Influences on Child Eating and Weight Development From a Behavioral Genetics Perspective

Tanja V. E. Kral, PhD; Myles S. Faith, PhD

Disclosures

J Pediatr Psychol. 2009;34(6):596-605. 

In This Article

Abstract and Introduction

Abstract

Childhood obesity is a strong risk factor for associated comorbidities such as type 2 diabetes, cardiovascular disease, and orthopedic abnormalities in youth and its increasing incidents thus represents a major public health concern. The following review provides evidence for a familial association between parental and child weight status, eating behaviors, and food preferences. It further draws the link between environmental influences, such as parent feeding practices, and the development of child eating behaviors and thereby elucidates how genetic and nongenetic influences can contribute to the familial transmission of obesity. We use eating in the absence of hunger, an eating trait which refers to children's susceptibility to eating in response to the presence of palatable foods in the absence of hunger, as an example to illustrate these associations. The review concludes with an outlook on possibilities for future research efforts in the field.

Introduction

The prevalence of overweight among children has more than tripled since the early 1960s (Ogden, Flegal, Carroll, & Johnson, 2002; Ogden et al., 1997; Strauss & Pollack, 2001). The most recent data from the National Health and Nutrition Examination Survey (NHANES) (2003-2004) indicate that approximately 14% of children 2-5 years and 19% of children 6-11 years are overweight, which represents a 25-35% increase since the beginning of this decade alone (Ogden et al., 2006). Children from certain ethnic subgroups are disproportionately affected by this increase in body weight. For example, among Mexican American and non-Hispanic Black youth the prevalence of overweight ranges from 10% to as high as 27% across different age and gender subgroups (Ogden et al., 2006).

Childhood overweight is a critical risk factor for associated comorbidities such as type 2 diabetes (T2D), cardiovascular disease, and orthopedic abnormalities (Berenson et al., 1998; Daniels et al., 1995; Hardy, Harrell, & Bell, 2004; Rosenbloom, Joe, Young, & Winter, 1999). There is currently great concern about the development of T2D in youth, which also is increasing in prevalence (Bloomgarden, 2004; Fagot-Campagna, 2000). As Cruz and colleagues noted, obesity and family history of T2D are two of the strongest risk factors for the development of the disease in youth (Cruz et al., 2005). Dietary factors have been shown to affect insulin dynamics and β-cell (i.e., cells which produce and release insulin) function in children. For example, in overweight Latino children, ages 10-17 years, total sugar intake (g/day) was found to be positively correlated with children's body mass index (BMI), BMI z-scores and total fat mass and negatively correlated with insulin sensitivity and disposition index (i.e., index of β-cell function) (Davis et al., 2007). These associations underscore the relationship between diet and disease risk and the need for dietary interventions to promote healthy eating habits in children, especially those who are at high risk for the development of T2D. The question of how children develop eating patterns, food preferences, and the ability to regulate energy intake during growth is fundamental to understanding the development of childhood obesity and its complications, including T2D.

Obesity-promoting dietary environments are thought to encourage excessive energy intake among children by offering convenient access to large portions of palatable, energy-dense foods. At the same time, genetic predispositions determine how individuals will respond to the environment. One behavioral eating trait which has been shown to be influenced by both genetic and environmental factors is eating in the absence of hunger (EAH). EAH, which refers to children's susceptibility to eating in response to the presence of palatable foods in the absence of hunger, has been shown to be a stable eating trait in young girls (Birch & Fisher, 2000; Birch, Fisher, & Davison, 2003; Fisher & Birch, 2002) and to be correlated with children's weight status during middle childhood (Birch & Fisher, 2000; Faith et al., 2006).

The aim of this review is to illustrate how factors relating to children's familial predisposition to obesity and to their home environment can act together to influence children's eating and weight development. Specifically, the first two sections of the paper highlight the extent to which parental weight status and (eating) behaviors and food preferences can impact children's weight status and their eating behaviors and food preferences. Next, using EAH as an example of an eating trait which promotes increased caloric intake in susceptible children, we illustrate how genetic and nongenetic factors can shape this trait. We present competing conceptual models which can be used to test these influences and their impact on EAH. We conclude the current review with a discussion of possible gaps in the literature on the study of child eating phenotypes and present an outlook on possibilities for future collaborations in the field. We note that this review focuses on "unmeasured genotype" studies (also referred to as behavioral genetics or quantitative genetics studies) that did not test specific genes, rather than molecular genetics studies that test specific genes. These latter studies will be critically important to future developments in the field, and merit their own review.

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