Huevos, Cholesterol
We get a lot of questions from clients about different foods: what to eat, how much, when, and is food X on the plan? Some of our recommendations run against USDA guidelines (which are influenced by Big Agriculture, i.e., financially engineered; pardon the political statement but it’s true) as well as everything we have been taught about food since around 1990, and we understand when people are uncomfortable and confused. In this vein, some of you are concerned when we extoll the virtues of the Mighty Egg and encourage consumption of three of the little miracles at a time in a single scrumptious serving. It really okay to eat a lot of whole eggs, especially if you have high cholesterol?
The short answer is that (a) dietary cholesterol is not a bad thing (contrary to “conventional wisdom”) and (b) once you cut sugar, grains, and other pro-inflammatory foods from your diet, both saturated fat and cholesterol are fine to eat – in fact, they are quite healthy when your body is able to use them as intended. Egg yolks have all kinds of great health benefits, and eggs work better as a system – your body can use the nutrients in the whole egg more effectively than in just the white (I think there’s a protein and enzyme involved but for the life of me have not been able to find the reference for that assertion). Therefore, as long as you’re not having toast or orange juice with your omelette / scramble / frittata, it’s fine.
A more thorough answer requires an explanation of the role of cholesterol in the body, and the reasons for the demonization of cholesterol – what can go wrong. Brace yourself – here we go on a scientific excursion…
Cholesterol is a structural component of cell membranes, essential for brain growth, cell creation and repair, and is a precursor for vitamin D and numerous hormones, including cortisol (stress), aldosterone, progesterone, estrogens, and testosterone. In other words, it’s required for human (and animal) life, and plays a key role in regulating metabolism. Some plants and all animals contain cholesterol, but plant cholesterol is poorly absorbed. The liver regulates cholesterol levels in the blood by synthesizing cholesterol when levels are low, and converting excess to bile and bile salts (which can be excreted) when levels get high. Cells throughout the body synthesize about 80% of your cholesterol, and the liver makes about 20%. Your body synthesizes about 1g of cholesterol each day, and most Americans eat 200-300mg (more if you eat a lot of meat). Since the liver balances total cholesterol from all sources, synthesized or dietary, people who eat meat may produce less cholesterol than vegetarians, but they have similar total amounts of cholesterol. That’s why cholesterol-rich eggs and meat are not the sole culprit of high cholesterol; the liver can remove excess dietary cholesterol. Turns out that there’s more to the story.
You have heard of LDL (low-density lipoprotein, also erroneously called “bad cholesterol”) and HDL (often called “good cholesterol”). Chylomicrons and VLDL are other lipoproteins, which play roles in energy delivery. The liver turns used VLDL into LDL, which delivers free cholesterol (easily absorbed) to the cells, as well as triglycerides (energy) and cholesteryl esters (not easily absorbed). LDL particles may bind to an LDL receptor on a cell and deliver some cholesterol, or it may go back to the liver. LDL also returns the majority of excess cholesterol from cells to the liver. Meanwhile, the liver and small intestine produce HDL, which picks up some of the excess cholesterol at the cells and carries it back to the liver. To oversimplify, LDL is like UPS (pickup and deliver), and HDL is the charity donation pickup van for unneeded cholesterol.
Wait a minute, you ask; so LDL and HDL aren’t cholesterol? No – they carry cholesterol. Blood panels can count the LDL and HDL particles or the cholesterol content in the particles, called LDL-C or HDL-C. The actual LDL count, or particle number, is called LDL-P.
Atherosclerosis – artery plaque – occurs when LDL particles embed in artery walls, triggering an inflammatory (immune) response, which creates more room for more LDL particles. Research and research interpretations conflict on whether particle size or particle count matters more. One theory suggests that small, dense LDL particles, which tend to occur in insulin resistant people, are the ones that embed in the artery walls. Other evidence shows that number of LDL particles is the most important number, suggesting that the chances of LDL particles embedding in the artery walls simply increases when more particles are present. HDL counts don’t seem to matter, and drugs that increase HDL have been shown to be ineffective, whereas statins that lower LDL-P can reduce heart disease risk. It’s a lot cheaper and healthier to lower LDL-P with good nutrition.
Here’s where the toast comes in. Regular consumption of simple sugars such as those found in desserts, breads, pasta, corn products, and fruit juices (pina coladas too!) can lead to insulin resistance, which tricks cells into behaving as if they are not getting fed enough and need to store more energy. Your body responds by sending more triglycerides (lipids) to the cells via the bloodstream. Your lipoprotein particles, including LDL, will be loaded up with more lipids, leaving less room in the UPS trucks for free cholesterol. Therefore, your body has to send out more trucks to deliver the same amount of cholesterol. If the trucks are bigger, each one can carry more triglyceride and more cholesterol, but you may still need more trucks. The jury is out on exactly how this works, but the result is a higher chance of getting LDL stuck in your artery walls and an increased risk of heart disease.
One more point: research has shown that saturated fat doesn’t increase heart disease risk when carbohydrate intake is low. That’s why you can eat bacon with your eggs, but we don’t recommend toast or orange juice with them.
Congratulations if you made it through our little foray into blood biochemistry. It’s an emerging area and this post just scratches the surface of a very complex set of processes. From here, you can look at the interaction between the metabolic processes that involve insulin and leptin, as well as the impact of cortisol and the nasty effects of stress and sleep deprivation, but for now let’s just say that all of these processes are interdependent and you can make things significantly better or worse by changing your training, nutrition, sleep, and stress exposure.
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This post was drawn from numerous studies and secondary sources based on the scientific literature. Bibliographies can be found in works by Taubes, and good old Wikipedia too. My apologies for being lazy about citing the sources.
If you really want to get into the science of cholesterol, check this blog post series by Dr. Peter Attia: http://eatingacademy.com/nutrition/the-straight-dope-on-cholesterol-part-i