Obesity and cancer

Symposia Abstracts S026 Obesity and cancer Anne-thea McGill University of Auckland, New Zealand Although there is much research on obesity, CVD, and cancer, often these research areas, and therefore management strategies, intersect somewhat clumsily. A more expansive view may show that much common ground is present and that these linkages may give rise to less confusing preventative strategies, and decrease those which are ineffective. A brief over view of epidemiology will track the trends (increases and decreases) in these three conditions over the last 125 years. Certainly, exposure to environmental pollutants, particularly tobacco smoking, but also industrial chemicals released uncontrolled in large mounts prior to the 1950—60s, was wide spread, and was found to be associated with CVD and cancers. Cancers have been studied in great detail, and various chemicals, including large numbers of plant chemicals have been studied for effects on disregulated metabolism in cancer: prevention, amelioration and cure. At the same time food was blamed for CVD as the still-used blood cholesterol/TG markers had been discovered and were thought to be related to fatty food, especially saturated fat. The cause for the rise in obesity has not clearly been elucidated. It may be that CVD, and later cancer, was largely caused by a multitude of toxic chemicals combined with poor food micronutrient intake and that obesity is more of problem of energy over load plus seriously low micronutrient/macronutrient ratios. The way food micronutrients, high dose vitamin therapy, toxicants and some metabolic medications, including Metformin, interact with the NRF2 system and other metabolic pathways in obesity and cancer will be examined.

13 ness of interventions. In children and adolescents BMI changes as part of normal growth and hence it is common to adjust BMI by converting it to an age and sex specific centile or z-score using population based BMI reference data. Yet, there are a number of limitations to measuring change in BMI z-score in the research environment, particularly in obese adolescents, which may lead to misinterpreting results. A reduction of 0.5 BMI z-score is often referred to as the minimum reduction to produce significant improvements in cardiometabolic indices. However, we need to consider what this means in terms of change in weight and BMI; changes in BMI z-score can represent a broad range of changes depending upon age, sex and initial BMI [1]. In particular, the CDC 2000 reference data have practical upper limit and only poorly distinguish weight status in severely obese; a high BMI is associated with a limited range of BMI z-score, such that change in BMI z-score has poor sensitivity in characterising weight changes [2]. Alternative measures to describe and track obese children have been suggested, including expressing BMI as a percentage of the 95 percentile [3]. Is it time to rethink our research methodology?

References [1] Berkey CS, Colditz GA. Adiposity in Adolescents: Change in actual BMI works better than change in BMI z-score for longitudinal studies. Ann Epidemiol 2007;17:44—50. [2] Woo JG. Using body mass index z-score among severely obese adolescents: A cautionary note. Int J Pediatr Obes 2009;4:405—10. [3] Flegal KM, Wei R, Ogden CL, Freedman DS, Johnson CL, Curtin LR. Characterizing extreme values of body mass index — for-age by using the 2000 CDC and Prevention growth charts. Am J Clin Nutr 2009;90:1314—20.

http://dx.doi.org/10.1016/j.orcp.2012.08.029 S028

http://dx.doi.org/10.1016/j.orcp.2012.08.028 S027 Measuring adiposity change in adolescents Sarah P. Garnett Institute of Endocrinology and Diabetes, The Children’s Hospital at Westmead. The Children’s Hospital at Westmead Clinical School, University of Sydney, Australia Serial measurements of BMI are widely used as a proxy measure of adiposity to assess effective-

The obese adolescent — Realistic expectations in paediatric care and the challenging transition to adult care Kate Steinbeck The Academic Department of Adolescent Medicine, University of Sydney, Australia The physiological events of puberty, the necessary completion of the psychosocial tasks of adolescence and the pace of cognitive development may all operate together to increase the severity of established childhood obesity, or to bring on obe-