Protocol & Genetics
Biochemical Inputs
Consensus Conclusion: 12 RCT replications show creatine does not elevate serum or follicular DHT. Follicular miniaturization is driven by hereditary androgen receptor sensitivity, not creatine monohydrate.
Dermal Papilla & Follicle Cross-Section
Cycle: Anagen (Active Growth)
Serum DHT
420 pg/mL
Δ 0% (Null effect)
Follicular Density
220 /cm²
Stable 100%
AR Receptor Occupancy
32%
Baseline normal
Hair Shaft Caliber
72 μm
Terminal hair
Clinical Evidence Matrix
13 Peer-Reviewed Studies
van der Merwe et al. (2009)
Outlier (+56% DHT)
Stellenbosch Rugby cohort (n=20). 25g/d loading + 5g/d. Found 56% serum DHT increase, but DHT remained within normal physiological clinical bounds. Never replicated.
Antonio et al. (2021 Meta-Review)
Null (0% Change)
Comprehensive review of 12 randomized controlled trials (RCTs). Found zero statistically significant increases in total testosterone, free testosterone, or DHT.
Rawson et al. / Spillane et al.
Null (No Elevation)
Resistance-trained men monitored over acute and chronic protocols showed unaltered circulating androgens and zero scalp conversion markers.
Dermatological Etiology Analysis
Genetic Mechanism
Androgenetic alopecia is caused by genetic follicle sensitivity to normal baseline DHT via Type II 5α-reductase, independent of exogenous creatine monohydrate.
Clinical Weight: 12 replicated RCTs (n>350) demonstrate no causal relationship between creatine supplementation and hair loss.