Iron Transport

This marker sits in Exchange -- moving iron across boundaries and handing it between carriers.

Serum iron is circulating iron at the moment of the draw; ferritin reflects iron stores (but is also an acute-phase inflammatory protein); TIBC reflects how much transferrin (the iron-carrier protein) is available; transferrin saturation is the percentage of that capacity currently in use.

Typical range: Ferritin ~15-150 ng/mL (women), ~20-250 ng/mL (men), lab-dependent; serum iron ~60-170 mcg/dL; saturation 20-50%; TIBC 250-450 mcg/dL (conventional ranges, consistent with mainstream lab medicine).

Food first: Heme iron (red meat, poultry, fish) is more bioavailable than plant iron; pair plant iron with vitamin C; ensure adequate riboflavin (dairy, eggs, leafy greens, organ meats) and copper (liver, shellfish) as supporting cofactors.

When to see someone: Iron overload -- from hereditary haemochromatosis or from sustained over-supplementation -- causes irreversible damage to the liver, heart and pancreas, so a confirmed deficiency should come before iron is added. A genuinely abnormal panel, particularly a raised transferrin saturation with a raised ferritin, warrants a standard workup including consideration of HFE genetic testing rather than a self-directed mineral protocol. Ferritin is always read alongside CRP.

This marker sits in Exchange -- moving iron across boundaries and handing it between carriers.

Total circulating copper, of which roughly 95% is normally bound to ceruloplasmin and about 5% is loosely bound to albumin and small peptides (the "free" or "non-ceruloplasmin-bound" fraction).

Typical range: Roughly 70-140 mcg/dL for men, 80-155 mcg/dL for women (ranges vary somewhat by lab/method).

Food first: Beef/chicken liver, oysters and shellfish, cacao are copper-dense whole foods the functional model favors; standard nutrition guidance agrees these are good copper sources for people with confirmed low intake or deficiency.

When to see someone: Copper has a genuinely narrow window in both directions. Overload is Wilson's disease, a genetic condition causing serious liver and neurological damage that needs hepatology or genetics management. A raised serum copper on its own should prompt checking ceruloplasmin and ruling out inflammation, pregnancy or oestrogen therapy -- all of which raise it -- before it is read as dysregulation.

This marker sits in Exchange -- moving iron across boundaries and handing it between carriers.

The major copper-transport protein made in the liver; it carries the large majority of circulating copper and functions as a ferroxidase enzyme, oxidizing ferrous iron (Fe2+) to ferric iron (Fe3+) so iron can bind to transferrin and be moved and stored safely. This ferroxidase role is well-established, mainstream biochemistry. **[SOLID]** (source: Vashchenko G, MacGillivray RT, Nutrients, 2013; StatPearls, NCBI Bookshelf)

Typical range: Roughly 20-40 mg/dL in most adult reference ranges (some labs cite 27-37 mg/dL); varies by assay.

Food first: Copper-rich foods (liver, shellfish) support the substrate side; retinol-rich foods (liver, egg yolk, dairy fat, cod liver oil) are the the functional model-favored vitamin A source, on the theory that preformed retinol (not beta-carotene) is what's needed.

When to see someone: A low ceruloplasmin together with a high non-ceruloplasmin-bound ("free") copper and/or neurological or liver symptoms warrants a Wilson's disease workup with a specialist -- this is a serious genetic condition, not something to self-manage with a mineral protocol.

This marker sits in Exchange -- moving iron across boundaries and handing it between carriers.

the functional model calculates a ratio between total serum copper and ceruloplasmin (or ceruloplasmin-bound copper) to estimate how much circulating copper is "unbound"/not carried by ceruloplasmin. The closest validated mainstream analog is **non-ceruloplasmin-bound copper (NCC)**, calculated as total serum copper minus the copper accounted for by measured ceruloplasmin, used in specialist hepatology/Wilson's-disease practice.

Typical range: There is no widely recognized, standardized "normal" copper:ceruloplasmin ratio in mainstream lab medicine. For the related NCC calculation used in Wilson's disease diagnostics, values above roughly 25 mcg/dL (with a low ceruloplasmin) are suggestive of Wilson's disease, but cutoffs vary meaningfully by lab and assay and are not standardized for general population screening. (source: Journal of Trace Elements in Medicine and Biology, non-ceruloplasmin-bound copper across laboratories)

Food first: No dedicated evidence-based nutrition protocol exists for "lowering the unbound copper fraction" outside the Wilson's disease context; general copper/retinol/magnesium sufficiency is the functional model's proposed lever.

When to see someone: A genuinely elevated unbound/free copper fraction, especially with low ceruloplasmin, is a marker of a serious medical condition (Wilson's disease) requiring a hepatologist or geneticist -- a self-calculated ratio from routine labs should never be used to diagnose or rule out Wilson's disease, and should not delay a proper specialist workup if clinically suspected.

This marker sits in Transform -- the cofactors enzymes need to turn fuel into usable energy.

Magnesium concentration inside red blood cells, which -- because RBCs live about 120 days -- reflects a longer-term, more stable snapshot of intracellular magnesium status than serum magnesium, which represents less than 1% of total body magnesium and can shift acutely with stress hormones. This physiological rationale (serum magnesium as a poor proxy for tissue status) is well-supported. **[SOLID]**

Typical range: Roughly 4.0-6.8 mg/dL depending on the lab (e.g., Quest ~4.0-6.4 mg/dL, LabCorp ~4.2-6.8 mg/dL).

Food first: Leafy greens, nuts, seeds, legumes, whole grains, dark chocolate; supplemental forms like magnesium glycinate or citrate are generally better tolerated than oxide.

When to see someone: Anyone with reduced kidney function (low eGFR) needs medical guidance before supplementing magnesium at the functional model-recommended doses -- magnesium is renally cleared and can accumulate to dangerous levels in kidney disease. High-dose oral magnesium commonly causes diarrhea before anything more serious in people with normal kidneys.

This marker sits in Maintain -- the cleanup and defence system, and whether it is switched on.

A liver-produced marker of systemic inflammation, standard in cardiology risk assessment.

Typical range: <1.0 mg/L low cardiovascular risk, 1.0-3.0 average, >3.0 high risk (standard AHA/CDC cutoffs).

Food first: Mediterranean-pattern eating, weight management, smoking cessation -- these move hs-CRP more reliably than any single mineral intervention.

When to see someone: hs-CRP rises with any acute infection, injury, or recent exercise/dental work -- a single elevated reading isn't meaningful in isolation.

This marker sits in Exchange -- moving iron across boundaries and handing it between carriers.

Serum zinc reflects circulating zinc status (an imperfect marker, since most zinc is intracellular); the zinc:copper (or copper:zinc) ratio compares the two minerals, which compete for absorption via intestinal metallothionein.

Typical range: Serum zinc roughly 60-120 mcg/dL. A reference interval for the plasma copper/zinc ratio of about 0.54-1.68 has been established in healthy women of childbearing age; the functional model and some functional-medicine sources cite a narrower "optimal" ratio of roughly 0.7-1.0, which is an opinion range, not a diagnostic cutoff. (source: Nutrients, 2021, PMC7999022)

Food first: Balance zinc-rich foods (oysters, red meat, seeds) with copper-rich foods (liver, shellfish, cacao) rather than supplementing either in isolation long-term without monitoring.

When to see someone: Chronic zinc supplementation above ~40 mg/day risks copper deficiency and its neurological/hematologic consequences; anyone on long-term zinc should have copper status periodically checked.

This marker sits in Transform -- the cofactors enzymes need to turn fuel into usable energy.

Hair tissue mineral analysis (HTMA) measures mineral and trace-element concentrations in a hair sample, marketed as a window into longer-term tissue mineral status; the functional model sometimes references whole-blood or hair testing as a supplementary way to assess mineral patterns beyond a standard serum panel.

Typical range: No standardized reference ranges exist across labs; each commercial HTMA lab uses its own ranges and often its own proprietary "ratio" interpretive system.

Food first: N/A.

When to see someone: Don't make major supplementation decisions (especially involving iron, copper, or high-dose minerals) based solely on an HTMA result -- confirm with standard serum/blood testing, since HTMA's inter-lab reliability for general mineral status is weak.

This marker sits in Build -- the raw material for making and renewing structure.

Serum retinol reflects circulating, "storage-form" vitamin A status, though serum levels are homeostatically buffered and don't fall until liver stores are substantially depleted.

Typical range: Roughly 20-60 mcg/dL in most adult reference ranges (some labs cite 28-86 mcg/dL); levels at or below ~20 mcg/dL suggest moderate deficiency, ≤10 mcg/dL suggests severe deficiency.

Food first: Liver, egg yolks, full-fat dairy, and (per the functional model) cod liver oil are preformed-retinol sources; orange/yellow vegetables provide beta-carotene, a precursor the body converts to retinol at a variable and self-limiting rate.

When to see someone: Preformed vitamin A (retinol, as in cod liver oil and liver) has real toxicity risk that beta-carotene does not. Intakes above roughly 10,000 IU/day (3,000 mcg RAE) of preformed retinol during pregnancy are linked to increased birth-defect risk, with clearer teratogenic signal above 25,000-30,000 IU/day; a single very high acute dose (>100,000 IU) in early pregnancy is a recognized teratogenic risk. (cite: Rothman KJ et al., NEJM, 1995; EFSA Scientific Opinion, 2024) Pregnant or potentially pregnant women should not start high-dose cod liver oil or retinol supplementation without discussing dose with a clinician. Chronic high-dose preformed vitamin A in anyone can cause liver toxicity, bone pain, and headaches (hypervitaminosis A).

This marker sits in Exchange -- moving iron across boundaries and handing it between carriers.

The hormone that controls how much iron enters the bloodstream at all. Made in the liver, hepcidin binds the iron exporter ferroportin on gut and macrophage cells and degrades it, which shuts the door on both dietary absorption and the recycling of iron out of storage. It is the master regulator, and it is the reason iron status is a question of traffic control rather than intake. **[SOLID]** (source: Hepcidin and Iron in Health and Disease, 2023)

Typical range: Assay-dependent and not yet standardised across laboratories, which is the main practical limitation of ordering it. Interpret it against the reporting range of the specific lab, and against ferritin and CRP drawn at the same time.

Food first: There is no food that lowers hepcidin directly. The honest answer is that this marker points upstream: it tells you to look for the inflammatory driver rather than to add iron, and adding iron against a high hepcidin is the specific mistake it exists to prevent.

When to see someone: A raised hepcidin with low serum iron is not a reason to supplement iron. Iron given into an inflammatory state is poorly absorbed and adds oxidative load. This is one of the clearest cases where the correct action is the opposite of the intuitive one.

This marker sits in Exchange -- moving iron across boundaries and handing it between carriers.

How loudly the tissues are asking for iron. Cells that need iron put more transferrin receptors on their surface, and a soluble fragment of those receptors appears in the blood. Unlike ferritin, sTfR is not an acute-phase reactant, so it does not rise with inflammation -- which is precisely why it is useful when ferritin cannot be trusted. **[SOLID]** (source: Iron-related Biomarkers in the Diagnosis and Management of Iron Disorders, 2024)

Typical range: Assay-specific. Frequently reported alongside the sTfR/log-ferritin index, which combines demand and storage into one figure and separates the two common pictures more cleanly than either number alone.

Food first: Where sTfR is genuinely raised, the tissues are asking for iron and the usual food levers apply: haem iron from red meat and shellfish, non-haem sources paired with vitamin C, and attention to whatever is limiting absorption.

When to see someone: sTfR is not affected by inflammation, but it IS raised by anything that increases red cell production, including haemolysis and recent altitude exposure. Read it beside a blood count rather than alone.

How much haemoglobin is actually being packed into the newest red blood cells, made in the last few days. Because reticulocytes are young, this is close to a real-time readout of the iron supply reaching the bone marrow, where ferritin reports a storage balance accumulated over months. **[SOLID]** (source: Transferrin saturation versus reticulocyte hemoglobin content for iron deficiency, 2003)

Typical range: Commonly reported around 28-35 pg depending on analyser, with values below roughly 28 pg treated as suggesting functional iron restriction. Analyser-dependent, so use the reporting laboratory's range.

Food first: The same levers as iron repletion, with the advantage that this marker will tell you within a couple of weeks whether they are landing.

When to see someone: Analyser-dependent, and not comparable between laboratories using different instruments. Track it in the same lab or the trend means nothing.