Complementary and alternative medicine for hair loss

Key points

Patients with androgenetic alopecia may be interested in exploring complementary and alternative medicine, including supplements, specialty diets, and essential oils.
There is insufficient evidence to support the use of any complementary and alternative medicine as monotherapy for androgenetic alopecia.
Patients who wish to forgo traditional therapies in favor of complementary and alternative medicine should be counseled that the latter are not considered an appropriate monotherapy for alopecia. These patients can be directed toward efficacious treatments that may be similarly perceived as “natural,” including platelet-rich plasma therapy, microneedling, and photobiomodulation.
Although many complementary and alternative medicine therapies have roots in ancient culture and are generally considered safe, certain products and practices place patients at risk of serious harm.
Patients with androgenetic alopecia and a serum ferritin less than 40 ng/mL should undergo repletion with an oral slow-release ferrous iron supplement for at least 3 to 6 months before laboratory reevaluation.
Most individuals have adequate biotin intake, and biotin supplementation may invalidate laboratory tests such as cardiac troponin and thyroid panel assays.
Alopecia patients experiencing psychosocial distress from hair loss may benefit from seeing a licensed mental-health professional, joining a patient support group, and scalp photography.

Introduction

Complementary and alternative medicine (CAM) includes treatments and practices that are distinct from traditional medical care. Patients with androgenetic alopecia (AGA) can feel distressed and may not respond to treatment, prompting them to explore CAM therapies. Many CAM therapies, including topical herbal preparations, massage, and specialty diets, have roots in ancient culture. CAM treatments for AGA include natural herbal products, mind-body practices, and homeopathy. ^, Patients report turning to CAM to gain a sense of control over their condition and from concern with side effects of traditional medications (level of evidence: 5). ^,

Increasing patient interest in CAM mirrors trending consumer demand for “natural” products and is estimated to be an annual $30.2-billion industry. However, less than half of patients using CAM therapies inform their physician (level of evidence: 2a). Although CAM is generally considered safe, certain products and practices place patients at risk of serious harm ( Pearl 11.1 ). ^, ^, This chapter will provide an overview of the medical literature on CAM therapies for AGA.

PEARL 11.1:

Alopecia patients who wish to forgo traditional therapies in favor of complementary and alternative medicines (CAMs) should be counseled that CAMs are not considered an appropriate monotherapy for alopecia and can be directed toward efficacious treatments that may be similarly perceived as ‘natural’ including platelet-rich plasma treatment, microneedling, and photobiomodulation.

Diet and supplements

Hair requires adequate intake of macronutrients and micronutrients for optimal growth. The association between nutrition and hair is so linked that anthropologists can measure the concentration of nitrogen isotopes specific to corn-fed animal-based proteins in a person’s hair and approximate their socioeconomic status (level of evidence: 2c). The well-known link between nutrition and hair prompts many distressed alopecia patients to start new diets and supplements, spurring the growth of a massive hair-related diet and nutraceutical industry. However, the literature examining hair and nutrition is conflicted. In this section, we review evidence regarding diet and supplementation in AGA.

Protein

Hair primarily consists of protein. The importance of dietary protein to hair growth is highlighted in conditions of inadequate protein intake. For example, children with kwashiorkor who have diets that are calorically adequate but protein poor experience increased hair shedding, decreased hair shaft diameter, hypopigmented fibers, and texture changes. Although dietary protein is readily available to people in developed countries, there is evidence to suggest that many patients with AGA may not have adequate protein intake.

A small cross-sectional study of 20 patients with AGA identified that 90% had inadequate protein intake and that 55% were “severely deficient” (consumed <30 g/day) despite self-reporting eating a regular diet (level of evidence: 4). Histologic comparison revealed increased perifollicular fibrosis in those with low dietary protein compared with those with normal dietary protein. The study found a positive association between consumption of breakfast and overall protein intake. A similar case-control study of 357 patients with AGA did not find a significant association between protein intake and AGA outcomes (level of evidence: 3b). The small size of these studies and conflicting results limit broad generalizations. However, they demonstrate that patients who are food secure may still have diets deficient in protein and could benefit from nutrition counseling.

The dietary reference intake (DRI) for protein is 0.8 grams per kilogram of body weight for sedentary adults. However, this can be increased for adults who are active. Long-term dietary protein intake exceeding 2 grams per kilogram of body weight can cause renal, cardiovascular, and gastrointestinal disease and should be avoided. The authors typically recommend 50 to 60 grams daily of dietary protein intake for patients with AGA and normal renal function.

Cystine

Keratin is the primary hair protein. Although many oral hair-growth supplements include keratin as an ingredient, it is poorly solubilized in water and not readily absorbed in the human digestive tract. Supplementation with keratin’s constituent amino acids, namely cysteine, to improve hair growth has been proposed in the treatment of AGA. Cystine is the oxidized form of cysteine responsible for disulfide keratin cross-linking. Various studies have examined the use of cystine in AGA and telogen effluvium (TE) and suggest a positive treatment response (level of evidence: 1b). However, cystine was combined with other minerals, vitamins, and proprietary formulations in these studies, preventing true determination of cystine’s efficacy. There is not sufficient evidence to support routine cystine supplementation for the treatment of AGA.

Iron

Hair matrix cells undergo rapid division, facilitating elongation of the anagen hair shaft. Iron is a cofactor of rate-limiting enzymes crucial to cell division and is involved in the regulation of multiple genes along the bulge region. ^, However, the mechanistic role of iron in hair growth remains to be established.

Iron deficiency is common. In the United States 12% to 16% of females ages 16 to 49 years and 2% of males ages 16 to 69 years are iron deficient (level of evidence: 2c). After age 50, fewer women are iron deficient (6% to 9% total) as a result of decreased menstrual blood loss, while more men (4% total) are iron deficient, presumably as a result of gastrointestinal blood loss. Several laboratory tests can be used to estimate iron status. However, serum ferritin is the most reflective of overall iron status.

It is important to distinguish iron depletion and iron deficiency anemia (IDA). Iron depletion occurs when total body iron reserves are decreased, indicated by a low serum ferritin (typically <40 ng/mL but may be lab-specific) and normal hemoglobin. There may not be overt clinical signs and symptoms in iron depletion. IDA is more severe and has the potential to cause functional limitations. In IDA, serum ferritin is less than 20 ng/mL, hemoglobin is low (9-12 g/dL), and total iron binding capacity (TIBC) is increased (350-400 mcg/dL). IDA should always be treated, and prompt referral is needed to investigate the cause of anemia and to prevent end organ damage. However, there is no consensus regarding iron supplementation for the treatment of patients who are iron depleted and have AGA.

Studies examining the relationship between iron deficiency and hair loss have been conducted in women with AGA and TE. A case-control study of 52 women with AGA and 11 without found that those with AGA had significantly lower serum ferritin (level of evidence: 3b). The association did not vary with respect to age, and there were no differences in hemoglobin between groups. A similar case-control study in 100 premenopausal women with AGA found that 72% had serum ferritin below the lowest serum ferritin of 40 ng/mL seen in the control group (n = 20) (level of evidence: 3b). However, there are conflicting reports in the literature. A case-control study of 43 women with AGA and 43 controls found no difference in serum ferritin between groups (level of evidence: 3b). A prospective cohort study identified 12 of 194 women with biopsy-proven AGA (level of evidence: 3b). All patients underwent treatment with spironolactone 200 mg daily or cyproterone acetate 100 mg daily for 10 days each month. The 12 patients with AGA underwent treatment with iron supplementation for 6 months, and all achieved a target serum ferritin greater than 20 ng/mL. The study authors concluded that there was no significant benefit observed in those who underwent iron repletion. However, no statistical analysis was published.

Several case-control studies have demonstrated that patients with AGA have a higher incidence of iron depletion than those without AGA. However, conflicting reports remain. Although there is no consensus statement on universal screening for iron deficiency in those with AGA, it is frequently an expert recommendation (level of evidence: 5). ^, The treatment of IDA is necessary and requires referral for further workup. However, the treatment of iron depletion in those with AGA has not been extensively studied, and more research is needed. Despite this, iron repletion is not costly, and the most common side effect is gastrointestinal intolerability.

Given the potential for benefit with minimal serious side effects, we recommend patients at risk for iron depletion including premenopausal women, those with a restrictive diet or history of eating disorders, those with a family history of anemia, those with a history concerning for depletion (e.g., fatigue, headache, restless leg syndrome, pica, renal disease), and patients with malabsorptive disorders or a history of bariatric surgery be screened for iron deficiency. In those with iron depletion (ferritin <40 ng/mL with normal hemoglobin), we recommend treatment with an oral slow-release ferrous iron supplement for at least 3 to 6 months before laboratory reevaluation ( Pearl 11.2 ).

PEARL 11.2:

Advise alopecia patients with iron depletion to purchase oral iron supplements with ferrous iron, as it is more readily absorbed than ferric iron.

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