NewAgeMayan
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SUP3R-EPI and SUP3R-EPI ELITE Q&A
- Thread starter NewAgeMayan
- Start date
NewAgeMayan
Well-known member
Epi-Andro
Epi-Andro, also known as Epiandrosterone, 3ß-androsterone, 3ß-hydroxy-5a-androstan-17-one, 5a-androstan-3ß-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 3ß-hydroxysteroid dehydrogenase (3ß-HSD) and 17ß-hydroxysteroid dehydrogenase (17ß-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 3ß-HSD into Androstanedione (5a-androstane-3,17-dione) and then converted by 17ß-HSD into DHT. And another conversion pathway for Epiandrosterone is to be converted by 17ß-HSD into Androstanediol (5a-androstane-3b,17b-diol) and then converted by 3ß-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-17ß-ol-3-one) or 17ß-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,17ß-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.
Epi-Andro, also known as Epiandrosterone, 3ß-androsterone, 3ß-hydroxy-5a-androstan-17-one, 5a-androstan-3ß-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 3ß-hydroxysteroid dehydrogenase (3ß-HSD) and 17ß-hydroxysteroid dehydrogenase (17ß-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 3ß-HSD into Androstanedione (5a-androstane-3,17-dione) and then converted by 17ß-HSD into DHT. And another conversion pathway for Epiandrosterone is to be converted by 17ß-HSD into Androstanediol (5a-androstane-3b,17b-diol) and then converted by 3ß-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-17ß-ol-3-one) or 17ß-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,17ß-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.
NewAgeMayan
Well-known member
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.
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.
BlackTiger22
Active member
in on this
Dragoninho
Member
Is it any possibility that we will see a Androsterone/Epiandro mix in the future?
Afi140
Legend
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.
BamBam0319
Well-known member
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
NewAgeMayan
Well-known member
Yes, but no moreso than other androgenic compounds.
NewAgeMayan
Well-known member
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).
NewAgeMayan
Well-known member
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.
Misfit28
Well-known member
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.
Oldnewb
New member
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.
Misfit28
Well-known member
How close to bedtime did you take it?
NewAgeMayan
Well-known member
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.
Oldnewb
New member
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!
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!
Misfit28
Well-known member
What time did you take the second dose?
NewAgeMayan
Well-known member
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.
Ash can certainly contribute to sleep difficulties for some, if dosed too close to bed.
Misfit28
Well-known member
My plan is about 30-60 minutes preworkout, then mid-day with lunch (2 caps per day).
Misfit28
Well-known member
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.
NewAgeMayan
Well-known member
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.
Misfit28
Well-known member
I agree wholeheartedly. I work two jobs M-F, so every minute of sleep is precious to me, LOL.
Oldnewb
New member
I generally work out around 3:00--3:30 generally for about 90 minutes give or take. So I first dosed at breakfast (8:30 am) then after dinner, at about 6:00 pm. Im just going to do a single dose after lunch, that way I have that spike during my workout.
Ashwaganda usually knocks me on my ass, literally drooling in beard before me and the wife finish watching our shows together, haha.
So would a lack of stable levels throughout the day influence shutdown/suppression negatively by creating a stressful daily hormonal loop? Or would it just be a fact that gains would be diminished? Sleep is more important to me, I spent years with sleep issues up until just a few months ago when I started with the ash.
Thanks for all the input btw guys!
Ashwaganda usually knocks me on my ass, literally drooling in beard before me and the wife finish watching our shows together, haha.
So would a lack of stable levels throughout the day influence shutdown/suppression negatively by creating a stressful daily hormonal loop? Or would it just be a fact that gains would be diminished? Sleep is more important to me, I spent years with sleep issues up until just a few months ago when I started with the ash.
Thanks for all the input btw guys!
NewAgeMayan
Well-known member
Its obviously difficult to put any kind of figures on these questions, given the amount of variables involved.
Furthermore, alot of this is somewhat relative.
If someone is limited to 250mg per day, are they worse off, will they experience less gains, dosing once pre wo compared to someone spreading that dose out in 50-100mg amounts?
Id be surprised if the differences/benefits were measurably significant. If anything, at a 250mg/d dose, Id wager the single dose to be 'better', if I had to choose a side.
Now, when we get to much larger doses, 500mg+, then I would expect to see some divergence between dosing schedules.
Again, you probably wont be shortchanging yourself dosing 250mg once /d, compared to someone dosing 125mg twice, or 50mg five times.
Furthermore, alot of this is somewhat relative.
If someone is limited to 250mg per day, are they worse off, will they experience less gains, dosing once pre wo compared to someone spreading that dose out in 50-100mg amounts?
Id be surprised if the differences/benefits were measurably significant. If anything, at a 250mg/d dose, Id wager the single dose to be 'better', if I had to choose a side.
Now, when we get to much larger doses, 500mg+, then I would expect to see some divergence between dosing schedules.
Again, you probably wont be shortchanging yourself dosing 250mg once /d, compared to someone dosing 125mg twice, or 50mg five times.
BamBam0319
Well-known member
I'm just gonna dose 10 pills a day. 12 day cycle FTW. Get on my level p*ssies.
Wkdsean88
New member
Just ordered this, just a quick question for others getting it. I'm still trying to decide whether to do 6 or 8 weeks and whether to stack it with 1 andro or 4 andro or solo.
Cheers
1. How long are you running it for
2. What dosage are you planning.
3. Are you running it solo, if not what are you stacking it with.
Cheers
1. How long are you running it for
2. What dosage are you planning.
3. Are you running it solo, if not what are you stacking it with.
NewAgeMayan
Well-known member
Hey,
1) prolly 8wks, dependant on if sides present
2) starting at 250mg/d, then will increase to 500mg if I feel it warranted
3) 30mg/d Ostar1ne
CJNator
Well-known member
Log?
NewAgeMayan
Well-known member
Nah, Ive already started the cycle.
BamBam0319
Well-known member
Damn, 30mg osta? What's your reasoning?
NewAgeMayan
Well-known member
Ive bought up a nice stock of the compound, enough to trial a range of doses in a variety of dietary contexts. So just to experiment really.
CJNator
Well-known member
Oh ok, hope you have a great run!
BamBam0319
Well-known member
NewAgeMayan
Well-known member
Cheers fellas.
Aiming for 12wks total on Ostar, at a fairly decent kcal deficit. Last 8wks with epi.
Aiming for 12wks total on Ostar, at a fairly decent kcal deficit. Last 8wks with epi.
YouBet33
Well-known member
I'm running similar but with LGD for 12 weeks, 8 weeks super epi and 4ad for base, and end with a bang with either d1methadrol, original tr1umph, or alpha 90
NewAgeMayan
Well-known member
I'm running similar but with LGD for 12 weeks, 8 weeks super epi and 4ad for base, and end with a bang with either d1methadrol, original tr1umph, or alpha 90
Deficit too?
I will certainly be doing similiar experiments with my LGD stock. Be boring to run it all identically
YouBet33
Well-known member
Deficit too?
I will certainly be doing similiar experiments with my LGD stock. Be boring to run it all identically
Yes, need to drop a few!
YouBet33
Well-known member
Not sure how high to run my LGD at tho, I have two bottles in stash and wanna save one for the future
NewAgeMayan
Well-known member
IMO, couple of things to consider.
LGD generally takes a couple weeks for benefits to manifest. Good time to dose low and conserve your supply.
After that, to reap the most benefits from the compound, I would recommend dosing at least 8mg/d.
YouBet33
Well-known member
Might just go 12 weeks at 4 mg since I'm adding in multiple other compounds at 4 weeks and 6 weeks , that way I have a whole bottle left
BamBam0319
Well-known member
Meh if it were me it would be impossible to resist bumping to 8mg after either 2 or 4 weeks. What else you running?
YouBet33
Well-known member
Super Epi and 4ad for 8 weeks, and d1methadrol for 6
Wkdsean88
New member
Strongsupps is doing 15% off the sup3r-1 and sup3r-4!!!!!
coupon code for the 1 is*SUP3R115 and the sup3r-4 is*SUP3R415
I just ordered both of these without the code half an hour ago. Doh!
edje007
Well-known member
Oooohhh noooo