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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Fifty patients with severe weight loss thought to be caused by anorexia nervosa were hospitalized for evaluation. On the basis of psychiatric history and mental state examination, they were divided into three diagnostic categories: anorexia nervosa; other. The MMPI of patients with anorexia nervosa was markedly abnormal, with highest peaks on the D (depression), PT (obsessionality and anxiety), and SC (schizophrenia) scales. This profile was similar to that of patients with obsessional symptoms and neurotic depression, but differed significantly from the profile of patients with low weight but normal mental state examination. These findings suggest that starvation alone does not explain the psychopathological symptoms similar to those with depressive and obsessional symptomatology. The MMPI is useful in differentiating anorexia nervosa from those with lowered weight from nonpsychiatric causes, but does not by itself provide a distinct diagnostic category when compared with neurotic disorders having similar symptom clusters.
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PMID:The MMPI in three groups of patients with significant weight loss. 652 72

The goal of this paper is to draw conclusions about the usefulness of the standard EEG in psychiatry. In general, two thirds of psychiatric referrals for an EEG are expected to provide useful information. The emphasis in schizophrenia is placed on left-sided abnormalities, especially on the left temporal area. In mood disorders the emphasis is on right-sided foci, in addition to the controversial 6/sec spike and wave complexes, small sharp spikes and positive spikes. In the acute stage of alcoholism, a relationship is seen between the degree of intoxication and the amount of slow activity, while in the chronic stage an increase in slow activity is seen, but another change is fast activity on the temporal areas. During withdrawal a low seizure threshold can be seen as irregular bilateral spike and wave complexes. During abstinence 2-4 yr may be required before slow wave sleep is normal in all regards. Among the organic mental syndromes, delirium shows slow activity, except in delirium tremens, which often is associated with a normal record with fast activity. In dementia the prevalence of EEG abnormalities is related to the degree of impairment. After five sessions of ECT diffuse slow waves are often seen. In other conditions, among developmental disorders about one half of autistic children show abnormalities and epileptiform activity is not uncommon. Mild nonspecific abnormalities are seen in about 40% of dyslexics and also in behavior disorders. Anxiety disorders include anorexia nervosa, showing abnormal background activity related to the effect of starvation on cerebral metabolism. In panic attacks paroxysmal activity can be seen. In borderline personality positive spikes have been (again) associated with impulsivity and 6/sec spike and wave complexes with interpersonal problems. Of the drugs of abuse psilocybin and phencyclidine are often associated with generalized epileptiform patterns and with marijuana the alpha shows a decreased frequency with increased amplitude. Typically, an increase in slow activity is seen with psychotropic drugs if there is a change in the level of awareness. Finally, distinctive personality traits are, at times, seen in temporal lobe epilepsy and the phenomenon of "forced normalization" may appear when seizures stop and psychotic symptoms appear.
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PMID:A review of the usefulness of the standard EEG in psychiatry. 871

The authors present the review of literature concerning schizophrenia, schizophrenia type and delusional disorders in patients with a lifetime diagnosis of anorexia nervosa (AN). The authors describe also 3 patients (2 cases of paranoid schizophrenia and 1 case of catatonic syndrome). The clinical features in all patients are discussed. In 1 patient the catatonic symptoms occurred within the context of AN, (perhaps due to metabolic disturbances) and in 2 other cases the psychotic features occurred after recovery from AN. The authors discuss the occurrence of psychotic features in AN, and the possible function of starvation and metabolic disturbances in their aetiology.
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PMID:[Schizophrenia, schizophrenia-like disorders and delusional disorders in patients with anorexia nervosa: literature review and report of 3 cases]. 973 79

Increased Apolipoprotein D (ApoD) expression has been reported in various neurological disorders, including Alzheimer's disease, schizophrenia, and stroke, and in the aging brain . However, whether ApoD is toxic or a defense is unknown. In a screen to identify genes that protect Drosophila against acute oxidative stress, we isolated a fly homolog of ApoD, Glial Lazarillo (GLaz). In independent transgenic lines, overexpression of GLaz resulted in increased resistance to hyperoxia (100% O(2)) as well as a 29% extension of lifespan under normoxia. These flies also displayed marked improvements in climbing and walking ability after sublethal exposure to hyperoxia. Overexpression of Glaz also increased resistance to starvation without altering lipid or protein content. To determine whether GLaz might be important in protection against reperfusion injury, we subjected the flies to hypoxia, followed by recovery under normoxia. Overexpression of GLaz was protective against behavioral deficits caused in normal flies by this ischemia/reperfusion paradigm. This and the accompanying paper by Sanchez et al. (in this issue of Current Biology) are the first to manipulate the levels of an ApoD homolog in a model organism. Our data suggest that human ApoD may play a protective role and thus may constitute a therapeutic target to counteract certain neurological diseases.
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PMID:Overexpression of a Drosophila homolog of apolipoprotein D leads to increased stress resistance and extended lifespan. 1658 12

Psychiatric studies of immigrants have yielded contradictory findings regarding rates of mental illness. Current evidence suggests that rates of schizophrenia (and probably other disorders) among immigrant groups are low compared with native-born populations when sending and receiving countries are socially and culturally similar. The rates for immigrants are higher when sending and receiving countries are dissimilar, probably because of multiple social problems faced by immigrants in the receiving country. Refugees who flee their own country because of fears of violence or starvation often have had extremely traumatic experiences, which may result in PTSD and sometimes chronic impairment. Asylum seekers who arrive illegally to seek refuge in a foreign country also may have multiple traumas and experience further distress from their uncertain residency and legal status. Although much is known about the effects of migration, competent culturally sensitive services for migrants remain inadequate to meet the need.
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PMID:Immigrants and refugees: the psychiatric perspective. 1716 47

It is well recognized that investigation into the relationship between early life programming and subsequent neurological disorders may have powerful implications for understanding the human vulnerability to psychopathology. The present article will propose that schizophrenia may be adaptively programmed by early environmental adversity permitting physiological and behavioral characteristics that would have created a fitness advantage in the ancestral environment under conditions of nutritional scarcity and severe environmental stress. This proposition will be analyzed in terms of phenotypic plasticity theory which explains how and why specific environmental stressors can alter normal gene expression resulting in an alternative phenotype that is better suited for an adverse environment. The primary neurophysiological symptoms of schizophrenia can be induced in animals through exposure to prenatal and postnatal stressors, and that schizophrenia itself is known to be associated with exposure to stress during development, supports the view that the "disorder" may represent a predictive, adaptive response to adversity. In fact, maternal malnutrition, maternal stress, multiparity, short birth interval and stress provoking postnatal events are well recognized epidemiological risk factors for schizophrenia that may represent cues for the initiation of epigenetic programming. Behavioral and physiological characteristics of schizophrenia will be analyzed and interpreted as protective in the context of environmental hardship. For instance, the hypometabolic areas of the schizophrenic brain--the hippocampus and the frontal lobes--are the same areas that are known to become adaptively hypometabolic in response to starvation, stress and variations in ecological rigor in birds and mammals. Individuals with schizophrenia are also highly genetically inclined to develop the metabolic syndrome, which is widely thought to allow developmentally deprived mammals to conserve energy under poor circumstances. It is well known that schizophrenia features an up-regulated hypothalamic-pituitary-adrenal axis and an exaggerated stress response--both alterations thought to represent predictive, adaptive responses to stress in mammals--which may have increased attentiveness to the environment and created a defensive, vigilance-based behavioral strategy. The habituation deficits characteristic of schizophrenia--which can be induced in other mammals through stress--may represent a cognitive strategy that alerts the organism to salient, potentially informative stimuli and that permits it to be more impulsive and vigilant. Inability to calm instinctual drives, ignore arousing stimuli, and inhibit transient desires are all core characteristics of the disorder, which predict social and vocational disabilities in modern times, but may have amounted to a robust, selfish strategy in prehistoric times.
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PMID:Schizophrenia and phenotypic plasticity: schizophrenia may represent a predictive, adaptive response to severe environmental adversity that allows both bioenergetic thrift and a defensive behavioral strategy. 1732 Oct 61

Bipolar disorder and schizophrenia share common chromosomal susceptibility loci and many risk-promoting genes. Oligodendrocyte cell loss and hypomyelination are common to both diseases. A number of environmental risk factors including famine, viral infection, and prenatal or childhood stress may also predispose to schizophrenia or bipolar disorder. In cells, related stressors (starvation, viruses, cytokines, oxidative, and endoplasmic reticulum stress) activate a series of eIF2-alpha kinases, which arrest protein synthesis via the eventual inhibition, by phosphorylated eIF2-alpha, of the translation initiation factor eIF2B. Growth factors increase protein synthesis via eIF2B activation and counterbalance this system. The control of protein synthesis by eIF2-alpha kinases is also engaged by long-term potentiation and repressed by long-term depression, mediated by N-methyl-D-aspartate (NMDA) and metabotropic glutamate receptors. Many genes reportedly associated with both schizophrenia and bipolar disorder code for proteins within or associated with this network. These include NMDA (GRIN1, GRIN2A, GRIN2B) and metabotropic (GRM3, GRM4) glutamate receptors, growth factors (BDNF, NRG1), and many of their downstream signaling components or accomplices (AKT1, DAO, DAOA, DISC1, DTNBP1, DPYSL2, IMPA2, NCAM1, NOS1, NOS1AP, PIK3C3, PIP5K2A, PDLIM5, RGS4, YWHAH). They also include multiple gene products related to the control of the stress-responsive eIF2-alpha kinases (IL1B, IL1RN, MTHFR, TNF, ND4, NDUFV2, XBP1). Oligodendrocytes are particularly sensitive to defects in the eIF2B complex, mutations in which are responsible for vanishing white matter disease. The convergence of natural and genetic risk factors on this area in bipolar disorder and schizophrenia may help to explain the apparent vulnerability of this cell type in these conditions. This convergence may also help to reconcile certain arguments related to the importance of nature and nurture in the etiology of these psychiatric disorders. Both may affect common stress-related signaling pathways that dictate oligodendrocyte viability and synaptic plasticity.
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PMID:eIF2B and oligodendrocyte survival: where nature and nurture meet in bipolar disorder and schizophrenia? 1732 32

Converging evidence suggests that a neurodevelopmental disruption plays a role in the vulnerability to schizophrenia. The authors review evidence supporting in utero exposure to nutritional deficiency as a determinant of schizophrenia. We first describe studies demonstrating that early gestational exposure to the Dutch Hunger Winter of 1944--1945 and to a severe famine in China are each associated with an increased risk of schizophrenia in offspring. The plausibility of several candidate micronutrients as potential risk factors for schizophrenia and the biological mechanisms that may underlie these associations are then reviewed. These nutrients include folate, essential fatty acids, retinoids, vitamin D, and iron. Following this discussion, we describe the methodology and results of an epidemiologic study based on a large birth cohort that has tested the association between prenatal homocysteine, an indicator of serum folate, and schizophrenia risk. The study capitalized on the use of archived prenatal serum specimens that make it possible to obtain direct, prospective biomarkers of prenatal insults, including levels of various nutrients during pregnancy. Finally, we discuss several strategies for subjecting the prenatal nutritional hypothesis of schizophrenia to further testing. These approaches include direct assessment of additional prenatal nutritional biomarkers in relation to schizophrenia in large birth cohorts, studies of epigenetic effects of prenatal starvation, association studies of genes relevant to folate and other micronutrient deficiencies, and animal models. Given the relatively high prevalence of nutritional deficiencies during pregnancy, this work has the potential to offer substantial benefits for the prevention of schizophrenia in the population.
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PMID:Prenatal nutritional deficiency and risk of adult schizophrenia. 1868 77

The neurodegenerative and neurotoxic aspects of schizophrenia and/or psychosis involve genetic, epigenetic, and neurotoxic propensities that impinge upon both the symptom domains and the biomarkers of the disorder, involving cellular apoptosis/excitotoxicity, increased reactive oxygen species formation, viral and bacterial infections, anoxic birth injury, maternal starvation, drugs of abuse, particularly cannabis, metabolic accidents, and other chemical agents that disrupt normal brain development or the integrity of brain tissues. Evidence for premorbid and prodromal psychotic phases, aspects of neuroimaging, dopamine, and psychosis vulnerability, and perinatal aspects provide substance for neurodegenerative influences. Not least, the agencies of antipsychotic contribute to the destructive spiral that disrupts normal structure and function. The etiopathogenesis of psychosis is distinguished also by disruptions of the normal functioning of the neurotrophins, in particular brain-derived neurotrophic factor, dyskinesic aspects, immune system disturbances, and metabolic aspects. Whether detrimental to neurodevelopment or tissue-destructive, or an acceleration of neurotoxic pathways, the notion of neurodegeneration in the pathophysiology of schizophrenia spectrum and psychotic disorders continues to gather momentum.
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PMID:Neurodegenerative aspects in vulnerability to schizophrenia spectrum disorders. 2480 34


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