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A Guide to Obesity and the Metabolic Syndrome: Origins and Treatment

2011 Edition, March 28, 2011

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ISBN: 978-1-4398-1458-1
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  • Revision: 2011 Edition, March 28, 2011
  • Published Date: March 28, 2011
  • Status: Active, Most Current
  • Document Language: English
  • Published By: CRC Press (CRC)
  • Page Count: 400
  • ANSI Approved: No
  • DoD Adopted: No

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Obesity: Origins and Solutions

How Did Americans Get So Fat?

If you have been to your local shopping mall recently and are older than 20 years of age, you have witnessed the growing girth of many Americans. The United States is now the fattest country in the world! The U.S. government regularly surveys the American public to put numbers on the face of fatness. These surveys are called the National Health and Nutrition Examination Surveys (NHANES). Between 1960 and 1976, there was a slow rise in the number of Americans who were overweight. This rise was similar to the slow increase in overweight that occurred from the time of the Civil War (in 1860) through 1976 (Bray 1976a). Between 1976 and today, however, there has been a big jump in the number of overweight and obese Americans. The number has more than doubled between 1980 to 2002 (from 14.5% to 33.5% obese) (Ogden et al. 2007). The increased rate at which people are becoming fat has led some to label this an "epidemic" (the World Health Organization [WHO], the National Heart, Lung, and Blood Institute [NHLBI]).

Figure 1 shows this pattern of increase for three levels of body weight. The upper limit of normal is 25 body mass index (BMI) units, a number we will describe in more detail in Chapter 2. People above a normal BMI of 25 have increased from 45% of the population to over 60% today-a rise of more than one-third. A BMI of 30 in Figure 1 is the dividing line for obesity. The number of adults above a BMI of 30 has grown from 14% in 1960 to over 30% today-a 100% increase. The final line at a BMI of 40 defined the dividing line for the very obese. Very obese people were uncommon in 1960 but are now more than 5%-a more than 400% increase.

Nearly 40 years ago, even before the "obesity epidemic" began in earnest, the plight of fat Americans became my life's work. Much of my office practice of medicine dealt with obese adolescents and young adults. Back in the 1960s, I was saddened and dismayed by the young people weighing more than 300 pounds who came to my office for help. The problem is much worse now. In the 1960s, the group with a body weight greater than 300 lbs was less than 0.1% of the American population. Now it is over 5% and growing rapidly. Thirty years ago, I published my first book on obesity, (Bray 1976a) followed by an update in 2007 (Bray 2007b). Twenty-five years ago, I published my first treatment program to help people manage their weight problem (Bray 1982). Many things have changed in the intervening years. Preparation of this book has been strongly influenced by my experiences at the Pennington Biomedical Research Center in Baton Rouge, Louisiana. When I became director of this center in 1989, the current obesity epidemic was in full swing. As director of this magnificent nutrition research facility, I had additional resources to tackle the problem that has been my life's work. This book incorporates many new ideas about weight management that I have learned through the help of many patients and professional colleagues.

Let me put my strategy of weight management forward for you and then fill in the details about how this approach came about. First, we know that in famines, and when food is in short supply, people don't gain weight-indeed, they lose weight (Ravelli et al. 1999; Franco et al. 2007). No food-no fatness. This means that food plays a key part in the problem (Swinburn et al. 2009)

Focusing on food and how its intake is regulated is the first step toward understanding the epidemic of obesity. Reasoning that some foods are playing a bigger role than others, we examined the data from the U.S. Department of Agriculture about changes in food supply during the twentieth century. One of the striking findings was that the epidemic of overweight occurred in parallel with the introduction of high fructose corn syrup (HFCS) into the American food supply (Bray 2004). The association between the rapid rise in obesity and the introduction of HFCS doesn't prove that HFCS is the cause of obesity-obesity clearly has a number of causes, many of which are related to eating more food than we need. But the evidence is growing that the fructose that comes from HFCS or sucrose (table sugar) may be one contributor to the rise in obesity rates (Vartanian et al. 2007; Malik et al. 2010).

Along with a major shift in the supply of caloric sweeteners in the American diet, a number of other changes have occurred over recent decades that impact the epidemic of obesity. These trends can be summed up under the five "Bs": Beverages, Burgers, Behavior, Being Active, Buyer Beware.

Beverages: I have already introduced you to beverages sweetened with fructose from either HFCS or sugar. There are a number of potentially harmful effects of fructose on body weight (Malik et al. 2010; Bray 2009). Thus, reducing fructose intake makes sense to me and soft drinks and sweetened fruit drinks that contain this sugar are easy targets. Several studies reviewing scientific publication (meta-analyses) have shown that soft drink consumption predicts energy intake and often weight gain and obesity (Vartanian et al. 2007; Olsen and Heitmann, 2009; Malik et al. 2009). Get as much of your fluid and beverage needs as you can from water, tea, or coffee-at least six to eight 8-ounce glasses a day and avoid beverages that have fructose in them.

Burgers: Everyone, or nearly everyone, has eaten at one of the fast food restaurants. They are ubiquitous in the United States and around the world. Burgers tend to be loaded with fat -but they are "tasty." Over the past 50 years, the size of most burgers has ballooned. A single large burger meal can provide 1000 calories or more, which is 50% or more of the calories needed by many Americans each day. These are problem foods for some people who want to lose weight and keep it off, as well as for people who do not want to gain weight. This threat to a healthy weight was shown dramatically in the documentary movie, Supersize Me. The director, Morgan Spurlock, gained over 25 pounds in 1 month while supersizing his meal every time it was offered. Grilling burgers at home without the "special" sauce is good advice.

Behavior: Eating and drinking are behaviors. One view has it that we become overweight because we have "faulty" behaviors. Whether true or not, this idea has been helping people plan what they eat, and with whom and where they eat, to get better control over their own personal eating. The Internet is one of the most striking developments of the past decade (Winett et al. 2005). The power of the Internet is being harnessed to use in behavioral weight management, and offers promise for the future. One of the most important concepts has been the control of portion size using "portioncontrolled" foods. I will explore behavioral techniques in Chapter 6 and focus on the types of foods and beverages to include in a diet plan.

Be as active as you can to counteract the tendency to be inactive. Society no longer requires much strenuous activity, unless we choose to do so. Television, video games, and comfortable automobiles all make the United States one of the most inactive societies on earth. Inactivity is the norm. We know that overweight people sit an average of 2 hours more per day than do thinner people. Standing up while talking on your cell phone uses more energy. The beauty of the cell phone is that you can talk anywhere and walk while doing so, all of which burns more energy. A step counter to count the steps you take, described in Chapter 6 is one way to set a goal of becoming more active.

Buyer Beware: We are all influenced by the prices of the things we buy, including food. Price reductions and sale items get our attention. Food pricing works the same way. Special deals, such as "two-for-the-price-of-one" and "supersizing" are ways of selling more for a "better deal"-a better deal for the seller maybe, but not necessarily a better deal for you. Buy healthy foods, not necessarily the cheap ones. Remember, you don't have to clean your plate. Put the waste in the garbage bin rather than on your own waist. Avoid combinations of fructose from HFCS or sugar and fat.

Isn't Obesity Just a Recent Problem?

Overweight was a problem long before I finished medical school 50 years ago. I found this out when I came across a short book from the nineteenth century that traced the origins of obesity. Although it was written in French by an American who was studying in Paris-something lots of young physicians did in the nineteenth century-it opened my eyes to the long history of overweight that is described in Chapter 1 (Worthington 1875). It is hard to believe that there was enough to fill an obesity book that far back. Yet there was, and this book stimulated me to learn more about the history of obesity and when it began (Bray 2007a).

Treatment for overweight people has been described for more than 5000 years (Bray 2007a). These descriptions can be found in medical writings from the Egyptian, Babylonian, Chinese, Indian, Meso-American, and Greco-Roman cultures. Many causes were proposed and many treatments suggested long before we had any modern medicines. In spite of this long history, the problem is still with us-and getting worse-meaning that we neither understand it well nor have completely effective treatments. We have greatly increased our knowledge and have much more to offer people working to manage their weight, yet, at this writing, the problem continues to worsen-we haven't even yet contained it-to use a firefighter's phrase.

The first English-language books devoted solely to the subject of obesity or corpulence as it was called were written in the eighteenth century, well before the American Revolution (Short 1727; Flemyng 1760). These were followed during the next two hundred years by books in many languages (Bray 2007a). The first American book dealing with the medical side of obesity was published in 1940, just prior to World War II. By the time Rony (1940) wrote this book, the basic concepts of energy balance and metabolism had been well established. Scientific studies at the time of the French Revolution (Lavoisier 1789; Boyle 1764) had clearly shown that metabolism was similar to burning a candle. Some 50 years later, the law of conservation of energy (von Helmholtz 1847; von Mayer 1842) was clearly stated by two German scientists. This work in Germany stimulated Americans to develop equipment that could measure human metabolism (Atwater and Rosa 1899). With this equipment, they showed that the idea of energy balance applied to human beings just as it did to other animals. We were metabolically part of the same evolutionary animal kingdom.

While the basic science behind fatness was developing, the first popular weight reduction "diet" was published in London in 1863 (Banting 1864). William Banting, its author, was a layman. The first edition of his small pamphlet, titled Letter on Corpulence Addressed to the Public was published because Banting was thrilled with the success he achieved using a diet given to him by his doctor (Harvey 1872). It was high in protein and low in carbohydrate, and it aroused the same fervor in England at the time of our Civil War as have some of the modern popular diet books.

We made a major step forward when we recognized that overweight had many causes-a major achievement in the twentieth century. One type of overweight, although rare, is due to brain tumors that are often associated with impaired vision and glandular disturbances (Frohlich 1901; Babinski 1900). Shortly after this discovery, a famous American neurosurgeon, Dr. Harvey Cushing, showed in 1912 that a tumor in the "master gland" (the pituitary) could also produce overweight (Cushing 1912).

For more than half of the twentieth century, the life insurance industry did its best to convince Americans that being overweight was dangerous to health and tended to shorten lifespan (The Association of Life Insurance Medical Directors 1913). Industry leaders knew this from the money they had to pay out to settle death-benefit claims for insurance on people who were overweight. We now know that even modest increases in excess weight are associated with shortened lifespan (Adams et al. 2007; Whitlock et al. 2009).

Two other observations in the twentieth century were key to understanding obesity. The first was the discovery in 1994 of leptin, a peptide produced in fat that is involved in the regulation of food intake and other functions when calorie intake is reduced during starvation, and possibly to predict weight gain. The second was the publication of two articles that showed that losing weight prolongs life (Sjostrom et al. 2007; Adams et al. 2007). This had been predicted from the improvements in risk factors for diabetes and heart disease that occur with weight loss. The direct demonstration that voluntary weight loss prolongs life, however, was a necessary step forward.

Lessons Learned about Obesity in the Past 30 Years

Overweight as a problem came of age in the 1970s. The National Institutes of Health (NIH) are funded by American taxpayers to support basic research aimed at curing heart disease, diabetes, arthritis, cancer, and other diseases. In the late 1960s, the Fogarty International Center for Preventive Diseases at the National Institutes of Health was established to honor Congressman John E. Fogarty (1913–1967), a US Congressional Representative from the State of Rhode Island, who had been a long-time and vocal supporter of expanded research at the NIH. One of the first activities of the new Fogarty Center was to organize a Conference on Prevention of Obesity. "Obesity" was perceived, even in the 1970s, to be a major public health issue. This Conference was held at NIH in 1973 (Bray 1976b).

The impetus for the study of overweight given by the Fogarty Center Conference on Obesity was followed by the first in a series of International Congresses on Obesity. The first was held in London in 1974 (Howard 1975) Along with the development of these international meetings came the publication in 1976 of the first journal devoted specifically to obesity-the International Journal of Obesity. Tucked away at the same time was the first edition of my first book about obesity, The Obese Patient, published in 1976 (Bray 1976a).

The most important advance in obesity in recent years was the discovery of leptin (Zhang et al. 1994). This peptide hormone is made predominantly in the fat cells. When leptin is absent, massive overweight occurs in human beings and in research animals. Defects in the leptin receptor, the "lock" that the leptin molecule "key" fits into, are also responsible for a small number of massively overweight people (Farooqi and O'Rahilly 2007). In addition to derangements in the leptin genes, defects in other genes can produce obesity in human beings. One of these genes, called the melanocortin-4 receptor gene, is defective in up to 5% of markedly overweight youngsters (Farooqu and O'Rahilly 2007). This is one of the most frequent genetic causes for a chronic human disease. Yet, collectively, these individuals are only a tiny fraction of all obese people.

Behavior modification could be used to treat overweight subjects (Stuart and Davis 1972). As this technique was developed in detail (Chapter 6), it became one of the "three pillars," along with diet and exercise, for the treatment of obesity. Efforts have been made to adapt these behavioral techniques to prevent development of weight gain in large groups of people, but they have often been disappointing. Behavioral strategies are cognitive strategies, that is to say, they require you to do something active, such as dieting, exercising, or modifying the way you live. We are slowly learning that these cognitive strategies do not translate into the prevention of overweight, and the weight that people initially lose using them is often regained. The alternative to "cognitive" approaches are the "noncognitive" approaches, that is, ways of dealing with obesity that do not require much active individual involvement. An analogy in the prevention of dental caries ("cavities") can be used to make this distinction. Tooth-brushing and flossing regularly will reduce dental disease. These procedures are "cognitive" strategies since the individual has to remember to do them and actually do them. The addition of fluoride to the water supply is a noncognitive strategy that accomplished the same end. When our water was fluoridated, dental caries were dramatically reduced, without our volitional activity.

Several things may help prevent obesity and don't require much effort. Taking more calcium may be one of them. People with higher intakes of calcium have lower body weight in some, but not all, studies. The use of low fat dairy products, which are a good source of calcium, lower blood pressure, and are part of one of the diets I describe in Chapter 6.

Less sleep is associated with higher body weights. Children who sleep less gain more weight in their preschool years (Bray 2007b) (Chapter 3). This also applies to adults, and there is now a potential explanation for this effect in the changes of sleep on hormones.

Another low-effort strategy for weight loss would be to buy foods for "health," not for "price." Turning off that natural desire to get more for your money when buying food may be hard, but what you get for your money when you buy cheap food may be fat and fructose and added sugar, which may simply become "waste on your waist." It is better to eat well than to eat cheaply.

The fat cell is much more than where fat is stored (Flier 2004). It is a cell that plays a part in the daily orchestra of life. It makes music through the chemicals it produces. Sometimes the notes are beautiful, but they can also be discordant. With the discovery that leptin is made almost entirely in the fat cell, it has become clear that the fat cell has very significant functions besides storing fat. Fat cells are part of the largest glandular (endocrine) tissue in the body. They produce numerous products that are released into the circulation and that act on other cells. Among these are molecules that cause inflammation, molecules that are involved in controlling blood pressure or influencing cell growth, and molecules that regulate fat metabolism and blood clotting (Chapter 3).

The past 30 years have seen the development of a plethora of new drugs for the treatment of many diseases. Some of these medications produce weight gain (Chapters 3 and 5). Switching to alternative medications that do not cause weight gain is one approach the physician can take to this problem.

The commonly observed "beer-belly" in men or "apple shape" in women is medically termed "central adiposity." We have learned that central adiposity is a risk to health. This was first noted nearly 100 years ago, but it wasn't until the early 1980s (Larsson et al. 1984) that it became widely appreciated that people with central adiposity were at high risk for diabetes and heart disease. Waist circumference has become the standard way to measure central adiposity. It is also one of a group of signs and symptoms related to heart disease and diabetes, including high blood pressure, high blood sugar, low levels of HDL-cholesterol, and high levels of triglycerides.

Diets can reduce your risk of disease and provide a way to treat some of them effectively. This was shown elegantly in a study comparing the effects of three different dietary patterns on blood pressure (Appel et al. 1997; Sacks et al. 2001). The first diet, the reference diet, was a standard American diet or Western-type of diet, with plenty of fat, meat, and normal amounts of fruits and vegetables. The second diet, one of the two experimental diets, was called the fruits and vegetable diet because it was enriched with fruits and vegetables. The aim was to increase dietary intake of magnesium and potassium from fruits and vegetables to the seventy-fifth percentile of normal, that is, a level above what three out of four people would normally get in their diet. The third diet-the Combination or DASH Diet-was enriched to the same degree as the second diet with fruits and vegetables. In addition, it had more low fat dairy products to increase calcium intake and also had lowered total fat intake (27% vs. 33% in the control diet), more fiber, higher protein (18%) from the extra 3% from vegetable sources, and reduced intake of calorically sweetened beverages and other sweets. Blood pressure was significantly reduced in people eating the fruits and vegetables diet and reduced even more in the people eating the Combination (fruits, vegetables, low fat dairy products) or DASH diet (Appel et al. 1997; Sacks et al. 2001).

Another large clinical trial, called the Diabetes Prevention Program, showed that weight loss through reduced intake of calories and fat plus more physical activity could significantly reduce the risk of diabetes mellitus in people at high risk for this disease (The DPP Research Group) (Chapter 4). Modest weight loss can have important health benefits for people at risk for diabetes and other chronic metabolic diseases.

Obesity is a stigmatized condition. That is, there is prejudice against and dislike for the obese. The efforts, particularly among women, to lose weight and avoid this stigma cost billions of dollars per year.

In addition to the health benefits from weight loss, including prolonging life (Sjostrom et al. 2007; Adams et al. 2007), there is an improvement in the quality of life. Weight loss improves the ability to move and to get around. When weight loss is not sufficient to give a cosmetic benefit and improvements in quality of life people may not be willing to continue the effort needed to maintain a program of weight management. Set goals that you can accomplish and take small steps toward these goals.

Surgical treatment for obesity began in the 1960s. The current popularity of these procedures is the result of the lowered risk from surgery with the use of newer, so-called laparoscopic surgeries. Using laparoscopic techniques reduces the risk and has increased the number of treated patients. It is estimated that more than 200,000 people had this surgery in 2010. This approach to obesity is discussed in detail in Chapter 8.

This book has been divided into two parts:

Part I. Origins of Obesity

The Introduction and Chapter 1 put the ideas behind the development of current theories of obesity into an historical context. The Introduction covers the period from the Old Stone Age to the onset of scientific science in the beginning of the 1500s. Chapter 1 covers the period from the sixteenth through the nineteenth century. With Chapters 2 through 5, we move into the twentieth century and provide definitions of obesity and establish the prevalence of obesity and the mechanisms involved in the energy imbalance that produces obesity. The ill-consequences to health associated with increasing body fat, and the evaluation and prevention of obesity that are essential for trying to deal with the problem, are also discussed.

Part II. Treatment of Obesity

Effective treatments for obesity have been slow in developing. Prior to the twentieth century, diet and physical activity had been mainstays of advice for those with weight problems dating back 2500 years or more. The idea that obesity might reflect a maladaptive behavior leads to the concept of modifying this lifestyle with a set of techniques that are now part of most treatment programs (Chapter 6). With the dawn of the twentieth century, drugs developed by organic chemists based on the concept of a "lock and key" fit were introduced for the treatment of many diseases, including obesity (Chapter 7). Chapter 8 deals with surgery, which dates its introduction to the ideas of surgeons after World War II. With the introduction of fiber optic instruments that allowed laparoscopic surgery, the number of patients receiving surgical treatment for obesity ballooned to well over 200,000 per year (Chapter 8).

This book could not have been written without input over the years from many people, and the particular help of those now working with me. I am grateful to CRC Press for inviting me to write this monograph some 35 years after I wrote my first monograph in 1976. Dr. Greenway, a long term colleague from my years in Los Angeles, has provided input to the text as has my colleague Dr. Donna Ryan who has worked with me for the 20 years that I have been at the Pennington Biomedical Research Center. Preparation of the manuscript has been under the careful supervision of my editorial assistant Ms. Robin Post, to whom I acknowledge my debt of gratitude.