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Yes indeed i made a few researches about the strongest sarm « S-23 » and its a dogshi compound that immitates badly test with around 60% of its binding affinity to ARs, Just blast Test BrootalWhy SARMs are dogshit
Introduction: First of all, i was inspired to make this thread by Dr Alex Tatem video on youtube bashing on SARMs so i decided i would join the trend and also add some more content to what he said on his video and to explain mechanistically why SARMs get brutally mogged by AAS, also because I've heard SARMs propaganda thousands of times, though the contents of this thread are pretty much water to anyone with surface knowledge about pharma, however, there is a lot of people who are seriously misinformed regarding these compounds, thinking they are "better" than steroids and have a superior ROI and are "safer" than AAS, also because SARMs have been promoted on other forums like .org for example, pneumo's trash SARMs thread is still up there and also other relevant content creators have openly "promoted them", so to resume this whole thread it's basically just me bashing SARMs.
What are SARMs?
SARMs (Selective Androgen Receptor Modulators) are synthetic research compounds designed to act like androgens but with a key difference, they work and bind to the same AR receptors and proteins than your classic AAS (like testosterone) but with a nuance as the word "selective" is present on its acronym as SARMs are designed to be extremely "selective" with tissue, so the main goal of pharmacies when developing them was to create a class of compounds that would do the same as AAS but exclusively activating androgen receptors in skeletal muscle and bone tissue, this in theory would avoid the classical androgenic side effects on AAS we all know about (aromatization, gyno, hair loss, prostate issues, acne etc)
Spoiler: They failed that premise.
AR mechanism pathway.
To explain the mechanism of SARM’s i will go over first of how normal androgens work first
Ligands Scientific definition: “A molecule that binds to another molecule, used especially to refer to a small molecule that binds specifically to a larger molecule, e.g., an antigen binding to an antibody, a hormone or neurotransmitter binding to a receptor, or a substrate or allosteric effector binding to an enzyme” (National Center for Biotechnology Information, MeSH ID: D008024).
Simple Explanation: A ligand is simply a molecule that binds and activates a receptor triggering a reaction, natural ligands are testosterone and its more potent metabolite dihydrotestosterone (aka DHT), produced via 5α-reductase conversion in specific tissues (prostate tissue for example).
AR Scientific definition: “The androgen receptor (AR) is defined as a ligand-activated transcription factor that mediates signaling by androgens and is a member of the nuclear receptor superfamily. It is unique for being encoded by a gene on the X chromosome and contains a polymorphic glutamine repeat in its N terminus that influences its activity” (“Androgen Receptor,” n.d., para. 1).
Simple Explanation: This means that the AR receptor is a protein found inside certain cells that when one of these hormones/ligands (Testosterone/DHT) enters the cell and binds to the receptor, it activates it, then the activated receptor proceeds to move into the cell’s nucleus, where the DNA is stored, and binds to specific parts of the DNA chain to modulate and control which genes are activated and deactivated (AREs), it’s like pressing keys in your keyboard when playing videogames, now, they do this by changing gene activity and expression, the AR tells the cell to produce proteins and to create effects associated with androgenic activity (aka, muscle growth, body hair development, libido etc).
AR Genomic activation pathway simplified:
1: An androgen (like testosterone/dihydrotestosterone (DHT)) enters the cell and binds to the ligand binding domain (LBD) of the AR.
2: This binding changes the shape of the receptor, specifically a region called helix 12, which closes around the hormone and creates an activation surface called AF-2.
3: Heat shock proteins (HSPs), which keep the receptor inactive and stable, detach from the receptor activating it.
4: The activated monomeric androgen receptors move rapidly from the cytoplasm across the nuclear membrane into the nucleus.
5: Once inside the nucleus, the activated receptors pair with one another to form a homodimer, which binds tightly to specific DNA sequences called androgen response elements (AREs). (Alberts et al.)
6: The receptor recruits coactivator proteins such as the SRC family and p300/CBP, these coactivators loosen and modify chromatin, making the DNA easier for the cell to read and interpret.
7: They also recruit RNA polymerase II, the enzyme responsible for transcribing genes into RNA.
8: Target DNA is transcribed into pre-mRNA.
9: mRNA is processed, exported to the cytoplasm As a result of this interactions this increases the transcription of androgen responsive genes that are involved in muscle protein synthesis, bone mineralization, recovery, strength, etc.
(Info obtained from https://pmc.ncbi.nlm.nih.gov/articles/PMC9837614/)
SARMs pathway and mechanism explained:
1: The SARM enters inside the cell and binds to the ligand-binding domain (LBD) of the AR in the cytoplasm.
2: When it binds this causes a unique shape change in the receptor (around helix 12 and the AF-2 surface), (which is different from the change induced by testosterone/dihydrotestosterone (DHT)).
3: Heat shock proteins detach, the receptor then dimerizes, and travels to the cell nucleus, in the nucleus, the SARM-AR complex binds to androgen response elements (AREs) on the DNA.
Now, here's the part where the mechanism changes:
4:Due to the unique shape of the AF-2 surface, the SARM-AR complex activates coregulator proteins in a very highly selective way, the shape perfectly matches and gathers potent coactivators (like the SRC family) in tissues like skeletal muscle and bones loosening chromatin for easier gene transcription..
5: In androgenic tissues such as the prostate or the sebaceous glands, the distinct conformation of helix 12 usually fails to gather and trigger these coactivators efficiently, or it favors the activation of corepressors. As a result this induces weak gene expression or actively blocks the receptor in those tissues (competitive antagonism and or partial agonism).
6: In the target anabolic tissues (skeletal muscles) where coactivators successfully gather and activate, RNA polymerase II is gathered to the promoter region of the gene.
7:Then the DNA is transcribed into pre-mRNA, which will specifically induce gene upregulation of genes that are connected to muscle hypertrophy (like IGF-1) and bone density, while minimizing the transcription of genes that induce androgenic side effects like (prostate enlargement, hairloss etc).
8:The mRNA is processed and exported to the cytoplasm, where it is converted into functional proteins.
9: This results in targeted increases in muscle protein synthesis, strength, and recovery and "theorically" with significantly reduced androgenic side effects.
Geometric differences explanation and their relevance:
SARMs differ from AAS because they are mostly non-steroidal and they induce distinct changes and effects compared to testosterone/dihydrotestosterone (DHT), this is because despite having completely different structural forms they still manage to fit the shape of the receptor and bind to it.
For comparison:
Testosterone skeletal form:
View attachment 54094
Ostarine (enobosarm, MK-2866, GTx-024):
View attachment 54095
Despite SARMs having different structures regarding their shape, the relevant binding interactions are still present because most SARMs preserve the correct the spatial arrangement of hydrophobic regions and hydrogen bonding groups (3D pharmacophore) needed to interact with the AR ligand binding pocket.
To achieve tissue selectivity while still remaining compatible with the AR, SARMs replace the common four ring steroidal structure present in AAS with bioisosteric (1) functional groups, these include aromatic rings (like benzene), bicyclic systems, nitriles, trifluoromethyl groups, ether linkages, and heterocycles.
1: (bioisosteric, refers to replacing a functional group in a drug molecule with another of similar shape, volume, or electronic properties).
In “theory” these modifications to their geometric structure should keep the relevant parts of the interactions with the AR needed for muscle growth and to get rid or minimize the rest that are causing the androgenic side effects, basically because the co activators and co repressors they trigger inside the cells nuclei for DNA expression and transcription are different than that classical AAS trigger inside cells.
This means their modified chemical structure will trigger different conformational changes inside the AR receptor in some tissues, making them behave like partial agonists on certain tissues and like full agonists on skeletal muscle and bones.
However, this selectivity is relative, failing the original premise of the creation of SARMs, as in practice SARMs can still produce some androgenic effects, more frequently at higher doses, this point in particular will be relevant when I disclose the rest of the cons of SARMs.
Additionally there are several discrepancies regarding the activation pathways of SARMs.
1: Why their selectivity Fails
The premise of SARMs assumes that you can strongly stimulate anabolic pathways in muscle, while minimally stimulating other androgen sensitive tissues like the skin, scalp and prostate tissue, the issue is the AR is a single nuclear receptor that is present throughout the whole body and integrated into many endocrine systems and tissues simultaneously, so once you strongly activate the AR signaling enough to create strong anabolic effects the common side effects such as test suppression, lipid profile changes, cardiovascular effects and CNS effects begin appearing regardless of whether the ligand is steroidal or nonsteroidal.
Another aspect worth mentioning is that selectivity is a meme. Their selectivity depends on the receptor conformation, tissue specific cofactors and differential gene transcription they trigger when binding the AR.
Scientific reviews explain that SARMs induce different AR conformational changes and recruit different co regulators in different tissues, however, this selectivity is flawed, even the most highly selective SARMs still activate hypothalamic AR, pituitary AR, hepatic AR. etc.
2: It’s also worth mentioning that SARMs will tank your E2 and total testosterone anyways, and regardless of what people think of E2, it is cardioprotective, neuroprotective and plays a huge role in your libido and also in BMD, E2 also is a key factor when it comes to anabolism, when you have an exogenous hormone with 0 aromatization you miss that key elements for pathways needed for anabolism, as E2 enhances hepatic IGF-1 production, local IGF-1 expression in muscle, growth hormone responsiveness, IGF-1 is also anabolic and it enhances PI3K/Akt/mTOR signaling, protein synthesis, satellite cell activation, muscle repair and so on, now let’s get over the neuroprotective benefits of E2, it influences, dopamine, serotonin, nitric oxide signaling and CNS excitation etc, i could go ahead and also explain why it’s relevant for joint health too but that’s water info, now this DOES NOT mean more estrogen equals more anabolism, but it’s definitely needed for proper anabolism.
3: The therapeutic doses deemed “safe” are significantly way lower than bodybuilding doses, SARMs might work reasonably well to treat sarcopenia, frailty, cachexia, osteoporosis,
where only mild anabolic support is needed, but they miserably fail when it comes to bodybuilding dosages, especially at the safety profile, it is not a coincidence the amount of severe liver injuries that can be seen from SARMs, and also fit a perfect correlation and causation, even at those dosages they still get obliterated by testosterone or almost all AAS, the ROI is simply not good enough to bother taking them.
View attachment 54096
Study: https://pmc.ncbi.nlm.nih.gov/articles/PMC5820696/
It’s important to note that this study should not be used as an absolute to claim “all SARMs sold online are fake and not really SARMs” but to use this as a reference to understand how mislabeled this market is. However, it is still something to consider.
Important Note: First of all, we need to mention that the doses used for SARMs on clinical trials vs the doses commonly used for bodybuilding are wildly different, for example;
RAD 140 bodybuilding doses (anecdotal information) : 20-30 mg per day, anecdotally users often repor 4-7 kg of lean mass after 8-10 weeks.
mostly is very likely to be glycogen/water combined.
Ostarine (enobosarm, MK-2866, GTx-024) bodybuilding doses (anecdotal information): 10–25 mg/day, anecdotally users often report: 2–4 kg total bodyweight gain, with maybe 1.5 -- 3 kg being lean tissue and the rest is very likely to be glycogen/water combined.
LGD-4033 bodybuilding doses (anecdotal information): 5–30 mg/day anecdotally users often report: 4–7 kg bodyweight gain over: 6–10 weeks, lot of it is likely to be glycogen, intracellular water, food mass, temporary fullness, not pure contractile tissue, which is again the usual thing with SARMs.
This highly affects the compound behaviour, just for reference, this were the clinical trial doses:
RAD 140: (no human data) (Monkeys doses was 0.01 mg, 0.1 mg, 1.0 mg).
study: https://pmc.ncbi.nlm.nih.gov/articles/PMC4018048/
Ostarine: Clinical trials of Ostarine showed: 1–1.5 kg lean body mass gain over about 8–12 weeks at doses around 1–3 mg/day.
study: https://pubmed.ncbi.nlm.nih.gov/22031847/
LGD-4033: Clinical trials of LGD-4033 showed: 1.21 kg lean body mass increase
in only: 21 days at: 1 mg/day.
study: https://pubmed.ncbi.nlm.nih.gov/22459616/
This is a drastic dose change which will affect their behaviour a lot compared to bodybuilding doses, but nyways, once we’ve cleared this it’s time to go to their study case profile and sides.
Ostarine (enobosarm, MK-2866, GTx-024):
https://link.springer.com/article/10.1186/s12885-018-5080-4
"We identified 19 articles (representing 20 RCTs) that focused on pharmacological management of cancer cachexia. Agents showing promising results included Anamorelin and Enobosarm. Anamorelin at 50 or 100 mg per day for 12 weeks showed a consistent benefit across all studies and resulted in significant improvement in weight as compared to baseline among cancer patients. Enobosarm at 1 and 3 mg per day was also effective in improving lean body mass and QOL symptoms among advancer stage cancer patients. Finally, use of combination agents provide evidence for targeting multiple pathways underlying cachexia mechanism to achieve maximum benefit. No agents showed functional improvement in cancer patients."
"Conclusion
Anamorelin as a single agent shows promising results in improving cachexia related weight loss among cancer patients. Further research on combination therapies may be helpful to address critical gaps in cachexia management."
View attachment 54122
Pure rape at a dose which is several times lower than a bodybuilding dose.
got beated by a fucking ghrelin agonist.
LGD-4033:
This first studies use the clinical trial doses (0.1 mg 0.3 mg and 1 mg/day)
View attachment 54097
View attachment 54098
View attachment 54100
Study: https://pmc.ncbi.nlm.nih.gov/articles/PMC4111291/#abstract1
Yes, take into account this was the behaviour of LGD-4033 at clinical doses, safe to say at bodybuilding doses all the shit mentioned will brutally exacerbate. We don’t have any human trial data for a 1:1 extrapolation regarding the safety profile at bodybuilding doses, but we do have a terrifying collection of liver injuries for LGD-4033:
Study: https://pmc.ncbi.nlm.nih.gov/articles/PMC7304490/
View attachment 54101
View attachment 54102
View attachment 54104
Yeah...Immediately no.
Note: This is the SARM with the least clinical data, therefore this next information needs to be taken with a nuance as the best we got is animal to human extrapolations.
View attachment 54107
Even tho we don’t have specifical human data, RAD 140 RAPES testosterone production in similar animals to humans such as monkeys.
https://pmc.ncbi.nlm.nih.gov/articles/PMC4018048/
"As shown in Figure 4, RAD140 increased the weight of the levator ani muscle above that of the intact control starting with the lowest tested dose (0.1 mg/kg). Interestingly, RAD140 demonstrated no stimulation of the prostate above the intact animal control level until the highest dose tested, 30 mg/kg. At 0.3 mg/kg, RAD140 demonstrated muscle efficacy similar to TP at 0.5 mg/kg, but a dose of 30 mg/kg of RAD140 was required to approximate the prostate efficacy of 0.5 mg/kg TP.24 From this study it is apparent that in young intact male rats RAD140 has a very wide range of selectivity relative to both TP-treated rats as well as sham-control rats."
The dose used by bodybuilders lol.
Same as any SARMs fuck ton of cases with cholestatic liver injury and other types of liver injuries, all of this at bodybuilding dosages.
Study: https://pubmed.ncbi.nlm.nih.gov/36561105/ =
View attachment 54106
More studies:
https://www.ochsnerjournal.org/content/early/2022/07/13/toj.22.0005
https://pmc.ncbi.nlm.nih.gov/articles/PMC10911832/
Mechanistical standpoint:
Enclomiphene stimulates your natural production via LH/FSH, this mechanism entirely depends on your HPTA axis being intact and not suppressed, AAS and SARMs suppress endogenous testosterone production by binding to the ARs in your hypothalamus, so with the hypothalamus suppressed and not secreting GnRH it won't travel to the pituitary gland (even if a tiny amount does, AAS and SARMs also directly suppress the anterior pituitary gland's sensitivity to GnRH), so without a strong GnRH signal, the pituitary gland won't secrete LH/FSH, so then the LH/FSH won’t travel to the testicles and bind to the Leydig cells which are the cells responsible for triggering endogenous testosterone production, the whole mechanism of Enclomiphene works exclusively by binding to ERs in the hypothalamus and anterior pituitary gland, acting as an antagonist to block estradiol (E2) from delivering its negative feedback signal.
Now the issue is that androgen receptor activation operates independently of estrogen receptor activation.
This means even if enclomiphene successfully blocks the ERs in the anterior pituitary gland and signals the hypothalamus that E2 is low and that GnRH secretion is needed, the ARs in the hypothalamus are completely flooded and saturated to the max so your body thinks that no GnRH secretion is needed due to the ARs in the hypothalamus being completely saturated.
Enclomephine and overall SERMs work OFF cycle because the HPTA axis is not suppressed anymore (hypothalamic ARs are not fully saturated anymore by AAS) so they receive the signal and respond releasing GnRH.
So no, it wouldn’t work, especially when the suppression is this strong:
View attachment 54107
We need to understand this is not a 1:1 extrapolation but can be used as a reference to understand how suppressive this compound is.
The "No risk of hyper responding or megadoses" is absolute bullshit, and it's once again overstating.
atrophicpyra said:
"the negative feedback system thats super irrleveant in the cycle since same could be said for 100mg of test e, u never know if that 100mg is gonna get u to 500nl of test e or 1,500nl of test e,"
Extremely backwards, you are confusing the raw bioavailability of a direct hormone with the responsiveness of a multi organ system feedback loop, also, when you inject 100mg of test e, you are introducing a fixed unchanging chemical mass into your body, the way your body responds is a whole other topic, and this whole "overshoot" thing would be cause of crushed SHBG.
atrophicpyra said:
"the variability of using a test e vial over 6.25mg ed enclo is alot higher"
Another backwards statement, again, testosterone has a cleaner mechanism that bypasses the HPTA axis and doesn't rely on LH/FSH to endogenously create this response, therefore from a mechanism standpoint it has a cleaner and simpler mechanism, again this wouldn’t work and i already explained why.
We don't need a specific study on RAD 140 with Enclomephine to know how the underlying mechanism works, we know how strongly RAD 140 binds to the AR, and we know how the hypothalamus responds to heavy androgenic signaling (which is the total shutdown of the GnRH) so no, this complete dumbfuck theory would not work.
RAD-140: Very limited human clinical trials, zero performance trial, (dose used in monkeys was 0.01 mg 0.1 mg and 1.0 mg)
study: https://pmc.ncbi.nlm.nih.gov/articles/PMC4018048/
RAD 140 Bodybuilding doses (anecdotal information): 0-30 mg per day, anecdotally users often repor 4-7 kg of lean mass after 8-10 weeks.
mostly is very likely to be glycogen/water combined.
Ostarine: Clinical trials of Ostarine showed: 1–1.5 kg lean body mass gain over about 8–12 weeks at doses around 1–3 mg/day.
Study: https://pubmed.ncbi.nlm.nih.gov/22031847/
Bodybuilding doses (anecdotal information) : At bodybuilding doses 10–25 mg/day, anecdotally users often report: 2–4 kg total bodyweight gain, with perhaps 1.5 -- 3 kg being lean tissue and the rest glycogen/water combined.
LGD-4033: Clinical trials of LGD-4033 showed: 1.21 kg lean body mass increase
in only: 21 days at: 1 mg/day.
Study: https://pubmed.ncbi.nlm.nih.gov/22459616/
Bodybuilding doses (anecdotal information): At common underground doses: 5–30 mg/day anecdotally users commonly report: 4–7 kg bodyweight gain over: 6–10 weeks, again, a lot is likely to be glycogen, again, just like with other SARMs, it’s probably just mostly intracellular water, food mass, temporary fullness, not pure contractile tissue.
VS
Testosterone:
View attachment 54108
https://pubmed.ncbi.nlm.nih.gov/11701431/
Anadrol:
View attachment 54110
https://journals.physiology.org/doi/full/10.1152/ajpendo.00363.2002
This is not to say anadrol is insanely mild, but definitely way safer than dogshit SARMs
Need to also mention this study was performed on 60 year old niggas that didn’t work out and they still gained 5kg of lean mass, once again, SARMs get mogged to death by AAS.
View attachment 54111
https://journals.physiology.org/doi/full/10.1152/ajpendo.00363.2002
View attachment 54112
https://www.researchgate.net/public...ed_phase_III_trial_in_eugonadal_men_and_women
First of all, i wanna clear this up, this is not to hate on pneumo anything, i could care less about him and i never met him or interacted with him, matter fact i invite you to read his thread on RAD 140 so you can see he was a fucking retard:
View attachment 54116
During his whole thread all he points out he experienced during the cycle was:
-A fuck ton ED during all the cycle.
-Broke out like crazy and lots of Acne.
-Super low energy.
-Irritability.
All that for this physique:
View attachment 54117
Especially when he could’ve gotten the same results avoiding the ED and acne and everything else just doing Test with proper ancillaries, he could’ve obtained the same gains and even way way better gains without risking the liver. Nothing else to say.
He was clearly mentally challenged.
Why AAS still mog?
This is not to deny the side effects or risks of AAS, however, we must comprehend why from a safety and performance standpoint AAS are much more superior, the vast majority of AAS have decades of research, and use, lot's of long term data, therefore we know their interactions and behaviour, which is not the case with SARMs as the long term data is non-existent.
From a ROI standpoint SARMs are simply not worth taking, high risk profile for sub-optimal results compared to almost any AAS,it's safe to say that AAS due to their predictability and the superior risk mitigation leverage they are by far your best bet, and if anything goes wrong you can always cruise on a TRT dose to stabilize your health.
Conclusion: Based on all the information available, including medical and scientific literature, we can conclude SARMs are a class of ineffective and unsafe compounds that failed their own premise, and that AAS are the superior and safer option based on a mechanistical, long term data, and side effects management standpoint.
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