Wednesday, August 10, 2022

Comments by Hermes

Showing 502 of 502 comments.

  • What kind of kills me is that he has these two parallel arguments based on his statistical studies.

    1. LAIs should be the first line treatment for psychosis/schizophrenia. (Except perhaps for pregnant women.)

    2. There’s no safe window to stop antipsychotics, at least in an eight year timeframe.

    => Once you get psychosis, it’s lifetime LAI for you.

    Also the comment that nurses get reward when they act according to guidelines.

  • Another argument from Tiihonen, around 5:00:

    Is there a safe place to stop antipsychotic medication? According to Tiihonen studies, there’s no safe point of stopping antipsychotic medication.

    “It seems to me that during the first eight years of the illness, it is not safe to say it would be safe to stop the antipsychotic medication”

    Then he goes on to LIA injections.

    The to clozapine. I’ve been updating this message while watching the video. It’s a very good English review of his views on the treatment.

    Results: “I would say it is the lack of antipsychotic treatment that is associated with the associated mortiality .. associated LAI most with reduced mortality .. no safe point in 8 years to stop the antipsychotic medication”

  • Tiihonen has a long track record of promoting the new drugs over years and decades in Finland. Latest is of course promotion of long lasting injectable antipsychotics (LAIs), for which the pharmacies have a new patent for. This work wasn’t mentioned in this article, but it’s there, at least in the Finnish media. Some examples are here. They’re in Finnish, but maybe you can make sense of them with Google translate.

    I’ll give some quick translations:

    “A Finnish professor would change the the treatment of schizophrenia: Injection medicine could lower mortality

    According to the results, injections were related to 20-30 % smaller risk of getting to a hospital treatment.

    In addition the injection drugs lowered mortality of schizophrenia patients by 30%


    – Almost all of the National treatment guidelines say that there are certain special instances, where you should consider using LAI.

    – In my opinion the recommendation should be backwards, so that in only special conditions you should consider using an oral formulation.

    “If Tiihonen had his say, the national guidelines should be something else.

    – There are some special cases, where you should consider using oral [instead of LAI]

    LAIs are expensive, but the price should be considered against cost of staying in hospital.”

    “I was expecting only 30 % difference. I was surprised to see a 60% difference. It’s very rare to see this big a difference in medicine.

    He can think of only a single group of patients where the oral form is preferable over LAI.

    “It’s the patient group considering pregnancy.”

  • Regarding the situation between US and Finland, well yes, we don’t at least yet have as strick forced commitment laws compared US from what I’ve read. I realise it may change in future. However without those rules, they often find other medias or ways to almost enforce the drugs to the patients they deem need them. There’s can be psychological pressure, and if they think you’re not complying or “treatable” in public, then they can send you involuntarily to a mental hospital for evalution, and often you’ll end up with injections there. Maybe more often these days because of the new patents around. They’re making the injection choice more acceptable among the stakeholders, and with stakefolders I refer to a diverse group of people, not only psychiatrists. Many of those people don’t have any great affiliations with pharma, but the consensus opinion just shifts to prefer the patented drugs over time.

  • I know the issues with LAIs, and I’d rather fight to the end before accepting them for myself, even if was of the customazible variety. I’d myself try to stay with the oral meds as long as possible for their customability, and I could stop them on my own if the situation insisted that. I don’t recommend it for others, but it’s what I kind of had to do on my own. When looking reasons for LAIs being described or marketed at sometimes less, now more, a large part of that influence does seem to come from marketing department in various ways. But it’s not only pharma, there are various other human interests in the game. Doctors, family members and other people with a stake to hold have also other interests in the products. They often want the patient to be predictably medicated, which can happen with injections. The Abilify with tracking devices for schizophrenia seems like a horrible product.

  • Clozapine has a low affinity for dopamine D2 receptor which explains why it doesn’t cause tardive dyskenisia and other similar issues as easily. I think it was sometimes though in the development cycle of SGAs that it was effective because of its HT2 effects. Not sure, but I guess much of its effect (for good or bad) may come from its antihistamine actions. Some people with actual experience taking the drug don’t always talk so favourably about it, so not sure if it’s the best.

  • Incidentally when I was looking at the low dose haloperidol studies, some stated that the haloperidol group got more additional anticholinergic drugs compared to controls… this may imply it was still blocking the dopamine receptors too hard, or other drugs mitigated to that issue with more anticholinergic effect (or perhaps with other receptor activity)

  • “Some people commenting on this site have mentioned the harms of anticholinergics for a long time. They were most likely introduced to the atypicals to hide visible movement disorders.”

    Some of the older low-potency antipsychotics such as chlorpromazine, the first neuroleptic drug, have much higher anticholinergic effect (block muscarine) than haloperidol. While the anticholinergic drugs can prevent (block? hide?) the effects of dopamine antagonism related EPS symtoms, drugs such as chlorpromazine also have a smaller affinity to dopamine receptors, so I’m not exactly sure how much it is about anticholinergic effect and how much about less dopamine antagonism.

    “I wonder if there is any information on chronic blocking of the 5HT receptors (I know it’s related to concentration and the forming of new memories).”

    I personally don’t really have opinion, or don’t understand properly how the 5HT blocking actually works. I don’t know what it feels like subjectively, or the clinical implications from any proper studies. Some studies with drugs majorily blocking the 5HT have been quite disappointing to the industry if I recall correctly.

    “The antihistamines are linked to sedation, chronically blocking that would mean the whole wake / sleep cycle is damaged.”

    On the other, I think I understand the antihistamine effect a lot better. A very low dose of Seroquel (quetiapine) is a very potent antihistamine, acting on H1 receptors. It’s what makes you drowsy and sedated. It also gives you “munchies” and may be one major factor why some of these drugs make you fat. Taking the traditional US variety of OTC Benadryl (diphenhydramine) would give you much of the same effects as a low dose of quetiapine. In Europe they often sell the same trademark Benadryl with another active ingredient, but the point is that the original Benadryl blocks highly the histamine H1 receptor just like quetiapine at a small dose.

  • I read one scientific article, I forget if it was about neuroleptic injections in general or specifically SGA injections. It stated that when the oral SGAs came around, injections in general (which were all FGA injections) got general criticism and bad reputation. That is, at that time SGAs had the patent, and the general opinion about injections became more negative. The article then went out to consider the benefits of long lasting injections (LAI). I’m not sure if that article was somehow trying to make the new LAIs more acceptable or if it was more trying to assess the topic in a more neutral manner. I’ve seen many articles though which seem to more clearly to promote the new LAIs (which are on patent of course) as some kind of a next major step in the treatment. Even if they don’t directly focus on SGA LAIs, it’s kind of implicit that they’ll often be of the patented SGA variety rather than haloperidol. Maybe in US there’s still some patient groups out of the insurance system that can’t afford Abilify LAI but can afford haloperidol. In Finland people with severe mental illness diagnoses in public health care get a code with which they can get drugs like this for basically no charge, which means the tax payers pay for it, and they can get really expensive.

    Even if one considers that LAI may be warranted in some situations, there’s clearly this drift on many fronts that turns out the favour the drugs currently on patent, or perhaps coming to patent in next years. I’m not even sure pharma is so much bothered about things such SSRI criticism these days, since the projected future revenue will come patented drugs such as the new LAI and maybe having some patented drugs used of “augmenting” depression treatment. All of this hinders from assessing the risks and benefits for the patient in as neutral or objective manner as possible.

  • As for the second point “The long acting drugs are being promoted because the newer ones are on patent.”

    Yes, I’ve followed this progression over the years and I’m frustrated by it. There may be some actually bad guys around, but more often it’s more gradual change in attitudes of all kinds of people. The “low beat drumming” is perhaps a good way to put it.

    For instance, lately there’s been some quite visible “swedish registry studies” come out from research groups which find injections are powerful, and the same persons also publish studies which say injections are the best choice for first episode psychosis, and then other studies which suggest there’s no safe window for stopping an antipsychotic once it’s started. For instance, professor Tiihonen has been quite visible in Finnish public press media, stating that the official national guidelines should be changed to state that neuroleptic injection should be the first line treatment for first episode psychosis.

    They’re not allowed to market medications directly to consumers in TV-ads and such here like in US, but the pharmaceutical companies can create “educational sites” about topics such as schizophrenia and bipolar. When you look at them, they’re doing things such as first giving a short history of neuroleptics; they enabled people to move away from hospitals, then came SGAs, etc. Move to the third page, there’s a kind of a crosswalk sign demonstrating the benefits of oral vs injections (long lasting it states) and lots of talk about this choice. It seems like it’s not direct marketing of these drugs as such, but there’s plenty of commercial interest behind all those sites, the images, words they have in.

  • Yes, I understand the argument that a low dose of haloperidol might be a better alternative for some people. It would presumably block less dopamine receptors than higher doses, and it would have much less effect on other receptors that relate to metabolic issues and so on. I don’t have clinical experience on how injections of haloperidol are administered. A low dose injection of haloperidol might work if it really is administered at the lowest dose for that person in the clinic.

    However, I guess it’s still possible that even with a low dose haloperidol strategy it will create more EPS symptoms over time than some of the other drugs because of its potent dopamine antagonism. After a quick look at articles of low dose haloperidol, some still suggested there was more ESP with low dose haloperidol compared to SGA in those studies. I also understand many of the studies from this field have been convoluted with pharmaceutical interests that are often not very direct, and other issues, as you mentioned. If I had no other choice, I might choose low dose haloperidol injection for its titratability over, say Abilify, provided I was part in the decision making.

    Antipsychotic drugs and extrapyramidal side effects in first episode psychosis: a systematic review of head–head comparisons

    Peter M Haddad1, Amlan Das2, Sarvenaz Keyhani1 and Imran B Chaudhry3

    “parkinsonism and akathisia. Six of athe seven haloperidol studies showed higher rates/severity of both syndromes as assessed by a standard rating scale at one or more time points versus at least one SGA comparator. This included two low-dose haloperidol stud- ies (maximum dose ≤ 4 mg) indicating that this is not simply an artefact of trials using inappropriately high doses of haloperidol. The data is consistent with a meta-analysis, largely in chronic schiz- ophrenia, in which low-dose haloperidol (< 7.5 mg) was associated with a higher EPS risk than SGA comparators (Leucht et al., 2009)."

  • Hi Sandra. I haven’t visited this site for a while. When I wrote about these issues as a kind of recovering person from Finland in response to your posts several years ago, I perhaps appeared a bit grumpy and not always correct, but I realise even at that time we shared some of the same interest in this issue. Still geeking out.

    It may be that kind of specifically directing dopamine receptors e.g. at a low dose with haloperidol is better than scattering them with drugs that go to dopamine and everywhere else. On the other hand, drugs such as Seroquel sedate people through H1-histamine receptors, etc, so they may may get more sleep and so on, without the need of excessive dopamine blocking, which can lead to nasty stuff. There may be some kind of a bike stabiliser effect with drugs such as Seroquel in the sense that the doctor cannot block the dopamine really hard even if she tried to, because of the receptor affinities involved. I mean, you can block dopamine really hard with increasing doses of haloperidol, but it’s much harder to do with say Seroquel. Also if you look at the receptor profiles of some the older neuroleptics such as chlorpromazine or perhenazine, they have less affinity to dopamine receptors and more to others. If you want only to block the dopamine receptors at a very certain amount with haloperidol, you perhaps also need to be really careful not to overshoot it as a doctor. Also there may be some benefits from the other sedating effects of other neuroleptics for sleep, etc. Thoughts?

    (As a personal note, I’d rather not touch any of the drugs of this class.)

  • Right. The patents of SSRI and “atypical” neuroleptics have already expired or will expire soon, which will reduce some of the financial pressure to prescribe them. However, now there’s something sinister in the pipeline, namely the new depot injection forms of the atypicals that are currently promoted and will be promoted in the coming years for things such as first psychotic episode, etc. When the atypical came to market, injections of older neuroleptics were downplayed as somewhat inhuman and so on. Now there’s a new campaign to make injections again more acceptable in standard care.

  • To give some idea, I’m a Finn, and I only heard about Open Dialogue after reading Whitaker’s book. It’s a small country too. I also kind of think it has been even over-sold in international groups like this. My experience with the public mental health care was that it was very low quality and abusive. I even had as my psychiatrist someone who had been working in the Open Dialogue group in Tornio, I think. I think there has been some interest in the approach lately, largely because of the international interest.

  • Stahl, an influential figure in psychopharmacology, tries to draw a line between “conventional” neuroleptics and “atypical” neuroleptics in his book Stahl’s Essential Psychopharmacology. You can read the chapter about conventional neuroleptics here: It details how high D2 blocking in conventional neuroleptics can lead to all these adverse effects. Haloperidol is a strong D2 blocker. Other conventional drugs, such as chlorpromazine or perphenazine, not so much. Instead of telling about the lower D2 blocking ability of these other conventional drugs, he just adds the side effects of these specific drugs to the side effect list of conventional drugs in chapter “Other pharmacologic properties of conventional antipsychotic drugs”. For instance:

    “Still other pharmacologic actions are associated with the conventional antipsychotic drugs. These include generally undesired blockade of histamine H1 receptors (Figure 5-9) causing weight gain and drowsiness, as well as blockade of α1-adrenergic receptors causing cardiovascular side effects such as orthostatic hypotension and drowsiness.”

    Nowhere he mentions that for instance Seroquel has very strong effect on those same specific receptors, in very low doses. Etc.

  • Fiachra: “Does Seroquel have anti neurological compounds added to it that block extrapyramidal effects?”

    Technically they don’t usually add different compounds to these drugs. The drugs are made of molecules and they have different effects because their molecules “prefer” to bind to different receptors. When there are lots of haloperidol molecules in one’s body, they often tend to go block dopamine receptors and comparatively not so much other receptors. The molecules of other neuroleptic drugs, such as Seroquel, tend to go less likely to block dopamine and often go to other receptors instead. A single Seroquel molecule can go to dopamine, histamine, noradrenaline, serotonin, etc, receptor.

    Major reason some of these drugs have less EPS is that they block dopamine more weakly, even at the doses they are used to treat psychosis. So, a dose of 600-800 mg of Seroquel is still likely to give you less dopamine blocking than moderate or high dose of haloperidol. In addition, I think for instance Seroquel (or, quetiapine molecule’s metabolite norquetiapine) binds to anticholinergic M1 receptors, which may prevent or mask some EPS.

  • All neuroleptic drugs work on dopamine receptors in “anti-psychotic” doses. But its not only dopamine, these drugs also play with other receptors with varying affinities. For instance, a low dose of Seroquel may give you munchies because of its strong antihistamine H1 effects at that dose. That sedating effect of the drug may also enable more sleep for those people who have not slept properly in a long time. Actually getting some sleep may help with many people who are diagnosed with psychosis. Etc.

  • So much of the comments put out by psychiatrists or psychologists seem like they’re promoting their own particular guild all the time. Psychologists sometimes think they get support from this modern criticism of psychiatry, but then get dismayed when they find out that some people in that party also criticise their own field. Psychology and CBT has its own problems, often as severe as those of psychiatry.

  • I don’t think it does this site favour in general either to take maybe too extreme positions.

    “Indeed, referring to them as though they are real, reliable, and valid entities — in the context of the citation of theory and statistics about heritability — is stunningly misleading. ”

    I don’t think it’s “stunningly misleading”. Currently Jay’s articles are some of the few ones published on this site I actually consider reading and thinking more thoroughly. Maybe it’s because I feel I don’t understand genetics and the related studies done it well enough.

  • Jay, thanks for the tips to what to read about this subject. I’ve been interested in this topic at least since I read a related book by Chorover. I live in Finland and I know there was plenty of eugenics movement here. Finland was even allied with Germany in much of the early parts of 20th century. I have some articles on my to-read list concerning this particular point in history.

  • I guess that with benzodiazepines and opioid painkillers there may be yet more confounding factors that explain the correlation, after all there are certain type of people who try to get prescription for these drugs. Antidepressants had +31% risk, benzodiazepines +45%, opioid painkillers +92% and non-opioid painkillers (NSAID, aspirin, ibuprofen, etc) +206%. Any ideas how to explain that correlation for non-opioid analgesics?

  • I think he means “11-year follow-up of mortality in patients with schizophrenia: a population-based cohort study (FIN11 study)”

    This study became quite popular. Psychiatrists of all kind started to use the study as an (often unconscious) propaganda tool or weapon in presentations. They still do that. As an example, they go out to a presentation to professionals, patients or patients, and then talk about how this Tiihonen cohort study says neuroleptics, injections of neuroleptics or clozapine show .. insert whatever self-justification in this part.

  • Tiihonen’s interests are clear:

    – Benzos, opiates, etc out, more SSRI and atypical neuroleptics instead
    – More widespread use of long-lasting neuroleptic injections
    – He’s a particular fan of clozapine

    Etc. Then he crafts these cohort studies that support this thinking. If there’s his name in the study, then it’s a huge predictor the study will support one of these points.

  • This same Jari Tiihonen has a voice on today’s largest newspaper in Finland. “Research: Pain medication and benzodiazepines connected to homicide”. It’s another cohort study. The article says that the most important result from this study is perhaps that antidepressants don’t cause homicidal behaviour. (sorry in Finnish)

    It seems that many if not most of the common people commenting to that article realized problems with causation, such as that the people who use benzos or opiates at the present society are as a group more likely to be just the persons who also act more violently. It almost seems that Jari Tiihonen’s job at Karolinska institute is to craft his psychiatry propaganda using big cohort studies. Maybe it’s possible to create almost all kinds of points from those kind of studies?

  • If you get a label of schizophrenic, bipolar, psychotic, psychosis level problem, etc, then in the current narrative those conditions require anti-psychotic drugs. Perhaps sometimes those labels are used in order to justify use of anti-psychotic drugs. It may be self-justifying for the prescriber too.

  • I’m looking to your new post. I’ve looked at all this push for LAIs and related talk about importance of “adherence” in first psychosis during the last years. I find it quite worrisome. I haven’t read that book from Whitaker and Cosgrove, so I’m also looking forward to the point of view they make concerning schizophrenia as a chronic disease. I think it’s a messy topic.

    I’ve been trying to figure out what happened to me when I got diagnosed with bipolar, then schizophrenia, then when I had quit all drugs and returned to work, the diagnoses was that I had had “severe depression with psychotic symptoms” when I had arrived to that psychiatric unit two year before, though their own check-in test at the time implicated to them that I did not have depression at that time. I don’t think I had any notable type of psychosis at the time, but of course no one believes that because they know people with psychosis are paranoid towards treatment, not adherent, have lack of insight, are treatment resistant and so on.

    I do think there’s biology behind much of what counts as mental illness, and diagnoses do have some validity or use. At the same time, in clinical practice psychiatric diagnoses and descriptions are somewhat hazy and cannot be proved to be strictly right or wrong, psychiatrist have plenty of power over their patients and so on. The diagnoses, words and descriptions are sometimes used as kind of tools in things such as behaviour control and self-justification.

    On my hiking and trail running sessions I’m currently listening to audiobook “Mistakes Were Made (But Not By Me)” which deals with the self-justification angle. It’s not a specialty of psychiatrist to try to find explanations to prove self-worthness, being a respectable citizen, etc. Most of us do it. Psychiatry is not the only place where it happens, but it’s one place where this self-justification can have particularly nasty consequences. Other places this kind of behaviour can have unfortunate consequences include forensic system, juridical system, psychological interventions and relationships. It happens everywhere.

    In my particular case I was rendered unable to work by the treatment. After two or three months of the treatment with neuroleptic drugs (and SSRI), I was sleeping 14-16 hours a day, my speech was very slow and I often answered with just “yes” and “no”. Just months before I was fully employed in a good job which required clear and logical thinking. My relatives and other people around me got very worried for my health at that point, after I was being treated for some months with neuroleptic drugs. My mental and physical health kept getting worse during the next months, and the descriptions I read from their notes show how self-justification may cause psychiatrists or psychologists to wrangle already loose diagnostic labels and descriptions so that it looks like they were doing great job and are respectable citizens.

    For instance, when at the two or three month mark I complained about the actual severe reaction to neuroleptic medication (Ability and quetiapine), they wrote in their papers “patient had paranoid though concerning current medication”. I never had any paranoid thoughts, but that’s a nice place to use that word, since it knocks out my criticism. After two years from starting the treatment, I was out of all meds and back to work, but the final report which they wrote and sent to public Finnish health care units said “patient had paranoid thinking when he arrived here”. No. Their own actual records say falsely that “patient had paranoid thoughts concerning his medications” two or three months after I arrived there, at a point when it was evident to almost anyone else that I was rendered disabled by their treatment.

    Confirmation bias is “the tendency to search for, interpret, or recall information in a way that confirms one’s beliefs or hypotheses”. In my case, it seems that the psychiatrist and psychologist had decided early on that I maybe had bipolar or psychosis of some kind. After that point, they started to interpret everything I said through that lens. When I told about the effects of the drugs on my brain, philosophy, etc, they were dismissed in their official notes in terms such as “patient claimed he prefers to think in scientific way, but his use of words was illogical”. When I objected to this treatment, the self-justification perhaps on both parts just escalated the situation. When I started to resist the treatment that I felt was destroying my health, that resistance itself became to them more proof of mental illness. If I disagreed with them, they interpreted that as more of delusional thinking and proof of their original hypothesis. And then I disagreed more.

  • David, I don’t know too much about EPS and anticholinergic or antihistamine drugs. They say newer antihistamines are less sedating because their molecules are less likely to cross the blood-brain barrier, and so they don’t affect the histamine receptors in brain as much. The original Benadryl (diphenhydramine) does work in a similar way as a very small dose of Seroquel, though at least here in Finland what they call Benadryl is not that same chemical anymore. In any case, I think diphenhydramine has been used as a sleep med, maybe even anti-anxiety, etc, in history.

  • When I got diagnoses of schizophrenia around 2010-2011 (of which I “recovered” as soon as I got it), I had a psychologist telling me I’d get a brain damage if I would not take neuroleptics. When I was waiting in a waiting room, I saw an advertisement to a drug-funded infomercial site paid by a pharma company.

    Pharma in Finland is not allowed to advert directly to customer like they are in USA, so pharma builds official looking info sites. The site had one of Finland’s top forensic psychiatrists answering to patients, in a “doctor answers to patient” kind of way. He told there things such as “Schizophrenia is considered a brain-degradring brain disease. Some studies suggest that newer neuroleptics may reverse this process.” When I emailed him for proof of this, he sent me back one of those studies comparing haloperidol and perhaps Zyprexa (I don’t remember for sure and can’t check). Blah blah, haloperidol with more dopamine blocking caused more brain shrinkage than the control, etc.

    In any case, there’s one top psychiatrist telling as an authority to schizophrenia patients that schizophrenia is a brain-degenerative brain disease. And that that atypical neuroleptics may reverse this process.

  • Daniel, much of what you have observed of Open Dialogue is true. It’s not a new “yoga” to heal people with schizophrenia diagnoses. To me, the most interesting thing in those and related studies (need-adapted, whatever) is that they tried to avoid neuroleptics, maybe diagnoses and other related stuff in first-episode patients.

  • As an example of “promotional sites”, when I was an inpatient in a Helsinki psychiatric clinic, I noticed in the waiting room that there was a large promotional for this site in the waiting room for patients: When you click it, yeah, it’s not direct promotion to patients, but it’s from Lundbeck Ab, makers of injectable neuroleptics. When you click the first link, it says in the end, quoting Heli Pilvilampi from Aurora hospital. I don’t have time to translate it myself, but you’ll get the idea with this Google translate:

    “Schizophrenia relapse fastest way to the situation in order to balance is usually achieved by modifying the person’s medication. Because relapse is often caused treatment interruption, Pilvilampi, the alternative is to practice therapy resumption of the old medication strengthening or replacement. In particular, long-term injections at this stage are recommended:” Pretty soon we will usually talk about these long-acting injections in favor – especially if the pre-drug therapy has been interrupted. Their advantage is the ease of use, efficiency and smooth effect on your body. ”

    Patients’ attitudes injections varies, but mainly they are perceived positively: “For some it’s just a matter of course, and a good thing, that once a month to get the injection, and that’s all. Of course, it also requires further staff motivation and merits emphasis. Family support is also changing the type of treatment is still very important, “Cloud Lake says.

  • I don’t know it makes a difference, but unlike USA, in Finland pharma is not allowed to directly advertise prescription drugs to consumers. What they do instead is to advertise directly to doctors in their conferences, papers, advertisements and so on. Other technique they use is to publish for public some “official information sites” about schizophrenia and the best ways to treat it (currently of course atypical drugs or injection forms of these drugs). There are chief psychiatrists going around teaching other psychiatrists about the awesome effects of these new injection medications.

  • Fiachra, here’s an article concerning QTc prolongation with neuroleptic drugs:

    QTc Prolongation and the Use of Antipsychotics: A Case Discussion

    “Despite the documentation of prolonged QT intervals with all of the above-mentioned antipsychotics, significant evidence of TdP is linked only to use of thioridazine (and possibly other low-potency antipsychotics), droperidol, and haloperidol. Among antipsychotics, thioridazine is most closely associated with TdP. Other low-potency antipsychotic medications may also be associated with TdP; however, thioridazine, unlike the other low-potency antipsychotic medications, acts as a calcium-channel blocker, and it may be this property that leads to elevated rates of TdP.”

  • Fiachra said:

    “The strange thing is that I did have occasional palpitations while on Mellaril, but not the scary straining on beats that I experienced on Seroquel.”

    These drugs work on many different receptors besides dopamine and histamine. Adrenergic, serotonin, acetylcholine, etc. Each drug has a bit different profile on which receptors they affect on. One drug also has different relative effect on different receptors based on dosage. For instance, 25 mg of Seroquel has lots of histamine effect relative to effects on other receptors, while 600 mg has much more dopamine effect yet not that much more histamine effect than 25-100 mg of Seroquel.

    For instance, I with thioridazine there are effects that are different from those of quetipine. For instance, the action of these drugs on alpha adrenergic 1 and acetylcholine receptors probably are involved in cardiovascular related issues. Each of these drugs work on a similar set of receptors, but they vary on which receptors they prefer to activate.

  • Fiachra:

    “At a small fraction of 25mg per day I was experiencing a type of straining on heartbeat effect, and I noticed when I woke in the morning my chest, ribcage area was reddish and the rest of my body was white. When I stopped the Seroquel completely these symptoms disappeared. My sleeping was then diminished but I got it back with more daytime exercise.”

    When I started quetiapine (same as Seroquel) at 25 mg, I started to get some weird heart issues just when going to bed. Just when I was falling asleep, I was awakened be some kind of heart shock. There also started to randomly appear some strong and large red spots around my body, meaning some type of issues with inflammation, immune systems and so on.

    It’s true that Seroquel at 25 mg does not really affect dopamine systems. At the same time, it’s a very strong antihistamine in H1 receptors, similar to Benadryl, in those doses.

  • Fiachra: “Seroquel has a half life of 6hrs and at 25 mg is a lot stronger on sleeping, so I cut the Seroquel right down. But eventually I found out that Seroquel at 25mg has no dopamine effect, so by switching to Seroquel I had ‘weaned’ myself.”

    Yes, Seroquel at 25 mg is very sedating because it works very strongly on histamine H1 receptors. That effect is possible useful in getting sleep, etc. In the long term, it may also havoc one’s metabolism, etc.

  • Exactly. I googled the receptor affinities of Mellaril (thioridazine), and for instance it binds strongly to antihistamine receptor H1, etc. It’s the same receptor that quetiapine binds strongly to. That effect gives the strong sedation, and possibly also part of the heart issues. Both Mellaril and Seroquel have strong sedating antihistamine activity on the same antihistamine receptors (H1, etc), and I can’t see any rational point to switch medications like what was done to you, Fiachra.

    If you want just the antihistamine sedation of H1, you can buy the the OTC (in USA, not in Finland) drug Benadryl which sedates persons just like Seroquel in low doses.

  • The patents of the so-called-atypical antipsychotics have run out, or are about to run out. They’ve been just waiting to market you these new injectable forms of the same drugs. Why? Because these forms have a new patent. Then the marketers of pharma, lay psychiatrists, etc, go out and spread the word that this is the way to treat the patients.

  • To elaborate, psychiatrists, psychologists and other people, even lay persons often use diagnoses and other technical terms such as anosognosia, bipolar, schizophrenia, lack of insight, etc, as tools of behaviour control. It’s true that some persons hear voices, have mental problems, etc, and that is related to whatever happens in their body. At the same time of course these diagnoses and other descriptions of patients are often used as kind of tools in behaviour control.

  • Markps2, yes. I haven’t read Szasz and from what I’ve read of his thoughts, I’m not sure I agree with all of it. I think many people diagnosed with schizophrenia have something wrong in their body, for instance. Stress hormones, metabolism, HPA axis, etc. On the other hand, these diagnoses, drugs and other techniques are also often used as tools of behaviour control. For instance, labelling someone with “schizophrenia” often is similar to labeling someone as a “witch”. I also got labelled as having “schizophrenia”, and it was only then that I realised how hazy the real clinical world of psychiatry was. Much of it has to do with behaviour control.

  • Currently I sleep 7-8 hours at a night and get up quite easily. There have been also many confounding factors, such as me getting off drugs, etc. But in any way, I think my body in a way got adapted to this type of diet, where I would take a very low amount of carbs, such as 20-30 mg in a day, over weeks. The body changed its metabolism, and after the adaptation phase, my body lost the hunger, so I can easily go over long periods without any hunger or cravings for food at all.

  • Also, in what I take as quite a great success in both losing weight and getting back mental focus, I think the most important issue was to reduce carbohydrates to minimum and increase fat intake. It may sound even paradoxical given the current dietary guidelines, but it worked for me at least. If you change your diet like that, your body, including your brain, transforms to using more of the ketone bodies made of fat for energy, instead of glucose. This shift can also produce different type of mental experience. Very low carb diets have been successfully used to treat epileptic patients, for instance.

    Of course, when I was reducing carbs, I also reduced my gluten intake at the same time, so I don’t know if gluten was causing some of my issues. But I’m skeptical about it being gluten in any meaningful way, in my case.

  • To elaborate further, I think when I switched to a quite low carb and higher on fat diet, my metabolism changed, and as a result things such as mental fogginess during the day, the thing I was often medicating myself on with legal or mental drugs, pretty much disappeared. My mental world changed quite drastically after that change in my diet. I can now keep a pretty constant focus throughout the day at work, and after work, with generally just two meals in a day, no snacks between.

  • I went low on all sugar and carbohydrates and higher with fat consumption originally as an effort to drop those 25 kg I gained with neuroleptic drug. It worked very well in that sense, I dropped those 25 kg in a year. However, another think I noticed in that process was that the kind of diet I was on gave me much more constant clarity in thought. I no longer needed sugar based snacks at work to give me energy, I had more constant and stable energy throughout the day, etc. I therefore keep eating this type of diet even after I lost that weight. However, I’m not overly promoting what I’m doing to other people. People have different types of bodies and situations, for instance, so I’m not telling everyone to follow what I did. I can just add one anecdote.

  • Heh. Yeah. It’s kind of funny or interesting that I used the term autonomously, at a time when I was a “zombie”, when I was not connected with other “zombies”. The psychiatrist nurse had actually literally written in my “plan for recovery sheet” very early on as one of my top goals to “get rid of the zombie state of mind”, just as I had told her. Maybe zombies have some group mind, like sometimes depicted in those movies, since they know to use that word so often with neuroleptics.

  • This “zombie” word in describing neuroleptic drugs is interesting. I have it in my records that “patient had problems describing his emotional states”, and soon in my “treatment plans” that I was feeling like a zombie. At that time, I had not read basically any sources from “anti-psychiatry” or “critical psychiatry”, or even good critical accounts from “service users”. I think I had kind of invented that word by myself. Later on I noticed there were lots of other persons describing the state of mind in the same manner.

  • Timothy, thanks for this piece. It’s probably true people in this “Whitaker camp” are simplifying issues and so on, but then again they are often not PhD students specialising in this type of thinking, reading and discussing Foucault and academic papers, etc.

    In any case, I agree with you that there are many factors besides just drugs that drive this increase in disability. I’ll give as an example my own experience of the psychiatric system. First, I live in Finland which has a somewhat different culture and history than USA. It’s a small and culturally homogenous country, with a relatively “egalitarian” social system, similar to other nordic countries of Europe, such as Sweden. The public health care is free for every citizen and people get paid for disabilities, including mental illness, by the state. Being somewhat distant and small country, Finland was also slower to follow with trends such as the increase in SSRI prescriptions for depression.

    I had quite severe issues related to anxiety, stress, depression, social phobia and so on from at least 13 years of age. At the same time, I also managed to somehow do quite well in school. Let’s just say that my symptoms were quite severe. Around 1998-2000, when I was roughly 20 years of age, I went to a university doctor to ask for SSRI, to try if it would help my quite severe symptoms. He was very reluctant to prescribe it, but eventually complied and gave me a prescription. I took it for some time, for some reason stopped it for a while, then wanted to try it again. I went back to the doctor to ask for new prescription of SSRI. This time he would not write a prescription and said that in his opinion, SSRI is not the answer to my issues. I protested and was angry, and he said I need to seek to the psychiatric part of the university health care if I wanted medicine.

    So, I then sought help from the psychiatric side. I had meetings with a psychologist who tried to ask about my issues. I wanted to get those SSRIs. The papers suggest I was suggesting maybe I have a bipolar, but they didn’t find any signs that suggest it. Finally I got to the psychiatrist, an older woman who also had a strong background in psychotherapy. I got her to prescribe SSRIs, but she was constantly saying that maybe I should eventually stop the drug, we don’t know much about the long term effects of these drugs and so on. I resisted and wanted to keep eating that SSRI. Eventually when I went to work, I stopped going to the university health care and also stopped taking SSRI.

    Fast forward to 2010 or so, when I was 33 years of age. I wanted to try SSRI again, to see if it would then again help with some of my symptoms. I went to the public health care this time, in a more suburban place I live in. I could have gone to a private health care, since in Finland the employer often pays for private health care for employees, but I think my idea was that I didn’t want the work related people to know about these issues. In the public health care, I saw a general doctor who readily prescribed me SSRI, asked some questions, and then also sent me for an evaluation. Long story short, they immediately added neuroleptic drugs, which caused severe issues which were intepreted as schizopohrenia, bipolar and so on within months. I was told I had a “progressive brain disease” which would impair my brain if I did not eat the drugs. When I complained of the very severe effects neuroleptics had on me, they wrote in their papers “patient had paranoidic ideas concerning his medication”. I was off the work for a year and they tried to push me to some “day hospital” And so on. After about half a year I finally figured out what was really going on, and then managed to fight my way out of the place.

    So, what was the difference between those years 1998-2000 and 2010-2012? I was actually in a worse condition in 1998 than in 2010. I can think of at least two major factors. One is that the kind of pharmaceutical health care with SSRI and “atypical” neuroleptics really broke through in Finnish care through that decade. This is similar to what Whitaker seems to address in Anatomy of an Epidemic. Other factor perhaps is that I went to the low quality public health care instead of health care of university or that paid by my employer. A lot of the health care in the public section seemed to be often focused on social and behaviour control. They had issues with getting psychiatrist work there, one psychiatrist handled a huge number of patients, a lot of the work was related to behaviour control with neuroleptic drugs, writing applications for disability and so on.

    I don’t know what that university health care looks like today. Probably they’re now more open to write prescriptions for SSRI, modern neuroleptic drugs. So, I think in part things have moved towards this direction in last decades because of the focus on this kind of treatment. It’s also probably true that even in a relatively egalitarian country such as Finland, people in different “classes” of people get different types of treatment. And so on.

  • Sa, you wrote:

    “One person told me that for these people, it is like their brain has `closed down’ temporarily into a a primal `freeze’ state (rather than flight or fight) -that when the person is extremely distressed, the emotional part of the brain is so over stressed that information can’t get up properly to the cortex. [please forgive my layman’s interpretation of the brain).”

    I personally had quite strong issues related to anxiety, panic attacks and this fight/flight/freeze thing you mention when I was a teenager and a young adult. For instance, sometimes when I was asked a question in a classroom I just couldn’t say a word – I very well understood I should say something but I simple couldn’t because of the anxiety. That seems pretty close to the “freeze” thing you mention. I also developed quite severe symptoms of depression, I now think a lot of it was related to things such as severe prolonged stress.

    I had already found different tools that worked for me in improving my condition, namely things such as meditation, hiking, exercise. I slowly but steadily improved over years. I was over 30 when I entered the public health care system and got prescribed with SSRI and neuroleptic drugs. As a result, I could not work, often slept 14-16 hours a day. When people, such as my family, would talk to me, I usually just listened to them and answered with single words such as “yes”, “no” and “ok”. I got anhedonia, for instance I no longer got those pleasant effects of exercise and meditation, so I stopped doing them. Then, after some months of this, I got diagnosis of schizophrenia, perhaps largely because my symptoms very closely mimicked those of negative and cognitive effects of schizophrenia! I most probably would be still an unemployed “schizophrenic” had I continued taking those drugs.

    In any case, the state I got in with neuroleptic drugs was qualitatively somewhat different from the experiences of depression, social phobia and fight/flight/freeze I had experienced. It’s possible that from an observer, they would have looked similar from outside. I was mute and I couldn’t function well socially, I was often mute. But in fight/flight/freeze, inside I still had intense experience. With neuroleptics, I became docile, lethargic and conforming. Inside in my mind, I was constantly tired and I had high constant anxiety in social settings. It wasn’t exactly like panic attacs.

    I don’t know of all the factors involved, but as an example human body secretes stress hormones, cortisol, norepinephrine, dopamine, etc, in stressful situations. This can help to give confidence in stressful or emergency situations, help in focus and so on. If this state is prolonged, it can lead to other health issues, such as hypertension, depression and so on. Perhaps in my case, the neuroleptic drugs in a way chronically prevented these natural bodily functions from taking place. I was highly stressed in social situations, and these dopamine, norepinephrine and stress hormones would no longer be there for aid. I was left silent, docile and highly anxious inside.

    I don’t see I could have in any way got out of that condition I was in with neuroleptic drugs. However, this is just another anecdote. It was essential for me to quit neuroleptic drugs and continue with the tools I’ve found to work for me: kind of a low carb paleo diet, hiking, exercise and meditation. I also understand that these tools I use probably won’t work for many other people in different situation, body and history, so I’m not promoting that to other people with same diagnoses. My technique was primarily to test and research many different things and keep those that eventually benefited me.

  • Also, I guess it’s this kind of knowledge of receptor affinities, etc, that is supposed to be the exact speciality of “biological psychiatrists”. What I noticed is that the psychiatrists I met had no clue about these issues, how their drugs work in brain and body to begin with. It’s supposed to be their speciality.

  • If you want the sedation of antihistamine H1 action, why not prescribe the OTC drug Benadryl. If you want muscarine effect, why not prescribe a drug that targets those receptors. Same with other receptors. All of these complex drugs play with the same receptors, having differences primarily in what receptors they affect on with different dosages or schedule.

  • When you increase the dosage of these drugs, the relative effect on different receptors varies widely. I mean, for instance with Zyprexa and Seroquel you get lots of antihistamine action on H1 receptor even with very low doses, which means you get lots sedation and other beneficial or adverse related to that action. If you increase the dosage, the antihistamine action reaches a plateau and effects on other receptors become more apparent.

    Likewise with with acetylcholine blocking, these drugs block muscarine receptors more or less, depending on dose. Some drug may cause lots of this effect on a relatively low dose, or may not. In the case of Seroquel (quetiapine) apparently it’s actually the active metabolite norquetiapine which has stronger affinity on muscarinic receptor M1. If instead of taking a single dose of, say, 600 mg Seroquel each day, you take that some amount in smaller doses during the day, you end up with more of the metabolite norquetiapine. This is similar to how Seroquel XR works. It also means more acetylcholine antagonism.

    I guess my point is that figuring out how much, for instance, acetylcholine antagonism you get from a drug is quite more complex than simply looking at the dosage of one a drug.

  • travailler-vous, thanks for your words and reading tip! I don’t need a Finnish translation, I prefer to read books in English if that was the original language they were written in. I’m also interested in genetics, but I don’t understand a lot of it. I think I need to read some good biology book about the cellular level mechanisms to understand it better. I also have one book from Jay Joseph in my book shelf that I haven’t read yet, it’s been sitting there for a long time, but not because I’m not interested in this topic, but because I have many different topics I’m interested as well.

    I think some people try to promote the idea that some other group of people are somehow “inferior by birth”, hence the huge interest in genetics of mental disease. It’s similar to the IQ and race issue. Ideas like this can be used for social or behaviour control.

  • Sleves, you’ve told a couple of “ax-murder” stories to scare people.

    “More often than not, our patients get the benefit of the doubt and aren’t “forced” to be treated… they end up off meds, and back in our hospital, sometimes dozens of times, after doing things like “shooting the cartel members” who are walking sown the sidewalk in their home towns. These are people who have never tested positive for substances of abuse or been on psych meds. In their paranoid psychosis, they know to ask for a jury trial (which our hospital cannot afford), so they go on their paranoid, hallucinatory way.”

    Also, shizophrenia is supposed to be this worst psychiatric disease world has known. It’s also supposed to be the crown of psychiatry, since psychiatrists have found a cure to it. Namely they found neuroleptics which sedate any human or mammal. Do you not understand that your “ax-murder” warnings may be highly “triggering” to many people who write around here, who have got the same diagnoses you accuse “ax-murderers” of?

    Also, as they are so crazy and hallucinating… how come they because of that craziness just know to ask for a jury trial? I’d imagine a truly crazy and hallucinating person wouldn’t know to ask for such a trial.

  • I also know that epileptic fits, for instance, can cause brain damage and “kindling”. It may be that some people with diagnoses of “schizophrenia” and “bipolar” also have brains or bodies that function unoptimally. However, I don’t think there’s any real proof that for instance “psychosis” itself or maybe taking LSD very directly causes any brain damage, I mean in the direct way that it is shown in the case of epilepsy.

  • sleves,

    You say “Please see my post below. Schizophrenia, bipolar disorder and depression also cause brain damage. Circuits are rewired making diseased states more likely after one recovers, and there is evidence that there is atrophy of brain areas in the untreated patients of these disorders. ”

    I’m not sure it makes sense to say that, for instance, “schizophrenia causes brain damage”. As if “schizophrenia” is one “entity”, or cellular disease, such as as some genetic problem in producing too much dopamine. It is not a single genetic disease with one cause. There are many different reasons why a person may get labeled schizophrenic. Same with bipolar and depression.

    If there are good studies that show that people labeled with schizophrenia have different brain areas compared to an average person, it doesn’t mean that one disease called “schizophrenia” caused that brain shrinkage. Poor nutrition, isolation from community, chronic stress, lack of play, teasing, spending all days indoors, lack of exercise, lack of sleep and so on probably affect all kinds of brain areas, functioning of body and so on. Do you see a difference between this point of view, versus the view that for instance schizophrenia is one cellular level brain disease that causes people to act like, um, lunatics?

  • Further on, you say that “ALL doctors understand the limitations of drugs, diet, exercise, talk therapy, ..”

    Then: “We have never seen a schizophrenic return to premorbid functioning”

    Let’s uppercase that never too, as is your style: “We have NEVER seen a schizophrenic return to premorbid functioning”

    I had a diagnosis of schizophrenia, and I’ve gone to a lot better functioning since that diagnosis. It’s simple logic that if you talk with absolute terms such as ALL and NEVER, it’s very easy to dismiss it. “ALL do this”, you can give one example to dismiss it. “We have NEVER”, again the same thing. Just one example and the argument is out.

  • “With all these people, as best I could tell, the only right new diagnosis was (and most likely always is and just will be) a worse one.”

    And I reached the bottom of the worst diagnoses in less than a year. According to their diagnoses and descriptions, I guess I’m basically so bad a case that I can’t possibly go worse. Hah, they no longer have any ammo against me.

  • travailler-vous, as you say:

    “Absolutely unexceptionably, I met no one who validated re-thinking a diagnosis or re-structuring it to include actual effects on the personality of trauma and abuse, in and of themselves, except that that also served to justify the existing treatment plan and make compliance even more important. With all these people, as best I could tell, the only right new diagnosis was (and most likely always is and just will be) a worse one.”

    Yes, I managed to collect all the hardest diagnoses they have on offer in the span of 2-3 years. It started with bipolar, then psychosis schizophrenia, then in when I left this public health care unit, the diagnosis said I had major depression with psychotic symptoms. I had paranoid thinking, my thinking was illogical, inconsistent and strange, based on what they wrote in their papers. They wrote all the worst diagnosis and observations about me in their papers one could imagine. Yet, during that time I actually quit all my psychiatric drugs and returned to a full time job, etc. If I had eaten their drugs and accepted their diagnosis, I would be an unemployed “schizophrenic”.

    I met two other psychiatrists after the first diagnosis of schizophrenia. It’s very hard to formulate an argument against the first diagnosis, if that diagnosis is “schizophrenia” with “paranoid thinking”. Anyway, concerning diagnosis, I got the worst of them in a short period, and now I don’t eat any drugs, I’m in a demanding full-time job, and I’m doing relatively fine. If any of those diagnosis is actually “true” in my case, I can go around telling people these diagnoses not that bad actually.

    Or whatever. When I see the next doctor or psychiatrist who has read these papers and diagnoses about me, the show will start again. Maybe I need to formulate some arguments to shut them down, or get some doctor to insert more favourable comments about me in their databases.

  • I guess all kinds of chronic stress, bad diet or even malnutrition, bad habits, lack of social contacts or other “play”, abuse of drugs, etc, can cause brain changes too. People who subsequently get diagnosed with schizophrenia often fall to this group of people. I don’t think there’s any one single (genetic, etc) disease “schizophrenia” which then “causes” these brain differences.

  • To give an example of “neural reasoning” done on this subject, I’ll give as an example a review done by our friend, Torrey.

    Studies of individuals with schizophrenia never treated with antipsychotic medications: a review.

    “A review of 65 studies of individuals with schizophrenia who had never been treated with antipsychotic medications indicates significant abnormalities in brain structure and function. Neurological and neuropsychological measures show the most consistent and largest group differences between those affected and normal controls. Measures of structural differences and cerebral metabolic function are significant but less impressive. Electrophysiological differences also are found, but most such studies are older and have methodological problems. The brain abnormalities implicate a variety of interrelated brain regions, primarily the medial temporal, prefrontal, thalamic, and basal ganglia areas. It is concluded that schizophrenia is a brain disease in the same sense that Parkinson’s disease and multiple sclerosis are, and that the brain abnormalities in schizophrenia are inherent in the disease process and not medication-related. The challenge for the future is to use the new molecular techniques to study these brain areas and elevate our understanding of schizophrenia’s etiology to the next level.”

    “It is concluded that schizophrenia is a brain disease in the same sense that Parkinson’s disease and multiple sclerosis are, and that the brain abnormalities in schizophrenia are inherent in the disease process and not medication-related. “

  • Here another new study. “Brain Structure and Function in First-Episode Schizophrenia”

    “Significant cortical thinning was identified in the medicated patient group relative to the control group in prefrontal (mean reduction [MR], 0.27 mm; P < .001), temporal (MR, 0.34 mm; P = .02), parietal (MR, 0.21 mm; P = .001), and occipital (MR, 0.24 mm; P = .001) cortices. The unmedicated patient group showed no significant cortical thickness differences from the control group after clusterwise correction."

    "Conclusions and Relevance These findings highlight the complex relationship between antipsychotic treatment and the structural, functional, and behavioral deficits repeatedly identified in schizophrenia. Although short-term treatment with antipsychotics was associated with prefrontal cortical thinning, treatment was also associated with better cognitive control and increased prefrontal functional activity. This study adds important context to the growing literature on the effects of antipsychotics on the brain and suggests caution in interpreting neuroanatomical changes as being related to a potentially adverse effect on brain function."

    Earlier they were using the brain shrinkage argument as a tool to use drugs. Now some try to say, with these short term brain studies and reasoning, that maybe the brain shrinkage is actually a good thing to happen in a schizophrenia patient.

  • Bah. This study sounds like promotion for “second generation antipsychotics” more than anything else. There are lots of differences in receptor affinities between among “first” and “second” generation neuroleptics. This is what they actually did:

    “The final sample used in this study comprised 25 FGA-treated subject .. who were admitted between 1994 and 1996 (except five who were admitted between 1997 and 1998( and 27 SGA-treated subjects … who were admitted between 1997 and 1999. Importantly, patients were all treated within the same first-episode service and hence the time difference reflected anti-psychotic prescription guidelines at the time the date were collected. This reduced the possibility of drug prescription on the basis of demographic (e.g. age, gender or intelligence) or symptom (e.g. diagnosis and specific symptoms) that may have biased the results.”

    Earlier psychiatrists were telling patients and other psychiatrists that they’ve seen brain shrinkage in schizophrenia, and then add that it’s seen even before patients have been given neuroleptic drugs. Some often added that the “second generation” neuroleptic have been shown to reverse this process in some studies. Now, after those long term studies from Andreasen and so on, they are trying to publish studies which admit that those crappy “first generation” neuroleptics apparently have these crappy effects, but our new, on patent (at least in depot version) actually improve the brain.

    Also, for instance, Andreasen studies have been over a decade, these talk about “differences seen in months”, and so on.

  • Julie, yes, for this winter I bought an alarm clock which gradually increases the level of light over 30 minutes before the alarm. Also also have a designed “bright light” on after that for breakfast. It seems to help me keep my sleep rhythm during this darkest time and also keep me more active during the day. On the other hand, I’ve heard some people in even more northern parts, such as in Lapland, tend to live more slowly, “hibernating” during the winter months.

    During the summer it’s the reverse, in the middle of summer it doesn’t really get dark at all. When I was eating Ability, my sleep quality became quite bad and I was awakened several times in night. At those times, I had to use a blindfold the type you can find for airplanes during summer. I tried curtains that block light, but it wasn’t enough since some light always got in through some opening. These days I no longer need to do that at home, but they still really help when I’m sleeping in a tent during summer here.

    Diet can also make difference. I personally don’t eat much carbohydrates and try to avoid all sugar in morning and during the day, and get the energy from fat and protein. For me, this creates a more lucid, focused state of mind. The carbs I get from vegetables, etc. In the evening a may eat a bit more carbs. Carbs can have a somewhat sedating effect on me, especially since my body is used to much lower amount than average.

    In any case, currently my sleeping schedule is entirely different it was earlier. I had always been up very late and getting up in mornings was very hard. Now I go bed early and wake up early, after 7 hours of sleep. There are many other factors besides those mentioned in this shift, such as more exercise, less stress, etc, but in any case, I think it’s possible that sleeping habits and schedule can change a lot even without drugs.

  • Julie, there’s just this issue:

    “After sunset, no matter where you live, don’t use artificial lighting. This means any artificial light. Use candlelight.”

    You know, here in very north, say Helsinki, at this time of the year the sun sets very early, say 15:00 or a bit later. F.lux starts setting the blue light off, I need to press it a couple of times to keep it doing it. The people in these northern parts of the world are supposed to work with eight hour work schedules throughout the year, just like the rest of the world. In even more northern parts of Finland, there are periods during the winter where the sun never goes up.

    So… If you happen to live in these more northern parts of the world, you can you “awakening bright light alarm clock (often with annoying bird sounds)” in morning. It might change your body to work a bit like when a natural sunrise would occur. I personally use one of those devices, and I’m quite happy with the results. When I get up for breakfast, I turn on a bright light which is somewhat similar to the light from sun.

    In a sense, I’m trying to follow a somewhat “natural” cycle in use humans. Where I live in, I like to use these other devices too, if I’m supposed to work in a modern work life as well.

  • Julie, I like what you wrote, and agree with most of what you wrote. I also love the application f.lux. I think it’s awesome if you need to work late on. It changes the colours of your monitor so that the blue light is reduced when the sun goes down. The screen will look more like candle light.

    To test how well this idea works. Well, if you frequently use the computer late in evening, and you live in a part of world where it gets dark late enough. Install this program called f.lux to your computer. Notice how it changes the grades of the screen when the sun goes down. Use computer with those settings for an hour or more, browsing, writing, whatever. Then turn it off for a while in those settings. The computer screen is suddenly like sunlight to your eyes. I think this effect of blue light often affects the way the body words in different circadian rhythms, etc.

  • I’ve thought that things such as psychiatric diagnoses and different types of psychotherapies are also often used as forms of behaviour control. Sometimes it may be for good, sometimes for bad. (Depending on the point of view.) It’s not just pharma and drugs.

    By the way, I just saw Joanna Moncrieff’s blog review of a book called “The Therapy Industry” in my RSS feed which deals with some of these issues. I haven’t read this book, but here’s the blog writing:

  • Antero,

    I’m sincerely sorry about those posts I made above. I had some bad experiences in public Finnish psychiatric system, and sometimes – especially when I’ve had wine – I start to rant about these issues. I will try to behave better from now on.

    In any case, I think your posts about Open Dialogue were some of the more interesting ones I’ve seen on these forums in a long time. I’ve thought that Open Dialogue is perhaps even too much idealised internationally. It’s true that it is created for the needs of a certain local area and culture, and it probably can’t be very easily just transferred to other areas. The studies are maybe not very high quality. As you say, there are other systems out there which may perform as well or better for certain purposes. One of the big reasons for the international interest in OD is because it was featured in the last chapter of Robert Whitaker’s book.

    I’m still somewhat interested in the short term use of benzodiazepines instead of neuroleptics in acute crisis. Maybe I’ll comment about it later on.

  • Also, from what I’ve seen in and about the public mental health services in more Southern parts of Finland… It’s more coercion, injections, etc. Patients get a cup of coffee if they get an injection. Active promotion of injections from the top psychiatrists. Etc. I have no clue where in Finland things in public psychiatry are actually getting *better*… it was horrible in there.

  • “I do not think that they would have manipulated the data regarding medication. It is more a question of poor reporting and lack of critical analysis. As to the suicides, it is an intentional concealment. Why this has happened, I do not know. We will hear about this later this year from a leading Nordic researcher on mortality in psychoses in the Nordic countries.”

    Perhaps we’re seeing cohort studies from Jari Tiihonen on this topic. Previously, he has published cohort studies to support use of two concurrent neuroleptics (but not benzo), clozapine, injections, etc. Let’s see if I’m pre-cognitive.

  • Antero, your writing seems quite polished. Maybe it’s not just “you” who is writing out there. In any case, for instance you say:

    “Just a couple of words about the “Open dialogue” method. It was originally developed in Turku, Finland while I was a resident. Most of us were enthusiastic about the project. But later it became a lot of trouble. Most of the staff were relieved when the method was stopped.”

    “In the Open Dialogue method benzodiazepines are also used in high doses. The study they made of the project was of weak quality but most of all the researhers concealed cases of suicides during the study period. Currently, the Keroputaa hospital area in Finland where the method is used has the highest suicide rate among schizophrenia patients in Finland.”

    For instance, you don’t make sense if the “method” was stopped or not. First, you were relieved when the “method” was stopped. Then you tell that the area where the “method” is used “has the highest suicide rate among schizophrenia patients in Finland”.

  • Thanks for your comments with perhaps some new perspectives or data on this issue. Watching the international hype around Open Dialogue, I’ve thought it’s almost certainly oversold. I was “treated” in a Helsinki state hospital for “psychosis” and “schizophrenia” by another “ex-Open Dialogue psychiatrist in Oulu”, and I can tell that was also a most horrible experience which entirely destroyed my life. Well, to be honest, she didn’t start it, but neither was she very willing to fix the issues with false diagnoses, etc.

    I do not think that they would have manipulated the data regarding medication. It is more a question of poor reporting and lack of critical analysis. As to the suicides, it is an intentional concealment. Why this has happened, I do not know. We will hear about this later this year from a leading Nordic researcher on mortality in psychoses in the Nordic countries.

    OMG, more propaganda from Tiihonen, I presume?

  • That is, Torrey, DJ Jaffe, and perhaps also Allen Frances, are machinating towards more “freedoms” to forcefully drug people. The “argument” they try to use about prisons and them needing homes, it’s often just a thing to try to collect people to support their cause. Their cause is to support more liberal forced-drugging of people, and so on.

  • This nick FaceOfChange has read too much of people such as Torrey, DJ Jaffe, and perhaps also Allen Frances. They are a political force driving for more forced control of behaviour with neuroleptic injections, etc.

    “Backward beliefs keep the public ignorant and as long as there is ignorance, people will never see the need to make war on psychotic illness like they have made war on cancer, and diabetes, and heart disease. Only enlightenment will dispel stigma. When people are educated out of this morass of discredited theories, they will see the need to provide supported housing and the complex – and expensive – infrastructure that will finally get the mentally ill out of prisons and off death row. This is serious!”

    In this piece, the “complex – and expensive – infrastructure” means legislations to force-inject neuroleptics to “suspect” people.

  • Johanna, you’re spot on with this ketamine issue. What you wrote in this first chapter is pretty much what I also think:

    “For what it’s worth, a single “trip” on this drug (well known both as a psychedelic plaything and a “twilight anesthetic” for minor medical procedures) strikes me as a safe bet. If someone gets temporary relief from this experience — and can use the experience to interrupt a crisis and start climbing off the floor — more power to them. That’s how ketamine was being used in the initial reports that sparked all this “possible breakthrough” chatter.”

    Thanks for it!

  • I had severe panic attacks when I was young, etc. I got diagnosed with schizophrenia, bipolar, etc, in my thirties. I had been on SSRI on and off for a long time. Actually, what I really feel bad about is the use of neuroleptic drugs. The prescription that you mention was actually almost exactly what worked for me. Hiking, exercise, diet, meditation. The really worked for me, in combination, but it may not work for everyone. SSRI may work for some people, for some time, who denies that?

  • I actually have the diagnosis of schizophrenia, bipolar and severe depression. I don’t really agree with prognosis and whatever you have. I’m not using any drugs, such as neuroleptics, etc. It’s possible for some people to live without the drugs… for some the drugs help. It’s OK if some people like to take the drugs. I just take the issue when some idiots or assholes come and try to force the drug to me.

  • An interesting article from Mental Elf:

    I think that drugs such as “first generation” haloperidol, which have much affinity on dopamine receptors, easily have many adverse effects related to them antagonising dopamine receptors very effectively. Haloperidol and some other older generation drugs block dopamine very effectively. Using smaller doses of haloperidol will cause smaller amounts of dopamine blocked, measured by receptor occupancy, etc. However, there are many other “first generation” drugs that don’t have so great affinity for dopamine receptors.

  • Are the second generation neuroleptics “better” than the first generation drugs? I think it would be best to forget the distinction about first and second generation drugs. The idea that the second generation drugs are much more effective, and have less side effects, has lead to doctors prescribing them for even more variety of patients. They’re now prescribed as a first-line treatment for insomnia, for instance. Sure, Seroquel is very sedating at 25-100 mg, because of the histamine effect, maybe some effect on other receptors as well. Doctor thinks, hmm, Seroquel was useful for this patient. When the same patient comes to doctor and complains she can no longer sleep, the doctor ups the dose of Seroquel, hoping it will give the same sedating effect. But it will not, that original sedating effect will not increase from that point on, and we end up with people asking help for sleep eating Seroquel in “dopamine blocking antipsychotic doses”.

  • Jonathan,

    “I have always wondered how doctors simply pick and choose meds- subjective preference, research, etc?…and what leads them to high dose polypharmacy. Is there literature that supports it?”

    I don’t think doctors or psychiatrists generally think much about such issues as how different drugs they prescribe function pharmacologically. Some may be interested in psycho-pharmacology, and know more about it, but that certainly is not the rule. In your example, the patient was given 800 Seroquel, among other drugs, for sleep, or so she said. A very small dose of Seroquel, such as 25-50 mg is very sedating and may help in sleep, because it’s a strong antihistamine at those doses. It works well at first, then after some time it no longer works. Doctor thinks, the patient responded well to a low dose of Seroquel, let’s increase it. They may in this process increase the dose of Seroquel up to 800 mg just for sleep, but the increases won’t work anymore for sleep in the same way it worked in 25-50 mg.

  • Haloperidol is a very potent drug on dopamine receptors and it’s easy to get lots of dopamine blocking with it, unless you stay in low doses. If you block dopamine receptors very effectively, you also get side effects. In comparison, for instance quetiapine binds much more weakly to dopamine, so that at 600-800 mg you get some dopamine antagonism that may be used in psychosis and you can’t really get to the max. dopamine antagonism that haloperidol can give. In that sense, it’s harder to give too much dopamine blocking with quetiapine than haloperidol. However, many other older neuroleptics are also weaker on dopamine receptor and stronger on other receptors compared to haloperidol, etc.

  • There are drugs and there are drugs. Some drugs calm the person down, some do not. Some drugs, such as NMDA antagonists and benzos, are usually pleasant and conforming to the person. He’ll like to take them. Other drugs, such as dopamine antagonists, often make the patient feel like shit. That’s one reason why psychiatrists have invented concepts such as “patient does not have adherence”, “he does not have insight”, etc. Neuroleptics make you feel like shit. That’s a major reason patients don’t like to eat them. I think there’s some actual reason to look again into laughing gas and ketamine.

  • “Again, I am not sure anyone has studied the effects of prolonged and repeated use of ketamine.”

    Well, there was at least John Lilly, who extensively studied effects of increasing uses of ketamine on himself. His results were.. different. In any case, he was shooting for some spiritual or extra-terrestrial stuff, he was not on a maintenance dose. I’m also interested in how one larger dose of ketamine (or similar drug) can produce a longer lasting ease from depression.

  • I found a short English description of this book I referred to: Mikko Ylikangas: Unileipää, kuolonvettä, spiidiä. Huumeet Suomessa 1800–1950 [Opium, death’s tincture, speed. Drugs in Finland 1800–1950]

    “This book presents an account of the history of drugs in Finland, as well as changes in legal and illegal drug use. Even in the early 19th century, the authorities were concerned about opium abuse. Medical doctor Elias Lönnrot – best known for collecting the folk poems that make up the Kalevala, the Finnish national epic – coined the name ‘unileipä’, ‘the staff of dreams’, for opium. A period of prohibition of alcohol in the 1920s spurred a huge increase in the sale of cocaine; in the 1930s Finland led the Western world in consumption of heroin as a cough suppressant. In the late 1940s, the United Nations investigated why Finland, with a population of four million, consumed as much heroin in a year as other countries did over an average of 25 years. This was explained by the severity of wartime conditions: drugs were used to maintain battle readiness and to combat anxiety, sleeplessness and tuberculosis. Social problems caused by misuse did not, however, get out of control. This book was awarded a prize for the best science book of the year in Finland in 2009.”

    There were issues with addiction and so on, but perhaps even the use of heroin was not entirely bad, at least in those conditions. There were people getting addicted, but there are perhaps many untold stories of people who got through from day to day life with drugs such as heroin, went to work and otherwise led a relatively normal life. The society did not get out of control, even in those severe conditions after the war, even though legal heroin was widely available.

  • The concept of original sin as such was formulated and developed by people such as Augustine, Luther and so on. It’s not in Bible as such. The concept of original sin can be used as a tool of behaviour control, by telling people they have this deficiency by birth. They are “broken”, therefore they need to act certain way, be controlled by others, etc. Some people are very interested in proving that things such as “shizophrenia” or “bipolar” are single genetic diseases that are inherited from birth, and then telling other people about it. Likewise with all this IQ and race reasoning.

  • Concerning use of drugs as medicine, I read an interesting book by Ylikangas about the history of drug use in Finland (the book is only available in Finnish). As many know, drugs such as opium, heroin and cocaine were commonly prescribed by doctors and quacks in 19th century and early 20th century in many parts of world. Ylikangas points out that a recurring theme with each new drug was that at first it was promoted as having no side effects or issues at all. It would take longer time to see the actual issues. For instance, heroin was first promoted as similar to opium but without addiction potential.

    Heroin, cocaine and opium were widely available. Heroin was used in cough medicine. Finland was actually the biggest consumer of legal heroin during 1930s. After the Second World War, Finland was dealing with poverty and other issues. UN or other such international body demanded an explanation from Finland for the huge use or import of legal heroin. The Finnish president at the time answered that we need lots of heroin because of our climate. It was not commonly said that there’s any problem in public talk. However, restrictions of heroin and other drugs were quite rapidly mandated after some international orders, and the public image of these drugs likewise changed quickly among doctors and general public.

  • Some people of every generation will use diagnoses, genealogical reasoning, biological reasoning, to tell that there’s this lower class of people. There’s one brilliant and little known book called From Genesis to Genocide (Chrorover), published in 1979, that deals with this issue. Some people are “inferior”, they have this “original sin”. It’s a recurring theme that will happen to the end of humanity. I don’t know if that a depressing idea to many of you.

  • James, I’m ashamed to admit I haven’t read your other articles. I didn’t know you’re a trail runner or marathoner. I came in this thread only to talk about the light issue. In any case, I’ll check your other threads! I’m really just getting in these new worlds of train running, and also ultra-light trekking. I’m a life-long nerd that’ll be 40 soon. I know I can conquer the nature as well, or maybe the nature will conquer me, but I hope I’ll enjoy the experience!

  • B, and James, I think that in general for my strength regular exercise has been even more useful than those tools that have to do with light. I live in a place where I’m close to the Helsinki centre, but there’s woods right next to where I live, and I’ve taken it as a habit to go out there in woods after work for an hour, whenever I can. It took some time of habit forming, study on habit forming and so on, but now I love it. It’s amazing how much you actually can change, train your body and so on. I was the biggest nerd who hated anything to do with exercise when I was a kid. 🙂

    I’m actually now interested in hiking quite light-weight in different kinds of areas. I’ve decided I’ll go out to test my clothes in any kind of weather, I’ve been practicing trail running for some time, and now I bought trail running shoes with spikes in them for winter running. 🙂

  • Also, I live so north, in Finland, that I can’t just stay in bed most of the day, at least if I work at the same time, in order to “synchronize my sleeping schedule with natural cycles”. I have at least these three tools that I think help be during these long and dark winter months:

    1. A “wake up alarm-clock light” that gradually increases the level of light for 30 minutes before the alarm. Then at full light, it outputs sounds of birds chirping, some slightly new ageys tunes, or plain old radio.

    2. At table, when having breakfast, I have a designed “bright light” on.
    3. I think at evenings, this f.lux appilication and other similar techniques are useful.

  • By the way, there’s a free program called f.lux which automatically tunes colors of your computers screen when the sun sets and rises, based on where your location is. I reduces blue light of the screen when the sun goes down, etc. It available for free for many different operating systems, such as Windows, OS X and Linux and also some mobile devices. Here:

    Currently here in Helsinki, when I’m at work, it goes yellow already soon after 15:00 or so already, but it has a button “disable for an hour”. I may need to press it a couple of times again, but it’ll get better from now on. 😉

    Some ebook readers also these days have options to invert colors to white on black. For instance, the new iOS for iPad and iPhone has iBooks that can switch those colors automatically when you’re in dark, so that in a dark room the background is black and text white.

  • This article talks about coercion in psychiatry, then compares it to other medicine. The coercion Datta refers to is forced restraint, forced medication and so on. But in reality, in psychiatry, people are using somewhat more subtle devices such as diagnoses, “he has a lack of insight”, “he has paranoid thinking”, “he is psychotic”, “he has anosognosia”, etc, etc, as a form of restraint or coercion. In the current world, this kind of coercion is quite common in psychiatry. I know it, I’ve seen it, I have a proof of it in my psychiatric papers. I think that generally, there is a lot more of this kind of thing happening inside psychiatry than in general medicine, if only because psychiatry is maybe.. more vague or whatever.

  • When I was a young and probably quite crazy teenager, I spent time in this psychedelic subculture too. There were people using, or more often perhaps abusing some other substances that block NMDA receptors like ketamine does. This subculture had a term “afterglow” for that great feeling you sometimes have after a good trip. I experienced something like this when I experimented with these drugs. When I tried LSD or mushrooms, they were similar in intensity of experience compared to ketamine like drugs, though of course different. However, they kind of left me “drowned out” for the next day or two, maybe because all the stress, etc, that I went through in that experience. At that time I was quite depressed and anxious anyway.

    Those NMDA blocking drugs, however, often resulted in some sort of rebirth effect the following days, when the chemical itself had supposedly already disappeared. I don’t think it was at least entirely something more psychological that I had resolved during my trip. I think there’s some biological explanation to that rebirth or afterglow experience I got, though I don’t know what it was. It may have something to do with NMDA receptors, glutamate, inflammation, whatever. Because of this experience I had when I was young and too reckless, I think ketamine may ease depression through some mechanism we don’t yet understand. That is, I’m interested in what new studies say about ketamine relating to mental health treatment, and I acknowledge much of the stuff out there is financed and motivated by pharma.

  • When I was younger, I was quite interested in “psychedelic sub-cultures”. Many of those people in MAPS, Shulgin, etc, were mostly very interested in the altered states of mind these chemicals bring on and so on. Much of the stuff those people talk about is not so directly related to modern psychiatry and pharmaceutical industry. Rather those people are actually very interested in effects of LSD, MDMA and so on, often through experiences. Pharma can’t even use chemicals such as LSD, ketamine or MDMA as a profit making chemical unless they invent some other chemical or other for they can patent, that’s probably what they’re trying to do with ketamine.

    I think the research of use of drugs such as LSD and MDMA for therapeutic purpose is quite hazy. There are not many good quality studies and many anecdotes. In any case, I perhaps kind of think that often there are adverse effects from psychiatric drugs because people use them each day, hour and year of their life. Body gets used to their effects, issues develop and so on. At least some types of psychedelic therapy ideas have the patient take one larger dose for one time, which creates an alternate mental state, which is perhaps supposed to create some transformation. I don’t know if it works well often, but it seems a different concept from taking SSRI or neuroleptic each morning.

  • Also, if it the case that some things such as the function of endocrines, immune system, metabolism and so on is inherited in some epigenetic manner, and it affects health of offspring, to me it sounds like maybe it’s also possible to try to change these things with things such as proper diet, exercise, meditation, better environment, etc. It doesn’t sound like the strict “original sin” concept; “you are inferior by birth”.

  • Ann, biology as a concept is neutral, like mathematics, cosmology and physics. It’s a natural science that studies living organisms. Of course, in practice scientists study and promote other things more than others, sometimes based on their own interests, sometimes based on funds, etc. For instance, in pharmacology what gets studied is often related to funds from pharma. Some people also use biological concepts, such as genetics or neuroscience, to reason that some groups of people are somehow inferior by birth. And so on.

  • If mental illnesses are propagated from mother to offspring through non-genetic ways, it doesn’t have to mean that, for instance, “schizophrenia” is any single issue in nervous system, such are broken dopamine receptors or malformed brain. What I’m thinking is maybe more that maybe if mother is constantly very stressed up, has starvation, uses drugs, etc, while pregnant, maybe these things can affect things such as how baby’s immune system functions, etc. I don’t think “schizophrenia” is any single neurological disease, but I guess things such as function of immune system, metabolism, stress hormones and so on can contribute to some cases. Same things with bipolar, depression, etc.

  • I actually think this “movement of survivors” would benefit if there were more people who actually know about biology and neuroscience. Biology and neuroscience as such is not bad or good, it’s at best just neutral information about what goes on in our bodies. Psychiatrists and other people often use some silly biological reasoning to promote their cause. It’s possible that some people in our “movement” who know more about biology will reason against those claims on more biological level as well. For instance, I guess the “movement” has also largely used those Andreasen claims about brain shrinkage from neuroleptics to promote their case. It’s biology too,

  • I also think that it will not work to say that all things related to biology has nothing to do with real issues. Psychological stress may cause elevated stress hormones, lack of sleep and so on, which may cause other issues in body, such as increase in inflammation related cytokines, “dysfunctional” HPA axis and so on. These things can often be mapped to what goes on in your mind and daily life as well. Each thought we have in our mind is also somehow directly related to changes in our body, including our brain.

  • Sorry that I have the opinion that things such as prolonged exposure to stress may cause elevated stress hormones and inflammation related cytokines, etc, and that kind of action can also cause several types of issues in body, including brain. I don’t think the wrong thing is in trying to explain all that goes on in body through biology. The wrong thing is when some people try to explain other people’s behaviour using bad biological reasoning, such as “some people are born biologically bad, because of this gene”, etc. Some people often use some concepts of biology to promote their agenda that some people are inferior to other, and so sone. It’s the “original sin” concept in a new dress.

    I do still think that for instance, the function of immune system and so on affects our mental state. For instance, when you have a flu, you don’t feel like moving around a lot. You may feel like you want to stay in bed a lot instead. Why do you feel like this when you have flu? Maybe it has to do with cytokines, hormones, etc, running around in your body?

  • Upbringing has a huge influence. But I think there are most probably many ways to propagate mental issues to offspring. And example: Inside a woman’s womb there is an embryo about to develop. At first it’s just a combination of molecules, or whatever. After that point, all of developments that go on in building that human baby inside the mother are affected by the hormonal, etc, chemical issues that go inside mother’s body. Hormones, cytokines, etc, of mother shape up how the cells will unfold to a real human being, before the human baby is even “out”.

  • Thanks for posting a link to this article, though unfortunately the whole article is not available, only the abstract which doesn’t talk about any actual mechanisms. In any case, I think this is an interesting issue. Things such as the environment (hormones, cytokines, etc) inside mother’s body and then later on upbringing, environment and so on all combined perhaps explains a chunk of why psychiatric problems often run in families.

  • New age bullshit generator here gives answers that are quite as good:

    “We exist as chaos-driven reactions.

    Nothing is impossible. Sharing is a constant.

    If you have never experienced this harmonizing on a cosmic scale, it can be difficult to self-actualize.

    Although you may not realize it, you are transformative. Have you found your mission? It can be difficult to know where to begin.

    You will soon be recreated by a power deep within yourself — a power that is high-frequency, magical. Through affirmations, our essences are transformed into faith. Naturopathy may be the solution to what’s holding you back from an unfathomable vector of synchronicity.”


    “There is a related metaphor in Western science. A molecule is not so much an object but a dynamical pattern. At the quantum level it is a pattern of energies which extend into the ground state of the entire cosmos. Absorbed into the body this dynamic energy pattern provokes a range of transformations of the body’s biochemical activities. Of course, the analogy can only go so long as Western science continues to fragment matter from ethical values, consciousness and spirit. …””

  • Hi David, I don’t have a reply button either. When the depth of replies goes too far on this board, there won’t be a reply button anymore. In any case, I think I’m relatively open minded to new ideas and so on. I read through that link you gave, and it was not very convincing.

    Saplosky’s Zebra book was a great listen, thought there are probably many new better theories and findings made since. It’s just one “level” of seeing things. People get elevated stress hormones during stress, long term stress may affect immunological issues in body and so on. That’s one level of seeing what goes on. There are other levels of seeing things, such as spiritual, social and psychological, and these levels are often related to each other in various kinds of ways. So, in short, though I evidently don’t like the effects neuroleptic drugs have on my body, I think it’s often quite useful to think about what goes on in body in this “neuroendocrinology” level. It’s one level to consider, there are many other levels as well.

    As for that link you gave, it seemed a bit like yet more of that new age stuff.

    “There is a related metaphor in Western science. A molecule is not so much an object but a dynamical pattern. At the quantum level it is a pattern of energies which extend into the ground state of the entire cosmos. Absorbed into the body this dynamic energy pattern provokes a range of transformations of the body’s biochemical activities. Of course, the analogy can only go so long as Western science continues to fragment matter from ethical values, consciousness and spirit. …”

  • There is nothing wrong in looking at human behaviour in a biological level, though there are psychological levels, and other levels as well, which levels are often quite related to each other. The trouble is not in looking at what goes on in biological level, the trouble is when some people start to use some of those findings to support their conquest of behaviour control and treating of mad. Even diagnosis can be often seen as tools of behaviour control.

  • During the last autumn, I listened to Sapolsky’s “Why Zebras Don’t Get Ulcers” when I was walking or running through the woods in my evenings. I remember listening to that audio book while I was running through the woods. It was a very interesting listen. I think Sapolsky’s level of reasoning is entirely valid and interesting, at least to me.

  • Here’s another new article: “Decarceration of u.s. Jails and prisons: where will persons with serious mental illness go?”

    “Decarceration (decreasing the number of persons incarcerated in U.S. jails and prisons) has begun. It is estimated that more than 350,000 persons with serious mental illness (SMI) are among those incarcerated in the United States and that many thousands of them will probably be among those released. Currently, the prison population in general is being reduced as a consequence of concerns about overcrowding and of policies and programs such as reclassification of drug possession, which would affect many persons with mental illness. Court-ordered diversion and changes in sentencing guidelines are also serving to reduce prison populations. In recent years, the mental health system did not have to manage as large a number of persons with SMI, especially those who were among the most difficult and expensive to treat, because many of them were incarcerated in jails and prisons. Now, with decarceration and the release of many such persons, the mental health system may be expected to assume more responsibility for them and should be prepared and funded to meet their needs. This population of persons with SMI needs structure and treatment that, depending upon their individual needs, may include 24-hour supportive housing, ACT and FACT teams, assisted outpatient treatment, psychiatric medication, and psychiatric hospitalization.”

    Perhaps at least part of this story from Allen and Torrey can be seen as a tactic to get more power to psychiatry by telling people these stories of all those mental ill people in prison (in USA). “Let’s start about housing, they don’t even have houses to live in.” The power they want is more ACT, more forced medication, more funds, etc.

  • Fianchra, I don’t know so much about how these drugs affect different receptors in body, but I’ve noticed that in practice, neither do the psychiatrists or other doctors who practice these drugs. You generally don’t get much interesting information about pharmacology, etc, of these drugs from psychiatrists, though it’s supposed to be their speciality.

  • I think it may be that many different factors may affect in things such as pro- and anti-inflammatory cytokines, stress hormones and so on. Psychological stress, lack of sleep and so on also affect the the body, or perhaps “enable” the body to get inflammatory and other responses. Infections from bacteria or viruses may very well be one factor in some cases of diagnosed mental illnesses.

  • Some thoughts on obesity effects of Zyprexa and other atypical neuroleptics. I don’t think there’s any kind of consensus on through what exact mechanisms these drugs cause weight gain. One thing is that they may cause binge-eating, or eating too much, or eating of trash food through some mechanism (maybe partly through histamine H1 receptor?). They don’t actually help in practicing exercise, I quit practicing kungfu and reduced other time spent walking or cycling in part because of the “anhedonia” kind, tiring and sedating effects these drugs had on me.

    I think that there’s perhaps also some more direct ways these drugs affect our bodies that cause weight gain. It’s perhaps not only that they cause you to eat more and be more sedentary. There are articles out there which suggest that drugs such as Zyprexa may cause more direct changes in stuff such as in fat/glucose metabolism. See for instance this arcticle from the blogger Last Psychiatrist and the study it references:

    Zyprexa caused the body of mice to utilise fat preferentially, which resulted in elevated glucose and insulin levels. Elevated glucose and insulin levels may lead to insulin resistance and metabolic syndrom.

    Other article:

    “Atypical antipsychotics may “directly” influence glucose homeostasis, increasing risk of type 2 diabetes independently of changes in adiposity. “

    I personally don’t think weight gain and loss is only just a “calories in, calories out” issue. The quality of food can have great effect. Perhaps with drugs such as Zyprexa, it’s especially important to be careful of the sugar and carb intake? Many people in modern world get huge amounts of carbs and sugar through bread, pasta, pizza, all kinds of food you find in supermarkets and so on. It’s perhaps not a very helpful combination with drugs such as Zyprexa which perhaps have quite severe effects on glucose and fat metabolism.

  • Fianchra, yes, I experienced that even very low doses of Seroquel are very sedating and even tiny doses such as 12.5 mg or even less can enable sleep. I also noticed a distinct difference in the sedation effect between 12.5 mg and 25 mg, 12.5 mg didn’t cause so much sedation but was enough to cause sleep.

    Both older and newer neuroleptics work in a similar manner on the same receptors in body. Each drug is made of molecules, and in body these molecules may affect different types of receptors. For instance, all neuroleptic drugs block dopamine D2 receptors in large doses where they are used for controlling psychosis. At doses of Seroquel 25 mg, the Seroquel molecules don’t go so much in dopamine receptors, but they go have a large effect in histamine H1 receptors, which causes much of the sedation in that dose. The Seroquel molecules also tick other receptors besides histamine H1 and dopamine, also based on dosage, which contribute to its effects.

    That drug Mellaril you mentioned affects on a similar set of receptors as Seroquel and other neuroleptics, but these drugs have differences in how much they act on different receptors and thus what effects they have. For instance, Seroquel is very strong in blocking histamine H1 receptors, so it’s very sedating in low doses. Other neuroleptics that are not so sedating usually have molecules that don’t go so likely to histamine receptors.

  • Sandra: “I think the sedating drugs may be harder because of the rebound insomnia but I have had people have trouble as well with the less sedating drugs.”

    Yes, in one discussion board I read about many people having issues with sleep when trying to quit a low dose of quetiapine, such as 25 mg – 100 mg. It’s already very sedating at 25 mg because of at least its actions on histamine H1 receptors, and their body was used to the sedating effect. I personally found that when tapering, 12.5 mg was enough to give me sleep when needed. After some time on 12.5 mg, I switched to melatonin. But yeah, different neuroleptics may have different issues when tapering because they affect different receptors or work in a bit different way. Abilify at full dose actually caused me to wake up several times at night and a low dose of quetiapine perhaps helped me sleep a bit better. I personally actually didn’t have much issues in stopping Abilify, though I don’t think I should have been eating it to begin with.

  • There’s a bit controversial book from Gary Taubes – “Good Calories, Bad Calories”. Or, an easier read, “Why We Get Fat”. They explain some basics of this “controversial” issue. In any case, I admit I’m kind of a fan and supporter. Zyprexa and other drugs may cause insulin resistance, the best bet is to restrict all carb and sugar intake, and eat fat instead.

  • As I said above, I’m totally biased about this issue, because of my own positive experiences. In any case, what worked for me was to throw away all sugar and carbohydrates that I can (there’s often sugar added in all kinds of food). It’s actually often good to take fats, such as the fats from olive oil, etc. I personally vote for getting energy from fat, and avoiding sugar and carbs as much as possible.

  • By the way, I personally started to gain weight rapidly after I was put on neuroleptics. I was perhaps on way to diabetes, there was something wrong with blood glucose levels at the time. However, I also kept gaining weight or at least not losing it while I was tapering or after I had had quit the drugs. I was after changes in diet and exercise that I started to steadily lose that weight. Of course it helped that I was no longer on drugs, but losing that weight didn’t come automatically for me after I quit the drugs.

  • I mean, I lost that 25 kg in a short time (a year) after going to a low carb diet. I admit that I also also tapered down or reduced the drugs during that time, the drugs that caused the weight gain in the fist place. At least in my case, the best solution was to go in a low carb high fat diet. I also started to exercise, etc. Also meditation, etc. Many factors, but I think that in reducing weight, reducing carbs/sugar was essential. I think that maybe drugs such as Zyprexa fuck up the sugar/fat metabolism so that one should avoid carbs even more that usual. ?

  • Doctors are supposed to know about metabolism that happens in body, how their drugs affect their patients, and other issues.

    Peter Attia’s “low carb” blog may not be directly related to the side effects of “atypical neuroleptics” .. He knows a lot more about biology than I do.

    Now I may be personally biased, but I gained 25 kg in a short time after taking the drugs .. and lost that 25 kg in a relatively short time too. I know I’m biased because of my personal experience, but still..

  • I actually think doctors who talk to overweight people who take these weight-creating and diabetes-creating drugs such as Zyprexa, would do great if they told their patients to eat a diet which restricts carbs and sugars severely, promotes fat, etc. It may sound crazy, but yes, what worked for me was to eat lots of fat and to avoid all sugar.

  • Yes, I have nothing against the idea that you can actually lose weight by quitting neuroleptics – I did so and lost those 25 kg I gained in the “process”. I lost that weight, and actually got interested in nutrition, in severely restricting my sugar intake. After all of that crap I experienced, I think that at least for me, it’s best to restrict my carb/sugar intake. I also think that the basic reason drugs such as Zyprexa and Seroquel cause weight gain is somehow related to sugar/carb metabolism. and stuff. Maybe.

  • To elaborate further, if there’s an issue in stopping drugs such as Zyprexa or Seroquel, maybe it’s because they’re very sedating already in low doses? This sedation also gives good sleep and so on, which tends to improve well being in longer term if that has been an issue. On lower doses, these drugs are not operating so much on “neuroleptic” dopamine receptors, and should perhaps be compared to other drugs, based on receptors they affect on those low doses.

  • I think that maybe when going down or up with low doses of Zyprexa, you largely change its effects on receptors such as histamine H1 and serotonin 5-HT2A, based on affinity data I just looked on. That is, maybe the effects of Zyprexa on these receptors reach a maximal potency, or “saturate”, on a relatively low dose. That is, when you increase the dose further, this effect won’t increase much anymore. For instance, you could get a similar sedating antihistamine effect from some older OTC (in USA) antihistamines such as diphenhydramine, then again they would perhaps have similar adverse effects!

    In any case, maybe part of the reason for drugs such as Zyprexa and Seroquel is that they sedate people, through their strong action in histamine and other receptors already in low doses. ?

  • Critics of “medical model” often call out about the “chemical imbalance” thing. Other people often answer that no one who knows anything at all ever really suggested it, or that doctors need to talk in a simple language to patients, and so on. But I guess you can often see the same or similar thing as the “chemical imbalance” story in articles like this one, where they use a slightly more elaborate “neuro-reasoning” to impress and convince doctors and other specialists reading it. I’m actually perhaps a weirdo in this board because I’m interested in learning how these drugs actually work in body on biological level and there are probably many interesting articles out there, but often these neuro-pharma-promo-articles don’t have anything interesting in them.

  • Our official (Finnish) guidelines also currently state things such as neuroleptic medication should be kept to a minimum dose in order to prevent unwanted effects, tapering down can be attempted after the patient has been symptom free for a year or two, etc. Not all of that actually sounds so bad for a disease so grave as psychosis, as it is described in those guidelines. It’s that what I saw and experienced there was something entirely different.

  • “I think it is less clear of dose impacts propensity to gain weight.”

    Sandra, are you referring to some specific studies which suggests dose reduction didn’t help with weight gain, or that there haven’t been studies of it?

    It probably depends on dosages, drug in question and other factors as well. For instance, I think some neuroleptic drugs that often cause weight gain affect strongly in histamine H1 receptors, and it has been suggested this is one factor why they cause weight gain. (They may cause weight gain in other ways too, this is just an example.) The effects a drug has on different kinds of receptors doesn’t grow linearly with dosage, so that even a relatively low dose of Seroquel or Zyprexa may “saturate” those histamine receptors, or other receptors, so that going from a massive dose to a big dose doesn’t necessarily have much effect on weight issues. As an example, 25 mg of Seroquel already caused me huge “munchies”, maybe because of the strong activity on histamine receptors at that dose. I don’t think the “muchies” effect would have grown linearly up to 600 mg or have had much change from 400 mg to 600 mg.

  • Oh, and I can tell people recovering from schizophrenia wasn’t actually that hard. Or, alternatively, if I actually have schizophrenia, I can tell people it’s not that bad after all. Psychiatrists like to talk of schizophrenia like it’s their holy speciality. I can just sneeze and say, well, I had it and I recovered. Or, I have it, but it’s not as bad as people make it be, it’s actually quite nice.

  • For me, neuroleptics caused almost exactly quite severe “negative symptoms”, such as sleeping 14-16 hours a day, and then being very tired and lethargic the rest of the day. I was only responding with single words, etc. Then the psychiatrist and psychologist perhaps somehow interpreted that as “schizophrenia negative symptoms” and “post-psychosis depression”. Their diagnosis were not “strict” and “objective” at all, they constantly used the diagnosis and other related concepts to validate their own delusional views. It was much worse in practice than what I had imagined it to be.

  • So, what do you think it means to “have a schizophrenia”? You seem to understand quite clearly when a person has a schizophrenia and when not. And you suggest there are perhaps other people, who also fall outside the narrow criteria, who also actually have schizophrenia, a disease which according to you is present with birth. No wonder some people these days prefer to say “schizophrenia” instead of schizophrenia.

  • 300 mg/day is a relatively low amount of Seroquel for psychosis. It maybe has some little effect on dopamine systems, lots of activity for tiring antihistamine, plenty of action on different types of receptors. For psychosis or schizophrenia it’s used at doses like 600-800 mg, and even then it’s not blocking dopamine very efficiently when compared to high doses haloperidol. In any way, of course those other receptor activities can be interpreted as “negative symptoms” by a patient or a psychiatrist.

    So, I pretty much developed negative and maybe cognitive symptoms of schizophrenia in some months when using these drugs. That type of experience is mostly resolved. Of course I sometimes have trouble concentrating on a task a need to do, but the experience and others’ reaction to it is entirely different. I realise this is an anecdote, but on the other hand, our brain systems are quite similar with their neurotransmitters, different brain areas, pathways and so on. Some may say I wasn’t originally schizophrenic, so I got those serious effects from neuroleptics, whereas in schizophrenics, they have some kind of an inborn problem with generating too much dopamine or having dysfunctional dopamine receptors, or whatever, and so in their case the use of a high dose of neuroleptic drugs “balances” their dopamine activity, instead of it going hypo. I just don’t find that kind of thinking very plausible.

    Our body, including brain, is a complex system with interacting hormones, sytokines, neurotransmitters, etc. When a human or an animal is stressed enough, in panic, etc, I guess there may plenty of dopamine, cortisol or other stress hormones utilised. Maybe some dopamine receptors go to a “high” state. Maybe their kind of a natural body regulation system has gone a bit awry. If you insert a drug which blocks enough of those dopamine receptors, of course those people get dulled so much that they start to act like those typical people people consider schizophrenia. At antipsychotic doses, those drugs are given in so large amounts that a big amount of all dopamine receptors are blocked, and it’s not really about balancing their dopamine levels to a normal level, especially when those drugs are given chronically.

  • When I was on Abilify 15 mg plus some Seroquel, I developed a condition which both looked like descriptions of negative (and maybe cognitive) symptoms of schizophrenia, and it felt like it subjectively too. The papers they wrote when I went there say things such as “patient was talking throughout most of the meeting and wouldn’t even stop when..”, whereas some months later they read “patient responds with single words”. Subjectively, it felt pretty dull and colourless, I didn’t get positive feelings from things such as exercise or meditation which I had earlier enjoyed. I remember once drinking two cups of coffee and taking nicotine capsules just before meeting with a psychologics, so that I’d appear at least a bit more fluent or lucid. I guess I at least developed much of what could be called negative or cognitive symptoms of schizophrenia from neuroleptics. However, I still think many people labeled with schizophrenia have something like negative or cognitive symptoms even without drugs. Even prolonged stress, bad nutrition, lack of sleep, etc, can cause all kinds of issues in many people.

  • I don’t know much about statistics, etc.. I only did one course in university and barely passed it. I’m getting more interested now in learning it. Anyway, this study seems to be of the same cohort as in this news:

    More Evidence Antipsychotics Reduce Brain Volume

    In that paper, they found out neuroleptic use is associated with brain volume decrease, but brain volume decrease is not associated with cognitive decline. In this other study of the same cohort, they found out that higher neuroleptic use was associated with cognitive decline.

  • I liked this part of the article:

    “I had to be cut off from my family, which made everything worse,” she tells me. Indeed, her performance is as much a political statement about America’s mental health care as it is a personal one. “I feel like people should be integrated into the community and we should have social rituals to support people who are going through that experience of madness.”

  • Perhaps these traditional hallucinogens may be useful for some people in the way that they can smear all one’s life and problems on face. “What! Why am I living like this!” .. followed by some kind of liberation, and perhaps a longer lasting change in lifestyle. However, at least in current drug culture this type of progress seems quite rare.

  • Yeah, I’d separate traditional hallucinogens from drugs such as antidepressants, alcohol, pot, speed, heroin, even ketamine, etc, at least in their addiction potential. Their effects can be very powerful and not necessarily pleasant, especially if one’s suffering from mental issues to begin with. They’re not drugs you can escape your problems easily with, and they can easily create extremely bad trips. People also develop tolerance rapidly.

    However, they’re clearly very powerful drugs with lots of potential. Perhaps if we as society had some proper (social) rituals to use them in a healing manner, they’d be useful. I don’t know what these rituals would be like, but I guess it’s possible.

  • I mean, in the mental health scheme, psychedelics such as LSD, shrooms, mescaline, etc, maybe can at times maybe blow your mind so that you figure out your problems, because they’re all smeared on your face, and then you’re supposed to start to work on it in your regular life. Doing too much of those drugs may lead to you being diagnosed as psychotic, bipolar or schizophrenic, and then you’ll get pumped with antipsychotics, which will make your experience the opposite of those good moments on psychedelics.

  • I did some hallucinogens such as shrooms and LSD in my early 20s, maybe more than a regular guy. I had actual quite severe problems with depression, anxiety, panic attacks, etc. I wouldn’t recommend people with this type of experiences to take hallucinogens. I had some very profound experiences and also some equally horrible experiences, often during the same trip. I’m still not against this type of drugs, but I’m not promoting them either. I used them maybe a bit too much and got a bit burned out too.

    After more than a decade of stopping experimenting with them, I see they had both beneficial and adverse effects on my later life. On one hand, I realised all the richness of experience, where I could be, and I started to appreciate some aspects of systems such as yoga, tai chi, chi kung, zen, etc. On the other hand, maybe I became a bit too eccentric in my social life because of in one part the drugs, and in one part reading too much of those 60’s gurus such as Leary and Lilly.

  • A continued saga of Boc5, the first non-peptidic glucagon-like peptide-1 receptor agonist with in vivo activities.
    He M1, Guan N, Gao WW, Liu Q, Wu XY, Ma DW, Zhong DF, Ge GB, Li C, Chen XY, Yang L, Liao JY, Wang MW.
    Author information

    Glucagon-like peptide-1 (GLP-1)-based therapy presents a promising option for treating type 2 diabetes. However, there are several limitations relative to the peptidic GLP-1 mimetics currently on the market or under development. This concern has led to a continued interest in the search for non-peptidic agonists for GLP-1 receptor (GLP-1R). Here, we briefly review the discovery, characterization and current status of a novel class of cyclobutane-derivative-based non-peptidic agonists for GLP-1R, including Boc5 and its newly discovered analogue WB4-24. Although the oral bioavailability of such compounds still poses great challenges, the progress made so far encourages us to identify a truly ‘druggable’ small molecule agonist for GLP-1R.

  • And to repeat, I positively think all that itching sounds like some kind of a “histamine rebound”. I’d try to go down a bit slower with those mini-doses of Seroquel, it’s primarily an antihistamine at those 12,5 mg-25mg levels. If you itch too much, maybe your body is telling you’re going down too fast.

  • I personally went for sleep reasons to 12,5 mg for six months, then quit it. I think much of that sedating effect of low doses of Seroquel is because it’s a strong “traditional” antihistamine at H1. If the itching is too strong, maybe you can think of taking a very low dose, such as 12,5 mg, for some time, then taper down from there. I think 25 mg is the lowest they start Seroquel for any reason (insomnia, etc), yet I found out 12,5 mg was quite effective for me as well. That is, maybe find the lowest dose you don’t get itch, etc, then taper down from there.

  • I mean… if you take Seroquel even at 0-50 mg, it’s a very potent antihistamine at H1 receptors. Your body probably will adjust to this antihistamine effect if you take it long enough.

  • Yes, it’s true that Seroquel is a strong antihistamine at H1 receptors at doses 0-50 mg. It is a strong antihistamine at even larges doses, but the antihistamine effect kind of levels out when the dose is increased and other receptor stuff comes more prominent. Note that this sedating effect of Seroquel at 0-50 mg is similar to older antihistamines like Benadryl which go easily to brain and to H1 receptors. Many later antihistamines don’t go so easily to those brain histamine receptors, for instance because they can’t pass the blood-brain barrier, so they’re not as sedating. In any case… I think the itching does sound like it’s because your body has kind of got used to Seroquel’s antihistamine effects. I remember getting kind of casual large red inflammation spots around my body when *starting* Seroquel. I think I also got later on insane itching when trying to sleep, and it might be related to quitting Seroquel. I’d have to check my diaries to be sure… But in any case, yes it’s a potent antihistamine at H1 receptors.

  • Yes, I definitely don’t disagree with any of that. At least my point of view is that inflammation, cytokines, etc, may be one thing that happens in the body of someone who has some severe mental issues such as not getting sleep. For instance, life circumstances such as prolonged stress, problems with people, getting isolated, etc, change all kinds of things inside the body too, such as they may increase stress hormones, change the proportion of cytokines and so on the biological level. I think the levels of social, biological, spiritual, subjective experience, political, etc, are all very much inter-related. For instance, in my own case, I think my “problems” were also in a big part caused by prolonged social issues (parenting, issues as a kid in school, etc).

  • For instance, after years of self-experiment and study, I’ve developed a system for myself which works quite well. It consists mainly of diet (low carb paleo style), meditation, zen and yoga style exercises, “science” of creating new habits, hiking and trekking, and related issues. Actually these all are related in some way or another. I think one possible way they have actually helped me may have to do with inflammation, through the effects caused in my body through diet, exercise, meditation, etc. I don’t know for sure, but it makes sense. Of course there are many other changes on many different levels as well. For instance, a low carb diet may in the end be more “energy efficient” way to supply energy for the brain, maybe it facilities more GABA. Not to mention, for instance, the social level issues, etc. These different levels and things are often interrelated in many ways. So of course I don’t think inflammation is the only explanation of depression, but it’s one interesting thing to consider in this mesh.

  • I for one am interested in the role of inflammation, immune system, cytokines, etc, in depression and other mental issues. It’s at least an interesting thing to think about. You don’t have to say it’s all about inflammation or cytokines, or that you’re kind of born with an unrepairable bad immune system and that makes go mad. Many of the more “extreme anti-biological anti-psychiatrists” admit that things such as prolonged stress, social issues, bad nutrition and lack of sleep may cause mental issues. Well, there’s certainly also some biological ways these social and other issues cause issues. Prolonged bodily inflammation, cytokines, immune system, etc, may be one thing that is being modulated by lack of sleep, social problems, etc. It may well be related to at least some cases of depression, psychosis5, etc.

  • Talking of irony or sarcasm. Before my last meeting with my psychiatrist, I had ordered and read through the records they had written during the two or three years in the out-patient or whatever it was. The last meeting actually became only because I had ordered those records a week before, and also because I supposedly had a private meeting with the doctor.

    Anyway, I read in my records that when I went to their place, “patient sleeps roughly 7,5 hours in night and gets up refreshed up”. After three months of treatment with Seroquel and Abilify, the records say I sleep sometimes maybe 14-16 hours in day, sometimes I sleep through a whole weekend. I also was constantly tired through the day, zombie, certainly not capable of full-time work, etc. Also some strange red “inflammation” areas on my skin, and “heart shocks” when falling to sleep. When I told about these issues to them, they wrote in their records that patient had, wait for this… paranoid thinking concerning his medication. And guess what, that word paranoid somehow got into my final records, after two or three years by entirely different doctor, who never had seen anything like that in me. It’s like those words can follow you like some parasites.

    During our last meeting I was quite angry and annoyed by all the things that had happened to me. I assertively told my doctor, referring to their claims and reports they had written: “You probably again think I’m paranoid, but … what what you’ve written and the diagnoses you’ve done may affect my chance of getting work, and so forwards” Guess what she said next to that? She asked in kind of a panicked voice: “You’re not thinking we’re thinking bad things of you?” Bah. A nice way to dodge that criticism and sarcasm. “It’s mad man’s talk.” But anyway. I don’t think she was doing it very consciously, and I could see her become quite nervous herself. They can use diagnoses, psychiatric terms and ideas, etc, as kind of tools in controlling, convincing, etc.

  • I’m fortunate enough not to have been in a hospital, but I did get my records from the time span of two or three years I was in the public treatment here in Finland. I’ve successfully tapered off neuroleptics and SSRIs mostly by my own means and with the help of people in internet. At the time I guess I also wanted to try SSRI and neuroleptics and I don’t feel grudge that I was given those drugs. I tried those drugs and fortunately I got off them before they caused further damage. I am a bit wiser about what works and doesn’t for me. I’m done with that.

    However, I’m still dealing every day with those things they said to me, the things they wrote in their records and the diagnoses they gave me. If you read the records, they paint me as perhaps one of the most insane people you’d ever meet. I also got during that time all the worst diagnoses they had on offer: bipolar, paranoia, severe depression with psychosis and schizophrenia. I got “cured” of this “schizophrenia” by stopping drugs, stopping seeing shrinks, going back to work, etc. Sometimes what they’ve written seems like straight out of some modern version Rosenhan experiment. They had made up their mind I was psychotic or had “schizophrenia”, after of which they seemingly tried to interpret and bend every possible thing so as to conform to this belief, and since this business of psychiatry is so “fuzzy”, “imprecise” or “loose”, there’s lots of freedom in bending things. Is there some term in psychology for this kind of thinking? Perhaps at least “confirmation bias” is similar to what I’m after.

    Now that those first psychologist and psychiatrist have writtenb their “delusional” records about me in the eight months or so they were “testing” me with Rorscach, etc, it seems the records will quite possibly influence the reasoning of doctors, psychiatrists and other professionals Iater on my life until the day I die. I’m just trying to figure out best approaches in neutralising those lies in my records.

  • Risperdal is a strong antagonist at those serotonin receptors. Basically a similar set of receptors as quetiapine, different affinities. Especially at the time of their marketing, many places suggested that it’s this serotonin receptor (5-HT2A, etc) antagonism that makes “atypical” drugs better than than old drugs such as perphenazine. It’s quite hard to get any good data from the studies done at this period, since so many of them have been basically pharma-funded promotional studies! “Our drug is better than your drug, because…”

  • Hi Johanna,

    “Once you’re on it, it appears to be wicked hard to stop, with “rebound” distress that may be worse than the distress you felt before the Seroquel. I do not know if it can actually cause “rebound” hallucinations or paranoia ”

    At least if Seroquel is taken in “antipsychotic” doses, say maybe 600 mg – 800 mg, withdrawing from that can cause at least in principle “supersensitivity psychosis” like other neuroleptics (see Seeman, etc). I’ve also observed some people trying to quit Seroquel and I’ve quit it myself too, and I think another thing is that at lower doses, even 25 mg or less, it has a very strong sedating effect, largely from its antihistamine action (similar to Benadryl). Because their bodies have got accustomed to these effects, people may have trouble sleeping without Seroquel, etc. Maybe some people find use for its sedating effects. Anyway, yes, I guess most people don’t find it very pleasurable or addictive in the sense of benzos or opiates, but maybe some people want to use it for its sedating effects.

  • Often the “official” rules state things such as neuroleptics could be withdrawn maybe after a year or two of the acute use, or that they should be used in the smallest possible dose in order to prevent detrimental effects, etc. Psychiatrists and other specialists often claim that this is what is done, but it simply does not seem to be the case in practice. In that Wunderink study they had a group where the amount of neuroleptics was intentionally kept to minimum. Sandra has made her own experiments, with her great intuition, insight, intelligence, etc. There we have people who had “intention” to do this. If the actual clinical practice usually seems to overshoot even the current “official” rules, how could we teach the current system to give these drugs more judiciously? It seems that there has been a constant “official propaganda” among doctors and public over many years that benzos should not be used except in some cases, and it may have worked. Perhaps I don’t see that kind of a “propaganda” happening inside of psychiatry among neuroleptics at least as long as the current neuroleptics are profitable. In short, I don’t see why the mass of the current care would strive to give people the minimum amount of neuroleptics, or how how to make it do so.

  • Hi Ron,

    I’m not sure what conclusions to make of this study. But in any way, in this paper Harrow divided the patients to three groups: those who ate neuroleptics all the time, those who at times ate neuroleptics and those who never ate neuroleptics (possibly seemingly). For instance, in that second graph, it seems it includes patients only from the first and third group, that is, those who took neuroleptics all the time and those who didn’t ever take it, maybe from the two year point. It still seems possible that people from first and third group jumped to the second group, that is, the group who sometimes used neuroleptics. Etc.

    I don’t see it’s any kind of a definite proof that neuroleptics make it worse in long term for every person with the diagnosis of schizophrenia. Often we haven’t even very clearly even defined what “better” or “worse” even mean, except through some psychologic tests.

    However, let’s begin with this: it’s common “wisdom” among psychiatrists and lay-people alike that “schizophrenia” is a single brain-degrading cellular level brain disease alike to Parkinson’s (often only reverse in the dopamine function), and that psychologists or psychiatrists can reliably determine its presence with their tests, etc, and often that perhaps only drugs can prevent that degration, and drugs should be given to every “schizophrenic”. This is a very common view of what “schizophrenia” “is”. By the law of contradiction, Harrow’s studies at least show this view of “schizophrenia” is not right. There’s something wrong in there somewhere, probably in many places.

  • I’ll add that one way I see this neuroleptic induced dopamine supersensitivity stuff could cause more psychotic symptoms or hospitalisations in patients eating a “maintenance dose of neuroleptic” is that some of them forgot to take their neuroleptic, or secretly didn’t take it. This explanation I can easily understand, the neuroleptic primed brains would cause “supersensitive psychosis”.

    Maybe one reason why I insist on this point is related to a quote someone mentioned, I think it was Maria Bradshaw.

    “The most perfidious way of harming a cause consists of defending it deliberately with faulty arguments.”

    — Friedrich Nietzsche

  • Sandra, you wrote:

    “You make a distinction between two notions: “the effectiveness of neuroleptics is reduced over time in some patients” which you consider supersensitivity explaining vs. ” more psychosis for people why[who] use neuroleptics at a constant or increasing dose”.

    I think others see that as the same thing. In his post, Whitaker equates the presence of psychotic symptoms over 20 years in the group who remained on neuroleptics as indication that supersensitivity occurs.”

    Yes. Even after reading those papers by Seeman, Chouinard, etc, I don’t see them talking about maintenance treatment causing more psychosis than there was to begin with. I understand that neuroleptic induced dopamine supersensitivity means roughly that neuroleptics block dopamine receptors, which causes body to adjust so that it postsynaptic neurons grow more dopamine receptors, or maybe some dopamine receptors go to a “high” affinity state, etc. That is, neuroleptics initially reduce dopamine related signalling, but later body makes compensations which may potentially undo at least some of the dopamine blocking effects of the neuroleptic. Because of the adjustment, the net dopamine signalling while on chronic neuroleptic treatment may become closer to the baseline. I don’t see why dopamine activity would shoot [i]over[/i] baseline as long as the same level of neuroleptic is maintained. If you lower the dose of neuroleptic after these adaptations, then I can see how these adaptations can cause symptoms.

    In that post from Whitaker, in c) he says that someone suggested neuroleptics made schizophrenic patients “more vulnerable to future relapse than would be the case in the natural course of the illness.” In d), he gives Chouinard supersensitivity as a possible biological explanation for this. I don’t really see those Chouinard or Seeman papers are a direct explanation of c). I agree that presence of psychotic symptoms over 20 years may be related to supersensitivity, as can withdrawal psychosis, etc.

    That’s basically my point. I’m not claiming neuroleptics do not cause more psychosis in long term through some mechanism. I just don’t directly see why neuroleptic induced dopamine supersensitivity would cause more psychosis in long term as long as the level of medication is maintained or increased, and I didn’t see those references claim it either. It’s possible supersensitivity is related to more psychotic symptoms in this way too, but I don’t see enough evidence to state it this way. In short, I see from the reasoning in those studies how a constant dose of a neuroleptic may cause supersensitivity, which may increase the net dopamine signalling closer to the baseline, and therefore psychotic symptoms may reoccur despite neuroleptic treatment. It doesn’t seem to directly explain why a constant dose of a neuroleptic would cause more psychotic symptoms than there was at the baseline.

  • Also, for instance, Seeman et al

    “Breakthrough” Dopamine Supersensitivity during Ongoing Antipsychotic Treatment Leads to Treatment Failure over Time

    It also talks about neuroleptic treatment maybe sometimes losing its effectiveness through supersensitivity, but not about treatment causing more psychosis through this mechanisms, as if the net dopamine activity would somehow rise above what it was before neuroleptics. I’m asking only because often in MiA I hear this argument that neuroleptic induced supersensitivity maybe means there are more psychosis in neuroleptic treated patients in long term, this claim is almost in the Harrow paper too, and that recent post from Whitaker. Does it? Why?

    “Although in the present study with rats haloperidol and olanzapine lost efficacy over time, not all treated patients develop therapeutic tolerance. However, a notable proportion of initially stabilized patients relapse during treatment and this cannot always be explained by nonadherence to treatment. For example, even when medication is guaranteed by depot injection, the average relapse rate at 1–2 years is still 18–55% (Carpenter et al., 1999; Schooler, 2003; De Graeve et al., 2005). Although relapse during continued treatment can be attributed to a number of reasons, our results suggest that an antipsychotic-induced increase in dopamine sensitivity might predispose certain individuals to psychotic relapse. This provides a discrete hypothesis that can be tested in patients.

    Together, the present findings allow us to propose the following: (1) initially, antipsychotics block D2 receptors, and increase dopamine and dopamine turnover in a system where levels of D2 receptors and D2High receptors are normal. At this stage the balance of agonist (i.e., endogenous dopamine-related) drive and receptor blockade allows the antipsychotic to exert a net anti-dopaminergic effect. (2) With continued treatment, there is a decrease in turnover on the presynaptic side, D2 blockade by antipsychotics is maintained, but both D2 receptor numbers and D2High sites are elevated. At this later stage, endogenous dopamine drive is potentiated and can more readily oppose the anti-dopaminergic effects of the antipsychotic. This might explain why antipsychotics so often fail. The challenge now is to identify the neural processes by which dopamine supersensitivity and antipsychotic treatment tolerance develop. At the same time, the biological (i.e., increases in D2 receptors and D2High sites) and behavioral (loss of efficacy in behavioral models) markers identified here provide targets that can be used to identify strategies to overcome or prevent antipsychotic treatment failure.”

  • One more comment to clarify what I was trying to articulate here about this dopamine supersensitivity. One sometimes hears it as a possible explanation for increased psychosis with neuroleptic treatment. I can easily see how neuroleptics might cause dopamine supersensitivity, which in turn might explain things such as why the effectiveness of neuroleptics is reduced over time in some patients, or why some patients get psychotic symptoms when they lower their dosages. However, it’s less clear to me why this mechanism would cause more psychosis for people why use neuroleptics at a constant or increasing dose. I just don’t see why this would be the case.

    I browsed some of those Seeman papers and also this Chouinard paper:

    “We have propposed [sic] that similar changes occur in the mesolimbic pathway in response to the chronic DA blockage by these drugs and that psychotic symptoms following withdrawal or decrease of neuroleptics could be the clinical expression of a mesolimbic DA postsynaptic receptor supersensitivity.”

    Is there any proposed mechanism or proof that neuroleptic dopamine supersensitivity causes more psychotic symptoms in patients who use a maintenance dose of neuroleptics? I can see that this kind of supersensitivity could, for instance, mean that some patients keep taking higher and higher amounts of neuroleptics and then they may stop working very well.

    I just mean that if one’s arguing that maintenance treatment with neuroleptics causes more psychosis in the end, is neuroleptic caused dopamine supersensitivity a valid argument given what we know?

  • I don’t know too much about Parkinson’s, or about anything actually, but to my mind there maybe these two kinds of thinking:

    1. Lack of dopamine signalling between neurons somehow causes Parkinson’s and related stuff. In Parkinson’s, maybe some dopamine producing cells die, etc. With neuroleptics, they block the dopamine pathways and thus cause the same issues “downstream”. This kind of thinking is kind of obvious.

    2. Because of the blocking of dopamine receptors, body tries to create even more dopamine, etc, and this overproduction kind of causes issues in some parts such as substantia nigra over time.

    Heh, I also must repeat that I don’t understand this body, biology or neurostuff at all. I’m just kind of trying to understand some of it.

  • From what little I know, I think the dopamine hypersensitivity thing is maybe even overstated in these conversations. This is almost “common wisdom” and I don’t have any data to back it up, but for instance in the case of neuroleptics used on high doses, they block the dopamine receptors. Cells may grow more dopamine receptors, more dopamine may be produced, dopamine receptors may go to a “high” state, etc, to compensate or maybe to find some kind of a homeostasis. In any case, if you block enough of those receptors, all those compensatory mechanisms won’t be enough to undo the effects of the drugs. Some compensations are made, but as long as you take the drug in a high dose, the tolerance won’t undo all of the effects. Certainly it’s not feasible to think that, if you’re taking the drug in a high constant level, the dopamine compensation will overcome the effects of the drug and eventually cause even more “dopaminergic activity” than there was to begin with. If you try to lower the dose of the drug, or quit it, then of course these compensatory effects may come to play.

    Still, there may be many effects of these drugs which lead to all kinds of problems and diagnoses. For instance, I think at the current day many of the “cognitive and negative symptoms of schizophrenia” are quite hard to distinguish from the actual “disease called schizophrenia”.

  • Yes, both patients and doctors, etc, can think “let’s not rock the boat” way. Many people diagnosed with schizophrenia, psychosis, bipolar and so on this way. Often when I’ve read what many patients write, they seem to prefer to take their drugs, and I’m not one to tell them not to take them.

    I wanted to rock my personal boat and they tried to deny it with any means and stories they could invent, and even pathologised my opinions on my own treatment. “Has paranoia concerning meds”, etc. I’m not saying anyone shouldn’t eat neuroleptics, but I guess I just want to save my own ass and that of people with similar issues.

    Harrow also says this about “adherence”. Many professionals think it’s very important to increase adherence and they try to do it with any means. Surely there are many patients who stop their drugs, return to hospital, etc. But “SZ” is not a single brain degrading reverse Parkinson’s disease like some seem to think. Some people do quite well without meds in longer term. With all this talk about increasing adherence, I wonder if all those people in the study who in the end didn’t take neuroleptics would do even better if their adherence was increased and they were made to use neuroleptics…


    “Lack of adherence to prescribed medications re- duces the effectiveness of antipsychotics for patients. In research on medication adherence for psychiatric patients with psychosis, the mean rate of adherence was estimated at 58% (Cramer & Rosenheck, 1998; Osterberg & Blaschke, 2005). Lack of adherence con- tributes to the very poor outcome in some patients in treatment. However, the very large significant differ- ences, in the opposite direction from that expected, found in rates of psychosis and rehospitalization when comparing unmedicated SZ to those prescribed antipsychotics is so striking and the timing consistent with other reports about antipsychotic effects dimin- ishing or even reversing after the 2–3-year period (Harrow et al. 2005, 2012; Harrow & Jobe, 2007; Wunderink et al. 2013) that it suggests adherence is not the main factor contributing to poor outcome.
    In addition, lack of adherence does not contribute to the relatively favorable outcomes of many SZ who were unmedicated for many years. Often, these unme- dicated SZ are not taken into account in estimates of outcome in schizophrenia. The field knows very little about this type of SZ. Cohen & Cohen (1984) have noted the bias that can arise from our more frequent clinical contact with chronic poor outcome patients.”

  • I think many “official” guidelines in US and Europe alike say things such as when a person has been symptom free for a year or longer, the dose of neuroleptics can be reduced or the neuroleptics can maybe stopped. Even this Harrow paper mentions it:

    “Association (APA) guidelines (Lehman et al. 2004) indicate clinicians should consider discontinuing antipsychotics for SZ who are symptom free for a year or longer. However, many clinicians assume that antipsychotics are important for continued stability and keep SZ on antipsychotics indefinitely.”

    I guess reductions in the dose or even discontinuation happens relatively rarely in practice, at least initiated by a doctor. “You’ve been doing so well for a year now after your psychosis, let’s try to taper the neuroleptic off!” No, the thinking is more often like “let’s not rock the boat”. There may be other related issues too, such as that if a person is heavily medicated, he’ll often never properly “recover” functionally, etc, to a level where it is considered that maybe now it’s time to reduce the dose. Often the reality seems to be that the patient eats some mix of drugs, if they start to get too serious effects or problems, then the doses are increased, maybe a new drug is added, maybe a neuroleptic is switched to another neuroleptic, and so on. Once the patient is “stabilised” on a certain set of medications and doesn’t whine too much, it probably often seems the safest and easiest thing to just keep taking the meds at those levels.

  • Benzos are perhaps the most efficient, safest and patient-comfortable psych-drugs out there when used in a controlled setting and temporarily, such as in temporary “psychosis”. The addiction may get quite bad in long term, so they should maybe used only short term. But still.. I guess there’s a use for them. I’d rather give those first-episode patients admitted to hospitals benzos instead of neuroleptics when possible. Or maybe some OTC drugs such as Benadryl. Just to give some sedation and sleep. Benzos can be most useful drugs when used in a controlled setting. Of course troubles may start out of it.. but still..

  • I guess I personally agree with Seth’s point. Benzos may be some of the most efficient and safe substances out there if used in a right manner in reducing anxiety and providing sleep. Maybe a safe environment to try them instead of neuroleptics would be in a hospital setting for something like first episode psychosis or related crisis. Maybe if they were used in such settings people wouldn’t get addicted to these drugs. Maybe there wouldn’t be so many chronic “schizophrenia” patients. Etc.

    I don’t think there’s nothing a priori kind of wrong with using drugs.

  • I know about the problems of consciousness in philosophy of mind, and as I said, I don’t have an answer to them. I don’t understand how we get this subjective consciousness. As for the gut thing, see what I wrote below:

    “Actually, when talking of biology, I’ve lately been much more interested in what’s happening in our bodies also outside the brain, things such as metabolism, liver, glucose, ketogenic amino acids, cytokines, inflammation, fatty acids, etc. Also things such as epigenetic changes in body. I guess some of that stuff has been more useful than much of the neurostuff related to psychiatry, since they at least can help a bit in navigating the optimal things that may help.”

  • I personally think almost all of what we experience in our normal (or abnormal) consciousness is very directly related to stuff that happens in our brain, the action potentials, etc. That’s why neuroleptics affect the experience, often in an adverse way! If there’s just the mind independent and strong, it shouldn’t be strongly affected by neuroleptics. But it is. I know about the problem of subjective experience and so on, and I don’t have a solution for it. At the same time, I don’t think the “mind outside of body” thing is a very good argument against neuroleptics in many or most cases.

  • I don’t see studies like this in so bad a light. We know things such as getting diagnosis in mental illness run in families. The “pure” genetic theory kind of says it’s an inherited disease, kind of an original sin a person gets on birth. However, if some problems are passed through things such as upbringing or epigenetic mechanisms, it kind of implies these problems maybe can also be fixed through various kinds of ways. Maybe another epigenetic or behavioural change will fix the problem.

  • I haven’t really tried any of these official therapies, but as an analogy, I’ve greatly benefitted from my own system of diet, exercise (trekking, hiking, train running), basic stuff about creating new habits and meditation, all of these interrelated. I’ve read through books such as James Austin’s Zen and the Brain, which I’ve found quite interesting, though they haven’t probably greatly influenced the way I practice. It’s mainly interesting to me, though I guess there are some general level ideas about how the body or brain work that have been useful, things such homeostasis, neuroplasticity, etc. Actually, when talking of biology, I’ve lately been much more interested in what’s happening in our bodies also outside the brain, things such as metabolism, liver, glucose, ketogenic amino acids, cytokines, inflammation, fatty acids, etc. Also things such as epigenetic changes in body. I guess some of that stuff has been more useful than much of the neurostuff related to psychiatry, since they at least can help a bit in navigating the optimal things that may help.

  • Yes, I at least agree with you that schizophrenia is a “placeholder”. Heh, I got that diagnosis for a while because of misunderstandings and severe effects of neuroleptics (“negative + cognitive”) even though I haven’t ever had any hallucinations or, in my opinion, any severe psychotic symptoms. And once they thought I had psychosis or “schizophrenia”, they started to interpret everything in a way that validated their belief. For instance, they thought my answers to Rorscach test meant I was hallucinating. Now that the stupid label is there in my official papers and will haunt me for the rest of my life. In a way, once you get a diagnosis like that, it’ll often influence the thoughts of professionals to the point where they start to see all kinds of things as symptoms of the disease. So in this sense I also agree with you that the diagnosis may often be harmful.

    But reading through all these things professionals and non-professionals write everywhere often makes me pessimistic. The view of schizophrenia as some kind of a reverse Parkinson’s disease is just so wide spread. And the same kind of thing is true with bipolar, etc. They’re all being treated the same way anyway, with SSRI and neuroleptics. Maybe it’d be easier if they simply created a single category “mental illness” and prescribed neuroleptics for it as the first line treatment.

  • You can easily see the social or behaviour control aspect of current psychiatry whenever you see an article in newspaper where someone has done something irrationally bad, and read the comments section. “Why they let these people walk out there without their meds”, “they won’t take these meds unless hospitalised or forced”, etc. Neuroleptics are definitely used as a device of social control also in this day.

  • “I do not know of any thoughtful person – in or out of psychiatry – that considers schizophrenia to be one “thing”. It is an umbrella term that captures many things and, to say it again, I have come to the belief that it has long out lived whatever usefulness it might have had at one time.”

    Sandra, I must admit you have a pretty strict filter on who you consider thoughtful. Maybe it’s a good thing. 😉

    In any case, yeah, in Finland the leading official authorities talk things to the public such as “schizophrenia is considered to be a brain degrading cellular level disease” .. “there’s also some proof that taking atypical neuroleptic drugs will reverse this condition”. When I sent email to this authority and asked about it, he sent me back one of those earlier monkey studies where they still thought Zyprexa was “more protective than haloperidol”, because it had less of brain shrinkage.

    In any case… of course there are many thoughtful people out there who believe schizophrenia is a single cellular level disease which forcibly causes people to act violent. They perhaps haven’t heard the dialogue! If even after that they insist it .. maybe they’re not very thoughtful.

  • Concerning the last part of this interview, where Robert says:

    “Yet, as you suggest, this is why it is going to be so hard for psychiatry to reform. Diagnosis and the prescribing of drugs constitute the main function of psychiatrists today in our society. From a guild perspective, the profession needs to maintain the public’s belief in the value of that function. So I don’t believe it will be possible for psychiatry to change unless it identifies a new function that would be marketable, so to speak. Psychiatry needs to identify a change that would be consistent with its interests as a guild.”

    I think I agree. Much of the way psychiatrists react is because they want to strengthen, defend, etc, their own status, credibility, etc, and by proxy that of their own profession. Maybe it’s similar to Nietzsche’s concept of “will to power”. It’s also one of the reasons some of the current psychologists have come to support the current critique of psychiatry – they see it may give more power to their guild. Psychiatrists likely won’t stop doing what they do because they suddenly understand through some kind of logical claims that it’s not “good”. Maybe psychiatry is now kind of aspirating for the next revolution to come, whether it’s a totally new kind of a drug, magnetic or other ways of stimulating brain, other ways to change the functioning of brain, maybe implanting things in brain and so on. That’s their hope and aspiration. Until the technology, I guess they’ll try to hang on to their current power as forcibly as they can.

    This same thing happens in physics and all kinds of “hard” sciences as well.

  • I’m not trying to get in the nutrition debate that is all over the place. I still think that in my personal case, going low carb/sugar helped me to at least lose those fats I gained from, well, basically modern psych meds which often mess up with with the metabolism of glucose/fat. I’m not everyone, but in my case, if I was still eating, for instance, the typical atypical drugs, I’d go very low carb/sugar just to save my body.

  • “Obviously what constitutes a “healthy” diet is not agreed upon, but people who are serious about their health and are only hearing “Paleo”/low-carb should at least be aware that there are other (better? I think so) approaches.”

    This obviously referred to what I wrote above. Going low carb benefited me greatly, and as I said, I only heard about “paleo” some months ago. I’ve never said this approach works with everyone, I’ve only talked about my own experiences. I think that in my case going low carb was the most crucial thing at least in losing weight. In my case! I never said it’s good for everyone. What is your “better” approach, going vegan?

  • I mean, a pure brain disease in my opinion would be something like a virus that goes to your brain and forcibly blocks maybe NMDA receptors so that you’ll fall into hallucinations despite what’s going on in your life or body otherwise. I haven’t seen much proof that, for instance, “schizophrenia” is a brain disease in this sense. There may be some cases of people diagnosed as schizophrenia or bipolar who have a brain disease in this sense.

  • Yes, I agree. Those people talk about these different psychiatric drugs and their effects on different receptors the same way some recreational drug enthusiastics talk about what receptors their drugs affect. It’s pretty much the way I see it. They are psychoactive substances that act on those receptors.

    However, I do think that there’s certain complexity with this thing. For instance, I think all things we think and experience are also related to our body. For instance, when someone is very stressed up and acting in a fight-or-flight-manner, etc, it’s entirely possible that, for instance, his dopamine receptors are acting in a high state, etc, and neuroleptics will dampen that thing quite crudely. Should that be seen as disease? As in, there may be so many different things in life that will cause different kinds of disturbances in body, such as dopamine activity or NDMA receptor blockage in the end, which may be related to certain types of behaviour or subjective experiences sometimes seen as mental illness. I guess it’s possible that there are many different pathways (social, trauma, nutrition, stress, lack of sleep, etc) that can lead to kind of disturbances in body, and those may involve more active dopamine receptors, NMDA, cytokines, etc. At times it may be “biological” in that sense. Often they have kind of claimed that, for instance, schizophrenia is one single cellular level disease. I haven’t seen much proof of that.

  • Though, some people like to experiment with these different receptors these drugs affect on, such as the people at There are many people who know so much about these different receptors and also often have experience about it. For instance, a short googling showed plenty of reports about akathisia related to lurasidone. It may be that drugs with more metabolic effects have less akathisia, because those exact effects help with akathisia. Or not. I don’t know, I’m done with self experiment on this field!

  • I mean, when I was actually in the “system”, I was given some SSRI first (I forgot its name), later Abilify. When in a meeting I pointed to them then I read that the metabolism of SSRI interacts with that of Abilify, the psychologist looked at the psychiatrist and after a while, the psychologist said “let’s stop the SSRI, Abilify also helps with depression”. !! Blocking your D2 sometimes does not help with depression, maybe it oftentimes causes it to a horrible degree, likewise as it causes social phobia, etc.

  • I dunno, lurasidone is just another “atypical” neuroleptic drug. It works the same way as other “atypical” neuroleptics, it blocks D2 and potentially gives the same adverse effects that Whitaker, etc, have reported upon. It doesn’t have some of those sedating histamine H1 effects (same as Benadryl). The sedation effects of Seroquel, etc, may very well help with the studies on depression, in the sense the patients with Seroquel get actual sleep, because of H1. I read this new drug may be sedating, or not, through some mechanism through some new serotonin receptor. In any case, the drug very generally works in a similar adverse or beneficial ways as other neuroleptics, of course depending on dose. Really cruel to give it as an antidepressant in my point of view.

  • My comment is on the “right” level, that is, not a reply to your post, even though they are at the same level. I never liked the hierarchical web forums at the time they were introduced.

  • I personally came out of the cave of psychiatry by testing many different things on myself, sometimes or often against official orders, walking many wrong roads, correcting the path when I realised it was a wrong path, etc. Hard to test this kind of thinking with RCT. I eventually found a system (low-carb diet, exercise, basic psychology on habits etc, some Eastern practices such as zen) that works very well for me. I could have chosen drugs such as neuroleptics or SSRI, but eventually I considered them not useful. I found the techniques that actually worked largely through my personal self-experiment, study, etc. Some other person may have another set of techniques or drugs that work for them. I also understand I had enough money, education, time, etc, to think and experiment like this.

  • In any case, I actually prefer to be in the TAU (treatment as usual) group in the sense of this study, which is stopping drugs & psychiatrists and not getting therapy of any kind either. Nice to hear it’s more effective in some senses compared to CBT. 😉

  • Yeah, two years ago or so I decided to go low carb based on just some basic advice I had read, and I studied more here and there while I was at it. I lost maybe a little over 20 kg in a year and now I’ve lost 27 kg. I’m pretty close to my ideal weight right now (BMI 22,5), though I can see a very slight bit of fat around stomach at times. In any case, I think I even heard about this pale stuff just some months ago and my diet was quite much of what that paleo crowd talks about already. Yeah, I’m now following that Mark’s Daily Apple blog with RSS, as well as some other “paleo” blogs. I also haven’t gone too much into details of nutrition, I’m just trying to get at least the macronutrients right and getting rid of too much processed foods. I’ll likely go further to it with time and experience. For me, Peter Attia’s blog has been a great source of info

  • I’ve been doing something similar to relatively low carb/high fat, real food, paleo, whatever diet for maybe two years. Besides losing all of the weight I gained while in psychiatry, I think it has had a great effect on my mind and general well-being as well. For instance, it’s much easier for me to maintain a constant focused state of mind throughout the day. This effect also helps with exercise, and those help with some more “advanced” zen practices. For me, these practices seem to boost each other in great ways. I remember being sceptical about diet when I was younger, but I’m not so much anymore. Even still, I haven’t taken or studied much about micronutrients. I do take some fish oil capsules and whatever comes from berries, vegetables, etc. If one eats lots of “toxic” food, I’m not sure loads of micronutrients will do much to fix it. In any case, I’m not sure what all of this stuff has done to my body and brain, maybe it’s something to do with inflammation, cytokines, ketosis-kind metabolism stuff, etc, but it’s working for me.

  • Good luck with your project! I personally don’t like to learn from videos and stuff, I often prefer to read stuff, stop on points I don’t understand, skip ones I understand, etc. Though I am actually trying to learn listening to podcasts while trekking through woods. I personally often don’t have enough time or interest to watch videos about stuff though. In any case.. enough about my preferences. I’ve noticed many people like to watch videos from YouTube, etc, maybe it’s similar to watching TV, so this kind of an approach may work for many people.

  • One of the most incredible statements of Ross: “Psychosis is caused by many factors, one of which is schizophrenia.” As if there’s some ghost-like but never proven entity called schizophrenia which then causes some of psychosis on people. LOL. He’s got his cause and effect totally wrong. Schizophrenia is more like a term they give to those people who have recurrent or longer lasting psychosis of any kind, and the meds complicate it a lot since they can give almost any person negative and cognitive aspects of schizophrenia.

  • 12,5 mg or 25 mg of Seroquel works very largely on histamine H1 receptors, that’s why it’s so sedating. One could try an older antihistamine such as Benadryl instead. I don’t think Seroquel at those doses necessarily causes those brain shrinkages, but hey why not use one of those older antihistamines instead, they’re often OTC. Though I wouldn’t personally use even those for a prolonged time such as many months or years… But it may be better than insomnia for some people.

  • Yes, sorry, I was just playing with these metaphors in this thread. After all, my psychologist determined my thinking is “concrete”, that is I can’t understand metaphors, so I can’t help it. In any case, I hope you keep whacking psychiatrists with your nails in their head to wake them up, I’m trying to do the same the best I can. 😀

  • Add to that, doctors are known to be very probable to experiment with drugs such as benzos. Why won’t you doctors experiment with neuroleptics at least once, just to know what the initial dose is like? You give it to anyone, and yet dare not test it on yourself?

  • It would be most useful for patients if psychiatrists tried their drugs even if once! But they won’t. If pushed, the argument is that they don’t have that disease so it’s not not sensible to take that drug, etc. Truth is the drugs affect everyone the same way. Some block dopamine receptors, some H1 receptors, etc. If you doctors so readily prescribe these drugs to almost anyone who walks at your meeting, why dare you not to experiment with these drugs your own body? Doctors force them to so many of their patients, yet dare not try the effects of these medicines on their own bodies for one single time, dare to speak that they try the effects upon a longer span of time.

    Some courageous Isreali researchers tried the effects of their medicines, and this is what they reported:

    “The Israeli researchers [Belmaker and Wald’s (1977) letter to the editor]( of the British Journal of Psychiatry reporting their personal experiences of haloperidol:

    “Haloperidol is an effective antipsychotic agent which is a relatively specific blocker of dopamine transmission in the brain (Anden et al, 1970). As part of the preliminary trials in a study of possible dopaminergic mechanism in affective disorder, the two authors each were given haloperidol 5 mg intravenously in a two-minute push. The effect was marked and very similar in both of us: within ten minutes a marked slowing of thinking and movement developed, along with profound inner restlessness. Neither subject could continue work, and each left work for over 36 hours. Each subject complained of a paralysis of volition, a lack of physical and psychic energy. The subjects felt unable to read, telephone or perform household tasks of their own will, but could perform these tasks if demanded to do so. There was no sleepiness or sedation; on the contrary, both subjects complained of severe anxiety.

    The present experience was similar to that previously reported of neuroleptic effects in normal subjects (DiMascio et al, 1963; Heninger at al, 1965), though previous studies used neuroleptics which block both dopamine and noradrenaline receptors (Anden et al, 1970).We used a relatively specific dopamine blocker, haloperidol, and experienced profound cognitive and emotional restriction. Dopamine blocking by neuroleptics may function to restrict cognitive and emotional processes in normals as well as in schizophrenics and thus it is possible that it does not specifically antagonize schizophrenic pathology. In the presence of psychotic anxiety or delusions, such cognitive or emotional restriction may be desirable and therapeutic. However, the restrictive effect may be a general one…”

  • Changing my diet has had not only a great effect on my body weight (currenly 27 kg down from my highest, BMI 22.7, right in middle of the normal range, though I think as a male I still have slightly too much fat around my waist instead of muscled for that BMI). I also think that the diet had a great effect on my mind, though it wasn’t the only factor. For myself, eating real food and getting the macronutrients right was most important – in my case, going low carb and eating vegetables and meat, etc instead of other stuff I was poisoning my body with.

    I also take some omega-3 supplements and try to eat fish regularly. But, I guess for many people it’s more urgent to get rid of “toxic” food and get to eat some better food. Taking omega-3 supplements often won’t get rid of the bad things you do to your body with the other food.

  • Seena Fazel’s comments about quite “quite eccentric” positions of Moncrieff:

    “On the penultimate page, she states that the current model of understanding antipsychotic action (‘the disease-centered model’ in which antipsychotics act to correct the underlying dopamine dysfunction) ‘has played a major part in the obfuscation of the social control function that has always been embedded at the heart of psychiatry’ (page 219). Elsewhere, Moncrieff writes that the view that antipsychotics act by correcting an underlying disease ‘kept the genie of social control firmly inside the psychiatric lantern…. [and] made the practice of forced drugging respectable’ (page 143). This is an extreme view. Clearly, psychiatry has occasionally been abused but psychiatrists have also been instrumental in challenging such abuses. To suggest that ‘social control’ has ‘always’ been at its ‘heart’ would be a surprise to most psychiatrists who one would reasonably think are mostly motivated by treating illness and reducing distress.”

    Seena’s kind of showing that Moncrieff is at least partly right when she talks about disease vs drug model. “Psychiatrists are motivated by treating illness and reducing distress.” It’s clear for anyone with a clear mind who has studied the history of psychiatry that part of it has always been about social and behaviour control. Whitaker’s books include some good history, one of my personal favourites is Chorover’s From Genesis to Genocide: The Meaning of Human Nature and the Power of Behavior Control. I think not only the current drugs and the previous tools of psychiatry (insulin shocks, lobotomy, ect, etc, lol) have been so clearly used for social control, psychiatry has also a myriad of other more subtle techniques of social control, including things such as diagnosis, lies about “inborn inferiority” such as genetic disease, biological determinism, etc. Social control has indeed always been at psychiatry’s heart. Maybe it’s a good thing the news finally got to Seena too.

    “Books for the defence need to be written that focus on key problems for patients and public health – underfunded and overstretched psychiatric services in high income countries, and the continued scarcity of such services in low and middle income countries. Even in America, the three largest institutions that treat psychiatric patients are jails, many of whom according to recent surveys by the Department of Justice are subject to appallingly high rates of sexual abuse. Books like Moncrieff’s that only target the drugs and their manufacturers miss the mark.”

    This book by Moncrieff was primarily about neuroleptics. Seena’s also worried about the scarcity of psychiatric service in low and middle income countries, but look at the WHO studies Whitaker mentioned – do they really need more psychiatrists who treat them with SSRI’s, Seroquel and Abilify?

  • Thanks for another great article!

    Yeah, I’ve seen some people who list “compliance” as one of their major research interests, etc. Some people think these things as their work. So many of psychiatric papers, articles, etc, are about compliance and related things. Schizophrenics have anosognosia, lack of insight and paranoia, so they won’t take meds. I just saw an advertisement of a new book by a psychiatrist about bipolar disorder, the back cover of which repeats twice the problem with medication; in the manic state bipolar patient is so exalted that he thinks he doesn’t need meds. They’re worried about adherence with depression too.

    Certainly part of it comes from pharma related marketing, like in your examples, but I think there are other issues as well, such as that doctors and psychiatrists these days feel they have been losing authority because of internet, alternative treatments and so on.

    In my case, I personally went to doctor and requested SSRI because I thought it might help with some stuff (maybe some depression, anxiety, etc). I got a very authoritative psychologist and psychiatrist to treat me, and I was almost immediately put on neuroleptics too and got diagnosis of bipolar and then finally schizophrenia within less than a year, after of which I was made basically incapable of doing any work and transferred to another doctor. Now, I hated how they treated me in a very authoritative style and saw the ill effects on me, so I began to fight back, tapered off neuroleptics, got back to work and so on. I had not read Whitaker or any other critique of psychiatry at this point, I realised that I had to act on my own mainly because it was so obvious to me they were treating me like shit.

    Afterwards I found Whitaker’s Anatomy of an Epidemic, MiA community, many interesting scientific papers and found out that there’s actually credible critique of psychiatry. I had thought earlier that just I had been misdiagnosed and that those people who tried to treat me were incompetent. I also hadn’t paid much attention to “anti-psychiatry”, even after what happened to me I thought the critique of psych drugs was by some “loonies”. There were those other people who really need their meds, they made a mistake on just my case.

    Connecting this personal story to the topic of the post, maybe if those first psychiatrists and psychologists weren’t so authoritative, paternal and controlling, if they were actually friendly people who I’d like and whose ideas seemed at least a bit more believable to me, I’d currently still be maybe eating SSRI and some neuroleptic and living a crappier life than I currently do, maybe with a diagnosis of bipolar. Maybe it was a blessing in disguise in my case that the first people I met weren’t very skilful with these other types of adherence techniques. 😉

  • Unfortunately, that’s often the way the world works. People, scientists, patients, etc, go to work each day and mostly act by their learned habits, etc. Science doesn’t happen so that one scientist makes a logical claim, other scientists see that as true, then all world sees that as true. Science, medicine, etc, is a lot dirtier, like all social games *snort*. Paul Feyerabend made a point or two about it some years ago. In any case, thanks so much for your very neutral and great article in so prominent a magazine.

  • Thanks for your explanation, mah3md. I like your knowledge and frankly opinionated style. However, I think I’ve personally succeeded in transforming my body, brain and mind with most happiest results through things such as nutrition (low carb, real food), exercise, meditation, etc. Just few years ago I had a bunch of diagnoses such as bipolar, severe depression, psychosis and schizophrenia. I had all the worst diagnoses psychiatry has to offer and here I am, totally out of the system, med free and doing pretty damn well in my own opinion. Nutrition has been a huge thing in getting my body and mind healthy, I think my body is soon close to ideal weight for my age, and I can feel pretty good well-being most of the day. Pretty amazing I should say. In a way, it seems I’ve figured out the rules for transforming my body and mind to something pretty good, and good nutrition is part of it. To get back to diagnosis and drugs of psychiatry would be total torture and insanity for me. But I still appreciate what you’re saying and find it interesting, mahm3d.

  • Monica, thanks for this beautiful piece! I have very similar experience myself about inner GPS, etc. When I was seeing my psychologist and psychiatrist, they constantly tried to enforce their authority upon me. For instance, when I said something about drugs they were giving me, they strictly warned me that I should not read or trust information from Internet, apparently I should only trust what they say. They even gave me a patient guide printed by a pharma company instead.

    “Ananda asked [Buddha]
    who would be their teacher after death.
    He replied to his disciple –

    “Be lamps unto yourselves.
    Be refuges unto yourselves.
    Take yourself no external refuge.
    Hold fast to the truth as a lamp.
    Hold fast to the truth as a refuge.
    Look not for a refuge in anyone besides yourselves.””

  • The site Current Psychiatry has this kind of idiotic polls for random psychiatrists. Many of them try to promote lurasidone between the lines.

    “Mr. P, age 25, has a history of schizophrenia. His psychotic symptoms respond well to olanzapine, but he gains 30 pounds in the first 2 months of treatment and his blood glucose level hovers in the pre-diabetic range. How would you treat Mr. P?
    votes: 446

    21.7 % Obtain baseline metabolic data and monitor him monthly 97 votes
    33.2 % Switch to a newer antipsychotic, such as lurasidone 148 votes
    11 % Lower Mr. P’s olanzapine dosage 49 votes
    34.1 % Recommend diet and exercise 152 votes”

    Ms. Z, age 31, has a history of bipolar I disorder, which has been well controlled with risperidone, 2 mg/d, for 5 years. She recently learned that she is 6 weeks pregnant and is concerned about risperidone’s effect on her baby. How would you treat her?
    votes: 0

    0 % Maintain Ms. Z’s risperidone dose and educate her about the risks of untreated illness No votes
    0 % Switch Ms. Z to quetiapine, 400 mg/d No votes
    0 % Switch Ms. Z to lurasidone, 40 mg/d No votes
    0 % Discontinue risperidone and schedule frequent follow-up appointments No votes

    … etc

    I’m afraid some IDIOT DOCTORS will soon start to prescribe lurasidone to their patients because of this kind of IDIOTIC PROMOTION.

  • Two days ago I for some reason googled for “lurasidone”, or whatever, I don’t remember what I googled. Google showed up a new article about lurasidone where the drug again “draws praise”. It was a recent one, released just a day or so ago. It got up to the most recent Google results.

    By: MITCHEL L. ZOLER, Clinical Psychiatry News Digital Network: “Lurasidone’s potential for bipolar depression draws praise”

    Here Mitchel L. Zoler tries to promote that luresidone is great for bipolar, never mind it works like haloperidol except it also works on 5-HTA. He’s getting funds from the makers of luresidone with a brand name Latuda.

    When researching this thing, I noticed there were some sites which immediately released this article or at least a reference from Mitchel Zoler. These sites all come from the same ip address and they all look the same next to next another.

    Non-authoritative answer: canonical name =

    Some of the sites under this scheme:

    * This is the place where Nasrallah “Draws praise” to Larusidone

    * This is the place where Nasrallah is the leading director or whatever. “Findings” about Larusidone were published here, or at least now a link to the next site ..

    * At the current time, here’s the article that draws praise:


    All of these sites come from the same ip address and all of them look like some crap shit made for idiot doctors.

  • If there’s one thing Nasrallah is certainly supporting for, it’s the use of “atypical” neuroleptic injections. They have a patent for many years. He suggests for a more wide use of “atypical” neuroleptic injections. He also suggests that as a psychiatrist, once you’ve started a patient on an injection, you should never stop, you should not even switch to an oral form of the same drug, because disaster will ensue. This is already known.

    However, he’s also promoting the oral form of a new neuroleptic Lusaridone, which is kind of haloperidol of atypicals. It hits dopamine D2 very hard, and also serotonin 5-HT2a which perhaps entitles some people to claim the drug “atypical”. It hits those receptors very hard but doesn’t work so much on histamine receptors, etc. Apparently, the results haven’t been very good. However, Nasrallah has been very excited about this particular drug:

    Nasrallah: Newer Atypical Antipsychotics Draw Praise

    “It has placebo-level metabolic effects,” said Dr. Nasrallah, professor of psychiatry and neuroscience at the University of Cincinnati. “The metabolic profile is better than for Geodon [ziprasidone] or Abilify [aripiprazole], which are currently accepted as the least metabolically adverse atypical antipsychotics.”

    Earlier on this thread I posted about Nasrallah’s opinion about weight gain and neuroleptics:

    “Dr. Nasrallah: Yes, I analyzed data from CATIE as part of the metabolic working group and am presenting the findings at the 2007 Society of Biological Psychiatry and American Psychiatric Association meetings.[13,14] Because several investigators had found that patients who gain weight seem to respond better, a statistician and I examined the relationship between weight gain and therapeutic response. We found a strong relationship between weight gain and improvement on PANSS positive-symptom and total scores across all the medications prescribed in CATIE, whether FGA or SGA. In each case, the more the weight gain, the lower the psychosis score at the end of the study.

    This finding suggests that weight gain is part and parcel of improvement, although excessive weight gain, which happens with some of the SGAs, is not necessary. We know that patients with schizophrenia already have high risk for metabolic syndrome with and without antipsychotic treatment, and they tend to be poorly treated for diabetes, hyperlipidemia, and hypertension.”

    Can’t you see, that with your own pharma propaganda of drug propaganda concerning lurasidene, you contradict the incredible suggestions you made earlier concerning weight gain and typical/atypical neuroleptics?

    Lurasidone is the haloperidol of atypicals (D2 Ki = 1.7 nM, 5HT2A Ki = 2.0 nM). If you think that haloperidol should be banned, then a ban on lurasidone should be considered as well. Yet Nasrallah promotes it.

  • Nasrallah has continued the discussion on his site, Current Psychiatry.

    A forum for haloperidol

    “The efficacy and neurotoxicity of haloperidol are independent mechanisms. Blocking dopamine receptors controls psychotic symptoms, but neurotoxicity involves triggering apoptosis, increasing free radicals, binding to sigma receptors, increasing intracellular calcium, decreasing neurotropic factors, increasing P53, T-box, Jun kinase, etc. Neurotoxicity is separate from extrapyramidal side effects. Similarly, the neuroprotective effects of atypical antipsychotics, such as enhancement, neuroplasticity, increasing neurogenesis, and growth factors, are separate from their antipsychotic efficacy.

    The assertion about the neurotoxicity of haloperidol is based on 28 published studies in neuroscience journals (which are rarely accessed or read by clinicians). Thus, the terms “premature and damaging” do not apply. I served as a messenger summarizing all these destructive properties of haloperidol1 and I certainly was prepared to parry and deflect some arrows.”

    You don’t do science by counting how many published studies you’ve found that support your case, or showing how huge list you can make of different chemicals that maybe relate to haloperidol neurotoxicity.

    “I served as a messenger summarizing all these destructive properties of haloperidol1 and I certainly was prepared to parry and deflect some arrows.”

    I guess in reality he wasn’t really prepared for the feedback that he’d get. If you do a Google search for for instance, “nasrallah haloperidol”, this thread comes up before his writings.

  • I just read this article from Science: Changing brains: why neuroscience is ending the Prozac era.

    It talks about what will perhaps be the next trend in psychiatry too. It’s about the new circuit based thinking of brain. Instead of causing changes in receptors all over the body and brain, perhaps it’s better to affect specific circuits in brain, or so the thinking goes.

    “Big money has already been committed. The Obama White House has promised $3bn to develop technology to help identify brain circuits, while the National Institute of Mental Health has promised to move its seven-figure funding away from research into conditions such as schizophrenia and depression towards a system that looks at how brain networks contribute to difficulties that are shared across diagnoses. This project, given the unspectacular name Research Domain Criteria or the RDoC Project, is being cited as an eventual replacement for the diagnostic system used by current-day psychiatrists.”

    Insel has clearly been promoting this RDoC program of NIMH. His famous criticism of DSM-5 just before the release promoted explicitly their own RDoC. Now here’s an idea. He has figured out that the criticism of current drugs (our “Whitaker empire”, etc) may actually be used to promote their RDoC program.

  • Of course the term “anti-psychiatry” is denigrating. I have nothing against people creating a new meaning for the word “anti-psychiatry” in our current or future culture, but in the mean time, perhaps from at least strategical point of view, it’s often more useful to say something like you’re not anti-psychiatry, you’re something else. Maybe you’re critical of psychiatry, etc.

  • So part of my point is that things such as chemistry and biology can be both used to advance the case of biological determinism and our case. We can perhaps explain how environment, meditation, exercise, etc, can change our body, brain, gene expression, etc. Biological explanations as such can be used for “good” or “bad”.

  • Even very large portion of common people who read newspapers these days are quite interested in natural sciences, physics, chemistry, biology, etc. I also think particles, molecules, cells, neurons, etc are involved in almost everything that we experience. If you think about meaning of words, I guess something like anti-biological psychiatry can also work against what many of us are trying to do. Many people who hear that these people are anti-biological psychiatry will instantly think that they’re idiots who think what happens in body or brain doesn’t matter at all. Of course what happens in body and brain matters, if you don’t sleep for several days your experience probably will be altered, maybe your body is flooding with stress hormones, etc, etc. If you take drugs that affect central nervous system, your experience often will be altered.

    What I agree is most harmful is something I’d perhaps call “biological determinism”, by which I mean explanations of people who are mentally inferior by birth, through explanations of genetics, schizophrenia and other mental illnesses as inherited cellular level brain disease, etc. Sociobiology was kind of a precursor to much of current biopsychiatry. Biological determinism is kind of like “biological explanation of natural sin” and it’s often used as a powerful tool of behaviour control.

    However, many people who think they are thinking “objectively” or in a “neutral scientific way” value a lot stuff from natural sciences. I see that ultimately natural sciences try – or should try – to study and explain parts of our common universe, without any social, psychological or political goals. Understanding of core natural sciences, such as physics, chemistry and biology, can be used when arguing for politics of different views. For instance, maybe the concept of neuroplasticity is useful for our movement. We can explain how central nervous system can change through exercises or environment, it’s not all inborn. Some people studying (epi)genetics are saying similar things about genes: environment and our experience of world (mind) can quite rapidly and radically change the expression of genes. See this nice article “The Social Life of Genes”

  • The word “anti-psychiatry” often has lots negative connotations to it, that’s why they use it. “They’re scientologists, they shouldn’t be taken seriously”. The word has come to have the connotations over time. Many people these days feel safer to say they’re critical of psychiatry, critical psychiatrists, etc, instead of saying they’re anti-psychiatry. But I don’t see why the same word can’t be polished and take yet again a more noble meaning in current or future generations.

  • She’s not “recommending” neuroleptics for psychosis. She’s has been attacking the use of psychiatric drugs and psychiatry with her books and articles. I personally think the core thing is that people are given most neutral or objective information possible and then they have absolute *choice* to take or not to the drug. I’ve read some typical mental health boards and some people there like to eat their neuroleptics. i think they have right for that decision, and I think I should have the right to never have neuroleptics inserted in my body without my will. Some people may perceive neuroleptics as useful for them, and it’s their right to perceive so. In my opinion, Moncrieff certainly is not trying to promote the use of neuroleptics in any cases, she’s attacking their use. In some older slides she showed how in some old studies benzos and opium were about as effective in treatment of psychosis as were neuroleptics.

  • I respect both Sandra and Moncrieff greatly, yet I think there’s a slight difference between them. Sandy is maybe trying to find the “neutral” position. Moncrieff has been working and publishing actively against use of drugs for years from many different points of view. She’s not trying to create “treatment guidelines”, most of her work is critique of psychiatry. For instance, she can probably have much greater effect if she as a doctor won’t go out raving about banning all neuroleptics in all cases, etc. If she did that, a large number of people would not take her seriously.

    See, for instance, this older article:

    Myth of the antipsychotic

    Other media had been talking about problems of SSRI use around 2008, but she got article in a popular newspaper where she criticises the use of neuroleptics as well. Etc. Etc. She has been actively campaigning against “chemical cures” for years, certainly not advocating their use. In a way, I don’t think she’s trying to build some kind of a general treatment guideline but is quite effectively criticising drugs and psychiatry with her articles and books. How is that bad?

  • I liked this description of self-experimentation in Joanna’s article:

    “For the first hour I didn’t feel too bad. I thought maybe this is okay. I can get away with this. I felt a bit light-headed … [After being asked to fill in a form] I couldn’t have filled it in to save my life. It would have been easier to climb Mt Everest … It was accompanied by a feeling that I couldn’t do anything, which is really distressing. I felt profoundly depressed. They tried to persuade me to do these cognitive tests on the computer and I just started crying.”

    Here’s another self-experiment:

    The Israeli researchers [Belmaker and Wald’s (1977) letter to the editor]( of the British Journal of Psychiatry reporting their personal experiences of haloperidol:

    “Haloperidol is an effective antipsychotic agent which is a relatively specific blocker of dopamine transmission in the brain (Anden et al, 1970). As part of the preliminary trials in a study of possible dopaminergic mechanism in affective disorder, the two authors each were given haloperidol 5 mg intravenously in a two-minute push. The effect was marked and very similar in both of us: within ten minutes a marked slowing of thinking and movement developed, along with profound inner restlessness. Neither subject could continue work, and each left work for over 36 hours. Each subject complained of a paralysis of volition, a lack of physical and psychic energy. The subjects felt unable to read, telephone or perform household tasks of their own will, but could perform these tasks if demanded to do so. There was no sleepiness or sedation; on the contrary, both subjects complained of severe anxiety.

    The present experience was similar to that previously reported of neuroleptic effects in normal subjects (DiMascio et al, 1963; Heninger at al, 1965), though previous studies used neuroleptics which block both dopamine and noradrenaline receptors (Anden et al, 1970).We used a relatively specific dopamine blocker, haloperidol, and experienced profound cognitive and emotional restriction. Dopamine blocking by neuroleptics may function to restrict cognitive and emotional processes in normals as well as in schizophrenics and thus it is possible that it does not specifically antagonize schizophrenic pathology. In the presence of psychotic anxiety or delusions, such cognitive or emotional restriction may be desirable and therapeutic. However, the restrictive effect may be a general one…”

    These days neuroleptics are prescribed very easily for all kinds of patients. Psychosis, insomnia, anxiety, depression, behaviour problems in elders and young people, etc, etc. If doctors are ready to give these drugs to all of these people, why don’t they more often test the same drugs on themselves to see how they actually work from a subjective point of view? That would probably help them to understand their patients better. In a way, I have much better understanding compared to doctors of what dopamine antagonism, etc, does, because I’ve done it for a long time, observed its effects, and then came back to the experience of not having these drugs in my body. Are doctors so much cowards that they dare not to try the drugs they prescribe daily to their patients for just one day? So that they’d understand much better how these drugs actually work?

    It’s like a person who has never taken any alcohol trying to describe the effects of alcohol from what he has read about it.

  • By the way, I read that book from Julian Jaynes in my youth, and it greatly shifted my thinking. Today I would be much more critical about the work, but i still can’t deny that the book is one very original and even inspirational one. I think I’ll have to read it again with a new mind, and with great respect to now deceased Julian Jaynes.

  • Heh, some of these current biopsychiatrists have some strange articles or interests in their past. For instance, Henry Nasrallah was interested in Julian Jayne’s theory of bicameral mind (The Origin of Consciousness in the Breakdown of the Bicameral Mind):

    Nasrallah, Henry (1985). “The Unintegrated Right Cerebral Hemispheric Consciousness as Alien Intruder: A Possible Mechanism for Schneiderian Delusions in Schizophrenia”. Comprehensive Psychiatry 26 (3): 273. doi:10.1016/0010-440X(85)90072-0. PMID 3995938.

  • I personally currently do use zazen (Zen meditation) for healing, transforming my mind, etc. I’m not saying it doesn’t work for that. There’s many kinds of Zen Buddhism and practices of zazen. I’m just saying that what they’re doing in many of those Zen Buddhism schools, and also other intensive meditation schools in Buddhism, may be too intense and not not really useful for people with severe mental problems or coming out of drugs. For instance, I went to one local Zen school and even the beginners had to sit 30 minutes in a strict single position watching the wall doing their practice (such as counting breath), then a short walk, then 30 minutes more. On some days, there was a third round of that. And after maybe six months the more enthusiastic people start to go to more intensive retreats, or even go living in a modern version of monastery.

    Maybe what I think is that the hardcore way zazen is practiced in many of these places is not the best bet for healing. Much of Zen comes from monasteric tradition and aims for enlightenment, not for curing “mental illnesses”. At the same time, it has many great practices which could be useful also for treating mental problems.

    I’ve not gone much down to this mindfulness therapy, but I’m not against it, I think it’s a positive thing that they’re trying this type of things in Western therapy situation. I really haven’t studied it more thoroughly, but for instance Jon Kabat-Zinn has been a serious Zen practitioner and he has been a great leading force behind this mindfulness therapy thing. But I admit I really haven’t studied him or this system of mindfulness therapy.

    In any case, I can say these Chinese practices of tai chi chuan, kungfu and and chi kung, and also the more Japanese kind of zazen, have all helped me in this path. I don’t need the stuff I think is included in that mindfulness therapy, because I think my current practice includes all or at least most if it.

    There can be many reason why that kind of therapy doesn’t work for everyone. Maybe some people just are too much “Western” in their nature, that kind of practices don’t help or interest them enough. They just don’t “get it” or in other ways don’t find it useful. Maybe some people expect too much too soon. Maybe people don’t have the understanding, life-situation or discipline to make it a daily habit. Maybe they expect too much too soon, then go back to their old habits. The point is creating new habits in your mind/brain! It won’t come with without effort.

    So in general, I’m positive about this mindfulness therapy movement, I’m also positive about thinking about how other Eastern techniques could be used for treating or, even better, preventing these Western mental illnesses.

  • I’m not you, but I gained 25 kg while on Seroquel and Abilify and while withdrawing from them. I guess I gained some weight after I had stopped them too, though it may have been because of bad eating habits I had developed. Then I lost those 25 kg in a year after I started to each low carb, real healthier food diet and increased exercise. Maybe your body needs to adjust again to this new situation and it takes some time.

    Here’s article “Why Zyprexa (And Other Atypical Antipsychotics) Make You Fat” which points to a study where Zyprexa makes body use fat instead of sugar travelling in your body, possible leading to insulin resistance, etc. If that’s true with Seroqual, then it may be one good reason to go low sugar/carb in diet if you’re taking or withdrawing from these drugs.

    I’m sure you’ll get your weight down eventually!

  • I won’t go very deeply on this topic, at least right now, but I was quite interested in this class of drugs (psychedelics such as LSD or shrooms) in my youth. When you’re under influence, a doctor would quite likely diagnose you psychotic. They’re enormously powerful drugs and the experience and outcomes are largely determined by several factors (“set & setting”). Sometimes, maybe used in some types of manner, they can certainly lead to big problems.

    In any way, here’s some thoughts to explain the results. One, perhaps quite large group of people interested in these drugs are interested because they are more “intelligent” in the sense of “thinking out of box”, they like to try new things, etc. So in a sense, the people who try these drugs are kind of a self selected group. Second, these drugs are not an easy way to escape if you are having emotional problems (“heaven or hell”), there are many other drugs that are easier to escape. They can make up for hours of total hell, and maybe the people who take them for years have their marbles and life together to begin with, and that enables them to take psychedelics repeatedly. It’s also possible that some of them have improved because of psychedelics. I don’t know. Etc.

  • I don’t have much experience with herbs and acupuncture, but I have more experience with chi kung (qi gong) and tai chi chuan. I’ve sometimes mentioned I currently practice zen meditation, but I try to also tell people it may be not be the best choice for treating mental problems or drug withdrawal as such, at least in the way it often practiced. It may too hard, ardous, “anvanced”, etc, for many situations like this, at least in the way it is currently practiced. I’ve now heard many stories of people getting admitted for psychosis after doing severe zen practice in my local school, even though these are often related to very hard practice, such as doing a daily practice or going to intensive retreats.

    I’ve also read similar comments from some “gurus” of this field. For instance, one of them said that you shouldn’t do zen meditation if you’re constantly depressed or anxious. He recommended to first practice kungfu to get your body in shape. Then later on you should move to chi kung, which when practiced in a right manner is kind of a combination of movement, meditation and mindfulness. There are actually a huge number of these techniques, some more relaxed and flowery, some done for improving martial efficiency. And then you should move to zen meditation. I don’t say I really have enough experience to confirm this though. I think there’s huge potential to change your mind and body with this type of exercises, just keep in mind that if you’re using them to heal yourself from great distress, anxiety, etc, some of the hardest techniques and authoritarian schools, etc, may not be the best technique in that situation. A gentler technique may work better at that point of life. I think that chi kung techniques could be developed to at least as efficient technique for therapy in Western society as current mindfulness therapies done. Well, they have lots in common to begin with.

    I know chi kung or tai chi chuan may look silly on video, but it’s not just those bodily movements. Just doing those movements like they’re done externally is not enough, you’re supposed to work inside your mind at the same time, learn to get into the relaxed state of mind, etc. In a way, it’s another system you can use to retrain your mind/body complex (neuroplasticity, etc). Maybe similar to hatha yoga.

  • “What did you think of my two part response below on informed consent and the possibility that Benzo prescriptions may actually be a causative factor in SSRI post withdrawal problems?”

    I read through those posts with great interest, but I feel it’s somehow out of my scope of understanding. I know things about mechanisms of some of these drugs on brain and mind, in part because studying the functioning of brain has been my hobby and interest for many years, in part because because I have direct experience of dopamine agonism and antagonism, etc, and their effects. For instance, I’m not saying much about lithium because I’ve never taken or researched it. In a similar way, I don’t have strong opinions about causal factors of SSRI/benzos in this case because I feel I just don’t have enough understanding or experience on this issue.

  • I just read through what I had written here and noticed I made silly mistake. Yrjö Kallinen is another significant person in the history of Finland, he publicly talked about Eastern systems, theosophy, etc, in early twentieth century. The influential person researching schizophrenia treatment in Finland was Yrjö Alanen. I don’t know how I did that.

    “I think the system of Open Dialogue, which has roots in at least 1970′s in the history of quite socialist Finland (Yrjö Kallinen, etc),” …

    Biography of Yrjö Alanen:ö-alanen

  • Ahahaha. Great link! Maybe next time some psychiatrist or psychologist suggests I have a mental illness, I can point them to this list and say that it’s actually eccentricity.

    “Nonconforming attitude
    Intense curiosity
    Happy obsession with a hobby or hobbies
    Knew very early in their childhood that they were different from others
    Highly intelligent
    Opinionated and outspoken
    Unusual living or eating habits
    Sometimes not interested in the opinions or company of others
    Strong moral obligations (against infidelity, strong family values, ultrareligious)
    Mischievous sense of humor”

  • I read the biography of Steve Jobs (Isaacson). He also had many eccentric qualities and many would say he often was an asshole, but at the same time he’s close to worshipped by many people, the eccentric qualities almost being a proof of his “brilliance”, etc.

  • Richard: “And Benzos are wonderful drugs in a hospital setting, but outside of a hospital they are perhaps the most dangerous and misused drugs in the world.”

    Yeah, I pretty much agree. In one sense, when used in a right manner, benzos are perhaps the most efficient and safe psych-medications out there. They hit the right button in brain to reduce anxiety and they’re not very toxic to the body. I’m not totally anti all drugs, I think there’s nothing a priori bad about ingesting chemicals which affect your nervous system. While I agree that they often cause severe problems when used chronically, at least I would like to write some statement that if I ever get hospitalised because of full-blown psychosis of any kind, I will not accept neuroleptics in any situation, but it may be OK to use benzodiazepines in the acute phase.

    Currently they claim that people in psychosis have anosognosia, etc, so they don’t understand what’s best for them. Why can’t I make a statement when I’m not considered psychotic that because of my understanding of the functioning of brain, mind, my own mind, and so on, if in future I get closed to a hospital because I’m considered psychotic, I still do not want to take neuroleptics. That way they couldn’t claim the choice is because of anosognosia or whatever, the decision was made in a “normal” state of mind. I read that in Finland, there’s some national program trying to improve the treatment of mental illness, and one part of it is that a person can fill some official sheet about his will if he gets hospitalised because of mental illness. When I looked at the sheet they proposed, it seemed totally useless for actually affecting your treatment. It had a checkbox “If you get hospitalised because of mental illness, do you want to get treatment according to the best known scientific information about mental illness? yes/no”. Ridiculous. If a person says yes to that, it means that they’ll still get treated with neuroleptics because those people claim it’s the best scientific information. If they don’t check that part, it doesn’t make any difference. Sheets like that only give people feel they are in control, they don’t change the treatment at all.

  • Part of effects of alcohol are because of their effects on GABA receptors, just like with benzos. In addition to this, alcohol is also for example NMDA antagonist. In a way, you could try to simulate being drunk by taking ketamine and benzodiazepine together. The ill effects of alcohol are well known. If you took a low dose of benzo, roughly equivalent of one or two cups of wine with dinner, you’d probably have no big problems.

  • “it’s just that the profession needs to admit that these problems are not primarily medical and they have to be able to be humble about the possible role of any medical approach and to acknowledge their own uncertainty about what is really going on, as do psychiatrists within Open Dialogue.”

    Ron, I like what you’re generally saying. But. I think the situation in Finland is just as fucked up as in Western European countries. I can say that much because I have liven all my life in Finland. I don’t think you foreign people totally understand the history and homogenous nature of Finland. The people up there in Northern Lapland are even more divorced from other kinds of cultures, though they see other cultures more and more through TV, internet, etc. There was just news that while in 2006 or so Keropudas was second lowest in forced treatment (binding, etc) in Finland, now it’s the second topmost. The manager of the hospital, Birgitta, explained that the types of patients have shifted during these years. They now get more and more of drug related cases and it’s the only place for this kind of patients to go in that province of Lapland. That is, maybe they’re kind of getting the torrent of current Western culture and it’s not all nice even with their family therapy.

    Some people living in that area also complain about weird people wandering around and demand a change in the system.

    I think the system of Open Dialogue, which has roots in at least 1970’s in the history of quite socialist Finland (Yrjö Kallinen, etc), is mostly interesting in that that particular place used neuroleptics in cautious manner. They had studies where one place used neuroleptics every time and other place used neuroleptics cautiously.

    Still, I’m not convinced Open Dialogue (kind of a family therapy) is the right answer. During the last meetings with my therapists here in Helsinki, I told her about all these problems in psychiatry, and mentioned Keropudas. She then told that she was working there earlier in her life. But she still was kind of cruel and non-enlightened even in our last meeting. For instance, when I tried to explain how they had made my life harder, she suddenly said “do you think we are thinking bad thoughts about us”, as if suggesting my critique is due to some illness in my brain or mind.

    In total, while I agree with most of you people write in this site, I think the system of Open Dialogue is currently almost too idealised and promoted in these circles. You don’t really understand the homogenous culture of Finland and Lapland, and their experiences can’t be totally extrapolated to other countries.

  • Yeah, the point of ‘more’ button kind of was that if you’re not interested in that topic or post, it doesn’t distract so much from what you’re trying to do. Circumventing ‘more’ button by breaking one long post in 12 or so different posts is worse than posting a long post with or without a ‘more’ button. Note that I’m not saying anything about claims made here, just the posting style. If other people posted their long posts like that, this would be a mess. “My argument is so important that every person needs to see every single word of it, if there’s a more button some of them see only part of it and that’s unacceptable.”

  • Exactly. I’ve mentioned Chorover’s book From Genesis to Genocide before, but I’ll do it once more. Published in 1979 and tracing the history and methods of sociobiology and behaviour control, the book somehow widened my thinking about the current state of psychiatry. I increasingly started to see current diagnosis systems, psych disclines, drugs, claims of biological determinism, claims of genetic or brain disease origin of mental illness, etc, as quite strictly following this historical tradition. There’s still this group of people claiming other group of people are inferior by birth and they are thus entitled to control the behaviour of this other group. Their claims about the mechanism change over time but the general idea stays the same.

    I’ll type some quotes from the book:

    “Measurements of facial angle were not White’s sole interest, however. He reported, and later measurements would subsequently confirm, that Africans have coarser and larger-caliber hair than Europeans. The fact the caliber of hair taken from African apes was closer in diameter to that of blacks than of whites led White to the familiar conclusion that blacks were “closer to apes”. That this is intended to mean, of course, is that blacks are, on the average, “behind” or “below” whites in terms of their biological, intellectual, and moral development.

    It is worth noting, in connection with this argument, that it is not necessary to emply explicitly perjorative stereotypes as a means of formulating questions about superior and inferior classes of human beings. All that is required is a system of measurement and an uncritical acceptance of the concept of biological hierarchy.

    In 1850, for example, Dr. Samuel A. Cartwrith, a respected physician who . . . to investigate and report upon “the diseases and physical pecularities of the negro race” . . . It begins by claiming that the biological and medical status of blacks “has not been the subject of much scientific investigation, and is almost entirely unnoticed in medical books and schools”. Cartwright proposed to remedy this lack with an ingenious psychobiological theory in which the “defective … atmospherization of the blood, conjoined with a deficiency of cerebral matter in the cranium,” was put forward as “the true cause of that debasement of mind, which has rendered the people of Africa unable to take care of themselves.”

    . . . Cartwright concluded by claiming to have demonstrated “… that there is a radical, internal, or physical difference between the two races, so great in kind as to make what is wholesome and beneficial for the white man … not only unsuitable to the negro race, but actually poisonous to its happiness.”

  • I also noticed that the number of views in “What’s Hot This Week” are in red. Red is a color that immediately takes the attention of people (except that of the truly crazy ones) and I personally wouldn’t use it like this, as if the number of times people have read the article compared to others is the important thing. No matter how small or big the numbers are individually or compared to each other, look at them!

    However, I also think this discussion would better fit here:

  • During the last 15+ years, I’ve withdrawn from SSRI several times, twice after three or more years of continuous use. I probably won’t have to withdraw no longer since I’m not gonna use them anymore. Anyway, even when on our last meeting with doctor last autumn, where I gave I gave heavy critique about what they had done and psychiatry in general, my psychiatrist, after I had at time withdrawn from neuroleptics, suggested that I could stop SSRIs (I had already done so without telling her) and said I might feel melancholic for a while and then it’d go away. My experience has been entirely different.

    First time I withdrew, I got brain zaps, etc, while going down. Otherwise, I think I felt quite good, as if I got my spirit back. However, similar to what Shipko said, I think I noticed quite early on that after a longer time, such as after three months, I started to get worse and even got effects that were different from what I started with. I think there were many different physiological things at play here, the body adapting to SSRI and the rebound, etc. I don’t know, or think, I would have got much better just by waiting for the effects to go away. I practiced and experienced years with different systems, similar to what Monica has been talking about, and gradually learned more about how my mind was connected to my body, I learned to listen my body and work with it in various means. Last years’s autumn when I quit SSRI after 3-4 years of use in a short time, it was no big deal compared to the times I did that earlier, and I think it’s because of what I had learned during all those years and my application of it. Still, at least in current time, there are no perfect systems which will tell you what will work for you, it often requires plenty of research, self-experimentation, practice, time, etc. I’m just getting grip of what works for *me* but I don’t claim it works for others.

  • Oh, and of course I forgot to mention places like Delphi. Delphi is located in a mountaneus place next to sea. There are the ruins of the places where the oracles used to see things and direct decisions of other important people. (You can also take a taxi ride up the mountains to the ancient cave of worship of Pan and take a walk down to Delphi through the old path. It’s a great day-hike.)

    I also traveled to the place of Eleysian Mysteries, an hour or so bus ride from Athens. Prominent people from Athens would travel there yearly to get an initiation of a kind, an initiation which perhaps involved visions, etc.

    Much of what took place there would maybe be considered as schizophrenia in today’s world.

  • Thanks for clarifying your point, Donna. I just asked because I’m quite interested in these old pagan gods, the ancient culture of Greece, Rome, Egypt, etc, the ancient philosophers, and generally what happened at the time. There is infinite amount of parallels to the modern, or should I say post-modern world, and metaphors to derive from there, etc. For instance, when I travelled in Pompeii and Santorini, I noticed they were quite packed cities, with one kind of temple for Venus (Aphrodite) who was a patron for love and many woman qualities. Walk 20 meters and there was a main street with statues of Zeus and Mars. Turn right, and there’s a temple for Isis, the Egyptian mother god. Of course these kinds places were for the elite and soldiers, etc, not for the slaves, but at least among them there seemed to be a great good-will towards worship of other gods.

    Nietzsche and other people have written interesting comments about the polytheism of pagan cultures. I just love to think about the ancient system. I just asked because in many ways, the world of those Greek and Roman gods was also totally different from the Orwellian/biopsychiatry world. For one, there were many different gods to choose from.

    Your explanation of the capricious, teen age, etc, nature helped to figure out what you were referring to. 🙂

  • I’m not officially a Buddhist, but before I was put on neuroleptics I regularly practiced zazen (the meditation system of Zen Buddhism) and also things such as Tai Chi Chuan. When I was put on neuroleptics, I quit all of these in some months. One reason was that they lost a point in a way. I stopped getting any kind of benefits of them and they became a huge burden. For instance, I remember being on a six-hour weekend camp where I was just so tired and uninspired that I just kept wishing it would stop. Now I’ve again started with zazen and hiking (not Chinese/Taoist techniques right now, but that’s in part because of other issues such as time).

  • “Do you bookmark things and collect links Hermes?”

    Actually, this is a thing I’ve been struggling for ages. I kept bookmarking links I thought I might need later and kept creating increasingly complex folder structures, but the result was so huge and complex that I never bothered to use it, usually Google found what I was looking for much faster. And the pages could also go away. Right now I have only services I visit quite regularly but are too hard to find with Google in my bookmarks. For instance, to get to this site I write “mad in america” in Google search bar or just the address bar, but to go to my work email, I use a bookmark.

    I’m bit of a geek too, so what I describe here is maybe not useful for everyone. When I find a scientific article (usually PDF) that I think is important, I save it to a scientific article management program called Mendeley. It has programs or apps at least for Windows, OS X, iPhone and iPad. The idea is that you download the PDF files to yourself in that program. Then you can do searches through the files, star them, tag them, organize them in groups (psychiatry, mathematics, etc), add other meta-information such as what was the original link, your own comments, etc. You can also sync all of this between, say, iPhone and computer. It’s free up to a limit.

    With just web pages and other stuff, not strict scientific PDF articles, I use Evernote for a similar purpose. I’m not totally satisfied with its user interface, but it works in a similar way to Mendeley for those things. You can take a “snapshot” of a web page to that program, create folders and tag files, etc. You can do searches through the pages you’ve saved, and if a page goes away from internet, you still have a copy of it.

    I have similar systems at least for my own plain text notes, images, etc. I also use Dropbox. There are many other programs or systems like Mendeley or Evernote as well. But yeah, I stopped bookmarking pages which I thought might be important later on. That system didn’t work very well for me personally, I just collected a huge number of links that I never used in practice.

  • I’m not talking for Anonymous, and I think we may disagree on this a bit, but .. I’m anarchistic on many levels of abstract, scientific, methodological, etc, thought, but a totally anarchistic society would not work until all people of the society had a high level of self-control, etc, which is not the case – it could easily lead in people creating even more oppressive police states, etc. Maybe in a sense I agree that the government should be kept to minimum and individual freedom maximised, is that a libertarian position? I also understand many of the arguments in some of the more social systems. Heh, maybe that’s the cause I’ve never been so interested in politics, I never find I clearly belong in left/right/whatever party. 🙂

  • Thanks, Richard. I made that comment about your age on a drunken weekend evening with wine, etc, and I understand that it may sound confusing. But what I meant, perhaps, was that you still seem to have some of that “rebel” spirit, or maybe the good kind of 60’s spirit in you, you’re still fighting for this cause. Many people are “rebels” in their 20s and then give in to the “regular” way of thinking, this happened even with many of the hippies of 60s. Many of them found a comfortable job later on and had no courage or interest to talk about different types of fundamental problems in our society later on. I’m not sure if it’s even about being “rebel”, but maybe some kind of awareness .. Still learning new things, still wanting to change the world, that kind of thing, see? It seems lots of people even of my age have already given up on that kind of thing. In a way, you are still carrying torch instead of bullshit, and that’s a great thing.

  • And I must highlight that reference by Richard to Bob Marley (“emancipate your mind from mental slavery”). Lately I’ve been listening to some reggae music, esperically Marley, and I think we need plenty of similar kind of rebel attitude in our movement. Someone said a while ago on this forum something akin that the battle concerning mental illness is the last great human rights battle.

    Bob Marley – Redemption Song Live In Dortmund, Germany

  • And yes, my position in this death rate issue is pretty much the same as that of Ron and Anonymous. Dying even 15 years earlier *on average* is a huge difference. A lot of it is because of drugs, especially in the current era of “atypical” neuroleptics. Telling about this huge problem is not the problem, I think it should be told even more widely. In mathematics, you can prove whole claim to be false with “proof by contradiction”. That is, for example, if you claim that “all people who start taking drugs die 25 earlier or more” and they find just one counter-example, your claim is refuted.

    People in this movement constantly talk about psychiatry being pseudoscience and so on, but claims like that are not very convincing if we claim “scientific” facts which are so easily dismissed. I once told one woman about studies such as Harrow, Andreasen, etc, and she asked her psychiatrist about these issues. He said to each question that “there are no such studies”. Then he gave her a lecture about Scientology. The term “anti-psychiatry” has also become a denigrating term in our society, so people like Lieberman use it. Also, even in our current society even common people think they are quite scientifically minded and objective. If they read claims which they can easily refute, it will decrease the effect of all that we have to say.

  • I haven’t read that paper from Healy, but Healy himself posted these things in MiA quite recently:

    La Reine Margot: Data Access, Ghostwriting, Suicide and Mad Reviewers

    “Patients with psychosis, just as they were 100 years ago, are now 4 times more likely to be dead after 5 years of treatment than the rest of us. Patients with schizophrenia are 11 times more likely to be dead – this is much worse than 100 years ago.”

    Mortality in schizophrenia and related psychoses: data from two cohorts, 1875–1924 and 1994–2010

    “We found a 10-year survival probability of 75% in the historical cohort and a 90% survival probability in the contemporary cohort with a fourfold increase in standardised death rates in schizophrenia and related psychoses in both historical and contemporary periods. Suicide is the commonest cause of death in schizophrenia in the contemporary period (SMR 35), while tuberculosis was the commonest cause historically (SMR 9). In the contemporary data, deaths from cardiovascular causes arise in the elderly and deaths from suicide in the young.”

    The causes of death in people diagnosed with schizophrenia or related psychosis between these time periods vary, but here even Healy is not saying this group of persons had a normal life span in the historical period.

  • Thanks, Donna. When talking about studies with schizophrenics and bipolars, I know very well about their vague nature. I personally have had both of those labels, and now that I’m totally out of the system, I don’t eat any meds and I’m not seeing any psychiatrists, I guess I don’t have either of these disorders anymore in a sense. If there’s no one to label me, I don’t have the label. When scientific studies talk about schizophrenics or bipolars, they mean people who some psychiatrist has classified as such. When talking about such studies, it’s often convenient to talk about studies done on bipolars or schizophrenics. I know it’s in other sense wrong, for instance there is no single disease called schizophrenia, it’s an umbrella term, but it’s also a valid term in the sense that they were all people who a psychiatrist had decided to label schizophrenic. So the studies were done on people labeled schizophrenia, bipolar, etc, by psychiatrists or psychologists. If I talk about people recovering from schizophrenia in this rate in this way, I mean schizophrenia in this vague way. They are people who some person has labeled with schizophrenia. That group includes many different types of people with different types of problems. That’s basically my position. I’m sorry if my use of terms has caused distress, but I think you’ll understand that with my history of getting labeled bipolar, schizophrenia, severe depression and psychosis and then quickly “recovering” by withdrawing from drugs and other means, I am extremely sceptical of all of these labels.

  • Does Whitaker’s book make your blood boil because he didn’t put terms schizophrenia and bipolar in quotes? I don’t see what is it that makes your blood boil with me since we share so much things. Is is that I’m also interested in biology, metabolism, neuroscience, the functioning of the brain and its relationship to mind? I see things such as biology and neuroscience at their core neutral, a study about how the world works. Psychiatry takes part of them and tries to use it as their advance. Similar data can be used against psychiatry, such as in showing chronic D2 blocking back make your life suck or atrophy your brain. Understanding of the metabolism of the body can help you eat more healthily (Peter Attia, etc).

    It’s just interesting that I get my fellow survivors’ blood boiling even though my position is very anarchistic on many levels and at the same time I’m trying to keep some kind of balance. Is it just because of my interest in biology?

    For instance, here I talked about my readings in sociobiology (Chorover: From Genesis to Genocide)

    It’s basically about the same thing that you say you’ve been spreading word in this recent article:

    If I still get your brain boiling boiling (beware, brain boiling could cause you brain inflammation which will shut your NMDA receptors), just give me a chance. I’m not all bad.

  • Donna, and I read and re-read about your disagreements, and I don’t really see where we really disagree with. For instance:

    “I also disagree that survivors or critics of biopsychiatry’s constant despicable lying and fraud in the guise of science which is evil pseudoscience created for the sole purpose to prey on the vulnerable and less powerful members of society as is the case with their constant despicable eugenics theories, should be required to fight this garbage with anything but firm rebuttals and exposure of the truth behind this monstrous evil and fraud per this article”

    To be honest, with my simple mind, I had to read and re-read this argument to understand our misunderstanding. My position is that I want to understand the “neutral truth”, whether it comes from survivors, science, neuroscience, etc. I know it’s constantly changing and we can newer achieve anything like “neutral truth”, but that’s a target, or a bridge and not an end. I attack the false statements made by silly psychiatrists, but I also attack false statements made by survivors. It’s just not true or at least proven that drugs cause 25 years or more reducement in lifespan in general. They do cause reducement, but not that much, or at least it is not proven by any means. And I have never said any psychiatrists are *required* for this this change. You make your sentences so incredibly complex that it takes a while to parse what you’re actually saying.


    “I agree with others here that the early deaths of those stigmatized with the worst, life destroying bogus labels with the bipolar fad fraud the latest justification for biopsychiatry’s fascist, predatory existence with Big Pharma/Government, are either directly or indirectly caused by biopsychiatry’s predation on the vulnerable, abused, traumatized and wounded. A majority of such people are able to rise above such adversity if they can avoid the further retraumatizing assaults of biopsychiatry and other social predators that guarantee general scapegoating, contempt, ostracism, stigma and destruction by most of society.”

    Do you claim I somehow disagree with you with all of this? How? I don’t. In what part exactly do you disagree with me?

  • I have to dispatch this to another level of talk because there’s no more a reply button provided in this level.



    You said,

    “Yeah. People with bipolar or schizophrenia die so much earlier than the general population and much of it is from drugs, but it’s not the only factor.”

    Actually, comments like this referring to “people with bipolar or schizophrenia” by supposed survivors drive me up the wall!

    Do you believe that these bogus, voted in stigmas exist in reality or is that a slip on your part that you are treating this “collective fantasy of science behind the DSM” per Dr. Allen Francis, ed. of DSM IV as something real?”

    Give me a break. I have tried to dutifully use quotiation marks whenever I remember to use to use them, though sometimes it seems like a burden. If I say some studies have found “bipolar and schizophrenics die this much earlier”, it doesn’t mean agree with their system of classifying people. I think I have made in many places clear my opinion that things such as “schizophrenia” or “bipolar” are not some discrete brain diseases. I have a very anarchistic position about this whole thing. That’s much of what I what I have been fighting for.

    My point was that that particular claim simply is not supported by science or other kinds of reasoning, and making such claims will make us look silly.

    Maybe when I told about schizophrenics and bipolars, it was a short-hand for “people who have been diagnosed with schizophrenia or bipolar by the current system”. Believe me, I understand the complexities. The studies talk about these groups, so I have to talk about the groups the studies talk about to make any sense of it.

  • Yeah. People with bipolar or schizophrenia die so much earlier than the general population and much of it is from drugs, but it’s not the only factor. Even things such as suicides are part of it, and though sometimes suicides can be seen in some ways to be caused as drugs, there are other factors too. Also, in those studies, 25 years has usually been the maximum estimated difference, studies saying things such as “they die 15-25 years earlier”. I haven’t looked too much into all these studies, but as I understand the schizophrenics have now been starting to earlier, maybe in part because of “atypicals” which can cause metabolical, etc, problems, which may cause cardiovascular, etc, problems. While ago there was a link to some study done on some Northern European countries (maybe Finland, Sweden, Denmark) about risks of patients dying from cardiovascular reasons. The paper noted that people with serious mental illness (schizophrenia or bipolar) die so much earlier. The bipolars had longer life-span and they suggested it’s in part because, even though neuroleptics seem to have come almost a first-line treatment of bipolar, bipolars still consume a lot less of “atypical” neuroleptics than do schizophrenics. I’m sure the drugs are causing more or less directly a lot of this gap in lifespan.

    However, the problem is that, for instance, if your opponent or even some lay people reads your story and notices something he can easily refute, they can use it as weapon against you or maybe they no longer take you seriously. I admit that I sometimes use this kind of techniques against my enemies, but it means I also need to be careful about what I actually claim myself. It’s similar to that discussion among survivor, etc, groups, if biology/neuroscience matters at all. If someone claims that biology/neuroscience doesn’t matter at all, there’s just our self/mind/soul, then it’s just so easy for them to dismiss you. “If biology/neuroscience doesn’t matter at all, why do you care about these drugs changing the function of your brain in the first place”, etc.

    In short, they can pick single claims, trivially dismiss them and by proxy dismiss all else you said. I agree there’s plenty of evidence that drugs often shorten the life, but there’s no evidence of the claim that they cause all of that 25 years. They notice there’s a claim that has no proof and they shoot it down.

  • Nice post, Nancy! I had never heard of this story. I love parallels, metaphors, analogies, fairy tales, etc, even though among all else my psychologist found with here tests that I have “concrete thinking” which presumably means I can only understand the literal meaning, not the abstract or metaphorical meaning. OK OK, I get it, these were real rats that really escaped from NIMH and we were not told about it! I just read the Wiki page of this story. I got many other parallels too, but I won’t go through them.

    Lastly, perhaps I’m so big nerd that I immediately combined badgers with this internet meme from a decade ago.

    What does the snake mean? Pharma or something even more sinister? Also, perhaps connecting mushrooms with drugs such as neuroleptics is not right since they often work in opposite ways in a sense. 😉

  • Yeah, I know that encrypting information can make you more suspect. Encrypting information can mean that they’ll keep it indefinitely, until they can maybe one day decrypt it. I read about this thing you posted about the day after I posted my comment. I personally haven’t been overly secret or concerned about my identity, though I’m not either directly revealing it all in public Facebook profile at this time, etc. I do encrypt my computers and backup drives, and also more sensitive data that I have in “cloud” such as Dropbox, but that’s more to block script-kiddies than NSA, etc.

  • Actually, I don’t think all of this is just pharma, just psychiatry, etc. All these fields are done by humans who have their own emotions, goals, etc. I think that I’ve observed that other kinds of doctors as well perhaps feel not too satisfied in part because they feel they have been losing some of their authority, respect and control. Some reasons for this are post-modern thought, internet, etc. But I’m sure many of them are annoyed by this.

  • By the way, I’m also currently reading Ben Goldacre and I do agree there are shaky things in other medicine too. I know doctors often have a lot wider base of information about different types of diseases and medications than I have. At the same time, I guess that many times if I got some disease, I’d listen to what a doctor says but also check and double check about it from articles other sources. I know that with time I could become quite knowledgeable of at least my own situation.

    When I was on neuroleptics, I gained 25 kg in weight and blood tests seemed to suggest problems with blood sugar, etc. So the general doctor gave me a lengthy speak about eating lots of fruit and bread, going low on fat, dairy and calories, etc. I did some research and experimentation and I lost those 25 kg by eating entirely differently than what they were suggesting. I restricted carbs and sugar (including fruit), didn’t count calories, didn’t go low fat, ate real food instead of processed, etc.

    For instance, I’ve seen how some people in ALS community do their own research with old off-patent drugs or other treatment. Some of the stuff is even quite promising, but pharma doesn’t seem at all interested in investigating those paths at all.

  • In this anti-anti-psychiatry article, Lieberman argues:

    “Being “against” psychiatry strikes me as no different than being “against” cardiology or orthopedics or gynecology—which most people, I think, would find absurd. No other medical specialty is targeted by such an “anti” movement.”

    But maybe this situation is not because of just those evil antipsychiatrists, maybe it’s because psychiatry is not the same as cardiology, orthopedics or gynecology! Maybe there are some *reasons* people still don’t think of psychiatry in the same terms as they think cardiology. I can at least walk away from a gynecologist or cardiologist without a fear that they’ll call cops who shut me down to an establishment where experts will forcibly perform gynaecological experiments, and I will stop the analogy before it gets out of hand. This besides many of those treatments actually have much more long term proof of their their beneficial effects vs adversal in long term use than have psych drugs.

  • Anonymous (can’t go further in thread because there’s no longer the reply button):

    subvet I’m not a mason but I’m a firm believer in self determination, individual liberty and personal responsibility.

    My favorite sculpture is this…

    Man carving himself out of stone. I look at this for minutes and remind myself that it is only me, not government, not some rescuer, not some random quack, that can sort this life out. It reminds me that the decisions I make each day, shape my life, and that ultimately I am in control.

    There is also female versions:

    Man, Anonymous. See, maybe three-four hours before I saw your post, I was at work, bored, without nothing to do, and for some reason decided to further research what my nick Hermes might represent. One of the first pictures from Google image search was a sculpture of Hermes where he was building a sculpure of another god or person.

    I had seen the picture before (I’ve been to Louvre, maybe I’ve seem the actual statue too), but it left me thinking about what the sculptor had thought about, etc. I don’t usually think about this kind of things and I don’t look at sculptures. It totally blew my mind to see after some hours the sculptures who were forging themselves. I can’t believe the synchonity. And I’m not suggesting I’m forging you people in any way, or whatever ideas you may get. 😉

  • Anyway, because of the unscientific qualities, and qualities of social and behavior control, psychiatry is a most vulnerable place. There is this problem in medicine, but it is not by just some random chance that psychiatry has become the biggest target of accusing of all this kind of fraud, like Lieberman seems to suggest. It really is the worst of all of medicine; it is not even real medicine.

    Lieberman: “Indeed, APA immediately and drastically reduced its relationships with the pharmaceutical industry.” No, pharma has drastically reduced its relationships with APA. It was not by APA’s choose.

  • They never did. But many of these organizations such as APA have been functioning with large amounts of money drawn from pharma. Lately the money from pharma to psycho drug research has been drying out and these organizations can’t maintain anymore the amount of research, etc, that they did earlier. This causes a panic reaction inside organizations: either start kicking people out or start getting more money.

  • Yeah, I haven’t read Szasz, but I have him on my quite long reading list.

    Today when I was walking in woods, I revisited the original suggestions in Harrow studies about locus of control related issues. I know Whitaker gave it another spin, suggesting that the other group fared much better because they were not taking neuroleptics, but there may still be something to Harrow’s suggestions about people having more internal locus of control, resilience, etc, survive because of these qualities. For instance, maybe in the current system you need these exact qualities to figure out on your own the drugs are not really helping.

    “In severe psychiatric disorders a more external locus of control is not specific to schizophrenia and after the acute phase is not associated with one particular diagnostic group. A more external locus of control is related to fewer periods of recovery, to both depressed mood and psychosis, and to various aspects of personality (p<.05)."

    It seems that the current psychiatry very radically tries to shift the locus of control from the person to themselves. Earlier people had demons, etc, controlling what happens to them. These days the demons are called bipolar, psychosis, etc. People talk about these as some demons external to them, demons which cause them to act in irrational ways. Then they go to witch-doctor who tries to banish demons with their mixture of frog skin and Datura. Yet they know that they can't ever live a real life in society because they have this demon living inside them. Demons control their mind and life and witch-doctors are their only hope in banishing demons.

    Since my teenage years I've been quite distrustful of official authorities and the common wisdom. I know there are people out there who have more knowledge or information about some special issue than I have, but I don't trust them because they have MD after their name, I decide if I should trust them based on what they are saying. Sometimes it even takes a "leap of faith" and constant evaluation of the current situation. At times, I've taken time to learn different areas of science, and after some time I've noticed that lots of the mainstream information is crap or boring. Often the most interesting and intelligent new information comes from the maverick or rebel part of the community, somewhat outside of the mainstream. Of course there are also plenty of true crackpots outside the mainstream. Feyerabend wrote a book on philosophy of science called Against Method about related issues.

    I personally got out of the system before reading any current or older critique of psychiatry, and I think it was in part because of my quite sceptical view of authorities. I think many current survivors of psychiatry have once bought the stuff psychiatry told them and then heard about alternative way of thinking through other channels, such as Whitaker's books or psychiatric survivors. In my case I didn't need even those, I hadn't heard of them, I just had this sceptical view of all professions and strong belief in my own abilities to change my own mind and even the universe. Maybe in a sense I have quite strong internal locus of control, tendency to methodological anarchism, etc, and that's what saved me. At the same time, current psychiatry and other psych-methods often try to strongly transform person's locus of control from internal to more external, to their hands.

  • Yeah, I’ve seen that list of things to block earlier. It seems to include lots of sites with ‘wrong’ information, such as web forums, anorexia and eating disorder websites, esoteric material and web blocking circumvention tools. Maybe with time more enlightened people will start to move to other kind of systems where there’s less control, such as Tor networks.

  • Lately there have been some comments comparing psychiatry to religion, with quotes from Szasz, etc. In a sense, many people and patients seem to view psychiatry in a similar way to the spiritual view of the world. They saw themselves likes leaves in wind, their life largely controlled by actions of spirits, universe, God, etc. Their locus of control was largely external. The primitive man had also another system called magic where the locus of control was more internal. These people believed they can change the universe according to their will with proper techniques. That kind of thinking can perhaps be seen as a precursor of science.

  • The Harrow studies suggest that the people who got of neuroleptics and later on fared much better than the other group had qualities such as a stronger locus of control, etc. Some years ago when I was given diagnosis such as bipolar and schizophrenia and treated with neuroleptics, I understood without very extensive research that the diagnosis and treatment were crap. I observed directly that neurileptics were ruining my life and from brain level I understood that chronic blocking of dopamine and other receptors is not a good idea for me. When I told about these issues to my psychiatrist and psychologist, I saw huge attempt in making me lose my own locus of control, etc. For instance, when the adverse effects of neuroleptics started to kick in (14-16 hours of sleep, yet tired, increased anxiety, social phobia, etc), they suggested that it’s because of “post-psychosis depression” or my disease. When I told about the adverse effects of drugs, they wrote things such as “patient had paranoid thinking towards medication”, “the patient uses a lot of scientific and philosophical terms, but they are not coherent”, etc. Psychologist said that if I don’t eat neuroleptics, it will cause damage to my brain. She also warned my several time about reading things form internet and gave me a guide published by a pharma company.

    In a sense, there was a huge pressure on me to accept that I have a serious brain disease which is controlling my mind and therefore I need to give in to drugs and the control of psychiatry. The reports and their talk constantly tried to paint a picture that my thinking was totally incoherent and illogical, I can’t do my current job, etc. Yet with my illogical and incohorent thought, I quit the neuroleptics and returned to my work. I had to dismiss massive amount of attempts to control me by these authorities. When I’ve read these regular mental health forums, I see that a huge number of people writing there have quite authoritarian view of the whole situation. For instance, if someone considers about lowering a drug that is causing problems, often someone comes warning that “you shouldn’t even consider doing that without approval from your doctor”, “you’re not a doctor!”, etc. Perhaps in the current situation, escaping from life-long neuroleptic treatment often requires enough resilience, anti-authoritarion attitude, capacity of doing research and self-experimentation, more internal locus of control, etc.

    Actually, I think I got out of the system pretty much on my own. At the time I didn’t read any stuff critical about psychiatry. I just thought that I was misdiagnosed and mistreated but still kind of believed that “real” psychosis, bipolar or schizophrenia definitely warrants for treatment with neuroleptics. It was only one year and a half ago when I read Whitaker’s Anatomy of an Epidemic that I started to see these problems from a wider perspective.

  • Thanks for this post, Anonymous. I personally would not take neuroleptics even if I was hallucinating pink elephants or whatever. If I was threatened by forcible injection of these drugs, maybe I’d travel to Goa or wherever. But I’m still interested in the way these drugs work in the brain or nervous system. In that sense, this new poster gave valuable information. There was not much that I disagree with.

  • By the way, in a sense there’s perhaps something good about SGAs compared to haloperidol. It’s much harder to cause very severe D2 antagonism and all the related crappy stuff on patients with SGAs, so in a sense they have training wheels for doctor. But then again, not every FGA is haloperidol either, drugs such as perphenazine and chlorpromazine also have different receptor profiles, etc, compared to haloperidol. So, I don’t know if it’s neutral to find all the bad things haloperidol can cause and then generalise it to mean all FGAs. Though I must admit that CATIE did a similar thing with perphenazine. Maybe instead of comparing FGAs with SGAs or brand names with each other, they should be studying things such as what are the adverse or beneficial effects of D2 antagonism with different receptor populations, time of use, etc.

    Perhaps these days when a doctor thinks he’s not getting the response he was looking for, he adds another neuroleptic to the soup. Or sometimes even third one. One person with schizophrenia diagnosis told that he was on large doses of two neuroleptics (Abilify and maybe Seroquel), and when he told the head psychiatrist of a clinic that he wanted to drop the other neuroleptic, the psychiatrist almost jumped over table and told that every schizophrenic takes at least two neuroleptics.

  • Thanks for this message, mah3md. It sounds like you have longer experience with him than I have. I know NMDA antagonist drugs can directly cause the “dissociative” part of some types of psychosis, but they don’t usually directly cause anxiety, etc. They’re actually very pleasant to many people. I’m thinking that maybe in some forms of paranoid psychosis prolonged stress, lack of sleep, etc, causes on the brain level something similar to NMDA antagonism or some related glutamate stuff. Stress, prolonged negative thoughts, etc, combined with NMDA antagonism type dissociation => a type of paranoid psychosis. But what causes what?

  • And yes, I understand that it’s a trade journal or whatever. In part, my interest is not at all what new information the paper claims (nothing), in this case I’m interested in this whole complex promotional system they are trying to perform.

  • Yes, it wasn’t an attack against you. I like your posts and way of seeing the world a lot. I just recalled that other post, the topic of which was neuroleptics/adherence or whatever. I just wondered if this really is the best that the current bio-psychiatry has to offer, then it’s pretty much crackpottery.

  • I don’t think Nasrallah’s editorial is considered very important at all (where does Sandra find all these silly persons? Is the case really that they’re the best of the breed?).

    However, I think there are many different axis to prescriptions of neuroleptics, for instance. One axis is the pharma axis. Another is the social/behaviour control axis. Etc. And all of these mesh in ‘interesting’ ways…

  • Thanks. And I’m talking about the subscription thing which takes place within the MiA site, not PayPal. For one, there are not any “states” in Finland. There are types of provinces but they’re never used in addresses.

  • Good luck with your efforts! I use many of those same techniques (diet, exercise, meditation, etc). In fact I’ve been experimenting with them on-off style for 15 years, but during the last year and a bit more I’ve been even more serious about it. This kind of techniques can transform one’s mind and body pretty profoundly, but at the present time it also often requires plenty (I’m talking of years) of careful self-experimentation, research and of course practice to draw even some kind of a personal map of this territory. For instance, some more rigorous Eastern practices may not be suitable for curing mental problems.

    “Everyone is just telling me I need the right combo of meds and then all will be fine, which I don’t believe.”

    Yeah, sometimes I’ve been just observing the way people talk in those mental health forums. If someone, for instance, with bipolar diagnosis complains about her current state or effects of medication, soon there’ll people giving the highest solace they know of: “Hang in there! Switching meds can suck, but I know you’ll find the right medications.”

  • If you regularly poll the front page of MiA and also other blogs, it may be worth it to invest time to learn about RSS and different kinds of RSS readers. The “hidden” blog posts in MiA will show there before they’re released to the front page and you may save plenty of time. The idea is that you subscribe to RSS feeds of different blogs with your reader and when one blog has a new post, it will appear in your reader.

    You can even subscribe to all comments in MiA blog posts, at first I found that a bit overwhelming but now I’m used to it. 🙂

  • I intentionally posted that quote quite vaguely, because I know people can get somewhat different meanings of it and it’s a good thing. Other main themes of Nietzsche were breaking and rearranging the table of values (morality) and eternal recurrence. Another way to read it: literally insert psychiatry to that quote from Nietzsche.

  • “God is dead. God remains dead. And we have killed him. How shall we comfort ourselves, the murderers of all murderers? What was holiest and mightiest of all that the world has yet owned has bled to death under our knives: who will wipe this blood off us? What water is there for us to clean ourselves? What festivals of atonement, what sacred games shall we have to invent? Is not the greatness of this deed too great for us? Must we ourselves not become gods simply to appear worthy of it?”

    — Nietzsche, Gay Science

    Just replace ‘God’ with ‘psychiatry’.

  • For some reason, psychiatrists have never been publishing numerous studies about adherence, treatment compliancy, anosognosia, etc, with drugs such as benzodiazepines, opiates, etc. “He doesn’t understand that he has a disease and therefore he doesn’t eat these benzos I prescribed him!” 😉

  • Also, the current idea is that schizoprenics (or bipolars, psychotics, etc) should take neuroleptics indefinitely. For instance, many of those people in Harrow’s study who quit neuroleptics probably did it without a consent from psychiatrists. Some of them were possibly also the people who would have been offered more injections just because they were not compliant if this adherence/injection system was more widespread. Or with injections they wouldn’t have been able to exit the system? I don’t know, just some ideas. But it resonates with what I experienced. I had to do it in secret.

  • Injections are usually used as a coercive way to give the drugs to patients who don’t want to take them. They last maybe two weeks and the psychiatrist can be sure that the patient has taken the drug. If the patient doesn’t arrive to have a new injection, the psychiatrist knows there’s a “problem”. That is, they are usually used by one party against one person’s will.

    For instance, the language in this paper from BJPsych is much more subtle than the trolling statements Nasrallah makes, but you can see what they say if you have ears and read it with a clear mind.

    “The concept of `recovery’ stresses the importance of working towards goals that are defined by the patient and not by the clinician.9 To achieve this, mental health professionals need to work in a patient-centred way to enable the patients to make choices that will help them to achieve their personal goals (for example, living independently, going back to college or finding a job). Medication management is therefore about a process of shared decision-making in which two experts (clinician and patient) share information and agree jointly the best treatment plan to enable patients to achieve their personal goals. Long-acting injections (LAIs) are one of the choices that patients and clinicians should consider to enable effective management of symptoms and promote recovery. Ultimately the choice about whether to stick to this plan is the patient’s. However, this does not mean that clinicians are passive; for example, if an appointment for an LAI is missed then it is important to follow up and explore with (but not blame) the patient the reasons why this was the case. Although the evidence base remains equivocal, many authors argue that unless we work with patients to make shared collaborative choices, clinical outcomes for patients will not improve.2,10,11”

    Then in the later part of the article there are all the delicate details of giving an injection.

  • Nasrallah: The Cutting Edge of Schizophrenia Treatment: An Expert Interview With Henry A. Nasrallah, MD

    Yeah, Nasrallah suggests you start giving schizophrenics chronic injections from the first episode. How do you even know if it’s psychosis or schizophrenia (basically chronic psychosis) in the first episode?

    “Dr. Nasrallah: Yes, I have long advocated for depot medications, even before CATIE, because as a clinician and researcher, I have no doubt that one of the greatest problems in the treatment of schizophrenia is lack of adherence and repeated psychotic relapse. My opinion, which is shared by many researchers, is that recurrent relapses are neurotoxic and may account for the deteriorating course of patients with schizophrenia.[4] It is of utmost importance to help patients with schizophrenia stay on their medications and avoid relapse.

    In community and outpatient settings, 70%-80% of patients are either partially or totally noncompliant.[5] This is unacceptable if the goal is to achieve recovery. Patients with schizophrenia would have much better outcomes than we usually achieve if they were protected from relapses by ensuring treatment adherence from the first episode. But we have no study of first-episode patients assigned to a guaranteed-adherence regimen, which would be depot medication, vs treatment as usual with oral medication.

    Now we have risperidone depot, the first long-acting SGA, and I hope others come to the market in the near future. In my experience with risperidone depot, it not only protects against relapse, it also helps restore function, especially after about 1 year of use. Patients have to stick with it, and in the second year they may experience a restoration of social functioning, such as a capacity for part-time employment or school enrollment, which may become even more striking in the third year. I have had patients stay on it for 4 years, and it is amazing to me how much better these patients function.

    Dr. Nasrallah: Cognition is the single most important area in schizophrenia right now, and cognitive deficits are a core feature of the illness, perhaps more than positive symptoms. Clinicians know how to eliminate or reduce positive symptoms — delusions and hallucinations — pretty quickly, yet are left with patients who cannot go back to school or work. Cognitive deficits are keeping patients from working and being socially adept. In fact, we have a whole body of literature now showing that patients with schizophrenia have cognitive deficits in several domains that place them at 1-2 standard deviations below the general population. They are not mentally retarded, but they are impaired in memory, attention, visuospatial abilities, learning abilities, and executive function.[9]

    Dr. Nasrallah: Yes, I analyzed data from CATIE as part of the metabolic working group and am presenting the findings at the 2007 Society of Biological Psychiatry and American Psychiatric Association meetings.[13,14] Because several investigators had found that patients who gain weight seem to respond better, a statistician and I examined the relationship between weight gain and therapeutic response. We found a strong relationship between weight gain and improvement on PANSS positive-symptom and total scores across all the medications prescribed in CATIE, whether FGA or SGA. In each case, the more the weight gain, the lower the psychosis score at the end of the study.

    This finding suggests that weight gain is part and parcel of improvement, although excessive weight gain, which happens with some of the SGAs, is not necessary. We know that patients with schizophrenia already have high risk for metabolic syndrome with and without antipsychotic treatment, and they tend to be poorly treated for diabetes, hyperlipidemia, and hypertension.

  • Nasrallah: The case for long-acting antipsychotic agents in the post-CATIE era

    “Conclusion: Long-acting agents represent a valuable tool for the management of schizophrenia and merit wider use, especially in light of emerging literature regarding the neuroprotective advantages of atypical antipsychotics over conventional agents in terms of regenerating brain tissue during maintenance therapy.

    In summary, long-acting antipsychotic agents that ensure continuous drug delivery and the provision of appropriate psychosocial therapy have the potential to address issues of all-cause discontinuation and poor compliance. Further- more, it has been reported that some patients prefer long-acting formulations, thereby suggesting that physicians should more often recommend and prescribe a long-acting agent when antipsychotic maintenance therapy is indicated (58).

    I didn’t even bother reading through that.

    This guy wants more patients on injections, which apparently should not be ever stopped. Everything he says should be taken with that purpose of his in mind.

  • Nasrallah: Newer Atypical Antipsychotics Draw Praise (2010)

    “It has placebo-level metabolic effects,” said Dr. Nasrallah, professor of psychiatry and neuroscience at the University of Cincinnati. “The metabolic profile is better than for Geodon [ziprasidone] or Abilify [aripiprazole], which are currently accepted as the least metabolically adverse atypical antipsychotics.”

    I don’t see if this guy is anything more than a pharma-marketing goon.

  • And note that I had never heard about haloperidol causing some kind of apoptosis through sigma2, and another idea is that it will metabolise to a toxic metabolite. I do not have any idea if these ideas are valid or crap or not practically applicable. It would take even more time from me and also most psychiatrists to determine this. Then there are all of those other studies. Nasrallah is not making any single argument, molecular mechanism, etc, about why haloperidol is neurotoxic and why “atypicals” fix this. He just throws at your face a huge number of papers which in different ways find adverse effect in haloperidol and via Nandra a bunch of papers which find beneficial effects of SGAs. One study finds SGAs increase BDNF in one part of brain, one finds that haloperidol metabolises to a toxic molecule, etc. These may not have anything to do with each other. It seems a mess and a smoke screen. But I’ll still go through what they claim in that Nandra paper about the beneficial effects of SGAs.

    I earlier posted a YouTube link about Nasrallah’s talk published April 2013. Listen with a clear mind the talk to the end. He who has ears, let him hear.

  • Yeah, I will still be looking at the 5HT thing when I get back from hiking. Earlier last year one person (Ed) brought about studies which said that the 5HT effect of SGAs increased the number of dopamine receptors in high-affinity state, and therefore it perhaps counteracted the dopamine antagonism effect of the same drug. In a way, some molecules of the drug would go to dopamine receptors and block them, while at the same time other molecules go to to 5HT which may cause effects which reverse some of the D2 antagonism. They said this may make SGAs less effective in treating psychosis and were thinking of a new drug which would prevent this effect of 5HT . .

    They’re pulling these studies about haloperidol and at least implicitly say that this is true for all FGAs. In CATIE they took perphenazine and talked of it as if it represents all FGAs.

    BTW, do you have any sense how in practice psychiatrists find the dose in clinical setting? Do they follow the official recommendations for doses, do they increase/decrease dose until they get a result they’re satisfied with, etc? I guess it’s a mix of these. They have the target doses and then test increasing/decreasing the dose, adding new drugs, etc.

    For instance, some say that to reach an equivalent response for psychosis the drugs should be given in a dose where they roughly antagonise D2 in the same receptor occupancy. On the other hand, I don’t think it’s impossible that if someone gets lots of H1 sedation, adrenergic effects, etc, from quetiapine, he can cope with less of D2 antagonism.

    In any case, it’s possible that for instance Abilify may cause less of some type of damage than “equivalent” (low enough but working) dose of haloperidol. I don’t know. In my opinion, from patient’s point of view more sinister thing is that these people are driving for increased use of injections which in many cases can be seen as increased coercion.

  • I went through some of those neuroscience papers about haloperidol. It is true that there may be some techniques that haloperidol can cause some forms of neuronal damage or changes in ways I hadn’t heard of. For instance, haloperidol seems to also act on sigma2 receptor which may cause some kind of cell death. Another thing is that haloperidol may metabolize to neurotoxic pyridium metabolites. I don’t know further what type of damage they may do. I don’t know, for instance, which other neuroleptic drugs also bind to sigma2 or metabolise to pyridium. But in any case, it’s possible that haloperidol has these, ehm, possibly additional mechanisms of causing damage.

    Note that these mechanisms may be additional to another types of damage or shrinkage. For instance, if the D2 antagonism causes the brain shrinkage via some unknown mechanism, then it’s potentially shared by all neuroleptics, depending on how much D2 antagonism you get. Or maybe they have other common ways to cause damage. As you know, in the monkey study both haloperidol and olanzapine (Zyprexa) groups got severe 8-11% reduction in brain mass in all major brain regions and most robust in frontal lobes and parietal lobes.

    I haven’t really gone through the references about the claims of atypical being neuroprotective, but many of them were of the type that they had seen increase of growth factor BDNF in some part of brain with some drug, etc. It’s hard to say what these mean in practice. They didn’t help the brains of those monkeys on olanzapine. Or maybe helped some particular part of the brain. Or not. But the thing about these claims is that when the general psychiatrist reads it, he gets the picture that haloperidol is very toxic and atypicals are the opposite, they’re actually neuroprotective. There are many different and often speculated mechanisms at play.

    OK. I hope you get something out of that.

  • Ahahaha.. I found a reply from the authors of the original study:

    “To the Editor: As Dr. Nasrallah notes, our data provide confirmation of the higher mortality associated with haloperidol when compared with atypical antipsychotics in patients with dementia (1). The main finding and unique contribution of our paper, however, is that there are mortality risk differences between atypical antipsychotics, with risperidone and olanzapine having higher mortality rates than quetiapine. Since the publication of our article, our findings of differential mortality among individual antipsychotics have been confirmed in another sample (2).

    Dr. Nasrallah also brings his pilot study (3) to our attention. This retrospective study at a single center reported higher rates of 2-year mortality for patients taking haloperidol in comparison with those taking atypical antipsychotics. However, as noted in a letter to the editor regarding that paper (4), the study did not control for the known selection biases that occur in patients treated with haloperidol compared with atypical antipsychotics. Haloperidol tends to be prescribed for patients older and sicker than those treated with atypical antipsychotics (5). In our study, we analyzed a wide array of potential confounding factors in addition to using propensity methods to control for potential treatment-by-indication bias. In doing so, we observed the mortality action of haloperidol occurring within the first 30 days of treatment. Therefore, it is unclear that one could conclude that neurotoxicity is the mechanism of mortality risk.

    In light of our data, the evidence from randomized controlled trials, and a number of retrospective database studies, we find no support for the idea that atypical antipsychotics are neuroprotective in patients with dementia. Randomized trials have shown atypical antipsychotics to have 1%–2% higher risk than placebo over 10- to 12-week study periods (6). Over the longer 6-month follow-up in our cohort, olanzapine and risperidone showed mortality rates of approximately 27 deaths per 100 person-years of treatment compared with 18.6–21 deaths per 100 person-years with quetiapine and valproic acid. In addition, we previously showed (7) that the absolute mortality risk over 12 months in patients taking atypical antipsychotics was 4.8% higher than in those not taking medication, which corresponds to a number needed to harm of 20.8. Therefore, if atypical antipsychotics are to be prescribed, then they should be used in conjunction with a risk-benefit approach taking into account the efficacy and safety evidence base for the agents under consideration.”

    Isn’t he even ashamed that he’s taking credibility away from more serious researchers?

  • At least in this case he’s more direct, instead of plain obvious, of what he’s trying to do:

    “Dr. Nasrallah says that he advocates for depot injections to combat nonadherence to medications and repeated psychotic relapses, which may lead to a worse outcome.

    Studies of FGA depots, although they show less relapses, do not show the improved functioning over time that SGA medications do. But, this may be due to the fact that studies using FGA depot injections are often done with patients who have already suffered repeated relapses and have a more severe illness course. Also, there is always the fear that the patients may get tardive dyskinesia from the FGA.

    SGA depot injections, on the other hand, may show that they will both prevent relapse and improve function over time. That has been his experience with his patients.”

  • Here’s a recent video where Nasrallah claims with recurrent episodes of psychosis the patient goes all the time to a worser state. He stresses that patients should be kept on neuroleptics so that the second episode doesn’t occur. He says fortunately there are ways to prevent the relapse. He then tells how some patients in South Africa were given injections for two years. When they were switched to oral by another doctor, one in seven patients relapsed and never recovered.

    Another obvious push from this guy for new injections. Everything I read and see from this guy is ridiculous. Maybe I should stop and start packing for my hiking trip.

  • This Nasrallah guy is clearly very angry towards haloperidol! When I googled for “haloperidol neurotoxicity”, the second result was a letter from Nasrallah: Does the Neurotoxicity of Haloperidol Explain the Higher Mortality in Dementia Patients Compared With the Second Generation Agents?

    He had found a study where dementia patients in haloperidol group had higher mortality than in those who got an “atypical”. He says the original article didn’t consider the possible reasons for the higher mortality risk with haloperidol. Then he again says studies indicate atypicals are neuroprotective and haloperidol and perphenazine are neurotoxic. And suggests that haloperidol neurotoxicity caused those deaths in dementia patients.

    He didn’t mention for instance:

    “Haloperidol users were significantly older and sicker (as evidenced by the highest Charlson comorbidity index scores, highest rates of concurrent delirium, and more inpatient days in the preceding year) than users of the other study medications. A higher percentage of African American patients were treated with haloperidol compared with the other agents. Those taking haloperidol were also significantly more likely to have used opioids or benzodiazepines and less likely to have used antidepressants during the year preceding the new antipsychotic start.”

    To me these seem much more plausible factors than haloperidol neurotoxicity somehow killing the patients.

  • Nasrallah: The antipsychiatry movement: Who and why

    “Finally, the antipsychiatry movement aggressively criticizes the pharmaceutical indus- try’s research, tactics, and influence on psychiatry. Also included in the attacks are academ- ic psychiatrists who conduct FDA clinical trials for new drugs and educate practitioners about the efficacy/safety and indications of new FDA-approved drugs. Although industry research grants are deposited at the investigators’ universities, critics mistakenly assume these psychiatrists personally benefit. The content of all educational programs about psy- chiatric drugs is strictly restricted to the FDA-approved product label, but critics assume that expert speakers, who are compensated for their time and effort, are promoting the drug rather than educating practitioners about the efficacy, safety, tolerability, and proper use of new medications. Part of the motive for attacking this collaboration is the tenet held by many in the antipsychiatry movement that medications are ineffective, unnecessary, or even dangerous. I wish antipsychiatrists would spend a week on an acute psychiatric unit to witness the need for and benefit from psychotropic medications for psychotic, manic, or depressed patients. Although psychiatric patients experience side effects, they are no worse than those experienced by cancer, arthritis, or diabetes patients.”

  • It’s often hard for me to argue about this tranquilizer thing. In high D2 blocking doses, I don’t don’t think it’s tranquilizer like benzos or alcohol. It doesn’t shut down the “anxiety axis” (amydala, etc) like they do. But it’s not specific either, it tunes down the dopamine pathways, which means it tunes down large part of higher brain areas such as frontal lobes.

  • Just in case some of you didn’t get it, that’s why they’re making up those idiotic “scientific” statements. It’s not done from a neutral position. It’s not trying to find the “truth” or “meaning” or whatever. They just scrap whatever crap they find with their computer and create a scientific paper that satisfies what they were asked for.

  • Currently, no one is starting with haloperidol oral. New patients all start with Seroquel or Abilify or whatever. There are maybe some older people who have stabilised taking haloperidol orally. There’s no explicit need to ban haloperidol. The oral use will die quite soon. Except that haloperidol has been one of the most popular injection drugs and now there’s injections of Abilify, etc.

  • “I think they were trying to suggest that the effects on the serotonin receptor mediates the effects on dopamine.”

    Oh, and when I talked about 5HT, 5HT means serotonin. Perphenazine and chlorpromazine work in this system pretty much like the “atypicals” work. So what to make of the claims of Nasrallah, etc, that typicals are very bad and atypicals are actually beneficial? Is it crap or not?

  • I looked the the editorial and the Nandra article a bit more. One thing is that all of their references about the neurotoxicity are about haloperidol, yet without a problem they then claim all older neuroleptics are the same when they are not. And at the same time they widen their various references about different newer neuroleptics as if they apply to each newer drug, even though the newer drugs have quite different receptor affinities, etc. For instance:


    Second-generation antipsychotics have been shown to be much safer for the brain than their older-generation counterparts (although they are not more efficacious). ..

    Evidence for the grave neurotoxicity of haloperidol and other older neuroleptics, compared with atypical antipsychotics, is substantial and multifaceted.

    Twenty-eight studies reporting the various destructive effects of older antipsychotics (especially haloperidol) on brain tissue have been published in prominent neuroscience journals, based on work in animal models, cell culture, and post-mortem human tissue.


    Even if efficacy is debatable, mechanism of action is much clearer cut. We know that typical drugs are D2 antagonists. We know that atypical drugs are 5HT receptor inverse agonists, but with actions on many other receptors.

    This is convoluted. The largest “antipsychotic” mechanism of all neuroleptics in higher doses is D2 antagonism. Haloperidol happens to be a very “pure” neuroleptic in the sense that its molecules go largely to D2 receptors instead of also to other receptors. In CATIE study they used perphenazine which is a more medium potency neuroleptic in that in addition to dopamine receptors, its molecules go also to other receptors so there tends to be less dopamine blocking and more effects on other receptors. These change the way it feel and how it works in the brain. It’s a bit like taking a smaller dose of haloperidol and then small doses of some other drugs. Chlorpromazine has relatively low binding to D2 and plenty of binding to other receptors, such as histamine. Chlorpromazine and maybe perphenazine are also strong antagonists at 5HT and they could be called atypicals if they had been released at the same as atypicals.

    One thing with haloperidol is that if you want lots of D2 blocking, then it’s quite possible to do it if you give a larger dose, and then you get lots of effects related to D2 blocking. Sometimes some patient might find a neuroleptic with lots of H1 blocking useful because of its highly sedating effect, someone might like more of just the D2 blocking. Etc.

    BTW, if he says this and it can be shown that the newer neuroleptics cause the same thing, we can use the same argument to ban all neuroleptics! Except it wouldn’t work.

    The FDA would never approve haloperidol today, given the serious harm it can do to the brain, despite its efficacy for psychosis. (It’s interesting how the FDA bans a drug immediately if it causes tragic birth defects, such as thalidomide, but not if a drug is destructive to the brain tissue of a disabled adult patient. Invisible damage can be less alarming or urgent than visible damage.)

  • I actually just read the Nasrallah editorial, earlier I was mostly reading through the linked article. 🙂

    But in that editorial he’s clearly promoting the banning of haloperidol and use of newer drugs. He’s right about haloperidol possibly causing these problems, though he’s not really explaining why. There’s a huge list of molecular mechanisms by which haloperidol causes damage to impress the psychiatrists who don’t understand what they mean. Then there’s only this one sketchy reference which tries to prove by molecule level handwaving that the atypicals are actually neuroprotective. And he’s pretending that during the last 15 years there has suddenly become huge amount of evidence of neurotoxicity of haloperidol and *that* is the reason he has stopped using it during the last 15 years. And even if the newer neuroleptics cause less shrinkage (it probably depends on dose), it still doesn’t mean they’re neuroprotective! If any of those molecular mechanisms of haloperidol toxicity are true, it’s very possible they’re true also about new drugs.

    But yeah, I’ll still have to go deeper to that Nandra study to see if I can find any convincing arguments in it.

  • I can’t talk for Sandy, but I like to go deeper into these articles and see how they’re manufactured. After you do it a while, sometimes you can spot good science from bad science almost from the style of writing. Maybe she is open to the idea that the newer drugs cause less damage than the older ones. I think it may often be a question of dose and amount of dopamine blockage.

  • By the way, I just noticed in the famous monkey study which found that both haloperidol and olanzapine “in a manner that mimics clinical use” cause brain shrinkage used the amount of D2 blockage to determine the doses of drug to each group of non-psychotic monkeys just as I suggested it should be done.

    However, more recent imaging studies of dopamine D2 receptor occupancy suggest that antipsychotic efficacy, without pronounced extrapyramidal symptoms or hyperprolactinemia, occurs when 65–72% of striatal dopamine D2 receptor are occupied.

    Consequently, in this study, we sought to obtain plasma levels of 1–1.5 ng/ml for
    haloperidol and of 10–25 ng/ml for olanzapine.


    That there are no consistent differences between atypicals and typicals, SGAs and FGAs, has been confirmed in a recent meta-analysis of 150 trials of these drugs: in 95 of these trials the FGA comparator was a high-potency FGA – haloperidol – frequently at high doses.14

    An example of the promotional studies, there are many similar:

    These preliminary results support the potential value of quetiapine for improving cognitive impairment in pa- tients with schizophrenia and emphasize the importance of further research with this promising atypical antipsychotic.

    Patients were then administered a series of neuropsychological tests and randomly assigned to double-blind treatment with quetiapine (300-600 mg/day) or haloperidol (10-20 mg/day) within a flexible dose schedule (determined by the clinician at each centre).

    Another study with a *low* dose of haloperidol (5 mg) compared to Risperidone:

    This study examined the neurocognitive effects of low-dose haloperidol compared with risperidone over a 2-year period.

    This study did not provide support for neurocognitive advantages of a newer antipsychotic med- ication over a low-dose conventional medication. We speculate that conventional medications may have neuro- cognitive benefits at low doses that are neutralized or reversed at higher doses.

    In any case, in that newer article from 2012, I couldn’t read the older references. It may well be that they’re now aware of this haloperidol trick and they’ve picked articles where it isn’t prominent. I can’t check it. They often just make claims but don’t explain why it is so, maybe the referenced article has some reasoning, but I don’t know.

  • Donna, I think Sandy in part wanted us to comment about parts where the reasoning of this article might be wrong, etc. She clearly was sceptical of its claims and even pointed out how there was those commercials for Abilify injection in the next page. Maybe there’s some promotional attempts again going behind the scenes. If there are, it may be useful to further understand how it happens. (See Ben Goldacre, etc)

  • Thanks. In what I wrote, I was mostly reading the reference to this recent paper in my comments instead of the recent editorial:

    I also agree that most of those studies he referenced are from the promotional phase of those atypicals. Unfortunately I can’t get to most of the actual papers, only the abstracts. I don’t know how they decided to measure the dose between those two drugs they gave to the rats, but one important thing to look would be how much dopamine receptors the given amount of drug molecules block. To do this even roughly, you’d need to do some math with receptor affinities, etc. That is, an easy trick is to give haloperidol in a dose where it blocks lots of dopamine to one group and another group a new drug in a level where it blocks less dopamine. Haloperidol causes bad things and the new drug causes less of the bad things, then they say the new drug causes increase of BDNF, etc.

  • Thanks Sandra. I’ll also try to go deeper to the article and references, provided I find the references. I’m not a neuroscientist but I’ve studied some neuroscience, and especially my passion has been a more network or algorithmic level view of the brain (by what logic neurons communicate and create connections, etc) and type of computational neuroscience (Jeff Hawkins, Hecht-Nielsen, etc). My thinking still is that the D2 antagonism between cells causes the brain atrophy seen in those monkeys, etc. Of course there are then other downstream cellular mechanisms, etc, which actually cause the cells to die and of which I don’t know too much. The receptor affinities of haloperidol is such that it very strongly blocks the dopamine receptors, but this is of course dose dependent. The newer neuroleptics such as Seroquel at lower doses block other receptors such as H1 and 5HT2A and at higher doses they start to block D2, and you can’t block D2 as much with them as you can with high doses of haloperidol.

    Many of those older studies which have found that, for instance, that Seroquel is neuroprotective or improves cognitive skills, have given perhaps one group 400 mg of Seroquel and other 15 mg of haloperidol. At those doses the haloperidol group has been getting hugely more D2 blocking.

    There are also other older neuroleptics which have a wider receptor profile and less affinity to D2.

    About the 5HT2A antagonism being protective, in our discussion forums there’s a post where the research has noticed that 5HT2A turn dopamine reseptors to a HI-state, meaning it works against the dopamine blocking effects of atypical neuroleptics. They were thinking about new drugs which prevent this process. But maybe this thing works against the dopamine antogonist thing of the same drugs and therefore increases the dopaminergic activity and therefore reduces the negative effects of dopamine blocking.

    I don’t know, but I’ll try to go through this path of thinking. Thanks for another puzzle, I learn so much going through them.

  • I agree with much of what Seth wrote here. Within three years I managet to get all the most severe diagnoses they have on offer (bipolar, schizophrenia, severe depression with psychosis) when all of my severe symptoms were obviously caused by neuroleptics. When I got to the system, in my papers it says I sleep 7,5 hours and wake up lucid. Three months later, after starting neuroleptics, my papers say I sleep 14-16 hours a day and am still tired during the day. I also got “heart shocks” when falling sleep, my skin all over the body would develop red “inflammation” or whatever spots, I became anhedonic. Heavy inner anxiety and depression like symptoms. The papers said that I had become very passive in conversation and replied only with single words. When I talked about these problems which obviously were because of neuroleptics, they for instance suggested that I have “post-psychosis depression” and wrote in their papers that “patient has paranoid thoughts concerning his current medication. Also when I said I have too much of Abilify, the psychiatrist just looked at me and said “it’s a good dose”. I developed symptoms that were very similar to “negative and cognitive symptoms of schizophrenia”, and they went gradually away when I stopped neuroleptics.

    I’m not anymore taking any meds but I’ve been taking SSRIs too. They have many problems too, but in my opinion they’re generally not even close to neuroleptics. One thing is that their use can lead to neuroleptics eventually. The psychiatrists, patients and general population still seem to think that these “atypical” neuroleptics are much safer and more efficient than the old neuroleptics, so there’s a low barrier to trying them.

  • It’s interesting that small Northern countries such as Finland, Sweden and Denmark have been giving so much hits to this site. I live in Finland and it often seems that in the public discussion there’s no discussion about the drugs, etc, at all. And for example in Finland, there’s only five million people living in the whole country! I hope I didn’t cause all of those clicks by myself. 😉

    The biggest problem for me to subscribing was the trouble of subscribing. Surely I can give a pint per month to MiA, but the subscribing process seemed too troublesome. I decided it’s worth it.

    (BTW, I keep on having issues with paying. It whines about the address – it might be a foreign country issue. I’ll try it again tomorrow and if it still doesn’t work, I’ll contact Matthew or someone.)

  • Sandy: “I agree that this seems likely to undermine the placebo effect. It is one of the things that make me wonder if I can keep working.”

    One thing about the placebo thing is that the people who got placebo also regularly went to talk to a doctor or whoever. Maybe just seeing someone regularly and talking to her about his problems helps. Feeling like one’s in best possible treatment or care, under safe wings, etc. I don’t know if it’s just the belief in that pill.

  • I didn’t watch the video, I usually prefer reading unless I just want to see what the person looks like, but:

    “Today, thanks to better early detection, there are 63% fewer deaths from heart disease than there were just a few decades ago. Thomas Insel, Director of the National Institute of Mental Health, wonders: Could we do the same for depression and schizophrenia? The first step in this new avenue of research, he says, is a crucial reframing.”

    There are, well, I don’t know how many percent more deaths from heart disease and other cardiovascular diseases now than there were just a few decades ago among mental patients, thanks to “atypical” neuroleptics, etc. Maybe to do the same thing, you could reduce the amount they’re prescribed or something? 😉

  • Paris, I haven’t yet read through much of what you wrote (these posts are long), but what small part I read it resonates pretty much with my own home-baken system I’ve grown over the years. For instance, I’ve been pretty interested in neuroscience and especially kind of a computational neuroscience where you try to learn the algorithms of neural networks. I’ve also been interested in mind and its relation to brain and body and environment and society and etc. I’ve practiced martial arts based on taoist stuff and also a little chi kung+kungfu. Also a little yoga. Right now I try to practice zazen (zen meditation, a form of mindfulness practice) daily and connect it with western science and also widen it to my daily life. This with hikes in nature and finding the right nutrition, and working about how new habits are created and old ones lost, and willpower .. maybe willpower can be seen as a habit/s .. and connecting all of these as kind of a mosaic .. wow.

  • The difference between American style and European style must be genetic. Between my country, Finland, and America the difference is even more pronounced. It could very well be that the people who fled Europe to America were people who didn’t cope with the society of the time. Maybe they were more of the ADHD type or maybe they just weren’t accepted in a civilised society. And now they’re passing their genes in a closed territory. This might be a problem but I’m sure Europe will eventually find the faulty genes of Americans and see the difference in brain scans and give drugs to control Americans and invent handy lies for it. One day, Europe will rise again!

    (Sarcasm alert)

  • Yes, they use the term anti-psychiatry because these days it has become a degrading term. Sometimes they make even references to scientologists. I don’t know if it’s possible to change the meaning of that word to a more positive one. Until then, maybe it’s easier to say it’s not anti-psychiatry, it’s something else.

    I told one woman about some of the studies such as brain shrinkage, Harrow, etc. She then told about them to her doctor and he said of each one that ‘there are no such studies’ and then talked about Scientology.

  • I don’t really understand this theory. The supposed supersensitivity thing relates to brain compensating for the dopamine blocking caused by drugs. It doesn’t mean that the dopamine systems become more active than normal when on neuroleptics. If neuroleptics cause use of drugs such as nicotine, I’d guess that it may be because neuroleptics make you feel like shit and people may use drugs to counter the dulling effects of neuroleptics, to get at least some reward, focus, etc.

  • I read from Stephan Chorover’s book From Genesis to Genocide this incredible lie from Plato’s Republic. Sociobiological determinism.

    Socrates: How then may we devise one of those needful falsehoods of which we lately spoke — just one royal lie which may deceive the (present) rulers, if that be possible, and at any rate the rest of the city?

    Glaucon: What sort of a lie?

    Socrates: Nothing new: only an old Phoenician tale of what has often occurred before now in other places (as the poets say, and have made the world believe) though not in our time, and I do not know whether such an even could ever happen again, or could now even be made probable if it did.

    Glaucon: How your words seem to hesitate on your lips!

    Socrates: You will not wonder at my hesitations when you have heard.

    Glaucon: Speak, and fear not.

    Socrates: Well then, I will speak, although I really know not how to look you in the face, or in what words to utter the audacious fiction, which I propose to communicate gradually, first to the rulers then to the soldiers, and lastly to the people. They are to be told that their youth was a dream, and the education and training which they received from us, an appearance only; in reality during all that time they were being formed and fed in the wind of the earth where themselves . . . were manufactured; when they were completed, the earth, their mother sent them up; and so, their country being their mother and also their nurse, they are bound to advise for her good, and to defend her against attacks. . . .

    Glaucon:You had good reason to be ashamed of the lie which you were going to tell.

    Socrates: True, but there is more coming; I have only told you half. “Citizens”, we shall say to them in our tale, “you are bothers, yet God has framed you differently. Some of you have the power of command, in the composition of these he has mingled gold, wherefore they also the greatest honour; others he has made of silver to be auxiliaries; others again who to be husbandmen and craftsmen he has composed of brass and iron; and the species will generally be preserved in children. But as all are of the same original stock, a golden parent will sometimes have a silver son, or a silver parent a golden son. And God proclaims as a first principle to the rulers, that above all else, there is nothing which they should so anxiously guard . . . as . . . the purity of the race. They should observe what elements mingle in their offspring; for if the son of a golden or silver parent has an admixture of brass and iron, then nature orders a transposition of ranks. . . . For an oracle says that when a man of brass or iron guards the state, it will be destroyed.” Such is the tale; is there any possibility of making our citizens believe it?

    Glaucon: Not in the present generation . . . but their songs may be made to believe in the tale, and their sons’ sons, and posterity after them.

  • “Your understanding the states of mind that get labeled ‘negative symptoms’ of ‘Schizophrenia’ and its relation to Ketamine is outrageously unsupported.”

    Yeah, when the ketamine blocks the NMDArs in high enough sub-anaesthetic doses, maybe it kind of prevents the sensory signals from eyes, ears, skin, etc from arriving to the mind or “reality creation loop”, so the mind is free create a new kind of reality that is not so much directed by input coming from sensory neurons and thus from the environment. If someone is given a very big dose of ketamine, he may become unresponsive looking at him, but he may experience things very intensively inside his mind. Much of currently documented negative symptoms of schizophrenia are related to neuroleptic type dopamine antagonism which is a totally different experience. Instead of experiencing an intense internal world, life is taken away from all things that make it good. Motivation is taken away, anhedonia, etc. They’re two totally different things, even though from outside it may seem that the persons are not responding in a similar way.

  • Actually, I personally would much prefer to take a low dose ofketamine over neuroleptics. When I was younger, I tried some other NDMA antagonist drugs similar to ketamine in high but sub-anaesthetic doses. Alcohol and nitrous oxide also work at least in part through NMDA antagonism. I also watched what other people in that “community” were doing. There seems to be some resemblance to some symptoms seen in some psychosis in NMDAr antagonist intoxication. They can also cause those symptoms more directly, amphetamine psychosis often requires more of a binge type use, so it seems there’s more complex processes going on than just dopamine activity in one part of the brain causing hallucinations. However, they also liked the effects and I don’t think they’re that crazy to ingest drug just to get the effects of current schizophrenic patients. They liked the experience and found it interesting.

    In 60s there was a researcher called John Lilly who experimented with isolation tanks and chronic use of large doses of ketamine, and these also in combination. He developed some things which most people would consider quite wacky, such as a cosmic coincide center affecting the human development through series of coincidences. On other hand, he didn’t develop the high anxiety, amotivation, etc now seen in schizophrenia. Maybe in some forms of more paranoid psychosis there has been prolonged anxiety, fear, sleeplessness which then cause things such as “dysfunction” of HPA axis, increased or decreased dopamine production or dopamine receptor levels, similar stuff with glutamate or NMDA receptors, etc. Maybe in a way, some paranoid psychosis have this ketamine type dissociation effect combined with high anxiety, fear, lack of sleep. And the latter in a way can cause the NMDA and dopamine stuff. And they can be caused by kinds of trauma, etc, etc. And the dissociation effect can maybe create a feedback loops with these others things in brain, in society and in mind which just increase the problem. Etc.

    Maybe one of my points is that to understand complex things such as brain function and how it relates to mind, society, madness, etc, we need to constantly jump from one level of explanation to another and see how they interrelate.

  • I found this article in Psychiatric News web site:

    He’s whining about a lot about how the psychiatry isn’t respected enough and so on. People on this site won’t need education about where he’s wrong, etc. It’s plain in out in eyes. But reading through it, I just had to facepalm every time he wanted something for psychiatry, and then in the same statement also said that we also need to reduce the stigma of mental disease. At times he also mentioned improving the mental health system. If he wanted to explicitly talk about about reducing the stigma of mental illness, he would have made it one part of the speech, and the problem of psychiatrists not getting enough respect and funds from pharma another part. Now he’s mingling the parts about the respect for psychiatrists, funds from pharma, and the stigma of psychiatrist patients in single sentences throughout the speech. It’s as if he’s trying to use the acknowledged stigma of mental patients to support their own case.

    Here’s a version of Lieberman’s speech from the above link where I’ve removed all the “and also to reduce the stigma of mental lllness” and other crappy parts. I have not added anything in there, I have just removed parts of it.



    This is “our time,” said incoming APA President Jeffrey Lieberman, M.D.—time for psychiatry to seize on its advantages and realize a long-deferred dream of equity.

    Speaking at the Opening Session of APA’s 2013 annual meeting in San Francisco last month, Lieberman said he was angry about the continued stigma associated with disparagement of psychiatry in some quarters.

    … I have recently thought about that scene in ‘Network’ because as I view what is happening to the field of psychiatry, I feel ‘mad as hell, and I don’t want to take it anymore.’ The truth be told, that is why I ran for APA president—because I felt mad and wanted to use all of the power and influence of APA to speak up and stick up for our profession.

    “Throughout my career, I have been acutely sensitive to the lack of respect toward psychiatry as a medical specialty,” Lieberman said. “I suppose there might have been a time when psychiatry wasn’t as scientifically based as it should have been. But that was then, and now is now. For such attitudes and practices to persist in the 21st century is nothing short of discriminatory and prejudicial.”

    “The pharmaceutical industry has all but abandoned the development of novel psychotropic drugs,” he said. “And DSM-5 has become a lightning rod for self-styled critics and the antipsychiatry movement. Psychiatry continues to be a punch line for jokes.”

    Yet at the same time, Lieberman said, he felt profoundly optimistic about the future.

    “It is for these reasons that despite the lingering effects of stigma and inequity, I say that this is our time, and our time is within our professional lifetimes,” Lieberman said. He urged members individually and collectively to fight for the respect for the psychiatric profession.

    He pointed out that APA has a key role to play in this process. “APA is our best weapon in the fight for respect and equality both for our profession,” he said. “Therefore, I am calling on APA to redouble its efforts in representing our profession both inside the Beltway and across the country at the grassroots level of the membership and district branches. This is the time for us to seize the moment, for psychiatry to take its rightful role in the field of medicine.” ■

  • In any case, I’ll add that I like much of neuroscience, in fact I’ve been studying it for maybe 15 years on and off. There’s lots of crap or useless stuff out there, but thinking about the function of brain and how it relates to human consciousness is one of my favourite topics. When in the last paragraph I talked about “them”, I wasn’t specifically targeting neuroscientists. I meant it more generally: for instance, some people inside psychiatry also may be worried about Whitaker’s, etc, books and articles, etc, and of the people with less name finding out, alone or in group, the lies they spread. It’s not just the grands, it’s also the general attitude towards them as persons, how much they and their professions are respected, taken seriously, obeyed, etc. Lest their profession is not called pseudoscience, bad science or fraud. Just like in ancient Rome where the street theatres mocked the people in power (did they really?), now we’re doing the same thing in the internet age.

    There’s something slightly ironic or whatever in that we’re also here scrutinising their paper with a suspicious eye, I hope it doesn’t lead to more censorship. 🙂 But in any case, this seems like a good article, worth reading.

  • Danke, Marilyn. I just skimmed through the study but added it to my reading list. Some of the more interesting bits were where they described about their own worry that, basically:

    1. The media says something concerning neuroscience.
    2. The public finds out it was a fraud, crap, useless, false or whatever.
    3. The public will start to devalue or disregard neuroscience.

    For instance, a quote:

    “As neuroscience findings are increasingly echoed by the media, we are now, and much more so than in the past, in the public eye. Distortions of neuroscience findings open the door to suspicious public attitudes towards neuroscience and this might result in a decrease of the resources that society will accept being allocated to future research. It is the responsibility of the neuroscience community, and in its long-term interest, to correct this as soon as possible.”

    (Um, they mostly were worried about media, they forgot doctors, psychiatrists, etc. I don’t know if that was a conscious decision or not.)

    Bottom line. They are worried about the public perception of their profession. They are worried about common people learning the simple chemical imbalance theory was not right and they were lied to. Etc. Etc. And the consequences. They are almost scared of people like us. And a nice thing about that study is that maybe some of them are thinking about about what their own profession is doing wrong, instead of just blaming media, etc, for telling lies about what they *really* do.

  • I haven’t seen any papers, but looking at how the brain, dopamine pathways, etc, work and the quality of the brain atrophy, etc, that’s how I currently see it. Andreasen herself said in the NYT article:


    A. Well, what exactly do these drugs do? They block basal ganglia activity. The prefrontal cortex doesn’t get the input it needs and is being shut down by drugs. That reduces the psychotic symptoms. It also causes the prefrontal cortex to slowly atrophy.”

  • The brain shrinkage/atrophy in humans haven’t been as drastic as 10% in that monkey study. Anyway. We don’t know for sure about the mechanisms of this shrinkage, but maybe one way to think of it is that heavy blocking of dopamine receptors reduces the use of dopamine pathways in the brain (to frontal lobes and other areas) and because these pathways don’t get used that much, they atrophy, kind of like unused paths in the woods gradually go away if they’re not used. Even adult human brains are malleable and plastic, so it’s possible to take an axe and hack new paths in the woods. OK, I’ll stop with this metaphor before it goes too far. 🙂

  • I think that maybe with their injection comments they are driving an approval for a new study or studies where they will be giving injections of neuroleptics to the patients so that they can measure the brains of the studies over years. I kid you not. It is sick that they seek out methods to make people more “adherent” to their power. It is even more sick that they call injections one method of “adherence”.

  • Parts of this paper suggesting politics of control make me sad.

    “Schizophrenia is one of the most important brain diseases that psychiatrists treat.

    Adherence can be maximized in a variety of ways: maintaining good rapport and frequent supportive con- tact, choice of medications that have the lowest aversive side effects (such as akathisia and extrapyramidal side effects), and use of long-acting injectable medications.

    Teasing apart the mechanisms by which relapse may lead to brain tissue loss will require rigorous clinical trials, preferably with random assignment of medications that enhance treatment adherence (e.g., long-acting injectable agents versus treatment as usual) …”

  • I haven’t very thoroughly examined it, but I find many of these inflammation theories interesting. There’s one study which found out that aspirin can reduce the effectiveness of SSRI and SSRIs can influence the cytokines through some mechanism. It also makes sense that the brain or behavior is modified by inflammation, for example in the sense that it’s good for a human or animal and the tribe if a sick person rests in relative seclusion until the inflammation goes away. Etc.

  • Biology and brain probably is involved with almost everything that goes in our normal mind. I don’t know how the brain/body creates the conscious experience, but every time we even think a mundane thing such as “should I get a coffee”, neurons are certainly part of that process.

    I don’t know about mental illness, that seems like a pretty general term and it’s part semantics, etc, if it should be used or not.

    However, the thing that psychiatrists currently often say it that, for instance, schizophrenia is currently considered a cell level brain disease which causes atrophy in brain (I took that definition straight from an “official” schizophrenia guide site for patients funded by a pharma company). This is not true. As you said, schizophrenia is an umbrella term and there are many different kinds of patients with that label. Maybe some have some kind of an encephalitis or virus or whatever which causes them visions despite psychological, social, etc, stuff. Maybe this is a brain disease.

    However, at the same time there probably is a huge number of people with the same label whose symptoms are caused by social issues, trauma, poverty, lack of sleep, prolonged stress, exploitation, etc. All of these things can change the way brain and body operates and the operation of the brain and body can cause psychotic symptoms. I still wouldn’t call it a brain disease. For instance, if you stay up for four days without sleeping, your brain will probably operate in an abnormal manner, maybe it’s flooding with stress hormones an so on. If you have a trauma, your mind or body may go to a stressed up state regularly from different cues and prolonged stress without rest can “wear out” healthy bodily functions. Etc, etc.

    I think there’s a difference here, one is caused by a cellular level pathology and you can’t much help it psychological means, other is a natural response of body/brain/mind to certain conditions. In this sense, often for instance neuroleptics resemble a brain disease much better than schizophrenia. 😉

  • Thanks for the link. However, I think the idea that ketamine may reduce the memory problems of ECT is not entirely strange. A stroke or brain injure can cause a glutamate storm in the brain which is known to cause excitotoxic damage. Ketamine, PCP and other glutamate NMDA antagonist drugs block NMDA receptors so that glutamate can’t activate them. It is known that this can prevent the glutamate excitotoxicity.

    The way I see it, if ketamine helps with the memory and other longer term problems of ECT, then it seems to imply that ECT causes a glutamate storm with excitotoxic damage, which causes the memory problems. I also wonder if the damage is the primary way ECT ‘works’ in the first place.

  • Thanks Monica! I am using very similar techniques myself. Diet, zen meditation, hikes in nature, also some chi kung and yoga style streching. Earlier I have been doing kungfu and tai chi chuan as well. BTW, I don’t necassarily recommend zen as it’s often done in schools before one’s in a better condition, it’s often considered somewhat austere and advanced practice.

    I’ve also been thinking about and using ideas from neuroplasticity, willpower, habits and so on. For instance, for me it has been very beneficial to create a morning ritual with washing, little yoga and zazen and then breakfast. Also, I have an evening ritual immediately when I get home from work: out to the woods for an hour, shower, little yoga and zazen, then dinner. It has become a lot easier when it became an automatic habit.

    I also do the zazen when I’m walking in the woods, etc. It’s like I’m etching new better pathways in my brain. The effects are not always immediate like with drugs and it required lots of time and effort, but I this kind of practices can bring about more permanent change.

    Maybe it’d be cool if there was more Eastern type possibilities targeted especially for mental health, withdrawals and so on. I mean exercises similar to zazen, chi kung, yoga and so on but stripped from more esoteric stuff, maybe easier at first and so on. The mindfulness stuff is perhaps a bit like it.

  • I don’t know why I have Allen Frances in my RSS feed. I usually collect good stuff to my RSS feed. I don’t even know who he is. Sometimes, though very rarely, I pick out RSS feeds that are inane, so that I can track what they are writing. Maybe this is what I get.

    “So what is a patient or potential patient or parent to make of the confusing struggle between NIMH and DSM-5 debacle?

    My advice is to ignore it. Don’t lose faith in psychiatry, but don’t accept psychiatric diagnosis or treatment on faith — particularly if it is given after a brief visit with someone who barely knows you. Be informed. Ask lots of questions. Expect reasonable answers. If you don’t get them, seek second, third, even fourth opinions until you do.

    A psychiatric diagnosis is a milestone in a person’s life. Done well, an accurate diagnosis is the beginning of increased self understanding and a launch to effective treatment and a better future. Done poorly it can be a lingering disaster. Getting it right deserves the kind of care and patience exercised in choosing a spouse or a house.

    Remember that psychiatry is neither all good or all bad. Like most of medicine, it all depends on how well it is done.

    Allen Frances”

    I think that the important message is that you “Don’t lose faith in psychiatry”!!

    I don’t why I’ve subscribed to this RSS, but I think it was to follow senile old men in their degeneration to nothing.

  • Yes, for instance “Three, ECT causes neurons to release large quantities of the neurotransmitter glutamate which releases more glutamate leading to excited toxicity and neuronal death.” Daniel Fisher

    So, yes, ketamine and other dissociative drugs can prevent this kind of damage by blocking the glutamate NDMA receptors. But I wonder if this damage is the main way ECT “works” in first place?

  • Excess amounts of excitatory neurotransmitter can cause neuronal damage. NMDA receptor antagonists such as ketamine can prevent this kind of damage by closing these glutamate receptors. If ketamine helps with memory problems of ECT, then does it mean that the memory loss of ECT is caused by excitotoxic damage done by excess glutamate release? Maybe.

  • “Can anyone comment on how in the world ketamine might prevent ECT caused memory loss?”

    I have no idea. Ketamine works largely by blocking the NMDA channels which are also related memory formation (LTP, etc). The action of ketamine and similar drugs is very interesting in my opinion. I’ll have to read the article a bit later and think about it.

  • When I was younger, maybe ten years ago, I hanged a lot in some forums for the abuse of cough syrups which work similar to ketamine (NMDA blocking, etc). The chemicals made us contact foreign forms of life, etc, so it can’t be all bad! It is just crazy, people are using cough syrups to get a ketamine like high.

  • Actually I am waiting on updates, they’ve got Whitaker, Moncrieff, Kirsch, Seikkula (the Open Dialogue man), etc, together in Vatican. What? Why have they all gone to Vatican? Well, obviously there’s a conference, but it’s not easy to get any important name like them to a single conference. How have they gathered all of them in that single place? Did pope personally invite them? OK, I admit that Healy is missing. And some other people.

    But anyway, the post just says that there’s a conference in Vatican but it doesn’t say what the conference is about and who has called it. It doesn’t make it divine if it’s in Vatican. Are they preaching to priests or is it scientific conference, what are they doing there?

  • They don’t just “include” persons to be in certain places. These persons are human beings with their own lifes. Maybe they weren’t asked, maybe they didn’t want to travel to Vatican, or whatever.

    I don’t even know what Whitaker, Moncrieff, etc, are doing there. I’ve travelled in Rome/Vatican twice. From outside, they’re both bubbling with both tourists and the general italian buzz. I like it also, but I’d like to know why is this happening brought about, who has brought it about, etc. Will the next pope preach about not using meds?

    In short, for what audience is this show of “superstars” of the best current critics of psychiatry for? For the major popes in Vatican? For more general public?

  • One of my points was that the psychotic patients maybe know from experience, etc, that their treatment with heavy doses of neuroleptics really suck. Start treating them with heavy doses of benzos or opiates and see if they get more compliant. 😉

    The people with anxiety or depression don’t get quite as severe effects from their drugs. The drugs may even help in some way, at least in the beginning.

  • I don’t know if anxiety/depression is so much different in many cases of psychosis, which word itself is not very rigorously defined. Prolonged stress, anxiety, lack of sleep, etc, can in some persons lead to what will be diagnosed as psychosis. It’s not all psychosis patients, but I think in psychosis patients it’s not all anosognosia, they know from experience or otherwise that their drugs (large doses of neuroleptics) can seriously suck subjectively, or in some cases they know of other dangers. The outward signs of misappropriate behaviour may calm down but often they’re trapped inside their mind in a miserable state. If the drugs made them “normal” they would gladly eat them.

  • I think I mentioned the Meditarranean diet in a previous thread. I must clarify that the mention of that was largely because I had just read an article which suggested that maybe we should look at the whole system of different cultures instead of focusing on different micro-nutrients. My own nutrition for the last year or so has been Mediterranean in the sense that instead of margarine or butter I prefer olive oil, and with food I often enjoy a glass of wine. And I eat a lot of cucumber, tomatoes, olives, etc. But I’ve been also going pretty low-carb, so in that respect it’s not that much pasta. And I love asian food, I do the same thing there, I eat just a little bit of rice. But! It’s just what I’m doing right now, I have no idea if it’s useful for other people, it just works for my personal body and situation.

    Low carb will drive your body to ketosis which may change your mind too, but I can’t be sure if it’s good for everybody. But I’m certain that nutrition can affect your mind too. 🙂

  • Nasrallah just when Risperdal Consta was coming to market.

    “Conclusion: Long-acting agents represent a valuable tool for the management of schizophrenia and merit wider use, especially in light of emerging literature regarding the neuroprotective advantages of atypical antipsychotics over conventional agents in terms of regenerating brain tissue during maintenance therapy.

    This study was supported by an unrestricted education grant from Johnson & Johnson.”

  • Both Subotnik and Robinson receive or have received funds from Janssen, the maker of Risperdal.

    In Finland, it’s not allowed to advertise meds directly to the public, so the pharma advertises in magazines for doctors instead. And, the companies are allowed to create official looking information sites as long as they don’t directly advertise their own drug. Thus we have a site from Janssen which tells information about schizophrenia. The site has many pages with information about neuroleptics.

    You can’t probably read Finnish but you can see that the pages are divided in two columns. Guess what the left and right column mean? No, it’s not not second generation neuroleptics, it’s regular vs depot/injection, right side listing all glorious benefits of long-lasting neuroleptics to the patient. “You don’t have to remember to take the med every day”, etc. That is, they’re trying to affect even the patient and his relatives so that they’d prefer the depot.

    ‘Patent expiries have been hitting the books of the big players across the industry, but careful management of the lifecycle of a drug, for example by developing improved formulations, can limit the impact. The recent US approval of Janssen Pharmaceutica’s Risperdal Consta (risperidone) for schizophrenia is a prime example of the value in this approach.

    Risperdal Consta is a two-week, intra-muscular injectable version of Risperdal (risperidone), first launched in the US in 1997 and due for patent expiry in 2007. Risperdal is Janssen’s most important product, bringing in sales of over $2.5 billion in 2002. Patent expiry in December 2007 will lead to a $1 billion-plus loss in revenues in 2008, due to generic sales erosion, according to analysts at market research firm Datamonitor.’

    Here’s one study that I found from Subotnik’s homepage, a study by him and other people. It’s incredible, now they say that long-lasting injections of Risperdal may help with the white matter loss and improve cognitive performance!

  • Yeah, I read though it here. Subotnik seemsto be pushing the idea how important it is to prevent even slight nonadherence of Risperdal.

    When the atypical neuroleptics were pushed to the market, there were lots of studies which seemed to suggest that they improve cognition, work better and so on compared to the old neuroleptics. They’re not doing those studies anymore so much. Why? The patents have dropped. I’m afraid that we’ll see more studies done on the importance of the atypical depot neuroleptics (such as Risperdal Consta) which of course may cause better adherence.

    Here Robinson comments on this same study and hpromotes the use long acting neuroleptics.

    ‘Another potential intervention to maintain adherence is the use of long-acting formulations of antipsychotics with recent-onset patients early in the course of treatment before nonadherence becomes established. Long-acting formulations eliminate the covert nonadherence that can occur with oral formulations. Knowing that patients are nonadherent allows for discussions between patients and their families and clinicians about the patient’s choice to suspend medication treatment and about making appropriate plans. Long-acting formulations have advantages that may be especially relevant with recent-onset patients. Young patients frequently do not wish to have their peers know that they are receiving medication and may live in situations, such as dormitories, that limit the ability to comply with oral medications without detection. Injectable medications can enhance confidentiality, since they only have to be taken within a health facility. Because recent-onset patients tend to be responsive to monotherapy with antipsychotics, they are more likely than multiepisode patients to only require injections, without supplementation with oral medications. Of specific interest in light of the data from the Subotnik et al. study, patients who accept injections are fully adherent in contrast with the partial adherence common with oral formulations. Preliminary data for long-acting formulations of newer antipsychotics suggest promise with these strategies. Two studies (5, 6) have demonstrated that agreement to injections can be obtained with a substantial percent of recent-onset patients. Weiden et al. (6) found that medication adherence, measured by time to a 2-week medication gap, was significantly longer in subjects who were randomly assigned to receive and also accepted long-acting risperidone treatment compared with subjects receiving oral maintenance medication. However, the number of recent-onset subjects studied with long-acting antipsychotic strategies remains relatively small, and further study is clearly indicated.’

    Here’s a reply from Green and Gordon, I think it’s much more in line with the opinions of people here.

  • Thanks Sandra. I wish that in these studies they would always publish the raw data they’ve used (at what time point the interviews were made, what the exact results were, etc) instead of just publishing the papers, so that the data could be interpreted in different ways by different parties. But I digress. 🙂

  • There probably wasn’t any protocols to measure that kind of thing, they just measured what they did and at max made some observations (I haven’t read this particular study that the table is based on). The uber non-compliants were without drugs for four weeks or more or dropped out of study.

  • I think so too, though I could have gone even half faster if I hadn’t slipped a bit, but I think it’s better to seek for lasting changes instead of speed diets anyway.

    More to the point of this article, at this time I’ve also started again with regular exercise, zen meditation and other changes in lifestyle, so I can’t exactly pinpoint how much the diet contributed to my clearer and more energetic mind, but I think it may have done at least a part of it. I haven’t so much experimented with different special supplements but rather changed my whole diet, though I do take some omega-3 fish oil capsules, vitamin D, etc.

    I also read recently that they’re investigating ketogenic diet for epilepsy and other neurological disorders.

  • Part of my current personal ‘system’ besides things like regular exercise and zen techniques is diet. I’ve been basically eating kind of low carb, maybe a bit Mediterranean style. Lots of tomato, cucumber, olives, olive oil and also pretty unprocessed meat (fish, chicken, etc). Little carbs. One or two pints or glasses of wine per day. I don’t know how good it really is but I’ve lost 24 kg in a year and my BMI is less than 24 currently, also my mind is clear and I no longer have any cravings for carbs.

  • One of the reasons that we still need psychiatrists is this:

    “Psychiatrists, alone among mental healthcare professionals, have worn the white coat of medicine, which forever will infuse our professional identity.”

    They just need a stethoscope hanging around their neck so that they’ll look even more professional!

  • After reading this post, I did a search for his posts on this this site. I found the most recent (I think).

    Why we still need psychiatrists!

    “Who has the best potential to lead this advance? By now, you should know the answer. It is still only psychiatrists that have the most comprehensive education and training in all aspects of mental health and mental illness.”

    And it goes on about listing the reasons why we still need psychiatrists. Reading through the list makes my brain ache: is this irony? Oh, it isn’t. Facepalm. Damn.

    Sorry, this may be off-topic, but I hadn’t facepalmed with this yet.

  • I haven’t ever really heard voices, but I’ve been testing and practicing Eastern techniques on and off for maybe 15 years. Currently I’m doing it more regularly than ever, 30 minutes of zazen (zen meditation) in the morning, then after work I go out for a hike in the woods for an hour and I often try to do the same thing while walking, then another 30 minutes of zazen. Also a little bit of yoga, etc. At this point, this is incredibly powerful exercise for me and my brain and body.

  • I think that the things that you listed (HPA axis, hippocampus, glutamate, etc) are often important factors in depression, psychosis and so on. Prolonged stress, etc, can lead to psychosis on some people. The thing is that neuroleptics don’t generally help even in getting the stress cascade or HPA axis in control, it just shuts down, for instance, the frontal lobes. It shuts down the “end results” but not the factor which caused them in the first place. So people are left inside their mind in great anxiety/depression/negative symptoms, they just took away the outward signs of aggression, etc, and perhaps many parts of the higher human mind.

    I have found a system of almost daily heavy walking in the woods, zen meditation, healthy diet, and other similar practices to be helpful for me, but I can’t generalise my practices for other people. Omega-3 may help but it may not if you otherwise don’t eat in an healthy way (see inflammation, etc).

    Even the traditional Chinese/Taoist treatment, though they didn’t have any science, had a better general idea. They incorporated body, mind, food, exercise, meditation, chi kung and basically everything between Yin and Yang to their system. Now we’re trying to nuke down some specific receptors and see what comes out.

  • One more thing. Note that I’m not trying to argue, merely trying to find some new ways to look at this issue.

    The Jin et al study found no significant change in psychopathology with the four atypicals (compared to what?). I suppose this is the same study that I read before. In any case, the people in that study were 40 or older. The first psychosis often comes with a young age. The experience and the life leading to that event and the hospitalisation was perhaps quite traumatic.

    Joanna Moncrieff gives some typical examples of experiences from a website in her slides. You can see the same kind of reasoning everywhere. The person had some distressing experiences at a young age and neuroleptics took the worst edge off. They often admit the meds are giving them problems and they live a very passive life, don’t work, can’t concentrate, etc. But they still believe the drug is keeping their “beast” in chains. So they take it for the rest of their lives, combined with maybe two other drugs.

    • “it makes me feel like a veggie, but that was better than what I was going through and it kept me out of the hospital” (olanzapine)
    • “Although I felt very well, I felt as if I had absolutely nothing to talk about. I kept wondering about whatever [it] was that had been so interesting during most of my life that I had suddenly lost… But I was very much in contact with reality and for that I was thankful” (haloperidol)

    They themselves think that they need to eat the drug, or else! and they’ll keep on taking the drug for the rest of their lives, never really improving but living some kind of a stabilised life. They often have had some strong experiences at an early point in their life and they’ll absolutely take the drug that they think will prevent it happening again indefinitely, even though it makes them feel like shit and gives other problems. And I’m not saying they should taper down, I’ve seen many people like that and I don’t know if it would be a good idea to try to taper them down anymore if they don’t want it. ?

    The official guides in Finland say that after psychosis, the patient should be treated for 2-6 years and if the patient has “recovered”, then the medications can be stopped. But the patients never “recover” because their dopamine pathways and other receptors are chronically altered, and at that point they already have at least two other drugs in their system and no one wants to change the drug induced homeostasis. So they’ll go like that to the rest of their shortened life. People are constantly told that neuroleptics or other drugs will be taken away if they recover, but that never happens in practice. The only times people practically get off neuroleptics is when they themselves for some reason or another decide to do it , and it’s sometimes done with help from officials, sometimes not.

  • Yes, I agree pretty much. Brain and body is full of different types homeostatic systems which try to do their best to adapt.

    “What that final post-drug homeostasis might feel like probably varies among individuals. Given the influence of the drugs and the passage of time, it is unlikely that the nervous system reverts to factory settings. You can’t step in the same river twice, especially if it’s been flooded with artificial hormones.”

    The huge neural network of brain, consisting of maybe 10^11 neurons (give or take some), each connected to other neurons, is the core of what the brain does and how mind operates. The neurons communicate with each other by sending downstream connected neurons signals with the mechanism of action potential (neuron will “launch” in certain different biochemical settings). The signal may or may not cause a new signal in the downstream neuron. The neurons also constantly change their connections to other neurons, new connections may grow according to new stimulus and old connections may die because they have not been used, etc.

    For instance, neuroleptics do not regulate the general amount of dopamine in the brain. It’s not like a thermostat, it’s not a brain in a soup of neurotransmitters.

    The molecules of neuroleptics go between two neurons, part of this network, and prevent the signal going from one neuron to the downstream neurons. Such connections of neurons are part of important dopamine pathways in the brain, one of which goes to the frontal lobes (the same frontal lobes that they used to cut or destroy with lobotomy), related to a “higher” level of functioning. Another pathway goes to the limbic regions, a more “emotional” part of the brain. (Note that gave those adjectives as a general guidelines, it’s not simple like in saying that emotions reside here, etc. But you probably knew that already.) There are also other pathways, blocking of one which causes men to grow tits. But I digress. Some have said that it’s the blocking of the “frontal lobe pathway” which helps in psychosis, others claim it’s the “limbic pathway” which helps. In any way, you can see that it blocks many dopamine pathways, which are actually a huge number of neurone connected to each other and sending signals to each other.

    When you insert the molecules of a neuroleptic into the brain, they will go between the neurons in these pathways and prevent the neurons from signalling to each other. The brain atrophy thing is basically because when the connections/neurons won’t be used for a long time, they will die away. If there is such a thing as a homeostasis for the whole neural network (or mind?) as a whole, it will have to get used to the new reality where the dopamine pathways are not so easily used. With time and living in this new depleted state, the neurons in the brain will grow others kinds of connections (paralleled by a new kind of a “slower lifestyle”, etc).

    If the neuroleptic is given for a long time in a sufficiently large state, taking the drug away will not cause the neural network to return to its original state automatically. Actually every experience changes the network and you can’t ever return to the previous network (that’s how the life is), but with neuroleptics especially the change can be pretty drastic. The old connections and neurons are dead and they have been replaced by some new connections. Taking he drug away will not grow back the old connections or neurons nor will the new connections go away.

  • After four months of eating neuroleptics, I complained of my severe symptoms, such as sleeping 14 hours a day or more yet being constantly very tired, getting heart shocks when falling asleep, red spots appearing all over my body at times, my hands getting numbed, hard depression/negative symptoms and anxiety. Now that I’m out of the place and meds, I ordered the papers they had written of me. The psychologist had written on a paper around that time: “The patient had paranoid thinking concerning his current medication.”

  • In this case of presynaptic and postsynaptic neurons, we’re talking only of two neurons! There may be kind of a homeostatic thing going on with the growing of receptors and transforming them to D2High on the postsynaptic neuron, and also changing the amount of dopamine released by the presynaptic neuron on the presynaptic side neuron, etc. But this is just between those two neurons, you can’t directly see from it what happens in the human mind. It’s about how easy it is for the presynaptic neuron to ignite an action potential in the postsynaptic neuron. But this doesn’t very directly transform to real world. There’s maybe 10^11 of interconnected neurons in the brain, forming different brain areas and connection between other neurons and brain areas, with different areas working in different ways.

    So, the homeostatis thing that I mentioned referred to just those two neurons, now the whole brain. There are similar things going on with so many other parts of the brain and body, but it’s not the only rule. There are other kinds of rules too, many of which we don’t know yet. How the neurons communicate with each other, what each brain area does, etc.

    Sandra wrote earlier:

    “What puzzles me, however, is that I do not observe many people who need more neuroleptic over time to sustain the same level of “remission”. Now that I look for it, I see it more but there are many others I know who have done fairly well over many years on the same dose. I have worked in the same place for 20 years and I have known a good number of people for that entire time. Believe, me, I am paying attention now.”

    Yeah, I think that study told about people needing to go up in neuroleptics. In practice there may be some increases needed to the dose but then people find a steady dose (which they often keep on taking indefinitely). In this particular case, for instance, we’re talking about those two two neurons and there’s natural limits about how much they can change their functioning. They can grow only a certain amount of new D2 receptors, etc. When the neuroleptics block enough of D2, there’s just no more that the two neurons can do between each other. And often it’s not useful to look at just the two neurons, and especially it’s not useful to just think about the brains in the “brain in a soup of neurotransmitters” kind of a way. 🙂

    Sometimes a better way to think about the action of neuroleptics is on a more systemic level. Here’s “What Doctors May Not Tell You About Psychiatric Drugs” by Grace E. Jackson:

    See Appendix E. That’s part of one of the dopamine pathways (neuroleptics block all four). The more there’s D2 blocking by neuroleptics, the less effective these pathways will work. Those arrows go towards the frontal cortex, etc. Neuroleptics will dampen the traffic in these pathways, in a way. The neurons in the dopamine pathways just cannot propagate the action potentials anymore, at least not as easily, depending on the dose.

  • Sandy,

    Yes, I entirely agree and believe that dopamine supersensitivity is one important factor in relapse. The brain and neurons usually try to maintain homeostasis, so when the D2 receptors get blocked, the neurons try to figure out a way around it. Actually, there may be several different ways they do this, such as in changes in dopamine turnover growing more D2 receptors and changing D2 receptors to a D2High state.

    ‘To explore potential mechanisms, we studied presynaptic and postsynaptic elements of the dopamine system and observed that antipsychotic failure was accompanied by opposing changes across the synapse: tolerance to the ability of haloperidol to increase basal dopamine and dopamine turnover on one side, and 20–40% increases in D2 receptor number and 100–160% increases in the proportion of D2 receptors in the high-affinity state for dopamine (D2High) on the other.’

    So, I think this adaptation may in part explain both treatment failure in long term and strong relapse when withdrawing.

  • Oh, they try to find TNF-α blocker for treatment resistant depression? Now others say that SSRI work by increasing TNF-α, etc, in the brain. If this is true, I hope they at least don’t try to treat TRD by giving both SSRI and Enbrel.

    It’s a bit confusing, some people say that inflammation in the body causes depression and some say that increasing these inflammation markers in the brain is the mechanism by with SSRI works.

    And then TNF-α is related to BDNF. Oh well, I just started to study this inflammation thing a while ago and don’t understand much of its mechanisms, but it’s interesting to learn about its mechanisms.

  • By the way, when people quit neuroleptics and then fall to psychosis which may be more severe than the original one, there may be many other reasons to this besides dopamine super sensitivity, increase in D2High receptors, etc. I have no doubt that neuroleptics can mess up with dopamine issues, long use of most other psychoactive drugs (alcohol, benzos, opium, SSRI, etc) cause the brain to seek for a homeostasis in similar ways, thus the withdrawals.

    But there’s also, for instance, a more system level or neural network level way to look at the brain. The brains constantly create new connections, remove old ones and so on based on our experiences, thoughts, almost anything. For instance, one of the four dopamine pathways that is blocked by neuroleptics leads to our frontal lobes which is part of much of our higher level processing. Andreasen et al say that the use of neuroleptics will cause these networks to atrophy because, essentially, they are not used. This may in essence reduce many important things related to our higher level thinking, maybe control of one’s actions or thoughts, etc. If this atrophy is already well developed and then you take the drugs off and the brain starts to operate without the D2 blocking, maybe with the super sensitivity, then maybe you no longer have the “mental skills” to control that at all. The D2 super sensitivity doesn’t increase continuously over the years, but the system level problems will. Thus, it may be already very hard to quit after 10 years of high dose neuroleptic use. I don’t have any references for this specific case, but that’s in principle how the brain operates.

    You don’t have to even think about it on the brain level at all. Subjectively, if you eat neuroleptics for a long time, you tend to change in the way you behave. Many people who eat neuroleptics life quite simple life often at home, maybe browsing the net, not striving towards much anything, not developing their personality so much. Over time, the person’s habits and personality become transformed because of the drugs. If you then remove the neuroleptic, he maybe doesn’t anymore have the inner capabilities to handle the situation with D2High or lack of D2 blocking, a situation which he maybe could have handled earlier.

    Anyway, these were some thoughts about the long term use of neuroleptics. I haven’t seen much talk about this issue: if someone wants to use neuroleptics for a longer period but not for the rest of the life, then how long should he eat it so that it doesn’t become practically impossible? Three months? Two years? Six years?

  • Yes, for instance, if you look at those studies where they’ve found many marvellous things about the new neuroleptics, such as that they are safer, more effective or they improve cognition or negative symptoms better than the old neuroleptics. Sometimes they even prevent brain damage from schizophrenia. If you look at the older studies which claim this, you’ll see that one trick that they often used is that they give other group a relatively small dose of a new neuroleptics (such as 430 mg of quetiapine) and the other group a large dose of haloperidol (such as 15 mg). The thing with this is that the dose of haloperidol blocks a lot greater amount of D2. If you lowed the haloperidol to a level where it blocks roughly the same amount of D2 as that new drug, then it might be roughly as effective for acute psychosis and it wouldn’t mess with all those other receptors and cause so many metabolic problems. In a way these studies point to the direction that lots of D2 blocking causes these other problems for which the new drugs were supposed to help.

    Sandra, did you notice that this post is not tagged as a “Featured Blog” so it doesn’t appear on the front page like the first part?

  • About the long term effects of neuroleptics, I think there are issues that are not easily captured by studies. I’ll give an example from my own life.

    I wasn’t originally psychotic, I don’t think I’ve really ever been. My problems are/were more related to anxiety and depression. In any way, they decided to put me on neuroleptics (Abilify 15 mg and quetiapine 25 mg). I wasn’t even in very bad state in the beginning. The reports read that I sleep 7,5 hours a night and wake up bright. After four months of treatment, the reports say I sleep 14-16 hours night. Despite this amount of sleep, I was continuous tired. I had became very depressed and had developed very severe symptoms which were indistinguishable from the so called negative symptoms of schizophrenia. At this point they had invented that I had psychosis in the beginning and when I told about my problems, they said it’s maybe post-psychotic depression. After maybe eight months I already supposedly had schizophrenia! The drugs were perfectly mimicking the negative and cognitive aspect of schizophrenia. I answered with single sentences and was very passive, and my subjective experience was just like what others describe about the negative symptoms. At this point I started to fight against it, stopped the meds and “recovered”.

    So, one point is that if you start the treatment with high enough doses of neuroleptics and continue it for a long enough time, people won’t usually “recover” because they have their dopamine pathways blocked, so it often does not happen so that doctor and patient agree that hey, now you’re recovered and doing fine, let’s try to quit the neuroleptics. Instead they often start to interpret the effects of the drugs as symptoms of a severe disease and maybe keep adding other drugs to help with symptoms. This is one reason why, in my opinion, it’s often dangerous to even start with neuroleptics.

  • David, thanks for this. I haven’t Bad Pharma yet, though it’s in my reading list. I don’t know the intricate details of this issue, so it was good to read another opinion about what to do about it.

  • I think that the problems in science aren’t only in psychiatry. Science in the end is just a bunch of people working together. Ben Goldacre has written a new book called Bad Pharma which consists also other drugs besides the psychiatric ones. I haven’t yet read it but from what I know, I think it’s a very good book. Because of the ambivalent nature of psychiatric drugging, the misdeeds may be greater than in other pharma. Lee Smolin wrote a book about the problems in the physics community (Big Trouble in Physics).

    Paul Feyerabend, a philosopher of science, wrote a book called Against Method where he rejected the rational process of science described by his teacher Popper and other authorities. He suggested that science does not go forward by those rational processes but it is instead a lot more ‘anarchistic’ process.

  • Robert, it sounds a bit that Harrow and Lobe are considering some of the things that you suggested in Anatomy and other places. It doesn’t seem like there’s anything really very new in that study, maybe the biggest thing is that it gets published in Schizophrenia Bulletin. But it’s a good thing anyway.

    They mention different mechanisms which may cause the supersensitive psychosis when withdrawing from neuroleptics, such as the drugs causing supersensitive dopamine receptors, etc. Of course these are just ideas and they don’t even mention more systemic changes the drugs may cause. We don’t even have a good systemic or neural network level understanding of how the brain operates and what the drugs do to that operation in long term. For instance, the Andreasen brain atrophy thing may be because neuroleptics block the major dopamine pathways (networks of communicating neurons). For example, the neurons in the frontal lobes don’t get any feedback and brain cells or their connections may die away because of this, that’s how the brain often operates. So one factor in how successful the attempt to get away from neuroleptics very possibly depends on how long one has been on these drugs. If you’re ten years on a large dose of neuroleptics, it may be very hard already to get off them because of the network level changes.

    Anyway. It seems that they’ve at least re-evaluated their data to see what happens when the patients quit the drugs and what happens to those patients who somehow persist through those months of withdrawal. This sounds like some good new information. It may also be that their original ideas about prognosis factors relate to this mess. The other new thing was that they found those people with good prognosis who stayed on meds and didn’t fare so well.

  • “Morphine and chemotherapy for cancer are accepted as effective short term treatments. There are no good arguments that either should be used long term. The science to justify neuroleptics belonging to the same category already exists.”

    Moncrieff also says than in some earlier studies, drugs such as benzodiazepines and even opium have been found to be as effective, I suppose short term, then neuroleptics. (I haven’t read these studies though.) But maybe it is not a good idea to start the neuroleptics in the first place even in many of the acute psychosis, given that their use usually or often simply sticks.

    * Barbiturates: 2 early studies showed chlorpromazine superior
    • Opium: 1 study. Opium equal to chlorpromazine for acute psychosis
    • Benzodiazepines: 6 trials: 3 trials AP=BZD; 2 trials BZD>AP; 1 trial CPZ>BZD=HAL

  • Jeremy from Finland mentioned Joanna Moncrieff and she’s often very good read. For instance, here’s her presentation paper about Antipsychotics: myths and realities. She has written a lot of different articles, etc, I’ve also read one of her books.

    And the situation in Finland seems to be more something like that Finland was still somewhat independent and distant from the European trends in the earlier part of the 20th century and there were some experiments here and there, but gradually at least the Western world has become and is becoming more and more alike. Same ways of acting, same drugs, etc. Same problems. The thing that those people are doing in Tornio is not so much some new discovery but kind of remnants or one final remote “island” of Finnish national development from 1960’s or 1970’s. During the 1980’s, the USA/Western thinking and media pushed more and more to Finland and replaced the studies on schizophrenia therapy done by this other group. A small number of people in Finland have since then continued with their studies, and those people in Tornio are a great number of those people who are left from this development.

  • Again, the reply button is gone and there’s no way to modify one’s broken reply. But I need to add one more point. 🙂

    altostrata: “Hermes, this is an endless discussion, and off-topic attached to Sandy’s blog post, but I would challenge that antidepressants have any magical effect on depression specifically.”

    I want to add one final point, and that is that it may be that using a chemical at one point to a some brain may be sometimes useful. I think that there’s some proof that it may be be in more severely depressed patients more beneficial to take SSRI in at least short term than placebo. I agree we don’t know if it’s a good idea for them to take it in a long term and it may be that the drug doesn’t work even short term for the mid or low depressed patient. But I don’t think it’s an a priori wrong idea that some chemicals may help some persons in some way if used in a right way. The important questions are such things as what they actually do in the brain, in what way they may help some people, etc.

  • altostrata: “Hermes, this is an endless discussion, and off-topic attached to Sandy’s blog post, but I would challenge that antidepressants have any magical effect on depression specifically.”

    I don’t think what I’m saying is an endless discussion or that what I’m saying is off-topic, well it may be off-topic in some reader’s view but directly related to the posts that Sandra made just before. Maybe that makes it somehow bad or off-topic.

    If you read what I actually wrote above, maybe you’ll also get the idea that maybe SSRI or monoamine antidepressants are maybe not a good idea in long term.

    Rather, like amphetamines and other psychoactive substances, they are stimulating or cause other neurological noise (such as emotional anesthesia) that some people report as relieving symptoms of “depression” (whatever that is). Others report effects that they feel as adverse, including — quite commonly — overstimulation.

    Yes, and I just tried to explain why they may cause a little bit of actual relief from one group of the severely depressed people.

    [quote]Antidepressants don’t “work” for depression any more than, say, LSD “works” for depression.[/quote]

    Actually I think that LSD or magic mushrooms or ecstasy may be a good thing in rewriring the brain in just one session, just if it’s given in a therapeutical context, not in a getting fucked up context. They may work just after one session. Actually I think LSD may have much potential for curing depression if it’s used in a proper manner.

  • There’s again no reply button present under altostrata’s message, so I have to reply to some other message.

    ‘Other neurologists view the increase in BDNF supposedly spurred by SSRIs as a response to injury, and not a good sign.’

    That is just part of what I was trying to suggest. That the good part in the ‘responding’ phase of the treatment in those severely depressed was because of in one way or other they ‘enabled’ the brain/mind to grow more positive connections or learn more positive thinking. Castren just found out an idea of window of learning and said that just enabling the window of learning is not sufficient for a better kind of thinking, you also need to grow those better connections with exercise or therapy or whatever.

    My additional point was that maybe the way SSRI and other amine antidepressants relieve depression in some of the patients is not a good idea to relieve the depression, at least in long term. The point is the same as what those neurologists say. My suggestion was that SSRI and other amine antidepressants maybe cause an inflammation kind of an effect in the brains of some of those people in who SSRI initially helps! And that effect also required some other internal/external therapy. A persisting inflammation caused by meds doesn’t sound like a good idea. I dont know if this reasoning is true idea, but maybe it is. No one explains why it isn’t a good idea, and I mean [i]theory[/i] and not practice, I already know that in practice the meds weren’t a good idea for me.

  • Donna, BDNF is short for brain-defined neurotrophic factor. It is a protein which may help neurons to grow new axons, connections, etc. According to these latest theories about how SSRI help some group of depressed people a bit just because of these. For example, a neuroscientist from Helsinki uni, not a psychiatrist, called Henry Castren is now saying that people use the SSRI meds in a wrong way. He says that they may increase the BDNF in some people which may help their growth of new neurons. No, in fact he claims with his rat studies and his theory that SSRI meds are used in a wrong way.

    His theory is that SSRI meds may cause in some unknown way this BDNF protein to increase. But his point that he has been driving is that if you just use SSRI, it may cause an increase in BDNF or whatever, but it will not itself cause any relief. It will at most kind of open a window of new learning in some of the patients, but even that won’t help just because there’s more BDNF. That merely enables or helps the brain to learn more connections, but just enabling is it enough, the brain also needs to learn those new connections. Castren also says in his studies that a rat who got a running wheel and otherwise a good environment grew new connections in his visual cortex like the rat in a dark room or whatever with fluoxetine, that is, it was just useful to give the rat a running wheel than it was to give him fluoxetine? They were closing the other eye of a rat, then testing how much his visual cortex will change, etc.

    Their point is that in their theory, because maybe of the growth of this protein called BDNF, or some other factor they do not yet know, depression meds may open a window of new learning in some specific patients who perhaps lack this type of growth factors. It may be in a way true. But it does not really even help of you increase the serotonin or SSRI or BDNF or whatever, you also need to give internal/external stimulus that creates the new better connections. That is, at max. it may create a new ‘window of learning’ in some patients, but even that window is useless if you don’t use it.

    My additional point was that, if these new theories about the SSRI, window of learning, BDNF, inflammation, etc, actually there is not a single theory … Well, one of my points is that if all this reasoning about opening the window of learning and increasing BDNF in some patients is in fact true, it may be, the mechanism through which it does that increase of BDNF may be a sick one indeed and not a good idea in long term. The basic idea: SSRIs increase inflammation or a process like that and that increases the molecules involved in inflammation and that increases BDNF and that may just kind of enable some of the worst patients maybe to learn to break out of the negative loop of thoughts. I don’t know if this kind of reasoning is true or not and I know it sounds like a crackpot thing after you’ve heard years and years about the serotonin theory. But still, or even less in my opinion it sounds like a good idea to eat SSRI especially long term, maybe in some specific cases it might help a bit with concurrent other new stimulation/training in cases where the patient just can’t learn to a better kind of thinking despite continuous efforts.

    There are actually many different points in what I wrote about. One of the final points is that if all that reasoning about why SSRI and other similar antidepressants help with patients, that mechanism may be a sick indeed. Those chemicals actually cause kind of an inflammation in the brain and that will cause in the end the release of BDNF and other growth factors. This sounds like a crazy theory to many and there is no theory about it, but why do the studies suggest that it is so?

    And my bigger point was not to suggest the BDNF theory or the other reasoning, just to point that when you figure out another way how the drugs may actually work, it may instantly change the whole way of thinking about how/when/why to use these drugs. I have found my own way of reasoning, which is also kind of based on these later reasonings of some neuroscientists and psychatrists, which also doesn’t at all depend on meds or any know therapy and which in the end works better for me.

  • I gained over 20 kg during the few years of my treatment. Less than a year ago I not only quit added sugar, I went on low carb diet. I eat just a little bit of rice or potatoes with meal, otherwise I try to eat plenty of vegetables, fish, chicken, etc. Now I’ve lost all those 20 kg I gained during the treatment and I feel great, and I don’t even feel like I want to eat any extra carbs anymore, the desire has dropped off.

    I can’t say how much this diet has changed my mood exactly, I’ve done plenty of other changes as well. For instance, after I get home after work, I try to go to woods for an hour or so of hiking. After that, I also do 30 minutes of zen meditation which is quite hard mental practice. (I don’t recommend zen for those very ill, it may be too hard and hardcore.) And other changes. But even besides all of this has been my own striving to understand how I can change my life, the pathways in my brain, I’ve been trying to understand this for 15 years already and I think I now have a good grip of the things that I can do to change my mind, body or brain without the help of shrinks at all.

    I mean, I think I have now found a good foundation for me, but it is not a general purpose system which will work for other people. But I think there are some things that are general. For instance, the effect of prolonged stress/inflammation/etc on the brain and maybe on neuroplasticity, for instance prolonged stress and bad health may deplete the brain from BDNF and other growth factors. Maybe, for instance, SSRI helps one group of severely depressed patients just because it, besides all its other unhelpful actions, it in one way or other reduces stress or increases BDNF or whatever so that the severely depressed patient can create more positive pathways to his brain. That is, in those cases where the drug works a little bit, maybe a subgroup of severely depressed patients, even in them the help doesn’t come directly from the drug but from the drug somehow allowing more BDNF, or whatever, and then at the same time kind of rewiring his brain networks or mind.

    There’s a recent study that anti-inflammation drugs can drastically reduce the effectiveness of SSRIs. Many sites nowadays say that SSRI may be anti-inflammatory, but if anti-inflammation drugs reduce the effectiveness of SSRI, it doesn’t sound so simple. SSRI has also been shown to increase cytokines related to inflammation in frontal lobes but now in the body in general, these cytokines can cause more release of BDNF, anti-inflammation drugs block these cytokines.

    I don’t claim this is the right way to think about the mechanism of SSRI, but it’s a good example of what some of the current neuroscientists are proposing. If you know the actual mechanism behind these drugs, it may give other ideas of whether it was a good idea to prescribe them in the first place, especially after a longer time.

    Do you know what is a good way to increase BDNF? Regular aerobic exercise. What is an efficient way to rewire the brain after you have your body in shape and all those good growth proteins abide in your brain? Zen meditation, self-determination, etc, etc. Donna said that something to the effect that people should become their own doctors. Sometimes it may be useful to go and see a specialist and ask questions about things you don’t know yet, maybe it would take too much time to figure it out and it’s more efficient to ask a specialist about the issue. But this shouldn’t be an authoritative system with psychiatrists trying to control their patients who won’t obey their orders, the patient and the doctor should be on a same level, the patient comes to his office and asks for objective information about the drugs and then the doctor tells what is known, and then then patient decides if he should try to the drug.

  • Bob mentioned in the sidebar!

    “Two of those books proved particularly influential for Johnson. Both Anatomy of an Epidemic: Magic Bullets, Psychiatric Drugs and the Astonishing Rise of Mental Illness by journalist Robert Whitaker and The Emperor’s New Drugs: Exploding the Antidepressant Myth by psychologist Irving Kirsch reject the theory that chemical imbalances in the brain cause mental illness, challenging the usefulness of the drugs routinely prescribed to treat such problems.”

  • Well, perhaps people like Torrey have an intelligence anosognosia. Perhaps partly because of their ageing brains and frontal lobes, they subjectively think they’re making some relevant thoughts and points, but they don’t understand that their ideas are totally idiotic. In their subjective mind they feel like they’re totally in control of things, making changes, etc, but the other world sees them in a different light. It’s a very sad condition indeed, the only cure that I know of is to chemically block the d2 receptors in their brain.

  • Well, first, I don’t live in America and I know people in America tend to deal a lot with attorneys, etc. But even still, I don’t think that it’s always wise to threat with law issues in a modern internet discussion. It can seriously backfire you in the eyes of the public. If someone attacks you like a foaming-mouth Rottweiler, sometimes it gives a better impression when you just respond to it in a cool manner, or perhaps even ignore it.

  • Emily: “If I were Torrey, I would be very jealous of what you have accomplished in such a short time with MIA. Well done, Bob!”

    Yeah, the fact that Torrey is constantly referencing and attacking Bob’s writings means that he’s taking them seriously, at least as a serious threat. Torrey’s like some character in the Batman franchise.

  • In trying to make a proof that the currect schizophrenia is really a brain disease, he gives a link to his own pdf, which consists of some random studies, without him ever making any point. The monkey studies and the Ho and Andreasen studies suggest the dopamine blocking of the neuroleptics atrophy also the frontal lobe pathways. Maybe this causes, as Breggin has suggested, an intoxication anosognosia where the patient can’t understand what detrimental effects the drugs have caused to him. Perhaps the Stockholm syndrome is also one factor. Also, in lay terms, a person who has committed to taking drugs kind of needs to believe that he’s getting the best possible treatment – and the relatives of the patients do the same, without experiencing the sucking adverse effects.

  • Some two years ago I was on neuroleptics and got diagnoses of schizophrenia. Since then I went off the neuroleptics and returned to work. Since then the nurses and psychiatrists I’ve seen have often commented that the other psychiatrist and psychologists probably made a misdiagnosis. I know of a woman who has had a diagnosis of psychosis or schizophrenia for years, who by herself went to a low dose of neuroleptics and then told about it to her doctor – the doctor looked at her older data and then said that the schizophrenia was probably a misdiagnosis.

    Heh, perhaps when a patient goes off the drugs, then a doctor can say that the earlier doctors have perhaps made a misdiagnosis. When it’s the same doctor who made the original diagnosis, it’s easier to say that the illness is now in remission.

  • Many prefer civil and conformist ways of influencing issues, maybe with negotiations and suggestions things will be changed. I’m not always with them. Nietzsche, Feyerabend, Sex Pistols, did they do wrong with their non-conformist ways? I think not. Decry me as an anti-psychiatrist, and I’ll proudly take the title and spit on your face. I can’t stand idiotic pseudo-science for social control.

  • The term anti-psychiatry has been made laughable, in order to make its proponents laughable as well. One woman here in Finland told her psychiatrist of several of studies well known for MiA crowd, such as Harrow’s studies, the neuroleptic brain atrophy studies, etc, and he denied them all, he said that there are no such studies. Then he wen’t on to describe Scientology and how they oppose the meds. I can’t see any other reason for him bringing on the subject of Scientology except as an attempt to ridicule these people by inference and association.

    Maybe it’s generally wise to avoid the label anti-psychiatry because of its negative connotations. However, I personally don’t care – I don’t get my money from psychiatry or pharma and I don’t care if they think I’m a crackpot, and I’m not looking for a huge following. In some ways it’s an apt term, maybe it’s time to vindicate some of it.

  • Well, I made just a quick browse through one article in that book. I’ll just jot some quick notes about it, I’m not expecting that many people here are very interested about the history of mental health care in Finland. 🙂

    OK, I’m from southern Finland, Helsinki, and I’ve noticed lots of talk here about a psychosis treatment here in Finland called Open Dialogue. People are flying over the big sea to the northern Finland to learn more about it. I even read that Sandra Steingard had asked the people there why this treatment isn’t done in the southern parts of Finland. Since there has been so much talk of this thing, I’ll give a native perspective from Helsinki. For starters, the first time I read about the whole method was in the final chapter of Anatomy of an Epidemic, this after I had been through and recovered from a typical pharma-abuse.

    During the times of war in 1900-1950, Finland used huge amounts of drugs such as amphetamine and heroin, sometimes the use of heroin was more than in other Northern European countries combined. When the precursor of UN questioned Finland about its use of heroin, Finland just told them that we need this much heroin because of, among other things, our climate.

    Since then, it seems to me, Finland (and other countries in Europe, etc) has been steadily aligning with the global regulations, policies and ways of doing things. Finland has also been following quite closely Swedish-type social welfare system. It’s also been a bit distant, not least geographically, from the rest of the Europe, though in the modern age much of that gap has disappeared.

    Anyway, I read a Finnish book called Reformin pirstaleet (“The Shatters of a Reform”) about the recent history of mental health care in Finland, which perhaps gives some ideas about how this Open Dialogue method is still done in the Northern Lapland.

    Some quick notes from browsing through the book. Most of it actually from one article inside the book, from Ilo Helen et al.

    * During the 1980’s and 1990’s there was a big dehospitalisation project. Finnish shrinks thought that the hospitals were shameful from a global perspective, etc. That is, this dehospitalisation seemed to happen much later than in many other countries. This was due to political changes started in 1970’s.
    * The “anti psychiatric” movement never caught up in Finland.
    * Instead, the biggest forces of reform started within the professionals, etc. In the beginning of 1960’s, psychiatrists such as Yrjö Alanen, Reino Elosuo, etc, proposed that the psychiatry should concentrate on helping the patients recover and get them back to the society with rehabilitation, psychotherapy and social support. From this grew in 1970’s a movement of reformist social psychiatry. This thought lead a lot of mental health system in the 1970’s and 1980’s.
    * The were two kinds of political movements, one “psychiatric-medicinal mental health work” and other “society-constructional mental health work” (I have no idea what the proper English terms for these are.) The latter included the idea of “de-psychiatry” or non-medical thinking and working which prevents mental problems and generates better mental health in society.
    * In the papers of mental health policy from 1970’s and 1980’s, there was widely issued the basic point of view that mental health work is not just about “fixing” already existing mental health problems. Even more important was “preventive work”, which meant preventing mental health problems with therapeutic and social interventions, etc. Also, there were issues about societal planning, etc.
    * The writers go on about how the psychiatric-medicinal model triumphed from 1980’s, etc.

    * This Yrjö Alanen developed individual and family psychotherapies for schizophrenia in 1970’s-1980’s which were employed in Turku of Southern Finland, among other places. His work resulted in something called need-adapted treatment. For instance, this slide about Open Dialogue says: Inspired by the work of Yrjö Alanen, M.D. in Turku: “Need-Adapted” Approach.

    That is, I’m not an expert on this, but it somehow seems to me that there were parties in Finland, not only in Lapland, which were going towards the direction of this Open Dialogue method. Then the medical model came and won, but in Northern Finland some people are still working with and developing some of those other models .

    Just don’t take my impressions as any kind of an authority, I don’t even really know what’s in these need-adapted and open dialogue approaches. 🙂

  • I’ll try to re-read the book I told about, it’s called Reformin pirstaleet (the shatters of reform) and tell about the main points in this development of (attempted) mental health reform in Finland, what happened therein, etc.

  • I’m from the southern Finland, namely Helsinki. I can tell you that the first time I read about the Open Dialogue method was in Anatomy of a Epidemic, after being battered with the pharma-treatment in Helsinki. Sandra, in your post you questioned why this kind of treatment isn’t done in the southern parts of Finland. I read a Finnish book about the history and the current situation of mental health-care in Finland. From what I got out, it seems that in the 70’s, etc, there was a striving to reform the mental health-care so that the sociaty is also involved, etc, and there were roots similar to Open Dialogue in southern Finland, such as Turku. I need to re-read it to get a fuller understanding of what happened.

    Anyway, I read another historical book about the drug use in Finland. During the wars between 1900-1945, Finns consumed a lot of drugs such as amphetamine and heroin. Heroin was available everywhere in cough syrups, etc. At one point Finland was consuming more heroin than other Northern European countries combined. The precursor of UN questioned Finland about its use of heroin, but even the president of Finland objected it. Finland told them, among other things, that because of our climate, we lots of heroin.

    As I see, at the time small distant countries could do more on their own way. During 1950-1990, or so, Finland also started to follow the regulations and way of doing things with the rest of Europe, and thus also USA. Finland is still geographically distant from the rest of Europe, and Northern Finland is even more so, so I guess that’s one of the reasons they still do their own thing in Lapland. Of course, in other countries in Asia and Africa, they’re doing yet more of their own things, but there’s usually no good data of the outcomes, etc. In general, most of Europe and USA are doing the same thing – if a new drug comes to the market, pushed by the manufacturer, all of these countries are more than happy to start using it.

  • Heh, I knew this. On the discussion forums, I talked a bit with Emily about how the pharma operates in Finland. The hospitals and health-care are much more socialised in Finland, my home country, compared to USA, yet the system still works according to the pharma rules.

    In Finland, the pharma is not allowed to advertise the meds directly to the consumers. Well, what they do instead is that they advertise directly to the doctors in the magazines for doctors. Another thing is that they print “official schizophrenia guides”, etc, and spread them to the patients. They can’t mention their own drug, but apparently they think that it’s still worth it to spread the “message” to the patients.

    One other thing that the pharma does in Finland is that they publish “official educational” web sites about schizophrenia, etc. These web sites then get advertised in the public, tax-payed hospitals.

    With this kind of propaganda, the pharma changed the general opinions so that that both the doctors and the patients now believe that the “second generation” neuroleptics are oh so much more better than the old ones.

    I know most of you can’t read Finnish, but I’ll explain. Here is a link to an “official educational” web site released a while ago. The site is run by a pharma company Janssen-Cilag. There is general blah blah kind of information about schizophrenia, this link takes directly to the medicine section.

    Well, instead of talking about the drugs, their function, side-effects, etc, when you go to the medicine section, first thing you see is a divider. Either you take the tablets (left side) or you take a depot (right side). Then there are a lot of benefits on the right side. Then on another page there’s a big banner “Because of the new techniques, new longer-lasting antipsychotics have been generated”.

    On the link “Different types of neuroleptics”, they’re no longer making the distinction between the “typical” and “atypical” neuroleptics. Instead the important distinction is whether it’s a tablet (left side) or a depot (right side).

    That is, instead of making it a patient-doctor decision of choosing between a typical or atypical neuroleptic, the big choice is now if the medicine is a tablet or a depot. That’s because pharma’s patents are going old, so they think they can more money with depots. Oh sure, you can’t advertise your depot medicine directly to the patient, but you can create an “official” web site which encourages the patient to ask the doctor for a depot neuroleptic. “You’re free to live your life to the fullest, you don’t even have to remember to take your daily doses”.

  • Stephen, yes, this is an interesting and complex topic. However, I don’t want to go too deep into it here, much because it’ll get buried and not many people people would read it. I hope we’ll get back to it in some other place! In my 20’s, I spent much of my time studying and practicing different Western and Eastern systems of attainment, so this is an interesting subject for me.

  • Sascha, thanks for this invitation. I first read Whitaker’s Mad in America somewhere this concurring year, then found this site, and then read about you in a blog which told about Seth Farber’s book. It had an interview of you as well.

    Seth had ideas about schizophrenics being dormant mystics. Or that schizophrenics swim in the same ocean as mystics, it’s just that they have not learned to swim yet. And the thing about them being prophets … Well, let me say that I very well understood your point of view in it. In any case, that’s where I learned of you. I’ve yet to learn more throughly about what you guys and gals have in the Icarus web site and community.

    We don’t have any movements or organisations about this kind of issues here in Finland, so I just try to follow what’s happening in the web and other countries. However, I wish I can “spiritually” be a part of this movement. Perhaps ordering a cool t-shirt will help. 😉

    Happy ten years to you!

  • Jeffrey, actually, now that I checked the article he referred to, the article itself is not so bad, it quite clearly admits that possibly the shrinkage is due to Haldol or neuroleptics.

    The study’s called Antipsychotic Drug Effects on Brain Morphology in First-Episode Psychosis.

    However, after reading the actual study, it’s even more strange that he writes to his patients that the neuroleptics may *save* the brain from the brain damaging effects of schizophrenia according to the scientific studies.

    I have another similar study somewhere which downright suggests that the atypical neuroleptic seems to protect the brain from the damage of schizophrenia better than the old neuroleptic. I’ll see if I find it.

  • The only interesting thing about this article is that they found that the use of neuroleptics correlate with the loss of brain volume (though that was already known). Otherwise they’re just throwing claims here and there without making any coherent point. There are sentences and then between them there are references to other studies.

    But anyway, I’ve been reading about this brain atrophy caused by neuroleptics since the last spring. I think there’s plenty of evidence to think that the neuroleptic drugs do cause a significant brain shrinkage. Some of the more interesting studies are the studies with macaque monkeys and the Andreasen-Choon-etc study “Long-term antipsychotic treatment and brain volumes.”

    Some of the scientists have made a model that there’s four or so dopamine pathways in the brain. Well, independent of how many of these pathways exist, they’re all blocked by the neuroleptics. One of the pathways leads to the frontal lobes. You know, if you take a dopamine blocking neuroleptic, then it blocks the pathways to the frontal lobes. An instant lobotomy! When you take the same drug for a longer time, the areas in the brain that don’t get any input – including the frontal lobes – start to deteriorate. A secondary, more longer lasting lobotomy!

    What makes this sad situation even more … should I say perverse? … is that they tell people that the neuroleptics save from the brain damage or shrinkage. When I told my psychologist that I’m feeling like a total crap from the meds, she said that *if I don’t take them it may cause me brain damage*.

    A while ago there was some doctor in an ‘official’ schizophrenia info site (funded by a pharma company) who told to the patients that sometimes schizophrenia causes brain damage/shrinkage (or that the brain damage causes schizophrenia), but there’s some scientific evidence that the second generation neuroleptics may help with this shrinkage.

    I wrote to him an somewhat angry mail, not expecting an answer. However, I surprisingly got a mail from him where he referred me to a study where they had scanned the brains of patients on an older generation neuroleptic and a second generation neuroleptic. They found out in the study that the patients on the old generation neuroleptics had brain shrinkage, whereas the patients on their new generation neuroleptics had less of a brain shrinkage. The conclusion was that the new neuroleptics in some unknown way *prevent* the brain shrinkage … Hey scientific geniuses, here’s another interpretation: The patients on the older neuroleptics had lots of brain shrinkage because of heavy dopamine blocking and the patients on the new neuroleptic had less of brain shrinkage because the new neuroleptic blocked less of dopamine.

    Most of the schizophrenia patients are on neuroleptics. It may be that some of the negative and cognitive symptoms that are claimed to be caused by the disease are actually caused by the neuroleptic drugs. My own belief that it most certainly is so.

    Oh well, maybe life is easier when you have a drain bammage.

  • From the article: “In our opinion, it is worse that a psychotic person is sentenced to preventative detention than a nonpsychotic person is sentenced to compulsory mental health care,” Svein Holden, one of the prosecutors, told the court.

    Heh, I kind of laughed out when I read this comment earlier. The prosecutor is telling that statement as if a self-evident truth, meant to change the opinions of nay-sayers. What is a fate worse for a sane person than be chemically lobotomized with neuroleptics and kept in a hospital? I just read some article which said that many psychiatric survivors have told that they’d rather be in jail than medicated to oblivion.

  • I’m from Finland, close to Norway, so I’ve been through some heated discussion around this topic. More and more I think about this case, the more I think that the common psychiatric diagnoses don’t make a sense.