Saturated Fat – the Devil is in the Details

Saturated fat is often stated in debates as a cause of heart disease, which is why you sometimes hear it’s bad to eat meat, eggs, coconuts, and other forms of saturated fat. But there is reason to dig a little deeper on the subject.

A fat is basically made from a long chain of carbon atoms that have single and double bonds. The double bonds can react with hydrogen and form a single bond. In chemistry, a saturated fat is a type of fat in which the fatty acids all have single hydrogen bonds. They are called “saturated” because thepalmitic-acid-3d-balls second bond is broken up with each half of the bond attached to, or “saturated with” hydrogen atoms. Don’t worry if you don’t understand the chemistry, we’ll go into more easier-to-understand details.

Most animal fats are saturated, while most plants and fish are generally unsaturated (think lard and coconut oil). Saturated fats have higher melting points and are solids at room temperature, whereas unsaturated fats are liquids at room temperature (think olive oil). The myth that saturated fats are solids at room temperature and thus are the same inside the body is simply a false misleading statement. Saturated fat increasing heart disease risk is a controversial topic. Many reviews recommend a diet low in saturated fat and argue it will lower risks of cardiovascular disease whereas other articles have found the opposite.

In fact, if you restrict saturated fat and replace it with carbs, not only do you not see a benefit, you actually increase your risk for heart disease. And this is not some odd dietary switch, this is exactly what the average American is doing. The sharp increase in dietary carbs is mind boggling at times, there isn’t enough evidence to change dietary guidelines.

A novel way that research scientists like Dr. Jeff Volek PhD and others have explored saturated fats and the risk of heart disease is by measuring the plasma levels of saturated fats. Researchers have found there is a very consistent association. A good example is palmitic acid, which is a good endogenous blood marker of lipogenesis (to make new fat). Palmitic acid is turned into palmitoleic acid (16-1), which has 16 carbons and one double bond. Increased palmitic acid is an endogenous marker of lipogenesis; which is in turn a marker of the first signs of insulin resistance and metabolic disease. So if you have more total saturated fat, or palmitic acid in your blood, this is consistently associated with a higher risk for heart attacks, and a higher risk for heart failure. There are dozens of studies showing this.

So the take away point here is, that it is what your body does with saturated fat that’s important. Whether you store the saturated fats in your cell membranes, or if they are processed and used as energy – this is the key. If you tend to store a lot of saturated fat, this is associated with diabetes, pre-diabetes and heart disease. Again, storing saturated fat is not good, but dietary saturated fat doesn’t seem to correlate to heart disease. This is confusing to many people because we tend to think “you are what you eat.”

So the question then becomes – What’s contributing to plasma saturated fat? This question has led researchers to start measuring specific types of fatty acids and saturated fat levels in people on a ketogenic diet (see this post).

One study measured the effects of the amount of saturated fat the body stored on a calorie restricted SAD (Standard American Diet) and WFKD. The saturated fat content of the SAD was three times the level of a WFKD (36 versus 12). And when the saturated fat was measured 12 weeks later, it went down more in a ketogenic diet.

And what was even more intriguing, was the fact that palmitoleic acid 16-1 (16 carbons and 1 double bond) which is a monounsaturated fat, consistently goes down on the ketogenic diet. This is why we can look at your levels of palmitic acid on a fatty acid test and know whether you are in early metabolic disease.

Another very interesting study prescribed a very intense feeding schedule to people with pre-existing metabolic syndrome (took about six months for each patient) and they were given various level of carbohydrates. There were six different levels of carbs, starting with a low level of carb, going up to a pretty moderate to high-carb diet. The study showed that there was no change in diet and plasma levels of saturated fat. There was a change in the level of palmitic acid, which went up with the addition of carbohydrates, and this is a marker of the denovo lipogenesis, which is very intimately connected to the dietary carbohydrate content. We have to keep in mind that within any given level of carbohydrate, you have a lot of variability between people, but as you increase carbs you see an increase in palmitic acid and an increase in the signs of early metabolic disease.

Some people can maintain a flat slope of palmitic acid when given carbs, and are probably the ones that are most carb-sensitive, where they don’t resort to denvo lipogenesis. This is an example of what the body does with saturated fat. When the slope increases, the palmitic acid goes up, and this signals that the person is not processing carbs very well.

Another reason palmitic acid is a good marker of denovo lipogenesis, is that it is not confounded by dietary intake (unless you eat a lot of macadamia nuts). Palmitoleic acid is very low in most foods, and when it goes up in concentration, it’s a pretty good indication of converting carbs to fat. And there are dozens of studies that have linked higher levels of palmitoleic acid in red blood cells to early metabolic syndrome and other problems.

Fatty acid composition is kind of a “rabbit hole,” but using palmitic acid as an indicator of how well carbs are being processed is a consistent way to detect a higher risk for various chronic diseases.