Diabetes and blood sugar
Diabetes is, at heart, a problem of fuel. Every cell in your body runs on glucose — sugar carried in the blood — and there is an exquisite system, built around a single hormone called insulin, that keeps the amount of it in a narrow, safe band hour by hour. Diabetes is what happens when that system breaks: either the hormone stops being made, or the body stops listening to it. The result is the same — sugar piles up in the blood where it does slow damage — but the two routes to it are almost opposite diseases that happen to share a name. This page is for anyone who wants to understand diabetes from first principles: what blood sugar and insulin actually are, how the types differ, how it is diagnosed and watched, why it matters, the extraordinary history of the cure that wasn't quite a cure, and how it is managed today. It is written to be useful whether you have just been diagnosed, love someone who has, or are simply curious.
What diabetes actually is
Start with the fuel. When you eat — especially carbohydrates — your gut breaks the food down into glucose, a simple sugar, which is absorbed into the bloodstream. Glucose is the body's universal currency of energy: your brain in particular runs on almost nothing else. But glucose cannot, for the most part, simply wander into cells on its own. Most cells need to be told to take it up, and the molecule that does the telling is a hormone called insulin.
Insulin is made by clusters of cells in the pancreas, a gland tucked behind the stomach. Scattered through it are perhaps a million tiny cell-islands called the islets of Langerhans, and within them the beta cells that manufacture insulin. When blood glucose rises after a meal, the beta cells sense it and release insulin into the blood. Insulin acts like a key: it docks onto receptors on muscle, fat and liver cells and signals them to open glucose channels and pull sugar out of the blood — burning it, or storing it as glycogen and fat for later. As the sugar moves out of the blood and into the cells, blood glucose falls back to baseline. The whole loop is a thermostat.
There is a mirror hormone too. When blood glucose drops too low — between meals, overnight, during exercise — the alpha cells in the same islets release glucagon, which does the opposite: it tells the liver to break stored glycogen back down and release glucose into the blood, pushing the level back up. Insulin lowers, glucagon raises, and between them they hold blood sugar in a remarkably tight range — roughly 4–7 mmol/L (about 70–130 mg/dL) in someone without diabetes — whatever you eat and whatever you do.
Diabetes is the failure of this thermostat. The name comes from the Greek for “to pass through” (the body seemed to pass water straight through) and the Latin mellitus, “honey-sweet”. When insulin is missing or ignored, glucose cannot get into cells, so two things happen at once: the cells starve in a sea of fuel they cannot reach, and the unused sugar builds up in the blood. Hyperglycaemia — high blood sugar — is the defining feature, and over years that excess sugar quietly damages blood vessels and nerves throughout the body. When it spills over a threshold the kidneys can no longer reabsorb, glucose pours into the urine, dragging water with it — hence the classic early symptoms: raging thirst, constant urination, weight loss and fatigue. You can read the NHS overview at nhs.uk/conditions/diabetes.
The types: Type 1, Type 2 and the rest
Two diseases, one name. The shared symptom — high blood sugar — is reached by two very different roads.
Type 1 diabetes is an autoimmune disease: the body's own immune system, for reasons still not fully understood, attacks and destroys the insulin-making beta cells in the pancreas. The factory is demolished. People with Type 1 make little or no insulin of their own and must inject or infuse it to live — before insulin was discovered, a Type 1 diagnosis was a death sentence within months. It usually appears in childhood or young adulthood (though it can begin at any age), comes on fast, and is not caused by diet or lifestyle. It accounts for roughly 8–10% of all diabetes. The NHS page is at nhs.uk/conditions/type-1-diabetes, and Breakthrough T1D (formerly JDRF) focuses on it specifically.
Type 2 diabetes is a different mechanism entirely. Here the factory keeps working — at first — but the body's cells stop responding properly to insulin, a state called insulin resistance. The pancreas compensates by making ever more insulin to force the message through, until eventually it cannot keep up and a relative deficiency sets in. It develops gradually, usually in adulthood (though increasingly in younger people), and is strongly linked to excess weight, inactivity, genetics and age — though plenty of people who are not overweight develop it too. Type 2 is the overwhelming majority, around 90% of cases worldwide, and it is rising fast: the WHO counts hundreds of millions of people affected. The NHS overview is at nhs.uk/conditions/type-2-diabetes.
| Type 1 | Type 2 | |
|---|---|---|
| Underlying cause | Autoimmune destruction of insulin-making beta cells — an absolute insulin deficiency | Insulin resistance plus a relative insulin deficiency as the pancreas tires |
| Typical onset | Often childhood / young adulthood; rapid (days to weeks) | Usually mid-life onward; gradual (years), often silent at first |
| Share of cases | ~8–10% | ~90% |
| Linked to lifestyle? | No — not caused by diet or weight | Strongly linked to weight, inactivity, genetics, age |
| Body weight | Often normal or low at diagnosis | Often (not always) overweight |
| Treatment | Insulin, always — injections or a pump, for life | Diet & weight first; then tablets (metformin and others), often later injectables or insulin |
| Can it remit? | No — the beta cells are gone | Yes — substantial weight loss can put it into remission in some people |
Beyond the headline two, the picture has texture:
- Gestational diabetes — high blood sugar that appears during pregnancy, when placental hormones drive insulin resistance. It usually resolves after birth, but it needs careful management to protect mother and baby, and it marks a raised lifetime risk of Type 2.
- LADA (latent autoimmune diabetes in adults) — sometimes called “Type 1.5”: a slow-burning autoimmune diabetes that begins in adulthood and is easily mistaken for Type 2 at first, until the person's own insulin fades.
- MODY (maturity-onset diabetes of the young) — a group of rare, inherited diabetes caused by a single gene fault, which runs strongly in families and can sometimes be treated with tablets rather than insulin once correctly identified.
- Prediabetes — not a disease so much as a warning light: blood sugar that is higher than normal but not yet in the diabetes range. It signals raised risk, and crucially it is often reversible with diet, weight loss and activity before Type 2 sets in.
The numbers: diagnosis and monitoring
Diabetes is, more than almost any other condition, a disease of numbers — living with it means watching them, and diagnosing it means measuring them. There are three main tests, and they look at blood sugar over different time-frames.
- HbA1c (glycated haemoglobin) — the workhorse. Glucose sticks irreversibly to the haemoglobin in your red blood cells, and because those cells live about three months, the proportion that is “sugar-coated” gives a running average of blood glucose over roughly the last 8–12 weeks. It needs no fasting. In the UK it is reported in mmol/mol; internationally the older % (DCCT) scale is still common. A diabetes diagnosis is usually drawn at 48 mmol/mol (6.5%) or above.
- Fasting plasma glucose — a single blood sugar measured after an overnight fast. A snapshot, not an average.
- Oral glucose tolerance test (OGTT) — you drink a standard sugary solution and blood glucose is measured two hours later, to see how well your body clears a known load. It is the standard test in pregnancy.
One of the most confusing things for anyone reading about diabetes is that the numbers come in different currencies. Day-to-day blood glucose is measured in mmol/L in the UK and much of the world, but in mg/dL in the United States — and the US numbers look about eighteen times bigger for the same blood sugar (7 mmol/L ≈ 126 mg/dL). HbA1c likewise comes as mmol/mol (UK) or % (DCCT, used in the US). Always check which scale a figure is on before comparing.
Once diagnosed, the numbers keep mattering. People on insulin in particular test their blood glucose many times a day — historically with a finger-prick and a meter, now increasingly with a continuous glucose monitor (more on those below) — and review their HbA1c every few months with a clinician to judge how well control is being held over the long run. The aim is to keep blood sugar close to the normal band as much of the time as possible without tipping into dangerous lows.
Why it matters: the complications
On a good day, well-managed diabetes is almost invisible. The reason it must still be taken seriously is that chronically high blood sugar does slow, cumulative damage — especially to small and large blood vessels and to nerves — and that damage is what eventually hurts people. The complications are usually grouped by what they affect.
- Eyes (retinopathy). High sugar damages the tiny vessels at the back of the eye; left unchecked, diabetic retinopathy is a leading cause of blindness in working-age adults. This is why people with diabetes are offered regular retinal screening.
- Kidneys (nephropathy). The kidneys' fine filters can be scarred over years, leading to chronic kidney disease and, at worst, the need for dialysis or a transplant. Diabetes is a leading cause of kidney failure.
- Nerves (neuropathy). Damage to nerves, classically in the feet and legs, causes numbness, tingling and pain — and the loss of sensation is itself dangerous.
- Feet. Numbness plus poor circulation means small cuts go unnoticed and heal badly, leading to ulcers and, in the worst cases, amputation. Diabetic foot care is a whole discipline for good reason.
- Heart and blood vessels. Diabetes roughly doubles the risk of heart attacks and strokes — cardiovascular disease is the biggest single cause of death in people with diabetes.
Alongside the slow damage are the acute dangers, when blood sugar swings too far either way in the short term. Hypoglycaemia (“a hypo”) is blood sugar dropping too low — usually from too much insulin, too little food, or unexpected exercise — causing shakiness, sweating, confusion and, if it falls far enough, seizures or unconsciousness. At the other extreme, very high blood sugar in Type 1 can tip into diabetic ketoacidosis (DKA): starved of usable glucose, the body burns fat for fuel and floods the blood with acidic ketones, a state that is life-threatening without urgent treatment.
A severe hypo — someone with diabetes who is confused, fitting or unconscious — is a medical emergency; if they can swallow, fast-acting sugar helps, and if they cannot, they need emergency help (and a glucagon injection if one is to hand). DKA — signalled by very high sugar with vomiting, deep rapid breathing, abdominal pain, a fruity smell on the breath and drowsiness — is also an emergency and needs hospital treatment straight away. Both can kill, and both are reasons to call for urgent medical help rather than wait.
The encouraging counterpoint is that these complications are not inevitable. The whole point of modern diabetes care is that keeping blood sugar (and blood pressure, and cholesterol) close to target dramatically lowers the chance of every one of them — a fact that took decades and two landmark trials to nail down.
A short history
Diabetes is one of the oldest diseases on record, and its history splits cleanly into the long era when it was a mystery, the short, miraculous moment when insulin was found, and the steady refinement since.
The disease was described in ancient Egypt, India, China and Greece. Indian physicians around 1,500 years ago noticed that the urine of some patients attracted ants and tasted sweet, and called it madhumeha, “honey urine”. For centuries, a sweet-taste diagnosis — a physician literally tasting the urine — was how diabetes was confirmed; the Latin mellitus, “honey-sweet”, is a fossil of that practice. Through all of it the cause was unknown and the disease, in its severe form, was untreatable: patients, especially children, simply wasted away.
Then came one of the great stories of medicine. By the late 1800s researchers had narrowed the trouble to the pancreas — remove a dog's pancreas and it developed diabetes — but no one could isolate the substance responsible. In 1921–22, in a Toronto laboratory, the surgeon Frederick Banting and the student Charles Best, working under J.J.R. Macleod and with the biochemist James Collip, managed to extract insulin from animal pancreas and purify it enough to use. In January 1922 they injected it into a dying fourteen-year-old, Leonard Thompson; his blood sugar fell, and he lived. Children who had been days from death sat up and recovered. It was as close to a resurrection as medicine gets. Banting and Macleod won the Nobel Prize the very next year, in 1923 — and, in a famous gesture, the discoverers sold the patent to the University of Toronto for a token sum, hoping to keep insulin cheap.
For sixty years, insulin was extracted from the pancreases of pigs and cattle. Then in the early 1980s came the next leap: recombinant DNA technology let scientists insert the human insulin gene into bacteria and yeast, which then brewed genuine “human” insulin in quantity — one of the first triumphs of biotechnology. Two huge trials then settled how it should be used: the DCCT (Diabetes Control and Complications Trial, 1993) in Type 1 and the UKPDS (UK Prospective Diabetes Study, 1998) in Type 2 proved that tight control of blood sugar genuinely prevents the eye, kidney and nerve complications — turning “keep your sugar down” from sound advice into evidence. The most recent chapter is the GLP-1 era: a class of drugs born from the biology of gut hormones that has, in the 2010s and 2020s, transformed the treatment of Type 2 diabetes and obesity alike.
Current approaches
There is no single treatment for diabetes, because there is no single diabetes. But the modern toolkit is rich, and it has improved enormously in a generation. The pieces fall into a few groups.
Monitoring. For decades the only way to know your blood sugar was a finger-prick: a drop of blood on a test strip read by a meter, several times a day. The biggest recent change in everyday life with diabetes is the continuous glucose monitor (CGM) — a small sensor worn on the arm or abdomen that reads glucose in the tissue fluid every few minutes and streams it to a phone, complete with trend arrows and alarms for highs and lows. It turns a handful of daily snapshots into a continuous film, and it has changed how well people can steer.
Insulin and pumps. Everyone with Type 1 (and some with Type 2) needs insulin, given either by injection — typically a long-acting “background” insulin plus fast-acting doses at meals — or by an insulin pump, a device that drips insulin continuously through a small cannula. The frontier here is the closed-loop or “artificial pancreas” system: a CGM and a pump talking to each other through an algorithm that adjusts insulin automatically, minute by minute, to keep glucose in range — a genuine step toward automating the broken thermostat.
Tablets and injectables for Type 2. The first-line drug is usually metformin, an old, cheap and well-proven tablet that lowers the liver's glucose output and improves insulin sensitivity. Beyond it sit several newer classes, two of which have reshaped treatment: SGLT2 inhibitors, which make the kidneys flush excess sugar out in the urine and, as a bonus, protect the heart and kidneys; and GLP-1 receptor agonists — the drugs sold as Ozempic, Wegovy and (as the related dual-agonist tirzepatide) Mounjaro — which mimic a gut hormone to lower blood sugar, slow the stomach and powerfully reduce appetite and body weight.
| Drug class | What it does | Examples |
|---|---|---|
| Insulin | Replaces the missing hormone directly; essential in Type 1 | Long-acting + fast-acting analogues |
| Metformin (biguanide) | Lowers the liver's glucose output, improves insulin sensitivity; first-line in Type 2 | Metformin |
| SGLT2 inhibitors | Make the kidneys excrete excess glucose in urine; protect heart & kidneys | Empagliflozin, dapagliflozin |
| GLP-1 receptor agonists | Mimic a gut hormone; lower sugar, suppress appetite, drive weight loss | Semaglutide (Ozempic / Wegovy), tirzepatide (Mounjaro) |
| Sulfonylureas | Squeeze more insulin out of the pancreas; older, cheap, can cause hypos | Gliclazide |
| DPP-4 inhibitors | Block the enzyme that breaks down the body's own GLP-1 | Sitagliptin, linagliptin |
Diet, weight and remission. For Type 2 in particular, diet and weight are not a footnote but central to treatment — and the most striking recent finding is that Type 2 diabetes can be put into remission by substantial weight loss. The UK DiRECT trial showed that an intensive, low-calorie diet leading to weight loss could return blood sugar to normal without medication in a large fraction of people, especially those treated early. Remission is not a guaranteed cure — the diabetes can return if weight does — but it overturned the old assumption that Type 2 only ever progresses. (None of this applies to Type 1, where the beta cells are gone and insulin is non-negotiable.) Diabetes UK and the US NIDDK both have practical guidance on diet and management.
What the research says & frontiers
Diabetes research is unusually active, and several frontiers are genuinely moving.
- Delaying Type 1 with immunotherapy. Because Type 1 is an immune attack, the dream is to call off the attack before the beta cells are destroyed. The drug teplizumab, an antibody that retrains the immune system, has been shown to delay the onset of clinical Type 1 in high-risk people by years — the first treatment to touch the disease process itself rather than just replace insulin.
- Replacing the beta cells. If insulin-making cells are gone, why not put new ones back? Islet transplants from donor pancreases already work for selected patients but are limited by donor supply and the need for lifelong immune-suppressing drugs. Stem-cell-derived beta cells — growing fresh insulin-producing cells in the lab — are now in clinical trials and could, in principle, remove the supply problem.
- Ever-smarter closed loops. The artificial-pancreas systems keep getting better — faster algorithms, dual-hormone designs that deliver glucagon as well as insulin, less need for the user to count carbohydrates — inching toward a system that simply manages itself.
- The prevention question. For Type 2, the biggest prize is preventing it at all. Trials have shown that diet, weight loss and activity can cut the rate at which prediabetes progresses to diabetes — the challenge is delivering that at the scale of a population, as cases climb worldwide.
Where to get help & more info
If you are worried about diabetes — your own or someone else's — the first step is a doctor, who can run the simple tests above. For trustworthy background and practical, plain-English guidance, these are good places to start:
- NHS — Diabetes (UK), with separate pages on Type 1 and Type 2.
- Diabetes UK — the leading UK charity, with a helpline, community and detailed guides.
- World Health Organization — Diabetes fact sheet, for the global picture.
- American Diabetes Association and the US NIH's NIDDK, for US-oriented information (note the different units).
- Breakthrough T1D (formerly JDRF) for Type 1 research and support, and the CDC for US public-health data.
Some of the figures and details on this page — typical ranges, statistics and the biology — were compiled with the help of AI tools and may contain errors or be out of date. They are shared in good faith for general interest only, and are not medical advice. Nothing here is a substitute for a doctor or a qualified health professional; if you are worried about your health, please seek professional help. Check claims against primary medical sources before relying on them.