Each marker below carries its technical name, what it measures in plain language, the limits of what it can tell you, and the nutrients known to move it. Where a framework and mainstream practice disagree, both views are shown rather than one being hidden.
Toxic Elements & Halogens (the overlooked half)
Whether something is occupying the seat a nutrient was meant to sit in. This is a tier-one entry not because everyone needs a full toxic-element workup, but because almost nobody is offered one at all -- and a standard panel is silent on it. Deficiency gets investigated. The other half of the equation usually does not.
Typical range: There is no single number here. Blood lead and mercury reflect recent exposure rather than what is stored in tissue; a normal blood level does not rule out a body burden accumulated over years. Aluminium and glyphosate are not on any standard panel at all. That absence is the point of this entry -- it is a gap in the usual workup, not a result.
Nutrients that move it
- Displacement is chemistry, not a hypothesissolid -- Elements that sit near each other on the periodic table share charge and size, and transport proteins select on charge and size. So the wrong element gets carried through the right door. This is established biochemistry with named machinery, not an association waiting for a trial. The sodium-iodide symporter is the thyroid's iodine door, and perchlorate, thiocyanate, nitrate and fluoride all compete at it (source: PMC6466022). DMT1, the divalent metal transporter, carries iron -- and also manganese, cadmium, cobalt and lead, because they present to it the same way (source: PMID 22736759). Metallothionein binds zinc and copper, and cadmium binds it harder and displaces them (source: PMC5486060, PMID 21462106).
- Being deficient makes you absorb more of the wrong thingsolid -- This is the part that joins the two halves of the model. DMT1 is upregulated when iron is low -- the body opens the door wider because it needs iron (source: PMID 25753988) -- and the same widened door admits lead and cadmium. So deficiency does not merely sit alongside toxicity; it actively increases uptake of it. Sufficiency is therefore the first line of defence: iodine against the halogen group, and adequate iron, zinc, calcium and selenium across the metals.
- Where to look if you suspect itemerging -- If exposure is plausible -- older housing, occupational contact, well water, heavy fish intake, dental history, agricultural proximity -- the honest move is to look at the whole set rather than one element, because they arrive together and compete together. Tier 3 on this page carries lead, mercury, aluminium and PFAS individually. Tissue-level elemental screening measures the whole panel at once rather than one at a time.
Food first: The protective pattern is unglamorous and consistent: sufficient minerals so there is no vacancy to fill, adequate protein for the conjugation pathways, sulphur-bearing vegetables such as brassicas, garlic and onions, and enough fibre to carry conjugated compounds out rather than allowing reabsorption. Iodine sufficiency specifically, because the halogen competition is at a single named door. Filtered water, and reducing the intake side wherever it is identifiable.
Read the studies on Toxic Elements & Halogens (the overlooked half)Lead
The level of a toxic heavy metal with no known safe or beneficial level in the body, accumulating in bone and affecting the brain, kidneys, and cardiovascular system with chronic exposure.
Typical range: Standard: under 3.5 mcg/dL is the current CDC reference/action level for adults -- there is no optimal nonzero level; lower is always better.
Nutrients that move it
- Calcium -- Competes with lead for absorption in the gut and for storage sites in bone; a randomized placebo-controlled trial in pregnant women found calcium supplementation reduced blood lead levels by about 11% compared to placebo.
- Iron -- Iron deficiency increases intestinal lead absorption (the gut appears to substitute lead for iron when iron is scarce); iron repletion in iron-deficient individuals modestly lowers blood lead.
- Vitamin C -- Observational data associates adequate vitamin C status with lower lead absorption, though dedicated high-quality RCT evidence is thinner than for calcium/iron.
- Zinc -- Observational data associates adequate zinc status with lower lead absorption, though dedicated high-quality RCT evidence is thinner than for calcium/iron.
Food first: Ensure adequate dietary calcium, iron, and vitamin C, especially in children and pregnant women (the highest-risk groups for lead's neurodevelopmental effects).
When to see someone: Nutritional strategies reduce absorption of *ongoing* low-level exposure -- they do not treat significant lead toxicity, which requires medical evaluation and, in some cases, chelation therapy. Any meaningfully elevated lead level needs a source investigation, not just a supplement response.
Read the studies on LeadMercury
The level of a toxic heavy metal, most commonly elevated in adults from eating fish/seafood higher on the food chain.
Typical range: Standard: under 10 mcg/L (whole blood) is a commonly used general-population reference, though this varies by lab and by whether inorganic vs. methylmercury is being measured; there is no optimal nonzero level.
Nutrients that move it
- Selenium -- Binds mercury (forming inert mercury selenide) and is a cofactor for antioxidant enzymes that counter mercury's oxidative damage; animal and cell studies show a clear protective relationship, but robust human RCT evidence that selenium supplementation reverses mercury toxicity in people is still limited.
Food first: Choose lower-mercury fish (salmon, sardines, shrimp, cod) over high-mercury species (swordfish, king mackerel, shark, bigeye tuna) to get omega-3 benefits without excess mercury load; adequate selenium intake is theoretically protective but shouldn't be a reason to eat high-mercury fish liberally.
When to see someone: Elevated mercury in pregnant women or young children warrants dietary source investigation and possibly medical guidance given fetal/childhood neurodevelopmental sensitivity; don't rely on selenium supplementation as a way to "offset" ongoing high-mercury fish consumption.
Read the studies on MercuryAluminum
Serum aluminum is the standard test, and what it means depends almost entirely on kidney function. With normal kidneys the body clears aluminum efficiently, so serum levels are usually low and not very informative about tissue burden. Urine aluminum reflects recent exposure and excretion capacity and is used in research protocols.
Typical range: There is no meaningful optimal level -- aluminum has no biological role. The marker becomes genuinely actionable in one specific population: people with impaired kidney function, especially dialysis patients, where aluminum is renally cleared and dialysis does not remove it efficiently. Periodic monitoring is standard of care there.
Nutrients that move it
- Silicic acid (silicon-rich mineral water)emerging -- Silicon appears to reduce aluminum's bioavailability and promote urinary excretion, probably by forming a complex the body does not absorb. A 12-week pilot gave 15 Alzheimer's patients 1 litre a day of silicon-rich water; urinary aluminum excretion rose without affecting iron or copper, and body burden fell. It was small, uncontrolled and unblinded, and the authors framed it as a preliminary test of a hypothesis -- not a treatment.
- Magnesiumcontested -- Magnesium and aluminum compete for some of the same intestinal transport sites, so adequate magnesium is sometimes proposed to reduce absorption. That is plausible chemistry and it is not backed by a dedicated human aluminum-reduction trial.
- Adequate hydrationsolid -- The kidney is the main clearance route for absorbed aluminum, so anything supporting normal renal function supports clearance. This is normal physiology working as intended rather than a targeted intervention.
Food first: Silicon-rich mineral water, adequate magnesium, and enough fluid to support normal kidney function.
Read the studies on AluminumPFAS (per- and polyfluoroalkyl substances)
A serum or plasma panel that sums seven to nine individually measurable PFAS compounds -- PFOA, PFOS, PFHxS, PFNA, PFDA, PFUnDA and MeFOSAA -- rather than reporting "PFAS" as one number. There are thousands of these chemicals and only a handful can be measured and interpreted reliably. They are called forever chemicals because the carbon-fluorine bond barely breaks down, so they persist in the body for years.
Typical range: The National Academies (NASEM, 2022) published numeric action tiers, which is unusual for a toxin panel: under 2 ng/mL summed is usual standard of care; 2 to under 20 ng/mL means counselling on exposure reduction plus screening for dyslipidemia and pregnancy hypertension; 20 ng/mL and above adds thyroid testing, and kidney assessment over 45.
Nutrients that move it
- Dietary fiberemerging -- An NHANES analysis of 6,482 adults found higher fiber intake associated with lower serum PFAS, plausibly because fiber binds bile acids and interrupts the recirculation that keeps PFAS in the body. This is a cross-sectional association, not a trial showing that adding fiber lowers an individual's level -- but it is low-risk and healthy regardless.
- Blood or plasma donationsolid -- The strongest evidence of anything tried. A randomized trial of 285 Australian firefighters found plasma donation every 6 weeks lowered mean serum PFOS by 2.9 ng/mL versus 1.1 for whole-blood donation, still present 3 months after the trial. It works by physically removing the blood proteins PFAS binds to -- it is direct removal, not a detox mechanism.
- Filtered drinking watersolid -- Activated carbon and reverse osmosis remove PFAS from water at the tap. This prevents FUTURE accumulation and does not lower what is already in the blood -- which makes it the most reliable lever available, and a different job from reducing existing burden.
Food first: Fiber-rich whole foods, filtered drinking water, and reduced exposure at source -- PFAS-free cookware and food packaging where practical, and care with fish from known-contaminated waters.
When to see someone: Any product marketed as a PFAS detox should be treated skeptically -- the evidence-backed list is short: donation, prescription bile-acid binders under supervision, dietary fiber, and removing the exposure source.
Read the studies on PFAS (per- and polyfluoroalkyl substances)Whole-Blood / Hair Mineral Analysis (HTMA)
Cellular Six: TransformThis 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.
How it is used clinically
HTMA's reliability is genuinely contested even outside the functional model specifically. **[CONTESTED]** A landmark study sent split samples from a single healthy volunteer to six US commercial hair-testing labs and found more than 10-fold differences in reported concentrations for 12 different minerals between labs. (cite: JAMA, 2001, PMID 11150111) More recent work confirms that intra- and inter-laboratory reliability for HTMA remains inconsistent and heavily dependent on which lab and methodology is used, and correlation between hair mineral levels and actual serum/tissue status is weak to moderate for most minerals (hair zinc versus serum zinc correlates only weakly, for example). (cite: PMC3582931) HTMA is on firmer ground for detecting toxic heavy metals (lead, mercury, cadmium, arsenic), where peer-reviewed and CDC/ATSDR biomonitoring methods have more established validity -- but using it to diagnose "metabolic types," mineral-ratio-based disease patterns, or to guide the functional model's specific mineral-dosing decisions is not supported by controlled clinical evidence.
What this framework claims
HTMA and mineral-ratio analysis are used by some the functional model-adjacent practitioners to infer "oxidation type," adrenal/thyroid patterns, and mineral dysregulation not visible on standard blood work.
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.
Read the studies on Whole-Blood / Hair Mineral Analysis (HTMA)