Cardarine talk

[Zarati]

I don't see a whole lot of talk about cardarine, apparently it's great for cholesterol. Up to 17% boost in HDL

I read the cancer studies, they seem exaggerated, talking big doses for yeaaaars

 

[Matsuo Munefusa]

what do you want to talk about it? Its been discussed for many many pages on the forum. Not being snarky just curious about your angle.

 

[Type-IIx]

I think people misunderstand the 2-year rodent bioassay, a valid standardized method for determination of carcinogenicity. Cardarine is definitely carcinogenic, and guys run it long-term. It might not be as bad as smoking, but it's highly carcinogenic.

 

[SOUR DIESEL]

what do you want to talk about it? Its been discussed for many many pages on the forum. Not being snarky just curious about your angle.

^^^clearly he's "shilling" .....cuz he sells the stuff

I don't see a whole lot of talk about cardarine, apparently it's great for cholesterol. Up to 17% boost in HDL

I read the cancer studies, they seem exaggerated, talking big doses for yeaaaars

^^^next time you want to start a thread; ..remember to PM Machu Picchu first to ask permission ..lol


.

 

[Zarati]

what do you want to talk about it? Its been discussed for many many pages on the forum. Not being snarky just curious about your angle.

I used the search button, remember couple of threads but not much on its effect on insulin sensitivity, lipids, etc.
Read some people get skin tags tho lol

 

[Zarati]

Brothers let's keep it civil here, I'm on superdrol, ima get angry and come kiss you on yo cheeks

 

[SOUR DIESEL]

I used the search button, remember couple of threads but not much on its effect on insulin sensitivity, lipids, etc.
Read some people get skin tags tho lol

^^^brother you don't owe him an explanation

"your angle" if you had one ..is not his concern ..that's what MODs are for ..and the MODs here are quite intelligent & experienced

Brothers let's keep it civil here, I'm on superdrol, ima get angry and come kiss you on yo cheeks

^^^we'r all good here ..no uncivilness going on
..Macho Pikachu just gets a lil high in his britches & starts trying to personifying a supremacy (..& appointing himself liberties) that he doesn't have
..& then he tries to leverage that "pseudo power" (..however subtly) on less experienced members to make them feel like they did something wrong/stupid
..it might make him feel better about himself, but he has no jurisdiction here ..the only power he has is what you give him

take a close look; he's not a "cool kid" or an authority on anything ..so you don't need his approval to post
..& there are many many many threads that rehash the same thing, that's what keeps the board revolving/progressing
..each thread can catch the attention, comments, experiences & contributions/new information of different members that were not present before & can serve to give us a new prospective & enlighten us all
..so don't worry

I don't see a whole lot of talk about cardarine, apparently it's great for cholesterol. Up to 17% boost in HDL

I read the cancer studies, they seem exaggerated, talking big doses for yeaaaars

^^^as far CARDARINE ..yes it does improve HDL ..& IME, it seems more than just 17%
..i remember bloodwork where my HDL went from 30 to 42 ..that's 28.5%+/-
^^^this is at a dose of 20mg/day

..it provides a noticeable rise in energy even when running TREN
(..actually won't run TREN without it anymore)
^^^i used it as a PRE-workout 20mg all at once 45mins prior to training ◄this give the best "boost"

..no i don't run it year round ..but maybe 6mos out of the year? ..never go over 20mg/day either


^^^IMO the carcinogenic effects don't really apply to our & are based on heavy dose & duration
..even "benign" things ..including water ..can have adverse effects in high enough doses ..sooo


^^^maybe Type-IIx can provide the studies & we can all delve deeper into topic as part of this discussion


.

 

[aphextwin]

It’s not going to cause cancer at an extremely low dose. If it did, I’m fucked. I just cycle it on and off…love it.

 

[Type-IIx]

^^^maybe Type-IIx can provide the studies & we can all delve deeper into topic as part of this discussion

Absolutely brother. When I get interested in a compound, before I put it in my body (or perhaps decide not to), I like to as objectively as possible assess the risk-reward of the compound. Here is what I came up with as a risk-reward profile for Cardarine. I've drawn up risk-reward profiles on a lot of compounds, @OuchThatHurts if ProM ever wanted to feature them or anything I do think they're decently thorough and objective.

This risk-reward profile is based largely on what I think was the best article I've read on Cardarine by Peter Bond. Aside from already being a succinct work, I essentially looked in to the cited data, learned about the particular benefit of Cardarine, which most guys probably don't even appreciate fully (increased cholesterol efflux, muscle oxidative capacity) before taking Cardarine. So here's just a risk-reward profile of many that I have drawn up for "objectivity."

Cardarine (GW501516)
PPAR: peroxisome proliferator-activated receptor; group of nuclear receptors ∴ affect gene transcription (e.g., PUFAs/FAs affect gene transcription via these receptors)

• α: lipid metabolism
• δ: delta; glucose metabolism and muscle oxidative capacity
• γ: formation of new fat cells, FA uptake and storage ∴ insulin sensitivity [3]

Broadly, activation of these receptors ⇒ antiartheriogenic and antiinflammatory state

• fibrates, class of compound that broadly activates PPAR subtypes
• glitazones/thiazolidinediones activate PPARγ ⇒ ameliorated insulin sensitivity [1]

Cardarine (GW501516): putative PPARδ agonist; initially showed promise for:

• partial ↓ hyperinsulinemia
• ↓ VL/LDL & fasting TGs
• ↑ HDL
• ↑ cholesterol efflux: reverse cholesterol transport, whereby HDL protects the arteries (purportedly specific to PPARδ) [1]

Clinical trials concluded that Cardarine:

• merely counteracts the ↓ HDL from switching to a sedentary lifestyle
• likely improves insulin sensitivity (Clinical Trial 1) [4]
• In abdominally obese/dyslipidemia:
  • ↓ HOMA-IR (∴ ↓ insulin resistance)
  • ↓ liver fat
  • ↓ NEFA (i.e., less circulating FAs) (Clinical Trial 2) [5 - 6]

Additional large study and summary of the clinical trials [7] mentions that due largely to the cancer risk, the product would not be pursued to market.

Substantial cancer risk
See [8 - 9] for rat cancer study discussion, "the infamous rat cancer study."

The 2-year rodent carcinogenicity bioassays showed worrying results

The pharmaceutical industry is expected, or pretty much mandated, to explore the carcinogenicity of new pharmaceuticals they intend to bring to market. Historically the FDA and it’s European equivalent the European Medicines Agency (EMA) required the 2-year rodent bioassay for this. Which boils down to giving mice and rats the substance for 2 years, and then assessing the cancers that have arised. This has been done for decades and there’s a wealth of data on the most commonly used rat strains for this type of studies. The bioassay has good sensitivity and specificity. Meaning that, if a substance is carcinogenic, there’s a good chance this bioassay will demonstrate this. Similarly, if a substance is not carcinogenic, there’s also a good chance this bioassay will demonstrate that.

The full data of the 2-year rodent bioassays have not been published by GSK, but a brief summary of their result has [8, 9].

In the rat study, male rats were given 0, 5, 20, or 40 mg/kg/day, whereas female rats were given 0, 3, 10 or 20 mg/kg/day. The results showed increased mortality in females at all doses, with neoplasms considered related to cardarine in various tissues at all dosages, namely:
Hepatocellular adenoma at >10 mg/kg/day
Urinary bladder transitional cell carcinoma in males at 20 and 40 mg/kg day
Thyroid follicular cell adenoma at >3 mg/kg/day and carcinoma in males at >20 mg/kg/day
Tongue squamous cell papilloma in males at 5 and 40 mg/kg/day
Stomach squamous cell papilloma in males at >5 mg/kg/day and a female at 20 mg/kg/day, and carcinoma in a male at 40 mg/kg/day and a female at 3 mg/kg/day
Skin inverted squamous cell papilloma in males at >5 mg/kg/day and females at 3 or 20 mg/kg/day
Harderian glands adenoma in males at >5 mg/kg/day and adenocarcinoma in a male at 40 mg/kg/day
Testes interstitial cell adenoma at 40 mg/kg/day
Ovary Sertoli cell adenoma at >10 mg/kg/day
Uterus polyp and endometrial adenocarcinoma at >3 mg/kg/day

In the mice study, mice were given 0, 10, 30, 60 or 80 mg/kg/day. The results showed increased mortality at doses >30 mg/kg/day and neoplasms considered related to cardarine in various tissues, namely:

Hepatocellular carcinoma at >30 mg/kg/day and adenoma at >10 mg/kg/day
Stomach squamous cell carcinoma at all dosages
Combined squamous cell tumours at all dosages (squamous cell papilloma and carcinoma, and keratoacanthoma)

[1]

Needless to say, these results demonstrating considerable carcinogenicity foreclosed pursuing bringing Cardarine to market.

Cholesterol efflux capacity
The capacity of HDL particles to accept cholesterol from macrophages which engulf oxidized LDL cholesterol [10]. In cholesterol efflux, HDL particles reuptake oxidized LDL particles from macrophages in the arterial wall and transport it back to the liver [10].

Macrophages can release their cholesterol by simple diffusion or through transporter proteins, the most important being the ATP-binding cassette transporter A1 (ABCA1) [10]. This is likely one of the main ways HDL cholesterol protects arteries from deterioriating [10].

Risk-reward Profile for Cardarine (GW501516)
Whether:
+ improved insulin sensitivity via increased skeletal muscle oxidation
+ increased cholesterol efflux (improved artery health via HDL & reverse cholesterol transport)
is worth:
--- substantial cancer risk
in consideration of:
availability of legal, cheap, effective fibrates; particularly glitazones/thiazolidinediones which effectively improve insulin sensitivity via PPARγ sans "cholesterol efflux" and significantly, cancer risk.

_____
**References**
[1] Bond, P. The Rise and Fall of Cardarine (GW501516). Sep 2021. Source: https://thinksteroids.com/articles/cardarine-gw501516/
[2] Grygiel-Górniak B. Peroxisome proliferator-activated receptors
and their ligands: nutritional and clinical implications--a review. Nutr J. 2014 Feb 14;13:17. doi: 10.1186/1475-2891-13-17. PMID: 24524207; PMCID: PMC3943808.
[3] Montaigne, David, Laura Butruille, and Bart Staels. “PPAR control of metabolism and cardiovascular functions.” Nature Reviews Cardiology (2021): 1-15.
[4] Sprecher, D. L., Massien, C., Pearce, G., Billin, A. N., Perlstein, I., Willson, T. M., … Johnson, T. G. (2006). Triglyceride:High-Density Lipoprotein Cholesterol Effects in Healthy Subjects Administered a Peroxisome Proliferator Activated Receptor Agonist. Arteriosclerosis, Thrombosis, and Vascular Biology, 27(2), 359–365. doi:10.1161/01.atv.0000252790.70572.0c
[5] Riserus, U., Sprecher, D., Johnson, T., Olson, E., Hirschberg, S., Liu, A., … Karpe, F. (2007). Activation of Peroxisome Proliferator-Activated Receptor (PPAR) Promotes Reversal of Multiple Metabolic Abnormalities, Reduces Oxidative Stress, and Increases Fatty Acid Oxidation in Moderately Obese Men. Diabetes, 57(2), 332–339. doi:10.2337/db07-1318
[6] Ooi, E. M. M., Watts, G. F., Sprecher, D. L., Chan, D. C., & Barrett, P. H. R. (2011). Mechanism of Action of a Peroxisome Proliferator-Activated Receptor (PPAR)-δ Agonist on Lipoprotein Metabolism in Dyslipidemic Subjects with Central Obesity. The Journal of Clinical Endocrinology & Metabolism, 96(10), E1568–E1576. doi:10.1210/jc.2011-1131
[7] Olson, E. J., Pearce, G. L., Jones, N. P., & Sprecher, D. L. (2012). Lipid Effects of Peroxisome Proliferator-Activated Receptor- Agonist GW501516 in Subjects With Low High-Density Lipoprotein Cholesterol: Characteristics of Metabolic Syndrome. Arteriosclerosis, Thrombosis, and Vascular Biology, 32(9), 2289–2294. doi:10.1161/atvbaha.112.247890
[8] Geiger, L. E., et al. “Rat carcinogenicity study with GW501516, a PPAR delta agonist.” The Toxicologist 108.1 (2009): 895.
[9] Newsholme, S. J., et al. “Mouse carcinogenicity study with gw501516, a PPAR delta agonist.” The Toxicologist 108.1 (2009): 896.
[10] Bond, P. Book on Steroids. (2020).

 

[warlock]

Absolutely brother. When I get interested in a compound, before I put it in my body (or perhaps decide not to), I like to as objectively as possible assess the risk-reward of the compound. Here is what I came up with as a risk-reward profile for Cardarine. I've drawn up risk-reward profiles on a lot of compounds, @OuchThatHurts if ProM ever wanted to feature them or anything I do think they're decently thorough and objective.

This risk-reward profile is based largely on what I think was the best article I've read on Cardarine by Peter Bond. Aside from already being a succinct work, I essentially looked in to the cited data, learned about the particular benefit of Cardarine, which most guys probably don't even appreciate fully (increased cholesterol efflux, muscle oxidative capacity) before taking Cardarine. So here's just a risk-reward profile of many that I have drawn up for "objectivity."

Cardarine (GW501516)
PPAR: peroxisome proliferator-activated receptor; group of nuclear receptors ∴ affect gene transcription (e.g., PUFAs/FAs affect gene transcription via these receptors)

• α: lipid metabolism
• δ: delta; glucose metabolism and muscle oxidative capacity
• γ: formation of new fat cells, FA uptake and storage ∴ insulin sensitivity [3]

Broadly, activation of these receptors ⇒ antiartheriogenic and antiinflammatory state

• fibrates, class of compound that broadly activates PPAR subtypes
• glitazones/thiazolidinediones activate PPARγ ⇒ ameliorated insulin sensitivity [1]

Cardarine (GW501516): putative PPARδ agonist; initially showed promise for:

• partial ↓ hyperinsulinemia
• ↓ VL/LDL & fasting TGs
• ↑ HDL
• ↑ cholesterol efflux: reverse cholesterol transport, whereby HDL protects the arteries (purportedly specific to PPARδ) [1]

Clinical trials concluded that Cardarine:

• merely counteracts the ↓ HDL from switching to a sedentary lifestyle
• likely improves insulin sensitivity (Clinical Trial 1) [4]
• In abdominally obese/dyslipidemia:
  • ↓ HOMA-IR (∴ ↓ insulin resistance)
  • ↓ liver fat
  • ↓ NEFA (i.e., less circulating FAs) (Clinical Trial 2) [5 - 6]

Additional large study and summary of the clinical trials [7] mentions that due largely to the cancer risk, the product would not be pursued to market.

Substantial cancer risk
See [8 - 9] for rat cancer study discussion, "the infamous rat cancer study."


[1]

Needless to say, these results demonstrating considerable carcinogenicity foreclosed pursuing bringing Cardarine to market.

Cholesterol efflux capacity
The capacity of HDL particles to accept cholesterol from macrophages which engulf oxidized LDL cholesterol [10]. In cholesterol efflux, HDL particles reuptake oxidized LDL particles from macrophages in the arterial wall and transport it back to the liver [10].

Macrophages can release their cholesterol by simple diffusion or through transporter proteins, the most important being the ATP-binding cassette transporter A1 (ABCA1) [10]. This is likely one of the main ways HDL cholesterol protects arteries from deterioriating [10].

Risk-reward Profile for Cardarine (GW501516)
Whether:
+ improved insulin sensitivity via increased skeletal muscle oxidation
+ increased cholesterol efflux (improved artery health via HDL & reverse cholesterol transport)
is worth:
--- substantial cancer risk
in consideration of:
availability of legal, cheap, effective fibrates; particularly glitazones/thiazolidinediones which effectively improve insulin sensitivity via PPARγ sans "cholesterol efflux" and significantly, cancer risk.

_____
**References**
[1] Bond, P. The Rise and Fall of Cardarine (GW501516). Sep 2021. Source: https://thinksteroids.com/articles/cardarine-gw501516/
[2] Grygiel-Górniak B. Peroxisome proliferator-activated receptors
and their ligands: nutritional and clinical implications--a review. Nutr J. 2014 Feb 14;13:17. doi: 10.1186/1475-2891-13-17. PMID: 24524207; PMCID: PMC3943808.
[3] Montaigne, David, Laura Butruille, and Bart Staels. “PPAR control of metabolism and cardiovascular functions.” Nature Reviews Cardiology (2021): 1-15.
[4] Sprecher, D. L., Massien, C., Pearce, G., Billin, A. N., Perlstein, I., Willson, T. M., … Johnson, T. G. (2006). Triglyceride:High-Density Lipoprotein Cholesterol Effects in Healthy Subjects Administered a Peroxisome Proliferator Activated Receptor Agonist. Arteriosclerosis, Thrombosis, and Vascular Biology, 27(2), 359–365. doi:10.1161/01.atv.0000252790.70572.0c
[5] Riserus, U., Sprecher, D., Johnson, T., Olson, E., Hirschberg, S., Liu, A., … Karpe, F. (2007). Activation of Peroxisome Proliferator-Activated Receptor (PPAR) Promotes Reversal of Multiple Metabolic Abnormalities, Reduces Oxidative Stress, and Increases Fatty Acid Oxidation in Moderately Obese Men. Diabetes, 57(2), 332–339. doi:10.2337/db07-1318
[6] Ooi, E. M. M., Watts, G. F., Sprecher, D. L., Chan, D. C., & Barrett, P. H. R. (2011). Mechanism of Action of a Peroxisome Proliferator-Activated Receptor (PPAR)-δ Agonist on Lipoprotein Metabolism in Dyslipidemic Subjects with Central Obesity. The Journal of Clinical Endocrinology & Metabolism, 96(10), E1568–E1576. doi:10.1210/jc.2011-1131
[7] Olson, E. J., Pearce, G. L., Jones, N. P., & Sprecher, D. L. (2012). Lipid Effects of Peroxisome Proliferator-Activated Receptor- Agonist GW501516 in Subjects With Low High-Density Lipoprotein Cholesterol: Characteristics of Metabolic Syndrome. Arteriosclerosis, Thrombosis, and Vascular Biology, 32(9), 2289–2294. doi:10.1161/atvbaha.112.247890
[8] Geiger, L. E., et al. “Rat carcinogenicity study with GW501516, a PPAR delta agonist.” The Toxicologist 108.1 (2009): 895.
[9] Newsholme, S. J., et al. “Mouse carcinogenicity study with gw501516, a PPAR delta agonist.” The Toxicologist 108.1 (2009): 896.
[10] Bond, P. Book on Steroids. (2020).

Nice info.

How much do you think it aims in improving insulin sensitivity?

 

[Type-IIx]

Nice info.

How much do you think it aims in improving insulin sensitivity?

It's not possible to say exactly, what is noted from the first clinical trial in healthy subjects were some effects on gene expression/mRNA expression of some HDL/TG pathways, with a proposed mechanism:
"changes in glucose tolerance (admittedly unlikely in healthy volunteer subjects) could have contributed to the observed TG and HDL changes. Lee et al and Tanaka et al have notes an improvement in insulin sensitivty when...GW501516...is administered to rodents (34, 35). This is hypothesized to be associated with reductions in the pool of skeletal muscle fat, a feature relevant to insulin resistance (36)."

Insulin and glucose were not measured directly in the healthy subjects, but they propose that if insulin sensitization did occur, an insulin-dependent impact on lipolysis (18) as well as on hepatic synthesis (37) might have contributed to the lipid trends observed.

Basically, I wouldn't hang my hat on there being huge improvements in insulin sensitivity without a bit more evidence, but the mechanism is sort of logically implicated and has been measured in rodents.

 

[Reno911]

I doubt anyone is using 3 or 5mg per KG of bodyweight.

 

[Type-IIx]

I doubt anyone is using 3 or 5mg per KG of bodyweight.

It's a universally accepted model of carcinogenicity, it's not intended for human equivalence because rather than being willing to sacrifice human beings to cancer by megadosing with compounds of uncertain risk, the scientific and medical community values human life over rodent life. So they run these tests, which can be interpreted. The interpretation, correct interpretation, is that cardarine is carcionogenic. I'm not proposing you test whether YOU survive Cardarine at megadoses, I'm just presenting evidence of a universally accepted model of carcinogenicity and its results.

 

[Reno911]

It's a universally accepted model of carcinogenicity, it's not intended for human equivalence because rather than being willing to sacrifice human beings to cancer by megadosing with compounds of uncertain risk, the scientific and medical community values human life over rodent life. So they run these tests, which can be interpreted. The interpretation, correct interpretation, is that cardarine is carcionogenic. I'm not proposing you test whether YOU survive Cardarine at megadoses, I'm just presenting evidence of a universally accepted model of carcinogenicity and its results.

You're saying in mice studies to determine carcinogenicity the universally accepted model is 100+ x's the human dosage?

 

[Type-IIx]

You're saying in mice studies to determine carcinogenicity the universally accepted model is 100+ x's the human dosage?

I'm saying human equivalence formulas are inapplicable. It's a model for carcinogenicity that is standardardized against the replicable 2-year rodent cancer assay. It's not intended for dose-response calculations in humans.

 

[oxandrin]

I'm saying human equivalence formulas are inapplicable. It's a model for carcinogenicity that is standardardized against the replicable 2-year rodent cancer assay. It's not intended for dose-response calculations in humans.

I appreciate your approach to this topic and you appear genuine in your beliefs. I will provide some additional insights. I agree that It seems there was a rush to lean on human equivalency.While the carcinogenicity of the rodent study was scientific we must also remember there is human data that revealed no reports of ANY cancer in ANY of the human subjects, which at face value appears to be a positive for cardarine safety yet these human studies doesn't appear to satisfy the safety determination of cardarine.

With respect to the highly debated rodent study a couple of parameters that I call into question aside from the administration is the question of the subjects themselves. These rodents are considered the gold standard for two year carcinogenic studies. I dont feel these outcomes are supported by the cleanest type of measurement> I would love to see the scientific community reevaluate the candidacy of the current subjects and if not replace them then certainly find an additional precursor to hold up the seemingly iron clad determination of a drug being carcinogenic and how that determination applies to humans. Im not suggesting that these rodents were substandard due to the fault of the "supplier", in that case we can question any study using Wistar rats-positive or negative.The goal would be to prevent scratching out viable drugs that can be brought to market.

Regarding genetic drift.
"Furthermore, it should be considered that SD and Wistar rats are delivered by different breeders that are breeding these animals for many generations. In this case, differences between substrains (e.g., Hsd: SD and Crl: CD(SD)) and even breeding colonies at different locations within a substrain may cause differences in control data"

https://insights.envigo.com/hubfs/White%20paper_Wistar%20Han%20rat%20for%20carcinogenicity%20studies.pdf

Study confirming the standard.

https://www.ahajournals.org/doi/10.1161/circ.140.suppl_1.15696

Study revealing the importance of the breeder providing the rats.

Food for thought....what says you guys?

 

[Type-IIx]

I appreciate your approach to this topic and you appear genuine in your beliefs. I will provide some additional insights. I agree that It seems there was a rush to lean on human equivalency.While the carcinogenicity of the rodent study was scientific we must also remember there is human data that revealed no reports of ANY cancer in ANY of the human subjects, which at face value appears to be a positive for cardarine safety yet these human studies doesn't appear to satisfy the safety determination of cardarine.

With respect to the highly debated rodent study a couple of parameters that I call into question aside from the administration is the question of the subjects themselves. These rodents are considered the gold standard for two year carcinogenic studies. I dont feel these outcomes are supported by the cleanest type of measurement> I would love to see the scientific community reevaluate the candidacy of the current subjects and if not replace them then certainly find an additional precursor to hold up the seemingly iron clad determination of a drug being carcinogenic and how that determination applies to humans. Im not suggesting that these rodents were substandard due to the fault of the "supplier", in that case we can question any study using Wistar rats-positive or negative.The goal would be to prevent scratching out viable drugs that can be brought to market.

Regarding genetic drift.
"Furthermore, it should be considered that SD and Wistar rats are delivered by different breeders that are breeding these animals for many generations. In this case, differences between substrains (e.g., Hsd: SD and Crl: CD(SD)) and even breeding colonies at different locations within a substrain may cause differences in control data"

https://insights.envigo.com/hubfs/White%20paper_Wistar%20Han%20rat%20for%20carcinogenicity%20studies.pdf

Study confirming the standard.

https://www.ahajournals.org/doi/10.1161/circ.140.suppl_1.15696

Study revealing the importance of the breeder providing the rats.

Food for thought....what says you guys?

Your argument is that the 3 clinical trials, whose durations were in terms of weeks, that did not measure any parameter of carcinogenicity as an outcome, are not only good evidence that cardarine is not carcinogenic in humans, but better than the standard that is actually used to determine that outcome?

Do you have evidence that the 2-year rodent carcinogenicity bioassays were susceptible to this theoretical genetic drift problem by actually sourcing from different breeders or colonies?

Have you considered the fact that if there was consensus that the carcinogenicity standard was not a good one; it wouldn't be used as a standard?

 

[narta]

Aren't Han Wistar rats prone to developing cancer anyway and have a lifespan of 3 years? So they gave cardarine for the 2/3 of their life expectancy to already cancer prone rats?

 

[jeroendebleser]

I think people misunderstand the 2-year rodent bioassay, a valid standardized method for determination of carcinogenicity. Cardarine is definitely carcinogenic, and guys run it long-term. It might not be as bad as smoking, but it's highly carcinogenic.

This + it doesn't do much imo so why risk cancer?

 

[Flex500]

Your argument is that the 3 clinical trials, whose durations were in terms of weeks, that did not measure any parameter of carcinogenicity as an outcome, are not only good evidence that cardarine is not carcinogenic in humans, but better than the standard that is actually used to determine that outcome?

Do you have evidence that the 2-year rodent carcinogenicity bioassays were susceptible to this theoretical genetic drift problem by actually sourcing from different breeders or colonies?

Have you considered the fact that if there was consensus that the carcinogenicity standard was not a good one; it wouldn't be used as a standard?

I’m with you on this topic, but let me take it from another angle…as an investor. I’m a big investor in small cap bios (not the GSK was a small cap). They could have made a ton of money off of this drug.

Statins came out in early 00’s (or maybe 05ish I don’t totally recall) and for me Cardarine works better than statins on my lipids. GSK could have potentially had the most impactful lipid modulator on the market + the impacts on insulin sensitivity.

From 2005 to now this could have been a $30-$50 billion drug during a time when this sort of drug was literally craved by the medical community.

Along with the info you posted, this is why I decided never to use it again.

It feels like as a bodybuilder community we are trying to convince ourselves it’s safe, but pharma companies don’t turn down billions revenue for nothing. And just as an fyi most pharma companies would agree that to make $50b they had to pay back $1-$6b down the road due to sides so there is an amount of risk many will take. This drug wasn’t even in the “borderline zone” for safety.