![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 15 of 15. This is the beginning of the thread.
Posted by jrbecker on July 1, 2003, at 14:27:42
So I got bored this weekend and started to compile an exhaustive list of drugs in development for depression, anxiety, and insomnia. The list is somewhat selfish in this regard, since I failed to make it an all-inclusive one that encompasses other indications such as bipolar disorder, ADHD and schizophrenia as well. But many of these compounds do have clinical over-lap for these conditions, so it should be informative to all of you.
I can’t guarantee that every one of these drugs trials are still going on, but I did make an effort to exclude compounds that seemed to show little reporting or progress as of late. Additionally, I’m quite sure I’m missing a few, the main reason for this is the fact that some of the pharm co’s keep their early research phases under the radar, so as to protect them from the competition.
Another thing to keep in mind, only about 1 in 5 drugs that enter clinical trials eventually get approved. So don’t expect to see the majority of these ever come to fruition in the marketplace. Of course, this list is quite long, so just by sheer numbers, there will a lot of new drugs in the treatment arsenal.
Lastly, I apologize in advance to anybody that has questions on the pharmacological actions of these drugs. I unfortunately did not take the time to explain in “friendlier” terms what these drugs actually do. Plans are most likely in the works to revise this list into a much more organized and resourceful manner. Shawn Thomas, of www.neurotransmitter.net mentioned some interest in possibly undertaking this arduous task. This might include detailed links about their pharmacological actions, study references, and the sections being broken down in a more digestible manner. So consider this an early rough draft. In the meantime, Shawn’s link might be of interest as such a resource: http://www.neurotransmitter.net/neurosignaling.html I’ll do my best to keep this list updated and timely.
If you have any additions to the list, or just comments or suggestions, please feel free to email me at jrbecker76@hotmail.com. Hope this provides some insight and optimism to you all.
JB
http://www.geocities.com/jrbecker76/jrbecker76.htm
Posted by Penny on July 1, 2003, at 14:45:09
In reply to List of Drugs in Development , posted by jrbecker on July 1, 2003, at 14:27:42
Let's just hope that some of these drugs go a long way toward fighting mental illness! Some of us are quickly exhausting the list of current meds...
thanks.
Posted by MB on July 1, 2003, at 17:45:36
In reply to Re: List of Drugs in Development , posted by Penny on July 1, 2003, at 14:45:09
Boy, it's nice to see that they're working on treatments for depression *other* than drugs that block serotonin transport. I mean, how many SSRIs do we need, already. Sheesh!
MB
Posted by Jack Smith on July 1, 2003, at 17:54:09
In reply to Nice to see...thank you, posted by MB on July 1, 2003, at 17:45:36
> Boy, it's nice to see that they're working on treatments for depression *other* than drugs that block serotonin transport. I mean, how many SSRIs do we need, already. Sheesh!
>
> MBI agree but notice that only the seratonin/norepinephrine drugs are in late stage trials. Fact is that they still have not been able to develop an effective AD that does not concentrate on seratonin, NE and to a lesser extent dopamine. I hope they will soon.
JACK
Posted by cubbybear on July 2, 2003, at 7:32:19
In reply to Re: Nice to see...thank you, posted by Jack Smith on July 1, 2003, at 17:54:09
>>
> I agree but notice that only the seratonin/norepinephrine drugs are in late stage trials. Fact is that they still have not been able to develop an effective AD that does not concentrate on seratonin, NE and to a lesser extent dopamine. I hope they will soon.
>
> JACKHi Jack,
Since it's been pretty well established that depression stems from problems with the serotonin, NE,and dopamine balance/depletion, I wonder how you could theoretically create an AD that does not concentrate on these. And why would you want to see such a development?
Posted by Jack Smith on July 2, 2003, at 12:59:03
In reply to Re: Nice to see...thank you » Jack Smith, posted by cubbybear on July 2, 2003, at 7:32:19
> Hi Jack,
> Since it's been pretty well established that depression stems from problems with the serotonin, NE,and dopamine balance/depletion, I wonder how you could theoretically create an AD that does not concentrate on these. And why would you want to see such a development?
>
>Well, because I think that seratonin, NE and dopamine are only part of the problem and there is a lot more to it. Hence, some people can find no relief from any AD's.
By the way, email me, I had been out of the country and my account automatically deleted all my emails. I was meaning to write back to you but when I got back (from Bali), my email account was cleaned out.
JACK
Posted by Caleb462 on July 2, 2003, at 13:03:44
In reply to Re: Nice to see...thank you » Jack Smith, posted by cubbybear on July 2, 2003, at 7:32:19
> >>
> > I agree but notice that only the seratonin/norepinephrine drugs are in late stage trials. Fact is that they still have not been able to develop an effective AD that does not concentrate on seratonin, NE and to a lesser extent dopamine. I hope they will soon.
> >
> > JACK
>
> Hi Jack,
> Since it's been pretty well established that depression stems from problems with the serotonin, NE,and dopamine balance/depletion, I wonder how you could theoretically create an AD that does not concentrate on these. And why would you want to see such a development?
>
>It has NOT been well established that depression stems from problems with serotonin/NE/dopamine balance/depletion.
Posted by cubbybear on July 3, 2003, at 1:32:09
In reply to Re: Nice to see...thank you » Jack Smith, posted by Caleb462 on July 2, 2003, at 13:03:44
>> It has NOT been well established that depression stems from problems with serotonin/NE/dopamine balance/depletion.
Well, maybe not WELL established, but so far, from all I've read, these chemicals definitely play a part. I would appreciate your citing an article or two that refutes the current hypothesis.
>
Posted by Caleb462 on July 3, 2003, at 2:25:17
In reply to Re: Serotonin, etc in Depression--your rebuttal » Caleb462, posted by cubbybear on July 3, 2003, at 1:32:09
> >> It has NOT been well established that depression stems from problems with serotonin/NE/dopamine balance/depletion.
>
> Well, maybe not WELL established, but so far, from all I've read, these chemicals definitely play a part. I would appreciate your citing an article or two that refutes the current hypothesis.
> >
>
>I've no doubt they play a part in psychiatric disorders, but how, why, and to what extent... who knows?
My personal belief is that the large majority of major depressive episodes stem from chronic, recurrent stress... which throws the system out of whack in some way... in what way, no one exactly knows. Excess cortisol release could certainly be one thing...
I've run across several articles refuting the "monoanime hypothesis" of depression, though I don't have them archived, unfortunately. I will find them again, and post thim when I do.
Posted by jrbecker on July 3, 2003, at 11:13:37
In reply to Re: Serotonin, etc in Depression--your rebuttal » Caleb462, posted by Caleb462 on July 3, 2003, at 2:25:17
It's needless to say that the underpinnings of affective disorders are multivariant, with multiple genetic loci and environmental causes at fault. The exact combination of these stressors in each individual are in fact probably quite different. This is why that after many genetic screening studies, there is not one specific genetic location that we can unilaterally point a finger at. In fact, new gene locis are being discovered all the time. See further below for a timely example.
Current affective disorder theory has moved beyond neurotransmitter depletion/dysfunction as the main culprit, rather it now looks at this dysfunction as much more biochemically ~downstream~ of the where the real problems start. It is now believed that the cogs in the wheel are much further up the biochemical pathways (e.g, cAMP-CREB dysfunction, neural cell death/neuroplasticity dysfunction, specific kinase or enzyme dysregulation, HPA dysfunction, and so on and so on). I've provided a few links below if you care to get immersed in this everchanging, and certainly no-where-near settled debate of what's really at fault. But I guess the good news is that we're slowly unraveling this stuff.
http://www.medscape.com/viewarticle/418726?WebLogicSession=PwROVofJKIbQXHZo1h7ZOs08XDTyom24Voc2i9AtKqZ8aX2BMgXX|-4114154987197810445/184161395/6/7001/7001/7002/7002/7001/-1
http://www.mcmanweb.com/article-234.htm
http://journals.endocrinology.org/joe/160/0001/1600001.pdf
http://hdlighthouse.org/research/brain/updates/0051neurogenesis.phtml
http://www.future-drugs.com/admin/articlefile/ern020310.pdf
http://www.mcmanweb.com/article-191.htm
http://www.nature.com/cgi-taf/DynaPage.taf?file=/nm/journal/v7/n5/full/nm0501_541.html
http://lokman.cu.edu.tr/psychiatry/derindex/kpb/fulltext/2002/12(4)/6.pdf
http://www.neurotransmitter.net
<><><>
And now for recent news...
http://www.biospace.com/news_story.cfm?StoryID=13155220&full=1
University of Pittsburgh Researchers Single Out Genes For Major Depression; Genes Implicated In Mood Disorders And Shorter Lifespan
PITTSBURGH, July 2 /PRNewswire/ -- Researchers at the University of Pittsburgh have completed the first survey of the entire human genome for genes that affect the susceptibility of individuals to developing clinical depression.George S. Zubenko, M.D., Ph.D., professor of psychiatry at the University of Pittsburgh School of Medicine and adjunct professor of biological sciences at Carnegie Mellon University and his team have located a number of chromosomal regions they say hold the genetic keys to a variety of mental illnesses, including major depression and certain addictions. The survey was done in 81 families identified by individuals with recurrent, early-onset, major depressive disorder (RE-MDD), a severe form of depression that runs in families. The Pitt team's findings are published today in the American Journal of Medical Genetics.
Finding the genetic roots of depression is important for many reasons. Depression is the second-leading cause of disability worldwide, affecting nearly 10 percent of the population. And while scientists have made significant progress developing new drugs to treat it, studies that identify specific risk genes may lead to even more effective drugs designed to target depression in specific individuals.
Twin studies have demonstrated that genetic factors typically account for 40 to 70 percent of the risk for developing major depression, but finding those genes has proven to be a challenge because, as in most diseases, there are likely numerous genes involved and only individuals with certain combinations of those genes develop the disorder.
Of equal interest is a secondary finding that - longevity in the families who carry these genes is significantly reduced.
The survey revealed 19 loci -- small regions on chromosomes where genes reside -- that appear to influence susceptibility to depressive disorders. The results extended the investigators' previous finding that a small region of chromosome 2q containing the CREB1 gene affects the vulnerability of women to developing depression. And at least some of the 19 depression vulnerability loci appear to work in concert to affect a person's risk of developing depression. According to Dr. Zubenko, "Greater scrutiny of the chromosome 2 locus has provided stronger evidence for the role of CREB1 as a risk gene for depressive disorders among women. In addition, five of the new genetic loci appear to interact with the CREB1 region to affect the risk of developing clinical depression in these families.
"Women are twice as likely as men to develop depression, and genetic differences appear to account for some of that disparity," said Dr. Zubenko. Sex-specific loci were common and preferentially affected the vulnerability of women to developing unipolar mood disorders. Evidence of at least one male-specific risk locus also was found. The sex-specific effects of particular risk genes for depression may result from the interactions of these genes and their products with sex hormones.
These findings suggest there are important differences in the molecular pathophysiology of mood disorders in men and women, or in the mechanisms that determine resistance to stressful stimuli. They may also help explain the vulnerability of women to depression during times of significant hormonal fluctuation including puberty, menstrual cycling, pregnancy and childbirth and menopause. Conversely, age-related reductions in hormone levels may contribute to a reduced proportion of familial cases of depression among depressions that arise later in life.
CREB1 is a gene that encodes a regulatory protein called CREB that orchestrates the expression of programs of other genes that play important roles in the brain and the rest of the body. The widespread importance of CREB as a genetic regulator may influence the development of additional psychiatric disorders related to depression, such as alcoholism and other addictions, as well as medical conditions outside of the nervous system that are associated with depression. For example, three of the new linkage regions affected the risk of developing a spectrum of depressive disorders including alcohol and other substance use disorders.
Remarkably, deceased members of the 81 families died at an age eight years younger than the general population and over 40 percent died before the age of 65. This difference in mortality was spread across the lifespan, including a five-fold increase in the proportion of children who died in the first year of life and several-fold increases in deaths by suicide, homicide and liver disease. However, most premature deaths occurred from "natural causes" including heart disease, cancer and stroke. "Tracking down the risk genes in these regions is an obvious priority, and we expect that the research will connect clinical depression and other medical disorders at their most fundamental levels," said Dr. Zubenko.
Information provided by the Human Genome Project is enabling the investigators to make important progress toward this goal. In 18 of the 19 newly identified genetic regions, the authors found candidate genes that participate in cell signaling pathways that converge on CREB. These observations provide an important new perspective on the biology of depression and its treatments that focuses on cell signaling pathways rather than particular neurotransmitters.
"The identification and characterization of susceptibility genes and their products will provide new opportunities for drug development and disease prevention, new information about the biology of mood and its regulation, and new insights into the interactions of mental illness and the human life span," said Dr. Zubenko. "Genotyping markers in chromosomal regions that harbor susceptibility genes may provide more immediate advances in the treatment of major depression. For example, individuals with particular genetic markers in these regions may respond better to particular current treatments than others. This strategy may enable clinicians to use genetic markers to better match individual patients to treatments to which they will optimally respond, while minimizing side effects."
Other researchers involved in this study include: Brion S. Maher, Ph.D.; Hugh B. Hughes III, M.S.; Wendy N. Zubenko, Ed.D., M.S.N.; J. Scott Stiffler, B.S.; Barry B. Kaplan, Ph.D.; and Mary L. Marazita, Ph.D.
The study received funding from the National Institute of Mental Health.
For more information on the Molecular Neurobiology and Genetics Lab at the University of Pittsburgh, please see http://www.zubenkolab.pitt.edu/.
CONTACT: Craig Dunhoff, DunhoffCC@upmc.edu, or Jane Duffield, DuffieldDJ@upmc.edu, +1-412-647-3555, or fax, +1-412-624-3184, both of UPMC.
University of Pittsburgh Medical Center
CONTACT: Craig Dunhoff, DunhoffCC@upmc.edu, or Jane Duffield,DuffieldDJ@upmc.edu, +1-412-647-3555, or fax, +1-412-624-3184, both of UPMCWeb site: http://www.zubenkolab.pitt.edu/
Web site: http://www.upmc.com/
similar article on same story...
http://www.psychiatry24x7.com/news/detail.jhtml?itemname=p0630057.4rw0
30/06/2003 - Pitt Researchers Single Out Genes for Major Depression; Genes Implicated in Mood Disorders and Shorter Lifespan - /CAUTION -- ADVANCE FOR RELEASE
/ADVANCE/PITTSBURGH, July 2 /PRNewswire/ -- Researchers at the University of Pittsburgh have completed the first survey of the entire human genome for genes that affect the susceptibility of individuals to developing clinical depression.
PR via NewsEdge Corporation : /ADVANCE/PITTSBURGH, July 2 /PRNewswire/ -- Researchers at the University of Pittsburgh have completed the first survey of the entire human genome for genes that affect the susceptibility of individuals to developing clinical depression.George S. Zubenko, M.D., Ph.D., professor of psychiatry at the University of Pittsburgh School of Medicine and adjunct professor of biological sciences at Carnegie Mellon University and his team have located a number of chromosomal regions they say hold the genetic keys to a variety of mental illnesses, including major depression and certain addictions. The survey was done in 81 families identified by individuals with recurrent, early-onset, major depressive disorder (RE-MDD), a severe form of depression that runs in families. The Pitt team's findings are published today in the American Journal of Medical Genetics.
Finding the genetic roots of depression is important for many reasons. Depression is the second-leading cause of disability worldwide, affecting nearly 10 percent of the population. And while scientists have made significant progress developing new drugs to treat it, studies that identify specific risk genes may lead to even more effective drugs designed to target depression in specific individuals.
Twin studies have demonstrated that genetic factors typically account for 40 to 70 percent of the risk for developing major depression, but finding those genes has proven to be a challenge because, as in most diseases, there are likely numerous genes involved and only individuals with certain combinations of those genes develop the disorder.
Of equal interest is a secondary finding that - longevity in the families who carry these genes is significantly reduced.
The survey revealed 19 loci -- small regions on chromosomes where genes reside -- that appear to influence susceptibility to depressive disorders. The results extended the investigators' previous finding that a small region of chromosome 2q containing the CREB1 gene affects the vulnerability of women to developing depression. And at least some of the 19 depression vulnerability loci appear to work in concert to affect a person's risk of developing depression. According to Dr. Zubenko, "Greater scrutiny of the chromosome 2 locus has provided stronger evidence for the role of CREB1 as a risk gene for depressive disorders among women. In addition, five of the new genetic loci appear to interact with the CREB1 region to affect the risk of developing clinical depression in these families.
"Women are twice as likely as men to develop depression, and genetic differences appear to account for some of that disparity," said Dr. Zubenko. Sex-specific loci were common and preferentially affected the vulnerability of women to developing unipolar mood disorders. Evidence of at least one male-specific risk locus also was found. The sex-specific effects of particular risk genes for depression may result from the interactions of these genes and their products with sex hormones.
These findings suggest there are important differences in the molecular pathophysiology of mood disorders in men and women, or in the mechanisms that determine resistance to stressful stimuli. They may also help explain the vulnerability of women to depression during times of significant hormonal fluctuation including puberty, menstrual cycling, pregnancy and childbirth and menopause. Conversely, age-related reductions in hormone levels may contribute to a reduced proportion of familial cases of depression among depressions that arise later in life.
CREB1 is a gene that encodes a regulatory protein called CREB that orchestrates the expression of programs of other genes that play important roles in the brain and the rest of the body. The widespread importance of CREB as a genetic regulator may influence the development of additional psychiatric disorders related to depression, such as alcoholism and other addictions, as well as medical conditions outside of the nervous system that are associated with depression. For example, three of the new linkage regions affected the risk of developing a spectrum of depressive disorders including alcohol and other substance use disorders.
Remarkably, deceased members of the 81 families died at an age eight years younger than the general population and over 40 percent died before the age of 65. This difference in mortality was spread across the lifespan, including a five-fold increase in the proportion of children who died in the first year of life and several-fold increases in deaths by suicide, homicide and liver disease. However, most premature deaths occurred from "natural causes" including heart disease, cancer and stroke. "Tracking down the risk genes in these regions is an obvious priority, and we expect that the research will connect clinical depression and other medical disorders at their most fundamental levels," said Dr. Zubenko.
Information provided by the Human Genome Project is enabling the investigators to make important progress toward this goal. In 18 of the 19 newly identified genetic regions, the authors found candidate genes that participate in cell signaling pathways that converge on CREB. These observations provide an important new perspective on the biology of depression and its treatments that focuses on cell signaling pathways rather than particular neurotransmitters.
"The identification and characterization of susceptibility genes and their products will provide new opportunities for drug development and disease prevention, new information about the biology of mood and its regulation, and new insights into the interactions of mental illness and the human life span," said Dr. Zubenko. "Genotyping markers in chromosomal regions that harbor susceptibility genes may provide more immediate advances in the treatment of major depression. For example, individuals with particular genetic markers in these regions may respond better to particular current treatments than others. This strategy may enable clinicians to use genetic markers to better match individual patients to treatments to which they will optimally respond, while minimizing side effects."
Other researchers involved in this study include: Brion S. Maher, Ph.D.; Hugh B. Hughes III, M.S.; Wendy N. Zubenko, Ed.D., M.S.N.; J. Scott Stiffler, B.S.; Barry B. Kaplan, Ph.D.; and Mary L. Marazita, Ph.D.
The study received funding from the National Institute of Mental Health.
For more information on the Molecular Neurobiology and Genetics Lab at the University of Pittsburgh, please see http://www.zubenkolab.pitt.edu/.
CONTACT: Craig Dunhoff, DunhoffCC
upmc.edu, or Jane Duffield, DuffieldDJ
upmc.edu, +1-412-647-3555, or fax, +1-412-624-3184, both of UPMC.
SOURCE University of Pittsburgh Medical Center
-0- 07/02/2003/0800
/CONTACT: Craig Dunhoff, DunhoffCC
upmc.edu, or Jane Duffield, DuffieldDJ
upmc.edu, +1-412-647-3555, or fax, +1-412-624-3184, both of UPMC/
/Web site: http://www.zubenkolab.pitt.edu /
CO: University of Pittsburgh Medical Center; University of Pittsburgh School
ST: Pennsylvania
IN: HEA MTC PUB
SU: SVY WOM
Posted by MB on July 3, 2003, at 21:28:41
In reply to Re: Nice to see...thank you, posted by Jack Smith on July 1, 2003, at 17:54:09
You're right. Blagh!
MB
Posted by MB on July 3, 2003, at 21:36:54
In reply to Re: Nice to see...thank you, posted by Jack Smith on July 1, 2003, at 17:54:09
> I agree but notice that only the seratonin/norepinephrine drugs are in late stage trials. Fact is that they still have not been able to develop an effective AD that does not concentrate on seratonin, NE and to a lesser extent dopamine. I hope they will soon.
>
> JACKWait, there is a tachykinin receptor (NK-1) antagonist, a glucocorticoid receptor antagonist, and a peptide ligand in phase III. That's not too bad is it?
MB
Posted by MB on July 3, 2003, at 21:48:52
In reply to Re: Nice to see...thank you » Jack Smith, posted by cubbybear on July 2, 2003, at 7:32:19
> Hi Jack,
> Since it's been pretty well established that depression stems from problems with the serotonin, NE,and dopamine balance/depletion, I wonder how you could theoretically create an AD that does not concentrate on these. And why would you want to see such a development?
There's one new theory that the common mecahnism by which antidepressants work is by modulating brain derived nerve growth factor (BDNF). I can't find that much data on it though. Check out this usenet thread:MB
Posted by sciutti on July 6, 2003, at 19:51:59
In reply to Re: Serotonin, etc in Depression--your rebuttal » Caleb462, posted by Caleb462 on July 3, 2003, at 2:25:17
> > >> It has NOT been well established that depression stems from problems with serotonin/NE/dopamine balance/depletion.
> >
> > Well, maybe not WELL established, but so far, from all I've read, these chemicals definitely play a part. I would appreciate your citing an article or two that refutes the current hypothesis.
> > >
> >
> >
>
> I've no doubt they play a part in psychiatric disorders, but how, why, and to what extent... who knows?
>
> My personal belief is that the large majority of major depressive episodes stem from chronic, recurrent stress... which throws the system out of whack in some way... in what way, no one exactly knows. Excess cortisol release could certainly be one thing...
>
> I've run across several articles refuting the "monoanime hypothesis" of depression, though I don't have them archived, unfortunately. I will find them again, and post thim when I do.
I still don't know how to use message boards. So I'll try this....I sent Dr. Bob a question. Is that "proper" cuz I haven't gotten any replies, but I understand that. Have been reading posts on causes, drugs, etc. and I have done a lot of research. The web site for the monamine hypothesis I think is - http://www.biopsychiatry.com/mechnov.htm. and very informative.
With long term use of AD there have been found to be increases in both serotonergic and dopaminergic function ie long term use induces adaptive changes in pts. system. To me, that sounds plausible and may explain why they work.
Sorry if I offended anyone in subject content, but it just popped into my head cuz does it really matter WHY they work or just that meds do work? I am so guilty of researching and wanting to know the why and this sounds so hypocritcal, so sorry. Joanne
Posted by Caleb462 on July 7, 2003, at 9:47:29
In reply to NO ONE HAS ANWSERED SO I'LL TRY THIS WAY - WGAS? » Caleb462, posted by sciutti on July 6, 2003, at 19:51:59
> > > >> It has NOT been well established that depression stems from problems with serotonin/NE/dopamine balance/depletion.
> > >
> > > Well, maybe not WELL established, but so far, from all I've read, these chemicals definitely play a part. I would appreciate your citing an article or two that refutes the current hypothesis.
> > > >
> > >
> > >
> >
> > I've no doubt they play a part in psychiatric disorders, but how, why, and to what extent... who knows?
> >
> > My personal belief is that the large majority of major depressive episodes stem from chronic, recurrent stress... which throws the system out of whack in some way... in what way, no one exactly knows. Excess cortisol release could certainly be one thing...
> >
> > I've run across several articles refuting the "monoanime hypothesis" of depression, though I don't have them archived, unfortunately. I will find them again, and post thim when I do.
>
>
> I still don't know how to use message boards. So I'll try this....I sent Dr. Bob a question. Is that "proper" cuz I haven't gotten any replies, but I understand that. Have been reading posts on causes, drugs, etc. and I have done a lot of research. The web site for the monamine hypothesis I think is - http://www.biopsychiatry.com/mechnov.htm. and very informative.
> With long term use of AD there have been found to be increases in both serotonergic and dopaminergic function ie long term use induces adaptive changes in pts. system. To me, that sounds plausible and may explain why they work.Yes. Anti-depressants do cause long term changes in monoanime function. This does not mean that the depression stemmed from a problem in monoanime function however. If you have an infection, and you take penicillin, the infection will go away. But does this mean you had a penicillin deficiency? Most certainly not.
> Sorry if I offended anyone in subject content, but it just popped into my head cuz does it really matter WHY they work or just that meds do work? I am so guilty of researching and wanting to know the why and this sounds so hypocritcal, so sorry. Joanne
>I'd say it certainly matters WHY they work. Figuring this out can lead to better, safer treatments. Knowledge IS power.
This is the end of the thread.
Psycho-Babble Medication | Extras | FAQ
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.org
Script revised: February 4, 2008
URL: http://www.dr-bob.org/cgi-bin/pb/mget.pl
Copyright 2006-17 Robert Hsiung.
Owned and operated by Dr. Bob LLC and not the University of Chicago.