This is Watkins, one of the senior authors of this paper on Lp(a) and heart disease:
"This is the most convincing evidence so far that this protein [Lp(a)] is directly part of the pathway that causes heart disease rather than a bystander. If we can target it through treatment, we might expect to lower the risk of disease," coauthor Dr Hugh Watkins (University of Oxford) told heartwire.
OK, we have known for quite a long time that Lp(a) is associated with heart disease. We also know that genetics has a big influence on the level of Lp(a) in the bloodstream. The basic rule is that if you have a small number of kringle IV repeats from your apo(a) genes you will have a large amount of Lp(a) in your blood stream. All of this is old news.
How many repeats of kringle IV you have is a genetic trait. The people at Oxford have used a very sophisticated search technique to locate a couple of changes, each involving a single base pair, in the region of the DNA which makes up the chromosome area coding for apo(a). Either of them affects the number of kringle IV repeats you have in your apo(a). Hence the amount of Lp(a) in your blood.
Finding two single point DNA variations which influence kringle IV repeats is a huge achievement. We now have a piece of genetic mechanism information. What puzzles me is how this is any different from simply counting the number of kringle IV repeats in apo(a) extracted from an ordinary blood sample, which we have been doing for years, without knowing exactly which change in the DNA affected the count.
What is assumed in this paper and the inferences drawn from it is that Lp(a) is intrinsically bad and that genes are the sole control of the level of Lp(a).
Both assumptions are probably wrong. We have to back to Tanzania to see what might actually influence Lp(a) in people with identical apo(a) kringle IV repeats. Hint, its not atrovastatin or ezetimbe.
But one thing came out of the abstract which is actually quite interesting. There is an association between these gene changes, "a small Lp(a) lipoprotein size" and heart disease.
I'm just wondering if a small Lp(a) particle is also a dense Lp(a) particle..........
Back to the Bantu next.