Only time will tell if this hypothesis ends up in that same graveyard, or changes the way we think about lipoproteins and atherosclerosis.
Let’s start with what we know, then fill in the connections, with the goal of creating an eating strategy for those most interested in delaying the onset of cardiovascular disease.
[This paper also reviews the clinical situation of mutations which builds a very compelling case for the causal model of apo B particles in the development of atherosclerosis].
Needless to say, she broke up with me on the spot (in the middle of a parking lot!
), despite me drawing a very cool picture illustrating the difference, which I’ve re-created, below.] The reason age is such a big driver of risk is that the longer your artery walls are exposed to the insult of apo B particles, the more likely they are to be damaged, for all the reasons we covered in Part IV of this series.
The figure below shows the changes in serum triglycerides via 3 different ways of measuring them.
Figure A shows the difference in 24-hour total levels (i.e., the area under the curve for serial measurements – hey, there’s our integral function again! Figure B shows late evening (post-prandial) differences.
Maybe it’s because I’m a math geek, but such models just seem intuitive to me because I think of most things in life in terms of calculus, especially integrals, the “area under a curve.” [I once tried to explain to a girlfriend who thought I wasn’t spending enough time with her that my interest in her should be thought of in terms of the area under the curve, rather than any single point in time.
That is, think in terms of the integral function, not the point-in-time function.
Many of you have asked about this, and my comments have always been the same.
It is entirely plausible that an elevated level of LDL-P or apo B in someone consuming a high-carb diet portends a greater risk than someone on a ketogenic or low-carb diet.
In other words, the “dream” study has not been done and won’t be done for a long time.