Welcome to Part 2 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. Today we look at the evidence (or lack thereof) linking total energy intake, fat intake, sugar sweetened beverage intake, and calcium intake with the childhood obesity epidemic. To skip to Part 3, which focuses on sleep, maternal age, and pollution, click here.
Increased Total Energy Intake
It is well established that intentional overfeeding results in significant weight gain [46–48]. For example, Levine and colleagues report that overfeeding volunteers by 1000 kcal/day results in an average weight gain of 5 kg in just 8 weeks . However, counterintuitively, recent reviews have noted that total EI has not been a consistent predictor of weight gain in prospective studies of children [19, 49]. It is worth noting however that this may be due to the limitations of self- or parent-reported caloric intake, as both adults and children are known to have great difficulty in accurately reporting EI [50–52]. For example, Huang and colleagues report that fully 55% of children aged 3–19 who participated in the Continuing Surveys of Food Intakes by Individuals study reported physiologically implausible values for energy intake, and that excluding these individuals resulted in dramatic improvements in both the strength and the consistency of the relationship between EI and body weight .
As with PA, there is currently little information regarding historical trends in the EI of Canadian children, and data from the United States are equivocal as some [53–56], but not all [57, 58], studies report increased EI during the past half century. For example, self-reported energy intake from the 1977-1978 Nationwide Food Consumption Survey and the 1999–2004 National Health and Nutrition Examination Survey suggest that the average daily EI of American children aged 1–10 in 1999–2004 was 15% higher than in 1977-1978, with similar increases observed in adolescents [54, 55]. In contrast to these findings, however, Troiano and colleagues report that between 1970 and 1994, EI in American youth was relatively stable . Thus, given the absence of Canadian data and the ambiguity of available data from our closest neighbour, there is currently insufficient evidence to conclude that EI has increased in Canadian youth during recent decades.
While prospective studies and historical trends may lend only weak support to the putative role played by EI in the Canadian childhood obesity epidemic, it remains extremely plausible biologically. As mentioned earlier, several trials have shown that intentional overfeeding results in dramatic weight gain in adults [46–48], and there is little reason to expect this relationship to be different in children. While it should be noted that there is evidence that over-consumption results in compensatory increases in EE in some individuals, , this would likely be insufficient to prevent an increase in obesity rates at the population level. Further, other consistent predictors of weight gain which lend themselves to more accurate self-reporting than total EI (e.g., television watching and sugar-sweetened beverages, which will be discussed below) are thought to exert their influence through their impact on EI. Thus, despite the weak evidence presented from observational studies, the strong biological plausibility and impressive results from studies of chronic overfeeding suggest that there is currently moderate evidence that increased EI has contributed to the childhood obesity epidemic.
Increased Sugar Sweetened Beverage Intake
While trends in total EI over the past 40 years are unclear, there is little ambiguity for trends in sugar-sweetened beverage (SSB) intake, which has increased dramatically in recent decades [58–60]. For example, the average self-reported soft-drink intake in American youth increased from roughly 150 mL/day in 1977 to more than 350 mL/day in 1998 , and recent studies suggest that total SSB intake has continued to increase into the 21st century . Interestingly, while this may be partially due to increased fast food consumption, available evidence suggests that SSB intake has also increased in the home environment in recent decades .
Several recent systematic reviews have also concluded that there is consistent evidence that excess consumption of SSBs is associated with an elevated risk of weight gain [19, 61, 62]. For example, among longitudinal studies, Vartanian and colleagues report significant effect sizes of 0.24 and 0.09 for the relationship of SSB consumption with total EI and body weight, respectively . Similarly, a 19-month prospective study of 548 school children reports that every serving of sugar-sweetened beverages at baseline was associated with a 0.18 kg/m2 increase in BMI at followup . Finally, it has recently been estimated that removing sugar-sweetened beverages from the diet of American children and youth would reduce caloric intake by an average of 235 calories per day , which has the potential to dramatically reduce the risk of positive energy balance in this age group. Thus, available evidence suggests that excessive consumption of SSBs plays a strong role in the etiology of the childhood obesity epidemic.
This relationship between SSB and prospective weight gain can be explained by multiple biological mechanisms. First and foremost, SSB intake is associated with increased EI, as described earlier . This is likely due to the fact that SSBs are both energy dense and have little impact on satiety, both of which could lead to increases in EI . Further, many SSBs are sweetened with high fructose corn syrup (HFCS) and therefore contain a fructose fraction. This fructose fraction may also contribute to weight gain through increased lipogenesis, inhibition of satiety signals, and reductions in EE, although it should be noted that the relative importance of HFCS in the etiology of obesity is still a matter of dispute [61, 65].
Increased Fat Intake
Not surprisingly, as the consumption of carbohydrates has increased during the past 30 years, the relative contribution of fat to total EI has decreased, although intake remains above recommendations [57, 58]. For example, Cavadini and colleagues report that between 1965 and 1996 fat intake decreased from 39% to 32% of EI for Americans aged 11–18 . However, it should be noted that this same study found that absolute fat intake actually increased by 4% during the 1990’s , suggesting that the relative changes in fat intake may have more to do with increased consumption of carbohydrates than with reductions in fat consumption.
The evidence linking fat intake and obesity in prospective studies is surprisingly equivocal and provides little support for the role of fat intake in the development of obesity . For example, Davis and colleagues report that of 15 longitudinal studies of childhood weight gain reviewed by the American Dietetic Association, just 4 supported the role of dietary fat intake, while 4 others showed mixed results, and 7 found no association . However, as with total EI, fat intake remains an extremely plausible mechanism biologically. Similar to SSBs, dietary fat is both energy dense and relatively nonsatiating per calorie ingested, lending itself to passive overconsumption . Further, increased fat consumption appears to have little impact on fat oxidation or overall EE, suggesting that excess EI related to increased fat intake is very likely to result in positive energy balance and weight gain . However, despite these plausible mechanistic links, available evidence provides only weak support of the role of dietary fat intake in the current childhood obesity epidemic.
Reduced Calcium Intake
Along with the changes in fat and SSB intake in recent decades, there has also been a well-documented reduction in the intake of dietary calcium [58, 68]. For example, between 1965 and 1996, Cavadini et al. report that the milk consumption of American youth decreased by 36%, while total calcium intake dropped by roughly 13% . Further, it has been suggested that high calcium intake may influence body weight through increases in fecal fat excretion, fat oxidation, and thermogenesis [69, 70]. However, a recent meta-analysis of childhood calcium supplementation studies reports no significant association between supplementation and any measure of weight or body composition , which is supported by the findings of a similar review in adults . Thus, while there is some evidence for plausible mechanisms linking reduced calcium with increased adiposity, the lack of evidence linking calcium intake with changes in actual measures of body composition suggests that reductions in calcium intake do not represent an important cause of the Canadian childhood obesity epidemic.
Coming Up Next
Come back tomorrow (now online here), when we’ll look at the potential role played by reduced sleep, pollutants, increased maternal age, breastfeeding, and adult obesity.
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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