Testosterone vs DHT: What Bodybuilders Need to Know

Testosterone and dihydrotestosterone (DHT) are the two primary male androgens. Testosterone is the precursor; DHT is its more potent metabolite, produced when the enzyme 5-alpha reductase converts testosterone in target tissues.

Both hormones bind the androgen receptor, but DHT does so with approximately five times greater affinity. This makes DHT the dominant androgen in tissues with high 5-alpha reductase activity: the scalp hair follicles, the prostate, and the skin. Testosterone, on the other hand, is the primary anabolic signal for skeletal muscle, bone, and erythropoiesis.

For bodybuilders on TRT or running cycles, this distinction has direct practical consequences. Muscle growth is driven primarily by testosterone (and its synthetic analogues), while side effects like hair loss, prostate enlargement, and acne are driven primarily by DHT. The ratio between these two hormones, and the route of testosterone administration, determines the side effect profile of any testosterone-based protocol.

Receptor binding affinity:

• Testosterone binds the androgen receptor with moderate affinity
• DHT binds approximately 5 times more strongly and dissociates more slowly, producing a more sustained androgenic signal in target tissues
• This difference in binding strength explains why DHT drives tissue-specific effects that testosterone alone does not

Tissue selectivity:

• Testosterone is the primary anabolic hormone for skeletal muscle, bone mineral density, erythropoiesis, and fat distribution
• DHT is the dominant androgen in the scalp (hair follicle miniaturisation), prostate (growth stimulation), sebaceous glands (acne), and external genitalia
• Blocking DHT with finasteride preserves testosterone's anabolic effects while reducing DHT-mediated side effects

Conversion pathway:

• Testosterone is converted to DHT by 5-alpha reductase (Types I and II) in target tissues
• This conversion is one-directional: DHT cannot be converted back to testosterone
• The rate of conversion depends on tissue type, 5-alpha reductase expression, and the route of testosterone administration

Aromatisation:

• Testosterone can be aromatised to oestradiol by the aromatase enzyme (CYP19A1)
• DHT cannot be aromatised. It is a "dead-end" metabolite in terms of oestrogen conversion
• This is why DHT-derivative steroids (Masteron, Winstrol, Primobolan) do not cause oestrogenic side effects like water retention or gynecomastia

Serum levels on TRT:

• Injectable testosterone enanthate raises serum DHT to approximately 2.2x baseline
• Transdermal testosterone (creams, gels) raises serum DHT to approximately 5.5x baseline
• The difference is due to first-pass conversion through 5-alpha reductase-rich skin tissue

When to focus on testosterone levels:

• Assessing TRT adequacy (target: mid-to-upper reference range, or symptom resolution)
• Evaluating muscle-building, recovery, and body composition changes
• Diagnosing hypogonadism (two morning draws below 300 ng/dL with symptoms)
• Monitoring alongside free testosterone and SHBG for a complete picture

When to focus on DHT levels:

• Investigating new or worsening hair loss on TRT
• Evaluating acne severity that does not respond to standard treatment
• Assessing prostate symptoms (urinary hesitancy, frequency, nocturia)
• Comparing delivery methods (switching from cream to injections, or vice versa)
• Before and after starting a 5-alpha reductase inhibitor (finasteride, dutasteride)

When to test both together:

• Pre-TRT baseline panel (establishes your personal ratio)
• When changing TRT delivery method (the DHT/testosterone ratio shifts significantly)
• When adding or removing a 5-alpha reductase inhibitor
• When running compounds that interact with 5-alpha reductase (e.g., nandrolone, which converts to the weaker DHN instead of DHT)