Androgenetic alopecia (AGA) is the most common form of hair loss in both men and women. It is a genetically determined, androgen-mediated condition in which specific follicles (those with higher androgen receptor expression) are progressively miniaturised by exposure to dihydrotestosterone (DHT). The follicle does not die; it shrinks. Each successive hair growth cycle produces a finer, shorter shaft, and the anagen phase shortens progressively over years until the follicle produces barely visible vellus hair.

The pattern is characteristic and reflects the regional distribution of androgen-sensitive follicles. In men, this typically means temporal recession and vertex thinning with occipital sparing: the classic Hamilton-Norwood pattern. In women, the picture is different: diffuse thinning over the crown with preservation of the frontal hairline is the most common presentation, graded by the Ludwig scale. The occipital region is generally spared in both sexes because those follicles have lower androgen receptor density and are largely resistant to DHT regardless of circulating levels.

AGA is progressive and permanent in the sense that miniaturised follicles do not spontaneously recover once the process is established. It does not resolve on its own, and the rate of progression varies considerably between individuals. The androgen pathway underlying AGA is covered in depth in the article on DHT and the follicle.

Telogen effluvium is a shedding disorder rather than a miniaturisation disorder. The follicles themselves are not damaged and do not shrink. Instead, a systemic trigger causes a disproportionate number of follicles to shift prematurely from the anagen (growth) phase into the telogen (resting) phase. Approximately two to four months later, those follicles shed their telogen hairs simultaneously, producing a noticeable increase in daily hair loss. The shed is the visible event; the shift in hair cycle dynamics is what caused it.

The triggers for TE span a wide range of systemic events: major illness, surgery, significant physiological stress, crash dieting or significant rapid weight loss, childbirth (postpartum TE is extremely common), thyroid dysfunction, iron deficiency, and some medications. The 2-4 month delay between trigger and shed reflects the time it takes for the follicles displaced into telogen to complete that resting phase and shed. This delay is why TE is routinely misattributed: the shed happens well after the event that caused it, and the connection is not immediately obvious.

Acute TE typically resolves within six to nine months once the trigger is addressed, as follicles return to anagen and produce new growth. Chronic TE, defined as lasting more than six months, is a distinct and less well-understood entity. It predominantly affects middle-aged women and can fluctuate for years without a clearly identified ongoing trigger, though nutritional factors and subclinical thyroid dysfunction are often implicated.

Before a formal clinical assessment, five observable signals provide useful initial guidance.

TE and AGA frequently coexist, which is why distinguishing them can be difficult. The scenario is common: someone has underlying AGA that has been progressing slowly and was perhaps not yet noticeable. A systemic trigger then precipitates a TE episode. The acute shed reveals the AGA that was already there, and the visible thinning after the shed has resolved may be partly the aftermath of TE (which will recover) and partly the AGA (which will not, without intervention).

This overlap produces a clinically ambiguous picture that is not reliably untangled without trichoscopy. Someone in this situation who treats only the TE trigger may find their density partially recovers but does not return to the level it was before the TE, because the AGA was already present. If that gap is attributed to "the TE not fully resolving," the underlying AGA goes untreated while the window for early intervention narrows.

The five signals above are indicators, not diagnostic tools. Confirmation requires a clinical assessment. The most informative is trichoscopy: a dermoscopic examination of the scalp that can directly visualise the proportion of miniaturised hairs in affected versus unaffected areas, identify the perifollicular changes associated with AGA, and assess hair calibre variation. A dermatologist can also perform a hair pull test to assess active shedding and interpret it in the context of the pattern and history.

For suspected TE, blood work is essential rather than optional. Ferritin (iron stores), thyroid function (TSH, free T4), full blood count, and in women, relevant hormonal panels, will identify the most common correctable causes. Ferritin in particular is routinely low in women with TE, and the threshold for "normal" varies significantly between laboratory reference ranges and clinical hair loss standards; a dermatologist familiar with hair loss will use a higher ferritin threshold than a standard lab range would suggest.

Scalp biopsy is the definitive investigation when the picture remains ambiguous after clinical assessment and trichoscopy, but is rarely the first step and is generally reserved for cases where other diagnoses such as scarring alopecia need to be excluded.

The treatment logic for each condition is almost entirely separate. For acute TE, the primary intervention is identifying and removing the trigger: correcting iron deficiency if present, stabilising thyroid function, improving nutritional status, or simply allowing time to pass after a one-off physiological event. No DHT-blocking medication is indicated for TE and none will address it. Time is often the most effective treatment for acute TE, provided the trigger is no longer active.

For AGA, the approach is fundamentally different. Because the condition is progressive and driven by an ongoing androgen signal in genetically susceptible follicles, addressing the trigger (there is no external trigger) is not the treatment. Intervention requires either reducing DHT availability (finasteride, dutasteride), supporting the follicular environment and anagen duration (minoxidil, topical actives), or both. The article on building a hair loss protocol covers how these approaches can be combined and sequenced.

Realistic timescales differ substantially. TE recovery, once the trigger is resolved, typically occurs over three to six months. AGA interventions require a minimum of three to six months before meaningful assessment is possible, and the goal in most cases is stabilisation rather than significant regrowth, though partial recovery is seen, particularly in early-stage AGA with prompt treatment. The article on how long before you see results from a hair loss serum covers this in more detail.

This article is provided for educational purposes and does not constitute medical advice. Hair loss has multiple potential causes and a confirmed diagnosis requires assessment by a qualified healthcare professional. AmpleLab products are cosmetic formulations and are not intended to diagnose, treat, cure, or prevent any condition.

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