Iron deficiency and hair loss: the ferritin threshold, the mechanism, and how to correct it

Iron deficiency is among the most correctable causes of hair loss — yet it is routinely missed because the laboratory threshold used by most standard reference ranges is far below the level required for optimal hair follicle function. Understanding the ferritin target, the mechanism of iron-related hair loss, and how to supplement effectively is essential for any woman with unexplained diffuse shedding.

Why iron matters for hair follicles

The biology

Hair follicles in the anagen (growth) phase are among the most rapidly dividing cell populations in the body. The matrix cells at the base of the follicle divide faster than almost any other tissue except bone marrow. This rapid cell division requires:

Iron for DNA synthesis: Iron is a cofactor for ribonucleotide reductase, the rate-limiting enzyme in DNA synthesis. Without adequate iron, rapidly dividing cells — including follicular matrix cells — cannot maintain their replication rate.
Iron for cellular respiration: Iron is central to the electron transport chain (cytochrome c, Fe-S clusters) — aerobic energy production that fuels the high metabolic demands of the actively growing follicle.
Iron for keratin production: Keratinocyte differentiation and keratin protein synthesis are impaired in iron-deficient follicles.

Net effect of iron deficiency on follicles: The follicle prematurely transitions from anagen to telogen — the metabolic demands of active growth cannot be sustained. This produces the classic picture of telogen effluvium — diffuse increased shedding from all over the scalp as more follicles than normal are in the resting/shedding phase simultaneously.

The ferritin distinction

Ferritin is the iron-storage protein — its serum level reflects the body's iron stores, not just current circulating iron. Serum ferritin is the most clinically useful marker for iron status in the context of hair loss because:
Serum iron and hemoglobin remain normal until iron stores are substantially depleted
Hair follicles are affected by iron store depletion before anemia develops
Normal hemoglobin + low ferritin = iron deficiency without anemia — still causes hair loss

This is why women can have normal CBC and hemoglobin but significant iron deficiency causing hair loss — the ferritin level is the correct test.

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The ferritin threshold problem

What standard labs report as "normal"

Most clinical laboratory reference ranges for serum ferritin list normal as >12 ng/mL for premenopausal women. This threshold was established to define anemia-level iron deficiency — the point at which iron stores are essentially absent and red blood cell production is compromised.

What the hair loss literature shows

The research literature on iron and hair loss consistently identifies a higher ferritin threshold for hair-relevant iron sufficiency:

*Rushton et al. (2002, Clinical and Experimental Dermatology):* This key study evaluated premenopausal women with diffuse hair loss. Those with ferritin &lt;30 ng/mL had significantly higher hair loss than those with ferritin >70 ng/mL. After iron supplementation in deficient women, significant improvement in hair density was observed at 6 months.

*Kantor et al. (2003, Journal of Investigative Dermatology):* Serum ferritin levels were significantly lower in women with telogen effluvium compared to controls; the threshold for hair loss association was ~40 ng/mL.

*Trost et al. (2006, Archives of Dermatology):* Systematic review confirming the association between low ferritin and hair loss in women, recommending ferritin >70 ng/mL as the target for hair-relevant iron sufficiency.

Clinical consensus: A ferritin level of 70 ng/mL is the widely used threshold among trichologists and dermatologists specializing in hair loss for "iron-sufficient" with respect to hair health. A ferritin between 12–70 ng/mL may be reported as "normal" by the lab but may be hair-loss-relevant deficiency.

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Who is at risk for hair-relevant iron deficiency

Premenopausal women with heavy menstrual bleeding

The most common cause. Monthly blood loss in women with menorrhagia (heavy periods) can exceed the amount of iron absorbed from the diet, creating a chronic negative iron balance. Even with a diet containing adequate iron, the monthly loss outpaces absorption capacity.

Clinical screen: Ask about pad/tampon use per cycle day; any period lasting >7 days with heavy flow; passage of clots. Menorrhagia warrants gynecologic evaluation (fibroids, von Willebrand disease, hormonal causes) in addition to iron supplementation.

Vegetarians and vegans

Dietary iron comes in two forms:
Heme iron (meat, fish, poultry): Highly bioavailable; absorbed at ~20–30%
Non-heme iron (plant sources, fortified foods): Much lower bioavailability; absorbed at ~2–10%

Vegetarians and vegans rely entirely on non-heme iron and may not achieve adequate intake even with iron-rich plant foods (legumes, tofu, fortified cereals, dark leafy greens). Phytates in grains and legumes further inhibit non-heme iron absorption.

Women after childbirth

Delivery involves significant blood loss; the fetus draws heavily on maternal iron stores throughout the third trimester. Postpartum iron deficiency is common and frequently underlies or prolongs postpartum hair loss beyond what estrogen withdrawal alone accounts for.

Women with gastrointestinal conditions

Celiac disease, Crohn's disease, atrophic gastritis, or any condition affecting the duodenum (the primary iron absorption site) impairs iron uptake regardless of intake. H. pylori infection reduces gastric acid → impairs non-heme iron absorption. Bariatric surgery (particularly gastric bypass with duodenal exclusion) dramatically reduces iron absorption capacity.

Athletes (particularly runners)

"Sports anemia" — a real phenomenon involving increased iron loss through sweat, increased red blood cell breakdown from footstrike hemolysis, and increased iron demand from training adaptation. Female endurance athletes are at particular risk for iron deficiency.

Frequent blood donors

Each whole blood donation removes ~200–250 mg of iron — roughly 2–3 months of dietary iron absorption for the average person. Regular donors can gradually deplete iron stores even without other risk factors.

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Work-up and diagnosis

Recommended tests

| Test | What it measures | Target |
|---|---|---|
| Serum ferritin | Iron stores | >70 ng/mL for hair health |
| Serum iron | Circulating iron | Normal range |
| TIBC (total iron-binding capacity) | Transferrin saturation | Normal; elevated TIBC = depletion |
| Hemoglobin / CBC | Anemia status | Normal (may be normal with low ferritin) |
| CRP or ESR | Inflammation | Important — ferritin is an acute-phase reactant; elevated in inflammation regardless of iron stores |

The CRP caveat: Ferritin is falsely elevated in active inflammation or infection — the body sequesters iron as part of the acute-phase response. A woman with active autoimmune disease, active infection, or chronic inflammation may have a "normal" ferritin that does not reflect actual iron stores. CRP helps identify this situation.

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Supplementation: what to take and how

Iron formulations

Ferrous sulfate (325 mg = 65 mg elemental iron): The most widely available and least expensive oral iron. Effective but has higher GI side effects (constipation, nausea, stomach cramping) than newer formulations.

Ferrous gluconate / ferrous fumarate: Slightly lower elemental iron per tablet (38 mg and 33 mg respectively); similar efficacy; somewhat better GI tolerability than sulfate.

Ferric pyrophosphate / liposomal iron: Newer formulations with significantly improved GI tolerability; may be better absorbed at lower doses. Appropriate for patients who cannot tolerate conventional ferrous formulations.

Polysaccharide-iron complex (PIC): Another well-tolerated alternative; fewer GI side effects; useful for patients requiring long-term supplementation.

Dosing strategy

Standard dose: 150–200 mg elemental iron per day is the classical repletion dose — but this is associated with significant GI side effects and may actually reduce absorption efficiency.

Alternate-day dosing: Moretti et al. (2015, Blood) demonstrated that alternate-day iron supplementation (every other day) achieves equivalent or superior absorption to daily dosing, with substantially fewer GI side effects. The mechanism involves hepcidin regulation — daily iron suppresses hepcidin initially then allows recovery on the off-day, improving net absorption. Alternate-day dosing at 65–100 mg elemental iron is now a reasonable standard approach.

Enhancing absorption

Take iron with vitamin C: Vitamin C (ascorbic acid 250 mg or more) taken simultaneously significantly enhances non-heme iron absorption by reducing Fe³⁺ to the more absorbable Fe²⁺ form
Take on an empty stomach: Iron absorption is highest on an empty stomach; GI side effects are also higher. A small amount of food (not dairy, not high-phytate grains) can moderate GI effects without substantially reducing absorption.
Avoid co-administration with: Calcium supplements (inhibit iron absorption), antacids/PPIs (reduce gastric acid → impair iron absorption), tannins in tea and coffee (chelate iron → reduce absorption), certain medications (levothyroxine, quinolone antibiotics — space by 4 hours)
Avoid dairy and high-phytate foods within 1–2 hours of iron dose

Timeline for response

Ferritin replenishment: After starting oral iron supplementation, ferritin levels begin rising within weeks, but reaching target levels (>70 ng/mL from a depleted baseline) typically takes 3–6 months of consistent supplementation.

Hair response: The hair follicle cycle lag means that improved iron stores do not immediately produce visible hair improvements. Expect:
3–4 months before reduced shedding is apparent
6 months for meaningful density improvement
12 months for full recovery in moderate deficiency cases

Recheck ferritin at 3 months to verify supplementation is working and adjust dose if needed. After achieving target ferritin, retest every 6 months to confirm maintenance — if the underlying cause (heavy periods, malabsorption) is not corrected, iron deficiency will recur after stopping supplementation.

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Diet sources of iron

Dietary iron alone is rarely sufficient to correct established iron deficiency efficiently (given the absorption limitations), but it is essential for maintaining iron status after supplementation achieves target levels:

| Food | Iron (mg) | Type | Notes |
|---|---|---|---|
| Beef liver (85g) | 5.2 mg | Heme | Highest density |
| Dark meat chicken (85g) | 1.1 mg | Heme | Common source |
| Oysters (85g) | 8.0 mg | Heme | Very high |
| Lentils (½ cup cooked) | 3.3 mg | Non-heme | With vitamin C |
| Tofu (½ cup firm) | 3.4 mg | Non-heme | With vitamin C |
| Spinach (½ cup cooked) | 3.2 mg | Non-heme | Phytates reduce absorption |
| Fortified cereals | 18 mg | Non-heme | Read label; with OJ |
| Pumpkin seeds (28g) | 2.5 mg | Non-heme | Reasonable plant source |

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