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Remember Sherri (photo above)? She shared her before and after Wheat Belly photos with us a few months ago, a striking example of the age-reversing effects of this lifestyle. (More on Sherri’s story can be found here.)

Follow the many conversations here in Wheat Belly land, and you will take notice of how often people look younger following this lifestyle. Turning the clock back 10, even 20, years is common. So I thought it would be relevant to bring back a conversation I provided in the original Wheat Belly book, a discussion of aging, why it happens, and what can be done about it.

People following the Wheat Belly lifestyle look younger, but there are real phenomena going on beneath the surface that reflect a slowed aging process. This is yet another example of an adverse effect of grain consumption that has nothing to do with “gluten,” as these youth-preserving effects are due to elimination of the amylopectin A carbohydrate of wheat and grains. Gram for gram, ounce for ounce, the amylopectin A starch of grains raises blood sugar higher than any other carbohydrate or sugar, even table sugar.


Cataracts, Wrinkles, and Dowager’s Humps: Wheat and the Aging Process

“The secret of staying young is to live honesty, eat slowly, and lie about your age.”
Lucille Ball


Wine and cheese may benefit from aging. But for humans, aging can lead to everything from white lies to a desire for radical plastic surgery.

What does it mean to get old?

Though many people struggle to describe the specific features of aging, we would likely all agree that, like pornography, we know it when we see it.

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 met 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 year 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 twentysomething, 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, advance 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 eight 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 phenomenon 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.


No country for old bread eaters

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. 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. 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.

(Discussion continued on page 135 of Wheat Belly.)