Ferritin and iron studies
Reads: Iron status
You want it adequate, not high: low stores are a documented cause of fatigue in some people and demonstrably not in others — see the conditional before supplementing.
What this marker reads
Iron status — body iron stores, read as ferritin, which carry oxygen and run the enzymes that make cellular energy.
What a named body publishes
Each line below is the sentence the issuing body wrote, carried with its own identifier. Nothing here interprets your result — it states what was published, for whom, and by whom.
Ferritin
“WHO: in apparently healthy adults aged 20-59 years, a serum or plasma ferritin concentration below 15 µg/L indicates iron deficiency.” 20-59
WHO guideline on use of ferritin concentrations to assess iron status in individuals and populations · World Health Organization, Geneva, 2020 — hosted on NCBI Bookshelf The document
“WHO: in apparently healthy older persons aged 60 years and above, a ferritin concentration below 15 µg/L indicates iron deficiency.” 60+
WHO guideline on use of ferritin concentrations to assess iron status in individuals and populations · World Health Organization, Geneva, 2020 — hosted on NCBI Bookshelf The document
“WHO Recommendation 1.3: in apparently healthy individuals, risk of iron overload is indicated by a ferritin concentration 'exceeding 150 µg/L in menstruating women'.” females, 20-59
WHO guideline on use of ferritin concentrations to assess iron status in individuals and populations · World Health Organization, Geneva, 2020 — hosted on NCBI Bookshelf The document
“WHO Recommendation 1.3: in apparently healthy individuals, risk of iron overload is indicated by a ferritin concentration exceeding '200 µg/L in men and non-menstruating women'.” males, 20-59
WHO guideline on use of ferritin concentrations to assess iron status in individuals and populations · World Health Organization, Geneva, 2020 — hosted on NCBI Bookshelf The document
“WHO: the same iron-overload-risk threshold of above 150 µg/L is listed for females in the older-persons (60+) stratum.” females, 60+
WHO guideline on use of ferritin concentrations to assess iron status in individuals and populations · World Health Organization, Geneva, 2020 — hosted on NCBI Bookshelf The document
“WHO: the same iron-overload-risk threshold of above 200 µg/L is listed for males in the older-persons (60+) stratum.” males, 60+
WHO guideline on use of ferritin concentrations to assess iron status in individuals and populations · World Health Organization, Geneva, 2020 — hosted on NCBI Bookshelf The document
“WHO: for pregnant women the guideline gives a ferritin threshold of below 15 µg/L in the FIRST TRIMESTER to indicate iron deficiency; it gives no threshold for the second or third trimester.” females, pregnancy, first trimester
WHO guideline on use of ferritin concentrations to assess iron status in individuals and populations · World Health Organization, Geneva, 2020 — hosted on NCBI Bookshelf The document
“WHO Recommendation 1.2: in the presence of infection or inflammation, 'a ferritin concentration below 30 µg/L in children and 70 µg/L in adults may be used to indicate iron deficiency.'” applies when infection or inflammation is present
WHO guideline on use of ferritin concentrations to assess iron status in individuals and populations · World Health Organization, Geneva, 2020 — hosted on NCBI Bookshelf The document
“WHO: the same inflammation-adjusted adult threshold of below 70 µg/L applies to older persons aged 60 years and above.” applies when infection or inflammation is present
WHO guideline on use of ferritin concentrations to assess iron status in individuals and populations · World Health Organization, Geneva, 2020 — hosted on NCBI Bookshelf The document
“WHO: in NON-HEALTHY adults a ferritin concentration above 500 µg/L may indicate risk of iron overload or other disease and calls for further clinical and laboratory evaluation (conditional recommendation, very low certainty of evidence).” stated for adults who are not apparently healthy
WHO guideline on use of ferritin concentrations to assess iron status in individuals and populations · World Health Organization, Geneva, 2020 — hosted on NCBI Bookshelf The document
Your laboratory reads your result against its own assay, and this page does not do that for it. What is above is what a named body published and for whom; what is below is the machinery the marker reads and the formulas witnessed on it.
What moves it
Parasite burden lowers it.
Five countries, three languages, unrelated groups. Vietnam 54-month WHO/Melbourne program; Cochrane screened-infected arm; Bolivia; Eritrea; Philippine pregnancy. Verbatim: “The prevalence of hookworm infection was reduced from 76% to 11%; mean hemoglobin rose from 122 g/L to 131 g/L and anemia prevalence fell from 38% to 18%.”. doi 10.1371/journal.pntd.0002146 · PMC3623698
Vitamin C raises it.
Enhances non-heme iron absorption. Carried by the intermediary-metabolism, micronutrient and clinical reviews. doi 10.3390/nu18132141 · PMC9967593
Copper status raises it.
Ceruloplasmin is required to mobilize iron - copper deficiency can present as anemia. Carried by the intermediary-metabolism, micronutrient and redox reviews. doi 10.3390/nu18132141 · PMC9967593
Iron gatekeeper hormone lowers it.
iron loading raises hepcidin — the negative feedback that limits further absorption. Hepcidin degrades ferroportin and blocks enteric iron uptake. PMID 835510 · PMC7005133
What it moves
It lowers Daily energy.
The positive trial is specific and the subgroup is the 144 non-anemic women aged 18-55 with unexplained fatigue, elemental iron daily for four weeks, double-blind and placebo-controlled. Fatigue fell 29 percent on iron versus 13 percent on placebo (difference 0.95 points, 95% CI 0.32 to 1.62, P = 0.004), and subgroup analysis showed that only women with ferritin at OR below 50 micrograms per liter improved. And the negative trials ARE why this edge is conditional rather than simple. 154 female blood donors, iron-deficient without anemia, four weeks of oral ferrous sulfate: hemoglobin and ferritin both rose significantly (P < 0.01) and fatigue did not move (-0.15 points, P = 0.697). Then a larger trial closed the obvious escape routes: 405 non-anemic donors with ferritin at or below 50, given a single intravenous dose of iron-carboxymaltose — which bypasses absorption and compliance entirely. Fatigue 3.9 versus 4.0, P = 0.819. And the pre-specified subgroups included ferritin below 25 and fatigue at OR above 4 points, with exploratory analyses at lower cut-offs: NO between-group differences anywhere. So the distinction is not about dose, route, OR how low the ferritin is. It is about WHO walked in. Women who presented with fatigue and had low ferritin improved. People selected for iron deficiency who were not complaining did not — and the donor trial supplies the reason it is easy to confuse the two: blood donation did not induce overt symptoms of fatigue in spite of the significant biological changes it produces. A low ferritin is not a symptom. the positive evidence is almost entirely in menstruating women. Nothing here establishes the effect in men or post-menopausal women. PMC7449957
It lowers Calm under stress.
A systematic review and meta-analysis of randomized placebo-controlled trials in non-anemic children, adolescents and menstruating adults, and the value is that it names which endpoints moved and which did not: supplementation improved symptoms of anxiety (d = 0.34), fatigue (d = 0.34), physical well-being (d = 0.42), cognitive intelligence (d = 0.46) and short-term memory (d = 0.53) — but not attention OR depression. The same meta-analysis, the same trials, the same population, and two endpoints did not move. An arrow into mood or focus would contradict the source this edge is built on. And the subgroup finding confirms the conditional on the Iron Status → Fatigue link from the other direction: supplementation effects were absent when excluding iron-deficient participants. Iron does nothing for people who are not short of it — which is the same lesson the blood-donor trials taught, arrived at by a different route. Note the design gap the authors themselves expose: pre-post studies showed much larger effects including depression (d = 0.93), fatigue (d = 1.01) and overall psychiatric symptoms (d = 1.13). Those ARE uncontrolled designs and the RCT column is the one this edge is drawn from. The gap between d = 0.93 uncontrolled and NO effect randomized is a measurement of how much placebo and regression to the mean are worth in this literature. doi 10.1016/j.neubiorev.2025.106276
It raises Sleep.
The route is restless legs syndrome, and the finding that makes it worth drawing is that the blood test can be normal while the brain is not: altered iron homeostasis appears to be a primary component underlying RLS pathology and is seen most prominently as decreased brain iron in the substantia nigra, demonstrated in MRI, brain ULTRASONOGRAPHY and post-mortem brain tissue — and these changes in brain iron ARE present despite normal blood levels of iron. And the intervention evidence does not require anemia: both oral and IV iron treatments significantly reduce RLS symptoms compared with placebo even in persons WHO ARE not anemic. Peripheral iron status relates to RLS severity, so the two compartments are connected without being the same. A second, independent arm: children with iron deficiency anemia show altered REM architecture — longer REM episodes in the first third of the night and shorter in the last, shorter latency to the first REM episode, and shorter non-REM stage 2. That is sleep structure, not sleep complaint. the RLS trials are in diagnosed RLS, and the REM architecture data are in anemic children. This edge is not evidence that iron improves ordinary sleep in iron-replete people. PMC8525689
It raises Iron & oxygen carriage.
The mechanism that makes iron supplementation fail: anemia of inflammation is characterized by the insufficient production of erythropoietin and decreased response of erythroid progenitors to EPO. In addition, it inhibits the release of iron from the body stores and alters the iron status after being stimulated by hepcidin. Inflammation locks iron away - so oral iron given into an inflammatory state does not reach the marrow. Anemia affects 1.62 billion people. And the periodontal link is measured: a meta-analysis of sixteen studies on hemoglobin and iron metabolism in periodontitis - though the authors call the association still controversial and ask for larger cohorts. PMID 835510 · PMC7005133
It lowers Liver.
PMC9593083 — https://www.merckmanuals.com/professional/hematology-and-oncology/iron-overload/hereditary-hemochromatosis — The aging outcome lists the thirteen hallmarks themselves, each mapped to its pathway and labeled with its hallmark number. (from the reviews of this outcome). PMC9593083
It raises Iron gatekeeper hormone.
Iron loading raises hepcidin - the negative feedback that limits further absorption. PMC7005133
It raises Thyroid.
The finding that reframes the whole node: the thyroid makes a pro-hormone, not the active hormone. T4 is activated to T3 by DIO1 and DIO2, and inactivated to rT3 by DIO3 - and the three types of deiodinases have variable tissue distribution, so active hormone level is set locally in each tissue, not centrally by the gland. A serum TSH does not tell you what a given tissue is seeing. Three trace elements, three different jobs: thyroid and deiodinase function depends on supply of the trace elements iodine, selenium and iron. Iodine is the substrate; selenium because the deiodinases ARE selenoproteins; iron because thyroperoxidase is a hemoprotein. A thyroid formula missing any one of the three has a hole in a different place. And selenium carries a documented harm: in a small fibrous gland with low iodine intake, SE supplementation for six months resulted in severe hypothyroidism with very low total T4 and highly elevated TSH - because activating previously-selenium-starved extrathyroidal deiodinases accelerated the loss of limited iodine stores. Selenium without sufficient iodine can make thyroid function worse. Genetic variation is named: the DIO2 Thr92Ala polymorphism may impair T4-to-T3 conversion in certain individuals. doi 10.1016/j.freeradbiomed.2022.09.024 · PMC9967593
It lowers Gum health.
The mechanism is a self-feeding loop and the fuel is your own tissue: inflammation and dysbiosis positively reinforce each other because inflammatory tissue breakdown products ARE used as nutrients by the dysbiotic microbiota - specifically collagen peptides and heme-containing compounds. The bacteria eat the damage the immune response causes, which causes more damage. And it is not an infection in the ordinary sense: periodontitis is caused mainly by dysbiosis of the bacterial community, rather than an infection by individual bacteria. Keystone pathogens, whose colonization is facilitated by accessory pathogens, initially subvert the host response, after which PATHOBIONTS - commensals turned pathogenic - over-activate inflammation. A keystone pathogen works at low abundance by changing the community, not by dominating it. The tissue-destruction route is specific: pathogens induce epithelial-mesenchymal transition via TGF-beta/Smad, Wnt/beta-catenin and Notch, causing loss of E-cadherin, junctional epithelial instability, pocket formation and attachment loss. doi 10.3390/jmp7010011 · PMID 25534621 · PMC5646588
It raises Nails.
NBK559311 — Drawn from reviews of neighboring outcomes rather than from studies of this outcome itself, which is weaker evidence, and the map marks it so.
It raises Body temperature control.
PMC6531837 — 8989508 — Drawn from reviews of neighboring outcomes rather than from studies of this outcome itself, which is weaker evidence, and the map marks it so. PMC6531837
Formulas that modulate it
Each formula page names this pathway and carries the study behind its claim.
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