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Childhood obesity and type 2 diabetes

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VOL: 98, ISSUE: 19, PAGE NO: 49

Matt Sabin, MB BS, BSc, MRCPCH, is a clinical paediatric research registrar;Elizabeth Crowne, MD, FRCPCH, is a consultant paediatrician in endocrinology and diabetes;Julian Shield, MD, FRCPCH, is a consultant senior lecturer, Royal Hospital for Children, Bristol

Childhood obesity is dramatically increasing in prevalence, and the complications of obesity, previously only seen in adulthood, are beginning to appear in children for the first time. Until now, type 2 diabetes had only been described in adults and children from ethnic minorities. The recent identification of four Caucasian UK children with type 2 diabetes related to severe obesity has led to fears that this is the ‘calm before the storm’ in terms of an epidemic of obesity-related type 2 diabetes and cardiovascular disease.

 

Childhood obesity is dramatically increasing in prevalence, and the complications of obesity, previously only seen in adulthood, are beginning to appear in children for the first time. Until now, type 2 diabetes had only been described in adults and children from ethnic minorities. The recent identification of four Caucasian UK children with type 2 diabetes related to severe obesity has led to fears that this is the ‘calm before the storm’ in terms of an epidemic of obesity-related type 2 diabetes and cardiovascular disease.

 

 

While knowledge of the numerous factors that are involved in the development of obesity increases, research to date has failed to provide any basis for effective treatment. However, current evidence points towards a family-based approach of education, in terms of diet and exercise, as being the most effective form of prevention and treatment. Initiatives from many quarters are necessary to combat the lifestyle changes that have led to the current situation. We need to find ways of reducing rates of childhood obesity and its complications if we are to avoid future obesity-related disease.

 

 

Obesity is increasing in adult and paediatric populations throughout the world (World Health Organization, 2000; Deckelbaum, 2001) leading the WHO in 1997 to describe the problem as ‘an escalating epidemic’. The increase in obesity prevalence rates was first noted in the USA more than 20 years ago and, linked with this, there was an increase in type 2 diabetes. The scale of the problem has been difficult to quantify, as there has been much debate regarding the most accurate way to classify the terms ‘overweight’ and ‘obesity’. The body mass index (BMI=weight/height2) has become the most widely used tool in adults and children and is now agreed to be a satisfactory index of adiposity in childhood. It also correlates with actual measures of body fatness and has been shown to correlate with long-term mortality (Must, 1996).

 

 

The problem with using the BMI in childhood is that it changes with age. After birth there is a gradual decline in BMI to a nadir at approximately six years of age (termed the time of ‘adiposity rebound’), following which there is a gradual increase to adult levels. Recent data regarding ranges of BMI for different populations has led to the creation of BMI growth charts representing normal ranges for age (Cole, 2000). This has allowed estimates of overweight and obesity rates to be calculated. UK children are quoted at approximately 10% and 1% respectively (Cole, 2000). However, there is now increasing evidence that these figures are underestimates and that figures are actually more like 30% and 10% respectively (Campbell, 2002). Whichever set of figures is more representative, it is now widely agreed that prevalence rates are increasing dramatically and that, if changes are not implemented quickly, significant illness can be predicted for today’s children.

 

 

Adult obesity is associated with increased risk of cardiovascular disease, hypertension and type 2 diabetes, and although the long-term implications of childhood obesity require clarification there is now strong evidence that it is associated with the development of the ‘metabolic syndrome’. This incorporates hypertension and abnormal glucose metabolism with high insulin and lipid levels. It is the abnormal glucose metabolism associated with the raised circulating levels of insulin (due to a resistance in peripheral tissues to the effect of insulin) that can lead to a failure of the pancreas to secrete enough insulin. This can lead to type 2 diabetes, with its attendant risks of cardiovascular disease, peripheral vascular disease, blindness, nephropathy and neuropathy later in life.

 

 

In Bristol, we have established a clinic for children with obesity and have seen worrying evidence of high insulin levels and even type 2 diabetes (Box 1). This is the first description of these effects in UK Caucasian children and we believe that this is the tip of the iceberg in terms of the prevalence of insulin resistance associated with childhood obesity. Research into interventions aimed at the treatment and future prevention of childhood obesity are needed now if we are to avoid an epidemic of diabetes and heart disease.

 

 

Latest research
The increase in obesity rates has been met by research initiatives, mainly from the USA, looking at interventions to reduce weight. These have been based on diet and exercise changes, and the best results have been associated with implementing this in a cognitive-behavioural therapy approach (Epstein, 2001). However, at a time when obesity rates are escalating there is an astonishing lack of evidence for any particular approach to either treatment or prevention (Campbell, 2002).

 

 

In contrast, there is an increasing amount of evidence from laboratory research into the complexities that underlie appetite, growth and a propensity to obesity. In fact, where adipose tissue was previously thought to be a non-descript entity that was present simply to store energy, there is now much data that supports it being a separate endocrine organ. We now know that adipose tissue has receptors that control its own growth and it also secretes factors, which have central effects on appetite and satiety.

 

 

Probably the best researched is the hormone leptin, which is secreted from adipose tissue and feeds back to the brain, reflecting the body’s current status of fat storage and, in turn, encouraging a reduction in intake. This is part of a loop involving many factors that link to control the body’s energy intake. As a balance to this, a hormone termed ‘ghrelin’ is secreted from the stomach and may be involved in feeding back a hunger signal to the brain in times of low energy intake. These are two factors in an enormously complex system that controls energy intake and adipose tissue growth and regulation. Other factors that are secreted by adipose tissue have been implicated in the process of obesity-related insulin resistance.

 

 

Of these the cytokine TNF alpha and a hormone called resistin have received much interest. Their role in insulin-resistance, secondary to obesity, is still to be finally elucidated but represents significant advances in our understanding of the development of obesity. However, initial excitement on discovery of these factors has led to disappointment because they do not individually hold the key to the progression of obesity or obesity-related insulin resistance.

 

 

Treatment and prevention
While research is under way and scientific advances are made into the understanding of obesity and its related disorders, lifestyle changes remain the mainstay of treatment and prevention. Nurses are ideally placed to deliver this information. There are currently no specific drug therapies for obesity that are used in the paediatric population. However, in those children developing type 2 diabetes our Bristol clinic initially uses metformin, which is an insulin-sensitising agent. The advantage of metformin over sulphonylureas or insulin is that there is no risk of hypoglycaemia and, therefore, blood sugars do not need to be monitored so vigorously. However, care should be taken in prescribing for those with liver or kidney disease, as lactic acidosis can occur.

 

 

Some factors that may be associated with increases in childhood obesity prevalence rates (National Audit Office, 2002) are outlined in Box 2 and may provide a practical basis for educating children with obesity and their families. This education should be available from all nurses and workers involved in the care of children. It can be seen from the list why cognitive-behavioural approaches in the USA have had the best results in terms of weight reduction and why prevention and treatment should be centred not only on the child but also their family.

 

 

Modern society may be responsible for many of these factors, rather than the children themselves, and acceptance of the child with obesity along with education and encouragement of lifestyle changes is essential if we are to avoid long-term consequences.

 

 

Discussion
Childhood obesity is a consequence of modern society, and many factors have contributed to the current situation. Therefore, prevention and treatment should not be confined to simple medical treatment - others must also take some responsibility, including government bodies, food manufacturers, the media, advertising companies and schools. Greater affluence has led to lifestyle behaviours centred on sedentary activities and eating as a leisure activity. However, individuals must shoulder some responsibility and encourage change wherever possible.

 

 

At our Bristol clinic we have seen that simple education and support in personal aspects of daily living provides a good basis for attempting weight changes. This is especially so in the younger child, where weight reduction is not encouraged. Often simple lifestyle changes, carried out by parents, have led to weight stabilisation that then falls into normal ranges as the child continues to grow. From the medical perspective, whether treatment is best implemented from community-based programmes, primary care or secondary care remains to be seen, but it is likely that all will need to be involved, with emphasis based on the home and school environments.

 

 

Conclusion
Increasing childhood obesity and a lack of evidence regarding the best approaches to tackle this has led to widespread concern. The increasing evidence of complications associated with childhood obesity and the presentation of the first cases of obese children with type 2 diabetes in the UK has taken many by surprise. However, this situation was predictable from US trends. If these trends are extrapolated we are set for a future of increasing obesity and with it an increase in the prevalence of type 2 diabetes and cardiovascular disease. While research efforts are made to investigate mechanisms underlying appetite and adipose tissue regulation, it is the responsibility of all to try and minimise childhood obesity with the available tools to hand. At present, the best of these is education regarding diet and exercise.

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