Insulin Resistance Prevention and Reversal
A standard carton holds 12 eggs, and when I try to add a 13th, we don’t consider the carton egg resistant when it won’t fit. It’s just full.
We either need a bigger carton, eat the eggs faster, or stop buying more eggs and expecting them to fit.
Insulin-friendly eating, low-processed food, consumption, and low-carb diets of any kind are a way we stop buying more eggs, exercise is how we create a bigger carton, and ketones from fat burning make up for the eggs we aren’t eating as frequently for energy.
Or, you can take medications, herbs, or supplements to try and force more than 12 eggs into a 12-egg carton and see how well that works.
“Insulin carries in glucose to feed our cells. Without it, they starve.” Ever heard that before?
It’s not true.
It’s time to update our language and metaphors used for insulin resistance and diabetes, specifically regarding what insulin is and does.
80% of our cells get glucose through facilitated diffusion, where as long as there is glucose in the system, our cells will not starve, with or without insulin’s help.
Glucose uptake is enhanced via the 14 Glucose Transport (GLUT) pathways for faster access in different tissues.
Only one of the 14 is insulin-dependent, the GLUT 4 pathway.
The GLUT 4 pathway depends on insulin to transport glucose from the blood and into storage in either liver or muscle glycogen or fat cells.
GLUT 4 insulin-dependent glucose transport does not bring glucose into cells to “feed” or use glucose for energy—the 13 other GLUT(s) do that.
For example, the brain is the largest consumer of glucose, and the brain cells called glial cells use GLUT 5, and neurons use GLUT 3. The heart uses GLUT 1. Muscle cells absorb glucose using GLUT 1 and 3.
This is why in untreated type 1 diabetes, people don’t die immediately without insulin or animals when their pancreas is removed completely. A type one diabetic can’t store glucose as glycogen or fat and, unfortunately, waste away regardless of what or how much they eat.
The bottom line, cellular glucose uptake in your body is not dependent on insulin.
Cells take up glucose whether there is insulin present or not.
Insulin does promote glucose utilization as insulin signals inside the cell….and the cell signals to the mitochondria, affecting the Krebs’ cycle directly to make more of the energy molecule ATP.
ATP can be made via the Krebs cycle from either glucose or ketones (the byproduct of fat-burning). Insulin promotes increased glucose use by turning off the fat-burning side, stopping the use of ketones, and, therefore, ketosis and fat-burning.
Blood sugar numbers drop when insulin is secreted or injected because it signals the liver to stop releasing more blood sugar into the bloodstream.
Less glucose being released into the bloodstream as the cells continue to use what is present will result in a net lowering of blood sugar.
Insulin doesn’t determine glucose uptake but storage and release for the liver. Insulin doesn’t drain the tub filled with glucose but instead turns the faucet that’s filling the tub off.
This is no slight distinction, and it means people are not resistant to insulin as much as they are maxed out in where to put extra glucose. At that point, the body has no choice but to turn that glucose into fat.
No amount of insulin can force extra eggs into a 12-egg carton.
When you’re full, you’re full, and the only option is to stop trying to force more glucose into your cells, increase your glycogen capacity with exercise to have a better blood sugar buffering system, and start using ketones more than glucose for energy production.
Never stop learning, my friends!
We can do better!