The Invisible Fire · Ask Your Body

The appointment that changes nothing

You know something is wrong.

You've been tired for years. Your weight has crept up despite trying. Your joints ache; your concentration isn't what it was. You can't quite explain it, but something is off.

Your doctor runs blood tests. A week later: everything's normal. Cholesterol borderline, blood sugar fine. Go home, come back in a year.

What your doctor didn't tell you — and, in most cases, genuinely doesn't know — is that the test which would have found your problem years before it turned serious was never ordered. It's called a fasting insulin test, and it isn't part of routine screening. The reason has nothing to do with science — and everything to do with what this piece is about.

This is the keystone of everything on this site. The other pieces show you single rooms; this one shows you the house. Once you see the fire, you'll recognise it under condition after condition — each with its own name, its own specialist, its own drug, and the same flame underneath.

Chapter one · the fire nobody's looking for

What the fire actually is.

Every time you eat carbohydrate — bread, pasta, rice, sugar, cereal, potatoes — it becomes glucose in your blood. Your pancreas releases insulin to escort that glucose into your cells. (If that machine is new to you, It's All Sugar walks through it slowly.)

The system works fine when it isn't overused. But on a modern diet, glucose floods in meal after meal, year after year — and the cells stop listening. They become resistant to insulin's signal. The pancreas compensates by shouting louder: making more and more insulin to get the same message across. Elevated insulin, cells not responding — that's insulin resistance, and it's the fire.

This isn't fringe or new. It was described as a coherent syndrome by Professor Gerald Reaven of Stanford in his landmark 1988 lecture to the American Diabetes Association — he called it Syndrome X; we now call it metabolic syndrome. That was 37 years ago. Reaven estimated it's present in about a quarter of apparently healthy, non-obese adults with normal blood glucose. In overweight or sedentary people, far more. [Ref 1]

The slow burn

What happens in the silent years.

Here's what's underway for years — sometimes decades — before a doctor diagnoses anything, all while your standard tests keep coming back "normal":

The liver overproduces cholesterol. High insulin flips a switch in the liver (SREBP) that turns on the very enzyme statins block. Cholesterol rises — not mainly from dietary fat, but because insulin is telling the liver to make more. [Ref 2] (This becomes important for cholesterol and statins.)
Fat packs around your organs. Insulin tells fat cells to store, not release — especially visceral fat, which itself pumps out inflammatory molecules that worsen the resistance. A self-feeding loop.
Chronic inflammation takes hold. Elevated insulin drives inflammatory signalling (NF-κB), raising cytokines like TNF-alpha, IL-6 and CRP. This low-grade fire damages blood vessels, raises cancer risk, and impairs immunity.
The gut and the mitochondria struggle. The gut balance tips toward inflammatory species; the cell's energy engines are worn by oxidative stress. The fatigue everyone calls "just getting older" has a biochemical cause.

And here's the trap: throughout all of this, standard blood tests read normal — because the test being ordered (HbA1c) only rises after the fire has burned long enough to overwhelm the pancreas. By the time HbA1c flags it, the fire has been burning for years.

The test that would catch it early

It exists. It's cheap. It's decades old.

A fasting insulin test measures insulin after an overnight fast. When insulin is high even while fasting — the pancreas over-producing with no food present — insulin resistance is there. Combined with fasting glucose it gives a score called HOMA-IR, a validated tool that has existed since 1985. [Ref 3] The calculation takes seconds.

There's an even earlier warning too: leptin resistance, the "smoke signal before the fire," where the brain stops hearing the hormone that says you've eaten enough. It's generally upstream of insulin resistance — the earlier signal. [Ref 4] Both tests are available privately; neither is routine.

Neither test requires new technology. Neither is experimental. Both have been validated for decades. Neither is routinely ordered — because neither leads to a prescription. The most effective response to what they detect is dietary, and there is no profitable drug that targets insulin resistance at its source. Hold that thought; it's the whole story.

Chapter two · what the fire produces

One fire. Many names.

The conditions linked to insulin resistance aren't a list of rare diseases — they're the most common causes of death and disability in the Western world. Each gets its own specialist, its own clinic, its own drug. But look closer and they're not separate diseases at all. They're one fire, surfacing in whichever part of you is weakest first.

Tap each one — see how the same fire causes it, which number the doctor chases, which drug manages that number, and what's left quietly burning.

🔥

Insulin resistance

the one fire underneath

Read down them and the pattern is impossible to miss: same fire, different flame, different specialist, different pill — and the fire itself measured by none of them, addressed by none of them. The cumulative burden of this single upstream problem is the majority of the health system's entire chronic-disease bill.

Chapter three · the drugs that mimic the diet

Managing the marker, not the fire.

Here's the most revealing part. Several of the biggest drugs don't oppose the diet that would fix the fire — they imitate it, from the outside, for as long as you keep paying:

SGLT2 inhibitors (the "-flozin" drugs) make you pee out glucose — a pharmaceutical approximation of what cutting carbohydrate does through food. Blood glucose falls, insulin demand falls, the body shifts toward fat-burning. Same destination as the diet; one costs billions and runs for life.
Statins block the cholesterol enzyme — at the wrong end of the chain. Insulin, through SREBP, switches that enzyme on; a low-carb diet turns the stimulus off at the start; the statin blocks it at the finish. Stop the statin and cholesterol climbs again, because the upstream driver was never touched. [Ref 2] (Statins, in depth.)
GLP-1 injections (Ozempic, Wegovy) mimic a gut hormone that makes you eat less — a £20-billion-a-year approximation of fasting. Real improvement, genuinely reaching the fire — but stop, and the driver is still there. (The diabetes drugs, in depth.)

The question every drug in this chapter raises is the same: why does a pharmaceutical approximation of a dietary state receive billions in investment and urgent adoption, while the dietary approach it's approximating stays marginal? And how big is the number the marketing hides? How Risk Is Sold shows you how to read that.

The answer isn't that the drugs don't work — some genuinely do. It's that they're aimed downstream, at the consequence, while the upstream cause keeps burning. A managed marker is a lifelong customer. An extinguished fire is not.

Chapter four · who is paid to manage the fire

Not a conspiracy. Something more ordinary.

None of this needs a secret plan. The institutions that should be shouting about insulin resistance have financial relationships pointing the other way — and all of it is published, disclosed, in plain sight.

The regulators are largely funded by the industry they regulate

Regulator	Industry-funded
MHRA (UK)	~75% from industry fees
TGA (Australia)	~93% (full cost recovery)
EMA (Europe)	~89%
Medsafe (NZ)	~84%
FDA (USA)	~48% overall; ~66% for human drugs

Sources: UK Parliament Written Answer 16 Jan 2023; TGA Cost Recovery Statement 2023-24; Demasi, BMJ 2022 [Ref 9]; official releases.

And the guideline-setters lean the same way

Seven years of academic research into NICE (the UK's cost-effectiveness body) documented what researchers call "neoliberal corporate bias" [Ref 10]: industry consulted on NICE's methods from its inception; clinical specialists declaring financial conflicts with the very manufacturer under appraisal in 56% of cases, none excluded; 84% of 485 drug appraisals ending in positive guidance; a senior staffer telling an industry meeting, "we see the industry as our clients." Medical school, meanwhile, gives UK doctors on average fewer than 20 hours of nutrition training across four years — and hundreds of hours of pharmacology.

The pharmaceutical companies are not ignorant of any of this. They employ superb biochemists; they fund the research that maps these pathways in molecular detail. They know the biology. What they've done with that knowledge is target the downstream consequences rather than the upstream cause — because consequences generate recurring revenue and prevention doesn't. It's produced not by a secret plan but by ordinary commercial incentives operating at every level at once.

It is not a conspiracy when it is true.

The people who tried to point this out

A remarkably consistent pattern.

The connection has been understood, in molecular detail, for decades. The scientists and clinicians who tried hardest to say so met a strikingly similar fate:

John Yudkin — the man who was rightIn 1972 he argued, with solid evidence, that sugar — not dietary fat — drove heart disease and diabetes. Ancel Keys, whose fat hypothesis suited the food industry, mounted a campaign that destroyed Yudkin's reputation; his book went out of print and he died largely forgotten. In 2016, internal sugar-industry documents in JAMA showed a 1965 review had been funded specifically to blame fat and downplay sugar. It shaped global guidelines for half a century. [Ref 7]
Dahlqvist, Noakes, FettkeA Swedish GP, a world-renowned South African sports scientist, an Australian surgeon — each reported to their medical authorities for recommending lower-carbohydrate eating. Each, after years of prosecution, was cleared — and in Fettke's case the regulator issued a written apology, the complaints having come from people with documented food-industry ties.
David Unwin — the exception that proves the ruleAn NHS GP who published his low-carb results relentlessly and transparently: 51% overall type 2 diabetes remission, 77% within a year of diagnosis, ~£68,000 saved in drugs a year in one surgery. [Ref 8] He wasn't prosecuted — because he published, framed it as service evaluation, built relationships, and saved the system money. Same science as the others; different institutional response.

Chapter five · putting the fire out

What you can actually do.

This isn't about rejecting medical care or refusing prescribed medicine. It's about understanding what the science supports and advocating for yourself while the system catches up.

Get the real tests

Ask about fasting insulin / HOMA-IR (the most direct measure), fasting leptin, and — available on any standard lipid panel — your triglyceride-to-HDL ratio (above ~2.0 in mmol/L strongly suggests insulin resistance; ask for the actual numbers, not just "normal"). An elevated fasting insulin on paper is much harder to dismiss than a verbal request.

Reduce the flood

The intervention with the most direct mechanistic relevance is cutting refined carbohydrate — sugary drinks, cereals, white bread, pasta, rice, processed snacks — and replacing those calories with protein, healthy fats and vegetables. Not a rigid protocol; just fewer, smaller insulin spikes. This is the approach behind Unwin's remission figures, achieved in an ordinary surgery. [Ref 8]

One firm rule, exactly as in the diabetes piece: if you take medication for diabetes or blood pressure, don't change it on your own. Cutting carbohydrate can lower blood sugar fast, so your doses may need to come down — a good problem, but one for your doctor to manage, together with you.

This is the short version. The full practical map — what to measure, what a day looks like, the levers that amplify it, and how to do it all safely with your doctor — is the capstone of this whole series: Putting Out the Fire →

The most important part

The synthesis is the thing that was missing.

None of the facts here are new. The biochemistry has been understood since 1988. The dietary science has been building since the 1970s. The clinical evidence is in peer-reviewed journals anyone can read.

What was never assembled — never handed to you in one place — is the synthesis: that these separate threads are connected; that the diseases share one upstream cause; that the cause is testable and addressable; and that the institutions who should be saying so have financial reasons not to.

If you've had a heart attack, or fatty liver, or a creeping blood sugar — it likely wasn't three unlucky diseases. It was one fire, surfacing three times.

That's what this whole site is for: not to tell you what to think, but to hand you the fire so you can see it for yourself — under the sugar, under the diabetes, under the cholesterol, under the number on every drug you're offered. Once you've seen it, you can't un-see it.

The information is free. The test is accessible. The primary intervention is food. Ask your body — and ask for the fasting insulin test.

Verified references

[1] Reaven GM (1988). Role of insulin resistance in human disease. Diabetes 37(12):1595-1607. PMID 3056758. Read →

[2] Horton, Goldstein & Brown (2002). SREBPs: activators of cholesterol and fatty-acid synthesis in the liver. J Clin Invest 109(9):1125-1131. PMC150968. Read →

[3] Matthews DR et al. (1985). Homeostasis model assessment (HOMA-IR). Diabetologia 28(7):412-419. PMID 3899825. Read →

[4] Lustig RH (2006). Childhood obesity: behavioral aberration or biochemical drive? Reinterpreting the First Law of Thermodynamics. Nat Clin Pract Endocrinol Metab 2(8):447-458. PMID 16932334. Read →

[5] Lee C-L et al. (2026). Machine-learning-predicted insulin resistance is a risk factor for 12 cancers. Nature Communications, 16 Feb 2026. ~500,000 UK Biobank participants. Read →

[6] Craft S (2009). Metabolic disorders in Alzheimer disease and vascular dementia. Arch Neurol 66(3):300-305. PMID 19273747. Read →

[7] Kearns, Schmidt & Glantz (2016). Sugar Industry and Coronary Heart Disease Research. JAMA Intern Med 176(11):1680-1685. PMID 27617709. Read →

[8] Unwin D et al. (2023). What predicts drug-free type 2 diabetes remission? BMJ Nutrition, Prevention & Health 6(1):46-55. PMID 37559961. Read →

[9] Demasi M (2022). From FDA to MHRA: are drug regulators for hire? BMJ 377:o1538. PMID 35768073. Read →

[10] Abraham J & Balendran G (2025). The Political Sociology of NICE. Sociology of Health & Illness 47(1):e13878. PMC11693927. Read →

[11] Rickard, Ozieranski & Lexchin (2021). The pharmaceutical industry's engagement with UK APPGs. PLOS ONE 16(6):e0252551. PMC8224875. Read →