Anyone try Cardarine?

[antipcman]

She asked for anecdotal proof. "Has anyone used..." qualified my answer. You don't seem to have used, so I simply said don't disregard or better yet don't waste her time with the varied results. There was no malapropisms in my writing.

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There definitely was malapropism that you clearly have yet to distinguish. "I simply told her not to waste her time with the varied results [RESULTS THAT WERE ENOUGH FOR THE IP HOLDER TO DISCONTINUE RESEARCH]."

Keep shilling your SARM-nonsense. The exaggerated claims have already been disproven. If OP was going to run a silly SARM, why wouldn't OP just stick with var at that price point? MK-677? Why not IPAM and Mod GRF 1-29.

"You're not doing OP any good." Really? You are? She already said the only thing she found of value in relation to SARMs was GW so you steer her in the direction of 2 products that have been found to be inferior to their more researched counterparts. Ironic because some of the logs I've seen have implied insulin resistance in MK-677 as well as a GH bleed. Sooooo explain to me why MK-677 works better than any GHRP. Explain to me how OP would benefit from a more expensive, more heavily shilled, less proven steroid that's the second coming of the ole "prohormone" in the sense that it doesn't have that dirty word "steroid" attached to it.

 

[MISSHULK]

Anyone?

[emoji23]

 

[antipcman]

OP, as stated previously, GW 501516 is a ppar "delta" agonist. To understand why its mechanism of action is detrimental to the human body, it is important to understand what a ppar agonist actually doe; this shed's some light on the ppar delta itself:

http://cancerres.aacrjournals.org/content/64/9/3162.full.pdf

”The nuclear receptor peroxisome proliferator-activated receptor [PPAR/ (NR1C2)] has been implicated in colorectal carcinogenesis by various molecular genetic observations. These observations have recently been supported by studies of activation of PPAR by pharmacological agents. Here we present the first report of the stimulation of breast and prostate cancer cell growth using PPAR selective agonists. Activation of PPAR with compound F stimulated proliferation in breast (T47D, MCF7) and prostate (LNCaP, PNT1A) cell lines, which are responsive to sex hormones. Conversely, we have found that several steroid-indepen-dent cell lines, including colon lines, were unresponsive to compound F. These findings were confirmed with an additional high-affinity PPAR agonist, GW501516. Conditional expression of PPAR in MCF7 Tet-On cells resulted in a doxycycline-enhanced response to GW501516, thus providing direct genetic evidence for the role of PPAR in the prolifera-tive response to this drug. Activation of PPAR in T47D cells resulted in increased expression of the proliferation marker Cdk2 and also vascular endothelial growth factor (VEGF) and its receptor, FLT-1, thus, suggesting that PPAR may initiate an autocrine loop for cellular prolif-eration and possibly angiogenesis. Consistent with this hypothesis, we demonstrated a pro-proliferative effect of GW501516 on human umbilical vein endothelial cell cultures and found that GW501516 also regulated the expression of VEGF and FLT-1 in these cells. *Our observations provide the first evidence that activation of PPAR can result in increased growth in breast and prostate cancer cell lines and primary endothelial cells and supports the possibility that PPAR antagonists may be of therapeutic value in the treatment of breast and prostate cancer.”

*Personal note: Very interesting that a ppar delta agonist is the mechanism in which propensity toward adipose as a source of energy is the means in which this compound actually works. Yet, in terms of cancer research, antagonism (i.e. the exact opposite) in seen as "therapeutic" in terms of treating both breast and prostate cancer.


This is another piece of research that shows cancer cell proliferation in humans. They used mice in the experiment in addition to using human cells not as the sole method of research but for illumination and verifiability, contrary to what many other folks suggest:


Methods

Animals
..........[eliminated for redundancy]






Cell Culture and Reagents.


LS-174T, HCT-116, HCA-7, SW480,HT-29, and SW620 cells were maintained in McCoy’s 5A medium with 10% FBS. PPAR-null HCT-116 cells were a gift from K. W.Kinzler (Johns Hopkins School of Medicine, Baltimore, MD) (11).GW501516 was obtained from Ramidus AB (Lund, Sweden). Ly294002 was obtained from Calbiochem (La Jolla, CA).
Real-Time Quantitative PCR.


VEGF, VEGFR1, VEGFR2, andVEGFR3 mRNA was quantified by real-time quantitative PCR using iCycler (Bio-Rad, Hercules, CA) and iQ SYBR green Su-permix (Bio-Rad). The assay was conducted previously described(39). Primers for VEGF, VEGFR1,VEGFR2,VEGFR3, and Actin genes were chosen by using the Beacon Designer 4 program.