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PubMed1984

Changes in amphetamine-induced anorexia and stereotypy during chronic treatment with antidepressant drugs.

Amphetamine-induced anorexia and stereotyped behaviour were studied in rats, following pretreatment with the antidepressants DMI, inprindole and mianserin. A complex drug-dependent and dose-dependent pattern of results was obtained. Acute pretreatment with DMI and iprindole enhanced amphetamine anorexia and stereotypy; at high doses only, the enhancement of anorexia disappeared during chronic treatment. Mianserin had no effects acutely, but chronic treatment with high doses attenuated anorexia and enhanced stereotypy. High doses of all three drugs attenuated anorexia and enhanced stereotypy during withdrawal. The most parsimonious account of these results is that the acute affects of DMI and iprindole are artefactual, and that chronic administration of all three antidepressants increased dopaminergic function and decreased beta-adrenergic function.

Animals↗
PubMed1992

Carboxyl-terminal tripeptide of alpha-melanocyte-stimulating hormone antagonizes interleukin-1-induced anorexia.

Interleukin-1 beta (IL-1), a cytokine released from inflammatory cells, is thought to be involved in the anorexia associated with severe infection. To assess a possible role of the amino acid sequence found in the supposed IL-1 receptor binding sites, we determined the antagonistic effects of alpha-melanocyte-stimulating hormone (MSH) and the carboxyl-terminal tripeptide of alpha-MSH-(11-13) (alpha-MSH-(11-13)) on the anorexia induced by intracerebroventricular (i.c.v.) administration of 0.5 pmol IL-1. The parent alpha-MSH molecule completely prevented the induction of anorexia by IL-1 at both doses tested, 0.5 and 5.0 pmol. In contrast, alpha-MSH-(11-13) prevented the IL-1-induced anorexia only at 5.0 pmol, but not at 0.5 pmol. Intracerebroventricular injection of 5 pmol of the parent alpha-MSH molecule alone temporarily decreased food consumption at 1-2 h; 5.0 pmol of alpha-MSH-(11-13) alone did not affect food consumption. These data indicate that alpha-MSH can antagonize the anorexic effects of IL-1. The carboxyl-terminal tripeptide portion of alpha-MSH may be important for the antagonistic action of alpha-MSH on the anorexia induced by IL-1.

Amino Acid Sequence↗
PubMed1990

Gastrointestinal symptoms in anorexia nervosa. A prospective study.

Neither the natural history of gastrointestinal symptoms in patients with anorexia nervosa nor their response to refeeding have been well studied. We hypothesized that gastrointestinal symptoms in anorexia nervosa will decrease during refeeding despite high caloric intake, suggesting that delayed gastric emptying, where present, is a result rather than a cause of anorexia nervosa. Study goals were (a) to determine the type and frequency of gastrointestinal symptoms, (b) to follow symptoms during refeeding prospectively, and (c) to develop guidelines for gastrointestinal testing and intervention in hospitalized anorectic patients. Sixteen consecutive patients with anorexia nervosa were rated on 12 gastrointestinal symptoms before and after nutritional rehabilitation and followed up throughout treatment. All patients reported multiple gastrointestinal symptoms on admission; all symptoms except belching improved during treatment despite large calorie increases (p less than 0.0002); significant improvements occurred in appetite, bloating, constipation, vomiting, and diarrhea; and no patients required endoscopy, x-ray evaluation, or antipeptic regimens. We conclude that although severe gastrointestinal symptoms are common in anorexia nervosa, they improve significantly with refeeding. Specific gastrointestinal studies should be reserved for patients who do not gain weight or who have indications of independent digestive disease.

Abdominal Pain↗
PubMed1985

Subgroups of anorexia nervosa and bulimia: validity and utility.

Sociodemographic and psychodynamic similarities and differences among four subgroups of eating disordered females seeking outpatient consultations for anorexia nervosa and bulimia are presented. Supporting the spectrum concept of eating disorders, the four diagnostic subgroups are: anorexia nervosa, restricting; anorexia nervosa with bulimic complications; normal weight bulimia with a history of anorexia nervosa; and normal weight bulimia without a history of anorexia nervosa. Overall, the 165 patients are white, middle to upper-middle class females in their early twenties. The highest levels of psychopathology, as measured by the Eating Disorder Inventory, was manifested by patients afflicted with both anorexic and bulimic symptomatology, either in the past or at time of consultation. Implications for diagnostic classification and clinical intervention are discussed.

Adolescent↗
PubMed1984

Plasma and brain cholecystokinin levels in cancer anorexia.

The syndrome of cancer anorexia includes early satiety in man and a reduction in the duration of feeding in experimental animals. These aberrations suggest dysfunction of peripheral and/or central nervous system satiety mechanisms in tumor-bearing individuals. Since the gut peptide, cholecystokinin (CCK), has been implicated as a potent satiety cue in man and animals, plasma and brain concentrations of CCK were measured by radioimmunoassay in anorectic tumor-bearing rats. Plasma concentrations of immunoreactive CCK were not significantly altered in either an acute Walker 256 carcinosarcoma or more chronic methylcholanthrene-induced sarcoma animal model of cancer anorexia. However, levels of immunoreactive CCK were significantly reduced in the hypothalamus and cerebral cortex of animals bearing the methylcholanthrene sarcoma during both mild and severe anorexia. These data demonstrate that elevations in immunoreactive CCK are not a major factor in the etiology of cancer anorexia. If brain CCK is involved in satiety, tumor-bearing rats may be attempting to compensate for their anorexia by down-regulating CCK production.

Animals↗
PubMed1987

Atypical responses to morphine in mice: a possible relationship to anorexia nervosa?

According to our previously proposed auto-addiction hypothesis of chronic anorexia nervosa, patients become addicted to an initial period of dieting through endogenous opioid mediated mechanisms. Morphine causes hyperactivity and anorexia in the mouse, symptoms of anorexia nervosa but responses opposite to those of most species including rats and normal human subjects. This suggests that the atypical opioid systems in the mouse may resemble those of the chronic anorexia nervosa patient in contrast to those of most species including the normal human. Characterization of this atypical opioid system may be useful in understanding the pathophysiology of anorexia nervosa.

Animals↗
PubMed1986

Adrenalectomy induced anorexia in gold thioglucose-treated obese mice: metabolic and hormonal changes.

Adrenalectomy of gold thioglucose (GTG)-treated hyperphagic obese mice had been shown by us earlier to result in anorexia, weight loss, hypoglycemia and subsequent death of all mice. More recent studies suggest that adipose tissue mass may not be the critical determinant of anorexia since a large proportion of GTG-treated non obese (pair-fed to curb obesity) mice when challenged with adrenalectomy also developed anorexia. The aim of the present studies was to determine whether the changes in circulating metabolites, namely, glucose, free fatty acids and hormones, including insulin, glucagon and ACTH, which accompany adrenalectomy, might provide a clue to the causative agent for the onset of anorexia in GTG obese and non obese mice. Accordingly, plasma levels of glucose, free fatty acids, insulin, glucagon and ACTH were measured in GTG-treated obese, non obese and in normal untreated mice following adrenalectomy or a sham operation. Preoperatively, plasma insulin levels were significantly elevated in GTG obese mice whereas plasma glucose, free fatty acids and glucagon levels were not appreciably different than those of untreated controls. Upon adrenalectomy and onset of anorexia, GTG obese mice exhibited a progressive decline in blood glucose and insulin levels; plasma free fatty acids increased precipitously but only after the first day. Plasma glucagon levels declined immediately following adrenalectomy, however, by the 6th day postoperatively they were significantly elevated above the sham operated obese and untreated controls. Prior to adrenalectomy, the pair-fed GTG non obese mice exhibited blood glucose and insulin levels well below the levels of untreated controls and GTG obese mice whereas plasma free fatty acids and glucagon levels were markedly elevated.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1991

Hyperammonemia and anorexia in Morris hepatoma-bearing rats.

Inoculation of Buffalo rats with Morris hepatoma produced significant anorexia within four weeks and reduced body weight within two weeks. Blood ammonia concentration was increased by 113% when the rats were euthanized, five days after the development of anorexia. Infusing ammonium salts into normal Buffalo rats also induced anorexia at a blood ammonia concentration comparable to that observed in the tumor-bearing rats. Although ammonia-infused rats exhibited expected increases in brain tyrosine, tryptophan, and metabolites of dopamine and serotonin, these alterations were attenuated in the tumor-bearing rats. These results indicate that hyperammonemia may be a general consequence of experimental cancer and that the increase in ammonia concentration may be of primary importance in the development of experimental cancer-induced anorexia. The rather small alterations in neurotransmitter metabolism in anorectic tumor-bearing rats deemphasize the role aberrations in DA and 5-HT systems in the development of experimental cancer anorexia.

Ammonia↗
PubMed1994

Changes of the corrected Q-T interval in the electrocardiogram of patients with anorexia nervosa.

Thirty patients with anorexia nervosa and 30 controls had an electrocardiogram with the corrected Q-T interval. The aim of the study was to analyse the corrected Q-T interval in patients with anorexia nervosa compared with the findings in the control group, to compare the body mass index between two groups and to measure underlying dispersion of the corrected Q-T interval in each of the 12 ECG leads in both groups. All corrected Q-T intervals were measured in each of the 12 ECG leads and the longest values of three consecutive intervals were used for this analysis. The prolonged corrected Q-T interval was found in 12 out of 30 patients with anorexia nervosa (40%), with the longest mean values of 0.421 s (range, 0.334-0.500 s), and in 2 out of 30 patients of the controls (7%), with the longest mean values of 0.390 s (range, 0.343-0.444 s). The difference was statistically significant (t = 4.453, P < 0.001). Relative risk for prolongation of the corrected Q-T interval in patients with anorexia nervosa was high: 12 compared with control subjects. The longest values of the corrected Q-T interval in both groups, and the longest values of the prolonged corrected Q-T interval in both groups were observed in the anteroseptal leads of the electrocardiograms. The mean serum potassium level in the group with anorexia nervosa was 3.97 and in the control group was 4.15 mmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMedDate not supplied

Cholecystokinin-induced hypophagia is not potentiated by cancer anorexia.

The interaction of cholecystokinin-induced hypophagia with cancer anorexia was investigated within both acute (Walker 256 carcinosarcoma) and chronic (methylcholanthrene-induced sarcoma) animal models of cancer anorexia. Cholecystokinin octapeptide (CCK8) effectively reduced feeding for at least one hour in both groups of rats. However, this peptide was no more effective in inducing hypophagia in tumor-bearing rats than in nontumor-bearing control rats when tested at a variety of doses (0.5, 5.0 and 50.0 microgram/kg; IP) both prior to and after the development of anorexia. Therefore, these data do not support a role of cholecystokinin in the mediation of experimental cancer anorexia, since no synergism of CCK8-induced hypophagia with the anorexia was observed.

Animals↗
PubMed1996

Neuropeptide Y blocks and reverses interleukin-1 beta-induced anorexia in rats.

Neuropeptide Y (NPY) increases feeding by direct action in the central nervous system (CNS). Interleukin-1 beta (IL-1 beta), on the other hand, induces anorexia when administered ICV at estimated pathophysiological (e.g., yielded by 1.0 ng/rat dose) and pharmacological (> or = 4.0 ng) concentrations in the cerebrospinal fluid (CSF). In the present study, we investigated NPY/IL-1 beta interactions using the ICV administration. ICV microinfusion of NPY (5.0 micrograms) significantly increased 2-h food intake (by 89%), whereas IL-1 beta decreased 2-h food intake (32% decrease with 1.0 ng/rat; 53% with 4.0 ng/rat; and 51% with 8.0 ng/rat). NPY (5.0 micrograms) blocked the anorexic effect induced by all doses of IL-1 beta when both compounds were administered concomitantly. Central infusion of NPY was also able to induce feeding in IL-1 beta-pretreated rats exhibiting marked anorexia. The results show that ICV-administered NPY blocks and reverses the anorexia induced by estimated pathophysiological and pharmacological concentrations of IL-1 beta in rats. A second interpretation of a data subset is that IL-1 beta attenuates or blocks NPY-induced increase in feeding depending on the IL-1 beta dose used. Blockage and reversal of IL-1 beta-induced anorexia by NPY suggest the importance in studying cytokine-peptide interactions in the regulation of feeding behavior. Understanding these endogenous interactions may produce strategies with potential therapeutic implications for chronic diseases associated with long-term anorexia.

Animals↗
PubMed2005

Early detection of cardiac dysfunction in patients with anorexia nervosa by tissue Doppler imaging.

BACKGROUND: Cardiac damage is a major complication of chronic starvation. The aim of this study was to evaluate the changes of left ventricular function in patients with anorexia nervosa by means of pulsed tissue Doppler imaging. METHODS: A total of 20 females (age 22.4+/-4.3 years) with overt anorexia nervosa, 20 matched healthy thin females with body mass index < 19 kg/m2 and 20 matched healthy normal-weight females underwent both standard echocardiography and tissue Doppler imaging. Myocardial systolic wave (Sm) and early (Em) and atrial (Am) diastolic waves were measured on the basal lateral segment and the basal interventricular septum from the apical four-chamber view. RESULTS: When compared with control groups, the anorexia nervosa group showed lower left ventricular mass (p < 0.0001), lower Sm peak of both lateral wall (6.5+/-0.9 vs. 9.4+/-2.1 and vs. 9.5+/-1.9 cm/sec, p < 0.001) and septum (5.6+/-1.5 vs. 8.6+/-1.6 and vs. 8.8+/-1.5 cm/sec, p < 0.001), and comparable Em, Am and Em/Am ratio. The ratio between transmitral peak E and Em was significantly greater in anorexic patients than in controls (lateral wall: 8.1+/-0.1 vs. 6.8+/-0.2 and vs. 6.9+/-0.2, p < 0.001; septum: 10.8+/-0.4 vs. 8.8+/-0.5 and vs. 8.8+/-0.3, p < 0.001). No differences were observed between thin and normal-weight females. In the anorexia nervosa group, S(m) peak was significantly related to left ventricular mass indexed, at both septum (r = 0.55, p < 0.02) and lateral wall (r = 0.49, p < 0.03) levels. CONCLUSIONS: These results show that anorexia nervosa is associated with left ventricular systolic dysfunction, which is related with the reduction of cardiac mass. Tissue Doppler imaging can give useful information in the identification of regional left ventricular dysfunction, in addition to traditional parameters.

Adult↗
PubMed2005

Bone loss associated with anorexia nervosa.

The objective of this study was to evaluate the epidemiology, diagnosis, pathophysiology, and treatment of bone loss related to anorexia nervosa. Earlier onset and longer duration of anorexia nervosa are associated with more severe bone loss. Osteoporosis develops in 38-50% of cases. Bone mineral density measurement by dual-energy X-ray absorptiometry is useful for assessing bone mass, and bone marker assays provide information on bone turnover. Bone loss in anorexia nervosa is probably multifactorial. Estrogen deficiency was long felt to be the major factor. However, in contrast to postmenopausal osteoporosis, bone loss associated with anorexia nervosa is related mainly to inadequate bone formation, with only a slight increase in bone resorption. This suggests a role for nutritional factors, such as disturbances in the growth hormone-somatomedin C axis (GH/IGF-I) related to malnutrition. The best treatment strategy for correcting bone mass in patients with anorexia nervosa is not agreed on. Resumption of menstrual cycles and weight gain seem necessary but not always sufficient. Studies found no benefits with estrogen therapy, but this was usually given as estrogen-progestin contraceptives. No vast studies evaluating hormone replacement therapy have been reported. Bone formation enhancers such as IGF-I seem to provide the best results, most notably when used in combination with estrogens. This suggests that complex treatment strategies combining bone formation enhancers and bone resorption inhibitors may deserve evaluation.

Absorptiometry, Photon↗
PubMed2005

"Starve a fever and feed a cold": feeding and anorexia may be adaptive behavioral modulators of autonomic and T helper balance.

Anorexia is a common symptom accompanying infections, but the teleology of the phenomenon remains unexplained. We hypothesize that anorexia may represent a prehistoric behavioral adaptation to fight infection by maintaining T helper (Th)2 bias, which is particularly vital in fighting bacterial pathogens. Specifically, we propose that anorexia may avert the reduction of Th2/Th1 ratio by preventing feeding-induced neurohormonal and vagal output from the gut. Emerging evidence suggests that the vagal and neurohormonal output of the gut during feeding promotes Th1 function, which is desirable in fighting viral infections. Since fever may be an adaptation to fight bacteria and "colds" are generally viral in origin, the adage "starve a fever and feed a cold" may reflect a sensible behavioral strategy to tilt autonomic and Th balance in directions that are optimal for fighting the particular type of infection. The ability to modulate T helper balance through the neurohormonal and autonomic axis by adjusting food intake may be the mechanism behind other unexplained clinical observations such as the improved outcomes of ICU patients after enteric versus parenteric feedings. Compared to the prehistoric period when bacterial infection was commonplace, the anorexic response may be less adaptive today when viruses and cancers have become common triggers of anorexia. By promoting host anorexia, cachexia, and insomnia, cancers and viruses can deter behaviors such as digestion and sleep that would raise vagal and Th1 activity against tumors and viruses. Hydration and sleep, unexplained but widely accepted recommendations for flu patients, may also work by promoting vagal and Th1 functions. Modulating feeding, hydration, and sleep may prove beneficial in treating other conditions associated with abnormal autonomic and Th balance.

Adaptation, Physiological↗
PubMed1997

Body image disturbances and their change with videofeedback in anorexia nervosa.

Disturbance in the way the body is experienced is a diagnostic criterion for anorexia nervosa, and impedes recovery. A method relatively free of external prompts, to reduce the potential for experimentally induced biases, evaluated body image distortions (BID) in 18 patients with anorexia nervosa soon after admission to an inpatient unit, and 18 normal controls, before and after a videofeedback session. The BID were assessed in the affective and self/social domains by visual analogue scales in which the instructional set oriented subjects to (a) the sensation of fatness (Affective Response, AR), and (b) size compared with other young women (Comparative Size Response, CSR). The AR and CSR were significantly greater than normal in anorexia but decreased significantly with videofeedback, while values for controls were stable. The AR and CSR were only partially independent, indicating overlap of the domains. In anorexia only, the responses were related to two DSM-IV diagnostic criteria for anorexia, fear of gaining weight and health-weight concerns, as well as to drive for thinness and body dissatisfaction. Fear of gaining weight occupied a central position in determining the magnitudes of BID and the other measures, including anxiety and depression.

Adult↗
PubMed1993

Mineral balance and bone turnover in adolescents with anorexia nervosa.

We evaluated seven female adolescents with anorexia nervosa to determine whether calcium metabolism was affected by their disorder. We measured calcium absorption, urinary calcium excretion, and calcium kinetics, using a dual-tracer, stable-isotope technique during the first weeks of an inpatient nutritional rehabilitation program. Results were compared with those from a control group of seven healthy adolescent girls of similar ages. The percentage of absorption of calcium was lower in subjects with anorexia nervosa than in control subjects (16.2% +/- 6.3% vs 24.6% +/- 7.2%; p < 0.05). Urinary calcium excretion was greater in subjects with anorexia nervosa than in control subjects (6.4 +/- 2.5 vs 1.6 +/- 0.7 mg.kg-1 x day-1; p < 0.01) and was associated with bone resorption rather than calcium hyper-absorption. Calcium kinetic studies demonstrated a decreased rate of bone formation and an increased rate of bone resorption. These results suggest marked abnormalities in mineral metabolism in patients with anorexia nervosa. From these results, we hypothesize that improvement in bone mineralization during recovery from anorexia nervosa will require resolution of hormonal abnormalities, including hypercortisolism, in addition to increased calcium intake.

Absorption↗
PubMed1984

Altered exercise performance and abnormal sympathetic responses to exercise in patients with anorexia nervosa.

We evaluated the cardiovascular and sympathetic responses to exercise in patients with anorexia nervosa to determine whether their bradycardia results from a high level of physical fitness. Twenty adolescent patients with anorexia nervosa underwent maximal exercise tests, and the results were compared with those in 15 age-matched adolescent girls. In the patients with anorexia, maximal values were heart rate 174 +/- 2.8 bpm, systolic blood pressure 127 +/- 3.4 mm Hg, oxygen consumption 31 +/- 1.1 ml/kg/min, and plasma norepinephrine concentration 1581 +/- 238 pg/ml (n = 16). In the controls, corresponding values were significantly higher (P less than 0.025): heart rate 193 +/- 2.1 bpm, systolic blood pressure 163 +/- 4.4 mm Hg, oxygen consumption 39.3 +/- 1.6 ml/kg/min, and plasma norepinephrine 2695 +/- 413 (n = 10). Anaerobic threshold occurred at the same percent of maximal work in patients and controls. Results of exercise ECGs in all controls were normal, but five patients with anorexia nervosa developed significant ST segment depression. Thus, in patients with anorexia nervosa there is abnormal working capacity and cardiovascular responses to exercise and abnormal sympathetic responses to the stimulus of exercise, and a myocardial abnormality manifested as ST segment depression during exercise in some.

Adolescent↗
PubMed1994

Disturbances in growth hormone secretion and action in adolescents with anorexia nervosa.

Women in whom anorexia nervosa develops during adolescence have failure of linear growth associated with low levels of insulin-like growth factor I (IGF-1). To investigate the pathophysiology of growth retardation in adolescents with anorexia nervosa, we measured basal growth hormone (GH), growth hormone-binding protein (GHBP), IGF-1, and insulin-like growth factor binding protein-3 (IGFBP-3) in three groups of patients: (1) 28 recently hospitalized female adolescents with anorexia nervosa, (2) 23 of the same patients after partial weight restoration, and (3) 28 healthy control subjects matched for age, sex, and pubertal stage. Fasting GH levels in group 1 did not differ significantly from those in group 3. In contrast, serum GHBP (p < 0.001), IGF-1 (p < 0.001), and IGFBP-3 (p < 0.01) were significantly lower in group 1 than in group 3. Serum GHBP and IGFBP-3 levels were positively correlated with body mass index. Serum GHBP levels were low in patients in all five pubertal stages and even in those shown to have adequate GH secretion. In group 2 (after refeeding) the serum IGF-1 concentration increased significantly and GHBP and IGFBP-3 returned to normal. We conclude that patients with anorexia nervosa have diminished GH action resulting in decreased secretion of IGF-1. The positive correlation with body mass index and the reversibility with refeeding suggest that these changes are secondary to malnutrition. Altered GH function that occurs during the years of active growth can explain the growth retardation seen in anorexia nervosa.

Adolescent↗