Drugs and Dementia

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This week, JAMA Internal Medicine published online an interesting paper, “Cumulative Use of Strong Anticholinergics and Incident Dementia: A Prospective Cohort Study.” They found that exposure to anticholinergic drugs significantly increased the risk of developing dementia. This study has important implications for those who prescribe and take psychiatric drugs but it is worthwhile describing the study in some detail before discussing those implications.

First, some context. Acetylcholine (ACh) is a neurotransmitter (a chemical that propagates a nerve signal from one cell to the next) that is found throughout the body. It is involved in gut motility, visual acuity, heart rate, and secretions. In the brain, its activity is linked to memory and movements. There are many drugs that blocked ACh receptors (the proteins that allow nerve transmission to occur). In psychiatry, anticholinergic drugs are used to combat some of the neurological effects of the neuroleptic drugs such as muscle stiffness and tremor. But there are also many drugs used to treat depression and psychosis that have anticholinergic effects.

Drugs that block the action of Ach – anticholinergics – often cause dry mouth, constipation, rapid pulse, urinary retention (difficulty emptying one’s bladder), and blurred vision. But these drugs can impair memory. What this study addressed was the extent to which these drugs are associated with a new diagnosis of dementia and also, of importance, whether individuals who discontinue these drugs remain at higher risk of developing dementia.

They evaluated adults 65 years or older who received their health care within one integrated system in Seattle. This allowed them to access records for all drugs the individuals had been prescribed for 10 years leading up to and during the study. They excluded individuals who had a prior diagnosis of dementia and they screened everyone for signs of dementia at the outset of the study and then biennially for the duration of the study. In total they followed 3434 individuals. They calculated total anticholinergic exposure in a way that took into account both the daily dose prescribed and the total number of days the dose was prescribed to determine a total standardized daily dose.

This was a careful study. To avoid what they call protopathic bias – the possibility that one of these drugs was prescribed to treat depression or insomnia that in retrospect was an early sign of dementia – they excluded from their calculations all drugs prescribed in the year prior to the onset of dementia. They statistically controlled for factors that could contribute to dementia: age, sex, smoking status, years of education, body mass index. They accounted for health care status and several specific health conditions that could impact the results – coronary heart disease, Parkinson’s disease, diabetes, stroke, hypertension, depression, and concurrent benzodiazepine use.

There were two major findings. The first is that total exposure to anticholinergic drugs increases the risk of developing dementia. But of further concern, these effects were seen even if the drugs had been stopped years before the onset of dementia.

They found that there was a dose response risk for developing dementia, i.e. those with greater exposure had an increased risk. The Hazard Ratio for those in the highest exposure group was 1.54 with a 95% confidence interval of 1.21-1.96. This means that those who had the highest exposure to the drug had a 1.5 greater likelihood of developing dementia than those who had no exposure.

This study has general implications since there are so many drugs on the market that have anticholinergic effects. In our age of increasing polypharmacy, especially as people age, this is a warning call to be judicious in our prescribing.

But the study has particular implications for psychiatry. First of all, many psychiatric drugs have anticholinergic effects. The older tricyclic antidepressants as well as some older neurolpetics were on the researchers’ list. But there were also some newer ones – paroxetine (Paxil), olanzapine (Zyprexa) and clozapine (Clozaril).

The paper is of particular interest to me because it relates to one of the very first research studies in which I participated. It was a study that tested the hypothesis that the dose of haloperidol that caused minimal neurological side effects – the neuroleptic threshold (NTH)– as measured with a simple, brief examination was also the effective dose. Going higher on the dose yielded more discomfort but no further reduction of psychotic symptoms. PET studies have supported this hypothesis: 70% blockade of dopamine receptors yields an anti-psychotic effect and 80% yields significant neurological side effects. Anticholinergic drugs are used to reduce the neurologic symptoms. But they should never be needed. If someone has these symptoms the thing to do is to lower the dose not add another drug. If the person still has psychotic symptoms on the lower dose, increasing it is not likely to yield any further improvement.

The NTH paper was published just before the newer neuroleptics were coming to the market. Whereas in the late 80’s, academic psychiatrists were talking about moderating dose, by the late 90’s everyone was talking about how safe the newer drugs were. Polypharmacy – once shunned in academic circles – came back into favor. Most psychiatrists in practice today were trained in the 1990’s or 2000’s.

Beyond that, my one gripe with this paper is that the list of drugs with anti-cholinergic effects did not seem complete. Another site, which appears to do a good job of tracking drugs’ anticholinergic burden, includes many more psychiatric drugs which are in common use. A recent study, reported the risk of dementia among people diagnosed with schizophrenia to be about double the risk of the general population. We know that many people are being exposed to psychiatric drugs at very young ages and then are often on them for many years. Although there is much discussion in the psychiatric literature about cognitive impairment in people who are diagnosed with schizophrenia it is most often discussed as a result of the psychiatric disorder not of the drugs the person is taking.

I sometimes wonder how we know what we know. For instance, a psychiatrist goes through extensive training and ends up with a sense of having a general grasp on the field. But no one can read everything that has been published. Much of our learning is still in the apprentice mode – we learn from those around us. Most residents never learn about the neuroleptic threshold. And many emerge with the belief that the cognitive impairments associated with schizophrenia are due to the “disease” rather than the drugs we give.

I have come back to this theme again and again. This is not an anti-drug discussion. It is a respect-the-drug discussion. We need to use these drugs with caution. Dose matters. Length of time a person is on them matters. Polypharmacy matters.

Acknowledgment: I want to thank the always insightful and incisive Nev Jones for discussing this paper with me and directing me to some helpful papers and websites pertinent to this topic.

 

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46 COMMENTS

  1. This was a study that caught the attention of a lot of people I know who aren’t particularly interested in issues related to psychiatry…mainly because of many articles highlighting Benadryl/dementia. Perhaps it will help people to further delve into the complications of long term use of anticholinergics.

    But I was not aware of that site that you link to that shows the breakdown in anticholinergic properties of most psych drugs. In the category that shows strong anticholinergics effects (scoring a 3), that is quite a list that includes most of the “1st generation” antipsychotics but also the very commonly prescribed seroquel and Zyprexa.

    Sadly, I assume this won’t have a great effect on prescribing patterns, but I wonder why. Will the APA try to dismiss these findings? Simply ignore them?

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  2. Thanks for this very informative article and for all your hard work.

    You write

    ‘But of further concern, these effects were seen even if the drugs had been stopped years before the onset of dementia.’

    Do you have any more information about this such as whether length of time or dosage strength related to these effects?

    Severe cognitive difficulties seem to be part of the picture for some people with psychosis right from the beginning. I am thinking the effects you are talking about are ones that are more gradual over time?

    Do you have any suggestions for further reading about pscychosis and cognitive difficulties?

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    • Hi Sa,
      This was a statistical finding. They controlled for the time period when people were on the anticholinergic drugs. They found that there was an effect even if people had stopped the drugs. This had the same impact as those who were still on them. In all instances, there was a dosing effect – the longer or higher dose people were on,. the higher the risk of developing dementia. Of course, not everyone developed dementiia. The risk was at most 1.5 times higher.
      You are correct that these are problems that emerge over time. No one in the study had any evidence of dementia at the beginning of the study. You are also correct that there are reports of cognitive difficulties for some people early on. What I have always wondered was to what extent this might be due to the crisis state. In my experience it can vary a lot from person to person. Many people who have psychosis, for example, do not seem to have any cognitive impairment (or none that is readily observable).

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      • Thank you for your response.
        You write
        “You are also correct that there are reports of cognitive difficulties for some people early on. What I have always wondered was to what extent this might be due to the crisis state.”

        I would so like to understand more about this. Are you able to explain this a little bit more?

        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).

        So another question I have is do you see psychotic people with these kinds of cognitive impairments, who are medicated, recover over time? The only recovery stories I have heard for people in this condition are from people who were not medicated. Thirdly, there is now a lot of mainstream literature that talks about the cognitive deficits that accompany schizophrenia and mood disorders, and I am left worrying that maybe we are hearing more about cognitive deficits accompanying pscyhotic disorders because the medication interferes with the cognitive recovery of this `freeze state’
        I apologize if this is a diversion from the topic but I long so much to try and figure this out; so any discussion or ideas of how I could research this more would be so helpful.

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          • Thank you …that is comforting to hear. And just to clarify – I am thinking these were people who also had ‘ catatonic’ like symptoms which presented like major cognitive difficulties in addition to positive symptoms, (and obviously if they are colleagues their cognitive impairments resolved).

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        • Sa-
          I am not going to discuss specific cases due to confidentiality but I was addressing the larger question – do people who experience what I would call psychotic states and who take drugs to treat the condition ever recover while on the drugs? The answer, in my experience, is yes. That group is underrepresented on this website but they are out there and I know some of them. I also know people who do not do so well. Outcomes are highly varied and that makes it hard to make sweeping generalizations about whether these drugs are “good” or “bad”.
          As I have said here and elsewhere is that there is good reason to be cautious with these drugs and, if they are used, to do everything one can to use them in the lowest dose possible and for the lowest duration possible.

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          • I think that also depends on your definition of recovery. These drugs don’t cure “schizophrenia” – they numb down the emotions and in some cases apparently switch of the psychotic experiences (I’ve heard people who say they don’t really even do that – they just make “voices” and other hallucinations less intrusive). In the same time they disable other cognitive and emotional capabilities. Maybe for some people the trade off is worth it – it’s not for me to judge but it’s hard to call this recovery, at best it’s symptom management. Also a good question is how often the “recovery” on these drugs is due to the drugs and how often is spontaneous recovery despite the drugs. It’s really hard to tell, especially because taking someone off the drugs often causes a withdrawal psychosis.

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        • 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.

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          • “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 attacks. ”
            Exactly. What psychiatrists don’t get – behaviour does not equal internal state. The fact someone “appears” calm does not mean they are. I remember trying to explain that to many psychiatrsist and they never seemed to get it. For them sedation was a good state – they have apparently never taken any of their wonder drugs. The type of emotional numbness that some of these drugs induce can turn one into a murderer – anything just to make you feel something internally. I was more “crazy” on these drugs because my brain was fighting back.

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          • Wow -thanks so much. I am always so grateful to people who give up their time to share personal information to help me try to understand how to best help my loved one.

            Hermes, your experiences really resonate with our situation. I am wondering if the ‘qualitatively different state’ you experienced with neuroleptic drugs changed back quickly after you stopped taking them or if it took quite a while? And also if your anxiety sometimes affected your comprehension of material [e.g.things you used to understand easily became more difficult to understand and thus setting off a whole cycle of increased anxiety)

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          • “if your anxiety sometimes affected your comprehension of material”
            I can speak of my experience here – it definitely did. You can’t really concentrate on reading anything when you are experiencing severe anxiety, since your mind is trying to evaluate all the potential threats. It’s a chronic hypervigilant state (completely different from short time stress which can have an opposite effect) in which it’s hard to sit down and think something over, read, watch or listen with comprehension since you’re constantly ready for fight or flight. Of course different people may have a different experience but this is how it was for me. It also took a long while to get to “baseline” – about half a year and after that happened I had an opposite reaction of sorts – my body crushed (I was physically and mentally sick to the point I could not get out of bed for more than 1/2h at a time), which lasted for a few months. These emotional states take a huge toll on the body and mind and it takes time to recover.

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  3. This reminds me of a woman who had a shield alert out some years ago after suffering a bad reaction to steroids given to her after surgery and winding up in the ER and being forcibly admitted to the psych unit. She wound up involuntarily comitted to a state mental hospital for many months if I recall, and the more they drugged her, the more signs of “dementia” she showed, and then they used that to make her a ward of the state and the forced drugging became permanent without even a need for court order. Someone here may know more about this tragic case than I do, but I only bring it up with vague recollection because it’s relevant to the reality behind the topic in this article. I’m sure it happens to many thousands of people a year. Added to the brain damage caused by neuroleptic drugs, and I’m sure this is happening to a million or more.

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  6. I have been taking some form of psychiatric drug for going on 26 years. I was institutionalized during two periods (1989) and (1990). I have either been a full time student or gainfully employed for the last 24 years. I realize that Soteria is designed for people with a first case episode, but given my fairly good track record and the accumulating evidence of the harm of these drugs, is there not some place to go to safely detox, even if it takes me six to nine months? I currently take 2.5mg of Zyprexa, and .5 mg of klonopin. I think that insurance should cover this, given the tens of thousands of dollars already down the rat hole for hospitalization, drugs, lab tests, psychiatry visits, monitoring for the abuse done by Lithium to my kidneys, not to mention the future medical dilemmas I face. I am 54, and I have a son who is a merit semi finalist. I think that I must be doing some things right, and deserve the opportunity to finally divorce myself from psychiatry, and still be able to eke out some of life’s pleasures in old age.

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      • 2.5mg of Zyprexa every day for years? It was a dose that made me fall asleep in the middle of a busy street within 1/2h of taking it, gave me restless leg syndrome, caused huge hunger (fortunately only for like 10 minutes until I fell asleep uncontrollably) and made me dead tired for 1-2 days after followed by 1-2weeks withdrawal (total emotional rollercoster).
        I don’t want to scare people (in fact even if your risk is 1.5x higher there’s still a good chance you’re going to be fine) but no amount of these drugs is safe.

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        • 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.

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          • 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.

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          • 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.

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          • Another problem is these drugs work differently on almost everyone. Because on top of the receptor binding affinities that you can reasonably show in the lab you have people who have different receptor isoforms, different endogenous neurotransmitter and hormone levels, different circuitry, different drug metabolism, different other drugs they consume etc., etc. The problem with these drugs is: the do not treat any underlying problem, they are mainly tranquilizing/ mood altering and their effect on any human is purely empirical and changing from dose to dose, day to day. This is not medicine it’s quackery.

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  8. I’m so not surprised. I’ve tried Zyprexa and the side effects I had, although I took a very small dose (cutting the smallest pills into 4) were horrific and the withdrawal reaction continued for at least a week after a single dose. These things are so toxic it’s incomprehensible to me why they are used in the first place (well, maybe the reason is: money).

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  9. I dealt with a whole bunch of anticholinergic intoxication poisoning, according to drugs.com.

    Initially, I had anticholinergic intoxication poisoning caused by Voltaren 50mg, Ultram 50mg, Risperdal .5 mg – 2 mg, Lithium, 900mg – 1200mg, Seroquel 50mg – 400 mg, and Zantac 150 mg – 300 mg. This lasted for about four months.

    I had anticholinergic intoxication poisoning caused by Voltaren 50mg, Ultram 50mg, Lithium, 900mg – 1050mg, Seroquel 50mg – 400 mg, and Zyprexa 10mg – 20 mg. This lasted for approximately four months.

    Then my psychiatrist created anticholinergic intoxication with Voltaren 50mg, Ultram 50mg, Lithium, 900mg, Zyprexa 10mg – 20 mg, Proxyl 200mg, Geodon 240 mg, and Tregretol 150 mg. This lasted for approximately four more months.

    Then my psychiatrist created anticholinergic intoxication poisoning with Voltaren 50mg, Ultram 50mg, Lithium, 300mg – 900mg, Geodon 20 mg – 240 mg, Wellbutrin 150mg – 300 mg, Topomax 25 mg, and Carbitrol 200 mg – 500 mg. This lasted approximately 21 months, although much of this was a prolonged weaning off all these major drug interaction laden drug cocktails.

    “We need to use these drugs with caution. Dose matters. Length of time a person is on them matters. Polypharmacy matters.” Think I’ll end up with dementia, Sandy? No family history of it.

    And lets hope the psychiatrists some day learn that creating anticholinergic intoxication in patients with massive drug interactions is not actually “appropriate medical care,” and it’s not “bipolar” either. It’s anticholinergic intoxication poisoning. My “bipolar” etiology was the common adverse withdrawal effects of Wellbutrin, given for smoking cessation, worsened by the Voltaren and Ultram adverse effects.

    Isn’t it great we can medically explain the etiology and causes of “bipolar” now, however?

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    • No answer for those of us who dealt with medically provable iatrogenesis, Sandy? I mean no disrespect, but this may be why some here doubt your motive when claiming it is appropriate to maintain the psychiatric industry’s right force medicate people. My pastor has already confessed that psychiatric stigmatization, tranquilization, and poisoning with major drug interactions is the historic “dirty little secret of the two original educated professions” way of covering up easily recognized iatrogenesis and clergy sins.

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        • Let me try to clarify as I understand Someone Else’s criticism here:
          I think she means (and I tend to agree) that it is highly irresponsible (aside from other ethical problems) to allow psychiatrists to take decisions about drugging people against their will because:
          a) most of them have no clue about the many problems with this drugs (you’d be a rare exception rather than a rule)
          b) they should not be charged with making such profound decisions for someone because these drugs are not safe and any time you use them you are putting a patient in danger – informed consent should apply to such dangerous drugs (it should apply to every treatment but psych drugs are among the most invasive)
          c) one often (always?) cannot distinguish between the effect of a drug and the effect of a person’s mental distress. In the real world that translates to patients getting worse despite of the treatment or “unmasking underlying illnesses” and other mind-blowing examples of ill-logic.
          That would be another layer on top of a purely ethical concern about the use of force in psychiatry.

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        • Thank you for your response, Sandy, and as I mentioned above it is not my intent to be disrespectful to you. To the contrary, I am very grateful you are speaking out against what I, for obvious reasons, believe are crimes being committed against humanity by today’s psycho / pharmaceutical industries. But I do believe your heart is basically in the right place, and thank you for the work you are doing.

          I do disagree that doctors should have a right to force and coerce the toxic psychiatric drugs onto other human beings. The UN agrees with this as well, they call it “torture,” and it is. I also believe absolute power has corrupted the psychiatric industry absolutely at this point, you being one of the few exceptions.

          I agree with B’s statements about the drugs, and the toxic drug cocktails I was put on prove that either my doctor was an extremely unethical man or incapable of checking for moderate and major drug interaction warnings, thus an idiot (probably both).

          However, I do concede I do not have your experience in the industry, in regards to the need to force treat people. I just know the doctor who hospitalized me against my will (those drugs are not listed above), has now been arrested by the the FBI for unnecessarily hospitalizing, “snowing,” and performing unneeded surgeries on many patients for profit.

          Personally I believe the psychiatric industry should stop worshipping the DSM “bible,” and instead, learn to garner a little wisdom from the real bible. For example, “… the love of money is a root of all kinds of evil.” And, “Love your neighbor as yourself.”

          My question was, “Think I’ll end up with dementia, Sandy?”

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          • Someone else,
            I have no way of answering that last question. In the group with the highest exposure, the risk among those who were on anti-cholinergic drugs was 1.5 times higher than those who weren’t. It is hard to do the calculations of the drugs you have to figure out what risk group you would be in. Not all of the drugs on that list have anti-cholinergic effects. And there are other factors that also contribute to risk – diabetes, family history, high blood pressure to name a few. I think it is hard to take a study like this and apply to any given individual but it informs us about relative risks.
            I am sorry for what you have been through although it sounds like there were consequences for at least one of the psychiatrists involved.
            I am not addressing what you and B have raised about forced drugs since this has been discussed pretty extensively in my last blog.

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          • Sandy,

            Thank you again for the response. You’re right, the drugs I was on don’t all have anticholinergic effects, but when you check the drug cocktails on drugs.com, most warn of anticholinergic intoxication, so it was the combinations of drugs that were particularly toxic.

            Thank you for this info, “there are other factors that also contribute to risk – diabetes, family history, high blood pressure to name a few.” Surprisingly, I didn’t end up with diabetes (I think my current doctor was shocked.) And this is good news for me since I don’t have a family history or high blood pressure either.

            Actually, the doctor who was arrested was an internist, not the “snowing” psychiatrist. But I’m very grateful that one psychiatrist has now expressed sorrow for the crimes committed against me by both mainstream doctors and psychiatrists, due to their personal greed. Thank you for your empathy.

            And as to your comment, “I sometimes wonder how we know what we know… many [psychiatrists] emerge with the belief that the cognitive impairments associated with schizophrenia are due to the “disease” rather than the drugs we give.

            I will tell you that I’d had 40 hours of psychological career testing done not long before I was railroaded into the system, and I had a borderline genius IQ and it was recommended I be a “judge” or “architect.” I was given a CPT test in the midst of the first group of drugs listed above, resulting in a score of 15.11. A boss of mine, after I was weaned off the drugs gave me a business psychology test prior to hiring me, he was a lawyer and took the test at the same time. I missed 1 on the IQ portion, he missed 5. It’s the drugs that cause the cognitive problems, not the scientifically invalid disorders.

            “In a time of universal deceit – telling the truth is a revolutionary act.” I know it takes strength to speak the truth in your industry right now, thank you for what you’re doing. Tell your parents they should be very proud of your courageous stance.

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  10. “I have come back to this theme again and again. This is not an anti-drug discussion. It is a respect-the-drug discussion. We need to use these drugs with caution.”

    … say the people who have never been subjected to the suffering of psychiatry and the horrors of psychotropic drugs. Respect people. Reject drugs.

    “Dose matters. Length of time a person is on them matters. Polypharmacy matters.”

    People matter. Lives matter. Slay the Dragon of Psychiatry.

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  11. Wow, great discussion. It amazes me how complex the brain is, and the multiple, varied effects of drugs on our brains. As an E.R. Nurse, I have also learned about the tremendous lack of knowledge that Physicians have for the side effects (and direct effects) of medications. They usually do not have the time, or interest to keep up. I fairly recently learned about the fact that histamines are also neurotransmitters in the brain. In a very informal survey, I mentioned this to some Physicians and it seems that about 1 in 3 are aware of this fact, but I have not asked that many. Almost zero nurses are aware of it. The public is entirely unaware of it in my experience. The topic comes up a lot, because people often mention that “antihistamines make me feel weird”. I personally use them sometimes for allergies and they make me feel weird too- I break the allegra in thirds and take is as needed. I have even noticed some decrease in inhibitions, and increased lack of self-control (although I know I am still ultimately responsible for that). I remember reading someone who suggested that antihistamines could have been marketed as anti-depressants because of their similarities had they come out at an opportune time, or had been marketed for such use. (I wonder how many violent outbursts/ suicides might be linked to antihistamines?) This is fascinating and alarming about their link to dementia. I have seen benadryl break the severe EPS reactions of neuroleptic use even prior to the administration of cogentin ( and even rarely be the only drug used for this). I assume this is because of their anticholinergic properties, although I am not certain if this is the primary drug action that breaks the dramatic tonic EPS reactions (Does anyone know this off hand?). This has big implications for the millions taking antihistamines daily for allergies along with their use for psychiatric problems. I love your thoughtful posts!!!

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    • 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.

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