I have been looking closely at the protocols for managing chronic disease, especially diabetes. Managing is an appropriate word choice, but not in a good way.
The finding that statins can contribute to insulin resistance (a core feature in diabetes), coupled with the fact they are the standard of care confirms my suspicions of the broad application of such standards.
Statins are a class of medications commonly used to decrease cholesterol synthesis. They lower cholesterol – effectively. The question is to what benefit, and what collateral damage might develop?
My studying of the topic results in not recommending statins for prevention in most cases although there may be some benefit (but NOT from lower cholesterol) for those who have had a cardiac event.
The mechanism used is not free of consequences. Every cell NEEDS cholesterol, which is why they make it. Further, the mevalonate pathway inhibited by statins involves other important endpoints that can cause DNA damage when manipulated1.
2019 Diabetes Standard of Care
This is from the 2019 version for the American Diabetes Association Standards of Care.
The percentage that falls into the “no statin” category are fractional (I can think of one Island Drug patient in the last number of years).
So, it is safe to say, if you get diabetes you will get recommended statin therapy.
But Statins Cause Insulin Resistance?
Yes, that is the Catch 22. Insulin is the hormone that instructs cells to take up glucose (blood sugar). Increase blood sugar, insulin signaling gets louder, but over time the cells listen less since they don‘t need any more sugar. So we secrete insulin in larger amounts to get the sugar out of the bloodstream. This is insulin resistance, driven by dietary inputs of foods that cause high blood sugar.
Studies, even as recently last month, have identified a mechanisms where statins can play a causal role in this scenario. There are a few different theories, but I will highlight the one involving decreased glucose utilization in the muscle cells.
They have found that muscle cells do not take up as much glucose during statin exposure.34
This is important because our muscle mass is typically a major glucose consumer. Glucose consumption allows good fuel uptake for growth/maintenance of the muscles and helps keep glucose out of the bloodstream. Both good things.
Further, we recognize muscle mass as a predictor of longevity5 – the more muscle, the longer we live. No doubt glucose metabolism is involved.
They have reported exercise capacity as diminished in statin users, as i wrote about here. Yet another factor that points to decreased muscular glucose uptake.
As I wrote about in the whitepaper, Avoiding Insulin in Type 2 Diabetes, insulin increases lipid synthesis. Carbohydrates also increase lipid synthesis in the liver. Sugar then independently changes cholesterol for the worse (see this previous article). Quite a circle of chaos.
With lipid dysfunction caused by dietary inputs, they prescribe statins.
Statins then cause LESS glucose utilization in the muscles, which makes insulin resistance WORSE.
High blood sugar->dyslipidemia->statins->HIGHER blood sugar!
While managing diabetes via the standard of care may seem good, I opt for a more progressive approach. Continuing to along the path of high carbohydrate diets while increasing pharmaceutical interventions to mitigate the consequences is inferior to addressing the causal factor on the dietary input side.
Please reach out for a free consultation if you are interested in exploring a path from the causal angle.
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