The Hair Playbook

Most people meet hair loss the same way: more strands on the pillow, a wider part in the bathroom mirror, a shower drain telling a story you did not want to read. The next move is usually a late-night search and a new shampoo or a bottle of "hair, skin, and nails" gummies. That rarely works, because it skips the only question that matters. What is the shedding pointing at?

Hair is one of the most metabolically demanding tissues you have. When the body is under pressure from low iron, a sluggish thyroid, a recent pregnancy, a crash diet, or a stretch of bad sleep, hair is one of the first luxuries it cuts from the budget. So the shedding is almost always a downstream signal. The job is to find the upstream driver and fix that. The right labs and a doctor who has time to read them beat a random supplement stack nearly every time.

Why is my hair falling out?

Your hair grows in a cycle. Each follicle spends 2 to 6 years in a growth phase (anagen), a short transition, then a rest phase (telogen) before the old hair sheds and a new one starts. Losing 50 to 100 hairs a day is normal. The problem starts when something pushes a big batch of follicles into the rest phase at once. That shows up as a wave of shedding 2 to 3 months after the trigger, which is exactly why the cause is so often missed. By the time you notice, the event that caused it has faded from memory.

The drivers we find most often:

• Low ferritin. Ferritin is your iron storage protein, and follicles slow down when it drops, often below 50 ng/mL, even when your hemoglobin reads normal. This is the single most common miss we see in women.
• Thyroid disease. Both an underactive and an overactive thyroid drive shedding, and the hair change can show up months before the diagnosis does. The classic tell is thinning at the outer third of the eyebrows.
• Telogen effluvium. A reactive whole-scalp shed triggered by illness (COVID included), surgery, childbirth, rapid weight loss, or a major stressor. It looks alarming and it almost always grows back once the trigger resolves.
• Hormonal shifts. Postpartum estrogen drop, perimenopause, and PCOS-driven androgens all change the picture.
• Genetic pattern loss. Androgenetic alopecia, where DHT-sensitive follicles miniaturize over time. This one is genuinely genetic and needs its own tools.

This guide covers all of them. For the deeper version of any one, the dedicated guides on hair loss in men, hair loss in women, and the overall hair loss workup go further.

What labs actually find the driver?

Most people who come to me about their hair have had "labs" before. Almost never the right ones. A TSH and a basic CBC are not enough for a complaint this sensitive. Here is the panel that earns its place:

• Ferritin and full iron studies. Lab "normal" for ferritin often starts at 15 ng/mL, which is far below where hair starts to suffer. I aim for above 50 ng/mL in most adults, and above 70 in a woman who is actively shedding.
• Full thyroid panel. Not just TSH. We run TSH, free T3, free T4, reverse T3, and TPO antibodies. A TSH technically in range (say, 3.5) with a low free T3 can still drive hair loss, and roughly 90% of low thyroid in the US is Hashimoto's, which only TPO antibodies catch. The deeper logic is in our thyroid optimization guide.
• 25-OH vitamin D, B12, folate, zinc. Deficiency is common through a Philadelphia winter and matters for the growth phase. We test rather than guess.
• Sex hormones. Total and free testosterone, DHEA-S, SHBG, estradiol, and progesterone (timed to the cycle in premenopausal women). If the picture fits PCOS, we add fasting insulin and HbA1c; if perimenopause, FSH and LH.
• Metabolic markers. Fasting insulin and HbA1c when insulin resistance is in the picture, since high insulin pushes androgen production up.

This is more lab work than most people have had run on their hair. It is also the lab work that actually finds the answer, which saves money and months compared to guessing your way through the supplement aisle.

What is different about hair loss in men?

For men, the most common cause by a wide margin is male pattern hair loss (androgenetic alopecia). More than half of men have some degree of it by 50, and for plenty it starts in the twenties. Two things are required: inherited follicle sensitivity to DHT (dihydrotestosterone, a metabolite of testosterone), and a normal amount of DHT in circulation. You do not need high testosterone. You just need follicles that listen too closely. DHT shortens the growth phase a little more each cycle until the follicle miniaturizes and stops making a visible hair. The pattern is usually the temples and crown, with the back and sides spared.

About 1 in 5 men I see for "hair loss" has something else going on, or pattern loss layered on top of a thyroid or iron problem. So we run the labs first. If the workup flags low ferritin or thyroid disease, we fix that, and sometimes the shedding settles without ever starting hair medication.

When it is pattern loss, two medications carry the evidence and they are worth doing together:

• Finasteride (oral, 1 mg daily). It blocks the enzyme that converts testosterone to DHT. In trials, it slows loss in about 90% of men and produces visible regrowth in roughly two-thirds, with peak effect at 12 to 24 months. It is generic and inexpensive. The sexual side effect rates in trials sit close to placebo (decreased libido around 1.8%), but a small fraction report symptoms that persist after stopping, and there is a weaker signal around mood in younger men. I ask about that before and during treatment, and we stop and reassess rather than push through.
• Minoxidil (topical 5%, or low-dose oral). It improves blood flow to the follicle and prolongs the growth phase. One detail worth knowing: topical minoxidil is a prodrug that needs an enzyme called sulfotransferase in the scalp to switch it on, and some men do not carry enough. If you used the topical faithfully for months and saw nothing, that is not necessarily a failure of the drug; the oral form is activated by the liver and skips that bottleneck.

The full men's protocol, including dutasteride, microneedling, and the honest data on post-finasteride syndrome, lives in hair loss in men.

What is different about hair loss in women?

For women it is rarely one thing, and it is almost never "just stress." The differential is wider: telogen effluvium, female pattern loss, postpartum shedding, thyroid disease, perimenopause, PCOS, iron deficiency, and occasionally scarring alopecias that need a dermatologist. The pattern in female pattern loss looks different from men's; it is usually a widening center part with diffuse thinning across the top, and the frontal hairline is usually preserved. Women very rarely go fully bald in these areas, which is part of why treatment can do so much.

A few drivers are specific to women and worth naming:

• Postpartum. During pregnancy, high estrogen holds extra hair in the growth phase. After delivery, those hairs shift to shedding together around month 3 to 6. It is dramatic and it is expected, and most women see real regrowth by 9 to 12 months. We still check iron and thyroid, because postpartum thyroiditis shows up at 3 to 6 months and gets dismissed as "just being a new mom."
• Perimenopause. Falling estrogen and progesterone shift the balance toward androgens, even when absolute androgen levels are normal, which can unmask genetic thinning at the temples and part.
• PCOS. High insulin signals the ovaries to overproduce testosterone, which can cause scalp thinning and unwanted hair growth at the same time. Treating it as the metabolic condition it is, with diet, inositol, sometimes metformin, often improves both. The full approach is in our PCOS guide.

The evidence-based tools for women are topical or low-dose oral minoxidil, and spironolactone (an oral medication that blocks androgen activity, typically 50 to 200 mg daily, especially useful in PCOS-driven loss). Spironolactone is a teratogen, so reliable contraception is required; we cover that clearly before starting. Finasteride is generally not first-line for women of childbearing age. The deeper version is in hair loss in women.

What do "hair" supplements actually do?

Here is the part the labels will not tell you. Most multi-ingredient hair supplements do very little unless you are actually deficient in something specific. The honest hierarchy is "test, then treat," not "stack and hope."

• Biotin. The real evidence is for brittle nails at 2,500 mcg daily, where it reduces splitting. For hair, it supports existing strands more than it grows new ones, and true biotin deficiency is rare. The bigger issue is safety: high-dose biotin (the kind in hair-and-nail gummies) can distort lab tests, pushing TSH falsely low and T4 and T3 falsely high (which can look like Graves disease) and falsely lowering troponin (which can mask a real cardiac event). The rule is simple: stop biotin 72 hours before any thyroid or cardiac blood draw. The full picture is in our biotin clinical guide.
• Iron. This is the supplement that actually moves the needle, but only when ferritin is low. We use ferrous bisglycinate, which is gentler on the gut than ferrous sulfate, dosed at 25 to 60 mg of elemental iron with vitamin C, often on alternate days (which absorbs better because it lets the blocking hormone hepcidin reset between doses). Never supplement iron without confirmed labs; iron overload is its own real risk.
• Saw palmetto. A plant extract with mild DHT-blocking activity, a gentler cousin of finasteride. The evidence is modest but reasonable for early pattern loss, and it is a fair option for someone who wants to avoid prescription anti-androgens. Details in the saw palmetto guide.
• Beta-sitosterol. A plant sterol with real trial data, but for cholesterol and prostate symptoms, not hair. It is a good example of using a supplement only where the evidence actually is. See the beta-sitosterol guide.
• Zinc, selenium, B vitamins. Worth supplementing only if labs or diet point to a gap. Zinc and selenium matter for thyroid hormone conversion, so they tie back to the hair story, but too much causes its own problems.

What we do not use: proprietary "hair growth" stacks with dozens of ingredients and no head-to-head data, biotin megadoses, or compounded peptides marketed for hair. We use individual targeted nutrients when your labs show a gap, full stop.

Why is my hair going gray, and can I change it?

Graying and shedding are different problems, but they land in the same conversation often enough to cover here. Each follicle has its own color factory: pigment cells (melanocytes) fed by a stem-cell reserve. With age, that reserve runs down and the pigment cells take oxidative damage, including a buildup of hydrogen peroxide that bleaches the strand from within. When a follicle stops making pigment, the strand grows in gray. It is essentially all-or-nothing per hair, which is why you go gray strand by strand.

The honest answer about gray hair has two parts. First, the timing is mostly written in your genes. If your parents grayed early, a perfect diet and every supplement on the shelf will not hold the line for long. Second, a few real levers exist at the margins:

• Real deficiencies. Low B12, folate, iron, copper, and vitamin D are linked to premature graying, and correcting a genuine deficiency sometimes restores some pigment, especially when caught early. Normal levels plus more vitamins does nothing.
• Thyroid disease. Both over- and underactive thyroid associate with early graying, which is one more reason to check it.
• Smoking and stress. Smokers gray earlier. And a careful study that mapped pigment along single hairs against people's life events found graying lined up with stressful periods, and some hairs regained color when the stress lifted. So stress appears to genuinely push graying along, and a portion may be reversible, though it will not override the genetic clock.

What does not work: there is no pill shown to reverse ordinary genetic graying. A bold promise to reverse gray is a reason for skepticism, not excitement. The reliable cosmetic answer is the one it has always been, which is to color it if it bothers you. The full version is in our gray hair guide.

How does a primary care workup beat guessing?

The difference is simple. A 10-minute dermatology or hair-restoration visit often ends with a minoxidil or finasteride prescription and very little testing. Those tools have a place, but they are band-aids if the real driver is thyroid, iron, or stress. We start the other way around. We measure first, find the upstream driver, and treat that. Often the medication dose ends up lower, or we avoid it entirely.

That order matters in Philadelphia specifically, because so much of what we see is layered: a nurse at Penn under-eating protein on rotating shifts, a chef in East Passyunk with low ferritin from a plant-forward diet, a new mom in Fishtown whose 4-month shed is tangled up with undiagnosed postpartum thyroiditis. The labs untangle it. Then we set honest expectations about timing, because the hair cycle is slow. Even when we fix the driver this month, the regrowth shows up as fine baby hairs at the part line 3 to 6 months later. Patience is part of the protocol, and it is a lot easier to be patient when you know you are treating the right thing.

Key Takeaways

• Hair shedding is usually a downstream signal. The job is to find the upstream driver (iron, thyroid, hormones, stress, rapid weight loss, or genetics) and treat that.
• The right labs (ferritin, full thyroid panel, sex hormones) find the answer that a lone TSH and CBC miss, and they save you months of guessing.
• For genetic pattern loss, finasteride plus minoxidil is the evidence-based answer in men; minoxidil and spironolactone in women.
• Biotin and most hair supplements do little unless you are deficient, and high-dose biotin distorts thyroid and cardiac labs, so stop it 72 hours before any draw.
• Gray hair is mostly genetic; correct a real deficiency, do not smoke, manage stress, and color it if it bothers you. No pill reverses ordinary graying.
• Regrowth follows the hair cycle, so expect shedding to slow at 3 months and visible regrowth at 6 to 12 months, even after the driver is corrected.

Scientific References

1. Trost LB, Bergfeld WF, Calogeras E. "The diagnosis and treatment of iron deficiency and its potential relationship to hair loss." Journal of the American Academy of Dermatology. 2006;54(5):824-844.
2. Kaufman KD, Olsen EA, Whiting D, et al. "Finasteride in the treatment of men with androgenetic alopecia." Journal of the American Academy of Dermatology. 1998;39(4):578-589.
3. Randolph M, Tosti A. "Oral minoxidil treatment for hair loss: A review of efficacy and safety." Journal of the American Academy of Dermatology. 2021;84(3):737-746.
4. Sinclair R. "Female pattern hair loss: a pilot study investigating combination therapy with low-dose oral minoxidil and spironolactone." International Journal of Dermatology. 2018;57(1):104-109.
5. Lipner SR. "Rethinking biotin therapy for hair, nail, and skin disorders." Journal of the American Academy of Dermatology. 2018;78(6):1236-1238.
6. Rosenberg AM, Rausser S, Ren J, et al. "Quantitative mapping of human hair greying and reversal in relation to life stress." eLife. 2021;10:e67437.
7. Vincent M, Yogiraj K. "A descriptive study of alopecia patterns and their relation to thyroid dysfunction." International Journal of Trichology. 2013;5(1):57-60.