Cholesterol- Friend or Foe?
Saturday, September 1, 2012 at 8:40AM Answer: You would not survive very long without the functions cholesterol performs. Found in every cell in the body, cholesterol manufactures Hormones, fights infections, aids fat digestion and absorption of fat soluble vitamins A, D, E, & K, produces Vitamin D from sunshine, maintains cell membrane integrity especially for water balance and nutrient transport (by this function cholesterol is linked to every cell function needing outside nutrients to enter cells), plus cholesterol helps prevent virus attachment onto cell membranes. Perhaps one of the most vital functions getting attention right now is that cholesterol supports learning and memory with important roles in the health of nerve tissues.
The Cholesterol story is one that could sustain a season of weekly TV shows and remain entertaining until the end. Cholesterol testing in Rabbits alone would provide more entertainment than many CSI episodes. Scientists create artery disease in rabbits by feeding massive cholesterol amounts, but did not find that this always resulted in heart attacks. Rabbits never suffer from heart attacks on their normal diet. A very revealing fact might support this observation. Rabbits make their own vitamin C. Vitamin C builds collagen. ref Collagen maintains artery wall membrane strength. Artery membranes separate cholesterol build up in artery walls from blood flow inside arteries. In humans this artery membrane tears open and pieces of the cholesterol laden plaque break off and float downstream until getting stuck when vessels narrow leading to a heart attack. This tearing of membranes did not happen in rabbits.
Here is an interesting observation. Humans with higher cholesterol levels tend to have more heart disease while humans that measure low cholesterol tend to get more infectious diseases and cancers. ref ref
CHECK OUT THE GRAPH ON THIS WEBSITE. IT IS A THINK-TWICE WORLD PLOT OF MORTALITY TO CHOLESTEROL LEVELS. Sure looks like a target cholesterol level of about 210 (range 200-240) might be the safest amount from the lowest mortality point of view. Interestingly, it is exactly the same as the Korean men's study found. BUT, quite a bit more than the 160 advocated by USA health officials.
This means at 160 total cholesterol there might be less heart disease, BUT almost a 2.5 times higher overall death rate. While this is just an association, there are far too many other factors and studies not to see a trend. Seems like a very easy choice to pick life and a cholesterol level just over 200 (making sure HDL is 50-60), and then deal with lifestyle choices to reduce heart disease risk.
Statins, vascular calcification, and vitamin K-dependent proteins: Is there a relation?
- PMID: 33634559
- DOI: 10.1002/kjm2.12373
Abstract
The present cross-sectional clinical study aimed to examine the connection between statin exposure, coronary artery calcification (CAC), and vitamin K-dependent proteins (VKDPs) in patients with cardiovascular (CV) conditions. Two groups of patients were studied: patients with established CV disease (CVD) and healthy patients at moderate risk for CVD (a control group). The groups were also split into statin users and non-users. The following VKDPs were measured in plasma: uncarboxylated Matrix Gla-protein (ucMGP), undercarboxylated (ucOC), and carboxylated osteocalcin (cOC), Gla-rich protein (GRP). CAC score (CACS) was determined by multislice computed tomography. Among all the participants in the study, CACS was more pronounced in statin users compared to non-users; the same was found also among the CVD patients and among the controls. While the levels of ucMGP and GRP did not differ between statin users and non-users, ucOC and ucOC/cOC were significantly elevated in statin users, indicating vitamin K deficiency. There was a positive correlation between the levels of ucOC and CACS in the entire population and in the group of statin users, but not in statin non-users. No association was found between ucMGP or GRP and CACS. Statins had also an impact on the international normalized ratio and interacted with vitamin K antagonists (VKAs). Our results are in agreement with the existing evidence about positive association between statins and vascular calcification. They enlighten to a certain extent the possible mechanisms through which statins may enhance calcium accumulation in arterial wall, namely, by inhibition of vitamin K dependent proteins and functions involved in vascular protection.
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