Hammilton
Bluelighter
- Joined
- Sep 2, 2008
- Messages
- 3,435
You'd have to take so much as to get rid of MAO-A and MAO-B.
While MAO-B is only effective against dopamine and phenethylamine and possibly one or two other very simple monoamines closely related to dopamine, MAO-A is effective against 5HT and NE-like monoamines, AND dopamine-like monoamines.
Sure, it's reasonable to believe that there is some variation on human MAO levels. However, the variation needed here would be pretty extreme. Possible, sure, but given that MAO is possibly one of the most important enzymes in the body, enabling us not to die from eating anything with much tyrosine and tyramine. Unfortunately, they're both rather ubiquitous in our diets.
It's not reasonable to believe that he had accidentally taken an MAO-I. If he had done so, four grams would have resulted in death. Both mitragyna, who I've been talking to about this, and I have overdosed on this drug. It's very easy to do, unfortunately- and our doses were no where near four grams. They were nowhere near a gram. Not even close to half a gram. Maybe a 250mg (1/4 gram).
Phenethylamine is a TAAR agonist, however. If there is any activity at all associated with PEA in un-deMAO'd people, it's likely to result only from TAAR agonism. TAAR agonism may produce some anxiolytic effect, but (so far) there's no indication that selective agonists will be recreational.
I'm not concerned with what Shulgin has to say about the subject; his analysis is useful in understanding the qualitative nature of psychedelics (where even with similar binding affinities and ratios, the qualitative nature may be consistently different and remarkably constant) but it's not really useful here. Sample size is much too small, there's no control, subjects aren't administered the drug blind (as far as I can tell, anyway). However, there is lots and lots of research on the subject of PEA.
Interestingly, while I was researching the subject, I came across this http://archpsyc.ama-assn.org/cgi/content/full/63/11/1209
It finds significantly elevated MAO-A levels in untreated depressed patients. I should look into comparisons between SSRIs, TCAs and MAO-A inhibitors in depression treatment. I wonder if MAO-A inhibitors are way more effective or not. I suspect not, given the efficacy of imipramine.
While MAO-B is only effective against dopamine and phenethylamine and possibly one or two other very simple monoamines closely related to dopamine, MAO-A is effective against 5HT and NE-like monoamines, AND dopamine-like monoamines.
I lean towards believing his claims. I have heard it said many times that PEA's effects are noticeable without an MAOI if administered at very high doses. (I know what Shulgin et al say on the matter, but presumably he didn't test it on that many people; some may have naturally fairly low levels of MAOs and others naturally high levels. Perhaps Shulgin's were all high end of the continuum in terms of MAO concentrations.)
Sure, it's reasonable to believe that there is some variation on human MAO levels. However, the variation needed here would be pretty extreme. Possible, sure, but given that MAO is possibly one of the most important enzymes in the body, enabling us not to die from eating anything with much tyrosine and tyramine. Unfortunately, they're both rather ubiquitous in our diets.
It's not reasonable to believe that he had accidentally taken an MAO-I. If he had done so, four grams would have resulted in death. Both mitragyna, who I've been talking to about this, and I have overdosed on this drug. It's very easy to do, unfortunately- and our doses were no where near four grams. They were nowhere near a gram. Not even close to half a gram. Maybe a 250mg (1/4 gram).
Phenethylamine is a TAAR agonist, however. If there is any activity at all associated with PEA in un-deMAO'd people, it's likely to result only from TAAR agonism. TAAR agonism may produce some anxiolytic effect, but (so far) there's no indication that selective agonists will be recreational.
I'm not concerned with what Shulgin has to say about the subject; his analysis is useful in understanding the qualitative nature of psychedelics (where even with similar binding affinities and ratios, the qualitative nature may be consistently different and remarkably constant) but it's not really useful here. Sample size is much too small, there's no control, subjects aren't administered the drug blind (as far as I can tell, anyway). However, there is lots and lots of research on the subject of PEA.
Interestingly, while I was researching the subject, I came across this http://archpsyc.ama-assn.org/cgi/content/full/63/11/1209
It finds significantly elevated MAO-A levels in untreated depressed patients. I should look into comparisons between SSRIs, TCAs and MAO-A inhibitors in depression treatment. I wonder if MAO-A inhibitors are way more effective or not. I suspect not, given the efficacy of imipramine.