en The hair cycle: why hair grows, falls out, then grows back
Summary
A hair does not grow indefinitely. It lengthens for a few years, stops, rests, then falls out to make room for its replacement. That back and forth has a name: the hair cycle. It plays out at the level of each individual follicle, the little pouch of skin that manufactures the hair, and it has been running on a loop since you were born.
Understanding the mechanism changes a great deal when you are worried about shedding. Some losses are simply the cycle doing its job. Others signal that it has been thrown off, or that it is running out. And telling them apart comes down to precise criteria, not to instinct.
The follicle, the factory that makes the hair
The scalp holds roughly 100,000 hair follicles. Each one is a tube-shaped cavity anchored in the dermis, the deep layer of the skin. At its base sits the bulb, and inside that bulb a structure called the dermal papilla: it receives the blood supply, and therefore the nutrients, and it gives the order to make hair or to stop.
What you see and style, the shaft, is dead material. Keratin, a fibrous protein, stacked up and hardened. Everything that matters happens below the surface, inside the follicle. That is why a shampoo cannot change a cycle: it works on the part that has already been produced.
Three phases, and a hair that lets go
The hair cycle runs through three successive phases, always in the same order, then starts again from the beginning. The durations below are the ones the clinic works with.
The anagen phase: growth
This is the active phase, and by a long way the longest: 2 to 5 years. Cells in the bulb divide at speed and the shaft lengthens by around a centimetre a month. How long this phase lasts is largely genetic, and it is what sets the maximum length your hair can reach. Someone whose anagen phase runs for two years will never have very long hair, whatever care they put in.
At any given moment, about 90 per cent of the hairs on the scalp are in anagen (Natarelli et al., 2023). It is that heavy imbalance in favour of growth that gives the impression of a stable head of hair.
The catagen phase: transition
A brief interlude of 2 to 3 weeks. The follicle stops producing, retracts to about a sixth of its length, and the connection between the bulb and the dermal papilla breaks. The hair no longer grows. It is still there, but it has been unplugged from its supply.
The telogen phase: rest
This one lasts 2 to 4 months. Dormancy was the word used for a long time, wrongly: a follicle in telogen stays actively on standby and responds to signals from its environment, ready to start a new cycle (Geyfman et al., 2015). The hair itself is still anchored, but nothing is feeding it any more.
The exogen phase: release
The expulsion of the dead hair has a name of its own, the exogen phase, and it is triggered at the end of telogen. The hair detaches and goes, often pushed out by the new one already emerging in the same follicle. Losing 50 to 100 hairs a day is this stage working normally, not a symptom. On the pillow, in the shower tray, in the brush: that is where you find them.
Every follicle keeps its own calendar
Here is the point almost nobody knows, and it explains everything else. Follicles are not synchronised. The one next to your parting can be in full growth while its neighbour has been resting for six weeks. Each follicle cycles independently of the others, which keeps overall density more or less constant despite the permanent turnover (Harrison & Bergfeld, 2009).
If follicles were synchronised, we would lose our hair in one block every three or four years, like an animal moulting. That is not what happens. The shedding is diluted, invisible, spread out. And it is precisely because it is usually invisible that shedding which becomes visible deserves to be taken seriously.
When the cycle is thrown off
Two very different mechanisms sit behind most cases of shedding, and confusing them leads to poor decisions.
Telogen effluvium: a massive, temporary switch
A shock to the body can tip a large number of follicles out of anagen and into telogen all at once. Two or three months later, all those hairs reach the exogen phase together and fall together. This is telogen effluvium. The lag explains why patients almost never connect their shedding to the event that set it off: it is already well behind them.
The usual triggers are surgery, a high fever, a restrictive diet, childbirth. Postpartum hair loss is the clearest example of all. The good news is that the follicles are not damaged, they have simply all gone to sleep at the same time. The cycle resumes.
Androgenetic miniaturisation: a permanent drift
Here the mechanism is a different one. Under the influence of dihydrotestosterone, a derivative of testosterone, genetically sensitive follicles see their anagen phase shorten cycle after cycle. Each new hair grows back a little finer, a little shorter, a little less pigmented, until it becomes vellus and then nothing. This is what is called miniaturisation, and it is the central mechanism of androgenetic alopecia (Cuevas-Diaz Duran et al., 2024). The role of DHT in hair loss is well established today, and sensitivity to that hormone is inherited.
This is not an effluvium. Nothing restarts on its own. The loss of hair density settles in along a recognisable pattern, graded by the Norwood-Hamilton scale.
The other factors that weigh on the cycle
Thyroid hormones set the speed at which cells in the bulb renew themselves. An imbalance in either direction shows up in the hair: thyroid problems and hair loss are directly connected.
Nutritional intake counts too, because the anagen phase is a demanding metabolic building site. Iron heads the list of deficiencies observed, and low iron translates quickly into hair loss. A vitamin D deficiency is another frequent suspect. One caution though: supplementing without a proven deficiency achieves nothing.
Some medicines block cell division and therefore strike the follicle in mid-anagen. Chemotherapy is the best known case, with rapid and heavy shedding that reverses once treatment ends.
Repeated mechanical tension damages the follicle from the outside. Tight braids, extensions and pulled-back buns worn year in year out end up producing traction alopecia, often along the frontal hairline and above the ears. Caught early, it recedes. Caught late, the follicle is gone.
Chronic stress, finally, is among the signals that push follicles towards telogen. The link between stress and hair loss is not a salon belief, it is documented. Seasonal shedding is also more marked in late summer and in spring, tied to hormonal variation that follows light exposure.
A follicle does not have an unlimited number of cycles
This is the limit rarely discussed. A hair follicle does not start over for ever: it goes through something in the order of 10 to 30 cycles across a lifetime (Harrison & Bergfeld, 2009). Eventually it wears out and stops producing.
That sheds light on two things. First, why density falls naturally with age even without alopecia. Second, why androgenetic miniaturisation does so much damage: by shortening every anagen phase, it burns through that stock of cycles far faster than expected. The follicle reaches the end of the line at forty instead of seventy.
And once a follicle has gone out, no treatment relights it. The tissue has turned fibrous, there is no structure left to stimulate. Which is why the calendar counts as much as the treatment you choose.
Have your cycle read before deciding anything
Shedding is diagnosed, not guessed at. In consultation, examining the scalp with a magnifying camera, trichoscopy, measures shaft diameter and the proportion of fine hairs zone by zone. That is what allows us to settle between an effluvium that will pass and a miniaturisation that is progressing.
Where miniaturisation is already advanced across an area, a transplant remains the most durable treatment for androgenetic alopecia. Its logic rests entirely on the hair cycle: follicles in the donor area at the back of the head are not sensitive to DHT. Moved to the top of the scalp, they keep their own programme and go on cycling normally.
Not every scalp lends itself to it, and the hair transplant guide sets out the criteria. The simplest step is to check beforehand whether you are suitable for a hair transplant: active, unstabilised shedding, for instance, is treated medically first. With Dr Emrah Cinik, every hair transplant Turkey project begins with this assessment of the cycle, area by area.
A last word on the durations. The scientific literature gives wider ranges than the ones used here, up to 8 years for anagen depending on the publication. Those gaps come from the populations studied and the measurement methods. The order of magnitude does not move: years of growth, a few weeks of transition, a few months of rest.
Sources
Natarelli, N., Gahoonia, N., & Sivamani, R. K. (2023). Integrative and Mechanistic Approach to the Hair Growth Cycle and Hair Loss. Journal of Clinical Medicine, 12(3), 893. https://doi.org/10.3390/jcm12030893
Harrison, S., & Bergfeld, W. F. (2009). Diffuse hair loss: Its triggers and management. Cleveland Clinic Journal of Medicine, 76(6), 361-367. https://doi.org/10.3949/ccjm.76a.08080
Geyfman, M., Plikus, M. V., Treffeisen, E., Andersen, B., & Paus, R. (2015). Resting no more: re-defining telogen, the maintenance stage of the hair growth cycle. Biological Reviews, 90(4), 1179-1196. https://doi.org/10.1111/brv.12151
Cuevas-Diaz Duran, R., Martinez-Ledesma, E., Garcia-Garcia, M., Bajo Gauzin, D., Sarro-Ramírez, A., Gonzalez-Carrillo, C., Rodríguez-Sardin, D., Fuentes, A., & Cardenas-Lopez, A. (2024). The Biology and Genomics of Human Hair Follicles: A Focus on Androgenetic Alopecia. International Journal of Molecular Sciences, 25(5), 2542. https://doi.org/10.3390/ijms25052542
