@MichGuy12 You included this in a post earlier this year. I am looking for studies on this point. Where did you get this information?
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I’ll do some research later this week, but here’s some info. This particular piece states "We saw that some folks who think they’re healthy actually are misregulating glucose — sometimes at the same severity of people with diabetes — and they have no idea,”
The study was in a Diabetic Journal. I’ll take a look around to see if I can find it.
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I think it is becoming clearer that T2D progresses over 10-20 years as undiagnosed insulin resistance before showing up as high HbA1c. I wouldn’t be surprised if a large majority of Americans have insulin resistance.
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As a marker of insulin resistance, high and extended glucose spikes after a meal are a good signal. That makes sense.
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Understanding obesity as a disease, with diabetes as a comorbidity versus diabetes with obesity as a comorbidity helps most people understand a difficult fact – if you are obese, even excessively overweight, you most likely have some form of insulin resistance. If you have insulin resistance, of any kind, you are walking an incredibly dangerous tightrope of increased cardiovascular risks, ongoing neurological and nephrological damage.
No debate
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The science behind the Randle Cycle, also known as the glucose fatty-acid cycle is a bit dense, even for those who understand obesity medicine (and I am by no means the experts, expert) so here’s some information on what I explained above!
Tldr; Fat Cells are insulin resistant
A simpler explanation below; Our body can use two types of fuel: glucose (like gasoline) and fatty acids (like diesel). The Randle cycle helps our body decide which fuel to use for energy.
When we have a lot of glucose available, such as after a meal, our body prefers to use glucose as its main source of fuel. Insulin helps transport glucose into our cells, where it can be used for energy.
But when glucose levels are low, like during fasting or intense exercise, our body needs an alternative fuel source. This is where the Randle cycle comes in. It promotes the breakdown of stored fatty acids, converting them into energy molecules called ATP.
The Randle cycle involves a complex interaction between insulin and hormones like glucagon and adrenaline. When insulin levels are low, these hormones signal our body to break down fatty acids for energy. At the same time, they inhibit the use of glucose, making fatty acids the primary fuel source.
So, in simpler terms, the Randle cycle helps our body decide whether to use glucose or fatty acids for energy, depending on what’s available and the signals from our hormones.
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Another factoid about adipose fat. It contains the highest density of senescent cells found in the human body. This then leads to higher inflammation. I wonder if a higher senescent cell burden would lead to diabetes as well?
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I think the issue is that as cells fail to differentiate properly they turn into adipocytes and store fat. IMO diabetes is in part caused by a failure of differentiation in the pancreas.
If you consider these two CGM readings roughly a year apart (the daily food cycle is the same)
https://twitter.com/johnhemming4mp/status/1650480078424244230
You can see that glucose peaks at 8 mmol/L rather than going over 10 mmol/L. That I think is as a result of improved gene expression and bettter differentiation (less senescence particularly in the pancreas).
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