Childhood obesity

Childhood obesity Epidemiology - Determinants and risk factors Differential diagnosis and complications Prevention Non-pharmacological treatment Pharmacological and surgical treatment Conclusion

Worldwide prevalence of childhood obesity has increased greatly during the past three decades. The increasing occurrence in children of disorders such as type 2 diabetes is believed to be a consequence of this obesity epidemic.

Much progress has been made in understanding of the genetics and physiology of appetite control and from these advances, elucidation of the causes of some rare obesity syndromes. However, these rare disorders have so far taught us few lessons about prevention or reversal of obesity in most children. Calorie intake and activity recommendations need reassessment and improved quantification at a population level because of sedentary lifestyles of children nowadays.

For individual treatment, currently recommended calorie prescriptions might be too conservative in view of evolving insight into the so-called energy gap. Although quality of research into both prevention and treatment has improved, high-quality multicentre trials with long-term follow-up are needed. Meanwhile, prevention and treatment approaches to increase energy expenditure and decrease intake should continue. Recent data suggest that the spiralling increase in childhood obesity prevalence might be abating; increased efforts should be made on all fronts to continue this potentially exciting trend.

Epidemiology
8 years have passed since the last Seminar on childhood obesity in The Lancet.¹ Our goal is to review new information and outline some of the remaining challenges. A review of secular trends in the number of overweight or obese children concluded that prevalence had increased during the past two to three decades in most industrialised countries, apart from Russia and Poland, and in several low-income countries, especially in urban areas.²

Prevalence doubled or trebled between the early 1970s and late 1990s in Australia, Brazil, Canada, Chile, Finland, France, Germany, Greece, Japan, the UK, and the USA.2 By 2010, more than 40% of children in the North American and eastern Mediterranean WHO regions, 38% in Europe, 27% in the western Pacific, and 22% in southeast Asia were predicted to be overweight or obese. However, that 2006 review pre-dates recent data, which, although still too soon to be certain, suggest that the increase in childhood obesity in the USA, the UK, and Sweden might be abating.^3-5

Internationally agreed thresholds of body-mass index (BMI) define underweight, normal weight, overweight, and obesity in adults, but in children, effects of age, sex, puberty, and race or ethnicity on growth make classification dificult. Definition of a standard age-related growth chart and clinically meaningful thresholds for overweight and obesity present challenges. The International Obesity Taskforce (IOTF) international standard growth chart enables global comparison of prevalence.⁶ However, many countries continue to use their own country-specific charts, including the USA, where standards are based on a national survey from the early 1960s, before the present epidemic.⁷

Widely used thresholds for being overweight or obese in childhood are: 110% or 120% of ideal weight for height; weight-for-height Z scores of higher than 1 or higher than 2, and BMI at the 85th, 90th, 95th, and 97th percentiles (on the basis of international or country-specific reference populations).² The IOTF recommend using their international growth charts and limits specific to age and sex that, on average, correspond to adult thresholds. The IOTF classification has high specificity, but low sensitivity.⁸

Determinants and risk factors
A historical convergence of forces, biological and technological, has led to the obesity epidemic. During millennia of frequent food scarcities, natural selection probably favoured people with parsimonious energy metabolism, known as the thrifty gene hypothesis.⁹

Although the advent of agriculture about 14 000 years ago ensured more stable food supplies, activities of daily living still needed substantial energy expenditure until about 50 years ago, when radical changes occurred in food availability and energy expenditure. The obesity epidemic is probably the result of evolutionary legacy interacting with our technologically advanced and consumerist society.

Population groups in North America who have preserved traditional lifestyles with substantial embedded physical activity have reduced prevalences of obesity.¹⁰ Likewise, in countries with low and middle incomes, the obesity epidemic is largely occurring in urban areas that have easy access to energy-dense cheap foods and low energy requirements in daily life.²

Obesity is a complex disorder that is affected by many interacting genetic and non-genetic factors. We focus mainly on prevention and treatment.

The table summarises determinants or risk factors that are associated with childhood obesity or variation in adiposity, and figure 1 shows a simplified model of leptin signalling, which is the key biological pathway controlling energy balance.^2,4,11-45

Figure 1: A simplified model of the leptin signalling pathway Lines with arrowheads show stimulatory action. Lines with perpendicular endblocks show inhibitory action. AgRP=agouti-related protein. BDNF=brain-derived neurotrophic factor. CART=cocaine-amphetamine related transcript. CPE=carboxypeptidase E. CRH=corticotropin-releasing hormone. GABA=gamma amino butyric acid.

GI=gastrointestinal. IR=insulin receptor. LR=leptin receptor. MCH=melanin-concentrating hormone. MSH=melanocyte-stimulating hormone. NPY=neuropeptide Y. PC1=prohormone convertase 1. POMC=pro-opiomelanocortin. PYY=peptide YY. TRH=thyrotropin-releasing hormone. TrkB=tropomyosin receptor kinase B.

Determinants or risk factors for development of childhood Obesity or increased adiposity

Since the discovery of leptin, understanding of the mechanisms controlling energy balance has rapidly advanced. Apart from leptin replacement therapy in a few leptin-deficient individuals, interventions that effectively prevent or treat obesity in the general population are yet to emerge. Both insulin and leptin are secreted in proportion to body fat and serve as adiposity signals, acting on the same neurons of the hypothalamic arcuate nucleus to regulate energy homoeostasis. Ghrelin, which is secreted by the stomach and duodenum, serves as a hunger signal at the hypothalamus and brainstem, whereas other peptides secreted by the gastrointestinal tract, including peptide YY, act as satiation signals.

The ligands leptin,⁴⁶ pro-opiomelanocortin,^47,48 cocaine-amphetamine related transcript,⁴⁹ and brain-derived neurotrophic factor (BDNF),^16,50 the receptors for leptin,^51,52 melanocortins,^53-56 and BDNF,⁵⁷ and the enzyme prohormone convertase 1^58,59 have function-changing mutations that are associated with obesity in children. Mutations in the ligands and receptors for neuropeptide Y,⁶⁰ agouti-related protein,⁶¹ carboxypeptidase E,^62,63 and melanin-concentrating hormome⁶⁴ change energy balance in rodents, but have not been convincingly associated with human obesity. For several risk factors, evidence is weak and, although important advances have been made, how to incorporate the information effectively and cost-effectively into prevention programmes for children is unclear.

Joan C Han, Debbie A Lawlor, Sue Y S Kimm
Lancet 2010; 375: 1737-48
Published Online May 6, 2010 DOI:10.1016/ S0140- 6736(10)60171-7

Unit on Growth and Obesity, Program on Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, DHHS, Bethesda, MD, USA (J C Han MD); MRC Centre for Causal Analyses in Translational Epidemiology, Department of Social Medicine, University of Bristol, Bristol, UK (Prof D A Lawlor PhD); and Department of Internal Medicine/Epidemiology, University of New Mexico School of Medicine, Albuquerque, NM, USA (S Y S Kimm MD)

Correspondence to: Dr Sue Y S Kimm, University of New Mexico Health Sciences Center, Department of Internal Medicine/Epidemiology, University of New Mexico, MSC 10 5550 Albuquerque, NM 87131-0001, USA kimm@pitt.edu

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