Relevant bibliographies by topics / Anorexia neurosa

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Anorexia neurosa'

Author: Grafiati
Published: 4 June 2021
Last updated: 9 February 2022

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Journal articles on the topic "Anorexia neurosa"

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Lima, Mônica Assunção Costa. "Anorexia e melancolia." Revista Latinoamericana de Psicopatologia Fundamental 15, no. 2 (June 2012): 251–64. http://dx.doi.org/10.1590/s1415-47142012000200003.

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O texto desenvolve a proposição freudiana, que se encontra no Rascunho G, de que a anorexia é a neurose paralela à melancolia. Propõe que o elo entre melancolia e anorexia deve ser buscado no campo do narcisismo. Explora quatro aspectos da melancolia que permitem a aproximação destas duas afecções, entre elas, a inibição, a perspectiva de uma instância crítica que se diferencia do eu e se volta contra ele, o sadismo com que essa instância crítica trata o eu, e a identificação do eu ao objeto.
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Cunha, Flávia Coutinho Campos, and Ângela Maria Resende Vorcaro. "Anorexia: "uma neurose paralela à melancolia"." Revista Latinoamericana de Psicopatologia Fundamental 16, no. 2 (June 2013): 232–45. http://dx.doi.org/10.1590/s1415-47142013000200004.

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Investiga-se a assertiva freudiana de que "a neurose nutricional paralela à melancolia é a anorexia". Percorreremos a obra freudiana para construir o paralelo entre essas duas afecções. O conceito de narcisismo e o mecanismo de identificação fundamentarão essa aproximação desdobrada nos seguintes pontos: a anestesia sexual, a autodepreciação e o sadismo.
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Sergeeva, A. "Energy and protein needs of patients with anorexia neuroza (AN)." Clinical Nutrition 37 (September 2018): S103. http://dx.doi.org/10.1016/j.clnu.2018.06.1396.

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Berlinck, Manoel Tosta, and Ana Cecília Magtaz. "Reflexões sobre O caso de Ellen West: estudo antropológico-clínico, de Binswanger." Revista Latinoamericana de Psicopatologia Fundamental 11, no. 2 (June 2008): 232–38. http://dx.doi.org/10.1590/s1415-47142008000200005.

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O relato do caso de Ellen West ilustra de forma magistral que a questão da anorexia não está somente ligada a um problema alimentar. Revela tratar-se de um conflito entre o ego e o superego e, portanto, representa uma neurose narcísica. A severidade do superego baseia-se nas regras de cumprimento dos ideais. Quanto mais esses forem elevados, menos poderão ser satisfeitos. Geralmente, para ser objeto de investimento amoroso do superego o ego tem que se mostrar como o que não é: o ideal.
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Silva, Alinne Nogueira, and Angélica Bastos. "Anorexia: uma pseudo-separação frente a impasses na alienação e na separação." Psicologia Clínica 18, no. 1 (2006): 97–107. http://dx.doi.org/10.1590/s0103-56652006000100008.

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O presente trabalho versa sobre a anorexia nos quadros de neurose e tem por objetivo detectar as dificuldades com que se defronta a psicanálise nos casos de sujeitos que recusam a alimentação. Segundo uma abordagem teórico-clínica, o artigo parte do sintoma anoréxico, tal como ele se apresenta no plano dos fenômenos, e investiga sua articulação com o plano estrutural na fantasia neurótica. Admite-se a premissa de que a anorexia, mais que uma recusa de comer, afirma-se como um "comer nada". Assim, procede-se a uma investigação sobre o "nada", aqui entendido como um objeto. A fim de conceituar essa modalidade de objeto, recorre-se à teoria lacaniana da constituição do sujeito segundo as operações de alienação e separação. Examina-se a fantasia de desaparecimento e discutem-se o êxito e o impasse da separação, quando esta se estabelece às custas de uma estratégia anoréxica.
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Liu, Wei, Dianyou Li, Fafa Sun, Xiaoxiao Zhang, Tao Wang, Shikun Zhan, Yixin Pan, et al. "Long-Term Follow-up Study of MRI-Guided Bilateral Anterior Capsulotomy in Patients With Refractory Anorexia Nervosa." Neurosurgery 83, no. 1 (August 18, 2017): 86–92. http://dx.doi.org/10.1093/neuros/nyx366.

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Abstract BACKGROUND Anorexia nervosa (AN) is one of the most challenging psychiatric disorders to treat. The poor clinical outcomes warrant novel treatments for AN, especially in severe and persistent cases. OBJECTIVE To explore the feasibility of magnetic resonance imaging-guided bilateral anterior capsulotomy in the treatment of refractory AN. METHODS Seventy-four patients diagnosed with refractory AN who underwent capsulotomy completed this 3-yr follow-up study. Outcomes included body mass index (BMI) and results from a series of psychiatric scales (for obsessive, depressive, and anxious symptoms) that were implemented at baseline (presurgery), and 1 mo, 1 yr, and 3 yr after surgery. RESULTS Compared to presurgical levels, BMI increased significantly at 1-yr and 3-yr follow-ups. Compared to presurgery scores, psychiatric scale scores were significantly improved at 1-mo postsurgery, and continued to remain low at the 1-yr and 3-yr follow-ups. In addition, Mini-Mental State Examination (MMSE) scores were in the normal range during the long-term follow-up. The most common short-term side effects included urinary incontinence (n = 7), sleep disorders (n = 8), and fatigue (n = 6). Long-term complications included disinhibition (n = 6), memory loss (n = 3), and lethargy (n = 4). No patient in this study experienced death or disability. CONCLUSION Capsulotomy enabled patients with refractory AN to normalize their weight, especially those in life-threatening conditions. While it appears to be an acceptable life-saving treatment, it is indicated only when fulfilling strict criteria given its complications and irreversibility.
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Zanello, Marc, Philibert Duriez, Johan Pallud, Alexandre Roux, Tarek Sharshar, Philip Gorwood, and Bertrand Devaux. "Letter: Long-Term Follow-up Study of MRI-Guided Bilateral Anterior Capsulotomy in Patients With Refractory Anorexia Nervosa." Neurosurgery 83, no. 1 (April 18, 2018): E39—E40. http://dx.doi.org/10.1093/neuros/nyy123.

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Zhang, Chencheng, Dianyou Li, Guozhen Lin, and Bomin Sun. "In Reply: Long-Term Follow-up Study of MRI-Guided Bilateral Anterior Capsulotomy in Patients With Refractory Anorexia Nervosa." Neurosurgery 83, no. 1 (April 18, 2018): E41—E42. http://dx.doi.org/10.1093/neuros/nyy124.

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Segreeva, A., V. Luft, A. Lapitsky, and E. Tyavokina. "Informativeness of the calculation of basal metabolic rate (bmr) in patients with anorexia neuroza (AN)." Clinical Nutrition 37 (September 2018): S103. http://dx.doi.org/10.1016/j.clnu.2018.06.1395.

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Gautron, Laurent. "Neurobiology of inflammation-associated anorexia." Frontiers in Neuroscience, 2009. http://dx.doi.org/10.3389/neuro.23.003.2009.

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Dissertations / Theses on the topic "Anorexia neurosa"

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Pimentel, Fernanda Freire de Carvalho. "Anorexia: um sintoma contemporâneo." Universidade do Estado do Rio de Janeiro, 2013. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=7653.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
Esta dissertação propõe investigar o sintoma anoréxico na estrutura neurótica como um sintoma contemporâneo em consequência da baixa operatividade da função paterna e da incidência avassaladora do Desejo Materno. A pesquisa foi iniciada por um levantamento histórico-bibliográfico do jejum e da recusa alimentar ao longo da história, até o estabelecimento da anorexia como uma psicopatologia. Para dar sustentação ao eixo central desta Dissertação, a pesquisa explora o conceito de pai na Obra de Freud e no ensino de Lacan, investigando a baixa operatividade desta função e seus efeitos na formação do sintoma. O conceito de pulsão é explorado com o objetivo de compreender a anorexia como uma invasão pulsional no corpo decorrente da precária sustentação da armadura simbólica que a lei paterna insere. Deste modo, esta Dissertação expõe duas hipóteses centrais: a anorexia como uma manobra de separação, operação que a função paterna não inscreve devidamente e desta forma um recurso diante da hegemonia materna; e a anorexia como estragos que apontam a invasão da mortífera pulsão no corpo, decorrentes da presença avassaladora do Outro materno e da inconsistência da função paterna
The purpose of this thesis is to investigate the anorexic symptom in the neurotic structure as a contemporary symptom resulting from the low operatibility of the paternal role and the overwhelming incidence of the Maternal Desire. The research was initiated by a historical-bibliographical survey of fasting and food refusing throughout history, until the establishment of anorexia as a psychopathology. Giving support to the control axis of this thesis, the research explores the father concept in the work of Freud and Lacans teaching, investigating the low operability of this function and its effects on symptom formation. The drive concept is explored in order to understand anorexia as an encroachment drive in the body due to the precarious support of the symbolic armor that the paternal law inserts. Thus, this thesis exposes two central hypotheses: anorexia as a separation ploy, an operation that the paternal function does not fulfil properly and, therefore, is not an appeal in the face of maternal hegemony, and anorexia as damages that point the invasion of deadly drive in the body, arising from the overwhelming presence of the Maternal Other and of the inconsistency of the paternal function
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Kuschewski, Ruth [Verfasser], Jens [Akademischer Betreuer] Brüning, and F. Thomas [Akademischer Betreuer] Wunderlich. "Gp130 Signaling In POMC Neurons Is Required For CNTF-Induced Anorexia / Ruth Kuschewski. Gutachter: Jens Brüning ; F. Thomas Wunderlich." Köln : Universitäts- und Stadtbibliothek Köln, 2011. http://d-nb.info/103801705X/34.

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Paues, Jakob. "Brain Stem Involvement in Immune and Aversive Challenge." Doctoral thesis, Linköping : Linköping University, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-7579.

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Zizzari, Philippe. "Implication de ghreline/obestatine, deux peptides issus du même précurseur, dans le contrôle de la sécrétion d'hormone de croissance et du comportement alimentaire." Phd thesis, Université Paris Sud - Paris XI, 2007. http://tel.archives-ouvertes.fr/tel-00129504.

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Dans cette thèse nous nous sommes intéressés aux relations entre ghreline (GHR) d'une part et sécrétion d'hormone de croissance (GH) et prise alimentaire (PA) d'autre part. Nous avons montré : a) que la sécrétion de GHR est rythmique ; b) que les pics de GHR, peu corrélés avec ceux de GH, sont en relation étroite avec les épisodes de PA. Néanmoins, un antagoniste du récepteur GHSR1a montre que la GHR endogène modulerait l'amplitude du pic de GH et que ses effets sur la PA mettraient en jeu soit le GHSR1a dans des états d'activation différente soit des récepteurs différents ; c) que les taux de GHR dépendent plus de l'état nutritionnel que de la masse grasse et seraient régulés par des facteurs présents dans l'intestin. Une dérégulation de ces derniers pourrait participer au développement de l'obésité ; d) que chez l'anorexique (AN) le polymorphisme Leu72Met présente un déséquilibre de transmission qui est plus marqué chez l'AN boulimique que chez l'AN restrictive.
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MARTINŮ, Veronika. "Problematika poruch příjmu potravy na 2. stupni ZŠ." Master's thesis, 2011. http://www.nusl.cz/ntk/nusl-80676.

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Thesis deals with the issue of food intake disorders in secondary school. The theoretical part of the work is focused on defining the terms anorexia nervosa and bulimia nervosa. Starting with historical development of these diseases, through complexity of causes and consequences of the disease and description of an endangered group of patients, I got to the contemporary medical treatment used. The practical part of this work consists of the questionnaire survey of adolescent students. Based on the results of this survey I proposed a brief prevention program, targeting in particular parents and teachers, including practical advices how to support the prevention of food intake disorder diseases of adolescents.
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Chen, Kuei-Mi, and 陳貴米. "Effect of estrogen on adenosine-induced anorexia and neuropeptide neuronal activities." Thesis, 2000. http://ndltd.ncl.edu.tw/handle/12772556010409698040.

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碩士
中國醫藥學院
醫學研究所
88
Adenosine induces vasodilatation, muscle relaxation and anorexia in animals. To investigate whether the anoretic effect of adenosine is modulated by estrogen, adult ovariectomized (OVX) rats primed with either estradiol (E2, 10μg/rat) or sesame oil (OIL) were deprived of food for 24h and subjected to peripheral adenosine injection (0, 10, 100 mg/kg) immediately prior to refeeding. The results showed that administration of 100 mg/kg adenosine reduced food intake at the first two hour of refeeding regradless of the steroid milieu of the rats, even though E2- primed rats had leaner body size. However, in E2-treated rats, this initial supression of food intake was compensated by 8h of refeeding, whereas in OVX+OIL animals cumulated food intake at the same time point was still significantly lower than that of saline-injected rats. I then investigated whether E2 could modulate the hypotensive and bradycardiac effects of adenosine by measuring blood pressure and heart rate in anesthetized OVX rats that had been treated with either estradiol (E2, 10μg/rat) or sesame oil for 2 days. Blood pressure and heart rate were significantly suppressed by every adenosine dose administered (P<0.0001). Statistic analysis revealed a main effect of E2 on heart rate (P=0.0002) and duration of bradycardia (P=0.0001). E2 also reduced the hypotensive response to adenosine. These data suggest that E2 can modulate adenosine-induced inhibition of cardiovascular functions in female rats. Immunohistochemical staining showed increased cFos expression in supraoptic nucleus (SON) after adenosine injection in a dose-dependent manner but not in paraventricular nucleus (PVN). cFos expression in oxytocin (OT) neurons in both PVN and SON and in vasopressin (VP) neurons in SON was also increased by adenosine, suggesting that adenosine preferentially activated OT neurons. However, E2 failed to have an impact on the induction of cFos. Expression of OT, VP, neuropeptide Y (NPY) and NADPH-diaphorase (NADPH-d) in the hypothalamus or cerebral cortex was not affected by estrogen either. The data indicated that although adenosine-induced anorexia or cFos expression in the central nervous system was not influenced by E2, E2 did play a modulatory role in the long-term control of body weight and food intake and in cardiovascular responses to adenosine. Nevertheless, these effects of E2 were unlikely mediated by hypothalamic OT, VP, NPY or NADPH-d neurons.
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Ye, Mei-Chen, and 葉玫真. "The role of neuropeptide Y neurons in adenosine receptor agonist-induced anorexia." Thesis, 2003. http://ndltd.ncl.edu.tw/handle/00814536097766229529.

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碩士
中國醫藥學院
醫學研究所
91
Our previously study indicated that the inhibitory effect of adenosine on feeding is not mediated by oxytocin neurons. The purpose of the present study was to investigate the role of NPY neurons in adenosine receptor agonist-induced anorexia. We found that intracerebral co-administration of 10 μg/5ul N6-cyclopentyladenosine（CPA, A1 receptor agonist）or 1 μg/5ul CGS21680（CGS, A2a receptor agonist）with 10 μg/5ul NPY did not block the inhibitory effect of CPA or CGS-on food intake in overnight fasted rats（P＞0.05）. Another set of animals were sacrificed 2h after icv injection of CPA or CGS（1, 5 and 10 μg）and brain tissues were subjected to immunocytochmistry of NPY . The results showed that adenosine failed to alter NPY levels in the hypothalamic Arcuate（ARC）and Paraventricular（PVN）nuclei. These data reveal that the anorectic effect of adenosine is not mediated by NPY neurons. In order to investigate whether NPY cell bodies express adenosine receptors, double-label immunocytochemistry was performed in brain tissues obtained from icv cholchicin-treated animals. The result showed that although NPY was in close apposition with adenosine receptor immunoreactivity, there was no evidence of colocalization of both antigens. To further investigate the role of endogenous adenosine in the modulation of food intake, satiated rats were treated icv with 1, 5 or 10 μg DPCPX（A1 receptor antagonist）or ZM-2413851（ZM, A2a receptor antagonist）. I found that 10ug DPCPX significantly increased food intake（P＜0.05）, but ZM failed to alter the feeding behavior （P＞0.05）. The data suggest that endogenous adenosine A1 receptor plays a role in normal feeding behavior and adenosine via A1 receptors may have the same target as NPY in PVN. However, exogenous adenosine-induced anorexia is not mediated by orexigenic NPY neurons.
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DelRusso, Tara Ann. "Eating Attitudes and Body Image in 7th, 9th, and 11th Grade Female Students." 2010.

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Stefano, Johanna. "Risk of Eating Disorders in Elite Female Pair and Single Figure Skaters and Ice Dancers." 2009.

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Books on the topic "Anorexia neurosa"

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Vries, Jan Maarten. By appointment only: Nerve problems, stress, fears, anxiety, depression, hypertension, hysteria, suicide, psychosomatic problems, alcoholism, allergies, diet, anorexia nervosa, deficiencies, communication. Edinburgh: Mainstream Pub., 1985.

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Wójcik-Gładysz, Anna. Ghrelin – hormone with many faces. Central regulation and therapy. The Kielanowski Institute of Animal Physiology and Nutrition, Polish Academy of Sciences, 2020. http://dx.doi.org/10.22358/mono_awg_2020.

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Discovered in 1999, ghrelin, is one of the peptides co-creating the hypothalamicgastrointestinal axis, otherwise known as the brain-gut axis. Ghrelin participates in many physiological processes and spectrum of its activity is still being discovered. This 28 amino acid peptide ‒ a product of the ghrl gene, was found in all vertebrates and is synthesized and secreted mainly from enteroendocrine X/A cells located in the gastric mucosa of the stomach. Expression of the ghrelin receptor has been found in many nuclei of the hypothalamus involved in appetite regulation. Therefore it’s presumed that ghrelin is one of the crucial hormones deciphering the energy status required for the maintenance of organism homeostasis. Ghrelin acts as a signal of starvation or energy insufficiency and its level in plasma is reduced after the meal. Neuropeptide Y (NPY) and agouti-related peptide (AgRP; NPY/AgRP) neurons located in the arcuate nucleus (ARC) area are the main target of ghrelin in the hypothalamus. This subpopulation of neurons is indispensable for inducing orexigenic action of ghrelin. Moreover ghrelin acting as a neurohormone, mainly in the hypothalamus area, plays an important role in the regulation of growth and reproduction processes. Indeed, ghrelin action on reproductive processes has been observed in the systemic effects exerted at both hypothalamus-pituitary and gonadal levels. Similarly the GH-releasing ghrelin action was observed both on the hypothalamus level and directly on the somatotrophic cells in the pituitary and this dose-related GH releasing activity was found in in vitro as well as in in vivo experiments. In recent years, numerous studies revealed that ghrelin potentially takes part in the treatment of diseases associated with serious disturbances in the organism energy balance and/or functioning of the gastrointestinal tract. It was underlined that ghrelin may be a hormone with a broad spectrum of therapeutic effect on obesity and anorexia nervosa, as well as may also have protective effect on neurodegenerative diseases, inflammatory disorders or functional changes in the body caused by cancers. In overall, ghrelin treatment has been tested in over 100 preclinical studies with healthy volunteers as well as patients with various types of cancer, eating disorders such as anorexia nervosa and bulimia nervosa. It was observed that ghrelin has an excellent clinical safety profile and emerging side effects occurred only in 3–10% of patients and did not constitute a sufficient premise to discontinue the therapy. In general, it can be concluded that ghrelin may be sufficiently used as a prescription drug.
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Book chapters on the topic "Anorexia neurosa"

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Treasure, Janet. "The Biology of Anorexia Nervosa." In Biological Basis and Therapy of Neuroses, 93–106. CRC Press, 2018. http://dx.doi.org/10.1201/9781351070249-5.

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MILLS, IVOR H. "THE NEURONAL BASIS OF COMPULSIVE BEHAVIOUR IN ANOREXIA NERVOSA." In Anorexia Nervosa and Bulimic Disorders, 231–35. Elsevier, 1986. http://dx.doi.org/10.1016/b978-0-08-032704-4.50027-9.

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Krassas, Gerasimos E., and Luigi Bartalena. "Endocrinology of eating disorders." In Oxford Textbook of Endocrinology and Diabetes, 280–87. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.2243.

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Eating disorders affect about five million Americans every year. There are three different eating disorders: anorexia nervosa, bulimia nervosa, and binge eating disorder. Eating disorders are complex conditions deriving from a complex interplay of long-standing behavioural, emotional, psychological, interpersonal, and social factors. The neuronal circuits that control the ingestion of food are mainly related to catecholaminergic, serotoninergic, and peptidergic systems. In this respect, while serotonin, dopamine and prostaglandin promote the ingestion of food, by contrast, neuropeptide Y, noradrenaline, γ‎-aminobutyric acid (GABA), and opioid peptides inhibit food ingestion, thus causing the development of eating disorders (1). Eating disorders typically occur in adolescent girls or young women, although 5–15% of cases of anorexia nervosa and bulimia nervosa and 40% of cases of binge eating disorder occur in boys and men. Approximately 3% of young women are affected with these disorders, and probably twice that number has clinically important variants. Although early disorders mostly develop in adolescence or young adulthood, they can occur after the age of 40 years and are increasingly seen in young children (2). Eating disorders are more prevalent in industrialized societies than in nonindustrialized societies, and occur in all socioeconomic classes and major ethnic groups in the USA. About half of those who have anorexia nervosa or bulimia nervosa fully recover, approximately 30% have a partial recovery, and 20% have no substantial improvement in symptoms (2). The aim of this chapter is to give an overview of the endocrinology of eating disorders leading to excessive weight gain or excessive weight loss in humans. It is of note that despite the strong association between obesity and eating disorders, the increase in obesity is not followed by an increase in eating disorders (3).
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Ferreira, Adaliene Versiani Matos, Laís Bhering Martins, Nayara Mussi Monteze, Geneviève Marcelin, and Karine Clément. "Immunology of Eating Disorders." In Immunopsychiatry, 241–50. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190884468.003.0014.

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Eating disorders (EDs) are characterized by dysregulation in eating behavior leading to extreme increase or decrease in food intake that, in turn, changes body weight, adiposity, and physical health. Anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorder (BED) are the three major eating disorders. Peculiar immune abnormalities occur in these conditions. Previous studies have reported a higher number of CD4+ T lymphocytes in patients with AN, which are related to a relative resistance to viral infections, even in the presence of leukopenia. It has also been proposed that a cluster of cytokines is altered in these patients. A chronic low-grade inflammation has been observed in obese people with BED and in patients with AN, but with a different profile in each condition. In this context, antagonist drugs of specific cytokines, such as anti-TNF, showed improvement of AN-related symptoms, but increased weight gain in obese subjects. The identification of specific molecules and/or immune cells that impair neuronal circuits implicated in eating behaviors may contribute to the development of pharmacological strategies for eating disorders.
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P. James, Steven, and Dena Bondugji. "Gamma-Aminobutyric Acid (GABA) and the Endocannabinoids: Understanding the Risks and Opportunities." In Gamma-Aminobutyric Acid - Neuropsychiatric and Therapeutic Implications [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.99242.

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The Gamma-aminobutyric acid (GABA) system is the main inhibitory neurotransmitter system in the central nervous system (CNS) of vertebrates and is involved in critical cellular communication and brain function. The endocannabioid system (ECS) was only recenty discovered and quickly recognized to be abundantly expressed in GABA-rich areas of the brain. The strong relationship between the GABA system and ECS is supported both by studies of the neuraoanatomy of mammalian nervous systems and the chemical messaging between neurons. The ECS is currently known to consist of two endocannabinoids, Anandamide (AEA) and 2-Arachidonyl Glycerol (2-AG), that function as chemical messengers between neurons, at least two cannabinoid receptors (CB1 and CB2), and complex synthetic and degradative metabolic systems. The ECS differs from the GABA system and other neurotransmitter systems in multiple ways including retrograde communication from the activated post-synaptic neuron to the presynaptic cell. Together, this molecular conversation between the ECS and GABA systems regulate the homeostasis and the chemical messaging essential for higher cortical functions such as learning and memory and may play a role in several human pathologies. Phytocannabinoids are synthesized in the plant Cannabis sativa (C. sativa). Within the family of phytocannabinoids at least 100 different cannabinoid molecules or derivatives have been identified and share the properties of binding to the endogenous cannabinoid receptors CB1 and CB2. The well-known psychoactive phytocannabinoid Δ9-tetrahydrocannabinol (THC) and the non-psychoactive cannabidiol (CBD) are just two of the many substances synthesized within C. sativa that act on the body. Although the phytocannabinoids THC and CBD bind to these endogenous receptors in the mammalian CNS, these plant derived molecules have little in common with the endocannabinoids in structure, distribution and metabolism. This overlap in receptor binding is likely coincidental since phytocannabinoids evolved within the plant kingdom and the ECS including the endocannabinoids developed within animals. The GABA and ECS networks communicate through carefully orchestrated activities at localized synaptic level. When phytocannabinoids become available, the receptor affinities for CB1 and CB2 may compete with the naturally occurring endocannabinoid ligands and influence the GABA-ECS communication. In some instances this addition of phytocannabinoids may provide some therapeutic benefit while in other circumstances the presence of these plant derived ligands for the CB1 and CB2 receptors binding site may lead to disruption of important functions within the CNS. The regulatory approval of several THC products for nausea and vomiting and anorexia and CBD for rare pediatric seizure disorders are examples of some of the benefits of phytocannabinoids. Concerns regarding cannabis exposure in utero and in the child and adolescence are shrill warnings of the hazards associated with disrupting the normal maturation of the developing CNS.
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Berga, Sarah L. "Disorders of gonadotropin secretion." In Oxford Textbook of Endocrinology and Diabetes, 1212–23. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.0838.

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Folliculogenesis and ovulation depend upon adequate gonadotropin stimulation, which in turn requires appropriate gonadotropinreleasing hormone (GnRH) input. There exists a group of related disorders in which GnRH drive to the pituitary is reduced, resulting in secondary diminution of follicle-stimulating hormone (FSH) and luteinizing hormone input to the ovary. Clinically, reduced GnRH drive results in a spectrum of ovarian compromise, ranging from luteal insufficiency to chronic anovulation. Variable menstrual patterns follow, including amenorrhoea, polymenorrhoea, with or without menorrhagia, and oligomenorrhoea, depending on the extent of follicular activity across time. Rarely, there is an organic or congenital cause for reduced GnRH drive, such as a brain tumour, coeliac disease, or migration of an insufficient number of GnRH neurons from the olfactory placode into the hypothalamus during fetal development. Typically, the cause is functional, that is, due to the endocrine consequences of certain psychological or behavioural variables. Anorexia nervosa provides the most dramatic example, but most women who develop functional hypothalamic anovulation do not meet criteria for an eating disorder and do not develop one subsequently. Because of the occult and heterogeneous nature of the behavioural variables that contribute to the genesis of this related group of disorders, a variety of names have been used to describe this syndrome, including exercise amenorrhoea, stress-related or stress-induced anovulation, functional hypothalamic amenorrhoea, functional hypothalamic chronic anovulation, and psychogenic amenorrhoea. Occasionally, psychiatric syndromes other than eating disorders such as depression coexist with functional hypothalamic anovulation, but unlike anorexia nervosa, in which amenorrhoea is almost universal, amenorrhoea is less common in women with bulimia and depression. Despite the multiplicity of names, the pathogenesis of anovulation in these diverse clinical settings is similar. In recognition of their common nature, I have chosen herein to refer to this group of disorders as ‘functional hypothalamic anovulation’ or FHA. As noted above, not all women have reduced gonadotropin secretion to the extent that they become amenorrhoeic or even persistently anovulatory, but most investigations have focused on subjects with the most complete expression of these related disorders, namely, those who are amenorrhoeic due to chronic anovulation. Generally, functional hypothalamic anovulation is considered to be a form of secondary amenorrhoea, but it can present as primary amenorrhoea. The diagnosis of functional hypothalamic anovulation is one of exclusion.
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Li, Jie Jack. "Duloxetine Hydrochloride (Cymbalta)." In Top Drugs. Oxford University Press, 2015. http://dx.doi.org/10.1093/oso/9780199362585.003.0014.

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“To live is to suffer, to survive is to find some meaning in the suffering.” Nietzsche’s words ring true to many. Depression is romanticized at times due to its association with poets and artists, but in reality depression, especially major depressive disorder (MDD), can be debilitating. There are two types of depression: MDD and bipolar, also known as manic–depressive illness. Severe changes in mood is the primary clinical manifestation of both disorders. MDD presents as feelings of intense sadness and despair with little drive for either socialization or communication; physical changes such as insomnia, anorexia, and sexual dysfunction can also occur. Mania is manifested by excessive elation, irritability, insomnia, hyperactivity, and impaired judgment. It may afflict as much as 1% of the population. MDD is among the most common psychiatric disorders in humans, affecting up to 10% of men and 20% of women over the course of their lives. Among those affected, 28% experience a moderate degree of functional impairment, while 59% experience severe reductions in their normal functional ability. About 19 million Americans suffer from depression per year. In terms of disease burden, MDD ranks as the fourth most costly illness in the world, with estimated annual costs of depression in the US amounting to approximately $43.7 billion. While we all agree that depression exists, we do not all agree on the causes of depression. The exact causes of depression are not definitively known. However, in the 1950s, it was observed that in addition to its other pharmacological properties, reserpine (a Rauwolfia alkaloid) induced a depressive state in normal patients and also depleted levels of neurotransmitters such as norepinephrine (NE) and serotonin (5-HT). This observation and others led to the hypothesis that the biological basis of major mood disorders may include abnormal monoamine neurotransmission. Substances such as NE, serotonin, and dopamine (DA) mediate neurotransmission. These substances are released from presynaptic neurons, cross the synaptic gap, and interact with receptors on the postsynaptic cells. The synthesis, transmission, and processing of these neurotransmitters provide a number of points of intervention through which a pharmacological agent may affect transmission.
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Conference papers on the topic "Anorexia neurosa"

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Goebel-Stengel, M., S. Scharner, P. Prinz, P. Kobelt, M. Rose, and A. Stengel. "Ratten mit Aktivitäts-basierter Anorexie zeigen eine erhöhte Aktivierung Nesfatin-1-haltiger Neurone in verschiedenen Gehirnkernen." In Viszeralmedizin 2017. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1605155.

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