Does heart disease run in your family?

As I see it

I have often heard people comment about how heart disease runs in their family. I wonder how many of them have heard of Lipoprotein(a)?

Lipoprotein(a) is a particle in our blood which carries cholesterol, fats and proteins. Compared with LDL and HDL, Lipoprotein(a) is a lesser known lipoprotein which is surprising given its role in cardiovascular health.

Having a high level of Lipoprotein(a), is a significant genetic risk factor for heart disease including coronary artery disease, peripheral vascular disease, aortic stenosis, thrombosis, and stroke.

Unlike LDL or HDL levels which can be influenced by diet and exercise and even reduced by medications, the amount of Lipoprotein(a) that we can make in the body is determined by genes that are passed on from our parents when we are born. It doesn’t change significantly as we age except for women when levels increase as the natural estrogen level declines with menopause. It’s interesting to note that diet and exercise have little impact on Lipoprotein(a) levels and currently there are no medications available in New Zealand, specifically aimed at reducing Lipoprotein(a) levels. This could be why there is very little said about this potentially very harmful molecule.

Given what is known about Lipoprotein(a), it’s surprising that the population at large is not offered a simple blood test to determine an individual’s level. The normal level for Lipoprotein(a) is less than 300 mg/L but in New Zealand it’s estimated that 20% of our population will have a level greater than 500 mg/L. If your doctor is unable to offer a blood test for Lipoprotein(a) it is possible to pay for this at any Labtests clinic. I understand that the cost is approx $44.00

It’s really interesting that Lipoprotein(a) is found primarily in humans and animals that do not make their own vitamin C. Dr Mathias Rath, a German doctor and researcher, together with double Nobel Laureate Dr Linus Pauling, developed a hypothesis connecting two evolutionary events. The first was the emergence of the apo(a) gene around 40 million years ago. Dr Rath and Dr Pauling say that this coincided with the ancestor of man losing the ability to make vitamin C due to the mutation of one of four genes responsible for the endogenous (in the body) production of vitamin C. Humans, guinea pigs, fruit bats and primates are not able to make their own vitamin C.

Dr Rath and Dr Pauling went on to further hypothesise that Lipoprotein(a) functions as a surrogate for vitamin C. They said that Lipoprotein(a) levels may be increased in some cases due to a vitamin C deficiency. They also noted that the Lipoprotein(a) and vitamin C possess some similar properties, such as in the acceleration of wound healing and other cell-repair mechanisms. Based on this, Drs Pauling and Rath suggested that humans intentionally synthesise Lipoprotein(a) when they are lacking adequate vitamin C.

Dr Rath says that Lipoprotein(a) is a very ‘sticky molecule similar to LDL but with an additional adhesive protein (apoprotein(a)) surrounding it. This, he says, makes it one of the stickiest particles in our body. He notes that Hamburg University studies conducted on atherosclerotic lesions in human arteries showed that they are largely composed of Lipoprotein(a) rather than LDL molecules.

Is there anything one can do to lessen the potential impact of Lipoprotein(a)? According to Drs Rath and Pauling, because Lipoprotein(a) is believed to bind to artery walls via Lysine binding sites, supplementing with two simple amino acids, L-Lysine and L-Proline, may put what they describe as a ‘teflon’ coating on the Lipoprotein(a) molecule thus reducing its stickiness. If New Zealand researchers were able to verify this, it would be great news for all of us.

John Appleton –

Ph: 09-489-9362