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    cAMPHIBOLIC "THE ANABOLIC THERMOGENIC" Instock and ready to ship at


    The compound known as forskolin was isolated from the herb Coleus forskohlii in the 1974. The herb itself however, native to India, Sri Lanka, Thailand, and Nepal, has been used for centuries in traditional medicine to treat heart disease, allergies, asthma, glaucoma, and a variety of other ailments.

    Outside of traditional Ayurvedic medicine, forskolin has found a use primarily as a laboratory tool to study the process known as lipolysis, or the mobilization of stored fat that can then be used as fuel by the body.


    Normally when the body requires the use of stored fat for fuel, hormones such as epinephrine or norepinephrine bind to receptors on fat cells and initiate a signaling cascade that eventually results in the activation of an enzyme within the fat cell called hormone sensitive lipase (HSL). Fat is stored in the form of triglycerides, composed of fatty acid chains bound to a glycerol backbone. HSL frees up the fatty acids so they can leave the fat cell, enter the bloodstream, and travel to wherever they are needed for fuel, primarily working muscle.

    Forskolin mimics the effects of the body's fat mobilizing hormones like epinephrine by entering fat cells and increasing levels of the enzyme adenylate cyclase, which in turn increases cyclic adenosine monophosphate (cAMP), an important compound involved in the signaling cascade described above. The increase in cAMP leads to activation of HSL, and fat is mobilized, ready to be used as fuel. Note as depicted in the illustration below that forskolin bypasses the hormonal receptor and enters the cell by traversing the cellular membrane. In the case of fat cells, epinephrine or a chemical analog of epinephrine such as clenbuterol or albuterol binds to these so-called beta adrenergic receptor sites and initiates the signaling cascade that ultimately results in fat release.

    Prolonged use of these chemical agents however ultimately leads to a desensitization of the receptor, and a loss of drug effectiveness. With beta-receptors desensitization occurs primarily by a decrease in cell surface receptor number. This is important clinically because beta2 receptor agonists such as clenbuterol and albuterol are commonly used to treat asthma by binding to beta-receptors in lung tissue. They lead to the relaxation of bronchial smooth muscle and decrease airway resistance. Hence the widespread use of forskolin to treat airway constriction in allergies and asthma.

    Note that since like beta agonists, forskolin too initiates the signaling cascade, but since it acts independently of beta receptors, even cells whose beta receptors have been severely downregulated by exposure to beta2 agonists are still responsive to forskolin (1). So a person who has been using clenbuterol or albuterol over an extended period might consider switching to a forskolin-based product, achieving the same net result of fat loss by bypassing the downregulated beta-receptors. Interestingly, beta2 receptors in tissue samples that had experienced this downregulation/desensitization (technically called tachyphylaxis) by continual exposure to salbutamol recovered sensitivity to the drug in vitro when exposed to forskolin (2) If this works in vivo it gives a person who wants to increase lipolysis several options for the combined or individual use of a beta agonist and forskolin.

    Fig. 1 Forskolin bypasses the hormone receptor to directly phosphorylate and hence activate HSL


    So far to summarize, we see that forskolin has the ability to activate Hormone Sensitive Lipase and release free fatty acids that can be used by the body for fuel. This lipolytic effect is obviously advantageous for a person seeking to lose fat. However, unless the fat mobilized by forskolin is actually burned for fuel, it will simply be redeposited as fat. One could obviously increase exercise levels to burn this mobilized fat, or go on a calorie restricted diet. These are certainly healthful approaches to weight loss, but forskolin itself can promote the burning of these liberated fats by virtue of its ability to elevate metabolic rate by stimulating the production of thyroid hormone.

    Thyroid Stimulating Hormone, or TSH, is a hormone released by the pituitary gland that signals the thyroid gland to produce T4 and T3. Forskolin, when added to thyroid tissue in culture, mimics the effect of TSH and stimulates the production of thyroid hormone (3). Thyroid hormone is well known to increase metabolic rate by way of several mechanisms, and this increased metabolic rate will lead to the use of the mobilized fatty acids for fuel.

    In addition to stimulating the secretion of primarily T4 from the thyroid, forskolin promotes the conversion of the relatively inactive T4 to its potent metabolite T3 via the action of type II deiodinase. Forskolin has been shown to induce the expression of type II deiodinase in peripheral tissue, especially skeletal muscle (4)

    Thyroid hormone has been shown to be helpful in treating depressive disorders. Also, several studies have shown that patients suffering from depression have reduced levels of activity of cAMP signaling in the brain. (4) Forskolin administration to depressed and schizophrenic patients has resulted in marked improvement in symptoms in these subjects (5). On the other hand, enhanced cAMP signaling in bipolar patients may contribute to manic episodes (6). So while possibly benefiting people suffering from depression, forskolin could exacerbate the symptoms of bipolar disorder. One should obviously consult with a medical professional here before self-medicating with forskolin.


    We have seen how forskolin relaxes bronchial smooth muscles in asthma. It also has the ability to relax cavernosal smooth muscles in the penis, allowing the organ to fill with blood (7). For those readers familiar with drugs like Viagra and Cialis, they would recognize that this is exactly how these drugs work, albeit in a somewhat different manner. These drugs are known as phosphodiesterase inhibitors, and prevent the breakdown of another second messenger, cGMP that is involved in signaling cascades similar to cAMP. In particular, in the penis the prevention of breakdown of cGMP leads to erections. So forskolin and Viagra (as well as Cialis) act via different pathways to stimulate erections. The authors in (7) observed a synergistic effect on erection when forskolin was combined with Viagra. So both agents alone promote erection, and when combined exhibit synergism, an effect greater than the sum of the two.


    Macrophages and monocytes are immune cells that secrete both pro inflammatory compounds (cytokines) as well as anti-inflammatory cytokines. Tumor Necrosis Alpha (TNF-alpha) is an example of the former, while Interleukin 10 (IL-10) exemplifies the latter. States of chronic inflammation are associated with high levels of TNF-alpha and low levels of IL-10. Both of these cytokines are dependent on cAMP for their control. Elevated cAMP suppresses TNF-alpha, while at the same time stimulating IL-10. (8) In animal models of rheumatoid arthritis, forskolin has been shown to dramatically shift the cytokine environment away from a pro-inflammatory one by suppressing TNF-alpha production. Of relevance to athletes and bodybuilders, overtraining leads to chronic inflammation associated with elevated TNF-alpha. Forskolin may help here as in arthritis.

    TNF-alpha is believed to play a central role in the development and progression of insulin resistance and type II diabetes. Many athletes supplement with R-ALA to improve insulin sensitivity. Forskolin may help as well in improving glucose tolerance

    Recent research has shown hypogonadism (low testosterone) to be an inflammatory condition associated with elevated levels of TNF-alpha (9). Testosterone administration normalizes the cytokine profile in these subjects. The elevated TNF-alpha in hypogonadism may be responsible for at least part of the diminished muscle mass in these patients, as well as their high incidence of inflammatory cardiovascular disease.

    Finally, but far from being the least significant effect of TNF-alpha, is that it suppresses the local production of IGF-1 in skeletal muscle (10).

    With regard to dosing, the typical dosage of forskolin is 25-60 mg per day divided between 2-3 doses, with 50-60 mg being considered the ideal range by the majority of users. The ideal drug to use in combination with forskolin would be the cAMP phosphodiesterase inhibitor Rolipram. Rolipram, prescribed as an antidepressant, slows the breakdown of cAMP, and this would prolong and amplify the effect of forskolin. Unfortunately Rolipram is not yet available in the United States, but is an option for our European and Japanese readers. In animal studies Rolipram has been shown to be a potent lipolytic agent (11). In countries where Rolipram is not available, other options might be ephedrine and caffeine, as well as yohimbine. In fact, caffeine is a weak cAMP phosphodiesterase inhibitor that might prolong cAMP activity and amplify the effect of forskolin in a fashion similar to the prescription drug Rolipram. In fact, one popular theory about how caffeine promotes lipolysis is that by acting as a phosphodiesterase inhibitor it too prolongs and amplifies the lipolytic effects of cAMP.

    Thus far everything we have discussed concerning forskolin stems from findings of published research. However, forskolin has developed a reputation, anecdotally, of having anabolic properties. Many people have reported making decent gains in terms of mass and strength, while at the same time remaining lean. The low body fat is certainly not surprising in terms of what we've learned about the fat burning effects of forskolin. The size and strength gains may be due in part to forskolin's suppression of TNF-alpha, and the consequent rise in IGF-1 that accompanies TNF-alpha suppression. Increased testosterone production, and decreased muscle catabolism, described below, likely contribute as well.

    It's been well established that the beta 2 agonist clenbuterol is a potent anabolic agent in animals. Like all beta-2 agonists, clenbuterol utilizes cAMP, as depicted in Fig 1 above. The data regarding the anabolic potential of clenbuterol and other beta-2 agonists are scantier in humans than in animals (12, 13, 14). Nevertheless, they do show an anabolic and ergogenic effect for this class of drugs. Since forskolin amplifies cAMP signaling, it would not at all be surprising if it too had anabolic characteristics.

    Forskolin is also well known as a vasodiltor; cAMP activation in the smooth muscles of vascular walls leads to relaxation and expansion of the blood vessels, allowing for more blood to travel into tissues, including skeletal muscle. Insulin shares forskolin's vasodilatory properties (15). Increased blood flow in response to insulin is believed to enhance both glucose and amino acid delivery to muscle tissue, helping to promote anabolism. To quote from one study (15),

    "Insulin-mediated vasodilation is an important physiological determinant of insulin action."

    So when one considers that forskolin is just as or even more potent a vasodilator than insulin, forskolin too should aid in the delivery of amino acids to muscle tissue, promoting anabolism.


    Testosterone is produced in testicular Leydig cells when LH binds to surface receptors and initiates a signaling cascade involving elevated levels of cAMP. This cascade leads ultimately to increased levels of an important Leydig cell cholesterol transfer protein (16) (testosterone is made from cholesterol) and activation of steroidogenic enzymes involved in testosterone production (17). So by elevating levels of cAMP, (with forskolin) an intermediate in the signaling cascade that ranges from LH binding to testosterone production, we should see an increase in testosterone output. This may be particularly important for those of us who are feeling the effects of aging. In a study by Chen,(18) the authors looked at cAMP levels in young and old rats, and found that testosterone production declined with age as a function of declining cAMP levels. So something is keeping LH from elevating cAMP and inducing steroidogenesis is aging rats. Notably, in the older rats, cAMP levels were restored to youthful levels upon administration of forskolin


    Thus far we have presented some possible mechanisms whereby forskolin, by elevating cAMP, promotes anabolism. Elevations in cAMP are also responsible for limiting catabolism of skeletal muscle as well. Muscle wasting is a characteristic of numerous disease states, as well as muscle disuse. AAS users are all too familiar with the latter effect, when hard-earned gains rapidly disappear post-cycle. Much of this atrophy is caused by the action of the so-called calpains. The calpains are a family of calcium dependent enzymes that degrade unused muscle tissue. Calpains in turn are inhibited by another endogenous compound called calpastatin. How is this related to forskolin? It turns out that calpastatin is upregulated by cAMP (19). Thus not only does forskolin promote anabolism, it slows muscle catabolism when muscle is not being used extensively. This would be expected to be important when a person is immobilized or unable to train due to injury, or is simply unable to maintain the rigorous training regimen off cycle that they adhered to while on AAS. So we have another potential mechanism whereby forskolin staves off post cycle muscle loss. It should be noted that even though reference (19) deals specifically with bovine calpains/calpastatin, the two are ubiquitous in all mammalian tissues, including human skeletal muscle, and calpastatin is cAMP dependent in all tissues thus far examined.

    So we see that not only is forskolin safe and legal, it acts as both a mild anabolic compound as well as an anticatabolic agent in skeletal muscle tissue. This is in to the fat burning properties we discussed in detail. It may be the ideal compound for some wishing to avoid the illegalities of anabolic steroids, especially since prohormones are on the way out. It should appeal to women due to its relatively mild anabolic nature compared to harsher anabolics.

    We mentioned a few agents that might potentiate the effects of forskolin. What might be some other good readily available supplements to stack with forskolin? Caffeine and green tea extract are two possibilities. As illustrated in Figure 1, caffeine itself and the caffeine in green tea both believed to act as phosphodiesterase inhibitors. This prolongs the action of cAMP, leading to increased lipolysis. It also turns out that the norepinephrine and epinephrine that began the lipolytic signaling process are broken down by an enzyme called catechol O-methyltransferase (COMT).The catechins are constituents in green tea which inhibit COMT, prolonging the life of the norepinephrine and epinephrine. So green tea has a much greater lipolytic effect that does caffeine alone (20).

    In animal studies green tea also seems to act as an appetite suppressant (21). The catechin believed responsible for the weight loss seen in animals is known as EGCG. Exactly how green tea reduces appetite is unknown, but it is evidently not due solely to the caffeine content since direct administration of EGCG results in appetite suppression. It's also possible that elevated levels of norepinephrine, described above, contribute to appetite suppression.

    Green tea also inhibits the enzymes that are responsible for the digestion of fats, so called lipases. The processes outlined above describe lipolysis, the liberation of fatty acids stored in adipocytes. However, unless energy expenditure (EE) is increased, or a diet undertaken, the fatty acids will simply be converted back to fat. It turns out that both caffeine, either alone or in green tea increases EE by inducing so-called futile cycling in adipocytes. Futile cycling involves the continual breakdown of fats into fatty acids and glycerol, with the subsequent reesterification of these components. This is an energy consuming process that elevates EE. So we see that green tea and caffeine contribute to fat burning via several mechanisms, some in conjunction with forskolin, and some independently of forskolin.


    Until recently, adipocytes were considered merely storage sites for fats. Now we realize that besides that familiar role, fat cells secrete a host of compounds with diverse and far reaching effects. Skeletal muscle has undergone a similar recharacterization and it is now regarded as a secretory organ. For example, up until recently it was unknown that muscle possesses aromatase and secretes estrogen into the circulation. Quoting from the study in which this was discovered,

    "Taking into account bulk in the body it is concluded that muscle can be an important source of estrogens in men and post-menopausal women and its contribution to the circulating pool of estrogens may be comparable to that of adipose tissue" (22). This is not necessarily a bad thing. There is ample evidence from animal and human studies that estrogen acts in a similar fashion as testosterone with respect to fat metabolism. And estrogen is important for cardiovascular health in both men and women. Quoting from one of the leading authorities on the metabolic roles of the sex hormones,

    "[with respect to adipose tissue metabolism] Oestrogens seem to exert net effects similar to those of testosterone." (23).

    According to the authors of (22), estrogen formation may be controlled cAMP-dependent promoters of the aromatase gene. So the possibility exists that forskolin may play a role in the production of estrogen from muscle tissue.

    Musclin is another protein produced and secreted by skeletal muscle tissue (24). Musclin seems to inhibit glucose uptake and glycogen formation . It too is cAMP dependent; forskolin, when administered to mice, reduced musclin levels. This would be expected to improve glucose uptake and glycogen storage.


    The above is in contrast to the effects of forskolin on glucose uptake in adipocytes, where it inhibits insulin stimulated glucose activity. Interestingly, this appears to be a cAMP independent phenomenon, with forskolin directly inhibiting the glucose transporter (25). This is likely another mechanism whereby glucose promotes fat burning. With limited glucose for use as fuel, fat cells must rely on their own stored fat to carry out the metabolic processes required for their survival. Other studies suggest that the inhibition of glucose uptake by adipocytes in the presence of forskolin is caused by direct inhibition of expression of the GLUT4 (glucose transporter 4) gene by cAMP (26). So there may be dual mechanisms through which forskolin acts to inhibit glucose uptake by adipocytes.

    1) Sartori C, Fang X, McGraw DW, Koch P, Snider ME, Folkesson HG, Matthay MA Selected long-term contribution: effects of beta(2)-adrenergic receptor stimulation on alveolar fluid clearance in mice J
    Appl Physiol. 2002 Nov;93(5):1875-80.

    2) Yousif MH, Thulesius O. Forskolin reverses tachyphylaxis to the bronchodilator effects of salbutamol: an in-vitro study on isolated guinea-pig trachea. J Pharm Pharmacol 1999 Feb;51(2):181-6

    3) Becks GP, Buckingham DK, Wang JF, Phillips ID, Hill DJ Regulation of thyroid hormone synthesis in cultured ovine thyroid follicles Endocrinology 1992 May;130(5):2789-9

    4) Hosoi Y, Murakami M, Mizuma H, Ogiwara T, Imamura M, Mori M. Expression and regulation of type II iodothyronine deiodinase in cultured human skeletal muscle cells. J Clin Endocrinol Metab 1999

    5) Reiach JS, Li PP, Warsh JJ, Kish SJ, Young LT. Reduced adenylyl cyclase immunolabeling an activity in postmortem temporal cortex of depressed suicide victims J Affect Disord 1999 Dec;56(2-3):141-51

    6) Bersudsky Y, Kotler M, Shifrin M, Belmaker RH. A preliminary study of possible psychoactive effectof intravenous forskolin in depressed and schizophrenic patients. Short communication. J Neural Transm.1996;103(12):146

    7) Seo KK, Kim SC, Jun IO, Oh MM, Lee MY Synergistic effects of sildenafil on relaxation of rabbit and rat cavernosal smooth muscles when combined with various vasoactive agents. BJU Int. 2001 Oct;88(6):596-601

    8) Foey AD, Field S, Ahmed S, Jain A, Feldmann M, Brennan FM, Williams R. Impact of VIP and cAMP on the regulation of TNF-alpha and IL-10 production: implications for rheumatoid arthritis. Arthritis Res Ther 2003;5(6):R317-28

    9) Malkin CJ, Pugh PJ, Jones RD, Kapoor D, Channer KS, Jones TH. The effect of testosterone replacement on endogenous inflammatory cytokines and lipid profiles in hypogonadal men. J Clin Endocrinol Metab. 2004 Jul;89(7):3313-8

    10) Lang CH, Nystrom GJ, Frost RA. Tissue-specific regulation of IGF-I and IGF-binding proteins in response to TNFalpha. Growth Horm IGF Res 2001 Aug;11(4):250-60.

    11) Nakamura J, Okamura N, Kawakami Y. Augmentation of lipolysis in adipocytes from fed rats, but not from starved rats, by inhibition of rolipram-sensitive phosphodiesterase 4. Arch Biochem Biophys. 2004 May 1;425(1):106-14

    12) van Baak MA, Mayer LH, Kempinski RE, Hartgens F. Effect of salbutamol on muscle strength and endurance performance in nonasthmatic men Med Sci Sports Exerc. 2000 Jul;32(7):1300-6

    13) Caruso JF, Signorile JF, Perry AC, Leblanc B, Williams R, Clark M, Bamman MM. The effects of albuterol and isokinetic exercise on the quadriceps muscle group Med Sci Sports Exerc. 1995 Nov;27(11):1471-6

    14) Oya Y, Ogawa M, Kawai M. Therapeutic trial of beta 2-adrenergic agonist clenbuterol in muscular dystrophies Rinsho Shinkeigaku 2001 Oct;41(10):698-700

    15) de Jongh RT, Clark AD, IJzerman RG, Serne EH, de Vries G, Stehouwer CD. Physiological hyperinsulinaemia increases intramuscular microvascular reactive hyperaemia and vasomotion in healthy volunteers. Diabetologia. 2004 Jun;47(6):978-86

    16) Baron AD, Steinberg HO, Chaker H, Leaming R, Johnson A, Brechtel G. Insulin-mediated skeletal muscle vasodilation contributes to both insulin sensitivity and responsiveness in lean humans. J Clin Invest.
    1995 Aug;96(2):786-92.

    17) Luo L, Chen H, Zirkin BR 2001 Leydig cell aging: steroidogenic acute regulatory protein (StAR) and cholesterol side-chain cleavage enzyme. J Androl 22:149-156

    18) Chen H, Hardy MP, Zirkin BR 2002 Age-related decreases in Leydig cell testosterone production are not restored by exposure to LH in vitro. Endocrinology.May;143(5):1637-42.

    19) Cong M, Goll DE, Antin PB. cAMP responsiveness of the bovine calpastatin gene promoter. Biochim Biophys Acta. 1998 Nov 26;1443(1-2):186-92.

    20) Dulloo AG, Duret C, Rohrer D, Girardier L, Mensi N, Fathi M, Chantre P, Vandermander J Efficacy of a green tea extract rich in catechin polyphenols and caffeine in increasing 24-h energy expenditure and fat oxidation in humans. Am J Clin Nutr 1999 Dec;70(6):1040-5.

    21) Kao YH, Hiipakka RA, Liao S. Modulation of endocrine systems and food intake by green tea epigallocatechin gallate. Endocrinology. 2000 Mar;141(3):980-7.

    22) Larionov AA, Vasyliev DA, Mason JI, Howie AF, Berstein LM, Miller WR. Aromatase in skeletal muscle. J Steroid Biochem Mol Biol. 2003 Mar;84(4):485-92

    23) Bjorntorp P. Hormonal control of regional fat distribution. Hum Reprod 1997 Oct;12 Suppl 1:21-5

    24) Nishizawa H, Matsuda M, Yamada Y, Kawai K, Suzuki E, Makishima M, Kitamura T, Shimomura I. Musclin, a novel skeletal muscle-derived secretory factor. J Biol Chem. 2004 May 7;279(19):19391-5

    25) Joost HG, Steinfelder HJ. Forskolin inhibits insulin-stimulated glucose transport in rat adipose cells by a direct interaction with the glucose transporter. Mol Pharmacol. 1987 Mar;31(3):279-83.

    26) Kaestner KH, Flores-Riveros JR, McLenithan JC, Janicot M, Lane MD. Transcriptional repression of the mouse insulin-responsive glucose transporter (GLUT4) gene by cAMP. Proc Natl Acad Sci U S A. 1991 Mar 1;88(5):1933-7.

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    Cissus quadrangularis

    Cissus quadrangularis is an ancient medicinal plant native to the hotter parts of Ceylon and India. It was prescribed in the ancient Ayurvedic texts as a general tonic and analgesic, with specific bone fracture healing properties. Modern research has shed light on Cissus' ability to speed bone healing by showing it acts as a glucocorticoid antagonist (1,2). Since anabolic/androgenic compounds are well known to act as antagonists to the glucocorticoid receptor as well as promote bone growth and fracture healing, it has been postulated that Cissus possesses anabolic and/or androgenic properties (1,3). In addition to speeding the remodeling process of the healing bone, Cissus also leads to a much faster increase in bone tensile strength. In clinical trials Cissus has led to a fracture healing time on the order of 55 to 33 percent of that of controls. That cissus exerts antiglucocorticoid properties is suggested by a number of studies where bones were weakend by treatment with cortisol, and upon administration of Cissus extract the cortisol induced weakening was halted, and the healing process begun.

    While the increased rate of bone healing may be of great significance to persons suffering from chronic diseases like osteoporosis (4), the antiglucocorticoid properties of Cissus are likely of much more interest to the average bodybuilder or athlete, since endogenous glucocorticoids, particularly cortisol, are not only catabolic to bone, but catabolize muscle tissue as well. Numerous studies over the years have suggested that glucorticoids, including the body's endogenous hormone cortisol activate pathways that degrade not only bone, but skeletal muscle tissue as well. A recently published report documented exactly how glucocorticoids (including cortisol) induce muscle breakdown: They activate the so-called ubiquitin-proteasome pathway of proteolysis (5). This pathway of tissue breakdown is important for removing damaged and non-functional proteins. However, when it is overactive during periods of elevated cortisol (e.g disease states, stress, and overtraining) excess amounts of normal tissue are broken down as well. By exerting an anabolic, antiglucorticoid effect cissus helps preserve muscle tissue during times of physical and emotional stress.

    Although the bulk of the research on Cissus centers around bone healing, the possibility exists that Cissus may act to improve bone healing it may improve the healing rate of connective tissue in general, including tendons. If this is the case it would be of great benefit to bodybuilders and athletes.

    Besides the above-mentioned properties of Cissus, the plant is also rich in the vitamins/antioxidants vitamin C and beta-carotene. As analyzed, Cissus quadrangularis contained ascorbic acid 479 mg, and carotene 267 units per 100g of freshly prepared paste in addition to calcium oxalate (6).

    The typical recommended daily dosage of Cissus extract is between 100 and 500 mg, depending on the concentration of the extract and the severity of symptoms. For the powder of the dried plant, the Ayurvedic texts recommend a dosage of 3 to 6 grams to accelerate fracture healing. Safety studies in rats showed no toxic effects at dosages as high as 2000 mg/kg of body weight. So not only is Cissus efficacious, it is also quite safe, in either the dried powder form or the commercially available extract.

    Cissus also possess analgesic properties on a mg per mg basis comparable to aspirin or anti-inflammatory drugs like ibuprofen. Cissus quadrangularis constitutes one of the ingredients of an Ayurvedic preparation, `Laksha Gogglu', which has been proved to be highly effective in relieving pain, reduction of swelling and promoting the process of healing of the simple fractures as well as in curing the allied disorders associated with fractures (7). The mechanism through which Cissus exerts its analgesic and anti-inflammatory properties has not been well characterized. It may act centrally, but the anti-inflammatory features suggest that it acts by preventing the conversion of arachidonic acid to inflammatory prostaglandins.

    1) Chopra SS, Patel MR, Awadhiya RP. Studies of Cissus quadrangularis in experimental fracture repair : a histopathological study Indian J Med Res. 1976 Sep;64(9):1365-8

    2) Chopra SS, Patel MR, Gupta LP, Datta IC. Studies on Cissus quadrangularis in experimental fracture repair: effect on chemical parameters in blood Indian J Med Res. 1975 Jun;63(6):824-8.


    4) Shirwaikar A, Khan S, Malini S. Antiosteoporotic effect of ethanol extract of Cissus quadrangularis Linn. on ovariectomized rat. J Ethnopharmacol. 2003 Dec;89(2-3):245-50.

    5) Combaret L, Taillandier D, Dardevet D, Bechet D, Ralliere C, Claustre A, Grizard J, Attaix D Glucocorticoids regulate mRNA levels for subunits of the 19 S regulatory complex of the 26 S proteasome in fast-twitch skeletal muscles. Biochem J. 2004 Feb 15;378(Pt 1):239-46.

    6) Chidambara Murthy KN, Vanitha A, Mahadeva Swamy M, Ravishankar GA. Antioxidant and antimicrobial activity of Cissus quadrangularis L. J Med Food. 2003 Summer;6(2):99-105.

    7) Panda, J Res Ayurv Siddha, 1990, 11, 7


  3. I think I'm going to give this a go both during and after my next T3 cycle. I figure if it really helps mobilize fat cells, then the bump in metabolism from the T3 (and the slight bump in T3 that the forskolin gives) should really help burn the fat... And I will run this along with Guggul afterwards to help get the thyroid rolling again afterwards. Sounds like good stuff.

  4. let us know how it works. would this work on pct from ph?
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    Quote Originally Posted by wastedwhiteboy2
    let us know how it works. would this work on pct from ph?
    Its a great product to use after pro hormones. I picture it as your body needs an alternative source of anabolic fuel after any cycle.


  6. Quote Originally Posted by wastedwhiteboy2
    let us know how it works. would this work on pct from ph?
    Will do. I won't be running another T3 cycle for a while though (probably not until April), hopefully there will be additional feedback from others before then.


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