Neurotransmitter and Hormonal Background of Hostility in Anorexia nervosa (original) (raw)

Anorexia Nervosa: Directions for Future Research NEUROENDOCRINE/NEUROTRANSMITTER ABNORMALITIES IN ANOREXIA NERVOSA

the Study Group on Anorexia Nervosa (AN): Basic Mechanisms, Clinical Approaches and Treatment met in Geneva, Switzerland to discuss recent progress in research on anorexia nervosa, and to identify directions for future studies. Anorexia nervosa is a disorder of unknown etiology, without a specific curative treatment, affecting mostly individuals in adolescence and early adulthood, with significant morbidity and mortality, and having a major impact on psychosocial and vocational development. In anorexia nervosa there are severe disturbances in virtually every endocrine system, such as the hypothalamic-pituitary-adrenal (HPA) axis, the hypothalamic-pituitary-gonadal (HPG) axis, the hypothalamic-pituitary-thyroid (HPT) axis, the growth hormone (GH)lsomatomedin C (IGF-1) system, and the central and peripheral arginine vasopressin (AVP) systems. Furthermore, classical neurotransmitter systems, such as the cholinergic noradrenergic, and serotonergic systems, are abnormally regulated in anorexia nervosa. New research data is also emerging on the abnor-maUregulation of immune function in this disorder. The Study Group concluded that even though several biological systems are abnormally regulated in anorexia nervosa, there is no biological test which is specific enough to make the diagnosis of the disorder. New directions for research in anorexia nervosa are identified and discussed in this report. Finally, the Study Group proposed future meetings to bring together clinical and pre-clinical (pharmacological, biochemical, and molecular) scientists studying topics, such as neuroendocrine function, which are important in the biology of anorexia nen/osa.

The hypothalamic-pituitary-adrenal axis in anorexia nervosa

1996

Studies examining the function of the hypothalamic-pituitary-adrenal (HPA) axis in anorexia nervosa are reviewed. A principal finding is that of hypercortisolism, associated with increased central corticotropin-releasing hormone levels and normal circulating levels of adrenocorticotropic hormone. Similarities between neuroendocrine findings in anorexia nervosa and in affective disorder are reviewed. The contribution of circadian rhythm disturbances and malnutrition to observed HPA axis abnormalities in anorexia nervosa is also considered. Directions for future research are discussed.

Aggressive Behavioral Characteristics and Endogenous Hormones in Women with Bulimia nervosa

Neuropsychobiology, 2000

Increased aggressiveness frequently occurs in patients with bulimia nervosa (BN), but its neurobiological correlates have been poorly investigated. In this study, we investigated possible relationships between such clinical measure and blood levels of endogenous hormones in patients with BN. Morning plasma levels of testosterone, 17β-estradiol, prolactin (PRL) and cortisol were measured in 33 bulimic women and 22 healthy female controls. The eating-related psychopathology, depression and aggressiveness were rated by specific psychometric scales. Bulimic patients showed decreased plasma levels of PRL and 17β-estradiol, and increased concentrations of cortisol and testosterone. Moreover, patients scored higher than healthy controls on rating scales assessing eating-related psychopathology, depressive symptoms and aggressiveness. A significant positive correlation was found between testosterone plasma levels and aggressiveness in patients but not in controls. These findings suggest tha...

Studies of serotonin function in anorexia nervosa

Psychiatry Research, 1996

Neuroendocrine, temperature, test-meal, and psychometric responses are reviewed following challenges with the post-synaptic S-HT receptor agonist m-chlorophenylpiperazine (m-CPP), the S-HT precursor L-tryptophan (L-TRP), and placebo in 12 patients with anorexia nervosa (AN) and 16 healthy controls. A subset of the AN patients (n = 8) were rechallenged 3-4 weeks after attaining a predetermined goal weight. AN patients had blunted prolactin (PRL) responses to both m-CPP and L-TRP at low-weight and at goal-weight in comparison to controls, although there was a tendency toward normalization with weight gain. There were trends for blunted growth hormone (GH) responses following both L-TRP and m-CPP in the low-weight but not the goal-weight AN patients. Cortisol (CORT) responses following m-CPP and L-TRP were not significantly different among any of the groups. Temperature and test-meal measures were largely unaffected by serotonergic agents in the patients, although m-CPP decreased meal size in the controls. Psychometric responses were variable and are briefly described. Taken together, these findings indicate that responsiveness in post-synaptic hypothalamic-pituitary serotonergic pathways is altered in AN patients. Although there were some trends toward normalization of responsiveness following goal-weight attainment, many differences tended to persist in the patients despite an average increase of 13 kilograms. These may represent changes in serotonergic function at levels in the CNS "above" the hypothalamus.

Behavioral neuroendocrinology and treatment of anorexia nervosa

Frontiers in Neuroendocrinology, 2008

The user has requested enhancement of the downloaded file. All in-text references underlined in blue are added to the original document and are linked to publications on ResearchGate, letting you access and read them immediately. This article appeared in a journal published by Elsevier. The attached copy is furnished to the author for internal non-commercial research and education use, including for instruction at the authors institution and sharing with colleagues.

Studies of serotonin function in anorexia nervosal

Neuroendocrine, temperature, test-meal, and psychometric responses are reviewed following challenges with the post-synaptic S-HT receptor agonist m-chlorophenylpiperazine (m-CPP), the S-HT precursor L-tryptophan (L-TRP), and placebo in 12 patients with anorexia nervosa (AN) and 16 healthy controls. A subset of the AN patients (n = 8) were rechallenged 3-4 weeks after attaining a predetermined goal weight. AN patients had blunted prolactin (PRL) responses to both m-CPP and L-TRP at low-weight and at goal-weight in comparison to controls, although there was a tendency toward normalization with weight gain. There were trends for blunted growth hormone (GH) responses following both L-TRP and m-CPP in the low-weight but not the goal-weight AN patients. Cortisol (CORT) responses following m-CPP and L-TRP were not significantly different among any of the groups. Temperature and test-meal measures were largely unaffected by serotonergic agents in the patients, although m-CPP decreased meal size in the controls. Psychometric responses were variable and are briefly described. Taken together, these findings indicate that responsiveness in post-synaptic hypothalamic-pituitary serotonergic pathways is altered in AN patients. Although there were some trends toward normalization of responsiveness following goal-weight attainment, many differences tended to persist in the patients despite an average increase of 13 kilograms. These may represent changes in serotonergic function at levels in the CNS "above" the hypothalamus.

A review of endocrine changes in anorexia nervosa

Journal of Psychiatric Research, 1999

Anorexia nervosa is a syndrome of unknown etiology[ It is associated with multiple endocrine abnormalities[ Hypothalamic monoamines "especially serotonin#\ neuropeptides "especially neuropeptide Y and cholecystokinin# and leptin are involved in the regulation of human appetite\ and in several ways they are changed in anorexia nervosa[ However\ it remains to be clari_ed whether the altered appetite regulation is secondary or etiologic[ Increased secretion of corticotropin!releasing hormone and proopiomelanocortin seems to be secondary to starvation\ however\ there is evidence that it may maintain and intensify anorexia\ excessive physical activity and amenorrhea[ Hypothalamic amenorrhea\ which is a diagnostic criterion in anorexia nervosa\ is not solely related to the low body weight and exercise[ Growth hormone resistance with low production of insulin!like growth factor I and high growth hormone secretion re~ect the nutritional deprivation[ The nutritional therapy of patients with anorexia nervosa might be improved by administering an anabolic agent such as growth hormone or insulin!like growth factor I[ So far none of the endocrine abnormalities have proved to be primary\ however\ there is increasing evidence that some of these might participate in a vicious circle[ Þ 0888 Elsevier Science Ltd[ All rights reserved[

Psychoneuroendocrinology of anorexia nervosa

Psychoneuroendocrinology, 2006

It is suggested that the symptoms of anorexia nervosa are physiological responses to starvation. There is no evidence of a neural or non-neural dysfunction that predisposes women for anorexia nervosa and the endocrine and psychological consequences of starvation are reversed once patients have re-learnt how to eat and regained a normal body weight. Because variability in the supply of food may be a common evolutionary condition, it is more likely that body weight is variable than constant in normal circumstances. The role of the neuroendocrine system in times of feast and famine is to allow the individual to adopt behavioral strategies as needed rather than maintaining body weight homeostasis. Treatment of anorexic patients should aim at reducing their high level of physical activity in order to facilitate eating.

Neurobiology of Anorexia Nervosa

Anorexia nervosa is a rare, yet dangerous and often deadly disorder that primarily affects young teenage women. Individuals with anorexia are driven to starvation, refuse to maintain a minimally normal body weight, posses distorted perceptions and beliefs of oneself, and demonstrate abnormal attitudes toward food and weight. Specifically the restricting type, a subtype of anorexia that does not involve binging or purging behavior, will be the focus of this paper. Within the anorexic brain there are many chemical changes and brain abnormalities that take place including hormonal and chemical imbalances and dysfunction in the insular cortex and frontal-striatal circuits. Many of these abnormalities are believed to intensify and prolong the duration of the disorder while others are a direct result of starvation. Medications provide some relief for certain symptoms of anorexia, but the most successful treatment options include forms of CBT and family therapy.