What ferritin actually is
Ferritin is your body's primary iron storage protein. It's the long-term reservoir — iron stored in cells, particularly in the liver, spleen, and bone marrow, waiting to be mobilised when needed.
When ferritin is low, it doesn't necessarily mean you're anaemic. You can have completely normal haemoglobin and red blood cell counts while your storage levels are significantly depleted. This is the distinction that gets missed in standard testing. The full blood count looks fine. The symptom picture doesn't match.
The reason is that ferritin is not just a passive storage tank. Iron from ferritin is required as a cofactor in dozens of enzymatic reactions throughout the body — reactions that don't wait for haemoglobin to drop before they start to be affected.
The reference range problem
The NHS reference range for serum ferritin in adult women is typically 13–150 ng/mL. For men it's broadly similar at 30–400 ng/mL. These are population reference ranges — they represent the middle 95% of people tested.
The problem with population reference ranges is that they include everyone — people who are tired, unwell, inflamed, post-viral, chronically stressed. The range reflects what's statistically common, not what's physiologically optimal.
A ferritin of 28 ng/mL falls within the NHS normal range. In clinical practice, it represents a storage level at which multiple body systems begin to be functionally compromised — not dramatically, not immediately, but measurably.
What low ferritin actually affects
This is where the picture becomes clinically interesting. Ferritin isn't just relevant to iron deficiency anaemia. It's a cofactor in systems that affect energy, mood, cognition, and metabolic function in ways that standard testing never connects.
Thyroid hormone conversion
Thyroid peroxidase, the enzyme that makes thyroid hormone, contains iron (haem). The enzymes that convert T4 to active T3 are selenium enzymes. In observational studies, iron-deficiency anaemia is associated with lower T4 and T3 — which points to reduced hormone production rather than a specific block in conversion.
A person with ferritin of 28 ng/mL and a TSH of 2.4 mIU/L — both within normal ranges — may have symptoms that overlap with low thyroid function, and iron deficiency is one of the things worth checking before anyone reaches for thyroid medication. The downstream effects — fatigue, cold intolerance, brain fog, weight resistance — appear exactly as they would in hypothyroidism.
Dopamine transport
The enzyme that makes dopamine, tyrosine hydroxylase, needs iron. In animal studies, iron deficiency lowers the density and function of the dopamine transporter. That has not been shown directly in humans.
The clinical presentation includes poor concentration, low motivation, difficulty with executive function, restless legs at night (a well-established iron-ferritin connection), and a flat or blunted mood that doesn't quite meet the criteria for depression but interferes significantly with daily function.
This is one of the reasons ferritin testing is particularly relevant in clients presenting with ADHD-type symptoms or unexplained cognitive difficulties. The neurological impact of low ferritin is underappreciated in standard medical practice.
Mitochondrial energy production
Iron is essential for the electron transport chain — the series of protein complexes in mitochondria that generates ATP, the cellular energy currency. Several of these complexes (I, II, and III in particular) are iron-sulphur proteins that cannot function adequately without sufficient iron stores.
The result is reduced cellular energy production that manifests as persistent fatigue disproportionate to activity levels — the fatigue that sleep doesn't fix, that rest doesn't resolve, that appears to have no obvious cause on a standard blood panel.
Immune function
Iron is required for the proliferation and differentiation of immune cells. Low ferritin impairs both innate and adaptive immune responses. This can present as frequent infections, slow recovery from illness, or a general sense of immune vulnerability that isn't explained by any specific pathogen or diagnosis.
The clinical pattern I see repeatedly is a client whose GP has run full blood count, thyroid panel, and basic metabolic markers — all within normal range — who presents with fatigue, brain fog, low mood, and poor recovery. Ferritin at 24 ng/mL. Iron saturation at 18%. The clinical picture resolves, slowly and measurably, as ferritin is repleted to 70–90 ng/mL over four to six months.
Allow three to six months: rebuilding stores is slow, and a retest at six to eight weeks shows direction, not the end point.
What's causing low ferritin when diet seems adequate?
This is a question worth asking. Low ferritin with apparently adequate dietary iron intake suggests something is interfering with absorption or increasing demand.
Gut dysfunction — iron absorption occurs primarily in the duodenum and upper jejunum. Gut inflammation, low stomach acid, and dysbiosis all impair iron absorption. This is why addressing gut health before iron supplementation often produces better results — and why GI-MAP stool analysis is a relevant companion investigation.
H. pylori infection — H. pylori is directly associated with iron deficiency through multiple mechanisms: blood loss from gastric irritation, competitive consumption of iron, and impairment of acid production needed for iron absorption. A client with persistent low ferritin despite supplementation should be screened for H. pylori.
Coeliac disease — intestinal damage from gluten impairs iron absorption. About 1 in 31 people with iron-deficiency anaemia turn out to have coeliac disease (Mahadev 2018), so it is worth testing for, via the GP, before going gluten-free.
Heavy periods — an obvious but frequently underestimated cause. Monthly blood loss in the absence of adequate dietary iron intake creates a chronic deficit that accumulates over years. Ferritin of 22 in a 38-year-old woman with heavy periods is not a coincidence.
Chronic inflammation — ferritin behaves as an acute phase reactant. It rises with inflammation, which can mask true iron deficiency. A client with ferritin of 65 ng/mL and elevated hs-CRP may actually be iron deficient once the inflammatory component is accounted for.
How to replete ferritin correctly
Not all iron supplements suit everyone. Ferrous sulphate — the standard NHS prescription — is well absorbed when iron is low, but commonly causes gastrointestinal side effects.
Ferrous bisglycinate causes fewer gut side effects and, in pregnancy trials, raised haemoglobin slightly more (Fischer 2023). Timing matters more than most people realise: a single morning dose on alternate days is absorbed better than daily or split doses, because each dose raises hepcidin, the hormone that blocks the next one (Stoffel 2017).
Vitamin C alongside iron enhances absorption. Tea with a meal can cut non-haem iron absorption by up to about 80–90%, and coffee by about 40% (Hurrell 1999; Morck 1983) — so take iron away from tea, coffee and calcium.
The timeline matters. Ferritin repletion from a level of 25 ng/mL to 80 ng/mL with appropriate supplementation typically takes four to six months. Testing at six to eight weeks gives an early indication of trajectory but isn't the endpoint.
The ferritin thresholds in this article are graded against published research, and my clinical target is labelled as mine. For the wider evidence base covering iron, blood chemistry optimal ranges, and 9 other clinical areas with 34+ PubMed referenced papers:
Read the TDG Evidence Base →The bottom line
A ferritin of 30 ng/mL and a ferritin of 80 ng/mL are both "within the normal range." They are not the same result. For some people — particularly women with fatigue or hair loss — the gap between them matters, and the one trial that tested it found fatigue improved with iron at ferritin of 50 or below.
Normal is not a destination. It's a floor. The clinical question is not whether your ferritin clears 13 ng/mL. It's whether it's high enough for the dozens of iron-dependent processes in your body to work the way they're designed to.
That's a different question — and it requires a different reference range to answer it.