![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 9 to 33 of 38. Go back in thread:
Posted by linkadge on February 6, 2007, at 19:50:11
In reply to Re: J+J and Janssen in trouble over Risperdal » linkadge, posted by SLS on February 6, 2007, at 18:33:39
About 3 weeks @ 1mg. It also gave me the worst akathesia, worse than seroquel @75 or zyprexa @ 5mg.
Linkadge
Posted by linkadge on February 6, 2007, at 19:51:11
In reply to Risperdal has been a life-saver for me..ALL, posted by Jay on February 6, 2007, at 19:15:11
I agree, one mans curse could be another mans cure. If it works for you then just take all else with a grain of salt.
Linkadge
Posted by SLS on February 7, 2007, at 5:31:28
In reply to Re: J+J and Janssen in trouble over Risperdal, posted by linkadge on February 6, 2007, at 19:50:11
> About 3 weeks @ 1mg. It also gave me the worst akathesia, worse than seroquel @75 or zyprexa @ 5mg.
I can see that happening, of course. I would just like to point out that some neuroleptics produce anxiety as a startup side effect rather than akathisia.
I agree with Jay, and hope that these drugs do not become demonized in the same way benzodiazepines were. With what else we have available, I don't think they deserve it.
- Scott
Posted by Jay on February 7, 2007, at 10:04:57
In reply to Re: J+J and Janssen in trouble over Risperdal, posted by SLS on February 7, 2007, at 5:31:28
Yep..Scott and Link, I certainly don't think people should just take the drugs if problems show up, and that people shouldn't be afraid to be critical. Like you said Linkadge, it mostly depends on individual reactions. And Scott, I was very much thinking of the demon/fear stirred up over benzo use in this case. So, basically, I think we'd all agree, start low and go slow, and don't shrug off any side effects. Actually, in the post where I read about (an exception from above) using 2 or so mg of Risperdal at once for a few days, being somewhat useful for dysphoric mania, the author (a pdoc) said they had the same experience with a 2-3 day script of Haldol, at about 5mg. Interesting, because these two meds have some chemical connections.
Best,
Jay
Posted by Chairman_MAO on February 7, 2007, at 11:18:32
In reply to Re: J+J and Janssen in trouble over Risperdal, posted by linkadge on February 6, 2007, at 14:32:30
No one drug should be "brought down", because I believe we should have a free-market economy. It's just that the so-called "antipsychotics" should have to compete with morphine, benzodiazepines, etc. which can be just as effective in the treatment of psychosis, if not more so. And the "patient" can still think!
However, I will agree with you that risperidone is the most horrid of all of the "atypicals". Gynecomastia and other endocrine problems are far too common, viz. they happen at all! The only reason the atypicals are "safer" with regard to tardive dyskinesia AFAIK is that they bind more weakly to and/or dissocate more rapidly from D2 receptors. That's it. There's nothing magical, except perhaps with cloazpine, which is IMHO the only one of the whole class of those drugs anyone should try, as if you have to get to the aypticals, you might as well use the best one.
But far fewer people should be prescribed these things than are. Seroquel seems to be the most benign, but also mostly ineffective for treatment of schizophrenia (which, incedentally, is an obsolete and stigmatizing diagnostic category that should be abandoned).Of course, we live in an age where, despite the fact that acetaminophen/paracetamol is now known to cause liver damage at _therapeutic doses_ in _otherwise healthy individuals_, it is still considered preferable to morphine, which is non-toxic.
Posted by med_empowered on February 7, 2007, at 15:05:57
In reply to Re: J+J and Janssen in trouble over Risperdal » linkadge, posted by Chairman_MAO on February 7, 2007, at 11:18:32
I agree. Think about it: the only reason a drug company can make $$$ off of something as unpleasant as Risperdal is b/c of the RX drug system. We're giving docs waaaay too much power here.
Consumers end up with all costs--some medication costs, doctor costs, costs of side effects, so on and so forth. We should be allowed to purchase and use (or NOT purchase and refrain from using) any drug(s) we see fit. Think about ADHD...amphetamines are old, and cheap. If they were over-the-counter, consumers would probably avoid Adderall XR and what not and go for generic versions...drug costs would be reduced, and we wouldn't have to pay doctors for visits that are solely designed to give us a permission slip("prescription") to have meds that would otherwise be illegal.
In mexico, a lot of pharmacies have doctors on hand--not for controlled rx's, but for basic stuff. So if you come in with minor problems--infections, allergies, colds, whatever--the doc will do a quick consult and recommend some meds to you, and you're done. That's it. Here, you have to make an appointment, pay lots of money to the doc, and then the prescription is likely to be for some expen$ive new drug that doesn't actually benefit the consumer, but does benefit the doctor and drug companies. Its a ridiculous situation.
Posted by Sebastian on February 8, 2007, at 19:15:25
In reply to Re: J+J and Janssen in trouble over Risperdal, posted by med_empowered on February 7, 2007, at 15:05:57
I have to agree with a lot of the things you people are saying.
Risperdal, made me worse than I was. I started holucinating on it, my mucles were stiff as a board when on it, made me hungry, and I thought the TV was talking to me. had some weird thoughts on that drug.
I don't work for zyprexa or nothing, but its the most helpfull med I ever took. For most of my symptoms. I even wonder if I ever would have ended up in the hospital 3 times, if they had just given me that one first.
Ivan
Posted by munificentexegete on February 8, 2007, at 20:55:22
In reply to Re: J+J and Janssen in trouble over Risperdal, posted by med_empowered on February 6, 2007, at 9:57:32
> One study I read compared zyprexa (dosed based on clinical judgement) to fixed-dose Haldol, 5mgs, with prophylactic benztropine.
to how much zyprexa?
5mg Haldol is almost twice as much required to induce serious eps, you would have to compare it to about 30mg of zyprexa to make a valid comparison.
>they can also create some tremendous problems, and many people with psychotic disorders can do well without them.
they don't fix an imbalance and they do result in permanent damage to brain structure and indeed every organ in one's body.
Posted by Dinah on February 9, 2007, at 14:06:54
In reply to Re: J+J and Janssen in trouble over Risperdal, posted by munificentexegete on February 8, 2007, at 20:55:22
Risperdal has been a godsend for me. It is calming without making me drowsy. And it's calming in a bone deep way that benzos just can't mimic. I'm often less tearful on it, although I'm not sure whether it's because it has antidepressant qualities or if it's mainly anxiety that causes my depression.
If I use it regularly, I tend to lose touch with my emotions. And it's not great for my diabetes. So it's not without costs.
I have used between .25 mg and 1.5 mg a day, I think, with .25 mg being the norm for me when I use it. When I don't need it I don't use it, and I have no problems with withdrawal.
I find it a bit energizing, but it doesn't cause that creepy itchy jumpy feeling that anything with NE does for me.
I think results vary widely from person to person. But whatever it offers appears to be exactly what I need.
Posted by Dinah on February 9, 2007, at 14:39:19
In reply to Re: J+J and Janssen in trouble over Risperdal » munificentexegete, posted by Dinah on February 9, 2007, at 14:06:54
That was a general comment, not a reply to anyone in particular.
Posted by munificentexegete on February 9, 2007, at 15:03:42
In reply to Re: J+J and Janssen in trouble over Risperdal » munificentexegete, posted by Dinah on February 9, 2007, at 14:06:54
> Risperdal has been a godsend for me. It is calming without making me drowsy. And it's calming in a bone deep way that benzos just can't mimic. I'm often less tearful on it, although I'm not sure whether it's because it has antidepressant qualities or if it's mainly anxiety that causes my depression.
>
> If I use it regularly, I tend to lose touch with my emotions. And it's not great for my diabetes. So it's not without costs.
>
> I have used between .25 mg and 1.5 mg a day, I think, with .25 mg being the norm for me when I use it. When I don't need it I don't use it, and I have no problems with withdrawal.
>
> I find it a bit energizing, but it doesn't cause that creepy itchy jumpy feeling that anything with NE does for me.
>
> I think results vary widely from person to person. But whatever it offers appears to be exactly what I need.
>isn't the damage from risperdal cumulative, so that if tardive dyskinesia develops after say 100mg of risperdal, then it doesn't matter how low the dose is?
Posted by linkadge on February 10, 2007, at 11:44:50
In reply to Re: low dose risperdal -- Dinah, posted by munificentexegete on February 9, 2007, at 15:03:42
>they don't fix an imbalance
They do and they don't. In the case of a medication which can say, ameliorate an overactive HPA axis, improve sleeping patterns, or improve social function, one is likely to see subsequent improvements in other aspects of brain health. Some studies suggest that treatment with certain agents can prevent hippocampal volume loss associated with mood disorders.
It is hard to say that the drug doesn't get to the root cause, when nobody really knows what the root cause is.
>they do result in permanent damage to brain >structure and indeed every organ in one's body
That is simply not true. The verdict is not in on the newer antipsychotics yet. While they may cause symptomatic movement problems, there is not much conclusive evidence that they cause irreversable brain dammage, let alone dammage to every organ in the body.
There are risks involved in treatment of course, just as there are risks involved in lack of treatment.
It is fair to say that a patient should be fully informed about risks, but unfair to blow risks out of proportion.
Linkadge
Posted by munificentexegete on February 10, 2007, at 16:10:16
In reply to Re: low dose risperdal -- Dinah, posted by linkadge on February 10, 2007, at 11:44:50
>>they don't fix an imbalance
> They do and they don't.which imbalance do they fix?
>>they do result in permanent damage to brain structure and indeed every organ in one's body
> That is simply not true.
> The verdict is not in on the newer antipsychotics yet.http://www.contac.org/contaclibrary/medications22.htm
> It is fair to say that a patient should be fully informed about risks
once TD is proved, it is simply as bad as a typical AP.
Posted by cb_psy on February 11, 2007, at 5:41:25
In reply to J+J and Janssen in trouble over Risperdal, posted by halcyondaze on February 5, 2007, at 14:41:53
Ive read that it has antidepressant and anti anxiety effects at lower dosage.
"The only receptor subtype that risperidone is likely or known to saturate at these lower doses (0.5-1 mg/day) is the 5-HT2A receptor" (Schotte et al, 1996; Nyberg et al, 1999; Talvik-Lofti et al, 2000).
Posted by linkadge on February 11, 2007, at 11:42:57
In reply to Re: low dose risperdal -- Dinah, posted by munificentexegete on February 10, 2007, at 16:10:16
>which imbalance do they fix?
Like I said, antipschotic treatment can oftentimes be associated with a normalization of the HPA axis. Some researchers think that psychosis in some people is fundimentally caused by HPA axis abnormalities, hence the strong antipsychotic actions of antiglutacortacoid drugs like RU-486.
>http://www.contac.org/contaclibrary/medications22>.htmA single case of something does not proove anything. The woman was taking lithium too, which has occasionally been asociated with TD. It is impossable to say that everybody treated with atypical antipsychotics is going to develop TD, even if there have been some cases of it.
There are going to be risks involved in treatment of any disease. The decision to take a medication or not is based on the personal cost/benifit ratio.
>once TD is proved, it is simply as bad as a >typical APIts not a matter of being proven or not. You have proved that TD *can* occur. That does not proove that TD will occur in any given patient.
Just as any given side effect for any drug will not occur in all patients.
Linkadge
Posted by Dinah on February 11, 2007, at 14:36:45
In reply to Re: low dose risperdal -- Dinah, posted by linkadge on February 11, 2007, at 11:42:57
Hmmm... That makes sense. I've long thought, from things totally unrelated from emotional disorders, that my HPA axis was involved in whatever was wrong with me.
Posted by rina on February 11, 2007, at 14:44:22
In reply to Re: J+J and Janssen in trouble over Risperdal, posted by SLS on February 7, 2007, at 5:31:28
> > About 3 weeks @ 1mg. It also gave me the worst akathesia, worse than seroquel @75 or zyprexa @ 5mg.
>
> I can see that happening, of course. I would just like to point out that some neuroleptics produce anxiety as a startup side effect rather than akathisia.
>
> I agree with Jay, and hope that these drugs do not become demonized in the same way benzodiazepines were. With what else we have available, I don't think they deserve it.
>
>
> - Scott
can someone tell me what akathesia is?
Posted by munificentexegete on February 11, 2007, at 15:24:42
In reply to Re: low dose risperdal -- Dinah, posted by linkadge on February 11, 2007, at 11:42:57
>>which imbalance do they fix?
> Like I said, antipschotic treatment can oftentimes be associated with a normalization of the HPA axis. Some researchers think that psychosis in some people is fundimentally caused by HPA axis abnormalities, hence the strong antipsychotic actions of antiglutacortacoid drugs like RU-486.
many people have many hypotheses about many things, some people think including myself that time travel is possible, although there is no reproducable evidence supporting the cause of psychosis meaning it is merely an unsupported hypothesis at best, not scientific fact.
> A single case of something does not proove anything. The woman was taking lithium too, which has occasionally been asociated with TD. It is impossable to say that everybody treated with atypical antipsychotics is going to develop TD, even if there have been some cases of it.
do you really think there is only one case of TD with risperdal. EPS, NMS, TD, dystonias, akathisia, parkinsonism its all there in risperidone and any side effect profile worth its salt points it out. I just pointed out that court cases have been won meaning it is also legal fact too.
> There are going to be risks involved in treatment of any disease. The decision to take a medication or not is based on the personal cost/benifit ratio.
what disease?
>> once TD is proved, it is simply as bad as a typical AP
> Its not a matter of being proven or not. You have proved that TD *can* occur. That does not proove that TD will occur in any given patient.most of the studies assume EPS including TD occurs and try to point out that it produces relatively less incidence of EPS/TD. They change the doses to make it seem this way.
> Just as any given side effect for any drug will not occur in all patients.
i think it is fairly well established that risperdal causes EPS including TD. So the next issue it what is the max single dose that can induce serious eps, i think it is about aorund 5 to 6 mg depending on size weight and sex of the patient. Then what is the risk of tardive dyskinesias from long term treatment, it may be a 2% chance with 300mg, 20% chance @ 600mg and a 50% chance at 900 mg (there hasn't been enough long term studies to confirm these numbers yet). then doctors and patients could make informed choices at least regarding the potential for serious permanent brain disease from antipsychotic medication. is psychosis even a medical issue?
Posted by linkadge on February 11, 2007, at 16:51:44
In reply to Re: low dose risperdal -- linkadge, posted by munificentexegete on February 11, 2007, at 15:24:42
For starters, nobody is forcing you to take any of these drugs. If you don't believe they are safe, then don't take them, no harm done.
>many people have many hypotheses about many >things, some people think including myself that >time travel is possible, although there is no >reproducable evidence supporting the cause of >psychosis meaning it is merely an unsupported >hypothesis at best, not scientific fact.
I am not saying that any one identifyable cause of psychosis has ever been established, nor do I think there will ever be. I am simply saying that people's suffering is real. Considering the lack of viable alternatives, I think the judicious use of antipsychotics is warrented.
>do you really think there is only one case of TD >with risperdal. EPS, NMS, TD, dystonias, >akathisia, parkinsonism its all there in >risperidone and any side effect profile worth >its salt points it out. I just pointed out that >court cases have been won meaning it is also >legal fact too.
Yes. it is a legal fact that these drugs *can* cause neurological problems. Just as cases have been won on the issue of antidepressnats causing people to commit suicide. Again, this does not conclude that everybody who takes these drugs will have this side effect.
>what disease?
It really doesn't matter what you want to call it, disease or otherwise. If you are saying that suffering is not real just because it cannot be observed under a microscope then I think we have lost the point.
>most of the studies assume EPS including TD >occurs and try to point out that it produces >relatively less incidence of EPS/TD. They change >the doses to make it seem this way.
I don't understand.
>i think it is fairly well established that >risperdal causes EPS including TD.
No. It is well established that risperidal *can* cause TD. The *numerical* indicence has not been established. I took risperidal, I did not develop TD. So therefore it is not true that risperidal causes TD in everybody.
>So the next issue it what is the max single dose >that can induce serious eps, i think it is about >aorund 5 to 6 mg depending on size weight and >sex of the patient. Then what is the risk of >tardive dyskinesias from long term treatment, it >may be a 2% chance with 300mg, 20% chance @ >600mg and a 50% chance at 900 mg
But, nobody takes that much risperidal.
>then doctors and patients could make informed >choices at least regarding the potential for >serious permanent brain disease from
>antipsychotic medication.>is psychosis even a medical issue?
Maybe not. But unforunately, there are no other established treatments for the problem. If it is not a medical issue what do you recomend? Excorcism? Studies suggest that these problem tend to get worse over time.
Linkadge
Posted by munificentexegete on February 11, 2007, at 18:53:18
In reply to Re: low dose risperdal -- linkadge, posted by linkadge on February 11, 2007, at 16:51:44
> For starters, nobody is forcing you to take any of these drugs. If you don't believe they are safe, then don't take them, no harm done.
true, however, most people will come into contact with these drugs on an involuntary basis at some point in their life such as in the foster care system, in a nursing homes, and even in the teen screen process.
>> many people have many hypotheses about many things, some people think including myself that time travel is possible, although there is no reproducable evidence supporting the cause of psychosis meaning it is merely an unsupported hypothesis at best, not scientific fact.
>I am not saying that any one identifyable cause of psychosis has ever been established, nor do I think there will ever be. I am simply saying that people's suffering is real. Considering the lack of viable alternatives, I think the judicious use of antipsychotics is warrented.
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.
>> do you really think there is only one case of TD with risperdal. EPS, NMS, TD, dystonias, akathisia, parkinsonism its all there in risperidone and any side effect profile worth its salt points it out. I just pointed out that court cases have been won meaning it is also legal fact too.
> Yes. it is a legal fact that these drugs *can* cause neurological problems.
yes, it is an established medical and legal fact that all antipsychotics typical and atypical cause EPS including TD.
> Just as cases have been won on the issue of antidepressnats causing people to commit suicide.
sad isn't it when many studies conclude the risk of suicide is higher with an AD than without.
> Again, this does not conclude that everybody who takes these drugs will have this side effect.
however, everyone is exposed to the risk of developing serious neurological damage with these drugs. it is about calculating the probablities given the size of the dose and the length of treatment.
>> what disease?
> It really doesn't matter what you want to call it, disease or otherwise. If you are saying that suffering is not real just because it cannot be observed under a microscope then I think we have lost the point.
well if it isn't a disease, then that means it isn't a medical issue doesn't it?
>> most of the studies assume EPS including TD occurs and try to point out that it produces relatively less incidence of EPS/TD. They change the doses to make it seem this way.
> I don't understand.
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.
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 think it is fairly well established that risperdal causes EPS including TD.
> No. It is well established that risperidal *can* cause TD. The *numerical* indicence has not been established. I took risperidal, I did not develop TD. So therefore it is not true that risperidal causes TD in everybody.
however, you were exposed to a risk of developing TD. That risk is exacerbated by increased doses and the total amount of risperidone injested. 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. 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.
>> So the next issue it what is the max single dose that can induce serious eps, i think it is about aorund 5 to 6 mg depending on size weight and sex of the patient. Then what is the risk of tardive dyskinesias from long term treatment, it may be a 2% chance with 300mg, 20% chance @ 600mg and a 50% chance at 900 mg
> But, nobody takes that much risperidal.
every milligram injested causes neurological damage, if overtime the total amount of risperidone injested by a patient from the time they first start taking the medication is more than say 100mg, that would be taking 2mg for 50 days, there may be a 0.05% chance that neurological decay caused by the risperidone displays as TD.
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.
>> is psychosis even a medical issue?
> Maybe not. But unforunately, there are no other established treatments for the problem. If it is not a medical issue what do you recomend?Excorcism?
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.
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.
> Studies suggest that these problem tend to get worse over time.
what problem are we talking about precisely, a disease, or something else?
Posted by linkadge on February 11, 2007, at 20:06:15
In reply to Re: low dose risperdal -- linkadge, posted by munificentexegete on February 11, 2007, at 18:53:18
>true, however, most people will come into >contact with these drugs on an involuntary basis >at some point in their life such as in the >foster care system, in a nursing homes, and even >in the teen screen process.
I don't agree with using medications in such ways.
>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, 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.
>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.
>however, everyone is exposed to the risk of >developing serious neurological damage with >these drugs. it is about calculating the >probablities given the size of the dose and the >length of treatment.
That sounds fair.
>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.
>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.
>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.
>However, you were exposed to a risk of >developing TD. That risk is exacerbated by >increased doses and the total amount of >risperidone injested.True.
>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.
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.
>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).
>every milligram injested causes neurological >damage,
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.
>if overtime the total amount of >risperidone >injested by a patient from the time they first >start taking the medication is more than say >100mg, that would be taking 2mg for 50 days, >there may be a 0.05% chance that neurological >decay caused by the risperidone displays as TD.
It does't work that way. Like I said before, the brain is able to deal with toxic agents quite well, so long as the dose is low, and its defences are high. Dammage only occurs when the system is overwhelmed.
Think of it this way. There are pesticides which are anticholinsterase inhibitors. They raise levels of acetycholine so high that the result is neurological dammage. But, low doses of anticholinsterase inhibitors are in many foods you eat. Green tea inhibits acetycholinsterase. Yet green tea is highly neuroprotective. So you cannot say that acetycholinsterase inhibition causes dose dependant neurotoxicity.
>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.
>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.
>what problem are we talking about precisely, a >disease, or something else?It doesn't matter. People need solutions.
Linakdge
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.
Posted by Phillipa on February 12, 2007, at 18:36:30
In reply to Re: low dose risperdal -- linkadge, posted by munificentexegete on February 12, 2007, at 4:55:50
To the best of my knowledge the serotonin in blood is not indicative to the brain or the serotonin in the spinal fluid. Most is in the gut. Love Phillipa
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
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.phpthanks *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.
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