Bulimia Nervosa in Thyroid Disorder

Ulrike Schmidt, Geoffrey 0’ Donogh ue

(Accepted 1 December 1990)

We describe three cases, in whom DSM-III-R bulimia nervosa developed subsequent to a thyroid disorder. Neither patient previously had had any eating pathology. Marked weight fluctuations occurred during the pretreatment phase and during treatment of the thyroid dis- order, and seem to have been an important trigger for the patients’ eating disorder. One patient with hypothyroidism abused her prescribed thyroxine in order to induce weight loss.

Thyroid disease typically leads to a disturbance of appetite and changes in weight (Ingbar & Woeber, 1980). Similar symptoms predominate in bulimia nervosa. Thyroid disorder and bulimia nervosa are relatively common, so comorbidity by coincidence should occur frequently. A few such cases have been described (Wong, Birmingham, & Tildesley, 1987; Krahn, 1990; Fonseca, Wakeling, & Harvard, 1990).

The prevalence of eating disorders in another endocrine disorder, diabetes, appears to be above that expected by chance, which has led to speculations that the rapid weight changes following diagnosis and at the beginning of treatment increase the risk for the development of an eating disorder (Steel, Young, Lloyd, & Macintyre, 1989). In a similar fashion one would expect that the weight fluctuations in thyroid disorder may lead to weight preoccupation and an increased risk of developing an eating disorder.

Below we describe three cases, which raise the possibility of such an etiological link between thyroid disorder and bulimia nervosa.

PATIENT 1

Miss L. was a 22 year old student of Hong Kong Chinese origin, the youngest of four siblings. She had a family history of obesity and hyperthyroidism. At age 17 the pa- tient’s weight was stable at 50 kg at a height of 155 cm. Shortly before her A-levels she began to develop a voracious appetite, eating increasingly larger meals, but never feel-

Ulrike Schmidt, Dr. med., M.Phil., M.R.C.Psych., is Research Worker and Honorary Senior Registrar, Institute of Psychiatry, London. Geoffrey O’Donoghue, M.B., B.Ch., D.C.H., M.R.C.Psych., is Senior Registrar and Research Worker, Maudsley Hospital, London. Address reprint requests to Dr. U. Schmidt, Institute of Psychiatry, De Cre- spigny Park, London 5t5 8AZ, England.

international journal of Eating Disorders, Vol. 12, No. 1 , 93-96 (1 992) 0 1992 by John Wiley & Sons, Inc. CCC 0276-3478192101 0093 -O4$04 .OO

Schmidt and O'Donoghue 94

ing full. She also felt hot and sweaty, had shaky hands, and palpitations. Her periods became irregular. Three months after the start of these symptoms she was diagnosed as hyperthyroid and treatment with carbimazole was started. At that point she weighed 56 kg. In order to lose some weight she exercised vigorously. Despite this, her weight increased to 59 kg over the next 6 months. She began to induce vomiting and also started to binge two to three times a day, eating large amounts of sweets. Her weight gradually settled back to its premorbid level of 50 kg. She stopped taking carbi- mazole 9 months later and was discharged from the endocrinology clinic in a euthyroid state. Bingeing and vomiting persisted, and she continued to be very worried about her weight and appearance. Two years later she told her General Practitioner about her eating disorder and was then referred for treatment.

PATIENT 2

Mrs. F. was a 42 year old divorced secretary with two adult sons. On presentation she weighted 73 kg at a height of 163 cm. She had a family history of obesity. Her problems had started 8 years previously. Until then she had weighed 60 kg. A bout of flu left her feeling ill, exhausted, and depressed. She lost 3 kg in weight. Laboratory investigations revealed hyperthyroidism. Treatment with carbimazole and thyroxine was started. Following this she began to binge-eat regularly several times per week and her weight increased by 15 kg to 72 kg over the next 6 months. Her weight gain was accompanied by increasing depression. She was treated with amitryptiline and a behavioral treatment program for her eating disorder, and made a partial recovery. She remained on carbimazole and thyroxine for 5 years. When these drugs were with- drawn she remained euthyroid. A year later she had a relapse of bingeing alternating with self-starvation. In addition, she had started to induce vomiting and was taking laxatives. She suspected that she might have again become hyperthyroid, but this was not the case.

PATIENT 3

Miss P. was a 26 year old single nurse who presented at a weight of 63 kg and a height of 160 cm. Until the age of 14 she had been slim. She then gained weight and her clothes size increased from size 10 to size 14. She tried to induce vomiting after meals but was unsuccessful. From age 16 onwards she went on different diets, but her weight continued to increase. At age 19 she reached 77 kg. A year later she was found to have type IIa familial hypercholesterinemia after the same diagnosis had been made in her mother. (Several other members of her family also suffered from this condition.) At the same time hypothyroidism was diagnosed. She was treated with thyroxine (150 micrograms) and lipid-lowering agents including cholestyramine, probucol, gemfi- brozil, and bezafibrate. She was also prescribed a low cholesterol diet. Over the next 3 years her weight fell to 67 kg. She became euthyroid, but her cholesterol levels re- mained high (up to 11.7 mmol/liter) despite treatment. She smoked regularly despite strict medical advice to the contrary.

Bulimia Nervosa in Thyroid Disorder 95

From age 23 onwards she began to take more than her prescribed dose of thyroxine as she realized that this made her lose weight. She also dieted, weighed herself several times a day, and felt guilty after eating. At age 24 she reached her lowest adult weight of 48 kg. She became amenorrheic for 6 months. At that point she was taking up to 250 micrograms of thyroxine daily. Her thyroid function tests were noticed to be abnormal (T4: 229 nmol/liter; thyroid stimulating hormone (TSH): 0.2 X lop3 IU/liter). She was advised to reduce her prescribed dose of thyroxine but she continued to take 250 mi- crograms daily. She was depressed, irritable, and experienced fleeting ideas of being attacked by strangers. She saw a psychiatrist who prescribed phenelzine (15 mg t.d.s.), on which her depression improved. Soon she began to have urges to overeat and would binge for days on end. Her weight increased by 12 kg to 60 kg over 3 months. She stopped the phenelzine and increased her thyroxine to 400 micrograms a day. Her depressive symptoms recurred. She was constantly tearful and unable to cope at work. Amitriptyline was started, which was later changed to trazodone. Her mood then lifted and for the first time she admitted to having abused thyroxine and to having an eating disorder. At present her eating behavior fluctuates between episodes of bingeing and episodes of severe food restriction. She continues to take more thyroxine than pre- scribed, and has also started to induce vomiting.

DISCUSSION

Unlike the earlier case reports, these subjects developed DSM-III-R bulimia nervosa after the onset of thyroid disease. Marked weight fluctuations during the pre-treatment phase and during treatment of the thyroid disorder preceded the onset of the eating disorder and seem to have been an important trigger for it, similar to the precipitants in diabetes mellitus. In case 3 the patient’s preoccupation with weight was reinforced by the treatment of her hyperlipidemia with a low fat diet and avoidance of obesity.

In all three cases the eating disorder persisted beyond the resolution of the original thyroid problem, and required treatment in its own right.

We suspect that many similar cases go unnoticed, as bulimic patients rarely sponta- neously report their symptoms. In our cases 1 and 3 the patients’ eating disorder went unrecognized for several years despite ongoing medical supervision. Our hypothyroid patient (case 3) continued to abuse thyroxine for over 3 years despite her professional knowledge of its dangers, accompanying marked depression, repeated laboratory evi- dence of raised thyroxine levels, and her physicians’ advice to reduce her thyroid med- ication. The deliberate abuse of thyroxine in order to induce weight loss in normal weight bulimia nervosa has been noted before (Fornari, Edleman, & Katz, 1990). It must be extremely tempting for patients with hypothyroidism struggling with their weight to abuse their medication in this way.

Clearly, on the basis of a small case series like the one presented here, one can reach no definite conclusions about these issues: it is possible that the coincidence of these two conditions is merely that expected by chance in two common disorders. An epide- miological study of eating disorders in thyroid disorders may answer these questions more fully.

We would like to thank Prof. G. Russell and Dr. Robin Jacoby for their permission to report these cases and Dr. Janet Treasure for her helpful comments on the manuscript.

96 Schmidt and O'Donoghue

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