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The Truth About Cholesterol

Cholesterol and cardiovascular disease

Cholesterol has been given so much attention by the medical profession over the last 40+ years that the word 'cholesterol' is automatically (and wrongly) equated with cardiovascular disease because it is often found deposited, along with fats, fibrin, and calcium in the inner lining of arteries where it narrows them. 

There are several theories about the theory of cardiovascular disease. A Unifying theory has been proposed by Drs. Rath and Pauling - Dr Pauling is the winner of 2 nobel prizes. Their theory suggests that thickening arteries and cardiovascular disease revolve primarily around the lack of vitamin C.

Vitamin C is necessary for the production of collagen and elastin, which keep our arteries, bones, teeth, cartilage, and other tissues strong. Lack of vitamin C results in weakened arteries and bleeding into the tissue spaces. 

Under survival pressure, according to Rath and Pauling, nature developed and selected for survival a way to protect us from early death due to weakened artery walls. This was to thicken our arteries using an adhesive repair protein called apoB made in our liver that is then attached to the VLDL particle. The VLDL transport protein contains cholesterol and triglicerides amongst other things which are delivered to different cells in the body. During this delivery the VLDL carrier is converted to ILDL, then to LDL and then to  a much smaller Lp(a) carrier.


The Lp(a) carrier ie lipoprotein(a) and it's ApoB protein is used to affect the repair to any damaged endothielium cells of the vascular system. High Lp(a) carrier proteins and the ApoB protein it is carrying is therefore a strong risk factor for cardiovascular disease whereas LDL is a weaker risk factor. HDL is the vehicle for collecting unused cholesterol and returning it back to the liver for re-cycling. 

Cholesterol particles travelling in the blood stream over time can become oxidized if exposed to free radicals or any other oxidants.  Oxidized cholesterol and certain long-chain fatty-acids found travelling in the blood play a part in making platelets more sticky, which makes narrowing of arteries and clotting more likely.

Rath and Pauling suggest that in killing us by apoB induced artery thickening, nature infers on us a survival advantage. For survival of the species, it is better to die from a heart attack after we have reproduced, than to die from weakened arteries before we have had a chance to reproduce.

Reversing the damage. 

When vitamin C ascorbate levels in our blood increases, this keeps the connective tissue in our arteries strong. ApoB levels then decrease because less repair protein is necessary. Low levels of antioxidants (vitamin C) lead to poor control of the free radicals that are normally produced in our cardiovascular system. Oxidization is also caused by affects of toxins in our food, drugs, pesticides, and chemicals that we are exposed to from the outside. Free radicals speed oxidation of cholesterol and triglycerides. Free radicals, oxidized cholesterol, and oxidized triglycerides can cause damage to arteries, especially ones that are weakened by deficient vitamin C.

Foods high in Vitamin C are: Kale, broccoli, brussels sprouts, lemons, strawberries, oranges, etc.

Exerpt from 'Fats that Heal, Fats that Kill' by Udo Erasmus.

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