Warm-up: 400m Run, 8 Wide, Normal, and Narrow Push-ups, 8 Wide, Normal, and Narrow Squats, 20 Lunges, 10 Backwards Lunges
Squat: 5×3 @ 70%
Work: 3×15 of ring push-ups, ring rows, and ring v-outs
Finisher: 20 strict knees to elbows
Have you ever wondered what exactly the doctor is testing or hoping to divine from your cholesterol score, make up of LDL vs HDL, or total triglycerides? Never even crossed your mind, eh? Well, as we have before, we are going to ask you to be a little more inquisitive when it comes to daily life regarding nutrition and health. Let us learn.
Cholesterol is only one of several fatlike substances that circulate through your bloodstream. All of the fatlike substances together are known as lipids or blood lipids. The collective blood lipids, henceforth referred to as just lipids, include free fatty acids and triglycerides. FFA and triglycerides are the molecular forms in which fat is found floating around your blood stream. Lipids could not be accurately measured until the 1950s when a young medical physicist named John Gofman published an article in Science that would launch our modern era of cholesterol pandemonium. You will see that, even six decades later, we are still somewhat confused as to what EXACTLY causes cardiovascular disease, atherosclerotic build up, and myocardial infarctions.
Continuing our cram session on blood lipids, we need to figure out just how in the world we came up with good and bad cholesterol. Both cholesterol and triglycerides are shuttled through the bloodstream in particles called lipoproteins. This is where we get LDL (bad) and HDL (good) cholesterol. LDL stands for low density lipoprotein while HDL stands for high density lipoproteins. The differentiation between them as good and bad is an oversimplification that we must address at some point as well. But for now we will plod along in our descriptions of what some cardiologists want you to think are two warring factions battling for your arterial walls.
Our imitable Gofman noted that, regarding cardiovascular disease, the problem may be caused not by cholesterol but by a defect or an abnormal concentration in a lipoprotein. He was really ahead of his time – way to go Cal Berkeley (go Bears)! His research found three lipoproteins that seemed to have some correlation (NOT CAUSATION) to cardiovascular disease. The two we are familiar with today are the aforementioned HDL and LDL, but the one that goes unheralded is VLDL, very low density lipoproteins. VLDL carries the vast majority of triglycerides while much of the cholesterol is found in the LDL.
In the 60 years since Gofman’s paper in Science, much research time and money have been spent on the problem of cardiovascular disease. What causes it? What prevents it? Which measurable factors give us the best idea of risk factor? Did I leave that electron microscope on in the lab? Maybe we have been asking the wrong questions though.
It is not all bleak, overcast skies out there though; a few things have been almost unequivocally proven. Saturated fats raise both LDL and HDL cholesterol. Monounsaturated fats lower LDL and raise HDL. Carbohydrates lower HDL. Vigorous exercise raises HDL. This list could go on ad nauseum. The problem comes from trying to tie this list back in with coronary artery disease (CAD) or cardiovascular disease (CD). HDL, particle numbers (numbers of HDL, LDL, VLDL), particle sizes (VLDL is very large and fluffy compared to HDL and LDL), and a slew of other parameters are more or less associated with CAD, but they are just covariant. These parameters are not necessarily, or usually, the direct mediators of increased or decreased risk for CAD or CD.
People telling you that your high LDL count is causing cardiovascular disease are basically telling you that Shaquille O’Neal’s large shoe size caused his extreme height. If by lowering your LDL you decrease your risk for CD, can we not by that same token cut off Shaq’s toes to make him shorter? None of the lipid hypotheses are biologically plausible, and all have failed to be proven despite decades of research and billions in expenditure.
Our attention to nutrition, and especially CD and the like, has pushed technology ahead, and we now have the ability to measure even more parameters that are purported to give us feedback on cardiovascular disease risk. HDL, LDL, total cholesterol, and triglycerides are no longer the particles du jour. Lipoprotein (a), cholesterol ester transfer protein (CETP), and calcium scores have become de rigueur as the new tests for CD. What I mean to convey with this is that as science becomes more sophisticated, we will be able to measure more and more parameters that we associate with CD. This can be good, and I am sure one day we will have a definitive answer to many questions we currently still have in the nutrition field. But as for now, we must be weary of our attempts to measure every single factor we think associates with CD in order to come up with some prescription to prevent or drug to suppress.
A great example of this was Pfizer’s attempt to control CETP through an inhibitor called torcetrapib. The drug purportedly cost Pfizer $800 million to develop. Torcetrapib brings HDL up while simultaneously lowering LDL, and they combined it with a statin to really lower the LDL – a veritable wonder drug! They took it to trials and they were getting levels of HDL and LDL that, according to most cardiologists, should have reduced risk of CD to zero. But the group that received the drug had all-cause mortality increases of 60%! Needless to say the trial was halted early.
I like this quote: “Everything should be made as simple as possible, but no simpler.” Albert Einstein supposedly said that, and he did big things if I have my histories correct. The problem with nutrition is that it is not simple. We cannot fall prey to trying to oversimplify it. We will keep this in mind as we move forward in this series.
A bit convoluted and all over the place, my sincerest apologies,