mandometer musings

European Eating Disorders ReviewEur. Eat. Disorders Rev. 11, 1–6 (2003)Published online in Wiley InterScience (www.interscience.wiley.com). DOI: 10.1002/erv.496

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Mandometer Musings

Ulrike Schmidt*Eating Disorders Section, Institute of Psychiatry, London, UK

I recently attended an eating disorders meeting in Helsinki. Onepresentation caused a real stir. This was a talk by Dr Cecilia Bergh on theeating disorder treatment pioneered by her and her colleagues at theKarolinska Institute in Stockholm with excellent results. Some Finnishpatients and carer organizations demanded that this new treatment bemade available in Finland too, as they perceived it as significantly moreeffective than anything else currently on offer, producing remissionrates of 75 per cent for anorexia nervosa (AN) and bulimia nervosa (BN).The frustration of people feeling that there is an exciting novel treatmentavailable ‘next door’ without being able to access it, is understandable.Moreover, the fact that specialist eating disorder services in Finland arefew and far between and those that exist are seriously under-fundedseemed to make this situation even more tantalizing for carers andpatients. I had vaguely heard about the Karolinska treatment before, butgot really curious about it. So what is in it?

THE KAROLINSKA MODEL OF EATING DISORDERS

Dr Bergh and colleagues’ model of anorexia nervosa (Bergh &Sodersten, 1996; 1998) is based on the notion that this is not a mentaldisorder, but a human analogue of the rat activity stress paradigm(Morrow et al., 1997). According to this model anorexia nervosa arisesfrom the combination of two risk factors, dieting and increased physicalactivity. Both of these are known to activate the mesolimbic dopami-nergic reward pathways and the locus coeruleus noradrenergicattention pathways in the brain. Their hypothesis is that anorexiadevelops because eating less and being physically more active are

European Eating Disorders ReviewCopyright # 2003 John Wiley & Sons, Ltd and Eating Disorders Association. 11(1), 1–6 (2003)

*Correspondence to: Dr Ulrike Schmidt, PO Box 059, Eating Disorders Section, Institute ofPsychiatry, De Crespigny Park, London SE5 8AF, UK. E-mail: [email protected]

initially rewarding and that later on anorexic behaviour becomesconditioned to the stimuli that originally provided the reward becausethe brain’s network for attention has been activated. The typicalpsychopathology of AN is seen as a consequence of starvation. It ispostulated that similar mechanisms operate in bulimia nervosa. Theirtreatment is based on this model, although it is not entirely clear to me,precisely how.

THE KAROLINSKA MODEL OF TREATMENT

The treatment focuses on four key symptoms of anorexia nervosa: (1) thedisordered eating behaviour and altered perception of satiety, (2)hypothermia, (3) physical hyperactivity and (4) the disordered social life(Bergh, Brodin, Lindberg, & Sodersten, 2002; Berg, Eklund, Eriksson,Lindberg, & Sodersten, 1996).

The core-piece of the treatment, addressing problems with eat-ing behaviour and satiety perception, is the Mandometer system.(Mandometer is a registered trademark). This is an interactive computersystem designed to help patients recover faster. It is aimed at teachingpatients to eat a healthy amount of food in a healthy amount of time byanalysing and processing interactive feedback during meals. Thepatient’s plate is put on a scale which is connected to the computer.Patients get feedback about their own rate of eating and can input satietyratings as they progress through the meal which are compared againstsatiety ratings of a normative control group. Over time anorexics aretrained to eat more food more quickly and bulimics less food moreslowly. This system is used once a day at lunch-time. It sounded to me asif this system combined elements of the behavioural technique of pacing(used previously in the treatment of obsessional slowness), bio-feedback(for which there is little evidence in eating disorders) and exposuretherapy (which has had mixed results in eating disorders).

For those who are reluctant or unable to use this system in the contextof starting treatment, initiation of eating is approached by adopting theSkinnerian principle of successive approximations.

The overall treatment programme at the Karolinska combinesmultiple components and uses flexible amounts of inpatient (reservedfor those with severe AN) and outpatient care. For patients with ANgradually increasing weight gain goals are set. Physical activity isinitially restricted and rest periods of 1 h in a warm room are observed.A feeding schedule of regular meals is supplemented with nutritionalsupplements and there is a social schedule, including graded short-termgoals. Drug treatment with cisapride is used in those with AN, but no

U. Schmidt Eur. Eat. Disorders Rev. 11, 1–6 (2003)

Copyright # 2003 John Wiley & Sons, Ltd and Eating Disorders Association. 2

other medications. (This medication has been withdrawn from themarket in many countries including the UK because of concerns over itssafety).

Some of these several components seem similar to what is used inmany specialist inpatient regimes in the UK and elsewhere in thetreatment of AN.

THE TREATMENT RESEARCH

The authors evaluated their treatment programme in a very smallrandomized controlled trial (n¼ 32) which includes 19 patients with ANand 13 with BN (Bergh et al., 2002). In this study the efficacy of thetreatment was compared against waiting list. It is not clear whatpopulation the clinic serves (secondary or tertiary care, catchment area-based or not etc.), and how patients were referred and recruited for thestudy. Inclusion and exclusion criteria were specified and five severelyill AN patients and 10 EDNOS patients were excluded from the study.Although the ages of AN patients range from 10 to 33 years, their meanage is 16 years and the mean duration of illness is short. (In general suchpatients tend to have a good prognosis). There is no mention of whoassessed outcome and whether the assessor was blind to treatmentgroup. The definition of remission is unusual as for anorexia nervosathis does not include restoration of menarche, nor does it for bulimianervosa, include abstinence from compensatory behaviours. In thoseanorexics who achieved remission the mean BMI was 18.6 ranging from15.4 to 19.9. This suggests that some of those defined as in remission maystill have been significantly underweight. The outcomes for participantswith BN are inadequately described. The average service consumptionof patients is not described in detail. However, treatment does seem tobe intensive with 4/16 patients requiring initial inpatient treatment andoutpatient treatment starting with five treatment occasions per weekgradually going down to one every other week.

In the same paper the authors describe a much larger observationalstudy of 168 patients who entered their treatment program between1993 and 2000. Of these 85 had AN, 38 BN and 45 EDNOS. The clinicaldetails given about this cohort are limited and are said to be similar tothose reported in the RCT. Eighty-three patients (49 per cent) went intoremission after a median of nearly 12 months, 23 (14 per cent) withdrewfrom treatment and 62 (37 per cent) were in treatment for a median of 6.8months (presumably this latter group had not yet lived through the fullfollow-up period at the time of reporting). The estimated time toremission was 14.7 months, irrespective of diagnosis. The estimated

Eur. Eat. Disorders Rev. 11, 1–6 (2003) Mandometer Musings


overall rate of remission was about 75 per cent. Of note, 52 of thepatients in the observational study were treated as inpatients. (If thosetreated as inpatients are mainly those with AN about two-thirds of thispatient population had a spell of inpatient treatment, i.e. a considerablyhigher proportion than in most UK-based centres).

COMMENT: SOUR GRAPES FROM A CATCHMENT AREAPSYCHIATRIST OR THE EMPEROR’S NEW CLOTHES?

I found the outcome paper not always easy to understand. Many detailswere not reported, or not reported in sufficient detail to be able to reallyknow how good the results of the Karolinska treatment are and todisentangle its effects and costs for different types of eating disorders.Some details are reported for the RCT, but not for the observationalstudy and by implication one is asked to extrapolate from one to theother, which may not be justified.

The discussion focuses mainly on anorexia nervosa, pitching thefindings from the present study against long-term outcome studies foranorexia nervosa. This is arguably an unfair comparison as many of thestudies they quote relate to adults with AN with a poorer prognosis thanthe AN patients in the Swedish study. Moreover, we must not forget thatboth the RCT and the observational study included patients with eatingdisorders other than AN.

Likewise, in the discussion the authors make another poorlysubstantiated claim i.e. that the estimated cost of their treatment isconsiderably below that of other methods. They base this claim on acalculation they conducted in an earlier paper (Bergh & Sodersten, 1998)where they estimated the cost for a patient with AN as £400,000 based on(a) published prognoses of recovery and chronicity, (b) a meantreatment length of 4 months, (c) a cost of 1 bed-day of £400, and (d) aloss of income due to a 60 per cent absence from work from the onset ofthe disorder at 14 years to retirement. The cost of their own treatment isestimated as £65,000 (approx. 100,000 Euros) per patient with no furtherdetails given.

Taken at face value the Swedish RCT compares a relatively intensivebroad-spectrum treatment against no treatment in young patients with ashort duration of illness and relatively mild AN and bulimic patientswhose symptom severity is not adequately described. So what is allthe hype about? There is solid research evidence to suggest thatyoung AN patients treated in other centres with family therapy or otherfamily-based interventions have a similarly good long-term outcome at



follow-up, with about 60 to 90 per cent of cases fully recovered (forreview see Eisler, LeGrange, & Asen, in press).

A somewhat surprising aspect of the RCT is that waiting list pa-tients really did stay on the waiting list and did not seek treatmentelsewhere. This is in contrast to the only other study that used asimilarly brave design, i.e. the study by Crisp et al. (1991), where themajority of those assigned to waiting list had the good sense to seektreatment elsewhere. The willingness of patients in this study to stay onthe waiting list may say something about the high expectations thatpeople have of the Karolinska treatment.

And what about the Mandometer? This clearly is the most intriguingand unusual aspect of the treatment. Would the package work equallywell if patients noted their satiety ratings on a piece of paper? We knowfrom research in other areas that computerized delivery of treatmentmay lend it additional authority (Burgoon et al., 2000; Nass, Fogg, &Moon, 1996). So, is the mandometer just an expensive placebo or is it ahelpful device that works through the postulated mechanisms that haveinformed its creation? It would be interesting to see how the use of theMandometer compared with a control condition where the computerdelivered different, bogus or irrelevant feedback. Certainly theMandometer attracts interest and publicity and perhaps more benefi-cially, faith in the patients who use it. Is this the ‘magic’ ingredient? Atpresent the treatment package has been shown to be better than awaiting list condition in which the subjects were—unusually—prepared actually to wait. The big question is how the treatment wouldcompare with an equally caring and intensive treatment costing around£65,000. At present we do not know the answer to this question. In theabsence of data, feelings tend to rule. Some greet the treatment withgreat enthusiasm. I too would welcome a truly new treatment approachin the field of anorexia nervosa. The Karolinska approach should beevaluated further. However, for the present I tend to view the wholething with the sceptical and perhaps even jaded eyes of an adultpsychiatrist working with a catchment area full of more reluctant andolder patients with longer lasting conditions. Only time and adequateresearch will tell where the truth lies. However, one way or another, Isuspect we are going to hear a lot more about the Mandometer in yearsto come.

REFERENCES

Bergh, D., & Sodersten, P. (1996). Anorexia nervosa, self-starvation and thereward of stress. Nature Medicine, 2, 21–22.

Eur. Eat. Disorders Rev. 11, 1–6 (2003) Mandometer Musings


Bergh, D., & Sodersten, P. (1998). Anorexia nervosa: rediscovery of a disorder.Lancet, 351, 1427–1429.

Bergh, C., Brodin, U., Lindberg, G., & Sodersten, P. (2002). Randomizedcontrolled trial of a treatment for anorexia nand bulimia nervosa.Proceedings of the National Academy of Sciences, 99, 9486–9491.

Berg, C., Eklund, S., Eriksson, M., Lindberg, G., & Sodersten, P. (1996). A newtreatment of anorexia nervosa. Lancet, 348, 611–612.

Burgoon, J. K., Bonito, J. A., Bengtsson, B., Cederberg, C., Lundeberg, M., &Allspach, L. (2000). Interactivity in human–computer interaction: astudy of credibility, understanding and influence. Computers in HumanBehavior, 16, 553–574.

Crisp, A. H., Norton, K., Gowers, S., Halek, C., Bowyer, C., Yeldham, D., Levett,G., & Bhat, A. (1991). A controlled study of the effect of therapies aimedat adolescent and family psychopathology in anorexia nervosa. BritishJournal of Psychiatry, 159, 325–333.

Eisler, I., LeGrange, D., & Asen, E. (in press). Family interventions. In J.Treasure, U. Schmidt, & E. Van Furth (Eds.), Handbook of eating disorders(2nd ed.). Chichester: John Wiley & Sons.

Morrow, N. S., Schall, M., Grijalua, C. V., Geiselman, P. J., Garrick, T., Nuccion,S., & Novin, D. (1997). Body temperature and wheel running predictsurvival times in rats exposed to activity-stress. Physiol Behav, 62, 815–825.

Nass, C., Fogg, B. J., & Moon, Y. (1996). Can computers be team mates?International Journal of Human Computer Studies, 45, 669–678.



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