Disclaimer: Long post incoming.
Wouldn't this in itself cause at least some noticable behavioural effects immediately? And even if this was the case the likelihood of it occurring from first-time low doses of MDMA is just quite simply miniscule.
I see that saying that neurotoxicity would cause 'instant' effects may have been premature. Especially since SSRI's sometimes take weeks to work. Nevertheless, I still find it difficult to entertain the hypothesis that acute low doses of MDMA (as is reported by a lot of LTC posters) can induce long-term destruction of neurons only manifesting in any behavioural symptoms weeks or even months later.
We're really not disputing the existence of a LTC. Nor are we downplaying any of it's effects or the impact it has on your life and I'm sorry if it comes across that way. What we are disputing is the contention that it is a result of neurotoxicity. Just like your example there doesn't necessarily point toward any reason why dilantin causes Steven-Johnson syndrome, it just does in a very select few.
I don't know, I kind of have problems with determining causation from such a minority population. If Diliantin was the 'cause' of Steven-Johnson syndrome then the incidence would surely be much higher? Or, and as I feel with LTCs, we're missing something here and it's not really the 'cause' but instead a tiny factor in a large host of other more plausible reasons. From brief research of the syndrome it outlines some similar reasons to LTCs such as genetic disposition and weakened immune systems. Isn't it far more likely that these reasons predict those who develop Steven-Johnson syndrome with the drug either being a tiny factor or even entirely coincidental? Basically, it's too near to correlational rather than causal evidence.
Your definition of 'damage' is missing a pretty critical component. By your logic, simply growing up is a form of damage since the maturation process causes permanent alterations in brain function. Change and damage are not the same thing. Changes in brain function can be a good thing so you can't define them as 'damage'. I think a better definition would be: 'Any permanent change in brain anatomy or function that causes detrimental effects'. If we use that definition then it's a little harder to conclude that MDMA causes neurological damage. Even in the biased review which included Ricaurte and all sorts of bad science, posted by the OP, they suggest that the human evidence for behavioural effects are 'subtle'.
You post some interesting theories and there's no doubt you've spent a lot of time thinking about it. Dare I say you've spent a lot of time 'self-diagnosing' and obsessing over it which was one of BlueBull's possible explanations for such long-term effects. While your theories may go some way to explaining the case studies on BL, what about Dawglow's after comments? He admits it himself that it was all anxiety. And that once he realized that and was able to work on it he eventually recovered. Now he's even been taking MDMA again and seems to be back to 100%. So could Dawglow's relatively quick recovery perhaps reflect the fact he found the true cause of his LTC quicker than others? Another guy who recovered and posts the same account is Futura101. I remember when he used to post pretty obsessively about MDMA and seemed to be constantly researching why he was experiencing what he was. Me and him used to have pretty similar discussions to what we are having now. Now he realizes that that very behaviour was a large part of the problem. All of the people I know that have 'recovered' ended up agreeing with the skeptics. That's not to say it's the same for everyone.
I did not mean to scare people. I just meant to put forward a different account of why these LTCs occur. It just appeared intuitive to me that if MDMA can treat PTSD then it could also cause it somewhat paradoxically depending on how it was used. Of course it's entirely speculative, just somewhat logical to me. I'd also say that propagating the idea that a LTC is PTSD is no more scary than saying it's neurotoxicity. At least to me, suggesting that it could be 'psychological trauma' is less scary than saying it's 'brain damage'. Perhaps you disagree.
We had some discussion about this a while back but I'm still not entirely sure what this theory is all about. Can you explain the theory and why it's more solid?
Wouldn't this in itself cause at least some noticable behavioural effects immediately? And even if this was the case the likelihood of it occurring from first-time low doses of MDMA is just quite simply miniscule.
I see that saying that neurotoxicity would cause 'instant' effects may have been premature. Especially since SSRI's sometimes take weeks to work. Nevertheless, I still find it difficult to entertain the hypothesis that acute low doses of MDMA (as is reported by a lot of LTC posters) can induce long-term destruction of neurons only manifesting in any behavioural symptoms weeks or even months later.
We're really not disputing the existence of a LTC. Nor are we downplaying any of it's effects or the impact it has on your life and I'm sorry if it comes across that way. What we are disputing is the contention that it is a result of neurotoxicity. Just like your example there doesn't necessarily point toward any reason why dilantin causes Steven-Johnson syndrome, it just does in a very select few.
I don't know, I kind of have problems with determining causation from such a minority population. If Diliantin was the 'cause' of Steven-Johnson syndrome then the incidence would surely be much higher? Or, and as I feel with LTCs, we're missing something here and it's not really the 'cause' but instead a tiny factor in a large host of other more plausible reasons. From brief research of the syndrome it outlines some similar reasons to LTCs such as genetic disposition and weakened immune systems. Isn't it far more likely that these reasons predict those who develop Steven-Johnson syndrome with the drug either being a tiny factor or even entirely coincidental? Basically, it's too near to correlational rather than causal evidence.
Your definition of 'damage' is missing a pretty critical component. By your logic, simply growing up is a form of damage since the maturation process causes permanent alterations in brain function. Change and damage are not the same thing. Changes in brain function can be a good thing so you can't define them as 'damage'. I think a better definition would be: 'Any permanent change in brain anatomy or function that causes detrimental effects'. If we use that definition then it's a little harder to conclude that MDMA causes neurological damage. Even in the biased review which included Ricaurte and all sorts of bad science, posted by the OP, they suggest that the human evidence for behavioural effects are 'subtle'.
You post some interesting theories and there's no doubt you've spent a lot of time thinking about it. Dare I say you've spent a lot of time 'self-diagnosing' and obsessing over it which was one of BlueBull's possible explanations for such long-term effects. While your theories may go some way to explaining the case studies on BL, what about Dawglow's after comments? He admits it himself that it was all anxiety. And that once he realized that and was able to work on it he eventually recovered. Now he's even been taking MDMA again and seems to be back to 100%. So could Dawglow's relatively quick recovery perhaps reflect the fact he found the true cause of his LTC quicker than others? Another guy who recovered and posts the same account is Futura101. I remember when he used to post pretty obsessively about MDMA and seemed to be constantly researching why he was experiencing what he was. Me and him used to have pretty similar discussions to what we are having now. Now he realizes that that very behaviour was a large part of the problem. All of the people I know that have 'recovered' ended up agreeing with the skeptics. That's not to say it's the same for everyone.
I did not mean to scare people. I just meant to put forward a different account of why these LTCs occur. It just appeared intuitive to me that if MDMA can treat PTSD then it could also cause it somewhat paradoxically depending on how it was used. Of course it's entirely speculative, just somewhat logical to me. I'd also say that propagating the idea that a LTC is PTSD is no more scary than saying it's neurotoxicity. At least to me, suggesting that it could be 'psychological trauma' is less scary than saying it's 'brain damage'. Perhaps you disagree.
We had some discussion about this a while back but I'm still not entirely sure what this theory is all about. Can you explain the theory and why it's more solid?
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