The burden of overweight and obesity-related ill health in the UK

This paper reviews previous cost studies of overweight and obesity in the UK. It proposes a method for estimating the economic and health costs of overweight and obesity in the UK which could also be used in other countries. Costs of obesity studies were identified via a systematic search of electronic databases. Information from the WHO Burden of Disease Project was used to calculate the mortality and morbidity cost of overweight and obesity. Population attributable fractions for diseases attributable to overweight and obesity were applied to National Health Service (NHS) cost data to estimate direct financial costs. We estimate the direct cost of overweight and obesity to the NHS at £3.2 billion. Other estimates of the cost of obesity range between £480 million in 1998 and £1.1 billion in 2004 [Correction added after online publication 11 June 2007: 'of the cost of obesity' added after 'Other estimates']. There is wide variation in methods and estimates for the cost of overweight and obesity to the health systems of developed countries. The method presented here could be used to calculate the costs of overweight and obesity in other countries. Public health initiatives are required to address the increasing prevalence of overweight and obesity and reduce associated healthcare costs.

Assessing the burden of overweight and obesity : an example from the United Kingdom

Introduction: In this paper I review previous cost studies for overweight and obesity in the UK. I propose a method for estimating the economic and health costs of overweight and obesity in the UK which could also be used in other countries.

Methods: Costs of obesity studies were identified via a systematic search of electronic databases. Information from the WHO Burden of Disease Project was used to calculate the mortality and morbidity cost of overweight and obesity.
Population attributable fractions for diseases attributable
to overweight and obesity were applied to National Health Service (NHS) cost data to estimate direct financial costs.

Results: We estimate the direct cost of overweight and obesity to the NHS at £3.2 billion. Other estimates range between £480 million in 1998 and £1.1 billion in 2004. There is wide variation in methods and estimates for the cost of overweight and obesity to the health systems of developed countries.

Conclusion: The method presented here could be used to calculate the costs of overweight and obesity in other countries. Public health initiatives are required to address the increasing prevalence of overweight and obesity and reduce associated healthcare costs.

Urban living and obesity : is it independent of its population and lifestyle characteristics?

OBJECTIVES: Living in an urban area influences obesity. However, little is known about whether this relationship is truly independent of, or merely mediated through, the demographic, socio-economic and lifestyle characteristics of urban populations. We aimed to identify and quantify the magnitude of this relationship in a Sri Lankan population.

METHODS: Cross-sectional study of adults aged 20-64 years representing the urban (n = 770) and rural (n = 630) populations, in the district of Colombo in 2004. Obesity was measured as a continuous variable using body mass index (BMI). Demographic, socio-economic and lifestyle factors were assessed. Gender-specific multivariable regression models were developed to quantify the independent effect of urban/ rural living and other variables on increased BMI.

RESULTS: The BMI (mean; 95% confidence interval) differed significantly between urban (men: 23.3; 22.8-23.8; women: 24.2; 23.7-24.7) and rural (men: 22.3; 21.9-22.7; women: 23.2; 22.7-23.7) sectors (P < 0.01). The observed association remained stable independently of all other variables in the regression models among both men (coefficient = 0.64) and women (coefficient = 0.95). These coefficients equated to 2.2 kg weight for the average man and 1.7 kg for the average woman. Other independent associations of BMI were with income (coefficient = 1.74), marital status (1.48), meal size (1.53) and religion (1.20) among men, and with age (0.87), marital status (2.25) and physical activity (0.96) among women.

CONCLUSIONS: Urban living is associated with obesity independently of most other demographic, socio-economic and lifestyle characteristics of the population. Targeting urban populations may be useful for consideration when developing strategies to reduce the prevalence of obesity.

The North-South gap in overweight and obesity in England

Regional differences in overweight and obesity levels in England have mirrored those of CVD, with higher levels in the North. It is unclear whether the increase in the prevalence of overweight and obesity over the last 15 years has been consistent in different regions of the country. BMI data from each of the health surveys for England conducted between 1993 and 2004 were analysed. Annual grouped estimates of the prevalence of overweight (BMI ≤ 25 kg/m²) and obesity (BMI ≤ 30 kg/m²) for the North and the South of England were produced by appropriately combining regional administrative authorities. Logistic regression analyses were performed to assess the independence of the geographical effect after adjustment for age and social class. The prevalence of both overweight and obesity in women has risen more quickly in the North than in the South between 1993 and 2004, leading to a widening of inequalities. The prevalence of both overweight and obesity in women in the South has remained reasonably stable since 1997. The prevalence rates of both conditions in men have risen in parallel in the North and the South between 1993 and 2004 by approximately 8%. The OR for obesity for young women increased between 1993/98 and 1998/2004 from 1·07 (1·00, 1·14) to 1·21 (1·13, 1·30). Widening geographical inequalities in overweight and obesity rates in women could lead to widening inequalities in cardiovascular and other diseases.

Diet, physical activity and obesity statistics

This publication provides statistics on diet, physical activity and obesity as these relate to the incidence and prevalence of CVD.

Risk of cardiovascular and all-cause mortality in individuals with diabetes mellitus, impaired fasting glucose, and impaired glucose tolerance. The Australian Diabetes, Obesity and Lifestyle Study (AusDiab)

Background--Diabetes mellitus increases the risk of cardiovascular disease (CVD) and all-cause mortality. The relationship between milder elevations of blood glucose and mortality is less clear. This study investigated whether impaired fasting glucose and impaired glucose tolerance, as well as diabetes mellitus, increase the risk of all-cause and CVD mortality.

Methods and Results--In 1999 to 2000, glucose tolerance status was determined in 10 428 participants of the Australian Diabetes, Obesity, and Lifestyle Study (AusDiab). After a median follow-up of 5.2 years, 298 deaths occurred (88 CVD deaths). Compared with those with normal glucose tolerance, the adjusted all-cause mortality hazard ratios (HRs) and 95% confidence intervals (CIs) for known diabetes mellitus and newly diagnosed diabetes mellitus were 2.3 (1.6 to 3.2) and 1.3 (0.9 to 2.0), respectively. The risk of death was also increased in those with impaired fasting glucose (HR 1.6, 95% CI 1.0 to 2.4) and impaired glucose tolerance (HR 1.5, 95% CI 1.1 to 2.0). Sixty-five percent of all those who died of CVD had known diabetes mellitus, newly diagnosed diabetes mellitus, impaired fasting glucose, or impaired glucose tolerance at baseline. Known diabetes mellitus (HR 2.6, 95% CI 1.4 to 4.7) and impaired fasting glucose (HR 2.5, 95% CI 1.2 to 5.1) were independent predictors for CVD mortality after adjustment for age, sex, and other traditional CVD risk factors, but impaired glucose tolerance was not (HR 1.2, 95% CI 0.7 to 2.2).

Conclusions--This study emphasizes the strong association between abnormal glucose metabolism and mortality, and it suggests that this condition contributes to a large number of CVD deaths in the general population. CVD prevention may be warranted in people with all categories of abnormal glucose metabolism.

The effectiveness of physical activity interventions for the treatment of overweight and obesity and type 2 diabetes

This review summarises current evidence relating to the effectiveness of physical activity (PA) interventions for treating overweight and obesity and type 2 diabetes. Interventions to increase PA for the treatment of overweight and obesity in both children and adults have primarily consisted of health education and behaviour modification strategies in clinical settings or with selected families or individuals. Although evidence is limited, strategies to reduce sedentary behaviours appear to have potential for reducing obesity among children and adolescents. Among adults, strategies that combine diet and PA are more effective than PA strategies alone. Combined lifestyle strategies are most successful for maintained weight loss, although most programs are unsuccessful in producing long-term changes. There is little evidence about compliance to prescribed behaviour changes or the factors that promote or hinder compliance to lifestyle changes. Limited evidence suggests that continued professional contact and self-help groups can help sustain weight loss. Most of the interventions for the treatment of type 2 diabetes have been conducted in clinical settings and have typically required the use of extensive resources. Evidence suggests that interventions can lead to small but clinically meaningful improvements in glycaemic control, even in the absence of weight loss. A recent study demonstrated that a multifactorial intervention (diet, PA and pharmaceutical) can reduce the risk of diabetes complications in individuals with type 2 diabetes. Nevertheless, there is little evidence about the effectiveness of community-based interventions in producing long-term changes in glycaemic control and reduced mortality in people with type 2 diabetes.

The inverse relationship between number of steps per day and obesity in a population-based sample - the AusDiab study

Background:
Physical activity (PA) is inversely associated with obesity but the effect has been difficult to quantify using questionnaires. In particular, the shape of the association has not yet been well described. Pedometers provide an opportunity to better characterize the association.

Methods:
Residents of households over the age of 25 years in randomly selected census districts in Tasmania were eligible to participate in the AusDiab cross-sectional survey conducted in 1999–2000. 1848 completed the AusDiab survey and 1126 of these (609 women and 517 men) wore a pedometer for 2-weekdays. Questionnaire data on recent PA, TV time and other factors were obtained. The outcomes were waist circumference (in cm) and body mass index (BMI) (kg/m2).

Results:
Increasing daily steps were associated with a decline in the obesity measures. The logarithmic nature of the associations was indicated by a sharper decline for those with lower daily steps. For example, an additional 2000 steps for those taking only 2000 steps per day was associated with a reduction of 2.8 (95% confidence interval (CI): 2.1,4.4) cm in waist circumference among men (for women; 2.2 (95% CI: 0.6, 3.9 cm)) with a baseline of only 2000, steps compared to a 0.7 (95% CI 0.3, 1.1) cm reduction (for women; 0.6 (95% CI: 0.2, 1.0)) for those already walking 10 000 steps daily. In the multivariable analysis, clearer associations were detected for PA and these obesity measures using daily step number rather than PA time by questionnaire.

Interpretation:
Pedometer measures of activity indicate that the inverse association between recent PA and obesity is logarithmic in form with the greatest impact for a given arithmetic step number increase seen at lower levels of baseline activity. The findings from this study need to be examined in prospective settings.

Effects of diets high in whey, soy, red meat and milk protein on body weight maintenance in diet-induced obesity in mice

This study examined the effects of different food sources of protein on energy intake, body weight maintenance, and on the responses of plasma leptin, insulin and adiponectin in chronic high-fat diet-induced obese mice. Obesity was induced in 47 mice with a high-fat diet for 20 weeks. They were divided into five diet groups to test the effects of a higher protein proportion (30% energy), achieved at the expense of carbohydrate. For the next eight weeks, four of the groups were fed diets of chow formulated with whey, soy, red meat or milk while the control group continued on their high-fat diet. The results showed that: (i) increasing the protein : carbohydrate ratio (both at 30% energy) in a high-fat diet did not reduce the level of obesity; (ii) the type of protein added, however, did have a significant effect on the level of obesity attained; (iii) whey protein stabilised weight gain the most, had the strongest satiety effects and also stimulated the highest production of adiponectin; and (iv) whey protein also was associated with the lowest insulin values among all proteins tested. Plasma leptin levels were not affected by any of the diets. Dietary fat remains a potent factor in weight management, but the type and amount of protein may also be important through its effects on food intake. In particular, the apparent decreased appetite associated with increased adiponectin in the whey-based high-protein diet may contribute to stabilised body mass in chronic high-fat diet-induced obesity.

Assessing cost-effectiveness in obesity (ACE-Obesity) : an overview of the ACE approach, economic methods and cost results

Background : The aim of the ACE-Obesity study was to determine the economic credentials of interventions which aim to prevent unhealthy weight gain in children and adolescents. We have reported elsewhere on the modelled effectiveness of 13 obesity prevention interventions in children. In this paper, we report on the cost results and associated methods together with the innovative approach to priority setting that underpins the ACE-Obesity study.

Methods : The Assessing Cost-Effectiveness (ACE) approach combines technical rigour with 'due process' to facilitate evidence-based policy analysis. Technical rigour was achieved through use of standardised evaluation methods, a research team that assembles best available evidence and extensive uncertainty analysis. Cost estimates were based on pathway analysis, with resource usage estimated for the interventions and their 'current practice' comparator, as well as associated cost offsets. Due process was achieved through involvement of stakeholders, consensus decisions informed by briefing papers and 2nd stage filter analysis that captures broader factors that influence policy judgements in addition to cost-effectiveness results. The 2nd stage filters agreed by stakeholders were 'equity', 'strength of the evidence', 'feasibility of implementation', 'acceptability to stakeholders', 'sustainability' and 'potential for side-effects'.

Results : The intervention costs varied considerably, both in absolute terms (from cost saving [6 interventions] to in excess of AUD50m per annum) and when expressed as a 'cost per child' estimate (from <AUD1.0 [reduction of TV advertising of high fat foods/high sugar drinks] to >AUD31,000 [laparoscopic adjustable gastric banding for morbidly obese adolescents]). High costs per child reflected cost structure, target population and/or under-utilisation.

Conclusions : The use of consistent methods enables valid comparison of potential intervention costs and cost-offsets for each of the interventions. ACE-Obesity informs policy-makers about cost-effectiveness, health impact, affordability and 2nd stage filters for important options for preventing unhealthy weight gain in children. In related articles cost-effectiveness results and second stage filter considerations for each intervention assessed will be presented and analysed.

Central obesity as a precursor to the metabolic syndrome in the AusDiab study and Mauritius

Evidence from epidemiologic studies that central obesity precedes future metabolic change and does not occur concurrently with the appearance of the blood pressure, glucose, and lipid abnormalities that characterize the metabolic syndrome (MetS) has been lacking. Longitudinal surveys were conducted in Mauritius in 1987, 1992, and 1998, and in Australia in 2000 and 2005 (AusDiab). This analysis included men and women (aged 25 years) in three cohorts: AusDiab 2000–2005 (n = 5,039), Mauritius 1987–1992 (n = 2,849), and Mauritius 1987–1998 (n = 1,999). MetS components included waist circumference, systolic blood pressure, fasting and 2-h postload plasma glucose, high-density lipoprotein (HDL) cholesterol, triglycerides, and homeostasis model assessment of insulin sensitivity (HOMA-S) (representing insulin sensitivity). Linear regression was used to determine which baseline components predicted deterioration in other MetS components over 5 years in AusDiab and 5 and 11 years in Mauritius, adjusted for age, sex, and ethnic group. Baseline waist circumference predicted deterioration (P < 0.01) in four of the other six MetS variables tested in AusDiab, five of six in Mauritius 1987–1992, and four of six in Mauritius 1987–1998. In contrast, an increase in waist circumference between baseline and follow-up was only predicted by insulin sensitivity (HOMA-S) at baseline, and only in one of the three cohorts. These results suggest that central obesity plays a central role in the development of the MetS and appears to precede the appearance of the other MetS components.

Expanding evidence for the multiple dangers of epidemic abdominal obesity

The waistline of America has been expanding now for decades,1 largely as a consequence of an obesogenic environment, with a car-worshipping culture and take-away lifestyle par excellence.2 No upper limit to the prevalence or extent of obesity is yet apparent, and many countries and communities worldwide are busily following the American lead. Accumulating research evidence suggests that the personal and economic costs of the obesity epidemic are immense,3 driven by the obesity-related increases in risk for conditions such as type 2 diabetes mellitus, the metabolic syndrome, cardiovascular disease (CVD), kidney disease, arthritis, cancer, asthma, and sleep-disordered breathing. In addition, decreases are apparent in self-esteem and quality of life.

HOMA insulin sensitivity index and the risk of all-cause mortality and cardiovascular disease events in the general population : the Australian diabetes, obesity and lifestyle study (AusDiab) study

Aims/hypothesis We assessed whether the relationships between insulin sensitivity and all-cause mortality as well as fatal or non-fatal cardiovascular disease (CVD) events are independent of elevated blood glucose, high blood pressure, dyslipidaemia and body composition in individuals without diagnosed diabetes.
Methods Between 1999 and 2000, baseline fasting insulin, glucose and lipids, 2 h plasma glucose, HbA1c, anthropometrics, blood pressure, medication use, smoking and history of CVD were collected from 8,533 adults aged >35 years from the population-based Australian Diabetes, Obesity and Lifestyle study. Insulin sensitivity was estimated by HOMA of insulin sensitivity (HOMA-%S). Deaths and fatal or non-fatal CVD events were ascertained through linkage to the National Death Index and medical records adjudication.
Results After a median of 5.0 years there were 277 deaths and 225 CVD events. HOMA-%S was not associated with all-cause mortality. Compared with the most insulin-sensitive quintile, the combined fatal or non-fatal CVD HR (95% CI) for quintiles of decreasing HOMA-%S were 1.1 (0.6–1.9), 1.4 (0.9–2.3), 1.6 (1.0–2.5) and 2.0 (1.3–3.1), adjusting for age and sex. Smoking, CVD history, hypertension, lipid-lowering medication, total cholesterol and waist-to-hip ratio moderately attenuated this relationship. However, the association was rendered non-significant by adding HDL. Fasting plasma glucose, but not HOMA-%S significantly improved the prediction of CVD, beyond that seen with other risk factors.
Conclusions/interpretation In this cohort, HOMA-%S showed no association with all-cause mortality and only a modest association with CVD events, largely explained by its association with HDL. Fasting plasma glucose was a better predictor of CVD than HOMA-%S.