Evaluating Bidirectional Predictive Pathways between Dietary Restraint and Food Addiction in Adolescents.

The relationship between food addiction, an important emerging construct of excessive eating pathology, and dietary restraint has yet to be fully understood. Eating disorder models commonly posit that dietary restraint exacerbates loss of control eating (e.g., binge episodes) and may also play a causal role in the development of food addiction. However, dietary restraint as a reaction to consequences of food addiction (e.g., uncontrollable eating or weight gain) represents another plausible pathway. Existing studies indicate that the association between food addiction and dietary restraint may be more significant during adolescence than adulthood, but are limited by cross-sectional study designs. A longitudinal study using an adolescent sample is ideal for investigating potential pathways underlying links between food addiction and dietary restraint. This study examined temporal pathways between food addiction and dietary restraint in a sample of one hundred twenty-seven adolescents (M = 14.8, SD = 1.1) at three timepoints spanning two years. This is the first study to examine longitudinal cross-lagged panel associations between food addiction and dietary restraint. In this adolescent sample, food addiction significantly predicted future dietary restraint (b = 0.25, SE = 0.06, p < 0.001), but dietary restraint did not significantly predict future food addiction (b = 0.06, SE = 0.05, p > 0.05). These findings support the theory that dietary restraint may be a reaction to deleterious effects of food addiction during adolescence.

Food addiction and dietary restraint in postpartum women: The role of childhood trauma exposure and postpartum depression.

The early postpartum period is a sensitive time for understanding women's high-risk eating (i.e., eating behavior associated with negative health outcomes) given potential long-term eating behavior implications for infants. Food addiction and dietary restraint are two high-risk eating phenotypes associated with long-term negative health outcomes that have been theoretically linked. Yet, no research has considered how much these constructs overlap during the early postpartum period. The present study sought to characterize these two high-risk eating phenotypes in postpartum women to examine whether these are distinct constructs with specific etiologies and to inform future targets of intervention. Women (N = 277) in the early postpartum period reported on high-risk eating, childhood trauma exposure, depression symptoms, and pre-pregnancy weight. Women's height was measured and pre-pregnancy BMI was calculated. We conducted bivariate correlations and path analysis to characterize the relationship between food addiction and dietary restraint, controlling for pre-pregnancy BMI. Results showed that food addiction and dietary restraint were not significantly associated and that women's childhood trauma exposure and postpartum depression were associated with food addiction but not dietary restraint. Sequential mediation revealed that higher levels of childhood trauma exposure were associated with worse postpartum depression and, in turn, greater food addiction during the early postpartum period. Findings suggest that food addiction and dietary restraint have distinct psychosocial predictors and etiological pathways, which suggests important construct validity differences between the two high-risk eating phenotypes. Interventions seeking to address food addiction in postpartum women and mitigate the impact of this high-risk eating phenotype on the next generation may benefit from treating postpartum depression, especially in women with histories of childhood trauma exposure.

Associations of maternal food addiction, dietary restraint, and pre-pregnancy BMI with infant eating behaviors and risk for overweight.

Maternal food addiction, dietary restraint, and pre-pregnancy body mass index (BMI) are associated with high-risk eating behaviors and weight characteristics in children and adolescents. However, little is known about how these maternal factors are associated with individual differences in eating behaviors and risk for overweight in infancy. In a sample of 204 infant-mother dyads, maternal food addiction, dietary restraint and pre-pregnancy BMI were assessed using maternal self-report measures. Infant eating behaviors (as measured by maternal report), objectively measured hedonic response to sucrose, and anthropometry were measured at 4 months of age. Separate linear regression analyses were used to test for associations between maternal risk factors and infant eating behaviors and risk for overweight. Maternal food addiction was associated with increased risk for infant overweight based on World Health Organization criteria. Maternal dietary restraint was negatively associated with maternal report of infant appetite, but positively associated with objectively measured infant hedonic response to sucrose. Maternal pre-pregnancy BMI was positively associated with maternal report of infant appetite. Maternal food addiction, dietary restraint, and pre-pregnancy BMI are each associated with distinct eating behaviors and risk for overweight in early infancy. Additional research is needed to identify the mechanistic pathways driving these distinct associations between maternal factors and infant eating behaviors and risk for overweight. Further, it will be important to investigate whether these infant characteristics predict the development of future high-risk eating behaviors or excessive weight gain later in life.

A narrative review of highly processed food addiction across the lifespan.

Evidence is growing that highly processed (HP) foods (i.e., foods high in refined carbohydrates and fat) are highly effective in activating reward systems and may even be capable of triggering addictive processes. Unlike traditional drugs of abuse, exposure to HP foods is common very early in development. HP food addiction has been associated with negative outcomes, including higher body mass index (BMI), more frequent binge eating, greater failure in weight loss treatment trials, and poorer mental and physical health. Although most research on HP food addiction has been conducted using adult samples, research on this topic now spans across the life span beginning in utero and extending through older adulthood. HP food addiction and related reward-based changes are associated with negative outcomes at every life stage, which has important implications for developmentally tailored prevention and treatment efforts. Using a developmentally informed approach, the current study comprehensively reviews the existing research on HP food addiction across the lifespan and highlights important areas of future research.

Behavioral Responses to Sucrose as an Indicator of Positive Hedonic Response Across the First Six Months of Infancy.

Behavioral responses to sucrose provide an index of positive hedonic response in newborns. In 118 infants, the current study used repeated assessments to explore behavioral responses to sucrose solutions (24%/50% sucrose) compared to water across the first six months of infancy. Lip smacking and bringing fingers to mouth are more likely to occur in response to 24% sucrose relative to water. Tongue protrusions are also more likely to occur for 50% sucrose relative to water. Behavioral responses to sucrose may provide an index of positive hedonic response and could be used to investigate individual differences in the first six months of infancy.

Integrating Mouse and Human Genetic Data to Move beyond GWAS and Identify Causal Genes in Cholesterol Metabolism.

Identifying the causal gene(s) that connects genetic variation to a phenotype is a challenging problem in genome-wide association studies (GWASs). Here, we develop a systematic approach that integrates mouse liver co-expression networks with human lipid GWAS data to identify regulators of cholesterol and lipid metabolism. Through our approach, we identified 48 genes showing replication in mice and associated with plasma lipid traits in humans and six genes on the X chromosome. Among these 54 genes, 25 have no previously identified role in lipid metabolism. Based on functional studies and integration with additional human lipid GWAS datasets, we pinpoint Sestrin1 as a causal gene associated with plasma cholesterol levels in humans. Our validation studies demonstrate that Sestrin1 influences plasma cholesterol in multiple mouse models and regulates cholesterol biosynthesis. Our results highlight the power of combining mouse and human datasets for prioritization of human lipid GWAS loci and discovery of lipid genes.