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BafangFan t1_itfc4xj wrote

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.

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Euda-monia t1_itfmw89 wrote

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.

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dv_ t1_itfwkpz wrote

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?

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OfLittleToNoValue t1_itfyewt wrote

Yep. Glycating happens when there's too much sugar in the bloodstream. Which usually happens when people get put on low fat diets.

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Buttons840 t1_ith9z83 wrote

> 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.

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Euda-monia t1_itfz5bs wrote

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.

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dv_ t1_itg8h7x wrote

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?

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OfLittleToNoValue t1_itfyc1n wrote

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.

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Euda-monia t1_itfziuy wrote

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.

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OfLittleToNoValue t1_itg1q0v wrote

Yes it is.

Abstract Background Endothelial function deteriorates after glucose ingestion.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2585377/

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Euda-monia t1_itg2hzq wrote

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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Nitz93 t1_itiotg5 wrote

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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sethonomics t1_itfbo42 wrote

I was just thinking about this stuff! Thanks!

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Meatrition OP t1_itfa2th wrote

Result The prevalence of Pre-DM was 9.77%.The median TG/HDL-C ratio was 0.671 (interquartile range, 0.468–1.010). After adjusting covariates, the results showed that TG/HDL-C ratio was positively associated with Pre-DM ((OR = 1.185, 95%CI 1.145–1.226). In addition, the TG/HDL-C ratio level has a non-linear relationship with the incidence of Pre-DM, in which the inflection point was 1.617. The effect sizes (OR) on the left and right sides of the inflection point were 1.312 (95%CI 1.242–1.386) and 0.980 (95%CI 0.898–1.070), respectively. And the sensitive analysis demonstrated the robustness of the results. Subgroup analysis showed a stronger association between TG/HDL-C ratio and Pre-DM in females and the population with 30 years  < age  < 40 years, 18.5 kg/m2 < body mass index  < 24 kg/m2, and ALT < 40U/L. Conclusion This study demonstrates a positive and non-linear relationship between TG/HDL-C ratio and Pre-DM in Chinese non-obese people with a normal range of low-density lipoprotein cholesterol. TG/HDL-C ratio is strongly related to Pre-DM when TG/HDL-C ratio is less than 1.617. It makes sense to reduce the TG/HDL-C ratio level below the inflection point from a treatment perspective.

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SerialStateLineXer t1_itlkwxh wrote

These seemed like extremely low ratios. At first I thought Chinese people were just really healthy, but then I realized that because cholesterol and triglycerides have different molar weights, the ratio is different depending on whether HDL and TG are expressed in mmol/L or mg/dL. You need to multiply by about 2.2 to convert mmol/L ratios to mg/dL ratios (the kind you typically get in the US).

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