A new paradigm for investigating the etiology of obesity in early childhood: Exposure to added sugars and hyper‐palatable foods in infancy and dysregulation of food reinforcement processes

Abstract

BACKGROUND 1.1 | The durability of the childhood obesity epidemicChildhood obesity is an epidemic in the United States. 1,2 In the past two decades, childhood obesity rates have continued to rise despite intensified prevention efforts. 2,3 Most recent estimates indicate that 19.7% of Americans between 2 and 19 years of age have obesity. 4 Furthermore, among infants, nearly 10% have excess weight for their height, 5 and 10%-50% experience a pattern of rapid weight gain in the first 24 months of life. 6 Notably, one recent national birth cohort found that rapid weight gain during the first 24 months of life resulted in a twofold increase in overweight or obesity at 3 and 5 years of age, respectively. 7 Hence, arresting rapid weight gain before early childhood (3-5 years) is vital for the prevention of child obesity. Consequences of obesity during infancy and early childhood span almost every health area and can lead to chronic health conditions in adulthood that cause significant impairments and disabilities. 3 Thus, further work is needed to identify mechanisms influencing the development of obesity at early critical life points.Recently, greater attention has recently been directed toward obesity prevention during the first 2 years of life (0-24 months). 8 However, randomized prevention approaches have yielded very limited effects. For instance, the Early Prevention of Obesity in Childhood (EPOCH) Collaboration conducted a prospective meta-analysis 9 on data accrued from four randomized controlled trials that addressed key targets identified for obesity prevention. Obesity prevention targets consisted of extended breastfeeding duration, introduction of table foods at the appropriate time (6 months), low intakes of nutrient-poor foods, responsive feeding practices, limited screen exposure, and ample amounts of sleep and activity. 9 Findings revealed that at 18-24 months, participants in the intervention condition displayed a mere 2% decrease in the prevalence of overweight and obesity relative to the control group. Similarly, in a recent review of 29 randomized controlled trials conducted among infants that included a minimum follow-up duration of 24 months, 10 only 7% of trials (2/29) found the intervention to have a positive effect on BMI zscores (with small effect sizes), and a third trial reported that children in the treatment condition had a lower prevalence of obesity than their control counterparts, yet mean BMI scores were comparable for all participants in the cohort. Taken together, this evidence demonstrates that sustained management of childhood obesity during infancy and early childhood years is modest, at best. Therefore, Tera L Fazzino and Kai Ling Kong have equal contribution.

Hyper-palatable foods in elementary school lunches: Availability and contributing factors in a national sample of US public schools

“…School cafeterias are a major point of influence for child nutrition and US federal legislation requires that school lunches contain important nutrients that support children’s dietary health [ 4 ]. However, the legislation does not regulate types of foods that may be difficult to stop eating, such as hyper-palatable foods, which are a hypothesized factor that may elevate child obesity risk [ 5 ]. The purpose of the current pilot study was to characterize the availability of HPF in a sample of lunch menus from US public elementary schools.…”

“…Current federal meal legislation does not regulate types of foods that may be difficult to stop eating, such as hyper-palatable foods, which are a hypothesized mechanism that may elevate child obesity risk [ 5 ]. Hyper-palatable foods (HPF) contain combinations of palatability-inducing nutrients (e.g., fat, sugar, sodium, and/or carbohydrates) that yield an artificially rewarding eating experience [ 6 ].…”

“…HPF may excessively activate brain reward neurocircuitry, while also dampening engagement of physiological satiety mechanisms, which may facilitate overeating [ 7 , 8 ]. When consumed repeatedly over time, HPF may dysregulate food reinforcement processes, skewing children’s food intake behavior toward HPF and away from foods such as fruits and vegetables [ 5 , 9 ]. Evidence indicates that there may be a dose response relationship between HPF intake and health consequences [ 10 ]; thus early and repeated consumption of HPF among young children is hypothesized to be a key risk factor for excess dietary HPF intake and child obesity risk [ 5 ].…”

“…When consumed repeatedly over time, HPF may dysregulate food reinforcement processes, skewing children’s food intake behavior toward HPF and away from foods such as fruits and vegetables [ 5 , 9 ]. Evidence indicates that there may be a dose response relationship between HPF intake and health consequences [ 10 ]; thus early and repeated consumption of HPF among young children is hypothesized to be a key risk factor for excess dietary HPF intake and child obesity risk [ 5 ]. Applied to the school food environment, if HPF are regularly available in and consumed in school lunches, school meals may be a key source of regular HPF exposure among young children that could increase their risk for excess dietary intake of HPF and obesity.…”

“…Given the widespread availability of HPF and documented regular dietary intake of HPF among infants, it stands to reason that HPF may also be regularly available in US public school settings, such as elementary school lunches. Thus, an examination of the availability of HPF in elementary school lunches is needed to understand the degree to which young children may be regularly exposed to HPF, a key factor that may increase children’s risk for excess dietary intake of HPF and childhood obesity [ 5 ].…”