A few people have been sending me queries recently about ApoB – the so-called ‘master-risk metric’ from the NMR test. We must question whether high ApoB is a problem in its own right. If ApoB is above ‘ideal’ – should one strive to lower it regardless? Should we attempt to lower it…’blindly’? Do we really believe that the Low Density Lipoproteins are inherently toxic to our bodies, regardless of the conditions in which they function?
Or…is there a concern only when the ApoB particles have actually become compromised; for example, oxidised? Biq question that. Huge question in fact. Luckily there are a suite of measurements that may exonerate the high ApoB in any given case. But these don’t seem to exert a hypnotic effect on the experts like ApoB does. Strange that – why place so much focus on ApoB as massively malign?
Well, here are a few links that question the universal evil of ApoB. We must ask has it EARNED it’s broad-brush demonic status. Or is it yet nother associational interactor, problematic only when compromised…by far more important causal issues. Should it never be judged alone, in other words? Anyway, here’s a sample of the ApoB black flock to ponder on:
Another thing I find quite shocking is the practice of looking at ApoB, without a simultaneous focus on ApoA1. How on earth can one be used for risk…without considering the other?? First take a quick look at this study pic (Women’s Health). On the right I’ve changed it from log scale to linear for clarity. Wow – ApoB on its own is kinda weak here, compared to other (better) measures. And many people who would appear high risk looking at APoB alone, would be low risk looking at their ApoB/ApoA1. So much for ApoB – major bum steer, eh? (some posts below addressing this also):
Finally, “say hello to my leetle friend”….El Pee Little Ay ( Lp(a) ). Apparently not such a clear-cut pantomime villain. It looks like high Lp(a)….just means you have to be even more careful to follow the LCHF/D/w3/w6/Mg/K2 prescription. Is all. :
So it appears to me that a lot of support for ApoB and Lp(a) has been inherently associational. Sure, an enormous edifice of mechanistic discussion has been built to support them as universal bad-actors (especially the old ApoB). And sure they partake in key roles within CHD. But the black swans will have their say. Good hypotheses should be borne out in Case Control study outcomes. Failures like these demand revisiting the hypothesis. Especially when there are so many interactions, so many more causal drivers of greater importance. So how big is ApoB as a risk, IN AND OF ITSELF? Without correcting for HDL/ApoA1/Insulin/glucose etc. etc.?
Well I for one wouldn’t waste too much time on it. Far bigger root-cause fish to fry.
In closing, if one must pick a single thing to fixate on for CVD (not a good idea btw) – I certainly wouldn’t have it be ApoB.
For those who still worry (with all-round good metrics but naturally high LDLp), Franziska has great discussion here: http://www.lowcarbdietitian.com/blog/lipid-changes-on-a-very-low-carb-ketogenic-diet-my-own-experience
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