INTRODUCTION

Obesity is defined as excess accumulation of adipose tissue. The World Health Organization describes the increase in obesity as a worldwide epidemic, with Western countries having a total number of 1.1 billion people overweight. The incidence of obesity in developed countries is increasing at an alarming rate and because obesity is associated with many chronic diseases, it has a dramatic effect on health costs in the present and will have in the future. Lowering the incidence of obesity in the community requires a multidisciplinary approach involving educators, urban planners and nursing and health practitioners. A recent survey found that 9.2% of Australians are members of weight-loss courses from companies such as Jenny Craig and Weight Watchers (Australian Institute for Health and Welfare [AIHW], 2005).

INCIDENCE IN AUSTRALIA

According to the Australian Society for the Study of Obesity (2007), the number of people who are obese is rising rapidly worldwide, making obesity one of the fastest developing public health problems. Recent studies estimate that more than half of all Australian women (54%) and two-thirds of men (68%) are overweight or obese. Almost 61% of the adult population in Australia is overweight or obese, and obesity has more than doubled in the past 20 years; the prevalence is 2.5 times greater than it was in 1980. Importantly, childhood obesity in Australia is the highest among developed nations. Twenty-seven per cent of Australian children are now overweight or obese (AIHW, 2005). The prevalence of obesity is higher among children of lower socioeconomic status (O’Dea, 2003).

A recent study of 20,347 Australian men and women showed that for the period 1980–2000 obesity increased by 250%, with the rate of growth in obesity higher in women than in men (34% compared to 27%). The study correlated obesity with lower socioeconomic status, higher television viewing time and lower physical activity (Cameron, 2003).

CLINICAL MEASUREMENTS

The most convenient way to measure overweight and obesity is by body mass index (BMI, kg/m²). A person is overweight if their BMI is between 25 and 29 and obese if their BMI is 30 or greater. Obesity is also classified according to the increased health risks associated with increasing BMI levels: class I (BMI 30–34.9), class II (BMI 35–39.9) and class III (BMI 40+). In clinical practice children are classified according to BMI-for-age growth charts (Baur, 2000).

Some practitioners use waist-to-hip ratios, as there is a greater risk of heart disease, diabetes, infertility and liver disease cancers associated with central adipose tissue accumulation (‘spare tyre’), and a single measurement can be used. Men with a waist circumference greater than 102 cm and women with a waist circumference greater than 88 cm are classified as obese (Baur, 2000).

There are also a number of electronic devices that can be incorporated into weighing scales or hand-held devices that can determine total adipose tissue but these have to be corrected for height, gender and athletic ability.

The obesity class into which a person falls determines the type of therapy and lifestyle changes that can be suggested. A reduction in dietary energy intake and an increase in physical activity would be considered for all obese people, and aggressive methods of weight reduction using drugs or bariatric surgery for people with class II or class III obesity, particularly if they have other risk factors (Katzmarzyk & Mason, 2006).

EPIDEMIOLOGY AND CAUSES OF OBESITY

A study of hospital and medical practice records found that of 14 preventable health risks examined, obesity was responsible for 7.5%, and physical inactivity 6.6% of the incidence of the major diseases in Australia (AIHW, 2005). The highest risk factor was smoking (7.8%).The study also showed that a strong upsurge in the number of people with diabetes is likely, mostly due to higher levels of obesity.

Other studies (AIHW, 2005) have shown that two-thirds of avoidable hospital admissions were due to chronic conditions, many from diabetes complications, heart and respiratory conditions caused by obesity. This places an economic burden on the health system as well as a stress on health workers, as obese patients are physically difficult to manage. The annual cost to the Australian community was estimated at $3 billion in 2007, so the cost-effectiveness and therapeutic benefits of management strategies must have a high priority.

Humans have evolved to consume food when it is available and store excess energy as adipose tissue while at the same time reducing physical activity, which maintains this store. Some individuals have ‘thrifty genes’, which are very efficient at conserving energy, but in Western society we do not experience the food scarcity that would reduce the energy stores. ‘Dieting’ in these individuals may be ineffective because of metabolic adaptation that conserves energy (Williams & Ness, 1991).

Men are less likely to regard themselves as overweight or to feel that they need to lose weight than are women. Women are likely to be concerned about their weight, particularly if they are in higher socioeconomic groups or are high-profile individuals such as models or movie stars. Social class is also correlated with other health risk factors associated with obesity and heart disease, the incidence of drug taking, alcohol and tobacco abuse increasing in lower socioeconomic groups (Skurray & Ham, 1999).

In recent years research studies have suggested that increased obesity incidence has occurred despite no apparent increase in food intake. This has been dubbed the ‘American paradox’. A decrease in physical exercise was suggested to be the cause of this obesity (Philips, 2004). However, the International Obesity Taskforce (IOT) (2002) has shown that the total amount of food may have remained constant but there has been an increase in the intake of energy-dense foods and drinks, as well as an environment that limits opportunities for physical activity. Australian national nutrition surveys have shown that in Australia the increase in energy consumption in recent years has come not from dietary fat but from carbohydrate in the form of sucrose in processed foods (Stubbs & Lee, 2004).

A common myth is that obese people have a lower-than-normal metabolic rate. However, a comparison of populations in Europe, Australia and the USA has shown that the total daily energy expenditure of obese people is the same as that of normal-weight individuals. The mass of the population has increased so that population total energy expenditure has increased (IOT, 2002).

Surveys investigating changes in physical activity over the period in which the incidence of obesity has increased have shown that the percentage of people undertaking 30 minutes of exercise per day decreased from 62% to 57% even though there is evidence that 45 to 60 minutes of exercise is needed on a daily basis to prevent weight gain on the present energy-rich diet (IOT, 2002). More recent studies in Australia and the USA have pinpointed the cause of obesity in children and young adults as an increase in consumption of soft drinks, with Australian data indicating a 240% increase over a 30-year period. Children who consumed the most soft drinks were obese and intervention studies showed that adults gained weight after ten weeks of normal consumption of soft drinks; another group who consumed artificially sweetened soft drinks lost weight. Soft drinks do not appease the appetite compared with solid energy-rich foods (Gill et al, 2006).

Other factors that have given rise to an ‘obesogenic’ environment are:

THE ASSOCIATED DISEASES OF OBESITY

Obesity has become one of the greatest health challenges in the Western world. It causes so much unnecessary morbidity and premature mortality and yet it is our most preventable cause of ill-health and chronic disability (O’Brien, Brown & Dixon, 2005).

In 2003, the AIHW reported on four major risk factors for ill-health and identified these as physical inactivity, overweight and obesity, tobacco smoking and alcohol consumption. ‘Risk factor’ is the term for a range of health-related behaviours that can have a positive or negative impact on individual health. It is also known as a ‘determinant of health’.

The term ‘malnutrition’ is more often associated with undernourishment and hunger than with obesity. However, the world is now seeing a dramatic increase in other forms of malnutrition characterised by obesity and the long-term implications of unbalanced dietary and lifestyle practices (World Health Organization (WHO), 2000).

Overweight or obesity is linked to numerous chronic health problems, including type 2 diabetes (AIHW, 2003), cardiovascular disease (Stanton (2006)), respiratory disease (Catford & Caterson, 2003), musculoskeletal problems and some cancers (IOT, 2002). The AIHW (2003) found that overweight or obesity during childhood and adolescence increases the risk of overweight or obesity in adulthood.

Notwithstanding genetic factors, overweight and obesity are caused by an energy imbalance. This imbalance of nutrient energy occurs when energy intake exceeds energy expenditure over a period of time. The AIHW (2003) found that good nutrition and levels of physical activity play an important role in the prevention of weight gain and weight loss. Good nutrition is a crucial preventative mechanism in the achievement of good health.

A positive energy balance (consuming more energy than you use) is relatively easy to achieve with our sedentary lifestyle and is largely due to overconsumption of energy-dense foods and foods high in fat (WHO, 2000). Alcohol consumption also contributes to weight gain, and excessive alcohol consumption is a major risk factor for morbidity and mortality in Australia. The AIHW (2003) estimated that the harm caused by excessive alcohol consumption accounted for 4.9% of the total burden of disease in 1996. Highly sweetened, high-strength ready-to-drink (RTD) alcopops deliberately mask the flavour of alcohol and encourage excess intake by making it easier to get drunk faster. The 2005 Australian Government survey of secondary schools students’ use of alcohol showed that 47% of 12–17-year-old girls and 13% of boys had consumed pre-mixed spirits in the last week and that the number of RTDs on the market had increased substantially (Australian Government Department of Health and Ageing, 2006).

A major consequence of our increasing overweight and obesity is the rising incidence of type 2 diabetes and the newly recognised metabolic syndrome. According to Zimmet, Alberti and Shaw, in 2001 the global incidence of people with diabetes was said to be 150 million and by 2025 this number will have risen to 300 million. This poses a massive health problem in both developed and developing countries. Mohan (2001) observed that in developed countries, overweight, obesity and diabetes correlate with lower socioeconomic groups, whereas the reverse applies in developing countries.

While the incidence of type 2 diabetes differs throughout the world, it is due to environmental, genetic and behavioural factors. People of Indian, Pacific Islander or Australian Aboriginal heritage are at particularly high risk of developing type 2 diabetes (Virtual Endocrine Centre, 2007). Indigenous peoples around the world are said to suffer diabetes at two to five times the rate of non-indigenous people (Menzies School of Health Research [MSHR], 2007).

One hypothesis proposes that a ‘thrifty gene’ is responsible for this increased susceptibility of indigenous peoples to type 2 diabetes. This genetic trait is said to help indigenous peoples survive extended periods without food, as it is associated with increased metabolic efficiency of nutrients. Now, a time of relative plenty, this ‘thrifty gene’ increases susceptibility to diabetes when indigenous populations migrate, urbanise or lead more modern, affluent and sedentary lifestyles. A media release from the MSHR (2007), however, suggests that the ‘thrifty gene’ is not responsible for the high rates of diabetes in indigenous peoples but that the high rates of diabetes are linked to aspects of the social environment:

Since 1981 the incidence of type 2 diabetes has doubled in Australia and the total number of cases has increased three-fold. According to Shaw and Chisholm (2003), more than 7% of Australian adults now have diabetes. Additionally, a further 16% of Australian adults have glucose intolerance. As the prevalence of diabetes increases with age, due in some part to degenerative processes, it is estimated that currently 20% of those aged over 60 years have type 2 diabetes. Alarmingly, more and more younger people, even children, are now developing type 2 diabetes. The increased number of obese young people will mean increased incidence of type 2 diabetes mellitus in this age group (Virtual Endocrine Centre, 2007).

Type 2 diabetes mellitus, also known as Non Insulin Dependent Diabetes Mellitus, is a complex metabolic disorder characterised by hyperglycaemia, a relative deficiency of insulin secretion, along with a reduced response of target tissues to insulin (insulin resistance). This, in turn, produces a deranged metabolism of carbohydrate, fats and proteins (Shaw and Chisholm (2003)).

According to Shaw and Chisholm (2003), insulin resistance is associated with a variety of cardiovascular risk factors, including central adiposity, glucose intolerance, dyslipidaemia and hypertension. When this association was realised, the concept of the metabolic syndrome was born, defined by WHO as having two components:

Early identification and diagnosis of metabolic syndrome, as a precursor to type 2 diabetes and as a risk indicator for cardiovascular disease, could have a marked impact on preventing the development of these diseases and the burgeoning obesity epidemic if crucial behavioural and lifestyles changes are enacted. Therein lies the complexity of the problem.

Shaw and Chisholm (2003) give the example of a 52-year old male with metabolic syndrome. Diagnosis was based on impaired glucose tolerance, central obesity, hypertension and dyslipidaemia. To halt this pre-diabetic state he needed to reduce all these risk markers in his lifestyle. To achieve this change he consulted with a dietitian to help reduce calories and saturated fat in his diet, to change the amount of food he ate. He undertook a 30-minute exercise regimen every day by alternating a brisk walk, swimming laps or riding an exercise bike before breakfast. After 6 months, while his weight had only decreased by 3 kg, his waist circumference had decreased by 6 cm and he felt generally better and more energetic and was enthusiastic to continue the diet and exercise regimen. Shaw and Chisholm emphasise that this type of lifestyle change needs to be ongoing, as discontinuing the program would put him (because of metabolic syndrome indicators) at high risk of developing type 2 diabetes, hypertension and cardiovascular disease.

Heart failure prevalence is increasing as a result of the ageing of the Australian population and also as a result of the increasing prevalence of overweight, obesity and diabetes. The risk of developing heart failure in Western countries is now about 20%. Campbell, 2003 says that while treatment of heart failure has seen many major advances in recent years it remains a major burden on the community. ‘Burden’ refers to the cost, care and disability associated with the cardiovascular diseases. Preventative approaches offer great benefits to the whole population. The prospect of reducing the incidence of heart failure, other cardiovascular diseases and diabetes through multi-tiered preventative strategies should be a major incentive for governments to fund this priority approach to healthcare (Campbell, 2003).

An interesting paradox in the alcohol debate is that low-to-moderate alcohol consumption has been found to have a protective effect against hypertension, ischaemic heart disease, stroke and gallstones for some subgroups of the population. The cardiovascular health benefit of low-to-moderate alcohol consumption relates mainly to men over 40 years of age and post-menopausal women (AIHW, 2007).

While diabetes and cardiovascular disease are potential major consequences of overweight and obesity, the chronic debilitating effects of overweight and obesity are often more insidious. The following three consequences highlight the complexity of the compounding effects of excess weight gain: obesity and the musculoskeletal system, obesity and reproductive health and obesity and depression.

To understand the effect of weight gain on the musculoskeletal system of the human body you need to imagine how it would feel if you added extra weight to your present condition. As an exercise you could try this: add a series of ever-increasing leaded weights to your ankles and go about your normal daily activities. As you increase the leaded weights you start to tire more quickly and your productivity reduces. Your legs may start to ache as a result of the added weight, as it becomes harder to carry the extra load around. Ultimately overweight or obesity is a burden that you carry around. This burden of weight gain adds stresses and strains to all systems in the body, as it overtaxes all anatomical and biochemical systems.

Over time, adding weight to the skeletal and articulation systems puts extra load on the spine and hips and particularly weight-bearing joints such as the knees. While normal degenerative changes often necessitate orthopaedic reconstructions and replacements, excess weight is often the main contributing factor to the rate of degeneration. Invasive surgery of any sort is fraught with risks and these risks are exacerbated with increasing levels of overweight and obesity. Within our elective surgery system we already have cases where surgery is delayed until an individual loses weight so as to enhance post-operative recovery and the operative intervention. If acceptable weight loss is not achieved then the individual may progressively become reliant on aids, such as walking sticks, to maintain mobility and independence.

It is in everyone’s interest to maintain a healthy weight range and thus reduce their own potential burden of chronic illness and disability.

A lesser documented effect of overweight and obesity is on reproduction function and obstetric outcomes (Nankervis et al, 2006). The ability to conceive spontaneously is reduced by obesity. Overweight and obese women are over-represented among sub-fertile groups and those presenting with menstrual irregularity and anovulation (Nankervis et al, 2006).

Pregnancy outcomes are also affected by overweight and obesity as risks to mother and baby are increased. These include increased risks of miscarriage, gestational diabetes, pregnancy induced hypertension, pre-eclampsia, thromboembolism, haemorrhage, caesarean section, sleep apnoea, wound infection and anaesthetic complications (Dietl, 2005; Andreasen et al, 2004).

Nankervis et al, 2006 confirm that congenital abnormalities, birth-related injuries and fetal death in utero are more common in the offspring of overweight and obese women. Babies are more likely to be macrosomic—large for gestational age—which complicates 10% of all births and increases risks of birth trauma and caesarean deliveries.

As overweight and obesity are occurring at a younger age, often increasing with time, and women are becoming pregnant later in life, the problems associated with reproductive health will escalate as the incidence of overweight and obesity increases (Nankervis et al, 2006).

Overwhelming evidence exists that overweight and obese people die earlier, suffer more damage to their body systems and functions, and are not the jolly individuals they are thought to be. Depression in the very obese is now well documented. Obese children and adults experience widespread prejudice, teasing and discrimination. As a group, they are less productive, accounting in Australia for some 4 million days away from work in 2001 (Colagiuri (2007)).

There are a number of possible reasons for the links between obesity, anxiety and depression. One reason might be that being obese is socially undesirable. Our culture is bombarded with the ‘thin is beautiful’ message and people not fitting that image may be seen as lazy or lacking in willpower, or having little regard for their health. Social undesirability might lead to greater anxiety and depression (Skilton et al, 2007). As obesity eventually causes ill-health and disability, the obese individual may be at risk of anxiety and depression, as we know that people who suffer from physical ill-health and disability are more prone to anxiety and depression (ASSO, 2004).

Overweight and obese people are less physically active. While it’s harder for them to be physically active and while lower physical activity might contribute to their obesity, we know that physical activity has an antidepressant effect. The irony is that physical activity tends to reduce depression (ASSO, 2004).

There is no doubt that obesity has a genetic component, and genes have always played a role in obesity and yet obesity is on the rise in epidemic proportions. Colagiuri (2007) asks Why? What has changed? What have we done? Do we have too much food and too little exercise, or have we changed the compositions of the food we eat? Is it our sedentary ‘touch of a button’ lifestyle, or is it our thoughtless urban design that reduces incidental physical activity? Perhaps it is television and e-games. Or let’s just blame our parents.

One thing we do know is that we need comprehensive public health strategies that are multi-tiered and intersectorial to encompass the environmental and social determinants of lifestyle. Caterson, 1999 believes we need to legislate for healthier environments and healthier communities, and we need education about healthy lifestyles throughout life, along with aggressive control of risk factors in high-risk individuals.

The solution to obesity is simple but it requires a long-term commitment to permanently change eating and exercise habits—and therein lies the problem, says Stanton (2006). Prevention is always the first choice when tackling obesity. However, individual commitment to lifestyle and behaviour change is difficult, as it is influenced by powerful commercial forces that promote eating and physical inactivity. To challenge the advertising of energy-dense foods during children’s TV viewing time would take strong political will (Brown & Siahpush 2007).

What should we do about obesity? One view, according to Caterson, 1999, is that weight loss and control are individual responsibilities, and another is that morbid obesity is inevitable because of genes, inherent appetite drives and metabolic set points, which need pharmacological or surgical weight-control help.

Brown & Siahpush (2007) suggest that the options for tackling overweight and obesity are:

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