mobro said:
So what happens when you come off of the Derma? I would start another cycle if able but what if? If the Derma raises your test what keeps the boys producing for real recovery over the long term? True we shouldn't be cheap on this but it's new and I am a skeptic. Let's hear it, and keep it simple for me(not the brightest bulb in the house)
Dermacrine is positively correlated to increase lean body mass and reduce fat mass through four main mechanisms: Combating cortisol dominance, increasing GH & IGF-1, increasing androgens, reducing estrogen, and increasing thermogenesis.
Cortisol dominance can be described as having an unbalanced hormonal profile favoring cortisol activity either by having high cortisol levels, low androgen levels, or both. This hormonal shift towards cortisol dominance can be caused by excessive physical or mental stress [↑cortisol], post steroid use [↓androgen], alcohol consumption [↓androgen↑cortisol] and old age [↓androgen↑cortisol]1-4 In all cases, cortisol dominance is a condition associated with decreased muscle mass, increased fat mass, and degradation of general well being.4, 5, 17, 18, 19 Excessive cortisol activity can also decrease production of steroid hormones and androgens creating further cortisol dominance.6In order to neutralize the negative effects of cortisol and avoid cortisol dominance, one must maintain optimum levels of critical androgens.24 [Illustrated on the “Hormones” page]
DHEA is an immediate precursor to the critical androgens known as androstenediol and androstenetriol.20,21 These metabolites of DHEA are known to have powerful anti-catabolic and anti-cortisol activity by counteracting the muscle wasting and immuno-suppressive effects of cortisol.23,24 Both androstenediol and androstenetriol act as anabolic hormones and have been shown to enhance recovery and tissue repair from injury.24,25 Furthermore, DHEA, androstenediol and androstenetriol have been found to be potent enhancers of the immune system, by helping to fight off infection, protect against lethal radiation, and restore immunity during times of stress.26-29
Studies using DHEA with elderly subjects and HIV patients have also shown restoration of immune system activity by increasing the division of immune promoting cells.30-32 Its been proposed that this increased division of immunogenic cells is a result of DHEA increasing the bioavailability of IGF-1 and enhancing cellular mitosis.31
DHEA’s stimulation of IGF-1 activity is supported by other human trials.33,34 These studies have also revealed that DHEA can stimulate GH release. Therefore, the increase in IGF-1 can be explained by the increase in GH, since GH is converted to IGF-1 in the liver. An explanation for the GH release can be explained here by Suarez et al. 2005,
“it can be inferred that DHEA may release GH in vivo by reducing somatotrope responsiveness to somatostatin, as well as by enhancing somatotrope sensitivity to GHRH.”
In general terms, DHEA sensitizes the pituitary to GHRH and boosts the release of GH.34
The increase in GH and IGF-1 with DHEA supplementation has shown to have real world benefits in muscle growth, fat loss and muscle strength in various human studies.35-37 Besides having a direct effect on body composition, IGF-1 plays an important role in steroidogenic hormone production. Most notably, IGF-1 stimulates the conversion of cholesterol to pregnenolone, otherwise known as the rate limiting step in steroid hormone synthesis. Enhancement of steroidal synthesis by IGF-1 is accomplished by IGF-1’s action upon the leydig cell and stimulation of CYP11A, 3b HSD, and StAR. 38-40 Direct stimulation upon the leydig cell from IGF-1 helps initiate the first steps in creating anabolic hormones such as androstenedione, androstenediol, and t estosterone.
Concerning the process of steroidogenesis, it is known by most steroid users that anabolic androgenic steroids (AAS) inhibit natural testosterone production. However, most do not realize that AAS also inhibit DHEA production along with all other beneficial androgens.9-12 Most assume that simply using an “anti-estrogen” and inhibiting estrogen will prevent testicular shutdown and restore testosterone production, however this is not the case for the heavy steroid users. High levels of testosterone (AAS) can actually inhibit and degrade the enzymes responsible for its own creation, such as the 17a-hydroxylase enzyme.13 It can be theorized then, that all testosterone derivatives and AAS's such as stanozolol, methandrostenolone, nandrolone and even oxandrolone can directly inhibit the enzymes responsible for steroid production and cause long term suppression of steroidogenesis, aside from causing direct hypothalamus and pituitary suppression via the androgen receptor.
On the contrary, DHEA and pregnenolone appear to encourage there own production by stimulating the enzymes and hypothalamus to increase androgen production. Pregnenolone has been found to increase the release of gonadotropin releasing hormone (GnRH) from the pituitary, and thereby increase luteinizing hormone (LH) and follicle stimulating hormone (FSH) release.7 DHEA has been shown to stimulate StAR at a cellular level, therefore enhancing uptake of cholesterol into the mitochondria and up-regulating the rate limiting step in hormone synthesis.8 These properties of DHEA and pregnenolone seem to make them an excellent choice for post cycle therapy (PCT) or hypogonadal men, but there remains a problem.
Plain ol DHEA and pregnenolone are limited in there supplemental usefulness due to there eventual conversion to estrogen through interaction with the aromatase enzyme (CYP 19). Excessive estrogen can inhibit the hypothalamus pituitary testicular axis (HTPA), and increase fat deposits and water retention41. Fortunately, Dermacrine limits estrogen synthesis by including the Phyto Aromatase Inhibitor complex, consisting of three potent plant based aromatase inhibitors, namely 7,8 benzoflavone, chrysin and resveratrol.42,43 These flavonoids directly compete with aromatizing androgens for interaction with the aromatase enzyme as well and inhibit the production of the aromatase enzyme itself.44,45 As a result, estrogen is kept down, and the steroidogenic enzymes are kept up, therefore making Dermcrine one powerful hormone rejuvenator.
As another benefit to controlling estrogen levels, fat burning is made much easier. The fat loss is further catalyzed by the ingredients DHEA and 7-keto DHEA. Both of these thermogenic hormones increase calorie burning and fat loss by directly activating the mitochondrial and cytosolic thermogenic enzymes in liver.46,47.
Numerous studies with animals and humans have shown dramatic increases in fat and weight loss with the use of DHEA and 7-keto DHEA.48-51 Since DHEA is not a stimulant, the fat loss is accomplished without the jitters, anxiety or heart palpitations associated with drugs like caffeine and ephedra.
In summery, Dermacrine may help improve body composition by antagonizing cortisol, stimulating GH & IGF-1 release, raising anabolic/androgenic hormones, reducing estrogens and eliciting a thermogenic response from liver enzymes.
Dermacrine is positively correlated to support libido, erectile function and fertility through three main mechanisms: Increasing androgens, reducing estrogens and promoting healthy blood flow.
As its been discussed before, low levels of DHEA can be caused by steroid use, alcohol abuse, poor diet, lack of sleep, old age and excessive physical or mental stress. Its well established that low levels of DHEA (and testosterone) is associated with reduced sexual interest and ability.60,61 Therefore, it can be inferred that supplementing with DHEA can help support sexual function. Other androgens such as androstenedione, testosterone and their 5a-reduced metabolites; androstanedione, dihydrotestosterone, and androsterone share a strong influence on sexual function. All of these androgens have important neurobiological effects and act directly on the central nervous system to initiate sexual interest and stimulus.52 Dermacrine can incre ase these critical androgens by providing the main precursor, DHEA.
Another mechanism by which Dermacrine increases androgen production is by reducing estrogens and preventing negative feedback upon the hypothalamus pituitary testicular axis (HPTA). Our proprietary Phyto Aromatase Inhibitor complex (Phyto AI) effectively inhibits the aromatase enzyme (CYP 19) and reduces estrogen.42-45 In fact, chrysin, 7,8 benzoflavone, and resveratrol have been successfully used in animal studies to increase sperm count and fertility by inhibiting estrogen, and increasing testosterone.53,54 These animal studies also noted an “aphrodisiac” like property from these flavones, which makes sense since chrysin and 7,8 benzoflavone are the main active constituents from passion flower (passiflora incarnate) which has long been known to posses aphrodisiac like properties and has been prescribed for sexual disorders in other countries.15,16
Most importantly, the above animal studies also noted increases in both LH & FSH. As you may be aware, LH is a hormone sent from the pituitary which stimulates the testis to produce androgens, such as testosterone. Less known by most, is the importance of FSH. Without adequate FSH, LH would quickly desensitize the testis and androgen production would come to a halt, since FSH sensitizes the testis to the effects of LH by increasing the number of LH receptors in the testis. Many steroid users and/or hypogonadal men will attempt to restore their testosterone production by administering hCG (LH mimicker). However, HCG can quickly desensitize the testis and lead to further suppression of testosterone production. A better protocol would be to administer hCG with FSH (if one could obtain it), or simply buy our product.
As a final benefit, the ingredients in Phyto AI have shown to be “vasorelaxants”, which may help promote blood flow to genitalia and support erectile function.55-57
Note: Several steroidal aromatase inhibitors such as formestane (4-OHA), 1,4,6-androstatriene-3,17-dione (ATD) and androstenetrione (6-OXO) can directly inhibit the HPTA by interacting with the androgen receptor leading to a sequential reduction in LH.58,59 We DO NOT recommend the use of these steroidal based aromatase inhibitors’s.
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