QJM vol. 97 no. 12 © Association of Physicians 2004; all rights reserved.
Commentary |
The obesity epidemic: prospects for prevention
From the 1Department of Health and Human Sciences, University of Essex, Wivenhoe, and 2Department of Epidemiology and Public Health, Queen's University of Belfast, Belfast, UK
| Summary |
|---|
|
|
|---|
Some 2025% of UK adults are obese according to the WHO criterion (BMI
30 kg/m2). Type 2 diabetes, increasingly recognized as a major complication of overweight and obesity, is beginning to appear in UK adolescents, following the trends in the US. Epidemiological data indicate that the prevalence of overweight and obesity has doubled or tripled in the past few decades in the US, in Europe, and even in many developing countries. Thus obesity is increasingly seen as a public health problem requiring concerted action by both governmental and non-governmental organizations. A sound understanding of the root causes is crucial, if strategies for the prevention and treatment of this epidemic are to be developed. Many epidemiological studies suggest that physical activity at work, school or at leisure has declined to minimal levels, and that sedentary behaviours such as television viewing and computer games have become major pastimes. Thus energy requirements are substantially less than those for recent generations. Further, the food industry produces high-calorie foods which children and adults consume as snack meals, giving a substantial surfeit to their daily energy requirement. In children, a few school-based, preventive intervention trials have shown some promising results. Many negative trials have also been reported, and practical difficulties remain in the widespread implementation of appropriate protocols. Initiatives have been introduced by the government to increase the physical education syllabus in school to a minimum of 2 h/week, and the promotion of fruit and vegetables. Further research is required on the physiological and psychological causes of overweight and obesity in children and adults, and randomized, controlled, school and community-based trials are required to pilot preventative initiatives. Monitoring of the progress in prevention at both organizational and outcome level is required, and also of adverse outcomes such as a rise in the prevalence of eating disorders. | Introduction |
|---|
|
|
|---|
We have always had fat patients, whose personalities are as varied as the next person's (see Figure 1), but increasingly excess weight is becoming seen as a public health problem rather than one just for the individual patient and their physician. Recognition of the complications of excess weight and of the scale of the problem has led to the forecast that obesity will soon overtake the smoking habit as the predominant preventable cause of death in Western countries.1,2
|
| Definition and complications |
|---|
|
|
|---|
Garrow has proposed a simple definition of overweight and obesity as a condition in which body fat stores are charged to an extent which impairs health.3 In the 1940s and 1950s, insurance companies published tables of desirable weights, which were based on their own mortality data. More recently epidemiological studies have used Quetelet's index of body weight standardized for height (kg/m2) and, on the basis of data from these studies, the normal (desirable) range lies between 18.5 and 24.9 kg/m2, with overweight defined as 25.0 to 29.9 kg/m2 and obesity as 30.0+ kg/m2. The World Health Organization (WHO) classification4 is shown in Table 1.
|
The subcategories of obesity (IIII) are more likely to be of clinical use, rather than for epidemiological monitoring, as the more severe grades of obesity are unlikely to be well represented in epidemiological surveys. There has been recent interest in central obesity as measured by the waist-hip ratio. But the evidence that central obesity provides a better risk marker than BMI for future cardiovascular disease and insulin resistance remains controversial,5,6 and secular trend data are lacking. Globally, 58% of cases of type 2 diabetes, 21% of coronary heart disease, and between 8% and 42% of some cancers are attributable to overweight and obesity.7
| Prevalence and trends: adults and children |
|---|
|
|
|---|
The International Obesity Task Force2 indicates that the prevalence of obesity in European adults is between 1025% in women and 1020% in men and that the prevalence has increased by 1040% in Europe in the past 10 years. The scale of the epidemic in England in adults and in children is shown in Box 1.
| Box 1 Obesity in England, 19802002: some summary facts
|
Whilst the BMI cut-points for adults of 25 kg/m2 and 30 kg/m2 for overweight and obesity have been established worldwide, there was no commonly accepted standard of determining overweight and obesity in children until Cole et al.11 published reference curves for children aged 218 years based on pooled data from several countries; cut-points for BMI at 6-monthly increments in age, which correspond to the percentiles of children with a BMI of 25 kg/m2 (overweight) or 30 kg/m2 (obese) at 18 years of age are used. Previously childhood obesity had been defined in various ways: weight for height percentiles, percent of ideal body weight and absolute weight,12 etc., and therefore it was difficult to make comparisons of prevalence and trends between and within populations. In the US, the Surgeon General has reported that 15.3% of 611-year-olds and 15.5% of 1219-year-olds are considered obese,13 and the heaviest children are getting heavier.14 In Australia, 23% children are overweight, with a further 6% being obese.15 The prevalence of overweight is also increasing in many countries with transitional economies such as Brazil and China;16 although in Russia, overweight decreased from 15.6% to 9.0% in children and adolescents, but this is more likely to be due to problems with food distribution and availability, than to good dietary practice.16 Trends in central obesity, measured by waist circumference, have greatly exceeded the trends in BMI in children aged 1116 years between 1977 and 1997 in Britain,17 but waist circumference has not been adopted as an international standard. A recent report to the World Health Organization by the International Obesity Taskforce recommends that BMI cut-points such as those proposed by Cole et al.11 be used as a standard definition for surveys, but that further research was required; also on waist circumference, and on the shorter-term health consequences of childhood obesity.18 While childhood obesity does not necessarily indicate adult obesity, epidemiological studies have found that about a third of obese preschool children and a half of obese school-age children become obese adults.19 The scale of the problem suggests that only a concerted sustained effort by health professionals in collaboration with many other disciplines and organizations will reverse this trend for future generations.
| Causes |
|---|
|
|
|---|
Overweight and obesity occurs when there is an imbalance between energy intake and expenditure. This imbalance can result in overweight and obesity in children in a matter of years or, in adults, often in the longer term, in decades. The regulation of energy balance is highly complex, involving societal, behavioural, genetic, hormonal, and neural influences.20 Results from twin studies suggest that the tendency to obesity is inherited,21,22 at least in part, and that responsiveness to dietary intervention is genetically determined.23 Children with overweight or obese parents have a greater risk of obesity,24,25 which may have both genetic and environmental components. The ability to taste seems to be fully functional before birth, and infants and children appear to develop a preference for salt and a dislike for bitter and strong tastes.26,27 The discovery of mutations in the gene encoding leptin in two obese Pakistani children,28 and the striking effects of leptin administration to those children with a deficiency,29 have stimulated interest in the role of genetics in obesity. Single genes are thought to produce a small effect at population level, and it is the interaction between the genetic defects associated with obesity and other factors, such as prenatal factors which may account for high levels of obesity.22 However the two main preventable causes of obesity are lack of physical activity and chronic consumption of excess calories.
The majority of obese adults were of normal weight as children, and it is a result of excess energy intake over a period of many years which leads to obesity. Therefore learning to eat healthily and to exercise is vital. However, being a thin child doesn't necessarily offer protection against later obesity. Indeed, it has been found that children who were the thinnest in childhood and became fat adults had the highest levels of adult ill health.30 This suggests that it is the change in relative size between birth and adulthood that is associated with increased risk of adult disease, rather than size itself.31 Therefore, getting the energy balance right is important, not only from birth, but from before conception. Both maternal undernutrition and overnutrition may affect later levels of obesity in offspring. Maternal overnutrition, leading to an increase of transfer of nutrients to the foetus, may change energy metabolism in the foetus, leading to obesity.32 However, there is a body of evidence linking low birth weight and other markers of foetal size to cardiovascular risk factors,33 including increased central fat distribution and waist-hip ratio.34,35
There seem to be critical periods even within gestation, as data from the Dutch famine cohort show that, in 19-year-old men, exposure to famine in the first two trimesters of pregnancy was associated with an almost two-fold increase in obesity, while those exposed to famine in the third trimester had reduced rates of obesity at 19 years.36 Also maternal smoking during pregnancy has been associated with later obesity in children.3739 Infant feeding is also important in the development of obesity, with children who were bottle-fed having higher rates of obesity than those who were breast-fed,40,41 but this relationship has been inconsistent in adults.42,43
Dietary intake
Growth rate in children and adolescents is a sensitive indicator of dietary adequacy, even though the energy required for growth is a minor component of total energy.44 Children are expected to gain around 12 kg in weight and 30 cm in height between the ages of 5 and 10 years, with the percentage of body fat remaining constant for boys and increasing for girls. Boys are heavier than girls until about 8 years, when girls become heavier with the onset of puberty and the associated deposition of fat.45 In order for the child's full potential for height and healthy weight to be achieved, adequate nutrition is essential. The National Diet and Nutrition Survey (NDNS) of young people in Britain aged 418 years46 found that mean energy intakes were lower than the estimated average requirement, but that children were taller and heavier than similar populations in previous studies.47 The most commonly eaten foods were white bread, savoury snacks, chips, biscuits, other forms of potatoes, and chocolate. These foods all contain a high proportion of refined carbohydrates which cause a large post-prandial insulin response; foods like these with a high glycaemic index (based on the physiological response to glucose) have been linked with the development of type 2 diabetes.48
The NDNS46 also found that children ate less than half the recommended five portions of fruit and vegetables per day. This is comparable to figures from the US, which show that only one in five children and one in four adults consume five portions daily.49 Sugared fizzy drinks were consumed by three-quarters of the NDNS children, compared to less than half who usually drank the sugar-free versions.46 Ebbeling et al.50 estimate that an excess calorie consumption of only 120 kcal per day (the equivalent of one sugared soft drink) would produce a 50 kg increase in body weight over 10 years. Consumption of fast food is also increasing worldwide. A large fast food meal such as a double cheeseburger, French fries, soft drink and dessert would contain 2200 kcal,50 which is equivalent to the recommended daily intake of calories for adults, and is unlikely to be the only food consumed in a day.
In NDNS, carbohydrate provided 51% of food energy intake in boys and girls, and fat provided about 35% of food energy, with saturated fat comprising 14% of energy which is above the adult recommendations of 11%. The relationship between fat intake and obesity is unclear,44 and studies in the US show that despite a decrease in the proportion of dietary fat, obesity is increasing.51,52 Since reported intakes in the NDNS were lower than the estimated average requirements, and under-reporting was considered unlikely, diet is clearly not the only factor implicated in the increase in obesity.46
Physical activity
Rates of physical activity have been declining and it has been estimated that between 4069% of British children over the age of 6 are spending <1 h/day being moderately active;45 in a recent study in 35-year-olds in Glasgow, total energy expenditure was significantly lower than the UK estimated average requirement for energy (by 837 kJ/day).53 In the US, >60% of adults do not meet the recommended targets for physical activity.13 More people are engaged in sedentary work than before, spend more time in traffic queues and in front of televisions and computer monitors in their spare time, and the amount of time spent walking and cycling has decreased.54 A large cohort study in American nurses found that in 50 000 non-obese and non-diabetic nurses, those who watched more television and had a sedentary lifestyle were at greater risk of developing obesity or diabetes during 6 years of follow-up. The authors estimated that 30% (95%CI 2436%) of new cases of obesity and 43% (95%CI 3252%) cases of type 2 diabetes could be prevented by adopting a relatively active lifestyle (<10 h/week TV viewing and
30 min of brisk walking per day).55 In American schools, many schoolyards are closed out of school hours because of the risk of litigation54 and the situation is similar in Britain. Here, in the 1980s, about 67% of children aged 510 years walked to school, just over 20% travelled by car and <10% by bus. By 2000, only 55% walked, 35% went by car and 10% by bus.45 In the US, one third of adolescents watched
5 h of television per day, and there was less obesity in those children who watched <1 h of television per day.56 Advertisements for food are scheduled most frequently when children are likely to be watching.57 A recent report from New Zealand which followed 1000 children until the age of 26 years found that television viewing in childhood and adolescence was associated with higher BMI, lower cardiorespiratory fitness, increased cigarette smoking and raised serum cholesterol.58 Schools play a vital role in providing physical activity for children and adolescents, but budget cuts have resulted in resulted in less, and sometimes no physical activity, on school timetables,54,59 despite the knowledge that children and adolescents who participate in team sports or exercise programmes are less likely to be overweight.60
Family environment also plays an important role in the development of obesity. Lengthy periods of television viewing, lack of family meals at home, eating out at restaurants, childhood neglect and depression have all been associated with increased childhood risk of obesity.50 Environmental risk factors for childhood obesity have been recently reviewed elsewhere.18
| Prevention and treatment |
|---|
|
|
|---|
The promotion of healthy eating and regular physical activity is essential both for the prevention of future obesity61 and also for treating those who are already overweight and obese.62 Recent large multi-centre trials have shown that significant weight loss is achievable using a contribution of diet and physical activity, and can prevent the onset of type 2 diabetes in subjects at risk.63 It remains to be seen whether similar protocols can be effectively introduced into public health and primary care practice. Guidelines for prevention and treatment have been introduced both in the US13 and in Britain,7 but implementation plans for these guidelines may take some years to be accepted and established given the number of organizations potentially involved, and the complex task of promoting collaboration between them. Given the scale of the epidemic the burden of treatment services will lie with primary care although a recent report from the Royal College of Physicians, Royal College of Paediatrics and Child Health and the Faculty of Public Health emphasizes the role of nutritional support services.64 The National Audit Office Report identified only 12 separate obesity clinics in England,65 and a Cochrane Review of the management and organization of care for overweight and obese people found that there were few solid leads about improving obesity management, and that further research was required to identify cost-effective strategies for improving the management of obesity.66 In the UK, guidelines for the use of Orlistat and Sibutramine as anti-obesity agents were issued by the National Institute for Clinical Excellence,67 and the Chief Medical Officer's Report7 noted that their use had trebled since these guidelines were issued. Surgical treatment for type II and III grades of obesity appears to be more cost-effective than medical therapy, and may be underutilized.68 As weight loss is more difficult to achieve and maintain in adulthood,69 prevention and treatment in childhood and adolescence is essential. However as children are less mature intellectually and psychologically than adults, treatment plans have been mainly based on the family or school in order to provide the extra support that children will need. In surveys in Northern Ireland it was found that the level of dieting among obese 13- and 14-year-olds was low (38% in girls and 15% in boys)70 but in 58-year-olds, overweight and obese children were reported by parents to be taking healthier food choices.71 However, as has been shown elsewhere46 there was a marked trend for children from poorer families to have unhealthy food choices, which may indicate that national health promotion should be particularly directed at less well-off parents.
Education on good nutrition is vital, as it may influence eating habits. This is a useful form of prevention when focused on families as, not only could it change adult dietary preferences, but those of children also; food preferences are formed in childhood, mainly through parental food choice, and affect childhood dietary intake. These preferences are carried through to adult life and can cause adult health effects.72 Educating parents of obese children has been shown to produce positive changes in the children's dietary intake.73
Current recommendations from the American Heart Association74 are: (i) All children age 2 and older should participate in at least 30 min of enjoyable, moderate-intensity activities every day. (ii) They should also perform at least 30 min of vigorous physical activities at least 34 days each week to achieve and maintain a good level of cardiorespiratory (heart and lung) fitness.
School-based initiatives to improve nutrition are being developed. In Britain, teaching about food and nutrition may occur in Science, Design and Technology or in Personal, Social and Health Education.45 The Healthy Schools Programme encourages awareness of local health issues and schools attempt to present consistent informed messages about healthy eating.75 School travel plans have also been developed, which encourage the reduction of car use, thus increasing physical activity. The National School Fruit Scheme will ensure that all 46-year-olds will receive a free piece of fruit on each school day; there are other initiatives, such as fruit tuck shops and food dudes, which are summarized in a British Nutrition Foundation review.45 Similar campaigns are also occurring in the US, which include programmes to increase the amount of physical activity in schools, sponsored walking to school, turn-off televisions campaigns, and also the introduction of salad bars in schools.45 There have also been school-based interventions for children who are overweight or obese. One such intervention showed that a 10-week education programme resulted in a 15.4% decrease in the percentage overweight in obese children. and caused a reversal in the steady weight gain that these children were experiencing.76 In the US, there are a large number of community-based strategies, including walking trails, working with owners of restaurants to increase the amount of healthy items on their menus, cookery classes and community gardens.
Despite all these initiatives in the US, in Britain and elsewhere, the results from education programmes have been disappointing.50 This may be due at least in part to the influence of the multi-national food industry and advertising.77 The food industry spends billions of pounds advertising, and the budget for promoting healthy nutrition is minute in comparison.77 Others have also suggested food marketing controls18 but governments may be reluctant to intervene too radically against a powerful food industry. However in the US, some new initiatives based on long-term changes combining comparatively small increases in physical activity and decreases in calories have been sponsored by the food industry.78 A recent initiative by the World Health Organization includes recommendations restricting the availability of high energy foods,79 but this may be resisted by the food industry. Fiscal policies to promote healthier foods have been proposed for the prevention of coronary disease80 but have not been encouraged by official scientific representatives of the US Department of Agriculture.81
Doctors and other health professionals also have a major role to play in the treatment of obesity. Data from the US show that 58% of obese patients have never had counselling for weight loss.49 Obesity is often not considered a serious medical condition by doctors, and is generally only treated when other disease risk factors are present, rather than before these risk factors develop or are made worse by obesity.2
A recent report by the Select Committee on Health for the UK Parliament, which consulted widely, made a number of major recommendations,82 including the establishment of a strategic framework for preventing and treating obesity within the NHS with a full range of treatment options. It also advised that children should have access to appropriate services and should be screened for overweight and obesity annually at school. The committee also noted the complexity of the task, the need to obtain the collaboration of the food industry and to review progress in 3 years.
| Future research |
|---|
|
|
|---|
Although increases in physical activity have been shown to reduce weight in children who are obese,73 it is not yet known what level of activity is needed.83 There is little known about the association of behavioural or environmental change with obesity. More evidence is required from longitudinal studies, particularly those based on cohorts of infants or children. A metaanalysis on the evidence for tracking of obesity into adulthood may provide useful information for public health strategies. There is also a need for small-scale trials that can measure the effects of behavioural and environmental change in both children and adults. A summary review of diet, physical activity and behavioural approaches to the management of obesity and overweight has been published recently.84 It will also be important to monitor for undesirable side effects of trials and public health initiativesfor example, a rise in the incidence of eating disorders such as anorexia nervosa and bulimia.85 These studies need to be followed up with large-scale intervention trials, and finally long-term trials that can assess the impact of changes over a period of many years. The role of genetics in overweight and obesity also needs further research and, in particular, the interplay between genes linked with obesity and major factors in the environment.
| Footnotes |
|---|
Address correspondence to Dr J.W.G. Yarnell, Department of Epidemiology and Public Health, Queen's University of Belfast, Belfast, UK. e-mail: h.porter{at}qub.ac.uk
| References |
|---|
|
|
|---|
1. Allison DB, Fontaine KR, Manson JE, Stevens J, Van Itallie Tb. Annual deaths attributable to obesity in the United States. JAMA 1999; 282:15308.
2. International Association for the Study of Obesity. About Obesity. [www.iotf.org]
3. Garrow JS. Chapter 34: Obesity. In: Garrow JS, James WPT, Ralph A, eds. Human Nutrition and Dietetics, 10th edn. Edinburgh, Churchill Livingstone, 2000.
4. WHO. Obesity: Preventing and Managing the Global Epidemic. Report of a WHO Consultation on Obesity. Geneva, World Health Organization, 1998.
5. Sowers JR. Obesity as a cardiovascular risk factor. Am J Med 2003; 115(Suppl. 8A):3741S.
6. Bray GA, Champagne CM. Obesity and the Metabolic Syndrome: implications for dietetics practitioners. J Am Diet Assoc 2004; 104:869.[CrossRef][ISI][Medline]
7. Department of Health. Annual Report of the Chief Medical Officer 2002. London Department of Health, 2002. [www.doh.gov.uk/cmo/annualreport2002]
8. Joint Health Surveys Unit (on behalf of the Department of Health). Health Survey for England, 2002. Norwich, The Stationery Office, 2003. [www.doh.gov.uk/stats/trends1.htm]
9. Bundred P, Kitchener D, Buchan I. Prevalence of overweight and obese children between 1989 and 1998: population based series of cross sectional studies. Br Med J 2001; 322:3268.
10. Joint Health Surveys Unit (on behalf of the Department of Health). Health Survey for England, 2000. London, The Stationery Office, 2001.
11. Cole TJ, Bellizzi MC, Flegal KM, Dietz WH. Establishing a standard definition for child overweight and obesity worldwide: international survey. Br Med J 2000; 320:12403.
12. Strauss RS. Comparison of measured and self-reported weight and height in a cross-sectional sample of young adolescents. Int J Obes Relat Metab Disord 1999; 23:9048.[CrossRef][ISI][Medline]
13. US Department of Health and Human Services. The Surgeon General's Call to Action to Prevent and Decrease Overweight and Obesity. Rockville, 2001.
14. Troiano RP, Flegal KM. Overweight children and adolescents description, epidemiology, and demographics. Paediatrics 1998; 101:497504.
15. Booth ML, Wake M, Armstrong T, Chey T, Hesketh K, Mathur S. The epidemiology of overweight and obesity among Australian children and adolescents, 199597. Aust NZ J Public Health 2001; 25:1629.[ISI][Medline]
16. Wang Y, Monteiro C, Popkin. Trends of obesity and underweight in older children and adolescents in the United States, Brazil, China and Russia. Am J Clin Nutr 2002; 75:9717.
17. McCarthy HD, Ellis SM, Cole TJ. Central overweight and obesity in British youth aged 1116 years: cross sectional surveys of waist circumference. Br Med J 2003; 326:6246.
18. IOTF Working Group (Editors Lobstein T, Baur L, Uauy R). Obesity in children and young people. A crisis in public health. Obes Rev 2004; 5(Suppl. 1).
19. Serdula MK, Ivery D, Coates RJ, Freedman DS, Williamson DF, Byers T. Do obese children become obese adults? A review of the literature. Prev Med 1993; 22:16777.[CrossRef][ISI][Medline]
20. Lustig RH. The neuroendocrinology of obesity. Endocrinol Metab Clin North Am 2001; 30:76585.[CrossRef][ISI][Medline]
21. Bray GA, Bouchard C, James WPT. Handbook of Obesity. New York, Marcel Dekker Inc, 1998.
22. Barsh GS, Farooqi IS, O'Reilly S. Genetics of body-weight regulation. Nature 2000; 404:64451.[Medline]
23. Perusse L, Bouchard C. Role of genetic factors in childhood obesity and in susceptibility to dietary variations. Ann Med 1999; 31:1925.
24. Whitaker RC, Wright JA, Pepe MS, Seidel KD, Dietz WH. Predicting obesity in young adulthood from childhood and parental obesity. N Engl J Med 1997; 337:86973.
25. Lake JK, Power C, Cole TJ. Child to adult body mass index in the 1958 British Birth cohort: associations with parental obesity. Arch Dis Child 1997; 77:37681.
26. Cowart BJ. Development of taste perception in humans: sensivity and preference throughout the life span. Psychol Bull 1981; 90:4373.[CrossRef][ISI][Medline]
27. Randall E, Sanjur D. Food preferencestheir conceptualisation and relationship to consumption. Ecol Food Nutr 1981; 11:15161.
28. Montague CT, Farooqi IS, Whitehead JP, Soos MA, Rau H, Wareham NJ, Sewter CP, Digby JE, Mohammed SN, Hurst JA, Cheetham CH, Earley AR, Barrett AH, Prins JB, O'Rahilly S. Congenital leptin deficiency is associated with severe early-onset obesity in humans. Nature 1997; 387:9038.[CrossRef][Medline]
29. Farooqi IS, Jebb SA, Langmack G, Lawrence E, Cheetham CH, Prentice AM, Hughes IA, McCamish MA, O'Rahilly S. Effects of recombinant leptin therapy in a child with congenital leptin deficiency. N Engl J Med 1999; 341:87984.
30. Wright CM, Parker L, Lamont D, Craft AW. Implications of childhood obesity for adult health: findings from thousand families study. Br Med J 2001; 323:12804.
31. Lucas A, Fewtrell MS, Cole TJ. Fetal origins of adult diseasethe hypothesis revisited. Br Med J 1999; 319:2459.
32. Whitaker RC, Dietz WH. Role of the prenatal environment in the development of obesity. J Pediatr 1998; 132:76876.[CrossRef][ISI][Medline]
33. Barker DJ. The developmental origins of adult disease. Eur J Epidemiol 2003; 18:7336.[ISI][Medline]
34. Gale CR, Martyn CN, Kellingay S, Eastell R, Cooper C. Intrauterine programming of adult body composition. J Clin Endocrinol Metab 2001; 86:26772.
35. Law CM, Barker DJ, Osmond C, Fall CH, Simmonds SJ. Early growth and abdominal fatness in adult life. J Epidemiol Community Health 1992; 46:1846.[Abstract]
36. Ravelli GP, Stein ZA, Susser MW. Obesity in young men after famine exposure in utero and early infancy. N Engl J Med 1976; 295:34953.[Abstract]
37. Vik T, Jacobson G, Vatten L, Bakketeig LS. Pre and post-natal growth in children of women who smoked in pregnancy. Early Hum Dev 1996; 45:24555.[CrossRef][ISI][Medline]
38. Von Kries Troschke AM, Koletzko B, Slikker W Jr. Maternal smoking during pregnancy and childhood obesity. Am J Epidemiol 2002; 156:95461.
39. Wideroe M, Vik T, Jacobsen G, Bakketeig LS. Does maternal smoking during pregnancy cause childhood overweight? Paediatr Perinat Epidemiol 2003; 17:1719.[CrossRef][ISI][Medline]
40. Toschke AM, Vignerova J, Lhotska L, Osancova K, Koletzko B, Von Kries R. Overweight and obesity in 6- to 14-year-old Czech children in 1991: protective effect of breast-feeding. J Pediatr 2002; 141:7649.[CrossRef][ISI][Medline]
41. Gillman MW, Rifas-Shiman SL, Camargo CA Jr, Berkey CS, Frazier AL, Rockett HR, Field AE, Colditz GA. Risk of overweight among adolescents who were breastfed as infants. JAMA 2001; 285:24617.
42. Parsons TJ, Power C, Manor O. Infant feeding and obesity through the life course. Arch Dis Child 2003; 88:7934.
43. Ravelli AC, van der Meulen JH, Osmond C, Barker DJ, Bleker OP. Infant feeding and adult glucose tolerance, lipid profile, blood pressure, and obesity. Arch Dis Child 2000; 82:24852.
44. Butte NF. Fat intake of children in relation to energy requirements. Am J Clin Nutr 2000; 72:124652S.
45. Buttriss J. Nutrition, health and schoolchildren. Nutr Bull 2002; 27:275316.[CrossRef]
46. Gregory J, Lowe S, Bates CJ, et al. National Diet and Nutrition Survey: Young people aged 418 years, Vol. 1. Report of the Diet and Nutrition Survey. London, The Stationery Office, 2000.
47. Department of Health. The Diets of British Schoolchildren. Report on Health Social Subjects 46. London, Her Majesty's Stationery Office, 1989.
48. Salmeron J, Manson JE, Stampfer MJ, Colditz GA, Wing AL, Willett WC. Dietary fibre, glycemic load, and risk of non-insulin-dependent diabetes mellitus in women. JAMA 1997; 277:4727.[Abstract]
49. Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Physical Activity and Good Nutrition, Essential Elements to Prevent Chronic Diseases and Obesity: At a Glance 2001. [www.cdc.gov/nccdphp/dnpa/]
50. Ebbeling CB, Pawlak DB, Ludwig DS. Childhood obesity: public-health crisis, common sense cure. Lancet 2002; 360:47382.[CrossRef][ISI][Medline]
51. Troiano RP, Briefel RR, Carroll MD, Bialostosky K. Energy and fat intakes of children and adolescents in the United States: data from the National Health and Nutrition Examination Surveys. Am J Clin Nutr 2000; 72:134353S.
52. Cavadini C, Siega-Riz AM, Popkin BM. US adolescent food intake trends from 1965 to 1996. West J Med 2000; 173:37883.[CrossRef][ISI][Medline]
53. Reilly JJ, Jackson DM, Montgomery C, Kelly LA, Slater C, Grant S, Paton JY. Total energy expenditure and physical activity in young Scottish children: mixed longitudinal study. Lancet 2004; 363:21112.[CrossRef][ISI][Medline]
54. Grantmakers in Health. Weighing in on obesity. America's growing health epidemic. Issue brief no. 11. Washington DC. Grantmakers in health, 2001. [www.gih.org]
55. Hu FB, Li TY, Colditz GA, Willett WC, Manson JE. Television watching and other sedentary behaviours in relation to risk of obesity and Type 2 Diabetes Mellitus in women. JAMA 2003; 289:178591.
56. Crespo CJ, Smit E, Troiano RP, Bartlett SJ, Macera CA, Andersen RE. Television watching, energy intake and obesity in US children: results from the third National Health and Nutrition Examination Survey, 19881994. Arch Pediatr Adolesc Med 2001; 155:3605.
57. Dibb S, Castell A. Easy to Swallow, Hard to stomach. London, National Food Alliance, 1995.
58. Hancox RJ, Milne BJ, Poulton R. Association between child and adolescent television viewing and adult health: a longitudinal birth cohort study. Lancet 2004; 364:25762.[CrossRef][ISI][Medline]
59. Fox KR, Riddoch CJ. Changing the physical activity patterns of contemporary children and adolescents. Proc Nutr Soc 2000; 59:497504.[ISI][Medline]
60. Pate RR, Trost SG, Levin S, Dowda M. Sports participation and health-related behaviours among US youth. Arch Pediatr Adolesc Med 2000; 154:90411.
61. Crawford D. Population strategies to prevent obesity. Br Med J 2002; 325:7289.
62. Noel PH, Pugh JA. Management of overweight and obese adults. Br Med J 2002; 325:75761.
63. Kriska AM, Delahanty LM, Pettee KK. Lifestyle intervention for the prevention of type 2 diabetes: translation and future recommendations. Curr Diab Rep 2004; 4:11318.[Medline]
64. Working Party. Storing up problems. The medical case for a slimmer nation. London, Royal College of Physicians, 2004.
65. National Audit Office. Tackling obesity in England. Report by the Comptroller and Auditor General. Norwich, The Stationery Office, 2001. [www.nao.gov.uk/guidance/chiefexec2b.htm]
66. Harvey EL, Glenny A-M, Kirk SFL, Summerbell CD. Improving health professionals management and the organisation of care for overweight and obese people (Cochrane Review). In: The Cochrane Library, Issue 2. Oxford: Update Software, 2001.
67. National Institute for Clinical Excellence. Published Appraisals Nos 22 (Orlistat) and 31 (Sibutramine). London, NICE, 2001. [http://www.nice.org.uk]
68. Steinbrook R. Surgery for severe obesity. N Engl J Med 2004; 350:10759.
69. National Institutes of Health. The Practical Guide: Identification, Evaluation and Treatment of Overweight and Obesity in Adults. Bethesda, Md: North American Association for the Study of Obesity, National Heart, Lung, and Blood Institute; 2000. NIH publication 004048. [http://www.nhlbi.nih.gov/guidelines/obesity/practgde.htm]
70. Yarnell JWG, McCrum EE, Patterson CC, Skidmore P, Shields MD, McMahon J, Evans AE. Prevalence and awareness of excess weight in 13 and 14 year olds in Northern Ireland using recent international guidelines. Acta Paediatr 2001; 90:14359.[CrossRef][ISI][Medline]
71. Skidmore PML, Yarnell JWG, Mc Geough GE, Mc Mahon J, Shields M, Scott A, Evans A. Gender differences in dietary habits in a population of primary school children. Proc Nutr Soc 2001; 60:66a (abstract).
72. Power C, Moynihan C. Social class and changes in weight for height between childhood and early adulthood. Int J Obes 1988; 12:44553.[ISI][Medline]
73. Golan M, Fainaru M, Weizman A. Role of behaviour modification in the treatment of childhood obesity with the parents as the exclusive agents of change. Int J Obes Relat Metab Disord 1998; 22:121724.[CrossRef][ISI][Medline]
74. American Heart Association. Exercise (Physical Activity) and Children, 2004. [http://www.americanheart.org/presenter.jhtml?identifier=4596]
75. Department for Education and Employment. White paper on Excellence in schools (1997). HMSO, London.
76. Brownell KD, Kaye FS. A school-based behaviour modification, nutrition education, and physical activity program for obese children. Am J Clin Nutr 1982; 35:27783.
77. Nestle M. The Ironic Politics of Obesity. Science 2003; 299:781.[Abstract]
78. Hill J. Physical activity and obesity. Lancet 2004; 1:182.[CrossRef]
79. WHO Technical Report Series, 916. Diet, nutrition and the prevention of chronic diseases. Report of a joint WHO/FAO expert consultation. Geneva, Switzerland, 2003. [http://www.who.int/hpr/NPH/docs/who_fao_expert_report.pdf]
80. Marshall T. Exploring a fiscal food policy: the case of diet and ischaemic heart disease. Br Med J 2000; 320:3014.
81. Kennedy E, Offutt S. Alternative nutrition outcomes using a fiscal food policy. Br Med J 2000; 320:3045.[CrossRef]
82. Select Committee on Health. Third Report. London. UK Parliament, 2004. [www.publications.parliament.uk/pa/cm200304/cmselect/cmhealth/23/2303.htm]
83. Schoeller DA. But how much physical activity? Am J Clin Nutr 2003; 78:66970.
84. Mulvihill C, Quigley R. The management of obesity and overweight: an analysis of reviews of diet, physical activity and behavioural approaches. London, Health Development Agency, 2003. [www.hda.nhs.uk]
85. Fairburn CG, Harrison PJ. Eating disorders. Lancet 2003; 361:40716.[CrossRef][ISI][Medline]
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
B. Mokhlesi, M. H. Kryger, and R. R. Grunstein Assessment and Management of Patients with Obesity Hypoventilation Syndrome Proceedings of the ATS, February 15, 2008; 5(2): 218 - 225. [Abstract] [Full Text] [PDF] |
||||
![]() |
M O'Flaherty, E Ford, S Allender, P Scarborough, and S Capewell Coronary heart disease trends in England and Wales from 1984 to 2004: concealed levelling of mortality rates among young adults Heart, February 1, 2008; 94(2): 178 - 181. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. Hypponen and C. Power Hypovitaminosis D in British adults at age 45 y: nationwide cohort study of dietary and lifestyle predictors Am. J. Clinical Nutrition, March 1, 2007; 85(3): 860 - 868. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. A. Rabin, T. K. Boehmer, and R. C. Brownson Cross-national comparison of environmental and policy correlates of obesity in Europe Eur J Public Health, February 1, 2007; 17(1): 53 - 61. [Abstract] [Full Text] [PDF] |
||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||




