Type 1 and type 2 diabetes are the two principal forms of diabetes mellitus, yet they differ fundamentally in their causes, onset, and treatment. Type 1 diabetes is an autoimmune condition causing absolute insulin deficiency, typically presenting acutely in younger people and requiring lifelong insulin therapy. Type 2 diabetes develops gradually due to insulin resistance and relative insulin deficiency, usually in adults, and can often be managed initially through lifestyle changes and oral medications. Understanding these key differences is essential for accurate diagnosis, appropriate treatment selection, and effective long-term management. Both conditions share similar complications, but their distinct underlying mechanisms necessitate tailored therapeutic approaches aligned with NICE guidance.

What Is the Difference Between Type 1 and Type 2 Diabetes?

Diabetes mellitus encompasses a group of metabolic disorders characterised by chronic hyperglycaemia resulting from defects in insulin secretion, insulin action, or both. The two principal forms—type 1 and type 2 diabetes—differ fundamentally in their pathophysiology, onset patterns, and management approaches.

Type 1 diabetes is an autoimmune condition in which the body's immune system destroys the insulin-producing beta cells in the pancreatic islets of Langerhans. This results in absolute insulin deficiency, meaning the pancreas produces little to no insulin. Without insulin, glucose cannot enter cells effectively, leading to elevated blood glucose levels whilst cells are starved of energy. Type 1 diabetes typically presents in childhood or adolescence, though it can occur at any age. When diagnosed in adults, it may initially be termed latent autoimmune diabetes in adults (LADA)—a slower-onset autoimmune form that may not require insulin immediately but progresses to insulin dependence, usually within months to a few years. Insulin therapy is essential for survival in type 1 diabetes; most individuals require it from diagnosis, though some adults with LADA may initially manage with other treatments before progressing to insulin.

Type 2 diabetes, by contrast, is characterised by insulin resistance combined with relative insulin deficiency. In this condition, the body's cells become less responsive to insulin, and over time the pancreas cannot produce sufficient insulin to overcome this resistance. Type 2 diabetes usually develops gradually in adults, particularly those over 40 years (or over 25 years in people of South Asian, African-Caribbean, or Black African descent), though increasing rates are now seen in younger populations due to rising obesity levels. Unlike type 1 diabetes, type 2 can often be managed initially through lifestyle modifications, oral medications, or non-insulin injectable therapies, though some individuals eventually require insulin.

Understanding these fundamental differences is essential for appropriate diagnosis, treatment selection, and patient education. Whilst both conditions result in hyperglycaemia and share similar long-term complications, their distinct underlying mechanisms necessitate different therapeutic approaches. NICE guidance (NG17, NG28) provides detailed UK-specific recommendations for diagnosis and management of both diabetes types.

Causes and Risk Factors: Type 1 vs Type 2 Diabetes

The aetiological factors underlying type 1 and type 2 diabetes are markedly different, reflecting their distinct pathophysiological mechanisms.

Type 1 diabetes arises from autoimmune destruction of pancreatic beta cells. The precise trigger for this autoimmune process remains incompletely understood, though it likely involves a combination of genetic susceptibility and environmental factors. Certain human leucocyte antigen (HLA) genotypes, particularly HLA-DR3 and HLA-DR4, confer increased risk. Environmental triggers that may precipitate the autoimmune response in genetically susceptible individuals include:

• Viral infections (particularly enteroviruses)

• Early dietary factors (though evidence remains inconclusive)

• Vitamin D deficiency (suggested but not definitively proven)

Importantly, type 1 diabetes is not caused by lifestyle factors such as diet or physical inactivity. Family history plays a modest role—having a first-degree relative with type 1 diabetes increases risk, but most people diagnosed have no family history of the condition.

Type 2 diabetes has a stronger genetic component, with higher concordance in identical twins than type 1 diabetes. However, environmental and lifestyle factors play a predominant role in disease expression. Major risk factors include:

• Obesity, particularly central (abdominal) adiposity—the single most important modifiable risk factor (BMI ≥25 kg/m² in White populations; ≥23 kg/m² in South Asian, African-Caribbean, Black African, and Chinese populations)

• Physical inactivity—sedentary behaviour independently increases risk

• Age—risk increases substantially after 40 years (25 years in certain ethnic groups)

• Ethnicity—people of South Asian, African-Caribbean, and Black African descent face 2–4 times higher risk

• Family history—having a first-degree relative with type 2 diabetes significantly elevates risk

• Impaired glucose regulation—HbA1c 42–47 mmol/mol (non-diabetic hyperglycaemia) substantially increases progression risk

• Gestational diabetes—women with previous gestational diabetes have up to 50% risk of developing type 2 diabetes within 5–10 years postpartum

• Polycystic ovary syndrome (PCOS)

• Certain medications—including corticosteroids and some antipsychotics

NICE guidance (PH38) emphasises the importance of identifying individuals at high risk through validated risk assessment tools such as the Leicester Practice Risk Score or QDiabetes, enabling targeted prevention strategies. The NHS Diabetes Prevention Programme offers structured lifestyle modification programmes for people at high risk, including those with non-diabetic hyperglycaemia.

Symptoms and Diagnosis of Type 1 and Type 2 Diabetes

Whilst both forms of diabetes can present with classical hyperglycaemic symptoms, the onset pattern and severity typically differ substantially.

Type 1 diabetes characteristically presents acutely over days to weeks with pronounced symptoms including:

• Polyuria (excessive urination)

• Polydipsia (excessive thirst)

• Unexplained weight loss (often rapid and significant)

• Fatigue and lethargy

• Blurred vision

• Recurrent infections (particularly thrush)

Approximately 25–30% of individuals with type 1 diabetes present in diabetic ketoacidosis (DKA)—a life-threatening emergency characterised by hyperglycaemia, ketosis, and metabolic acidosis. DKA symptoms include nausea, vomiting, abdominal pain, rapid breathing, and altered consciousness. Any suspicion of DKA requires immediate emergency assessment.

Urgent referral is essential for suspected type 1 diabetes: adults should have same-day specialist diabetes team contact (within 24 hours); children and young people require same-day emergency referral to paediatric diabetes services.

Type 2 diabetes often develops insidiously, with many individuals remaining asymptomatic for years. When symptoms occur, they tend to be milder and more gradual than in type 1 diabetes. Many cases are identified through opportunistic screening or investigation of complications such as retinopathy or neuropathy. Some individuals present with hyperosmolar hyperglycaemic state (HHS), though this is less common than DKA in type 1 diabetes and also requires emergency assessment.

Diagnostic criteria are identical for both types and based on plasma glucose or HbA1c measurements:

• Fasting plasma glucose ≥7.0 mmol/L

• Random plasma glucose ≥11.1 mmol/L (in presence of symptoms)

• HbA1c ≥48 mmol/mol (6.5%)

• 2-hour plasma glucose ≥11.1 mmol/L during oral glucose tolerance test

Important limitations of HbA1c for diagnosis: HbA1c should not be used for diagnosis in children and young people, pregnancy, suspected type 1 diabetes or rapid-onset symptoms (within 2–3 months), haemoglobinopathies, chronic kidney disease, HIV, recent steroid therapy, or conditions affecting red cell turnover. In these situations, glucose-based diagnostic tests should be used.

In asymptomatic individuals, diagnosis requires confirmation with a repeat test. Following biochemical confirmation, distinguishing between type 1 and type 2 diabetes relies on clinical features (age, body habitus, presentation acuity) and, where uncertainty exists, additional investigations including:

• C-peptide measurement—low or undetectable levels suggest type 1 diabetes (most informative outside the immediate post-diagnosis period)

• Diabetes-associated autoantibodies—including anti-GAD, anti-IA2, and anti-ZnT8 antibodies; positivity rates are high in children with type 1 diabetes but lower in older adults with LADA

These tests are not routine but should be used when classification is uncertain, as accurate classification is essential and fundamentally determines treatment approach. When diagnostic uncertainty persists, specialist diabetes team input should be sought promptly.

Long-Term Complications and Management Strategies

Both type 1 and type 2 diabetes share similar long-term complications arising from chronic hyperglycaemia, though the management strategies to prevent these complications differ according to diabetes type.

Microvascular complications affect small blood vessels and include:

• Diabetic retinopathy—the leading cause of blindness in working-age adults; the NHS Diabetic Eye Screening Programme invites all people with diabetes from age 12 (type 2 diabetes at or soon after diagnosis), with annual screening thereafter

• Diabetic nephropathy—progressive kidney damage potentially leading to end-stage renal disease; monitored through annual urine albumin-creatinine ratio and estimated glomerular filtration rate

• Diabetic neuropathy—nerve damage causing pain, numbness, or loss of sensation, particularly in feet; annual foot examinations are essential

Macrovascular complications affect large blood vessels, substantially increasing risk of:

• Coronary heart disease and myocardial infarction

• Cerebrovascular disease and stroke

• Peripheral arterial disease

People with diabetes face 2–4 times higher cardiovascular risk than the general population, necessitating comprehensive cardiovascular risk management including blood pressure control, lipid management, and antiplatelet therapy for secondary prevention (not routinely for primary prevention in diabetes).

Management of type 1 diabetes centres on insulin replacement therapy, which must be individualised. Options include:

• Multiple daily injection regimens—combining long-acting basal insulin with rapid-acting bolus insulin at mealtimes

• Continuous subcutaneous insulin infusion (insulin pump therapy)—recommended by NICE for individuals meeting specific criteria

• Hybrid closed-loop systems—increasingly available, offering automated insulin delivery adjusted by continuous glucose monitoring

Structured education programmes such as DAFNE (Dose Adjustment For Normal Eating) empower individuals to adjust insulin doses based on carbohydrate intake, promoting flexibility whilst optimising glycaemic control. NICE (NG17) recommends HbA1c targets of ≤48 mmol/mol (6.5%) for most adults, though individualised targets may be appropriate.

Management of type 2 diabetes follows a stepwise approach:

1. Lifestyle modification—dietary changes emphasising reduced refined carbohydrates and saturated fats, increased physical activity (≥150 minutes moderate-intensity exercise weekly), and weight loss (particularly beneficial for those with BMI ≥25 kg/m², or ≥23 kg/m² in South Asian and other high-risk ethnic groups). For some people with recent-onset type 2 diabetes, structured weight management programmes may support remission.

2. Metformin—first-line pharmacotherapy unless contraindicated, improving insulin sensitivity

3. Additional glucose-lowering therapies—selected based on individual factors:

4. SGLT2 inhibitors are prioritised (with or without metformin) for people with established cardiovascular disease, chronic heart failure, or chronic kidney disease

5. GLP-1 receptor agonists offer weight loss and cardiovascular benefits and are recommended for people with obesity or established cardiovascular disease

6. Other options include DPP-4 inhibitors, sulfonylureas, or insulin, selected according to hypoglycaemia risk, weight considerations, and individual circumstances

NICE (NG28) recommends HbA1c targets based on therapy-related hypoglycaemia risk: ≤48 mmol/mol for adults managed by lifestyle and diet or with drugs not associated with hypoglycaemia (e.g., metformin, SGLT2 inhibitors, GLP-1 receptor agonists); ≤53 mmol/mol when treatment includes drugs associated with hypoglycaemia risk (e.g., sulfonylureas, insulin).

Patient self-management is crucial for both diabetes types. Individuals should:

• Monitor blood glucose as recommended by their healthcare team

• Attend annual diabetes reviews including retinal screening (via NHS Diabetic Eye Screening Programme from age 12), foot examinations, and kidney function assessment

• Maintain healthy lifestyle habits

• Recognise and respond appropriately to hypoglycaemia (blood glucose <4 mmol/L)—treat with 15–20 g fast-acting carbohydrate, retest after 15 minutes

• Contact their GP urgently if experiencing persistent hyperglycaemia, recurrent hypoglycaemia, or symptoms suggesting complications

• Seek immediate medical attention for suspected DKA (particularly in type 1 diabetes) or HHS

• Seek same-day urgent specialist foot care for active foot problems including ulceration, infection, ischaemia, or new severe neuropathic pain

Multidisciplinary diabetes care, involving specialist nurses, dietitians, podiatrists, and physicians, optimises outcomes. With appropriate management and regular monitoring, individuals with both type 1 and type 2 diabetes can minimise complication risk and maintain excellent quality of life.

Frequently Asked Questions