Submitted by Meatrition t3_yb8wo4 in science
LDL cholesterol is frequently believed to be the "bad" cholesterol, and is also the cholesterol that is affected by saturated fat consumption.
Anywhere from 50-75% of people who have heart attacks have normal cholesterol levels, including LDL cholesterol.
So how good of a predictor of heart disease is LDL, and why have we put so much emphasis on lowering LDL when it seems to have little bearing on our heart disease risk?
My triglycerides were at one point 1,200 (whatever the unit is). I have lowered that by 80% through low carb, high fat diets and fasting.
Carb intake has had a far greater impact on my cholesterol ratios than protein and fat does - and yet the advice is to always avoid fats - especially saturated fat.
LDL is called the bad cholesterol because it can clog your arteries. Saturated fats can trigger your liver to make far more LDL than it would normally do. LDL isn't really "bad" - it's just the 'bad' part of a problem - an imbalance of lipoproteins. It's bad to have too much if you don't have enough HDL to clean it up.
But you're right, carbs can influence cholesterol negatively. You need to keep your carbs as unprocessed and complex as possible.
The whole cholesterol = heart attack thing is kinda old school now. We live and learn.
From what I recall, LDL can clog your arteries when it becomes glycated, because then, the liver's LDL receptors don't recognize the glycated LDL molecules and the liver won't take those particular molecules out of circulation. Is this correct?
Yep. Glycating happens when there's too much sugar in the bloodstream. Which usually happens when people get put on low fat diets.
> too much sugar in the bloodstream usually happens when people are on low fat diets
I would guess the vast majority of people with too much sugar in their bloodstream are not on any specific diet at all.
That's part of the picture, yes. There are still a lot of unknowns but what we do know is that both the glycation and oxidation of LDL reduce its ability to be recognised for recycling by the liver. Higher circulating LDL means higher risk of it entering into the artery wall where macrophages gorge on them resulting in foam cells.
When the macrophages pull in the damaged LDL particles, do they ever go away? Are there self-repair mechanisms in the body that clean that up over time?
LDL doesn't just clog your arteries because it exists.
Sugar ablates endothelial cells in the arteries. LDL binds to the damage to repair it.
Eating less fat means eating more sugar which causes more damage.
Blaming LDL for blockage is like saying gauze pads cause gunshot wounds.
It's not damage that allows LDL into the artery. There are proteins that carry it across.
>Eating less fat means eating more sugar which causes more damage.
It's not that simple.
Yes it is.
Abstract Background Endothelial function deteriorates after glucose ingestion.
What the abstract actually says: "Endothelial function after high-sugar food ingestion is improved by endurance exercise performed on the previous day"
But, I wasn't referring to this when I said it's not that simple. I was referring to your comment about eating less fat means eating more sugar.
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VLDL is the better marker!
Also one should exclude all patients with elevated lipoprotein A from such studies. Overall it's the best marker but you can't really act upon the result.
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