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PubMed1988

Determinants of delayed gastric emptying in anorexia nervosa and bulimia nervosa.

Gastric emptying was measured using a gamma camera in 22 patients with anorexia nervosa, in 10 patients of normal or high weight with bulimia nervosa and in 10 controls. Patients with anorexia nervosa were tested (1) while underweight and selecting their own diet (10 patients); (2) underweight, but receiving an adequate diet on an inpatient unit (refeeding diet) (12 patients); and (3) under refeeding diet conditions after weight gain (eight patients). Three meals, each labelled with technetium 99m-sulphur colloid, 3.7 MBq were used: (1) a mixed solid meal containing labelled poached egg; (2) 200 ml d-glucose solution, 0.5 kcal/ml, and (3) 200 ml physiological saline. Only gastric emptying rates of the solid meal and glucose solution were significantly delayed. Gastric emptying of saline was normal. The gastric disturbance was confined to patients with anorexia nervosa selecting their own diet. Patients receiving adequate nutrition on the ward had normal gastric emptying and weight gain in this group had no significant effect on emptying. Slow emptying was observed in patients who maintained a low weight solely by food restriction as well as in patients whose anorexia nervosa was complicated by episodes of bulimia. Thus, slow gastric emptying occurred when the quantity of food reaching the duodenum was sufficiently reduced to result in severe weight loss. Moreover, abnormal gastric emptying was seen only after the two meals that contained calories and were hypertonic to plasma, either of which properties could mediate the disturbance. Gastric emptying in bulimia nervosa was normal. Slow gastric emptying could exacerbate undereating in starving patients with anorexia nervosa by enhancing satiety.

Adult↗
PubMed2000

Causes of anorexia in untreated hyperthyroidism: a prospective study.

Seventeen consecutive patients (mean (SD) 46 (11) years) with untreated hyperthyroidism and anorexia and 29 patients (35 (9) years) with untreated hyperthyroidism without anorexia were studied. The study was conducted at the thyroid clinic of the PUMC Hospital, Beijing, China from March to August 1997. The patients' ages, serum free calcium, liver function and emotional state, specifically the level of anxiety (using the self anxiety scale, Chinese version), were compared before and/or after antithyroid drug treatment in the two groups. This prospective study suggested that the causes of anorexia in untreated hyperthyroidism are complicated. Older age, abnormal liver function, and the level of anxiety are significantly related to anorexia in untreated hyperthyroidism, but hypercalcaemia was not confirmed to be related to anorexia in the study.

Adult↗
PubMed1978

Anorexia nervosa: recent investigations.

In this paper, I have: 1. described the typological diagnosis of anorexia nervosa, 2. discussed recent hematological, lipid, electrolyte, gastrointestinal, and electrocardiographic studies in anorexia nervosa, and 3. reviewed recent endocrine investigations including thyroid, adrenal cortical, gonadotropin, growth hormone, and catecholamine studies in anorexia nervosa. Although all of the reviewed studies have contributed greatly to the formation of descriptive criteria for anorexia nervosa, they have not supported any single hypothesis concerning the etiology of anorexia nervosa. Further studies are needed to ascertain relationships between the typical anorectic behavior and the endocrine and catecholamine changes observed in this disorder.

Adolescent↗
PubMed1989

Anorexia induced by interleukin 1: involvement of corticotropin-releasing factor.

It has recently been demonstrated by three independent research groups including ours that interleukin 1 (IL-1), a polypeptide hormone produced by activated monocytes or macrophages, or both, stimulates the release of hypothalamic corticotropin-releasing factor (CRF). Since CRF acts centrally in the brain to reduce food intake, we hypothesized that IL-1 might induce anorexia through this central action of CRF. The present study was carried out to examine the hypothesis, using male Wistar rats. Based on three lines of evidence, we report here that IL-1, both endogenously released and exogenously administered, induces the suppression of food intake in rats and that endogenous CRF in the brain is involved in the IL-1-induced anorexia. First, lipopolysaccharide (LPS), a potent stimulant of the release and production of endogenous IL-1, caused anorexia in a dose-related manner, and this effect was significantly blocked by pretreatment with glucocorticoid hormones, which have been shown to inhibit the production of endogenous IL-1 by LPS. Second, intraperitoneal injection of IL-1 resulted in a dose-related suppression of food intake. Third, anorexia induced by IL-1 was diminished by the immunoneutralization of endogenous CRF in the brain. These results provide further evidence of the existence of bidirectional communication between the immune and neuroendocrine systems. Furthermore, this connection between IL-1 and CRF may represent a mechanism by which anorexia results from the activation of the immune system by such immunological challenges as acute infectious diseases.

Animals↗
PubMed1996

Dissociation of temperature changes and anorexia after experimental colitis and LPS administration in rats.

The acute phase of inflammation induces both anorexia and fever. Because several analyses suggest a linkage between the meal size and body temperature, we assessed whether temperature changes were causal to anorexia in situations involving acute inflammation. Specifically, we evaluated whether elevations of body temperature could account for the reduced food intake after induction of experimental colitis [via intrarectal infusions of trinitrobenzene sulfonic acid (TNB)] or injection of 100 micrograms/kg lipopolysaccharide (LPS). Temperature was monitored telemetrically in rats via implanted temperature transmitters. TNB-treated rats demonstrated a 5-day anorexia that resulted specifically from a decrease in meal size. Although TNB-treated rats were hypothermic on the day of treatment, no other body temperature changes were noted. LPS reduced food intake and elevated temperature, but these two effects were uncorrelated temporally. Although these results do not identify the mechanisms of anorexia, the findings indicate clearly that the anorexia associated with the acute inflammatory response is not secondary to fever.

Animals↗
PubMedDate not supplied

Bullae, bronchiectasis and nutritional emphysema in severe anorexia nervosa.

STUDY OBJECTIVES: Pulmonary complications of anorexia nervosa are rarely documented. The case of a patient with anorexia nervosa and pulmonary disease is presented, a new quantitative computed tomography (CT) method for the detection of emphysema is employed, the literature is reviewed and the concept of 'nutritional' emphysema is discussed. RESULTS: The case of a 34-year-old, nonsmoking woman with long-standing severe anorexia nervosa who was evaluated for cough and progressive shortness of breath is reported. Pulmonary function testing showed a predominant restrictive pattern with a marked reduction in carbon monoxide transfer and respiratory muscle strength, and an elevated residual volume. Imaging revealed bullae and bronchiectasis, and quantitative analysis of the CT scan was consistent with mild, generalized emphysema. Bronchial washings grew Pseudomonas aeruginosa. Known causes for bronchiectasis were excluded. A literature review disclosed few reported noninfectious pulmonary complications of anorexia nervosa. CONCLUSIONS: To the authors' knowledge, this is the first report of bullae and bronchiectasis in a patient with anorexia nervosa, and the CT analysis was consistent with mild emphysema. Malnutrition has been associated with emphysematous changes in animals and may be the primary insult in the development of emphysema, bullae and bronchiectasis in the present patient.

Adult↗
PubMedDate not supplied

Neuropeptide Y counteracts interferon-alpha-induced anorexia.

Interferon-alpha (IFN-alpha) immunotherapy is associated with significant adverse neurological effects, including anorexia, which can be a limiting factor in immunotherapy. Thus, it is important to develop strategies that could ameliorate IFN-alpha-induced neurological manifestations without significantly affecting its immunomodulating properties. In this study, we tested the hypothesis that an endogenous feeding-enhancing peptide, neuropeptide Y (NPY), could inhibit IFN-alpha-induced anorexia in rats. The results show that IFN-alpha induced significant anorexia when administered centrally into the third cerebral ventricle at an immunotherapeutically relevant dose (1,350 IU/rat). Heat-inactivated IFN-alpha had no effect. NPY (5.0 microg/rat) counteracted the IFN-alpha-induced anorexia when administered 3 or 10 h following IFN-alpha, or when it was concomitantly administered with IFN-alpha. The data suggest that NPY and its agonists could represent a potential novel intervention for IFN-alpha immunotherapy-associated anorexia.

Animals↗
PubMed1986

Hypothalamic-pituitary-thyroidal dysfunctions in anorexia nervosa.

There are clinical similarities between anorexia nervosa and hypothyroidism. Circulating levels of T4 and particularly T3 have been reported to be low in this eating disorder. Previous reports have, however, shown normal basal levels of serum TSH with normal or delayed responses to TRH. To assess thyroid function and the hypothalamic-pituitary axis in 21 women with anorexia nervosa, serum levels of free and total thyroid hormones, binding proteins, and TSH employing an extremely sensitive assay (detection limit = 0.02 microU/ml) were measured. Serum T4, free T4, T3, free T3, TSH, TBG and TBPA concentrations were significantly lower and rT3 levels were significantly higher in anorexia nervosa patients than in normal controls. A delayed TSH response to TRH was noted in 66% of patients, hyporesponsiveness was seen in another 24%, and a normal response in only 10%. In 10 anorexia nervosa patients studied after weight gain, T4, T3, free T3, TSH, TBG and TBPA were significantly increased, and rT3 was significantly decreased. No change in mean free T4 levels with weight gain was noted. Other parameters of hypothalamic dysfunction in anorexia nervosa have been reported and the present data suggest that apparent hypothalamic hypothyroidism occurs perhaps as an adaptation to prolonged starvation.

Adolescent↗
PubMed1998

Transplantable rat glucagonomas cause acute onset of severe anorexia and adipsia despite highly elevated NPY mRNA levels in the hypothalamic arcuate nucleus.

We have isolated a stable, transplantable, and small glucagonoma (MSL-G-AN) associated with abrupt onset of severe anorexia occurring 2-3 wk after subcutaneous transplantation. Before onset of anorexia, food consumption is comparable to untreated controls. Anorexia is followed by adipsia and weight loss, and progresses rapidly in severity, eventually resulting in reduction of food and water intake of 100 and 80%, respectively. During the anorectic phase, the rats eventually become hypoglycemic and hypothermic. The tumor-associated anorexia shows no sex difference, and is not affected by bilateral abdominal vagotomy, indicating a direct central effect. The adipose satiety factor leptin, known to suppress food intake by reducing hypothalamic neuropeptide Y (NPY) levels, was not found to be expressed by the tumor, and circulating leptin levels were reduced twofold in the anorectic phase. A highly significant increase in hypothalamic (arcuate nucleus) NPY mRNA levels was found in anorectic rats compared with control animals. Since elevated hypothalamic NPY is among the most potent stimulators of feeding and a characteristic of most animal models of hyperphagia, we conclude that the MSL-G-AN glucagonoma releases circulating factor(s) that overrides the hypothalamic NPY-ergic system, thereby eliminating the orexigenic effect of NPY. We hypothesize a possible central role of proglucagon-derived peptides in the observed anorexia.

Animals↗
PubMed1991

50-year trends in the incidence of anorexia nervosa in Rochester, Minn.: a population-based study.

OBJECTIVE: The aim of the study was to determine incidence and prevalence rates and long-term trends in incidence of anorexia nervosa by identifying all persons residing in the community of Rochester, Minn., during the 50-year period 1935 through 1984 who had the disorder. METHOD: From a community-based epidemiologic resource, 13,559 medical records with diagnoses of amenorrhea, starvation, weight loss, anorexia nervosa, or other conditions were screened to identify true cases of anorexia nervosa determined by using standard diagnostic criteria. RESULTS: One hundred eighty-one residents (166 female and 15 male) fulfilled the diagnostic criteria for anorexia nervosa; these were the incidence cases. Due to a quadratic trend in the rates for girls 10-19 years old, the incidence rate among female residents fell from 16.6 per 100,000 person-years in the 1935-1939 period to a low of 7.0 in 1950-1954 and increased to 26.3 in 1980-1984. The incidence rates for women 20 years old and older and for males remained constant. For females 15-24 years old, there was a linear increase. The overall age-adjusted incidence rate per 100,000 person-years was 14.6 for females and 1.8 for males. The prevalence rate per 100,000 population was 269.9 for females and 22.5 for males. CONCLUSIONS: Anorexia nervosa is more common than previously recognized. Among girls 15-19 years old it is a very common chronic illness. Its incidence has increased among females 15-24 years old but not among older women or among males.

Adolescent↗
PubMed1998

Does fluoxetine augment the inpatient treatment of anorexia nervosa?

OBJECTIVE: While pharmacological interventions are of established utility in bulimia nervosa, medications have no clear role in the treatment of anorexia nervosa. Because patients with anorexia nervosa frequently exhibit mood disturbances and symptoms of obsessive-compulsive disorder, the authors tested the utility of fluoxetine in the treatment of women participating in an inpatient program for anorexia nervosa. METHOD: The authors conducted a randomized, placebo-controlled, double-blind, 7-week study of fluoxetine at a target daily dose of 60 mg in 31 women with anorexia nervosa receiving treatment for their eating disorder on a clinical research unit. Body weight and measures of eating behavior and psychological state were obtained at baseline and at termination. RESULTS: There were no significant differences in clinical outcome on any measure between patients receiving fluoxetine and patients receiving placebo. CONCLUSIONS: Fluoxetine does not appear to add significant benefit to the inpatient treatment of anorexia nervosa.

Adolescent↗
PubMed2002

The outcome of anorexia nervosa in the 20th century.

OBJECTIVE: The present review addresses the outcome of anorexia nervosa and whether it changed over the second half of the 20th century. METHOD: A total of 119 study series covering 5,590 patients suffering from anorexia nervosa that were published in the English and German literature were analyzed with regard to mortality, global outcome, and other psychiatric disorders at follow-up. RESULTS: There were large variations in the outcome parameters across studies. Mortality estimated on the basis of both crude and standardized rates was significantly high. Among the surviving patients, less than one-half recovered on average, whereas one-third improved, and 20% remained chronically ill. The normalization of the core symptoms, involving weight, menstruation, and eating behaviors, was slightly better when each symptom was analyzed in isolation. The presence of other psychiatric disorders at follow-up was very common. Longer duration of follow-up and, less strongly, younger age at onset of illness were associated with better outcome. There was no convincing evidence that the outcome of anorexia nervosa improved over the second half of the last century. Several prognostic features were isolated, but there is conflicting evidence. Most clearly, vomiting, bulimia, and purgative abuse, chronicity of illness, and obsessive-compulsive personality symptoms are unfavorable prognostic features. CONCLUSIONS: Anorexia nervosa did not lose its relatively poor prognosis in the 20th century. Advances in etiology and treatment may improve the course of patients with anorexia nervosa in the future.

Adolescent↗
PubMed2004

Comorbidity of anxiety disorders with anorexia and bulimia nervosa.

OBJECTIVE: A large and well-characterized sample of individuals with anorexia nervosa and bulimia nervosa from the Price Foundation collaborative genetics study was used to determine the frequency of anxiety disorders and to understand how anxiety disorders are related to state of eating disorder illness and age at onset. METHOD: Ninety-seven individuals with anorexia nervosa, 282 with bulimia nervosa, and 293 with anorexia nervosa and bulimia were given the Structured Clinical Interview for DSM-IV Axis I Disorders and standardized measures of anxiety, perfectionism, and obsessionality. Their ratings on these measures were compared with those of a nonclinical group of women in the community. RESULTS: The rates of most anxiety disorders were similar in all three subtypes of eating disorders. About two-thirds of the individuals with eating disorders had one or more lifetime anxiety disorder; the most common were obsessive-compulsive disorder (OCD) (N=277 [41%]) and social phobia (N=134 [20%]). A majority of the participants reported the onset of OCD, social phobia, specific phobia, and generalized anxiety disorder in childhood, before they developed an eating disorder. People with a history of an eating disorder who were not currently ill and never had a lifetime anxiety disorder diagnosis still tended to be anxious, perfectionistic, and harm avoidant. The presence of either an anxiety disorder or an eating disorder tended to exacerbate these symptoms. CONCLUSIONS: The prevalence of anxiety disorders in general and OCD in particular was much higher in people with anorexia nervosa and bulimia nervosa than in a nonclinical group of women in the community. Anxiety disorders commonly had their onset in childhood before the onset of an eating disorder, supporting the possibility they are a vulnerability factor for developing anorexia nervosa or bulimia nervosa.

Adolescent↗
PubMed2005

Anorexia nervosa mortality in Northeast Scotland, 1965-1999.

OBJECTIVE: Most previous studies of mortality in anorexia nervosa patients have shown an increased risk of premature death but have been limited by methodological constraints. This study aimed to overcome some of these constraints by having a large original sample size, diagnosis confirmed by case note review, a long duration of follow-up, and a clear base population. METHOD: The authors identified 524 anorexia nervosa cases seen in specialist services in Northeast Scotland; anorexia nervosa diagnosis was confirmed by scrutinizing case notes. Those who had died were identified from the National Health Service register or register of deaths. The death rates and causes of death were analyzed. RESULTS: Twenty-three patients died, giving a crude death rate of 4.4% and a standardized mortality rate of 3.3 (95% CI=2.2-4.9). In only one-third of the cases was anorexia nervosa on the death certificate, but an eating disorder or other psychiatric pathology probably contributed to several of the other deaths. Older age at the time the patient was seen at the specialist service was the only identifiable risk factor in the group of patients who died. The median length of time between diagnosis and death was 11 years. CONCLUSIONS: Anorexia nervosa is associated with increased risk of premature death. It is possible that death rates could be reduced by early diagnosis and by long-term specialist care.

Adolescent↗
PubMed2002

Assessing guilt in adolescents with anorexia nervosa.

OBJECTIVE: This study explores the role of guilt in adolescents with anorexia nervosa. Numerous clinical observations have suggested guilt in adolescents or parents contributes to the development of anorexia nervosa, though systematic assessment of this phenomenon has not been undertaken. METHODS: The Interpersonal Guilt Questionnaire was used to assess types and levels of guilt in adolescents with anorexia nervosa and their parents. RESULTS: We found significantly elevated levels of self-hate guilt in adolescents with anorexia nervosa compared to adolescent norms. However, parents had lower levels of guilt compared to adult norms. CONCLUSION: Self-hate guilt is elevated in adolescents with anorexia nervosa. Treatment strategies should take this phenomenon into consideration when developing clinical approaches.

Adolescent↗
PubMedDate not supplied

Nutrition in advanced cancer: anorexia as an outcome variable and target of therapy.

The endpoints used as outcome variables in clinical cancer treatment trials, including nutrition intervention studies, should contain items that are meaningful to the patient. Variables to consider are appetite, food intake, physical performance, psychological and social functioning, response to cancer therapies, survival time, nutrition status, associated morbidity, and costs. Ideally, the design and conduct of nutrition trials should be carried out by a multidisciplinary team comprising medical oncologists, physician specialists in nutrition, dietitians, and social scientists. Anorexia has not been a focus of nutrition support trials in the past partly because of the lack of effective strategies to reverse it. Anorexia is one important cause of cancer starvation, and it also causes patient discomfort. This paper describes outcome variables that include patient derived subjective factors such as anorexia, and outlines new strategies to reverse anorexia. Pharmacologic strategies tested to reverse anorexia include corticosteroids, anabolic steroids, cyproheptadine, hydrazine sulfate, cannabinoids, and megestrol acetate. Of these, only the latter has been consistently well tolerated and effective, with significant improvements in appetite and food intake demonstrated in large-scale, randomized, controlled trials involving more than 600 cancer patients. Dose-response studies have demonstrated increasing efficacy with increasing doses of megestrol acetate from 160 to 800 mg/day. Doses in excess of 800 mg/day are not currently recommended. The mechanisms of action of megestrol acetate involve both behavioral and metabolic effects, and its impact on energy expenditure, appetite, body composition, endocrine function, and lipid metabolism is the subject of ongoing research.(ABSTRACT TRUNCATED AT 250 WORDS)

Anorexia↗
PubMed1998

Neuroendocrine, appetitive and behavioural responses to d-fenfluramine in women recovered from anorexia nervosa.

BACKGROUND: Increased central serotonin (5-HT) function has been hypothesised to be a vulnerability trait in anorexia nervosa. METHODS: Eighteen women with a history of DSM-III-R anorexia nervosa and 18 female controls were examined. The subjects had recovered weight and menstrual function. A placebo-controlled d-fenfluramine test was used. Subjects ingested d-fenfluramine or placebo and after three hours were offered a 'free' meal. The amounts eaten were recorded and plasma cortisol and prolactin levels were measured. Questionnaires related to eating attitudes and behaviour, to personality, and to mood were administered. RESULTS: Unlike the control subjects, those recovered from anorexia nervosa did not show the expected appetite-suppressing responses to d-fenfluramine; their eating attitudes and behaviour were more restrained, 'negative' perfectionism was more pronounced, and post-meal plasma cortisol levels did not rise as expected. CONCLUSIONS: Our results do not suggest that increased central 5-HT function is a trait marker in anorexia nervosa, but dysregulation in part of the central 5-HT system may be a vulnerability factor. The flattened post-meal response to cortisol in the subjects who had recovered from anorexia nervosa suggests that their hypothalamic pituitary--adrenal axis may be altered and deserves further investigation.

Adult↗
PubMed1984

The role of endogenous opiates in the mechanism of inhibited luteinizing hormone (LH) secretion in women with anorexia nervosa: the effect of naloxone on LH, follicle-stimulating hormone, prolactin, and beta-endorphin secretion.

The aim of this study was to evaluate the role of endogenous opiates in the mechanism of decreased LH secretion in women with anorexia nervosa. For this purpose the effect of opiate receptor blockade with naloxone on LH, FSH, PRL, and beta-endorphins secretion was studied in 24 women with anorexia nervosa and 7 normal women. Serum LH, FSH, PRL, beta-endorphin-like substance, ACTH, and cortisol concentrations were measured before and after opiate receptor blockade after a single iv dose of 0.2 mg/kg naloxone or saline. Mean serum LH and FSH concentrations increased significantly after naloxone in the normal women. Eleven patients had a significant increase in serum LH concentrations in response to naloxone and 13 did not respond to naloxone with an increase in LH concentration. In the first group the basal LH values were higher than those in the second group. In the majority of patients in the first group amenorrhea preceded the wt loss, whereas in most patients in the second group amenorrhea appeared during the phase of wt loss. Naloxone did not alter pulsatile LH secretion in 6 women. No effect of naloxone on serum FSH and PRL concentrations was found. A significant increase in beta-endorphin-like substance levels after naloxone administration occurred in patients with anorexia nervosa. However, serum ACTH and cortisol concentrations were not altered in response to naloxone. In conclusion, the increase in LH release after opiate receptor blockade by naloxone suggests that endogenous opiates may play a role in the mechanism of inhibited LH secretion at least, in the majority of those women with anorexia nervosa in whom amenorrhea preceded wt loss. The results also point to a different mechanism of ACTH and beta-endorphin secretion in patients with anorexia nervosa.

Adolescent↗