The HbA1c Target: The Evidence Behind the Tool

A 74-year-old retired schoolteacher from Karkala comes for her diabetes review with her son. She has had type 2 diabetes for 18 years and takes glimepiride and insulin glargine. Last month she fell in the bathroom; the glucometer read 52 mg/dL. Her eGFR is 48, her haemoglobin 10.2 g/dL with a low ferritin, and her HbA1c 6.3 per cent. Her son is delighted. “Doctor, her sugar is finally below 7.” This is an illustrative case, not a real patient.

Is it good news? By the end of this article you will know why the HbA1c we treat towards is not the normal value, and why lower is not always better. You will also see why her 6.3 may not be telling the truth.

1. A normal HbA1c and a target HbA1c are different numbers

The ADA and the ICMR draw the same three bands: normal below 5.7 per cent, prediabetes 5.7 to 6.4, diabetes at 6.5 and above. For the bands themselves, see the queue’s article Diagnosing Diabetes and Prediabetes. Yet for most adults with diabetes the treatment target is 7.0, above the diabetic threshold.

“Why not aim for normal?” Because lowering glucose has a benefit and a cost, and the two grow at different rates. Three trials taught us this.

• The benefit side. UKPDS took newly diagnosed type 2 patients from 7.9 to 7.0 per cent and cut microvascular endpoints by 25 per cent. DCCT took type 1 patients from about 9 to about 7 and cut retinopathy, neuropathy and kidney disease by 50 to 76 per cent.
• The cost side. ACCORD took a high-risk type 2 population with a median duration of 10 years towards normal, reaching 6.4 per cent against 7.5, and mortality rose (hazard ratio 1.22, 95 per cent CI 1.01 to 1.46). The trial was stopped at 3.5 years.

Put together, the curve is steep at the top and flat at the bottom. Most of the protection comes from bringing a very high HbA1c down to about 7. The further step from 7 to 6 adds a much smaller gain, and on insulin or a sulfonylurea, hypoglycaemia can outweigh it.

2. The seven factors

Ismail-Beigi and colleagues proposed the framework in 2011 and the ADA and EASD position statement of 2012, updated in 2015, drew it as seven wedges. Five are usually fixed for a given patient and two can be worked on.

The factors are the risk of hypoglycaemia, the duration of diabetes, life expectancy, important comorbidities, established vascular complications, the patient’s attitude and expected effort, and the resources and support around them. Each one pushes the target tighter or looser. The 2026 ADA figure keeps the factors but starts from health status: a healthy adult begins at 7.0, a complex one at 8.0, and a very complex one has no HbA1c target at all. The tool follows that order, then applies the factors.

Look at our schoolteacher. She is on insulin and a sulfonylurea and has had a hypoglycaemic fall: the hypoglycaemia risk is high. Her diabetes is long-standing. Her kidneys are impaired. Every one of these moves her target looser, not tighter.

3. What the cardiovascular trials did and did not show

Six trials sit behind every argument about how low to go. The table is worth reading once, slowly.

Two readings follow. Early, near-normal control in a new diagnosis pays for decades; the UKPDS benefit lasted, and reached deaths and heart attacks, long after the HbA1c difference had gone. Late, near-normal control in an established, high-risk patient on insulin and secretagogues has not paid, and in ACCORD it cost lives. The ACCORD hypoglycaemia analysis found that severe hypoglycaemia raised mortality in both arms but did not by itself explain the difference between them, so the harm is not fully understood.

“So the newer drugs change this?” They change one part of it. None of these trials used an SGLT2 inhibitor or a GLP-1 receptor agonist, whose cardiovascular benefit does not depend on the HbA1c. The trials above are about how low to push the number, not about which drug to choose.

Our schoolteacher is the ACCORD patient, not the UKPDS one: 18 years of diabetes, insulin and a secretagogue, already a severe low.

4. Where the guidelines disagree

The guidelines agree more than they differ, but the differences are real. Read across each row for the question you are facing.

The tool prints the ADA target and then any other figure that differs. For our patient the American College of Physicians row matters most: on a drug that causes hypoglycaemia, consider de-intensifying below 6.5 per cent.

5. The HbA1c is a red cell measurement before it is a glucose measurement

Glucose sticks to haemoglobin slowly, over the whole life of the red cell. So anything that changes how long red cells live changes the HbA1c without changing the glucose. Iron deficiency raises it. In 75 non-diabetic adults with iron deficiency anaemia in Chennai the HbA1c was 6.84 per cent against 5.12 in controls, and it rose with the severity of the anaemia. In Pune, HbA1c called 23.3 per cent of 116 young adults prediabetic where the glucose tolerance test called 7.8 per cent, in a group of whom a third were anaemic.

“Then which way is her 6.3 wrong?” Her low ferritin pushes the HbA1c up, so her real average glucose may be even lower than 6.3 suggests. Shortened red cell survival pushes it down: haemolysis, transfusion, erythropoiesis-stimulating agents, kidney failure and pregnancy. When the red cells cannot be trusted, use something else: glucose profiles, fructosamine, or the glucose management indicator and time in range from continuous monitoring.

6. The Indian picture

In India the usual problem runs the other way.

• ICMR-INDIAB-13, 2022: of 4834 adults with known diabetes across all states, 36.3 per cent had an HbA1c below 7.0; 7.7 per cent met the glycaemic, blood pressure and LDL targets together; 16.7 per cent self-monitored glucose, 36.9 per cent of those on insulin. The commonest departure from target in India is upward, not downward.

That is exactly why a patient like our schoolteacher is missed. When most patients are above target, a low number looks like success. The tool keeps the Indian caveat at the bedside: a raised HbA1c in a menstruating woman or a vegetarian with a low ferritin should be read beside a fasting and a post-prandial glucose before therapy is escalated.

Back to our patient

An HbA1c well below the goal on insulin or a sulfonylurea in a complex older adult is over-treatment, and over-treatment is common enough to have a name. If her health status is complex, the ADA goal is below 8.0 per cent, with a fasting glucose of 90 to 150 mg/dL. The ADA recommends de-intensifying, or switching to a class that does not cause hypoglycaemia. Her son’s good news is a warning. Her fall was the message.

Try this

A 32-year-old man, newly diagnosed with type 2 diabetes and on metformin alone, comes back with an HbA1c of 6.4 per cent. Is he over-treated? Illustrative case.

Answer. No. Metformin alone does not cause hypoglycaemia, and a low HbA1c on metformin alone is not over-treatment: NICE says to maintain it. For a type 2 adult on lifestyle or metformin, the ADA target is below 7.0, with below 6.5 possibly appropriate, and NICE sets 6.5. He is the UKPDS patient: early, near-normal control in a new diagnosis pays for decades.

Take-home points

• The treatment target for most adults is 7.0 per cent, above the diagnostic threshold of 6.5; the gap is deliberate.
• Early tight control in a new diagnosis pays for decades; late tight control on insulin or a sulfonylurea did not, and in ACCORD it cost lives.
• An HbA1c well below goal on insulin or a sulfonylurea in a complex older adult is over-treatment: de-intensify.
• A low HbA1c on metformin alone is not over-treatment.
• Iron deficiency raises the HbA1c and shortened red cell survival lowers it; check the glucose before acting on the number.

For what a fasting insulin and C-peptide can tell you about the beta cell behind the number, see the companion article Beta Cell Function and Insulin Resistance: The Evidence Behind the Tool.

Declaration: the author built and maintains the tool. It is free to use. The figures in this article are those the tool carried in its Evidence tab on 5 November 2026, each from the source the tool names. The illustrative cases follow the tool’s rules; check the tool’s result for a real patient.

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