SUP3R-EPI and SUP3R-EPI ELITE Q&A

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  1. SUP3R-EPI and SUP3R-EPI ELITE Q&A


    SUP3R-EPI:
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    SUP3R-EPI ELITE:
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  2. Epi-Andro



    Epi-Andro, also known as Epiandrosterone, 3-androsterone, 3-hydroxy-5a-androstan-17-one, 5a-androstan-3-ol-17-one and Isoandrosterone, is a steroid hormone with weak androgenic activity. The name Epiandrosterone is due to it being an epimer of Androsterone (3a-hydroxy-5a-androstan-17-one). Epiandrosterone and Androsterone (sometimes referred to as 'R-DHEA') are almost identical in structure, with Epiandrosterone being the 3-beta isomer (thus why it may also be referred to as Isoandrosterone) and Androsterone being the 3-alpha isomer. It is naturally occurring in most mammals, including pigs, and was first artificially synthesized over 80 years ago in 1934 by Nobel prize-winning Croatian chemist Leopold Ružicka, who also first successfully synthesized Testosterone. It was not until four years after being synthesized that in 1938 it would be first identified in humans. It is a naturally produced metabolite of the adrenal hormone Dehydroepiandrosterone (DHEA) by the enzyme 5a-reductase.

    Most notably Epiandrosterone is a precursor/prohormone to the androgen Dihydrotestosterone (commonly abbreviated to DHT) through a two-step conversion process in vivo by the enzymes 3-hydroxysteroid dehydrogenase (3-HSD) and 17-hydroxysteroid dehydrogenase (17-HSD). According to data from Julius Vida when Epiandrosterone is injected it is almost entirely inactive, resulting in only a very mild androgenic effect and must be taken orally to convert to an active hormone. There are two possible pathways of conversion, both requiring two conversion steps each to transition from Epiandrosterone to DHT. One conversion pathway for Epiandrosterone is to be converted by 3-HSD into Androstanedione (5a-androstane-3,17-dione) and then converted by 17-HSD into DHT. And another conversion pathway for Epiandrosterone is to be converted by 17-HSD into Androstanediol (5a-androstane-3b,17b-diol) and then converted by 3-HSD into DHT. It is quite difficult to calculate percentages for conversion rates due to the fact that these conversions are reversible, as Epiandrosterone can convert to DHT, and DHT can also convert to Epiandrosterone.

    Whichever pathway Epiandrosterone takes in vivo, we arrive at the target hormone Dihydrotestosterone. And this is what makes Epiandrosterone interesting, as DHT is typically synthesized in the prostate, testes, hair follicles, and adrenal glands by the enzyme 5a-reductase which reduces the 4,5 double-bond of the hormone Testosterone. So what is DHT? Dihydrotestosterone (DHT), also referred to as 5a-Dihydrotestosterone (5a-DHT), Androstanolone (5a-androstan-17-ol-3-one) or 17-hydroxy-5a-androstan-3-one, is a naturally occurring sex steroid and androgen hormone in the human body. It has two to three times greater androgen receptor affinity than Testosterone and 15-30 times greater affinity than adrenal androgens. It plays a significant role in the development of secondary sex characteristics and unlike Testosterone it cannot be converted by the enzyme aromatase to estradiol.

    It is more androgenic than it is anabolic, with claims of an anabolic/androgenic ratio of 152/268. In fact, it exhibits relatively little direct anabolic effects on muscle in men, with Testosterone being the primary active androgen in muscle. That is not to say DHT is without any anabolic effect, it does have some anabolic activity in the muscle, but such anabolic activity is significantly weaker than that of an equal amount of Testosterone. This is due to its quick breakdown by an enzyme called 3alpha-hydroxysteroid reductase (3a-HSD) into the weak metabolite 3a-androstanediol (5a-androstane-3a,17-diol), thus why it is not an effective anabolic in muscle tissue. But despite the fact that Epiandrosterone's target hormone has little direct anabolic effect on its own, DHT is still very important as it has potent effects on the central nervous system. These effects lead to increased neurological efficiency (increased strength) enabling you to lift more weight, and increased resistance to psychological and physical stress, as well as optimal libido and sexual function such as improved duration of erections and frequency of orgasms. This allows for higher intensity workouts that when paired with a proper diet and exercise program should allow for increased muscle mass.

    To illustrate the importance DHT has in the body, there are anecdotal reports of individuals using Finasteride (a 5a-reductase inhibitor which inhibits the conversion of Testosterone to DHT) with Testosterone and noticing a significant reduction in performance enhancement effects as compared to Testosterone alone. This isn't due to the inhibition of the direct anabolic activity of Testosterone on muscle anabolism, as that would not occur. Instead it is likely due to the reduction of androgenic effects in other areas of the body that contribute to the ergogenic effects, specifically the CNS which is stimulated primarily by DHT which leads to increased neural output and thus greater strength and recovery. DHT is also an important androgen in the liver where its inhibition could lead to a reduction in the production of androgen dependent liver growth factors such as IGF-1.

    DHT also functions as an antagonist of estrogen, which can be seen with the drug Finasteride which may cause gynecomastia in some men by reducing DHT levels in the body, and thus reducing DHT’s antagonism of estrogen in the body. DHT directly inhibits estrogens activity on tissues, either by acting as a competitive antagonist to the estrogen receptor or by decreasing estrogen-induced RNA transcription at a point subsequent to estrogen receptor binding. It also directly blocks the production of estrogens from androgens by inhibiting the activity of aromatase. Studies done in breast tissue showed that DHT, Androsterone, and 5alpha-Androstandione inhibit the formation of Estrone from Androstenedione.

    However, DHT is not without the possibility of side effects. It is thought to be the primary contributing factor in male pattern baldness, and since its precursor Epiandrosterone is already 5a-reduced, the use of 5a-reductase inhibitors such as Finasteride with the intention to prevent or mitigate androgenic side-effects like hair-loss will not work. It may also play a role in the development and exacerbation of benign prostatic hyperplasia (BPH) by enlarging the prostate gland, and may induce male secondary sex characteristics in women, such as a deepened voice and facial hair. Though these side effects are not limited to DHT, and are in fact a possibility with many AAS/PH/DS that exert androgenic effects.

    Since many Anabolic Androgenic Steroids (AAS), Prohormones (PH) and Designer Steroids (DS) are incapable of converting to DHT like Testosterone to fulfill the biological demands the body has while also suppressing endogenous Testosterone production and thus DHT production as well, it is extremely common to see reports of lethargy and libido crash while on cycle. This is why it is also common to see recommendations for Epiandrosterone to be used as a 'Test Base', because it helps mitigate lethargy and low libido by fulfilling the body’s biological demands. The only other legal compound capable of this is 4-Androsterone though it does not convert to a significant amount of DHT, which is why you will often see the two 'stacked' together to address the need for both DHT and Testosterone while on a suppressive cycle.

    It is possible that Epiandrosterone may cause some HPTA suppression, and therefore it is always recommended to run a properly planned Post-Cycle Therapy (PCT) following any supplementation regimen containing Epiandrosterone.

    So what do we know about Epiandrosterone?

    •Non-Methylated/Non-Liver Toxic (Doesn't require liver support such as TUDCA or NAC)
    •Dry Compound/Non-Aromatizing (Won't convert estrogen nor cause water retention or bloating)
    •Anti-estrogenic Effect
    •Increases Aggression
    •Increases Energy/Combats Lethargy
    •Increases Muscle Hardness and Density
    •Increases Strength via CNS Activation
    •Increases Vascularity
    •Reduces Water Weight (Leading to a drier/tighter appearance)
    •Supports Libido
    •Excellent for Cutting/Recomping
    •Excellent Stacker



    Conversion Processes: (Two step conversion to Dihydrotestosterone)
    Epiandrosterone -> {via 3b-HSD enzyme to} Androstenedione -> {via 17b-HSD enzyme to} Dihydrotestosterone
    Epiandrosterone -> {via 17b-HSD enzyme to} Androstenediol -> {via 3b-HSD enzyme to} Dihydrotestosterone
    Though the risk of estrogenic side effects are essentially non-existant while on Epi-Andro, we always recommended that you have an AI, such as Exemestane, on hand.

    Epi-Andro Example Cycles:
    Beginner:
    Epi-Andro - 500/500/500/500/500/500
    *Space capsules out with meals containing fats.

    Advanced/Experienced:
    Epi-Andro - 500/500/750/750/1000/1000
    *Space capsules out with meals containing Fats.
    Epi-Andro - 1000/1000/1000/1000/1000/1000/1000/1000
    *Space capsules out with meals containing fats.

    Post Cycle Therapy (PCT):
    Clomid - 50/50/25/25 (Or SERM of your choice)
    Olympus Labs Sup3r PCT (As indicated on label)
    AI of choice on hand (E.g. Exemestane)

    Andros also have synergy, when stacked together. Here are a few example stack cycles...

    Ultimate Epi/4 Cycle:
    Epi-Andro - 1000/1000/1000/1000/1000/1000/1000/1000
    4-Andro - 330/330/330/330/330/330/330/330
    *Space capsules out with meals containing fats.


    Dry Epi/1 Cycle:
    Epi-Andro - 1000/1000/1000/1000/1000/1000/1000/1000
    1-Andro - 330/330/330/330/330/330/330/330
    *Space capsules out with meals containing fats.

    Elite Cycle:
    Epi-Andro - 1000/1000/1000/1000/1000/1000/1000/1000
    1-Andro - 330/330/330/330/330/330/330/330
    4-Andro - 330/330/330/330/330/330/330/330
    *Space capsules out with meals containing fats.
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  3. Our Andro line utilises S-SEDDS...what is this?


    Self-emulsifying drug delivery systems (SEDDS). SEDDS have been proven in the last two decades to be a phenomenal success. They are able to overcome some of the biggest challenges confronting contemporary delivery science today by improving on the oral bioavailability of compounds with poor and inconsistent gastrointestinal absorption. SEDDS do so by facilitating absorption of compounds via the intestinal lymphatic system and thus circumnavigating the hepatic first-pass effect. The lymphatic system is a drainage network that extends throughout the entire body in proximity to the circulatory system and is a logical target since orally administered compounds can work more effectively when transported selectively to the intestinal lymphatic system. The bioavailability of compounds that undergo significant first-pass metabolism in the liver, as Andros do without enhanced delivery methods, can be improved dramatically by utilizing the lymphatic system for absorption in the intestine, thus avoiding the destructive first-pass effect in the liver.

    However SEDDS are typically prepared in a liquid form, which can result in some disadvantages, for example, low stability, large volume of dose and issues with handling and portability. To overcome these issues, solid-SEDDS (S-SEDDS) has emerged to improve upon an already excellent delivery system. Through solidification of liquid self-emulsifying systems into powders the liquid SEDDS can be converted into solid dosage form without affecting compound release property. Thus, S-SEDDS combines the advantages of SEDDS (i.e., enhanced solubility and bioavailability) with those of solid dosage forms (e.g., high stability and reproducibility, compact dosage form and ease of handling and portability). Though it has little, if any, current presence in the world of supplementation, S-SEDDS is a cutting edge and highly effective delivery system utilized by the pharmaceutical industry. It is without a doubt one of the most effective means by which to deliver any compound at this point in time, and stands to replace other more antiquated methods delivery in the very near future.

  4. in on this

  5. Is it any possibility that we will see a Androsterone/Epiandro mix in the future?
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  6. Anyone experienced with this, what's the likelihood that this will cause high blood pressure given that it converts to DHT?

    Thanks,

    Crowbar

  7. Quote Originally Posted by crowbar46 View Post
    Anyone experienced with this, what's the likelihood that this will cause high blood pressure given that it converts to DHT?

    Thanks,

    Crowbar
    It will be individual. Most don't experience a real rise in BP but I do notice some increase (not enough to cause concern). Monitor it and go from there. Hawthorn berry can help alleviate some of the issue if there is one.
    *strong supplement shop rep*

    Find the latest supplements at the best prices at strongsupplementshop.com

  8. I definitely get a BP spike when I'm on epiandro and I see a really hot girl or I'm scrolling through Chuck Diesel's Jugs 4 Jugs thread
    Training & everything else log: http://anabolicminds.com/forum/workout-logs/275307-bam-bam-goes-30.html

  9. Subbed. Did I read somewhere that taking other things alongside the S-SEDDS delivery may also improve their absorption? I.E. taking another compound at the same time as Sup3r Epi Elite.

    Forgive me if this was already answered, can't remember where I saw it!

  10. I assume hair loss would be a notted side effect especially to someone that is prone to it?

  11. Does anyone know how hard epiandro tanks your good cholesterol?

  12. Quote Originally Posted by CJNator View Post
    I assume hair loss would be a notted side effect especially to someone that is prone to it?
    Yes, but no moreso than other androgenic compounds.

  13. Quote Originally Posted by Oldnewb View Post
    Does anyone know how hard epiandro tanks your good cholesterol?
    Difficult to put black and white figures on this, as severity will depend on the individual. Best approach is to do all you can via diet (olive oil, garlic, etc) and, if you wish to be extra cautious, supplementation (fish oil, pantethine, coq10, etc).

  14. Quote Originally Posted by Misfit28 View Post
    Subbed. Did I read somewhere that taking other things alongside the S-SEDDS delivery may also improve their absorption? I.E. taking another compound at the same time as Sup3r Epi Elite.

    Forgive me if this was already answered, can't remember where I saw it!
    Dont know if you read Yates talking about this elsewhere, but no. To use a comparison, S-SEDDS is more like phytofuse than, say, bioperine.

  15. Quote Originally Posted by NewAgeMayan View Post
    Dont know if you read Yates talking about this elsewhere, but no. To use a comparison, S-SEDDS is more like phytofuse than, say, bioperine.
    Yeah, I saw that after I posted lol.

    Thanks for the clarification! Someone else posted that they had felt a difference with either another supp or medication.

  16. Started my 500 mg a day cycle yesterday, this is a completely new experience for me. The epi kicked in a lot harder than I expected. Unfortunately I seem to be one of those lucky ones whose bloodpressure shoots up while on it, gave me damn insomnia, lol. Im giving it a few more days, but my strategy may be to grab a weaker dosed epi and use that as my 2nd dosing of the day.

  17. Quote Originally Posted by Oldnewb View Post
    Started my 500 mg a day cycle yesterday, this is a completely new experience for me. The epi kicked in a lot harder than I expected. Unfortunately I seem to be one of those lucky ones whose bloodpressure shoots up while on it, gave me damn insomnia, lol. Im giving it a few more days, but my strategy may be to grab a weaker dosed epi and use that as my 2nd dosing of the day.
    How close to bedtime did you take it?

  18. Quote Originally Posted by Oldnewb View Post
    Started my 500 mg a day cycle yesterday, this is a completely new experience for me. The epi kicked in a lot harder than I expected. Unfortunately I seem to be one of those lucky ones whose bloodpressure shoots up while on it, gave me damn insomnia, lol. Im giving it a few more days, but my strategy may be to grab a weaker dosed epi and use that as my 2nd dosing of the day.
    Sounds like you split dose the 2 caps? If so, good.

    One other option, before you go buy more, could be to stick with just the 1 cap for a few days before bumping up to 2. This may (and I stress the may, no guarantees) allow some CNS acclimatisation where you eventually dont experience such a pronounced acute reaction.

    Itd be handy if you had a bp/hr monitor, too. Gives you an objective measure of where things are at.

  19. Absolutely, that's a great idea, sticking to one a day for a while...what would be the drawbacks of staying at that dose with this high dosage and better delivery system?

    My bp generally runs from about 110 over 75 to 120 over 85, this was annoying as hell considering half the time if Im not lifting or whatever I don't even know if Im dead or alive, lol.

    I was wired for sound until about 2 am. I had also taken 500 mg of ksm-66 (ashwaganda) around 8:30, didn't help at all. This stuff is pretty darn potent.

    Edit: Also starting on arimicare pro today, hopefully that helps!

  20. Quote Originally Posted by Oldnewb View Post
    Absolutely, that's a great idea, sticking to one a day for a while...what would be the drawbacks of staying at that dose with this high dosage and better delivery system?

    My bp generally runs from about 110 over 75 to 120 over 85, this was annoying as hell considering half the time if Im not lifting or whatever I don't even know if Im dead or alive, lol.

    I was wired for sound until about 2 am. I had also taken 500 mg of ksm-66 (ashwaganda) around 8:30, didn't help at all. This stuff is pretty darn potent.

    Edit: Also starting on arimicare pro today, hopefully that helps!
    What time did you take the second dose?

  21. Ideally, you want a blood spike around workout, but you also want stable levels throughout the day if possible. If youre only dosing 1c/d, the former is obviously your main priority.

    Ash can certainly contribute to sleep difficulties for some, if dosed too close to bed.

  22. Quote Originally Posted by NewAgeMayan View Post
    Ideally, you want a blood spike around workout, but you also want stable levels throughout the day if possible. If youre only dosing 1c/d, the former is obviously your main priority.

    Ash can certainly contribute to sleep difficulties for some, if dosed too close to bed.

    When you first start on Arimacare, it is quite likely that you will experience an increase in BP for a week or so.
    My plan is about 30-60 minutes preworkout, then mid-day with lunch (2 caps per day).

  23. Quote Originally Posted by Misfit28 View Post
    What time did you take the second dose?
    I just realized I may have projected my workout times on him, LOL. I work out in the early AM, so dosing shouldn't be as much an issue for me as it might be for those that work out in the evening.

  24. Quote Originally Posted by Misfit28 View Post
    My plan is about 30-60 minutes preworkout, then mid-day with lunch (2 caps per day).
    Im planning something similiar when I go up to 2c.

    If you train in the evening, Id imagine dosing 1-2hrs pre wo isnt going to stifle efficacy. Besides, nothing worse than disrupted sleep.

  25. Quote Originally Posted by NewAgeMayan View Post
    Im planning something similiar when I go up to 2c.

    If you train in the evening, Id imagine dosing 1-2hrs pre wo isnt going to stifle efficacy. Besides, nothing worse than disrupted sleep.
    I agree wholeheartedly. I work two jobs M-F, so every minute of sleep is precious to me, LOL.
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