DAA - Q&A with Dr. Dana Houser

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  1. DAA - Q&A with Dr. Dana Houser


    I figured I'd help you out in regards to starting a new thread for DAA.

    Here is the question posted over in the other thread:

    I love DAA but it causes my existing estro gyno to flare up big time. I have read where others have this same problem. I have also seen bloods where it is shown that DAA increases both estro and prolactin and reduces the T/E ratio. Have you seen any of these issues with your experimentation? Moreover, would you suggest the continued use of DAA in individuals with documented low T having gyno issues with the addition of a good AI?

    I, and I'm sure many others, would love your input/insight to this regard. Do you suggest stacking anything w/ DAA if you're prone to any of these sides, or even just nervous about them?


  2. Thanks for the thread assistance. DAA has generated a LOT of interest in the body composition world and that is perhaps needless to say, but the original studies were VERY intriguing and it seemed like finally we had a true "holy grail" as the dust settled on yet another crop of PH/PS/DS agents. "Slowly" but surely, sports nutrition companies began using this compound and with fever trying to jump on perhaps the next big thing. When I gave a presentation at the ISSN meeting in 2010, 13 products had already been introduced on the sports nutrition side probably in about an 8-month timeframe that included this ingredient or were solo products!

    Anyone who is shifting the HPGA (for people familiar with my writing, you know I do not care for the term HPTA as "T" can mean "Testicular" but also "Thyroid" axis in that setting; so I reserve HPGA for the testes where "G" stands for "Gonadal" and then I leave the HPTA in tact for the thyroid side) can certainly be susceptible to side effects and this is dependent (as many other things) on so many different variables. We'll take estrogen and prolactin in turn because those were the things mentioned.

    Estrogen: if we increase testosterone, there is a good chance you will be susceptible to aromatic conversion (the so-called diversification pathway in androgen metabolism)...this is dependent upon a host of things; one more prominent among them would be bodyfat % and keeping in mind that the higher the bodyfat%, the higher the levels of aromatase and higher test levels converting. The unfortunate thing is that the picture doesn't stop there...there are 1000s of things in the environment that increase SHBG. If you suffer concomitant SHBG increases which is even impacted by compounds some companies think they are putting in to make their DAA product "different" may wreak further havoc on the system. See, the unfortunate thing is that SHBG has a higher affinity for testosterone as compared with estrogen. Hopefully you can see how this would be a problem. Picture the coupling now of increased aromatic conversion with higher levels of SHBG with a higher affinity for androgen as opposed to estrogen. So, higher levels of E + lower levels of Free T is a pretty bad pairing I think you'd agree.

    Prolactin: This appears to be an issue with long-term administration; not necessarily the short term. We just don't accurately know how to define long-term and short-term. Is long-term defined as anything greater than 12 days (original Italian study data); my suspicion is not from my own data...but probably greater than about 1.5-3 months of straight use. This is not to suggest everyone will have issues. I myself used 3.12 grams of DAA for a full year without concomitant changes in prolactin levels. Keep in mind, prolacin will act as an inhibitor of GnRH at the level of the hypothalamus and LH and FSH at the level of the pituitary. Jesus, now picture this coupled with increased SHBG and estrogen! Needless to say, our T:E ratio has changed precipitously in that setting.

    But this is not meant to strike fear in the hearts of men and suggest it a poor test-promoting agent; at least not if cogniscent of the potential for all this to happen. The issue with just employing an AI is perhaps obvious UNLESS you are using it in the short term. If using it in the long-term, then we have the issue of prolactin to now contend with...that said, should we employ agents that stimulate dopamine which sounds very good on paper? Dopamine inhibits prolactin.

    But now, what to do about long-term use of a dopamine agonist. Well - pharmaceutically speaking, cabergoline can cause grief with heart valves - NO WAY MAN! Bromocriptine has a lot of uncomfortable effects (nausea and orthostatic hypotension being big ones); possibly less pertient with short-acting forms. Plus, you could see lowering of blood sugar which will lower inert insulin levels and could at least hypothetically-speaking make SHBG levels increase...WTF! Now what? How about long-term use of dietary supplements that would act as a dopamine agonist? Well, now we have the final concern...if keeping dopamine agonist on board keeps dopamine secretion in the "on" postition, what's going to stop downregulation of dopamine receptors?

    WOW - so how to summarize all of that?


    Probably what would be best is a scheme that looks more like this:

    (1) < 1 month: add AI
    (2) > 1 month: add intermittent use of dopamine agonist to DAA + AI in a 5 on, 2 off -or- 3 on, 1 off fashion (I prefer the 5 on, 2 off "Weekend Holdiay" pattern for most things micro-cycled).
    (3) Consider stopping at a max of 3 months (for now, until I can grab cummulative data - it will be on-going) if you do see a flare in side effects.


    * What people think is that they can alter the system (their own system) to get a good end result without the potential for sides. What might be a reasonable offering is to make people understand that it's also ok to use other things, not necessarily every day alongside your primary ergogenic aid...but in mico-cycle fashion to avoid even further side effect by the addition of the "side effect protector." This is just not realistic.

    Any takers in partaking in some closer monitoring of this protocol? Feel free to contact me VIA PM; do not post this in this thread.

    Thanks,


    D_
    Anabolicminds.com Featured Author
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  3. As far as dopamine agonists go how do you feel about pramipexole? It is supposed to be better than caber with less sides, I've only used it to reduce the refractory period(non existent) Would it be a better choice in the above scenario?

  4. Well, in the department of cardiac valvular sides that may be true - unfortunately, I am unaware of data that has explicitly looked at this. It does harbor predilection for D3 receptors, the receptor responsible for many of Bromocriptine's effects (HA, dizziness, Orthostatic Hypotension, etc...). So, it may take out Caber's cardiac stuff; but not Bromo's "generally annoying" stuff. That said, there is a very unique hyperalgesia (probably the most exquisite as far as dopamine agonists go) associated with pramipexole...kind of a very sensitive all-over muscle pain. I am uncertain anyone would want to experience this. It may be avoided with Dexpramipexole, the enantiomer of pramiproxole - but again, there are a lot of unknown variables here.

    Now, all this said...I would have trouble recommending anything of this status in self-medication circles. It'd just be irresponsible of me as I don't have the data to back up anything here. What I am saying is that it is very much so interesting discussion only.


    D_
    Anabolicminds.com Featured Author

  5. Quote Originally Posted by dinoiii View Post
    Well, in the department of cardiac valvular sides that may be true - unfortunately, I am unaware of data that has explicitly looked at this. It does harbor predilection for D3 receptors, the receptor responsible for many of Bromocriptine's effects (HA, dizziness, Orthostatic Hypotension, etc...). So, it may take out Caber's cardiac stuff; but not Bromo's "generally annoying" stuff. That said, there is a very unique hyperalgesia (probably the most exquisite as far as dopamine agonists go) associated with pramipexole...kind of a very sensitive all-over muscle pain. I am uncertain anyone would want to experience this. It may be avoided with Dexpramipexole, the enantiomer of pramiproxole - but again, there are a lot of unknown variables here.

    Now, all this said...I would have trouble recommending anything of this status in self-medication circles. It'd just be irresponsible of me as I don't have the data to back up anything here. What I am saying is that it is very much so interesting discussion only.


    D_
    I totally understand, the effects of this substance are most certainly noticeable and all the unpleasant sides that you stated are immediately apparent. Tiny doses. but I was speaking in hypothetical terms only, I know you could not recommend any such protocol
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  6. Yeah, my experience with pramipexole isn't there. If relying on pharmaceutical versions of dopamine agonists to treat things of a neuroendocrine order considering the HPGA, then I would have to stick with tried and true agents like Caber and Bromocriptine; but I hear you. It does offer interesting conceptualization of the situation; but I am just unsure how best to respond without having experience with it myself.

    I can likely say it MAY very well avoid some issue, but the narrow therapeutic index concerns me. If you take into consideration volume of distribution, I am uncertain what kind of "tiny" dose you are talking about. While tiny may be very nice in terms of side effects; it doesn't mean you'd ever hit the therapeutic realm...so unfortunately, I don't know how best to direct you here and that's kind of what I was getting at. I don't like sounding "wishy-washy" in response and MAY is a junky word to use, but it's all I have at this time.


    D_
    Anabolicminds.com Featured Author

  7. I cant wait for all of this.... im giddy.
    By believing passionately in something that still does not exist, we create it. The nonexistent is whatever we have not sufficiently desired.
    Franz Kafka

  8. .25 milligram but again I wasn't using it to reduce prolactin long term only for the weekend if you catch my drift. It is indeed potent stuff

  9. so for 90 days run of DAA i can add this?

    Stimulate removal of estrogen from the body

    calcium-D-glucarate, tocotrienols and I3C

    Block estrogen receptor binding

    7,8-benzoflavone are effective in blocking estrogen receptor-binding sites and reducing aromatase activity.

    Prolactin

    Mucuna Pruiens (40%L-Dopa) "250mg EOD"?

  10. Quote Originally Posted by MAxximal
    so for 90 days run of DAA i can add this

    Stimulate removal of estrogen from the body

    calcium-D-glucarate, tocotrienols and I3C

    Block estrogen receptor binding

    7,8-benzoflavone are effective in blocking estrogen receptor-binding sites and reducing aromatase activity.

    Prolactin

    Mucuna Pruiens (40%L-Dopa) "250mg EOD"?
    Interesting summary. Let's see what the D says. I'm subbed.
    RecoverBro ELITE

  11. Quote Originally Posted by mattrag View Post
    Interesting summary. Let's see what the D says. I'm subbed.
    Yes! I can`t wait to start and thinking about add some Resveratrol to the mix with the above goodies (Red wine and lecithin make resveratrol stay more time in the blood)

    Red Wine Extract 50% Polyphenols
    Grape Seed Extract 95%
    Lecithin powder

  12. This table is a good example
    Attached Images Attached Images  

  13. Quote Originally Posted by MAxximal
    This table is a good example
    Nice post!! I'd rep but my phone doesn't let me lol

    So this shows all the pathways we can use to get rid of estrogen right?
    Is increasing shbg good?
    RecoverBro ELITE

  14. Quote Originally Posted by mattrag View Post
    Nice post!! I'd rep but my phone doesn't let me lol

    So this shows all the pathways we can use to get rid of estrogen right?
    Is increasing shbg good?
    No increasing Shbg is bad, it reduces your free testosterone by binding it and making it unable to attach to androgen receptors

  15. Quote Originally Posted by truthornothin
    No increasing Shbg is bad, it reduces your free testosterone by binding it and making it unable to attach to androgen receptors
    Yea that's what I figured. So I'm guessing fiber is both good and bad?
    RecoverBro ELITE

  16. I have personally been on DAA since june 2010 !!
    rare breaks would stretch out from 3 days to 1 week.

    no problems except some acne and not at a constant rate (i take a week A.I. probably 2 or 3 doses in a month max and it deals with that)

    You do realise >1 month on DAA basically abolishes drug tolerance? for ephedrin, mdma, ketamine etc etc. (perhaps it was just me but my circle is n=5 friends all reporting the same thing so whatever)

    For whatever is worth i notice the above effect pretty much on on PA's chelated DAA / DAA+sarcosine too. the regular bulk powder does work but to a very very noticibale weakness of effect!

    lastly, taking chelated TF2 in the morning and a strong ph in the evening(SD+Hdrol combo) resulted in a noticable delay in the appearance of hpta shutdown effects. without above they would be evident on day 7 to 10 on similar sd doses in the past. with this it was extended to 20 days before i felt any real signs(no blood tests sorry but 10 years of experience with cycles should give me a decent idea)

    in your 1 year trial did you notice any of the above d?

    Thanks

  17. What about DAA causing severe anxiety in some individuals? I had to stop it completely because of this.... when confronted with a challenging or stressful scenario, my brain would wild and panic set in like never before.

  18. maybe I will add Sarcosine (N-methylglycine) or Calcium lactate gluconate to DAA?

    any experience with both?

  19. I have read where Dinoii is not a big fan of Resveratrol. It can act as an estrogen agonist in some instances and an estrogen antagonist in others, depending on the environment. There still very little human testing with this product.

  20. Probably what would be best is a scheme that looks more like this:

    (1) < 1 month: add AI
    (2) > 1 month: add intermittent use of dopamine agonist to DAA + AI in a 5 on, 2 off -or- 3 on, 1 off fashion (I prefer the 5 on, 2 off "Weekend Holdiay" pattern for most things micro-cycled).
    (3) Consider stopping at a max of 3 months (for now, until I can grab cummulative data - it will be on-going) if you do see a flare in side effects.


    Would Man sport primal male be a good AI option ?

  21. Primal Male is a test booster with I3C (estrogen channeling agent) added. I doubt if it would do much for estrogen modulation in the presents of DAA. At least not from my experience. I would recommend either Formestane or possibly Erase. I have tried several others including Formadrol without much success. Formestane at low dosage I think would be best.

  22. Quote Originally Posted by BBB View Post
    Primal Male is a test booster with I3C (estrogen channeling agent) added. I doubt if it would do much for estrogen modulation in the presents of DAA. At least not from my experience. I would recommend either Formestane or possibly Erase. I have tried several others including Formadrol without much success. Formestane at low dosage I think would be best.
    I3C used correctly like (DIM @ correct dose *high doses is toxic*) works wonders for me

  23. Quote Originally Posted by MAxximal View Post
    I3C used correctly like (DIM @ correct dose *high doses is toxic*) works wonders for me
    What do you mean by wonders? What dosage and for how long? I have used I3C, didn't notice much, not that I was expecting much.

  24. Quote Originally Posted by dontknowaboutme View Post
    What do you mean by wonders? What dosage and for how long? I have used I3C, didn't notice much, not that I was expecting much.
    i used this and other goodies for prostate purposes due a high dose of epiandrosterone.

    http://cebp.aacrjournals.org/content.../2477.full.pdf

  25. I was asking about primal male, since if my memorie is right i read on another board that he was the or one of the formulator behind Primal male, I can be wrong do.

  26. Quote Originally Posted by alvin1 View Post
    Probably what would be best is a scheme that looks more like this:

    (1) < 1 month: add AI
    (2) > 1 month: add intermittent use of dopamine agonist to DAA + AI in a 5 on, 2 off -or- 3 on, 1 off fashion (I prefer the 5 on, 2 off "Weekend Holdiay" pattern for most things micro-cycled).
    (3) Consider stopping at a max of 3 months (for now, until I can grab cummulative data - it will be on-going) if you do see a flare in side effects.


    Would Man sport primal male be a good AI option ?
    Would dopamine agonist be something like drive or igf-2 by appnut? I'm running Alpha Mass by FRL and when I'm done with this cycle was planning on running TF2 with Bioforge V3 as pct.

  27. every body reacts differently.
    i only take the AI when i feel my skin begins to act up. and not for any other reason

  28. This thread absolutely blew up! I suppose that's a good thing seeing how it ended up being the first topic on the chopping block. It may take me a moment to respond to everyone and with that I apologize in advance. There are just far many more of you than there are of me.

    D_
    Anabolicminds.com Featured Author

  29. This is a very active site Doc. Not like LB. You may be getting more than you bargined for.

  30. Quote Originally Posted by MAxximal View Post
    so for 90 days run of DAA i can add this?

    Stimulate removal of estrogen from the body

    calcium-D-glucarate, tocotrienols and I3C

    Block estrogen receptor binding

    7,8-benzoflavone are effective in blocking estrogen receptor-binding sites and reducing aromatase activity.

    Prolactin

    Mucuna Pruiens (40%L-Dopa) "250mg EOD"?

    Uhhh, that might be overkill and I am unsure what I would do with some of the agents. I do agree that if this is what you have gotten out of my previous posts, then this is an "interesting" summary as one author in this thread stated...

    Biotest tried to make calcium D-glucarate (CDG) important in one of their products from the past known as "M." There's probably a reason it never went anywhere. I have my own suspicions and it is more mechanistic: Following administration, glucarate is converted to d-glucaro-1,4-lactone, which inhibits beta-glucuronidase. Inhibition of beta-glucuronidase surely CAN be a good thing in various estrogen cascades; but in some androgen pathways...this is not a good thing at all. I am unaware of any studies nor do I have data on the impact with males and androgen levels (please feel free to point us in a direction if you are able). So, I probably dub this one a PASS.

    7, 8 benzoflavone is interesting on paper though I admittedly cannot suggest I have a lot of experience with it. My fear, as with any bioflavanoid is that you do have an optimization curve to follow. For people unfamilar with the term, its that there is a consistently "optimal" dose to see suggested effects and above it, things fall off quickly. See, Benzoflavone's parent compound Passiflora incarnata did show worrisome effects [prolonged QT on cardiac studies and Ventricular arrhytmias) at the efficacious dose. [see Toxicity of Passiflora incarnata L. J Toxicol Clin Toxicol. 2000]. Now, I am unsure who is using this compound in the industry, but if the toxicology studies are correct, I can assure you they are likely not using an efficacious dose - which is probably fortunate.

    I am fine with use of the other three; the only issues I would suggest being careful of is with long-term use of dopamine agonists like mucuna puriens. I also do not know where the protocol of "250mg EOD" came in, but that is NOT my recommendation...it needs to be a DAILY DOSE for a serum steady state to be achieved. Dependent upon the L-Dopa percentage is where you can rest your hat on milligram dosage.

    D_
    Anabolicminds.com Featured Author
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