The Primal Blueprint (20 page)

Cholesterol is a little waxy lipid (fat) molecule that happens to be one of the most important substances in the human body. Every cell membrane has cholesterol as a critical structural and functional component. Brain cells need cholesterol to make synapses (connections) with other brain cells. Cholesterol is the precursor molecule for important hormones such as testosterone, estrogen, DHEA, cortisol, and pregnenolone. Cholesterol is needed for making the bile acids that allow us to digest and absorb fats. Cholesterol is made into all-important vitamin D in the presence of sunlight. Bottom line is that you can’t live without cholesterol, which is why your liver actually makes up to 1,400 milligrams a day regardless of how much food-borne cholesterol you consume—or how much you avoid it like the plague—in your diet.

Because cholesterol is fat-soluble (it does not dissolve in water—think balsamic vinegar remaining intact in a dish of olive oil) but must travel to and from cells in the watery environment of the bloodstream, it needs to be carried by special spherical particles called lipoproteins (the name means “part protein and part lipid”). There are several varieties of lipoproteins with different transporting functions—chylomicrons, LDLs, IDLs, HDLs, and VLDLs (as well as subfractions of those)—but the three we are concerned with here are VLDLs, LDLs, and HDLs (very low-density, low-density, and high-density lipoproteins, respectively). Each of these lipoproteins carries a certain percentage of cholesterol, triglycerides, and other minor fats. Your blood test values for triglycerides and HDL, LDL, and VLDL cholesterol represent the combined total in your bloodstream of what all the lipoproteins are transporting.

VLDLs, the largest of these cholesterol complexes, are manufactured in the liver in the presence of high levels of triglycerides (triglycerides are also made in the liver—from excess carbohydrates and fats). Hence, VLDLs comprise 80 percent triglyceride (and a little cholesterol). After leaving their birthplace in the liver, these lipoproteins deliver their cargo to fat and muscle cells for energy. Once these VLDLs have deposited their triglyceride load inside a fat or muscle cell, their size decreases substantially and they become LDLs. At this point, they bear mostly cholesterol and a little bit of remaining triglyceride. In a healthy person, most of these LDL molecules are called “large fluffy” or “buoyant” LDLs. As such, they are generally harmless, even at relatively high levels, as they go about their assigned task of delivering cholesterol to the cells that need it.

The real trouble starts when triglycerides are unusually high in the bloodstream. This condition can occur routinely when you eat a high-carb diet (even if it’s a low-fat diet), because, as you learned in the “It’s All About Insulin” section, excessive insulin production drives the conversion of ingested carbohydrate into fat (triglycerides). Obviously, the condition can also occur when you eat a moderate-carb, high-fat diet, because insulin will see to it that both excess carbs and fat get circulated in the bloodstream and stored in fat cells.

Dr. Dean Ornish and other proponents of low-fat eating will tell you that reducing fat intake reduces cholesterol and triglyceride levels. This is absolutely true, as confirmed by numerous best-selling books as well as newspaper and magazine feature stories touting quick and dramatic results (lowered cholesterol and triglyceride levels) from fat-restrictive diets. But one reason is this: your liver makes cholesterol as a raw material for the bile salts that help you digest fat, so if you aren’t eating fat, your genes will be given the signal to down-regulate cholesterol production.

“
Low-fat eating requires you to consume excessive carbs, by default, to obtain your daily energy requirements
”

However, low-fat eating requires you to consume excessive carbs, by default, to obtain your daily energy requirements. This leads to excessive insulin production and, as you recall, kick-starts the cycle that eventually leads to heart disease. Any way you slice it, consuming too many carbs leads to high triglycerides (not to mention the other risk factors detailed in the sidebar “How to Sneeze at Heart Disease”).

With high triglycerides in your blood, VLDL production skyrockets to handle the extra load. This can cause some of the VLDL particles to become altered into a more sinister form of LDL that has been shown to be a major factor in atherosclerosis and heart disease. These “small, dense LDLs” (why can’t all medical nomenclature be this easy?) are thought to initiate the majority of atherosclerosis problems when they become
stuck in the spaces between cells lining the artery and then become oxidized. This oxidative damage causes inflammation and begins a process of destruction that I will detail shortly. Research has shown that people with Metabolic Syndrome or type 2 diabetes all have elevated levels of both triglycerides and these small, dense LDL particles. Of course, these same people have substantially increased risks for heart disease and stroke.

The remaining cholesterol complex with which you might be familiar is the high-density lipoprotein (HDL), which takes cholesterol back to the liver for recycling. HDLs also clean up any damaged or oxidized cholesterol that might cause problems later—including removing the small, dense LDL particles and oxidized cholesterol that have become stuck in the artery wall. These tiny but powerful HDL cholesterol complexes are often called the “good cholesterol” or “nature’s garbage trucks.” Medical researchers generally agree that the more HDL you have, the lower your risk for heart disease. As you might have imagined, people with Metabolic Syndrome and type 2 diabetes also typically have low levels of beneficial HDL. Exercise is one of the cheapest, easiest, and most effective ways to raise HDL.

As mentioned earlier, because lipoproteins have a lipid surface, they are subject to oxidation. Like oils left open in your kitchen, they can go rancid when they come in contact with oxygen. When this happens they—and the cholesterol inside—can become damaged. Of course, oxidation happens all the time throughout the body, and we have evolved some effective antioxidant enzyme systems (namely catalase, superoxide dismutase, and glutathione) to prevent too much of this damage from getting out of control. Furthermore, consuming ample levels of high-antioxidant foods (fruits, vegetables, nuts and seeds, dark chocolate, red wine, as will be detailed in
Chapter 4
) and antioxidant supplements (such as vitamin E, CoQ10, beta-carotene, and lycopene) can help mitigate some of the damage. It’s also extremely convenient that HDLs can remove some of the damaged cholesterol and take it back to the liver for recycling.

Your cholesterol processing system clearly has evolved to expect a certain range and quality of dietary fat, protein, carbohydrate, and antioxidants, as well as a certain level of exercise (to help promote insulin sensitivity in the muscles and maintain high levels of HDL) to provide appropriate gene signals and avoid artery disease. And because HDL particles are very small, they can get into the spaces between arterial wall cells and clean up the oxidized cholesterol. That’s why Big Pharma has tried—so far unsuccessfully—to create an effective drug to raise HDL and address existing atherosclerosis (some physicians prescribe the combination of prescription fibrates and over-the-counter niacin to raise HDL, but this treatment can be problematic and is not widely used).

The system has served humans and most all other mammals well for millions of years—until recently, when processed carbohydrates and partially hydrogenated fats entered the picture. As a result of unique gene signaling from consuming too much of these unnatural foods, small, dense LDLs are created and can become trapped in the spaces between endothelial cells lining the artery (sometimes called a gap junction). Even if they are not oxidized to begin with, once trapped, they can oxidize in place because they are sitting there continually exposed to oxygen passing by attached to hemoglobin in the red blood cells. Either way, this oxidation eventually causes injury and inflammation to the arterial wall, prompting the body’s immune system to send macrophages (scavenging white blood cells) to gobble up the oxidized LDLs at the site where the first particles were trapped.

The immune system tries hard to do its job, but the macrophages are overwhelmed by absorbing so much oxidized LDL. Their gorging on oxidized LDLs signals specific genes to transform the macrophages into foam cells that attach to the arterial lining, laying the foundation for future trouble. The resulting lesion prompts more macrophages to come to the rescue. They try to gobble up more and more oxidized LDLs floating by, increasing the severity of the lesion over time. This is the familiar saga of plaque accumulation on the arterial wall. The plaque grows and eventually compromises the inner diameter of the artery. If allowed to continue, it can eventually occlude blood flow or break off as a clot, preventing blood—and oxygen—from reaching a vital organ (resulting in your classic heart attack or stroke).

The oxidation of these small, dense LDLs most likely happens for a variety of reasons that have to do with modern dietary habits more than anything else: a high intake of unstable polyunsaturated fats from vegetable oils in the diet (PUFAs incorporated into the lipid layer are much more prone to oxidation than are saturated fats); a reduced intake of natural antioxidants in the diet, which would otherwise mitigate oxidation; the presence of fewer HDL particles to remove oxidized lipids (low HDL cholesterol readings may be partly caused by high-carb diets); and the fact that small, dense LDL particles do not bind as easily to the normal LDL receptors on muscle and fat cells. Unable to release their cholesterol load and with typically fewer HDL particles to gobble them up, these small, dense LDL particles linger longer in the oxygen-rich bloodstream until they oxidize. By the way, the reason atherosclerosis happens in the arteries and not the veins is because venous blood has very little oxygen.

Note that the oxidation and inflammation process described has little or nothing to do with your total cholesterol or even your total LDL cholesterol levels. In most cases, atherosclerosis is a result of the oxidation of a small fraction of the total amount of LDL in your blood—the small, dense LDL particles. If you have little or none of these in your blood, your risk for heart disease drops dramatically. Also, if your HDL is high, it’s very
unlikely that you’ll encounter a problem, because HDL does a great job of scavenging the oxidized cholesterol from LDL in the bloodstream.

Unfortunately for some of us, poor diet, lack of exercise, stress, certain drug therapies, and, yes, family genetic history can all contribute to the increased production of the dangerous small, dense LDL particles. Your doctor can test for them if you ask, but most common blood tests don’t yet distinguish between the benign “fluffy” forms of LDL, sometimes called pattern A, and the small, dense particles, called pattern B. A comprehensive lipid blood panel will typically provide values for total cholesterol, HDL, LDL, VLDL, and triglycerides.

A physician will generally dispense medication if your total LDL levels exceed a certain figure (this varies by doctor and individual patient profile), knowing it will respond to the statins with a quick overall reduction. Statins will indeed lower all forms of LDL (including both the good stuff and the bad stuff), but it’s a much more sensible—and safe—option to simply alter dietary and exercise habits and minimize insulin production, thereby preventing excess accumulation of triglycerides in the blood and allowing the cholesterol system to work as intended. In fact, the combination of low carbs and good fats in a
Primal Blueprint
eating plan, along with
Primal Blueprint
exercise habits, will generally raise HDL, lower both triglycerides and small, dense LDL, and allow you, regardless of your genetic predisposition, to essentially have no participation in this heart disease saga whatsoever. The choice is yours.

“
HDL does a great job of scavenging the oxidized cholesterol from LDL in the bloodstream… if your HDL is high, it’s much less likely you’ll encounter a [heart disease] problem
.
”

Isn’t it ironic, then, to discover that statins and other cholesterol-lowering meds do not have any ability to influence LDL particle size and can only lower total LDL by reducing both the good and the bad versions? The fact that some people taking statins experience a dramatic reduction in total cholesterol or in LDL means very little in the context of the true oxidation and inflammation nature of heart disease. To be clear, statins do slightly reduce the risk of additional heart attacks among men under the age of 65 who have had a prior heart attack. However, many doctors now believe that these benefits are independent of their “cholesterol-lowering” properties and instead come from an anti-inflammatory effect that addresses the more proximate cause of heart disease. A cheaper and more effective anti-inflammatory effect can be achieved by eating foods high in omega-3, taking fish oil supplements, or popping a small dose of aspirin daily.

By simply adopting the
Primal Blueprint
laws, you can enjoy superior results without the perilous side effects and huge expense of drug therapy. In the case of statins, known side effects include muscle pain, weakness and numbness, chronic fatigue, tendon problems, cognitive problems, impotence, and blood glucose elevations. These side effects are believed to be due in large part to statins’ interference with the normal production of a critical micronutrient known as coenzyme Q10 (CoQ10). CoQ10 is essential to healthy mitochondrial function and defending our cells against free radical damage. Statin therapy is believed to lower CoQ10 levels by up to 50 percent. Ironically, CoQ10 plays a particularly important role in the healthy function of the cardiovascular system, and heart attack patients show depressed levels of CoQ10! Some researchers suggest that statins’ depletion of CoQ10 may nullify any potential benefits of statin therapy.