by Steve Hickey
Joe had terminal lung cancer. He was constantly coughing up blood and I talked with him in the living room of his small suburban home because Joe was too sick to come to my office. In fact, he was too sick to get out of his recliner. It was in this chair that his life was played out, day and night. He could not walk and he was in too much pain to even lie down. He spent the night in his chair. He did not want to eat. But he did still want to live, and he was willing to try even vitamins if they would help him feel any better.
It was October and the leaves, orange and bright yellow, were falling outside the picture window as we talked. It is never easy to work with the dying. As a counseling student, I’d seen plenty of them at the Brigham Hospital in Boston. Then, I had listened and watched—now, I listened and watched and suggested vitamin C.
“How much?” Joe croaked.
“As much as humanly possible under the circumstances,” I replied. I explained bowel tolerance to him, and answered the usual questions from his family. Most centered on how well would it work. Some were understandably skeptical; some were in overly optimistic denial. “Vitamin C is very much worth using, with due consideration of how sick Joe really is.” All agreed that Joe had nothing to lose.
Joe kept a big jug of water and a bottle of vitamin C crystals on the table right next to his recliner. Within days, Joe stopped coughing up the blood. This alone would have been more than enough benefit, but there was more good news within the week. His wife reported that Joe’s appetite was back and he was able to lie down in bed. He was sleeping much better and in much less pain. Over and over, I have seen profound pain relief and dramatic improvement in sleeping in terminal patients that take huge doses of vitamin C. If the vitamin did nothing else, these benefits would be indisputable arguments for using it.
A week or so later, Joe was able to walk around the house with a cane and he was even walking around the yard. His wife was quite emotional as she reported his progress. She knew, at some level, that Joe was not likely to survive such severe cancer. And in the end, he didn’t. But he added to his length of life, and the quality of that life was extraordinarily enhanced by the vitamin C.
How much did he take? About 4,000 mg every half hour when he was awake, day or night. That approaches 100,000 mg a day. Joe never got diarrhea. As time passes and our knowledge increases, we realize that the benefits of vitamin C for cancer patients can be greatly increased by its combination with other nutrients. Vitamin C works most effectively by driving a redox synergy with other nutrients, such as alpha-lipoic acid and vitamin K3. Had this information been available at the time, Joe might have lived even longer and felt even better.
Cancer is one of the most feared diseases and its incidence and devastation has been increasing throughout modern history. The causes of this disease lie in the balance of oxidants and antioxidants in the cell. Humans are complex multicellular animals and have evolved numerous defenses against carcinogenesis and malignancy. A critical element in this defense is vitamin C.
CHAPTER 8
Heart Disease
“One sometimes finds what one is not looking for.”
—ALEXANDER FLEMING
Vitamin C is critical for a healthy heart. People need not be dying from coronary heart disease or occlusive stroke because evidence suggests that an adequate intake of vitamin C and other antioxidants would prevent and potentially eliminate these conditions. Orthomolecular physicians have claimed for decades that the cause of heart attacks and strokes is low-grade scurvy. Ignoring this suggestion may have made these diseases the biggest killers in the Western world.
Strangely, however, deaths from these diseases were rare in the past—this is a new epidemic. It is not normally acknowledged that coronary heart disease is a relatively recent problem restricted to some humans living under modern conditions. Most animals do not suffer coronary heart attacks. Where it does occur in animals, it is rare and is associated with a lack of vitamin C. Something in the way people live has changed over the last hundred years or so, causing an epidemic of heart disease and stroke. These particular changes are not fully established or, more importantly, understood. The most that has been achieved is a statistical association with risk factors. However, there is a common clue—risk factors for heart disease directly or indirectly increase the body’s need for vitamin C and other antioxidants.
The Heart and Circulation
In simple terms, the heart is the pump and the blood vessels are the piping used to transport blood about the body. The cardiovascular system has to be largely self-regulating and be able to repair itself quickly. It has many functions, but a single critical requirement is to deliver oxygen to the tissues.
Blood consists of cells in a surrounding fluid called plasma. Blood carries oxygen in red blood cells bound to a protein called hemoglobin. When bound to oxygen, hemoglobin is red, giving the blood its color. Red cells are the most abundant cells in the blood, consistent with their purpose in supplying the body with oxygen. When the blood supply to an organ is prevented, the tissues are deprived of oxygen for generating energy and can rapidly suffer damage. Lacking oxygen, the cells’ primary energy supply is lost, as is their ability to generate antioxidants, and they are rapidly subject to oxidation and free radical damage.
Oxygen powers oxidation and reduction (redox) reactions, providing energy and a continuous source of antioxidants. Oxygen is required for generation of energy from the burning of our food in a series of free radical reactions. Absence of oxygen means that these oxidation reactions are interrupted, and sensitive cells, such as those in the brain, rapidly run out of energy. Our bodies run on a series of redox reactions: oxidation removes electrons from molecules and its opposite, reduction by vitamin C and other antioxidants, provides electrons. Tissue damage and death results if this function is prevented, even for a short time.
The heart has four chambers, two collecting chambers (atria) and two pumping chambers (ventricles). The rate of contraction of heart muscle is modified by signals from the nervous system or by hormones such as adrenaline. A specialized section of the nervous system called the autonomic system keeps control of these basic bodily functions without the necessity of conscious attention. Vitamin C protects the autonomic system and is absolutely necessary for the synthesis of adrenaline.1 Indeed, your body’s highest concentrations of ascorbate are found in the adrenal glands.2 An adequate supply of vitamin C is thus essential for the body to respond appropriately to stress and prevent shock. This action of vitamin C may be one of the main mechanisms for its action in protection against disease, infection, and toxins.3
Heart Attacks, Blood Clots, and Strokes
Inappropriate clotting of the blood causes heart attacks and strokes. A blood clot is the result of blood coagulation and is an essential mechanism in the repair of damaged blood vessels. Blood clots are formed when platelets aggregate at the site of an injured blood vessel. While clots are essential to prevent unnecessary blood loss and maintain the integrity of the cardiovascular system, clots occurring at the wrong time or place can block blood vessels, leading to a heart attack. Abnormal blood clotting occurs in conditions that disrupt the normal blood flow. In atrial fibrillation, when the smaller upper chambers of the heart beat rapidly and ineffectively, blood flow slows and clots can form in the stationary blood. Other conditions that can lead to blood clots include heart failure or sitting for long periods on a long flight.
Most people who die of a heart attack seem to enter a period of ventricular fibrillation shortly before death. If a clot in the coronary arteries prevents the blood supply to the heart muscle, the resulting damage can overload the control of ventricular contraction. The wavelike signal to contract is disturbed by the damaged area of the heart wall. As a result, the deflected signal reaches muscle fibers at the wrong time, leading to an uncoordinated contraction. When the ventricles fibrillate, different parts of the main heart muscle contract at dissimilar rates simultaneously and the muscle enters an irregular spasm. These writhing
spasms effectively stop the pumping action. Since the cardiac muscle also provides its own blood supply, the muscle can rapidly run out of energy and the ventricles eventually dilate with the resulting relaxation.
Blockage of a vessel supplying the brain will cause an occlusive stroke. Other essential organs with fine capillaries can also be affected, such as a pulmonary embolism blocking the blood supply to a section of lung. These blockages are essentially the same as those occurring in a heart attack or occlusive stroke.
The heart muscle and tissues are supplied by a system of local blood vessels (the left and right coronary arteries). Blood flow through these vessels is largely under local control and responds to increasing demand by raising blood flow. Local hormones, such as the free radical nitric oxide (NO), dilate the coronary arteries. While blocking one of the coronary arteries with a blood clot will rapidly kill or damage the supplied heart muscle, if the blood flow is restricted more slowly, collateral blood vessels may accommodate the change and provide an alternative supply. Small arteries in the heart are often interconnected (anastomosed) and can compensate when minor vessels are blocked. Unfortunately, the larger arteries are independent and blockages are consequently life threatening.
We have a good understanding of the human cardiovascular system as a result of decades of scientific research. A buildup of fat blocking blood flow does not cause heart attacks, as is often erroneously described. Heart attacks and many strokes are a result of a blood clot forming on an inflamed area inside an arterial wall and breaking away to block a coronary vessel. This pathological process depends on a deficiency of vitamin C and related antioxidants.
Atherosclerosis
Atherosclerotic plaques consist of fatty tissues and cells that accumulate within the arterial wall. The early stages of plaque formation involve the attraction of white blood cells and the proliferation of cells in the arterial tissue. Within the developing arterial plaque, cell behavior is disrupted and cholesterol is deposited. Unlike the furring up of water pipes, plaque formation is an active process depending on the response of cells to local injury. Initially, the artery wall responds by thickening locally and expanding in diameter, which keeps the blood flowing as the plaque grows. Thickening of the wall of an artery supplying the heart can prevent it from expanding with increased blood pressure when a person exercises; the result is angina pectoris, a feeling of tightness and pressure in the chest. In other arteries, it can lead to tightening and pain in the legs (intermittent claudication). Eventually, the plaque begins to obstruct the vessel and reduce blood flow; this gradual constriction is called stenosis.
In some cases, the plaque can continue to expand until it totally blocks the artery, preventing the flow of blood. However, only about 15 percent of heart attacks result from direct blockage by a growing plaque; most are caused when the plaque ruptures. Plaques typically cause heart attacks indirectly by causing blood clots.
There are essentially two forms of plaque, stable and unstable. Stable plaques are relatively safe: they may grow slowly and completely block an artery, but this is a rare occurrence. Unstable plaques, as the name implies, are much more dangerous. They have a thin, fibrous cap overlying a soft core of fat and white blood cells, which helps strengthen and contain the plaque’s inflamed fat, providing increased stability for a time. But these unstable plaques contain a high level of free radicals, which can lead to splitting of the fibrous cap. Once the cap is damaged, the body attempts to heal this wound as it would attempt to heal any wound—by clotting. Clotting is a primary mechanism to prevent loss of blood and maintain the integrity of damaged blood vessels.
Plaque-associated clotting can rapidly block the artery. More often, pieces of the clot break free and travel through the bloodstream before coming to rest in an artery too small for the lump to pass through. When this happens in an artery supplying the heart, it deprives the muscle tissue of oxygen and causes a heart attack. Sometimes the clot ends in the brain and kills an area of tissue in an occlusive stroke.
All of the processes leading to a catastrophic event can be slowed or stopped with vitamin C. Heart attacks may simply reflect a shortage in supply of vitamin C and related antioxidants. Dr. William J. McCormick and other early vitamin C researchers first explained the dependency of heart disease on vitamin C levels over half a century ago.4 This was later elaborated upon by Linus Pauling and others.5 However, we have yet to see an appropriate research effort into this area despite the alarming levels of atherosclerosis leading to disability and death. Conventional medicine’s infatuation with dietary fat and cholesterol has stifled research into vitamin C and heart disease since the middle of the twentieth century.
The Real Cause of Heart Disease—Lifestyle Factors or Inflammation?
Searching for the cause of heart disease involves numerous pathways that end in shortage of vitamin C, inflammation, and oxidative damage. Smoking, high blood pressure, and a high-fat diet may contribute to atherosclerosis, but they are not the cause. Some people will live a long life despite being at high risk from all the major lifestyle risk factors. Others will die early from rampant atherosclerosis but be nonsmoking vegetarians who have a particular aversion to animal fats. The key feature linking the main risk factors is that they produce free radical damage and increase the requirement for vitamin C.
An objection to the idea that conventional risk factors do not explain heart disease might be that genetic factors are also involved. The changing incidence of heart disease in the twentieth century is not explained or reflected by the traditional risk factors, even when considered along with genetic factors.6 Finding genes for the disease provides pointers to the underlying biochemical problem, but these genes do not by themselves provide an explanation or a therapy. Suggesting the involvement of a genetic component simply means that some people susceptible to heart disease are born with an abnormal biochemistry. However, the human requirement for vitamin C is one of the most ubiquitous genetic abnormalities for our species. The major genetic change in humans—the loss of the ability to synthesize vitamin C—is generally ignored by conventional medicine. But lack of the ability to synthesize vitamin C appears to be the explanation for the human susceptibility to cardiovascular disease.
The concentration on risk factors often obscures the relationship between cardiovascular disease and inflammation. Most risk factors have a pro-inflammatory component. The risk factors for atherosclerosis include disordered lipid (fat) profiles, such as high levels of low-density lipoprotein (LDL) cholesterol in the blood. Autoimmunity and infection are also associated with increased risk, as are high levels of homocysteine, oxidative stress, genetic predisposition, C-reactive protein, and various metabolic diseases.7 The effects of these risk factors can combine by acting synergistically on separate parts of the inflammatory response. Typically, they stimulate the release of a number of active molecules involved in inflammation, including reactive oxygen species and immune cells that respond to injury.
Risk factors do not directly point to a cause of the disease. They are, however, indicators of inflammation and an increased need for vitamin C. When risk factors are combined, the relative risk increases, which is consistent with the person experiencing chronic inflammation and low-grade scurvy.
The conventional risk factors seem to affect three main cell types that act together in arterial function.8 Endothelial cells line the inner surface of blood vessels and control flow of hormones and other chemicals into the blood vessel wall.9 They act as a boundary between the blood vessel and the blood. Deeper in the artery wall, smooth muscle cells maintain the structure and vascular tone of the blood vessel, contracting and expanding to decrease or increase flow. White blood cells can enter the vessel wall to help defend the arteries from chemical and biological insults, but oxidative damage to these white blood cells can result in inflammation of the arterial wall and atherosclerosis. Chronic inflammation in an area of the blood vessel wall interferes with the normal activities of these cells.
S
ome of the common risk factors for heart disease, such as smoking and high blood pressure, promote oxidation and inflammation in the arterial wall. Oxidation associated with stress can cause white blood cells to adhere to the arterial wall, an early stage of plaque formation.10 Mechanical and other stresses on the artery produce inflammation and stimulate plaque formation. A sufficient supply of vitamin C is the most important factor in preventing this inflammation and subsequent heart disease. Orthomolecular vitamin C supplementation may be the best way in which an individual can prevent heart disease and stroke. The common factor for the conventional risk factors is their relationship to inflammation and free radical damage. High intakes of vitamin C and related antioxidants can prevent this damage.
It becomes clear that improved prevention and treatment are possible when it is appreciated that atherosclerosis is an inflammatory disease. However, medicine has for decades been transfixed by the idea that cholesterol or other “bad” fats are the underlying cause, even though there was never any hard evidence for this view, merely the presence of cholesterol as a component of the arterial plaque and statistics indicating their association as risk factors. The realization that plaques are areas of an inflamed artery has taken decades to come to the forefront. Inflammation may be considered a rather odd feature to overlook, as inflammation is a characteristic of damaged tissues. Interestingly, persons with inadequate vitamin C are more likely to suffer from both inflammation and high cholesterol.
Plaque inflammation can be active or relatively dormant. Active plaques with acute inflammation are the most dangerous. Plaques can remain dormant for years but flare up occasionally to put the person at risk of clot formation, heart attack, or stroke. Often, inflammation in plaques is associated with infection. Many drugs currently in use for the treatment of heart disease, such as aspirin and the statins, have anti-inflammatory, antioxidant, or antimicrobial properties, although they are often given for other reasons.11 Most of the conventional risk factors for heart disease and stroke cause inflammation and free radical damage. The transition of the low-grade inflammation of a dormant plaque to the active dangerous form occurs when there are insufficient antioxidants. High intakes of vitamin C may prevent this transition and prevent heart attacks completely.