SSRIs

Question:

BULLSHIT Joe

Response:

> BULLSHIT > Joe

Therapy can be very good. I know because I have tried it. I know about this sort of thing. Really.

Response:

WASHINGTON (Reuters) – Therapy is at least as effective in treating depression as drugs are, and its effects last longer, scientists said on Thursday in a report sure to annoy drug companies that make millions selling antidepressants. The cost of therapy is about the same as drugs short-term, and cheaper over the long term, the researchers told a meeting of the American Psychiatric Association. "This will be a surprising, controversial finding for many psychiatric professionals," Robert DeRubeis, chair of the psychology department at the University of Pennsylvania, said in a statement. "Most believe quite strongly in the efficacy of medication, and psychiatric treatment guidelines call unequivocally for medication in cases of severe depression." An estimated 20 million Americans suffer from depression, which can lead to suicide. DeRubeis and Steven Hollon of Vanderbilt University in Nashville studied 240 patients with depression to see if drugs or therapy worked better. "The question that has most often been asked in studies is, ‘What gets people better faster?"’ DeRubeis said. "We asked, ‘What will keep depression away over the long term?"’ Their patients got one of three treatments — 16 weeks of cognitive therapy, 16 weeks of antidepressants plus visits to a professional, or 16 weeks of placebo pills plus visits. Cognitive therapy is a type of talking-out treatment in which patients are helped to question their negative views of themselves. "By the 16-week post-treatment assessment, response rates were identical (57 percent) for both pharmacotherapy and cognitive therapy," the researchers said in their report. "Thus, these findings suggest that cognitive therapy may work more slowly in effecting change than does pharmacotherapy, but that by the end of a four-month course of treatment, patients who receive cognitive therapy fare as well as those who receive pharmacotherapy." Most — 75 percent — of the patients who got cognitive therapy avoided a relapse, compared to 60 percent of patients on medication and 19 percent of those receiving a placebo pill, they told the group’s annual meeting in Philadelphia. "These results suggest that even after termination, a brief course of cognitive therapy may offer enduring protection comparable to that provided by ongoing medication," DeRubeis said. THERAPY IS CHEAPER The 16 weeks of drugs cost an average of $2,590, compared with $2,250 for cognitive therapy, the researchers said. Over time, therapy may prove to be cheaper because patients have to continue taking antidepressants, the researchers said. "Some proponents of medication for severely depressed patients have suggested that cognitive therapy is impractical on the basis of cost," DeRubeis said. "Our study indicates that isn’t true, especially over the long term." The study is a sharp contrast to dozens of others being presented at the meeting that show the efficacy of one antidepressant over another. The market for antidepressants is huge — and profitable. Eli Lilly and Co. earned nearly $2 billion in 2001 from Prozac and Sarafem, two brand names of a drug known generically as fluoxetine used to treat depression and severe premenstrual syndromes. The study is not the first to challenge the assumptions underlying the use of drugs to treat depression. The idea behind the drugs is to change levels of brain chemicals — in the case of fluoxetine and related drugs the targeted chemical is serotonin, linked with mood. But two recent reports suggest that placebos not only work as quickly as drugs short-term, but affect the same areas of the brain.

Response:

BULLSHIT Joe

Response:

> BULLSHIT > Joe

Therapy can be very good. I know because I have tried it. I know about this sort of thing. Really.

Response:

WASHINGTON (Reuters) – Therapy is at least as effective in treating depression as drugs are, and its effects last longer, scientists said on Thursday in a report sure to annoy drug companies that make millions selling antidepressants. The cost of therapy is about the same as drugs short-term, and cheaper over the long term, the researchers told a meeting of the American Psychiatric Association. "This will be a surprising, controversial finding for many psychiatric professionals," Robert DeRubeis, chair of the psychology department at the University of Pennsylvania, said in a statement. "Most believe quite strongly in the efficacy of medication, and psychiatric treatment guidelines call unequivocally for medication in cases of severe depression." An estimated 20 million Americans suffer from depression, which can lead to suicide. DeRubeis and Steven Hollon of Vanderbilt University in Nashville studied 240 patients with depression to see if drugs or therapy worked better. "The question that has most often been asked in studies is, ‘What gets people better faster?"’ DeRubeis said. "We asked, ‘What will keep depression away over the long term?"’ Their patients got one of three treatments — 16 weeks of cognitive therapy, 16 weeks of antidepressants plus visits to a professional, or 16 weeks of placebo pills plus visits. Cognitive therapy is a type of talking-out treatment in which patients are helped to question their negative views of themselves. "By the 16-week post-treatment assessment, response rates were identical (57 percent) for both pharmacotherapy and cognitive therapy," the researchers said in their report. "Thus, these findings suggest that cognitive therapy may work more slowly in effecting change than does pharmacotherapy, but that by the end of a four-month course of treatment, patients who receive cognitive therapy fare as well as those who receive pharmacotherapy." Most — 75 percent — of the patients who got cognitive therapy avoided a relapse, compared to 60 percent of patients on medication and 19 percent of those receiving a placebo pill, they told the group’s annual meeting in Philadelphia. "These results suggest that even after termination, a brief course of cognitive therapy may offer enduring protection comparable to that provided by ongoing medication," DeRubeis said. THERAPY IS CHEAPER The 16 weeks of drugs cost an average of $2,590, compared with $2,250 for cognitive therapy, the researchers said. Over time, therapy may prove to be cheaper because patients have to continue taking antidepressants, the researchers said. "Some proponents of medication for severely depressed patients have suggested that cognitive therapy is impractical on the basis of cost," DeRubeis said. "Our study indicates that isn’t true, especially over the long term." The study is a sharp contrast to dozens of others being presented at the meeting that show the efficacy of one antidepressant over another. The market for antidepressants is huge — and profitable. Eli Lilly and Co. earned nearly $2 billion in 2001 from Prozac and Sarafem, two brand names of a drug known generically as fluoxetine used to treat depression and severe premenstrual syndromes. The study is not the first to challenge the assumptions underlying the use of drugs to treat depression. The idea behind the drugs is to change levels of brain chemicals — in the case of fluoxetine and related drugs the targeted chemical is serotonin, linked with mood. But two recent reports suggest that placebos not only work as quickly as drugs short-term, but affect the same areas of the brain.

Response:

Question:

http://www.sciencenews.org New antidepressant medications have gained widespread use in the past decade, and more await approval from the Food and Drug Administration following clinical trials. Much debate currently concerns whether it’s ethical for physicians to give placebo pills to depressed volunteers in such studies, instead of providing either the drug being tested or an FDA-approved antidepressant. An analysis of the FDA’s clinical-trial database on recently approved antidepressants now promises to enliven the controversy further. It finds that depressed patients assigned to 4 to 8 weeks of placebo treatment

Question:

Here is a link to the 7 May 2002 article in The Washington Post regarding placebos versus antidepressants. http://www.washingtonpost.com/wp-dyn/articles/A42930-2002May6.html Cut and paste it into the address spot in your Internet browser.

Response:

As if you didn’t know?

Response:

> But hasn’t EACH ONE of these anti depressants undergone trials for > effectiveness before approval and use by the general public? Part of that is > to be better than placebo. What am I missing?

Evidently the FDA requires that the drug manufacturer furnish data from at least 2 studies (so usually only data from 2 studies are provided) showing the drug to be better than placebos.  Sometimes manufacturers must conduct 5 studies (maybe even more!) to obtain 2 that show their drug has qualities that exceed those of the placebo. The studies not sent to the FDA to gain approval for the drug may show that the placebo performed better than the drug, or that the drug was not found to be better than the placebo with suitable statistical significance (based on the number of patients involved in the study, etc.). Evidently patients who learn they improved using the placebo are prone to sudden reversal of the gains of the non-drug placebo!  So how much of "getting better" is in the mind of the patient, that "thinking one has gotten better" is a major part of "getting better"?  We must all wonder…

Response:

But hasn’t EACH ONE of these anti depressants undergone trials for effectiveness before approval and use by the general public? Part of that is to be better than placebo. What am I missing?

– Hide quoted text — Show quoted text -> Placebos & Antidepressants Work the same Way > Antidepressants also cause additional brain changes > http://mentalhealth.about.com/library/weekly/aa050502a.htm > We have known for some time that patients given placebos (pills with no > active ingredient) often respond the same way that patients given > antidepressants. Their depression often lifts as a result of either > treatment. A new study (5/02) shows us that these two treatments both > cause similar changes in the brain. > Helen Mayberg, M.D., and her colleagues at the University of Texas > Health Science Center, San Antonio, used functional brain imaging to > study glucose metabolism in different parts of the brain following > treatment with either fluoxetine or placebo. The study was a > randomized, double-blind trial of 17 middle-aged men who were > hospitalized for unipolar depression. The researchers found that their > depressed male subjects who got better (four in each condition) > responded with increased cortical activity and decreased limbic > activity after six weeks of either treatment. Patients receiving > fluoxetine also showed changes in lower parts of the brain – in the > brainstem, striatum and hippocampus. These changes were not seen in > patients who received placebo. > A graphic illustration of the changes shows the similarities and > differences between the two conditions. > Composite PET (positron emission tomography) scan data, superimposed on > MRI (magnetic resonance imaging) scans, show brain areas that increased > (red) or decreased (yellow) in activity in men who responded to placebo > (top row) and fluoxetine (bottom row). Both groups shared a pattern of > increased activity in the cortex (e.g., prefrontal, posterior > cingulate) and decreased activity in limbic regions (e.g., subgenual > cingulate), which the researchers suggest is necessary for therapeutic > response. Men who responded to the active medication, in addition, > experienced decreased activity in certain lower brain areas (e.g., > hippocampus, anterior insula) thought to sustain the cortical/limbic > changes and prevent relapse. (Graphic and key courtesy of NIMH, 2002) > What does this all mean? There are several ways to think about this > study. One conclusion that we can draw is that the placebo effect is > real – and that the act of taking an inert substance (along with other > aspects of a hospital treatment program) can trigger certain changes in > the brain. In an interview with NIMH Dr. Mayberg cautioned against > equating antidepressants and placebos. "Our findings do not support > the notion that antidepressants work merely via a placebo effect. > Patients on active medication who failed to improve did not sustain the > brainstem, striatal and hippocampus changes unique to antidepressant > responders." Rather, the authors speculate that "clinical improvement > in the group receiving placebo as part of an inpatient study is > consistent with the well-recognized effect that altering the > therapeutic environment may significantly contribute to reducing > clinical symptoms. The additional subcortical and limbic metabolism > decreases seen uniquely in fluoxetine responders may convey additional > advantage in maintaining long-term clinical response and in relapse > prevention" (Mayberg, et.al., 2002). > This study is important because it helps us begin to understand how > antidepressants and other treatment techniques change the brain. We > are just beginning to understand the brain at this level, and further > research will undoubtedly build upon this foundation. We already know > that both psychiatric medications and psychotherapy result in changes > in the brain. This study begins to tell us how the brain changes. > Reference: > Helen S. Mayberg, J. Arturo Silva, Steven K. Brannan, Janet L. Tekell, > Roderick K. Mahurin, Scott McGinnis, and Paul A. Jerabek, The > Functional Neuroanatomy of the Placebo Effect, Am J Psychiatry 2002 > 159: 728-737. [Abstract available Online]

Response:

This surprises me. Worries me for some reason also. On one hand I think that my anti depressant probably works for me. (Indeed, speculation is that too much antidressants can set off a manic cycle.) On the other hand I KNOW that my other medications do control my mania.

– Hide quoted text — Show quoted text -> Placebos & Antidepressants Work the same Way > Antidepressants also cause additional brain changes > http://mentalhealth.about.com/library/weekly/aa050502a.htm > We have known for some time that patients given placebos (pills with no > active ingredient) often respond the same way that patients given > antidepressants. Their depression often lifts as a result of either > treatment. A new study (5/02) shows us that these two treatments both > cause similar changes in the brain. > Helen Mayberg, M.D., and her colleagues at the University of Texas > Health Science Center, San Antonio, used functional brain imaging to > study glucose metabolism in different parts of the brain following > treatment with either fluoxetine or placebo. The study was a > randomized, double-blind trial of 17 middle-aged men who were > hospitalized for unipolar depression. The researchers found that their > depressed male subjects who got better (four in each condition) > responded with increased cortical activity and decreased limbic > activity after six weeks of either treatment. Patients receiving > fluoxetine also showed changes in lower parts of the brain – in the > brainstem, striatum and hippocampus. These changes were not seen in > patients who received placebo. > A graphic illustration of the changes shows the similarities and > differences between the two conditions. > Composite PET (positron emission tomography) scan data, superimposed on > MRI (magnetic resonance imaging) scans, show brain areas that increased > (red) or decreased (yellow) in activity in men who responded to placebo > (top row) and fluoxetine (bottom row). Both groups shared a pattern of > increased activity in the cortex (e.g., prefrontal, posterior > cingulate) and decreased activity in limbic regions (e.g., subgenual > cingulate), which the researchers suggest is necessary for therapeutic > response. Men who responded to the active medication, in addition, > experienced decreased activity in certain lower brain areas (e.g., > hippocampus, anterior insula) thought to sustain the cortical/limbic > changes and prevent relapse. (Graphic and key courtesy of NIMH, 2002) > What does this all mean? There are several ways to think about this > study. One conclusion that we can draw is that the placebo effect is > real – and that the act of taking an inert substance (along with other > aspects of a hospital treatment program) can trigger certain changes in > the brain. In an interview with NIMH Dr. Mayberg cautioned against > equating antidepressants and placebos. "Our findings do not support > the notion that antidepressants work merely via a placebo effect. > Patients on active medication who failed to improve did not sustain the > brainstem, striatal and hippocampus changes unique to antidepressant > responders." Rather, the authors speculate that "clinical improvement > in the group receiving placebo as part of an inpatient study is > consistent with the well-recognized effect that altering the > therapeutic environment may significantly contribute to reducing > clinical symptoms. The additional subcortical and limbic metabolism > decreases seen uniquely in fluoxetine responders may convey additional > advantage in maintaining long-term clinical response and in relapse > prevention" (Mayberg, et.al., 2002). > This study is important because it helps us begin to understand how > antidepressants and other treatment techniques change the brain. We > are just beginning to understand the brain at this level, and further > research will undoubtedly build upon this foundation. We already know > that both psychiatric medications and psychotherapy result in changes > in the brain. This study begins to tell us how the brain changes. > Reference: > Helen S. Mayberg, J. Arturo Silva, Steven K. Brannan, Janet L. Tekell, > Roderick K. Mahurin, Scott McGinnis, and Paul A. Jerabek, The > Functional Neuroanatomy of the Placebo Effect, Am J Psychiatry 2002 > 159: 728-737. [Abstract available Online]

Response:

Question:

- Hide quoted text — Show quoted text -> > > >Correct me if I’m wrong, but I know that benzodiazepines work by > >  suppressing > > > >the CNS. So why are they addictive? And first of all, what is the > >  definition > > > >of addiction? Effexor and Paxil has terrible withdrawal symptoms; why >are > > > >they not considered addictive, for example?? > > > There are two kind, psychological and physical. Which do you mean? > > both > I agree with all the above about benzos.  However, antidepressants are > not addictive. > Basically, addictive psychiatric drugs (i.e. benzodiazepines) are all > like alcohol and all the other well known addictive drugs.  The exact > reason they are addictive, on a molecular/biochemical level, is a > mystery. >OK. I drop my request for a molecular/biological level description of >addiction. All I ask is, why do you call alcohol and benzos addictive, and >the AD’s not addictive! What is the behavioural difference between the >addicts to benzos and patients strugling to withdraw Effexor? >cem

I suppose you could start with saying you can’t take xanax for a year and NOT have withdrawal, but can stop Paxil abruptly and be just fine. It doesn’t fit.

Response:

>I suppose you could start with saying you can’t take xanax for a year >and NOT have withdrawal, but can stop Paxil abruptly and be just fine. >It doesn’t fit.

But people have sued the manufacturers of Paxil and won because they didn’t reveal the severity of withdrawal.  There have been scores of Paxil anecdotes here, some people have no problem while others say it was the worst experience of their lives. One subtle difference between Xanax and Paxil is that one produces a mildly euphoric experience while the other simply restores a normal state of being.  But Xanax is HIGHLY addictive!!!  I can’t describe the sensation, but Xanax made me feel like I always had to take another dose.  There was no pain or suffering, just a mental compulsion to take another dose.  I was lucky that I only took it for 5-6 months, long-term users report absolute hell in withdrawal.

Response:

> But people have sued the manufacturers of Paxil and won because they > didn’t reveal the severity of withdrawal.  There have been scores of > Paxil anecdotes here, some people have no problem while others say > it was the worst experience of their lives.

I’m one of the former, although I had such horrible side-effects when I was taking it that any withdrawal may have been compensated for by the diminished side-effects once I’d given it the boot. > One subtle difference between Xanax and Paxil is that one produces a > mildly euphoric experience while the other simply restores a normal > state of being.  But Xanax is HIGHLY addictive!!!  I can’t describe > the sensation, but Xanax made me feel like I always had to take > another dose.  There was no pain or suffering, just a mental > compulsion to take another dose.  I was lucky that I only took it > for 5-6 months, long-term users report absolute hell in withdrawal.

I’m curious about this one.  I’d taken lorazepam for about 2 years, which is supposedly one of the most "addictive" benzos, and when I decided it wasn’t really useful so I may as well stop it I experienced 2 or 3 weeks of slightly increased anxiety, agitation and so on, but certainly a long way from "absolute hell."  I’m wondering if I’m somehow more resistant to withdrawal than most others, or if it’s more a case of how much aggro someone’s prepared to tolerate?  In my case I think I took the rather morbid line that life was already so crap that some extra horribleness was no big deal. Chris.

Response:

> >Correct me if I’m wrong, but I know that benzodiazepines work by suppressing >the CNS. So why are they addictive? And first of all, what is the definition >of addiction? Effexor and Paxil has terrible withdrawal symptoms; why are >they not considered addictive, for example?? >cem > They all are addictive.

Before proceeding on this, does anyone know why the ASAP people, of whom one at least has visited here, are vociferously against the position that benzos are addicting?  And why, this group does not go bezerk if you mention benzo addiction? Squiggles

Response:

- Hide quoted text — Show quoted text ->Before proceeding on this, does anyone know >why the ASAP people, of whom one at least has >visited here, are vociferously against the position >that benzos are addicting?  And why, this group >does not go bezerk if you mention benzo addiction? > Because unlike you, they just can’t admit addiction. It’s like walking > in a bar at 11 a.m. and telling people they are alcoholics. > It’s the flip side of anti-med —- pro-med. So blinded and in denial > they can’t see the forest for the trees. > Did you notice they now have a message board for people who want to > debate things that may be "disruptive", IOW – addiction? > Just go to ASAP and ask if benzos are addictive, and report back your > results.

I’ve been there – if you check the Google correspondence between Ian and me, you will see the acrimonious nature of the debate. It’s hard to believe that all of them are blinded to the possibility of addiction.   Interesting that they now have a "disruptive" room – maybe I should go there, LOL!   Squiggles

Response:

>Correct me if I’m wrong, but I know that benzodiazepines work by suppressing >the CNS. So why are they addictive? And first of all, what is the definition >of addiction? Effexor and Paxil has terrible withdrawal symptoms; why are >they not considered addictive, for example??

I can only say from personal experience that benzos are incredibly addictive.  Especially Xanax.  In a way they are similar to methamphetamine, neither makes you think you’re addicted.  Like meth, benzos create a pure mental desire to take another dose, you always find some rationale to do more, thee is no actual physical withdrawal involved.  Perhaps there is some withdrawal, it tends not to be painful, just a dramatic increase in anxiety, the very thing benzos are prescribed to treat.

Response:

>Correct me if I’m wrong, but I know that benzodiazepines work by suppressing >the CNS. So why are they addictive? And first of all, what is the definition >of addiction? Effexor and Paxil has terrible withdrawal symptoms; why are >they not considered addictive, for example?? > There are two kind, psychological and physical. Which do you mean?

both

Response:

> Not true, Chris.  The benzodiazepine Klonopin (clonazepam HCl) has a > half-life of between 30-40 hours–a half life typical of the SSRIs (except > fluoxetine).

Okay, maybe I missed out the phrase "generally speaking."  Of course there are exceptions with a minority of benzos with atypically long half-lives and antidepressants with very short ones, but IMHO using one of the exceptions to say the basis is "not true" is nitpicking (of course it may be inaccurate in other more valid aspects) Chris.

Response:

> > >Correct me if I’m wrong, but I know that benzodiazepines work by >  suppressing > >the CNS. So why are they addictive? And first of all, what is the >  definition > >of addiction? Effexor and Paxil has terrible withdrawal symptoms; why are > >they not considered addictive, for example?? > There are two kind, psychological and physical. Which do you mean? > both

I agree with all the above about benzos.  However, antidepressants are not addictive. Basically, addictive psychiatric drugs (i.e. benzodiazepines) are all like alcohol and all the other well known addictive drugs.  The exact reason they are addictive, on a molecular/biochemical level, is a mystery. Antidepressants aren’t.  They seem to work by putting a floor under one’s mood state, so that you don’t go spiraling downwards.  But you won’t see people on the street because of being hooked on antidepressants – it just doesn’t happen. The people who deny that benzos are addictive are either in an addictive denial state or in some other peculiar denial state. There’s no doubt that benzos are highly addictive.

Response:

- Hide quoted text — Show quoted text -> > >Correct me if I’m wrong, but I know that benzodiazepines work by >  suppressing > > >the CNS. So why are they addictive? And first of all, what is the >  definition > > >of addiction? Effexor and Paxil has terrible withdrawal symptoms; why are > > >they not considered addictive, for example?? > > There are two kind, psychological and physical. Which do you mean? > both > I agree with all the above about benzos.  However, antidepressants are > not addictive. > Basically, addictive psychiatric drugs (i.e. benzodiazepines) are all > like alcohol and all the other well known addictive drugs.  The exact > reason they are addictive, on a molecular/biochemical level, is a > mystery. > Antidepressants aren’t.  They seem to work by putting a floor under > one’s mood state, so that you don’t go spiraling downwards.  But you > won’t see people on the street because of being hooked on > antidepressants – it just doesn’t happen. > The people who deny that benzos are addictive are either in an > addictive denial state or in some other peculiar denial state. > There’s no doubt that benzos are highly addictive.

I think the word "addiction" has a special pharmaceutical meaning and a literal one; it is the literal one that gets people or riled up.  Regarding the ADs however, it seems that some of the new ones leave their mark, if you discontinue the drug; hence the neologism:  "discontinuation syndrome" – how similar that is to "addiction" is something a competent pharmacologist should be able to figure out. Squiggles — Truth has become a commodity.              - Squiggles

Response:

– Hide quoted text — Show quoted text -> > >Correct me if I’m wrong, but I know that benzodiazepines work by >  suppressing > > >the CNS. So why are they addictive? And first of all, what is the >  definition > > >of addiction? Effexor and Paxil has terrible withdrawal symptoms; why are > > >they not considered addictive, for example?? > > There are two kind, psychological and physical. Which do you mean? > both > I agree with all the above about benzos.  However, antidepressants are > not addictive. > Basically, addictive psychiatric drugs (i.e. benzodiazepines) are all > like alcohol and all the other well known addictive drugs.  The exact > reason they are addictive, on a molecular/biochemical level, is a > mystery.

OK. I drop my request for a molecular/biological level description of addiction. All I ask is, why do you call alcohol and benzos addictive, and the AD’s not addictive! What is the behavioural difference between the addicts to benzos and patients strugling to withdraw Effexor? cem

Response:

Correct me if I’m wrong, but I know that benzodiazepines work by suppressing the CNS. So why are they addictive? And first of all, what is the definition of addiction? Effexor and Paxil has terrible withdrawal symptoms; why are they not considered addictive, for example?? cem

Response:

> Correct me if I’m wrong, but I know that benzodiazepines work by suppressing > the CNS. So why are they addictive? And first of all, what is the definition > of addiction?

Because the CNS adapts to compensate after prolonged suppression, so once the suppression ends the CNS becomes overactive resulting in various nasties like anxiety and insomnia.  Or something like that. > Effexor and Paxil has terrible withdrawal symptoms; why are > they not considered addictive, for example??

Much longer half-life.  Benzos wear off after a few hours leading to the chronic user to be continuously aware that they need to take another dose.  Most ADs take several days (at least) before any withdrawal effects are likely to appear, which doesn’t have quite the same immediacy about it. Chris.

Response:

>Correct me if I’m wrong, but I know that benzodiazepines work by suppressing >the CNS. So why are they addictive? And first of all, what is the definition >of addiction? Effexor and Paxil has terrible withdrawal symptoms; why are >they not considered addictive, for example?? >cem

They all are addictive.

Response:

Not true, Chris.  The benzodiazepine Klonopin (clonazepam HCl) has a half-life of between 30-40 hours–a half life typical of the SSRIs (except fluoxetine).

– Hide quoted text — Show quoted text -> Correct me if I’m wrong, but I know that benzodiazepines work by suppressing > the CNS. So why are they addictive? And first of all, what is the definition > of addiction? > Because the CNS adapts to compensate after prolonged suppression, so > once the suppression ends the CNS becomes overactive resulting in > various nasties like anxiety and insomnia.  Or something like that. > Effexor and Paxil has terrible withdrawal symptoms; why are > they not considered addictive, for example?? > Much longer half-life.  Benzos wear off after a few hours leading to > the chronic user to be continuously aware that they need to take > another dose.  Most ADs take several days (at least) before any > withdrawal effects are likely to appear, which doesn’t have quite > the same immediacy about it. > Chris.

Response:

Question:

This is Serzone, according to www.medbroadcast.com here is the link for you reading pleasure; http://drugs.medbroadcast.com/ASP/DrugInfo.asp?BrandNameID=379 Carrie

– Hide quoted text — Show quoted text -> I`ve been on 600 mg of this stuff for a couple of years. > When I looked in a worthy book recently, it listed 4 types of > antidepressants : >         MAOIs >         SSRIs >         Benzedrines >         Others. >  nefazodone was listed under `others,` but no description was given. The net > hasn`t been much help. > I get very bad headaches when I cut down (and for 3 weeks when I srarted on > it .)

Response:

I`ve been on 600 mg of this stuff for a couple of years. When I looked in a worthy book recently, it listed 4 types of antidepressants :         MAOIs         SSRIs         Benzedrines         Others.  nefazodone was listed under `others,` but no description was given. The net hasn`t been much help. I get very bad headaches when I cut down (and for 3 weeks when I srarted on it .)

Response:

Question:

Hello Group, I don’t have insurance, so I pay for my fluoxetine (generic prozac) myself. Does anyone have any experience with buying their meds through the internet? Healthmeds.com sells 20 mg fluoxetine for less than $1 per unit.  That’s half what my local pharmacy charges. Comments welcome, Thanks

Response:

The most reliable pharmacy is #1 Online Pharmacy.  I’ve gotten all my antidepressants from there (I live in US): http://www.1drugstore-online.com/showproducts.asp?gcode=005

Response:

Thanks for the info!   Their prices are very low. You haven’t had any problems?   No problems with dosages being screwed up, or anything like that?    I’ve heard stories of internet drug companies selling sugar pills.

– Hide quoted text — Show quoted text -> The most reliable pharmacy is #1 Online Pharmacy.  I’ve gotten all my > antidepressants from there (I live in US): > http://www.1drugstore-online.com/showproducts.asp?gcode=005

Response:

> Thanks for the info!   Their prices are very low. > You haven’t had any problems?   No problems with dosages being screwed up, > or anything like that?    I’ve heard stories of internet drug companies > selling sugar pills. > The most reliable pharmacy is #1 Online Pharmacy.  I’ve gotten all my > antidepressants from there (I live in US): > http://www.1drugstore-online.com/showproducts.asp?gcode=005

I’ve been buying all my meds (bp, cholesterol, antidepressants) from drugstore.com.  Never had a problem.  They’re owned by Rite-Aid, so if you have one nearby you can pick it up at the store.

Response:

Question:

Having nothing to say, himself Eric has resorted to outright copying of other groups. If we wanted to read Dr. Bobs we would be there. – Hide quoted text — Show quoted text -> I copied and pasted this off the Dr. Bob’s tips and tricks section. One of the > main theories as to why antidepressants "poop out" and stop working is because > of dopamine depletion. This can be remedied by adding a dopamine agonist like > Amantadine, Ritalin, Mirapex, bromocriptine, etc. > "Patients who lose response to antidepressants > —— > When encountering patients who do well for the first few weeks on an SSRI > (especially Prozac) but then seem to lose their response after a few weeks I > have to decide whether to increase or decrease the dose. If the patient, at > that point, seems to have *new* sedation or apathy I conclude the dose is too > high and decrease it. If not, I increase it. Most of the time I end up > increasing the dose. If the patient seems to require a dose of the SSRI which > produces sedation or apathy in order to have an antidepressant effect then I > consider changing the time of day of administration (usually doesn’t help) or > adding a stimulant. > I confess that I have not seen many patients whose depression does better on > lower SSRI doses, but I have seen a bunch who get fewer side effects that way. > —— > It has been hypothesized by Don Klein and others that what looks like decreased > antidepressant effectiveness is really a state of akinesia resulting from > depletion of dopamine with continuing use of the SSRIs. Based on this > understanding one can treat the apparent fall-off in SSRI effectiveness with DA > agonists such as bupropion, amantadine, methylphenidate, dextroamphetamine, > etc. I have done this on many occasions, often with excellent results. > —— > I have often observed that patients who respond well to low doses of an > antidepressant, and lose the effect after a month or so, may regain the > therapeutic effect if their dose is increased to more usual doses. > This may be a manifestation of an initial placebo response followed by a > pharmacological response, or possibly something related to the pharmacokinetics > or pharmacodynamics of the drug. > —— > It seemed to me that once virtually no one developed tolerance to the > antidepressant effects of SSRIs. That was when all we had available was > fluoxetine. Nowadays, I prescribe more of the short-acting SSRIs, and it is my > impression that more than 5% to 10% of my patients develop tolerance to their > meds after taking them from one to twelve months. My patients seem to improve > with an incremental increase in dose; however, one increase usually predicts > that they will later need a second increase as the same phenomenon occurs. When > we reach the upper limit of the recommended dosage range, I switch to an > alternate antidepressant, which often works — but not always. Sometimes such a > patient will creep up on their dose of the second SSRI and then return to the > first one, usually with renewed effectiveness at the initial starting dose. > This phemnomenon seems so common that I mention to patients that it can happen > and that if it does I want them to contact me. > The data is impressionistic, but it seems to me that I see much more of this > "dosage creep" (and don’t you hate that terminology!) than I used to see. > —— > I have had a very similar experience. This is now spoken about in many > psychopharm conferences as "poop out." In my experience it sometimes happens as > late as 3 years into an SSRI (typically Prozac, since it’s been around the > longest), in as many as 20% of patients. > What is to be done? There is talk among "poop out" veterans of adding > bromocriptine since there is speculation that this might be a dopaminergic > depletion phenomenon. People have said this helps, but I haven’t used it yet > myself. > —— > I have a lot of experience seeing people who have failed to respond to a series > of antidepressants and/or are failing to respond to a medication which used to > help. I have found that evaluating four factors will usually get things back on > track: > sleep problems > alcohol use > thyroid problems and > subsyndromal bipolar symptoms. > Alcohol use, even in small amounts, can disrupt sleep in sensitive individuals > and I usually recommend complete abstention from alcohol. > The most common problem I have found, however, is the presence of subtle, > subsyndromal bipolar symptoms, current or past, which may or may not meet > criteria for mania or hypomania. These patients do best with the addition of > lithium or another mood stabilizer. > —— > This wearing off phenonemon seems to be an all too frequent occurence with the > new antidepressants, in particular moclobemide. Rather than increasing the > dosage, a few of my colleagues down here paradoxically suggest a day or two to > a week without medication, with good results! Maybe it’s got something to do > with enzyme induction. Although others have suggested that this wearing off > merely reflects an initial placebo response, I don’t think it fully explains > this phenomenon. > —— > Lee Dante wrote, in part: > This phenomena of the SSRI "poop out" can usually be reversed by adding 25 mg > of naltrexone (marketed in the US as Revia), usually on top of supper to avoid > transient nausea. In anywhere from two weeks to five of once daily dosing the > SSRI regains the full effect and often is perceived as working better than it > did at first. I have done this in over forty cases where this has been most > gratifying. At this dose of naltrexone the incidence of side effects is very > low, and the improvement is sustained over a period of years. It has been the > end of poop out in my practice. > —— > That reminds me of a patient with opiate dependence in the post-detox phase. He > was receiving 20 mg of fluoxetine for a comorbid major depression and was > improving when naltrexone 50 mg/day was added. Within 4 days, he was hypomanic. > On discontinuation of fluoxetine (on the presumption of a SSRI-induced > hypomania), he returned to his previous baseline over a period of one week. At > that time, I did not think much of a possible interaction between fluoxetine & > naltrexone. Now, I begin to wonder! > —— > I’ve used Remeron (mirtazapine) fairly often for Paxil "poop-out". > Eric > "Oh you didnt get better cause you didnt work hard enough in talk therapy. Its > YOUR fault!." Quote from Typical talk therapy asshole after therapy fails to > relieve severe depression > http://groups.yahoo.com/group/MergePsychiatryIntoNeurology/

Response:

- Hide quoted text — Show quoted text – > Having nothing to say, himself Eric has resorted to outright copying of > other groups. > If we wanted to read Dr. Bobs we would be there. > I copied and pasted this off the Dr. Bob’s tips and tricks section. One of the > main theories as to why antidepressants "poop out" and stop working is because > of dopamine depletion. This can be remedied by adding a dopamine agonist like > Amantadine, Ritalin, Mirapex, bromocriptine, etc. > "Patients who lose response to antidepressants > —— > When encountering patients who do well for the first few weeks on an SSRI > (especially Prozac) but then seem to lose their response after a few weeks I > have to decide whether to increase or decrease the dose. If the patient, at > that point, seems to have *new* sedation or apathy I conclude the dose is too > high and decrease it. If not, I increase it. Most of the time I end up > increasing the dose. If the patient seems to require a dose of the SSRI which > produces sedation or apathy in order to have an antidepressant effect then I > consider changing the time of day of administration (usually doesn’t help) or > adding a stimulant. > I confess that I have not seen many patients whose depression does better on > lower SSRI doses, but I have seen a bunch who get fewer side effects that way. > —— > It has been hypothesized by Don Klein and others that what looks like decreased > antidepressant effectiveness is really a state of akinesia resulting from > depletion of dopamine with continuing use of the SSRIs. Based on this > understanding one can treat the apparent fall-off in SSRI effectiveness with DA > agonists such as bupropion, amantadine, methylphenidate, dextroamphetamine, > etc. I have done this on many occasions, often with excellent results. > —— > I have often observed that patients who respond well to low doses of an > antidepressant, and lose the effect after a month or so, may regain the > therapeutic effect if their dose is increased to more usual doses. > This may be a manifestation of an initial placebo response followed by a > pharmacological response, or possibly something related to the pharmacokinetics > or pharmacodynamics of the drug. > —— > It seemed to me that once virtually no one developed tolerance to the > antidepressant effects of SSRIs. That was when all we had available was > fluoxetine. Nowadays, I prescribe more of the short-acting SSRIs, and it is my > impression that more than 5% to 10% of my patients develop tolerance to their > meds after taking them from one to twelve months. My patients seem to improve > with an incremental increase in dose; however, one increase usually predicts > that they will later need a second increase as the same phenomenon occurs. When > we reach the upper limit of the recommended dosage range, I switch to an > alternate antidepressant, which often works — but not always. Sometimes such a > patient will creep up on their dose of the second SSRI and then return to the > first one, usually with renewed effectiveness at the initial starting dose. > This phemnomenon seems so common that I mention to patients that it can happen > and that if it does I want them to contact me. > The data is impressionistic, but it seems to me that I see much more of this > "dosage creep" (and don’t you hate that terminology!) than I used to see. > —— > I have had a very similar experience. This is now spoken about in many > psychopharm conferences as "poop out." In my experience it sometimes happens as > late as 3 years into an SSRI (typically Prozac, since it’s been around the > longest), in as many as 20% of patients. > What is to be done? There is talk among "poop out" veterans of adding > bromocriptine since there is speculation that this might be a dopaminergic > depletion phenomenon. People have said this helps, but I haven’t used it yet > myself. > —— > I have a lot of experience seeing people who have failed to respond to a series > of antidepressants and/or are failing to respond to a medication which used to > help. I have found that evaluating four factors will usually get things back on > track: > sleep problems > alcohol use > thyroid problems and > subsyndromal bipolar symptoms. > Alcohol use, even in small amounts, can disrupt sleep in sensitive individuals > and I usually recommend complete abstention from alcohol. > The most common problem I have found, however, is the presence of subtle, > subsyndromal bipolar symptoms, current or past, which may or may not meet > criteria for mania or hypomania. These patients do best with the addition of > lithium or another mood stabilizer. > —— > This wearing off phenonemon seems to be an all too frequent occurence with the > new antidepressants, in particular moclobemide. Rather than increasing the > dosage, a few of my colleagues down here paradoxically suggest a day or two to > a week without medication, with good results! Maybe it’s got something to do > with enzyme induction. Although others have suggested that this wearing off > merely reflects an initial placebo response, I don’t think it fully explains > this phenomenon. > —— > Lee Dante wrote, in part: > This phenomena of the SSRI "poop out" can usually be reversed by adding 25 mg > of naltrexone (marketed in the US as Revia), usually on top of supper to avoid > transient nausea. In anywhere from two weeks to five of once daily dosing the > SSRI regains the full effect and often is perceived as working better than it > did at first. I have done this in over forty cases where this has been most > gratifying. At this dose of naltrexone the incidence of side effects is very > low, and the improvement is sustained over a period of years. It has been the > end of poop out in my practice. > —— > That reminds me of a patient with opiate dependence in the post-detox phase. He > was receiving 20 mg of fluoxetine for a comorbid major depression and was > improving when naltrexone 50 mg/day was added. Within 4 days, he was hypomanic. > On discontinuation of fluoxetine (on the presumption of a SSRI-induced > hypomania), he returned to his previous baseline over a period of one week. At > that time, I did not think much of a possible interaction between fluoxetine & > naltrexone. Now, I begin to wonder! > —— > I’ve used Remeron (mirtazapine) fairly often for Paxil "poop-out". > Eric > "Oh you didnt get better cause you didnt work hard enough in talk therapy. Its > YOUR fault!." Quote from Typical talk therapy asshole after therapy fails to > relieve severe depression > http://groups.yahoo.com/group/MergePsychiatryIntoNeurology/

Can  someone with glaucoma or hypertension safely take ritalin for ADD?

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Question:

> Hello, > I’ve just started taking Celexa, and I have a question about the > potential for (unwanted) weight gain.  Is the weight gain side effect > associated with SSRIs a consequence of a change in eating habits > induced by the drug, or directly due to a change in metabolism?  In > other words, if I carefully monitor what I eat, can I avoid gaining > weight or even be able to lose weight?

 Hi Tom, Welcome to the ng. Antidepressants may increase or decrease basal metabolic rate without changing caloric intake or they may affect hormonal changes and increase appetite. The best course of action is to increase physical activity….aerobic nonstop activity daily for at least 30 min a day. Peace, Lynda I believe it alters carbohydrate metabolism

Response:

hi Tom… the SSRI (Prozac) that I was on for years caused me to have an initial weight loss, although the loss eventually evened itself out. My Pdoc says that regarding weight gain, unfortunately it is not so much eating habits changed by the drug as it is a metabolical change (I had asked him about this too). However, Prozac and Celexa do have pharmacological differences (Celexa is a newer breed of drug), so my Pdoc may have just been giving me info specific to Prozac. Regards, compucat

– Hide quoted text — Show quoted text -> Hello, > I’ve just started taking Celexa, and I have a question about the > potential for (unwanted) weight gain.  Is the weight gain side effect > associated with SSRIs a consequence of a change in eating habits > induced by the drug, or directly due to a change in metabolism?  In > other words, if I carefully monitor what I eat, can I avoid gaining > weight or even be able to lose weight? > Tom L.

Response:

Hello, I’ve just started taking Celexa, and I have a question about the potential for (unwanted) weight gain.  Is the weight gain side effect associated with SSRIs a consequence of a change in eating habits induced by the drug, or directly due to a change in metabolism?  In other words, if I carefully monitor what I eat, can I avoid gaining weight or even be able to lose weight? Tom L.

Response:

Question:

Hello – I’m Peter and I’m new to this newsgroup. I had been on Prozac for 6 years and then it stopped working for me. The doc put me on Effexor, and it worked a treat-all the old anger and anxiety went away and then I began to notice things. I had real trouble reaching orgasm, and when I did the ejaculation and orgasm were separated, which was really weird. My wife thought it was her fault, but I begin to realise it wasn’t. The worst effect by far is when I miss a tablet-that’s right, JUST ONE !! I begin to get confused and my eyes begin to, well, how can I put it, buzz and hurt, as if some extra fluid had just been pumped in. The other day I was driving back from Coventry to Bradford (150 miles) and I began to feel the eyes going, and that’s when I realised I’d forgotten the tablet. Now I know it has a short half life, but this is crazy – how can I ever hope to get off it, as I am trying to do now with the help of therapy. It’s really horrible; some people might say that these are symptoms of my condition reappearing, but I say NO! This never happened before Effexor. Does this ring any bells with anyone? Can anyone say that any of the above has happened to them? Thanks everyone, I know you can ease my mind and I really appreciate you help and input. Bye for now, Peter Finan

Response:

> Paxil and Effexors half life make them the worse antidepressants to stop… > people frequently get horrific withdrawal  especially where they stop > abruptly…  you have to taper off very very gradually..

I’ve been on both at one time or another for prolonged periods of time. I stopped each one of them cold turkey without any noticeable adverse effects. > As people get down to lowest possible dosage of Paxil or Effexor…..some > have used Prozac then,   tapering off that…then as well, ..to keep the > worse of the symptoms of withdrawal at bay…and reported it works to do > that.. > Sexual dysfunction as you reported is Frequent side effect of the SSRI et al

Effexor is not an SSRI, and has notably fewer sexual side effects than the SSRIs. Dave – Hide quoted text — Show quoted text -> or modern class of Antidepressants.. > Hello – I’m Peter and I’m new to this newsgroup. I had been on Prozac for > 6 > years and then it stopped working for me. The doc put me on Effexor, and > it > worked a treat-all the old anger and anxiety went away and then I began to > notice things. I had real trouble reaching orgasm, and when I did the > ejaculation and orgasm were separated, which was really weird. My wife > thought > it was her fault, but I begin to realise it wasn’t. The worst effect by > far is > when I miss a tablet-that’s right, JUST ONE !! I begin to get confused and > my > eyes begin to, well, how can I put it, buzz and hurt, as if some extra > fluid > had just been pumped in. The other day I was driving back from Coventry to > Bradford (150 miles) and I began to feel the eyes going, and that’s when I > realised I’d forgotten the tablet. Now I know it has a short half life, > but > this is crazy – how can I ever hope to get off it, as I am trying to do > now > with the help of therapy. It’s really horrible; some people might say that > these are symptoms of my condition reappearing, but I say NO! This never > happened before Effexor. Does this ring any bells with anyone? Can anyone > say > that any of the above has happened to them? Thanks everyone, I know you > can > ease my mind and I really appreciate you help and input. > Bye for now, > Peter Finan

Response:

> Now I know it has a short half life, but > this is crazy – how can I ever hope to get off it, as I am trying to do now > with the help of therapy. It’s really horrible; some people might say that > these are symptoms of my condition reappearing, but I say NO! This never > happened before Effexor. Does this ring any bells with anyone? Can anyone say > that any of the above has happened to them? Thanks everyone, I know you can > ease my mind and I really appreciate you help and input.

I took Effexor XR for quite a while, and I don’t recall having any trouble going off it nor having particularly adverse reactions to missing a single dose. It is possible and not necessarily an unpleasant experience. I probably had the sexual dysfunction, but I didn’t get a sufficient response to it to be interested in having sex in the first place. Fiona — If we had no winter, the spring would not be so pleasant: if we did not sometimes taste the adversity, prosperity would not be so welcome.      – Anne Bradstreet, Meditations Divine and Moral, 1664

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Question:

3 years ago my G.P. dianosed me as being clinically depressed and prescribed Cipramil tablets. I have once tried to come off them but within 4 weeks I was having my original symptoms and was advised to go back on them. I am now at my wits end as I have a complete loss of libido which I am aware is a side effect of  antidepressants and as a result am considering to once again try to manage without the help of the Cipramil. Has anyone experienced a similar problem and if so how have you managed to overcome it ? P.S. also known as Citalopram Hydrobromide.

Response:

Why not try another anti-depressant?  There are many out on the market today & I would think you should be able to find one with minimal side effects.  It might take some trial & error, however. >3 years ago my G.P. dianosed me as being clinically depressed and prescribed >Cipramil tablets. I have once tried to come off them but within 4 weeks I >was having my original symptoms and was advised to go back on them. I am now >at my wits end as I have a complete loss of libido which I am aware is a >side effect of  antidepressants and as a result am considering to once again >try to manage without the help of the Cipramil. Has anyone experienced a >similar problem and if so how have you managed to overcome it ? P.S. also >known as Citalopram Hydrobromide.

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