I came across an interesting statin study the other day. It’s from last year, but I hadn’t seen it until recently. The study, entitled “Statins Do Not Decrease Small, Dense Low Density-Lipoprotein,” sought to understand the effect of statin therapy on small, dense LDL, the truly “bad” kind of “bad” cholesterol, the stuff that’s strongly associated with increased heart disease risk in many studies. We know that statins reduce LDL cholesterol – they are extremely effective at curtailing the cholesterol-synthesizing hydroxy-methyl-glutaryl-coenzyme A reductase, if you’re into that sort of thing – but their effectiveness at lowering sdLDL is unknown. They reduce the rate at which cholesterol is produced and that’s as specific as it gets.
Researchers at the Cardiovascular Center of Korea University’s Guro Hospital assembled a group of 612 heart patients, some with confirmed coronary artery disease (CAD) but most without. They were divided into two groups on the basis of statin use; subjects who had been taking statins were put in one group, while subjects with no prior statin use formed the control group. Both groups were again divided based on CAD. In the statin-treated group, 119 had CAD and 53 didn’t. In the control group, 130 had CAD and 310 didn’t.
Overall, statin users saw drops in absolute LDL and sdLDL numbers (as expected), but the proportion of sdLDL to large fluffy LDL increased when taking statins. This effect was particularly pronounced in non-CAD patients. Among CAD patients, statins had a smaller effect on the sdLDL:large LDL ratio, but it was still present. Statins had the definite effect of increasing the proportion of sdLDL, regardless of CAD status.
How much does this even matter? Is it proportion of sdLDL or absolute count of sdLDL that we should concern ourselves with – or neither? I know where I lean.
Besides, if it’s reducing sdLDL you’re interested in, you might just consider intermittent fasting. In a new study just released, researchers put obese adults on an alternate day fasting protocol for eight weeks and monitored their blood lipids. The results were pretty dramatic. You got all the usual improvements that go with fasting – reduced LDL and triglycerides, weight loss, lowered waist circumference – plus a big drop in small, dense LDL. To my knowledge, fasting has never been shown to explicitly lower sdLDL. It’s not that surprising, sure, but it’s certainly nice to see it confirmed. Best of all, subjects saw the biggest improvements in the third phase of the study, when they graduated from alternate day fasting with controlled feeding to alternate day fasting with free feeding.
Speaking of fasting, a few people wondered aloud in last week’s comment section for my sample week post about why I choose to fast after working out instead of immediately feed my starving muscles crying out for sustenance. I gave a quick account why (at this stage in my life, I’m not too worried about putting on muscle or refilling glycogen right away, and I prefer the fat burning, growth hormone promoting effects of post-workout fasting) but I came across a study that kind of addresses this. While the post-workout “protein synthesis” window is a real thing, it’s not fleeting. No matter what the biceps specialists down at the gym tell you, your muscles won’t atrophy just because they don’t receive an immediate protein infusion; according to the results of this study, you actually have about twenty four hours of heightened muscle sensitivity after working out. So, don’t stress out about getting in that food right away post-workout. If you feel best doing it, by all means: eat. In fact, if you’re looking to bulk up, go ahead and eat a big meal after your workout. Just don’t worry about wasting away if you don’t. Cause you won’t.
One more thing before I go: Oprah and her team of staffers are currently on a vegan challenge. Or maybe they just wrapped it up; I’m not sure. I didn’t – and still don’t – plan on saying much about the whole fiasco, since the woman could erase me from the face of this planet with a single phone call, but I enjoyed reading that one of the biggest beneficial outcomes attributed to the new diet was that the staff was going through a record amount of toilet paper. Isn’t that a lovely bit of data on a Monday morning? I thought so too.
Mark Sisson is the founder of Mark’s Daily Apple, godfather to the Primal food and lifestyle movement, and the New York Times bestselling author of The Keto Reset Diet. His latest book is Keto for Life, where he discusses how he combines the keto diet with a Primal lifestyle for optimal health and longevity. Mark is the author of numerous other books as well, including The Primal Blueprint, which was credited with turbocharging the growth of the primal/paleo movement back in 2009. After spending three decades researching and educating folks on why food is the key component to achieving and maintaining optimal wellness, Mark launched Primal Kitchen, a real-food company that creates Primal/paleo, keto, and Whole30-friendly kitchen staples.