Creatine monohydrate is one of the most thoroughly researched and widely used dietary supplements among athletes and fitness enthusiasts. It is known for its proven ability to enhance strength, performance, and muscle mass. Despite decades of data supporting its safety and efficacy, a persistent concern circulates regarding its potential impact on androgen levels. Many people search for evidence linking creatine intake to elevated levels of Dihydrotestosterone (DHT). This article explores the scientific evidence to determine how creatine supplementation affects circulating DHT.
Dihydrotestosterone and Its Biological Role
Dihydrotestosterone (DHT) is a potent androgen synthesized from testosterone (T) via the enzyme 5-alpha reductase (5-AR). DHT is several times more biologically active and potent than testosterone.
The enzyme 5-AR is highly expressed in tissues like the prostate, skin, and hair follicles. DHT binds strongly to androgen receptors, driving biological processes such as acne development and oil production regulation.
The relevance of DHT often centers on its link to androgenetic alopecia, or male-pattern baldness. DHT’s action on genetically susceptible hair follicles causes them to miniaturize, leading to hair loss. It is also implicated in prostate growth and conditions like benign prostatic hyperplasia.
The Initial Research Findings on Creatine and DHT Levels
The widespread concern about creatine and DHT levels stems almost entirely from a single 2009 study by van der Merwe and colleagues. This research, conducted on college-aged male rugby players, was a double-blind, placebo-controlled crossover trial measuring changes in androgen hormones.
The study protocol involved a seven-day loading phase (25 grams daily) followed by a 14-day maintenance phase (5 grams daily). During the loading phase, researchers observed a substantial 56% increase in serum DHT levels above baseline measurements, a finding statistically significant compared to the placebo group.
Even during the maintenance phase, DHT levels remained significantly elevated, registering 40% above the original baseline. Total testosterone levels did not change significantly throughout the 21-day period. The ratio of DHT to testosterone increased by 36% after loading and remained elevated by 22% during maintenance, suggesting an enhanced rate of conversion.
Mechanism of Hormonal Interaction and Follow-up Studies
The mechanism proposed by the initial researchers suggested that creatine supplementation might enhance the activity of the 5-alpha reductase enzyme, facilitating a greater conversion of available testosterone into DHT. Since total testosterone levels did not increase, the rise in DHT was hypothesized to result from a shift in the metabolic pathway.
Despite the percentage increases, the absolute DHT concentrations remained within the normal physiological range for healthy adult males. The significant percentage change was measured against the participants’ individual baseline, meaning the subjects were not elevated to pathologically high levels.
Subsequent human studies investigating the link between creatine and androgen levels have largely failed to replicate the initial 2009 findings. Multiple controlled trials using standard creatine doses have reported no significant changes in total testosterone or DHT levels. For instance, a 12-week randomized controlled trial found no difference in DHT or the DHT-to-testosterone ratio between men supplementing with creatine and those taking a placebo. Other studies measuring free testosterone, the form directly converted to DHT, also found no statistically significant increase. This lack of consistent replication suggests creatine does not reliably or significantly alter androgen profiles in most users.
Clinical Relevance and Practical Takeaways
Translating the scientific data suggests that the temporary DHT increase observed in the single study is unlikely to be clinically meaningful for the average user. Although the 40% to 56% increase sounds dramatic, the resulting hormone levels remained within the established normal range. To cause noticeable androgenic side effects, such as hair loss or acne, an individual would need to be genetically predisposed and cross a pathological threshold.
The primary driver of male-pattern baldness is not simply the amount of circulating DHT, but rather the genetic sensitivity of the hair follicles to the hormone. If an individual is not genetically susceptible to androgenetic alopecia, a modest increase in DHT within the normal range is unlikely to initiate hair loss. The lack of replication across numerous studies provides reassurance.
The safety profile of creatine monohydrate remains excellent, supported by extensive long-term research that has not demonstrated any consistent link to adverse health effects. For those concerned about elevated DHT, a practical approach is to skip the high-dose loading phase and simply begin with a standard maintenance dose of 3 to 5 grams per day. This approach mitigates any potential initial hormonal spike while still allowing the user to gain performance benefits.