The Need for Complex Ideas in Anorexia Nervosa

The Need for Complex Ideas in Anorexia Nervosa:Why Biology, Environment, and Psyche All Matter, WhyTherapists Make Mistakes, and Why Clinical Benchmarks

Are Needed for Managing Weight Correction

Michael Strober, PhD, ABPP1,2*Craig Johnson, PhD3,4

ABSTRACT

Anorexia nervosa remains an enigma and

its clinical challenge is intimidating. But the

potential for new insights has been advanc-

ing, largely as a result of elegant research

in the neurosciences that has modeled be-

havioral processes resembling key features

of the illness. Unfortunately, many in the

eating disorder field seem to know little of

this work or the implication it holds for

treatment philosophy. Instead, the knowl-

edge void has been taken up recently by a

host of misguided notions about etiology,

blatantly dismissive attitudes toward psy-

chological concepts, and ill-conceived

beliefs about therapy priorities. This article

is a clinical perspective on these issues.VVC 2012 by Wiley Periodicals, Inc.

Keywords: anorexia nervosa; treatment;

training

(Int J Eat Disord 2012; 45:155–178)

Introductory Comments

This article has a long history. It dates back to a Julymorning in 1974, when the lead author walkedthrough the doors of the UCLA NeuropsychiatricHospital and was welcomed almost immediately bya 13-year old patient whose ghoulish appearancewas so horrifying I could do little more than stareincredulously. My greeter was unfazed by the reac-tion—as though she had seen it so many times it nolonger touched her own sensibilities; if it ever did.After the introductions, she said—a bit over-proudlyI thought—that she had anorexia nervosa (AN) andweighed 52 pounds. I distinctly remember thinking Ihad seen something like this before; then I remem-

bered. It was 1960. I was 11 years old and had cometo my grandmother’s hospital bed to say goodbye forthe very last time; she died the following day fromcolon cancer. When I asked my mother what madeher so thin, she said it was the cancer; on the day mygrandmother died she weighed only 69 pounds. Iremember thinking this had to be a mistake—agrown person couldn’t be that thin.

As for my new acquaintance, she was only a frac-tion as old as my grandmother, but ‘‘thin’’ didn’teven come close to describing the skeleton thatstood before me. Her skin had all but melted intothe bones beneath and her head—it appeared soshrunken that her eyes dangled perilously from theirorbits, seemingly held in place only by a singleremaining sliver of muscle; I was certain they weregoing to drop at any moment. Like the memory ofmy grandmother’s appearance on her final day, myfirst encounter with AN remains equally well pre-served; you never forget images like these. I alsorecall the brief exchange we had. She asked if I knewwhat AN was. I said I didn’t, so she volunteered toteach me. She described the illness as a way of con-trolling things. When I asked how, she said, ‘‘by los-ing weight,’’ as if the answer was obvious. But whenI asked, ‘‘What exactly is it you’re trying to controland why did you lose so much weight?’’ she juststared blankly. After a brief pause she went on to saythat everyone—hospital staff, friends, teachers, andfamily—is worrying about her—her father especially(who I soon learned suffered from manic depres-sion)—but they’re exaggerating the danger, sheadded; then she abruptly walked away.

Dr. Strober receives support from the Franklin Mint Chair in Eat-

ing Disorders. Both authors receive support from the National

Institute of Mental Health. Dr. Strober has received support from

SmithKline Beecham and Abbott Laboratories. The authors thank

Dr. Cynthia Pikus for editorial comments.

*Correspondence to: Michael Strober, PhD, UCLA Semel Institute,

760 Westwood Plaza, Los Angeles, CA 90024.

E-mail: [email protected]

Accepted 10 January 2012

1 Department of Psychiatry and Biobehavioral Sciences and

Semel Institute for Neuroscience, David Geffen School of Medicine

at UCLA, Los Angeles, California2 Stewart and Lynda Resnick Neuropsychiatric Hospital at UCLA,

Los Angeles, California3 Eating Recovery Center of Denver, Denver, Colorado4 Department of Psychiatry, University of Oklahoma College of

Medicine, Oklahoma City, Oklahoma

Published online 28 January 2012 in Wiley Online Library

(wileyonlinelibrary.com). DOI: 10.1002/eat.22005

VVC 2012 Wiley Periodicals, Inc.

International Journal of Eating Disorders 45:2 155–178 2012 155

EXTENDED CLINICAL FORUM

This, I thought, was extraordinary—and intimi-dating. I had no idea what to make of it, or how togo about helping someone like this.

I first became interested in the nature and causesof mental illness in high school. Now, standingright in front of me was something tangible; tangi-ble, but too complex for an inexperienced clinicianto comprehend. Ironically, 6 months before settingout to write this article I received an email from mygreeter; I had neither seen nor heard from her sinceshe discharged from UCLA more than 36 years ago.She said she didn’t know why, but that she wantedeveryone to know (several members of the originaltreatment team remain) that at 49 years of age shewas long recovered, had two healthy children, andenjoyed working as a nurse in a community hospi-tal near her home; she included a picture. Thenshortly thereafter, as if I needed a reminder aboutAN’s less merciful side, another message came; thisone from the husband of kindly 49-year-old patientwhose recent treatment at UCLA was her first.Unfortunately, traveling to California seeking treat-ment 34 years after her illness began, it was toolate. He thanked us for trying, but said his wiferecently told him and their two sons that she hadgrown weary from the struggle; a week ago shewent to sleep for the last time, the three of them byher side.

The purpose of science is to advance knowledgeabout phenomena not well understood. In theprocess, certain ideas gain prominence, skepticalattitudes emerge, and resulting conflicts of opinionare debated. That theoretical ideas diverge is to beexpected, especially in the clinical sciences; in psy-chiatry, it almost seems a given. Even when knowl-edge of illness and treatment appear to approachthe problem adequately, arguments in psychiatrycan linger without any single resolution enjoyinggeneral acceptance. For some it’s a frustrating stateof affairs; others see it as incentive for extendingmore rigorous analyses to novel ideas. Then again,in a far different way, the conflict of ideas some-times justifies in the minds of still others that allbeliefs are created equal. But their argument ofequivalence arises only because the clinicalphenomena we study and treat are not easilygraspable.

This article focuses on controversies that haverecently emerged in regard to AN. As the subtitlestitles make clear, it is a long one, and the questionswe take up are touchy. On the face of it, it reflects arenewed interest in AN that many in the eating dis-order community take as reason for optimism thatprogress is at hand. Progress is indeed being made,but serious concerns overshadow what should be

an opportune time for new learning. They arebroadly related to the different sources of informa-tion that clinician and academician access toincrease their fund of knowledge, and how eachgeneralizes empirical and experiential knowledgeto the clinical setting.

It is an exciting time for eating disorders researchbecause the opportunities for advancing knowledgeare now rich. But ironically, there is also a knowl-edge chasm that is wide. Simply stated, in spite of awealth of empirical and experiential knowledgethat brings attention to the complexities embeddedin AN, a counter-intuitive view now prevails in theminds of many, one that portrays the illness and itstreatment in ways that do not suffice as truth. Thetwo main sources of controversy center on (1) theexplanatory role of causal genes and abnormalbiology, and (2) whether family-based treatmentfor weight correction should have primacy in man-aging younger patients. That these are importanttopics for empirical investigation with implicationswe need to take seriously is not in question. Ourconcern is how quickly this research came to legiti-mize, through some unknown parity of reasoning,faulty propositions about causality and mentalfunction in AN, and attitudes that many insist mustcommand its treatment. This article offers an anal-ysis of these beliefs—not only in relationship toother areas of scientific study, but also in the con-text of our clinical work—and show why they lackplausibility and thus fail to satisfy any acceptablecriterion of a priori knowledge. We will not be argu-ing that a case can be made at this time for a spe-cific theory about AN, only that certain increasinglypopular ideas present an unbalanced picture of theillness, lack believability, and risk having undesir-able consequences should therapists predicateinterventions on their acceptance as irrefutabletruths. The key point we will present is that what-ever the origins of AN, the processes involved arequite intricate. We will stress this premise repeat-edly, because we think the repetitions are neces-sary. Many of the points we will be making applyequally well to bulimia nervosa, but since we knewthe article would be lengthy we elected to focus onAN alone.

In essence, the article asks which notions aboutAN—concerning vulnerability and psychopathol-ogy on the one hand, and subjectivity and therapyon the other—are rational to believe. In framingour answer, we will make reference to new researchfindings—because knowledge that accrues fromscience should inform clinical practice—and theevery day challenges we confront taking care ofpatients—because inferences we draw about these

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156 International Journal of Eating Disorders 45:2 155–178 2012

encounters can refine theoretical knowledge ofhow the human psyche forms and adapts to its sur-round.

That conflicts of opinion exist about causal fac-tors in AN and what therapy attitude is the mostjustified is an interesting point, but unsurprisinggiven how clinicians form beliefs about psychopa-thology and treatment; which leads to touchy ques-tions: What brings well-intentioned researchers ortherapists to disparage certain concepts withoutfirst considering whether it’s rational to do so?We’ve witnessed it in the past 2 years—an insist-ence that they be retracted, as if the only conceiva-ble reason for invoking them in the first place isself-interest or bias. And why do well-intentionedtherapists wind up doing bad things? The reasonour subtitles are apt is because the conflicts ofopinion that have risen to the center of debate inour field actually lost validity some time ago—afact many in our field seem unaware of.

Well conceived scientific investigation createsknowledge and theory that have plausibility. Onewould hope, then, that unity of opinion should fol-low as new understanding is disseminated to prac-titioners, patients, and the public; unfortunately,it’s not so easy. Making the case for credible knowl-edge in psychiatry when different views of abnor-mality vie for primacy has long been challengingand it will remain so if rival theories are defendedtoo narrowly, if research focuses on one element ofknowledge to the neglect of others, and if new find-ings quickly generalize without waiting for corrob-oration from other sources. This is precisely whypatience and skepticism are indispensable virtueswhen it comes to making sense of human actionsthat spin a story of puzzling complexity; whenthere is no single, sufficiently adequate testimonyto their nature, when evidence is often overriddenby counter-evidence, and when presumed truthsare, in fact, assumptions devoid of evidential sup-port. Applied to AN, these are hardly subtle distinc-tions considering that the narrowest of conceptionsabout its nature and treatment have taken hold inthe opinion of many.

How much about AN can be spelled out by theeffects of genes and biology and whether or notthere is sufficient justification at this time for fam-ily-based management of weight restoration toreplace other treatment models in the care ofpatients (in particular children and teens, as well asyoung adults still residing at home), are intriguingquestions. As we already stated, each notion hasbeen supporting ground for real progress. Clearly, asignificant body of research shows that inheritedvulnerability is an individually necessary compo-

nent of AN, justifying the idea that eating disordersshould be seen in the same light as other biologi-cally based mental illnesses (BBMI; see Klumpet al.1 for background). Likewise, the well-executedstudy by Lock et al.,2 showing a greater benefit offamily-based therapy (FBT) compared with individ-ual therapy in promoting short-term remission inyouth with AN, represents a meaningful contribu-tion to clinical care. Unfortunately, the implicationsof these paradigms were quickly overstated andthey are now being invoked by many as single, de-fensible solutions to the thicket of clinical chal-lenges that AN presents. So questions arise: Do theBBMI and FBT paradigms, at least in the way theyare being justified, offer coherent and substantiveframeworks for approaching the illness? And canthe divisive controversies that have emerged overtheir meaning and treatment implications be sensi-bly resolved? We believe they can.

But it will require adopting an overarchingnotion about human motivation that is inarguablyfactual. Simply stated, that to understand why inthe long arc of human development some peoplethrive while others remain beholden to oddmotives and self-defeating acts requires thesubtlest appreciation of how complex processesshape behavior and self-concept; the complexity ofhuman life, including its deviancies, is fact. So doesit not stand to reason that broadly conceivedapproaches to behavior change should also occupya prominent place in our attitudes about treatmentwhen it comes to an illness that is emblematic ofhow challenging psychiatric treatment can be?

The need for openness to new knowledge hasanother important subtext: that some of the morenotable successes in psychiatric therapeutics overthe last half-century arose from a serendipity thatturned conventional notions about biology upsidedown. Even empirically validated psychologicaltherapies have been ‘‘hijacked’’ unexpectedly byprinciples of their own, corresponding little to orig-inal ideas about mechanisms and mediators ofchange (best illustrated by early studies of cognitivebehavioral therapy for depression). This doesn’tmean theory should be set aside when discussingtreatment models for AN, as some have argued; tothe contrary. As knowledge of human developmentstrengthens, shining a brighter light on how normaland abnormal behavior evolves through environ-mental regulations of gene expression and a myriadof other complex processes, we have more to takeaccount of. This is why it isn’t closure around sim-ple models that’s needed, but rather efforts thatseek connections between once separate lines ofinquiry. So the good thing is that eating disorders

COMPLEX IDEAS IN ANOREXIA NERVOSA


have finally entered the research mainstream; thenot so good thing is that many in the field havebecome entrenched in single-sided notions, over-looking the value of combining insights from differ-ent theoretical and clinical traditions.

The Illusion of Consensus

It isn’t that consensus among us is completely lack-ing; it’s that it’s illusive. Witness any discussion ofAN and points of agreement are many; or so itseems. Regarding psychopathology, we agree thatits symptoms quickly assume a will of their ownand that in its more severe form the consequencesare grave. We also appreciate that the illness has astubbornness so persuasive it brings patients to dothings different from what we plan for them.Parents describe it best: a transformation of theirchild’s manner seemingly out of nowhere, as mysti-fying as it is frightening, often leaving them ex-hausted, in despair, and resentful. AN can not beexplained simply, nor is the remedy predictable,because so many of its features—the suddenness ofits onset, the rapidly peaking intensity, its ego-syn-tonic character—are inaccessible to single-focusedideas.

Also uncontroversial is that heritable factors op-erate at an important level in etiology. It’s when dis-cussion turns to equally strong evidence fromresearch outside of eating disorders that environ-mental factors also play a role in pathologicalbehavior, sometimes enhancing, sometimes miti-gating, the vulnerabilities conferred by genes thatconsensus frays. Why acrimony ensues as soon asthis notion is introduced is an intriguing question,especially when evidence of gene-by-environmentinteraction in psychological development is incon-trovertible, and given that the evidence is strongestfor phenotypes having a plausible clinical parallelto AN: stress sensitivity, cognitive bias towardthreat, neuroticism, anxiety—even activity-basedanorexia.3,4 To frame the irony differently, here weare bickering about whether or not rearing influen-ces should be included in causal and treatmentparadigms, at the same time that neuroscience-based models of psychiatric disorder elegantlyshow why inheritance shouldn’t receive singularattention any more than early attachment deficitsor family discord should. Simply put, the more welearn about molecular codes that play a role in vul-nerability, the better is our appreciation that theorigins of abnormal behavior travel a far distancefrom inherited variations of DNA.

Clinically, we easily agree that AN is an intimidat-ing challenge and that therapists who take it onshould have the highest level of skill developmentto help patients battle its emotional sway. But thisis hardly the prevailing ideology in our professionaldialogue. Instead, many in the field are attemptingto reduce complex challenges to rudimentary ideaswhich then quickly take on such broad significancethat a treatment model is born impromptu—someeven insisting it should be adopted as our treat-ment of choice. Why? If complexity is bluntlyetched not only in the psychopathology of AN butalso in the challenges it creates, shouldn’t this verysame notion be a constant thread in the ideas weintroduce during treatment? And if narrow ideassufficed, why does the treatment of AN often veeroff course and prove disappointing? As an example,consider the notion that eating and restoringweight to normal weight while preventing compen-satory behaviors models extinction learning; in themost rudimentary sense this is true, but to thinkthis rises to the level of an explanatory paradigm isshort-sighted.

So we are not saying that opinions about ANshouldn’t vary. It’s when the intensity with whichthey are defended rests on assumptions too narrowto represent a powerful conceptual principle thatknowledge suffers, along with patient care. If clearthinking is what we want in our professional andpublic discourse—it’s certainly what our patientsand families deserve—then entrenched viewpointsthat ignore the many levels of analysis needed forexplaining an illness layered in complexity must beset aside. And there is another point. Since errors inmanaging AN are sometimes set in motion beforetreatment actually begins (an assertion less incon-gruous than it sounds), modifying attitudesfounded on sweeping generalizations may help toavoid these blunders from occurring in the firstplace. This article is, in effect, a dialectic thatunderscores why our field is wracked by confusion,mistrust, and divisiveness when it need not be.

The Impetus for This ClinicalPerspective

It arose from a heated conversation that took placeover dinner at a recent national meeting of eatingdisorder professionals. Present were the authors,several practitioners, and the founding member ofa parent advocacy group with ties to the Academyfor Eating Disorders (AED). The conversation even-tually fixed on a question that was of particularconcern to this parent, ironically enough harkening

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back to the lament of 19th century pioneers—Wil-liam Gull and Ernest-Charles Lasegue—that bothpractitioner and family often went too far inindulging the patient’s wish to manage eating ontheir own. Listening to this parent’s account of herdaughter’s treatment by a ‘‘specialist’’ she initiallyassumed trustworthy, it was clear how the treat-ment went awry and why her anger was deserved.‘Why do therapists wait too long before realizingtheir patient can not gain weight?’ was the questionshe put to us.

Unfortunately, therapist complacency inaddressing malnutrition remains, giving credenceto this parent’s belief that clear thinking about howto approach AN’s intransigence is still lacking. So asthe conversation came to a close our dinner com-panion suggested, with further encouragementfrom others at the table, that the authors—friendsand colleagues for nearly four decades—write acommentary on this issue and that it be accompa-nied by a proposal: that outpatient managementfollow definable benchmarks for determining whena therapist should stop doing what has not beenhelpful and replace it with something that mightbe; specifically, a level of care offering greater sup-port for weight gain and reduction of psychopa-thology. We acknowledged this was a worthy sug-gestion because as far as we know, little has beenwritten about specific, treatment-focused bench-marks in AN.

But as we began to write, we felt that a discussionfocused on benchmarks alone would not sufficebecause while they can be plausibly described,implementing them at a point in treatment whensymptoms are worsening or progress has stalled isa unique challenge; and as our key point argues,not many challenges in AN can be managed with-out convincing insights and strong clinical skills.We wanted our younger colleagues to understandthis; it became an important part of the reason weare writing this article.

Our Backgrounds

Obviously, we wouldn’t have written it if we didn’tconsider the question posed to us at dinner to bemeaningful and answerable. Still, a perspective ispersonal, so we thought a brief summary of ourbackgrounds would be important.

Our careers have been long, nearing 40 yearsnow. We were fortunate that our doctoral trainingin clinical psychology crossed several theoreticaldomains—social learning theory, cognitive and de-

velopmental psychology and psychopathology,principles of behavioral and psychodynamictheory, and brain–behavior relationships—and thatafter graduating we devoted much time to connect-ing research with patient-based experience; also,bio-phobic we’re not. The lead author’s mastersand dissertation research investigated sleep elec-trophysiology in newborns at risk for severe mentaldisorder, and both of us have collaborated withauthors of the AED Position Paper on Eating Disor-ders as Biologically Based Mental Illness1 in thePrice Foundation and National Institute of MentalHealth funded studies of genetic factors in eatingdisorders.5 In addition, MS was a founding Fellowof the American Academy of Clinical Psychophar-macology and is a longstanding member of the So-ciety of Biological Psychiatry, and CJ is a PrincipalInvestigator in an NIMH-funded multicenter studycomparing family behavioral treatment to systemicfamily therapy in adolescents with AN. Similarly,our academic and postdoctoral experiences werefurther strengthened by supervised experience ininterdisciplinary clinical settings from multipletherapeutic viewpoints. Finally, we have spent ourentire career working in combined service andresearch environments that provide care to themost seriously ill children and adults (and fami-lies), as well as to those less impaired. Between us,the number of patients and families we havetreated privately, treatments that we have super-vised directly in the centers we direct, and consul-tations we have conducted with juvenile and adultpatients (and families), is on the order of 12,000.

The summary will strike some as overly self-regarding, but seeing how ideas on etiology andtreatment are now as easily accepted as they aredismissed, there is no stand-in for theoretical diver-sity and depth of clinical experience when takingon matters about which so many in the Academydisagree. Thus, we feel well prepared to address thedisciplinary blinders and doctrinaire attitudes nowhindering the rapprochement of ideas our fieldurgently needs.

Our Framework

Modeling treatment on advances in our under-standing of pathological processes in AN has longproven difficult; this is why controversy can be agood thing. But the sort of debate we need is notpossible if arguments depend on fixed beliefs thatare at odds with the very research cited in theirdefense, and if new treatment ideas are greeted ei-ther with gushing enthusiasm or disdain, rather



than caution and humility. To be clear, we are fo-cusing on the BBMI and FBT paradigms notbecause we disagree with them—there is good em-pirical support for the original concepts—butbecause a larger body of research shows that theinterpretation of each needs softening, and becausemany have come to see the BBMI paradigm as jus-tifying a therapy philosophy we believe is not onlyunwarranted, but contrary to good clinical care.What we mean here is that an increasingly geno-centric view of AN is being overinterpreted to meanthat weight correction is an absolute biological pre-requisite for any treatment that is more ‘‘psycho-logical’’ in character. At first blush, this seems areasonable notion; but it needs to be nuanced.Obviously, if low body weight continues so will psy-chopathology and no therapy-derived insight iscompelling enough to stand on its own in reversingthe disease; behavior change is, of course, crucialto anyone’s definition of recovery; without weightcorrection the prospect for sustained recovery isnil. Just the same, there is no evidence—empiricalor clinical—showing that normal weight is a neces-sary prerequisite for initiating meaningful psycho-logical dialogue, or that psychotherapeutic dia-logue can not be facilitative of weight change. It’s abit like mixing apples and turnips. A patient 50pounds below a BMI of 19—confused, disorgan-ized, unable to retain short-term information, andemotionally erratic—is unquestionably ill-suitedfor psychotherapy of any sort. But this patient isconsiderably different from one who is 30 poundsunderweight, ingesting food, and though com-pelled by similar fears is nevertheless committed toan examination of the conflict that has taken holdof his or her mind. Simply stated, normalization ofweight is not the absolutely essential starting pointfor using thought, reason, and insight as founda-tions for change.

There is another paradox of sorts that needsmention here. A fundamental principle of FBTholds that parents must separate the symptoms ofAN from the person who bears them. It’s an emi-nently sensible concept because the separation, ifsuccessful, can buffer against additional personaland family strain; especially for the patient, whosealready harsh self-disparagement is injury enough.Just the same, there are histories in which parentalattitudes, environmental strain, and psychopathol-ogy are not so easily segregated and the interven-tional efforts needed are more involved.

So our concerns are (1), the absence of supportfor many of the clinical assumptions the BBMI andFBT paradigms have given rise to, and (2), a philo-sophical attitude about treatment that is becoming

far too circumscribed, moving in a direction thatsuggests—we now hear it stated often—that onlytechniques supported by controlled, empiricalstudy deserve consideration. Again, to eliminateany misunderstanding, we are not contrariansassailing empirical research on biology or treat-ment techniques. Biology is an essential field of in-quiry and the study of FBT by Lock et al. is a signaldevelopment with important implications. Whatwe worry about is that many therapists have reifiedthe effects of genes and took the results reported byLock et al. to mean that FBT is the only justifiedtreatment for young people with AN, overlookingthe fact that 50% of the participants who received itwere unremitted. In our view, the present disunityin our field underscores three worrisome trends:(1) that many therapists apparently see no place forthe sort of clinical wisdom that can never bemanualized; (2) that the emphasis on empiricallyvalidated interventions is drawing attention awayfrom more broad-based training experiences; and(3) that therapists who will one day encounter veryill patients are not being prepared adequately fortaking on the many complex predicaments theywill face. In short, although it is without questionthat FBT will suffice as a first-line intervention forsome young patients with AN (most likely thosewhose vulnerability load is less extreme), to insist itis the only treatment modality that deserves con-sideration doesn’t translate well for clinicians whohave seen AN’s many faces over many years.

So the dialect underscores the need for attitudesabout the BBMI and FBT paradigms to move in thedirection of perspective taking: an appreciation oftheir value, but with finer distinctions that take intoaccount knowledge gained from long-term clinicalexperience and translational research showingwhy a more inclusive vision of its complexity isimperative.

In one sense, that we have come to this criticaljuncture isn’t unexpected. In a field where softideas have long taken precedence, paradigms sup-ported by empirically verified observations will nat-urally demand strong attention, as they should. Butas we said earlier, there is a caveat: that belief aboutcomplex clinical issues is useful only if it portraysknowledge accurately and comprehensively. On thesurface, the proposition is straightforward; in real-ity, it’s anything but; because debate over what weshould or should not believe inevitably takes placein an interpersonal context of one person (orgroup) trying to convince another that the ideathey have invested time and effort in is a fallacy.This is where the intellectual analysis of ideasbecomes tricky, because human nature being what

STROBER AND JOHNSON


it is it doesn’t take much to violate the operativenotion that this form of discourse must be emotionneutral. Realistically, the only viable solution to theproblem of close mindedness is to carefully con-sider if the ideas we justify as knowledge are defen-sible regardless of personal ideology, and to resistturning a blind eye to ideas we may be inclined toreject spontaneously and uncritically. As a concreteexample, it would mean that if we held strongly topsychoanalytic principals, we would not reject outof hand evidence of a cognitive mechanism operat-ing in symptom formation. Cutting straight to thepoint, however strong our commitment might beto an ideology it should never cordon us off fromconsidering the possible relevance of other con-cepts about human behavior.

So we unapologetically acknowledge that a pur-pose of this article is to challenge ideas tied to theBBMI and FBT paradigms that many now assumeto be fact; to offer an understanding of why theyhold only a piece of truth about AN—an importantpiece to be sure—but not a whole truth, and to seethat when a less demanding theoretical and clinicalcalculus is applied to causal biology and psychopa-thology that is complex it inevitably faces disap-pointment. Our objective thus brings us to severaltouchy questions: Why do our treatments helpsome but not others? What brings well-intentionedcare givers to do unwise things? And why has therebeen preciously little discussion at recent Academymeetings about the importance of approaching ANwith diverse treatment skills?

The Challenge and Its Complexities

That the questions are timely should be clear toanyone who has attempted to fully understand theillness. AN expresses a more or less lawful historyand clinical presentation, but once it takes hold itsclinical borders shift quickly in directions not easilyanticipated. We do our best to warn patients thatthey are feeling the pull of misguided ideas, butthey are tone deaf to the standard logic applied tohealth. To them, only one wisdom matters: what-ever actions succeed in losing more weight is a sen-sible alliance to strike. Of course the search forinherited genes should continue; because the effortis as important to AN as to any other psychiatric ill-ness. AN is certainly a multilocus condition whoseeventual expression depends on multiple predis-posing traits, chief among which are anxious worryand hypervigilance, reward deficits, compulsive-ness of habits, and an obsessional thought struc-ture. But to assume that everything about it is

encoded in the genome, that a single biological cal-culus will crack open the mystery because environ-mental influences are trivial, that our culture’sembrace of a thin body ideal is the primary nonge-netic trigger that warrants focus in preventionefforts are notions that seriously misjudge all ofwhat the illness embodies.

Another facet of AN particularly unnerving, espe-cially for the less seasoned therapist, is that theclinical acumen therapists need builds slowly butthe fear the illness incites is instantaneous. And it’sa different sort of fear, one that cares little to noth-ing about our background—student, beginner,scholar, or therapy veteran—what we look like, thegentleness of our manner, even the dedication webring to the work is immaterial. AN is maddeningbecause the interpersonal context it creates isimpersonal and insolent, which is why it doesn’ttake long for patients to turn uncooperative and forthings to feel out of our hands. And when it does,the risk for treatment to lurch back and forth inways perceived by patient and family as incoherentor needlessly inflexible—or, maybe too flexible—will be great. This much is certain: when the fearstrikes, challenges will mount quickly and beforelong skeptical loved ones will start questioning ourevery move; this is when we learn never to presumethat treatment approach in AN is straightforward;not because it never is, but because in so manycases it isn’t. The common lesson learned in clinicalwork is that the skill set needed to keep the man-agement of AN on track transcends what is por-trayed in the most rigorously articulated treatmentmanual.

Historical Footnotes

In 1982, Paul Garfinkel and David Garner pub-lished a highly regarded discussion of the multidi-mensional character of AN.6 Johnson and Connorfollowed in 19877 with a similar book exploringbulimia nervosa from a bio-psycho-social perspec-tive. Thus, well over two decades ago there wasawareness that eating disorders would requireanalyses that kept multiple levels of discourse inplay, each having unique value. But history fadesquickly and this bit of seminal discourse now sitson the side lines, paid little more than lip service—acknowledged, but more as an afterthought. So atthe same time that our annual workshops and ple-nary titles are stressing integration and synthesis,resistance to setting aside favored ideas remainsstrong. Again, we are not decrying differences ofopinion—it is a sacred part of scientific and clinicaldebate. But there is no opportunity for sober dia-logue about ideas relevant to issues of causality or



our treatments when arguments are laced with vit-riol and the points argued have been shown byother science to be false or overstated. If the unciviltone of arguments that scrolled across the AED ListServe last year is indication of our field’s readinessfor synthesis and integration, we are in trouble.

On the Importance of Integrative Models of

Etiology and Treatment

Returning to our keynote, complexity is the fore-most principle of human development, as crucialto understanding how healthy behavior evolves asit is to decoding how behavior turns pathological.Because of this truism, paradigms that ignore com-plexity inevitably sacrifice real world applicability,not because their broad outline is incorrect, butbecause they do not go far enough in their explana-tions. In our view, the reason we are in the throes ofrancorous argument about BBMI and FBT isbecause the implications of this complexity arebeing ignored.

It is not an inherent contradiction to argue thatparadigms can be informative at the same timethey are incomplete. BBMI warrants attentionbecause in addition to advancing knowledge ofpossible causal mechanisms it has had far rangingimplications for health care policy in the UnitedStates—the inclusion of eating disorders among thelist of insurance parity diagnoses being a case inpoint. Similarly, though only a single controlledstudy, the report on FBT by Lock et al. was well exe-cuted and its main result is straightforward; but thestudy’s safety parameters required participants tobe medically stable for outpatient treatment and tobe 75% or greater of ideal body weight. These arenot criticisms, merely clarifications meant to drawa contrast between what is, and what is not, indi-cated by a single study and why good sense mustguide its interpretation; clearly, good sense in itsinterpretation has, thus far, been missing.

This is how scientific advances often come withunfortunate trade-offs, and why a measured inter-pretation of their meaning is needed to lower therisk of pronouncements the research neverintended. We know the authors of the AED PositionPaper on BBMI and are confident they do not holdto some, or most, of the ideas the paradigm imme-diately gave rise to. As for FBT, the clinical insightsgained by the research were almost immediatelymuddied by inexcusably sharp-tongued criticismand undeserved pronouncements about treatmentphilosophy. So let’s take a breath, step back, andremember that both praise and criticism must becautiously and smartly rendered. Genes and biol-

ogy matter greatly in vulnerability to AN, but envi-ronmental influences can matter too. As for FBT, itis neither the Holy Grail of AN treatment nor some-thing villainous.

Revisiting Predisposing Biology

By their very nature, all psychiatric disorders areextremes of human nature. However, the phenome-nology of AN stands apart from other mental disor-ders, not simply its strangeness, but more the easewith which patients shrug off its seriousness. Mor-ton smartly drew attention to this more than threecenturies ago8 in his treatise on tuberculosis, whenhe attributed an odd indifference to malnutritionamong certain of his wasted patients not to apathogen, but rather to ‘‘passions of the mind.’’Modern epidemiological research confirms, withcold facts, the implications: should AN progress inseverity the risk of premature death from starvationor suicide rises dramatically. To be in the presenceof someone so withered yet so driven, who insiststheir wasted appearance—if they acknowledge it atall—is more illusion than omen of approachingdeath, triggers a suffocating fear. Then, to watchhelplessly as this unforgiving madness stretchesstarvation to a degree of physical endurance thatseems inconceivable, even taking precedence overthe frantic pleas of loved ones to try one morebite—it’s a grimly visceral tragedy not justlydescribed; to think biology is not involved in someway is hard to fathom.

But the more common menace of AN is notdeath; it is the risk of a long, persisting illness, usu-ally with symptoms of lesser intensity but that stillimpact quality of life. Why the illness is fatal tosome but not others, why some recover fully whileothers struggle a lifetime, are critically importantquestions for which there are no immediateanswers. But one generalization stands up to rea-son: that when vulnerability is at the tail of the bell-shaped curve the risks of symptom persistence,and possibly death, are greater. Even before evi-dence of genetic influence in eating disorders cameto light there were other commonsense reasons topresume biology was at play; it is hard to imagineotherwise with a madness that comes on quicklywithout any truly rational explanation. But now,with decades of evidence showing that inheritedinfluences are present in most, if not all, major psy-chiatric illness, the evidence pertaining to AN isincontrovertible: (a) eating disorders are transmit-ted in families; (b) concordance is greater inidentical compared to nonidentical twin pairs; (c)characteristics associated with AN (regimentedbehavior and perfectionistic attitudes, aversion to

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risk and low reward seeking, anxious worry and ele-vated vigilance) appear to be tags of vulnerabilityas they are present before signs of weight loss andare also reflected in its core diagnostic symptoms;(d) anxiety states are not limited to patients only,but also occur more frequently in relatives of per-sons with AN compared to relatives of non-AN con-trols; (e) as common as body image concerns andweight dissatisfaction are in the general femalepopulation, AN is, by comparison, rare; (f) altera-tions in brain physiology mediating reward seekingand anxiety have been reported, some persistingafter normal weight has been restored. Thisconcisely summarizes the strength of the BBMIparadigm (supporting references can be foundelsewhere.9–11

It’s when it comes to the question of what spe-cific elements of AN and its outcome are encodedin the genome and where other sources intervenethat we are at a loss. Indeed, if there is a single,overarching seminal idea emerging from recentneuroscience research it is that psychiatric illnessreveals processes more elusive than the effects ofvulnerability genes alone. So we turn next to thestriking contrast between this body of new knowl-edge and what many in the Academy deem to bejustified beliefs. Some of the statements listedbelow were made at the 2010 and 2011 Academymeetings, others we picked up from the AED ListServe. They are paraphrased—some are embel-lished—but only to make the point that it hasbecome easy in our field for misunderstanding,misattribution, and plain lack of knowledge tostand in for clinical wisdom.

1. It is now proven that AN is a brain disease;this explains why patients behave strangelyand say illogical things—their actions, per-ceptions, and utterances are irrationalbecause their brain is.

2. AN is a genetic disorder; this is why you haveit forever and why psychosocial factors areless relevant in causation or in determiningoutcome; features once thought to be part ofits psychological realm are really effects of itsgenetic underpinnings, having no unique sig-nificance of their own.

3. The BBMI model doesn’t deserve the strongattention it is receiving because the methodsnow used to study brain biology are prone toover-interpretation.

4. Because AN is a brain-based illness, familyturmoil should be viewed only as a byproductof the frustration the illness sows; weightcorrection needs to take priority for thesetensions to resolve; things said by patients

about their relationships, family ones included,should not to be taken too seriously.

5. Psychotherapy cannot, and should not, takeplace until the brain is mended by restoringweight to normal.

6. Family-based behavioral therapy is the onlyacceptable method for treating young patients.

7. The FBT approach to weight restoration iscrude and atheoretical, unjustly divertingattention away from critical psychologicalneeds of the patient; it disparages psychother-apy.

What is instructive about this list of duelingassertions, and worrying, is that it didn’t take longfor biology to be turned on its head in ways theKlump et al.1 Position Paper never intended, andfor treatment research focused on FBT to be wildlygeneralized. It is little wonder that so manypatients and families tell us they feel at a loss, notknowing who to turn to for sound, factual advice.

Expanding the Vistas of Biology, Development,

and Environment

We shouldn’t forget that opinions about causalityand treatment of mental illness from the early 20thcentury forward were as wide ranging and conten-tiously debated as were attitudes about AN. What’sdifferent today is that ideologies take hold rapidlybecause science technology and the conceptualprinciples on which it rests are more sophisticated,and new research findings now appear almost daily.The wrinkle is that while the roles of inheritanceand biology in AN are now well accepted, the trans-lational implications of research findings in alliedfields have been slow to enter our dialogue. As wesaid earlier, the good thing is that research on eat-ing disorders has entered the biomedical and psy-chological mainstream; the not so good thing isthat many Academy members are woefully unfami-liar with this new science. This, we believe, is whythe BBMI and FBT paradigms have needlesslybecome crucibles for dissention and acrimony andwhy it is important that our field become better ac-quainted with the bullet points that follow (inter-ested readers are referred elsewhere for a summaryof primary sources11):

1. Not only are genes and environment corre-lated, the effects of each coevolve and inter-act, which is to say that neither influence isfully deterministic. Regarding the tempera-ment that underlies AN, these correlations



explain why anxious, worry prone, and stub-bornly perfectionistic children not only seekout certain types of social environments, theyalso ‘‘invite’’ them; because genes and thebiology they express make it so. By the sametoken, because genes and environments alsomeet randomly, they can clash. For this rea-son, everyday experiences never guaranteethe predictability that children vulnerable toAN prefer and need, which they mistakenlybelieve they can achieve by imposing strictorder on their daily routines. The ultimate‘‘failure’’ of their innately formed discipline toachieve the unfailingly ordered world theyseek is difficult for people with AN to concedeand it may be one reason they are prone tothe harsh self-judgments of inadequacy, pas-sivity, and mediocrity they bear.

2. Brain circuitry is not fixed, but rather adaptsfunctionally to the environment and thendepends on it for its continuing expression.Moreover, neural circuits have plasticity andthus support different, and at times contrast-ing, motivational drives depending on theenvironment’s emotional tone; this is why cir-cuit activity is a less than reliable biomarkerfor abnormal behavior. The search for generaland specific indicators of AN risk should con-tinue, but none presently exist nor have weyet identified neurobehavioral correlates ofdiscrete treatment responsive or unrespon-sive subgroups.

3. Neurochemical changes brought on by stress(including exposure to adverse rearing envi-ronments) not only strengthen the encodingof memories for negative emotional events,they also reshape brain morphology inregions linked to anxiety, fear learning, andreward seeking. Particularly intriguing in thisregard is recent evidence (see12 for back-ground) that even less extreme variations inhuman care giving can impact the trajectoryof developing brain systems that mediateaffective and motivational characteristics. Forexample, whereas the left and right frontalhemispheres are differentially specialized forprocessing appetitive versus aversive stimuli,respectively (the left frontal region mediatingapproach and appetitive behavior; the rightfrontal region promoting avoidance, fear, andbehavioral inhibition), a greater rightcompared with left frontal activation occurswhen children are reared in adverse environ-ments—a shift that is associated withincreased risk for internalizing behaviors

(some of the very same phenotypes charac-teristic of AN).

4. It is now clear that environmental stressmechanistically increases anxiety pronenessby over-sensitizing fear-generating structuresin the limbic brain (amygdala nuclei) and dis-rupting prefrontal modulation of this region.But the converse is equally powerful: thatrearing in environments characterized by pa-rental warmth can silence genes that other-wise promote anxiety,13 a finding that maypossibly shed at least some light on why posi-tive family relations have been linked to bet-ter short- and long-term outcomes in AN.14,15

In short, the social world plays an impres-sively large role in shaping behavioral out-comes. Referring back to points 2 and 3, thisis why it has been recently argued16 that so-called vulnerability genes might actually sup-port adaptation in a context dependent man-ner: programming fear/avoidance when rear-ing has been adverse so the child can respondwith increased vigilance and avoidance whenlater facing environments that are anxiogenic(i.e., stress-inducing, novel, or generating dis-comfort in any way; also note here that dis-comfort with novelty and diminished motiva-tion by reward are common in AN), but pro-moting appetitive motivation when rearing isfavorable (note again, the link between posi-tive family relationships and more favorableoutcome in AN).

5. A final point concerns a newly describedgenetic mechanism—epigenesis—whoseeffects may underlie at least some of the pat-terns described above. In contrast to inheri-tance of a nucleotide sequence, epigenesisrefers to a heritable, nonstructural modifica-tion of the genome in which gene expressionis set-off by environmental events. A classicillustration13 is the developmental effect onhippocampal–hypothalamic regulation ofstress that results from variation in lickingand grooming of newborn rat pups by moth-ers (a model of maternal care). The effect isrobust, with high grooming mothers produc-ing offspring with less stress reactivity (i.e.,less nervousness). Interestingly, epigeneticstudies have also shown that stress to a parentalters not only their behavior, but that offuture generations—even when these off-spring receive no direct exposure to environ-mental stress themselves.17 Exactly how thiscross-generation transmission of susceptibil-ity occurs isn’t known—behavioral modeling

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of parenting behavior from one generation tothe next, or stress effects on germ cells whichare then transmitted across generations arepossibilities—but whatever the mechanismthe effect supports the provocative idea thatenvironmental programming is operativeeven at the embryonic level. The take homemessage is that continuities between stress,development, and parent behavior begin toform early and the dynamic processesinvolved can suddenly activate feelings ofthreat in offspring when novel environmentsare encountered later in life. But the converseis equally true: when a rearing environmentsignals a low likelihood of stress, fear behavioris less automatic and the potential negativeconsequences of later stress exposure arereduced because HPA and limbic arousal isbetter regulated by learning experiences thatpromote inhibitory brain processes.

The general implication of this body of researchis obvious: that for paradigms of AN to be completerequires their studious appraisal of the manystrands of vulnerability involved in symptom devel-opment and illness progression, including: suscep-tibility genes; the effects exerted by environmentalstress on the expression of inherited traits; andother nongenetic effects in the programming oflong-lasting behavioral patterns. What is significanthere is not only the heuristic value of this science,it is that when translated appropriately it can fur-ther help therapist, patient, and family make bettersense of an illness that seems ungraspable. And forthis very same reason it justifies what should al-ready be a common sense notion: that our thera-pies should not overlook the strains of life thatpotentially maintain or accentuate vulnerability,and that interventions targeting the family, school,or interpersonal environment can have benefit.Indeed, evidence from outside our field (researchon youth with mood disorders) is showing thatmultifocus, family-based therapies for stress-rid-den, emotionally reactive families can buffer sensi-tivities that high risk genes lay down.18

In sum, the reason long-term outcomes in patho-logical behavior are not easily predicted is becausewhile genes influence the outline of our tempera-ment, environmental conditions program andmoderate inherited tendencies through complexfeedback loops that determine how behavioral pat-terns eventually stabilize; simple and linear our de-velopment is not. Inheritance wires biology, biologyexpresses behavior and is also substrate for theexperiences behavior generates, experience then

rewires biology in order that behavioral phenotypesadapt optimally to unique environmental ‘‘demands,’’and from this dizzying cascade of interweavingevents the mind’s consciousness forms.

So after taking account of how genes constrainadjustment, why would we dispute clinical formu-lations that properly reflect other far reachinginfluences that shape the mental subtleties inher-ent to self-concept and motivated acts? Why shouldthis be, when science now shows that whatevergenetic predisposition to psychological illness setsin motion, the effects unfold in a social milieuwhose imprints of learning, experience, and expec-tation also enter into the long, cumulative causalchain from which a host of ideas arise—somerational, others imagined and far-fetched? This iswhy we submit that AN can not be understoodcomprehensively unless the fundamentally impor-tant notion of complexity is given credence; that af-ter biology, the rearing environment—the largersocial context too—can imbue symptoms withdeeply felt, personal undertones that if not takenseriously can significantly short-change our treat-ments.

We now offer three vignettes which makes thepoint. We include them as an integral part of thediscussion because through the lens of our per-spective each is a perfectly good acid test of howwe are doing at reflecting the synthesis that wehold to be crucially important to our daily work.

Clinical Illustrations

S is a 17 year female whose illness has lingeredwithout remission for 3 years; at the commence-ment of this round of treatment her BMI was 12.8.The youngest of three children, S excelled inschool—an independent thinker who stubbornlyresisted outside assistance even when confrontedwith challenges that stymied her; insisted that herday be strictly organized from the time she roseuntil her bedtime and that certain routines wereessential for ‘‘correct’’ behavior; and exhibitednervousness from an early age, especially at thepossibility of making mistakes or not knowing theanswer to a question a teacher might unexpectedlythrow her way. Everyone in the family described Sas unusually disciplined in all aspects of her behav-ior and would unhesitatingly sacrifice personalneeds for the wellbeing of others. S had friends, butshe secretly disdained any peer who, in her eyes,squandered their free time, preferring to fill herown free time with a myriad of ‘‘worthy’’ goals andobjectives she believed would hone skills thatwould prepare her for future pursuits. S vehemently



insisted her self-esteem was strong. But followingthe start of her illness she admitted to a feelingdescribed as ‘‘hollowness,’’ causing her to fear thather once steely resolve was weakening. She chas-tised herself for secretly wishing she could relaxmore and be spontaneous like her friends. As treat-ment progressed, she started to acknowledge,begrudgingly at first, that she first longed for agreater sense of freedom—‘‘to just be like everyoneelse’’—around age 11, and that her self esteem was,in truth, always shaky. It was at roughly this sametime in her life that her father, who described him-self as painfully shy and nervous, was suddenly laidoff due to the economic downturn and though thefamily was well set financially, he grew withdrawnand sullen. Witnessing this, S felt torn between car-ing for him and seeking greater personal comfortand support from friends and other family. Strug-gling to reconcile the conflicting urges, she reignedherself in more, refocused on school, and gave her-self unselfishly to family needs; it was not the firsttime she felt so inclined. When she was 8 an oldersibling took seriously ill, a family-wide strain thatlingers. Looking back, her father volunteered thatthe stress of this illness was probably aggravated byhis inherent nervousness, which he was sureimpacted S more than anyone else. Adding to thestory, S’s older sibling described both her parentsas worriers, but that mother covered it better byperiods of excessive drinking, which S admitted shehad witnessed but never felt comfortable talkingabout. S described her parents’ as being prone toworry over even minor matters and assuming theworst of all possible outcomes when challenged inany way. Two weeks following her hospital admis-sion she spontaneously expressed an opinion thather illness served many purposes: suppressinghunger made her feel her character was strong; eat-ing as little as possible enhanced her discipline,which, she asserted, was crucial to aiding her fam-ily to cope with her sibling’s illness; and that losingweight was not only key to excelling in school—ir-refutable proof of self-restraint and single-minded-ness—it also pulled her attention away from worryand anger over her mother’s drinking and herfather’s passivity. In a family session roughly threeweeks post-admission, the therapist unexpectedlypushed hard for each family member to discuss, indetail, the nature and content of every one of theirstrains; to describe not only the specific points ofconflict within the family’s shared experience thatincited their emotions, but also what issues intensi-fied their worry the most. S appeared instantane-ously uncomfortable. This was noticed by thetherapist, who asked that S not interrupt the flow of

discussion but rather sit quietly, observe, takenotice of anything that stood out, and feel whateverdiscomfort she was having; but first, S was askedwhy she blanched. She said she was afraid that herparents would not welcome this line of question,would grow uncomfortable, and that later at homethe adverse effects of being challenged in this waywould spill out and that she would feel compelledto pick up the pieces by calling her motherthroughout the next day to see how she was man-aging. The therapist’s response was, ‘‘Then let thishappen.’’ The following day, S spoke of the session.She described the unease it generated as she lis-tened to her parents’ revelations, and the need shealso felt to keep her unease in check. Nevertheless,she and her family appreciated the importance ofwhat they were asked to jointly experience. Whatunfolded in subsequent sessions was further dis-cussion of the role discipline had long played inher development, her instinctive unease wheneveremotion—of any sort—was triggered by social oracademic challenge or excitement, the alarm trig-gered by seeing her family in distress, and the con-viction that food avoidance was not only a measureof the discipline needed to effectively reign herselfin so should could offer an anchor of support toher parents, but also an effective distraction froman array of personal and family related concerns. Sand her family are working well together, engagedin treatment with openness and commitment. Salso states she is more accepting of the need for herfamily to play a supervisory role in her eating andweight gain now that they are speaking more hon-estly about things that had been buried for yearsand managing their emotional life more effectively.Her weight gain is still triggering, but the wisdomshe is expressing in her individual and group ther-apy is genuine.

L is a 14-year-old girl with an 8-month history ofillness. Very petite, people think she is 11 years old;she finds this comforting and is equally unfazed byher BMI of 11.2, hoping she can lose 10 additionalpounds. L is unusually frank when discussing this,attributing her wish to be small to constant self-doubt, anxiety, and resentment at having to growolder when, in her view, her living skills are stillpoor. She has been compliant with meals, but shefrets daily about not being prepared for what othersnaturally expect of a teenager; she would muchprefer living with her parents forever. Her parentsstate these characteristics have shadowed L’s devel-opment from an early age. They are supportive andloving people and came to treatment eager toexplore anything and everything the treatmentteam thought might help them, and their daughter.

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Two weeks following the start of treatment L con-fided to her therapist that there was something inher history that her parents were not acknowledg-ing: her father’s heavy night time drinking, which,for several years, she witnessed with extreme fear.When she was 12, L divulged to her mother whatshe had seen, and that she was constantly afraidbecause her father was obviously ignoring the seri-ousness of this problem; mother assured L every-thing was okay. L told her therapist that as she waslosing weight she caught herself wondering if itmight compel her father to take better care of hisown health. Shortly after revealing this in her indi-vidual therapy she discussed it openly in a familysession. Choosing her words carefully, she said sheknew her body image was its own problem, tied insome way to her anxieties, but there was hypocrisyin her father worrying so much about her appear-ance while ignoring his own health. Father wasgenuinely moved by L’s directness, especially asneither he nor her mother had ever seen thisbefore. He admitted he had ignored the impact ofhis behavior on his family, and L’s mother acknowl-edged, as well, that she had been reluctant to con-front her husband. L also asked her father whetherher weight gain would cause him to see her as a‘‘stronger’’ person and, if so, would this encouragehim to start drinking again? His assurance that itwould not happen—that he would seek treatmentand stay with it—was welcomed by L. Although herweight concerns did not sharply lessen, she saidher father’s response to her emotions helped easewhat had been a powerful anxiety. As a result shefelt more at ease taking meals with them.

M is 29 years old, haunted by an 18-year historyof uninterrupted AN. Her drive to excel surfacedearly and it remains unrelenting, usually leavingher exhausted and unfulfilled; M says she knows itssource is innate. She also remembers being a ‘‘highstrung’’ child, a trait she shares with both parents;anxiety and alcohol abuse are prevalent acrossthree generations of relatives on both sides. Whensigns of puberty emerged at age 11, she remem-bered recoiling, apprehensive that adolescencewould be a distraction, dulling her drive to achieveexcellence in every sphere and reducing her pro-ductivity. So when her weight jumped severalpounds when she 11, she was convinced her disci-pline had indeed collapsed. In less than 3 monthsher weight had dropped to 61 pounds. Speaking ofthis period in her life M remembered feeling star-tled by puberty because it was unnervingly sudden;so were the changes emerging in her school friends,and at home: strange new hair styles, risinghem lines, flirting with boys and adopting odd new

curiosities, and her parents’ constant squabblingwithout either one asking for a reprieve. It was,according to M, too much for her rigid character totake in. And the strain didn’t stop here. When Mwasn’t fretting about her homework, her calories,or how to relate to an adolescent world she couldn’tfathom, she worried about each of her parent’swellness. Her father was a reclusive, emotionallylimited man without friends, her mother a diabeticsince childhood who was significantly overweightand who neglected herself; her fear was that eachwould desert her. M recognized that her relation-ship with her parents was ‘‘complicated.’’ Althoughthey were neither emotionally nor physically ex-pressive and rarely did they make attempts toengage with her, she loved them deeply and consid-ered them unique and special people. At the sametime, it disturbed her that it was always a nonrela-tive adult who set in motion each of her three hos-pital admissions when her weight dropped toalarming levels. Reflecting on this part of the his-tory, M said she learned early on to care for herselfand believed that isolation and rigid over-control ofdependency was normative; however, as adoles-cence crossed over into adulthood she grew rest-less, bitter, and torn when pondering why herparents said little about her emaciated appearance.At present, M is nearing completion of a PhD inpublic health administration. She has returned totreatment in despair, questioning if her life has pur-pose and feeling the deep void that isolation fromothers has left in its wake. It has been an achingpain she has covered with fits of anger, convincedthat any desire for intimate connection is, in theend, farcical; that if her own parents neglected theseriousness of her illness since she was 11, howcould any other human being deem her worthy ofcare now? She is compliant with meals, but she dis-dains eating, regarding it not as a quintessentiallyhuman need but rather a ‘‘mortifying’’ admissionof ‘‘passivity,’’ no different than wishing desperatelyfor something that will never be—human connec-tion. She says that the conflict of ideals raging inher head has become tyrannical—between self-denial and disdain for nurturing (and nourishment,which she regards as it symbolic equivalent) on theone hand, and wanting to be free of the misery herillness on the other. ‘‘The more I think back to howlonely I was growing up and how empty our familylife was, the angrier I become; that’s when my ob-session to lose more weight starts screaming soloud I can’t stand it. It’s crazy. What I alwaysadmired about my father was his discipline. Andnow he doesn’t seem to care that this is what’sgoing to kill me.’’ From the time she was young, M,



like many others with AN, felt in her bones, ‘‘If I’mnot everything, I’ll be nothing.’’

These are complex case histories drawn fromcountless others. They have been included not onlybecause they give voice to the struggle that AN of-ten is, but also to provide context for the points wehave been discussing, and those that will follow.The complexities illustrated are not seen in everycase of AN, but when they are we need to thinktwice before offering pronouncements about themeaninglessness of events in the nonbiologicalrealm and insisting that one-sided notions of deter-minism and illness pathways are adequate. Theindelible mark of genes is obvious here, not only inthe temperamental anxiety, rigidity, and lowhedonic drive that mark the development of theseyoung women, but also in the psychological envi-ronment their parents have shaped. But beyondthis, rearing environments and the demands theyplace on children can also be less than optimal forpsychological health and for this reason must betaken into account. It is a factual point, not anaccusation, and to mention the obvious counter-point—family rearing in other cases of AN is com-pletely unremarkable—almost seems superfluous.Clearly, family rearing is not causal in any primarysense, nor is there any evidence to suggest it isrequired for every case AN to emerge; but neither isit irrelevant. Genes are surely the starting point forthese life trajectories, selecting for particular traitsthat, depending on environmental conditions, willreact to the psychological ‘‘demands’’ of the envi-ronment within a predetermined range and with aparticular phenomenology. Whatever the demandis (to lessen the load brought on by a member’s ill-ness; an imagined, or overtly imposed, ‘‘duty’’ tomake up for a misbehaving sibling’s negativeimpact on family life; a perceived—rightly orwrongly—parental short-coming; adjusting to rear-ing low in nurturing or one burdened by instability,harshness, or trauma), the strain and hardship itcan set off should not be relegated in importance.Good science proves the point: symptoms ofpsychological illness do not exist in an impersonalvacuum. The unfortunate fact of development forpeople vulnerable to AN is that it represents atrade-off: inherited genes program for certainforms of adaptation (rigid control, avoidance, andrestraint) when novelty, stress, and emotional dis-cord are encountered, but the benefits patients at-tribute to these patterns are illusory and their futureconsequences can be grim. In short, to hold to thenotion that biology explains most of what is core inAN and FBT is the only treatment that matters willexplain too little to really help patient and family

resolve struggles that are achingly complex. This iswhy a broad vision of treatment is needed and whyour concern with therapeutic nihilism is a real one.

The concern is hardly cheap hyperbole (also seeWaller’s19 thoughtful appraisal of how motivation iscurrently viewed in eating disorder circles). Inrecent consultations we have listened to patientscomplain that anger they had been expressing intheir therapy had been discounted—‘‘a part of thedisorder,’’ said their therapists, who assured it willcease once weight increased. Yes, some outburstsare just that—irrational anger set off by the reason-able efforts of loved ones or therapists to maintaina steady hand. But every upset emotion a distortionwrought by starvation? The patients we are refer-ring to here had upsets completely unrelated to theneed for weight gain. This increasingly popularnotion—that the heated emotion of patients andthe seemingly volitional nature of their actions isdriven by biology alone and will be tempered byrefeeding—deserves a heavy dose of skepticismbecause it is too superficial a notion to permitunderstanding of the reactive processes that, overtime, link biology to its context and shape ideasthat are also central to AN: about motivation, iden-tity, conflict, and maturational fears. The three casehistories make the point that AN is an adaptationthat biology alone can not wrap itself around.

Other Clinical Challenges: WhyExperience, Skill, and Complex IdeasMatter

Thus, the question arises: How well are the currentemphases on biology and manualized treatmentspreparing young therapists for the challenges theywill soon encounter? And given recent attention onoutpatient, family-based therapy and the strong al-legiance pledged by many therapists to the model,let’s also consider the question of whether or notAN’s more extreme morbidity is being taken toolightly. Unfortunately, here, too, the concerns arejustified.

We have recently crossed swords with providersoddly opposed to hospital-based care, not only forpatients at low weight for periods ranging frommonths to years, but also for those whose weightwas on the decline. The argument has been thatinpatient treatment is ‘‘known’’ to be ineffective (infact, there isn’t a stitch of evidence that supportsthis statement), and that if their patient is exposedto ones hospitalized they will only learn dishonestyand deviousness; yes, this can happen. But the

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logic here is so obviously tortured you wonder howit leaves someone’s mouth uncensored: ‘‘I insist onprotecting my patient by maintaining the presenttreatment course at the risk of even greater weightloss, further bone decay, more psychological mal-aise, and an even stronger conviction that weightloss is the ultimate salvation.’’ It’s this sort of fool-ishness that leaves anyone experienced in the careof very ill patients scratching their head in baffle-ment and dismay. Perhaps more irritating is thatthis absurdity is almost always argued by therapistswho have never worked in a hospital setting. Ofcourse hospitalization carries significant risk; wehear the horror stories quit often. But the problemsarise mainly in settings where the treatmentapproach is either incoherent or coercive; becausethe program’s leadership and staff are minimallyskilled and the treatment philosophy is superfi-cially narrow and pedestrian. Sadly, the effects ofpoor treatment, no matter where it takes place, canbe far reaching. Beyond the branding effect—allhospitals/day hospitals/therapists should beavoided—the lack of geographically accessible,high-quality inpatient programs (or limited avail-ability of skilled therapists), only compounds theproblem. But shrill attacks from practitioners whoknow little to nothing about the high quality of carethat is possible in well-regarded treatment centersand who fail to grasp the urgency of interveningwith more intense levels of management when ANadvances are difficult to stomach.

The Therapist’s Task

Judging the intensity of the dispositional traitsthat foreshadow AN is a critical task; this is becauseonce irrational attitudes about weight, appearance,and dietary restraint unfold these factors play arole in driving symptom intensities, their resistanceto rational argument, and the strength of thereward weight loss brings. To have this knowledgeis to be forewarned because when extreme habit ri-gidity and anxiety converge, AN’s remedy is farmore difficult and the self-belittling ideas, shame,and convictions of inadequacy that patients harborare highly resist to challenge. So taking into consid-eration how difficult it is to predict the future, wecome to the question: How, and when, should wereact to malnutrition that is not reversing? Inter-vening early offers a potential advantage, but eventhen treatment is beset by challenges for which im-mediate, easy to effect, solutions are sometimelacking. This is why the question is a crucial one.But first we consider some other treatment-relatedchallenges for which solutions are not always im-mediate.

One is the grim reality of finite resources. Motiva-tion for treatment may be strong and family sup-port unwavering, but if funds needed to support anextended period of care for a dangerously under-weight person at a respected treatment programare not available, alternative solutions may be few;this is a circumstance that can only be described asheart wrenching.

A second is no less urgent, but is more universal:that of treatment refusal or nonadherence, a chal-lenge that becomes especially worrisome whenpatients are at the age of consent. Avoidance ofcare in AN is not so much a battle of wills as a con-frontation between opposing values and perspec-tives—of patient, family, and practitioner. Havingbeen a part of the struggle more than once, it ishard to capture in words the urgency of a family’sdesperation, our own as well, when a dangerouslywasted person enters a courtroom to serve as aplatform for legal debate about mental competencyand the freedom to choose one’s fate. The debate isless contentious when risk of death is imminentand mental deterioration is indisputable, but onlybecause there is no legal barrier to physician inter-vention within a medical facility when risk is immi-nent; even the most zealous patient rights advocateshies away from a defense of free choice underthese circumstances. It’s when the sufferer appearscapable of satisfying the broad legal definition ofcompetency in spite of malnutrition that the out-come is less certain. Having sat through the pro-ceedings many times, there isn’t prose strongenough to describe the tension—parents and lovedones, therapist, too—all obliging court etiquette bygritting teeth in order to remain silent witness tolegal arguments that defy reason.

This is why the question of what can be donebefore the opinions of attorneys and judges areengaged is so important. And shouldn’t these issuecome up for detailed discussion in the very firstcontact with a potential patient (and family)? Isn’tthis the logical time to prepare them for what is tocome, both in general and in the many particularsof the illness, in the hope that a travesty can beaverted—to discuss the nature of AN, what drivesincomprehensible objections to weight gain, whatin the case history might impact on long-term out-come, and the different levels of care that may beneeded? This is the role of consultation, a task fardifferent from motivational enhancement (again,see Waller’s19 cautionary points). We would argue,and strongly, that for an illness as challenging andenigmatic as AN consultation is an essential pre-requisite to the initiation of treatment; unfortu-nately, it is frequently ignored, as we will show. Our



point in citing these examples is that given thechallenge they entail, it is difficult to sustain a casefor teaching about AN that focuses on narrow ideasand narrow clinical training.

We naturally hope for our science to becomemore generative, but in the meantime it isn’t as ifwe are completely in the dark. Managing AN ishard, but at least some of the challenges can betempered if met by a clinical wisdom that is appro-priately balanced by humility; unless we are toohostile to some ideas and too favorably disposed toothers. What we hope we have made clear is that tosuccessfully integrate pragmatic strategies sup-ported by clinical research and experience into anoverarching management that better assists patientand family, clinicians must know about the scienceoutlined above, learn how it applies, and come tothe work very well prepared. It’s when the challengeis met by inexperience and skills narrowly devel-oped that fear takes hold, and the impulse to seethe illness in more categorical terms—to insist onthe superiority of single, specific interventions—will be strong; we have seen this many times insupervising the casework of less experienced thera-pists. Maintaining poise as symptoms escalate isdifficult under any circumstance, but when trainingand experience lack diversity and depth thestraightforwardness of less abstract conceptsbecomes appealing. Simply put, experience toolimited and clinical training too selective will bringfrustration and fear should the initial presentationbe severe, should progress stall, and should weightstart to decline.

At the Margins: What Patients andParents Are Not Being Told

Exactly what are parents and patients being toldabout the ‘‘new’’ paradigms for understanding AN?Well, they certainly hear more about genes and thebrain; but unfortunately, without much clarifica-tion or context, the result of which has been nosmall measure of confusion and misunderstandingas they are to wonder in private if they were justtold they/their child has ‘‘brain damage’’ or a‘‘genetic defect.’’ It goes without saying that explan-ations serve a clinical purpose only if they are au-thoritative and complete; if not, they do harm sincefragments of truth are never a good substitute forno explanation at all.

This is why it is not a good thing for patients andthe public to be told that AN is a genetic disorder,but little else; not to be told: obstacles stand in the

way of identifying causative genes and determininghow genes, brain physiology, and behavior interre-late; what genetic risk actually means; that stress inthe environment can worsen vulnerabilities by pro-gramming anxiety proneness and negative reac-tions to later occurring stressful events; what con-nection causative genes may have to core featuresof the illness (anxiety and fear proneness, compul-siveness of habits, and low appetitive motivation);that genetic effects are not necessarily permanent;that predisposing genes can also have positiveadaptive effects—i.e., discipline and regimentationare virtues, but in AN these virtues are ‘‘high-jacked’’ in an effort to restore a veneer of compe-tence as the strains of maturation become toomuch to live with; that behavior is shaped by envi-ronment too, because genes, biology, and the socialcontext, which includes family life, are interde-pendent.

On top of these omissions, we now hear thera-pists insist that giving credence to environmentalinfluences in AN is outdated, a theory refuted longago, and that doing so amounts to unjustifiedscolding of parents for being malevolent and caus-ative. This is so patently at odds with science it sug-gests that the BBMI and FBT paradigms’ most ar-dent defenders know the least about it (again, weare not referring to any of the authors of the BBMIand FBT papers1,2). It’s another oddly inverted,contradictory logic—pitting a general premise(genes and biology play a role in risk; FBT can beeffective) against others also well supported by ele-gant research (how natural processes inevitablylink genes, brain function, and environmental ad-versity together; FBT is not universally effective).

Our point is that a growing, integrative scienceconvincingly shows there is no basis whatsoever toclaim that reference to environmental conditions isresurrecting outdated theories of psychogenic eti-ology. Rather, it argues:

1. AN frequently involves more (in psychologicalterms) than what is transmitted by heredity.

2. Invoking an interplay of biology and environ-ment does not vilify families any more than itargues family disturbance is a causal prereq-uisite.

3. The notion of stress engendered vulnerabilityis not at odds with treatment models that seefamilies as critical partners in care; it arguesthat broad attention must be given to sourcesof intrafamilial strain and the need for otherforms of therapeutic dialogue to reduce it.Ignoring the potential adverse effects of envi-ronments that can increase childhood anxiety

STROBER AND JOHNSON


is not helpful to families or patients given cur-rent scientific data showing these effects can belong lasting, and that changing a rearing envi-ronment’s emotional tone can be beneficial.

Importantly, our experience has been that nearlyevery family who has heard this broadly sketchedviewpoint has been entirely receptive to the con-cepts outlined, did not feel vilified, and welcomedknowing about their implications. So from the clin-ical perspective, the message that modern neuro-science underscores is: (1) that an invigorated focuson therapy skill is warranted, addressing not onlythe individual’s belief structure, but also the socialcontext in which they live; and (2) applying tech-nique, whether in manual form or instructed, canbe valuable, but more is needed, especially when itcomes to work with difficult cases. In our view, thefurther needed element is not easily measured, butpatients and families feel its presence and theyspeak of it often. It is not one single thing, butrather a set of skills with different facets: theuniquely refined ability of the therapist to sit longhours sifting patiently and thoughtfully throughstrains and secrets the human psyche can easilycloak; insight into what this messy tangle of con-flicting tensions, puzzling emotions, and disparag-ing self-beliefs reveals about a patient’s (and fam-ily’s) misery; the ability to translate this under-standing into prose eloquent enough, anddelivered with the strength of conviction needed,for our patient (and family) to ‘‘feel’’ they best giveit deeper thought; and then to steer the treatmentin the direction needed and escalate its intensityshould progress lag. To appreciate science is onething, but in the clinical realm there is no substi-tute for well-honed skills, intuitiveness, and deci-siveness when facing AN’s challenge.

Other Research Relevant to TreatmentManagement

We know that our treatments are imperfect, butintervening soon after illness onset probably has abetter chance of restoring health in persons withAN than when treatment waits until middle or lateadulthood, at least judging from the poor results ofadult treatment trials. This being the case, there arethree crucially relevant empirical observations thatinform the use of benchmarks in treatment man-agement:

1. Because weight gain during the course oftreatment is often partial, psychopathological

symptoms can persist for years. For some, thepattern remains stable, for others symptomswax and wane in intensity through adult life.

2. Prospective research in other psychiatric con-ditions—e.g., schizophrenia20 and majoraffective illnesses21—shows that even whenvery mild symptoms persist, the risk of laterrelapse is greatly increased. For an illustrationin AN, the reader is referred to Lowe et al.22

and Strober et al.23

3. There is literature in the pharmacotherapy andcognitive behavior therapy (CBT) of depres-sion,24 CBT for bulimia nervosa,25 and FBT forAN26 showing that greater symptom reductionin the very early weeks of these (time limited)therapies predicts a more robust end-of-treat-ment outcome. In other words, if early treat-ment improvement is nil the likelihood of afavorable short-term outcome is low. Theimplication for managing the trajectory ofweight gain in the early phase of outpatienttherapy couldn’t be more obvious.

Benchmarks and the Context for TheirApplication

Having laid out a strong justification for treating ANas a complex set of deterministic processes and foradopting a comprehensive attitude toward its treat-ment, we come to what may seem a technically sim-ple question: What definable benchmarks can besensibly used to determine when a course of outpa-tient treatment in AN has reached its limit of benefitand should give way to a higher level of care? But wealso hope the reader now better appreciates why thequestion is not so straightforward; because it’s noteasily separated from the perspective taking wehave been stressing, or from the connecting linksbetween the research cited above and the keynote ofthis article. There are several points:

1. Even when clinical improvement is notewor-thy, the continuing presence of mild symp-toms should not be taken lightly as an inher-ent destabilizing process remains active.

2. Lack of early weight gain in outpatient ther-apy may place a limit on what can beachieved over time, at least in the short-term.

3. Complex processes are in play; to assume thatsingle interventions are by themselves satis-factory is assuming too much.



4. Therapist inexperience can be iatrogenic, itseffects swinging in directions that seementirely haphazard: extreme laxity when con-tainment is needed, rigidly enforced controlwhen additional time is warranted to see ifthe treatment course can evolve withoutadverse consequence. And let’s not forget inthis regard that a patient’s avowed enthusi-asm for eating is often the last refuge for afear that a more intense treatment is coming.This is why it is important to understand thatthe appearance of change is not necessarilymeaningful change and why failure to recog-nize the distinction can have serious reper-cussions.

5. As illness lengthens so does its perniciouseffect on physical health and self efficacy; thisis why allowing low body to linger is not onlyinexcusable, it is dangerous. In short, itbehooves therapists to be aware of observa-tions both within and outside our field thatdraw attention to why it is important to setboundaries that may have practical clinicalrelevance.

Still, it’s easy to miss the context of the message:benchmarks will not have the consequenceintended unless they are a seamless part of a largerideology; specifically, the many premises that jus-tify seeing AN as a complex illness requiring vari-able aspects of management and therapeuticapproach. Benchmarks should not be treated as de-scriptive criteria; rather, they are elements in anoverarching concept of care, transmitting knowl-edge about the illness and its management thatpatients and families should learn from. Even ifthey are systematically imposed they will be onshaky grounds if attempted by clinicians whosetheoretical and clinical perspectives are narrow.

And there is yet another crucial point: that partialimprovement in AN is often heralded as an impor-tant achievement for patients. This is a tricky issuebecause depending on the context of the illnessand its course, it may be; in fact, it’s a more touchyand complicated matter. Patients need to feel thereis hope for change and that their therapist appreci-ates how hard the struggle to gain weight is; evenwhen it seems effortless it rarely is. But empathywith what is an agonizing struggle needs to be cau-tiously reconciled with the danger of complacency.Many times we hear patients say—their therapiststoo—that the illness has been stable for some time;that this is a good thing given how bad things usedto be. Perhaps, but stasis is not justification forcomplacency, especially when the patient is a child

or young adult. As the research just highlightedshows, symptoms that linger confer more than theeventual risk of bone disease and relapse; in time italso brings a rise in psychological inertia. We hopefor a therapy that will one day prove transforming,but for now AN is frustrating because change typi-cally comes in orders of magnitude too small todiscern. It’s a clinical fact that underscores oneother: as the duration of a stably low weight length-ens, insidious shaping processes are evolving thatcontinue to feed an already ruthless self judgment,ultimately forming the belief that ‘‘I can neveradapt to adult life unless I am thin.’’ And sincemany patients remain underweight for long periodsof time while continuing in the same outpatienttreatment, how can we not wonder if the eating dis-order community is aware of this?

Add to this concern two more examples of howpatients equivocate when they receive a recom-mendation that they intensify their care. Theycome from many hundreds of consultations (someinitiated by parents, some requested by the thera-pist, some from patients themselves) that soughtour advice on the status of a current therapy. Weare referring specifically to consultations that beginwith the assertion: ‘‘Things now are so much betterthan before.’’ Maybe so, but sometimes the wordsare less a comment on progress and hope for a bet-ter future than an unskillfully cloaked fear that ahigher level of care is precisely what the consultantwill advise. Patients may be clumsy in how theyminimize the seriousness of their illness, but thisdoesn’t mean they lack intuition. What better wayto soften the fear of being told they need somethingmore than by ending the consultation before itbegins with a pretext for why it wasn’t needed inthe first place.

A second obfuscation (some related statistics tofollow) is seen with patients who are not currentlyunder treatment by a mental health professional(some having discontinued this treatment) butinstead are receiving supportive care from othercare givers (e.g., nutritionist, spiritual counselor,pediatrician, school guidance counselor, or nurse),often for lengthy periods in spite of negligibleweight gain; it is a common scenario. Why this isbegs many questions, but as AN is fundamentally apsychological/psychiatric illness, this form of solo,nonpsychological ‘‘counseling’’ is not, and shouldnever be, a trade-off for mental health treatment,even when the patient has declined it. Many ofthese care givers have taken strong exception toour criticism of the arrangement, but we stand bythe reproach. Apart from the incongruity (not tomention the expense) of sustaining such contact

STROBER AND JOHNSON


when the patient’s commitment to, or tolerance of,

weight gain is nil, the idea that it is vital because it

remains the only available support may be a nobleone, but a contact that lacks neither reference to

the facts of the patient’s psychopathology, nor one

able of probing the varied, complex reasons why

self-examination is shunned, only fosters the illu-

sion that care and support is actually being given; it

is not. It isn’t that the arrangement lacks benefit

whatsoever; it’s that, at best, it’s a superficial one.

We have known far too many patients, stable but

with attenuated symptoms for many years, who

ultimately paid a heavy price for the relapse that

eventually came. Simply stated, it’s our view—anda strong one—that nonmental health allied care

should never be initiated or continued without a

patient having first established a treatment that is

psychological in nature. And should that relation-

ship end referral of the patient for consultation

should be arranged immediately and the allied care

should cease. Patients may refuse, but the idea that

this is a de facto justification for sustaining an

arrangement that offers little further therapeutic

challenge is setting a dangerous precedent. Theopinion may strike some as harsh, maybe even tan-

tamount to an unethical abandonment of the

patient (it is not), but as Vandereycken and Meer-

man note in their excellent book on AN,27 it is far

better to interrupt the illusion of ‘‘treatment’’ when

conditions for a genuine therapy are absent than to

press forward when resistance to change is too

great. How to approach the dilemma is considered

below.

As the above examples imply, benchmarks serve

the purpose of holding off the adverse complica-

tions that lack of weight gain, or weight decline,

eventually bring. But they will have the greatest

utility when they rest on a comprehensive attitude

toward care, in the same way that their public

health implications hinge on their wider dis-

semination. So we hope the reader will see accept

their utility and apply them widely in outpatient

practice.

Having said this, we are not claiming there is a

general theory that lends validity to the bench-

marks we will describe, or that implementing them

guarantees that the hold AN has on patients will be

decisively broken. Benchmarks are merely a frame

of reference for approaching a particular problem,

not a set of testable hypotheses. Still, they have an

association with scientifically supported observa-

tions and because an immense amount of clinical

experience provides further testimony, we believe

the general rationale for their application is broadlycorrect and that significant adverse consequencesfollow when outpatient care lacks a framework ofwhich benchmarks are a part. The time points inthe algorithms described were not empiricallyderived, but neither are they entirely arbitrarily.Again, their objective is to avoid blunders via apragmatic frame of reference for approaching aparticular problem.

Low Body Weight and Other Foundations for

Benchmarks

Obviously, the prime reason for linking bench-marks to a time line for deciding when outpatientcare should transition to one more intensive is themalignant effects of unremitting malnutrition; buta brief caveat concerning the relationship betweenlow weight and outcome warrants comment.Clearly, people who stay ill naturally have pooreroutcomes, but what mediates the association oflow weight and long-term outcome is not yetunderstood. For example, we don’t know if themechanisms involved are at a cellular level;whether low weight is reinforced over time in wayspsychological, interpersonal, or biological, or viainteractions between all three; whether low weightis a proxy for other factors more discreetly linked totreatment failure and chronicity; or how manyyears of unremitting illness are required before re-covery can be declared unfeasible. In our experi-ence, it is common for patients and families to betold that a very low BMI is predictive of poor out-come; but as Steinhaussen14 shows, this pro-nouncement is incorrect. It isn’t body mass at thebeginning of treatment that predicts poorer long-term outcome, it’s the persistence of low bodyweight that does.

Some Personal Observations as Testimony to

the Need of Benchmarks

They are drawn from many consultations withboth adolescents and adults, of which three standout.

First, it is striking how many patients remain inoutpatient care for extended stretches of time, frommonths to decades, without anyone in the treat-ment team ever having advised referral to a higherlevel of care for weight restoration and a morecomprehensive treatment. And we are not referringhere to patients for whom such a recommendationwas made but refused.

Second, many adolescents (as well as youngadults who still reside with parents) enter treat-ment without any assistance being offered to



parents—no preparation, assistance, guidance, ordiscussion whatsoever, even when families wereasking to participate and fully capable of doing so.The rationale typically given for separating parentsfrom the child’s therapy—to preserve the child’sconfidentiality—is difficult to defend since main-taining a strong individual psychotherapy and giv-ing direction to parents need not be mutuallyexclusive.

Third, among the 226 consultations conductedby MS between January 2007 and December 2010where treatment involved a multidisciplinary teamof professionals, lack of cohesion in the team’sleadership structure along with poorly articulatedrationales given for decisions that were renderedover the course of treatment were frequent com-plaints. Indeed, when patients/families wereasked, ‘‘Who in this team is in charge, and who doyou turn to for guidance?’’ there were blank stares.Moreover, critically important and complex deci-sions (e.g., timing of calorie changes; whether itwas, or was not, appropriate to participate in exer-cise or recreational activities; setting of the targetweight and prescribed weekly weight gain; whento back off temporarily on calorie increases toallow symptoms to stabilize; whether vacationsshould be permitted or delayed) were often dele-gated to certain members of the team withoutinput from others and rendered without anyinvolvement of the therapist, the effect of whichwas that clinical factors of central importance didnot inform decision making in any logically con-sistent or sensible way. Indeed, the irritation ofparents, ‘‘We never know who is in charge,’’ waspalpable. For an illness so baffling, this state ofaffairs is not simply counterintuitive, it is just plainwrong. If we accept that AN is an inherently com-plex illness, why undertake its treatment withoutfirst laying out clear, a priori rules governing howdecisions that clearly require an account of howpsychological, pathological, physical issues inter-act will be rendered? And given that many inter-acting factors are at play in AN, it is imperativethat all treatment decisions reflect knowledge ofthese deterministic trends, what they mean, andthe function—in psychological terms—they serve.Naturally, certain decisions depend uniquely onthe patient’s physical condition and here thephysician’s authority is absolute. But outside ofthis general point, treatment decisions that ariseoften in AN can not, in our opinion, be renderedclearly without a single person guiding the pro-cess. And in our view, the single best resource forunderstanding the complexities at play is, ofcourse, the therapist; but ironically, rarely is the

therapist involved in this way. To the contrary, inthese consultations many therapists told MS theypreferred to defer management decisions toothers, which, as the consultation ultimately madeclear, proved a tactical and conceptual error;because for patient and family, uncertainty andmistrust arose as a result. Decision making in ANis inevitably a reactive process because it shifts assymptoms wax and wane; this is why collaborativediscussion is essential. But at day’s end the clini-cian with the single greatest knowledge of the caseand its context must construct the narrative andbring coherence to whatever overarching decisionsare needed. Who else can realistically do this butthe therapist? The idea that extending the thera-pist’s role in this way can contaminate the therapyis not new, and we are not making light of thepotential for conflict. Still, we have worked con-jointly with patient and family members for deca-des and the occasions when therapy shut downbecause boundaries were muddled were few. Butthis was because the nature, parameters, rationale,and transference implications of the arrangementwere thoroughly discussed before treatmentactually began.

Last, and perhaps most disconcerting in the lightof what we have discussed, rarely do either patientor family receive a formal and detailed introductionto the nature of AN, including the challenges tocome if treatment is to be attempted. Among the226 families referred to above who were currentlyreceiving outpatient care and who sought consulta-tion with MS about the viability of this treatment, Iasked whether they had received, at any time fromany treating therapist, an initial consultation thatdiscussed in depth: (a) the defining characteristicsof AN; (b) what background factors precede itsonset; (c) how and why it is believed to be self rein-forcing; (d) why patients often state they can notaccept life without it; (e) what is known about riskfactors and how these factors collectively shape thesymptoms that unfold; (f) why symptoms becomeso resolute, and so quickly; (g) the different coursepatterns and outcomes the illness takes, includingthe risks of chronicity and premature death; (h)what bench marks would guide decisions aboutwhen to stop one treatment in order to consideralternatives; (i) how parents/significant others canassist their child/partner in managing the symp-toms and in promoting weight restoration; (j) whatinfluences in the environment are favorable, andthose that might hinder progress; (k) short- andlong-term medical effects; (l) and what is known atpresent about the value and purpose of differenttherapeutic modalities. To our amazement, in only

STROBER AND JOHNSON


two cases – less than one percent – was such acomprehensive pre-treatment preparation given.This is simply inexcusable.

Benchmark Algorithms

When to Consider Inpatient Care as a First-Line

Intervention

No attempt has yet been made to determine ifthere is a specific clinical boundary that warrantsinpatient versus outpatient care; neither is there aspecific weight threshold (below 75% of ideal bodyweight is frequently cited) nor an infallible courseindicator that supports the imperative of hospitali-zation, beyond, of course, trending signs of cardiac,hematologic, kidney, or liver function abnormality.However, based on experience with patients whoenter into outpatient care first, the likelihood offailing this treatment is high when any of the fol-lowing clinical features are present, and especiallywhen they co-occur.

1. A steeply declining trajectory in body weight,especially when weight is already below 75%of expected weight for age and height.

2. Irrefutable insistence that further weight lossis needed, or justifiable, because of an over-weight or ‘‘obese’’ appearance.

3. History of an extreme degree of regimentationor compulsiveness in behavioral routinesfrom early in life; extreme fear of matura-tional challenge; a history of trauma, extremehyperactivity (multiple hours of unrestrainedactivity), or comorbidity with major depres-sion or obsessive compulsive disorder whentheir symptom intensity results in impair-ment on their own, or is compromisingweight restoration.

Some will ask how these indicators are to beoperationalized so they can be applied systemati-cally; but this is where the sort of clinical judg-ment that experience hones is important. Simi-larly, it is intuitive that when more than one ofthe listed features is present concurrently theimpairment this results in is too difficult to inter-rupt in the outpatient setting. For these reasonsthe rationale for moving sooner rather than laterto inpatient care is sound. We are not saying it isabsolutely impossible for outpatient care to suc-ceed when very low body weight (or these otherclinical features) is present—we know of cases—but it is rare.

When to End Outpatient Care

This is by far the most crucial scenario forbenchmark application because it is the morecommon one. Our recommended algorithms forescalating the level of care are as follows; theyare broken down by the presenting circum-stance.

Scenario 1: When Outpatient Care Has Been

Attempted for an Underweight Child/

Adolescent/Young Adult, Regardless of

Previous Treatment History

Beginning treatment de novo with an under-weight child or teen is the paradigmatic illustra-tion of benchmarking the level of care needed tominimize risk of a deeper and more entrenchedpsychopathology. In fact, we are increasinglybeing asked by parents, ‘‘When do we know whatwe’re doing is not working?’’ It is a complicatedquestion for several reasons: because the treat-ment of AN requires time, so changing course toosoon isn’t always a good thing; there is no uni-formity in how ‘‘low weight’’ is defined; andswitching to another therapist, one more skilled,can sometimes reverse the course dramatically.But knowing that a spontaneous remission isextremely rare, that bone demineralizationaccrues quickly, and that as symptoms intensifyself-esteem and adaptive competency suffer, weurge that outpatient therapy be stepped up tohospital care when any of the following circum-stances apply:

1. If weight declines steadily over the first 3weeks of treatment (or following consultationif no treatment was initiated). In our experi-ence, this trajectory becomes difficult tointerrupt thereafter.

2. Weight is initially stable, but there is a negligi-ble average weight gain (or a waxing and wan-ing pattern of increases and decreases) by theend of month two of treatment (or followingan initial consultation). In our experience, asteady, uninterrupted increase in weight backto normal body mass becomes increasinglyless likely after this point.

3. There is initial weight gain, but the slope ofthe increase levels off prior to the patientachieving full weight restoration, and this flat-tened pattern remains unaltered for at least 6continuous weeks.

If, per chance, there is a change of therapist, thealgorithms recycle immediately.



Scenario 2: Initiating Outpatient Treatment for

the First Time in an Older Adult at Low Body

Weight

Here, we are presuming the patient has been illfor at least 5 years. It might be argued that becauseillness duration is longer the urgency of more in-tensive treatment is proportionately greater; but sois the patient’s language of resistance, and sincetime will be needed before we have a good sense ofthe precise issues involved in the history of such apatient a more lenient algorithm is prudent. Soassuming the patient is judged by a physician’s ex-amination to be medically stable, the algorithmneeds to allow greater time for the patient’s struggleto play out. Accordingly, we recommend the transi-tion to a higher level of care when:

1. Weight is declining steadily in the first threeweeks after commencing treatment.

2. Weight is initially stable, but the patient isunable to initiate, and then sustain, a steadyincrease in weight by the end of month threeof treatment; in our experience, uninter-rupted weigh gain after this point is increas-ingly unlikely with such a patient.

3. Weight increases initially, but the slope of thisincrease then levels off and remains so for 3continuous months.

Scenario 3: Initiating Outpatient Treatment

with a Young Adult Who Has Had a Prior

Failed Treatment

Here we recommend the same criteria as in Sce-nario 1.

It is also legitimate to ask whether these shouldbe explicit rules; but it should be remembered thatthe time points derive from experience. Beyond thequestions that naturally arise about algorithms,what these address in a fundamental sense, and wethink reasonably given the material reviewed, is thedanger of passivity in decision making; becauseover time, the pull of irrational habits, conflictedmotivation, and the mind’s attitude in AN growstronger and as they do the resistance to changebecomes more formidable.

What to Do When Patients/Families Reject the

Recommendation of a Higher Level of Care?

As Vandereycken and Meerman note,27 therapistshave as much ‘‘right’’ to discontinue treatment aspatients do; except here, the rationale is stronger asit is informed by an important clinical wisdom.Patients withdraw from treatment due to fear ofwhat they are being asked to confront and the emo-

tional discomfort that results (we are not speakinghere of ending a treatment that is poorly executedor one attempted by an unskilled therapist). But fortherapists, the decision comes after a lack of mean-ingful progress over an extended period, or upon apatient’s refusal to step up their level of care whenit is deemed acutely necessary. There is no questionthese are difficult, sometimes painful, decisions;we consider them reluctantly because of the origi-nal commitment we made to the patient’s well-being and our abiding hope that one day ourpatient will enjoy a future less encumbered bywithering self-deprivation. But returning to an ear-lier caution, continuing a level of care that isunprofitable and not likely to have benefit in theforeseeable future is not treatment, and to carry onas if it is carries significant risk. For this reason, dis-continuing treatment may well be the only actionpersuasive enough to convey the urgency of whatthe therapist feels, and what the patient needs,regardless of what they ultimately decide to do.

But it is not a finite decision, and this is an im-portant point. Instead, we recommend for the timebeing only a temporary interruption of care; specif-ically, if an impasse has been reached we recom-mend reconvening in 1 month’s time for furtherassessment of the patient’s circumstances. The ra-tionale of the interruption is explained by incorpo-rating the premises discussed throughout this arti-cle; hope is expressed that the patient (and/or fam-ily) will soon reconsider the refusal of a higher levelof care; the risks of further refusal are discussedstraightforwardly; interim follow-up with a physi-cian is strongly recommended; possible underlyingreasons for the patient’s reluctance to contemplatetreatment of greater intensity are outlined, empha-sizing the psychopathological issues involved,including as much detail in the explanation as pos-sible; and finally, the possibility that the treatmentmay end at this time is acknowledged. Should thepatient return, laboratory results and symptomintensities are reviewed and signs indicating a wor-sening of the patient’s physical or clinical state arediscussed in detail, along with the patient’s/family’scurrent worries, or, perhaps, their professed lack ofconcern (but rarely is a blase attitude seen). If theoriginal recommendation is rebuffed at the 1-month follow-up, a second follow-up in 3 monthsis offered and if the patient agrees the therapistagain expresses hope that the return visit will takeplace. Yet a third, but final, 3-month follow-up isscheduled if the refusal persists.

In our experience, the outcomes are entirelyunpredictable: some patients reconsider quickly,accepting the higher level of care because their

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condition has worsened, or the intensity of theirmisery has greatly increased; some continue to re-fuse, but ultimately reconsider at a later time;others seek treatment elsewhere, sometimes show-ing noteworthy improvement; and still others neverreturn and we never hear from them again. Finally,as discussed elsewhere,28 for some adult patientsthe only recourse is a supportive managementwhere the interventions and objectives are carefullymeasured.

Concluding Words and a Postscript onConsultation

We have presented an argument for understandingthe mystery and danger of AN in the broadest con-text possible. In doing so, we have highlighted les-sons being taught by numerous credible studiesabout biology, development, and life experience –lessons germane to psychopathology and to itstreatment. We made the point that genes and biol-ogy are the fundamentally important starting pointfor understanding, because compulsiveness ofhabit, anxiety, low reward seeking, and behavioralregimentation are heritable phenotypes that‘power’ the illness and sustain its self-rewardingproperties. But equally important to this under-standing is that these traits can be ‘opportunisti-cally exploited’ by the psyche of AN to sustain itsadaptive, self-rewarding effects. Whether we thinkthe transformative process is unconscious or voli-tional is beside the point since the dividing line istoo faintly drawn to determine where one ends andthe other begins. Still, even though vulnerabilitybegins with genes and biology, to assume there isneither intentionality nor volition involved at anylevel of the illness is a fallacy; biology and willful-ness are not mutually exclusive processes. So whatisn’t beside the point is that genes and biologyshould be viewed in functional terms, that the clin-ical implications of this viewpoint are many, andthat molecular neuroscience reminds us that lifeexperiences play a role in illness because even irra-tional mental states adapt to social pressures in acausal chain that shapes the course of developmentover many years. This is why throughout the articlewe stressed that a narrow conceptual vision of ANcan never suffice as clinical theory because makingpragmatic interventions the centerpiece of therapyis not only too deliberate, it is insufficiently sensi-tive to the contextual factors that can either pro-mote or arrest symptom progression.

So coming to the end, we return to the touchyquestion of where things go wrong and why. Also,

why is it that in preparing to treat a psychiatric ill-ness we unhesitatingly agree is more complex andpotentially threatening to health than any other,therapists rarely begin with a detailed, comprehen-sive, authoritative empirical and clinical accountthat establishes: what, exactly, is being treated; howthe illness evolves and what processes underlie itsself-perpetuating character; why the treatment islikely to be challenging and in what ways; how longa period of care may be needed, the elements ofthat care, and what risks result if the treatmentshould end prematurely; what benchmarks need tobe followed to decide when more intense interven-tion is essential, and why; what behavioral, psycho-logical, and life style changes signal that the end oftreatment is at hand; and what personal, parent,family, and social strains may be important to con-sider, and to address therapeutically? Why does thisrarely occur? We believe the reasons are several:

1. insufficient clinical experience; lack ofbreadth in academic and clinical training;and little exposure to other areas of psycho-pathology relevant to eating disorders;

2. a commitment to doctrinaire ideas and quick-ness to write off alternative possibilities for care;

3. lack of training and experience in combinedclinical and academic settings that offer com-prehensive, multidisciplinary, and higher lev-els of care, and a misguided disdain for hospi-tal-based treatment.

How to put into words unfamiliar to eitherpatient or family the many reasons why weightgain has become a fear so paralyzing it is resisted atall costs, and how to give far ranging explanationsof what gives rise to the illness and the absurdlywild beliefs that become attached to its symptoms,are questions that underscore the essential wisdomof making far ranging clinical skills and diverse the-oretical knowledge our foundation. Not only does itallow for answers to the questions patients andfamilies surely have, it also articulates the unspo-ken resistances to change and the withering emo-tional highs and lows that may soon erupt forwhich everyone, therapist too, must prepare. This,in our experience, is the dialogue that has provedthe most robustly effective means of helpingparents (and other loved) separate illness from theperson who bears the affliction; any other prepara-tion is sterile and incomplete.

Who doesn’t wish for a treatment that can allevi-ate suffering quickly? But to think there is a decisiveway of accomplishing it is risky and naıve. Teachingparents skills to assist with weight gain is a good



thing; we should do it. What is not a good thing isfailing to recognize it must coincide with a seas-oned ability to infer when the conditions for itssuccess may not be present and how other inter-ventions can assist. We know from colleagues,many interactions with therapists, and quite exten-sive experience with patients and families, that inthe torrent of excitement that greeted FBT, it, and italone, has assumed center stage in the care beingdelivered by many practitioners and many treat-ment centers whose knowledge of the illness ismarginal. We understand this; when treatmentservice options are limited, a pragmatic solution isneeded, and quickly. Still, it shouldn’t overshadowthe need for platforms of teaching and skill build-ing that are more comprehensive. And let us notforget another basic truth about people who strug-gle and the loved ones who understand little ofhow to help. Ultimately, it is the therapist’s knowl-edge of the mysteries involved and the wisdomthey display in rendering their clinical judgmentsthat instills hope and builds faith that what is beingdone follows a rationale that must be honored.Without this, the bond that tethers our patient toour treatment is a fragile one.

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Health & Medicine

The Need for Complex Ideas in Anorexia Nervosa