The post itself and the exchange of comments on Dr Davis' blog about genetic causes of sdLDL piqued the interest of many of us. You need to have read the post and comments to make sense of this particular post here. I'm not keen on decrying the concept of genetic sdLDL out of hand but, obviously, there is a great deal that can be thought about around the non genetic concept. My thoughts are down here as I don't want to go cluttering Dr D's post up with comments that are clearly mine, from my biased viewpoint, and very probably not congruent with those of Dr D. The situation is too interesting not to expand a little though...
I roughed out Stan and Ollie on Fitday, very crudely and making big guestimates.
Here they are:
Very crudely for Stan
I gave them both half a kilo of cabbage each, nuts as almonds, (slightly more for Stan as he is weight stable) and chicken, again slightly more for Stan to keep him weight stable. I also allowed Stan some cannola oil to make his total calories up to 2000kcal/d.
And here is a guess for Ollie
I assumed Ollie was burning 0.34lb/d of his own fat and entered this as lard. I allowed him a total (including the lard from his butt/belly) of 2,300kcal/d as he was carting a fair bit more weight around than Stan. Probably an underestimate.
Saturated fat "consumption" for Ollie (who near eliminated sdLDL) worked out as 67g/d, total fat was 83% of 2300kcal, MUFA 105g and PUFA 31g. Most of this fat was from belly-fat plus almonds.
Fat for Stan (who retained sdLDL) was from his diet only as he, quite correctly, lost very little weight over 6m. Results were saturated fat 17g/d, total fat 70% of 2000 calories eaten, MUFA 84g/d and PUFA 53g/d.
I find it hard to see that Stan's saturated fat is the reason for his sdLDL, unless one posits that 17g/d of saturated fat as chylomicrons (apoB48 labelled, gut produced) causes sdLDL in some way (sdLDL is apoB100 labelled and produced by the liver). While at the same time Ollie's 67g/d of saturated fat, available as FFAs after release by hormone sensitive lipase from his adipocytes, behaves differently to Stan's 17g/d saturated fat released from chylomicrons by lipoprotein lipase....
It's possible, but it seems implausible to me.
Dr Davis mentioned the tendency of this sub group of his patients to be borderline diabetic. This to me is far more interesting and makes my ears prick up. Both apoB100 and apoB48 have glycation-predisposed sites which, once glycated, inhibit their uptake by the LDL receptor (certainly for the apoB100 particles, probably something similar works for the apoB48 particle, I've not chased this).
If apoB100s are not taken up because they are glycated due to a borderline diabetes tendency we have a very plausible mechanism for "atherogenic" remnant particles both being formed and "remaining". It just needs a little sugar to get them there. And of course, some of us think sugar and arteriosclerosis might be linked anyway...