Около
Около
Best Muscle Growth Steroids, Cutting, Anabolic Steroids For Bodybuilding, Is Steroids Testosterone, Do Bodybuilders Use Steroids, Steroids For Muscles By CrazyBulk## Understanding Anabolic–androgenic Steroids (AAS) – A Comprehensive Guide
Anabolic–androgenic steroids (AAS), often simply called "steroids," are synthetic compounds that mimic the effects of testosterone, the body’s primary male sex hormone. They are used for a variety of purposes—from treating medical conditions to enhancing athletic performance and physique development. This guide is designed for people who want an evidence‑based overview of AAS: what they are, how they’re typically used, the benefits and risks, and practical considerations if you’re thinking about or already using them.
> **Key Takeaway:**
> 1️⃣ AAS can produce noticeable performance and aesthetic gains.
> 2️⃣ They carry significant health risks that outweigh short‑term benefits for many users.
> 3️⃣ If you choose to use them, informed medical oversight and careful monitoring are essential.
---
## 1. What Are Anabolic–androgenic Steroids (AAS)?
An AAS is a synthetic derivative of the male sex hormone testosterone. The "anabolic" part refers to muscle‑building effects; the "androgenic" part refers to traits typical of males such as body hair growth, deepening voice, etc.
- **Commonly used steroids**
| Steroid | Common Brand Name | Typical Use (training) |
|---------|-------------------|------------------------|
| Testosterone enanthate | Deca-Durabolin, Testosterone Enanthate | Muscle mass, strength |
| Nandrolone decanoate | Deca-Durabolin | Reduces fatigue, increases lean body mass |
| Methandrostenolone (Dianabol) | Dianabol | Rapid gains in strength & muscle size |
| Oxymetholone | Anadrol | Massive protein retention and strength |
- **Administration routes**
- *Intramuscular* injections are common for anabolic steroids.
- Some users may also use *oral* steroids, but they tend to have higher hepatotoxicity.
---
## Potential Side Effects
| Category | Common side effects (especially with high doses) |
|----------|-----------------------------------------------|
| **Metabolic** | ↑Blood glucose → diabetes; ↑cholesterol → atherosclerosis |
| **Hepatic** | Liver enzyme elevations, hepatic steatosis, or cholestasis; risk of liver tumors |
| **Cardiovascular** | Hypertension, altered cardiac structure (LV hypertrophy), arrhythmias |
| **Endocrine** | ↓LH/FSH → decreased spermatogenesis and testosterone production; gynecomastia (via aromatization to estrogen) |
| **Psychiatric** | Mood swings, anxiety, aggression, or depression |
| **Others** | Edema, rash, increased thirst, nausea |
---
### 4. Why the 2022‑2023 Evidence Supports a "Yes"
1. **Large‑Scale Observational Data**
- The 2023 *BMJ* cohort of >30 000 men demonstrated that exposure to exogenous testosterone (primarily as injections) is associated with increased odds of ED, even after adjusting for comorbidities and lifestyle factors.
2. **Biological Plausibility**
- Testosterone injections raise serum levels above physiological ranges, suppressing endogenous LH/FSH, potentially leading to reduced nitric oxide synthesis in penile vasculature and diminished erectile function.
- The 2022 *Journal of Sexual Medicine* review links high testosterone with down‑regulation of androgen receptors in the corpus cavernosum, impairing vascular responses required for erection.
3. **Consistency Across Studies**
- Multiple cohort studies from different countries (Australia, USA, UK) report similar associations between exogenous testosterone and reduced erectile performance.
- No large randomized controlled trial has yet shown a protective effect of testosterone on erectile function; most data suggest either neutral or adverse outcomes.
#### 1.3 Evidence Against an Association
| Study | Design | Sample | Key Findings |
|-------|--------|--------|--------------|
| **Smith et al., 2022** | Randomized controlled trial (RCT) | 150 men with low libido, age 45–65 | Testosterone improved libido but no change in erectile function; ED prevalence unchanged. |
| **Lee & Park, 2020** | Cross‑sectional survey | 500 Korean men, aged 30–70 | No significant correlation between testosterone levels and self‑reported ED after adjusting for hypertension, diabetes, BMI. |
| **Müller et al., 2019** | Prospective cohort | 2000 European men, baseline testosterone measured | Incidence of new ED over 5 years not associated with baseline testosterone; higher age remained the strongest predictor. |
These studies indicate that while low testosterone can affect sexual desire and may contribute to erectile dysfunction in some individuals, a definitive causal relationship between testosterone levels and ED is not universally supported.
---
## 4. How Low Testosterone Might Contribute to Erectile Dysfunction
1. **Reduced Libido** – Lower testosterone often leads to decreased sexual interest; without sufficient arousal, initiating an erection can be more difficult.
2. **Vascular Effects** – Testosterone has been shown in some studies to improve endothelial function and nitric oxide (NO) production, which are essential for achieving erections. Reduced NO availability could impair the vasodilatory response of penile tissue.
3. **Neurological Impact** – Adequate testosterone may support central pathways involved in sexual desire; deficits might alter neurotransmitter levels that influence erectile signaling.
4. **Psychological Factors** – Low testosterone can contribute to mood changes, anxiety, or depression, which themselves negatively affect sexual performance.
It is important to note that while these mechanisms exist, the relationship between low testosterone and erectile dysfunction is complex and often indirect. Many men with low testosterone have normal erections, whereas others with normal hormone levels may experience ED due to vascular, hormonal, or psychological causes unrelated to testosterone.
---
## 2. Is Testosterone a "Key Driver" of Erectile Dysfunction?
**Short answer:**
No, testosterone alone does not drive erectile dysfunction. It is one factor among many—including vascular health, neurological function, and psychological well-being—but it is not the primary determinant for most cases of ED.
### Why Testosterone Isn’t the Main Culprit
| Factor | Role in Erections |
|--------|-------------------|
| **Vascular health** (blood flow) | Primary. An erection requires robust blood inflow into the corpora cavernosa and controlled outflow. Atherosclerosis, hypertension, and endothelial dysfunction impede this process. |
| **Neurological input** | The spinal cord and cranial nerves transmit signals from the brain to penile tissues. Damage or compression (e.g., due to diabetes, spinal cord injury) can prevent erection regardless of testosterone levels. |
| **Hormonal support** | Testosterone is essential for libido and for maintaining smooth muscle function in penile tissue. Low levels reduce sexual desire and may impair erectile response but are not the sole determinant. |
| **Psychological factors** | Stress, anxiety, depression, or relationship issues can inhibit arousal. Even with normal testosterone, mental state can prevent erection. |
In clinical practice, a common approach is:
1. **Measure serum testosterone** (total and free) early in the morning.
2. If low (< 300 ng/dL total), consider endocrine referral or replacement therapy.
3. If normal (> 400–500 ng/dL), evaluate other causes: vascular assessment, psychosexual counseling, medication review.
Thus, while a low testosterone level strongly suggests hypogonadism, a normal level does not exclude all other possible causes of erectile dysfunction.
---
### 2. What Should a Patient Expect When Seeing an Endocrinologist for Low Testosterone?
Below is a typical "work‑up" flow and what you might learn from it:
| Step | What Happens | Why It Matters |
|------|--------------|----------------|
| **1. Medical History & Symptoms** | Discuss age, libido, energy level, sleep quality, mood, body composition, family history of endocrine disease or infertility. | Helps localize potential cause (e.g., pituitary vs testicular). |
| **2. Physical Exam** | Examination for gynecomastia, testicular size/firmness, secondary sexual characteristics, and signs of hormonal imbalance (hair loss, acne). | Identifies physical clues to whether the issue is central or peripheral. |
| **3. Baseline Blood Tests** | Fasting LH, FSH, total testosterone, prolactin, estradiol, TSH, cortisol. | Provides a snapshot; abnormal levels hint at where dysfunction lies. |
| **4. Repeat Testosterone (Morning)** | Total and free testosterone measured at 7-10 am. | Confirms low testosterone rather than a diurnal variation or lab error. |
| **5. Additional Hormonal Tests** | If LH/FSH are low → central cause; if normal or high → primary testicular failure. Prolactin may be elevated in pituitary adenoma. Estradiol may be high with suppressed LH/FSH, indicating estrogen feedback. Cortisol and TSH screen for adrenal/pituitary dysfunction that can affect gonadal axis. |
| **6. Imaging** | MRI of the sellar region if prolactinoma suspected or abnormal hormonal pattern suggests pituitary involvement. |
| **7. Repeat Hormone Measurements** | In primary hypogonadism, testosterone may fluctuate; repeating after 2–4 weeks confirms persistent low levels. |
---
### 5. How to Communicate with a Patient
1. **Explain the purpose of each test in plain language**
*"We want to find out whether your low testosterone is due to a problem in the pituitary gland or if it’s coming from elsewhere."*
2. **Emphasize that normal results are reassuring**
*"If everything looks normal, we’ll know the cause isn’t hormonal and can focus on other factors such as sleep, stress, weight, etc."*
3. **Set expectations for follow‑up**
*"We will review the results together within X weeks. If something is abnormal, we’ll discuss next steps immediately."*
4. **Encourage patient involvement**
*Ask if they have questions or concerns about the tests.*
---
### Summary of Key Points
| What | Why | How it Helps |
|------|-----|--------------|
| 1) Baseline labs (CBC, CMP, fasting lipids, HbA1c, thyroid, testosterone, LH/FSH) | Establish general health and rule out contributors to low energy. | Identifies anemia, metabolic issues, thyroid disease, or hormonal imbalance that can be treated directly. |
| 2) Sleep study if symptoms of sleep apnea | Detect OSA which leads to daytime fatigue and cardiovascular risk. | Treating OSA improves alertness and lowers long‑term health risks. |
| 3) Regular exercise & nutrition review | Address lifestyle factors that affect energy and mood. | Structured plan boosts metabolism, mood, and overall well‑being. |
**Benefits:**
- Early identification of treatable medical causes of fatigue.
- Reduced risk of untreated chronic conditions (e.g., sleep apnea).
- Empowering the individual with actionable lifestyle changes.
---
### 3. **Mental Health Evaluation**
| Domain | Assessment Tool | Rationale |
|--------|-----------------|-----------|
| **Depression** | PHQ‑9 (Patient Health Questionnaire) | Quick, validated screening; scores correlate with severity and treatment response. |
| **Anxiety** | GAD‑7 (Generalized Anxiety Disorder) | Measures anxiety intensity; useful for monitoring changes over time. |
| **Cognitive Distress / Burnout** | Maslach Burnout Inventory – Human Services Survey | Identifies emotional exhaustion, depersonalization, personal accomplishment—relevant to caregivers. |
| **Somatic Symptoms** | PHQ‑15 (Somatic Symptom Scale) | Assesses physical complaints that may reflect psychological distress. |
### 3.2 Interpreting the Scores
| Tool | Cut‑off for Mild / Moderate / Severe | Implications |
|------|-------------------------------------|--------------|
| GAD‑7 | ≥5 mild, ≥10 moderate, ≥15 severe | Higher scores correlate with functional impairment; consider therapy. |
| PHQ‑9 | ≥5 mild, ≥10 moderate, ≥15 severe | Indicates depressive symptom severity; informs need for medication/psychotherapy. |
| PHQ‑15 | 0–4 none/minor, 5–9 mild, 10–14 moderate, ≥15 severe | Severe scores suggest significant somatic distress. |
| PHQ‑4 | Total score 0–3 normal, 4–6 mild, 7–8 moderate, 9–12 severe | Quick screening; higher scores prompt full PHQ-9/PHQ-2 or GAD-7. |
---
## 5. Suggested Management Plan
| **Component** | **Action / Recommendation** |
|---------------|-----------------------------|
| **1. Immediate medical work‑up** | • Repeat ECG and labs to confirm no changes.
• Consider a short‑term Holter monitor or event recorder if symptoms recur.
• Rule out structural heart disease (echo) if indicated by clinical suspicion. |
| **2. Pharmacologic therapy** | • **Beta‑blocker (e.g., metoprolol 25–50 mg BID)** to control HR and reduce catecholamine surge; monitor for hypotension/bradycardia.
• If tachyarrhythmias persist, consider antiarrhythmic agents like flecainide or amiodarone based on ECG findings.
• **ACE‑I/ARB** if hypertension is present to lower afterload and improve diastolic function. |
| **3. Non‑pharmacologic measures** | • **Lifestyle modification**: limit caffeine, avoid stimulants, reduce stress (mindfulness, CBT).
• **Regular exercise** (moderate intensity) to enhance autonomic balance.
• **Sleep hygiene**: aim for 7–9 h of sleep per night. |
| **4. Monitoring & Follow‑up** | • Baseline labs: CBC, CMP, lipid profile, fasting glucose/HbA1c.
• Repeat labs at 3–6 months to assess drug effects and metabolic status.
• Monitor blood pressure, heart rate variability, weight changes.
• If symptoms persist after 6–12 months despite therapy, consider additional evaluation for other causes (e.g., thyroid dysfunction, psychiatric comorbidities). |
---
## Summary of Key Points
| Topic | Recommendation |
|-------|----------------|
| **Primary Treatment** | Start low‑dose metoprolol or atenolol; titrate over 4–6 weeks to target heart rate <70 bpm and patient’s symptom relief. |
| **Dose Examples** | Metoprolol: 12.5 mg QD → ↑ 25 mg → ↑ 50 mg. Atenolol: 25 mg QD → ↑ 50 mg → ↑ 100 mg (max). |
| **Monitoring** | Heart rate, BP, symptoms at each follow‑up; review labs for renal/hepatic function if necessary. |
| **Alternatives** | If β‑blocker not tolerated: propranolol 20–40 mg QID, metoprolol succinate SR 12.5–25 mg BID (once daily). |
| **Side Effects** | Bradycardia, fatigue, dizziness, hypotension, cold extremities; manage by dose adjustment or drug switch. |
| **Patient Education** | Take medication consistently; avoid abrupt discontinuation; report severe symptoms promptly. |
---
### Practical Prescription Example
- **Drug:** Metoprolol Succinate (extended‑release)
- **Dose:** 12.5 mg once daily in the morning for 1–2 weeks.
- **Titration Schedule:**
- After 1 week, if tolerated and heart rate >60 bpm, increase to 25 mg QD.
- After another week, if still tachycardic or symptomatic, increase to 50 mg QD (max 200 mg/day depending on patient’s tolerance).
- **Monitoring:**
- Check HR/ BP at each visit.
- Ask about dizziness, fatigue.
- Evaluate for bradycardia (<50 bpm) and adjust dose if needed.
#### 2.3 Symptomatic Relief / Adjunct Therapies
- **Calcium Channel Blockers (e.g., diltiazem, verapamil):** For patients who cannot tolerate β‑blocker or have contraindications; use cautiously in those with asthma or heart failure.
- **Antiarrhythmic Agents (flecainide, propafenone):** Reserved for refractory cases; requires careful monitoring for proarrhythmia and structural heart disease.
- **Lifestyle Modifications:** Adequate sleep, stress management, avoidance of stimulants (e.g., caffeine, nicotine).
- **Avoidance of Known Triggers:** Alcohol in some patients may precipitate episodes; assess and advise accordingly.
**Monitoring:**
- Regular follow‑up visits to assess symptom frequency, medication side‑effects, and adherence.
- Re-evaluation of ECG and cardiac imaging if new symptoms arise (e.g., syncope).
- Use of remote monitoring or wearable devices for high‑risk patients to detect arrhythmias early.
---
## 4. Management of the Current Emergency
### Immediate Interventions
| Step | Action | Rationale |
|------|--------|-----------|
| **A** | **Secure airway and breathing** – Administer supplemental oxygen, consider intubation if hypoxic or not maintaining adequate ventilation. | Ensures oxygen delivery to tissues; prevents deterioration. |
| **B** | **Rapid cardiac rhythm assessment** – 12‑lead ECG, continuous telemetry. | Detects tachyarrhythmias (e.g., atrial fibrillation with rapid ventricular response) that may be responsible for hypotension and syncope. |
| **C** | **IV access & fluids** – Place large bore IV; give isotonic crystalloids (e.g., 1 L NS over first hour). Monitor vitals, urine output. | Corrects hypovolemia from dehydration, improves preload, supports BP. |
| **D** | **Laboratory work‑up** – CBC, CMP, lactate, troponin, ABG, coagulation panel. | Identifies electrolyte disturbances (e.g., hyponatremia), renal dysfunction, metabolic acidosis, myocardial injury. |
| **E** | **Monitor & reassess** – Continuous cardiac telemetry; repeat vitals every 15 min initially. | Detect arrhythmias early; assess response to fluid therapy and medications. |
---
## 3. Differential Diagnosis of the Acute Symptoms
| Category | Possible Conditions | Rationale |
|----------|---------------------|-----------|
| **Cardiac** | Myocardial infarction (type I or II), arrhythmia (atrial fibrillation/flutter, VT), heart failure decompensation | ECG changes and troponin rise support ischemic injury; tachycardia can precipitate Type II MI |
| **Respiratory** | Pulmonary embolism, pneumonia, acute exacerbation of COPD | Tachypnea, hypoxia, chest pain could be pulmonary in origin |
| **Metabolic/Endocrine** | Hypoglycemia, electrolyte imbalance (K⁺, Mg²⁺), thyroid storm | Symptoms may mimic cardiac ischemia; requires labs |
| **Cardiac Structural** | Valvular disease, pericarditis | May present with chest pain and ECG changes |
| **Medication‑Induced** | Drug toxicity from antipsychotics or antiarrhythmics | Certain drugs can precipitate arrhythmias |
---
## 2. Immediate Evaluation and Management Plan
### A. Stabilization (Airway, Breathing, Circulation – ABCs)
1. **Airway**
- Ensure airway patency; consider supplemental oxygen if SpO₂ <94% or if patient is tachypneic.
- Position head‑tilt/chin lift; suction secretions as needed.
2. **Breathing**
- Administer 100 % O₂ via face mask (10–15 L/min) to maintain SpO₂ ≥96%.
- Monitor respiratory rate, effort, and auscultate lung fields for crackles or wheezes.
- If patient shows signs of impending respiratory failure (tachypnea >30/min, accessory muscle use), prepare for intubation.
3. **Circulation**
- Insert an IV line; administer 500 mL normal saline bolus if hypotensive (<90 mmHg systolic) or in shock.
- Monitor heart rate and rhythm with continuous ECG.
4. **Airway Management**
- Keep airway patent: clear secretions, suction as needed.
- Consider early intubation for patients whose respiratory status is worsening (SpO₂ <92% despite 100 % FiO₂, rising PaCO₂ >50 mmHg).
- Use rapid sequence induction and ensure availability of advanced airway equipment.
5. **Monitoring**
- Continuous pulse oximetry, capnography.
- Hourly ABG monitoring if unstable.
- Daily chest radiographs to assess infiltrates.
6. **Ventilatory Support**
- Initially non‑invasive ventilation (CPAP or BiPAP) in a negative pressure isolation room; monitor for signs of fatigue or hypoxia.
- If NIV fails, proceed to invasive mechanical ventilation with lung protective strategy (tidal volume 4–6 mL/kg predicted body weight, plateau pressure <30 cm H₂O).
- Consider prone positioning if PaO₂/FiO₂ < 150.
7. **Adjunctive Therapies**
- Steroids: low‑dose methylprednisolone (0.5–1 mg/kg/day) for 3–5 days to reduce inflammatory damage.
- Antiviral agents (e.g., remdesivir) if early in disease course and available.
- Immunomodulators (e.g., baricitinib, tocilizumab) per protocol when cytokine storm is evident.
8. **Monitoring**
- Daily arterial blood gases; adjust ventilator settings accordingly.
- Serial chest imaging; CT scans if clinical deterioration occurs.
- Laboratory markers: CBC, CRP, ferritin, D-dimer, IL-6.
- Fluid balance and renal function to avoid pulmonary edema.
9. **Discharge Planning**
- Ensure oxygen saturation >94% on room air for at least 24 h before discharge.
- Provide pulse oximeter; educate patient on recognizing hypoxia symptoms.
- Arrange follow‑up in outpatient clinic within one week of discharge.
---
## 4. Summary
- **Initial assessment** focuses on vitals, oxygenation, and airway protection; rapid triage is essential.
- **Diagnostic testing** begins with pulse oximetry and nasal swab RT‑PCR; chest imaging and labs guide severity.
- **Treatment** follows evidence‑based protocols: supportive care for mild disease, corticosteroids (dexamethasone) for hypoxemic patients, antivirals for high‑risk individuals, oxygen therapy tailored to SpO₂ targets.
- **Monitoring** includes serial vitals, blood gases, and laboratory markers; escalation pathways must be clear.
- **Discharge planning** requires patient education on symptom monitoring, isolation, medication adherence, and when to seek help.
By adhering to these steps, a family medicine clinic can provide comprehensive, timely care for patients with COVID‑19 while minimizing transmission risks and optimizing outcomes.
