Understanding diabetes
Diabetes mellitus is a group of metabolic diseases characterised by chronically elevated blood glucose (hyperglycaemia). To understand what goes wrong, you first need to understand insulin — the key that unlocks your cells to allow glucose in.
When you eat carbohydrates, your digestive system breaks them down into glucose, which enters your bloodstream. Your pancreas detects rising blood sugar and releases insulin. Insulin acts like a key, binding to receptors on cells throughout your body and allowing glucose to enter and be used for energy.
In diabetes, this system breaks down in one of two fundamental ways: either the pancreas produces little or no insulin (Type 1), or cells stop responding normally to insulin — insulin resistance — and the pancreas cannot produce enough to compensate (Type 2). Without adequate insulin action, glucose accumulates in the bloodstream, and over time this persistent hyperglycaemia damages blood vessels and nerves throughout the body.
HbA1c (glycated haemoglobin) measures the percentage of haemoglobin molecules that have glucose attached. Because red blood cells live for about 3 months, HbA1c reflects your average blood sugar over the preceding 2–3 months. Normal: below 5.7%. Prediabetes: 5.7–6.4%. Diabetes: 6.5% or above. Treatment target for most people with diabetes: below 7.0%.
Types of diabetes
Type 1
- Autoimmune beta cell destruction
- 5–10% of all diabetes cases
- Often onset in childhood
- Requires lifelong insulin
- Not preventable
- Strong genetic component
Type 2
- Insulin resistance + beta cell dysfunction
- 90–95% of all cases
- Typically adult onset (rising in youth)
- Managed with lifestyle, oral drugs, ± insulin
- Largely preventable; can enter remission
- Strongly linked to obesity and inactivity
Gestational
- Develops during pregnancy
- ~7–10% of all pregnancies
- Usually resolves post-delivery
- Managed with diet, sometimes insulin
- Increases T2D risk later in life
- Risks to baby if uncontrolled
LADA
- Latent Autoimmune Diabetes in Adults
- "Type 1.5" — often misdiagnosed as T2
- Slower beta cell destruction
- Initially responds to oral medications
- Eventually requires insulin
- GAD antibody test confirms diagnosis
Prediabetes: the critical intervention window
Prediabetes affects 96 million American adults — roughly 1 in 3 — and the vast majority don't know they have it. The landmark Diabetes Prevention Program showed that intensive lifestyle intervention (7% weight loss + 150 minutes/week of physical activity) reduced progression to Type 2 diabetes by 58% over 3 years — far superior to metformin (31% reduction). Prediabetes does not have to become diabetes.
Symptoms and warning signs
The classic triad of diabetes symptoms reflects the body's response to high blood sugar: glucose spills into the urine, pulling water with it (causing frequent urination and thirst), and cells starved of glucose signal hunger and trigger fat and muscle breakdown (causing weight loss).
| Symptom | Why it happens | Type 1 | Type 2 |
|---|---|---|---|
| Excessive thirst | Dehydration from glucose-driven urination | Very common | Common |
| Frequent urination | Kidneys flush excess glucose | Very common | Common |
| Unexplained weight loss | Body breaks down fat and muscle for fuel | Very common | Less common |
| Extreme fatigue | Cells cannot access glucose for energy | Common | Common |
| Blurred vision | High glucose alters fluid balance in the lens | Common | Common |
| Slow-healing wounds | Impaired immune function and circulation | Moderate | Common |
| Tingling / numbness | Nerve damage from hyperglycaemia | If uncontrolled | Often first sign |
| Darkened skin (acanthosis nigricans) | Sign of insulin resistance | Absent | Common — neck, armpits |
Type 2 diabetes typically develops over years with minimal symptoms. By the time of diagnosis, up to 50% of patients already have evidence of complications — retinopathy, neuropathy, or kidney disease. This is why the ADA recommends screening everyone aged 35–70 who is overweight or obese, and earlier in those with additional risk factors.
DKA: Nausea, vomiting, abdominal pain, fruity breath, rapid breathing, confusion — mainly Type 1. Severe hypoglycaemia: Seizure, unconsciousness, or inability to self-treat low blood sugar — any type on insulin or sulfonylureas.
Diagnosis and screening
| Test | Normal | Prediabetes | Diabetes |
|---|---|---|---|
| Fasting plasma glucose | <100 mg/dL | 100–125 mg/dL | ≥126 mg/dL |
| HbA1c | <5.7% | 5.7–6.4% | ≥6.5% |
| 2-hr glucose (OGTT) | <140 mg/dL | 140–199 mg/dL | ≥200 mg/dL |
| Random glucose + symptoms | — | — | ≥200 mg/dL |
A diagnosis requires two abnormal results on separate occasions — unless classic symptoms are present with a random glucose ≥200 mg/dL, which is sufficient alone. HbA1c and fasting glucose are preferred for screening because they require no special preparation beyond overnight fasting.
Who should be screened?
- All adults aged 35–70 who are overweight (BMI ≥25) — every 3 years if normal
- Adults of any age with BMI ≥25 plus any risk factor (family history, hypertension, dyslipidaemia, PCOS, prior gestational diabetes, physical inactivity)
- Asian Americans: screen at BMI ≥23 due to higher metabolic risk at lower BMI
- All pregnant women: screen for gestational diabetes between 24–28 weeks
Complications of diabetes
Chronic hyperglycaemia damages blood vessels in two ways. Microvascular complications affect small vessels — eyes (retinopathy), kidneys (nephropathy), and nerves (neuropathy). Macrovascular complications arise from accelerated atherosclerosis — heart attack, stroke, and peripheral artery disease. People with diabetes have a 2–4× higher risk of cardiovascular events than the general population.
| Complication | Mechanism | Prevalence | Prevention |
|---|---|---|---|
| Diabetic retinopathy | Small vessel damage in retina | #1 cause of blindness in working-age adults | Annual eye exams; tight glucose + BP control |
| Diabetic nephropathy | Glomerular damage | #1 cause of end-stage renal disease in U.S. | ACE inhibitors/ARBs; SGLT2 inhibitors strongly protective |
| Diabetic neuropathy | Nerve damage from glucose toxicity | ~50% of people with diabetes | Glucose control; foot care; pain management |
| Diabetic foot / amputation | Neuropathy + vascular disease | ~100,000 amputations/year in U.S. | Daily foot inspection; podiatry care; footwear |
| Cardiovascular disease | Accelerated atherosclerosis | Leading cause of death in T2D | GLP-1/SGLT2 drugs; statins; BP control; lifestyle |
Treatment: medications
Type 1 diabetes requires insulin replacement therapy — there is no alternative. The goal is to mimic normal insulin secretion: a low background (basal) level plus mealtime (bolus) spikes.
- Basal-bolus regimen (MDI): Long-acting basal insulin once or twice daily plus rapid-acting insulin at each meal. Flexible and effective with carbohydrate counting training.
- Insulin pump (CSII): Continuous subcutaneous insulin infusion via a small pump. Delivers programmable basal rates and mealtime boluses with greater precision.
- Closed-loop / Artificial Pancreas: Pump linked to a CGM via an algorithm that automatically adjusts insulin in real time. Leading systems — Omnipod 5, Tandem Control-IQ — reduce hypoglycaemia and improve time-in-range significantly.
- Adjunct therapy: Some T1D patients benefit from adding a GLP-1 or SGLT2 inhibitor to reduce insulin doses — requires careful monitoring for DKA risk with SGLT2 inhibitors.
| Drug class | Key examples | HbA1c reduction | Weight effect | Key benefit |
|---|---|---|---|---|
| Metformin | Glucophage | 1–1.5% | Neutral / mild loss | First-line; inexpensive; CV-neutral |
| GLP-1 agonists | Semaglutide (Ozempic), Tirzepatide (Mounjaro) | 1–2%+ | Significant loss (5–22%) | CV benefit proven; now first-line with CVD or obesity |
| SGLT2 inhibitors | Empagliflozin (Jardiance), Dapagliflozin | 0.5–1% | Mild loss | Strong kidney and heart failure protection |
| DPP-4 inhibitors | Sitagliptin (Januvia) | 0.5–0.8% | Neutral | Well-tolerated; no hypoglycaemia; once daily |
| Sulfonylureas | Glipizide, Glimepiride | 1–1.5% | Weight gain | Inexpensive; risk of hypoglycaemia |
| Insulin | Glargine, Aspart, Lispro | Variable — very effective | Weight gain | Most powerful glucose-lowering agent |
For most patients with T2D and established cardiovascular disease or high CV risk, GLP-1 receptor agonists with proven CV benefit should be prioritised regardless of baseline HbA1c. For patients with heart failure or chronic kidney disease, SGLT2 inhibitors are preferred.
| Type | Onset | Peak | Duration | Use |
|---|---|---|---|---|
| Rapid-acting (Aspart, Lispro) | 10–20 min | 1–3 hr | 3–5 hr | Mealtime bolus — take just before eating |
| Ultra-rapid (Fiasp, Lyumjev) | 2–5 min | 1–2 hr | 3–5 hr | Can be taken at or after meals; ideal for pumps |
| Regular (short-acting) | 30–60 min | 2–4 hr | 5–8 hr | Older formulation; IV drips in hospital |
| Intermediate (NPH) | 1–2 hr | 4–12 hr | 14–24 hr | Less used; twice daily; hypoglycaemia risk |
| Long-acting (Glargine, Detemir) | 1–2 hr | No peak | 20–24 hr | Once-daily basal — backbone of T1D and many T2D regimens |
| Ultra-long-acting (Degludec) | 1 hr | No peak | 42+ hr | Very stable; lower hypoglycaemia risk |
| Inhaled (Afrezza) | 12–15 min | 30 min | 2–3 hr | Rapid-acting alternative — no injection at meals |
GLP-1 drugs explained: Ozempic, Mounjaro, and beyond
GLP-1 (glucagon-like peptide-1) is a hormone naturally released by cells in the gut after eating. GLP-1 receptor agonists mimic its actions: stimulating insulin secretion (only when blood sugar is elevated — minimal hypoglycaemia risk), suppressing glucagon, slowing gastric emptying, and acting on brain appetite centres to reduce hunger.
| Drug | Type | Dosing | HbA1c↓ | Weight loss | CV benefit |
|---|---|---|---|---|---|
| Semaglutide (Ozempic) | GLP-1 agonist | Weekly SC | ~1.5–2.0% | ~6–15% | Yes (SUSTAIN-6) |
| Semaglutide (Wegovy) | GLP-1 agonist (higher dose) | Weekly SC | Weight indication | ~15–17% | Yes (SELECT) |
| Tirzepatide (Mounjaro) | GLP-1 + GIP dual agonist | Weekly SC | ~2.0–2.4% | ~15–22% | Trial ongoing |
| Liraglutide (Victoza) | GLP-1 agonist | Daily SC | ~1.0–1.5% | ~5–8% | Yes (LEADER) |
| Semaglutide oral (Rybelsus) | GLP-1 agonist (oral) | Daily tablet | ~1.0–1.4% | ~3–4% | Neutral |
| Dulaglutide (Trulicity) | GLP-1 agonist | Weekly SC | ~1.1–1.6% | ~2–4% | Yes (REWIND) |
Most common side effects are gastrointestinal — nausea, vomiting, diarrhoea — which typically improve as the dose is gradually escalated. GLP-1 drugs should generally be avoided in patients with a personal or family history of medullary thyroid carcinoma or MEN2, or active pancreatitis.
Rapid significant weight loss from any cause can lead to facial volume loss and a more aged appearance. This is not unique to semaglutide. The appropriate response is not to avoid effective treatment for a serious metabolic condition, but to discuss the options with a healthcare provider if cosmetic concerns arise.
Nutrition and lifestyle for diabetes
There is no single "diabetic diet." The evidence supports several dietary patterns that share core principles: emphasising whole foods, limiting ultra-processed foods and refined carbohydrates, and matching carbohydrate intake to individual metabolic capacity.
- Mediterranean diet: Olive oil, fish, vegetables, legumes, whole grains, nuts. Strongest overall evidence for cardiovascular risk reduction in diabetes.
- Low-carbohydrate (<130g carbs/day): Produces the largest short-term HbA1c reductions. Particularly effective for Type 2 — some patients achieve remission. Requires careful medication adjustment to avoid hypoglycaemia.
- Very low-calorie diet (800 kcal/day): Used in structured programmes like the DiRECT trial to produce rapid weight loss and T2D remission. Requires medical supervision.
- Physical activity: Exercise takes up glucose independently of insulin. The ADA recommends 150+ minutes/week of moderate aerobic exercise plus resistance training 2–3 days/week.
Diabetes technology
Continuous Glucose Monitors (CGM)
CGM systems use a small sensor inserted under the skin that measures glucose every 5 minutes, transmitting readings to a smartphone. Leading systems include Dexcom G7, Abbott FreeStyle Libre 3, and Medtronic Guardian 4. The key metric is Time in Range (TIR) — percentage of readings between 70–180 mg/dL. Target: >70% for most adults.
Hybrid closed-loop systems (artificial pancreas)
Connect an insulin pump to a CGM via an algorithm that automatically adjusts basal insulin delivery based on real-time glucose readings. Leading systems: Tandem t:slim X2 with Control-IQ, Omnipod 5, Medtronic MiniMed 780G. Clinical trials consistently show improved TIR, reduced hypoglycaemia, and better quality of life compared to manual regimens.
Frequently asked questions
Type 1 is an autoimmune condition where the immune system destroys insulin-producing beta cells — requiring lifelong insulin therapy. It is not caused by diet or lifestyle and is not preventable. Type 2 is a progressive metabolic condition where cells become resistant to insulin and the pancreas cannot compensate — managed initially with lifestyle changes and oral medications. Type 2 is strongly linked to obesity, inactivity, and genetics, and can often be prevented or put into remission with intensive lifestyle intervention.
Yes — significant weight loss (10–15% of body weight) through intensive dietary intervention or bariatric surgery can achieve remission of Type 2 diabetes in many patients, meaning normal blood sugar without medications. The DiRECT trial showed 46% of participants achieved remission at one year with a structured very low-calorie diet. Remission is more likely in those with shorter duration of diabetes and less beta cell damage.
Classic early symptoms include excessive thirst, frequent urination, unexplained weight loss, blurred vision, and fatigue. In Type 1, these can develop rapidly over days to weeks. In Type 2, symptoms often develop slowly over years — or are completely absent. Many people with Type 2 are diagnosed incidentally during routine blood tests.
No. Ozempic (semaglutide) is a GLP-1 receptor agonist — a completely different class from insulin. It mimics the gut hormone GLP-1, stimulating insulin release only when blood sugar is elevated, suppressing glucagon, slowing gastric emptying, and reducing appetite. It cannot replace insulin for Type 1 diabetes. When used alone, it does not cause dangerous hypoglycaemia — a significant advantage over many diabetes medications.
Diabetes is diagnosed by any of: fasting plasma glucose ≥126 mg/dL; 2-hour glucose ≥200 mg/dL during an OGTT; HbA1c ≥6.5%; or random glucose ≥200 mg/dL with classic symptoms. Prediabetes is fasting glucose 100–125 mg/dL or HbA1c 5.7–6.4%. A single abnormal result requires confirmation on a separate day unless symptoms are present.
- International Diabetes Federation. IDF Diabetes Atlas, 10th edition. 2021.
- American Diabetes Association. Standards of Care in Diabetes — 2024. Diabetes Care. 2024;47(Suppl 1):S1–S321.
- Diabetes Prevention Program Research Group. Reduction in Type 2 Diabetes with Lifestyle Intervention or Metformin. NEJM. 2002;346(6):393–403.
- Lean MEJ, et al. Primary care-led weight management for remission of type 2 diabetes (DiRECT). Lancet. 2018;391(10120):541–551.
- Marso SP, et al. Semaglutide and Cardiovascular Outcomes in Type 2 Diabetes (SUSTAIN-6). NEJM. 2016;375:1834–1844.
- Zinman B, et al. Empagliflozin, Cardiovascular Outcomes, and Mortality in Type 2 Diabetes (EMPA-REG). NEJM. 2015;373:2117–2128.
- Jastreboff AM, et al. Tirzepatide for Obesity (SURMOUNT-1). NEJM. 2022;387:205–216.