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Coleus Forskohli
Forskolin-hGH and cAMP stimulator
This "power" herb has an active ingredient in it called forskolin. It has been used in ayruvedic medicine for many years. Forskolin's basic mechanism of action is that it increases the amount of cyclic AMP (adenosine monophosphate) in cells by activating an enzyme called adenylate cyclase. Cyclic AMP (cAMP) is one of the most important secondary messengers in the cell. It is considered to be one of the most important cell regulating compounds.
Under normal circumstances, cAMP forms by adenylate cyclase activation due to hormonal stimulation at the cell receptor site. However, forskolin seems to bypass this reaction and allows for an increase in intracellular cAMP to occur. Why is it important to increase cAMP levels? Well, there are several benefits of this to athletes including relaxation of the arteries and smooth muscles, lowering blood pressure, enhanced insulin secretion (which can help drive carbohydrates and protein into muscle cells for energy and recovery), increased thyroid hormone function (which can help enhance metabolic rate), and significantly increase lipolysis (fat burning). Forskolin also seems to benefit other cellular enzymes as well.
The breakdown of fat for fuel (lipolysis) is actually regulated by cAMP. Forskolin has been shown to not only enhance lipolysis but it may also inhibit fat storage from occurring. This is very good news for individuals trying to lose body fat and get lean. Another way that forskolin may allow for fat loss to occur is by stimulating thyroid hormone production and release. Thyroid hormone controls metabolism and can enhance metabolic rate, which may translate into more fat loss.
One of the overlooked benefits of forskolin includes its stimulation of digestive enzymes, which can allow individuals to digest and assimilate their food better. It has been shown to increase nutrient absorption in the small intestine.
Forskolin has been shown to be safe and effective and has a great amount of potential as a sports supplement. As with most dietary supplements, more human research is needed but the future looks bright for this compound.
Dosage and Administration
Commonly coleus extracts come in standardized dosage of about 15% forskolin. Some medical professionals have recommended taking 50-100 mg of standardized coleus extract two to three times per day but these amounts have not been confirmed by clinical research. Most studies have used injected forskolin; therefore, the amount that should be taken orally to have the same effect is still unknown.
Stimulating cAMP
Brain Nerve. 2008 Jul;60(7):717-24.
[cAMP/PKA signaling underlies age-related memory impairment]
Yamazaki D, Saitoe M.
Tokyo Metropolitan Institute for Neuroscience, Fuchu, Tokyo 183-8526, Japan.
Physiological aging of the brain is inevitable, regardless of the occurrence of pathological diseases such as Alzheimer disease or cerebral vascular disorders. AMI (age-related memory impairment) is an important phenotype of brain aging. In contrast to organismal aging, the molecular mechanisms underlying AMI are poorly understood and hindered by the lack of specific mutants for AMI. We used the fruit fly Drosophila as a novel model for genetic analyses of AMI since it has a short lifespan and is suitable for quantitative analysis of learning and memory. The molecular mechanisms underlying learning and memory in Drosophila are similar to those in mammals. In a screen for AMI mutants, we found that heterozygous mutations of DC0 gene, which encodes the major catalytic subunit of PKA (cAMP-dependent kinase), delayed AMI onset by more than 2-fold without affecting lifespan and memory at young age. The first identification of AMI mutant provides provocative insights into the role of cAMP/PKA signaling and the genetic relationship between organismal aging and brain aging.
Coleus Forskohlii (Forskolin) Enzyme and Hormone Activator
Coleus Forskohlii, a member of the mint family, has a long history of use in Ayurvedic medicine, being applied to a variety of conditions including hypertension, asthma, eczema, psoriasis, congestive heart failure, and angina. The beneficial effects of this herb have been well-researched in both animal and human clinical studies. It acts by increasing levels of cyclic adenosine monophosphate (cAMP) in cells. This cAMP activates many other enzymes which are involved in diverse cell functions. Some of the effects that have been observed and studied include:
A powerful anti-spasmodic action on smooth muscle. This makes it useful for the relief of intestinal colic, uterine cramps, painful (cramping) urination, angina and hypertension. This antispasmodic effect also relaxes airways, resulting in bronchodilation, decreased airway resistance, and increased vital capacity and forced expiratory volume of the lungs, making it a very useful treatment for asthma and allergies.
Increased contractility of the heart muscle, which makes it valuable in the treatment of congestive heart failure, while at the same time it lowers blood pressure by relaxing the arteries. Increased cerebral (brain) blood flow. This indicates that it may be helpful in improving post-stroke recovery.
Inhibition of platelet aggregation (blood clotting) also adds to its value in the treatment of cardiovascular and cerebrovascular disorders. It is felt that the cAMP elevating effects of forskolin may result in an improvement in glaucoma and conditions of increased intraocular pressure. Symptoms of psoriasis have been improved through the use of forskolin, thought to be due to an improvement in the cAMP/cGMP ratio. Depression may also be responsive to the effects of forskolin through it's action of increasing cAMP and inhibiting phosphodiesterase. Researchers stopped short of recommending forskolin for the treatment of depression, but did state that "elevated brain cAMP levels are closely linked to antidepressant activity..."
Scientists at the Penn State University College of Medicine found significant weight loss and reduction of blood pressure levels in subjects of a recent study, indicating that forskolin may be a useful and safe herb for those seeking to lose weight. Related to the above is the effect that forskolin has on the thyroid: it serves to increase thyroid hormone production and stimulates thyroid hormone release. This mechanism may be one way in which forskolin promotes a normal body weight. It's effects in normalizing thyroid function may also contribute the antidepressant effects seen with forskolin use.
Scientists at Brown University have suggested that forskolin may have a place in the prevention of tumor metastasis due to its effect as a potent inhibitor of platelet aggregation and inhibition of tumor colonization. Finally, forskolin has been shown to enhance and boost the immune system by activating macrophages and lymphocytes which are valuable tools in the body's battle against infection.
Induction of increased cAMP levels in articular chondrocytes blocks matrix metalloproteinase-mediated cartilage degradation, but not aggrecanase-mediated cartilage degradation.
Arthritis Rheum. 2007 May;56(5):1549-58.
Karsdal MA, Sumer EU, Wulf H, Madsen SH, Christiansen C, Fosang AJ, Sondergaard BC.
Nordic Bioscience Diagnostics, Herlev, Denmark. mk@nordicbioscience.com
OBJECTIVE: Calcitonin has been suggested to have chondroprotective effects. One signaling pathway of calcitonin is via the second messenger cAMP. We undertook this study to investigate whether increased cAMP levels in chondrocytes would be chondroprotective.
METHODS: Cartilage degradation was induced in bovine articular cartilage explants by 10 ng/ml oncostatin M (OSM) and 20 ng/ml tumor necrosis factor (TNF). In these cultures, cAMP levels were augmented by treatment with either forskolin (4, 16, or 64 microM) or 3-isobutyl-1-methyl xanthine (IBMX; 4, 16, or 64 microM). Cartilage degradation was assessed by 1) quantification of C-terminal crosslinking telopeptide of type II collagen fragments (CTX-II), 2) matrix metalloproteinase (MMP)-mediated aggrecan degradation by (342)FFGV- G2 assay, 3) aggrecanase-mediated degradation by (374)ARGS-G2 assay, 4) release of sulfated glycosaminoglycans (sGAG) into culture medium, 5) immunohistochemistry with a monoclonal antibody recognizing the CTX-II epitope, and 6) toluidine blue staining of proteoglycans. MMP expression and activity were assessed by gelatin zymography.
RESULTS: OSM and TNF induced an 8,000% increase in CTX-II compared with control (P < 0.001). Both forskolin and IBMX dose-dependently inhibited release of CTX-II (P < 0.001). OSM and TNF induced a 6-fold increase in (342)FFGV-G2, which was abrogated by forskolin and IBMX (by >80%). OSM and TNF stimulated MMP expression as visualized by zymography, and MMP expression was dose-dependently inhibited by forskolin and IBMX. The highest concentration of IBMX lowered cytokine-induced release of sGAG by 72%.
CONCLUSION: Levels of cAMP in chondrocytes play a key role in controlling catabolic activity. Increased cAMP levels in chondrocytes inhibited MMP expression and activity and consequently strongly inhibited cartilage degradation. Specific cAMP modulators in chondrocytes may be potential treatments for cartilage degenerative diseases.
Effect of forskolin on beta-adrenergic hyporesponsiveness in skin.
De Vries GW, Amdahl LD, Lowe N, Wheeler LA. Skin Pharmacol. 1988;1(2):106-14.
Discovery Research, Allergan, Inc./Herbert Labs, Irvine, Calif.
Beta-Adrenergic receptor hyporesponsiveness has been observed in psoriasis and after exposure of epidermis to phorbol esters. It was the purpose of our studies to determine if forskolin, which is known to act synergistically with receptor agonists in elevating endogenous levels of cyclic AMP, could return these responses to those seen under control conditions. It was observed that topical application of phorbol ester to mouse ears in vivo led to a significant reduction in isoproterenol stimulation of cyclic AMP in vitro. Low doses of forskolin (10(-7) M) were able to enhance isoproterenol's effect under these conditions. Similarly, human keratinocyte cell cultures treated with phorbol esters and human psoriatic epidermis in vitro were both hyporesponsive to isoproterenol. Again, pretreatment of these samples with forskolin restored the beta-agonist stimulation to control values. These data indicate that forskolin is still able to act synergistically with beta-agonists in hyporesponsive systems and suggest that forskolin may be a useful probe in defining the mechanism of this decreased responsiveness both in phorbol-ester-treated skin and in psoriasis.
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