How Bad is Saturated fat and Cholesterol? The Final Word.

The conventional idea that saturated fat is bad is now very outdated and incorrect.

Polyunsatruated fats are highly unstable and oxidize very easily, which is the actual cause of atherosclorosis and heart disease.

Cholesterol is a moot point. It actually has nothing to do with heart disease whatsoever. It is also a myth that eating cholesterol will increase blood levels of cholesterol. (Understand that HDL and LDL particles are not cholesterol, they only contain cholesterol. Cholesterol itself really does not play a functional role in forming atherosclorotic plaques, and is in fact a necessary nutrient in our bodies).

Saturated fat is actually protective, because it increases protective HDL particles, while increasing the size of the LDL particles, making it more difficult for them to infiltrate the arterial wall and contribute to forming atherosclorotic plaques. The saturated nature of Saturated fat also makes it very resistant to oxidation, since all available carbon bonds are tied up with a hydrogen atom (Saturated fat has no double bonds). Monounsaturated fats share this trait as well.

Plus, saturated fat is the method our bodies use to store excess energy, which is an evolved survival mechanism for our hunter-gatherer ancestors when times were tough. Obviously, saturated fat plays a very important role in Human survival.

Polyunsaturated fat contains two or more pairs of double bonds without hydrogen atoms occupying the open space, and it’s the carbon that lies between the double bonds that is wide open to oxidation.

Yes, this means fish oil supplemetation is not as protective as is commonly believed. It’s benefits have been vastly exagerated.

Therefore you should only eat the whole food. Consuming fish as a food will ensure the other nutrients (vitamins, antioxidants) are in place that may protect you from the oxidative damage of excess PUFAs. It’s important to note that all studies showing the benefits of fish oil supplementation have been less than 2 years, and the one that lasted 4 years showed an increase in heart disease and sudden death. So don’t supplement! Eat the whole food!


These double bonds allow systemic inflammation to develop, because the more Polyunsaturated fat you have circulating in your system, the longer it is allowed to “hang out” on the small dense LDL particles, leaving lots of time and opportunity for it to oxidize. Once the LDL particles are oxidized, they become smaller and penetrate the arterial wall, where they initiate the atherosclorotic process:

The membrane of LDL contains polyunsaturated fatty acids (PUFA), which are highly vulnerable to oxidation. Cells continuously make antioxidant enzymes and other antioxidant compounds to protect their membrane PUFA. If PUFA start to oxidize, the cell ramps up its antioxidant production. When the liver packs cholesterol into a VLDL particle and secretes it into the blood (where it eventually becomes an LDL particle after delivering some of its nutrients to other tissues), it puts some antioxidants into the package. The PUFA have now left the comparative safety of the liver cell and have only a limited supply of antioxidants. When those antioxidants are used up, the PUFA begin to oxidize, and their oxidation products proceed to damage other components of the lipoprotein. When the oxidation becomes severe, the oxidized LDL winds up in a foam cell in an atherosclerotic plaque.

So? Saturated=Good, Polyunsatruated=Bad.

What foods should we eat? What should we avoid?

This easy to follow list of foods should form the foundation of your diet. It’s the easiest way to avoid inflammation and promote health, lean body mass, and mental clarity.

How do arthersclorotic plaques form?

Here is how most doctors and “health professionals” will have you believe is the process by which “cholesterol and arterycloggingsaturatedfat clogs your arteries”


It shows cholesterol flowing through the blood and just glomming on to the inner lining of a blood vessel as if it were grease clogging up a pipe.  Is that how it happens?  Not at all.

Growing evidence supports the role of local and systemic

inflammation as a common pathophysiological

mechanism in different cardiovascular diseases, including

congestive heart failure or CAD (coronary artery

disease). Indeed, it is well established that atherosclerosis

is an inflammatory disease [33]. [reference]

First of all, the plaque grows behind the layer of the blood vessel in contact with the blood, not on top of it.  The plaque develops within the inner and outer walls of the blood vessel:

The proinflammatory cytokines aggravate plaque instability by inhibiting extracellularmatrix synthesis and promoting smooth muscle cell apoptosis. IL-8, a CXC chemokine produced by neutrophils, smooth muscle cells and ECs, induces the migration and proliferation of ECs and smooth muscle cells. [reference]

Second, the plaque doesn’t initially progress inward to obstruct the blood vessel.  It initially progresses outward, pushing backwards into the middle of the blood vessel:
It doesn’t begin occluding the blood vessel until it’s already occupying about 40 percent of the blood vessel wall.  What happens to make it start occluding the blood vessel?  It appears to be the successive rupturing and re-healing of highly inflamed plaques:
On the left we see a secondary plaque forming on the surface of an initial plaque that had ruptured.  On the right we see that the worst plaques may have as many as four sites of rupture and re-healing.
 In lay-terms, these plaques develop as the surplus of circulating LDL (you ate too many polyunsaturated fats) particles begin to oxidize and cause inflammation. The LDL are small and easily infiltrate the arterial wall. Macrophages within the arterial wall induce an immune response by “gobbling up” the oxidized LDL into “foam cells” that begin to expand and eventually lead to rupture and heart attack.
This discussion only covers inflammation as it relates to atherosclorosis. In this post, I get into how inflammation relates to other problems, like obesity and depression.

So, in conclusion 

  • Saturated fat is good, because it increases protective HDL and increases the size of the LDL. It’s also a good source of energy, and highly resistant to oxidation.
  • Cholesterol is also good, because it is a health-promoting substance. It is a critical component of cell membranes, the precursor to all steroid hormones, a precursor to vitamin D, and the limiting factor that brain cells need to make connections with one another called synapses, making it essential to learning and memory. 
  • Polyunsaturated fat is bad, because it makes the LDL particles smaller, and is easily oxidized, leading to inflammation and atherosclorotic plaques that form within the cellular walls of the blood vessel, leading to buildup and rupture.

You may also want to read:

Paleo/Primal diet is a high-fat, high-cholesterol diet. And that’s a good thing…

What the heck is inflammation? How does it affect me?

Paleo for one year. Understanding the Paleo concept.

Meal timing for stubborn fat loss. Intermittent Fasting.

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