Hair Loss: The Functional Medicine Approach

Reading the Roots

A single hair strand is a biological time capsule. It records three months of nutritional status, hormone levels, heavy metal exposure, and stress load in its structure. When hair falls, it is not a cosmetic inconvenience — it is a systemic signal. The follicle is one of the most metabolically active structures in the body, with a turnover rate second only to bone marrow. It requires iron, zinc, biotin, amino acids, thyroid hormone, adequate blood flow, and a stable hormonal environment to sustain itself. When any of these falter, the follicle is among the first structures the body sacrifices — because unlike the heart or brain, hair is not essential for survival.

This is why hair loss is so diagnostically valuable in functional medicine. It forces us to look under the hood.

The Hair Growth Cycle

Every hair follicle cycles independently through three phases:

Anagen (growth phase): 2-7 years. This is when the hair is actively growing at approximately 1 cm per month. Roughly 85-90% of scalp hairs are in anagen at any given time. The length of anagen determines maximum hair length — this is genetically determined and varies by body region (eyelashes have a much shorter anagen than scalp hair).

Catagen (transition phase): 2-3 weeks. The follicle shrinks, the hair shaft detaches from the blood supply, and growth stops. The hair is now a “club hair” — dead but still anchored.

Telogen (resting phase): 3-4 months. The club hair sits in the follicle while a new anagen hair begins forming beneath it. Eventually, the new hair pushes the old one out — this is the hair you find on your pillow or in your brush. Losing 50-100 hairs per day is normal cycling.

Understanding this cycle explains a critical clinical pattern: the trigger for hair loss often occurred 2-4 months before the shedding begins. The patient presents in panic at month 4, but the insult — surgery, illness, crash diet, emotional trauma, medication change, postpartum hormone shift — happened at month 1.

Types of Hair Loss

Androgenetic Alopecia

The most common form. In men: receding hairline and vertex thinning (the classic “male pattern”), driven by DHT (dihydrotestosterone) converting terminal hairs to vellus hairs (miniaturization). Genetic sensitivity of follicle androgen receptors determines pattern and severity. In women: diffuse thinning across the crown with preserved frontal hairline (“Christmas tree pattern” on part), driven by a combination of androgen excess and estrogen decline. Female androgenetic alopecia is often under-recognized.

Telogen Effluvium

Diffuse shedding — hair coming out in handfuls, clogging the shower drain. Not patchy. Triggered by a systemic stressor that pushes a disproportionate number of follicles from anagen into telogen simultaneously. Common triggers: surgery, high fever, childbirth (postpartum — usually peaks at 3-4 months), crash dieting, severe emotional stress, medication changes, thyroid dysfunction, iron deficiency. Usually self-limiting — resolves within 6-12 months after the trigger is addressed. Chronic telogen effluvium (>6 months) suggests an ongoing systemic issue.

Alopecia Areata

Autoimmune attack on the hair follicle. Presents as smooth, round patches of complete hair loss — “exclamation point” hairs at the margins (short, broken hairs that taper at the base). Can progress to alopecia totalis (entire scalp) or alopecia universalis (entire body). The follicle is not destroyed — the immune attack targets the anagen phase, forcing premature catagen. This means regrowth is always possible if the immune dysregulation is resolved.

Other Types

• Traction alopecia: Chronic tension from tight hairstyles (ponytails, braids, extensions). Frontal and temporal hairline. Reversible if caught early; permanent if follicles are scarred
• Scarring (cicatricial) alopecias: Lichen planopilaris, frontal fibrosing alopecia, discoid lupus — inflammatory conditions that destroy the follicle permanently. Requires dermatology evaluation and biopsy
• Anagen effluvium: Rapid shedding during anagen — typically chemotherapy. Hair regrows after treatment ends

The Root Cause Evaluation

Iron

The most commonly missed cause of hair loss in women. Standard lab reference ranges allow ferritin as low as 10-15 ng/mL — but Kantor (2003) demonstrated that ferritin below 40 ng/mL is associated with increased hair shedding, and David Rushton’s research at the Institute of Trichology suggests that optimal hair growth requires ferritin above 70 ng/mL. Many women with “normal” iron labs are functionally deficient for hair growth.

Iron is required for ribonucleotide reductase, the rate-limiting enzyme in DNA synthesis — and hair follicle matrix cells are among the fastest-dividing cells in the body. Without adequate iron, they cannot sustain the replication rate anagen demands.

Supplement: iron bisglycinate 25-50mg every other day (better absorption than daily per Stoffel 2017), taken with vitamin C 200mg on an empty stomach. Target ferritin 70-90 ng/mL. Recheck every 3 months. Rule out heavy menstruation, GI blood loss, celiac disease, and poor absorption as ongoing causes.

Thyroid

Both hypothyroidism and hyperthyroidism cause hair loss, but hypothyroidism — particularly Hashimoto’s thyroiditis — is the more common culprit. T3 (triiodothyronine) is directly required for hair follicle proliferation and differentiation. Low T3 prolongs telogen and shortens anagen. Hair becomes dry, brittle, and thin.

The trap: TSH may be “normal” (within reference range) while free T3 is suboptimal. Many patients with Hashimoto’s have adequate T4 production but impaired T4-to-T3 conversion due to selenium deficiency, chronic stress, gut dysfunction, or inflammation.

Test: TSH, free T4, free T3, reverse T3, TPO antibodies, thyroglobulin antibodies. Optimize free T3 to upper third of range.

Hormonal

• DHT: The primary driver of androgenetic alopecia. 5-alpha reductase converts testosterone to DHT in the follicle. Genetically susceptible follicles respond to DHT by miniaturizing
• Estrogen decline: Menopause, perimenopause, oral contraceptive withdrawal — the shift in estrogen-to-androgen ratio unmasks androgen effects
• PCOS: Hyperandrogenism → excess DHT → hair loss on the scalp (paradoxically, excess hair on face and body)
• Postpartum: High estrogen during pregnancy keeps hair in anagen. After delivery, estrogen plummets, and all those hairs enter telogen simultaneously — massive shedding at 3-4 months postpartum. Self-limiting but terrifying
• DHEA-S elevation: Adrenal androgen excess, sometimes from chronic stress (adrenal hyperactivity), supplements (DHEA supplementation in women is a common iatrogenic cause)

Stress

Not just emotional — physiological. Surgery, illness, caloric restriction, overtraining, sleep deprivation. Cortisol pushes follicles from anagen to catagen prematurely. Chronic stress also depletes zinc, B vitamins, magnesium, and iron — nutrients the follicle requires. Check cortisol (salivary 4-point) and DHEA-S. The cortisol:DHEA ratio reflects adrenal resilience.

Nutrients

• Zinc: Essential for DNA synthesis, immune function, and protein structure. Deficiency causes telogen effluvium and impaired keratin formation. Test: serum zinc or RBC zinc. Target 80-120 mcg/dL
• Biotin (B7): Cofactor for carboxylase enzymes involved in amino acid and fatty acid metabolism. True deficiency is uncommon but supplementation at 5000 mcg appears to support hair growth. Critical caveat: biotin interferes with immunoassay lab tests — it falsely lowers TSH and falsely elevates free T4, mimicking hyperthyroidism. Stop biotin 48-72 hours before any thyroid blood work
• Vitamin D: Deficiency (<30 ng/mL) is associated with alopecia areata (Aksu Cerman 2014) and telogen effluvium. Vitamin D receptors are present in hair follicles and are essential for anagen initiation. Target 50-80 ng/mL
• Selenium: Required for T4-to-T3 conversion and glutathione peroxidase (protects follicle from oxidative damage). Deficiency contributes to both thyroid-related hair loss and direct follicle damage. Dose: 200 mcg daily
• B12: Deficiency impairs DNA synthesis in rapidly dividing follicle cells. Common in vegans, those on metformin or PPIs. Test methylmalonic acid for functional deficiency
• Protein: Hair is 95% keratin. Inadequate protein intake (common in restrictive diets, elderly, GLP-1 agonist users) starves the follicle. Minimum 1.0-1.2g per kg body weight

Gut Connection

• Celiac disease: Autoimmune gluten reaction causes malabsorption of iron, zinc, B12, folate, and vitamin D — all critical for hair growth. Even non-celiac gluten sensitivity may contribute
• SIBO: Malabsorption + inflammation + nutrient competition with bacteria
• Low stomach acid: Impaired protein digestion and mineral absorption (iron, zinc). Common in hypothyroidism (circular causation)

The Functional Hair Loss Protocol

Foundational Supplements

Supplement	Dose	Target
Iron bisglycinate	25-50mg every other day	Ferritin >70 ng/mL
Zinc picolinate	30mg	Support keratin synthesis, 5AR inhibition
Biotin	5000 mcg	Keratin support (stop before labs)
Vitamin D3 + K2	5000-10,000 IU to target	50-80 ng/mL
Selenium	200 mcg	Thyroid conversion, antioxidant
B12 (methylcobalamin)	1000-5000 mcg	If deficient
Collagen peptides	10-15g	Amino acids for hair structure
Silica (from horsetail or bamboo)	10-20mg	Structural support
MSM (methylsulfonylmethane)	1-3g	Sulfur for keratin/collagen

Anti-DHT Natural Approach

• Saw palmetto 320mg standardized extract: inhibits both type I and type II 5-alpha reductase. Rossi (2012) — 38% improvement in hair growth over 2 years. Fewer sexual side effects than finasteride
• Pumpkin seed oil 400mg daily: Cho (2014) randomized controlled trial — 40% increase in hair count after 24 weeks compared to placebo. Likely works through 5-alpha reductase inhibition
• Stinging nettle root 300-600mg: binds SHBG, may reduce free DHT at the follicle
• Green tea extract (EGCG): inhibits 5-alpha reductase in vitro, anti-inflammatory
• DIM 200mg: modulates estrogen metabolism, may shift androgen balance
• Reishi mushroom: contains 5-alpha reductase inhibitors (Grant 1999)

Topical Treatments

• Minoxidil 2% (women) or 5% (men): FDA-approved. Vasodilator that prolongs anagen and increases follicle size. Results in 4-6 months. Must be continued indefinitely (hair loss resumes upon stopping)
• Rosemary essential oil: Panahi (2015) — rosemary oil applied topically was comparable to 2% minoxidil after 6 months, with less scalp itching. Dilute in carrier oil (jojoba), massage into scalp daily
• Pumpkin seed oil topical: Emerging evidence for direct follicle stimulation
• Caffeine shampoo: Stimulates hair follicle growth in vitro (Fischer 2007), counteracts DHT suppression. Leave on 2 minutes before rinsing
• Microneedling (dermaroller): 1.5mm depth, once weekly — activates wound healing and growth factors in the scalp. Dhurat (2013) — microneedling plus minoxidil significantly outperformed minoxidil alone

PRP (Platelet-Rich Plasma)

Gentile (2015) demonstrated significant improvement in hair density with PRP injections — the patient’s own blood is drawn, centrifuged to concentrate platelets and growth factors, then injected into the scalp. Typical protocol: 3-4 sessions at 4-6 week intervals, then maintenance every 6-12 months. Growth factors released include PDGF, VEGF, EGF, and IGF-1 — which stimulate follicle stem cells and prolong anagen. Cost is the primary barrier ($500-1500 per session, typically not covered by insurance). Results are variable but promising — works best for early-stage thinning before follicles are fully miniaturized.

Alopecia Areata: The Autoimmune Protocol

• Autoimmune elimination diet (remove gluten, dairy, soy, corn, eggs, nightshades for 90 days)
• Vitamin D optimization to 60-80 ng/mL
• Gut healing protocol (L-glutamine, probiotics, zinc carnosine)
• Stress reduction (the autoimmune component is often stress-triggered)
• Low-dose naltrexone (LDN) 1.5-4.5mg at bedtime — modulates immune function, case reports and small studies show benefit in alopecia areata
• JAK inhibitors: baricitinib (Olumiant) FDA-approved for severe alopecia areata in 2022, ruxolitinib topical approved — these target the Janus kinase pathway that drives the T-cell attack on follicles. Significant side effect profile for systemic JAK inhibitors requires careful monitoring

The Timeline

Hair has a long memory but a slow response. Addressing root causes today produces visible changes 3-6 months from now. Full results typically require 12-18 months of consistent intervention. The follicle needs to complete an entire telogen-to-anagen transition with optimized nutrients, hormones, and inflammatory status before the new growth becomes visible.

Patience is part of the protocol. The hair is telling you the truth about what happened inside your body three months ago. What truth would you like it to tell three months from now?