I am fascinated by the convergence of seemingly unrelated evidence to form a new model of thought. For example, in mammals, gonadal failure induces bone loss,1 whereas obesity appears to prevent bone loss through an unknown mechanism.2 New discoveries recently have provided evidence that a small polypeptide hormone called leptin, which is secreted by fat cells, controls body weight and, directly or indirectly, gonadal function after binding to a specific receptor located in the hypothalamus.3 All this leads me to wonder if brain function could control obesity, gonadal function and osteoporosis.
In this column, I explore the significant risks of obesity and highlight the counterintuitive relationship between obesity, brain and gonadal functions, and osteoporosis. Osteoporosis is the most common disease in the Western Hemisphere, and its prevalence is increasing in both men and women. This is of particular significance to the part of our society that is becoming older, less physically active and more often obese. Ironically, these diseases and conditions start during childhood and adolescence.
Humans did not evolve as sedentary mammals, but our present human condition appears to provide fewer opportunities for physical exertion than ever before. We are increasingly "auto-centered"; only 10 percent of U.S. trips are by bicycle or on foot, compared with 40 percent of trips in European cities.4 Each day, men average 81 minutes behind the wheel of an automobile, and women average 64 minutes.5
Coupled with our choice to be sedentary is our continued affinity for certain tastes, which once helped us find the calories necessary to stay alive. We like sweet things; to our prehistoric ancestors sweet meant fruits and nutritious and nonpoisonous foods. We also like the taste of fat; our prehistoric ancestors needed all the calories they could get, and fats are packed with them—nine calories per gram, compared with four calories per gram in proteins and carbohydrates.
Throughout human history, the basic desires for sweets and fats were not so different from what they are today. As little as a century ago, however, people exercised often by necessity. Townships and urban centers were designed and built for foot travel. Children walked to school and played outdoors until darkness fell. In 1900, most Americans lived in rural communities and worked at hard labor in fields such as agriculture or mining. And sweet and fatty foods were harder to come by.
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OBESITY
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The body mass index, or BMI, is calculated from a person’s weight in kilograms divided by the square of the person’s height in meters (pounds and inches can be substituted for the metric units if the number of pounds is multiplied by 704.5, a conversion factor).7 BMIs between 18.5 and 24.9 define "normal," BMIs between 25 and 30 define "overweight," and BMIs greater than 30 define "obesity."
Obesity is the result of a complicated mix of social, cultural, behavioral, genetic and physiological factors. In the United States, a link exists between weight and socioeconomic status: the proportion of adolescents from low-income households who are overweight is almost twice that of adolescents from middle- and high-income households.6 In women, being overweight is more prevalent among women with lower incomes and less education.7
In the United States, being overweight and obese now affects 107 million adults7,8—nearly three out of every five—an increase of nearly 25 percent over the past 30 years.7 These are epidemic proportions.
In 1900, the leading cause of death was pneumonia; tuberculosis and diarrhea were second and third, respectively. Heart disease was fourth and was responsible for 6.1 percent of all deaths in the United States. Today, heart disease is the leading cause of death, responsible for 31.4 percent of all deaths. Cancer, stroke and pulmonary disease follow. Together, these four diseases kill two out of every three Americans.8 As many as 30 health conditions have been associated with obesity, including heart disease, diabetes, high blood pressure, stroke and some forms of cancer.9
Children and excess weight.
Today, one in five children are overweight—a 50 percent increase over the past three decades.10 Overweight children are at high risk of becoming overweight or obese adolescents and adults, and obese children 10 to 13 years of age have a 70 percent chance of becoming obese adults.10,11 Since 1975, the prevalence of obesity in children 6 to 11 years of age has nearly tripled for boys and increased nearly 2.5 times for girls. In adolescents—children 12 to 17 years of age—the obesity rate has doubled for boys and increased 1.5 times for girls.
Obesity is the result of a complicated mix of social, cultural, behavioral, genetic and physiological factors.
Childhood obesity is much more common among minorities than among whites; African-Americans, Hispanics, Pacific Islanders and Native Americans have high rates of childhood obesity.10,12 Beyond increasing the likelihood of being overweight adults, the consequences of obesity in children and adolescents are not as well-defined as are those in adults, but adverse health effects have been observed. Overweight and obese children are more likely to have severe asthma, orthopedic complications, Type II diabetes and high blood pressure.12 Type II diabetes accounted for as little as 2 percent of all childhood diabetes in 1992; two years later it accounted for 16 percent. Overweight children are more than 12 times as likely to have high fasting blood glucose levels—a risk factor for diabetes—than are normal-weight children. They also are nine times more likely than normal-weight children to experience elevated blood pressure levels.10–12
Healthy People 2010.
Improving the health of children and adults is the aim of the Healthy People plan. In January, the Department of Health and Human Services presented the Healthy People 2010 plan, or HP 2010, a next step from the Healthy People 2000 plan. With 467 objectives in 28 focus areas—including oral health—the evidence-based plan is wide in scope and impressive in its goals.8 Reducing the prevalence of obesity and increasing physical activity are two focuses of the plan.
Not surprisingly, children in our nation are not choosing to exercise as much as in the past. Today, only 20 percent of high-school students engage in moderate physical activity at least five times a week. School-based physical activity also has been on the decline. As part of HP 2010, Surgeon General David Satcher, M.D., Ph.D., has asked for an increase in physical activity during school hours, and for schools to provide after-school and year-round access to playing fields and gymnasiums.8
All too often, adults also are not choosing to exercise. According to HP 2010,8 in 1997 only 15 percent of adults engaged in regular moderate activity such as walking, swimming or dancing, and 23 percent engaged in vigorous activity such as jogging or swimming laps. Forty percent of adult Americans engaged in no leisure-time physical activity,6 and the remaining 22 percent exercised infrequently. Regular physical activity is not an absolute requirement to control weight, but it does enhance the management of body weight and well-being. Moderate exercise is associated with lower death rates, decreases the risk of death from heart disease, lowers the risk of developing diabetes and is associated with a decreased risk of colon cancer. It also reduces and controls blood pressure.8
Overall in our society, neither children nor adults eat well. According to HP 2010, only 3 percent of Americans are eating at least the three recommended servings of vegetables a day, and only 28 percent eat at least the two recommended servings of fruit per day. The HP 2010 goals include increasing these numbers to 50 and 75 percent, respectively, by the end of this decade.8
Dentistry is well-positioned to motivate, inform and educate the families and communities we serve to make health choices that include regular exercise and healthy foods. The dental profession fully understands the challenge of modifying human behaviors for oral hygiene; for example, brushing, flossing and tobacco cessation are simple in theory, yet seemingly difficult in practice. Benefits of healthy behaviors may take weeks, months or years to be seen, and months can feel like eons to many in our high-speed, hyperscheduled, instant-gratification society.
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EFFECTS OF OBESITY ON HEALTH
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Being overweight or obese substantially raises a person’s risk of developing diseases and illnesses such as high blood pressure, high cholesterol, Type II diabetes, heart disease and stroke, gallbladder disease, arthritis, sleep disturbances and breathing problems, as well as endometrial, breast, prostate and colon cancers. For example:
- – Men with a BMI of at least 40 have 18 times the prevalence of Type II diabetes and 21 times the prevalence of gallbladder disease as do normal-weight men.7
- – Women with BMIs of at least 40 have 13 times the prevalence of Type II diabetes and five times the prevalence of gall-bladder disease as do normal-weight women.7
- – Obese adults are at a sixfold risk of developing hypertension compared with normal-weight adults.
- – More than 75 percent of hypertension cases can be directly attributable to excess weight.10
- – Among patients with obstructive sleep apnea, up to 70 percent are obese.10
Thwarting weight gain and obesity is a challenge for health professionals and for their patients. Socially, overweight and obese people also can suffer from stigmatization, discrimination and low self-esteem.8 Contrary to statistics suggesting that many people who lose weight gain it back, other studies have found that many people succeed in losing weight and keeping it off.13–15
The consequences of not reducing or eliminating obesity are dire beyond the health effects. The 1995 costs of obesity in medical costs and lost productivity were $99 billion.8,9,14
Obesity: a network of genes in fat cells, brain, gonads and bone? Why can some people seemingly eat whatever they wish and remain thin, while others eat healthy meals and are overweight? How much of a tendency for being overweight is in the genes, and how much is related to learned behaviors? These are not simple questions with simple answers. The American Obesity Association states that although obesity is "a chronic disease with a familial component," the tendency toward obesity is "fostered by ... lack of physical activity combined with abundant, tasty, high-fat food."15 Like any nature vs. nurture question, the best answer is not one or the other, but both. Results from studies of twins and adopted children show a heritability of obesity of 30 to 40 percent; 30 to 40 percent of their obesity is caused by said genes and the rest is from poorly controlled behaviors. This heritability comes from multiple genes, each exerting its own effects. More than 70 genes have been chronicled as having an effect on obesity, either in animal models or humans.16
One of these genes is the obesity gene, or ob, found on human chromosome 7; it encodes for the small polypeptide hormone leptin, which has been studied extensively with regard to obesity.16 Leptin is synthesized and secreted from fat cells and acts as a signal or ligand that binds to a specific receptor located predominantly in the hypothalamus; this signal transduction appears to control appetite and energy expenditure.16 Studies in humans suggest that some obese people are less sensitive to leptin-mediated instructions; they don’t recognize when they are no longer hungry. In some types of obesity, loss of function mutations in either the leptin hormone gene or the leptin receptor gene may be the cause of the disease or condition.17
In January, scientists reported that leptin inhibits bone formation through a hypothalamic relay mechanism that provides a centralized control for bone mass.18 Using transgenic mouse models that represent either leptin deficiency or leptin-receptor deficiency, these investigators discovered a novel regulatory loop or network that integrates obesity, brain and gonadal functions, and osteoporosis into a new thought model.18
Agouti-related protein, or AGRP, also seems to be involved in appetite regulation. AGRP and leptin seem to work against one another; AGRP induces food intake, while leptin comes into play when appetite has been satiated.19 In leptin-null mutation mice that exhibit leptin deficiency and are obese, AGRP is consistently produced at high levels, which drop when normal leptin is given. In normal mice, AGRP is produced at high levels during fasting but not at other times.19 Neuropeptide Y and the melanocortin 4 receptor, or MC4-R, are additional candidate genes that may become very important for gene-based drug discovery to manage obesity, as well as osteoporosis. Neuropeptide Y stimulates increased appetite and decreased energy use.20 MC4-R reduces appetite and increases energy use.21
Clearly, obesity is a complex human disease. Obesity likely reflects multiple mutated or variant genes, multiple gene-gene interactions and multiple gene-environment interactions that result in a predilection to store excess calories as fat, in conjunction with behavioral effects such as overeating and low levels of physical activity. Of course, a few types of obesity result from predominant loss-of-function genetic mutations. When administered leptin, a child with a mutation in the leptin gene lost weight and reduced food intake.17 Although such cases are relatively rare, the study provides possible solutions to the complicated problems involved in the molecular physiology of weight regulation and the relationship of weight regulation with osteoporosis.
Future research will increasingly use molecular biology tools that are fueled by emerging technologies such as bioinformatics and coupled with DNA microarray gene chips that enable dissection of thousands of gene functions at one time. The completion of the Human Genome Project by 2003 will offer a complete human genetic lexicon. These and many other scientific and technological advances will drive the fields of functional genomics and proteomics and perhaps lead to treatments for obesity, brain and gonadal functions, and osteoporosis that can be used in combination with behavior interventions that result in healthy choices for foods and physical exercise.
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CONCLUSION
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Dental health professionals must become more involved in opportunities to promote health and reduce disease. A recent study found that of more than 9,000 adults only one-third reported being counseled about exercise at their last physician visit. Women, older patients, higher-income (above $50,000 annually) patients and patients with a college education were more likely to be counseled compared with their counterparts. Those already overweight and obese, as well as those with heart disease and diabetes, also were more likely to be counseled.22
It is in the best interest of patients, particularly those who most need and can benefit from our counsel—those with lower education and income levels, as well as children and adolescents—that dental professionals promote diet and exercise programs that inform, educate and motivate.
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OBESITY
EFFECTS OF OBESITY ON...
