remedy for ssri induced brain damage?

[BilZ0r]

^ Yeah, I was going to bite on that one too, but I had better things to do.

 

[Kris Kristofferson]

wow. um... wow
you are an idiot
you took MDMA once a month for three years, and you are saying prozac harmed you?
if you want to give advice to people, READ about the topic at hand. Obviously experience has taught you nothing.

i apologize for this

 

[Kris Kristofferson]

You have to take the MDMA and the SSRI at the same time (or even the SSRI just a bit before) to get full protection, at 6 hours you get about 50% neurotoxicity...

is this true?
'full' protection sounds a little optimistic

 

[VelocideX]

is this true?
'full' protection sounds a little optimistic

Sounds good, but its not. Taking SSRI before MDMA almost completely blocks the effect. Failing that, it substantially attenuates it

 

[VelocideX]

modafinil is too expensive for me, so i take adrafinil, which is the same (adrafinil is broken down by your liver into modafinil) which is much cheaper, but a bit more work for your liver --- dont worry, your liver is evil and needs to be punished !

That's a really healthy philosophy =\

 

[Dr. Beat]

That's a really healthy philosophy =\

do i have to spell out sarcasm ?

 

[Dr. Beat]

Um dude. No. Not even close. If you take SSRIs 6 hours after MDMA you get a protection that is just able to be detected statistically, i.e. it is tiny. And their haven't been many (not that I doubt the results). You have to take the MDMA and the SSRI at the same time (or even the SSRI just a bit before) to get full protection, at 6 hours you get about 50% neurotoxicity...

...and still, this is all rat data, using IP dosing, rat-neurotoxicity doses, and likewise, huge fluoxetine doses.

Kris Kristofferson is completely correct, and I agree with him, though if I see either of you flaming in the Advanced Drug discussion I'm going to CLAWs you.

i would take 1 pill, NEVER more, and 3 hours later take an SSRI.

We would always take 2 litres of green tea with us, and eat prunes, or other friut high in anti-oxidents, and eat healthy food through out the night. People used to think we were crazy. So i dont think i burnt my brain out on MDMA like you are suggesting.

did that for 3 years, and after that i have had extremely high levels of seratonin compared to most people, and compared to what i used to have 10 years ago.

after hanging around the rave scene for 7 years, i have seen MANY people come and go, and when the 'leave' the scene, they generally have VERY low levels of seratonin, the opposite of me, so it was hard to relate to them on any level.

they started with high seratonin the first few months, and then went down hill each few months.

i started with low seratonin, and each year it kept going up and up.

lucky me !

 

[Dr. Beat]

How on earth do you know what your "dopamine level" is? Sure, selegiline will raise your dopamine levels in the short term, but after that how do you have any idea what it is? Homeostasis is going to operate to some degree.

that seems like a really dumb question, but i will answer it.

when my dopamine is high, i feel great, my mind is clear, my body feels light and energised, i get brain tingles, i talk alot, my face is expressive, my thoughts are quick, music sounds great, i am motivated.

when my dopamine is low, my mood is flat, a bit negative, my mind feels groggy, i am not excited about anything, music all sounds flat, my body feels like double gravity is on it, it is an effort to talk, i have low motivation.

i could go on, but you get the idea.

Since when was selegiline supposed to be a mood booster? It's not. It's used as an adjunct to levodopa for parkinson's patients. Either you're talking about the nootropic effect, which probably isn't related to dopamine levels and is related to propargylamine-like antiapoptic effects, or you're mistakenly trying to use it as a sustainable mood booster. There's certainly some mood boosting effect for the first week or two, but after that it declines.

it is often sold on internet sites as a mood booster. look them up if you dont believe me.

 

[BilZ0r]

^ Dude, what the hell...

when my dopamine is high, i feel great, my mind is clear, my body feels light and energised, i get brain tingles, i talk alot, my face is expressive, my thoughts are quick, music sounds great, i am motivated.

When you get those feelings, how the hell do you know that that coincides with "high dopamine" (whatever that means). Have you had a PET to tell you. You can't intuitively know when your dopamine is high.

after that i have had extremely high levels of seratonin compared to most people

Likewise, unless you've had a PET scan, or another kind of radiolabelling experiement, you can't know this.

Meanwhlie, if we closely examine the experimental evidence, Schmidt 1987, showed that a large dose (and I mean, massive 5mg/kg SC) fluoxetine, provided partial protection against MDMA induced 5-HT depletion, but as Schmidt and Taylor reported three years later, this was not mirrored in tryptophan dehydroxylase levels... and hence that neurotoxicity was still happening.

I mean think about it. You were taking a know neurotoxin, and a trying to prevent that neurotoxicity with a known, non-serotonergic neurotoxin. You ended up feeling bad. It makes sense, even excluding the scientific evidence, that it was caused by the neurotoxic drug, and not the non-neurotoxic drug.

 

[BilZ0r]

is this true?
'full' protection sounds a little optimistic

Nope, that's what the paper shows.
http://thedea.org/neurotoxicity.html#prozac

 

[VelocideX]

Just because selegiline is sold as a mood booster doesn't make it a mood booster.

It is, for a week or two, then tolerance sets in and you're back where you started.

 

[Dr. Beat]

^ Dude, what the hell...



When you get those feelings, how the hell do you know that that coincides with "high dopamine" (whatever that means). Have you had a PET to tell you. You can't intuitively know when your dopamine is high.

Likewise, unless you've had a PET scan, or another kind of radiolabelling experiement, you can't know this.

Meanwhlie, if we closely examine the experimental evidence, Schmidt 1987, showed that a large dose (and I mean, massive 5mg/kg SC) fluoxetine, provided partial protection against MDMA induced 5-HT depletion, but as Schmidt and Taylor reported three years later, this was not mirrored in tryptophan dehydroxylase levels... and hence that neurotoxicity was still happening.

I mean think about it. You were taking a know neurotoxin, and a trying to prevent that neurotoxicity with a known, non-serotonergic neurotoxin. You ended up feeling bad. It makes sense, even excluding the scientific evidence, that it was caused by the neurotoxic drug, and not the non-neurotoxic drug.

a year ago I was on Reboxatine everyday for 6 months, so I know what a NARI feels like and what it feels like to come off it.

I tried Survector a few years ago, so i know what a DARI feels like, and what it feels like to come off it.

I have trieds most SSRI's like Prozac (the least selective), Zoloft, Paxil, and Cipramil (the most selective) so i know what serotonin feels.

When people I know take l-tryptophan, they act a lot more like I do, and feel like I do a lot more.

i have also done stuff like take speed and after a few hours take propranolol (beta blocker) and low doses of chlorpromazine (strong alpha blocker) together to get maximum dopamine with minimum noradrenaline - it is a great combo !

right now i am on Ritalin and a very small dose of amisulpride which gives me lots of dopamine with very little noradrenaline - another great combo !

but i am sure my experiences mean nothing to you because they were not done in a lab - i give my subjective experiences more weight than your scientific experiments done in an artificial lab done on very unhappy rats. Each to their own truth i guess.

 

[BilZ0r]

Or many these drugs don't selectively "increase" any levels of any neurotransmitter. They have downstream effects, on many systems. How does selective DRIs feel? Do they feel like L-DOPA? No they don't. Do they feel like VTA stimulation? No they don't. Do they feel like dopaminergic selective amphetamines? No. Do they feel like dopaminergic agonists? No. All of these drugs which in your view should all feel the same in some cases feel very different (infact different selective DRIs can feel very different depending on their pharmacokinetic parameters). Hence your logic to me, makes no sense.