Dr. Joanna Moncrieff: Challenging the New Hype About Antidepressants

James Moore

This week on MIA Radio, we interview Dr. Joanna Moncrieff. Dr. Moncrieff is a psychiatrist, academic and author. She has an interest in the history, philosophy and politics of psychiatry, and particularly in the use, misuse and misrepresentation of psychiatric drugs. As an author, Dr. Moncrieff has written extensively on psychiatric drugs and her books include The Myth of the Chemical Cure, A Straight Talking Introduction to Psychiatric Drugs and The Bitterest Pills: the troubling story of antipsychotic drugs.

She is one of the founding members of the Critical Psychiatry Network which consists of psychiatrists from around the world who are sceptical of the idea that mental disorders are simply brain diseases and of the dominance of the pharmaceutical industry.

We talk about the recent meta-analysis of the efficacy and tolerability of 21 antidepressant drugs, widely reported in the UK news media on February 22nd.

In the episode we discuss:

  • The approach taken in the largest ever meta-analysis of efficacy and tolerability of 21 common antidepressant drugs.
  • The problems inherent in comparing antidepressants with each other, as opposed to trials that compare the active drug to a placebo.
  • That the main conclusion reached was that all the antidepressants studied were better than placebo at reducing depressive symptoms.
  • The limitations of the study, particularly how response rate was selected as the primary outcome measure.
  • That ‘response’  is mostly defined as a reduction in the Hamilton Depression Rating Scale (or other scale) rating of 50% or more during the study.
  • That the response rate can artificially inflate the difference between drug and placebo.
  • The problems with blinding in the supporting trials and the effects of including people who are already receiving antidepressant treatment.
  • That the study did not include adverse effects or withdrawal difficulties, only dropout rates which are not representative of the whole picture of taking the drugs.
  • The short-term nature of the supporting trials, mainly 8 weeks, with a range of 4 to 12 weeks, which cannot be easily compared with the real world experience of people taking the drugs for much longer periods.
  • That, when the primary data is analysed (the depression rating scale scores) the differences between placebo and antidepressants are very small and probably clinically insignificant.
  • The uncritical and sensational nature of the media reporting of the study and the link to the Science Media Centre.
  • The concerns about the reporting that depression is under-treated in the UK which is not supported by the results of the study.
  • That people should carefully consider the balance of benefit versus risk, taking into account the potential for adverse effects or difficulties stopping the drugs.

Relevant links:

Comparative efficacy and acceptability of 21 antidepressant drugs for the acute treatment of adults with major depressive disorder: a systematic review and network meta-analysis

Challenging the New Hype About Antidepressants

The Hamilton Depression Scale

Empirically derived criteria cast doubt on the clinical significance of antidepressant-placebo differences

Efficacy of antidepressants in adults

The Science Media Centre

To get in touch with us email: [email protected]

© Mad in America 2018

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James Moore
James Moore has experienced the psychiatric system and psychiatric drugs firsthand following a stress-related breakdown. Believing himself to be fundamentally broken, he spent many years on psychiatric drugs before awakening to the reality that psychiatry has few answers for human difficulties. James produces and hosts the Mad in America podcast, in which he interviews experts and those with lived experience to challenge some common misconceptions about psychiatry, psychiatric drugs and the bio medical model.

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  1. The whole article is here.

    It is so short I thought it was the abstract. The whole article is quite strange.
    Here is a quote: “We contacted all the pharmaceutical companies marketing antidepressants and asked for supplemental unpublished information about both premarketing and post-marketing studies, with a specific focus on second-generation antidepressants. We also contacted study authors and drug manufacturers to supplement incomplete reports of the original papers or provide data for unpublished studies.”
    That means the drug companies could provide any data they wanted and exclude whatever was not in their favor.
    Another problem is that all these studies rely on patients who are taking antidepressants before the study and stop taking the drug cold turkey. Then, after 10 days half of them get back a drug very similar to what they were taking. The placebo group continues their cold turkey withdrawal. It is quite obvious that people feel a lot better when they get back a similar drug compared to being in withdrawal.
    So all of these studies are not testing if antidepressants work, they are just showing the obvious: that getting back a drug is more pleasant than abrupt cold turkey withdrawal.
    In addition, the placebo group reaches the same level as the drug group one week later. Why not wait?

    What is Really strange with this Research is the standard mesn difference which is a messure of how much higher the response to the antidepressants is. The authors admit it is modest: 0.31. 0.2 is considered low. 0.5 modest. This is actually LOWER than what Kirsh et al got when they determined that antidepressants don’t have any clinically significant effect.
    It doesn’t matter that the antidepressants all beat placebo when the difference is so small that neither the patient nor the doctors can notice it. It is only when you test thousands of patients lie this study does that the very small difference will show up.

    And almost all the studies were done by the manufacturers.

    Another strange effect is that when a company tests their antidepressant against another, their drug always becomes the winner. Here the authors call this «the novelty effect”
    It is just like Pepsi and Coca Cola are running their own trials to find which is more tasty.

  2. Heard tell Wessely and his gang are sending a posse to Birmingham this year. What do you bet they’ll be diagnosing the Brummy accent as a precursor to having ‘ADHD’ children and a life of crime ∴ in need of early intervention drugging?

    It’s gonna get worse. I implore Fiddaman and the brummies, to take Wessely and his gang hostage at the town hall.

  3. I haven’t listened to every broadcast (they started before I was aware of them) but those I have listened to have always been full of valuable information. I thank you, James, once again, for taking the time to make these broadcasts available to us all.

    I want to also thank Dr. Moncrieff for taking the time to make her views clear. I have read many articles on MIA (and increasingly in the wider-spread media) that are critical of antidepressants and other drugs. As a psychiatric survivor who was on antipsychotics for many years (during which time I degraded and was turned into a zombie), I am still learning about the effects that all of these drugs — antidepressants, antipsychotics, anti-ADHD — have on the people who are unfortunately either convinced or forced to take them. Thank you.

    Eric Coates

  4. Brilliant! Thank you so much for this, I will be sending the link out to people who heard the hoopla and wondered what to make of it all.

    Just a couple questions, Joanna. You said… (about people choosing to take antidepressants)

    “That’s fine as long as people are aware of what the research evidence actually says and can make up their own minds […] I think what’s really important is that people know that the story that’s being told us by the institutions that created those headlines on Thursday is not the only view…”

    1. All well and good in theory… but when the institutions that feed such press releases to the mainstream media also write the official guidelines on antidepressant prescribing for GPs*, what chance does anyone really have of making an informed choice?

    2. Your situation applies only to adults who are able to make their own decisions and reject medical advice if they choose. What about children, or patients on Community Treatment Orders? How do parents of children who have been prescibed antidepressants go about challenging doctors and official medical advice?

    My feeling is that Psychiatry’s PR juggernaut is only just warming up its engine. Plenty more in the pipeline, I fear.

    *perfectly explained by Dr Andrew Green in this youtube clip at 1hr19mins30secs https://www.youtube.com/watch?v=vejVt1fNYQk

  5. Thank you for this. The co-ordinated press campaign cherry picked the data when the overall answer was plain to see: no clinical effect, despite the inevitable commercial bias in the data. I hope NICE aren’t fooled, and I hope people have the courage and presence of mind to ask their Doctors what the evidence is for what they are prescribing.

  6. what a very good podcast again…thanks james and dr Moncrieff…..
    when I was depressed I would have taken anything for relief…
    that is a problem…and my friends believe doctor knows best..
    with all their pills for all the suffering…we are not dealing with causes..
    and the anti-psychiatry talk is making it worse for me…

  7. Why do we continue to call neurotoxic chemicals “medications” or “antidepressants” or “antipsychotics”? As Moncrieff well knows, and as Breggin has pointed out, these psychotropic, neurotoxic drugs have nothing to do with medication or healing. They are DRUGS. Why do we continue to use euphemisms such as “medication”? And as Auntie rightly notices, hardly any one will really be able to make an informed choice about psychotropic drugs because hardly anyone knows the real history of these drugs. Even if they did, hardly anyone knows the true history of psychiatry. Thus, no one is making an informed choice about these neurotoxins. They are making choices based on deception and misinformation. They are making choices based on psychiatric propaganda. This is not informed decision making. The information will come later, when in their drug induced, zombie like state, they realize that they have been duped by psychiatry and the pharmaceutical industry. But even that will be difficult because of what Breggin has shown in his descriptions of “medication spellbinding,” namely, the difficulty of perceiving the iatrogenic harm that is caused by psychotropic drugs.

    • I object to the term antipsychotic, as it labels the person consuming the drugs as psychotic. Where as the drugs are not antipsychotic, they are disabling.

      At times these drugs can create explosive reactions and at times the drugs can create very risky indifference. I took these drugs voluntarily for many years at very low doses and eventually stopped taking them.

  8. Every time I read an article like this, it only confirms what I already KNOW! Psychiatry is a pseudoscience, a drug racket, and a means of social control. It’s 21st Century Phrenology, with potent neuro-toxins. Psychiatry has done, and continues to do, far more harm than good. Years ago, now, I was working very closely with an excellent licensed clinical psychologist, and a general practitioner/family doctor. For over a year each, I tried “Wellbutrin”, and “Zoloft”. As far as I’m concerned, they were both a waste of time & money. My psychologist said he, “thought they might have helped somewhat”, but he couldn’t be sure! The other psych drugs I’d been given earlier definitely did me far more harm than good! The longer I stay away from psychiatry and psych drugs, the more whole, healthy, and happy I become! Gee, Doc, what happened to my “mental illness”….????….
    For extra credit points, try to find even *ONE* mass-casualty school shooter who was documented to NOT be on psych drugs, especially antidepressants…. Go ahead, I dare you!….

  9. To understand this you have to understand what SSRI’s are good at…. reduction of libido….it’s about an attempt at population reduction. This is the new role for psychiatry. They all know, full well, that AD’s are no good for depression nor anxiety. The ‘guardian’ got into bed with multi billionaire Gates and that is his game. From their perspective MH is the perfect method… there is no diagnostic test, so almost any excuse will do, once on the drugs people fear coming off them, if they have akathisia…..suicide ideation or kill themselves or someone else, it’s the ‘mental’ illness and please understand Joanna, akathisia is not just a young persons ‘illness’. They have made sure the word akathisia is not in any drug box insert . Expect the guardian to go full-steam ahead on normalising the drugging of UK children and schools using anxiety depression and ADHD on-going MH assessments to justify it.

    What are you going to do…more philosophy, that will suit them just fine ?

    • The difference between now and then, apart from the different age-group obviously, is that they changed the measure from SMD, ie average efficacy in the whole population, to “response rate” in a subcategory. Or in other words, they mainly reported on 18% group of responders who had got substantially better in 8 weeks. A totally different and controversial way of looking at the data. The adult meta-analysis had many more patients (116,000 vs 5,000), and the authorship has changed substantially as well.

      The comparison in the 2 papers is striking. Fluoxetine (Prozac) goes from easily being top of the league in children and adolescents to near the bottom in adults.

      Then there is the amazing case of Amitriptyline, which goes from next-to-bottom of the league in under 18’s (SMD=.08 ie next to useless), to being top of the league in adults by a distance, but based on relative response rate.

        • The 18% is probably the mania kicking in and then they get out at 8 weeks before the patient becomes completely delusional or stops taking the drug completely or ends up being hospitalized.

          The side effects are the most reliable part of these prescriptions. Take a look at Viagra and it’s launch if you don’t believe me. It was first introduced as a blood pressure pill. Oops!

          • Side effects look like they are an influence. I think it might be more to do with sedation though.

            I think a statistician would confirm that the main reason that 18% got substantially better must be either the placebo effect of the drug, or natural remission. That would explain why quite a lot of both drug users and placebos end up in that 18% category.

            Now, the reason why there seems to be more drug users in that group must be down to that small (but real) effect size of 0.3. And the reason for this effect could either be a genuine but small therapeutic effect, or unblinding, or perhaps simply sedation -meaning you aren’t actually totally with it when someone asks you how your depression is going. The top two performers in the adult study are also two of the biggest sedaters.

            There is so much that they did not report, but it seems to me they could have. Why didn’t they report the response rate by individual drug/placebo? Why didn’t they report the effect size by drug, like they did for the under-18 study?

  10. Thank you for this very helpful and thorough interview. The only thing I would question is the statement that it may not be possible to design research that would definitively answer the question of antidepressant efficacy. I think it’s very possible that long-term research, following people over the course of years and looking at both positive and negative effects, would show a clear long-term deleterious effect. It’s just so common to find people who benefitted greatly at first, and then reverse tolerance creeps up, and side effects creep up…my bet would be that if you extend the time scale to real-life scenarios, the results might just become pretty clear.

    I realize that isn’t too likely to happen, but strategically I think there’s a strong case to be made–a very plausible hypothesis to be put forth–that would strengthen the argument against the drugs. Well, not just strategically, as opening up the debate beyond the narrow confines of current research actually helps to expand people’s understanding. And who knows, maybe more discussion like that could actually open up the possibility of careful research?

  11. Have been reminded of the UK guidance of prolonged QT interval (you just drop down dead) and citalopram/escitalopram and it being dose dependent. Well in the context of pharmacogenetics and all the inhibitors/activators of metabolising enzymes, there is no such thing as ‘dose dependent’.


    “The potential for citalopram and escitalopram to cause QT interval prolongation has been known for some time and is reflected in the product information. However, recent data have further defined this risk and have clarified that their effects on the QT interval are dose dependent.”

    And unless your rigged up to an ECG just before you drop down dead, no one is going to know what caused it, as far as I’m aware.

  12. Is everyone forgetting that benzodiazepines also “work” when you first start taking them? But then they turn on you and become your worst nightmare and destroy your life. So even if antidepressants do “work” for the first couple of weeks (and that’s a big “if”), that doesn’t mean anything. The wording by The Lancet is extremely misleading. They might as well have said that it’s good to take benzos since they “work”, because for about 1-2 weeks they acutally do! In fact, I bet benzos work much better for depression during those 1-2 weeks than antidepressants do. And so does alcohol, and probably many illicit drugs.

      • My point is that 8-week trials don’t give any clues on how a drug performs, because any psychoactive substance is likely to have an effect, some positive and perhaps desired, and some very bad. One could compare antidepressants to benzodiazepines as an acute treatment for depression and I’m willing to bet the benzos will actually come out the better of the two! Especially if the depression is accompanied by anxiety, tension and insomnia. Actually, antidepressants take some time to “kick in” so it is 100% certain that benzos perform better in short-term trials. Obviously, it would be insane to tell people that we should all use more benzos when we’re depressed as that would be quite catastrophic to say the least. Yet psychiatry is now promoting antidepressants without considering the long-term outcomes, which do not speak in favor of the drugs. Not to mention the same dr. Cipriani concluded only 20 months ago, also in The Lancet, that antidepressants are not suitable for the use in children and teens, which clearly contradicts the “antidepressants work” conclusion of his recent meta analysis, but nothing about this contradiction is mentioned in his latest paper, nor in the media coverage.

  13. Do antidepressants work?
    Comments on the latest Lancet study

    On February 21 2018, The Lancet published a large meta-analysis (MA) led by Dr. Andrea Cipriani of the National Institute for Health Research, Oxford, on the efficacy and acceptability of 21 antidepressants (AD). According to the study, all AD’s were superior to placebo (PBO). The results of the MA were hyped by many media outlets. The English newspaper The Guardian called it a «groundbreaking study» that «will put to rest doubts about the medicine». «The drugs do work», so says the title (https://www.theguardian.com/science/2018/feb/21/the-drugs-do-work-antidepressants-are-effective-study-shows).
    But even the authors of The Lancet article don’t go as far as sharing this kind of «jovialism», of cheerful enthusiasm, when they write: «certainty of evidence is moderate to low», and then again: «the effect sizes were mostly modest» (http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(17)32802-7/fulltext).
    One of the weakest points of this MA is its failure to report anything on harms, which are numerous and well documented (see among others, « A.F. Carvalho et al., //www.karger.com/Article/Pdf/447034; C. Cartwright, «Long-term antidepressant use: patient perspectives of benefits and adverse effects, Patient Preference and Adherence», 2016, and many articles by psychiatrist David Healy).
    There are many more weaknesses. First of all the MA says nothing about the Number Needed to Treat (NNT); nothing about difficulty coming off AD’s; 78% of the randomized controlled trials (RCT’s) part of this MA were sponsored by the pharmaceutical industry; four authors declared conflicts of interest (COI), (but we don’t know how many of the authors of the studies included in the MA were in COI?); it was way too short (around 8 weeks); according to The Lancet, 73% had «moderate risk» of bias, 9% «high risk»; no information about run-in periods (which allow to cherry-pick participants and exaggerate efficacy); many trials had no information about randomization and allocation concealment; no evaluation of global functioning; one of the primary outcomes was response rate, a very weak criterion to judge efficacy; likely no active placebo; so-called a «considerable amount of unpublished data»… for 8 drugs out of 21 (were clinical study reports included , how many participants were concerned by these unpublished studies, and can you trust pharma giving negative studies?). Moreover, in AD studies the blind is broken because AD’s are active substances giving rise to adverse events. In a systematic review of 21 trials in a variety of areas that had both blinded and nonblinded assessors, the effect was exaggerated by 36% on average by nonblinded assessors (Hróbjartsson et al, BMJ 2012;344:e1119).
    Many studies have shown that RCT’s sponsored by industry and/or reported by authors in COI inflate efficacy. A study in the Am. J. of Psychiatry (2005), estimated that articles in four psychiatric journals, by authors in COI were 4.9 times more likely to estimate the drug was superior to PBO than authors who declared no COI (Roy H. Perlis et al., <http://ajppsychiatryonline.org/doi/full/10.1176/appi.ajp.162.10.1957). Sometimes efficacy is purely invented. This is what the famous and manipulated 329 study on paroxetine for depression in adolescents did (J.D. Amsterdam et al., «Industry-corrupted psychiatric trials», https://gallery.mailchimp.com/a6a198ec28f476496d9945891/files/470b3922-de15-4e23-ba5f-7769b2e404f0/Industry_corrupted_trials.pdf ).
    A MA led by Erik Turner looked at 74 FDA-registered studies of AD’s. Almost half (49%) failed to prove the drugs were superior to PBO (N Engl J Med 2008;PMID: 13199864). We are allowed to hypothesize that those studies were the «best» the makers of AD’s submitted to FDA.
    The authors of The Lancet article say the «great majority» had MODERATE to severe depression as measured by the Hamilton scale, or HAMD (mean score 25.7, standard deviation 3.97). Whatever criticism can be made about HAMD, this statement seems to be incorrect: according to the American Psychiatric Association, 8-13 is mild depression, 14 to 18 moderate, 19-22 severe, 23 + very severe. So the participants in this MA were very very severely depressed.
    Many MA’s by independent researchers (I. Kirsch, J.C Fournier, psychiatrist Joanna Moncrieff) show that efficacy for mild to moderate depression is no better than PBO. And the great majority of AD’s are prescribed to people who have mild to moderate depression. According to Kirsch, for very very severe depression (28 +), the mean difference on HAMD between AD and PBO is 4.36, slightly more than the 3 considered clinically significant by the National Institute of Clinical Excellence (NICE) (Kirsch, I., Zeitschrift für Psychologie, 222(3), https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4172306/, 2014).
    J. Undurraga and well known psychiatrist Ross Baldessarini (107 RCT’s) found, for second-generation antidepressants an NNT of 8.7 for SSRI’s, 10.2 for SNRI’s, and 6.2 for first-generation antidepressants called TCA’s (deadly in overdose and likely to cause heart rhythm disturbances that may be fatal )–(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3280655/, 2012, Table 2). Of course, these are means.
    The MA points out correctly that depressive symptoms tend to improve spontaneously. Industry sponsored RCT’s of fluoxetine and venlafaxine show no significant difference by week 8 between AD and PBO (Gibbons et al, Arch Gen Psychiatry, doi:10.1001/archgenpsychiatry.2011.2044). Moreover, a study comparing the efficacy of psychotherapy assigned 340 persons to a wait list (10 weeks). They gained 4 points on HAMD (Rutherford, B.R., Roose, S. P., https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3628961/, July 2013). Furthermore, a 3-year study carried in the US showed that 50.7% of people with depression, anxiety and drug abuse remit without any treatment (Sareen, J., et al., http://jamanetwork.com/journals/jamapsychiatry/fullarticle/211213, 2013, 43). Of course, it does not mean they don’t need help. Some of the same researchers did another study (1 year) in the Netherlands and found a greater number of remitters (some had residual symptoms).
    Moreover, AD’s may worsen depression. In this MA, the relapse rate for PBO is 24.7% versus 48.7 for SSRI’s (Andrews, P. et al., https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3133866).
    And what about overdiagnosis, which does not seem to be the case for this MA (see Thombs, B. D., et al., (2018). «Addressing overestimation of the prevalence of depression based on self-report screening questionnaires», Canadian Medical Association Journal. DOI: 10.1503/cmaj.170691, and R. Mojtabai who determined that 61,4% of people, almost all on AD’s, did not meet DSM so-called «criteria» (R. Mojtabai, Psychother Psychosom, 2013).
    The Guardian article quotes one of the authors, Dr. Geddes: «we don’t have very precise treatments for depression». True for AD’s; false for psychotherapy, at least for mild to moderate depression, and no side effects as long as you don’t end up in the hands of a charlatan.
    The Guardian piece quotes Dr. Cipriani saying that 80% stop their AD within one month. How do you reconcile this with the fact that those who defend their efficacy declare that it takes a few weeks (more or less 6 to 8) before AD’s show efficacy. But, unfortunately it takes just a few days for adverse events to manifest in many users, including suicidality and homicidal thoughts in a small percentage.
    As Joanna Moncrieff points out, media coverage of AD’s focusses on people who say they were helped by those molecules and this question is important to address. As Dr. Moncrieff says, if they decide that AD’s are worth trying, they should be aware that they will have to put up with the risks of side effects, understand that the difference between drug and PBO is very small (clinically null for mild to moderate depression) and the idea that the chemical imbalance theory, is not at all supported by research (https://www.madinamerica.com/2018/03/dr-joanna-moncrieff-challenging-new-hype-antidepressants/).
    I would add that alternatives exist (psychotherapy, peer and community support, exercise, acupuncture, etc.). If antidepressants show some efficacy in a minority, it is most likely not by virtue of their antidepressive qualities. It is by virtue of their activation effect (some clinicians adjust the dose to «create a controlled hypomania»), or the opposite, their sedative effects. They numb emotions, bad and in many instances good, as a New Zealand study has shown (C. Cartwright, op. cit.).
    This MA may look impressive with 522 RCT’s, but adds nothing new, just more smoke and mirrors. Including more biased studies in a MA does not make it better.
    J.-C. St-Onge, author: Tous fous? L’influence de l’industrie pharmaceutique sur la psychiatrie.