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Does Smoking Affect HbA1c? Causes, Risks, and UK Guidance

Written by
Bolt Pharmacy
Published on
16/3/2026

Does smoking affect HbA1c? The evidence is clear: smoking raises HbA1c levels through multiple metabolic mechanisms, including increased insulin resistance and stress hormone release, leading to higher average blood glucose readings. For people with or without diabetes, this has real implications for diagnosis, monitoring, and long-term health outcomes. This article explains how smoking influences HbA1c, what UK clinical guidelines say about interpreting results in smokers, how stopping smoking affects your readings, and when to seek advice from your GP.

Summary: Smoking raises HbA1c levels by increasing insulin resistance and stimulating stress hormones that elevate blood glucose, and is recognised by NICE as a modifiable risk factor in diabetes management.

  • Nicotine promotes insulin resistance and stimulates catecholamine and cortisol release, both of which raise circulating blood glucose and contribute to higher HbA1c readings.
  • Carbon monoxide in cigarette smoke can alter red blood cell lifespan, which may influence HbA1c results independently of blood glucose changes.
  • Smokers with diabetes have higher HbA1c levels, greater insulin requirements, and elevated risk of complications including nephropathy, neuropathy, and cardiovascular disease.
  • NICE guidance (NG28) lists smoking cessation as a priority intervention in diabetes management for both type 1 and type 2 diabetes.
  • Stopping smoking may cause a short-term transient rise in HbA1c, often linked to weight gain, but medium- to long-term glycaemic control typically improves.
  • NHS Stop Smoking Services, nicotine replacement therapy, and pharmacological options such as varenicline are available free of charge and are recommended under NICE NG92.

How Smoking Affects HbA1c Levels

Smoking raises HbA1c by promoting insulin resistance and stimulating stress hormone release, which increases circulating blood glucose; carbon monoxide may also alter red blood cell lifespan, further influencing results.

Smoking has a well-documented influence on HbA1c levels, the blood test used to measure average blood glucose over the preceding two to three months. Research consistently shows that smokers tend to have higher HbA1c readings compared to non-smokers, even when other factors such as diet and physical activity are accounted for. Understanding why this happens requires looking at the direct metabolic effects of smoking and its broader impact on glucose regulation.

The primary mechanisms are metabolic rather than analytical. Nicotine and other compounds in tobacco smoke promote insulin resistance — a state in which the body's cells respond less effectively to insulin — leading to higher circulating blood glucose levels over time. Smoking also activates the sympathetic nervous system, stimulating the release of catecholamines (adrenaline and noradrenaline) and cortisol. These hormones stimulate the liver to release glucose into the bloodstream and impair insulin signalling, further raising blood sugar levels.

A secondary consideration involves red blood cell (RBC) biology. Carbon monoxide in cigarette smoke binds to haemoglobin to form carboxyhaemoglobin, which can alter RBC lifespan. Because HbA1c reflects glycation of haemoglobin over the lifespan of red blood cells (approximately 90–120 days), changes in RBC turnover can influence the result — though the direction and magnitude of this effect varies between individuals. This is a biological rather than a direct analytical interference, and its contribution to HbA1c changes in smokers is generally considered secondary to the effects of insulin resistance and raised blood glucose.

The cumulative effect of these mechanisms means that smokers are at greater risk of both developing type 2 diabetes and experiencing poorer glycaemic control if diabetes is already present. NICE guidance (NG28) recognises smoking as a modifiable risk factor in diabetes management, and smoking cessation is recommended as a priority intervention.

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Smoking, Red Blood Cell Turnover, and HbA1c Interpretation

Carbon monoxide from smoking can alter red blood cell lifespan and affect HbA1c readings, but smoking is not listed by NICE as a contraindication to HbA1c testing; discordant results should prompt complementary testing such as fasting plasma glucose or OGTT.

Beyond the genuine rise in blood glucose that smoking can cause, there are biological reasons why HbA1c results in smokers may require careful interpretation. This distinction matters clinically, as it can affect how results are used in diagnosis and monitoring.

Carbon monoxide from cigarette smoke binds to haemoglobin, forming carboxyhaemoglobin. This can alter red blood cell lifespan and turnover. Since HbA1c reflects glycation of haemoglobin over the lifespan of red blood cells, any change in RBC turnover can influence the result. A shorter RBC lifespan tends to lower HbA1c (as cells are replaced before accumulating as much glycation), while a longer lifespan may raise it. The net effect in any individual smoker depends on the degree of these changes.

It is important to note that, according to NGSP and IFCC analytical guidance, the principal recognised causes of HbA1c assay interference are haemoglobin variants (such as HbS or HbC), carbamylated haemoglobin (as seen in renal failure), and certain haematological conditions — not carboxyhaemoglobin directly interfering with immunoassay or HPLC methods. Smoking is not listed by NICE as a contraindication to using HbA1c for diagnosis. Modern HPLC methods are generally robust, though laboratories should be aware of haemoglobin variants in any patient.

Clinicians should therefore bear in mind that:

  • A smoker's HbA1c result should be interpreted alongside the full clinical picture, including smoking history

  • Where HbA1c results appear discordant with symptoms or clinical findings, complementary tests such as fasting plasma glucose or an oral glucose tolerance test (OGTT) may be appropriate, in line with NICE and WHO guidance

  • Smoking status should be documented at every diabetes review and factored into clinical decision-making

Impact of Smoking on Blood Sugar Control in Diabetes

Smokers with diabetes consistently show higher HbA1c levels, greater insulin requirements, and significantly elevated risk of complications including cardiovascular disease, nephropathy, and retinopathy.

For people already living with diabetes — whether type 1 or type 2 — smoking presents a significant additional challenge to achieving good blood sugar control. Studies have consistently demonstrated that smokers with diabetes have higher HbA1c levels, greater insulin requirements, and a higher risk of diabetes-related complications compared to non-smoking counterparts.

The mechanisms are multifactorial. Nicotine stimulates the release of catecholamines (adrenaline and noradrenaline), which promote glycogenolysis (the breakdown of glycogen to glucose) and gluconeogenesis (the production of new glucose in the liver). These effects can acutely raise blood glucose via catecholamine-mediated pathways following smoking. Over time, repeated glucose elevations contribute to a sustained rise in HbA1c.

Insulin resistance is another critical factor. Smoking impairs the signalling pathways through which insulin facilitates glucose uptake into muscle and fat cells. For people with type 2 diabetes, this worsens an already compromised system. For those with type 1 diabetes, it can lead to unpredictable glucose fluctuations and may increase the insulin doses needed to achieve the same glycaemic effect.

The consequences extend beyond HbA1c. Smokers with diabetes face a significantly elevated risk of:

  • Diabetic nephropathy (kidney disease)

  • Peripheral neuropathy (nerve damage)

  • Cardiovascular disease, including heart attack and stroke

  • Diabetic retinopathy (eye disease)

NICE guidance (NG28 for type 2 diabetes and NG17 for type 1 diabetes) highlights smoking cessation as a priority intervention for people with diabetes, recognising that stopping smoking can meaningfully improve both glycaemic control and long-term outcomes. NICE NG92 (Stop Smoking Interventions and Services) provides the evidence base for cessation support options.

What NHS and NICE Guidelines Say About Smoking and HbA1c Testing

NICE NG28 sets an HbA1c diagnostic threshold of 48 mmol/mol for diabetes; smoking is not a contraindication to testing, but results should be interpreted alongside the full clinical picture including smoking status.

NICE and NHS guidance provides a clear framework for HbA1c use in diabetes diagnosis and monitoring. HbA1c is the preferred diagnostic test for type 2 diabetes in the UK, with a threshold of 48 mmol/mol (6.5%) or above indicating diabetes, and 42–47 mmol/mol (6.0–6.4%) indicating non-diabetic hyperglycaemia (prediabetes), in line with NICE NG28 and WHO diagnostic criteria.

NICE guidance specifies that HbA1c may not be appropriate as a sole diagnostic tool in certain circumstances — principally where conditions affect red blood cell turnover or where haemoglobin variants are present (for example, haemoglobinopathies, haemolytic anaemia, or recent blood transfusion), and in pregnancy. Smoking is not explicitly listed as a contraindication to HbA1c testing for diagnosis. However, clinicians are advised to interpret all HbA1c results in the context of the patient's full clinical picture, which should include smoking status. Where results are discordant with symptoms or clinical findings, fasting plasma glucose or an OGTT should be considered per NICE and WHO guidance.

For ongoing monitoring in people with established diabetes, NICE recommends HbA1c testing every three to six months until levels are stable, then every six months thereafter (NG28 for type 2; NG17 for type 1). Smoking status should be recorded at every diabetes review, and cessation support offered proactively.

NHS Stop Smoking Services, nicotine replacement therapy (NRT), and pharmacological options such as varenicline or bupropion are available through the NHS, in line with NICE NG92. Prescribers should check current local formulary guidance and MHRA communications regarding product availability, as supply of some cessation medicines has been subject to periodic disruption. The MHRA and EMA support the broader evidence base recommending smoking cessation as part of comprehensive diabetes management.

Mechanism / Factor Effect on Blood Glucose / HbA1c Clinical Significance Guidance Reference
Nicotine-induced insulin resistance Impairs cellular glucose uptake; raises circulating blood glucose and HbA1c over time Primary driver of elevated HbA1c in smokers; worsens type 2 diabetes control NICE NG28
Catecholamine & cortisol release Stimulates hepatic glucose output (glycogenolysis, gluconeogenesis); acutely raises blood glucose Contributes to sustained HbA1c elevation; increases insulin requirements in type 1 and type 2 diabetes NICE NG28, NG17
Carboxyhaemoglobin & RBC turnover Alters red blood cell lifespan; may raise or lower HbA1c depending on net RBC turnover change Biological interference; HbA1c should be interpreted alongside full clinical picture in smokers NGSP / IFCC analytical guidance
Smoking as diagnostic confounder Smoking is not a contraindication to HbA1c testing; discordant results warrant fasting plasma glucose or OGTT Smoking status should be documented at every diabetes review and factored into result interpretation NICE NG28; WHO diagnostic criteria
Smoking cessation — short term Transient HbA1c rise possible due to weight gain, increased appetite, and metabolic changes Temporary effect; patients should be counselled not to be discouraged from continuing cessation NICE NG92
Smoking cessation — medium to long term Reduced insulin resistance, lower stress hormones; HbA1c trends towards levels seen in never-smokers Improves glycaemic control, insulin sensitivity, microvascular health, and cardiovascular risk NICE NG92, NG28, NG17
Cessation support options (NHS) NRT, varenicline, bupropion; integrated dietary and physical activity advice to mitigate weight gain Most effective when combined with behavioural support; check local formulary and MHRA supply updates NICE NG92; MHRA / EMA

How Stopping Smoking Influences Your HbA1c Reading

Stopping smoking may cause a short-term rise in HbA1c due to weight gain and metabolic changes, but long-term cessation improves insulin sensitivity and blood glucose regulation, with HbA1c levels gradually improving.

Quitting smoking can have a meaningful — though sometimes initially counterintuitive — effect on HbA1c levels. In the short term, some studies have observed a transient rise in HbA1c following smoking cessation. This is thought to be partly due to weight gain, which is common after stopping smoking, as well as changes in appetite and metabolism. Nicotine suppresses appetite and increases metabolic rate, so its removal can lead to increased caloric intake and reduced energy expenditure, both of which can temporarily affect glycaemic control. The timeframe and magnitude of this effect vary between individuals, and the evidence base continues to develop.

However, the medium- to long-term picture is considerably more positive. As the body recovers from the physiological effects of smoking — including reduced insulin resistance, lower levels of stress hormones, and improved cardiovascular function — blood glucose regulation tends to improve. Longitudinal data suggest that HbA1c levels in ex-smokers can gradually move towards those seen in people who have never smoked, particularly when cessation is accompanied by healthy lifestyle changes.

For people with diabetes, the benefits of stopping smoking extend well beyond HbA1c. Improvements in:

  • Insulin sensitivity, which may reduce the doses required

  • Microvascular circulation, benefiting kidney, eye, and nerve health

  • Cardiovascular risk, which is disproportionately elevated in people with diabetes who smoke

...are all well-evidenced outcomes of cessation. To help mitigate weight gain after quitting, NICE NG92 recommends that cessation support is integrated with dietary and physical activity advice, and referral to dietetic or weight management services should be considered where appropriate.

Healthcare professionals should counsel patients that any short-term worsening of HbA1c after quitting is typically temporary and should not discourage them from persisting with cessation efforts. The long-term gains far outweigh the transient challenges.

When to Speak to Your GP About HbA1c and Smoking

Smokers with an HbA1c in the prediabetes range, those struggling to meet diabetes targets, or anyone noticing glucose changes after quitting should contact their GP for further assessment and cessation support.

If you are a smoker — whether or not you have a diagnosis of diabetes — there are several situations in which it is important to speak to your GP about how smoking may be affecting your HbA1c and overall metabolic health.

Seek urgent or emergency care immediately if you experience:

  • Severe vomiting, abdominal pain, rapid or laboured breathing, confusion, or extreme drowsiness — these may be signs of diabetic ketoacidosis (DKA) or severe hyperglycaemia and require same-day urgent assessment. Call 999 or go to your nearest A&E if you are very unwell.

Contact your GP if:

  • Your HbA1c result has come back in the non-diabetic hyperglycaemia range (42–47 mmol/mol) and you are a current smoker — your result may warrant further investigation with a fasting plasma glucose or oral glucose tolerance test, in line with NICE and WHO guidance

  • You have been diagnosed with diabetes and are struggling to achieve your HbA1c target despite following dietary and medication advice, as smoking may be a contributing factor

  • You have recently stopped smoking and noticed changes in your blood glucose readings, or received an unexpectedly higher HbA1c result at your next review

  • You are experiencing symptoms suggestive of raised blood glucose, such as increased thirst, frequent urination, fatigue, or blurred vision

Your GP can arrange repeat or confirmatory testing, review your diabetes management plan, and refer you to NHS Stop Smoking Services if you are ready to quit. Smoking cessation support is available free of charge through the NHS and is significantly more effective when combined with behavioural support and pharmacotherapy, as outlined in NICE NG92.

It is also worth raising smoking at your annual diabetes review if you have not already done so. Diabetes care teams are well placed to offer tailored advice and can coordinate support across dietetics, pharmacy, and specialist nursing. Addressing smoking is one of the most impactful steps you can take to protect your long-term health — and your HbA1c is one measurable way to track the benefit.

Frequently Asked Questions

Does smoking directly raise HbA1c levels?

Yes. Smoking raises HbA1c by increasing insulin resistance and stimulating the release of stress hormones such as adrenaline and cortisol, which elevate blood glucose over time. Carbon monoxide may also alter red blood cell lifespan, further influencing the result.

Will my HbA1c improve if I stop smoking?

In the medium to long term, yes — stopping smoking reduces insulin resistance and lowers stress hormone levels, which typically improves blood glucose control and HbA1c. A short-term transient rise may occur due to weight gain after quitting, but this is usually temporary.

Should my GP know I smoke when interpreting my HbA1c result?

Yes. NICE guidance advises that HbA1c results should always be interpreted alongside the full clinical picture, including smoking status. If your result appears discordant with your symptoms, your GP may arrange a fasting plasma glucose or oral glucose tolerance test for clarification.


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