Addressing Causes of Female Hair Loss and Exploring Preventative Measures

Grade 5 female pattern hair loss | Image credit: © DermNet

Hair loss is a common problemfor women, with more than 50% of postmenopausal women and up to 40% of healthy women experiencing frontal/parietal hair loss, often beginning around reproductive age.¹ The most common type of female hair loss is androgenetic alopecia (AGA), or female pattern hair loss (FPHL). Other forms of alopecia affecting women include alopecia areata (AA), telogen effluvium (TE), lichen planopilaris, central centrifugal cicatricial alopecia, frontal fibrosing alopecia, and traction alopecia. It has also been shown that female hair loss can have a psychosocial impact, contributing to lower self-image, anxiety, and depression.²

There are limited FDA-approved medications to address female hair loss. These include topical minoxidil for FPHL and 3 oral Janus kinase inhibitors indicated for the treatment of AA.³ Given the dearth of options, supplements, and nonprescription therapies could help fill a gap in managing cases of female hair loss.

When discussing the pathophysiology of female hair loss disorders, it is helpful to consolidate etiologies into a few broad categories. These include hormone imbalance, systemic and localized inflammation, nutrient and vitamin deficiencies, aging and cellular senescence, and oxidative stress. The origins of hair loss vary, and each cause has interventions that may serve as mediators impacting disease progression and reversal.

Hormone Imbalance and Sensitivities

Hair loss in women is often influenced by hormonal factors, such as the production of dihydrotestosterone (DHT), polycystic ovary syndrome (PCOS), thyroid disorders, menopause, pregnancy, and hormone replacement therapy (HRT). Although the role of DHT, a potent androgen, is established in male pattern baldness, DHT may also contribute to FPHL by miniaturizing hair follicles, particularly in genetically predisposed individuals.^4,5 In PCOS, hormone dysregulation and elevated androgen levels lead to scalp hair thinning. Thyroid imbalances, both hyperthyroidism and hypothyroidism, can disrupt the hair growth cycle, leading to diffuse hair loss.⁵ During menopause, estrogen levels decline, exacerbating hair thinning, whereas postpregnancy hormonal shifts often trigger TE. HRT may alleviate or exacerbate hair loss depending on individual hormonal responses.⁵

These insights highlight the complexity of managing hair loss in women, which requires individualized approaches and consideration of hormonal profiles and related endocrine disorders. Although pharmacologic therapy remains the cornerstone of treatment, nonpharmacologic options are available as complementary and alternative treatments.

Saw palmetto (SP), also known as Serenoa repens, is a natural treatment that has shown efficacy in addressing FPHL and TE. SP functions as a nonselective inhibitor of 5α-reductase, comprising primarily fatty acids and phytosterols, that reduces DHT binding to androgen receptors by nearly 50%.⁶ Additionally, SP promotes the conversion of DHT to its weaker metabolite, androstanediol, further minimizing hair follicle damage.⁷ Studies show that SP can improve hair count, density, and overall quality in patients with FPHL and TE, with some reporting up to 83.3% improvement in hair density.⁸

Horsetail (Equisetum arvense) has also demonstrated efficacy in inhibiting 5α-reductase. In a recent study, the ethyl acetate extract of horsetail was the most effective among several Equisetum debile extracts, exhibiting inhibition of 5α-reductase activity (approximately 35%), although it remains less potent than finasteride.⁹ This inhibition is believed to be associated with palmitic acid, making horsetail a promising natural alternative for reducing DHT levels and promoting hair regrowth.¹⁰

Pumpkin seed oil has antiandrogenic and anti–5α-reductase activity. A randomized controlled trial of pumpkin seed oil capsules used among 76 patients with AGA demonstrated superior hair growth and patient-reported satisfaction among the intervention vs the control group.^11,12

Systemic and Localized Inflammation

Systemic inflammatory diseases also contribute to hair loss. Patients with connective tissue diseases, autoimmune disorders, and metabolic syndromes can experience cutaneous manifestations that often include alopecia.¹³ On a localized level, the role of inflammation in AGA, AA, and scarring alopecia is well documented. Historically, AGA was considered a noninflammatory alopecia. However, biopsies of balding scalps in patients with AGA demonstrated an inflammatory infiltrate and perifollicular fibrosis.¹⁴ Studies have demonstrated that the extent of inflammation correlates with the most severe clinical forms of AGA, and the addition of anti-inflammatory therapies to AGA treatment has led to improved treatment outcomes.¹⁵

The active constituent of turmeric, curcumin, shows promise as an ingredient to promote hair health. It has been shown to have therapeutic effects, including antioxidant protection against free radicals, anti-inflammation by lowering histamine levels and possibly by increasing the production of natural cortisone by the adrenal glands, and antimicrobial activity.¹⁶

Pea sprout extract (Pisum sativum)has been shown to improve hair density when applied topically through its anti-inflammatory and antioxidant properties. Results of a study from 2019 demonstrated that the supplementation of 100 mg of pea sprout extract daily decreased hair loss in individuals experiencing hair shedding.¹⁷

Frontal fibrosing alopecia | Image credit: © DermNet

Nutrient and Vitamin Deficiencies

Rapidly dividing hair matrix cells in the follicular bulb require micronutrients for cellular turnover. Nutrient and vitamin deficiencies can significantly impact hair health and contribute to hair loss. Iron deficiency is one of the most recognizable causes of TE due to its role in oxygen transport and cellular metabolism. Low serum ferritin levels are often associated with hair shedding​. Vitamin D plays a crucial role in hair follicle cycling. Low levels are linked to various hair disorders, primarily AA, with weaker evidence for TE and AGA. Supplementation in cases of deficiency may improve these conditions^​.18

Vitamin A is necessary for the growth and differentiation of hair follicles. Both vitamin A deficiency and toxicity may lead to hair loss. A deficiency can lead to dry, brittle hair and hair loss​. Excess vitamin A can disrupt the hair cycle, resulting in reduced density and fewer anagen-phase hairs​.¹⁸ Vitamins C and E, known for their antioxidant properties, support hair health by protecting follicles from oxidative stress and aiding in collagen synthesis, which is essential for hair structure.¹⁸ Zinc, copper, and selenium deficiencies are known to manifest as alopecia. Excessive selenium intake may also contribute to hair loss​.¹⁹

Certain components of the vitamin B complex are associated with hair loss, including riboflavin, niacin, biotin, folate, and vitamin B12. Riboflavin deficiency is rare in the US. Biotin is the only B vitamin produced by the body; as such, healthy individuals do not require biotin supplementation. Although adequate biotin supports hair growth and maintenance by promoting healthy keratin production, high doses can contribute to abnormalities in diagnostic tests for thyroid hormones and troponins.²⁰ Niacin and folate are vital for cellular growth and hair follicle function, and deficiencies can lead to reduced hair growth and loss.¹¹ Groups at risk for folate deficiency include those experiencing alcoholism, poor diets, and malabsorption disorders. Otherwise, folate deficiency is uncommon.

Although vitamins and minerals are essential for hair health, supraphysiologic doses of these nutrients can be harmful. Many supplements contain doses beyond the recommended daily amounts, which can lead to toxicity or other adverse effects. For most individuals, meeting the recommended daily intake of these nutrients through a balanced diet or conservative supplementation​ is sufficient to support hair health without risking the consequences of excessive supplementation​.

Aging and Cellular Senescence

The scalp and hair follicles are subject to intrinsic, extrinsic, and natural aging, all of which contribute to hair loss. Intrinsic factors are related to genetic and epigenetic mechanisms, whereas extrinsic factors can be secondary to UV radiation, chemical treatments, pollution exposure, and other causes.²¹ Natural aging is phenotypically and histologically characterized by weathering of the hair shaft, a decrease in melanin and overall hair production, and development of increasingly dry, thin, dull, and brittle hair.²² Senescent alopecia has been described as a distinct process and is characterized histologically by a modest reduction in the size of otherwise normal hair.²³

Nicotinamide adenine dinucleotide (NAD+) is a fundamental molecule in human life and health as it participates in energy metabolism, cell signaling, mitochondrial homeostasis, and dictating cell survival or death. This small molecule lies at the center of cell metabolism, mitochondrial function, and the biological processes of aging by serving as a substrate for the electron transport chain.²⁴ Cellular NAD+ levels are strongly correlated with aging.²⁵

Nicotinamide mononucleotide (NMN), a precursor to NAD+ in cells, has been studied for hair growth. A 2024 murine study by Chuntao Xu et al showed that NMN can promote hair health by significantly lowering inflammatory markers such as IL-6 and tumor necrosis factor–α, which are expressed under states of high DHT activity, and by reducing oxidative stress. Furthermore, it can enhance human dermal papilla cells’ VEGF expression equivalent to that achieved by minoxidil.²⁶ In 2019, Khadka et al suggested that the modulation of NAD+ levels may be a novel therapeutic approach to prevent chemotherapy-associated hair loss. ²⁷

Taurine is a naturally occurring amino acid. Studies have shown that taurine supplementation protects against pathologies associated with mitochondrial defects, such as aging, and serves as a major antioxidant, anti-inflammatory, and antiapoptotic factor in the body.²⁸ Taurine has been shown to promote hair survival and prevent hair growth inhibition in vitro. It can also prevent TGFB1 from negatively affecting hair follicles.²⁹

Oxidative Stress and Free Radicals

Oxidative stress has been linked to the pathogenesis of AGA, AA, and TE.³⁰ Oxidative stress can disrupt normal hair follicle maturation and growth cycles. Reactive oxygen species are created during normal cellular function and have important physiologic functions, including maintenance of signaling pathways during hair follicle development.³¹ In vitro studies of AGA have shown increased markers of and increased sensitivity to oxidative stress in dermal papilla cells from balding scalps compared with nonbalding scalps.³²

Vitamins such as E and C are potent antioxidants. Supplementation with these vitamins can affect hair loss. A randomized controlled trial of fish oil, black currant seed oil, vitamin E, vitamin C, and lycopene supplementation compared with no supplementation showed increased hair density and thickness in the intervention group.³³

Ashwagandha (Withania somnifera) is a common ingredient in hair health products. It is a natural antioxidant and anti-inflammatory herb that has been shown to fight free radicals and strengthen hair follicles to promote hair growth.³⁴

Biotin-Free Matters

Biotin, often marketed for hair growth, can interfere with several laboratory values, causing inaccurate results. Examples include cardiac markers such as troponin; sex hormones including estradiol, testosterone, and sex hormone–binding globulin; other B vitamins such as folate and vitamin B12; parathyroid hormone; and hepatitis A and B antibodies/antigens.³⁵ High doses of biotin can lead to falsely elevated free T4 and T3 levels while lowering TSH, resulting in potential misdiagnosis of thyroid conditions​.³⁶ The FDA has issued warnings about this interference, particularly in lab assays​. Additionally, biotin deficiency is rare in individuals with a balanced diet, and evidence supporting its role in hair growth is limited to cases of true deficiency​. Thus, choosing biotin-free supplements can be beneficial for avoiding diagnostic complications.³⁶

Conclusion

Given more than half of postmenopausal women experience some form of hair loss, the lack of FDA-approved treatments contributes to a growing demand for nonpharmaceutical therapies. By considering the root causes, we can identify key ingredients and interventions that may benefit women experiencing hair loss. Evidence shows that although some nutritional deficiencies may cause or exacerbate alopecia, nutritional overdosing may also have harmful effects. Additional studies should be performed to explore ingredient benefits and safety profiles.

Adam Leavitt, MD, is a board-certified dermatologist at Advanced Dermatology and Cosmetic Surgery in Orlando, Florida, and a core faculty member of the Kansas City University - Orlando.

Spencer D Hawkins, MD, FAAD, is a board-certified dermatologist and Mohs micrographic surgeon at Advanced Dermatology and Cosmetic Surgery in East Greenwich, Rhode Island, and an ISHRS fellowship-trained hair restoration surgeon at the Hair Medicine Institute in Sandy Springs, Georgia.

Chesahna Kindred, MD, MBA, FAAD, is the owner of and a board-certified dermatologist at Kindred Hair & Skin in Marriotsville, Maryland, and an associate professor at Howard University in Washington, DC.

Cheri Frey, MD, FAAD, is a board-certified dermatologist at Howard University in Washington, DC, and an assistant professor and director of the university's residency program.

Madeliene Gainers, MD, FAAD, is the owner of and a board-certified dermatologist at Madeliene Elaine in Chevy Chase, Maryland.

Steven K. Grekin, DO, FAAD, is the founder of the Grekin Skin Institute in Wyandotte, Michigan, program director of the dermatology residency program at Beaumont Health Systems in Royal Oak. Michigan, and a board-certified dermatologist at Advanced Dermatology and Cosmetic Surgery in Warren and Wyandotte Michigan.

Matt Leavitt, DO, FAAD, is the executive chairman, founder, and board-certified dermatologist at the Advanced Dermatology and Cosmetic Surgery in Orlando, Florida. He is also the chairman of the Orland Dermatology Residency Program, and assistant professor of dermatology at the University of Central Florida and Kansas City University - Orlando.

Disclosures

A. Leavitt: Pfizer (abrocitinib)

Hawkins: No disclosures

Kindred: AbbVie, Aerolase (lasers), Aerolase and Selphyl medical boards, Arcutis, Arcutis (roflumilast), Galderma (nemolizumab), Janseen, Lilly, Lilly (baricitinib), Novartis, Pfizer, Pfizer (ritelcitinib), Regeneron, Regeneron (dupilumab), Sanofi, Sanofi (dupilumab) speaker, Sun Pharmaceuticals, UCB advisory boards, xtressé founding adviser

Frey: Beiersdorf, Benev, Galderma, L’Oreal, Novartis, Nutrafol, Procter & Gamble, Sun Pharmaceuticals

Gainers: No disclosures

Grekin: No disclosures

M. Leavitt: Founder and CEO, Restore Biologics

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