Eating Disorder Paradigms for the New Millennium: Do “Attachment” and “Culture” Appear on Brain and Genome Scans?
Bibliographic record
Abstract
Arguably, eating disorders have inspired more shifts in explanatory paradigms, over a shorter span of time, than have any other class of syndromes in the history of psychiatry. We once understood anorexia nervosa (AN) to be a response to well-meaning but overbearing intrusions of anxious parents (usually mothers) that drove affected children into a compensatory stance of food refusal-presumably, the sole means of self-assertion left to these unfortunate children. This construal was tempting, partly because the parents of children with AN all seemed to be so anxious and partly because daughters with AN all seemed to be so obstinate and oppositional. However, careful attention to family interaction and attachment patterns showed that the parents in question were often anxious for no other reason than that watching one's child starve herself provokes anxiety. These anxious parents often enough failed to accommodate their daughters' simultaneous calls for protection, validation, and autonomy.' Likewise, we understood bulimia nervosa (BN) to be a misguided protest against parental dysempathy, hostility, and indeed sometimes, cruelty-a desperate grappling on the part of developmentally damaged children to gratify need through unbridled bingeing and then reject what was obtained through purging.2 These metaphors had emotional appeal but did not have sufficiently universal application. There followed the era of defining eating disorders as culture-bound syndromes or social epidemics.3 Clearly, cultural messages about the importance of dieting and slimness have a lot to do with eating disorders. However, emerging cross-cultural and historical data began to reveal a startling truth: eating disorders, especially AN, have occurred throughout the history of civilized societies, and indeed, in societies not even brushed by pressures to be thin. AN, at least, began to look less like a socioculturel creation and more like a hereditary syndrome akin to such entities as schizophrenia or bipolar disorder.4 Indicating a swing to yet another etiologic concept, prototypic opening phrases in articles from the late 1990s often read something like the following: Once thought to embody a cultural preoccupation with dieting, AN and BN have come to be increasingly defined as neuropsychiatrie disorders with strong genetic determinants. This shift in perspective has reflected some central additions during the past 10 to 15 years to the knowledge base on eating disorders. Family epidemiologic and twin data have shown that the eating disorders are heritable, whereas neurobiological, genetic association, and linkage studies have provided clues as to what factors might transmit vulnerability.5-7 Important changes in weightings assigned to psychological-developmental and neurobiological-genetic factors have clearly been in order. Another competition among concepts has also unfolded as an undercurrent, relating to the question of whether to view the eating disorders as disturbances of self-, mood, and impulse regulation or as disturbances of mechanisms governing appetite and weight control. In other words, are eating disorders feeding disorders, or are they variants of anxiety, mood, and impulse control disorders? Proponents of the first view search for causes among agents known to influence eating behaviour directly (such as leptin, ghrelin, and brain-derived neurotrophic factor) and among neurotransmitters that regulate satiety and reward from food (such as serotonin and dopamine).8 Advocates of the second perspective emphasize the ways in which the eating disorders resemble mood, anxiety, and impulse control disorders and construe eating symptoms as secondary or epiphenomenological aspects of phobic food avoidance. The problem is that exponents of the feeding disorder model sputter when asked to explain why eating disorders coincide so frequently with other psychiatric problems (such as affective or personality disorders), whereas adherents of the second camp never give a satisfying answer a deceptively simple question: Why is it an eating disorder? …
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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 | 0.006 | 0.008 |
| Meta-epidemiology (narrow) | 0.001 | 0.000 |
| Meta-epidemiology (broad) | 0.001 | 0.001 |
| Bibliometrics | 0.003 | 0.003 |
| Science and technology studies | 0.003 | 0.013 |
| Scholarly communication | 0.007 | 0.019 |
| Open science | 0.001 | 0.004 |
| Research integrity | 0.004 | 0.009 |
| Insufficient payload (model declined to judge) | 0.009 | 0.001 |
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".