Hyperinsulinemia and Chronic Pain: How High Insulin Makes You Hurt

This talk was delivered to a clinical audience at LowCarbUSA. It is more technical than most articles here, and the concepts underneath it matter to patients.

Most patients with chronic pain are told their problem is structural. A disc, a joint, a nerve being compressed. Sometimes that is true.

But a large proportion of the patients who arrive at our clinic have something else running underneath the structural finding: chronically elevated insulin. Not diabetes — most have never been given that diagnosis. High insulin, with blood glucose still in the normal range.

This article explains the proposed mechanism connecting the two, and is honest about which parts are established and which are inference.

Insulin is not just a blood sugar hormone

Insulin’s textbook job is moving glucose out of the bloodstream. That description undersells it considerably.

Insulin is an anabolic growth and storage hormone. It influences fat storage, sodium retention, sympathetic nervous system tone, vascular smooth muscle behavior, and inflammatory signaling. When it is chronically elevated, all of those systems sit in a shifted state.

That is the reason a hormone most people associate only with diabetes turns up in a discussion about back pain.

Four routes from high insulin to more pain

Here is how elevated insulin plausibly amplifies a pain problem. I want to be clear about the epistemic status: these mechanisms are individually well described in the literature, and the combination as an explanation for a given patient’s pain is clinical reasoning, not a proven causal chain.

Inflammation. Insulin resistance and the visceral adipose tissue that accompanies it produce a chronic low-grade inflammatory state. Adipose tissue is not inert storage — it is metabolically active and secretes inflammatory signaling molecules. A nervous system marinating in inflammatory cytokines is a more sensitive nervous system.

Nerve health. Elevated glucose and insulin over time damage small nerve fibers and the tiny blood vessels that feed them. This is the same process that produces diabetic neuropathy — but it does not politely wait for the diabetes diagnosis. Small-fiber changes are measurable in people with pre-diabetes.

Impaired healing. Microvascular dysfunction means less oxygen and fewer nutrients reaching tissue that is trying to repair. An injury that should resolve in six weeks takes six months, and a tissue stuck in a prolonged inflammatory phase keeps producing pain signals.

Central sensitization. Persistent peripheral input plus systemic inflammation encourages the spinal cord and brain to amplify signals — the volume-control problem covered in central sensitization.

Why standard testing misses this entirely

The routine metabolic panel measures glucose. It does not measure insulin.

Because the pancreas compensates for insulin resistance by producing progressively more insulin, glucose can remain normal for years while insulin climbs. A patient can be substantially hyperinsulinemic with a fasting glucose their physician describes as perfect.

This is not a fringe observation. It is the point Dr. Joseph Kraft made with more than 14,000 glucose tolerance tests performed with insulin measurement — abnormal insulin responses were common in patients whose glucose curves looked unremarkable. His population was patients referred for testing rather than a random sample, so his percentages should not be applied to the general public, but the principle holds.

If you want the earlier signal, it has to be requested: fasting insulin alongside glucose, and the triglyceride-to-HDL ratio. More on what to ask for in insulin resistance before diabetes.

What this changes about treatment

If a patient’s pain is being sustained partly by metabolic inflammation, then the metabolic problem is a treatment target — not a separate issue for a different doctor.

Practically, that means an interventional procedure is more likely to hold when the terrain underneath it is improving, and less likely to hold when it is not. It also means that dietary change is not lifestyle advice bolted onto pain care; for some patients it is the part doing the most work.

What it does not mean is that pain is caused by insulin in every patient, or that metabolic care replaces appropriate structural diagnosis and treatment. A compressed nerve root still needs to be identified. The two questions are asked together, not instead of each other.

Frequently asked questions

Key takeaways

• Insulin is a growth and storage hormone that affects inflammation, vascular tone and nerve health — not only blood sugar.
• Four plausible routes from high insulin to worse pain: inflammation, small-fiber nerve damage, impaired healing, and central sensitization.
• Glucose can stay normal for years while insulin climbs, so standard panels miss the early stage.
• Ask for fasting insulin and triglyceride-to-HDL, not glucose alone.
• The mechanisms are established; the causal chain in an individual patient is clinical reasoning, not proven fact.

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. 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.
2. Araújo J, Cai J, Stevens J. Prevalence of optimal metabolic health in American adults: NHANES 2009–2016. Metabolic Syndrome and Related Disorders. 2019;17(1):46–52.
3. Woolf CJ. Central sensitization: implications for the diagnosis and treatment of pain. Pain. 2011;152(3 Suppl):S2–S15.
4. Eddy D, Schlessinger L, Kahn R, Peskin B, Schiebinger R. Relationship of insulin resistance and related metabolic variables to coronary artery disease: a mathematical analysis. Diabetes Care. 2009;32(2):361–366.

Dr. Gurpreet Singh Padda, MD, MBA, MHP