Ferritin and Hair Loss: What Level Is Optimal, and Does the 70 ng/ml Rule Make Sense?

Ferritin stores iron inside cells (mainly in the liver, spleen and bone marrow), and a small amount of it circulates in the blood. In the absence of inflammation, the blood concentration reflects the body's iron stores well: a low result confirms deficiency even if haemoglobin is still normal (so-called iron deficiency without anaemia, which we discuss in a separate entry). Typical laboratory thresholds are around 15 ng/ml for diagnosing depleted stores, and values below 30 ng/ml are sometimes treated as iron deficiency in clinical practice, but the limits differ between laboratories and guidelines.

The problem is that ferritin is also an acute-phase protein: it rises in infections, inflammation, liver disease, obesity, after intense exercise and in cancers. So a ferritin of 60 ng/ml in a person with chronic inflammation may correspond to real deficiency, while in a healthy person it means normal stores. When interpreting the result it is worth assessing CRP at the same time (we describe it in the entry on CRP and hsCRP) and a blood count, including haemoglobin and MCV, MCH and RDW.

In addition, the result depends on sampling conditions and the phase of the menstrual cycle, which we discuss in the article on low ferritin with normal haemoglobin and pre-analytics. A single result without context is not enough to decide on supplementation, let alone that ‘ferritin must be 70’.

Hair follicles are among the fastest-dividing tissues in the body, and cell division requires DNA synthesis, in which an iron-dependent enzyme (ribonucleotide reductase) takes part. Iron is also a component of cellular respiratory enzymes and a cofactor of many metabolic reactions. The authors of a review published in the Journal of the American Academy of Dermatology described iron-dependent genes in the ‘bulge’ region of the hair follicle, where stem cells reside, and suggested that iron deficiency could disturb the hair cycle.

In terms of mechanism: deficiency may prematurely end the growth phase (anagen) and push more follicles into the resting phase (telogen), which shows up as increased, diffuse shedding 2–4 months after the trigger. This is, however, a biologically plausible mechanism, not one demonstrated directly in humans in a way that would allow identifying a ferritin threshold below which hair starts to fall.

In 2026 a systematic review with meta-analysis covering 29 papers was also published, which found significantly lower ferritin in people with telogen hair loss than in healthy controls (standardized mean difference −0.57; 95% CI −1.01 to −0.12), with high heterogeneity of results. This means the general direction is consistent — lower ferritin more often accompanies telogen shedding — but the spread between studies is large, and the association alone does not prove that iron deficiency caused the shedding.

This study is especially important for judging the popular threshold of 40 or 70 ng/ml: the proportion of women with ferritin ≤40 µg/l in the group without hair loss was as high as 72.3% before menopause. If ferritin below 40 by itself caused hair loss, most healthy premenopausal women would have a hair problem, and that is not the case. Conclusion: low (but not extremely low) ferritin is very common in women and does not in itself determine hair loss.

The difference in results between this and the earlier studies comes partly from the choice of control group (in the Olsen study controls were recruited from women around the university, with no hair loss in history or examination), sample sizes, the definition of hair loss and the presence of inflammation. Such a discrepancy is typical for a topic in which there are no large randomized trials.

The value of 70 µg/l (ng/ml) appears in Rushton's 2002 review, in which the author recommends ferritin at 70 µg/l with a normal ESR (<10 mm/h) in people with marked hair shedding, while admitting that the level to adopt ‘has not been definitively established’. It is therefore an expert opinion based mainly on clinical observation, not on a study in which people with ferritin of 40 were randomly divided into groups supplemented to 70 and not.

In turn, the authors of another review (St Pierre et al. 2010) explicitly note that the published studies have small patient numbers and different designs, that there are no randomized treatment trials, and call for a well-designed trial of the effect of iron supplementation in iron-deficient women with persistent hair loss. To our knowledge no study has appeared to date that would settle this question unambiguously.

Most studies concern women, because they more often have iron deficiency (menstruation, pregnancy, diet). In men iron deficiency is rare, and when it appears it requires looking for a source of blood loss, especially from the gastrointestinal tract — as the authors of the Trost review stress. For men with typical androgenetic alopecia (receding temples, crown), low ferritin is rarely the cause, and iron supplementation without deficiency will bring no effect on the hair and carries a risk of overload.

In androgenetic alopecia the main factor is the sensitivity of follicles to DHT, not iron stores; treatment relies on finasteride, minoxidil and other methods, which we discuss in separate articles. Ferritin may, however, coexist and aggravate diffuse shedding on top of the androgenetic pattern. In telogen shedding, which appears 2–4 months after a trigger (fever, childbirth, a restrictive diet, surgery, chronic stress), iron deficiency is one possible element of the picture, but usually not the only one.

A special group is people after bariatric surgery, on vegan or very restrictive diets, with heavy periods, coeliac disease or inflammatory bowel disease — here iron deficiency is a real, common and potentially reversible factor in hair loss and is worth actively checking. A related topic, alopecia areata and its determinants, is described in a separate article.

A similar myth is the belief that iron supplementation ‘strengthens hair’ regardless of the state of stores. In people with normal stores extra iron does not improve hair condition, and may cause gastrointestinal complaints and, with long-term excess, overload.

Ferritin deserves to be tested in diffuse hair loss, especially in women, but it does not deserve the role of a magic number. A sound approach is to treat documented iron deficiency and its cause, look for other coexisting factors (thyroid, vitamin D, diet, stress, drugs) and not turn a result ‘in the lower half of normal’ into a diagnosis that promises hair regrowth after taking a supplement. If, after stores have been replenished and causes removed, hair still falls, other diagnoses must be considered, including androgenetic alopecia.