Type 2 Diabetes

Intro

Type 2 diabetes (T2D) is a chronic metabolic condition characterised by insulin resistance and a progressive decline in the pancreas’s ability to produce enough insulin to compensate. It is by far the most common form of diabetes, accounting for approximately 90—95% of all cases worldwide.

Unlike Type 1 diabetes, Type 2 typically develops over years and is strongly associated with modifiable risk factors such as excess body weight, physical inactivity, and dietary patterns — though genetics, age, and ethnicity also play substantial roles. Many people have elevated blood glucose for years before diagnosis, during which time organ damage may already be occurring.

This guide provides a plain-language, evidence-based overview of Type 2 diabetes: who is at risk, how it is detected and diagnosed, what treatment options exist, and why cardiometabolic risk management is central to modern care. It is not a substitute for individual medical advice. If you’re unsure how Type 1 and Type 2 diabetes differ, see our overview explaining the distinction.

Key Points

Type 2 diabetes is driven by insulin resistance — the body’s cells respond less effectively to insulin — combined with a gradual decline in insulin production.
It is strongly linked to overweight and obesity, physical inactivity, and family history, though it can occur in people of any body size.
T2D often develops silently; many people have no symptoms at diagnosis and are identified through routine screening.
Lifestyle modification (diet, physical activity, weight management) is the foundation of treatment at every stage.
Several medication classes are available, including metformin, GLP-1 receptor agonists, SGLT2 inhibitors, and insulin, each with different mechanisms and benefits.
People with T2D face elevated cardiometabolic risk — heart disease and stroke are the leading causes of death in this population.
Early detection and sustained glucose, blood pressure, and lipid management significantly reduce the risk of complications.

Deep Dive

What Type 2 diabetes is

In a healthy metabolism, the hormone insulin — produced by beta cells in the pancreas — enables cells throughout the body to take up glucose from the bloodstream and use it for energy. In Type 2 diabetes, two interrelated problems develop:

Insulin resistance: Muscle, liver, and fat cells become less responsive to insulin’s signal, so more insulin is needed to achieve the same effect.
Beta-cell dysfunction: Over time, the pancreas cannot keep up with the increased demand for insulin, and blood glucose levels rise.

This process is gradual. Most people pass through an intermediate stage called prediabetes (impaired fasting glucose or impaired glucose tolerance) before meeting the diagnostic threshold for diabetes. Prediabetes is itself associated with increased cardiovascular risk.

Key features of T2D include:

Relative insulin deficiency — the pancreas still produces insulin, but not enough to overcome resistance.
Strong genetic component — having a first-degree relative with T2D substantially increases risk.
Modifiable risk factors — excess visceral adiposity, sedentary behaviour, and certain dietary patterns are well-established contributors.
Variable presentation — some people are diagnosed with significant symptoms; many are identified through routine blood tests with no symptoms at all.

Type 2 vs Type 1

Type 2 and Type 1 diabetes both result in elevated blood glucose, but they differ in their underlying cause, typical onset, and management approach:

Feature	Type 2	Type 1
Underlying cause	Insulin resistance with progressive beta-cell decline	Autoimmune destruction of beta cells
Insulin production	Initially normal or elevated; declines over time	Little to none
Typical onset	Adulthood (increasingly seen in younger populations)	Childhood / young adulthood (any age possible)
Body habitus at diagnosis	Frequently associated with overweight/obesity	Often normal weight
Primary treatment	Lifestyle changes, oral medications, injectables, and sometimes insulin	Insulin (always required)
Proportion of diabetes cases	~90—95%	~5—10%
Autoantibodies	Absent	Present (GAD65, IA-2, ZnT8, IAA)

It is worth noting that the distinction is not always clear-cut. Some adults diagnosed with apparent T2D may actually have latent autoimmune diabetes in adults (LADA), a slower-onset form of autoimmune diabetes. Autoantibody testing can help clarify the diagnosis when there is clinical uncertainty.

Screening & diagnosis

Because Type 2 diabetes can be asymptomatic for years, screening plays a critical role in early detection.

Who should be screened (consistent with ADA recommendations):

All adults aged 35 and older (repeated at least every 3 years if results are normal).
Adults of any age who are overweight or obese and have one or more additional risk factors, including:
- First-degree relative with diabetes
- High-risk racial/ethnic background (e.g., African American, Hispanic/Latino, Native American, Asian American, Pacific Islander)
- History of gestational diabetes
- Polycystic ovary syndrome (PCOS)
- Physical inactivity
- Hypertension, dyslipidaemia, or cardiovascular disease
People with prediabetes (tested annually).

Diagnostic tests and thresholds:

Test	Prediabetes	Diabetes
Fasting plasma glucose	5.6—6.9 mmol/L (100—125 mg/dL)	7.0 mmol/L (126 mg/dL) or higher
HbA1c	39—47 mmol/mol (5.7—6.4%)	48 mmol/mol (6.5%) or higher
2-hour OGTT	7.8—11.0 mmol/L (140—199 mg/dL)	11.1 mmol/L (200 mg/dL) or higher
Random plasma glucose	—	11.1 mmol/L (200 mg/dL) or higher with classic symptoms

A diagnosis of diabetes generally requires two abnormal results from the same or different tests, unless unambiguous hyperglycaemia is present with classic symptoms.

Common symptoms (when present):

Increased thirst and frequent urination
Fatigue
Blurred vision
Slow-healing wounds or frequent infections
Tingling or numbness in the hands or feet
Darkened skin patches (acanthosis nigricans), especially around the neck or armpits

Treatment options

Type 2 diabetes management is progressive — treatment intensifies over time as the condition evolves. The overarching goals are to maintain blood glucose within a target range, reduce cardiometabolic risk, prevent complications, and support quality of life.

Lifestyle modification:

Lifestyle change is the cornerstone of T2D management and is recommended at every stage, including alongside medication.

Dietary approaches: No single “diabetes diet” is prescribed. Evidence supports several patterns, including Mediterranean, DASH, and low-carbohydrate approaches. The emphasis is on whole foods, adequate fibre, controlled portions, and limiting ultra-processed foods and added sugars.
Physical activity: Guidelines generally recommend at least 150 minutes per week of moderate-intensity aerobic activity (e.g., brisk walking), plus resistance training 2—3 times per week. Activity improves insulin sensitivity independent of weight loss.
Weight management: For people with T2D and overweight or obesity, even modest weight loss (5—10% of body weight) can meaningfully improve glycaemic control, blood pressure, and lipid levels. Greater weight loss (15% or more) has been associated with diabetes remission in some studies.
Smoking cessation: Smoking worsens insulin resistance and substantially increases cardiovascular risk. Cessation is strongly recommended.

Metformin:

Usually the first-line pharmacological therapy for T2D.
Works primarily by reducing hepatic glucose production and improving insulin sensitivity.
Well-established safety profile, low cost, and weight-neutral or mildly weight-reducing.
Most common side effects are gastrointestinal (nausea, diarrhoea), which often improve with time or extended-release formulations.

GLP-1 receptor agonists (e.g., semaglutide, liraglutide, dulaglutide, tirzepatide):

Injectable (and in some cases oral) medications that mimic the incretin hormone GLP-1.
Stimulate insulin secretion in a glucose-dependent manner, suppress glucagon, slow gastric emptying, and reduce appetite.
Associated with significant weight loss in addition to glucose lowering.
Cardiovascular outcome trials have demonstrated reductions in major adverse cardiovascular events (heart attack, stroke, cardiovascular death) with several agents in this class.
Common side effects include nausea, vomiting, and diarrhoea, which typically diminish over time.

SGLT2 inhibitors (e.g., empagliflozin, dapagliflozin, canagliflozin):

Oral medications that block glucose reabsorption in the kidneys, causing excess glucose to be excreted in the urine.
Provide modest glucose lowering, weight reduction, and blood pressure reduction.
Cardiovascular and renal outcome trials have shown benefits in reducing heart failure hospitalisations and slowing progression of chronic kidney disease, independent of glucose-lowering effects.
Notable side effects include genital mycotic infections and, rarely, diabetic ketoacidosis (euglycaemic DKA).

Insulin:

May be needed when other therapies are insufficient to achieve glycaemic targets, or at diagnosis if blood glucose is very high.
T2D insulin regimens vary widely — from a single daily injection of basal insulin to more intensive regimens with mealtime doses.
Insulin is effective at lowering glucose but carries risks of hypoglycaemia and weight gain.
The decision to start insulin is individualised and does not represent a “failure” of management.

Other medication classes:

Sulfonylureas (e.g., gliclazide, glimepiride) — stimulate insulin secretion; effective and low-cost but carry a higher risk of hypoglycaemia and weight gain.
DPP-4 inhibitors (e.g., sitagliptin, linagliptin) — enhance incretin activity; well tolerated and weight-neutral but provide more modest glucose lowering.
Thiazolidinediones (e.g., pioglitazone) — improve insulin sensitivity; effective but associated with weight gain, fluid retention, and bone fracture risk.

Treatment selection increasingly considers not just glucose control but also cardiovascular and renal benefit profiles, weight effects, side-effect burden, cost, and patient preference.

Cardiometabolic risk

Cardiovascular disease is the leading cause of morbidity and mortality in people with Type 2 diabetes. T2D rarely exists in isolation — it frequently clusters with other metabolic risk factors in a pattern sometimes called metabolic syndrome:

Central (abdominal) obesity
Elevated blood glucose
Hypertension
Dyslipidaemia (elevated triglycerides, low HDL cholesterol)

Why cardiometabolic risk matters:

Adults with T2D have a 2- to 4-fold higher risk of cardiovascular events compared to those without diabetes.
Heart attack, stroke, heart failure, and peripheral arterial disease are all more common.
Chronic kidney disease frequently coexists with T2D and is both a consequence of and a contributor to cardiovascular risk.

Managing cardiometabolic risk:

Modern T2D guidelines emphasise a comprehensive approach that goes beyond glucose alone:

Blood pressure management: Target levels are generally below 130/80 mmHg for most people with diabetes (specific targets are individualised). ACE inhibitors or ARBs are often first-line, particularly when kidney disease is present.
Lipid management: Statin therapy is recommended for most adults with T2D based on cardiovascular risk assessment. LDL cholesterol targets depend on overall risk profile.
Antiplatelet therapy: Aspirin may be considered for secondary prevention (after a cardiovascular event) and in some primary prevention scenarios, based on individualised risk-benefit assessment.
Medication selection for glucose lowering: GLP-1 receptor agonists and SGLT2 inhibitors are now preferred add-on therapies for people with T2D who have established cardiovascular disease, heart failure, or chronic kidney disease, because of their demonstrated organ-protective benefits beyond glucose control.
Weight management: Sustained weight loss reduces blood pressure, improves lipids, and lowers glucose — addressing multiple risk factors simultaneously.

FAQ

Q: Can Type 2 diabetes be reversed or put into remission? A: In some cases, yes. Significant weight loss — through lifestyle changes, structured programmes, or bariatric surgery — has been shown to achieve diabetes remission (defined as HbA1c below the diabetes threshold without glucose-lowering medication) in some people, particularly those diagnosed recently. However, remission is not guaranteed, may not be permanent, and ongoing monitoring is still recommended.

Q: Is Type 2 diabetes caused by eating too much sugar? A: Not directly. T2D is caused by insulin resistance and beta-cell dysfunction, which develop through a combination of genetic predisposition, excess body weight, physical inactivity, and other factors. While high sugar intake can contribute to weight gain and overall metabolic burden, no single food causes diabetes.

Q: Do all people with Type 2 diabetes eventually need insulin? A: Not necessarily. Many people manage T2D effectively with lifestyle changes and non-insulin medications for years or decades. However, because beta-cell function tends to decline over time, some people will eventually need insulin to maintain adequate glucose control. This is a natural progression of the disease, not a failure of treatment.

Q: What is HbA1c and what should it be? A: HbA1c (glycated haemoglobin) reflects average blood glucose over the preceding 2—3 months. For most adults with T2D, guidelines suggest a target of below 53 mmol/mol (7.0%), though targets are individualised based on age, duration of diabetes, comorbidities, and risk of hypoglycaemia. Less stringent targets may be appropriate for older adults or those with significant comorbidities.

Q: Is metformin safe long-term? A: Metformin has been used for decades and has an extensive safety record. It is generally well tolerated. Long-term use can reduce vitamin B12 absorption, so periodic monitoring is recommended. It should be used with caution in people with significant kidney impairment, and dosing may need to be adjusted based on kidney function.

Q: Why are GLP-1 receptor agonists and SGLT2 inhibitors increasingly prescribed? A: Beyond their glucose-lowering effects, several GLP-1 receptor agonists and SGLT2 inhibitors have shown cardiovascular and/or renal benefits in large clinical trials. Guidelines now recommend them preferentially for people with T2D who have or are at high risk of cardiovascular disease, heart failure, or chronic kidney disease.

Q: Can young people get Type 2 diabetes? A: Yes. While T2D has traditionally been considered an adult-onset condition, rising rates of childhood obesity have led to increasing diagnoses in adolescents and young adults. T2D in younger people tends to progress more aggressively and may be harder to manage than in older adults.

Q: How often should someone with Type 2 diabetes see their doctor? A: This varies by individual circumstances, but most guidelines recommend HbA1c testing every 3—6 months and at least annual comprehensive reviews that include blood pressure, lipid panel, kidney function, eye examination, and foot assessment. People on insulin or with unstable glucose levels may need more frequent contact.