Glossary

An enzyme present in skeletal muscle tissue that inactivates DHT before it can bind to androgen receptors. This is why blocking DHT conversion does not impair muscle hypertrophy — muscle tissue renders incoming DHT inactive before it can act on receptors. This is the mechanistic reason TRT + finasteride preserves muscle mass.

The enzyme responsible for converting testosterone into DHT (dihydrotestosterone). Two main isoforms: Type I (found primarily in skin and sebaceous glands) and Type II (dominant in scalp hair follicles and the prostate — the primary pharmaceutical target). Inhibiting this enzyme is the mechanism behind finasteride, dutasteride, saw palmetto, EGCG, and pumpkin seed oil.

The medical term for male pattern baldness. "Androgenetic" refers to the combined contribution of androgens (like DHT) and genetics (AR gene CAG repeat length and other inherited factors). AGA affects approximately 50% of men by age 50. It is characterised by progressive follicle miniaturisation in a characteristic M-shaped or crown-loss pattern driven by DHT sensitivity.

The active growth phase of the hair cycle. Normal anagen lasts 2–6 years, during which the follicle produces a growing hair shaft. DHT progressively shortens anagen duration across successive hair cycles in susceptible follicles — this is the central mechanism of AGA. Hair eventually enters telogen (resting) and falls out, but the shortened anagen means each successive hair is thinner and shorter.

A class of hormones that regulate the development and maintenance of male characteristics. The primary androgens in the body are testosterone and DHT, though DHEA and androstenedione are also classified as androgens. Androgens act by binding to androgen receptors (AR) inside cells.

The protein that testosterone and DHT bind to in order to exert their effects. Sensitivity to DHT is determined by the AR gene variant — specifically the number of CAG repeats in the gene's N-terminal domain. Shorter CAG repeat sequences produce a more transcriptionally active receptor, making hair follicles hypersensitive to DHT at normal serum concentrations.

Non-cancerous enlargement of the prostate gland, driven in part by DHT. Type II 5α-reductase is highly expressed in the prostate; finasteride was originally developed as a BPH treatment before its hair loss applications were recognised. High prostate DHT levels contribute to urinary symptoms in older men. This shared mechanism is why finasteride treats both conditions.

The primary androgenic driver of male pattern baldness. DHT is produced from testosterone by the enzyme 5α-reductase. It is 5–10× more potent than testosterone at androgen receptors. In hair follicles genetically predisposed to DHT sensitivity, DHT progressively shortens the growth cycle and shrinks follicles (miniaturisation) until terminal hairs are replaced by fine, unpigmented vellus hairs. DHT also plays roles in prostate function and body hair growth.

A compound produced in the body when cruciferous vegetables (broccoli, cauliflower, Brussels sprouts) are digested. DIM supports healthy estrogen metabolism and has been studied for its role in maintaining favourable androgen balance. It does not directly inhibit 5α-reductase but supports the overall hormonal environment conducive to high testosterone and lower DHT activity.

The principal bioactive polyphenol in green tea. EGCG competitively inhibits both Type I and Type II 5α-reductase isoforms, reducing testosterone-to-DHT conversion. It is the primary mechanism by which green tea functions as a natural DHT blocker. EGCG does not affect testosterone production directly. Available as a supplement (typically 400mg/day) or through 2–3 cups of brewed green tea daily.

A synthetic Type II 5α-reductase inhibitor approved for both BPH (5mg/day, brand name Proscar) and androgenetic alopecia (1mg/day, brand name Propecia). Finasteride reduces serum DHT by approximately 70% without lowering testosterone. Clinical trials demonstrate that muscle gains and physical performance are fully preserved when finasteride is combined with TRT. Available by prescription only. Side effects — primarily sexual — occur in approximately 3–5% of users and resolve in most cases upon discontinuation.

A tunnel-like structure in the skin from which a hair grows. Each follicle cycles through growth (anagen), transition (catagen), and resting (telogen) phases. Follicle size — and therefore hair fibre thickness — is genetically determined but influenced by androgens. DHT-sensitive follicles undergo progressive miniaturisation across successive cycles in AGA. Once a follicle reaches a critically miniaturised state, it may become permanently non-functional.

The increase in muscle cell size (not number) in response to resistance training and adequate androgen stimulation. Testosterone — not DHT — is the primary anabolic signal driving skeletal muscle hypertrophy. Because muscle tissue inactivates DHT via 3α-HSD, blocking DHT conversion does not reduce hypertrophy in clinical trials. This is the key finding that makes the TRT + finasteride combination viable.

A carotenoid pigment found primarily in tomatoes, watermelon, and grapefruit. Lycopene has documented 5α-reductase inhibitory activity. Bioavailability is significantly higher from cooked tomatoes (tomato paste, sauce, passata) than from raw tomatoes. Consuming cooked tomatoes 3–4× per week with a fat source (olive oil) provides a practical dietary source of lycopene for DHT management.

The hallmark process of androgenetic alopecia. Under repeated DHT stimulation, susceptible hair follicles progressively shrink across successive hair cycles — each cycle producing a thinner, shorter, and less pigmented hair shaft. Terminal hairs (thick, pigmented, visible) are gradually replaced by vellus hairs (fine, nearly colourless, barely visible). Advanced miniaturisation is difficult to reverse; early intervention produces the best outcomes.

Plant-derived compounds structurally similar to cholesterol, found in high concentrations in pumpkin seeds, sunflower seeds, and sesame seeds. Phytosterols have documented competitive inhibition of 5α-reductase. They are a primary mechanism behind pumpkin seed oil's efficacy in the only RCT of a natural supplement for androgenetic alopecia. Pumpkin seed oil is the most phytosterol-dense supplement commonly available.

A flavonoid found in onions, apples, capers, and berries. Quercetin has in vitro evidence for 5α-reductase inhibitory activity and antioxidant properties that reduce systemic inflammation. It is not the primary driver of any food in the protocol, but onions and apples are included in the diet section partly for their quercetin content alongside other beneficial compounds.

A palm plant whose berry extract is the most extensively studied natural 5α-reductase inhibitor. The fatty acids in saw palmetto extract competitively inhibit the enzyme's active site. Standard dose for DHT management is 320mg/day of a standardised liposterolic extract. Multiple systematic reviews confirm a consistently favourable safety profile. Clinical efficacy data for AGA specifically is promising, though larger dedicated RCTs remain needed to match the evidence level of pharmaceutical comparators.

A protein produced by the liver that binds to testosterone (and DHT) in the bloodstream, rendering the bound fraction biologically unavailable. Only "free" testosterone that is not bound to SHBG can enter cells and activate androgen receptors. High SHBG lowers free testosterone even when total testosterone appears normal. Factors that raise SHBG include excess alcohol, low zinc intake, and elevated cortisol. This is why reducing alcohol and supplementing zinc are part of the protocol.

The primary male sex hormone produced primarily in Leydig cells of the testes. Testosterone is the direct precursor to DHT via 5α-reductase conversion. It is the principal anabolic signal for skeletal muscle. The protocol's objective is not to lower testosterone — it is to inhibit the enzyme that converts it to DHT, leaving testosterone itself elevated or unchanged. Sleep, resistance training, adequate zinc, and vitamin D3 are evidence-based methods of optimising testosterone production.

A medical treatment for clinically low testosterone (hypogonadism) consisting of exogenous testosterone administration (injection, gel, or patch). TRT raises testosterone and, proportionally, DHT — since more substrate is available for 5α-reductase conversion. Men on TRT who are concerned about hair loss can combine it with finasteride, which reduces DHT by ~70% while leaving the elevated testosterone intact. This combination preserves muscle and performance outcomes in clinical trials.

A variable sequence of cytosine-adenine-guanine (CAG) trinucleotide repeats in the N-terminal domain of the androgen receptor (AR) gene. The number of CAG repeats inversely correlates with AR transcriptional activity — shorter repeats produce a more active receptor that is more sensitive to both testosterone and DHT. This is the primary genetic determinant of individual DHT sensitivity, explaining why two men with identical DHT levels can have radically different hair loss trajectories. CAG repeat length cannot be changed; it defines your baseline susceptibility level.