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Anabolic Steroids: Uses, Abuse, And Side Effects


 An Evidence‑Based Overview of Steroids in Health and Medicine


Prepared for: General public, school teachers, parents, and health educators (ages ≥ 13)

Purpose: To provide a clear, balanced, and up‑to‑date summary that can be used in classrooms, community talks, or personal learning.




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1. What Are "Steroids"?



Term Meaning Example


Corticosteroid Synthetic hormones that mimic cortisol (the body’s natural stress hormone). Prednisone, Dexamethasone


Anabolic steroid Hormones that promote muscle growth; often abused for athletic performance or bodybuilding. Testosterone enanthate, Nandrolone decanoate


Glucocorticoid Sub‑class of corticosteroids that mainly reduce inflammation and immune activity. Hydrocortisone


Mineralocorticoid Sub‑class that helps regulate salt & water balance. Fludrocortisone


> Note: The terms "steroid" and "glucocorticoid" are often used interchangeably in medical contexts, but they refer to different substances.



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2. When You’re Prescribed a Glucocorticoid



Situation What’s the risk? How can it happen?


Short‑term (days–weeks) – e.g., oral prednisone for asthma exacerbation, or a single dose of methylprednisolone in an ER setting. Usually no significant adrenal suppression if total cumulative dose 1 mg/day). Risk of suppression rises if cumulative dose >2–3 g over 30 days or continuous exposure >4–6 weeks. The axis is down‑regulated: ACTH production decreases; adrenal cortex reduces its responsiveness; cortisol secretion may be blunted under stress, leading to adrenal crisis.


High doses (e.g., >50 mg/day prednisone) – even for a few weeks can suppress the axis. The suppression can last for several months after discontinuation. Patients may present with fatigue, dizziness, low blood pressure; they need steroid cover until recovery.


These thresholds are derived from studies of adrenal function in patients on glucocorticoid therapy (e.g., Fabbri et al., 2006; Rachakonda et al., 2017). They serve as a practical guide for clinicians to decide when an HPA‑axis assessment is necessary.



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3. How to Assess the HPA‑Axis



3.1 Timing of Assessment



After Cessation: Perform tests after at least 4–6 weeks off oral glucocorticoids, if possible, because many patients will have recovered endogenous cortisol production by this time.


During Ongoing Therapy: If the patient must continue therapy (e.g., severe asthma), a stimulation test can still provide useful information. However, results may be suppressed and require interpretation with caution.




3.2 Standard Tests



Test Principle Procedure Typical Thresholds


Cosyntropin (Synacthen) Stimulation – low-dose (1 µg) Measures adrenal reserve by stimulating ACTH receptor. Blood cortisol at baseline, 30 min, and 60 min after IV/IM cosyntropin. 20 µg/dL normal.


High-dose Cosyntropin Alternative if low-dose ambiguous. 250 µg dose; same sampling times. >18 µg/dL at 30 min indicates adequate reserve.


Insulin-Induced Hypoglycemia Test Gold standard for adrenal insufficiency. Induce hypoglycemia with insulin; measure cortisol response (should rise to >20 µg/dL). 3 time zones Hydrocortisone 5–10 mg PO at bedtime for 1–2 days Ensure sleep cycle adjustment


Emergency kit In case of accidental discharge Dexamethasone 4 mg PO + Hydrocortisone 50 mg IV if necessary Keep with patient’s primary care provider


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6. Monitoring and Follow‑Up



Parameter Frequency Target / Action


Blood pressure At each visit (or home monitoring) 140/90


HbA1c Every 3–6 months 8%


Serum creatinine / eGFR Every 6 months (or quarterly if CKD stage 4) If decline >10% in 3 months, consider nephrology referral


Urine albumin-to-creatinine ratio Every 6 months If persistent ≥300 mg/g, intensify ACEi/ARB dose


Lipid panel Annually or more often if unstable LDL

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