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Comment by hombre_fatal | Hacker News Reader

There is a whole mountain of evidence that saturated fat increases LDL cholesterol and better markers like Apo B. Placebo controlled, double-blind interventions. You can even run the experiment on yourself with monthly blood panels.

Are you contesting that?

That's pretty settled science. Low-carb influencers don't even deny that, so they instead try to hand-wave that high LDL/ApoB aren't a problem. Usually with some quackery over how atherosclerosis works, usually claiming that lipids only pass through the arterial endothelium when it's inflamed (false, they pass through anyways).

The balance of evidence showing that LDL cholesterol and better markers like Apo B cause CVD and atherosclerosis is so huge I'm not sure where I'd start if I wanted to deny it.

What research do you think is so convincing that it supersedes this balance of evidence?

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You have tapped into a logical fallacy. A is associated with B. B is associated with C. This in no way indicates that A causes C. It just doesn’t. You have to show that A and C are associated, then you have to determine causation. You can’t skip steps.

I see this all the time in nutrition “science”, and it is just bad science.

Do you think there is no research into saturated fat and heart disease (A->C)? I beg you to google it instead of washing your hands of it because one guy on HN doesn't have the time to walk you through the literature.

https://en.wikipedia.org/wiki/Saturated_fat#Association_with...

My understanding of the low carb argument here is that LDL isn't inherently bad, but oxidized LDL is and that LDL requires a high blood sugar environment for oxidation. I don't have any reason to know if that's right or wrong. I hope it's right, but I also have made efforts to avoid processed meats high in saturated fats (like salami, cold cuts) just in case.

Oxidation is what makes LDL recognizable to scavenger receptors. It's immediately eliminated from the blood.

We can actually wash our hands of LDL discussion because we have a better marker for atherosclerosis: Apolipoprotein B.

Even though LDL is a proxy for Apo B (you basically can't have high LDL and low Apo B nor vice versa), it's better to focus on Apo B which is carried by lipoproteins like LDL and is more causally linked in CVD.

I was going to ask what you think "LDL" cholesterol means with regard to its actual fractional measurement instead of calculated volumetric level, but then I decided you seemed content with your worldview and it wasn't really disturbing me personally.

As I get older, I find more enjoyment using my magnifying glass for discovery than burning

Well, I'll do you one better: I'll dismiss the whole conversation about LDL concentration and focus only on the better marker most causally linked to CVD that's carried by LDL and other lipoproteins. (LDL concentration is merely a proxy)

So, don't put that magnifying glass away too fast: https://en.wikipedia.org/wiki/Apolipoprotein_B#Role_in_lipop...

> What research do you think is so convincing that it supersedes this balance of evidence?

You seriously need to ask yourself that question before asking it of others.

If you're asking me what the scientific consensus is or what the balance of evidence shows, start with this article:

https://en.wikipedia.org/wiki/Saturated_fat#Association_with...

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