Welcome to Part 3 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, and in Part 2 we looked at changes in food intake. Today we look at the evidence (or lack thereof) linking sleep, pollution, maternal age and breastfeeding with the pediatric obesity epidemic. To skip to Part 4, which looks at the relative contributions of all the risk factors discussed in this series, click here.
Available evidence suggests that short-sleep duration may be another important risk factor for childhood overweight and obesity. A recent systematic review and meta-analysis by Cappuccio and colleagues reports that children who sleep less than 10 hours per night are at 89% greater risk than their peers who sleep more than 10 hours/night . Using this same data, it has been estimated that 5 to 13% of all childhood obesity could be due to short-sleep duration . Although the vast majority of the research to date has been cross-sectional , there is evidence of sleep as a predictor of weight gain in prospective studies as well. For example, Reilly and colleagues report that toddlers who slept less than 11 hours per night at age 2.5 years were 35–45% more likely to be obese at age 7 than toddlers who averaged more than 12 hours of sleep , with similar findings reported by Bell and Zimmerman .
Secular trends in sleep duration also support the putative role of sleep duration in the childhood obesity epidemic. Since the 1970’s, the average sleep duration of children has decreased significantly among industrialized nations. Between 1974 and 1986, the average sleep time of 2-year olds in the Zurich Longitudinal Studies decreased by 45 minutes , while Dollman and colleagues report a 30-minute decrease from 1985 to 2004 among South Australian teenagers . Similarly, the prevalence of sleep-onset difficulties has also increased dramatically in recent years .
Finally, a putative role for shortened sleep in the etiology of the obesity epidemic is also supported by plausible mechanisms which are thought to influence both EE and EI [80, 81]. For example, it has been reported that sleep restriction in adults results in significant increases in hormones which promote EI including cortisol and ghrelin, along with decreases in anorectic hormones such as leptin and PYY [80,82–84]. Not surprisingly, short-sleep duration has also been shown to result in increased hunger and appetite, both of which were strongly associated with the changes in ghrelin and leptin mentioned earlier . Given that leptin and ghrelin are thought to, respectively, promote and inhibit physical activity, it has been suggested that sleep debt could potentially result in reductions in EE as well [81, 85]. However, recent experimental evidence in young men suggests that acute sleep restriction results in relatively little change in EE . Thus, at present it appears very likely that sleep deprivation results in increased EI, while there is little direct evidence that it results in reduced EE. When these biological mechanisms are considered alongside the consistent relationship between shortened sleep and obesity in prospective studies, and secular trends in sleep duration, there is currently strong evidence that shortened sleep plays a role in the childhood obesity epidemic.
Endocrine Disrupting Chemicals
Endocrine-disrupting chemicals (EDCs) are any “compound, either natural or synthetic, which alters the hormonal and homeostatic systems that enable the organism to communicate with and respond to its environment” , several of which (known as obesogens) may influence body weight . Limited evidence suggests that EDCs may exert a negative influence on aspects of EE. For example, it has been reported that mothers who have high levels of polychlorinated biphenyls (PCBs) in their breast milk also have low levels of plasma triiodothyronine, a thyroid hormone which is known to stimulate basal metabolism . Similarly, interventions in adults which increase plasma organochlorine concentrations result in significant decreases in both triiodothyronine and resting metabolic rate  and may also reduce skeletal muscle oxidative capacity . However, despite this limited biological evidence linking EDCs and EE, at present it is unclear whether prenatal exposure to EDCs predisposes to future weight gain . For example, while some reports suggest that the concentration of PCBs in cord blood is positively associated with BMI in early childhood , other reports suggest no relationship , or even a negative relationship  between prenatal PCB exposure and prospective weight gain. Similar inconsistencies have also been observed for other EDCs such as DDE . Thus, while being an interesting area for future research, at present there is very little evidence that EDCs play a causal role in the childhood obesity epidemic.
Increased Maternal Age
The average age of first pregnancy has increased dramatically in recent decades in both Canada [95–97] and around the world [98–100], and several plausible mechanisms have been suggested, which could link maternal age with increased risk of childhood obesity. For example, older mothers are known to give birth to smaller infants, which is itself a risk factor for the development of obesity [96, 101]. Similarly, older women are also likely to have both higher plasma concentrations of EDCs and higher BMIs, both of which may also predispose their children to future weight gain, as discussed elsewhere in this review [102–104]. Finally, research in sheep suggests that older maternal age may result in increased fat deposition , which may be related to accelerated reductions of proteins responsible for thermogenesis-related energy expenditure , although it is not immediately clear how or if this relates to humans.
Although the mechanisms described above are all at least somewhat plausible, the relationship between maternal age and childhood obesity in observational studies is inconsistent. For example, while Patterson and colleagues report that the odds of obesity in a cohort of American girls increased by 14% for every 5-year increase in maternal age , a more recent study of 8234 British children found no relationship between maternal age and risk of obesity at age 7 . Given this conflicting evidence, there is currently only weak evidence that maternal age plays a role in the childhood obesity epidemic, and future prospective studies are needed to clarify this relationship.
Duration of breastfeeding has been strongly and consistently linked with reduced risk of childhood overweight and obesity . For example, Harder and colleagues performed a meta-analysis which examined the association between duration of breastfeeding and the risk of childhood overweight in 17 independent observational studies . In comparison to children who were breastfed for less than 1 month, they report that children who were breastfed for 1–3 months had 19% reduced risk of overweight. The risk of being overweight continued to decrease as the duration of breastfeeding increased—risk was reduced by 24% among those breastfed for 4–6 months, 33% among those breastfed for 7–9 months, and by 50% for those breastfed for more than 9 months. On average, each additional month of breastfeeding reduced the risk of being overweight by 4%.
Despite consistent reports of the relationship between breast feeding and reduced risk of overweight and obesity, the mechanisms underpinning this relationship remain unclear. It has been suggested that it may be due to alterations in the neuroendocrine control of appetite, although this has yet to be verified in human participants . Thus, it is not possible at present to determine the precise mechanisms linking the duration of breastfeeding to body weight in childhood.
While breastfeeding appears to have a strong relationship with the risk of excess weight gain in childhood, trends in the prevalence of breastfeeding suggest that it is not a major contributor to secular increases in childhood obesity rates during the 20th century. Since the 1970’s, the prevalence of breastfeeding has remained constant or increased among most western nations for which data is available [108, 109]. For example, in the early 1970’s roughly 20% of American women exclusively breastfed while in the hospital, but this increased to 45% by the year 2000 . Given that obesity rates continued to increase steadily throughout this period despite increases in the prevalence of breastfeeding, there is currently weak evidence that breastfeeding plays a primary role in the childhood obesity epidemic.
Come back tomorrow (now available here) when we look at a counter-intuitive contributor to the pediatric obesity epidemic: the adult obesity epidemic. We will also compare the relative contributions of all the risk factors we’ve discussed so far. See you then!
Saunders, T. (2011). Potential Contributors to the Canadian Pediatric Obesity Epidemic ISRN Pediatrics, 2011, 1-10 DOI: 10.5402/2011/917684
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