Anabolic Androgenic Steroids and IPED Agents

011 Anabolic Androgenic Steroids and IPED Agents

 40 MINUTE COURSE TRAINING VIDEO 

With Thomas O'Connor, M.D.  Founder / CEO Testosteronology Society® 

Video Lesson Takeaways

 ◉ Think in ecosystems, not single drugs. The moment someone stacks agents, the clinical risk profile changes faster than most people expect.

◉ Start by sorting what they are actually using into families, because testosterone-derived, DHT-derived, and nandrolone-derived compounds tend to carry different predictable problem sets.

◉ Oral-heavy plans deserve immediate attention, since liver strain can pile up quietly, especially when someone adds “side meds” that also stress hepatic metabolism.

◉ “Selective” does not mean “safe.” SARMs and similar agents still show up alongside cardiovascular, renal, and hepatic concerns when you look at real-world patterns.

◉ Expect the non-hormone add-ons. Clenbuterol, thyroid agents, diuretics, stimulants, and cosmetic meds often end up being the difference between a stable patient and a messy physiology picture.

◉ DHT-derived cutting compounds can be brutal for acne and hair loss in the wrong genetics, and the user often normalizes it until it becomes unmanageable.

◉ Nandrolone exposure is its own counseling lane, because sexual side effects commonly trigger panic-driven self-treatment with dopamine agonists and other risky “fixes.”

◉ Keep your eyes on the long game. People can feel great while their cardiovascular and kidney risk quietly drifts the wrong direction.

◉ Hematocrit is not a “nice to watch” marker here. Rising viscosity risk is one of the clearest safety signals that the exposure pattern needs to change.

◉ Peaks and troughs matter as much as the weekly milligrams. Missed doses, catch-up dosing, and unstable schedules can create symptoms and labs that look like new disease.

◉ Shutdown and recovery need to be discussed plainly, especially with younger users, because prolonged suppression is not always a clean rebound story.

◉ Treat “reported dose” as a starting hypothesis, not a fact. Underground and veterinary supply chains increase mislabeling, contaminants, and unexpected pharmacology that can flip your interpretation.

◉ The most useful stance is harm-reduction plus defensible documentation: get the real exposure history, pick the few monitoring priorities that actually prevent harm, and make the plan realistic enough that the patient will follow it.

 COURSE 011 TEXT 

① Modern AAS And IPED Use Beyond Elite Sport

The modern anabolic androgenic steroid (AAS) and image- and performance-enhancing drug (IPED) user does not always match the stereotype clinicians were trained to imagine. Many are not professional athletes, and many do not describe themselves as steroid users. They may be recreational lifters, strength athletes, physique competitors, hybrid athletes, older adults pursuing optimization, adolescents shaped by social media, women pursuing body composition change, or men trying to preserve an identity built around strength, leanness, libido, or appearance.[1] The older public story was shaped by elite sport, including the 1988 Seoul Olympics and subsequent U.S. scheduling of anabolic steroids in 1990, but the modern clinical reality is now much broader than formal doping.

The first clinical mistake is asking too narrowly. “Are you using steroids?” misses patients who believe selective androgen receptor modulators (SARMs) are not steroids, peptides are wellness tools, human chorionic gonadotropin (hCG) is fertility support, thyroid medication is a “cutting agent,” or testosterone is simply optimization. An accurate exposure history should ask about hormones and any ancillary agents used as part of the patient’s “stack”. 

② Patient Motivations, Disclosure Barriers, And Failed Cessation

AAS and IPED use is usually driven by appearance, strength, body image, or perceived quality of life rather than formal sport.[1] Clinicians should not frame every case as cheating or competition. Many patients are responding to gym culture, online comparison, sexual confidence, masculinity concerns, aging fears, or fear of losing a physique they worked hard to build.
 

Patients often avoid disclosure to their clinician due to fear of judgment or discrimination and perceived lack of education.[1] Patients also often attempt to stop using but fail to do so.[5] These patients may fear withdrawal, loss of muscle, decreased strength, sexual dysfunction, depression, or lack of medical support. A clinician can discourage unsafe use while still recognizing that stopping may require structure, trust, and follow-up.

③ Core AAS Categories: Testosterone, DHT-Derived Agents, and 19-Nor Agents

For practical clinical history-taking, AAS can be organized into three major classes. Testosterone-derived agents commonly include injectable testosterone, oral testosterone undecanoate, metandienone, CDMT, fluoxymesterone, and boldenone. Testosterone is often the base of a regimen because it is familiar, available, easy to combine with other drugs and is a substrate for aromatase. DHT-derived agents include oxandrolone, stanozolol, drostanolone, methenolone, mesterolone, oxymetholone, and methasterone. Users may describe these agents as dry, hardening, cosmetic, or safer because they are less estrogenic. That language is misleading. These drugs may worsen lipids, blood pressure, acne, androgenic alopecia, mood symptoms, and virilization risk in women. Classic 17-alpha-alkylated oral AAS add hepatic risk, while oral testosterone undecanoate is a distinct TRT product because it is not 17-alpha-alkylated and is absorbed primarily through the lymphatic system.

19-nor agents include nandrolone esters and trenbolone esters. These agents often appear in mass, strength, joint-comfort, and aggressive recomposition contexts. They should raise concern for prolonged suppression, fertility disruption, sexual dysfunction, mood volatility, sleep disruption, and difficult post-use recovery. Oral AAS such as methandrostenolone, stanozolol, oxymetholone, fluoxymesterone, and designer oral compounds should be asked about separately because patients may fail to disclose short-term “kickstart” use despite hepatic risk.[1,2]

④ Cycles, Stacking, Blast-And-Cruise Patterns, And Post-Cycle Therapy

The use pattern often explains the clinical presentation better than the drug name alone. Cycling means planned periods of use. Stacking means combining multiple AAS or IPEDs at the same time. Post-cycle therapy refers to user-directed attempts to restore endogenous testosterone production, often with selective estrogen receptor modulators (SERMs), hCG, or other agents. Blast-and-cruise means the patient never truly comes off, but alternates higher-dose exposure with lower-dose continued androgen use. These patterns change lab interpretation. A suppressed LH and FSH after recent AAS exposure does not prove primary hypogonadism. A high testosterone level may reflect injection timing, undisclosed exposure, or intentionally supraphysiologic dosing. A patient who is “off cycle” but using hCG, clomiphene, tamoxifen, SARMs, thyroid drugs, or peptides may not be physiologically off. The history should identify last dose, current compounds, true off periods, withdrawal symptoms, PCT attempts, and prior recovery failure.[4,5,7]
 

⑤ SARMs, Prohormones, Peptides, And Growth Hormone Pathway Agents

SARMs are challenging because of the marketing language used to describe them. Patients may describe ostarine, ligandrol, RAD-140, andarine, YK-11, S-23, or blends as selective, mild, modern, or not really steroids. That claim should not reassure the clinician. SARMs are commonly purchased online as research chemicals, long-term safety data are limited, and the product identity is often unreliable. Products marketed as SARMs have been found to be mislabeled, with some containing other substances, including anabolic steroid compounds.[2,9]

Prohormones and designer precursors follow the same formula. DHEA-related products, androstenedione-type products, 1-DHEA, 4-DHEA, 19-nor-DHEA, epiandrosterone, trendione, boldione, and designer products may be sold with supplement-like language while functioning as androgenic exposures. These should not be dismissed because they came from a supplement website. The same concern about unreliable product identity applies to them.

Peptides require a different kind of caution. Recombinant growth hormone, IGF-1 products, GHRH analogs, GHRP agents, MK-677, GH fragments, BPC-157, TB-500, melanotan products, PT-141, kisspeptin, gonadorelin, hCG, and HMG may be used for recovery, fat loss, sleep, tissue repair, injury narratives, libido, tanning, or fertility support. The word peptide often sounds benign to patients, but many products have uncertain sterility, purity, approval status, and safety data. In practice, “peptide” often functions as a marketing umbrella rather than a single coherent drug class, covering recovery agents, tanning agents, sexual-function drugs, growth hormone pathway products, fertility-related agents, and research chemicals. Many of these products, including SARMs and prohormones, are sold as research chemicals and may even be labeled “not for human consumption,” despite patients injecting or ingesting them.
 

⑥ Estrogen, Fertility, Hair-Loss, Acne, And Sexual Function Agents

Estrogen and fertility-modulating drugs often reveal that the patient is treating the side effects of the stack while continuing AAS or IPED use. Aromatase inhibitors may be used for nipple sensitivity, water retention, gynecomastia fear, or a dry look. SERMs may be used for gynecomastia, PCT, or attempts to restart the axis. hCG, HMG, recombinant FSH, and related agents may be used for testicular size, fertility, or perceived recovery support. These medications can be appropriate in the right context, but informal cycle management is not medical treatment.[2,3]

Hair-loss, acne, and sexual function agents can expose the burden of androgenic exposure. Finasteride, dutasteride, minoxidil, isotretinoin, topical acne regimens, sildenafil, tadalafil, PT-141, and similar agents may appear to manage side effects. Severe acne may suggest high androgenic burden. Erectile dysfunction may reflect vascular disease, estradiol mismanagement, prolactin-related side effects, stimulant use, sleep collapse, withdrawal, anxiety, or relationship stress.

⑦ Metabolic And Fat-Loss Agents: GLP/GIP Drugs, Insulin, Thyroid Drugs, Stimulants, And DNP

Metabolic and fat-loss agents may create some of the most urgent risks in modern IPED use. GLP/GIP-related drugs such as semaglutide and tirzepatide, along with investigational agents such as retatrutide, may be medically appropriate in one patient and risky in another depending on context. A supervised metabolic patient is not the same as a physique patient using appetite suppression during aggressive cutting while also using thyroid drugs, stimulants, AAS, or diuretics. Insulin is high risk when misused. Non-diabetic users may take rapid-acting insulin, regular insulin, or long-acting insulin for mass gain, nutrient partitioning, or recovery. Hypoglycemia can occur quickly and can cause confusion, syncope, seizure, coma, or death. If the patient refuses to stop, safety counseling should still address life-threatening hypoglycemia, glucose monitoring, and emergency treatment planning.[2]

Thyroid drugs and stimulants can distort the clinical picture. T3, T4, desiccated thyroid, clenbuterol, ephedrine, caffeine stacks, yohimbine, amphetamines, methylphenidate, modafinil, and cocaine may produce tachycardia, hypertension, insomnia, anxiety, tremor, panic symptoms, arrhythmia risk, heat intolerance, and muscle loss. DNP deserves the most direct warning because it is used for fat loss by uncoupling oxidative phosphorylation and has been associated with severe hyperthermia and death.[10] No cosmetic or performance goal makes DNP use medically reasonable.
 

⑧ Diuretics, Contest Prep, Looksmaxing, Testosterone-Maxing, And Appearance-Driven Use

Diuretics and water manipulation are common in contest preparation and appearance-driven settings. Furosemide, torsemide, bumetanide, thiazides, potassium-sparing diuretics, and other drying agents may be combined with sodium restriction, water restriction, laxatives, stimulants, thyroid drugs, and final-week pressure. Patients may describe this as drying out, tightening up, or peaking. Clinicians should hear electrolyte risk, arrhythmia risk, kidney injury, syncope, rhabdomyolysis, paralysis, and possible death, including hyperkalemia risk when potassium-sparing diuretics are used. Contest-prep histories should be direct. Ask about show dates, weigh-ins, photoshoots, diuretics, water loading, sodium restriction, thyroid drugs, clenbuterol, insulin, growth hormone, GLP/GIP agents, stimulants, laxatives, cramping, weakness, palpitations, syncope, dark urine, and emergency visits. The patient may not volunteer these details because the practices are normalized inside physique culture.

Looksmaxing and testosterone-maxing are newer cultural patterns that deserve clinical recognition. Looksmaxing may include low-dose AAS or SARMs, GLP/GIP agents, thyroid drugs, clenbuterol, diuretics, isotretinoin, finasteride, dutasteride, minoxidil, melanotan products, PT-141, PDE-5 inhibitors, Botox, fillers, and cosmetic procedures. Testosterone-maxing is the pursuit of higher testosterone for masculinity, libido, dominance, body composition, confidence, or anti-aging, often without classic hypogonadism.[2,3]

⑨ Strength, Powerlifting, CrossFit, And Performance-Specific Exposure Patterns

Strength and functional-fitness communities create different drug signatures than contest bodybuilding. Powerlifting and strongman patterns may include testosterone, trenbolone, nandrolone, oxymetholone, Dianabol, Halotestin, boldenone, insulin, growth hormone, stimulants, NSAIDs, and pain-masking drugs. The immediate reward is performance, so patients may normalize severe blood pressure, sleep apnea, tendon pain, aggressive bodyweight gain, chronic NSAID use, and stimulant load.

Renal risk should not be overlooked. AAS exposure, hypertension, dehydration, heavy body mass, intense training, and NSAID use can converge in strength athletes. Proteinuria may appear before kidney function looks alarming on routine labs, and focal segmental glomerulosclerosis has been described after anabolic steroid abuse.[8] Urinalysis, urine albumin-creatinine ratio, blood pressure trends, and longitudinal renal assessment may reveal risk earlier than a single creatinine value.

CrossFit-style and functional-fitness users may combine physique drugs, endurance-adjacent drugs, stimulants, recovery peptides, SARMs, thyroid drugs, beta-agonists, and weight-loss agents. They may deny steroid culture while still using IPEDs. Training style, event demands, injury history, competition schedule, and recovery practices help make sense of the exposure history.
 

⑩ Physician Red Flags Across Cardiovascular, Hematologic, Renal, Hepatic, Reproductive, Psychiatric, And Dermatologic Domains

AAS and IPED exposure should trigger organized red-flag screening, not scattered lab ordering. Cardiovascular concerns include hypertension, severe dyslipidemia, exertional chest pain, dyspnea, palpitations, syncope, arrhythmia symptoms, left ventricular hypertrophy, cardiomyopathy, coronary plaque, myocardial infarction risk, and sudden cardiac death risk. The harm-reduction review emphasizes cardiovascular assessment because AAS use is associated with dyslipidemia, hypertension, LVH, arrhythmia, atherosclerosis, polycythemia, thrombosis, infertility, endocrine dysfunction, tendon rupture, and sexual dysfunction.[2,3,6]

Hematologic and renal red flags include erythrocytosis, polycythemia, thrombosis history, repeated phlebotomy with iron depletion, proteinuria, rising albumin-creatinine ratio, edema, uncontrolled hypertension, dehydration practices, rhabdomyolysis risk, heavy NSAID use, and kidney markers that do not fit the patient’s baseline. Hepatic red flags include jaundice, dark urine, pruritus, right upper quadrant pain, cholestatic patterns, oral AAS exposure, designer oral compounds, alcohol, isotretinoin, and hepatotoxic supplements.[2,3]

Endocrine and reproductive red flags include HPG-axis shutdown, testicular atrophy, infertility, prolonged post-cycle hypogonadism, gynecomastia, estradiol mismanagement, sexual dysfunction, prolactin-related symptoms when relevant, thyroid-axis disruption, and fertility urgency. Psychiatric and dermatologic red flags include severe depression, suicidal ideation, hypomania, aggression, panic, insomnia, stimulant misuse, substance use disorder, body dysmorphia, severe acne, scarring acne, androgenic alopecia, injection-site abscesses, unexplained masses, fever, and localized pain.[2,3]

⑪  Harm Reduction, Monitoring, Documentation, And Longitudinal Clinical Strategy

Harm reduction is not cycle management, permission, or optimization support. It is medical care for a patient who is already exposed to risk. The clinician should discourage unsafe AAS and IPED use, but should not abandon the patient who is not ready or able to stop. The harm-reduction review emphasizes nonjudgmental care, patient education, risk reduction, and support for cessation guided by the specific compounds being used.[2]

The first visit should answer the following questions:

• What is the patient using now?
• What was used previously?
• What does the patient believe the drugs are doing?
• What adverse effects have appeared?
• Is the patient trying to stop, unwilling to stop, or afraid to stop?
• Is there immediate danger from blood pressure, chest symptoms, psychiatric instability, insulin, DNP, diuretics, infection, or severe withdrawal?

Boundaries must be clear. Treating hypertension, dyslipidemia, infection, erythrocytosis, psychiatric disease, cardiac disease, renal injury, or hypoglycemia risk is harm reduction. Prescribing drugs to help maintain an unsafe illicit cycle is not. Monitoring should match exposure and may include blood pressure, CBC, CMP, lipids, glucose or A1C, renal markers, urinalysis, urine albumin-creatinine ratio, liver markers, testosterone-related labs when clinically useful, LH and FSH when suppression classification matters, estradiol when indicated, semen analysis when fertility matters, ECG when appropriate, echocardiography when concern exists, and referral when findings exceed scope.

Documentation should be clinically honest. The note should record current and past compounds, source, route, timing, dose if known, cycling pattern, PCT attempts, withdrawal symptoms, adverse effects, comorbidities, psychiatric risk, fertility goals, patient motivation, readiness to stop, counseling provided, and follow-up plan. Unknown product identity is not a detail to clean up. It is part of the risk. Longitudinal care moves the patient from secrecy and informal advice into medically accountable monitoring, treatment of adverse effects, safer decision-making, and eventual cessation or stabilization when possible. ABCDS™ provides a practical harm-reduction structure for organizing cardiovascular, hematologic, renal, symptom, and screening risks in patients exposed to AAS and IPED polypharmacy. 

 COURSE 011 SUMMARY 

AAS and IPED use are a multi-agent exposure syndrome rather than a single-drug behavior. Patients may use these agents for appearance, strength, leanness, masculinity, confidence, contest preparation, recovery, or self-directed optimization rather than formal sport. Clinicians learned to ask beyond “steroids” and identify testosterone-derived agents, DHT-derived agents, 19-nor compounds, oral AAS, SARMs, prohormones, peptides, growth hormone pathway agents, estrogen modulators, fertility drugs, GLP/GIP agents, insulin, thyroid drugs, stimulants, DNP, diuretics, sexual function drugs, hair-loss drugs, acne drugs, and research chemicals.

The course emphasized that exposure pattern drives risk interpretation. Cycles, stacking, blast-and-cruise behavior, PCT attempts, continuous use, failed cessation, and withdrawal symptoms affect the meaning of labs, symptoms, and recovery expectations. Clinicians learned to screen cardiovascular, hematologic, renal, hepatic, endocrine, reproductive, psychiatric, dermatologic, and musculoskeletal risk domains. The course also separated harm reduction from facilitation. Clinicians should discourage unsafe use while still treating adverse effects, monitoring risk, maintaining clear boundaries, documenting exposure accurately, and supporting safer long-term care.

 COURSE 011 EVALUATION 

 COURSE 011 REFERENCES 

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2. Bonnecaze AK, O’Connor T, Burns CA. Harm reduction in male patients actively using anabolic androgenic steroids (AAS) and performance-enhancing drugs (PEDs): a review. J Gen Intern Med. 2021;36(7):2055-2064.
3. Pope HG Jr, Wood RI, Rogol A, Nyberg F, Bowers L, Bhasin S. Adverse health consequences of performance-enhancing drugs: an Endocrine Society scientific statement. Endocr Rev. 2014;35(3):341-375.
4. Bhasin S, Brito JP, Cunningham GR, et al. Testosterone therapy in men with hypogonadism: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2018;103(5):1715-1744.
5. Kanayama G, Brower KJ, Wood RI, Hudson JI, Pope HG Jr. Anabolic-androgenic steroid dependence: an emerging disorder. Addiction. 2009;104(12):1966-1978.
6. Baggish AL, Weiner RB, Kanayama G, Hudson JI, Lu MT, Hoffmann U, Pope HG Jr. Cardiovascular toxicity of illicit anabolic-androgenic steroid use. Circulation. 2017;135(21):1991-2002.
7. Rahnema CD, Lipshultz LI, Crosnoe LE, Kovac JR, Kim ED. Anabolic steroid-induced hypogonadism: diagnosis and treatment. Fertil Steril. 2014;101(5):1271-1279.
8. Herlitz LC, Markowitz GS, Farris AB, et al. Development of focal segmental glomerulosclerosis after anabolic steroid abuse. J Am Soc Nephrol. 2010;21(1):163-172.
9. Van Wagoner RM, Eichner A, Bhasin S, Deuster PA, Eichner D. Chemical composition and labeling of substances marketed as selective androgen receptor modulators and sold via the internet. JAMA. 2017;318(20):2004-2010.
10. Grundlingh J, Dargan PI, El-Zanfaly M, Wood DM. 2,4-dinitrophenol: a weight loss agent with significant acute toxicity and risk of death. J Med Toxicol. 2011;7(3):205-212.
     

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