Insulin resistance

A state in which cells respond poorly to insulin, so more is needed to do the same job.

Insulin resistance is the state in which cells respond less readily to insulin, so more of it is needed to move the same glucose out of the blood. The pancreas compensates by producing more, and for years that compensation holds.

That silent period is the important part. Fasting glucose and HbA1c can look entirely normal while insulin is climbing, so testing glucose alone finds the problem late. It is the reason fasting insulin, or the HOMA-IR estimate that combines the two, adds information.

It sits upstream of a great deal: type 2 diabetes, fatty liver disease, raised triglycerides with low HDL, higher blood pressure, polycystic ovary syndrome and a substantial share of cardiovascular risk. Metabolic syndrome is largely a description of its consequences.

The main drivers are excess visceral and liver fat, inactivity, low muscle mass, poor sleep and, in some people, genetics that set the starting point. Muscle is the largest destination for glucose in the body, so having less of it and using it less often shifts the whole system.

It is unusually reversible for something so consequential. Exercise improves glucose disposal after a single session and cumulatively with training, partly through a route that does not require insulin at all. And weight loss where there is weight to lose is powerful: in the DiRECT trial a primary care programme achieved remission of type 2 diabetes in 46% of participants at one year, rising to 86% among those who lost 15 kg or more.

Supplements marketed to reverse it, berberine, cinnamon, chromium and the rest, show small and inconsistent effects on glucose measures and nothing resembling those numbers.

In practice: train regularly, keep or build muscle, watch the waist rather than only the scale, sleep, and get glucose and HbA1c checked rather than inferred.

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