- Email: [email protected]
The downside of our technological revolution? An obesity-conducive environment
The Downside of Our Technological Revolution? An Obesity-Conducive Environment Barry A. Franklin, uring a recent flight to a scientific meeting, I was seated next to a pleasant 300-plus pound passenD ger. Both of us requested diet Cokes. Ironic, I thought. Considering the plethora of artificially sweetened beverages, diet, “light,” low-fat, no-fat, reduced calorie, and Olestra-laden products that are currently available—and yet, as a nation, we’re getting fatter and fatter. The latest figures show that more than half of all Americans are overweight or obese.1 Accordingly, there is a national obsession to be slim, with an astonishing 25 ⫾ 10% of Americans trying to lose weight at any given time of the year.2 Even the pharmaceutical industry has offered “solutions,” from amphetamines and thyroxine in the 1960s, to fenfluramine and phentermine (fen-phen), and now sibutramine in the 1990s. No nation in the history of the world has experienced the Y2K obesity problem that we have in the United States (US). In recent years, fashion designers have increasingly responded with elastic waistbands, “big and tall sizes,” and “loose-fit” styles. Moreover, the airlines have successfully marketed altered seat alignments and “more leg room” for their expanding passenger populations. In Baltimore, 19-inch seats in the old Memorial Stadium were replaced with 22-inch seats in their newly constructed ballpark, Camden Yards. Convenience or necessity? The proportion of US adults who are classified as obese (defined as a body mass index ⱖ30 kg/m2) rose 49% between 1991 and 1998, with the greatest increases among the youngest age group, college-educated, and those of Hispanic ethnicity.3 During this time period, obesity increased in every state, in both sexes, and across all age groups, races, educational levels, and smoking statuses. The skyrocketing prevalence of obesity has created a major public health concern,4 because it is strongly associated with several chronic diseases, including type 2 diabetes, coronary heart disease, and metabolic syndrome X, or, as it is also known, cardiac dysmetabolic syndrome.5 This syndrome, which increases the risk of coronary atherosclerosis, is related to insulin resistance, in which obesity is a primary factor. A From the Department of Medicine, Division of Cardiology (Cardiac Rehabilitation), William Beaumont Hospital, Royal Oak, Michigan. Manuscript received September 21, 2000; revised manuscript received and accepted November 27, 2000. Address for reprints: Barry A. Franklin, PhD, Cardiac Rehabilitation and Exercise Laboratories, Beaumont Rehabilitation and Health Center, 746 Purdy Street, Birmingham, Michigan 48009. E-mail: [email protected]. ©2001 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 87 May 1, 2001
PhD
higher prevalence of hypertension, osteoarthritis, and gallbladder disease is also associated with increasing obesity.6 In 1998, in response to an emerging body of scientific evidence, the American Heart Association reclassified obesity as a major modifiable risk factor for coronary heart disease.7 Moreover, it is currently estimated that mortality due to overweight and obesity is second only to cigarette smoking in the number of deaths that could be prevented by behavioral change.8 However, researchers cannot agree on why there has been an outbreak of obesity. Is it genes, the campaign to reduce cigarette smoking, gluttony, or sloth? Unquestionably, genetic factors predispose a significant portion of the population to becoming overweight. Available data suggest that the genetic contribution to individual variations in body weight and fat stores lies somewhere between 25% and 70%.9 –12 Nevertheless, there’s no evidence to suggest that the American genotype has changed over the past decade. Perhaps the campaign to reduce cigarette smoking, which has been effective, may be partly responsible? Smoking cessation is associated with a modest increase in caloric intake. Researchers have also shown that smoking 24 cigarettes over a 24-hour period increases the daily caloric expenditure by about 10%.13 Thus, caloric intake and energy expenditure can be expected to increase and decrease, respectively, when people stop smoking, thereby favoring a gain in body weight. Yet, the decrease in smoking itself is unlikely to explain the exponential rise in obesity, because the effect of smoking on weight is rather small and transient.14,15 Furthermore, it applies to ex-smokers only—a fraction of the population. Recently, a provocative report suggested that technologic advances provide the most likely explanation for the current rise in obesity.16 According to the theory, our current high-tech milieu has increasingly emphasized comfort and convenience with the development of time-saving and labor-saving devices, focusing on speed, rapid communication, improved efficiency, and increased productivity. In the current obesity-conducive environment, food has become readily accessible and, simultaneously, we have “engineered” physical activity out of our vocational and leisure-time pursuits. Our increased reliance on technology has resulted in constant pressure toward positive energy balance by promoting energy intake and discouraging physical activity (Figure 1).17 Food has become abundant and relatively inexpen0002-9149/01/$–see front matter PII S0002-9149(01)01467-9
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FIGURE 1. Influence of environmental factors on energy balance. When energy intake equals energy expenditure, the system is in energy balance. In the current obesity-conducive environment, factors (circled) on the left are driving energy intake up, and factors on the right are driving energy expenditure down, creating a state of positive energy balance, with a concomitant increase in body weight and fat stores. Adapted with permission from Hill and Melanson.17
sive. Vending machines dot our workplaces, distributing cheap, high-fat, high-calorie snacks. Most service stations now tempt us with an array of junk foods when we’re especially vulnerable, i.e., when we’re hungry, after work, or traveling long distances. In fact, proprietors estimate that 20% to 40% of all cash customers succumb to the aromatic and visual stimuli. Consequently, many of us end up fueling our cars and ourselves with “economy” grades. We have access to portions that dwarf those of past generations, which can be seen in “supersizing” (for a few pennies more) in fast-food restaurants, pizzapizza promotions (2 for the price of 1), and in the “giant” candy bars, oversized bagels (4 to 7 oz), and “big gulp” soft drinks (32 oz) that are currently available. Restaurant servings of 22- to 38-oz steaks and fish are no longer unusual, and appear to support the notion, “bigger is better.”18 In some movie theaters, a “medium” popcorn now contains 16 cups—and many order it “buttered.” Moreover, on an average day, nearly half of all adults are restaurant patrons and 21% of US households use some form of takeout or delivery. Because an increasing number of snacks and meals are now being eaten outside the home (or via carry-out), it has created an environment that promotes overeating. Yet, studies suggest that compared with the past few decades, when people were engaged in more physically demanding lifestyles, there has been only a slight increase or a very modest decline in total energy and fat intake.7,19 –22 Several investigators have pointed out an apparent paradox whereby obesity in the US has increased during this period, while cholesterol levels and dietary fat, expressed as a percentage of total calories, have slightly declined.19,21 Although the available self-reported data are suspect,23 because overweight people often underreport their caloric intake and overreport their caloric expenditure,24,25 it 1094 THE AMERICAN JOURNAL OF CARDIOLOGY姞
VOL. 87
appears the most likely explanation for the current obesity epidemic is a continued decline in energy expenditure that has not been matched by an equivalent reduction in energy intake.17 Physical education has been reduced or eliminated in many schools. Daily participation in physical education classes has declined among high school students from 42% in 1991 to 25% in 1995.26 Children seldom walk or ride bikes anymore (parents drive them), and physically demanding work has been largely ousted from the workplace. Household-related physical activity has also markedly declined with the proliferation of prepared foods and energy-saving devices such as washing machines, dishwashers, microwave ovens, self-propelled lawn mowers, and automatic garage door openers. Even these modern conveniences are becoming increasingly antedated and replaced by dry cleaners, restaurant eating or drivethroughs, and professional lawn services. Today, we can even order our groceries or do our shopping on-line. Physical labor has been and continues to be technologically engineered out of the American lifestyle.27 For example, in contrast to a decade ago, our luggage is now easily transported on wheels, guided by retractable handles. Moreover, modern airports are now strewn with parking lot shuttles, moving walkways, golf cart transport vehicles (for elderly, overweight, and unfit persons), elevators, and escalators. Many of us walk just 3,000 ⫾ 500 steps/day, corresponding to ⬃1.5 miles or 150 kilocalories! Much of our days involve extended driving time, desk work, sitting on or waiting for airplanes, meetings, teleconferences, computer interactions, or operating machines or conveyors that have replaced physically demanding work. Cellular phones, dictaphones, and laptop computers have become part of our vocational garb, exacerbating our hypokinetic state. Increasingly, we are paid to think, to provide specific sedentary skills, or to communicate or process information. Relative to our leisure-time activities, the US is the world’s leading innovator in passive entertainment,16 which generally involves sitting for extended periods. About half the leisure time of the average American is spent watching television—more often than not, using a remote control device. Other popular pasttimes include reading, video games, e-mailing others, searching the Internet, and gambling. Even the handles on our casino’s slot machines have been replaced or complemented by push buttons—to increase the speed and ease of gaming. According to the Physical Activity and Health report by the Surgeon General, low levels of activity, resulting in fewer kilocalories used than consumed, contribute to the high prevalence of obesity in the US.26 Recent physical activity prevalence data are particularly troubling. More than 60% of American adults are not regularly physically active, and 25% of the adult population report no physical activity in their leisure time.26 Moreover, it appears that vigorous exercise is not unlike other health-related behaviors in MAY 1, 2001
that only a fraction of those who initiate the behavior will continue, irrespective of initial health status or the type of conditioning regimen.28 The evidence supporting physical inactivity as a major cause of obesity in the US is overwhelming. The issue is not information but methods, motivation, and behavioral changes; everyone knows how to lose weight— either you eat less, exercise more, or do both (ideally)— but few are able to muster the strategies and sustained self-discipline to cope with an increasingly challenging environment. Those who do should be able to successfully achieve and maintain an ideal body weight.29 Those who do not? More than likely, they will continue to embrace the opinion of an earlier observer who stated, “There is a divinity that shapes our ends.”30 1. Expert Panel. Executive summary of the clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults. Arch Intern Med 1998;158:1855–1867. 2. Kassirer JP, Angell M. Losing weight—an ill-fated New Year’s resolution. N Engl J Med 1998;338:52–54. 3. Mokdad AH, Serdula MK, Dietz WH, Bowman BA, Marks JS, Koplan JP. The spread of the obesity epidemic in the United States, 1991–1998; JAMA 1999: 282:1519 –1522. 4. Booth FW, Gordon SE, Carlson CJ, Hamilton MT. Waging war on modern chronic diseases: primary prevention through exercise biology. J Appl Physiol 2000;88:774 –787. 5. Jung RT. Obesity as a disease. Br Med Bull 1997;53:307–321. 6. Must A, Spadano J, Coakley EH, Field AE, Colditz G, Dietz WH. The disease burden associated with overweight and obesity. JAMA 1999;282:1523–1529. 7. Eckel RH, Krauss RM. American Heart Association call to action: obesity as a major risk factor for coronary heart disease. Circulation 1998;97:2099 –2100. 8. McGinnis JM, Foege WH. Actual causes of deaths in the United States. JAMA 1993;270:2207–2212. 9. Bouchard C, Savard R, Despres JP, Tremblay A, Leblanc C. Body composition in adopted and biological siblings. Hum Biol 1985;57:61–75. 10. Cardon LR, Carmelli D, Fabsitz RR, Reed T. Genetic and environmental correlations between obesity and body fat distribution in adult male twins. Hum Biol 1994;66:465– 479. 11. Stunkard AJ, Foch TT, Hrubec Z. A twin study of human obesity. JAMA 1986;256:51–54. 12. Stunkard AJ, Sorensen TI, Hanis C, Teasdale TW, Chakraborty R, Schull WJ,
Schulsinger F. An adoption study of human obesity. N Engl J Med 1986;314: 193–198. 13. Hofstetter A, Schutz Y, Je´quier E, Wahren J. Increased 24-hour energy expenditure in cigarette smokers. N Engl J Med 1986;314:79 – 82. 14. Green MS, Harari G. A prospective study of the effects of changes in smoking habits on blood count, serum lipids and lipoproteins, body weight and blood pressure in occupationally active men. The Israeli CORDIS Study. J Clin Epidemiol 1995;48:1159 –1166. 15. Flegal KM, Troiano RP, Pamuk ER, Kuczmarski RJ, Campbell SM. The influence of smoking cessation on the prevalence of overweight in the United States. N Engl J Med 1995;333:1165–1170. 16. Franklin BA. Losing weight without vigourous exercise: unfounded gadgets, gimmicks, and fraudulent claims. J Hong Kong Coll Cardiol 2001;9(suppl.):71– 77. 17. Hill JO, Melanson EL. Overview of the determinants of overweight and obesity: current evidence and research issues. Med Sci Sports Exerc 1999;31: S515-S521. 18. Young LR, Nestle M. Variation in perceptions of a medium food portion: implications for dietary guidance. J Am Diet Assoc 1998;98:458 – 459. 19. Ernst N, Obarzanek DE, Clark MB, Briefel RR, Brown CD, Donato K. Cardiovascular health risks related to overweight. J Am Diet Assoc 1997;97:S47–S51. 20. Federation of American Societies for Experimental Biology, LS, Research Office. Food Consumption and Nutrient Intake. In: Third Report in Nutrition Monitoring in the United States. Document No. A77.2:N95/2/V.1-2.Washington, DC: US Government Printing Office, 1995:148 –149. 21. Heini AF, Weinsier RL. Divergent trends in obesity and fat intake patterns: the American paradox. Am J Med 1997;102:259 –264. 22. De Castro JM. Socio-cultural determinants of meal size and frequency. Br J Nutr 1997;77(suppl 1):S39 –S55. 23. Jebb SA. Aetiology of obesity. Br Med Bull 1997;53:264 –285. 24. Lichtman SW, Pisarska K, Berman ER, Pestone M, Dowling H, Offenbacher E, Weisel H, Heshka S, Matthews DE, Heymsfield SB. Discrepancy between self-reported and actual caloric intake and exercise in obese subjects. N Engl J Med 1992;327:1893–1898. 25. Jakicic JM, Polley BA, Wing RR. Accuracy of self-reported exercise and the relationship with weight loss in overweight women. Med Sci Sports Exerc 1998;30:634 – 638. 26. United States Department of Health, and Human Services. Physical activity and health: a report of the Surgeon General. Document No. S/N 017-02300196-5. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, 1996. 27. Koplan JP, Dietz WH. Caloric imbalance and public health policy. JAMA 1999;282:1579 –1581. 28. American College of Sports Medicine. ACSM’s Guidelines for Exercise Testing, and Prescription. 6th ed. Baltimore, MD: Lippincott Williams & Wilkins, 2000. 29. Roberts WC. Obtaining and maintaining an ideal body weight. Am J Cardiol 1999;83:639. 30. Shakespeare W. Hamlet, Prince of Denmark, Act V, Sc 2.
EDITORIAL
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PhD
higher prevalence of hypertension, osteoarthritis, and gallbladder disease is also associated with increasing obesity.6 In 1998, in response to an emerging body of scientific evidence, the American Heart Association reclassified obesity as a major modifiable risk factor for coronary heart disease.7 Moreover, it is currently estimated that mortality due to overweight and obesity is second only to cigarette smoking in the number of deaths that could be prevented by behavioral change.8 However, researchers cannot agree on why there has been an outbreak of obesity. Is it genes, the campaign to reduce cigarette smoking, gluttony, or sloth? Unquestionably, genetic factors predispose a significant portion of the population to becoming overweight. Available data suggest that the genetic contribution to individual variations in body weight and fat stores lies somewhere between 25% and 70%.9 –12 Nevertheless, there’s no evidence to suggest that the American genotype has changed over the past decade. Perhaps the campaign to reduce cigarette smoking, which has been effective, may be partly responsible? Smoking cessation is associated with a modest increase in caloric intake. Researchers have also shown that smoking 24 cigarettes over a 24-hour period increases the daily caloric expenditure by about 10%.13 Thus, caloric intake and energy expenditure can be expected to increase and decrease, respectively, when people stop smoking, thereby favoring a gain in body weight. Yet, the decrease in smoking itself is unlikely to explain the exponential rise in obesity, because the effect of smoking on weight is rather small and transient.14,15 Furthermore, it applies to ex-smokers only—a fraction of the population. Recently, a provocative report suggested that technologic advances provide the most likely explanation for the current rise in obesity.16 According to the theory, our current high-tech milieu has increasingly emphasized comfort and convenience with the development of time-saving and labor-saving devices, focusing on speed, rapid communication, improved efficiency, and increased productivity. In the current obesity-conducive environment, food has become readily accessible and, simultaneously, we have “engineered” physical activity out of our vocational and leisure-time pursuits. Our increased reliance on technology has resulted in constant pressure toward positive energy balance by promoting energy intake and discouraging physical activity (Figure 1).17 Food has become abundant and relatively inexpen0002-9149/01/$–see front matter PII S0002-9149(01)01467-9
1093
FIGURE 1. Influence of environmental factors on energy balance. When energy intake equals energy expenditure, the system is in energy balance. In the current obesity-conducive environment, factors (circled) on the left are driving energy intake up, and factors on the right are driving energy expenditure down, creating a state of positive energy balance, with a concomitant increase in body weight and fat stores. Adapted with permission from Hill and Melanson.17
sive. Vending machines dot our workplaces, distributing cheap, high-fat, high-calorie snacks. Most service stations now tempt us with an array of junk foods when we’re especially vulnerable, i.e., when we’re hungry, after work, or traveling long distances. In fact, proprietors estimate that 20% to 40% of all cash customers succumb to the aromatic and visual stimuli. Consequently, many of us end up fueling our cars and ourselves with “economy” grades. We have access to portions that dwarf those of past generations, which can be seen in “supersizing” (for a few pennies more) in fast-food restaurants, pizzapizza promotions (2 for the price of 1), and in the “giant” candy bars, oversized bagels (4 to 7 oz), and “big gulp” soft drinks (32 oz) that are currently available. Restaurant servings of 22- to 38-oz steaks and fish are no longer unusual, and appear to support the notion, “bigger is better.”18 In some movie theaters, a “medium” popcorn now contains 16 cups—and many order it “buttered.” Moreover, on an average day, nearly half of all adults are restaurant patrons and 21% of US households use some form of takeout or delivery. Because an increasing number of snacks and meals are now being eaten outside the home (or via carry-out), it has created an environment that promotes overeating. Yet, studies suggest that compared with the past few decades, when people were engaged in more physically demanding lifestyles, there has been only a slight increase or a very modest decline in total energy and fat intake.7,19 –22 Several investigators have pointed out an apparent paradox whereby obesity in the US has increased during this period, while cholesterol levels and dietary fat, expressed as a percentage of total calories, have slightly declined.19,21 Although the available self-reported data are suspect,23 because overweight people often underreport their caloric intake and overreport their caloric expenditure,24,25 it 1094 THE AMERICAN JOURNAL OF CARDIOLOGY姞
VOL. 87
appears the most likely explanation for the current obesity epidemic is a continued decline in energy expenditure that has not been matched by an equivalent reduction in energy intake.17 Physical education has been reduced or eliminated in many schools. Daily participation in physical education classes has declined among high school students from 42% in 1991 to 25% in 1995.26 Children seldom walk or ride bikes anymore (parents drive them), and physically demanding work has been largely ousted from the workplace. Household-related physical activity has also markedly declined with the proliferation of prepared foods and energy-saving devices such as washing machines, dishwashers, microwave ovens, self-propelled lawn mowers, and automatic garage door openers. Even these modern conveniences are becoming increasingly antedated and replaced by dry cleaners, restaurant eating or drivethroughs, and professional lawn services. Today, we can even order our groceries or do our shopping on-line. Physical labor has been and continues to be technologically engineered out of the American lifestyle.27 For example, in contrast to a decade ago, our luggage is now easily transported on wheels, guided by retractable handles. Moreover, modern airports are now strewn with parking lot shuttles, moving walkways, golf cart transport vehicles (for elderly, overweight, and unfit persons), elevators, and escalators. Many of us walk just 3,000 ⫾ 500 steps/day, corresponding to ⬃1.5 miles or 150 kilocalories! Much of our days involve extended driving time, desk work, sitting on or waiting for airplanes, meetings, teleconferences, computer interactions, or operating machines or conveyors that have replaced physically demanding work. Cellular phones, dictaphones, and laptop computers have become part of our vocational garb, exacerbating our hypokinetic state. Increasingly, we are paid to think, to provide specific sedentary skills, or to communicate or process information. Relative to our leisure-time activities, the US is the world’s leading innovator in passive entertainment,16 which generally involves sitting for extended periods. About half the leisure time of the average American is spent watching television—more often than not, using a remote control device. Other popular pasttimes include reading, video games, e-mailing others, searching the Internet, and gambling. Even the handles on our casino’s slot machines have been replaced or complemented by push buttons—to increase the speed and ease of gaming. According to the Physical Activity and Health report by the Surgeon General, low levels of activity, resulting in fewer kilocalories used than consumed, contribute to the high prevalence of obesity in the US.26 Recent physical activity prevalence data are particularly troubling. More than 60% of American adults are not regularly physically active, and 25% of the adult population report no physical activity in their leisure time.26 Moreover, it appears that vigorous exercise is not unlike other health-related behaviors in MAY 1, 2001
that only a fraction of those who initiate the behavior will continue, irrespective of initial health status or the type of conditioning regimen.28 The evidence supporting physical inactivity as a major cause of obesity in the US is overwhelming. The issue is not information but methods, motivation, and behavioral changes; everyone knows how to lose weight— either you eat less, exercise more, or do both (ideally)— but few are able to muster the strategies and sustained self-discipline to cope with an increasingly challenging environment. Those who do should be able to successfully achieve and maintain an ideal body weight.29 Those who do not? More than likely, they will continue to embrace the opinion of an earlier observer who stated, “There is a divinity that shapes our ends.”30 1. Expert Panel. Executive summary of the clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults. Arch Intern Med 1998;158:1855–1867. 2. Kassirer JP, Angell M. Losing weight—an ill-fated New Year’s resolution. N Engl J Med 1998;338:52–54. 3. Mokdad AH, Serdula MK, Dietz WH, Bowman BA, Marks JS, Koplan JP. The spread of the obesity epidemic in the United States, 1991–1998; JAMA 1999: 282:1519 –1522. 4. Booth FW, Gordon SE, Carlson CJ, Hamilton MT. Waging war on modern chronic diseases: primary prevention through exercise biology. J Appl Physiol 2000;88:774 –787. 5. Jung RT. Obesity as a disease. Br Med Bull 1997;53:307–321. 6. Must A, Spadano J, Coakley EH, Field AE, Colditz G, Dietz WH. The disease burden associated with overweight and obesity. JAMA 1999;282:1523–1529. 7. Eckel RH, Krauss RM. American Heart Association call to action: obesity as a major risk factor for coronary heart disease. Circulation 1998;97:2099 –2100. 8. McGinnis JM, Foege WH. Actual causes of deaths in the United States. JAMA 1993;270:2207–2212. 9. Bouchard C, Savard R, Despres JP, Tremblay A, Leblanc C. Body composition in adopted and biological siblings. Hum Biol 1985;57:61–75. 10. Cardon LR, Carmelli D, Fabsitz RR, Reed T. Genetic and environmental correlations between obesity and body fat distribution in adult male twins. Hum Biol 1994;66:465– 479. 11. Stunkard AJ, Foch TT, Hrubec Z. A twin study of human obesity. JAMA 1986;256:51–54. 12. Stunkard AJ, Sorensen TI, Hanis C, Teasdale TW, Chakraborty R, Schull WJ,
Schulsinger F. An adoption study of human obesity. N Engl J Med 1986;314: 193–198. 13. Hofstetter A, Schutz Y, Je´quier E, Wahren J. Increased 24-hour energy expenditure in cigarette smokers. N Engl J Med 1986;314:79 – 82. 14. Green MS, Harari G. A prospective study of the effects of changes in smoking habits on blood count, serum lipids and lipoproteins, body weight and blood pressure in occupationally active men. The Israeli CORDIS Study. J Clin Epidemiol 1995;48:1159 –1166. 15. Flegal KM, Troiano RP, Pamuk ER, Kuczmarski RJ, Campbell SM. The influence of smoking cessation on the prevalence of overweight in the United States. N Engl J Med 1995;333:1165–1170. 16. Franklin BA. Losing weight without vigourous exercise: unfounded gadgets, gimmicks, and fraudulent claims. J Hong Kong Coll Cardiol 2001;9(suppl.):71– 77. 17. Hill JO, Melanson EL. Overview of the determinants of overweight and obesity: current evidence and research issues. Med Sci Sports Exerc 1999;31: S515-S521. 18. Young LR, Nestle M. Variation in perceptions of a medium food portion: implications for dietary guidance. J Am Diet Assoc 1998;98:458 – 459. 19. Ernst N, Obarzanek DE, Clark MB, Briefel RR, Brown CD, Donato K. Cardiovascular health risks related to overweight. J Am Diet Assoc 1997;97:S47–S51. 20. Federation of American Societies for Experimental Biology, LS, Research Office. Food Consumption and Nutrient Intake. In: Third Report in Nutrition Monitoring in the United States. Document No. A77.2:N95/2/V.1-2.Washington, DC: US Government Printing Office, 1995:148 –149. 21. Heini AF, Weinsier RL. Divergent trends in obesity and fat intake patterns: the American paradox. Am J Med 1997;102:259 –264. 22. De Castro JM. Socio-cultural determinants of meal size and frequency. Br J Nutr 1997;77(suppl 1):S39 –S55. 23. Jebb SA. Aetiology of obesity. Br Med Bull 1997;53:264 –285. 24. Lichtman SW, Pisarska K, Berman ER, Pestone M, Dowling H, Offenbacher E, Weisel H, Heshka S, Matthews DE, Heymsfield SB. Discrepancy between self-reported and actual caloric intake and exercise in obese subjects. N Engl J Med 1992;327:1893–1898. 25. Jakicic JM, Polley BA, Wing RR. Accuracy of self-reported exercise and the relationship with weight loss in overweight women. Med Sci Sports Exerc 1998;30:634 – 638. 26. United States Department of Health, and Human Services. Physical activity and health: a report of the Surgeon General. Document No. S/N 017-02300196-5. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, 1996. 27. Koplan JP, Dietz WH. Caloric imbalance and public health policy. JAMA 1999;282:1579 –1581. 28. American College of Sports Medicine. ACSM’s Guidelines for Exercise Testing, and Prescription. 6th ed. Baltimore, MD: Lippincott Williams & Wilkins, 2000. 29. Roberts WC. Obtaining and maintaining an ideal body weight. Am J Cardiol 1999;83:639. 30. Shakespeare W. Hamlet, Prince of Denmark, Act V, Sc 2.
EDITORIAL
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