What Is DHT?
Dihydrotestosterone (DHT) or more specifically 5α-Dihydrotestosterone is derived from testosterone by a reaction with the enzyme 5-alpha-reductase; reducing the 4,5 double-bond of Testosterone..
Testosterone is converted to dihydrotestosterone upon interaction with the 5-alpha reductase enzyme. More specifically, this enzyme removes the C4-5 double bond of testosterone by the addition of two hydrogen atoms to its structure (hence the name di-hydro-testosterone). The removal of this bond is important, as in this case it creates a steroid that binds to the androgen receptor much more avidly than does its parent steroid. 5-alpha reductase is present in high amounts in tissues of the prostate, skin, scalp, liver and various regions of the central nervous system, and as such represents a mechanism for the body to increase the potency of testosterone specifically where strong androgenic action is needed.(DHT is formed primarily in the prostate gland, testes,adrenal glands and hair follicles, and DHT is produced by male embryos during development in the womb and is responsible for the formation of male gender-specific characteristics.DHT is associated with other male characteristics such as: facial hair, body hair, voice and muscle development and contributes to the male sex drive.)
Dihydrotestosterone (DHT) plays an important role in the organization and functioning of the central nervous system. Many neural cells contain active androgen receptors, and it is thought that there may even be a specific importance of dihydrotestosterone in this area of the body. Studies have shown DHT to have a profoundly greater impact in these cells compared to testosterone. Animal models demonstrated that both testosterone and DHT would result in increased androgen receptor proliferation in neural cells three and seven hours after being administered, however only DHT was able to sustain this increase at the twenty-one hour mark.
The strong interaction between the central nervous system and skeletal muscles, collectively referred to as the neuromuscular system, is of key importance to the athlete. There appears little doubt that the ability of the body to adapt to training and its ability to activate nerve endings in muscle tissue are reliant on the interactions of the neuromuscular system. Inhibiting the formation of DHT during a testosterone cycle may therefore inadvertently interfere with strength and muscle mass gains.
Testosterone is the active androgen in muscle
Skeletal muscle is unique from other androgen dependent tissues in the body. It actually contains little or no 5-AR, so little or no DHT is actually formed in the muscle. In addition to this, any DHT that is formed, or that is already present in the blood and travels to the muscle, is quickly deactivated by an enzyme called 3alpha-hydroxysteroid reductase (3a-HSD).
So at least as far as muscle is concerned, testosterone is the primary active androgen. This is not to say that administering exogenous DHT is not without any anabolic effect. It actually does have some anabolic activity in the muscle, albeit significantly weaker than that of an equal amount of testosterone. This is due to its quick breakdown by 3a-HSD into the weak metabolite 5alpha-androstan-3a,17b-diol. If this enzyme were somehow blocked, it is likely that DHT would exhibit very potent anabolic effects on muscle.
It is important to understand that even though testosterone is the active androgen in muscle, and DHT exhibits relatively little direct anabolic effects on muscle in men, DHT is still very important for the full performance enhancement effects from testosterone. What I specifically mean here are the effects of DHT on the central nervous system, which lead to increased neurological efficiency (strength), and increased resistance to psychological and physical stress – not to mention optimal sexual function and libido.
Anti–Estrogen effects of DHT
One important function of DHT in the body that does not get much discussion is its antagonism of estrogen. Some men that take Proscar learn this the hard way – by developing a case of gynecomastia. By reducing DHT’s protection against estrogen in the body, these men have fallen victim to its most dreaded ramification – bitch tits!
How does DHT protect against estrogen? There are at least three ways that this likely occurs. First of all, DHT directly inhibits estrogens activity on tissues. It either does this by acting as a competitive antagonist to the estrogen receptor or by decreasing estrogen-induced RNA transcription at a point subsequent to estrogen receptor binding.
Second of all, DHT and its metabolites have been shown to directly block the production of estrogens from androgens by inhibiting the activity of the aromatase enzyme. The studies done in breast tissue showed that DHT, androsterone, and 5alpha-androstandione are potent inhibitors of the formation of estrone from androstenedione. 5alpha-androstandione was shown to be the most potent, while androsterone was the least.
Lastly, DHT acts on the hypothalamus / pituitary to decrease the secretion of gonadotropins. By decreasing the secretion of gonadotropins you decrease the production of the raw materials for estrogen production – testosterone and androstenedione (DHT itself cannot aromatize into estrogens).
How Does DHT Lead To Baldness
Genetic Disposition to Male Pattern Baldness
The exact mechanism causing Male Pattern Baldness (MPB) in men is, as yet, unknown although it is believed to be an inherited pre-disposition for hair follicles to shrink in the presence of DHT.
Hair follicles with genetic sensitivity to DHT begin to contract or reduce in size. This forms progressively finer hair while shortening the normal lifespan of the sensitised hair follicle.
Ultimately, the hair follicles cease producing hair.
Hair on the crown seems to be most sensitive; while hair follicles on the sides of the head are not as susceptible to DHT, leading to the characteristic Male Pattern Baldness.
It is possible to Block or Inhibit the conversion of Testosterone to DHT within the body using 5-α-Reductase Inhibitors.
How Does Hair Grow?
Hair Follicle Structure and Ultimate DHT Sensitivity
A hair follicle is a special site of the skin that packs old cells into a structure that grows into a hair.
Hair growth phases
Hair grows in cycles going through several transition phases:-
Anagen - Active Phase - Hair growth occurs
Catagen - Intermediate Phase - Hair growth ceases and a club is formed at the base
Telogen - Dormant Phase - No Hair Growth.
Scalp hair can take up to 6 years to complete this cycle. Typically 3-4 Years Growth cycles are initiated and controlled by a chemical signal or growth factor.
The dermal papilla is responsible for hair growth. It divides, differentiating to form new hair follicles. It is nourished by the blood capillaries of the skin for active hair growth and posseses many receptors for androgens such as DHT and Growth Factors.
DHT may influence the hair growth phases by shortening the active hair growth anagen phase and also prolonging the dormant telogen phase.
DHT also initiates follicular size reduction or follicle miniaturisation in susceptible individuals so that hair becomes progressively finer leading to hair loss.
DHT can also form wax like substances that bind around the hair roots preventing hair re-growth.
