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TCC502: Calories, Obesity, and Diabetes

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Certificate in Plant-Based Nutrition Course Two: Diseases of Affluence

Calories, Obesity, and Diabetes



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Chapter 1: Introduction Today’s lecture is on one of the most talked-‐about problems of recent times; namely, obesity and overweight problems—and their sequel, a disease that tends to occur along with obesity; namely, diabetes. If you have heard the news perhaps you have even caught a glimpse of the staggering statistics that now exist on obesity among Americans: two thirds—two out of three adult Americans—are now considered to be overweight, and one third of the adult population is considered to be obese. In other words, about half of the people who are considered to be overweight are classified as being obese. Not only are these numbers high, but the rates at which they have been rising are ominous, as you can see in the adjoining chart. Let’s take a look at this chart a little bit. 1 [See slide number 3.] You will see that from 1960 to the year 2000, the percentage of people who were obese increased from around 13% or so in 1960 to now at least 30% in the year 2000. Let’s look a little more closely. From 1960 to 1980 it didn’t seem that the percentage of people with overweight problems was that different; it went from 13% to 15%, more or less, in that 20-‐year period. But in the next 20-‐year period, from 1980 until the year 2000, essentially it doubled, so what we are really seeing here is the emergence of what many people would call an epidemic. But what do “overweight” and “obesity” really mean? The standard expression of body size is referred to as the “body mass index.” What this means is that we take the body weight, which is measured in kilograms, and express it relative to the height of the individual. So we take into consideration the height of people before we determine the relationship of weight to height. According to most official standards, being overweight is having a body mass index of about 25, but those who have a body mass index above 30 are considered to be obese. Now, you can determine your own body mass index using charts that are fairly widespread, and we have one here with us. [See slide number 4.] This information is expressed in pounds and inches, and kilograms and meters, for your convenience. The numbers in this chart are consistently the same for both females and males, and so either men or women can use the same numbers. Chapter 2: Overweight and Obesity in Children Perhaps the most depressing element of our so-‐called super-‐size or excess weight is the growing number of overweight and obese children. About 15% of children—or young people between the ages of 6 and 19 years—are now considered to be overweight, and another 15% are at risk2 of becoming overweight.3 In other words, a total of 30% of young people now are either overweight or closely at risk of being overweight. When people are

1 Flegal KM, Carroll MD, Ogden CL, et al. “Prevalence and trends in obesity among US adults, 1999-‐2000.” JAMA. 288(2002):1723-‐1727. 2 The term “at risk” refers to the attribute of this population (in this case, 15% of children) who are capable, or more likely, to develop obesity because of various factors such as dietary consumption or activity level. 3 Ogden CD, Flegal KM, Carroll MD, et al. “Prevalence and trends among overweight US children and adolescents.” JAMA. 288 (2002):1728-‐1732.



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overweight, young people in this particular case, they are likely to face a host of medical problems. For example, they can have increased cholesterol levels, and that in turn can translate into increased risk for heart disease; yes, even at a young age. We have evidence, for example, that atherosclerosis is now being seen in very young children, even younger than ten years of age, which in turn is associated with these increased cholesterol levels, which are oftentimes associated with being overweight. Overweight children can also have a condition called glucose intolerance, which is reflective of a diabetes-‐like condition. Their blood pressure can be elevated as well, and then there is the condition among some people called sleep apnea, which can cause neurological or cognitive problems. Most importantly, however, overweight young people are much more likely to be obese adults compared to young people who are not obese.4 So seeing this much obesity, this much overweight in young people actually indicates an increasing likelihood of there being lifelong health problems for these folks. Chapter 3: Overweight and Obesity in Adults Now, we know that there are problems for adults as well, of course, who are overweight. There are practical, everyday problems. Obviously, people who have too much weight to carry around aren’t able to have the same degree of physical activity, and that only compounds the problem. In people who are consistently and substantially overweight, just regular routine and mundane things that most of us take for granted are compromised. The ability to even tie shoes, for example, really strikes home the consistent problems that these people have. That is the short-‐term, practical, everyday situation. In the longer term, obesity is an indication of diseases to come. I mentioned briefly the fact that diabetes is one such disease, although we also know that obesity tends to be reflective of future disease like the cancers and heart disease as well. The American Obesity Association has given us some numbers to show the size of the problem. The medical costs attributed to obesity are now said to be $100 billion per year.5 In addition, we spend another $30 to 40 million out-‐of-‐pocket money to keep the weight off in the first place.6 Buying various and sundry products and doing gimmicks of all kinds, simply to try to keep the weight off or get the weight down, at least in the short term. Together that is a lot of money. An economic black hole essentially is sucking our money away without really offering anything in return, if we look at those increasing rates of obesity that we saw in the previous chart. Clearly no one really wants to be overweight. That is very clear. So why is it that two out of every three Americans are, in fact, overweight? Why is one third of the population obese? I applaud people for trying to achieve a healthy weight, and I know that there are major personal impediments for many people to reduce their weight. A lot of personal and societal issues seem to get in the way. I know it is not easy for people who are overweight 4 Dietz WH. “Health consequences of obesity in youth: childhood predictors of adult disease.” Pediatrics 101(1988):518-‐525. 5 Adcox S. “New state law seeks to cut down on obesity.” Ithaca Journal (Sept. 2002):5A. 6 Colditz GA. “Economic costs of obesity and inactivity.” Med Sci Sports Exerc. 31(1991):S663-‐S667.



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to really bring their weight under control. I also know that overweight people really don’t want to be overweight. So, why are so many people overweight? Aside from the personal difficulties of people coming to terms with their overweight problems, I am concerned with our societal system that allows and even encourages this problem. We are essentially drowning in an ocean of very bad information coming from all kinds of sources: newspapers, radios, television, just conversation of all kinds. We are really just getting an awful lot of bad information. Too much of it is intended to put money into someone else’s pockets—taking advantage of us, essentially, instead of honestly helping people to lose weight. We actually need a new solution—that is very clear. We need better information, and particularly we need a system that tells people what they can do for themselves at an affordable price. This seems like a simple idea to me, but that in fact is not really being delivered. We need to stop telling people the latest gimmick that only costs money [and] creates problems that cost even more money in the long run. Chapter 4: Proposed Solutions I am convinced that the most practical solution for losing weight is a whole food, plant-‐ based diet—coupled, of course, with a reasonable but regular amount of exercise. This means a long-‐term lifestyle change. It does not mean a quick-‐fix fad. This lifestyle change is a practice that [yields] sustained weight loss while minimizing the risk of chronic disease. If we only think about losing weight in the short run, we oftentimes lose sight of what this is all really about: our long-‐term health. So thinking about short-‐term magic tricks is really not going to do the job for us. Solving this problem does not require these magic tricks and complex equations involving blood types or carbohydrate counting or calorie counting, as so many people think, or soul-‐searching. Take a look around and you can see for yourself who is slim and vigorous and healthy, and who is not. Also, while you are at it, consider some impressive research studies large and small that consistently show that vegetarians and vegans are slimmer than their meat-‐eating counterparts. We have a lot of evidence on that now. According to a recent summary of seven studies, vegetarians or vegans are somewhere around 10 to 30 pounds slimmer than their fellow citizens, and this really applies to most vegetarians or vegans except for a small but significant minority, and I will have a word about that in a moment. 7 8 9 10 11 12 13

7 Ellis FR, Montegriffo VME. “Veganism, clinical findings and investigations.” Am J Clin Nutr. 23 (1970):249-‐255. 8 Sacks FM, Castelli WP, Donner A, et al. “Plasma lipids and lipoproteins in vegetarians and controls.” New Engl J Med. 292 (1975):1148-‐1151. 9 Key TJ, Fraser GE, Thorogood M, et al. “Mortality in vegetarians and nonvegetarians: detailed findings from a collaborative analysis of 5 prospective studies.” Am J Clin Nutri. 70(Suppl.) (1999):516S-‐524S. 10 Bergan JG, Brown PT. Nutritional status of ‘new’ vegetarians.” J Am Diet Assoc. 76(1980):151-‐155. 11 Appleby PN, Thorogood M, Mann J, et al. “Low body mass index in non-‐meat eaters: the possible roles of animal fat, dietary fibre, and alcohol.” Int J Obesity 22(1998):454-‐460. 12 Dwyer JT. “Health aspects of vegetarian diets.” Am J Clin Nutr. 48(1988):712-‐738. 13 Key TJ, Davey G. “Prevalence of obesity is low in people who do not eat meat.” Brit Med J. 313(1996):816-‐817.



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In one study, people were told to eat as much as they wanted of the foods that were mostly low-‐fat, whole food, and plant-‐based. In only three weeks these people lost an average of 17 pounds.14 In other words, what that really indicated [was] that they could just eat foods as much as they wanted and not think about being on a diet and still lose weight. At the Pritikin Center, which is an old established wellness clinic that has been around since the 1960s and 1970s, they looked at the information on some 4,500 patients who [were] run through their clinic over a period of time—4,500 patients who were on a three-‐week program at the center. While there, consuming a mostly plant-‐based diet and engaging in some regular exercise, the clients lost a total of 5½% (on average) of their body weight—again, over a period of only three weeks. An intervention study, of course, is [one in which] you take individuals and actually get them to change, and then see what has happened. For example, one study showed a loss of 2 to 5 pounds after only 12 days of switching the diet;15 another one, 10 pounds in three weeks,16 17 16 pounds over 12 weeks,18 and 24 pounds over a year.19 All studies having to do with switching over to a whole food, plant-‐based diet. Chapter 5: Will It Work for Everyone? While a plant-‐based diet works for most people, it seems, as I said before, not to work for every individual. First and foremost, losing body weight on a plant-‐based diet is much less likely to occur when these individuals are consuming too much of the refined carbohydrate foods. Sweets, pastries, and pastas simply won’t do it. Although they are considered to be vegetarian or vegan, if you will, in reality those are not the kinds of foods we are talking about.20 These foods are high in readily digested sugars and starches—in other words, refined carbohydrates, and the pastries are often also very high in fat as well. This is one of the main reasons that I usually refer to the optimal diet as a whole food, plant-‐based diet, where the entire food is present and [where] the carbohydrates that are being consumed are the complex natural kind.

14 Shintani TT, Hughes CK, Beckman S, et al. “Obesity and cardiovascular risk intervention through the ad libitum feeding of traditional Hawaiian diet.” Am J Clin Nutr. 53(1991):1647S-‐1651S. 15 McDougall J, Lizau K, Haver E, et al. “Rapid reduction of serum cholesterol and blood pressure by a twelve day, very low fat, strictly vegetarian diet.” J Am Coll Nutr. 14(1995):491-‐496. 16 Ornish D, Scherwitz LW, Doody RS, et al. “Effects of stress management training and dietary changes in treating ischemic heart disease.” JAMA. 249(1983):54-‐59. 17 Shintani TT, Beckham S, Brown AC, et al. “The Hawaii diet: ad libitum high carbohydrate, low fat mult-‐cultural diet for the reduction of chronic disease risk factors: obesity, hypertension, hypercholesterolemia, and hyperglycemia.” Hawaii Med J. 60(2001):69-‐73. 18 Nicholson AS, Sklar M, Barnard ND, et al. “Toward improved management of NIDDM: a randomized, controlled, pilot intervention using a lowfat, vegetarian diet.” Prev Med. 29(1999):87-‐91. 19 Ornish D, Scherwitz LW, Billings JH, et al. “Intensive lifestyle changes for reversal of coronary heart disease.” JAMA. 280(1998):2001-‐2007. 20 Some of my physician friends who care for vegan and vegetarian patients (including Drs. Michael Klaper, Neil Barnard, John McDougall, and Hans Diehl) have told me that upwards of 5% or even 10% of their patients have difficulty keeping their weight down, even when they continue on a diet comprised only of plant foods. There seems to be a consensus among these practitioners that most of these “failed” cases can be explained as given in the text.



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In addition to eating the wrong kind of plant-‐based diet, weight loss may be elusive if a person never engages in any physical activity. A reasonable amount of physical activity sustained on a regular basis, of course, can pay important dividends. Keeping body weight off is a long-‐term lifestyle choice—and in fact, what I will be consistently [saying] throughout these lectures is that this kind of dietary lifestyle is one that we should be thinking of as a lifestyle practice, not a short-‐term dietary situation. Gimmicks that produce impressively large, quick weight loss—such as the high-‐protein, high-‐fat, low-‐carb diets—don’t work in the long term. Short-‐term losses in body weight should not come along, [as they do] in those kinds of diets, with long-‐term pain—which will include kidney problems, heart disease, cancer, bone or joint ailments, and other problems that may be brought on as people persist in using high-‐protein, high-‐fat, low-‐carb diets. One very large study of more than 21,000 vegetarians and vegans21 found that the body mass index of these folks was lower among those who adhered to their diet for five or more years compared to people who used this diet for less than five years. In other words, this really goes to the point I am trying to make—namely, that one should not only not be using this diet just for quick weight loss, but should stay on it. And those who stay on it for five years or more become accustomed to it and enjoy it, and they are going to have additional benefit compared to those who don’t. Generally speaking, throw away those simplistic ideas about counting calories. I have found that counting calories (as people tend to advocate that idea) is a simplistic recommendation often used by those who oppose a change in the type of food to be consumed. In other words, people who tend to be opposed to switching over to a plant-‐based diet are likely to say things like, “Oh, it’s just the amount of food that we consume,” and that is about all there is really to it—or in other words, the total amount of calories we consume. I think it is a very simplistic view to simply talk about calories being consumed as being largely related to our weight problems. With a whole food, plant-‐based diet, we can eat as much as we want and still lose weight, as long as we eat the right type of food. In some studies, those who follow a whole food, low-‐fat, plant-‐based diet consume somewhat fewer calories, but [it is] a rather small incremental decrease in calorie intake. They actually spend more time eating—there has been research on this—and they eat a larger volume of food than their meat-‐eating counterparts, while still consuming slightly [fewer] calories.22 Fruits, vegetables, and grains as whole foods are much less energy-‐dense than animal foods and added fats. There are few calories in each spoonful or cupful of these whole foods. Remember that [the] fats present in animal foods (and, of course, added fats) have nine calories per gram, whereas carbohydrates and protein have only four calories per gram. In addition, the whole fruits, vegetables, and grains have a lot of fiber, which makes you feel full21 23—again, there has been good research on that—and yet the fiber in these kinds of foods contributes almost no calories to the meal. So if you eat a healthy meal, you may reduce the calories you consume, digest, and absorb, even if you eat significantly 21 Key TJ, Davey G. “Prevalence of obesity is low in people who do not eat meat.” Brit Med J. 313(1996):816-‐817. 22 Duncan KH, Bacon JA, Weinsier RL. “The effects of high and low energy density diets on satiety, energy intake, and eating time of obese and nonobese subjects.” Am J Clin Nutr. 37(1983):763-‐767. 23 Heaton KW. “Food fibre as an obstacle to energy intake.” Lancet (1973):1418-‐1421.



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more food. [These are] just some of the observations that people who consume a vegetarian—or, better yet, a vegan— type of diet are likely to consume a little [fewer] calories, although we know at the same time [with] that kind of food we can, in fact, consume actually more food and get the same benefit, more or less. However, this [approach] of just counting calories, as I said before, is not quite good enough—not yet, anyway. The same criticisms I would make against the high-‐protein, high-‐fat, low-‐carb diet, such as the Atkins diet—which initially induces a much lower calorie intake—can also be applied to short-‐term studies [in which] subjects consume fewer calories while eating a plant-‐based diet. Short-‐term calorie reduction means little or nothing, as people find it very difficult to continue consuming fewer calories, and if weight loss is due to calorie restriction, the diet will not likely lead to long-‐term weight loss. That is why other studies form a crucial link in this story. Studies show that the weight loss effect of a whole food, plant-‐based diet is not due to calorie restriction alone. These studies document the fact that vegetarians who consume the same amount [of], or even significantly more calories than, their meat-‐eating counterparts actually will be slimmer. The China Study demonstrated that rural Chinese consuming a plant-‐based diet actually consumed significantly more calories per pound of body weight than Americans. Of course, as we said before, some of that is due to the fact that they are more active. Even the least active Chinese tend to be more active than the average American. Most people will automatically assume that these rural Chinese are going to be heavier by consuming more calories—heavier than [their] US meat-‐eating counterparts. Not so—the rural Chinese are still slimmer while consuming a greater volume of food and more calories.24 25 26 What is the secret? One factor is the process that we refer to as “thermogenesis,” which refers to our production of body heat during metabolism—namely, the calories that are being consumed under these conditions. In the case of consuming a plant-‐based diet, some of those calories are going to be burned off as body heat, instead of being laid down as body fat. Vegetarians have been observed to have a slightly higher rate of metabolism during rest,27 and that is reflective of this thermogenesis phenomenon. Thus they burn up slightly more of their ingested calories as body heat, rather than [depositing] them as body fat.28 A relatively small increase in metabolic rate translates surprisingly to a significant number of calories over the course of 24 hours. If we actually are capable in our metabolism [of losing] an extra 50 calories a day—which, incidentally, is not an amount that is easily measured; in fact, it hardly can be measured at all—this has been shown to be related to a loss of about 8 to 10 pounds of body weight per year. Now that may sound like a fairly slow 24 Appleby PN, Thorogood M, Mann J, et al. “Low body mass index in non-‐meat eaters: the possible roles of animal fat, dietary fiber, and alcohol.” Int J Obesity 22(1998):454-‐460. 25 Levin N, Rattan J, Gilat T. “Energy intake and body weight in ovo-‐lacto vegetarians.” J Clin Gastroentrol. 8(1986):451-‐453. 26 Campbell TC. “Energy balance: interpretation of data from rural China.” Toxicol Sci. 52(1999):87-‐94. 27 Pochlman ET, Arciero PJ, Melby CI, et al. “Resting metabolic rate and postprandial thermogenesis in vegetarians and nonvegetarians.” Am J Clin Nutr. 48(1988):209-‐213. 28 The study by Pochlman et al. showed high oxygen consumption and higher resting metabolic rate but was badly misinterpreted by the authors. We had very similar results with experimental rats.



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rate of body weight loss, but if one is losing 8 to 10 pounds of body weight per year—let’s say over a period of three, four, or five years—you can see that this really adds up. It really is a very small differential in the amount of calories that are being laid down as body weight as opposed to calories that are being burned off. Chapter 6: The Role of Exercise Many studies have shown that sustaining an exercise program on a regular basis helps to keep off the weight that is initially lost. Starting and stopping exercise programs is not really a very good idea. It should be on a regular basis.29 In regards to the amount of exercise we need, a mere 15 to 45 minutes per day, every day, will maintain a body weight (according to some very good research) that is 11 to 18 pounds lighter than it would otherwise be. The idea of combining diet and exercise to control body weight really works wonders. Recall for example the studies on our experimental animals, which were fed diets containing either the traditional 20% casein or 20% protein. The animals consuming the 5% casein diets had strikingly less cancer. They had lower blood cholesterol levels and longer lives.30 They also, surprisingly, consumed slightly more calories, but they burned off those calories as body heat. [We] actually did some fairly detailed studies and measured the amount of body heat that was being lost, and then determined the kinds of mechanisms that were at play to cause this to happen. I then wondered, after seeing those early studies in experiments with animals: would these impressive benefits of a low-‐protein diet affect their physical activity? Some of us had noticed over the course of these experiments that the 5% casein animals (getting less cancer, of course) seemed to be more active than the 20% casein animals. To test this idea, we housed rats in cages with little exercise wheels and then fed them either the 5% or 20% diet, and these exercise wheels could record the number of turns when they got into the wheel and turned it. Within the very first day the 5%-‐casein-‐fed animals voluntarily exercised in the wheel about twice as much as the 20%-‐casein-‐fed animals, and exercise remained considerably higher for the 5%-‐casein animals throughout the two weeks of the study.31 Now, we can take these results and combine them with some very interesting observations on body weight. A plant-‐based diet—lower in protein, of course (certainly [in terms of] plant protein as opposed to animal protein)—operates on calorie balance in two ways to keep body weight under control. First, as we have just discussed, it discharges calories as body heat through the process of thermogenesis, instead of storing these calories as body fat, and as I said before, it doesn’t take many calories to make a big difference over a year or so. Second, a plant-‐based diet encourages more physical activity. I think most of you know that when you are consuming a heavy meal—oftentimes high in fat and high in protein—

29 Fogelholm M, Kukkonen-‐Harjula K. “Does physical activity prevent weight gain—a systematic review.” Obesity Rev. I(2000):95-‐111. 30 Gibney MJ, and Kritchevsky D, eds. Current Topics in Nutrition and Disease, Volume 8: Animal and Vegetable Proteins in Lipid Metabolism and Atherosclerosis. New York, NY: Alan R. Liss, Inc., 1983. 31 Krieger E, Youngman LD, Campbell TC. “The modulation of aflatoxin (AFB1) induced preneoplastic lesions by dietary protein and voluntary exercise in Fischer 344 rats.” FASEB J. 2(1988):3304 Abs.



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you feel sluggish. You don’t feel like the same kind of physical activity [you do when] consuming a light meal, generally meaning a diet low in fat and plant-‐based. So a plant-‐based diet basically encourages more physical activity, therefore more calorie expenditure. As body weight goes down, it becomes easier to be more physically active. So diet and exercise are operating in harmony to achieve the same thing. This is really what a healthy lifestyle is all about. Moreover, while this is going on, we know that we can prevent chronic diseases like cancer, heart disease, and diabetes. Of course, this whole lifestyle notion of combining exercise with diet and getting the long-‐term result is a far cry from the usual quick weight loss kind of achievements that people get using high-‐protein, high-‐fat diets. Chapter 7: Closing Remarks on Obesity Obesity, as I indicated before, is really an ominous indicator of poor health that Western nations are currently facing, and I just thought we might keep in mind a couple of ideas that have been widely discussed. First, be aware of diets and potions and pills that create rapid weight loss with no promise of good health in the future. The diet that helps to reduce weight in the short run needs to be the same diet that creates and maintains health in the long run. Another thought: considering obesity as an independent specific disease is misplaced.32 33 In recent years, for example, medical authorities have created a specific code for obesity, considering it as a separate disease. I think that was an error. It gives us the wrong impressions. If we think of obesity as a separate disease, we tend to lose sight of the fact that it really is related to many other diseases. In other words, we lose the notion of the larger context. As a result of thinking of obesity as a separate disease, we tend to look for specific cures to take care of this disease. A third notion: forget the promise of there being a specific gene or even a few genes that can be manipulated to control obesity.34 35 36 At present, for example, the last count that I heard said more than 20 genes had been discovered to be related in some way to weight control. There is no way under the sun, as we discover these genes and go forward, that we are really ever going to know how all of these genes coordinate their activities to control obesity. Discovering genes for obesity is primarily for the purpose of developing a drug to knock out or inactivate those genes. We can control the cause of overweight and obesity without changing our genes. It is right at the end of our fork. 32 Heshka S, Allison DB. “Is obesity a disease?” Int J Obesity Rel Dis. 25(2001):1401-‐1404. 33 Kopelman PG, Finer N. “Reply: is obesity a disease?” Int J Obesity 25(2001):1405-‐1406. 34 Campbell TC. “Are your genes hazardous to your health?” Nutr Advoc. I(1995):1-‐2,8. 35 Campbell TC. “Genetic seeds of disease. How to beat the odds.” Nutr Advoc. I(1995):1-‐2, 8. 36 Campbell TC. “The ‘Fat Gene’ dream machine.” Nutr Advoc. 2(1996):1-‐2.



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Chapter 8: Overview of Diabetes The one disease that we hear a lot about these days is diabetes. Diabetes tends to occur in people who are overweight, so the two go hand-‐in-‐hand. From 1990 to 1998, just a mere eight or nine years, the incidence of diabetes in the United States increased by 33%.37 Over 8% of American adults are now diabetic, and over 150,000 young people now have the disease. Diabetes is classified as either type 1 or type 2. Type 1 is the really serious kind. Type 2 is less serious, but nonetheless in the long run can cause just as much damage. Type 1, the serious type, develops in children and young people, and thus is sometimes referred to as juvenile-‐onset diabetes. This form accounts for about 5 to 10% of all diabetes cases. Type 2, which accounts for the remaining 90 to 95% of all cases, used to occur in adults aged 40 years and up, and thus type 2 diabetes was called adult-‐onset diabetes.38 But because up to 45% of the new diabetes cases in children are now type 2 diabetes39—in other words, the adult type of diabetes is now occurring in children—the age-‐specific names are being dropped and the two forms of diabetes are simply referred to as type 1 and type 2. In both of these types of diabetes, the disease begins with an impaired or dysfunctional glucose metabolism—that is, the metabolism of the blood sugar that is circulating and providing much of the energy for our bodies. In type 1, there is a loss of the ability to produce insulin. Insulin, you may recall, is a hormone produced by the pancreas that is required for the utilization of glucose, specifically for the ability of glucose (as it circulates in the blood) to penetrate and enter into the cells where it does its business. So insulin is critically important to being able to utilize glucose. Type 1 individuals have lost their ability to produce insulin. The cells that actually produce the insulin in the pancreas have been damaged, often in very severe ways so never again can they produce insulin, even when plenty of glucose is present. In type 2 diabetes, the so-‐called adult-‐onset diabetes, there is a loss of the control of using the glucose. Blood levels become high in individuals who are consuming simple refined carbohydrates—the carbohydrates are quickly absorbed, and higher glucose levels result. Among people who persistently consume these kinds of foods, blood glucose levels tend to remain fairly high, and in response insulin is overproduced to try to help the glucose get into the cells. This continuous production of high levels of insulin eventually leads to a resistance on the part of the cells to actually use the insulin. This ends up being a condition called insulin resistance. So in these cases, even though there is plenty of insulin around, and ample supplies of glucose (as in the case of type 2 diabetes), it still ends up as a diabetes-‐like condition because the glucose is simply not getting into the cells to do what it should be doing. 37 Mokdad AH, Ford ES, Bowman BA, et al. “Diabetes trends in the US 1990-‐1998.” Diabetes Care 23(2000):1278-‐1283. 38 Center for Disease Control and Prevention. “National diabetes fact sheet: general information and national estimates on diabetes in the United States, 2000.” Atlanta, GA: Centers for Disease Control and Prevention; 2000. 39 American Diabetes Association. “Type 2 diabetes in children and adolescents.” Diabetes Care 23(2000):381-‐389.



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Chapter 9: Complications Due to Diabetes The complications of diabetes can be quite serious.40 There is two to four times as much heart disease among people with diabetes. There is two to four times the risk of stroke among diabetics. Over 70% of the people with diabetes have high blood pressure. Diabetes, incidentally, is the leading cause of blindness in adults, and one that many people know about is that diabetes is the leading cause of end-‐stage kidney disease, which often requires kidney dialysis, a very expensive procedure. Over 100,000 diabetics underwent kidney dialysis or kidney transplantation in 1999 alone. And other very serious conditions can result in those who have diabetes, such as serious nervous system disorders, which may require [the] amputation of limbs. In fact, over 60% of all lower limb amputations have been performed on diabetics. 41 This list is long enough to show that diabetes is very serious. The disease has many complications, and often it is the overweight who tend to get it. Modern drugs and surgery really offer no cure for diabetics. At best, current drugs may help to maintain a reasonably functional lifestyle, but these drugs will never offer substantial improvement. As a consequence, diabetics face lifetimes of drugs and medications, making diabetes an enormously costly disease. The economic toll of diabetes [in the US] is over 130 billion dollars a year.42 Chapter 10: There Is Hope But there is hope. In fact, there is much hope. The food we eat has enormous influence over this disease. The right diet not only prevents but also has been shown to treat diabetes, and of course that diet is the same diet that is used to control obesity. Like most chronic diseases, diabetes shows up more often in some parts of the world than in others. This has been known for 100 years. It has also been well documented that populations with low rates of diabetes eat different diets [from] populations with high rates of diabetes. In the adjoining chart,43 44we have some figures that were accumulated now over 70 years ago to illustrate this point. [See slide number 24.] As carbohydrate intake goes up and fat intake goes down, diabetes rates decline rapidly from around 20.4 to 2.9 deaths per 100,000 people. Of course, the carbohydrate intake we are talking about here, as I pointed out in the previous lecture, is [of] the complex carbohydrates that come along with the consumption of plant-‐based food. So a high-‐carbohydrate, low-‐fat diet—what I call a whole food, plant-‐based diet—actually helps to prevent diabetes. This was 70 years ago, and I find it really surprising that we knew so much so long ago and so few people really seem to know or to take up this idea. Thirty 40 Centers for Disease Control and Prevention. “National Diabetes Fact Sheet: General Information and National Estimates on Diabetes in the United States, 2000.” Atlanta, GA: Centers for Disease Control and Prevention. 41 Centers for Disease Control and Prevention. “National Diabetes Fact Sheet: General Information and National Estimates on Diabetes in the United States, 2000.” Atlanta, GA: Centers for Disease Control and Prevention. 42 Centers for Disease Control and Prevention. “National diabetes fact sheet: general information and national estimates on diabetes in the United States, 2000.” Atlanta, GA: Centers for Disease Control and Prevention; 2000. 43 Himsworth HP. “Diet and the incidence of diabetes mellitus.” Clin. Sci. 2 (1935): 117–148. 44 Himsworth HP. “Diet and the incidence of diabetes mellitus.” Clin Sci. 2(1935):117-‐148.



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years later the question was reexamined—in this case, using 11 countries. [See slide number 25.] We can see the results in the adjoining chart.45 Very clearly, the relationship between diabetes and obesity is very impressive. Increasing amounts of overweight and obesity are associated with increasing incidence of diabetes. Yet both of the studies in the previous two charts are often considered to be kind of crude because we are really comparing populations. Populations are rather diverse, and so many people who don’t want to think about these relationships point out that these kinds of studies are unreliable since they involve populations. Some critics of the notion of this relationship between diet and diabetes quite frankly will never be convinced. According to them, [because] diabetes [is] a genetics-‐based disease, there may be unmeasured cultural factors that we have to think about, there are uncertain physical activity [factors], and of course some of this can play a role. But that tends to focus people’s attention on those factors, and we lose sight of the dietary effect. So instead of looking at diverse populations across the broad range of dietary conditions, let’s look at diabetes rates within single populations. Chapter 11: Findings from Seventh-‐day Adventists The Seventh-‐day Adventist community shows up in a lot of research. They are an interesting group to study because of their dietary habits. Their religion encourages them to stay away from meat, fish, eggs, coffee, alcohol, and tobacco. As a result, about half [of] Seventh-‐day Adventists are vegetarians, but 90% of this half still consumes dairy and egg products, deriving a significant amount of their calories from animal sources. It should be noted that the meat-‐eating Adventists (the other half) are not really the meatiest of eaters. They consume about three servings of beef a week and less than one serving of fish and poultry.46 I know plenty of people who consume this amount of meat every couple of days. So in these Adventist studies, scientists are comparing moderate vegetarians to moderate meat eaters. This really is not a big difference to discern what relationship diet may have with diabetes. Even so, the Adventist vegetarians are much healthier than their meat-‐eating counterparts. Those Adventists who deprive themselves of meat also deprive themselves of the ravages of diabetes. The vegetarians in these studies have shown about half the rate of diabetes41 47 of the meat eaters, even though the nutritional differences between these groups of people are not nearly as large as they might be. The vegetarians also have about half the rate of obesity. There are actually dozens, if not hundreds, of studies that have shown the same thing. 45 West KM, Kalbfleisch JM. “Influence of nutritional factors on prevalence of diabetes.” Diabetes 20(1971):99-‐108. 46 Fraser GE. “Associations between diet and cancer, ischemic heart disease, and all-‐cause mortality in non-‐Hispanic white California Seventh-‐day Adventists.” Am J Clin Nutr. 70(Suppl.)(1999):532S-‐538S. 47 Snowdon DA, Phillips RL. “Does a vegetarian diet reduce the occurrence of diabetes?” Am J Publ Health 75(1985):507-‐512.



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Chapter 12: Intervention Research on Diabetes Now, if you are still not convinced of this relationship, consider the more rigorous kinds of experimental study—the so-‐called controlled or intervention studies where the experimentalist may, in fact, take a group of people who are diabetic and actually change their diet to see what happens. Professor James Anderson at the University of Kentucky is one of the most prominent scientists studying diet and diabetes and has been doing this for many years. He has published impressive results using dietary means alone. One of his studies examined the effects of a high-‐fiber, high-‐carbohydrate, low-‐fat diet on 25 type 1 diabetics (that is the serious kind) and 25 type 2 diabetics, and he did this in a hospital setting, so it was a good study. None of his 50 patients was overweight, and all of them were taking insulin shots to control their blood sugar levels. After just three weeks, the type 1 diabetic patients were able to lower their insulin medication by an average of 40%.48 This is truly remarkable because most people in the field even today would deny that diet really had much if anything to do with type 1 because these are the people who allegedly are not able to produce insulin, and so should be unresponsive to dietary change. Nonetheless, he was able to show that with a dietary change to a plant-‐based diet they were able to lower their insulin medication by an average of 40%. Their blood sugar profiles also improved dramatically. Just as importantly, their cholesterol levels dropped by 30%. I think this study, although a single study, is really quite remarkable in terms of its effect, and needs to be explored further. Of the 25 type 2 patients (that is the adult-‐onset type), 24 were able to discontinue their insulin medication during the course of this study. 49 In another study of 14 lean diabetic patients, total cholesterol levels decreased by 32% in just two weeks,50 as shown in the adjoining chart. [See slide number 29.] These benefits, representing a decrease in blood cholesterol from around 206 mg/deciliter down to about 141, are truly astounding, especially considering the speed with which they appear. Professor Anderson also found no evidence that this cholesterol decrease was temporary. As long as people continued consuming this high-‐carbohydrate, low-‐fat, plant-‐based diet, it remained low for an additional four years,51 as far as his study was concerned. Another group of scientists—at the rather famous Pritikin Center—achieved equally spectacular results by prescribing a low-‐fat, plant-‐based diet and exercise program to a group of diabetic patients. Of [the] 40 patients on medication at the start of the program, 34 were able to discontinue all medication after only 26 days.52 As you can see from these studies, we can actually beat diabetes and keep it under control, and save some of that 130

48 Anderson JW. “Dietary fiber in nutrition management of diabetes.” In: Vahouny GV, Kritchevsky D, eds. Dietary Fiber: Basic and Clinical Aspects. New York: Plenum Press, 1986:343-‐360. 49 Anderson JW. “Dietary fiber in nutrition management of diabetes.” In: Vahouny GV, Kritchevsky D, eds. Dietary Fiber: Basic and Clinical Aspects. New York: Plenum Press, 1986:343-‐360. 50 Anderson JW, Chen WL, Sieling B. “Hypolipidemic effects of high-‐carbohydrate, high-‐fiber diets.” Metabolism 29(1980):551-‐558. 51 Story L, Anderson JW, Chen WL, et al. “Adherence to high-‐carbohydrate, high-‐fiber diets: long-‐term studies of non-‐obese diabetic men.” J Am Diet Assoc. 85(1985):1105-‐1110. 52 Barnard RJ, Lattimore L, Holly RG, et al. “Response of non-‐insulin-‐dependent diabetic patients to an intensive program of diet and exercise.” Diabetes Care 5(1982):370-‐374.



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billion dollars a year that we spend on it. And as we are doing these kinds of treatments and employing these procedures, we also will (as we spoke about in the first part of the lecture) begin to control obesity as well. So the results are really remarkable in terms of the effects of diet on both obesity and diabetes.

TCC502: The Pleasure Trap


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The Pleasure Trap



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Chapter 1: The Greatest Philosophical Question of All Time My name is Doug Lisle. I am a psychologist. I am here to talk about a very important problem we face today: when it comes to diet and lifestyle issues, why is it that once we know the right thing to do, it is very difficult to do it? To figure this out and to attack this problem, we have to ask and answer the greatest philosophical question of all time. Why does a shark have teeth? Why does a shark have teeth? To eat. A shark has teeth to eat. Why does a shark eat? A shark eats to survive. It survives so that it can reproduce so that little tiny sharkies can do this all over again, and this has been going on for millions upon millions upon millions of years. Chapter 2: Guidance System And this is why a shark has teeth. A shark has teeth, actually, because he is not reproducing himself; he is actually reproducing DNA, or strands of DNA, that we call genes. Those genes actually build the teeth and the rest of that shark so that it can manage to survive and reproduce within its natural habitat. Now, how does a shark know when to eat? When it is hungry. What do we call things like that, little signals from within the shark’s body that tell it what to do? Instincts, and instincts are actually neural circuits. An instinct is, in fact, the pattern of neurons or the way that the “vine” is built through these effective electrical circuits. As the shark goes about its business, it has inputs from the environment coming in through its eyes or its nose, for example, and that shark can smell one drop of blood in a million gallons of seawater. That shark is literally designed by nature to take that information from the environment and have that information activate specific neural circuits. The neural circuits of a shark are absolutely unique to that shark’s body. Just as a glove fits a hand perfectly, the shark’s particular set of neural circuits fits the shark’s body and encourages shark-‐like behavior. So, for example, suppose that it’s a couple hundred years from now and we have a poor shark that has lost its olfactory circuitry so it can’t smell anymore. We also have a big hippopotamus in the zoo that had an accident and he didn’t make it. We did some bypass surgery on the hippo and we actually took from that hippopotamus some neural circuits of its olfactory system. If we wired those circuits into that shark, would they work? They wouldn’t work, because those specific sets of circuits are actually for sharks, for no other creature. Those circuits are part of the shark’s nature. Now, it turns out that across the animal kingdom we find that the different kinds of neural circuits for different kinds of organisms are actually patterned in a very similar way. So sharks are being encouraged to do certain kinds of behavior. That shark could in principle just circle around and around in the water. It could find a sea wall and bang its nose into it, and then circle back around and bang its nose into it again. But that is not what the shark will do. The shark will actually perform a certain set of stereotypic behaviors that will increase the statistical likelihood of its survival and reproduction. To do so, it needs a guidance system, and this is that guidance system.



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Chapter 3: The Motivational Triad The guidance system consists of three parts. The first one is pleasure, and pleasure is a signal to the shark’s nervous system to tell it when it has, in fact, maneuvered its body into circumstances with respect to the environment that are in the best interest of the survival and reproduction of its genes. So let’s talk about what that might be. We already know that the shark is doing what he needs to eat and to survive, and that he needs to survive to reproduce. The number-‐one job of this creature is to take care of its need to eat. So a top priority behavior is going to be seeking food to make sure that this shark survives. When the shark eats, it activates what we now know as the pleasure pathway. It causes a set of dopamine circuits to go off near the pleasure centers of the brain, so this shark will know when it has done something that was good for its long-‐term best interest. Inside an animal’s nervous systems are two primary systems that help this organism know when they are maneuvering in the environment in a way that is in their best interest biologically. The first is food—it needs to eat. It is made out of stuff [cells], and it needs to take in things from the environment to keep the cells going. Taking in good food activates pleasure systems in the brain. Engaging in sexual activity also causes the pleasure centers of the brain to go off, and in a more intense fashion. Both activities produce dopamine rushes in the pleasure centers of the brain. Now it is not enough for this creature to know when it is headed for good things. It also needs to know when it has run into problems. When it moves through water and the water is a little too cold or too hot, or it rubs against some fire coral and may tear some tissue, it is going to need to have another set of signals to tell it when its relationship to the environment is not in its best interest. Those signals are quite diverse, and they fall under what we are going to call pain. So this creature is actually designed by nature to do two processes at the same time as it goes about trying to survive and reproduce. Number one is to try to feel good with pleasure activities. Those can be considered something like the “profits” of biology. And then it is going to have avoidance circuitry that is going to let it know when it is actually losing points. It is trying to get positive points and avoid losing points. So pleasure seeking and pain avoidance are the two primary guidance systems that help creatures maneuver around this planet so that they can survive and reproduce. Now, for several thousand years, philosophers and natural scientists and others have tried to analyze this pleasure seeking and pain avoidance. They have talked a lot about it, and they have come pretty close to understanding motivation. However, a third part of motivation has recently been identified that we now understand to be a key component of why creatures do what they do. It isn’t enough for this shark to simply seek pleasure and avoid pain. It has to do as good a job of it as it possibly can. If there is a tuna flopping in the



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water 20 feet away and another tuna flopping in the water 40 feet away, we know intuitively, all other things being equal, the reason why the shark is going to go for the tuna that is 20 feet away. The reason is energy conservation, and this is important because it prevents him from being sloppy in his behavior and not getting as much profit as he could. This is why all over the world predators go after the weak, the sick, the slow, the young, the isolated, and the injured. They do that for a reason—they do that because they have preferential neural circuits that look for creatures that are compromised, which increases their likelihood of survival and reproduction. This principle has also helped us understand a great deal more about why creatures do what they do. Chapter 4: More to Life Now, you might be saying to yourself, my life seems a little more complicated than this. My life seems more complex than just seeking pleasure, avoiding pain, and conserving energy. Surely there’s more! And in fact, there is more.

This is a gray shrike. [See slide number 11.] This is a proud bird of prey of Middle Eastern desert. This is a male. You can tell by the distinctive markings. Now this male flies around all spring long and gathers up bugs—kills bugs and things like this—and impales them on thorns inside of his territory. Now, why would he do such a thing? To attract a mate. The reason he has to go through all this trouble is that a little bit later in the spring, the females cruise into town, and after the weather has turned nice and warm and everything is kind of cushy, they fly around and see which guys have more stuff in their trees. They mate with the guys who have the most stuff. Now, isn’t it strange that he knows what to do? How would he know in advance—weeks in advance, before any females get there—what he must do to win a female? Well, biologists have said that the answer is instinct. How does such an instinct work? This creature is going to make a lot of choices. He might have a good period where he puts a lot of stuff in his tree, but then a rainstorm may come and knock it out of the tree. Then he might put more stuff into his tree, only to have a competitor come and try to fight him for his territory and just take it. His life is a big circus, and it lasts for weeks. How does his behavior remain orchestrated so intelligently that he continually uses the best judgment he can to get the most stuff possible into his tree? Well, you might think that nature gives him a little jolt of pleasure as a guidance system; every time he kills a bug and puts it on a thorn, he might get a little dopamine hit to remind him of the big dopamine hit to come. You might think that that’s what nature did, but that’s not actually what nature did.



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Chapter 5: Moods of Happiness What nature did was to invent an entirely different guidance system completely independent of pleasure: the moods of happiness. The moods of happiness are a guidance system that works in the following way. Suppose you are a kid and you have a piñata, and you and your brother and sister are playing Hide the Piñata. You would be blindfolded and move this way and that, and they would say, “You are getting cold,” when you move away from the piñata, and they’d say, “You are getting warm,” when you move toward it. A guidance system. This guidance system will help you move very efficiently toward your goal. Whereas without this guidance system, you would just wander around hoping that you get to the right place. This guidance system is the moods of happiness, and an associated psychological experience: moods of unhappiness. The moods of happiness involve completely different circuits in the brain. They are actually located in a different place. They involve serotonin circuitry and norepinephrine circuitry, and experiences such as pride, satisfaction, and romantic love. These are actually parts of the guidance system to tell creatures when they are on their way to very important goals. Now, suppose we did something kind of unusual with this shrike, and we put him in a cage. Suppose that in this cage we had two buttons. If he pushed one button, a little door would open, and he could fly out into the aviary and start to kill bugs and put them on thorns. If he pushed the other button, we [would] present him with a female all ready to go. Now, which button will he choose? He will choose the female. The motivational triad dictates what he will do. We know he is pursuing pleasure, trying to avoid pain, and he’s trying to conserve energy. So the conservation of energy principle determines what he is going to do, and that is what he will do. Now, let’s suppose we put him back in his cage. This time he has a different set of buttons. The first button produces a female all ready to go, but pressing the second button produces a little catheter filled with cocaine, which we stick in his head. Cocaine actually causes the dopamine release of pleasure, just like what happens with food and sexual activity. It’s an absolute mimic for that. If he hits that button, he gets the same amount of dopamine as he would get from sexual activity. Now what is he going to do? He will hit the cocaine button. Why is that? The conservation of energy principle once again. It will turn out that a typical laboratory animal given that paradigm actually dies within 10 to 12 days. If given unlimited access to that kind of chemical, even as the circuits in the nervous system are screaming that they are starving or dehydrated and in serious trouble, they will continue to hammer on that circuitry, because we have trapped the motivational system.



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Chapter 6: What Motivates Creatures We now understand what motivates creatures: the motivational triad. Pleasure seeking, pain avoidance, and energy conservation. We can track that motivational system quite effectively and make it so that this creature can actually end its life in the pursuit of pleasure. Now, suppose that before he got into serious trouble we stopped and let him recover. We fed him and let him go through the process, and then we let him go right back again to the same process. We could see to it that we could have in this gray shrike’s life more dopamine hits than any gray shrike that had ever lived. At the end, would that have been a good life? What would have been missing from that life? The up and down, the moods of happiness. If you short-‐circuit the system directly to the ultimate goal, the pleasure activation of dopamine, what you leave behind are the moods of happiness. In this country in about 1950, a young man came of age who was incredibly talented, very handsome, and fortunate. He came of age at just the right time. The movie industry, the recording industry—everything was just ready to heap adulation on one person, and Elvis was the one. By 1992, his recordings had sold billions of copies more than any other artist in history, and yet Elvis was miserable, and by the time he was middle-‐aged, he was six feet under the ground. He had been a martial arts enthusiast in his youth. He really liked to do that a lot, and liked to work out with people, but toward the end of his life, because of the pleasure trap, he had short-‐circuited himself right to pleasure instead of using the process of the moods of happiness. Chapter 7: Pleasure Trap Let’s look at how this works. We can trap the motivational triad. We can do it in animals very easily, and we don’t need to spend a lot of time and energy trying to figure out how to do it. But there’s a problem. In modern society, we work very hard to figure out how to trap each other. We now have very sophisticated mechanisms, very sophisticated products and services, [with which] we are trying to help people take a short cut to the pleasure, because that is the way we compete in the marketplace. There are actually three general processes that can cause this problem. We might call it the pleasure-‐seeking trap when we artificially stimulate dopamine production through things such as drugs and processed foods. A pain-‐avoidance trap would be where modern medicine, despite its tremendous successes and great utility, can also encourage people to use pain-‐blocking medications that actually help them toward destruction. The pleasure-‐seeking trap, the pain-‐avoidance trap, [and] the energy-‐conservation trap I just call the pleasure trap. The pleasure trap is what happens to a creature when it faces novel environmental circumstances for which it was not designed. As a result of that, it makes poor choices that can disrupt or destroy its health and happiness.



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Chapter 8: Unrefined Plant Food Consumption Now, let’s look at the biggest pleasure trap in the modern world. 1 What this is, is a schematic. [See slide number 24.] This is not a detailed scientific paper, but rather a schematic of a very important paper produced by the National Institutes of Health and the World Health Organization, published in 1999. Let me tell you what this picture shows us. We see countries and epidemiological events that have been recorded with respect to dietary excellence and diseases such as heart disease, congestive heart failure, and cancer. Those are depicted in red for each country. What is depicted in green are the amounts of all unprocessed and minimally processed plant foods. So this is an extraordinary graph. This is just about all the science anybody needs to see to understand what direction to go. We see that in countries where people consume very little whole natural food, the death rates from heart disease and cancer are extraordinarily high. They reach about 90% in Hungary. Right next to Hungary is the United States, a close second, the second-‐worst in the world with respect to these diseases. We see an amazing crisscross—as mortality rates fall from these diseases, there is an increase in the extent to which fruits and vegetables, whole grains, legumes, and starchy materials form the basis of a health-‐promoting diet. As a former statistics professor at Stanford University, I can tell you that after looking at a great deal of science, you rarely get the chance to see something this beautifully presented, this clear, this convincing. And I am not talking about 50 subjects or 100 subjects; I’m not talking about some little paper someone published for some untoward reason. We are talking about major epidemiological work involving millions of people, and when we examine it closely, we see a beautiful pattern of results telling us which way to go. Chapter 9: Whole Natural Foods It is pointing toward a diet of whole natural foods. The basis of the diet is fresh fruits and vegetables, whole grains, legumes, and starchy materials. We are now going to try to understand why this is difficult for people to embrace. Let’s look at something that should be a very important tip to a creature wandering around in an environment looking for pleasure and trying to understand what it should be going for and what it shouldn’t be going for. The caloric density of food is going to be an important variable in determining how valuable that material is for that creature’s survival. So when we consider salad, and when you actually taste salad, you might think to yourself, “It’s okay.” That salad is about 100 calories a pound, so it is not bad. But I would have to eat about 15 or 20 pounds of salad a day, and since I am not really designed that way, something that has greater caloric density will probably taste better. Consider vegetables such as corn and carrots and broccoli. These are tastier at 200 calories a pound, and you can tell the difference. As you are tasting it, you can tell the difference between a raw salad vegetable and carrots or corn. 1 Produced by the National Institutes of Health (NIH) and the World Health Organization (WHO), 1999.



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But if we move on to fruit, we find that it is very tasty and that it is about 300 calories a pound. So we can start to see that this amazing signaling device, this amazing pleasure-‐seeking compass inside of us, is actually telling us what direction to go by letting us know how much caloric density there is in food. As we get to the starches that form the basis of a health-‐promoting diet—rice and potatoes and beans—these are about 500 calories a pound. And then the most calorically dense whole natural foods in nature are nuts and seeds, at 2000 or maybe 2500 calories a pound. So now we start to see that the basis of a health-‐promoting diet is built around these sorts of foods with this degree of caloric density. Chapter 10: Popular Foods Let’s look at popular foods, because these foods form a very large percentage of the standard American diet. Consider chocolate. What is in chocolate that people like? Pure sugar. We took a whole natural food, sugar cane, and separated out all the fiber, water, mineral, and vegetable matter and what was left was this pure crystalline substance that carries 1800 calories a pound. Think about that relative to your raw salad at 100 calories a pound, or your fruit at 300 calories a pound. Sugar, the pure carbohydrate, is what the pleasure centers of the mouth are designed by nature to respond to. A pure 1800 calories a pound is going to hit that system pretty hard. Then we take fat from either milk or some other source. Pure fat is 4000 calories a pound, the most calorically dense substance there is. Chocolate, then, is pure sugar and pure fat to produce an amazingly concentrated substance all the way up at 2500 calories a pound. Let’s look at potato chips and French fries. What is in French fries that people like? What we have, we have 2 substances: fat and salt, and a little bit of potato. It is a little bit of vegetable matter dipped into the deep fryer filled with 4000-‐calorie-‐a-‐pound oil. When we eat it, it is going to be 2500 calories a pound. And people salt it on the way, so it is only a little healthier than if you stick the straw straight in the deep fryer. What about cheese? What is in cheese that people like? Fat and salt. They take trucks full of salt and they just roll right up there and pour it in those bins to make cheese, and what you have is a super-‐high-‐fat food that came from a milk product. That milk product was actually designed by nature to take a little baby cow that is about 60 pounds and turn it into a big animal of 600 pounds in about six months. So we wonder why we have all these health problems. Again, the caloric density in cheese is very high, 1700 calories a pound. Now let’s look at ice cream. What have we got in ice cream that people like? Fat and sugar. Because there is a little bit of water in it, the actual caloric density of ice cream is theoretically only 1200 calories a pound, but the truth is that the water passes through the gut very quickly. This is basically a completely concentrated food on the order of 3,000



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calories a pound. No surprise that it bangs the human pleasure center so hard. It was introduced in Paris in 1677 to rave reviews for the next 300 years. Chapter 11: The Dietary Pleasure Trap (Part I) And here is the actual American diet: 51% oil and refined carbohydrates, and 42% animal food. 7% percent is left over for fruits and vegetables, and of that, 2% (or a third) is the potatoes in potato chips and French fries. [See slide number 28.] You have a diet in America that has completely left its roots, to the point that basically 95% is things we shouldn’t be eating. The things we should be eating have become the decorations on the plate. Let’s look at why this has happened so that we can understand it. This is the pleasure trap. [See slide number 30.] Our species has now created a whole set of artificial inputs—foods—that bear no relationship to how our motivational system was designed. Let’s look at why this gets us into such trouble. This is a schematic pleasure diagram that shows how much dopamine circuits in the brain are being activated depending on what kind of substance we are interacting with, and we’re talking about people here. With a whole natural foods diet, a McDougall-‐style diet 2(discussed later), we find that people experience pleasure in what I am going to call the normal range because that was the diet for which you were designed. How much pleasure you experience in your food depends on a couple things. If you are very hungry, then the nervous system is designed by nature to activate your pleasure circuitry more; the degree of activation depends on how important the survival problem is. So, of course, the hungrier you are, the more pleasure you get from the same food, all other things being equal. Another variable is the caloric density of the food. A salad might be nice at 100 calories a pound, but fruit at 300 is a little better, and if you are very hungry things like beans and rice at 500 calories a pound provide a robust meal that really starts to activate the pleasure centers. So both caloric density and how hungry you are interact to determine how much you enjoy your food. Now, when we introduce foods that were not designed by nature, we find the following: we are designed by nature to get more concentrated foods. Those are our instincts, the signals that evolved to save our lives in an environment of scarcity. When we introduce foods that are not consistent with our natural history, and we move away from whole natural foods, it enhances activation of the pleasure centers. The result is the junk food diet that people in America eat today. Chapter 12: The Dietary Pleasure Trap (Part II) Now, the problem is that if we continue to eat this way, a remarkable phenomenon occurs. Neuroscientists call this neuroadaptation—nerves adapting. Psychologists call it habituation, which simply means that you get used to it, and that’s what it really is. So, for 2 Dr. Lisle is referring to a whole food, plant-‐based diet that is low in fat.



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example, when you walk into a home during the holiday season and smell the fragrance of a Christmas tree, you have gone from a low concentration of that smell outside to a higher concentration inside, and it smells great. But after 10 or 15 minutes, you get used to it. Or if you are in a theater and you walk outside, it seems really bright at first, but then you get used to it. Or if you have some friends splashing around in a pool, you may stick your toe in the water and say, “Oh, that’s cold.” But if you jump in, you may find that 15 minutes later it seems nice. The temperature of the water didn’t change—you changed. Your nervous system changes its signaling depending on the nature of the stimulus you are giving it. This is a very difficult thing for people to grasp when they are in this motivational dilemma, which we are going to call the dietary pleasure trap. This goes in stages. Stage I is the diet we were designed to eat, and our responses to it are those that our nervous system evolved to have. In Stage 2, we introduce unnatural foods, and these are very exciting by comparison. They have a drug-‐like effect on the system. You are getting hyperactive levels of dopamine in your circuitry, and it convinces your nervous system that, in fact, it is in your best interest to pursue that food. In Stage 3, we’ve gotten used to it. [See slide number 31.] Now, if you are very lucky you have come across a book by John McDougall or Dean Ornish or Joel Furman. Even if you are fortunate enough to understand what direction to go in, you still find yourself in an extraordinary motivational dilemma. In Stage 3 of the dietary pleasure trap, what happens if you do the right thing is that as you move from a highly concentrated diet to a less concentrated diet based on whole natural foods, the sensing mechanisms in your tongue tell you that you are moving in the wrong direction. This is what makes the pleasure trap such a devastating problem. We now are starting to see the reasons we have the problem that we began this lecture with. Why is it that once we know the right thing to do, it is still difficult to do the right thing? The answer is that the pleasure trap has trapped the motivational system of human beings into a 180-‐degree spin. When you do the right thing it feels wrong, and when you do the wrong thing it feels right. Now we start to see why this is so difficult. Chapter 13: The Dietary Pleasure Trap (Part III) Now it turns out that if you stick with it for several weeks, you are going to wind up right back where you started, right where you belong. [See slide number 33.] But it is not easy. It’s not easy to do this. We need some techniques and guidance to try to recalibrate what I call an internal compass. Our internal compass is this whole motivational system—the motivational triad that helps us move in the right direction in life, toward what is, in fact, in our biological best interest. The problem is, it can be disrupted and it can take us for quite a spin. If you stick to this process through Stage 4, you will in fact recover and come to Stage 5. But it is not an easy battle. It may last 8 to 12 weeks. It is not nearly as difficult as the battle of drug addiction. In fact, what is happening with cocaine addiction, alcohol addiction, and cigarettes is exactly the same process, and the nervous system goes through exactly the



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same recovery phase. We’ve actually seen that the recovery curves for drug and alcohol addiction can be not 8 to 12 weeks, but 17 years. That is how long it can take to recover. I have not seen any more heroic fight in my work in clinical psychology than watching people caught in the pleasure trap, in an addictive cycle, fight to get their systems turned right-‐side up. This is a very difficult problem, and it’s difficult whether we are talking about food or about a chemical that shouldn’t be in the system the way it is. Chapter 14: Escaping the Trap This is a tough road, but a few things can help you move in the right direction. Let’s look at how it is that we escape the pleasure trap. Number one is knowledge. We need to know that the trap is there. We need to know that it is giving us false feedback as we go in the right direction. Even though it doesn’t seem as exciting, even though it doesn’t seem as good, we have to stick with it and get to the right direction. If we do that, we will in fact recover. Some of you are saying, “Great, but that isn’t going to get it done for me. You had better have something else.” And we do have something else. A few other things that can be useful. One thing that can be useful is to actually get yourself hungry. If you have been trying to do well and yet you have a weekend and the wheels just come off and you’re back in the dietary pleasure trap and you know that really healthy meals just aren’t going to taste good, on Monday morning don’t eat for a while. Go all the way to Monday night. What will happen is that the sensitivity of your taste receptors will increase, your motivation for eating is going to rise, and then once you have a meal that you know is healthy and that you have liked before, you increase the likelihood that you will actually enjoy that meal. So getting hungry is a very short way to try to move through this trap. Another technique is to use something like juice fasting, where you might go two or three days on juices. If you use something like carrot and apple juice, you are taking all the fat and salt out of the diet, leaving just the carbohydrate in there. In doing so you are resting those receptors and increasing their sensitivity. This can be a very useful short-‐term maneuver to help you recover on your way out of the pleasure trap. Sometimes attempting these things on our own is not enough. Sometimes we need to be locked up. I am involved in two “prison” programs. The first is at the True North Health Center, operated by Dr. Alan Goldhamer.3 4 5 At the True North Health Center, we take people on water only. People go perhaps a week or ten days on water. Let me tell you something: nothing motivates people to eat whole natural foods better than giving them a prison diet for a week—bread and water, except with no bread. The taste nerves in the

3 Goldhamer A, Lisle D, Parpia B, Anderson SV, Campbell TC. Medically supervised water-‐only fasting in the treatment of hypertension. J Manipulative Physiol Ther. 2001 Jun;24(5):335-‐9. 4 Goldhamer AC, Lisle DJ, Sultana P, Anderson SV, Parpia B, Hughes B, Campbell TC. Medically supervised water-‐only fasting in the treatment of borderline hypertension. J Altern Complement Med. 2002 Oct;8(5):643-‐50. 5 McCarty MF. A preliminary fast may potentiate response to a subsequent low-‐salt, low-‐fat vegan diet in the management of hypertension -‐ fasting as a strategy for breaking metabolic vicious cycles. Med Hypotheses. 2003 May;60(5):624-‐33.



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tongue recover very quickly, and people will really enjoy that food. A woman recently told me that after about three or four days she was dreaming about carrots. I like the True North Health Program. It is a little bit uncivilized, but it gets the job done. But it is not my favorite program. My favorite program is run by Dr. John McDougall, the internist who has been a trailblazer in helping us understand what direction to go. He is a master of explaining the details in a way that we can understand. The McDougall program is a terrific experience. People experience ten days of really good, healthy food, and they get a great educational experience. We need to recover our way. We need to understand why we have lost our way. This is a very difficult problem that we have in the modern environment. It isn’t just that some of us are obsessed with talking about healthy food; no, this is, in fact, the biggest problem people face in terms of undermining their health and happiness. This is a big claim—that both health and happiness are affected, but I can support it with Duke University surveys going back five decades. They tell us that the most important predictor of happiness in life is our health. When the pleasure trap is disintegrating the natural relationship between the pursuit of pleasure and the moods of happiness, when that is undermined so that we do things that harm our health, we wind up undermining our happiness as well. The dietary pleasure trap is the biggest problem that most of us face in a modern environment, the one that most threatens our individual and collective well-‐being. Programs like this, where we get together with like-‐minded folks who are trying to head in the right direction, can be a terrific source of support. But I have to tell you this is a difficult journey, one that each of us must walk alone. It is likely to be the most difficult and yet ultimately the most rewarding path to choose. Thank you very much.

TCC502: Heart Disease


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Heart Disease



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Chapter 1: Introduction My name is Dr. Caldwell B. Esselstyn, Jr., and I am absolutely delighted to be with you today. As you will see as this lecture proceeds, my interest since 1985 has been to prevent and reverse cardiovascular disease, the number-‐one killer of women and men in all of Western civilization. But let us go on to the rest of this story. While I was at the Cleveland Clinic at the top of my career in thyroid surgery, parathyroid surgery, and breast surgery, along came this other interest. Chapter 2: Prevent and Reverse Heart Disease It was around the late 1970s and early 1980s that I began to get a little disillusioned with what I was doing in surgery. Not that I wasn’t perfectly delighted to orchestrate resolution of a problem that had to be resolved surgically. But no matter how many of these breast operations I was doing, I wasn’t doing one single thing for the next victim. That is what really sparked my drive in searching the world literature and finding that in other cultures, breast cancer was very infrequently seen. For instance, it was 20 times less frequently seen in Kenya than in the United States.1 In the 1950s in rural Japan, breast cancer was practically unheard of, but by the time Japanese women migrated to the United States, by the second and third generation, they had the same rate of breast cancers as their Caucasian counterparts.2 Many other diseases had a similar echo, but I had the feeling that if I tried to do a study of nutrition and cancer, my bones would be dust long before I got some results. I think in retrospect that that was probably incorrect, but I decided therefore at that time to tackle cardiovascular disease, which was benign, but still it was the leading killer of women and men in Western civilization. Back there in 1981, 1982, 1983, even before I think I met John, I had stumbled upon the McDougall plan, which was to me very exciting, very inspirational reading, and I think it threw down some hard guidelines that really helped in my ultimate decision to really focus on heart disease. My dream was, quite simply: if we can show that heart disease is nothing more than merely a toothless paper tiger that need never, ever exist—and if it does exist it need never, ever progress—if people would start eating to save their hearts, then the rest of this common chronic killing disease disappears. So it was very exciting, and that was the dream that many of us today, who still have our shoulders to the wheel in this area, still feel very strongly about. Chapter 3: Absence of Coronary Artery Disease Let’s just do a little background quickly. Even today, as much as we are trying to destroy the rest of the world with our American way of eating, even today there are nations that seem to have escaped. For instance, we see it in rural China, and among the Papua Highlanders, the people of central Africa, and the Tarahumara Indians in northern Mexico.

1 Government Accountability Office. 2 Lewis H. Kuller, et al., Archives of Internal Medicine, January 9, 2006: “10-‐year Follow-‐up of Subclinical Cardiovascular Disease and Risk of Coronary Heart Disease in the Cardiovascular Health Study.”



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If you are a heart surgeon and you go to these places to earn a living, forget it. You are going to have to sell pencils. It is just not there. There are some basics that we know, for instance. If you look carefully at our children, by age 12 they have internal medial thickening of their carotid artery to the brain.3 Now have you heard about giving statin drugs to children? Then all that old business we heard three, four, or five years ago about putting statins in the drinking water is suddenly beginning to almost seem realistic. How powerful are the drug companies going to be? So if you are giving statins to children and they already have thickening of their carotid arteries, what happens to them six or eight years later? We know from autopsies of Korean and Vietnam War soldiers that 80% of our GIs who are age 20 already have gross evidence of coronary artery disease.4 5 If you don’t like that study, we have a more recent one. Some people will say it was the war that made the disease come on so suddenly. All right, let’s look at the civilians. We look at today’s study, “The Pathobiologic Determinance of Atherosclerosis in the Young,” and what do we see? In those who died of accidents, homicides, and suicides between the ages of 16 and 34, the disease is ubiquitous. Even in a 16-‐year-‐old woman now you see the early signs of the disease. So maybe we are doing something wrong, because these other nations don’t ever seem to have this problem. Now, last spring in a conference in Los Angeles that I was moderating, I asked Lew Kuller to be on the panel because he had done a wonderful ten-‐year cardiovascular health study. He is from the University of Pittsburg School of Public Health, where he is a professor. Lew Kuller said at that panel, “All males who are 65 and all females who are 70 who have been exposed to the traditional Western diet have cardiovascular disease and should be treated as such.” Now that is pretty powerful. We were saying that this is the case in our children and our young GIs and it is not a great surprise that everybody now has it when they are in their 60s and 70s. They may not have had their stroke yet. They may not have had their heart attack yet. The other gifts of cardiovascular disease, if you don’t have a heart attack or stroke, are dementia and frailty. We will talk about frailty a little bit, and hypertension. It is interesting that in the Framingham Study, if you took a thousand participants in the Framingham Study who at age 50 were measured and found to have normal blood pressure—when you look at that same group at 70, 20 years later, 90% have hypertension.6 7 Not a good track record. 3 Berenson G, Srinivasan S, Bau W, Newman WP, Tracy RE, Wattingney WA. Association between multiple cardiovascular risk factors and atherosclerosis in children and young adults. N Engl J Med 1998;338:1650-‐1656. 4 Enos, WF, Holmes RH, Beyer J. Coronary disease among United States soldiers killed in action in Korea. JAMA 1953;152:1090-‐1093. 5 McNamara JJ, Molot MA, Stremple JF, Cutting RT. Coronary artery disease in combat casualties in Vietnam. JAMA 1971;216:1185-‐1187. 6 Castelli W. Take this letter to your doctor. Prevention 1996;48:61-‐64. 7 Castelli, W., Doyle, J, Gordon,T. et al. “HDL Cholesterol and Other Lipids in Coronary Heart Disease.” Circulation. (May, 1977).



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Chapter 4: Plant-‐Based Nutrition Here is where we as a profession totally blew it, just totally blew it. [See slide number 17.] One of the great public health experiments of all time occurred in World War II. Recall when the Axis powers of Germany took over the low countries of Holland and Belgium, and occupied Denmark and Norway. Characteristically, their troops took away their livestock—their cattle, their sheep, their goats, their pigs, their chickens. These populations were now subsisting on plant-‐based nutrition, and lo and behold, what do you think happened? Let’s look at Norway and the deaths from heart attack and stroke. 8 If we look here at 1927, 1930, and 1935, they are going up and up and up. In 1939, here they come—the Germans, the greatest public health officers that Norway has ever seen. Suddenly, in 1940, 1941, 1942, 1943—if the Germans had stayed any longer they would have totally obliterated all the cardiovascular disease in Norway. When have we ever seen a population with this degree of plummeting of disease because of a statin? When have we ever seen this plummeting of disease in a population when there has been angioplasty or stents or coronary artery bypass surgery? No, the most powerful thing of all that ever happened in the Westernized nation was when suddenly, perhaps not with their own blessing, they went plant-‐based, and profound things occurred. Look what happened in 1945. Cessation of hostilities, bingo, we are going back up. It is so powerful that Neil Picard, a pathologist in Belgium, was telling his students at the autopsy table, “See this plaque in these coronary arteries, we didn’t see this during the war years. They weren’t there.” Very powerful stuff. [See slide number 18.] Now, obviously you are going to say that on the left that’s kind of normal, and you are right; and you are going to say on the right it is kind of bad. When you have a coronary angiogram, and the interventional cardiologist sees this 90% blockage, here is what is going to come out of his mouth—it is almost a guarantee: “You are a walking time bomb.” But nothing is probably further from the truth, because in actual fact, this plaque has been around a long, long time. It is not a young juvenile plaque filled with mostly fat and cholesterol that is so much at risk for rupture. This is a stable plaque, which is very unlikely to rupture. As a matter of fact, what often happens here with the slow chronic onset, these patients are very likely to have angina and are very likely to have developed little vascular threads that run around outside of the artery feeding this downstream heart muscle. We call these collaterals, and the collaterals, of course, are never going to equal something like this [normal artery], but they can be enough that when the artery finally blocks off, the patient will not have had a heart attack. Maybe the angina will have gotten a lot worse or they often will have 100% blockage with absolutely no damage to the downstream heart muscle. No heart attack. 8 Strom A, Jensen RA. Mortality from circulatory diseases in Norway 1940–1945. Lancet 1951;1:126–129. http://jama.ama-‐assn.org/cgi/content/full/295/17/2018



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On the other hand, if you can say that 10% of heart attacks occur this way, where do the other 90% occur? The 90% are with these young small juvenile plaques that are occupying no more than 10, 30, 40, 50% of the lumen of the artery. What seems to occur is that as you eat this typical American diet, very, very hazardous things happen to these plaques. [See slide number 19.] When you start eating this fat diet, the first thing that occurs is that things begin to get sticky. The cellular elements of your blood flow become very sticky. Your white cells get sticky. Your platelets responsible for clotting get sticky. Your endothelial cells are sticky; even your LDL particles, your bad cholesterol, get to be sticky. When that stickiness develops, a nasty, nasty cascade of events begins to [occur]. I am going to take some time on this because in my opinion the next three or four slides are where I really try to do what I call throw in the hook, grasp somebody. Because I think when people understand these next four or five slides they are never going to want to eat the American way. Chapter 5: Birth of a Plaque Let’s just do this, let’s sort of start here from the left and work our way slowly across to the right. [See slide number 20.] Let’s say now everything has gotten sticky. As you look here, the blood is supposed to be flowing through there (this drawing is from Peter Libby of Harvard), and the blood is flowing up here, and here is the arterial wall, and the muscle is here. These are the endothelial cells, these little purple single-‐layer endothelial cells. When you are young and healthy and everything is fine, it is estimated that if you spread out your endothelial cells one layer thick, you will cover six to eight tennis courts. If you were to gather them all together, you would have something as large as your liver. It is the largest endocrine organ in the body. Now, with these endothelial cells and everything getting sticky, we start over here and we have this bad LDL cholesterol (this is what we call the fluffy, puffy LDL cholesterol), which migrates and crosses into the subendothelial space, and you see it here. Now, sadly, what happens once it is in this subendothelial space is that it is oxidized by free radicals. Now, what is oxidation? Let’s get that term cleared up. If you take a bite out of an apple and now you put it down and have two minutes of conversation and then you go back to take another bite, what happened to that apple? It got brown on you, it got oxidized. What causes the oxidizing? These free radicals. Free radicals are molecules that are really sort of unstable. They either have an extra electron or they lack an electron, and being unstable they are very potent oxidizers. Where do they come from? Well, they come from eating the oil, the dairy, the meat, etc. It is so characteristic of this American diet, and once this bad cholesterol is oxidized, it goes from orange to yellow. Now it is the small, hard, dense molecule that is really a rascal, but the body recognizes how lethal this is and so it calls upon the SWAT team, which happens to be the white cells, which, of course, are blue. Now the white cells also go across into the subendothelial space, where they become like a Pac-‐Man. It starts gobbling up this bad oxidized LDL molecule, and as we follow it across, look what we finally get over here. We get a white cell that is so filled up with bad cholesterol that we do what we often do in medicine to confuse people so



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that we don’t understand what we are talking about: we change the name. We don’t call it just the white cell that is gobbling up bad cholesterol; we now call it a foam cell. Now the foam cell is really the Darth Vader of this whole sequence, because this foam cell elaborates these nasty, nasty chemical substances that we call metalloproteinases—bear with me—stromelysin, elastase, collagenase, myeloperioxidase. These rascals, these bad metalloproteinases, selectively begin to erode this cap over the plaque, and it erodes it and erodes it, often selectively in the upstream border of the plaque where the shoulder of the plaque meets the vessel wall. When that cap gets to be as thin as a cobweb and we have this sheer force of blood racing over that cobweb, it tears. When it tears, we have the extravasation, or shall we say, the oozing out of plaque content into the flowing blood, where it activates our clotting factor platelets. It is highly thrombogenic, meaning it is likely to cause a clot, and lo and behold we now go to B. The clot is formed. We try to mend and repair this tear, but the clot is in and of itself self-‐propagating, and so in a matter of minutes we can go from here to here. There is no time, obviously, for collaterals to develop, which would take months. Suddenly the entire vessel is blocked, and all the downstream heart muscle is immediately deprived of oxygen and nutrients, and that sadly is the case that John McDougall wrote up so beautifully.9 10 This man clearly ruptured his plaque, and at autopsy it showed that he had many of these. These are never treated with bypasses or angioplasty because the patient can have literally hundreds of these. But by the same token, the very fact that you see this cascade and how terrible it is tells us the answer. It gives us the absolute positive clue about what you can do to never have a heart attack. Why, this disease is nothing more than a toothless paper tiger that need never exist, and if it does exist it need never progress. We want you to know what you can do so that you never rupture your plaque. You strengthen this cap over the plaque, and it interrupts the whole cascade of events. Chapter 6: Endothelial Cells One of the great breakthroughs in our understanding of endothelial cells has a very interesting history. In 1980, Dr. Furad began to identify the fact that the endothelial cells were not just lovely little cells that were sort of an inside barrier to these pipes that we call blood vessels. In actual fact, the endothelial cell is a metabolic dynamo, changing minute by minute, and when they first began to see that the endothelial cell was manufacturing something that was allowing the vessel to dilate, nobody knew what it was. So we in medicine, as usual, chose a word that was very easy for everybody to remember: the EDRF factor, the endothelial derived relaxation factor. Fortunately, that term only lasted six years because other great scientists went to work and discovered that that was in actual fact a gas: nitric oxide. Your endothelial cells, your healthy endothelial cells, are making a gas that is only there for milliseconds, but that is absolutely the key to the health of your vessels.

9 A Posthumous Interview by Tim Russert, Former Host of Meet the Press. McDougall newsletter, volume 7, June 2008. Accessed online 4/12 at http://www.drmcdougall.com/misc/2008nl/jun/russert.htm 10 Commentary on My Posthumous Interview with Tim Russert. McDougall newsletter, volume 7, July 2008. Accessed online 4/12 at http://www.drmcdougall.com/misc/2008nl/jul/080700.pdf



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What jobs does nitric oxide do? The most important is that it dilates the vessel. When you run upstairs, the coronary arteries dilate, the arteries in your legs will dilate. At the same time, it keeps things from getting sticky. If you’ve got plenty of nitric oxide, then you don’t start this whole process because it doesn’t get sticky. You’ve got plenty of nitric oxide if you are eating correctly. You don’t have the free radicals. If you’ve got plenty of nitric oxide, nitric oxide will absolutely destroy and kill Darth Vader, the foam cell. Well now, you are saying to yourself, I’ve got this great system, this great nitric oxide system; why should I ever have to have a heart attack in the first place? Well, maybe you do something that injures the system. So we have to look at that, and some very interesting science. Robert Vogel from the University of Maryland and his team did some very interesting experiments to help us understand how we injure the endothelial cells.11 They did something called the brachial artery tourniquet test, where you place an ultrasound probe over the brachial artery and get a nice measurement. Then for five minutes you have a blood pressure cuff encircling your upper arm and it is elevated above systolic blood pressure, so for five minutes you have zero blood flow to your lower arm. Then you release the cuff and you remeasure the diameter of the brachial artery and it will have gone “whoop” in response to that period of occlusion by the cuff. The nitric oxide is just pouring out. Vogel did a brilliant thing. He took these young subjects to a certain fast food restaurant. Half the group got cornflakes, and their brachial artery tourniquet test was normal. The other half had hash browns and sausage, and within 120 minutes they couldn’t dilate the blood vessel. They had so tortured, so absolutely assaulted their endothelial cells that they could not manufacture enough nitric oxide after that meal to dilate the artery. Now, in young subjects a number of hours later, it began to come back and recover, but you and I know that the next morning they are going to have scrambled eggs and bacon. At lunch they’ll have white bread with mayonnaise and cold cuts, and at suppertime they’ll have a baked potato with sour cream, vegetables in butter, a lamb chop, ranch dressing on the salad, and ice cream and cake. We just hammer and hammer and hammer away at those endothelial cells in this typical American diet. So by the time you are 12, you have carotid artery thickening. By the time you are 18 or 20, if you die in combat we find that you have coronary artery disease, and everybody has it, of course, when they are 60 and 70. Not a good plan. It doesn’t happen just with hash browns. It has been repeated with dairy products, and repeated with oil. Ever hear me say no oil? No oil! We don’t want you to injure your endothelial cells. You are doing it with oil and you are doing it with dairy, and you are doing it with anything that has a mother or a face. As John McDougall says, “All muscle, whether it paws with a hoof, flaps a wing, or wiggles a fin,

11 Brachial artery ultrasound: A noninvasive tool in the assessment of triglyceride-‐rich lipoproteins. Robert A. Vogel M.D., F.A.C.C., Clinical Cardiology Article first published online: 3 FEB 2009. DOI: 10.1002/clc.4960221407 http://onlinelibrary.wiley.com/doi/10.1002/clc.4960221407/abstract



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is made up of animal cholesterol, animal protein, and animal fat, all of which are bad for you.” So we understand how you injure the endothelial cells. Now we should go one step further, in case you really want to know, anatomically, exactly where these are located. [See slide number 25.] Chapter 7: Nitric Oxide My wife always gets annoyed with me. Ann is very patient, but she gets annoyed, saying that you are spending too much time on the biochemistry. Well, I am going to be guilty again because I think it is so important, and I am going to use a phraseology that you all will be able to grasp. First, let’s just look here, one, two, three: arginine, nitric oxide synthase, and nitric oxide. [See slide number 26.] Think of it this way: you have raw material, the factory, and the end product. Arginine your body makes, and you get it from beans. You are not ever going to be short on arginine. Nitric oxide synthase, this is a factory. This is going to work well, and for those of you who exercise it works even better, and then we get the nitric oxide. If it were only so straightforward, one, two, three, we would have no problem. However, here we have ADMA—asymmetric dimethylarginine. All of us make it. It is sort of a normal byproduct of protein metabolism. Now, the problem with ADMA is that it also wants a spot in the factory, and it seems to have a greater affinity in being more powerful for displacing arginine. So nature has given us two good ways to get rid of ADMA. You get rid of it through the urine and you get rid of it through this very, very wonderful and powerful enzyme that we call DDAH, dimethyl arginine, dimethyl amino hydrolase. What does it do? It destroys, it metabolizes away, it gets rid of ADMA. Now, as an example of how important both these pathways are, you may or may not know that people in renal failure who go on living on chronic dialysis and have lost the ability to make urine on a regular basis have a very, very high rate of vascular disease. Why? Because they have so much ADMA that is always filling up the factory, and arginine can’t get in there. They can’t make nitric oxide. Now what about the rest of us, who do have adequate and normal urinary output? How does it work with us? Well, I have said that this is a very powerful enzyme, but it is delicate. What do we do that destroys this so that our urine can’t keep up with it and we get too much ADMA? What do we do that destroys this? Every single cardiovascular risk factor destroys DDAH and makes too much ADMA. What are these risk factors? Hypertension will destroy DDAH. High cholesterol destroys DDAH. High homocystine does it. High triglycerides do it. Insulin resistance is one of the worst. This is of course in people who have diabetes. You may do wonderful things with their cholesterol, but if they are diabetic they still are destroying their DDAH; they are making so much of this and can’t get rid of it that we can’t have them make nitric oxide to protect their arteries. So if you are treating somebody who is diabetic, be sure you get them to understand and buy into the fact that they have to do everything they can to control and get rid of their diabetes to spare DDAH.



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The other thing that does it is, of course, tobacco smoke. So you can see if you take a statin, you are really not attacking all of those things at all. You are just getting one. Now, I am famous for being totally unsympathetic with physicians who tell me, “Ess, you are a little bit too strict. You are extreme; I believe in moderation.” And I say, what is moderation? One person will say, “Well, I don’t think I will have any tonight,” and another person will say, “Well, I’ll just have a little bit.” But moderation is a term that I don’t like to use here. If you were to go to the Tarahumara Indians who never have this heart disease and they are eating corn and beans and vegetables in moderation, they are perfectly happy; the Papua Highlanders are perfectly happy. The key here is that we decided to go ahead and look at what happened in the past. When you look collectively at all these statin studies, here is what you end up with—the great pills that came forward in the 1990s. 30% fewer new heart attacks, 30% fewer new heart attack deaths, 30% less need for intervention such as bypass and angioplasty.12 Well my question was, what about the other 70%? This is not cancer. What is going on here? The downside of this present approach is that we have significant mortality. Let’s say there are going to be a million angioplasties and stents in this country this year. Now, everybody probably points to the fact there is only 1% mortality. What is 1% of a million? Ten thousand, and if you do that in ten years, that is 100,000 people who have been killed by the procedure. I don’t know if that is a great record. If we lost 10,000 GIs in Iraq this year, I think there would be some sort of an outcry. It would be called carnage. Now, what about morbidity? There is a significant morbidity with these procedures. The expense is absolutely inordinate, and the sad thing is that even those who do these procedures recognize that all they are doing is a stopgap patch job, the benefits of which are going to continue to erode with the passage of time. We think that is a little bit scary. Recently, there was a great rethink. In 2006, when coated stents began to go haywire, there was big panel suggesting that we better be more cautious about it, and when you do force in a stent sometimes these clots are released downstream. These patients often have a small heart attack when this occurs. So, they wanted to get a better drug. So along came this great blockbuster. If only we could raise the HDL, they said. So they did. They got a drug, torcetrapib. It raised the HDL just out of sight, and at the same time Lipitor was taking the bottom out of the LDL. Ideal drug. Everything was going to be wonderful. But the chairman of Pfizer got a little phone call two weeks before the end of this last trial and the independent monitoring committee said, Mr. Chairman we have a problem. Really, what’s the problem? Well, in the torcetrapib group there were 81 deaths, whereas in the control group, or the placebo rather, there seemed to be only 50, so they had to scrub it. They did look at the trials that were underway with it, and even with these fantastic numbers there was absolutely zero benefit to patients who had a look before and after with coronary angiograms or ultrasounds, and the same was true of the carotid artery in British

12 “The Bypass Angioplasty Revascularization Investigation (BARI) Investigators. Comparison of coronary bypass surgery with angioplasty in patients with multivessel disease.” N Engl J Med. 335 (1996) 217-‐225.



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studies with this drug. So we had these wonderful numbers, but there was really no benefit and quite a bit of setback. Chapter 9: We Are Going to Put the Fire Out This slide I have to put up because I do poke a little fun at my friends from Harvard. [See slide number 35.] Now, I have great respect for Harvard and for Boston. Through the years, they have contributed great things to medicine. But I get the Harvard Heart Letter every month, and in the back of it there are often patient comments to the editor. This 75-‐year-‐old gentleman was asking the following question. He said, look, when I was 65 I had this coronary artery bypass, triple bypass, and I have done absolutely everything that they asked that I should do and now I am told at 75 that I have to have another bypass. The editor replied, “Dear sir, you should congratulate yourself. The best that can be hoped for in this disease is to slow the rate of progression.” I don’t think he was very excited about that answer, but I would respectfully disagree. I ask patients when I see them with their heart disease to think of it as a low-‐grade brush fire. Their house is on fire, and I have a little arrangement beforehand. I try to talk to all the patients over the phone before I see them and say, “Look, I am more than happy to try to help you, but we have to have two things that you must understand. One, we have to have the same shared vision for your disease if I am going to treat you, and that shared vision has to be that I am not interested in slowing the rate of progression of your disease. This disease is a toothless paper tiger. We have to agree that we are going to abolish this disease. The second thing I have to have from you is a request. Are you and your spouse willing to give up the following phrase, which is, “This little bit can’t hurt”? Can you imagine. When I get through four hours of counseling somebody—this happened once this summer. They were leaving, going out the door, and the husband said, “Well, two weeks from now Ruth and I have an anniversary, I guess I might do a little cheating.” I said, “Get back in here. You mean to tell me you love Ruth so much that on your anniversary you are going to celebrate and destroy a few of those last remaining endothelial cells?” Come on. Three things that I want my patients to know that I never want to hear from them. Don’t ever let any of my patients tell me they were pretty good. I never want to hear that that was all they had. What would happen if you missed a meal? Your endothelial cells will rejoice, and I don’t ever want to hear “Dr. Esselstyn, there just wasn’t time.” No, if I am treating this disease, the patient and I together have an understanding that they are not going to add one single thimbleful of gasoline to the fire. We are going to put the fire out. That has to be the goal. Chapter 10: Review of the First 12 Years So, just a little review of the first 12 years of the study when we were following it pretty intensely. [See slide numbers 37 and 38.] As you know, I have given you the background epidemiological data on this, and with these patients they were really kind of the walking dead. They had serious disease, triple-‐vessel disease. Most had either failed their first or second bypass, or failed their first or second angioplasty, or they were too sick for these



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procedures, or they had refused. The goal was to keep their total [cholesterol] under 150 and their LDL 80 or under, and this is what we wanted to avoid: No oil, no fish, fowl, meat, or dairy. No oil, no oil, no oil. Why no oil, for those who are still skeptical? There is a paper out of [Vilano Group and Research Institute, Cardiovascular Foundation of Colombia].13 Looking at olive, soybean, and palm oil intake, they have a similar acute detrimental affect on the endothelial function in healthy young subjects. Whether the olive oil was taken at room temperature, partially heated, or fully heated to frying, there was the same damage to the endothelial cells. Chapter 11: Arrest and Reversal Treatment Regimen Now, these next few slides I have purloined, with his help, from Jeff Novik, so I give Jeff full credit for that. [See slide number 41.] Now, I am a bit of a taskmaster to patients who have coronary disease. I don’t like them to have nuts, and I don’t like them to have oil. Why not these oils? You can see that olive oil, Omega-‐6 and Omega-‐3. We need Omega-‐6 and we need Omega-‐3, but something happened in the 20th century, and I don’t know quite when it occurred. I am just going to guess it might have been in the early 20s. Suddenly, everything you began to purchase had oil in it. The bread had oil in it, all spreads had oil in them, and everything that was often canned had oil in it. So suddenly we were getting far more than the Omega-‐6 we should have. The ideal ratio of Omega-‐6 and Omega-‐3 is somewhere around 1:1, 2:1, or 3:1 of Omega-‐6 to Omega-‐3, but today in the United States it is 10:1, 20:1, or 30:1. When that ratio gets so far out of whack, it really does begin to injure our vessels, produce insulin resistance and a lot of inflammation. Things that we don’t want. So when I ask people to stop the oils, immediately what we are doing is that we are greatly reducing this. You can see how much more Omega-‐6 to Omega-‐3 there is. Except for the one thing—I do like my patients to have, in the morning, ground-‐up flaxseed meal. But look at here: sunflower, 15:1 Omega-‐6 to Omega-‐3, and corn oil 79:1. This is showing how high the ratio is of the essential fatty acid 6. The essential fatty ratios of nuts and seeds, again, 4:1, 16:1, 16:1, 20:1, 37:1, filberts 88:1, more nuts, again 117:1, 300:1, 1,000:1, 1,800:1. And now saturated fat, here are the nuts. The American Heart Association doesn’t like you to have more than 8% in your diet.14 Well look at here, we have all these nuts filled with all this saturated fat, which is obviously horrible for us. [See slide number 43.][Note: All ratios in the chart are presented as 06:03 except those for flaxseed and chia seed, which are presented in the reverse (03:06).]

13 Rueda-‐Clausen CF, et al. Olive, soybean and palm oils intake have a similar acute detrimental effect over the endothelial function in healthy young subjects. Nutr Metab Cardiovasc Dis. 2007 Jan;17(1):50-‐7. 14 Jeff Novick: http://drmcdougall.com/forums/viewtopic.php?f=22&t=6796&start=0.



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Now, we want to have people have all their whole grains from their cereal, breads and pasta, legumes, lentils, vegetables, and fruit. It ended up that this is about an 11% fat diet. So my patients often were taking a little cholesterol-‐lowering medication. When we started, we didn’t have any statins, but on the other hand some of our best results recurred in patients who never took any statins. The exercise was unstructured, and I think exercise is wonderful, but I learned something from Dr. James Prochaska, who is a great psychologist from Rhode Island. When you are talking about behavioral psychology and getting patients to change, if you ask them to do four things—exercise, meditate, relax, and the most significant food change that they will ever have in their lives—chances are it is going to be difficult, and you are going to have recidivism of some of these things. I think each of us has within us just so many behavioral modification units, and therefore, since food trumps it all, if you go out and use moderation in your diet and yet you are an exercise fiend like Jim Fixx, that doesn’t spare you, doesn’t save you. Food trumps it all. I have patients with strokes who never could exercise and yet they did absolutely beautifully over 20 years. They couldn’t exercise a lick. But that is not my message—I want people to exercise, but I want them to understand that I will not punish them or be angry with them or upset if they can’t exercise or they occasionally miss times or if they have injuries to their extremities and can’t exercise. But boy if they stray on the food, I am going to be over them like a tent. The key is to have that initial interview with the patient and spouse and get them to understand this whole endothelial cascade. You can get patients to get their arms around this pathophysiology, get patients to understand the endothelial cells and how they injure them and how exciting it can be and how rapidly they can restore when they treat these kindly. When I was seeing patients originally, I didn’t know how I would get to them. They were leaving their cardiologist and coming over to a general surgeon who had this wild idea. The mantra that I decided to use with them, since I was not a trained psychologist, I used the same mantra that I did with my cancer patients. I learned this mantra years ago from Bert Dunphy, a surgeon from the West Coast who was a surgeon for whom I had great respect. Bert used to say that patients with cancer are not afraid to suffer. Patients with cancer are not afraid to die, but patients with cancer are afraid of being abandoned by their physician or by their family. The first five years I saw every patient myself every two weeks, the next five years I saw every patient myself every four weeks, and then the next three years they are on autopilot. After 10 years we were seeing them quarterly. We had group gatherings as we started. They liked the fact that my wife and I were eating the same way. Chapter 12: Monell Chemical Senses Study The Monell Chemical Senses Center15 has shown us [slide number 48] that you can get those people and cradle them through those first 12 weeks; that is when you can have them lose and down-‐regulate their receptor for fat.

15 Mattes RD. Fat preference and adherence to a reduced-fat diet. Am J Clin Nutr. 1993 Mar;57(3):373-81.



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We have receptors for cocaine, heroin, nicotine, sugar, and fat. It takes about 12 weeks to down-‐regulate the receptor for fat. Then they no longer have that craving and they are in good shape. We started with an average mean cholesterol of 237, and at five years you can see they were pretty darn good, and this was the absolute key right here—the LDL, and even at 12 years keeping it right down here where we wanted it. Don’t be upset—many of the patients who reversed their disease had HDL cholesterols under the 40 that you usually see on a standard lab handout. Now that standard lab handout, I really don’t pay any attention to that. Many, many of my patients have cholesterols under 40, which would drive the average cardiologist apoplectic. They don’t need that much HDL. If you are going to lower the cholesterol that is part of what comes down, but I will be very fussy about trying to help them get the LDL down. Now, what about angiograms? Angiograms are kind of interesting. All these angiograms that I am going to share with you have been reviewed in triplicate in the Cleveland Clinic Angiography Core Laboratory, where these two individuals do nothing all day long except review angiograms for national medical trials. [See slide number 49.] They review these, and when they give the percentage I know it is accurate because of the degree of review that they received. Now, this is as small an improvement that your eye can see in a 67-‐year-‐old pediatrician with a 10% improvement in 1987 to 1992. Now, that isn’t how long it took for that to happen. That is when we happened to do the angiogram. This is in a 58-‐year-‐old factory worker. [See slide number 50.] The circumflex vessel [is] here and you can see, I think, there is quite [a] difference here when you compare to over here. This happens to be in a 54-‐year-‐old retired security guard, where this was described as a 30% improvement. [See slide number 51.] Now this wonderful young surgeon, Joe Crowe [slide number 52], replaced me as chairman of the Breast Cancer Task Force. In 1996, at age 44 with cholesterol of 156—no family history, not hypertensive, not diabetic, not a smoker—Joe began to get chest pains, and throughout October, cardiology worked him up. Everything was fine, no problem. It came to November—first week, he finished his surgical schedule. He sat down, was writing post-‐op orders—“Shew!” Splitting headache, immediately followed by this elephant that was just sitting crushing his chest, pain in his jaw and down his arm. Joe had a heart attack. He was whipped down to the cath lab. They started his catheterization and cardiac arrest. Got him going again, finished the catheterization, another cardiac arrest. Got him going again, stabilized, up to the floors. Three days later, everything was fine and he was discharged, but he was very depressed because they found that his arteries were in pretty good shape but the entire lower third of his left anterior descending artery was so diseased he couldn’t have stents. You just can’t stack up stent after stent after stent after stent. That doesn’t work. It was too far down the artery to have a bypass. So here he was at 44, thinking that nothing could be



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done, very depressed. So Ann and I had him out to the house two weeks after his heart attack. “Joe, look, you have been eating this toxic American diet. You have the typical disease. You gotta go plant-‐based.” He said, “Ess, I’ll do it. I have no other options, but I’m not going to take any of the cholesterol-‐lowering drugs. I am just leery about them.” Hey, fine, that is your call, no problem. For the next two and a half years, Joe became the absolute personification of commitment to the plant-‐based diet. His total cholesterol went from 156 to 89. He was like a rural Chinese. His bad cholesterol went from 98 to 38, and then not five years or seven years later but 30 months after his heart attack, he had another angiogram. I knew it was coming and my office was three doors down, and on the day that he had it, I walked in at noon and said “Joe, I understand you had an angiogram this morning. Want to share with me? How did it go?” He got up from his desk, walked past me, closed the door, and put his arms around me and a couple of little tears and he said, “You know you saved me.” [See slide number 53.] Joe, wait a minute, I’m the cheerleader—whatever happened, you did it. Can you show the angiogram? So it is kind of exciting. Although I used to get a big boot out of doing surgery and having some complicated procedure come out successfully, I don’t think there is anything quite as exciting or rewarding [as] when you can shepherd somebody through this sort of coronary disease and have this kind of a result. I think that the key is to really spend the time when you are counseling these people with passion. I think it was a little tough when we started the first three or four years, we didn’t have a database, but I think now when we see patients and they can see the experience and what can happen and what they themselves can do, it is so powerful. Chapter 13: Summary, and Shift to the Brain Here we look at the summary of 12 years. [See slide number 54.] These are the dropouts. These are the patients that despite all my persuasive powers within the first 12 months, I recognized that these wonderful guys, six guys, just weren’t cutting it, and with their understanding I returned them at full time to their expert cardiologists with the understanding that I would peek in from time to time to see how they were doing. They kind of became my control group, and what did we see? Lo and behold, these six patients over the next 12 years had 13 new coronary events: increasing angina, cardiac arrhythmias, bypass, angioplasty, congestive heart failure, and a death. Now what about the other 18 during that 12 years? [See slide number 55.] Well, first we decided we’d see how many coronary events they had had before I ever saw them. In the eight years prior to seeing them while they were with their expert cardiologist, [there were] 49 coronary events in these 18 people. In the 12 years on the program, there were no further events in 17 of the patients. One sheep wandered from the flock and had increasing angina and a bypass, but now he is back with the flock. So if you don’t comply then you have the problem. Now, as we compare what we saw earlier, there is no mortality from the diet. There is no morbidity from the diet, and most



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exciting of all, the benefits continue to improve with the passage of time. I think the greatest gift that we can give patients with heart disease is the following. There is nothing that a patient who has had a heart attack fears more, as does his family, than wondering when the other shoe is about to fall. When is grandpa or my husband going to have that next heart attack? You never have to have another heart attack. You just keep eating this way and keep the numbers right, and you have made yourself heart attack-‐proof. We know this because of the database, now over 20 years. Now we shifted to the brain. We know that about 50% of Americans by age 85 have dementia.16 What, are you going to work hard all your life and have that be a reward? Not a good plan. Now we know that the normal brain is going to be uniformly dark. [See slide number 60.] The areas that are light here are the cerebral ventricles that you see here. There was a good study in 2001 by Megan [Leary] and her team.17 Megan Leary, from the West Coast, and her team had looked at MRIs of the brains of Americans, and what did they begin to see at age 50? These little white spots, which we now know are little strokes. Whether you are playing tennis, driving a car, sleeping—zappo, you get a little stoke. Not a problem. Lots of reserve in the brain, small stroke, but now you are 65 and you continue to eat this way. You find yourself saying more often than before, “Sweetheart, where did I leave the car keys?” No problem. Now you are 75 and you have continued to eat the same way, and now you might say, “Sweetheart where did I leave the car?” So you continue to eat this way and now you are 85, and you look at her and you say “Are you my sweetheart?” That doesn’t have to happen. Here is a rascal. This poor gentleman, 90 of these hits—ding, ding, ding, ding, ding, ding. Can you imagine the brain trying to send beautifully coordinated synaptic messages? Zap, hit at a scar, back up [and] try another, scar, another scar. Not a good plan. A wonderful organ, but we really ought to take care of it, and the time to do it is, of course, in middle age or much earlier. Chapter 14: Brain Debris I want to say a word about the work of Pierre Amarenco. He is a physician from Paris. He took as patients men who were most likely to have vascular disease. He had them do transesophageal echocardiography. The esophagus has such anatomical proximity to the ascending aorta that he was able to get precise pictures of whether the aortas in those Frenchmen had 1 mm of atherosclerotic debris, 1–3.9 mm of debris, or over 3.9 mm of debris. He then followed them for three years. Which group had the highest rate of stroke? Yes, the group with the greatest amount of debris, because when your heart beats, blood goes rushing into that aorta, and this loosely applied debris breaks off.

16 Skoog,I, Nilsson, Palmertz, L. et al. “A Population-‐Based Study of Dementia in 85-‐year-‐olds.” NEJofM. (Jan 21, 1993): http://www.nejm.org/doi/full/10.1056/NEJM199301213280301. 17 Leary, M. "Annual Incidence of First Silent Stroke in the U.S" Cerebrovasc Dis 2003;16(3):280-5. Accessed online 3-12 at http://www.happyhealthylonglife.com/happy_healthy_long_life/2011/07/brain_on_exercise.html



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It doesn’t go down around into your abdomen, your intestine, or your feet. The path of least resistance is right up into your head. You see this in spades, although it isn’t something that is often talked about with the patient beforehand, when surgeons have to place the Satinksy clamp on the side of that aorta to pinch up the little cuff so they can sew in the vein bypass graft. When they do that, if at the time he is clamping this aorta on the side, with the nurse up here monitoring the middle cerebral artery with an ultrasound, he says clamping, she hears “schwu,” and if it is four bypasses it is “schwu” four times. Sadly, if the patient dies and you have someone do an autopsy and look in the brain as Dr. Guy Macon did at Johns Hopkins Hospital in Baltimore, you see that debris. Which explains why these patients often have flank encephalopathy, personality changes, and inability to hold a job. When they are carefully studied with neurocognitive studies before and after surgery, 22% of the people will permanently lose over 22% of their cognition.18 Not a good reward. And what about the legs? One patient coming to my office for his heart evaluation had to stop five times crossing the skyway because he had angina in his calf. We call it claudication, you know, just to confuse the public. So I said, “Don, over you go to the vascular lab.” And this was the ankle pulse volume when I first saw him. [See slide number 62.] Forgot all about his leg, we were so focused on his heart, and about eight months later he said, “Remember, Dr. Esselstyn, I used to stop those five times coming to your office because of the ankle angina and calf pain?” Yup. “You know the last month it got to be four times, three, two, one, and I don’t stop anymore.” Okay Don, back you go to the vascular lab. As you can see, the amplitude was markedly different. So with no operative procedures in the leg, this change in diet obviously restored the circulation. Chapter 15: Finally—Endothelial Cells Now, finally, we come back to the endothelial cell. One thing I couldn’t get the cardiologists to accept was the fact that I said often patients will say that their angina is improving rapidly or they are getting rid of it within 4 to 6 to 8 weeks. “Patients will tell you anything, Ess. You can’t believe that.” Well, I believed it. So I wanted to get some science. [See slide number 63.] This was a PET, a PET rubidium dipyridamole scan, but a PET scan, nevertheless, where we label the red cell, and if the red cell got into the heart muscle here, it showed up as either yellow or orange, and we knew we were in good shape, but here, not good, very poor perfusion. So, with this 58-‐year-‐old school bus driver from Youngstown who entered first with a cholesterol of 261, I counseled him an hour after he had this, and then 10 days later his cholesterol was down to 126, and then six weeks later we got another scan and it is all back.

18 Newman, M. et al. “Longitudinal Assessment of Neurocognitive Function after Coronary-‐Artery Bypass Surgery.” NEJofM. (Feb 8 2001). http://www.nejm.org/doi/full/10.1056/NEJM200102083440601



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Does he need an angioplasty or bypass? And here was an older fellow; [slide number 64] this was a 75-‐year-‐old retired tool and die maker who had a 248 cholesterol. This whole wall of his heart was not perfusing well. I counseled him an hour afterwards and 10 days later 137—12 weeks later (takes longer when you are older), got it back. This was a 65-‐year-‐old retired barber from Sandusky. [See slide number 65.] The only thing higher than his cholesterol of 290 was his weight. He was lying beached in the Intensive Care Unit of the clinic, having failed two bypass operation operations with angina at rest. You are supposed to look like a donut in this view, and here he wasn’t even filling it out at all. I counseled him, 10 days later, my all-‐time champ, 160 points in 10 days it came down. Six weeks later got it back. Pretty exciting. Finally, we have a 58-‐year-‐old stockbroker [slide number 66] with cholesterol of 248 and close again—might be [a] donut here but not closing the loop right here. He has an area of ischemia, not good flow. I counseled him. After an hour he had this, and 10 days later 137—not six weeks later, not 12 weeks later, but 3 weeks later, he got it back. Why does that happen? Remember it’s those powerful cells lining your arteries that are going to do it. [See slide number 67.] The endothelial cells. It seems that when you profoundly lower their cholesterol, most importantly when you give them the right food and take away the wrong food and you stop punishing the endothelial cells and you nourish them, back they come in force, and now they dilate and even the diseased arteries can carry more flow. So if you recall Pascal’s law in physics, flow is related to the fourth power of the radius. So for a tiny increase in diameter, you get a huge increase in flow, and you have these people locked in. If you get rid of their angina within a few weeks, boy, are they believers. So here we go, a little bit different than we saw earlier. As you eat correctly, notice how this is going to get straightened. That is wider, it’s thicker, it’s firmer, and the plaque is getting smaller. I don’t care if you go any further than this; you are home free now. Oh, if you want to get a bonus that is wonderful too. Chapter 16: Old and Frail—A Matter of Heart Ed Underwood is from the University of Pittsburg, Dr. Tamara Harris the NIH. Together they did a thing called the 400-‐meter walk study.19 [See slide number 68.] Take patients over the age of 70, walk 20 meters out and 20 meters back ten times, 400 meters. They timed them. These were all patients over 70. Followed them for six years, and then they divided them into core groups—fastest, next fastest, next fastest, slowest. Then they compared the fastest to the slowest at the end of six years. The slowest now had the 19 Newman, A, Harris, T. Association of Long-‐distance corridor walk performance with Mortality, cardiovascular disease, mobility limitation and disability. (AKA 400 Meter Walk Study) JAMA: http://jama.ama-‐assn.org/cgi/content/full/295/17/2018.



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greatest onset of new partial disability, the greatest onset of new total disability, and the greatest difference in mortality. If you go back to those pictures that I showed you earlier of the brain, where there were all those little strokes, there is a strip at the top of our brains called the motor strip. As you begin to infarct and have little strokes in the motor strip that controls our ability to use our arms and legs, we are no longer able to use our arms and legs as freely or with as much alacrity in dispatch. And as our muscles whither and shrink and atrophy, at the same time our brain is withering and shrinking and atrophying. So frailty, where people can no longer hold their balance and they have lost all their muscle strength, appears to be a vascular disease. But there is good news with the exercise. Several institutions have now clearly shown that in the elderly, instead of having your brain shrink, your brain can grow. [See slide number 70.] The parts of the brain that grow with exercise are the hippocampus, which is responsible for memory, and the frontal lobes, which control executive thinking. But what is the exercise that does it? You can’t wash the car or plant a few flowers. The exercise that does it is at least three to four times a week at least 30 minutes really getting the heart rate up and getting a sweat. That’s really exercise. Given the present way that most Americans live, this is a rather exciting but very scary platform. It is really exciting how things suddenly change. When I was in training in surgery and when I first came to work on the staff at the Cleveland Clinic, one of the most common operations that I did was for duodenal ulcer. We did all kinds of different operations for duodenal ulcers, from taking out half of the stomach to cutting vagus nerves. Every day there were surgeons who had ulcer operations on their list, and yet, these wise guys from Australia, Warren and Matthews, said wait a minute. They were looking at these specimens and they said, you know I think we see some bacteria here in these ulcer patients. And of course, the surgeons said, nonsense, what are you talking about. No organism can live in one-‐tenth normal hydrochloric acid that we have in our stomach. Oh yes, I think we see some. So they stuck with it and stuck with it and stuck with it despite the resistance that they were encountering, and lo and behold they put a name to it. What you’re seeing here is the artist’s description of Helicobactor pylori, which cause duodenal ulcers. [See slide number 72.] There are bacteria in the stomach, and you can get rid of them in about two weeks with some antibiotics. What happened to all those operations we used to do for duodenal ulcers? Well, they are now in the history textbooks. So what happened to Warren and Matthews? Well, they do what all Australians do—they had a little good time about it all. They even did it better than most. They went over to Nobel’s country and got the Nobel Prize for making that significant contribution. Now, the Cleveland Clinic, where I hail from, has been touted 12 years in a row—and now it is actually I think 14 or 15—for being the best heart center. When it says that, though, it is talking about invasive procedures, and I am sure that if I had to have an angioplasty or a bypass I would probably want to have it done there. But that is mostly done on the second floor. What we do on the first floor in our hospital is we create the disease. I did have my blood drawn today. I don’t take any cholesterol-‐lowering medication except what Ann



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feeds me. The total was 123. The triglycerides were 32. The HDL was 40. The LDL was 77. Blood glucose was 80. So, I think it is important that if we are going to ask you to do some of these things, we really sort of have to do some of these things ourselves. There is a little epicenter of wonderful things that are happening in Wooster, Ohio. There is a little branch down there of the Cleveland Clinic, a wonderful cardiologist, endocrinologist, and family physician. They embrace this whole idea, and this is David Shewmon’s work as you can see, down here his name. [See slide number 76.] He is an endocrinologist there. I implored him to let me use his slide and give him credit. He had a patient who resisted and resisted with diabetes and finally suddenly began to eat the plant-‐based diet, and within days in the gray area that glucose was in the normal range. Pretty powerful and very exciting. This is another of his patients. [See slide number 77.] When you are in Wooster, Ohio, where he is from, you are in some serious dairy country. This dairy maiden was a little overweight. This is his patient, and you’re normal in the blue. This was her urinary calcium eating all this meat and dairy. Finally, he implored her. Would you please just give us a little try and see what we can do. She went on a plant-‐based diet and within one week, zappo, she is down in the normal range. Kind of exciting, isn’t it? I mean, just diet.

TCC502: Diet and Cancer I


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Diet and Cancer I:

Chemical Causes of Cancer



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Chapter 1: Cancer—How It Begins and How It Progresses Cancer is a disease that is often dreaded, but that need not be the case if we better understand how this disease begins and how it progresses. This is a matter of exchanging fear for the hope that arises when we have reliable knowledge. Lack of knowledge encourages fear, an emotion that seems to permeate every level of what has now become a cancer industry. In this first of a series of three lectures, we will begin by considering what many believe to be the chief cause of cancer, the chemicals that pollute our environment—especially those that arise from the harvesting, packaging, and processing of our food. Many of these cancer-‐causing chemicals—or carcinogens, as we generally call them—are those that are man-‐made; that is, they are not normally found in nature. We begin with the topic of cancer-‐causing chemicals because they have dominated the discussion of cancer for at least four to five decades. We spend large amounts of money testing chemicals for their cancer-‐causing properties, and then we spend excessive time and emotion debating how we should regulate and control them. Although much has been learned, especially about the biological and biochemical properties of cancer, there are also what I consider to be serious misunderstandings. Some we will consider here, and some in the next lectures. Chapter 2: Cancer Is Traditionally Studied in Stages I want to point out that researchers traditionally divide the development of cancer into stages, admittedly for the convenience of their own thought processes. Although the lines dividing these stages are somewhat arbitrary, each state is considered to have certain unique characteristics that help us identify events that may help us treat or even cure this disease. Although these stages have unique characteristics, they also have some common features, as we shall see. Chapter 3: The Stages of Cancer There are three stages of cancer: initiation, promotion, and progression. Initiation, as the name implies, begins the process; promotion pushes it along, and progression describes the more serious stage of cancer, as it begins to spread from its primary site into other tissue sites. We begin by considering initiation. This is the initial stage where chemicals are primarily thought to act. At least that is [what has been thought] in recent years. Chemicals capable of causing cancer, as we said before, are called carcinogens. Following consumption, and after passing into the intestinal tract, they are absorbed into the bloodstream. Because most of these chemicals are soluble in fat, they tend to seek storage in our body fat. However, the body also likes to rid itself of these chemicals. Through enzymes, mostly in the liver, it converts them to water-‐soluble metabolites, which are much more readily excreted from the body.



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Unfortunately, during this enzymatic conversion of these chemicals into water-‐soluble and of course less toxic metabolites, a small amount also may escape the process and be converted into intermediate metabolites, which are (chemically speaking) highly reactive. These intermediate products are so reactive that they can non-‐enzymatically attack crucially important molecules like DNA, RNA, and protein. Attacking DNA to form what we call covalent chemical bonds is especially troublesome, because DNA is the stuff of genes. Although the cell has a highly efficient process of repairing most of this damaged DNA within the genes, small amounts may escape repair. If the damaged DNA remains unrepaired and permanently changed for future cell generations, it is considered to be what we call a mutation. Chapter 4: Initiation and Promotion In this slide [slide number 9] we show that if the cells containing this damaged DNA divide (or replicate, as we say) into a new generation of cells before they are repaired, the damaged, mutated DNA will be retained in the genes of the new cells. These mutations are rarely if ever reversed, and thus fix the destiny of these new cells and their progeny. Some of them may give rise to cancer. This slide [slide number 10] describes how promotion begins with the replication of initiated or mutated cells into clones of these cells. These new clones will continue to multiply or replicate as the years pass, if the conditions are right. Eventually they cluster together to form so-‐called “foci” of cells that can be seen under a relatively low-‐power microscope. Promotion may be a years-‐long process. Most importantly, this stage of cancer development may be reversible under certain conditions. Chapter 5: Progression In this slide [slide number 11] we see how these early clusters or foci, or so-‐called pre-‐cancer cells, gradually grow into small and then ever-‐larger tumors, eventually to be diagnosed as cancer itself. Tumors may stay at their site of origin and remain benign and relatively harmless in many cases. Or they may begin to invade neighboring tissues, some of which may be elsewhere in the body. This property of invasiveness is called “metastasis.” The term “malignancy” describes the property of cancer cells becoming independent, aggressive, and relatively resistant to destruction. “Rugged individualism” might be a good phrase to describe this property. Chapter 6: Cancer Development Over Time Here we see a schematic summary of the three stages of cancer development. [See slide number 12.] Although these stages are arbitrarily divided in this chart, note the gradual color change, which is meant to convey that these stages also share some common features that gradually change in degree. Note also the time dimension for these stages. Initiation, at least from the perspective of a single cell, occurs within a very short period of time—



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merely the time required for the absorption of the carcinogen into the cell, where it is metabolized to a form that tightly balances the DNA, now called a DNA adduct. Promotion, in contrast, may take years from the time the initiated mutated cell first replicates itself until the time it grows into a troublesome tissue mass. One of the most important features of promotion is its reversibility, as we said before. This implies a push-‐pull kind of process that is controlled by the relative amounts and activities of so-‐called promoters and anti-‐promoters. When promoters are more active, the process goes forward toward cancer. When anti-‐promoters are more active and prominent, the process regresses. This concept cannot be overstated, because it suggests that if the identities of these promoters and anti-‐promoters are known and can be controlled, of course then the cancer process can be kept in a stable state of regression even if and when mutated cells remain in the tissue. The final stage, progression, is often considered with foreboding and is relatively short. Perhaps also a time when the process can be only prevented by harsh treatments—hopefully treatments that selectively target destruction of cancer cells without damaging normal neighboring cells. But there is essentially little or no reason to believe that the reversible process occurring during promotion does not also operate during progression, a very exciting concept indeed. Chapter 7: The Causes of Cancer This summarizes many different kinds of cancer causes, some of which are unequivocally proven and some of which are a little more speculative. [See slide number 13.] But first, I need to define what I mean by the word “cause.” Namely, I consider any factor or any condition that favors cancer development at any of its stages a cause. Chemicals and certain viruses have been shown to initiate cancer. Many of these agents also promote cancer. Family history implies the presence at birth of cells already initiated; that is, the genes have been mutated, implicating genetics as a cause of cancer. Excessive radiation either from sunlight or from radioactive substances may act both to initiate and to promote cancer. Stress is a more speculative cause, although it is widely thought to be significant. The biochemical and physiological bases of stress, of course, are very complex. Nonetheless, most researchers would agree that stress compromises in some way the very complex immune system that otherwise keeps the development of cancer under control. Stress may act during any of the three stages of cancer development. Nutritional imbalances are the most significant causes of cancer. Many nutrients consumed above or below their optimal levels have been experimentally shown to promote cancer. In contrast, returning to optimum levels of consumption of these nutrients will halt promotion and perhaps even reverse it, perhaps all the way back to (but not including) the initiation stage. Keep in mind, of course, that reversal of initiation in theory requires a back-‐mutation, a rare event. Nutritional control of cancer during its promotion stage may also act during the progression stage, although the supporting evidence is much less developed. Incidentally, nutritional control of cancer should be considered within the



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context of food, not [within the context of] supplements of individual nutrients. And of course with food, the nutritional effect depends mostly on the integrated activities of a very large number of highly active nutrient-‐like substances in food. Chapter 8: Chemical Causes of Cancer This summarizes a few of the more important points made so far. [See slide number 14.] During the past five to six decades, most people—and this includes researchers and the public alike, by the way—have assumed that cancer is caused by chemicals found in our food, water, and environment. Furthermore, researchers have assumed that these chemicals primarily act during the initiation stage—thus being considered initiators. As a result, there has long been considerable public pressure to identify which of the many environmental synthetic chemicals might, in fact, cause cancer. This very public concern and pressure led to a government-‐led research program to test these chemicals for such activity, and to regulate how much if any of these substances might be allowed in our environment. The primary regulation for testing and controlling these chemicals was a 1958 amendment added to the food and drug regulations, called the Delaney Amendment, after Congressman James Delaney of New York. Although this amendment was rescinded in 1996, its underlying presumption continues to this day. For this reason, we need to understand how the carcinogenicity of chemicals has been experimentally determined. Chapter 9: 1958 Delaney Amendment This shows the actual wording of this amendment. [See slide number 16.] The wording leaves no doubt that these chemicals should not be added to food in any amount. This necessity for their absence has been referred as zero tolerance. This begins our consideration of the limitations of this regulation, and there were many. Most importantly, the number of environmental chemicals to which we are being exposed is far higher than can reasonably be tested. Early estimates during the 1960s and 1970s, not long after the Delaney Amendment was passed, quickly demonstrated that testing a single chemical would cost a few hundred thousand dollars. Moreover, the time required to conduct these tests and evaluate the results was prohibitively long, perhaps three to four years per chemical. It thus was clear from a very practical perspective that this regulation made little or no sense. There were also other concerns that emerged, that continue to linger in the public mindset even today. Most importantly, the focus on chemicals as the main causes of cancer diverted attention away from other possible causes, especially those concerning nutrient imbalances. Also, the experimental requirements to do these chemical tests turned out to be seriously flawed. Chapter 10: Carcinogenicity Testing these chemicals in humans was clearly not allowed, so experimental animals (specifically rats and mice, for the most part) were required. The slide shows that there are several important criteria for testing chemical carcinogens. [See slide number 19.] First, multiple groups of animals—one group used as a control and three to four used as



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treatment groups—had to be included to determine whether there was a so-‐called dose-‐response relationship for chemicals shown to cause cancer. That is, when a chemical experimentally causes cancer, there should be increasing numbers of tumors with increasing doses of the chemical. As an aside, if the number of tumors observed in the treatment groups is not related to dose, then the results are seriously in doubt. Second, the results are more convincing if the observed tumors are the same type, because specific chemicals being tested usually don’t cause a variety of tumors. Third, there is a need to have enough animals per group to detect relatively small but statistically significant increases in tumor development. And fourth, the length of the study is about two years, the normal lifetime of the animals. This, of course, is considered to be equivalent to 70 years of lifetime for humans. Chapter 11: Positive Lab Animal Test This graph [slide number 20] illustrates schematically a typical tumor response where increasing chemical doses are associated with increasing tumor responses. Note that the doses chosen for study are intentionally set very high to maximize the detection—statistical detection, I should say—of a potential response. And finally, the doses also span a very wide range, perhaps two to three orders of magnitude, as shown by the logarithmic nature of the doses in this chart in the 110 and 100 scale that is being used. This schematically illustrates two serious problems with this type of testing: the experimental doses are usually far higher than the practical doses normally experienced by humans in everyday life. [See slide number 21.] Therefore, it is necessary to know: what is the so-‐called dose-‐response relationship for humans? This requires knowing how to extend the line from the high experimental doses to the much lower practical doses, an exercise called interpolation. For example, [does] the slope of the line observed at the upper doses extend in the same linear manner all the way down to the zero dose? Or does it slope downwards to indicate a dose below which no cancer might be expected? This uncertainty has led to a serious and acrimonious debate in science for many years, mostly with little consensus. Thus, regulatory authorities, politically playing it safe, so to speak, have assumed a linear line extending to zero, but others have objected, specifically when it became known that certain chemicals tested using this methodology were already present in nature. Chapter 12: How to Predict Human Response from Animal Data This is a new dimension of difficulty. In addition to the difficulty of knowing how to interpolate high dose-‐response to low dose-‐response, as we already discussed, there is the problem of knowing how to extrapolate the response from one species—for example, rodents—to another, humans. Again, this is a highly arbitrary exercise, as illustrated by the fact that even for closely related rat and mouse species, there is only a 50% correspondence. That is, of the chemicals causing cancer in rats, only about 50% are likely



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to cause cancer in mice. It is anyone’s guess what the correspondence might be when extrapolating from rodents to humans. Chapter 13: In the Interim (Post 1958) This summarizes the evolution of some of the main ideas that have occurred since the adoption of zero tolerance [through] the Delaney Amendment of 1958. [See slide number 24.] As a result of these concerns and the other difficulties mentioned earlier, the original Delaney Amendment was eventually abolished in 1996. However, keep in mind, although these regulations may have gradually changed, the focus on single chemicals as primary causes of cancer remains with us. This slide summarizes a couple of the main points that we have been making during this lecture. First, cancer development is typically considered as an ordered sequence of three stages: initiation, promotion, and progression. Secondly, chemical carcinogens mostly (but not always) have been considered as initiators. Thus, conditions that promote (for example, nutrient imbalances) have been underemphasized and even ignored as causes of cancer.

TCC502: Diet and Cancer II


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Diet and Cancer II:

Initiation versus Promotion



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Chapter 1: Cancer—Initiation Versus Promotion You will recall from the first lecture that I spent some time talking about the different stages of cancer, especially the role of chemicals and their being able sometimes to cause cancer, primarily during the so-‐called initiation stage. You will also recall that there are two additional stages: promotion and progression. I spent much of my early career investigating in experiments the effect of a particular chemical carcinogen on the development of early cancer cells—studying various factors that could affect the way that carcinogen acted—and eventually got into the second stage, called promotion. What arose from those early studies were some ideas that were really quite provocative, especially in regard to the role of nutritional imbalances and how they could affect these different stages. So this lecture focuses on a specific question: Are nutritional imbalances important in the cancer process? The question we raised in my research group was: Is there a difference in nutrition’s effect on initiation as opposed to promotion, for example? So I want to spend this lecture talking about a comparison of the features of initiation and the features of promotion, and particularly about the role of a particular nutrient on the activity of those two stages. Chapter 2: Cancer Development Over Time This is a repeat of the slide seen in the previous lecture, simply showing the different stages of cancer: the initiation stage, the promotion stage (which is reversible, and that is a thought to keep in mind as we go through this), and the final stage: progression. [See slide number 6.] This is somewhat repetitive of what we generally talked about in the first lecture, but showing a little bit more detail, which is important as we get into this comparison of initiation and promotion. [See slide number 7.] This is the stage of initiation showing how, when a chemical that causes cancer comes into the body, it eventually goes to cells and gets metabolized to eventually damage DNA or genes. These chemicals that can cause cancer are very toxic, and it is natural for the body to want to get rid of them. These chemicals also tend to be lipid-‐soluble—that is to say, they are more soluble in fatty tissue than in aqueous or water tissue. So when the chemical comes into the body it is metabolized by a very complex enzyme system called the mixed function oxidase enzyme system, or MFO system. That enzyme, primarily located in the liver but also in a few other tissues, is responsible for converting the chemical to less toxic metabolites. In that process it is converting a fat-‐soluble chemical into a more water-‐soluble chemical, with additional enzyme steps, incidentally, to eventually produce metabolites that are less toxic that then can be excreted. But that enzymatic process, which we studied extensively and in considerable detail, is a very complex system. In that process it turns out that the enzyme, as it converts the carcinogen to less toxic metabolites, also produces a very small amount of an intermediate referred to as an epoxide. That epoxide only has a minute fraction of a lifetime; essentially,



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it is extremely reactive. For the chemist who may be listening to this, it is so reactive that it is electrophilic in nature—it can bind as an electrophile, it can bind to so-‐called nucleophilic substances, one of the most important being the DNA component of the gene. Once that material forms, it very quickly binds chemically to the DNA in a very tight bond called a covalent bond, to lead to what we consider a damaged gene. Chapter 3: Carcinogen Activity During Promotion This shows what eventually becomes of this so-‐called damaged DNA—we also call it a carcinogen DNA adduct. [See slide number 8.] What becomes of these damaged genetic components as they progress to the promotion stage? Most of the damaged DNA is repaired. Some estimate that in the neighborhood of 99 to maybe 99.9% of it actually gets repaired. But if this cell actually divides into daughter cells before some of the damaged DNA is repaired, then in a sense the damaged DNA gets fixated into the so-‐called daughter cells, the progeny of the parent cell. And once it is fixed into the DNA, then it is going to remain there for all subsequent generations of cells coming from that original cell. That is considered to be the process of mutation. In other words, the carcinogen comes into the cell and gets enzymatically metabolized to cause a reactor product that then binds the DNA, alters the DNA permanently to give rise to a mutation. That mutated cell or damaged cell, which is [otherwise] a clone of the original cell, eventually grows into clusters of little cells, which eventually become larger and larger and form tumors. And of course that is the process of promotion. So now the question is, since we know a little bit about initiation and something about promotion, how do they compare in terms of actually producing the ultimate1 tumor? Chapter 4: An Experimental Role for Nutrition in Cancer Development I’m simply drawing our attention to the idea that henceforth, in the remaining slides, I want to talk about some experimental results that we obtained over a number of years showing the effect of nutrition on the development of cancer. In the process we learned a great deal about the relative importance of nutrition—affecting promotion on the one hand and initiation on the other. I am basically outlining some ideas that led to this area of research. The initial observation arose in the Philippines when I was there helping to coordinate a nationwide program of feeding malnourished children. It was widely assumed in those days—and of course assumed by myself and my senior colleagues—that these children most of all needed to consume more protein, as we would be doing here in the West. They were said to be consuming very low-‐protein diets, and that was certainly true. They also were consuming protein that was not so-‐called “high-‐quality,” which is the term often used to describe animal protein.

1 By “ultimate”, Dr. Campbell is referring to an eventual tumor.



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In any case, one of our efforts in the Philippines was to make sure that these children got enough protein. However, it turned out that in a happenstance manner, I learned [that] a few children in the Philippines, a very few, were actually getting primary liver cancer at a very young age, four years of age and younger. That could have been just an anomalous observation, I guess, except for the fact that when I started inquiring about who these children were and inquiring about their families, it turned out that the families of these children were the ones who were already consuming the higher levels of protein, which we were attempting to provide to the rest of the children. And so the idea arose that somehow higher-‐protein diets like we might be consuming here in the West were more likely to create conditions in which the children were susceptible to primary liver cancer. So the remaining research then focused on the question concerning how did protein relate to primary liver cancer. Chapter 5: Dietary Protein and AFB1-‐Induced Liver Cancer Here are some interesting results published by some researchers in India on the question of higher protein intake and primary liver cancer.2 3 [See slide number 11.] Of course, the observation that higher-‐protein diets tend to promote liver cancer seemed obviously somewhat provocative and somewhat anomalous until I saw this report that came from India. In that case, the researchers were studying the effect of regular protein diets compared with low-‐protein diets on the development of liver tumors in rats. (Incidentally, the liver tumors in rats that were being observed were actually caused—or initiated, if you will—by a chemical carcinogen that was being widely studied at the time, including [through] some work in our own lab, a chemical called aflatoxin, a metabolite of a mold that grows on peanuts and corn in particular.) These researchers divided their animals into two groups: those fed regular levels of protein (that is to say, 20% of total energy), and another group fed 5%, which was considered to be an inadequate level of protein. They thought initially that feeding the animals the higher levels or the regular-‐to-‐good levels of protein would help to repress the development of liver tumors that might be caused by this chemical carcinogen. In actual fact, what they learned was that the animals given the regular levels of protein were the ones that produced the tumors, and the ones given the lower levels of protein did not. You can see in the results here that the difference between the 20% protein diets and the 5% protein diets in terms of their ability to affect tumor development was really substantial. It was essentially 100% in the case of the animals fed the regular levels of protein and only 0% in the case of the animals fed 5% protein. So this was consistent with what I thought I was seeing with the children.

2 Madhavan TV, and Gopalan C. “The effect of dietary protein on carcinogenesis of aflatoxin.” Arch. Path. 85 (1968): 133–137. 3 Confirmed by Wells et al., 1974.



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Chapter 6: Two Objectives There were two objectives that we set for ourselves in a long series of experiments that were to be continued over the next 25 to 30 years in my laboratory research, which was primarily funded by the National Institute of Health and a bit by the American Cancer Society and the American Institute for Cancer Research. The first objective was to confirm these unusual findings from the laboratory animal experiments that were conducted in India. We simply wanted to know if it was true that higher-‐protein diets promoted tumor development in animals exposed to aflatoxin. And secondly, since this observation was basically quite different from what one would otherwise expect, we wanted to learn how the protein worked. We do in science want to know how things work because understanding how they work gives us a lot more confidence in the original observations we make. Here I am showing just one sample of findings45 that we obtained over the next many years on the effect of protein on tumor development initiated by this chemical carcinogen, aflatoxin (or AF as abbreviated here). [See slide number 13.] In this slide, I am simply showing the effect of protein feeding on the development of early precancerous foci. If you recall, I talked about clusters of cells that would emerge early during promotion, which would eventually lead to tumor development. This is simply a display of results comparing the effect of 20% protein diets and 5% protein diets on the development of these early precancerous clusters—as I refer to them here, foci. Now, if we look at the dotted line as shown there over the first 12 weeks of this early tumor development, you see that in the animals fed the 20% protein diet, these early foci began to increase and continued to increase over that 12-‐week period, if in fact the animals were fed that 20% protein diet. In contrast, if we went back then and decided to switch the diet from 20% to 5% and back to 20% and back to 5% again—in other words, if we did what is called a dietary intervention study—we got some really interesting results. For the first three weeks, animals fed the 20% protein diets—those are the regular levels—would grow the foci as expected, as you can see with the dotted line. If the animals were then switched to a low-‐protein diet for three weeks, the development of those early foci were turned off. Then, for the following three weeks, going up to nine weeks, if the animals were put back on the 20% protein diet, these cells continued to grow—they were turned on again. What we learned, in effect, with this kind of study, is that we can virtually turn tumor development on and off, as expressed here by these early precancerous foci. I probably shouldn’t say tumors—they are precancerous foci indicative of tumor development. We can essentially turn on and turn off the development of these early foci over the first 12 weeks of the experiment simply by feeding them 20% protein diets or 5% protein diets. 4 Youngman LD, and Campbell TC. “High protein intake promotes the growth of preneoplastic foci in Fischer #344 rats: evidence that early remodeled foci retain the potential for future growth.” J. Nutr. 121 (1991). 5 Youngman LD, and Campbell TC. “Inhibition of aflatoxin B1-‐induced gamma-‐glutamyl transpeptidase positive (GGT+) hepatic preneoplastic foci and tumors by low protein diets: evidence that altered GGT+ foci indicate neoplastic potential.” Carcinogenesis 13 (1992): 1607–1613.



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Chapter 7: Dietary Protein-‐ and Chemical Carcinogen-‐Induced Lifetime Liver Cancer Here is an extension of what we looked at with respect to early foci development.6 [See slide number 14.] What we were looking at was the effect of protein intake or protein consumption on the development of tumors over the lifetime of the animal—not just early foci formation, but full tumor growth during that period. In this experiment, these animals were exposed to a chemical carcinogen in the beginning that could cause liver cancer, but then were fed two different levels of protein (again the 5% and the 20%) and we measured to see what kinds of tumors actually formed after 100 weeks—or about two years, which is the normal lifetime of the animals. And you can see that the animals fed the 20% protein diets had a very large amount of tumor activity. We refer to it as tumor severity, which considers both the percentage incidence—that is, the numbers of animals that actually get the tumors—and the tumor weight. The tumor severity index shows that the animals given the 20% protein diet got lots and lots of tumor activity. The animals given the 5% protein diets had almost no tumor activity. But what was really interesting about this study was that when the animals were given the 5% protein, they were all living at 100 weeks, were very thrifty, alive, well, had sleek hair coats, very energetic and active and jumping around the cages as if they were still reasonably young, with no observable tumors. In contrast, the animals fed the 20% protein diets were all dead at 100 weeks with liver tumors.7 8 This really remarkable difference was consistent with what the Indian workers had reported.9 So we achieved objective number one, showing that animals fed the regular levels of protein did indeed grow tumors far more dramatically than animals fed the lower levels of protein. Chapter 8: Effects of Protein Feeding on Viral Carcinogenesis What we just saw in the previous slide was the effect of protein feeding on the development of tumors initiated by a chemical. The next question we were able to ask in part because some research had been done in other laboratories. We wanted to ask whether the protein feeding might have an effect on the development of liver tumors initiated not by a chemical, but by a virus. So we were asking about the effect of protein feeding on viral carcinogenesis.

6 Youngman LD, and Campbell TC. “Inhibition of aflatoxin B1-‐induced gamma-‐glutamyl transpeptidase positive (GGT+) hepatic preneoplastic foci and tumors by low protein diets: evidence that altered GGT+ foci indicate neoplastic potential.” Carcinogenesis 13 (1992): 1607–1613. 7 Youngman LD, and Campbell TC. “Inhibition of aflatoxin B1-‐induced gamma-‐glutamyl transpeptidase positive (GGT+) hepatic preneoplastic foci and tumors by low protein diets: evidence that altered GGT+ foci indicate neoplastic potential.” Carcinogenesis 13 (1992): 1607–1613. 8 Youngman LD. The growth and development of aflatoxin B1-‐induced preneoplastic lesions, tu•mors, metastasis, and spontaneous tumors as they are influenced by dietary protein level, type, and intervention. Ithaca, NY: Cornell University, Ph.D. Thesis, 1990. 9 Madhavan TV, and Gopalan C. “The effect of dietary protein on carcinogenesis of aflatoxin.” Arch. Path. 85 (1968): 133–137.



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In the case of the chemical (in the previous studies), we knew that in rats aflatoxin gets metabolized, attacks genes, and initiates liver cancer. In the study on the virus, we took advantage of some work that had been done by others showing that when animals were exposed to hepatitis B virus, this virus (comprised of DNA, incidentally) was capable of inserting a portion of its DNA or its gene into the liver DNA, in this case with mice. That was a means by which the virus initiated the development of liver cancer in these animals. So, the question we wanted to ask was whether the protein feeding could affect the subsequent development of the tumors that would emerge from this hepatitis B virus initiation. Chapter 9: Protein Nutrition Predominates Over Viral-‐Induced Cancer Genes In this slide [slide number 16] we see some results—from feeding different levels of protein—on the development of liver tumors in the mice that have been exposed to the hepatitis B virus gene.10 11 Just a word by way of background on what this picture is really showing. These are four tissues—we refer to them as sections—that have been prepared from essentially a biopsy of the livers of these mice. You will see that two of these pictures have big white holes in them. Ignore that—it means nothing. It is just a cross section of a vessel passing through the tissue. I want to draw your attention to the idea that when animals are transfected with the virus—they were considered transgenic—and then fed different levels of protein, the protein had a really substantial effect on the development of these lesions. In the panel in the upper right quadrant, you can see some dark stained areas. It is the dark staining that really matters here. That is what indicates the emergence and development of tumor material in these animals. You can see a lot of it in the animals that had 20% protein. In contrast, in the panel on the lower left, from animals fed 12% protein (that is quite a bit less, just enough to satisfy development of growth and a little more), you can see that there is somewhat less tumor activity. In the animals fed 6% protein, there was essentially no staining. So this is telling us that the 20% animals really were actively growing early tumors, the 6% animals were not, and the 12% protein animals were somewhat intermediate. These three panels can be compared with the one on the upper left. This is a section of a normal liver in an animal that has not been transfected but has been fed 20% protein, and you can see that there is no tumor activity in that animal. Chapter 10: Multiple Explanatory Mechanisms In this slide [slide number 17] I summarize some of the so-‐called explanatory mechanisms that we learned about as the protein affected the development of the tumors. 10 Hu J, Cheng Z, Chisari FV, et al. “Repression of hepatitis B virus (HBV) transgene and HBV-‐induced liver injury by low protein diet.” Oncogene 15 (1997): 2795–2801. 11 Cheng Z, Hu J, King J, et al. “Inhibition of hepatocellular carcinoma development in hepatitis B virus transfected mice by low dietary casein.” Hepatology 26 (1997): 1351–1354.



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You recall that we satisfied objective number one, showing that higher-‐protein diets turned on tumor development far more than low-‐protein diets. The second question was: how does it work? This is a brief summary of some of the so-‐called mechanisms we examined. You will see that during both initiation and promotion, the level of protein affected the development of early and later tumors in a number of different ways. It was almost as if every time we looked for an explanatory mechanism we found one, and at first I found that observation somewhat frustrating and troubling because it was hard to know which one really mattered. But eventually it became quite clear that the protein was acting in such a way on both of these stages that it seemed to cause the emergence of a whole host of different kinds of mechanisms that were very likely to be highly integrated as they produced the final response. I will come back to this point a little bit later when I talk about how nutrients work as they affect the development of cancer. We were learning that the effect on promotion was apparently much greater than the effect on initiation, and we will see in the subsequent findings how that really works. Chapter 11: Experimental Protein Casein In this slide I am simply summarizing a very provocative part of our research, which arose when we asked about the kind of protein we were using in these animal studies. [See slide number 18.] Throughout these studies, we had been using casein, which represents about 87% of the protein in cow’s milk. It was really quite remarkable to realize that something so commonly consumed and so regarded as important was capable, when fed in excess of what is actually needed, of having this rather remarkable effect on tumor development. What made it more remarkable was the fact that when we tested soy protein and wheat protein, two plant proteins, also at 20% of total diet calories, we did not see tumors being developed at all. It only happened when we were using casein, an animal-‐based protein. In this slide and the next one, I want to just point out a couple more features about the way in which protein works that we need to bear in mind. In this slide [slide number 19] I am showing the effect of the percentage of dietary protein on the development of these early cancer cells.12 You can see that as we explored this relationship, when casein represented from 4 to 10% of the total dietary protein, essentially there was no effect on the development of these early foci. However, when the level of protein exceeded 10% in the diet, there was a fairly sharp dose-‐response relationship when you went from 10% to 20% protein.13 You can see these remarkable differences in the two figures of 20% and the 4-‐6% at the bottom. So what really was interesting about this particular finding was that about 10% protein was the amount required for maximizing growth rates in these young animals. In fact, they 12 Dunaif GE, and Campbell TC. “Dietary protein level and aflatoxin B1-‐induced preneoplastic hepatic lesions in the rat.” J. Nutr. 117 (1987): 1298–1302. 13 Remember that in the context of this experiment, casein represented 100% of total protein intake, and 100% of the % calories from protein in the diet. In a human context, adding animal protein to the diet easily takes the % calories from protein above 10%.



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can do with less than 10% as they become older, but in any case, 10% is the amount that is needed of this very important nutrient. It was the amount consumed in excess of the amount needed that actually caused the cancerous response. To put this in the context of human nutrition, I should point out that the amount of protein required by humans is approximately the same as by rodents. We also need about 10% protein, more or less—in fact even less, possibly. It turns out that most humans, in fact almost all humans, are consuming diets that are considerably in excess of the 10% amount we actually need. So this, if it [relates to] humans, is a very important observation. Chapter 12: Liver MFO Activity in Rats Fed 5% and 20% Dietary Protein In this slide I am showing yet another feature of this protein effect that is really quite interesting. 14 [See slide number 20.] I could show a lot of effects of protein on various and sundry activities. Here I am showing just a couple that are particularly significant. In this case, we are looking at the effect of 20% dietary protein and 5% dietary protein on the principal enzyme responsible for metabolizing that initiating chemical carcinogen, aflatoxin. That enzyme is very, very important. It has all kinds of activities, but what was really interesting is that we saw essentially a twofold difference in that enzyme activity within one day after feeding the protein meals. Other studies indicated that this enzyme activity could change very rapidly, even after a meal of consuming high or low protein. And as you can see from this presentation, it becomes very, very different over a four-‐day period, as one feeds a 20% versus a 5% protein diet. From my perspective, this is an extremely rapid response, which reflects the ability of food to alter important activities that may influence cancer development. And food can cause this effect in a very short period of time. Chapter 13: Heresy? In this slide I want to pause for a moment and summarize what we have observed so far, pointing out three observations that many would regard as virtual heresy. [See slide number 21.] They involve a very, very important protein that people think is healthy: namely, casein, but when fed at higher than the amount required, it actually promotes cancer. Second, a reasonable shift in the level of dietary protein—from 5% to 20% or 10% to 15%—is the kind of shift that people make from day to day, or that occurs among individuals. A reasonable shift in the level of dietary protein consumed turns cancer on and off even at relatively advanced stages of disease. That is a very provocative thought, if one

14 After Maso and Campbell, 1978. It was mainly published in Martha Maso's undergraduate honors thesis, but is also supported by similar studies that we did and never published. The arrow in the chart refers to the 2-‐fold difference in the enzyme activity within the first day after starting the diets. At the time, I [Dr. Campbell] thought it was remarkable that a dietary change like that could cause such a rapid change in an enzyme activity that is so critical to many reactions, including carcinogenesis.



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stops and thinks about it a bit. And finally, protein feeding as it causes these changes can act very swiftly, perhaps within hours after consuming the meal. In this slide [slide number 22] I want to draw our attention to one more observation that many would regard as heresy, but I don’t. I think we established this information very carefully and from many different perspectives. Only a part of the data is shown here. In any event, consider the traditional regulatory criteria regarding what a chemical carcinogen is and is not, according to the Delaney Amendment that we talked about in the first lecture. If we observe these traditional rules of the day, we have to conclude that casein is the most significant chemical carcinogen ever discovered. In the minds of most people, that would be absolutely heretical, but we did it very carefully and from multiple different perspectives, and published the results in the very best cancer research journals. Chapter 14: Nutrition Controls the Expression of Genes Involved in Cancer Development In this slide we see another observation that subsequently turned out to be very, very important, in my view—an observation illustrated by the studies we just talked about. [See slide number 23.] Nutrition controls the expression of genes involved in the development of cancer. In other words, if we have genes that can give rise to cancer, we can use nutrition to control the expression of these genes. This was demonstrated in the information I provided here, for genes altered by chemical carcinogens or by viruses. The effect is somewhat broad, but it brings into focus the idea that it is not necessarily the kinds of genes we have that give rise to cancer, and perhaps other diseases as well. Rather, it is nutrition and the food we consume that become important in controlling the expression of these genes. In this slide I am simply summarizing very quickly the effects of some other nutrients on other kinds of cancers that we also studied in our laboratory. In addition to the work we did, of course, other laboratories were doing research that really expanded the scope of what we were beginning to understand about the role of nutrition in the development of experimental cancer. [See slide number 24.] In our laboratory, for example, diets that were higher in fat tended to increase the development of early pancreatic cancer clusters, or lesions. We also note from larger human studies that high-‐fat diets are associated with a higher risk for pancreatic cancer. We also studied the effect of a very low intake of carotenoids, things like beta-‐carotene, for example—the colored components of vegetables. As the intake of those carotenoids—those plant-‐based anti-‐oxidants—decreased, the liver cancer increased. So that was a nutritional imbalance, in a sense, that stimulated tumor development. And finally, we also studied the effect of diets high in fat on transplanted mammary tumors. Similarly, high-‐fat diets increased the ability of these mammary tumors, once they were transplanted into animals, to take hold and to grow. Therefore this summary, together with the earlier work that I discussed, addresses this whole concept of nutritional imbalance. In some cases, it is related to inadequate intake of nutrients; in other cases it is related to an excessive intake of some nutrients, and these



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comparisons divided along plant-‐ versus animal-‐based nutrients. Animal-‐based nutrients, when fed in excess, tended to stimulate cancer. Plant-‐based nutrients, in contrast, tended to decrease tumor development, and the effects that we saw in these experimental studies were really substantial. Chapter 15: Cancer as a Function of Diet (Diet Constant) In this slide I summarize schematically what we have talked about during this lecture, especially in regards to the question I posed at the beginning: Which is more important as far as the effect of nutrition is concerned? [See slide number 25.] Is it more important during the process of promotion, or is it more important during the process of initiation? Or I could simplify the question still further: which is the more important process—promotion or initiation? In this slide I show normal cells in blue at the top. When initiated either with a high dose of carcinogen—that is, a high C—or a low dose of carcinogen, we get different amounts of cells that have been converted to cancer cells. We get more cancer cells with a high dose of carcinogen than with a low dose of carcinogen, as indicated by the red cells in that cluster. If we continue on this course—that is to say, the only difference between these two groups is the level of carcinogen being consumed or administered—all the way to the end of the study, the animals that are given the high dose of carcinogen have more initiation, more so-‐called DNA adducts, more mutagenesis, and in effect more initiation. This in turn gives rise to more clusters or foci, and eventually to more tumors. In contrast, if we look at the right-‐hand pathway, the animals given the lower levels of carcinogen have fewer DNA adducts, fewer mutations, and of course less initiation, fewer clusters, and fewer tumors. So the amount of tumors that we get at the end of the experiment is strictly a function of how much carcinogen we get exposed to. This goes back to the concept of the dose-‐response relationship between chemical carcinogens that initiate and the ultimate tumor response we see at the end. Chapter 16: Cancer as a Function of Diet (in Spite of C Dose) This slide is a follow-‐up to what we just described, except that we have done something here that really is quite remarkable. [See slide number 26.] Two groups of animals are given either a high dose of carcinogen or a low dose of carcinogen. But instead of continuing on the same diet, we took the animals that had more preneoplastic cells in the beginning because of a high dose of carcinogen and put them on a low-‐protein diet, which I call an optimum diet (shown in green). In effect, we get fewer foci and tumors. In contrast, if we take the animals that are given only a low dose of carcinogen, that produces much less initiation, but then give them a diet that is considered to be excessive—that is, high in protein—and we get more foci and more tumors.



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This only shows schematically this effect, but the results that we got were really remarkable in this regard. That is to say, the level of carcinogen that we got exposed to in the beginning or that we were using in these experiments didn’t make any difference. The dose of carcinogen made no difference if we subsequently fed diets that had different levels of protein—diets that could affect the growth of these tumors after they were present. The animals that had the highest amount of initiation were the ones that were getting few or no tumors. The animals that received the lowest level of carcinogen, when given the high-‐protein diet, in fact got more foci and more tumors. This really does show very dramatically that the effect of promotion supersedes what goes on during initiation. More particularly, it shows that simply altering diet during the promotional stage can have a dramatic effect on whether tumors grow, regardless of the carcinogen dose in the beginning. Chapter 17: Main Points In this slide I am simply summarizing the points I just made. [See slide number 27.] I need not dwell on this except to point out that these two observations, in my view, really summarize a lot of research, only a small portion of which has been shown here. It shows primarily that nutrition, especially in the form of protein intake but also in the form of intake of other nutrients, plays a very important role in the development of cancer, and the role is played primarily during promotion rather than during initiation. I should point out, however, and I didn’t show the results of that here, that high-‐protein diets actually increase initiation—increase the activation of the carcinogen, for example, and increase the formation of the DNA adducts. And so the high-‐protein diet actually increases initiation as well as promotion, but the effect of protein on promotion activity supersedes whatever may have occurred during initiation.

TCC502: Diet and Cancer III


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Diet and Cancer III:

Human Studies on Diet and Cancer



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Chapter 1: Types of Human Studies In the first two lectures, I talked about the experimental and theoretical basis of cancer. I talked about the stages of cancer that researchers like to use for studying this disease: initiation, promotion, and progression; and the biological and clinical characteristics of these three stages. I ended by talking about the evidence that we obtained in our laboratory showing the extremely important effect of nutrition on the development of experimental cancer in laboratory animals. This basic information is very important, but it means little if we are not showing its practical significance for human cancer. Thus, this presentation begins a discussion on the more practical evidence on diet and cancer when we study humans. Human studies are also referred to as epidemiology studies, which by definition are designed to determine the distribution and causes of disease in populations of people. There are three different kinds of epidemiology studies, as shown here in this chart. [See slide number 4.] The first kind of study is observational, which simply means that we observe diet and disease associations among different populations to see how they compare. Many diet and lifestyle characteristics can be measured and then recorded and compared, or correlated, with disease rates. Comparing dietary fat with breast cancer rates for different countries is an example of this type of study. It is observational because we simply observe and record how dietary fat is related to breast cancer rates under practical conditions. It is not the kind of study, though, that proves cause-‐and-‐effect associations, whether it concerns dietary fat or something else. It can, however, provide hints about what might be causes of disease. The second kind of study directly analyzes whether a specific diet or lifestyle factor actually causes disease. This is done in randomized clinical trials, which are widely used for drug development. The researcher gives an agent to one group of people and compares its effects with the effects observed in a control group not given the agent. The third group of studies is partly analytical, partly observational. There are two kinds of studies in this group. A case-‐control study simply compares the diet and lifestyle characteristics of people who have the disease with control people who do not have the disease to see which diet and lifestyle factors are associated with the disease. Cohort studies are very similar, except that subjects who are healthy at the start of the study are followed over time to see which diet and lifestyle practices, which are usually measured in advance, are associated with disease occurrence. The main message I want to convey in this slide is simply that most researchers doing these studies have a very strong tendency to discover specific causes of specific diseases. Here I show the methods used to determine how one dietary or lifestyle factor among many such factors is associated with disease. In the first method, used in observational studies—although we know that many dietary and lifestyle factors may be involved in disease occurrence—in reality, we still try to find the disease-‐producing effects of single factors as if they were acting alone. We do this by statistically adjusting or mathematically controlling for the simultaneous or confounding effects of all but the one factor we are most interested in.



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Chapter 2: Assuming Single-‐Factor Causes of Disease In the second case, we design randomized clinical trials to study the independent effects of single agents by actually directly testing them. Regardless of which type of experimental study and analytical methods we use, the underlying assumption used for most of these studies is that single diet and lifestyle factors, perhaps even acting alone, cause the disease being studied. Most investigators ignore that this is an assumption because they truly believe that single factors actually cause disease. Most of us tend to look for magic bullets and simple cures because they are easier to understand, often because this is the way to make money, as with drugs. In any case, this assumption has consequences that seriously violate the concept of nutrition, and in fact this is a major cause of confusion about diet and disease relationships. Nutrition, as we shall see, represents the highly integrated effects of countless dietary lifestyle factors acting together. Chapter 3: Breast Cancer (cases/100,000/yr) Here I am using one of the best-‐known examples, the association of dietary fat with breast cancer, to illustrate my ideas about human studies of diet and disease. [See slide number 6.] What is true in this example is often true for most other diet and disease studies as well. The late professor Ken Carroll, at the University of Western Ontario in Canada, published this information, although other researchers reported similar findings.1 Total dietary fat is shown on the X axis, rates of breast cancer on the Y axis. We see a very impressive association: the higher the fat consumption, the higher the breast cancer rates. An interesting feature of this graph is the threshold level of dietary fat. Theoretically speaking, this suggests that there is a level of fat consumption below which no breast cancer is seen. This actually is a reasonable conclusion because there is a need for a certain amount of fat to be consumed. Chapter 4: Breast Cancer (cases/100,000/yr) This is an observational study involving countless different diet and lifestyle factors2. [See slide number 7.] Thus we cannot conclude that dietary fat alone is the cause of breast cancer. Many dietary lifestyle factors also change in parallel with dietary fat, even factors such as the number of telephone poles or the amount of paved highway, both of which are unlikely to cause this cancer. Here we get a hint as to whether dietary fat is acting alone. When breast cancer rates are compared with dietary plant fat, we see no meaningful relationship.

1 Carroll KK, Braden LM, Bell JA, et al. “Fat and Cancer.” Cancer 58 (1986): 1818-‐1825. 2 Carroll KK. Experimental evidence of dietary factors and hormone-‐dependent cancers. Cancer Res. 1975 Nov;35(11 Pt. 2):3374-‐83.



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For example, Ceylon has a relatively high intake of plant fat and a low rate of breast cancer. New Zealand, on the other hand, has a low intake of plant fat and a high rate of breast cancer. Chapter 5: Breast Cancer (cases/100,000/yr) In contrast, when we compare breast cancer rates with dietary animal fat, we again see a strong relationship. [See slide number 8.] In this case, however, there is no threshold effect, as we saw for total fat3. That is, the consumption of even small amounts of animal fat is associated with increasing breast cancer rates. Thus, the question arises in this and the previous slide of whether animal fat causes breast cancer but plant fat does not. On the basis of other studies not shown here, however, this is not a reasonable assumption. Plant fat, in fact, has been shown experimentally to stimulate breast cancer development more than animal fat. It is important to know, however—and this is a very important point—that this effect of plant fat shows up only when the total fat intake becomes relatively high. This, by the way, is some of the important evidence showing that total dietary fat should be low and that added plant fat, usually oils (outside the context of whole plant-‐based food) should be minimized or even avoided. An answer to this apparent dilemma—of whether it is plant fat or animal fat that is best related to breast cancer—can be much more reliably [found when we consider] foods, not just fat. In foods, a large number of nutrients play a role, and fat intake merely describes these foods. For example, animal fat represents animal-‐based food and plant fat represents plant-‐based food. Chapter 6: Evidence that Dietary Fat Alone Is Not the Cause of Breast Cancer Several types of evidence show that dietary fat alone, either animal-‐ or plant-‐based, is not the sole cause of breast cancer. Here we show the first of three such kinds of evidence. [See slide number 9.] We know that among other nutrients, total dietary fat for different countries almost perfectly parallels dietary animal protein consumption, which parallels animal food, of course. In other words, the association of breast cancer with total dietary fat, shown here and in our earlier slide, could just as easily be described as an association with animal-‐based foods. Dietary fat consumption increases in these countries as animal protein and animal-‐based food consumption also increase.4 This is shown in the yellow inset [slide number 10] by the very high correlation—90%—between fat and animal protein—or, of course, animal-‐based foods.5 At the same time, consumption of plant-‐based foods tends to decrease as animal-‐based foods tend to increase. The original focus on total fat as the specific cause of this disease (as shown here) 3 Carroll KK. Experimental evidence of dietary factors and hormone-‐dependent cancers. Cancer Res. 1975 Nov;35 (11 Pt. 2):3374-‐83. 4 Chart based adapted from: Carroll KK. Experimental evidence of dietary factors and hormone-‐dependent cancers. Cancer Res. 1975 Nov;35 (11 Pt. 2):3374-‐83. 5 Chart adapted from: Carroll KK, Braden LM, Bell JA, et al. “Fat and cancer.” Cancer 58 (1986): 1818–1825.



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was misplaced. It should have been on increasing consumption of animal-‐based foods and decreasing consumption of plant-‐based foods. Taking this approach, we can now assume that a large number of nutrients in these foods, not just fat, combine to play a role in breast cancer development. Chapter 7: Evidence that Dietary Fat Alone Is Not the Cause of Breast Cancer The second kind of evidence shows that altering the level of fat in our diets has no effect on breast cancer development. This is evidence produced by the well-‐known Nurses’ Health Study at Harvard University.6 This study is a cohort study of about 90,000 American nurses who have been followed for about 20 years for disease associations with their dietary practices. For analytical purposes, these nurses were divided into ten groups according to the dietary fat [they were consuming]. These results show that as dietary fat increases from less than 29% of calories to more than 49% of calories, the risk of breast cancer does not change. Also, note the correlation of dietary fat with dietary animal protein. A correlation of approximately zero, which is shown in the yellow box, means the dietary fat bears no relationship to dietary animal protein. This indeed is typical of the American diet, as shown in the next slide. [See slide number 12.] Chapter 8: Nurses’ Health Study (8 years) In addition to there being no relationship between dietary fat and breast cancer in this study, it was also shown that decreased fat consumption was accompanied by increased protein consumption, the vast majority of which was animal-‐based. Increased consumption of protein, especially animal-‐based protein, would offset any benefits that might theoretically result from lower-‐fat diets. At the same time, even though dietary fat varies widely in this study with no breast cancer effect, vegetable and fruit consumption remained unchanged and [was] very low for all groups, regardless of fat intake. Researchers found other evidence supporting this tradeoff of total fat and animal based-‐foods in another very large group of American women in the Women’s Health Initiative Trial.7 For two years, these women received intensive coaching on how to specifically reduce their fat intake. They responded by decreasing their consumption of high-‐fat red meat, but in doing so increased their consumption of low-‐fat poultry and fish. This trade-‐off looks unequal but it is not, because the consumption of poultry and fish was higher than red meat at the start of the study. Exchanging red meat for poultry and fish decreases total fat without altering the already low consumption of fruits and vegetables. Thus, they retain their high overall consumption of animal-‐based foods without altering their overall consumption of fruits and vegetables. 6 Willett WC et al. Dietary fat and fiber in relation to risk of breast cancer. An 8-‐year follow-‐up. JAMA. 1992 Oct 21;268(15):2037-‐44. 7 Writing Group for the Women’s Health Initiative Investigators. “Risks and benefits of estrogen plus progestin in healthy postmenopausal women: principal results from the Women’s Health Initiative Randomized Controlled Trial.” JAMA 288 (2002): 321–333.



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Chapter 9: Women’s Health Initiative Feasibility Trial Here we show the effects of these changes on nutrient intake after two years of coaching. [See slide number 15.] In the intervention group, dietary fat decreased from 37% to 23%, but their already high dietary protein intake increased another 20%.8 Incidentally, one year after the coaching was over, dietary fat started to creep back upwards from 23% to 28%. At this juncture, we should pause to take note of the results of these two very influential but very different studies. The international study of Carroll and the Nurses’ Health Study at Harvard long presented a dilemma. The [apparent contradiction] now can be reconciled. In both cases, the hypothesis that dietary fat alone might be a major cause of breast cancer was incorrect. Rather, dietary fat was only an indicator or surrogate marker for animal-‐based foods. Chapter 10: Breast Cancer Risk Factors Keyed to Diet In addition to the first two kinds of evidence, we should note that many other diet and lifestyle factors have been found to alter breast cancer risk. [See slide number 17.] Each of the factors shown in this slide can either directly or indirectly trace their effect on breast cancer risk to the consumption of plant-‐ or animal-‐based foods. In other words, there are many ways to show that plant foods tend to decrease, while animal-‐based foods tend to increase, breast cancer risk. It is important to note, therefore, that it is the full complement of nutrients present in these foods that plays a role in breast cancer risk. It is not only dietary fat, or for that matter any other single nutrient, acting independently. An additional word on these arrows in the slide: When age at menarche, or age at first menses, increases, breast cancer risk decreases. When body weight increases, breast cancer risk increases. When meat intake increases, so does breast cancer risk. When legume and grain intakes increase, breast cancer risk decreases, and when percentage of body fat increases, so too does the risk of breast cancer. These summaries are based on a report by the World Cancer Research Fund published in 1997.9 The evidence that plant-‐based foods protect [against] and animal-‐based foods enhance breast cancer risk is now convincing. However, it also is important to know that breast cancer risk, especially for women most at risk, can only be reduced substantially when there is a substantial—perhaps even total—switch to plant-‐based foods. A summary of 144 studies showing statistically significant associations of vegetable and fruit consumption with all cancer rates was published by an expert panel in 1997 [by the World Cancer Research Fund]; all 144 studies showed a

8 Writing Group for the Women’s Health Initiative Investigators. “Risks and benefits of estrogen plus progestin in healthy postmenopausal women: principal results from the Women’s Health Initiative Randomized Controlled Trial.” JAMA 288 (2002): 321–333. 9 Expert Panel. Food, nutrition and the prevention of cancer, a global perspective. Washington, DC: American Institute for Cancer Research/World Cancer Research Fund, 1997.



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protective effect.10 It is fair, therefore, to conclude that consuming fruits and vegetables can only lead to lower cancer risk. In contrast, there are no studies showing a protective effect of animal-‐based foods on cancer risk. Chapter 11: Main Lessons from the Example of Dietary Fat and Breast Cancer Here is a summary of the main lessons to be drawn from this example of dietary fat and breast cancer. [See slide number 19.] Lesson 1 is simply that fat alone does not explain the effect of the overall diet on breast cancer risk. Lesson 2 says virtually the same for animal protein, or for that matter any other single nutrient. Overall, the lessons from this fat versus breast cancer model briefly show that increased consumption of animal-‐based foods increases breast cancer risk, while increased consumption of plant-‐based foods decreases breast cancer risk. Based on many other kinds of evidence, this can be assumed to be the same for other cancers as well. There have been many different kinds of human studies as well as many different kinds of other studies in the laboratory. In the case of human studies, every effort should be made to avoid making conclusions about the effects of single nutrients. Furthermore, these studies alone rarely, if ever, prove a cause-‐and-‐effect association. Rather, proof is much more a question of considering the total weight of all the evidence, especially when the evidence is gathered under a wide variety of conditions. Chapter 12: Establishment of Weight of Evidence When establishing the weight of the evidence, some very useful, well-‐accepted rules or criteria have been developed over the past few decades. I show some of the more important of these here [slide number 21]. An example of a strong cause-‐and-‐affect association [can be found in] the dietary fat versus breast cancer relationship that we just considered. 11 A consistent association for individual factors within the same food groups basically means that the various factors commonly present in plant foods should act in a consistent manner to help reduce disease risk. Consistent association for different kinds of studies has been illustrated here with the Carroll international study and the Nurses’ Health Study at Harvard. And biological plausibility is a very important consideration. It basically means that we understand something about how these things work. In other words, we begin to understand how it all makes sense.

10 Expert Panel. Food, nutrition and the prevention of cancer, a global perspective. Washington, DC: American Institute for Cancer Research/World Cancer Research Fund, 1997. 11 As fat increases, breast cancer risk also increases. Total fat intake is highly correlated with animal food intake, except in cases where free oil has been added to the diet in significant quantities.

TCC502: Chronic Diseases


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Chronic Diseases



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Chapter 1: Review and Introduction First let me start this lecture by summarizing some of the previous lectures, because this is an outgrowth of those lectures. As I went through my research career, I first realized that animal protein, when tested in an experimental cancer model in animals, was substantially different from plant protein in its ability to promote tumor development. It turned out also that animal protein’s effect was quite dramatic, operating through a whole constellation of mechanisms that seemed to be working together. At that point in time, I was aware that working on the effects of single nutrients on single diseases (even if they operated through multiple mechanisms) was not the whole answer. But the distinction between animal protein and plant protein certainly was a signpost, in a way, [that indicated] the kinds of foods that might be having an effect on cancer, and perhaps other diseases. But more importantly, it [raised] the question of the effect of multiple nutrients operating together, and that is when the human study in China came into view and we decided to look at dietary patterns, and to look at more than just protein—to look at the effects of nutrients or the associations of nutrients with multiple disease outcomes, and whether they tended to be associated with animal based-‐foods or plant-‐based foods. By the time we got done with that study, and with considering the effect of foods on major diseases like breast cancer, colon cancer, a few other cancers, obesity, diabetes, and the heart diseases, the evidence was really quite provocative and quite impressive—not just because of the work that I had been involved in, but because of the work that existed in the literature by so many other people. At that point in time, plant-‐based diets—and I should emphasize whole food, plant-‐based diets—really seemed to be very impressive in their effect on promoting health and preventing a whole host of different kinds of diseases, and the diseases that had been considered up to this point seemed to have a lot in common. They shared similar kinds of mechanisms at the cellular level within the body. They seemed to occur in the same kinds of populations, and some of the same nutrients that seemed to operate on one set of diseases also operated on other sets of diseases. It was then that I began to ask questions about how broad really was this plant-‐based effect. Was it just for those diseases that we had so far studied, or perhaps were there others? At that point I sat down with my son and decided to write a book, and to consider more carefully some of the other diseases that we had from time to time considered in our policy panels, but that I didn’t know a whole lot about. So, we systematically got involved in looking at the effect of diet on a range of diseases. The information was, quite frankly, explosive. It seemed that the effects of a plant-‐based diet existed not only for the diseases that I just mentioned, but also seemed to exist (operating, of course, by somewhat different mechanisms) for a wide variety of other diseases too.



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Chapter 2: Overview of Autoimmune Diseases There is one cluster of diseases that seemed to really stand out, and to be quite interesting and impressive. These were the so-‐called autoimmune diseases. Now, as their name indicates, “autoimmune” [means] something gone awry with the immune system, and the prefix “auto” refers to the fact that the immune system has been disrupted in such a way that it turns around and attacks the body itself. Now, there are a lot of people who have autoimmune diseases, and there are many diseases that are fairly well known but not necessarily [recognized] by the public to be autoimmune in nature. There are about a quarter of a million people in the United States each year who get diagnosed with one of these autoimmune diseases, and there are about 40 different kinds, at least—maybe more according, to some lists. 1 Women are somewhere in the neighborhood of 2-‐3 times as likely to get one of the diseases as men, and although these diseases tend not to kill quite like the previous diseases we talked about, they are very debilitating, very serious, and very costly in terms of not only financial dollars, but also in terms of the pleasantries of life. It is said, for example, that there are at least 8 ½, maybe 9 million people in the United States who have an autoimmune disease, and some estimates go as high as 12-‐13 million.2 That is a lot of people. Now, as I indicated, there are some 40 different kinds of autoimmune diseases. Many of them are somewhat rare, but some of them are much more common, and some of the autoimmune diseases shown in the accompanying chart are ones we have heard a lot about.3 [See slide number 10.] Rheumatoid arthritis is an autoimmune disease. Grave’s disease, or hyperthyroidism, is an autoimmune disease; so is multiple sclerosis, or as some people refer to it, MS. Type 1 diabetes, we talked about that a little bit before. It is the kind of serious diabetes that accounts for 5-‐10% of the total diabetics in the country, and it is the kind where people are not able to produce the insulin that is required for the utilization of glucose. And then there is the condition called lupus, or its more extensive name: systemic lupus erythematosus. All of these diseases and many, many more are autoimmune diseases [in which] the immune system has basically gone awry and turned on itself. Now, as far as these autoimmune diseases are concerned, there is one unique characteristic that seems to apply, at least to the ones so far studied: they tend to exist in the northern climates. They also tend to exist in the industrialized countries, and of course, in the populations that also tend to get heart disease and cancer. So we see this sort of commonality between the autoimmune diseases and the other so-‐called degenerative diseases. 1 Mackay IR. “Tolerance and immunity.” Brit. Med. Journ. 321 (2000): 93–96. 2 Jacobson DL, Gange SJ, Rose NR, et al. “Short analytical review. Epidemiology and estimated population burden of selected autoimmune diseases in the United States.” Clin. Immunol. Immunopath. 84 (1997): 223–243. 3 Ibid



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Chapter 3: A Word on the Immune System Before I talk a little bit about autoimmune disease, I should say a word about the immune system itself. Some people think, rather simplistically, that the immune system is fairly simple—like an organ, like the liver, the heart, or lung. Nothing could be further from the truth. The immune system is extraordinarily complex. It is comprised of a large variety of different kinds of cells that are produced as needed. It is comprised of a lot of different kinds of chemical products that are produced by these cells, and the system operates throughout the body. Basically what it is intended to do is respond to the presence of foreign proteins that enter our blood stream and our bodies. Foreign proteins that otherwise would do damage. So the body in a sense is defending itself against these strange proteins that come in and otherwise would be doing harm. The interesting thing about this is that the immune system, because it has such enormous flexibility and is able to respond to all kinds of foreign materials that may enter our body, basically looks at these foreign proteins as they come in. It looks at them fairly closely, and then determines how to make a product that interacts with the foreign protein. Each of the proteins, as you may recall, is unique in terms of the sequence of amino acids that comprises the polypeptide chain. That gives each of the proteins a very unique and specific characteristic, and the immune system in turn looks at that pattern of amino acids and makes a product that is essentially the mirror image of that, and so can bind to those proteins. Now, the [foreign] proteins that are entering the body are called antigens, and the products that are being produced in general by the immune system are called antibodies. So antigens are the substances that enter our bodies and cause harm, and antibodies are the substances that are produced by the immune system to counteract these antigens. Chapter 4: Diseases in Greater Detail Now there are some of these autoimmune diseases that I want to discuss, just to illustrate what we know so far about them in a broader context. Autoimmune diseases like type 1 diabetes, multiple sclerosis, and arthritis have actually been examined more carefully, I think, and in more depth than some of the others. Basically, the antigen comes from the food, gets into the blood stream, and is seen by the immune system as something to attack. It makes a very specific antibody against these proteins, and then turns around and discovers that the same sequence of amino acids in the antigen coming into the body can also be found in some of the tissues in our bodies (that are otherwise operating normally). So the antibodies that are being produced to tackle these foreign proteins in a sense turn on [the body], find exactly the same kind (or at least a portion of the same kind) of protein somewhere in our bodies, and attack it. In the case of type 1 diabetes, for example, the protein that enters the body causes the production of an antibody that finds exactly the same amino acid sequence on the cells in the pancreas that produce insulin. So the antibodies begin to attack the cells producing



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insulin and wipe out the ability of the pancreas to produce insulin. Of course, that can be a relatively permanent process. Multiple sclerosis is a condition where the nerve system—especially the central nervous system and the main nerve cord that is surrounded by a so-‐called “myelin sheath”—the autoimmune process operating there is that the antigen coming into the body essentially mimics the proteins in the myelin sheath. The body makes the antibodies to attack the proteins coming in, then turns around and discovers exactly the same amino acid sequence is present in some of the proteins that surround the myelin sheath, and destroys them. So we get a condition called demyelination. Obviously, that disrupts the nerve function and its conduction of signals, and therein actually leads to a rather serious problem that is progressive, usually. Arthritis is similar. [In the case of rheumatoid arthritis], proteins in the tissues of joints are destroyed because of the presence of antibodies that are being produced against a substance coming in from the outside. Chapter 5: Foreign Invaders and the Immune System Now, in terms of the proteins coming from the outside that I referred to as foreign invaders, it also develops that the immune system is not only able to see a protein and make an antibody against it. It should be noted that these antibodies are really quite remarkable, and the system is quite remarkable because oftentimes it will be seeing a protein that it has never seen before. Maybe something altogether new that perhaps we have even synthesized through our industrial processes. So the immune system is so flexible, so adaptable, and so creative that it can actually make antibodies against these substances, and take care of them and then in turn save (essentially, memorize) the process in the sense that if ever again those same kinds of chemicals were to come into our system, the immune system could quickly get up to speed, produce some antibodies, and take it on once again. Now, let me just illustrate a little more detail about a couple of these autoimmune diseases; namely, type 1 diabetes and multiple sclerosis [and discuss] what kinds of foods seem to be involved in or related to the incidence and production of these diseases. Chapter 6: Type I Diabetes Type 1 diabetes tends to occur in very young children, at least it first starts in infants, basically, and at first the whole story about type 1 diabetes and its relationship to food began with the observation that infants who were not breast-‐fed for a sufficient length of time—perhaps not even breast-‐fed at all—and then given foods like dairy seemed to have a higher risk for type 1 diabetes. Further research, as time went along, [showed] that it wasn’t necessarily just that they weren’t getting the native mother’s milk, but more to the point, they were being exposed to cow’s milk. Subsequently, some researchers started to take apart the cow’s milk to have a look at what might be causing this problem, and indeed they found some proteins in cow’s milk that had this unique amino acid sequence that, when entering the bloodstream of a



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new-‐born infant (especially if it wasn’t being breast-‐fed) was inducing the production of an antibody. The original discovery involved a so-‐called 17 amino acid sequence. A very specific sequence of amino acids that generated production of the antibody, and once the antibody was produced and supposedly only recognized that 17 amino acid sequence, it discovered exactly the same 17 amino acid sequence on the cells of the pancreas that was producing insulin. That set in motion a train of events that destroyed that child’s life, in the sense that it was never again able to produce insulin. One of the more remarkable reports of this cow’s milk effect was reported in 1992, not so long ago, in the New England Journal of Medicine.4 In that particular study, done in Finland, 142 diabetic children were tested to see if they might have the antibody that would have been produced only if those children had been exposed to cow’s milk early in life. They were compared against 79 normal children, so in other words we have 142 diabetic children and 79 normal children, and the test was to see if the diabetic children might have the antibody that would indicate [previous] exposure to cow’s milk, as opposed to those who didn’t. And sure enough, as the adjoining chart shows, virtually all of the children who were diabetic had the antibody that was specific for one of the cow’s milk protein fractions. [See slide number 18.] The level of those antibodies in the blood of those [diabetic] children was across-‐the-‐board higher than it was in the normal children. There was no overlap. It was really quite a remarkable study, almost clearly pointing to the idea that the diabetic children had not only been exposed to the cow’s milk early in life, but also had suffered the consequences of that protein, because that protein had been shown in more intricate studies to be able to bind to the islet cells of the pancreas that produce insulin. Okay, [it] was quite a controversial finding to suggest that cow’s milk actually could cause this very serious disease in infant children, but as time passed, not only was it provocative and somewhat controversial, but there were other studies at the same time that started to show the same thing. It turned out that the disease was a little more complex than the simple fact of cow’s milk causing type 1 diabetes. Chapter 7: More on Type I Diabetes It is now known, for example, that cow’s milk seems to operate primarily on those children who are genetically susceptible in the first place, and also on children who—perhaps this is not so well confirmed—perhaps had been exposed to a particular kind of virus. So it was the combination of genetically susceptible children being exposed to cow’s milk, and perhaps also to a certain kind of virus, that led to the production of the disease. After that there were some additional studies focusing on the risk of diabetes in these genetically susceptible children—which, in this case could be assessed at the beginning [of their lives]—and it turned out that for the children who were genetically susceptible and exposed to cow’s milk, their risk of type 1 diabetes was in the neighborhood of 11-‐13 times

4 Karjalainen J, Martin JM, Knip M, et al. A bovine albumin peptide as a possible trigger of insulin-‐dependent diabetes mellitus. N Engl J Med. 1992 Jul 30;327(5):302-‐7.



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what it would have been in children who were not genetically susceptible. An 11-‐ to 13-‐fold increased risk of type 1 diabetes is truly huge. In fact, as shown in the adjoining chart5 [slide number 20], if we compare the level of risk that cow’s milk causes type 1 diabetes with, let’s say, the risk of some other sort of cause-‐and-‐effect association we are more familiar with, it turns out that cow’s milk has a more pronounced effect on its ability to cause or at least be associated with type 1 diabetes than, for example, the relationship between smoking and lung cancer, or the relationship between the very well-‐known high blood pressure and cholesterol association with heart disease. In other words, we know well that high blood pressure and high cholesterol levels are associated with heart disease. We know well now that smoking is closely related to lung cancer, and we can determine the relative risk. But it turns out that the association of cow’s milk (in children who have the high-‐risk genes) with type 1 diabetes is even greater than is the relationship between smoking and lung cancer, according to the data that have so far been published. That is really quite remarkable. It would be nice, of course, if we wanted to be very specific and determine which infants were susceptible and which were not; perhaps we could screen out those individuals who were genetically susceptible and pay particular attention not to give them cow’s milk, but the fact of the matter is we can’t really discern that that well yet. So we really don’t know which children are likely to be susceptible to this effect of cow’s milk, but rest assured, we do know that cow’s milk seems to have this very prominent effect in causing this very serious kind of diabetes. That kind of finding would have been quite convincing for a lot of people. It certainly was very impressive, but obviously it still didn’t convince everyone, especially given the enormously impressive so-‐called good effects of cow’s milk that a lot of people presumed. So let’s look at some other kinds of studies to see what really might exist. [See slide number 22.] In the next chart6, if we look at the relationship between cow’s milk consumption and the incidence of type 1 diabetes in different countries, as was done in a study in France, we see this again this impressive relationship. That is, the higher the cow’s milk consumption, the higher the type 1 diabetes. It is really a very impressive and almost linear type of relationship, and furthermore, it turns out that although we see different levels of type 1 diabetes in different countries, it turns out that if people move from one risk area—just like the cancer, just like the heart disease—if they move from one risk area to another risk area (especially earlier in life), it turns out that their risk of getting the full-‐blown disease is somewhat attenuated if they move to an area where there is less milk being consumed. 5 Hammond-‐McKibben D, and Dosch H-‐M. “Cow’s milk, bovine serum albumin, and IDDM: can we settle the controversies?” Diabetes Care 20 (1997): 897-‐901. 6 Dahl-‐Jorgensen K, Joner G, and Hanssen KF. “Relationship between cow’s milk consumption and incidence of IDDM in childhood.” Diabetes Care 14 (1991): 1081-‐1085.



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Chapter 8: Faulty Numbers Game

Now, as far as the controversy was concerned, I really became quite interested in the nature of it, because I find that in much of the [scientific] literature—not only involved in this particular case, but in other diet and disease cases—much of the controversy that tends to erupt relates to people’s having other kinds of interests and being essentially impacted in a negative way because of information like this. Even if the industry, of course, becomes quite concerned about this, or perhaps individuals [become] concerned about this, it is a fertile ground for the development of controversies.

Having said that, in this particular case of the controversy involving type 1 diabetes and cow’s milk, if one looks at a summary of some of the studies that have been done in the last 12-‐15 years on this—and I have looked, and there have been some really major and very good summaries of multiple studies—it turns out that if one compares all of these studies [to see] which ones showed a relationship between cow’s milk consumption and type 1 diabetes and which ones did not, something happens in terms of the analysis of the data that I need to share with you. Because it is this kind of relationship, this kind of analysis, that is too often used in science that ultimately leads to confusion and controversy.

If we have, let’s say, 20 studies where we are studying the hypothesis of the relationship between cow’s milk consumption and type 1 diabetes, before we know anything else we can at the outset assume that we are going to get three kinds of answers. Either we get an increase in type 1 diabetes with an increase in cow’s milk consumption and it is statistically significant, or we get a decrease in type 1 diabetes with an increase in cow’s milk consumption. We either get an increase or a decrease, and let’s assume we are just talking about statistically significant results in both of those cases.

And then there is a third group of possible results. Namely, we don’t see anything one way or the other. It turns out that if we can look at it that way and we look at all the results of these studies and just compare the statistically significant results of diabetes going up or diabetes going down in those who have been exposed to cow’s milk, every single study that has so far been done, in effect (and there are about 20-‐some studies that have been analyzed in this way), in every single study for which there is a statistically significant result, as cow’s milk consumption goes up type 1 diabetes is statistically significantly increased, as far as risk is concerned.

Now, I think that is straightforward enough. But the problem with this whole analysis is that those who do not want to believe this and have reasons to find something wrong with these kinds of studies, what they tend to do is, they say, “Ok, let’s say of the 20 studies there are 10 of them that show a statistically significant positive effect, and then there are another 10 that show no effect.” Mind you, none of them show the inverse effect. That is, of the 10 that show the statistically significant effect in the example I am using, they were all positive. There were none that were statistically significant in the reverse direction, but there were 10 that didn’t show any effect at all, and so what they end up saying, these critics, is that 10 studies showed an effect and 10 did not; therefore, it is a washout. That is



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really incorrect, because the 10 studies that were found to be statistically significant all showed the same direction; the 10 studies that did not, did not.

So when one analyzes this information this way, it turns out that when we look at studies that showed no effect, we can find all sorts of good reasons—in fact, oftentimes in the studies themselves—why we would not have actually detected an effect that really was there in the first place. I simply point this out because a lot of studies or relationships that become somewhat confusing and controversial unfortunately have been analyzed in this way, without taking into consideration the so-‐called “null effect,” where one see no relationship at all, and in the case of type 1 diabetes and cow’s milk, that is exactly what has happened.

I also point this out because as I was becoming familiar with this literature and reading all the material and mentioning it to some colleagues, the remark I got from people who really didn’t know that much about it (but they certainly had heard something about it) was, “Oh, that has already been disproven.” It turns out that the people who were saying that were referring to a very specific paper where, in fact, [there was a] rather serious flaw. So my conclusion is, at the present time, based on this very high risk observed for genetically susceptible children, that cow’s milk certainly has an effect on causing type 1 diabetes, but it may be quite selective for certain individuals under certain conditions. So much for type 1 diabetes.

Chapter 9: Multiple Sclerosis (MS)

In the case of multiple sclerosis, which of course is another very serious autoimmune disease, we should point out that there are about 400,000 people in the United States alone who have the disease.7 That is a lot of people. 400,000 people, according to the National Multiple Sclerosis Society. Now, the word “sclerosis” stopped us for a second, so let’s think about the [term] multiple sclerosis itself. “Sclerosis,” of course, is basically the destruction of tissue; it is the loss of function of tissue, and in this particular case, it is nerve tissue. The “multiple” part of the phrase really refers to the multiple kinds of symptoms that occur as a result. People who get MS often will have all sorts of problems, and the kinds of symptoms that tend to occur in one kind of person don’t necessarily exist in exactly the same way in other kinds of people. So you get a whole variety of different kinds of outcomes in MS, and it has been considered all these years to be a sort of degrading disease that progresses over time, and eventually people with MS often end up not only immobile in wheelchairs, but actually bedridden for the later years of their lives.

One of the remarkable things about MS, however—and it is a relationship that I recall was basically pooh-‐poohed because it was often thought [to be] a quack kind of finding—was the work of a certain Dr. Roy Swank. Dr. Swank, way back in the 40s working in Norway, found that MS tended to occur in rather different levels in the different communities of Norway. For example, people living along the coast tended to have substantially less MS than people living inland. People living inland were consuming lots of dairy. People along 7 Reingold SC. “Research Directions in Multiple Sclerosis.” National Multiple Sclerosis Society, November 25,2003. Accessed at http://www.nationalmssociety.org%5Cbrochures-‐Research.asp



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the coast were consuming much less dairy, but more fish. At the same time, MS (like type 1 diabetes) tends to be very high where sunlight exposure is less, and Norway over the course of the year tended to have less constant sunlight and so [MS rates] seemed to be quite a bit higher, let’s say, than countries around the equator. But in any case, setting aside the sunlight exposure question, what Dr. Swank noticed was that the people living inland—subsisting on dairy products, to a considerable extent—had much more MS than people living along the coast.

One interpretation of that finding, of course, was that fish consumption was protective against MS, and in fact there is some evidence that fish oils in particular might have some beneficial effects in reducing the symptoms of MS. But the relationship that concerned Dr. Swank was this relationship between the consumption of foods in the inland and consumption of foods along the coast, and what he focused on at that time—and this is back in the 1940s, early 1950s—given the information he had in front of him, was the question concerning the consumption of saturated fat. Saturated fat, of course, is much higher in dairy foods, certainly, than in plant materials, and so he focused on the idea that maybe this differential in the amount of MS inland as opposed to the coast was really related to the amount of saturated fat that people were consuming. So, he embarked on a really ambitious trial that has now lasted for more than 35 years.8

In fact, Dr. Swank himself moved on from the University of Montreal, where he was when he was doing this work in Norway, to become the Director of the Department of Pathology at Oregon Medical Center in Portland, Oregon. So, Dr. Swank followed these individuals, some 144 individuals that he recruited in the study, for the next 35+ years, and published a sequence of reports as the results started to come in. Finally, in the early 1990s, he published a paper, which is the summation of the effects over all those years, and I will quote. He says: “About 95% of the patients on the low-‐fat diet during the early stages of the disease remained only mildly disabled for approximately 30 years.”9 95% remained mildly disabled, only 5% of these patients died. These are the people, of course, consuming much less fat—in this particular case, less than 20 grams of saturated fat. In contrast, 80% of the patients with early-‐stage MS who consumed a poor diet with higher saturated fat died of MS. So, over the years, he followed these people for all this time, and divided them into groups who, on the one hand, consumed diets that contained less than 20 grams of saturated fat as opposed to those [consuming diets] that contained more than 20 grams of saturated fat. He saw this substantial difference in the rates of disease progression. Only 5% of the people on the low-‐fat diet died; 80% of the people on the higher-‐fat diet died. Now, as I said, he focused on saturated fat, but saturated fat levels in these diets were basically an indication of the animal-‐ versus plant-‐based foods being consumed by these two different groups of people. So, once again, we see essentially a result, at least in a broad sense, that is very similar to the effect of diet on type 1 diabetes, another autoimmune disease.

8 Dr. Swank died in 2008, but the study continues to the present day at Oregon Health & Science University (in Portland, OR) under the direction of John McDougall, MD. The diet study group is currently following the low-‐fat McDougall Diet. Data analysis has begun and results should be available in 2013. 9 Swank RI. “ Effect of low saturated fat diet in early and late cases of multiple sclerosis.” Lancet 336[1990]:37-‐39.



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Chapter 10: More on Multiple Sclerosis

Since that time, [as with] type 1 diabetes, there has been a publication showing that there is a strong and impressive relationship between milk consumption in different countries and MS. 10 [See slide number 31.]

That is, the higher the milk consumption, the higher the MS. As far as the details of the effect of milk, or even perhaps other kinds of foods, on the development of MS (and there are some other foods that do have some constituents that have been shown to possibly be related to MS), it turns out that this relationship is very impressive, very similar to type 1 diabetes. That is to say, the higher the consumption of dairy, the higher the rates of diabetes and of MS as well.

Now, it turns out, from the studies that have so far been done on the various autoimmune diseases, that they seem to have a lot in common. As I said before, they tend to occur in the same kinds of populations. They tend to occur in the northern climates where there is less sunshine, and there is considerable work showing that also might be related to the production of vitamin D in the skin (by the sun); in any case, they [have] a lot in common. Sometimes they tend to occur in the same people, not only in the same populations. Furthermore, they tend to have other things in common: the basic biochemistry that underlies the development of these diseases, for these different groups of people, for these different kinds of diseases.

The basic biochemistry, it turns out, is remarkably similar and involves a role for animal protein in particular, in its effect on significantly and negatively affecting the contribution of vitamin D. I don’t really have an opportunity to get into the details of that, but suffice it to say that the mechanisms that seem to exist in these various autoimmune disease conditions, as so far studied—these mechanisms and the integration of reactions that we so far know about—seem to have a lot of commonalities. So, we have a rather distinctive contribution of animal foods to the production of these individual autoimmune diseases that have been studied in considerable depth, and these include type 1 diabetes, lupus, rheumatoid arthritis, and MS. Among those four, at least, as they are being studied at the present time, we see the very distinctive differentiation between the effects of animal foods and plant foods. Animal food, of course (largely through the protein content, but surely involving other nutrient characteristics as well), seems to raise the risk of these diseases.

So, this brings us to a whole new group of diseases that seem to be influenced, broadly speaking, in the same way as were the degenerative diseases like cancer, heart disease, and diabetes. Once again, it is the distinction between the plant-‐ and animal-‐based food.

10 Malosse D, Perron H, Sasco A, et al. “Correlation between milk and dairy product consumption and multiple sclerosis prevalence: a worldwide study.” Neuroepidemiology 11 (1992): 304-‐312.



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Chapter 11: Osteoporosis

What about some other diseases that seem not to necessarily fall in this particular category? One such disease is osteoporosis. Osteoporosis commanded a lot of attention in the last two or three decades in the United States. Osteoporosis, of course, is the disease that results in increased risk for bone fracture, and so the prevalence of osteoporosis and the risk of osteoporosis in various societies and countries tends to be measured by the prevalence or percentage of people who actually experience bone fractures.

The dairy industry has been promoting for years, as we all know, greater consumption of dairy to make stronger our bones and teeth, largely because dairy has calcium and calcium is a major component of bones, and so that notion, simplistic as it may be, nonetheless sounds somewhat reasonable. The higher the consumption of dairy, the lower the rates of osteoporosis, because we are making strong bones, after all. However, it turns out that if one begins to examine the relationship between intake of calcium and animal foods in general—and specifically dairy food—the higher the consumption of dairy foods, the higher the consumption of animal protein in calcium-‐containing foods, there is no evidence that osteoporosis rates are decreased. In fact, the higher the consumption of animal protein, the higher the consumption of calcium, and the higher the consumption of dairy which contributes in a major way to those two nutrients, the higher the risk of osteoporosis, not the lower. Certainly a very alarming kind of finding, at least as far as the dairy industry is concerned.

Now, let’s look a little more in a little more detail of some of these relationships. If one examines, for example, an increase in protein intake over what people otherwise would consider basal, one of the things that has been observed for a long time is the greater the excretion of urinary calcium—or the excretion of calcium in the urine. We know something about that and have known something about that—it goes back all the way to the 1920s. That is to say, animal protein tends to create an acid-‐like condition—albeit somewhat modest, but nonetheless significant—in the blood and the urine of the body. That occurs because the amino acids present in protein (as opposed to the amino acids present in most plant proteins), as they get metabolized and altered and excreted and changed, give rise to products that are somewhat more acidic.

A more acid-‐like condition in the body is not tolerated, and what the body wants to do is to reduce that acidity, so to speak. It does so by adding a buffer. The best buffer it can get its hands on, essentially, is the calcium present in the bone. So as individuals tend to consume more protein and experience more fracture rates, as we know, that relationship is strongly related to the acid condition that is produced in the body, resulting from the metabolism of animal protein. The acid [is then neutralized] by the calcium present in the bone, and of course as that tends to occur (as protein tends to go up and animal protein tends to go up), one tends to lose more calcium in the urine and thereby to weaken the bone. The adjoining



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chart shows this clearly in a study of some human subjects in the United States.11 [See slide number 34.]

As protein intake goes up, let’s say, 100% or 200% over what the lowest level might be, we see a significant and very impressive increase in urinary calcium. Incidentally, a six-‐month study recently funded by the Atkins Center (the Atkins people, of course, are promoting high intakes of animal protein) found that people who adopted the Atkins diet actually excreted 50% more calcium in the urine after six months on the diet, which of course is just one more strike against that kind of diet—at least in the long run, this is going to lead to problems were it to continue.

The question concerning the acidity produced by animal protein consumption, however, became somewhat controversial. Some thought it was a little bit narrowly focused, thought also that animal protein specifically was not the whole answer. It was known, for example, that exercising regularly—especially doing weight-‐bearing exercises, as they say—was helpful to reduce the risk of osteoporosis, and so the question concerning the effect of animal protein on the induction of acidity in the body (and of course the loss of calcium in the urine) many have thought to be a little bit narrow, not necessarily that significant, although it certainly has been noted and generally accepted. So it has rested as a somewhat controversial, and maybe at times almost insignificant, observation amongst some people.

Chapter 12: More on Osteoporosis

However, some recent studies have really put that idea, I think, now to rest. There is a study out of the University of California at San Francisco done by a group that has been spending many years working on this question concerning the role of body acid—referred to as metabolic acidosis—on the production of osteoporosis. They, for example, summarized a total of 87 surveys in 33 countries12 (that is a lot of studies, a lot of people) where they were able to compare the ratio of vegetable to animal protein on the induction of bone fractures in these different countries. The argument being that maybe it wasn’t just the animal protein alone that created this acid. By the same token, it could be that the amount of acid produced by consuming animal-‐based food could be alleviated and attenuated, to some extent, if people at the same time consumed more vegetables and fruits.

So, what came to mind for these researchers was whether it was the ratio of the animal to vegetable protein that might give a better indication of the acidity that would otherwise result, and therefore the bone fracture rate. We can see indeed, in the accompanying chart [slide number 36], a most impressive set of data—as the vegetable-‐to-‐animal protein ratio increases for these 33 countries, you can see that the rate of bone fracture (or hip fracture in this particular case) in these different 33 countries dramatically decreases.13

11 Hegested DM. “Calcium and osteoporosis.” J. Nutr. 116 (1986): 2316-‐2319. 12 This is known as a meta-‐analysis, in which scientist review research that has been previously done and compare the results of studies that have similar study design. 13 Frassetto LA, Todd KM, Morris C, Jr., et al. “World incidence of hip fracture in elderly women relation to consumption of animal and vegetable foods.” J. Gerentology 55 (2000): M585-‐M592.



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I’ve hardly seen any data that could be more impressive than this. So there is more to the story than just, I would say, animal protein specifically giving rise to an acidic condition that is chiefly responsible for osteoporosis; rather, it is also the ability of plant-‐based foods to be able to attenuate that effect. So it is really the balance of animal to plant foods that plays a major role in this. The same group at the University of California also moved from comparing a bunch of different societies of different countries over to a study of their own, where they were looking at more than 1,000 women age 65 and up, and were asking questions concerning the ratio of animal to plant protein in that case. It turned out that as they followed these women in the study for a period of about seven years, the women with the highest ratio of animal protein to plant protein had 3.7 times more bone fractures than the women with the lowest ratio.14

So I think we are finally coming to terms with what initially might have been considered somewhat controversial, somewhat narrowly focused—we are coming to terms with the idea that as we change the ratio of plant-‐ to animal-‐based foods, it certainly can have a dramatic effect on whether or not we are going to get osteoporosis. As far as osteoporosis is concerned, incidentally, I think most people know it tends to occur much more in women than men, and also in women who are post-‐menopausal. That is the time when their estrogen levels have declined, and as estrogen levels decline the risk of osteoporosis tends to go up—and that is another whole story in itself. The levels of estrogen, for example—I mentioned this before in the breast cancer case—amongst women consuming high animal-‐based foods tend to be substantially higher than amongst women consuming plant-‐based foods. So as women consuming animal-‐based foods approach menopause, their estrogen levels come crashing down—more so than, let’s say, women who are consuming a plant-‐based diet. As estrogen levels decline—estrogen tends to protect against calcium loss, to some extent—that is another mechanism that seems to come into play in explaining all of this.

Incidentally, in our China Project, where the animal-‐to-‐plant ratio was about 10%, the fracture rate, as far as we could tell (but we didn’t have really good data on this), was only about one fifth that of the United States. But subsequently there has been another study that has compared a number of different countries, insofar as this animal-‐to-‐plant ratio is concerned, and gotten some remarkable results.

Nigeria, for example, where the animal-‐to-‐plant ratio is only about 10% that of Germany—in other words, in Nigeria they are mostly consuming plant material; in Germany they are mostly consuming animal material.15 So, in Nigeria where the animal-‐to-‐plant protein ratio is only about 10%, the hip fracture rate is lower by over 99%. So I think now we have evidence that not only helps to clarify the confusion and controversy that previously existed, we also have evidence to show that the relationship of diet, and particularly of dairy, with osteoporosis is overwhelmingly impressive.

14 Sellmeyer DE, Stone KL, Sebastian A, et al. “A high ratio of dietary animal to vegetable protein increases the rate of bone loss and the risk of fracture in postmenopausal women.” Am. J. Clin. Nutr. 73 (2001): 118–122. 15 Frassetto LA, Todd KM, Morris C, Jr., et al. “Worldwide incidence of hip fracture in elderly women: relation to consumption of animal and vegetable foods.” J. Gerontology 55 (2000): M585–M592.



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Ok, so let’s now turn our attention. Incidentally, there is another whole sort of consideration here that I wish I could cover, but I won’t be able to. It has to do with bone density. Bone density is commonly tested these days in women as an indication of osteoporosis risk. It goes as follows: the higher the bone density, the lower the risk of osteoporosis. So, women are being told that, or being advised that they should try to keep their bone density up. Bone density naturally declines with age to a considerable extent, so the idea is to keep bone density up. However, there are a lot of chinks in the armor of that argument that are now beginning to appear, and I am not at all convinced that the bone density measurement tells [us] exactly what it should be telling [us], but I won’t have a chance to really get into those details.

Chapter 13: Kidney Stones

So now we have information on the autoimmune diseases and osteoporosis. What about some others? And I will just quickly mention some of these, because as one looks at the literature on these diseases, again we see this very strong distinction between animal-‐ and plant-‐based foods.

Kidney stones, for example. Something that anyone who has experienced the passing of a kidney stone will tell you is the worst kind of pain they have ever experienced, but kidney stones tend to be quite common—more so than one might imagine. It is said, for example, that 15% of Americans (usually more men than women) will experience a kidney stone sometime in their lifetimes.16 The question becomes: what about kidney stones and diet—is there anything going on there?

Well, the majority of kidney stones that occur are made up of calcium and oxalate, and there is a man who previously was at the University of Glasgow—in fact, much of his career was with the University of Glasgow—by the name of Dr. Robertson, who had been studying this in great detail, and publishing lots of studies on the question concerning the effect of diet on kidney stone formation.

What he was able to find was that the higher the animal protein intake, the higher was the likelihood of kidney stones. In fact, his data was so impressive as he started to compare different communities around Great Britain, for example, that he started to apply that idea to men who came into his medical practice to see if he could do something about it. He found something really quite remarkable. With men who tended to have a recurrence of kidney stone formation, he simply took them off of animal protein; switch the diet and it went away. It was that simple. The adjoining chart shows the relationship among protein intake— animal protein intake—and the discharge, so to speak, of the stones per 100,000 people. 17[See slide number 39.]

16 Stamatelou KK, Francis ME, Jones CA, et al. “Time trends in reported prevalence of kidney stones.” Kidney Int. 63 (2003): 1817–1823. 17 Robertson WG, Peacock M, and Hodgkinson A. “Dietary changes and in the incidence of urinary calculi in the UK between 1958 and 1976.” Chron. Dis. 32 (1979): 469-‐476.



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The amount of animal protein that seems to begin to increase the risk for kidney stone formation is only about 20 grams per person per day. Obviously this is not going to influence everyone, but for those who are susceptible, 20 grams and up can be a problem. If you stop to think about that, on average in the United States and Great Britain, for example, men are consuming 100-‐110 grams of protein a day, with about 70% of that (let’s say 70 grams or so) in the form of animal protein.

What Dr. Robertson found was that with about only 20 grams or so, risk could start to increase. We are consuming a very high level of animal protein, and unfortunately, for about 15% of the men in our society, sometime in their life they are going to experience this awful condition called a kidney stone passing. It is not necessarily fatal, but can in fact lead to kidney problems later in life, serious kidney problems, and it certainly is extraordinarily, excruciatingly painful.

Chapter 14: Two More Diseases

Two more diseases I will just mention quickly that seem to segregate according to whether animal-‐ or plant-‐based food is consumed: one has to do with the eyes, and the other has to do with the brain.

In eye problems there are a couple of conditions, one of which is chiefly responsible for blindness among people age 65 and over; that is called macular degeneration. The other condition that is commonly seen, and reasonably correctable for most people, is cataracts. If we look at the relationship of macular degeneration—which causes blindness—and cataracts, which as I say are correctable to some extent, it turns out in both cases there are now very impressive studies showing that in people who consume more plant-‐based material, and more antioxidants in particular, the lower is the risk for macular degeneration and cataracts. Figure something like in the neighborhood of 50, 60, 70, even 80-‐90% of all the blindness due to macular degeneration could be prevented, according to the evidence that is now coming out, simply if people were to consume a plant-‐based diet.18

Similarly, in the case of brain function, there are a couple conditions (one of which is much less serious than the other, and more common, and the other which is very serious) that seem to show the same thing. I am referring to cognitive dysfunction, our ability to remember what we have been doing, essentially. Cognitive dysfunction tends to be much higher, as we get older, among people who are consuming an animal-‐based diet than among those consuming a plant-‐based diet. In other words, consuming a plant-‐based diet, you are going to keep your mind for a longer period in your life, and not have to suffer this cognitive dysfunction.

It also turns out that people with cognitive dysfunction have been shown to have about a six-‐fold increased risk of Alzheimer’s disease, and of course these days we have heard a lot about Alzheimer’s. It seems to be increasing in its prevalence. It is worrisome. Most everybody knows that for people who have Alzheimer’s, it is a very, very serious problem,

18 Seddon JM, Ajani UA, Sperduto RD, et al. “Dietary carotenoids, vitamins A, C, and E, and advanced age-‐related macular degeneration.” JAMA 272 (1994): 1413–1420.



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especially for the family that has to care for them. And similarly, in the case of Alzheimer’s disease—which some people have referred to as a cardiovascular disease of the brain because of the presence of cholesterol and the occlusion of blood flow in the brain—it turns out that Alzheimer’s disease also is being strongly linked to the consumption of animal-‐based food. So, naturally, we tend to see Alzheimer’s travel along with heart disease. As people consume more meat-‐based diets, get more heart disease early in life (and of course later in life), they are the ones who are at much higher risk for getting Alzheimer’s diseases as well.

So we have cognitive dysfunction and Alzheimer’s disease in the case of the brain; we have macular degeneration and cataract formation in the case of the eyes; we have this kidney stone problem amongst those who have to suffer with that.

In the case of bones, we have osteoporosis and fracture rates, and of course then we have this whole host of diseases called the autoimmune diseases.

In all of these diseases (obviously the list is becoming very large, especially when you consider it in the context of cancer, heart disease, diabetes, and obesity) we see the same trends. Plant-‐based diets protect against these diseases. Animal-‐based diets do not. Animal-‐based diets tend to promote these diseases; plant-‐based diets tend to protect against these diseases, and I just find that kind of separation of effects to be extremely impressive. We tend to see all these diseases in the same societies. We tend to see sometimes the same diseases in the same people, and when we look at the sort of underlying biochemistry and clinical relationships, we see a lot of commonality amongst these diseases. Obviously, the mechanisms are going to be somewhat different. The organs clearly are different in these different cases, but what is common to all of these is what we decide to put in our mouth.

TCC502: Principles of Nutritional Health


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Principles of Nutritional Health



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Chapter 1: Benefits of a Healthy Lifestyle In this course I have talked a lot about the evidence that plant-‐based eating is a superior way of eating. I have talked very briefly about some of the underlying biochemistry and pointed out how consistent the effect is for a whole variety of different diseases. I could also talk about many other benefits from eating this way. I have found that many people who are hearing this evidence for the first time eventually become quite impressed and say yes, okay, I understand, this is impressive evidence. But to go away and actually do something about it is sometimes another question. I have found that it can be helpful to create some take-‐home ideas that reduce the issues to principles. So I have put together eight principles that gather in all this information in ways that tell us how we should be doing science, how we should be treating the sick, how we should feed ourselves, how we should think about health, and even how we should perceive the world. I find that this evidence is so broad-‐based, so profound, that the more I look at it from many different perspectives, the more impressed I become. This is really about much more than just deciding what kind of food we put in our mouths and how we feel about it. So I’ve reduced some of these notions down to principles. Let’s consider them. Chapter 2: Principle #1 Principle #1. Nutrition represents the combined activities of countless food substances. The whole is greater than the sum of its parts—you have heard that before. Foods contain an enormous number of chemical substances. Most of their total weight is in the form of nutrients, and all of these elements work together in marvelous ways. Foods are not just a handful of different nutrients—we should measure the nutrients in each food perhaps in the tens of thousands, maybe the hundreds of thousands. What is interesting about the nutrients in foods is that they work together as they get absorbed and then become highly integrated [through] metabolism. The combined activities of countless food substances are what nutrition is really all about. To get a glimpse of what we mean by that, let us develop a meal—let’s say spinach with ginger, and whole-‐grain ravioli shells stuffed with butternut squash and spices, and topped with a walnut tomato sauce. Let’s think about all the different kinds of nutrients that are present. Let’s just consider spinach, for example. In the adjoining table you will see that there are amino acids of all kinds. 1 [See slide number 8.] Most amino acids are present, and the fatty acids that make up lipids. There are vitamins and minerals, and of course the macronutrients. We also have a catchall group of substances that are typically present in plants, called phytosterols. Many of these participate in anti-‐oxidation reactions, and all sorts of other things. I should emphasize that this is only a partial list of some of the nutrients whose structures we have determined. Then think about how all these things work together to create a response. And of course,

1 U.S. Department of Agriculture. “USDA Nutrient Database for Standard Reference.” Washington, DC: U.S. Department of Agriculture, Agriculture Research Service, 2002. http://www.nal.usda.gov/fnic/foodcomp/cgi-‐bin/nut_search_new.pl



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we are only talking about one food, spinach. Spinach has a lot of good stuff in it, and when it is ingested, these nutrients are ultimately absorbed in our intestines and together produce a response. It is the whole food. The nutrients tend to mutually support each other as they do their work inside the body. Chapter 3: Principle #2 Principle #2 is a sort of follow-‐up to Principle #1: Vitamin supplements are not a panacea for good health. That doesn’t mean that vitamin supplements never have a beneficial effect in [any] cases, at least in the short term. That may be true, but in the long term—and that is what we are talking about here: long-‐term health, the prevention of disease, and the promotion of health—using vitamin supplements is simply not going to work. If we continue to consume the typical Western diet—high in animal protein, low in fiber, and high in fat—we are not going to avoid the consequences by using a handful of different kinds of supplements. Evidence that that is a good course to follow simply doesn’t exist. I have followed the development of the vitamin supplement industry quite closely for the last 20 or 30 years, and have been involved in several cases developing policy on the marketing, sale, and promotion of these sorts of materials. I once served for three years as the chief consultant to the Federal Trade Commission as they were putting together their recommendations in the early days regarding what health claims were permissible for vitamin supplements. I found that there is tremendous pressure in the marketplace, resulting in a multibillion-‐dollar market, to develop very specific individual chemical substances and call them supplements and nutrients that do various things. Dr. Atkins, for example, and others like him, have promoted the high-‐protein, low-‐carb diet that we know so much about. It turns out that many of the people who are doing this kind of promotion actually have a lucrative marketing activity on the side promoting supplements. If I may say so, it is almost as if they were promoting sickness and then hoping that they could sell the supplements to make people feel they were getting better. So supplements really don’t work. Consider the biochemistry and go back to Principle #1, where everything is working together. The idea of taking a single nutrient out of context, putting it in a pill, and consuming it to achieve what all these nutrients together achieve is kind of mindless, terribly superficial, and it doesn’t make a lot of sense. The whole idea, the enthusiasm for supplements, began in the late 70s and continued into the 80s, but it began to unravel to some extent around the middle of the 1990s, when the results of a study of beta-‐carotene and lung cancer were released. Beta-‐carotene, as I am sure you know, is a precursor to vitamin A. It is found only in plants, and it is a good antioxidant. Diets containing beta-‐carotene have been shown across the board to reduce various diseases. Sometimes people have speculated that many of the benefits of a plant-‐based diet are really due to the consumption of beta-‐carotene. So in the late 80s beta-‐carotene became quite an exciting nutrient, and pills were being made and people were starting to take them rather extensively.



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So a study was organized to see if taking beta-‐carotene supplements might prevent one kind of cancer, lung cancer.2 3 That was considered the one to study because lung cancer, generally promoted by cigarette smoking, of course, tends to occur because of the induction of free radicals, which we talked about before. Free radicals are more likely to occur where there is lots of oxygen, and in the lung tissue itself there is a high degree of oxygenation, and therefore a high degree of free radical formation. If beta-‐carotene were acting the way most people thought it would, as an antioxidant, it should have an effect on lung cancer. So the study was organized basically in Finland, and people were followed for a total of eight years. The results caused an enormous storm, both in the public mind and in the science community. It turned out that taking beta-‐carotene supplements was associated with an increase in lung cancer rates, not a decrease. The same study found that beta-‐carotene consumption from foods was associated with a decrease in lung cancer rates. So adding beta-‐carotene supplements to the diet did not, in fact, reduce lung cancer; it significantly increased it. It almost brought an end to the entire marketing scheme for the use of beta-‐carotene supplements. This was an early indication that taking supplements out of context to do something like prevent cancer simply wasn’t working. Since then, an enormous number of studies have been reported, and as far as we now know, the effect of these supplements on preventing serious long-‐term diseases such as heart disease and cancer are simply not standing up. In fact, just recently a report came out that resulted in two major reviews of all the trials that have been conducted so far.4 5 This report basically concluded that, and I’ll quote: “The researchers could not determine the balance of benefits and harms of routine use of supplements of vitamin A, C, or E, or vitamins with folic acid [which is something that comes in plant material] or antioxidant combinations for the prevention of cancer or cardiovascular disease.” This was a major report reviewing a vast amount of literature that had been conducted over 15 or 20 years, and they concluded that these really important vitamins that everybody assumed were to have a beneficial effect, and that had been reported from time to time to have a beneficial effect—mainly vitamins A, C, and E—simply were not working. This release of information in recent years, I think, is beginning to raise some serious questions even in the public mind about the use of supplements.6 7 It is not the way to go to get long-‐term health. Indeed, in a recent article in the New York Times, some of this new evidence on nutrient supplements was reviewed and caused quite a lot of discussion. 2 The Alpha-‐Tocopherol Beta Carotene Cancer Prevention Study Group. “The effect of vitamin E and beta carotene on the incidence of lung cancer and other cancers in male smokers.” New Engl. J. Med. 330 (1994): 1029–1035. 3 Omenn GS, Goodman GE, Thornquist MD, et al. “Effects of a combination of beta carotene and vitamin A on lung cancer and cardiovascular disease.” New Engl. J. Med. 334 (1996): 1150–1155. 4 U.S. Preventive Services Task Force. “Routine vitamin supplementation to prevent cancer and cardiovascular disease: recommendations and rationale.” Ann. Internal Med. 139 (2003): 51–55. 5 Morris CD, and Carson S. “Routine vitamin supplementation to prevent cardiovascular disease: a summary of the evidence for the U.S. Preventive Services Task Force.” Ann. Internal Med. 139 (2003): 56–70. 6 Long-‐term study finds vitamin E supplements raise the risk of prostate cancer. Oncology (Williston Park). 2011 Nov 15;25(12):1236-‐7. 7 Mursu J, Robien K, Harnack LJ, Park K, Jacobs DR Jr. Dietary supplements and mortality rate in older women: the Iowa Women's Health Study. Arch Intern Med. 2011 Oct 10;171(18):1625-‐33.



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Chapter 4: Principle #3 Principle #3. There are virtually no nutrients in animal-‐based foods that are not better provided by plants. Now we know that a number of different nutrients exist in animal versus plant foods to a very different extent. In fact, some nutrients might be present in one and not the other. If we look at the adjoining chart at some nutrients as they exist in a mixture of plant-‐based foods and a mixture of animal-‐based foods, we see some very distinctive differences. 8 9 10 [See slide number 11.] Cholesterol, of course, is only found in animal-‐based food. Dietary fat tends to be more common, or at least [occur] at higher levels, in animal-‐based foods. Protein is about even, but I have already pointed out that the protein present in animal-‐based foods tends to have different characteristic effects. Beta-‐carotene, which we just talked about, is technically only present in plant-‐based foods. Only plants can make beta-‐carotene. There is a tiny trace of beta-‐carotene in animal flesh, but apparently this is only because animals had consumed food that contained beta-‐carotene. Dietary fiber, of course, is only found in plant-‐based food. Vitamin C and folate, as I mentioned before, and vitamin E, all tend to have much higher concentrations in plant-‐based foods than in animal-‐based foods. And on down the list we see the different minerals and vitamins, and there is a really interesting relationship here. So we see this major difference between plant-‐ and animal-‐based foods. As far as Principle #3 is concerned, there are virtually no nutrients in animal-‐based foods that are not better provided by plants. This chart is intended to show that all the nutrients we really need are present in plant-‐based foods. We don’t need to consume animal-‐based foods to get any of these nutrients. This is not to say that the animal-‐based foods don’t have these nutrients. They do have some, and in some cases fairly generous amounts, as with protein, for example. But there is no evidence that we need to consume any animal-‐based food to get our supply of good nutrition. Now there are a couple examples that, one might argue, are present primarily in animal-‐based foods and not in plant-‐based foods, so we should therefore consume animal-‐based foods. I am thinking of vitamin B12 and vitamin D, which tends to be present in animal-‐based foods, although it is primarily present in milk because it has been added to milk. So vitamin D and vitamin B12 are anomalies. Vitamin D is not really a vitamin. A vitamin is a nutrient that we have to consume because we can’t make it. In reality, we can make vitamin D. All we need to do is to go out and get some sunshine and we get all the vitamin D we need. So the idea that you must consume

8 Holden JM, Eldridge AL, Beecher GR, et al. “Carotenoid content of U.S. foods: an update of the database.” J. Food Comp. Anal. 12 (1999): 169–196. 9 U.S. Department of Agriculture. “USDA Nutrient Database for Standard Reference.” Washington, DC: U.S. Department of Agriculture, Agriculture Research Service, 2002. http://www.nal.usda.gov/fnic/foodcomp/cgi-‐bin/nut_search_new.pl 10 The exact food listings in the database were: Ground Beef, 80% lean meat/20% fat, raw; Pork, fresh, ground, raw; Chicken, broilers or fryers, meat and skin, raw; Milk, dry, whole; Spinach, raw; Tomatoes, red, ripe, raw, year-‐round average; Lima Beans, large, mature seeds, raw; Peas, green, raw; Potatoes, russet, flesh and skin, raw.



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animal foods, and dairy in particular, to get vitamin D is really nonsense. We can get the vitamin D we need by getting adequate sunshine. This isn’t to say that a little vitamin D can’t be helpful, particularly for people who simply can’t get the sunshine. But it is not otherwise essential. It is often said that we must consume some animal-‐based foods because only they have B12. In reality, the B12 present in any food, plant or animal, is only there because of synthesis by microorganisms. In the case of animals, the microorganisms producing the B12 reside in the large intestine, or in the case of ruminants, in the lumen. The microorganisms there make some B12, and then end up putting a lot of it in the liver and some other tissues. So it is argued that we perhaps need some animal-‐based food from time to time to get some B12. But we can actually get B12 from supplements if we really need it. People who rely entirely on plant-‐based foods do have lower levels of B12. The question arises, however, of how we could have evolved on plant-‐based foods. It turns out that plants previously thought to be unable to take up B12 can actually do so. However, those plants must be growing in organic soil where there are lots of microorganisms to produce the B12. The B12 can get into the plant, and so we can get some B12 that way. Also, in olden days, before we became so scrupulous about cleaning our foods, having a little soil attached to the plants grown in organic soils always gave one enough B12. So there wasn’t really a distinction between B12 being present in animal-‐based foods and not in plant-‐based foods. It is really all from microorganisms, and the question is the extent to which those organisms contribute to the B12 in those two different foods. One more point is probably worth noting concerning the differences between animal-‐ and plant-‐based foods. The protein level of nuts and seeds can be quite high compared to that of animal-‐based foods. Nuts and seeds have quite a lot of fat and quite a lot of protein. I previously said that animal foods in general have more fat and more protein than plants—not so much more protein, but certainly more fat. The important point is that the fat and the protein in nuts and seeds are distinctively different, and more healthful. Cholesterol is not a nutrient, and it is only present in animal-‐based foods. We need cholesterol to do certain things, especially to maintain membranes in our cells. It is particularly important in some of the tissue that surrounds our nerves. So cholesterol is important, but we can make all the cholesterol we really need, and we don’t need to consume one gram of it. Chapter 5: Principle #4 Principle #4. I find this one quite interesting. Genes do not determine disease on their own. The genes function only by being activated or expressed. Nutrition plays a critical role in determining which genes, whether they are good or bad, are being expressed. We have heard a lot about genes. In fact, I think the majority of the basic medical research budget is now concerned either directly or indirectly with trying to discover the genes responsible for producing this or that kind of disease, whether it is obesity, diabetes, heart disease, or



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breast cancer. The inference is being made that if we just knew which genes did what, then we might be able to—in the case of bad genes—intercept them. If we know something about the structure of the proteins that are produced from the genes and can be a little bit creative, we can come up with drugs to intercept the activities of these bad genes. Unfortunately, I find that whole approach to understanding biology and the promotion of health to be very, very mischievous. It is going in the wrong direction, as far as I am concerned. But let’s get back to the question of genes and health or disease. Genes are required to produce health. Every biological event that occurs essentially originates from the activity of some gene or a cluster of genes. If we didn’t have genes, we wouldn’t have life. Obviously, some genes, if they act in the wrong way, might give rise to disease, but we are now discovering that the idea of a single gene’s causing a single disease has passed by the wayside. I don’t think there are many people around anymore who subscribe to that idea, although as recently as 5 to 10 years ago many people even in science did subscribe to it. But with our ability to determine the contribution of genes to disease, we have discovered that for any one disease, more and more genes seem to be involved. 11 The China Project and other studies of people with different dietary lifestyle practices around the world concluded that genes didn’t comprise more than, let’s say, 2 to 3% of cancer risk, or perhaps of heart disease risk. These are very low contributions. So on the one hand, genes are at the root of these diseases’ getting started, but they are not alone responsible for the disease. What is really happening is our understanding of the role of nutrition. If a certain gene would give rise, perhaps in combination with other genes, to certain diseases, it is easy to control the activities of these genes simply by eating the right kind of nutrients. One of the fascinating things that has come up in recent years is that the nutrients present in plant-‐based foods tend to keep mischievous genes, the bad genes, under control. That is why we tend to get much less of these diseases when we consume the nutrients in that way. To give you some idea of how foolish this genetic research is in terms of its focus on single genes and single outcomes, I should point out a recent little study published in a well-‐known medical journal on a little worm that has some 16,000-‐plus genes. We have perhaps 30 [thousand], or about twice that many genes. The researchers basically scored the ability of each of these genes, when turned on or turned off, to contribute to body weight. This is obviously interesting and important, as far as obesity is concerned, if in fact it worked the same way in humans. In any case, by turning each one of these 16,000-‐plus genes on and off, they discovered 417 genes that actually affected weight. Now, I would ask anyone working in this field, how in the world can we assume that if there are at least 400 genes in that little worm, and probably twice that many in the case of humans, involved in causing something like obesity, then how ridiculous would it be to think about reaching in and getting a drug from one of those genes, or maybe a couple of them? That is really quite

11 Ashrafi K, Chang FY, Watts JL, et al. “Genome-‐wide RNAi analysis of Caenorhabitis elegans fat regulatory genes.” Nature 421 (2003): 268–272.



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foolish, and I think this discovery really says a lot about the whole idea of genes causing disease. It is not genes; it is nutrition. Chapter 6: Principle #5 Principle #5. Nutrition can substantially control the adverse effects of noxious chemicals. This is an area that my own research group worked in for many years. We were particularly interested, as you will recall, in a very potent carcinogen, aflatoxin, and its ability to cause liver cancer. We found that regardless of the dose of the carcinogen being given, we could control whether that carcinogen actually led to the cancer. Incidentally, genetics come into play here, too, because these carcinogens often begin their activity by modifying a gene, so in a sense we are talking not only about a chemical carcinogen’s possibly causing a disease, but about the contribution of the gene (that has been altered by the carcinogen) to cause the disease. What we discovered, at least in the initial experiment, was that we could basically keep under control even the most noxious chemical carcinogen. I have become quite interested in exploring that literature for many years now, looking at various kinds of toxic agents that get into our diet, especially small amounts of toxic agents. I should point out that I subscribe to the idea that we should control exposure to noxious agents, especially the kind that we synthesize and that nature has never seen before. But sometimes we get terribly excited and make a lot of news about this chemical or that chemical possibly being present in the environment and causing this problem or that problem, when we tend to ignore what really makes the difference as far as many of these diseases are concerned. Think of breast cancer and heart disease and the like—it is really the balance of nutrients being consumed that can sequester the toxicity that would otherwise occur with the consumption of small amounts of these so-‐called chemical carcinogens. I want to emphasize that I do not mean we should be unconcerned about getting exposed to some of these noxious chemicals. We should be concerned because it is not only cancer that we have to be thinking about. Some other unknown phenomena could well occur that maybe nutrition couldn’t control so well. But in my view, nutrition has an enormous ability to control the noxious agents that we otherwise get. A good example is cigarette smoking. Cigarettes are loaded with chemical carcinogens, especially kinds that tend to promote the formation of tumors. That has been well demonstrated. We know that, but we also know that if people who are heavy smokers consume a plant-‐based diet, their risk of getting lung cancer is substantially reduced. In one of the biggest studies done along this line, people who were heavy smokers and consumed the most vegetables reduced their risk of getting lung cancer almost equal to that of the nonsmoker.12 I don’t want that to be taken out of context, because smoking also promotes heart disease, and we don’t know too much about that. But it does demonstrate once again

12 Shekelle RB, Raynor Jr. WJ. Dietary vitamin A and risk of cancer in the Western Electric Study. Lancet 1981;2:1185-‐1190.



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that nutrition plays a major role in keeping the effects of these noxious chemicals under control. Chapter 7: Principle #6 Principle #6. The same nutrition that prevents disease in its early stages—that is, before diagnosis—can also halt or reverse disease in its later stages, after diagnosis. The best way to illustrate this is what I saw evolve over the last 30 to 40 years with respect to heart disease. When I was a student, the hypothesis was being put forward that we could prevent heart disease by consuming a diet low in saturated fat and low in cholesterol—that is, a diet higher in fruits and vegetables. When some eminent researchers came to our school, Cornell University, to talk about their notion that a plant-‐based diet could prevent these diseases from occurring in the first place, I remember that many of the professors were rather reluctant to accept this idea that eating had anything to do with prevention of heart disease. As the years passed, they finally came, somewhat begrudgingly in some cases, to accept the idea that a more plant-‐based diet low in saturated fats and cholesterol could possibly prevent heart disease. But they often said at the same time that although this disease might be prevented, there was no way that the disease could be reversed once it was already present. That was an idea that virtually everyone subscribed to. Some 10 years ago, we learned that with heart disease in particular, people with seriously advanced disease could bring that disease under control, and even reverse it, by consuming a plant-‐based diet. It is really quite remarkable. What I have taken away from this history, from the evidence that I have seen myself over the years—and experimentally, even up until the final stages—is that diet is responsible for preventing the disease in the first place, and can help to stop it wherever it may be, and perhaps in many cases actually reverse it. We know for type 2 diabetes, adult-‐onset diabetes, that if we take diabetics and give them a plant-‐based diet, we can sometimes reverse the disease and take them off the medicine. I have actually been at clinics on several occasions now where I have met people who have had that experience. It is really very dramatic. In Professor Anderson’s work from the University of Kentucky, which I mentioned in the lecture on diabetes, he was able to show that even type 1 diabetics, who absolutely need insulin, when put on a plant-‐based diet, were able to reduce their drug needs by 40% or more.13 How that works I am not sure. But in any case the plant-‐based diet has that nutritional effect on diseases at fairly late stages of the disease, whether it is heart disease, diabetes, perhaps even cancer. There is a fairly well-‐known study now that indicates that melanoma, a very deadly cancer, can be kept largely under control through the use of a plant-‐based diet. Chapter 8: Principle #7 Principle #7. Nutrition that is truly beneficial to one chronic disease will support health across the board. The last bit of discussion in [Chronic Disease] was an attempt to

13 Anderson JW. “Dietary fiber in nutrition management of diabetes.” In: G. Vahouny, V. and D. Kritchevsky (eds.), Dietary Fiber: Basic and Clinical Aspects, pp. 343–360. New York: Plenum Press, 1986.



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show that a plant-‐based diet has very broad effect. It influences a large variety of different diseases, and now we are beginning to understand why that is so. This is due in part to the fact that these diseases share a common biochemistry that causes disease to occur in the first place. Nutrition seems to act through that medium to affect a wide variety of diseases. Chapter 9: Principle #8 Principle #8. Good nutrition creates health in all areas of our existence, and all parts are interconnected. As I have been involved in research over the years, I have become more and more aware that science tends to focus on one little itsy-‐bitsy part of the puzzle. Some people spend their entire lives working on just one part, maybe one enzyme, one kind of cause-‐effect relationship, what have you. That research is very interesting and very productive in the sense that it gives us an insight into how things work, so I don’t want to belittle it. But we can’t just focus on details. If we make an observation on one detail and then ask broader questions and keep on asking broader questions every time, it turns out that all of these parts are really interconnected. Initially, I considered this notion of interconnectedness as having to do with the interplay between different nutrients—let’s say in the same food, or operating within the cell. But now it turns out that that idea of interconnectedness goes beyond biology; it goes beyond what is going on in the cell. It operates between organs. Hormones conduct messages from one organ to another, for example. We have a lot of interplay between organs in the body. There is also interplay between individuals, people who are choosing to eat this way and those who don’t. So a plant-‐based diet really has an impact far beyond biology, far beyond our health and the risk of our getting disease. It also affects our ability to be physically active, and our emotional and mental health. It comes into play in a major way with respect to our environment—if anyone would like to know more about that, I would highly recommend reading some of the books by people such as Professor David Pimentel, or John Robbins, who wrote Diet for a New America, and more recently, The Food Revolution. Excellent books now show that consuming animal-‐based foods is often at the root of environmental problems. I would actually argue that it even goes beyond the environment. It involves political and economic considerations. I am referring to the fact that rich countries tend to go to poor countries, take some of their valuable land, cut down their forests, put cattle on the land, and chase away the local peasantry just so we can eat meat. In doing this, we create a terrible economic and political disequilibrium, which in many cases eventually leads to violence and wars, and the rest of the progression of the story is fairly well known. So I think that interconnectedness is an important concept to keep in mind. It involves a much larger domain in how we choose to live and to interact with each other.

TCC502: Coconut Oil


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Coconut Oil: Healthy or Hazardous?

TCC502: Coconut Oil


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Chapter 1: Coconut Oil Hi, I’m Dr. Matt Lederman, a board-‐certified internist who specializes in nutrition and lifestyle medicine. I’m not quite sure why people think there is something magically healthy about coconut oil. I think it is because it tastes good, and therefore the misinformation is easier to swallow. For several years now, coconut oil has been marketed as the new wonder oil, a cure-‐all with health benefits ranging from antimicrobial properties (such as fighting viruses and bacteria, including HIV), to fighting cancer (by supporting our immune system), to reducing heart disease (by reducing cholesterol and benefiting our arteries), to promoting weight loss, to treating hyperthyroidism, to many other things. Its uses are also varied—it’s a cooking and baking oil, an ingredient in many packaged foods, and a component used in biodiesel fuel, soaps, and skin products. So what’s the scoop? Well, it is true that coconut oil contains some medium-‐chain fatty acids called MCFAs, which are less readily absorbed compared to longer-‐chain fatty acids. And these MCFAs have been shown to have less of an effect on LDL, bad cholesterol. But is that not similar to saying that burning your hand with a 300-‐degree flame has less of an effect on your skin than burning your hand with a 400-‐degree flame? Oil and fat are oil and fat. That being said, I have read that MCFAs are absorbed directly into the liver, and as a result, have the potential [to promote] weight loss. Even if true—this was only theoretical in the study—this reductionist view misses the point that people don’t eat MCFAs. Rather, they eat coconut oil, and half the saturated fat in coconut oil is not MCFAs. At over 90% saturated fat, taking away the portion of MCFAs in coconut oil—which still requires us to make the huge assumption that MCFAs are all good and can’t be negated—then you are still left with 45% of the saturated fat. So even subtracting all of the theoretical goodness of MCFAs from the total saturated fat content, coconut oil is still worse than lard, which is only 43% saturated fat. And we all know that lard is not a health food. In many cases, the minimal amount of beneficial MCFAs in coconut oil are isolated and removed from the oil to be used medicinally or in beauty products. So many people are risking their hearts and their lives and not even getting the little theoretical benefit they thought they were getting. Yes, it is true that some of these MCFAs, like loric and capric acid, have been shown to have antifungal and antiviral properties, but we don’t eat foods because of their antimicrobial properties. We eat foods to provide healthy fuels, which as a result strengthen our immune system, which then fights microbes. Now, food doesn’t fight infection; rather, our immune system does. With that argument we could recommend alcohol as a health food because alcohol kills some microbes. More importantly, we shouldn’t approve of a food just because one part of it has a specific property we like. This reductionist view is sort of like saying cigarettes are great because

TCC502: Coconut Oil


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they have found some antioxidants in the tobacco. The take-‐home message is that the whole food serves no purpose and does pose a serious risk. There are no omega-‐3 fats, the essential fats people actually need, in coconut oil. And furthermore, if people on a no-‐added-‐oil, low-‐fat, plant-‐based diet added coconut oil to their diets, the fat load on their vessels would cause serious damage. Inflammation and blood vessel flow decrease when exposed to any fat, including coconut oil. Overall, health takes a beating. When looking at the whole package, the numbers just don’t lie. Take a look at the nutritional content of one tablespoon of coconut oil. [See slide number 7.] There are 116 calories, which all come from fat, which is easily stored as fat on your body. The mostly saturated fat is 12 grams, half of which are not MCFAs, this theoretically good medium-‐chain fatty acid. There are no carbohydrates and no protein; there are no vitamins except 0.1 micrograms of vitamin K. And just so you get this in perspective, one romaine leaf has 30 micrograms of vitamin K. Are we sensing a theme here? The bottom line is that coconut oil is devoid of vitamins, minerals, and most other nutrients. It is pure fat, and worse than that, it’s over 90% saturated fat. The same saturated fat that raises our cholesterol, clogs our arteries, and contributes to our heart attacks. In the 1980s, the American Heart Association recognized coconut oil’s high saturated fat content as being overall destructive to heart health, as well as specifically promoting heart damage and disease. As a result, they continued to advise the reduction of all saturated fats, including coconut oil, to less than 7% of dietary calories. This opinion is shared by the World Health Organization and the FDA, both recommending decreasing intake of saturated fats, because the reduction of saturated fat, including coconut oil, has been shown to benefit our overall health. In light of this information, coconut oil seems better served in our cars and on our skin, and really should never be used in our food. Having said that, if you enjoy the taste of coconut, or if a little bit of coconut is helping you stay on this healthy new diet and lifestyle, then using a little bit of the whole plant food, not the oil, once in a generous while, is okay.

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