I’ll put links to reading resources here.



The straight dope on cholesterol – Part I

This is a difficult read for anyone who isn’t already familiar with the relevant biology, but it’s comprehensive.

It is a great demonstration of how complex the systems of the body are, and thus how easy it is to oversimplify conclusions and advice about health topics.

It also highlights how historic technologies and their limitations can establish advice that later becomes ingrained misinformation, which may be difficult to supersede with more complex but accurate information.

For example, the first blood cholesterol tests only gave a value for the total cholesterol.
More recently, we established the LDL vs. HDL (“bad” vs. “good” cholesterol) distinction, diminishing the perceived merits of a simple total cholesterol value.
Still more recently, we found that LDL comes in small, dense (“harmful”) and larger, buoyant (“harmless”) variations*.
Again more recently, LDL-p (lipoprotein particle count) is recognised as a much stronger predictor of cardiovascular disease risk than the previously used LDL-c (cholesterol concentration).
While we’re digging into CV risk in context of cholesterol (well, lipoproteins): Glycation (reaction with sugar) and oxidation in general of LDL particles has huge mechanistic implications in the cause of atherosclerosis (the build-up of fatty plaque in the arteries that causes heart disease and stroke). Accordingly, eating in a way that induces chronically high blood sugar (as can be measured with an HbA1c test) seems worse for cardiovascular disease risk compared to the long-reported saturated fat consumption.

In all cases, context is very important, and the trends seen for each individual‘s blood profile over time should be as useful in treating them as a comparison to the population.
Different people, even identical twins, can react very differently to the same foods due to the huge variation in gut bacteria between individuals.

*Interestingly, saturated fat consumption has been shown to convert small, dense (“harmful”) LDL into large, buoyant (“harmless”) LDL; this could be considered to offset the perceived risk of cardiovascular disease from the increased total blood cholesterol induced by saturated fat consumption.



I changed the descriptions of LDL subtypes from “fluffy” to “buoyant”, since Dr Ronald Krauss doesn’t like the term “fluffy”, and he’s a pioneering researcher in the field, so props to him.
Here’s an interview with him.

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