Bibliographic record
Abstract
Development of an eating disorder involves an interplay of factors, which may be environmental, biological, developmental, genetic, and/or psychological. All eating disorders are more prevalent in females, have an increased propensity for adolescent onset, and are, in most instances, precipitated by stressful life events. The value inherent in using an animal model to investigate the etiology of disordered eating lies in the real-life validity of such a model. Despite clinical evidence that early-life stress and heightened anxiety frequently precede the onset of pathological eating, animal models of eating disorders have not incorporated these findings to any great extent. Nor do most models take into account that the largest population of eating-disordered individuals is comprised of adolescent females and young women. The goals of this thesis were: (i) to present an overview of the physiological mechanisms that underlie stress-induced alterations in feeding systems and eating behaviours; and (ii) to examine potential factors that influence susceptibility to develop binge eating and anorexia using the most well-established animal models of these disorders. The research presented demonstrates that low levels of maternal care in early life are associated with greater vulnerability to the later development of stress-induced binge eating of highly-palatable food and, further, that this heightened vulnerability manifests in females during adolescence. In an activity-based animal model of anorexia nervosa (ABA), young adult animals that experienced early-life maternal separation lost weight faster, ate less, ran more, and required fewer days to reach removal criterion compared to their handled counterparts, with females, in particular, showing increased vulnerability. Finally, using a milder version of the ABA paradigm, early-life maternal separation increased females' susceptibility to ABA during adolescence, but not in adulthood, whereas males' susceptibility to ABA was increased only in adulthood. Together, these findings highlight the interplay between environmental, biological, and developmental factors in the etiology of binge eating and ABA.
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.000 |
| Meta-epidemiology (narrow) | 0.001 | 0.000 |
| Meta-epidemiology (broad) | 0.000 | 0.001 |
| Bibliometrics | 0.001 | 0.000 |
| Science and technology studies | 0.000 | 0.001 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.001 |
| Research integrity | 0.000 | 0.002 |
| Insufficient payload (model declined to judge) | 0.002 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".