High Lp(a) level, .. more difficult to break down blood clots
L-Carnitine can reduce Lp(a)
https://drmalcolmkendrick.org/2017/01/16/what-causes-heart-disease-part-xxiv/
---------------------------------------------------------------------------------
On the positive side, after sixty-one million years, or so, evolution came up with a partial solution to the early stages of scurvy. Namely, the synthesis of a substance to block the cracks in the blood vessel walls, and control the bleeding. This substance is, or course, lipoprotein (a).
Lipoprotein (a) (Lp(a)) is synthesized in the liver, and it travels around in the bloodstream, looking for any cracks in blood vessels walls a.k.a. damaged endothelium. When a crack is spotted Lp(a) is attracted to the area and sticks very firmly, and cannot easily be removed. Of course, the rest of the blood clotting system also moves into action, so all hell breaks loose. Therefore Lp(a) becomes mixed up with platelets, red blood cells, fibrin, and almost everything else in the blood, including all the other lipoproteins.
However, Lp(a) has a very special trick up its sleeve. It mimics plasminogen.
After a blood clot forms, anywhere in the circulation, it has to be broken down, and removed – once the blood vessel underneath it has repaired. I liken this (not very accurately) to road works. If the road surface is damaged, the repair team comes in, sets up barriers and traffic lights and suchlike, then they repair the road. Then all the barriers, and traffic lights, and suchlike, must be removed.
....
Which means that if you have a high Lp(a) level, you will develop bigger and more difficult to break down blood clots. Exactly what evolution had in mind for creatures that cannot manufacture vitamin C, and need to plug cracks in artery walls when the vitamin C level falls. However, not so good, if you want to stop atherosclerosis from developing.
Because these Lp(a) rich blood clots have to go somewhere, and the only place that they can go is to be absorbed into the artery wall itself, and then broken down. However, these clots are more difficult to break down, so, with repeated clots over the same area of artery wall, bigger and bigger plaques will grow.
...
However, there is one way to definitely reduce Lp(a) levels, and that is to take l-carnitine. Here, from a study called ‘
L-carnitine reduces plasma lipoprotein(a) levels in patients with hyper Lp(a)’
‘L-carnitine, a natural compound stimulating fatty acid oxidation at the mitochondrial level, was tested in a double blind study in 36 subjects with Lp(a) levels ranging between 40-80 mg/dL, in most with concomitant LDL cholesterol and triglyceride elevations. L-carnitine (2 g/day) significantly reduced Lp(a) levels… the reduction being more dramatic in the subjects with the more marked elevations. In particular, in the L-carnitine group, 14 out of 18 subjects (77.8%) had a significant reduction of Lp(a) vs only 7 out of 18 (38.9%) in the placebo group. In a significant number of subjects the reduction of Lp(a) resulted in a return of this major cardiovascular risk parameter to the normal range.’ 4
Does this then result in a reduction in CVD risk? The answer is that I do not know, for sure. A meta-analysis of L-carnitine supplementation has been done. This consisted of five trials on three thousand people. L-carnitine supplementation did show some benefit – which did not reach statistical significance, but came very, very close.
For those of you who like a bit of statistics, here we go
‘The interaction test yielded no significant differences between the effects of the four daily oral maintenance dosages of L-carnitine (i.e., 2 g, 3 g, 4 g, and 6 g) on all-cause mortality (risk ratio [RR] = 0.77, 95% CI [0.57-1.03], P = 0.08)’5
CI [0.57 to 1.03] – close, but no cigar.
To put this into figures anyone can understand. In the intervention groups (those taking L-carnitine) there were 83 deaths. In the control group (those not taking L-carnitine) there were 106 deaths. Total study population was 3108, split in two groups: control and intervention. This gets as close to statistical significance as you can get (virtually). In fact, if this had been a statin trial, you would never have heard the end of it. ‘
Ladies and gentlemen a 22% reduction in overall mortality with L-carnitine supplementation.’ [Oh, what fun statistics are].
...
What would I now recommend? If you have a high Lp(a) level take lots of vitamin C and l-carnitine and see if your Lp(a) level falls. If it does, keep taking lots of vitamin C and l-carnitine for the rest of your life. If it does not fall? Not sure.
----------------------------------------------------------------------------------