The health authorities have been telling us for decades that saturated fat raises the risk of heart disease.
For this reason, we’ve been told to avoid foods like meat, eggs, coconuts and dairy products.
The theory goes like this:
Saturated fat raises LDL cholesterol in the blood.
LDL cholesterol lodges in the arteries, causing atherosclerosis and eventually, heart disease.
This is also known as the diet-heart hypothesis. This theory has never been proven, despite it having been the cornerstone of dietary recommendations since 1977 (1).
When referring to cholesterol, be it LDL or HDL, we’re actually not talking about the cholesterol itself.
LDL stands for Low Density Lipoprotein and HDL for High Density Lipoprotein.
The lipoproteins are proteins that carry fat, cholesterol, phospholipids and fat soluble vitamins around in the bloodstream.
The thing with cholesterol (or more accurately, the lipoproteins that carry around the cholesterol) is that elevated blood levels of it are associated with an increased risk of heart disease.
This graph from the massive MRFIT study (4) clearly shows that in men, total cholesterol above 240 mg/dL (6.2 mmol/L) is associated with an increased risk of death, specifically from heart disease.
It is now well acknowledged that the type of cholesterol matters.
However, the situation gets even more complicated than that. It turns out that there are subtypes of LDL, specifically relating to the size of the particles.
It is now known that the size of the LDL particles is of critical importance.
Scientists now realize that the number of LDL particles (LDL-p) is more important than their total concentration (LDL-c). The greater your LDL particle number, the more likely you are to have mostly small, dense LDL particles (23, 24, 25).
Bottom Line: The relationship between cholesterol and heart disease is complex. HDL is associated with a lower risk, while small, dense LDL particles are associated with a greater risk.
The first part of the diet-heart hypothesis is that saturated fats raise blood levels of LDL cholesterol.
However, despite this idea being so deeply ingrained in the minds of laypeople and health professionals alike, there is no clear link.
Some short-term feeding trials do in fact show that increased saturated fats raise LDL in the short term.
If saturated fats were such a dominant factor in LDL, the association should be strong and consistent in observational studies, but it’s not.
Both of these populations have low cholesterol and an absence of heart disease.
Bottom Line: If saturated fat really raises LDL, then the effect is weak and inconsistent. Saturated fat is certainly not a dominant factor in LDL levels.
If you take into account the size of the LDL particles, you see that saturated fat doesn’t actually harm the blood lipid profile… it improves it!
Studies show that:
If saturated fats reduce the small, dense LDL particles and raise HDL, then they should decrease the risk of heart disease, not the other way around.
Bottom Line: Saturated fats shift the LDL particles from small, dense to Large and raise HDL. If anything, this should decrease the risk of heart disease.
The low-fat diet that is commonly recommended by the health authorities is a miserable failure. In the beginning, there were only observational studies backing it up. Since then, many controlled trials have been conducted.
This diet actually makes the blood lipid profile worse, not better.
For this reason, low-fat diets have a net harmful effect on the blood lipid profile, while low-carb diets have a positive effect.
Low HDL and high triglycerides are two components of the metabolic syndrome, which is a stepping stone towards obesity, type II diabetes and heart disease.
Bottom Line: A decrease in HDL cholesterol and LDL particle size, along with an increase in triglycerides, should all lead to an increased risk of heart disease.
If saturated fats caused heart disease, then people who eat more saturated fats should be at a greater risk… but they aren’t.
Review articles of prospective observational studies don’t see any associations.
One study published in 2010 that looked at 21 studies with a total of 347.747 individuals concluded (56):
“A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD.”
But observational studies can’t really prove anything, they can only demonstrate correlation. So we can’t exonerate saturated fat based on such studies alone.
Fortunately, we do also have randomized controlled trials. Such studies are considered the “gold standard” of research.
The Women’s Health Iniative is the largest randomized controlled trial on diet in history. In this study, 48.835 postmenopausal women were randomized into a low-fat diet group and a control group who continued to eat the standard western diet.
After a period of 8.1 years, there was no difference in the rate of cardiovascular disease between the two groups (59). The diet did not work for weight loss, breast cancer or colorectal cancer either (60, 61, 62).
Another massive study, the Multiple Risk Factor Intervention Trial (MRFIT) involved 12.866 men at a high risk of heart disease. This is the group of people most likely to see a benefit if the low-fat diet actually worked.
However, after 7 years, there was no difference between the men randomized to a low-fat diet and the group eating the standard western diet, despite the fact that more men in the low-fat group also quit smoking (63).
The low-fat diet got tested, it didn’t work. Period.
Overall, there is zero evidence that saturated fat causes heart disease, or that reducing saturated fat leads to a reduction.
Just for fun, I’d also like to show you this graph of how the obesity epidemic started at the exact same time the low-fat dietary guidelines were released to the American public:
Obesity is a major risk factor for heart disease, diabetes and other chronic diseases.
Of course, this graph only shows a correlation and doesn’t prove that the low-fat guidelines caused the obesity epidemic, but it’s still an interesting observation.
Despite having been repeatedly proven to be ineffective, mainstream health authorities and many nutrition professionals still continue to peddle the low-fat diet.
Bottom Line: There is no evidence that saturated fat increases the risk of heart disease, or that diets low in saturated fat reduce the risk.
Another important cause of death that doesn’t get mentioned often in discussions about saturated fat, is stroke… otherwise known as a cerebrovascular accident.
A stroke happens when there is a disruption in blood flow to the brain, either due to a blockage or bleeding.
Strokes are actually the second most common cause of death in the world, accounting for 6.15 million deaths in the year 2008 alone (64).
In 2008, strokes killed 6.15 million, while heart disease killed 7.25 million… judging by these numbers, stroke is almost as significant as heart disease when it comes to mortality in the population.
Bottom Line: Consumption of saturated fat is associated with a lower risk of stroke in many studies. Stroke is the second most common cause of death worldwide.
Of course, there are some bad fats in the diet that actually DO raise the risk of heart disease.
Trans fats are monounsaturated fats that have been put through a hydrogenation process.
This increases the shelf life of the fats and makes them resemble saturated fats in consistency.
To lower your risk, eat healthy foods with plenty of saturated and monounsaturated fats. Eat some Omega-3s from fish and grass-fed animals, but stay away from trans fats and vegetable oils.
It’s time to retire the decades old myth that saturated fat is in any way related to heart disease.
It wasn’t proven in the past, it hasn’t been proven today and it never will be proven… because it’s just flat out wrong.
Article by By Kris Gunnars