Psycho-Babble Medication | about biological treatments | Framed
This thread | Show all | Post follow-up | Start new thread | List of forums | Search | FAQ

Re: low dose risperdal -- linkadge

Posted by munificentexegete on February 13, 2007, at 8:44:41

In reply to Re: low dose risperdal -- linkadge, posted by linkadge on February 12, 2007, at 19:57:40

>> yes, doctors should be upfront when a patient comes to them with anxiety or some other non disease, and point out that from a medical point of view they don't have anything wrong with them.

> It is difficult to say. While it is true that anxiety is a common human emotion, there is no way to prove that all humans experience it to the same degree. Just as every human experiences pain, but not all humans experience chronic pain.

Sure, however, there is nothing physically wrong with them, anxiety in the absence of biological markers is just a feeling nothing more is it not? There should be biological markers in the case of chronic pain: epinephrine, norepinephrine, cortisol levels, and beta-endorphins, insulin production, glucagon, growth hormone, prolactin, heart rate, blood pressure, vagal tone, oxygen saturation, breathing, intracranial pressure, and sweating can all be used to measure the stress response and pain. I am sure there are many more markers for pain.

>> then they should point out that drug treatments are the highest risk route for dealing with problems in living.

> If the anxiety is a result of environmental conditions then I would say yes. However, not all anxiety is a result of ones environment. Just as one can breed mice to be hyper anxious all the time with little environmental provocation.

Well the doctor isn't really there to deal with anything other than medical issues are they? If you prescribe medications for a non disease isn't that malpractice? If your doctor prescribed you chemotherapy if you didn't have cancer; would that be malpractice?

>> then objectively detail all the potential risks of the medication. a significant problem is the drug company research is as far from objective and independent as anything I've ever seen.

> I will agree with that.

>> I have been looking for some good research on antidepressants, you know things like the dose impact on serotonin levels, overall receptor occupancy, akathisia risk at different doses, however, there is a seeming black hole in this regard. is there a good site for this sort of research?

There has been a lot of research on relative binding affinities of drugs to certain sites.
The following website allows one to look for entries of drug binding to various receptors. I don't know what data has been but together regarding how this translates to side effects like akathesia.

> http://pdsp.cwru.edu/pdsp.php

thanks *puts on research glasses & grabs a cuppa*, I hope i can finally get some answers...

>> Well understanding that problems in living are not medical diseases is an important understanding to reach.

> True, but for many people with 'schizophrenia', there is no identifiable environmental cause or trigger.

Trigger for what? Delusions (retreating into fantasy worlds, overactive imaginations and apparently even using metaphors in one's speech is a sign of delusion), voices (doesn't everyone have an internal dialog), paranoia (being scared is a natural emotion like anxiety or depression), disorganised speech (not having perfect grammar is apparently a sign of disease), talking too quickly, showing too much emotion, showing too little emotion, talking too slowly, blunted emotions, having a messy haircut, wearing “odd” clothes, facial hair, not doing the dishes, quirky personality, not working for extended periods of time, not agreeing with the government. Some times even when none of these emotions or behaviours are present the person is diagnosed with “prodrome”. As schizophrenia is a medical delusion as it cannot be shown to exist by medical science and arguably a doctor diagnosing an imaginary disease is in much worse shape than their “patient”, then a prodrome is a delusion of a delusion is it not?

>> At the moment people incorrectly believe they have a medical condition when they get anxious or depressed, they see their doctor and he incorrectly tells them it is due to a chemical imbalance and then goes on to talk about reuptake mechanisms.

>> If they have biological depression on the other hand, then they can take blood and spinal fluid tests and measure their serotonin and dopamine levels to prove the existence of a disease that needs treatment.

> I agree, but such tests are not commonplace. In addition, there may be psychiatric manifestations that fall outside the realm of imbalances in serotonin or norepinephrine. Perhaps it is wrong to conclude that somebody is chemically imbalanced without proof. But, I fear that many people with true biological depression would not show so on any currently available tests. Just like there are no tests to prove migraine, but that doesn't make a persons suffering any less real.

How can one have biological depression without any evidence?

Some doctors won't prescribe even painkillers unless they have evidence of disease, like a lady I know who was involved in a car accident and has a permanent migraine as a result of her head injury which you could see on the MRI scan. With a migraine there is probably something to measure I would have thought, I could be wrong though, however, I would imagine there would be some enzyme or some identity to be traced, even the pain and stress markers that I listed above would probably be enough to guide a doctor in identifying a true migraine patient from a morphine addict. Otherwise couldn't we all just see the doctor for our weekly barbituate script?

>> less binding and looseness are hard to understand, are you referring to receptor occupancy, reversible vs irreversible binding, or half life or a combination thereof?

> Atypical antipsychotics at therapeutic doses have a higher Ki affinity for dopamine receptors than typical antipsychotics, ie less receptor occupancy. For atypical antipsychotics, certain additional binding properties are thought to contribute to antipsychotic efficacy, such as 5-h1a agonism (clozapine, seroquel, ziprazadone), 5-ht2a antagonism (all atypicals), sig-1r antagonism, (certain atypicals) etc.

ah ok, now i understand where you are coming from, they usually compare a dose of Atypical that creates a lower level of dopamine block than the Typical, and conclude it is a safer drug head to head. Problem is if you compare an equivalent dopamine block in an atypical v typical comparison one gets all the traditional side effects + a lot of new ones from blocking all the other receptors as well. So they are if anything more potent and more dangerous than the old ones, if the studies were actually performed on a truly comparable basis. Although I agree that due to the long half life of some of the typicals, overtime the dopamine block and neurological damage from them could be progressively amplified, although there are short half life typical antipsychotics as well such as molindone and thiothixene. Risperidone does have a particularly short half life while olanzapine has a medium half life which could build up in the brain tissue over a couple of days. So this means that psychiatrists can up the doses of Atypicals as high as they wish whenever they wish, and the neurological damage they can exact is now even more severe. Notwithstanding the half life issue, they are portraying more potent and toxic drugs as less potent and less toxic to gain acceptance when they are not that at all. I believe they are the presenting to us a pack of wolves and via the design of the research studies, dressing them as sheep.

>> That would be a good outcome, except for that to hold true low dose therapy should never result in TD. However, this isn't the case, not even for risperidone.

I would tend to think that lower doses have less likelihood of causing TD. Note I said less likelihood, not no likelihood. If you have data to suggest otherwise...

>>157/7/1150" target="_blank">http://ajp.psychiatryonline.org/cgi/content/full/>157/7/1150

>> so extrapolating from that study every single milligram is causing brain damage.

> Nice try. You are going to have to give a little more proof than..."extrapolating". Anyhow, the main results of this study were:

> 1) The 1-year cumulative incidence of persistent emergent tardive dyskinesia among the 255 patients without dyskinesia at baseline was 2.6%.

> 2) Patients with dyskinetic symptoms at baseline experienced significant reductions in the severity of dyskinesia.

> 3) Patients who received 0.75–1.5 mg/day of risperidone showed a significant improvement in psychopathologic symptoms over the 1-year period

That's a high rate of TD for a 1mg daily dose for less than a full year of treatment, think about it! I wonder what the 1 year TD score would be at a dose of 6mg+?

>> I guess it may depend on many things like a persons height, weight, sex and age, however, the main factors affecting the development and progression of tardive dyskinesia is obviously the size of the daily dose as well as the total amount of the drug consumed since beginning treatment.

> Again, this does not prove that every milligram of antipsychotic is causing brain damage. Even if we agree that TD may be related to daily dose, or total drug consumed does not prove that those who don't get TD have sustained any brain damage.

> You would need to show me data that proves that all antipsychotics cause brain damage in all patients who take them that is directly proportional to the amount of drug taken. No such data exists.

They have all been shown to cause TD, I have pointed to a study regarding low dose risperidone as this thread is about risperidone, and is often seen by many to be one of the least damaging atypicals, but TD data exists for all APs atypical or typical and all the drug company information admits as much. Unfortunately there have not been any definitive long term studies done using an equivalent level of dopamine blockade across all APs typical and atypical; with such a study we could definitively say which ones cause the most and which ones cause the least TD for a given level of antipsychotic activity.

My guess would be, everything else being equal, the longer half life drugs will cause the most TD. Although as has been already shown the atypicals also come with a whole new array of side effects from their wider receptor profile and effects, including more significant metabolic disorders such as diabetes and heart disease.

>>here read the section on TD from Janssen's web >site (page 2) common/company/pi/risperdal.pdf;jsessionid=W4L3A" target="_blank">http://www.janssen.com/active/janus/en_US/assets/>common/company/pi/risperdal.pdf;jsessionid=W4L3A

> Ok, so it says that the risk of TD is thought to increase with duration of treatment. That does not prove that all doses cause brain damage, only that if brain damage occurs, it may be related to duration of treatment.

I think you'll agree that when the drug company itself admits this to be the case in their drug information pamphlet, then it is fairly well established.

>> You'll have to elaborate on that one, I don't quite understand that point. Schizophrenia is not a medical disease, it is not a medical condition, it is a medical delusion.

> You see. Just because I lack proof that Schizophrenia is a medical illness, is not proof that it isn't a medical illness.

Of course it is. Without any medical evidence that schizophrenia is real, it can only be an imaginary disease. Without evidence seeing an imaginary disease in a healthy patient is a medical delusion.

>It may well be a medical illness whose biological underpinnings have yet to be elucidated.

Now we have moved from the scientifically based world of medical science into the alternate universe of theoretical medicine. From reality to imaginary, from fact to fiction we go. We can hypothesize that a person may have some sort of unknown disease, however, such a disease is hypothetical, imaginary, unproved, unsupported, not based on evidence, not scientific fact. A person cannot be diagnosed with an imaginary theoretical disease, it is an unsupportable diagnosis, it is not medical science.

Without evidence of disease we cannot ever be justified in treating anyone against their will; imagine getting a foot or a hand amputated if there was no proof of necrosis, or insulin poisoning if you didn't have diabetes. Speaking of necrosis have you seen pictures of the gangrene that people with diabetes get? Horrifying stuff when you consider that risperidone now has a FDA warning for diabetes. Is involuntary treatment of a patient by a doctor without evidence of disease a criminal activity?

The medical profession, the psychiatrists are the main culprits but gps do it too, shouldn't be allowed to go around diagnosing people with imaginary diseases and treating them for it by giving them pesticides, lobotomies or electricity, but that's exactly what they do.

We can merely point out that some people have overactive imaginations, feel strong emotions, behave oddly, or wear strange or old clothes or have an eccentric haircut. To diagnose a healthy patient as diseased is prima facie malpractice. To treat a healthy person for a disease they don't have is also malpractice. Sometimes the best medicine is no medicine at all.

> It doesn't really help those afflicted with the condition to go up to them and tell them..."hey, you don't have a medical disease". So what? It is easy to raise a flag, but much harder to offer viable, and practical alternative solutions.

How can you help someone without a disease? from a medical point of view you can't, in fact if you treat a healthy person, then you run the risk of introducing iatrogenic disease in an otherwise healthy person.

If a patient feels depressed or anxious then they shouldn't necessarily think that it is due to a disease. If there is something genuinely wrong with the patient, it will be possible to find it, there will be changes in brain structure or activity, enzyme, chemicals, t cell or cortisol changes, something indicating that something is amok with the body or brain. Without any hard evidence, it is not possible to confirm a diagnosis of disease and treating a medical delusion may only serve to injure an otherwise healthy patient.

Once a patient starts taking the antipsychotics they can measure all manner of iatrogenic disease, including brain, blood and heart diseases.


Share
Tweet  

Thread

 

Post a new follow-up

Your message only Include above post


Notify the administrators

They will then review this post with the posting guidelines in mind.

To contact them about something other than this post, please use this form instead.

 

Start a new thread

 
Google
dr-bob.org www
Search options and examples
[amazon] for
in

This thread | Show all | Post follow-up | Start new thread | FAQ
Psycho-Babble Medication | Framed

poster:munificentexegete thread:730044
URL: http://www.dr-bob.org/babble/20070213/msgs/732375.html