Cholesterol Phobia

Cholesterol research is difficult, esoteric and accessible in journals that seldom make it beyond their target audience – other people doing the same type of work. One theory about the relationship of cholesterol and heart disease has dominated medical practice for over half a century, but there has always been dissension in the ranks of scientists, some of whom labor away in obscurity, slowly building a case that may one day topple the current dogma. I have attempted to make this subject accessible to a non-medical audience because the current paradigms for thinking about heart disease and treating it affect everyone who sees a doctor, listens to the news or reads the popular press – even children, because they eat what their parents believe is healthy for them.   
Cholesterol phobia: is the end in sight?

       Cholesterol earned a villain’s reputation because it got caught at many criminal scenes where victims succumbed to heart attacks. It was found lurking in the walls of arteries too narrowed by “plaques” to allow blood passage. Even in young healthy men, cholesterol- laden “fatty streaks” were surprise findings at autopsy after accidental or war-related death. Experimentally, fat choked arteries were easy to produce in experimental animals by feeding them food pellets saturated with fat – even olive oil worked. The laboratory work bolstered attempts to show that different populations consuming different amounts of fat had different rates of heart disease. Though both the laboratory and epidemiology studies were fraught with contradictory results, and the dietary cholesterol theory of heart disease was initially rejected by the American Heart Association, the personalities and scientific politics involved eventually catapulted the theory into the lives of all Americans, over 20 million of whom are now on potent drugs to combat the evil substance. 

The dietary theory of heart disease

       After more than half a century of war on cholesterol, the dietary theory remains just that – a theory – no matter how many commercials remind you that you need to lower your cholesterol. You may be surprised to hear that cholesterol could be absolved of its villainous status, within your lifetime. But don’t expect your doctor to agree, at least not yet. The cholesterol theory has a grip on our culture that is almost religious. The current dogma, advertised everywhere, is simple: there is good cholesterol, labeled HDL, and bad cholesterol, labeled LDL and anyone who cares a whit about his health will do whatever it takes to get those numbers in line with the current recommendations of the American Heart Association –eat a low fat diet, exercise, and take the right drugs. 

Inconvenient facts

Inconvenient facts have always dogged the theory. Cholesterol levels plummet in seizure patients treated with high fat, no carbohydrate diets. Heart attacks occur despite normal cholesterol levels. Low fat diets raise cholesterol levels -President Eisenhower was one of the most famous examples. And buried in the literature of the last half century are many clues pointing a blaming finger away from cholesterol and toward the complex lipoproteins that ferry it around the body. As more and more questions are raised about the efficacy and dangers of drugs that reduce cholesterol, more attention may turn to these lipoproteins. After all, like cholesterol, they have been part of the statistic most closely associated with heart disease – the LDL (low-density lipoprotein) cholesterol. 

What are lipoproteins? 

       Total cholesterol measures cholesterol attached to lipoproteins. Lipoproteins are combinations of phospholipids (fats that dissolve in water) and specialized proteins that fit like keys into receptors on cells. Lipoproteins function like cargo ships, carrying fats to cells for fuel, to fat tissue for storage, and back to the liver for reprocessing when demanded. More or less cholesterol crowds aboard each boat depending on the number of boats available. The size of the fleet, in turn, depends on the amount of triglycerides (another type of fat), awaiting shipment. 

Triglycerides rule

        Triglycerides and cholesterol are very different fats. Triglycerides provide the fatty acids that fuel most cells and are stored in fat tissue for later energy demands. Cholesterol yields no energy at all. It is a building block, used in the construction of all cell membranes and in the making of hormones and bile. Not all cholesterol comes from fat in the diet. The brain makes its own, and the liver and skin make whatever the body needs – raising production whenever dietary intake is low. Cholesterol and triglycerides attached to lipoproteins are like citizens of two different countries travelling together on one of the country’s boats. That country that builds the boats belongs to the triglycerides. The more triglycerides present in the body, the more lipoproteins in the fleet.    

The varying density of lipoproteins 

Lipoproteins fully loaded with cholesterol and triglycerides are fluffy and buoyant (fat floats) and called very low density lipoproteins, VLDL for short. They dock at cells in need of fuel or cholesterol, unload some cargo, lose some buoyancy, and become a little denser. Eventually they become low-density lipoproteins (LDL) and , with no energy or building material left to give up, they return to the liver for recycling. Another particle type called high-density lipoprotein (HDL) is even less buoyant – and less well understood. In contrast to cholesterol bound to LDL and VLDL, the cholesterol carried by HDL particles, like the cholesterol carried away from the intestines by chylomicrons (very large lipoproteins) does not contribute to the storage of fat in any tissues so is not associated with plaque formation in arteries. 

What do the anti-cholesterol drugs do? 

       The widely prescribed statin drugs block the body’s ability to make cholesterol, which makes less cholesterol available to be loaded on to the lipoprotein boats. But boat make proceeds apace because it is driven by the amount of triglyceride awaiting transport- and the triglycerides, remember, come from dietary carbohydrates. Lowering cholesterol manufacture does not lower  lipoprotein production  – the lipoprotein boats will simply carry less cholesterol per lipoprotein particle, making each particle smaller and denser. Will this magically keep cholesterol out of artery walls? Not a good bet. Lipoprotein research labs have identified seven different particle types within the LDL fraction of total cholesterol. Heart risk appears to be correlated with the smallest and densest sub-fraction – the kind carrying the least amount of fat per molecule. (The anti-cholesterol drugs do have an independent anti-inflammatory effect which may be the way they diminish risk of a cardiac event in people with heart disease.) 

Take-away message

       So how does this complicated information change your life? Triglycerides, the stimulus for VLDL and LDL production, are a product of carbohydrate processing – especially of sugars and refined grains. Lowering VLDL production and hence LDL production requires lowering dietary carbohydrates – not fat, not cholesterol. Blood cholesterol isn’t even a good marker for total body cholesterol, which includes cholesterol squirreled away in artery walls. Cholesterol in arteries behaves much like cholesterol stored in fat tissue. It is responsive to the entire array of interconnected feedback loops involve not only fats, but carbohydrates and insulin and all the other hormones. It is time to respect its complexity and quit expecting that coaxing the body to make less cholesterol by taking drugs to block its production, or by eliminating it form the diet will end the scourge of heart disease. 

The Sweet Tooth: Pathway to a Broken Heart?

For the last half a century or more we have believed the dietary cholesterol theory about heart disease, a hypothesis (idea to be tested by experiment) that found favor with researchers, grant makers, doctors and drug makers. What if this theory is wrong? What if cholesterol in artery walls has less to do with dietary fat than with the way the body processes carbohydrates? What if refined sugars and grains are the dietary culprits? Could insulin, the master hormone at the center of all energy processing, be a better marker than cholesterol for heart disease?

What is blood sugar?

The first thing to understand about sugar is that the blood sugar is not the same thing as the sugar in your pantry. Or the sugar in soft drinks or the sugar in fresh fruit. Blood sugar is a simple molecule called glucose – a product of plants’ ability to convert the energy of the sun into starches, long chains of glucose linked together. When you eat a starch, the digestion process breaks down the chains into simple glucose molecules which circulate in your blood. Glucose is used by every cell in the body for energy, and is also made into glycogen for storage in liver and muscle.The sugar in your pantry is sucrose extracted from plants, specifically cane grasses and beets, by a refining process that concentrates and crystallizes it. Each sucrose molecule is a combination of one glucose molecule with another of fructose, a chemically different plant sugar molecule.

The taste for sweetness is innate and possibly addictive. Before the advent of refined sugar, indulging the sweet tooth was difficult. The only edible sources were berries and fruits and small amounts of honey guarded by nasty bees – all confined by climate and geography. Sugar made its way into the human diet slowly, spreading from the East to the West as the secret of this “liquid gold” made its way along routes of commerce.

Sugar and the diseases of civilization

With time and commerce, consumption of sugar and refined grains skyrocketed. The diseases of civilization – diabetes, heart disease and obesity – followed refined sugar, flour and rice around the world, appearing wherever old dietary staples were replaced by these “white” foods. By the 1920s, the Americans averaged 110-120 pounds of sugar per person per year. We inched up to 124 pounds by the late 1970s. Then came the Japanese chemical innovation that made high-fructose corn syrup (HFCS) a dietary staple. By 2000, HFCS bumped sugar consumption up to 150 lbs. per year, largely in the form of sweetened drinks.

High fructose corn syrup 

HFCS differs from sucrose because the ratio of fructose to glucose in corn syrup is 10% higher than in table sugar – 55:45 instead of 50:50. Some scientists believe that it is the remarkable increase in fructose consumption in modern times that correlates with the appearance of the metabolic syndrome – abdominal obesity, high fasting blood sugar, high triglycerides, abnormal lipoprotein levels and high blood pressure. If so, a 10% increase in fructose combined with a recent, large jump in overall sugar consumption may spell real trouble.
How can fructose cause trouble? Isn’t it the primary sugar of fruits? Yes, but eating an apple with a small amount of fructose combined with absorption-slowing fiber hardly nudges blood sugar up – a far cry from the blood sugar spike after 20 ounces of an HFCS sweetened beverage. Drink a coke, and about 60% of the glucose in the HFCS goes directly into the blood for immediate use, and 40 % into the liver for storage as glycogen. The fructose all goes to the liver for conversion into fat – released into the blood as triglycerides. The higher the fructose in the diet, the higher the triglycerides in the blood. Fructose is a “lipogenic” or fat-producing sugar, and long term consumption also raises LDL or bad cholesterol.

The problems with too much sugar

Once sugar consumption exceeds the small amounts nature provides without refining techniques, trouble begins. The different ways the body processes fructose and glucose combine to produce very efficient fat production. A rise in blood glucose prompts the pancreas to put out insulin to help ferry glucose into cells for energy use or storage. Insulin, like fructose, is “lipogenic” because it helps move fats into storage depots in three areas – the liver, fat tissue, and the walls of arteries. And as triglycerides are formed from fructose, insulin busies itself shuttling them around the liver and out into the blood. The pancreas then produces even more insulin to take care of the glucose – this is the phenomenon known as insulin resistance, part of the metabolic syndrome associated with heart disease.

Is it the cholesterol or the sugar?

The theory that cholesterol in dietary fat is the direct cause of cholesterol deposits in arteries requires a leap over the metabolic pathways that process simple sugars and are intimately involved in fat formation and storage – and over the fact that many people with low cholesterol levels have heart disease. Over the last half century, many researchers and doctors made the leap because they believed the theory. Just as important to widespread acceptance, though, were less scientific influences like the cheap availability of a test for blood cholesterol, the difficulty and expense of measuring insulin, and the dominance of researchers devoted to the dietary cholesterol theory over those who questioned it.

Medical history books contain an embarrassing array of once-unassailable theories and practices that have fallen by the wayside. Despite a modern sense of scientific invincibility, current medical ideas are not immune from error. Sugar and refined carbohydrates are not yet the poster children for the scourge of heart disease, but they may be a far better target than cholesterol. If the dietary fat theory gives way to the sugar theory, the massive push to lower cholesterol by diet and drugs may go into the books as one of those once-unassailable ideas that eventually fell.

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