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Recovery from anorexia nervosa: a Durkheimian interpretation.

Attempts to explain "eating disorders" in contemporary western society have concentrated on aetiology at the expense of resolution. Most "recovered" anorectics, however, question medical definitions of "anorexia nervosa" and clinical criteria for recovery. This article refers to a study of 32 people at different stages of the recovery process, to reconceptualize the problem in sociological terms. Durkheim's account of asceticism offers a fresh interpretive framework in which anorexia and recovery are understood as the negative and positive phases respectively of a ritual of self-transformation. In western culture, where appropriate myths and rituals of re-incorporation are not readily available following a period of symbolic fasting, it is not surprising that recovery from anorexia is not automatic. Participants in this study referred to anorexia as a spiritual quest and for them recovery involved a re-discovery (or creation) of a threefold connection: inner, with others and with "nature". These connections are, for them, the defining features of spirituality. The negative phase of the ritualistic quest (anorexia) involves a confrontation with the inevitability of death as a condition of the positive phase (recovery) in which people actively choose life. This new theoretical approach provides a non-medicalized understanding of anorexia and simultaneously enables a re-interpretation of the fasting of medieval women saints. Recent scholarship in this area is re-evaluated to demonstrate that the continuity between asceticism and anorexia lies in the use of food as a metaphorical attempt to confront the universal problem of one's own mortality. In certain historical situations, asceticism served a socially valuable symbolic purpose. In contemporary society, however, this meaning is no longer available. Instead, it is recovery which constitutes the active and metaphorical "rebellion" against forces of social control. Finally, the work of Van Gennep is used to explore some of the specific ritual processes through which people effect the self-transformation from suffering to recovery, providing further insights into how recovery takes place from a wide range of other sufferings as well.

Anorexia Nervosa↗

Lack of association between anorexia nervosa and D3 dopamine receptor gene.

BACKGROUND: Evidence from family and twin studies suggests a genetic contribution to the etiology of anorexia nervosa. Different genes could contribute to the vulnerability to anorexia nervosa, but dopamine could be more specifically implicated in anorexia nervosa because of pharmacologic, endocrine, and neurobiological specificities. The dopamine receptor D3 (DRD3) may be of additional interest, since it is specifically located in the limbic area, an area implicated in reward and reinforcement behavior. METHODS: We performed an association study between 39 patients with severe (requiring hospitalization and with young age at onset) anorexia nervosa (DSM-III-R), and 42 controls, with the Bal I polymorphism in exon I of the DRD3 gene. RESULTS: There was no significant difference between patients with anorexia nervosa and controls in allele frequencies or genotype count. The association was still negative between subgroups separated according to family history of anorexia nervosa or comorbid mood disorders. CONCLUSIONS: Despite the fact that the number of patients tested is small, there is good evidence that the Bal I DRD3 polymorphism does not play a major role in the genetic component of anorexia nervosa. It would be useful to test polymorphisms of the other genes coding for dopamine receptors.

Adolescent↗

Plasma concentrations of interleukin-1-beta, interleukin-6 and tumor necrosis factor-alpha, and of their soluble receptors and receptor antagonist in anorexia nervosa.

Interleukin-1beta (IL-1beta), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) induce anorexia, and multiple behavioral and biochemical alterations that mimic those of anorexia nervosa. Reports in the literature, however, contain contrasting data on the pattern of secretion of the three cytokines and on the downstream activities of their receptors and receptor antagonists in anorexia nervosa. We measured plasma concentrations of IL-1beta, IL-6, TNF-alpha, soluble IL-6 receptor (sIL-6-R), soluble TNF-alpha receptors I and II (s-TNF-alpha-R-I and II), and soluble IL-1beta receptor antagonist (s-IL-1beta-R-A) in 14 female patients with anorexia nervosa (nine restricters, five binge/purgers) and in 13 age- and sex-matched healthy control subjects to see whether the circulating cytokine concentrations and the downstream steps of cytokine activity were impaired, and if these alterations were correlated with some aspects of the disease. Concentrations of IL-1beta, IL-6, TNF-alpha, s-TNF-alpha-R-I and -II and sIL-1beta-RA in plasma did not differ significantly in patients with anorexia nervosa compared with control subjects. Concentrations of sIL-6-R were significantly lower in the patients than in the control subjects, but there were no differences between the two sub-types of anorexia nervosa. The etiopathogenetic significance of the sIL-6-R alteration is not clear, but together with recent data in the literature on cytokine function, the finding suggests that an impairment of the pro-inflammatory cytokine pathway might be involved in the development of anorexia nervosa.

Adolescent↗

[Cardiac disorders in young women with anorexia nervosa].

INTRODUCTION AND OBJECTIVES: The objective of this study was to compare heart abnormalities in young women with anorexia nervosa and in a control group of the same age and sex. Patients and method. We report a matched case-control study of 30 adolescents with anorexia nervosa and 30 healthy women of the same age with normal weight. An electrocardiogram and echocardiogram were done. Heart parameters were measured on the electrocardiographic tracings, and QT dispersion was defined as the difference between maximum QT and minimum QT in any of the 12 leads. Diameter, mass and left ventricular mass index were measured. RESULTS: QT and corrected QT intervals were significantly greater in patients with anorexia nervosa than in the control group. QT dispersion and corrected QT dispersion were significantly greater in anorexia nervosa than in the control group (QTd, 59.3 23.0 vs 38.4 8.0 ms; p = 0.000; QTcd, 56.5 24.2 vs. 40.3 21.8 ms; p = 0.011). Left ventricular mass was significantly lower in young women with anorexia nervosa. We found a significant relationship between body mass index and left ventricular mass index, and between the former and corrected QT dispersion. CONCLUSIONS: Adolescents with anorexia nervosa show significant cardiac disorders in comparison to healthy women of the same age. This finding may be a useful indicator of the risk of arrhythmia and sudden death in patients with anorexia nervosa.

Adolescent↗

Update on anorexia and cachexia.

Declining physical, emotional, and social function as a result of anorexia and cachexia are considerable contributors to discomfort for cancer patients and their families, and they impair the patient's ability to express optimal physical and psychosocial potential as long as possible. This decline no longer has to be accepted as an indispensable sequel to advanced cancer, just as pain is no longer considered to be unavoidable. A routine screening for anorexia and cachexia and associated symptoms is necessary, as is a careful, comprehensive assessment, because the condition is not always obvious. Decisions about anorexia and cachexia treatment are guided by prioritizing the different, concurrent physical, psychosocial, and existential problems and by considering the natural course of the cancer and the effects of antineoplastic therapies. Reversible causes for anorexia and cachexia need to be identified and treated, if appropriate. Nutritional interventions are often indicated; patients with a predominant starvation component and without inflammation may profit the most. New pharmacologic therapies for primary anorexia and cachexia syndrome are expected to enter clinical practice soon; however, until then, treatment with corticosteroids, progestins, or prokinetics may be indicated for some patients. To understand a multicausal syndrome, multimodal and interdisciplinary therapy is required. Specialist palliative care services can be helpful to provide, hand-in-hand with the disease specialists [172], assessment and management of psychophysical symptoms and sociospiritual needs of patients during the course of the illness and at the end of life [173]. Research efforts aim to better characterize subgroups of patients suffering from secondary causes of anorexia and cachexia and to elucidate the mechanisms involved in the primary anorexia and cachexia syndrome. Increasingly individualized treatments are expected with combination treatments that involve different mechanisms including nutrition.

Anorexia↗

Genetic factors in anorexia nervosa.

Anorexia nervosa is a severe and complex disorder with incompletely known vulnerability factors. It is generally recognized that anorexia nervosa is a familial disorder, but the majority of twin studies have shown that the concordance rate for monozygotic twins is higher (on average 44%) than for dizygotic twins (on average 12.5%). This difference in concordance rates shows that genetic factors, more than common familial environment, may explain why the 'anorexia nervosa' phenotype runs in families. In order to estimate the heritability in the broad sense of anorexia nervosa according to published familial and twin studies, we first assessed the intrapair correlation between monozygotic and dizygotic twins, and secondly calculated the deviation threshold of relatives of affected probands from the relative mean. In this review, we obtained an estimation of the heritability at 0.72 according to all published controlled familial studies (six references quoted in MEDLINE(R)), and 0.71 for all published twin studies (59 references quoted in MEDLINE(R)). This estimation is close to the ones previously proposed, between 0. 5 and 0.8. Familial and twin studies may also help to define the boundaries of the phenotype, shedding light on the complex relationship between anorexia nervosa on the one hand, and bulimia nervosa, mood disorders, and alcoholism on the other. Demonstrating the importance of genetic factors in anorexia nervosa, and more specifically for anorexia of the restrictive type, requires not only prospective and adoption studies (which are still lacking), but also genetic polymorphisms analyses, which began very recently.

Anorexia Nervosa↗

Socio-cultural factors in the development of anorexia nervosa.

A population of professional dance (N = 183) and modelling (N = 56) students, who by career choice must focus increased attention and control over their body shapes, was studied. Height and weight data were obtained on all subjects. In addition, a questionnaire that is useful in assessing the symptoms of anorexia nervosa, the Eating Attitudes Test (EAT), was administered. Results of these tests were compared with those of normal female university students (N = 59), patients with anorexia nervosa (N = 68), and music students (N = 35). Anorexia nervosa and excessive dieting concerns were overrepresented in the dance and modelling students. Twelve cases (6.5%) of primary anorexia nervosa were detected in the dance group. All but one case developed the disorder while studying dance. Within the dance group those from the most competitive environments had the greatest frequency of anorexia nervosa. These data suggest that both pressures to be slim and achievement expectations are risk factors in the development of anorexia nervosa. The influence of socio-cultural determinants are discussed within the context of anorexia nervosa as a multidetermined disorder.

Anorexia Nervosa↗

Energy expenditure and physical activity in relation to bone mineral density in women with anorexia nervosa.

OBJECTIVES: To assess sleeping metabolic rate (SMR), average daily metabolic rate (ADMR), and total bone mineral density (TBMD) in women with anorexia nervosa, and to evaluate the effect of daily physical activity on TBMD. DESIGN: We compared women with anorexia nervosa and controls using measurements on body composition, and energy expenditure. Relations between these measurements were investigated. SETTING: Daily living environments in The Netherlands, and body composition and energy expenditure laboratory of the Department of Human Biology. SUBJECTS: Twelve adult, non-hospitalized women with anorexia nervosa, and sixteen adult normal weight women. INTERVENTIONS: Average daily metabolic rate was measured with the doubly labeled water method and sleeping metabolic rate in a respiration chamber. TBMD was measured by dual energy X-ray absorptiometry, and percentage body fat was calculated combining the results from underwater weighing and deuterium dilution. RESULTS: TBMD was significantly lower in anorexia than in controls (0.989 +/- 0.081 vs 1.144 +/- 0.054 g/cm2). Also ADMR and SMR were reduced in anorexia. The physical activity index (PAI = ADMR/SMR) was not significantly different from PAI in controls. In anorexia, TBMD was related to the PAI (R2 = 0.35, P < 0.05). Finally, stepwise multiple regression revealed that PAI together with the study groups as dummy variables could explain 69% of the variation in TBMD. CONCLUSION: These findings show that in anorexia TBMD is reduced, but that nonetheless physical activity has a significant positive effect on bone density.

Absorptiometry, Photon↗

Absence of desensitization by hexarelin to subsequent GH releasing hormone-mediated GH secretion in patients with anorexia nervosa.

OBJECTIVE: Both the basal levels and the neuroregulation of GH secretion are perturbed in patients with anorexia nervosa. It is unknown if these alterations are due to severe undernutrition or if they reflect basic neurotransmitter alterations of the patient's neural pathways. On the other hand, prior administration of the GH secretagogue hexarelin in normal subjects blocks the GH-releasing capability of GH releasing hormone (GHRH) administered 2 hours later. In the present work a sequential test was performed using the administration of hexarelin as first stimulus followed 120 minutes later by GHRH. The two aims of the study were: (a) to evaluate the interaction of GHRH and hexarelin, and (b) to further understand the alterations in GH neuroregulation in patients with anorexia nervosa. DESIGN: The GH stimuli used were hexarelin (1 micrograms/kg i.v.), a GH stimulus whose main action is hypothalamic, followed 120 minutes later by GHRH (1 micrograms/kg i.v.) as a pituitary stimulus. Each woman was tested once. PATIENTS: Thirty-two woman matched for age participated in the study: six normal-weight women as controls, 14 women with anorexia nervosa, seven women with secondary amenorrhoea due to voluntary weight loss for aesthetic reasons, and five normal-weight women after 72 hours of a controlled hypocaloric diet (800 cal/day). MEASUREMENTS: Plasma GH levels were measured by time-resolved fluoroimmunosasay, each value shown is the mean +/- SE in mU/l. RESULTS: The administration of hexarelin to the normal-weight women induced a clear-cut GH secretion (expressed as mean +/- SE of GH peak in mU/l of 77.5 +/- 21.8, but blocked the GH-releasing capability of GHRH administered 120 minutes later (6.6 +/- 2.8, P < 0.05). In contrast, the women with anorexia nervosa showed a normal GH response after the two stimuli: hexarelin 64.8 +/- 9.2. GHRH 71.1 +/- 14.2. The absence of heterologous desensitization was specific to anorexia nervosa, because the women with amenorrhoea due to voluntary weight loss but with a normal energy intake showed a pattern similar to the controls (GH after hexarelin 60.3 +/- 9.5 and to GHRH 120 minutes later 6.2 +/- 1.0 (P < 0.05)). Similarly, the women after the short-term hypocaloric diet showed a hexarelin-mediated GH secretion of 99.6 +/- 17.8, which blunted the subsequent administration of GHRH (GH mean peak of 9.9 +/- 2.9, P < 0.05 vs hexarelin). CONCLUSIONS: In the normal subjects, the administration of hexarelin induced clear-cut GH secretion, but inhibited the action of GHRH when administered 120 min later, while this heterologous desensitization was not observed in the patients with anorexia nervosa. This sequentially delayed test may be of some value in the clinical setting for assessing the status of patients with anorexia nervosa.

Adult↗

Body composition in adolescents with anorexia nervosa.

BACKGROUND: Malnourished patients with anorexia nervosa have altered body composition characterized by depletion of fat and fat-free mass. OBJECTIVES: The objectives of this study were to assess the body composition of adolescents with anorexia nervosa compared with that of control subjects and to investigate the relation between simple anthropometric measures and reference techniques for measuring body composition. DESIGN: Twenty-three adolescent females with anorexia nervosa aged 15.46 +/- 1.34 y (x +/- SD) were studied. Body composition was measured by anthropometry, dual-energy X-ray absorptiometry (DXA) (for body fat), and prompt gamma in vivo neutron activation analysis [for total body nitrogen (TBN)]. Twenty-five female subjects provided the control DXA data. TBN measurements were compared with prediction equations based on sex, height, age, and weight. RESULTS: Anorexia nervosa patients had significantly lower weight (40.2 +/- 4.6 kg), body mass index (in kg/m(2): 15.3 +/- 1.2), percentage of body fat (DXA) (13.8 +/- 5.8%), percentage of TBN predicted for age (73 +/- 10%), trunk fat (2.1 +/- 1.0 kg), leg fat (2.6 +/- 1.1 kg), and trunk-to-leg fat ratio than did control subjects (P < 0.05). In anorexia nervosa patients, significant correlations were found between triceps skinfold thickness and percentage of body fat (r = 0.83), body mass index and percentage of body fat (r = 0.46), and body weight and TBN (r = 0.84, P < 0.05). CONCLUSIONS: Hospitalized adolescent females with anorexia nervosa are depleted of total body fat and protein. We identified 3 simple anthropometric measures (triceps skinfold thickness, BMI, and body weight) that can be used to assess body composition and nutritional status in malnourished adolescents with anorexia nervosa.

Absorptiometry, Photon↗

The growth hormone response to insulin induced hypoglycaemia in anorexia nervosa and control underweight or normal subjects.

Hypoglycaemic stimulation of growth hormone (GH) secretion has been measured in 12 anorexia nervosa patients, 11 adolescents approximately matched for weight and age, 14 underweight adults with no history of anorexia nervosa and 27 normal patients. The results showed a high proportion of blunted growth hormone responses among the anorexia nervosa patients as compared to normal subjects, underweight adolescents or adults. In the group of underweight adults, diminshed growth hormone responses were most frequently seen in patients with depressive illness. The complex pathogenesis of the diminshed growth hormone response in anorexia nervosa involves many factors; undernutrition itself, possible hypothalamic insufficiency related to the psychopathological background and other endocrine abnormalities like hypogonadism, relative hypercorticism and hypothyroidism. The interference of the nutritional, psychological and endocrine factors could not be dissociated in our investigation or from the review of the literature on this subject. It is suggested that hypothalamic insufficiency plays a prominent role in the growth hormone hyporesponsiveness in anorexia nervosa. Although diminished, the stimulated growth hormone response remains higher in anorexia nervosa than in true hypopituitarism. This phenomenon coupled to a preserved or even increased suprarenal function enables one to differentiate cachexia resulting from anorexia nervosa and hypopituitarism leading eventually to cachexia.

Adolescent↗

Anorexia induced by the parasitic nematode, Nippostrongylus brasiliensis: effects on NPY and CRF gene expression in the rat hypothalamus.

Infections of the gastrointestinal nematode, Nippostrongylus brasiliensis, in the laboratory rat result in a characteristic biphasic anorexia which is followed by hyperphagia once the worm burden has been cleared. Despite the importance of parasite-induced anorexia, relatively little is known of the underlying mechanisms. We have investigated the involvement of the central appetite drive in this anorexia by studying the gene expression of two neuropeptides with opposing actions on energy balance, NPY and CRF. Gene expression was assessed by in situ hybridization at 2, 8 and 16 days post-infection (p.i.) in infected rats, in uninfected controls, and in a group with food intake restricted to match that taken voluntarily by the parasitize animals. The sampling intervals corresponded to each of the two phases of maximum anorexia and the period of compensatory hyperphagia. Surprisingly, we found that increases in NPY gene expression in the hypothalamic arcuate nucleus (ARC) accompany anorexia in rats infected with N. brasiliensis; there was a significant relationship between degree of anorexia and induction of NPY mRNA after 8 days of infection. Furthermore, ARC NPY mRNA levels in parasitized animals were similar to those in pair-fed individuals with food intake restricted to match the infected rats. The number of larvae used to establish the infection affected both the degree of anorexia and the level of NPY mRNA at 8 days p.i. in a dose-dependent manner. NPY gene expression remained elevated in infected rats during at least the initial stages of compensatory hyperphagia. This suggests that animals detect a state of energy deficit during the early stages of the infection, yet do not feed, but become hyperphagic coincident with worm loss. The failure of anorectic parasitized animals to feed in response to activation of the NPYergic system makes this a novel system in which to study the regulation of hypothalamic NPY by physiological challenge. There were no significant differences in CRF gene expression between the groups at any of the sampling intervals.

Animals↗

Birth outcomes and pregnancy complications in women with a history of anorexia nervosa.

OBJECTIVE: To examine birth outcomes and pregnancy complications in women with a history of anorexia nervosa. DESIGN: Prospective cohort study. SETTING: Nationwide study in Sweden. POPULATION: All primiparous women--discharged from hospital with a diagnosis of anorexia nervosa during 1973 to 1996--who gave birth during 1983 to 2002 (n = 1000) were compared with all non-anorexia nervosa primiparous women who gave birth during the same years (n = 827,582). METHOD: Register study with data from Medical Birth Registry and National Patient Discharge Register. MAIN OUTCOME MEASURES: Pre-eclampsia, instrumental delivery, prematurity, small for gestational age, birthweight, Apgar score and perinatal mortality. RESULTS: Main birth outcome measures in women with a history of anorexia nervosa were very similar to the main population. The only observed differences were a slightly lower mean birthweight and lower adjusted odds ratios for instrumental delivery in the anorexia nervosa group compared with the main population. Neither severity of the disease nor a shorter recovery phase after first hospitalisation was related to pregnancy complications or birth outcomes. CONCLUSION: A history of anorexia nervosa was not associated with negative birth outcomes. Thus, special obstetric monitoring of pregnant women with history of anorexia nervosa does not seem to be warranted in a country with a satisfactory maternity surveillance.

Adolescent↗

Normal gastric antral myoelectrical activity in early onset anorexia nervosa.

Anorexia, epigastric discomfort, nausea, and vomiting may result from disordered gastric motility and emptying. These features have been found in many adults with anorexia nervosa, but have never been investigated in early onset anorexia nervosa. In 14 patients with early onset anorexia nervosa (eight of whom had upper gastrointestinal tract symptoms), six children with other eating disorders, four children with non-ulcer dyspepsia, and 10 controls matched for age and sex, the non-invasive technique of surface electrogastrography was used to measure fasting and postprandial gastric antral electrical control activity, which underlies antral motility. The electrical signal was recorded by four bipolar silver/silver chloride electrodes attached to the upper abdomen, amplified and low pass filtered at 0.33 Hz before being displayed on a polygraph, digitised at 1 Hz, and stored on the hard disk of a personal computer for later offline analysis. Patients with non-ulcer dyspepsia had gastric antral dysrhythmias. No significant difference was found in the mean (SD) dominant frequency of the antral electrical control activity between patients with early onset anorexia nervosa (2.86 (0.35) cycles/minute (cpm)), patients with other eating disorders (3.14 (0.65) cpm), and controls (3.00 (0.46) cpm). The amplitude of electrical control activity increased postprandially in all but one subject and the fasting/postprandial amplitude ratio did not significantly differ between patients with early onset anorexia nervosa and controls, though patients with longer established disease had a smaller increase in amplitude. Gastric antral electrical dysrhythmias are not a feature of early onset anorexia nervosa and therefore do not induce or perpetuate food refusal in this disorder.

Adolescent↗

Cardiac abnormalities in young women with anorexia nervosa.

OBJECTIVE: To identify the characteristics of cardiac involvement in the self-induced starvation phase of anorexia nervosa. METHODS: Doppler echocardiographic indices of left ventricular geometry, function, and filling were examined in 21 white women (mean (SD) 22 (5) years) with anorexia nervosa according to the DSMIII (Diagnostic and Statistical Manual of Mental Disorders) criteria, 19 women (23 (2) years) of normal weight, and 22 constitutionally thin women (21 (4) years) with body mass index < 20. RESULTS: 13 patients (62%) had abnormalities of mitral valve motion compared with one normal weight woman and two thin women (p < 0.001) v both control groups). Left ventricular chamber dimension and mass were significantly less in women with anorexia nervosa than in either the women of normal weight or the thin women, even after standardisation for body size or after controlling for blood pressure. There were no substantial changes in left ventricular shape. Midwall shortening as a percentage of the values predicted from end systolic stress was significantly lower in the starving patients than in women of normal weight: when endocardial shortening was used as the index this difference was overestimated. The cardiac index was also significantly reduced in anorexia nervosa because of a low stroke index and heart rate. The total peripheral resistance was significantly higher in starving patients than in both control groups. The left atrial dimension was significantly smaller in anorexia than in the women of normal weight and the thin women, independently of body size. The transmitral flow velocity E/A ratio was significantly higher in anorexia than in both the control groups because of the reduction of peak velocity A. When data from all three groups were pooled the flow velocity E/A ratio was inversely related to left atrial dimension (r = -0.43, p < 0.0001) and cardiac output (r = -0.64, p < 0.0001) independently of body size. CONCLUSIONS: Anorexia nervosa caused demonstrable abnormalities of mitral valve motion and reduced left ventricular mass and filling associated with systolic dysfunction.

Adult↗

The clinical features of late onset anorexia nervosa.

This study examines clinical features of late onset anorexia nervosa. This involved the scrutiny of a large database of patients with anorexia nervosa comprising data gathered at standardized initial assessments over the period 1960-1990. Patients with a late onset were compared to other selected patient samples. The population comprised 12 patients with a first onset of anorexia nervosa at or after the age of 30, 415 patients with an onset after 15 but before 20 and 9 patients with an onset after 15 but before 20 and matched for age at presentation with the late onset group. Features studied included age at menarche, age at onset of anorexia nervosa, age at presentation, duration of illness, weight at presentation, lowest adult weight, highest weight, weight at onset of illness, marital status and parity. Patients with an onset of anorexia nervosa after the age 30 comprised 2% of the total female patient sample. Though such patients were rare, their clinical features were very similar to those of typical patients with adolescent onset. Notably, young and late onset patients had similar durations of illness prior to presentation, and similar proportions had bulimia and defensive vomiting. Feared sexuality, no longer necessary for childbearing, emerged as being of apparent aetiological significance in the late onset group, with the disorder embodying its rejection, as often also seems to be the case with earlier onset. The late onset cases were hard to diagnose and had a poor outcome. The study underlines the importance of considering the diagnosis of anorexia nervosa in older patients, even if there is no earlier history of anorexia nervosa. Such patients are likely to find it easier to conceal the psychological origins of their problem behind the possibility of a primary physical illness, or behind psychiatric diagnoses such as depression, the treatment of which may not threaten their avoidance of normal body weight.

Adult↗

LPS-induced anorexia in leptin-deficient (ob/ob) and leptin receptor-deficient (db/db) mice.

Administration of endotoxin (lipopolysaccharide, LPS) induces profound anorexia. Injection of leptin decreases food intake in mice. Recently, we reported that LPS and cytokines increase leptin levels in hamsters. To further investigate the role of leptin in the LPS-induced anorexia, we administered LPS to leptin receptor-deficient (db/db) and leptin-deficient (ob/ob) mice. We found that LPS caused anorexia in both db/db and ob/ob mice. As might be predicted if leptin had a role in anorexia, the db/db mice were somewhat resistant to LPS-induced anorexia. However the ob/ob mice were more sensitive to LPS-induced anorexia. No differences between db/db and ob/ob mice and their respective littermate were observed in circulating tumor necrosis factor levels after LPS. These data suggest that leptin per se is not essential for LPS-induced anorexia.

Analysis of Variance↗

Anorexia nervosa in monozygotic twins.

Which is more important, hereditary factors or psychological environment factors, in the etiology of anorexia nervosa? The question is studied by considering 7 cases of anorexia nervosa in monozygotic twins of the authors' own practice. In 5 of 7 cases, only 1 of a set of twins was found to be suffering from anorexia nervosa. On the other hand, in 2 of 7 cases, both twins were diagnosed as having anorexia nervosa. Even in the concordant cases studied by the authors, however, the quality or degree of anorexia nervosa in each case was different. Therefore, even given the existence of concordant cases, without inquiring precisely into the quality or degree of anorexia nervosa, it is not possible to conclude that hereditary factors play a determining role in the etiology of anorexia nervosa.

Adolescent↗