Has anyone switched from Prozac to generic fluoxetine? If so, have you noticed any differences. thanks, marks
hi Mark – both had worked exactly the same. The generic Prozac (called Fluoxetine) was fine with me, and it was cheaper to boot! — regards, Compucat
– Hide quoted text — Show quoted text -> Has anyone switched from Prozac to generic fluoxetine? If so, have you > noticed any differences. > thanks, > marks
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
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
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
> 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.
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/
- 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?
Duloxetine is a medication used to treat depression and anxiety. Buy duloxetine fibromyalgia and feel better today!
has anyone heard of that new anti-depressant on the radio?i was trying to remember what it was called.thanks
.."that" new antidepressant on the radio? Geez, you’re not giving us much to go on. I haven’t heard of anything new available here in the US, sadly.
>: Re: new anti-depressant?
The only new one I’ve heard about recently is Duloxetine and, quite frankly, I don’t think it’s much to get excited about, but you be the judge. I think Eli Lilly markets it, and that would make sense because their Prozac patent just ran out and generic companies have scooped up generic prozac (fluoxetine), so that is that much less money in Eli Lilly’s pockets. Interesting that they timed the news about Duloxetine right after the prozac patent ran out.
The article, "Bromocriptine Treatment of Relapses Seen During Selective Serotonin Re-uptake Inhibitor Treatment of Depression" mentions why bromocriptine might be effective for those who had SSRI poop-out: "Some patients relapse while taking previously effective doses of selective serotonin reuptake inhibitor antidepressants (SSRI), as they do with other antidepressants. Possible explanations of this include the loss of a nonspecific or placebo response and the possible loss of pharmacodynamic effect due to tachyphylaxis. Extrapyramidal disorders have been reported with the clinical use of fluoxetine, suggesting alterations in striatal dopaminergic neurotransmission. A review of the literature concludes that serotonin modulates dopamine neurotransmission, although the details of this interaction are yet to be elucidated. Further, a recent preclinical study found that chronic fluoxetine treatment caused decreases in dopamine levels in the nucleus accumbens and striatum in rats of between 60 and 70% that persisted up to 14 days after fluoxetine was discontinued. Another laboratory has published preliminary results of decreased synthesis of dopamine in rat forebrain with chronic fluoxetine treatment, consistent with this finding, although further experiments were not able to confirm the original finding. Nonetheless, the weight of evidence to date suggests that there are important functional interactions between the ascending projections from serotonergic raphe nuclei and dopaminergic neurons in the striatum and limbic forebrain. Therefore, the loss of SSRI’s benefit may be related to secondary deficiencies in dopamine neurotransmission caused by SSRI treatment, possibly in patients especially vulnerable because of relatively low dopaminergic tone. We hypothesized that this might be alleviated by postsynaptic dopaminergic agonists like bromocriptine…"
I’d like to see how you do on bromocriptine or the dopaminergic MAOI’s/RIMA’s.
>>ubject: Re: SSRI’s and Dopamine Depletion >I’d like to see how you do on bromocriptine or the dopaminergic >MAOI’s/RIMA’s. >Bromocripine alone…or in combo with an SSRI >cause I will NEVER ever take an SSRI again
An ap is what you need Gem. Remove the **** from my address for email replies…. —–= Posted via Newsfeeds.Com, Uncensored Usenet News =—– http://www.newsfeeds.com – The #1 Newsgroup Service in the World! —–== Over 80,000 Newsgroups – 16 Different Servers! =—–
STUDIES ON PERSISTENT EFFECTS OF SSRI USE The following new study is very significant. It finds that very young rats exposed to Prozac for just 2 weeks had brains changes that persisted into adulthood. It concludes: "This is the first empirical demonstration of long-lasting effects of the administration of a selective serotonin reuptake inhibitor during juvenile life on the maturation of the central serotonergic system." J Child Adolesc Psychopharmacol 1999;9(1):13-24; discussion 25-6 Persistently increased density of serotonin transporters in the frontal cortex of rats treated with fluoxetine during early juvenile life.
– Hide quoted text — Show quoted text -> STUDIES ON PERSISTENT EFFECTS OF SSRI USE > The following new study is very significant. It finds that very young rats > exposed to Prozac for just 2 weeks had brains changes that persisted into > adulthood. It concludes: "This is the first empirical demonstration of > long-lasting effects of the administration of a selective serotonin reuptake > inhibitor during juvenile life on the maturation of the central serotonergic > system." > J Child Adolesc Psychopharmacol 1999;9(1):13-24; discussion 25-6 > Persistently increased density of serotonin transporters in the frontal cortex > of rats treated with fluoxetine during early juvenile life.
This must be the study that Steve was talking about. – Hide quoted text — Show quoted text –
YES YES!!!! thanks so much, bob! – Hide quoted text — Show quoted text -> STUDIES ON PERSISTENT EFFECTS OF SSRI USE > The following new study is very significant. It finds that very young rats > exposed to Prozac for just 2 weeks had brains changes that persisted into > adulthood. It concludes: "This is the first empirical demonstration of > long-lasting effects of the administration of a selective serotonin > reuptake > inhibitor during juvenile life on the maturation of the central > serotonergic > system." > J Child Adolesc Psychopharmacol 1999;9(1):13-24; discussion 25-6 > Persistently increased density of serotonin transporters in the frontal > cortex > of rats treated with fluoxetine during early juvenile life. > This must be the study that Steve was talking about.
Thats really interesting Jim.. Ill try to get a copy.. That so little research of this sort is done in the US isnt suprising when most is sponsored by the multi-billion dollar pharmaceutical multinationals. – Hide quoted text — Show quoted text – > X-No-Archive: yes >YES YES!!!! thanks so much, bob! > See comments below. > I believe the Rat study does not in itself "prove" things > But I do believe that the comibination of some > circumstantial information, including the Rat study, does > indicate that there could be long term damage in the brain > due to the SSRIs. > And that is something both important and worthy of > discussion in substance. >> > STUDIES ON PERSISTENT EFFECTS OF SSRI USE >> > The following new study is very significant. It finds that very young rats >> > exposed to Prozac for just 2 weeks had brains changes that persisted into >> > adulthood. It concludes: "This is the first empirical demonstration of >> > long-lasting effects of the administration of a selective serotonin >> > reuptake inhibitor during juvenile life on the maturation of the central >> > serotonergic system." >> > J Child Adolesc Psychopharmacol 1999;9(1):13-24; discussion 25-6 >> > Persistently increased density of serotonin transporters in the frontal >> >cortex of rats treated with fluoxetine during early juvenile life. >> This must be the study that Steve was talking about. > Glad Steven found his reference. Steven or others might > consider reading (or rereading if you already read it), the > Prozac Backlash Book by Josepth Glenmullen M.D. copyright > 2000 which comes after the 1999 rat article referenced. > Glenmullen mentions the rat study and quite a bit more. > However the case he makes for potential braindamage, > rests not on the rat study, but rather on the page after > page of circimumstantial information (not proof). > In addition to the straifforward support for patients rights > and other factors, the information relative potential brain > damage provided by Gelenmullen (not proved) , is > sufficiently convincing to me that it enhances my support > for at least some patients who desire to be off the meds. > Some Doctors manage to get people on the drugs who do not > seem to be needing them in the first place. And some who > might need the drugs at least for some time, seem to get > stuck with the "drug for life" thing even when that does > not seem reasonable. Only emphasis of some Drs, books etc, > seems to be on the potential of "remission" , rather than > a balance of all factors including remission. > A discussion of potential brain damage as developed in the > Glenumllen book (or others) would be useful. especially to > those who might be marginal as to real need or not need for > the drugs. Or might lnfluence the dosage if people go for > the most allowed, rather than the least needed. > ——- > Very rough discussion of the book relative the rat study, > and other factors /hypothesis – observations brought out > by Glenmullen (not facts). Relative potential brain damage. > . > Paraphrases – not direct quotes. > o Glenmllen discusses the rat study page 201 and beyond in > a subparagraph called "Test Tube Studies of Blenderized Rat > Brains" > . > Indicates that serotonin levels cannot be measured in the > brain of any patient etc. And to circumvent the problems > with human subjects, pharmaceutical companies turn to animal > models. He acknowleges that the results may bear little > resemblence to what the drugs do in the living brain. So > this is not offered as "proof". > So the rat study all by itself is not offered as proof, but > but it is interesting in addition to and in context with > other conjectures. . > Some other circumstantial items. > o Page 16 there is mention of how both former and > currently popular anitdepressents appear to boost > neurotransmitter beyond ordinary circumstances. That > includes cocaine, amphetamines, prozac group etc. > o Page 20 he indicates how a reaction to artificially > elevated serotonin lowers dopamine. And notes that drugs > reducing dopamine are known to produce side effects which > are now appearing with Prozac and other drugs in its class. > He notes (page 20) how the earlier drugs the brain damage > could progess slowly and often silent. And that the degree > of damage relates to the total cumulartive exposure to the > drugs. > This point seems to be that drugs were once OK and took > many years to discover problems with, have some of the same > side effects which occur in the SSRIs. . And how long it > was before the older drugs were discovered to be not good. > Would note that it did seem odd to me, that the Dopramine > drop was only relatively recently discovered. Which does > leave open the question of what all else might be going on, > and not yet noticed. > The implication that brain damage if it exists, would be > likely to be total dose related (based on other drugs) , > would leat one towards thinking about minimum dosage needed, > ratther than maximum dosage. And the potential > desireability of getting off the drugs sooner rather than > later as some books – doctors indicatee. Especially if that > is what an individual might desire.. > o page 22. Mentions some withdrawal items and how the > drug companies try to avoid negative connotations of > withdrawal, by using the term antideprssant discontinuation > syndrome. > More about that on page 87 – 88 where there are > recommendatins for physicions to tell the public there is > no dependence problem etc. And discontinuance will not be a > problem. > Yet we have seen how it is a problem via many articles on > the internet. > o page 57 – 59 A subportion called "Silent Brain > Damage". Not much proof here, but some conjectures. > o page 84 - 85 Mention of antidepressants chemically > altering , distorting , stifle feelings etc. . Leaving > patients "bland" and "tranquillize" etc. > Hope that some of the people here might be not this way > even with the drugs . However, the patients on drugs > that I have seen, seem to be bland. Nice, quiet, and even > happy (after some recovery). But not lively. This might > or might not be permanent. But if the drugs are never lifter > per the pyschitrists drug for life scenarios, that can > become the equivalent of permanent. > If someone is put on drugs "for life", and if that person > is misdiagnosed, does not really need the drugs, or > receives an unfavorable risk – reward decision relative to > remission and what the patient wants. there can be a > problem therm. Which gets bigger to the extent that there > might or might not be something to the potential of > permanent brain damage. > . > o page 88 – 94 etc. Mentions the wearing off of the > drugs. Increased doses etc until it no longer work. Poop > out etc. Page 94 mentions how the wearout appears > permanent and how that raises concer about the long temr > effects of the drugs on the brain. > page 94 + Mentions a possiblity of drugs being toxic to the > brain destroying critical parts of brain cells. And how > there is a lack of adequate studies of the prozac gp etc. > And therefore needs to turn to studies of the drugs. > On page 97 – 99 that the drugs might be toxic via high > levle of neurotransmitters.. Few published studies but not > conclusive. This brings us back to the animal studies. > page 101 analogy to other drugs such as cocaine etc. > Etc The list could go on. > This is a small sample of the items in just one 584 page > book. There are other books etc, but the Prozac Backlash > book is the only book I have that referenced the Rat study. > And the only book I have with so much information about > potential brain damage even if it is not proven,and does not > claim to be proven. But there is also no proof that there > is not long term damage to the brain. And not much > evidence that anyone is going to study that. > It does seem like a shame that the US does not study that > kind of thing (the potential of brain damage). > While all this gets sorted out, I will continue to beleive > that it is a good idea for the patients to have rights of > choice (except maybe for the usual danger type of thing),, > and not be pushed into the drugs by what seems to be a drug > society. > This is based on a number of factors, and the potential of > long term brain damage is just one of those factorsr. The > better that item gets discussed – sorted out, the better > people will be able to make their risk – reward decisions. > Glad to see good discussions going or here for that reason.
X-No-Archiev: yes >Thats really interesting Jim.. >Ill try to get a copy.. >That so little research of this sort is done in the US isnt suprising when >most is sponsored by the multi-billion dollar pharmaceutical multinationals.
That looks like it could be the situation. It seems to be difficult to find a doctor in the US that is not so brainwashed by the drug industry and or others, as to provide mental treatment which passes the test of common sence. When it comes to the drug situation. Have read about, and seen some, situations where the patient is not informed, not listened to. And where concent is coerced via a number of ways into taking the drugs they don’t want. Have been puzzeled as to how come people can go to doctors for tens of years for regular medical treatment, and not run into problems with what doctors do .When it comer to mental health, I am gradually finding out the he US system appears to be a basket case . Have postulated that maybe it is because anyone who graduated in the order of 10 years or more, would be learning about the newer mental health drugs from the drug company’s representatives themselves. Or from drug company approved research articles. It is unfortunate that the way doctors actions can make it necessay for regular people to become their own doctors. Problems I have read about and or witnessed in the US.: People are ambushed by MDs with free samples, and no explanations of side effects etc. And pushed to take the drugs sometimes even if the item is not deprsssion. And a pushiness to continue to take them . Or the opposite. A willingness to prescribe them just because someone saw a drug company advertisement, or wants one for reasons which are not sound. And a lack of knowledge. When it comes to the Pysciatrists they seem to know much more about it than the regular MDs. . But many of them also push the the drugs at times that defy common sence. Refuse treatement without drugs, coerce people to do what the doctor says etc. And there is a tendency to try to keep people on the drugs for life. Even it it is the first round of depression. . Would be nice if the pyschologist PH Ds could help the US regualar people out, when they try to fight against the medicine being shoved at them . But have seen where they too will sucomb to the drug thing by telling people to do whatever the pyschiatrists say. Even including the drug for life bit when their own fine therapy might be all that is needed. It would help if more of them would stand up for the regular people but few do.. All that would not matter as much if there was no potential of permanent damge. But there does seem to be a danger of potential permanent damage , and that danger increases with the total dose. So those who don’t need the drugs are being exposed to that potential damage needlessly . Even those who really need the drugs and where the benefits potential benefits outweigh the dangers, can be exposed to higher doses than needed. . The book contains more items than just potential brain damage .. For example in the very first pages in the introduction Glenmullen descirbes how he saw a patient he calls Anne. Just moving from Chicago to the Univ of Cambridge (Mass where he is a pyschiatrist). She had come to him because she was running out of medication. . She had been on 150 mg of Zoloft for 3 years. She had been given the serotonin lifter by her primary care doctor because she was upset over her boyfriend’s breaking up with her. And at that time had only mild symtoms which wouldn’t even qualify for depression diagnosis. Seems like she got together with her boyfriend a few months later and they have now been happily maried for 2 years. She got her medication for a year and then just kept getting more by calling the office for a refill. An exposure to a high dose of Zoloft for 3 years until he helped her stop.. Later on mentioned how she was surprised that the pills cost so much ($150 per month), since she was getting them paid for by her HMO. Then there was a discussion of withdrawal problems which she thought was return of symptoms but Glenmullen indicated was withdrawal and not return to her original symptons. Much later in the book there is a discussion of how HMO’s push the drugs to save therapy costs etc. —- So there seems to be many pressures here in the US to use the antidepressent drugs. At least some times not justified by symtoms etc. The drug companies , the doctors, the HMOs, the advertisements, and even family members who can be brainwashed by the doctors to try to make the patient take the pills.. Glenmullen indicates how for patients whose symptoms aer more severe he still recommends medication. Even though the book is critical of the way the drugs are prescribed and the potential dangers he is still for the drugs when needed. After this first situation description (Anne) of one of his patients, the book continues to describe many more situations where people have been incorrectly given the drugs . Also much more useful information not found in a number of other books I have looked at. One point not being picked up by others is contained on page 208 where he indicates that when a placebo is used which has side effects (but not an anti depressant), the performance of the placebo climbs to where there is no difference. —- As I mentioned in my prior aritcle, discussion of the potential or non potential for brain damage is important. Not proven, but enough information to be well worth discussing the potential of non potential of that. Even if just a little bit true, it would be of value in decisions made for dosages which might be higher than needed,. Or decisions for patients as to whether or not to use them at all for the minor situations . And , for decisions relative support for those who might not want ot do drugs for life, when they had at most one depression. Patients should have the right to refuse treatment from the doctors. With the usual special considerations when involved in situations of danger. . All of that hopefully consistent with the needs of the many people here in this usenet gp and elsewhere, who need the drugs and want to be able to continue to be able to get them . —- Hope you and some others might get the book. I have seen it a few times in the bookstores here in the US, but it is not that easy to find. Should it be difficult to find in the UK, possibly it could be ordered special. Prozac Backlash. Josepth Glenmllen. M.D. Copyright 2000 A touchstone Book published by Simon and Shuster New York, London,, Toronto, Sydney, and Singapore. Some background of prior posts left in for context. Some snipped. – Hide quoted text — Show quoted text -> X-No-Archive: yes > >YES YES!!!! thanks so much, bob! > See comments below. > I believe the Rat study does not in itself "prove" things > But I do believe that the comibination of some > circumstantial information, including the Rat study, does > indicate that there could be long term damage in the brain > due to the SSRIs. > And that is something both important and worthy of > discussion in substance. > >> > STUDIES ON PERSISTENT EFFECTS OF SSRI USE > >> > The following new study is very significant. It finds that very young > >> > rats exposed to Prozac for just 2 weeks had brains changes that persisted > >> > into adulthood. It concludes: "This is the first empirical demonstration > >> > long-lasting effects of the administration of a selective serotonin > >> > reuptake inhibitor during juvenile life on the maturation of the > >> > central serotonergic system." > >> > J Child Adolesc Psychopharmacol 1999;9(1):13-24; discussion 25-6 > >> > Persistently increased density of serotonin transporters in the > >> > frontal cortex of rats treated with fluoxetine during early juvenile life. > >> This must be the study that Steve was talking about. > Glad Steven found his reference. Steven or others might > consider reading (or rereading if you already read it), the > Prozac Backlash Book by Josepth Glenmullen M.D. copyright > 2000 which comes after the 1999 rat article referenced. > Glenmullen mentions the rat study and quite a bit more. > However the case he makes for potential braindamage, > rests not on the rat study, but rather on the page after > page of circimumstantial information (not proof). > In addition to the straifforward support for patients rights > and other factors, the information relative potential brain > damage provided by Gelenmullen (not proved) , is > sufficiently convincing to me that it enhances my support > for at least some patients who desire to be off the meds.
snip – Hide quoted text — Show quoted text -> It does seem like a shame that the US does not study that > kind of thing (the potential of brain damage). > While all this gets sorted out, I will continue to beleive > that it is a good idea for the patients to have rights of > choice (except maybe for the usual danger type of thing),, > and not be pushed into the drugs by what seems to be a drug > society. > This is based on a number of factors, and the potential of > long term brain damage is just one of those factorsr. The > better that item gets discussed – sorted out, the better > people will be able to make their risk – reward decisions. > Glad to see good discussions going or here for that
… read more »
- Hide quoted text — Show quoted text – > X-No-Archiev: yes >Thats really interesting Jim.. >Ill try to get a copy.. >That so little research of this sort is done in the US isnt suprising when >most is sponsored by the multi-billion dollar pharmaceutical multinationals. > That looks like it could be the situation. > It seems to be difficult to find a doctor in the US that is > not so brainwashed by the drug industry and or others, as > to provide mental treatment which passes the test of common > sence.
GPs are often more independently minded in the UK and have a attitude of care for the patient as a person and arent wannabe scientists in white coats.. they are often quite happy to be doctors. – Hide quoted text — Show quoted text -> When it comes to the drug situation. Have read about, and > seen some, situations where the patient is not informed, > not listened to. And where concent is coerced via a > number of ways into taking the drugs they don’t want. > Have been puzzeled as to how come people can go to doctors > for tens of years for regular medical treatment, and not > run into problems with what doctors do .When it comer to > mental health, I am gradually finding out the he US system > appears to be a basket case . > Have postulated that maybe it is because anyone who > graduated in the order of 10 years or more, would be > learning about the newer mental health drugs from the drug > company’s representatives themselves. Or from drug company > approved research articles.
reports of side-effects have the drug company salesmen picking up reports..they are not always circulated for obvious reasons > It is unfortunate that the way doctors actions can make it > necessay for regular people to become their own doctors.
not neccessarily unfortunate.. partners with the doctor providing information and resources is a good model.. > Problems I have read about and or witnessed in the US.: > People are ambushed by MDs with free samples, and no > explanations of side effects etc. And pushed to take the > drugs sometimes even if the item is not deprsssion. And a > pushiness to continue to take them .
Luckily, the provision of free medication for the economically deprived as part of all treatment universally available and free at point of treatment precludes such things in the UK > Or the opposite. A willingness to prescribe them just > because someone saw a drug company advertisement, or wants > one for reasons which are not sound. And a lack of > knowledge.
We have no direct advertisments… Im pretty sure iys illegal and its certainly unconscionable > When it comes to the Pysciatrists they seem to know much > more about it than the regular MDs. . But many of them also > push the the drugs at times that defy common sence. Refuse > treatement without drugs, coerce people to do what the > doctor says etc. And there is a tendency to try to keep > people on the drugs for life. Even it it is the first round > of depression. .
Sadly economic factors Physical treatments for the poor and pychotherapy for the rich has a long history. Psychotherapy without charge available albeit with a waiting list.. > Would be nice if the pyschologist PH Ds could help the US > regualar people out, when they try to fight against the > medicine being shoved at them . > But have seen where they too will sucomb to the drug thing > by telling people to do whatever the pyschiatrists say. > Even including the drug for life bit when their own fine > therapy might be all that is needed. It would help if more > of them would stand up for the regular people but few do..
It would be professional suicide … as doctors with the legal right to cut into bodies(the big divide).. and the right to prescribe the psychiatrists are at the top of the totem pole.. – Hide quoted text — Show quoted text – > All that would not matter as much if there was no potential > of permanent damge. > But there does seem to be a danger of potential permanent > damage , and that danger increases with the total dose. > So those who don’t need the drugs are being exposed to that > potential damage needlessly . Even those who really need > the drugs and where the benefits potential benefits > outweigh the dangers, can be exposed to higher doses than > needed. . > The book contains more items than just potential brain > damage .. > For example in the very first pages in the introduction > Glenmullen descirbes how he saw a patient he calls Anne. > Just moving from Chicago to the Univ of Cambridge (Mass > where he is a pyschiatrist). > She had come to him because she was running out of > medication. . She had been on 150 mg of Zoloft for 3 > years. She had been given the serotonin lifter by her > primary care doctor because she was upset over her > boyfriend’s breaking up with her. And at that time had only > mild symtoms which wouldn’t even qualify for depression > diagnosis. > Seems like she got together with her boyfriend a few months > later and they have now been happily maried for 2 years. > She got her medication for a year and then just kept getting > more by calling the office for a refill. An exposure to a > high dose of Zoloft for 3 years until he helped her stop.. > Later on mentioned how she was surprised that the pills cost > so much ($150 per month), since she was getting them paid > for by her HMO. Then there was a discussion of withdrawal > problems which she thought was return of symptoms but > Glenmullen indicated was withdrawal and not return to her > original symptons. Much later in the book there is a > discussion of how HMO’s push the drugs to save therapy costs > etc. > —- > So there seems to be many pressures here in the US to use > the antidepressent drugs. At least some times not justified > by symtoms etc. The drug companies , the doctors, the > HMOs, the advertisements, and even family members who > can be brainwashed by the doctors to try to make the patient > take the pills.. > Glenmullen indicates how for patients whose symptoms aer > more severe he still recommends medication. Even though the > book is critical of the way the drugs are prescribed and > the potential dangers he is still for the drugs when needed. > After this first situation description (Anne) of one of > his patients, the book continues to describe many more > situations where people have been incorrectly given the > drugs . > Also much more useful information not found in a number of > other books I have looked at. One point not being picked up > by others is contained on page 208 where he indicates that > when a placebo is used which has side effects (but not an > anti depressant), the performance of the placebo climbs to > where there is no difference. > —- > As I mentioned in my prior aritcle, discussion of the > potential or non potential for brain damage is important. > Not proven, but enough information to be well worth > discussing the potential of non potential of that. > Even if just a little bit true, it would be of value in > decisions made for dosages which might be higher than > needed,. Or decisions for patients as to whether or not to > use them at all for the minor situations . And , for > decisions relative support for those who might not want ot > do drugs for life, when they had at most one depression. > Patients should have the right to refuse treatment from the > doctors. With the usual special considerations when > involved in situations of danger. > .
I believe it promises to get worse rather than better with hysteria and misinformation driving forced community treatment plans and NAMI taking vast amounts of drug company cash to help force it through.. > All of that hopefully consistent with the needs of the many > people here in this usenet gp and elsewhere, who need the > drugs and want to be able to continue to be able to get > them . > —- > Hope you and some others might get the book. > I have seen it a few times in the bookstores here in the US, > but it is not that easy to find. Should it be difficult to > find in the UK, possibly it could be ordered special.
Its available with a one to two week wait http://www.amazon.co.uk/exec/obidos/search-handle-form/202-5814657-72… at Amazon (uk) – Hide quoted text — Show quoted text -> Prozac Backlash. Josepth Glenmllen. M.D. Copyright 2000 A > touchstone Book published by Simon and Shuster New York, > London,, Toronto, Sydney, and Singapore. > Some background of prior posts left in for context. Some > snipped. >> X-No-Archive: yes >> >YES YES!!!! thanks so much, bob! >> See comments below. >> I believe the Rat study does not in itself "prove" things >> But I do believe that the comibination of some >> circumstantial information, including the Rat study, does >> indicate that there could be long term damage in the brain >> due to the SSRIs. >> And that is something both important and worthy of >> discussion in substance. >> >> > STUDIES ON PERSISTENT EFFECTS OF SSRI USE >> >> > The following new study is very significant. It finds that very young >> >> > rats exposed to Prozac for just 2 weeks had brains changes that persisted >> >> > into adulthood. It concludes: "This is the first empirical demonstration >> >> > long-lasting effects of the administration of a selective serotonin >> >> > reuptake inhibitor during juvenile life on the
… read more »
Hi I’m new to this NG – so please excuse if this ha been asked before. My doctor has just prescribed Felicium (fluoxetine hydrochloride) and I read the box and accompanying leaflet which contained all sorts of horrific warnings re possible side effects Are they just covering all possibilities? Or do many of these actually occur? My doctor says that there should be no side effects. It worries me as fear of the drugs was the primary reason I did not seek assistance for many years. Any thoughts would be appreciated. David Probett
> My doctor has just prescribed Felicium (fluoxetine hydrochloride) and > I read the box and accompanying leaflet which contained all sorts of > horrific warnings re possible side effects > Are they just covering all possibilities? Or do many of these actually > occur? > My doctor says that there should be no side effects. It worries me as > fear of the drugs was the primary reason I did not seek assistance for > many years. > Any thoughts would be appreciated. > David Probett
Your doctor prescribed Prozac. The package insert exists because of laws that require giving patients complete information about all of the adverse events observed in clinical trials. Some are related to the drug; some are not. If a patient in the trial develops pneumonia and dies, that data must be collected and reported. Did the drug give the patient pneumonia? Almost certainly not. There is a lengthy disclaimer prior to the "everything that happened to patients" section that informs you the drug may not have been the cause. Fear of drugs kept me out of treatment for many years as well. I’ve had headaches and dry mouth, diminished and increased libido, constipation and diarrhea…rarely did any side effect rise above merely inconvenient. Psych meds don’t hurt. They won’t give you heart or liver problems. Lots and lots of people around the world take what you’ll be taking. I suggest you relax a little, weigh your options as dispassionately as you can, and if you trust your doctor, try the drug for a month. The likelihood is very high that you’ll feel markedly better. Good luck.
Has anyone had any success trying high doses of folate/folic acid as a supplement to Prozac/other SSRIs? FOLIC ACID SUPPLEMENTS FOR DEPRESSION A November 2000 study shows that folic acid supplements are a simple way to greatly improving the antidepressant action of fluoxetine (Prozac) and probably other antidepressants. In addition to improving the effectiveness of fluoxetine, folic acid supplements also greatly reduced the side effects of fluoxetine. This study concludes that folic acid levels used should be sufficient to decrease plasma homocysteine and that men require a higher dose of folic acid to achieve this than do women. Coppen & Bailey (2000) Enhancement of the antidepressant action of fluoxetine by folic acid: a randomized, placebo controlled trial. Journal of Affective Disorders 60, p121-130
>Has anyone had any success trying high doses of folate/folic acid as a >supplement to Prozac/other SSRIs?
I haven’t used them for depression, but my folate level (along with B12) is one of the things that my pdoc screened for the first time he saw me. And when my depression recently got worse again, he got another level, because he said that anticonvulsants, which I take for bipolar, often decrease folate levels. However, mine was fine. But I do take B-complex. Emily – Hide quoted text — Show quoted text ->FOLIC ACID SUPPLEMENTS FOR DEPRESSION >A November 2000 study shows that folic acid supplements are a simple way to >greatly improving the antidepressant action of fluoxetine (Prozac) and >probably other antidepressants. In addition to improving the effectiveness >of fluoxetine, folic acid supplements also greatly reduced the side effects >of fluoxetine. This study concludes that folic acid levels used should be >sufficient to decrease plasma homocysteine and that men require a higher >dose of folic acid to achieve this than do women. >Coppen & Bailey (2000) Enhancement of the antidepressant action of >fluoxetine by folic acid: a randomized, placebo controlled trial. Journal of >Affective Disorders 60, p121-130
I’m not familiar with use of folic acid. But I do know women respond better to different B vitamins than men do. B-6 is one that most women find very effective. Christina
– Hide quoted text — Show quoted text -> Has anyone had any success trying high doses of folate/folic acid as a > supplement to Prozac/other SSRIs? > FOLIC ACID SUPPLEMENTS FOR DEPRESSION > A November 2000 study shows that folic acid supplements are a simple way to > greatly improving the antidepressant action of fluoxetine (Prozac) and > probably other antidepressants. In addition to improving the effectiveness > of fluoxetine, folic acid supplements also greatly reduced the side effects > of fluoxetine. This study concludes that folic acid levels used should be > sufficient to decrease plasma homocysteine and that men require a higher > dose of folic acid to achieve this than do women. > Coppen & Bailey (2000) Enhancement of the antidepressant action of > fluoxetine by folic acid: a randomized, placebo controlled trial. Journal of > Affective Disorders 60, p121-130
mental case! Who has as she put it, "a delicate mental condition!" 
Do not listen to this piece of shit! She’s a mental case! All fucked up in the head! A piece of shit! – Hide quoted text — Show quoted text -> I’m not familiar with use of folic acid. But I do know women respond better > to different B vitamins than men do. B-6 is one that most women find very > effective. > Christina > Has anyone had any success trying high doses of folate/folic acid as a > supplement to Prozac/other SSRIs? > FOLIC ACID SUPPLEMENTS FOR DEPRESSION > A November 2000 study shows that folic acid supplements are a simple way > to > greatly improving the antidepressant action of fluoxetine (Prozac) and > probably other antidepressants. In addition to improving the effectiveness > of fluoxetine, folic acid supplements also greatly reduced the side > effects > of fluoxetine. This study concludes that folic acid levels used should be > sufficient to decrease plasma homocysteine and that men require a higher > dose of folic acid to achieve this than do women. > Coppen & Bailey (2000) Enhancement of the antidepressant action of > fluoxetine by folic acid: a randomized, placebo controlled trial. Journal > of > Affective Disorders 60, p121-130
I don’t know the ideal dose of folate supplementation. It looks like 500 microgram of folate per day is sufficient for most women, according to the trial (below), with men requiring more. Folate is usually sold by pharmacists in tablets of around 500 microgram — typically taken once daily by women (for pregnancy/menstruation). But it’s also sold by pharmacies in 5 milligram tablets, which is 10X that dose. There are no adverse effects from taking a high dose of folate in a healthy person — it’s a water-soluble vitamin. So men could probably do with taking that sort of dose (5 mg) daily. Enhancement of the antidepressant action of fluoxetine by folic acid: a randomised, placebo controlled trial. Coppen A, Bailey J MRC Neuropsychiatry Laboratory, West Park Hospital, KT19 8PB, Surrey, Epsom, UK. BACKGROUND: A consistent finding in major depression has been a low plasma and red cell folate which has also been linked to poor response to antidepressants. The present investigation was designed to investigate whether the co-administration of folic acid would enhance the antidepressant action of fluoxetine. METHODS: 127 patients were randomly assigned to receive either 500 microg folic acid or an identical looking placebo in addition to 20 mg fluoxetine daily. All patients met the DSM-III-R criteria for major depression and had a baseline Hamilton Rating Scale (17 item version) score for depression of 20 or more. Baseline and 10-week estimations of plasma folate and homocysteine were carried out. RESULTS: Patients receiving folate showed a significant increase in plasma folate.This was less in men than in women. Plasma homocysteine was significantly decreased in women by 20.6%, but there was no significant change in men. Overall there was a significantly greater improvement in the fluoxetine plus folic acid group. This was confined to women where the mean Hamilton Rating Scale score on completion was 6.8 (S.D. 4. 1) in the fluoxetine plus folate group, as compared to 11.7 (S.D. 6. 7) in the fluoxetine plus placebo group (P<0.001).A percentage of 93. 9 of women, who received the folic acid supplement, showed a good response (>50% reduction in score) as compared to 61.1% of women who received placebo supplement (P<0.005). Eight (12.9%) patients in the fluoxetine plus folic acid group reported symptoms possibly or probably related to medication, whereas in the fluoxetine plus placebo group 19 (29.7%) patients reported such symptoms (P<0.05). LIMITATIONS AND CONCLUSIONS: Folic acid is a simple method of greatly improving the antidepressant action of fluoxetine and probably other antidepressants. Folic acid should be given in doses sufficient to decrease plasma homocysteine. Men require a higher dose of folic acid to achieve this than women, but more work is required to ascertain the optimum dose of folic acid. J Affective Disorders 2000 Nov;60(2):121-30
– Hide quoted text — Show quoted text -> I used to take a B-100 capsule everyday and when I did that I noticed I would > get a very mildly better antidepressant response from my meds. It was nothing > spectacular but I noticed a slight improvement. I never tried supplementing > with higher doses than that. > How much folate is needed for AD supplementation do you know? > Eric
> Folate is usually sold by pharmacists in tablets of around 500 microgram — > typically taken once daily by women (for pregnancy/menstruation). But it’s > So men could probably do with taking that sort of dose (5 mg) daily. > Enhancement of the antidepressant action of fluoxetine by folic acid: a > randomised, placebo controlled trial.
Yeah the ideal dose of folate is a mystery to me too. I’d like to thank whoever posted the original reference. I chow down 10 or more 400 mcg folates whenever I remember; I’d like to take a higher dose supplement but for some reason the federal legislature thought they could be better health care providers than doctors and limited pill forms to that amount. Andy
>Yeah the ideal dose of folate is a mystery to me too. I’d like to thank >whoever posted the original reference. I chow down 10 or more 400 mcg >folates whenever I remember; I’d like to take a higher dose supplement but >for some reason the federal legislature thought they could be better >health care providers than doctors and limited pill forms to that amount.
Andy, The amount you’re taking is a huge overdose and can be harmful! Please, cut it down to 1000 or maybe 1500 mcg at most. Here’s an abstract that should be of interest (emphasis added): Prog Neuropsychopharmacol Biol Psychiatry 1989;13(6):841-63 Folic acid and psychopathology. Young SN, Ghadirian AM Department of Psychiatry, McGill University, Montreal, Quebec, Canada. 1. The incidence of folic acid deficiency is high in patients with various psychiatric disorders including depression, dementia and schizophrenia. 2. In epileptics on anticonvulsants, folate deficiency often occurs because anticonvulsants inhibit folate absorption. In these patients folate deficiency is often associated with psychiatric symptoms. 3. In medical patients psychiatric symptoms occur more frequently, and in psychiatric patients symptoms are more severe, in those with folate deficiency than in those with normal levels. 4. Many open studies have demonstrated therapeutic effects of folate administration on psychiatric symptoms in folate deficient patients. 5. SEVERAL PLACEBO-CONTROLLED STUDIES HAVE NOT DEMONSTRATED THERAPEUTIC EFFECTS, POSSIBLY BECAUSE THE DOSES THEY USED (15-20 mg/day) ARE KNOW TO BE TOXIC AND TO CAUSE MENTAL SYMPTOMS. 6. Two placebo-controlled studies have demonstrated beneficial effects of folic acid administration, one in patients with a syndrome of psychiatric and neuropsychological changes associated with folate deficiency and the other in patients on long-term lithium therapy. In the latter study the dose was only 0.2 mg/day. 7. Folic acid deficiency is known to lower brain S-adenosylmethionine and 5-hydroxytryptamine. S-Adenosylmethionine, which has antidepressant properties, raises brain 5-hydroxytryptamine. Thus, depression associated with folate deficiency is probably related to low brain 5HT. 8. S-Adenosylmethionine is involved in many methylation reactions, including methylation of membrane phospholipids, which influences membrane properties. This may explain the wide variety of symptoms associated with folate deficiency. 9. Because the costs and risks associated with low doses of folic acid (up to 0.5 mg/day) are small, folic acid should be given as an adjunct in the treatment of patients with unipolar or bipolar affective disorders and anorexia, epileptics on anticonvulsants, geriatric patients with mental symptoms and patients with gastrointestinal disorders who exhibit psychiatric symptoms. 10. Although the majority of the patients listed above will probably not be helped by folic acid therapy, a significant minority are likely to have folate-responsive symptoms. good to "see" you <g>, -elizabeth
Some studies have shown that people who are nonresponsive to SSRIs, in particular, tend to improve with folate — that folate deficiency is what keeps them from responding to the ADs. As many as 2/5 of patients with major depression may be folate deficient (probably more like 1/4). Men appear to require higher doses than women. In general, around 500-1000 mcg is probably adequate for anyone with a folate deficiency. (That’s *micrograms*, not milligrams (the equivalent in mg is 0.5-1000 mg). Don’t take 5 mg of folic acid! It can be toxic.) I think most folate supplements you can get in drug stores over the counter are 400mcg (0.4mg); my dad takes a 1mg supplement by prescription (he has well-controlled heart disease, thanks to meds, surgery, dietary changes, and exercise). I don’t think it works terribly well except in people who are deficient in folate so you shouldn’t expect miracles if your folate levels are normal. BTW, this might be a first step in explaining the connection between depression and cardiovascular disease. That’s pretty cool. Here’s an abstract that explains a little about the current theories regarding folate and depression: Nutr Rev 1996 Dec;54(12):382-90 Folate, vitamin B12, and neuropsychiatric disorders. Bottiglieri T, Kimberly H. Courtwright and Joseph W. Summers Institute of Metabolic Disease, Baylor University Medical Center, Dallas, Texas, USA. Folate and vitamin B12 are required both in the methylation of homocysteine to methionine and in the synthesis of S-adenosylmethionine. S-adenosylmethionine is involved in numerous methylation reactions involving proteins, phospholipids, DNA, and neurotransmitter metabolism. Both folate and vitamin B12 deficiency may cause similar neurologic and psychiatric disturbances including depression, dementia, and a demyelinating myelopathy. A current theory proposes that a defect in methylation processes is central to the biochemical basis of the neuropsychiatry of these vitamin deficiencies. Folate deficiency may specifically affect central monoamine metabolism and aggravate depressive disorders. In addition, the neurotoxic effects of homocysteine may also play a role in the neurologic and psychiatric disturbances that are associated with folate and vitamin B12 deficiency. -elizabeth
>Don’t take 5 mg of folic acid! It can be toxic.
Folate 5 mg tablets should not be toxic to a healthy person. The 5 mg tablets are sold over-the-counter in Australia. It is a water-soluble, B vitamin. However, folate interacts with the trimethoprim/sulphonamide antibacterials, some anticonvulsants, sulphasalazine, methotrexate and other drugs.
– Hide quoted text — Show quoted text -> Some studies have shown that people who are nonresponsive to SSRIs, in > particular, tend to improve with folate — that folate deficiency is what > keeps them from responding to the ADs. As many as 2/5 of patients with major > depression may be folate deficient (probably more like 1/4). > Men appear to require higher doses than women. In general, around 500-1000 > mcg is probably adequate for anyone with a folate deficiency. (That’s > *micrograms*, not milligrams (the equivalent in mg is 0.5-1000 mg). Don’t > take 5 mg of folic acid! It can be toxic.) > I think most folate supplements you can get in drug stores over the counter > are 400mcg (0.4mg); my dad takes a 1mg supplement by prescription (he has > well-controlled heart disease, thanks to meds, surgery, dietary changes, and > exercise). > I don’t think it works terribly well except in people who are deficient in > folate so you shouldn’t expect miracles if your folate levels are normal. > BTW, this might be a first step in explaining the connection between > depression and cardiovascular disease. That’s pretty cool. > Here’s an abstract that explains a little about the current theories > regarding folate and depression: > Nutr Rev 1996 Dec;54(12):382-90 > Folate, vitamin B12, and neuropsychiatric disorders. > Bottiglieri T, Kimberly H. > Courtwright and Joseph W. Summers Institute of Metabolic Disease, Baylor > University Medical Center, Dallas, Texas, USA. > Folate and vitamin B12 are required both in the methylation of homocysteine > to methionine and in the synthesis of S-adenosylmethionine. > S-adenosylmethionine is involved in numerous methylation reactions involving > proteins, phospholipids, DNA, and neurotransmitter metabolism. Both folate > and vitamin B12 deficiency may cause similar neurologic and psychiatric > disturbances including depression, dementia, and a demyelinating myelopathy. > A current theory proposes that a defect in methylation processes is central > to the biochemical basis of the neuropsychiatry of these vitamin > deficiencies. Folate deficiency may specifically affect central monoamine > metabolism and aggravate depressive disorders. In addition, the neurotoxic > effects of homocysteine may also play a role in the neurologic and > psychiatric disturbances that are associated with folate and vitamin B12 > deficiency. > -elizabeth
> Andy, > The amount you’re taking is a huge overdose and can be harmful! Please, cut > it down to 1000 or maybe 1500 mcg at most. Here’s an abstract that should be > of interest (emphasis added): > Prog Neuropsychopharmacol Biol Psychiatry 1989;13(6):841-63 > Folic acid and psychopathology. > Young SN, Ghadirian AM > Department of Psychiatry, McGill University, Montreal, Quebec, Canada. > patients. 5. SEVERAL PLACEBO-CONTROLLED STUDIES HAVE NOT DEMONSTRATED > THERAPEUTIC EFFECTS, POSSIBLY BECAUSE THE DOSES THEY USED (15-20 mg/day) ARE > KNOW TO BE TOXIC AND TO CAUSE MENTAL SYMPTOMS. 6. Two placebo-controlled
Elizabeth, Thanks for taking the time to point this out to me. I had no idea and will cut the dose down to 2X 400mcg a day. I hope all is well. Andy
– Hide quoted text — Show quoted text -> Andy, > The amount you’re taking is a huge overdose and can be harmful! Please, cut > it down to 1000 or maybe 1500 mcg at most. Here’s an abstract that should be > of interest (emphasis added): > Prog Neuropsychopharmacol Biol Psychiatry 1989;13(6):841-63 > Folic acid and psychopathology. > Young SN, Ghadirian AM > Department of Psychiatry, McGill University, Montreal, Quebec, Canada. > patients. 5. SEVERAL PLACEBO-CONTROLLED STUDIES HAVE NOT DEMONSTRATED > THERAPEUTIC EFFECTS, POSSIBLY BECAUSE THE DOSES THEY USED (15-20 mg/day) ARE > KNOW TO BE TOXIC AND TO CAUSE MENTAL SYMPTOMS. 6. Two placebo-controlled > Elizabeth, > Thanks for taking the time to point this out to me. I had no idea and > will cut the dose down to 2X 400mcg a day. I hope all is well. > Andy
The reference below says that 15-20 mg folate/folic acid is toxic. But not 5 mg, or 10 X 400 micrograms. I have the label of the over-the-counter folic acid 5 mg tablets from Sigma Pharmaceuticals, 1408 Centre Rd, Clayton, Vic 3168, Australia — a reputable manufacturer of ethical pharmaceuticals: "Dose: Take one tablet daily or as directed by physician." There is a rigorous Poisons Act in Australia. If folic acid was toxic at this sort of dose, it would certainly not be available in pharmacies over-the-counter, to say the least. The B-vitamins (including folate) are water-soluble. It is generally the fat-soluble vitamins (eg A and D) that can have serious toxicity problems. The trial below states that: "Folic acid should be given in doses sufficient to decrease plasma homocysteine. Men require a higher dose of folic acid to achieve this than women, but more work is required to ascertain the optimum dose of folic acid." The dose given in the trial was 500 microgram daily, but this was insufficient for most men in the study. A significantly higher dose may be required. – Hide quoted text — Show quoted text -> Elizabeth, > Thanks for taking the time to point this out to me. I had no idea and > will cut the dose down to 2X 400mcg a day. I hope all is well. > Andy > Andy, > The amount you’re taking is a huge overdose and can be harmful! Please, cut > it down to 1000 or maybe 1500 mcg at most. Here’s an abstract that should be > of interest (emphasis added): > Prog Neuropsychopharmacol Biol Psychiatry 1989;13(6):841-63 > Folic acid and psychopathology. > Young SN, Ghadirian AM > Department of Psychiatry, McGill University, Montreal, Quebec, Canada. > patients. 5. SEVERAL PLACEBO-CONTROLLED STUDIES HAVE NOT DEMONSTRATED > THERAPEUTIC EFFECTS, POSSIBLY BECAUSE THE DOSES THEY USED (15-20 mg/day) ARE > KNOW TO BE TOXIC AND TO CAUSE MENTAL SYMPTOMS. 6. Two placebo-controlled
Enhancement of the antidepressant action of fluoxetine by folic acid: a randomised, placebo controlled trial. Coppen A, Bailey J MRC Neuropsychiatry Laboratory, West Park Hospital, KT19 8PB, Surrey, Epsom, UK. BACKGROUND: A consistent finding in major depression has been a low plasma and red cell folate which has also been linked to poor response to antidepressants. The present investigation was designed to investigate whether the co-administration of folic acid would enhance the antidepressant action of fluoxetine. METHODS: 127 patients were randomly assigned to receive either 500 microg folic acid or an identical looking placebo in addition to 20 mg fluoxetine daily. All patients met the DSM-III-R criteria for major depression and had a baseline Hamilton Rating Scale (17 item version) score for depression of 20 or more. Baseline and 10-week estimations of plasma folate and homocysteine were carried out. RESULTS: Patients receiving folate showed a significant increase in plasma folate.This was less in men than in women. Plasma homocysteine was significantly decreased in women by 20.6%, but there was no significant change in men. Overall there was a significantly greater improvement in the fluoxetine plus folic acid group. This was confined to women where the mean Hamilton Rating Scale score on completion was 6.8 (S.D. 4. 1) in the fluoxetine plus folate group, as compared to 11.7 (S.D. 6. 7) in the fluoxetine plus placebo group (P<0.001).A percentage of 93. 9 of women, who received the folic acid supplement, showed a good response (>50% reduction in score) as compared to 61.1% of women who received placebo supplement (P<0.005). Eight (12.9%) patients in the fluoxetine plus folic acid group reported symptoms possibly or probably related to medication, whereas in the fluoxetine plus placebo group 19 (29.7%) patients reported such symptoms (P<0.05). LIMITATIONS AND CONCLUSIONS: Folic acid is a simple method of greatly improving the antidepressant action of fluoxetine and probably other antidepressants. Folic acid should be given in doses sufficient to decrease plasma homocysteine. Men require a higher dose of folic acid to achieve this than women, but more work is required to ascertain the optimum dose of folic acid. J Affective Disorders 2000 Nov;60(2):121-30
I’m on Fluoxetine injections weekly, percocet X4/day,diazepam max dose, cogentin X2/day and Ativan 2-3mg every 2 hours. Any info would help. Thx
Are you a tad bit addicted? Why does your doctor prescribe percocet, diazepam and ativan in those high doses? Do you have other medical problems besides depression? Nikki
Ihttp://biz.yahoo.com/rf/001019/n19235986.html Sepracor shares tumble on Lilly change By Ransdell Pierson NEW YORK, Oct 19 (Reuters) – Sepracor Inc., one of the country’s highest-profile biotech companies, lost more than a third of its market value on Thursday after it and partner Eli Lilly and Co. dropped plans to develop Sepracor’s second-generation version of Lilly’s blockbuster antidepressant Prozac. The two companies decided to abandon further development of the compound, which is closely related to the key chemical in Prozac (fluoxetine), following clinical studies in which a heart irregularity was detected using high doses of the drug. Shares of Sepracor (NasdaqNM:SEPR – news) fell $44-7/16 to $76-3/8, or 36 percent, in heavy trading on the Nasdaq market, while Lilly’s stock (NYSE:LLY – news) slipped $5-3/8 to $83-7/8 on the New York Stock Exchange. Sepracor said it will lose out on annual royalties of up to $100 million it had expected from Lilly by 2003 on sales of the still-experimental drug, R-fluoxetine, now that Lilly has bailed out. “Clearly that is going away. There is no way to sugar coat that that disappears from our (earnings) model,” a Sepracor official said in a telephone conference with analysts. Prozac boasted global sales of $2.6 billion in 1999, but its U.S. patent expires in August 2001. The Sepracor version would have allowed Lilly to offer a patent-protected alternative to generic forms of Prozac expected to hit the market late next year. Sepracor said the heart irregularity, called QTc prolongation, was statistically significant, meaning it was likely related to the drug. But the company described it as a “clinically insignificant effect.” Nevertheless, further development was not being considered because trials to prove its safety would delay Lilly’s marketing application for the drug at least another two years, Sepracor said. Lilly’s key Prozac patent is slated to expire next year following a court ruling in August that trimmed its life by two years. Corey Davis, an analyst for Chase Hambrecht & Quist, said on Thursday that Lilly and Sepracor had hoped to get R-fluoxetine to market by 2002 — in time to convince millions of patients taking Prozac to switch to the follow-up drug. But, Davis said, the court ruling threw a monkey wrench into their strategy because generic rivals to Prozac will probably now spring up years before Sepracor and Lilly would be able to complete new clinical trials of R-fluoxetine to verify its safety. Lilly licensed rights to R-fluoxetine in 1998 from Sepracor, a Marlborough, Mass.-based firm that specialises in making slightly altered versions of currently marketed drugs, which are intended to be safer than the original versions. Although Sepracor has abandoned R-fluoxetine, the company said it plans to become profitable by 2003 — enabled by its planned launch in the next four years of 10 new drugs that will be sold by Sepracor’s own salesforce. They include a different anti-depression compound called R-DDMS, which Sepracor is testing in Phase II trials, as well as treatments for allergies, incontinence and hypertension. It said QTc prolongation has not cropped up as a side effect in trials of other drugs in its extensive pipeline. R-fluoxetine is a so-called “chiral” version of Prozac, meaning that the original molecule has been split, with removal of the half suspected of causing side effects. Sepracor has patents on altered forms of a score of existing compounds, including Prozac and Schering-Plough Corp.’s (NYSE:SGP – news) top-selling allergy drug Claritin. The company’s share price had skyrocketed in the past two years after Sepracor licensed its version of Prozac to Lilly and rights to a derivative of Claritin to Schering-Plough. Analysts are expecting Schering-Plough to win U.S. marketing approval this year for the follow-up version of Claritin, desloratadine. Meow, The only true Eric in North Carolina (The official defender of drug- and radiation-free Ukrainian women) WARNING TO PARENTS: Jew-hating Austrian Nazi Peter "Guardian" Schrenk
Wow. Now it’s your turn to SUCK MY DICK.