Losing Hair?
The Cause Is In Your Blood.

Ferritin is an acute-phase reactant, meaning it rises during inflammation. A ferritin of 40 in a healthy person might genuinely reflect adequate stores. A ferritin of 40 in someone with chronic inflammation could be masking a true deficiency, because inflammation artificially elevates the reading. This is why ferritin must be interpreted alongside hs-CRP (inflammation marker) and transferrin saturation. Without both, the ferritin number on its own can be misleading in either direction.

The Murphy et al. 2025 audit of 16,889 NHS fatigue requests found ferritin was ordered in only 9.4% of cases. Hair loss patients fare slightly better because NICE NG145 does recommend ferritin as first-line, but GPs typically use the standard laboratory reference range (15 to 300 µg/L) rather than the dermatological optimal range (70+). A result of 18 gets filed as "normal." A trichologist would call it severely depleted.

Telogen effluvium from iron deficiency is reversible. But the recovery timeline is 6 to 18 months once ferritin reaches optimal levels. Every month spent with suboptimal iron is a month of preventable shedding. Early testing shortens the recovery window dramatically.

Both underactive and overactive thyroid cause diffuse hair thinning. The British Association of Dermatologists lists thyroid function testing as a standard investigation for anyone presenting with diffuse hair loss. But the NHS tests TSH only with reflex Free T4, meaning Free T4 is only checked if TSH is abnormal. Free T3 and thyroid antibodies are almost never included.

This matters because Hashimoto's thyroiditis (autoimmune thyroid destruction) can cause hair loss for years before TSH moves out of range. Anti-TPO antibodies are elevated, the thyroid is being progressively damaged, but the compensatory mechanisms keep TSH "normal." The hair loss is one of the earliest visible signs, long before the full hypothyroid picture develops.

Subclinical hypothyroidism affects 8 to 10% of the UK population (British Thyroid Association). It is more common in women and increases with age. Treating confirmed thyroid dysfunction typically leads to gradual hair regrowth over 6 to 12 months, but only if it's detected. A TSH-only test misses the autoimmune and conversion components that a comprehensive panel catches.

A 2024 meta-analysis found vitamin D deficiency in over 50% of people with alopecia areata and telogen effluvium. Vitamin D receptors are present on hair follicles, and vitamin D plays a direct role in the anagen (growth) phase of the hair cycle. Deficiency shortens the growth phase and accelerates the transition to shedding.

NDNS data shows 23% of UK adults are vitamin D deficient at the strict threshold of below 25 nmol/L. At the more clinically useful threshold of below 50 nmol/L, the prevalence is significantly higher, particularly from October to April when UVB radiation in the UK is insufficient for cutaneous synthesis. Most people losing hair in the UK have never had their vitamin D tested.

Vitamin D deficiency also compounds iron deficiency and thyroid dysfunction. Low vitamin D impairs thyroid hormone receptor binding and worsens autoimmune thyroid processes. It also affects calcium metabolism, which influences follicle cycling. This is why testing vitamin D in isolation tells a partial story. It needs to be measured alongside ferritin, thyroid markers, and inflammatory markers to understand the full contribution to hair loss.

DHT (dihydrotestosterone) is the hormone behind androgenetic alopecia in both sexes. Testosterone is converted to DHT by the enzyme 5-alpha reductase at the hair follicle. The amount of free testosterone available for this conversion depends on SHBG (sex hormone binding globulin). Low SHBG means more free testosterone, more DHT production, and faster pattern hair loss.

In women, low SHBG is common with insulin resistance, PCOS, and obesity. Hormonal contraception (particularly progesterone-only methods) can lower SHBG. Coming off the combined pill can cause a temporary SHBG drop that triggers shedding. In men, SHBG naturally declines with age, obesity, and insulin resistance, increasing free testosterone and DHT exposure at the follicle.

This is another reason why isolated testing fails. A "normal" total testosterone tells you nothing about DHT exposure without knowing the SHBG level. A low SHBG with normal total testosterone means high free testosterone and high DHT production. The comprehensive panel that includes testosterone, SHBG, free testosterone calculation, and oestradiol reveals the full androgenic picture that a single testosterone test cannot.

Chronic low-grade inflammation (measured by hs-CRP) damages hair follicles directly and worsens every other cause of hair loss. Inflammation at the scalp disrupts the follicle microenvironment. Systemic inflammation impairs iron absorption, worsens thyroid autoimmunity, and increases insulin resistance. It is the connective thread between seemingly unrelated causes of shedding.

Cortisol, the stress hormone, pushes hair follicles from the growth phase into the resting phase prematurely. This is the mechanism behind stress-related telogen effluvium. The typical pattern: a period of intense stress is followed 3 to 6 months later by noticeable shedding. If the stress is chronic (work, relationship, financial, health anxiety), the shedding becomes ongoing.

Post-covid hair loss is a well-documented example. COVID-19 triggers both systemic inflammation and a cortisol stress response. Hair shedding peaks 3 to 6 months after infection and can persist for 12 months or more. Testing inflammation markers, cortisol, ferritin, and vitamin D after covid reveals which pathways are still active and which need support.