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The current author comments on the articles from the April 2007 American Psychologist special issue on eating disorders. The current author states that the contributors to this special issue are to be commended for acknowledging lack of progress in understanding, classifying, and treating anorexia nervosa (AN). They highlighted the acute need to refine diagnosis (see record 2007-04834-004), understand comprehensive causal mechanisms to tune treatments and transcend "hodgepodge diagnoses" (see record 2007-04834-005), study functional neural circuits and link behavior with "genomic, cellular, and systems data" (see record 2007-04834-003), and develop effective treatments (see record 2007-04834-006).
Guisinger on Special Issue on Eating Dis-
orders ...................................................199
Applebaum on Mann et al. ................200
Herman et al. on Mann et al. .............202
Tomiyama & Mann reply ....................203
Competing Paradigms for
Anorexia Nervosa
Shan Guisinger
Missoula, Montana
The contributors to the April 2007 Ameri-
can Psychologist special issue on eating
disorders are to be commended for ac-
knowledging lack of progress in under-
standing, classifying, and treating anorexia
nervosa (AN). They highlighted the acute
need to refine diagnosis (Wonderlich,
Joiner, Keel, Williamson, & Crosby,
2007), understand comprehensive causal
mechanisms to tune treatments and tran-
scend “hodgepodge diagnoses” (Striegel-
Moore & Bulik, 2007, pp. 181–182), study
functional neural circuits and link behavior
with “genomic, cellular, and systems data”
(Chavez & Insel, 2007, p. 164), and de-
velop effective treatments (Wilson, Grilo,
& Vitousek, 2007, p. 201). Specifically,
Chavez and Insel (2007) wrote that
“present-day treatments are significantly
limited” and that identifying underlying
pathophysiology “will be critical for devel-
oping more effective treatments and pre-
ventive strategies” (p. 160). This state of
the field could suggest that a new paradigm
is needed, but new paradigms are often
resisted by the established scientific com-
munity (Kuhn, 1962), of which the contrib-
utors to the special issue are internationally
recognized leaders.
People with AN restrict food, see fat
on their emaciated bodies, and often exer-
cise energetically although they are at least
15% below normal weight. Any dieter can
attest that these are remarkable abilities. In
fact, energy regulation researchers believe
it is normally impossible for individuals to
maintain weight below normal for long.
However, the established point of view as-
sumes that AN is caused by “successful
pursuit of thinness through dietary restric-
tion and other measures” (Wilson et al.,
2007, p. 199), attributing cause to putative
faulty cognitions or disturbed relationships
that lead someone to have excessive weight
concerns and restrict food and exercise ex-
This view overlooks considerable ev-
idence that the cognitive and behavioral
symptoms are not strictly volitional and are
themselves caused by weight loss in the
genetically vulnerable, rather than the other
way around (Guisinger, 2003; Hebebrand,
Casper, Treasure, & Schweiger, 2004), as
well as evidence that symptoms are biolog-
ically “engineered.” In fact, Keel and
Klump (2003) found that the odd beliefs
and behaviors characteristic of AN are re-
markably similar across age, sex, and his-
torical era. Neuroimaging finds that body
image distortion results from specific
changes: When underweight anorexics
look at their own bodies, the brain region
responsible for body schema is activated,
but only in response to the patient’s own
image and only when underweight (Wag-
ner, Ruf, Braus, & Schmidt, 2003). An-
orexics receive strong signals both to eat
and to fast because normal starvation-in-
duced increases in orexigenic (hunger) sig-
nals are compromised by simultaneous ex-
cesses in anorexigenic signaling (Inui,
2001). AN is heritable, with some symp-
toms linked to genetic polymorphisms of
appetite regulators. The ability to develop
AN is activated at puberty in some girls by
genetic changes perhaps involving !-estro-
gen receptors (Klump & Gobrogge, 2005).
Yet the apparent functional coherence of
specific psychobiological evidence is often
ignored in “hodgepodge” diagnosis and ex-
A candidate for a new paradigm for
AN and perhaps the other eating disorders
sees them as evolutionary adaptations to
starvation gone awry. The adapted-to-flee-
famine hypothesis (AFFH) proposes that
when hunter-gatherers’ weight loss was
due to local famine, normal responses—
hunger, lethargy, and despair—would have
interfered with crucial efforts to migrate.
Then, individuals with abilities to ignore
hunger, move energetically, and deny star-
vation could flee local depletion (Guis-
inger, 2003), resulting in selection for the
abilities (or symptoms) that now comprise
the AN syndrome.
Researchers may dismiss adaptationist
arguments as untestable, but reasonable
conclusions can be reached by weighing
evidence and judging probabilities. Decid-
ing which competing explanation provides
the best explanatory fit and the most coher-
ence is called inference to the best expla-
nation (Lipton, 2004). If one applies this
method, an evolutionary explanation for
AN symptoms has more evidentiary sup-
port than other explanations (Guisinger,
2003). The AFFH accounts for the broad
array of phenomena and is supported
by evidence from multiple independent
sources. Psychosocial explanations explain
little biological data and are undermined by
observations that symptoms are similar
across era, sex, and culture (Keel & Klump,
2003) as well as by twin studies showing
little influence of family environment
(Striegel-Moore & Bulik, 2007).
Why has the evolutionary perspective
been overlooked? In 2003, I wrote,
Eating disorder specialists have overlooked the
adaptive significance of these symptoms because
current theories were developed when the pen-
dulum in psychology and psychiatry had swung
away from evolutionary explanations. For exam-
ple, as late as the 1960s researchers had diffi-
culty publishing findings showing that rats have
innate abilities to learn to easily associate taste
with subsequent nausea because reviewers as-
sumed the rat mind, as well as the human mind,
was essentially a tabula rasa at birth. . . . Twen-
tieth century clinicians were not trained to look
for evolutionary adaptive processes.
Furthermore, it has been difficult to see a con-
nection between the behavior of starved animals
and dieting girls because humans tend to explain
behaviors and beliefs in psychological terms.
Today’s anorectics often attribute their self-star-
vation to a desire to be thin, while medieval
women with holy anorexia explained the same
behaviors with reference to piety. Humans try to
199April 2008
American Psychologist
Copyright 2008 by the American Psychological Association 0003-066X/08/$12.00
Vol. 63, No. 3, 199 –204
make sense of their behavior post hoc, even
when it emanates from sub-cortical structures.
(Guisinger, 2003, p. 757)
Kuhn (1962) wrote that normal sci-
ence is “a strenuous and devoted attempt to
force nature into the conceptual boxes sup-
plied by professional education” (p. 5). In
the case of anorexia in this special issue,
commitment to psychosocial causation led
to some odd omissions and errors. Wonder-
lich et al. (2007) failed to mention the
many critiques of the claim made in the
Diagnostic and Statistical Manual of Men-
tal Disorders (American Psychiatric Asso-
ciation, 2000) that hyperactivity is second-
ary to desire for weight loss (Hebebrand et
al., 2004), which is important because it
obscures the applicability of several animal
models (Epling & Pierce, 1988).
Wilson et al. (2007) and Chavez and
Insel (2007) downplayed or gave an odd
twist to a psychotherapy outcome study
that found that the control group’s nutri-
tional counseling and supportive manage-
ment fared better than specialized cogni-
tive– behavioral therapy for AN and
interpersonal therapy for AN (McIntosh et
al., 2005). These and other results (a) sug-
gest that treatment succeeds (when it does)
despite popular theories of AN, (b) empha-
size the importance of communal or famil-
ial refeeding, and (c) indicate that assum-
ing symptoms are caused by individual or
interpersonal psychopathology is counter-
AN-biopsychosocial therapy (A-
BPST) combines traditional psychotherapy
with a theoretically intuitive explanation
for the symptoms—for example, that con-
trolling hunger, denying starvation, and
moving made sense in the context of a
desperate journey. Preliminary clinical re-
search suggests that A-BPST can improve
treatment outcome (Guisinger & Schuld-
berg, 2007).
American Psychiatric Association. (2000). Diag-
nostic and statistical manual of mental disor-
ders (4th ed., text rev.). Washington, DC:
Chavez, M., & Insel, T. R. (2007). Eating disor-
ders: National Institute of Mental Health’s
perspective. American Psychologist, 62(3),
159 –166.
Epling, W. F., & Pierce, W. B. (1988). Activity
based anorexia: A biobehavioral perspective.
International Journal of Eating Disorders, 5,
475– 485.
Guisinger, S. (2003). Adapted to flee famine:
Adding an evolutionary perspective on an-
orexia nervosa. Psychological Review, 110,
Guisinger, S., & Schuldberg, D. (2007, May
2–5). Preliminary examination of a biopsy-
chosocial treatment for anorexia nervosa. Pa-
per presented at the International Conference
on Eating Disorders, Baltimore, MD.
Hebebrand, J., Casper, R., Treasure, J., &
Schweiger, U. (2004). The need to revise the
diagnostic criteria for anorexia nervosa. Jour-
nal of Neural Transmission, 111, 827–840.
Inui, A. (2001). Eating behavior in anorexia ner-
vosa—an excess of both orexigenic and an-
orexigenic signalling? Molecular Psychiatry,
6, 620 624.
Keel, P. K., & Klump, K. L. (2003). Are eating
disorders culture-bound syndromes? Implica-
tions for conceptualizing their etiology. Psy-
chological Bulletin, 129, 747–769.
Klump, K. L., & Gobrogge, K. L. (2005). A
review and primer of molecular genetic stud-
ies of anorexia nervosa. International Journal
of Eating Disorders, 37(Suppl), S43–S48; dis-
cussion, S87–S89.
Kuhn, T. S. (1962). The structure of scientific
revolutions. Chicago: University of Chicago
Lipton, P. (2004). Inference to the best explana-
tion (2nd ed.). London: Routledge.
McIntosh, V. V., Jordan, J., Carter, F. A., Luty,
S. E., McKenzie, J. M., Bulik, C. M., et al.
(2005). Three psychotherapies for anorexia
nervosa: A randomized, controlled trial.
American Journal of Psychiatry, 162, 741–
Striegel-Moore, R. H., & Bulik, C. M. (2007).
Risk factors for eating disorders. American
Psychologist, 62, 181–198.
Wagner, A., Ruf, M., Braus, D. F., & Schmidt,
M. H. (2003). Neuronal activity changes and
body image distortion in anorexia nervosa.
NeuroReport, 14, 2193–2197.
Wilson, G. T., Grilo, C. M., & Vitousek, K. M.
(2007). Psychological treatment of eating dis-
orders. American Psychologist, 62, 199 –216.
Wonderlich, S. A., Joiner, T. E., Jr., Keel, P. K.,
Williamson, D. A., & Crosby, R. D. (2007).
Eating disorder diagnoses: Empirical ap-
proaches to classification. American Psychol-
ogist, 62, 167–180.
Correspondence concerning this comment
should be addressed to Shan Guisinger, 4624
Aspen Drive, Missoula, MT 59802-5220.
Why Diets Fail—Expert Diet
Advice as a Cause of Diet
Michael Applebaum
FitnessMed, Inc., Chicago, Illinois
In “Medicare’s Search for Effective Obe-
sity Treatments: Diets Are Not the An-
swer,” Mann et al. (April 2007) offered the
following broad, sweeping conclusion:
“The benefits of dieting are simply too
small and the potential harms of dieting are
too large for it to be recommended as a safe
and effective treatment for obesity” (p.
230). This statement is provocative and
unproven in the text.
According to the laws of thermody-
namics, which appear to apply everywhere
in the known universe, anytime one con-
sumes fewer Calories than one burns, there
will be weight loss (Brooks, Fahey, &
Baldwin, 2005, p. 22), despite the claims of
some diet gurus and MDs (Cruise, 2005, p.
55; Katz, 2005). Any and every diet must
work so long as a person voluntarily sus-
tains a condition of fewer Calories in than
out for a sufficient duration. Yet the arti-
cle’s conclusion denies this simple univer-
sal truth. This is a failing.
A major key to its failing is found in
Mann et al.’s (2007) Footnote 3: “The term
dieting has been used to refer to a wide
range of behaviors, but we use it solely to
refer to the specific behavior of severely
restricting one’s calorie intake in order to
lose weight” (p. 221). Rather than explore
what they term severe Calorie restriction
and its ramifications, Mann et al. (2007)
glossed over the matter. Perhaps an explo-
ration of this issue should be undertaken
before arriving at a media-sensational con-
clusion that is potentially of great harm,
that is, dissuasive of Calorie limitation for
weight loss.
Virtually all diets are based on the
“fact” that a “safe” 1–2 pounds (0.45– 0.91
kg) per week weight loss can be achieved
by a daily intake reduction of 500–1,000
This is false. It is impossible to
lose only 1–2 pounds per week following
this advice (McArdle, Katch, & Katch,
2001, pp. 840, 849).
Consequent to this approach are rec-
ommendations by acknowledged diet ex-
perts for energy intakes in a very interest-
ing range of Calories. Table 1 shows some
diet experts’ schemes (in bold) and their
Calorie intake recommendations compared
with intakes in instances of attempted/suc-
cessful murder and intentional infliction of
suffering by starvation: None of the intake
advice listed includes the recommended
approximately 300 Calories per day to be
For examples, see Berning (2005), President’s
Council on Physical Fitness and Sports (2004),
Medical Encyclopedia: Losing Weight (n.d.),
and U.S. Food and Drug Administration, Federal
Trade Commission, and National Association of
Attorneys General (1992).
200 April 2008
American Psychologist
... The unknown etiology of anorexia and the lack of understanding of the pathogenesis have hindered the development of effective interventions (Wagner et al., 2007). More recently, Guisinger (2008) commended Wonderlich, Joiner, Keel, Williamson, & Crosby (2007 for an article in which they acknowledged a " lack of progress in understanding, classifying and treating anorexia nervosa " and the need to refine diagnosis through the study of neural biology and its link to behaviour (Guisinger, 2008, p.199). Guisinger suggests there is a need for a new paradigm as it is usually impossible for an individual to maintain weight below normal, for any period of time. ...
... is, the anorexic person is remarkable. He disagrees with Wilson, Grilo & Vitousek, (2007) and the more established view that assumes anorexia is " caused by a successful pursuit of thinness " resulting in restricting and excessive exercise and weight concerns, and attributes this to " putative faulty cognitions or disturbed relationships " (p.199). Guisinger (2008) believes the evidence shows that this is not volitional; but is instead a genetic vulnerability, and the restrictive behaviour results in cognitive and behavioural symptoms caused by weight loss not the other way around (Guisinger, 2008; Hebebrand, Casper, Treasure & Schweiger, 2004). Some researchers suggest that Anorexia Nervosa is an ...
... He disagrees with Wilson, Grilo & Vitousek, (2007) and the more established view that assumes anorexia is " caused by a successful pursuit of thinness " resulting in restricting and excessive exercise and weight concerns, and attributes this to " putative faulty cognitions or disturbed relationships " (p.199). Guisinger (2008) believes the evidence shows that this is not volitional; but is instead a genetic vulnerability, and the restrictive behaviour results in cognitive and behavioural symptoms caused by weight loss not the other way around (Guisinger, 2008; Hebebrand, Casper, Treasure & Schweiger, 2004). Some researchers suggest that Anorexia Nervosa is an " unusual variant " of mood disorder to which the female population is particularly vulnerable (Salbach-Andrae et al., 2007) showed consistently that this also included more extreme behavioural constraint, avoidance of novelty and emotionality, regimentation, and perfectionism in early life compared with those without the illness. ...
The intention of this dissertation was to review the existing literature on the topic of movement from deadness to aliveness in the anorexic client and the countertransferential experience of this. Psychodynamic approaches recommended for this client group are reviewed through this directional lens. A literature review was conducted from a holistic framework looking at the approaches which utilise counter transference to integrate psychoanalysis, psychodynamic and mind/body psychotherapy. Although there is a wide body of literature relating to aliveness and deadness in the therapeutic space, it seems within the literature on eating disorders, the theme of death and deadness has been largely overlooked. It was found that clients with Anorexia Nervosa have complex presentations related to the puzzling path physiology of this illness. Improved outcome for the client may be enhanced by focusing the psychotherapeutic interventions to support the client to work through deadened states and access the self towards a more enlivened state and integral self.
... Given the similar weights it is likely that this finding reflects greater body dysmorphia in those with higher eating pathology. Indeed, many researchers suggest that inaccurate self-assessment of body size is an important symptom of eating disorders (APA, 2000; Guisinger, 2008). This appears particularly well-documented for Anorexia Nervosa (Guisinger, 2008). ...
... Indeed, many researchers suggest that inaccurate self-assessment of body size is an important symptom of eating disorders (APA, 2000; Guisinger, 2008). This appears particularly well-documented for Anorexia Nervosa (Guisinger, 2008). These findings lend support to this already large body of literature and suggest that such body dysmorphia may also be present in a sample overrepresented with bulimics. ...
... Berrocal Moya, Rivas, Bersabé, y Castro, 2003). De especial relevancia son los escasos avances en la comprensión, clasificación y tratamiento de la anorexia nerviosa (Guisinger, 2008). ...
Full-text available
Resumen El presente artículo presenta los resultados obtenidos tras desarrollar y validar el Cuestio-nario de Imagen Corporal, con una muestra de 395 personas pertenecientes a población clínica o general. El instrumento permite valorar la po-sible existencia de trastornos de la conducta ali-mentaria relacionados con la bulimia, anorexia, obesidad, vigorexia y ortorexia. Todos los facto-res y la escala en su conjunto mostraron ade-cuada consistencia interna y el análisis facto-rial confirmó la multidimensionalidad de la escala y por tanto, avala su validez de construc-to. Los resultados obtenidos de la aplicación del instrumento sugieren que la existencia de ante-cedentes personales o familiares relacionados con estos trastornos o con ansiedad o depre-sión, incrementan la probabilidad de presentar problemas de conducta alimentaria. Ello es con-sistente con la literatura y apoya su validez experimental. Abstract This paper presents the results obtained after developing and validating the Body Image Questionnaire with a sample of 395 persons belonging to clinical or general population. The instrument allows assessing probable eating disorders related to bulimia, anorexia, obesity, ort-horexia, and bigorexia. All the factors and total scale showed good internal consistency. Factor analysis confirmed the multidimensionality of the scale and therefore, its construct validity. The results of the instrument implementation suggest that the existence of personal or family history related to these disorders or to anxiety or depression, increase the likelihood of developing eating disorders. This is consistent with the literature and supports the experimental validity of the measure.
... Being such a complex phenomena, eating disorders are difficult to evaluate and this field currently faces several challenges (Sepulveda, 2007). First, the persistence of conceptual issues related to the actual diagnosis of these disorders and their medical criteria of severity (Berrocal, Rivas, Bersabé, & Castro, 2003;Guisinger, 2008). Second, studies have focused on classical ED, leaving other disorders unexplored. ...
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Eating disorders adversely affect physical health, eating habits, social and family relationships, mood, work and school performance. We tested for cross-cultural validity of the Body Image Screening Questionnaire (BISQ), a screening measure validated in Spain, which assesses potential eating disorders related to anorexia, perception of obesity, orthorexia and vigorexia, in a Romanian sample from both clinical and general populations. The measure showed adequate internal consistency and allowed distinguishing clinical vs. general subsamples. Significant differences based on clinical characteristics were obtained. The measure can be utilized as screening tool of individuals who need further assessment and prioritize primary intervention strategies with at risk population.
How is genetic involvement interpreted for disorders whose medicalisation is contested? Framing psychiatric and behavioural disorders in terms of genetics is expected to make them seem more medical. Yet a genetic aetiology can also be used to frame behaviour as acceptable human variation, rather than a medical problem (for example, sexual orientation). I analyse responses to the idea that there is a genetic component in anorexia and bulimia nervosa (AN or BN) via semi-structured interviews with a sample of 50 women diagnosed with an eating disorder (25 had recovered). All but three volunteered that genetics would medicalise AN or BN by (i) making eating disorders seem more like 'real diseases'; implying that these disorders need (ii) professional treatment or (iii) a biologically based treatment. The results also indicate there are several counter-logics by which genetic framing could support non-medical definitions of AN or BN. I argue that genetic framing reduces perceived individual responsibility, which can support definitions of behaviour as either a reflection of disease (which entails intervention) or a reflection of normal human diversity (which does not). In the context of public scepticism as to the 'reality' of AN or BN, genetic involvement was taken as evidence of disease in ongoing negotiations about the medical and moral status of people with eating disorders.
The purpose of this review was to update and complement part 1 of this study. Clinical, ethical and legal approaches to forced treatment in patients with anorexia nervosa were considered in the light of recent literature. The first comparison of compulsorily detained adolescents and those treated under parental consent shows mainly advantages in the short and medium term of using the Mental Health Act. In a qualitative study, a pathway for advance decisions has been developed. Implications of the Human Rights Act for clinical practice have been elucidated. A case report of a pregnant anorexic woman shows the risk for her foetus. The ethical dilemma of treating a woman with cerebral palsy and chronic anorexia nervosa has been reported and an ethical re-evaluation of treatments for (especially chronic) anorexia nervosa recommended. The treatment of adolescents with severe anorexia nervosa may be improved by detention under the Mental Health Act. The Human Rights Act has implications for the treatment of anorexia nervosa. Guidelines for treating anorexia nervosa should include recommendations for pregnant sufferers as well as for those with severe physical comorbidity. A shift from cure to care for chronic anorexia nervosa might improve ethical conduct.
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Anorexia nervosa (AN) is commonly attributed to psychological conflicts, attempts to be fashionably slender, neuroendocrine dysfunction, or some combination of these factors. Considerable research reveals these theories to be incomplete. Psychological and societal factors account for the decision to diet but not for the phenomenology of the disorder; theories of biological defects fail to explain neuroendocrine findings that suggest coordinated physiological mechanisms. This article presents evidence that AN's distinctive symptoms of restricting food, denial of starvation, and hyperactivity are likely to be evolved adaptive mechanisms that facilitated ancestral nomadic foragers leaving depleted environments; genetically susceptible individuals who lose too much weight may trigger these archaic adaptations. This hypothesis accounts for the occurrence of AN-like syndromes in both humans and animals and is consistent with changes observed in the physiology, cognitions, and behavior of patients with AN.
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In this paper I explore the prospects of applying inference to the Best Explanation (TIBE - sometimes also known as 'abduction') to an account of the way we decide whether to accept the word of others (sometimes known as 'aliens'). IBE is a general account of non- demonstrative or inductive inference, but it has been applied in a particular way to the management of testimony. The governing idea of Testimonial IBE (TIBE) is that a recipient of testimony ('hearer') decides whether to believe the claim of the informant ('speaker') by considering whether the truth of that claim would figure in the best explanation of the fact that the speaker made it.
A biobehavioral model of activity-based anorexia is examined in terms of recent evidence. Strenuous exercise reduces the value of food reinforcement and results in decreased food intake. Reduction of food intake increases the motivational value of physical exercise. This produces an escalation in activity that further suppresses appetite. Cultural practices of diet and exercise initiate this anorexic cycle, and once started the process is resistant to change. These anorexias may be the result of natural selection favoring those organisms that became active in times of food scarcity. Proximate physiological mechanism(s) appear to involve the endogenous opiate system that mediates the relationshp between running and eating. It is argued that classification of human self-starvation should be based on environmental and/or biological conditions that control food regulation. Activity anorexia may be one instance of such a classification that could account for many instances of “an orexia nervosa”.
Recent research on anorexia nervosa (AN) has focused on examining the genetic underpinnings of its etiology. The current article reviews molecular genetic studies that have focused on this aspect of AN development. Medline and PsychInfo literature searches, in addition to close inspection of study reference sections, were used to identify studies that examined the genetic diathesis for AN. Findings from association studies indicate some role for the serotonin system in the development of AN. Genomic regions on chromosomes 1 and 10 are also likely to harbor susceptibility genes for AN as well as a range of eating pathologies. Findings corroborate those of neurobiologic studies suggesting that alterations in serotonergic functioning may contribute to the pathogenesis of AN. Nonetheless, future molecular genetic research would benefit from larger and more sustained investigations of candidate genes in homogeneous phenotypes. © 2005 by Wiley Periodicals, Inc.
Anorexia nervosa (AN) is a disorder characterized by abnormal eating behavior, weight regulation, and disturbances in attitudes and perceptions toward body weight and shape. Although progress has been made in the treatment of AN, a substantial portion of patients have a limited response to treatment. Multiple endocrine and metabolic changes occur after prolonged starvation, conserving energy and protein. A number of the endocrine findings in patients with AN may be secondary to adaptive mechanisms. However, AN differs from simple starvation in that excess of both feeding-stimulatory (orexigenic) and feeding-inhibitory (anorexigenic) signalling is characteristic, producing the "mixed" signal about satiety and desire to feed. This leads to a failure of the adaptive feeding response that is initiated by a decrease in leptin, an adiposity signal from fat tissue, and the resultant increase and decrease of orexigenic and anorexigenic signalling, respectively. The hypothesis of unbalanced shift of feeding-regulatory circuitry places anorexigenic corticotropin-releasing factor and orexigenic neuropeptide Y in the final common neurobiological substrate for AN. Therapeutic intervention using such receptor antagonists may lead to more successful and targeted psychopharmacological treatment.
The authors explore the extent to which eating disorders, specifically anorexia nervosa (AN) and bulimia nervosa (BN), represent culture-bound syndromes and discuss implications for conceptualizing the role genes play in their etiology. The examination is divided into 3 sections: a quantitative meta-analysis of changes in incidence rates since the formal recognition of AN and BN, a qualitative summary of historical evidence of eating disorders before their formal recognition, and an evaluation of the presence of these disorders in non-Western cultures. Findings suggest that BN is a culture-bound syndrome and AN is not. Thus, heritability estimates for BN may show greater variability cross-culturally than heritability estimates for AN, and the genetic bases of these disorders may be associated with differential pathoplasticity.