Monday, March 20, 2023

Comments by Hermes

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  • 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.