The Clot Thickens: The Enduring Mystery of Heart Disease

Written by Dr. Malcolm Kendrick, a general practitioner in England, The Clot Thickens is a book about heart disease. Dr. Kendrick puts forward an alternative to the cholesterol hypothesis.

Notes

The diet-heart hypothesis or cholesterol hypothesis was first proposed back in the late 19th century, but didn’t really gain any traction until the 1950s due to the work of Ancel Keys.

Kendrick states that heart disease has nothing to do with eating saturated fat, nor does it have anything to do with cholesterol in the bloodstream.

Specifically, this book is about atherosclerosis, sometimes called “hardening of the arteries.” The most likely place to find atherosclerotic plaques is in the coronary arteries though it can occur in other arteries (never in the veins).

The Cholesterol Hypothesis has two parts –

  1. Saturated fat in the diet raises blood cholesterol.
  2. A raised cholesterol level causes CVD.

Cholesterol has to be transported in lipoproteins (lipid + protein).

There are several different types, the biggest is a chylomicron, the smallest is HDL. The one blamed for CVD is LDL.

Senator McGovern’s Dietary Committee of 1977 was the single most important event in the demonisation of saturated fat. The dietary guidelines from this committee were taken up around the world despite a complete lack of any real evidence.

Kendrick states that it is now “beyond doubt that saturated fat consumption cannot raise LDL levels.” The body utilizes a negative feedback loop to regulate the level of all substances in the blood. This system of keeping everything under control is called homeostasis.

What happens when we eat saturated fat?

  1. It binds to bile salts in the bowel.
  2. Once bound with bile salts, it’s absorbed into the gut wall and packed into a chylomicron.
  3. The chylomicron travels through the thoracic duct and released directly into the bloodstream.

It does not, at any point, pass through the liver.

As chylomicrons travel around the body, they are stripped of their fat content by cells they encounter (primarily fat cells). They continue to shrink in size until they are about the size of a LDL molecule, at which point they are called chylomicron remnants. These remnants are absorbed back into the liver. Which means that only a very small percentage of the fat that you eat can end up in the liver. This is what happens to all types of fatty acids: saturated, polyunsaturated, or monounsaturated.

Nothing in the absorption, transport, and storage of dietary fat, saturated or otherwise, has anything to do with LDL a.k.a. ‘bad cholesterol’ in any way shape or form.

Where do LDL’s come from?

The liver makes VLDL’s (also called triglycerides). The role of VLDL is to transport fatty acids and deliver them to fat cells. A LDL molecule is simply what is left of VLDL once it has been stripped of most of its fat content.

VLDL –> shrinks –> IDL –> shrinks –> LDL

Most LDL molecules are pulled out of circulation by the liver, though a certain amount does remain free in the blood. They can deliver cholesterol to cells that need it.

In whatever way you view these lipoproteins, the key takeaway fact is that VLDLs are the only source of LDLs. Thus, for the LDL level to rise, the VLDL level must go up first. Which leads to the next question. What makes VLDL levels go up? Well, as I hope is now clear, it is not, and never could have been saturated fat consumption.

Instead, what causes VLDL levels to rise is eating carbohydrates.