Anabolic Steroids: Uses, Abuse, And Side Effects

# Understanding the Health Implications of Anabolic Steroids

Anabolic–androgenic steroids (AAS), often referred to as anabolic steroids, are synthetic derivatives of the male sex hormone testosterone. While they have legitimate medical uses—such as treating hormonal deficiencies, certain types of anemia, and muscle-wasting conditions—they are also widely misused for performance enhancement and body‑building purposes. Misuse can lead to a host of acute and chronic health problems.

Below is an evidence‑based overview of the potential short‑term and long‑term risks associated with AAS misuse, along with key points that healthcare professionals should consider when counseling patients or www.kornerspot.com managing care.

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## 1. Short‑Term (Acute) Effects

| Category | Symptoms / Conditions | Typical Onset |
|----------|----------------------|---------------|
| **Hormonal** | Acne, oily skin; increased body hair (hirsutism); voice deepening in females | Within days to weeks |
| **Psychological** | Irritability, mood swings, aggression ("roid rage") | Days to weeks |
| **Cardiovascular** | Elevated blood pressure; palpitations; tachycardia | Hours to days |
| **Renal** | Fluid retention leading to edema, particularly in lower limbs | Within days |
| **Gastrointestinal** | Nausea, stomach upset when taking high doses | Immediate after ingestion |

> *Tip*: Encourage users to monitor blood pressure at home; a sudden spike could indicate an emerging problem.

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## 4. Long‑Term Physiological Consequences

### 4.1 Endocrine and Reproductive System Effects

| Organ/Function | Effect of Chronic Steroid Use |
|----------------|--------------------------------|
| **Testes** | Atrophy, decreased spermatogenesis → infertility or reduced libido |
| **Ovaries** | Disruption of follicular development; amenorrhea in females |
| **Pituitary Gland** | Suppression of endogenous gonadotropin release (LH/FSH) |
| **Adrenal Cortex** | Inhibition of natural cortisol synthesis, leading to adrenal insufficiency |

> **Key Point:** The suppression of the hypothalamic-pituitary-gonadal axis can persist long after cessation of steroids, necessitating hormone replacement or assisted reproductive techniques.

### 3.2 Hormonal Imbalances

#### 3.2.1 Testosterone Excess
- Elevated free testosterone → increased DHT (dihydrotestosterone) via 5α-reductase.
- DHT binds androgen receptors more strongly, promoting sebaceous gland activity and hair follicle miniaturization.

#### 3.2.2 Estrogen Production
- Aromatase enzyme in adipose tissue converts excess androstenedione to estrone.
- Elevated estrogen can disrupt the balance of testosterone/estrogen, leading to gynecomastia (breast tissue enlargement).

#### 3.2.3 Prolactin Elevation
- High prolactin levels inhibit gonadotropin-releasing hormone (GnRH), further suppressing LH and FSH.
- Resultant low testosterone exacerbates androgen deficiency.

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## Clinical Manifestations

### A. Hair Loss Patterns

| Area | Typical Pattern |
|------|-----------------|
| **Scalp** | Thinning at vertex and frontal region; receding hairline. |
| **Facial (Moustache, beard)** | Patchy loss or complete absence of facial hair. |
| **Armpit & Chest** | Reduced density of pubic hair. |

### B. Physical Symptoms

- **Decreased libido**
- **Erectile dysfunction**
- **Mood changes: depression, irritability**
- **Anemia (low hemoglobin) leading to fatigue**
- **Loss of muscle mass**

### C. Hormonal Imbalances

| Hormone | Normal Range (Men) | Typical Level in Affected Men |
|---------|--------------------|--------------------------------|
| Testosterone | 300–1000 ng/dL | < 250 ng/dL (hypogonadism) |
| LH (Luteinizing hormone) | 1.5–9.4 IU/L | ↑ due to feedback inhibition |
| FSH (Follicle stimulating hormone) | 1.5–12.4 IU/L | ↑ |

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## 3. How do we Diagnose?

### A. Clinical History & Physical Examination

- **Symptoms**: decreased libido, erectile dysfunction, fatigue, depression.
- **Physical Signs**: reduced body hair, gynecomastia, testicular atrophy.

### B. Laboratory Tests (First-Line)

| Test | Reference Range (male) |
|------|------------------------|
| Testosterone (total) | 300–1000 ng/dL |
| Free testosterone (calculated or measured) | ~9–30 pg/mL |
| LH | 1–10 IU/L |
| FSH | 1.5–12.4 IU/L |
| Estradiol | <40 pg/mL |
| Prolactin | 2–17 ng/mL |
| TSH | 0.4–4.0 mU/L |

**Interpretation:**

- **Low testosterone + low LH/FSH** → Central hypogonadism (pituitary/hypothalamic).
- **Low testosterone + normal/high LH/FSH** → Primary testicular failure.
- **Isolated LH deficiency** → Suggests a pituitary or hypothalamic lesion; may present with other pituitary hormone deficits.

### 2. Imaging Studies

| Study | Purpose | Findings Suggestive of LH Deficiency |
|-------|---------|-------------------------------------|
| **MRI Brain (Pituitary Focus)** | Detect pituitary adenoma, hypoplasia, stalk interruption, or infiltrative disease. | <1 mm pituitary size, empty sella, thickened pituitary stalk (>3 mm), absent posterior pituitary bright spot, mass lesion compressing the pituitary |
| **CT/MRI of Skull Base** | Identify sellar/parasellar lesions (e.g., craniopharyngioma). | Mass causing hypophyseal dysfunction |
| **Ultrasound (Testis)** | Evaluate testicular volume and echotexture. | <2 mL volume, hypoechoic parenchyma |

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### 4. Hormonal Tests to Confirm GHD

#### A. Baseline Serum Hormones
- **TSH** – normal in isolated GHD (unless combined pituitary deficiency).
- **Free T4** – should be normal.
- **LH/FSH** – typically low or normal; gonadotropin axis may also be affected but often less severely than GH axis.
- **Testosterone** – low‑normal to low for age.
- **IGF‑1 (Insulin‑like Growth Factor‑1)** – the most reliable screening marker.

> **Interpretation**
> - IGF‑1 below age‑specific lower reference limit strongly suggests GHD.
> - IGF‑1 may be normal in mild GHD; thus stimulation tests are required for definitive diagnosis.

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### 3. GH Stimulation (Dynamic) Testing

Because basal GH secretion is pulsatile and can be suppressed by stress, a dynamic test that provokes GH release is mandatory to confirm or exclude GHD.

| Test | Principle | Procedure | Interpretation |
|------|-----------|------------|----------------|
| **Insulin‑Tolerant Hypoglycaemic Stimulation (ITT)** | Induces hypoglycaemia → counter‑regulatory GH surge. | • Baseline blood glucose, insulin, GH levels.
• Give 0.1–0.15 U/kg IV regular insulin.
• Monitor glucose every 5 min; maintain ≤40 mg/dL (2.2 mmol/L).
• Collect serum at 30‑60 min for GH measurement. | Peak GH ≥10 µg/mL → normal response; <10 µg/mL suggests hypopituitarism.
In children, thresholds may be lower (~5–8 µg/mL) due to higher basal GH. |
| **Glucagon Stimulation Test** | Alternative when insulin test contraindicated (e.g., severe hypoglycemia risk). | • 1 mg IV glucagon over 3‑5 min.
• Baseline serum cortisol, ACTH, and glucose measured.
• Repeat measurements at 10, 20, 30, 45 min. | • Normal adrenal reserve: cortisol rise ≥250 nmol/L from baseline within 20–30 min.
• In children with chronic disease, a smaller increase (≥200 nmol/L) may be acceptable due to altered stress response. |
| **Pituitary Function** | *Dynamic testing for secondary adrenal insufficiency.* | • Insulin‑induced hypoglycaemia test or CRH stimulation test to assess ACTH release. | • In children, insulin tolerance test is standard: after inducing hypoglycaemia (blood glucose <2.5 mmol/L), measure cortisol and ACTH at 0, 15, 30, 60 min.
• A rise in cortisol >20% over baseline indicates intact pituitary‑adrenal axis. |
| **Other Pituitary Hormones** | *Assess for broader hypopituitarism.* | • Growth hormone stimulation tests (arginine, clonidine), thyroid function tests, sex steroids, prolactin. | • In children with craniopharyngioma or similar lesions, it is common to evaluate the entire pituitary axis due to risk of multiple deficiencies. |

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## 3. Interpretation & Clinical Reasoning

| Parameter | Expected Result if **normal** | What a *lower* value suggests |
|-----------|------------------------------|--------------------------------|
| Serum cortisol (morning) | ~10–20 µg/dL (≈ 275–550 nmol/L) | Possible adrenal insufficiency; could be due to pituitary failure or primary adrenal disease. |
| DHEA‑S | 100–400 µg/dL (≈ 3–12 μmol/L) | Low levels may indicate diminished adrenal androgen output, pointing toward adrenal hypofunction. |
| Testosterone | ~200–300 ng/dL (≈ 7–11 nmol/L) in men; <30 ng/dL (≈ 1 nmol/L) in women | Low male testosterone suggests hypogonadism; low female levels may reflect ovarian failure or generalized endocrine dysfunction. |

> **Key point**: A pattern of *low* adrenal androgens (DHEA‑S, testosterone), coupled with a normal/normal-high gonadal axis, is most consistent with primary adrenal insufficiency.

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## 2. Which Hormones Should We Measure?

| Category | Key hormones to assess | Rationale |
|----------|------------------------|-----------|
| **Adrenal Axis** | **Serum cortisol** (baseline, preferably early morning)
**Plasma ACTH** | To establish whether the adrenal glands are producing sufficient cortisol and whether ACTH is appropriately elevated. |
| **Androgens** | **Dehydroepiandrosterone‑sulfate (DHEA‑S)**
**Free testosterone** (or total T + SHBG) | DHEA‑S declines sharply in adrenal insufficiency; testosterone may fall if cortisol deficiency is severe or with concurrent hypogonadism. |
| **Sex Hormones** | **LH, FSH**, **Estradiol** (men), **Progesterone** (if relevant) | To assess gonadal function and potential pituitary involvement. |
| **Pituitary Hormones** | If a central cause is suspected: **TSH, FT4**, **Prolactin**, **Growth hormone axis** (IGF‑1)
**MRI pituitary imaging** if indicated | To rule out pituitary disorders such as hypopituitarism or macroadenoma. |

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## 2. Interpretation of Findings

| Finding | Interpretation | Clinical Significance |
|---------|-----------------|-----------------------|
| **Low cortisol (baseline)** | Suggests adrenal insufficiency (primary or secondary). | Must be confirmed with ACTH stimulation test; treat if confirmed. |
| **Low serum sodium (<135 mmol/L)** | Hyponatremia typical of adrenal crisis or SIADH. In the setting of low cortisol, often due to decreased free water clearance from lack of glucocorticoid action. | Treat underlying cause; correct electrolytes cautiously. |
| **Normal potassium** | Rules out primary hyperaldosteronism or hypoaldosteronism (which would raise K⁺). | Points toward secondary adrenal insufficiency where aldosterone is preserved. |
| **Low/normal ACTH with low cortisol** | Suggests secondary adrenal insufficiency due to pituitary failure, not primary adrenal disease. | Further evaluate pituitary function; consider MRI imaging. |
| **Normal or high renin activity** | Indicates intact RAAS system, supporting secondary rather than primary adrenal failure. | Confirms that aldosterone production remains functional. |

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## 5. Summary of Findings

- **Pituitary Function:** Normal anterior pituitary hormone levels (TSH, ACTH, LH/FSH, prolactin).
- **Adrenal Function:** Cortisol suppressed after ACTH stimulation; low cortisol with normal ACTH → secondary adrenal insufficiency.
- **Renin Activity:** Normal or slightly elevated, indicating intact RAAS and functional aldosterone production.

**Conclusion:** The patient has isolated secondary adrenal insufficiency (pituitary failure to produce adequate ACTH) with preserved mineralocorticoid function. Management should include glucocorticoid replacement; monitor for hyponatremia and potential pituitary dysfunction progression.