The Fasting Insulin Test: Why It Matters for Nerve Pain

A fasting insulin test measures the hormone your pancreas is pushing out to keep blood sugar normal. That matters because blood sugar can look fine for more than a decade while insulin climbs. And the nerves that carry pain are among the first tissues to pay.

The video for Chapter 4 of The Pained Brain, The Hormone Nobody Measured Is Starving Your Nerves, walks through how it works. The book is by Dr. Gurpreet Singh Padda, MD, MBA, MHP, and Dr. KrisJay Fucanan, MD. This page covers what the video could not. What does the number mean? Where is the test weak? What does the nerve evidence show once you look past glucose? The metabolic background is in how high insulin makes you hurt.

What does a fasting insulin test show that glucose misses?

The Whitehall II cohort followed British civil servants. People who later got diabetes were already 34.2 percent less sensitive to insulin in the years 13 to 5 before diagnosis. Their fasting glucose drifted only from 5.47 to 5.79 mmol/L. Their pancreas overworked the whole time. Its output crashed only near diagnosis. The gland strained for a decade while the sugar barely moved.

Nine European cohorts were pooled. They compared 3,309 people who went on to get diabetes with 13,963 matched controls. One to six years before diagnosis, the insulin-resistant group had a fasting insulin-to-glucose ratio 88 percent above controls. That held after adjusting for age, sex and body size. Then there is the clamp test, the gold standard, run in 80 hospital patients. Normal glucose with high insulin looked the same as impaired glucose tolerance and new diabetes. Glucose clearance was 6.23, 6.37 and 6.19 mg/kg/min.

What is a normal fasting insulin level, and how reliable is the test?

A lab’s normal range is not a danger line. In 21,684 healthy Brazilian adults, the middle fasting insulin value was about 6.6 microU/mL. The normal range topped out at 13.14. In 4,942 Tehran adults followed for 9.2 years, the level that best predicted diabetes was 9.16 in men and 11.13 in women. So a result printed as normal can still sit above the line that predicted disease.

The test has limits, and I would rather say so than oversell it. The same samples read 1.8-fold apart across eight commercial lab tests. In 2025, only one of twelve immunoassays agreed fully with mass spectrometry, the reference method. Among 26,976 adults without diabetes, fasting insulin alone barely predicted death, at 1.13. The top HOMA-IR group, which pairs insulin with glucose, reached 1.34. Repeat values on the same lab test are the ones worth reading.

That measuring gap is why the test is rarely ordered. A 2010 work group found no rules to label a person insulin resistant. It laid out three steps. Standardize the test. Let research set cutoffs. Then write guidelines. The first step never finished. Today’s standards define prediabetes by glucose and HbA1c alone. They make no fasting insulin recommendation. No standard means no guideline. No guideline means nobody is prompted or paid to ask.

How does high insulin damage nerves?

Insulin opens blood vessels through nitric oxide. It tightens them through endothelin. In insulin resistance, the opening side goes deaf. The tightening side keeps working. So more insulin means a narrower vessel. In 40 obese adults without diabetes, the most insulin-resistant third widened their arteries 9.2 percent. The least resistant third widened them 18.0 percent.

Inside the nerve, the small vessels narrow early. A Swedish study took nerve biopsies (samples) eleven years apart. Men who later got diabetes already had tiny vessel channels of 5.5 square micrometers. Men who stayed healthy had 22.8. Their glucose was still normal or only a little high. The key comparison was tiny, a signal rather than a rate.

Insulin also acts on the pain nerve directly. That proof comes from lab and animal work, not people. In rat sensory nerves, insulin raised acid-sensing channel currents by 46.2 percent. It made pain behavior worse through insulin receptors outside the brain. No one has tested whether that happens at the insulin levels a patient with high insulin carries. In human volunteers, the picture is clearer on inflammation. Raising insulin while glucose was held steady raised interleukin-6 messenger RNA in fat elevenfold at two hours.

Does prediabetes damage nerves, and why do tests miss it?

Nerve damage does not wait for a diagnosis. In a Michigan weight-management cohort, obese people with normal glucose and no nerve disease on exam already had fewer small nerve fibers in the leg than lean controls. They had 4.5 against 6.4 fibers per millimeter. Among people with severe obesity, waist size split those with nerve damage from those without, 139.3 against 129.1 centimeters. Body mass index did not.

How you test decides what you find. Across 29 studies, nerve damage in prediabetes ranged from 2 percent to 77 percent. The highest numbers came from small-fiber tests and mixed methods. In 28 people with prediabetes at Heidelberg, a full set of sensory tests found nerve damage in 71 percent. More than half showed hyperalgesia: nerves turning up, not down. A normal nerve conduction study may simply be the wrong test for small fibers. That is what nerve testing can and cannot measure.

Not every cohort agrees. In Olmsted County cohorts, prediabetes brought no extra nerve symptoms or sensory changes. One large study found metabolic syndrome had no link of its own once prediabetes was counted. The evidence leans one way. It is a majority, not a consensus. Where a marker other than glucose was measured, the body’s own insulin output stands out. Among 5,249 Danes with new type 2 diabetes, a high C-peptide carried a prevalence ratio of 1.72 for possible nerve damage. A high HbA1c carried only 1.42.

The loop: pain and its treatments push insulin up

Pain itself raises insulin resistance. Thirty minutes of painful skin stimulation cut glucose uptake 22 percent in ten healthy young men. Two weeks of prednisolone lowered insulin sensitivity, more so at higher doses. It also cut the opening of tiny vessels by insulin by up to 17 percent. In national survey data, adults on prescription opioids averaged a fasting insulin of 15.5, above the normal range. That comparison was not adjusted. It may reflect who takes opioids rather than the drug. When I use a steroid injection as a bridge, I want the patient’s insulin already in hand. That loop between pain and metabolism is why chronic pain costs years, not only comfort.

What lowers insulin and helps nerves grow back?

Movement has the clearest nerve signal. In one randomized trial, 100 adults with type 2 diabetes got either a year of supervised exercise or counseling alone. Leg nerve fibers rose 1.5 fibers per millimeter with exercise. They fell 0.1 without it. HbA1c did not change. In 14 adults with painful diabetic nerve damage, sixteen weeks of aerobic exercise cut how much pain got in the way of life, from 4.65 to 2.97. HbA1c and body mass index did not change. The likeliest route runs through blood flow. Insulin-driven flow to muscle makes up 25 to 40 percent of insulin’s effect on glucose uptake. Nerves depend on the same small vessels. That link is my reading of the pattern, not any single trial’s conclusion.

Weight and diet push the same way. In Look AHEAD, adults with type 2 diabetes put on an intensive lifestyle program reported less burning pain in the feet and legs. Each kilogram lost moved the symptom score. Driving sugar down with more insulin did not do the same. In ACCORD, 10,251 patients on tight glucose control showed no real gain on the combined outcome that included nerve damage. The hazard ratio was 0.95. Speed matters too. In reported cases of nerve injury during fast weight loss on newer drugs, the typical loss was 3.7 kilograms a month. Any medication decision belongs with your physician.

In our practice, every new patient has a fasting insulin drawn before any needle goes in. Fewer than one in a hundred of our chronic pain patients turns out to be metabolically healthy. That figure comes from our own patients, not a trial, and individual results vary. Ask for the number itself. Ask which lab test ran it. Repeat it on the same one. Pair it with a fasting glucose so HOMA-IR can be figured. The studies and their limits are in the Deep Dive to Chapter 4. What the wear and tear on a spine report really records is in the post on abnormal MRI findings.

Frequently asked questions

What is a normal fasting insulin level?

It depends on the lab and the test it uses. In 21,684 healthy adults, the middle value was about 6.6 microU/mL. The top of the normal range was 13.14. In a nine-year cohort, the level that best predicted diabetes was 9.16 in men and 11.13 in women. That is below many printed upper limits. Read your result against your own lab’s range and your last value. Why a glucose test misses insulin resistance.

Can prediabetes cause nerve pain?

It often travels with it. Some patients have painful nerve damage labeled as having no known cause. About a third of them had impaired glucose tolerance (high blood sugar found only on a two-hour sugar drink test). Their fasting glucose and HbA1c were normal. Prediabetes cohorts show small-fiber damage that routine tests often miss. But two studies found no prediabetes signal. Why diabetic nerve pain burns at night.

What is hyperinsulinemia?

Hyperinsulinemia means insulin that stays high. Usually the pancreas is making up for cells that respond poorly to the hormone. Blood sugar can stay normal for years while insulin climbs. Among American adults without diabetes, the share with fasting insulin above 10 uU/mL rose from 28.2 percent to 41.4 percent across two decades of national surveys. Why we treat insulin before we treat the joint.

Why don’t doctors routinely test fasting insulin?

Because the test was never standardized. When first compared, the same samples on commercial insulin tests varied by a typical 24 percent. In 2025, only one of twelve immunoassays agreed fully with mass spectrometry. Without a standard there are no agreed cutoffs. Today’s standards make no fasting insulin recommendation. The test is still useful when repeated on one lab test. What a first interventional pain appointment includes.

Can exercise reverse nerve damage from insulin resistance?

It can regrow small nerve fibers. In a randomized trial of adults with type 2 diabetes, a year of supervised exercise raised leg nerve fibers 1.5 fibers per millimeter. The counseling group lost 0.1. HbA1c did not change. In people with prediabetes and nerve damage, a year of diet and exercise coaching regrew thigh fibers. Those who regrew most had the biggest drop in pain. Why losing muscle switches off the body’s own anti-inflammatory signals.

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Medically reviewed by Dr. Gurpreet Singh Padda, MD, MBA, MHP, board certified in anesthesiology, pain medicine, interventional pain management, addiction medicine and obesity medicine. Adapted from Chapter 4 of The Pained Brain by Dr. Padda and Dr. KrisJay Fucanan, MD. Last reviewed September 2026.

Dr. Gurpreet Singh Padda, MD, MBA, MHP