The Hormone Nobody Measured Is Starving Your Nerves | The Pained Brain, Chapter 4

High insulin · normal blood sugar

High Insulin, Normal Blood Sugar: What Your Nerves May Be Showing

A normal glucose and a normal A1c can sit on top of years of rising insulin. The nerves that carry pain are often among the first tissues to show the cost, and a routine checkup looks at neither.

High insulin, normal blood sugar: a pattern most checkups are not built to catch. Blood sugar stays in range because the pancreas releases more and more insulin to push sugar into cells that have stopped responding well. The glucose number looks reassuring. The effort behind it never appears on a standard panel, and small nerves can be paying for that effort for years.

The video The Hormone Nobody Measured Is Starving Your Nerves covers Chapter 4 of The Pained Brain, by Dr. Gurpreet Singh Padda, MD, MBA, MHP, and Dr. KrisJay Fucanan, MD. Measura [Cardiometabolic and Autonomic Health Analysis] takes the measurement side of it: what a normal result can hide, which parts of the damage can be measured before any diagnosis, and what to ask for at your next visit.

How long can insulin run high before blood sugar rises?

Long-term studies answer this by looking backward from the day diabetes was diagnosed. British civil servants who later developed diabetes were already 34.2% less sensitive to insulin thirteen years earlier, while their fasting glucose barely budged, from 5.47 to 5.79 mmol/L. In a Japanese cohort of 27,392 adults, people who would later be told they had prediabetes already showed lower insulin sensitivity ten years before that label, with fasting sugar of 91.8 mg/dL against 89.6 in people who never progressed. No one would flag a gap that small.

A glucose tolerance test with insulin measured at the same time shows the hidden half. Among 4,185 people whose glucose handling was entirely normal, 2,079 were producing abnormal amounts of insulin to keep it that way. Roughly half of “normal” was compensating, and a glucose-only result could not tell them apart.

Can high insulin damage your nerves and their blood supply?

Insulin opens blood vessels through one signal and tightens them through another. When the body becomes resistant, the opening signal weakens while the tightening one keeps working. In 40 obese adults with no diabetes, the most insulin-resistant third widened their arteries by 9.2% on testing, compared with 18.0% in the least resistant third.

Nerves are fed by tiny vessels that run inside them. Swedish researchers biopsied a leg nerve in a group of men and came back eleven years later. The men who went on to develop diabetes had, at the first biopsy, capillaries inside the nerve with an open channel of 5.5 square micrometers, against 22.8 in the men who stayed healthy. The nerve was short of blood before any diagnosis existed.

The front of the eye shows the same process, and shows that it can turn around. People with impaired glucose tolerance already had fewer corneal nerve fibers than controls, 24.4 against 30.7 per square millimeter. The five who reversed their glucose intolerance grew nerve back, from 25.4 to 29.8. Laboratory work adds a second effect: insulin makes pain-sensing nerve cells fire more readily. That evidence comes from animal tissue, not people, but it explains how a metabolic hormone can turn up the volume on pain.

Why can a routine nerve test come back normal?

Small nerve fibers, the ones that carry pain and temperature, tend to fail before the large fibers that standard nerve conduction studies measure. When Heidelberg researchers tested people with prediabetes, a full sensory battery found nerve damage in 71%. The usual bedside score found it in 11%, and nerve conduction studies missed 58% of what the battery caught. More than half had nerves that were oversensitive rather than numb.

Weight and waist matter even without a diabetes diagnosis. In a Michigan cohort, nerve damage turned up in 3.8% of lean adults, 11.1% of obese adults with normal glucose and 29.0% of obese adults with prediabetes. In a German cohort followed for six and a half years, every five centimeters of waist added 22% to the odds of developing neuropathy, with or without diabetes. And in a 2001 study of patients told their painful neuropathy had no known cause, 34% had impaired glucose tolerance that only a sugar drink revealed.

That is where sudomotor testing fits. Tiny nerve fibers switch on the sweat glands in your hands and feet, and this test checks how well that signal works, something a conduction study does not assess. Burning or tingling feet are covered in numbness, burning and tingling.

Why isn’t fasting insulin on a routine blood test?

The honest reason is that the test was never standardized. When the same blood samples were run on twelve commercial insulin assays, results varied by a median of 24%. By 2025, just one of twelve methods matched the laboratory gold standard. Without a standard there are no agreed cutoffs, and current diabetes diagnostic standards define prediabetes by glucose and A1c without naming fasting insulin at all. No standard, no guideline, no routine order. The gap is institutional, not biological.

The number is still useful when it is read with care. In an Iranian cohort followed for nine years, future diabetes became more likely once fasting insulin passed about 9.16 for men or 11.13 for women, well under the top of many printed reference ranges. A value repeated over time on the same assay is the comparison that means something.

What tests show high insulin with normal blood sugar?

A measurement plan for this pattern has several parts, and none of them is a diagnosis on its own:

Blood work. Laboratory panels can include fasting glucose, HbA1c and triglycerides. Ask whether fasting insulin is on the requisition, because insulin and glucose drawn together allow HOMA-IR to be calculated. C-peptide is the body’s own record of how much insulin it is making, and among 5,249 Danes newly diagnosed with type 2 diabetes it tracked neuropathy more strongly than A1c did.
Small-fiber nerve function. Sudomotor testing, described above.
Vessel function. Arterial stiffness and endothelial function testing describes how the artery wall responds, the property insulin resistance wears down.
Body composition. Bioimpedance body composition separates fat from lean tissue, which a bathroom scale cannot do.

Findings go to your physician. They describe terrain; what to do about it is a clinical conversation. The research on reversal is encouraging. In a randomized trial of 100 adults with type 2 diabetes, a year of supervised exercise regrew small nerve fibers in the leg by 1.5 fibers per millimeter while A1c stayed flat. In 32 people with prediabetes and neuropathy, those whose fibers regrew most after a year of diet and exercise counseling had the largest drop in nerve pain. Movement and food are biology, and they are also schedules, neighborhoods and habits, which is why a measured baseline helps: it turns a vague warning into a number that can be tracked. The full evidence, including the studies that disagree, is in the book companion for Chapter 4, and the imaging side of the same argument is in what degenerative disc disease means.

Frequently asked questions

Can you have high insulin with a normal A1c?

Yes. A1c reflects average blood sugar, and blood sugar can stay normal for years while the pancreas works harder to hold it there. In a large database of glucose tolerance tests with insulin measured, about half of people with entirely normal glucose handling were producing abnormal amounts of insulin. Only measuring insulin shows that extra effort. Insulin resistance and metabolic health.

What fasting insulin number should concern me?

There is no single agreed cutoff, because insulin assays were never standardized. In a healthy Brazilian reference population the median sat near 6.6 microU/mL with an upper limit of 13.14, while a nine-year Iranian study linked future diabetes to levels as low as 9.16 in men and 11.13 in women. Your physician reads your value against your laboratory and your earlier results. Understanding your results.

Can prediabetes damage nerves?

The evidence says it often does, though not every study agrees. In a population survey near Beijing, neuropathy was present in 3.25% of people with normal sugar and 6.29% of people with prediabetes, and a German sensory study found measurable nerve damage in 71% of people with prediabetes. The small fibers that carry pain are usually affected first. Small-fiber versus large-fiber neuropathy.

Does sudomotor testing diagnose neuropathy?

Not on its own. It measures how well the small nerve fibers that control sweat glands in the hands and feet are working. That is one objective piece of a picture that also includes your symptoms, an examination, blood work and sometimes other nerve tests. Results go to your physician, who decides what they mean alongside everything else. Sudomotor dysfunction.

Why hasn’t my doctor ordered a fasting insulin?

Mostly because the system never built the tools around it. Insulin assays from different manufacturers disagree, so no agreed cutoffs exist, and diabetes diagnostic standards rely on glucose and A1c alone. That does not make the number useless. It makes it a number to request, repeat on the same assay and interpret with your physician. What insulin resistance looks like before diabetes.

Can you have high insulin and not be diabetic?

Yes, often for years. The pancreas releases more insulin to keep blood sugar in range, so the glucose number looks normal while the effort behind it climbs. British civil servants who later developed diabetes were already 34.2% less sensitive to insulin thirteen years before diagnosis, while their fasting glucose barely moved. A glucose-only test cannot see that stage.

What should I do if my insulin is high?

Get a measured baseline and review it with your physician. Fasting insulin drawn with fasting glucose lets HOMA-IR be calculated; repeat it on the same assay so the trend means something. Small-fiber nerve, vessel and body-composition testing show whether the terrain is already paying a cost. In trials, a year of supervised exercise, or of diet and exercise counseling, regrew small nerve fibers.

Ask for the number behind the normal sugar

Request a Measura testing plan that looks at blood work, small-fiber nerve function and vessel health together. Results go to your physician.

Send a message

4477 Woodson Rd, Suite 201, St. Louis, MO 63134. Monday to Friday, 9:00 a.m. to 5:00 p.m. Please do not send symptoms, diagnoses or images through a web form — a website form is not a secure medical channel. Send your name and number and we will call you back.

References

Tabák, A. G., Jokela, M., Akbaraly, T. N., Brunner, E. J., Kivimäki, M., & Witte, D. R. (2009). Trajectories of glycaemia, insulin sensitivity, and insulin secretion before diagnosis of type 2 diabetes: an analysis from the Whitehall II study. Lancet, 373(9682), 2215–2221. https://doi.org/10.1016/S0140-6736(09)60619-X
Crofts, C., Schofield, G., Zinn, C., Wheldon, M., & Kraft, J. (2016). Identifying hyperinsulinaemia in the absence of impaired glucose tolerance: An examination of the Kraft database. Diabetes Research and Clinical Practice, 118, 50–57. https://doi.org/10.1016/j.diabres.2016.06.007
Galvao, R., Plavnik, F. L., Ribeiro, F. F., Ajzen, S. A., Christofalo, D. M. de J., & Kohlmann, O. (2011). Effects of different degrees of insulin sensitivity on endothelial function in obese patients. Arquivos brasileiros de cardiologia, 98(1), 45–51. https://doi.org/10.1590/s0066-782×2011005000119
Mohseni, S., Badii, M., Kylhammar, A., Thomsen, N. O. B., Eriksson, K.-F., Malik, R. A., Rosen, I., & Dahlin, L. B. (2017). Longitudinal study of neuropathy, microangiopathy, and autophagy in sural nerve: Implications for diabetic neuropathy. Brain and behavior, 7(8), e00763. https://doi.org/10.1002/brb3.763
Azmi, S., Ferdousi, M., Petropoulos, I. N., Ponirakis, G., Alam, U., Fadavi, H., Asghar, O., Marshall, A., Atkinson, A. J., Jones, W., Boulton, A. J. M., Tavakoli, M., Jeziorska, M., & Malik, R. A. (2015). Corneal Confocal Microscopy Identifies Small-Fiber Neuropathy in Subjects With Impaired Glucose Tolerance Who Develop Type 2 Diabetes. Diabetes care, 38(8), 1502–8. https://doi.org/10.2337/dc14-2733
Kopf, S., Groener, J. B., Kender, Z., Fleming, T., Bischoff, S., Jende, J., Schumann, C., Ries, S., Bendszus, M., Schuh-Hofer, S., Treede, R.-D., & Nawroth, P. P. (2018). Deep phenotyping neuropathy: An underestimated complication in patients with pre-diabetes and type 2 diabetes associated with albuminuria. Diabetes Research and Clinical Practice, 146, 191–201. https://doi.org/10.1016/j.diabres.2018.10.020
Callaghan, B. C., Xia, R., Reynolds, E., Banerjee, M., Rothberg, A. E., Burant, C. F., Villegas-Umana, E., Pop-Busui, R., & Feldman, E. L. (2016). Association Between Metabolic Syndrome Components and Polyneuropathy in an Obese Population. JAMA Neurology, 73(12), 1468–1476. https://doi.org/10.1001/jamaneurol.2016.3745
Christensen, D. H., Knudsen, S. T., Gylfadottir, S. S., Christensen, L. B., Nielsen, J. S., Beck-Nielsen, H., Sørensen, H. T., Andersen, H., Callaghan, B. C., Feldman, E. L., Finnerup, N. B., Jensen, T. S., & Thomsen, R. W. (2020). Metabolic Factors, Lifestyle Habits, and Possible Polyneuropathy in Early Type 2 Diabetes: A Nationwide Study of 5,249 Patients in the Danish Centre for Strategic Research in Type 2 Diabetes (DD2) Cohort. Diabetes Care, 43(6), 1266–1275. https://doi.org/10.2337/dc19-2277
Marcovina, S., Bowsher, R. R., Miller, W. G., Staten, M., Myers, G., Caudill, S. P., Campbell, S. E., & Steffes, M. W., for the Insulin Standardization Workgroup (2007). Standardization of insulin immunoassays: report of the American Diabetes Association Workgroup. Clinical Chemistry, 53(4), 711–716. https://doi.org/10.1373/clinchem.2006.082214
Singleton, J. R., Marcus, R. L., Jackson, J. E., K Lessard, M., Graham, T. E., & Smith, A. G. (2014). Exercise increases cutaneous nerve density in diabetic patients without neuropathy. Annals of Clinical and Translational Neurology, 1(10), 844–849. https://doi.org/10.1002/acn3.125