Cholesterol Down: Ten Simple Steps to Lower Your Cholesterol in Four Weeks--Without Prescription Drugs [NOOK Book]

Read an Excerpt

1

Cholesterol 101

The doctor of the future will give no medicine, but will interest his patients in the care of the human frame, in diet, and in the cause and prevention of disease.
—Thomas Alva Edison, American scientist and inventor (1847–1931)

CARDIOVASCULAR DISEASE:

WILL IT BE YOUR CAUSE OF DEATH?

Odds are that you will die from some form of cardiovascular disease— our nation’s deadliest epidemic—be it a heart attack, stroke, high blood pressure, or other disease of the heart and blood vessels. In the United States, one person dies from cardiovascular disease approximately every thirty-five seconds. Combine that overwhelming death toll with the staggering $403 billion estimated direct and indirect cost of cardiovascular disease for 2006, and you begin to grasp the magnitude of this huge public health concern.

More fearful that you will die of cancer? Recent American Heart Association statistics reveal that you are much more likely to succumb to a disease of the heart or blood vessels. In 2003, almost twice as many Americans died of cardiovascular disease as of cancer. In fact, cardiovascular disease claims more lives than the next four leading causes—cancer, respiratory diseases, accidents, and diabetes— combined.

If you are a woman and think your gender will protect you, you should know that in 2003 almost half a million American women died of cardiovascular disease, mainly heart disease. In fact, according to the American Heart Association’s 2003 statistics, a woman’s odds of dying from heart disease far surpassed her chances of dying from breast cancer (1 in 30 women who died did so of breast cancer, while 1 in 2.6 died of cardiovascular disease). Furthermore, more women succumbed to cardiovascular disease than men—approximately 60,000 more women than men. The truth is that women are different from men, both in their symptoms of heart disease and in the propensity of women to exhibit a different but just as deadly type of heart disease, “coronary microvascular disease” or a hardening of the minute arteries that feed the heart (but are too tiny to show up on a typical angiogram). According to new findings, high cholesterol and high blood pressure are among the leading causes of this condition.

The good news is that lifestyle modifications will provide you with a powerful measure of protection against diseases of the heart and blood vessels, including microvascular disease. By following the easy ten-step Cholesterol Down Plan outlined in Part II of this book, you can lower your “bad” cholesterol and maybe even save your life.

According to the World Health Organization’s report Global Strategy on Diet, Physical Activity, and Health, various forms of cardiovascular disease resulted in an estimated 16.7 million deaths globally in 2003. Most of these deaths were from heart disease (7.2 million) and stroke (5.5 million), with the rest attributed to high blood pressure and other vascular illnesses.

Source: who.int/dietphysicalactivity/publications/facts/ cvd/en/print.html.

What causes a heart attack or stroke?

A heart attack or stroke is ultimately caused by a corroding of LDL particles that accumulate within the inner arterial wall, resulting in inflammation and eventual thickening of the arterial walls leading to the heart or brain, a process called atherosclerosis. This slow, progressive disease typically starts in childhood, when cholesterol, cellular debris, fat, calcium, and other compounds begin building up in the large arteries. Over time, a poor diet and sedentary lifestyle predispose our arteries to clogging up with this thick mass of gunk, called plaque, with often fatal consequences. Eventually the plaque ruptures and a blood clot forms; the flow of blood, oxygen, and nutrients is blocked, and a heart attack or stroke ensues.

Fortunately, there are a number of simple lifestyle changes that can protect your arteries from atherosclerosis. In later chapters, you will see how the Cholesterol Down Plan works to dramatically cut your cholesterol and reduce your chances of developing cardiovascular disease, including atherosclerosis.

WHAT IS CHOLESTEROL, ANYWAY?

Everyone talks about cholesterol, but few people actually understand what it is. In physical terms, it is a white fat-like substance with a consistency like candle wax that can be found nearly everywhere in the body: in the membranes of all cells, in the bile stored in the liver, in steroid hormones, and—most important for the purposes of this book—floating through the bloodstream in transport vehicles known as lipoproteins. Despite its bad rap, some cholesterol is vitally important for good health, as it is a major building block for many structures within our bodies—even our bones and teeth, as cholesterol is a precursor for vitamin D.

The cholesterol transit system

Oil doesn’t mix with water, so it shouldn’t be a surprise that oily cholesterol doesn’t mix with blood, which is basically salty water. The body solves this problem by producing waterproof cholesterol transporters called lipoproteins. In addition to cholesterol, lipoproteins also ferry around dietary fat (known in scientific circles as triglyceride, or triacylglycerol) and the fat-soluble vitamins E, D, A, and K. If you were to assemble a lipoprotein, you would need four building blocks: protein, cholesterol, triglycerides, and phospholipids (another type of waxy fat-like material found in high concentration in cell membranes). The amount of each substance varies depending on the class of lipoprotein.

THE FOUR TYPES OF LIPOPROTEINS

Lipoproteins are divided into four main classes according to density: chylomicrons, VLDL, LDL, and HDL (Figure 1.1). Lower-density lipoproteins are characterized by a higher fat-to-protein ratio (fat is lighter) and therefore float more easily in the blood. Here are the basics about the four classes of lipoproteins in order of increasing density:

• Chylomicrons are the least dense of all the lipoproteins and are basically just big balls of fat (triglycerides), with a makeup of about 90 percent fat, a touch of phospholipids, some cholesterol, and a smidgin of protein.

• VLDL (very low-density lipoprotein) carries a great amount of fat, some phospholipids, and cholesterol. The high fat content of VLDL makes a large quantity of this lipoprotein in the blood undesirable.

• LDL (low-density lipoprotein, or “bad” cholesterol) has only a fraction of the fat and double the protein of VLDL and is very high in cholesterol. This lipoprotein carries the majority of cholesterol in the blood and is considered the unhealthy one.

• HDL (high-density lipoprotein, or “good” cholesterol) is a spherical blob of mostly protein (albeit a type different from that found in LDL), some cholesterol, phospholipids, and very little fat. The densest of all the lipoproteins, HDL is the healthy one.

MEASURING YOUR CHOLESTEROL

Your doctor will ask you to fast overnight before having your blood drawn to measure your lipoprotein levels. Fasting ensures that the chylomicrons are gone and have no effect on the sum total of cholesterol or triglycerides swimming around your bloodstream. The lab report will analyze your blood specimen for HDL, LDL, and VLDL. It will show the amount of “good” cholesterol (HDL), “bad” cholesterol (LDL), and triglycerides (blood fat) in the bloodstream. Your doctor may also test you for some risky particle characteristics— such as small and dense LDLs, small HDLs, or big VLDL particles—if you are at high risk for heart disease.

The key to a healthy blood test lies in the cholesterol transport: where the cholesterol goes, how it gets there, and how much of it accumulates. The blood test measures the quantity of cholesterol transport vehicles (aka lipoproteins). A healthy blood test shows a high number of HDL cholesterol transporters (the lipoprotein that carries cholesterol out of the arteries back to the liver for degradation). Too much LDL is unhealthy because it can build up in the inner arterial wall that feeds the heart and brain. In combination with other substances, the cholesterol in LDL forms plaque, which clogs the arteries (atherosclerosis). If a blood clot forms, cells downstream die and a heart attack or stroke occurs. Atherosclerosis is therefore a disease related to problems with cholesterol transport.

HDL, THE LIFESAVING LIPOPROTEIN

HDL is manufactured in the small intestine and the liver, its primary source. As it moves through the bloodstream, it takes in excess cholesterol that leaches out of tissue cells and, most important, excess cholesterol building up in the inner arterial wall. HDLs unload this cholesterol in the liver, where it is then excreted via bile, a process referred to as “reverse cholesterol transport.” Other lipoproteins bring cholesterol into the cells, so it is this reverse transport from the cells to the liver that distinguishes HDL as the “good” cholesterol. An elevated level of HDL has been associated with a reduced risk for heart disease. HDL confers heart-protective benefits in four ways:

1. HDL circulates around the body, picking up excess cholesterol and bringing it back to the liver for disposal (reverse cholesterol transport).

2. HDL is an antioxidant, capable of dismantling rogue free radical molecules that oxidize the protein in the LDL particles—a contributing factor to atherosclerosis. (Oxidation is the same process that produces rust on metals.)

3. HDL is an anti-inflammatory (like aspirin) and can decrease the inflammation linked with the atherosclerotic process.

4. HDL lessens the ability of the blood to form clots, thus reducing the risk of heart attack or stroke.

LDL, THE DEADLY LIPOPROTEIN

LDL is the chief cholesterol carrier in the blood, ferrying approximately 70 percent of all the blood cholesterol around the network of arteries. Basically, this lipoprotein is loaded with cholesterol. Unlike HDL, LDL is not directly manufactured in the liver. Instead, a different type of lipoprotein is first produced by the liver, the parent molecule called VLDL. After circulating around the bloodstream, VLDL loses much of its fat (triglyceride) cache to various bodily cells to become LDL. LDL is designed to take cholesterol to cells that have run short, as cells require some cholesterol to maintain proper functioning. Typically, the LDL is taken into the cell and broken down, and then the cholesterol is used to make membranes or hormones. However, when the amount of LDL in the blood gets too high, the situation can become injurious.

Why is LDL so dangerous?

LDL is commonly referred to as the “bad” cholesterol because high levels of circulating LDL have been linked to an increased risk for atherosclerosis and cardiovascular disease. LDL is the most dangerous lipoprotein, not only because each particle is made up of mostly cholesterol (roughly 45 percent) but also because of its destination. LDL carries cholesterol to the arteries, infiltrates their walls, and goes through a series of transformations that trigger plaque buildup.

What does this “bad” cholesterol look like?

LDL cholesterol is a round lipoprotein that shuttles the bulk of the cholesterol in the blood. The inner core contains oily cholesterol molecules, each with a fatty acid chain dangling from it. Also found within the core is a lesser amount of triglyceride molecules intermingling with the cholesterol esters. Seventy-five percent of the cholesterol within the LDL is in this bound-up (esterified) form, concentrated within the inner core. The greater the concentration of these “chained” cholesterol molecules in the LDL, the more susceptible the LDL molecule is to oxidation (which instigates the catastrophic events that make up the atherosclerotic process), and the higher your risk for developing heart disease.

Surrounding the fatty core of LDL is an outer shell consisting of many fat-like molecules called phospholipids, plus some “unchained” cholesterol. The entire LDL ball is encircled by one big spaghetti- like strand of protein called Apo B (apolipoprotein B-100) (Figure 1.2). This protein molecule plays a crucial role in mooring the LDL molecule onto LDL receptors (more on these later).

EATING YOUR WAY TO A HEART ATTACK

What most people don’t realize is that cholesterol comes from two sources: from food and from our own cells. In fact, we actually make three times more cholesterol (about 1,000–1,200 milligrams per day) than we typically eat. So we don’t need to eat cholesterol because the body is perfectly capable of manufacturing enough of this waxy substance on its own. Still, Americans continue to consume an appreciable amount of cholesterol from dietary sources, which can raise “bad” cholesterol levels and increase our risk of heart disease. The average American ingests approximately 300–400 milligrams of cholesterol every day from animal sources. This amount exceeds the government’s cholesterol-lowering dietary recommendation of no more than 200 milligrams a day. It is simple to eat this much cholesterol: seven ounces of liver (providing 762 milligrams of cholesterol) or two egg yolks (424 milligrams) will easily put you over the top.

In the intestine is a reservoir of cholesterol called the cholesterol pool. The amount of cholesterol that enters the pool from bile is up to five times greater than the amount of cholesterol derived from our diet. Where does all that cholesterol floating around in the intestine go? About half of the approximately 2,000 milligrams in the pool is excreted and half is reabsorbed into the intestinal cells, ultimately going back to the liver. If you could block reabsorption of some of the cholesterol in the intestinal pool so that it gets excreted and not returned to the liver, then you would decrease your circulating LDL level. One class of cholesterol-lowering drugs in particular capitalizes on this concept.

How is cholesterol absorbed from the intestinal pool into the body?

For cholesterol, the gateway into the body is a layer of cells lining the upper intestine known as enterocytes. The only way for cholesterol to get to this layer is to attach itself to a transporter called a micelle. Micelles are small, round transport packages formed by bile salts and phospholipids that carry cholesterol and fat (triglycerides) to the intestinal cell wall. The cholesterol must then take a second transport vehicle—a protein carrier called Niemann- Pick C1 Like 1, or NPC1L1 for short. The NPC1L1 travels through the wall and into the intestinal cell where the cholesterol is packaged into chylomicrons for travel in the lymph system and ultimately the bloodstream. Zetia, the new cholesterol-lowering drug, blocks cholesterol absorption from the intestine by targeting the NPC1L1 protein.

Once in the bloodstream, chylomicrons off-load lots of triglycerides to needy cells, eventually arriving at the liver as small, cholesterol-rich particles known as chylomicron remnants. These remnants signal to the liver cells that they don’t have to make more cholesterol, as a new cholesterol shipment has arrived—cholesterol that may have come from your breakfast omelet. The liver extracts the cholesterol from the remnants to make whatever is required for the day. Typically, the cholesterol is converted into bile acids for its launch into the body’s cholesterol recycling system. But the liver could instead package the cholesterol up as a lipoprotein (primarily VLDL) and send it back into the bloodstream, ultimately increasing the amount of “bad” LDL cholesterol. Eat a huge amount of cholesterol and you increase the delivery of cholesterol to the liver by chylomicron remnants. Therefore, you should avoid foods with high cholesterol in order to lower the amount of cholesterol in your intestinal pool. Less cholesterol overloading the liver means less VLDL exported and less LDL produced.


From the Trade Paperback edition.