REV-Blog


When we started on this journey, this new WOE (way of eating), we were both pretty clueless. But we learned from the best. Like anyone, we didn't start out perfect. Hey, we aren't even close to perfect now. No one starts out as an expert, everyone is a beginner at some point.

In this blog, we want to share mostly what we have learned, our experience, our progress, our struggles. We will also feature guest blogs. If you have something worth sharing, please contact us.

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A few thoughts on ApoB by Tucker Goodrich



 

A few thoughts on ApoB

It's something we're programmed for, genetically. It's a fundamental component of digestion and energy distribution. (Dave Feldman - @realDaveFeldman)

So if it causes CVD, then CVD is a genetic disease.

#lcl6 h/t @jimolsen717

If CVD is genetic, then we should see the current rate of CVD (~50% of deaths) in all human populations. We don't. This is demonstrated repeatedly, best here:

Where various genetic populations have near-zero CVD in their natural environment.

We only see CVD in populations consuming higher amounts of linoleic acid, and, best, low levels of animal fats.

United States Dietary Trends Since 1800: Lack of Association Between Saturated Fatty Acid Consumption and Non-communicable Diseases

There are various confounders that affect this, like smoking, pollution, or FH, but all do so though that variable.

'Mendelian randomization': can genetic epidemiology contribute to understanding environmental determinants of disease?

So it seems, clearly, that when linoleic acid is low, ApoB is not harmful. Populations with ApoB levels higher than US levels, for instance, but no industrial seed oil consumption, have near-zero rates of CVD.

Linoleic acid (LA) itself, however, isn't a problem. It's only when it becomes oxidized that it's a problem.

This is roughly like saying spilled gasoline in a match-testing facility isn't a problem...

Since it's going to get oxidized, sooner or later. We know that eating LA leads to increased oxidized LA in the body, as we can measure a carrier of LA, LDL. LDL with oxidized LA is called oxLDL.

ApoB is just a protein, you have quadrillions of them in your body right now. LDL contains one ApoB, as do some other things in your body.

When LA gets oxidized, it attaches to and oxidizes the ApoB in LDL—along with everything else in the neighborhood.

This is why ApoB is such a poor risk marker.

Along with those populations that don't have CVD, it's a poor indicator for CVD risk even in populations that have high LA consumption.

It's not causing it, it's just a vehicle.

Physicians and scientists who have been following the science for the last few decades are figuring this out.

If you're curious, while consuming LA to prevent CVD is still recommended by certain Stone-age physicians and professional organizations, LA increases ApoB.

And yes, the oxidized LA that you eat is delivered throughout your body, causing all sorts of mayhem.

Including to your arteries, to give you CVD.

Written by Tucker Goodrich
Published April 22nd, 2023

Twitter: @TuckerGoodrich
Blog: Yelling Stop
Reflections on barefoot-style running, healthy diets, and moving in the right direction.
YouTube: @TuckerGoodrich0
Original thread on Twitter by Tucker Goodrich

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