DMAA Alternative

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  1. Quote Originally Posted by lronFist View Post
    Coclaurine is the main metabolite via COMT, and it is a peripheral anti-stimulant (1). It won't make it pass the human BBB either. The first point is important because higenamine, which is indeed stimulatory to adrenergic receptors, has an incredibly short half-life and its main metabolite is distinctly anti-stimulatory.

    (1) jstage. jst. go. jp/article/jphs1951/50/1/50_1_75/_pdf
    Great find!

    Note: a www. addition is mandatory for that link to open. Reading now.

    So it appears it might not only be anti-stimulatory but also ergolytic during exercise...


  2. Quote Originally Posted by mr.cooper69 View Post
    Great find!

    Note: a addition is mandatory for that link to open. Reading now.
    My post count needs to be 150 before I can post links.
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  3. Quote Originally Posted by lronFist View Post
    Coclaurine is the main metabolite via COMT, and it is a peripheral anti-stimulant (1). It won't make it pass the human BBB either. The first point is important because higenamine, which is indeed stimulatory to adrenergic receptors, has an incredibly short half-life and its main metabolite is distinctly anti-stimulatory.

    (1) jstage. jst. go. jp/article/jphs1951/50/1/50_1_75/_pdf
    Yes, that article I have seen. Some comments on the ACD/I-Lab predictions for crossing BBB are unfortunately only on rodent model.

  4. Quote Originally Posted by lronFist View Post
    My post count needs to be 150 before I can post links.
    I have the same problem, and find it annoying.

  5. DMAA is irreplaceable!!
    Anabolicminds.com Featured Author
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  6. Quote Originally Posted by lronFist View Post
    Coclaurine is the main metabolite via COMT, and it is a peripheral anti-stimulant (1). It won't make it pass the human BBB either. The first point is important because higenamine, which is indeed stimulatory to adrenergic receptors, has an incredibly short half-life and its main metabolite is distinctly anti-stimulatory.

    (1) jstage. jst. go. jp/article/jphs1951/50/1/50_1_75/_pdf
    So I reread the pointed out article. Now, biochemistry is only my hobby so I am sorry if my following speculation is totally wrong.

    The test in that article has been conducted on the heart muscle and I presume you ware referring to the results in influence of calcium ion channels by higenamine and coclaurine? I have reread numerous times the chapter 5 (pp. 65-77) in book called Voltage-Gated Ion Channels as Drug Targets (ISBN 3-527-31258-7) and also found well summarized info on wiki about different types of calcium channels. It appears that L-type channels are mostly concentrated in cardiac muscle (the tissue used in the article), while in brain there are mostly P-type, Q-type and N-type of channels. Is it therefore correct to judge the possible CNS activities of Higenamine and Coclaurine in the brain, based on the test performed on L-type of channels?

  7. Quote Originally Posted by Kelt View Post
    So I reread the pointed out article. Now, biochemistry is only my hobby so I am sorry if my following speculation is totally wrong.

    The test in that article has been conducted on the heart muscle and I presume you ware referring to the results in influence of calcium ion channels by higenamine and coclaurine? I have reread numerous times the chapter 5 (pp. 65-77) in book called Voltage-Gated Ion Channels as Drug Targets (ISBN 3-527-31258-7) and also found well summarized info on wiki about different types of calcium channels. It appears that L-type channels are mostly concentrated in cardiac muscle (the tissue used in the article), while in brain there are mostly P-type, Q-type and N-type of channels. Is it therefore correct to judge the possible CNS activities of Higenamine and Coclaurine in the brain, based on the test performed on L-type of channels?
    In cardiac tissue, activating the beta-1 receptor increases cAMP which enhances calcium release from the sarcoplasmic reticulum via PKA. This is why higenamine is an inotrope. The study cited above notes that the 6-OH on the tetrahydroisoquinoline is a necessary constituent for beta receptor activation. COMT removes this constituent by way of creating a methoxy group (i.e. creating coclaurine).

    cvpharmacology. com/cardiostimulatory/beta-receptors-Gs.gif <---(This image may help).

    As I have already mentioned, neither higenamine nor colclaurine have access to the CNS, and probably do not interact directly with calcium channels.

  8. Quote Originally Posted by lronFist View Post
    In cardiac tissue, activating the beta-1 receptor increases cAMP which enhances calcium release from the sarcoplasmic reticulum via PKA. This is why higenamine is an inotrope. The study cited above notes that the 6-OH on the tetrahydroisoquinoline is a necessary constituent for beta receptor activation. COMT removes this constituent by way of creating a methoxy group (i.e. creating coclaurine).

    cvpharmacology. com/cardiostimulatory/beta-receptors-Gs.gif <---(This image may help).

    As I have already mentioned, neither higenamine nor colclaurine have access to the CNS, and probably do not interact directly with calcium channels.
    Oh, I see, this is how it goes when I read something outside of my area after midnight.

    However, I cannot stop wondering that the prediction in ACD/I-Lab can be so wrong. They use predictions of LogPS (rate of brain penetration), LogPB/LogBB (extent of brain penetration) and Log(PS*fu, brain) (Brain/plasma equilibration rate) as a measure of “brain penetration sufficient for CNS activity”. There are numerous nicely writer articles about efforts on estimating accurate predictions of new compounds’ properties.

    Did you have a look at this tool?
    ilab.acdlabs.com/iLab2 (I use your trick )

  9. PA what led you to look for DMAA in the first place? Was it a quest to find an ephedrine alternative? Do you have an interest in finding an alternative to DMAA? If no what would it take to generate an interest in such?

    Thank you for your time.



  10. Quote Originally Posted by pushinweightw View Post
    PA what led you to look for DMAA in the first place? Was it a quest to find an ephedrine alternative? Do you have an interest in finding an alternative to DMAA? If no what would it take to generate an interest in such?

    Thank you for your time.
    +1
    These are really good questions.

  11. Quote Originally Posted by Patrick Arnold

    In Sweden u can be apprehended by police if they suspect you are using anabolic steroids. suspicion can be simply having extraordinary muscle mass. this happened to IFBB bodybuilders that were visiting sweden recently.
    At least one (Tony Freeman) was arrested and forced to submit urine if i recall
    The X-man had been to Holland a couple of days before going to Sweden. In Holland he smoked a joint, which explains the narcotics. He also had prescriptions for his aas, which cleared him from the drug use. I think he lost a contract with a supplement company because of his arrest.

    Norway is more strict than Sweden, but one is allowed to use aas.

  12. Quote Originally Posted by Patrick Arnold
    DMAA is irreplaceable!!
    Before a workout with ......?
    As a fatburner?

  13. Quote Originally Posted by HITFrank View Post
    Before a workout with ......?
    As a fatburner?
    both, Clear Shot, its all you need
    E-PHARM Nutrition Representative
    Better one ugly truth than a million pretty lies
    Check Out Ur-Spray and D-Serine at Prototype Nutrition




  14. Quote Originally Posted by pushinweightw View Post
    PA what led you to look for DMAA in the first place? Was it a quest to find an ephedrine alternative? Do you have an interest in finding an alternative to DMAA? If no what would it take to generate an interest in such?

    Thank you for your time.
    +1
    I've got an add-odd question for PA: How long did it take you to finally settle on DMAA and how many different substances did you research before deciding DMAA was the way to go?

  15. Quote Originally Posted by HITFrank View Post
    Norway is more strict than Sweden, but one is allowed to use aas.
    Interesting, is it not that essential amino acids in the free form are considered as pharmaceutics in Norway?

  16. Quote Originally Posted by pushinweightw View Post
    PA what led you to look for DMAA in the first place? Was it a quest to find an ephedrine alternative? Do you have an interest in finding an alternative to DMAA? If no what would it take to generate an interest in such?

    Thank you for your time.
    it was to find a replacement for ephedrine yes

    and i was researching a different area when i came across a reference that mentioned dmaa. since i had never heard of it and was curious i did a literature search on the chemical and found articles that suggested it might be a decent cns stimulant

    i have tried to find an alternative to dmaa. i have come across candidates, but none of them have evidence of being natural. thats the problem
    Anabolicminds.com Featured Author

  17. Quote Originally Posted by HITFrank View Post
    Before a workout with ......?
    As a fatburner?
    nothing makes you feel like dmaa makes you feel. thats what i mean
    Anabolicminds.com Featured Author

  18. Quote Originally Posted by Ceredumbellum View Post
    +1
    I've got an add-odd question for PA: How long did it take you to finally settle on DMAA and how many different substances did you research before deciding DMAA was the way to go?
    i had tried a few out such as halostachine and found they sucked. i also tried NMT back then. when we tried dmaa we knew immediately it was great
    Anabolicminds.com Featured Author

  19. Quote Originally Posted by Kelt View Post

    Interesting, is it not that essential amino acids in the free form are considered as pharmaceutics in Norway?
    They used to, you can buy junk L-Glutamine now. When it comes to supplements Sweden is still more liberal..

  20. Quote Originally Posted by Patrick Arnold View Post
    nothing makes you feel like dmaa makes you feel. thats what i mean
    Pat, how safe do you think it is to take DMAA and ephedrine together but without any caffeine? I would like to get the bronchodilation effects of ephedrine and the "feeling" of DMAA...

  21. Quote Originally Posted by Patrick Arnold View Post
    i had tried a few out such as halostachine and found they sucked. i also tried NMT back then. when we tried dmaa we knew immediately it was great
    I presume that what is special with DMAA is that the molecule is methylated on the alpha position protecting the amine from MAO? Also due to only a partial phenyl ring structure it cannot be considered as amphetamine analog?

    The pity with most PEA analogs (including halostachine) is the lack of the amine protection, due to the “nakedness” on alpha position.

  22. Quote Originally Posted by Patrick Arnold View Post
    i had tried a few out such as halostachine and found they sucked. i also tried NMT back then. when we tried dmaa we knew immediately it was great
    On a side note, as I see that you also experimented with NMT which is a tryptamine with poor oral bioavailability (according Shulgin, #50 in Tihkal).

    Now I do not exactly know the laws around tryptamines, but did you researched the possibility of finding a legal and natural tryptamine with good oral bioavailability and use it as a stimulant? Do you know about Dr. James Fadiman’s work on micro dosing psychedelics? It seems that a micro dose have a good stimulant with anti-depressive properties. Now, I understand that you cannot use what Fadiman experimented with, but I suppose, that there may be a similar compound in structure and properties as of those that are already scheduled?

    EDIT: Hmmm, I probably was too quick with assuming that NMT is N-Methyltryptamine, while you probably meant N-Methyltyramine? However, the question still stands, since tickling the serotonergic receptors seems to produce very noticeable stimulatory effects.

  23. Quote Originally Posted by Kelt View Post
    On a side note, as I see that you also experimented with NMT which is a tryptamine with poor oral bioavailability (according Shulgin, #50 in Tihkal).

    Now I do not exactly know the laws around tryptamines, but did you researched the possibility of finding a legal and natural tryptamine with good oral bioavailability and use it as a stimulant? Do you know about Dr. James Fadiman’s work on micro dosing psychedelics? It seems that a micro dose have a good stimulant with anti-depressive properties. Now, I understand that you cannot use what Fadiman experimented with, but I suppose, that there may be a similar compound in structure and properties as of those that are already scheduled?

    EDIT: Hmmm, I probably was too quick with assuming that NMT is N-Methyltryptamine, while you probably meant N-Methyltyramine? However, the question still stands, since tickling the serotonergic receptors seems to produce very noticeable stimulatory effects.
    What serotonergic drugs do you find stimulating?

  24. Sheeezus, well, most of that is waaay over my head. But what i do know is, when using DMAA and a strong coffee i can sit and read and really focus and take in what i'm reading OR i can go to the gym and do a 1 1/2 hour super-intense leg and ab workout!!!

    Not many other stimulants can give me those options.

  25. Quote Originally Posted by lronFist View Post
    What serotonergic drugs do you find stimulating?
    Well Dr. Fadiman was experimenting with LSD in 25mcg doses, or rather he asked volunteers to report their experience with such a small doses. This due to the fact that LSD was already scheduled. The same effect has been reported from users of psilocybe mushrooms, where the definition of micro dose is a fifth of the normal dose. Both LSD and Psilocin/Psilocybin are agonists of 5-HT_2A, 5-HT_2C and 5-HT_1A serotonergic receptors. If you spend some time searching the net there is plenty of anecdotal reports from people who tried it and it worked for them. There are unfortunately no legit published papers about this is due to the halting of all research with psychedelic compounds in 60ies. However I am convinced that if there is an unscheduled natural and active compound stimulating these three types of serotonergic receptors, it will produce a quite notable stimulant like (full off energy, focused, well productive) effect at very small doses.

    EDIT: Double checked on the dose Fadiman used for the study, it was 10mcg not 25mcg.
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