chapter 37 Obesity
BACKGROUND
Increased prevalence of obesity is an issue confounding health policy makers across the developed and developing world (Fig 37.1). In medicine, disciplines that have not had to deal with obesity-related illness are having to change management practices to counter it, and the role of cigarette smoking as our leading preventable cause of illness is rapidly being supplanted by overweight. Population surveys in Australia and internationally, while varying depending on the populations studied,1,2 show that starting from the paediatric age group, the prevalence of obesity increases in all age groups up to about the sixth decade.
In the United States in 2007–2008, the age-adjusted prevalence of obesity was 33.8% overall, 32.2% among men and 35.5% among women. The corresponding prevalence estimates for overweight and obesity combined (BMI ≥ 25) were 68.0%, 72.3% and 64.1%.4 A review of prevalence estimates in European countries found that the prevalence of obesity based on measured weights and heights varies widely from country to country, with higher prevalences in central, eastern and southern Europe.5
The Ausdiab Study showed a prevalence of overweight and obesity in Australia of over 50%.6 Data for children and adolescents are incomplete but from a demographic point of view at least, the progression from normal weight to overweight and obesity seems to be progressive rather than reversible, so that patients who develop weight problems are more likely to develop further weight problems than undergo substantial improvement. A significant percentage of obese adolescents will be expected to become obese adults.7
According to the UK Counterweight Trial, obese patients are more frequent presenters to general practitioner (GP) clinics8 and more likely to be actively treated with medications9,10 than the average patient, so the population prevalence of obesity will usually under-represent the number of obese patients that a practitioner will actually see. Normalisation of obesity in the community allows it to be chronically under-recognised, and many patients who could benefit from intervention by a GP will miss out if active screening and action are not part of practice policy.11,12 Table 37.1 shows BMI and waist circumference values for the Caucasian population. Risk stratification by BMI for non-Caucasian populations is more difficult, and because they may be at risk of adverse metabolic problems at a lower weight, any evidence of excess abdominal adiposity may warrant formal assessment for the metabolic syndrome (Box 37.1). Estimation of childhood and adolescent weight disorders relies on using growth charts created by the American Centers for Disease Control and Prevention, with patients classified as overweight when above the 85th percentile, and obese when above the 95th percentile.
TABLE 37.1 Classification of obesity and overweight in Caucasians13
| Classification | BMI (kg/m2) | Waist circumference (cm) |
|---|---|---|
| Normal range | 18.5–24.9 | |
| Overweight | 25–29.9 | > 94 (male) > 80 (female) |
| Obese | > 30 | > 102 (male) > 88 (female) |
| Class I | 30–34.9 | |
| Class II | 35–39.9 | |
| Class III | > 40 |
BOX 37.1 Diagnosis of the metabolic syndrome14,15
2005 International Diabetes Federation definition of the metabolic syndrome:
WHAT CAUSES OBESITY?
While the underlying force driving weight gain in an individual is chronic energy imbalance, the seeming simplicity of weight maintenance hides multiple layers of complexity that relate as much to genetic and environmental factors16–19 as to voluntary food and exercise choices. Evolution has given us physiological systems that work to maintain ‘current weight’ without voluntary control and offer significant resistance to weight change (Fig 37.2). In both overfeeding and underfeeding studies there is resistance to changes in body composition, so that diets of energy surplus or restriction, while changing weight in the short term, will usually have little long-term effect on weight. Long-term positive energy imbalance gradually wears down the relatively weak metabolic defences against weight gain and this leads to creation of extra fat stores. These extra stores are rigorously defended when they are threatened by attempts at voluntary weight loss (Box 37.2), and thus chronic weight gain is encouraged and weight loss seemingly unobtainable. Environmental changes leading to increasing availability of energy-dense food, combined with a decline in opportunities to expend calories in everyday activities, have disengaged the ‘brakes’ that have previously allowed most people to remain weight stable.20 Failing societal cues for eating and exercise are yet to be replaced by effective public health policy, and lessons learned from successful public health campaigns relying on legislative changes to bolster education (i.e. tobacco smoking) have yet to be applied in obesity prevention. Studies looking at preventing weight gain in ‘at-risk’ populations are plagued by compliance and methodological problems, but patients who are frequent users of healthcare, such as pregnant women21 and patients with depressive illness,22 can benefit from weight management programs, and therefore these patients and others who are regular attendees at GP clinics are ideal candidates for intervention.
FIGURE 37.2 (and Box 37.2) The relationship between energy intake and weight is not linear.17,23–26 Most people’s weight varies within a 3–5 kg range, and once they leave this range a number of mechanisms are triggered,27,28 which return that person to their previous range, or, if the energy changes are long-lasting, act to reduce weight change by either increasing (energy excess) or decreasing (energy deficit) metabolic rate29–32 and altering hunger signals33,34 to help return the individual to their earlier range.35 Weight loss triggers a complex array of metabolic and behavioural changes. Patients losing weight often find that they manage early weight loss without great difficulty, then reach a plateau beyond which they cannot go without great effort. They become progressively psychologically distressed the longer the diet persists,36 and when they cease dieting they recover their lost kilos at a rapid rate, often overshooting their start weight.37
BOX 37.2 Measured physiological responses to weight loss
OBESITY-RELATED ILLNESS
Weight-related comorbidities are often a mixture of both metabolic and ‘mass-related’ physical changes (Table 37.2). An overweight patient’s expanded adipocyte mass functions as an active endocrine organ, with production of endocrine and paracrine substances as well as cytokines, which affect the systemic and portal circulations, leading to the metabolic effects of insulin resistance, including lipid and glucose abnormalities, reproductive hormone changes and hypertension. The physical manifestations of obesity, such as gastro-oesophageal reflux, sleep apnoea and arthritis, probably have metabolic associations also, but these are not well understood, and although obesity is significantly associated with cancers of the uterus, breast, colon and oesophagus, the mechanisms behind this are also not well understood.
INTEGRATIVE MANAGEMENT
DEFINING GOALS
Despite the diversity in patients needing weight management, and regardless of the resources available to the GP and the patient, the goals need to be health based. Some patients will be seeking weight loss, some will be undergoing treatment for metabolic or physical conditions, and some will be unaware of, or resistant to, linking their weight with their health. When devising a weight control strategy, weight loss itself needs to be viewed as the least effective measure of success and is the least likely outcome. Obtaining and maintaining a reduced-calorie diet combined with any degree of exercise will prevent weight gain, help control cholesterol and blood pressure problems, reduce abdominal girth, prevent progression of impaired glucose tolerance to type 2 diabetes, and potentially reduce mortality risk.38 Discussing weight issues in terms of health will significantly reduce the risk that the patient will treat your advice in the same manner that they treat the varied, conflicting and erroneous advice they receive from various forms of the dieting ‘industry’. Most diet-induced weight loss is invariably followed by weight regain, as the dietary process creates an artificial and unsustainable approach to food and exercise, rather than teaching the skills necessary to manage weight and maintain health in the long term.
MANAGEMENT OPTIONS
A range of weight management tools is available to the GP and can be used depending on the circumstances of the patient. Some obesity treatments may not be freely available, but most of those used in hospital-based obesity clinics are available in the community (Box 37.3). Guiding patients towards healthy eating habits and sustainable exercise patterns is the ultimate goal, but there will be times when weight loss itself is viewed as important, and if this is the case it is useful to know the nature and effects of obesity therapies. While occasional patients will have dramatic results from non-lifestyle treatments, it is unusual for these to persist, and weight regain usually leaves the patient in worse mental and physical health.
BOX 37.3 Nature and effects of readily available obesity treatments13,39–45
Reduced-energy diet
Very-low-energy diet
Exercise therapy
Successful weight loss
Box 37.4 shows data obtained from groups of patients who have not only lost weight, but kept it off in the long term. The medical data are primarily from the National Weight Control Registry,61 which is an observational study of patients who have maintained > 13.6 kg of weight loss for more than 12 months, and is the largest non-surgical weight-loss cohort in the world. Regardless of the route taken to weight loss, the destination is the same. Patients who lose large amounts of weight consume a diet that is significantly reduced in calories, food choice and spontaneity. They undertake about an hour of aerobic exercise a day, and if they ever regain weight they struggle to lose it again. As patients with weight problems are used to eating more and exercising less than their weight-normal peers, it is no surprise that so few can manage the self-imposed deprivation that this entails.
