I’ve been reading about cholesterol recently and I’ve come to a conclusion: Blaming cholesterol for heart disease is like blaming crime scene investigators for crime.
Imagine the government hired a researcher to look into the reasons behind an increase in crime rates. Every time a crime is reported, this researcher goes to the local area and petitions the local residents for their version of events leading up to and after the crime. After months of collecting data, the researcher starts analysing the data and notices that the one common factor in all accounts is that there are always a lot of crime scene investigators at the scene of a crime just after it has happened. The logical conclusion: Crime scene investigators cause crime. With great excitement, the researcher presents his findings to the government who respond by reducing the number of CSIs within the police force. Of course, we know that CSIs don’t cause crimes (at least I don’t think so), and in fact the action taken would have the very opposite effect to the one desired. A reduction in CSIs would mean less solved crime which would lead to an increase in the crime rate.
This is the situation we are in with cholesterol. The above example is of course ridiculous, but that is because we can easily see the other factors at work in crime and crime prevention. This has not always been the case with cholesterol.
Back in the day (about 1950), when cholesterol came under suspicion of causing heart disease, the only measurements available at the time were of total cholesterol (TC). It wasn’t until a few years later that cholesterol was divided into its sub-groups of HDL (high density lipoprotein), LDL (low density lipoprotein), IDL (intermediary density lipoprotein), VLDL (very low density lipoprotein) and chylomicrons. However, in the meantime, very expensive studies, investigating the effects of TC and saturated fat on heart disease had begun and by the time this new research was presented the agencies responsible (NIH, AHA etc) couldn’t change these studies or afford to start new ones. These studies were largely inconclusive, but this didn’t stop the American government making health care policy. The US government had to do something as heart disease was on the rise, and in the light of disappointing evidence it went with what it thought would be the best approach. Lower intake of saturated fats and increase the intake of carbohydrates. The main idea being that there probably isn’t any harm in recommending A to prevent B, so we’ll recommend A. Unfortunately there has been a lot of harm done.
The following is an overly simplified view of cholesterol and heart disease (as that’s how I understand it). If you want to read the facts for yourself from someone who is actually qualified, then I’d recommend a series of blog posts on cholesterol written by Peter Attia MD on his excellent blog, The Eating Academy. The first blog in the series can be found here. You can also read about the history behind this in the excellent book The Diet Delusion (Good calories, bad calories in the US) by Gary Taubes.
Cholesterol (shown above courtesy of wikipedia) is one of several fat like substances that circulate in the blood called lipids, other lipids include free fatty acids and triglycerides. Cholesterol (along with saturated fat) is essential for life as it is used within the construction of cell membranes in our body. This is a good thing. No cholesterol = no life. Also, the amount of cholesterol in our body is very finely tuned and dietary cholesterol has very little or no effect on blood serum cholesterol.
As cholesterol is a fatty substance, it repels water so it can’t travel in the blood stream by itself (try mixing olive oil with water), so it needs to be carried to its destination. This is where the lipoproteins come in. These lipoproteins (HDL, LDL etc) carry cholesterol within the blood stream, think of them like a cholesterol train. In my oversimplified world the LDL train takes the cholesterol to work, the HDL train brings it back home again. This is why having low LDL cholesterol (LDL-C) and high HDL-C is considered a good thing.
So surely we should all be eating diets that lower our LDL-C and raise our HDL-C. Well, not so fast.
It turns out it’s not the cholesterol that causes the problem (in this case, heart disease), but rather it’s the LDL particles themselves. The LDL particles can make their way into the arterial wall and when they do this triggers an immune and inflammation response which can result in the build up of plaques. Bad news. The more LDL particles (LDL-P) you have, the greater risk you have of developing heart disease. Depending on the circumstances, these LDL particles can carry different amounts of cholesterol, so it’s possible that someone with a high LDL-C has a low risk of heart disease because they have low LDL-P and someone with a low LDL-C has a high risk of heart disease because they have high LDL-P.
Shown below is a graph taken from a paper published in the Journal of Clinical Lipidology in 2011.
This graph is plotting the cumulative incidence of cardiovascular events for groups with concordant or discordant levels of LDL-C and LDL-P. As you can see, the greater the LDL-P, the greater the occurences, the lower the LDL-P, the lower the occurences. You’ll also notice that those with higher LDL-P had a lower LDL-C than those with concordant LDL-C and LDL-P.
So what determines how many LDL particles are produced and how much cholesterol they carry? Genetics obviously comes into it, but the major controlling factor of risk is our diet.
When we eat a carbohydrate rich meal, this raises our blood glucose levels. In response, the liver takes some of this glucose and turns it into fat i.e. triglycerides – essentially an oil droplet. These triglycerides are fused with an apo B protein and cholesterol to form a lipoprotein. This resulting lipoprotein is of the VLDL variety as the triglycerides are lighter than either the apo B protein or the cholesterol. The liver secretes this triglyceride rich VLDL into the blood stream where it starts depositing the triglycerides around the body. As the triglyceride content of the VLDL reduces, it transitions into a small dense LDL particle. The rate at which triglycerides accumulate in the liver dictates the amount of triglycerides loaded onto the lipoprotein. Diets that are restricted in calories or carbohydrates produce fewer triglycerides resulting in lipoproteins that are less dense than LDL but more dense than VLDL – IDL. These IDL particles, as they deposit triglycerides turn into large fluffy LDL particles. The more triglycerides, the more small dense LDL particles, the less triglycerides then fewer large fluffy LDL particles.
There has been a lot of discussion about whether small dense LDL particles present a greater risk than large fluffy LDL particles, but the greatest predictor of risk is the number of LDL particles rather than their size.
From studies it has been show that eating sugar increases levels of triglycerides, VLDL and apo B. Removing sugar from the diet reverses this affect. Also, eating fat in the absence of sugar and starches does not raise triglycerides or other bio-markers for cardiovascular disease.
So when it comes down to it, the best diet for the prevention of heart disease is one that restricts sugar and keeps blood glucose low, which will in turn keep the levels of triglycerides low, i.e. a low carb/high fat diet.