Several hormones can cause hair loss, but the most common culprit is DHT (dihydrotestosterone), a potent form of testosterone responsible for the gradual thinning seen in both male and female pattern baldness. Beyond DHT, thyroid hormones, estrogen, cortisol, insulin, and even growth hormone all play roles in keeping hair follicles healthy or pushing them toward shedding. Here’s how each one works.
DHT: The Primary Driver of Pattern Baldness
DHT is converted from testosterone by an enzyme in your skin and hair follicles. In people genetically prone to hair loss, DHT binds to receptors on hair follicles and gradually shrinks them, a process called miniaturization. Each growth cycle produces a thinner, shorter, lighter hair until the follicle eventually stops producing visible hair altogether. This is the mechanism behind androgenetic alopecia, which affects roughly 50% of men over 50 and a significant number of women as well.
The growth phase of hair (called anagen) normally lasts two to six years. DHT shortens this phase, meaning hair spends less time growing and more time resting or falling out. Genetics determine how sensitive your follicles are to DHT, which is why two people with similar testosterone levels can have very different hairlines. Medications that block the enzyme converting testosterone to DHT can reduce scalp DHT levels by about 64% to 69%, which is enough to slow or partially reverse hair loss in many people.
Cortisol: How Stress Shuts Down Hair Growth
Cortisol, your body’s main stress hormone, directly interferes with the signals that tell hair follicle stem cells to start growing. Research from Harvard’s Stem Cell Institute showed the mechanism in detail: elevated cortisol acts on a cluster of cells beneath the hair follicle called the dermal papilla. Under chronic stress, these cells stop releasing a specific signaling molecule (called Gas6) that normally activates hair follicle stem cells. Without that signal, stem cells stay dormant and new hair doesn’t grow.
This creates what’s essentially an “adrenal gland to hair follicle axis.” Your body always has some baseline cortisol activity that naturally slows hair cycling during rest periods. Chronic stress amplifies this system, making it far harder for follicles to enter the growth phase. The clinical result is telogen effluvium, a condition where large numbers of hairs shift into the resting phase simultaneously and then shed a few months later. Unlike pattern baldness, stress-related hair loss is typically diffuse across the entire scalp and often reversible once cortisol levels normalize.
Thyroid Hormones: Too Much or Too Little
Your thyroid gland produces T3 and T4, hormones that directly regulate hair follicle function. Both hormones prolong the growth phase of hair by stimulating the cells in the hair bulb to multiply and by suppressing signals that would otherwise shut growth down prematurely. T4 specifically blocks a growth-inhibiting protein in the follicle, keeping hair in its active growing state longer. Both T3 and T4 also support hair pigmentation, which is why thyroid problems sometimes affect hair color as well as density.
When your thyroid is underactive (hypothyroidism) or overactive (hyperthyroidism), this balance breaks down. Hypothyroidism is the more common cause of noticeable hair loss: without enough thyroid hormone, follicles lose the signal to keep growing, and hair becomes dry, brittle, and thin. The thinning is usually diffuse rather than patchy. Because thyroid disorders develop gradually, many people don’t connect their hair changes to a thyroid problem until other symptoms like fatigue, weight changes, or temperature sensitivity appear.
Estrogen and Progesterone: Postpartum and Menopause
Estrogen extends the growth phase of hair, which is why many women notice thicker, fuller hair during the last trimester of pregnancy, when estrogen levels surge. The hormone keeps a larger-than-normal percentage of hairs in the active growing phase simultaneously, reducing the usual daily shedding.
After childbirth, estrogen drops sharply. All those hairs that were held in the growth phase suddenly shift to the resting phase at once. A few months later, they start falling out in what can feel like alarming clumps. This postpartum shedding typically peaks around three to four months after delivery and resolves on its own within six to twelve months as hormone levels stabilize. It’s not true hair loss in the sense that follicles are damaged; the hair cycle is simply recalibrating.
A similar but more gradual process happens during menopause. As estrogen and progesterone levels decline permanently, hair loses the protective effect those hormones provided. Follicles also become relatively more exposed to the androgens (like DHT) that were previously counterbalanced by estrogen. The result is often diffuse thinning across the top of the scalp, sometimes with a widening part line.
Insulin and Androgens in PCOS
Polycystic ovary syndrome (PCOS) creates a hormonal chain reaction that can lead to hair thinning. The sequence starts with insulin resistance: when your cells don’t respond well to insulin, your body produces more of it. High insulin levels lower a protein called sex hormone-binding globulin (SHBG), which normally binds to testosterone and keeps it inactive. With less SHBG circulating, more testosterone is free and available to be converted into DHT at the hair follicle.
This is why women with PCOS can develop a pattern of hair loss that resembles male pattern baldness, typically thinning at the crown and along the part. Treatment often involves a two-pronged approach: reducing insulin resistance to restore SHBG levels, and using medications that block androgen effects at the follicle. Oral contraceptives are sometimes part of this strategy because they increase SHBG production, binding up more of the free testosterone that would otherwise reach hair follicles.
DHEA-S: The Adrenal Androgen
Your adrenal glands produce a hormone called DHEA-S that serves as a building block for more potent androgens. On its own, DHEA-S doesn’t directly shrink hair follicles. But once it reaches the skin and hair follicles, it gets converted into testosterone and eventually DHT. Women with elevated DHEA-S levels (above the normal range of roughly 0.3 to 3.2 micrograms per milliliter) can develop a female pattern of hair thinning even without PCOS.
DHEA-S also interferes with an enzyme in the hair follicle that’s essential for building the nucleic acids hair cells need to grow. This disruption, combined with its role as a precursor to stronger androgens, makes elevated DHEA-S a meaningful contributor to hair loss in women. Blood testing for DHEA-S is a standard part of evaluating unexplained female hair loss, since elevated levels point toward an adrenal source rather than an ovarian one.
Growth Hormone and IGF-1
Growth hormone doesn’t act on hair follicles directly, but it triggers the liver and other tissues to produce IGF-1, one of the most powerful signals for keeping hair in the growth phase. IGF-1 receptors sit on the cells of the hair matrix and the outer sheath of the follicle, where they drive cell multiplication and maintain active growth. Low circulating IGF-1 levels have been associated with hair loss in middle-aged women, and balding scalp follicles show decreased IGF-1 activity compared to non-balding follicles on the same head.
The clearest evidence comes from a rare genetic condition called Laron syndrome, where growth hormone is produced normally but the body can’t respond to it, resulting in very low IGF-1 levels. People with this condition have sparse hair growth, various degrees of thinning, frontal hairline recession, and structural hair defects visible under a microscope. While most people’s IGF-1 levels aren’t this dramatically low, the finding illustrates how important this hormonal pathway is for healthy hair. IGF-1 levels decline naturally with age, which likely contributes to the gradual loss of hair density that most people experience over time.