When we break the natural laws, they break us. In this chapter, you are going to read about some things that you may hold very dear as part of what you see as your identity. It is very important that you acknowledge the healthy part of yourself that does not want diabetes, or the diet and lifestyle that create it, to be your life experience anymore. Any attachment we had to the diabetic that we were, and the diet and lifestyle we lived that created it, need to be transformed. “My precious burdens,” Walt Whitman said, “My precious burdens I carry them wherever I go.”
What we will investigate now are our precious burdens, and in Chapter 4, we will develop a mental space and life practices that will help us let go of these for a life that draws in the best things possible. Chapter 5 will show you how to eat a Culture of Life anti-diabetogenic diet that is accessible and tasty, no matter what your busy life schedule may bring. If you are having any doubt as you read this book cover to cover, see the client results in Chapter 4. What you will see is the reality that you want for yourself, for your family, and for society. Hold in your mind the potential that you can be one of the healthiest, most vibrant people you know. We are going to guide you to achieving just that. With this in mind, let’s look at these precious burdens, these lifestyle attachments that need to be transformed to help reverse Type-2 diabetes.
Risk factors associated with the Culture of Death are listed below. We’ll look at them one by one in this chapter, along with other issues of diabetes as an accelerated aging reality, genetics, diabetes in children, insulin resistance, gestational diabetes, Alzheimer’s associated diabetes, and cancer associations. The personal lifestyle habits, choices, and predisposing diseases that are diabetogenic include:
According to the U.S. Centers for Disease Control (CDC), 37.7 percent of diabetics report being physically inactive. Inactivity promotes Type-2 diabetes, and even increases insulin needs in Type-1 by not accessing the benefit of special proteins that transport glucose into the cells. Essentially, exercise works like taking an insulin shot, because it reduces blood glucose levels. Working your muscles more often and making them work harder improves their ability to use insulin and absorb glucose. This puts less stress on your insulin-making pancreatic beta cells.
A new theory on how exercise serves to work like insulin stems from the special proteins called GLUT-4 transporters that usher glucose into the muscle cells. Exercise causes GLUT-4 transporters to rise to the surface of the cellular membrane, where they can shuttle circulating glucose into the cell, increasing insulin sensitivity and decreasing insulin needs. Findings from the Nurses’ Health Study and Health Professionals Follow-Up Study suggest that walking briskly for a half hour every day reduces the risk of developing Type-2 diabetes by 30 percent. The benefits of exercise, with suggestions and data, will be presented at greater length in Chapter 3.
Let’s look at television watching specifically. A study by the American Diabetes Association followed 41,811 men ages 40 to 75 over a ten-year period. A direct association was observed between television watching and risk of developing diabetes. The men who reported sitting in front of a TV more than nineteen hours per week were more than 150 percent more likely to become diabetic than those who watched less than three hours a week. “Bubble gum for the eyes,” Steve Allen called it. Television watching is another form of inactivity, and increasing evidence suggests that exercise is protective against the development of Type-2 diabetes mellitus.
Every two hours per week you spend watching TV instead of pursuing something more active increases the chances of developing diabetes by 14 percent.1
It is important to understand overweight and obesity, taken together or separately, as a reflection of the Culture of Death diet and lifestyle, as an underlying cause of insulin resistance and diabetes. Data from the CDC shows that among diabetics, 82.1 percent are overweight or obese, and 48.1 percent are obese based on self-reported height and weight. Overweight or obesity is a precondition for many of the preventable causes of death now experienced in the developed world. A special report in the New England Journal of Medicine found that obesity is now such a significant factor that “it is larger than the negative effect of all accidental deaths combined (e.g., accidents, homicide, and suicide), and there is reason to believe that it will rapidly approach and could exceed the negative effect that ischemic heart disease or cancer has on life expectancy.”2 They continue: “From our analysis of the effect of obesity on longevity, we conclude that the steady rise in life expectancy during the past two centuries may soon come to an end.”
Let’s look at some of the theoretical underlying causes of overweight and obesity.
There is no necessity to sell out our health and shorten our lives so that someone else can profit from marketing longer-shelf-life, so-called “convenient” foods. To continue to eat these foods is to reaffirm membership in the Culture of Death.
When you cook food, according to the Max Planck Institute, you coagulate 50 percent of the food’s protein. Other research shows that 70–90 percent of vitamins and minerals and up to 100 percent of phytonutrients are destroyed when food is cooked. Processing, cooking, pasteurization, and irradiation are all food handling methods that destroy the anti-diabetogenic qualities of our foods given to us in their natural state. Because of these processes that destroy the nutritional value of the food by at least 50 percent, we end up needing to eat more food to get the nutritional value that we would have gotten with the uncooked food in its whole state. This additional eating leads to overweight. This has significant implications for why we use a nutrient-dense live-foods diet, as discussed in Chapter 4. In addition, the junk food diet fills us with empty calories, leaving us more hungry and further craving food.
For example, to make this point crystal clear, shopping the center of the supermarket (where the processed foods are) can create diabetes. Adam Drewnowski, an obesity researcher at the University of Washington, wanted to figure out why it is that the most reliable predictor of obesity in America is a person’s low economic status. Drewnowski gave himself a hypothetical dollar to spend, using it to purchase as many calories as he could. He discovered that he could buy the most calories per dollar in the middle aisles of the supermarket, among the towering canyons of processed food and soft drinks. Drewnowski found that a dollar could buy 1,200 calories of cookies or potato chips, but only 250 calories of carrots; that his dollar bought 875 calories of soda but only 170 calories of orange juice.3 This is a potential insight into why people of low economic means have the highest rates of diabetes in Western cultures.
Going deeper into the psychospiritual level, as we contrast the Culture of Death with the Culture of Life, it is my teaching that “there is never enough food for the hungry soul.” The Culture of Death creates a hungry, empty soul experience, which we try to fill with food as a substitute for love and connection. The Culture of Life fills our souls with love.
A high-glycemic diet is one that includes any white sugar, any white flour, white rice, honey, maple syrup, alcohol, coffee, wheat, any junk food, and most fruit (some fruit, such as berries and cherries, is moderate to low on the glycemic index). A high-glycemic diet also includes cooked beets and carrots, rutabaga, summer squash, cooked yams, pumpkin, parsnips, white potatoes, apricots, figs, grapes, raisins, melons, mangos, bananas, papaya, pears, peaches, plums, pineapple, kiwi, sapote, cherimoya, rambutian, durian, dates, and dried fruits. All fruit juices, carrot juice, and beet juice are also high-glycemic foods. High insulin index foods, which are low on the glycemic index but still diabetogenic, include meat, fish, chicken, and dairy.
We recommend against fruit for three to six months until the fasting blood sugar (FBS) stabilizes at 85 or below, and then only low-glycemic fruit such as berries, cherries, citrus, goji berries, cranberries, and an occasional apple.
Fiber is the part of the plant that cannot be digested or absorbed by the body. It is a carbohydrate that is obtained from vegetables, fruits, nuts, and seeds. Fiber is either water soluble or water insoluble. Water-soluble fiber is especially good for people with diabetes, because it delays the pace at which food passes through the stomach. This allows a slower rate of absorption of glucose into the bloodstream, which reduces the glycemic roller-coaster. It also improves insulin sensitivity, combating insulin resistance and helping insulin do its job of ushering glucose into the cells.
According to Dr. Julian Whitaker, MD:
One of the earlier studies demonstrating the power of dietary fiber in the treatment of diabetes was conducted by Perla M. Miranda, RD, MS, and David L. Horwitz, MD, PhD, FACp, and published in the Annals of Internal Medicine in 1978. Each of eight subjects who had insulin-dependent diabetes consumed either 20 grams of dietary fiber per day in the form of high-fiber bread or a mere 3 grams of fiber. All other factors of the diet were kept constant, as was the patients’ insulin dosage. On the low-fiber intake, the average blood glucose level of the patients was 169.4 mg/dl. During the period of higher fiber intake, the mean blood sugar level was 120.8 mg/dl.4
Figure 1: Effects of fiber in Type-1 diabetics (Source: Reversing Diabetes by Julian Whitaker, p. 116)
A potential diabetic can be transformed into a completely diabetic individual by administration of the time-honored carbohydrate-free meal of meat and fat.
DR. I. M. RABINOWICH, 1930
A quarter pound of beef raises insulin levels in diabetics as much as a quarter pound of straight sugar.
DIABETES CARE 7, 1984, P. 465
Cheese and beef elevate insulin levels higher than “dreaded” high-carbohydrate foods like pasta.
AMERICAN JOURNAL OF CLINICAL NUTRITION 50, 1997, P. 1264
A single burger’s worth of beef, or three slices of cheddar cheese, boost insulin levels more than almost two cups of cooked pasta.
AMERICAN JOURNAL OF CLINICAL NUTRITION 50, 1997, P. 1264
We have been hinting that a successful reversal of diabetes takes us back to high-enzyme live food and unprocessed food, which is part of the Culture of Life. This is a diet similar to what the human organism has been eating for perhaps 3.2 million years. A shift happened about 10,000 years ago, when farming and herding came into the forefront of the tribal cultures and we began to switch to a grain-based and herding civilization. Herding meant the introduction for the first time in history of high amounts of flesh food on a regular basis. Before that the human species really did not eat a lot of meat. According to Robert Leakey, one of the leading medical anthropologists in the world, the human diet was primarily a vegan chimpanzee diet with an occasional bite of meat. Through simple logic, we can see that a brown bear is clearly more carnivorous than a human by looking at its claws and teeth, and yet a brown bear eats a diet of 95–97 percent raw plant food. The longest-living Hunza people of northern Pakistan live on a diet that contains less than 1 percent meat. Consider that between 1840 and 1974, the quantity of meat eaten per person in the United States increased five times over. During roughly the same time, the United States went from being the healthiest nation in world in 1900, out of 100 surveyed, to dead last in 1990.5
The diet that historically has been best for health and prevention of Type-2 diabetes really is one that is high-complex-carbohydrate, non-animal-fat, and moderately low-plant-fat (15–20 percent); low-glycemic and low-insulin; and high in fiber. In World War II, Professor H. P. Himsworth noted that when food shortages removed the white flour, white sugar, and excessive meat protein and fats from the typical British diet, the death rate from diabetes fell 50 percent.
Studies have shown that Seventh-Day Adventist men who ate meat six or more days a week had 3.8 times greater risk of having diabetes mentioned on the death certificate as compared with those Seventh-Day Adventists who were lacto-ovo-vegetarians.6 This would not be unexpected since meat contains considerable cholesterol and saturated fat, which would result in higher risk of atherosclerosis, the major cause of death among diabetics. However, the unexpected finding was that twenty years prior, at the outset of the study, those who were nondiabetic were more apt to get diabetes if they were customarily in the habit of consuming meat.
England and Wales. Diabetic Mortality indices. The figures for 1946 and 1947 supplied by Dr. Percy Stocks. Drawn by Thomas L Cleave in The Saccharine Disease.
In The China Study, T. Colin Campbell, PhD, relates a study that measured diets and diabetes in a population of Japanese American men in Washington state. These men, sons of Japanese immigrants to the U.S., remarkably had more than four times the prevalence of diabetes than the average rate found in similar-age men who stayed in Japan. For Japanese Americans, the ones who developed diabetes also ate the most animal protein, animal fat, and dietary cholesterol, each of which is only found in animal-based foods.7 Total fat intake also was higher among the diabetics. These same dietary characteristics also resulted in excess weight. These second-generation Japanese Americans ate a meatier diet with less plant-based food than men born in Japan. The researchers wrote: “Apparently, the eating habits of Japanese men living in the United States resemble more the American eating style than the Japanese.” The consequence: four times as much incidence of diabetes.8
The benefits of a diet of plant foods is professionally recognized. The American Dietetic Association (ADA), the world’s largest organization of professional dieticians, published the following statements in June 2003 on a vegetarian diet and lifestyle:9
Vegetarians have been reported to have lower body mass indices than nonvegetarians, as well as lower rates of death from ischemic heart disease; vegetarians also show lower blood cholesterol levels; lower blood pressure; and lower rates of hypertension, type 2 diabetes, and prostate and colon cancer. Well-planned vegan and other types of vegetarian diets are appropriate for all stages of the life cycle, including during pregnancy, lactation, infancy, childhood and adolescence.
Vegetarian diets offer a number of nutritional benefits, including lower levels of saturated fat, cholesterol, and animal protein as well as higher levels of carbohydrates, fiber, magnesium, potassium, folate, and antioxidants such as vitamins C and E and phytochemicals….
It is the position of the American Dietetic Association and Dietitians of Canada that appropriately planned vegetarian diets are healthful, nutritionally adequate, and provide health benefits in the prevention and treatment of certain diseases.
Meat eating is diabetogenic on all accounts, and meat is by no means an ideal food or protein source for humans. Meat eating creates the preconditions for diabetes, and accelerates the complications of the condition once it has manifested. Research cited in Spiritual Nutrition shows that meat protein can increase insulin resistance, a precondition for diabetes and the diabetic degenerative process. Let’s investigate the negative aspects of meat eating, and consider whether these realities should be included or excluded from a Culture of Life anti-diabetogenic diet and lifestyle designed to completely reverse diabetes.
According to T. Colin Campbell, PhD, numerous studies have shown that vegetarians and vegans are slimmer than their meat-eating counterparts. People in these studies who are vegetarian or vegan are anywhere from 5 to 30 pounds slimmer than their fellow citizens.10,11,12,13,14,15,16 Our results in the Tree of Life 21-Day+ Program bear this out. During the thirty-day program for the film, participants, who were meat eaters, lost between 20 and 32 pounds.
Cardiovascular disease is significantly higher in meat eaters. In 1961 the AMA stated that 97 percent of heart disease would be eliminated if people gave up eating meat and ate a vegetarian diet.
Udo Erasmus reports in his book Fats That Heal, Fats That Kill that several species of fish actually contain toxic fats and oils. An example is the toxic cetoleic fatty acid, found in herring, capelin, menhaden, anchovetta, and even in cod liver oil!
Younger women who regularly eat red meat appear to face an increased risk for a common form of breast cancer, according to a large, well-known Harvard study of women’s health published in the Archives of Internal Medicine November 2006. The study of more than 90,000 women found that the more red meat the women consumed in their twenties, thirties, and forties, the greater their risk for developing breast cancer fueled by hormones in the next twelve years. Those who consumed the most red meat had nearly twice the risk of those who ate red meat infrequently.17
Men whose mothers have low beef intake, compared to men of mothers with high beef intake, are more virile. Sons of mothers with low beef consumption have sperm concentrations 24.3 percent higher than those of high-beef-consumption mothers. Eighteen percent of sons of mothers with high beef consumption had sperm levels lower than what the World Health Organization considers the lower limit of subfertility—this rate of infertility is three times higher than sons of mothers with low beef consumption. Extrapolating, we have two theoretical potentials: sons of vegan mothers are more virile, and vegan men are more virile.
Research has also shown that removing meat from your diet and eating a plant-sourced diet can reduce or eliminate asthma. Thirty-five patients who had suffered from bronchial asthma for an average of twelve years, all receiving long-term medication, twenty including cortisone, were subject to a plant-source-only diet for one year. In almost all cases, medication was able to be withdrawn or drastically reduced. There was a significant decrease in asthma symptoms. Twenty-four patients (69 percent) fulfilled the treatment. Of these, 71 percent reported improvement at four months and 92 percent at one year.18
Osteoporosis is significantly higher in meat eaters or even women who drink three or more glasses of milk per day. Research suggests that the higher amounts of protein create an acidity that forces the bones to give up calcium to neutralize the acidity.
The high phosphorus content in meat actually pulls calcium from the bones. In essence, from the perspective of health and diabetes in particular, animal flesh sourced protein—fish included—is inferior to vegetable protein as a quality protein source. This undisputed scientific fact is confirmed by the China Study by T. Colin Campbell and the epidemiological evidence of 6,500 Chinese across 65 provinces. A meat-based protein is a poorer quality protein source than a plant-based protein, as evidenced by cancer data from that study showing that the more animal protein was consumed, the higher the rates of cancer. According to the Max Planck Institute, cooking coagulates approximately 50 percent of the protein, making the food less digestible, more coarse, and more inflammatory. In essence, cooking meat protein creates a situation in which one actually gets one-half the protein that is eaten and the other half acts as an inflammatory toxin.
The best and most assimilable sources of protein are the algaes (about 70 percent protein), nuts and seeds, bee pollen, and greens, grains, and beans. Spirulina, blue-green algae, chlorella, hemp seeds, olives, durian, all sprouts (including sprouted grains and beans), bee pollen, green vegetables (especially spinach, watercress, arugula, kale, broccoli, brussel sprouts, collard greens, and parsley), powdered grasses, and green superfood powders are examples of relatively high-protein live foods.
Animals concentrate plant foods to form their tissues. And if there is toxicity in their air, water, and/or food environment—such as chemicals, pesticides, herbicides, larvicides, fungicides, detergents, bleaches, toxic solvents—then these toxins accumulate in the animal. Dairy products contain five times as many pesticides as commercial fruits and vegetables. And flesh foods, such as fish or chicken, which are higher up on the food chain, contain fifteen times as many pesticide residues as commercial fruits and vegetables.
From a practical point of view, eating fish is potentially dangerous because of the widespread, ever-increasing pollution of the waters of the world. The biggest water contaminants are PCBs and mercury. PCBs, along with dioxin, DDT, and dieldrin, are among the most toxic chemicals on the planet. According to John Culhane, in his 1980 article “PCBs: The Poisons That Won’t Go Away,” only a few parts per billion of these substances can cause cancer and birth defects in lab animals.19 The tenth annual Council on Environmental Quality, sponsored by the U.S. government, reported PCBs in 100 percent of all human sperm samples. According to a Washington Post article in 1979, PCBs are considered one of the main reasons that the average sperm count of the American male is approximately 70 percent of what it was thirty years ago. This same article also points out that 25 percent of college students were sterile at the time as compared to 0.5 percent thirty-five years earlier. Most toxicity experts agree that the main source of human contamination comes from eating fish from waters in which the PCB levels are high, which today can be almost anywhere. The Environmental Protection Agency estimates that fish can accumulate up to nine million times the level of PCBs in the water in which they live. PCBs have been found in fish from the deepest and most remote parts of the world’s oceans.
Fish and shellfish are natural accumulators of toxins, because they live and are flushed by the water in which they dwell. Shellfish such as oysters, clams, mussels, and scallops filter ten gallons of water every hour. In a month, an oyster will accumulate toxins at concentrations that are 70,000 times greater than the water they are living in. The problem isn’t solved by not eating fish—after all, half the world’s fish catch is fed to livestock. According to Diet for a New America by John Robbins, more fish are consumed by U.S. livestock than by the entire human population of all the countries in Western Europe. Periodic testing in the U.S. has found eggs and chickens highly contaminated with PCBs after being fed fish contaminated with PCBs.
Mercury toxicity from ingesting fish is another well-known source of illness. Two forms of mercury are the most dangerous: quicksilver mercury and methylmercury, which is about fifty times more toxic. Although there is general agreement that mercury in plants is a less toxic form, experts do not agree on whether the mercury in fish is stored primarily in the form of the more toxic methylmercury. In any case, children and adults who ate fish from mercury-contaminated waters in Minamata Bay, Japan, in 1953, along the Agano River in Niigata, Japan, in 1962, and other locations in Iraq, Pakistan, and Guatemala, all have suffered death, coma, or a variety of brain and neurological damage.
Researchers in Taiwan say they have established for the first time that the mercury compound present as a contaminant in some seafood can damage the insulin-producing cells in the pancreas. In their experiments, Shing-Hwa Liu and colleagues exposed cell cultures of insulin-producing beta cells to methylmercury. They used concentrations of methylmercury at about the same levels as people would consume in fish under the U.S. Food and Drug Administration’s recommended limits.20
Contamination of fish is widespread. According to Rudolph Ballentine, MD, mercury toxicity is being reported with increasing frequency by physicians as well as dentists. The two main contributing factors seem to be a diet high in fish and the common use of silver-mercury amalgams for dental work. Fish consumption alone may be enough to cause mercury toxicity. An article by the Canadian Medical Association in 1976 reported that Indians in Northern Canada, who ate more than a pound of fish per day, had symptoms of mercury poisoning. A 1985 study in West Germany of 136 people who regularly consumed fish from the Elbe River found a correlation between the blood levels of both mercury and pesticides and the amount of fish eaten.
In a study published in the Diet and Nutrition Letter of Tufts University, it was reported that the more fish pregnant mothers ate from Lake Michigan, the more their babies showed abnormal reflexes, general weakness, slower responses to external stimuli, and various signs of depression. They found that mothers eating fish only two or three times a month produced babies weighing seven to nine ounces less at birth and with smaller heads.21 Jacobsen, in a 1986 follow-up study reported in Child Development, found that there was a definite correlation between the amount of fish the mothers ate and the child’s brain development, even if fish was eaten only once a month. He found that the more fish the pregnant mothers ate, the lower was the verbal IQ of the children.22 These children also had lower SAT scores seventeen to eighteen years later. Children are usually the most sensitive to toxins, and they are prime indicators of what may be happening to adults on a more subtle level. A Swedish study in 1983 found that the milk of nursing mothers who regularly ate fatty fish from the Baltic Sea had higher levels of PCBs and pesticide residues than even meat-eaters. Lactovegetarians were found to have the lowest pesticide residues in this study.
For everyone who lives on milk, being still an infant, is unskilled in the word of righteousness. But solid food is for the mature, for those whose faculties have been trained by practice to distinguish good from evil.
HEBREWS 5:13–14
Children with diabetic genetic tendencies who drink cow’s milk have an 11–13 times higher rate of juvenile diabetes than children who are breastfed by their own mothers for at least three months. Although many are not aware of it, milk consumption is directly associated with juvenile diabetes. The American Academy of Pediatrics made a decision, based on this data, in 1994 to strongly encourage families with a diabetic history not to give their children cow’s milk or cow’s milk products for at least two years. The key to understanding this is that there are more than 100 antigens found in milk. The reason for the increase in juvenile diabetes is that the children have much higher formation of antibodies to the cow’s milk antigens. According to a 1999 study reported in the journal Diabetes by Outi Vaarala, researchers found up to eight times the number of antibodies against milk protein in dairy-product-consuming children who also developed juvenile diabetes.23 Finland, which has the world’s highest milk consumption, also has the world’s highest per capita rate of insulin-dependent diabetes.24 The problem is that the antibodies to the milk antigens cross-react with the beta cells of the pancreas, creating inflammation and scarring. This consequently blocks or destroys beta cell production of insulin.
This is not new information. In 1992 the New England Journal of Medicine reported a study done in Finland on children ages 4–12. They measured the antibodies in these children against BSA (bovine serum albumin). Of the 142 children with juvenile diabetes every one one had an antibody titer greater that 3.55 and not one of the 79 nondiabetic children had an antibody titer greater than 3.55. The complete lack of overlap of serum antibodies of these two populations lead to some very productive studies in understanding the relationship of cow’s milk intake and incidence of juvenile diabetes. One study in Chile25 found that genetically susceptible children who were weaned too early onto cow’s milk—before three months of age—had a risk factor for juvenile diabetes of 13.1 times greater than children who did not have a genetic proclivity, or who were breastfed for at least three months. Another significant study in the U.S.26 found that children with a genetic tendency who were weaned onto cow’s milk before three months had a Type-1 diabetes incidence of 11.3 times greater than those who did not have a genetic tendency and who were breastfed for at least three months. The general statistical view is that anything more than 3–4 times higher is considered a significant finding.
Charting the degree of milk consumption from ages 0 to 14 against the onset of Type-1 diabetes reveals the correlation between milk consumption and Type-1 diabetes.27 It is no accident that Japanese children, who have the lowest milk consumption, have 1/36th the incidence of Type-1 diabetes than do the children from Finland, who had the highest consumption of milk.
Figure 2: Association of cow’s milk consumption and incidence of Type-1 diabetes in different countries (Source: T. Colin Campbell, The China Study)
When the data for both the genetically susceptible and non-susceptible are merged, there is an increased risk for children who are weaned and put on cow’s milk before three months of approximately 1.5 times, which is approximately a 50 percent increase in incidence of Type-1 diabetes. One additional study in Finland showed that the consumption of cow’s milk increased the rate of Type-1 diabetes by 500–600 percent.28
The overall results strongly suggest that cow’s milk, especially in children who are genetically susceptible and who are weaned before three months, significantly increases the risk of developing Type-1 diabetes. Milk consumption has many other health and spiritual problems, which are beyond the scope of this book.
Cow’s milk is the number one cause of food allergies among infants and children, according to the American Gastroenterological Association.29 Most people begin to produce less lactase, the enzyme that helps with the digestion of milk, when they are as young as 2 years old. This reduction can lead to lactose intolerance.30 Millions of Americans are lactose intolerant, and an estimated 90 percent of Asian Americans and 75 percent of Native-and African Americans suffer from the condition, which can cause bloating, gas, cramps, vomiting, headaches, rashes, and asthma.31 Studies have also found that autism and schizophrenia in children may be linked to the body’s inability to digest the milk protein casein; symptoms of these diseases diminished or disappeared in 80 percent of the children who were switched to milk-free diets.32 A UK study showed that people who were suffering from irregular heartbeats, asthma, headaches, fatigue, and digestive problems “showed marked and often complete improvements in their health after cutting milk from their diets.”33
Walter Willett is chairman of the Nutrition Department at the Harvard School of Public Health, and co-authored a major study of more than 75,000 American nurses, which found that women with the highest calcium consumption from dairy products actually had substantially more fractures than women who drank less milk. Citing a 1980 study in the journal Clinical Orthopedics and Related Research, Mark Hegsted of Harvard University makes the point that people in the U.S. and Scandinavian countries consume more dairy products than anywhere else in the world, yet they have the highest rates of osteoporosis.34 As pointed in out in Conscious Eating and the American Journal of Clinical Nutrition, there is a problem of excessive protein in the diet. This excessive animal protein creates acidity and a high phosphorus content that pulls calcium out of the bones, and therefore is a plausible explanation for why those with the highest dairy intake have the highest rates of osteoporosis. A 1985 study in The American Journal of Clinical Nutrition suggests that dairy products offer no protection against osteoporosis, probably due to the high protein content of milk.35
The bottom line is that calcium deficiency is not a threat to someone eating a plant-source-only cuisine. In fact, inadequate calcium intake appears not to be a problem at all. A scholarly review of the subject in the Postgraduate Medical Journal in 1976 revealed that calcium deficiency caused by an insufficient amount of calcium in the diet is not known to occur in humans at all.36
T. Colin Campbell did a twenty-seven-year study, published as The China Study, jointly arranged by Cornell, Oxford, and the Chinese Academy of Preventive Medicine. Funded by the National Institutes of Health, the American Cancer Society, and the American Institute for Cancer Research, the study was called by the New York Times the “Grand Prix of Epidemiology.” His research team investigated the role of protein in promoting cancer. They found one protein that consistently and strongly promoted cancer—casein in cow’s milk. Casein is 87 percent of the proteins in dairy, and it promotes all stages of the cancer process.
What were the safe proteins? Those from plant sources. In fact, their research found that the people who ate the most plant-based foods were the healthiest and tended to avoid chronic disease. More important, they discovered through the findings of other researchers and clinicians worldwide, as we have, that “the diet that has time and again been shown to reverse and/or prevent [diseases caused by animal protein consumption] is the same whole-foods, plant based diet found to promote optimal health in laboratory research and in the China Study. The findings are consistent.”37
In Norway, 15,914 individuals were followed for eleven and a half years. Those drinking two or more glasses of milk per day had 3.5 times the incidence of cancer of the lymphatic organs.38 One of the more thoughtful articles on this subject is from Allan S. Cunningham of Cooperstown, New York, writing in The Lancet, November 27, 1976 (page 1184), in an article entitled “Lymphomas and Animal-Protein Consumption.” Cunningham tracked the beef and dairy consumption in terms of grams per day for a one-year period, 1955–1956, in fifteen countries. New Zealand, United States, and Canada had the highest consumption, respectively. The lowest meat and dairy consumption was in Japan. The difference between the highest and lowest was nearly thirty-fold: 43.8 grams/day for New Zealanders versus 1.5 for Japan. Cunningham found a highly significant positive correlation between deaths from lymphomas and beef and dairy ingestion in the fifteen countries analyzed. The reason for the role of dairy is that the dairy intake creates a chronic immunological stress that tends to cause lymphomas in laboratory animals and also possibly in humans. We know that ingestion of cow’s milk can produce generalized lymphopathy, swollen liver, swollen spleen, and significant adenoid hypertrophy. It can be hypothesized that meat protein adds its general carcinogenic effect to the specific carcinogenic effect on the lymph from dairy.
Drinking more than one glass of milk a day, or its equivalent, has been shown to give women a 3.1 times greater risk of ovarian cancer than non-milk drinkers. Harvard Medical School did a study and analyzed data from twenty-seven different countries, to find the same increased amount of ovarian cancer associated with dairy.
A positive relationship between ovarian cancer and dairy products was first reported in The Lancet by Cramer et al. in 1989, when it was suggested that lactose consumption may be a dietary risk factor for ovarian cancer.5239 More recently, data collected from the Harvard Nurses Health Study was used to assess the lactose, milk, and milk product consumption in relation to ovarian cancer risk in more than 80,000 women. Over sixteen years of follow-up, 301 cases of one particular type of ovarian cancer were confirmed in this study group. Results showed that women who consumed the most lactose had twice the risk of this type of ovarian cancer than women who drank the least lactose. It was suggested that galactose (a component of lactose) may damage ovarian cells, making them more susceptible to cancer.40
In 2004, Susanna Larsson and colleagues of the Karolinska Institute in Stockholm, Sweden, published a study41 in the American Journal of Clinical Nutrition that examined the association between intake of dairy products and lactose and the risk of ovarian cancer. In this study of 61,084 women age 38 to 76 years, the diet was assessed over three years. After 13.5 years 266 participants had been diagnosed with ovarian cancer. Results showed that women consuming four or more servings of dairy a day had double the risk of ovarian cancer, compared to those consuming low or no dairy. Milk was the dairy product with the strongest positive association with ovarian cancer.
A study by Curtis Mettlin, funded by the American Cancer Society and cited in the International Journal of Cancer, April 15, 1989, showed that people drinking three or more glasses of whole milk a day had a twofold increase in lung cancer.42
The journal Cancer in 1989 reported that men drinking three or more glasses a day of whole milk were shown to have a 2.49 times increase in prostate cancer.43 A 2001 Harvard review of the research put a finer point on it:
Twelve of … fourteen case-control studies and seven of … nine cohort studies [have] observed a positive association for some measure of dairy products and prostate cancer; this is one of the most consistent dietary predictors for prostate cancer in the published literature [italics added]. In these studies, men with the highest dairy intakes had approximately double the risk of total prostate cancer, and up to a fourfold increase in risk of metastatic or fatal prostate cancer relative to low consumers.44
We see this data corroborated in world data for breast and prostate cancer rates in China, Japan, England, Scotland, and Canada (by the International Agency for Research), and in the U.S. (by the Surveillance Epidemiology and End Results Program of the National Cancer Institute). Figure 3 illustrates that the lowest rates of breast and prostate cancer are consistently in China and Japan, where dairy and animal meat are rarely consumed. As Jane Plant, PhD, remarks in The No Dairy Breast Cancer Prevention Program:
The Japanese cities of Hiroshima and Nagasaki have similar rates of breast cancer: and remember, both cities were attacked with nuclear weapons, so in addition to the usual pollution-related cancers, one would also expect to find some radiation-related cases. If, as a North American woman, one was living a Japanese lifestyle in industrialized, irradiated Hiroshima, you would slash your risk of contracting breast cancer by a half to a third. The conclusion is inescapable. Clearly, some lifestyle factor not related to pollution, urbanization, or the environment is seriously increasing the Western woman’s chance of contracting breast cancer.45
Looking at the chart below, you can see that a black man in the United States is 280 times more likely to develop prostate cancer than a man in rural Quidong, China, and 70 times more prone than a man in urban Tianjin, China.
Figure 3: Age-standardized rates of incidence for breast and prostate cancer
Plant continues:
We know … that whatever causes the huge difference in breast and prostate cancer rates between Eastern and Western countries, it isn’t genetic. Migration studies show that when Chinese or Japanese people move to the West, within one or two generations their rates of incidence and mortality from breast and prostate cancer approach those of their host community.46
Over the next couple of years, Plant and her husband Peter examined the results of the China-Cornell-Oxford Project of T. Colin Campbell, and credited the fact that Easterners do not eat dairy products for their low rates of breast and prostate cancer. Pick up an Asian recipe book at the store—you’ll find no mention of dairy products.
One cubic centimeter (cc) of commercial cow’s milk is allowed to have up to 750,000 somatic cells (common name, “pus”) and 20,000 live bacteria before it is kept off the market. That amounts to a whopping 20 million live, squiggly bacteria and up to 750 million pus cells per liter. According to Robert Cohen, author of Don’t Drink Your Milk, the average liter of milk in Florida has 633 million pus cells, the highest in the nation. Montana is the lowest, with 236 million pus cells per liter. This is not a healthy thing, whether it is 236 or 633 million. Besides pus cells and blood, which are now normal in milk produced during machine suckling, the milk is also high in pesticides, herbicides, antibiotics, hormones, radioactive iodine, and disease factors such as mad cow prion and bovine leukemia virus. In addition, research cited by Robert Cohen has made the point that there is up to a gallon of extra mucus in the body created as a result of drinking dairy. The mucus problem is associated with the fact that 87 percent of milk protein is casein, the main ingredient of Elmer’s Glue.
All animal foods raise the blood cholesterol; that includes beef, fish, chicken, dairy, and eggs. Plant-source foods do not contain cholesterol. Caldwell B. Esselstyn, MD, author of Prevent and Reverse Heart Disease, in a private communication in July 2007 said that an LDL of greater than 80 increases your risk for heart disease, and levels lower than 80 are safe. Dr. Esselstyn said that LDL levels are the most important cholesterol indicator for propensity to heart disease. According to the Centers for Disease Control, 55.9 percent of diabetics reported that their cholesterol was high, placing them at an increased risk for heart disease and poor glucose control.
In our Tree of Life program, which includes the moderate use of healthy, raw nuts and seeds and a 100 percent live-food diet, we had dramatic drops in 21–30 days in LDL cholesterol. For example, one person went from 148 to 86, another from 86 to 46, a third from 216 to 88, a fourth from 153 to 105, and a fifth from 142 to 85, for an average 67-point drop in LDL cholesterol on a plant-sourced live cuisine including nuts and seeds in just 21–30 days. This is an average drop of 44 percent of LDL in one month. There is no other diet that comes anywhere close to these dramatic drops in LDL, which is why we recommend a 100 percent live-food plant-based diet. To place these numbers in perspective, at the University of Toronto Dr. David Jenkins applied a vegan diet with standard cooked vegan elements such as nuts, seeds, oat bran, soy products, and plant sterols. In a four-week period, he achieved a 29.6 percent drop in LDL cholesterol. On a natural live-food vegan diet, our results in four weeks were 50 percent better, without the use of oats or soy.
When the body is under stress, many hormones are released that indirectly increase insulin excretion and indirectly create insulin resistance, a precursor to a diabetic physiology. These hormones release energy in the form of glucose and fat, which is made available to the cells of the body. This provides fuel for what has been traditionally referred to as the “fight or flight” response. With stress, one sees increases in the secretion of catecolamines, especially from the adrenals, resulting in an increased glucose release from the liver into the blood stream, and glucocorticoid or steroid hormones secreted by the adrenal glands and growth hormone produced by the pituitary gland. Extreme stress for months at a time has been known to trigger the onset of a diabetic physiology.
In the U.S., 62.5 percent of adults with diabetes reported having hypertension (source: CDC). Hypertension is part of the basket of symptoms seen in Syndrome X, discussed below.
Candida is also commonly associated with diabetes and is a larger symptom of a Culture of Death diabetogenic diet and lifestyle. Candida is a fungal parasite that excretes toxic waste that can get into the bloodstream and cause symptoms of bloating, clouded thinking, depression, diarrhea, exhaustion, halitosis (bad breath), menstrual pains, thrush, unclear memory recall, recurring vaginal or bladder infections, anxiety, constipation, diarrhea (or both), depression, environmental sensitivities, fatigue, feeling worse on damp or muggy days or in moldy places, food sensitivities, insomnia, low blood sugar, mood swings, premenstrual syndrome, ringing in the ears, and sensitivities to perfume, cigarettes, or fabric odors. Diets high in cooked starches (bread, baked potato, cakes, cookies, pasta) and diets loaded with refined or hybridized (seedless) fruit sugars both feed candida. Diabetes with its higher blood sugar levels makes people good candidates for candida.
Rainbow Green Live-Food Cuisine examines the pathogenic microorganism candida and how its presence in the body pushes the recycling button or “composting button” as the candida functions to recycle the organism it inhabits back to the soil. In essence, candida accelerates the rate of fermentation of the system. At the turn of the nineteenth century, candida yeast was primarily seen in people who were dying of cancer and other very serious diseases, as fungation is the seventh stage of disease (we will discuss the Seven Stages of Disease in Chapter 3). Depending on the degree of toxicity, this composting process leads to chronic disease, misery, and ultimately death. The key to restoring health is minimizing or eliminating the toxic conditions so that the composting button is turned off. A low-sweet, live-food, non-acidic diet and healthy lifestyle are the key factors to reversing the aging-degenerative process of chronic candidiasis. The diet and lifestyle to do this is exactly the anti-diabetogenic diet and lifestyle of the Culture of Life that we are outlining in this book.
According to an evaluation of twenty studies over the past ten years, the prevalence rate of diabetics with major depression is three to four times greater than in the general population. While depression affects 3–5 percent of the population at any given time, the rate is 15–20 percent in patients with diabetes, according to the American Diabetic Association. Women in particular are at greater risk, according to other studies.47
For many years it has been hypothesized that depression is a diabetic complication, which is almost certain given that the diabetogenic diet and lifestyle is the same diet and lifestyle that creates a biologically altered brain, fatty-acid and amino-acid deficiencies, and toxemia, and thus gives rise to depression. More recent research, however, points to depression as a possible cause or trigger for diabetes. Researchers at Kaiser Permanente’s Center for Health Research in Portland, Oregon, looked at 1,680 diabetic members of its health maintenance organization. They found that when compared with nondiabetics, those with diabetes were more likely to have been treated for depression within six months before their diabetes diagnosis. About 84 percent of those diabetics also reported a higher rate of earlier depressive episodes than those in the control group. Gregory Nichols, a Kaiser researcher who conducted the study, said the study suggests depression frequently precedes the onset of diabetes, rather than vice versa.48
A major study in 2004 by Johns Hopkins and other centers tracked 11,615 initially nondiabetic adults age 48–67 over six years, and found that “depressive symptoms predicted incident Type-2 diabetes.” In prospective analyses, after adjusting for age, race, sex, and education, individuals in the highest quartile of depressive symptoms had a 63 percent increased risk of developing diabetes compared with those in the lowest quartile.49
The good news is that I have developed a five-step program for treating depression naturally that seems to work in about 90 percent of patients. It is detailed in my book, Depression-Free for Life.
Syndrome X was first coined as a term by Gerald Reaven, MD, at Stanford University to describe a group of symptoms that arise from an overall metabolic disorder. These symptoms may include Type-2 diabetes, obesity with an inability to lose weight, high cholesterol, high blood pressure, high triglycerides, low HDL cholesterol, and coronary heart disease. Some 655,000 people are newly diagnosed each year, and it is estimated that an equal 655,000 cases are not diagnosed. Some estimates cite some 47 million people with the basket of symptoms known as Syndrome X. A classic symptom and hint of the metabolic syndrome is the accumulation of fat in the abdomen and the inability to lose fat and weight. Dr. Simeon Margolis, co-author of a Johns Hopkins report on Syndrome X, says that abdominal obesity is often the first outward sign of Syndrome X. It seems to be associated with insulin resistance. Some long-term studies have suggested that the higher the fasting blood insulin levels and the greater the amount of abdominal fat, the greater likelihood of death from Syndrome X.
The metabolic disorder that we’ve created through unnatural ways of living from the lifestyle and diet of the Culture of Death has a significant effect on people’s health. Some researchers estimate that we age one-third faster when blood sugar levels are high. Some of the negative impact is related to the glycation process, in which glucose fuses with protein. It disorganizes the protein function, creating cross linkages and disrupting the protein function in the cell membrane and enzymes. The glycation process also results in greatly increased free radical production. Untreated or even poorly managed Syndrome X and diabetes produce an accelerated aging and death process.
Syndrome X and diabetes also create a chemical change in the nerves. These changes impair the nerves’ ability to transmit signals. Symptoms of nerve damage include numbness, tingling, increased sensitivity to touch, insensitivity to pain and temperature, and loss of coordination. The excess sugar also damages blood vessels that carry the oxygen and nutrients to the nerves. People with Syndrome X are more likely to develop obstruction to the arteries and therefore increased or decreased blood flow to the extremities, which creates increased rates of amputations. Up to 70 percent of people with Syndrome X have some form of nerve damage. It is even worse in smokers. Some people feel the metabolic syndrome is not reversible, but with the Tree of Life program, we have seen a high frequency of the reversal of this syndrome over a three-week cycle.
The development of insulin-dependent diabetes mellitus is thought to be dependent on the interaction of environmental agents with the pancreatic beta cells.50
UNIVERSITY OF CALGARY
Just as consuming organic foods is a way to avoid ingesting toxins, becoming aware of the quality of water one drinks and uses is increasingly essential in today’s polluted world, since water can be a major source of toxins. According to Diet for a Poisoned Planet, less than 1 percent of the Earth’s surface water is safe to drink. In some places in the United States and other countries, the term “drinking water” for tap water should be considered nothing more than a euphemism.
The water that the general public uses comes from two sources: underground sources, such as springs and wells, and surface water, such as rivers and lakes. Presently, both these sources are becoming more and more polluted as toxic chemicals, acid rain, raw sewage, agricultural herbicides, pesticide runoff, chlorination, fluoridation, sewage landfills, and radioactive wastes are either dumped into or seep into them. One of the best-known examples of toxic water pollution to date is the infamous Love Canal, where according to the New York Times in 1984, thousands of tons of toxic chemicals were dumped, including 60 pounds of the deadly poison dioxin.
The pollution situation is so out of control that in monitoring cancer rates in Philadelphia, one researcher was able to correlate the different rates and types of cancer in the population with the specific river the people lived near. According to Steve Meyerowitz, in his book Water, the Environmental Cancer Prevention Center found that residents drinking from the west side of the Schuylkill River had 67 percent more deaths from esophagus cancer than those on the east side. Those drinking from the Delaware River on the east side suffered 59 percent more deaths from cancer of the brain, 83 percent more malignant melanoma, and 32 percent more colorectal cancers than those on the west side. This is just one of many studies linking specific water pollution to an increase in cancer rates.
Medical science has discovered how sensitive the insulin receptor sites are to chemical poisoning. Metals such as cadmium, mercury, arsenic, lead, fluoride,51 and possibly aluminum may play a role in the actual destruction of beta cells through stimulating an auto-immune reaction to them after they have bonded to these cells in the pancreas. It is because mercury52 and lead attach themselves at highly vulnerable junctures of proteins that they find their great capacity to provoke morphological changes in the body. Changes in pancreatic function are among the pathogenetic mechanisms observable during lead intoxication.53
Cadmium, a widespread heavy metal contaminant found in air, soil, and water, can accumulate in the pancreas and exert diabetogenic effects in animals. In a large cross-sectional study, urinary cadmium levels are significantly and dose-dependently associated with both impaired fasting glucose and diabetes.54 Such accumulations increase the likelihood of kidney damage and failure, spur free radical activity, and exacerbate neuromuscular complications of Type-2 diabetes.55,56,57,58 Cadmium sources include tap water, fungicides, marijuana, processed meat, rubber, seafood (cod, haddock, oyster, tuna), sewage, tobacco, colas (especially from vending machines), tools, welding material, evaporated milk, airborne industrial contaminants, batteries, instant coffee, incineration of tires/rubber/plastic, refined grains, soft water, galvanized pipes, dental alloys, candy, ceramics, electroplating, fertilizers, paints, motor oil, and motor exhaust.
Because mercury is increasingly becoming elevated in all forms of life, we can assume that more people will have some defects in pancreatic function. Pancreatic support is increasingly necessary for optimal health.
FROM A PERSONAL COMMUNICATION WITH DR. GARRY GORDON
In August 2006, the American Chemical Society published research that showed conclusively that methylmercury induces pancreatic cell apoptosis and dysfunction.59 Mercury is a well-known toxic agent that produces various types of cell and tissue damage, yet billions of people are exposed to levels of mercury harmful to pancreatic health. In the case of diabetes mercury is especially telling, for it affects the beta cells, the insulin itself, and the insulin receptor sites, setting off a myriad of complex disturbances in glucose metabolism.60
Mercury leads the pack in the potency of its toxicity and in the pervasiveness of it presence in the environment through fish, air, and water, medicine through vaccines, and dentistry with dental amalgams. Some say we are all receiving, just through our air, water, and food about a microgram of mercury a day. Sounds like a little until you calculate that a microgram contains 3,000 trillion atoms with each of them holding the potential to deactivate insulin and the receptor sites crucial to their function.61
Studies out of Taiwan and Bangladesh show that individuals who are exposed to higher amounts of arsenic—in their soil and/or drinking water—have a higher independent risk of developing Type-2 diabetes.62,63 Arsenic in tap water is common; this hormone disruptor is suspected of playing a role in diabetes. Arsenic interferes with the action of glucocorticoid hormones, which belong to the same family of steroid hormones as estrogen and progesterone. Glucocorticoids turn on many genes that help regulate blood sugar and even ward off cancer. Repeatedly drinking water containing certain amounts of arsenic has been linked to increased rates of cancer and diabetes. The underlying mechanism is now thought to be hormone disruption.64
Lead exposure has been associated with an increased risk of hypertension, and is a well-established risk factor for kidney disease. Lead either affects blood pressure indirectly through alterations in kidney function or via more direct effects on the vasculature or neurologic blood pressure control. Researchers at Harvard Medical School state:
Our findings support the hypothesis that long-term low-level lead accumulation (estimated by tibia bone lead) is associated with an increased risk of declining renal function particularly among diabetics or hypertensives, populations already at risk for impaired renal function.65
According to “Fluoride in Drinking Water: A Scientific Review of EPA’s Standards,” made public by the National Research Council in 2006:
The conclusion from the available studies is that sufficient fluoride exposure appears to bring about increases in blood glucose or impaired glucose tolerance in some individuals and to increase the severity of some types of diabetes. In general, impaired glucose metabolism appears to be associated with serum or plasma fluoride concentrations of about 0.1 mg/L or greater in both animals and humans. In addition, diabetic individuals will often have higher than normal water intake, and consequently, will have higher than normal fluoride intake for a given concentration of fluoride in drinking water. An estimated 21 million people in the U.S. have diabetes mellitus; therefore, any role of fluoride exposure in the development of impaired glucose metabolism or diabetes is potentially significant.66
Compressed, activated, charcoal block filters are an inexpensive way to get protection from the carbon-based organic pollution, pesticides, herbicides, insecticides, PCBs, cysts, heavy metals, asbestos, VOCs (volatile organic chemicals), and THMs in our water. They also eliminate chlorine and foul odors. They do not, however, absorb inorganic mineral salts such as chloride, fluoride, sodium, nitrates, and soluble minerals. For this reason, they are best for city water systems but not for well water systems, which have a potential to be polluted with high amounts of nitrates from agricultural wastes. A concern regarding granular charcoal filters is their tendency to be a gathering ground for bacteria, yeasts, and molds, and their inability to remove pollutants found in some drinking water. Some of the more sophisticated charcoal filters do have a reverse wash system in an attempt to compensate for this. Another problem with charcoal filters is that the charcoal can break down with age or from hot water and release the contaminants back into our drinking water. The best way to avoid this is to pay attention to any change in taste, smell, or color of the water, or a reduction in water flow rate. Duane Taylor, a water expert from North Coast Waterworks in Sonoma County, California, suggested in a personal communication that the main problem with charcoal filters is that the user does not replace the filter often enough. He recommends purchasing a filter unit that will stop the flow and make the user change the filter when its filtering capacities are used up. If one does not have such a filter, then he recommends changing the filter at 75 percent of the manufacturer’s suggested lifetime. If one waits until there is a taste change, decrease in rate of flow, or smell to the water, the filter may already be dumping contaminants back into the water. Activated carbon is rated on its ability to remove iodine and phenols. The iodine number should be greater than 1,000 on the measuring scale, and the phenol number should be 15 or less. Another important consideration for carbon filter effectiveness is the contact time of water with the filter. The slower the flow rate and the more carbon there is in the filter, the better job the filter does.
Reverse osmosis (RO) is one of the best methods to get pure water without using up a lot of energy. RO units remove bacteria, viruses, nitrates, fluorides, sodium, chlorine, particulate matter, heavy metals, asbestos, organic chemicals, and dissolved minerals. They do not remove toxic gases, chloroform, phenols, THMs, some pesticides, and low-molecular-weight organic compounds. When combined with an activated carbon filtration system, however, they can remove the entire spectrum of impurities from the drinking water, including organic and inorganic chemicals. Many RO units now have pre-and post-filters to take care of any residual impurities that the RO unit does not remove.
In RO, the water to be filtered is forced through a semi-permeable membrane by the moving elements from more-concentrated to less-concentrated solutions. The membrane is permeable to pure water but not to most of its impurities. If conditions are right for sufficient water pressure and the water is not excessively hard, almost no energy is needed for the operation of RO systems. A pressure pump is needed if the total dissolved solids are greater than one thousand parts per million. The water is as pure as distilled, yet it is not heated as in distilled water and therefore not destructured, which is a great advantage. Sometimes a pressure pump is needed for extremely hard water, and this does require electrical energy. The main problem with an RO unit is the fragility of the semi-permeable membrane. Some membranes can be destroyed by chlorinated water, highly alkaline water, or temperatures above 100° Fahrenheit. If the water is chlorinated, a cellulose membrane is needed. A polymer membrane can be used if the water is not chlorinated.
Some people have had the membrane break in less than the expected three years. For this reason, it is good to check the water purity regularly. Newer and stronger membranes are now available on the market, but we are still in the habit of checking the water purity every four months and/or whenever there is a change in the taste. While RO units are similar in appearance and claimed performance, there are many complex, interdependent choices regarding pre-treatment, membrane selection, and post-treatment. To select a system that fits your water filtration needs and to develop the best maintenance plan, it is best to talk with someone who has in-depth knowledge of the many factors involved. If properly selected and maintained, an RO unit may be the most energy-efficient and best way to protect your water. In the past, RO units required a lot of water to work properly, which is a disadvantage, particularly during times of drought. Some of the newer models have been designed to operate with minimal water usage.
Water distillers, although generally more expensive, remove most everything from the water, including bacteria, fluoride, nitrates, radionuclides, and/organic and inorganic toxins, as well as heavy metals such as lead, mercury, and cadmium, and soluble minerals such as calcium and magnesium. Some toxic organic compounds, such as THMs and dioxin, have the same as or a lower boiling point than water and therefore are not filtered out by the distillation process. The heating of the water also disrupts potential homeopathic patterns of toxins that are left in the water in reverse osmosis filtration. Some of the more expensive distillers have built-in pre-boiler or post-boiler filters as options to eliminate this problem.
There are two major drawbacks to water distillers. One is that they are energy-intensive and expensive unless one has a solar water distiller. The other problem is that distilled water is dead, unstructured water so foreign to the body that one actually gets a temporarily high white blood cell count in response to drinking it. It is, however, possible to revive this dead, destructured water by the use of a product called Crystal Energy. I feel that the water distiller is the safest way to approach the water toxicity problem and have outlined in detail how to reactivate distilled water in my book Spiritual Nutrition.
In the May 24, 1996 New Zealand Medical Journal, J. Bart Classen, MD, a former researcher at the National Institutes of Health, reported a 60 percent increase in Type-1 diabetes following a massive campaign in New Zealand from 1988 to 1991 to vaccinate babies six weeks of age or older with hepatitis B vaccine. His analysis of a group of 100,000 New Zealand children followed since 1982 showed that the incidence of diabetes before the hepatitis B vaccination program began in 1988 was 11.2 cases per 100,000 children per year, while the incidence of diabetes following the hepatitis B vaccination campaign was 18.2 cases per 100,000 children per year.68
In the October 22, 1997 Infectious Diseases in Clinical Practice, Dr. Classen presented more data further substantiating his findings of a vaccine-diabetes connection. He reported that the incidence of diabetes in Finland was stable in children under 4 years of age until the government made several changes in its childhood vaccination schedule. In 1974, 130,000 children age 3 months to 4 years were enrolled in a vaccine experimental trial and injected with hepatitis B vaccine or meningococcal vaccine. Then, in 1976, the pertussis vaccine used in Finland was made stronger by adding a second strain of bacteria. According to the National Vaccine Information Center’s (NVIC) report, “Juvenile Diabetes and Vaccination: New Evidence for a Connection,” during the years 1977–1979, there was a 64 percent increase in the incidence of Type-1 diabetes in Finland compared to the years 1970–1976.69
Doctors started reporting in the medical literature as early as 1949 that some children injected with pertussis (whooping cough) vaccine (now part of the DPT or DTaP shot) were having trouble maintaining normal glucose levels in their blood. Lab research has confirmed that pertussis vaccine can cause diabetes in mice.
As diabetes research progressed in the 1960s, 70s, and 80s, there were observations that viral infections may be a co-factor in causing diabetes. The introduction of live virus vaccines, such as live MMR vaccine made from weakened forms of the live measles, mumps, and rubella viruses, has raised questions about whether live vaccine virus could be a co-factor in causing chronic diseases such as diabetes.
In 1982, another vaccine was added to the childhood vaccination schedule in Finland. Children age 14 months to 6 years were given the live MMR (measles-mumps-rubella) vaccine. This was followed by the injection of 114,000 Finnish children 3 months and older with another experimental Hib vaccine. In 1988, Finland recommended that all babies be injected with the hepatitis B vaccine.
The introduction of these new vaccines in Finland was followed by a 62 percent rise in the incidence of diabetes in the 0–4 years age group and a 19 percent rise of diabetes in the 5–9 years age group between the years 1980 and 1982 and 1987 and 1989. As shown in the NVIC report, Classen concluded:
The net effect was the addition of three new vaccines to the 0–4 year old age group, and a 147 percent increase in the incidence of IDDM. The addition of one new vaccine to the 5–9 year olds resulted in a 40 percent rise in diabetes incidence. With no new vaccines added to the 10 to 14 year olds, a rise in the incidence of IDDM was seen by only 8 percent between the intervals 1970–1976 and 1990–1992. The rise in IDDM in the different age groups correlated with the number of vaccines given.70
The Centers for Disease Control published data supporting a link between timing of immunization and the development of diabetes.71 The data from the CDC’s preliminary study supports published data that immunization starting after 2 months is associated with an increased risk of diabetes. The U.S. government study showed that hepatitis B immunization starting after two months was associated with an almost doubling of the risk of IDDM.
According to Hal Huggins in It’s All in Your Head, one cup of coffee can elevate the glucose level enough to need three units of insulin to counteract it. Researchers at Queen’s University in Ontario investigated the effect of caffeine ingestion on insulin sensitivity in sedentary lean men and obese men with and without Type-2 diabetes. They also examined whether chronic exercise (a three-month aerobic exercise program) influences the relationship between caffeine and insulin sensitivity in these individuals. Their results showed that caffeine ingestion was associated with a significant reduction in insulin sensitivity by a similar magnitude in the lean (33 percent), obese (33 percent), and diabetic (37 percent) groups in comparison with those given placebo. After exercise training, caffeine ingestion was still associated with a reduction in insulin sensitivity by a similar magnitude in the lean (23 percent), obese (26 percent), and Type-2 diabetic (36 percent) groups in comparison with those given placebo.
Figure 4 shows that with exercise, insulin sensitivity did go up, but in all groups, whether lean, obese, or Type-2 diabetic, caffeine intake significantly reduced insulin sensitivity. The researchers concluded that caffeine consumption is associated with a substantial reduction in insulinmediated glucose uptake independent of obesity, Type-2 diabetes, and chronic exercise.72
Figure 4: Insulin sensitivity in lean, obese, and Type-2 diabetic groups with and without caffeine intake, before and after three months of exercise
According to the CDC, 17.7 percent of U.S. adults with diabetes smoke, and the dangers are very real for diabetics. Smoking affects both carbohydrate and lipid metabolism. In one study of diabetics, 114 smokers were compared to 49 nonsmokers. The smokers had a 15–20 percent higher insulin requirement and serum triglyceride concentration. In heavy smokers the insulin requirement was 30 percent higher. Researchers have found that chronic smokers were likely to be more insulin resistant, hyperinsulinemic, and dyslipidemic compared to matched groups of nonsmokers. It is believed that catecholamines, a type of hormone, are produced in greater quantity in smokers and act as an antagonist to insulin action.73 A study of forty patients with Type-2 diabetes found insulin resistance was markedly aggravated among those who smoked.74
A contributing factor to insulin resistance is nicotine-containing products. Please understand that insulin resistance is a precursor to diabetes, so anything that contributes to insulin resistance encourages a move from pre-diabetes to diabetes, or makes an existing diabetic condition worse. Chronic cigarette smoking has been found to markedly aggravate insulin resistance for Type-2 diabetics.75 Lack of exercise certainly helps to activate the expression of Type-2 diabetes.76 The good news is that even mild exercise can help stave off cigarette cravings and withdrawal symptoms as well as decrease a smoker’s chance of reaching for a cigarette, according to a study published in the journal Addiction. Researchers from the University of Exeter and the University of Toronto reviewed fourteen previously published studies and compared the results. They found that twelve of the studies demonstrated that a session of exercise caused a rapid decrease in cigarette cravings, withdrawal symptoms, and other negative effects of cigarette addiction. As little as five minutes of simple exercises such as walking, isometrics, or muscle flexing proved as effective as a nicotine patch in decreasing an immediate craving.77 Not only does exercise reduce cravings for cigarettes, but it seems to dramatically improve endurance and fitness, decreases body fat stores, and decrease insulin resistance.
A prospective study of Japanese men concluded that age of smoking initiation and number of cigarettes smoked were major risk factors for developing diabetes.78 Similarly, data from the U.S. Cancer Prevention Study found that as smoking increased so the rate of diabetes increased for both men and women.79
Nicotine has also been associated with decreasing peripheral circulation and thus increasing the tendency for amputation. Smoking increases adrenaline secretions by 23 percent and thus increases blood sugar. Obviously, smoking decreases lung function, and therefore oxygen in the system, and this lack of oxygenation to the tissues decreases peripheral circulation and leads to a greater tendency for gangrene and amputation. Smoking is a documented risk factor for both the development and progression of various types of neuropathy (damage to the peripheral nervous system). A retrospective study of Type-1 and Type-2 diabetic patients found that current or ex-smokers were significantly more likely to have neuropathy than individuals who never smoked (64.8 percent compared to 42.8 percent).80 A later study found that cigarette smoking was associated with a twofold increase in risk.81 Studies also show that smoking increases the chances of developing gum disease, a contributing factor in poor glycemic control. In fact, smokers are five times more likely than nonsmokers to have gum disease. For smokers with diabetes, the risk is even greater. If you are a smoker with diabetes, age 45 or older, you are twenty times more likely than a person without these risk factors to get severe gum disease.82
Often diabetes doesn’t get diagnosed until its complications begin to arise. Major chronic complications include: retinopathy, which leads to blindness; neuropathy, degeneration of the nervous system; nephropathy, or kidney disease; atherosclerotic coronary disease; and atherosclerotic vascular disease. About 85 percent of all diabetics develop retinopathy, 20–50 percent develop kidney disease, and 60–70 percent have mild to severe forms of nerve damage. Diabetics are two to four times more likely to develop cardiovascular disease (which is a factor in 75 percent of diabetes-related deaths) and two to four times more likely to suffer stroke. Multiple studies show that insulin resistance doubles the risk of heart attack as early as fifteen years before diabetes is diagnosed, along with risk of stroke. Middle-age people with diabetes have death rates and a heart disease rate two times higher than those without diabetes. Diabetics are also three-four times more likely to develop clinical depression than nondiabetics.
The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) reported in 1993 that diabetes is the leading cause of new cases of blindness among adults 20 to 74. Somewhere between 12,000 and 24,000 new cases of blindness per year are caused by diabetic retinopathy. About 60–70 percent of the people with diabetes have mild symptoms to severe forms of diabetic nerve damage. Neuropathy is the major cause of nontrauma lower limb amputation, and studies suggest that as many as 70 percent of amputees die within five years.83 Many people with diabetes have a “slow stomach” or gastric paresis. These conditions all seem to be associated with hyperinsulinemia (high blood insulin) and hyperglycemia (high blood sugar).
Diabetes, in essence, is an accelerated aging. So hyperinsulinemia becomes a part of the continuum of developing diabetes. It is a tip-off point before we get to diagnosable diabetes and the accelerated aging pattern known as chronic disease. Hyperinsulinemia is telling us that we have a higher risk of developing chronic degenerative diseases. Our carbohydrate metabolism requires attention and is one of the most important life extension factors. The diet and lifestyle we are suggesting helps us maintain healthy blood sugar levels.
Proper management of carbohydrate metabolism is key to a healthy life and longevity. A normal fasting blood sugar, according to ADA data, is 100. However, as we have already pointed out, the latest research shows that if you have a blood sugar of 86 or higher you are already entering into the first stages of an abnormal metabolism, an accelerated aging process, and are beginning to lose control of a healthy carbohydrate metabolism.
A major twelve-year study at Harvard University of 42,500 male health professionals ages 40 to 75 who did not initially have diabetes, cardiovascular disease, or cancer found two dietary patterns. One diet was characterized as prudent, with medium to higher concentrations of vegetables, fruit, fish, poultry, and whole grains. The other, characterized as Western, had a high consumption of red meat, processed foods, fat, dairy products, refined grains, sweets, and desserts. The researchers found that the Western dietary pattern was associated with substantially increased risk of Type-2 diabetes. They found that high blood sugar levels led to complications such as blindness, kidney failure, and heart disease. The key factors were being overweight and physically inactive, as well as having a diet that was not prudent. They concluded that all three were important and it was difficult to separate the risk of diet from the risk of being overweight and physically inactive. The study made crystal clear the importance of all three in creating Type-2 diabetes.84
Hyperinsulinemia, a metabolic time bomb, is associated with a whole series of chronic degenerative diseases. Not only is it a major risk factor for coronary heart disease, but is linked with the rise in plasma free radicals associated with oxidative stress, which contributes to heart disease and actually decreased brain function. Cell damage resulting from elevated insulin and blood sugar levels can lead to degenerative diseases such as hypertension and cancer.
Chronically elevated blood sugar contributes also to the formation of advanced glycation end products, also known as AGEs. These result from the non-enzymatic glycosylation of proteins. Once the proteins become glycosylated, they lose their function and contribute further to chronic disease including atherosclerotic cardiovascular disease (ASCVD) and renal failure. They cause part of what we call cross linkages, which are, in essence, an accelerated aging process. This glycosylation also produces sugar alcohols. The AGEs in sugar alcohols are associated with nerve damage to blood vessels, kidneys, lenses of the eyes, and the pancreas, and generally accelerate the aging process. The sugar alcohol formation is associated with cataract development and diminished nerve function. Therefore at a minimum, what we want to do is to try to control the high blood sugar.
Type-2 has a much stronger genetic component than Type-1. A lot of research on diabetes was done in England, where they have 1.9 million diabetics. Findings explain up to 70 percent of the genetics involved. In Type-2 diabetes, family histories and obesity are major risk factors for the condition. One genetic mutation has been identified as a possible cause of Type-2 diabetes. The mutation was a particular zinc transporter, known as SLC 30 A8, which is involved in regulating insulin secretion.
In another genetic study, a UK team found that people with two copies of the mutant TCF7L2 gene were twice as likely to develop Type-2 diabetes.85 According to Professor Stephen Humphries, the gene “seems to be causing as many cases of diabetes in the UK as obesity.” The researchers discovered that those who carry one variant of the TCF7L2 gene were 50 percent more likely to develop Type-2 diabetes. But those men who carried two copies of the gene were 100 percent more likely to develop diabetes. Professor Humphries, lead researcher on the study for the University College of London Center for Cardiovascular Genetics, said, “Although being overweight is a major risk factor for the development of diabetes, it is clear that an individual’s genetic makeup has a big impact on whether or not they will develop diabetes.” Professor Humphries said 40 percent of the population carries one mutation of the gene while 10 percent carry both. Again, the message is clear: The genes load the gun, and our lifestyle pulls the trigger. We are not determined by our genes. We are affected by our genes. Our genes have a certain tendency to make us more susceptible to our lifestyles. It is our lifestyle that makes the difference.
Another gene, ENPP-1, disrupts the way the body stores energy and handles sugar by blocking the hormone insulin. Research by a French and UK team showed that children with a faulty version of ENPP-1 often were obese as young as 5 years old.
The gene called SUMO-4 helps regulate the body’s immune system, which defends against infection. It was found in the U.S. at the Medical College of Georgia. The gene enables more cytokines to be made and directs the revved-up immune response in the cells of the pancreas that make insulin. In other words, it amplifies inflammation.
Although there is a genetic component, we do not need to use that as an excuse and move into fatalism. We have control of our destiny and need the courage to live a lifestyle that makes us immune to diabetes. This is what this book is about.
Type-2 diabetes, which we have been describing, is self-inflicted, manifesting in an ever-increasing proportion of young people. Because of poor diet and lifestyle, we are seeing Type-2 diabetes in more and more 5-year-olds and 10-year-olds. The Culture of Death diet and lifestyle is obviously accelerating the expression of a poor genotypic tendency for diabetes. In Type-1 diabetes, 85 percent of the people do not have a genetic predisposition, but a genetic predisposition still does play some role. The Type-1 diabetes is called insulin-dependent diabetes mellitus (IDDM) because the beta cells of the pancreas are destroyed by some sort of inflammatory process. Research has suggested that 75–90 percent of the people with Type-1 diabetes have a much raised antibody titer against their own beta cells. These B-cell antibodies seem to be associated with cow’s milk. Two specific proteins in the milk cause the cross-reaction with the beta cells of the pancreas. The drinking of milk in the first few months has been associated with eleven to thirteen times higher rates of Type-1 diabetes than those people who don’t drink milk in genetically predisposed children who are weaned before three months.
The symptoms of diabetes may come on very quickly. High levels of sugar in the blood and urine, frequent urination, and/or bedwetting may be seen readily in children. Other symptoms include extreme hunger, extreme thirst, weight loss, weakness, tiredness, irritability, mood swings, and nausea. Type-1 has also been associated with a variety of viral infections. This is in contrast to Type-2 diabetes, which is slow to develop with many of the same symptoms, but with hard-to-heal infections, blurred vision, itchy skin, candida, and the mind not working so clearly. Cases of Type-1 can arise from exposure to viruses that have been documented, including measles, mumps, infectious mononucleosis, infectious hepatitis, Coxsackie virus, and cytomegalovirus. These viruses cause an immune inflammation response that destroys the beta cells of the pancreas in an infant. Infant research suggests that exposure to German measles in the womb may have a 40 percent greater chance of developing Type-1 diabetes.
Type-1 diabetes can run in families, but there is a weak association. About 85 percent of people who develop Type-1 diabetes do not have an immediate family member who is diabetic. If you’re a twin with diabetes, you have a one-in-three risk factor for Type-1. Figure 5 shows the risk factors associated with other family member diabetics.
Figure 5: Family risk factors for diabetes (Source: Rotter, J I, Anderson, C E, Rubin, R, Congleton, J E, Terasaki, P I, and Rimoin, D L. “HLA genotypic study of insulin-dependent diabetes the excess of DR3/DR4 heterozygotes allows rejection of the recessive hypothesis.” Diabetes, Feb. 1983, 32(2):169–174.)
In the early stages, Type-2 diabetics or NIDDM diabetics, do produce insulin, but the cells are unable to use it properly as they are resistant to the signaling of the insulin. Normal insulin production is about 31 units per day on average in the blood. In insulin-resistant diabetes, the pancreas may overwork to produce about 114 units of insulin.86 The underlying cause of insulin resistance is a breakdown in the communication between the insulin, a chemical messenger, and the receivers of that signal called GLUT-4 transporters. GLUT-4 transporters are proteins within the cell that rise to the cell’s membrane, take hold of the glucose, and bring it inside the cell. Insulin resistance means that the cells do not receive the message. Because the cells are not hearing the message from the insulin and thus receiving the sugar, blood glucose levels remain high, causing the pancreatic beta cells to pump out more insulin to “knock” louder on the cell walls. Early in this disease process, the glucose is let in. This is called compensated insulin resistance, as the pancreas has put out more insulin and glucose levels stabilize for a while. As this continues, over time the beta cells of the pancreas wear out from producing up to four times the normal insulin levels. Glucose levels remain elevated in this state of uncompensated insulin resistance, and over time the person experiences an advanced case of Type-2 with beta cell inflammation and eventually “beta cell burnout.” About 30 percent of the people with Type-2 diabetes do inject insulin on a daily basis because their insulin-producing cells become burned out from excessive use. Then these Type-2 (NIDDM) diabetics become insulin-dependent diabetics (IDDM).
There are multiple reasons for insulin resistance. Insulin receptors on the outside of the cells may not accept insulin, or there are too few receptors as the glucose enters the cells, or the cells don’t use it properly, or excess dietary fat accumulates in the cell and disrupts glucose absorption. Part of the issue is that the ability to move from glycogen to glucose is blocked within the cells and there is a backup.
This whole system is somewhat affected by free radical production associated with hyperinsulinemia. This elevated free radical production activates Nuclear Factor kB, which is a DNA regulator that acts within the cell nucleus. NFkB activation intensifies inflammatory responses, resulting in more production of free radicals and eventually beta-cell death. So we begin to see that diabetes is also associated with inflammation. In essence inflammation occurs, not only through the autoimmune inflammation that we get in Type-1 but also as the more chronic low-level inflammation we may see in Type-2.
N-acetyl cysteine is a precursor to glutathionine (GSH) and is a powerful antioxidant to moderate cell metabolism and gene expression. GSH is thought to prevent the oxidation that causes beta cell damage, and it does this by inhibiting NFkB activation. So it’s possible that the inflammation from the NFkB activation plays an important role in the development of diabetes. And if that’s the case n-acetyl cysteine, which inhibits NFkB activation, has the potential to prevent or delay the onset of the disease. In the presence of other oxidants, NFkB can activate the vascular cell adhesion molecules (VCAM-1). This molecule helps these plasma cells attached to the endothelium and therefore creates more clogged arteries. The VCAM-1 increase has been shown to be one of the most important events initiating atherosclerosis. Type-2 diabetes and glucose intolerant hypertensive patients have been found to have elevated levels of plasma VCAM-1.87 In diabetics n-acetyl cysteine may synergize with the antioxidant vitamins C and E; these three together seem to reduce blood glucose levels in mice. They also increase beta cell mass and preserve insulin content.
Type-1 diabetes is rising alarmingly worldwide, at a rate of 3 percent per year. Some 70,000 children age 14 and under develop Type-1 diabetes annually.
Increasingly, children are also developing Type-2 diabetes, in both developed and developing nations, with reports of Type-2 diabetes in some children as young as 8 years old. Approximately 2 million children ages 12–19 have a Type-2 diabetic condition directly related to obesity and inactivity. About one in fourteen boys seem to have this condition.
In a study reported in the November 2005 issue of Pediatrics, based on data involving 950 children in a 1999–2000 national health survey, researchers found that among roughly 177,000 Americans under age 20, both Type-1 and Type-2 have increased. About 25 percent of the diabetic children now have Type-2, compared with just 4 percent ten years ago. Approximately 7 percent of the children in the study were pre-diabetic—that translates to 2 million children. About 16 percent of the kids in the study were obese. The study supports the idea that our children are heading more seriously in the direction of a diabetes disaster.
Figure 6: Top ten countries for incidence rate of Type-1 diabetes in children, 0–14 years (Source: Diabetes Atlas, third edition, International Diabetes Federation, 2006)
About 5 million children are overweight in the U.S. Overweight is being described as a new epidemic in the American pediatric population, with an overall 33 percent increase in diabetes incidence and prevalence seen in the last ten years. Type-2 diabetes has changed from a disease of our grandparents and parents to a disease of our children. In 1994 Type-2 diabetes accounted for 16 percent of new cases of pediatric diabetes, and by 1999, it accounted for 8 percent to 45 percent, from state to state.88 In Ohio and Arkansas, African American children with Type-2 diabetes represented 70–75 percent of new pediatric diabetes cases.89 In Ventura, California, 31 percent of new adult-onset diabetes were Mexican American youths. Among the Pima tribe, pediatric diabetes is seen in 20 to 40 per 1000. Unlike Type-1 diabetes, most children with Type-2 diabetes have a family member with Type-2 diabetes; 45 to 80 percent have a parent with Type-2 diabetes90 and 70 to 90 percent report at least one affected first-or second-degree relative. Up to 60 to 90 percent of youth who develop diabetes have ancanthosas, a thickening and hyperpigmentation of skin at the neck. This seems to be associated with insulin resistance. Once Type-2 diabetes is established, the persistence of obesity exacerbates the complications of hypertension, dyslipidemia, atherosclerosis, and polycystic ovarian syndrome, which start to appear despite the fact that these patients are still young.91
Figure 7: Estimated number of prevalent cases of Type-1 diabetes in children (0-14 years) by region (Source: Diabetes Atlas, third edition, International Diabetes Federation, 2006)
Investigators reviewed national health surveys of more than 6,000 U.S. children ages 6 to 18 between 1988 and 1994. They also looked at the data from 3,000 children in China and 7,000 in Russia. In the U.S. about 11 percent of the children were obese and slightly more than 14 percent were overweight, compared to 6 percent in Russia obese and 10 percent overweight. In China 3.6 percent were obese and 2.4 percent were overweight.92 In contrast to the U.S. and England, the Chinese and Russian children from the wealthiest families tended to be more heavy.
Figure 8: Overweight and obesity among school-age children (5–17 years) worldwide (Source: Diabetes Atlas, second edition, International Obesity Task Force, 2003)
Our children are fed daily propaganda to eat foods that are causing them harm. A Kaiser Family Foundation study analyzed more than 8,000 advertisements using detailed data about the viewing habits of children in three age groups. Researchers found that children of all ages are bombarded with promotions for fast food, junk food, and soda, with 8-to 12-year-olds seeing the most food advertisements. This market, the “tweens,” is especially important to advertisers because it encompasses the ages at which youngsters typically begin to make some of their own buying decisions. According to Dr. Susan Linn of the Campaign for a Commercial-Free Childhood (CCFC): “We know that marketing is a factor in the childhood obesity epidemic. It is unconscionable that 8–12-year-olds see, on average, more than 7,600 food commercials a year—the vast majority for candy, snacks, cereals, and fast food.”93
We understand that overweight is a risk factor for heart disease in adults, but the situation is more ominous still. Autopsy data from the conflicts in Korea94 and Vietnam,95 the Bogalusa study,96 and the PDAY Study97 all testify to the ubiquitous nature of the disease in young Americans. The 1992 Bogalusa Heart Study examined autopsies performed on children killed in accidental deaths. Researchers found the initial stages of atherosclerosis in the form of fatty plaques and streaks in most children and teenagers.98
Research by Dr. Milagros G. Huerta has suggested that magnesium deficiency is related to Type-2 diabetes in obese children, who are more likely to have insulin resistance.99 This study was performed to see if obese children get enough magnesium in their diets and if a lack of magnesium can cause insulin resistance and thus Type-2 diabetes. Researchers found that 55 percent of obese children did not get enough magnesium from the foods they ate, compared with only 27 percent of lean children. The results showed that obese children got 14.4 percent less magnesium from the foods they ate than lean children, even though obese and lean children ate about the same number of calories per day. Children with lower magnesium levels had a higher insulin resistance. Obese children typically eat more calories from fatty foods than lean children. In addition to not eating enough foods rich in magnesium, obese children seem to have problems using magnesium from the foods they eat. Extra body fat can prevent the body’s cells from using magnesium to break down carbohydrates.
Characteristic signs of Type-2 diabetes in children include: overweight, early stages of heart disease, magnesium deficiency, and insulin resistance. Chlorophyll through a plant-sourced diet is high in magnesium. Chlorophyll is an amazing food that is essential for humans, and at the center of every chlorophyll molecule is the element magnesium. Plant blood (chlorophyll) and human blood (hemoglobin) are not so different, as shown in Figure 9.
Magnesium is seventeen times as prevalent in the human heart as any other tissue in the body. Famous research scientist Dr. Max Oskar Bircher-Brenner called chlorophyll “concentrated sun power” and said:
Chlorophyll increases the functions of the heart, affects the vascular system, the intestines, the uterus, and the lungs. It raises the basic nitrogen exchange and is therefore a tonic which considering its stimulating properties cannot be compared with any other.100
Figure 9: Plant chlorophyll and human blood hemoglobin
One of the reasons chlorophyll is so effective may be its similarity to hemin. Hemin is part of hemoglobin, the protein fraction of human blood that carries oxygen. Studies done as long ago as 1911 show that the molecules of hemin and chlorophyll are surprisingly alike, with the difference being that chlorophyll is bound by an atom of magnesium and hemin is bound by iron.101 Experiments have shown that severely anemic rabbits make a rapid return to a normal blood count once chlorophyll is administered.102 Although the exact chemical transaction has not been proven, the human body seems to be able to substitute iron and rebuild the blood. It is as if the anemic patient has had a transfusion.
The diagnosis of insulin resistance is not the same as diabetes. It is associated with pre-diabetes, and exists in many Type-2 diabetics. Insulin resistance starts before diabetes and is a whole metabolic shift. About 25 to 35 percent of the population have a degree of insulin resistance and suffer from the health consequences of hyperglycemia.103 Insulin resistance seems to be a common feature of, and possibly contributing factor to, a variety of interlinking health problems including diabetes mellitus,104 polycystic ovarian syndrome,105,106,107 dyslipidemia,108 hypertension,109,110 cardiovascular disease,111,112,113,114,115 sleep apnea,116 certain hormone-sensitive cancers,117,118,119 and obesity.120,121, 122,123 One key sign to diagnose Type-2 is called abdominal obesity, which is almost a clinical marker for this metabolic dysregulation.
Magnesium deficiency is very common in my clinical experience, and is found in about 90 percent of people with diabetes. Insulin resistance is also associated with hypertension. Experimental work with magnesium deficiency showed that giving magnesium reduces tissue sensitivity to insulin. If the diet is depleted in potassium, it can also lead to insulin resistance at post-receptor sites.124 Zinc and chromium play a role in decreasing insulin resistance, as well as does vanadium. Biotin does appear to decrease insulin resistance according to research.125 Vitamin E plays a role. About 600 mg was all that was needed to make a difference in insulin resistance.
Taurine and glutathione all seem to decrease insulin resistance. CoQ10, which seems to be quite good for this, also results in improvements in blood sugar, blood pressure, and uptakes of C, E, and beta-carotene. Alpha lipoic acid is specifically good for improving insulin resistance (sensitivity). Fiber creates an improved insulin resistance. Saturated fats make the insulin resistance worse. Vegetables decrease fasting insulin. Vitamin A-rich foods decrease insulin resistance.
Stress also plays a role at the insulin resistance level. Acute stress seems to be clearly associated with severe, although reversible, insulin resistance.126 We should pay attention to stress, and the treatment of stress.127 A study by Nelson showed that psychosocial stress played a role in the chronic elevation of cortisol, which results in increased plasma insulin levels. A hormone called leptin is secreted by the fatty tissues. High leptin levels appear to act on the hypothalamus to decrease body fat. But as the percentage of body fat increases, even high levels of leptin are unable to stimulate the metabolic processes. So in obesity, we have a leptin resistance.128 Leptin resistance decreases as a person becomes more sensitive to insulin.
In summary, factors that may contribute to insulin resistance and thus to diabetes include: high-fat diet; low-protein diet; deficiencies of the omega-3 and omega-6 fatty acids; a diet high in simple carbohydrates; high-glycemic meals filled with refined sugar and starches; stress; low fiber intake; deficiencies of the minerals calcium, magnesium, chromium, vanadium, potassium, and zinc; deficiency of carotenoids; low intake of vegetables; lack of exercise; watching television; and nicotine.
Gestational diabetes is a third major category of diabetes that needs to be addressed. It occurs in 5 to 14 percent of pregnant women. It is important to diagnose this effectively and treat it because it plays a big role in the onset of Type-2 diabetes five to ten years later. Half of women who’ve had gestational diabetes eventually develop Type-2.129 It is associated with the metabolic changes that take place during a normal pregnancy. To conserve sugar for the baby, mom’s placenta produces hormones that naturally increase insulin resistance, thus rerouting some of the sugar to her fetus that before pregnancy would have gone to her cells. Early in pregnancy maternal estrogen and progesterone increase and promote pancreatic beta cell hyperplasia and increased insulin release.130
This rise in insulin increases peripheral glucose utilization and glycogen storage and lowers glucose levels but this shifts as the pregnancy progresses. There are increased levels of human chorionic gonadatropin (HCG) which also leads to insulin resistance. Cortisol, which has the highest diabetic creating potency, peaks at twenty-six weeks. Progesterone, with anti-insulin qualities, peaks at thirty-two weeks. These two milestones, twenty-six and thirty-two weeks, encompass an important time during which the pancreas releases 1.5 to 2.5 times more insulin to respond to the resistance.131
Figure 10: The diabetogenic potency of hormones in pregnancy
Gestational diabetes is the most common medical complication in pregnancy. Women who have it face a significantly greater risk of developing diabetes later in their life. It may be immediate or long-term, in terms of complications. Statistically associated with gestational diabetes is an increase in preeclampsia and resulting increased C-sections. A study by Coustan and Associates showed that 6 percent were tested with irregular glucose tolerance at zero to two years post-partum; 13 percent were irregular at three to four years; 15 percent at five to six years; and 30 percent at seven to ten years post-partum.132 Other studies have documented Type-2 diabetes at three to five years post-partum in 30 to 50 percent of the women.133,134 Repeated insulin resistance physiologies, due to additional pregnancies, lead to an increase in the rate of developing Type-2 diabetes later. The relative risk for Type-2 diabetes was 1.95 for each 10 pounds gained during pregnancy. This is also associated with greater risk for developing hypertension, hyperlipidemia, EKG changes, and mortality.135 Women with gestational diabetes (GDM) had higher triglycerides and fatty acids, beta hydroxy butyrate, and LDL, and lower HDL cholesterol than normals. Their offspring have an increased rate of perinatal mortality and morbidity. One study showed a fourfold increase in perinatal mortality in pregnancies complicated by improperly managed GDM.136 Other studies have suggested an increased rate in stillbirths associated with GDM.
Maternal hyperglycemia leads to fetal hyperglycemia and fetal hyperinsulinemia with increases in fetal growth. Growth is bigger in the fatty and the liver tissues.
In studies of children of women with pre-gestational diabetes and GDM, they found that irregular glucose tolerance (IGT) was thirteen times higher than in controls. It appears that children of mothers with GDM have a higher incidence of obesity. They saw that Type-2 diabetes occurred in 8.6 percent of children with pre-diabetic mothers and 45 percent of infants with diabetic mothers.137
Approximately 4.5 million Americans have Alzheimer’s Disease, and that figure may triple in less than fifty years, according to the Alzheimer’s Association. More than 65 percent of Americans are overweight or obese, and the Centers for Disease Control and Prevention (CDC) estimates that some 54 million people are considered pre-diabetic. Pre-diabetes and diabetes mean high blood sugar, greatly increasing the chance of developing diabetes, obesity, heart disease, and, according to new research, Alzheimer’s. This link could foretell a dramatic increase in Alzheimer’s cases, unless dietary and lifestyle interventions are made now.138
Researchers are beginning to connect Alzheimer’s with diabetes, obesity, and heart disease. It is such a strong connection that Alzheimer’s is being referred to by scientists at Brown Medical School as Type-3 diabetes.139 A variety of studies have shown that people with Type-2 diabetes have about double the average incidence of Alzheimer’s. One study out of the Karolinska Institute in Sweden found that even people with borderline diabetes, meaning people with high blood sugar, had a 70 percent greater risk of developing Alzheimer’s.140 Apparently the risk of dementia rises in people with high blood sugar. Speculation is that the poor brain circulation caused by diabetes is a primary factor. An eight-year study out of Kaiser Permanente tracked 22,582 patients age 50 or above with Type-2 diabetes, and found that diabetic individuals with high blood sugar experience an increased risk of dementia and Alzheimer’s. Compared to those with normal glycosylated hemoglobin levels (HgbA1c less than 6), those with HgbA1c levels greater than 12 were 22 percent more likely to develop dementia, and those with HgbA1c levels above 15 were 78 percent more likely to develop dementia. As with peripheral vascular disease going to amputations, there may be a vascular dementia that is triggered by low blood flow to the brain.
New research linking diabetes and Alzheimer’s suggests that the high blood sugar of diabetes can lead to the formation of advanced glycation end products, or AGEs.141 AGEs are sugar-derived substances that form in the body through an interaction between carbohydrates and proteins, lipids, or nucleic acids such as DNA. AGEs adversely affect the structure and function of proteins and the tissues that contain proteins.142 Recent studies have shown that both the formation and accumulation of AGEs are enhanced in diabetes.143 According to evidence provided by Edward R. Rosick, DO:
Advanced glycation end products become even more destructive when coupled with free radicals formed during cellular energy production. These highly reactive agents produce oxidative stress that can cause cellular damage. Researchers now believe that oxidative stress may be involved in the formation of AGEs, which in turn may induce even more oxidative stress. Most AGEs that accumulate in proteins are produced under conditions of high oxidative stress. New evidence shows that oxidative stress may be an important causative factor in both insulin resistance and Type-2 diabetes.144,145
Brain autopsies of Alzheimer’s patients find signs of significant oxidative damage by free radicals, and new research indicates that AGEs may initiate this damage.146 It is the oxidative damage and the accumulation of AGEs in both diabetes and Alzheimer’s that is the biochemical similarity between these two diseases.
We do have nutritional protection against oxidative stress of this kind. Studies show that alpha-lipoic acid (ALA) helps protect the brain against damage caused by free-radical-induced oxidative stress, which has important implications for its potential role in protecting against Alzheimer’s disease.147,148
Other good news is that the high blood sugar of diabetes and the increased risk for Alzheimer’s is related to consumption of processed high-glycemic foods, not natural foods. Juicy new research suggests that antioxidants in fruit and vegetable juices may lower the risk of Alzheimer’s disease. The Kame Project, a long-term study of more than 1,800 Japanese Americans conducted in Seattle, began in 1992–1994 to study participants who had no dementia, and averaged 71 years of age. The group was followed through 2001. During that time, eighty-one cases of probable Alzheimer’s were diagnosed in participants who had completed the food surveys. Those who reported drinking fruit or vegetable juices at least three times per week were 73 percent less likely to have developed Alzheimer’s as those who drank juice less than once a week.149 This is great news, as the Culture of Life anti-diabetogenic diet includes ample amounts of fresh vegetable juice.
In addition to diabetes, there is a strong link between high insulin levels and some types of cancer. In one study, ten post-menopausal women with endometrial cancer had significantly higher fasting serum insulin levels than the controls. Researchers found insulin receptors in the post-menopausal ovaries, which is a unique place to find them.150 In a study of 752 women with endometrial cancer and with 2,606 controls, an association was confirmed between NIDDM and an increased risk of endometrial cancer.151 Insulin is thought to affect the development of endometrial cancer through its hormonal stimulating properties. In twenty-two endometrial cancer patients in one study, those with high hyperinsulinemia had significantly more steroid hormone receptors in the tumor area, compared with patients with low insulin anemia.152,153 Researchers also discovered a link between colon cancer and insulin levels and it may be associated with insulin’s role as a growth factor in the colon. In 102 cases of colorectal cancer researchers found that those with the highest level of fasting glucose had almost twice the increased risk of colon cancer. Those with the highest fasting insulin levels also were associated with the increased risk of colon cancer.154
A recent study in the American Journal of Clinical Nutrition has shown that people who consume a large amount of processed sugar each day are at a much higher risk for pancreatic cancer, which kills about 30,000 Americans each year. Of nearly 80,000 men and women whose diets were studied during 1997–2005, 131 developed pancreatic cancer. Those who drank carbonated or corn-syrup laden drinks even twice a day were 90 percent more likely to contract pancreatic cancer than those who never drank them. Those who added sugar to their foods or beverages at least five times daily had a 70 percent higher risk of developing pancreatic cancer than those who did not.155 Clearly, increased insulin demand due to high sugar consumption burdens the pancreas and increases pancreatic cancer risk.
In Chapter 1 overwhelming data was presented that diabetes is a worldwide pandemic. In Chapter 2 the reader can see that by living in the Culture of Death (expressed by: a diet and lifestyle of highly refined carbohydrates, dairy products, processed white flour, processed white sugar, cooked animal and other saturated fats, trans fats, nicotine, coffee, commercial foods high in agrochemicals, heavy metal toxicity, vaccinations, poor air and water quality, and high stress), we have created the pandemic of diabetes. In other words, diabetes is a symptom of the Culture of Death.
In addition to the Culture of Death tendencies that aggravate and pull the trigger on the loaded gun of genetic propensities, there are also economic considerations. Those people living in weaker economic conditions seemed to also be more susceptible, with the exception of China, Russia, and India, where those of greater affluence have more access to junk foods and are running higher rates of obesity, which is associated with diabetes.
In general, what we are saying is that it is a world diet and lifestyle that is a Crime Against Wisdom. The point is clear. The reader is given the option to choose the Culture of Life over the Culture of Death. Chapters 3 through 6 of this book give you the wisdom to no longer suffer the Crimes Against Wisdom in the Culture of Death. These chapters will show how to do this in a straightforward, uncomplicated way that enables you to live a life of abundance, free of diabetes.
We want to make it perfectly clear that in Western societies, a lower-class economic status does not sentence individuals or families to a cheap, highly processed diet that brings diabetes, although it does make it harder to change the diabetic trend. Being empowered by the message of this book to eat organic, whole, live foods, of which you only need to eat half as much to get the nutrients as compared with cooked food, can prevent and reverse diabetes. I have yet to find a person, no matter how difficult their economic status, who could not switch over to this Culture of Life diet and lifestyle. And the exciting thing about this in our advanced Western culture is that we are able to acquire foods and food concentrates that are allowing us to access more powerful forms of nutrition than our ancestors ever dreamed possible. This means that we can do even better than just achieve a nondiabetic physiology, but a post-diabetic physiology in which one’s health is better than it was before the diabetes, and better than most people in the world who have never developed diabetes.
Even in developing societies, where urbanization with its diet and lifestyle has increased rates of diabetes, moving back to a rural agrarian lifestyle can make accessible the indigenous diets which for centuries have protected people from having diabetes. It is useful to remind the reader that the Pima Indians, who are now running a 51 percent rate of diabetes, had only one single documented case of diabetes by 1920 when they were still living on their land and eating their indigenous diet. Their cousins, the Tarahumaras, who have stuck with a natural diet and remained on their land, have only 6 percent incidence of diabetes.
I believe that these healthy results will be repeated in all indigenous cultures who give up white flour, white sugar, cooked hydrogenated and animal fats, and return to the land and their indigenous diets and lifestyles.
In the next chapter we will be discussing a comprehensive theory of the causes of diabetes which will give you more insight into how to effectively manage your metabolism. This is a theory that explains the effectiveness of the clinical results. As a scientist, one understands, as with all theories, they must be proven. Theories give us a way to investigate what is going on. Further research is then needed to disprove or prove them. The key is that there are potentially significant results and in the next chapter we will be presenting a theory that helps us develop and understand the rationale for the 21-Day+ Program for healing diabetes, especially Type-2 and gestational, as well as providing a path for future research. To prove something is more difficult than theorizing. For example, it took more than thirty years to prove that smoking was directly linked to lung cancer. The beautiful thing is that the approach is both safe and outstanding for developing high-level wellness. It is a win/win proposition.