Sunday, April 15, 2018

LDLp is how cholesterol is transported to cell through normal endothelial walls




In the book Eat Rich Live Long the authors Ivor Cummings and Jeffrey Gerber write on pgs 352 & 353,  "so higher number of these (LDLp) would cause more damage to the arteries.  But the evidence suggests that this only happens in cases where the artery wall is already damaged.   LDLp -the count of LDL  particles- especially may have little or no relevance if there is no arterial damage or inflammation present. If your system is already fireproofed, then extra boats ferrying around will not have any impact."


The authors don't reflect on concentration gradient.  

I keep my LDLp less than 750 with atorvastatin 10 mg and endur-acin(OTC niacin) 1,000 mg.

Many people with LDLc less than 200 will have LDLp of 1500. 

The over abundance of particles in the blood by concentration gradient pushes the particles through the artery wall in higher number. 

This is simple biology/chemistry.  






"Attention was first drawn to the early origin of atherosclerosis :
1-by an autopsy study conducted on young soldiers killed in the Korean War.
Their average age was 22 years, and over 70% of them had evidence of atherosclerosis in their coronary arteries.
2- Postmortem coronary angiography and dissection of hearts from 105 United States soldiers killed in Vietnam demonstrated that 45% had some evidence of atherosclerosis and 5% had gross evidence of severe coronary atherosclerosis. 
3-Another study demonstrated a very high incidence of lipid-laden macrophages in the intima of the aorta and coronary arteries of young American children killed in motor accidents, with over 50% of children aged 10-14 years having some evidence of early atherosclerosis.
4-A nation-wide autopsy-based study of atherosclerosis in young Japanese (1 month-39 years) disclosed the presence of fatty streaks in 29% of aortas in those aged less than 1 year and in 3.1% of coronary arteries of children aged 1-9 years. 
5-Another examination 13 years later revealed an increased prevalence and extent of coronary artery lesions in autopsied subjects who died in their third and fourth decade of life.
6- In the Bogalusa Heart Study, the extent of fatty streaks and fibrous plaques in the aorta and coronary arteries were examined in 204 young patients 2-39-years-of-age. The prevalence of fatty streaks in the coronary arteries increased with age from approximately 50% at 2-15-years-of-age to 85% at 21-39-years-of-age, and the prevalence of raised fibrous-plaque lesions increased with age from 8% at 2-15-years-of-age to 69% at 26-39-years-of-age. 
The prevalence and the extent of atherosclerosis was greater with increasing age, body mass index (BMI), blood pressure, and levels of serum total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C). 


                                                 



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