![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
[email protected]Shown: posts 14 to 38 of 38. Go back in thread:
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.
Posted by linkadge on February 14, 2007, at 18:55:44
In reply to Re: low dose risperdal -- linkadge, posted by munificentexegete on February 13, 2007, at 8:44:41
>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.
Unfortunately these are not always practical diagnostic markers. It is possable for an individual to experience chronic pain in the absense of such indicators.
The same thing goes with depression. I believe there are probably dozens of biochemical imbalances which have not yet been fully discovered let alone have accuate diagonostic tests for.
I would not deny a person medicaton for chronic pain based on the fact that no test indicates they are in pain. That could be a grave mistake.
>Well the doctor isn't really there to deal with >anything other than medical issues are they?
Yes, they are there to deal with medical issues. Due to the unfortunate imperfections of modern science however, they must also work within the rhelm of presumed medical illnesses. Its like parkinsons disease. You can treat parkinsons without seeing anything but physical symptoms. There are no accurate "dopamine" tests or anything to indicate parkinsons. The same thing goes with alhzheimer's. You cannot truly diagnose alzheminer's untill after death. But doctors will still medicate for what they presume is alzhemiers. Is that wrong. Maybe some would say so, but I wouldn't.
>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?
It would only be malpractice if there wasn't good reason to suspect it was cancer. If all the conventional diagonostic tests were utilized and pointed to cancer, then chemotherapy is indicated.
Unfortunately, in depression, there are no usefully diagonistic tests, because it is very unlikely that it is one singal disease. Not all depressed patients are hypersecretors of cortisol. Not all blood tests, or even post mortem tests indicate low levels of monoamines. But it would be unethical to assume that a person's suffering is artificial just because science lacks the tools to identify the problem.
You do realize, that even if a spinal fluid test indicates low serotonin, that SSRI's or MAOI's are not correcting the problem. So, even for those who can be identified by monoamine tests, all medications are still only working on a symptomatic level. As such, there is no such thing as anyones disease being more physical than another's.
>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),How much do these people have to suffer for somebody to help them out? You can excuse their disease, but what does that do? When I was a child, I used to look at my grandfather with Parkinson's and ask my mother "why doesn't he just keep his hands still??"
If you are able to mentally write off the symptoms of schizophrenia, then clearly you do not have it, and should never need antipsychotic medication. But, why do that to people who do have the disorder? If they kill themselves because of their delusions, would you still blame that on an "overactive imagination". Clearly there are degrees of the illness, but trying to write off human suffering is not right IMHO.
Everybody knows that these people disever better than antipsychotics. But what?>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.
Let those who can get by without drugs do so.
>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.
Thousands of studies have failed to indicate any consistent changes in the levels of monoamine transporters in affective disorders. I agree. When and if the drugs work, they work for unknown reasons.
> I agree, but such tests are not commonplace. In>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.
Whats the lesser of two evils? Prescribing painkillers to somebody who doesn't need them, or
not prescribing them to somebody who does?>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.
You don't treat migranes with morphine. They can be treated with other drugs which are generally not abusable. Patients generally don't fake migrane to get on triptans, beta blockers, or anticonvulsants. Just as most people don't fake depression to get on SSRI's. SSRI's are not that good. I found SSRI' therapy very disagreeble, even when I was very depressed.
Sure, there could be some yet unidentified biological cause of all migrane. Unfortunately, we *do not( have any test which identifies migrane with a high degree of accuracy.
>Otherwise couldn't we all just see the doctor >for our weekly barbituate script?I would not want to live life on barbiturates. I do not find sedatives enjoyable at all, they make me depressed, and use them as infrequently as possable. I am fortunate that they are there when I need them, and am glad that a doctor trusts me to prescribe them, since I know we could go through 1000s of tests and come up with no idenifyable cause of anxiety.
Why should the few people who abuse these drugs ruin it for the rest?
>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,Not necessarily. We have not yet identified significant negative consequence of say histamine blockade, or 5-ht2a receptor blockade. This does not mean that the drugs are perfectly safe, it just means that it by conventional tests, they could be safer than traditional drugs. For instance, 5-ht1a agonists generally have little toxicity. In very high doses they can cause hypothermia, but many food substances are 5-ht1 agonists, such as olemide.
>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.
High doses of atypicals are very rarely used for anxiety disorders. In low doses, drugs like risperidal probably achieve their so called anti-anxiety effect through serotonin receptor blockade. I never said the drugs were perfectly safe.
>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.
We do not know whether the drugs are more toxic, or less toxic at this point. Only time will tell.
>I believe they are the presenting to us a pack >of wolves and via the design of the research >studies, dressing them as sheep.You could be right.
>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+?
But that rate was not accounting for the what dyskinesias people had on startup. The study highlights said that dyskinesease dropped in some patients switched from typicals.
When I took risperidal for anxiety, I took like 0.25-0.5 mg.
>They have all been shown to cause TDYes that is a possability.
>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.
I personally didn't think that study was all that scarry.
>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.
Again, I never said they were perfectly safe. There are risks to treatment as well as risks to nontreatment. I understand that sorting things out can be maddening.
>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.
I never doubted that TD is a possable side effect of antipsychotic treamtment.
>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.Well then I guess alzheimers, migrane, parkinsons etc, CFS, are just medical delusions too.
There is medical evidence that shizophrenia is a medical disease. There are usually a number of physical alterations/abnormalities of the brain's of those with schizophrenia, namely hippocampal and temporal lobe abnormalties, grey matter abnormalities. Disorder of the prefrontal cortex, mitochonidial dysfunction, abnormalties of glutamatergic function. Abnormalties in intracellular activity, PKC, GSK-3b, GAP-43, calcuium, etc. Those who research the genetics and anatomy of shizophrenia have little doubt that it is a disease, however there is not a whole lot of take home points from these findings, nor any clear tests to identify it in living patients.
>Now we have moved from the scientifically based >world of medical science into the alternate >universe of theoretical medicine.Nobody is forcing you to believe that this is infact a disease. If you want to believe that schizophrenia is just a figment of the imagination, then go right ahead.
This affliction will still continue to plague humanity whether people want to believe that it a result of some brain abnormality, or possesion by spawn of Lucfer.
>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.Of course it is not a scientific fact. There are a lot of things in life that we respond to without having to beforehand establish them as scienfific fact.
>A person cannot be diagnosed with an imaginary >theoretical disease, it is an unsupportable >diagnosis, it is not medical science.
It is supportable, just not 100% conclusive. There are a lot of things in life that are not 100% conclusive. Scientists are still in the realm of collecting data and formulating hypothesis about many of these problems. But in the meantime, I urge you to establish a treatment modality which is more efficatous than the one at present.
But, if you feel there is nothing wrong, then this conversation is pointless. If your reason for visiting this site is simply to tell us that we are all perfectly healthy people, then your comment is duely noted.
>Without evidence of disease we cannot ever be >justified in treating anyone against their will;
I agree with you 110%.
>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?
I think that anybody has the legal right not to take medication if they so choose. But legality is a separate issue.
>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.
For starters I don't even think the lobotomy occurs anymore. So we can stratch that one off the list. I agree with you 100% that people should never be treated against their will. But for those who concentually want to be treated with antipsychotics, antidepressants, or ECT, I beleive they should have the right.>Sometimes the best medicine is no medicine at all.
I agree.
>How can you help someone without a disease?
Thats a good question. I don't know why TCA antidepressants worked when they did. I don't know why sedatives work. Do I not have a disease? I don't really care. I'm here because medications have helped me in the past.
>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.
What is your defintion of a healthy person? When I was getting 2 hourse of sleep, vomiting from anxiety, crying 3+ hours a day, shaking, eating nothing, hiding in a courner and activly suicidal, I suppose there was nothing at all wrong with me. Just a healthy person going about their daily living. All I care was that the medications helped me to get better.
>If a patient feels depressed or anxious then >they shouldn't necessarily think that it is due >to a disease.
I agree.
>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.
Sorry, but I totally disagree with you. There are *no* conventional diagnostic tests for depressive or anxiety disorders. Like I said above, only a fraction of depressed patients show cortisol abnormalities. There is some evidence of regional brain hypofunction in depressed patients, but it is not unique to depression, ie it occurs in all sorts of other psychiatric disorders. The levels of monoamine metabolities in the cerebral spinal fluid is only a measure of monoamine breakdown, it says nothing about how well a particular monoamine is functoning. It says nothing about the inegrity or responsivness of the receptors.
>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.
Or it may help. I was diagnosed with depression without any "hard" evidence. I was not injured by treatment, and I believe the treatment aided in my recovery. I am no longer on any medications.
>Once a patient starts taking the antipsychotics >they can measure all manner of iatrogenic >disease, including brain, blood and heart >diseases.I reiterate. Those are possable side effects. There is no data to proove that all patients will get such side effects.
Linkadge
Posted by munificentexegete on February 15, 2007, at 7:42:15
In reply to Re: low dose risperdal -- linkadge, posted by linkadge on February 14, 2007, at 18:55:44
>>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.
> Unfortunately these are not always practical diagnostic markers. It is possible for an individual to experience chronic pain in the absence of such indicators.
How is that possible? Pain is a pathophysiological process. Some of the chemicals involved include prostaglandins and a protein called cyclooxygenase 2 (COX-2), these can be measured. It also affects other metabolic pathways and systems operating within the body, it can be identified directly or indirectly, you can test for it with the test I listed above, there are probably many more. A doctor has many lab test to prove the presence and persistence, even the severity of pain.
> I would not deny a person medication for chronic pain based on the fact that no test indicates they are in pain. That could be a grave mistake.
Let's take asprin, it binds to COX2 proteins and stops them from producing protaglandins. If you measured the patient's prostaglandins and found that their levels were not elevated, then prescribing asprin would not reduce the patient's pain, and by disrupting the patient's normal biochemical pain process, actually cause it to malfunction and not operate to produce pain as appropriate, in addition what if the patient dies from internal bleeding from the asprin?
> The same thing goes with depression. I believe there are probably dozens of biochemical imbalances which have not yet been fully discovered let alone have accurate diagnostic tests for.
Yes, however, isn't altering the serotoninergic system when there is no evidence of abnormality introducing iatrogentic disease?
>> Well the doctor isn't really there to deal with anything other than medical issues are they?
> Yes, they are there to deal with medical issues. Due to the unfortunate imperfections of modern science however, they must also work within the realm of presumed medical illnesses. Its like Parkinson's disease. You can treat Parkinson's without seeing anything but physical symptoms. There are no accurate "dopamine" tests or anything to indicate Parkinson's. The same thing goes with Alzheimer's. You cannot truly diagnose Alzheimer's until after death. But doctors will still medicate for what they presume is Alzheimer's. Is that wrong. Maybe some would say so, but I wouldn't.
Well actually the pathophysiology of both Parkinson's and Alzheimer's are well documented. There are two components to consider. The first is diagnosis. In the case of Parkinson's can be diagnosed by physical symptoms such as slowness in movement as well as resting tremor together with MRIs to confirm the existence of damage to the substantive nigra portion of the brain as well as urine, blood, or spinal tests as well as PET scans to confirm changes in the patient's dopamine levels or dopamine receptor performance. The same can be said of Alzheimer's disease where a diagnosis can be made on the basis of biomarker tests such as Beta-amyloid measured in cerebrospinal fluid, Tau protein measured in cerebrospinal fluid, and neural thread protein/AD7C-NTP measured in cerebrospinal fluid and in urine. This can be augmented with FDDNP PET scans and psychological testing. Those tests are necessary to confirm the diagnosis. What a surgeon's scalpel can do to the dead, PET can easily or even more accurately do to a living brain.
Now moving on to the treatment of Parkinson's disease, there are several options. Depending on which part of the dopaminergic system is identified as damaged, dopamine agonists and levodopa may be used. Treatment of Parkinson's with Atropine without evidence that ACh levels are too high, is unsupported. The treatment of Alzheimer's without evidence that ACh levels being too low is also unsupported with the some of the drugs like donepezil acting as nerve toxins, although reversible in nature.
>> 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?
> It would only be malpractice if there wasn't good reason to suspect it was cancer. If all the conventional diagnostic tests were utilized and pointed to cancer, then chemotherapy is indicated.
Yes, they would need to provide evidence to support their diagnosis, if the patient died, would that be manslaughter as well?
> Unfortunately, in depression, there are no usefully diagnostic tests, because it is very unlikely that it is one single disease. Not all depressed patients are hypersecretors of cortisol. Not all blood tests, or even post mortem tests indicate low levels of monoamines. But it would be unethical to assume that a person's suffering is artificial just because science lacks the tools to identify the problem.
Sure there are, how many times have you read about Ki bindings, receptor occupancy, even receptor firing rates, dopamine levels, etc, there are literally hundreds of potential diagnostics. Finding disease in a healthy patient without evidence is a medical delusion.
> You do realize, that even if a spinal fluid test indicates low serotonin, that SSRI's or MAOI's are not correcting the problem. So, even for those who can be identified by monoamine tests, all medications are still only working on a symptomatic level. As such, there is no such thing as anyones disease being more physical than another's.
Well if a problem with the serotogenic system is identified, the SSRIs and MAOIs help the brain to increase its use of available serotonin by blocking the reuptake of serotonin. MAOI's work by inhibiting the enzyme monoamine which then stops serotonin and other chemicals from being broken down by the brain.
>> 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),> How much do these people have to suffer for somebody to help them out? You can excuse their disease, but what does that do? When I was a child, I used to look at my grandfather with Parkinson's and ask my mother "why doesn't he just keep his hands still??"
What are they suffering from? Overactive imaginations and internal dialog? Your grandfather obviously had Parkinson's, however, that has a pathophysiology that can be identified. Can you show me any evidence that anyone diagnosed with schizophrenia has a disease, that their brain will somehow decay overtime, can you show me the malfunctioning or damage to the dopaminergic or serotogenic system, can you show me a gene that proves the disease, can you show me any evidence of any pathophysiology at all? something more than imagination and internal dialog? You don't expect me to trust a diagnosis made without any evidence at all do you? By that definition of disease every human on this planet has schizophrenia. Is medicine a matter of trust, or is it based on science? When we see disease in healthy individuals without any evidence then we have moved from medical science to a medical delusion.
> If you are able to mentally write off the symptoms of schizophrenia, then clearly you do not have it, and should never need antipsychotic medication.
Does a doctor need to have had a disease to diagnose it? He does however need medical evidence to support a medical diagnosis.
> But, why do that to people who do have the disorder?
What disorder? Schizophrenia is a medical delusion.
> If they kill themselves because of their delusions, would you still blame that on an "overactive imagination". Clearly there are degrees of the illness, but trying to write off human suffering is not right IMHO. Everybody knows that these people deserve better than antipsychotics. But what?
People have suicidal thoughts from problems in living, intense stress and severe depression are medically identifiable and treatable. Imagination and internal dialog are not.
There have been many studies performed on the extreme violence induced by akathisia. I believe it is the neurological disease most likely to trigger violence and suicide in otherwise calm and tranquil people, and it occurs in more than 75% of patients injected with 10ml of haloperidol. If you wanted a healthy person to commit suicide, giving them a single medium to large dose of antipsychotic is the only medication I can think of that would be most likely to elicit a suicidal response. I wonder what the suicide rate would be for healthy people from a single dose of haloperidol at 10, 20, 30 and 40mg, do you think we would reach the Ld50, not from toxicity, but from suicide? Btw 40mg is seen as a therapeutics dose for a persons diagnosed with “schizophrenia”.
On the other hand, if you have the PET scan / lab results in front of you and can see the overactivity of the dopaminergic system, then you may well in such a circumstance be justified in suggesting such a medication.
>> 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.
> Let those who can get by without drugs do so.
Medical intervention is only justified if evidence of a medical disease exists.
>>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.
> You don't treat migraines with morphine. They can be treated with other drugs which are generally not abusable. Patients generally don't fake migraines to get on triptans, beta blockers, or anticonvulsants. Just as most people don't fake depression to get on SSRI's. SSRI's are not that good. I found SSRI' therapy very disagreeable, even when I was very depressed.
Many prescription medications are abused and painkillers and stimulants like ritalin are among the most common. How does a doctor know he is treating a bonafide disease and a bonafide patient as opposed to a malingerer or an addict? As a patient all I would have to do is complain about a migraine, then he'll eventually get to the barbituates, morphine, codine, or whatever else I have in mind.
> Sure, there could be some as yet unidentified biological cause of all migrane. Unfortunately, we *do not( have any test which identifies migrane with a high degree of accuracy.
Well there are many established causes of migraines such as head trauma, influenza, encephalitis, tumors etc, however, in the absence of any known diseases I think you would have to test for evidence of pain and stress biomarkers in order to confirm a diagnosis and target the pain relief medication.
>>Otherwise couldn't we all just see the doctor for our weekly barbituate script?> I would not want to live life on barbiturates. I do not find sedatives enjoyable at all, they make me depressed, and use them as infrequently as possible. I am fortunate that they are there when I need them, and am glad that a doctor trusts me to prescribe them, since I know we could go through 1000s of tests and come up with no identifiable cause of anxiety.
Are you sure, how many tests have you had done? If it is that much of a problem in your life, surely you would have had a PET scan by now to look at how all of your receptors are functioning? How many did you have before you were prescribed any medications? I wouldn't take a drug that effected my serotonin system without evidence it was diseased, otherwise I would be introducing extra disease into my body.
> Why should the few people who abuse these drugs ruin it for the rest?
They don't, testing ensures an actual disease is treated. Feeling anxiety is also a natural emotion, are you sure that you are not just a naturally anxious person?
>> 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,> Not necessarily. We have not yet identified significant negative consequence of say histamine blockade, or 5-ht2a receptor blockade. This does not mean that the drugs are perfectly safe, it just means that it by conventional tests, they could be safer than traditional drugs. For instance, 5-ht1a agonists generally have little toxicity. In very high doses they can cause hypothermia, but many food substances are 5-ht1 agonists, such as olemide.
You are smart enough to know they are almost certainly more toxic, we just don't have the comprehensive independent research as the drug companies sponsor the trials.
>> 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.
> High doses of atypicals are very rarely used for anxiety disorders. In low doses, drugs like risperidal probably achieve their so called anti-anxiety effect through serotonin receptor blockade. I never said the drugs were perfectly safe.
I can see a use for short term use of them if tests provide evidence of abnormal overactivity in the dopamine and serotonin systems but how often is that likely to occur?
>> 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.> We do not know whether the drugs are more toxic, or less toxic at this point. Only time will tell.
Drug companies will never sponsor trials to properly compare the typical to atypicals, although you know and I both know atypicals have a significantly greater receptor activity and are thus far “dirtier” than typicals. There is no proof that the atypicals are less toxic for a given level of dopamine blockade either. In the absence of any proper head to head comparisons with equivalent D2 blockades, I will lay the gauntlet down and suggest that notwithstanding the long half life typicals, the atypicals are more toxic and more potent chemicals that take toxic nerve seizing medications to new levels, I redub them the first of the antibrain family.
>> I believe they are the presenting to us a pack of wolves and via the design of the research studies, dressing them as sheep.You could be right.
> 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+?
> But that rate was not accounting for the the dyskinesias people had on startup. The study highlights said that dyskinesias dropped in some patients switched from typicals.
Yes it was, they measured “persistent emergent dyskinesias”.
> When I took risperidal for anxiety, I took like 0.25-0.5 mg.
Against your will or with your consent?
>>They have all been shown to cause TD
>Yes that is a possibility.
>> 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.
> I personally didn't think that study was all that scarry.
Really, do you like horror flicks then? Seen “firestarter” :)?
>> 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.
> Again, I never said they were perfectly safe. There are risks to treatment as well as risks to nontreatment. I understand that sorting things out can be maddening.
Safe, they one of the most toxic medications available and applied to people without evidence of disease as mood stabilisers, anxiety medication or even for better “sleep architecture”. The term neuroleptic chemotherapy is in wide use. Used on persons without identifiable disease, IMHO they are nothing short of the worst example of medicine in modern history. Just because a series of nerve toxins affects dopamine, serotonin, and ardenaline receptors doesn't make them good medications to use on healthy people without evidence of disease. IMHO the iatrogenic neurological disease these medications cause is unprecedented; a universe of devastation.
>> 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.
> I never doubted that TD is a possible side effect of antipsychotic treatment.
Agreed then.
>> 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.
> Well then I guess alzheimers, migrane, parkinsons etc, CFS, are just medical delusions too.
They all have specific pathophysiologies that can be identified with relevant medical tests. There is no doubt that those diseases can be identified in a patient.
> There is medical evidence that schizophrenia is a medical disease. There are usually a number of physical alterations/abnormalities of the brain's of those with schizophrenia, namely hippocampal and temporal lobe abnormalities, grey matter abnormalities. Disorder of the prefrontal cortex, mitochonidial dysfunction, abnormalities of glutamatergic function. Abnormalties in intracellular activity, PKC, GSK-3b, GAP-43, calcuium, etc. Those who research the genetics and anatomy of schizophrenia have little doubt that it is a disease, however there is not a whole lot of take home points from these findings, nor any clear tests to identify it in living patients.
Unlike Alzeihmer's and Parkinson's, Schizophrenia does not have any proven pathology. There is literally no lab test for schizophrenia. Those abnormalities you mentioned may indeed exist in a patient diagnosed with schizophrenia, however, they do not define Schizophrenia. Ironically if the pathophysiology if schizophrenia were to be identified it would be reclassified as a neurological disease and treated by neurologists. Although I can guarantee you that day will never come, as the pathology of an overactive imagination is not a disease and so it will never be discovered. IMHO Schizophrenia is nothing short of the biggest delusion in medical history.
>> Now we have moved from the scientifically based world of medical science into the alternate universe of theoretical medicine.> Nobody is forcing you to believe that this is in fact a disease. If you want to believe that schizophrenia is just a figment of the imagination, then go right ahead.
Thanks I refuse to agree to a delusion. I need some medical evidence.
> This affliction will still continue to plague humanity whether people want to believe that it a result of some brain abnormality, or possession by spawn of Lucifer.
I don't consider an overactive imagination, or having internal dialog a disease, a plague or even a problem. We all have imagination, we all have internal dialog. Sure we might have some problems, get fired from work, break up with our girlfriends, and our internal dialog might change to being more negative, our feelings from happy to scared, but that is a normal human brain reacting in a normal way to the pressures of normal life. Some people even retreat into an imaginary world as a coping mechanism, but that still a disease does not make. A doctor is a medical scientist, he demands evidence that disease exists or he can no longer be defined as a doctor.
>> 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.> Of course it is not a scientific fact. There are a lot of things in life that we respond to without having to beforehand establish them as scientific fact.
*Gasps in shock*
>> A person cannot be diagnosed with an imaginary theoretical disease, it is an unsupportable diagnosis, it is not medical science.
It is supportable, just not 100% conclusive. There are a lot of things in life that are not 100% conclusive. Scientists are still in the realm of collecting data and formulating hypothesis about many of these problems. But in the meantime, I urge you to establish a treatment modality which is more efficacious than the one at present.
Can we diagnose everyone schizophrenic and treat them to antipsychotic medication? They all have imagination, and all have internal dialog? We can say we are not 100% certain, however, early treatment prevents worsening of the disease. Perhaps we should add antipsychotic medication into the water supply?
> But, if you feel there is nothing wrong, then this conversation is pointless. If your reason for visiting this site is simply to tell us that we are all perfectly healthy people, then your comment is duely noted.
No, I find medicine an infinitely fascinating topic of interest, and this site is a valuable source of information. However, I do think that some areas of medicine seemed to have blurred the line between evidence based science and fantasy, and so I bring an interesting perspective as do you.
>Without evidence of disease we cannot ever be justified in treating anyone against their will;
I agree with you 110%.
thumbs up
>>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?
>I think that anybody has the legal right not to take medication if they so choose. But legality is a separate issue.
Never mind probably a legal not medical question anyway.
>> 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.
> For starters I don't even think the lobotomy occurs anymore. So we can scratch that one off the list. I agree with you 100% that people should never be treated against their will. But for those who concentually want to be treated with antipsychotics, antidepressants, or ECT, I believe they should have the right.Sure lobotomies still occur in Australia, UK, and most states of America to the best of my knowledge. However, I am saddened when I read all the posts of a patient who had “an eating disorder” who within 2 months is on antipsychotics, or someone else is on them for insomnia, or even for people who find they chat to themselves every now and find themselves feeling scared and alone. Do they deserve to be diagnosed with imaginary diseases and treated with some of the most toxic medications available?
>Sometimes the best medicine is no medicine at all.
I agree.
>How can you help someone without a disease?
> Thats a good question. I don't know why TCA antidepressants worked when they did. I don't know why sedatives work. Do I not have a disease? I don't really care. I'm here because medications have helped me in the past.
Is it possible you did have a problem with serotonin and so the antidepressants worked as a result?>> 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.
> What is your definition of a healthy person? When I was getting 2 hours of sleep, vomiting from anxiety, crying 3+ hours a day, shaking, eating nothing, hiding in a corner and actively suicidal, I suppose there was nothing at all wrong with me. Just a healthy person going about their daily living. All I care was that the medications helped me to get better.
I am sorry to hear you went through all that. I am sure that in that state your receptors, and catecholamine levels would have been all over the place even your glucose levels would have been much lower than usual, with good testing I feel confident they could have identified problems and treated you with the best medications for your condition. That combined with therapy would have been a good solution imho.
>> If a patient feels depressed or anxious then they shouldn't necessarily think that it is due to a disease.
I agree.
>> 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.
> Sorry, but I totally disagree with you. There are *no* conventional diagnostic tests for depressive or anxiety disorders. Like I said above, only a fraction of depressed patients show cortisol abnormalities. There is some evidence of regional brain hypofunction in depressed patients, but it is not unique to depression, ie it occurs in all sorts of other psychiatric disorders. The levels of monoamine metabolities in the cerebral spinal fluid is only a measure of monoamine breakdown, it says nothing about how well a particular monoamine is functioning. It says nothing about the integrity or responsiveness of the receptors.
Like i said before, you know the technology they use for testing the drugs is available, MRI, Pet, urine, blood. Everything you ever wanted to identify even the tiniest abnormality in your brain or body. They can even show all the chemical changes and receptor activities that occur in response to social stimulus for example, you can literally see that some people have a negative impact on our brain's chemistry.
>>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.
> Or it may help. I was diagnosed with depression without any "hard" evidence. I was not injured by treatment, and I believe the treatment aided in my recovery. I am no longer on any medications.
Maybe you were just lucky? What about those that die from the iatrogenic disease such treatments methodology certainly introduces?
>>Once a patient starts taking the antipsychotics they can measure all manner of iatrogenic disease, including brain, blood and heart diseases.> I reiterate. Those are possible side effects. There is no data to prove that all patients will get such side effects.
We both know what they really do to a brain.
Posted by med_empowered on February 15, 2007, at 16:34:32
In reply to Re: low dose risperdal -- linkadge, posted by munificentexegete on February 15, 2007, at 7:42:15
I think its good that scientists have tried to develop safer, better drugs for schizophrenia BUT I think to truly help "schizophrenics," we're going to need to move beyond our concepts of "mental illness" and definitely get past this idea that blocking dopamine is **the** way to help people who have psychosis.
What I find ridiculous is that when someone sees a shrink--even voluntarily--they go from being "people" to being "patients". Suddenly, problems or undesirable behaviors/thoughts are "diseases" or "symptoms" or "conditions," and psychiatry is really into this idea of maintaining people--there's not much room allowed for recovery, or even allowed for the possibility that thoughts/behaviors might be understandable reactions to a given situation. In fact, in my own experiences, I've found that there isn't much attention paid to a patient's life at all--its assumed that the unwell will always be unwell, and that the best that can be done is to drug them up into a state of either semi-wellness or at least less disturbing un-wellness. The problem is that behaviors are not diseases, and thoughts are not diseases, yet these are the criteria by which people are "diagnosed" and turned into "patients". I imagine with more minor diagnoses--anxiety, panic attacks, some forms of depression--there is more attention paid to patient's lives, but once a line is crossed into bipolar/schizo-land, its all symptoms, symptoms, symptoms, and drugs, drugs,drugs.
Neuroleptics are still damaging and toxic and the incredible dishonesty surrounding their widespread use is appalling. We have kids taking them for ADHD, people taking them for anxiety, for sleep, for depression, for bipolar disorder...we have "schizophrenic" patients being loaded up on high doses, or sometimes given complex cocktails with multiple antipsychotics plus various other drugs. Its madness, pure madness, and it costs money and damages lives.
Posted by munificentexegete on February 16, 2007, at 5:48:16
In reply to Re: low dose risperdal -- linkadge, posted by med_empowered on February 15, 2007, at 16:34:32
> I think its good that scientists have tried to develop safer, better drugs for schizophrenia BUT I think to truly help "schizophrenics," we're going to need to move beyond our concepts of "mental illness" and definitely get past this idea that blocking dopamine is **the** way to help people who have psychosis.
true, what about if we redefined schizophrenia as an overactivity of the dopaminergic system? Then they could test for it, and treat it with antidopaminergic meds.
> What I find ridiculous is that when someone sees a shrink--even voluntarily--they go from being "people" to being "patients". Suddenly, problems or undesirable behaviors/thoughts are "diseases" or "symptoms" or "conditions," and psychiatry is really into this idea of maintaining people--there's not much room allowed for recovery, or even allowed for the possibility that thoughts/behaviors might be understandable reactions to a given situation. In fact, in my own experiences, I've found that there isn't much attention paid to a patient's life at all--its assumed that the unwell will always be unwell, and that the best that can be done is to drug them up into a state of either semi-wellness or at least less disturbing un-wellness. The problem is that behaviors are not diseases, and thoughts are not diseases, yet these are the criteria by which people are "diagnosed" and turned into "patients". I imagine with more minor diagnoses--anxiety, panic attacks, some forms of depression--there is more attention paid to patient's lives, but once a line is crossed into bipolar/schizo-land, its all symptoms, symptoms, symptoms, and drugs, drugs,drugs.
> Neuroleptics are still damaging and toxic and the incredible dishonesty surrounding their widespread use is appalling. We have kids taking them for ADHD, people taking them for anxiety, for sleep, for depression, for bipolar disorder...we have "schizophrenic" patients being loaded up on high doses, or sometimes given complex cocktails with multiple antipsychotics plus various other drugs. Its madness, pure madness, and it costs money and damages lives.I get the feeling with the current approach every single human being qualifies for a diagnosis of a significant number of the illnesses in the DSMIV, including bipolar and schizophrenia. It's not uncommon for some patients to obtain at least half a dozen to a dozen different diagnoses in quite a short space of time without a single diagnostic test or scan showing an abnormality; how often does that happen with regular medicine?
Posted by linkadge on February 18, 2007, at 8:34:11
In reply to Re: low dose risperdal -- Med, posted by munificentexegete on February 16, 2007, at 5:48:16
>true, what about if we redefined schizophrenia >as an overactivity of the dopaminergic system? >Then they could test for it, and treat it with >antidopaminergic meds.
There only very weak proof that schizophrenia is related to an overactivity of dopamine. New research suggests that the disease is intercellular. Dopamine only acts as a signal to activate intercellular second messenger systems.
And there are no tests that can measure dopamine levels acuratly in the brain. Without entering the brain iteslf, one can only test for metabolite levels. But metabolite levels are only an indicator of dopamine metabolism not overall brain dopamine functionality.
In addition, even if dopamine levels were abnormally high, a dopamine receptor blocker is not going to correct that. It simply blocks the receptors, which upregulates their sensitivity.
Linkadge
This is the end of the thread.
Psycho-Babble Medication | Extras | FAQ
Dr. Bob is Robert Hsiung, MD,
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Script revised: February 4, 2008
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