JUST WHAT EXACTLY About Arteriosclerosis?

This is my car, Milano. He’s oldish, high mileage, quite stylish, and is somewhat ambivalent about whether he could be a son car or a girl car. He’s also some kind of Italian derivative which means that spares can be an issue. Anyway, this post is actually about another Milano, the magical apoA1 Milano. Everybody knows that a low HDL is associated with an elevated threat of CHD. We know this from a massive amount of observational evidence.

In general, people with low HDL are more likely to suffer a coronary attack. Totally convincing association. This has led to the hypothesis that HDL protects against heart attacks. To the main point where experts are developing HDL-like particles as drugs now. Pour them in and suck out that arteriosclerosis.

I assume the first spanner in the works was apoA1 Milano. The initial study was published in 1985 and is available as a pdf download here back. It’s worth emphasizing that apoA1 Milano was within a residential area which had a low prevalence of heart disease and, within that grouping community, it had not been regarded as the reason for that low incidence of CVD. Everyone locally was protected.

A hypothesis I might suggest, produced from the lipid hypothesis patch of “HDL is good”, is that under high CVD risk conditions that apoA1 Milano may be bad news. There was no selection effect to remove the gene in Limone sul Gardo because the population here was already doing something very right.

Probably living on Lardo. The impression I get from Franceschini is that he is proposing the contrary hypothesis. There’s another hereditary error leading to low HDL, a problem with the gene for LCAT (Lecithin Cholesterol Acyltransferase). LCAT takes free cholesterol from tissue/lipoproteins and esterifies it ready for putting into HDL particles. The mutation leads to cholesterol build-up in some tissues and very low HDL levels in the blood.

If you can’t put cholesterol into HDL, there won’t be much HDL cholesterol. And what little HDL is present will have a normal apoA1 on it’s surface. Nothing Milanesque about any of it. It’s a dribble of this same HDL that helps to keep anyone with high HDL free of CVD, if you believe that. You would have thought this is an absolute cert of a recipe for atherosclerosis.

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Franceschini’s group do the work and were again sufficient to create in a journal with free access. The abstract is here. Just click on the PubMed link for full-text message. Just what exactly about arteriosclerosis? The analysis used carotid intima-media thickness as a surrogate for arteriosclerosis. This seems reasonable if you ask me.

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