Why is black women’s hair so hard to grow? (part 2)
Updated: Sep 6, 2025
In today's world, our hair and scalp are exposed to countless ingredients, and it's time to talk about something crucial, yet often overlooked: Endocrine Disrupting Chemicals (EDCs). The journey to vibrant, healthy hair is deeply intertwined with your hormonal balance, and EDCs, found in many everyday products, can subtly but significantly interfere, potentially leading to hair thinning and other concerns.
What Are Endocrine Disrupting Chemicals (EDCs)? The Hidden Impact
Endocrine Disrupting Chemicals (EDCs) are substances that can interfere with the body's endocrine (hormone) system. They can mimic hormones, block natural hormones, or alter hormone synthesis, transport, metabolism, and elimination, thereby disrupting normal bodily functions. The critical point is that these chemicals can disturb the delicate hormonal symphony that governs so many biological processes, including hair growth.
The Unsettling Truth: EDCs in Your Hair Products
A preliminary study investigating hair products used by U.S. Black women revealed a concerning reality: these products frequently contain mixtures of endocrine disrupting and asthma-associated chemicals. The study tested 18 hair products across six categories popular among Black women—hot oil treatment, anti-frizz/polish, leave-in conditioner, root stimulator, hair lotion, and relaxer—and found that a staggering 84% of detected chemicals were not listed on the product label. This lack of transparency means you might be unknowingly exposing yourself to substances that can impact your health.
Specific EDCs commonly found in these hair products include:
• Fragrances: All tested products contained fragrance chemicals. Fragrances are often proprietary blends that can hide a multitude of undisclosed chemicals, some of which are EDCs.
• Parabens and Diethyl Phthalate: A significant 72% of the tested products contained parabens and diethyl phthalate. Parabens (like methylparaben, ethylparaben, propylparaben, butylparaben) are commonly used as preservatives in cosmetics and can mimic estrogen in the body. Phthalates, like diethyl phthalate (DEP), are used to help fragrances last longer and can also act as endocrine disruptors.
• Other Chemical Classes: The study also found ultraviolet (UV) filters, cyclosiloxanes, glycol ethers, alkylphenols, ethanolamines, antimicrobials, and bisphenol A (BPA). These are all classes of chemicals known to include substances with endocrine-disrupting properties.
• Formaldehyde and Formaldehyde-Releasing Preservatives: These are known carcinogens and allergens that can be found in personal care products, particularly hair smoothing and straightening products. While the immediate link to hair thinning isn't explicitly stated, their presence highlights the overall chemical burden and potential for systemic impact. The frequency of use for certain products, like hair oils, which are typically used more often and not rinsed out quickly, can increase exposure compared to products like dyes or relaxers.
This situation points to an issue of "environmental injustice of beauty," where certain populations, including Black women, may face higher exposures to harmful chemicals due to specific product use patterns. This underscores the critical need for greater transparency in product labeling and the development of safer alternatives.
The Hormonal Tapestry of Hair Growth: How EDCs Pull at the Threads
Hair growth is a highly regulated biological process controlled by a complex interplay of hormones, growth factors, and signaling pathways within the hair follicle, which is described as a "complex miniorgan". The hair cycle itself consists of four primary phases:
Anagen (Growth Phase): The active growing phase, where hair shafts are produced by terminally differentiated keratinocytes. This is the longest phase, lasting years.
Catagen (Regression Phase): A short transitional phase where the hair follicle regresses.
Telogen (Resting Phase): A resting period where the hair is retained in the follicle but no active growth occurs.
Exogen (Shedding Phase): The phase where the old hair shaft is shed, making way for a new anagen hair.
Many hormones profoundly influence this delicate cycle, impacting hair growth, density, and follicle structure. When EDCs interfere with these hormones, the consequences can directly manifest as hair thinning or loss.
Key Hormones and EDC Interference:
Androgens (Testosterone, Dihydrotestosterone - DHT): Androgens are crucial regulators of hair growth. While often associated with male pattern baldness (androgenetic alopecia, AGA), they play a significant role in female pattern hair loss (FPHL) as well. Specifically, DHT is a potent androgen derived from testosterone via the 5-alpha-reductase enzyme. In androgen-sensitive areas like the scalp in genetically predisposed individuals, DHT can lead to follicular miniaturization, shortening the anagen phase and causing hair to become progressively finer and eventually disappear.
EDC Link: EDCs can interfere with androgen signaling in several ways:
Androgen Receptor Modulation: Some EDCs can act as anti-androgens, blocking the action of natural androgens, or, conversely, as androgen mimics, potentially over-stimulating pathways. This disruption can impact hair follicle sensitivity and contribute to conditions like FPHL.
Enzyme Inhibition: EDCs might affect enzymes involved in androgen metabolism, such as 5-alpha-reductase, altering the balance of testosterone and DHT.
PCOS Connection: Polycystic Ovary Syndrome (PCOS), a common endocrine disorder characterized by androgen excess, is frequently associated with FPHL and hirsutism (excessive hair growth in androgen-sensitive areas). While not directly caused by EDCs, exposure to EDCs might exacerbate hormonal imbalances that contribute to PCOS-related hair thinning.
Estrogens: Estrogens generally promote hair growth and extend the anagen phase. Hair density and anagen percentage tend to be higher in women compared to men, and hair loss can increase during menopause when estrogen levels decline.
EDC Link: Many EDCs are known as "xenoestrogens" because they mimic estrogen's actions. While mimicking estrogen might sound beneficial for hair, the disruption of the natural hormonal balance can be detrimental. EDCs can bind to estrogen receptors (ER-alpha and ER-beta) and activate or inhibit them inappropriately. This "fake estrogen" signal can confuse the body, potentially leading to dysregulation of the hair cycle. Research suggests that genetic variants in estrogen receptor genes (ESR2) and aromatase (CYP19A1), an enzyme that converts androgens to estrogens, are associated with FPHL. EDCs could interfere with these genetic pathways or hormonal conversions.
3. Thyroid Hormones: Thyroid hormones (THs) are essential regulators of cell growth, differentiation, and metabolism, and the skin is a significant target organ for THs. Both hyperthyroidism (overactive thyroid) and hypothyroidism (underactive thyroid) can cause diffuse hair shedding (telogen effluvium). THs directly influence human hair follicle functions, prolonging the anagen phase and stimulating hair matrix keratinocyte proliferation and pigmentation.
EDC Link: Many EDCs are known to disrupt thyroid function. They can interfere with thyroid hormone synthesis, transport, and metabolism, or directly interact with thyroid hormone receptors, leading to either hypothyroid or hyperthyroid states. Given the clear link between thyroid dysfunction and hair loss, exposure to EDCs that impact the thyroid gland or thyroid hormone signaling pathways presents a significant, though indirect, pathway to hair thinning. For instance, certain EDCs might affect deiodinases, enzymes crucial for activating or inactivating thyroid hormones at a local cellular level, including in hair follicles.
4. Cortisol (Stress Hormone): Chronic psychological stress is a well-established factor that can induce hair loss, primarily telogen effluvium. Cortisol, the primary stress hormone, can directly disrupt the hair growth cycle, pushing follicles prematurely into the resting phase.
EDC Link: While stress is often perceived as purely psychological, EDCs can exacerbate the body's stress response. Some EDCs might interfere with the hypothalamic-pituitary-adrenal (HPA) axis, which regulates cortisol production. This could lead to chronic elevated cortisol levels, or an altered stress response, indirectly contributing to hair thinning. Additionally, some EDCs can induce oxidative stress, which is also implicated in hair growth inhibition and premature hair follicle regression.
The UNWYLD Commitment: Your Hair, Your Health, Our Priority
The connection between endocrine disrupting chemicals and hair thinning is not always a direct, linear cause-and-effect relationship in scientific literature specifically on hair. However, by understanding:
1. The proven presence of EDCs in hair products, particularly those marketed to Black women.
2. The well-documented impact of EDCs on the body's hormonal systems.
3. The critical role of hormones in regulating the hair growth cycle and follicle health.
You have the power to choose products that honor your body and your hair. By opting for clean, natural formulations, you are reducing your exposure to EDCs and giving your hair the best possible environment to flourish. We are here to support you every step of the way on your journey to truly healthy, resilient, and glorious hair.
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Selected References
1. Wall, D., Meah, N., Fagan, N., York, K. and Sinclair, R. (2022) ‘Advances in Hair Growth’, Faculty Reviews, 11(1), p. 1.
2. Hasan, R., et al. (2022) ‘Effects of Hormones and Endocrine Disorders on Hair Growth’, Cureus, 14(12), p. e32726.
3. Chen, J., et al. (2023) ‘Endocrine disrupting chemical-associated hair product use during pregnancy and gestational age at delivery: a pilot study’, BMC Pregnancy and Childbirth, 23(1), p. 74.
4.(2023) ‘Formaldehyde and Formaldehyde Releasing Preservatives in Personal Care Products Used by Black Women and Latinas | Environmental Science & Technology Letters’.
5. Llanos, A.A., et al. (2017) ‘Hair product use and breast cancer risk among African American and White women’, Carcinogenesis, 38(9), pp. 883–892.
