JR, Roose SP. Does study design influence outcome?. The effects of placebo control and treatment duration in antidepressant trials. Psychother Psychosom 2009;78:172-81.
  7. Walsh BT, Seidman SN, Sysko R, Gould M. Placebo response in studies of major depression: variable, substantial, and growing. JAMA 2002 Apr 10;287(14):1840-7.
  8. Pigott HE, Leventhal AM, Alter GS, Boren JJ. Efficacy and effectiveness of antidepressants: current status of research. Psychother Psychosom 2010;79(5):267-79.

58 COMMENTS

  1. I’ve read Irving Kirsch’s book “The Emperor’s New Drugs” https://www.amazon.com/Emperors-New-Drugs-Exploding-Antidepressant/dp/0465022006

    It’s a good book, and it’s great that people are exposing the flaws in so-called “antidepressant” studies.

    But let’s be honest. As bean counters and number crunchers do these studies in the comfort of their offices, there are millions of people whose brains are being DESTROYED by psychotropic drugs and who suffer in ways that these bean counters and number crunchers can’t even begin to fathom. Not only that, but the people who suffer as guinea pigs, if they survive the ordeal, are made to pay for their own suffering.

    As Peter Breggin and others have so eloquently shown, there is no such thing as an “antidepressant.” These brain destroying chemicals are not “meds” or “medication.” They are brain-DESTROYING drugs. The term “antidepressants” is a misleading euphemism for dangerous and toxic chemical compounds. All of these studies are useless in the face of the myth of mental illness. As long as the myth of mental illness reigns supreme, it doesn’t matter what kind of “remedies” or “treatments” are studied.

    Almost daily I learn of yet another “mentally ill” person who took his or her own life. Many people assume that these poor “mentally ill” people commit suicide because they don’t get the right “treatment” or they don’t take their “meds.” NONSENSE! The brain-DESTROYING drugs are CAUSING these innocent people to commit suicide in ever increasing numbers, and no one is doing anything about it except call for more psychiatry, more drugs, more involuntary incarceration.

    Enough is enough. Slay the Dragon of Psychiatry.

  2. Slaying the Dragon of Psychiatry:

    I agree with you that we urgently need to take action and that there is a social justice aspect to the problem of unbiased data trickling out through back channels that may never see the light of day as it concerns the general public. One gets a sense that this is a part of a systemic problem that is not limited to psychiatric and pharmaceutical corruption. One gets a sense that this is related to a larger problem of lack of morality and ethics in business and the lack of connectedness of wealthy business owners to their customers. A parallel can be found in mining companies that capitalize the short term gains and socialize the clean-up costs (Noam Chomsky).

    The vast majority of people are taking anti-depressants voluntarily. If people who are depressed were offered different options such as support rebuilding their lost social connections, help spending time in nature, etc. they may not always go for the ‘magic bullet’ solutions. But whose job is it to educate people about the wealth of unfunded alternatives? Whose job is it to pay for them? Is it my job to educate my neighbors? Is it the government’s job? We certainly can no longer rely on professionals.

    Should alternative professionals (the people who ‘first do no harm’) such as naturopathic doctors, somatic practitioners, music therapists, art therapists, peer specialists, massage therapists, life coaches, process psychologists, cognitive behavioral therapists, personal trainers, yoga instructors, nutritional counselors, etc. be offering their services for free to accommodate the high number of people who can’t afford such services?

    Special interest groups are waiting in the wings to fill the void with other magic bullet solutions but most people know deep down inside that personal mental and physical wellness is achieved by de-cluttering the mind and de-toxifying the body, ridding oneself of the myriad of bad habits acquired by dealing ineffectively with pain and trauma which everyone experiences. This is a personal process that everyone must make, rich or poor.

  3. I’m really pleased you highlighted this paper, and I hope some more academics read and respond to it, because, if it’s right, it’s a bombshell. I say if it’s right because we are all wondering incredulously how the placebo in an RCT can massively outperform the drug in real life. I know it’s apples and oranges, but then we are saying RCTs of psychiatric drugs are so riddled with placebo effects we can’t use them for anything.

    We all understand how Irving Kirsch proved the drugs were basically useless as drugs but possibly useful as (rather damaging) placebos. Now it seems that in and of themselves they aren’t even much of a placebo. Even I’m having trouble believing it’s this bad.

  4. A big problem I have with studies of anti-depressants – other than the obvious damage it does to the brains of the people involved – is that every person reacts differently to each anti-depressant. That much was proven to me with the first anti-depressant I ever used – Prozac. The first time I used it, the weight of the world was lifted off my shoulders. I lost my job and so could not afford to continue using it. When I finally got back on it, NOTHING happened! No relief At All! In fact, I never experienced that relief ever again – over nearly 30 years on anti-depressants. I weaned off them this year.

  5. I have three problems with the way Dr Moncrieff comments on antidepressant trials, including this piece.

    To enter Star D, patients had to have DSM Major Depression, of at least moderate severity. But Dr Moncrieff has repeatedly stated that she believes ‘psychiatric disorder’ is scientifically and conceptually invalid: http://www.criticalpsychiatry.co.uk/docs/LanguageOfDisorder.pdf

    Most of her piece assumes that measuring the depression, whether with the originally published flawed measure, or the now ‘unburied’ one, is valid. But by her own arguments, neither set of measures are. How can an invalid concept, or ‘construct’, be validly measured?

    Let us assume, for the sake of my second point, that Dr Moncrieff abandons one of her mutually incompatible opinions and accepts diagnosis is valid and depression can be measured, albeit imperfectly. She tends to assert, with Kirsch, that small improvements on the Hamilton scale are ‘clinically insignificant’: that phrase is not used here, where she writes ‘it is difficult to believe that people treated with antidepressants do any better than people who are offered no treatment’.

    However, the small improvements on the depression scale are in groups, not in individuals. As I understand how statistics operate in randomised controlled trials, we have no way of knowing to what extent the small improvements are shared out, in any treatment group which does better than a placebo or other comparator group. It may well be that only a small number of treated patients are getting the improvement (beyond placebo/natural remission/comparator), and if they are then their treatment-associated improvement could be very significant clinically.

    That is a key reason why I think Dr Moncrieff and others should stop saying ‘there’s no such thing as an antidepressant’, which in my view is a form of ‘pillshaming’: https://drnmblog.wordpress.com/2018/04/18/pillshaming-is-real-heres-a-newish-way-to-reduce-it-and-to-reduce-antidepressant-use/

    Thirdly, it is not true that people in the placebo arms of antidepressant trials ‘are offered no treatment’, as Dr Moncrieff implies here. They are in fact provided with a good deal of interpersonal interaction which amounts to supportive psychotherapy. This is likely to be very helpful to all people in such trials, whether they have a ‘real’ pharmacological response or not, and by downplaying the need for it Dr Moncrieff shows herself to be on the side of those looking to shave a few more percentage points off public funding for mental health services: https://drnmblog.wordpress.com/2018/05/23/how-drop-the-disorder-colludes-with-the-neoliberalism-it-claims-to-oppose/

      • This is my point: ‘It may well be that only a small number of treated patients [in the group] are getting the improvement (beyond placebo/natural remission/comparator), and if they are then their treatment-associated improvement could be very significant clinically.’

        I think Dr Moncrieff routinely and misleadingly omits to point this out: she failed to comment on the issue below.

        There is evidence that people with more severe depression do respond more to certain physical treatments. The best RTA I know on this was the 1989 NIMH study which was not directly Pharma-funded: https://www.ncbi.nlm.nih.gov/pubmed/2684085

        Dr David Healy appears to hold that antidepressants are wholly placebo for mild-moderate depression. I am not convinced that we can be so sure about this.

        For mild-moderate I am NOT saying ‘there IS such a thing as an antidepressant’. Just: ‘we don’t know, but what is the point of pillshaming? Let’s offer antidepressants only after providing proper information, including that most episodes naturally remit, and for those who choose the drug offer a 50% chance of having a placebo’.

        • My understanding is that Dr Moncrieff does not point out that a small number benefit from the chemical in the drug, for the simple reason that she cannot find evidence to support this, and nor can the rest of us.

          I do not think that, as yet, there is such a thing as an antidepressant, but I am not shaming those who come to a different conclusion and take the drugs. Shame implies that they are doing something I consider morally wrong or stupid, or they have let themselves down and should know better. Far from it. They are told by experts like those whose names appear on the Science Media Centre that the drugs “work” and are “much better than placebo”. Their NHS psychiatrists say unblinkingly that the drugs reverse a chemical balance. I don’t blame them for trying anything that might make them feel better when they are in grave distress, nothing seems to help, and everyone around them tells them it will work. There is no shame in believing what experts tell you. We know where the real shame should lie.

          Why is the onus of proof always on those who believe antidepressants don’t work? I thought that you didn’t have a drug until you proved it worked, which the drug companies originally succeeded in doing, but now the results no longer seem to hold up. Where’s the evidence-based argument that they work? There must be some scientific justification, where is it? Do you have any reason to believe they might work? Is it the idea that efficacy must exist because there are some people whose response is on the right hand end of the of the bell curve? Because that applies equally to placebos and just isn’t science.

          You are saying we should use them out of a hunch they might work when the data is strongly suggesting the opposite. Thats rather odd, but amidst all the statistics, have we even got a credible drug mechanism or is that guesswork as well?

          Dr Moncrieff is highlighting an important paper that is reporting what was intended to be the primary outcome of an expensive study which for some reason was never reported. It is indeed dismal and researchers should be trying to figure why.

          • Yes, the ‘burden of proof’ has not been properly applied, because of Pharma marketing and other activities, and it is certainly reasonable to be suspicious about this paper.

            I think antidepressants are overprescribed by 10x and maybe more, in the UK, but that was the position of Dr David Healy and others before Dr Moncrieff came onto the scene 10 years ago

            People with clinical depression should get some support (as they do in the placebo arm of a clinical trial), and if they do not recover within a few months, either psychotherapy or medication is reasonable.

            However, ‘support’ costs money because it involves paying people for their work, and in fact is more expensive than medication overseen by very brief visits to doctors.

            Dr Moncrieff does not advocate providing such support, because she does not believe in depression as a mental disorder. She believes money should be generally redistributed. That is socialism combined with ‘Drop the Disorder’, and what I pointed out in my ‘neoliberalism’ piece is that it is also attractive to tax-cutting right-wing politicians, who cherry-pick the ‘Drop the Disorder’ but leave out the socialist redistribution.

        • I do not think that, as yet, there is such a thing as an antidepressant

          And let’s hope there never is. Other than socialism, which has nothing to do with taxes or political parties, but people having control over the product of their labor, and the rest of their lives as well. Neoliberalism is the same as neoconservatism, it’s just which bourgeois party is spouting the rhetoric; psychiatry serves both as required.

        • At the risk of getting a battering I will say that the talk of political ideology has no place in assessing the efficacy of antidepressants. We need approaches to “it” regardless of where you are on the political spectrum.

          I don’t think there is evidence for a subset we can identify for whom antidepressants “work”, so statements like “10 times too many” have no evidential underpinning.

          There are approaches that respect and empower the patient, like open dialogue and psycho social and recovery projects, but the current psychiatric profession has either turned away from these or shown luke-warm support and they would need to turn their training on its head to embrace them.

          Psychologists need a bigger role because they “get it” and psychiatrists need to lose some of their power because they have abused it. This can start by NHS psychologists undertaking to keep your conversations private and not just act as note-taker for the psychiatrist.

          • I disagree with the idea that “political ideology has no place in assessing the efficacy of antidepressants” because I agree with you when you say “I don’t think there is evidence for a subset we can identify for whom antidepressants work”.

            “Open dialogue and psychosocial and recovery projects” exist within the “middle health” bubble, but most professionals, let alone psychiatrists, just aren’t there, that is, they aren’t there in the ‘alternative medicine’ corner of that bubble. The “mental health” bubble pops when medicalization, exposed for the fraud that it actually is, given public education campaigns, meets massive populist physical resistance.

            I don’t think the vast majority of psychologists, as you say, “get it”. Psychologists don’t have such a big role because they don’t want a bigger role. They have restricted their activities, in the main, to treating less “serious mental illness”, so-called, leaving the business of playing a prominent role in the more totalitarian institutions to psychiatrists.

          • I am not against or for socialism (which I mean in the ordinary sense current in the UK, not the Marxist sense of ‘real socialism’). It is Dr Moncrieff and her anti-diagnosis colleagues who stress political reform as being of primary importance, so I do think anyone wanting to scrutinise their statements needs to take politics into account.

            Let me try again to address: “[no]…evidence for a subset we can identify for whom antidepressants work”. There may be such a subset, but the point is that with published RCTs we have now, we cannot identify the characteristics of that subset.

            I would go further and say that because there is evidence for antidepressants working in severe depression (https://www.ncbi.nlm.nih.gov/pubmed/2684085, repasted from above) then to me that does support the idea of a ‘subset’ in people with mild-moderate. Many conditions have a spectrum of severity from subclinical and mild to moderate and severe.

            For mild I guestimmate the chances of you being in this subset might be 1 in 1000. For moderate it might be 1/100. But the longer your depression goes on the more likely you would be in it.

            My own depression lasted 2-3 years and I didn’t try antidepressants (or formal psychotherapy). I am pleased that I did not expose myself to the risk of being on them for a long time, but cannot be 100% sure that I did not lose out on the chance of making the episode shorter.

          • The way you discuss this makes it appear that “depression” and “episodes” are the problem, rather than symptoms of other difficulties. “Depression” is not a scientific entity, it’s a lay-person’s description of a state of the mind at a particular time. “Depression” as described in the DSM can result from early childhood trauma, thyroid dysfunction, nutritional deficiencies, a dead-end job, relationship instability, lack of sleep, lack of a sense of purpose, side effects of other drugs, a range of actual physiological illnesses, and more. It is ABSURD to consider “depression” as a unitary “disorder” and try to “treat it” without bothering to discover what is actually going on. Sure, drugs can make anyone feel better, if it’s the right drug at the right time. That’s why people go out drinking after work or smoke some weed when they get home. But no one thinks drinking alcohol is “treatment” for “anxiety disorders”. It’s a drug, plain and simple. Same with SSRIs or any other “medication.” They are drugs, plain and simple. They can’t “treat” depression any more than they could “treat” boredom or excitement or pain or irresponsibility. Depression isn’t a “treatable” entity. It is usually an indication of something else going on, and “treating” it without consideration of the causes is about as smart as “treating” pain without looking for the source of it.

          • Abilify has been advertised as a “treatment” for “treatment resistant depression”. Abilify is, of course, a neuroleptic. My point is that if you are drugging 1000 or 100 people for every one person you might, according to theory, be able to “help”, that doesn’t make much sense. I would also suggest that there has to be a question as to how deeply entrenched, in that one percent, their “ailment” is lodged. We don’t know, for instance, how much of it might be antidepressant related, that is, maintained by a certain degree of toxicity in their treatment.

          • Concerned Carer — Your confusion lies in your belief that psychiatry is a health field, as evidenced by your use of terms such as “patient.” As long as you try to understand things in such a context they will never make sense. You seem to equate the drugs “working” with people feeling less pain, which seems to be a moral/philosophical issue, not a medical one. Why should being detached from one’s feelings be considered “working”? Are you claiming people’s feelings are not grounded in material reality?

        • none of it matters mate- what matters is that some people think their ok and some don’t- that’s their reality- and that’s what matters to them people- whats right or wrong for them- and what matters to them is them- their choice- not some drug dealer/ or pusher employed by the state. The reality is all drugs can help or harm some people- a fool knows that- yet we’ve got fools who force them into people in contrast to the reality of their report, when in reality, it doesn’t matter what anyone says about the medication and its benefits- their not going to be there for everyone- because their different, for everyone- reality again- the only way anyone promoting or pushing “their drugs” on anyone- can know, is by the “report of the person having them”- being forced to have them- that’s the bottom line- and if they’re saying they make them feel bad or sick-er– that’s what they do- in reality- and for anyone to say their crap or whatever, however, is the same as anyone saying they don’t like beer- or cigarettes- their crap-or anything else- and when they say that are they shaming those people- or just trying to save them. Cuts both ways mate.

  6. All public funding for “mental health” disservices should be eliminated (and no, housing and nutrition are not “mental health services”). Nothing serves neoliberalism more than psychiatry.

    I also believe in pill-shaming, though it should be directed at pharma, not its victims.

    How can an invalid concept, or ‘construct’, be validly measured?

    He does have a point here.

    • Praise the pills by shaming patients. That’s how psychiatry works.

      Did an SSRI make you psychotically manic? Your fault. You’re a bipolar monster who deserves to have your life ruined. The pills are safer than aspirin and never hurt anyone who wasn’t a crazy SMI already who deserves a lifetime of segregation on a disabling cocktail.

      Psych docs whine about “pill shaming” but pills have no feelings. These same people have no qualms about shaming their patients/victims by calling them bipolar or schizophrenic and going on TV to tell the public how dangerous all “bipolars” and “schizophrenics” are. (There is no other medical profession that routinely maligns its patients on national television.)

      It’s not pill shaming or patient shaming psychiatrists are worried about it seems, but the shaming of their own profession. Cruel, pointless experiments on trusting people and libelous slander are pretty shameful behaviors.

    • I don’t see any evidence for a subset in severe, and why on earth that would mean there is a subset in mild as well escapes me. Its another hunch with no coherent mechanism of action.

      The bottom line is that we can’t find a clinically significant separation from placebo in anyone. These Star*D results suggest it’s even worse when used in real life. And we still don’t have a credible mechanism of action, do we? I mean, is there a coherent argument left supporting their usage?

      So, knowing what we know now, that Fluoxetine and Citalopram have effect sizes some 20% below what NICE at one stage considered clinically significant (0.30), and knowing the increased risk of suicidality, should they ever have been approved in the first place? Shouldn’t they be taken off NICE’s list of approved medications until someone somewhere produces credible evidence to support their use?

    • Oldhead: for the record, I have never said the drugs work, psychiatry is in fact currently a health field that claims to make people better, and people that either choose or are forced to receive psychiatric treatment need a name and whilst “patient” isn’t the best i can’t think of a better one at this moment.

      Posters on here should really read what others say and stop assuming that everyone apart from them is a baddie. Most of us here are basically on the same side, even people I’ve sometimes disagreed with. There is a difference between critical psychiatry and anti psychiatry to be sure, but it’s a spectrum.

      Let’s move on and listen respectfully to the important views and insights everyone has to offer and not simply say “you are confused” – after all, we know that tactic all too well, don’t we?

      • I’m saying if the drugs did “work” that would NOT be a good thing.

        There are many better terms than “patient,” which is the absolute worst and the most disempowering; “survivor” and “psychiatric inmate” are the most preferred.

        People here are NOT “basically on the same side,” btw. Some want to “reform” psychiatry, some want to end it; I would call that diametric opposition.

  7. So funny and gone wrong…. two psychiatrists.. pillshaming for saying there is no such thing as an ‘antidepressant’ and the other one who says there is no such thing as an ‘antidepressant’ who works in the NHS therefore must prescribe the ‘antidepressant’. I feel slightly better – ‘antidepressant’ ? – for that laugh after looking at the horror of a blown down tree in my garden this morning.

  8. From Chapter 4 of Grace E Jacksons Drug Induced Dementia :

    “To date, the investigation by Kalia et al is the only animal study which has analyzed the appearence of serotonin nerve fibers following exposure to pharmaceutical inhibitors of serotonin reuptake.

    Unexpectedly, these reseachers found that fluoxetine and sertraline were toxic to serotonin neurons in multiple regions of the brain.

    Based upon dose-equivalent levels of medication in the peripheral bloodstream, the antidepressant regimes used in this experiment were comparable to those consumed by humans.

    Although the four-day exposures to fluoxetine and sertraline did not fully deplete serotonin, both drugs contributed to reductions of serotonin content (12% and 4% respectively) within the prefrontal cortex of the brain.

    Flouxetine and sertraline produced the same quality and distrubution of structural defects caused by two other drugs (Ecstasy and dexfenfluramine) whose toxicities preclude sale on the US market.

    Damage to the structural integrity of the serotonin network cannot be regarded as a trivial phenomenon. Most notably, the anatomical changes which occured in rats in response to fluoxetine and sertraline were similar to the defects observed in humans in association with serveral neurodegerative conditions.”

    • Yes, these reports add to other evidence about unwanted effects and dependence, and should be included in any full ‘informed consent’.

      But to respond to Frank Blankenship’s point above, depression is so common that the numbers of people who do not remit spontaneously within 6 months, say, are still quite high in absolute terms.

      He writes ‘if you are drugging 1000 or 100 people for every one person you might, according to theory, be able to “help”, that doesn’t make much sense.’ But in the case of mild-moderate depression it is usually much more about patient choice (better-informed, I hope) than anything coercive which is what ‘drugging’ can imply. If your depression has gone on for 6 months or longer then those (crudely guesstimated) odds will be better.

      I hope everyone accepts that similar arguments apply for psychotherapy. Like most people (I think) I would prefer psychotherapy, but it can be negative too, and it is a fact that quite a few people are very sceptical about it and see many psychotherapists as charlatans.

        • If you talk your problems to death and don’t do anything different counseling won’t work.

          I believe once you have an SMI label the counselor or therapist will view you as hopeless and encourage you to view yourself as hopeless. Most counselors want to help folks but the power imbalance makes it hard as well as the inherent pessimism.

          A lot of counselors get depressed since no one gets better (unless they flee the funny farm.) They get depressed themselves or quit caring. I feel sorry for the well-meaning ones who work at a community mental illness center.

          A lot are mystified at how those they treat become more childish and impaired over the years “despite” the best neurotoxins available.

  9. Am I a hermit in the psychological wilderness because I support the proper use of select nutrients for certain depressive states where appropriate selective features present themselves? Such contributing things as overconsumption of various stimulants (B1), presence of diverse perceptual distortions (B3 and/or B6+zinc), “bipolar” symptoms (B12), suicidal ideation (B1 and/or B12), alcohol abuse (B3 in niacin form, maybe accompanied by glutamine) frequently aren’t dealt with successfully by psychotherapy or antidepressants alone, but can be ameliorated by non-drug means directed by proper questioning and/or a few tests that can properly direct therapeutic interventions (a term I don’t really like).

    • What you’re talking about is analyzing what is actually happening to a person’s body, rather than just saying “all anxious people need B1” or other such generalizations. I’m right there with you. Everyone is different, and pretending that all people need therapy or B1 or meditation or ANY single intervention based on how they feel is never going to work. But for some, nutritional interventions have been very successful. It needs to be case by case.

      • Steve…regarding different causes of depression, you are exactly right. But everything I have said above is criticising that current state of affairs in the UK, where a GP can prescribe an antidepressant after a ten-minute consultation.

        I have not prescribed anything for four years, but working as an independent psychiatrist I only prescribed after a minimum 90 minute consultation, and because psychosocial factors were often identified that led to less prescribing not more.

        • It seems like we’re coming from a similar place. I’m only pointing out that talking about “depression” as if it were a real clinical entity implicitly supports the worldview we’re trying to break down. Joanna Moncrieff writes well about using the “drug-based model” of intervention – we’re using a drug because some people like its effects, not because we’re “treating” some medical entity. I think language is very important at this stage – we need to make folks conscious of the implicit assumptions in suggesting that someone “has depression” that “can be treated.” It’s part of the marketing scheme to use such language.

          That being said, if doctors or anyone else spends 90+ minutes actually listening and asking compassionate questions, the client is much more likely to actually get something they need. I just think it’s important to convey to them that there isn’t something “wrong” with them for feeling or reacting as they do – it’s just their current condition, and if they want to work to change it, that’s their decision. It’s not up to me to “diagnose” them with some spurious “condition” and pretend that means I know something that they don’t. The client is the one who has the answers.

    • If bizarre thoughts are caused by lack of micro nutrients the person will benefit from supplements like you recommend Bcharris. I suffer from lack of B12 and iron. I believe years on those safe and effective toxins has ruined my digestive system. Blood work shows the deficit but the doctor doesn’t know the cause. Or isn’t telling.

  10. Earlier this year my father was suddenly taken ill, the GP said it was a urinary infection. It was very obvious that it was very much more serious than that. The GP didn’t want to know about speeding up the ambulance and insisted I drive him home and wait for the ambulance there while with every passing minute he was worsening. I spent the rest of the day and almost all night at the hospital while they did tests and scans. Early the next morning I went back in. One look at the senior nurse and I knew it wasn’t good. She didn’t even take me into a private room, just said almost casually from her desk in the ward, that his gall bladder had burst, there were lesions on his liver and he would be in hospital for the foreseeable future. Straight away I realised this was the beginning of the end. The next thing I remember were people rushing towards me in slow motion, loads and loads of them, then someone put a mask on me and others were pulling my coat off. They told me I had passed out and smashed my head on the floor. There was no memory of this then nor now. I felt much much better quickly, got up off the floor and wanted to see the consultant about my father. Next morning this happened and he said basically your father is not going to live. They were only going to make him comfortable, there was an operation but at his age he wouldn’t survive it. The next twelve days would prove to be some of the most harrowing days of my life and I knew it would be the memory of those days that could affect me in the future. And sure enough I relive those days in the middle of the night, but I’m in control of it. Long Term Potentiation has a control mechanism. A biology control mechanism. If you not only don’t believe in any of this but think that this is buying onto psychiatry, fine, you may suffer. I know otherwise and do not.

    btw what I went through – with respect to my father – was nothing compared to the horror of psychiatry. The kind of horror that people outside of all this will never grasp unless it happens to them and it can happen to anybody.

    Psychiatry needs to be abolished, psychiatrists put out of a job, convicted of forced drugging with neurotoxins and their pay packets given to their victims.

  11. Found this interesting:

    https://www.scienceandmediamuseum.org.uk/whats-on/early-birds

    And yet they turn down the work of someone who has indepth experience and knowledge of the truth of all this, is also a sufferer and survivor. Work that is in no way controversial.

    These are the appauling drugs used in young peoples ‘autism’ units in the UK, that includes children:

    Apiriprizole (Abilify atypical ‘antipsychotic’)

    Lithium (mood stabaliser – out right posion)

    Clonazepam (benzodiazepeine)

    Asenapine (atypical ‘atipsychotic’)

    Chlorpromazine (‘antipsychotic’)

    Paliperidone (atypical ‘antipsychotic’)

    Quetiapine (atypical ‘antipsychotic’)

    Risperidone (atypical ‘antipsychotic’)

    Ziprasidone (atypical ‘antipsychotic’)

    I’ll pick out and project the truth of just one: Risperidone –

    https://www.youtube.com/watch?v=K12jE7TH7zQ