Anabolic Androgenic Steroids and iPED Agents

Course Overview

Modern anabolic androgenic steroid and iPED use is no longer limited to elite sport, professional bodybuilding, or obvious high-risk gym culture. Patients may be recreational lifters, physique competitors, strength athletes, CrossFit athletes, social media-influenced adolescents, women pursuing body composition changes, older adults seeking “optimization,” or men who entered testosterone use through self-directed enhancement rather than medical diagnosis. The clinician’s task is not to memorize every underground drug name. The task is to recognize the exposure pattern, understand what category of risk it creates, and ask questions that reveal what the patient is actually using.

AAS and iPED care requires a broader medication history than “Are you using steroids?” Modern exposure may include testosterone esters, DHT-derived agents, 19-nor compounds, oral anabolic steroids, SARMs, prohormones, peptides, growth hormone pathway agents, GLP/GIP drugs, insulin, thyroid drugs, stimulants, diuretics, fertility drugs, aromatase inhibitors, SERMs, acne drugs, hair-loss drugs, erectile dysfunction drugs, and psychiatric or cognitive agents. Many patients do not disclose use because they expect judgment, believe clinicians lack knowledge, or fear legal and insurance consequences. A large survey of 2,385 men using AAS found that 56.1% had never disclosed use to a medical professional, 55.3% of those who disclosed felt discriminated against, and more than 60% of those who attempted cessation were unsuccessful.[1] Course 011 trains clinicians to approach these patients with informed skepticism, nonjudgmental history-taking, risk-based monitoring, and clear harm-reduction boundaries.

Learning Objectives

After completing this course, clinicians should be able to:

➀ Recognize how modern AAS and iPED use presents in recreational, physique, strength, appearance, optimization, and self-directed health communities.

➁ Distinguish major AAS categories, including testosterone-derived agents, DHT-derived agents, 19-nor agents, and oral 17-alpha alkylated compounds.

➂ Identify common iPED categories layered with AAS, including SARMs, prohormones, peptides, growth hormone pathway agents, GLP/GIP drugs, insulin, thyroid drugs, stimulants, diuretics, fertility drugs, SERMs, and aromatase inhibitors.

➃ Explain how cycles, stacking, blast-and-cruise patterns, post-cycle therapy, and failed cessation attempts change clinical interpretation.

➄ Screen for cardiovascular, hematologic, renal, hepatic, endocrine, reproductive, psychiatric, dermatologic, and musculoskeletal risks associated with AAS and iPED exposure.

➅ Apply a harm-reduction approach that discourages unsafe use while still providing appropriate evaluation, monitoring, counseling, treatment of adverse effects, and referral.

➆ Document exposure history, patient goals, adverse effects, cessation attempts, current risk, and monitoring rationale in a way that supports safe longitudinal care.

Course Topics

The following topics will be covered in the course text, video, diagrams or downloadable documents:

➀ The Modern AAS And iPED Patient

➁ Core AAS Categories Clinicians Must Recognize

➂ Use Patterns: Cycling, Stacking, Blast-And-Cruise, And Failed Cessation

➃ Accessory Endocrine Agents: AIs, SERMs, hCG, SARMs, And Prohormones

➄ Metabolic, Appearance, And Contest-Prep iPEDs

➅ Red-Flag Risk Domains In AAS And iPED Care

➆ Harm Reduction Without Facilitating Misuse

➇ Documentation, Monitoring, And Longitudinal Clinical Strategy

Video Lesson Takeaways

◉ Modern AAS and iPED use is no longer limited to elite athletes or competitive bodybuilders, because many patients now use these agents for appearance, strength, confidence, leanness, recovery, or self-directed optimization.

◉ Clinicians should ask beyond “Are you using steroids?” because patients may not consider SARMs, peptides, thyroid drugs, insulin, diuretics, GLP/GIP agents, estrogen blockers, or research chemicals to be steroid use.

◉ Many patients do not disclose AAS or iPED exposure because they fear judgment, legal consequences, insurance concerns, or a clinician who does not understand the drugs they are using.

◉ Testosterone esters often form the base of AAS regimens, but the same molecule can represent legitimate replacement therapy or supraphysiologic exposure depending on indication, dose, monitoring, and stacking.

◉ DHT-derived agents, 19-nor compounds, and oral anabolic steroids each create different clinical concerns involving lipids, blood pressure, liver markers, fertility, sexual function, mood, sleep, and recovery after discontinuation.

◉ Cycles, stacking, blast-and-cruise patterns, post-cycle therapy attempts, and failed cessation histories are clinically important because they change how symptoms and laboratory findings should be interpreted.

◉ Aromatase inhibitors, SERMs, hCG, SARMs, and prohormones should not be treated as harmless support tools because they may reveal deeper endocrine disruption, informal cycle management, or uncertain product exposure.

◉ Metabolic and contest-prep iPEDs such as thyroid drugs, insulin, clenbuterol, diuretics, GLP/GIP agents, stimulants, and DNP can create acute risk that may be more dangerous than the androgen itself.

◉ Cardiovascular, hematologic, renal, hepatic, endocrine, reproductive, psychiatric, dermatologic, and musculoskeletal screening should be organized around the patient’s actual exposure pattern.

◉ Harm reduction does not mean helping a patient optimize an unsafe regimen, but it does mean treating adverse effects, monitoring risk, keeping the patient engaged, and continuing to support safer choices.

◉ Clinicians should avoid moralizing language because trust determines whether patients disclose the real exposure history needed for safe care.

◉ The core clinical standard is informed, nonjudgmental, medically serious care that brings patients out of secrecy and into structured monitoring, clear boundaries, and safer long-term recovery.

➀ The Modern AAS And iPED Patient

The modern AAS and iPED patient is often missed because clinicians still imagine a narrow stereotype. Many patients using these agents are not professional athletes, and most are not presenting because they failed a drug test. They may present for fatigue, infertility, erectile dysfunction, acne, blood pressure elevation, anxiety, poor sleep, abnormal liver enzymes, high hematocrit, “routine labs,” or concern that something is wrong after stopping a cycle. Appearance and strength are often more relevant motivations than organized sport. In a survey of 2,385 men using AAS, 82.2% reported improving appearance or gaining muscle as a motive, 50% reported strength gain, and fewer than 10% reported organized athletic performance.[1]

The first clinical skill is asking better questions. “Are you on steroids?” is too narrow and often fails. Patients may not consider SARMs, peptides, hCG, thyroid drugs, insulin, clenbuterol, GLP drugs, aromatase inhibitors, or diuretics to be steroid use. Some will answer no because they only use “research chemicals,” “peptides,” “test boosters,” or “optimization” agents. Others will withhold the truth because they expect judgment. The clinician should ask specifically about hormones, testosterone, oral or injectable anabolic agents, SARMs, peptides, fat-loss drugs, fertility drugs, estrogen blockers, thyroid drugs, insulin, diuretics, stimulants, erectile dysfunction drugs, hair-loss drugs, acne drugs, and products bought online.

Trust is not a soft issue in this population. It determines whether the clinician gets accurate data. Men using AAS often rate physicians poorly for knowledge of AAS and may rely more heavily on coaches, forums, other users, and underground sources.[1] That does not mean the clinician should validate unsafe advice. It means the clinician must be informed enough to ask precise questions, recognize common terms, and avoid a moralizing tone that ends the conversation. Nonjudgmental care keeps the patient in the medical system long enough to identify harm, treat disease, and support safer decisions.[2]

➁ Core AAS Categories Clinicians Must Recognize

AAS pharmacology can be clinically organized into a few major categories. Testosterone-derived agents include injectable esters such as testosterone cypionate, enanthate, propionate, undecanoate, and mixed-ester preparations, along with non-injectable testosterone products that may be medically used or misused in optimization settings. Testosterone remains the base of many AAS regimens because it is familiar, available, highly anabolic, and easily combined with other drugs. The same molecule can represent legitimate replacement therapy or supraphysiologic exposure depending on indication, dose, target level, monitoring, and whether other agents are stacked on top.

DHT-derived agents include drugs such as oxandrolone, stanozolol, drostanolone, methenolone, mesterolone, and oxymetholone. Users often describe these drugs as “dry,” “hardening,” cosmetic, or less estrogenic. That language can mislead both patients and inexperienced clinicians. Lower aromatization does not equal lower risk. DHT-derived and oral agents may worsen lipids, acne, androgenic alopecia, blood pressure, mood symptoms, hepatic markers, and virilization risk in women. Oral 17-alpha alkylated AAS deserve particular attention because hepatotoxicity is primarily associated with these oral agents rather than all AAS equally.[1,2]

19-nor and nandrolone-related agents include nandrolone decanoate, nandrolone phenylpropionate, trenbolone esters, and related compounds. These are commonly associated in user communities with mass, strength, aggression, body recomposition, and joint-comfort narratives. Clinically, they should raise concern for prolonged HPT-axis suppression, fertility disruption, sexual dysfunction, mood volatility, sleep disturbance, blood pressure changes, and difficult post-use recovery. Trenbolone exposure should sharpen the history because users frequently report severe insomnia, sweating, irritability, libido changes, and cardiovascular strain.

The clinician does not need to recite every underground brand name, but must recognize class signals. “Test and deca,” “test and tren,” “anavar,” “winny,” “d-bol,” “primo,” “masteron,” “blast,” “cruise,” and “PCT” are not casual gym slang in the medical office. They are data. Each term tells the clinician something about androgen exposure, suppression risk, liver risk, cardiovascular risk, fertility risk, and likely patient beliefs about what is safe.

➂ Use Patterns: Cycling, Stacking, Blast-And-Cruise, And Failed Cessation

AAS and iPED exposure is usually a pattern, not a single drug. “Cycling” refers to planned periods of use, often lasting weeks to months. “Stacking” refers to combining multiple AAS and iPED agents during the same period. “Post-cycle therapy,” or PCT, refers to attempts to restore endogenous testosterone production after stopping, commonly using SERMs, hCG, or other endocrine agents. “Blast-and-cruise” refers to higher-dose exposure followed by lower-dose continued androgen use rather than true cessation. These distinctions matter because they change whether the patient has a recoverable baseline, ongoing suppression, recurrent relapse, or continuous exposure.

The survey of 2,385 men found that two or three AAS or prohormone compounds were commonly used during a cycle, nearly half reported continuous use without PCT, and a similar proportion reported an on-and-off cycle approach with PCT.[1] Those patterns should change how clinicians interpret labs. A low LH and FSH after recent exposure may not mean primary hypogonadism. A high testosterone level may reflect timing, supraphysiologic dosing, or undisclosed use. A normal lab value during active use may not mean the patient is safe. The exposure timeline is essential.

Cessation is often harder than clinicians expect. In the survey, 46.16% had attempted to stop AAS use, but 60.22% of those attempts were unsuccessful.[1] Common reasons for not stopping included fear of decreased quality of life, loss of muscle or worsened appearance, decreased strength, lack of medical support, withdrawal symptoms, and perceived dependence.[1] A clinician who simply says “stop using” may be medically correct in principle but ineffective in practice. Patients may relapse because withdrawal feels intolerable, because their identity is tied to appearance and strength, or because their social environment reinforces continued use.

The visit should document the patient’s pattern clearly. The clinician should ask what was used, when it started, whether the patient is still using, whether there were true off periods, whether PCT was attempted, what symptoms occurred after stopping, and what caused resumption. That history often explains the patient’s current presentation better than the current lab panel alone.

➃ Accessory Endocrine Agents: AIs, SERMs, hCG, SARMs, And Prohormones

Accessory endocrine agents are commonly used to manage the side effects of AAS exposure while the exposure continues. Aromatase inhibitors such as anastrozole, letrozole, and exemestane are used to reduce estradiol-related symptoms or to chase a drier appearance. SERMs such as tamoxifen and clomiphene are used for gynecomastia concerns or attempted recovery. hCG is used to preserve testicular volume or support Leydig cell stimulation. These drugs can provide important clues, but they do not make the underlying AAS pattern safe.

The survey found frequent use of anastrozole, tamoxifen, exemestane, hCG, clomiphene, and similar agents during or after AAS cycles.[1] This matters because patients often treat these drugs as routine cycle-management tools rather than medications with their own risks and limitations. Aromatase inhibitors may contribute to sexual dysfunction, adverse body composition changes, and bone density concerns when estrogen is suppressed excessively.[2] SERMs and hCG may be part of medically supervised recovery in selected cases, but high-quality evidence for many informal PCT practices remains limited.[1,2]

SARMs and prohormones require a particularly careful history because patients often believe they are safer than AAS. SARMs are commonly marketed online as selective, modern, mild, or “not steroids.” Prohormones and designer precursors may be sold as supplement-like products even when their physiologic intent is androgenic. The harm-reduction review notes that SARMs lack adequate long-term safety data and that products sold online may be mislabeled or contaminated.[2] The clinician should treat SARM or prohormone exposure as clinically meaningful androgen exposure until proven otherwise.

The boundary is important. Harm reduction does not mean prescribing AIs, SERMs, hCG, or other agents to help a patient continue an unsafe illicit regimen. It may mean recognizing what the patient is already taking, identifying adverse effects, treating diagnosed conditions, counseling on risk, and planning supervised cessation or recovery when the patient is ready. The note should distinguish patient-reported self-use from clinician-prescribed treatment.

➄ Metabolic, Appearance, And Contest-Prep iPEDs

Modern iPED exposure extends well beyond classic AAS. Patients may use growth hormone, IGF-1-related products, secretagogues, peptides, GLP/GIP drugs, insulin, thyroid hormone, clenbuterol, ephedrine, caffeine stacks, diuretics, DNP, melanotan products, erectile dysfunction drugs, hair-loss drugs, acne drugs, and cosmetic-adjacent compounds. The transcript and outline both emphasize that modern iPED use can appear in bodybuilding, strength sports, CrossFit-type communities, looksmaxing, testosterone maxing, contest preparation, and social media-driven body transformation.

Metabolic and fat-loss agents can create high-risk presentations. T3, T4, clenbuterol, ephedrine, stimulants, GLP/GIP drugs, and DNP may be used for cutting, leanness, appetite control, or rapid visual change. Clenbuterol and thyroid misuse can produce tachycardia, anxiety, hypertension, arrhythmia, heat intolerance, insomnia, and muscle loss. DNP deserves direct warning because it can produce fatal hyperthermia.[2] Insulin misuse is another major danger because non-diabetic users may take it for mass gain or nutrient partitioning and develop severe hypoglycemia, seizures, coma, or death.[2]

Diuretic use is one of the most dangerous contest-prep behaviors. It may be combined with sodium restriction, water manipulation, laxatives, heat exposure, stimulants, and final-week dehydration. The clinician should ask about contest dates, photoshoots, weigh-ins, recent cramping, syncope, palpitations, weakness, dark urine, or emergency visits. Potassium and magnesium assessment may be necessary when diuretics are used in this setting.[2] The patient may call it “drying out,” but the physiologic risk is electrolyte collapse, arrhythmia, kidney injury, rhabdomyolysis, and death.

Peptides and growth hormone pathway agents often sound less threatening to patients because “peptide” has become a wellness term. That language should not reassure the clinician. Products marketed for recovery, sleep, fat loss, injury healing, tanning, libido, or anti-aging may have uncertain identity, purity, sterility, and human safety data. The clinician should document source, route, claimed purpose, adverse effects, and whether the product was prescribed, compounded, purchased online, or obtained through an underground source.

➅ Red-Flag Risk Domains In AAS And iPED Care

AAS and iPED exposure should trigger organized risk screening. The most important domains are cardiovascular, hematologic, renal, hepatic, endocrine, reproductive, psychiatric, dermatologic, and musculoskeletal. More than 94% of survey respondents reported side effects from AAS use.[1] Frequently reported issues included testicular atrophy, acne, hypersexuality, hypertension, mood changes, erectile dysfunction, dyslipidemia, gynecomastia, hair loss, polycythemia, injection-site abscess, infertility, tendon rupture, and left ventricular hypertrophy.[1] These findings are not rare side notes. They are expected clinical surveillance targets.

Cardiovascular risk requires early attention. AAS use has been associated with dyslipidemia, hypertension, left ventricular hypertrophy, arrhythmias, atherosclerosis, and impaired cardiac function.[2,3,6] Initial assessment should include blood pressure, lipid profile, cardiometabolic risk review, family history, symptom assessment, and ECG when appropriate.[2] Echocardiography should be considered when chronic exposure, symptoms, suspected LVH, cardiac dysfunction, strong family history, or other risk features are present.[2] Coronary calcium assessment may be appropriate when atherosclerotic risk factors or long-term exposure raise concern.[2]

Hematologic and renal screening should not be superficial. CBC and hematocrit are needed because androgen exposure can increase erythropoiesis and lead to erythrocytosis. Kidney assessment may require more than creatinine in heavily muscled patients, because muscle mass and supplements can complicate interpretation. Urinalysis, urine albumin-creatinine ratio, blood pressure, and longitudinal renal markers can help identify early injury. AAS use has been associated with focal segmental glomerulosclerosis and other renal concerns in some users.[8]

Hepatic risk depends heavily on the agent. Oral 17-alpha alkylated AAS are the most relevant direct hepatotoxicity concern.[1,2] Liver function testing should be obtained when oral AAS, prohormones, designer compounds, or hepatically relevant co-exposures are present. Alcohol, isotretinoin, supplements, acetaminophen, and other hepatotoxic agents can increase concern. The clinician should not assume that a short oral course is harmless simply because the patient calls it a “kickstart.”

Reproductive and psychiatric risk must be asked directly. AAS exposure can suppress gonadotropins, impair spermatogenesis, cause testicular atrophy, and contribute to anabolic steroid-induced hypogonadism.[1,2,7] Fertility goals, testicular symptoms, sexual function, gonadotropins, testosterone timing, and semen analysis may be relevant. Psychiatric screening is equally important when patients report anxiety, irritability, hypomanic symptoms, aggression, depression, body dysmorphia, stimulant use, substance use, or withdrawal symptoms. Behavioral health referral is not an afterthought when mood instability, suicidality, or dependence features appear.

➆ Harm Reduction Without Facilitating Misuse

Harm reduction begins when the patient is already using or recently exposed and is not ready, willing, or able to stop immediately. The clinician should discourage unsafe AAS and iPED use, but should not abandon the patient because the patient is not ready for cessation. Refusing evaluation can push the patient back to forums, coaches, underground labs, or other users. The harm-reduction review argues for nonjudgmental care focused on education, adverse-effect screening, risk treatment, and support for cessation.[2]

The first visit should clarify the patient’s concern. Some patients want blood work. Some want fertility help. Some want to stop but fear withdrawal. Some want reassurance that their current plan is safe. Some want a physician to prescribe medications that help maintain the cycle. These are not the same clinical requests. The clinician can provide evaluation and treatment for adverse effects while refusing to assist ongoing misuse. Treating hypertension, dyslipidemia, erythrocytosis, infection, psychiatric symptoms, hypoglycemia risk, or cardiac disease is harm reduction. Prescribing an aromatase inhibitor, SERM, hCG, or erectile dysfunction drug simply to support an illicit cycle is facilitation, not harm reduction.

A practical harm-reduction plan should be exposure-specific. Injectable AAS exposure requires cardiovascular, hematologic, endocrine, reproductive, and psychiatric surveillance. Oral AAS exposure adds hepatic assessment. Thyroid and clenbuterol exposure require cardiovascular and thyroid-axis attention. Insulin misuse requires hypoglycemia counseling and a safety plan if the patient refuses to stop. Diuretic use near contest preparation requires urgent electrolyte and renal risk awareness. SARMs and peptides require counseling about unknown safety, mislabeling, contamination, and lack of reliable product identity.

The clinician’s tone should be direct and calm. The patient should hear that the clinician does not endorse unsafe use, but also that medical care remains available. That balance is what keeps the patient engaged. It also creates repeated opportunities to revisit cessation, identify new harm, and move the patient toward safer physiology over time.

➇ Documentation, Monitoring, And Longitudinal Clinical Strategy

Documentation is part of the treatment. The note should record the patient’s stated goals, current and past compounds, source, route, dose if known, timing, cycling pattern, PCT attempts, prior cessation attempts, adverse effects, comorbidities, and readiness to stop. It should distinguish confirmed facts from patient-reported information and unknown product identity. A patient using “research peptides” from an online vendor should not be documented as if they are taking a known, regulated prescription product.

Monitoring should be matched to exposure rather than ordered randomly. Common baseline and follow-up considerations include blood pressure, CBC, CMP, lipids, glucose or A1C, liver markers, renal markers, urinalysis, urine albumin-creatinine ratio, testosterone-related labs when clinically useful, LH and FSH when suppression classification matters, estradiol when clinically indicated, semen analysis when fertility matters, ECG when appropriate, echocardiography when concern exists, and specialty referral when findings exceed the clinician’s scope. ABCDS™ can help organize glycemic status, blood pressure, cardiovascular and lipid risk, hematologic response, symptom experience, and screening duties over time.

Longitudinal care should repeatedly reassess cessation readiness. Some patients will stop quickly once risk is identified. Others will need multiple visits before they trust the clinician enough to attempt recovery. Some will relapse after prolonged cessation. The survey’s poor cessation success rate reinforces that the clinician should not treat a single failed attempt as moral failure.[1] The plan should account for withdrawal symptoms, fertility goals, mood stability, social environment, body image drivers, and the patient’s fear of losing function or identity.

AAS and iPED care is safest when it is clinically honest. The clinician should document that unsafe use was discouraged, that risks were explained, that harm-reduction monitoring was offered or performed, that urgent warning signs were reviewed, and that referral was recommended when needed. The goal is not to normalize AAS or iPED use. The goal is to bring patients out of secrecy and into medically accountable care, where harm can be identified, treated, and reduced.

COURSE SUMMARY

This course trained clinicians to recognize AAS and iPED use as a multi-agent exposure syndrome rather than a single-drug behavior. Modern patients may use these agents for appearance, strength, masculinity, leanness, confidence, contest preparation, recovery, or optimization rather than formal sport. The clinician must therefore ask beyond “steroids” and identify testosterone esters, DHT-derived agents, 19-nor agents, oral AAS, SARMs, prohormones, peptides, growth hormone pathway agents, thyroid drugs, insulin, stimulants, diuretics, fertility drugs, SERMs, aromatase inhibitors, and other accessory agents.

Clinicians learned that exposure pattern drives risk interpretation. Cycles, stacking, blast-and-cruise patterns, PCT attempts, continuous use, failed cessation, and withdrawal symptoms affect the meaning of labs, symptoms, and recovery expectations. The course emphasized cardiovascular, hematologic, renal, hepatic, endocrine, reproductive, psychiatric, dermatologic, and musculoskeletal red flags. It also separated harm reduction from facilitation. The clinician should discourage unsafe use while still treating adverse effects, monitoring risk, maintaining clear boundaries, and supporting eventual cessation when possible. The core clinical standard is informed, nonjudgmental, medically serious care that brings patients out of secrecy and into structured monitoring.

REFERENCES

Bonnecaze AK, O’Connor T, Aloi JA. Characteristics and attitudes of men using anabolic androgenic steroids: a survey of 2385 men. American Journal of Men’s Health. 2020;14(6):1557988320966536.
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. Journal of General Internal Medicine. 2021;36(7):2055-2064.
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.
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.
Kanayama G, Brower KJ, Wood RI, Hudson JI, Pope HG Jr. Anabolic-androgenic steroid dependence: an emerging disorder. Addiction. 2009;104(12):1966-1978.
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.
Rahnema CD, Lipshultz LI, Crosnoe LE, Kovac JR, Kim ED. Anabolic steroid-induced hypogonadism: diagnosis and treatment. Fertil Steril. 2014;101(5):1271-1279.
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.
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.
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.

Anabolic Androgenic Steroids and iPED Agents

Course Overview

Learning Objectives

Course Topics

011 Anabolic Androgenic Steroids and iPED Agents

Video Lesson Takeaways

➀ The Modern AAS And iPED Patient

➁ Core AAS Categories Clinicians Must Recognize

➂ Use Patterns: Cycling, Stacking, Blast-And-Cruise, And Failed Cessation

➃ Accessory Endocrine Agents: AIs, SERMs, hCG, SARMs, And Prohormones

➄ Metabolic, Appearance, And Contest-Prep iPEDs

➅ Red-Flag Risk Domains In AAS And iPED Care

➆ Harm Reduction Without Facilitating Misuse

➇ Documentation, Monitoring, And Longitudinal Clinical Strategy

Recommended Grand Rounds Case Reviews

Advanced Clinical Training Insights