Background: Worldwide, the prevalence of obesity among children has increased dramatically. Although the etiology of childhood obesity is multifactorial, to date, most preventive interventions have focused on school-aged children in school settings and have met with limited success. In this review, we focus on another set of influences that impact the development of children's eating and weight status: parenting and feeding styles and practices. Our review has two aims: (1) to assess the extent to which current evidence supports the hypothesis that parenting, via its effects on children's eating, is causally implicated in childhood obesity; and (2) to identify a set of promising strategies that target aspects of parenting, which can be further evaluated as possible components in childhood obesity prevention.Methods: A literature review was conducted between October 2006 and January 2007. Studies published before January 2007 that assessed the association between some combination of parenting, child eating and child weight variables were included.Results: A total of 66 articles met the inclusion criteria. The preponderance of these studies focused on the association between parenting and child eating. Although there was substantial experimental evidence for the influence of parenting practices, such as pressure, restriction, modeling and availability, on child eating, the majority of the evidence for the association between parenting and child weight, or the mediation of this association by child eating, was cross-sectional. Conclusion:To date, there is substantial causal evidence that parenting affects child eating and there is much correlational evidence that child eating and weight influence parenting. There are few studies, however, that have used appropriate meditational designs to provide causal evidence for the indirect effect of parenting on weight status via effects on child eating. A new approach is suggested for evaluating the effectiveness of intervention components and creating optimized intervention programs using a multiphase research design. Adoption of approaches such as the Multiphase Optimization Strategy (MOST) is necessary to provide the mechanistic evidence-base needed for the design and implementation of effective childhood obesity prevention programs.

Rates of overweight in North American children and adolescents have increased dramatically since the 1970s. Childhood obesity has reached epidemic proportions and calls for prevention and treatment programs to reverse this trend have been made. However, the evidence base needed for effective action is still incomplete, especially for childhood obesity prevention programs. This paper focuses on primary prevention of childhood obesity and has three aims: (1) to briefly describe current primary prevention approaches for childhood obesity and the evidence for their impact; (2) to elucidate promising, but untested intervention strategies using an ecological framework and evidence from experimental and epidemiological research on factors influencing children's eating and weight status; and (3) to introduce a multiphase strategy for screening intervention components and building and evaluating potent interventions for childhood obesity. Most childhood obesity prevention programs have focused on school-aged children and have had little success. We suggest that, given these findings, prevention efforts should be expanded to explore other contexts in which children live as possible settings for intervention efforts, including the family and childcare settings. Given that 25% of preschool children are already overweight, intervening with children before school entry should be a priority. A review of experimental research on the developing controls of food intake in infancy and childhood suggests possible intervention strategies, focusing on parenting and aspects of the feeding environment. Epidemiological findings point to even earlier modifiable risk factors, including gestational weight gain, maternal prepregnancy weight, and formula feeding. However, the potential impact of altering these risk factors remains to be evaluated. In response to this problem, we suggest a new, multiphase method for accomplishing this, including screening intervention components, refining intervention designs and confirming component efficacy to build and evaluate potent, optimized interventions.

The ability to perceive flavors begins in utero with the development and early functioning of the gustatory and olfactory systems. Because both amniotic fluid and breast milk contain molecules derived from the mother's diet, learning about flavors in foods begins in the womb and during early infancy. This early experience serves as the foundation for the continuing development of food preferences across the lifespan, and is shaped by the interplay of biological, social, and environmental factors. Shortly after birth, young infants show characteristic taste preferences: sweet and umami elicit positive responses; bitter and sour elicit negative responses. These taste preferences may reflect a biological drive towards foods that are calorie- and protein-dense and an aversion to foods that are poisonous or toxic. Early likes and dislikes are influenced by these innate preferences, but are also modifiable. Repeated exposure to novel or disliked foods that occurs in a positive, supportive environment may promote the acceptance of and eventually a preference for those foods. Alternatively, children who are pressured to eat certain foods may show decreased preference for those foods later on. With increasing age, the influence of a number of factors, such as peers and food availability, continue to mold food preferences and eating behaviors.

An examination of the basic biology of sweet taste during childhood provides insight, as well as new perspectives, for how to modify children's preferences for and intakes of sweet foods to improve their diet quality.

This study describes qualitatively distinct trajectories of BMI change among girls participating in a longitudinal study of non‐Hispanic, white girls (n = 182) and their parents, assessed at daughters' ages 5, 7, 9, 11, 13, and 15 years. Height, weight, body fat, fasting blood glucose and lipids, blood pressure, waist circumference, and pubertal status were measured, and participants self‐reported dietary, physical activity, and television (TV) viewing patterns. Growth mixture models were used to model heterogeneity in girls' BMI trajectories over 10 years. Statistical support was strongest for four distinct BMI trajectories: (i) upward percentile crossing (UPC; n = 25, 14%); (ii) delayed downward percentile crossing (DDPC; n = 37, 20%); (iii) 60th percentile tracking (60PT; n = 52, 29%); and (iv) 50th percentile tracking (50PT; n = 68, 37%). Girls in the UPC group had more metabolic risk factors at age 15 years, even after adjusting for concurrent weight status. Girls in the UPC group had mothers with the highest BMIs at study entry and were breast‐fed for a shorter duration. This novel approach for examining differences in growth trajectories revealed four distinct BMI trajectories that predicted adolescent metabolic health outcomes in girls. The present study provides support for BMI monitoring in girls and for the potential utility of combining data on BMI tracking with data on familial characteristics for the early identification of girls at elevated risk for obesity and metabolic syndrome.