Question:
broken link
– Hide quoted text — Show quoted text -> The story is on : > www.observer.co.uk/magazine/story/0,11913,846295,00 >I haven’t noticed any comments on the article in the Observer about >the use of Tricyclic Antidepressants in the alleviation of some forms >of chronic pain .
Response:
I’m sure you realize that there is a difference between physical dependence and addiction. If you don’t, search the Google archives for numerous posts on the topic. Benzos are excellent medications. You taper on, become physically dependent, and if you want to go off, you taper off. As the analogy goes: are insulin-dependent pateints addicted? Are the many people on this ng who take pain meds daily addicted? Are people on antidepressants addicted? Please think about and learn the difference between "addiction" and proper use of medication before you tell someone not to take an effective medicine. Jennifer – Hide quoted text — Show quoted text – >Martin >"I need to take Ambien for sleep, but, my doctor would rather >have me take it than a low dose of elavil – he sees Ambien as a much safer >drug." >If this is true then your doctor is a real moron. While not a benzo, it >works in similar fashion and is just as addicting and has a very short half >life. Want problems similar to benzo addiction ? >www.benzo.org.uk > I took large doses of Elavil for about ten years to help with daily > headaches and migraines (3-4 per month). Was up to about 200 mg daily. I > moved from Dallas to Ogden, Utah and started seeing a new psychiatrist. >He > asked about the Elavil (I was really depressed) and I told him that it was > for both depression and pain. His personal opinion (and one shared by >many > of his colleagues – he also was a professor of psychiatry for about 10 > years) is that the pain relieving affect of Tricyclic Anti-Depressants is > much overrated. My doctor said that the mood benefits of anti-depressants > is very helpful in pain management, but that the TCAs have too many side > affects. > He took my off the Elavil and Serzone (newer anti-depressant that sucks) >and > put me on Prozac. My mood improved. My headaches did not get any worse, > but over time have gotten much better. > My personal experience with Elavil is that I gained weight, had a hard >time > waking up in the morning, and got really constipated. I’ll never go back >to > the stuff. I need to take Ambien for sleep, but, my doctor would rather > have me take it than a low dose of elavil – he sees Ambien as a much safer > drug. > My psychiatrist still, with the addition of my back pain, has not >mentioned > Elavil or any of its buddies. He interviews me much closer with my back >to > see how my life is going with the pain. He sees how pain can be a monster > in people’s lives unless treated properly. He is totally supportive of me > taking Oxycontin and other meds for breakthrough. (He is an avid skier > also, I really like the guy.) > Martin > > I haven’t noticed any comments on the article in the Observer about > > the use of Tricyclic Antidepressants in the alleviation of some forms > > of chronic pain .
Response:
Martin ….and your wife glad you both found it as thought provoking as I did…and I certainly agree with your feelings…these CAN be wonder drugs,,,when prescribed carefully and monitored closely…not handed out like candy to shut people up… I will keep you in mind as I peruse other sources…but that was a real eye opener to me…as obviously it was to you two…not that it represented "studies" but more like "common sense" that maybe more medical practitioners need to remember they still have… cheers..Martin.. rb Hawki
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Martin "I need to take Ambien for sleep, but, my doctor would rather have me take it than a low dose of elavil – he sees Ambien as a much safer drug." If this is true then your doctor is a real moron. While not a benzo, it works in similar fashion and is just as addicting and has a very short half life. Want problems similar to benzo addiction ? www.benzo.org.uk – Hide quoted text — Show quoted text -> I took large doses of Elavil for about ten years to help with daily > headaches and migraines (3-4 per month). Was up to about 200 mg daily. I > moved from Dallas to Ogden, Utah and started seeing a new psychiatrist. He > asked about the Elavil (I was really depressed) and I told him that it was > for both depression and pain. His personal opinion (and one shared by many > of his colleagues – he also was a professor of psychiatry for about 10 > years) is that the pain relieving affect of Tricyclic Anti-Depressants is > much overrated. My doctor said that the mood benefits of anti-depressants > is very helpful in pain management, but that the TCAs have too many side > affects. > He took my off the Elavil and Serzone (newer anti-depressant that sucks) and > put me on Prozac. My mood improved. My headaches did not get any worse, > but over time have gotten much better. > My personal experience with Elavil is that I gained weight, had a hard time > waking up in the morning, and got really constipated. I’ll never go back to > the stuff. I need to take Ambien for sleep, but, my doctor would rather > have me take it than a low dose of elavil – he sees Ambien as a much safer > drug. > My psychiatrist still, with the addition of my back pain, has not mentioned > Elavil or any of its buddies. He interviews me much closer with my back to > see how my life is going with the pain. He sees how pain can be a monster > in people’s lives unless treated properly. He is totally supportive of me > taking Oxycontin and other meds for breakthrough. (He is an avid skier > also, I really like the guy.) > Martin > I haven’t noticed any comments on the article in the Observer about > the use of Tricyclic Antidepressants in the alleviation of some forms > of chronic pain .
Response:
The story is on : www.observer.co.uk/magazine/story/0,11913,846295,00 – Hide quoted text — Show quoted text – >I haven’t noticed any comments on the article in the Observer about >the use of Tricyclic Antidepressants in the alleviation of some forms >of chronic pain .
Response:
If the stuff you’ve been reading is on the web, could you send me the links?? thanks, Martin
– Hide quoted text — Show quoted text -> Martin > I’m sorry…what I meant to say..do you have a link to the Observer or > whatever..that talked about TCA and pain relief link…personally I have been > reading more and more that other than maybe their help in sleep > disturbances…TCA’s really are not all that effective..if at all..in pain > relief..tho..as with anything..we all are different..so am sure there are some > here who will have different experience.. > Actually I read this week..not sure if it was in a journal or the LA Times > that there is even a lot of controversary about "antidepressants" and what they > actually afford the human organism…perhaps trading the "depression,,,ie > negative for sure response" for a "flat..ie also a negative response"…not to > mention the sexual side effects (which this source quoted as being > significantly higher than previously reported)…I sorta got a mental image of > a sort of zombie…it described how writers had lost the initiative to > write..painters to paint..etc..you know..creativity..while of course not in a > black depression …and also not to mention the weight gain issues…problems > getting off some of these meds…etc etc.. > funny how things change….hopefully for the better?? > rb > Hawki
Response:
Martin.. Actually the LA times on Mondays has a Health section…I am quite sure that is where I read the most recent stuff…will have to see if we still have it…I know the times is available online.. NO..I get a gazillion medical/nursing journals coming thru the house each month..which is why I lose track of what I read WHERE….from now on..I will try and KEEP the article and can at least give you an idea of how to track it down… I must admit I was a bit surprised (no..not personally…since I had experienced all the negative side effects of antideps)…to read that MAYBE it isn’t always such a good idea to just "smother" if that is what we are doing…the emotions//chemicals..whatever…only to later discover that the "zest for life" has also been smothered…has to be a better way… will search for that article..and keep you in mind as I read further…it surely is a fascinating..if not.."depressing" topic (not funny!) rb Hawki
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thanks rb Hawki
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Martin Only for you (grin) would I actually dig thru the trash on thanksgiving Day…but it was the LA Times!!! and I did find it…I can’t provide a link..alas.. But I entered LATimes.com into my browser..hit Health on the left column…then a list of the articles eventually came up…title is "life with depression,,or life with dull feeling"… Unfortunately..when I clicked on the title..I got a screen that said I had to "register"..but that it was free…so I stopped there…but you may want to take the time to do the register stuff…it is an intersting piece..and leaves much to think about…not a scientific study…written by a psychiatrist in Boston.. Just an a clip…"While prozac and others ….increases specific chemical tramissions in some parts of the brain,,it inhibits others elsewhere"……"the cursed feelings are gone…but so are the blessed ones." I found that statement alone to be profound… If you would like…I would be happy to snail mail it to you…but it is just a short piece and you should be able to access it online.. peace…Martin rb Hawki
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I am honored that you’d dig through the trash for me!! (grin – LOL) I registered on latimes.com and looked up this article – very good article. The findings that the journalist wrote out just confirm to me that these are powerful medicines and should only be used when needed. I see some of the folks who post comments in our group who are trying to self-medicate with some of the "internet pharmacies" that require no prescription and I see that this could be disasterous. My wife and I spoke about this article for awhile last night. This stuff is important to us – we have two kids – our older son is 14 and has bipolar disorder, our younger is 10 and has autism. We’ve spent a lot of time and money with psychiatrists, psychologists, the pharmacy, and psychiatric hospitals. For me, anti-depressants (prozac for me) have been a godsend. But, prior to being put on this medicine, my doctor took a long time making sure that the diagnosis of depression was accurate. (A psychiatrist in Dallas started me on anti-depressants 10 years ago, my good doc in Utah changed me to Prozac 4 1/2 years ago.) With me, the "joyous" parts of life weren’t possible anymore, but with proper medication, the joy came back. I’ve known of doctors prescribing anti-depressants without taking time to diagnos the patient or to follow up to see how it is doing. Depression is a very serious disease with a mortality rate of about 10-15% if not treated properly. That is what the medicine is for. There are times when somebody is just "down" for a short period but not truly "depressed". There is a big difference. We have also learned with our son Ben that anti-depressants can be extremely dangerous for somebody with bi-polar disorder. They can "push" the person into a manic phase, which can have deadly consequences. The psychiatric medicines have saved my little family. I have extended family members whose physicians write out Zoloft to be taken "prn" with a prescription that allows enough refills for a year. Pretty scary. There is no monitoring of the patient who is being treated for a disease with that high of a mortality rate. Enough rambling. I’ll print this article and take it to my psychiatrist in January. He’ll find it interesting too! Martin
– Hide quoted text — Show quoted text -> Martin > Only for you (grin) would I actually dig thru the trash on thanksgiving > Day…but it was the LA Times!!! and I did find it…I can’t provide a > link..alas.. > But I entered LATimes.com into my browser..hit Health on the left column…then > a list of the articles eventually came up…title is "life with depression,,or > life with dull feeling"… > Unfortunately..when I clicked on the title..I got a screen that said I had to > "register"..but that it was free…so I stopped there…but you may want to > take the time to do the register stuff…it is an intersting piece..and leaves > much to think about…not a scientific study…written by a psychiatrist in > Boston.. > Just an a clip…"While prozac and others ….increases specific chemical > tramissions in some parts of the brain,,it inhibits others
elsewhere"……"the – Hide quoted text — Show quoted text -> cursed feelings are gone…but so are the blessed ones." > I found that statement alone to be profound… > If you would like…I would be happy to snail mail it to you…but it is just a > short piece and you should be able to access it online.. > peace…Martin > rb > Hawki
Response:
Martin I’m sorry…what I meant to say..do you have a link to the Observer or whatever..that talked about TCA and pain relief link…personally I have been reading more and more that other than maybe their help in sleep disturbances…TCA’s really are not all that effective..if at all..in pain relief..tho..as with anything..we all are different..so am sure there are some here who will have different experience.. Actually I read this week..not sure if it was in a journal or the LA Times that there is even a lot of controversary about "antidepressants" and what they actually afford the human organism…perhaps trading the "depression,,,ie negative for sure response" for a "flat..ie also a negative response"…not to mention the sexual side effects (which this source quoted as being significantly higher than previously reported)…I sorta got a mental image of a sort of zombie…it described how writers had lost the initiative to write..painters to paint..etc..you know..creativity..while of course not in a black depression …and also not to mention the weight gain issues…problems getting off some of these meds…etc etc.. funny how things change….hopefully for the better?? rb Hawki
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I’ll see if my psychiatrist (does not believe that they have the trycyclics (sp???) have the pain benefits) can point me to any literature that supports his views, other than his clinical experience. I don’t see him for 6 weeks, but I’ll drop him a note. He’s a great doc. Martin
– Hide quoted text — Show quoted text ->he article in the Observer about >the use of Tricyclic Antidepressants in the alleviation of some forms >of chronic pain . > Hmmm > A lot of us have gone…or still are on this route…for some time now…so > unless they discovered something "new"….do you have a link I can check out??? > thanks > rb > Hawki
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>he article in the Observer about >the use of Tricyclic Antidepressants in the alleviation of some forms >of chronic pain .
Hmmm A lot of us have gone…or still are on this route…for some time now…so unless they discovered something "new"….do you have a link I can check out??? thanks rb Hawki
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I haven’t noticed any comments on the article in the Observer about the use of Tricyclic Antidepressants in the alleviation of some forms of chronic pain .
Response:
I took large doses of Elavil for about ten years to help with daily headaches and migraines (3-4 per month). Was up to about 200 mg daily. I moved from Dallas to Ogden, Utah and started seeing a new psychiatrist. He asked about the Elavil (I was really depressed) and I told him that it was for both depression and pain. His personal opinion (and one shared by many of his colleagues – he also was a professor of psychiatry for about 10 years) is that the pain relieving affect of Tricyclic Anti-Depressants is much overrated. My doctor said that the mood benefits of anti-depressants is very helpful in pain management, but that the TCAs have too many side affects. He took my off the Elavil and Serzone (newer anti-depressant that sucks) and put me on Prozac. My mood improved. My headaches did not get any worse, but over time have gotten much better. My personal experience with Elavil is that I gained weight, had a hard time waking up in the morning, and got really constipated. I’ll never go back to the stuff. I need to take Ambien for sleep, but, my doctor would rather have me take it than a low dose of elavil – he sees Ambien as a much safer drug. My psychiatrist still, with the addition of my back pain, has not mentioned Elavil or any of its buddies. He interviews me much closer with my back to see how my life is going with the pain. He sees how pain can be a monster in people’s lives unless treated properly. He is totally supportive of me taking Oxycontin and other meds for breakthrough. (He is an avid skier also, I really like the guy.) Martin
– Hide quoted text — Show quoted text -> I haven’t noticed any comments on the article in the Observer about > the use of Tricyclic Antidepressants in the alleviation of some forms > of chronic pain .
Response:
November 27, 2002
Question:
Just like to point out from my own personal experience that both times I have been on Prozac my craving for alcohol has increased quite dramatically. Although I have remained reasonably happy I have gone into a really heavy drinking binge. It also seems to lessen the hangover in some way as well. NOT good news for drinkers. dan 
Response:
> The so called "selectivity" of SRI’s was a marketing ploy, never a > fact in reality.
Bullshit. > (See Stephen Stahl’s article "Not so Selective SRI’s"
Here’s what he says in his opening paragraph: "Selective serotonin reuptake inhibitors (SSRIs) got this name from their greater selectivity (10-fold or more) for blocking serotonin reuptake rather than norepinephrine reuptake. They also lack the sodium channel blocking properties of the tricyclic antidepressants, making them safe in overdose. In addition, SSRIs have less affinity for alpha1-receptors, muscarinic cholinergic receptors, and histamine-1 receptors compared with the tricyclic antidepressants, leading to the greater tolerability profile of SSRIs." Historically, in the context of their origins, SSRIs were "selective for serotonin-receptor binding" when compared to the other antidepressants then available. Any other meanings of SSRI arise from ignorance. > The not so selective SRI, incite a flooding of serotonin receptor > sites with 20 times the normal level of serotonin there.
That is utter fucking bullshit. First you say they are not serotonin-selective. Then you create some fantasy that serotonin release is enhanced. These are REUPTAKE inhibitors, binding to receptors. There is no increase in serotonin release. > This pathological overstimulation and activation in the brain, would > put people into a manic or psychotic state, if the brain didnt react > to such pathological overstimulation by DESTROYING receptor cells for > all stimulating neurotransmitters RIGHT QUCK.
There is no evidence for apoptosis in any region of the brain. In fact, there is evidence of enhanced growth of the hippocampi during SSRI treatment. > Most peoples brain performs this brain cell kill, rather than allow a > person go into a state of mania or psychosis. > The brain cell kill includes receptor cells for not only serotonin, > but dopamine and epineprinin…etc etc.
Etc. etc ? Please share your evidence with us all. > So. Serotonin boosters are not so selective at all, since they effect > more than serotonin.
Only the ignorant would mistake the original meaning of SSRI. Even Stahl acknowledges that much. We don’t even know why they work. It could be that the antidepressant effect requires these secondary binding affinities that you are criticizing so. Maybe you *need* to have suppression of liver enzymes for them to help you obtain a remission from depressive symptoms. Maybe that’s *why* it takes weeks for there to be any effect. Serotonin-receptor binding takes place within hours, but nothing happens for weeks. Why? > And, the effect on dopamine cells is such, a lot of previously non > drinkers wind up craving alchohol, and other stimulants shortly after > begining a course of treatment of SRI’s
You have certainly failed in demonstrating a factual basis for your hypothesis. If SSRIs kill these brain cells, as you suggest, they certainly could no longer induce dopamine-dependent cravings, now could they?
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> This pathological overstimulation and activation in the brain, would > put people into a manic or psychotic state, if the brain didnt react > to such pathological overstimulation by DESTROYING receptor cells for > all stimulating neurotransmitters RIGHT QUCK.
Just to put the focus on this one issue alone, let’s see what your hero Mental Illness May Be Damaging to Your Brain Stephen M. Stahl, M.D., Ph.D. "A new and unanticipated role is emerging for psychopharmacologic agents. That is, they may even be rescue workers, salvaging neurons from imminent death caused by fire, thus preventing these neurons from being turned into ashes. By putting out the fire, coupled with preventing future outbreaks, these agents thereby prevent a cumulative destructive process (see Phase III in the Figure). The rescue role is evident in the effects that the long-term administration of antidepressants and antipsychotics are having on disease progression. For example, the ability of antipsychotics to prevent future psychotic breaks appears to arrest the downhill course of schizophrenia.6 Sufficiently clear evidence in this area has generated debate on whether conducting placebo-controlled trials in schizophrenia is ethical.6 That is, those on placebo risk a relapse and possibly incremental brain destruction. Similarly, the "kindling" of future episodes of affective illness that are linked to reproductive events in women might be halted with antidepressant treatment.7 Could prevention of symptoms of obsessive-compulsive disorder, panic, and social phobia similarly prevent the apparent treatment unresponsiveness of chronic uncontrolled anxiety disorders? Are these implications even more profound for the treatment of young patients with early-onset episodes of depression, mania, or psychosis? Is the flip side of early intervention that long-term suppression of symptoms will allow the brain to "heal" so that long-term treatment can eventually be discontinued? The child’s and adolescent’s brain may be more vulnerable than mature, possibly less plastic, brains to destructive ravages of the illness processes. " Clearly, ma’am, you don’t know a thing about what you’re rambling on about.
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its hard to understand whos saying what, but nonetheless reinforces my belief that these drugs do nothing slaughter out body, but create temporary relief.. Similar to illegal drugs wouldnt you say?
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> babbled : >> The so called "selectivity" of SRI’s was a marketing ploy, never a >> fact in reality. >Bullshit. > Such hostility is typical of either drug co shills, or those with a > psychotoxic drug dependency. > which are you?
There’s nothing hostile in that term. You’re full of shit, that’s all. Such stupidity is typical of either alcoholics or pathological gamblers. Which are you? – Hide quoted text — Show quoted text ->> (See Stephen Stahl’s article "Not so Selective SRI’s" >Here’s what he says in his opening paragraph: >"Selective serotonin reuptake inhibitors (SSRIs) got this name from their >greater selectivity (10-fold or more) for blocking serotonin reuptake rather >than norepinephrine reuptake. > They also lack the sodium channel blocking >properties of the tricyclic antidepressants, making them safe in overdose. >In addition, SSRIs have less affinity for alpha1-receptors, muscarinic >cholinergic receptors, and histamine-1 receptors compared with the tricyclic >antidepressants, leading to the greater tolerability profile of SSRIs." >Historically, in the context of their origins, SSRIs were "selective for >serotonin-receptor binding" when compared to the other antidepressants then >available. Any other meanings of SSRI arise from ignorance. > White wash! > The ignorance surrounding SSRI’s is the direct result of their makers, > lies, omissions, failure to disclose etc.
The term was defined quite clearly. Your ignorant misuse of the term is understandable, given your lack of formal eductaion. >> The not so selective SRI, incite a flooding of serotonin receptor >> sites with 20 times the normal level of serotonin there. >That is utter fucking bullshit. First you say they are not >serotonin-selective. Then you create some fantasy that serotonin release is >enhanced. These are REUPTAKE inhibitors, binding to receptors. There is no >increase in serotonin release. > SSRI’s binding to receptor cells to block or dam the serotonin from > escaping, MEANS that serotonin is pooling up in the area surrounding > the blocked off receptors. This pooling up was demonstrated in studies > to be 20 times the amount of serotonin pooling normally seeking access > to receptor cells, a truly PATHOLOGICAL condition.
References? How about something scientific. >> This pathological overstimulation and activation in the brain, would >> put people into a manic or psychotic state, if the brain didnt react >> to such pathological overstimulation by DESTROYING receptor cells for >> all stimulating neurotransmitters RIGHT QUCK. >There is no evidence for apoptosis in any region of the brain. In fact, >there is evidence of enhanced growth of the hippocampi during SSRI >treatment. > Where are you from? Mars?
LOL. Mol Pharmacol 2002 May;61(5):1017-24 Related Articles, Books, LinkOut Antidepressant treatments induce the expression of basic fibroblast growth factor in cortical and hippocampal neurons. Mallei A, Shi B, Mocchetti I. Department of Neuroscience, Georgetown University Medical Center Washington DC; and Department of Toxicology, University of Cagliari, Cagliari, Italy. New experimental evidence suggests that the mechanism of action of antidepressants includes the induction of neurotrophic factor synthesis in selected brain areas. The present study is aimed at establishing whether prolonged antidepressant treatments increase the expression of basic fibroblast growth factor (FGF2), a polypeptide growth factor that has a broad neurotrophic activity in the adult central nervous system. Rats received a single dose or long-term (3 weeks) administration of desipramine (DMI), fluoxetine (FLU), and mianserin (MIA), then were sacrificed at 5 and 24 h after the last injection. RNase protection assay and Western blot analysis revealed that all antidepressant drugs elicited an anatomically specific increase in FGF2 mRNA and protein. The increase in FGF2 mRNA after a single injection was seen only at 5 h after the injection and was restricted to the entorhinal cortex, whereas the effect of the long-term treatments lasted up to 24 h and occurred in the entire cortex and hippocampus. Immunohistochemical analysis of FGF2 immunoreactivity was carried out to investigate which cell types responded to the antidepressant treatments. DMI and MIA increased FGF2 proteins predominantly in neurons of layer V throughout the cerebral cortex and in some neurofilament-positive cells of the hippocampus. FLU increased FGF2 immunoreactivity mainly in neurofilament-positive cells of the hippocampus. These findings may explain the therapeutic efficacy of antidepressants in affective disorders. PMID: 11961119 [PubMed - in process] Mol Psychiatry 2001 Nov;6(6):610, 725-8 Related Articles, Books, LinkOut Fluoxetine enhances cell proliferation and prevents apoptosis in dentate gyrus of maternally separated rats. Lee HJ, Kim JW, Yim SV, Kim MJ, Kim SA, Kim YJ, Kim CJ, Chung JH. Kohwang Medical Research Institute, College of Medicine, Kyung Hee University, 1 Hoegi-Dong, Tongdaemoon-Ku, Seoul, 130-701, Korea. The mother-infant relationship is an instinctive phenomenon, and loss of maternal care in early life influences neonatal development, behavior and physiologic responses.(1,2) Furthermore, the early loss may affect the vulnerability of the infant to neuropsychiatric disorders, such as childhood anxiety disorders, personality disorders and depression, over its lifespan.(3,4) Fluoxetine is prescribed worldwide for depression and is often used in the treatment of childhood mental problems related to maternal separation or loss of maternal care.(5,6) In the present study, fluoxetine was administrated to rats with maternal separation to determine its effects on neuronal development, in particular with respect to cell proliferation and apoptosis in the dentate gyrus of the hippocampus. Rat pups were separated from their mothers and socially isolated on postnatal day 14 and were treated with fluoxetine (5 mg kg(-1)) and 5-bromo-2′-deoxyuridine (BrdU) (50 mg kg(-1)) for 7 days, after which immunohistochemistry and a terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining were carried out. In the pups with maternal separation treated with fluoxetine, the number of BrdU-positive cells was significantly increased and that of TUNEL-positive cells was significantly decreased in the dentate gyrus compared to pups with maternal separation that did not receive fluoxetine treatment. These findings indicate that fluoxetine affects new cell proliferation and apoptosis, and we propose that fluoxetine may be useful in the treatment of maternal separation-related diseases. PMID: 11673802 [PubMed - indexed for MEDLINE] Eur J Pharmacol 2001 Jan 5;411(1-2):67-70 Related Articles, Books, LinkOut Antidepressants alter cell proliferation in the adult brain in vivo and in neural cultures in vitro. Manev H, Uz T, Smalheiser NR, Manev R. Department of Psychiatry, The Psychiatric Institute, University of Illinois at Chicago, 1601 West Taylor Street MC912, 60612, Chicago, IL, USA. The action of antidepressants on cell proliferation (bromodeoxyuridine (BrdU) or [3H]thymidine incorporation) was studied in the adult rat hippocampus in vivo and in neural precursors (immature rat cerebellar granule cells) in vitro. In vivo, prolonged (21 days) but not acute (single) intraperitoneal treatment with fluoxetine (5 mg/kg) resulted in a 3.4-fold increase of bromodeoxyuridine-positive cells in the subgranular zone of the dentate gyrus. In cell cultures, at 1 and 10 days in vitro, 48-h fluoxetine exposure (1 microM, which is comparable to therapeutic plasma concentrations) reduced thymidine incorporation when initiated at 1 day in vitro, but increased cell proliferation when initiated at 10 days in vitro. Clomipramine and imipramine produced similar action in vitro; desipramine was ineffective. PMID: 11137860 [PubMed - indexed for MEDLINE] > The evidence that SRI destroy brain cells in the frontal lobe been > around for ages.
You can’t even get that part right, can you? Decreased prefrontal activity is associated with *successful* antidepressant treatment. Semin Clin Neuropsychiatry 2001 Apr;6(2):113-20 Related Articles, Books, LinkOut Prefrontal changes and treatment response prediction in depression. Cook IA, Leuchter AF. Quantitative EEG Laboratory and Clinical Neurophysiology Program, Department of Psychiatry and Biobehavioral Sciences, Neuropsychiatric Institute and A continuing challenge in the treatment of depression is how to determine whether an effective drug has been selected for a particular patient, given that individuals will respond to some antidepressants but not others. The factors that contribute to response for each person have been examined from a variety of perspectives, both psychological and physiological. Advances in neuroimaging and in quantitative electroencephalography (QEEG) have made it possible to examine features of brain activity that are associated with response. A new QEEG measure, cordance, is correlated with regional cortical perfusion, and has been used with retrospective and prospective studies to evaluate specific findings that are predictive of clinical response in major depression. We present here a series of depressed subjects treated with antidepressants of different classes; decreases in prefrontal activity were seen as early as 48 hours into treatment in responders and were absent in nonresponders. These findings suggest a role for the prefrontal region in mediating … read more »
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one other thing, do you think that St. Johns Wort, as it works simillarly to SSRI’s, has the same negative effect on the brain/body, or any similar negatives?
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> how the their ekleits > Again, the slander, fl
Ok, you win. I’m no match for you…..LOL. Navel fluff 1, Critic no score. Tee hee.
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Your message made my penis pulsate with desire
– Hide quoted text — Show quoted text – > babbled : >> The so called "selectivity" of SRI’s was a marketing ploy, never a >> fact in reality. >Bullshit. > Such hostility is typical of either drug co shills, or those with a > psychotoxic drug dependency. > which are you? >> (See Stephen Stahl’s article "Not so Selective SRI’s" >Here’s what he says in his opening paragraph: >"Selective serotonin reuptake inhibitors (SSRIs) got this name from their >greater selectivity (10-fold or more) for blocking serotonin reuptake rather >than norepinephrine reuptake. > They also lack the sodium channel blocking >properties of the tricyclic antidepressants, making them safe in overdose. >In addition, SSRIs have less affinity for alpha1-receptors, muscarinic >cholinergic receptors, and histamine-1 receptors compared with the tricyclic >antidepressants, leading to the greater tolerability profile of SSRIs." >Historically, in the context of their origins, SSRIs were "selective for >serotonin-receptor binding" when compared to the other antidepressants then >available. Any other meanings of SSRI arise from ignorance. > White wash! > The ignorance surrounding SSRI’s is the direct result of their makers, > lies, omissions, failure to disclose etc. >> The not so selective SRI, incite a flooding of serotonin receptor >> sites with 20 times the normal level of serotonin there. >That is utter fucking bullshit. First you say they are not >serotonin-selective. Then you create some fantasy that serotonin release is >enhanced. These are REUPTAKE inhibitors, binding to receptors. There is no >increase in serotonin release. > SSRI’s binding to receptor cells to block or dam the serotonin from > escaping, MEANS that serotonin is pooling up in the area surrounding > the blocked off receptors. This pooling up was demonstrated in studies > to be 20 times the amount of serotonin pooling normally seeking access > to receptor cells, a truly PATHOLOGICAL condition. >> This pathological overstimulation and activation in the brain, would >> put people into a manic or psychotic state, if the brain didnt react >> to such pathological overstimulation by DESTROYING receptor cells for >> all stimulating neurotransmitters RIGHT QUCK. >There is no evidence for apoptosis in any region of the brain. In fact, >there is evidence of enhanced growth of the hippocampi during SSRI >treatment. > Where are you from? Mars? > The evidence that SRI destroy brain cells in the frontal lobe been > around for ages. >> Most peoples brain performs this brain cell kill, rather than allow a >> person go into a state of mania or psychosis. >> The brain cell kill includes receptor cells for not only serotonin, >> but dopamine and epineprinin…etc etc. >Etc. etc ? Please share your evidence with us all. > Common knowledge which only drug co shills, and those addicted to the > stimulating SRI are in denial about it. >> So. Serotonin boosters are not so selective at all, since they effect >> more than serotonin. >Only the ignorant would mistake the original meaning of SSRI. Even Stahl >acknowledges that much. > "Even Stahl" LOL > Stahl has been conducting clinical trials and research FOR the > pharmaceutical companies for ages, and is about as compromised a > scientist as there is. > So it was actually quite a shock for someone as compromised as Stahl > to author the "Not So Selective SRI’s" paper. > At least until he followed up that paper with the one about How to > make use, and market the various SRI’s on the basis of each of their > being NOT SO SELECTIVE! > http://www.psychiatrist.com/pcc/brainstorm/br5912.htm > the first paper is very hard to find. > While the second one, instructive of how to make marketing use of the > secondary binding properties of the NOT SO SELECTIVE SRI’s is > beautrifully displayed on WWW in the above link. >We don’t even know why they work. > WE know they do NOT work > Regards depression, they are no more effective than a sugar pill. > too bad they are not as benign as a sugar pill, because though > ineffective as AD’s. even CAUSING depression, on them, and most > especially rebound depression upon stopping them, they cause all > manner of psychiatric disturbance, compulisve behaviors and cravings > for alchohol. . > It could be that the antidepressant effect >requires these secondary binding affinities that you are criticizing so. > The secondary binding occuring such that the dopamine receptor cells > also get blocked or dammed up, so that dopamine in also pooling up > around receptor cells is NOT a good thing, darling. > Having 20 times amount of serotonin pooling up is BAD, but having > excess dopamine pooling up is CATASTROPHIC, activating psychosis, > mania, aggression, violence, paranoia, which a healthy brain will NOT > allow for very long. > Hence, the activation and overstimulation will TRIGGER a huge brain > cell kill, destroying large areas of the frontal lobe to STOP > activation caused by all this excess serotonin and dopamine and lord > knows what else, a brain kill whic is a neuroleptic type action.. > the so called therapeutic effect reached on SRI’s after six weeks, > is not an antidepressant one…but a tranqulizing one of a > neuroleptic > or partial chemicla lobotomy of the frontal lobe, upon 40 % of its > cells being destroyed or made unusable. >Maybe you *need* to have suppression of liver enzymes for them to help you >obtain a remission from depressive symptoms. > SRI’s do inhibit and impair liver function by suppressing enzyme 2d6. > Impairing the liver so it can no longer detoxify the blood of all the > many environmental toxins 2D6 break down, leaving SRI users > susceptible ot all manner of CANCER. > Maybe that’s *why* it takes >weeks for there to be any effect. Serotonin-receptor binding takes place >within hours, but nothing happens for weeks. Why? > Who you kidding? The first six weeks on an SRI is the most happening > of times…SRI induced anxiety, agitation, ahathesia, hypomania, > mania, paranoid delusions, suicidal ideations, homocidal ideations, > OCD, PSYCHOSIs, weight loss, and on and on, until the poor brain cant > take it, and KILLS its cells off to TRANQUILE itself in good old > neuoleptic like action. >> And, the effect on dopamine cells is such, a lot of previously non >> drinkers wind up craving alchohol, and other stimulants shortly after >> begining a course of treatment of SRI’s >You have certainly failed in demonstrating a factual basis for your >hypothesis. If SSRIs kill these brain cells, as you suggest, they certainly >could no longer induce dopamine-dependent cravings, now could they? > Now you play dumb about the paradoxical reactions of the brain to > psychotoxic chemcial.. > How convenient! .
Response:
> Your message made my penis pulsate with desire
Joe Parsons? – Hide quoted text — Show quoted text -> babbled : > >> The so called "selectivity" of SRI’s was a marketing ploy, never a > >> fact in reality. > >Bullshit. > Such hostility is typical of either drug co shills, or those with a > psychotoxic drug dependency. > which are you? > >> (See Stephen Stahl’s article "Not so Selective SRI’s" > >Here’s what he says in his opening paragraph: > >"Selective serotonin reuptake inhibitors (SSRIs) got this name from their > >greater selectivity (10-fold or more) for blocking serotonin reuptake > rather > >than norepinephrine reuptake. > They also lack the sodium channel blocking > >properties of the tricyclic antidepressants, making them safe in > overdose. > >In addition, SSRIs have less affinity for alpha1-receptors, muscarinic > >cholinergic receptors, and histamine-1 receptors compared with the > tricyclic > >antidepressants, leading to the greater tolerability profile of SSRIs." > >Historically, in the context of their origins, SSRIs were "selective for > >serotonin-receptor binding" when compared to the other antidepressants > then > >available. Any other meanings of SSRI arise from ignorance. > White wash! > The ignorance surrounding SSRI’s is the direct result of their makers, > lies, omissions, failure to disclose etc. > >> The not so selective SRI, incite a flooding of serotonin receptor > >> sites with 20 times the normal level of serotonin there. > >That is utter fucking bullshit. First you say they are not > >serotonin-selective. Then you create some fantasy that serotonin release > is > >enhanced. These are REUPTAKE inhibitors, binding to receptors. There is > no > >increase in serotonin release. > SSRI’s binding to receptor cells to block or dam the serotonin from > escaping, MEANS that serotonin is pooling up in the area surrounding > the blocked off receptors. This pooling up was demonstrated in studies > to be 20 times the amount of serotonin pooling normally seeking access > to receptor cells, a truly PATHOLOGICAL condition. > >> This pathological overstimulation and activation in the brain, would > >> put people into a manic or psychotic state, if the brain didnt react > >> to such pathological overstimulation by DESTROYING receptor cells for > >> all stimulating neurotransmitters RIGHT QUCK. > >There is no evidence for apoptosis in any region of the brain. In fact, > >there is evidence of enhanced growth of the hippocampi during SSRI > >treatment. > Where are you from? Mars? > The evidence that SRI destroy brain cells in the frontal lobe been > around for ages. > >> Most peoples brain performs this brain cell kill, rather than allow a > >> person go into a state of mania or psychosis. > >> The brain cell kill includes receptor cells for not only serotonin, > >> but dopamine and epineprinin…etc etc. > >Etc. etc ? Please share your evidence with us all. > Common knowledge which only drug co shills, and those addicted to the > stimulating SRI are in denial about it. > >> So. Serotonin boosters are not so selective at all, since they effect > >> more than serotonin. > >Only the ignorant would mistake the original meaning of SSRI. Even Stahl > >acknowledges that much. > "Even Stahl" LOL > Stahl has been conducting clinical trials and research FOR the > pharmaceutical companies for ages, and is about as compromised a > scientist as there is. > So it was actually quite a shock for someone as compromised as Stahl > to author the "Not So Selective SRI’s" paper. > At least until he followed up that paper with the one about How to > make use, and market the various SRI’s on the basis of each of their > being NOT SO SELECTIVE! > http://www.psychiatrist.com/pcc/brainstorm/br5912.htm > the first paper is very hard to find. > While the second one, instructive of how to make marketing use of the > secondary binding properties of the NOT SO SELECTIVE SRI’s is > beautrifully displayed on WWW in the above link. > >We don’t even know why they work. > WE know they do NOT work > Regards depression, they are no more effective than a sugar pill. > too bad they are not as benign as a sugar pill, because though > ineffective as AD’s. even CAUSING depression, on them, and most > especially rebound depression upon stopping them, they cause all > manner of psychiatric disturbance, compulisve behaviors and cravings > for alchohol. . > It could be that the antidepressant effect > >requires these secondary binding affinities that you are criticizing so. > The secondary binding occuring such that the dopamine receptor cells > also get blocked or dammed up, so that dopamine in also pooling up > around receptor cells is NOT a good thing, darling. > Having 20 times amount of serotonin pooling up is BAD, but having > excess dopamine pooling up is CATASTROPHIC, activating psychosis, > mania, aggression, violence, paranoia, which a healthy brain will NOT > allow for very long. > Hence, the activation and overstimulation will TRIGGER a huge brain > cell kill, destroying large areas of the frontal lobe to STOP > activation caused by all this excess serotonin and dopamine and lord > knows what else, a brain kill whic is a neuroleptic type action.. > the so called therapeutic effect reached on SRI’s after six weeks, > is not an antidepressant one…but a tranqulizing one of a > neuroleptic > or partial chemicla lobotomy of the frontal lobe, upon 40 % of its > cells being destroyed or made unusable. > >Maybe you *need* to have suppression of liver enzymes for them to help > you > >obtain a remission from depressive symptoms. > SRI’s do inhibit and impair liver function by suppressing enzyme 2d6. > Impairing the liver so it can no longer detoxify the blood of all the > many environmental toxins 2D6 break down, leaving SRI users > susceptible ot all manner of CANCER. > Maybe that’s *why* it takes > >weeks for there to be any effect. Serotonin-receptor binding takes place > >within hours, but nothing happens for weeks. Why? > Who you kidding? The first six weeks on an SRI is the most happening > of times…SRI induced anxiety, agitation, ahathesia, hypomania, > mania, paranoid delusions, suicidal ideations, homocidal ideations, > OCD, PSYCHOSIs, weight loss, and on and on, until the poor brain cant > take it, and KILLS its cells off to TRANQUILE itself in good old > neuoleptic like action. > >> And, the effect on dopamine cells is such, a lot of previously non > >> drinkers wind up craving alchohol, and other stimulants shortly after > >> begining a course of treatment of SRI’s > >You have certainly failed in demonstrating a factual basis for your > >hypothesis. If SSRIs kill these brain cells, as you suggest, they > certainly > >could no longer induce dopamine-dependent cravings, now could they? > Now you play dumb about the paradoxical reactions of the brain to > psychotoxic chemcial.. > How convenient! .
Response:
> ->one other thing, do you think that St. Johns Wort, as it works simillarly to > ->SSRI’s, has the same negative effect on the brain/body, or any similar negatives? > St. John’s Wort was recently tested and found to be no more effective > than a placebo.
not quite true. There are numerous studies out there that do show a difference from placebo but those are not always replicable. — "It was, of course, a lie what you read about my religious convictions, a lie which is being systematically repeated. I do not believe in a personal God and I have never denied this but have expressed it clearly. If something is in me which can be called religious then it is the unbounded admiration for the structure of the world so far as our science can reveal it." – Albert Einstein in Albert Einstein: The Human Side, edited by Helen Dukas (Einstein’s secretary) and Banesh Hoffman, and published by Princeton University Press http://home.gwi.net/~mdmpsyd/index.htm
Response:
> babbled : >one other thing, do you think that St. Johns Wort, as it works simillarly to >SSRI’s, has the same negative effect on the brain/body, or any similar negatives? > SJW certainly does NOT have the STIMULANT profile of adverse reactions > and side effects the SSRI’s have. > SJW has few side effects.
It has some mild MAOI effects; I’d watch my diet. > SJW is a safe and effective remedy for mild to moderate depression. > OTC products for depression with side effects profiles similiar to the > SSRI’s, or stimulants are products like 5-HTP and SAM-e. > .
– "It was, of course, a lie what you read about my religious convictions, a lie which is being systematically repeated. I do not believe in a personal God and I have never denied this but have expressed it clearly. If something is in me which can be called religious then it is the unbounded admiration for the structure of the world so far as our science can reveal it." – Albert Einstein in Albert Einstein: The Human Side, edited by Helen Dukas (Einstein’s secretary) and Banesh Hoffman, and published by Princeton University Press http://home.gwi.net/~mdmpsyd/index.htm
Response:
> ->one other thing, do you think that St. Johns Wort, as it works simillarly to > ->SSRI’s, has the same negative effect on the brain/body, or any similar negatives? > St. John’s Wort was recently tested and found to be no more effective > than a placebo.
Id have to disagree, that was one test.. ive seen noticable changes in my body physically from it, as well as mentally.. and if its a placebo, why does my body react very differently when i take different dosages. either a very very creative body, or it might be working? but id have to say its not very strong.. so it wouldnt work in all cases….
Response:
> your knowledge of the subject is so limited and superficial, you cant > even sustain a discussion of the SUBJECT,
When you’re ready to debate the science, Linda Gore, we can discuss this further. You said: >> >> This pathological overstimulation and activation in the brain, would >> >> put people into a manic or psychotic state, if the brain didnt react >> >> to such pathological overstimulation by DESTROYING receptor cells for >> >> all stimulating neurotransmitters RIGHT QUCK.
But the truth is: – Hide quoted text — Show quoted text ->Mol Pharmacol 2002 May;61(5):1017-24 Related Articles, Books, LinkOut >Antidepressant treatments induce the expression of basic fibroblast growth >factor in cortical and hippocampal neurons. >Mallei A, Shi B, Mocchetti I. >Department of Neuroscience, Georgetown University Medical Center Washington >DC; and Department of Toxicology, University of Cagliari, Cagliari, Italy. >New experimental evidence suggests that the mechanism of action of >antidepressants includes the induction of neurotrophic factor synthesis in >selected brain areas. The present study is aimed at establishing whether >prolonged antidepressant treatments increase the expression of basic >fibroblast growth factor (FGF2), a polypeptide growth factor that has a >broad neurotrophic activity in the adult central nervous system. Rats >received a single dose or long-term (3 weeks) administration of desipramine >(DMI), fluoxetine (FLU), and mianserin (MIA), then were sacrificed at 5 and >24 h after the last injection. RNase protection assay and Western blot >analysis revealed that all antidepressant drugs elicited an anatomically >specific increase in FGF2 mRNA and protein. The increase in FGF2 mRNA after >a single injection was seen only at 5 h after the injection and was >restricted to the entorhinal cortex, whereas the effect of the long-term >treatments lasted up to 24 h and occurred in the entire cortex and >hippocampus. Immunohistochemical analysis of FGF2 immunoreactivity was >carried out to investigate which cell types responded to the antidepressant >treatments. DMI and MIA increased FGF2 proteins predominantly in neurons of >layer V throughout the cerebral cortex and in some neurofilament-positive >cells of the hippocampus. FLU increased FGF2 immunoreactivity mainly in >neurofilament-positive cells of the hippocampus. These findings may explain >the therapeutic efficacy of antidepressants in affective disorders. >PMID: 11961119 [PubMed - in process] >Mol Psychiatry 2001 Nov;6(6):610, 725-8 Related Articles, Books, LinkOut >Fluoxetine enhances cell proliferation and prevents apoptosis in dentate >gyrus of maternally separated rats. >Lee HJ, Kim JW, Yim SV, Kim MJ, Kim SA, Kim YJ, Kim CJ, Chung JH. >Kohwang Medical Research Institute, College of Medicine, Kyung Hee >University, 1 Hoegi-Dong, Tongdaemoon-Ku, Seoul, 130-701, Korea. >The mother-infant relationship is an instinctive phenomenon, and loss of >maternal care in early life influences neonatal development, behavior and >physiologic responses.(1,2) Furthermore, the early loss may affect the >vulnerability of the infant to neuropsychiatric disorders, such as childhood >anxiety disorders, personality disorders and depression, over its >lifespan.(3,4) Fluoxetine is prescribed worldwide for depression and is >often used in the treatment of childhood mental problems related to maternal >separation or loss of maternal care.(5,6) In the present study, fluoxetine >was administrated to rats with maternal separation to determine its effects >on neuronal development, in particular with respect to cell proliferation >and apoptosis in the dentate gyrus of the hippocampus. Rat pups were >separated from their mothers and socially isolated on postnatal day 14 and >were treated with fluoxetine (5 mg kg(-1)) and 5-bromo-2′-deoxyuridine >(BrdU) (50 mg kg(-1)) for 7 days, after which immunohistochemistry and a >terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling >(TUNEL) staining were carried out. In the pups with maternal separation >treated with fluoxetine, the number of BrdU-positive cells was significantly >increased and that of TUNEL-positive cells was significantly decreased in >the dentate gyrus compared to pups with maternal separation that did not >receive fluoxetine treatment. These findings indicate that fluoxetine >affects new cell proliferation and apoptosis, and we propose that fluoxetine >may be useful in the treatment of maternal separation-related diseases. >PMID: 11673802 [PubMed - indexed for MEDLINE] >Eur J Pharmacol 2001 Jan 5;411(1-2):67-70 Related Articles, Books, LinkOut >Antidepressants alter cell proliferation in the adult brain in vivo and in >neural cultures in vitro. >Manev H, Uz T, Smalheiser NR, Manev R. >Department of Psychiatry, The Psychiatric Institute, University of Illinois >at Chicago, 1601 West Taylor Street MC912, 60612, Chicago, IL, USA. >The action of antidepressants on cell proliferation (bromodeoxyuridine >(BrdU) or [3H]thymidine incorporation) was studied in the adult rat >hippocampus in vivo and in neural precursors (immature rat cerebellar >granule cells) in vitro. In vivo, prolonged (21 days) but not acute (single) >intraperitoneal treatment with fluoxetine (5 mg/kg) resulted in a 3.4-fold >increase of bromodeoxyuridine-positive cells in the subgranular zone of the >dentate gyrus. In cell cultures, at 1 and 10 days in vitro, 48-h fluoxetine >exposure (1 microM, which is comparable to therapeutic plasma >concentrations) reduced thymidine incorporation when initiated at 1 day in >vitro, but increased cell proliferation when initiated at 10 days in vitro. >Clomipramine and imipramine produced similar action in vitro; desipramine >was ineffective. >PMID: 11137860 [PubMed - indexed for MEDLINE]
And, you said: >> The evidence that SRI destroy brain cells in the frontal lobe been >> around for ages.
But, the truth is: – Hide quoted text — Show quoted text ->Semin Clin Neuropsychiatry 2001 Apr;6(2):113-20 Related Articles, Books, >LinkOut >Prefrontal changes and treatment response prediction in depression. >Cook IA, Leuchter AF. >Quantitative EEG Laboratory and Clinical Neurophysiology Program, Department >of Psychiatry and Biobehavioral Sciences, Neuropsychiatric Institute and >A continuing challenge in the treatment of depression is how to determine >whether an effective drug has been selected for a particular patient, given >that individuals will respond to some antidepressants but not others. The >factors that contribute to response for each person have been examined from >a variety of perspectives, both psychological and physiological. Advances in >neuroimaging and in quantitative electroencephalography (QEEG) have made it >possible to examine features of brain activity that are associated with >response. A new QEEG measure, cordance, is correlated with regional cortical >perfusion, and has been used with retrospective and prospective studies to >evaluate specific findings that are predictive of clinical response in major >depression. We present here a series of depressed subjects treated with >antidepressants of different classes; decreases in prefrontal activity were >seen as early as 48 hours into treatment in responders and were absent in >nonresponders. These findings suggest a role for the prefrontal region in >mediating response to medications with different mechanisms of action and >raise the possibility of using new QEEG measures to identify changes in >brain activity that are predictive of clinical outcome from antidepressant >treatment. Copyright 2001 Copyright by W.B. Saunders Company.
Response:
> The evidence that SRI destroy brain cells in the frontal lobe been > around for ages.
Functional neuro-imaging gives a different perspective: Ann N Y Acad Sci 1999 Jun 29;877:614-37 Related Articles, Books, LinkOut Prefrontal cortical-amygdalar metabolism in major depression. Drevets WC. Department of Psychiatry, University of Pittsburgh School of Medicine, Functional neuroimaging studies of the anatomical correlates of familial major depressive disorder (MDD) and bipolar disorder (BD) have identified abnormalities of resting blood flow (BF) and glucose metabolism in depression in the amygdala and the orbital and medial prefrontal cortical (PFC) areas that are extensively connected with the amygdala. The amygdala metabolism in MDD and BD is positively correlated with both depression severity and "stressed" plasma cortisol concentrations measured during scanning. During antidepressant drug treatment, the mean amygdala metabolism decreases in treatment responders, and the persistence of elevated amygdala metabolism during remission is associated with a high risk for the development of depressive relapse. The orbital C metabolism is also abnormally elevated during depression, but is negatively correlated with both depression severity and amygdala metabolism, suggesting that this structure may be activated as a compensatory mechanism to modulate amygdala activity or amygdala-driven emotional responses. The posterior orbital C and anterior cingulate C ventral to the genu of the corpus callosum (subgenual PFC) have more recently been shown in morphometric MRI and/or post mortem histopathological studies to have reduced grey matter volume and reduced glial cell numbers (with no equivalent loss of neurons) in familial MDD and BD. These data suggest a neural model in which dysfunction of limbic PFC structures impairs the modulation of the amygdala, leading to abnormal processing of emotional stimuli. Antidepressant drugs may compensate for this dysfunction by inhibiting pathological limbic activity. Publication Types: Review Review, Academic PMID: 10415674 [PubMed - indexed for MEDLINE] Arch Gen Psychiatry 2001 Jul;58(7):631-40 Related Articles, Books, LinkOut Comment in: Arch Gen Psychiatry. 2001 Jul;58(7):649-50. Arch Gen Psychiatry. 2001 Jul;58(7):651-3. Regional brain metabolic changes in patients with major depression treated with either paroxetine or interpersonal therapy: preliminary findings. Brody AL, Saxena S, Stoessel P, Gillies LA, Fairbanks LA, Alborzian S, Phelps ME, Huang SC, Wu HM, Ho ML, Ho MK, Au SC, Maidment K, Baxter LR Jr. Department of Psychiatry and Biobehavioral Sciences, University of BACKGROUND: In functional brain imaging studies of major depressive disorder (MDD), regional abnormalities have been most commonly found in prefrontal cortex, anterior cingulate gyrus, and temporal lobe. We examined baseline regional metabolic abnormalities and metabolic changes from pretreatment to posttreatment in subjects with MDD. We also performed a preliminary comparison of regional changes with 2 distinct forms of treatment (paroxetine and interpersonal psychotherapy). METHODS: Twenty-four subjects with unipolar MDD and 16 normal control subjects underwent resting F 18 ((18)F) fluorodeoxyglucose positron emission tomography scanning before and after 12 weeks. Between scans, subjects with MDD were treated with either paroxetine or interpersonal psychotherapy (based on patient preference), while controls underwent no treatment. RESULTS: At baseline, subjects with MDD had higher normalized metabolism than controls in the prefrontal cortex (and caudate and thalamus), and lower metabolism in the temporal lobe. With treatment, subjects with MDD had metabolic changes in the direction of normalization in these regions. After treatment, paroxetine-treated subjects had a greater mean decrease in Hamilton Depression Rating Scale score (61.4%) than did subjects treated with interpersonal psychotherapy (38.0%), but both subgroups showed decreases in normalized prefrontal cortex (paroxetine-treated bilaterally and interpersonal psychotherapy-treated on the right) and left anterior cingulate gyrus metabolism, and increases in normalized left temporal lobe metabolism. CONCLUSIONS: Subjects with MDD had regional brain metabolic abnormalities at baseline that tended to normalize with treatment. Regional metabolic changes appeared similar with the 2 forms of treatment. These results should be interpreted with caution because of study limitations (small sample size, lack of random assignment to treatment groups, and differential treatment response between treatment subgroups). Publication Types: Clinical Trial Controlled Clinical Trial PMID: 11448368 [PubMed - indexed for MEDLINE] Biol Psychiatry 2001 Aug 1;50(3):171-8 Related Articles, Books, LinkOut Brain metabolic changes associated with symptom factor improvement in major depressive disorder. Brody AL, Saxena S, Mandelkern MA, Fairbanks LA, Ho ML, Baxter LR. Department of Psychiatry and Biobehavioral Sciences, UCLA School of Medicine, Los Angeles, California 90095, USA. BACKGROUND: Symptoms of major depressive disorder (MDD) have been linked to regional brain function through imaging studies of symptom provocation in normal control subjects and baseline studies of subjects with MDD. We examined associations between change in depressive symptom factors and change in regional brain metabolism from before to after treatment of MDD. METHODS: Thirty-nine outpatients with MDD underwent 18F-fluorodeoxyglucose positron emission tomography scanning before and after treatment with either paroxetine or interpersonal psychotherapy. Associations were determined between changes in regional brain metabolism and changes in four Hamilton Depression Rating Scale factors (anxiety/somatization [ANX], psychomotor retardation [PR], cognitive disturbance [COGN], and sleep disturbance) and two corresponding Profile of Mood States subscales (tension [TENS] and fatigue [FATIG]). RESULTS: Improvement in ANX, PR, TENS, and FATIG factors was associated with decreasing ventral frontal lobe metabolism. Improvement in ANX and TENS was also associated with decreasing ventral anterior cingulate gyrus (AC) and anterior insula activity, whereas improvement in PR was associated with increasing dorsal AC activity. COGN improvement was associated with increasing dorsolateral prefrontal cortex metabolism. CONCLUSIONS: Brain regions that show significant relationships with symptom provocation in normal control subjects have similar relationships with MDD symptoms as they improve with treatment. PMID: 11513815 [PubMed - indexed for MEDLINE]
Response:
– Hide quoted text — Show quoted text – >: >> your knowledge of the subject is so limited and superficial, you cant >> even sustain a discussion of the SUBJECT, >When you’re ready to debate the science, Linda Gore, we can discuss this >further. >Science? >I was discussing facts, Larry. >The fact being discussed here, is SSRI’s inducing of cravings for >alchohol in the non-drinking population of SSRI users. >The fact that SSRI’s induce alchohol cravings is a NON-disputable >fact. .
During the "flying" block of my TM Sidhis course one lady started having an intensive craving for booze….
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> ->Science? > -> > ->I was discussing facts, Larry. > You blew Larry’s cover.
Cover? LOL.
Response:
>When you’re ready to debate the science, Linda Gore, we can discuss this >further. > Science? > I was discussing facts, Larry.
Science is Latin for knowledge. > The fact being discussed here, is SSRI’s inducing of cravings for > alchohol in the non-drinking population of SSRI users.
I don’t dispute that happens. > The fact that SSRI’s induce alchohol cravings is a NON-disputable > fact. .
Agreed. > I have used known facts, to construct a working hypothesise to explain > the phenonmonon. of these out of character cravings for alchohol on > SSRI’s in the non drinking population.
You have misused and invented facts to explain something that needs no explanation. > Do you have an alternative explanation as to why the non drinking > population of SSRI users are besieged by cravings for alchohol upon > SSRI use?
Why individuals might experience this is beyond our current understanding, IMHO. Your hypothetical mechanism is not consistent with observations of brain function in response to SSRI intake. > Or, do you self servingly, plan on continuing to ignore the FACT > that SSRI’s are inducing cravings for alchohol in non drinking > population of SSRI users?
I do not dispute the existence of the phenomenon. Quite the contrary, I have observed it at close quarters. What I dispute are the "facts" you have presented.
Response:
id still have to disagree… i cant imagine a placebo is gonna wake me up on the our every night, make me have deeper dreams, restore sexual function, improved concentration and about 100 other things… and id have to say this is the first time its worked for me, ive tried using it 4 times before, only reason its working this time is coz i doubled the dose.. but no point arguing.. if u think ure right, you are 
and whatever works really..
– Hide quoted text — Show quoted text – > ->Id have to disagree, that was one test.. ive seen noticable changes in my > ->body physically from it, as well as mentally.. and if its a placebo, why > ->does my body react very differently when i take different dosages. either a > ->very very creative body, or it might be working? but id have to say its not > ->very strong.. so it wouldnt work in all cases…. > That test was a pretty huge test. Placebo’s, and the very act of > taking medication, make one feel better.
Response:
typed: > one other thing, do you think that St. Johns Wort, as it works > simillarly to SSRI’s, has the same negative effect on the brain/body, > or any similar negatives?
It’s not very useful, actually, for people with severe depression. Have you read it? You have to take like 6/day. That’s expensive. If I feel screwed by anyone, it’s the vitamin/natural pills for several reasons. They’re expensive, you have to take a lot of them, and they realy don’t have to tell you what’s in them. Oh yes. They come in non-recyclable plastic, which is a bit hypocritical. —- —–BEGIN PERL GEEK CODE BLOCK—– P+++>++++c–>*P6 >?R >++M+>++O++MA+E PU BD++C++D++S++X WP MO PP n+CO?PO-o+G+A-OLC+OLCC+OLJ+OLP–OLR–OL CO–OLS–OLL–OLA–Ee Ev-Eon+Eot!Eob Eoa!uL++>+++uB!uS!uH!uo!w—m!osA!osBE! ——END PERL GEEK CODE BLOCK—— elizabeth at psy dox dot com
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When I was first put on Paxil my craving for alcohol increased dramatically as well. I was bing drinking 6 days out of 7 for a good while.
Response:
> >It’s not very useful, actually, for people with severe depression. >Have you read it? You have to take like 6/day. That’s expensive. >If I feel screwed by anyone, it’s the vitamin/natural pills for >several reasons.
Because they’re expensive, you have to take a lot and they aren’t very effective. Hello. > You missed the latest on the SJW clinical trial? > http://www.nih.gov/news/pr/apr2002/nccam-09.htm
That one?: Study Shows St. John’s Wort Ineffective for Major Depression of Moderate Severity An extract of the herb St. John’s wort was no more effective for treating major depression of moderate severity than placebo, according to… —- —–BEGIN PERL GEEK CODE BLOCK—– P+++>++++c–>*P6 >?R >++M+>++O++MA+E PU BD++C++D++S++X WP MO PP n+CO?PO-o+G+A-OLC+OLCC+OLJ+OLP–OLR–OL CO–OLS–OLL–OLA–Ee Ev-Eon+Eot!Eob Eoa!uL++>+++uB!uS!uH!uo!w—m!osA!osBE! ——END PERL GEEK CODE BLOCK—— elizabeth at psy dox dot com
Response:
Have there been any empirical tests on the natural products like St. John’s Wort? If not I think that would be something to push hard for. Maybe FDA sponsered research at a university. Richard – Hide quoted text — Show quoted text – > babbled : >one other thing, do you think that St. Johns Wort, as it works simillarly to >SSRI’s, has the same negative effect on the brain/body, or any similar negatives? > SJW certainly does NOT have the STIMULANT profile of adverse reactions > and side effects the SSRI’s have. > SJW has few side effects. > SJW is a safe and effective remedy for mild to moderate depression. > OTC products for depression with side effects profiles similiar to the > SSRI’s, or stimulants are products like 5-HTP and SAM-e. > ..
Response:
I am on 60 mgs. of Paxil and have no lack of desire, pulsing and otherwize. – Hide quoted text — Show quoted text – > babbled : >Your message made my penis pulsate with desire > Your definitely not on any SSRI! >>babbled : >>>>The so called "selectivity" of SRI’s was a marketing ploy, never a >>>>fact in reality. >>>Bullshit. >>Such hostility is typical of either drug co shills, or those with a >>psychotoxic drug dependency. >>which are you? >>>>(See Stephen Stahl’s article "Not so Selective SRI’s" >>>Here’s what he says in his opening paragraph: >>>"Selective serotonin reuptake inhibitors (SSRIs) got this name from their >>>greater selectivity (10-fold or more) for blocking serotonin reuptake >rather >>>than norepinephrine reuptake. >>They also lack the sodium channel blocking >>>properties of the tricyclic antidepressants, making them safe in >overdose. >>>In addition, SSRIs have less affinity for alpha1-receptors, muscarinic >>>cholinergic receptors, and histamine-1 receptors compared with the >tricyclic >>>antidepressants, leading to the greater tolerability profile of SSRIs." >>>Historically, in the context of their origins, SSRIs were "selective for >>>serotonin-receptor binding" when compared to the other antidepressants >then >>>available. Any other meanings of SSRI arise from ignorance. >>White wash! >>The ignorance surrounding SSRI’s is the direct result of their makers, >>lies, omissions, failure to disclose etc. >>>>The not so selective SRI, incite a flooding of serotonin receptor >>>>sites with 20 times the normal level of serotonin there. >>>That is utter fucking bullshit. First you say they are not >>>serotonin-selective. Then you create some fantasy that serotonin release >is >>>enhanced. These are REUPTAKE inhibitors, binding to receptors. There is >no >>>increase in serotonin release. >>SSRI’s binding to receptor cells to block or dam the serotonin from >>escaping, MEANS that serotonin is pooling up in the area surrounding >>the blocked off receptors. This pooling up was demonstrated in studies >>to be 20 times the amount of serotonin pooling normally seeking access >>to receptor cells, a truly PATHOLOGICAL condition. >>>>This pathological overstimulation and activation in the brain, would >>>>put people into a manic or psychotic state, if the brain didnt react >>>>to such pathological overstimulation by DESTROYING receptor cells for >>>>all stimulating neurotransmitters RIGHT QUCK. >>>There is no evidence for apoptosis in any region of the brain. In fact, >>>there is evidence of enhanced growth of the hippocampi during SSRI >>>treatment. >>Where are you from? Mars? >>The evidence that SRI destroy brain cells in the frontal lobe been >>around for ages. >>>>Most peoples brain performs this brain cell kill, rather than allow a >>>>person go into a state of mania or psychosis. >>>>The brain cell kill includes receptor cells for not only serotonin, >>>>but dopamine and epineprinin…etc etc. >>>Etc. etc ? Please share your evidence with us all. >>Common knowledge which only drug co shills, and those addicted to the >>stimulating SRI are in denial about it. >>>>So. Serotonin boosters are not so selective at all, since they effect >>>>more than serotonin. >>>Only the ignorant would mistake the original meaning of SSRI. Even Stahl >>>acknowledges that much. >>"Even Stahl" LOL >>Stahl has been conducting clinical trials and research FOR the >>pharmaceutical companies for ages, and is about as compromised a >>scientist as there is. >>So it was actually quite a shock for someone as compromised as Stahl >>to author the "Not So Selective SRI’s" paper. >>At least until he followed up that paper with the one about How to >>make use, and market the various SRI’s on the basis of each of their >>being NOT SO SELECTIVE! >>http://www.psychiatrist.com/pcc/brainstorm/br5912.htm >>the first paper is very hard to find. >>While the second one, instructive of how to make marketing use of the >>secondary binding properties of the NOT SO SELECTIVE SRI’s is >>beautrifully displayed on WWW in the above link. >>>We don’t even know why they work. >>WE know they do NOT work >>Regards depression, they are no more effective than a sugar pill. >>too bad they are not as benign as a sugar pill, because though >>ineffective as AD’s. even CAUSING depression, on them, and most >>especially rebound depression upon stopping them, they cause all >>manner of psychiatric disturbance, compulisve behaviors and cravings >>for alchohol. . >> It could be that the antidepressant effect >>>requires these secondary binding affinities that you are criticizing so. >>The secondary binding occuring such that the dopamine receptor cells >>also get blocked or dammed up, so that dopamine in also pooling up >>around receptor cells is NOT a good thing, darling. >>Having 20 times amount of serotonin pooling up is BAD, but having >>excess dopamine pooling up is CATASTROPHIC, activating psychosis, >>mania, aggression, violence, paranoia, which a healthy brain will NOT >>allow for very long. >>Hence, the activation and overstimulation will TRIGGER a huge brain >>cell kill, destroying large areas of the frontal lobe to STOP >>activation caused by all this excess serotonin and dopamine and lord >>knows what else, a brain kill whic is a neuroleptic type action.. >>the so called therapeutic effect reached on SRI’s after six weeks, >>is not an antidepressant one…but a tranqulizing one of a >>neuroleptic >>or partial chemicla lobotomy of the frontal lobe, upon 40 % of its >>cells being destroyed or made unusable. >>>Maybe you *need* to have suppression of liver enzymes for them to help >you >>>obtain a remission from depressive symptoms. >>SRI’s do inhibit and impair liver function by suppressing enzyme 2d6. >>Impairing the liver so it can no longer detoxify the blood of all the >>many environmental toxins 2D6 break down, leaving SRI users >>susceptible ot all manner of CANCER. >>Maybe that’s *why* it takes >>>weeks for there to be any effect. Serotonin-receptor binding takes place >>>within hours, but nothing happens for weeks. Why? >> Who you kidding? The first six weeks on an SRI is the most happening >>of times…SRI induced anxiety, agitation, ahathesia, hypomania, >>mania, paranoid delusions, suicidal ideations, homocidal ideations, >>OCD, PSYCHOSIs, weight loss, and on and on, until the poor brain cant >>take it, and KILLS its cells off to TRANQUILE itself in good old >>neuoleptic like action. >>>>And, the effect on dopamine cells is such, a lot of previously non >>>>drinkers wind up craving alchohol, and other stimulants shortly after >>>>begining a course of treatment of SRI’s >>>You have certainly failed in demonstrating a factual basis for your >>>hypothesis. If SSRIs kill these brain cells, as you suggest, they >certainly >>>could no longer induce dopamine-dependent cravings, now could they? >>Now you play dumb about the paradoxical reactions of the brain to >>psychotoxic chemcial.. >>How convenient! .
Response:
May 2, 2002
Question:
I have used neurontin for two years to relieve symptoms of depression. This drug is expensive but it is the most effective drug I have ever used. I do not respond well at all to antidepressants (they generally make me more anxious or far too ‘flat’ in mood, or in the case of tricyclics I get very angry and irritable/restless.). Recently I have been scaling down my neurontin dose, gradually. I am seven days, if not more, at my present dose, meaning there ought to be no withdrawal from the neurontin affecting me at present. However, I have become more depressed, fearful (‘terrorized’ is a word I prefer) and irritable than I have been in many months, possibly years. Here is the part I don’t understand: I am worse off now on a low dose of nuerontin (800 mg. or 400mg twice a day) than I was prior to the time I ever used neurontin (1998, 1997, using zero mg — none at all). So I am wondering if long term use of neurontin causes a permanent increase in severity of depression. In other words, if a person uses neurontin for many months, does that person alter his brain chemistry or body in some permanent way, in a way that makes that person forever dependent on neurontin? Put simply, is neurontin a drug that makes a person more sick over the long run? Is it nothing more than "booze" in a capsule? My questions are basically these: Does anyone here know of anyone who has suffered from long term use (2 years or more) of neurontin? Are there any studies or research out yet that suggest long term use of neurontin is damaging to a person’s emotional state? Is there any evidence, anywhere, that neurontin is useful for treating mood disorders? Put more directly, is it STUPID for anyone to be taking neurontin, despite the fact that it offers temporary relief, given that we (or I) know almost nothing about its long term effects? I ask these questions for a few reasons. One, neurontin is not a well understood drug (at least not here in the States) when used to treat emotional disorder. Two, I am one of those people who is highly suspicious of drug companies, a person who often believes that drug companies care only about cash flow, and will sell whatever they can with complete disregard to the health of their customers. Realize that the FDA here in the States has, in recent years, become more lax concerning what drugs are considered safe or legal. Realize also that the United States is in an incredible amount of debt, and that the basic idea here in the States at this time is "anything that is good for the economy is good." And what better way to generate commerce for a nation with a grave amount of debt than to get people ‘hooked’ on useless (or untested) drugs, if only to prop up the pharmaceutical companies for a few more years? If only to prop up the American economy a bit longer? Greed is a strong motivator, so I don’t consider myself paranoid. If people can get rich, legally, they will do it, with complete disregard of others. Most of the history of western civilization proves this to be true. The tobacco industry proves this to be true. No one needs to respond to those last remarks of mine (I don’t want to start a debate about the industry) but it is the way I envision the mental health industry here in the USA. I’m deeply suspicious of it (as well as everyone and everything else). I really do not believe, at the moment, that any institution of any kind here in the States, or any person, really wants to improve anyone else’s quality of life. I SEE no evidence of it. What I believe instead is that those in the mental health industry enjoy the money that flows in from people like me who are "sick" or from people who are purposely misdiagnosed or NEGLECTED so that they (me, and possibly you) can remain a permanent source of revenue (and be a "perpetual client") to whatever agency they choose for assistance, with greed being the motivator for all this. I mean, what better way to make money than to purposely mismanage someone’s mental health care? With a little luck, I may be hospitalized someday. More money for them. That’s how it all works, right? All that said, just having had a terrible day, I have taken an extra 400mg of neurontin two hours ago. I feel (and, I actually AM) ten or 100 times less worse than I was throughout this day. BUT…my experience with neurontin tells me that in 3 or 4 weeks, should I continue to take 1200mg of neurontin daily (instead of the 800mg I’ve been on for about a week), my experience with this drug tells me that after 3 or 4 weeks I will need to raise the dose yet again (to 1600mg). So what I am saying is that neurontin offers a great deal of relief (in my case) but only for a few weeks (possibly two months, maybe three at most). Short term relief, long term…BAD. Clearly I am very confused about what good neurontin actually is, so anyone who wishes to shed any light on this or share their experiences with this drug, please do. I will check back tomorrow. I see my "pill doctor" on Thursday. And thanks in advance to anyone who posts a timely reply to this. Bryan a severely depressed guy who just feels he is just a guinea pig, most of the time, and really hates those drug companies because they don’t seem to know, or care, what they are selling us, and that fucking pisses me off. And have a good day out there, each one of you. Or if you cannot have a good day, just please tell me what the F is going on. I don’t know who to believe. No one has convinced me they know anything at all. But maybe you guys got some ideas out there. And just to clarify things a little, my therapist, my psychiatrist and my two best friends are all saying, in essence, "take the damn pills, Bryan." But what do they really know? Not enough, that’s my guess. Thanks for reading.
Response:
hi Bryann… I take Neurontin, 2400 mg. daily. It’s combined with a couple of anti-depressants though (Celexa – 60 mg. and Remeron 10 mg.). I’ve been on this combination since mid February, but have been taking Neurontin since December. So far, this combo seems to be lifting me out of what is/was a very treatment resistant bout of depression. So for now, I am delighted something is working – but is it the Neurontin or Celexa? I can’t answer that. Your post really caught my eye, because I am HOPING that Neurontin is going to be a saving grace for me. I took Prozac for over 10 years, only to find that since last August it was pooping out on me. My pdoc got me up to 60 mg. a day and didn’t want to go any further. So I suspect by my recent history, and what I am reading on this newsgroup and elsewhere, that a lot of our psychiatric drugs have an "expiry date" for each individual. I believe what you are saying, regarding taking these (psychiatric) drugs and winding up being dependent on them. Although I haven’t read it yet, the book "Prozac Backlash" goes into how these drugs alter our neurotransmitters and receptors, potentially changing them forever. However, after struggling with being Bipolar II for about 20 years, if these drugs are "booze" then I guess I will have to call myself an alcoholic, as I really do need them to keep my life on track, and I will continue to take them. Your thoughts regarding drug companies are thoughts I have had as well. I too wonder if these drugs are being pushed to either make someone rich or pave the financial way for new drugs that will do the same. My cynical mind follows that theory, especially when you hear that many of the drugs sold in North America for dollars each are sold for pennies each elsewhere, substantiating that the cost to the consumer is based on what the economy can/will afford. So where does this leave me? Well, I still choose to have faith in the doctors treating me. I try to turn a blind eye to what I hear regarding drug company profits, etc. I try to focus on my health. If Neurontin doesn’t wind up being good long term for me (and it’s interesting that my pdoc is starting to talk about Depakote) I will move onto the next drug. Sorry I didn’t have any information regarding long term use… just wanted to share my thoughts with you. regards, Compucat >^+^<
> I have used neurontin for two years to relieve symptoms of depression. This > drug > is expensive but it is the most effective drug I have ever used. I do not > respond well > at all to antidepressants (they generally make me more anxious or far too > ‘flat’ in > mood, or in the case of tricyclics I get very angry and
irritable/restless.). – Hide quoted text — Show quoted text -> Recently I have been scaling down my neurontin dose, gradually. I am seven > days, > if not more, at my present dose, meaning there ought to be no withdrawal from > the neurontin affecting me at present. However, I have become more depressed, > fearful (‘terrorized’ is a word I prefer) and irritable than I have been in > many > months, possibly years. > Here is the part I don’t understand: I am worse off now on a low dose of > nuerontin > (800 mg. or 400mg twice a day) than I was prior to the time I ever used > neurontin > (1998, 1997, using zero mg — none at all). So I am wondering if long term use > of neurontin causes a permanent increase in severity of depression. In other > words, > if a person uses neurontin for many months, does that person alter his brain > chemistry or body in some permanent way, in a way that makes that person > forever > dependent on neurontin? Put simply, is neurontin a drug that makes a person > more sick over the long run? Is it nothing more than "booze" in a capsule? > My questions are basically these: Does anyone here know of anyone who has > suffered from long term use (2 years or more) of neurontin? Are there any > studies or research out yet that suggest long term use of neurontin is damaging > to a person’s emotional state? Is there any evidence, anywhere, that neurontin > is useful for treating mood disorders? Put more directly, is it STUPID for > anyone to be taking neurontin, despite the fact that it offers temporary > relief, > given that we (or I) know almost nothing about its long term effects? > I ask these questions for a few reasons. One, neurontin is not a well > understood > drug (at least not here in the States) when used to treat emotional disorder. > Two, > I am one of those people who is highly suspicious of drug companies, a person > who often believes that drug companies care only about cash flow, and will > sell whatever they can with complete disregard to the health of their > customers. > Realize that the FDA here in the States has, in recent years, become more lax > concerning what drugs are considered safe or legal. Realize also that the > United States is in an incredible amount of debt, and that the basic idea here > in > the States at this time is "anything that is good for the economy is good." > And > what better way to generate commerce for a nation with a grave amount of debt > than to get people ‘hooked’ on useless (or untested) drugs, if only to prop up > the pharmaceutical companies for a few more years? If only to prop up > the American economy a bit longer? > Greed is a strong motivator, so I don’t consider myself paranoid. If people > can get rich, legally, they will do it, with complete disregard of others. > Most > of the history of western civilization proves this to be true. The tobacco > industry proves this to be true. > No one needs to respond to those last remarks of mine (I don’t want to start a > debate about the industry) but it is the way I envision the mental health > industry here in the USA. I’m deeply suspicious of it (as well as everyone and > everything else). I really do not believe, at the moment, that any institution > of any kind here in the States, or any person, really wants to improve anyone > else’s quality of life. I SEE no evidence of it. What I believe instead is > that > those in the mental health industry enjoy the money that flows in from people > like me who are "sick" or from people who are purposely misdiagnosed or > NEGLECTED so that they (me, and possibly you) can remain a permanent source > of revenue (and be a "perpetual client") to whatever agency they choose for > assistance, with greed being the motivator for all this. > I mean, what better way to make money than to purposely mismanage > someone’s mental health care? With a little luck, I may be hospitalized > someday. More money for them. That’s how it all works, right? > All that said, just having had a terrible day, I have taken an extra 400mg > of neurontin two hours ago. I feel (and, I actually AM) ten or 100 times less > worse than I was throughout this day. BUT…my experience with neurontin > tells me that in 3 or 4 weeks, should I continue to take 1200mg of neurontin > daily (instead of the 800mg I’ve been on for about a week), my experience > with this drug tells me that after 3 or 4 weeks I will need to raise the dose > yet > again (to 1600mg). So what I am saying is that neurontin offers a great deal > of relief (in my case) but only for a few weeks (possibly two months, maybe > three at most). Short term relief, long term…BAD. > Clearly I am very confused about what good neurontin actually is, so anyone > who wishes to shed any light on this or share their experiences with this > drug, please do. I will check back tomorrow. I see my "pill doctor" on > Thursday. And thanks in advance to anyone who posts a timely reply to this. > Bryan > a severely depressed guy who just feels he is just a guinea pig, most of the > time, and really hates those drug companies because they don’t seem to know, > or care, what they are selling us, and that fucking pisses me off. And have > a good day out there, each one of you. > Or if you cannot have a good day, just please tell me what the F is going on. > I don’t know who to believe. No one has convinced me they know anything at > all. > But maybe you guys got some ideas out there. And just to clarify things > a little, my therapist, my psychiatrist and my two best friends are all > saying, in essence, "take the damn pills, Bryan." > But what do they really know? Not enough, that’s my guess. > Thanks for reading.
Response:
Thanks Sharon, because what you took the time to write (below) makes good sense, but it also tells me that I ain’t the only one who is busy weighing the pro’s and cons. I hear you loud and clear when you say "while depressed, I’m not really living at all" (paraphrased). Ain’t that the truth. While I’ve been decreasing my neurontin, I haven’t been living as well as I had been. I don’t know where the last month and a half went, but I sure as hell know I didn’t do much of anything. My doubts about medications are a daily struggle. Each time I take any pill I feel somewhat "foolish" for lack of a better word, and each time I take a pill I wonder if that pill is one too many. For reasons I can’t articulate well, I want to completely break free of the mental health system (no drugs, no nothing). I’ve tried three times to go "med-free." Each time was hell. So, sure, I’m damn desperate for relief ("sick of being sick") and so I will increase the dose again, probably from 800mg to 1600mg (and my doc will advise me to take 2400mg, as he always does). The Prfizer story I haven’t read yet, but I’ll check it out. And BTW, my diagnoses, for what they’re worth, range from severe depression to PTSD to schizoaffective to gender dysphoria (among others (!)), and I’ve tried about 15 drugs over about 10 years. What a mess this mental health business is. Neurontin, for me, certainly offers the best short term (and possibly long term) relief. Sadly, it dulls my thinking, limits and restrains my imagination, and I don’t have many dreams while sleeping. When taking neurontin at a high dose, I’m calm, but I’m not all there. It’s as if much of my brain function is curtailed. And when I begin resenting what the drug is doing to me, I cut back on the dose. And so, I’m always on this roller coaster, raising the dose and lowering it again. But overall my quality of life is better on a higher dose, at least in the short term (a few weeks or so). It’s my resentments about what the drug does to me, and my suspicions about the drug makers (Pfizer, eh?) — it’s these things that inevitably drag me down and wish I’d never heard of neurontin. Especially after a few months fly by and I say to myself, with my 2400mg of neurontin in my system, I say to myself "where did all of those months go?" I feel that high doses of neurontin for long periods of time (many months) do little more than rob me of time. And straying off topic a bit, there are some semi-political things here too. I’m a survivor of a horribly abusive mother. I’ll no doubt be angry at her as long as I live. Neurontin dulls my anger. Conceivably (though I have no criminal record or history of violence) neurontin isn’t helping me so much as it is protecting my mother. In other words, though I have no wish to go to prison or do any crimes, I wonder if the purpose of neurontin is simply to drug me into a passive state, so that the truth about what my mother did to me, and the severity of the damage she did, are neatly swept under the carpet. I see this as almost Orwellian. Drug the victims. Shut them up, with any drug, to protect the perpetrators: the true causes of so much mental illness in adults. No, I gain nothing by remaining angry at my mom. But last year I had this long talk with her throughout the summer. The gist of the discussion was me asking her "hey, why do I have to take drugs for something *you* did?" So, each time I take these pills, I feel as if I am not helping myself as much as I am helping my mother by erasing my anger. My mother was a terrorist. She terrorized me when I was young. I want her to pay for that. We have a place for terrorists, down there in Camp X-Ray. But no, American culture is one where we silence the victims. I take the drugs; my mother still enjoys her freedom. And that’s ass backwards, if anything is. It makes it all the more difficult for me to keep taking these drugs, and that’s the point I’m trying to make here. To be blunt, if America’s culture is making people sick, let’s stop drugging the people who are getting sick. Let’s, instead, imprison and drug the people who dictate how America works. I realize this is wildly idealistic (probably fantasy) but it’s how we should all think. Let’s attack mental health problemd at their sources. Let’s ask: what is causing so many people to have anxiety and emotional distress, to the point where people cannot function? Let’s not, as Americans so often do, resort to cleaning up the mess after the damage is done (drugging the wounded, the damaged, the "sick). I just keep wondering, every day, why me and people like me need to take medications in order to live good lives in the "best" nation on the planet. A nation with a lot of drug abuse and violence. A nation that seems to be set up in a way that makes people sick. There are, I’ve read, more and more cases of depression and mental health problems each year in this country (even prior to 9-11). This is not so in Mexico, a poor country, a place I don’t wish to go to. Does the industry create its own clients? Does Mexico have low rates of suicide and depression (and so forth) because it *lacks* the kind of mental health care system the USA has? Is American culture unhealthy and damaging? These are the things I wonder about each time I drug myself. And if any doc calls me paranoid, I reject such assessments. Maybe it’s time for Congress to investigate the entire U.S. mental health system. Or maybe that time has long passed. Who knows. I’ll read about what Pfizer is up to. Thanks for writing, Sharon, and good luck out there, and I’m sorry for rambling on so long. (This letter was posted to the newsgroup and e-mailed too.) – Hide quoted text — Show quoted text ->I won’t get into a debate over the good, bad, and the ugly over drug >companies, but you my find the following story of interest, as Pfizer >is under investigation for pushing Neurontin for disorders on which it >is not approved: >http://money.cnn.com/2002/03/14/news/companies/neurontin.reut/index.htm >Neurontin isn’t even approved in the U.S. for treatment of Bipolar and >other mood disorders such as depression, so I doubt if there is much >credible long term research out there on it’s effectiveness. >I think the part you don’t understand, can long term use of Neurontin >make depression worse, really can’t be answered, at this point anyway. >It boils down to would your depression be worse or progressed if you >had never taken Neurontin, or does long term Neurontin actually cause >one’s depression to become worse. I don’t think anyone knows the >answer to that question. I haven’t seen any evidence that it does make >it worse, but that does not mean it doesn’t exist. >I’m not going to tell you to "take the damn pills, Bryan", that would >be reckless and foolish on my part, but will however just give you the >take on my thinking. >I weigh the pitfalls of suffering chronic depression with the pitfalls >of taking medications for which the long term effects are not fully >understood or revealed. For me, and please note the caveat me, it’s a >no brainer. I take the pills. Some may think of me as a drug company >stock holder for doing so, but that is fine with me. >I choose to live my life as depression free as possible, with the main >relief coming from medication. I’ll take relief from depression, with >all of it’s ugly symptoms. If the long term use of psychiatric >medications takes 5-10 years off of my life, or causes an unknown >disease or condition down the road, I’m willing to take that risk. The >reason? When suffering from depression, I’m not really living anyway, >and am just a shell of my "normal" self. It’s a quality of life issue >for me. >I didn’t post the link to the news article to fuel any suspicion about >drug companies. I think knowledge is a good thing, and we should base >our decisions on as much factual information as possible, without the >hype and scare tactics one side or the other try to use to sway you to >their point of view. >I’m not trying to give you a lame non-answer, but in the end, it’s >Bryan’s decision, and Bryan’s decision only, and hopefully based on as >much factual evidence as possible. >Maybe those people saying "take the damn pills" see a difference in >you, that you can’t see. However, they don’t have to live with the >side effects, and possible long term effects of the meds. I would be >as bold as to tell you to get the prescription Thursday. That doesn’t >mean you have to get it filled, but it is there in case you decide to. >Explain to your Dr. how you feel, and if he/she can’t understand, they >are probably not a very good Dr. IMHO >Since you asked, Neurontin is an anti-convulsant. Other >anti-convulsants are used in the treatment of mood disorders, more >commonly bipolar disorder, such as Depakote and Tegretol, with varying >degrees of success. Some will say they are heavenly, others pure crap. >Anyway, I’m sure my rambling didn’t provide much help, but good luck >with your decision, whatever it may be. >Sharon
Response:
>Sorry I didn’t have any information regarding long term use… just wanted >to share my thoughts with you.
No problem. Hey, I tried Celexa and could hardly stay awake. I agree about these drugs having ‘expiry’ dates. I did okay on a tricyclic for almost 3 years, then hit the cellar, and can now no longer tolerate that one drug. It seems logical that all psychoactive things would work that way: if one uses enough of them, they no longer do as advertised. I hope the U.S. Surgeon General just read that. I can’t overstate the money thing, though, living in a country where not a single alcohol bottle or beer can has any kind of warning on it, with alcohol being more deadly, and certainly more debilitating, than tobacco. Well I got off topic. See y’all around.
Response:
March 20, 2002