The Antioxidant Prescription – Chapter 2

via Bryce Wylde



In the spirit of the latest controversy around antioxidants and whether they may contribute to cancer, and today’s Dr OZ show, I have posted the first three chapters of my first book The Antioxidant Prescription: How to Use the Power of Antioxidants to Prevent Disease and Stay Healthy for Life. It is available in full from your local Indigo or Chapters book store or online at and (soft cover, kindle, and e-book all available)

The Antioxidant Prescription
How to Use the Power of Antioxidants to Prevent Disease and Stay Healthy for Life


Bryce Wylde BSc, RNC, DHMHS, HD


Random House Canada

Chapter 2: The Radical Truth

Part One

Chapter 2

The Radical Truth

In the first chapter I introduced you to free radicals and their dedicated opponents, the antioxidants. The relationship between these two classes of molecules is a curious one and one important to our health status. As you progress from chapter to chapter, I’m going to help you make the diet and lifestyle choices that will positively influence that relationship.
If we’re going to learn how to deal with free radicals, we need to know something about their background and the background of their adversaries, the antioxidants. Bad guys and their opponents are always interesting. If they indeed have a truly intimate connection to humankind, how did that connection come about? How did we come to recognize them and their numerous but almost unfathomably tiny crimes and heroic rescues? That’s the subject of this chapter.

Oxygen: An Unreliable Friend

Some time ago—two billion years, give or take a few hundred million—life was much simpler. Among the inhabitants of the Earth during that Paleoproterozoic or “old-first-life” era, some minuscule but plentiful organisms called anaerobes busily went about their lives, most of them in swampy fluid. Anaerobe means “without oxygen.” But as living creatures, they still consumed nutrients and excreted wastes. Their waste was in fact oxygen, a gas that percolated up through the slimy sludge they inhabited. Much as we now risk suffocating ourselves with carbon dioxide emissions, these plentiful anaerobes smothered in oxygen. There was nothing willing or able to clean this new oxygen stuff up as it accumulated to the point at which the anaerobes were simply swimming in it. Eventually, many of them died. Some of them managed to survive the “oxygen catastrophe” and still exist today—in our gut, for example, where they render great service to our digestion and our immune system.
This waste oxygen saturating the previously oxygen-free atmosphere turned out to be highly reactive, chemically speaking. It readily combined with other molecules, and in due course a new type of creature evolved that could actually use oxygen’s eager reactions as a power source—a highly efficient power source, too. The rest, as they say, is prehistory.
But oxygen has forever proven to be a bit of a two-faced friend to living things. Its tendency to lively interactions made it perfect for fueling the little energy plants called mitochondria that were floating around in almost every one of the newly evolving organisms. But the same quality caused it to make mischief when it reacted with things it shouldn’t—and still does. A perfect example is the spark that leaps from a fireplace to burn down a house. Without oxygen, there can be no fire—for better and worse. So oxygen is already a bit of a hyperactive party atom, but some kinds of oxygen carry this to extremes. Your average well-balanced atom has a nucleus at the centre, and whizzing around the nucleus is the familiar cloud of electrons—just the right number of them. Under certain circumstances, however, atoms can lose an electron or two, and such atoms then wander around looking everywhere for replacement electrons attached to other atoms. These are the needful characters we call radicals—and sometimes free radicals. None of them are more reactive than the oxygen radicals.
As I said, life—that always resourceful form of matter—eventually found a way to exploit, or at least co-opt, oxygen radicals. They could be sent in to blow up bacteria that invaded a living creature. They could be used as signal runners from cell to cell within larger multicelled creatures. But oxygen radicals could never be trusted, then or now; they’re just too radical. Living creatures have struggled to evolve ways and means of neutralizing these feckless allies since the very beginnings of life. How successful have we been? That’s part of the message of this book.

The Seekers

In 1954, in the depths of the Cold War, Dr. Denham Harman was studying the effects of radiation on human biological systems at the University of Berkeley in California. He was searching for viable antidotes to the sort of radiation poisoning that would result from an atomic attack.
Free radicals had been studied by chemists since the first one was discovered in 1900, and Harman understood that complex free radical reactions could result from radiation exposure. He also understood that what made radiation exposure so dangerous was that it triggered the production of the hydroxyl radical, the most powerful and deadly oxygen radical known—one that cannot be neutralized by the evolved defence systems of the human body. Large doses of radiation, of course, cause cancer or death, but Harman noticed that mild radiation poisoning produced symptoms similar to premature aging. Since low levels of radical molecules occur naturally in the human body, he wondered if the slow release of naturally occurring free radicals might be responsible for aging and for disease processes. In other words, though radiation-produced radicals were quicker, and therefore deadlier, there might be a connection between them and the free radicals produced by the day-to-day metabolism of the body.
I’ve mentioned that antioxidants are molecules that (as their name suggests) neutralize oxygen radicals without becoming unstable themselves. During the early years of Harman’s research, certain antioxidants were already known to provide protection against radiation exposure. Harman took the next conceptual step. In 1956 he published his free radical theory of aging, which became one of the most widely accepted explanations for the aging process. Harman’s theory proposed that a by-product of oxygen metabolism in the human body—free radical molecules—can react chemically with the molecules of cells and their DNA, breaking necessary links and chains and disrupting structures and eventually bringing about the process we call aging—and ultimately death. By 1957, Harman had demonstrated that antioxidants, by neutralizing free oxygen radicals, could extend the average lifespan of laboratory mice.
Despite Harman’s pioneer work, at the time most biochemists were interested in free radicals only for their important role in the manufacture of plastics. These molecules were regarded as too short-lived and too uncontrollable to play any role in serious life-and-death processes. But then, in 1961, Leonard Hayflick and Paul Moorhead, working at the Stanford University School of Medicine, determined that normal cells can divide only a limited number of times, after which cells effectively commit suicide. The number of times a cell is genetically programmed to reproduce, dubbed the “Hayflick limit,” varies from species to species. In the case of human cells, the Hayflick limit is about fifty and is directly linked to the lifespan of individuals. Put bluntly, it’s difficult for you and me to live on when our cells are preprogrammed to conk out after so many recycles. Here, suggested Hayflick and Moorhead, might be the truth about aging.
As work in this area progressed, it turned out that free radicals played a role in this programming. In fact, free radicals have turned out to be nature’s preferred mechanism of self-destruction when a cell’s time is up. The scientific name for this programmed death is “apoptosis.”
In the last thirty years, free radical research has led to profound biochemical, biological and medical advances. Our knowledge of radicals has grown, and as it has grown, it has enhanced our understanding of how DNA mutates and the important role radicals play in cancer, cardiovascular disease, stroke, Alzheimer’s disease, Parkinson’s disease and autoimmune diseases.
Meanwhile, the study of antioxidants has also moved forward. Dr. Lester Packer, a senior scientist at Lawrence Berkeley Laboratory, was among the first to describe the role of antioxidants in the health of organisms. He proposed that antioxidants function not singly but as a network to balance overall free radical activity. Packer demonstrated that antioxidants synergize with one another and, even more importantly, recycle one another. In order to neutralize free radicals, antioxidants need to work like a team of firemen putting out a fire: some man the pumper truck, some are up the ladder, some are at the hose. Some move right in close to the fire to put out the flames, where others help the victims of smoke inhalation back away from the fire. You can’t get away with sending only one antioxidant—say Vitamin E—into the fray: that would be like having all the firemen rush to the end of the hose, with no one left to turn on the water. As you’ll learn later in this book, using single antioxidants in high doses can actually do you more harm than good.
Dr. Packer has focused, rightly, on the synergy of antioxidants. He has described five pivotal antioxidants, which he calls network antioxidants: lipoic acid, coenzyme Q10, vitamin C, the naturally occurring forms of vitamin E, and glutathione. His conclusion: there’s a synergy between these antioxidants that slows aging and prevents and treats disease.
No one disputes the value of antioxidants in diet, where nature provides them in useful combinations. Recent studies have suggested that high doses of certain antioxidants (especially taken without their necessary “network”) may have marginally increased mortality in some studied groups. Packer’s seven hundred scientific papers and seventy books on every aspect of antioxidants and health have exposed the shortcomings of those studies and maintain the importance of the network effect. The clear message that emerges from Packer’s review of the literature and from his own work is that antioxidants should be taken as a balanced network and at doses specific to the individual case or condition.
A case in point. Acne often improves with a therapeutic dose of Vitamin A, somewhere in the range of 10,000 IU twice daily with food depending on an individual’s age and weight. However, the antioxidant vitamins C and E are also indicated for healthier skin and collagen formation and aid vitamin A in helping to get rid of the free radicals that are the cause and the result of acne formation. Cardiovascular disease, especially artherosclerosis (plaque formation), responds very well to vitamin E, but vitamin E works much better to sweep up the mess left from artery injury and plaque formation if vitamin C is also there to “recycle” its potency.
Support for the critical role of antioxidants in human health now flows in from many sources. Dr. Bruce Ames, currently project director at Children’s Hospital Oakland Research Institute, is widely recognized for his pioneering research in the field of micronutrients—that is, nutrients we consume in small amounts—and antioxidant therapy. Dr. Ames has suggested that when antioxidant and micronutrient intake is low over a long period of time and damage to the cells’ DNA begins to multiply, the body exercises a sort of triage system that may actually accelerate degenerative diseases and aging, eventually putting an end to the compromised organism—you—before you can pass on your DNA imperfections. This may be equally true whether you’re a starving African refugee or an overfed but undernourished North American.
As a result of an intensive burst of investigation into free radicals, we now know much more about the personalities of these chemical brothers. We know that certain of these molecules—the Abels, as it were—are essential components of the body’s enzymes and immune system. Others—the Cains—damage DNA and lead to cancer and other diseases.
We know now that there’s a link between an excessive burden of free radicals (called oxidative stress) and aging, as when free radicals formed by excessive exposure to the sun’s ultraviolet light lead to cataracts. We know that cholesterol is only one component of plaque formation, the other component being the first step: free radical damage to the arteries. (Only then do plaque deposits begin to form.) We know that free radical disruption of the brain may lead to Alzheimer’s and Parkinson’s diseases. And we know that once our body is in self-attack mode—think of autoimmune conditions such as arthritis—free radicals dominate.
This new knowledge has already made itself felt. The shelves of our local pharmacy are laden with antioxidants, and growing numbers of medical practitioners urge us to include antioxidant-packed citrus and berries in our diet and take as many as dozens of antioxidant supplements every day.
As I said in the first chapter, free radicals are directly or indirectly related to every medical condition known to us. At the molecular level, free radical damage is the cause of all disease. What we have yet to take on board in mainstream health circles is that what happens at the molecular level inevitably affects our overall health. I hope by the time you’ve finished the book, I’ve persuaded you of that fact.
Radicals and Antioxidants Up Close
When I was a kid, I saw a movie called Fantastic Voyage, about a submarine and its crew that were miniaturized and sent into a human body to save the patient’s life. Never mind the scientific and logical problems the story presented, I’ll always remember those scenes where the submarine cruised upstream through the arteries. Even today, when I think about what goes on inside the human body at the cellular and molecular level, I like to picture that submarine. I can’t think of a better way to imagine free radicals and antioxidants in action, so perhaps you’ll join me now on my own brief but fantastic voyage into the inner workings of a woman I’ll call Rhea Gretts. Like Will Powers, she’s a busy person. But unlike Will, she’s uneasy about her health and much more worried about the impact of some of her bad habits. I’ve treated many women like Rhea in my practice. They have good instincts about what will make them healthier, and good intentions about trying to shed those last bad habits, but they’ve hit stumbling blocks on the way to good health.
Our journey begins as our submarine, the Corpuscle, is injected into Rhea’s bloodstream as part of a new investigative procedure that allows patients to go about their daily lives while the medical detectives do their work.
We white-knuckled first-time investigators struggle to look calm, cling to our armrests and stare out the portholes. At the helm, the commander barks orders into a speaking tube as the Corpuscle tumbles through the dark surge of the heart’s right atrium, the turbulence of the right ventricle, the straits of the pulmonary semilunar valve and with a final rushing roar enters the massive pulmonary artery. The blood here, depleted in oxygen, is tinted a dark blue. In the seat beside me, a young scientist states the obvious: “We’re being swept into the lung. See? The blue is already turning to red as oxygen dissolves back into the blood.”
We slow as we enter the smaller arteries. Outside our portholes a stream of tumbling shapes dance past us.
“The round red ones are the red blood cells,” she says.
“I know.” I try to smile.
“Look!” She points out the window. The artery walls are pale here and appear closer to the ship. “A plaque deposit!”
Our captain pulls back on the throttle as we slip through the narrowed passage.
“Oh dear,” says my companion. “I hope this person is being careful with her diet.” The artery widens again and we motor forward. The path forks, and again the walls close in. Seemingly from nowhere, a fleet of immense and ghostly spheres crowd by us and stream ahead. One slows, lingers, then extends a tentacle-like arm. I shrink from the porthole. A leukocyte apparently wants to sample us.
“Damn these white cells!” snarls our captain. “Hold on!” Our ship lurches left, evading the pseudopod, then accelerates away. An instant later we’re jolted by a pulsing shriek that fills the ship.
“The smoke alarm!” shouts the skipper. “Damn! Our patient has gone out for a cigarette!” He throws a series of switches and a desperate quiet descends on us.
The young scientist whispers. “The lungs are in spasm and the alveoli are paralyzed. She’s inhaled.”
“We have to dive!” the captain warns. “We can’t risk being caught by a cough.”
I tighten my seatbelt, and the view outside our portholes fades to grey as we shrink down, descending from the anatomical level to the cellular level where the gross movements of the body will affect us less. A moment later the scene clears to reveal a breathtaking vista. The artery wall that had seemed so close when we were larger is now a far and glittering skyscape of individual cells. Every cell in the array looks like an immense and translucent airship. Around and between these huge shapes and on every side of us, molecules swarm.
“Damn smokers.” Our captain’s voice rumbles in the quiet. “Free radicals everywhere.” Sure enough, we hear a hail of pings on the hull as free radicals spew from unseen reactions around us. A host of these wildly reactive molecules, indistinct except for flashing spikes and prongs, collides with the distant artery wall and cuts a swath through the helpless cells that comprise it, broken cells drifting free as a tear opens in the artery. Yet further on, the scything radicals simply disappear as if by magic.
“Now that’s surprising,” I say. “Those radicals are being absorbed harmlessly in the artery walls. There’re no holes at all.”
My companion nods. “There have got to be lots of antioxidants around here for those walls to take that sort of punishment.” She squints at a drifting flock of identical molecules. “Yes! Look! Those are vitamin Es! I can tell by the shape. Maybe we’re in the body of a smoker who’s trying to eat right.”
“That’s a start,” I admit. “Maybe she remembers to take her ACES”—
which are the great antioxidants and radical killers, vitamins A, C and E, and selenium. They might be doing the job here.
The captain squeezes us through the narrow entrance to a lymph duct. Without warning, the ship lurches in a sickening arc and is dashed against the duct walls. The lights flicker.
“That damn cough again!” the captain mutters. “Hold tight!”
The Corpuscle is seized by a force of indescribable fury. The hull groans, the lights flicker again and go out. Darkness.
A diffuse glow outside the porthole. The captain is peering at his screens. “Yes,” he says. “That cough shot us right through a lymph node and into a breast duct.”
“Look at those big things over there!” My companion is pointing. “Know what they are?”
“Of course,” I say. “Molecules.”
She shoots me a pitying glance. “Those are estrogen hormones,” she says. “They’re trying to communicate instructions by docking in the duct cells, but they can’t. Plastic molecules have got here first and they’re mimicking the estrogen. I hate to see this!”
We’ve drifted into a spacious cavern. As the ship turns, a cluster of strange-looking cells comes into view off the starboard bow.
“Oh dear!” Her voice is tinged now with real alarm. “Those cells are multiplying out of control. That’s a cancer starting.” Even as she speaks, a dark shadow falls across the scene. I look up to see the great sprawl of a macrophage approaching. This is the big eater of the cellular defence army. One tentacle gropes tentatively towards us and two reach towards the multiplying cells. The Corpuscle draws back as the macrophage extends its pseudopods on either side of the cancer cells and with excruciating slowness engulfs them.
“I never get tired of seeing that,” mutters our skipper.
The young scientist is enthusiastically explaining. “Those cancer cells are finished. The macrophage cell will dissolve them in a flood of free radicals.”
“And do you think that the macrophage cell will itself be destroyed by the radicals it releases?” I ask just to see if she knows her stuff.
She shakes her head. “Not if this person is getting enough antioxidants in her diet to sweep up the aftermath.” And she’s right. But as the Corpuscle heads for the surface and the outside world, I reflect that even if that macrophage and all the rest of Rhea’s white blood cells survive, all the vitamin C in the world won’t keep her healthy if she doesn’t stop smoking.
Free Radicals: Rust under the Hood
On our excursion into Rhea’s cellular realm, we got a glimpse of this fact: every cell in the body—heart cell, liver cell, blood cell—functions like a miniature chemical factory. Besides the many battles between immune system cells and bacteria, viruses and cancers, a huge number of varied and necessary chemical reactions occur inside our cells during regular metabolism. These chemical reactions break large molecules down into smaller molecules or synthesize new molecules from smaller building blocks. Other reactions transfer electrical charges from one chemical substance to another. In the course of these reactions, oxygen atoms are routinely stripped of electrons and free radicals are born at an astonishing rate. If free radicals are the cause of all disease, they must be everywhere—and so they are. Where there is life, there is the free radical—friend and foe.
The best documented formation of free radicals is those that occur when we are exposed to environmental toxins: automotive emissions, industrial pollutants, cigarette smoke, various sources of radiation (including x-rays and the sun’s ultraviolet rays) and food additives, to name just a few. Study after study over recent decades has shown that lifestyle factors also contribute heavily to the formation of free radicals. Emotional stress, physical trauma, pollution, alcohol, cigarette smoke, deep-fried foods and overly strenuous exercise—these and a host of other things contribute to higher levels.
Free radicals are also formed as a not-so-obvious by-product of routine metabolism and inflammation processes. Such radicals may go largely undetected, yet they too contribute to the onslaught of oxidation that causes damage to our cells—even their destruction. If these electron-robbing, disease-causing molecules are not neutralized quickly, degenerative diseases and faster aging are the result. In many respects, the damage done by free radicals in the human body is similar to the rusting of a machine. Rusting is, after all, the reaction of the iron with those very oxygen radicals that “rust” our bodies. Here’s a homey example: we’ve all noticed that apples turn brown after their flesh is exposed to air. That too is oxidation. To slow down these oxidation processes, we apply protective paint to the iron and squeeze lemon juice on the apple. Paint temporarily keeps the oxygen at bay; lemon juice contains vitamin C and limonoids, both of which are powerful antioxidants.

Antioxidants: Nature’s Armour

We’ve seen how life is continually exposed to oxidative stress from inside and outside the body, and how living cells and entire organisms have developed defence mechanisms—various types of ingenious “antioxidant armour”—to protect them against free radicals. Essentially, antioxidants work by neutralizing free radicals, donating their own electrons to the hungry radicals while simultaneously maintaining their own stability as molecules. It wouldn’t do if antioxidants neutralized free radicals and were radicalized themselves in the process.
Our trillions of cells are abundantly equipped with these free radical defence mechanisms. But when we’re on the receiving end of an onslaught by chemicals, viruses, bacteria or mutant cancer cells, our defences are often overwhelmed. If we’re to prevent this cellular struggle from erupting as an actual disease, our cells require extra help. When it comes to our personal health, we don’t have another ten thousand—or a hundred thousand—years to evolve that help. That’s why we can benefit from eating certain foods and taking certain antioxidant supplements that help our cells do their jobs without sustaining significant damage. Of course some damage happens as we age, just that little bit, day by day, but it’s the small and acceptable amount of aging that we must think of as inevitable.
There it is then—one of the most important messages in this book: Sufficient antioxidant protection helps prevent ill health by stopping the chain reactions of free radical damage that underlie all disease.

The Balancing Act

Radicals cause great harm, yet paradoxically, we cannot exist without them. At the molecular level, every time we fight a cold, try to remember something or feel sexually aroused, we’re putting free radicals to use. Our immune cells produce copious numbers of the free radicals nitric oxide and superoxide, which are indispensable to such good deeds as opening blood vessels and “poisoning” invasive viruses and bacteria. Our immune system employs certain free radicals to kill cancer cells before the cancer grows, as we imagined on our submarine adventure.
In fact, many cancer drugs work by temporarily increasing the production of free radicals in the body. Oncologists also use focused radiation to generate powerful free radical activity and so destroy a cancer tumour. Yet free radicals in great numbers—those generated by our immune systems, say, or by too much unfocused radiation—can eventually cause diseases such as cancer. What are we to do with this contradictory evidence?
The governing principle behind all biological processes is homeostasis, a Greek-derived word meaning balance. We’ll have cause to refer to balance again and again throughout this book. The body must maintain an internal free radical balance. Unfortunately, for reasons we’ve already glimpsed, most of us are very imbalanced indeed, with far too many free radicals loose in our systems. So new is this knowledge, few people—including doctors—yet know what a free radical balance really means or how it might be achieved.
In the chapters that follow, we’ll explore the phenomenon more deeply. And then we’ll turn to real-world no-guess ways by which you can determine the current levels of free radicals in your body and establish that life-enhancing (and life-prolonging) balance.

Are Free Radicals Really the Root of All Disease?
A skeptical lay researcher once bet a bottle of good red wine that he could stump me on my contention that free radicals are involved in all disease. He proceeded to present me with the following scenarios.
Skeptical Investigator: A nurse is pricked by an HIV-contaminated needle and eventually dies of AIDS. How does she die of free radicals?
Bryce Wylde: The role that free radicals play in the case of HIV and AIDS is variable throughout the disease. From initial infection to full-blown AIDS to death—every step includes free radical bombardment at the cellular level. As an acquired immune-deficiency virus, HIV attacks the body by using a process of illusion so that the body can’t recognize it as a foreign invader. Paradoxically, in the first stages, the immune system doesn’t initiate enough free radicals in order to kill off the virus. When a person develops full-blown AIDS, death doesn’t come from the AIDS virus itself, but from the onslaught of free radical-related injury caused by every other disease that the person is now unable to fight off. This can include conditions otherwise as benign as the common cold.
S.I.: How about someone sickened by the malaria parasite?
B.W.: The malaria parasite sparks the body’s immune system response into employing the necessary free radicals. This attack on the parasite inevitably damages many other nearby tissues and organs. As one example, free radical overload can cause kidney failure and ultimate death if the person doesn’t receive immediate help.
S.I.: Okay, take heart failure from a purely mechanical clogging. What do free radicals have to do with a 103-year-old man dying of heart failure?
B.W.: No matter the person’s age, a heart attack or heart failure or heart disease always involves free radicals. As blood is the carrier of free radicals as well as their neutralizers, the antioxidants, the linings of the arteries are often the site of free radical “thunderstorms” that cause everything from plaque accumulation to heart attacks. Interestingly, it’s not the cholesterol itself that causes the plaque accumulation. The culprit is the original injury to the artery lining caused by a cascade of free radicals that then causes plaque to deposit at the site of injury.
S.I.: What about a woman who dies of an aortic aneurysm?
B.W.: In nearly every case of aortic dissection or aortic aneurysm, free radicals are the initial cause of the compromised vasculature. Years of free radical damage eat away at and weaken the walls of the artery or outpouch them enough that you may bleed outright into your body or brain.
S.I.: Okay, so take a fellow bitten by a cobra. He dies. Surely…?
B.W.: Death from a snakebite is a case of toxic shock governed by free radical overload. Nearly every toxin found in cobra venom initiates a tremendous amount of free radical damage and interrupts blood-clotting platelet-aggregating factor. At the molecular level, this causes major, irreversible damage by instigating “reperfusion injury.” Your organs melt from intense free radical onslaught as if you were exposed to nuclear radiation and you end up bleeding to death from the inside out. If the fellow is lucky enough to survive, it would be because a heroic dose of antivenom stopped the free radical cascade. He’d also need some significant doses of antioxidants to clean up the rest of the free radical inflammation that may continue for years after the actual encounter with the snake.
S.I.: A depressed person commits suicide…
B.W.: Free radicals are almost always involved in depression. As one example, some forms of psychoses and mental disillusionment can result from improper “methylation.” Methylation defect is a deficiency of specific antioxidants, including folic acid, the antioxidant B vitamins and vitamin C, especially in cases of schizophrenia. Free radicals are notorious for their attack on the nerve fibres in cases of depression caused by chronic stress, dementia and Alzheimer’s disease.
S.I.: (flipping through his notes) An air traveller dies of deep vein thrombosis. How could that be caused by free radicals?
B.W.: In this situation, a person may occasionally die of end-state organ necrosis or infection, both of which are free radical induced. But generally, the cause of death is acute. The most obvious example is thrown emboli, carried in the blood into the brain or heart or lung tissue, which causes immediate restriction of blood flow. The real question is what causes the emboli in the first place. The most frequent causes are oxidation of cholesterol, homocysteine or some other pro-inflammatory agent that instigated free radical damage at the arterial level. These and other free radical events can all lead to emboli, and emboli cause deep vein thromboses.
S.I.: All right, how about the case of a two-year-old child who dies of polio?
B.W.: Polio cannot be prevented or treated with antioxidants, but polio is a viral disease just like the common cold except that polio puts out a free radical toxin that destroys anterior horn cells in the spinal canal. Polio, as with many other deadly viruses, is also the cause in this case of a flurry of other free radical attacks by the body’s own immune system on the virus—all too often such an intense attack that the body can rarely ever regain balance. In the end, the nervous system is severely impaired or the poor child dies.
S.I.: And if the child dies instead of cancer of the retina?
B.W.: Any cancer, neoplasm or cell mutation is initiated by an attack on the genetic code.
S.I.: An attack by…?
B.W.: By free radical molecules. Often the result is a battle for control between free radicals and antioxidants. Due to an imbalance of cell regulation, natural killer-cell activity springs into full action. An entire host of other DNA and immune-related oxidative stress ensues.
S.I.: Forget cancer then. A fifty-year-old dies of amyotrophic lateral sclerosis—Lou Gehrig’s disease. Now what will your radicals and antioxidants do?
B.W.: Free radicals are the cause of the nerve death due to an autoimmune attack sequence. This causes loss of function, and can end up causing the untimely demise. No doubt you see no way antioxidants could help here. But they might surprise you. Strong antioxidants such as phosphatidylserine and N-acetylcysteine don’t offer a cure, but may help slow the progression of the disease by slowing down the deterioration of the nervous system.
S.I.: What if an automobile accident victim dies of shock? That’s something we can all understand. It’s basic. It’s down to earth.
B.W.: In this case, the body shuts down—and fast—due to a process known as cellular “autolysing.” In hypoxia—lack of oxygen from asphyxiation or extreme cold—cells begin releasing a huge number of deadly enzymes that destroy all other surrounding cells and injure tissues by initiating a cascade of free radicals. It’s as if we all at once “rust” thousands of times faster than we do via the natural aging process.
S.I.: Okay, okay. But allow me to pose my coup de grâce. A stabbing victim dies of blood loss.
B.W.: Clearly a tragedy, but obviously this situation does not qualify as disease, and of course I acknowledge the point at which disease and trauma separate.

Read Chapter 3

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