AAS exert their anabolic effects by binding to and activating androgen receptors located in the cytoplasm of muscle cells, this stimulates the release of the complex which then travels to the nucleus of the cell and begins transcribing genes important to increasing muscle protein synthesis and decreasing proteolysis, on top of this AAS also increases the release of other anabolic agents, such as growth hormone and IGF-1, and inhibits the release of IGFBP-4 which inhibits the actions of IGF-1, androgen receptors are also found in myoblasts and other evidence suggests that AAS can increase satellite cell function, in fact, it is believed that certain AAS help to increase myonuclei donation from satellite cells to a far larger degree than what is achieved naturally, so this means that through AAS you can gain muscle mass quicker and obtain more muscle mass than you ever could naturally. Although, evidence suggests that when testosterone is suppressed anabolic agents do not decrease, but hypertrophy is still severely inhibited so testosterone and AAS may stimulate hypertrophy through another process which doesn’t rely on anabolic agents or an anabolic agent which we are not yet aware of. Testosterone is believed to be so largely responsible for muscle growth that it is believed to be the reason for the age-related drop in muscle mass in men as testosterone levels decline. There is limited evidence supporting that testosterone elevations within the normal physiological range of 264-916 ng/dL have any effects on the body but supraphysiological levels of testosterone certainly do, these effects include an increase in muscle mass, strength, power output, work capacity and recovery rate.

Every AAS comes with many potential side effects, life-threatening side effects are rare but subjective side effects are incredibly common, almost to the point where you can guarantee a user of AAS that they will experience some side effects, some of these side effects may be reversible but some are not. Most early deaths from steroids appeared to be from those who abuse AAS and from those who use black-market compounds, and the most common causes of death from AAS use are related to the cardiovascular system. The side effect of the AAS can be the cause of the steroid in its intended form once it has entered the body, or it can be the result of the AAS being converted to another steroid in the body, such as estrogen, DHT, progesterone, glucocorticoids or mineralocorticoids, the increase of these steroid hormones in the body to superphysiological levels comes with a long line of health risks, additionally, the steroid can often still bind to steroid receptors other than the androgen receptors leading to health risks, and side effects from AAS use can be due to the suppression of gonadotropic hormones which is caused by AAS use, many of these specific side effects involve the reproductive system in both men and women.

Cardiovascular risks:

• Disturbed lipid metabolism
• Hypertension 
• Cardiac arrhythmias
• Myocardial hypertrophy
• Cardiomyopathy
• Thrombosis
• Early myocardial infarction
• Sudden cardiac death

Endocrine/ reproductive risks:

• Decrease of libido
• Decrease of fertility 
• Decreased LH and FSH
• Altered glucose metabolism
• Hypogonadism 

Male-specific risks:

• Testicular atrophy
• Erectile dysfunction
• Subfertility
• Prostatic hypertrophy
• Impaired spermatogenesis 
• Gynecomastia
• Testicular cancer

Female-specific risks:

• Virilization
• Voice deepening
• Menstrual irregularities
• Clitoral enlargement
• Reduced breast size
• Male pattern baldness

Liver risks:

• Jaundice
• Peliosis hepatis
• Neoplasia
• Gall bladder stones

Infection-related risks:

• Hematoma
• Infection
• Fibrosis 
• Neuro-vascular injury 
• Hepatitis B or C and HIV infection

Behavioural risks:

• Mood swings
• Depressive symptoms
• Manic symptoms
• Sleep disturbances
• Withdrawal
• Psychosis

Kidney risks:

• Pollakisuria 
• Increase of serum creatinine 
• Kidney stones

Skin risks:

• Acne
• Urticaria 
• Striae
• Alopecia

Gastrointestinal risks:

• Queasiness
• Emesis
• Diarrhoea
• Hematemesis

Musculoskeletal risks:

• Tendon damage 
• Bone pain 
• Premature epiphyseal closure

Other risks:

• Edema
• Fever
• Anaphylactic shock
• Cognitive decline

Most AAS are taken in cycles and post-cycle therapy (PCT) is used following a cycle to reduce the risk of side effects, withdrawal symptoms and gradually return the body, and particularly the hypothalamic-pituitary-gonadal axis, back to normal function. Following a cycle, the release of GnRH, luteinising hormones (LH) and follicle-stimulating hormones (FSH) is all typically greatly reduced, which decreases the production of testosterone, although estrogen levels still remain high due to large amounts of testosterone being produced being converted to estradiol. Hormones typically will naturally return to their normal level when u stop a cycle, but before that happens many side effects are likely to occur. There are several supplements which can, and often should be used by those who take AAS to minimise their side effects, these include nootropics, 5α-Reductase inhibitors, aromatase inhibitors, selective estrogen receptor modulators (SERMs), testosterone boosters, human chorionic gonadotropin (hCG), phosphatidylserine and acetyl-l-carnitine, and testosterone replacement therapy (TRT), a lot of these supplements can be taken on cycle as well as part of PCT in order to minimise the negative side effects associated with AAS.

Nootropics are a type of supplement which is meant to cause cognitive enhancements in some way, whether this be through enhancing learning and memory, through enhancing the resistance of learned behaviours and memories from things which would otherwise disrupt them, through protecting the brain against injury, through improving the efficiency of the tonic cortical control mechanism or the nootropic should lack the usual cognitive effects of the drug but have fewer adverse effects. Most nootropics marketed do not perform any piece of the criteria previously mentioned and many are marketed falsely, although some nootropics do have a beneficial cognitive effect. There are several classes of nootropics, these being central nervous system stimulants, racetams and cholinergics. Central nervous system stimulants are ones which alter the brain, these are the most popular type of nootropic, examples of these include caffeine and nicotine. Only certain types of racetams also fit into the category of nootropics, and their mechanism of action is poorly understood, of the racetams, the best-understood ones include piracetam and aniracetam, which are both said to be positive allosteric modulators of AMPA receptors and modulate cholinergic systems. Cholinergics are compounds or analogues of choline which are precursors of acetylcholine and phosphatidylcholine, the effects of cholinergics are still very much in question. Nootropics can be used tactfully by those taking AAS to help curb the negative psychological effects of the steroids and to help with neuroprotection, although the evidence for this is lacking, the one nootropic which I feel we can confidently say is beneficial to the brain is omega-3 fatty acids.

5α-Reductase inhibitors work to inhibit the conversion of certain androgens to DHT by binding to and inhibiting the enzyme 5α-Reductase in certain cell types, this reduces the side effects associated with elevated DHT levels such as male pattern baldness and acne. One of the downsides of this drug is that it means that more testosterone and whatever AAS which the individual is taking is aromatised to estrogen, if the individual also takes aromatase inhibitors however it means that testosterone and the AAS can be used more for its anabolic effects.

Aromatase inhibitors are a class of anti-estrogen drug which work by binding to and inhibiting the enzyme aromatase, this means that the process of aromatisation can’t occur, this is where androgens are converted to estrogens, and therefore the production of estrogen is inhibited. These are often taken on and off cycle to help mitigate estrogenic side effects from AAS, such as gynecomastia and water retention. Aromatase inhibitors are often taken off cycle as well because during the cycle the body's natural production of estrogen usually rises to balance out the effects. Slightly off-topic, I would like to dismantle a popular misconception that estrogen in some way makes people weak physically and even mentally. Estrogen is an important hormone in both men and women, and it in fact increases muscle mass rather than decreasing it, high estrogen levels are common amongst those who are obese, and it is associated with anxiety, fatigue, depression and low sex drive, which is likely responsible for estrogens bad reputation for males. Aromatase inhibitors, and other anti-estrogens, do when taken alone increase testosterone levels by as much as 50%, however, aromatase inhibitors have no evidence to suggest that they increase muscle mass, although side effects from low estrogen are still prevalent.

SERMs work by blocking or activating certain estrogen receptors in the body. The most popular ones used in PCT are Clomid and Novadex. Clomid works by targeting the estrogen receptors of the hypothalamus and pituitary gland, this stimulates the release of LH and FSH which is important for fertility and the production of testosterone. Nolvadex is useful in reducing estrogen levels and the associated symptoms of high estrogen levels, it also prevents estrogen surges which can lead to stroke, heart problems and prostate disease.

Testosterone boosters are used with the hope to boost the body's natural production of testosterone, through ingredients such as zinc, ashwagandha, maca and fenugreek, although evidence suggests that they are ineffective. If testosterone boosters was effective it would help to counteract the side effects of low testosterone levels which typically occur post cycle. 

TRT is the use of any prodrug of testosterone, most commonly testosterone undecanoate, in order to treat hypogonadism which is common post cycle, TRT will help testosterone levels remain in the normal range and help to stop any negative side effects of low testosterone levels. However, TRT should be used with caution post cycle, testosterone levels usually return to normal within 12-14 weeks however TRT can further suppress the natural production of testosterone and ensure that the body's natural production of testosterone is shut down for good.

Phosphatidylserine and acetyl-l-carnitine are two other supplements which are both used to lower cortisol levels which are typically high following a cycle, this helps to reduce catabolism and preserve an impressive physique post-cycle.

An important part of PCT is regular blood testing, to ensure that hormones are returning to normal levels, and also proper resistance training, nutrition, rest, and recovery. Resistance training should continue but at less volume, as your body will not be able to handle as much volume but you do not want to lose much mass which was put on during the cycle, this may be the perfect time for a maintenance phase or a reduced volume phase. Good nutrition includes an adequate amount of macros and micronutrients, while typically being in a calorie maintenance phase while recovering from the cycle. Rest and recovery is important, this includes adequate amounts of high quality sleep, while minimising stress and strain put on the body.

PCT should start roughly one week after you have ended a steroid cycle, when the AAS has left your body. Before starting PCT it is also important to stop the use of selective androgen receptor modulators (SARMs) and prohormones. PCT typically takes 4-6 weeks, but it can be extended longer if necessary. 

When talking about anabolic steroids there are several key terms which will often pop up including:

Cycle - the use and disuse of different AAS during different periods, often depending on bulking, cutting, proximity to competition, currently presented side effects and the current length of the use of a particular AAS.

Stacking - using several different AAS at once in order to increase the potency of each drug and gain the benefits each AAS has to offer.

Pyramiding - the gradual increase in an AAS dose often over several weeks in order to monitor the effects of the AAS. Following this the athlete will begin to drop the dose.

Growth hormone

Growth hormone (GH) is typically injected once per day at a dose of roughly 200-400mcg. The hormone is banned by WADA, but testing positive for GH is uncommon because GH levels typically return to baseline within 8-16 hours after intramuscular injection and 11-20 hours after subcutaneous injection, on top of this GH levels in the body vary greatly, exercise can raise GH levels by 500-1000%, other things which can raise GH levels include a rise in body temperature, third stage sleep, fasting, fever, certain amino acids and stress, while obesity, a high carbohydrate diet and the use of β2 adrenergic agonists decreases GH levels.

mRNA levels of MGF appear to greatly increase when elderly men performed resistance training and performed recombinant GH treatment, but similar results were not found in young men, it is therefore hypothesised that exogenous GH administration is only needed when natural GH levels drop due to ageing or due to other causes, which is necessary to reach the threshold to stimulate a large release of MGF, this will improve body composition, exercise quality, bone mass, renal and cardiac function as well as improve the overall quality of life. Normal physiological levels of GH likely have anabolic properties through other mechanisms, such as potentiating the effects of IGF-1, increasing collagen synthesis, increasing the uptake rate of amino acids and their transformation into proteins inside of cells, and also through increasing myoblast fusion within muscle cells and also potentially through testosterone-mediated muscle protein synthesis. GH also stimulates lipolysis which may improve body composition by lowering body fat, however, GH also appears to increase total body extracellular water levels due to its antinatriuretic properties which may counteract this. Interestingly GH has been shown to cause fat redistribution from central to peripheral depots.

Recombinant GH administration consists of one isoform, whilst over 100 isoforms of GH have been found to be produced endogenously, for this reason, recombinant GH administration likely does not enhance muscle growth, in fact, it has even been shown to reduce the natural GH production post-workout, which is necessary to get the other GH isoforms, this may diminish the rate of muscle growth. A method of testing for recombinant GH use involves testing for different GH isoforms in the blood, if there is a proportionally large amount of the GH isoform which is injected (the 22kDA monomer) then this points to recombinant GH use. It’s also important to note that the use of androgens already increases GH levels, so I wouldn't likely recommend the recombinant use of GH, and GH is very rarely used alone anyway, although it likely helps to aid recovery slightly and improve sleep.

Fascinatingly a rare condition known as acromegaly, results in an abnormally large production of GH in the body, this causes tissues of the body to grow very quickly resulting in the development of very large hands, face and feet, as well as other symptoms. Long-term recombinant GH use can result in fluid retention, hypertension, diabetes, cardiomyopathy, osteoporosis, menstrual irregularities, decreased HDL levels and impotence, thankfully some of these side effects are reversible if recombinant GH use is stopped.

Insulin

Insulin’s main purpose in the body is to transport glucose in the bloodstream into cells in order for them to be used for energy or stored as glycogen, but insulin has also shown to have a large anti catabolic and likely even anabolic effect. Insulin regulates various eIFs and eEFs which helps the translation process of protein synthesis. Insulin also activates the mammalian target of rapamycin (mTOR), increasing muscle mass. Insulin also has an ability to inhibit protein breakdown, however, the exact mechanism, by which insulin achieves this is unknown, for this reason insulin is often injected soon post workout to minimise muscle damage and transport glucose into cells which will help fatigue fade faster and may have some anabolic effects.

Hyperinsulinemia is caused by high amounts of insulin in the blood, this can occur if insulin is injected into the blood. A rather major side effect of insulin use, especially in those who are not diabetic or prediabetic, is hypos, this is when blood sugar drops too low due to excessive amounts of insulin which are quickly transports glucose into cells and rapidly depleting blood glucose levels, this can cause shaking, dizziness, anxiety, irritability, sweating, heart palpitations and weakness. Elevated insulin levels can also lead to insulin resistance and diabetes, which brings with it a long list of additional symptoms including feeling very thirsty, fatigue, urinating more than usual, weight loss, cuts or wounds taking a long while to heal and blurred vision. High insulin can additionally cause fat gain, increase the risk of cardiovascular disease and increase the risk of cancer. To stop these side effects it is important to have a high carb meal shortly after taking insulin.

Insulin use as a PED is banned under WADA, however, testing for insulin is difficult due to most forms of recombinant insulin use being very short lasting in comparison to other PEDs.

IGF-1

IGF-1 is typically injected at a dose of roughly 3-8mg 3 or 4 times per week, and methods of detection for abuse of the substance is tedious. 

IGF-1 naturally in the body has been shown to initiate protein synthesis, inhibits protein breakdown, promotes glycogen synthesis, increase satellite cell differentiation, increase fusion of myoblasts to muscle fibres, increase myotube diameter and increase the number of nuclei per myotube, however, recombinant use of IGF-1 has only been shown to reduce proteolysis rather than increase protein synthesis.

Recombinant IGF-1 use has been shown to have limited side effects, with the most common ones being erythema and lipohypertrophy due to the injection. Due to GH ability to increase IGF-1, recombinant IGF-1’s side effects are very similar. The IGF-1 and the insulin receptor are very similar and so some of the side effects of IGF-1 use involve insulin resistance. 

Selective androgen receptor modulators (SARMs)

SARMs can be injected or taken as a tablet, typically at a dose of anywhere between 10-200mg depending on the particular SARM taken. SARMs have very similar anabolic properties to AAS but with reduced androgenic effects, this is because SARMs bind to certain androgen receptors in the body rather than all of them, these include receptors in muscle and bone, leading to increased muscle mass and denser bones. SARMs androgenic to anabolic properties ratio is somewhere between 1:3 and 1:90 in different individuals. SARMs are banned by WADA under the category “other anabolic agents”.

Beta-blockers

Beta blockers are a rather interesting PED used for different purposes of others. Epinephrine or norepinephrine is able to carry out its effects by binding to adrenergic receptors, such effects include the vasoconstriction of arteries and the increase in blood pressure once epinephrine or norepinephrine binds to the α1 receptors of the arteries, the increase in heart rate and stroke volume, causing a further increase in blood pressure once epinephrine or norepinephrine has bound to the β1 receptors of the heart, and also the relaxation and dilation of the lungs once adrenaline has bound to the β2 receptors inside of the lungs. Beta-blockers work by binding to certain beta receptors and work as an antagonist stopping them from being activated by epinephrine or norepinephrine. Some Beta-blockers only block the β1 and β2 receptors while other beta-blocking agents can block the β1, β2 and α1 receptors, thus also making them alpha-blockers, these are often used to lower blood pressure. As a PED beta-blockers are used to calm the athlete and prevent muscle tremours which are useful in sports such as darts, although whether they cause any major impact is still in question although they are banned under WADA.

Side effects of beta-blockers include hypotension, fatigue, bronchospasms and it can also mask hypoglycemia meaning that it can go undetected in those who take beta-blockers. To minimise the side effects of beta-blockers it is important to slowly reduce the dose before completely stopping their usage.

Their are many types of beta-blockers but a typical dose is anywhere between 25-200mg, taken as a tablet often timed before a competitive sporting event.

Clenbuterol 

Clenbuterol is available as an injectable, syrup or tablet, often taken daily at a dose of about 100-300mcg. Clenbuterol has been shown to increase resting energy expenditure by 21% and fat oxidation by 39% making it very effective for weight loss. Clenbuterol also has the ability to increase maximum heart rate and exercise output which may indirectly lead to an increase in muscle mass due to more growth prompting workouts, however, despite its reputation clenbuterol has no evidence surrounding it suggesting that it is effective as an anabolic agent. Its use as an anabolic agent originated from Daniel Duchaine, commonly known as the steroid guru, who popularised the drug in 1988 in the sport of bodybuilding. 

Clenbuterol’s mechanism of action is not fully understood, what is better understood is the effects it has as a long-lasting β2 agonist. Like all β2 agonists, clenbuterol binds to β adrenergic receptors which leads to the relaxation of smooth muscles through a number of mechanisms and thus the widening of the airways, for this reason, like all other β2 agonists, it is banned by the World Anti-Doping Agency (WADA). Although those with asthma are allowed certain β2 agonists under WADA, this does not include clenbuterol.

Clenbuterol side effects include nervousness, hyperthyroidism, tachycardia, subaortic stenosis, hypertension, muscle tremors, headache, dizziness, gastric irritation, mood swings, nausea, vomiting, heart palpitations, diaphoresis and myocardial infarction.

Clenbuterol is a food contaminant in some countries and so doping control must determine between accidental and intentional intake. This is because clenbuterol is sometimes given to animals in hopes of them achieving a higher muscle-to-fat ratio, but this practice has been banned in the US since 1991 and since 1996 in the European Union due to health concerns. Consuming large amounts of meats containing clenbuterol may result in increased heart rate, muscular tremors, headaches, nausea, fever, and chills.

Human chorionic gonadotropin (HCG)

HCG’s main purpose comes when it is produced during pregnancy, almost exclusively in the placenta in order to maintain pregnancy. HCG is also partly responsible for the production of testosterone in the testes and ovaries, along with LH, this is why HCG can also be used as a PED, and it is why the use of HCG and LH is banned under WADA, and is tested for in men, however, recombinant HCG use is not tested for in females because it has not been shown to significantly increase testosterone levels and the procedure is invasive to females privacy because of its unintended screening for pregnancy. HCG can also be used to treat hypogonadism. HCG is typically injected at a dose of 500-1500 units 1-3 times per week.

But why would someone wish to increase testosterone through HCG in the bloodstream when AAS are available with far greater anabolic properties, this is because is far less likely to shut down natural testosterone production and the difficulty of detecting the use of HCG in the bloodstream is far greater as long as testosterone levels remain within a normal physiological range, although there are likely no or minimal differences in strength and muscle mass for those with high or low testosterone levels as long as they fall within this normal physiological range, on top of this the use of HCG and other PED’s which increase blood testosterone levels can still be detected through finding the ratio between testosterone and its inactive epimer epitestosterone, which is produced in equal amounts to testosterone in the body, also other androgens can be used for this method, however, this method is also flawed because the evaluation and quantification of steroids in urine are prone to variation due to a number of different factors, some genetic factors even make it very hard for some individuals who use HCG or a testosterone prodrug to fail this type of test to the standards of WADA.

Erythropoietin (EPO)

EPO is produced primarily in the kidneys. EPO travels in the bloodstream to the bone marrow and binds to EPO receptors on proerythroblasts (also known as immature red blood cells) and stimulates them to mature into erythrocytes (also known as red blood cells), it does this by stopping them from undergoing apoptosis. If the delivery of oxygen to the kidneys is low the kidneys will detect this and increase the production of EPO, on the other hand, if the delivery of oxygen to the kidneys is high the kidneys will decrease the production of EPO. If oxygen delivery to the kidneys is low this can be due to decreased blood flow or decreased blood oxygen content. If tissues of the body are not receiving enough oxygen because of decreased blood flow then an increase in EPO will not help this, thankfully the kidneys are able to detect when this is the case because a decrease in blood flow means that the kidneys are less perfused and therefore less fluid is filtered by the glomeruli, less fluid filtered means that fewer solutes need to be reabsorbed from the tubular cells of the kidneys and saved from being urinated out, this is a process which requires oxygen to be carried out, however, oxygen delivery to the kidneys is low due to low blood flow to the kidneys, although there are fewer solutes which need reabsorbing and so the oxygen demand is also reduced and the kidneys, therefore, do not increase the production of EPO. On the other hand, if blood flow to the kidneys is normal but oxygen levels are low, the demand for oxygen is high due to the amount of solutes which need reabsorbing but this demand is not met due to low blood oxygen levels and the kidneys will therefore increase the production of EPO. To get into more detail it is hypoxia-inducible factor 1 (HIF1) which is responsible for the increase in EPO. HIF1 has an alpha and beta group, in the presence of oxygen the enzyme HIF-prolyl hydroxylase will add an OH group to the alpha group of HIF1 in a process known as hydroxylation, HIF1 is then ubiquitinated, this is when ubiquitin molecules is added to the alpha group, HIF1 will now be destroyed by proteosome, however, if there is not enough oxygen present in the kidneys HIF1 will not be hydroxylated or ubiquitinated, HIF1 will then enter the nucleus of cells and induce the transcription for EPO and EPO in the bloodstream will therefore increase.

Exogenous EPO use will increase red blood cell count and thus increase endurance. EPO is typically injected at a dose of 100-300 units per kg of body weight 3 times per week. Side effects of EPO use include feeling sick, diarrhoea, blood clots, headaches, hypertension, muscle or joint pain, flu-like symptoms, cough, strokes, fluid build-up and skin rash. EPO use as a PED is banned and tested for under WADA.

Diuretics

Diuretics are taken orally and they work by decreasing sodium reabsorption in the nephrons of the kidneys and thus increase the amount of fluid urinated from the body, there are different types of diuretics which do this in different ways. Osmotic diuretics work by increasing the solute concentration inside of the nephrons at the proximal convoluted tubial and the loop of henleg and thus less water will defuse out of the nephrons and more water and solutes will be urinated out of the body. Loop diuretics work by acting on a certain transporter in the nephrons at the loop of henley stopping it from being able to reabsorb sodium, chloride and potassium. Thiazide diuretics work by acting on a certain transporter in the nephrons at the distal convoluted tubial to stop the reabsorption of sodium and chloride. There are two classes of potassium-sparing diuretics, one works by acting on the end of the distal convoluted tubule and collecting ducts whilst the other kind works by acting on the collecting ducts inhibiting aldosterones ability to bind to the aldosterone receptor, which will otherwise signal for the transcription of sodium potassium transporters which imbed themselves in the membrane of the cell, these diuretics have a unique property from the others because they do not cause an increase in potassium absorption from the blood stream which is a very important electrolyte in the body. The final type of diuretic is the weakest and these are carbonic anhydrase inhibitors, these act on the proximal convoluted tubule to prevent the reabsorption of sodium bicarbonate.

As a PED diuretics are used to excrete large amounts of fluid in order to lose weight, which is useful in sports with weight classes such as boxing, diuretics are also commonly used to mask the use of other PEDs by increasing the excretion of doping agents, this is why Diuretic use is banned under WADA and it is tested for, on top of this hydration levels are also often tested for using urine, however, urine tests for hydration are easy to fool simply by drinking distilled water before the test, and typically before any extreme measures to cut water weight such as using the sauna. This is very common practice in combat sports where a body weight cut of more than 5% is common and this will almost always lead to a failed hydration test otherwise. 

The most common side effect of diuretic use is hyponatremia, which is when sodium levels in the blood drop too low. Hypokalemia is a risk with potassium-sparring diuretics, this is when potassium levels in the blood drop too low, and, dehydration is another risk. These issues related to diuretic usage can lead to nausea, headache, muscle weakness and spasms, hypotension, heart palpitations, constipation and fatigue. 

Drug testing

Drug testing typically involves collecting urine and performing gas chromatography/mass spectrometry to find any AAS which are not naturally found in urine and to find evidence of endogenous androgens and their metabolites which may be in abnormally high amounts indicating AAS use, these types of AAS are much harder to test for, this process typically involves measuring the ratio of testosterone to epitestosterone, which are both produced in a similar manner and at a similar ratio, with a ratio of between 0.4 and 2 in the urine. Administration of exogenous testosterone will reduce the synthesis of both testosterone and epitestosterone via negative feedback but does overall result in an increase in the testosterone to epitestosterone ratio. A ratio of above 4 is now considered evidence of PED use by WADA. First tests of the testosterone to epitestosterone ratio occurred in the 1983 pan american games, where a ratio of above 6 was considered evidence of PED use, athletes however soon discovered that taking epitestosterone will reduce the ratio and lead to a negative test result, and so WADA now classes epitestosterone as a banned substance.

A more costly and often inconvenient yet effective method of exogenous AAS detection is the monitoring of an individuals steroid profile. This process involves gathering an athletes urine sample and finding the concentrations and ratios of many endogenously produced steroids, their precursors and metabolites, multiple urine samples are gathered over time and tested for changes in the individuals urinary steroid profile which may indicate AAS use, this is particularly useful to detect doping in athletes who genetically are less prone to testing positive for PED use in the urine, such as for those who excrete far less testosterone in the urine, these types of athlete will then often have their urine analysed via carbon isotope ratio (CIR) if their urinary steroid profile expereinces substantial change, in this process a steroid is combusted to carbon monoxide after exiting a gas chromatograph, the percentage of 13C is then measured for in an isotope ratio mass spectrometer, this is because their a consistent difference in 13C content between endogenous and exogenous steroid use and its metabolites.

With the prevalence of PED use in professional sport it may make you wonder how so many athletes manage to pass through drug testing, but there are several strategies used to do so. One strategy to avoid AAS detection is through the therapeutic use exemption (TUE) mechanism, this works by claiming that doping with testosterone is necessary due to a medical condition. A second method is the use of “designer steroids” which are slightly modified AAS which retain their biological activity but the steroid or its metabolites are unknown and so can not be tested for. “Designer steroids” still often cause changes in the urinary steroid profile but it is hard to gather concrete evidence of PED use for individuals using “designer steroids”. Other strategies of avoiding AAS detection is through doping with an enzyme inhibitor which blocks the production of the AAS associated metabolites, such as by taking a 5α-reductase inhibitor, and through using diuretics to decrease the concentration of any AAS related substances to below detection levels.

Conclusion

The potential side effects of PED use is often intentionally overstated by the medical community this unfortunately has led those interested in the use of PED use to turn to unreliable sources such as friends and family which is likely causing more harm then good, I will like readers to use this article for information regarding PED use but to certainly not use this for their own or others PED use guidelines as this was not the intention of this article and it is not my area of expertise. There are many more substances banned by WADA then what is covered in this article, and I never recommend the use of PEDs although if you are interested in the use of PEDs I highly recommend doing your own in depth research into PED use and ideally use the expertise of some sensible individuals with first hand experience of PED use.