anorexia nervosa: to investigate or to treat?

2
563 Anorexia Nervosa: to Investigate or to Treat? THE LANCET THE patient with anorexia nervosa may be referred for treatment to a psychiatrist, a phys- ician, or a gynaecologist. Whereas the psychiatrist is unlikely to request many diagnostic tests, his col- leagues may pursue exhaustive investigations of en- docrine function. The latter practice has been criti- cised on the grounds that the diagnosis of anorexia nervosa is a straightforward matter requiring only careful history-taking and physical examination, and that the endocrine disturbances are merely secondary to the loss of weight. Moreover, these in- vestigations may be time-consuming and may delay the start of correct treatment. The recent aware- ness of a sharp increase in the incidence of anorexia nervosa2-4 and its tendency to run a chronic course,5,6 has led to a greater sense of urgency to provide effective treatment. The question at issue, therefore, is whether a conflict need exist between treating the patient and investigating her endocrine status. . In all patients with anorexia nervosa there is evi- dence of an endocrine dysfunction, now known to originate in the hypothalamus and not in the an- terior pituitary as was formerly thought. Its most obvious clinical manifestation in the female is the cessation of menstrual function. (The correspond- ing symptoms in the much rarer male patients are a loss of sexual interest and activity.) The amenorrhoea is often an early symptom which may precede the loss of weight7-a finding which weakens the conclusion that the former is merely a consequence of the latter. Elucidation of the under- lying endocrine disturbances is a substantial 1. Beumont PJV. The endocrinology of anorexia nervosa. Med J Aust 1979; i: 611-13. 2 Theander S. Anorexia nervosa: a psychiatric investigation of 94 female pa- tients. Acta Psychiat Scand 1970; Suppl 214. 3. Kendell RE, et al. The epidemiology of anorexia nervosa. Psychol Med 1973; 3: 200-03. 4 Crisp AH, Palmer RL, Kalucy RS. How common in anorexia nervosa? A prevalence study. Br J Psychiatry 1976; 128: 549-54. 5. Morgan GH, Russell GFM. Value of family background and clinical features as predictors of long-term outcome in anorexia nervosa: four-year fol- low-up study of 41 patients. Psychol Med 1975; 5: 355-71. 6. Hsu LKG, Crisp AH, Harding B. Outcome of anorexia nervosa. Lancet 1979, i: 61-65. 7 Kay DWK, Leigh D. The natural history, treatment and prognosis of anor- exia nervosa, based on a study of 38 patients. J Ment Sci 1954; 100: 411-31. advance in our understanding of this mystifying ill- ness. The first clear evidence of a disorder of the hypothalamic-pituitary-gonadal axis came from the observation that urinary and blood levels of gona- dotropins and oestrogens are always low or undetec- table.8,9 It was later established that the anterior pituitary remains responsive to the administration of synthetic gonadotropin-releasing hormone (LHRH), as shown by rises in the serum levels of luteinising hormone (LH) and follicle-stimulating hormone (FSH), confirming that the site of the dis- order is in the hypothalamus rather than in the pituitary The loss of weight is undoubtedly an important contributory cause of the endocrine dis- order, as shown by a return to normal hypothala- mic, pituitary, and gonadal activity in a definite sequence after the return to a normal weight. First there is a rise in the circulating levels of LH, FSH, and aestrogens.8,9 Then follows a return of the capacity of the hypothalamus to respond to the negative-feedback effects of oestrogen. And the final step in the sequence is the return of the hypothala- mic response to the positive-feedback effects of oestrogen, with a resulting ovulatory surge of LH and a later resumption of regular menstruation and ovulation." However, this final step in the sequence may be delayed for several months, with persistence of the amenorrhoea despite weight gain. This is additional evidence that non-nutritional factors contribute to the hypothalamic disorder. Their nature is not clear, but a more fundamental disorder of hypothalamic function12 or the effects of the psychological disturbance itselp1 have been proposed. The only endocrine disorder regularly found in anorexia nervosa is that affecting the hypothalamic-pituitary-gonadal axis. In contrast, prolactin activity is normal, thyroid function is only slightly altered,13 and raised growth-hormone levels return to normal on refeeding. 14 How valuable is our new knowledge of the hypothalamic disturbances in the treatment of anorexia nervosa? The administration of LHRH can restore the cyclical secretion of gonadotropin 8. Bell EG, Harkness RA, Loraine JA, Russell GFM. Hormone assay studies in patients with anorexia nervosa. Acta Endocrinol 1966; 55: 140-48 9. Crisp AH, MacKinnon PCB, Chen C, Corker CS. Observations of gonado- trophic and ovarian hormone activity during recovery from anorexia ner- vosa. Postgrad Med J 1973; 49: 584-90. 10. Mortimer CH, Besser GM, McNeilly AS, Marshall JC, Harsoulis P, Tun- bridge WMG, Gomez-Pan A, Hall R. Luteinizing hormone and follicle sti- mulating hormone releasing test in patients with hypothalamic-pituitary- gonadal dysfunction. Br Med J 1973; iv: 73-77. 11. Wakeling A, DeSouza VFA, Beardwood CJ. Assessment of the negative and positive feedback effects of administered oestrogen on gonadotrophin release in patients with anorexia nervosa. Psychol Med 1977; 7: 597-405. 12. Russell GFM. The present status of anorexia nervosa. Psychol Med 1977; 7: 363-67. 13. Wakeling A, DeSouza VFA, Gore MBR, Sabur M, Kingstone E, Boss AMB. Amenorrhœa, body weight and serum hormone concentrations, with par- ticular reference to prolactin and thyroid hormones in anorexia nervosa. Psychol Med 1979; 9: 265-72. 14. Brown GM, Garfinkel PE, Jeuniewic N, Moldofsky H, Stancer HC. Endo- crine profiles in anorexia nervosa. In: Vigersky R, ed. Anorexia nervosa New York: Raven. 1977: 123-35.

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563

Anorexia Nervosa: to Investigate orto Treat?

THE LANCET

THE patient with anorexia nervosa may bereferred for treatment to a psychiatrist, a phys-ician, or a gynaecologist. Whereas the psychiatrist isunlikely to request many diagnostic tests, his col-leagues may pursue exhaustive investigations of en-docrine function. The latter practice has been criti-cised on the grounds that the diagnosis of anorexianervosa is a straightforward matter requiring onlycareful history-taking and physical examination,and that the endocrine disturbances are merelysecondary to the loss of weight. Moreover, these in-vestigations may be time-consuming and may delaythe start of correct treatment. The recent aware-ness of a sharp increase in the incidence of anorexianervosa2-4 and its tendency to run a chronic

course,5,6 has led to a greater sense of urgency toprovide effective treatment. The question at issue,therefore, is whether a conflict need exist betweentreating the patient and investigating her endocrinestatus.

.

In all patients with anorexia nervosa there is evi-dence of an endocrine dysfunction, now known tooriginate in the hypothalamus and not in the an-terior pituitary as was formerly thought. Its mostobvious clinical manifestation in the female is thecessation of menstrual function. (The correspond-ing symptoms in the much rarer male patients area loss of sexual interest and activity.) Theamenorrhoea is often an early symptom which mayprecede the loss of weight7-a finding whichweakens the conclusion that the former is merely aconsequence of the latter. Elucidation of the under-lying endocrine disturbances is a substantial

1. Beumont PJV. The endocrinology of anorexia nervosa. Med J Aust 1979; i:611-13.

2 Theander S. Anorexia nervosa: a psychiatric investigation of 94 female pa-tients. Acta Psychiat Scand 1970; Suppl 214.

3. Kendell RE, et al. The epidemiology of anorexia nervosa. Psychol Med 1973;3: 200-03.

4 Crisp AH, Palmer RL, Kalucy RS. How common in anorexia nervosa? Aprevalence study. Br J Psychiatry 1976; 128: 549-54.

5. Morgan GH, Russell GFM. Value of family background and clinical featuresas predictors of long-term outcome in anorexia nervosa: four-year fol-low-up study of 41 patients. Psychol Med 1975; 5: 355-71.

6. Hsu LKG, Crisp AH, Harding B. Outcome of anorexia nervosa. Lancet1979, i: 61-65.

7 Kay DWK, Leigh D. The natural history, treatment and prognosis of anor-exia nervosa, based on a study of 38 patients. J Ment Sci 1954; 100:411-31.

advance in our understanding of this mystifying ill-ness. The first clear evidence of a disorder of the

hypothalamic-pituitary-gonadal axis came from theobservation that urinary and blood levels of gona-dotropins and oestrogens are always low or undetec-table.8,9 It was later established that the anterior

pituitary remains responsive to the administrationof synthetic gonadotropin-releasing hormone

(LHRH), as shown by rises in the serum levels ofluteinising hormone (LH) and follicle-stimulatinghormone (FSH), confirming that the site of the dis-order is in the hypothalamus rather than in thepituitary The loss of weight is undoubtedly animportant contributory cause of the endocrine dis-order, as shown by a return to normal hypothala-mic, pituitary, and gonadal activity in a definitesequence after the return to a normal weight. Firstthere is a rise in the circulating levels of LH, FSH,and aestrogens.8,9 Then follows a return of the

capacity of the hypothalamus to respond to thenegative-feedback effects of oestrogen. And the finalstep in the sequence is the return of the hypothala-mic response to the positive-feedback effects of

oestrogen, with a resulting ovulatory surge of LHand a later resumption of regular menstruation andovulation." However, this final step in the

sequence may be delayed for several months, withpersistence of the amenorrhoea despite weight gain.This is additional evidence that non-nutritionalfactors contribute to the hypothalamic disorder.Their nature is not clear, but a more fundamentaldisorder of hypothalamic function12 or the effectsof the psychological disturbance itselp1 have beenproposed. The only endocrine disorder regularlyfound in anorexia nervosa is that affecting thehypothalamic-pituitary-gonadal axis. In contrast,prolactin activity is normal, thyroid function is

only slightly altered,13 and raised growth-hormonelevels return to normal on refeeding. 14How valuable is our new knowledge of the

hypothalamic disturbances in the treatment ofanorexia nervosa? The administration of LHRHcan restore the cyclical secretion of gonadotropin

8. Bell EG, Harkness RA, Loraine JA, Russell GFM. Hormone assay studiesin patients with anorexia nervosa. Acta Endocrinol 1966; 55: 140-48

9. Crisp AH, MacKinnon PCB, Chen C, Corker CS. Observations of gonado-trophic and ovarian hormone activity during recovery from anorexia ner-vosa. Postgrad Med J 1973; 49: 584-90.

10. Mortimer CH, Besser GM, McNeilly AS, Marshall JC, Harsoulis P, Tun-bridge WMG, Gomez-Pan A, Hall R. Luteinizing hormone and follicle sti-mulating hormone releasing test in patients with hypothalamic-pituitary-gonadal dysfunction. Br Med J 1973; iv: 73-77.

11. Wakeling A, DeSouza VFA, Beardwood CJ. Assessment of the negative andpositive feedback effects of administered oestrogen on gonadotrophinrelease in patients with anorexia nervosa. Psychol Med 1977; 7: 597-405.

12. Russell GFM. The present status of anorexia nervosa. Psychol Med 1977; 7:363-67.

13. Wakeling A, DeSouza VFA, Gore MBR, Sabur M, Kingstone E, Boss AMB.Amenorrhœa, body weight and serum hormone concentrations, with par-ticular reference to prolactin and thyroid hormones in anorexia nervosa.Psychol Med 1979; 9: 265-72.

14. Brown GM, Garfinkel PE, Jeuniewic N, Moldofsky H, Stancer HC. Endo-crine profiles in anorexia nervosa. In: Vigersky R, ed. Anorexia nervosaNew York: Raven. 1977: 123-35.

564

by the pituitary and induce normal ovulatorycycles in the amenorrhoeic patient. This treatmentis effective even in the underweight patient butsince her mental state does not get better such en-docrine therapy is of limited value. 5 As the basiccause of anorexia nervosa is unknown the best

approach to treatment is an empirical one. Thefirst essential goal is to restore the patient’s weightto normal. This can readily be achieved by trainednursing staff who rely on establishing a therapeuticrelationship with the patient and thus persuade herto accept a food intake of 3000-5000 calories dailyfor six to eight weeks.16 Because the nurses do mostof the work it seems unimportant whether the pa-tient is treated in a medical or a psychiatric unit.In Britain this treatment has been developedmainly in psychiatric units, usually in teachinghospitals because the resources necessary for thismore intensive care are seldom available elsewhere.

- BEUMONTI urges that, as soon as the diagnosis hasbeen established, the patient should be referred forpsychiatric treatment. Thus the first goal of thistreatment, restoring body weight to normal, shouldideally be followed by a second phase aimed attackling underlying psychological disturbances.Some workers maintain that inclusion of psycho-therapeutic measures17 and family therapy18 willimprove the late prognosis by more specifically cor-recting the psychopathology of anorexia nervosa.The evidence is still far from conclusive and thesetreatments merit further investigation-includingwork on their mode of action, if they do proveeffective.

Accident Prevention in Childhood

THE pattern of disease in childhood has altered

greatly in the past few decades, with a reduction inthe amount of infectious disease and a diminutionin the numbers of children handicapped by con-genital abnormality or birth trauma. As a result,accidents emerge starkly as an important cause ofmortality and morbidity. In Britain they are re-sponsible for about - half the deaths of school-children, for one in six of all admissions of childrento hospital, and for the attendance of one-sixth ofinner-city children at their local accident-and-

emergency department every year. Many of the in-

15. Nillius SJ, Wide L. The pituitary responsiveness to acute and chronic admin-istration of gonadotropin-releasing hormone in acute and recovery stagesof anorexia nervosa. In: Vigersky R ed. Anorexia nervosa. New York:Raven. 1977: 225-41.

16. Russell GFM. Anorexia nervosa. In: Beeson PB, McDermott W, Wyn-gaarden JB eds. Cecil’s Textbook of Medicine. 15th ed. Philadelphia:Saunders. 1979: 1699-1703.

17. Bruch H. The eating disorders: obesity, anorexia nervosa and the personwithin. London: Routledge and Kegan Paul. 1974.

18. Minuchin S, et al. A conceptual model of psychosomatic illness in childrenArch Gen Psychiatry 1975; 32: 1031-38.

juries are slight and can be seen as the means

whereby a young child learns some of the dangersof life, but a proportion are the cause of much per-sonal and family distress and handicap.

Health workers have been slow to respond to thechallenge presented by childhood accidents, per-haps feeling that their responsibility begins andends with the management of the injury. In addi-tion, few people have been able to obtain an overallview since orthopaedic surgeons deal with fractures,general surgeons with internal injuries, accident-and-emergency consultants with lacerations,neurosurgeons with head injuries, and poediatri-cians with poisonings. Gradually, however, peedia-tricians and paediatric surgeons have begun to ap-preciate the breadth of the problem, and theMedical Commission on Accident Prevention hastaken an important step in establishing the JointCommittee for Childhood Accident Prevention.The need for a national authoritative body wasfirst recognised in Sweden twenty years ago, whenthe Swedish Joint Committee on the Prevention ofChildhood Accidents was formed and on which theBritish committee is modelled. Although the PublicHealth Committee of the Council of Europe drewattention to the value of such a committee in

1972,1 other European countries have still not

established their national counterpart, as the Euro-

pean Society for Social Paediatrics has latelypointed out to the European Office ofW.H.O.2Many of the efforts in accident prevention work

have been unstructured, the approach being gener-ally "educational". However, there is increasingdoubt about the cost-effectiveness of large-scalecampaigns aimed at altering human behaviour-especially in adult spheres such as seat-belt wearingand drinking and driving. Adults are of course re-sponsible for the environment in which childrenare brought up, as well as for their training andeducation, and it is disappointing that, for ex-

ample, a direct educational approach to mothers inimproving the safety of their homes seemed almostworthless. The Rockland County project,3 in theU.S.A., showed no significant difference be-

tween the "educational" and "control" groups overa three-year period, and a small study by DER-SHEWITZ and WiLLIAMSON4 was similarly discour-aging about the efficacy of a short educational cam-paign. Even when safety propaganda is directedtowards carefully selected target groups the resultsare less than cheering. Several American workershave examined the efficacy of health education in

1. Accidents in childhood as a public health problem. Council of Europe, Stras-bourg, 1972.

2. Anonymous. Research needed on childhood accidents. Lancet 1979; ii: 1093. Schlesinger ER, et al. A controlled study of health education in accident pre-

vention: the Rockland County child injury project. Am J Dis Child 1966.111: 490-96.

4. Dershewitz RA, Williamson JW. Prevention of childhood household injuriesa controlled clinical trial. Am J Publ Health 1977; 67: 1148-53.