The concept of metabolic individuality is not new. What has never existed is a laboratory test that identifies which sort of metabolism you have. I want to be clear about that before the markers, because earlier versions of this article were not.
Here is the division of labour as Metabolic Natures actually applies it. The questionnaire captures the pattern you recognise in yourself — long-standing tendencies in appetite, energy, thermoregulation and stress response. It is a starting hypothesis, not a measurement, and nothing measures constitution. The panels below describe something different and more concrete: what your biochemistry is doing now.
That is not a lesser question. It is the question that decides where a protocol starts, because the current constraint governs the protocol until it clears. But a panel taken today reports today. Bicarbonate, triglycerides and total protein all move with recent diet, hydration, illness and training load, and a marker that moves with last week's eating cannot be a window onto anything constitutional.
What follows is an orientation to the markers most used in this framework, with the evidence for each stated at the strength it actually has. Where a claim is mechanistic and untested, it says so.
What this is, and what the evidence for it actually is
Metabolic Natures is a framework for deciding where to start, not a test result.
The general idea is well supported: people do better on different balances of food, and the balance someone can actually sustain is the one that works. Dansinger and colleagues randomised 160 people to four named diets for a year and found weight loss correlated with how well people stuck to the plan (r = 0.60) and essentially not at all with which plan it was (r = 0.07, not significant). DOI
The specific categories are not validated by controlled trials, and we do not claim they are. No trial has tested whether assigning someone to an oxidative or autonomic category, and matching a macronutrient ratio to it, produces a better result. The closest test of that shape of argument is DIETFITS — 609 adults, healthy low-fat against healthy low-carbohydrate, twelve months, a difference of 0.7 kg between arms, and neither a genotype pattern nor baseline insulin secretion predicted which diet suited whom. DOI DIETFITS did not test oxidation rate or autonomic tone, so it is not a direct refutation — but it tested the logic, and the logic did not hold up.
So what are we claiming? That a structured way of recognising your own long-standing pattern, adjusted from what your test findings currently show, gives you an approach you can recognise yourself in and therefore sustain. And one thing more, which is the part that can be wrong: we write down, before your protocol starts, what we expect to change and by when — and we check it at retest. That prediction can come back not met. Nothing else in the framework can.
And what we are not selling. Metabolic Natures recommends no proprietary formula, and no product is required for the method to work. The lineage this framework comes from did the opposite — it defined its own efficacy as depending on a sole-source supplement range. That is named here because the same standard has to apply to a tradition we came from as to one we did not.
Read the corrections to the book, dated →Blood chemistry: the metabolic foundation
A comprehensive blood chemistry panel, interpreted with optimal ranges rather than reference ranges, is the most accessible way to describe how someone’s metabolism is currently running. Several markers are consistently informative about that. None of them assesses type — which is the whole point of this article, and the sentence that used to sit here said the opposite.
The markers most often looked at
These are the blood chemistry markers most commonly used in this framework to describe how a person's metabolism is running. They describe current function. None of them has been shown to predict who does better on which balance of food, and they should be read as a description of the present state rather than as an identification of type.
| Marker | What it describes now |
|---|---|
| CO₂ / Bicarbonate | Acid–base balance, held in range mainly by the kidneys and breathing. A result outside the range points to the lungs, the kidneys or a metabolic cause, not to a type. |
| Total Protein | Albumin plus the globulins. Moves with hydration, liver function, nutrition and immune activity. |
| Triglycerides | Fat carried in the blood. Moves with the last meal (so fasting matters), alcohol, carbohydrate intake and insulin resistance. |
| HDL | The “good” cholesterol fraction. Tends to rise with activity and fall with insulin resistance and smoking. |
| Glucose (fasting) | Glucose regulation at one moment. Read alongside fasting insulin and HbA1c, not alone. |
| Uric acid | The end product of purine breakdown, cleared by the kidneys. Raised by alcohol, fructose, some diuretics and reduced kidney clearance. |
Updated 4 October 2026. Earlier versions of this table gave each marker a “faster-oxidative” and a “slower-oxidative” direction. Those directions came from the metabolic typing tradition and have never been tested against oxidative rate, or against which balance of food suits whom. Laid out as two columns, they read as a key for assigning a type, which is what this article says the markers cannot do, so they have been removed. The dated correction records the change.
No single marker is definitive, and taken together they are still not a type assignment. What a pattern of markers gives you is a description of current function — which is what you need in order to decide what to address first.
Two claims that used to appear in this table have been removed. Where they came from matters, so this says it rather than deleting them quietly.
The calcium-to-phosphorus ratio reached this framework through hair tissue mineral analysis, and its source is David L. Watts of Trace Elements Inc — not George Watson, whose oxidation-rate work is a different body of material by a similarly named author. In HTMA as it is actually taught, Ca/P is a hair measure, not a blood one; it is read as an autonomic ratio rather than an oxidative one; around 2.6 is considered the ideal, with the flags at above 3.6 and below 1.6; and a high ratio is taken to indicate parasympathetic dominance, while fast oxidation is the sympathetic state and drives hair calcium down.
This page carried it as a serum marker of fast oxidation above 2.5:1. That is the wrong specimen, the wrong axis, the wrong direction, and a figure closer to the middle of the range than to either edge — so “above 2.5 equals fast oxidiser” classified roughly everyone above average as a fast oxidiser. Four errors in one line.
Two further points, and they apply whatever the interpretation. Wolcott explicitly kept Metabolic Typing separate from HTMA, so the claim cannot lean on Healthexcel — and it cannot lean on Trace Elements without adopting HTMA wholesale. And in 2001 JAMA published a study in which a single hair sample from one volunteer, split between the six laboratories handling most US samples, returned between-laboratory differences exceeding tenfold for twelve minerals, with the labs issuing conflicting dietary advice from the same hair. DOI If split samples disagree that far, no ratio computed from them is reliable, whether or not the interpretation attached to it is sound.
The eosinophil-to-basophil ratio goes the same way for a simpler reason. Searched properly, no paper uses such a ratio as an index of anything, and the one study touching on these cells and autonomic function found both counts moving in the same direction — which is not what a ratio would predict. DOI
Neither has been tested against macronutrient response, and we no longer present either as a marker. A correction this specific is worth more than the claim ever was.
A note on the ranges themselves. Where a marker has a recognised clinical cutoff, that is the figure used and it is labelled as such. Where the figure is a functional range, that is a different kind of number with a different basis, and it is labelled as such too. The distinction matters more than it is usually given credit for.
"Reference ranges tell you whether you'll be admitted to hospital. Optimal ranges tell you how your metabolism is actually functioning. These are very different questions."
Organic Acids Test: inside the mitochondria
The OAT reaches metabolic processes blood chemistry cannot — mitochondrial function, neurotransmitter metabolism, nutrient cofactor status, and the efficiency of the Krebs cycle. It is genuinely informative about how energy production is currently running. What follows should be read as pattern description, not as type assignment: the type-specific Krebs signatures below come from clinical observation and no published validation of them has been found.
What the intermediates reveal
Elevated citrate with normal or low downstream intermediates (isocitrate, alpha-ketoglutarate, succinate) suggests a bottleneck in the cycle, and magnesium or B-vitamin insufficiency suppressing enzymatic activity is a common and correctable reason for it. Normal or low citrate with adequate downstream flow but elevated pyruvate suggests the cycle is running with substrate entry from glycolysis poorly channelled. Multiple simultaneous elevations suggest a congested cycle rather than a single bottleneck. Each of these is a description of current mitochondrial function and a pointer to what to address. Mapping them onto named types is clinical observation, and it is not evidence that the cycle pattern predicts which balance of food will suit someone.
Adipate, suberate, and ethylmalonate
Elevated adipate and suberate with normal ethylmalonate points to impaired mitochondrial fatty acid oxidation. This is the most directly actionable finding on the whole panel: it says the machinery for burning fat is not currently running well enough to process a large fat load, whatever anyone's recognised pattern suggests. It is a common and unglamorous explanation for feeling worse on a ketogenic approach. Elevated ethylmalonate alone suggests carnitine insufficiency, which is likewise a present-tense constraint rather than a type.
Pyroglutamate and glutathione demand
Elevated pyroglutamate on OAT is read as a marker of high glutathione demand — the body cycling through glutathione rapidly, which points to oxidative stress or toxic load. That makes it a useful flag for a blocking factor worth addressing. It is not an axis marker. It says nothing about oxidation rate or autonomic position, and the previous version of this paragraph attached it to two named types on two different axes, which cannot both be right. Evidence grade: mechanistic, and reasonable as a pointer to glutathione demand; no published validation of it as an indicator of any metabolic category has been found.
DUTCH hormone assessment: the adrenal-metabolic link
The relationship between adrenal function and metabolic rate is inseparable. Cortisol is not just a stress hormone — it is a primary regulator of glucose availability, fat mobilisation, protein catabolism, and mitochondrial biogenesis. Its diurnal pattern, and the pattern of its metabolites, describe a significant part of where autonomic load currently sits — which is a present-tense reading, not a type.
Putting the picture together
No one of these tests identifies your type, and neither do all of them together. That is not a hedge; it is the design. Running them together — as the TDG Five-Test Programme does — gives you convergent evidence about what is currently constraining function, and that is what sets the clinical priorities. It is a real and useful convergence. It is just an answer to a different question from the one the older systems claimed to answer.
This still matters enormously for intervention design. Two people can present with identical chief complaints — fatigue, weight gain, brain fog, poor sleep — with entirely different things in the way. One cannot digest protein; the other cannot oxidise fat; a third has thyroid function sitting in the upper part of the laboratory reference range and neither problem. (On that last one: upper reference limits for TSH differ between laboratories, commonly somewhere between 4.0 and 5.5 mIU/L, and no cut-off below a laboratory’s own upper limit has been validated against clinical outcomes. It is a reason to look harder, not a diagnosis.) The intervention that helps one will often worsen another. Without the data you are making expensive guesses about which.
"The tests do not tell you who you are. They tell you what is currently in the way, which is the only thing you can actually do something about this month."
The blocking factor complication
One thing that follows from all of the above and is usually left implicit: a blocking factor makes both instruments less trustworthy at once. It is not a case of one reliable reading and one distorted one. Sustained HPA activation pushes the questionnaire and the panels in the same direction together. Significant gut dysbiosis or a heavy toxic load does something similar. Under those conditions there is no clean measurement available from either side, and the honest position is that the starting point is provisional until the block clears — at which point it is re-examined, one step at a time, with the response itself treated as the test.
Volume 1 of Metabolic Natures covers blocking factors for readers; Volume 2, the Practitioner’s Manual (in progress), covers the specific OAT, GI-MAP and blood chemistry markers that point most clearly to whether a blocking factor or the recognised pattern should set the starting point.