Prediabetes is often a footnote in primary care, flagged inconsistently on lab reports, mentioned briefly or ignored for ‘watchful waiting’. This passive approach fails to reflect the biological reality. Long before HbA1c reaches the diagnostic threshold for type 2 diabetes (T2D) (≥ 48 mmol/mol or ≥ 6.5%), the disease process is active: insulin resistance, hyperinsulinaemia and β-cell stress drive early microvascular and cardiovascular damage.^1,2

Prediabetes (HbA1c 39–46 mmol/mol or 5.7% – 6.4%) is not benign; it is early T2D, and primary care must treat it as such.

Mechanistically, insulin resistance in muscle, liver and adipose tissue forces β-cells to overproduce insulin, leading to hyperinsulinemia, a hallmark of early metabolic dysfunction.³ This initially masks rising glucose but stresses β-cells, causing defects mirroring T2D. Hyperinsulinaemia often precedes glucose abnormalities by up to 24 years, affecting up to 75% of those with normal glucose tolerance.⁴ These early defects matter: 30% – 50% of individuals with prediabetes progress to T2D within 5–10 years.²

The consequences extend well beyond glycaemia. Prediabetes increases all-cause mortality and cardiovascular risk by 13% – 20%.⁵ Endothelial dysfunction, a driver of atherosclerosis, is evident early, with insulin resistance and hyperinsulinaemia promoting vascular damage.^6,7 Retinal damage already affects ~10%,⁸ neuropathy up to 20%,⁹ kidney disease risk is doubled¹⁰ and non-alcoholic fatty liver disease (NAFLD) occurs in up to 70% of cases.^6,11 Emerging evidence also links prediabetes to an increased risk of dementia and stroke.¹² In short, complications attributed to diabetes often begin during so-called ‘prediabetes’.

The good news is that prediabetes is highly reversible. Therapeutic carbohydrate reduction (TCR) not only prevents progression but has also been shown to restore normal glucose regulation. Therapeutic carbohydrate reduction reduces insulin demand, improves β-cell function and normalises glucose levels, often within weeks, typically without medication.¹³ Studies collectively show 77% – 97% of patients with prediabetes can return to normal HbA1c and dramatically improve metabolic health.^14,15,16,17 Early intervention not only prevents T2D but also reduces the risk of its comorbidities, with the potential to save healthcare systems billions.

Yet this opportunity is routinely wasted. Patients newly diagnosed with T2D often have years of documented prediabetes in their records that were never discussed. When this is understood, patients’ frustration is justified: why wasn’t action recommended when intervention would have been most effective? Failing to act on prediabetes is not just a missed opportunity; it is an ethical failure. Part of this inaction reflects institutional resistance. Reclassifying prediabetes as early T2D expands treatment populations, triggering concerns about medicalisation and resource allocation. Funders baulk at covering interventions for ‘pre-disease’. But this short-term thinking ignores the economics: treating early T2D with lifestyle intervention costs substantially less than managing late-stage complications. The question isn’t whether to treat, but when treatment is most effective and least expensive.

The term itself sabotages action. ‘Prediabetes’ signals a waiting room, not a treatment window. Primary care must reframe this as early T2D, establish concrete targets (HbA1c < 39 mmol/mol or 5.7%) and provide or refer for tailored dietary and lifestyle intervention.

Language determines response. ‘Prediabetes’ encourages surveillance; ‘early T2D’ demands treatment. Retiring the term ‘prediabetes’ aligns clinical language with pathophysiology and ensures intervention begins when it can prevent, rather than merely delay, irreversible complications.