Hormone Amplifying Stack - Raise Testosterone and Growth Hormone!
Applied Nutriceuticals Free Test (100 capsules)Applied Nutriceuticals HGH Up (150 capsules)
Applied Nutriceuticals HGH Up - Promotes Radical Increases in Growth Hormone and Testosterone Production!
HGHup is so unique it falls into a new category altogether. HGHup♂ is the world’s first hANh™ (Hybrid Anabolic / Near Hormonal); which is defined as a product that engages a synchronization of natural and exogenous factors to produce a pronounced anabolic and hormonal response. The distinct advantage of a hANh is that the user is able to obtain maximal physiological benefits comparable to that of fully hormonal products while minimizing potential side effects and disruption of endogenous factors post-usage.
HGHup♂ promotes radical increases in serum HGH and testosterone levels without a prescription. It is the only orally viable compound that is proven to increase HGH AND testosterone in human subjects.
PRODUCT CHARACTERISTICS:
• Increases the output of growth hormone and local IGF-1 levels• Increases the duration/viability of growth hormone pulse mass
• Increases androgen receptor structure, function, and number
• Increases natural production of testosterone
EFFECTS RELATED TO PHYSIQUE AND LIFE ENHANCEMENT:
• Greater lean muscle mass• Lowered body fat
• Increased strength
• Faster healing of injuries and better recovery from physical stress/training
• Better skin tone
• Deeper, more restful sleep
MAIN MECHANISMS OF ACTION:
Mucuna Pruriens, Vitamin B6 and L-Dopa: Increase Growth Hormone Output and Testosterone Production While Concurrently Decreasing Somatostatin and Prolactin.• HGHup♂ contains highly concentrated L-Dopa derived from Mucuna Pruriens. Mucuna Pruriens is an Ayurvedic Herb that has both anti-hypoglycemic and L-Dopa-increasing qualities. (32). L-Dopa has been shown to significantly increase levels of growth hormone in human subjects when administered orally. (1, 2, 3, 33).
• Oral viability in HGHUP♂ critical for product effectiveness, as growth hormone cannot be absorbed and is rendered ineffective due to the fragility of the ingredients. Several good examples are synthetic growth hormone (see Fig. 1) and growth hormone releasing hormone (GHRH, see Fig. 2). These compounds cannot be administered orally; because of their fragile amino acid sequence is destroyed by stomach acids. This also holds true with the vast majority of the so-called “GH Boosters” and “Peptides” commonly found in sports nutrition products.
• L-Dopa and Dopamine have also been shown to inhibit prolactin, a hormone that suppresses male testosterone production. Prolactin also has a positive correlation with a second hormone called somatostatin, which decreases the both amount and effectiveness of circulating growth hormone. Therefore, by lowering prolactin (and consequently somatostatin) levels, HGHUP♂ increases both testosterone and GH production; leading to greater recovery and lean body mass (38, 39).
• Vitamin B6 is also included in the formula for HGHUP♂, as it can also help further lower prolactin levels and increase the night-time peak of GH release pulse, while at the same time increasing the rise in GH associated with exercise by as much as 23% (7).
• Huperzine-A: Increasing AChE Inhibition and Mean serum GH by decreasing somatostatin. Huperzine-A is a strong acetylcholine esterase (AChE) inhibitor. Acetylcholine esterase inhibitors have been shown in numerous scientific studies to inhibit somatostatin via a variety of synergistic biomechanisms; all of which contribute to increased levels of growth hormone (9, 10, 11, 12, 13, 14, 15, 16, 17, 18). Consequently, the Huperzine-A, in HGHUP♂ increases the length, intensity, duration of growth hormone pulses and increases mean serum GH levels, therefore allowing for more of the positive anabolic and anti-aging benefits associated with GH.(8, 10, 12-17, 19-20).
• Somatostatin is a hormone that exerts effects on anterior pituitary as well as pancreatic, liver and gastrointestinal function (40, 41, 42, 43) . Somatostatin is of extreme importance because it directly effects growth hormone release and is the major regulating factor in slowing or even stopping growth hormone output. Therefore, by inhibiting somatostatin, overall mean serum GH will increase (41, 42). Somatostatin inhibits GH secretion indirectly via antagonizing GHRH secretion (41, 42, 43).
Green Tea Extract, and (−)-epigallocatechin-3-O-gallate (EGCG): Increasing Dopa Decarboxylase Inhibition and the AChE-inhibiting Effects of HGHUP
• Dopamine crosses the blood/brain barrier poorly, and cannot exert optimal effects on target receptors unless enough of the compound reaches the brain. L-Dopa is freely absorbed across this barrier, and when L-dopa crosses the barrier readily, growth hormone levels increase. (1-6, 32-33)• L-Dopa is most effective when conversion of L-Dopa to dopamine is mediated by a decarboxylase inhibitor. A decarboxylase inhibitor is a substrate that inhibits the metabolism of one biological entity into another biological entity (2, 3, 4, 5, 19, 20, 37).
• A decarboxylase inhibitor is generally administered at the same time as L-Dopa / Mucuna in order to reduce conversion of the L-dopa into dopamine in the periphery. (−)-epigallocatechin-3-O-gallate (EGCG), which is found in high amounts in the green tea extract used in HGHUP♂, is a potent decarboxylase inhibitor. The decarboxylase-inhibiting qualities of EGCG have been documented in several recent studies, in that EGCG seems to prevent L-dopa from converting into dopamine; allowing more significant levels of L-dopa to reach the brain and increase growth hormone levels (1, 2, 3, 4, 5, 37).
• EGCG has also been shown to significantly increase the effects of Huperzine A on acetylcholine esterase inhibition by increasing the transport of Huperzine-A by serum albumin. This allows for greater amounts of acetylcholine to be present, therefore allowing for greater mean serum growth hormone. Increased serum GH from HGHUP♂ allows for increased anabolism, better recovery, and increased muscle mass (19, 20).
HGHUP♂ INCREASES ANDROGEN RECEPTOR QUANTITY AND DENSITY AND CREATES A BETTER BINDING ENVIRONMENT FOR EXISTING ANDROGENS
L-Carnitine-L-Tartrate and Magnesium: Increasing Androgen Receptor Number and Density, and the Creation of a Better Binding Environment
• L-Carnitine L-Tartrate is an amino acid that has been shown to increase the number of androgen receptors in skeletal muscle, creating a better binding environment for testosterone and other androgens by allowing for a greater number of intact receptors available for hormonal interactions. (21-23)• Magnesium has been shown in more recent studies to inhibit the binding of steroid hormone binding globulin (SHBG) and free testosterone. SHBG binds free testosterone and allows it to be excreted from the body, without binding the androgen receptor. Magnesium keeps this from happening by altering the binding affinity of testosterone to SHBG; thereby allowing for increased amounts of free testosterone to remain active in the bloodstream. (24)
• Other human research has shown that supplemental magnesium, when taken along with other ingredients like DHEA and Zinc, can significantly increase free testosterone. (25-27). Therefore, HGHUP♂ allows for greater numbers of androgen receptors and a better binding environment for testosterone in skeletal muscle. This is a new breakthrough in sports supplementation as HGHUP♂ creates a better target for circulating free testosterone, allowing for greater binding of testosterone to the extra receptors which leads to increased protein synthesis, better recovery, and increased muscle mass.
HGHUP♂ INCREASES TESTOSTERONE
Mucuna Pruriens, Selenium, and Chlorophytum Borivillanum Ethanolic/Sapogenic Extract: Increasing Testosterone Levels• Mucuna Pruriens has been shown in several recent human studies to improve testosterone levels and spermatogenesis in animal studies and humans, via prolactin inhibition. Prolactin, as mentioned earlier, is a hormone that suppresses male testosterone production (30-31, 34-36, 38-39).
• The ethanolic and sapogenic extracts of Chlorophytum Borivaillanum have also been shown in animal studies to increase testosterone, and anecdotal data from products containing this compound also point to increased testosterone and lean body mass for users of this phyto-androgenic compound. However, the mechanism of action of Chlorophytum is poorly understood. (28- 29)
• Selenium has been shown in several studies to have direct effects on the biosynthesis pathways of testosterone. Selenium is rate-limiting in testosterone production in men, and if enough selenium (selenium deficiency is very common) is not available, testosterone will not be produced in optimal levels (27).
Administration, Timing, and Dosing
• Normal GH pulses (see chart below) occur throughout the day. For a normal male in an average day, there are 10 pulses of GH secretion lasting on average 96.4 mins with 128 mins between each pulse. The largest GH pulse occurs during stages 3 and 4 of the sleep cycle. GH pulses during sleep (see Fig. 5) occur at nearly triple the rate of GH pulses during the day (44-45)• Somatostatin release is controlled in large part by the cholinergic system. The cholinergic system is responsible for regulating the amount of acetylcholine found in the body at any given time. Acetylcholine is a neurotransmitter responsible for muscular activation in the peripheral nervous system, and tends to be excitatory in the central nervous system (CNS) (10, 11, 12, 13).
• The CNS component of acetylcholine mediates the cholinergic system, and this is important because the cholinergic system is responsible for mediating growth hormone response (11, 12, 13, 14, 15).
• The mechanism through which this is accomplished is simple: by increasing acetylcholine levels, there will be an increase in mean serum GH. HGHUP♂ increases acetylcholine via lowering levels of acetylcholine esterase or AChE (an enzyme that breaks down acetylcholine) (11, 12, 13, 14, 15).
• Taking an acetylcholine esterase inhibitor (in the case of HGHUP♂, Huperzine-A) before sleep will result in dramatically reduced somatostatin levels and dramatically increase serum GH levels (1-4, 5, 9-17,19, 20, 44, 45).
Somatostatin seems to be the major inhibitory factor in sleep-related GH pulses. When AChE is inhibited by pryridostigmine (an AChE inhibitor very similar to Huperzine-A) GH pulse mass is increased, and mean serum GH almost doubled. In terms of potency, Huperzine-A has actually been shown to be more potent than pyridostigmine bromide in terms of AChE inhibition (9-17, 19-20) .
• There has also been a very popular trend recently of bodybuilders taking Huperzine-A along with injectible synthetic growth hormone, because the compound is so effective at inhibiting somatostatin and increasing serum GH (46)
Taking (−)-epigallocatechin-3-O-gallate (EGCG) along with Huperzine-A will increase Hup-A’s effectiveness in inhibiting acetylcholine esterase, and its ability to allow the cholinergic system to suppress somatostatin. This has been verified in several scientific studies (19-20).
• Taking a supplement containing L-Dopa with a decarboxylase inhibitor before sleep can allow for dramatically increased levels of GH (1-5, 32- 33, 37-39).
• Hypoglycemia (low blood sugar) can also increase the amount of GH released. Insulin and GH are antagonistic, and the lower the insulin level, the higher the GH level (see chart below, 44-45).
• Timing of the dose and manipulating insulin levels before sleep is the key getting great results with HGHUP♂ (44-45, 47)
• Best results occur when a 4-6 capsule dosage is taken on an empty stomach (fasted state) 30 minutes before bedtime (44-45, 47)
Why Most OTC GH Products Are Ineffective, and How HGHUP Differs
• Over the last 20 years, a variety of products that claim to boost HGH orally have been promoted in the US sports supplement market. The vast majority of these products have been completely ineffective for several reasons:• Growth hormone is a peptide (a long chain amino acid structure), that cannot be taken in an oral form, due to the destruction of the sequence by the acidic environment of the stomach. Any supplement containing “oral growth hormone” is a scam (47).
• Many products use a combination of amino acids such as arginine and lysine in “kitchen sink” formulas, and claim that their combination is “scientifically proven” to work. Many amino acids boost growth hormone levels, but most of the time, it is only when taken intravenously, or in completely unattainable dosages that would make a normal person extremely sick. And the correct dosage is in gram amounts, not in the milligram range offered in many of these products (47).
• Even if these products allow for a viable release of GH, there is nothing present to inhibit somatostatin, which has been found to be the biggest factor in controlling GH levels (47)
• Many of these products are powdered mixes that contain sugar, sweeteners, or other compounds that may increase blood sugar. As discussed above, this will render the product virtually useless due to the inverse relationship between glucose and growth hormone (47).
• HGHUP♂ differs from these compounds because of the nature of the formulation. Every compound in the product is designed to work in concert with the other components; no filler or ineffective components are found in this product (47).
• HGHUP♂ utilizes the latest research on compounds which have been overlooked by other companies. The secret of the product is in the complexity, effectiveness and synergism of the blend (1-47).
• HGHUP♂ is the first product to positively manipulate somatostatin; this alone puts it in a class by itself.
• HGHUP♂ also utilizes components that boost androgen levels, increase the number and function of androgen receptors, and create an overall BETTER anabolic environment in which levels of testosterone and GH are optimized, leading to better recovery, increased lean body mass, and lower body fat (1-47).
Stacks and Tips to Maximize the Product
• Take Bio-Mend Anti-Oxidant formula• High ORAC Value
• Protects cellular membrane
• Protects transcriptional factors (mRNA and DNA)
In general, maintain a healthy diet and lifestyle:
• Drink Plenty of water; at least 64 oz. per day• Ingest at least 1 gram of protein per lb. of body weight daily
• Sleep at least 7 hours per night
• Eat lots of fruits and vegetables
• Eat lots of complex carbs
• Eat 5-6 smaller protein and carb-rich meals throughout the day
• Increase calories to at least 500 Kcal/day over your normal intake
• BCAAs and Creatine will be helpful
• Avoid alcohol and tobacco
• Take HGHUP♂ on an empty stomach before going to sleep, or take it with an all-protein meal. Remember, carbohydrates/insulin decrease the effectiveness of the product.
• HGHUP♂ can be stacked with synthetic growth hormone and will make it more effective
• In conclusion, HGHUP♂ in the most effective orally administered HGH and Testosterone agonist yet to be offered in the history of sports nutrition. For more information, you can contact Applied Nutriceuticals at info@appliednutriceuticals.com.
Studies and Clinical Info
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3. Schönberger W, Ziegler R, Brodt B, Grimm W. HGH secretion after oral application of L-dopa and L-carbidopa. Eur J Pediatr. 1976 Jun 8;122(3):195-200.
4. Fevang FO, Stoa RF, Thorsen T, Aarskog D. The Effect of L-dopa with and without decarboxylase inhibitor on growth hormone secretion in children with short stature. Acta Paediatr Scand. 1977 Jan; 66(1):81-84
5. Philippi H, Pohlenz J, Grimm W, Koffler T, Schönberger W. Simultaneous stimulation of growth hormone, adrenocorticotropin, and cortisol with L-dopa, carbidopa, and propranolol in children of short stature. Acta Paediatr, 2000 Apr;89(4):442-446.
6. Gordon M, Markham J, Hartlein JM, Koller JM, Loftin S, Black KJ. Intravenous levodopa administration in humans based on a two-compartment kinetic model. J. Neurosci Methods, 2007 Jan 30:159(2):300-307. Epub 2006 Aug 24
7. Pyridoxine (B6) suppresses the rise in prolactin and increases the rise in growth hormone induced by exercise. 1982 Aug 12;307(7):444-5.
8. Barletta C, Sellini M, Bartoli A, Bigi C, Buzzetti R, Giovannini C Influence of administration of pyridoxine on circadian rhythm of plasma ACTH, cortisol prolactin and somatotropin in normal subjects. Boll Soc Ital Biol Sper. 1984 Feb 28;60(2):273-8
9. Gordon RK, Haigh JR, Garcia GE, Feaster SR, Riel MA, Lenz DE, Aisen PS, Doctor BP. Oral administration of pyridostigmine bromide and huperzine A protects human whole blood cholinesterases from ex vivo exposure to soman. Chem Biol Interact. 2005 Dec 15;157-158:239-46. Epub 2005 Oct 26.
10. Wang R, Yan H, Tang XC. Progress in studies of huperzine A, a natural cholinesterase inhibitor from Chinese herbal medicine. Acta Pharmacol Sin. 2006 Jan;27(1):1-26
11. Kelijman M, Frohman LA. The role of the cholinergic pathway in growth hormone feedback. J Clin Endocrinol Metab. 1991 May;72(5):1081-7
12. Liang YQ, Tang XC. Comparative studies of huperzine A, donepezil, and rivastigmine on brain acetylcholine, dopamine, norepinephrine, and 5-hydroxytryptamine levels in freely-moving rats. Acta Pharmacol Sin. 2006 Sep;27(9):1127-36
13. Giustina A, Bossoni S, Bodini C, Doga M, Girelli A, Buffoli MG, Schettino M, Wehrenberg WB. The role of cholinergic tone in modulating the growth hormone response to growth hormone-releasing hormone in normal man. Metabolism. 1991 May;40(5):519-23
14. Friend K, Iranmanesh A, Login IS, Veldhuis JD Pyridostigmine treatment selectively amplifies the mass of GH secreted per burst without altering GH burst frequency, half-life, basal GH secretion or the orderliness of GH release. Eur J Endocrinol. 1997 Oct;137(4):377-86
15. Dinan TG, O'Keane V, Thakore J. Pyridostigmine induced growth hormone release in mania: focus on the cholinergic/somatostatin system. Clin Endocrinol (Oxf). 1994 Jan;40(1):93-6
16. Thakore JH, Coffey I, Dinan TG. Time dependency of pyridostigmine-induced growth hormone response.
J Basic Clin Physiol Pharmacol. 1994 Apr-Jun;5(2):117-2
17. Li YX, Zhang RQ, Li CR, Jiang XH. Pharmacokinetics of huperzine A following oral administration to human volunteers.
Eur J Drug Metab Pharmacokinet. 2007 Oct-Dec;32(4):183-7.
18. Haigh JR, Johnston SR, Peppernay A, Mattern PJ, Garcia GE, Doctor BP, Gordon RK, Aisen PS. Protection of red blood cell acetylcholinesterase by oral huperzine A against ex vivo soman exposure: next generation prophylaxis and sequestering of acetylcholinesterase over butyrylcholinesterase. Chem Biol Interact. 2008 Sep 25;175(1-3):380-6.
19. Xiao J, Chen X, Zhang L, Talbot SG, Li GC, Xu M. Investigation of the mechanism of enhanced effect of EGCG on huperzine A's inhibition of acetylcholinesterase activity in rats by a multispectroscopic method. J Agric Food Chem. 2008 Feb. 13:56(3) 910-915.
20. Zhang L, Cao H, Wen J, Xu M. Green tea polyphenol (-)-epigallocatechin-3-gallate enhances the inhibitory effect of huperzine A on acetylcholinesterase by increasing the affinity with serum albumin.
21. DI MARZIO L. (1) ; MORETTI S. (2) ; D'ALO S. (1) ; ZAZZERONI F. (1) ; MARCELLINI S. (2) ; SMACCHIA C. (3) ; ALESSE E. (1) ; CIFONE M. G. (1) ; DE SIMONE C. (1) ; Acetyl-l-carnitine administration increases insulin-like growth factor 1 levels in asymptomatic HIV-1-infected subjects : Correlation with its suppressive effect on lymphocyte apoptosis and ceramide generation.
22. Kraemer WJ, Spiering BA, Volek JS, Ratamess NA, Sharman MJ, Rubin MR, French DN, Silvestre R, Hatfield DL, Van Heest JL, Vingren JL, Judelson DA, Deschenes MR, Maresh CM. Androgenic responses to resistance exercise: effects of feeding and L-carnitine. Med Sci Sports Exer., 2006 Jul: 38(7): 1288-96.
23. Kraemer WJ, Volek JS, French DN, Rubin MR, Sharman MJ, Gómez AL, Ratamess NA, Newton RU, Jemiolo B, Craig BW, Häkkinen K. The effects of L-carnitine L-tartrate supplementation on hormonal responses to resistance exercise and recovery. J Strength Cond. Res. 2003 Aug: 17(3): 455-462,
24. André C, Berthelot A, Robert JF, Thomassin M, Guillaume YC. Testimony of the correlation between DHEA and bioavailable testosterone using a biochromatographic concept: effect of two salts. J Pharm Biomed An., 2003 Dec 4: 33(5): 911-21.
25. Excoffon L, Guillaume YC, Woronoff-Lemsi MC, André C. Magnesium effect on testosterone-SHBG association studied by a novel molecular chromatography approach. J Pharm Biomed An. 2009 Feb. 20: 49(2). 175-180.
26. Age-Related Eye Disease Study Research Group (2001). “A Randomized, Placebo-Controlled, Clinical Trial of High-Dose Supplementation With Vitamins C and E, Beta Carotene, and Zinc for Age-Related Macular Degeneration and Vision Loss. Arch Opthalmology. 119(10): 1417.
27. Berdanier, Carolyn D.; Dwyer, Johanna T.; Feldman, Elaine B. (2007). Handbook of Nutrition and Food. Boca Raton, Florida: CRC Press.
28. Thakur M. and Dixit V.K.* EFFECT OF CHLOROPHYTUM BORIVILIANUM ON ANDROGENIC & SEXUAL BEHAVIOR OF MALE RATS Indian Drugs 2006 April 43(4): 300-306
29. Kothari S.K., Safed Musli (Chlorophytum borivilianum) revisited, Journal of Medicinal and Aromatic Plants. 2004, 26, 60-63.
30. Saxena S and Dixit V.K: Role of total alkaloids of Mucuna pruriens Baker in spermatogenesis in male rats, Indian Journal of Natural Products. 1987, 3(2), 3-7.
31. Unnithan A.R. and Tandon V.L: Role of growth hormone in spermatogenesis in male rats. Indian Journal of Experimental Biology. 1982,20,734-737.
32. Modi KP, Patel NM, Goyal RK. Estimation of L-dopa from Mucuna pruriens LINN and formulations containing M. pruriens by HPTLC method Chem Pharm Bull (Tokyo). 2008 Mar: 56(3): 357-359.
33. Tharakan B, Dhanasekaran M, Mize-Berge J, Manyam BV. Anti-Parkinson botanical Mucuna pruriens prevents levodopa induced plasmid and genomic DNA damage.Phytother Res. 2007 Dec;21(12):1124-6.
34. Ahmad MK, Mahdi AA, Shukla KK, Islam N, Jaiswar SP, Ahmad S.
Effect of Mucuna pruriens on semen profile and biochemical parameters in seminal plasma of infertile men. Fertil Steril. 2008 Sep;90(3):627-35. Epub 2007 Nov 14.
35. Shukla KK, Mahdi AA, Ahmad MK, Shankhwar SN, Rajender S, Jaiswar SP. Mucuna pruriens improves male fertility by its action on the hypothalamus-pituitary-gonadal axis. Fertil Steril. 2008 Oct 28. [Epub ahead of print]
36. Shukla KK, Mahdi AA, Ahmad MK, Jaiswar SP, Shankwar SN, Tiwari SC .Mucuna pruriens Reduces Stress and Improves the Quality of Semen in Infertile Men .Evid Based Complement Alternat Med. 2007 Dec 18. [Epub ahead of print
37. Bertoldi M, Gonsalvi M, Voltattorni CB. Green Tea polyphenols: Novel irreversible inhibitors of dopa decarboxylase Biochem Biophys Res Commun. 2001 Jun 1;284(1):90-3.
38. Vaidya RA, Aloorkar SD, Sheth AR, Pandya SK. Activity of bromoergocryptine, Mucuna pruriens and L-dopa in the
control of hyperprolactinaemia. Neurol India. 1978 Dec;26(4):179-82.
39. Vaidya RA, Sheth AR, Aloorkar SD, Rege NR, Bagadia VN, Devi PK, Shah LP. The inhibitory effect of the cowhage plant- mucuna pruriens-and L-dopa on chloropromazine-induced hyperprolactinemia. Neurol India. 1978 Dec;26(4):177-8.
40. Epelbaum J, Guillou JL, Gastambide F, Hoyer D, Duron E, Viollet Somatostatin, Alzheimer's disease and cognition: An old story coming of age? C. Prog Neurobiol. 2009 Jul 10.
41. Nikolaeva AA, Koroleva SV, Ashmarin IP. [Research of interactions in the dopamine-serotonin-somatostatin system promises new outlook in fundamental and practical respects] Nikolaeva AA, Koroleva SV, Ashmarin IP. Eksp Klin Farmakol. 2009 Mar-Apr;72(2):60-4. Review
42. Cordido F, Isidro ML, Nemiña R, Sangiao-Alvarellos S.Ghrelin and growth hormone secretagogues, physiological and pharmacological aspect. Curr Drug Discov Technol. 2009 Mar;6(1):34-42.
43. Strowski MZ, Blake AD. Function and expression of somatostatin receptors of the endocrine pancreas. Mol Cell Endocrinol. 2008 May 14;286(1-2):169-79.
44. Haff, G. Lecture Notes for Graduate Study: Hormonal Parameters Relevant to Training. Appalachian State University, 2000.
45. Khoo, B. and Grossman, A. Normal Physiology of the Hypothalamus and Anterior Pituitary. St. Bartholomew’s Hospital, West Smithfield, London. Neuroendocrinology, Hypothalamus, and Pituitary. 2007 Ch. 1 Lecture.
46. Various sources. Anecdotal Information concerning the usage of AChE inhibitors with synthetic GH.
47. Applied Nutriceuticals Research. Unpublished alpha testing for new somatotropin-enhancing sports supplement. Charlotte, NC. 2009
Applied Nutriceuticals Free Test - Turbo-Charges Free Testosterone Output!
What's better than a Pro-Hormone? FREE TEST™!!!
The prohormone ban has come and gone. Yeah, there are a few still out there…the ones nobody wants because they don’t work. There might be a few dirty compounds floating around the internet from some shady companies too – and they’re not even remotely worth the risk. So what’s a guy who looking for REAL, HARDCORE gains supposed to do NOW?
Enter the era of the hANh™ (Hybrid Anabolic / Near Hormonal); which is defined as a product that engages a synchronization of natural and exogenous factors to produce a pronounced anabolic and hormonal response. The distinct advantage of a hANh is that the user is able to obtain maximal physiological benefits comparable to that of fully hormonal products while minimizing potential side effects and disruption of endogenous factors post-usage. Applied Nutriceuticals® pioneered this product category with HGHup♂™ and now takes it a step further with FREE TEST™.
FREE TEST cranks your testosterone levels like no other product because it hits the problem from two separate directions: On one hand it focuses on decreasing the body’s mechanisms that lower endogenous (natural) testosterone production – the most prominent one being cortisol. On the other hand it increases the testicular output of testosterone. The net result? An exponential improvement in the Anabolic / Catabolic Ratio (the proportion of Testosterone vs. Cortisol) – and even more importantly - it targets increases in the amount of FREE (direct) TESTOSTERONE, which is unbound and readily available to exert it’s anabolic effects on your body! And THAT, my friends, is what directly leads to huge increases in massive, rock-hard muscle. (Not to mention your sex life will go on turbo as well…you can thank us for that later!)
Below are actual test results from 6 test subjects after taking FREE TEST:
Here’s the best part: FREE TEST IS NOT A PROHORMONE nor does it convert to any hormone - so it is completely safe. So, if you were bummed when the prohormone ban went down…don’t be. We’ve got you covered.
Here’s a little of the “techie” stuff about how it works:
- *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!
Furthermore, the subjective feedback from the FREE TEST beta testers was nothing short of amazing. Within the first week users experienced feeling more motivated and assertive with shirt-splitting pumps, big-time strength increases, and revved up libido…all within the first week!
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 anabolic/catabolic ratio in skeletal muscle, catabolic principles, and how they relate to homeostasis. During an anabolic steroid or prohormone cycle, testosterone levels rise, creating an anabolic 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 anabolism 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).
Figure 2: TESTOSTERONE AND CORTISOL LEVELS DURING A PROHORMONE OR ANABOLIC / ANDROGENIC STEROID CYCLE:
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).
Figure 3: THEORETICAL TESTOSTERONE AND CORTISOL LEVELS DURING A FREE TEST™ CYCLE:

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 anabolic ratio (T:C), with anabolism far outweighing catabolism throughout the cycle, with minimal disruption of hormone levels post-cycle (53).
Figure 4: OVERVIEW OF THE HYPOTHALAMIC PITUITARY TESTICULAR AXIS:

Figure 5: POTENCY OF AROMATASE INHIBITORS, INCLUDING 3-DESOXY 7-KETO DHEA (KI VALUES):

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 anabolism 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 anabolic. 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 an anabolic 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 anabolic 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).
FIGURE 6: Forskolin-Induced Lean Body Mass Gains (Badmaev et al. 2001)

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 anabolism and protein synthesis (14-15).
Numerous other studies have shown parallels between increased cAMP levels and increased anabolism, 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)
Mitigating the factors that decrease testosterone, and how FREE TEST™ combats them via N-Acetyl-Cysteine and Selenium:
FREE TEST offers yet another benefit in the production and elevation of free testosterone, as it serves as a strong anti-oxidant in the reproductive system.
Cytokines are substances secreted by the immune system that carry signals between cells, and have effects on the function of many different bodily systems, including the function of endogenous testosterone modulation (25-26,35). Cytokines can be disruptive to the endocrine system, in that they can be involved in feedback inhibition during the production of testosterone, which can result in a downgrade of natural testosterone production. Under conditions such as systemic or testicular stress, the systemic and local (within the testis) amounts of pro-inflammatory cytokines (TNF, IL-1, and IL-6) will be increased significantly. Elevated amounts of cytokines can therefore be associated with decreased testicular function. Elevated levels of these cytokines will effect the endocrine system and alter the amount of hormones released by the system (mainly GnRH, LH and FSH), which regulate the spermatogenic process. Cytokines (mainly IL-6) can also significantly raise cortisol levels, which can also lead to a reduced anabolic stimulus (13,25,35).
In addition, Pro-inflammatory cytokines can suppress the cells of the testis, and lead to a decrease in spermatogenesis and thus to affect the function and/or viability of the testes in the production of testosterone (33-34).
Figure 7: ALTERATION OF HORMONAL PRODUCTION VIA CYTOKINES:

A recent study involving men taking a combination of N-Acetyl-Cysteine (or NAC, a precursor to glutathione), and selenium, (a trace mineral that has been shown to have direct effects on the biosynthesis pathways of testosterone), found that the combination of the two compounds has a mild synergistic effect on increasing testosterone levels in men. Selenium is rate-limiting in testosterone production in men, and if not enough selenium (selenium deficiency is very common) is available, testosterone will not be produced in optimal levels (25-26,49). The researchers also believe that the combination has an antioxidant effect in the testes via increasing glutathione levels. Glutathione is a tripeptide thiol found in all cells of the body, and is responsible for regulating protein synthesis and detoxifying cell structures. Selenium is needed for the detoxifying enzyme glutathione peroxidase, and NAC significantly increases glutathione levels. Increases in glutathione and glutathione peroxidase seem to be negatively correlated with cytokine release; as levels of these anti-oxidants increase, cytokine levels decrease. This effect is readily apparent in the male reproductive system, as several studies have shown that NAC can reverse testicular damage cross-indicated with cytokine release and cytokine-related testicular suppression. This characteristic alone promotes conditions that are extremely favorable for optimal testosterone production (25.49).
FIGURE 8: INCREASED TESTOSTERONE LEVELS RELATED TO N-ACETYL CYSTEINE AND SELENIUM SUPPLEMENTATION: STUDY DATA:

Modulating glucocorticoid and cortisol: Another way FREE TEST™ preserves the anabolic environment:
Glucocorticoids are a class of hormones that bind to the glucocorticoid receptor, and serve to prevent inflammation in the body. Cortisol is the most prevalent of the glucocorticoid hormones. It is a corticosteroid produced in the adrenal cortex of the kidney, and is used by the body as a response to stress. The release of cortisol is controlled by adreno-corticotropin-releasing hormone (45-47, 53).
Cortisol does have some benefits; for example cortisol is necessary for obtaining an optimal response to stimulant products, along with many body processes. The main function of cortisol is to increase blood sugar, but it can also counteract several different anabolic hormones in the body, including insulin and testosterone, thus acting in a catabolic function by tearing down muscle tissue when it is present in excessive amounts (53).
A negative Testosterone:Cortisol (T:C) ratio essentially starves muscle cells of nutrients by reducing muscle glycogen and potassium and weakening the immune system which can cause a general loss of muscle mass. A positive T:C ratio is necessary to produce an anabolic environment in the human body (53).
7-Keto DHEA, DHEA, and most derivations of this molecule have been found in many research studies to have the ability to significantly reduce glucocorticoid levels by altering cytokine levels, as discussed earlier in this article. They also modulate the negative immune effects of glucocorticoids on skeletal muscle that occur via competition for the 11beta-hydroxysteroid dehydrogenase 1 enzyme. The finding from initial pilot studies strongly suggest that 3, 7-Keto DHEA will produce potent immuno-modulating and cortisol-lowering effects similar to or possibly even greater than those associated with 7-Keto DHEA (22-23,45-47).
One of the aforementioned means through which 7-Keto DHEA and its metabolites serve this function is via acting on 11beta hydroxysteroid dehydrogenase 1 (11beta-HSD1), which is an enzyme that converts inactive glucorticoids to active substrate. 7-Keto DHEA and its analogs have been shown to compete with inactive glucocorticoids for the 11beta-HSD1 enzyme, thus reducing the conversion of inactive glucocorticoids to their active, muscle-catabolic form via receptor site antagonism. A good example would be a reduction in the conversion of cortisone to cortisol, which is a process dependant on the 11beta-HSD1 enzyme. 7-Keto DHEA has been shown to reduce this conversion; thereby lowering cortisol levels (45-47).
FREE TEST™ creates a superior binding environment for existing androgens: The role of Zinc and Magnesium in promoting a better binding environment for Free Testosterone:
Magnesium has been shown in more recent studies to inhibit the binding of steroid hormone binding globulin (SHBG) and free testosterone. SHBG binds free testosterone and allows it to be excreted from the body without binding the androgen receptor. Magnesium keeps this from happening by altering the binding affinity of testosterone to SHBG, and thereby allowing for increased amounts of free testosterone to remain active in the bloodstream (41-43).
Other human research has shown that supplemental magnesium, when taken along with other ingredients like DHEA and Zinc, can significantly increase free testosterone. Low magnesium levels have been found to be correlated with high cortisol levels, and this can lead to a negative skewing of the T:C ratio (20,41-43) .
Zinc is involved in over 200 enzymatic reactions, allowing for the action of several different hormones: GH, testosterone, and insulin all require zinc for synthesis (42-43,53).
The inclusion of these elements in FREE TEST allows for greater numbers of androgen receptors and a better binding environment for testosterone in skeletal muscle, hence creating a better target for circulating free testosterone and allowing for greater binding of testosterone to the additional receptors. All of these factors contribute to the multiple, synergistic mechanisms that lead to the dramatically increased protein synthesis, better recovery, and increased muscle mass users experience while taking FREE TEST.
Administration, Timing, and Dosing:
Under normal conditions, diurnal cortisol levels tend to be highest shortly after waking, and these levels tend to decline during the day, reaching their lowest point in the evening. Although cortisol levels tend to decline during the day, stressful events punctuate spikes into said decline (see Figure 9). Similarly, diurnal testosterone levels tend be highest in the early morning, and tend to wane as the day goes on, also spiking in a periodic fashion. Taking this into account, the timing of the Free Test™ dosage is crucial in contributing to the effectiveness of the product (53).
Dosing the product within 1-2 hours of waking will allow the product to be most effective, in regards to both diurnal hormone regulation, and also the relative half-lives of the compounds included in FREE TEST™. This will allow for a reduction in heightened cortisol levels associated with diurnal fluctuations, and will allow for a continued time period of increased testosterone levels, for up to 12-18 hours after the AM dosage (See Figure 9).
Figure 9: THEORETICAL DIURNAL CORTISOL LEVELS WITH AND WITHOUT FREE TEST™:

A second dose of the product most likely will not be required later in the day due to the inclusion of 3, 7-Keto DHEA, as suicide aromatase inhibitors normally only require dosing every 18-24 hours (21-22).
A dosage of 4-6 Capsules per day of Free Test™ is recommended, with food, within 1-2 hours of waking, depending on body weight.
Research involving blood testing of free and serum testosterone levels indicates heightened levels of testosterone within 1-2 weeks of the first dosage, with increases occurring up to weeks 3-4, and possibly longer (55).
FREE TEST can be run for much longer periods of time than conventional prohormones due to its effects on endogenous (naturally produced) testosterone, and the fact that it does not directly antagonize the androgen receptor. Instead, the product minimizes the homeostatic mechanisms in your own body that lower testosterone levels, and increases testosterone via secondary mechanisms of anabolism (manipulation of T:E and T:C). This allows the user to be able to run the compound for longer periods of time, up to 4-5 months while remaining safe and effective.
Stacks and Tips to Maximize the Product:
Stack product with HGH-Up♂- While each is extremely potent and effect on their own, there are distinct synergies with taking these product simultaneously. Their combined effects with rival that of even the most powerful prohormones without any of the risk associated with them.
Take Bio-Mend Anti-Oxidant formula
- *High ORAC Value
- *Protects cellular membrane
- *Protects transcriptional factors (mRNA and DNA)
In general, maintain a healthy diet and lifestyle:
- *Drink Plenty of water; at least 64 oz. per day
- *Ingest at least 1 gram of protein per lb. of body weight daily
- *Sleep at least 7 hours per night
- *Eat lots of fruits and vegetables
- *Eat lots of complex carbs
- *Eat 5-6 smaller protein and carb-rich meals throughout the day
- *Increase calories to at least 500 Kcal/day over your normal intake
- *BCAAs and Creatine will be helpful
- *Avoid alcohol and tobacco
In conclusion, FREE TEST™ is the most effective DSHEA compliant Testosterone enhancement product yet to be offered in the history of sports nutrition.
FAQ:
Q: When is the best time to take FREE TEST?
A: FREE TEST works best when taken early in the day, with food. This is the best way to simultaneously suppress cortisol and boost testosterone and maintain optimal levels throughout the day.
Q: How is FREE TEST different from other test boosters?
A: FREE TEST increases muscle anabolism via 7 mechanisms of action that work the problem two main directions: On one hand it stimulates endogenous testosterone production and androgen receptor quantity; on the other hand it suppresses muscle-destroying cortisol. The end results are dramatic.
Q: What are the main benefits of taking FREE TEST?
A:
- *Increased lean muscle mass
- *Lowered body fat
- *Better/Faster recovery from training
- *Increased muscular strength
- *Heightened libido and sexual drive
Q: Do I need a PCT (Post-Cycle Therapy) product after I cease taking FREE TEST?
A: No! In fact, FREE TEST is a strong aromatase inhibitor that triggers your natural production of testosterone; so it can actually be used AS a PCT.
Q: How long should I cycle on / off FREE TEST?
A: Typical cycles are 8-12 weeks, with at least 4 weeks off in-between.
References:
- Young ME, Leighton B.(1998) Evidence for altered sensitivity of the nitric oxide/cGMP signaling cascade in insulin-resistant skeletal muscle. Biochem J. Jan 1;329 ( Pt 1):73-9
- Aghdasi B, Reid MB, and Hamilton SL. (1997) Nitric oxide protects the skeletal muscle Ca2+ release channel from oxidation induced activation. J Biol Chem 272:25462-25467
- Balon TW, Nadler JL. (1997)Evidence that nitric oxide increases glucose transport in skeletal muscle. J Appl Physiol. 1997 Jan;82(1):359-63.
- Etgen GJ Jr, Fryburg DA, Gibbs EM. (1997) Nitric oxide stimulates skeletal muscle glucose transport through a calcium/contraction- and phosphatidylinitric oxidesitol-3-kinase-independent pathway. Diabetes Nitric oxide; 46(11):1915-9.
- Asano Tsuguyoshi (2001). Clinical report on root extract of perilla plant (Coleus forskohlii) ForsLean ® in reducing body fat. Asano Institute. Tokyo , Japan.
- Kreider RB, et al. Effects of Coleus forskohlii supplementation on body composition and markers of health in sedentary overweight females. Experimental Biology 2002 Late Breaking Abstracts. LB305: 2002.
- LEAMON, KB; PADGETT, W; DALY, JW. "Forskolin: Unique diterpene activator of adenylate cyclase in membrane and intact cells" Proc. Natl. Acad. Sci. USA 1981,78,3363-67
- DE SOUZA, NJ; DOHADWALLA, AN; REDEN, J; Forskolin, A. "Labdane Diterpenoid with Antihypertensive, Positive Inotropic, Platelet Aggregation Inhibitory, and Adenylate Cyclase Activating Properties" Medicinal Research Reviews 1983, 3(2), 201-219
- Badmaev, V. Majeed, M. Conte, A, Parker, J. “Diterpene Forskolin (Coleus forskohlii, Benth.): A possible new compound for reduction of body weight by increasing lean body mass” Sabinsa Corporation http://www.b5srl.com/articles/nu/2002/marapr/badmaev.htm 1/21/2004
- Ding X, Staudinger J. Induction of Drug Metabolism by Forskolin, the Role of The Pregnane X Receptor and the PKA Signal Transduction Pathway. J Pharmacol Exp Ther. 2004 Sep 30
- Forskolin, a diterpene compound isolated from the roots of Coleus forskohlii, activates adenylate cyclase in membranes from a variety of mammalian tissues. adenylate cyclase in human basophils and mast cells. Biochem Pharmacol. 1987 Jan 1;36(1):13-20.
Asif AR, Ljubojevic M, Sabolic I, Shnitsar V, Metten M, Anzai N, Müller GA, Burckhardt G, Hagos Y. Regulation of steroid hormone biosynthesis enzymes and organic anion transporters by forskolin and DHEA-S treatment in adrenocortical cells. Am J Physiol Endocrinol Metab. 2006 Dec;291(6):E1351-9. Epub 2006 Jul 11.
- Tsai SC, Lu CC, Lin CS, Wang PS. Antisteroidogenic actions of hydrogen peroxide on rat Leydig cells. J Cell Biochem. 2003 Dec 15;90(6):1276-86.
- Cronin MJ, Evans WS, Hewlett EL, Thorner MO. LH release is facilitated by agents that alter cyclic AMP generating system. Am J Physiol. 1984 Jan;246(1 Pt 1):E44-51.
- Andric SA, Janjic MM, Stojkov NJ, Kostic TS. Protein kinase G-mediated stimulation of basal Leydig cell steroidogenesis. Am J Physiol Endocrinol Metab. 2007 Nov;293(5):E1399-408. Epub 2007 Sep 11.
- Manna PR, D



