In part 1 we were introduced to the life-saving, ninja-like qualities of cholesterol and we ended with the task of looking at cholesterol as a smaller piece of a much larger puzzle that is heart (and overall) health. While cholesterol has gained the reputation of being a, if not, the force in the path towards disease, let's think of it more as that impressionable kid who is friends with everyone. Sometimes those friends are great, supportive and play well with others. And sometimes: not so much. Lipoproteins are those friends.
Cholesterol is fat-soluble, which means that it in order to get where it needs to go, it can’t just tromp into the primarily watery-base that is our blood stream (Kresser, 2013); it needs a buddy, or rather, a vessel. Enter: apoproteins. When apoproteins bind to fat, they become, apolipoproteins (lipo= fat), and the vessel that is created to transport our fat-soluble friend, cholesterol, along with fatty acids (FAs), antioxidants, and fat soluble-vitamins around the body, is called a lipoprotein (Kresser, 2103).
Think of these lipoproteins as little balls of different shapes and weights (or densities). What’s becoming apparent is that in the great ball pit that is our blood stream, it’s not the presence of cholesterol that is the problem, but rather the size and number of the balls (Moore, 2013 & Kresser, 2031). Continuing on with the ball pit analogy (like the kind you jumped into when you were 5 and it totally changed your life), imagine jumping into a pit filled with light, fluffy balls: super sweet, right? You’d just nestle into that pit of awesome without a scratch. Now imagine that there were some balls that weren’t so soft and fluffy, let’s go with more of the dense and hard variety. Probably not a big deal if the light and fluffy ones balanced out the hard and dense. But, what if there were a whole lot of not so soft balls – kiss goodbye to that delightful, cloud-like landing and say hello to a whole lot of bumps, bruises, and cuts. With several degrees of separation, move this analogy inside the arterial wall. We want a balance in our blood stream between lipoproteins that are smaller and denser, and ones that are lighter and fluffier. Otherwise we risk damaging our arterial walls. Balls aside, let’s meet the actual players:
High Density Lipoprotein (HDL): Let’s look at cholesterol transport being a round-trip (both away from and back to the liver) (Bauman, 2014). HDL is involved in both trips, bringing cholesterol from the cells and tissues back to liver to be cleared out of the body, but also bringing cholesterol to the adrenal, testes, and ovaries for hormone production (Bauman, 2014 & Attia, 2102). HDL is touted as “good cholesterol,” and that isn’t off base as it helps us to clear the endothelium, which is the inner lining of blood vessels (Moore, 2013). Atherosclerosis (or the accumulation of plaque in the endothelium of the artery wall (Bauman, 2014)) occurs when the endothelium gets clogged and damaged – thus we want plenty of HDL acting to continuously sweep the scene (Moore, 2013).
HDL Lab Ranges:
Standard Medical Range:
- Poor: below 40 mg/dL (men) or below 50mg/dL (women)
- Better: 40-49 mg/dL (men) or 50-59 mg/dL (women)
- Best: 60+ mg/dL
- Ideal: 70+ mg/dL
Low Density Lipoprotein (LDL): Here’s where size and the ball analogy become relevant. LDL is often condensed into a singular number on most standard lab tests (LDL-C or total cholesterol), but there are in fact two types of LDL particles: Pattern A = large & fluffy, and Pattern B = small & dense (Moore, 2013). LDL particles on a whole carry cholesterol from the liver out to the cells and tissues (Bauman, 2014). It's crucial that these particles be packaged with antioxidants, as they are quick and easy to oxidize and become damaged (Bauman, 2014).
Small LDL-P: These are those Pattern B particles mentioned above. Let’s take a second to dive into these a little bit deeper, as they will be important in the over-arching discussion of atherosclerosis. We can gain a pretty solid understanding of why these particles are problematic just by thinking of them as small and dense objects careening around beneath the one-cell thick layer of the endothelium – that just straight-up doesn’t sound like a good idea. Small LDL-P are more prone to oxidation (Moore, 2013). They can also be involved in glycation (a process that makes them sticky – you don’t want sticky and the arterial wall to mix) (Moore, 2013). Small LDL-P tend to be longer lived than their counterparts, sticking around in our systems for weeks rather than hours or days (Moore, 2013). Finally, small LDL-P are recognized and attacked by our immune system, meaning that if they are constantly moving through our system, our immune system is always on high alert (Moore, 2013). It’s these guys that are behind the declaration: size matters!
LDL-C Lab Ranges:
Standard Medical Ranges: (LDL-C, aka: total number)
- People at very high risk of heart disease: below 70 mg/dL
- People at high risk of heart disease: below 100 mg/dL
- Near ideal: 100-129 mg/dL
- Borderline high: 130-159 mg/dL
- High: 10-189 mg/dL
- Very High: 190 mg/dL+
- In general, LDL-C is looked at as an overly-simplistic view of heart health since it does not take into account particle size.
- More Comprehensive markers
- LDL-P / ApoB: below 1000nmol/L, but exact ranges not known for those eating a high fat/low cab diet.
- Small LDL-P: 20% or less than LDL-P & ideally less than 200 nmol/L
Very Low Density Lipoprotein (VLDL): Made in the liver and converted to LDL when in the blood stream, VLDL carry triglycerides (TGs), cholesterol, and phospholipids (Bauman, 2014 & Moore, 2013). VLDL are also in the “bad cholesterol” camp because their presence denotes a higher level of TGs in the blood (Moore, 2013). To provide some perspective, HDL is made up of 4% TGs; LDL is 8% TGs, and VLDL is 50% TGs! (Attia, 2012).
Triglycerides (TGs): Lets take a second to talk about TGs, as they are crucial in our understanding about how our cholesterol particle numbers can become unbalanced. When we have a high concentration of TGs on our body we need a way to transport them, and that is the job of LDL particles (Kresser, 2013). Here’s the thing, TGs out-compete cholesterol for a seat on LDL, which means that our body must produce more LDL particles in order to accommodate both the high TGs level as well as cholesterol transport (Kresser, 2013). Thus the more TGs we have, the more LDL particles we have in our blood. And what raises TGs in the blood: high consumption of carbohydrates (Moore, 2013).
High TGs levels in the blood are inversely correlated to high HDL, and put you at a greater risk of atherosclerosis (Moore, 2013). High TGs are also associated with metabolic syndrome and Type II Diabetes (Moore, 2013).
Triglycerides Lab Ranges
Standard Medical Ranges:
- Desirable: below 150 mg/dL
- Borderline High: 150-199 mg/dL
- High: 200-499 mg/dL
- Very High: 500 mg/dL and above
Holistic / Functional Ranges:
- Ideal = 50 - 100 mg/dL
Intermediate Density Lipoprotein (IDL): Made from degraded VLDL and can be made back into LDL (Bauman, 2014).
Total Cholesterol = sum of HDL, LDL, VLDL, & IDL
*Note: you can see just by looking at this “cholesterol equation” how simplified total cholesterol is an indication for health as a stand-alone measure, as it provides no sense of particle size and HDL vs. LDL etc.
So hold up, what does all this mean? When we begin to look at cholesterol as a passenger, a single player in a larger scheme, we start to get at the root of the issues. It comes down to a question of layers. If we merely look at total cholesterol, we are only looking at the first layer of issues. Attacking that layer alone doesn’t create a substantial shift. It would be like throwing pebbles at a giant. Ain’t no thang. The next layer is cholesterol’s vehicle. While addressing the ratio of LDL vs. HDL gets us one step closer, we’ve really only given that giant a big shove. We need to go bigger. We need to take that giant out at the knees. We do that by asking, “why?” Why is total cholesterol so high? Is it because I have tons of fluffy HDL particles or because I have way too many small and dense LDL particles? Why do I have an army of destructive LDLs on my hands? Why, Why, Why? This persistence leads us deeper down the rabbit hole, bringing us face-to-face with that theoretical giant himself: inflammation.
Next Week: Part 3 & The Giant, Inflammation
The information on this site is not meant to diagnose or treat, but rather to provide perspective. Please refer to your medical practitioner before changing or stopping any medication.
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