Insulin resistance: what it is, how to measure it and what helps

Insulin resistance means your cells respond less well to insulin, so your pancreas has to make more and more of it to keep your blood sugar normal. For as long as that extra insulin covers the work, your glucose stays neatly inside the reference range. You notice nothing.

That is what makes this condition so hard to catch. The test your GP runs as standard, fasting glucose, is often the last value to move.

Anyone who wants to know earlier looks at insulin itself, and at the ratio between two fat values already printed on any lipid panel.

What is insulin resistance exactly?

Insulin resistance is reduced sensitivity of your muscle, liver and fat cells to insulin. Insulin is the key that lets glucose into your cells. When that key works less well, your pancreas makes more insulin to achieve the same effect.

The result is a normal blood sugar sitting on top of an abnormally high insulin.

That situation is called hyperinsulinaemia and it can last for years. Your pancreas compensates, and while it manages, your result looks healthy. Only when the gland can no longer keep up does your fasting glucose start to climb. By then you are well into the process.

Fat tissue around your abdomen plays its own part. That tissue is hormonally active and releases substances that lower insulin sensitivity further. So the pattern keeps itself going.

What symptoms come with insulin resistance?

Usually none. Insulin resistance rarely produces clear symptoms in its early years, and that is the main reason it gets noticed so late. Where people do notice something, it tends to be tiredness after carbohydrate-heavy meals, a growing waistline and weight that will not shift.

Those complaints prove nothing. They fit dozens of other causes.

One physical sign is more specific than the rest: acanthosis nigricans, a velvety darkening of the skin on the neck, in the armpits or in the groin. That discolouration is associated with sustained high insulin levels. It is not proof, but it is a reason to raise the subject with your GP.

In women an irregular cycle can play a part. In men the waistline tends to show first. In both cases symptoms are poor guides here, and numbers are better ones.

How do you measure insulin resistance?

With a combination of values, not with one test. No single blood value demonstrates insulin resistance. What laboratories and doctors do is lay several values side by side and see whether the pattern fits. Drawn fasting, because eating disturbs almost everything in this list.

The cut-offs below are the Dutch ones, in mmol/l. Many foreign pages quote mg/dl, and those numbers cannot be laid over a Dutch report.

The glucose thresholds come from the WHO criteria applied by the Dutch College of General Practitioners in its NHG guideline on type 2 diabetes: below 6.1 mmol/l normal, 6.1 to 6.9 mmol/l an impaired fasting glucose, and 7.0 mmol/l or above measured twice fitting diabetes.

Take two people with exactly the same fasting glucose of 5.4 mmol/l. In the first, insulin is 5 mU/l; in the second, 18 mU/l. Both reports show a normal blood sugar, and both are told their value is fine.

Yet the second person's pancreas is doing more than three times the work for precisely the same result.

Run it through the index and the gap appears: the first lands at 1.2, the second at 4.3. None of that shows on the report when insulin is not drawn alongside. Same glucose, an entirely different story behind it.

Note the order in which these values move. Insulin rises first, HbA1c follows, glucose comes last. Anyone testing glucose alone is measuring the end of the story.

How to work out that index yourself is covered in calculating HOMA-IR.

What does the triglyceride/HDL ratio tell you?

That ratio is the cheapest signal available, because both numbers already sit on any standard lipid panel. You divide your triglycerides by your HDL cholesterol, both in mmol/l. A result around 1.8 or higher is statistically more common in people with reduced insulin sensitivity.

That figure did not come out of nowhere.

Stanford researchers compared ordinary laboratory values against a direct measurement of insulin sensitivity in people carrying excess weight. The triglyceride/HDL ratio emerged as one of the most usable simple markers, with an optimal cut-point of 1.8 in SI units, alongside a triglyceride value of 1.47 mmol/l (McLaughlin et al., 2003).

What strikes me is that almost no Dutch page mentions this ratio. Meanwhile half the country has a lipid panel in a drawer with both required numbers printed on it.

It remains an indirect measure. The ratio does not replace a fasting insulin, and it says little in people without excess weight. As a first orientation using material you already hold, it is hard to beat. Your cholesterol/HDL ratio is a different ratio, aimed at cardiovascular risk.

How does metabolic syndrome fit in?

Insulin resistance is the engine underneath metabolic syndrome. That syndrome is not a disease but a cluster of five risk factors: waist circumference, triglycerides, HDL cholesterol, blood pressure and fasting glucose. With three or more abnormal factors, doctors speak of the syndrome.

The international definition was harmonised by seven organisations in 2009 (Alberti et al., 2009).

What those five factors share is that nearly all of them track insulin sensitivity. That is why doctors see them appear in groups so often. Someone with high triglycerides, a low HDL and a growing waistline rarely has a fat problem alone.

The full criteria with the Dutch values are in metabolic syndrome.

How is it different from prediabetes?

Prediabetes is a measurable outcome, insulin resistance is the mechanism underneath it. In prediabetes your fasting glucose sits between 6.1 and 6.9 mmol/l, or your glucose tolerance is impaired. Insulin resistance can precede that by years, with glucose values that are still entirely normal.

Put differently: prediabetes is the point where your pancreas stops quite keeping up.

That distinction has practical consequences. Someone with a fasting glucose of 5.4 mmol/l is told the value is normal, and that is true. The same person can have a sharply raised insulin. The term impaired glucose tolerance describes something else again, namely how your sugar responds to a glucose drink during a tolerance test.

Which values belong to that stage, and what is still winnable there, is covered in prediabetes.

Can insulin resistance be reversed?

Often yes, and that is the most encouraging part of this subject. Insulin sensitivity responds to weight loss, to movement and to the composition of your diet. Unlike many chronic conditions, this is a process that can move in both directions.

The hard numbers come from two large studies.

In the American Diabetes Prevention Program, 3,234 participants with impaired glucose tolerance received a lifestyle programme, metformin or a placebo. The lifestyle programme cut new diabetes cases by 58 percent, metformin by 31 percent (Knowler et al., 2002).

The Finnish Diabetes Prevention Study independently found the same figure: 58 percent less diabetes in the lifestyle group, over an average of 3.2 years (Tuomilehto et al., 2001).

Two studies, two continents, exactly the same percentage. That is rare in medicine.

Both programmes turned on modest things: a few kilos of weight loss, roughly half an hour of movement a day, less saturated fat and more fibre. The Dutch Voedingscentrum describes the same principles for the Dutch situation. Muscle mass weighs heavily here, because muscle takes up most of your glucose. What happens to that muscle during rapid weight loss is covered in the crash diet.

What part does diet play?

Diet works here mainly through two routes: how much you take in, and how fast your blood sugar responds to it. No diet cures insulin resistance. There is, though, a pattern that keeps recurring in the prevention trials: more fibre, less saturated fat, fewer fast sugars.

Fibre is the most underrated part of that list.

Two things respond strikingly quickly to change. Your triglycerides often fall within a few weeks once you cut alcohol and sugary drinks. What else helps there, and how to track it, is covered in lowering triglycerides.

The second is satiety. Your brain learns how much fat tissue you carry through the hormone leptin, and in obesity that signal appears to land less well. Why that happens, and what the term leptin resistance does and does not mean, is covered in leptin resistance.

What does GLP-1 medication do to insulin resistance?

These drugs act indirectly. Semaglutide and tirzepatide improve insulin sensitivity mainly through the weight loss they cause, not by making your cells directly more sensitive. Less fat tissue means less of the substances that push sensitivity down.

That has one practical consequence that is rarely written down.

Your fasting insulin and your HOMA-IR can fall considerably during such a course while your underlying predisposition does not change. Stop the drug and regain the weight, and those values often move back with it. What else happens on stopping is covered in stopping Ozempic.

That is why a baseline before the first injection is so useful. Without it you cannot tell later whether a good result is your own gain or the effect of the drug.

Which values are worth measuring together?

The ones that show the pattern together. Isolated numbers are close to worthless here: a normal glucose rules nothing out, and a raised insulin means little on its own. What counts is glucose, insulin, HbA1c and the lipid panel in a single draw.

Drawn fasting, because otherwise half the comparison does not hold.

The GLP-1 baseline panel contains that combination and records your starting point before you begin a course. Anyone who only wants the insulin question answered can use the standalone HOMA-IR test. A BIG-registered doctor assesses the result in both cases.

Always discuss an abnormal result with your GP before changing anything about your treatment. According to RIVM figures, more than 1.2 million people in the Netherlands had diagnosed diabetes in 2024, and your GP is the one who decides what your values mean in your situation.

What I would look at myself

The order. Insulin moves first, HbA1c next, glucose last, and yet glucose is the only value most people ever have drawn. That is why insulin resistance so often surfaces only after years have already passed.

What strikes me most about this subject is how cheap the alternative is.

The triglyceride/HDL ratio costs nothing extra and is probably already printed on a result you have lying around. Work it out, put it next to your glucose, and discuss the combination with your GP. That is a more concrete first step than any symptom list.

References

• Matthews DR et al. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985. PMID 3899825
• McLaughlin T et al. Use of metabolic markers to identify overweight individuals who are insulin resistant. Ann Intern Med. 2003. PMID 14623617
• Knowler WC et al. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med. 2002. PMID 11832527
• Tuomilehto J et al. Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. N Engl J Med. 2001. PMID 11333990
• Alberti KGMM et al. Harmonizing the metabolic syndrome. Circulation. 2009. PMID 19805654
• NHG guideline on type 2 diabetes, cut-off values for fasting glucose.
• RIVM, figures on diabetes mellitus in the Netherlands (2024).
• Voedingscentrum, information on fibre, saturated fat and weight loss.

Every blood test result includes a professional assessment from a BIG-registered doctor. Discuss your result with your GP before changing anything about your treatment.