Hair loss: causes, which biomarkers to check and what to do about it

Iron deficiency and low ferritin

Iron deficiency is the most common nutritional cause of hair thinning, and ferritin (the iron storage protein) is the single most important blood marker for hair loss in women. Research consistently shows that women with diffuse hair shedding have significantly lower ferritin levels than matched healthy controls. In one study, women with ferritin levels at or below 30 ng/mL had 21 times higher odds of experiencing telogen effluvium (diffuse hair shedding) compared with women with adequate levels. A large clinical series found that iron deficiency accounted for 70% of cases of female alopecia.

The critical issue with standard testing is the reference range. The NHS defines iron deficiency anaemia using haemoglobin below 12 g/dL in women, with a corresponding ferritin well below 15 ng/mL. But research on hair loss consistently finds that the ferritin level needed for optimal hair growth is between 40 and 70 ng/mL, substantially higher than the threshold used to diagnose clinical deficiency. This means a person can receive a GP result described as normal while having ferritin levels that are actively impairing hair follicle function. Approximately 31% of UK women show signs of absolute iron deficiency, and 54% of UK girls have iron intakes below recommended levels, according to the National Diet and Nutrition Survey.

Thyroid dysfunction

Both underactive and overactive thyroid conditions cause diffuse hair loss, and thyroid disorders are among the leading medical causes of hair shedding in women. Thyroid hormones regulate the hair growth cycle directly: T3 (the active form) supports the growth phase, and when T3 is insufficient, follicles shift prematurely from the growth phase (anagen) to the resting phase (telogen), producing accelerated shedding. The pattern typically emerges 2 to 3 months after the onset of thyroid dysfunction and may persist or worsen until the underlying condition is addressed.

A critical point for hair loss testing: TSH alone is not sufficient. Free T4 and Anti-TPO antibodies need to be included alongside TSH because Hashimoto's thyroiditis (autoimmune thyroid disease) can produce active hair loss while TSH remains within the standard reference range, particularly in earlier stages. Thyroid disorders frequently coexist with iron deficiency because hypothyroidism impairs iron absorption and reduces ferritin, and because both conditions share common demographic risk factors.

Vitamin D deficiency

Vitamin D plays a role in hair follicle cycling, and deficiency is associated with telogen effluvium and alopecia areata. A 2024 meta-analysis found vitamin D deficiency in over 50% of people with alopecia areata. The mechanism appears to involve vitamin D receptors in hair follicle cells that regulate the transition between growth and resting phases. UK vitamin D deficiency rates are high across the year, with particular prevalence in winter months and in people with limited sun exposure, darker skin, or indoor lifestyles.

Hormonal causes: androgens, PCOS, and DHT

Androgenetic alopecia (pattern hair loss) in both sexes is driven by sensitivity of hair follicles to dihydrotestosterone (DHT), which is converted from testosterone by an enzyme called 5-alpha reductase. In women, this pattern is typically diffuse thinning at the crown rather than the receding hairline seen in men. PCOS, which affects around 1 in 10 UK women, is associated with elevated free testosterone and reduced SHBG (sex hormone binding globulin), increasing the amount of testosterone available for conversion to DHT. Testosterone and SHBG together determine the biological androgen load on hair follicles, making both markers necessary for a complete hormonal hair loss assessment.

B12 deficiency and its role in follicle function

B12 supports the production of red blood cells that deliver oxygen to hair follicles, and its deficiency impairs the energy metabolism within follicle cells. B12 deficiency frequently coexists with iron deficiency and thyroid dysfunction, making it part of the standard hair loss panel rather than an optional add-on. Vegetarian and vegan diets, certain gut conditions affecting absorption (including coeliac disease and low stomach acid), and increasing age all raise B12 deficiency risk.

Autoimmune causes

Alopecia areata is an autoimmune condition in which the immune system attacks hair follicles, producing patchy hair loss that can progress to complete scalp loss (alopecia totalis) or full body hair loss (alopecia universalis) in some cases. CRP (C-reactive protein) and thyroid antibody testing can provide some context for autoimmune-driven hair loss, and thyroid autoimmunity is significantly more common in people with alopecia areata than in the general population.

Physiological stress and telogen effluvium

Telogen effluvium is a form of diffuse hair shedding triggered by a physiological stress event approximately 3 months before the shedding begins. Common triggers include illness, surgery, significant weight loss, childbirth, or psychological stress. The mechanism involves a proportion of actively growing follicles shifting simultaneously into the resting phase in response to the stress signal, producing a wave of shedding when these follicles release their hair shafts approximately 3 months later. Ferritin and B12 deficiency often coexist with or amplify telogen effluvium, which is one reason why testing these markers is important even when a stress trigger seems to explain the shedding.

Standard GP testing for hair loss typically includes a full blood count and TSH, and occasionally serum ferritin. This misses Free T3, Free T4, Anti-TPO antibodies, vitamin D, B12, and androgen markers, which are the markers most clinically useful for identifying treatable causes of hair thinning. A home hair loss blood test UK that covers all relevant markers simultaneously provides the most complete picture with the fewest blood draws.

Ferritin is the most important single marker for hair loss in women. Levels should be interpreted against the hair-health threshold (40-70 ng/mL) rather than the anaemia prevention threshold (15 ng/mL).

TSH is the starting point for thyroid assessment. An elevated TSH indicates underactive thyroid, which causes diffuse hair loss and changes in hair texture.

Free T4 and Free T3 complete the thyroid picture. Free T3 is the active form that directly regulates hair follicle cycling; low Free T3 can cause hair loss even when TSH appears normal.

Anti-TPO antibodies identify Hashimoto's thyroiditis, which can drive hair loss before TSH shifts out of range.

Vitamin D should be included given its role in follicle cycling and its very high prevalence of deficiency in the UK.

Vitamin B12 supports red blood cell production and follicle energy metabolism; deficiency frequently coexists with the other markers above.

CRP provides context for inflammatory and autoimmune-driven hair loss.

Restoring iron and ferritin

If ferritin is below the hair-health threshold (40-70 ng/mL), iron restoration is the single highest-priority intervention. Dietary iron from haem sources (red meat, liver, seafood) is substantially more bioavailable than non-haem iron from plant foods. Consuming vitamin C alongside iron-rich plant foods significantly improves absorption. Iron supplements should only be taken with confirmed deficiency, as excess iron carries its own health risks. Retesting ferritin at 3 months of consistent supplementation or dietary change confirms whether levels are improving, and again at 6 months to verify that the target range has been reached. Hair regrowth after restoring optimal ferritin typically becomes visible at 3 to 6 months.

Thyroid treatment and monitoring

Hypothyroidism is treated with levothyroxine (T4 replacement), titrated to bring TSH into the therapeutic range. For people whose hair loss continues despite TSH normalisation, Free T3 testing is particularly important, as some people have adequate T4 but suboptimal T3 conversion that continues to impair follicle function. Correcting concurrent nutrient deficiencies, particularly ferritin and selenium, can improve T4-to-T3 conversion and support the hair recovery process alongside thyroid medication.

Nutrition for hair follicle health

Hair follicles are among the most metabolically active cells in the body, and their function is sensitive to nutritional status. Beyond the primary markers of iron and B12, zinc supports follicle structure and keratin production; dietary sources include meat, shellfish (particularly oysters), pumpkin seeds, and legumes. Biotin, while heavily marketed for hair health, is unlikely to benefit people who are not specifically deficient. Protein adequacy is critical: hair is approximately 95% keratin, and insufficient dietary protein directly impairs follicle function. At least 1.2 to 1.6 grams of protein per kilogram of body weight provides adequate substrate for hair protein synthesis.

Managing physiological and psychological stress

Telogen effluvium driven by stress resolves as the triggering event recedes and the follicle cycle normalises, typically over 6 to 12 months. Supporting the recovery process involves addressing any concurrent nutritional deficiencies (which amplify stress-related shedding), ensuring adequate sleep, and managing ongoing stress load. Tracking ferritin, B12, and vitamin D during this period confirms whether the nutritional foundation for recovery is in place.