Posted by linkadge on February 12, 2007, at 19:57:40
In reply to Re: low dose risperdal -- linkadge, posted by munificentexegete on February 12, 2007, at 4:55:50
>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 proove that all humans experience it to the same degree. Just as every human experinces pain, but not all humans expericne chronic 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 cen breed mice to be hyperanxious all the time with little environmental provokation.
>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.>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 idenfyable environmental cause or trigger.
>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.
I agree. So called 'anxiety disorders' are for the most part manufactured. Serious psychotic disorders are not IMHO. While a person with an anxiety disorder may be able to get by with exercise, behavioral modication, and valerian root, psychotic disorders often do not respond very well such inteventions.
>That approach is misleading as a person then >incorrectly believes they have a medical >condition which they medication for, when in >reality they do not.
For the most part I would say you are correct.
>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 additon, there may be psychiatric manifestations that fall outside the rhelm of imbalances in serotonin or norepinephrine. Perhaps it is wrong to conclude that somebody is chemically imballanced without proof. But, I fear that many people with true biolocial depression would not show so on any currently available tests. Just like there are no tests to proove migrane, but that doesn't make a persons suffering any less real.
>less binding and loosness are hard to >understand, are you referring to receptor >occupancy, reversible vs irreversible binding, >or half life or a combination thereof?Atypical antipsychotics at theraputic doses have a higher Ki affinity for dopamine receptors than typical antipsychotics, ie less receptor occupancy. For atpyical 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.
>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 likelyhood of causing TD. Note I said less likelyhood, not no likelyhood. If you have data to suggest otherwise...
>http://ajp.psychiatryonline.org/cgi/content/full/>157/7/1150
>so extrapolating from that study evey 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
>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 proove that every miligram of antipsychotic is causing brain dammage. Even if we agree that TD may be related to daily dose, or total drug consumed does not proove that those who don't get TD have sustained any brain dammage.
You would need to show me data that prooves that all antipsychotics cause brain dammage in all patients who take them that is directly proportional to the amount of drug taken. No such data exists.
>here read the section on TD from Janssen's web >site (page 2) >http://www.janssen.com/active/janus/en_US/assets/>common/company/pi/risperdal.pdf;jsessionid=W4L3AOk, so it says that the risk of TD is thought to increase with duration of treatment. That does not proove that all doses cause brain dammage, only that if brain dammage occurs, it may be relted to duration of treatment.
>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 Schizohprenia is a medical illness, is not proof that it isn't a medical illness. It may well be a medical ilness whose biolocial underpinnings have yet to be elucidated. It is the same as chronic fatigue syndrome. No one identifyable cause has been established, that does not mean that the disease has no underlying biological abnormality.
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 disase". So what? It is easy to raise a flag, but much harder to offer viable, and practical alternative soltions.
Linkadge
poster:linkadge
thread:730044
URL: http://www.dr-bob.org/babble/20070207/msgs/732267.html