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Anabolism: An Honest Risk Framework for PEDs

By Nootopics July 3, 2026

Research and education, not medical advice.

Bodybuilding is associated with considerable health deterioration marked by infertility, decreased lifespan, and at times failure of vital organs like the liver and heart. No, that shouldn’t matter as much as heavily weighing the risks of anabolics before deciding to use them.

This page compiles my own posts into one organized reference. My main incentive is to be as right as I can about what is the most optimal way to biohack.

The framework

On one hand, everyone can appreciate how effective anabolics are at improving physique and athletic ability, but on the other there is a well established danger to this way of life. In this post, I will attempt to construct the most carefully planned list of drugs to satisfy the best of both worlds: anabolism on par with established protocols, and preservation of health.

The most relevant steroids and SARMs from the time of me writing this post are the following: Testosterone (4,412 human trials, ~2,885 as monotherapy, 4 used 600mg/ week or above), Oxandrolone (106 human trials, 62 as monotherapy), Nandrolone (73 human trials, 51 as monotherapy), LGD-4033 (4 human trials, all monotherapy), RAD-140 (1 human trial, monotherapy), Methenolone (1 human trial, 0 monotherapy), Trenbolone (0 human trials).

For calculating the lean mass gains which each compound, we will have to extrapolate some metrics. To first establish a baseline, the clinical trial wherein LGD-4033 or placebo was given to 76 healthy young men for 21 days will be used for comparison.[1]

To derive this data, we have done a few things. First of all, weight gain in clinical trials closest in comparison to the study on LGD-4033 (Ligandrol) were prorated for Oxandrolone (Anavar), Nandrolone Decanoate (Deca) and Testosterone Enanthate (Test E) with the following formula:

Prorated 21-day Gain (kg) = Total Clinical Lean Mass Gain x (21 ÷ Trial Duration in Days)

Then, additional estimations were made for when the subjects were not young and healthy. In the case of Oxandrolone, a 20% increase was seen when accounting for age-related anabolic disparities. With Nandrolone Decanoate, there was a huge increase when adjusting for responsiveness between young healthy men and those suffering from HIV. To do this, a 300mg dose of testosterone was evaluated in healthy, and HIV-suffering patients, creating a multiplier of 1.49. With this adjustment, we get an estimated 1.45kg per 21 days. That being said, these are just estimations, so it’s best interpreted as a range; Oxandrolone under these circumstances could increase weight by 0.75-0.9kg, and Nandrolone could increase weight by 0.97-1.45kg. But it’s not known if that is true.

Moving on to our preclinical data, which was specific to Methenolone (Primobolan), RAD-140 (Testolone), and Trenbolone (Tren). This is where a ton of speculation happens, so the accuracy of these numbers isn’t clear, however an attempt was made to loosely predict their anabolic effect in humans. Pharmacodynamic Emax saturation was calculated by using the highest recorded weight gain, 1.85kg (using high dose testosterone, and this time alongside weight training) and multiplied it by the dose divided by the dose added to an estimated dose based on the drug achieving 50% occupation from assay data. Please note that for the occupation-estimated dose, AI was used, so it may be inaccurate - feel free to check it. The final value is then multiplied again by 0.85 as a penalty if the drug an injectable ester that takes time to build up in the system.

21 day Pharmacodynamic Emax Saturation Model = 1.85 x (Dose + Dose ÷ Affinity-Predicted Dose) x Ester Value

When this was conducted with testosterone and LGD-4033, values of 1.18, and 1.23 were achieved, respectively, suggesting this formula could be accurate, as it was close to the actual results from clinical trials.

In short, 1mg LGD-4033 shows the highest weight gain in clinical trials when the time period is reduced to 21 days, followed by 600mg Testosterone Enanthate, 600mg Nandrolone Decanoate, and 20mg Oxandrolone. This would make LGD-4033 34-60% stronger in terms of muscle growth than Oxandrolone when adjusting for a difference in responsiveness in samples. When trying to compensate for the subjects having HIV-induced muscle wasting, Nandrolone ranks the highest at 1.45kg/ 21 days, followed by Trenbolone at 1.43kg/ 21 days (extrapolated from rodent data) and RAD-140 at 1.33kg/ 21 days (extrapolated from non-human primate data). Under these circumstances, Nandrolone would have 18% greater anabolic effects than LGD-4033.

Comparative safety of legacy anabolics

In general, targeting the androgen receptor has its consequences across the entire body. However, there are major differences in the relative safety of these compounds. Trenbolone in particular is not only lacking in clinical data entirely, but has evidence strongly linking it to neurotoxicity independent of AR activation.[11] Nandrolone also displayed neurotoxic symptoms in the same study, albeit to a lesser extent and only through AR-mediated processes.

Despite likely being CNS-penetrating, LGD-4033 displays the lowest relative CNS MPO Score,[12] making its profile at least somewhat selective to peripheral tissue. Despite androgen receptor activation itself being at least somewhat neurotoxic, circumstantial preclinical evidence exists like in the case for Alzheimer’s for both RAD-140 and Testosterone.[13]

SARMs (Selective Androgen Receptor Modulators) were designed primarily as a class of orally bioavailable, non-aromatizing AR agonists that show less preference towards prostate binding, with the main goal of preserving the anabolic function associated with steroids, while reducing the side effects. Steroids follow a similar concept, although they have decreased selectivity due to being structurally derived from cholesterol.

Prostate growth can compress prostatic urethra, causing serious urinary problems. These can be transient, or with continued growth, permanently affected. In addition, prostate cancer may accelerate, which is a concern particularly in older populations who’s growth has naturally decelerated due to age. Aromatization of testosterone into estrogen causes a negative feedback loop resulting in the combined inhibition to testosterone synthesis by both, as well as estrogenic side effects such as gynecomastia (gyno), the enlargement of glandular breast tissue in males, edema (swelling caused by water retention that can potentially become dangerous), secondary hypertension caused by increased blood volume, and emotional volatility. Nandrolone converts into a weaker estrogen, estradiol-3-methyl ether, and at a reduced rate compared to testosterone; from this list, only Nandrolone and Testosterone aromatize into estrogenic compounds. 5α-reductase metabolizes testosterone into dihydrotestosterone (DHT). In the case of testosterone, DHT acts as a natural aromatase inhibitor, in turn reducing estrogen. However, DHT is the primary androgen driving androgenic alopecia (male pattern baldness). Unlike testosterone, nandrolone’s 5α-reduced form is much less active than its parent molecule. Progesterone receptor binding is a particularly dirty effect of both Nandrolone and Trenbolone, because of multiple factors. Firstly, it accelerates breast tissue growth from estrogen and IGF-1,[14] and amplifies estrogenic signaling.[15] Second, it triggers the localized release of dynorphin to shut down gonadotrophin-releasing hormone (GnRH), reducing LH and FSH.[16]

Testosterone possesses the strongest prostate binding, followed by trenbolone, Nandrolone and Methenolone. This can cause temporary or permanent urination obstruction, and accelerate prostate cancer in aging populations. LGD-4033 and RAD-140 performed best in this category.

Under normal circumstances, slightly reduced SHBG levels are not a huge concern, as it increases free testosterone. However, SHBG regulates hepatic lipogenesis by reducing acetyl-coenzyme A carboxylase levels. Severely low SHBG is marked by increased LDL and total cholesterol, which may form arterial plaques, representing a significant cardiotoxicity concern outside of cardiac hypertrophy. Agonists at the androgen receptor can reduce SHBG, with estrogen generally exerting the opposite effect. Oxandrolone showed the most significant suppression, around twice as strong when compared to Methenolone’s predicted suppression.

Despite having a much higher cardiotoxicity coefficient versus testosterone, the comparatively lower dose of Trenbolone at 10.3mg/ day reduces the risk percentage closer to that of Oxandrolone’s in this model. Interestingly, one study in mice with metabolic syndrome shows Trenbolone actually being far less cardiotoxic than testosterone and even circumstantially cardioprotective.[23]

When comparing Hepatotoxicity and Nephrotoxicity, Oxandrolone and RAD-140 are by far the worst offenders as their predictive hepatoxicity is clinically confirmed. Nephrotoxicity data here is strictly predictive, and highest in Trenbolone, followed by RAD-140 and testosterone. Predicted values for hepatotoxicity and nephrotoxicity were derived from a structural understanding of the molecules and their metabolism, and animal data wherever possible. Since these predicted risk values aren’t based on real data, they should be taken with a grain of salt.

Weighted risk assessment and the ranking

To establish a singular number representing the overall risk of each drug, the data should be weighted and then pooled based on the damage and unpleasantness of the side effect, as well as the strength of the data provided. The side effect priority will first estimate the clinical danger relative to the other side effects, as well as the unpleasantness of the side effect. The unpleasantness value will be divided by 2, then added to the danger value, and then the sum divided by 2. While this step may seem arbitrarily calculated, it’s the most convenient way to derive a singular risk value for the anabolics. Next, risk data for each compound was standardized to a 0-5 baseline scale and multiplied by the concern value. In the case of nephrotoxicity and hepatotoxicity, predicted toxicity was counted as half its value due to lack of evidence. Neurotoxicity was calculated based on brain penetration and direct literature.

After creating a comprehensive weighting of the overall side effects, and contrasting it with anabolism from our 7 drug candidates, we see a clear trend in the data: the side effects of anabolic-androgenic steroids (AAS) scale with the potency of their anabolic effect, possibly with the exception of Nandrolone if we do not adjust for their disease. SARMs on the other hand did not represent this trend, and performed slightly weaker, or superior to the steroids, while having the lowest total risk, with LGD-4033 having the greatest lean mass-to-risk ratio. From these drugs, Trenbolone was the least studied, and Testosterone the most studied.

Believe it or not, the only narrative I had going into this was that I knew about harm-mitigation strategies for anabolics and people’s general opinions on these compounds. I was genuinely surprised at how good LGD-4033 performed relative to these other drugs, and how poorly HGH and IGF-1 performed. It goes to show how in-the-know its chemists were with LGD-4033, and how continued development of these drugs has yielded a massive improvement to safety with time. Now all they need to do is make a derivative that doesn’t interfere with SHBG and ITT and we’re set for life.

HGH, IGF-1 and myostatin reality

The most relevant in this category from the time of me writing this post are the following: HGH, GHr agonist (492 clinical trials, 431 as monotherapy), rIGF-1, IGF-1 mimetic (34 clinical trials, 27 as monotherapy), BVS857, IGF-1 mimetic (3 clinical trials, all monotherapy), ACE-031, myostatin inhibitor (3 clinical trials, 2 as monotherapy).

While there is clearly lean mass gained by these compounds, it is relatively minimal when scaling for water weight and risk. Further, IGF-1 nor HGH influences androgen receptor-mediated anabolism in vivo,[44] meaning it is not expected that mixing these with an AR agonist would amplify the effects of AR agonists. This is on top of the fact that they are far less selective to muscular tissue than AR agonists, and lean mass gains purely as muscle tissue would make this an even smaller value. In addition to this, HGH, IGF-1 and mTOR are all extremely relevant to lifespan, with HGH restriction resulting in a ~+40-70% extension to lifespan, and IGF-1 ~+5%.[61]

It’s also not very well known that HGH essentially speed-ages you. But some people also claim HGH helps with recovery, so that could also be part of it. Because they confuse weight with muscle, and there are older studies where AR relied on IGF-1, but as I showed that doesn’t actually happen in vivo.

ACE-031 yielded the most lean mass out of any anabolic in this writeup, and simultaneously carried an extreme risk. It can not be stressed enough the difference in risk but it should have the highest net myogenesis out of anything else I covered in this post while simultaneously giving the highest muscle tissue ratio. Unlike HGH, it is expected that the myostatin inhibition of ACE-031 would amplify the anabolic effect of AR agonists. Two drugs in this category were pulled from clinical trials due to severe adverse effects, that being ACE-031 and BVS857. rhIGF-1, HGH and BVS857 all had exceptionally poor muscle-to-risk ratios, whereas high dose testosterone had the best.

Cholesterol adjuncts

The most relevant cholesterol modifying drugs from the time of me writing this post are the following: Atorvastatin, Rosuvastatin, Ezetimibe, Pitavastatin, Evolocumab, Berberine, Inclisiran, Lycopene, Red Yeast Extract, Pantethine, Citrus Bergamot.

When clinical data wasn’t available, it was predicted based on those four drugs with the following formula:

LDL-C Impact = 0.3784 x (SHBG Suppression Percentage) - 14.2297%

The resulting numbers are an 18% increase with Oxandrolone, 13.01% increase with RAD-140, 12.2% increase with Nandrolone, 7.71% increase with Trenbolone, 6.6% increase with LGD-4033, 1.66% increase with Methenolone, and a 0% increase with high dose Testosterone. It should be noted that this low value for testosterone was not expected until this portion of the writeup, and likely means that Testosterone’s risk value was over-predicted to an unknown extent if using LDL-C increases as the determining factor for SHBG’s risk. That being said, the consequences to SHBG suppression are beyond that of just LDL-C, as it causes increased hormone fluctuation and reduces HDL-C, so the value would probably only reduce moderately.

Oxandrolone had the most negative effect on LDL-C, whereas high dose testosterone had the least effect. Evolocumab had the strongest reduction to LDL-C and also showed the most favorable safety profile. Citrus Bergamot reduced LDL-C almost to the same extent as statins, despite having a drastically improved safety profile, and is a supplement that is widely available. Lycopene had the least effect, and Atorvastatin was the most risky of the substances analyzed.

The next generation

The current anabolics are already riddled with well-known issues. So for that reason, I will be creating some novel solutions seeking to revolutionize anabolics and potentially start fundraising for experiments to be conducted by university campus regarding these ideas of mine.

MEPB, AR Positive Allosteric Modulator (SARM PAM)

MEPB is an experimental drug, and safety data is isolated to rodent studies. It’s by far the riskiest thing I’ve invested into for that reason - however, when it comes to anabolics, you’re stuck between a rock and a hard place. MEPB is an agonist at BF-3, and BF-3 allosterically modulates the androgen receptor, and it does this at a molecular level. BF-3 antagonists are potent anti-androgen drugs, basically acting as NAMs at the AR, and BF-3 seems to specifically modulate Activation Function 2/ AF2, which has been named the “SARM” site, or selective androgen receptor modulator site, and contrary to the misleading name, SARMs as we know them bind there as agonists, not PAMs.

However, MEPB is not an anabolic drug at all by itself. It will instead modulate the response of androgens, increasing their safety, selectivity to muscle tissue and have a larger all around metabolic effect. AF2 is weaker than AF1, and SARMs were designed around testosterone, and testosterone binds preferentially to AF2, and DHT to AF1. MEPB, by shuffling endogenous androgens towards AF2, will detract from AF1, thereby making all androgens more SARM-like (more testosterone-like). This is significant, as DHT is thought to be a significant cause for androgen-induced side effects, suppression, and balding. However, it would mean that the pro-anabolic effects of MEPB, by virtue of enhancing net androgen binding, is in direct competition with AF2’s relative weakness over AF1 - and this unfortunately would make MEPB’s anabolism potential reliant on AF1 remaining activated and not being inhibited too much.

While it’s possible that MEPB in isolation would be on the longevity/ healthspan side of things, that’s only one half of the dynamic, because it could be made into a pretty efficient anabolic too. One potential route here would be to raise the biosynthesis of androgens by activating StAR (the rate limiting stage in the production of hormones).

The StAR / oxidative point

It starts with StAR, which shuffles cholesterol through the mitochondrial membrane. StAR is thought to be one of the leading targets in endocrine disruption. Various environmental toxins have been shown to impair it, in different ways. Going back to the steroidogenesis flowchart, after StAR activation, it’s not just going to selectively increase testosterone and everything is fine. Activation of StAR can become toxic when expressed under oxidative conditions by importing 7-OOH instead of just cholesterol. Here an antioxidant, such as a Nrf2 activator, could work to offset that damage. I chose Carnosic Acid due to being one of the only antioxidants that selectively protects healthy cells and kills cancer cells. But you’ll also see that estrogen will get produced - of course that would then demand blood monitoring, and perhaps application of an aromatase inhibitor to keep it within range. Everything has checks and balances, you also don’t want to completely shut down estrogen as it’s pretty important, even for anabolism.

MCB-613, What if we just bypassed DHT and went right to the coactivators?

If targeting the SARM site is really that limited - thus limiting AF2’s feasibility as a target, but DHT is also pretty undesirable, then what if we just went straight to the coactivators? To be clear, if MEPB seemed experimental, then MCB-613 is actually that much more obscure. It’s not entirely clear to me where it’s binding to induce SRC induction, but SRC1 was described as the necessary coactivator induced by DHT to unlock the maximum potential of the androgen receptor.

What’s funny about MCB-613, is that it was picked up from the scrapyard of searching for SRC inhibitors, after all, these are considered oncogenic genes that contribute greatly to cancer. But MCB-613 selectively kills cancer cells, exploiting the expansionism of cancer to basically rapidly grow itself to death. Another paper also describes MCB-613 as binding to Keap1, which produces an antioxidant effect. Interestingly, this might have crossover with how Carnosic Acid stimulates cancer cell death selectively, despite being protective to healthy cells.

Weight gain seems minimal in the MCB-613 group, much like MEPB, however that’s to be expected; what’s going to be interesting is how MCB-613 and MEPB interact in the same rat - would MEPB then become selectively anabolic? Would there be a lifespan extension from reduced cancer incidence? And what about balding, would this be the first route towards having cake and eating it too?

The main thing here is nuance. If we can create an anabolic that can be used basically forever, then we really should. Of course this is where things will get complicated, but for people who don’t want to ruin their reproductive or cognitive capabilities, maybe it’s worth exploration. I’m not saying I can predict the outcome, but the current methods are causing problems. I want to see where this goes. If not others then at least my own selfish reasons. Because I don’t want to castrate myself with drugs.

ORG-43902 vs HCG in depth

In our analysis, LGD-4033 is by far the safest anabolic agent despite still yielding a considerable increase to lean mass. However, the vast majority of anabolics severely impair the biosynthesis of androgens, to the extent that they act like contraceptives, and this too is true for LGD-4033. This side effect is mediated by the testis, as androgen receptor agonists limit the amount of intratesticular testosterone (ITT) and LH, and prolonged AR agonism can cause testicular atrophy if it’s not reversed. LH being shut down also impairs neurosteroids, which likely caused the cognitive impairment seen with high dose testosterone administration.

The largest downside to TRT is that it typically requires injection, and frequent doctor visits for some. In addition to that, with testosterone injections, natural production is suppressed, causing dependence and infertility. HCG is generally much more sustainable, albeit still requiring injection, which is the basis of my interest in ORG-43902.

ORG-43902 (aka ORG-41841) is an oral testosterone synthesis enhancer. HCG activates LHr to signal cAMP, and then StAR in leydig cells, which then causes steroidogenesis, and ultimately an increase in testosterone, but other hormones as well. LHr doesn’t get desensitized much with HCG compared to LH, which is due to it signaling cAMP and not recruiting calcium and PLCβ, hence why HCG is able to significantly increase testosterone in men but not LH. ITT was suppressed by 94% in the Testosterone enanthate group. Administration restored values to healthy controls. 400IU of HCG significantly raised total testosterone in healthy subjects with functioning testicles.

TP03 is a derivative in the same class as ORG-43902, both of which behaving as allosteric agonists at LHr at a distinct region of the receptor which does not compete with endogenous ligands. The main distinction is that ORG-43902 is a weak partial agonist at TSHr (however it did not increase thyroid levels in clinical trials), and acts as a pharmacoperone for FSHr which rescues misfolded proteins and increases its binding activity. Another major point of contention with HCG, is that prolonged LHr stimulation is toxic to leydig cells, this is for two reasons: LHr stimulates oxidative stress which is typical of cAMP-dependent pathways, but more importantly, and the leading theory, is that under oxidative conditions, StAR activation can transport 7-hydroperoxide into the mitochondria and cause cellular damage.

Strategic advantages of ORG-43902 over HCG:

  • ORG-43902 is orally bioavailable, whereas HCG requires injection.
  • ORG-43902 is likely to carry the “reverse tolerance”, and low receptor desensitization/ internalization as demonstrated with other LHr allosteric agonists in its class, such as TP03.
  • ORG-43902 has a shorter half life, which would allow more downtime during sleep, likely leading to less opportunities for leydig cell toxicity which is linked to prolonged LHr activation.
  • ORG-43902 is a stable small molecule, whereas HCG is a bulky protein with strict storage conditions.
  • ORG-43902 is less likely to cause hyperthyroidism than HCG, as it didn’t raise thyroid levels in its clinical trial.
  • ORG-43902 has unique activity as pharmacoperone for FSHr, which contributes positively to testicular function.

The effective dose for ovulation in women is 300mg, and HCG’s effective dose is 250ug r-hCG (2,325IU). Extrapolating from this, that would mean 350IU HCG would equate to around 45mg of ORG-43902. Since ORG-43902’s half life is nearly exactly half that of HCG, that would make ORG-43902’s equivalent dose relative to 350IU HCG, taken 3x per week, roughly 22.5mg per day.

Cons to ORG-43902: Firstly would be price. Second, it’s still increasing testosterone, and it’s expected that some testosterone may convert to estrogen, so one would need to monitor blood levels of estradiol and ensure it stays within range. Lastly, ORG-43902’s clinical data is limited to one phase 1 study in women.

Unfortunately, ORG-43902 turned out to be ineffective as monotherapy when used alongside anabolics in our group (data not shown), as only one person achieved supraphysiological testosterone levels on it, and they were not using an AR agonist, leading us to believe it is a true PAM and its effect is dependent on LH levels. This would mean that a LH promoter like Kisspeptin-10 would need to be administered twice a week alongside it for it to work properly. Since HCG and Kisspeptin can bypass the LH inhibition by anabolics, they have an edge over Enclomiphene in this regard. However, Enclomiphene can be used to further disinhibit the estrogen-mediated impairment to steroidogenesis caused by either adjunct. While Enclomiphene’s effect is lasting, any LH-mediated process will inherently develop tolerance unlike ORG-43902.

Appetite: ART27.13

The most relevant appetite stimulants from the time of me writing this post are the following: Mirtazapine, Ginger extract, THC, MK-677, ART27.13.

Naturally, with weight training and anabolic drugs, nutritional requirements increase to satisfy an increased muscle protein synthesis rate. However, a subset of the population cannot naturally obtain this level of appetite, which can greatly contribute to anabolic responsiveness. In terms of appetite stimulants, the two strongest in this category were THC, which can cause cognitive impairment and neurotoxicity, and MK-677, which can cause severe pancreatic insulin insensitivity, edema, tachyphylaxis and other longevity-related harm associated with elevated HGH. In fact, MK-677 has one clinical trial that needed to be terminated after multiple people nearly suffered congestive heart failure.[1] This was the inspiration for having ART27.13 carried on Everychem. It’s our hope that people eventually stop selling and consuming MK-677. See What To Avoid.

MK-677 was mainly used to promote HGH. HGH-related growth is incredibly non-selective and even if it’s not characterized by fat mass per se, that doesn’t mean it’s particularly myogenic, like in this study MK-677 didn’t improve muscular strength or function and somehow reduced the lean:fat mass ratio in limbs.[link] So I don’t really agree with the purported uses of MK-677 as a bodybuilding drug.

ART27.13 (also known as AZD1940), is a non BBB-penetrant CB1/2 agonist that was in clinical trials both as an appetite stimulant drug, and at one point an analgesic. Accordingly, only 0.7% of the compound was found within the brain, making it peripherally selective[1] - because of this, it did not impair cognition in clinical trials. It appears CB1 stimulation increases the size of meals consumed, instead of prompting meal consumption.

It would appear as little as 100mcg could promote appetite, with 800mcg creating a sedated state with more frequent side effects. 200-400mcg seems to have the most reasonable outcome with respect to side effects, and 1.3mg having the strongest result overall. There’s many mechanisms by which peripheral CB1 agonism can promote appetite, including but not limited to: a direct effect in taste buds influencing taste sensations and receptiveness to sweetness, stomach-stimulated ghrelin release, reduced cholecystokinin secretion in the small intestine, reduced GLP-1 and GIP, and vagal nerve stimulation. Importantly, vagal nerve ablation reversed the appetite-promotion of peripheral CB1 agonism, meaning vagal nerve stimulation could be the direct-acting mechanism of peripheral CB1, rather than an indirect reliance on commonly recognized pathways like GLP-1 and Ghrelin it also intersects with.

ART27.13 shows the highest effect when adjusted to match a healthy person, at 3.23kg in weight gain, but matches Mirtazapine’s results when using raw clinical data. Risk was calculated on the basis of obesity, heart failure and cognitive impairment, with heart failure holding the most weight; ART27.13 due to not penetrating the CNS and thus having less side effects than THC resulted in the lowest risk score, whereas MK-677’s was the highest due to evidence of cardiovascular events in previous clinical trials, followed by THC given it’s cognition impairment and neurotoxicity. Of these drugs, only ART27.13 was intentionally designed to stimulate appetite. Thus it should probably go without saying, consuming low quality food on ART27.13 would be ill-advised.

Carnosic Acid

AR-dependent anabolics exacerbate oxidative stress,[62] which in turn could cause widespread aging and reduced lifespan independent of the aforementioned risks. Many antioxidants promote cancer growth, but this is not the case for at least Astaxanthin and Carnosic Acid, with Carnosic Acid killing cancer cells is nearly every type of cell culture. It is thus recommended that someone on an anabolic cycle uses antioxidants if hoping to maintain their health.

Carnosic acid protected mouse primary neuronal cell cultures against hydrogen peroxide-induced damage more efficiently than edaravone or ebselen. Of the three compounds tested, CA displayed the most consistent neuroprotective effects. This correlates with its superiority over various synthetic antioxidants which is super rare for most natural vs. synthetic comparisons.

I wish someone else would begin dispelling rumors like this since it feels like it’s always me. In the study where Carnosic acid degraded androgen receptors, it was only in cancer cells. They literally show it not happening in normal cells. Carnosic acid also kills cancer cells but not normal cells. So they probably degrade due to it being toxic to cancer cells. The DHT inhibitor in rosemary extract isn’t Carnosic acid, it’s other constituents like 12-methoxycarnosic acid and rosemarinic acid. That’s why on everychem I am trying to sell carnosic acid that’s 95%+ pure, which isn’t as cheap to buy in bulk.

Methodology caveats

I supervised most of this data, a lot of it is driven by extrapolations on subject differences, species differences and drug predictions made with AI (I even subscribed to Google’s AI Ultra $100/mo because I was being limited on how much I could generate) and thus is sure to have a degree of inaccuracy. If anyone has any corrections to make for this post, let me know, however I’d request you only do so if you are absolutely able to prove it.

  • Limitations to lean mass calculations: Lean mass is not limited to muscle tissue, and a large portion of it is often represented as water weight. It is not clear how much the prorated numbers are skewed by this fact, and if LGD-4033 would perform worse had the trial been extended to multiple months.
  • Limitations to legacy anabolics conclusion: Where clinical data did not exist, extrapolation from preclinical data and speculation around the structure/ binding of the molecule was performed. Clinical data did not perfectly match among drugs and required adjustments to draw comparisons, which may cause a conflict in the drug’s pharmacokinetic differences or inaccuracies attempting to account for subject differences. Total risk combines clinical danger and unpleasantness, and weighting was not based on strict scientific methodology. Bodybuilders may abuse these drugs, like in the case of Trenbolone, and have risks that far exceed high dose Testosterone. Further, there is vasty disproportionate clinical data which could invalidate some of these findings as drugs receive greater study. This graph includes only 7 drug candidates and 10 major risk profiles, and so it’s not all-inclusive in its representation of this class of drugs, or overall risks. Lastly, AI was used to speculate on compound’s affinity and structural implications, meaning the validity of those pieces of data aren’t confirmed in this post. Other side effects, such as immunosuppression, are also valid and were not measured in this analysis.
  • Limitations to appetite stimulant calculations: Trenbolone’s fat reduction is preclinical and may not carry over to humans. While the estimated lean mass gains from eating more are added to the lean mass gained from anabolics, it’s not clear if this would be the case in practice. Lastly, no direct comparison exists using appetite stimulants alongside potent anabolic drugs, therefore the entire relationship is speculative.
  • Limitations to cholesterol-drug comparisons: Risk analysis was comparatively much less supervised when generating numbers for cholesterol-modifying drugs, and thus should be taken with a grain of salt. However the current predictions suit their reputation at present. LDL-C increasing, and SHBG decreasing with anabolics is highly dependent on dose and may not match self-reported data on suppression when using these drugs.
  • Limitations to other anabolics calculations: Risk analysis was performed with AI, and less rigorous than what was provided for legacy anabolics. Further, some extrapolations were made around trial length and subjects’ health status.

I’ve been making posts like these since before I would sell anything. I would appreciate it if you didn’t cast doubts on me due to this, as I did my best to rigorously explain these outcomes, and it’s all openly explained. I genuinely did not expect LGD-4033 to perform this positively. It just did.

Sources

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