Samuelg
Bluelighter
I've done amphetamine, MDPV, alpha-PVP, caffeine (high doses), 2C-E, 2C-D (it, 2C-E, and amphetamine were the best stimulants on the list, and it and amphetamine were the best), 2C-I, 2C-P, 2C-T-2, 2C-C-NBOME, 2C-I-NBOME, and 5-MEO-MIPT. I've consumed about a gram of 2C-E and 400 mg or so of 2C-P, 2C-I, 2C-T-2, AND 2C-D. I've consumed over 100 mg of 25C-NBOME and about half as much 25I! (Not all at once of course, I mean in my whole life) All of those stimulants that were also psychedelics were oftentimes taken as a stimulant rather than a psychedelic (not recommended, felt really good, but it can cause heart valve damage via 5HT-2B agonism and I can ACTUALLY feel my heart beating in my chest especially if I lay on my left side, before phenethylamine and pyrovalerone use this was not noticed, for whatever reason (placebo effect is entirely possible)). I've probably done more stimulants than a lot of people in this thread, and I certainly do like the feeling of stimulants. I do have interest in stimulants, there just doesn't appear to be any good ones on the research chemical market, besides amphetamine analogs. Just because I don't do shit stims like MPA doesn't mean my comments are backhanded or condescending. Your post sounds condescending to me, in fact. That's why I go on places like Bluelight, Pihkal, Tihkal, Erowid, so I can know if a chemical is shit before I acquire it. Not the best choice however, because you have to study Bluelight hard to get the proper warnings, and Erowid or Pihkal don't say shit about heart valve damage from 5HT-2B agonism.
wow, without the word almost this would be one of the worst posts on the board. When you say bad effects I assume you mean instant gratification, because the real bad effects from a drug like this come years later, or from overdose. Don't encourage people to get so inebriated they do not notice the damage they cause themselves.
Bluelight, Erowid and Pih/Tikhal dont say much if anything about the possible heart damage due to 5-HT2b agonism because it is something that accumulates over time and usually with constant and excessive use of a compound which is a known agonist. As such you can't expect such long term studies to exist for something like MPA for which only a few minor studies even mention. Any mentions of the pharmacodynamics of MPA would likely be speculation or fabricated, hence the lack of them.
Furthermore from what i understand of of the 5-HT receptors, and I'm perfectly happy to admit I could be wrong if anyone knows otherwise, the most common agonists that are used recreationally that affect the any of the 5HT receptors (non-selective) are psychedelics Psilocin and LSD. The agonists that affect the 5-HT2b receptors which as you pointed out linked to valvular damage by a mechanism that is unclear tend to be more in the empathogenic class of recreational drugs with MDMA and MDA being the most viable but also psychedelics such as DMT and Bromo-dragonfly.
The link between certain drugs and Cardiac fibrosis (thickening of the valves which is what i assume bloodshed is referring to) was first noted during the fen-phen withdrawl and deaths, the ingredient Fenfluramine was discovered to be powerful agonist of the then little known 5-HT2b receptor however studies show that whilst it was far too often to be considered safe in a prescribed drug often to be taken 3 times a day indefinitely, the actual incident rate of cardiac fibrosis from fen-phen were fairly rare.
The main problem i see with your seemingly slightly aggressive post is that no one knows if MPA is a 5-HT2b agonist, for all we know it could be an antagonist and the next cure of all heart disease but hasn't been noticed yet. Its relatively low euphoric quality would indicate it has moderately less serotonergic effects than some stimulants and substantially less than MDMA and the fact that it is chemically not a phenethylamine or amphetamine its a fairly hasty assumption to jump to that it has 5-HT agonist qualities at all let alone 5-HT2b.
Take for example sumatriptan, which i take at least 3 times a week for migraines, it is a close analogue of DMT (which is a strong agonist) sumatriptan has no psychedelic and a medically negligible agonistic quality on the 5-HT2b receptors.
Considering that MPA is a minor analogue separated from the nearest known 5-HT2b agonist by a considerable amount its reasonable to assume that its agonistic affect on the 5-HT2b is minor/negligible if it exists.
That being said I'm not saying it doesn't, given the appetite suppressing qualities of it and the occasional report of bowel issues (read:MPA shits

I would suggest that when it comes to being concerned about the cardiac effects of drugs 25i(presumably 25i-NBOMe), of which you have taken 50mg has a known 5-HT2b binding affinity of 231±73* and 25c (again, presumably 25c-NBOMe) of which you have consumed 100mg+ as it is part of the NBOMe phenethylamine family presumably (possibly not) has similar a similar binding affinity to 5-HT2b receptors should be more of a concern than MPA which thus far hasn't been found to be receptor binding or a ant/agonist to any of the 5-HT receptors.
*I'm aware binding affinity values have little impact on whether and to what degree something is an agonist or antagonist however if something cannot bind to a receptor the risk of stimulating or blocking that receptor is significantly reduced.