Anabolic steroid

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A vial of pharmaceutical grade testosterone cypionate, one of the most commonly used anabolic steroids.

Anabolic-androgenic steroids (AAS), commonly called steroids or just roids include endogenous (naturally produced by the body), exogenous (of external origin) and synthetic chemicals able to increase muscle and bone mass. These chemicals are responsible for the maintenance and development of several important metabolic processes (in both sexes) and the development of sexually dimorphic secondary sexual characteristics in males.

The administration of supraphysiological amounts (far above what can be produced naturally by the body) of AAS has been proven to greatly increase both the speed and total possible rate and amount of lean tissue growth and recovery from strenuous training; as such, they are often used by athletes, bodybuilders, and security and military personnel to attain these positive effects despite the potential for adverse side effects and their illegal status in many jurisdictions.

Many individuals in the looksmaxxing community also use and advocate using AAS as a looksmaxxing aid. The use of these substances for cosmetic (or other) purposes is also fairly common in the general public, though varying quite a bit by socioeconomic status, gender, age, race, mental health and (potentially) relationship status.[1][2] AAS usage seems particularly common among male users of online dating apps.[3]

Potential positive effects[edit | edit source]

  • Lean muscle tissue growth and non-muscle tissue growth (water retention, which visually increases the muscle's size and improves strength).
  • Enhanced strength and muscular endurance.
  • Increased cardiovascular endurance.
  • Deeper, more masculine voice (in rare instances).
  • Increased libido and erectile potency.
  • Increased focus, aggression and drive (anecdotal report of some users).
  • In what could be viewed as a positive or negative effect based on one's circumstances, a long enough AAS usage also results in nearly complete infertility in most men. This is typically reversible after several months of ceasing AAS usage. Some men appear more resilient to this effect, as they require concomitant administration of progestins for this effect to be apparent (though these doses are much lower than what is typical for recreational steroid users).[4]
  • Permanent slight increase in natural muscle growth cap observed in some users long after administration is discontinued. Likely due to the positive effects of AAS on the number of myonuclei in muscle tissue, which endure for long periods (perhaps permanently) and aid muscle growth and recovery.[5]

Potential negative effects[edit | edit source]

  • Acne.
  • Accelerated male-pattern baldness among those genetically prone to experiencing this.
  • Body hair growth.
  • Mood-swings and depression.
  • Increased blood pressure.
  • Liver toxicity (most pronounced among 17α-alkylated AAS. This includes the majority of orally administered AAS, apart from oxandrolone, which, despite being a 17α-alkylated AAS, is somewhat milder in this regard, potentially due to differences in this drug's metabolism compared to others of its class).[6]
  • Gynecomastia (breast tissue growth, which can be permanent if not swiftly treated).
  • Natural testosterone suppression. In extreme and rare cases this can apparently result in permanent shutdown of the HPTA axis, thus resulting in AAS induced hypogonadism. This typically necessitatates the permanent use of exogenous hormones to mitigate the symptoms of low testosterone levels.
  • Increased risk of cardiovascular failure, especially when used in high amounts and over the long term. Likely attributable to the increase in hematocrit levels that follow prolonged AAS usage (thus thickening the blood and increasing the risk of cardiac infractions) and possibly due to the negative effects AAS have on levels of arterial plaque.
  • Potentially negative neurological changes with long term and/or abusive use (observational research only).[7]
  • Potential for physiological addiction, due to the administration of AAS having the potential to alter the brains endogenous dopaminergic reward system, in a similar fashion to the process of addiction to other illicit substances (rodent studies only).[8]

Side effect prevention[edit | edit source]

Androgenic side-effects[edit | edit source]

Anabolic steroid users commonly take 5-α-reductase inhibitors such as finasteride or dutasteride to prevent hair loss (this will only be effective in the case of androgens that are converted via 5-α reductase to DHT, such as testosterone). It is important to note that this will not work in users who are particularly sensitive to the hair-loss related effects of androgens, as even weak androgens can still exert some direct negative effect on the hair growth cycle among these individuals. Topical compounds such as minoxidil (Rogaine) are also used in less severe cases.

In case the testosterone user experiences acne as a side effect, they may utilize topical anti-acne treatments such as retinoids (substances derived from, or chemically related to vitamin A), benzoyl peroxide, or they can take oral retinoids such as isotretinoin in the most severe cases (as these drugs can have harsh side effects).

Estrogenic/progesteronic side effects[edit | edit source]

As many AAS exhibit the potential to be aromatized by the enzyme aromatase into estrogen (or other related compounds), the concurrent administration of drugs with anti-estrogen properties is pursued by those sensitive to the sometimes negative effects of elevated levels of these hormones. It is important to note that these ancillary drugs themselves often exhibit the potential to cause adverse side effects.[9][10] There is some mechanistic evidence that some AAS (such as oxymetholone or trenbolone) can directly act on the estrogen receptor (ER) or the progesterone receptor (PR) by themselves, thus leading to the potential to induce these kinds of side effects in sensitive individuals, without elevated systematic levels of estrogens or progestins being at play directly. Therefore, the choice of AAS naturally influences what ancillary drugs users select in the attempt of ameliorating these unwanted side effects.

Aromatase inhibitors (AIs) or selective-estrogen receptor modulators (SERMS) are commonly used to prevent gynecomastia (breast tissue growth) during the cycle. Many users prefer the latter class of drugs as these substances are selective in how they affect the utilization of estrogen by the body, preserving some of the positive effects of estrogen (such as on mood, libido and bone tissue) while inhibiting the agonism of the estrogen receptors in the breast tissue by the hormone, thus preventing gynecomastia in many cases. Aromatase inhibitors strongly inhibit the bodies' production of estrogen and are thus generally recommended by users only in emergencies related to estrogenic side-effects, to have 'on hand' as needed.

It is also important to note that, in some cases, gynecomastia can occur in some sensitive individuals even when levels of estrogens are controlled, likely owing to the ability of some AAS (most notably nandrolone and trenbolone) to act as agonists of the progesterone receptor (PR), which is theorized to potentiate the effects of estrogen in the breast tissue. In these cases, AI usage alone would not suffice to control gynecomastia, and SERM usage may be necessary to block estrogen's local effects on the breast tissue. It has been found that progesterone and estrogen stimulate the production of IGF-1 (insulin-like growth factor 1) and that IGF-1 interacts with compounds that have estrogenic and progesteronic effects in mediating breast growth. Progesteronic compounds may also have direct stimulatory effects on the breast tissue, mainly via stimulating alveolar (breast tissue ducts) development.[11] Thus, individuals who are very sensitive to developing gynecomastia often limit their use of highly progesteronic and estrogenic compounds or avoid them altogether.

Some users that are sensitive to estrogen-related side-effects of AAS also forgo the usage of SERMS or AIs during the cycle and instead utilize lighter aromatizable compounds together with the AAS drostanolone (commonly referred to by the tradename for drostanolone propionate, Masteron), which does not aromatize to estrogen and also seems to exhibit some peculiar inhibitory effects on the growth of breast tissue that may be unique to this specific AAS.[12] The drug was previously administered to female breast cancer patients before the development of therapies that presented no risk of virilization related side-effects (hence the brand name's reference to breasts, the -mast prefix) namely AIs and SERMs.

Some steroids such as trenbolone, oxandrolone, stanozolol and metenolone enanthate (Primobolan) are not acted upon by the enzyme aromatase and therefore often do not require the administration of agents such as SERMs or aromatase inhibitors to negate any potential estrogenic or progestational effects (though the latter has been reported anecdotally among some users of trenbolone, and trenbolone indeed exhibits a high affinity for the progesterone receptor). However, suppose these substances are taken without aromatizing steroids. In that case, this will result in low or non-existent estrogen levels, which can often lead to several highly unpleasant side effects.

In some cases, these side effects are deliberately endured by users, such as when a pre-contest bodybuilder limits his anabolic steroid usage to these compounds for them to exert a 'hardening' effect on the muscles and increase muscular definition (due to the more exclusive lean tissue promoting effects of these steroids due to the lack of water retention experienced when taking them compared to more estrogenic/progesteronic substances).

General side effects[edit | edit source]

Sylimarine (milk thistle), TUDCA (tauroursodeoxycholic acid… ), NAC (N-acetyl cysteine) and other hepatoprotective compounds are often used in an attempt to prevent the potential for liver damage owing to the use of certain types of hepatotoxic AAS (though it is unclear how effective this is in the long term, many chronic users strictly limit their usage of liver toxic 17α-alkylated oral steroids due to this reason or restrict their usage to more mild compounds such as oxandrolone).

In terms of mitigating the potentially negative long-term effects on the cardiovascular system possibly associated with chronic AAS usage,[13] it is likely that only harm-reduction practices such as limiting one's usage to less harsh substances such as testosterone, nandrolone decanoate, and Primobolan and limiting the dosages of these substances would prove efficacious in the long term here. Following a regular program of cardiovascular exercise, eating a whole-food-based diet that excludes hydrogenated oils, added sugar, and ceasing any other activities that are risk-factors for cardiovascular disease, such as smoking, would likely be recommended. The supplementation of ω-3 fatty acids (fish oil) and garlic (and other substances that improve endothelial function in general) may also aid in maintaining healthy cardiovascular function, though evidence for this not overly robust.[14][15]

As the administration of even modest amounts of exogenous AAS is enough to cause substantial or total suppression of endogenous testosterone in most men, it is considered necessary by most users to implement PCT (post cycle therapy) after the completion of a steroid 'cycle' to reestablish the endogenous production of testosterone, as without this therapy, it takes a long-time for the HPT axis (hypothalamic–pituitary–thyroid axis) to recover from the negative feedback induced suppression of the gonadal function induced by the prolonged administration of AAS, leaving one prone to the negative effects of hypogonadism (low T). To this purpose, SERMS and HCG (human chorionic gonadotropin) are commonly administered to restore/maintain reproductive ability and the general function of the gonads during/after a steroid cycle (the latter is typically used as an adjunct, the former sometimes as monotherapy or, more commonly, using a combination of different SERMS).

Steroid usage among male population[edit | edit source]

According to an online survey on a sample of American online dating users, 36.4% of male users reporting using steroids, as opposed to only 3.8% of non-online dating men who reported AAS use.[16] This suggests that due to the highly competitive nature of online dating for men, men are being driven to increasingly extreme measures to improve their looks in order to compete. Steroid usage is widespread in PSL community because users often consider a lean muscular body a key to attract women.

Anabolic vs androgenic steroids[edit | edit source]

The term anabolic refers to the so-called "anabolic ratio" of the various androgenic substances. Substances developed for medical use were specially designed to have less androgenic activity on tissues such as the scalp, the prostrate, the skin and so forth, and greater androgenic activity on the muscle cells. The idea was that this would reduce the harsh side-effects many abusers of the newly-developed injectable testosterone were experiencing, such as members of the American Olympic weight lifting team at the time, via the development of synthetic alternatives that would be more targeting in terms of maximizing the anabolic effects of the drugs on the skeletal muscle tissue and minimizing the (often) adverse effects that resulted from these drugs agonism of the androgen receptor in other bodily tissues.

The ratio of the androgenic to anabolic effects of these new drugs was typically tested by administering AAS to castrated rodents (though primates were used in some studies). The resulting tissue growth was them compared by examining the levator ani muscle (thought to be representative of the effects of these compounds on the skeletal muscle tissue) vs. reproductive system tissues such as the seminal vesicles, and comparing this growth to that produced by the administration of testosterone, the reference compound.

From this method, a ratio of anabolic/androgenic effects vs testosterone was derived for many androgens. However, this procedure has been criticized as lacking scientific rigor due to the dissimilarity between the supposed levator ani muscle targeted in rat studies as compared to the human counterpart to the muscle. The levator ani was likely not the ideal muscle to utilize for this purpose. It is part of the rodent reproductive system and is thus not strictly homologous with skeletal muscle tissue in other mammals, such as humans. In fact, it was subsequently 'discovered' that this muscle is completely different to the levator ani in humans, with this muscle being properly named the dorsal bulbocavernosus, a muscle unique to rodents. This finding led to claims that this method of determining the relative anabolic/androgenic effects of the various AAS was completely useless, with it being asserted to data was lacking in regards to whether the hypertrophy of this muscle was strongly correlated with global nitrogen retention at all.[17]

However, there is biochemical evidence that the levator ani muscle does exhibit several characteristics that make it similar to skeletal muscle tissue for this purpose; for example, it has been discovered that the androgen receptor density in rodent prostate tissues is many times greater than in this muscle and that 5α-reductase activity (the compound that converts testosterone to DHT and is thus primarily responsible for the expression of male secondary sexual characteristics) is much lower in the levator ani as compared to the prostatic tissue of rodents, thus making the levator ani muscles similar to the skeletal muscle tissue in these regards, and therefore likely a decent proxy for skeletal muscle tissue.[18]

Another major issue with these studies is that many of them were quite brief (for reasons of expediency). The subjects were sacrificed well before the differential effects of AAS on the body's various tissues were fully apparent. As some androgens produce their androgenic effects on reproductive tissues such as the seminal vesicles more slowly than they do on the skeletal muscles, this may have lead to the anabolic/androgenic ratios of several of these compounds being distorted in favor of overstating anabolic effects and understating androgenic effects that may be more pronounced with prolonged usages.

This would mean that some of these compounds' low androgenic ratios would tend to understate their risk of producing the side-effects often associated with greater androgenicity, such as hair loss, prostate enlargement, acne and possibly aggression and mood swings.

It is important to note that even so-called 'anabolic steroids' can still exert strong androgenic effects (and therefore lead to the side effects associated with AAS use) in high enough doses or in those who are especially sensitive to their effects. The long quest of chemists (mainly driven by the desire to create AAS that could be safely administered to women and children) to completely disassociate the anabolic and androgen effects of synthetic AAS failed, with the research in this area now moving toward SARMs, which appear to have the promise of achieving the goal of substantial disassociation between these effects.

It is also important to note that not all androgenic effects are undesirable. The androgenic actions of AAS are needed to maintain a healthy libido, a stable mood, and other desirable effects. It is also commonly anecdotally asserted by many AAS users that cycles that only utilize relatively weak androgens tend to be less productive in terms of muscle growth as compared to those that use or add compounds with stronger androgenic effects. What substances a user utilizes tends to be driven by their goals, tolerance for side effects, and sensitivity to the side effects of AAS use, with those prone to experiencing strong androgen-related side-effects (such as acne and hair-loss) tending to avoid strong androgenic substances and those with a sensitivity to estrogenic side effects (such as gynecomastia and harsh water retention) avoiding the particularly estrogenic substances and so forth.

The following is a table listing the androgenic/anabolic ratios of various AAS, as derived from early animal studies (largely conducted on castrated rodents) that attempted to approximate the varying targeted effects of these compounds on the skeletal muscle tissue as compared to the reproductive tissues (used as a proxy of androgenic activity elsewhere in the body), using the methodology described above:

Anabolic/androgenic ratios for commonly used AAS. Sources: Llewellyn (2017) & Potts et al. (1976).
Ratios are in comparison to the reference compound, either testosterone propionate, oral testosterone (17α-MET) or a combination of the two.
Ranges are generally approximate, and averages of different studies were used in cases that exhibited a large amount of variance per sample.
Also included are the rough levels of estrogenic/progesteronic activity of these compounds.
Compound Anabolic ratio Androgenic ratio Estrogenic activity Progesteronic activity
Testosterone (reference) 1 1 Moderate Low
Methandrostenolone (Dianabol) 2-3 .6 Moderate to high
Very low
Nandrolone decanoate 3.29-4.29 .31-.41 Low High
Trenbolone acetate 5 5 None High
Oxymetholone (Anadrol) 3-4 .6 High (disputed) Low (disputed)
Stanozolol 2-3 .3 None Low
Drostanolone propionate (Masteron) .62-1.3
.25-.45 None No reliable data but likely low
Oxandrolone (Anavar) 3.2 .24 None Very low to none
Methenolone (Primobolan) .88 .44-.57 None No reliable data but likely low
Boldenone undecylenate (Equipoise) 1 .5 Low Low

Non-steroid anabolic agents[edit | edit source]

Some substances like SARMs (selective androgen receptor modulators), such as LGD-4033, RAD 140 and Ostarine, have been theorized to exert similar effects to anabolic steroids in the scientific literature. However, clinical reports and anecdotal accounts from users of these mainly untested substances indicates the anabolic effects of the current generations of these substances is typically much more modest,[19] at least compared to the administration of the more potent anabolics such as trenbolone, testosterone and oxymetholone. These substances are treated as PEDS (performance-enhancing drugs) by most international sports doping regulatory bodies, with penalties to the athlete when use is discovered being analogous to the penalties that exist for the use of AAS (anabolic-androgenic steroids).[20]

The long-term effects of these novel substances' administration are also understudied, with properly conducted and large scale clinical trials investigating these substances being severely lacking. This is true for many synthetic anabolic steroids also (though not for testosterone, at least in modest doses, and AAS that are still common in clinical use, such as nandrolone decanoate and oxymetholone), many of which were (such as the various varieties of trenbolone, a very popular anabolic steroid among recreation steroid users and athletes due to its potency and dramatic effects of muscle gain and overall body composition) not developed or intended for human use. However, it is important to note that many of these substances have been tested on humans throughout several clinical trials and have previously been approved by regulatory bodies such as the FDA in the United States for medical use in human patients, which is not true for any SARM as of 2021.

Several anabolic agents are not steroids or do not mimic the actions of steroids on the androgen receptor (what SARMs do) such as Cardarine (a PPARδ receptor agonist, often incorrectly labelled a SARM). This research chemical was abandoned by its manufacturer after experiments found that extreme doses of the substance are often carcinogenic in rats.[21]

Insulin, IGF-1 (insulin-like growth factor 1), and HGH (human growth hormone) and its several analogues also have anabolic effects, but don't have a steroidal chemical structure. This different mechanism of effect can give them a synergistic effect with AAS, and it is not uncommon for bodybuilders to administer these substances concurrently with AAS. Clenbuterol, a bronchodilator originally developed to treat asthma, can also exhibit weak to moderate anabolic effects and fat loss promoting properties, together with the more commonly used bronchodilator salbutamol (Ventolin). The anabolic effects of these drugs appear to be mediated by their agonism of the β2-adrenergic receptors of the muscle cells and seem modest in effect based on the results of limited human trials.[22]

Chads[edit | edit source]

Chads have been known to use steroids. It isn't uncommon for popular celebrities to have used heavy and copious amounts to attain physically aesthetic and muscular bodies and appearances. Many notable celebrities such as Ryan Reynolds, Zac Efron, Hugh Jackman, Vin Diesel, Henry Cavil and Tom Hardy have been accused of using anabolic steroids at some stage of their career. Several male video game characters, such as Duke Nukem, have physiques that are impossible to approximate in reality without the use of copious amounts of anabolic substances.

Many of the celebrities listed above have muscular bodies that otherwise would be difficult to achieve without the use of steroids, especially when one considers the amount of lean mass they often gain in short periods to fulfill the requirements of a certain role.

One major indicator of steroid use is when an individual (especially a previously trained one) has a suspiciously large jump in lean mass gains over a narrow window of time (nearly impossible to achieve in natural individuals due to the typical rate of lean mass growth, unless one is recovering from prolonged periods of calorie restriction, which can result in some 'rebound' gains).[23] Very dramatic 'body transformations' such as these are not uncommon in Hollywood. Other indicators include disproportionate development of the deltoids, neck and trapezius muscles, as these muscles exhibit greater androgen receptor density than the other upper body muscles, and thus they are particularly sensitive to the effects of anabolic steroids.

An individual's FFMI (fat-free mass index, or their overall amount of lean body mass in relation to their height) is also an indicator, especially at extremes, however it is important to note that there is significant overlap in FFMI between natural and AAS using athletes,[24] and thus there is no easy threshold of lean mass at which is it possible to ascertain 100% whether or not a person has used steroids, apart from obvious extremes.

References[edit | edit source]

  1. https://onlinelibrary.wiley.com/doi/abs/10.1046/j.1365-2605.1997.d01-285.x
  2. https://www.sciencedirect.com/science/article/abs/pii/S0306987716302158
  3. https://jeatdisord.biomedcentral.com/articles/10.1186/s40337-019-0244-4#Sec10
  4. https://www.ncbi.nlm.nih.gov/pubmed/15266528
  5. https://www.sciencedaily.com/releases/2019/01/190125084106.htm
  6. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1959346/
  7. https://onlinelibrary.wiley.com/doi/full/10.1111/add.14629
  8. https://pubmed.ncbi.nlm.nih.gov/32873724/
  9. https://www.breastcancer.org/treatment/hormonal/serms
  10. https://www.accessdata.fda.gov/drugsatfda_docs/label/2011/020541s026lbl.pdf
  11. https://www.ncbi.nlm.nih.gov/books/NBK279105/
  12. https://europepmc.org/article/med/576855
  13. https://doi.org/10.1016/j.drugalcdep.2015.04.013
  14. https://academic.oup.com/jn/article/136/3/736S/4664300?
  15. https://www.bmj.com/content/368/bmj.m456.long
  16. https://jeatdisord.biomedcentral.com/articles/10.1186/s40337-019-0244-4#Sec10
  17. https://eje.bioscientifica.com/view/journals/eje/48/3/acta_48_3_001.xml
  18. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2439524/
  19. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2907129/
  20. https://www.smh.com.au/sport/anti-doping-bodies-have-been-throwing-the-book-at-ligandrol-positives-20190803-p52djh.html
  21. https://doi.org/10.1517%2F14656566.2014.876992
  22. https://pubmed.ncbi.nlm.nih.gov/18374884/
  23. https://muscleandbrawn.com/celebrities/hugh-jackman-steroids/
  24. https://www.strongerbyscience.com/your-drug-free-muscle-and-strength-potential-part-1/

See also[edit | edit source]

Looks

Looks

Looks theoryLooksRegression toward the meanBeautyGolden RatioDecileFacial Aesthetics: Concepts and Clinical DiagnosisThe WallScientific BlackpillPhysiognomyBody dysmorphic disorderCheerleader effectGait

Lookism communities

Looksmax.meLookism.netLooksmax.net (defunct)

Looksmaxxing

GymmaxxingHeightmaxxingStatusmaxxingMoneymaxxingSurgerymaxxingWhitemaxxingAnabolic steroidsHGHSARMsJelqing

Looks levels

ChadChadliteBradGigachadTannerPretty BoyBeckyStacyMegastacyGigastacyWitch

Racepill

EthnicelJBW theoryRicecelCurrycelBlackcelArabcelWhitecel

Inceldom

AcnecelWristcelBaldcelEyecelNosecelOldcelUglycelFatcelShortcelSkinnycel

Body Parts

EyesBulging eyesLateral orbital rimLipsLower thirdMandibleMaxillaEyebrowMoustacheBoobsButtocksLeggingsFeetBrowridgeCheeksPenisBonepressedVagina

Body Characteristics

MacrophallismMidface ratioNeotenySexual attractivenessSexual dimorphismFacial Aesthetics: Concepts and Clinical DiagnosisFashionAntefaceFiveheadFrameFacial width-to-height ratioChinCanthal tiltCompact midfaceDeep-set eyesHunter eyesFacial masculinityFacial asymmetry