What Influences Us to Eat More Than We Need to Peer Reviewed Article
Prev Chronic Dis. 2009 Jul; half dozen(three): A94.
Published online 2009 Jun xv.
Peer Reviewed
Developmental Perspectives on Nutrition and Obesity From Gestation to Adolescence
Terry T. Huang, PhD, MPH, 
Layla Esposito, PhD, Jennifer O. Fisher, PhD, Julie A. Mennella, PhD, and Deanna M. Hoelscher, PhD, RD, LD, CNS
Terry T. Huang
Eunice Kennedy Shriver National Found of Child Wellness and Human Development
Layla Esposito
Eunice Kennedy Shriver National Institute of Child Health and Human being Development, Bethesda, Maryland
Jennifer O. Fisher
Temple University, Philadelphia, Pennsylvania
Julie A. Mennella
Monell Chemic Senses Middle, Philadelphia, Pennsylvania
Deanna M. Hoelscher
University of Texas School of Public Wellness, Houston, Texas
Abstract
Obesity results from a complex combination of factors that act at many stages throughout a person'southward life. Therefore, examining babyhood diet and obesity from a developmental perspective is warranted. A developmental perspective recognizes the cumulative effects of factors that contribute to eating behavior and obesity, including biological and socioenvironmental factors that are relevant at different stages of evolution. A developmental perspective considers family unit, schoolhouse, and customs context. During gestation, take a chance factors for obesity include maternal diet, overweight, and smoking. In early on babyhood, feeding practices, gustatory modality acquisition, and eating in the absence of hunger must be considered. As children get more independent during middle childhood and adolescence, school nutrition, food marketing, and social networks get focal points for obesity prevention or intervention. Combining a multilevel approach with a developmental perspective can inform more constructive and sustainable strategies for obesity prevention.
Introduction
Obesity results from a combination of factors that occur at unlike stages during a person's lifetime. Therefore, babyhood diet and obesity should be examined from a developmental perspective. First, prenatal and early life experiences influence the trajectory of weight into machismo (one). Second, during certain critical periods, vulnerabilities are intensified to specific maternal and ecology exposures that tin can lead to obesity (ii). Finally, the cumulative effects of multiple factors contribute to eating behavior and obesity (3).
Growing prove suggests that prenatal and maternal interactions and influences must be considered along with biological and ecology variables throughout infancy, childhood, and adolescence that may lead to — or prevent — obesity. Examining diet and obesity from a developmental perspective combines social context and biological influences with individual behavior (iv,5). Social context can range from family, to school, to the broader customs. We describe where these contexts collaborate with biological processes to bear upon food behavior and obesity. Although a person is at take a chance for obesity throughout his life, nosotros focus on specific developmental susceptibilities for obesity from gestation through adolescence (Table).
Table.
Risk Factors for Obesity in Childhood and Adolescence
| Variable | Gestation | Early Babyhood (Birth Through Age 5 y) | Center Childhood (Ages half dozen-12 y) | Adolescence (Ages thirteen-18 y) |
|---|---|---|---|---|
| Biological evolution | • Risk for metabolic syndrome increases with exposure to glucocorticoids, protein brake, maternal diet and obesity • Exposure to nutrient flavor in utero • Maternal smoking | • Heightened preferences for sweetness, salts, fats; rejection of bitter • Heightened sense of smell • Variation in sense of taste receptor genes • Breast-feeding, exposure to nutrient season in breast milk • Low nativity weight and BMI rebound • Weaning process • Portion size and meal timing • Conditioned nutrient preferences, associative learning | • Adiposity rebound • Conditioned nutrient preferences • Portion size | • Change in composition of body mass (fat and nonfat tissue) • Change in distribution of fat • Portion size |
| Cerebral development | NA | NA | • Physical operational thought • Decision making | • Formal operational thought (abstract thought) • Decision making and problem solving • More prone to impulsivity • Invincibility • Problems considering long-term consequences of deportment |
| Psychosocial development | NA | • Parental feeding practices, family mealtime routine • Presence of adult, modeling during feeding • Foods develop sociocultural meaning • Exposure to media • "Balance of power": children strive for increasing autonomy and control | • Parental feeding practices, family mealtime routine • Presence of adult, modeling during feeding • Peer influences • Foods develop sociocultural meaning • Increasing exposure to media • Evolution of trunk prototype • Eating exterior the home • Quality of school nutrient/vending | • Family mealtime routine • Peer influences, greater social network influences • Foods develop sociocultural meaning • Increasing exposure to media • Heightened awareness of body image • Eating exterior the home • Quality of school food/vending • Coping with stress • Style of intake control (eg, dieting, eating disorders, disinhibited eating) |
| Intervention strategies that have been tried | • Promote breast-feeding • Encourage healthy prenatal nutrition | • Increase parenting skills and instructor involvement in education healthful behaviors • Increment fruit, vegetable, fiber consumption • Encourage meals at home • Increase daily action/practice | • Involve family unit in treatment • Use age-advisable dietary modification • Reduce screen time • Utilize behavior-based strategies and curricula • Increment opportunities for concrete activity and availability of healthy foods at schools | • Involve family in treatment • Reduce caloric intake and increase physical activity • Reduce screen time • Utilise beliefs-based strategies and curricula • Increase opportunities for physical activity and availability of healthy foods at schools |
Gestational Period
Risk for obesity and metabolic disorders begins during gestation (1). Obesity is linked to in utero exposure to glucocorticoids, poly peptide restrictions, and maternal diet and obesity. Exposing fetal rats to high levels of glucocorticoids reduces birth weight and results in adults with high blood levels of insulin and glucose. Male offspring of female rats with a history of fetal exposure to glucocorticoids also showroom low birth weight and glucose intolerance — a multigenerational event (vi).
Feeding low-protein diets to pregnant rats produces a wide spectrum of disorders in their offspring (7): hypertension and vascular defects (8,nine), altered fetal pancreatic development and construction (10), altered glucose tolerance (eleven), altered liver structure and function (12), contradistinct gene expression (13), and perchance type 2 diabetes mellitus (10). In humans, low protein intake by women in late pregnancy has been associated with depression birth weight, a marker of risk for obesity and other metabolic disorders later in life (14).
A maternal diet loftier in fat also causes long-term harm to the offspring. Female rat pups born to and suckled by fat-fed mothers have high blood pressure, even afterwards being placed on a balanced diet subsequently weaning. The offspring are hypertensive, show vascular changes, and have high blood insulin levels. Such changes in early on life are probable to lead to metabolic syndrome in adult animals (xv).
Many studies take indicated a link between smoking during pregnancy and the offspring's subsequent obesity, only the underlying mechanism has not been established. Children born to women who smoke during pregnancy typically weigh less at birth, and they frequently accept a catch-up flow during their first year, although studies have not consistently found a link betwixt catch-upward growth and greater childhood body mass index (BMI). Other hypotheses postulate mechanisms such as poor placental blood supply because of nicotine-induced vasoconstriction, poor maternal nutrition, and fetal exposure to carbon monoxide. Whatever the mechanism, the relationship between smoking during pregnancy and children's overweight is well documented (sixteen,17)
In 1 report, for example, babies born to mothers who smoked during pregnancy weighed less than did babies born to nonsmokers (18). However, as they reached adolescence (age xi years for girls, 16 for boys), children exposed to tobacco in utero had a significantly greater risk of existence in the highest 10% of BMI for their age group. This tendency continued to strengthen with age (participants were followed through historic period 33) and could not be explained by other factors in their childhood, adolescence, or adulthood (18).
A recent 27-year study of children whose mothers smoked during pregnancy found larger annual changes in cholesterol levels; high-density lipoprotein cholesterol levels decreased and low-density lipoprotein cholesterol levels increased more than than in children not exposed to tobacco in utero. This was the get-go study to propose that smoking during pregnancy is linked to adverse changes in the lipoprotein levels of children (19). In an analysis of questionnaire data from 8,765 children aged v to 7 years, smoking after pregnancy was not associated with childhood obesity but intrauterine exposure was (20). Another report found that smoking during the 12 months before nascency of a child was associated with boyish overweight (21).
Studies take found a meaning clan between maternal prepregnancy overweight or obesity and overweight in children. This clan indicates that overweight mothers are more probable to have overweight children, and these odds increment with the age of the child. For children anile 24 to 47 months, just maternal prepregnancy obesity had a significant outcome; for children anile 48 to 71 months, either maternal prepregnancy overweight or obesity increased take chances; and in children aged 72 to 95 months, maternal overweight or obesity imparted an fifty-fifty higher risk (21,22). Chest-feeding reduced the likelihood of early on boyish overweight in children whose mothers' prepregnancy BMI was 25 or higher, although the effect of breast-feeding was not pregnant in children of healthy-weight mothers (21,22). Thus, both prenatal and maternal variables can increase the risk of obesity in even the youngest children, long earlier social factors have an influence. Obesity prevention efforts at this stage of development have typically focused on encouraging healthy prenatal nutrition and breast-feeding; nonetheless, interventions to reduce maternal obesity during pregnancy take been express.
Infancy and Early Childhood
Taste acquisition and preference
The biological substrate that underlies the taste and rewarding properties of foods is relevant because the best predictor of food preference is whether a child likes the gustation (23). Whether a food tastes practiced or bad and the pleasure of eating is a circuitous process mediated by chemical senses in the periphery and multiple brain substrates, which are remarkably well conserved phylogenetically (24).
The degree to which taste and aroma are agreeable is adamant by innate factors (25), learning and experience, and the interactions among these. From an evolutionary perspective, these senses, which are well developed at birth, function as gatekeepers throughout life (26). The small number of gustatory modality qualities may have evolved because of the functional importance of the primary stimuli (eg, sugars, sodium chloride, bitter toxins) in nutrient pick, specially in children. The heightened preference for sweetness gustatory modality, which is evident inside hours later on birth and persists until adolescence (27,28) most likely evolved because sugariness-tasting foods are high in energy. Children's heightened preference for salty tastes (29) attracts them to necessary minerals, and rejecting bitter-tasting substances protects them from poisons because most poisonous compounds taste bitter (30). Even so, although biting tastes are innately disliked, with repeated exposure, infants can come to similar sure foods that are bitter, particularly some vegetables (31-34).
The 2002 Feeding Infants and Toddlers Study, designed to update knowledge on the feeding patterns of the youngest Americans, found that even before their second altogether, many American toddlers develop the unhealthy eating habits of adults (35). Although toddlers were more likely to eat fruits than vegetables, 1 in iv did non consume any vegetables on a given day. Instead, like older children, they were more likely to swallow fat foods such every bit french fries, salty snacks, and sugariness beverages and less likely to eat bitter-tasting vegetables (36,37). None of the acme 5 vegetables eaten by toddlers was a nighttime green vegetable.
Our knowledge is growing of how, first very early in life, early on sensory experience can shape and modify flavor and food preferences. For instance, fetuses exposed to flavors, unremarkably detected by the sense of smell, in amniotic fluid and infants exposed to flavors in breast milk (both of which reverberate flavors of the mother's nutrition) (38) larn to similar those flavors as they brand the transition to eating adult foods (39). The foods that women eat when they are meaning and nursing are precisely the ones that their infants should adopt because the mothers' eating them teaches the child that these foods are available, safe, and nutritious. At this time, however, how the protective factor of breast-feeding interacts with transmitting flavor preference for energy-dense foods in overweight mothers is unclear.
These sensory and biological considerations shed light on why lifestyle changes are hard for young children to make. We cannot hands change the basic ingrained biology of liking sweets and avoiding bitterness — preferring candy to spinach. What we can do is modulate children'due south flavour preferences by providing early exposure, starting in utero and early infancy, to a diversity of salubrious flavors. The first emotional attachment to flavors should be exploited to try to reduce the prevalence of obesity in future generations. For this reason, preventive interventions may be most effective during pregnancy and postpartum, when women are highly motivated to change for the benefit of their children. Pregnant and lactating women should widen their food choices to include as many flavorful and healthy foods equally possible. These experiences, combined with repeated exposure to nutritious foods and flavor multifariousness (31-34), should make children more than probable to choose a healthy nutrition.
Eating in the absence of hunger
Infants (40,41) and young children (42,43) can adjust their nutrient intake in response to changes in the caloric content of their nutrition, and biological sensations involving ambition probably underlie this ability. This power has been documented at meals (42,43) and during the course of a day (44). The complex interaction of nature and nurture in the regulation of ambition (45) is exemplified by a beliefs known as eating in the absence of hunger (EAH), a behavioral mark of impaired satiety (46-49). Children ranging in age from iii (50) to 19 years (51) have been observed in laboratory settings to eat big amounts of palatable food in the absence of hunger, after a repast. The corporeality of free energy consumed in the absence of hunger is variable and related to kid weight. EAH is seen more than often in children who are overweight (39,47,49,52) and in children with college ane-year weight gains (53). This behavior is coordinating to external (53) or disinhibited (54) eating behavior in adults.
Genes influence many aspects of eating behavior, including gustatory modality sensitivity (55), food preference (56), intake of specific foods (57), meal patterns (58), energy density (59), macronutrient intake (60,61), and repast (61-63) and daily energy intake (61). Behaviors such as EAH may also be heritable (64), although testify is express. Genetic influences on EAH (49,65) and other eating behaviors such as emotional eating (66) are supported by findings that the behavior is more than common when 1 or both parents are overweight, even after certain environmental factors (eg, parental eating habits) accept been controlled for. Evidence for genetic influence on intake regulation is also reflected in the relative stability of behaviors like EAH within people during two- to six-year periods in childhood (47,67).
The biological underpinnings of EAH and other ambition-related behaviors are non well understood. EAH in children is associated with higher fasting insulin and leptin levels (64), ii hormones that regulate appetite and torso weight (68). Satiety responsiveness, a split up dimension of child intake regulation, has recently been linked to variations in the FTO gene (69), which confers obesity take a chance and is highly expressed in the hypothalamus, a eye of appetite regulation in the encephalon.
Similar to other aspects of appetite regulation (lxx,71), EAH appears to go more problematic throughout childhood (45,72). Though the causes are not known, socioenvironmental influences contribute to developmental shifts in intake regulation by overriding biologically based cues of hunger and satiety. Factors that modify intake regulation include the types and amounts of food to which children are exposed, social modeling of eating behaviors, and child feeding styles and practices (73). For instance, experimental inquiry has demonstrated social modeling influences on both the types (74) and amounts of food eaten by young children (75-77). Studies of EAH amid girls accept shown positive associations with mothers' simply not fathers' disinhibited eating (52,65).
EAH has too been associated with restrictive feeding practices, although non consistently. Restricting children'southward access to a preferred nutrient has been associated with higher levels of EAH in girls aged 3 to v years (49,78) and in not-Hispanic white girls aged 5 to nine years (47,72,79). Laboratory studies of preschool-aged children accept also demonstrated that restrictions placed on children's admission to palatable, free energy-dense foods can lead to increased nutrient intake when restrictions are lifted and food becomes available (lxxx,81). Other studies, yet, found no link between feeding restriction and EAH (54). In many ways, inconsistencies in the literature on EAH parallel those observed in the full general literature on child feeding, which may reverberate the early stage of the piece of work in the field. Knowledge of child feeding has largely evolved from laboratory studies that accost cause and effect merely provide limited insight on the usual environments and social interactions surrounding children's behavior. The approach parents take to feeding their children reflects their goals for their children'due south eating and wellness, and these goals are influenced by culture and socioeconomic condition (82). To some extent, the effect of child feeding practices on children's wellness requires careful consideration of context.
Middle Childhood
Another critical period for the development of obesity is during middle childhood. BMI tends to decrease during early childhood and then, typically between the ages of 6 and eight, begins to rise once more (adiposity rebound). Excessive rebound and early rebound (before age 5) are related to higher BMI in machismo (83). An early rebound may reflect the child'southward taking more than control of intake, exposure to gestational diabetes, or early maturation (84).
Children's patterns of weight gain vary by sex activity and age (85), and during stages of rapid growth, caloric requirements increase. These stages are opportunities for interventions to preclude obesity past decision-making caloric intake and increasing energy expenditure. In add-on, considering the prevalence of obesity increases among children after puberty, as the age of sexual maturity decreases in the population (86) obesity will probably become more prevalent among elementary school students.
Children of school historic period are highly susceptible to environmental stimuli such as marketing and food availability. Studies suggest that children who are exposed to food advertisements consume more. Several studies of advertizement on children's television programs establish that the foods promoted increased the gamble of becoming obese. In i report, at to the lowest degree half of food advertisements during children's television programming were for energy-dense, low-nutrient foods such as cereal, candy, snacks, soda, and fast food (87). Not only do such advertisements promote eating, just eating while watching television as well oftentimes leads to overeating because children do non find how much they are eating (88). A recent written report showed that for each hour of television watched, children consumed an extra 167 kcal/d (89). This susceptibility is mainly considering decision making, disquisitional thinking, and abstruse thinking are underdeveloped in childhood. For example, children in Piaget's preoperational stage of cognitive evolution (ages 2-7) are characterized by casuistic and egocentric idea, while children in the concrete operational stage (ages 7-xi) cannot think abstractly, reason logically, or make inferences based on available information (90). Exposure to advertisements would decrease by restricting food advertisements that target children, particularly during times, such as Sat mornings, when many children are watching television (87).
The school environment is an opportunity for study and intervention in children's wellness behaviors because multiple factors can influence obesity in this context. For example, the Coordinated School Health Plan model from the Centers for Disease Command and Prevention proposes a multilevel arroyo in which 8 unlike school components (eg, health education, nutrition services, healthy school environment, family unit and community involvement) interact to influence pupil wellness (91).
Few studies of school eating patterns take focused on kindergarten and early simple years, but in tertiary grade, schoolhouse lunch choices begin to influence children'due south overall diets (92). Schools' nutrient policies affect student BMI; in 1 study, as the number of schoolhouse food policies increased, students' mean BMI decreased (93).
The United states of america educational system has typically fallen brusque in considering health a priority for bookish emphasis or outcomes. Health outcomes must be included in the educational agenda and go office of school accountability to obtain support and funding for health-based policies and interventions, such every bit physical education, comprehensive wellness education, or BMI monitoring. A survey of the 100 largest schoolhouse districts in 2006 found that, amongst the local wellness policies implemented, 99% dealt with nutrition standards of school meals, 97% required diet education for at least some grades, and 65% set standards for when teachers tin can apply food to reward children for good behavior or academic accomplishments (94). School programs intended to convalesce the obesity crisis need funding, partnerships, and evaluation. In 2007, the Registered Nurses' Association of Ontario set along school policies that would prevent childhood obesity; these policies included promoting physical education classes for all students, requiring concrete educational activity specialists to be involved in physical education classes, selling healthy foods in cafeterias and vending machines, and promoting walking or biking to and from school (95).
Adolescence
In addition to developmental risks carried from earlier life, by adolescence the cumulative effects of social disadvantage on obesity become apparent. Analysis of data from the National Longitudinal Survey of Youth Child-Mother File found that having an unmarried mother increased the risk for adolescent overweight. Education and current income were not significantly associated with boyish overweight, and lifetime income was only marginally significant (21).
The Growing Upwardly Today Study establish that subjective social status in the schoolhouse environs predicted BMI in adolescent girls (96). Girls who ranked themselves at the depression end of school social status were 69% more likely to have a BMI two kg/10002 higher than that of girls of higher subjective social condition. The authors ended that college subjective social standing in schoolhouse might protect against weight gain in boyish girls. The feedback loop in which depression self-esteem increases the take chances of overweight and overweight contributes to depression cocky-esteem could be a critical point of intervention.
An assay of data from 12,067 people in the Framingham Middle Study revealed an association betwixt people's weight gain and weight proceeds in their social networks (97). Rather than occurring randomly throughout social networks, people with BMI ≥30 kg/m2 were clustered in the 32-year data set. This finding was not explained solely by social ties between people who were already obese. The chance of becoming obese during a given menses increased with development of obesity in a friend (57% increase), a sibling (40% increase), or a spouse (37% increase). The effect was stronger between same-sexual practice friends and siblings. This association did not extend to neighbors, nor was it associated with changes in smoking beliefs. A more recent written report examined the peer effects on adolescent BMI by using the National Longitudinal Study of Adolescent Health (98). This study constitute an effect of social networks on obesity in adolescents, and the effect was more than pronounced among girls and heavier adolescents. Social networks seem to play a role in the spread of obesity in both adults and adolescents. Therefore, programs that target peer norms may be constructive in preventing overweight in adolescents.
Cognitive evolution during adolescence should also be considered. Although the developmental stage of formal operational thought enables skills such every bit enhanced problem solving, decision making, and abstract reasoning (90), the underdeveloped prefrontal cortex (99) still leaves adolescents at risk for behaviors that may increase the risk of obesity. For instance, adolescents tend to exist decumbent to impulsivity and the fallacy of invincibility and to have problems considering long-term consequences of their beliefs. These factors tin can contribute to poor judgment when it comes to nutrient option and other wellness-related behaviors.
Conclusions
Traditional interventions for child and adolescent obesity often focus on the individual kid, with or without family involvement, and include didactics, modification of nutrition, and increases in concrete action. Cognitive behavioral strategies are ofttimes used to help children make improve decisions, solve problems, and monitor their own progress. A recent movement suggests minimizing screen time for youth because television, computers, and video games contribute to sedentary behavior. However, few obesity interventions show clinically or statistically significant weight loss across the intervention period (100), which suggests that new and more comprehensive interventions are needed.
To annul the growing incidence of obesity, interventions must adopt an arroyo that grasps the coaction of economic, social, behavioral, biomedical, and environmental influences. Such an approach would have to encompass emerging knowledge well-nigh how obesity is the upshot of complex factors acting at many stages throughout a person's lifetime. The claiming of intervening in the obesity epidemic becomes fifty-fifty more daunting with the realization that, in children and adolescents, these influences must be considered separately at each stage of development.
This overview of the developmental influences on childhood overweight and obesity suggests opportunities for intervention. To combat prenatal influences on child obesity, pregnant women should be strongly discouraged from smoking and encouraged to consume a diet low in fat with adequate poly peptide. Additionally, breast-feeding may decrease the risk of overweight, especially in children born to overweight mothers. Considering women are more motivated to change behaviors during pregnancy and immediately postpartum, these intervals can be targeted to shape eating patterns of both mother and child.
Interventions to prevent child and adolescent obesity should focus on multiple settings, including the home and school. Farther research should investigate variables in family relationships, the home, and the extended environment that influence eating. Schools can intervene past offering healthy nutrient choices in their breakfast and lunch programs and vending machines. Empowering families and schools and giving them resource to engage in obesity prevention efforts and to provide environments that support salubrious behaviors are critical issues that governments and social institutions need to address.
Footnotes
The opinions expressed by authors contributing to this journal do non necessarily reverberate the opinions of the Us Section of Health and Human Services, the Public Health Service, the Centers for Disease Control and Prevention, or the authors' affiliated institutions. Use of trade names is for identification only and does non imply endorsement by any of the groups named above. URLs for nonfederal organizations are provided solely as a service to our users. URLs do not plant an endorsement of whatsoever organisation by CDC or the federal government, and none should exist inferred. CDC is not responsible for the content of Web pages found at these URLs.
Suggested citation for this commodity: Esposito L, Fisher JO, Mennella JA, Hoelscher DM, Huang TT. Developmental perspectives on nutrition and obesity from gestation to adolescence. Prev Chronic Dis 2009;6(three). http://www.cdc.gov/pcd/issues/2009/jul/09_0014.htm. Accessed [appointment].
Contributor Information
Terry T. Huang, Eunice Kennedy Shriver National Institute of Child Wellness and Human being Development. 6100 Executive Blvd, 4B11, Bethesda, MD 20892-7510, Telephone: 301-594-1846, Email: vog.hin.liam@retgnauh .
Layla Esposito, Eunice Kennedy Shriver National Found of Kid Health and Human Development, Bethesda, Maryland.
Jennifer O. Fisher, Temple Academy, Philadelphia, Pennsylvania.
Julie A. Mennella, Monell Chemic Senses Center, Philadelphia, Pennsylvania.
Deanna One thousand. Hoelscher, University of Texas School of Public Health, Houston, Texas.
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