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Testosterone is not neuroprotective, estrogen is.A common myth circulating in the bodybuilding and TRT community is that testosterone is inherently neuroprotective and is unique from all other anabolic steroids in that regard.The reason why testosterone is neuroprotective is simply because it aromatizes at a rate that provides a sufficient amount of estradiol to balance out the androgenicity in the body.Data in rodent models using cortical cells suggests this very convincingly by showing how the aromatase inhibitor Anastrozole (Arimidex) completely eliminated the neuroprotective effects of testosterone [R].[embedded content]Table of ContentsAre Synthetic Anabolic Steroids More Dangerous Than Testosterone?There have been tons of studies published suggesting how much worse synthetic anabolic steroids are in contrast to testosterone for cardiovascular disease, neurotoxicity, and a myriad of other deleterious outcomes. I believe that a significant amount of this data is exaggerated based on the fact that exogenous estrogen is never co-administered in these studies.At the end of the day, testosterone is the safest androgen at physiologic dosages. However, I theorize that many synthetic anabolic steroids are not as dangerous as we are led to believe. My theory is that some compounds are not inherently significantly more dangerous than testosterone, rather, it is their lack of aromatization, 5-alpha reduction, or differing affinity for off-target receptors that makes them more dangerous.The effect on estrogen receptors and how potent of a substrate an anabolic steroid is for aromatase is the main factor that impacts how viable a hormone is for consideration in a monotherapy context.DHT derivatives cannot be converted by the enzyme aromatase into an estrogen like estradiol.Nandrolone (19-nortestosterone) and its derivatives (19-nors) each have their own individual affinity (or lack thereof) for estrogen receptors and interaction with aromatase, often resulting in subpar estrogen levels (exceptions to this exist such as Trestolone/MENT).Basically, I believe that some steroids may show to be significantly more cardiotoxic and neurotoxic in the data because they are always used on their own with an insufficient amount of estrogen to balance out the androgenicity in the body.The Importance Of Sufficient Estrogen LevelsHealthy estrogen levels are needed for libido, erection quality, vasodilation, cardiovascular health, brain health, bone health and several other critical functions.In women the risk of cardiovascular disease spikes significantly after menopause.It isn’t a coincidence that the majority of women who develop heart disease have it occur after their estrogen production has dropped to sub-male levels.If you don’t have a sufficient amount of estrogen relative to androgen levels in the body, cardiotoxicity and neurotoxicity levels will be significantly higher than they would be if healthy estrogen levels were sustained.From a bodybuilding perspective, estrogen is needed to optimize muscle growth, fat loss, as well as IGF-1 and growth factor production/cellular signaling.This is why heavily aromatizing steroids may indirectly result in greater growth potential and are often classified as “bulking” compounds.Anecdotally, many bodybuilders report that the most they’ve ever grown was during off-season mass building phases when their estrogen levels were through the roof.The Point Of A Testosterone BaseTestosterone is not tissue selective and is actually a poor muscle builder milligram for milligram when compared to other synthetic anabolic steroids developed in the years following its discovery.When it comes to nitrogen retention, on paper it is not superior to many anabolic steroids.However, it aromatizes into estradiol at a very tightly regulated rate, it is bioidentical, and our body knows exactly what to do with it.In addition, our body knows how much testosterone to bind up with SHBG, how much to free up and make available to tissues, as well as how much DHT to 5-alpha reduce to antagonize estrogen receptor activation should it get out of control.From a bodybuilding perspective, testosterone is subpar in many aspects.However, in an overall health, longevity AND bodybuilding context, testosterone cannot be beat at therapeutic dosages.By using a testosterone base or a source of sufficient estrogen the shortcomings of other anabolic agents can be attenuated to some extent, hence why testosterone is the base of most steroid cycles.The Balancing Act Of Testosterone, DHT and EstrogenSteroidogenesis in the body is carried out like a massive orchestra to regulate countless functions.It’s far more elaborate than simply testosterone, estrogen and DHT production.Even at a snapshot view, the balancing act of androgens and estrogens in the body is tightly regulated and is carried out to ensure health remains optimized.This balancing act gets more and more dysfunctional with age, poor lifestyle, poor diet, poor sleep hygiene and numerous other factors.However, the body still knows exactly what to do with testosterone, how to create an optimal opposing amount of estrogens, and how much testosterone to 5-alpha reduce into DHT to oppose excessive estrogens and support male secondary sex characteristics.When you compare clinical data on a synthetic anabolic steroid to testosterone in a monotherapy context, you have to consider that these studies are utilizing that synthetic steroid on their own, not with exogenous estrogen or any supplementary hormones that may be needed to balance out its androgenicity, lack of estrogenic activity and/or interaction with aromatase.Obviously if you take a compound that doesn’t aromatize sufficiently to estrogen and compare it head to head with the bioidentical androgen that our body knows how to aromatize and 5-alpha reduce at a perfectly balanced rate, you can just imagine which is going to come out on top in a cardiotoxicity and neurotoxicity context.Does this mean that a synthetic anabolic steroid compared to testosterone would not potentially be more efficacious than testosterone should those other backend pathways be supplemented to fill the gaps though?Synthetic Anabolic Steroids With Exogenous Estradiol For HRTSome individuals have underlying genetic polymorphisms and defects in sex hormone metabolism that may throw off the tightly regulated steroidogenesis pathway in a way that skews too heavily in favor of estrogen, or too heavily in favor of androgens.There are many cases in which synthetic anabolic steroids may beat out testosterone, despite testosterone on paper being the candidate of choice for most men at therapeutic dosages, and still the candidate of choice for many men at supraphysiological dosages too in a bodybuilding context.Nandrolone is a great compound to exemplify this in my opinion.It has a much lower level of androgenicity in the body due to its 5-alpha reduction into DHN, and it is also far less estrogenic than testosterone.Those who are prone to gyno, hair loss, acne or other common testosterone related side effects typically prefer nandrolone for this reason.This is why many female oral contraceptives are nandrolone analogs as well.Unfortunately, your heart and brain don’t care if you have hair loss, acne, or gyno, so there can be deleterious outcomes as a result of androgen use without a sufficient amount of unopposed estrogens, or an estrogen excess without sufficient androgen opposition.In regards to nandrolone, I don’t believe it has a sufficient amount of opposing estrogen to balance out its androgenicity.It activates estrogen receptor alpha (ERα) a bit via its inherent estrogenicity and it can aromatize to estrone, which can then convert to estradiol, but the amount of overall estrogenic activity it provides does not appear to be sufficient to offset its neurotoxicity or cardiotoxicity.I believe this is why most of the data found in nandrolone studies shows how horrible it is for the brain and the heart.Nandrolone is always evaluated on its own without a sufficient amount of estrogen present to provide cardiovascular and neurological support.If you shut down your natural endogenous testosterone production with an exogenous steroid, you will also shut down your natural endogenous estrogen production.Any estrogen production (or lack thereof) would then be derived from whatever exogenous steroids are being administered.This is why some synthetic steroids may not necessarily be as dangerous as we once thought, as the data we use to review their safety profiles are skewed by their lack of estrogenic support in the tissues that would otherwise be supported by testosterone aromatizing into estradiol.In the presence of sufficient estrogen, it is entirely possible that the deleterious effects of certain synthetic steroids in the body may be attenuated to some extent.The Neurotoxicity Of Testosterone, Nandrolone And WinstrolComparing the effect of testosterone with that of 19-nortestosterone (nandrolone) and stanozolol (Winstrol) on neurotoxicity we can clearly see that estrogen is what protects neurons in the brain, not testosterone itself.In this study, a physiologic dosage of testosterone was neuroprotective [R].Testosterone only amplified neurotoxicity at supraphysiological dosages.The neuroprotective effect of a physiologic dosage of testosterone was completely eliminated when the aromatase inhibitor anastrozole (Arimidex) was co-administered, suggesting that the intrinsic toxicity of testosterone as an androgen is only counterbalanced by its aromatization into 17β-estradiol.As opposed to testosterone, nandrolone does not appear to aromatize sufficiently into estrogen, and Winstrol does not interact with aromatase at all.As you would expect, nandrolone and Winstrol were both neurotoxic at every single dose evaluated regardless of Arimidex being co-administered or not.The anti-androgen flutamide was able to attenuate the neurotoxicity of all three androgens, thus further reinforcing that physiologic dosages of androgens without a sufficient amount of opposing estrogens, or supraphysiological dosages of androgens may facilitate neuronal death.None of the anabolic androgenic steroids in this study were toxic in the absence of NMDA, therefore suggesting that the mechanism by which unopposed androgens facilitate neuronal death is by increased vulnerability to excitotoxic insults.TestosteroneNeuroprotective Effect Of Testosterone At Physiologic Dosages Without ArimidexAt physiologic dosages without an aromatase inhibitor present, testosterone has shown to have a neuroprotective effect.Neuroprotective Effect Of Testosterone At Physiologic Dosages Is Eliminated By ArimidexIt is often assumed that the androgen itself (testosterone) is what protects the brain.However, the aromatase inhibitor Arimidex completely eliminated all neuroprotective effects of testosterone at that same physiologic dosage.Arimidex (anastrozole) exacerbated neurotoxicity at every single testosterone dosage when it was co-administered.This suggests that testosterone is not a unique androgen that is more neuroprotective than all other steroids, rather, it is its aromatization into estrogen that is neuroprotective.Neurotoxicity Of Testosterone At Suraphysiological Dosages With And Without ArimidexAt supraphysiological dosages, testosterone has shown to exacerbate neurotoxicity.While its aromatization into estrogen still prevents a significant amount of neuronal death, we can clearly see that supraphysiological testosterone concentrations exacerbate neurotoxicity regardless, and supraphysiological estrogen levels will not provide dose-dependent increases in neuroprotection.What is the takeaway from this?The data suggests that physiologic concentrations of testosterone facilitate neuroprotection in the brain via aromatization into estrogen, but there is a threshold to that neuroprotection, and supraphysiological concentrations will still be unhealthy.Nandrolone (19-nortestosterone)Neurotoxicity Of Nandrolone Regardless Of Arimidex UseNandrolone exacerbated neurotoxicity at all dosages, regardless if it was a low concentration or a high concentration being evaluated.In addition, co-administering Arimidex had no impact on how neurotoxic nandrolone was in this model at any dosage.This suggests that nandrolone does not aromatize into a sufficient amount of estrogen, or activate estrogen receptors on its own at an amount satisfactory to provide the neuroprotective effects of healthy estrogen levels.A source of estrogen would likely be necessary to co-administer with nandrolone for it to be considered a viable monotherapy alternative in a HRT context, or as a “healthy” cycle.Winstrol (Stanozolol)Neurotoxicity Of Winstrol Regardless Of Arimidex UseWinstrol exacerbated neurotoxicity at all dosages, regardless if it was a low concentration or a high concentration being evaluated.In addition, co-administering Arimidex had no impact on how neurotoxic Winstrol was in this model at any dosage.We already know that Winstrol does not aromatize into estrogen at all.This data suggests that a source of estrogen would be necessary to co-administer with Winstrol for it to even be considered as a viable monotherapy alternative in a HRT context, or as a “healthy” cycle.Anti-Androgens Attenuate The Neurotoxicity Of Anabolic Androgenic SteroidsUnopposed androgens with an insufficient amount of estrogen present will be cardiotoxic and neurotoxic.This is why Flutamide (an anti-androgen) was able to eliminate the neurotoxicity of nandrolone and Winstrol.Anti-androgens have a dose-dependent response just like anabolic androgenic steroids, so there will be androgen receptor (AR) competition occurring between anti-androgens and androgens for AR binding and activation.Anti-androgens will act as competitive antagonists for AR, or as makeshift synthetic steroids themselves, albeit with significantly reduced androgenicity.Basically, depending on the anti-androgen used, they will work either by suppressing endogenous androgen production, and/or by competing for androgen receptors.How effective the anti-androgen will be at inhibiting androgens from binding to AR will be based on binding affinity, binding constant, half-life, the dosage used, and a myriad of other factors.Flutamide is non-steroidal and acts as a selective, competitive, silent antagonist of the AR.It is a primitive and subpar anti-androgen relative to more recent developments in medicine, however, it is still effective at preventing androgens from binding to androgen receptors.This is why flutamide was able to eliminate all of the neurotoxicity of nandrolone and Winstrol at all dosages.By preventing nandrolone and Winstrol from binding to androgen receptors, they are no longer able to transcribe their effects in tissues.The flutamide and Arimidex data reinforces the fact that nandrolone does not produce enough estrogen to provide the neuroprotection needed to stave off neuronal death.With or without an aromatase inhibitor, nandrolone exacerbates neurotoxicity just the same.Without an aromatase inhibitor but with an anti-androgen, the neurotoxicity of Nandrolone is eliminated entirely.I suspect that the same applies for the inherent cardiotoxicity of nandrolone as well.Expectedly, the same applies for Winstrol as it is not a substrate for aromatase at all.This is where all the studies showing how terrible nandrolone is for the heart and brain come into question, as those negative outcomes found in the data may not have been so drastic if an exogenous source of estrogen was co-administered.The same dosage of flutamide was unable to fully offset the neurotoxicity of testosterone at supraphysiological dosages without Arimidex present.Once testosterone dosages exceed physiologic concentrations, the vulnerability to neurotoxicity and cardiotoxicity skyrockets.Too much of anything in the body is going to be bad, and testosterone is not exempt from this just because its the bioidentical hormone we naturally produce and aromatize into estrogen.The Aromatization Of Androgens Into Estrogen Is What Regulates NeurotoxicityReflecting on the data with and without an aromatase inhibitor we can see quite clearly that estrogen is what facilitates neuroprotection, not testosterone.Many assume that testosterone is a unique androgen that binds to AR in some special way that’s going to protect the brain and other steroids are going to destroy the brain.I don’t think it’s as cut and dry as that.I think it’s pretty clear in the data that with anastrozole co-administered the neuroprotective effect is wiped out, and without anastrozole there is a neuroprotective effect.What is the difference between aromatase being inhibited and aromatase not being inhibited?It is the estrogen level in the body.If you have a sufficient amount of estrogen to balance out androgens in the body, you get a good stable level of neuroprotection, which is reflected in how our body regulates endogenous androgen aromatization as is.But, if you have a supraphysiological level of androgens, or inhibit aromatase from providing the estrogen needed to carry out necessary functions in the body, neurotoxicity spikes up regardless of the fact that it is testosterone being evaluated, not a non-bioidentical synthetic anabolic steroid.This all circles back to the rationale behind using a testosterone base on cycle, or having a sufficient source of exogenous estrogen if you are deficient.It also reinforces that aromatase inhibitors are horrible for you if used unnecessarily.My Stance On Aromatase InhibitorsYou would be well served by doing whatever you can to avoid using aromatase inhibitors.If you even need an aromatase inhibitor in the first place you’re likely either using too much testosterone to begin with (or other aromatizing steroids), you’re too fat (more fat = more aromatase), your diet sucks, your lifestyle choices are poor, or you’re injecting too infrequently.Or you might have a genetic polymorphism that results in subpar sex hormone metabolism.At the end of the day, the likelihood that you would need an AI to handle a truly therapeutic dose of testosterone if you’ve optimized everything is extremely low.In a bodybuilding context at supraphysiological dosages, I also think that in most cases using an AI just so you can use “too high” of a testosterone dose is a poor strategy.Should You Take Exogenous Estrogen To Prevent Neurotoxicity And CardiotoxicityJust because estrogen is what provides neuroprotection, not testosterone, it absolutely does not mean that you should start popping your girlfriend’s birth control pills like candy.Unopposed estrogen in the body is carcinogenic.There is a reason why the first go to treatments for breast cancer are SERMs and aromatase inhibitors.Also, estrogen does not provide neuroprotection in a dose dependent manner.There is a sweet spot for everything in the body, and too much of anything is going to be bad.A 4-day pretreatment with low concentrations 0.01 μM (10 nM) of 17β-estradiol was substantially neuroprotective against NMDA toxicity.However, you can clearly see that there was not a dose dependent decrease in neurotoxicity in this study.Neuroprotection was significantly lower with 1 μM 17β-estradiol than with the much lower dosage of 0.01 μM 17β-estradiol. More is not better with anything in the body.The body has a tightly regulated system in place whereby a certain amount of estrogen is needed for physiologic functions.Too much estrogen without enough androgens can result in cancer development, gynecomastia (gyno), and a myriad of other issues.Too little estrogen and excessive androgens can result in cardiovascular disease, neuronal death, and a myriad of other issues.So, if you are using an androgen without a sufficient amount of opposing estrogen to balance it out, you will not only be inhibiting muscle growth and fat loss, but you will be putting your body in an even more quickly deteriorating state of health than you would have already been in regardless simply as a result of supraphysiological androgen levels.If you are using a TRT dose of testosterone, you would be best served by not unnecessarily inhibiting aromatase.Also, if you are using an anabolic steroid that is not a potent substrate for aromatase, you would be best served by adding a testosterone base or a source of adequate estrogen to your cycle.The interesting thing to evaluate would be whether all of the anabolic steroids previously described by the literature as horrendous for the heart and brain would still be described as such if an adequate dosage of exogenous estrogen was used in conjunction with them in the corresponding studies.It certainly opens the mind up to potential hormone replacement therapy alternatives, hence my experimentation in the past with Trestolone monotherapy, low dose Nandrolone with exogenous estradiol, and SARMs with exogenous estradiol.Related

Kevin Levrone is among professional bodybuilders like Dorian Yates who have opened up about their steroid cycles and dosages.In an interview with Muscular Development Kevin Levrone outlined his first and second steroid cycles with specific details, which gives us great insight into what kind of compounds and dosages he used to build his physique up.Levrone went through only a handful of cycles before he ended up on the Olympia stage.It’s insane to think that within just a couple years of steroid use Kevin was already standing on stage beside Dorian Yates placing 2nd at the 1992 Mr. Olympia.Kevin Levrone story is one of the best examples in history of elite genetic response to steroids.[embedded content]Kevin Levrone’s First Steroid CycleKevin Levrone started his first steroid cycle at 24 years old, six weeks out of his first competition (the 1990 NPC Maryland State Championship).Kevin first steroid cycle was comprised of:During that went from 198 pounds up to 206 pounds six weeks later while simultaneously burning fat.[embedded content]Although we are only able to have a glimpse of what his physique looks like after that first cycle due to the limited number of available photos, we can get a fair idea of the kind of musculature he was displaying at that first show.When it comes to testosterone use (and steroids in general), an increase in fat-free mass doesn’t necessarily mean that the body weight is comprised of only contractile tissue.This is often overlooked and is evidently exaggerated in the clinical data on graded dose response to testosterone in healthy young men.Because of this, we need to speculate a bit on how much weight Kevin actually gained during this first cycle of actual pure muscle.Based on an 8 pound gain, the simultaneous drop in body fat, and Kevin’s body composition he showed on stage at that first show, we can surmise that he probably gained around 10 pounds of muscle during that 6 week cycle.Kevin Levrone’s Second Steroid CycleAfter winning the 1990 NPC Maryland State Championship, Kevin had some time to eat in a calorie surplus and actually have a full off-season before his next pro qualifier show.Kevin’s second steroid cycle is far more indicative of his genetic response to anabolics as his first cycle was only six weeks long and didn’t have as much leniency in regards to his calorie allotment.Kevin’s second steroid cycle was comprised of:That comes to 1700 mg per AAS per week for his second cycle.Despite that being a fairly aggressive second cycle, Kevin claims he has never experienced negative side effects throughout his entire career.This second cycle is what allowed Kevin to pack on 30 pounds of fat-free mass between 1990 and nationals in 1991.Kevin Levrone’s Contest Prep CycleFor contest prep Kevin would add in androgenic hardening agents and let the more water retensive drugs work out of his system.At the start of contest prep Kevin added in four amps of Winstrol per week, split into twice weekly administration (2 amps administered twice per week).Winstrol V came in 50-milligram amps, so his weekly Winstrol dosage was 200 milligrams.At four weeks out, Kevin dropped the Testosterone, Nandrolone and Anadrol.At two weeks out Kevin added in 20 milligrams per day of Halotestin tabs, and would go into shows on Winstrol and Halo only.Between 1990 and 1991, Kevin’s stage weight increased from 206 pounds to 236 pounds.A 10 pound stage weight increase per year I would consider a VERY successful off-season.[embedded content][embedded content]Kevin managed to put on 30 during his first off-season, and found himself on the Olympia stage placing second to Dorian Yates within 2 years of his first steroid cycle.[embedded content]Related

As more and more IFBB pros and past Mr. Olympia winners like Dorian Yates start to open up over social media about their steroid use, we have started to get incredibly detailed insight into things like their genetic response to their first steroid cycle.From a very early age, it was pretty obvious that Dorian Yates was different from the rest and had a hyper-response to training and anabolics.A lot of people look to Dorian Yates as the pinnacle example of “hard work beats talent” and how “genetics aren’t everything”.A bit of delusion has been created stemming from Dorian’s training philosophies whereby many have truly started to believe that you can just grind harder than the next guy in the gym and completely make up for lacklustre genetics.The reality is that Dorian actually has some of the most insane bodybuilding genetics of all time.His biceps were a bit average compared to the rest of him, but other than that there was literally nothing wrong with his genetics at all, and the reason he became Mr. Olympia in the first place was his incredibly superior genetics.This is what Dorian looked like prior to training.Dorian Yates After 6 Months Of Natural TrainingDorian stepped on stage for his first bodybuilding event only 6 months after starting training at 21 years old.This event was at the Temple Hotel across the street from the gym that he worked out at.This is a picture of him posing at that event at the Temple Hotel Birmingham in 1984.According to him, this is after 6 months of natural training.6 MONTHS!He’s already bigger than almost every single person you would see at your local gym who have been training years.After 9 Months of Natural TrainingAfter only 9 months of natural training, Dorian already looked like a bodybuilder and had surpassed 99.9% of the population who has been working out for years.I see guys on gear constantly who look much worse than this that have been cranking for years.This is not something that can be attributed solely to “hard work beats talent”.Dorian Yates’ Progress From His First Steroid CycleMoving forward to 1985, Dorian did his first steroid cycle to prepare for his first official bodybuilding competition, the Novice West Coast (England).This is what he looked like at that first show.At the Novice West Coast Dorian placed first and shortly thereafter went to the World Games in London and placed 7th.This is after his first cycle, which was only 18 months after starting training.Within a year and a half, Dorian had already packed on what appears to be upwards of 40-50 pounds of pure muscle.Dorian Yates’ First Steroid CycleQuoting Dorian from an interview he did on his steroid use, his first cycle was as follows:[embedded content]It was 1985.I was 23 years old and had decided to enter my first competition after a year and a half of training, in which I had made excellent progress.I knew the others who would be competing would be using gear, and I wanted to even the playing field.It was a very deliberate decision that I didn’t take lightly, and I did as much reading as I could first.At 23, I feel I was old enough.At that age, you are fully matured physically, you’ve reached your full adult height, and so on.Even though I hadn’t been training terribly long, I had already managed to develop my physique to a decent level.Looking back, I may have been able to win that contest without using anything.I did one six-week “building” cycle of 20 milligrams of Dianabol a day, which took me from 215 at 5’11” to 235.Those were the most dramatic results I ever saw from steroids.I took six weeks off the gear, then at eight weeks out from my contest I began using 15 milligrams of Anavar per day, as well as one shot of Primobolan a week, which was 200 milligrams.I competed at around 210-215 and won that contest.EFBB [Britain’s equivalent of the NPC] officials were there and convinced me to represent the United Kingdom the following weekend as our heavyweight at the IFBB World Games.I placed seventh, and competed with men like Berry de Mey and Matt Mendenhall, both of whom were the top amateur heavyweights in their respective nations at that time.– Dorian YatesDorian Yates Rate Of Muscle GrowthAt the 1985 show, we see Dorian displaying an insane level of progression relative to what he looked like in the Temple Gym photoshoot in 1984.There’s a reason he became Mr. Olympia in the first place, and anyone who wants to argue that his training intensity, workout split, and training past failure is the reason he made such ridiculous progress is delusional in my opinion.Dorian gained upwards of what looks to be 20-30 pounds of stage weight per year until he won the Olympia.Even on what many would consider baby dosages of gear, he still easily swept high level bodybuilding shows and gained muscle at an incredibly fast rate.You can’t attribute that progress to just “he trained harder than everyone else”.Related

After reviewing the molecular weight of some of the most promising SARMs developed, I theorized that they could potentially be prepared in a topical solution for hair loss prevention.As you probably already know, Selective Androgen Receptor Modulators (SARMs) are a class of androgen receptor ligands that bind to androgen receptors and exert tissue selective anabolic effects with a relative lack of androgenicity when compared to traditional anabolic steroids.The end goal of their continued development is more or less to create the ultimate anabolic agent that can completely offset tissue loss as a result of musculoskeletal degenerative diseases, with a complete absence of androgenic activity in the body.While certain SARMs are closer to reaching this goal than others, the perfect SARM has yet to be developed.However, that doesn’t mean that the SARMs currently developed cannot be leveraged in some capacity for a variety of potential applications.As alternatives to oral SARMs, topical SARMs may be a promising area of research in the fight against hair loss.This article highlights the reasons why I believe there is such therapeutic promise in topical SARMs for hair loss prevention.[embedded content]Table of ContentsRole Of Androgens In Causing Hair LossDespite there being a cascade of events that lead to hair loss, the presence of too many androgens is ultimately what causes follicular miniaturization.However, the effects of exogenous androgens on the human body will inevitably vary between individuals due to several dependant factors in this cascade.As a rule of thumb, raising androgen levels via exogenous androgens will generally initiate or accelerate hair loss for someone who is hair loss prone.Unfortunately, anabolic steroids will unavoidably bring along some degree of concurrent androgenic activity.Our natural endogenously produced steroids are not an exception to this, and the androgen load in the body needs to be addressed in some capacity to attenuate, or even reverse hair loss.Standard Treatments For Hair Loss: Finasteride And DutasterideFinasteride and Dutasteride are medications designed to treat hair loss by inhibiting the enzymatic process responsible for DHT production.This means that they are not anti-androgens that bind to androgen receptors, but rather they prevent the body from converting testosterone into the much more androgenic metabolite dihydrotestosterone (DHT) by inhibiting the enzyme 5-alpha reductase.A 5 mg dose of Finasteride per day will inhibit approximately 70 percent of the body’s systemic DHT, in comparison to 0.5 mg Dutasteride; which inhibits 90 to 99 percent of the body’s systemic DHT.For most individuals, androgenic activity caused by DHT will be minimized after Dutasteride serum concentrations have peaked in the body, as there will simply be barely any DHT left.However, even with a high dose of Dutasteride, scalp DHT levels may not be diminished enough to completely deprive the tissues of DHT, and there is a substantial concurrent spike in scalp testosterone levels as a result of the blockade created at 5-alpha reductase.Not only is there potential for residual scalp DHT, but you if you rely on a 5-alpha reductase inhibitor as a form of hair loss prevention monotherapy you will still have a significant amount of testosterone unaccounted for in your body that still has its own inherent androgenic activity.I’ve posted a video on this before, where I review my over one year long experiment with Dutasteride where I lowered my DHT to undetectable levels and increased my testosterone levels into borderline supraphysiological territory.[embedded content]The inherent androgenicity of testosterone was still substantial enough to progress my androgenic alopecia.In fact, I still had all the characteristics of androgenic activity:facial hair growthbody hair growth (albeit notably reduced, which is to be expected)high libidomorning wood and good erectile qualityhair lossIn contrast to 5-alpha reductase inhibitors, a compound that reduces androgenic activity in the scalp by effectively targeting the androgen receptors would be more efficacious in staving off further hair loss progression.This is what prompted the development of anti-androgens.Transgender Hormone Therapy (Male-To-Female) For Hair Loss PreventionDuring the process of male-to-female gender transitioning, one of the first things doctors would do is prescribe estrogen or an estrogen analog to crush endogenous testosterone levels while increasing feminine hormones.They may also introduce anti-androgens to the protocol to further reduce the amount of androgenic activity in the body.One of the side effects of gender transitioning via anti-androgen and estrogen therapy is significant scalp hair regrowth, and complete reversal in even some of the most extreme cases.In some instances, men with nearly slick bald heads have grown back pre-puberty heads of hair via this kind of protocol.While this is clearly the most extreme method of reversing androgenic alopecia, you can’t argue with the results it produces in individuals who feel the risk/reward is worth it, or simply desire to become more feminine.Certain non-steroidal anti-androgens that interact with androgen receptors are designed to compete with testosterone and DHT for androgen receptor binding, while other steroidal anti-androgens work through slightly different mechanisms, albeit still working around the biological target of endogenous androgens (the androgen receptor).For the sake of not overcomplicating this section with too much scientific jargon, I’m going briefly summarize the pharmacodynamics of the two most commonly used anti-androgens in the hair loss prevention community, and elaborate on how SARMs may stack up to them.BicalutamideBicalutamide is a non-steroidal anti-androgen that is recognized for its affinity to androgen receptors, thus preventing testosterone and DHT from binding and transcribing their effects in tissues.Bicalutamide is a highly selective competitive silent antagonist of the androgen receptor, and is often utilized in androgen deprivation protocols, both clinically and experimentally.A common feature of pure anti-androgens, such as Hydroxyflutamide and Casodex (Bicalutamide), is their relatively weak binding affinity for the androgen receptor, 50–100 times less than that of Testosterone [R].On paper, it doesn’t seem like Bicalutamide would be very effective at preventing hair loss because of its weak binding affinity.However, the typical prescribed dosages of Bicalutamide are high enough that so much of the drug gets into the system that it essentially overpowers testosterone and DHT for androgen receptor binding.The logic behind this protocol is basically that the drug is poor at what it is designed to do, and for it to work it needs to be dosed extremely high until there is just so much of it circulating in the body that it overpowers testosterone and DHT by sheer volume.The half-life of Bicalutamide is 5-10 days as well (depending on single vs. continuous dosing), consequently allowing serum concentrations of the drug to accumulate far more over time.By creating a blockade of the androgen receptor, bicalutamide prevents the negative feedback androgens would normally create via the hypothalamic–pituitary–gonadal axis (HPG axis) in men.As a result of this, luteinizing hormone (LH) spikes in the body as the body recognizes a need to produce more androgens.After LH spikes, the gonads produce more testosterone, and more of that testosterone 5-alpha reduces into DHT, as well as aromatizes into estrogen.150 mg Bicalutamide per day in men has shown to increase testosterone levels by 59-97%, increase estrogen levels by 65-146%, as well as increase DHT, SHBG and prolactin to a less significant degree.This significant spike in estrogen will often lead to estrogenic side effects during Bicalutamide monotherapy.Gynecomastia is a very common occurrence during Bicalutamide monotherapy.Cyproterone AcetateIn contrast to the non-steroidal anti-androgen Bicalutamide, the steroidal anti-androgen Cyproterone acetate works by suppressing testosterone production directly, as well as competing for androgen receptors.Cyproterone acetate is one of the first anti-androgens developed, but it is still one of the most effective to date for hair loss prevention.With that being said, it has also shown to be one of the most side effect ridden compounds used for this purpose.Cyproterone acetate was originally clinically deployed to “treat” hypersexuality and sexual deviation.It was also used to delay precocious puberty.When puberty begins before age 8 in girls and before age 9 in boys, it is considered “precocious puberty”.As cyproterone acetate was used both in full grown men as well as pre-pubescent children, the conflicting findings in its pharmacodynamics have led to differing conclusions on how it works in the body, but for the sake of this article being about full grown men preventing hair loss, we will obviously be evaluating the clinical data on full grown men.Cyproterone acetate causes a prompt drop in LH and FSH levels, and consequently a massive drop in testosterone levels.In a study conducted on healthy male sexual offenders, dosing 50 mg cyproterone acetate twice daily caused testosterone levels to fall to subnormal levels within 1 week [R].Cyproterone acetate has the highest anti-androgenic activity of any other clinically used progestin.Despite it having a fairly weak binding affinity when compared to DHT and testosterone, Cyproterone acetate works similarly to Bicalutamide in that it accumulates during daily dosing because of its 1.6–4.3 day half-life, and also is dosed high enough clinically to increase serum concentrations high enough to a point whereby it can effectively compete for AR via sheer volume.In addition, because Cyproterone acetate significantly reduces testosterone production (and by extension DHT production) via its progestogenic activity, there are less endogenous androgens for Cyproterone acetate to compete with for AR as it accumulates, consequently making it very effective at displacing androgens at AR and inducing systemic anti-androgen activity.Cyproterone Acetate Vs. BicalutamideSteroidal anti-androgens have largely been replaced now by non-steroidal anti-androgens clinically, but cyproterone acetate and spironolactone are still commonly used in the management of feminizing hormone therapy.Cyproterone acetate is more effective at reversing hair loss than Bicalutamide anecdotally, but also comes with a significantly elevated risk profile associated with its use.Maintaining Masculinity Vs. Your HairWhile oral anti-androgens certainly work to reduce androgenic activity in the scalp, they also will often cause a variety of undesired side effects.Aside from the actual health concerns in regards to hepatotoxicity, musculoskeletal degeneration, and more, the main thing we are going to focus on is the effect anti-androgens have on your literal manhood.Expectedly, anti-androgens can cause feminization, loss of libido, erectile dysfunction, as well as muscle and bone loss.Now, like I mentioned, non-steroidal anti-androgens like Bicalutamide are substantially better in this regard, whereby they will not cause musculoskeletal degeneration, will maintain relatively normal sex hormone levels, and do not have many of the drawbacks of steroidal anti-androgens [R].However, that doesn’t mean that they are ideal, as they can still throw off the balance of androgens to estrogens in the body and prevent you from improving your body composition.Anything inhibiting testosterone from binding to androgen receptors in muscle and bone and transcribing anabolic effects will get in the way of your body composition goals at the end of the day.Inhibiting DHT and testosterone from binding to androgen receptors systemically will also impede countless physiologic processes that are facilitated via endogenous androgens in the body.This isn’t a flaw of the drug necessarily, as it is doing exactly what it was designed to do.However, androgen deprivation does not complement most of our goals as men, nor does it complement our health and quality of life.We want androgen deprivation in the scalp only, with no alteration of our systemic hormones or health markers.Obviously this is easier said than done, or else we would already have a topical anti-androgen available that stays localized, has a higher binding affinity than DHT, and has no systemic absorption.This compound does not exist, so we have to make do with our current pharmacology and understanding of pharmacodynamics.Oral Anti-Androgens Vs. Topical Anti-AndrogensMany would question why we don’t just use Cyproterone acetate or Bicalutamide topically to achieve this.The reason why these fall short as topical treatments essentially boils down to the fact that their binding affinity is poor, and their success as anti-androgens is largely achieved via their accumulation in the body systemically.When it comes to topical treatments, we don’t want something with a week long half-life, as it will start to accumulate in the body and cause systemic anti-androgen effects.The ideal compound would be something that has a short half-life, a high binding affinity for androgen receptors, and acts as a highly selective competitive silent antagonist in the scalp exclusively.The closest we have come to this so far is RU58841, with CB-03-01 showing therapeutic promise as well despite having a much lower binding affinity.[embedded content]A compound that does not convert to deleterious metabolites systemically is also advantageous, as there will unavoidably be some level of systemic absorption with any molecule that is small enough to penetrate the stratum corneum after topical application.While current topical anti-androgens commercially available do work for some individuals, there are limitations to each which I have delved into before.There is no perfect treatment at the moment, but in this article I elaborate on something I feel is worth further exploration when it comes to creating a strong localized androgen receptor blockade with as minimal of a systemic impact as possible.How Anti-Androgens Are Related To SARMs For Hair LossAt the end of the day, how does this all intertwine with SARMs?The bodybuilding community, the hair loss prevention community, and the research between them actually intersects in many ways that are commonly overlooked.I first realized the therapeutic promise of SARMs in a hair loss prevention capacity when I saw someone stop their hair loss cold turkey with the SARM S4 and exogenous Estradiol.What many don’t realize is that non-steroidal SARMs like S4 were synthesized using the chemical structure of traditional anti-androgens like Bicalutamide as their backbone.The most promising SARMs exhibit binding affinities several times higher than these anti-androgens, and I feel are an extremely promising area of untapped research for hair loss prevention.Some SARMs at certain dosages have shown to be as anti-androgenic as compounds like Bicalutamide and Hydroxyflutamide, more anti-androgenic than Finasteride, but with the benefit of actual tissue selective anabolic activity in muscle and bone.[embedded content]Basically, some SARMs can prevent hair loss better than Finasteride, as well as traditional anti-androgens, all while allowing supraphysiological muscle growth.The reason this is possible is that most SARMs have much higher binding affinities than traditional anti-androgens and can be far more effective at competing with endogenous androgens for AR binding and activation.In addition, because they are tissue selective, once they bind to androgen receptors, they induce anabolic activity in muscle and bone with a relative lack of androgenicity in other tissues like the prostate and scalp.I detail how this works further in one of my older articles called “Do SARMs Cause Hair Loss? | Can SARMs Prevent Hair Loss“.Oral SARMs also lower SHBG and can have a suppressive effect on endogenous androgen production at high enough dosages (and even low dosages with some SARMs).Through this suppression, SARMs can lower the androgen load in the body even further.With long-term use, certain SARMs may suppress endogenous testosterone production enough that the use of estrogen alongside the SARM becomes a necessity if aromatization is no longer satisfactory to maintain healthy estradiol levels.This presents an interesting scenario whereby androgen levels can be crushed to nearly undetectable levels via a non-steroidal SARM, and the additional negative feedback provided by the exogenous estradiol being added to the protocol to maintain therapeutic estrogen levels.The end result of this is essentially a heavy duty anti-androgen protocol that can maintain significantly more muscle mass than what is possible via traditional androgen deprivation therapy.However, oral SARMs obviously have their limitations as suppression of endogenous androgens is going to result in decreased libido, drive, and overall masculinity.While many who use traditional anti-androgens don’t care about this as they simply want the most efficacious way to nuke their hair loss, there are going to be many individuals who want to minimize the systemic impact of any treatment they deploy to keep their hair.This is where I believe there is therapeutic promise in topical SARMs.Difference Between Topical SARMs For Hair Loss And Topical Anti-AndrogensSARMs and anti-androgens are both effective at inhibiting gene transcription via androgen receptor competition.By competing against endogenous androgens for androgen receptor binding, topical anti-androgens like RU58841 and CB-03-01 are effective at preventing hair loss completely for some individuals with mild hair loss, and moderately effective at providing at least a decent foundation of protection for some individuals with more aggressive hair loss.One limitation of topical anti-androgens is that they work in a dose-dependent manner, but can wreak havoc if they get systemic.As I showed earlier with Bicalutamide, the higher volume of drug present, the more difficult it is for testosterone and DHT to bind to vacant androgen receptors.With anti-androgens its not as simple as increasing the dose until it works though, as topical solutions will go systemic to some extent, and the more drug you introduce to your system, the more anti-androgen activity you will get systemically.For someone with aggressive hair loss, chasing the volume approach with topical anti-androgens to overwhelm the endogenous androgens present in the scalp may lead to significant systemic side effects before adequate androgen receptor competition to prevent hair loss is even achieved.SARMs on the other hand will have a negligible impact on endogenous androgen production when trickling into the system in trace amounts, and will not induce anti-androgen activity in muscle and bone even if a substantial amount of it does get into the bloodstream.SARMsAnti-AndrogensComparable Binding Affinity To Testosterone For Androgen ReceptorsSOMESOMETranscription Of Anabolic AffectsYESNOTranscription Of Androgenic AffectsMINIMIZEDNOSide Effects To Systemic IntroductionMINORMAJORHow SARMs May Complement Finasteride Or DutasterideAs DHT has a binding affinity higher than all SARMs, and significantly higher than all anti-androgens, if sufficient AR competition could not be achieved locally via a SARM or anti-androgen to stave off androgenic alopecia, then a 5-alpha reductase inhibitor could then be looked at as a potential adjunct treatment to use concurrently.By dropping systemic DHT levels via 5-alpha reductase inhibition, competing for AR becomes significantly easier for us as we have compounds at our disposal that are actually comparable to testosterone in binding affinity.The 500 Dalton Rule For The Skin Penetration Of Chemical Compounds And DrugsThe molecular weight of a compound must be under 500 Dalton to allow skin absorption [R].Larger molecules cannot pass the corneal layer.The Dalton is used as a unit of molar mass, especially in biochemistry.1 Da (dalton) = 1 g/mol.The Most Promising SARMs For Hair Loss PreventionTaking S4 (Andarine) as an example, you can see that the molecular weight is 441.4 g/mol [R].Because S4 has a molecular weight of 441.4 daltons, it can pass the corneal layer and work to some extent topically.I’m using S4 as an example simply because it seems to be the most hair safe SARM of all to date via oral administration, and is also the only SARM I have seen used topically so far.It is also the only SARM I’ve seen used orally in conjunction with exogenous estradiol for over a year straight so far with great success and no notable deleterious effects to liver enzymes or other health markers that are commonly impaired with high dosages of oral SARMs.With that being said, S4 isn’t without its potential issues itself.SARMs are still uncharted waters, but there are several that have been well tolerated in a clinical setting at dosages several times higher than what we would be using for hair loss prevention, or even for muscle growth in a bodybuilding context in a few token scenarios.While S4 has shown to be the most promising SARM in a hair loss prevention context to date, I am confident that other alternatives with improved binding affinities, high tissue selectivity, and high tolerability clinically in actual human subjects would likely result in similar positive outcomes if the dosing was nailed down.For example, LGD-4033 has a molecular weight of 338.25 daltons and has shown to be well tolerated in humans at dosages as high as 22 mg per day orally [R].It has also binds to the androgen receptor with an extremely high affinity (Ki of ~1 nM), which is superior to every other SARM tested on humans with comparable tissue selectivity.In addition, a preclinical rodent model showed that it has greater than 500-fold selectivity of muscle tissue to prostate when compared to testosterone.LGD-4033 Selectivity For Muscle To Prostate Compared To TestosteroneA greater than 500:1 anabolic to androgenic selectivity would make LGD-4033 the most tissue selective SARM to date.However, in practical application, LGD-4033 seems several times more androgenic than S4, although it is also several times more anabolic milligram for milligram.Some individuals even report hair loss with LGD-4033 use.Context is key here though, as the individuals reporting hair loss are using dosages 10x higher than the dosage being evaluated in humans clinically, and it is not clear whether this is telogen effluvium or actual androgenic alopecia progression even in these mega-dosing cases.This is what I mean by the dosing needs to be nailed down with these compounds, as haphazard overdosing could easily lead to unexpected androgenic activity, or induce telogen effluvium via a significant shift in endogenous hormones.There is no SARM that is completely devoid of androgenic activity, so dose response needs to be carefully assessed when experimentation is done with these compounds.Anabolism as a Systemic Effect of Topical SARMs for Hair LossOne of the limitations of anti-androgens is that when they go systemic they can induce anti-androgenic activity in other tissues.SARMs on the other hand bind to androgen receptors and induce tissue selective anabolic activity.So, the theory here is that we can potentially use a lower dose of a SARM topically than we would need with an anti-androgen, and achieve a substantial anti-androgenic effect via a much lower dosage, and even if it were to go systemic to some extent, then the worst that happens is we get some anabolic activity in muscle and bone.In theory, it sounds great, but SARMs will still suppress endogenous androgen production to some extent, lower SHBG, and potentially induce some hepatic stress when systemic.However, the degree to which this occurs should be much lower than what occurs with traditional anti-androgens.This is all theoretical at the end of the day, as SARMs may not even compete for AR activation in the scalp.However, anecdotally via oral administration it seems fairly obvious that they do in all tissues in the body, despite having “selective” action.If a topical anti-androgen works, then a topical SARM should work in a similar way.SARMs are essentially just chemically modified anti-androgens with better binding affinity and anabolic activity after all.Efficacy Profile Of Topical SARMs For Men Wanting To Retain MasculinityFor many men, hair is a huge part of their identity and plays a massive role in looking good.Unfortunately, we’ve been put in a position biologically where the more androgens in our body, the more expedited our hair loss progression will be, and all effective anabolic agents have some level of androgenicity.So, in a perfect world, we would be able to utilize SARMs (or something like SARMs) to selectively occupy androgen receptors in the scalp, and leave the rest of the body alone.Topical SARMs For Hair Loss Prevention: A Viable Long-term Strategy?While SARMs are still very new, there are already SARMs with comparable binding affinities to testosterone that have shown to have no virilizing effects in women at fairly high dosages orally.Topically, we may be able to achieve more localized action on androgen receptors and minimize the systemic impact in the body.I believe there are better ways to manage hair loss than blindly crushing androgen levels with primitive medications.SARMs may or may not be the answer, but they are certainly a step forward and could very likely be used effectively as a form of monotherapy in some users, or as an adjunct treatment alongside tried and true compounds that do a significant amount of the heavy lifting, and then let a SARM clean up the mess leftover.Are SARMs perfect?No, they aren’t.However, some of the SARMs currently developed may already have more therapeutic promise for some individuals than traditional anti-androgens used for hair loss prevention.At the very least, they are worth exploring more in this context, and I believe are potentially a more progressive way to go about handling excessive androgenic activity via AR activation in the scalp.In addition, injectable SARMs are a new area I’m researching that may also have therapeutic promise as well.How To Create A Topical SARMThe ideal scenario would be that we mix a SARM into a topical solution that has shown to not only be very tissue selective with a high binding affinity, but has also shown to be well-tolerated in humans in a clinical setting with no deleterious outcomes, and then apply that solution topically to bind locally to androgen receptors and compete with testosterone and DHT for AR activation.Standard vehicles (the carrier solution you mix the compound in for topical application) should work similarly to anti-androgens.My guess is that a 70% ethanol/30% propylene glycol vehicle would suffice.A PEG 400 mixture may be a useful alternative vehicle for those with intolerance to propylene glycol, or those with vehicle-dependent contact allergy to SARMs in either propylene or hexylene glycol [R].Adding a bit of DMSO or daily microneedling with a short length pretreatment may need to be incorporated for absorption for those with less permeable skin.What concentration the solution should be remains up in the air and will need to be determined via experimentation.Following the dosage outlines used in a therapeutic setting, we can get a well-tolerated starting point.For example, with LGD-4033, orally it has a tissue selective anabolic effect at dosages as low as 0.1 mg per day, and has shown to be well-tolerated as high as 22 mg per day.The most notable clinical trial on LGD-4033 utilized 0.5 mg, 1 mg and 2 mg orally for 12 weeks.LGD-4033 exhibited encouraging safety and tolerability, and there were no drug-related serious adverse events in the study [R].A good starting point would be 0.5 mg LGD-4033 per day topically, with the dosage titrated up accordingly based on dose-response.The only SARM I’ve seen used topically to date is S4.As S4 does not have any human data, we had to design the protocol based around anecdotal findings and extrapolated clinical data on rodent models.Anecdotally, orally administered S4 does not induce night vision side effects until around 30-50 mg per day.A topically administered dosage of 25 mg per day produced a very quick reduction in sebum in the scalp, which is a very obvious marker of reduced androgenic activity.Scalp itch was also severely decreased, with no notable side effects.Notably, the individual who I oversaw who did this experiment gets horrible side effects from every single hair loss prevention compound he has tried.He’s one of the unfortunate ones who gets brutal 5-alpha reductase inhibitor side effects, systemic anti-androgen side effects with topical anti-androgen use, and even severely impaired sleep with PGD2 inhibitors.The fact that he had no issues with topical S4 was very promising, and piqued my interest in the area even more (which is partially what has led me to my current injectable SARMs experiment I am conducting on myself).Does that mean this is a viable long-term strategy?That remains to be seen with further experimentation.To be clear, this is still a theoretical approach to topical hair loss prevention, and is geared mostly towards individuals who have experienced negative side effects with 5-alpha reductase inhibitors, RU58841 and CB-03-01.Where To Buy SARMsMost companies do not third party test their products, nor do they have any satisfactory level of quality control whatsoever.I strongly advise that before you buy SARMs from a company online you thoroughly evaluate their track record, their third party test results, and how they are marketing their products in general.These Are My Current Trusted/Go To Companies For Third Party Tested 99%+ Pure SARMs:Science.bio – 10% off coupon code “DC10”Chemyo – 10% off coupon code “DC10”Amino Asylum – 20% off coupon code “DC20”Swiss Chems – 25% off coupon code “DC25”Disclaimer: The information included in this article is intended for entertainment and informational purposes only. It is not intended nor implied to be a substitute for professional medical advice. Prior to buying anything, check that it is compliant where you live with your current government laws.Related

There’s a misconception that Finasteride is a reliable source of remedy for hair loss prevention caused by the intake of all anabolic steroids.For anyone who has reviewed the downstream mechanisms of Finasteride in the body, it is clear that this is not true.Below are the details to a realistic set of expectations from Finasteride use with anabolic steroids.[embedded content]Table of ContentsNot All Steroids Convert to DHT via 5-Alpha ReductaseAn assumption that must be ruled out is the idea that dihydrotestosterone (DHT) will always be the by-product of metabolic reactions between 5-alpha reductase and an anabolic steroid.5-alpha reductase is an enzyme involved in steroid metabolism that can create androgenic metabolites (e.g. DHT) via a process called “5-alpha reduction”.While several studies indeed support the idea that DHT is an influencer for hair-loss and that anabolic steroids all have a certain tendency to interact with 5-alpha reductase, most of the steroids used for bodybuilding and powerlifting are not potent substrates for 5-alpha reductase, if they interact at all.Testosterone is the only anabolic steroid that is converted to DHT via 5-alpha reductase, which is contrary to the common misconception that all other anabolic steroids would also be converted to DHT.Other steroids that are substrates for 5-alpha reductase are converted to unique metabolites with their own individual anabolic and androgenic potency.For example, Boldenone (Equipoise) can be converted to dihydroboldenone (DHB) via 5-alpha reductase.Nandrolone can be converted to dihydronandrolone (DHN) via 5-alpha reductase.The two metabolites DHB and DHN each have their own unique anabolic and androgenic potency and will not be equal to one another, nor will they be equal to DHT.Testosterone vs. Other Anabolic Steroids as a Catalyst for Hair LossExcessive intake of testosterone can definitely result in an increased susceptibility to hair loss due to its interaction with 5-alpha reductase to produce DHT, as well as via its inherent anabolic activity, albeit to a much lesser extent.Meanwhile, certain synthetic anabolic steroids such as Primobolanare designed to maximize the anabolic activity in the body with a lower incidence of androgenic activity and do not interact with 5-alpha reductase at all. However, just because a steroid does not interact with 5-alpha reductase that does not mean that the parent hormone is hair safe whatsoever.There are several other steroids that do not interact with 5-alpha reductase that will still cause hair loss.The overarching concept that needs to be remembered is that all steroids have their own individual level of anabolism and androgenicity in tissues.Regardless if a steroid is a 5-alpha reduced metabolite, or a parent hormone, they are all still steroids at the end of the day with their own anabolic and androgenic impact on affected tissues in the body, and they need to all be accounted for.Anabolic Steroid Interaction With 5-Alpha ReductaseFinasteride is essentially a downstream androgen synthesis inhibitor.This particular medication reduces the formation of the potent androgen, dihydrotestosterone (DHT), from its precursor testosterone by successfully inhibiting the 5-alpha reductase enzyme.Since DHT is several times more androgenic than testosterone, this would significantly decrease the amount of androgenic influence on the body.An important aspect to take into consideration is that the parent hormones themselves are inherently androgenic to a significant extent.In fact, with some steroids, the metabolites could be far less androgenic than the parent hormone, in which case 5-alpha reduction could actually be more hair loss sparing.[embedded content]Nandrolone is an example of this, where the parent hormone (nandrolone) is more androgenic than its metabolite produced via 5-alpha reduction (DHN); subsequently making concurrent Finasteride use an accelerant of androgenic alopecia.Finasteride Only Prevents DHT Derived Hair LossTo sum up, Finasteride may meaningfully prevent hair loss only if the cause is due to excess DHT.This is because DHT is more several times more androgenic than testosterone.DHT exhibits such poor anabolic tissue selectivity that it is one of the few steroids that actually features an androgenic rating several times higher than its anabolic rating.In short, DHT sucks at building muscle.In a study conducted to determine whether the intake of Dutasteride would affect muscle mass accrual, those treated with the medication had similar results to the untreated control group; meaning that the decreased DHT level had no significant anabolic impact on muscle growth.Even by nearly wiping out the participants’ DHT levels with Dutasteride, they did not experience hindered muscle growth at all in response to graded testosterone doses [R].In fact, an argument can be made that inhibiting 5-alpha reductase can mediate supraphysiological muscle growth due to a higher ratio of testosterone to DHT.This is apparent in pseudohermaphrodites who are inherently 5-alpha reductase-deficient due to genetic mutations [R].In this particular study involving brothers with different DHT levels, the male with 5-alpha reductase deficiency experienced reduced sexual development throughout puberty, but also gained more muscle mass than his brother.In the image below, the man on the left has a 5-alpha reductase deficiency, and his brother on the right doesn’t have a deficiency.The man on the left has a higher testosterone level, is more muscular, and has less androgenic alopecia than his brother on the right who has normal DHT levels.The Steroids Finasteride Or Dutasteride Can Protect Your Hair FromFinasteride and Dutasteride do not occupy or inhibit androgen receptors, but rather they inhibit the 5-alpha reductase enzyme primarily responsible for converting testosterone to DHT.These medications are extremely effective at reducing DHT levels, hence why natural athletes and those on mild doses of exogenous testosterone typically experience the attenuation of hair loss progression with it, or at least some degree of slow down (dependent on the individual’s androgen receptor density, sensitivity, residual DHT levels, free testosterone levels, and a myriad of other less relevant factors).Those who blast Trenbolone, or any other anabolic steroid, will not be protected from the androgenic activity of those hormones on the scalp.It is essential to thoroughly understand the mechanism of action of everything going into your body prior to haphazardly popping pills in attempts to blindly remedy a side effect like hair loss, as you may be wasting your time, or even potentially make the situation worse.Related