Pillar 02 · Metabolism

Metabolic health starts years before the diagnosis

The core of metabolic disease is insulin resistance and the visceral (intra-abdominal) fat that drives it. Long before fasting glucose or A1C cross a diagnostic line, the body compensates by secreting more insulin, so fasting insulin and the ratio of fat-related markers shift first, and the lab values clinicians watch are late indicators. Clustering these abnormalities together is exactly what the metabolic-syndrome definition captures [Alberti KGMM, 2009], and it roughly doubles cardiovascular risk. The prevention angle is the same as for the heart: the damage accumulates over a lifetime, so catching the trend early, and reversing it, matters more than any single reading.

Insulin resistance: HOMA-IR

The Homeostasis Model Assessment turns a paired fasting glucose and fasting insulin into a single index of insulin resistance [Matthews DR, 1985]. Because it uses fasting insulin, it can flag the compensatory phase while glucose still looks normal.

Cut-points are population-, age-, and sex-dependent and are not a clinical diagnosis. The reference point here is the 90th-percentile value from a general adult population [Gayoso-Diz P, 2013]. A rising HOMA-IR over time is more informative than any one value.

A1C and estimated average glucose

A1C reflects average blood glucose over the prior ~3 months. The ADA thresholds (normal under 5.7%, prediabetes 5.7–6.4%, diabetes 6.5% and above) define where you sit [American Diabetes Association Professional Practice Committee, 2024]. The estimated average glucose (eAG) restates that A1C in the mg/dL units a glucometer shows, using the ADAG study’s regression [Nathan DM, 2008].

Prediabetes is the actionable window: it is common, often silent, and frequently reversible with the same diet, weight, and exercise changes that reduce visceral fat.

Metabolic syndrome (3 of 5)

Metabolic syndrome is a cluster: meeting any 3 of 5 criteria flags the combination of central adiposity, dyslipidemia, blood pressure, and glucose dysregulation that travels with insulin resistance. The 2009 harmonized definition unified the competing thresholds into one set [Alberti KGMM, 2009].

Waist circumference is intentionally population-specific in the harmonized statement; the widget uses the AHA/NHLBI (US) cut-points. Drug treatment for a component (blood pressure, lipids, or glucose) counts as meeting that component.

Triglyceride/HDL ratio

A high triglyceride-to-HDL ratio is a cheap, widely available surrogate for insulin resistance. It tends to rise as insulin sensitivity falls [McLaughlin T, 2003]. It is a marker, not a diagnosis, and the cut-point is unit-specific (the value below is for mg/dL).