Lab result explainedVitamins and mineralsLast updated November 8, 2026

Iron saturation (transferrin saturation): what low and high levels mean

Transferrin saturation (iron saturation) (TSAT) · Iron panel (serum iron, TIBC, transferrin saturation, ferritin) · reported in Percent (%); calculated from serum iron (µg/dL) ÷ TIBC (µg/dL) × 100

Transferrin saturation, often printed as iron saturation, TSAT or % saturation, is the percentage of your blood's iron-carrying capacity that is actually carrying iron. It is calculated, not measured directly: serum iron divided by total iron-binding capacity (TIBC), multiplied by 100. Normal is about 20 to 50 percent. A low saturation means little iron is on its way to the bone marrow; a high saturation means transferrin is nearly full and surplus iron is spilling into tissues.

The test matters at both ends. Below 20 percent is the working definition of iron deficiency in kidney disease and heart failure guidelines, and below 15 to 16 percent is the classic cut-off in otherwise healthy people; it is the marker that catches iron deficiency when ferritin has been pushed up by inflammation, and it falls in pregnancy, heavy menstruation, gut blood loss, celiac disease and after bariatric surgery. Above 45 percent is the screening threshold for hereditary hemochromatosis, the most common genetic disorder in people of Northern European ancestry, in which the gut absorbs too much iron for decades until it damages the liver, joints, pancreas and heart.

Saturation is the most volatile number on the iron panel. Serum iron is highest in the morning and falls by up to 30 percent through the day, swings by 20 to 30 percent from day to day, and rises for several hours after an iron tablet, a multivitamin or a large red-meat meal, so a single high or low saturation is confirmed on a fasting morning repeat before any conclusion is drawn. Ferritin tells you about stores; saturation tells you about supply today; the two together, with a CRP, make most of the diagnosis.

TSAT at a glance

What it is: the percentage of transferrin's iron-binding sites that are occupied; calculated as serum iron ÷ TIBC × 100.
Normal (adults): about 20–50% (some labs 15–50% or 20–45%); women tend to run a few points lower than men.
Low saturation (below 20%, and especially below 15–16%) means iron deficiency or iron locked away by inflammation; causes include blood loss, pregnancy, poor absorption, kidney disease, heart failure and obesity.
High saturation (above 45% on a fasting repeat) is the first laboratory sign of hereditary hemochromatosis and also occurs with iron supplements, transfusions, liver disease, thalassemia and some marrow disorders.
Read it with ferritin: low saturation + ferritin below 30 ng/mL = iron deficiency; low saturation + ferritin above 100 = inflammation; high saturation + ferritin above 300 (men) or 200 (women) = probable overload.
Next step: repeat fasting in the morning with iron supplements held for 24 hours; then ferritin and CRP, a search for blood loss if low, or HFE gene testing if persistently above 45%.

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What TSAT measures

Iron travels in blood bound to transferrin, a liver-made protein with two binding sites per molecule. The laboratory measures serum iron (the iron bound to transferrin, in µg/dL) and either TIBC or transferrin itself, then calculates what fraction of the binding sites are filled. At a normal serum iron of 100 µg/dL and a TIBC of 330 µg/dL, saturation is 30 percent: roughly a third of the seats are taken. Because it is a ratio, saturation can be abnormal when either number moves: a low serum iron lowers it, but so does a high TIBC, which is why iron deficiency (low iron, high TIBC) produces very low values, often under 10 percent.

The hormone hepcidin sets saturation from hour to hour. Made by the liver, hepcidin blocks the iron exporter ferroportin on gut cells and on the macrophages that recycle old red cells, so when hepcidin is high (inflammation, infection, obesity, kidney disease) iron is trapped inside cells and saturation falls even though stores are full, a state called functional iron deficiency. When hepcidin is inappropriately low (hereditary hemochromatosis, thalassemia and other conditions with ineffective red cell production) iron floods out of the gut and macrophages, transferrin fills up, and once saturation passes about 60 to 70 percent, free non-transferrin-bound iron appears and is taken up by the liver, heart and endocrine glands, where it causes oxidative damage.

Serum iron, and therefore saturation, has a marked daily rhythm and day-to-day variation. Values are highest between about 6 and 10 in the morning and fall by 20 to 30 percent by evening; a single oral iron dose raises serum iron for 4 to 8 hours and can briefly produce a saturation near 100 percent; a multivitamin with iron does the same on a smaller scale. For screening and for diagnosing hemochromatosis, guidelines specify a fasting morning sample with no iron taken for 24 hours, and a repeat before genetic testing is ordered.

Normal range for TSAT

Reference ranges vary between labs and by age, sex and pregnancy. Use the range printed on your own report.

Group	Typical range (Percent (%); calculated from serum iron (µg/dL) ÷ TIBC (µg/dL) × 100)	Notes
Adults, normal	About 20–50%	Labs differ: 15–50% and 20–45% are also common; men average a few points higher than women. Use the range on your report.
Iron deficiency	Below 15–16% (below 20% is used in kidney and heart failure guidelines)	With ferritin below 30 ng/mL (or below 100 with inflammation) this confirms absolute iron deficiency.
Functional iron deficiency (inflammation)	Below 20% with ferritin above 100 ng/mL	Iron is present but trapped by hepcidin; seen in chronic kidney disease, heart failure, infection, autoimmune disease and cancer.
Chronic kidney disease, iron treatment threshold	TSAT at or below 30% with ferritin at or below 500 ng/mL	KDIGO 2012 threshold for a trial of iron in people with anemia on or off erythropoiesis-stimulating agents.
Heart failure, iron deficiency definition	Ferritin below 100 ng/mL, or 100–299 ng/mL with TSAT below 20%	European Society of Cardiology definition used in trials of intravenous iron; TSAT below 20% alone also predicts worse outcomes.
Hemochromatosis screening threshold	Above 45% on a fasting repeat	ACG 2019 and AASLD guidance to proceed to HFE genotyping. Above 50% in men and 45% in women detects over 90 percent of C282Y homozygotes.
Marked elevation	Above 60–70%	Non-transferrin-bound iron appears and tissue loading accelerates; typical of untreated hemochromatosis, transfusional overload and thalassemia.
After an iron tablet or infusion	Can reach 80–100% for hours (tablet) to days (infusion)	Not a true measure of iron status; hold iron for 24 hours before a tablet-free panel and avoid testing within 1 to 2 weeks of an infusion.

High iron saturation

A high transferrin saturation means more iron is circulating than transferrin was built to carry comfortably, and the first job is to decide whether that reflects the body's true state or the timing of the sample. A tablet of iron, a multivitamin or a prenatal vitamin taken in the previous day, a recent iron infusion or a large meal of red meat or liver can all push saturation above 50 percent for hours. A value above 45 percent is therefore repeated on a fasting morning sample with no iron for 24 hours before it is acted on.

If the high saturation persists, hereditary hemochromatosis is the leading explanation in people of European ancestry. About 1 in 200 to 300 Northern Europeans is homozygous for the HFE C282Y mutation, which lowers hepcidin and lets the gut absorb two to three times the normal amount of iron. Saturation rises first, often in the twenties or thirties for men and after menopause for women, and ferritin follows as stores build over years. Roughly a quarter to a third of homozygous men, and a much smaller share of women, go on to develop iron-related disease (liver fibrosis or cirrhosis, arthritis of the knuckles, diabetes, low testosterone, heart failure, bronzed skin), and the point of early detection is that regular venesection before organ damage gives a normal life expectancy.

Other causes of a high saturation are secondary iron overload (transfusions, prolonged unnecessary iron supplementation), conditions in which iron absorption is driven up by an overactive but ineffective marrow (thalassemia, myelodysplasia, sideroblastic anemia, untreated B12 deficiency), and liver disease, where damaged hepatocytes release iron and make less transferrin so the ratio rises even if total body iron is only modestly increased. Alcohol-related and fatty liver disease, chronic hepatitis C and aplastic anemia (where the marrow cannot use the iron it receives) all fit here. Ferritin, liver enzymes, a CBC and the clinical picture separate these from hemochromatosis, and HFE genotyping settles the question.

Common causes

Recent iron intake or infusion
An oral iron dose raises serum iron and saturation for 4 to 8 hours (sometimes to 80 to 100 percent); multivitamins with iron and a large red-meat or liver meal do so more modestly. Intravenous iron distorts the panel for 1 to 2 weeks. Always confirm on a fasting, tablet-free morning sample.
Hereditary hemochromatosis (HFE)
C282Y homozygosity (about 0.4 percent of non-Hispanic white Americans) or C282Y/H63D compound heterozygosity lowers hepcidin and increases absorption. Saturation is usually above 45 percent, often 60 to 90 percent, before ferritin climbs; men present at 40 to 60, women later.
Non-HFE hemochromatosis
Rarer mutations in hemojuvelin, hepcidin, transferrin receptor 2 and ferroportin cause overload in people of any ancestry, including juvenile forms presenting in the teens and twenties with heart failure and hypogonadism.
Transfusional iron overload
Each unit of red cells adds 200 to 250 mg of iron with no way to excrete it; after 20 or more units (thalassemia major, sickle cell disease on chronic transfusion, myelodysplasia, aplastic anemia) saturation approaches 100 percent and ferritin exceeds 1,000 ng/mL.
Ineffective erythropoiesis
Thalassemia intermedia and major, myelodysplastic syndromes, sideroblastic anemias and untreated B12 or folate deficiency suppress hepcidin through marrow signals (erythroferrone), so absorption rises even without transfusion.
Liver disease
Alcoholic liver disease, chronic hepatitis C, fatty liver disease and cirrhosis release iron from injured hepatocytes and reduce transferrin production, raising saturation and ferritin; about a third of people with chronic liver disease have mild iron excess without HFE mutations.
Aplastic anemia and marrow failure
When the marrow cannot make red cells, iron delivered by transferrin is not used and saturation runs high even before transfusions begin.
Hemolysis
Rapid red cell destruction releases iron into plasma faster than it can be stored, producing a transient high saturation alongside high LDH and bilirubin and low haptoglobin.
Long-term unnecessary iron supplementation
Years of iron tablets or heavily fortified supplements without a deficiency gradually raise saturation and ferritin, particularly in men and post-menopausal women, who have no regular iron loss.

Symptoms that can go with it

Usually none until iron has accumulated for years; the result is often found on a routine test
Persistent fatigue and weakness
Joint pain and stiffness, characteristically in the second and third knuckles, and later the hips, knees and ankles
Loss of libido, erectile dysfunction or loss of periods from pituitary and testicular iron
Right upper abdominal discomfort, an enlarged liver or raised liver enzymes
New diabetes or worsening blood sugar without the usual risk factors
Bronze or grey skin tone, especially on sun-exposed areas
Breathlessness, swollen ankles or palpitations from iron in the heart muscle

Low iron saturation

A low transferrin saturation means the marrow is being offered less iron than it needs. When ferritin is low as well (below 30 ng/mL, or below 45 to 100 if there is inflammation), the body's stores are empty and this is absolute iron deficiency, the most common nutritional deficiency in the world. Saturation typically falls below 15 to 20 percent before hemoglobin drops, so a low saturation with a normal hemoglobin and a low ferritin is iron deficiency without anemia, which still causes fatigue, poor exercise tolerance, hair shedding and restless legs and still needs a cause found.

When ferritin is normal or high but saturation is below 20 percent, iron is present but unavailable: functional iron deficiency. Inflammation from infection, autoimmune disease, chronic kidney disease, heart failure, obesity or cancer raises hepcidin, which traps iron inside macrophages and gut cells. This is the mechanism of anemia of chronic disease, and in kidney disease and heart failure a saturation below 20 percent predicts poorer outcomes and is the trigger for intravenous iron in guidelines, because oral iron is poorly absorbed when hepcidin is high.

The two states often coexist. A woman with heavy periods and rheumatoid arthritis, or a man with a bleeding colon polyp and heart failure, can have a ferritin of 80 ng/mL that looks reassuring while saturation is 12 percent and the marrow is starved. In those settings clinicians use the saturation, the reticulocyte hemoglobin content (below 28 to 29 pg) and sometimes the soluble transferrin receptor to decide whether iron is needed, and a trial of iron with a repeat panel at 4 to 6 weeks is itself diagnostic.

Common causes

Blood loss
Heavy menstrual bleeding (the commonest cause in women under 50), slow gastrointestinal bleeding from ulcers, gastritis, polyps, bowel cancer, inflammatory bowel disease, angiodysplasia, aspirin and NSAIDs, hemorrhoids, and frequent blood donation. Each millilitre of blood carries about 0.5 mg of iron.
Pregnancy and breastfeeding
The fetus, placenta and expanded red cell mass need about 1,000 mg of iron over a pregnancy; saturation falls in the second and third trimesters, helped along by a rising TIBC. Closely spaced pregnancies deplete stores further.
Poor absorption
Celiac disease, Helicobacter pylori infection, atrophic gastritis, gastric bypass or sleeve surgery, long-term proton pump inhibitors or antacids, and inflammatory bowel disease reduce uptake in the duodenum, where most iron is absorbed.
Inadequate intake
Unplanned vegetarian or vegan diets, restrictive eating, toddlers on large volumes of cow's milk, and diets high in tea, coffee and phytate-rich unleavened grains limit absorbable iron. Needs are highest in infancy, adolescence, menstruation and pregnancy.
Chronic kidney disease
Reduced iron absorption, blood loss through dialysis circuits and blood tests, and high hepcidin from reduced clearance and inflammation all lower saturation; iron is given when TSAT is 30 percent or below with ferritin up to 500 ng/mL.
Heart failure
Around half of people with heart failure have iron deficiency by the ferritin/TSAT definition, through gut congestion, poor absorption, aspirin and inflammation; intravenous iron improved symptoms and exercise capacity in randomised trials (FAIR-HF, AFFIRM-AHF).
Inflammation and chronic disease
Infection, rheumatoid arthritis, inflammatory bowel disease, lupus, cancer and chronic infection raise hepcidin and lower saturation while ferritin stays normal or high: functional iron deficiency.
Obesity
Fat tissue produces interleukin-6, raising hepcidin and lowering iron absorption; people with obesity have lower saturation for the same intake, and saturation improves after substantial weight loss or bariatric surgery despite reduced intake.
Endurance exercise
Foot-strike hemolysis, gut blood loss, sweat losses and a hepcidin surge for several hours after hard training lower iron status; female endurance athletes have iron deficiency rates of 20 to 50 percent in surveys.
Erythropoiesis-stimulating agents
EPO treatment in kidney disease or chemotherapy drives the marrow to consume iron faster than it can be mobilised, producing functional iron deficiency with a sharp fall in saturation unless iron is given alongside.

Symptoms that can go with it

Fatigue, low energy and reduced exercise tolerance, often before anemia develops
Breathlessness on exertion and palpitations
Pale skin, brittle nails, hair shedding
Restless legs at night (iron deficiency is a common, treatable cause)
Cravings for ice or non-food substances (pica)
Sore tongue, cracked mouth corners, difficulty swallowing
Headaches, poor concentration, feeling cold, low mood
Heavy periods, black stools or other signs of the source of loss

Read it alongside

Ferritin — low saturation with ferritin below 30 ng/mL is absolute iron deficiency; low saturation with ferritin above 100 is functional deficiency from inflammation; high saturation with ferritin above 300 (men) or 200 (women) suggests overload.
TIBC and serum iron — the two numbers saturation is built from; a high TIBC with low iron (deficiency) and a low TIBC with high iron (overload or liver disease) produce the extremes.
CRP — explains a high ferritin and warns that ferritin up to about 100 ng/mL may be masking iron deficiency when saturation is low.
Hemoglobin, MCV and RDW — show whether the iron problem has reached the red cells; small cells with a high RDW mean established iron-deficiency anemia.
Reticulocyte hemoglobin content (Ret-He) — below 28 to 29 pg confirms the marrow is short of iron today, useful when ferritin and saturation disagree.
ALT, AST and GGT — raised in hemochromatosis and in the liver diseases that mimic it; ferritin above 1,000 ng/mL with raised enzymes prompts assessment for fibrosis.
HFE genotype (C282Y, H63D) — the confirmatory test when fasting saturation stays above 45 percent, and the screening test for first-degree relatives.
Glucose or A1C, testosterone and an echocardiogram — assess the organs iron damages when overload is confirmed.

What usually happens next

Any abnormal saturation is confirmed on a fasting morning sample with iron supplements and multivitamins held for 24 hours, together with ferritin and CRP if they were not already measured.
For a confirmed low saturation, the questions are the source of loss and the state of absorption: menstrual history, diet, gut symptoms, aspirin or NSAID use, a celiac antibody test, and, in men and post-menopausal women, upper and lower gastrointestinal endoscopy to exclude a bleeding lesion. Treatment is iron, oral first unless inflammation, kidney disease, heart failure or intolerance makes intravenous iron the better route, with a repeat panel and CBC at 4 to 6 weeks.
For a confirmed saturation above 45 percent, expect HFE genotyping and liver enzymes; if you are C282Y homozygous or compound heterozygous and ferritin is raised, venesection (removing about 450 to 500 mL of blood weekly or fortnightly until ferritin is 50 to 100 ng/mL, then a few times a year) is the treatment, and ferritin above 1,000 ng/mL prompts elastography or biopsy for liver fibrosis.
If you have hemochromatosis, your parents, siblings and children should be offered iron studies and genotyping, since siblings have a 1 in 4 chance of being affected.
If saturation is low but ferritin is normal and you have kidney disease, heart failure or an inflammatory condition, ask whether you meet the guideline thresholds for iron treatment (TSAT below 20 to 30 percent), since oral iron works poorly in these settings and intravenous iron improves symptoms.

Diet, lifestyle and natural levers with evidence

What can move TSAT once the cause is known. Nothing here replaces finding the cause.

Iron-rich foods paired with vitamin C (for low saturation from deficiency)

Strong evidence

Heme iron from red meat, poultry, fish and shellfish is absorbed at 15 to 35 percent; non-heme iron from lentils, beans, tofu, fortified cereals, pumpkin seeds and dark greens at 2 to 20 percent, and this second figure is the one you can change. In isotope studies, 25 to 100 mg of vitamin C eaten with a plant-based meal raised non-heme iron absorption two- to fourfold by keeping iron in its absorbable ferrous form, while meat in the same meal roughly doubled it. A vitamin C tablet taken with an iron supplement, however, added nothing to the hemoglobin response in a 2020 randomised trial of 440 adults, so the lever is about meals. Dietary change corrects mild deficiency over 3 to 6 months; established anemia usually needs a supplement.

Confirm deficiency with ferritin first. Extra iron, and vitamin C supplements above about 500 mg a day, should be avoided in hemochromatosis, thalassemia and chronic liver disease.

Oral iron: dose and alternate-day timing (for confirmed deficiency)

Strong evidence

Ferrous sulfate, fumarate or gluconate providing 60 to 120 mg of elemental iron raises hemoglobin by about 1 g/dL every 2 to 3 weeks and brings saturation back above 20 percent within 1 to 2 months, with ferritin recovering over 3 to 6 months. Stable-isotope trials from Zurich showed each dose raises hepcidin for 24 to 48 hours and blocks the next, so a single morning dose every other day is absorbed about a third more efficiently per dose than daily dosing; follow-up randomised trials in iron-deficient women found alternate-day dosing produced hemoglobin and ferritin gains comparable to daily dosing over 2 to 3 months with fewer gastrointestinal side effects. Splitting a dose into twice daily lowers total absorption.

Nausea, constipation and black stools are common. Take 1 to 2 hours away from tea, coffee, dairy, calcium, antacids and levothyroxine. Iron tablets are a major cause of accidental poisoning in children under 6; store them out of reach. Oral iron works poorly when CRP is high or in kidney disease and heart failure, where intravenous iron is used.

Timing iron away from tea, coffee and calcium

Moderate evidence

Single-meal isotope studies found black tea with a meal reduced non-heme iron absorption by 60 to 90 percent and coffee by 40 to 60 percent, through polyphenols that bind iron in the gut; 300 to 600 mg of calcium (a large glass of milk, a slice of cheese or a calcium tablet) roughly halved absorption of both heme and non-heme iron in the same meal, although long-term studies suggest the body partly adapts. Taking tea, coffee and calcium 1 to 2 hours away from iron-rich meals or supplements removes most of the effect, and vitamin C in the meal offsets much of the rest. For someone with a low saturation on oral iron, this is often the difference between a response and no response.

Cooking in cast-iron cookware

Moderate evidence

Acidic, moist foods simmered in cast iron pick up several milligrams of iron per serving, more with longer cooking and newer pans. A randomised trial in Ethiopian children found meals from iron pots raised hemoglobin about 1.3 g/dL more than meals from aluminium pots over a year, and a systematic review of trials found a positive effect on hemoglobin or iron status in most low-income settings, though a Cambodian trial of iron ingots added to cooking pots showed no benefit. It is a maintenance measure for marginal intake rather than a treatment for established deficiency.

Avoid in hemochromatosis and other iron-overload conditions.

Diet measures in hemochromatosis (for high saturation): tea with meals, limiting alcohol and vitamin C supplements, avoiding raw shellfish

Moderate evidence

Venesection is the treatment for hemochromatosis, and no diet replaces it, but a few measures reduce iron absorption or risk. In a controlled study of 18 people with hemochromatosis followed for a year, drinking black tea with meals reduced iron absorption and slowed iron re-accumulation enough to cut the number of venesections needed by about a third. Alcohol increases iron absorption, lowers hepcidin and multiplies liver damage, so guidelines advise keeping intake low and avoiding it entirely with liver fibrosis. Vitamin C supplements above about 500 mg a day increase absorption and mobilise iron and are not recommended, and raw or undercooked shellfish carries a risk of Vibrio vulnificus infection, which is far more severe in people with iron overload. Red meat and iron-fortified foods need not be eliminated, since their contribution is small compared with weekly venesection.

These measures are adjuncts to, not substitutes for, venesection and specialist follow-up. People with hemochromatosis should avoid iron and vitamin C supplements and check multivitamin labels.

Weight loss in obesity-related low saturation

Preliminary evidence

Obesity raises hepcidin through interleukin-6 from fat tissue, lowering iron absorption and saturation independent of intake. Small prospective studies found that hepcidin fell and transferrin saturation and iron absorption rose within 6 months of bariatric surgery despite reduced food intake, and diet-induced weight loss of around 10 percent lowered hepcidin and improved iron markers in overweight women in short trials. The effect is modest and the evidence is limited to small studies, so it complements rather than replaces treating any deficiency.

When to see a clinician promptly

A fasting transferrin saturation above 45 percent with a raised ferritin, particularly with joint pain, fatigue, raised liver enzymes, diabetes, low libido or a family history of hemochromatosis: HFE testing and, if confirmed, venesection prevents organ damage.
A ferritin above 1,000 ng/mL with high saturation, which raises the risk of liver fibrosis and needs specialist assessment.
Low saturation with iron deficiency in a man or a post-menopausal woman, or with black or bloody stools, weight loss or a change in bowel habit: a gut bleeding source must be excluded.
A hemoglobin below 7 to 8 g/dL, or anemia with chest pain, breathlessness at rest, fainting or a racing heart.
Iron deficiency that has not improved after 4 to 6 weeks of oral iron, suggesting ongoing loss, malabsorption or the need for intravenous iron.
Breathlessness, ankle swelling, palpitations or new diabetes in someone known to have iron overload, which can signal heart or pancreatic involvement.

Frequently asked questions

What is a normal iron saturation percentage?

About 20 to 50 percent in adults, with some laboratories using 15 to 50 or 20 to 45 percent; women average a few points lower than men. Below 20 percent (and especially below 15 to 16 percent) points to iron deficiency or iron trapped by inflammation, and above 45 percent on a fasting morning sample points to iron overload. Because serum iron swings through the day, a value just outside the range is repeated before anything is concluded.

What does low iron saturation with normal ferritin mean?

Most often that inflammation is holding iron in storage: ferritin rises with infection, autoimmune disease, kidney disease, heart failure, obesity and cancer, so a 'normal' ferritin of 60 to 100 ng/mL can coexist with a marrow that is short of iron. It can also be early iron deficiency in someone whose ferritin has not yet fallen below the cut-off, an afternoon sample, or pregnancy. A CRP, a reticulocyte hemoglobin content and sometimes a trial of iron sort it out; in kidney disease and heart failure a saturation below 20 percent is treated regardless of ferritin.

Is an iron saturation of 50 or 55 percent high?

Mildly, and worth repeating. Values of 45 to 55 percent are common for a few hours after an iron tablet, a multivitamin or a large red-meat meal, and are a few points higher in the morning. If a fasting morning repeat with no iron for 24 hours is still above 45 percent, guidelines recommend HFE genotyping and a ferritin and liver enzyme check, because this is the earliest sign of hereditary hemochromatosis. Saturations of 70 to 100 percent are typical of untreated hemochromatosis or transfusional overload.

What iron saturation indicates hemochromatosis?

A fasting saturation above 45 percent is the screening threshold used by the American College of Gastroenterology and the American Association for the Study of Liver Diseases; above 50 percent in men and 45 percent in women identifies more than 90 percent of people homozygous for the C282Y mutation. Saturation alone does not diagnose the condition: it leads to HFE gene testing, and iron overload is confirmed by a raised ferritin (above 300 ng/mL in men or 200 in women) with other causes excluded.

Can iron saturation be low but ferritin high?

Yes, and the combination is common in hospital and in chronic illness. It is the signature of anemia of chronic disease or functional iron deficiency: hepcidin, raised by inflammation, traps iron in storage cells, so ferritin (storage) is high while saturation (delivery) is low. It also occurs in chronic kidney disease, heart failure, liver disease and cancer, and after intravenous iron when ferritin has been pushed up. In these settings ferritin cannot be used alone to decide whether iron is needed.

How do I raise my iron saturation?

By correcting the deficiency and its cause. Oral iron (60 to 120 mg elemental iron daily or on alternate days, away from tea, coffee and calcium) raises saturation above 20 percent within 1 to 2 months in most people with absolute deficiency, alongside iron-rich meals with vitamin C. If inflammation, kidney disease, heart failure or malabsorption is the reason, oral iron is often ineffective and intravenous iron is used. Raising saturation without finding out why it was low, especially in men and post-menopausal women, risks missing a bleeding source.

Does iron saturation change during the day?

Yes, more than most blood tests. Serum iron, the numerator, is highest between about 6 and 10 in the morning and falls by 20 to 30 percent by evening, varies by 20 to 30 percent from one day to the next, and rises for 4 to 8 hours after an iron tablet or an iron-rich meal. TIBC is stable, so the saturation swings with serum iron. Fasting morning samples with iron supplements held for 24 hours give the most reliable result and are what hemochromatosis guidelines specify.

Should I stop taking iron before an iron saturation test?

Usually yes, for 24 hours, unless your clinician wants to see the effect of treatment. A dose taken that morning or the night before can push saturation to 80 to 100 percent and serum iron far above normal, giving a false impression of overload. Multivitamins and prenatal vitamins with iron have the same effect on a smaller scale. After an iron infusion, wait 1 to 2 weeks before testing. Ferritin is less affected by a single dose but still rises for days after an infusion.

References

Iron tests. MedlinePlus, US National Library of Medicine (2023)View source
Hemochromatosis. Mayo Clinic (2023)
Hereditary hemochromatosis. Merck Manual Professional Version (2024)
Kowdley KV, Brown KE, Ahn J, Sundaram V. ACG clinical guideline: hereditary hemochromatosis. American Journal of Gastroenterology (2019)
Bacon BR, Adams PC, Kowdley KV, Powell LW, Tavill AS. Diagnosis and management of hemochromatosis: 2011 practice guideline by the American Association for the Study of Liver Diseases. Hepatology (2011)
Adams PC, Reboussin DM, Barton JC, et al.. Hemochromatosis and iron-overload screening in a racially diverse population (HEIRS). New England Journal of Medicine (2005)
Ganz T. Hepcidin and iron regulation, 10 years later. Blood (2011)
Kidney Disease: Improving Global Outcomes (KDIGO) Anemia Work Group. KDIGO clinical practice guideline for anemia in chronic kidney disease. Kidney International Supplements (2012)
Anker SD, Comin Colet J, Filippatos G, et al.. Ferric carboxymaltose in patients with heart failure and iron deficiency (FAIR-HF). New England Journal of Medicine (2009)
Dale JC, Burritt MF, Zinsmeister AR. Diurnal variation of serum iron, iron-binding capacity, transferrin saturation, and ferritin levels. American Journal of Clinical Pathology (2002)
Kaltwasser JP, Werner E, Schalk K, Hansen C, Gottschalk R, Seidl C. Clinical trial on the effect of regular tea drinking on iron accumulation in genetic haemochromatosis. Gut (1998)
Stoffel NU, Cercamondi CI, Brittenham G, et al.. Iron absorption from oral iron supplements given on consecutive versus alternate days and as single morning doses versus twice-daily split dosing in iron-depleted women: two open-label, randomised controlled trials. Lancet Haematology (2017)

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This page is educational and is not medical advice or a diagnosis. Lab results have to be interpreted together with your history, symptoms and other results by a clinician who knows you. Do not start or stop a supplement to change a lab value before the cause is known.