Myeloperoxidase Test

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)


Iodine Deficiency

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.

Lipid Levels on Hospitalization for CAD

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.

LDL Receptor Activity

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.

India South & North

India has far greater incidence of heart disease in the north than in the south and yet looking at the lipid levels of the two populations seems to show that LDL may not be the culprit. Average levels of LDL for 40 to 50 year olds stood at 3.05 mmol in both regions. Not outrageously high by most standards. HDL however in the south averaged at 1.6 mmol whilst in the north it averages at a miserable 0.8 mmol. Triglycerides are also high in the north at 1.8. There is no data for the south generally but in Gujarat it stands at 1.2.

This seems to add weight to the hypothesis that HDL and Triglycerides are more important than LDL cholesterol in connection with heart disease. Drug companies have not surprisingly focused on LDL as it is more easily manipulated by chemical means.

You can take a look at the data here

More Vitamin C

I have posted before about the Linus Pauling Vitamin C hypothesis to curing heart disease. The idea that heart disease is really a form of arterial scurvy and that as one of a handful of species that cannot produce its own vitamin C we are more vulnerable than those that can. In fact species that produce their own Vitamin C do not seem to get heart disease.

here are some supporting figures taken from a large scottish study and published in the British Medical Journal

Ascorbic acid intake (mg/day)
14.9 34.7 44.2 54.5 70.2 116.1 50 10.9 30.5 42.1 55.2 72.3 118.5 30
All CHD 1 0.87 0.83 0.63 0.52 0.85 (0.80 to 0.91) *** 1 0.59 0.85 0.81 0.56 0.92 (0.82 to 1.02) NS
CHD deaths 1 0.98 1.03 0.86 0.72 0.93 (0.83 to 1.04) NS 1 1.17 2.12 1.61 0.76 0.99 (0.81 to 1.21) NS
All deaths 1 1.09 1.00 0.87 0.85 0.95 (0.88 to 1.02) NS 1 0.98 0.79 1.03 0.72 0.95 (0.86 to 1.04) NS

You can take a look at a neater version here (apologies for messy presentation above)

or the full report where you can click on the last pop table to get the Vit C data at

The figures from left to right show hazard ratios for different levels of intake of Vitamin C among the study subjects. The more Vitamin C taken the lower the hazard for Cardio Vascular Disease and CVD death. The 3 stars *** mean that the data for Vit C is highly statistically significant. There are 3 stars next to Vit C and men and incidence of CVD meaning the less men took the more likely they were to suffer from CVD.

My policy is to take a pink grapefruit with my breakfast every day and a Vit C supplement. Doing this has resulted in my own lowest reading of Lp(a), a well documented risk factor for heart disease.

The confusing aspect of the study is that Total cholesterol levels were also shown to be an increasing hazard as levels increased and were also statistically significant.

Gut Microbiome

Eat lots of veggies, fruits and whole foods. Avoid processed foods, grains and sugar. All seems like good advice but why are veggies better for us. What is the mechanism behind the digestion of these foods that eventually results in better heart health ?.

Dr Rhonda Patrick gives a pretty good explanation here about how a compromised gut microbiome might be the underlying cause of heart disease.

RCT’s and 2005

Reading the book ‘Fat and Cholesterol don’t cause heart attacks’ found here

It becomes clear that 2005 is a pretty important date in the debate about heart disease and in particular Statins. Most doctors will swear that Statins are beneficial in primary and secondary care (meaning you have not had a heart attack and you have had a heart attack). Of the remaining doctors most will swear that they are beneficial in secondary care. Even Doctor Kendrick has raised his hand to this question. A few will be brave enough to doubt that they are of use to anybody. This latter small group may well be correct when we look at the data from a different viewpoint.

In 2005 the regulations regarding randomised control trials, that’s the kind of trials that doctors like to label as ‘gold standard’ and the kind of trials they bring up when trashing epidemiological studies (studying populations without controls in place). It seems that there was plenty to get worried about pre 2005 when it came to the quality of RCT’s, and there’s me thinking that all RCT’s run by big pharma were clean and above board :). The FDA decided that the way trials were run needed tightening up, I cannot quite remember which medical disaster took place that forced their hand but it must have been compelling to get the FDA to squeeze Pharma. The net result is that when you are told that Statins are good for secondary prevention it is invariably based on meta analysis done on numerous studies both pre and post 2005. In some cases its just pre 2005. If on the other hand you focus on just post 2005 when RCT’s presumably became more reliable the benefits of Statins disappear for secondary prevention. The section in the book on this also highlights some of the dodgy practices that go on with trials and big pharma. For example they usually run numerous identical trials in different locations so that they can bin the ones that do not turn out as they would like and simply quote the one that does. This has been tightened up post 2005. There has even been an example where a trial going well for Pharma was pulled early which is quite puzzling, only to find on deeper examination that the incidence of diabetes amongst Statin users was becoming a thorn in the side of Pharma at the time and they probably pulled the study while the results looked OK for the reason that to take it to completion would have meant running the risk of uncovering type II diabetes rates increasing amongst the users of Statins in the trial.

I can strongly recommend the book, its a little more technical in parts than your average book on Cholesterol but do not let that put you off. There are plenty of excellent readable chapters.

Coffee Heart Friendly ?

I am mainly a green tea and hibiscus tea drinker these days but I have to admit I love the taste of coffee. Despite the fact that service in modern coffee bars has reduced to almost handing you a kettle and asking you to make your own I still like an occasional Americano. I am not tempted by the virtual desert menu of alternative coffee’s so that’s a good thing but is coffee heart friendly ?. Latest research says yes and no. It seems that coffee can increase your chance of a heart attack if you are a slow metabolizer of caffeine. If on the other hand you are a swift metabolizer then it is heart protective. Details of this discovery here

The determining factor with regard to the am I fast or slow is the CYP1A2 gene. If the rs762551 variant of this gene happens to be AA then you are a fast metabolizer (coffee is ok for you). If you are AC or the even slower CC then you are a slow metabolizer and should avoid coffee. You can get a breakdown of this gene and a whole host of others at 23andme.

I appear to be AA which means drinking coffee should not increase my heart attack risk but could help with lowering Alzheimers risk which is good news because I have one APOE e3 and one APOE e4 gene which means a higher risk of Alzheimers. This does not mean I am about to start packing the coffee in but its good to know that the occasional cup is probably fine. By the way there is research that shows that coffee increases LDL whilst green tea lowers it. I have found this to be true so if you are not a cholesterol sceptic and want to lower your LDL then perhaps coffee should be avoided.

Latest Tests

Whilst out in Portugal I had my blood tests done at the considerably cheaper rate than is available in the UK. The test came in at 180 euros which at today’s miserable post Brexit rate still comes in at around £165 and a £450 to £500 saving on what they would cost in the UK.
I included a couple of new tests and dropped the test for Vit D levels which in my case seem to be consistently good. In fact I have dropped my Vit D + K2 tablet down to 1,000mg rather than the original 5,000.
The test results were as follows.

Fibrigonen This came in at 290 mg/dl. Fibrigonen produced by the liver can increase Platelet aggregation and blood viscosity making it an increase risk for clotting. My reading was well under the levels shown in trials to increase risk and you really want it to be below 300mg/dl. Maybe my Fruitflow supplement is doing the trick here. There is a good account of Fibrigonen at

Apo A1 135 mg/dl
Apo B 89 mg/dl

The number to look at here is the Apo B to Apo A1 ratio. In other words ApoB divided by Apo A1. In my case its 0.66 which is way below the suggested 0.9 for men. In more than one trial this ratio has been shown to be a better predictor of Cardio disease than LDL counts, HDL counts or even Total Cholesterol to HDL ratio. Many people have pressed for this to be included within the standard lipid panel you get from your GP for this very reason. Of course it would muddy the waters and probably reduce the number of people needing Statins (does anyone need Statin ?), so don’t expect this to happen anytime soon. The Quebec Cardio Study makes a strong case for this ratio, read more about it at×2007000600014&script=sci_arttext&tlng=en

Lp(a) I have covered this on previous blog entries. Considered by many to be a substitute for Vit C and only produced by those species who cannot manufacture their own Vit C like us humans. In my case my Vit C intake seems to be keeping it down at 18.3 mg/dl (ideal is below 30)

MPO (Myeloperoxidase) This newcomer to me is a test of an enzyme made by white blood cells within the artery wall and is a good indicator of inflamation levels and hence vulnerable plaque. That’s vulnerable in the sense that its likely to burst and spill its gunge into your blood stream which with the help of your systems natural defences, will turn into a thrombus. Mine came in way below the reference of less than 3.5 KUA/L at somewhere less than 0.2. Don’t you just wish all these various test currency units were in just one currency like Euro’s?. Thinking about it maybe not Euro’s, perhaps Bitcoins.
A link here for MPO readers
Also some evidence supporting veggies have lower levels of MPO

Homocyteine This one came in slightly higher than the reference range of 0.5 to 1.88 mg/L at 1.93. This was a bit of a surprise as my previous two readings were 1.27 and 1.18. There are two possible explanations for this. First of all for the past 2 or 3 months I have leaning far more in the direction of Vegananism simply because I have cut down on fish a tad. I still eat fish but not as often. The second explanation is that I now take a Vit B12 lozenger instead of the multi vit B with Folate pill that I originally took. Homecysteine is lowered in the blood stream via 3 pathways.

1. Vitamin B6
2. Choline
3. Vitamin B12 and Folate

For Vegans B6 and Choline is not usually a problem but B12 in particular is as the main source is meat. Given that it works in conjunction with Folate it could be that I need at least to have a B12 and Folate supplement or to revert back to the multi Vit B tablet even if it does turn your piss green.

Footnote – 1 week back on the Jarrow B Right supp’s and my Homocystein dropped to 1.74 which suggests that with a few more weeks it will be back at the 1.27 range. I am however going to switch to a B12 and Folate supp’. As I stated earlier I want to avoid Niacin which is in the multi B supp as there is some evidence that Niacin can increase Lp-PLAC2. I will retest in January after a good spell on B12 plus Folate.

Update – It is now January and I can report that on the B12 and Folate from Life Extension my Homocysteine is back down to 1.42 mg/L that’s 10.5 um/ol. Not quite as low as when I was on the Jarrow tab’s originally but I am pretty happy with that.