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It must be noted that the vast majority of the studies demonstrating Cardarine’s apparent capacity to cause tumorigenesis and cell proliferation have been conducted in vitro, and appear to be equaled in number by those demonstrating the activation of PPARd to actually inhibit such cancerous phenomena. Furthermore, the former studies are not without criticism:
“The development of peroxisome proliferator-activated receptor-d ligands for the treatment of diseases including metabolic syndrome, diabetes and obesity has been hampered due to contradictory findings on their potential safety. For example, while some reports show that ligand activation of PPARd promotes the induction of terminal differentiation and inhibition of cell growth; other reports suggest that PPARd ligands potentiate tumorigenesis by increasing cell proliferation. Some of the contradictory findings could be due in part to differences in the ligand examined, the presence or absence of serum in cell cultures, differences in cell lines, or differences in the method used to quantify cell growth.”
“It is notable that synthetic PPAR agonists, which have been extensively used in human subjects, enhance colon polyp formation in the Apcmin model yet have not been demonstrated to cause cancer in humans. Similarly, PPAR activators cause hepatocarcinomas in rodents but fail to have such deleterious effects in humans. These findings cast doubt on the predictive power of mouse models to determine the human carcinogenicity of PPAR-targeted drugs.”
“Results from the present studies demonstrate that ligand activation of PPARd inhibits the growth of both MCF7 (BREAST CANCER) and UACC903 (MELANOMA) cell lines and provide further evidence that PPARd ligands are not mitogenic in human cancer cell lines.
“Evidence from a large number of independent laboratories also shows that cell growth is inhibited by PPARd and its ligands in colonocytes, keratincytes, cardiomyocytes, fibroblasts, endothelial cells and a variety of cancer cell lines.”
“Results from the present study demonstrate with the use of two highly specific PPARd ligands and the most reliable method for quantifying cell number, that ligand activation of PPARd modestly inhibits cell growth in either MCF7 or UACC903 cells. This work is consistent with past studies showing that ligand activation of PPARd inhibits cell growth in human liver and colon cancer cell lines.”
“The quantitative natures of the present findings are inconsistent with the hypothesis that cancer cell lines respond differentially as compared with normal cells, and provide further evidence that PPARd ligands do not potentiate tumorigenesis.”
To examine the effect of PPARd ligands on cell growth of human cancer cell lines, cell proliferation was quantified in three different colon cancer cell lines and two liver cancer cell lines in the presence of either GW0742 or GW501516, in the presence or absence of serum. No significant increase in cell proliferation was observed in any of the human cancer cell lines with either potent PPARd ligand:
Gastric tumor occurrence after treatment with DMBA and GW501516:
Treatment group No. animals No. animals with tumors
DMBA 10 0
GW501516 10 0
DMBA + GW501516 15 12
Mice maintained on a diet supplemented with PPARd agonist GW501516 following carcinogen administration resulted in the rapid development of gastric tumors in 12/15 animals, whereas treatment with either GW501516 or DMBA alone was not tumorigenic.
In perhaps the most infamous ‘study’, rats were administered up to 40mg/kg/d for two (2) years. That dose is roughly equivalent to 650mg/d for a human, dosed for two years.
In conclusion, if Cardarine is dosed responsibly, then given the current evidence and data it would seem unlikely that ingestion will result in the formation of tumors.
References can be found here on CARDARINE page.
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