• obesity;
  • weight;
  • stress;
  • child


  1. Top of page
  2. Abstract
  3. Does stress play a role in paediatric obesity?
  4. Understanding stress in the context of paediatric obesity
  5. Summary and directions for future research
  6. Clinical implications

Childhood obesity is a public health epidemic and is associated with substantial negative physical and psychosocial health consequences. Stress is thought to be one contributor to the development and maintenance of obesity in children and adolescents, yet the linkage between stress and paediatric obesity is a poorly understood phenomenon. This paper furthers the understanding of stress in the context of paediatric obesity by firstly presenting a focused review of what is known about links between chronic and acute stress and paediatric obesity risk and then synthesizing important areas from the literature. These critical areas of focus include the following: (1) physiological stress reactivity; (2) stress-induced eating; (3) stress and physical activity; (4) parent and family influences; and (5) stress in at-risk populations. This review is geared toward facilitating future research on the stress–obesity connection in youth. Copyright © 2013 John Wiley & Sons, Ltd.

Paediatric obesity is a public health epidemic. Nearly one-third (32%) of children and adolescents (ages 2–19 years) are currently classified as overweight [>85th percentile body mass index (BMI) for age and gender]. Over half of those youth (17%) are classified as obese (>95th percentile BMI for age and gender) (Ogden, Carroll, Kit, & Flegal, 2012). Youth from certain ethnic minority backgrounds (e.g. Latino and African American) and youth from low-income families are at an even greater risk for obesity (Gundersen, Mahatmya, Garasky, & Lohman, 2010; Ogden et al., 2012; Strauss & Knight, 1999). Obesity in childhood and adolescence has been associated with serious psychosocial and physical consequences. Psychosocial difficulties include impaired quality of life (Zeller, Roehrig, Modi, Daniels, & Inge, 2006), decreased self-concept (Israel & Ivanova, 2002) and poorer social functioning (Janssen, Craig, Boyce, & Pickett, 2004). Physically, overweight and obese youth are at increased risk for type 2 diabetes, high blood pressure, metabolic syndrome and cardiovascular disease (Eisenmann, 2003; Ogden et al., 2012). Furthermore, paediatric obesity often continues into adulthood and obesity may reduce overall adult life expectancy (Fontaine, Redden, Wang, Westfall, & Allison, 2003).

Emerging research implicates stress as one potential contributor to the development and maintenance of paediatric obesity (De Vriendt, Moreno, & DeHenauw, 2009; Dockray, Susman, & Dorn, 2009; Roemmich, Smith, Epstein, & Lambiase, 2007; van Jaarsveld, Fidler, Steptoe, Boniface, & Wardle, 2009; Yin, Davis, Moore and Treiber, 2005). Stress is defined in this paper as the negative response that results from threatening stimuli, external events or conditions that adversely affect a person's well-being (De Vriendt et al., 2009; Gundersen et al., 2010). Whereas a fairly substantial body of research suggests that chronic stress (e.g. financial strain, job-related stress and family relationship strain) is associated with increased risk for obesity in adults (e.g. Block, He, Zaslavsky, Ding, & Ayanian, 2009; Kivimaki et al., 2006), researchers have argued that there is currently a need to better understand the linkage between stress and obesity in children and adolescents (van Jaarsveld et al., 2009). One way to do this is to explore some critical areas from the growing body of research linking paediatric obesity and stress. The goal of this paper is to better understand the role of stress in the context of paediatric obesity by firstly examining what is known about links between stress and obesity risk and then presenting what is known on the basis of the existing literature.

Does stress play a role in paediatric obesity?

  1. Top of page
  2. Abstract
  3. Does stress play a role in paediatric obesity?
  4. Understanding stress in the context of paediatric obesity
  5. Summary and directions for future research
  6. Clinical implications

Links between chronic stress and paediatric obesity

A small number of studies have directly explored the relationship between chronic stress, described as prolonged exposure to stress over time (Pervanidou & Chrousos, 2011), and obesity in children and adolescents. Overall, findings from these studies suggest that a positive association exists between chronic stress and paediatric obesity risk (Lohman, Stewart, Gundersen, Garasky, & Eisenmann, 2009; Sweeting, Wright, & Minnis, 2005; Yin et al., 2005). See Table 1 for a description of selected studies included within this review examining the link between chronic stress and obesity.

Table 1. Descriptive characteristics for selected literature examining links between chronic and acute stress, and paediatric obesity
 Sample size (N)Age (years)Gender (%M)Stress measurement
  1. Note: CFSM: Core Food Security Module; PSS: Perceived Stress Scale; TSST: Trier Social Stress Test; TSST-C: Trier Social Stress Test for Children.

Chronic stress and paediatric obesity
Donoho et al., 2011238–110Life events checklist developed for and validated in multiethnic urban adolescent children
Lohman et al., 2009101110–1548CFSM; author-created indices of stressors: individual, maternal and family
Ravaja et al., 199667112, 15 and 1850Author-created life events questionnaire
Sweeting et al., 2005219611 and 15Baseline sample was representative of the populationAuthor-created questionnaires including weight-related items, self-image items and peer-related items
Van Jaarsveld et al., 2009406511–1658PSS
Yin et al., 200530312–24; M = 16.650Adolescent Resource Challenge Scale; median rent or mortgage in neighbourhood
Acute stress and paediatric obesity
Dockray et al., 20091118–1350TSST-C; cortisol
Eisenberg et al., 200347467th–12th grade50Survey designed by Project EAT investigators
Roemmich et al., 2003258–1256Speech stressor; heart rate; visual analogue scale
Roemmich et al., 200763M men = 9.857Speech stressor; heart rate; visual analogue scale
M women = 9.3
Stroud et al., 2000Study 1: 50Study 1: 18–20Study 1: 0Yale Interpersonal Stressor; Revised Restraint Scale; cortisol; blood pressure
Study 2: 25Study 2: 18–22Study 2: 52

Although the link between stress and obesity is complex, findings from a handful of cross-sectional studies and a fewer number of longitudinal studies are available.

Cross-sectional studies

A small number of cross-sectional studies have explored the relationship between chronic stress and obesity risk in adolescents and have found that higher levels of self-report stress are associated with an increased risk for obesity (Sweeting et al., 2005; Yin et al., 2005). For example, one study observed that stressful life events (e.g. people fighting on my street) predicted objectively measured BMI and waist circumference among adolescents (Yin et al., 2005). In another study involving adolescents ages 11 and 15 years, youth at both ages who acknowledged more weight-related worries (e.g. ‘Are you worried about putting on weight?’) were more likely to be obese (Sweeting et al., 2005). One of the only cross-sectional studies to examine the relationship between chronic stress and obesity risk in younger children used a sample of Hispanic peripubertal girls and measured stress related to school, family, personal and peer domains (Donoho, Weigensberg, Emken, Hsu, & Spruijt-Metz, 2011). The results were mixed, suggesting that only school stress was significantly related to body fat, such that children who reported more school-related stressors had a greater percentage of body fat (Donoho et al., 2011).

Longitudinal studies

A small number of studies have adopted a longitudinal approach to explore how stress affects obesity risk and weight gain across the school years (Ravaja, Keltikangas-Jarvinen, & Viikari, 1996; van Jaarsveld et al., 2009). Findings from these studies are mixed. Among youth aged 11–16 years, measures of self-reported perceived stress and objectively measured adiposity were taken across 5 years. At baseline, the higher-stress group had higher BMI and waist circumference than the lower-stress group, and this difference persisted across the 5-year period (van Jaarsveld et al., 2009). However, there were no significant differences in rates of increase in adiposity between the groups across the 5 years, suggesting that greater stress was not promoting faster weight gain (van Jaarsveld et al., 2009). There may also be gender differences. For example, in a longitudinal study examining associations between daily stressors and BMI in adolescents, self-reported stressors at 3- and 6-year follow-up were associated with increases in BMI among girls but not boys (Ravaja et al., 1996).

Links between acute stress and paediatric obesity

In contrast to the research examining the role of chronic stress in the context of paediatric obesity, fewer studies have focused upon the role of acute stress, defined as relatively brief periods of stress that do not continue across an extended period (Dickerson & Kemeny, 2004). Whereas chronic stress has generally been measured by self-report, the acute stress literature is based primarily on laboratory-based studies and examines both subjective self-report stress and objective, physiological measures of stress (e.g. cortisol and heart rate reactivity). Descriptive characteristics for selected studies examining the link between acute stress and obesity are presented in Table 1.

Three cross-sectional studies have demonstrated greater stress responses to a standardized speech stressor task among children with a higher BMI (Dockray et al., 2009; Roemmich et al., 2007; Roemmich, Gurgol, & Epstein, 2003). Although there is an absence of longitudinal studies exploring how acute stress reactivity may relate over time to paediatric obesity risk, this cross-sectional research on stress reactivity is important because of the demonstrated linkages between anthropometric variables (e.g. BMI percentile and percentage body fat) and because of findings suggesting implications of stress reactivity for key weight management behaviours (eating, exercise) in children. Roemmich et al. (2007) examined physiological reactivity (heart rate reactivity) and perceived stress in school-age children and found that children with larger increases in heart rate reactivity to a speech stressor had a greater percentage body fat, BMI percentile and central adiposity. Greater increase in perceived stress was associated with higher BMI percentile and a greater percentage of body fat (Roemmich et al., 2007). A second study also examined associations between objective stress reactivity and BMI, but used salivary cortisol response as the marker of stress. Higher cortisol reactivity to the speech stressor task was positively associated with objectively measured BMI for girls but not boys (Dockray et al., 2009). A third study found that school-age children characterized by greater heart rate reactivity to a speech stressor task participated in less exercise following the stress task than on a control day. Conversely, children in the low heart-rate-reactive group participated in similar amounts of exercise on both days (Roemmich et al., 2003).

In addition to the link between acute physiological stress reactivity and paediatric obesity risk, a couple of studies suggest specific links between acute stress and key behaviours associated with weight management (i.e. snack food consumption and physical activity). One study explained responses to a social ostracism stressor in adolescents aged 12–14 years. Research using both objective and subjective measures of stress has shown that even single episodes of ostracism, the intentional ignoring and excluding of individuals, are very stressful and can lead to impaired self-regulation, which can lead to unhealthy eating behaviours in youth (Eisenberg, Neumark-Sztainer, & Story, 2003; Salvy et al., 2011; Stroud, Tanofsky-Kraff, Wilfley, & Salovey, 2000; Zadro, Williams, & Richardson, 2004). This is especially troublesome for overweight and obese youth because they are more likely to be ostracized by peers and are more likely to eat in response to stress (Salvy et al., 2011; Temple, Legierski, Giacomelli, Salvy, & Epstein, 2008). Salvy et al. (2011) observed that overweight adolescents who experienced a social ostracism stressor consumed more food than both normal-weight adolescents in the ostracism condition and overweight adolescents in the control condition.

In summary, overall, findings from research exploring the roles of chronic and acute stress supports a stress–paediatric obesity risk linkage. However, there are inconsistencies and gaps in the literature, and more research is needed to disentangle the complex stress–obesity association. A selective review of the literature (Table 2) points to some critical areas that may aid researchers interested in further disentangling the stress and obesity linkage in youth and moving our field forward.

Table 2. Descriptive characteristics for literature examining the roles of physiological stress reactivity, stress-induced eating, parent and family influences, at-risk populations and physical activity
 Sample size (N)Age (years)Gender (%M)
Physiological stress reactivity
Buske-Kirschbaum et al., 1997Study 1: 16Study 1: 8–14Study 1: 56
Study 2: 15Study 2: 9–14Study 2: 47
Dockray et al., 20091118–1350
Newman et al., 200750M = 340
Ozier et al., 200882218–8327
Ravaja et al., 199667112, 15 and 18; followed up for 6 years50
Roemmich et al., 200763M men = 9.857
M women = 9.3
Van Jaarsveld et al., 2009406511–1658
Weigensberg et al., 20082058–1358
Yin et al., 200530312–24; M = 16.650
Stress-induced eating
Balantekin & Roemmich, 2012308–1250
Epel et al., 20015930–450
Newman et al., 200750M = 340
Nguyen-Michel et al., 2007617M = 13.424
Nguyen-Rodriguez et al., 2008517M = 12.524
Ozier et al., 200882218–8327
Roemmich et al., 2011408–1220
Roemmich et al., 2002408–1158
Rutters et al., 2008129M = 2850
Vannucci, et al., 20121508–18Not reported
Webber et al., 20094067–1246
Parent and family influences
Garasky et al., 200921375–11 and 12–1752 for 5–11 years
49 for 12–17 years
Gibson et al., 20073296–13Not reported
Koch et al., 200874431–652
Lohman et al., 2009101110–1548
Parks et al., 201221193–1752
Roemmich et al., 2003258–1256
Stenhammar et al., 2010Parents of 873 childrenChildren age 3865 mothers; 746 fathers
Strauss & Knight, 199929130–851
Zeller et al., 20071498–1641
Stress in at-risk populations
Goodman et al., 20051209M = 15.149
Grow et al., 201086166–1852
Jyoti et al., 2005~11,400 for Kindergarten through 3rd gradeKindergarten through 3rd grade~51 for Kindergarten through 3rd grade
Ievers-Landis et al., 20088198–1151
Lohman et al., 2009101110–1548
Powell et al., 2012898412–1754
Strauss & Knight, 199929130–851
Stress and physical activity
Balantekin & Roemmich, 2012308–1250
Norris et al., 199214713–1748
Yin et al., 2005303M = 16.650

Understanding stress in the context of paediatric obesity

  1. Top of page
  2. Abstract
  3. Does stress play a role in paediatric obesity?
  4. Understanding stress in the context of paediatric obesity
  5. Summary and directions for future research
  6. Clinical implications

Physiological stress reactivity

Previous methods used to measure stress

Easy-to-administer self-report instruments have been the most commonly used measures of stress (Newman, O'Connor, & Conner, 2007; Ozier et al., 2008; Ravaja et al., 1996; van Jaarsveld et al., 2009). However, critiques of these self-report measures include failure to assess objective threat, failure to obtain information regarding the date or timing of the stressor and inability to make a distinction between behaviour-dependent and behaviour-independent stressors (Grant, Compas, Thurm, McMahon, & Gipson, 2004). In contrast, stressor interviews can gain more information than checklists and other self-report instruments (i.e. information about timing of the stressor) but are more costly and time intensive and, therefore, are used less in stress research (De Vriendt et al., 2009). Similarly, well-validated stress-induction paradigms (e.g. the Trier Social Stress Test for Children; Buske-Kirschbaum et al., 1997) provide an effective method of eliciting a stress response within children and adolescents. This type of laboratory paradigm provides a unique opportunity to study the acute effects of stress, including objective, physiological responses to stress.

Importance of objective measures of stress with youth

Recently, work has been carried out to show physiological reactivity (e.g. the stress hormone cortisol and heart rate reactivity) as a marker of stress response and a predictor of BMI in children and adolescents (Dockray et al., 2009; Oskis, Loveday, Hucklebridge, Thorn, & Clow, 2009; Roemmich et al., 2007). For example, objectively measured heart rate reactivity during stress is positively associated with percentage body fat and abdominal girth (Roemmich et al., 2007). Salivary cortisol, which is relatively easy to collect and non-invasive, has consistently been documented as one of the best biomarkers of stress response in the literature (De Vriendt et al., 2009; Greaves-Lord et al., 2007; Kirschbaum & Hellhammer, 1994). Cortisol reactivity to stress is of particular interest given that activation of the hypothalamic–pituitary–adrenal (HPA) axis, specifically the release of glucocorticoids from the adrenal cortex, is a key biological mechanism through which chronic stress may lead to obesity (Adam & Epel, 2007; Bjorntorp, 2001; Dallman, 2010; Newman et al., 2007). Chronic elevations in cortisol may interfere with appetite regulation, which could lead to increased food intake and greater risk for overweight. Cortisol can affect appetite regulation by two mechanisms: (1) increasing secretion of neuropeptide-Y, leading to greater food intake, and (2) impairing the sensitization of satiety signals produced by leptin and insulin, thereby lessening the efficiency of the leptin system and impairing the inhibition of food intake (Adam & Epel, 2007; Bjorntorp, 2001).

Research demonstrates a link between relative hypercortisolemia (higher cortisol levels) and presence of metabolic syndrome among children and adolescents. Morning serum cortisol levels were associated with presence of the metabolic syndrome in overweight Latino youth, independent of body fat and insulin sensitivity. Furthermore, an increasing number of features of the metabolic syndrome (e.g. systolic blood pressure) were associated with higher cortisol levels (Weigensberg, Toledo-Corral, & Goran, 2008). There remains a need for research including physiological measurements of stress, such as cortisol and heart rate reactivity (van Jaarsveld et al., 2009; Yin et al., 2005).

Stress-induced eating

Roughly 30% of humans decrease food intake when stressed, whereas the majority of individuals increase their intake (Adam & Epel, 2007). ‘Stress-induced eating’ refers to the concept that increased food intake is a response to stress and that intake of highly palatable food has the capacity to shut down stress-induced HPA axis activation and diminish the distress (Adam & Epel, 2007; Bjorntorp & Rosmond, 2000; Greeno & Wing, 1994). Elevations in cortisol due to stress play a critical role in stress-induced eating. Stress-induced cortisol secretion influences food choices toward intake of highly palatable and energy dense, high-fat and sweet foods that provide relief from stress but may lead to weight gain (Dallman, 2010). Among those who increase their intake, chronic life stress may increase preference for foods that are higher in sugar and fat (Torres & Nowson, 2007). Stress may also decrease the inhibition produced by dietary restraint, defined as an attempt to inhibit food intake (Lowe, 1993), thereby leading to increased energy intake (Roemmich, Wright, & Epstein, 2002). A small but consistent body of research suggests that adults and children higher on dietary restraint are more prone to eat in response to stress (Balantekin & Roemmich, 2012; Roemmich, Lambiase, Lobarinas, & Balantekin, 2011; Roemmich et al., 2002).

In addition to increased food intake in response to stress, youth who report higher levels of perceived stress appear to engage in greater levels of emotional eating [defined as a behavioural pattern of eating in response to negative emotions (e.g. anger, anxiety and depression) not limited to stress; Faith, Allison, & Geliebter, 1997; Nguyen-Rodriguez, Chou, Unger, & Spruijt-Metz, 2008]. Previous research demonstrates that overeating is often an emotional defence for youth, and negative affect pre-meal predicts excessive food intake in children and adolescents scoring high on the Emotional Eating Scale, irrespective of BMI (Nguyen-Rodriguez et al., 2008; Vannucci et al., 2012). Therefore, emotional eating and stress-induced eating are likely related, and research should continue to examine this relationship, extending the focus to objectively measured stress.

Lessons from the adult literature

A small group of studies with adult samples suggests that stress leads to increased food intake, which increases the risk for weight concerns (Epel, Lapidus, McEwen, & Brownell, 2001; Newman et al., 2007; Ozier et al., 2008; Rutters et al., 2008). Snack intake was significantly associated with number of daily hassles and intensity of hassles in a group of pre-menopausal Kwomen (Newman et al., 2007). A second study concluded that adults with the greatest tendency to eat in response to emotions and stress were 13 times more likely to be overweight or obese than adults that were the least likely to eat in response to emotions and stress (Ozier et al., 2008). Furthermore, women who had a stronger response to stress (identified by high cortisol reactivity) consumed more calories and had a greater preference for sweet, high-fat foods, which could have a significant impact on weight over time (Epel et al., 2001). Given these findings among adults, it appears important to understand the acute effects of stress on dietary intake in youth. This is particularly salient given the possibility that a pattern of eating in response to stress during childhood or adolescence has the potential to persist into adulthood, and the cumulative effects of eating in response to stress may lead to weight gain and eventual overweight.

Lessons from the child and adolescent literature

Emerging research has examined associations between stress and eating among children and adolescents. Two studies have used self-report and parent report to link emotional and stress eating to a preference for energy-dense snack foods and increased weight status in youth (Nguyen-Michel, Unger, & Spruijt-Metz, 2007; Webber, Hill, Saxton, Van Jaarsveld, & Wardle, 2009). In a study involving Latino adolescents, youth who were categorized as emotional eaters had significantly more frequent intake of both salty and sweet high-calorie foods than those not categorized as emotional eaters (Nguyen-Michel et al., 2007). A longitudinal study concluded that child emotional overeating was positively associated with objectively measured child weight, although this study was limited by reliance on parent report on behalf of their child (Webber et al., 2009).

Perhaps more compelling evidence can be drawn from three experimental studies in children that examined associations between dietary restraint, stress reactivity and eating and found that the proclivity to eat following stress may also be related to dietary restraint (Balantekin & Roemmich, 2012; Roemmich et al., 2002; Roemmich et al., 2011). The first study examined changes in perceived stress in school-age children and observed that, following a speech stressor, low-restraint/low-reactive youth ate fewer snacks and high-restraint/high-reactive youth ate more snacks compared with the control conditions (Roemmich et al., 2002). A second study sought to explore whether children eat more when stressed, even when they have access to other coping behaviours (Balantekin & Roemmich, 2012). In this study, children completed a speech stressor on 1 day and were not given any stressful tasks on a control day. On both days, children were given access to television programmes, food and exercise equipment. Consistent with previous findings, children high in restraint and highly reactive to the stressor increased both eating time and calorie consumption on the stress day. This suggests that some children eat more when stressed even when alternative coping behaviours are available (Balantekin & Roemmich, 2012) and that dietary restraint in combination with stress reactivity may be important for identifying a pattern of eating in response to stress. Finally, acute stress reactivity has been tied to preference for comfort foods in children. Following a stressor, school-age children who were high in stress reactivity and dietary restraint consumed more calories and chose more energy-dense comfort foods (potato chips and M&M's) compared with healthier foods (pretzels and grapes) (Roemmich et al., 2011).

Stress and physical activity

In addition to the importance of considering the impact of stress on dietary intake, it is important to keep in mind that physical activity is a critical component of the energy balance equation and to recognize the effects of stress on physical activity. Indeed, one possible pathway through which chronic stress may be associated with obesity is through decreased physical activity, which tilts the energy-intake/energy-expenditure equation in the negative direction (De Vriendt et al., 2009). The aforementioned study by Balantekin and Roemmich (2012) found that 8- to 12-year-old children were more likely to watch television than engage in physical activity following a stressor. However, there is not a consistent association between perceived stress and the amount of physical activity a person obtains. For example, a person who perceives multiple life stressors (e.g. employment difficulties, parenting stressors, health care struggles and financial strain) may feel that there is not enough time to devote to physical activity. Research has shown time demands to be related to behaviours implicated in obesity risk (e.g. increased reliance on fast foods and less food preparation in the home) (Jabs & Devine, 2006). Conversely, some people consider physical activity a stress reliever and may overindulge in exercise when stressed.

A small body of research suggests physical activity can serve as a buffer against the harmful effects of stress (Holmes, Ekkekakis & Eisenmann, 2010). In one study, adolescents participating in high-intensity aerobic training reported significantly less psychological stress than a control group (Norris, Carroll, & Cochrane, 1992). A second study of adolescents and young adults ages 12–24 years found that the interaction between stress and physical activity significantly predicted BMI. Specifically, physical activity buffered the effect of chronic stress on adiposity, lending support for exercise as a protective factor for weight management (Yin et al., 2005).

Parent and family influences

A broader examination of the role of stress for childhood obesity risk suggests that, in addition to the effects of child stress on obesity risk at the individual child level (i.e. child stress affects child obesity risk), there is likely a link between parent/family stress and obesity risk in youth (Garasky, Stewart, Gundersen, Lohman, & Eisenmann, 2009; Gundersen et al., 2010; Koch, Sepa, & Ludvigsson, 2008; Lohman et al., 2009; Stenhammar et al., 2010; Zeller et al., 2007). There are at least two ways in which it is important to consider the family context with respect to the stress–obesity link. Firstly, it is important to consider research linking self-reported parent stress to child obesity risk. Secondly, it is important to understand how stressors within the broader home structure and family environment may be linked to child weight status.

Parent stress and paediatric obesity risk

Previous research suggests that there is a positive relationship between parental report of stress and paediatric obesity risk (Parks et al., 2012; Stenhammar et al., 2010; Zeller et al., 2007). Research in this area emphasizes two interesting points. Firstly, when exploring the effects of parental stress on child obesity risk, it is important to examine linkages with specific obesity-risk behaviours (e.g. fast food consumption and television viewing). Recently, Parks et al. (2012) found that greater parent perceived stress was related to greater child fast-food consumption, which is an important behavioural indicator of obesity risk. A second study found that not only were maternal stress scores associated with risk for childhood overweight but also greater child television-viewing time per day was also associated with this risk (Stenhammar et al., 2010). Parents experiencing higher levels of stress may have less energy or resources necessary to engage their children, potentially resulting in increased television viewing and risk for overweight (Stenhammar et al., 2010). Furthermore, it appears that parents of obese youth may experience greater mealtime-specific stress (e.g. arguments over eating) (Zeller et al., 2007).

A second message from research in this area is that, just as parent stress can be measured across a range of domains (e.g. parental worries, mealtime challenges and serious life events), it appears that experiencing stress across a greater number of domains may predict greater risk for child overweight. One study examined parental stress in four domains, serious life events, parenting stress, perceived social support and parental worries, and found that obesity risk increased as the number of domains of parent stress increased (Koch et al., 2008). Similarly, a second study found number of parental stressors to be significantly related to child obesity (Parks et al., 2012).

Family stress and paediatric obesity risk

In addition to the importance of examining parent stress, the existing research also suggests that it is important to examine how stress related to the broader family and home structure may affect the likelihood of becoming overweight (Bjorntorp, 2001; Garasky et al., 2009; Strauss & Knight, 1999). Whereas parent stress focuses on personal stress experienced by a parent, family stress more broadly describes stress across the entire home environment (e.g. family environment and family conflict).

Garasky et al. (2009) examined associations between stress in the home environment/family structure and child obesity in two age groups: 5–11 and 12–17 years. The stressors of interest (family disruption and conflict, mental and physical health problems, housing issues, health care struggles, financial strain, and lack of cognitive stimulation and emotional support) were chosen because they were common stressors related to the home environment. In the younger age group, lack of cognitive stimulation and emotional support in the household was associated with child overweight. For the older group, parental mental and physical health problems and financial strain were predictive of child overweight (Garasky et al., 2009). These specific stressors have both biological and behavioural linkages to increased weight status. Firstly, increased family or household stress can lead to lack of energy in parents, which results in unhealthy eating and/or a lack of physical activity in youth, both of which are precursors to obesity (Garasky et al., 2009; Roemmich et al., 2003). Secondly, from a biological perspective, family stress (i.e. financial strain) can lead to an increase in cortisol levels in the child or adolescent, resulting in a greater risk of overweight (Bjorntorp, 2001).

Consistent with these findings, other research has utilized the well-established Home Observation for Measurement of the Environment (HOME) scale, which measures stressors related to the family environment and parenting abilities, to determine whether a lack of cognitive stimulation and emotional support are associated with childhood overweight and obesity (Strauss & Knight, 1999). These factors are thought to increase obesity risk by restricting the child's physical activity and producing negative mental health outcomes, which are often co-morbid with unhealthy weight status (Garasky et al., 2009; Strauss & Knight, 1999). Low cognitive stimulation HOME scores, but not scores on the emotional support subscale, were associated with increased risk for child obesity (Strauss & Knight, 1999). Other studies have found that children residing in a single-parent home are at greater risk for higher BMI, overweight and obesity (Gibson, Byrne, Davis, Jacoby, & Zubrick, 2007; Strauss & Knight, 1999).

Stress in at-risk populations

Youth from racial and ethnic minorities backgrounds and low-income families are at an increased risk for obesity (Gundersen et al., 2010; Ogden et al., 2012; Strauss & Knight, 1999). However, there is a gap in the literature regarding the role of stress for youth in these paediatric obesity at-risk groups. Monitoring the weight status of children and adolescents from low-income households is particularly important given that psychosocial stressors are more common in these households (Finkelstein, Khavjou, & Will, 2006; Goodman, McEwen, Dolan, Schafer-Kalkhoff, & Adler, 2005; Gundersen et al., 2010). Specific stressors often seen in paediatric obesity at-risk populations include financial strain, poor housing quality, neighbourhood violence, food insecurity and stress stemming from ethnic or racial discrimination. Although the effect of these stressors has yet to be thoroughly understood, they may contribute to the high rates of childhood obesity in underrepresented youth worldwide. We will briefly consider linkages between stress and obesity risk in children from low-income families and then children from racial/ethnic minority backgrounds. Although we treat these as separate entities for the purposes of this review, we acknowledge that these are often overlapping groups of children.

Low-income youth and obesity risk

Low-income status, marked by financial strain, can be conceptualized as a major stressor and has generally been linked to higher obesity risk in children and adolescents (Grow et al., 2010; Jyoti, Frongillo, & Jones, 2005; Ievers-Landis, Storfer-Isser, Rosen, Johnson, & Redline, 2008; Lohman et al., 2009; Strauss & Knight, 1999). For example, compared with children from the high-income families, children in low-income families were nearly three times as likely to become obese at a 6-year follow-up (Strauss & Knight, 1999). Low-income families often experience stressful living conditions (e.g. housing quality, violence, low walkability and lack of recreation sites for physical activity) that could increase the risk for paediatric obesity (Grow et al., 2010). In previous research, median neighbourhood income was significantly associated with obesity status such that children from neighbourhoods with the lowest median incomes had greater odds of being obese (Ievers-Landis et al., 2008). Grow et al. (2010) synthesized neighbourhood contextual factors that could lead to child and adolescent obesity and found that social disadvantage (as defined by a combination of income, home ownership, education and race) was associated with increased risk of obesity. The odds of a child being obese increased for each $10,000 decrease in median household income, 10% decrease in percent of homeowners, 10% increase in percentage of women with high school education or less, single-parent households and non-White race (Grow et al., 2010).

Another stressor for low-income families that has been linked to paediatric obesity risk is food insecurity, defined as ‘limited or uncertain availability of or inability to acquire nutritionally adequate, safe, and acceptable foods due to financial resource constraint’ (Jyoti et al., 2005, p. 1). Kindergarteners experiencing current food insecurity, indicated by parent interview, had higher BMIs than children from food-secure households at kindergarten (Jyoti et al., 2005). Furthermore, children from persistently food-insecure households during kindergarten and third grade had a significantly greater increase in BMI (from kindergarten to third grade) compared with children from persistently food-secure households (Jyoti et al., 2005).

Racial/ethnic minority youth

Children and adolescents from racial and ethnic minority groups are at an increased risk for overweight (Ogden et al., 2012; Strauss & Knight, 1999). As of 2009–2010, significantly more Hispanic (21%) and non-Hispanic Black (24%) youth were obese compared with White children and adolescents (14%) (Ogden et al., 2012). Although it is important to recognize that children from certain racial/ethnic minority groups (e.g. Black and Latino) are more likely to come from a low-income family than White children (Powell, Wada, Krauss, & Wang, 2012) and that low-income is one contributor to the increased risk for obesity among racial/ethnic minority youth, there are several other potential contributors to the increased risk for obesity in racial/ethnic minority youth. A few of these contributors include media influences, neighbourhood food availability and increased stress.

Media influences are one dimension that may be contributing to excessive food intake among racial/ethnic minority youth. Previous research found that minority children watch more television than White children and are more susceptible to television advertising including high-calorie food commercials. Ethnic minorities have rated these ads more favourably than their White counterparts (Kumanyika & Grier, 2006). On top of this, content analyses have determined that low-nutrient food advertisements are more common during television programming that features African Americans and that African American magazines contain fewer health-focused advertisements. These difficulties are media influences are compounded by minority children's likelihood to live in neighbourhoods with more fast-food restaurants and fewer health-conscious options (Kumanyika & Grier, 2006).

Summary and directions for future research

  1. Top of page
  2. Abstract
  3. Does stress play a role in paediatric obesity?
  4. Understanding stress in the context of paediatric obesity
  5. Summary and directions for future research
  6. Clinical implications

Taken together, this selected review of the literature on the role of stress for paediatric obesity risk dovetails with directions for future research, including a need for more objective and physiological measurements of stress, continued emphasis on stress and eating, understanding the relationship between stress and physical activity, focus on stress in a family context and examining the stress–obesity linkage in at-risk populations. Conclusions based on the current paper should be evaluated with consideration that this paper was based on a selected versus systematic inclusion of articles. Systematic reviews (e.g. meta-analyses) examining the interrelationships between stress and obesity risk are important for advancing the field. Furthermore, although we present directions for future research in a number of domains, it is important to keep in mind that directions for future research in these areas are not mutually exclusive. For example, objective stress measurement may be especially important to consider for those children at higher risk for stress due to low socioeconomic status (Lupien, King, Meaney, & McEwen, 2001). Additional studies that measure stress objectively in underrepresented populations should be one focal point of future research. Furthermore, conclusions drawn in the present review do not differentiate the direct and likely reciprocal impacts of stress on obesity from the linkage between stress and obesity-related behaviours (e.g. decreased physical activity, emotional eating and television watching). However, findings presented in this review do provide strong evidence for the relationship between stress and obesogenic behaviours.

Although the available research suggests that a link between chronic stress and adiposity may emerge as early as late childhood or early adolescence, this research has been limited largely by the reliance on subjective reports of stress. Inclusion of objective, physiological measurements of stress response is necessary for better understanding the link between stress and obesity. Preliminary studies (e.g. Dockray et al., 2009; Oskis et al., 2009; Roemmich et al., 2007) speak to the need to include more objective measurements of stress. However, despite this need and despite the great utility in objective physiological measures of stress, these do not always correlate well with subjective experiences of stress, and it is nearly impossible (due to costs, adherence to protocol in youth, etc.) to assess stress physiologically in large-scale studies, which are needed. Thus, there is a need to develop measures of stress for youth populations that would allow for feasible epidemiological studies that can provide much needed data. Further, since objective measures of stress do not necessarily align with subjective experiences, studies that use a combination of subjective and objective stress measures are needed.

This review highlights several studies utilizing subjective and objective measurements of stress-induced eating that suggest that youth who are more likely to eat in times of stress are at an increased risk for overweight and are more likely to have a preference for unhealthy foods. It appears that children higher in dietary restraint may be at particular risk for eating in response to stress. However, more research is needed to examine the relationship between dietary restraint, stress reactivity and emotional eating. The small body of research with children, taken together with the known associations between stress and eating and obesity risk in adults, underscores the need for further research in this area.

In order to understand the connection between stress and paediatric obesity risk, we need to look at stress in a family context. Despite the research support that a connection exists between parent stress and paediatric obesity risk, not all studies have found a definitive linkage. For example, Moens et al. (2009) observed that families of overweight children and adolescents report more parenting stress, but did not find effects of stress on child BMI (Moens, Braet, Bosmans, & Rosseel, 2009). Interestingly, parental stress was tied to both parenting stress and stress due to parents' personal health status (Moens et al., 2009). This serves as a reminder of the need for future research to look beyond single predictors of stress. Additionally, although research in this area has been conducted with youth from all age ranges (i.e. young children, school-aged children, adolescents and their parents), most available studies have relied primarily on mother report. The role of parent-level and family-level stress for paediatric obesity risk could be better understood by future research that includes both mother report and father report and adopts longitudinal methodologies that are conducive to deciphering the temporal relationships between stress and obesity risk (e.g. does early parent stress predict later child obesity or does child obesity predict later parent stress).

In addition to the role of parents' own stress, it appears that stressors in the broader home and family environment may increase paediatric obesity risk. This suggests that it may be particularly important to be aware of and understand how the effects of stress on obesity risk operate among groups at a heightened risk for these stressors (e.g. low-income youth). Research utilizing objective measures of stress and longitudinal methodologies is needed to fully understand the reasons that children in these populations are at an increased risk for obesity.

Additional research is also needed to examine the moderating effect of physical activity on the stress–obesity linkage, especially in youth. Although a number of studies have looked at some aspect of the physical activity, stress and obesity triad, there is significant variability between results (Holmes et al., 2010). This inconsistency may be due, in part, to many studies assessing stress and physical activity via self-report. A combination of physiological, objective measures and subjective ratings may bring more clarity to the relationship. Finally, more prospective randomized experimental trials would improve the methodological quality of research in this area.

Whereas previous studies demonstrated a link between greater acute stress response and BMI percentile in children and young adolescents, these studies did not examine the link between stress response and risk for being in an overweight or obese category. Research is needed that compares differences in stress reactivity in lean versus overweight children. Research examining the link between acute stress and paediatric obesity is quite limited, and findings point to the need for more research in this area (Dockray et al., 2009; Roemmich et al., 2007). In relation to stress reactivity, future work should also explore patterns of eating in response to stress, whether there is a particular developmental stage at which patterns of stress eating are established and the extent to which these patterns may persist throughout childhood and be associated with risk for obesity.

Another important area for future research is to examine the impact of stress on other psychosocial (e.g. quality of life, peer relationships) and physical (e.g. diabetes and high blood pressure) consequences of obesity. For example, further investigation is warranted to explore whether obese children who experience high levels of stress report a more impaired quality of life than obese children with low levels of stress. Given that stress and obesity both influence multiple domains of functioning, and that there is overlap in the dimensions of physical and psychosocial health affected by stress and obesity, there is a need for longitudinal research aimed at disentangling the temporal sequences of the experience of stress, obesity/weight gain in youth and the emergence and maintenance of negative physical and psychosocial health consequences.

There are both direct and indirect links of stress and obesity, and more research is needed to identify the mediators and moderators that connect these two concepts. For example, although studies have examined how the stress–obesity linkage is moderated by weight control behaviours (e.g. decreased physical activity and increase in snack food consumption), fewer have looked at the direct link between stress reactivity and adiposity (Roemmich et al., 2007). Additionally, individual differences (e.g. usual time spent watching television or engaging in physical activity) and biological mechanisms (e.g. cortisol awakening response) have been examined as moderators between stress and obesity, but more research is needed to provide more depth on the relationships (Balantekin & Roemmich, 2012; Donoho et al., 2011; Garasky et al., 2009). Objective measures of stress, such as cortisol, do not necessarily capture subjectively experienced stress and thus may be a primary mediator of how psychological stress leads to obesity (De Vriendt et al., 2009; Donoho et al., 2011; Garasky et al., 2009). Further, family and parental factors (e.g. maternal stress) have been implicated as mediators in the stress–obesity linkage in youth (Zeller et al., 2007). Finally, although in many cases the linkage has been described as stress leading to obesity, most studies do not examine the directionality of the stress–obesity linkage. Although a small body of emerging research suggests that obese children may be more stress responsive (e.g. Dockray et al., 2009; Roemmich et al., 2007), the cross-sectional nature of the available research limits the ability to draw conclusions regarding the temporal relationship between obesity risk and stress. Future research adopting longitudinal designs is warranted.

Clinical implications

  1. Top of page
  2. Abstract
  3. Does stress play a role in paediatric obesity?
  4. Understanding stress in the context of paediatric obesity
  5. Summary and directions for future research
  6. Clinical implications

The research on stress and paediatric obesity provided in this review highlights the potential importance of targeting stress management as part of obesity prevention and intervention efforts. Paediatric weight management programmes may benefit from including psychoeducation and skill building related to the stress management and weight control behaviours addressed in this review. For example, youth could benefit from learning strategies to reduce emotional eating in response to stress, including learning alternative coping strategies and improving identification of stress-induced eating. Clinicians could also promote the role of physical activity in stress management while educating families that youth with higher levels of stress may be at increased risk for greater television viewing, which in turn increases the risk for obesity.

Others have noted that paediatric obesity prevention programmes should not only provide stress-reduction techniques but should also include coping strategies for stress (Gundersen et al., 2010). Learning to cope with stress is an especially integral skill for youth experiencing environmental (e.g. community-level) or family stress that is outside their control. Support for programmes aimed at reducing family-level stressors (e.g. managing financial stress) is imperative (Gundersen et al., 2010). This may be especially important for at-risk populations, including youth from low-income backgrounds. Encouraging mental health or other psychological services for parents could be beneficial as parental mental health problems have been associated with child overweight and obesity (Garasky et al., 2009). In addition, school health education classes could serve as an important forum for these programmes, as the classroom can be a highly stigmatizing and stressful environment where size discrimination occurs toward obese youth (Hague & White, 2005).


  1. Top of page
  2. Abstract
  3. Does stress play a role in paediatric obesity?
  4. Understanding stress in the context of paediatric obesity
  5. Summary and directions for future research
  6. Clinical implications
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