Research reportAdrenocortical regulation, eating in the absence of hunger and BMI in young children☆
Highlights
► We examined links between stress reactivity, eating behavior and body mass index in 5- to 9-year-old children. ► Greater increases in cortisol in response to stress were related to dysregulated eating and higher body mass. ► Stress reactivity may be a marker for energy balance dysregulation.
Introduction
In the past two decades, a major focus in developmental science has been to advance our understanding of why, when exposed to stressful experiences or circumstances, some children are placed at risk for emotional and behavioral problems but others are resilient (Boyce and Ellis, 2005, Cicchetti, 2002, Rutter et al., 1997). The effects of stress on children’s health and developmental outcomes are well-documented (Evans and English, 2002, Gunnar and Quevedo, 2007), and these effects extend across the lifespan (Anda et al., 2006, Dube et al., 2003, Evans and Kim, 2007). Obesity is one such health outcome whose biobehavioral underpinnings have been linked with stress (Bjorntorp and Rosmond, 2000a, Bjorntorp and Rosmond, 2000b, Chrousos, 2000, Gundersen et al., 2011).
Research attention has been drawn to the adrenocortical component of the physiological stress response as a potential mechanism in the development of obesity through its effects on the accumulation of central adiposity and dysregulated eating behavior, or eating in the absence of hunger (Bjorntorp and Rosmond, 2000a, Bjorntorp and Rosmond, 2000b, Drapeau et al., 2003, Kyrou et al., 2006, Rogers, 1999). Disruptions in the hypothalamic pituitary adrenocortical (HPA) axis and sympathetic nervous system (SNS) functioning, as indicated by cortisol and cardiovascular responses to stress, are linked to the accumulation of central adiposity, increased energy intake, and appetite regulation (Adam and Epel, 2007, Bjorntorp, 1997, Gluck, 2006, Gluck et al., 2004, Gluck et al., 2004b, Nieuwenhuizen and Rutters, 2008, Tataranni et al., 1996, Wallerius et al., 2003). Adrenocortical regulation (i.e., cortisol) may be an underlying mechanism for the development of energy balance problems in children (Spencer & Tilbrook, 2011).
Findings from a study in preadolescent youth (average age ∼10 years) show that cardiovascular reactivity (i.e., heart rate) to a laboratory-based stressor was linked to a higher percent body fat; increases in perceived stress after exposure to the stressor was also related to higher levels of body fat (Roemmich, Smith, Epstein, & Lambiase, 2007). Dockray, Susman, and Dorn (2009) confirmed a link between cortisol reactivity and obesity in 8- to 13-year-old boys and girls. A large majority of the studies that have provided evidence for a link between cortisol and obesity or eating behavior have been conducted with adult populations of men and women (Gluck et al., 2004b, Epel et al., 2000, Evans et al., 2008, Gluck et al., 2004, Rowland and Antelman, 1976, Steptoe et al., 2004). These studies suggest that cortisol reactivity may be linked to dysregulated eating, and eating in response to stress (Epel et al., 2001, Gluck et al., 2004, Gluck et al., 2004b).
Eating in the absence of hunger, a measure of dysregulated eating behavior, has consistently been associated with weight gain, overweight, and obesity, in both adults and children (Bellisle et al., 2004, Fisher and Birch, 2002). As such, eating in the absence of hunger has been proposed as a behavioral phenotype of obesity (Faith et al., 2006). Findings from a study by Rutters and colleagues (Rutters, Nieuwenhuizen, Lemmens, Born, & Westerterp-Plantenga, 2009) revealed that men and women ate more in the absence of hunger after exposure to an acute stressor; these effects were particularly strong for those participants with a disinhibited eating style. Similar findings have been reported more recently, in a sample of non-overweight women (Born et al., 2010). Stress, both perceived and manipulated, also has been found to affect eating/dietary choices and behaviors in youth (Cartwright et al., 2003, Jenkins et al., 2005, Roemmich et al., 2002) and adults (Born et al., 2010, Gibson, 2006, O’Connor et al., 2008, Zellner et al., 2006). Roemmich et al. (2002) found that preadolescent boys and girls (average age ∼9 years) who reported high levels of dietary restraint, reported higher levels of perceived stress, and increased energy intake on days in which they were exposed to stress, compared to non-stress days. Findings from a study with boys and girls as young as age 8 show that perceived stress was positively related to children’s reports of unhealthy eating behaviors, and the use of food as a coping mechanism for stress, nervousness and worry (Jenkins et al., 2005). There is a dearth of information on the biobehavioral processes underlying these dysregulated eating behaviors in young children. Understanding individual differences in the sensitivity of the physiological stress response may provide more information on the factors that contribute to the development of dysregulated eating and obesity in children.
Findings from recent studies show that eating appears to be a coping response to stress in youth (Balantekin and Roemmich, 2012, Roemmich et al., 2011). In these studies, adolescents ages 8–12 years consumed more calories on a stress day compared to a non-stress day, and this finding was particularly pronounced in adolescents with greater adiposity, and those who reported lower levels of dietary restraint. Similar findings from animal and human models studies suggest that eating may be a coping response to stress, particularly when the food is a comfort food (Dallman et al., 2003, Greeno and Wing, 1994, Tomiyama et al., 2011). Ulrich-Lai et al. (2010) showed that intake of palatable foods can buffer the biobehavioral effects of stress via reward pathways in the brain. The maladaptive, long-term outcome of this biobehavioral dysregulation is the weight gain and fat accumulation that may result from consumption, or overconsumption, of energy-dense foods.
Using a longitudinal sample of youth in the US, Francis and Susman (2009) examined links between behavioral regulation (measured using laboratory-based self-control and delay of gratification tasks) and BMI changes from age 3 to 12 years. Results revealed that youth who showed self-regulation failure at ages 3 and 4 had the most rapid increases in BMI from age 3 to age 12, compared to those who showed evidence of self-regulatory success at ages 3 and 4. We propose that cortisol output in response to a stressor is not only a marker for HPA-axis functioning, but may also be linked to regulation across domains, particularly as it relates to biobehavioral regulation of eating and body mass. Given that childhood obesity is a major public health concern, with more than 30% of children ages 6 to 11 years in the US classified as overweight or obese (Ogden, Carroll, Kit, & Flegal, 2012), a better understanding of the biobehavioral factors involved in the etiology of childhood obesity is needed. The purpose of this study was to examine adrenocortical regulation (as indexed by cortisol output in response to psychosocial stress) as an underlying mechanism for the development of problems with energy balance in 5- to 9-year-old children, through its effects on eating in the absence of hunger and body mass index (BMI). We tested the hypothesis that greater cortisol output in response to psychosocial stress would be linked to more eating in the absence of hunger and higher BMI scores.
Section snippets
Participants
Participants included 43 children (61% boys; 68% White, 16% Black, 16% other) ages 5- to 9-years (mean age = 7.1 + 1.5 years) and their biological parents, recruited for a study on growth and development in young children in a mid-Atlantic state; the sample was not recruited or selected based on weight status, stress levels, or eating behavior. Eligibility criteria for participation included living with at least one biological parent, and the absence of any biological, physical or developmental
Sample characteristics
Table 2 presents descriptive data on children in the sample. Overall, children in the sample were within the normal weight range based on BMI percentiles; approximately 19% of children in the sample were categorized as overweight (BMI percentile > 85th). On average, children consumed just over 250 kcals during the Free Access procedure, although some children consumed very little (20 kcals) while other consumed upwards of 700 kcals during the 10-min period.
Figure 2 displays the overall pattern of
Discussion
This study was designed to examine associations between individual differences in cortisol output in response to stress, eating in the absence of hunger and BMI z-scores in 5- to 9-year-old children. The results from the study provide evidence for adrenocortical output as a potential marker for problems beyond general behavioral and psychological domains of child development. Area under the curve with respect to increase (AUCi) was related to children’s eating in the absence of hunger and BMI,
Disclosure
In the interest of full disclosure, Dr. Granger is the founder and Chief Scientific and Strategy advisor at Salimetrics LLC (State College, PA) and this relationship is managed by the policies of the committee on conflict of interest at the Johns Hopkins University School of Medicine. The authors have no additional conflicts of interest to declare.
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Children's inhibitory control abilities in the presence of rewards are related to weight status and eating in the absence of hunger
2021, AppetiteCitation Excerpt :Gram weights were converted to kcal using information from the Nutrition Facts Panel. Eating in the absence of hunger (EAH) was assessed 20 min after consumption of the standard meal (Francis et al., 2013). During this paradigm, children were left alone in a room for 15-min with a range of palatable snacks and treats (e.g., candies, cookies, cakes, chips) as well as games and toys (food descriptions and amounts are published elsewhere Shana Adise et al. (2018)).
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Acknowledgements: We would like to thank the families who participated in this study for their time. The services provided by the General Clinical Research Center of The Pennsylvania State University are greatly appreciated. The study was supported by funding from the Children, Youth and Families Consortium at The Pennsylvania State University and NIH Grant M01 RR 10732. We appreciate the feedback we received on this manuscript from Drs. Laura Klein and Sheila West at the Pennsylvania State University.