Iron
Iron deficiency (ID) is the world’s most common nutritional deficiency and is a well-known cause of hair loss. What remains unclear is what degree of ID may contribute to hair loss.
While the mechanism of action by which iron impacts hair growth is not known, hair follicle matrix cells are some of the most rapidly dividing cells in the body, and ID may contribute to hair loss via its role as a cofactor for ribonucleotide reductase, the rate-limiting enzyme for DNA synthesis [14]. In addition, multiple genes have been identified in the human hair follicle [15], and some may be regulated by iron [16]. In a mouse model, reversal of ID led to restoration of hair growth [17].
Certain populations are at higher risk for ID, and a medical and dietary history may reveal risk factors. Premenopausal women are at higher risk due to menstrual blood loss, while postmenopausal women and men may present due to gastrointestinal blood loss. Other risk factors include malabsorption disorders (such as celiac disease) as well as achlorhydria or the use of H2 blockers, as iron requires an acidic pH for absorption.
Vegans and vegetarians are also at higher risk for ID, as their requirements for dietary iron are considered to be 1.8 times higher than for meat consumers [18]. Non-heme iron, found in plants, has a lower bioavailability than heme iron, found in meat and fish [19].
Patients with more advanced ID develop iron deficiency anemia and require replacement. ID may also result in a reduction of storage iron, measured by serum ferritin. A normal ferritin level does not exclude ID, however, as it is an acute phase reactant.
Although multiple research studies have been conducted, it is unknown if a deficiency of storage iron contributes to hair loss, as conflicting results have been noted. Some studies have found that low serum ferritin is more prevalent in patients with chronic TE, FPHL, AGA, and AA. Other studies have found no such link. Two excellent review articles have summarized these results and note considerable variations in study design, controls, and ID definitions [16,20]. There are few intervention trials, and they are limited by small numbers, lack of controls in some, and variable ferritin levels. These have utilized different interventions, including iron alone [21], iron with L-lysine [8,22], and iron with spironolactone [23].
One study used a control population that excluded patients at risk for ID [24] and found no statistically significant increase in the prevalence of ID in premenopausal or postmenopausal women with chronic TE or FPHL.
At this time, there are no definitive answers. Patients must be approached on a case-by-case basis. In the aforementioned review articles, the researchers present their approach. Both groups test patients with iron studies, including serum ferritin. Both recommend treatment of ID, with or without anemia, with dietary sources and oral iron supplementation when necessary, with a goal of ferritin levels above 50 μg/L [16] or 70 μg/ml, respectively [20].
Patients are monitored to measure their response—an important point. Patients who take iron supplements without monitoring are at risk for potentially severe complications, as iron supplementation leading to iron overload can cause toxicity. This can occur even at low levels if taken over a long period [25].