MDA vs. MDMA

[unodelacosa]

Could somebody who had both MDA and 6-APB compare their effects?

They are similar, and if you have the hydrochloride salt, they are about the same in dose with 6-APB maybe slightly more potent. But if you have the succinate salt, do note that it's ~36% less potent by weight compared to the HCl. Both drugs are mildly psychedelic but large doses of MDA get pretty trippy whereas 6-APB has more of a stimulant factor to it. MDA can get derpy and I pass out at the end of the roll, but 6-APB has more of an amphetamine-like kick to it. Also, the recovery from MDA afterward is harsher than 6-APB which I didn't feel was much challenge at all.

I've never been totally sold on any of the benzofuran ring-class ecstasy substitutes like it, including 5-APB, its n-methyl derivative, 5-MAPB, and 6-MAPB which switches the location of the solo oxygen atom in the furan ring to the opposite side of the ring. I've tried the "Borax combo" that's supposed to mimic MDMA, but it comes up short in my opinion. Nothing does what MDMA does in terms of sheer empathy and living in the present moment whilst being bathed in a wonderful anxiolysis, first and foremost, with MDA as a close runner-up (though distinct ☞ more psychedelia, less empathy). Yes, MDMA and MDA are neurotoxic, but then so is drinking ethyl alcohol. Brain cells die every single time one drinks booze, and it's a class 1 carcinogen to boot.

Benzofury drugs are probably cardiotoxic as they cause a good bit of tachycardia and show preference for the 5-HT2B serotonin receptor subtype. If you use them, avoid large doses and use very sparingly. Most people will consider 6-APB either "mellow" and "weak" with small to medium doses, or with larger doses, "speedy" and/or "gritty".

Dr. David Nichols and his group at Purdue studied 6-APB to determine if it could be a good, less-neurotoxic stand-in for MDMA that still affords a clinical utility for therapy. The trouble is, like I was saying it shows some 100 fold increase in affinity for the 5-HT2B receptor which regulates heart function while its norepinephrine/adrenergic activity leads to tachycardia. As such, just to reiterate the point: 6-APB is likely cardiotoxic, especially w/chronic use. But again, to be fair, cocaine is cardiotoxic, too, so occasional use of 6-APB probably won't dole out significant enough cardiotoxicity to worry about, in my estimate anyway, but I'm no cardiac specialist, and more research on this topic needs to be done to come to better conclusions regarding the extent of cardiotoxicity…

Despite all of this, demand for benzofury drugs has risen and accordingly so has the price most vendors I've seen are charging for them. We're not supposed to discuss exact drug prices per the forum rules, so I won't get into the details here beyond saying that the value proposition doesn't warrant the price, especially when one considers how the market value for the original compounds these would replace has dropped, likely thanks to an increase in global supply. Whenever this happens, the less scrupulous types start seeing dollar signs (or Euro marks, whatever, you get the gist), and it's important to test your drugs and consider doing "allergy test" amounts at first.

From Psychonautwiki:

6-APB is a serotonin–norepinephrine–dopamine reuptake inhibitor (SNDRI) with Ki values of 117, 150, and 2698 nM for the norepinephrine transporter (NET), dopamine transporter (DAT), and serotonin transporter (SERT), respectively.[4] 6-APB also possesses additional activity as a releasing agent of these monoamine neurotransmitters.[5]

6-APB is a potent full agonist of the serotonin 5-HT2B receptor (Ki = 3.7 nM)[4], with higher affinity for this target than any other site.[6] Moreover, unlike MDMA, 6-APB shows 100-fold selectivity for the 5-HT2B receptor over the 5-HT2A and 5-HT2C receptors.[6][7]

Aside from the 5-HT2B receptor, 6-APB has also been found to bind with high affinity to the α2C-adrenergic receptor subtype (Ki = 45 nM), although the clinical significance of this action is unknown.[4]

The potent agonism of the 5-HT2B receptor makes it likely that 6-APB would be cardiotoxic with chronic or long-term use, as seen with other 5-HT2B receptor agonists such as the withdrawn serotonergic anorectic fenfluramine

 

[Pastel]

They are similar, and if you have the hydrochloride salt, they are about the same in dose with 6-APB maybe slightly more potent. But if you have the succinate salt, do note that it's ~36% less potent by weight compared to the HCl. Both drugs are mildly psychedelic but large doses of MDA get pretty trippy whereas 6-APB has more of a stimulant factor to it. MDA can get derpy and I pass out at the end of the roll, but 6-APB has more of an amphetamine-like kick to it. Also, the recovery from MDA afterward is harsher than 6-APB which I didn't feel was much challenge at all........

This was a fantastic write-up! Thank you very much!

 

[someguyontheinternet]

5ht2b agonism doesn't lead to tachycardia but rather valvular fibrosis. It causes the heart valves to become stiffer which is irreversible at this point in time, that's the basis for the cardiotoxicity of 2b agonists. Tachycardia is mostly caused by the release of norepinephrine, NE release increases heart rate

 

[unodelacosa]

5ht2b agonism doesn't lead to tachycardia but rather valvular fibrosis. It causes the heart valves to become stiffer which is irreversible at this point in time, that's the basis for the cardiotoxocott of 2b agonists. Tachycardia is mostly caused by the release of norepinephrine, NE release increases heart rate

Yes, thanks for clarifying that, and I edited my comment to make clear it's the adrenergic activity that causes tachycardia. I didn't mean to conflate the two. However, it does increase the chances of cardiotoxicity, if not from being coupled with the 5HT2B agonism then if/when the heart experiences tachycardia from two separate sources, even including cardio activity. I understand this creates some kind of micro-tearing of the heart muscles which weakens it over time and could lead to infarction eventually. There's a paper on this somewhere; it even mentions the combination of Adderall and caffeine as being cardiotoxic. If you're interested in the paper and can't find it I'll try to search for it again.

This was a fantastic write-up! Thank you very much!

Sure thing. And again, I mean, don't get me wrong: I like the stuff and would probably use it again if the price is reasonable and the opportunity arises. It's kind of a Diet MDA, or perhaps MDA Lite™, if you will. "It's what E-mongers take when they're not rolling E!"® Lol. And the serotonin depletion hangover is so mild it's not a problem; you could even do it on a work night and be fine the next day at work more or less (depending on what you do, of course). That's probably the nicest thing about it. It's gentle on the afterglow, comedown, and feeling the following day. It doesn't murder my motivation like MDA and/or especially MDMA tend to do the following day.

 

[someguyontheinternet]

Myocardial infarction is a state of hypoxia whereas tears weakening the heart muscle make the person more prone to heart failure with reduced ejection fraction. Heart failure is different from a heart attack (infarction) where heart attacks are usually caused by blockage of some sort or if the person is experiencing tachycardia, independent of any tearing, the heart muscle uses more oxygen than can be supplied. This effect is worsened by vasoconstriction.

Heart failure from stretching of the heart muscle, causes a dilation of the left ventricle which is the chamber that pushes oxygenated blood into the aorta for general circulation. When the heart is stretched and weakened, it is no longer able to push blood through the system effectively which is sensed by the kidney activating the renin angiotensin system to drive vasoconstriction because the kidneys aren't sensing enough flow. This causes more stress on the heart and more stretching because its already weak leading to failure to pump.

Side note, there is another type of heart failure which is failure with preserved ejection fraction. This just means that the left ventricle is pushing out the correct proportion of blood but the amount is too small, this is the type commonly seen in users of anabolic steroids. The left ventricle undergoes hypertrophy just like any other muscle and thickens with regular exposure to cardiac load.

 

[unodelacosa]

tears weakening the heart muscle make the person more prone to heart failure with reduced ejection fraction

Oh yeah you're right. It's arterial blockage from a blood clot caused by plaque buildup that leads to a heart attack typically IIRC.

So heart failure with reduced ejection fraction would more likely be the result of damage to the heart muscle?
And you're saying stretching of the heart muscle is a separate form of heart failure?
And finally preserved ejection fraction is yet another form commonly seen with anabolic steroid users in which the left ventricle hypertrophies and thickens? And this is different from being "stretched and weakened", or is this essentially the same thing, you're saying when the heart muscle is stretched?

Muy interesante. Thank you for clarifying this.

@AutoTripper Check out this write-up, lol. Made me think of you: https://www.erowid.org/experiences/exp.php?ID=192

 

[someguyontheinternet]

Sorry I'm a little high rn so my writing is probably all over the place a bit lol

Heart attacks are usually caused by blockages yes, but they can be caused by tachycardia in an extreme enough fashion for extended periods because MI (myocardial infarction) in the end is hypoxia of the heart muscle. A blockage can prevent oxygenation but so can overuse of the muscle beyond the oxygen that the blood supply can handle, so tachycardia can lead to the heart running out of oxygen just like a blockage can but the damage these can cause are different but both are still MI.

Heart failure comes in two flavors like you said, with and without preserved ejection fraction. I'm not a cardiologist so there may be more nuance here but ejection fraction simply describes how much blood leaves the left ventricle divided by how much it holds which is why its a proportion, a fraction. When the muscle stretches and is too weak to fully contract, EF is reduced but when its too muscular, its preserved. The result of both situations is not enough blood being pushed through circulation.

To clarify the difference between the two in terms of change in the heart muscle, in preserved EF the heart muscle is strong but the chamber is too small. When its stretched and weak, the chamber is too big and can't push all of the blood out.

This diagram uses the older terms, systolic and diastolic heart failure where systole is the contraction phase where blood is pushed out of the ventricles and diastole is relaxation and filling of the ventricles.

Diastolic heart failure describes failure to fill sufficiently to support circulation.

Systolic heart failure describes failure to push enough blood out to support circulation.

 

[Holdan Caulfield]

I>

Myocardial infarction is a state of hypoxia whereas tears weakening the heart muscle make the person more prone to heart failure with reduced ejection fraction. Heart failure is different from a heart attack (infarction) where heart attacks are usually caused by blockage of some sort or if the person is experiencing tachycardia, independent of any tearing, the heart muscle uses more oxygen than can be supplied. This effect is worsened by vasoconstriction.

Heart failure from stretching of the heart muscle, causes a dilation of the left ventricle which is the chamber that pushes oxygenated blood into the aorta for general circulation. When the heart is stretched and weakened, it is no longer able to push blood through the system effectively which is sensed by the kidney activating the renin angiotensin system to drive vasoconstriction because the kidneys aren't sensing enough flow. This causes more stress on the heart and more stretching because its already weak leading to failure to pump.

Side note, there is another type of heart failure which is failure with preserved ejection fraction. This just means that the left ventricle is pushing out the correct proportion of blood but the amount is too small, this is the type commonly seen in users of anabolic steroids. The left ventricle undergoes hypertrophy just like any other muscle and thickens with regular exposure to cardiac load.

When you mention anabolic steroids causing this, would you include prescribed testosterone gel for legit low T from your GP?

 

[someguyontheinternet]

I>

When you mention anabolic steroids causing this, would you include prescribed testosterone gel for legit low T from your GP?

No, those therapies generally get people into the normal physiological range where anabolics go far above and beyond

 

[MedicinalUser247]

How come some people prefer MDA over MDMA ?

 

[Mr. Krinkle]

because it lasts longer and it makes you halookinate

 

[MedicinalUser247]

So, can an MDA like molecule that has a shorter chain be designed, but still have a psychoactive effect ? Or is MDA as short as it gets ?

 

[Esperighanto]

So, can an MDA like molecule that has a shorter chain be designed, but still have a psychoactive effect ? Or is MDA as short as it gets ?

You'd be referring to MDPEA here and as far as I'm aware it's inactive.

 

[MedicinalUser247]

What if it was 3,4-Methylenedioxy-phenyl-1-methanamine ?

 

[Esperighanto]

What if it was 3,4-Methylenedioxy-phenyl-1-methanamine ?

I'm curious as to where the 1 is on the phenethylamine skeleton, typically I refer to positions alpha, beta, N, 2, 3, 4, 5 and 6. By the name I'm assuming you're implying an extra methyl group on the N position, so the MDMA relative to MDPEA 's relationship to MDA, if that makes sense.

Idk if it's ever been bioassayed but I don't think expecting much would be smart given MDPEA 's low potency, and NMPEA's also low potency.

 

[MedicinalUser247]

Just thinking about stuff.

 

[Inspirialx9987]

Like once my old buddy said to me that some of the best nights of his party life were when he got his hands on a batch of Ecstasy pills that had a 70/30 ratio of MDMA/MDA. And now remembering those early millennium days of joy I definitely would say that as well. Especially when in the first 2-3 years 1-1,5 pills was more than enough to be a whole night me being everywhere in the club, in beginning mostly came alone in the club but never went out without at least 10+ new friends

 

[Mr. Krinkle]

i think these new pressed pills i got recently have both MDA and MDMA in them

sometimes it's hard to tell the difference - but usually the length of the trip is the main indicator


i have both separate mdma and mda and when i took them both a couple hours apart a few weeks ago, it was excellent

 

[Inspirialx9987]

I don´t have any more such amount of free time like 10-15 years ago and the last time I took some fine MDMA crystals, one good e pill what was a phenomenal time that night. But later days, as needed to travel back to work I had a nasty down experience, a depletion of serotonin and almost had a nervous breakdown because in the end, some minor shit happen that moment.. So decided it's enough for me what I eat I eat it. It´s ok when after a weekend of use I can have 3-4 days of sleep, relax and just take some time without any potential stress, giving my brain that build up again serotonin.

 

[unodelacosa]

I don´t have any more such amount of free time like 10-15 years ago and the last time I took some fine MDMA crystals, one good e pill what was a phenomenal time that night. But later days, as needed to travel back to work I had a nasty down experience, a depletion of serotonin and almost had a nervous breakdown because in the end, some minor shit happen that moment.. So decided it's enough for me what I eat I eat it.

It sounds like you took too much MDMA. That's when I get the worst hangovers – it's because I was chasing after a high that had already come and gone. I always end up paying for it whenever I attempt redosing more than just one ~80 mg booster.

I also have a regimen of vitamins and whatnot I take to ease the comedown and nourish my body. This includes magnesium chelate, CoQ-10, zinc, vitamin A & D, vitamin C and sometimes a mild benzo, and I do not do this when I have shit going on the next day. It isn't worth the strugglefest that it can cause.

Also worth noting: there's an idea I've read that opines that roughly 10 - 15% of MDMA is demethylated into MDA in the gut, and this is what leads to MDMA's psychedelia. I'm not so sure I believe this, but it's still interesting to consider, and not impossible that the body might demethylate MDMA and methamphetamine for that matter (demethylating into amphetamine).

It´s ok when after a weekend of use I can have 3-4 days of sleep, relax and just take some time without any potential stress, giving my brain that build up again serotonin.

That's a lot of sleep, just skipping the entire work week… lol, sounds nice though if highly unproductive following a decadent weekend of unproductive recreational drug use… just sayin'.