After reading considerably about the alternative carbohydrate hypothesis by Gary Taubes, I felt comfortable with the mechanisms behind obesity (and more importantly) metabolic syndrome. However what I still wasn’t sure about was the role that cholesterol plays in all of this. Well it turns out my confusion was well grounded, as popular medicine’s understanding of cholesterol has been clouded with poor science and lobbyist agenda. In this post I attempt to go through the science of cholesterol, as I understand it. However to really do the subject justice I’d recommend reading around, a great resource being Cholesterol Clarity by Jimmy Moore.
Introduction to Cholesterol
Heart disease is the biggest killer in the USA and the UK each year. The main cause of this is atherosclerosis, a thickening of the artery walls caused by the accumulation of fatty materials. Typically you’ll hear this attributed to “high cholesterol”. This isn’t correct. Cholesterol is a lipid, essential to the human body. Cholesterol itself isn’t problematic, instead it’s the particles transporting cholesterol, called lipoproteins, that we need to be wary of. The low density lipoproteins, specifically, are capable of burying themselves in the artery walls, causing a build up of plaque, and consequently atherosclerosis.
When misinformed doctors test cholesterol they focus on two numbers; LDL-C and HDL-C. HDL being “good” cholesterol, LDL being “bad”. Actually the cholesterol contained in these particles is the same type. What’s more important is the number of particles rather than the amount of cholesterol in them. There’s no direct correlation between a low LDL-C count and a low LDL-P count. LDL-P being the number that isn’t typically tested and refers to the number of low density lipoprotein particles. It’s possible to have a ‘perfect’ LDL-C number and yet have high a LDL-P number.
Summary so far:
- Cholesterol itself isn’t “bad”
- The issue is the size of the containers (lipoproteins) transporting it around the body
- The standard cholesterol tests used by doctors (measuring LDL-C and HDL-C) don’t tell us much
What causes high levels of low density lipoproteins (the problem)
Answer: The liver having to process copious triglycerides (TGs).
Solution: Cut out high carbohydrate foods and drinks.
See this article for the science.
In addition Gary Taubes explains the mechanism of creating low density lipoproteins very concisely in his book Good Calories, Bad Calories:
“After we eat a carbohydrate-rich meal, the bloodstream is flooded with glucose, and the liver takes some of this glucose and transforms it into fat—i.e., triglycerides—for temporary storage. These triglycerides are no more than droplets of oil. In the liver, the oil droplets are fused to the apo B protein and to the cholesterol that forms the outer membrane of the balloon. The triglycerides constitute the cargo that the lipo-proteins drop off at tissues throughout the body. The combination of cholesterol and apo B is the delivery vehicle. The resulting lipoprotein has a very low density, and so is a VLDL particle, because the triglycerides are lighter than either the cholesterol or the apo B. For this reason, the larger the initial oil droplet, the more triglycerides packaged in the lipoprotein, the lower its density.”
How do we measure our cholesterol risk?
There are two sound ways to measure atherogenic lipoproteins (the bad guys). The optimal test is the NMR Lipoprofile which gives a count for the number of each type of lipoprotein (LDL-P, HDL-P, VLDL-P and IDL-P). The test for this was created by LipoScience Inc. The NMR LipoProfile test is relatively easy to obtain in the USA. It’s somewhat harder in the UK. A company called Genova Diagnostics Europe offer a test called CV Health for £239 which appears to use LipoScience’s NMR tech. LipoScience have a great sheet for how to interpret the test results here.
Measuring Apolipoprotein B (ApoB, in particular the hepatic ApoB100) is the next best option. This test gives the total number of IDL-P, LDL-P and VLDL-P (but no breakdown). This is because each of these lipoproteins has one molecule of ApoB100.
I’ve tried to keep this article brief, and consequently may have missed important information out. If you have any questions please do ask in the comments or on Facebook. I welcome arguments, as long as they’re backed by science. I intend to add more references to this article in time.
Jimmy Moore’s Podcast ‘Ask the low carb experts’ with Dr. Thomas Dayspring. Highly recommended.
Gary Taubes’ Book – Good Calories, Bad Calories.
Perhaps the best primer to the alternate hypothesis of adiposity. Particuarly love this analogy Taubes makes regarding cholesterol:
“Measuring the LDL/HDL-C and then making potentially life-changing health decisions based on the number is like counting the number of people riding in vehicles on a freeway to determine the severity of traffic. It’s data, and it might give you a rough approximation of the situation, but it’s not as useful as actually counting the number of vehicles. A reading of 100 could mean you’re dealing with a hundred compact cars, each carrying a single driver, or it could mean you’ve got four buses carrying 25 passengers each. Or it could be a couple buses and the rest cars. You simply don’t know how bad (or good) traffic is until you get a direct measurement of LDL and HDL particle number.”
Peter Attia’s Blog Post Series – Straight Dope on Cholesterol. Attia goes into some real depth on the subject – interesting if you can keep up with the science. I struggled, but still took some good stuff away from it.