Contributors to the Pediatric Obesity Epidemic Part 4: Adult Obesity, and Relative Contributions of All Risk Factors

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Welcome to Part 4 in a series on potential contributors to the pediatric obesity epidemic. This series is based on a recent paper in the journal ISRN Pediatrics, which is available for free here. Big thanks to the University of Ottawa Author Fund for covering the Open Access publication costs.

Throughout the week we will examine the following potential contributors to the pediatric obesity epidemic:

  • Reduced sleep
  • Reduced physical activity
  • Increased total energy intake
  • Increased fat intake
  • Increased sedentary time
  • Exposure to endocrine-disrupting chemicals
  • Increased consumption of sugar-sweetened beverages
  • Inadequate calcium intake
  • Increased maternal age
  • Reduced breastfeeding
  • Increased adult obesity rate

In Part 1 we examined the impact of changes in physical activity and sedentary behaviour, in Part 2 we looked at changes in food intake, and in Part 3 we looked at sleep, breastfeeding, maternal age and pollution. Today we look at the evidence (or lack thereof) linking adult obesity with the pediatric obesity epidemic, then examine the relative contributions of all of the risk factors we’ve discussed so far.

Adult Obesity

Available evidence suggests that both parental obesity and gestational weight gain are risk factors for childhood obesity [75, 110, 111]. For example, Reilly and colleagues examined the relationship between parental and childhood obesity in a prospective study of nearly 9,000 British children [75]. In comparison to children born to two nonobese parents, they report that children were 2.5 times more likely to be obese when they had an obese father, and 4.3 more likely to be obese if they had an obese mother. Further, children born to two obese parents were more than 10 times more likely to develop obesity by age 7 than those born to two non-obese parents [75]. It has been reported that gestational weight gain is also a predictor of childhood obesity, and that this impact is stronger in women who were obese prior to becoming pregnant [111]. Finally, recent reports suggest that surgical weight loss prior to pregnancy dramatically reduces the risk of childhood obesity in babies born to obese women [112]. These relationships suggest that any putative cause of the increasing prevalence of adult obesity [113] including those that are unlikely to play a direct role in the epidemic of childhood obesity (e.g., iatrogenic weight gain [25]) may nonetheless play important indirect roles.

The relationship between parental and childhood obesity is likely to be linked via numerous mechanisms. For example, genetic factors are reported to account for roughly 25% of the variance in fat mass [114], which is likely to mediate some of the relationship in body composition between parent and child. Further, learned behavioural characteristics such as food choices, PA, and sedentary behaviours are also likely to mediate the transmission of intergenerational obesity [75, 115]. Finally, studies of animal models suggest that obesity or excessive weight gain during pregnancy is likely to predispose childhood obesity through deleterious changes in the central regulation of energy balance [116]. For example, lambs born to overfed ewes are less sensitive to signals of excess nutrient supply or fat mass than lambs born to control animals [116]. Taken together, the strong association between parental and childhood obesity and the numerous plausible mechanisms underlying these associations suggest that one of the most important drivers of the childhood obesity epidemic may in fact be adult obesity.

Relative Contributions to Childhood Obesity

As has been noted by others, there is currently insufficient information to make a truly objective ranking of the putative causes of an issue as complex as the current obesity epidemic [25]. However, the evidence presented above does allow some general conclusions to be made. This review has identified 4 factors—reduced sleep, increased sedentary time, increased consumption of sugar-sweetened beverages, and secular increases in adult obesity—which are likely to have made an important contribution to Canada’s childhood obesity epidemic. Each of these factors has shown strong and consistent associations with childhood weight gain, has increased in prevalence during the obesity epidemic, and results in either biological or behavioural changes that are likely to promote positive energy balance. Of these, adult obesity appears to have the most powerful impact on childhood obesity levels, while reducing the consumption of sugar-sweetened beverages may be among the simplest ways to prevent future weight gain in individuals of all ages.

Available evidence provides only moderate support for the role of either total EI or PA in the etiology of childhood obesity. This is likely due to methodological limitations of self-reported intake and expenditure, as both of these factors are biologically plausible and have been shown to have impressive effects on adiposity in experimental studies. It is possible that methodological limitations may also explain the inconsistent relationships seen between obesity and dietary fat intake. Future studies employing more objective methods of measurement are important to determine the true role of these factors in the etiology of the childhood obesity epidemic.

Finally, although each has been linked in some way with childhood obesity, there is currently weak evidence supporting the role of maternal age, breastfeeding, exposure to endocrine disrupters, or calcium insufficiency in the etiology of the childhood obesity epidemic. Of these, maternal age, breastfeeding, and endocrine disruptors appear worthy of future study, while there is sufficient evidence to conclude that calcium intake plays little role in pediatric obesity rates at the population level.

Coming Soon

Tomorrow (now available here) we will take a brief look at some potential contributors that didn’t make it into the review – poverty, fast food intake, increased food palatability, and stress.  If there are any others that you’d like covered, feel free to add them in the comments below and I will do my best!


ResearchBlogging.orgSaunders, T. (2011). Potential Contributors to the Canadian Pediatric Obesity Epidemic ISRN Pediatrics, 2011, 1-10 DOI: 10.5402/2011/917684

108. A. Yngve and M. Sjöström, “Breastfeeding in countries of the European Union and EFTA: current and proposed recommendations, rationale, prevalence, duration and trends,” Public Health Nutrition, vol. 4, no. 2, pp. 631–645, 2001.

109. A. S. Ryan, Z. Wenjun, and A. Acosta, “Breastfeeding continues to increase into the new millennium,” Pediatrics, vol. 110, no. 6, pp. 1103–1109, 2002.E.

110. Oken, E. M. Taveras, K. P. Kleinman, J. W. Rich-Edwards, and M. W. Gillman, “Gestational weight gain and child adiposity at age 3 years,” American Journal of Obstetrics and Gynecology, vol. 196, no. 4, pp. 322.e1–322.e8, 2007.

111. C. M. Olson, M. S. Strawderman, and B. A. Dennison, “Maternal weight gain during pregnancy and child weight at age 3 years,” Maternal and Child Health Journal, vol. 13, no. 6, pp. 839–846, 2009.

112. J. G. Kral, S. Biron, S. Simard et al., “Large maternal weight loss from obesity surgery prevents transmission of obesity to children who were followed for 2 to 18 years,” Pediatrics, vol. 118, no. 6, pp. e1644–e1649, 2006.

113. M. Shields, M. S. Tremblay, M. Laviolette, C. L. Craig, I. Janssen, and S. C. Gorber, “Fitness of Canadian adults: results from the 2007–2009 Canadian Health Measures Survey,” Health Reports, vol. 21, no. 1, pp. 21–35, 2010.

114. C. Bouchard, “Current understanding of the etiology of obesity: genetic and nongenetic factors,” American Journal of Clinical Nutrition, vol. 53, no. 6, pp. 1561S–1565S, 1991.

115. L. A. Francis, Y. Lee, and L. L. Birch, “Parental weight status and girls’ television viewing, snacking, and body mass indexes,” Obesity Research, vol. 11, no. 1, pp. 143–151, 2003.

116. I. C. McMillen, L. Rattanatray, J. A. Duffield et al., “The early origins of later obesity: pathways and mechanisms,” Advances in Experimental Medicine and Biology, vol. 646, pp. 71–81, 2009.

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