In this, the third and final post in the series, ‘What You Really Need to Know About Cholesterol’, I’ll be discussing HDL cholesterol, VLDL cholesterol, and how we can delay the onset of atherosclerosis. If you haven’t yet read part 1, or part 2, consider giving them a read, as this post is a continuation of those. In part 1, I discussed the cholesterol basics, and in part 2, I described how LDL cholesterol causes atherosclerosis.
The most important take away from part 1, part 2, and indeed this entire series on cholesterol is the importance of measuring LDL-P or total LDL particle count, as opposed to measuring LDL-C, or total serum LDL cholesterol levels, as most conventional cholesterol tests tend to do.
Why is measuring total LDL-P important? Because, it is LDL-P, not LDL-C that determines risk for atherosclerosis. The more LDL particles in circulation, the higher the risk. Two of the largest studies done following the link between cholesterol and atherosclerosis are the MESA trial (Multi-Ethnic Study of Atherosclerosis) and the Framingham study. What these studies show is that the higher the LDL-P, the higher the incidence of atherosclerosis. In particular, when LDL-P is higher compared to LDL-C (LDL-P > LDL-C), the incidence of atherosclerosis (including risk of death) increases. Conversely, when LDL-P is lower compared to LDL-C (LDL-P < LDL-C), the incidence of atherosclerosis (including risk of death) decreases.
What these studies also show us is that LDL-P and LDL-C values don’t predict risk equally. In fact, what they show is that LDL-C is simply not relevant when determining risk. It also shows that a sizable portion of the population will have high total serum levels of LDL (LDL-C) while having little risk of atherosclerosis. Just how many people are put on statins each year due to high LDL-C measurements when they actually have little risk of atherosclerosis should make us all curious.
Perhaps most interesting is that these studies showed that, often, those with the lowest LDL-C levels had the highest risk. In fact, this is highly prevalent among those with metabolic syndrome (a large portion of the United States population), including diabetics and those suffering from insulin resistance. A recent study in the American Journal of Cardiology, showed that, out of 2,000 diabetic patients presented with ideal cholesterol numbers, only 22% were actually in the very low risk range for developing atherosclerosis, and more than a third of the patients were actually at risk. The reason, of course: LDL-P > LDL-C.
Not only is measuring LDL-C levels completely useless in determining the risk of atherosclerosis, but doing so may be dangerous. Not only might some people be put on statins and encouraged to make useless and even harmful lifestyle changes, but others that are at risk may fly under the radar.
But, what about HDL cholesterol? If you have lots of LDL particles, does having lots of HDL particles help? The short answer is, more than likely, yes, especially if LDL-P is high. However, it’s important to note that the raising of HDL cholesterol levels through artificial means has shown no benefit whatsoever. HDL cholesterol particles, in part due to their small size, do an excellent job at cleaning up cholesterol around the artery walls. Notice that I said, HDL cholesterol “particles”. Just like the particle count matters for LDL cholesterol, it also matters for HDL cholesterol. Obviously, the higher the HDL-P, the more arterial scavenging. However, even though HDL cholesterol, like LDL cholesterol, plays an essential role in the body, when it comes to atherosclerosis, LDL cholesterol, specifically LDL-P, is what matters most. After all, higher HDL-P count hasn’t been shown to prevent atherosclerosis. It’s undeniable that it cleans up the LDL debris in our arteries, but as you will remember from part 2, this is a numbers game, and too many LDL particles will overwhelm, not only your HDL cholesterol, but your bodies other defenses as well. LDL-P truly is the be-all and end-all, when it comes to atherosclerosis. Which brings us to the much maligned VLDL cholesterol.
VLDL cholesterol is highly linked to diet. But, don’t jump to any conclusions! It has nothing to do with the cholesterol we eat! What’s at play here is a high intake of carbohydrates that is responsible for excess formation of VLDLs. Moreover, excess carbohydrates, plus excess fat, exacerbates VLDL formation dramatically. If you have been following my blog you know that I have spent a lot of time debunking the myth that saturated fat leads to heart disease. However, in the presence of excess carbohydrates, and even excess calories in general, excess fat can be a contributor to VLDL formation.
The average person can hold about 400 grams of glycogen in his or her liver, and perhaps up to another 150 or so in his or her muscles. Glycogen is essentially the storage version of glucose. When you eat carbohydrates, your body stores the extra sugar as glycogen in the liver and muscles to be used as needed. But, if your liver and muscles are full of glycogen, your body will turn a lot of that excess sugar into triglycerides, and then pack the triglycerides off into a transport vehicle to be used where they are needed around the body. As was discussed in part 1, this transport vehicle is a lipoprotein, and in this case, a very low-density lipoprotein (VLDL). Now, if you’re consuming excess fat at the same time you’re consuming excess carbohydrates, your body will be producing even more VLDLs, since there is more triglycerides that need to be packed away for transport.
It’s important to note that VLDLs contain about 5 times the amount of triglycerides as they do cholesterol. Compare that to a regular LDL particle that has close to 5 times as much cholesterol as triglycerides (See image above). So, where do all of these triglycerides go? Some of them will go to the muscles and other areas of the body to be used as energy, the rest, and probably the majority, will end up in your fat cells as storage. Now, at this point, VLDLs are just serving their natural function, which is delivering excess energy to where it belongs; this would be just fine if we were only eating to excess every once in a while, but such is often not the case. And it’s what happens after all of these VLDLs have delivered their triglyceride load that the real problem occurs.
After VLDLs deliver their triglyceride load, they shrink dramatically and become plain old LDL. That’s right, all of those VLDLs add to your LDL-P count. And these aren’t just any LDLs. Remember, VLDLs are formed mainly due to excess carbohydrate consumption, which means the body didn’t make them because it needed cholesterol, it made them mainly to move excess triglycerides around in the body. If you have excess VLDLs, you are almost certainly at a higher risk for developing atherosclerosis, as you almost certainly have high levels of LDL-P. Once VLDLs lose their triglyceride load and turn into LDLs, they are almost useless. They have very little cholesterol to contribute, so they do a lot of hanging around, so to speak. And when they hang around in your arteries, that’s bad news, as you well know by now.
Not only do these VLDLs turned LDLs increase your LDL-P number, but because these VLDLs are created via the foods we eat, they often oxidize far easier than regular LDLs. For one, having lost all of their triglycerides, when VLDLs turn into LDLs, they are often very small, which makes it easier for them to get stuck in between the spaces of the artery wall. Of course, when it comes to atherosclerosis, particle size matters little, it’s all about particle count. But, when particle count is high the presence of these tiny little VLDLs turned LDLs can spell catastrophe. On top of that, since VLDLs formed in the liver in response to excess food, their lipid layer is often made from polyunsaturated fats. Polyunsaturated fats (PUFAs) are highly unstable and oxidize easily. Over the last 50 years or so, Americans have been eating loads of PUFAs from industrial seed oils, prompted to do so by the “saturated fat is bad” crowd. It’s time for you to replace that tub of margarine with real butter, it may literally increase your life expectancy.
Yes, VLDLs are bad, very bad. But, let’s turn our attention to how we can delay the onset of atherosclerosis.
The older we get the greater our risk for developing atherosclerosis. The main reason is that our arteries have had all the more time to be assaulted by LDL particles. If you are in your 70′s and your LDL-P is in the top 5th percentile, you still have a greater risk of death from atherosclerosis than a 20 year old in the bottom 5th percentile. As we age, our bodies don’t produce or utilize antioxidants as efficiently, and as a result, we are more prone to oxidative assault, be it cancer or atherosclerosis. The older we get the greater our increase in triglycerides in the presence of glucose, as well. In other words, as we age, our bodies can’t handle glucose as efficiently, and this leads to an increase in triglycerides, which translates to more VLDLs, which ultimately means a higher LDL-P.
Even though the cholesterol we eat has little to do with our cholesterol levels, the food we eat often does have an effect. The consumption of high fructose corn syrup, for instance, increases blood levels of triglycerides considerably, which translates into more VLDLs, and hence higher LDL-P. Sure, this all seems repetitive, but some things are worth repeating.
What about saturated fat, does it raise LDL-P?
Perhaps nothing has been more misguided and caused more health problems than the anti-saturated fat crusade of the last half century. This crusade by many in the medical community has changed the diets of Americans dramatically. Over the past 4 or 5 decades Americans have replaced saturated fats, essentially animal products, with industrial seed oils and excess carbohydrates. And no, when I say carbohydrates I don’t mean fruits and vegetables. I mean processed carbs, such as sugar and grains (if you eat grains, you are eating processed carbohydrates). But what about saturated fat and cholesterol?
First, it’s important to understand that saturated fat is actually made up of a number of saturated fatty acids. The most common saturated fatty acids are, palmitic, stearic, lauric, and myristic acid. So, let us look at the complete fatty acid profile of a grass-fed New York strip steak. Around 40% of the fat in a grass-fed New York strip is made up of the monounsaturated fat, oleic acid. This is the same oleic acid that you’ll find in olive oil. That’s right, nearly half the fat in a New York strip steak is made from the same fat that is found in olive oil! 50% of the fat in the New York strip is saturated. However, a third of the saturated fat is of the stearic acid variety. Stearic acid is the same saturated fat found in dark chocolate…this fat is supposed to be good for your blood pressure and has even been associated with high HDL.
There is no evidence that saturated fat leads to heart disease of any kind. You can eat your beef, egg yolks, and shrimp without having to worry about that heart attack. These foods are nutritious and we’ve been eating them for millions of years. It’s the processed grains and industrial seed oils that have entered our diets in the last half century that have been killing us.
So what can we do to delay the onset of atherosclerosis? Avoid HFCS as much as possible, as not only will HFCS raise LDL-P, but most of the time HFCS comes as part of a highly processed meal or snack. Avoiding most added sugar is a must, especially as we age. Your basic table sugar is half fructose and half sucrose, and it also raises triglycerides and LDL-P.
With the exception of whole fruits and vegetables, carbohydrates should be rather limited for those at risk. The average American diet consists of about 50% carbohydrates. Which means the average American is consuming between 300-400 grams of carbohydrates per day. However, when you consider all those who already eat less carbs, that number can easily be between 400-500 grams of carbohydrates per day for many who aren’t cognizant of their intake. Keep in mind that all carbohydrates turn to sugar (glucose) in the blood stream. Not only do these extra carbs incur an insulin response in the body that is responsible for weight gain, they also increases triglyceride levels, and, you guessed it, LDL-P.
So, to sum it up: 1) You should avoid HFCS and added sugar. 2) Be aware of total carbohydrate intake, and limit carbohydrate intake especially if you are at risk.
Sure, there are other things you can do, like exercise, but removing carbohydrates from the diet seems to have the largest impact. In fact, cutting down on the carbohydrates will more than likely increase your metabolic health. And as the Framingham study shows, the worse your metabolic health, the worse your LDL-P.
So, now that we’ve concluded this three part series, I hope you’ve gained a better understanding of cholesterol. Specifically, I hope you’ve realized the importance of total LDL particle count, or LDL-P. Feel free to share your comments or contact me via the contact form or email button as well. If you’d like to look at the MESA trial and Framingham analysis more closely, you can do that here.