Critical Mistakes by Beginners During Their First Anabolic-Androgenic Steroid Course: A Medical Analysis
Introduction
A first anabolic-androgenic steroid (AAS) course is a critical period that determines not only athletic performance but also the athlete's long-term health. Unfortunately, the vast majority of novice users make systemic errors that can lead to serious and often irreversible consequences for the body.
Mistake #1: Lack of Pre-Cycle Laboratory Diagnostics
The Essence of the Problem
The most fundamental mistake is starting a cycle without prior comprehensive screening. A typical "mild" first course (250-500 mg of testosterone enanthate weekly + 20-40 mg of oxandrolone or another oral anabolic) is perceived as safe, creating a false sense of security.
Hidden Risks
Without baseline tests, it is impossible to identify pre-existing conditions that exogenous hormones will exacerbate:
Liver Markers (ALT/AST): If baseline transaminases are already elevated (non-alcoholic fatty liver disease, chronic hepatitis), adding hepatotoxic oral steroids can lead to acute drug-induced hepatitis with bilirubin >100 µmol/L and symptoms of jaundice.
Gilbert's Syndrome: Present in 3-10% of the population. Characterized by chronic elevation of indirect bilirubin. Adding alkylated steroids can cause bilirubin to reach critical levels (>150 µmol/L), creating a risk of bilirubin encephalopathy.
Lipid Profile: Pre-existing dyslipidemia (LDL >3.5 mmol/L, LDL/HDL >4) combined with AAS transforms into a high-risk atherogenic profile. Oxandrolone, despite its reputation as a "mild" steroid, can lower HDL by 40-50% and raise LDL by 20-30%. For a patient with initially high LDL, this creates conditions for accelerated atherogenesis, acute coronary syndrome, and thrombosis.
Estradiol: Individual variability in aromatase activity is enormous. For some athletes, even 250 mg of testosterone weekly can cause estradiol >200 pmol/L (normal 40-160), manifested as gynecomastia, water retention, and emotional lability. Without pre-cycle estradiol measurement, it is impossible to predict the need for aromatase inhibitors.
Prolactin: Pituitary reactivity is individual. In stress-sensitive individuals, even without using 19-nor-testosterones (nandrolone, trenbolone), prolactin can rise >1000 mIU/L, causing galactorrhea, erectile dysfunction, and suppressed libido.
Clinical Consequences
The lack of monitoring turns a manageable process into medical roulette. Typical scenarios:
Acute myocardial infarction in a 28-year-old athlete with undiagnosed familial hypercholesterolemia during the 8th week of a cycle.
Liver failure requiring transplantation in a patient with undiagnosed chronic hepatitis C.
Severe gynecomastia requiring surgical treatment due to ignored estradiol levels.
Mistake #2: Unrealistic Expectations and Dosage Escalation
Psychological Aspect
The first cycle is often accompanied by inflated expectations, fueled by marketing and misinformation on social media. Athletes expect a body transformation in 12 weeks comparable to that of professionals using gram-level dosages for several years.
Reality of the First Cycle
Physiologically justified results of a first course (250 mg testosterone enanthate + 20-40 mg oxandrolone for 12 weeks):
Muscle mass gain: 3-5 kg
Fat mass loss: 1-3 kg
Increase in strength indicators: 15-25%
These are solid results, but far from Instagram transformations.
Dangerous Escalation
Disappointment by weeks 8-10 leads to impulsive decisions:
Scenario: Increasing testosterone to 500-750 mg/week, raising oxandrolone to 60-80 mg, adding nandrolone decanoate 200-400 mg/week, and extending the cycle to 20-24 weeks.
Medical Consequences:
Cardiovascular: Left ventricular hypertrophy begins to develop with use of >500 mg testosterone for more than 16 weeks. Adding nandrolone worsens myocardial remodeling.
Hematological: Polycythemia (hematocrit >54%) develops in 20-30% of high-dose users, increasing the risk of thromboembolism by 3-4 times.
Endocrine: Suppression of the hypothalamic-pituitary-gonadal axis becomes deeper. Recovery after a 20-week course can take 6-12 months compared to 3-4 months after a 12-week course.
Psychological: Formation of a pattern of "solving problems by increasing dosages," which is a predictor of abuse.
Pharmacological Reality
The dose-effect relationship for AAS is not linear. Doubling the dose does not double the result but exponentially increases side effects. This is due to:
Saturation of androgen receptors
Proportional increase in aromatization
Progressive suppression of endogenous testosterone
Mistake #3: Ignoring Supportive Pharmacology and Nutraceuticals
The Problem of Underestimating Support
Athletes who neglect bloodwork also tend to ignore protective therapy, considering it "unnecessary overcaution." This is a systemic thinking error.
Critical Deficiencies and Their Consequences
1. Magnesium:
Mechanism: AAS increase magnesium utilization by 20-40% through enhanced protein synthesis and metabolism. Deficiency is worsened by sweat loss during intense training.
Clinical Signs: Night leg cramps, fasciculations, tremor, arrhythmias (ventricular extrasystoles), insulin resistance.
Prevention: Magnesium glycinate 200-400mg mg of elemental magnesium daily.
2. Sleep and Nervous System:
Problem: Supraphysiological androgens hyperactivate the CNS, causing insomnia, anxiety, and irritability in 30-40% of users.
Mechanism: Androgens modulate GABAergic transmission, reduce deep sleep (stages 3-4).
Solution:
Niacinamide 500 mg before bed (GABAergic effect)
Taurine 3-5 g (GABA receptor modulator, neuroprotector)
Ashwagandha (KSM-66 extract) 600 mg (anxiolytic, cortisol reduction)
Lion's Mane (Hericium erinaceus) 1-2 g (neurogenesis, sleep quality improvement)
3. Blood Rheology and Lipid Profile:
Problem: AAS increase hematocrit, blood viscosity, thrombogenicity, lower HDL, raise LDL and Lp(a).
Risks: Myocardial infarction, stroke, deep vein thrombosis (especially during long flights).
Protection Protocol:
Statins: Pitavastatin 1-2mg daily LDL >3.0 mmol/L or its significant increase during the cycle.
Bergamot Citrus: 500-1000 mg of standardized extract (polyphenols inhibit HMG-CoA reductase, increase HDL by 15-20%).
Omega-3: EPA+DHA 2-4 g daily (anti-inflammatory effect, improved rheology).
Aspirin: 75-100 mg if hematocrit >50% (antiplatelet).
4. Blood Pressure:
Mechanism: Sodium and water retention, increased sympathetic tone, 10-15% increase in blood volume.
Clinical Signs: BP can increase by 10-20 mm Hg, up to 160-180/100-110 mm Hg in predisposed individuals.
Protocol:
Sartans (Telmisartan): 40-60 mg daily. Advantages: cardioprotection, PPAR-γ activation (improves insulin sensitivity), no impact on workouts.
Taurine: 3-6 g (RAAS modulator, mild diuretic)
Magnesium: synergistic with sartans.
Clinical Case
An athlete, 26 years old, first cycle (300 mg testosterone + 30 mg oxandrolone), without supportive therapy. By week 7:
Night cramps (magnesium deficiency)
BP 155/95 (baseline 125/80)
Insomnia, anxiety
HDL dropped from 1.2 to 0.6 mmol/L
LDL increased from 3.2 to 4.8 mmol/L
Result: Cycle termination, 3 months of recovery, lost results, disappointment.
With proper support, the cycle could have been completed successfully.
Mistake #4: Lack of Post-Cycle Therapy (PCT)
The Misconception of "Natural Recovery"
The most common belief among young athletes (18-25): "I have high natural testosterone, my body will recover on its own." This is a dangerous misconception based on a misunderstanding of physiology.
Physiology of HPTA Suppression
Mechanism: Exogenous androgens via negative feedback suppress the secretion of GnRH by the hypothalamus. LH and FSH secretion by the pituitary decreases. The testes atrophy (25-40% volume reduction), cease testosterone production and spermatogenesis.
After a 12-week testosterone course:
Endogenous testosterone production: <50-100 ng/dL (normal 300-1000 ng/dL)
LH & FSH: suppressed or undetectable
Testosterone enanthate half-life: 7-10 days
Without PCT, recovery takes:
First signs of LH/FSH recovery: 4-6 weeks
Return of testosterone to lower limit of normal: 12-16 weeks
Full recovery: 6-12 months
Clinical Consequences of Hypogonadism
Weeks 1-4 after the last injection:
Testosterone drops to <100-150 ng/dL
Severe asthenia, depression
Complete loss of libido, erectile dysfunction
Catabolism: loss of 40-60% of gained muscle mass
Decreased motivation to train
Sleep disturbances
Increased anxiety, emotional lability
Weeks 4-12:
Gradual recovery, but testosterone remains suboptimal (200-400 ng/dL)
Reduced performance persists
Possible fat gain (cortisol remains elevated with low testosterone)
Psychological instability
PCT Protocol: Scientific Rationale
Goals of PCT:
Rapid restoration of LH/FSH secretion
Restoration of endogenous testosterone
Minimization of muscle mass loss
Preservation of quality of life and training capacity
Preserving Results
Proper PCT allows for:
Preservation of 70-85% of gained muscle mass (vs. 40-50% without PCT)
Restoration of testosterone to 500-700 ng/dL within 4-6 weeks (vs. 3-4 months)
Maintenance of normal well-being and libido
Continuation of effective training (albeit with reduced intensity)
Long-Term Risks of Avoiding PCT
Repeated cycles without PCT lead to:
Chronic hypogonadism (irreversible in 15-20% of cases)
Necessity of lifelong testosterone replacement therapy
Infertility
Osteoporosis
Increased risk of cardiovascular disease
Metabolic syndrome
Conclusion: Principles of Responsible Use
A first AAS course is not an experiment or entertainment. It is a serious medical intervention into the endocrine system, requiring:
1. Comprehensive Pre-Cycle Diagnostics: At minimum: CBC, biochemistry (ALT, AST, bilirubin, creatinine, glucose), lipid profile, testosterone, estradiol, prolactin, TSH.
2. Regular Monitoring: Tests at weeks 4-6 of the cycle and upon completion.
3. Adequate Dosages: The first cycle is a time to study the body's response, not chase maximal results.
4. Comprehensive Supportive Therapy: Protection of the cardiovascular system, liver, and CNS is not an option but a necessity.
5. Competent PCT: Refusing PCT guarantees loss of results and risks chronic health problems.
Problems arising during the first course due to an irresponsible approach can haunt one for life: from chronic heart disease to lifelong hormonal dependence.
Health is the only asset that cannot be bought with money. A sensible approach to the first course lays the foundation for years of safe AAS use and achieving athletic goals without destroying the body.
Even if blood testosterone levels are still not “zero,” locally within the testes testosterone is nearly absent