The Sugar in the Blood

Why this article exists

The average person with Type 1 is told the opposite — that diet doesn't matter, just count carbs and dose insulin — and quietly figures out on internet forums that a lot of what they eat matters. This piece tries to put the science, the missed nuances, the patient experience, and the resources in one place.

By the end you should be able to tell the types apart, recognise the emergency signs that mean stop reading and call an ambulance, understand why movement is one of the most powerful drugs you'll never be prescribed, make sense of the remission conversation — and walk into your next appointment with the questions that change your care.

The story most patients live

For most people with Type 2, it starts as nothing. Maybe you're tired more often. Thirsty in a way that doesn't quite go away. You pee at night when you didn't used to. Your vision blurs for a week and then clears. A small cut takes too long to heal.

A blood test lands a result you weren't expecting: “pre-diabetes,” or “Type 2.” Your doctor is calm, almost casual. They hand you a pamphlet about eating less sugar, suggest you “try to lose some weight,” and start you on metformin. The message — sometimes spoken, sometimes between the lines — is: this is your life now. Another pill in a few years. Eventually, maybe, insulin.

For most people with Type 1, the story is the opposite — fast and brutal. A child or young adult is suddenly drinking gallons, urinating constantly, losing weight despite eating. Sometimes the diagnosis comes in an ER, in diabetic ketoacidosis: vomiting, deep panting breaths, a fruity smell on the breath, sliding toward unconsciousness. From that day on, life is insulin, finger-pricks or a sensor, and the constant arithmetic of food plus activity plus insulin plus sleep.

And then there's the third story, the one almost no one tells. A lean, otherwise healthy adult in their thirties or forties is diagnosed with “Type 2.” They follow the rules. Their numbers won't budge. Metformin doesn't really work. They lose weight they didn't want to lose. A year, two years, sometimes longer pass before someone finally tests for GAD antibodies and realises they actually have LADA — Type 1 in slow motion, misdiagnosed for years.

Each of those stories has, somewhere in it, a moment where the patient could have pushed harder, asked a different question, or known one more thing. This article is for that moment.

— the humanistic core of this piece

What diabetes actually is

For everyone

Every cell in your body runs on glucose. After you eat, glucose enters your bloodstream. To get out of the blood and into your cells, it needs a key called insulin, made by beta cells in your pancreas. Diabetes is what happens when that system breaks — either the key isn't being made (the pancreas is damaged), or the locks have rusted (your cells stop responding to insulin), or both.

When glucose can't get into cells, two things happen at once: your blood sugar rises (the glucose is stuck in the blood), and your cells starve (they can't reach the fuel). Over years, that high blood sugar damages nerves, eyes, kidneys and blood vessels. That's why diabetes is dangerous — not the sugar number itself, but everything it slowly does.

The types — and why the type matters most

• Type 1An autoimmune disease: the immune system destroys your beta cells, so you make little or no insulin and need it from outside, for life. You cannot reverse Type 1 with diet — you can manage it beautifully, but you cannot replace missing insulin with broccoli.
• Type 2Primarily insulin resistance layered on an exhausted pancreas — around 90–95% of all diabetes. This is the type where food, weight and movement can do extraordinary things, including long-term remission for many people.
• LADA · 1.5Latent autoimmune diabetes in adults — Type 1 in slow motion. Looks like T2 at first, resists T2 treatment, eventually needs insulin. Roughly 10% of adults diagnosed “Type 2” actually have this, and most don't know it.
• gestationalAppears during pregnancy and often resolves after birth — but flags higher long-term risk of T2.
• MODYA rare set of genetic forms; some respond beautifully to sulfonylureas instead of insulin. A strong family pattern of young diagnoses is the clue — ask.
• Type 3cPancreatogenic diabetes, caused by pancreas damage — pancreatitis, surgery, cystic fibrosis. Frequently misclassified as T2.

For the scientist

The deep mechanism of T2D was reframed by Professor Roy Taylor at Newcastle as the twin-cycle hypothesis: excess fat accumulates inside the liver and pancreas — not just around them. Liver insulin resistance drives chronic over-production of glucose, and pancreatic fat suffocates the beta cells, suppressing insulin secretion. Lose enough of that organ fat — not just body weight, organ fat — and the beta cells can wake back up.

In T1D the story is immunological — HLA-linked autoimmunity destroys the beta cells, and newer drugs such as teplizumab can delay onset in high-risk relatives. None of that means dietary intervention reverses T1D; it doesn't. The gut microbiome, chronic inflammation, sleep and stress all sit on top of these mechanisms and modulate them.

Diabetes is no longer a “blood sugar disease” in any sophisticated model. It's a metabolic systems disease — and the blood sugar is the smoke, not the fire.

The alarm: when to act

This section is structured by urgency. Read all three levels — the first one is the difference between a hospital visit and a funeral.

Push for a diagnosis — or rethink your label — this week

• Increased thirst and urination, especially at night
• Unexplained weight loss, especially with normal or increased eating (a big T1 / LADA red flag)
• Constant fatigue, blurred vision, slow-healing cuts, recurrent yeast infections
• Numbness or tingling in the feet or hands
• A family member with Type 1, Type 2, or another autoimmune disease
• A child or young adult unusually thirsty, tired, and losing weight — get them tested this week

And if you already carry a “Type 2” label but you're lean, were under 50 at diagnosis, your oral medications barely move the numbers, you have another autoimmune disease, or you're losing weight you can't explain — ask explicitly: “Could this be LADA? Can we test GAD antibodies and C-peptide?” Naming it changes the conversation.

The self-advocacy script (use it every appointment)

• 01 · the trend“What's my HbA1c trend over time, not just today's number?” Direction matters more than any single value.
• 02 · the type“What's my actual diagnosis — Type 1, Type 2, LADA, or something else — and how sure are we?” Especially if your story is atypical.
• 03 · remission“Is remission a realistic goal for me, and if so, what's the plan?” For early-diagnosis T2D this is now an evidence-based question, not a fringe one.
• 04 · a CGM“Could I try a continuous glucose monitor, even short-term?” Two weeks of your own data teaches more than any pamphlet.
• 05 · the rest“What are my numbers for kidneys, eyes, feet, blood pressure and cholesterol?” Diabetes is managed by these too, not just sugar.
• 06 · the plan B“What does my care plan look like if my numbers don't change?” Get the next two steps in writing.
• 07 · a dietitian“Can I see a diabetes-trained dietitian, not just be handed a leaflet?”

Movement is medicine

You have likely been told to “exercise more.” That advice is correct and useless. Here is the version your doctor probably won't give you — starting with the timing trick almost nobody mentions.

The post-meal walk

Glucose spikes after meals — postprandial spikes — are a huge driver of HbA1c and long-term damage. A 15-minute brisk walk starting about 15 minutes after each main meal blunts those spikes dramatically. In a randomised crossover trial in people with T2D, three short post-meal walks outperformed one longer pre-breakfast walk for glycemic control.

The mechanism is elegant: contracting muscles pull glucose out of the bloodstream through an insulin-independent pathway, so you're sweeping sugar out without needing more insulin. For T2D patients, post-meal walking has been shown to be about as effective as adding a prandial insulin injection for blood-sugar control.

Three walks of fifteen minutes. That's it. If you only act on one thing in this entire article, act on this.

— the single highest-leverage habit

The two other legs

• resistance ×2/wkMuscle is your largest glucose sink — the more lean muscle you carry, the more buffer your metabolism has. Bodyweight squats, lunges, push-ups, kettlebells, weights. Any of it counts.
• aerobic 150/wkWalking, cycling, swimming, hiking — anything that gets you breathing harder for half an hour, several times a week. It improves insulin sensitivity for up to 48 hours after each session, which is why consistency beats intensity.

The carbohydrate question

This is the part where lived patient experience and mainstream guidelines have been at war for thirty years — and where the evidence is finally catching up. Let's handle it honestly, because honesty is what makes it useful.

Three real stories

• 1982 · New YorkRichard Bernstein, a Type 1 engineer showing early complications, bought his own glucose meter (then a $1,000 hospital device), measured dozens of times a day, and cut carbs hard. His sugars normalised; his complications reversed. At 45 he went to medical school to be taken seriously. His insight: the Law of Small Numbers — small meals, small doses, small errors, small swings.
• 2011 · NewcastleRoy Taylor's Counterpoint study showed a brief very-low-calorie diet emptied fat from the liver and pancreas and restored insulin secretion in early T2D. It grew into DiRECT — in The Lancet, 2018 — where 46% of participants were in remission at one year, off all diabetes medication.
• 2012 · SouthportGP David Unwin, after a furious patient reversed her own diabetes on low-carb, tried it with his next patients, then a hundred. Twelve years on, his NHS practice reaches roughly 50%+ remission in patients who stick with it — saving the surgery tens of thousands a year in drugs.

In one sentence

Carbohydrates raise blood glucose; protein raises it modestly; fat barely raises it at all. Less carbohydrate means less glucose load, less insulin needed, and — over time — less insulin resistance. In T2D that often means less disease. In T1D it means smaller swings, more time in range, and lower long-term complication risk.

What the data really supports

How to try low-carb safely, like a scientist

• 01 · tell your teamIf you're on insulin, sulfonylureas or SGLT2 inhibitors, doses likely need to drop quickly as carbs drop — otherwise you risk a hypo or DKA. This isn't optional.
• 02 · get a baselineHbA1c, fasting glucose, lipids, kidney function, blood pressure, weight, waist. You can't measure progress without a starting line.
• 03 · get a CGMEven two weeks of CGM data will teach you which foods your body tolerates and which spike you. Personal data beats generic advice every time.
• 04 · pick one protocolDiRECT meal-replacements (supervised), Unwin low-carb plates, the Virta ketogenic protocol, or Bernstein for T1 control. Commit to it for 8–12 weeks. Don't half-do three of them.
• 05 · track & reviewWeekly weight, fortnightly fasting glucose, quarterly HbA1c. With a CGM, post-meal time-in-range is your daily scoreboard.
• 06 · de-prescribe with your doctorAs your numbers respond, reduce medications with your doctor — don't stop drugs on your own, and don't get left on drugs you no longer need. That's the whole point.

The four-legged stool

For ankylosing spondylitis the metaphor was a three-legged stool. Diabetes needs four — and a stool missing a leg is just a stick.

• diagnosis & medsT1 needs insulin, always. T2 needs the lightest pharmaceutical toolkit that controls the disease — and modern options (metformin, GLP-1 agonists, SGLT2 inhibitors) are powerful and often cardioprotective. Don't refuse medicine out of ideology; do question drugs you've outgrown.
• movementEvery day, on purpose. Post-meal walks first, resistance training twice a week, an aerobic base. Cheap, no side effects, works in every type of diabetes.
• food as a toolNot a punishment. Reduce the glucose load enough that your physiology can heal — for most T2 that means lower carbohydrate in some sustainable form; for T1, smaller carb loads mean smaller swings.
• sleep, stress, dataPoor sleep tanks insulin sensitivity overnight; chronic stress raises cortisol and blood sugar; a CGM turns vague advice into personal feedback. Treat all three as medical interventions.

And running underneath all four: self-advocacy. The right diagnosis. The right type label. The right questions in the appointment. The willingness to say “I'd like to aim for remission” out loud. The community that keeps you going on month nine, when it's hard.

That is the difference, over a lifetime with diabetes, between drifting toward complications and pushing the disease backwards.

The mini-directory

Real, working starting points across the spectrum — from peer-reviewed science to community support. Treat forums and social media as hypotheses to test with your medical team; treat the trial papers and clinical sites as ground truth. Especially with insulin doses.

The story is no longer only one

For most of the last century, the dominant story of diabetes was managed decline — a slow accumulation of pills, then insulin, then complications. That story is no longer the only one available.

If you have Type 2 and you're newly diagnosed, the door is open: there is now serious, peer-reviewed evidence that aggressive early weight loss, by whichever sustainable route fits your life, can put your disease into long-term remission. Ask for that conversation. Don't accept “progressive” as your only option.

If you have Type 1, the story is different but no less hopeful: with modern insulins, CGMs, pumps, the law of small numbers, and a smart relationship with food, your time-in-range and your life expectancy can rival anyone's. You can't reverse it. You can absolutely outlive the projections. And if you suspect LADA or that your label is wrong — push. The right diagnosis is the prerequisite for the right life.

Walk after your meals. Lift something heavy twice a week. Sleep. Watch what you eat with curiosity, not shame. Find your community. Ask the next question.

— whatever your type

References

1. Lean MEJ, Taylor R, et al. — Primary care-led weight management for remission of T2D (DiRECT). The Lancet. (2018)
2. Taylor R, et al. — DiRECT 5-year outcomes. Lancet Diabetes & Endocrinology. (2024)
3. Taylor R, et al. — ReTUNE — remission in T2D at lower BMI; the twin-cycle & personal fat threshold. (2023)
4. Reynolds AN, et al. — Advice to walk after meals vs other times for glycemic control. Diabetologia. (2016)
5. Suntornlohanakul O, et al. — Post-meal walking vs prandial insulin for glycemic control — crossover RCT. (2020)
6. Athinarayanan SJ, et al. — Sustained T2D reversal on a ketogenic protocol (Virta), 2- and 5-year data. (2019–2022)
7. Unwin D, et al. — Low-carbohydrate diet in NHS general practice — multi-year evaluation. BMJ NPH. (2023)
8. Cleveland Clinic Journal of Medicine. — Latent autoimmune diabetes in adults (LADA): recognition & management. (2025)
9. American Diabetes Association. — Standards of Care in Diabetes; DKA & sick-day guidance. (2024–2025)