
Back to Blog
Lisa Patterer · 2 min read

A widely cited review of the molecular mechanisms behind insulin resistance describes a typical sequence: muscle and liver cells become less responsive to insulin first. The pancreas's beta cells compensate by releasing more insulin, which keeps blood sugar looking unremarkable for a while. This compensation phase can last years to decades before the beta cells can no longer keep up and blood sugar starts rising measurably.
Current diagnostic criteria for diabetes rely primarily on fasting glucose, the oral glucose tolerance test, and HbA1c — not on fasting insulin. That makes sense clinically, since these are well-validated markers, but it comes with a trade-off: they only become abnormal once the pancreas's extra compensatory effort is no longer enough. Fasting insulin, by contrast, reflects exactly that earlier phase of strain — a value the current diagnostic standard doesn't build in, even though it could complement it.
Evidence suggests chronically elevated insulin isn't only a byproduct — it appears to actively influence metabolic processes itself: insulin promotes fat storage and sodium reabsorption in the kidney, which can affect blood pressure. For some of the other associations discussed, such as with inflammatory processes, the evidence base is still developing, and more controlled studies are needed before clear clinical recommendations can be drawn.
An aging population with rising diabetes rates needs diagnostics that step in earlier than the point where damage is already visible. Fasting insulin — combined with fasting glucose in the HOMA index — can be an additional piece of the puzzle for spotting insulin resistance while there's still time to act through lifestyle change. That's the real shift in mindset in preventive medicine: not waiting for a value to become alarming, but looking earlier where that's already possible today.
