Prednisone
Prednisone is a synthetic oral glucocorticoid prodrug (converted in the liver to prednisolone) with roughly four times the anti-inflammatory potency of cortisol. It is one of the most widely prescribed anti-inflammatory drugs in medicine. For athletes it is double-edged: powerful for suppressing injury-related inflammation, but overtly catabolic to muscle and bone, immunosuppressive, and suppressive of the HPA axis with any sustained use.
01 Overview
Prednisone is inert until hepatic 11-beta-hydroxysteroid dehydrogenase converts it to active prednisolone, which binds the glucocorticoid receptor and broadly downregulates inflammatory gene transcription. Clinically it treats asthma, autoimmune disease, allergic reactions and inflammatory flares. A short 'burst' of a few days is generally well tolerated; the problems accumulate with dose and duration.
In a physique or recovery context prednisone is unambiguously catabolic: chronic use promotes proteolysis in skeletal muscle, drives visceral fat gain and a Cushingoid fat pattern, causes bone loss and blunts the immune response. It also suppresses the hypothalamic-pituitary-adrenal axis, so courses beyond roughly two to three weeks must be tapered rather than stopped abruptly to avoid adrenal insufficiency. It is prohibited in-competition by WADA when taken by oral, intravenous, intramuscular or rectal routes.
02 Mechanism
Prodrug converted to prednisolone, which activates the glucocorticoid receptor to suppress pro-inflammatory transcription factors (NF-kB, AP-1) and upregulate anti-inflammatory proteins, while promoting gluconeogenesis and protein catabolism.
03 Dosing
| Tier | Dose | Route | Notes |
|---|---|---|---|
| Short burst | 20–60 mg/day | Oral | Typical 3-7 day anti-inflammatory burst; usually needs no taper if brief. |
04 Effects
| Effect | Magnitude | Evidence | |
|---|---|---|---|
| Suppression of inflammationPotent reduction of swelling, pain and inflammatory flares within hours to days. | rapid, broad | Clinical | |
| Muscle catabolismPromotes skeletal muscle protein breakdown and proximal myopathy with sustained use — the opposite of an anabolic agent. | dose/duration dependent | Clinical | |
| Fat redistributionCentral/visceral fat gain, moon face and buffalo hump with chronic dosing. | Cushingoid pattern | Clinical |
05 Side effects
| Effect | Severity | Frequency | Evidence | Countermeasures |
|---|---|---|---|---|
| HPA axis suppressionSuppression of endogenous cortisol production; abrupt cessation after prolonged use can precipitate adrenal crisis. | Severe | Universal with prolonged use | Clinical | |
| Bone lossGlucocorticoid-induced osteoporosis and increased fracture risk with prolonged therapy. | Severe | Common with chronic use | Clinical | |
| ImmunosuppressionIncreased susceptibility to infection and impaired wound healing. | Severe | Common with dose | Clinical | |
| HyperglycaemiaElevated blood glucose and worsened insulin resistance. | Moderate | Common | Clinical |