Posted by munificentexegete on February 12, 2007, at 4:55:50
In reply to Re: low dose risperdal -- linkadge, posted by linkadge on February 11, 2007, at 20:06:15
>> on a voluntary basis, with proper elucidation of the true risks, meaning proper independent long term studies, I agree with you. but that sounds like an alternative universe to the one we currently live in.
> Well, thats what boards like this are for. I agree that doctors don't educate patients fully about the risks of the drugs they push. I was not made aware about some of the side effects of drugs which harmed me.
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. then they should point out that drug treatments are the highest risk route for dealing with problems in living. 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.
>> yes, it is an established medical and legal fact that all antipsychotics typical and atypical cause EPS including TD.
> No. It is an established fact that they *can* cause TD and EPS. Like I said before, if they caused TD and EPS in everybody who took them, then I would have got TD or EPS from them which I didn't.you are right.
>> sad isn't it when many studies conclude the risk of suicide is higher with an AD than without.
> It is difficult to say, because many of the studies which concluded an increased risk of suicide were short term studies. It is not clear how they affect the rate of suicide in the long term.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?
>> well if it isn't a disease, then that means it isn't a medical issue doesn't it?
> Regardless of wheather it is a medical issue, it is a problem. For many people with this "manifestation", there is little apparent other way to improve symptoms. Even if it isn't a medical disease, if a medicine can aid in the treatment, and is justified in its risks, then it makes sense to take it.
Well understanding that problems in living are not medical diseases is an important understanding to reach. 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.
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.
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.
problems in living are confused with medical disease all the time.
>> for example EPS is generally thought to be a dopamine receptor issue, so they compare a dose of new antipsychotic that induces a dopamine block of 50%, to a dose of old antipsychotic that blocks 80%+ of dopamine.
> Yes. Atypicals have less binding to dopamine receptors that typical antipsychotics. They also bind more loosely to the receptor.
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?
>> although as a side note much EPS could also be due to anticholinesterase activity hence why atropine is often a successful treatment for things like dystonias.
> I had no idea that antipsychotics had binding to cholinsterase.http://cat.inist.fr/?aModele=afficheN&cpsidt=15105808
>> actually you have almost certainly incurred brain decay from the risperidone, although you have not yet incurred enough damage for the damage to be obvious.> Not necessarily. The side effects from many medications are not always linear. Damage occurs when the drug ofsets natural chemistry so much that dammage occurs. The brain is able to deal with a variety of toxins so long as they don't acumulate to high enough doses. Like bacteria. Your body can deal with germs so long as the they are not at too high a level, and you won't get sick.
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.
http://ajp.psychiatryonline.org/cgi/content/full/157/7/1150
so extrapolating from that study evey single milligram is causing brain damage.
> The progression of TD may also depend on things like antioxidant enzyme status. Nutritional status. Level of neuroprotective growth factors etc. The level of the growth factor BDNF, is often related to the development of brain dammage after the administration of neurotoxins.
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.
>> As has been established, every milligram of antipsychotic causes progressive irreversible neurological damage, in the same way that a neurological disease would cause if say you had Parkinson's disease.
> I don't think that has been established. If it has, you would be able to easily present me with data that specifically shows that all antipsychotics induce brain damamge at *all* doses (including low doses).
> There is absolutely no data to support that claim.> That is like saying that valproate damamges the liver at all doses, which is not true. Yes, valproate can dammage the liver, but many people take high doses of valproate for long periods of time without any evidence of liver damamge.
that's another discussion.
>> with cumulative dose of 300mg, say 2 mg for 150 days the risk of TD may be 3%, and so on. 3% is a very high probablity given the seriousness of TD for only consuming 300mg, but that is the risk I have seen from some studies of risperidone in the elderly.
> I don't think it works that way. Show me one study that concludes that the occurance of TD is related to cumulative drug ingested, and not maximum daily dose.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=W4L3A
>> well if psychosis is not a disease it falls outside the ambit of the medical profession, as a result medical intervention can never be justified on an involuntary basis.
> I never agree with the use of these drugs on an involtentary basis.>> on a voluntary basis, by contrast, a person should be free to pursue as many different treatment alternatives, for whatever non disease they have, as they desire.
> While there may not be direct proof that schizophrenia is a medical illness, there is no proof that it is not a medical illness.
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.
poster:munificentexegete
thread:730044
URL: http://www.dr-bob.org/babble/20070207/msgs/732037.html