“Everything should be made as simple as possible, but not simpler.” – Albert Einstein
The fields of science, health, and medicine have a tricky problem on their hands when it comes to getting information across to the general public. Information must be simplified enough so that the individual can understand it, but not simplified too far, such that the information is lost. Unfortunately for much information regarding health choices, often, by the end of this process, the information received has been so simplified that the final message bears very little resemblance to the biological process that actually occurs in our bodies.
Today I plan to decode the misinformation surrounding atherosclerosis. Atherosclerosis is a complex process composed of numerous molecular interactions. Unfortunately it has been simplified down to a couple buzzwords, such that the entire process has been lost, and health choices aimed at preventing atherosclerosis often end up backfiring. To do this, we have to learn about the lipid system in our bodies, and how it relates to health functioning, as well as how it contributes to cardiovascular disease.
As the nation’s number one killer, cardiovascular disease should be at the forefront of our efforts to figure out. Fortunately, it is. Armies of doctors, scientists, and engineers are working to find solutions to this problem. Unfortunately, this isn’t going so well, because heart disease is still responsible for about 1/3 of all deaths, nationally. The problem is that, while medical advancements have done wonders to extend the life of those that do suffer from heart disease, we’ve really done very little to address the actual causes. Personally, I think we can do better.
In this article I wish to do two things:
1. Express my thoughts on why our efforts to reduce cardiovascular disease are failing.
2. Teach you, the individual, what is really going on to clog your arteries so that you are equipped to fight off our number one killer.
As with the entire spectrum of chronic disease, it comes down to lifestyle factors. We all know this – if we could just eat healthy diets and exercise properly then most of these cases would disappear. The question, though, is what does it require to be healthy, and how do we get ourselves to get there?
In my opinion, fixing this problem means getting the general public to understand the progression of atherosclerosis, along with the choices that cause the progression of the disease, and of course, getting the motivation to do something about it.
The progression of atherosclerosis understood by the general public is incredibly simplified, such that it has created a very flawed perspective on what causes the disease. This article is going to be technical, but I will do my best to simplify an incredibly complex topic. Don’t wirry about absorbing all of the technical details. As long as you come away from this article with an understanding of how the lipid transport system is so much more than cholesterol, LDL, and HDL, then I will have done my job.
A Lesson on the Lipid Transport System
Have you ever stopped to wonder how everything gets shipped around your body? All the nutrients, energy, and other resources that individual cells need to maintain proper functioning – where do they come from? If you know a little bit about biology, you know that the answer is the blood. Some molecules (i.e. water soluble molecules) are directly mixed in with the blood, which carries them where they need to go. But many of the resources the body needs are not soluble in water. Therefore they need some sort of transportation device to take them where they need to go, sort of like a boat to ship them around. This transportation device would be absolutely crucial for proper functioning throughout the body, as its cargo contains the resources that the body needs for basic functioning. Furthermore, any damage to the boat or the cargo would send dangerous reverberations throughout the entire system. The repercussions would be disastrous.
Unfortunately this is not common knowledge, and even worse than that, it seems to be a rather well-kept secret, such that the typical individual has no idea how any component of this system works, let alone the big picture. This shouldn’t be a problem, as knowledge of how our body works is not a pre-requisite for it to function properly. However, we do have a problem, because our oversimplified version of this system leads to health choices that put both the cargo and the boat in a risky state.
My goal is to fix that.
To understand atherosclerosis we need to discuss the lipid system, an extremely important system in your body, one that has been forgotten and has lost respect, despite it being one of the key processes keeping you alive and well.
For the past few decades, up through the present time, what you hear on the news and what you hear from your doctors all revolve around a few terms: cholesterol, LDL, and HDL. Out of all of these, LDL is the main villain from today’s perspective, as it is literally nicknamed “bad cholesterol.” According to mainstream knowledge, LDL is the ultimate evil particle wreaking health on the body, and as the logic goes, anything that raises levels of LDL should absolutely be eliminated. The truth is, the lipid system is absolutely crucial for healthy functioning, and LDL is a main component working to distribute important molecules throughout the body.
Listen closely, because this is important: Yes, LDL has some inherent detrimental properties, resulting in the build-up of plaque in arteries – but it is part of an incredibly important system. Molecules that increase LDL may be dangerous because LDL can be dangerous, BUT most of these molecules play other beneficial roles, and therefore it is very dangerous to jump straight to advising cutting out these molecules based solely on this one property. Most importantly, LDL is an important particle that plays a crucial role in healthy functioning, so labeling it as an evil, disease-causing particle is not only wrong but even dangerous.
A quick note on terminology. Lipids are simply the general term for fat and oil. I will use the term “lipid” throughout this article, so if this confuses you, just think “fat” when you read “lipid.” Another term is triglyceride, which is how lipids are stored and transported in the body (3 lipids bonded to a glycerol molecule). Another important term is the lipoprotein – this breaks down into “lipid protein,” because it is made of lipids and a protein molecule, whose job is to keep the particle intact. You know the terms LDL and HDL – these are actually different types of lipoproteins: LDL = low density lipoprotein; HDL = high density lipoprotein. LDL and HDL are particles containing different molecules, cholesterol being only one of them. Since they contain cholesterol, and there has been much research examining the cholesterol in LDL, the term “LDL cholesterol” has arisen. This should not be confused with LDL, which is a particle. LDL cholesterol (LDL-C) is the amount of the cholesterol residing in the LDL particles. If you’re confused, don’t worry, I’ll get into a more specific description of the particles soon.
To begin, we first need a brief lesson on lipids themselves, including how the body stores them and how the body uses them. Lipids are one of the body’s energy sources. The body uses glucose, from carbohydrates, as its quick energy, but it can only store around 2,000 calories of it. However it has an unlimited storage of fat, which is the form in which the body stores both carbohydrates and fat. Eat too much carbohydrate and it gets stored just like fat does – as fat.
Bodies store this fat as triglycerides – these are just 3 lipid molecules bound to a glycerol backbone. When the individual lipids are not bound, they are called free fatty acids. An important thing to remember is that fat is not soluble in water. Think about when you mix oil and water in your daily life, such as while cooking, and droplets of oil form. When we consume any sort of lipid, and it later gets digested in the gut and transported throughout the body, that oil forms droplets in the water-based solutions in our bodies, like the blood and digestive juices. We need to be able to transport these lipids around, so nature designed us an incredible mechanism to do so: lipoproteins.
Now the main process itself is very straightforward. Special particles, called lipoproteins, pick up the lipid cargo and ship it to where it needs to go in the body. These lipoproteins know what to do, such as where to drop off some cargo, based on signaling proteins throughout the body. For example, if a lipoprotein is traveling by a muscle that has the specific signaling proteins expressed, then the lipoprotein will bind to these proteins, that muscle cell will welcome the lipoprotein into the cell, and it will then drop its cargo, so that the cell can use it for whatever function it needed. The lipoprotein will then continue on its way, to either drop off more cargo elsewhere, or otherwise be recycled in the liver. For example, if a cell is in need of extra cholesterol, to make hormones or repair a damaged membrane, then it will express receptors for LDL, allowing LDL to bind to the cell and drop off cholesterol.
Lipoproteins are mostly made by the liver, come in many different sizes, and are classified by their density. The lowest density particles, the largest ones filled up with the most lipids, are the very-low density lipoprotiens (VLDL). Other forms are low-density lipoproteins (LDL) and high-density lipoprotein (HDL). One other lipoprotein, called a chylomicron, is made in the gut and transports fats from the gut to the body.
Three main molecules make up these particles. The main cargo is the triglycerides, which all cells all over the body need for a number of reasons, such as for energy, structural functions, or to make other lipid-based molecules. Cholesterol is the second main component of these particles, which is a second crucial piece of cargo, because the body uses cholesterol for an incredible number of functions (e.g. hormones and cell structure integrity). Finally, a protein keeps the particle together. Again, since these particles are made up of lipids (triglycerides) and a protein, they get the simple name, lipoprotein.
Cross section of a lipoprotein, containing cholesterol and triglycerides, bundled up in a lipid coating by an apoprotein.
There are two main starting points for this system – the gut and the liver. When we consume lipids, our bodies create chylomicrons, and these particles ship lipids from the gut around the body. The liver also makes its own triglycerides from carbohydrates. Once these homemade lipids are created, the liver makes its own particle, VLDL, and the homemade lipids, including triglycerides and cholesterol, get shipped around the body in these particles. When these particles have fulfilled their duties, they head back to the liver for recycling.
As the triglycerides empty from the VLDL particles, the VLDL becomes smaller and denser. When the system works properly, the VLDL gets converted to IDL (intermediate density), then into LDL, and the LDL gets recycled by the liver. This is essential for the triglycerides to get shipped around the body to where they need to go, while the LDL particles become smaller and denser until they are recycled.
VLDL —(loss of triglycerides)—> IDL —(loss of triglycerides)—-> LDL
The liver creates VLDL particles to ship lipids throughout the body. As VLDL loses cargo, it becomes ILDL, and later LDL. The cycle is completed when LDL is recycled by the liver.
Now sometimes when these particles are traveling around, they encounter various situations. One situation may be a damaged vein or artery. These particles have a secondary job, and that is to patch up these holes. To do this the particle unloads some cholesterol, making a sort of band aid to patch up the hole, and then continues on its way. Please note here that the particle was not doing an evil deed – it was actually repairing the body! There was a wound that needed bandaging, so it did so using the materials that were given to it. And there is no need to worry, because there is another particle, HDL, that will come along later once the wound has healed, and it will pick up that cholesterol so it can be used elsewhere.
Let’s recap: Triglycerides get shipped around the body in VLDL, and as this cargo gets unloaded the particle shrinks, until it eventually becomes LDL and gets recycled by the liver. A secondary function of these particles is to repair wounds it comes across by making cholesterol bandages. HDL will later come through once this wound heals and pick up the cholesterol. Note that everything up through now is well-known. It is textbook material that has been around for decades.
Now we know that this process gets more complicated, because obviously this system doesn’t always work so well. Clearly the process goes awry, which leads to a number of problems, and of primary interest is heart attacks. To understand the rest of the process, we are going to have a get a bit more technical. This is also where debate comes into the picture.
To discuss the rest of the process, let’s talk about everything that can go wrong.
Damage to the Lipid Transport System
The following are different methods by which the lipid transport system can go awry, resulting in the progression of atherosclerosis.
1. Failure to Recycle LDL
One of the main causes of harm is when LDL can’t get recycled by the liver. This may occur if the receptor on the liver that recognizes this particle gets blocked. If the particle can’t inform the liver that it needs to be let in, then the liver obviously can’t recycle it. This may also occur if the liver is at full capacity. If the liver already has too many triglycerides to deal with, it won’t be able to let the LDL back in. In either of these cases, the LDL then has no other choice than to continue through the bloodstream.
As LDL flows along through the bloodstream, it continues to lose its cargo, which makes it smaller, and denser. When it can’t get recycled by the liver, it continues circulating, dropping off cargo, and getting even smaller and denser. This process is amplified because as the particle gets smaller and denser, it has a lower chance of getting recognized by the liver. At this point let’s start calling it by its name, sdLDL, for small, dense, LDL. sdLDL is doomed to circulate through the blood until it gets consumed by the immune system.
2. Too Much Cargo
Another important problem to discuss starts with too many triglycerides that require shipment, via VLDL. Lipoproteins were designed such that they can only handle so much cargo, which is probably based on how much we ate while we evolved. So when our liver is filled with too many triglycerides, this system gets overloaded, leading to numerous consequences.
The presence of too many triglycerides results in the formation of many, large VLDL particles (2,7). To make large VLDL particles carry all these triglycerides, the liver must use extra cholesterol. As these special, large particles make their way through the body dumping triglycerides, they, like before, get smaller and smaller, until eventually they are relatively depleted of triglycerides. At this point, the particles are smaller, but they contain a much higher proportion of cholesterol. Because cholesterol is much denser than triglycerides, these particles end up being much denser. Sound familiar? This is another mechanism by which these sdLDL particles may form (7).
A second problem arises from the formation of too many triglycerides. To understand this we have to talk a little about HDL. We know HDL as the good guys. These are the particles that go around scavenging for cholesterol to pick up. Well these HDL particles are really friendly, and want to help of their VLDL and LDL friends, so when they see that these particles are overfilled with triglycerides, they take some of those triglycerides, and give them some cholesterol in return. But this isn’t good for the HDL, and actually causes destruction of these particles, resulting in lower levels of HDL (what we know to be a bad thing). Now this same exchange that occurs between HDL and VLDL can occur between LDL and VLDL. The LDL can also exchange triglycerides for cholesterol, which is a second mechanism for which LDL gets smaller (loses triglycerides) and denser (gains cholesterol), morphing into sdLDL (7).
In summary, high levels of triglycerides cause an overproduction of VLDL, which in turn causes low levels of HDL and high levels of sdLDL.
3. Dangerous Cargo
The third problem involves not the quantity of triglycerides, but the quality. Remember, these particles are basically made up of a lot of triglycerides, some cholesterol, and a protein. If the triglycerides themselves are damaged or reactive, they can do a lot of damage to the particles themselves, particularly to the triglycerides and protein.
Imagine a boat shipping cargo across the ocean. Now imagine that there is a variety of goods being shipped Some are perfectly benign, like bricks. However, some of that cargo is a little more dangerous, like gasoline, which is perfectly fine if left in a stable environment. Now imagine being told that there are new orders that dictate the best way to ship this cargo is to ignite it, then ship it across the ocean. How do you think any of these goods on that boat, along with the boat itself, is going to do?
Fatty acids (bound up as a triglyceride), the LDL’s cargo, comes in a variety of forms. Saturated fatty acids are perfectly stable because they are completely saturated with hydrogen atoms and therefore won’t react with other molecules. However, unsaturated fatty acids are greatly unstable because they readily react with other molecules. Unsaturated fatty acids are so named because they have at least one double-bond. You can think of a double bond as an opportunity to react with other molecules, and when an unfavorable reaction does occur, it leaves the unsaturated fatty acid in a state where it can react with other fatty acids and other molecules.
In chemical terms, this reaction is called oxidization, which is the stripping away of electrons. It’s the same term used for describing other chemical processes, such as rusting, which occurs when electrons are stripped away from iron. When discussed in the context of the lipid cycle, oxidization is a very dangerous word. Without getting too technical, reactive triglycerides are arguably one of the most dangerous problems that can go wrong. Reactive triglycerides can do damage to the particles themselves, which could lead to damaged signaling and the inability for these particles to drop off triglycerides where they are needed, and cause them to be unrecognizable by the liver, so they can’t be recycled. Remember from above that when the LDL can’t be recycled, it eventually turns into the dangerous sdLDL particles.
To summarize, problems arise in the lipid system when too many particles are produced, due to too many triglycerides accumulating in the liver. This is not so much a problem arising from too much fat consumption, but rather too much carbohydrate consumption, particularly sugar consumption (3). This overproduction of VLDL leads to sdLDL (2,7), the most dangerous particles (1,5). In addition, reactive triglycerides can damage the particles, impairing their ability to deliver cargo or be recycled, causing the formation of sdLDL and oxidized particles.
How do Damaged Lipoproteins cause Atherosclerosis
Now that you understand how the lipid system can get damaged, we can talk about how exactly these damaged particles cause problems like atherosclerosis and heart attacks.
In case you had forgotten, let me remind you that when this system functions properly, the particles circulate through the vessels, dropping off triglycerides as they go and occasionally dropping off cholesterol to repair damage in the vessel wall. Remember, liproteins deliver cholesterol to damaged arteries to, in a sense, bandage up the wounds. Again, this is a good thing, because gaping wounds in arteries lead to a leakage of toxic substances through the artery wall. Also, this is not a huge problem, because HDL will come around later to pick up the cholesterol one the wound is healed.
This mechanism – dropping off cholesterol, is not the culprit for heart disease. In the situation above, where LDL drops off cholesterol, the particle is just doing its job, just like it has been doing for millions of years, when heart disease wasn’t a problem.
The fault lies somewhere else – with the LDL particle getting stuck in the lining of the artery and getting attacked by the immune system. While the development of arterial plaques is complicated, it can be broken down to a few key ideas, which will be the focus here.
To summarize:
The process begins when damage is done to the artery wall, creating a gap in the normally sealed wall. This allows for LDL particles to slip through into the intima, the space beneath the outer layer of cells. Sometimes, an LDL particle is retained in the lining of the artery wall, due to binding to molecules called proteoglycans. Once an LDL particle gets suck in the lining of the artery wall, a cascade of immune and inflammatory responses occur. Note a key thing here – smaller, denser particles are more likely to find their way into the lining of the artery, and are also more likely to stick around because of a stronger interaction with proteoglycans (Packard). However, any LDL particle is capable of finding its way into the artery wall and playing a role in the formation of the plaque.
This process is combined with a secondary process that occurs due to the damaged artery wall: inflammation. The body’s inflammatory response is initiated whenever the body senses damage to tissue, such as a damaged artery wall. This response includes a cascade of particles which come to clean up anything it thinks might be a danger to the body. It also involves a cascade of other molecules (e.g. cytokines) which amplify the inflammatory signal.
The key component of the combination of these processes is engulfment of the LDL particle by macrophages. Macrophages are one of the main cells of the immune system, whose job is to scoop up particles that it recognizes as dangerous to the body. Well, LDL particles aren’t supposed to be stuck in the wall of the artery, so macrophages are recruited to scoop them up. Moreover, if these particles are damaged (i.e. oxidized), then the macrophages are absolutely going to want to scoop them up. These macrophages, filled up with LDL and all the lipids contained within, are referred to as foam cells. Clusters of these foam cells are the cause of the fatty streaks on the wall of the artery.
The final step is for the immune system to initiate growth of smooth muscle cells to cover up this fatty streak. This creates a cap for the plaque, with all the lipids and debris contained within. The finished product is a stable plaque, resulting in a narrowing of the artery, yet a healed up wound. It is important to note that these plaques, in their stable state, are not very dangerous. While they may disrupt blood flow that can result in further problems, the body is good at adapting, even creating new vessels to circumvent arteries to narrow for adequate blood flow (cite).
However, sometimes the structure of this cap is unstable or weakened by chemical reactions or shear stresses When this occurs it can lead to the possibility of rupture of the plaque. If the body didn’t have the materials (e.g. collagen) to create a strong cap, then the plaque is much more likely to rupture. This is what you don’t want to happen. This is what most often causes heart attacks.
When the plaque ruptures it sends all of that debris into the bloodstream, which is then free to wreak all sorts of havoc. The most dangerous result is the formation of a blood clot, resulting in a blocked artery, causing a heart attack. This blocking of the artery due to a ruptured plaque is the final step causing a heart attack.
How to avoid atherosclerosis
Now that you have a basic idea of the overall process, let’s examine the different ways that this rupturing can be avoided. I’ll dive into some specific points to address how the development of a plaque can be affected by our choices. However, I will keep each point very brief, as all we need is a general idea of each of these. There is plenty of information on each point that is just a google search away, which I encourage you to examine further if you feel the need.
1. Avoid damage to the artery wall
First, you can avoid the initial damage done to the artery wall. This is key because if no damage is done in the first place, the rest of the process won’t matter, because it can’t occur! Let’s look at how damage to the artery wall can be avoided. A few ways to do this are by avoiding systemic inflammation, oxidization, and high blood glucose levels.
Systemic Inflammation
If the body is inflamed, due to any sort of stressor (e.g. lifestyle stresses, smoking, overexercising, or poor dietary choices), then the vessels can become inflamed. Inflammation of the vessels allows for gaps in the arterial lining, allowing LDL to slip through and initiate a plaque.
To reduce the risk of plaque formation, we could work on lowering systemic inflammation. This could involve changing lifestyle factors, such as avoiding smoking, getting adequate sleep, and avoiding over-stressful exercise patterns. Additionally, this could involve avoiding industrial foods, such as vegetable oils and processed meats, and by eating more antioxidant-rich foods (i.e. plants).
Oxidized Particles
Oxidized particles can react with the lining of the artery wall, causing their own damage to the wall. Particles become oxidized when they react with free radicals. Also, if you remember from the discussion above, consumption of toxic lipids can cause oxidization of the particle containing them. For example, the process of creating vegetable oil, which requires unstable polyunsaturated fats to go through an intense process including high heat and strong chemicals, results in a mixture of highly reactive lipids. When we consume these toxic lipids, by consuming vegetable oil, these oxidized lipids then react with the particles, creating a reactive particle that can damage your artery wall.
A great way to get rid of free radicals is by increasing antioxidants, which again, is best done by eating lots of whole plant foods and limiting industrial foods.
High Blood Glucose Levels
High blood glucose levels are a chief cause of the destruction of the body. One general method of damage is the toxic nature of high levels of glucose, which is an additional method of inducing inflammation in the arteries. One specific method by which high blood glucose levels can lead to atherosclerosis is via the activation of clotting factors, leading to tiny blood clots (4). These blood clots can cause a restriction of blood flow to the artery wall, resulting in the death of artery wall tissue, and creating an opening for LDL.
2. Modification of Plaque Development
A second method for avoiding atherosclerosis is by modifying the development of the plaque itself. You could attempt to intervene to ensure that either:
- a stable plaque develops, by providing our body with nutrients it needs to create strong cap (e.g. collagen or its building blocks)
- the plaque gets cleaned up properly, which is the work of HDL
3. Lower LDL
Or third, we could attempt to decrease the amount of LDL getting into the wall. We can do this in a few different ways:
Particle Size
Smaller, denser LDL particles increase your risk of heart attack, compared to larger LDL particles (5). If you can increase the size and buoyancy of your LDL particles, then they have a lower chance of sneaking through the artery wall. This can be done in a number of ways, but most significantly by eating more whole plants foods. https://nutritionfacts.org/video/avocados-lower-small-dense-ldl-cholesterol/
When we move away from industrial foods that overload the liver with too many carbohydrates and toxic oils, then the liver can properly create healthy levels of VLDL, while being fully capable of recycling LDL particles. When properly sized VLDL particles are formed, and LDL particles are recycled at the proper rate, then sdLDL particles don’t appear to form (1).
Tackling the size of LDL particles definitely appears to improve risk for heart disease, but don’t fall into the trap of thinking that LDL size is all that matters. There is a common belief that if you have large, fluffy LDL, then you don’t have to worry about plaques forming, which is untrue (5). Yes, increasing size of particles helps, but at the end of the day, having high levels of LDL particles still increases chances of a heart attack (5). Remember this: larger LDL particles can still find their way into the artery wall – they just aren’t as quite as capable as smaller, denser ones.
2. Amount of LDL
Therefore, it is important to think about decreasing the LDL. If high levels of LDL particles strongly correlate with heart disease, which they do, then it is important to get those levels down.
Here’s where things get completely mixed up, so pay close attention. When we talk about lowering LDL, there are two different things we’re talking about: particle count and particle number.
Generally, when LDL is discussed, people talk about LDL cholesterol. When you’re given a statin because of high LDL, it is because statins lower the amount of cholesterol available, thus decreasing the amount of cholesterol in your LDL.
However, when it comes to what really matters for promoting atherosclerosis, it is the number of LDL particles, not the cholesterol content in them (5,6).
Lower Particle count:
LDL particle count is, once again, a great predictor of heart disease (5,6). This makes sense because higher levels of LDL particles means there is more opportunity for particles to sneak into the artery wall.
Remember from the discussion above that more VLDL particles are made when high levels of triglycerides require vessels for shipment out through the body. High levels of triglycerides mean high levels of LDL particles. Also remember that when these overly-stuffed particles are made, they have a higher chance of becoming damaged, making their chances of being recycled decrease.
Here is the main takeaway: to lower levels of LDL particles, avoid anything that leads to high triglycerides, because high triglycerides require high levels of VLDL particles, leading to the formation of more LDL particles.
Lower LDL Cholesterol
Now I’ll talk about the other form of “lowering LDL” – by lowering the cholesterol levels contained in LDL. Note that this is the chosen method society has taken. It is what we hear about on the news, in the doctor’s office, and everywhere else for that matter. Most significantly, it is what 20% of those over age 40 take a daily pill to prevent. When it comes to atherosclerosis, it is all about the LDL cholesterol – or so it would seem. We have chosen to focus on the need to lower LDL cholesterol to solve our heart disease problem, and from what I’ve seen, this has been a very dangerous choice.
Note that it wasn’t a bad idea to start here. LDL-C is a likely culprit, as cholesterol is the main component making up a plaque, so lowering it is a logical answer to solving heart disease. The question though, is how did it turn out?
Let’s look at the methods used to lower LDL cholesterol
1. First off, there’s the good old-fashioned dietary advice that everyone is familiar with: avoid saturated fat. What happens when you eat less saturated fat? Yes, LDL-C goes down. But the important question is, what did we do to get there?
Well, we need fat, so if we ditch the butter, then we need something to substitute it. And what is a better substitute than polyunsaturated fats like vegetable oils, which not only decrease LDL but also increase HDL. What a great idea!
Except, from what we learned earlier, what actually happens when we substitute butter, a nutritious, stable fat, for vegetable oil, a toxic polyunsaturated fat? Remember my boat example from earlier: there is a cargo ship shipping goods like brick and gasoline, which can both be kept safe, as long as nothing is ignited. You can think of cholesterol as brick and triglycerides as gasoline. If you ignite the brick, nothing will happen, but if you ignite the gasoline, well, you get the picture.
When you add toxic fats, like vegetable oil, to the mix, it is exactly like adding in ignited gasoline. Vegetable oil is made of fragile polyunsaturated lipids, which have been through harsh processing conditions, rendering them oxidized and primed for starting a reaction. By lowering saturated fat and increasing consumption of vegetable oil, you take out a stable lipid, and add in already ignited fuel, primed to start a fire.
What else happens when we eat less saturated fat? Well the advice over the past several decades has been to eat less saturated fat and eat more carbs.
Well, it turns out that the easiest way to disrupt your entire lipid profile is to consume excess carbohydrate. Remember this, as it is one of my main points – if you haven’t let it sink in yet, do that now. Excess carbohydrate has to be stored, and therefore it gets converted by the liver to triglycerides. High levels of triglycerides cause overproduction of VLDL, leading to high levels of LDL, particularly sdLDL.
So we see that the seemingly intelligent idea to cut back on saturated fat really just led to consumption of more vegetable oils, leading to more oxidization and damage to the particles, and more carbohydrate, which disrupted the entire lipid profile.
Now it’s important to note that this doesn’t have to be the case. We could switch from a diet higher in saturated fat to one of whole plant foods. This side-steps the problems of too much vegetable oil and too much carbohydrate. Undamaged polyunsaturated fats, ones that come from whole foods, are crucial for healthy functioning, and carbohydrate in low amounts are an important fuel source. The key is that these come in reasonable amounts from whole food sources.
So if you are taking the advice to eat more carbohydrate by eating more whole plant foods, then you’re on the right track to good health! Unfortunately though, this is not the common practice. Because the concern is only on the saturated fat, it is too common to make poor dietary choices like consuming more vegetable oils and processed carbs to avoid it.
2. Statins
To end this article, I’ll briefly talk about the easiest way to lower cholesterol. And, well, since we love to choose the easiest way out, it is the most widely used method of lowering cholesterol – the statin.
Simply put, statins lower cholesterol by blocking the synthesis of the molecule. If cholesterol can’t be synthesized, levels of it will obviously drop, and therefore statins become a wonder drug.
But here’s the interesting thing – they don’t really work for decreasing risk of heart attack. Clinical trials consistently show that statins only reduce the risk of heart attack by 1-2%. I don’t know about you, but when we’re talking about lives, that number doesn’t sound so great.
However, 1-2% can end up being a lot of people, especially when millions of people take them. So proponents of statins will argue that it is worth giving the drug to millions of people, even if it only saves 1 or 2 out of every 100 of them. The question, though, is is it worth it? Does taking a statin have any draw-backs? Any side effects that we should worry about?
You probably already know the answer, but before I get into it, just think about it for a moment. Statins decrease the amount of cholesterol available for our bodies. Now cholesterol is a very important molecule. It is part of the cell membrane, so the integrity of every single cell in your body relies on this molecule. All hormones in the body are made of cholesterol, so the signaling capabilities are highly reliant on it. I’ll stop with these two before I get carried away, because I think it’s enough for you to get the picture. Cholesterol is an essential molecule that numerous structures and functions of the body rely on.
So when we take a drug to decrease its synthesis, then, of course, it is going to have widespread effects. And it does.
For example, statins have been shown to cause insulin resistance (8,9), cause muscle pain, liver damage, and memory loss.
All for a lousy percentage point.
It gets even worse, because our efforts to lower LDL cholesterol may be all for naught. Many studies (5,6) have been conducted over the past years showing that LDL cholesterol is not even correlated with heart disease. A recent analysis (6) of 19 trials, including 30 cohorts, found, “either a lack of an association or an inverse association between LDL-C and both all-cause and CV mortality.” More specifically, they found:
“Inverse association between all-cause mortality and LDL-C was seen in 16 cohorts (in 14 with statistical significance) representing 92% of the number of participants, where this association was recorded. In the rest, no association was found. In two cohorts, CV mortality was highest in the lowest LDL-C quartile and with statistical significance.”
Now I find this interesting because the common method to address heart disease is to lower LDL-C, but from this analysis of the literature, it appears that lower levels of LDL-C don’t correlate with higher levels of heart disease. Moreover, it was demonstrated that in 92% of the participants, lower levels of LDL-C correlated with a higher risk of death!
So here we are, putting all this energy into lowering LDL-C, which actually might not even matter! But wait, it does matter, because the methods used to lower LDL-C are actually causing more damage. Why, because cholesterol is a crucial molecule for healthy functioning, both within every single cell in your body, along with communication throughout the entire body. If you get rid of cholesterol, you get rid of the body’s ability to create healthy, functioning cells.
Maybe this is why our rates of heart disease have been going nowhere? Maybe this is why heart disease is still our number one cause of death.
As we discussed, LDL clearly plays a role. The problem is how we address the LDL problem, and addressing it by doing all we can to lower LDL-C clearly isn’t working. Rather, if we focus our efforts on some of the direct causes of the disease progression, maybe we can get somewhere.
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“Everything should be made as simple as possible, but not simpler.”
I began this article with this quote by the great Albert Einstein. It is a theme that seems to continuously appear as we continue to work through previous mistakes in the health field.
If I know one thing, it is that biology is extremely complicated. Once again, we have a case where we tried to simplify it down to a handful of molecules (mainly, cholesterol and LDL). But biology isn’t ruled by a handful of molecules. It is run through complex systems with numerous molecular systems working together.
It isn’t a bad thing to simplify processes down in an attempt to understand it. It isn’t a bad thing to try to target one suspecting culprit. But this is one case where we were clearly wrong.
Our efforts focusing on LDL cholesterol do not prevent heart attacks. These methods even often lead to drugs and dietary choices that actually make matters worse.
It’s about time to change our perspectives on what really causes heart disease, so we can get around to actually saving lives.
Disclaimer: As always, I am not a doctor, and make no recommendations to stop taking any medicine. The information contained in this article should be used only as information to be used at your own discretion. Any concerns should be discussed with a trusted doctor before making any major decisions that could impact your health.
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