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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ketogenic diet is a high-fat diet that maintains the body's starvation mechanism, with exogenous fat provided for metabolism in lieu of stored fat. Mild dehydration is important to prevent dilution of the level of ketones in circulation at any given time. It is not known why or how ketosis affects seizure activity, so the principles behind the therapy have been developed from years of clinical experience and theoretical assumptions. Dietitians are essential providers of ketosis therapy, but the dietitian must work with a physician who understands the theories behind the therapy and is an active member of the ketosis therapy team.
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PMID:The ketogenic diet revisited. 933 88

Juvenile neuronal ceroid lipofuscinosis or Batten disease (JNCL) is a neurodegenerative disorder characterized by blindness, seizures, cognitive decline and early death. Brain atrophy and retinitis pigmentosa ensue because of neuronal and photoreceptor apoptosis. The CLN3 gene defective in JNCL encodes a novel 438 amino acid protein. Most affected genes harbor a deletion resulting in a truncated protein. CLN3 overexpression in NT2 cells enhances growth, reverses growth inhibition induced by serum starvation and protects from apoptosis induced by vincristine, staurosporine, and etoposide but not from death caused by ceramide. CLN3 modulates endogenous and vincristine-activated ceramide, and therefore suppresses apoptosis by impacting generation of ceramide.
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PMID:CLN3 defines a novel antiapoptotic pathway operative in neurodegeneration and mediated by ceramide. 1019 Nov 18

The effect of 24 h of fasting and changes in blood glucose and beta-hydroxybutyrate (BHB) level on latency to seizures in hyperbaric oxygen (HBO2) was studied. Conscious, unrestrained rats implanted with cortical electroencephalogram electrodes were exposed to 0.5 MPa (gauge pressure) O2 until seizures were observed. Fasting for 24 h significantly (P < 0.01) decreased blood glucose (from 8.6 +/- 0.9 in fed to 6.9 +/- 0.7 mM in the fasted group), increased blood BHB (0.07 +/- 0.02 mM to 0.38 +/- 0.10 mM, respectively), and prolonged the latency to seizures compared with normally fed animals (21.0 +/- 9.8 vs. 34.6 +/- 17.7 min, P < 0.05). Injection of the ketone precursor 1,3-butanediol (BD) to the fed animals increased blood BHB level to 0.72 +/- 0.32; however, seizure latency remained the same as in fed animals. Restoration of blood glucose in fasted animals to the same level as in the fed group did not reverse the protection achieved by fast; instead it increased the latency to seizures. The results indicate that the protection against HBO2 seizures by fasting in short starvation is not related to the increase in circulating ketone bodies or decrease in blood glucose.
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PMID:Attenuation of brain hyperbaric oxygen toxicity by fasting is not related to ketosis. 1037 29

Porphyrias are inherited defects of heme synthesis with manifestations that can mimic surgical diseases; they can be provoked by administration of certain drugs. Manifestations such as abdominal pain, vomiting, tachycardia, hypertension, neuropathy, fever, confusion, and seizures have been described. Management of patients with porphyria is designed to avoid triggering drugs, such as barbiturates, and perhaps, benzodiazepines and ketamines. Nontriggering drugs should be used in the management of patients with porphyria. Because starvation can induce an attack, glucose infusions are important in the prevention and treatment of porphyria.
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PMID:Anesthetic considerations in hepatic porphyrias. 1050 4

The ketogenic diet is a high-fat, adequate protein, low carbohydrate diet that has been used for the treatment of intractable childhood epilepsy since the 1920s. The diet mimics the biochemical changes associated with starvation, which create ketosis. Although less commonly used in later decades because of the increased availability of anticonvulsants, the ketogenic diet has re-emerged as a therapeutic option. Only a decade ago the ketogenic diet was seen as a last resort; however, it has become more commonly used in academic centres throughout the world even early in the course of epilepsy. The Atkins diet is a recently used, less restrictive, therapy that also creates ketosis and can lower the number of seizures. Dietary therapies may become even more valuable in the therapy of epilepsy when the mechanisms underlying their success are understood.
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PMID:More fat and fewer seizures: dietary therapies for epilepsy. 1532 19

Insulinoma tumors are often difficult to detect, as the symptoms largely precede occurrence of a visualized tumor. We report the case of an insulinoma patient with long delayed diagnosis and marked adaptation to extreme hypoglycemia. The patient with a 7-yr history of seizures was found to have plasma glucose concentration during a starvation test as low as 16 mg/dl, with no clinically significant symptoms and concomitant normal plasma insulin levels: 10-30 microIU/ml. All attempts to localize a tumor with repeated abdominal ultrasound examinations or computed tomography scanning were unsuccessful. The patient did not tolerate the introduced oral treatment with diazoxide. Once it had become technically available, endoscopic ultrasonography of the pancreas was performed. It revealed a 10 mm tumor in the pancreatic head. The tumor was subsequently removed surgically. During the operation plasma insulin concentration rose almost 15-fold, which confirmed the insulin-secreting character of the growth. Microscopic examination revealed benign insulinoma, with partially trabecular structure. One month after the operation the patient had normal plasma glucose values of 60-120 mg/dl, but she constantly complained of excessive thirst, which occurred soon after the operation and slowly subsided in the following weeks. In conclusion, the present report demonstrates that insulinoma should be considered and searched for in every case of hypoglycemia associated with normal insulin levels. It also confirms the essential role of endoscopic ultrasonography in the diagnosis of insulin-secreting tumors.
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PMID:Diagnostic difficulties in long-standing insulinoma with near-normal plasma insulin levels. 1588 65

The tragic life of Vincent van Gogh is summarized, emphasizing his early departure from formal education, failure as a successful salesman in the art world, attempt at religious studies, difficulty with female and family relationships, return to the art world, and tendencies toward extremes of poor nutrition or near self-starvation and excessive drinking and smoking. In Paris he joined the Impressionists, but drank very heavily both absinthe and cognac. Southward he went to Arles and was joined by Paul Gauguin, with whom he had major personality problems, causing van Gogh to cut off part of his left ear. He experienced paranoid ideation and confinement in mental institutions in Arles, and then returned to Paris and onto Auvers-sur-Oise, where he committed suicide at age 37. Possible physical diagnoses include glaucoma, Meniere's disease, acute intermittent porphyria, and chronic lead poisoning, but these diagnoses seem unlikely. Possible psychiatric diagnoses include borderline personality disorder, anxiety-depressive disorder with episodes of depression and hypomania, and also paranoid schizophrenia. Van Gogh did not have spontaneous seizures and, therefore, did not have epilepsy. Before he began to drink heavily, when he was near starvation, he had "fainting fits," and after drinking, especially absinthe, a convulsant drug, he continued to have similar attacks. His episodes of unconsciousness can be well explained by chronic malnutrition and alcohol abuse, only possibly exacerbated by drinking large quantities of absinthe. Although van Gogh is an excellent example of the Geschwind syndrome, at times associated with temporal lobe epilepsy, this fact does not establish such an epilepsy. Thus, the syndrome is an orphan without the parent condition.
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PMID:A reappraisal of the possible seizures of Vincent van Gogh. 1590 45

The gene encoding dARC1, one of three Drosophila homologs of mammalian activity-regulated cytoskeleton-associated protein (ARC), is upregulated in both seizure and muscular hypercontraction mutants. In this study we generate a null mutant for dArc1 and show that this gene is not involved in synaptic plasticity at the larval neuromuscular junction or in formation or decay of short-term memory of courtship conditioning, but rather is a modifier of stress-induced behavior. dARC1 is expressed in a number of neurosecretory cells and mutants are starvation-resistant, exhibiting an increased time of survival in the absence of food. Starvation resistance is likely due to the fact that dArc1 mutants lack the normal hyperlocomotor response to starvation, which is almost universal in the animal kingdom. dARC1 acts in insulin-producing neurons of the pars intercerebralis to control this behavior, but does not appear to be a general regulator of insulin signaling. This suggests that there are multiple modes of communication between the pars and the ring gland that control starvation-induced behavioral responses.
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PMID:The Drosophila ARC homolog regulates behavioral responses to starvation. 1770 55

For many years, the ketogenic diet, including recent variants such the medium-chain triglyceride (MCT) diet, has been used with good clinical results in the management of refractory epilepsies, particularly in children. The antiepileptic effects of the diet, like the antiepileptic effects of starvation, have been attributed to accumulation of ketones, and there are experimental data in animal models to support this hypothesis. Recently, new data about the neuroendocrine response to the acute phase reaction (stress) have emerged, indicating involvement of various neuropeptides, including neuropeptide Y (NPY), which is considered as an endogenous anticonvulsant. The release of NPY is also stimulated by nutrients in the gut, particularly fats. Long-chain and, to a greater extent, medium-chain triglycerides, which are components of the ketogenic diet, stimulate NPY secretion. This effect may explain the improvement in seizure control after starvation, use of the classical ketogenic diet, and use of the MCT diet.
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PMID:Is the antiepileptic effect of the ketogenic diet due to ketones? 1771 80

Wernicke's encephalopathy (WE) or thiamine deficiency is fatal if left untreated. We report a case of a 3-year-old boy with infantile autism and a severe eating disorder who developed WE after 3 weeks of starvation without thiamine supplementation. The eating disorder started when he entered preschool. He presented with unconsciousness and a cluster of seizures. Cranial magnetic resonance imaging (MRI) showed high-intensity signal changes in the basal ganglia on T2-weighted images and fluid-attenuated inversion recovery (FLAIR). Treatment with high-dose intravenous thiamine was effective. Pediatric patients with WE tends to show no typical symptoms or brain lesions on MRI as seen in adult WE patients typically along alcoholics. Brain lesions similar to those in hypoxia or mitochondrial diseases such as Leigh's encephalopathy, are observed in patients with pediatric WE, and this makes diagnosis difficult. WE should be considered when patients with severe eating disorders present with unconsciousness and/or frequent seizures, and show basal ganglia lesions on MRI, differential diagnosis should include WE.
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PMID:[Case of infantile autism with pediatric Wernicke's encephalopathy due to severe eating disorder]. 1917 16


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