Question:

Linda I go off on some posts.. I think its not really a healthy thing to rub some bodies face in the ground or accuse them of being villainous. There just people with problems. Let things go Linda. Imho – Hide quoted text — Show quoted text – >Snip > I don’t know who’s Linda, who’s not > Linda, and I’m not going to try and figure it out. I do > appreciate  your ability, however. >Anna has no ability in that regard, at least as she is currently blinded by >so much hatefulness… >For you to suggest such, you seek to inflame me..since you certainly had no >problems yourself knowing I was posting as B’sCyberMistress! Going so far as >to attribute more to me than I actually posted,  falsely accusing me of >being Reclaim as well.. >So please do not carryon your efforts to bully emotionally  vulnerable >single mothers with medically fragile children in tow who seek a voice and >support here.. indirectly now, by encouraging Anna’s effort to keep things >divisive in this NG.. posting nonsense wherein she continues to attempt to >so hatefully alienate and isolate one of the posters this NG is intended to >support. >Its your and her continuing to post so hatefully after everyone else agreed >to stop leaving a unipolar depressive like Eric out in the cold.. support >wise..from where he became accustomed to being supported.  support he could >have really used right now..going through a difficult time >..you and Anna have no shame, even the events of the last few days seems to >have incited a change of priorties in Peter.. >Linda >.

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Response:

> Yup, that’s one thing prolactin does. I think that’s part of the problem of > medical science today, they can’t see the forest for the trees. > I’ve always doubted the simple but plausible serotonin-reuptake explanation > for the action of this class of antidepressants. Why? Because it takes weeks > before there’s any response.

that is kinda true….. Consider the serotoninergic street drugs MDMA > (Ecstacy) and LSD. All it takes is the time for them to migrate from the > digestive tract into the blood, and then across the blood-brain barrier. > Boom! They’re active.

i =knew= it. back in the ’80’s mda and extasy (the real stuff) were legal……. and we did *quite* lots of it….. ive long wondered if a lot of these meds were invented during the same experiments…… when i took the first paxil, i felt it within two hours. but then as i say, im sensitive to that stuff. but i felt considerably, completely ‘better’ in just a few hours. i knew it  wasnt placebo cause i took other meds that just made me sick, or made me feel worse. so i knew i could trust what i was feeling. i was able to feel the effect of paxil in just a few hours. but most people arent. i know they have no idea what it is or how it really actually works.  either way, its interesting to think about. > We’re just too damn complicated to make simplistic assumptions. > One decent theory of SSRI action involves the second-messenger known as a > G-protein. Kind of like a hormone that acts only inside one neuron, it > carries the signal from an activated receptor complex into the operating > machinery of the cell, perhaps telling it to begin making more or less of > some other chemical (probably an enzyme), which in terms makes another > chemical (a protein), which then itself might be active, or which may in > turn regulate yet another system. All this takes time.

its so much more complicated than we know right now, thats for sure. > There’s my philosophical stance. If you have any sort of question you’d like > me to try and answer, fire away. I need the distraction.

me too!!!!!! > Lar > P.S. I don’t know who’s who around here. I don’t know who’s Linda, who’s not > Linda, and I’m not going to try and figure it out. I do appreciate your > ability, however. Maybe I’m dyslexic in that regard.

it doesnt bother me. i just put out information like i said :)  it made some good friends of mine get angry with me and im sorry about that. but, i guess i felt it was important to let my friends know something about whats going on. i just put out what i see and know. thats what everyone does. its up to others to make their decisions from that. anna — blackbird singin in the dead of night take these broken eyes and learn to see all your life you were only waiting for this moment to be free ~

Response:

- Hide quoted text — Show quoted text -> Center for Study of Suicidal Behavior, Department of Neuroscience, New York > State Psychiatric Institute, 1051 Riverside Drive, 10032, New York, NY, USA > The prolactin response to dl-fenfluramine (an indirect central serotonin > agonist) challenge has been used to assess serotonergic function and appears > to > be blunted in depressed patients. We used this method to determine whether > the > serotonergic deficit in depressed patients is corrected by treatment with > paroxetine. > now ive taken paxil for the past 5 years. its made me non-suicidal > =many= times, as well as non-homicidal. if it wasnt from serotonin, was > it from prolactin? isnt prolactin the same chemical thats released when > a woman nurses her baby? > must have more info. > anna

Yup, that’s one thing prolactin does. I think that’s part of the problem of medical science today, they can’t see the forest for the trees. I’ve always doubted the simple but plausible serotonin-reuptake explanation for the action of this class of antidepressants. Why? Because it takes weeks before there’s any response. Consider the serotoninergic street drugs MDMA (Ecstacy) and LSD. All it takes is the time for them to migrate from the digestive tract into the blood, and then across the blood-brain barrier. Boom! They’re active. We’re just too damn complicated to make simplistic assumptions. One decent theory of SSRI action involves the second-messenger known as a G-protein. Kind of like a hormone that acts only inside one neuron, it carries the signal from an activated receptor complex into the operating machinery of the cell, perhaps telling it to begin making more or less of some other chemical (probably an enzyme), which in terms makes another chemical (a protein), which then itself might be active, or which may in turn regulate yet another system. All this takes time. There’s my philosophical stance. If you have any sort of question you’d like me to try and answer, fire away. I need the distraction. Lar P.S. I don’t know who’s who around here. I don’t know who’s Linda, who’s not Linda, and I’m not going to try and figure it out. I do appreciate your ability, however. Maybe I’m dyslexic in that regard. L

Response:

> Center for Study of Suicidal Behavior, Department of Neuroscience, New York > State Psychiatric Institute, 1051 Riverside Drive, 10032, New York, NY, USA > The prolactin response to dl-fenfluramine (an indirect central serotonin > agonist) challenge has been used to assess serotonergic function and appears > to > be blunted in depressed patients. We used this method to determine whether > the > serotonergic deficit in depressed patients is corrected by treatment with > paroxetine.

now ive taken paxil for the past 5 years. its made me non-suicidal =many= times, as well as non-homicidal. if it wasnt from serotonin, was it from prolactin? isnt prolactin the same chemical thats released when a woman nurses her baby? must have more info. anna Prior to treatment with paroxetine sixteen depressed patients – Hide quoted text — Show quoted text -> received a placebo challenge followed by a dl-fenfluramine challenge the > next day. The same two challenges were repeated after treatment. Prolactin > baseline levels were measured before pill administration, and then hourly > for 5 > hours. Fenfluramine/norfenfluramine levels were assayed at each time point > after drug administration. Treatment with paroxetine > significantly increased the baseline prolactin level independently of > treatment > response but positively correlated with paroxetine dose. We found that > pre-treatment prolactin response to dl-fenfluramine challenge did not > predict > clinical response to paroxetine, nor did the prolactin > response change significantly after treatment. There was no significant > difference in the post-treatment prolactin response between treatment > responders and treatment non-responders. We found evidence of increased > prolactin levels that may reflect effects of paroxetine in enhancing > serotonin > levels. Acute release of serotonin as measured by the prolactin response to > fenfluramine is not altered by paroxetine treatment. > — > Larry Hoover > de-blob before using ;-)

– blackbird singin in the dead of night take these broken eyes and learn to see all your life you were only waiting for this moment to be free ~

Response:

This article suggests that serotonin responsiveness is not altered by the SSRI Paxil. Food for thought. Prolactin Response to dl-Fenfluramine Challenge before and after Treatment with Paroxetine (Paxil). Dulchin MC, Oquendo MA, Malone KM, Ellis SP, Li S, Mann JJ. Center for Study of Suicidal Behavior, Department of Neuroscience, New York State Psychiatric Institute, 1051 Riverside Drive, 10032, New York, NY, USA The prolactin response to dl-fenfluramine (an indirect central serotonin agonist) challenge has been used to assess serotonergic function and appears to be blunted in depressed patients. We used this method to determine whether the serotonergic deficit in depressed patients is corrected by treatment with paroxetine. Prior to treatment with paroxetine sixteen depressed patients received a placebo challenge followed by a dl-fenfluramine challenge the next day. The same two challenges were repeated after treatment. Prolactin baseline levels were measured before pill administration, and then hourly for 5 hours. Fenfluramine/norfenfluramine levels were assayed at each time point after drug administration. Treatment with paroxetine significantly increased the baseline prolactin level independently of treatment response but positively correlated with paroxetine dose. We found that pre-treatment prolactin response to dl-fenfluramine challenge did not predict clinical response to paroxetine, nor did the prolactin response change significantly after treatment. There was no significant difference in the post-treatment prolactin response between treatment responders and treatment non-responders. We found evidence of increased prolactin levels that may reflect effects of paroxetine in enhancing serotonin levels. Acute release of serotonin as measured by the prolactin response to fenfluramine is not altered by paroxetine treatment. — Larry Hoover de-blob before using ;-)

Response: