Title: Cardiovascular Disease & Lipoprotein A

Key words: lipoproteins, fibrinogen, apoprotein, Vitamin C, deficiency

Date: July 2000

Category: 13. Specific Conditions

Type: Article

Author: Dr M Draper

 

Cardiovascular Disease & Lipoprotein A

Evolutionary Rationale and Role

Introduction

Lipoprotein A {Lp(a)} is a unique lipoprotein particle composed of an LDL particle onto which a high-molecular-weight glycoprotein termed apo (a) is linked via a disulphide bridge. High concentrations of Lp(a) have been associated with an increased risk of cardiovascular disease, possible because of the homology of apo (a) with plasminogen. Concentrations of Lp(a) are highly heritable and less affected by environmental factors than are other lipoproteins.

We may have developed the ability to deposit lipoproteins (fat-protein complexes) along the artery wall in order to increase our chances of surviving during vitamin C-deficient times. Two groups of proteins that normally accumulate at injury sites to carry out repairs are fibrinogen and apoprotein. Apoproteins have a natural affinity with fat (lipids) and become lipoprotein A (LpA), which can repair damaged or leaky blood vessels. However, it also increases the risk of heart disease by building up deposits on the artery wall. In fact, of all the factors that can be measured, a person's level of lipoprotein A is the best indicator of risk.

Genetic research is now strongly suggesting that the development of lipoprotein A was most likely a genetic response to a species threatened with extinction through leaky blood vessels. Could this have been nature's way of dealing with life-threatening scurvy? The estimated dates for the development of lipoprotein A in monkeys correlate with the period in which primates are thought to have lost the ability to produce vitamin C.

How well does the theory of vitamin C deficiency as a root cause for cardiovascular disease fit with the facts? Vitamin C deficiency raises cholesterol, triglycerides (fats if the blood), bad LDLs, apoprotein and lipoprotein A , and lowers the beneficial HDLs. Conversely, increasing vitamin C intake lowers a high-cholesterol, triglyceride, LDL or LpA level and raises HDLs.

The significance of all these beneficial effects for our ancestors could have been that, during the summer when they could take in enough vitamin C, the increased HDL production would remove excess cholesterol. Vitamin C also inhibits excessive cholesterol production and helps convert cholesterol to bile. All this would lead to a decrease in unnecessary atherosclerotic deposits.

In one study it was shown that a daily 500mg of vitamin C can lead to a reduction in atherosclerotic deposits within two to six months. This concept also explains why heart attacks and strokes occur today with a much higher frequency in winter than during spring and summer, the seasons with increased ascorbate intake.