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Abstract

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).
Comment
Contents
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
DOI:10.1037/0003-066X.63.3.199
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-
cessively.
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-
planation.
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-
therapeutic.
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).
REFERENCES
American Psychiatric Association. (2000). Diag-
nostic and statistical manual of mental disor-
ders (4th ed., text rev.). Washington, DC:
Author.
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,
745–761.
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
Press.
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.
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Striegel-Moore, R. H., & Bulik, C. M. (2007).
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Wagner, A., Ruf, M., Braus, D. F., & Schmidt,
M. H. (2003). Neuronal activity changes and
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Wilson, G. T., Grilo, C. M., & Vitousek, K. M.
(2007). Psychological treatment of eating dis-
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Correspondence concerning this comment
should be addressed to Shan Guisinger, 4624
Aspen Drive, Missoula, MT 59802-5220.
E-mail: shan.guisinger@mso.umt.edu
DOI:10.1037/0003-066X.63.3.200
Why Diets Fail—Expert Diet
Advice as a Cause of Diet
Failure
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
Calories.
1
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
1
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. ...
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... 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. ...
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