The accumulated data show that the lower the LDL, the lower the incidence of MACE events, with as yet no indication of side effects to contraindicate use of statins, ezetimibe, or PCSK-9 inhibitors. Why not have a target of less than 20, or 15, or 10, especially when plaque is established and will only worsen?
I generally follow a low-ish carb diet, but every once in a while I will eat some slow carbs, such as rolled oats. If I had to pick one of the three, when would be the most appropriate time to eat those - after strength training, zone 2 cardio or intense cardio exercises?
A couple of weeks ago I did an indirect calorimetry, primarily in order to assess my metabolism at rest. It turns out I have a pretty fast metabolism, significantly higher than what standard formulas would predict for my height and weight. What was more interesting and somehow puzzling, though, was the part regarding substrate utilization: 99.1% carbohydrates. At rest, of course. Now, I’m a cyclist and I train a lot, and over the last 2 years I’ve managed to take my HR aerobic threshold from 145bpm to 160bpm (2mmol lactate, tested in a lab as well); and I can cycle at that intensity for hours with no carb intake (fasted training), with no meaningful sign of "bonking". How can I reconcile this kind of "aerobic function", to quote Maffettone, with that kind of extreme carb "burning" at rest? I genuinely don’t understand how it can be possible (ie., I thought I had dramatically improved my fat oxidation capacity). Thanks a lot.