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Free Test is a state-of-the-art formulation that utilizes 7 different mechanisms of action to increase testosterone, lower estrogen and cortisol, burn body fat, and build a leaner, more muscular physique.
PRODUCT CHARACTERISTICS:
•FREE TEST positively alters 7 homeostatic mechanisms of action that effect free and total testosterone output:
•Contains a natural suicide inhibitor of aromatase, and will improve the Testosterone : Estrogen (T:E) profile while concurrently increasing testosterone levels
•Increases NO/cGMP levels, which leads to increases in lutenizing hormone (LH) and greater endogenous testosterone production.
•Increases testicular Acetyl L-Carnitine (ALCAR) levels. High testicular ALCAR levels are conducive to heightened spermatogenesis.
•Lowers levels of cytokines IL-6, IL-1, and TNF-alpha- cytokines, which inhibit endogenous testosterone production by reducing levels of LH.
•Lowers cortisol levels and heightens Testosterone : Cortisol (T:C) ratio via competitive inhibition processes.
•Increases cAMP levels, which also increase LH levels.
•Influences/Increases androgen receptor (AR) binding via altering receptor electro-negativity.
After 8 weeks of usage of FREE TEST, test subjects were observed to have increased levels of free testosterone ranging from 50-200% over baseline. Impressive results for any product – especially one with no negative side effects!
EFFECTS RELATED TO PHYSIQUE AND LIFE ENHANCEMENT:
•Greater lean muscle mass
•Lowered body fat
•Better/Faster recovery from training
•Increased muscular strength
•Heightened libido and sexual drive
The basics of how FREE TEST works:
The main mechanism of action in FREE TEST has to do with the mytropic/catabolic ratio in skeletal muscle, catabolic principles, and how they relate to homeostasis. During a steroid or prohormone cycle, testosterone levels rise, creating a muscle growth state; as the testosterone to cortisol ratio (T:C) will become very positive. (See Figure 2: Notice the separation between the blue and pink lines at the beginning of the cycle). This allows for increased protein synthesis, and increases in lean body mass. However, due to homeostatic mechanisms in the body, cortisol levels begin to rise along with the increase in testosterone after the first 1-2 weeks (Note how the blue and pink lines come closer and closer together). The body seeks to gain balance (homeostasis) over the increased muscle building via modulating cortisol levels. The body recognizes that it cannot be in a state in which it requires such large amounts of nutrients for protein synthesis and lean tissue accretion for very long (a very high positive nitrogen balance), so it essentially tries to put the brakes on, via increasing cortisol levels to meet heightened testosterone levels (53).
This phenomenon occurs during every cycle and it is why, after week 6 of a cycle, gains slow dramatically, or stop altogether due to the homeostatic rise in cortisol. When this occurs, the user has one of two options: (1) Cessation of the cycle, followed by post-cycle therapy ((PCT) - note the pink line above the blue in wks. 10-12, indicative of a catabolic state), or: (2) Increase the dosage, and take the level of testosterone up even higher (not recommended for safety reasons).
Neither option is very good for keeping gains. The mechanism of action of Free Test seeks to circumvent this via manipulating the T:C ratio via non-androgen receptor mediated means. One key ingredient, 3, 7 keto DHEA plays a key role in accomplishing this. Here’s how it works: 7-Keto derivatives competitively interact with the 11beta-HSD1 enzyme, which is the enzyme that allows the transfer of inactive glucocorticoids to active ones. This is important as it therefore helps keep cortisol levels lower than normal by slowing (but not stopping) the conversion of inactive cortisol to active cortisol - allowing for mitigated levels of this catabolic hormone. (46-48).
Non-androgen receptor (AR) mediated methods of increasing testosterone are extremely crucial to the inner workings of Free Test. Another mechanism of action is that it exerts its effects through deceased estrogen levels, increased testicular function, and increased levels of luteinizing hormone (LH) (53). Since these controls are non-AR mediated (at least not directly), the rise in testosterone is more gradual and not as traumatic, consequently the body will not try to maintain homeostasis as stringently as with the dramatic increases seen with an AR-mediated cycle (see Figure 3 below).
These more gradual increases in testosterone levels allow for cortisol levels to remain relatively low during the cycle. Additional factors that directly suppress cortisol further improve the myotropic ratio (T:C), with muscle building far outweighing catabolism throughout the cycle, with minimal disruption of hormone levels post-cycle (53).
FREE TEST™ MAIN MECHANISMS OF ACTION:
Regulating Estrogen and Increasing Testosterone via Suicide Aromatase Inhibition: The Role of 3, 7-Keto DHEA:
3, 7-Keto DHEA is a naturally-occurring metabolite of dehydroepiandosterone (DHEA), and is a potent aromatase inhibitor with some very unique qualities. Aromatase is an enzyme that transforms testosterone into estrogen, and the more active aromatase is, the more estrogen will ultimately be present. Therefore, aromatase inhibitors significantly decrease the level of estrogen in the body. This is important as increased estrogen in men can signal the hypothalamic pituitary testicular axis (HPTA) to shut down the release of gonadotropin-releasing hormone (GnRH). GnRH signals the production of luteinizing hormone (LH), which signals the production of testosterone. Therefore, increased estrogen levels can lower endogenous testosterone production (21,29,31).
3, 7-Keto DHEA has demonstrated strong ability to lower estrogen, thus mitigating this effect. It has a high binding affinity (Ki value = 0.22 mM) to the aromatase enzyme, and binds in an irreversible manner, making it a suicide inhibitor of aromatase. Ki Values measure how efficiently a compound binds to its associated receptor. The lower the Ki value; the higher the binding affinity. This inhibition allows for the production of less estradiol (E2) and estrone (E1) and allows the user of the compound to maintain a higher level of testosterone; hence improving the Testosterone: Estrogen (T:E) ratio. The mechanism through which aromatase inhibitors raise testosterone is fairly simple; the HPTA senses low levels of estrogen, and because the body seeks to maintain homeostasis (it likes to maintain at least some estrogen, even in men), there is a concurrent increase in the amount of testosterone that is being produced, as a way to compensate for the low estrogen levels. The increased testosterone levels normally will result in increased estrogen since there is no estrogen being produced. Essentially, the brain is tricked into trying to produce more estrogen, so it releases more luteinizing hormone releasing hormone (LHRH) and subsequently more LH, leading to even higher testosterone levels (20,21-23).
All aromatase inhibitors share this characteristic of positively altering the T:E ratio, and all will raise serum testosterone levels in men, which has been referenced in numerous studies. 3,7-Keto DHEA is comparable in potency to several other commonly available aromatase inhibitors. As explained above, a lower Ki value means higher potency, making it more potent than both Formestane and Exemestane, and very similar to androstentrione (ATD) (31,55). (See Figure 5)
3,7-Keto DHEA is unique from other commonly used aromatase inhibitors in sports supplements in that it is a natural metabolite of 7-Keto DHEA and it cannot directly bind to the androgen receptor. 3,7-Keto DHEA (like 7-Keto DHEA) also cannot convert to testosterone, estrogen, or progesterone via any type of enzymatic reaction, so by strict definition it cannot in any way be considered a prohormone. This clearly differentiates it from other recently banned products that allow for the direct conversion to a controlled substance in the body (in either in trace amounts or full-scale conversion). This can not occur with 3,7-Keto DHEA, as it is formed naturally in humans from 7-Keto DHEA and can be readily found in humans in the amount of 5-7 ug/day (23-24).
Increasing luteinizing hormone via elevating nitric oxide and cyclic Guanosine Monophosphate (cGMP): The role of Acetyl-L-Carnitine, Resveratrol, and their interaction with the male reproductive system and StAR:
FREE TEST™ strongly influences testosterone production through the nitric oxide pathway and cGMP by increasing luteinizing hormone levels. Luteinizing Hormone (via receptors found on the surface of Leydig cells) is important as it controls the production and secretion of testosterone (1-4).
The inclusion of Acetyl L-Carnitine (ALCAR) (a derivative of L-Carnitine which is an amino acid that is crucial for fatty acid metabolism and male reproductive function) allows for this manipulation of cGMP, as does Resveratrol. cGMP is classified as a second messenger, meaning that it exerts its effects by acting in a manner secondary and in response to a first messenger signaling molecule. When a first messenger signaling molecule binds to a cell surface, another secondary pathway is activated that increases cGMP production (1,15,19,27).
Increasing cGMP is extremely important to the action of FREE TEST, in that increased cGMP levels equate to increased levels of luteinizing hormone (LH). LH has a stimulatory action on endogenous testosterone production; so when cGMP levels increase, so do LH levels, and when LH levels increase, so does endogenous testosterone production. This effect has been well documented in recent research on PDE5 inhibitors (compounds that increase cGMP levels such as slidenafil (Viagra®). Researchers found that high cyclic GMP levels ultimately equate to higher testosterone levels.
ALCAR has also been shown to be an acetate donor to coenzyme A, allowing it to aid in the synthesis and function of acetylcholine, both peripherally and centrally. 7-Keto derivatives of DHEA (like 3,7-Keto DHEA) antagonize GABA-A receptors and functionally increase cholinergic expression. Through this mechanism of action, ALCAR and 3,7-Keto DHEA can increase cGMP levels, through increasing the amount of available acetylcholine- as mentioned above, more cGMP, more LH, more testosterone. (18,20,32).
ALCAR levels are very important for testicular function, in that low testicular ALCAR and L-Carnitine levels are strongly associated with testicular dysfunction and infertility. (28,30,33)
ALCAR has also been shown to have a significant effect on increasing Leptin levels, and has also been shown to be a potent factor in the male reproductive system. Leptin releases LHRH (luteinizing releasing hormone) by activating nitric oxide synthase (NOS), an enzyme that speeds the formation of nitric oxide (NO) from the amino acid L-Arginine. LHRH controls the release of luteinzing hormone (LH), and greater amounts of LHRH release equal greater amounts of luteinizing hormone (LH) release, which can allow for higher amounts of endogenous testosterone. Therefore, by increasing leptin levels and boosting LHRH release, ALCAR can have some additional positive effects on endogenous testosterone production (1-4,18).
L-Carnitine, ALCAR, and several derivations thereof have been shown to elevate Nitric Oxide (NO) levels. NO is important in that it regulates vascular tone, central nervous system stimulation, induces the release of LHRH and regulates cGMP levels. ALCAR and 7-Keto derivatives of DHEA have also been shown to elevate acetylcholine levels, which allow for a concurrent increase in cGMP production. NO also activates the release of LHRH which reaches the pituitary and activates the release of gonadotropins via the activation of neural NO synthase (NOS) in the pituitary gland (1-4, 15, 33-34).
The fact that cGMP has a stimulatory action on steroidogenesis via increased LH production is an important one. In numerous pathway studies, increases in cGMP increased phosphorylation of the steroidogenic acute regulatory protein (StAR). Increased phosphorylation of StAR is important, in that (StAR) is a Leydig cell cholesterol transfer protein that provides the building blocks for testosterone synthesis. Increased phosphorylation allows for increased StAR activation, and increased StAR activation is necessary for the stimulation of steroidogenic enzymes involved in the transfer of cholesterol to testosterone. This increase in StAR, and the greater transfer of cholesterol to testosterone can result in greater endogenous testosterone synthesis (15,33-34).
By increasing the intermediary between these two processes, a resulting positive shift in muscle growth can occur. Therefore, high cGMP levels also equate to high levels of luteinizing hormone (the hormone responsible for mediating endogenous spermatogenesis), and when cGMP levels are elevated it serves as an intermediate in the signaling cascade that ranges from LH binding to testosterone production (15,33-34).
These results suggest that cGMP contributes to the control of basal steroidogenesis (endogenous testosterone production) in Leydig cells through the protein kinase G (PKG, and enzyme responsible for the activation of second messengers) -dependent modification of the StAR protein and interaction with LH. LH controls the production and secretion of testosterone, and the subsequent binding of LH with its receptor allows signaling through the cyclic AMP pathway through GTP binding proteins. Signal transduction occurs through the protein kinase A pathway as its principal signal transduction mechanism, and this ultimately allows for the release of testosterone after 30-60 minutes of LH stimulation (15-17,33-34).
To summarize, FREE TEST™ contains several potent direct mechanisms of action that strongly influence the production of increased testosterone via the NO / cGMP pathway, through a cascade of regulatory proteins and second messengers.
Forskolin and Resveratrol: Increasing endogenous testosterone production via increasing Cyclic AMP (cAMP) levels:
Forskolin has been the subject of research in the supplement industry since the early 1980s. Scientific studies have discovered that along with increasing thyroid activity and thermogenesis, forskolin is also a potent muscle enhancer. This occurs primarily through elevation of 3,5 cyclic adenosine monophosphate (cAMP) which is another second messenger that is important in hormone signaling (14,16).
cAMP elevation is a crucial piece of the puzzle in creating both a muscle building and thermogenic state, and forskolin is one of the best compounds available for triggering dramatic increases in cAMP levels. One study showed that forskolin was able to increase cAMP levels 4.82 times more than a placebo. Another study demonstrates that forskolin can raise cAMP levels in fat cells. This is important because it demonstrates the ability of the compound to enhance lipolysis; meaning that forskolin exerts powerful fat-burning effects as well as being a potent myotropic agent; plus forskolin can also enhance endurance capacity as well (5-10,14,16).
Another added bonus of forskolin and resveratrol are that they both increase cAMP independently of epinephrine, thus providing increased energy without the need to take any type of traditional stimulant. Increased cAMP also is a signal for steroidogenesis (testosterone production) in the Leydig cells of the testes by increasing levels of steroidogenic acute regulatory protein (StAR- as mentioned above) (14,16,36-38).
As mentioned earlier, StAR activation is necessary for the stimulation of the transfer of cholesterol to testosterone. By this process, and the fact that high cAMP levels also equate to high levels of luteinizing hormone, significant increases in endogenous testosterone production can occur along with a resulting increase in muscle growth and protein synthesis (14-15).
Numerous other studies have shown parallels between increased cAMP levels and increased muscle growth, and a ground-breaking 2005 study in The Journal of Obesity Research found that obese men taking 250 mg of 10% forskolin a day for 12 weeks (roughly the dosage included in the daily dosage of Free Test™) experienced an averaged 33% increase in free testosterone levels, averaged a 10 lbs. fat loss per person and increased lean mass an average of 8 lbs! A 2001 study by Badmaev (see Figure 6) also yielded similar results (6,8,54).
Quercetin is a citrus bioflavanoid that has been shown to boost the effects of resveratrol (this is the primary rationale for its inclusion in the formula) via prevention of precocious glucorindiation (deactivation of the compound) by the liver. Similarly, quercetin has also been shown to have some estrogen-antagonizing effects. Quercetin has also been shown to have some additional anti-oxidant effects, and has been shown to lower cortisol levels in several animal studies. Lastly, the combination of resveratrol and quercetin also has been shown in some cellular studies to actually destroy fat cells. (39,40,44)
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