Primo: risk-reward profile... is it 'conspicuous consumption' or does it really only 'shine' with long-term use?

[Cdave.aol]

His channel is garbage now geared towards brain dead teenagers who use mommy and daddy credit card to buy their SARMS. Don’t believe me? Look at the comment section of his videos, full of retards trying to make memes and be funny

And he wonders why now guys subscribed to his channel are running gear and other stupid shit, like bro that’s what you get for trying to appeal to the most viewers rather than focus on quality videos that may get less views

 

[Cdave.aol]

Well, duh, who is going to mention that they were in special ed?

I know he mentioned having a business degree and I honestly think he’s knowledgeable and intelligent. But he’s become a slave YouTube “algorithm” and social media making himself look really stupid

 

[Iron_Yuppie]

Derek got famous because he really, really didn’t want to lose his hair. From there he figured out that if you have a decent grasp of how to read clinical data you can sell the shit out of SARMs to people who are too lazy to do the research themselves. (That is a large population)

 

[Cdave.aol]

Derek got famous because he really, really didn’t want to lose his hair. From there he figured out that if you have a decent grasp of how to read clinical data you can sell the shit out of SARMs to people who are too lazy to do the research themselves. (That is a large population)

It’s not really SARMS but this Turkish crap whatever tf it’s called apparently it’s like anavar lite with no Hpta suppression

 

[CooSee]

Name another steroid you can run at high doses and have absolutely no idea that you’re using them because the side effects are nonexistent. That’s the appeal of primo. 600mg feels approximately the same as 0mg in terms of sides. It was quite literally designed to have the most favorable side effect profile that could be achieved while still being efficacious.

If you want tren-like results then primo will disappoint you. But you also won’t go two months without sleep, sweat like a stuck pig all day, and give yourself dementia. The risk/reward is thus: the reward is the lack of risk.

It’s like the treasury bond of steroids and Tren is Bitcoin.

 

[Type-IIx]

For the “Pros column” with a caveat:

Some evidence of Primo (methenolone)’s relative beneficial effect versus comparable AAS on cardiac health via the apparent absence of competitive inhibition of cortisol oxidation, perhaps tipping the balance in favor of less oxidative stress in cardiac cells (putative mechanism):

11β-HSD2 is an enzyme that controls the oxidation of cortisol. Its inhibition leads to glucocorticoid-mediated MR activation, potassium excretion, sodium and water retention, and increased blood pressure (Ferrari, 2010; Ferrari et al., 2001; Serra et al., 2002) [3].

Primo showed no significant alteration of glucocorticoid activity as a unique attribute. AAS that inhibit 11β-HSD2, or alternately (perhaps similarly to tren) inhibit cortisol oxidation and exert MR action, may aggravate atherosclerosis via MR activation and inflammatory processes in the vascular endothelium (Glazer, 1991; Thompson et al., 1989) [3].

CONCLUSION
+++ evidence (published) of some relative benefit versus comparable AAS for cardiac health (the absence of a harm does not imply a net positive, but rather an aspect of Primo that is comparably favorable)

-- some evidence (published) of relatively weakened anticatabolism of Primo.

_________________________________
References:
(continued from first post)
[3] Furstenberger, C., Vuorinen, A., Da Cunha, T., Kratschmar, D. V., Saugy, M., Schuster, D., & Odermatt, A. (2012). The Anabolic Androgenic Steroid Fluoxymesterone Inhibits 11 -Hydroxysteroid Dehydrogenase 2-Dependent Glucocorticoid Inactivation. Toxicological Sciences, 126(2), 353–361. doi:10.1093/toxsci/kfs022

 

[Jet Labs]

100mgs ed of primo-ace along with low dose test dose will give awesome results even after just 4 weeks of use and the results will be even better if you use primo-ace inject rather than oral. That's my experience at least.

 

[Ambusher]

His channel is garbage now geared towards brain dead teenagers who use mommy and daddy credit card to buy their SARMS. Don’t believe me? Look at the comment section of his videos, full of retards trying to make memes and be funny

And he wonders why now guys subscribed to his channel are running gear and other stupid shit, like bro that’s what you get for trying to appeal to the most viewers rather than focus on quality videos that may get less views

It's funny you mention that, because when I started watching him a couple months back and after having read his comment section, it's the exact same conclusion I drew. Nothing but children and teenagers in his comments thinking they're cute and seeing who can get the most likes. I even made a comment where I thought that his content would attract a higher-caliber quality of viewer, instead of the silly brats that are always trying to meme their way to fame in a comment section. Also, it's called Turkesterone.

 

[Ambusher]

Few things:

The study makes no mention of how well either the Primobolan or testosterone was tolerated by the breast cancer patients. Moreover, 44 % reported acne, 52 % reported hirsutism (more about this further down), 40 % reported flushing, and 76 % reported hoarseness in the Primobolan group. Mind you; if you're a postmenopausal woman with advanced breast cancer, a lot of stuff is considered to be 'tolerable' for the means of treating it.


Nowhere in the paper do they mention something about tolerability. The women who weren't continued on the 300 mg of testosterone per week weren't discontinued because they couldn't tolerate it, they were discontinued because it didn't lead to regression of their cancer. Moreover, perhaps 1200 mg of testosterone would. Who knows? Not that it matters, because I don't expect any of his readers to read this for treatment of their advanced breast cancer.


Yes, since most people who use Primobolan are of the opposite sex. Although I think he differs in his view from mine on exactly why that's interesting.


Again, the study mentions nothing about how the women tolerated it, and if you have advanced breast cancer A LOT is considered to be tolerable for the means of treating it. Actually, nothing safety-wise was measured other than the progression of the breast cancer and some self-reported side effects. Moreover, nothing with regard to its anabolism was measured.


Perhaps because 48 % of the patients treated with Primobolan saw regression of their cancer? That sure as hell would raise my well-being.


The onset of hirsutism is slow. In most trials in which women receive AAS, it takes about 4 to 6 months to become apparent. Given that only 16 of 27 patients (59%) patients received Primobolan for longer than 4 months, this implies that nearly every single woman receiving Primobolan long enough for hirsutism to become apparent, reported it as a side effect.

Anyhow, this study mostly seems utterly irrelevant to say anything about Primobolan. It didn't measure anything a bodybuilder should be interested in.

I've been reading his articles, because I'm quite ignorant of AAS and I'm trying to learn as much as I can, but it's fascinating to see someone dismantle someone else who presents themselves as "scientific" to their large audience. The thing that always bugged me about him is his talk of genetics. It honestly seems like he's passing down bro-lore statements about genetics, instead of actually understanding genetics. Do you not recommend his articles, at all? I bought your book and I am currently reading through it.

 

[Methyl Mike]

Name another steroid you can run at high doses and have absolutely no idea that you’re using them because the side effects are nonexistent. That’s the appeal of primo. 600mg feels approximately the same as 0mg in terms of sides. It was quite literally designed to have the most favorable side effect profile that could be achieved while still being efficacious.

If you want tren-like results then primo will disappoint you. But you also won’t go two months without sleep, sweat like a stuck pig all day, and give yourself dementia. The risk/reward is thus: the reward is the lack of risk.

It really does take a long time to get going. About 6 weeks for me. I won't comment on how effective it is because my body fat was not extremely low but it did not help me keep muscle when I started my new job. It's not as great as some people claim.

 

[PeterBond]

I've been reading his articles, because I'm quite ignorant of AAS and I'm trying to learn as much as I can, but it's fascinating to see someone dismantle someone else who presents themselves as "scientific" to their large audience. The thing that always bugged me about him is his talk of genetics. It honestly seems like he's passing down bro-lore statements about genetics, instead of actually understanding genetics. Do you not recommend his articles, at all? I bought your book and I am currently reading through it.

It's a bit hard for me to comment on that, as I've only read this article and his article on cardarine, and not any of his other writings. But based on those 2 articles I would definitely not recommend his articles no.

Hope you're liking the book! I'm currently in the process of writing a second edition, feel free to drop your email address on my website for when it's released (somewhere in 2023 if I'm being a bit optimistic):

2nd edition Book on Steroids? And some more coming up

peterbond.org

 

[Ambusher]

It's a bit hard for me to comment on that, as I've only read this article and his article on cardarine, and not any of his other writings. But based on those 2 articles I would definitely not recommend his articles no.

Hope you're liking the book! I'm currently in the process of writing a second edition, feel free to drop your email address on my website for when it's released (somewhere in 2023 if I'm being a bit optimistic):

https://peterbond.org/post/2nd-edition-book-on-steroids-and-some-more-coming-up[/URL

I certainly am and I'll defintiely do that so I can get an update when it drops. Also, was he drawing conclusions that weren't supported or was it some logical fallacy that he seems keen on committing? I think the worst thing someone ignorant of any topic can do is to start reading articles by someone that presents themselves in a "scientific" manner, while those articles contain numerous errors in logic and outright false information. They think they're getting good information, but it turns out it's as useless as bodybuilding dot com articles.

 

[PeterBond]

I certainly am and I'll defintiely do that so I can get an update when it drops. Also, was he drawing conclusions that weren't supported or was it some logical fallacy that he seems keen on committing? I think the worst thing someone ignorant of any topic can do is to start reading articles by someone that presents themselves in a "scientific" manner, while those articles contain numerous errors in logic and outright false information. They think they're getting good information, but it turns out it's as useless as bodybuilding dot com articles.

Just a few examples, in his cardarine article he writes:
"Via activating PPARδ, the liver switches its energy source from glucose to fatty acids, which can in turn reduce blood sugar levels [R]."
The reference being this study:

PPARδ regulates glucose metabolism and insulin sensitivity

The metabolic syndrome is a collection of obesity-related disorders. The peroxisome proliferator-activated receptors (PPARs) regulate transcription in response to fatty acids and, as such, are potential therapeutic targets for these diseases. We show ...

www.ncbi.nlm.nih.gov

In this study they examined the expression of several genes and blood measures in PPARδ knockout mice, db/db mice (a strain of diabetic mice) and wild-type in response to GW501516.
But does this study support what he says?
They find:
"Molecular and functional analyses suggest that PPARδ activation reduces hepatic glucose output by increasing glycolysis and the pentose phosphate shunt and promoting fatty acid synthesis in the liver."
Surrogates of hepatic fatty acid oxidation were not measured in this study.

While it's true that PPARδ activation induces hepatic fatty acid oxidation, his reference doesn't demonstrate it, and I don't think it's the reason why it has the potential to decrease blood glucose levels. (Mind you: blood glucose did not significantly decrease compared to controls in the clinical trials)

The next sentence: "This in turn upregulates the body's expression of proteins involved in energy expenditure, improves insulin sensitivity and body composition, which can lower the overall incidence of type II diabetes and cardiovascular disease [R, R]."
Neither of these studies subscribe to the claim that an increase in hepatic fatty oxidation leads to the effects he describes.

He's also misleading in representing the clinical trial results imo, he writes about this trial Triglyceride:high-density lipoprotein cholesterol effects in healthy subjects administered a peroxisome proliferator activated receptor delta agonist - PubMed:
"Cardarine significantly improved HDL Cholesterol levels and reduced Triglycerides [R]."
Triglycerides only showed a statistically significant within-group decrease, it showed no significant change compared to placebo.

Similarly he writes: "Lipolytic activity was gauged to assess the efficacy of Cardarine relative to placebo and the data revealed that the placebo group's Triglyceride levels went up significantly from high-fat meals, and the 2.5 mg and 10 mg treated groups both respectively lowered Triglyceride levels, even in the presence of the fat dense meals."
It would be honest to mention that the decrease in the 2.5 mg group was not statistically significant compared to the placebo group.

About a second clinical trial he writes:
"Treatment with Cardarine showed statistically significant reductions in fasting plasma triglycerides, apolipoprotein B, LDL cholesterol, and insulin [R]."
This is imo also misleading, as all these changes were only statistically significant in a within-group comparison. Compared to placebo, none of these changes was significant.

About the cancer issue he writes:
"Without being administered any chemicals at all, the median life expectancy of Han Wistar rats is between 30 and 33 months for females, and between 33 and 36 months for males.

The reason for their short life expectancy is the number of adenocarcinomas that they develop [R]."
This strain of rats actually live a bit longer than other common strains, such as the Sprague Dawley rats and Fischer 344 rats. They also have a lower overall tumour incidence: Differences in Types and Incidence of Neoplasms in Wistar Han and Sprague-Dawley Rats - PubMed

The study he cites is from 1980. The study I just cited is a recent one which covers a lot more data on these rats. Importantly, this strain has changed over time (there are actually several different colonies of it, depending on the supplier). The results of the 1980 trial do not match with what's seen by several other laboratories as can be seen in the paper I linked. I'm unsure what the cause of it is, perhaps simply more inbreeding within the colonoy the 1980 paper received the rats from. It's been common practice for quite some time now to minimize inbreeding by using rotational breeding systems.

"Prior to even looking at the animal models for Cardarine, we know that these rats are not expected to live longer than 3 years already, irrespective of what they are administered, due to their high probability of developing cancer."
Not just these rats, ALL rats. 3 years is about the life expectancy of a rat. How is this a critique?

"The first thing to note is the fact that the aforementioned study involved administering Cardarine to Han Wistar rats for almost 2 years straight (1.99 years to be exact)."
Spoilers: 2-year rodent bioassays always take 2 years. They're mandated as such by the FDA to get your meds approved for chronic conditions. This is how carcinogenicity has been screened for for decades.

He continues with calculating a human equivalent dose (HED). This is not what these HED formulas are meant for. These formulas are meant to come up with an educated guess of a proper dose for an initial clinical trial! Once more clinical data pours in, you can more accurately assess what would be an appropriate dose. These formulas are NOT meant for what he's doing here. You do your animal experiments, you assess a dose with no observed adverse effects, and then you use a formula like that one to derive a dose you could use in your first clinical trials. From thereon forward you refine your dose depending on pharmacokinetic and pharmacodynamic data in humans, as there can be vast differences in absorption and metabolism of a drug.
We don't have that data, GSK does.

The main point is that the 2-year rodent bioassay has a good sensitivy and specificity to determine whether or not a compound causes cancer:

The 2-year rodent bioassay in drug and chemical carcinogenesis testing: Sensitivity, according to the framework of carcinogenic action - PubMed

The long-term rodent bioassay (RCB) has been the gold-standard for the pre-marketing prediction of chemical and drug carcinogenicity to humans. Nonetheless, the validity of this toxicity test has remained elusive for several decades. In the quest to uncover the performance of the RCB, its...

pubmed.ncbi.nlm.nih.gov

I can go on and on, but yeah. You get the point I think.

 

[Ambusher]

Just a few examples, in his cardarine article he writes:
"Via activating PPARδ, the liver switches its energy source from glucose to fatty acids, which can in turn reduce blood sugar levels [R]."
The reference being this study:

PPARδ regulates glucose metabolism and insulin sensitivity

The metabolic syndrome is a collection of obesity-related disorders. The peroxisome proliferator-activated receptors (PPARs) regulate transcription in response to fatty acids and, as such, are potential therapeutic targets for these diseases. We show ...

www.ncbi.nlm.nih.gov

In this study they examined the expression of several genes and blood measures in PPARδ knockout mice, db/db mice (a strain of diabetic mice) and wild-type in response to GW501516.
But does this study support what he says?
They find:
"Molecular and functional analyses suggest that PPARδ activation reduces hepatic glucose output by increasing glycolysis and the pentose phosphate shunt and promoting fatty acid synthesis in the liver."
Surrogates of hepatic fatty acid oxidation were not measured in this study.

While it's true that PPARδ activation induces hepatic fatty acid oxidation, his reference doesn't demonstrate it, and I don't think it's the reason why it has the potential to decrease blood glucose levels. (Mind you: blood glucose did not significantly decrease compared to controls in the clinical trials)

The next sentence: "This in turn upregulates the body's expression of proteins involved in energy expenditure, improves insulin sensitivity and body composition, which can lower the overall incidence of type II diabetes and cardiovascular disease [R, R]."
Neither of these studies subscribe to the claim that an increase in hepatic fatty oxidation leads to the effects he describes.

He's also misleading in representing the clinical trial results imo, he writes about this trial Triglyceride:high-density lipoprotein cholesterol effects in healthy subjects administered a peroxisome proliferator activated receptor delta agonist - PubMed:
"Cardarine significantly improved HDL Cholesterol levels and reduced Triglycerides [R]."
Triglycerides only showed a statistically significant within-group decrease, it showed no significant change compared to placebo.

Similarly he writes: "Lipolytic activity was gauged to assess the efficacy of Cardarine relative to placebo and the data revealed that the placebo group's Triglyceride levels went up significantly from high-fat meals, and the 2.5 mg and 10 mg treated groups both respectively lowered Triglyceride levels, even in the presence of the fat dense meals."
It would be honest to mention that the decrease in the 2.5 mg group was not statistically significant compared to the placebo group.

About a second clinical trial he writes:
"Treatment with Cardarine showed statistically significant reductions in fasting plasma triglycerides, apolipoprotein B, LDL cholesterol, and insulin [R]."
This is imo also misleading, as all these changes were only statistically significant in a within-group comparison. Compared to placebo, none of these changes was significant.

About the cancer issue he writes:
"Without being administered any chemicals at all, the median life expectancy of Han Wistar rats is between 30 and 33 months for females, and between 33 and 36 months for males.

The reason for their short life expectancy is the number of adenocarcinomas that they develop [R]."
This strain of rats actually live a bit longer than other common strains, such as the Sprague Dawley rats and Fischer 344 rats. They also have a lower overall tumour incidence: Differences in Types and Incidence of Neoplasms in Wistar Han and Sprague-Dawley Rats - PubMed

The study he cites is from 1980. The study I just cited is a recent one which covers a lot more data on these rats. Importantly, this strain has changed over time (there are actually several different colonies of it, depending on the supplier). The results of the 1980 trial do not match with what's seen by several other laboratories as can be seen in the paper I linked. I'm unsure what the cause of it is, perhaps simply more inbreeding within the colonoy the 1980 paper received the rats from. It's been common practice for quite some time now to minimize inbreeding by using rotational breeding systems.

"Prior to even looking at the animal models for Cardarine, we know that these rats are not expected to live longer than 3 years already, irrespective of what they are administered, due to their high probability of developing cancer."
Not just these rats, ALL rats. 3 years is about the life expectancy of a rat. How is this a critique?

"The first thing to note is the fact that the aforementioned study involved administering Cardarine to Han Wistar rats for almost 2 years straight (1.99 years to be exact)."
Spoilers: 2-year rodent bioassays always take 2 years. They're mandated as such by the FDA to get your meds approved for chronic conditions. This is how carcinogenicity has been screened for for decades.

He continues with calculating a human equivalent dose (HED). This is not what these HED formulas are meant for. These formulas are meant to come up with an educated guess of a proper dose for an initial clinical trial! Once more clinical data pours in, you can more accurately assess what would be an appropriate dose. These formulas are NOT meant for what he's doing here. You do your animal experiments, you assess a dose with no observed adverse effects, and then you use a formula like that one to derive a dose you could use in your first clinical trials. From thereon forward you refine your dose depending on pharmacokinetic and pharmacodynamic data in humans, as there can be vast differences in absorption and metabolism of a drug.
We don't have that data, GSK does.

The main point is that the 2-year rodent bioassay has a good sensitivy and specificity to determine whether or not a compound causes cancer:

The 2-year rodent bioassay in drug and chemical carcinogenesis testing: Sensitivity, according to the framework of carcinogenic action - PubMed

The long-term rodent bioassay (RCB) has been the gold-standard for the pre-marketing prediction of chemical and drug carcinogenicity to humans. Nonetheless, the validity of this toxicity test has remained elusive for several decades. In the quest to uncover the performance of the RCB, its...

pubmed.ncbi.nlm.nih.gov

I can go on and on, but yeah. You get the point I think.

Yeah, I definitely get the point and I thank you for doing this. He presents himself in such a well-educated manner and stated that he has done thousands upon thousands of hours of research on these topics, yet falls prey to things he shouldn’t have, had he actually done the amount of research he claims. it’s just rather disappointing that when one thinks they’ve found a decent source of information, it turns out to be as relatively useless as the more dogmatic BB articles. Though, I look forward to finishing your book.

 

[malfeasance]

Just a few examples, in his cardarine article he writes:
"Via activating PPARδ, the liver switches its energy source from glucose to fatty acids, which can in turn reduce blood sugar levels [R]."
The reference being this study:

PPARδ regulates glucose metabolism and insulin sensitivity

The metabolic syndrome is a collection of obesity-related disorders. The peroxisome proliferator-activated receptors (PPARs) regulate transcription in response to fatty acids and, as such, are potential therapeutic targets for these diseases. We show ...

www.ncbi.nlm.nih.gov

In this study they examined the expression of several genes and blood measures in PPARδ knockout mice, db/db mice (a strain of diabetic mice) and wild-type in response to GW501516.
But does this study support what he says?
They find:
"Molecular and functional analyses suggest that PPARδ activation reduces hepatic glucose output by increasing glycolysis and the pentose phosphate shunt and promoting fatty acid synthesis in the liver."
Surrogates of hepatic fatty acid oxidation were not measured in this study.

While it's true that PPARδ activation induces hepatic fatty acid oxidation, his reference doesn't demonstrate it, and I don't think it's the reason why it has the potential to decrease blood glucose levels. (Mind you: blood glucose did not significantly decrease compared to controls in the clinical trials)

The next sentence: "This in turn upregulates the body's expression of proteins involved in energy expenditure, improves insulin sensitivity and body composition, which can lower the overall incidence of type II diabetes and cardiovascular disease [R, R]."
Neither of these studies subscribe to the claim that an increase in hepatic fatty oxidation leads to the effects he describes.

He's also misleading in representing the clinical trial results imo, he writes about this trial Triglyceride:high-density lipoprotein cholesterol effects in healthy subjects administered a peroxisome proliferator activated receptor delta agonist - PubMed:
"Cardarine significantly improved HDL Cholesterol levels and reduced Triglycerides [R]."
Triglycerides only showed a statistically significant within-group decrease, it showed no significant change compared to placebo.

Similarly he writes: "Lipolytic activity was gauged to assess the efficacy of Cardarine relative to placebo and the data revealed that the placebo group's Triglyceride levels went up significantly from high-fat meals, and the 2.5 mg and 10 mg treated groups both respectively lowered Triglyceride levels, even in the presence of the fat dense meals."
It would be honest to mention that the decrease in the 2.5 mg group was not statistically significant compared to the placebo group.

About a second clinical trial he writes:
"Treatment with Cardarine showed statistically significant reductions in fasting plasma triglycerides, apolipoprotein B, LDL cholesterol, and insulin [R]."
This is imo also misleading, as all these changes were only statistically significant in a within-group comparison. Compared to placebo, none of these changes was significant.

About the cancer issue he writes:
"Without being administered any chemicals at all, the median life expectancy of Han Wistar rats is between 30 and 33 months for females, and between 33 and 36 months for males.

The reason for their short life expectancy is the number of adenocarcinomas that they develop [R]."
This strain of rats actually live a bit longer than other common strains, such as the Sprague Dawley rats and Fischer 344 rats. They also have a lower overall tumour incidence: Differences in Types and Incidence of Neoplasms in Wistar Han and Sprague-Dawley Rats - PubMed

The study he cites is from 1980. The study I just cited is a recent one which covers a lot more data on these rats. Importantly, this strain has changed over time (there are actually several different colonies of it, depending on the supplier). The results of the 1980 trial do not match with what's seen by several other laboratories as can be seen in the paper I linked. I'm unsure what the cause of it is, perhaps simply more inbreeding within the colonoy the 1980 paper received the rats from. It's been common practice for quite some time now to minimize inbreeding by using rotational breeding systems.

"Prior to even looking at the animal models for Cardarine, we know that these rats are not expected to live longer than 3 years already, irrespective of what they are administered, due to their high probability of developing cancer."
Not just these rats, ALL rats. 3 years is about the life expectancy of a rat. How is this a critique?

"The first thing to note is the fact that the aforementioned study involved administering Cardarine to Han Wistar rats for almost 2 years straight (1.99 years to be exact)."
Spoilers: 2-year rodent bioassays always take 2 years. They're mandated as such by the FDA to get your meds approved for chronic conditions. This is how carcinogenicity has been screened for for decades.

He continues with calculating a human equivalent dose (HED). This is not what these HED formulas are meant for. These formulas are meant to come up with an educated guess of a proper dose for an initial clinical trial! Once more clinical data pours in, you can more accurately assess what would be an appropriate dose. These formulas are NOT meant for what he's doing here. You do your animal experiments, you assess a dose with no observed adverse effects, and then you use a formula like that one to derive a dose you could use in your first clinical trials. From thereon forward you refine your dose depending on pharmacokinetic and pharmacodynamic data in humans, as there can be vast differences in absorption and metabolism of a drug.
We don't have that data, GSK does.

The main point is that the 2-year rodent bioassay has a good sensitivy and specificity to determine whether or not a compound causes cancer:

The 2-year rodent bioassay in drug and chemical carcinogenesis testing: Sensitivity, according to the framework of carcinogenic action - PubMed

The long-term rodent bioassay (RCB) has been the gold-standard for the pre-marketing prediction of chemical and drug carcinogenicity to humans. Nonetheless, the validity of this toxicity test has remained elusive for several decades. In the quest to uncover the performance of the RCB, its...

pubmed.ncbi.nlm.nih.gov

I can go on and on, but yeah. You get the point I think.

That post took a lot of time. Thank you for putting it together.

 

[Ridethelightningbarefoot]

Im really surprised about dbol in this study. It comes up last in every category compared to nandrolone and primo. Im kind of confused about anadur coming out ahead of deca when its just a different ester..
So is this study then superior in gauging the overall anabolism of a compound?

 

[Type-IIx]

Im really surprised about dbol in this study. It comes up last in every category compared to nandrolone and primo. Im kind of confused about anadur coming out ahead of deca when its just a different ester..
So is this study then superior in gauging the overall anabolism of a compound?

From the chart (Fig. 1G & 3G) yielding a positive Nitrogen balance of 10.2g, the patient was 52kg b.w., fed 1,754 calories daily >BMR by 29%, 1.34g/kg protein (70g, 16%), C 48%, F 36%, and was administered daily Dbol orally in doses of 15mg for 14 days.

For Fig. 5D & 6D from the chart yielding a positive Nitrogen balance of 11.4g, the patient was 66.5kg b.w., fed 1,986 calories daily, >BMR by 27.5%, 1.18g/kg protein (79g, 15.9%), 52.4% C, 31.7% F, administered Dbol orally daily doses of 10mg over 2 week period (Figs 5D & 6D) and during the following 11 days, dosage increased to 15mg (Figs 5F & 6F) yielding positive Nitrogen balance of 9.6g before he was released from hospital.

The study is pretty good at reducing inter- and even minimizing intra- subject variability, though you must consider adaptations to feeding, prior AAS exposure, immobilization, and the macronutrient/energy balance.

 

[GuerillaPete]

Primo is overrated and not worth its price !
Needs to be ran high and for long to be effective and has typical dht sides like acne, hair loss , pimples and lipids !
4 weeks winstrol at 50 mg did more fore me than 600 mg primo a week for 6 moths!

 

[Turbo charged]

Primo is a feel good drug and is great at preserving muscle mass on a deficit probably the best drug for it.This is the reason why body builders love it and makes you hard as a rock. A drug wich is not very well know wich has the same identical profile as primo was made in the united states and 3 times more stronger with just as minimal sides was stenbalone. A great aas that has got forgotten but is still available. I ran it and it is primo times 3 no side effects at all same great feeling but put on nice muscle mass.it is a Acetate so you have to pin it atleast every other day.

 

[ludi_janez]

Primo is overrated and not worth its price !
Needs to be ran high and for long to be effective and has typical dht sides like acne, hair loss , pimples and lipids !
4 weeks winstrol at 50 mg did more fore me than 600 mg primo a week for 6 moths!

From primo you will not get any acne... im very very prone to acne, and primo actually improves the texture of the skin, because it counteracts the effects of testosterone on skin, and doesn't make it worse.
I have run now primo at 600mg per week, and i must also say that i expected more... i did get a really nice physique and good pumps without paying much attention to diet, but yeah, i didn't turn into a mass monster. But that is also not my goal to begin with. For me, at the price i get it, i think its worth it. The effects are much better if you run high test with it, but with that also the sides come - depends on a person, of course.