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- By Howard E. LeWine, MD, Chief Medical Editor, Harvard Health Publishing
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One side effect of statins that struck me was type 2 diabetes, 2 presumably being associated with weight gain. Now the diagnostic test of diabetes is as good as useless, 1.75 grammes of glucose per Kg of body weight taken at 9 am after a fast from the previous evening and after taking the first blood test, then one EACH HOUR, three all up. Now I’ve done quite a few 5 hr GTT’s and I found that I HAD to do a test each 15 minutes to start off or miss the peak. One woman I tested went from around 6.5 to SIXTEEN then fell to a low of 4 (a 400% fall) in a bit over an hour and had glucose in her urine. Ok, the standard test will detect glucose in urine but that peak is every bit as important as far as arteriosclerosis is concerned because the arteriosclerosis of diabetes is every bit as much about hyperglycaemia as it is about hypercholestertolemia. It called non-enzymatic glycosation of protein, glucose acting like a glue binding to proteins on epithelial cells lining blood vessels and trapping cholesterol in this glue.
Now looking at the metabolic pathways the central molecule is acetyle Co enzyme A or acetyl CoA (vinegar with an enzyme) the CENTRAL molecule of all major metabolic pathways in almost all cells. Ethanol (alcohol) is converted to acetyle Co A (via acetaldehyde), as are ketones from the breakdown of fatty acids. But the liver doesn’t import fatty acids to convert to ketones except with ketosis. However, look up what’s called the glycolytic pathway and you’ll see glucose coming in from one side, Here it can go up to be synthesised to glycogen, the storage form of glucose. Come back down to acetyle CoA and it can enter the TCA or citric acid cycle to make energy in the form of ATP, as well as intermediate molecules in the TCA cycle. But too much acetyle CoA into the TCA cycle and citric acid builds up and it inhibits glycolysis, But what happens if glycogen stores are topped to the brim, made worse by liver pathology limiting storage and no more energy production is needed other than a base level to keep the cell running. There is ONLY one way out, turn acetyle CoA into cholesterol. So the synthesis of excess cholesterol is an emergency BLOOD SUGAR REGULATING MECHANISM that would lower osmotic blood pressure etc. Block it and up goes blood glucose, DIABETES. Neat eh!! According to this irrefutable hypothesis cut back on the carb intake and the blood cholesterol level will come down accordingly so you can flush the statins down the loo where they belong.
What really matters is whether cholesterol is as bad as assumed. That’s right- it is an assumption. We need to see data showing the number of heart attacks and deaths vs LDL, HDL and Total Cholesterol levels. Then we need to see the CRP levels- a measure of inflammation. Then data with and without statins. I predict you will find that those with high CRP (inflammation) have the higher heart attack death rates, not those with high cholesterol levels. And those that take statins that have high CRP have lower death rates. Then there is research showing that statins have an antiinflammatory benefit, which is the true cause of the select benefits in those with increased inflammation, and the amount of statin needed to get most of that benefit is fractional of current dosages, just a few milligrams, with no side effects. But one can get the same benefit by eating more vegetables and less vegetable oil (inflammatory omega 6 oils found in plaques). Data has shown that lowering LDL is not beneficial and increases pneumonias and other deaths. Please be more thorough in your reporting. You are steering people in the wrong direction.
my father passed away when i’m 15 years old. he had problem with his liver. Now, i am very excited information about health for Liver. and i won’t like my father. thanks 😀
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