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Table of Contents
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Arguments for Cancer
Rodent Studies
In just about every thread you can find about the use of GW-501516 (GW or Cardarine) in humans, somebody always feels the need say it causes cancer. This is mainly based on a study in which rodents who were subjected to GW developed cancer during the clinical trials, which is partially true. Though, the information these people tend to leave out is under what conditions were these rodents developed cancer during the study. This argument is either because they are repeating something they read online, or realized if they cited the actually study their argument would lose all validity. The study, that is so often referred to, subjected rats to supraphysiological dosages of 10mg/kg of body, or to put that in perspective, a 200lb man (roughly 90 kg) dosing around 900mgs of GW-501516 per day. These doses defy any sensible logic and, therefore, hold no standing at the suggested dosage of 20mg a day.
The study cited above, rats were given the equivalent of a 900mgs dose of GW; this would be comparable to taking 14,625 mgs of aspirin per day. Usually, 325 mgs of aspirin is 1 dose (1 pill). This dose of aspirin could literally KILL you, forget cancer!
Fig 1. GW-501516 Chemical Structure
Flawed Testing Methods
Certain studies supporting the claim that GW causes cell proliferation in human cancer cell lines were flawed from the very beginning. These studies set out to prove an increase growth of cancer cells by estimating the number of cells using a method that tested for enzyme activity, increased activity would indicate more cells. The issue with this testing method is the very substance that they are testing with actually increases enzyme activity within cells. One can quickly see that judging cell proliferation by enzyme activity, while introducing a substance that increases enzyme activity, can give skewed results in regards to an increase in cells. Even if no increase in cells occurred, the increased enzyme activity could lead one to believe it had. In layman terms, it's like testing if your water is contaminated with bacteria by adding bacteria to it!
Scientific Basis for the Link to Cancer
There are reports that claim GW-501516 increases carcinogenesis through a number of ways: increasing cell growth due to the inhibition of apoptosis (cell death), promoting cell proliferation (cell growth) by increasing cyclooxygenase-2 (COX2) and/or vascular endothelial growth factor (VEGF). These reports claim GW can lead to inhibition of apoptosis in human colon cancer cell lines; stimulate proliferation of human liver, breast, and prostate cancer cell lines; increases COX2 expression in human liver cancer cell lines and increased expression of VEGF in breast and colon cancer cell lines. Mainly, the reports link to the above mentioned flawed study done on rodents.
Fig 2. Tumor Progression vs. Tumor Suppression
Arguments Against Cancer
Scientific Basis Against Link to Cancer
Although some reports do provide an argument for cancer, there are many other findings that are inconsistent with the viewpoint. For example, GW is an-501516 anti-inflammatory in many cell types; colon epithelium, macrophages, cardiomyocytes, immune cells, keratinocytes, myoblasts, endothelial cells, and hepatocytes. Evidence also suggest that GW-501516 (cardarine) promotes differentiation in intestinal epithelium, breast and colon cancer cell lines, trophoblasts and primary keratinocytes. This means it allows cells to become more specialized cells maintaining a natural limitation of certain cell types, without such a limitation, basic cells would run rampant invading areas they typically do not belong. GW has also been demonstrated inhibition of cell growth in a number of cells.
Summary of arguments against cancer:
- GW is an anti-inflammatory in many cells
- GW limits cancers
- GW inhibits high cell growth
- GW reduces cancer risks
Studies
A study was done in an attempt to discover why so many inconsistencies existed about GW. This study took three human colon cancer cell lines and two human liver cancer cell lines and tested using different models. Model 1, in the presence of or lack of serum, and, model 2, in the presence of or lack of GW, and studied them over culture period. The results were quantified using the Coulter Method, which is the gold standard of counting, to determine cell proliferation. Under the testing methods for this experiment, all five samples showed no changes in cell proliferation and failed to offer any evidence that PPARs such as GW increased cancer growth.
Fig 3. The Coulter Principle
Research Material
References
- PPARβ/δ a potential target in pulmonary hypertension blighted by cancer risk
- PPARβ/δ Agonist GW501516 Inhibits Tumorigenicity of Undifferentiated Nasopharyngeal Carcinoma in C666-1 Cells by Promoting Apoptosis
- Crosstalk between peroxisome proliferator-activated receptor δ and VEGF stimulates cancer progression
- Metformin inhibits PPARδ agonist-mediated tumor growth by reducing Glut1 and SLC1A5 expressions of cancer cells
- PPARδ regulates multiple proinflammatory pathways to suppress atherosclerosis
- Apoptotic effect of the selective PPARβ/δ agonist GW501516 in invasive bladder cancer cells
