Fascinating discussion, and I'll add that book to my list. Sorry, article...
@Melgar - For comparison, my triglyceride levels were 1.5mmol/L at the end of Feb; I would say that with roughly half that, you probably just don't need to look at any other lipid level.. you have almost no visceral fat, period.
I should mention that I'm only a 'convert' to the Malcolm Kendrick view of Cholesterol - I have zero actual medical knowledge; but I would thoroughly recommend reading any of his books - there is a lot of detail on all the data and science behind the connection between diet, cholesterol and heart disease, but any level of poking around will start to make you question some of the things we 'know' - and I would think, should make you far more relaxed about your levels of LDL..
Fundamentally, our thinking today is still an evolution of the interpretation of what doctors first saw under a microscope when they were investigating what was rapidly being described as heart disease - stuff that looked fatty and tested for cholesterol - therefore:
We need to eat less cholesterol, because then there will be less cholesterol in our blood, therefore, less to clog up our arteries and give us heart disease.
This led directly to the guidelines shifting to - eat less fat and more carbs. I mean literally - you can look up the guidelines in 1977 - there is a lot of detail, but fundamentally this led to the idea that we should eat less fat and more carbs.
However, the essential theory is full of holes, and even the original, when written out like I've done, doesn't hold water any more... so a more modern interpretation is now;
We need to eat less saturated fat, because there is a connection between saturated fats and cholesterol, so that we have less cholesterol in the form of 'bad' cholesterol, ie, LDL which can become oxidised, thus finding its way past the endothelium and getting stuck in the artery walls, causing plaque and thus heart disease.
However - all of that is
still full of holes...
The most obvious thing is that even way back when, there was significant argument about what the composition of arterial plaque actually is, and how it forms - it's horrendously complicated, and there are whole sections of medical science that just were not understood at the time, but there was definitely a counter argument that all plaques were essentially blood clots, and we should be looking at what was causing the blood clots in the arterial walls in the first place, not focussing on one of the ingredients (which turns out to be virtually identical to LDL but totally different in function, and utterly indistinguishable in the day)
It really makes as much sense as, - most of the composition of arterial plaque seems to be red blood cells, so we should eat less food which has red blood cells in it...
Anyway - the next problem with the dietary approach we all 'know' is that you need much more cholesterol to survive than you can possibly eat, and the liver produces most of it. If you eat less food high in cholesterol, your liver simply produces more.... You simply cannot control your level of cholesterol by just changing diet - (in your case, where you are clearly generally fit and eating well)
The next problem is that - the dietary fats we eat - whether saturated, mono saturated, Omega-3, poly unsaturated - whatever, are all packaged up indiscriminately as triglycerides in the intestine (despite what you might think, your body doesn't really care, the 'tri' refers to three fatty acid chains, and they are made up of any combination at hand) and transported around, dropping off the triglycerides as they go. But these have nothing to do with LDL - LDL, or low density lipids, start off life as very low density lipids, because they are stuffed with triglycerides, and carry them, along with a cholesterol molecule. Critically - all the triglicerides in these VLDLs are saturated, because they are all created by the liver - from carbs.
So - there is not, nor can be - any link between dietary fat and LDL. Diary - maybe, but only because of the level of carbs.. eating more carbs as a way of reducing LDL, though - well, that just cannot help.
Back to the Very low-density Lipid - or transport for Triglyceride - when they have done their job of distributing triglycerides, they are like deflated balloons, with only the cholesterol left - this obviously raises the density and is now known as .... an LDL.
The main distinguishing feature of an LDL is that when you take statins, they go down in number. Otherwise, the amount of LDL in your body is totally a function of your liver, and the amount of LDL receptors in your endothelium - the layer of cells that lines your arteries and veins - and which need cholesterol.
The other main feature of LDLs is that when an endothelial cell expresses an LDL receptor, it then (and only then) enters the cell, drops off its precious cholesterol, and is consumed in the process. There is no mechanism which would explain how an LDL can somehow get past the endothelial layer and 'get stuck' in the arterial wall... just none. It was best described as 'sticking a harpoon in the side of a whale, and then going around to the other side of the whale, and expecting the harpoon to come out' - just cannot happen.
That's just the tip of the iceberg. Get into what the Glycocalyx is, read about the work of Ancel Keyes, before and after he testified to congress, the study that Pfizer nearly published that talked about blood clots, just before they bought the company that developed Atorvastatin, Note that the phraseology around 'bad' cholesterol and 'good' cholesterol (neither of which are really cholesterol, but still emotionally connect to the 'eat less cholesterol' theory) just popped into existence at the same time as statins, which are very good at reducing 'bad' cholesterol... but not really anything else - save making a ton of money..
But, what do I know...
