A person with a fasting plasma glucose of 6.4 mmol/L is not "a little bit diabetic". They have impaired fasting glucose — one of three laboratory doors into the zone that ADA calls prediabetes. Prediabetes is not a disease in its own right in the sense of ADA organ criteria, but a range in which the risk of future T2DM and, observationally, of cardiovascular events is higher than with normoglycaemia.
Criteria for prediabetes in non-pregnant individuals according to ADA 2026 Table 2.2:
| Test | Range |
|---|---|
| HbA1c | 5.7–6.4% (39–47 mmol/mol) |
| Fasting plasma glucose (impaired fasting glucose, IFG) | 100–125 mg/dL (5.6–6.9 mmol/L) |
| 2-hour glucose during a 75 g oral glucose tolerance test (OGTT) (impaired glucose tolerance, IGT) | 140–199 mg/dL (7.8–11.0 mmol/L) |
ADA specifically states: risk is continuous and does not stop at the lower bound of the range, and at the upper end it is disproportionately higher. One test in the "grey zone" is not yet a verdict and not a reason to tell a person "you have diabetes".
For normal values and diabetes, the MoH RK 2022 protocol gives a table in mmol/L and distinguishes capillary whole blood from venous plasma. Normal fasting: capillary <5.6; venous plasma <6.1; 2 hours after OGTT <7.8 for both media. Diabetic range fasting: capillary ≥6.1; venous plasma ≥7.0; at 2 hours or random ≥11.1. Between normal and diabetes lie IFG (impaired fasting glucose) and IGT (impaired glucose tolerance). Note: the ADA fasting "normal" threshold (FPG <5.6 mmol/L) coincides with the capillary normal of the RK protocol and does not coincide with the venous normal of the RK protocol (<6.1). This is not a "translation error". The WHO historically set IFG from 6.1 mmol/L, ADA from 5.6. A student in Kazakhstan must state which medium and which document they are using. Mixing up capillary 6.2 with venous plasma 6.2 is a way to make a diagnosis that does not exist.
The global size of this zone. The IDF Atlas 11th edition estimates for 2024: 635 million adults with IGT (12.0%) and 488 million with IFG (9.2%). These are not "people with diabetes who have not yet been found". This is a separate high-risk population. An article in Diabetes Care (2025;48:e142) refines the same Atlas estimates.
Whether progression to diabetes can be shifted is no longer an observational question. The Diabetes Prevention Program (Knowler WC et al. N Engl J Med. 2002;346:393–403. PMID 11832527) randomised 3234 adults without diabetes but with elevated fasting and post-load glucose (essentially IGT plus elevated FPG), mean age 51 years, mean BMI 34.0. Three arms: placebo; metformin 850 mg twice daily; a lifestyle programme with goals of ≥7% body weight loss and ≥150 minutes of activity per week. Mean follow-up 2.8 years. Diabetes incidence: 11.0, 7.8 and 4.8 per 100 person-years in the placebo, metformin and lifestyle groups. Lifestyle reduced incidence by 58% (95% CI 48–66) and metformin by 31% (17–43) relative to placebo. To prevent one case over three years, 6.9 people needed to be enrolled in the lifestyle programme and 13.9 on metformin. The population was US adults with overweight and IGT, not "everyone with an HbA1c of 5.8% at an Almaty outpatient clinic". Extrapolation to isolated IFG or to prediabetes defined "by HbA1c alone" is limited: ADA 2026 explicitly notes that the effectiveness of prevention has been better demonstrated in people with IGT.
What prediabetes does not permit. It does not permit diagnosing T2DM "with a margin". It does not make metformin mandatory for everyone with an HbA1c of 6.0%. DPP showed a reduction in diabetes incidence, not a reduction in myocardial infarctions as the primary endpoint. It does not replace discussion of weight, activity and repeat testing.
The boundary of the lesson. Prediabetes is the place where a risk factor is already measurable in the laboratory, while the organ criteria for diabetes are not yet met. The next module begins where at least one test has crossed the diabetic threshold.