Not medical advice. I am a software engineer, not a physician. This page documents my own protocol and the research I read while building it. Talk to a qualified clinician before changing your supplementation, diet or any treatment. Lab reference ranges quoted here vary by laboratory and by individual.
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Hair loss affects roughly 50% of men by age 50 and up to 40% of women during their lifetime. While genetics play a dominant role — androgenetic alopecia (AGA) accounts for over 95% of male pattern hair loss — the process is far from inevitable. Nutritional deficiencies, hormonal imbalances, thyroid dysfunction, and chronic inflammation all accelerate hair thinning. This means there are multiple modifiable levers: blocking DHT at the follicle, stimulating blood flow to the scalp, providing structural building blocks (keratin, collagen, sulfur), and correcting underlying deficiencies detected by lab work.
Key insight: Hair loss is rarely caused by a single factor. An effective protocol combines DHT management, growth stimulation, structural nutrition, and lab-guided correction of deficiencies.
Each hair follicle cycles through three phases: anagen (active growth, 2–7 years), catagen (regression, 2–3 weeks), and telogen (rest/shedding, 2–4 months). At any given time, 85–90% of scalp hairs are in anagen. Hair loss occurs when the anagen phase shortens progressively, producing thinner, shorter hairs until the follicle miniaturizes completely.
The primary driver of follicle miniaturization is dihydrotestosterone (DHT). Testosterone is converted to DHT by the enzyme 5-alpha reductase (5-AR), which exists in two isoforms: Type I (skin, liver) and Type II (prostate, hair follicles). DHT binds to androgen receptors in genetically susceptible follicles, triggering a cascade that shortens anagen and eventually kills the follicle. This is why 5-AR inhibitors (saw palmetto, dutasteride) are a cornerstone of treatment: they reduce DHT production at the source.
Meanwhile, minoxidil works through a completely different pathway: it is a potassium channel opener and vasodilator that increases blood flow to the follicle and prolongs anagen. It also upregulates vascular endothelial growth factor (VEGF), promoting new capillary formation around the follicle. This is why combining minoxidil (growth stimulation) with a 5-AR inhibitor (DHT blockade) produces superior results to either alone.
Olsen, E. A., et al. (2002). A randomized clinical trial of 5% topical minoxidil versus 2% topical minoxidil and placebo in the treatment of androgenetic alopecia in men. J Am Acad Dermatol, 47(3), 377-385. PMID: 11702361
The following supplements target different mechanisms of hair loss — from DHT blockade and follicle stimulation to structural support. For full dosing and timing details, see the Supplement Stack article.
| Supplement | Role | Timing | Link |
|---|---|---|---|
| Minoxidil 5% (topical) | Follicle stimulation, vasodilation, prolongs anagen phase | Twice daily (AM & PM) | Stack → |
| Saw Palmetto | Natural 5-AR inhibitor, reduces DHT conversion | With breakfast | Stack → |
| Dutasteride (Rx) | Dual 5-AR inhibitor (Type I + II), strongest DHT blocker | With breakfast | Stack → |
| Biotin (B7) | Keratin infrastructure, strengthens hair shaft | With breakfast | Stack → |
| BioSil (ch-OSA) | Collagen and silicon for hair elasticity and thickness | Fasted (AM) | Stack → |
| MSM | Sulfur donor for keratin cross-linking and disulfide bonds | With breakfast | Stack → |
| Zinc | Growth cofactor, supports cell division in follicle matrix | With dinner | Stack → |
| L-Lysine | Essential amino acid for collagen synthesis, enhances iron absorption | With breakfast | Stack → |
| Collagen Peptides | Provides proline and glycine for hair structural protein | Fasted (AM) | Stack → |
Biotin and lab tests: High-dose biotin (>5 mg/day) can interfere with immunoassay-based lab tests, producing falsely low TSH and falsely high free T4. Discontinue biotin 48–72 hours before any blood draw that includes thyroid panels or troponin.
Patel, D. P., et al. (2017). A review of the use of biotin for hair loss. Skin Appendage Disord, 3(3), 166-169. PMID: 28879195
Hair loss is frequently a symptom of underlying metabolic or hormonal issues. The following lab tests help identify root causes and track progress. See the Preventive Lab Tests guide for complete reference ranges and ordering details.
| Test | What It Measures | Frequency | Link |
|---|---|---|---|
| Ferritin | Iron stores — ferritin <30 ng/mL strongly associated with telogen effluvium | Every 6 months | Details → |
| TSH | Thyroid function — both hypo- and hyperthyroidism cause diffuse hair loss | Annually | Details → |
| Total Testosterone | Baseline androgen level; low T can cause thinning in both sexes | Annually | Details → |
| DHT | Dihydrotestosterone — direct driver of follicle miniaturization | Baseline + 6 months after starting 5-AR inhibitor | Details → |
| DHEA-S | Adrenal androgen precursor; elevated levels in women suggest hormonal hair loss | Annually | Details → |
| Zinc (serum) | Zinc deficiency impairs cell division in the hair follicle matrix | Every 6 months | Details → |
| Vitamin D (25-OH) | Low vitamin D linked to alopecia areata and telogen effluvium | Every 6 months | Details → |
| Iron Panel (serum iron, TIBC, saturation) | Full iron status — rules out iron-deficiency anemia as hair loss cause | Every 6 months | Details → |
Target ferritin for hair health: While the lab "normal" range starts at 12 ng/mL, dermatologists specializing in hair loss recommend maintaining ferritin above 70 ng/mL for optimal hair growth. Many patients see significant improvement simply by correcting low ferritin.
Esfandiari, A., & Kelly, A. P. (2005). The effects of tea polyphenolic compounds on hair loss among rodents. J Natl Med Assoc, 97(8), 1165. — Olsen, E. A., et al. (2006). The importance of dual 5alpha-reductase inhibition in the treatment of male pattern hair loss. J Am Acad Dermatol, 55(6), 1014-1023. PMID: 17110217
A 2025 network meta-analysis published in Frontiers in Medicine analyzing randomized controlled trials confirmed that finasteride combined with minoxidil was identified as the most effective treatment for male androgenetic alopecia. A separate 2025 systematic review of seven RCTs (396 patients) comparing topical minoxidil-finasteride combination (3-5% minoxidil + 0.1-0.25% finasteride) against minoxidil monotherapy showed significant increases in hair density and diameter. The oral "all-in-one" formulation of low-dose minoxidil (2.5 mg) + finasteride (1 mg) is gaining clinical traction for improved patient compliance.
A 2025 Frontiers in Pharmacology systematic review and meta-analysis of oral minoxidil safety confirmed its efficacy at low doses (2.5-5 mg) for alopecia treatment with manageable side effects, primarily hypertrichosis (excess hair growth elsewhere) and mild cardiovascular effects. This represents a shift from topical-only use toward oral low-dose protocols supervised by dermatologists.
Frontiers in Medicine (2025). Relative efficacy of minoxidil in combination with other treatments for androgenic alopecia: a network meta-analysis. Frontiers