One of the biggest hesitations people have around starting a ketogenic diet is a concern that the diet will give you dangerously high cholesterol. Or, more specifically, that eating a high-fat diet will increase your serum cholesterol and, in turn, increase your risk for developing heart disease. This article separates the fact from the fiction, explaining why this concern is often incorrect and how eating a high-fat diet may actually decrease your bad cholesterol and risk for various types of heart disease.
Cholesterol is made of a few types of fatty structures made by the body and found in many foods. It’s essential to proper homeostasis (normal functioning of the human body and the cellular constructs within), because the body employs it for a number of natural functions; it’s used to create cell walls, synthesize vitamin D, and to help produce a number of different hormones. In fact, without cholesterol, the body would be incapable of proper cellular development and intercellular communication.
But if you’ve ever had a lipid panel test, you know that not all cholesterol is created equal.
There are a number of different types of cholesterol made and utilized by the body. The ones you hear most about are those discussed in your typical lipid (cholesterol) panel, which we will go over below.
The main components of a lipid panel lab test are:
Though triglycerides are directly influenced by the intake of carbohydrate-rich foods and not associated at all with the ingestion of dietary fat. It’s also typically associated with increased body-fat percentages, particularly in individuals who carry most of their fat in the belly area. Studies that evaluate prognostic data (long-term risk of poor outcomes) have shown that high levels of triglycerides play a key role in the development of and worsening of coronary artery disease. A ketogenic diet typically has a positive effect on reducing triglycerides as you significantly reduce your carbohydrate consumption. The normal range for triglycerides is considered under 150, but ideally under 90.
HDL (high density lipoprotein), known as “good” cholesterol, is associated with decreased risk for coronary atherosclerosis (heart disease) and therefor is seen to reduce risk of heart attack and even stroke. The ideal HDL range is typically around 60, but a value greater than 40 is considered normal.
LDL (low-density lipoprotein), is the part of the lipid panel that is blamed for coronary disease, strokes, and other issues surrounding atherosclerosis throughout the body. Below 130 is considered to be a normal LDL, while the ideal is under 100. However, if you’ve already been diagnosed with coronary disease or diabetes, your cardiologist will likely aim to get this below 70. But not all LDL is created equal. We’ll get to that in a minute.
In many respects, the “total cholesterol” is fairly unhelpful in determining whether or not you’re at risk for coronary disease or if your “bad” cholesterol is too high because total cholesterol includes both HDL and LDL. However, according to most healthcare institutions, the target for acceptable cholesterol levels is usually below 200 (and that was lowered from 300 in 1996 when lipid-lowering drugs like statins came to the market). Unfortunately, cardiovascular outcomes and changed for the better by lowering that vale.
The above are the primary components of a typical lipid panel. However, it’s not the whole picture. Most lipid panels do not include VLDL (very low-density lipoprotein) and do not differentiate the LDL particle into its two primary sizes (large and small particle). Why is this important? Because particle size matters.
Identifying the LDL particle size gives a better risk analysis foratherosclerosis (a disease in which plaque builds up inside your arteries). This is because large particle LDL has not been shown to be associated with coronary artery disease, while small particle LDL has a very strong association with the development of coronary artery disease.
Why isn’t LDL particle size being evaluated and discussed? The most logical answer is cost; evaluation of different types of LDL can be quite expensive. The conventional thinking is that by lowering your total LDL, you should lower small-particle concentration and therefore decrease risk for coronary disease. However, patients with well-controlled lipid panels on statin therapy with serum-LDL concentrations of less than 70 continue to develop and experience a worsening of existing coronary artery disease.
To start, it’s important to know that 80 percent of the cholesterol in the normal human body is generated by the body and not influenced by the intake of food, including dietary fat. The remaining 20 percent may be influenced by dietary fat intake and the intake of other macronutrients, such as carbohydrates. The reason we make the distinction of a “normal human body” is because this may not apply to individuals diagnosed with congenital hypercholesterolemia (a disorder that causes LDL levels to be very high).
Individuals with this diagnosis have fewer cholesterol receptors, and, consequently have more free-floating cholesterol in the bloodstream. Because there are fewer receptors, the body actually thinks it’s getting less cholesterol than it needs, so it makes more cholesterol (even if your levels are actually normal). This becomes problematic because most people with hypercholesterolemia don’t burn off this cholesterol, largely because their bodies are reliant on dietary carbohydrates for energy rather than dietary fat. In these individuals, their serum cholesterol will be slightly more influenced by their dietary choices. However, an individual with normally functioning cholesterol receptors would not have their serum cholesterol level influenced by increased dietary-fat intake, particularly if that individual is following a lower-carbohydrate diet focused on using fats for energy.
It’s also worth noting that hyperlipidemia (an abnormally high concentration of fats or lipids in the blood) can be the result of other factors like steroids, exogenous hormones, other medications, low thyroid function and kidney disease. And fructose is one of the worst offenders of fatty liver disease and high triglycerides.
A number of studies have looked at the difference between the ketogenic diet compared to a low fat diet for weight loss and diabetic control. In these studies, there was a consistent reduction of triglycerides in the ketogenic group and not in the low fat group. There was also greater improvement of HDL (good cholesterol) compared to the low fat group. And when particle size was evaluated, the ketogenic group almost always had a greater reduction in small particle LDL, the one associated with increase risk for heart disease or stroke.
To summarize, which part of the lipid panel we pay the most attention to is important. The focus should be on triglycerides and HDL and research is showing that a low-carb ketogenic diet usually results in improved cholesterol profile by lowering triglycerides and increasing HDL. Slightly higher LDL cholesterol is typically offset by having lower small particle LDL (associated with heart disease) and higher large particle LDL (not associated with heart disease).