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)

In abuse dwarfism the behavioral signs include some or all of the following: (1) a history of unusual eating and drinking behavior, reversible on change of domicile, such as eating from a garbage can and drinking from a toilet bowl, stealing food, alleged picky eating and rejecting food at the table, polydipsia and polyphagia, possibly alternating with vomiting and possibly also with self-starvation; (2) a history of such behavioral symptoms as enuresis, encopresis, social apathy or inertia, defiant aggressiveness, sudden tantrums, crying spasms, insomnia, eccentric sleeping and waking schedule, pain agnosia, and self-injury, all occurring only in the growth-retarding environment; (3) retarded motor development, with improvement on removal of the child from the domiclle of abuse; (4) retarded intellectual growht, reversible on change of domicile by as much as 30 to 50 IQ points; and (5) a history of pathologic family relationships, including unusual cruelty and neglect, either somatic or psychic or both.
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PMID:The syndrome of abuse dwarfism (psychosocial dwarfism or reversible hyposomatotropism). 85 51

This short review updates information on the release mechanisms of the systemic response to surgical injury and the modifying effect of pain relief. Initiation of the response is primarily due to afferent nerve impulses combined with release of humoral substances (such as prostaglandins, kinins, leukotrienes, interleukin-1, and tumor necrosis factor), while amplification factors include semi-starvation, infection, and hemorrhage. The relative role of the various signals in producing the complex injury response has not been finally determined, but the neural pathway is probably most important in releasing the classical endocrine catabolic response, while humoral factors are important for the hyperthermic response, changes in coagulation and fibrinolysis immunofunction, and capillary permeability. The modifying effect of pain relief on the surgical stress response is dependent upon the technique of analgesia. However, the effect on humoral-mediated responses is small, regardless of the technique used. Afferent neural blockade with local anesthetics is the most effective technique for reducing the endocrine-metabolic response, but only in operations in the lower part of the abdomen, probably because of insufficient afferent blockade during thoracic epidural analgesia. Systemic opiate administration, as well as non-steroidal antiinflammatory drugs, exert only a small modifying effect on the response. Low-dose combined analgesic regimens may provide total pain relief, but exert no important effect on the stress response. In summary, pain alleviation itself may not necessarily lead to an important modification of the stress response, and a combined approach with inhibition of the neural and humoral release mechanisms is necessary for a pronounced inhibition or prevention of the response to surgical injury.
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PMID:The stress response to surgery: release mechanisms and the modifying effect of pain relief. 265 70

Diet clearly influences neurotransmission. This can be important in grossly undernourished children. It can also be important in children in whom normal homeostatic mechanisms governing food intake are bypassed. Subtle differences in behavior can occur with physiologic variation in food intake. Components of foods can also be used as drugs. Starvation can impair neuronal maturation and can have lasting effects upon behavior and intellectual performance. The extent of starvation's impact upon the brain depends upon whether undernutrition occurred during a critical phase in brain development. Short-term fasting has small, but significant, effects upon intellectual performance. Even when gross malnutrition is not present, subtle changes in diet may modulate brain function. Tryptophan, tyrosine, and choline in the diet are used as precursors for neuronal synthesis of serotonin, dopamine and norepinephrine, and acetylcholine, respectively. It is likely that the brain's sensitivity to certain components of the diet exists to permit monitoring of food intake by the central nervous system. Tryptophan, tyrosine, and choline may be useful in treatment of humans with sleep disorders, pain depression, mania, hypertension, shock, or dyskinesias. Other components of the diet that may affect behavior include food additives, sugar, and caffeine. Food additives may exacerbate hyperactive symptoms in a small proportion of children with attention deficit disorder. Given that there is little potential for harm and that there is a subpopulation that may respond, a trial of a diet that contains no food additives may be a valid diagnostic approach for children with attention deficit disorder who do not respond to stimulant therapy or for children for whom stimulant therapy is not desired. Refined sugar has been blamed for many behavioral abnormalities. Subtle effects of carbohydrate upon behavior have been reported, but the existing data do not support the hypothesis that sucrose or fructose exert special effects upon neurotransmission. Caffeine is easily detected as a stimulant by humans, but it has little effect upon cognitive function. Administration of large doses of vitamins has no beneficial effect in most humans with schizophrenia, attention deficit disorder, autism, Down's syndrome, or drug addiction. Large doses of niacinamide may even be harmful, as they may cause hepatic damage.
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PMID:Dietary influences on neurotransmission. 302 51

A group of 47 patients suffering from chronic recurrent duodenal ulcers was subdivided into two groups according to whether the first manifestation of the disorder occurred early or late in the life of each individual. A comparison of the two groups revealed that the patients in group I (early manifestation) had a larger number of constitutional handicaps along with a higher incidence of dispositional prior experience with regard to object loss and that they assumed social responsibility at an early age. Group II (late manifestation) was characterized by a larger number of depressive psychoses, a higher incidence of alcohol abuse, and by attempts at suicide. Apart from this, the patients in group II often complained of muscular pain syndromes. Patients in group I frequently exhibited the characteristics of the ulcer type described by Alexander as well as chronic anger. Patients in group II most often had the personality structure of so-called psychosomatic patients or suffered from depressive disorders affecting their personalities and from chronic anxiety. The two characteristics which were most typical for recidivation were: 1. Actualization of experienced bereavement and 2. unspecific activation as a result of the will to assert themselves in stress situations. In 41% of the cases there was evidence of somatic factors as e.g. starvation, abuse of alcohol or abuse of analgetics. Long-term prophylaxis has been effected by psychopharmacological agents as well as by psychotherapeutic techniques.
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PMID:[Ulcer disease. Studies of patients with chronic recurrent duodenal ulcer in an attempt to differentiate subgroups based on age at disease onset, psychopathologic and biographical data]. 376 11

Parenterally administered substance P suppressed stress-induced eating (resulting from mild tail pinch) in a dose-related manner, whereas at similar or higher doses of substance P starvation-induced eating was uneffected. This specific effect of substance P on stress-induced eating is possibly associated with alterations of exogenous substance P of the normal modulation of pain transmission.
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PMID:Substance P suppresses stress-induced eating. 616 30

In anorexia nervosa the pain of hunger or, alternatively (in bulemia), of glut recalls Freud's aphorism that the man with toothache cannot fall in love. But object longing remains and stimulates such envy that the anorectic must project her wishes; she is not be found wanting. The use of projection, in turn, complicates self-other boundaries, with the result that she experiences not only people but even food as overpowering. This, then, excites more envy, indeed an envy so ruinous that self-starvation or compulsive evacuations are employed additionally to make reparation. Because all of this condenses into Less is More, the anorexic poses particular problems for analytic treatment, which is the subject of a companion paper.
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PMID:The problem of anorexia nervosa. 657 8

For most women, childbirth is associated with very severe pain often exceeding all expectations. Some childbirth education groups and popular texts on the subject, however, seem disposed to encourage unrealistic expectations: claiming that labour is other than painful and that pharmacological analgesia is both unnecessary and harmful. All too often, those who promote such views witness women in labour only occasionally and are rarely responsible for patient care. Pain associated with uterine contractions should be distinguished from that associated with delivery: for there are important differences in the clinical characteristics, neural pathways and physiological responses. In the first stage of labour pain is largely visceral in origin, whereas during the transitional and second stages somatic pain becomes more pronounced. As described in this review, it is now well established that uterine contraction pain evokes a generalised neuroendocrinal stress response producing widespread physiological effects during the first stage of labour. They include increased oxygen consumption, hyperventilation and respiratory alkalosis; increased cardiac output, systemic peripheral resistance and blood pressure; delayed gastric emptying; impaired uterine contractility and diminished uterine perfusion; and metabolic acidaemia. While other factors (such as anxiety, starvation and physical exertion) are also partly responsible for inducing some of these effects, pain appears to be the most potent source because they are all obtunded by effective epidural analgesia.
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PMID:The nature and consequences of childbirth pain. 755 28

Anorexia nervosa (AN) is a chronic eating disorder characterized by self-imposed semi-starvation that affects 1% of adolescent females. AN predisposes to osteoporosis through hypothalamic dysfunction, which may lead to elevated cortisol as well as diminished estrogen and progesterone. The osteoporosis associated with AN affects both trabecular and cortical bone and increases the risk of osseous fracture. Fractures in this population may go unrecognized, because planar X-rays may be nondiagnostic for 6 weeks or more. Four women with AN ranging in ages from 22 to 34 with skeletal pain and nondiagnostic roentgenographs are described. Stress fractures in these patients were subsequently identified by bone scan. Although moderate exercise in patients with AN-associated osteoporosis may be beneficial, strenuous exercise can be detrimental, with its potential risk of stress fractures and exacerbation of the underlying neurohormonal abnormalities. This risk for fracture may persist well after improvement in the patient's AN.
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PMID:Osteoporotic stress fractures in anorexia nervosa: etiology, diagnosis, and review of four cases. 766 64

The cachexia-anorexia syndrome occurs in chronic pathophysiologic processes including cancer, infection with human immunodeficiency virus, bacterial and parasitic diseases, inflammatory bowel disease, liver disease, obstructive pulmonary disease, cardiovascular disease, and rheumatoid arthritis. Cachexia makes an organism susceptible to secondary pathologies and can result in death. Cachexia-anorexia may result from pain, depression or anxiety, hypogeusia and hyposmia, taste and food aversions, chronic nausea, vomiting, early satiety, malfunction of the gastrointestinal system (delayed digestion, malabsorption, gastric stasis and associated delayed emptying, and/or atrophic changes of the mucosa), metabolic shifts, cytokine action, production of substances by tumor cells, and/or iatrogenic causes such as chemotherapy and radiotherapy. The cachexia-anorexia syndrome also involves metabolic and immune changes (mediated by either the pathophysiologic process, i.e., tumor, or host-derived chemical factors, e.g., peptides, neurotransmitters, cytokines, and lipid-mobilizing factors) and is associated with hypertriacylglycerolemia, lipolysis, and acceleration of protein turnover. These changes result in the loss of fat mass and body protein. Increased resting energy expenditure in weight-losing cachectic patients can occur despite the reduced dietary intake, indicating a systemic dysregulation of host metabolism. During cachexia, the organism is maintained in a constant negative energy balance. This can rarely be explained by the actual energy and substrate demands by tumors in patients with cancer. Overall, the cachectic profile is significantly different than that observed during starvation. Cachexia may result not only from anorexia and a decreased caloric intake but also from malabsorption and losses from the body (ulcers, hemorrhage, effusions). In any case, the major deficit of a cachectic organism is a negative energy balance. Cytokines are proposed to participate in the development and/or progression of cachexia-anorexia; interleukin-1, interleukin-6 (and its subfamily members such as ciliary neurotrophic factor and leukemia inhibitory factor), interferon-gamma, tumor necrosis factor-alpha, and brain-derived neurotrophic factor have been associated with various cachectic conditions. Controversy has focused on the requirement of increased cytokine concentrations in the circulation or other body fluids (e.g., cerebrospinal fluid) to demonstrate cytokine involvement in cachexia-anorexia. Cytokines, however, also act in paracrine, autocrine, and intracrine manners, activities that cannot be detected in the circulation. In fact, paracrine interactions represent a predominant cytokine mode of action within organs, including the brain. Data show that cytokines may be involved in cachectic-anorectic processes by being produced and by acting locally in specific brain regions. Brain synthesis of cytokines has been shown in peripheral models of cancer, peripheral inflammation, and during peripheral cytokine administration; these data support a role for brain cytokines as mediators of neurologic and neuropsychiatric manifestations of disease and in the brain-to-peripheral communication (e.g., through the autonomic nervous system). Brain mechanisms that merit significant attention in the cachexia-anorexia syndrome are those that result from interactions among cytokines, peptides/neuropeptides, and neurotransmitters. These interactions could result in additive, synergistic, or antagonistic activities and can involve modifications of transducing molecules and intracellular mediators. Thus, the data show that the cachexia-anorexia syndrome is multifactorial, and understanding the interactions between peripheral and brain mechanisms is pivotal to characterizing the underlying integrative pathophysiology of this disorder.
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PMID:Central nervous system mechanisms contributing to the cachexia-anorexia syndrome. 1105 8

Denying food and water to profoundly impaired people who may not be conscious, or may only be "minimally" conscious, raises challenging ethical issues. While there is growing support for withdrawing/withholding food and water (assisted nutrition and hydration, or "AHN") from people described as being in a "persistent vegetative state" ("PVS") and people with other profound neurological impairments, such as advanced dementia, the issue remains controversial, and for many, unresolved. In this article, the author argues that if a profoundly impaired person is not imminently dying from a disease process, denying food and water causes him or her to die of dehydration and starvation. When provision of food and water does not create excessive burdens (such as extreme pain and discomfort), and if the food and water can be digested and absorbed, denying such nourishment is immoral and unethical. Under these circumstances, this denial (by commission or omission) is motivated by a real intention to cause death, whether or not that intention is explicitly recognized.
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PMID:Masked intentions: the masquerade of killing thoughts used to justify dehydrating and starving people in a "persistent vegetative state" and people with other profound neurological impairments. 1113 Sep 27


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