Stage 0 · Starting Point
Normal Insulin Sensitivity — What Healthy Looks Like
Cells respond normally to insulin signalling. Glucose enters cells efficiently after meals. Post-meal glucose returns to baseline within 2 hours. Fasting insulin below 8 µIU/mL. Fasting glucose below 5.0 mmol/L. No symptoms. No clinical flags on standard blood tests.
Fasting insulin <8 · FG <5.0 · HbA1c <5.5%
Year 0
Years 1–3
Stage 1 · Early Insulin Resistance
Cellular Resistance Developing — Insulin Rising, Glucose Still Normal
Cells begin downregulating insulin receptor expression in response to chronic glucose and insulin elevation. The pancreas compensates by producing more insulin to achieve the same glucose clearance. Fasting glucose remains normal. Fasting insulin begins to rise — typically 8–14 µIU/mL. Post-meal glucose is higher than it should be but still within range. Standard blood test shows nothing abnormal. The process is invisible without measuring insulin directly.
Fasting insulin 8–14 · FG normal · HbA1c normal
Stage 2 · Compensatory Hyperinsulinaemia
Insulin High, Glucose Still Normal — The Most Dangerous Invisible Stage
The pancreas is now working significantly harder to maintain normal glucose levels. Fasting insulin rises above 14 µIU/mL — sometimes reaching 20-30 in significant resistance. This is the stage of maximum intervention opportunity — the process is fully reversible with diet, exercise, and targeted support. But it is also the stage most likely to be missed, because fasting glucose and HbA1c remain normal. Symptoms begin: energy crashes after meals, sugar cravings, difficulty losing weight despite effort, central fat accumulation, disturbed sleep.
Fasting insulin >14 · Post-meal glucose elevated · FG still normal
Years 3–7
Years 7–10
Stage 3 · Beta-Cell Fatigue
Pancreatic Output Begins to Decline — Glucose Starts to Creep
The pancreatic beta-cells, under sustained demand for compensatory hyperinsulinaemia, begin to fatigue. Insulin production capacity starts to decline. For the first time, fasting glucose begins to rise — typically into the 5.5–6.9 range (impaired fasting glucose / pre-diabetes). HbA1c may reach 5.7–6.4%. Post-meal glucose is now clearly elevated on a glucose tolerance test. The symptoms intensify: brain fog, fatigue, increased thirst, more frequent urination, poor wound healing, recurrent infections.
FG 5.5–6.9 · HbA1c 5.7–6.4% · Insulin may normalise or fall
Stage 4 · Impaired Fasting Glucose
Pre-Diabetes — The Last Clear Intervention Window
Fasting glucose consistently above 6.1 mmol/L. HbA1c 6.0–6.4%. The GP may now flag this, though many practices do not test HbA1c until symptoms are more pronounced. Intervention at this stage can still reverse the trajectory entirely — but it requires significant dietary restructuring, exercise programming, gut microbiome support, and often targeted supplementation (berberine, magnesium, chromium, alpha-lipoic acid). Organ-level consequences of chronic hyperinsulinaemia are accumulating: early cardiovascular changes, beginning of retinal changes, early renal glomerular changes.
FG 6.1–6.9 · HbA1c 6.0–6.4% · HOMA-IR elevated
Years 10–13
Year 13+
Stage 5 · Type 2 Diabetes Diagnosis
Fasting Glucose ≥7.0 or HbA1c ≥6.5% — The Process That Took a Decade
The diagnosis that standard medicine treats as the beginning of the problem is the endpoint of a 10-15 year process. Beta-cell function is now significantly reduced. Fasting glucose consistently at or above 7.0 mmol/L. HbA1c at or above 6.5%. Insulin may now be falling as beta-cell capacity declines. The standard response — metformin, dietary advice, monitoring — addresses the downstream glucose number but not the underlying insulin signalling failure, gut dysbiosis, chronic inflammation, or HPA axis dysfunction that drove the progression.
FG ≥7.0 · HbA1c ≥6.5% · Standard diagnosis threshold
When Each Marker Changes — The Diagnostic Window
Fasting Insulin
Rises first — Years 1–3
Post-meal glucose
Rises before fasting — Years 3–7
HbA1c
Enters pre-diabetes range — Years 7–10
Fasting glucose
Last to change — Years 10–13
Standard NHS screening checks fasting glucose and HbA1c. These are the last two markers to become abnormal. A decade of progressing insulin resistance is invisible to standard screening — which is why fasting insulin measurement is the single most important addition to any metabolic health assessment.
The clinical point
Type 2 diabetes is diagnosed when fasting glucose reaches 7.0 mmol/L. But the insulin resistance that causes it begins a decade earlier, when fasting glucose is still completely normal. Every year of insulin resistance before diagnosis represents a year of cardiovascular risk accumulation, chronic inflammation, visceral fat deposition, and progressive beta-cell decline — none of which shows on a standard annual blood test. Measuring fasting insulin costs approximately the same as measuring fasting glucose. It provides ten years more warning.
Testing That Identifies Each Stage
Blood Chemistry
Fasting insulin · Fasting glucose · HbA1c · HOMA-IR (calculated) · Triglycerides · HDL ratio
Post-meal test
1-hour and 2-hour post-meal glucose · The most sensitive early marker — normal fasting glucose with elevated post-meal response is Stage 1-2
DUTCH / OAT
Cortisol pattern (HPA drives insulin resistance) · OAT mitochondrial markers · Inflammation indicators via organic acids
Fasting insulin — the marker most GPs don't test
The TDG blood chemistry assessment includes fasting insulin, fasting glucose, HbA1c, and the full lipid picture that together identify which stage of the blood sugar timeline you are at — a decade before a standard annual review would flag anything.