Article on LDL Modification - by yours truly


(Siobhan) #1

Hello again, all :slight_smile:
I posted originally when I published part one of the series I’m writing for @DaveKeto’s blog cholesterolcode.com
That one was about the development of foam cells, all the way to plaque blockage or rupture. I mentioned in that one that scavenger receptors only take in modified LDL (not native/healthy) and as a result had quite a few people ask “well, then, what modifies LDL?”
As a result I wrote up part two which goes over exactly that. Not only what can cause the oxidation, but also what results in LDL being more vulnerable to that oxidation.
I also showed up on the 2ketodudes podcast to discuss lipids and clearance pathways as well :smile:
I hope you all enjoy, and if anyone has any corrections feel free to @ me
Thank you!!!


(Mark Rhodes) #2

I understand that it is not the same thing and the issues you are referring to are usually compounded over a length of decades but this point in your article

"Meaning that C. Pneumonia and Cytomegalovirus appears to contribute directly, through the aforementioned mechanisms, as well as peripherally " made me think of Tom. Is this what Tom was talking about in Scary Heart stories podcast recently? He got pneumonia and then very quickly got a racing pulse?

“…increase oxidative stress and LDL modification including high intake of Polyunsaturated Fatty Acid (PUFA) such as those found in seed oils,as well as high refined carbohydrate intake” The same heart healthy oils found in the SAD.

@siobhan , your research into this field are just amazing.


(Siobhan) #3

I’m sure @TomSeest could speak on this better than I could, but I don’t think foam cell formation (as a result of fighting the infection) is likely what caused his A-fib. As he mentioned in the podcast, his heart actually (used to) have scarring on it, so I suspect what happened is that the virus or bacteria (depending on type) actually infected his heart and damaged the muscle there.
This is talked about in this article.

However, respiratory infection can increase your chances of having a heart attack. There was a study done on exactly that which you can read here - and an article if you don’t feel like sitting down with a bona fide study on it.
Basically, they say that “something” about the respiratory infection destabilizes already-present plaque leading to a heart attack. I suspect that this “something” is actually the result of more stress on clearance pathways (LDL’s role in immune defense -> becomes damaged -> must be pulled out of the system and leads to foam cell formation; OR direct capture of bacteria/etc by scavenger receptors leading to the same stress on the system).

There’s also this study which found that people who came to the hospital with pneumonia, in particular, were at an increased risk for heart disease down the line. They mention that pneumonia increases pro-inflammatory cytokines, inflammation, etc

So let’s say you eat a very atherosclerosis-promoting diet (high sugar, refined carb, and omega 6 vegetable oils let’s also throw some stress, lack of sleep, and smoking in there too just from the examples I gave in the article). This is putting your body on high alert - constantly. There is no rest up and clear up debris (oxysterol, efflux from foam cells, repair, etc) period.

Then: add in an infection to that. Yet more is piled on due to fighting the infection (directly or indirectly). If you continue with the never-ending onslaught on your clearance system then this would obviously speed you even closer towards your body’s breaking point. As you said, however, these things almost certainly take decades, so even though it may further progression of the disease I’m not sure it could cause it in itself, alone, with no other contributing factors. I could be wrong though.

I make sure to say that infection, etc, if chronic or acute enough could lead to damage. That’s because I’m not 100% sure that you can’t have someone with 100% plaque/foam cell free arteries go to heart attack from just an infection. You would probably have to look at kids to really determine that (or very healthy adults). We can see, however, that infection leads to intimal (endothelial/arterial wall) thickening in children, and over thickening of the intimal layer is one of the first symptoms of developing heart disease (though how it fits in to the whole picture, I’m not sure yet).

The very same. I’ll let that statement stand on its own. But I will say that once you start viewing as saturated and mono vs polyunsaturated fats/oils as, at its most basic level “stable fats vs unstable fats” or “stable fats vs easily oxidized fats” you start to see seed oils in a very different light.
I think the evidence for these things at the very least not being helpful is pretty strong at this point.


(Mandi) #4

Another excellent article/post Siobhan. Well done!


(zee) #5

so i cook in olive oil all my low carb meals. So does olive oil considered oxidized fats?


(Siobhan) #6

Olive oil is mostly monounsaturated fat so should be fine as long as it isn’t extra virgin olive oil (this kind shouldn’t be heated) and not cooked at very high temps. If you’re worried use a more stable fat like coconut oil. There are lists of stable cooking oils on places like Diet Doctor etc too if looking for more options.