Drugs for Weight Loss, Psychoanalysis for Weight Gain

A Dimensional Analysis of Eating Disorders in the SAE Framework

Han Qin

Self-as-an-End Research · ORCID: 0009-0009-9583-0018

DOI: (pending)

Abstract

This paper applies the Self-as-an-End (SAE) dimensional framework to eating disorders, analyzing obesity and anorexia nervosa (AN) as two phases of a single layered system. A preliminary note: obesity is clinically a multifactorial chronic disease requiring treatment; binge eating disorder (BED) and obesity overlap substantially but are not equivalent. The SAE analysis targets the shared dimensional structure, not the clinical multifactorial picture.

The core thesis: overeating is primarily driven by 12DD (the drive layer), while AN is generated by a cultural implant that has colonized the 14DD position — a pseudo-14DD. 13DD (the conscious layer) is not the decisive force in either direction; it serves mainly as an execution bridge. A treatment principle follows: for 12DD problems, go lower (rewrite the 11DD habit substrate); for pseudo-14DD problems, go higher (identify and clear the colonizer from the 14DD position with the aid of 15DD, allowing authentic 14DD to emerge). Direct confrontation is always the worst strategy.

The paper covers non-pharmacological obesity intervention (eating rituals as 11DD inscription), the structural impasse of AN treatment (drugs cannot reach the pseudo-14DD), and — as a speculative extension — identifies AN and nihilism as structurally isomorphic pseudo-14DD pathologies. A running subtheme is the tragedy of 13DD: consciousness is the most lucid and most powerless layer, yet awareness of its own powerlessness is precisely the gateway to 15DD.

Keywords: SAE, eating disorders, anorexia nervosa, binge eating, obesity, GLP-1, 11DD, 12DD, 13DD, pseudo-14DD, 15DD, ritual, habit, nihilism

1. Why "Eat Less" Does Not Work

Everyone knows the answer to obesity: eat less. The answer is nearly useless. The gap between knowing and executing exposes a dimensional structure problem.

In the SAE framework, hunger is a 12DD-level broadcast signal. 12DD is the drive layer; it reaches behavior without passing through understanding. "Eat less" is a 13DD instruction. The problem: the energy cost of 13DD suppressing 12DD always exceeds the energy cost of the 12DD signal itself. This is a fundamental inequality — higher-layer suppression of a lower layer runs at a net deficit.

Worse, each suppression event does not weaken 12DD. 12DD has no learning mechanism; it fires identically next time. But 13DD fatigues. One side does not deplete; the other does. The outcome is determined from the start.

This is the structural reason willpower-based dieting inevitably fails. Not insufficient discipline — the dimensional architecture does not permit it.

2. Obesity as Emergence: An Outdated Calibration Projected onto a New Environment

The gain parameter of 12DD's hunger signal was calibrated in an evolutionary environment characterized by "the next meal is uncertain." 12DD faithfully executes this calibration: eat as much as possible, store as much as possible. In scarcity, this is a survival advantage.

The modern environment has become "the next meal is always certain." But it is not merely that food became abundant. The modern food industry systematically exploits 12DD's vulnerabilities: ultra-processed foods are engineered to hijack 12DD's dopamine pathways (the "bliss point"), artificially amplifying hunger signals that the environment alone would not sustain. Emotional eating follows the same structure: workplace and life stress drive the subject to seek chemical comfort from 12DD. The epidemic scale of modern obesity is therefore not simply an evolutionary mismatch — it is the industrialized exploitation of 12DD's design weaknesses. Willpower-based dieting becomes even more hopeless: 13DD faces not only its own biology but an entire industrial system armed to the teeth.

12DD lacks reflexivity. It has only feedforward, no feedback from outcomes to itself. At 100 kg, 12DD issues the same hunger signals as at 60 kg — or stronger, since larger mass requires more energy, and 12DD scales up accordingly.

Obesity is therefore not 12DD malfunctioning; it is 12DD performing too well against an environment it was not calibrated for. Obesity is emergence, not entity — the projection of an outdated calibration onto a new environment. A necessary caveat: this is the SAE causal-structural positioning. Clinically, obesity remains a chronic disease requiring treatment; its complications (cardiovascular, metabolic syndrome) are real medical problems. SAE analysis does not deny the necessity of treatment but identifies the generator layer that treatment should target.

The same mechanism, in an underweight individual, is life-saving. 12DD's high gain pulling a malnourished person back to normal weight is called "recovery." The same high gain continuing to pull in an already overweight person is called "obesity." 12DD does not distinguish. Emergence has no intrinsic valence — only degree of match with the environment.

3. GLP-1 Drugs: Intervention at the Correct Layer

GLP-1 receptor agonists (semaglutide, tirzepatide) have achieved breakthrough results. In STEP-1, semaglutide produced a placebo-adjusted weight loss of approximately 12.4 percentage points at 68 weeks. In SURMOUNT-1, tirzepatide produced placebo-adjusted losses of approximately 11.9% to 17.8% at 72 weeks depending on dose.

In SAE terms, these drugs directly modify 12DD signal strength. They do not make 13DD try harder; they make 12DD's hunger broadcast weaker. Patients commonly report that "food no longer occupies my mind" — a phenomenological description of reduced 12DD broadcast power.

This is "a priori guides, a posteriori assists": the a priori identifies the structure as a 12DD-13DD conflict; the a posteriori (pharmacology) finds an intervention at the correct layer.

But GLP-1 drugs have a critical limitation. In STEP-4's randomized withdrawal design, those continuing semaglutide lost a further 7.9% from week 20 to 68, while those switched to placebo regained 6.9%. A 2026 BMJ systematic review likewise reports weight regain after discontinuation. The drug changes 12DD signal strength but does not permanently rewrite 12DD's calibration parameters. When the drug stops, the old calibration returns.

4. The Symmetric Face: Dimensional Structure of Anorexia Nervosa

If obesity is the phase where 12DD dominates, AN is its symmetric counterpart. But the symmetry requires finer structural analysis.

AN's generator is not in 12DD, not in 13DD. It is a cultural implant that has colonized the 14DD position — a pseudo-14DD. "Thin is beautiful," "thin is right" — these signals enter the system through 12DD-level repeated broadcasting (media images, social evaluation, peer comparison), get processed by 13DD as "my own judgment," and then occupy the 14DD position. But they lack the structural characteristics of authentic 14DD.

In SAE Learning Series Paper 3 (Qin, DOI: 10.5281/zenodo.19490707), three distinctions between calling and 14DD are established. "Thin is right" perfectly fits calling: it originates externally, has not survived via negativa locking (has not been found to be ineliminable under negative scrutiny), and disappears when the social environment is stripped away. It is a pseudo-14DD — it occupies the 14DD position but is not a direction the subject cannot eliminate after 13DD scrutiny.

Once installed, the pseudo-14DD acquires the structural authority of the 14DD position: continuous broadcast, 13DD drawing power from it without fatigue. The suppression of 12DD is sustained not by 13DD's willpower but by the pseudo-14DD's unceasing signal.

13DD is merely the bridge. When 12DD's drive overpowers the pseudo-14DD signal, the result is overeating (clinically presenting as obesity or BED — overlapping but not identical; BED itself frequently involves strong pseudo-14DD-level shame and self-evaluation, not simply "12DD dominance"). When pseudo-14DD overpowers 12DD, the result is AN. 13DD is conscripted by whichever side wins.

The healthy state is one where 12DD is appropriately constrained and the 14DD position is not colonized; 13DD need not be conscripted by either side.

Both conditions carry intense shame. After a binge, the pseudo-14DD returns and generates shame. When an AN patient eats even a little, the pseudo-14DD punishes immediately. Shame is the tearing 13DD endures as the two signals alternate dominance. Many patients oscillate between the two — diagnostic crossover from restrictive AN to binge/purge behaviors is well-documented, with transition rates varying widely but directionally consistent. These are not two diseases but the same system jumping between two attractors.

5. Drugs Can Reach 12DD; Drugs Cannot Reach Pseudo-14DD

This is the structural reason AN is harder to treat than binge eating.

12DD is biological; drugs can reach it. Pseudo-14DD occupies a sociocultural position; drugs cannot reach it. Binge eating has the GLP-1 pathway; AN has no corresponding pharmacological route.

No FDA-approved drug for AN exists. Over 15 years (2010-2025), among 24 compounds registered on ClinicalTrials.gov, only one (lisdexamfetamine) received FDA approval — for BED, not AN. Olanzapine shows a modest BMI increase in AN meta-analyses (approximately 0.67 kg/m2), far insufficient to counter pseudo-14DD. This modest effect confirms the structural point: drugs can nudge 12DD, but when pseudo-14DD broadcasts continuously, the nudge is negligible.

This chronic impasse can be more precisely diagnosed using SAE Methodology VI (Qin, DOI: 10.5281/zenodo.19464507). Methodology VI identifies a systematic "promising but insufficient evidence" pattern: small studies inflate the crossing fraction through selection; large RCTs revert to population base rates, diluting the signal. AN treatment meets nearly all diagnostic criteria. The flip point for AN is the moment pseudo-14DD is identified as a colonizer (see section 9), and population-level crossing fraction for this event is extremely low. Any binary design that does not measure whether this identification has occurred will be systematically diluted below detection.

13DD also cannot clear pseudo-14DD. This is an energy problem, not a directionality problem. In SAE's chisel-construct cycle, each layer's remainder bridges to the next — 13DD's remainder ("I know my predictions are uncertain") is the generative pathway to 14DD, so layers are not strictly unidirectional. But in pathological contexts, 13DD's cognitive negation force ("I know this is wrong") is insufficient to dislodge a program already stably running at the 14DD position — the same class of energy inequality as 13DD's inability to suppress 12DD (section 1). Simultaneously, pathological maintenance loops create bidirectional coupling: once pseudo-14DD fires, sustained hunger and semi-starvation lock down cognition, emotion, and behavior — starvation itself (12DD) impairs cognitive flexibility (13DD), reinforcing pseudo-14DD's control. This is why weight restoration and nutritional rehabilitation are not peripheral measures but necessary steps in breaking the pathological loop. APA guidelines list medical stabilization, nutritional rehabilitation, weight restoration, and psychotherapy as core components of AN treatment, noting that many symptoms — including food preoccupation and cognitive difficulties — improve with weight restoration. The SAE argument is "12DD-layer drugs alone are not enough," not "renourishment can be bypassed."

Once pseudo-14DD occupies the 14DD position, 13DD cannot discern whether the judgment is implanted or its own; it can only receive and execute. The commonly reported "I know I have a problem but I can't stop" receives a more precise phenomenological description: not "14DD conflicts with me," but "something occupies the 14DD position; I think it is mine but it is not mine, and I cannot tell the difference." 13DD senses something is wrong but lacks the energy to dislodge an installed program.

6. A Necessary Correction: The Genetic Substrate of 12DD

A posteriori data provide an important correction. Large-scale genomic studies show AN has significant heritability and genetic correlations with metabolic traits (lipid, glycemic, anthropometric), independent of BMI-associated variants. This means 12DD also contributes: some individuals' 12DD is natively set at low gain.

The more precise structure: pseudo-14DD is AN's generator, but 12DD's gain parameter determines the threshold. Under the same cultural pressure, a low-gain 12DD is more easily overpowered. This does not mean AN is "actually biological" — it means 12DD individual variation determines vulnerability.

This correction strengthens the framework: obesity and AN are not simply two extremes of pseudo-14DD vs 12DD. The 12DD gain spectrum and pseudo-14DD pressure are two continuous variables whose combination determines which phase an individual falls into.

7. Loosening 13DD: Alcohol and Psychedelics

If pseudo-14DD suppresses 12DD through the 13DD bridge, can loosening 13DD work?

Temporarily, yes. Alcohol is the oldest 13DD loosening agent. AN patients may eat after drinking: 13DD loosens, pseudo-14DD's commands cannot pass through, 12DD's hunger signals can finally execute. Clinical literature documents high comorbidity between alcohol use disorders and binge/purge eating disorder subtypes, directionally consistent with 13DD loosening followed by 12DD release — though the literature more strongly supports comorbidity/co-occurrence than the specific causal chain described here.

Upon sobering, pseudo-14DD returns with doubled punishment: "you ate" plus "you lost control." Net effect is negative.

Psilocybin is currently being investigated for AN, hypothesized to increase cognitive flexibility. A Phase I feasibility study has been published in Nature Medicine. UCSF and UCSD trials are underway. Ketamine is also being tested.

From SAE's perspective, if these drugs merely loosen 13DD, they are sophisticated versions of alcohol: temporarily disconnecting the bridge while the upstream pseudo-14DD remains. Unless the loosening window allows patients to see that pseudo-14DD is implanted — but this hypothesis currently lacks sufficient evidence.

Loosening 13DD can provide temporary relief but not lasting resolution. Pseudo-14DD remains at the 14DD position.

8. Going Lower: 11DD Inscription and Eating Rituals

Returning to obesity. Beyond drugs targeting 12DD directly, there is a non-pharmacological path: bypass 12DD and rebuild the 11DD substrate beneath it.

11DD is the unconscious broadcast layer; 12DD sits atop it. If a behavioral pattern is inscribed into 11DD, it becomes automatic — 12DD reads from it directly, no 13DD involvement required.

This is the structure of habit. 13DD holds on temporarily, executing the pattern repeatedly until it sinks into 11DD. 13DD is temporary scaffolding; 11DD is the permanent foundation.

A posteriori evidence supports this. In a controlled experiment, chewing 40 times per bite versus 15 reduced total intake by 11.9%, with lower postprandial ghrelin and higher GLP-1/CCK — physiological satiety signals independent of caloric awareness. A meta-analysis found 10 of 16 experiments showed reduced intake with increased chewing.

More critically, hunger signals can be temporally recalibrated. A human study shifting fixed breakfast from 0700 to 0900 found acylated ghrelin patterns delayed by approximately 120 minutes within one week and total ghrelin aligned within two weeks. This directly demonstrates 11DD rewritability: hunger follows rhythm, and rhythm can be reset through repetition.

Intermittent fasting can be understood as 11DD inscription. The first two weeks, 13DD holds on. After sufficient repetition, 11DD records the rhythm, and 12DD's hunger signal during the fasting window automatically decreases. Experienced 16:8 practitioners reporting "I'm simply not hungry in the morning" describe 11DD inscription completion, not improved willpower. IF's rule is maximally simple — a binary signal 11DD can rapidly absorb.

Notably, RCT meta-analyses have not found IF to show clear appetite advantages over continuous energy restriction; a 2025 TRE meta-analysis even reports increased hunger in some overweight/obese adults. This fits the signal dilution pattern predicted by SAE Methodology VI. 11DD inscription has phase-transition structure with asymmetry ratio r >> 1 (long sprouting, rapid establishment). Most IF RCTs use binary designs not measuring whether 11DD inscription has been completed. Treatment-arm adherence is highly heterogeneous: some cross the flip point, others remain in the sprouting zone. Binary analysis pools both, systematically diluting the real effect. Methodology VI recommends: use cumulative time-in-zone as the analysis variable, and before declaring IF ineffective, determine what fraction of participants completed 11DD inscription.

Eating rituals are another 11DD inscription mechanism. Setting the table, arranging tableware, sitting properly, starting with soup — repeated enough, 11DD binds this sequence to "entering eating mode." Once ritualized, 12DD's response is constrained: it triggers only with ritual, not without. Standing snacking leads to overconsumption precisely because it bypasses the ritual, leaving 12DD unframed.

Rituals also create thresholds. Wanting to eat but having to set the table first — low cost, but sufficient to block most impulsive eating. Not 13DD blocking you; 11DD's program requiring sequence completion, during which the impulse may pass.

Cross-cultural evidence provides directional support. France's three-meal structure remains rooted; over 90% of American adults snack on any given day. OECD data show the US significantly higher in obesity than France. Although cross-national differences involve many confounders, the directional consistency holds. Traditional elaborate mealtime rules were not formality — they were 11DD management. Modernity dismantled the rituals, stripping away 11DD's framework.

Bedtime routine research provides a direct analogy. A cross-national study of over 10,000 children found consistent bedtime routines associated with better sleep outcomes dose-dependently. The shared structure: timing and sequencing cues entrain physiological rhythms.

From the SAE framework, non-pharmacological obesity intervention can be reconceived as an 11DD inscription checklist: simple body-level rules that, through repetition, indirectly modify 12DD's parameters. This is currently a high-potential structural hypothesis, not an RCT-validated strategy — evidence strength varies — but the structural direction is consistent. The optimal combination: use drugs to lower 12DD gain first, then inscribe new patterns into 11DD during the window, then discontinue the drug. The drug is scaffolding for the scaffolding.

9. Going Higher: 15DD as Structural Hypothesis

13DD cannot clear pseudo-14DD. Drugs cannot clear it. What can?

In the SAE framework: identification with the aid of 15DD.

The issue is not "suppressing 14DD" or "auditing 14DD" — pseudo-14DD is not authentic 14DD. It is a colonizer occupying the 14DD position without 14DD's structure. The target is: identify the occupant as implanted, clear the colonizer, allow authentic 14DD the space to emerge.

13DD senses something is wrong but lacks the discriminating power to confirm "this is not mine." 15DD provides this. The core of 15DD is not "understanding the other's cannot-not" (understanding is 13DD's business), but acknowledging that the other has a cannot-not you cannot fully understand (Qin, SAE Learning Series Paper 4, DOI: 10.5281/zenodo.19491926). When you acknowledge another's situation as one you cannot comprehend yet must respect, you gain an external reference point — from which the pseudo-14DD is exposed as an environmentally written program, not an ineliminable direction.

This is the structural reason depth-oriented psychoanalysis may work for AN: not teaching "eat more" at the 13DD level, but providing, through relational experience, the reference point from which pseudo-14DD can be seen as pseudo. Once seen, pseudo-14DD's signal continues but you no longer take it as your own; 13DD need not execute. The 14DD position is vacated; authentic 14DD — locked through via negativa — can develop.

This provides an SAE explanation for FBT efficacy in adolescents: parental love provides the external reference point. The patient senses "my mother is afraid I will die" — not a 13DD judgment but a 15DD-level acknowledgment of the other's situation.

Clinical data are directionally consistent. FBT has the strongest evidence base for adolescent AN. For adults, no behavioral therapy shows clear superiority; all leave substantial proportions symptomatic.

To be clear: 15DD-assisted pseudo-14DD identification is a strong structural hypothesis, not clinical consensus. It does not imply "one person's love" is the only pathway. For patients without family support — or where family is a trauma source — 15DD conditions may require therapeutic relationships, support communities, or other relational forms. Nutritional rehabilitation and weight restoration are necessary steps; pseudo-14DD identification cannot bypass foundational medical intervention. In severe physiological collapse (severe malnutrition can cause brain atrophy and severely impaired cognition), patients lack the minimum cognitive resources for 15DD. Medical intervention at 12DD must first pull the patient from the brink; 15DD activation presupposes minimum cognitive recovery.

A hard boundary: 15DD cannot be forcibly activated. It requires the subject to willingly acknowledge the other's situation. 12DD needs no consent. Pseudo-14DD needs no consent. But 15DD requires you to walk in, because "acknowledging that the other has a cannot-not you cannot understand" presupposes subjecthood.

The therapist can only be present, provide conditions, and wait. Those unwilling remain unwilling. Not treatment failure — the boundary of free will.

10. The Tragedy of 13DD

A running subtheme deserves explicit statement.

13DD is the most lucid and most powerless layer. Downward, it cannot overpower 12DD — energy inequality. Upward, it cannot clear pseudo-14DD — the same inequality. Its only role is execution: 12DD wins, it eats; pseudo-14DD wins, it starves; 15DD arrives, it relays; 11DD inscribes, it supervises temporarily. All the work, none of the credit.

Its unique suffering: it is the only layer that knows. 12DD does not know it has overdriven. Pseudo-14DD does not know it is implanted. 11DD does not know it is being rewritten. Only 13DD watches lucidly, powerless.

"I know I have a problem but I can't stop." More precisely: "Something occupies the 14DD position; I think it is mine but it is not mine, and I cannot tell the difference." Consciousness and reason — humanity's pride — are the most useless layer on this battlefield.

But "most useless" is not "completely useless." 13DD (including CBT) cannot change 12DD signals or clear pseudo-14DD, but it can map the battlefield: which layer, what enemy, and that powerlessness is structural, not moral. This mapping prepares for 15DD identification — you must first know something at the 14DD position is not yours before you can, with 15DD's aid, identify it. 13DD is the war correspondent, not the main force — but without the correspondent's reports, the main force does not know where to strike.

Yet when the self finally realizes the self is useless, something shifts. "Seeing 13DD's limitation" is a capacity already belonging to 15DD. The tragedy of 13DD is precisely the gateway to 15DD.

11. General Treatment Principle

For lower-layer pathology, go lower still. For higher-layer pathology, go higher still. Direct confrontation is always the worst strategy.

Obesity (12DD): go down — rewrite 11DD, pull the ladder from under 12DD. Drugs lower 12DD gain; in the window, inscribe new 11DD patterns.

Anorexia nervosa (pseudo-14DD): go up — with 15DD's aid, identify and clear the colonizer, allow authentic 14DD to emerge. Relational experience provides the external reference point.

13DD is not the protagonist — merely a temporary worker. Wu-wei is not inaction; it is 13DD stepping aside.

Before prescribing, determine which layer. For 12DD, drugs and habit reconstruction. For pseudo-14DD, relational intervention — while not bypassing nutritional rehabilitation. Layer mismatch is a possible structural reason modern medicine repeatedly encounters difficulty in psychiatric illness.

12. Coda: Pseudo-14DD Pathology (Speculative Extension)

The following is offered as speculative extension.

AN is the most visible instance of pseudo-14DD occupying the 14DD position and crushing 12DD — because the body dies. But the same structure may operate elsewhere. Nihilism: "nothing matters" occupying the 14DD position; 13DD executes "then do nothing"; 12DD's vitality is crushed. Certain depression subtypes may contain this structure. Certain addiction maintenance mechanisms may contain pseudo-14DD ("you are worthless") driving 13DD to self-abandonment.

Common feature: none are directions surviving via negativa; all are environmentally written programs occupying the 14DD position, preventing authentic 14DD from emerging.

If this isomorphism holds, these pathologies share the same impasse: drugs act on 12DD, cognitive therapy on 13DD, neither reaches the colonizer. 15DD's reference point is the structural pathway — but this is theoretical, lacking clinical validation outside AN. AN provides a visible model because its pseudo-14DD source and 12DD consequence are both measurable. Generalizability is an open question.

In these pathologies, drugs and cognition serve their own layers. SAE's core claim: at the generator layer, relational intervention — providing the reference point for pseudo-14DD identification — plays an irreplaceable role.

Self as an End: value yourself, so pseudo-14DD does not starve you. Treasure yourself, so 12DD does not stuff you. Release yourself, so 13DD stops clinging to control. Look toward the other: 15DD activates, pseudo-14DD is identified, authentic 14DD emerges.

Kant stated the principle 260 years ago: treat persons as ends, never merely as means. SAE fits gears to this sentence so it can engage with concrete persons. With the dimensional structure, this sentence tells you which layer obesity occupies, which layer AN occupies, where drugs belong, where rituals belong, where love belongs.

The destiny of philosophy is to engage with concrete persons.

Acknowledgments

Thanks to Zesi Chen for 18 years of sustained negation and dialogue in the development of the SAE framework.

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