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.
Fasting Insulin
The level of insulin in your blood after an overnight fast. When cells respond well to insulin, it takes only a little to keep glucose in line, so the number is low; when cells respond less well (insulin resistance), the pancreas compensates by releasing more, and fasting insulin rises long before glucose does. This is why it is treated as an early-warning marker rather than an afterthought -- a large pooled analysis of prospective cohort studies found that a higher fasting insulin level tracks with greater long-term risk of high blood pressure and coronary heart disease. (cite: fasting insulin and incidence of hypertension, stroke, and coronary heart disease -- meta-analysis of prospective cohort studies, PMID 24132974)
Typical range: Conventional lab range: roughly 2-25 microIU/mL (varies widely by lab and assay; many labs flag values above ~25). Functional optimal (opinion): a fasting insulin in the low single digits (often cited as ~2-6 microIU/mL) is described by functional-medicine practitioners as ideal -- this is an opinion range, not an official diagnostic cutoff, and fasting insulin is meant to be read alongside glucose (as HOMA-IR), not in isolation.
Nutrients that move it
- Soluble fibersolid -- summarizing dozens of meta-analyses covering tens of thousands of people, higher dietary fiber intake was linked to lower fasting insulin (alongside lower fasting glucose, HOMA-IR, and HbA1c), partly by slowing how fast a meal's sugar arrives. (cite: dietary fiber intake and cardiovascular risk factors -- umbrella review of meta-analyses of RCTs, PMC9511151)
- Magnesiumemerging -- a cofactor the body uses throughout normal glucose and energy metabolism, and one of the more common shortfalls in a modern diet; a meta-analysis of RCTs in type 2 diabetes found magnesium supplementation modestly improved fasting glucose and HbA1c, and low magnesium status tracks with insulin resistance. (cite: magnesium and glycemic control, meta-analysis of RCTs, PMC7784187)
- Chromiumcontested -- a trace mineral involved in normal carbohydrate metabolism; best thought of as adequacy rather than a lever to push, because the RCT evidence in glycemic markers is genuinely conflicting. (cite: conflicting meta-analyses of chromium picolinate RCTs, clinical-nutrition systematic reviews)
Food first: Front-load fiber and protein, put vegetables first in a meal, and choose slower (lower-glycemic) carbohydrates more often than not -- the plate is where the insulin signal is made easier to hear. Ensure dietary magnesium adequacy (leafy greens, nuts, seeds, legumes) rather than empiric megadosing.
When to see someone: Fasting insulin assays vary a lot between labs, so track trend on the same lab rather than comparing a single number across labs. A single reading is a piece of a picture a clinician interprets, never a self-diagnosis. Insulin supplements do not exist over the counter -- nothing here raises or lowers insulin as a treatment; the levers work by improving how the tissues respond to it.
Read the studies on Fasting InsulinHOMA-IR (calculated -- a derived value, not a measured one)
HOMA-IR is not a blood test drawn on its own -- it is a small calculation from two fasting values, roughly (fasting glucose in mg/dL x fasting insulin in microIU/mL) / 405, that estimates insulin resistance. Because it uses both glucose and insulin together, it can pick up a change that either one alone would hide: in a year-long lifestyle program, the HOMA-IR index detected improvements in insulin sensitivity that fasting glucose by itself did not register. (cite: fasting serum insulin and the homeostasis model of insulin resistance (HOMA-IR) in monitoring lifestyle interventions, PMID 17583689)
Typical range: No universal cutoff exists, because HOMA-IR shifts with the population and the insulin assay used. Values under roughly 2.0 are commonly read as insulin-sensitive and values above roughly 2.5-2.9 as suggesting insulin resistance, but these thresholds are population-dependent conventions, not a single validated diagnostic line. Because it is derived from fasting insulin, it inherits that marker's assay variability -- interpret the trend on one lab, not an absolute number.
Nutrients that move it
- Soluble fibersolid -- higher dietary fiber intake was linked to lower HOMA-IR in the same umbrella review of RCT meta-analyses that covered glucose, insulin, and HbA1c. (cite: dietary fiber intake and cardiovascular risk factors -- umbrella review, PMC9511151)
- Magnesiumemerging -- adequacy supports normal insulin signaling and glucose disposal; deficiency tracks with a higher HOMA-IR, and RCT supplementation modestly improved glycemic markers. (cite: magnesium and glycemic control, meta-analysis of RCTs, PMC7784187)
- Alpha-lipoic acidemerging -- a naturally occurring cofactor for mitochondrial bioenergetic enzymes with antioxidant properties; relevant to the energy-handling side of insulin sensitivity as a building-block input rather than a proven lever for this specific value (see the ingredient page for the actual evidence).
Food first: HOMA-IR follows fasting insulin and glucose, so the levers are the same: fiber and protein first, slower carbohydrates, a post-meal walk to let working muscle clear glucose, resistance movement to expand the muscle glucose sink, and protected sleep. Re-measure after working the loop -- HOMA-IR is sensitive enough to show the change while it is still early.
When to see someone: HOMA-IR is an estimate, not a gold-standard measurement of insulin resistance, and it is only as reliable as the fasting insulin it is built from. It is a screening/monitoring tool a clinician interprets in context, not a stand-alone diagnosis.
Read the studies on HOMA-IR (calculated -- a derived value, not a measured one)Fasting Glucose
The level of sugar in your blood after an overnight fast -- a tightly defended number the body works hard to keep in range. Because the body will defend a normal glucose for a long time by simply producing more insulin, glucose is among the LAST things to move, not the first; it is one of the five findings bundled into the metabolic-syndrome definition precisely because it clusters with the others around shared insulin-resistance physiology. (cite: a comprehensive definition for metabolic syndrome (NCEP ATP III), PMC2675814)
Typical range: Conventional: roughly 70-99 mg/dL is the range labs report as normal; 100-125 mg/dL is the band clinicians label "impaired fasting glucose," and ≥126 mg/dL on repeat is the clinical diabetes cutoff. These are the ranges labs and clinicians use for interpretation -- reading them at home is not a diagnosis. Functional optimal (opinion): some practitioners prefer a fasting glucose in the low 80s mg/dL; this is opinion, not an official target.
Nutrients that move it
- Soluble fibersolid -- higher fiber intake was linked to lower fasting glucose across the RCT-meta-analysis umbrella review, largely by flattening the post-meal glucose curve. (cite: dietary fiber intake and cardiovascular risk factors -- umbrella review, PMC9511151)
- Magnesiumemerging -- a meta-analysis of RCTs in type 2 diabetes found magnesium supplementation modestly improved fasting glucose; adequacy matters more than megadosing. (cite: magnesium and glycemic control, meta-analysis of RCTs, PMC7784187)
- Chromiumcontested -- involved in normal carbohydrate metabolism, but the RCT evidence for moving glucose is mixed and inconsistent. (cite: conflicting meta-analyses of chromium picolinate RCTs, clinical-nutrition systematic reviews)
Food first: Eating vegetables (fiber) before the carbohydrate portion of a meal measurably reduces the after-meal glucose rise; leading with protein and choosing slower carbohydrates does the same. A 10-minute walk after eating blunts the spike directly, because working muscle pulls glucose from the blood through a route that does not even require insulin to be working well.
When to see someone: A normal fasting glucose is a real reassurance about today and a poor guide to the trend -- it can sit right on top of a rising insulin level. This is exactly why fasting insulin/HOMA-IR is the higher-value addition when glucose still looks normal. Never read a glucose value as a diagnosis on its own.
Read the studies on Fasting GlucoseHbA1c (Glycated Hemoglobin)
A measure of how much sugar has stuck to your red blood cells, used as a stand-in for average blood sugar over roughly the previous three months. That three-month memory is genuinely useful, but it is still a record of where glucose has already been, and it can be skewed by anything that changes red blood cells -- low iron, or a condition that shortens red-cell lifespan -- which is why it should be read alongside the rest of the picture rather than alone. (cite: HbA1c and factors other than diabetes mellitus affecting it, PMID 20848057)
Typical range: Conventional: below 5.7% is the range reported as normal; 5.7-6.4% is the intermediate band clinicians watch; ≥6.5% is the clinical diagnostic cutoff. These are interpretation bands, not a home diagnosis. Functional optimal (opinion): some practitioners prefer HbA1c in the low-to-mid 5% range -- opinion, not an official target.
Nutrients that move it
- Soluble fibersolid -- higher dietary fiber intake was linked to lower HbA1c in the umbrella review of RCT meta-analyses, moving with the other glucose markers in the right direction together. (cite: dietary fiber intake and cardiovascular risk factors -- umbrella review, PMC9511151)
- Magnesiumemerging -- a meta-analysis of RCTs in type 2 diabetes found magnesium supplementation modestly improved HbA1c alongside fasting glucose. (cite: magnesium and glycemic control, meta-analysis of RCTs, PMC7784187)
- Ironemerging -- iron status changes red-cell turnover, so iron deficiency can push HbA1c up and iron repletion can bring it down independent of true average glucose; this makes iron a reason to interpret HbA1c cautiously more than a nutrient to move HbA1c with. (cite: HbA1c and factors other than diabetes mellitus affecting it, PMID 20848057)
Food first: The same curve-flattening levers as fasting glucose -- fiber and protein first, slower carbohydrates, post-meal movement -- lower average glucose over time and so lower HbA1c, which is a three-month average that changes slowly. Re-measure no sooner than about three months apart to see a real change.
When to see someone: HbA1c is unreliable in anyone with altered red-cell lifespan (recent blood loss, hemolysis, certain anemias, recent transfusion, pregnancy, or some hemoglobin variants) -- flag any of these to the ordering clinician, because a "normal" or "high" HbA1c in that setting can be an artifact of the red cells, not the blood sugar.
Read the studies on HbA1c (Glycated Hemoglobin)Triglycerides
The main fat carried in the blood. When insulin is not working well, the liver tends to pour out more triglycerides, so a rising triglyceride level is part of the insulin-resistance fingerprint -- and it is one of the five metabolic-syndrome findings for that reason. (cite: a comprehensive definition for metabolic syndrome (NCEP ATP III), PMC2675814)
Typical range: Conventional: below 150 mg/dL is desirable, 150-199 mg/dL borderline-high, and ≥200 mg/dL high. Functional optimal (opinion): some practitioners prefer triglycerides under ~100 mg/dL (or even ~70) as a sign of good insulin sensitivity -- opinion, not an official cutoff. Triglycerides are strongly affected by recent food and alcohol, so this should be a true fasting value.
Nutrients that move it
- Omega-3 (EPA and DHA)solid -- the long-chain omega-3 fats are well established to lower serum triglycerides in a dose-dependent way and are relevant to the body's normal inflammatory balance; this is one of the better-supported nutrient effects on any marker in this file (see the ingredient page for the trial evidence).
- Soluble fiberemerging -- fiber's curve-flattening and lipid effects tend to nudge triglycerides down as part of the broader improvement in glucose and insulin handling. (cite: dietary fiber intake and cardiovascular risk factors -- umbrella review, PMC9511151)
Food first: Oily fish (or an EPA/DHA source) for the omega-3 side, less refined and liquid sugar (which the liver converts efficiently to triglycerides), less alcohol, and the same fiber-first plate. Movement and reducing excess refined carbohydrate move triglycerides more than most single supplements.
When to see someone: A non-fasting draw or recent alcohol can inflate triglycerides substantially -- confirm the sample was truly fasting before reading it. Very high triglycerides are a medical matter (pancreatitis risk) that belongs with a clinician, not a nutrition experiment.
Read the studies on TriglyceridesHDL Cholesterol
The cholesterol carried in high-density lipoprotein particles. HDL tends to fall when insulin is not working well, so a low HDL is the other half of the insulin-resistance lipid fingerprint and is one of the five metabolic-syndrome findings. (cite: a comprehensive definition for metabolic syndrome (NCEP ATP III), PMC2675814)
Typical range: Conventional: the low-HDL flags used in the metabolic-syndrome definition are below 40 mg/dL in men and below 50 mg/dL in women; higher HDL is generally viewed favorably, though the picture at the very high end is nuanced and HDL is best read as part of a ratio and a cluster rather than chased in isolation.
Nutrients that move it
- Omega-3 (EPA and DHA)emerging -- can modestly raise HDL as part of its broader lipid effect, though its headline effect is on triglycerides (see the ingredient page).
Food first: HDL responds most to movement (especially aerobic activity and building muscle), to replacing refined carbohydrate with fiber and healthy fats, and to reducing excess visceral fat -- not to a specific pill. Read it together with triglycerides as a ratio.
When to see someone: Do not treat HDL as a number to maximize with supplements; its protective association is not the same as "more is always better," and it is most useful inside the triglyceride-to-HDL ratio and the wider cluster, interpreted by a clinician.
Read the studies on HDL CholesterolTriglyceride : HDL Ratio (calculated -- a derived value)
A calculated ratio (triglycerides divided by HDL cholesterol, both from an ordinary lipid panel) that serves as a cheap proxy for insulin resistance -- when insulin is not working well, triglycerides rise and HDL falls, so the ratio climbs. In nondiabetic overweight adults, the triglyceride-to-HDL ratio (with triglycerides and insulin) identified insulin-resistant individuals about as well as the formal metabolic-syndrome criteria did. (cite: use of metabolic markers to identify overweight individuals who are insulin resistant, DOI 10.7326/0003-4819-139-10-200311180-00007)
Typical range: No official clinical reference range exists. Using US (mg/dL) units, a ratio under roughly 2 is commonly described as favorable and above roughly 3-3.5 as a flag for insulin resistance, but these are community conventions, not validated diagnostic cutoffs, and the ratio performs differently across ancestries (it is a weaker marker in some populations). It also depends entirely on the units used -- mg/dL and mmol/L give very different numbers, so match the cutoff to the units.
Nutrients that move it
- The components' levers apply, not the ratio'semerging -- no dedicated trial has tested nutrient supplementation against this specific ratio as an endpoint; the practical approach is to move triglycerides down (omega-3, less refined sugar and alcohol) and HDL in the right direction (movement, less refined carbohydrate), using the evidence for each component separately. (cite: use of metabolic markers to identify insulin-resistant individuals, DOI 10.7326/0003-4819-139-10-200311180-00007)
Food first: This is the most underused number on a common lab -- it costs nothing extra. Move it by working its two parts: the omega-3 and refined-sugar levers on triglycerides, and the movement and refined-carbohydrate levers on HDL.
When to see someone: The ratio is a proxy, not a diagnosis, and its cutoffs are unit- and population-dependent -- do not port a mg/dL cutoff onto a mmol/L value, and do not let a single ratio override the fuller picture a clinician reads.
Read the studies on Triglyceride : HDL Ratio (calculated -- a derived value)TyG Index (Triglyceride-Glucose Index, calculated -- a derived value)
A calculated insulin-resistance marker built from two routine fasting labs -- the natural log of (fasting triglycerides in mg/dL x fasting glucose in mg/dL) / 2. Like HOMA-IR it estimates insulin resistance, but it uses triglycerides and glucose instead of insulin, so it can be derived from an ordinary panel without an insulin assay. It is well supported as a risk marker: even in people without diabetes, a higher TyG index at baseline was linked to greater 10-year cardiovascular disease risk beyond traditional risk factors (cite: TyG index and cardiovascular disease in a non-diabetic population -- 10-year prospective cohort, HH-3115, PMC9700958); in nearly 20,000 adults followed over eight years it tracked with all-cause and cardiovascular mortality in a non-linear pattern (cite: TyG index and all-cause and cardiovascular mortality in the general population, HH-3116, PMC7840600); and across two large cohorts a higher TyG index tracked with stiffer arteries and greater long-term risk of diabetes and cardiovascular disease (cite: TyG index as a predictor of arterial stiffness, diabetes, and cardiovascular disease -- two-cohort analysis, HH-3117, PMC9846351).
Typical range: No universal cutoff -- the validating cohort studies analyze it in tertiles or quartiles rather than against a single line, so it is read as "higher versus lower within a population" more than as a fixed threshold. Treat any specific TyG cutoff seen online as a research convention, not a validated clinical target.
Nutrients that move it
- The components' levers applyemerging -- TyG is built from triglycerides and fasting glucose, so the nutrient levers are those markers' levers: omega-3 and reduced refined sugar/alcohol on the triglyceride side, and fiber, magnesium adequacy, and post-meal movement on the glucose side. No nutrient trial has used TyG itself as an endpoint. (cite: dietary fiber intake and cardiovascular risk factors -- umbrella review, PMC9511151)
Food first: Work the triglyceride and glucose levers already described -- there is no separate "TyG diet."
When to see someone: TyG is a research-grade and emerging clinical marker, not a routine diagnostic test, and it requires a true fasting sample (both triglycerides and glucose move with recent food). It is a proxy a clinician interprets in context, never a stand-alone diagnosis.
Read the studies on TyG Index (Triglyceride-Glucose Index, calculated -- a derived value)hs-CRP (High-Sensitivity C-Reactive Protein)
Cellular Six: MaintainThis marker sits in Maintain -- the cleanup and defence system, and whether it is switched on.
A high-sensitivity measure of C-reactive protein, a liver-made protein that rises with inflammation. It is included on a metabolic panel as an inflammation adjunct, because insulin resistance and the visceral fat that accompanies it are low-grade inflammatory states -- so a higher hs-CRP often travels with the rest of the metabolic picture rather than standing apart from it.
Typical range: Conventional cardiovascular-risk bands (AHA/CDC): below 1.0 mg/L is the lower-risk band, 1.0-3.0 mg/L is average, and above 3.0 mg/L is the higher-risk band. A value above ~10 mg/L usually signals acute infection or injury rather than the chronic low-grade signal this panel is interested in -- it should be re-drawn once the acute event has passed before being read as a metabolic marker.
Nutrients that move it
- Omega-3 (EPA and DHA)emerging -- relevant to the body's normal inflammatory balance and commonly associated with lower inflammatory markers; a building-block input rather than a proven lever for a specific hs-CRP target (see the ingredient page).
- Soluble fiberemerging -- higher fiber intake is associated with a better cardiometabolic and inflammatory profile as part of its broad effect on the same physiology. (cite: dietary fiber intake and cardiovascular risk factors -- umbrella review, PMC9511151)
- Magnesiumemerging -- low magnesium status tracks with higher inflammatory markers, so adequacy is supportive; this is an association-and-adequacy point, not proof that repletion lowers hs-CRP. (cite: magnesium and glycemic control, meta-analysis of RCTs, PMC7784187)
Food first: The strongest levers on chronic low-grade inflammation overlap with the whole-panel levers -- reducing excess visceral fat, movement, sleep, an omega-3-adequate and fiber-rich diet -- rather than a single anti-inflammatory supplement.
When to see someone: hs-CRP is non-specific: it rises with any infection, injury, recent illness, or intense exercise, so a single high value is not a metabolic verdict. Draw it away from acute illness, and if it is above ~10 mg/L, repeat it before reading it as part of the metabolic picture. Interpretation belongs to a clinician reading the cluster.
Read the studies on hs-CRP (High-Sensitivity C-Reactive Protein)