Read Wheat Belly: Lose the Wheat, Lose the Weight and Find Your Path Back to Health Online
Authors: William Davis
Wheat Belly: Lose the Wheat, Lose the Weight and Find Your Path Back to Health (21 page)
If glycation accelerates aging, can
not
glycating
slow
aging?
Such a study has been performed in an experimental mouse model, with an AGE-rich diet yielding more atherosclerosis, cataracts, kidney disease, diabetes, and shorter life spans compared to longer-lived and healthier mice consuming an AGE-poor diet.
33
The clinical trial required for final proof of this concept in humans has not yet been performed, i.e., AGE-rich versus AGE-poor diet followed by examination of organs for the damage of aging. This is a practical stumbling block to virtually all anti-aging research. Imagine the pitch: “Sir, we will enroll you in one of two ‘arms’ of the study: You will either follow a high-AGE diet or a low-AGE diet. After five years, we are going to assess your biological age.” Would you accept potential enrollment in the high-AGE group? And how do we assess biological age?
It seems plausible that, if glycation and AGE formation underlie many of the phenomena of aging, and if some foods trigger AGE formation more vigorously than others, a diet low in those foods should slow the aging process, or at least the facets of aging that advance through the process of glycation. A low HbAlc value signifies that less age-promoting endogenous glycation is ongoing. You will be less prone to cataracts, kidney disease, wrinkles, arthritis, atherosclerosis, and all the other expressions of glycation that plague humans, especially those of the wheat-consuming kind.
Perhaps it will even allow you to be honest about your age.
MY PARTICLES ARE BIGGER THAN YOURS: WHEAT AND HEART DISEASE
IN BIOLOGY, SIZE
is everything.
Filter-feeding shrimp, measuring just a couple of inches in length, feast on microscopic algae and plankton suspended in ocean water. Larger predatory fish and birds, in turn, consume the shrimp.
In the plant world, the tallest plants, such as 200-foot kapok trees of the tropical forest, obtain advantage with height, reaching high above the jungle canopy for sunlight required for photosynthesis, casting shadows on struggling trees and plants below.
And so it goes, all the way from carnivorous predator to herbivorous prey. This simple principle predates humans, precedes the first primate who walked the earth, and dates back over a billion years since multicellular organisms gained evolutionary advantage over single-celled organisms, clawing their way through the primordial seas. In countless situations in nature, bigger is better.
The Law of Big in the ocean and plant worlds also applies within the microcosm of the human body. In the human bloodstream, low-density lipoprotein (LDL) particles, what most of the world wrongly recognizes as “LDL cholesterol,” follow the same size rules as shrimp and plankton.
Large LDL particles are, as their name suggests, relatively large. Small LDL particles are—you guessed it—small. Within the human body, large LDL particles provide a survival advantage to the host human. We’re talking about size differences on a nanometer (nm) level, a level of a billionth of a meter. Large LDL particles are 25.5 nm in diameter or larger, while small LDL particles are less than 25.5 nm in diameter. (This means LDL particles, big and small, are thousands of times smaller than a red blood cell but larger than a cholesterol molecule. Around ten thousand LDL particles would fit within the period at the end of this sentence.)
For LDL particles, size of course does not make the difference between eating or being eaten. It determines whether LDL particles will accumulate in the walls of arteries, such as those of your heart (coronary arteries) or neck and brain (carotid and cerebral arteries)—or not. In short, LDL size determines to a large degree whether you will have a heart attack or stroke at age fifty-seven or whether you’ll continue to pull the handle on casino slot machines at age eighty-seven.
Small LDL particles are, in fact, an exceptionally common cause of heart disease, showing up as heart attacks, angioplasty, stents, bypass, and many other manifestations of atherosclerotic coronary disease.
1
In my personal experience with thousands of patients with heart disease, nearly 90 percent express the small LDL pattern to at least a moderate, if not severe, degree.
The drug industry has found it convenient and profitable to classify this phenomenon in the much-easier-to-explain category of “high cholesterol.” But cholesterol has little to do with the disease of atherosclerosis; cholesterol is a convenience of measurement, a remnant of a time when it was not possible to characterize and measure the various lipoproteins (i.e., lipid-carrying proteins) in the bloodstream that cause injury, atherosclerotic plaque accumulation, and, eventually, heart attack and stroke.
“Drink me.”
So Alice drank the potion and found herself ten inches tall, now able to pass through the door and cavort with the Mad Hatter and Cheshire Cat.
To LDL particles, that bran muffin or ten-grain bagel you had this morning is just like Alice’s “Drink me” potion: It makes them small. Starting at, say, 29 nm in diameter, bran muffins and other wheat products will cause LDL particles to shrink to 23 or 24 nm.
2
Just as Alice was able to walk through the tiny door once she had shrunk to ten inches, so the reduced size of LDL particles allows them to begin a series of unique misadventures that normal-size LDL particles cannot enjoy.
Like humans, LDL particles present a varied range of personality types. Large LDL particles are the phlegmatic civil servant who puts in his time and collects his paycheck, all in anticipation of a comfortable state-supported retirement. Small LDLs are the frenetic, antisocial, cocaine-crazed particles that fail to obey the normal rules, causing indiscriminate damage just for laughs. In fact, if you could design an evildoing particle perfectly suited to form gruel-like atherosclerotic plaque in the walls of arteries, it would be small LDL particles.
Large LDL particles are taken up by the liver LDL receptor for disposal, following the normal physiologic route for LDL particle metabolism. Small LDL particles, in contrast, are poorly recognized by the liver LDL receptor, allowing them to linger much longer in the bloodstream. As a
result, small LDL particles have more time to cause atherosclerotic plaque, lasting an average of five days compared to the three days of large LDL.
3
Even if large LDL particles are produced at the same rate as small LDL, the small will substantially outnumber the large by virtue of increased longevity. Small LDL particles are also taken up by inflammatory white blood cells (macrophages) that reside in the walls of arteries, a process that rapidly grows atherosclerotic plaque.
You’ve heard about the benefit of antioxidants? Oxidation is part of the process of aging, leaving a wake of oxidatively modified proteins and other structures that can lead to cancer, heart disease, and diabetes. When exposed to an oxidizing environment, small LDL particles are 25 percent more likely to oxidize than large LDL particles. When oxidized, LDL particles are more likely to cause atherosclerosis.
4
The glycation phenomenon, discussed in chapter
9
, shows itself with small LDL particles as well. Compared to large particles, small LDL particles are eightfold more susceptible to endogenous glycation; glycated small LDL particles, like oxidized LDL, are more potent contributors to atherosclerotic plaque.
5
The action of carbohydrates is therefore twofold: Small LDL particles are formed when there are plentiful carbohydrates in the diet; carbohydrates also increase blood glucose that glycates small LDL. Foods that increase blood glucose the most therefore translate into both greater
quantities
of small LDL and increased
glycation
of small LDL.
So heart disease and stroke are not just about high cholesterol. They are caused by oxidation, glycation, inflammation, small LDL particles … yes, the processes triggered by carbohydrates, especially those made of wheat.
So it’s not really about cholesterol. It’s about the particles that cause atherosclerosis. Today you and I are able to directly quantify and characterize lipoproteins, relegating cholesterol to join frontal lobotomies in the outdated medical practice garbage dump in the sky.
One crucial group of particles, the granddaddy of them all, is very low-density lipoproteins, or VLDL. The liver packages various proteins (such as apoprotein B) and fats (mostly triglycerides) together as VLDL particles, so-called because abundant fats make the particle lower in density than water (thus accounting for the way olive oil floats above vinegar in salad dressing). VLDL particles are then released, the first lipoprotein to enter the bloodstream.
Large and small LDL particles share the same parents, namely VLDL particles. A series of changes in the bloodstream determines whether VLDL will be converted to big or small LDL particles. Interestingly, the composition of diet has a very powerful influence over the fate of VLDL particles, determining what proportion will be big LDL versus what proportion will be small LDL. You may not be able to choose the members
of your own family, but you can readily influence what offspring VLDL particles will have and thereby whether or not atherosclerosis develops.
At the risk of sounding tedious, let me tell you a few things about these lipoproteins in your bloodstream. This will all make sense in just a few paragraphs. At the end of it, you will know more about this topic than 98 percent of physicians.
“Parent” lipoproteins of LDL particles, VLDL, enter the bloodstream after release from the liver, eager to spawn their LDL offspring. On release from the liver, VLDL particles are richly packed with triglycerides, the currency of energy in multiple metabolic processes. Depending on diet, more or less VLDLs are produced by the liver. VLDL particles vary in triglyceride content. In a standard cholesterol panel, excessive VLDL will be reflected by higher levels of triglycerides, a common abnormality.
VLDL is an unusually social being, the lipoprotein life of the party, interacting freely with other lipoproteins passing its way. As VLDL particles bloated with triglycerides circulate in the bloodstream, they give triglycerides to both LDL and HDL (high-density lipoproteins) in return for a cholesterol molecule. Triglyceride-enriched LDL particles are then processed through another reaction (via hepatic lipase) that removes triglycerides provided by VLDL.
So LDL particles begin large, 25.5 nm or greater in diameter, and receive triglycerides from VLDL in exchange for cholesterol. They then lose triglycerides. The result: LDL particles become both triglyceride- and cholesterol-depleted, and thereby several nanometers smaller in size.
6,
7
It doesn’t take much in the way of excess triglycerides from VLDL to begin the cascade toward creating small LDL. At a triglyceride
level of 133 mg/dl or greater, within the “normal” cutoff of 150 mg/dl, 80 percent of people develop small LDL particles.
8
A broad survey of Americans, age 20 and older, found that 33 percent have triglyceride levels of 150 mg/dl and higher—more than sufficient to create small LDL; that number increases to 42 percent in those 60 and older.
9
In people with coronary heart disease, the proportion who have small LDL particles overshadows that of all other disorders; small LDL is, by far, the most frequent pattern expressed.
10
That’s just triglycerides and VLDL present in the usual fasting blood sample. If you factor in the increase in triglycerides that typically follows a meal (the “postprandial” period), increases that typically send triglyceride levels up two- to fourfold for several hours, small LDL particles are triggered to an even greater degree.
11
This is likely a good part of the reason why nonfasting triglycerides, i.e., triglycerides measured without fasting, are proving to be an impressive predictor of heart attack, with as much as five- to seventeen-fold increased risk for heart attack with higher levels of nonfasting triglycerides.
12
VLDL is therefore the crucial lipoprotein starting point that begins the cascade of events leading to small LDL particles. Anything that increases liver production of VLDL particles and/or increases the triglyceride content of VLDL particles will ignite the process. Any foods that increase triglycerides and VLDL during the several hours after eating—i.e., in the postprandial period—will also cascade into increased small LDL.
CONVERTING BREAD TO TRIGLYCERIDES
So what sets the entire process in motion, causing increased VLDL/triglycerides that, in turn, trigger the formation of small LDL particles that cause atherosclerotic plaque?
Simple: carbohydrates. Chief among the carbohydrates? Wheat, of course.
As noted earlier, wheat consumption increases LDL cholesterol; eliminat-wheat reduces LDL cholesterol, all by way of small LDL particles. But lay not look that way at first.
Here’s where it gets kind of confusing.
The standard lipid panel that your doctor relies on to crudely gauge risk for heart disease uses a calculated LDL cholesterol value—
not
a measured value. All you need is a calculator to sum up LDL cholesterol from the following equation (called the Friedewald calculation):
LDL cholesterol = total cholesterol - HDL cholesterol - (triglycerides 4 5)
The three values on the right side of the equation—total cholesterol, HDL cholesterol, and triglycerides—are indeed measured. Only LDL cholesterol is calculated.
The problem is that this equation was developed by making several assumptions. For this equation to work and yield reliable LDL cholesterol values, for instance, HDL must be 40 mg/dl or greater, triglycerides 100 mg/dl or less. Any deviation from these values and the calculated LDL value will be thrown off.
13,
14
Diabetes, in particular, throws off the accuracy of the calculation, often to an extreme degree; 50 percent
inaccuracy is not uncommon. Genetic variants can also throw the calculation off (e.g., apo E variants).
Another problem: If LDL particles are small, calculated LDL will
underestimate
real LDL. Conversely, if LDL particles are large, calculated LDL will
overestimate
real LDL.
To make the situation even more confusing, if you shift LDL particles from undesirably small to healthier large by some change in diet—a good thing—the calculated LDL value will often appear to go
up,
while the real value is actually going
down.
While you achieved a genuinely beneficial change by reducing small LDL, your doctor tries to persuade you to take a statin drug for the
appearance
of high LDL cholesterol. (That’s why I call LDL cholesterol “fictitious LDL,” a criticism that has not stopped the ever-enterprising pharmaceutical industry from deriving $27 billion in annual revenues from sales of statin drugs. Maybe you benefit, maybe you don’t; calculated LDL cholesterol might not tell you, even though that is the FDA-approved indication: high
calculated
LDL cholesterol.)
The only way for you and your doctor to truly know where you stand is to actually measure LDL particles in some way, such as LDL particle number (by a laboratory method called nuclear magnetic resonance, or NMR, lipoprotein analysis) or apoprotein B. (Because there is one apoprotein B molecule per one LDL particle, apoprotein B provides a virtual LDL particle count.) It’s not that tough, but it requires a health practitioner willing to invest the extra bit of education to understand these issues.