Eating disorders in adolescents and young adults☆

Increased physical activity is a common feature of anorexia nervosa (AN). Although high activity levels are associated with greater risk of developing AN, particularly when combined with dieting, most individuals who diet and exercise maintain a healthy body weight. It is unclear why some individuals develop AN while most do not. A rodent model of resilience and vulnerability to AN would be valuable to research. Dopamine, which is believed to play a crucial role in AN, regulates both reward and activity and may modulate vulnerability.

Adolescent and young adult female C57BL/6N mice were tested in the activity-based anorexia (ABA) model, with an extended period of food restriction in adult mice. ABA was also tested in dopamine transporter knockdown mice and wild-type littermates. Mice that adapted to conditions and maintained a stable body weight were characterized as resilient.

In adults, vulnerable and resilient phenotypes emerged in both the ABA and food-restricted mice without wheels. Vulnerable mice exhibited a pronounced increase in running throughout the light cycle, which dramatically peaked prior to requiring removal from the experiment. Resilient mice exhibited an adaptive decrease in total running, appropriate food anticipatory activity, and increased consumption, thereby achieving stable body weight. Hyperdopaminergia accelerated progression of the vulnerable phenotype.

Our demonstration of distinct resilient and vulnerable phenotypes in mouse ABA significantly advances the utility of the model for identifying genes and neural substrates mediating AN risk and resilience. Modulation of dopamine may play a central role in the underlying circuit.

Unhealthy weight control behaviors (UWCBs) can lead to numerous health problems. Adolescents who engage in UWCB are more likely to abuse substances than other adolescents. However, few studies have examined the relationship between UWCB and substance use, despite the fact that their co-occurrence can result in greater morbidity and mortality. The aim of this study was to examine the association between UWCB and substance use patterns among Korean adolescents using nationally representative data.

This study involved an analysis of statistical data collected from 27,284 adolescent participants (13–18 years old) in the 2017 Korean Youth Risk Behavior Web-based Survey.

The Chi-squared test and multiple logistic regression analysis were performed to demonstrate the association between substance use patterns (energy drink intake, alcohol use, cigarette smoking, electronic cigarette use, and drug use) and UWCB (one-food diets, fasting, diet pill use, and purging). All statistical analyses were performed to reflect complex sampling weights.

More female than male adolescents reported to be engaged in any of the following UWCBs: one-food diets (female: 9.6%, male: 4.8%), fasting (female: 11.6%, male: 7.4%), diet pill use (female: 2.9%, male: 1.5%), and purging (female: 4.1%, male: 2.2%). The prevalence of all UWCBs tended to increase as energy drink intake (P < 0.001), cigarette smoking (P < 0.001), and electronic cigarette use (P < 0.001) increased.

Health professionals who work with adolescents need to be aware of the importance of screening for UWCB, including one-food diets, fasting, diet pill use, and purging, especially as a co-occurrence with substance use.

The female bias in eating disorder prevalence is the largest in all of psychiatry. Binge eating on palatable food (PF) is a core, maladaptive symptom that cuts across all major types of eating disorders and can be studied via animal models. Using an individual differences rat model of binge eating that identifies binge eating prone (BEP) and binge eating resistant (BER) phenotypes, we previously showed that, compared with males, females consume more PF and are more likely to be classified as BEP. One potential explanation for this sex difference is that PF is inherently more rewarding to females, leading to higher rates of binge eating. Here we tested the hypothesis that females have more robust behavioral and neural responses to PF reward than males. Adult male (N = 18) and female (N = 17) Sprague-Dawley rats were exposed to the Conditioned Place Preference paradigm using PF as the unconditioned stimulus. Select males (N = 9) and females (N = 9) were video-recorded during three of the PF-paired conditioning sessions to score feeding behavior. Following CPP, 13 male and 12 female rats were exposed to PF just prior to sacrifice to induce expression of the neural activation marker Fos, and Fos expression was quantified in mesocorticolimbic, hypothalamic, and amygdalar circuits. In the CPP paradigm, females displayed a more robust shift in preference for the chamber paired with PF compared with males, and behavioral analyses revealed that average duration of individual feeding bouts during pairing sessions was longer in females than in males. Fos expression was significantly higher in females vs. males in select regions of the mesocorticolimbic reward circuit, with no sex differences in hypothalamic or amygdalar regions. These results provide initial evidence that PF may be more rewarding to females than to males, possibly due to heightened responsiveness of neural substrates that mediate the hedonic and motivational responses to PF, which in part, may underlie sex differences in binge eating proneness.

Compensatory exercise and fasting behavior, in the absence of binge eating and purging, appear to be important eating disorder behaviors that are associated with dysfunction, but little is known about these behaviors in youth. We studied the trajectories of their development in non-binge eating and non-purging girls during early adolescence. Using a longitudinal design, we assessed 564 girls six times over the three years of middle school (grades 6 through 8) and developed trajectories specifying different developmental patterns in relation to the behaviors. Prior to this period, when the girls were in 5th grade (elementary school), we assessed risk factors to predict girls' subsequent trajectory group membership. Compensatory exercise trajectory groups included a non-engagement group, a group that increased in the behavior, and a group that decreased in the behavior. There were two fasting trajectory groups, one consistently engaging in the behavior and the other consistently not. Elementary school levels of depression, eating expectancies, and thinness expectancies predicted subsequent trajectory group membership. Risk for compensatory exercise and fasting should be evaluated as early as in 5th grade. Targeted interventions should focus on girls in late elementary school or middle school, as this appears to be a critical developmental and maintenance period for compensatory exercise and fasting behavior.

This article is part of a Special Issue “Puberty and Adolescence”.

Puberty is one of the most frequently discussed risk periods for the development of eating disorders. Prevailing theories propose environmentally mediated sources of risk arising from the psychosocial effects (e.g., increased body dissatisfaction, decreased self-esteem) of pubertal development in girls. However, recent research highlights the potential role of ovarian hormones in phenotypic and genetic risk for eating disorders during puberty. The goal of this paper is to review data from human and animal studies in support of puberty as a critical risk period for eating disorders and evaluate the evidence for hormonal contributions. Data are consistent in suggesting that both pubertal status and pubertal timing significantly impact risk for most eating disorders in girls, such that advanced pubertal development and early pubertal timing are associated with increased rates of eating disorders and their symptoms in both cross-sectional and longitudinal research. Findings in boys have been much less consistent and suggest a smaller role for puberty in risk for eating disorders in boys. Twin and animal studies indicate that at least part of the female-specific risk is due to genetic factors associated with estrogen activation at puberty. In conclusion, data thus far support a role for puberty in risk for eating disorders and highlight the need for additional human and animal studies of hormonal and genetic risk for eating disorders during puberty.