- Email: [email protected]
Obesity: causes and consequences
OBESITY AND DIETING
Obesity: causes and consequences
Defining overweight WHO classification of overweight Classification BMI (kg/m2) Normal 18.5–24.9 Overweight 25.0–29.9 Obese class I 30.0–34.9 Obese class II 35.0–39.9 Obese class III > 40
Susan Jebb
Body mass index (BMI) = weight (kg)/height (m)2
Obesity is a condition of excess body fat, although it is usually defined on the basis of body mass index (BMI) or waist circumference (Figure 1). Obesity is arguably a predictable response to the modern world for an organism whose evolution is characterized by periods of famine. The broad public health problem of obesity can be usefully described as a failure of innate physiological body weight control mechanisms in the face of overwhelming environmental influences that favour sedentary lifestyles and energy-dense diets. It is increasingly necessary for individuals to develop cognitive strategies and practical skills to control their weight and avoid the adverse consequences of excess weight. The prevalence of obesity is rising around the world, but the rate of increase in the UK is generally greater than in other parts of north-western Europe. • In 1980, 8% of women (6% of men) were clinically obese, with a BMI >30. In 2002, this had trebled to 23% of women (22% of men). The prevalence of overweight (BMI 25–30) is also rising, but overweight is less common in women than men, affecting 33.7% and 43.4% respectively • The prevalence of morbid obesity (BMI >40) is also increasing sharply and now exceeds 2% of the female population. Figure 2 illustrates the trends in overweight and obesity in women (aged 16–64 years). The gender differences in the UK are modest, but in other parts of the world there is often a higher level of obesity among women. This is particularly true in the Middle East and Africa, where social and cultural values account for differences in the preferred body shape and size. In the Gambia in West Africa, the prevalence of obesity in urban women (35–50 years old) is 50% and in men (35–50 years old) only 6%. In recent years, there has been an increase in the prevalence of obesity in children and young people. Data from the Health Survey for England 2002 show that 7.2% of girls (5.5% of boys) aged 2–15 years are obese, and a further 16.3% and 20.3% overweight.1 The development of excess weight at a young age raises particular concerns for later health risks. Obesity is more common in individuals and families with low levels of education, low income or low social class. Parental obesity is a strong predictor of obesity in children, and obesity in children is strongly influenced by parental social class. In the UK, there are
Waist circumference in women Normal healthy range <80 cm (<31.5 inches) Health risks increasing 80–88 cm (31.5–35 inches) High risk > 88 cm (35 inches) 1
also important ethnic differences; Pakistani women are 60% more likely to be obese than their white counterparts and similar trends are emerging in young people. This underpins later differences in the prevalence of type 2 diabetes and cardiovascular disease.
Health risks of obesity It has long been known that obesity is associated with premature death. This has been confirmed in a number of prospective studies (Figures 3 and 4). Obesity increases the risk of a number of diseases including the two major killers, cardiovascular disease and cancer (Figure 3). It is estimated that, on average, obesity reduces life expectancy by between 3 and 13 years, the excess mortality being greater the more severe the obesity and the earlier it develops. In public health terms, however, the greatest burden of disease arises from obesity-related morbidity. Obesity affects almost every organ of the body (Figure 5). Its effects include metabolic syndrome
Trends in prevalence of overweight and obesity in women aged 16–64 years1 100 90
Obese
Overweight
80
Prevalence
70 60 50 40 30 20 10
Susan Jebb is Head of Nutrition and Health Research at the Medical Research Council Human Nutrition Research Centre in Cambridge. She is a nutrition scientist and a registered dietitian and has a particular interest in the role of dietary risk factors in the aetiology and treatment of obesity and its related metabolic diseases.
WOMEN’S HEALTH MEDICINE 1:1
0
1993 1994 1995 1996 1997 1998 1999 2000 2001 2002
Year 2
38
© 2004 The Medicine Publishing Company Ltd
OBESITY AND DIETING
Predicted survival of women according to BMI2
Problems caused by overweight and obesity. (The figures indicate approximate relative risks at BMI > 27–30 kg/m2)
Kaplan-Meier curves for non-smoking women 100
Hirsutism 2 Sweating ↑
90
Stroke 1.6 Low mood, poor self-esteem ↑
Proportion alive
80
Hypertension 2.9 Coronary heart disease 2.5 Thromboembolism 1.5 Heart failure 1.5
70 60
Hypoventilation ↑ Sleep apnoea ↑ Breathlessness 3.5
50 40
Normal weight (BMI 18.5–24.9 kg/m2) Overweight (BMI 25–29.9 kg/m2) Obese (BMI <29.9 kg/m2)
30 20 10
Breast cancer 1.3 Infertility ↑ Pregnancy problems 2 Cancer of uterus 4.6 Menorrhagia 1.8
0 0
10
20
30
40
Years from start of study Gallstones 2.7 Cancer of colon 1.5 Cancer of pancreas 1.6 Kidney disease ↑
3
(insulin resistance, hyperlipidaemia and hypertension), mechanical disorders (e.g. osteoarthritis, respiratory problems, sleep apnoea) and psychosocial disorders. Diabetes and cardiovascular disease: ‘metabolic syndrome’ comprises the cluster of metabolic disorders listed in Figure 6, all of which are risk factors for atherosclerotic disease. The development and severity of all the components depend on weight (fat) gain, so obesity is a key feature. Metabolic syndrome is strongly linked to a ‘Western’ lifestyle, characterized by low levels of physical activity and a diet rich in saturated fat and refined carbohydrate. • The link between obesity and type 2 diabetes is particularly striking. For women, a BMI of just 25 is associated with a five-fold increase in risk of type 2 diabetes, and the risk increases to more than 40-fold for a BMI in excess of 35. The risk is especially high for women with a central pattern of fat distribution, characterized by a large waist circumference (often described as ‘apple-shaped’), the risk is less for women with a similar BMI who tend to deposit
Diabetes mellitus 10 Dyslipidaemia 1.5 Hyperinsulinaemia ↑↑
5
their excess fat on the hips and thighs (‘pear-shaped’)(Figure 7).5 • Coronary heart disease (CHD) is also associated with weight gain and obesity. The Nurses’ Health Study showed a clear relationship between CHD and elevated BMI, even when controlling for age, smoking, menopausal status and family history. The risk of CHD increased from BMI 22–23, and was doubled at 25–28.9 and more than three times higher above 29, compared with the risk at BMI less than 21.5. The link between obesity and metabolic disease is not fully understood. High concentrations of circulating free fatty acid concentrations may inhibit efficient glucose uptake leading to insulin resistance. Recent research has shown that a number of proteins and other factors secreted by adipose tissue may also contribute to disease. Indeed, adipocytes are now recognized as an important endocrine organ. Adipose tissue is an important site of production of a number of cytokines including interleukin (IL)6 and tumour necrosis factor (TNF)-alpha. Sub-clinical levels of raised inflammatory markers (such as C-reactive protein, which is produced by the liver when stimulated by cytokines) may be important predictors of metabolic disease. Cancer: in recent years there has been a growing recognition of the increased risk of most types of cancer (with the exception of lung cancer), particularly postmenopausal breast cancer and colon and kidney cancer. Obesity is estimated to account for 20% of cancer deaths in women. Reproductive problems: obesity, especially severe obesity, is linked to infertility and an increased risk of complications during
Effect of increasing BMI on premature mortality3
Relative risk of death
2.5
2.0
All other causes Cancer Cardiovascular disease
1.5
1.0
0.5
40
1 18 8.5 .5 –2 0. 4 20 .5 –2 1. 9 22 .0 –2 3. 4 23 .5 –2 4. 9 25 .0 –2 6. 4 26 .5 –2 7. 9 28 .0 –2 9. 9 30 .0 –3 1. 9 32 .0 –3 4. 9 35 .0 –3 9. 9
0
Body mass index 4
WOMEN’S HEALTH MEDICINE 1:1
Osteoarthritis 2 Gout 3 Varicose veins ↑
39
© 2004 The Medicine Publishing Company Ltd
OBESITY AND DIETING
Features of metabolic syndrome
a Total energy expenditure in lean and obese subjects 10
Overt pathophysiological conditions • Obesity • Central fat distribution • Type 2 diabetes mellitus • Coronary heart disease • Hypertension • Polycystic ovary syndrome
9 8 7
MJ/d
Endocrine and biochemical abnormalities • Glucose intolerance • Hyperinsulinaemia • Insulin resistance • Hypercortisolism • Hypertriglyceridaemia • Low high-density lipoprotein (HDL) cholesterol • Raised small dense lowdensity lipoprotein (LDL) cholesterol
6 5 4 3 2 1 0
Lean
Obese
b Energy expenditure in lean and obese subjects expressed per kg fat-free mass (mean + SE) 50 45
6
40
Kj/kg/d
35
pregnancy. This includes hypertension, pre-eclampsia, gestational diabetes and an increased risk of foetal abnormalities including neural tube defects. Reductions in body weight of even 5–10% are associated with symptomatic improvements in many of these conditions and a significant reduction in the risk factors for chronic disease. Recent studies show as little as 4 kg weight loss over 4 years halved the incidence of type 2 diabetes in patients with impaired glucose tolerance. More dramatic decreases in diabetes are associated with the greater weight loss achieved as a result of bariatric surgery. However, improvements in hyperlipidaemia and hypertension may be transient and the impact of overall morbidity and life expectancy is less clear. This puts the emphasis on the primary prevention of excess weight gain.
5 0
Lean
obesity include mutations in the leptin gene and its receptor, or the melanocortin system. Other genetic syndromes occur in which obesity is a common element of the phenotype (e.g. Prader–Willi, Bardet–Biedl). However, these account for only a small proportion of the total cases of obesity and usually manifest as pronounced obesity from a relatively early age. Interestingly, in each case, obesity results primarily from over-eating rather than defects in energy expenditure. A large number of other candidate genes have been associated with obesity. Heritability studies suggest that approximately one-third of the variance in BMI may be due to genetic factors. The potential for some behavioural traits to have a genetic component is increasingly recognized, for example, food preferences or exercise habits.
Incidence/100,000 person-years
Relationship between obesity, fat distribution and coronary heart disease4
Metabolism For many years, obesity research focused on the search for a metabolic defect in obese people that limited their capacity to utilize energy and increased the propensity for fat storage. This was because some obese people ate a similar quantity of food, or perhaps even less, than their lean counterparts. Many obese people believe they have a lower metabolic rate than others, but the opposite is the case. Detailed studies have observed that obese people have a higher metabolic rate than their lean counterparts, which is proportional to the increase in lean tissue mass (Figure 8a and b). These findings have also been confirmed by studies using the doubly-labelled water method to make objective measurements of total energy expenditure in free-living conditions. In fact, community-based studies have demonstrated that obese people under-report their energy intake, typically recording at least
Waist tertiles High Medium Low
100
50
Medium
High
BMI tertiles 7
WOMEN’S HEALTH MEDICINE 1:1
Obese
8
Genes A small proportion of cases of obesity arise from genetic factors, leading to specific clinical syndromes. Monogenic causes of
Low
20 10
The causes of obesity are multi-factorial.
0
25 15
Aetiology of obesity
150
30
40
© 2004 The Medicine Publishing Company Ltd
OBESITY AND DIETING
a third fewer calories than the energy expended. The low levels of self-reported intake commonly observed in obese people and in other restrained eaters, are now recognized as a physiologically implausible record of habitual energy consumption. This has refocused attention on energy intake and the control of appetite and eating behaviour.
There is some evidence that high levels of physical activity may also enhance the sensitivity of the innate appetite control system making it easier to subconsciously balance energy intake and energy needs. This coupling between energy intake and energy expenditure is a key issue. Increases in obesity cannot be simply attributed to over-eating or inadequate activity, rather it represents a failure of the homeostatic mechanisms to precisely match energy intake to the body’s energy needs. However, research into the causes of obesity helps to develop individual strategies for the prevention and treatment.
Behaviour Obesity is a consequence of a period of prolonged positive energy balance when energy intake exceeds energy needs. Food intake and physical activity are two key behaviours which affect this energy balance and research has addressed their specific role in the aetiology of obesity. Fat (9 kcal/g) contains more than twice as many calories as protein or carbohydrate (4 kcal/g) making high-fat meals particularly energy dense. Studies in the 1990s revealed that dietary fat readily undermines innate appetite control systems. Studies among habitually lean subjects offered ad libitum access to foods in which the fat content was covertly manipulated, showed a positive association between energy intake and the proportion of fat in the diet. In other words, the higher the fat content, the greater the calories consumed. In studies, in which the energy density of foods is kept constant despite differences in the fat content, individuals were able to control their energy intake to match their energy needs and not exhibit hyperphagia. In the ‘real-world’ setting, energy-dense diets are high in fat, high in added sugars and low in vegetables and fruit. This type of diet is likely to increase the risk of obesity through a process described as passive over-consumption, implying that the quantity of food consumed may be unaltered but the net energy intake is increased because of the high energy density of the food. Sugar-rich soft drinks are an easy way to consume excess calories without realizing. Concerns about diet are compounded by the trend towards larger portions of many food items, notably soft drinks, savoury snacks and confectionery. Food eaten outside the home is frequently offered in extra-large portions, often at minimal additional cost. Research shows that large portions increase the energy consumed at a single eating episode but fail to illicit increased satiety or to suppress subsequent eating. Together, this results in an increased risk of excess weight gain. It is increasingly recognized that broader aspects of behaviour contribute to an individual’s risk of obesity. Many overweight people report that they rarely eat in response to a specific feeling of hunger, but as a consequence of boredom, loneliness or stress. Understanding these behavioural determinants of eating habits is important in helping to devise rational treatment strategies.
Environment: obesity is not just a concern for individuals. The increases in obesity linked to economic development suggest that we have a latent susceptibility to obesity. Around the world there are examples of communities following traditional lifestyles who, when exposed to 21st century Western culture, rapidly gain weight and develop diabetes. Closer to home, overweight tends to run in families, a result of both shared genes and a shared family lifestyle. Changes in society mean greater reliance on convenience foods and more food consumed outside the home; these tend to be higher in fat and sugar than home-prepared food. People increasingly depend on time-saving gadgets, which reduce effort, and then reward themselves after a hard day at work with hours spent in front of the TV or computer. u
REFERENCES 1 Sproston K, Primatesta P, eds. Health Survey for England, 2002. London: The Stationery Office, 2003. 2 Peeters A, Barendregt J J, Willekens F et al. Obesity in adulthood and its consequences for life expectancy: a life-table analysis. Ann Intern Med 2003; 138: 24–32. 3 Calle E E, Tuhin M J, Petrelli J M et al. Body-mass index and mortality in a prospective cohort of U.S. adults. N Engl J Med 1999; 341: 1097–105. 4 Rexrode K M, Carey V J, Hennekens C H et al. Abdominal adiposity and CHD in women. JAMA 1998; 280: 1843–8. 5 Manson J E, Willet W C, Stampfer M J. The Nurses’ Health Study: body weight and mortality among women. N Engl J Med 1997; 333: 677–85. FURTHER READING Garrow J. Obesity: report of the British Nutrition Foundation’s task force. Oxford: Blackwell Science, 1999. Jebb S A. Aetiology of obesity. Br Med Bull 1997; 53: 264–85. Packianathan I, Finer N. Medical consequences of obesity. Medicine 2003; 31: 8–11. WHO/FAO. WHO Technical Report Series 916. Diet, nutrition and the prevention of chronic diseases. Geneva: WHO, 2003.
Physical activity: levels of physical activity are also important. Daily activities now demand so little effort that voluntary physical activity is a major determinant of energy needs. A woman leading a sedentary life, using a car as the major form of transport, with an office-based job and no active leisure pursuits may expend only 30% more than their basal metabolic rate. Conversely, a moderately active adult may expend some 60% more and a very active sports person can double her basal energy needs. Physical activity brings important health benefits, independent of body weight, in particular helping to maintain insulin sensitivity and reduce the risk of type 2 diabetes.
WOMEN’S HEALTH MEDICINE 1:1
41
© 2004 The Medicine Publishing Company Ltd
Obesity: causes and consequences
Defining overweight WHO classification of overweight Classification BMI (kg/m2) Normal 18.5–24.9 Overweight 25.0–29.9 Obese class I 30.0–34.9 Obese class II 35.0–39.9 Obese class III > 40
Susan Jebb
Body mass index (BMI) = weight (kg)/height (m)2
Obesity is a condition of excess body fat, although it is usually defined on the basis of body mass index (BMI) or waist circumference (Figure 1). Obesity is arguably a predictable response to the modern world for an organism whose evolution is characterized by periods of famine. The broad public health problem of obesity can be usefully described as a failure of innate physiological body weight control mechanisms in the face of overwhelming environmental influences that favour sedentary lifestyles and energy-dense diets. It is increasingly necessary for individuals to develop cognitive strategies and practical skills to control their weight and avoid the adverse consequences of excess weight. The prevalence of obesity is rising around the world, but the rate of increase in the UK is generally greater than in other parts of north-western Europe. • In 1980, 8% of women (6% of men) were clinically obese, with a BMI >30. In 2002, this had trebled to 23% of women (22% of men). The prevalence of overweight (BMI 25–30) is also rising, but overweight is less common in women than men, affecting 33.7% and 43.4% respectively • The prevalence of morbid obesity (BMI >40) is also increasing sharply and now exceeds 2% of the female population. Figure 2 illustrates the trends in overweight and obesity in women (aged 16–64 years). The gender differences in the UK are modest, but in other parts of the world there is often a higher level of obesity among women. This is particularly true in the Middle East and Africa, where social and cultural values account for differences in the preferred body shape and size. In the Gambia in West Africa, the prevalence of obesity in urban women (35–50 years old) is 50% and in men (35–50 years old) only 6%. In recent years, there has been an increase in the prevalence of obesity in children and young people. Data from the Health Survey for England 2002 show that 7.2% of girls (5.5% of boys) aged 2–15 years are obese, and a further 16.3% and 20.3% overweight.1 The development of excess weight at a young age raises particular concerns for later health risks. Obesity is more common in individuals and families with low levels of education, low income or low social class. Parental obesity is a strong predictor of obesity in children, and obesity in children is strongly influenced by parental social class. In the UK, there are
Waist circumference in women Normal healthy range <80 cm (<31.5 inches) Health risks increasing 80–88 cm (31.5–35 inches) High risk > 88 cm (35 inches) 1
also important ethnic differences; Pakistani women are 60% more likely to be obese than their white counterparts and similar trends are emerging in young people. This underpins later differences in the prevalence of type 2 diabetes and cardiovascular disease.
Health risks of obesity It has long been known that obesity is associated with premature death. This has been confirmed in a number of prospective studies (Figures 3 and 4). Obesity increases the risk of a number of diseases including the two major killers, cardiovascular disease and cancer (Figure 3). It is estimated that, on average, obesity reduces life expectancy by between 3 and 13 years, the excess mortality being greater the more severe the obesity and the earlier it develops. In public health terms, however, the greatest burden of disease arises from obesity-related morbidity. Obesity affects almost every organ of the body (Figure 5). Its effects include metabolic syndrome
Trends in prevalence of overweight and obesity in women aged 16–64 years1 100 90
Obese
Overweight
80
Prevalence
70 60 50 40 30 20 10
Susan Jebb is Head of Nutrition and Health Research at the Medical Research Council Human Nutrition Research Centre in Cambridge. She is a nutrition scientist and a registered dietitian and has a particular interest in the role of dietary risk factors in the aetiology and treatment of obesity and its related metabolic diseases.
WOMEN’S HEALTH MEDICINE 1:1
0
1993 1994 1995 1996 1997 1998 1999 2000 2001 2002
Year 2
38
© 2004 The Medicine Publishing Company Ltd
OBESITY AND DIETING
Predicted survival of women according to BMI2
Problems caused by overweight and obesity. (The figures indicate approximate relative risks at BMI > 27–30 kg/m2)
Kaplan-Meier curves for non-smoking women 100
Hirsutism 2 Sweating ↑
90
Stroke 1.6 Low mood, poor self-esteem ↑
Proportion alive
80
Hypertension 2.9 Coronary heart disease 2.5 Thromboembolism 1.5 Heart failure 1.5
70 60
Hypoventilation ↑ Sleep apnoea ↑ Breathlessness 3.5
50 40
Normal weight (BMI 18.5–24.9 kg/m2) Overweight (BMI 25–29.9 kg/m2) Obese (BMI <29.9 kg/m2)
30 20 10
Breast cancer 1.3 Infertility ↑ Pregnancy problems 2 Cancer of uterus 4.6 Menorrhagia 1.8
0 0
10
20
30
40
Years from start of study Gallstones 2.7 Cancer of colon 1.5 Cancer of pancreas 1.6 Kidney disease ↑
3
(insulin resistance, hyperlipidaemia and hypertension), mechanical disorders (e.g. osteoarthritis, respiratory problems, sleep apnoea) and psychosocial disorders. Diabetes and cardiovascular disease: ‘metabolic syndrome’ comprises the cluster of metabolic disorders listed in Figure 6, all of which are risk factors for atherosclerotic disease. The development and severity of all the components depend on weight (fat) gain, so obesity is a key feature. Metabolic syndrome is strongly linked to a ‘Western’ lifestyle, characterized by low levels of physical activity and a diet rich in saturated fat and refined carbohydrate. • The link between obesity and type 2 diabetes is particularly striking. For women, a BMI of just 25 is associated with a five-fold increase in risk of type 2 diabetes, and the risk increases to more than 40-fold for a BMI in excess of 35. The risk is especially high for women with a central pattern of fat distribution, characterized by a large waist circumference (often described as ‘apple-shaped’), the risk is less for women with a similar BMI who tend to deposit
Diabetes mellitus 10 Dyslipidaemia 1.5 Hyperinsulinaemia ↑↑
5
their excess fat on the hips and thighs (‘pear-shaped’)(Figure 7).5 • Coronary heart disease (CHD) is also associated with weight gain and obesity. The Nurses’ Health Study showed a clear relationship between CHD and elevated BMI, even when controlling for age, smoking, menopausal status and family history. The risk of CHD increased from BMI 22–23, and was doubled at 25–28.9 and more than three times higher above 29, compared with the risk at BMI less than 21.5. The link between obesity and metabolic disease is not fully understood. High concentrations of circulating free fatty acid concentrations may inhibit efficient glucose uptake leading to insulin resistance. Recent research has shown that a number of proteins and other factors secreted by adipose tissue may also contribute to disease. Indeed, adipocytes are now recognized as an important endocrine organ. Adipose tissue is an important site of production of a number of cytokines including interleukin (IL)6 and tumour necrosis factor (TNF)-alpha. Sub-clinical levels of raised inflammatory markers (such as C-reactive protein, which is produced by the liver when stimulated by cytokines) may be important predictors of metabolic disease. Cancer: in recent years there has been a growing recognition of the increased risk of most types of cancer (with the exception of lung cancer), particularly postmenopausal breast cancer and colon and kidney cancer. Obesity is estimated to account for 20% of cancer deaths in women. Reproductive problems: obesity, especially severe obesity, is linked to infertility and an increased risk of complications during
Effect of increasing BMI on premature mortality3
Relative risk of death
2.5
2.0
All other causes Cancer Cardiovascular disease
1.5
1.0
0.5
40
1 18 8.5 .5 –2 0. 4 20 .5 –2 1. 9 22 .0 –2 3. 4 23 .5 –2 4. 9 25 .0 –2 6. 4 26 .5 –2 7. 9 28 .0 –2 9. 9 30 .0 –3 1. 9 32 .0 –3 4. 9 35 .0 –3 9. 9
0
Body mass index 4
WOMEN’S HEALTH MEDICINE 1:1
Osteoarthritis 2 Gout 3 Varicose veins ↑
39
© 2004 The Medicine Publishing Company Ltd
OBESITY AND DIETING
Features of metabolic syndrome
a Total energy expenditure in lean and obese subjects 10
Overt pathophysiological conditions • Obesity • Central fat distribution • Type 2 diabetes mellitus • Coronary heart disease • Hypertension • Polycystic ovary syndrome
9 8 7
MJ/d
Endocrine and biochemical abnormalities • Glucose intolerance • Hyperinsulinaemia • Insulin resistance • Hypercortisolism • Hypertriglyceridaemia • Low high-density lipoprotein (HDL) cholesterol • Raised small dense lowdensity lipoprotein (LDL) cholesterol
6 5 4 3 2 1 0
Lean
Obese
b Energy expenditure in lean and obese subjects expressed per kg fat-free mass (mean + SE) 50 45
6
40
Kj/kg/d
35
pregnancy. This includes hypertension, pre-eclampsia, gestational diabetes and an increased risk of foetal abnormalities including neural tube defects. Reductions in body weight of even 5–10% are associated with symptomatic improvements in many of these conditions and a significant reduction in the risk factors for chronic disease. Recent studies show as little as 4 kg weight loss over 4 years halved the incidence of type 2 diabetes in patients with impaired glucose tolerance. More dramatic decreases in diabetes are associated with the greater weight loss achieved as a result of bariatric surgery. However, improvements in hyperlipidaemia and hypertension may be transient and the impact of overall morbidity and life expectancy is less clear. This puts the emphasis on the primary prevention of excess weight gain.
5 0
Lean
obesity include mutations in the leptin gene and its receptor, or the melanocortin system. Other genetic syndromes occur in which obesity is a common element of the phenotype (e.g. Prader–Willi, Bardet–Biedl). However, these account for only a small proportion of the total cases of obesity and usually manifest as pronounced obesity from a relatively early age. Interestingly, in each case, obesity results primarily from over-eating rather than defects in energy expenditure. A large number of other candidate genes have been associated with obesity. Heritability studies suggest that approximately one-third of the variance in BMI may be due to genetic factors. The potential for some behavioural traits to have a genetic component is increasingly recognized, for example, food preferences or exercise habits.
Incidence/100,000 person-years
Relationship between obesity, fat distribution and coronary heart disease4
Metabolism For many years, obesity research focused on the search for a metabolic defect in obese people that limited their capacity to utilize energy and increased the propensity for fat storage. This was because some obese people ate a similar quantity of food, or perhaps even less, than their lean counterparts. Many obese people believe they have a lower metabolic rate than others, but the opposite is the case. Detailed studies have observed that obese people have a higher metabolic rate than their lean counterparts, which is proportional to the increase in lean tissue mass (Figure 8a and b). These findings have also been confirmed by studies using the doubly-labelled water method to make objective measurements of total energy expenditure in free-living conditions. In fact, community-based studies have demonstrated that obese people under-report their energy intake, typically recording at least
Waist tertiles High Medium Low
100
50
Medium
High
BMI tertiles 7
WOMEN’S HEALTH MEDICINE 1:1
Obese
8
Genes A small proportion of cases of obesity arise from genetic factors, leading to specific clinical syndromes. Monogenic causes of
Low
20 10
The causes of obesity are multi-factorial.
0
25 15
Aetiology of obesity
150
30
40
© 2004 The Medicine Publishing Company Ltd
OBESITY AND DIETING
a third fewer calories than the energy expended. The low levels of self-reported intake commonly observed in obese people and in other restrained eaters, are now recognized as a physiologically implausible record of habitual energy consumption. This has refocused attention on energy intake and the control of appetite and eating behaviour.
There is some evidence that high levels of physical activity may also enhance the sensitivity of the innate appetite control system making it easier to subconsciously balance energy intake and energy needs. This coupling between energy intake and energy expenditure is a key issue. Increases in obesity cannot be simply attributed to over-eating or inadequate activity, rather it represents a failure of the homeostatic mechanisms to precisely match energy intake to the body’s energy needs. However, research into the causes of obesity helps to develop individual strategies for the prevention and treatment.
Behaviour Obesity is a consequence of a period of prolonged positive energy balance when energy intake exceeds energy needs. Food intake and physical activity are two key behaviours which affect this energy balance and research has addressed their specific role in the aetiology of obesity. Fat (9 kcal/g) contains more than twice as many calories as protein or carbohydrate (4 kcal/g) making high-fat meals particularly energy dense. Studies in the 1990s revealed that dietary fat readily undermines innate appetite control systems. Studies among habitually lean subjects offered ad libitum access to foods in which the fat content was covertly manipulated, showed a positive association between energy intake and the proportion of fat in the diet. In other words, the higher the fat content, the greater the calories consumed. In studies, in which the energy density of foods is kept constant despite differences in the fat content, individuals were able to control their energy intake to match their energy needs and not exhibit hyperphagia. In the ‘real-world’ setting, energy-dense diets are high in fat, high in added sugars and low in vegetables and fruit. This type of diet is likely to increase the risk of obesity through a process described as passive over-consumption, implying that the quantity of food consumed may be unaltered but the net energy intake is increased because of the high energy density of the food. Sugar-rich soft drinks are an easy way to consume excess calories without realizing. Concerns about diet are compounded by the trend towards larger portions of many food items, notably soft drinks, savoury snacks and confectionery. Food eaten outside the home is frequently offered in extra-large portions, often at minimal additional cost. Research shows that large portions increase the energy consumed at a single eating episode but fail to illicit increased satiety or to suppress subsequent eating. Together, this results in an increased risk of excess weight gain. It is increasingly recognized that broader aspects of behaviour contribute to an individual’s risk of obesity. Many overweight people report that they rarely eat in response to a specific feeling of hunger, but as a consequence of boredom, loneliness or stress. Understanding these behavioural determinants of eating habits is important in helping to devise rational treatment strategies.
Environment: obesity is not just a concern for individuals. The increases in obesity linked to economic development suggest that we have a latent susceptibility to obesity. Around the world there are examples of communities following traditional lifestyles who, when exposed to 21st century Western culture, rapidly gain weight and develop diabetes. Closer to home, overweight tends to run in families, a result of both shared genes and a shared family lifestyle. Changes in society mean greater reliance on convenience foods and more food consumed outside the home; these tend to be higher in fat and sugar than home-prepared food. People increasingly depend on time-saving gadgets, which reduce effort, and then reward themselves after a hard day at work with hours spent in front of the TV or computer. u
REFERENCES 1 Sproston K, Primatesta P, eds. Health Survey for England, 2002. London: The Stationery Office, 2003. 2 Peeters A, Barendregt J J, Willekens F et al. Obesity in adulthood and its consequences for life expectancy: a life-table analysis. Ann Intern Med 2003; 138: 24–32. 3 Calle E E, Tuhin M J, Petrelli J M et al. Body-mass index and mortality in a prospective cohort of U.S. adults. N Engl J Med 1999; 341: 1097–105. 4 Rexrode K M, Carey V J, Hennekens C H et al. Abdominal adiposity and CHD in women. JAMA 1998; 280: 1843–8. 5 Manson J E, Willet W C, Stampfer M J. The Nurses’ Health Study: body weight and mortality among women. N Engl J Med 1997; 333: 677–85. FURTHER READING Garrow J. Obesity: report of the British Nutrition Foundation’s task force. Oxford: Blackwell Science, 1999. Jebb S A. Aetiology of obesity. Br Med Bull 1997; 53: 264–85. Packianathan I, Finer N. Medical consequences of obesity. Medicine 2003; 31: 8–11. WHO/FAO. WHO Technical Report Series 916. Diet, nutrition and the prevention of chronic diseases. Geneva: WHO, 2003.
Physical activity: levels of physical activity are also important. Daily activities now demand so little effort that voluntary physical activity is a major determinant of energy needs. A woman leading a sedentary life, using a car as the major form of transport, with an office-based job and no active leisure pursuits may expend only 30% more than their basal metabolic rate. Conversely, a moderately active adult may expend some 60% more and a very active sports person can double her basal energy needs. Physical activity brings important health benefits, independent of body weight, in particular helping to maintain insulin sensitivity and reduce the risk of type 2 diabetes.
WOMEN’S HEALTH MEDICINE 1:1
41
© 2004 The Medicine Publishing Company Ltd