I have mentioned before that pretty much all my ratios and markers are good eg Total to HDL ratio, ApoB/Apo A ratio, Lp(a), Homocysteine. One marker that I have found on two occasions to be too high is Lp-PLA2. This is a marker that is believed to signify unstable plaque within the arteries. So far I have not managed to lower it. I have however just got the results back for another test that looks at oxidative stress and a predictor of unstable plaque, namely Myeloperoxidase. I was kind of expecting this one might come back on the high side given that it appears to be a close cousin of Lp-PLA2 or at least testing a similar condition. I was very happy therefore to find that my reading was super low. Greater than 5 IU/ml is considered positive but I came back at less than 0.01.
The test was done with Blue Horizon and cost around £95. I will retest Lp_PLA2 later in the year and if it has not diminished perhaps try a spell on aspirin and see if that puts a dent in it or perhaps take solace from this test, surely they can’t both be right.
Good explanation here of the difference between Myeloperoxidase and Lp-PLA2
It would appear that the obvious approach to lowering Lp-PLA2 would be Niacin (Vit B3)
A couple of posts ago I mentioned Leptin resistance and its role in causing problems for getting LDL particles out of the blood stream when they have done their job of delivering cholesterol to cells. Iodine deficiency is one of the possible reasons for this problem with the Thyroid and Leptin resistance and it ties in nicely with a at least a couple of population studies.
The Japanese have very low rates of heart disease, even lower before they started to discover westernised food. We are usually quick to credit this to their consumption of fish but it may not only be this sole source of sea food. The Japanese consume large quantities of sea weed using it as an additive in stews and soups such as Miso soup. Sea weed is a very rich source of Iodine and perhaps their super rich Iodine content diet is a big factor in their heart protection.
Backing this up was a studies in the 1950’s in Finland which had very contrasting levels of heart disease were although both east and west were poor the east was far unhealthier when it came to cardio vascular health. This prompted an in depth study of the dietary habits of east and west and the most significant disparity was that the west consumed significantly more Iodine which may be why they have less heart disease than the East. More on this at the link below.
Needless to say I now take a 200mcg Iodine supplement daily via a Sea Kelp tablet and so far my stomach seems to tolerate these quiet well with no irritation.
Given the current guidelines for getting your LDL as low as possible to reduce heart disease risk you would naturally expect that when patients are wheeled into hospitals for Coronary Heart Disease ailments such as heart attacks or angina attacks, their LDL levels would on average be rather high. If we looked at a thousand such patients what percentage would you expect to have LDL levels above 2.6 mmol ?. Maybe 60% or perhaps 70%, surely it has got to be above 50% given that we are advised to get our levels below 3 mmol. Well according to a large study done on nearly 137,000 hospitalisations in America for CAD symptoms it was only 50.4%. Taking only those who were admitted for the first time for CAD symptoms did not really change the underlying message that much.
The other interesting thing is that when you talk to cholesterol advocates about the stats showing that low cholesterol means greater all risk of dying ie from all causes, they tend to shout reverse causation. What they mean by this is that disease, including heart attacks, tend to lower cholesterol levels thus giving a false low impression of cholesterol levels on death. Would this really skew the results shown in the study to the degree shown ? and if it did move the spread you would still have less people in the higher ranges of LDL than the lower ranges maintaining the underlying message in the study that more people are coming in with ‘low’ LDL than ‘high’. The real culprits within the data seem to be low HDL and high Trig’s.
Try this: the LDL particle is a cargo ship. It is supposed to land at various docks to deliver over the goods. However, it is also supposed to protect the goods so that they are in good shape when the ship gets to the dock. However, there are often pirates at sea, and they may attack both the people at shore as well as the cargo ships. If they block entry to the dock, the ship cannot refuel or purchase more ammunition for defense. If the ship is thus left at sea, it runs out of ammunition and the pirates are then able to effectively sabotage it, ruin its goods, and purposefully plant explosives and release infectious diseases on the boat. Then, when it does get near shoreline, the folks at the dock catch illnesses and are caught in terrorist explosions. Thus, the immune system, like a navy and national guard, rescues the cargo ships that have been attacked (oxidized LDL), and quarantines them and any toxic factors released from them in something like a superfund site, where the surrounding community is protected as best as possible.
The above is quoted from Chris Masterjohn, an expert on lipids and someone who does not appear to be selling anything. I like guys who are not flogging me supplements or Statins and clearly have something interesting to say.
The above is taken from an interview he did with Chris Kresser. What he is saying in the above is that landing at docks simply means delivering cholesterol to the various cells that need it and also being taken eventually and promptly out of the blood stream by the liver. The ammunition and defence taken on board are antioxidants needed to fight off oxidisation of the LDL membrane which has a polyunsaturated element to it. The LDL is capable of fighting off this oxidisation for a while but if it stays in the blood stream too long this ability breaks down and then oxidised LDL, the main cause of heart disease via plaque build up (quarantine), prevails.
This prolonged stay in the blood stream of LDL happens when we have a deficient LDL receptor activity and one of the main promotors of this is leptin resistance. Notice we have not mentioned Cholesterol at all. He makes a fascinating point when he cites the guy (name escapes me) who probably got the whole ball rolling on cholesterol back in the 1920’s when he performed experiments on rabbits. He induced plaque build up very similar to that found in humans by feeding them a high cholesterol diet. This experiment has been much criticised as irrelevant to humans as rabbits do not normally consume cholesterol and are therefore bound to have ill effects. However what he also found was that when you injected cholesterol into the rabbits nothing happened. The processing of cholesterol into LDL particles was required to induce plaque build up hence the clue that the LDL particle is the main problem not the cargo on board.
If all this Somalian pirate talk sounds pretty confusing then simply get the DVD out with Tom Hanks in the lead role. Eat some sea weed (iodine) and Brazil Nuts (selenium) whilst watching the film, your Leptin will thank you.