03-22-2007, 02:15 PM
While leafing through Alexander Shulgin's book TIHKAL (a treatise on psychedelic tryptamines), I came accross a reference, to acid hydrolysis of caseine, producing some fairly fruity bits and pieces, among them, three caught my eye, namely 1-methyl-1,2,3,4-beta-carboline,1,3-dicarboxylic acid, and harman, harmalan and the last two compounds tetrahydro derivatives.
Harman, and the like, are beta-carbolines, basically, 3-(2-aminoethyl)indoles (tryptamines, such as serotonin, melatonin, acting as neurotransmitters, and some such as n,n-dimethyl-T acting as fairly potent hallucinogens), cyclized with an amino acid, or aldehyde, now, assuming some biological process is capable of performing such a hydrolysis of caseine, which us auties are known sometimes to be intolerant to, then a decarboxylation in vivo, of the above dicarboxylic acid to give 1-Me-1,2,3,4-beta-carboline, is quite probable.
Ok, thats the chemistry out of the way, beta carboline alkaloids occur naturally in many plants, some fungi, and some marine creatures, and quite a few act as monoamine oxidase inhibitors, or MAOIs, inhibiting the enzymes that detoxify dietary amines such as tyramine, and affecting metabolism of such neurotransmitters as serotonin and dopamine, MAOIs are clinically used as antidepressants, although rarely used nowadays, because of some fairly severe side effects, including CNS stimulation, and if food containing tyrosine is eaten, which gets decarboxylated in the body to tyramine, causing a severe hypertensive crisis.
So, anyone got any input to share on this idea? caseine is known to be a culprit in causing hyperactivity and dietary sensitivity, I propose that instead of hydrolysis to form endogenous peptides with opioid-like activity, which being big, bulky protein chains, would be pretty unlikely to cross the lipophillic blood-brain barrier, even if they did "leak" from a compromised intestine, caseine might just instead, or even alongside the opioid peptide theory, be getting metabolised to some of these beta-carboline MAOIs, and from then, going on to cause the hyperactivity.
My apologies in advance for being unable to provide references, I haven't had the ability, or time, since getting out of prison, to get online and dig them up, if they exist, as my sole internet access is through the local library, this is just an idea, based on some chemical references, that although not in any way geared towards autism, are quite feasibly interacting in this way.
Harman, and the like, are beta-carbolines, basically, 3-(2-aminoethyl)indoles (tryptamines, such as serotonin, melatonin, acting as neurotransmitters, and some such as n,n-dimethyl-T acting as fairly potent hallucinogens), cyclized with an amino acid, or aldehyde, now, assuming some biological process is capable of performing such a hydrolysis of caseine, which us auties are known sometimes to be intolerant to, then a decarboxylation in vivo, of the above dicarboxylic acid to give 1-Me-1,2,3,4-beta-carboline, is quite probable.
Ok, thats the chemistry out of the way, beta carboline alkaloids occur naturally in many plants, some fungi, and some marine creatures, and quite a few act as monoamine oxidase inhibitors, or MAOIs, inhibiting the enzymes that detoxify dietary amines such as tyramine, and affecting metabolism of such neurotransmitters as serotonin and dopamine, MAOIs are clinically used as antidepressants, although rarely used nowadays, because of some fairly severe side effects, including CNS stimulation, and if food containing tyrosine is eaten, which gets decarboxylated in the body to tyramine, causing a severe hypertensive crisis.
So, anyone got any input to share on this idea? caseine is known to be a culprit in causing hyperactivity and dietary sensitivity, I propose that instead of hydrolysis to form endogenous peptides with opioid-like activity, which being big, bulky protein chains, would be pretty unlikely to cross the lipophillic blood-brain barrier, even if they did "leak" from a compromised intestine, caseine might just instead, or even alongside the opioid peptide theory, be getting metabolised to some of these beta-carboline MAOIs, and from then, going on to cause the hyperactivity.
My apologies in advance for being unable to provide references, I haven't had the ability, or time, since getting out of prison, to get online and dig them up, if they exist, as my sole internet access is through the local library, this is just an idea, based on some chemical references, that although not in any way geared towards autism, are quite feasibly interacting in this way.

