Recognising insulin resistance years before the diabetes diagnosis

The clinical convention is to screen for diabetes with fasting glucose and to reassure patients whose result falls within range. The difficulty is that fasting glucose is a late marker. The pancreas compensates for insulin resistance by producing more insulin, and it can hold glucose within range for years while doing so.

This means a patient can be told repeatedly that their sugars are fine while the process that will eventually produce diabetes is well advanced. In a country carrying the diabetes burden that India carries, that lost decade matters.

What to look for before the numbers move

Much of the earliest evidence is clinical rather than biochemical, and most of it is visible in an ordinary consultation.

• Central adiposity, particularly increasing waist circumference in a patient whose weight has been stable
• Acanthosis nigricans, the velvety darkening at the neck, axillae or knuckles, which is easy to miss and easy to see once you look
• Skin tags in the same distribution
• Pronounced postprandial somnolence and afternoon energy collapse
• Raised triglycerides with low high density lipoprotein cholesterol, a pattern that often precedes glycaemic change
• Raised alanine aminotransferase or fatty liver reported incidentally on imaging
• Polycystic ovary syndrome, gestational diabetes in the past, or a first degree relative with type 2 diabetes
• Hypertension appearing in a young adult

Any one of these in isolation means little. Three or four together in the same patient describe a metabolic trajectory, regardless of what the fasting glucose says.

Measuring more usefully

Where further assessment is warranted, a fasting glucose in isolation is the least informative option available. Glycated haemoglobin adds a longer window. A fasting insulin alongside fasting glucose allows an estimate of insulin resistance. A two hour post load glucose will reveal impairment that fasting values conceal.

A caution belongs here. Insulin assays vary between laboratories, reference ranges are inconsistent, and calculated indices were developed largely for research rather than for individual clinical decisions. These are supporting measures that refine a clinical judgement. They are not a diagnosis, and they should not be sold to patients as one.

What actually changes the trajectory

The interventions with the strongest evidence in this space are also the least proprietary. Sustained reduction in visceral fat, resistance training alongside aerobic activity, adequate sleep, reduction in refined carbohydrate and added sugar intake, and management of alcohol.

What makes this difficult is not the content of the advice but its delivery. Telling a patient to lose weight is not an intervention. Structured, reviewed, individually negotiated change with follow up is. This is where a health coach working alongside a physician earns their place in the team, and it is why IAFM treats coaching as a professional discipline rather than an accessory.

The prize is considerable. Metabolic dysfunction identified at this stage is more amenable to change than the same process identified after a decade of compensation and beta cell decline. The window is real, and it is currently being missed in a great many patients whose test results were described as normal.

This article is written for education and professional discussion. It is not medical advice and it is not a substitute for consultation with a clinician who knows your history. Nothing here should be used as a reason to stop or alter prescribed treatment without the involvement of the doctor who prescribed it.