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Methylone & 5-HT2B agonism

Several posts on this board and others say 'don't worry, doing 6-APB a few times a year isn't going to get you valvular hypertrophy'.

How is that? It is a very strong full agonist with a somewhat longish half life. Sound like a disaster hiding in the shadows to me.
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Go look at the fenfluramine debacle. It was initially thought to be safe and nobody noticed the cardiac valvular issues until people were taking it on a multi-dose-per-day regimen lasting months to years. (Also, people do use ergoloids with 5ht2b agonism, don't they?) So occasional use of APBs is probably going to be no more of an insult than any other serotonergic that hits 2b.

5HT2B, or not 5HT2B, that is the question?


(I'm here all week guys, try the veal and remember to tip your waitress.)
 
nickfurry said:
But I'm still curious about the very potent 5HT2b agonism of 6-APB etc. Isn't it quite likely that a lot of so called MDMA being sold these days is really a mix of benzofurans?

Several posts on this board and others say 'don't worry, doing 6-APB a few times a year isn't going to get you valvular hypertrophy'.

How is that? It is a very strong full agonist with a somewhat longish half life. Sound like a disaster hiding in the shadows to me.
Click to expand...

actually, at least in pills, we see that the quality right now is the best since ten years ago. up to now i also haven't seen any apb turn up in pills in the test results of the european test centers i check from time to time. it's a little surprising, but i guess it just isn't worth it if good mdma is doing the rounds anyway...

i'm also a bit sceptical because we haven't yet seen a high affinity full agonist like that. so while sekio should be correct, the 6-apb i bought will stay in the freezer for a few more years until we have more data ;)
 
If it makes you feel any better, consider that one A. T. Shulgin who had a habit of eating compounds with rather high affinity for 5ht2b (MEM is one of them) managed to evade valvulopathy for his whole life a long time.
 
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Didn't he have one of his valves replaced in his later years? Does anyone actually know why? Not that I think his valves were proliferated... just curious.
 
Taken from Wikipedia...
The chemistAlexander Shulginfirst popularized MDMA and MDA, and he invented DOI and many other recreational drugs that are also 5HT-2B receptor agonists. In 2008 Shulgin underwent surgery to replace a defective aortic heart valve. It is unknown whether or not Shulgin's lifelong use of psychedelic drugs caused the failure of his heart valve
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Well, fwiw Aortic valve problems are a "significant problem" in people of older age acording to the study below, but "aortic defect" is vague and the study below shows that aortic and mitral regurgitation are the two most common complications seen in fenfluramine users as a result of damaged valves.

It seems the aortic abnormalities are typically milder than what's seen with the mitral valve, in most cases at leasthttp://m.circ.ahajournals.org/content/101/17/2071.full). Not sure where I'm going with this, but I thought it's worth mentioning that aortic stenosis is common in the elderly. Even if his valves were proliferated, he had a good run!

Aortic regurgitation, mostly mild, was found in 29% of the entire study cohort.Conclusions. Calcific aortic valve stenosis constitutes a significant health problem in the elderly. Only a minority of those with potentially operable aortic valve stenosis undergo surgery.
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http://content.onlinejacc.org/mobile/article.aspx?articleid=1118660
 
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Sekio: you are not making your point very effectively %)

In any case, norfenfluramine (fenfluramine metabolite belived to be the cause of cardiopathy) is actually only a partial agonist, and its affinity for 5HT2b is less than half as strong as 5-APB, and ten times weaker than 6-APB! Further, clinical doses of fenfluramine seem to have been around 20-40 mg / day, which is obviously a much lower acute dose than typically used recrational doses of the benzofurans.

I'm not fully convinced of the 5HT2b agonism -> valvular hypertrophy hypothesis though. From what I gather, the original 1999 paper [1] warning of VH caused by fenfluramine was the origin of this hypothesis, they only did in vitro testing and it is not difficult to imagine other possible mechanisms. It doesn't seem impossible to me that evidenced fenfluramine-caused cardiopathy and a hypothesized general 5HT2b agonist caused cardiopathy are inadvertedly thrown together and confused.

I was unable to find further publications with in vivo data, but then I hardly know how to use google. So perhaps it's presumptious for a druggie nobody like me to second guess the scientists and doctors.

1) Possible Role of Valvular Serotonin 5-HT2B Receptors in the Cardiopathy Associated with Fenfluramine, Fitzgerald et al 1999, http://www.ncbi.nlm.nih.gov/pubmed/10617681
 
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About Shulgin, didn't he say he only tried each of his compounds once or twice? 2CB, supposedly one of his favorites, he only tried a handfull of times. I think it was in that Hamilton interview.
 
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