The studies to date have achieved proof of concept: Reduction of carbohydrates improves blood sugar, reducing the diabetic tendency. It is possible to eliminate diabetes medications in as little as a few weeks to months. In many instances, I believe it is safe to call that a cure, provided excess carbohydrates don’t make their way back into the diet. Let me say that again: If sufficient pancreatic beta cells remain and have not yet been decimated by long-standing glucotoxicity, lipotoxicity, and inflammation, it is entirely possible for some, if not most, prediabetics and diabetics to be cured of their condition, something that virtually never happens with conventional low-fat, plentiful grain diets such as that advocated by the American Diabetes Association.
It also suggests that prevention of diabetes, rather than reversal of diabetes, can be achieved with less intensive dietary efforts. After all, some carbohydrate sources, such as blueberries, raspberries, peaches, and sweet potatoes, provide important nutrients and don’t increase blood glucose to the same extent that more “obnoxious” carbohydrates can. (You know what I’m talking about.)
So what if we follow a program not quite so strict as the Westman “cure diabetes” study, but just eliminate the most ubiquitous, diet-dominating, blood sugar–increasing foods of all? You will drop blood sugar and HbA1c, lose visceral fat, and free yourself from the risk of participating in this nationwide epidemic of obesity, prediabetes, and diabetes. It would scale back diabetes to pre-1985 levels, restore 1950s dress and pants sizes, even allow you to again sit comfortably on the airline flight next to other normal-weight people.
“IF IT DOESN’T FIT, YOU MUST ACQUIT”
The wheat-as-guilty-culprit in causing obesity and diabetes reminds me of the O. J. Simpson murder trial: evidence found at the scene of the crime, suspicious behavior by the accused, bloody glove linking murderer to victim, motive, opportunity…but absolved through clever legal sleight of hand.
Wheat looks every bit the guilty party in causing diabetes: It plays a dominant role in the breakfast, lunch, dinner, and snacks of the majority of Americans, just as government advice advised. It increases blood sugar more than nearly all other foods, providing ample opportunity for glucotoxicity, lipotoxicity, and inflammation. It promotes visceral fat accumulation. There is a fits-like-a-glove correlation with weight gain and obesity trends over the past forty years—yet it has been absolved of all crimes by the “Dream Team” of the USDA, the American Diabetes Association, the Academy of Nutrition and Dietetics, etc., all of whom agree that wheat and its grain cousins should be consumed in generous quantities. I don’t believe that even Johnnie Cochran could have done any better.
Can you say “mistrial”?
In the court of human health, however, you have the opportunity to redress the wrongs by convicting the guilty party and banishing wheat and its co-conspirators from your life.
CHAPTER 9
CATARACTS, WRINKLES, AND DOWAGER’S HUMPS: WHEAT AND THE AGING PROCESS
The secret of staying young is to live honestly, 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 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 emphatic. 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 seventy-something and not twenty-something, 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 with 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 measure 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 track a measure of cumulative oxidative injury. Others have proposed that cellular debris accumulates from genetic misreading and leads to aging; measuring cellular debris would therefore 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. 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, dementia, 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 product, 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.1 The older we get, the more AGEs accumulate in the 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 see evidence of some AGE accumulation—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 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, brittleness 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 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 proteins, 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.2 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 70 to 90 mg/dl.) Blood glucose can range much higher at times; following a bowl of slow-cooked organic oatmeal without sugar, 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 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 non-diabetics.4
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 can be delayed.) Large studies, such as the Diabetes Control and Complications Trial (DCCT),5 have shown that strict reductions in blood glucose yield reduced risk for diabetic complications.
WHAT HAPPENS WHEN YOU AGE?
Outside of the complications of diabetes, serious health conditions have been associated with excessive or accelerated production of AGEs.
Kidney disease—When AGEs are administered to an experimental animal, it develops all the hallmarks of kidney disease.6 AGEs can also be found in human kidneys from persons suffering from kidney disease.
Atherosclerosis—Oral administration of AGEs in both animals and humans causes constriction of arteries, abnormal excessive tone (endothelial dysfunction) that lays the groundwork for atherosclerosis.7 AGEs also modify LDL particles, blocking their normal uptake by the liver and routing them for uptake by inflammatory cells in artery walls, the process that grows atherosclerotic plaque.8 AGEs can be recovered from tissues and correlated with plaque severity: The higher the AGE content of various tissues, the more severe the atherosclerosis.9
Dementia—In Alzheimer’s dementia sufferers, brain AGE content is threefold greater than in normal brains, accumulating in the amyloid plaques and neurofibrillary tangles that are characteristic of the condition.10 In line with the marked increase of AGE formation in diabetics, dementia is 500 percent more common in people with diabetes.11
Cancer—While the data are only spotty, the relationship of AGEs to cancer may prove to be among the most important of all AGE-related phenomena. Evidence for abnormal AGE accumulation has been identified in cancers of the pancreas, breast, lung, colon, and prostate.12
Male erectile dysfunction—If I haven’t already gotten the attention of male readers, then this should do it: AGEs impair erectile capacity. AGEs are deposited in the portion of penile tissue responsible for the erectile response (corpus cavernosum), disabling the penis’s ability to engorge with blood, the process that drives penile erections.13
Eye health—AGEs damage eye tissue, from the lens (cataracts) to the retina (retinopathy) to the lacrimal glands (dry eyes).14
Many of the damaging effects of AGEs work through increased oxidative stress and inflammation, two mechanisms underlying numerous disease processes.15 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.16
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 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 accelerate 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, increasingly 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.
The story doesn’t end at greater levels of AGEs. Higher AGE blood levels spark the expression of oxidative stress and inflammatory markers.17 The receptor for AGEs, or RAGE, is the gatekeeper to an assortment of oxidative and inflammatory responses (such as inflammatory cytokines, vascular endothelial growth factor, and tumor necrosis factor).18 AGEs therefore set an army of oxidative and inflammatory responses in motion, all leading to heart disease, cancer, diabetes, and more.
AGE formation is consequently a continuum. AGEs form at normal blood glucose levels, but they form faster at higher blood sugar levels. The higher the blood glucose, the more AGEs form. All it takes is a little extra blood sugar, just a few milligrams above normal, and—voilà—you’ve got AGEs doing their dirty work, gumming up your organs.
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