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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 25 of 41. This is the beginning of the thread.
Posted by AndrewB on April 21, 2000, at 15:10:01
This is a quote for m a depression study abstract:
Chronic treatment with amineptine induces downregulation of dopamine d2, beta- and alpha 2 adrenergic receptors.....
What does this imply, 'downregulation'?
AndrewB
Posted by michael on April 21, 2000, at 16:31:46
In reply to Amineptine: what does this mean: Scott, CamW, posted by AndrewB on April 21, 2000, at 15:10:01
Hey everyone -
I'm just trying to find out/establish if amineptine is a "dead-end" or not (i.e.: if it is currently manufactured, and if will be in the future). So this is what I've found so far
****************Amineptine : marketing authorization suspended : drug abuse and dependence
France. The Medicines Agency has announced that the marketing authorization for the antidepressant, amineptine (Survector : Servier) has been suspended in France and marketing voluntarily discontinued.
These actions have been taken after an evaluation of amineptine revealed a potential for abuse and risk of dependence. In addition, patients may develop significant weight loss and micro- and macrocystic acne that may be extensive and serious, leading to cutaneous sequelae after discontinuation of amineptine. Amineptine is also registered in Greece, Italy, Luxembourg, Portugal and Spain and it is marketed in 66 other countries worldwide in Africa, Asia and South America.
Further to the announcement of these measures in France, amineptine has been withdrawn in Thailand and it is being reviewed in the light of this information in Malaysia where it is currently under evaluation for registration.
***********************I know it's still available in some places (for the moment), but can anyone say for certain if continues to be mfg'd? Just wondering.
Posted by Cass on April 21, 2000, at 16:34:17
In reply to Amineptine: what does this mean: Scott, CamW, posted by AndrewB on April 21, 2000, at 15:10:01
> This is a quote for m a depression study abstract:
>
> Chronic treatment with amineptine induces downregulation of dopamine d2, beta- and alpha 2 adrenergic receptors.....
>
> What does this imply, 'downregulation'?
>
> AndrewBI read in a previous thread that Amineptine is most similar in action to the old drug, Meritol. I asked my pdoc about it, and he had never heard of it. Is this drug available in the U.S.?
Posted by Scott L. Schofield on April 21, 2000, at 17:23:39
In reply to Amineptine: what does this mean: Scott, CamW, posted by AndrewB on April 21, 2000, at 15:10:01
> This is a quote for m a depression study abstract:
>
> Chronic treatment with amineptine induces downregulation of dopamine d2, beta- and alpha 2 adrenergic receptors.....
>
> What does this imply, 'downregulation'?
>
> AndrewB
"Downregulation" means roughly the same thing as "desensitization". Downregulation is the process by which the neuronal cell membrane becomes less sensitive to stimulation by the neurotransmitter. There are two mechanisms by which this may occur:1. Reduction in the numbers of receptors along the membrane; decreased receptor density.
- measured as maximum binding sites (Bmax)2. Decrease in the binding affinity of receptor for the transmitter molecule; decreased receptor "stickiness".
- measured as the dissociative constant (Kd)Downregulation can be the result of increased levels of neurotransmitter within the synapse or exposure to ligand receptor agonists. Downregulation of receptors can also be brought about through mechanisms other than exposure to substrate. It can be thought of as the neuron's attempt to compensate for changes in its environment or workload.
That amineptine seems to cause a downregulation of noradrenergic receptors indicates that this drug may inhibit the reuptake of norepinephrine, as was initially described in early studies.
Basic results of downregulation at the synapse:A downregulated postsynaptic membrane requires a greater concentration of synaptic neurotransmitter to stimulate that neuron to fire (induce an action potential). The membrane is considered to be subsensitive. Neurotransmission is decreased.
A downregulated postsynaptic membrane requires a greater concentration of synaptic neurotransmitter to engage the negative feedback loop, and thus inhibit neurotransmitter synthesis and vesicular release. Neurotransmission is increased.
Upregulation and its consequences can be regarded as the reverse.Example: Upregulation of postsynaptic striatal D2 receptors is the result of their blockade by chronic administration of neuroleptic antipsychotics such as Haldol. The resulting supersensitivity of these membranes is thought to account for the development of tardive-dyskinesia.
Is depression the result of the abnormal regulation of neural activity brought about by inappropriate adjustments of membrane receptor sensitivities - dysregulation?
Hmmm. :-)
Thing get more interesting when specific receptor subtypes are selectively upregulated or downregulated. For more, see film at eleven.
- Scott
P.S. Andrew, I want a FREE autographed first edition copy of your upcoming book.
Posted by Scott L. Schofield on April 21, 2000, at 17:34:44
In reply to More questions about Amineptine, posted by Cass on April 21, 2000, at 16:34:17
> I read in a previous thread that Amineptine is most similar in action to the old drug, Meritol. I asked my pdoc about it, and he had never heard of it. Is this drug available in the U.S.?
No.
Merital (nomifensine), like amineptine, inhibits the reuptake of both dopamine and norepinephrine. It was marketed around the world, including in the U.S. in the mid 1980's.
Nomifensine was discontinued and withdrawn from market worldwide when a large number of reports appeared describing occurrences of hemolytic anemia in patients taking it. Some of these were fatal. Hemolytic anemia is a condition in which the red blood cells lyse (split or explode).
I experienced an initial robust response to nomifensine.
- Scott
Posted by Scott L. Schofield on April 21, 2000, at 21:29:23
In reply to Re: More questions about Amineptine, posted by Scott L. Schofield on April 21, 2000, at 17:34:44
Oops. Sorry.
I didn't read your question properly. I guess you were asking about the availability of amineptine. This drug has also been withdrawn from market in most, if not all countries.
There are a whole bunch of threads regarding this subject. You can find them in the archives and on the current page. I have yet to dig around a little more to find out if it is still being manufactured. Check out the postings of AndrewB.
- Scott
Posted by Scott L. Schofield on April 21, 2000, at 21:53:11
In reply to Re: Amineptine: what does this mean: Scott, CamW, posted by Scott L. Schofield on April 21, 2000, at 17:23:39
Please pardon my unpardonably deficient proofreading.
One "postsynaptic" should have been a "presynaptic".
-----------------------------------------------------
> This is a quote for m a depression study abstract:
>
> Chronic treatment with amineptine induces downregulation of dopamine d2, beta- and alpha 2 adrenergic receptors.....
>
> What does this imply, 'downregulation'?
>
> AndrewB"Downregulation" means roughly the same thing as "desensitization". Downregulation is the process by which the neuronal cell membrane becomes less sensitive to stimulation by the neurotransmitter. There are two mechanisms by which this may occur:
1. Reduction in the numbers of receptors along the membrane; decreased receptor density.
- measured as maximum binding sites (Bmax)2. Decrease in the binding affinity of receptor for the transmitter molecule; decreased receptor "stickiness".
- measured as the dissociative constant (Kd)Downregulation can be the result of increased levels of neurotransmitter within the synapse or exposure to ligand receptor agonists. Downregulation of receptors can also be brought about through mechanisms other than exposure to substrate. It can be thought of as the neuron's attempt to compensate for changes in its environment or workload.
That amineptine seems to cause a downregulation of noradrenergic receptors indicates that this drug may inhibit the reuptake of norepinephrine, as was initially described in early studies.
Basic results of downregulation at the synapse:A downregulated POSTSYNAPTIC membrane requires a greater concentration of synaptic neurotransmitter to stimulate that neuron to fire (induce an action potential). The membrane is considered to be subsensitive. Neurotransmission is decreased.
A downregulated PRESYNAPTIC membrane requires a greater concentration of synaptic neurotransmitter to engage the negative feedback loop responsible for inhibiting neurotransmitter synthesis and vesicular release. Neurotransmission is increased.
Upregulation and its consequences can be regarded as the reverse.Example: Upregulation of postsynaptic striatal D2 receptors is the result of their blockade by chronic administration of neuroleptic antipsychotics such as Haldol. The resulting supersensitivity of these membranes is thought to account for the development of tardive-dyskinesia.
Is depression the result of the abnormal regulation of neural activity brought about by inappropriate adjustments of membrane receptor sensitivities - dysregulation?
Hmmm. :-)
Thing get more interesting when specific receptor subtypes are selectively upregulated or downregulated. For more, see film at eleven.
- Scott
P.S. Andrew, I want a FREE autographed first edition copy of your upcoming book.
Posted by glenn on April 21, 2000, at 17:27:42
In reply to Amineptine: what does this mean: Scott, CamW, posted by AndrewB on April 21, 2000, at 15:10:01
> This is a quote for m a depression study abstract:
>
> Chronic treatment with amineptine induces downregulation of dopamine d2, beta- and alpha 2 adrenergic receptors.....
>
> What does this imply, 'downregulation'?
>
> AndrewB
i beleive it means that the body/brain responds by reducing the number of available receptors in response to the increased amount of the particular amine , in other words if theres so much dopamine available theres not the need for so many receptors or so the body thinks, a bit like the process of accomodation in nerve functioning, but im not absolutely sure about this as it would imply that almost all ads should do this and they dont , do they?!
glenn
Posted by Cass on April 21, 2000, at 18:41:54
In reply to Re: More questions about Amineptine, posted by Scott L. Schofield on April 21, 2000, at 17:34:44
Thanks for your response. Where can one buy Aminteptine? Like I said, my pdoc had never heard of it.
Posted by KarenB on April 22, 2000, at 0:47:32
In reply to Re: More questions about Amineptine/Scott, posted by Cass on April 21, 2000, at 18:41:54
> Thanks for your response. Where can one buy Aminteptine? Like I said, my pdoc had never heard of it.
Hi Cass,
Please refer to my post on 4-10-00 titled "amineptine available!" It has the address and website for a pharmacy in India with availability, along with instructions on how to order.
Good luck!
Karen
Posted by AndrewB on April 22, 2000, at 20:39:27
In reply to Re: More questions about Amineptine/Scott, posted by KarenB on April 22, 2000, at 0:47:32
I received an email from a user of amineptine in India. They have already stopped production of amineptine in India.
Posted by KarenB on April 22, 2000, at 20:47:55
In reply to Oh No! Amineptine Manufacture Halted, posted by AndrewB on April 22, 2000, at 20:39:27
> I received an email from a user of amineptine in India. They have already stopped production of amineptine in India.
Andrew,
Well, that was NOT what I wanted to hear - but thanks for the update.
Karen
Posted by KarenB on April 22, 2000, at 23:31:52
In reply to Oh No! Amineptine Manufacture Halted, posted by AndrewB on April 22, 2000, at 20:39:27
> I received an email from a user of amineptine in India. They have already stopped production of amineptine in India.
Oh buddy - that is NOT what I wanted to hear...but thanks for the update, Andrew.
Karen
Posted by AndrewB on April 23, 2000, at 9:47:42
In reply to Re: Oh No! Amineptine Manufacture Halted, posted by KarenB on April 22, 2000, at 23:31:52
Is the adderall still working for you. Is it similar to amineptine. Is it a possible substitute for amineptine.
Posted by michael on April 23, 2000, at 10:59:24
In reply to Oh No! Amineptine Manufacture Halted, posted by AndrewB on April 22, 2000, at 20:39:27
> I received an email from a user of amineptine in India. They have already stopped production of amineptine in India.
Does anyone know if it is still approved anywhere? Mfg'd anywhere? Like what country
Posted by KarenB on April 23, 2000, at 17:13:22
In reply to Q for KarenB, posted by AndrewB on April 23, 2000, at 9:47:42
> Is the adderall still working for you. Is it similar to amineptine. Is it a possible substitute for amineptine.
Andrew,
I'm on Ritalin SR, 20mg 2x a day. I thought it was poasitively affecting my mood but not so the past few days. I intend to try Adderall next if tweaking the dosage doesn't help.
By the way, what would you suggest as a US-available replacement for sulpiride, to augment the stimulant? As you know, that type of blend has been good for me.
Karen
Posted by KarenB on April 23, 2000, at 18:09:19
In reply to Re: Q for KarenB, posted by KarenB on April 23, 2000, at 17:13:22
Hey Everyone,
I just e-mailed Servier, the manufacturer of Survector to ask them if they are still producing ANYWHERE in the world and where I could purchase it.
I'll let you know what I find out.
Karen
Posted by AndrewB on April 23, 2000, at 20:17:10
In reply to Re: What up w/Amineptine??, posted by KarenB on April 23, 2000, at 18:09:19
Karen,
That was a very good idea to email Servier. That ought to give us a definitive answer.
You asked about substitutes for sulpiride that are US available. Mirapex might have a similar effect. Myself, I would just order the sulpiride or amisulpride from overseas since they are cheaper than Mirapex.
Let me know if adderall is similar to aminpetine.
AndrewB
Posted by micahel on April 23, 2000, at 21:56:55
In reply to Re: What up w/Amineptine??, posted by KarenB on April 23, 2000, at 18:09:19
> Hey Everyone,
>
> I just e-mailed Servier, the manufacturer of Survector to ask them if they are still producing ANYWHERE in the world and where I could purchase it.
>
> I'll let you know what I find out.
>
> KarenGood idea Karen - I couldn't find an e-mail address for them - well done. Looking forward to hearing what they say. Btw - if you need any assistance w/french, let me know. michael
Posted by PeterJ on April 25, 2000, at 3:44:51
In reply to Re: Amineptine: what does this mean: Scott, CamW, posted by Scott L. Schofield on April 21, 2000, at 17:23:39
May I add a few comments to Scott's excellent response.
(I am sure Scott knows all this, but it's an interesting topic.)Many antidepressants down-regulate beta-adrenergic receptors
by inhibiting NE uptake and thus increasing NE levels at the synapse.
However, other antidepressants may down-regulate beta receptors by
more indirect means. For exampe sulpiride down regulates beta
receptors. This is believed to occur because it blocks pre-synaptic
dopamine heteroreceptors on NE neurons. The DA receptors inhibit
NE release so blocking them may increase NE release.
The most important indirect effect on NE receptors occurs via
the serotonin system. Most, if not all, SSRIs (there is some variation
among studies) down-regulate beta adrenergic receptors after chronic
administration in animals. If you lesion the serotonergic system, this
down-regulation does not occur. What is even more interesting is that
serotonergic lesions also prevent the down-regulation produced by
noradrenergic antidepressants such as desipmramine and other TCAs.
It appears that 5-HT2 receptors have a necessary role in the
regulation of beta adrenergic receptors.
One antidpressant which still produces beta receptor down-
regulation in serotonin lesioned animals is clorgyline. It is
hypothesized that clorgyline has such a powerful effect on serotonin
levels that it overcomes the effect of the lesions of the sertonin
system (Aulakh et al. Role of serotonergic input in the down-regulation
of beta-adrenoceptors following long term clorgyline treatment.
Eur J Pharmacol 1988 Oct 26;156(1):63-70)
ECT and Transcranial Magnetic Stimulation also down-regulate
these receptors.
Early on (1975) it was proposed that beta adrenergic down-regulation
was a common factor in all effective antidepressant treaments. This may
not be the case as at least one antidepressant does not seem to down-
regulate beta receptors--bupropion. It is still true, however that almost
all effective antidepressants down-regulate beta adrenergic receptors in
rats. It's assumed this happens in humans as well, but we really don't know.Peter
Posted by Cam W. on April 25, 2000, at 6:41:00
In reply to Beta Receptor Down-Regulation, posted by PeterJ on April 25, 2000, at 3:44:51
Peter - Nice expalanation. Downregulaton of beta receptors may be a step in normalizing CRH release by hypothalamic cells by decreasing CRH's gene expression. But then again, all antidepressants, except citalopram, modify glucocorticoid receptor responsivity to cortisol (or corticosterone in animal models). Celexa (citalopram) modifies mineralocorticoid receptor responsivity to cortisol. Anyway, all seem to "re-couple" the HPA axis, the body's main stress response system and resolve the symptoms of depression.I believe that the area of breakdown of the HPA axis (or closely linked systems - eg endorphin system) determines which antidepressant will "resplice" the appropriate dysconnection of the HPA axis (eg desipramine or reboxetine for norepinephrine dysfunction; clomipramine or SSRIs for serotonin dysfunction. - Cam W.
Posted by AndrewB on April 25, 2000, at 13:19:25
In reply to Beta Receptor Down-Regulation, posted by PeterJ on April 25, 2000, at 3:44:51
Peter,
Thank you Peter for your excellent explanation of beta receptor down-regulation. It seems that the physiological changes to neurotransmitter neurons due to down-regulation are used by researchers as evidence of increased neurotransmitter receptor stimulation when trying to determine the actions (direct or indirect) of a drug or another neurotransmitter.
I hope you can answer my questions, I’m wondering if tolerance to a drug ever occurs due to down-regulation. Specifically I’ve read that tolerance to amphetamines is due to down-regulation of the alpha and beta andrenergic receptors due constant innervation of the post synaptic receptors. But I also have read a contradicting explanation for amphetamine tolerance. This explanation says amphetamine promotes the release of NE from nerve endings, specifically the cytoplasmic stores of NE. Tolerance in this scenario develops because only a limited amount of NE is available in this ‘mobile pool’. Which of these explanations sounds correct?
I realize that with SSRIs you don’t need ever increasing doses, so whatever down-regulation they create doesn’t cause tolerance. However if you stop taking an SSRI, are some people going to feel more depressed than ever before because their serotonergic and adrenergic systems have been down-regulated.
The reason I’m asking these questions is because I am trying amineptine. It is a dopamine reuptake blocker and is classified as a mild psychostimulant. I am wary of any psychostimulant causing tolerance. Amineptine is able to sharpen one’s mind among other things, but today I have not taken amineptine and I feel foggy headed. My mind is less sharp than it was before I started amineptine. Is this fogginess due to down-regulation (of either the dopaminergic or NE system). Can drug holidays counteract tolerance. If so, is there any standard protocol for the timing and spacing of drug holidays.
Thank you very much,
AndrewB
Posted by Scott L. Schofield on April 25, 2000, at 23:11:41
In reply to Beta Receptor Down-Regulation, posted by PeterJ on April 25, 2000, at 3:44:51
Dear Peter,
You couldn't possibly be more wrong. :-)> (I am sure Scott knows all this, but it's an interesting topic.)
I didn't. But I do now. Thank you for this wonderfully lucid explanation.
> One antidepressant which still produces beta receptor down- regulation in serotonin lesioned animals is clorgyline. It is hypothesized that clorgyline has such a powerful effect on serotonin levels that it overcomes the effect of the lesions of the sertonin system.Q: What is the proposed mechanism here? Are these chemical lesions? Do these lesions interfere with vesicular release, but spare postsynaptic processes? Is serotonin released passively from serotonergic nerve terminals? Does this serotonin stimulate nerves along the lesioned pathway to fire via local synapses, or does it migrate interstitially to remote sites?
I took clorgyline for about a year through an IND protocol administered by the NIMH of the National Institutes of Health. It is an amazing drug. It is arguably the most effective antidepressant in the world, and certainly the most potent MAO-inhibitor. Dr. William Potter and his colleagues considered it to be their "ace-in-the-hole" when treating refractory cases. As monotherapy, I found that it exerted the strongest persistant antidepressant effect of any drug I have taken. Unfortunately, I was only partially responsive, and was not permitted to combine it with anything else as per the protocol. My doctor was understandably reluctant to add desipramine, which I considered to be my best prospect. I wish I had forced the issue.
Clorgyline was never available as a pharmaceutical anywhere in the world. I don't know why. It had two things going for it as an antidepressant for treatment-resistant cases. It is extremely selective for MAO-A and it is irreversible. I spoke to a couple of doctors at the NIMH last week regarding its availability. I wanted to use it again and twist my doctor's arm to augment it with other antidepressants. Who knows, maybe having Lamictal on-board would have done the trick. I was informed that the chemical company that manufactures clorgyline no longer produces a preparation for human consumption. The three people who had been maintained on it for over a decade were forced to discontinue it. It remains available for animal experiments.
Crap.
The previous word is a very poor expletive for conveying excruciatingly painful emotions. I am very afraid.
- Scott
Posted by PeterJ on April 26, 2000, at 1:46:17
In reply to Re:Down-Regulation and Tolerance: Qs for PeterJ, posted by AndrewB on April 25, 2000, at 13:19:25
The greatest NE and 5-HT receptor changes produced by antidepressant
drugs appear to take place during the first few weeks of drug use, which
is coincident in time with the initial therapeutic effect. While later
changes can occur and might be associated with loss of antidepressant
effect ("poop out") this is not typical. Some depressed persons do
tend to develop tolerance in this way and thus don't respond well
to antidepressants. (Curiously, they may also improve transiently
during drug withdrawal.)With DA, the story is different. DA drugs tend to produce more rapid
beneficial effect, however it has been clinically observed that loss
of benefit with continued use is also more common. It's not inevitable
-- many people benefit from DA drugs for years -- but it can occur.The reason for tolerance to DA drugs is complex and not fully understood.
In the late 80s, Gold and others advocated the catecholamine depletion
explanation. I don't think this has been conclusively disproven, but
recent research has concentrated on receptor changes. These however
are very complex and dependant on the exact schedule of drug
administration.Chronic treatment of rats with stimulants may produce post-synaptic
DA receptor sensitization (kindling) or desensitization (tolerance).
Intermittent administration tends to sensitize while continuous
administration tends to lead to tolerance.Another newly revealed source of tolerance to DA drugs is super-
senisitivity of pre-synaptic DA autoreceptors (D2). These super
sensitive receptors inhibit DA output during the drug withdrawal
period.It's not clear why this supersensitivity develops.
In the case of Amineptine, if the initial benefit is dopaminergic, then
tolerance to that benefit is a theoretical concern. As I said, it's
not inevitable, but if you think you are observing tolerance, then
you may be right.Drug holidays might help, but there is no standard protocol for this.
Some patients with narcolepsy use drug holidays, but they are usually
pretty miserable during the "holiday". Your own observations
may be the best guide.Intermittent use may produce sensitization. This may be good--if
sensitization to the benefits occurs. On the other hand, sensitization
to adverse effects of DA (irritiablity, psychosis) may also occur, which
is not so good.If pre-synaptic DA supersensitivity is the problem, then sulpiride, which
blocks those receptors, would be ideal. The use of amineptine +
sulpiride ,which some have suggested on this board, makes perfect sense.
On the other hand, if you observe withdrawal symptoms from amineptine alone,
then withdrawal from amineptine + supliride may be a double whammy.Finally, despite my cautions about amineptine, I think it verges on a
crime against humanity to remove it from production when there are
at least some people who might benefit from it who have not responded
to other drugs.Peter
Posted by PeterJ on April 26, 2000, at 1:57:52
In reply to Re: Beta Receptor Down-Regulation, posted by Scott L. Schofield on April 25, 2000, at 23:11:41
>
> > One antidepressant which still produces beta receptor down- regulation in serotonin lesioned animals is clorgyline. It is hypothesized that clorgyline has such a powerful effect on serotonin levels that it overcomes the effect of the lesions of the sertonin system.
>
> Q: What is the proposed mechanism here? Are these chemical lesions? Do these lesions interfere with vesicular release, but spare postsynaptic processes? Is serotonin released passively from serotonergic nerve terminals? Does this serotonin stimulate nerves along the lesioned pathway to fire via local synapses, or does it migrate interstitially to remote sites?The lesions are produced by 5,7-dihydroxytryptamine which destroys serotonergic axons.
It is believed that clorgyline boosts the remaining levels of serotonin, but it is not
kown for sure if this is due to a small number of surviving axons or due to diffusion
of serotonin from other sites.
> I took clorgyline for about a year through an IND protocol administered by the NIMH of the National Institutes of Health. It is an amazing drug. It is arguably the most effective antidepressant in the world, and certainly the most potent MAO-inhibitor. Dr. William Potter and his colleagues considered it to be their "ace-in-the-hole" when treating refractory cases. As monotherapy, I found that it exerted the strongest persistant antidepressant effect of any drug I have taken. Unfortunately, I was only partially responsive, and was not permitted to combine it with anything else as per the protocol. My doctor was understandably reluctant to add desipramine, which I considered to be my best prospect. I wish I had forced the issue.
>
> Clorgyline was never available as a pharmaceutical anywhere in the world. I don't know why. It had two things going for it as an antidepressant for treatment-resistant cases. It is extremely selective for MAO-A and it is irreversible. I spoke to a couple of doctors at the NIMH last week regarding its availability. I wanted to use it again and twist my doctor's arm to augment it with other antidepressants. Who knows, maybe having Lamictal on-board would have done the trick. I was informed that the chemical company that manufactures clorgyline no longer produces a preparation for human consumption. The three people who had been maintained on it for over a decade were forced to discontinue it. It remains available for animal experiments.
>
> Crap.
>
> The previous word is a very poor expletive for conveying excruciatingly painful emotions. I am very afraid.
>
>
> - ScottYour frustration is understandable. There ought to be some kind of
provision that allows people who have not responded to standard
medications access to experimental chemicals. I am sure you
would be willing to sign a waiver saying the responsiblity
was yours if you could only try it. The situation now is...
well, you put it best...crap.Peter
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Dr. Bob is Robert Hsiung, MD,
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Script revised: February 4, 2008
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