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

In a previous paper, I have proposed that the deficiency of an endogenous caffeine-like substance is the underlying pathogenic mechanism in schizophrenia (1). In the present paper, my new concept is used to explain many of the clinical, biochemical, radiologic and pharmacologic facts about schizophrenia.
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PMID:Exploring the role of an endogenous caffeine-like substance in the pathogenesis of schizophrenia. 177 20

This article addresses itself to the apparent conflict between those reports indicating that caffeine affects schizophrenic behavior and the present study which failed to show substantial behavior or medication changes with caffeine. It is suggested that there are important subgroups of schizophrenic patients who are unusually sensitive to caffeine's apparent psychotogenic actions as reported in case reports and data on violence and destruction. It is also suggested that there are subgroups of schizophrenia which seem to require increased medication doses to "cover" caffeine effects.
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PMID:Response to "Effects of caffeine on behavior of schizophrenic inpatients". 274 92

Abnormal smooth pursuit eye movement (SPEM) has been proposed as a trait marker in schizophrenia. We utilized high resolution infra-red oculography to measure SPEM in 11 neuroleptic-treated schizophrenic patients, 10 drug-free schizophrenic patients, and 11 normals. The most characteristic abnormality was a significant increase in saccadic intrusions during SPEM in schizophrenic patients (p less than .001). SPEM gain was reduced in schizophrenic patients (p less than .005). No significant effects of neuroleptic treatment on SPEM were found, including analysis of seven patients in whom paired data was available. We also measured SPEM prior to and after caffeine ingestion (10 mg/kg) in 10 normals. We found reduced saccadic interruptions as a result of caffeine ingestion compared with placebo (p less than .05). As caffeine has been shown to selectively increase dopaminergic neurotransmission in mesocortical neurons, further study utilizing dopamine agonists during SPEM in schizophrenic patients is warranted.
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PMID:Smooth pursuit eye movements in schizophrenia: effects of neuroleptic treatment and caffeine. 257 22

As most diet therapy texts provide little information about psychiatric illnesses and their treatment, this article is intended as a brief introduction for dietitians. Several psychiatric illnesses, including schizophrenia, mood disorders, eating disorders, and substance abuse, may adversely affect food intake and nutritional status. The drugs used to treat those disorders similarly have effects on appetite and gastrointestinal function and interact with food and nutrients. Antipsychotics, antidepressants, and monoamine oxidase inhibitors (MAOIs) cause dry mouth, constipation, and weight gain. Lithium may cause nausea, vomiting, diarrhea, polydipsia, and weight gain. MAOIs have well-known interactions with foods containing tyramine. Lithium interacts with dietary sodium and caffeine; decreasing dietary intakes of those substances may produce lithium toxicity. Despite claims to the contrary, major psychiatric illnesses cannot be cured by nutritional therapies alone. Dietitians can, however, play an important role as part of a multidisciplinary team in the treatment of patients with psychiatric illness. Such a role includes nutrition assessment and monitoring, nutrition interventions, patient and staff education, and some forms of psychotherapy, including supportive and behavioral therapies for patients with eating disorders.
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PMID:Nutritional aspects of psychiatric disorders. 267 98

According to a recent hypothesis, the restless legs syndrome is thought to be due to a caffeine-like substance produced by the human body (1). Some researchers have reported a case of familial restless legs that had high concentration of free dopamine in the cerebrospinal fluid (2). Other researchers have noticed the beneficial effect of opioids in the treatment of the restless legs syndrome (3). In this article, I am compiling information reconciling the findings of those researchers with the hypothesis that proposes that the restless legs syndrome is due to a caffeine-like substance produced by the human body. Also, I am addressing the pathogenesis of the restless legs syndrome at the level of the dopamine receptors in the central nervous system. Understanding this pathogenesis probably will help in identifying the neurochemical deficiency causing schizophrenia.
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PMID:Understanding the pathogenesis of the restless legs syndrome at the level of the dopamine receptor. Are we about to identify the neurochemical deficiency causing schizophrenia? 271 21

Use of nonprescribed mood altering substances is pervasive and problematic in young adults with serious mental illnesses in community care. Fifty-eight percent of young adult clients with clearly defined schizophrenia or schizophrenia-related disorders participating in a long-term community treatment study were rated by staff or themselves as using alcohol, cannabis, or other street drugs several times a week or more. We interviewed in depth a random sample of these "significant users" to obtain their perspective on their frequencies, patterns, histories, contributing factors to, and effects of substance use and their related treatment experiences. Results revealed these clients' substance use to be of long duration and deeply entrenched, with current use often involving multiple substances including both street drugs and substances of "everyday life" (e.g., caffeine, nicotine). Clients reported compelling reasons for use including anxiety reduction, relief of boredom, and a means for social contact. Staff and clients clearly view substance use quite differently, with the latter focusing at least as much on consequences of symptom relief as symptom exacerbation. Treatment implications are discussed.
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PMID:Substance use in young adults with schizophrenic disorders. 281 75

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

We reviewed studies measuring unsupervised use of psychoactive substances in schizophrenic and control populations and organized the results by substance class. Despite much variation in their methodologies, these studies broadly agreed that schizophrenic groups' use of amphetamines and cocaine, cannabis, hallucinogens, inhalants, caffeine, and tobacco was significantly greater than or equal to use by control groups consisting of other psychiatric patients or normal subjects. Schizophrenic groups' use of alcohol, opiates, and sedative-hypnotics was significantly less than or equal to use by control groups. We discuss the implications of this nonrandom pattern of drug choice for the hypothesis of substance abuse as a form of self-medication in schizophrenia.
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PMID:A review of psychoactive substance use and abuse in schizophrenia. Patterns of drug choice. 331 90

A dexamethasone suppression test (DST) was administered to 31 inpatients with a severe acute schizophrenic exacerbation 4 or 5 days following admission and repeated after 4 weeks or prior to discharge. We identified 15 patients (48%) who were nonsuppressors on the DST at the first test. To exclude major confounders of DST results we monitored weight constancy and plasma concentrations of dexamethasone. In a subgroup of patients also plasma caffeine contents were determined. Our results indicate that DST nonsuppression occurs frequently among patients with schizophrenic crisis. Since caffeine plasma levels were indistinguishable between suppressors and nonsuppressors we reject that excessive caffeine intake accounts for DST nonsuppression among individuals with schizophrenia. Nonsuppressors had lower plasma dexamethasone levels than suppressors and reversal of the DST status from nonsuppression to suppression was associated with an increase of plasma concentrations of the test drug.
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PMID:Dexamethasone suppression test in severe schizophrenic illness: effects of plasma dexamethasone and caffeine levels. 361 83

Cerebral blood flow (CBF) measurements and mental status examinations were performed before and 30 min after oral administration of 250 mg of caffeine or a placebo given under double-blind conditions, in two groups of patients with schizophrenia. Caffeine produced significant CBF reductions but no changes in the patient's clinical condition.
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PMID:Caffeine-induced cerebral blood flow changes in schizophrenia. 369 74


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