Insulin Resistance Comes Years Before Diabetes — and Your Glucose Test Will Miss It

Your fasting glucose came back normal. Your physician said your labs looked fine. And you still feel exhausted, still carry weight around your middle, and still hurt.

Those things are not in conflict. A normal fasting glucose does not tell you that your metabolism is healthy — it tells you that the late stage of a metabolic problem has not arrived yet. The earlier stage can run for a decade or more underneath a normal glucose reading, and it is the stage where the damage starts.

This article explains what that earlier stage is, how common it actually is, and what can be measured instead.

Fewer than one in eight adults is metabolically healthy

Researchers analysing the National Health and Nutrition Examination Survey for 2009 to 2016 asked a simple question: what proportion of American adults have healthy blood sugar, blood pressure, triglycerides, HDL cholesterol, and waist circumference — all five, without medication?

The answer was 12.2%.¹

That means roughly 88% of adults fail on at least one of those five measures. Not 88% are diabetic — that is a different and smaller number. But 88% are carrying some degree of metabolic dysfunction, and most of them have never been told so, because no single test on a routine panel is designed to detect the pattern.

There is an older observation behind this. Between 1972 and 1998, Dr. Joseph Kraft performed more than 14,000 oral glucose tolerance tests with simultaneous insulin measurement. He found that a large majority of the patients he tested had abnormal insulin responses — many of them while their glucose curves looked entirely normal.²

An important qualification, because this finding is routinely overstated: Kraft’s patients were people referred for glucose tolerance testing, not a random sample of the population. His percentages describe a clinic population, not the country. What his work established was not a prevalence figure but a principle — you can be hyperinsulinemic long before you are hyperglycemic, and only measuring insulin reveals it.

Why glucose is the last thing to go wrong

Think of insulin as the signal that tells cells to take glucose out of the bloodstream. When cells respond less readily to that signal — insulin resistance — the pancreas compensates by producing more insulin. More signal, same result.

And it works. For years, sometimes decades, blood glucose stays in the normal range because the pancreas keeps raising the dose.

What that means clinically is that glucose is a late symptom. By the time fasting glucose or HbA1c drifts upward, the compensation has been running a long time and has begun to fail. A physician measuring only glucose is watching the last domino, not the first.

Meanwhile the elevated insulin itself is doing things. Insulin is a storage hormone — while it is high, fat goes into the cell and does not come out easily. It is also involved in inflammatory signalling. This is why the phrase “pre-diabetes” is misleading: it sounds like a warning about the future, and it is actually a description of a process already well underway.

Why a pain physician is talking about this at all

Almost every patient who comes to our clinic in chronic pain is also carrying an unnamed metabolic problem.

That is not a coincidence, and it changes treatment. Systemic inflammation raises the sensitivity of the nervous system. Elevated glucose impairs tissue healing. Visceral adipose tissue is metabolically active and produces inflammatory signalling molecules. A patient whose terrain is inflamed will hurt more from the same amount of tissue damage, will heal more slowly, and will get less durable benefit from an interventional procedure.

Treating the pain while ignoring the metabolic terrain is treating the loudest part of the problem rather than the most modifiable part.

What the evidence does and does not support

Here is where honesty matters more than enthusiasm.

Well established: cardiovascular risk does not begin at the diagnostic threshold for diabetes. There is a continuum of increased microvascular and macrovascular risk extending well below the glucose cutoffs used to diagnose it. Waiting for a formal diagnosis means acting after damage has accumulated.

Not established: that treating pre-diabetes reduces heart attacks or death. A meta-analysis of randomised trials in more than 23,000 people with pre-diabetes found that intervention did prevent or delay progression to diabetes — a relative risk of 0.83 — but produced no reduction in mortality or myocardial infarction, with a possible exception for stroke.³

So the argument for acting early rests on preventing diabetes itself and on the risk continuum. It does not yet rest on proven mortality benefit, and anyone who tells you otherwise is going beyond the evidence.

What can actually be measured

If a standard panel is not designed to catch this, what is? These are the measures worth discussing with your own physician:

• Fasting insulin, alongside fasting glucose rather than instead of it
• Triglyceride-to-HDL ratio, a widely used surrogate marker of insulin resistance
• HbA1c, which reflects roughly three months of average glucose
• Waist circumference, which tracks visceral fat better than weight alone

None of these is exotic or expensive. They are simply not on the default panel, so they must be requested.

Frequently asked questions

Key takeaways

• Only 12.2% of US adults meet all five criteria for metabolic health; roughly 88% fail at least one.
• Insulin rises years to decades before glucose does, so a normal fasting glucose does not rule out a metabolic problem.
• Cardiovascular risk climbs on a continuum below the diabetes diagnostic cutoff — the threshold is administrative, not biological.
• Trials in pre-diabetes have prevented diabetes but have not yet shown reduced heart attack or death; act early for the right reasons.
• Ask about fasting insulin, triglyceride-to-HDL ratio, HbA1c and waist circumference together.

Medically reviewed by Gurpreet Singh Padda, MD — Board Certified in Anesthesiology, Pain Medicine, Interventional Pain Management, Addiction Medicine, and Obesity Medicine. Last reviewed July 2026.

This article is educational and is not a substitute for evaluation, diagnosis, or treatment by a physician. Individual results vary. Do not start, stop, or change any medication without consulting your physician. To be evaluated, request an appointment or call (314) 481-5000.

References

1. Araújo J, Cai J, Stevens J. Prevalence of optimal metabolic health in American adults: National Health and Nutrition Examination Survey 2009–2016. Metabolic Syndrome and Related Disorders. 2019;17(1):46–52.
2. Kraft JR. Detection of diabetes mellitus in situ (occult diabetes). Laboratory Medicine. 1975;6(2):10–22. Referred clinical population; not a population prevalence sample.
3. Hopper I, Billah B, Skiba M, Krum H. Prevention of diabetes and reduction in major cardiovascular events in studies of subjects with prediabetes: meta-analysis of randomised controlled clinical trials. European Journal of Cardiovascular Prevention & Rehabilitation. 2011;18(6):813–823.

Dr. Gurpreet Singh Padda, MD, MBA, MHP