Obesity: The Problem and its Treatments Prepared by John Dixon, March 2002 extract follows. 1.1 Definition
Obesity can be defined as a disease in which excess fat has accumulated such that health may be adversely affected (Kopelman, 2000) and mortality increased. Obesity is a serious public health threat. After smoking it is the second leading cause of preventable premature death in the U.S.A.(1998). Obesity causes and exacerbates many health problems. It is an independent risk factor for coronary heart disease (Hubert et al, 1983) and associated with hypertension, dyslipidaemia and impaired glucose metabolism, which are also independent risk factors for coronary artery disease. Increasing levels overweight and obesity are positively associated with reduced life expectancy (Katzmarzyk et al, 2001; Lew, 1985). The Framingham study found that any weight gain after the age of 30 years, regardless of the initial weight, was associated with increased risk of death (Hubert et al, 1983). 25-12-2006
1.2 The size and cost of the problem
The World Health Organization (WHO) has recognized an epidemic of obesity throughout most of the developed and developing world (2000). The prevalence of obesity has at least doubled in the majority of developed countries over the last 2 decades. In Australia, obesity (BMI > 30 kg/m2) in adult Australians over 20 years of age has increased from 8% in 1980 to 15% by 1995 (Australian Institute of Health and Welfare, 1998) and is currently estimated to be 20.5% (Dunstan et al, 2001). Similarly in the USA the prevalence of obesity is currently 28% and in some regions and among specific ethnic groups, much higher (National Institute of Health, 2001). There is no evidence that this epidemic in Australia or elsewhere has reached its peak. The increase in overweight and obesity is not confined to wealthy countries. The WHO consultation on obesity clearly demonstrates that developing countries experiencing improved socioeconomic conditions undergo a rapid population transition from underweight to overweight (2000). In addition the increasing prevalence of obesity in children is alarming (Bundred et al, 2001) and heralds a life long disorder with great risk of obesity related disease (Dietz, 1994; Dietz, 1998).
The direct cost of obesity is 2-5% of most developed countries, including Australia (Levy et al, 1995). In 1995 the total cost of obesity in the U.S.A. was estimated to be US$ 99 billion with US$ 52 billion representing direct health costs, 5.7% of total health cost (Wolf and Colditz, 1998). If the direct cost of physical inactivity is combined with that of obesity, in the USA, the estimated cost is 9.4% of the national health budget (Colditz, 1999). The most costly elements are those of managing the obesity comorbidies of hypertension, type 2 diabetes and coronary artery disease (Birmingham et al, 1999; Swinburn et al, 1997; Wolf, 1998). It is estimated that obesity accounts for 85% of the total cost of treating type 2 diabetes and 45% for hypertension (Oster et al, 2000).
The burden of obesity not only includes the direct health cost, but indirect cost through lost output due to reduction in or cessation of productivity (Levy et al, 1995). In addition there are intangible costs. The individual burden of obesity comprises reduced quality of life, increased morbidity and premature mortality and these will be discussed in detail later. There is also society’s stigmatization of the obese resulting in decreased opportunities in education, housing and employment (Hutton, 1994).
1.3 Measuring Obesity
The most commonly used measure of obesity, excessive body fat, is body mass index (BMI) which is calculated from the weight and height. BMI = weight (kg) / height (m)2. The assumption is that variation in weight for subjects with the same height is due to fat mass. BMI provides an easily measured continuous variable that allows comparisons of weight status and classification of normal, overweight and grades of obesity. While BMI gives some general information about body fatness, it does not measure fat and cannot accurately reflect fat mass or fat distribution in any person or group of people. The WHO has proposed classification of overweight and obesity based on BMI for adult men and women (2000) (Table 1.1). The popular descriptions are also shown and reflect those generally used in the current bariatric literature. Other methods are used to measure fat mass and distribution. These vary from simple anthropometric measures such as waist circumference and skin-fold thickness to more sophisticated techniques using bioimpedance, hydrodensiometry, whole body composition, dual-energy x-ray absorptiometry, computed tomography and magnetic resonance imaging. All have their various advantages and disadvantages with respect to accuracy, practicality, availability and cost (Heymsfield et al, 1998). A focus of this thesis has been the use of simple clinical measures and their relation to obesity comorbidity. Waist circumference has been used as a simple clinical predictor of metabolic risk, identifying those at greater risk of coronary heart disease. A waist circumference of greater than 94 cm for men and 80 cm for women are associated with increased risk and measures of greater than 102 and 88 respectively represent substantially increased risk (Han et al, 1995; Kannel et al, 1991).
Table 1.1: WHO classification and popular descriptions of obesity, measured as BMI, for adult men and women.
Body mass index (kg/m2) WHO classification Popular description
<18.5 Underweight Thin
18.5-24.9 Normal “Healthy” or “normal”
25-29.9 Overweight Overweight
30-34.9 Obese Class I Obese
35-39.9 Obese Class II Severe Obesity
40 or greater Obese Class III Morbid obesity (40-49.9)
Super Obesity (50+)
1.4 Cause of the obesity epidemic
Obesity is not a single disorder. It is a result of a complex interaction of genetic, developmental, environmental and psychosocial factors leading to an imbalance between energy intake and expenditure. While it is estimated that genetic factors are major determinants of an obesity risk (Bouchard, 1991; Bouchard and Tremblay, 1997), the expression of obesity usually requires environmental or behavioural factors. Certainly, considering the time and geographic trends, the current epidemic of obesity is best explained by environmental and behavioural changes associated with social and technological changes.
There are a number of single gene abnormalities causing obesity that have been described in rodent models, for example the leptin deficient ob mouse (Zhang et al, 1994). Obesity can also be a consistent finding in single gene abnormalities in humans, for example Prader-Willi syndrome. However, it is unlikely that any single gene is responsible for the tendency to obesity in the majority of obese humans. There is an ongoing search for possible candidate genes associated with obesity and its metabolic consequences in order to develop suitable biochemical or genetic interventional therapies that may be tailored to a specific genetic abnormality.
The evidence that modern western lifestyle provides an obesogenic environment surrounds us and is perhaps most evident in populations where modern technological advances and food practices have recently been introduced. The rapid development of obesity and a very high prevalence of associated comorbidity have produced major health problems in indigenous populations in Australia, USA and the Pacific Islands (Fitzgerald et al, 1997; McDermott et al, 2000; Zimmet et al, 1997). Migration studies have frequently shown increases in BMI (VanItallie, 1994). The changes in these populations are examples of the social and environmental effects on the genetically predisposed.
Determining the exact characteristics of the technologically advanced environment that predispose to obesity is important as changes to these provide the only practical way of preventing obesity and curtailing the obesity epidemic. Obesity develops as a result of positive energy imbalance. The technologically advanced environment provides both a plentiful supply of energy rich foods and the opportunity to minimise human activity. Teasing out important modifiable factors can be a challenge. Many studies demonstrate the importance of physical activity with a negative relationship between activity and obesity (DeLany, 1998; Klesges et al, 1995). Longitudinal studies show that those more physically active are less likely to gain weight (Rissanen et al, 1991; Schmitz et al, 2000). Sedentary leisure activities have been strongly associated with obesity. For example a major risk factor for the development of obesity in children is prolonged time watching television each day (Gortmaker et al, 1996; Robinson, 1999). Modern sedentary lifestyles may well be the dominant environmental factor in the development of obesity (Prentice and Jebb, 1995; Weinsier et al, 1998). This is supported by the evidence that energy intake has not increased in many developed countries where the prevalence of obesity is rising (Weinsier et al, 1998). There are many factors influencing the sedentary nature of society: labor saving devices, television, less emphasis on physical education in schools, lack of safe parks, footpaths and road ways to allow pedestrian and bicycle traffic (Koplan and Dietz, 1999). Many modern urban environments are considered unsafe and do not encourage physical activity. The answer to the obesity epidemic may more likely to lie with changes in urban design and public policy, rather than with the health professions.
Measuring energy intake in large epidemiological studies is difficult, as under-reporting of energy intake is a widely recognised feature of obesity. This may partly explain why there is no reported direct correlation between the prevalence of obesity and energy intake in developed nations (Kopelman, 2000). However weight gain in adults has been associated with increased dietary intake, especially high fat intake (Klesges et al, 1992). Observational cross-sectional and longitudinal studies suggest that a high fat diet and physical inactivity are independent risk factors for weight gain and obesity (Astrup, 1999). There is good evidence that different macronutrient have varying effects on satiety and that simple sugars and fatty foods stimulate appetite whereas a protein rich diet increases satiety (Johnstone et al, 1996; Lawton et al, 1993; Westerterp-Plantenga et al, 1999). However, the effect of long term lower fat intake on body weight is equivocal (Lew, 1985). A study of weight maintenance following weight loss showed that a diet low in fat and increased physical activity were indicators of long term success (Wing and Hill, 2001).
Suggested public health approaches to reduce the prevalence of obesity include (Nestle and Jacobson, 2000):
• Education on lifestyle and physical activity.
• Food labelling of nutrient content.
• Lower prices for healthy foods.
• Health care providers teach healthy diet and exercise.
• Funding for recreational activities, and urban planning to promote physical activity in the community.
• Tax high calorie foods.
• Develop national policy to prevent obesity.
Factors related to fetal and neonatal nutrition may also be important. There is now wide spread epidemiological evidence that fetal undernutrition may predispose to obesity and the metabolic syndrome in later life (Barker, 1990; Barker, 1993). These, and many other studies, provide evidence of fetal programming increasing the risk of the obesity, type 2 diabetes and other metabolic risks in association with low rates of fetal growth (Forsen et al, 2000). Twin studies have confirmed an increase in subcutaneous and abdominal fat and lower lean body weight in adulthood for the twin of lower birth weight (Loos et al, 2001). There is a also a positive relationship between birth weight and later body mass index. This is largely accounted for by maternal weight – heavier mothers have heavier babies and these tend to become heavier adults. The fathers’ weight, however, does not influence the risk of adult obesity in his children (Parsons et al, 2001). In addition to the importance of fetal programming there is evidence in rats of early neonatal programming where feeding a highly palatable diet induces obesity. In those genetically predisposed, higher weight set points are established and defended into adult life (Levin and Keesey, 1998). The importance of fetal and early childhood nutrition may therefore play an important role in obesity prevention.
Source: Obesity – The Problem and its Treatments Prepared by John Dixon, March 2002
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