Read Wheat Belly: Lose the Wheat, Lose the Weight and Find Your Path Back to Health Online
Authors: William Davis
The rate of aging varies from individual to individual. We’ve all known a man or woman at, say, age sixty-five who still could
pass for forty-five—maintaining youthful flexibility and mental dexterity, fewer wrinkles, straighter spine, thicker hair. Most of us have also known people who show the reverse disposition, looking older than their years.
Biological
age does not always correspond to
chronological
age.
Nonetheless, aging is inevitable. All of us age. None will escape it—though we each progress at a somewhat different rate. And, while gauging chronological age is a simple matter of looking at your birth certificate, pinpointing biological age is another thing altogether. How can you assess how well the body has maintained youthfulness or, conversely, submitted to the decay of age?
Say you meet a woman for the first time. When you ask her how old she is, she replies, “Twenty-five years old.” You do a double take because she has deep wrinkles around her eyes, liver spots on the back of her hands, and a fine tremor to her hand movements. Her upper back is bowed forward (given the unflattering name of “dowager’s hump”), her hair gray and thin. She looks ready for the retirement home, not like someone in the glow of youth. Yet she is insistent. She has no birth certificate or other legal evidence of age, but insists that she is twenty-five years old—she’s even got her new boyfriend’s initials tattooed on her wrist.
Can you prove her wrong?
Not so easy. If she were a caribou, you could measure antler wingspan. If she were a tree, you could cut her down and count the rings.
In humans, of course, there are no rings or antlers to provide an accurate, objective biological marker of age that would prove that this woman is really seventysomething and not twentysome-thing, tattoo or no.
No one has yet identified a visible age marker that would permit you to discern, to the year, just how old your new friend is. It’s not for lack of trying. Age researchers have long sought such biological markers, measures that can be tracked, advancing a year for every chronological year of life. Crude gauges of age have been
identified involving measures such as maximal oxygen uptake, the quantity of oxygen consumed during exercise at near-exhaustion levels; maximum heart rate during controlled exercise; and arterial pulse-wave velocity, the amount of time required for a pressure pulse to be transmitted along the length of an artery, a phenomenon reflecting arterial flexibility. These measures all decline over time, but none correlate perfectly to age.
Wouldn’t it be even more interesting if age researchers identified a do-it-yourself gauge of biological age? You could, for instance, know at age fifty-five that, by virtue of exercise and healthy eating, you are biologically forty-five. Or that twenty years of smoking, booze, and French fries has made you biologically sixty-seven and that it’s time to get your health habits in gear. While there are elaborate testing schemes that purport to provide such an aging index, there is no single simple do-it-yourself test that tells you with confidence how closely biological age corresponds to chronological age.
Age researchers have diligently sought a useful marker for age because, in order to manipulate the aging process, they require a measurable parameter to follow. Research into the slowing of the aging process cannot rely on simply
looking.
There needs to be some objective biological marker that can be tracked over time.
To be sure, there are a number of differing, some say complementary, theories of aging and opinions on which biological marker might provide the best gauge of biologic aging. Some age researchers believe that oxidative injury is the principal process that underlies aging and that an age marker must incorporate a measure of cumulative oxidative injury. Others have proposed that cellular debris accumulates from genetic misreading and leads to aging; a measure of cellular debris would therefore be required to yield biologic age. Still others believe that aging is genetically preprogrammed and inevitable, determined by a programmed sequence of diminishing hormones and other physiologic phenomena.
Most age researchers believe that no single theory explains all the varied experiences of aging, from the supple, high-energy, know-everything teenage years, all the way to the stiff, tired, forget-everything eighth decade. Nor can biologic age be accurately pinpointed by any one measure. They propose that the manifestations of human aging can be explained only by the work of more than one process.
We might gain better understanding of the aging process if we were able to observe the effects of
accelerated
aging. We need not look to any mouse experimental model to observe such rapid aging; we need only look at humans with diabetes. Diabetes yields a virtual proving ground for accelerated aging, with all the phenomena of aging approaching faster and occurring earlier in life—heart disease, stroke, high blood pressure, kidney disease, osteoporosis, arthritis, cancer. Specifically, diabetes research has linked high blood glucose of the sort that occurs after carbohydrate consumption with hastening your move to the wheelchair at the assisted living facility.
Americans have lately been bombarded with a tidal wave of complex new terms, from collateralized debt obligations to exchange-traded derivative contracts, the sorts of things you’d rather leave to experts such as your investment banking friend. Here’s another complex term you’re going to be hearing a lot about in the coming years: AGE.
Advanced glycation end products, appropriately acronymed AGE, is the name given to the stuff that stiffens arteries (atherosclerosis), clouds the lenses of the eyes (cataracts), and mucks up the neuronal connections of the brain (dementia), all found in abundance in older people.
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The older we get, the more AGEs can be recovered in kidneys, eyes, liver, skin, and other organs. While
we can see some of the effects of AGEs, such as the wrinkles in our pretend twenty-five-year-old following Lucille Ball’s advice, it does not yet provide a precise gauge of age that would make a liar out of her. Although we can see evidence of some AGE effects—saggy skin and wrinkles, the milky opacity of cataracts, the gnarled hands of arthritis—none are truly quantitative. AGEs nonetheless, at least in a qualitative way, identified via biopsy as well as some aspects apparent with a simple glance, yield an index of biological decay.
AGEs are useless debris that result in tissue decay as they accumulate. They provide no useful function: AGEs cannot be burned for energy, they provide no lubricating or communicating functions, they provide no assistance to nearby enzymes or hormones, nor can you snuggle with them on a cold winter’s night. Beyond effects you can see, accumulated AGEs also mean loss of the kidneys’ ability to filter blood to remove waste and retain protein, stiffening and atherosclerotic plaque accumulation in arteries, stiffness and deterioration of cartilage in joints such as the knee and hip, and loss of functional brain cells with clumps of AGE debris taking their place. Like sand in your spinach salad or cork in the cabernet, AGEs can ruin a good party.
While some AGEs enter the body directly because they are found in various foods, they are also a by-product of high blood sugar (glucose), the phenomenon that defines diabetes.
The sequence of events leading to formation of AGEs goes like this: Ingest foods that increase blood glucose. The greater availability of glucose to the body’s tissues permits the glucose molecule to react with any protein, creating a combined glucose-protein molecule. Chemists talk of complex reactive products such as Amadori products and Schiff intermediates, all yielding a group of glucose-protein combinations that are collectively called AGEs. Once AGEs form, they are irreversible and cannot be undone. They also collect in chains of molecules, forming AGE polymers that are especially disruptive.
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AGEs are notorious for
accumulating right where they sit, forming clumps of useless debris resistant to any of the body’s digestive or cleansing processes.
Thus, AGEs result from a domino effect set in motion anytime blood glucose increases. Anywhere that glucose goes (which is virtually everywhere in the body), AGEs will follow. The higher the blood glucose, the more AGEs will accumulate and the faster the decay of aging will proceed.
Diabetes is the real-world example that shows us what happens when blood glucose remains high, since diabetics typically have glucose values that range from 100 to 300 mg/dl all through the day as they chase their sugars with insulin or oral medications. (Normal fasting glucose is 90 mg/dl or less.) Blood glucose can range much higher at times; following a bowl of slow-cooked oatmeal, for instance, glucose can easily reach 200 to 400 mg/dl.
If such repetitive high blood sugars lead to health problems, we should see such problems expressed in an exaggerated way in diabetics … and indeed we do. Diabetics, for instance, are two to five times more likely to have coronary artery disease and heart attacks, 44 percent will develop atherosclerosis of the carotid arteries or other arteries outside of the heart, and 20 to 25 percent will develop impaired kidney function or kidney failure an average of eleven years following diagnosis.
3
In fact, high blood sugars sustained over several years virtually
guarantee
development of complications.
With repetitive high blood glucose levels in diabetes, you’d also expect higher blood levels of AGEs, and indeed, that is the case. Diabetics have 60 percent greater blood levels of AGEs compared to nondiabetics.
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AGEs that result from high blood sugars are responsible for most of the complications of diabetes, from neuropathy (damaged nerves leading to loss of sensation in the feet) to retinopathy (vision defects and blindness) to nephropathy (kidney disease and kidney failure). The higher the blood sugar and the longer blood sugars stay high, the more AGE products will accumulate and the more organ damage results.
Diabetics with poorly controlled blood sugars that stay high for too long are especially prone to diabetic complications, all due to the formation of abundant AGEs, even at a young age. (Before the value of “tightly” controlled blood sugars in type 1, or childhood, diabetes was appreciated, it was not uncommon to see kidney failure and blindness before age thirty. With improved glucose control, such complications have become far less common.) Large studies, such as the Diabetes Control and Complications Trial (DCCT)
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, have shown that strict reductions in blood glucose yield reduced risk for diabetic complications.
Outside of the complications of diabetes, serious health conditions have been associated with excessive production of AGEs.
Many of the damaging effects of AGEs work through increased oxidative stress and inflammation, two processes underlying numerous disease processes.
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On the other hand, recent studies have shown that reduced AGE exposure leads to reduced expression of inflammatory markers such as c-reactive protein (CRP) and tumor necrosis factor.
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AGE accumulation handily explains why many of the phenomena of aging develop. Control over glycation and AGE accumulation therefore provides a potential means to reduce all the consequences of AGE accumulation.
This is because the rate of AGE formation is dependent on the level of blood glucose: The higher the blood glucose, the more AGEs are created.
AGEs form even when blood sugar is normal, though at a much lower rate compared to when blood sugar is high. AGE formation therefore characterizes normal aging of the sort that makes a sixty-year-old person look sixty years old. But the AGEs accumulated by the diabetic whose blood sugar is poorly controlled cause
accelerated
aging. Diabetes has therefore served as a living model for age researchers to observe the age-accelerating effects of high blood glucose. Thus, the complications of diabetes, such as atherosclerosis, kidney disease, and neuropathy, are also the diseases
of aging, common in people in their sixth, seventh, and eighth decades, uncommon in younger people in their second and third decades. Diabetes therefore teaches us what happens to people when glycation occurs at a faster clip and AGEs are permitted to accumulate. It ain’t pretty.