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SUPERPCT_92985.1435807445.1280.1280_33959.1441812756.1280.1280__94259
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super_epi_perfect_cycle__01224Sup3r Epi Perfect Cycle by Olympus UKar1macarepronew_45204.1435699731.1280.1280_33029.1441811083.1280.1280__01534SUP3R_EPI__15566

Sup3r Epi Perfect Cycle by Olympus UK

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$144.77 $115.19

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-1 Bottle of Sup3r ELite 60ct

-1 Bottle of Ar1macare pro

-1 Bottle of Sup3r PCT

 

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.

It is also worth noting that Epi-Andro, just as with 1-Andro and 4-Andro, undergoes significant first-pass metabolism in the liver. This, in addition to other factors, contributes to the low bioavailability of Epi-Andro. There are many delivery systems that have been utilized in attempts to enhance bioavailability, with the most recent advancements being with the pharmaceutical delivery system commonly abbreviated as S-SEDDS which stands for Solid Self-Emulsifying Drug Delivery Systems. S-SEDDS enhances absorption via the intestinal lymphatic system which circumnavigates the destructive hepatic first-pass metabolism.

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

In the world of supplementation, Andros reign supreme as today’s legal prohormones of choice. For those who are unaware of these compounds, the term Andro specifically pertains to the naturally occurring DHEA metabolites known as Epiandrosterone, 1-Androsterone and 4-Androsterone. There are a wide variety of Andros available utilizing different delivery methods, each with claims regarding improved bioavailability, half-life, and so on. It can be confusing, even overwhelming, when trying to choose a product that meets your needs. So let’s try to clear up some of that confusion by reviewing a few of the different delivery methods currently available.

 

Let’s begin with Cyclodextrins. Cyclodextrins use a carbohydrate-enveloping effect with compounds. The idea is that they are complexed in a structure which makes them water soluble. And they are in general designed to be taken sublingually (placed under the tongue to dissolve) with the intention to bypass first pass metabolism (liver breakdown). In 2002 a paper published in the Journal of Applied Physiology showed that a cyclodextrin complex of 4-Androstenediol did indeed result in increases in serum testosterone levels. However 4-Androstenediol, commonly referred to as 4-AD, converts directly to testosterone (1-step conversion) and since been banned in the United States. Now the legal prohormone 4-Androsterone, which converts to 4-Androstenedione and 4-Androstenediol and then convert to Testosterone (2-step conversion), is being seen released in the same manner of delivery along with 1-Androsterone and Epiandrosterone. But there’s an issue, they are completely different compounds. The difference between 1-step and 2-step conversion prohormones is significant enough that we cannot assume that the results of a study done on a 1-step conversion prohormone will translate to a 2-step conversion prohormone. There are also claims that because of the limited surface area, the amount of prohormone that can be absorbed at one time sublingually appears to be 25mg or less, which is an extremely low dosage.

 

So, let’s move on to Liposomes. Liposomes act in a similar manner to Cyclodextrins, but instead of using a carbohydrate-enveloping effect it uses a fat-enveloping effect, they fold upon themselves, giving a shell with a water-soluble exterior and an oil soluble interior (somewhat similarly to cyclodextrins). When a liposome is ingested, it passes through the stomach and into the small intestine where it comes into contact with the non-polar intestinal cell lining, merging with it. When this happens, the compound trapped in the interior of the liposome is transferred into the intestinal lining and from there it travels into the portal circulation to the liver. Liposomes and Cyclodextrins work very similarly; you put the compound in a water-soluble shell, and then deposit it in the lipid-like surface of the oral or intestinal mucosa. However, the flux between the cavity of the cyclodextrin molecule and the mucosa is far more efficient and faster than liposomes. A liposome must first merge and dissolve into the mucosal cell membrane before its contents are delivered. In contrast, the cyclodextrin molecule undergoes no such interaction at the mucosal membrane, and does not disintegrate; it simply instantaneously delivers its payload. An industry expert has commented in the past that that single-layered liposomes are great oral products, and may also be effective sublingually (under the tongue) but likely don’t work as well as cyclodextrin-complexed products.

 

Now let’s discuss Esters. Adding an ester group to a compound makes it less soluble in water and more soluble in fat. The main claimed benefit of adding such an ester is potential lymphatic delivery (through the small intestine into the lymphatic system and thus bypassing the liver) for overall improved bioavailability. Whether or not this works for Andros has yet to be proven. There are a number of different esters, for example the enanthate ester, which you may see hidden in a compounds nomenclature as “enanthoxy” if the enanthate ester is attached to an oxygen atom. Now it’s worth pointing out that esters varying in their length, and due to this, take up a varying percentage of the compounds weight that is essentially inactive, resulting in less active hormone milligram for milligram. A good way of illustrating how different esters result in different amounts of active compounds is by looking at various esterified testosterone preparations. In this instance, the esters Enanthate, Caprylate and Undecanoate:

 

-100mg Testosterone Enanthate = 71.99mg Testosterone (28.01mg Enanthate)

-100mg Testosterone Caprylate = 69.56mg Testosterone (30.44mg Caprylate)

-100mg Testosterone Undecanoate = 65.15mg Testosterone (34.85mg Undecanoate)

 

As you can see around 1/3rd of the compound is inactive, and though these numbers don’t necessarily reflect those of esterified Andros the principal is the same, less Andros by weight. There is also a misconception that orally ingested esterified compounds will match intramuscularly injected esterified compounds in the ability to provide a sustained release, but this is simply not the case. For example, an intramuscular injection of Testosterone Undecanoate provides a sustained release of Testosterone into the bloodstream for up to 10 weeks, but if orally administered it is eliminated from the body in just 3 to 4 hours. To what extent, if any, esterification improves bioavailability or half-life has yet to be proven, while increasing cost and providing lower doses of the active hormone by weight.

 

And finally, let’s talk about 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.

 

So when choosing an Andro product to help you reach your goals, ask yourself, do you want a product that is backed my theories and hypotheticals, or by cutting edge pharmaceutical science?

Additional information

Weight2 lbs
Dimensions8 x 8 x 8 in
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