In What Way Is LDL That Came from PUFA That Has Been Oxidized and Forms Part of Arterial Plaque Harmful?

yerrag

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After all, it has already oxidized. The oxidative stress from it is a thing of the past, or is it?

Will it cause further oxidation and even be a seed that begins another round of lipid peroxidation?

And if not, what harm does it cause to just leave the oxidized LDL alone in a foam cell that is part of the necrotic core in plaque?

The reason I ask is I've always assumed the oxidized LDL to be a source of lipid peroxidation. thinking that as long as it exists, there would continue to be a source of lipid peroxidation, long after a person has stopped taking PUFAs in his diet. Now I'm questioning this assumption so I'm asking this.

Thanks for your reply.
 
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yerrag

yerrag

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I'm going to answer myself on this.

It's probably because the oxidized LDL isn't totally oxidized, so it continues to be a source of lipid peroxidation, which would create oxidative stress and inflammation.

Why there are so many problems doctors cannot fix is because the medical system doesn't ask these questions. When I search, I don't get answers.
 
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yerrag

yerrag

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View: https://paulsaladinomd.libsyn.com/how-high-cholesterol-can-be-healthy-and-low-cholesterol-could-be-harmful-with-dave-feldman


I think you might find this interesting.
I know it's quite a long podcast and you should disregard the fact they are talking about carnivore keto diets .....the most important context is metabolic health .
They discussed quite a bit about oxidised LDL towards the end

Thank you. I caught the discussion on oxidized LDL at around the 1:29:30 mark. So it confirms that people with arteriosclerotic plaque gets to have higher serum levels of markers of lipid peroxidation, and that these levels go higher as one gets older. The implication being that there is more plaque accumulated as one ages for a population where PUFAs in their diet is the norm.

It still does not answer why oxidized LDL in plaque would continue to be a source of lipid peroxidation, but at least I know that it is sage to assume as much.

I posed this question to Ray and I hope he would reply to this.

But for now, I am inclined to think that the term oxidized LDL needs to be more accurately named as partially oxidized LDL.
 

LLight

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I'm not sure it answers your question but could the immune system be the source of the continuing damages?


These sequestered lipoproteins are susceptible to modification by oxidation, enzymatic cleavage, and aggregation [11]. Immune response to these modified lipoproteins drives the pathogenic evolution of the plaque by releasing proinflammatory mediators leading to a chronic inflammatory reaction. Oxidized LDL induces the formation of foam cells and fatty streaks in the vessel wall which is the hallmark of initiation of atherosclerosis [12]. Macrophages from the host immune system try to clean up cholesterol deposits in arteries, but once they are loaded with the unhealthy form of cholesterol, they get stuck in the arteries, triggering the body's inflammatory response.
 
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yerrag

yerrag

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I'm not sure it answers your question but could the immune system be the source of the continuing damages?

I don't see why the immune system should be implicated.

It is a given that the immune acts that way, and that is normal. And the dysfunction is not in the immune system. I would rather ask why the immune system acts that way. And if the oxidized LDL is a source of lipid peroxidation, and the immune system is merely doing what it's supposed to do and causing the inflammatory response due to the oxidative stress, then I'm going to give the immune system a pass, and train my sights on the culprit, which is the oxidized LDL.
 

LLight

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I guess it's not the final explanation of heart disease but a part of the mechanism.

For example, when they say:
Macrophages from the host immune system try to clean up cholesterol deposits in arteries, but once they are loaded with the unhealthy form of cholesterol, they get stuck in the arteries, triggering the body's inflammatory response.
we can wonder why macrophages get stuck in the arteries if their goal is to remove cholesterol deposits. The reason why would be another cause of the issue.
 
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yerrag

yerrag

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I guess it's not the final explanation of heart disease but a part of the mechanism.

For example, when they say:

we can wonder why macrophages get stuck in the arteries if their goal is to remove cholesterol deposits. The reason why would be another cause of the issue.
the macrophages that try to remove the oxidized ldl fail and they turn into foam cells that contain the oxidized ldl, and they accumulate as the necrotic core that forms the plaque (in the media layer of the blood vessel) grows and this adds to the atherosclerotic plaque.

But that wouldn't happen if there isn't a lot of PUFA in the system to cause LDL to become oxidized.

The cause is still PUFA that gets into becoming oxidized LDL. You still can't blame the macrophages for failing to remove the oxidized LDL. It wasn't made to remove oxidized LDL. Blame the person for not treating his body as a temple for putting the bad stuff into his body.

And blame the American Heart Association for telling the poor guy that PUFAs are heart-healthy.
 
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yerrag

yerrag

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@Elderflower j58 So glad to hear back from Ray.

Me:
If oxidized ldl is already oxidized, does it continue to cause lipid peroxidation in our blood vessels and cause inflammation and oxidative stress? Or is oxidized LDL only partially oxidized, and being so, it would continue to have a pathological effect?
Ray:
Yes, the oxidized fragments keep spreading the oxidation, with the smaller products often being the most toxic.

_______________________________________________________________________________________________________________________

No wonder that the older one gets, the more lipid peroxidation occurs from the accumulation of oxidized LDL and their fragments becoming more toxic as well.
 

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‘Bad’ Cholesterol May Have a Bad Rap
The research team — comprised of experts from seven different countries — evaluated data collected from 19 studies on a total of 68,094 older adults. The team was seeking to determine if LDL cholesterol is associated with death in the older adults.

According to the cholesterol hypothesis, it should directly relate. According to the BMJ study, it doesn’t.

Researchers say almost 80 percent of the participants in the studies who had high LDL cholesterol did not die because of their cholesterol level.

On the other hand, researchers discovered people with low levels of LDL cholesterol, or LDL-C, had the highest rates of death related to cardiovascular disease, the leading cause of deathTrusted Source for both men and women in the United States.

“These findings provide a paradoxical contradiction to the cholesterol hypothesis,” researchers wrote. “The cholesterol hypothesis predicts that LDL-C will be associated with increased all-cause and [cardiovascular disease] mortality.”

Overall, the researchers — four of whom have published books criticizing the cholesterol hypothesis — say, “the benefits from statin treatment have been exaggerated.”
 

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