Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Symptoms of depression that are temporary or caused by physical illness can be difficult to differentiate from those that represent a depressive disorder. A diagnosis of depressive disorder depends on the underlying cause, and on the nature, severity and duration of symptoms. Management involves accurate diagnosis and treatment of medical illness, practical interventions to resolve concurrent family, social and economic stressors, and emotional support. Cognitive, behavioral and brief psychodynamic therapies may be helpful in selected cases. Antidepressants and electroconvulsive therapy have a role in the treatment of severe or persistent depression associated with suicidal behavior, marked psychomotor retardation, starvation or other life-threatening symptoms. Suicidal thoughts are frequent in older patients with concurrent major depression and chronic illness, and measures to ensure patient safety are a priority.
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PMID:Depressive disorders in older medical inpatients. 192 39

Recent pharmacological studies have more precisely characterised the nature of the inhibitory effect of brain serotonin (5-hydroxytryptamine) on feeding behaviour. Thus, the brain sites and receptors involved have been identified, and a possible physiological role of endogenous serotonin in controlling natural patterns of eating and nutrient selection has been defined. The medial hypothalamus is believed to be a critical location in the mediation of serotonin's action. Specifically, the paraventricular and ventromedial nuclei are known to be involved in controlling energy balance, while the suprachiasmatic nucleus determines circadian patterns of eating. Serotonergic stimulation of these 3 nuclei with exogenous serotonin or drugs that release endogenous serotonin, preferentially reduces carbohydrate intake in naturally feeding animals through satiety mechanisms involved in the termination of feeding. This phenomenon is mediated by serotonin and possibly serotonin receptors, in contrast to serotonin autoreceptors which potentiate feeding possibly by inhibiting serotonin release. The activity of serotonergic function in the medial hypothalamus exhibits a circadian rhythm which is characterised by a peak at the beginning of the active cycle when the motivation to eat is strongest and is triggered by deficits in energy stores. At this time, carbohydrate is found to be the naturally preferred macronutrient, and it appears that serotonin becomes most activated under these conditions to terminate the carbohydrate-rich meal, possibly by activating satiety neurons localised in the medial hypothalamus. In this process, serotonin may interact antagonistically with noradrenaline (norepinephrine) and its alpha 2-noradrenergic receptors that normally function to enhance carbohydrate intake at the onset of the natural feeding cycle. Moreover, while inducing satiety for carbohydrate, serotonin may also play a role in switching the animal's preference towards protein. The regulation of this macronutrient is closely linked to that of carbohydrate, and it is normally preferred in the second meal of the natural feeding cycle. Most of the pharmacological evidence to date generally supports the hypothesis that disturbances in serotonin function occur in eating disorders. Decreases in plasma tryptophan, urinary 5-hydroxyindoleacetic acid (5-HIAA), platelet serotonin binding and basal cerebrospinal fluid 5-HIAA in anorexia nervosa normalise upon weight restoration and appear to be starvation effects. These alterations in serotonergic function may however perpetuate the symptomatology of anorexia nervosa once the illness is set in motion. Some drugs which in part affect serotonergic function facilitate weight gain in conjunction with an integrated psychotherapeutic and behavioural programme. Patients with bulimia nervosa, regardless of the presence of anorexia nervosa or major depression, who have been relatively weight stable and free of binge/vomit episodes for at least 3 weeks, have significantly blunted prolactin responses to the serotonin agonists. These findings indicate that post-synaptic responsiveness in hypothalamic-pituitary serotonergic pathways is reduced in bulimia. Similar alterations in other serotonin pathways at or above the level of the hypothalamus may contribute to binge eating and other behavioural symptoms in bulimic patients. The clinical response to several psychotropic agents known to potentiate serotonergic transmission further substantiates a serotonin dysregulation hypothesis of bulimia nervosa.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The role of serotonin in eating disorders. 219 74

To investigate the relationship between weight deficit and depressive symptoms, 48 adolescent patients (41 females, 7 males) fulfilling DSM III R criteria for anorexia nervosa were also assessed for DSM III diagnosis of major depressive disorder (MDD). Patients who met diagnostic criteria for MDD had a significantly lower body weight than those without a current episode of MDD. In turn patients with high weight loss had higher mean depression scores (HAMD, SDS) than patients with less weight deficit. With increase of body weight we found a highly significant decrease of depressive symptoms. The authors hypothesize that the DSM III criteria for MDD may not specifically distinguish between starvation-related psychopathology in anorexia nervosa and primary affective disorder.
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PMID:[Anorexia nervosa and depression. On the relation of body weight and depressive symptoms]. 279 33

Sleep research on eating disorders has addressed two major questions: (1) the effects of chronic starvation in anorexia nervosa and of rapidly fluctuating eating patterns in bulimia nervosa on the sleep regulating processes and (2) the search for a significant neurobiological relationship between eating disorders and major depression. At present, the latter question appears to be resolved, since most of the available evidences clearly underline the notion that eating disorders (such as anorexia and bulimia nervosa) and affective disorders are two distinct entities. Regarding the effects of starvation on sleep regulation, recent research in healthy humans and in animals demonstrates that such a condition results in a fragmentation of sleep and a reduction of slow wave sleep. Although several peptides are supposed to be involved in these regulatory processes (i.e. CCK, orexin, leptin), their mode of action is still poorly understood. In opposite to these experimentally induced sleep disturbances are the findings that the sleep patterns in eating disorder patients per se do not markedly differ from those in healthy subjects. However, when focusing on the so-called restricting anorexics, who maintain their chronic underweight by strictly dieting, the expected effects of malnutrition on sleep can be ascertained. Furthermore, at least partial weight restoration results in a 'deepening' of nocturnal sleep in the anorexic patients. However, our knowledge about the neurobiological systems (as well as their circadian pattern of activity) that transmit the effects of starvation and of weight restoration on sleep is still limited and should be extended to metabolic signals mediating sleep.
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PMID:Sleep in eating disorders. 1503 50

Several studies have shown that olanzapine is effective in weight restoration and maintenance for patients with anorexia nervosa (AN). However, major depression is a very common comorbid psychiatric disorder associated with AN. Additional antidepressant therapy may be required for treating anorexic patients with major depression. The authors present a case of AN associated with major depression, who responded well to the combination treatment of olanzapine and mirtazapine. A 27-year-old Taiwanese woman was admitted because of severe weight loss, poor nutrition, amenorrhea, major depression, and starvation complications including hematological dyscrasis, electrolytes and endocrine imbalance, and sinus bradycardia. In additional to nutritional and medical treatments, the patient was given olanzapine 10 mg/day and mirtazapine 30 mg/day. She took the combined medications for six months. Meanwhile she received cognitive behavior therapy and family therapy. With these treatments, the patient's depression was in remission, her body weight was increased from 24 to 38 kg, and her body mass index was increased from 9.8 to 15.5. Our case suggests that the combined treatment of olanzapine and mirtazapine can be used in the treatment of AN associated with major depression.
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PMID:Combined treatment of olanzapine and mirtazapine in anorexia nervosa associated with major depression. 1631 20

Acute intermittent porphyria (AIP) is a metabolic disease characterized by recurrent attacks of neurological and psychiatric dysfunction. It is a rare disorder of heme metabolism that usually presents with abdominal pain, gastrointestinal symptoms and autonomic nervous system disturbances. Exposure to certain drugs, dieting, starvation and infection during pregnancy may precipitate AIP attacks. Psychiatric manifestations of AIP include mood changes, organic brain syndrome and psychosis. Here, we present a 21-year-old female patient with AIP and major depression. She had a caesarean section under general anesthesia with pentothal and her recovery time from anesthesia took longer than usual. She had a blood transfusion because of severe anemia following the operation. Three days after her discharge she was readmitted to the hospital with confusion and seizure. It was her first AIP attack and it started 6 days after caesarean section. Two months after her first attack, we saw her for anxiety and depressive symptoms. She was in severe anxiety and depression and she was put on fluoxetine (20 mg/day liquid form). Following the treatment she did not develop any other porphyria attack. Her symptoms vanished and she improved functionally. She stayed on fluoxetine for 6 months without any new AIP attack. Despite limited data regarding fluoxetine therapy in porphyria patients, it seems to be safe for the treatment of depressive and anxiety symptoms in these patients.
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PMID:Safety of fluoxetine treatment in a case of acute intermittent porphyria. 2493 Apr 16

Major depressive disorder constitutes one of the leading causes of disability worldwide. However, it is not a unitary disease-it is a heterogeneous syndrome, with patients differing remarkably in symptom profile, pathophysiology and treatment responsiveness. Previous attempts to subtype major depressive disorder have showed limited clinical applicability. We present a classification of major depressive disorder episodes based on the proximate mechanisms that led to the original mood change that caused the depressive episode. We identify discrete depression subtypes that are induced by: 1) infection, 2) long-term stress, 3) loneliness, 4) traumatic experience, 5) hierarchy conflict, 6) grief, 7) romantic rejection, 8) postpartum events, 9) the season, 10) chemicals, 11) somatic diseases and 12) starvation. We further examine the ultimate functions of these subtypes and show that not all types of mood changes that trigger depression are adaptive. Instead, some are clearly maladaptive and some are byproducts of other adaptations. In modern societies, low mood after adverse life events may turn into a pathological depressive state. Modern lifestyle increases susceptibility to inflammatory dysregulation and chronic stress, both of which increase the amount of proinflammatory cytokines in peripheral blood, leading to low mood and sickness behaviour. Proinflammatory cytokines may aggravate the previously adaptive short-term mood changes to a chronic maladaptive depressive state by preventing the normalization of mood after adverse life events. Subtyping depression enables an effective and intelligent long-term treatment of patients in each subtype by treating the underlying causes of depression.
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PMID:Depression subtyping based on evolutionary psychiatry: Proximate mechanisms and ultimate functions. 2922 54

"Comfort women" refers to young women and girls who were forced into sexual slavery by the Imperial Japanese military during World War II. They were abducted from their homes in countries under Imperial Japanese rule, mostly from Korea, and the rest from China, Philippines, Malaysia, Taiwan, Indonesia, the Netherlands, etc. "Comfort women" endured extreme trauma involving rape, sexual torture, physical abuse, starvation, threats of death, and witnessed many others being tortured and killed. This article reviews all the studies that have investigated the psychiatric or psychosocial sequelae of the survivors of the Japanese military sexual slavery. Most importantly, a recent study which conducted a psychiatric evaluation on the former "comfort women" currently alive in South Korea is introduced. The participants' unmarried rate was relatively high and their total fertility rate was relatively low. Majority of the participants reported having no education and being the low economic status. They showed high current and lifetime prevalence of posttraumatic disorder, major depressive disorder, somatic symptom disorder, social anxiety disorder, panic disorder, and alcohol use disorder. Participants showed high suicidality and majority of the participants still reported being ashamed of being former "comfort women" after all these years. This article high-lights the fact that the trauma has affected the mental health and social functioning of former "comfort women" throughout their lives, and even to the present day.
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PMID:Psychiatric Sequelae of Former "Comfort Women," Survivors of the Japanese Military Sexual Slavery during World War II. 2966 7

Multiple sclerosis, currently incurable and potentially profoundly disabling demyelinating central nervous system disease, is associated with higher occurrence of suicide as affected individuals are prone to major depression and psychosis. Despite progressively incapacitating neurologic impairment, well-staffed institutions, and limited repertoire of methods of suicide, which prevents patients from purposefully ending their lives, suicide-determined patients typically commit suicide resulting from a medication overdose, sharp force traumata, self-neglect, or deliberate starvation. Here we describe a successful suicide committed by a 39-year-old wheelchair-bound, institutionalized, quadriparetic male patient with a diagnosis of multiple sclerosis with secondary progressive clinical course who utilized his motorized wheelchair to terminate his life. He tied a rope between his neck and wall bars and then propelled the wheelchair forwardly. The acceleration of the wheelchair resulted in ligature self-strangulation. This case report, with a review of the literature, is noteworthy for the rareness of the wheelchair-related fatality combined with an unusual, if not entirely unseen, suicidal mechanism in severely disabled adult.
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PMID:Wheelchair-Assisted Ligature Strangulation: An Unusual Suicide by a Quadriparetic. 3092 Apr 5