Editorials

Obesity in children and adolescents

BMJ 2012; 345 doi: http://dx.doi.org/10.1136/bmj.e5457 (Published 25 September 2012) Cite this as: BMJ 2012;345:e5457
  1. Lee Hudson, research fellow,
  2. Russell M Viner, professor
  1. 1UCL Institute of Child Health, London WC1N 1EH, UK
  1. r.viner{at}ucl.ac.uk

New data help to shed light on scale of future disease burden

As the epidemic of childhood obesity in high income countries has developed over the past 20 years, questions have emerged about the implications of adiposity in children and adolescents for current and future health. In a linked systematic review (doi:10.1136/bmj.e4759), Friedemann and colleagues report that obese children and adolescents aged 5-15 years have raised serum lipids, blood pressure, glucose, and insulin as well as increased left ventricular mass compared with children with a healthy weight.1 This is worrying, but what exactly does it mean?

The long term outcomes for the current generation’s obese children and adolescents remain to be seen. However, the current study will help build a more accurate picture of the cardiometabolic risk that these young people are likely to face. Most worrying is that these findings indicate that end organ effects in the form of increased left ventricular mass are already present in obese children. Despite high heterogeneity in many of the meta-analyses, the current review provides a stark illustration of the probable threat that childhood obesity poses to disease burden in the population.

These data are welcome because surprisingly few population based data exist on the prevalence of cardiovascular risk factors in overweight and obese children and adolescents outside the United States.2 We know that small reductions in cardiovascular risk factors in adult populations, of the order of the difference seen in this study, can lead to reductions in death from cardiovascular disease.3

Concerns about the health effects of childhood obesity have looked mainly at the implications of excess adiposity in childhood and adolescence for disease burden in adulthood, but the current data focus attention on the immediate health risks of obesity for children. Systematic reviews confirm that higher body mass index (BMI) in childhood and adolescence increases the risk of cardiovascular disease in adulthood.4 However, the mechanisms by which early obesity has this effect remains unclear. The question of whether childhood obesity exerts its effects through tracking into adult obesity or by a mechanism that is independent of adult weight is not yet clear.4 A recent systematic review found little evidence that childhood BMI affected cardiovascular risk in adults independently of adult BMI.4

A lack of tools and evidence for assessing health risk in overweight and obese children and adolescents, as well as patchy and often ineffective services, hamper clinical responses to childhood obesity. For adults, cardiovascular risk algorithms have been routinely implemented to guide clinical decision making in many settings. For children, expert opinion alone guides assessment and treatment decisions, so there is marked variation between countries. Existing risk algorithms cannot be applied to children, and child specific risk scores have so far not been thought feasible or desirable by many, owing in part to fears about the implications of “medicalising” obesity in children. This problem is compounded by the use of multiple definitions to identify childhood obesity. Childhood obesity is generally defined on the basis of a greater or smaller tip of a normative pyramid of BMI, rather than being directly linked to increased disease risk, as is the case for adults.5 The definitions of childhood and adolescent obesity from the International Obesity Task Force, which track definitions of adult obesity back through childhood growth centiles,6 provide the most robust basis for determining risk status for children with high BMI. This is particularly true when they are informed by data that link the task force’s obesity categories with cardiovascular risk.

A key question that Friedemann and colleagues’ review does not answer is whether the association between BMI and cardiovascular risk is relatively linear, or whether there are thresholds of adiposity above which risk increases. This is important not only for understanding individual risk, but also for assessing the potential benefits of any interventions. Currently, no clear weight loss targets are available for child and adolescent obesity, and we do not know how much obese children or adolescents should reduce their BMI to improve their cardiometabolic risk profile.

Further work needs to tease out the effects of age and pubertal status on cardiovascular risk. Evidence that early puberty, itself associated with childhood obesity,7 increases later cardiovascular risk raises the possibility that critical windows exist in which adiposity during growth may variably influence later risk.8 Further studies, in ethnic minority populations in high income countries and in populations in middle and low income countries, are also needed.

Childhood obesity, perhaps like climate change, is at times in danger of inciting an ennui borne out of a repetition of problems without answers, a long latency before problems become apparent, and a perception that solutions are out of reach. Friedemann and colleagues’ data, and findings from large clinical samples,9 challenge us to rethink our approaches to identifying cardiometabolic abnormalities in obese children. Children in most countries visit primary care about once a year, and parents often do not recognise obesity or the associated risks.10 Opportunistic measurement of BMI and comorbidities related to obesity in primary care may be a useful first step in helping families move towards tackling childhood obesity.

Notes

Cite this as: BMJ 2012;345:e5457

Footnotes

  • Research, doi:10.1136/bmj.e4759
  • Competing interests: Both authors have completed the ICMJE uniform disclosure form at www.icmje.org/coi_disclosure.pdf (available on request from the corresponding author) and declare: no support from any organisation for the submitted work; no financial relationships with any organisations that might have an interest in the submitted work in the previous three years; no other relationships or activities that could appear to have influenced the submitted work.

  • Provenance and peer review: Commissioned; not externally peer reviewed.

References