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PubMed1987

Immobilisation stress-induced anorexia is not due to gastric ulceration.

The relationship between the anorexia following immobilisation and the associated gastric pathology in male and female rats was investigated. Male rats were injected with saline or the histamine-H2. antagonist, ranitidine, which inhibits gastric acid secretion but does not readily enter the brain. Thirty minutes later, the animals were immobilised for 2 hours. Ranitidine pretreatment reduced the number of gastric lesions but had no effect on the degree of stress-induced anorexia. The number of gastric lesions did not correlate significantly with the degree of anorexia or weight loss. Previous studies have reported that female rats (unlike males) exhibit anorexia after repeated daily immobilisations and have greater gastric pathology following stress. Therefore, in a second experiment, female rats were pretreated with saline or ranitidine and immobilised for 2 hours/day for 4 days. The drug did not decrease the number of lesions observed after this treatment. However, as in the first experiment, the number of lesions did not correlate significantly with anorexia or weight loss. It is therefore unlikely that immobilisation stress-induced anorexia in either male or female rats is merely a consequence of gastric ulceration.

Animals↗

PubMed1986

Anorexia after adrenalectomy in gold thioglucose-treated obese mice: role of adipose tissue mass.

We have previously shown that following adrenalectomy, gold thioglucose (GTG)-treated hyperphagic obese mice exhibit anorexia, weight loss and a pronounced hypoglycemia which leads ultimately to their death. In the present study, we sought to determine whether the increased adipose tissue mass which is characteristic of GTG-treated obese mice exerted a role in the onset and development of anorexia after adrenalectomy. Accordingly, the effects of adrenalectomy on food intake, weight gain, plasma glucose and corticosterone levels were investigated in normal untreated controls, GTG-treated hyperphagic obese mice and GTG-treated non obese mice. The GTG-treated non obese mice were prepared by restricting their daily intake of chow (pair-feeding) to that consumed by normal untreated mice. After adrenalectomy, all mice were allowed free access to food. As expected, all GTG-treated hyperphagic obese mice exhibited anorexia and weight loss following adrenalectomy. In contrast, about half (52%) of the GTG-treated non obese mice exhibited anorexia and weight loss after adrenalectomy. The response of the GTG-treated non obese adrenalectomized mice was not due to differences in adrenal insufficiency since all adrenalectomized mice had blood levels of corticosterone of less than 0.5 microgram%. These findings indicate that whereas the increased adipose tissue mass of the GTG-treated obese mice appears to be associated with an increased incidence of anorexia following adrenalectomy, increased adipose tissue mass alone does not appear to be essential for the occurrence of anorexia.

Adipose Tissue↗

PubMed1984

Anorexia and brain serotonin: development of tolerance to the effects of fenfluramine and quipazine in rats with serotonin-depleting lesions.

The acute and chronic effects of the "serotonergic anorectics" quipazine and dl-fenfluramine were examined in rats with substantial and specific depletions of brain 5-hydroxytryptamine (5-HT) induced by 5,7-dihydroxytryptamine (5,7-DHT). A "dessert" test which did not involve food deprivation was used to assess anorexia. Markedly increased sensitivity to the L-5-HTP-induced behavioral syndrome in 5,7-DHT-lesioned rats indicated postsynaptic 5-HT receptor supersensitivity. We found low (2 mg/kg) and intermediate (5 mg/kg) doses of fenfluramine, a putative presynaptic agent, were more effective in producing anorexia in lesion rats versus controls. A higher dose of fenfluramine (10 mg/kg) was less effective in lesion rats, suggesting that high dose and low dose fenfluramine anorexia are mediated by different mechanisms. We found quipazine, a putative 5-HT postsynaptic agonist, in a dose range of 2-10 mg/kg, to be no more effective in producing anorexia in lesion rats compared to controls. The development of tolerance to both fenfluramine and quipazine anorexia was similar for lesion and control rats showing that an intact brain 5-HT system is not necessary for tolerance. Tolerance to the "behavioral syndrome" induced by high doses of these agents developed rapidly in controls but not at all in lesion rats. This suggests that the behavioral syndrome and anorexia are independent effects of fenfluramine and quipazine. These results also challenge the popular notion that the primary anorectic action of fenfluramine is via brain serotonin.

5,7-Dihydroxytryptamine↗

PubMedDate not supplied

The dipeptide Lys-Pro attenuates interleukin-1 beta-induced anorexia.

The carboxyl-terminal tripeptide of alpha-MSH(1-13), Lys-Pro-Val, antagonizes anorexia induced by interleukin-1 beta (IL-1). The present studies were undertaken to determine if the Lys-Pro dipeptide portion of this tripeptide likewise antagonizes anorexia induced by ICV administration of 0.5 pmol IL-1 in rats previously deprived of food. This dose of Lys-Pro did significantly attenuate the IL-1-induced anorexia, but only for 1 h after infusion. Simultaneous administration of a larger dose (5.0 pmol) of Lys-Pro reversed the IL-1-induced anorexia during both the 0-1-h and 2-4-h periods. In addition, both 0.5 and 5.0 pmol of the D-substitute tripeptide, Lys-D-Pro-Thr (LDPT), similarly attenuated the IL-1-induced anorexia. The ICV administration of 5.0 pmol Lys-Pro also did not have any significant effects on food consumption. These results indicate that the dipeptide Lys-Pro may have a short-term antagonistic action against the anorexia induced by IL-1, and it is possible that this action may be partially mediated by the blockade of IL-1 on its own receptor.

Amino Acid Sequence↗

PubMed1988

Superior mesenteric artery syndrome presenting as an anorexia nervosa-like illness.

Anorexia nervosa is often overdiagnosed in adolescent females with anorexia and extreme weight loss. In some cases, an anorexia nervosa-like illness is due to a treatable organic disorder. We describe a 16-year-old female with anorexia, vomiting, extreme weight loss, and amenorrhea who was referred as an anorexia nervosa case and was subsequently found to have superior mesenteric artery syndrome that was causing a duodenal obstruction. Conservative treatment with oral hypercaloric liquid feeding resulted in optimal weight gain and complete recovery. This syndrome should be considered in adolescents with an anorexia nervosa-like illness associated with vomiting and postprandial epigastric discomfort.

Adolescent↗

PubMed1996

Cancer anorexia: new pathogenic and therapeutic insights.

During tumor growth, anorexia and reduced food intake markedly contribute to the development of malnutrition, thus worsening overall patients' survival. A better understanding of the pathophysiology of eating behavior may lead to new and more effective therapies, aiming at counteracting the detrimental effects of anorexia and reduced food intake on nutritional status and survival in cancer patients. Brain tryptophan and serotonin concentrations seem to play a pivotal role in the regulation of eating behavior. Increased brain serotonin activity is indeed associated with a reduction of food intake. It has been recently hypothesized that increased availability of tryptophan to the brain and the consequent increased serotonin activity may represent the pathogenic mechanism for cancer-associated anorexia. According to this hypothesis, the modulation of brain serotonin activity may result in an improvement of anorexia. Reducing brain tryptophan availability represents a possible mechanism to restore brain serotonin activity to normal. There is evidence that the oral administration of neutral amino acids competing with tryptophan for brain entry results in a significant improvement of cancer anorexia. The same treatment may also be effective in improving secondary anorexia, which is associated with other chronic illnesses, including renal and liver failure, sepsis, and so forth, sharing a similar pathogenic mechanism.

Animals↗

PubMed2006

[Infantile anorexia: from birth to childhood].

Young child's anorexia (0-4 years) may have organic or psychological origin, when parents-child relationships are concerned. The most complex and earliest forms often have unspecified aetiology. Psychopathological classifications, which emphasize the mother-child relationships, are essential reference marks. But there is now a consensus in the definitions: the diagnosis of infantile anorexia requires criteria of acute or chronic malnutrition. We mainly distinguish anorexia by early disorder of homeostasis, anorexia resulting from serious disorder of attachment, anorexia by disorder of mother-child interactions, and finally early and complex anorexia, mixing an organic vulnerability and a bonding trouble, which can be secondary. Treatments differ according to the selected aetiology. Even if the origin is not mainly the fact of a relational mother-child dysfunction, parents-child's relations require a support to avoid aggravation by interactive vicious circles (force feeding). More than other diseases of early childhood, feeding disorders require a good knowledge of the working hypotheses both in the field of the paediatrics and the child psychiatry.

Anorexia↗

PubMed2006

Illness-induced anorexia and its possible function in the caterpillar, Manduca sexta.

Although many animals exhibit illness-induced anorexia when immune-challenged, the adaptive significance of this behavior remains unclear. Injecting Manduca sexta larvae (caterpillars) with live bacteria (Serratia marcescens), heat-killed bacteria or bacterial lipopolysaccharides resulted in a decline in feeding, demonstrating illness-induced anorexia in this species. We used M. sexta to test four commonly suggested adaptive functions for illness-induced anorexia. (1) Food deprivation did not reduce the iron content of the hemolymph. (2) Immune-challenged M. sexta were not more likely to move to a different part of the plant. Therefore, the decline in feeding is unlikely to be an adaptive response allowing the animal to move away from a patch of contaminated food. (3) M. sexta force-fed S. marcescens bacteria were not more susceptible to a S. marcescens systemic infection than were M. sexta force-fed nutrient broth. (4) Force-feeding infected M. sexta during illness-induced anorexia did not increase mortality and short-term food deprivation did not enhance survival. However, force-feeding M. sexta with a high lipid diet (linseed oil and water) resulted in an increase in mortality when challenged with S. marcescens. Force-feeding sucrose or water did not reduce resistance. Force-feeding a high lipid diet into healthy animals did not reduce weight gain, suggesting that it was not toxic. We hypothesize that there is a conflict between lipid metabolism and immune function, although whether this conflict has played a role in the evolution of illness-induced anorexia remains unknown. The adaptive function of illness-induced anorexia requires further study in both vertebrates and invertebrates.

Adaptation, Physiological↗

PubMed2005

Effects of omega-3 fatty acids on orexigenic and anorexigenic modulators at the onset of anorexia.

In cancer anorexia, a decrease in food intake (FI) occurs concomitant with changes in orexigenic peptides such as neuropeptide Y (NPY) and anorexigenic peptides such as alpha-melanocyte-stimulating hormone (alpha-MSH) and anorexigenic neurotransmitter serotonin. omega-3 Fatty acid (omega-3FA) inhibits cytokine synthesis, and delays tumor appearance, tumor growth, and onset of anorexia in tumor-bearing rats. We hypothesize that, in cancer anorexia, omega-3FA is associated with quantitative reversal of hypothalamic NPY, alpha-MSH, and serotonin receptor (5-HT(1B)-receptor) enhancing FI. Fischer rats were divided into: MCA tumor bearing fed chow (TB-Chow) or omega-3FA diet (TB-omega-3FA) and controls: non-tumor bearing fed chow (NTB-Chow) or omega-3FA diet (NTB-omega-3FA). Rats were euthanized at anorexia and brains were removed for hypothalamic immunohistochemical study, using NPY, alpha-MSH, and 5-HT(1B)-receptor-specific antibodies and slides assessed by image analysis. Immunostaining specificity was controlled by omission of primary or secondary antibodies and pre-absorption test. At anorexia, FI decreased (P < 0.05) in TB-Chow but did not change in TB-omega-3FA rats. In TB-omega-3FA vs. TB-Chow, NPY immunoreactivity increased 38% in arcuate nucleus (ARC; P < 0.05), and 50% in magnocellular paraventricular nucleus (mPVN; P < 0.05). alpha-MSH decreased 64% in ARC and 29% in mPVN (P < 0.05). 5-HT(1B)-receptor immunoreactivity decreased 13% only in supraoptic nucleus (P < 0.05). No immunoreactivity was found in the control sections. omega-3FA modified hypothalamic peptides and 5-HT-(1B)-receptor immunoreactivity at anorexia, concomitant with an increase in FI, were probably mediated by omega-3FA inhibition of tumor-induced cytokines.

Analysis of Variance↗

PubMed2006

Anorexia in chronic obstructive pulmonary disease--association to cachexia and hormonal derangement.

BACKGROUND: In patients with chronic obstructive pulmonary disease (COPD) weight loss frequently occurs that may ultimately lead to cachexia as a serious co-morbidity, indicating severely impaired functional capacity, health status and increased mortality. Increased energy expenditure due to mechanic and metabolic inefficiency and systemic inflammation are determinants of a hypermetabolic state that is not balanced by dietary intake. Anorexia may importantly contribute to weight loss in COPD, however, the association between immune and hormonal derangement and altered appetite has not been studied in detail. AIM: The aim of the present study was to investigate whether anorexia in COPD is related to inflammation and hormonal derangement in association to weight loss. METHODS: We prospectively enrolled 103 consecutive patients with COPD (age 59.8+/-1.3 years, 35% female, mean FEV1 38.3+/-1.7%) in comparison to healthy controls of similar age (n=15). RESULTS: In 34 patients (33%) cachexia was diagnosed (weight loss >7.5%, BMI < or = 24 kg/m2). Cachectic COPD patients had lower BMI (19.0+/-0.5 vs 25.6+/-0.7 kg/m2) and impaired lung function (FEV1 31+/-2% vs 42+/-2%, FVC 51+/-3 vs 59+/-3%, both p<0.001). Inflammatory immune activation (IL-6 and IL-6/IL-10 ratio) was significantly higher in cachectic COPD patients. Analysis of the extent of anorexia (visual analogue scale) revealed that cachectic COPD patients had significantly decreased subjective desire to eat compared to non-cachectic patients (3.5+/-0.3 vs 6.3+/-0.2, p<0.001). Patients with COPD and cachexia showed evidence of acquired GH resistance (decreased IGF-1/GH ratio) and insulin resistance (HOMA). Anorexia showed a direct correlation with the IGF-1/GH ratio (r=0.34, p<0.05) and was further related to BMI and % weight loss (both p<0.001). CONCLUSION: In COPD anorexia relates to hormonal derangement and inflammatory immune activation. Anorexia contributes to development of cachexia. The concept of appetite stimulating therapy emerges as a novel therapeutic option in cachectic COPD patients.

Anorexia↗

PubMed2004

Perfectionism dimensions in children and adolescents with anorexia nervosa.

PURPOSE: To assess the dimensions of perfectionism in adolescents with anorexia nervosa in comparison with adolescents from the general population and to validate the Spanish versions of two measures of perfectionism. METHODS: The Child and Adolescents Perfectionism Scale (CAPS), the Perfectionistic Self-Presentation Scale (PSPS) scale, the Eating Attitudes Test (EAT), and the Beck Depression Inventory (BDI) were administered to a group of 71 anorexia nervosa patients (mean age 15.3 years). Moreover, the CAPS and the PSPS were also administered to 113 adolescents from the general population (mean age 14.6 years). The CAPS and the PSPS were administered again after 1 week in 68 subjects to evaluate test-retest reliability. RESULTS: Both the CAPS and the PSPS demonstrated good internal consistency (Cronbach alpha for anorexia nervosa patients = .91; Cronbach alpha for general population = .85) and the two scales of the CAPS also had alpha coefficients in excess of .7. One-week test-retest reliability was also adequate (r = .80). Anorexia nervosa patients had higher mean scores in Self-oriented perfectionism (p < .001) and Perfectionistic self-presentation (p < .001) but not in Socially prescribed perfectionism (p = .292). There were significant correlations among perfectionism and the EAT and the BDI. A percentage of anorexia nervosa patients between 39% and 42% obtained a score higher than the mean in the comparison group plus two standard deviations in Self-oriented perfectionism and Perfectionistics self-presentation. CONCLUSIONS: The Spanish version of the CAPS and the PSPS showed good psychometric properties. A percentage of 40% of adolescent patients with anorexia nervosa show high Self-oriented perfectionism and Perfectionistic self-presentation.

Adolescent↗

PubMed2005

Differences of cortical 5-HT2A receptor binding index with SPECT in subtypes of anorexia nervosa: relationship with personality traits?

OBJECTIVE: Using single photon emission computed tomography and the 5-HT2A receptor antagonist, 123I-5-I-R91150, we explored differences in 5-HT2A binding index in anorexia nervosa patients with and without bulimic features. We also searched for associations between temperament dimensions and cortical 5-HT2) binding. METHOD: About 9 restrictive and 7 bulimic anorexia nervosa patients were examined and cortical 123I-5-I-R91150 binding index values were compared between the two subgroups. Open explorative correlation analysis was used to examine any relationships between binding index values and temperament scores, as assessed with the Temperament and Character Inventory. RESULTS: 5-HT2A binding index was significantly reduced in the parietal cortex in bulimic anorexia nervosa patients in comparison with restrictive anorectics. Further, a positive correlation was documented between reward dependence and parietal 5-HT2A binding index across patients in the two subgroups. DISCUSSION: Restrictive anorexia nervosa patients differ from binging/purging anorexia nervosa patients on the basis of a reduced parietal 5-HT2A binding index in the latter. We speculate that the finding of a positive correlation between parietal 5-HT2A binding and reward dependence might reflect an association between these two variables, at least in anorexia nervosa patients.

Adolescent↗

PubMed2004

Fenfluramine treatment in female rats accelerates the weight loss associated with activity-based anorexia.

Serotonin plays an important role in controlling food intake and regulating body weight. Thus, altered serotonergic function may be involved in the etiology of anorexia nervosa. To investigate this hypothesis, we examined whether activation of the serotonin system increases the severity of activity-based anorexia, an animal model of anorexia nervosa in which food-restricted rats are housed with access to running wheels. This paradigm promotes symptoms of anorexia nervosa, including hypophagia, hyperactivity, and weight loss. Food-restricted rats received injections of a serotonin agonist, fenfluramine, or saline 1.5 h prior to their daily 2-h period of food access. A third saline-injected group was pair-fed to the fenfluramine group. Drug treatment and food restriction were terminated following a 25% weight loss. During food restriction, each group developed symptoms of activity-based anorexia. Although similar reductions in food intake were observed in fenfluramine-treated and pair-fed rats, only fenfluramine-treated rats displayed an accelerated rate of weight loss, relative to saline-treated rats. Thus, some other nonanorexic aspect of fenfluramine, perhaps its influence on metabolism, must underlie the accelerated rate of weight loss in this group. Our results suggest that increased activation of the serotonin system exacerbates the weight loss associated with activity-based anorexia.

Animals↗

PubMed2003

Development of, and recovery from, activity-based anorexia in female rats.

Activity-based anorexia occurs in rats maintained on a restricted-feeding schedule while given free access to running wheels. These conditions induce high levels of wheel running and rapid weight loss. Although this procedure was developed as an animal model of anorexia nervosa, it has been studied primarily in male rats. Our goal was to examine the development of, and recovery from, activity-based anorexia in female rats. Food intake, wheel running, body weight, and phase of the estrous cycle were monitored daily prior to, during, and after a period of restricted feeding in which access to food was limited to 2 h/day. Food intake, body weight, and estrous cyclicity were also monitored in a control group housed without access to running wheels. Prior to food restriction, rats with wheels displayed high levels of wheel running and consumed more food than rats without wheels. Despite that both groups consumed similar amounts of food during the restricted-feeding phase, only rats with wheels developed symptoms of activity-based anorexia, including increased wheel running, rapid weight loss, and disruptions in estrous cyclicity. Recovery from activity-based anorexia was associated with hypoactivity and hyperphagia. Resumption of estrous cycles occurred when the weight lost during food restriction was regained. Hyperphagia, but not hypoactivity, was maintained following resumption of estrous cycles; however, this hyperphagia was limited to nonestrous phases. Our findings suggest that recovery from activity-based anorexia is mediated primarily by an increase in orexigenic signaling that promotes pronounced hyperphagia, and that the increase in satiogenic signaling during estrus abolishes this compensatory hyperphagia.

Animals↗

PubMed2004

Estradiol-mediated increases in the anorexia induced by intraperitoneal injection of bacterial lipopolysaccharide in female rats.

Lipopolysaccharide (LPS) derived from the cell walls of gram-negative bacteria causes a robust acute phase response (APR) that includes fever, anorexia, and many other elements. Because immune system function, including some models of illness anorexia, is sexually differentiated, we investigated the sexual differentiation of the anorexia induced by intraperitoneal LPS injections in rats. Cycling female Long-Evans rats tested either during diestrus or estrus ate less following 6.25 microg/kg LPS than did intact males. Following 12.5 microg/kg LPS, females in estrus ate less than either females during diestrus or males. Similarly, a more pronounced anorexia occurred following 12.5, 25, and 50 microg/kg LPS in ovariectomized females that received cyclic estradiol treatment and were tested on the day modeling estrus than in untreated ovariectomized rats. LPS also increased the length of the rats' ovarian cycles, usually by a day, especially when injected during diestrus. As in male rats, when LPS injections were repeated in the same rats, both estradiol-treated and untreated rats failed to display any significant anorexia. The inhibitory effects of LPS on eating in intact and ovariectomized rats were expressed solely as decreases in spontaneous meal frequency, without significant alteration of spontaneous meal size. These data indicate that anorexia following peripheral LPS administration is sexually differentiated and that estradiol is sufficient to produce this response. The mechanism of the pathophysiological effect of estradiol on meal frequency appears to be different from the physiological effect of estradiol on food intake because the latter is expressed solely as a change in meal size.

Acute-Phase Reaction↗

PubMed1998

Lipopolysaccharide (LPS)- and muramyl dipeptide (MDP)-induced anorexia during refeeding following acute fasting: characterization of brain cytokine and neuropeptide systems mRNAs.

We investigated the effectiveness of lipopolysaccharide (LPS) and muramyl dipeptide (MDP) administered into the brain to induce anorexia in acutely fasted Wistar rats allowed to refeed. We also assayed for changes in mRNA levels of IL-1 system components, TNF-alpha, TGF-beta1, glycoprotein 130 (gp 130), leptin receptor (OB-R), pro-opiomelanocortin (POMC), neuropeptide Y (NPY), glucocorticoid receptor (GR), and CRF receptor (CRF-R) in selected brain regions. The data show that LPS and MDP induced anorexia differentially during refeeding. LPS-induced anorexia was of a stronger magnitude and duration than that of MDP. RNase protection assays showed that LPS and MDP significantly increased the expression of IL-1beta, IL-1 receptor type I, and TNF-alpha mRNAs in the cerebellum, hippocampus, and hypothalamus; LPS was more potent in all cases. MDP treatment, on the other hand, induced a stronger increase in hypothalamic levels of IL-1 receptor antagonist (IL-1Ra) and TGF-beta1 mRNAs relative to LPS. In addition, competitive RT-PCR analysis showed that LPS induced an eleven-fold increase in IL-1alpha mRNA in the hypothalamus relative to vehicle. These findings suggest that LPS and MDP mediate anorexia through different cytokine mechanisms. A stronger up-regulation of anti-inflammatory cytokines (IL-1Ra and TGF-beta1) mRNA expression by MDP may be involved in the weaker MDP-induced anorexia relative to LPS. No significant changes were observed in the peptide components examined except for an up-regulation in cerebellar gp 130 mRNA and down-regulation of hypothalamic GR mRNA expression in response to LPS or MDP. This study shows that LPS and MDP induce anorexia in fasted rats allowed to refeed, and suggests an important role for endogenous cytokine-cytokine interactions.

Acetylmuramyl-Alanyl-Isoglutamine↗

PubMedDate not supplied

Specificity of eating disorders diagnoses in families of probands with anorexia nervosa and bulimia nervosa.

This study examines the prevalence of anorexia nervosa and bulimia nervosa in relatives of probands, and examines the probandwise specificity of any familial clustering. Data were collected from probands using the family history method. Probands were recruited in a sequential cohort fashion. Information collected from probands was rated semiblindly by two of the authors, and a diagnostic hierarchy applied to arrive at a diagnosis for each of the relatives assessed. Data are reported on 2,125 family members, collected from 93 probands. Diagnostic agreement between raters was high, with serious disagreement present in three of 167 possible cases of an eating disorder. Rates of anorexia nervosa, bulimia nervosa, major depression, and substance abuse declined from first- to third-degree relatives, which is consistent with genetic clustering, and there was evidence of a cohort effect operating for anorexia nervosa and bulimia nervosa. The rates of anorexia nervosa and bulimia nervosa in all family members were 5.1%, and 4.3% respectively. An analysis of maternal and paternal descent showed no evidence for X-linked dominant transmission in these families. Preliminary analysis of the clustering of diagnoses in relatives showed a tendency (chi 2 = 14.47, P = .006) for family members to be affected by the same diagnosis as was the proband. This trend was strongest for anorexia nervosa, but there was overlap when the proband had a lifetime diagnosis of bulimia nervosa, with or without anorexia nervosa. These results are compatible with the existence of genetic factors influencing predisposition to eating disorders, but do not prove such.

Anorexia Nervosa↗

PubMed1986

Anorexia nervosa, athletics, and amenorrhea.

We examined menstrual function in two groups of patients meeting the DSM III criteria for anorexia nervosa who differed only in their physical activity. Sixteen athletes with anorexia nervosa were compared with eight sedentary patients who had anorexia nervosa. Athletic patients with anorexia were found to have lower gonadotropin levels, a longer period of amenorrhea both before significant weight loss and after weight rehabilitation, and a higher weight at the time of resumption of menses than patients with anorexia who were sedentary. However, both groups were markedly undernourished, had amenorrhea before significant weight loss and after weight rehabilitation, and had lower gonadotropin levels than normal subjects. These data suggest that the increased physical activity often seen in patients with anorexia nervosa worsens, but does not cause, menstrual dysfunction.

Adolescent↗