The Hair Growth Cycle

Hair follicles are mini organs that repeatedly build, break down, shed and then rebuild again. That regenerative rhythm is unusual biology: most tissues do not run a lifelong programme of rapid cell division, structural remodelling, controlled shutdown, and then reactivation on loop. Each cycle is a coordinated handover between stem cell activity, matrix keratinocyte proliferation, vascular support, immune signalling, and extracellular matrix remodelling. When this system runs smoothly, hair density is stable and shedding stays within a narrow range. When the system is off balance, there is a very different outcome, including shorter growth phases, longer resting phases, or a more active shedding phase.

The hair growth cycle

Anagen (growth): The anagen phase is the active growth stage of the hair cycle, where hair follicles produce new cells which grow, divide and differentiate into keratin cells that make up the hair fibre.  This leads to hair growth of roughly 1 cm per month.  This phase lasts for 3-5 years for most people, but depending on other factors such as genetics can span 2-7 years.  Roughly 80-90% are in this phase on a healthy head of hair and the amount of time spent in this hair phase determines how long your hair will grow.

Catagen (transition): The catagen phase is a brief 2-3 week transitional stage in the hair growth cycle that follows anagen stage.  During this phase the hair follicle shrinks, the hair follicle starts to detach from blood supply, the base of the hair fibre hardens and growth stops.  The base of the hair fibre forms a club shape.  About 1-3% of hairs are in this phase at any time.  The hair is still in the follicle, but as it has been detached from blood supply it stops growing and prepares to enter the resting stage.

Telogen (rest): The resting stage of the hair growth cycle.  Here follicles are inactive and hair strands stop growing but remain anchored 3-4 months.  Roughly 10-15% of hairs are in this phase.  Here the follicle is anchored to the follicle, the new club shape is surrounded by ‘mooring cells’ [moor] that help mechanical retention so that it sits within the follicle more like a fitted plug than a straight hair fibre, the club shape helps by giving a broader keratinised base that is harder to dislodge than without the club shape.  But the main anchoring is provided by the adhesion machinery around it, especially junctional proteins. 

Exogen (shedding): Exogen is the final stage in the hair growth cycle where 50- 100 hair fibres a day are released.  Exogen is an active and controlled process, where the adhesive bond between the hair follicle and the club hair breaks via a proteolytic process (protein breakdown).  Proteases (such as serine proteases) break down the adhesion bonds that anchor the club hair in the follicles during the telogen to exogen transition, allowing the hair to fall out.  Proteolytic degradation of adhesion is usually tightly regulated by protease inhibitors.

Once you understand these phases, hair loss becomes easier to interpret because the visible symptom is usually downstream of cycle biology.  Internal factors like iron handling, vitamin D status, thyroid signalling, androgen activity, insulin sensitivity, inflammation, and stress physiology can alter growth signalling or recovery capacity. External and local factors like scalp barrier status, microbial load, sebum composition, irritant exposure and friction can add mechanical and inflammatory complications. 

This is why hair loss responds best to a diagnosis-led approach backed by proper biomarker evaluation with blood tests. The same level of shedding, thinning and loss of density, can sit on top of very different biology for one person when compared to another, and the drivers are often layered rather than single-cause. 

Most hair loss investigations come down to a simple question: what is shifting the distribution of follicles across the cycle, or changing the timing of transitions? The drivers are not complex, but they are often layered.