A1c and glucose levels (e.g., via CGM) tell you about sugar in the blood. Insulin levels tell you how hard your body is working to keep those numbers in range. Managing insulin resistance isn’t just about lowering glucose – it’s about lowering the insulin required to lower glucose.
We now know that (in an everyday, low-activity, frontcountry context) that frequent, small dosing of carbs may help us manage glucose (by keeping insulin elevated) – but those elevated levels of insulin may not improve insulin resistance.
Backpacking is a little bit different here, because the physical activity (fat burning HR ranges) can help keep insulin in check in response to frequent carb feeding.
Both CGM responses and A1c can miss insulin resistance. Two people with the same A1c may have very different insulin sensitivity. And two people who show the same glucose spike and time-to-return-to-baseline on a CGM may still differ dramatically in how much insulin their bodies had to produce to make that happen.
That’s why focusing only on glucose seems to be inadequate to me, and possibly give us a false sense of security. Insulin resistance (not glucose) may actually be the underlying driver of both the acute issues backpackers care about (bonking, mental fog). In addition, the past decade of insulin resistance research has pretty much implicated insulin and not glucose as the driver of chronic issues that affect long-term health (inflammation, visceral fat accumulation, cardiovascular disease, etc.).
It’s a fascinating set of metabolic dynamics and complex. But managing T2D (or anywhere on the spectrum of insulin resistance) via A1c or acute blood glucose or CGM feels inadequate to me – especially if we want to send insulin resistance into true remission.