ascorbic-acid and Schizophrenia

Studies have shown that oxidative stress (OS) is related to the pathophysiology of schizophrenia (SCZ), but whether antipsychotics can induce OS has not been investigated well. Moreover, antipsychotics have differential effects on the OS level modulation, i.e., different types of antipsychotics have different effects on the cellular antioxidants or pro-oxidants.. We followed the Preferred Reporting Items for Systematic Review and Meta-Analysis (PRISMA) guidelines and investigated the OS indicators including both enzymatic and nonenzymatic markers, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), malondialdehyde (MDA), glutathione (GSH), vitamin C, etc., of SCZ patients at baseline and follow-up of mono-medication.. Twenty studies met the inclusion criteria, with a total of 1162 patients enrolled at baseline, and 1105 patients completed the follow-up. OS markers were changed after a period of antipsychotic treatment in SCZ patients. The GPx activity and MDA level decreased in the whole blood (P<0.05), also the serum MDA level decreased (P<0.05). For the first-episode SCZ patients, the activity of GPx and the level of MDA decreased, while the level of vitamin C increased (all P<0.05). The levels of MDA in patients receiving atypical antipsychotics decreased (P<0.05), while the level of GSH in patients with typical antipsychotics decreased (P=0.05).. Antipsychotic medication may cause changes in the levels of OS markers in different blood samples of SCZ patients. However, the available studies might not be sufficient to reveal the underlying facts accurately due to the poor quality of experimental designs in the published literature.

Topics: Antioxidants; Antipsychotic Agents; Ascorbic Acid; Biomarkers; Glutathione; Glutathione Peroxidase; Humans; Oxidative Stress; Schizophrenia

There is accumulating evidence that progressive changes in brain structure and function take place as schizophrenia unfolds. Among many possible candidates, oxidative stress may be one of the mediators of neuroprogression, grey matter loss and subsequent cognitive and functional impairment. Antioxidants are exogenous or endogenous molecules that mitigate any form of oxidative stress or its consequences. They may act from directly scavenging free radicals to increasing anti-oxidative defences. There is evidence that current treatments impact oxidative pathways and may to some extent reverse pro-oxidative states in schizophrenia. The existing literature, however, indicates that these treatments do not fully restore the deficits in antioxidant levels or restore levels of oxidants in schizophrenia. As such, there has been interest in developing interventions aimed at restoring this oxidative balance beyond the benefits of antipsychotics in this direction. If antioxidants are to have a place in the treatment of this serious condition, the relevant and up-to-date information should be available to clinicians and investigators.. To evaluate the effect of antioxidants as add-on treatments to standard antipsychotic medication for improving acute psychotic episodes and core symptoms, and preventing relapse in people with schizophrenia.. We searched the Cochrane Schizophrenia Group's Study-Based Register of Trials which is based on regular searches of CINAHL, BIOSIS, AMED, Embase, PubMed, MEDLINE, PsycINFO, and registries of clinical trials. There are no language, time, document type, or publication status limitations for inclusion of records in the register. We ran this search in November 2010, and again on 8 January 2015. We also inspected references of all identified studies for further trials and contacted authors of trials for additional information.. We included reports if they were randomised controlled trials (RCTs) involving people with schizophrenia who had been allocated to either a substance with antioxidant potential or to a placebo as an adjunct to standard antipsychotic treatment.. We independently extracted data from these trials and we estimated risk ratios (RR) or mean differences (MD), with 95% confidence intervals (CI). We assessed risk of bias for included studies and created a 'Summary of findings' table using GRADE.. The review includes 22 RCTs of varying quality and sample size studying Ginkgo biloba, N-acetyl cysteine (NAC), allopurinol, dehydroepiandrosterone (DHEA), vitamin C, vitamin E or selegiline. Median follow-up was eight weeks. Only three studies including a minority of the participants reported our a priori selected primary outcome of clinically important response. Short-term data for this outcome (measured as at least 20% improvement in scores on Positive and Negative Syndrome Scale (PANSS)) were similar (3 RCTs, n = 229, RR 0.77, 95% CI 0.53 to 1.12, low quality evidence). Studies usually reported only endpoint psychopathology rating scale scores. Psychotic symptoms were lower in those using an adjunctive antioxidant according to the PANSS ( 7 RCTS, n = 584, MD -6.00, 95% CI -10.35 to -1.65, very low quality evidence) and the Brief Psychiatric Rating Scale (BPRS) (8 RCTS, n = 843, MD -3.20, 95% CI -5.63 to -0.78, low quality evidence). There was no overall short-term difference in leaving the study early (16 RCTs, n = 1584, RR 0.73, 95% CI 0.48 to 1.11, moderate quality evidence), or in general functioning (2 RCTs, n = 52, MD -1.11, 95% CI -8.07 to 5.86, low quality evidence). Adverse events were generally poorly reported. Three studies reported useable data for 'any serious adverse effect', results were equivocal (3 RCTs, n = 234, RR 0.65, 95% CI 0.19 to 2.27, low quality evidence). No evidence was available for relapse, quality of life or service use.. Although 22 trials could be included in this review, the evidence provided is limited and mostly not relevant to clinicians or consumers. Overall, although there was low risk of attrition and selective data reporting bias within the trials, the trials themselves were not adequately powered and need more substantial follow-up periods. There is a need for larger trials with longer periods of follow-up to be conducted. Outcomes should be meaningful for those with schizophrenia, and include measures of improvement and relapse (not just rating scale scores), functioning and quality of life and acceptability and, importantly, safety data.

Topics: Acetylcysteine; Allopurinol; Antioxidants; Antipsychotic Agents; Ascorbic Acid; Dehydroepiandrosterone; Drug Therapy, Combination; Free Radical Scavengers; Ginkgo biloba; Humans; Oxidative Stress; Randomized Controlled Trials as Topic; Schizophrenia; Selegiline; Vitamin E; Vitamins

Schizophrenia is a chronic condition that impacts significantly not only on the individual and family, but the disorder also has wider consequences for society in terms of significant costs to the economy. This highly prevalent condition affects approximately 1% of the worldwide population, yet there are few therapeutic options. The predominant treatment strategy for schizophrenia is anti-psychotic medication (with or without additional talking therapy) even though this approach lacks efficacy in managing the negative symptoms of the condition, is not effective in one-third of the patient group and the side effects of the medication can be severe and debilitating. In recent years, a number of pathophysiological processes have been identified in groups of people with schizophrenia including oxidative stress, one-carbon metabolism and immune-mediated responses. A number of studies have shown that these altered physiological mechanisms can be ameliorated by nutritional interventions in some individuals with schizophrenia. This review briefly describes the aforementioned processes and outlines research that has investigated the utility of nutritional approaches as an adjunct to anti-psychotic medication including antioxidant and vitamin B supplementation, neuroprotective and anti-inflammatory nutrients and exclusion diets. Whilst none of these interventions provides a 'one-size-fits-all' therapeutic solution, we suggest that a personalised approach warrants research attention as there is growing agreement that schizophrenia is a spectrum disorder that develops from the interplay between environmental and genetic factors.

Topics: Acetylcysteine; Antipsychotic Agents; Ascorbic Acid; Databases, Factual; Diet, Gluten-Free; Dietary Supplements; Fatty Acids, Unsaturated; Folic Acid; Glutamates; Humans; Melatonin; Oxidative Stress; Randomized Controlled Trials as Topic; Schizophrenia; Thioctic Acid; Vitamin B Complex; Vitamin D; Vitamin E

Accumulating evidence suggests that oxidative stress associated with impaired metabolism of the antioxidant glutathione (GSH) plays a key role in the pathophysiology of schizophrenia. Magnetic resonance spectroscopy (MRS) is one of the brain-imaging techniques that can quantitatively measure bioactive substances such as GSH in the intact human brain. Four different measurement sequences including double quantum coherence (DQC) filtering, MEscher-GArwood Point-RESolved Spectroscopy (MEGA-PRESS), Stimulated Echo Acquisition Mode (STEAM), and PRESS have been used to evaluate the (1)H-MRS measurement of GSH in the brains of patients with schizophrenia. Although the results of these studies were somewhat diverse, a negative correlation between brain GSH levels and the severity of negative symptoms in schizophrenia patients suggests that increasing the brain GSH levels might be beneficial for schizophrenia patients with negative symptoms. Moreover, a recent double-blind, placebo-controlled study demonstrated that add-on of N-acetyl-l-cysteine (NAC), a precursor of GSH, to antipsychotics improved the negative symptoms and reduced the side effects (akathisia) in patients with chronic schizophrenia. MRS study of the antioxidant defense system in schizophrenia still remains in the infantile stage; future studies are needed to examine the brain GSH level before and after NAC treatment, and thereby to provide direct evidence of the induced production of GSH in the living brain.

Topics: Ascorbic Acid; Brain; Glutathione; Humans; Magnetic Resonance Imaging; Schizophrenia

Schizophrenia is a devastating and poorly understood disease for which the only accepted therapy is nonspecific antipsychotic and anti-seizure medication. This article summarizes the evidence that certain vitamin deficiencies likely worsen the symptoms of schizophrenia, and the evidence that large doses of certain vitamins could improve the core metabolic abnormalities that predispose some people to develop it; it recounts the history of a controversial vitamin-based therapy for schizophrenia called orthomolecular psychiatry; and it concludes by advocating a process for discovering promising new schizophrenia therapies that involves small, carefully conducted clinical trials of nutrient combinations in appropriately selected patients.

Topics: Ascorbic Acid; Avitaminosis; Folic Acid; Humans; Niacin; Schizophrenia; Vitamins

Topics: Animals; Ascorbic Acid; Bipolar Disorder; Brain; Dopamine; Feeding Behavior; Humans; Hypothalamus; Milk; Mixed Function Oxygenases; Norepinephrine; Pargyline; Phenethylamines; Phenothiazines; Propranolol; Punishment; Rats; Reward; Schizophrenia

Topics: Acute Disease; Adult; Age Factors; Ascorbic Acid; Child; Clinical Trials as Topic; Evaluation Studies as Topic; Humans; Nicotinic Acids; Phenethylamines; Recurrence; Schizophrenia; Schizophrenia, Childhood; Tranquilizing Agents

Topics: Ascorbic Acid; Diet; Edible Grain; Humans; Methionine; Niacinamide; Nutritional Physiological Phenomena; Schizophrenia

Topics: Amino Acids; Ascorbic Acid; Dihydroxyphenylalanine; Humans; Methionine; Niacinamide; Nicotinic Acids; Phenylalanine; Psychotic Disorders; Pyridoxine; Schizophrenia; Tryptophan; Tyrosine

There is need for more efficient treatment of neurocognitive deficits in schizophrenia. In this 16 weeks randomised, placebo-controlled trial, we examined neurocognitive effects of adding ethyl-eicosapentaenoate 2g/day and/or vitamins E 364mg/day + C 1000mg/day to antipsychotics in 53 patients aged 18-39 years with acute schizophrenia. For the sake of validating neurocognitive tests, healthy subjects, not taking trial drugs, were also included in the study. Ethyl-EPA given alone to patients with low baseline RBC polyunsaturated fatty acids (PUFA), and Vitamins E+C given alone to high PUFA patients, impaired sustained attention (Continuous Performance Test, CPT-IP d prime score), standardised effect sizes d = 0.78 and d = 0.69, respectively. These adverse effects were paralleled by excessive increases in long-chain PUFA and serum alpha-tocopherol, respectively. They were counteracted by combining ethyl-EPA and vitamins, d = 0.80 and d = 0.74 in low and high PUFA patients, respectively. No other neurocognitive tests yielded significant results. Plausible mechanisms of harmful effects are oxidative stress and lipid raft disruption.

Topics: Adult; Antipsychotic Agents; Ascorbic Acid; Attention; Eicosapentaenoic Acid; Executive Function; Fatty Acids, Omega-3; Female; Humans; Male; Mental Status and Dementia Tests; Schizophrenia; Schizophrenic Psychology; Treatment Outcome; Vitamin E; Young Adult

Membrane lipid metabolism and redox regulation may be disturbed in schizophrenia. We examined the clinical effect of adding an omega-3 fatty acid and/or vitamins E+C to antipsychotics. It was hypothesized that lower baseline levels of polyunsaturated fatty acids (PUFAs) would predict more benefit from the add-on treatment. The trial had a multicenter, randomized, double-blind, placebo-controlled 2 × 2 factorial design. Patients aged 18-39 years with schizophrenia or related psychoses were consecutively included at admission to psychiatric departments in Norway. They received active or placebo ethyl-eicosapentaenoate (EPA) 2 g day⁻¹ and active or placebo vitamin E 364 mg day⁻¹+vitamin C 1000 mg day⁻¹ (vitamins) for 16 weeks. The main outcome measures were Positive and Negative Syndrome Scale (PANSS) total and subscales scores, analyzed by linear mixed models. Ninety-nine patients were included. At baseline, erythrocyte PUFA were measured in 97 subjects. Given separately, EPA and vitamins increased drop-out rates, whereas when combined they did not differ from placebo. In low PUFA patients, EPA alone impaired the course of total PANSS (Cohen's d=0.29; P=0.03) and psychotic symptoms (d=0.40; P=0.003), especially persecutory delusions (d=0.48; P=0.0004). Vitamins alone impaired the course of psychotic symptoms (d= 0.37; P=0.005), especially persecutory delusions (d=0.47; P=0.0005). Adding vitamins to EPA neutralized the detrimental effect on psychosis (interaction d=0.31; P=0.02). In high PUFA patients, there were no significant effects of trial drugs on PANSS scales. In conclusion, given separately during an acute episode, EPA and vitamins E+C induce psychotic symptoms in patients with low levels of PUFA. Combined, these agents seem safe.

Topics: Adolescent; Adult; Antipsychotic Agents; Ascorbic Acid; Double-Blind Method; Drug Therapy, Combination; Eicosapentaenoic Acid; Fatty Acids, Omega-3; Fatty Acids, Unsaturated; Humans; Schizophrenia; Schizophrenic Psychology; Treatment Outcome; Vitamin E; Vitamins; Young Adult

Oxidative stress may be a contributing factor in the etiopathophysiology of schizophrenia, which may be exacerbated by the treatment with antipsychotics with pro-oxidant properties. Increased levels of S100 B are associated with neurodegenerative disorders, including schizophrenia. The aim of the present study was to investigate the role of oxidative cell damage in the pathogenesis of schizophrenia. Forty patients who fully met the fourth Diagnostic and Statistical Manual of Mental Disorders criteria for schizophrenia and 35 healthy control subjects were included in the study. Serum S100 B level was determined to investigate brain damage. Plasma malondialdehyde (MDA) levels and susceptibility of red blood cell (RBC) to oxidation were determined to investigate the oxidative status and plasma vitamin E, vitamin C, serum total carotenoid levels and total antioxidant capacity and RBC superoxide dismutase (SOD) and whole blood glutathione peroxidase activities were measured to investigate the antioxidative defence before and after 6 weeks of antipsychotic treatment. Plasma MDA and serum S100 B levels and RBC-SOD activity were significantly higher in the schizophrenia group than those of the control group. Treatment did not modify any of the oxidative-antioxidative system parameters or serum S100 B levels. S100 B level was significantly higher in patients with negative symptoms than the patients with positive symptoms and the control subjects. S100 B levels were significantly reduced after 6 weeks of treatment in patients with negative symptoms. The results of the present study might support the oxidative cell injury hypothesis of the schizophrenia. Furthermore, the underlying mechanisms of the subgroups of schizophrenia might be different as suggested by the increased S100 B levels and its decrement after treatment in patients with negative symptoms.

Topics: Adult; Antipsychotic Agents; Ascorbic Acid; Carotenoids; Case-Control Studies; Female; Humans; Male; Malondialdehyde; Middle Aged; Nerve Growth Factors; Oxidative Stress; S100 Calcium Binding Protein beta Subunit; S100 Proteins; Schizophrenia; Superoxide Dismutase; Vitamin E

Classical antipsychotics like haloperidol are suggested to increase oxidative stress and oxidative cell injury in the brain. Pro-oxidant effect of haloperidol may influence the course and treatment outcomes of schizophrenia. Dietary supplementation of either antioxidants or omega-3 fatty acids was found to improve symptoms of schizophrenia. Thus we decided to assess the impact of combining omega-3 fatty acids, vitamins E and C supplementation on treatment outcome and side effects in schizophrenia patients treated with haloperidol. Ongoing haloperidol treatment of 17 schizophrenia patients was supplemented with 1000 mg capsule of omega-3 fatty acids (180 mg EPA+120 mg DHA) bid, vitamin E 400 IU bid and vitamin C 1000 mg/day. Patients were assessed with Brief Psychiatric Rating Scale (BPRS), Scale for the Assessment of Negative Symptoms (SANS), Simpson Angus Scale (SAS) and Barnes Akathisia Rating Scale (BARS) over a 4 month period. Gluthatione peroxidase, superoxide dismutase, malondialdehyde, vitamin E and C levels were also evaluated at baseline and at the end of study. BPRS, SANS, SAS and BARS scores obtained at follow-up visits were significantly lower compared to baseline. Superoxide dismutase level was significantly lower at the end of study. No significant differences were detected in other laboratory parameters. Our results support the beneficial effect of the supplementation on positive and negative symptoms of schizophrenia as well as the severity of side effects induced by haloperidol. The effect of supplementation on akathisia is especially noteworthy and it has not been investigated in previous studies.

Topics: Adolescent; Adult; Akathisia, Drug-Induced; Antioxidants; Antipsychotic Agents; Ascorbic Acid; Erythrocytes; Fatty Acids, Omega-3; Female; Haloperidol; Humans; Lipid Peroxidation; Male; Malondialdehyde; Middle Aged; Pilot Projects; Schizophrenia; Schizophrenic Psychology; Superoxide Dismutase; Treatment Outcome; Vitamin E

Several investigators implicated role of free radical-mediated pathology in schizophrenia. No study has ever examined the effect of vitamin C with atypical antipsychotics in the treatment of schizophrenia.. The aim of this study was to examine the effect of oral vitamin C with atypical antipsychotics on serum malondialdehyde (MDA), plasma ascorbic acid levels, and brief psychiatric rating scale (BPRS) score in schizophrenic patients.. Forty schizophrenic patients participated in a prospective, double-blind, placebo-controlled, noncrossover, 8-week study. The patients with schizophrenia were divided randomly into placebo and vitamin C group of 20 each. Serum MDA and plasma ascorbic acid were estimated by methods of Nischal and Aye, respectively.. Increased serum MDA and decreased plasma ascorbic acid levels were found in schizophrenic patients. These levels were reversed significantly after treatment with vitamin C along with atypical antipsychotics compared to placebo with atypical antipsychotics. BPRS change scores at 8 weeks improved statistically significant with vitamin C as compared to placebo.. Oral supplementation of vitamin C with atypical antipsychotic reverses ascorbic acid levels, reduces oxidative stress, and improves BPRS score, hence both the drugs in combination can be used in the treatment of schizophrenia.

Topics: Adult; Analysis of Variance; Antipsychotic Agents; Ascorbic Acid; Female; Humans; Male; Middle Aged; Oxidative Stress; Prospective Studies; Psychiatric Status Rating Scales; Schizophrenia; Time Factors; Treatment Outcome

There is evidence to suggest the derangement of the oxidant and antioxidant defense system in schizophrenia. The present study examined the effect of atypical antipsychotics on lipid peroxidation, superoxide dismutase (SOD) and ascorbic acid. For this purpose, a prospective, open-label, 8-week study design was utilized. Serum SOD, serum malondialdehyde (MDA) and plasma ascorbic acid were estimated. Schizophrenic patients (n = 48) were compared with age- and sex-matched healthy volunteers (n = 40). There was a significant increase in serum SOD, serum MDA and a decrease in plasma ascorbic acid in schizophrenic patients as compared to control subjects. The trend altered significantly after the treatment with atypical antipsychotics. The results of the Brief Psychiatric Rating Scale for schizophrenia also improved with the treatment. The findings indicate an involvement of free radicals in schizophrenia and its modification by treatment with atypical antipsychotics. This study can also be used as a predictor of drug response by atypical antipsychotics in schizophrenia.

Topics: Adult; Antipsychotic Agents; Ascorbic Acid; Brief Psychiatric Rating Scale; Case-Control Studies; Chi-Square Distribution; Female; Humans; Male; Malondialdehyde; Middle Aged; Oxidative Stress; Prospective Studies; Schizophrenia; Superoxide Dismutase

Topics: Ascorbic Acid; Clinical Trials as Topic; Humans; Nutritional Physiological Phenomena; Schizophrenia; Vitamins

After reviewing the literature on nicotinic acid in the treatment of schizophrenia, the authors present the results of the Canadian collaborative study. The data indicate that nicotinic acid has no therapeutic effect of schizophrenia.

Topics: Adrenochrome; Antipsychotic Agents; Ascorbic Acid; Clinical Trials as Topic; Drug Evaluation; Drug Therapy, Combination; Humans; NAD; Nicotinic Acids; Pellagra; Phenothiazines; Pyridoxine; Schizophrenia

Topics: Ascorbic Acid; Chlorpromazine; Clinical Trials as Topic; Female; Humans; Male; Schizophrenia; Sex Factors; Vitamin B Complex

Topics: Ascorbic Acid; Ascorbic Acid Deficiency; Clinical Trials as Topic; Humans; Nutritional Requirements; Schizophrenia

Topics: Aged; Aggression; Antipsychotic Agents; Ascorbic Acid; Behavior; Clinical Trials as Topic; Dementia; Drug Synergism; Female; Hospitals, Psychiatric; Humans; Male; Middle Aged; Neurocognitive Disorders; Phenothiazines; Placebos; Psychiatric Status Rating Scales; Schizophrenia; Vitamin B Complex

Topics: Acute Disease; Adult; Age Factors; Ascorbic Acid; Child; Clinical Trials as Topic; Evaluation Studies as Topic; Humans; Nicotinic Acids; Phenethylamines; Recurrence; Schizophrenia; Schizophrenia, Childhood; Tranquilizing Agents

Low levels of vitamin C have been observed in patients with schizophrenia and psychosis, and vitamin C may affect the dopaminergic system. Likewise, antipsychotic medication modulates striatal dopamine D2 receptors. We measured vitamin C levels in 52 patients with first-episode psychoses (24 females, age 23.1 ± 5.2 years) and 57 matched HCs (20 females, age 22.7 ± 4.3 years) before and after 6 weeks where patients received aripiprazole monotherapy (mean dose 10.4 mg ± 4.8 mg). At baseline, patients displayed lower levels of vitamin C (57.4 ± 25.9 µM) than controls (72.7 ± 21.4 µM) (t = 3.4, P = .001). Baseline symptoms and vitamin C levels were not correlated. Higher baseline vitamin C levels were associated with more improvement in negative symptoms (n = 39, R2 = 0.20, F = 8.2, P = .007), but not with age, sex, or p-aripiprazole. Because negative symptoms are generally considered challenging to alleviate, a potential adjunctive effect of vitamin C on treatment response should be tested in future randomized clinical trials.

Topics: Adolescent; Adult; Antipsychotic Agents; Aripiprazole; Ascorbic Acid; Female; Humans; Psychotic Disorders; Schizophrenia; Young Adult

Schizophrenia is a chronic neuropsychiatric disorder with a poorly understood pathophysiology. The theories about the disorder are mainly about dysregulation in one or more systems of neurotransmitters, and the progression triggers the presence of inflammatory markers indicates the possibility that the disorder is initially an inflammatory disease. The objective was to evaluate the ascorbic acid supplementation in an animal model of schizophrenia, on behavioral parameters, and cytokines involved in inflammation IL-1β, IL-10. Wistar rats with 60 days of age were used which were supplemented with ascorbic acid at 0.1, 1, and 10 mg/kg or saline for 14 days via orogastric gavage. Subsequently, four groups were given ketamine (25 mg/kg) and four groups received intraperitoneal saline from the 9th-15th day of the experiment. After 30 min of the last administration of ketamine/saline, and behavioral test, rats were killed by guillotine decapitation and the brain structures were carefully dissected for biochemical analysis. Results showed that ascorbic acid supplementation prevented motor sensory loss but nor alter other parameters evaluated. We concluded that ascorbic acid may be used as a therapeutic adjuvant in schizophrenia and may help to improve the schizophrenic patient's life quality.

Topics: Anesthetics, Dissociative; Animals; Ascorbic Acid; Behavior, Animal; Brain; Cytokines; Dietary Supplements; Dose-Response Relationship, Drug; Interleukin-10; Interleukin-1beta; Ketamine; Male; Rats; Rats, Wistar; Schizophrenia; Schizophrenic Psychology; Vitamins

Inflammation is a risk factor for the onset and progression of schizophrenia, and dietary factors are related to chronic inflammation. We investigated whether the dietary inflammatory index (DII) is associated with schizophrenia in the Korean population. Of the 256 subjects who responded to the questionnaire, 184 subjects (117 controls; 67 individuals with schizophrenia) were included in this case-control study. A semi-quantitative food frequency questionnaire was used to evaluate the dietary intakes of the study participants. The energy-adjusted DII (E-DII) was used to assess the inflammatory potential of the participants' diets. Dietary intakes of vitamin C, niacin, and folate were significantly reduced in the patients with schizophrenia. The patients with schizophrenia had higher E-DII scores than the controls (

Topics: Adolescent; Adult; Ascorbic Acid; Case-Control Studies; Diet; Dietary Carbohydrates; Dietary Fats; Dietary Proteins; Energy Intake; Female; Folic Acid; Humans; Inflammation; Male; Micronutrients; Middle Aged; Niacin; Republic of Korea; Schizophrenia; Vitamins; Young Adult

Inappropriate dietary intake and poor nutritional status are reported to be associated with metabolic syndrome and psychopathology in patients with schizophrenia. We hypothesized that inappropriate dietary habits and insufficient dietary intake of specific nutrients are associated with schizophrenia. To test the hypothesis, we assessed the dietary habits and nutritional intake of patients with schizophrenia and then developed suitable dietary guidelines. In total, 140 subjects (73 controls and 67 patients with schizophrenia from community mental health centers) were included, and dietary intakes were analyzed using a semi-quantitative food frequency questionnaire. As a result, the proportion of overweight or obese patients was significantly higher in schizophrenia subjects (64.2%) compared with control subjects (39.7%) (P=.004). The male schizophrenia patients had significantly lower dietary intakes of protein, polyunsaturated fatty acids (PUFAs), vitamin K, niacin, folate, and vitamin C than the male control subjects. In all multiple logistic regression models, subjects with the "low" dietary intake of protein, n-3 PUFAs, niacin, folate, and vitamin C had a significantly higher odds ratios for schizophrenia compared with those with the "high" dietary intake category of each nutrient. Therefore, maintenance of a healthy body weight and sufficient dietary intake of protein, PUFAs, niacin, folate, and vitamin C are recommended for Korean patients with schizophrenia.

Topics: Adult; Ascorbic Acid; Diet; Fatty Acids, Omega-3; Feeding Behavior; Female; Folic Acid; Humans; Male; Middle Aged; Minerals; Niacin; Nutrition Policy; Nutritional Status; Obesity; Overweight; Schizophrenia; Vitamins

Glutathione (GSH) metabolism dysfunction is one risk factor in schizophrenia. A transitory brain GSH deficit was induced in Wistar (WIS) and mutant (ODS; lacking ascorbic acid synthesis) rats using BSO (l-buthionine-(S,R)-sulfoximine) from post-natal days 5-16. When GSH was re-established to physiological levels, juvenile BSO-ODS rats were impaired in the water maze task. Long after treatment cessation, adult BSO-WIS/-ODS rats showed impaired place discrimination in the homing board with distributed visual or olfactory cues. Their accuracy was restored when a single cue marked the trained position. Similarly, more working memory errors were made by adult BSO-WIS in the radial maze when several olfactory cues were present. These results reveal that BSO rats did not suffer simple sensory impairment. They were selectively impaired in spatial memory when the task required the integration of multimodal or olfactory cues. These results, in part, resemble some of the reported olfactory discrimination and cognitive impairment in schizophrenia.

Topics: Aging; Animals; Animals, Newborn; Ascorbic Acid; Brain; Cognition Disorders; Cues; Disease Models, Animal; Female; Glutathione; Male; Maze Learning; Memory Disorders; Nerve Degeneration; Olfaction Disorders; Orientation; Oxidative Stress; Rats; Rats, Mutant Strains; Rats, Wistar; Schizophrenia; Sex Characteristics; Smell

A 53-year-old woman, known with a schizophrenic disorder and a history of drug addiction, was referred because of progressive hematomas of the lower extremities and fatigue. Her medical history included hyperplastic gums, tooth hypermobility and anaemia. Scurvy was diagnosed as a result of an insufficient diet due to drug addiction and a paranoid psychosis. After suppletion of vitamin C and starting highly nutritious food a rapid amelioration of the scurvy related complaints was observed. While dreaded and often fatal in earlier eras, in the 21st century scurvy is easily treatable if this diagnosis is recognised.

Topics: Anemia; Antioxidants; Ascorbic Acid; Female; Humans; Middle Aged; Schizophrenia; Scurvy; Substance-Related Disorders; Tooth Mobility; Treatment Outcome

A 53-year-old woman was referred because of progressive haematomas of the lower extremities and fatigue. Her medical history included hyperplastic gums and tooth loss. Scurvy was diagnosed; this was the result of an insufficient diet due to a paranoid psychosis. There was a dramatic improvement within a few days after addition of vitamin C and starting highly nutritious food. Scurvy is easily treated, but is not a disease of the past.

Topics: Ascorbic Acid; Ascorbic Acid Deficiency; Contusions; Diet; Fatigue; Female; Humans; Middle Aged; Schizophrenia; Schizophrenic Psychology; Tooth Loss; Treatment Outcome

Topics: Ascorbic Acid; Ascorbic Acid Deficiency; Contusions; Fatigue; Humans; Schizophrenia; Tooth Loss

Topics: Ascorbic Acid; Ascorbic Acid Deficiency; Humans; Schizophrenia; Tooth Loss; Vitamins

Reduced levels of membrane essential polyunsaturated fatty acids (EPUFAs), namely, arachidonic acid (AA), eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA) and docosahexaenoic acids (DHAs), and their association with psychopathology have been consistently reported in both chronic-medicated schizophrenic patients as well as in never-medicated patients soon after the first episode of psychosis. Past supplementation studies with either omega-6 or omega-3 or both EPUFAs generally in chronic-medicated-older patients have reported varying degrees of therapeutic effects, and have suggested that supplementation with primarily omega-3 EPUFAs (EPA>DHA) may be preferable. We report the supplementation with a mixture of EPA/DHA (180:120 mg) and antioxidants (vitamin E/C, 400 IU:500 mg) orally morning and evening to schizophrenic patients (N=33) for 4 months. The red blood cell (RBC) membrane fatty acid levels, plasma lipid peroxides and clinical measures were carried out by established procedures at pretreatment, posttreatment and after 4 months of postsupplementation period to determine the stability of treatment effects within patients. Levels of fatty acids and lipid peroxides were compared with their levels in normal controls (NC) (N=45).Posttreatment levels of RBC EPUFAs were significantly higher than pretreatment levels as well as levels in normal controls without any significant increase in plasma peroxides. Concomitantly, there was significant reduction in psychopathology based on reduction in individual total scores for brief psychiatric rating scale (BPRS) and positive and negative syndrome scale (PANSS), general psychopathology-PANSS and increase in Henrich's Quality of Life (QOL) Scale. The EPUFA levels returned to pretreatment levels after 4 months of supplementation washout. However, the clinical improvement was significantly retained. Future studies need be done in placebo-controlled trials and also with a comparison group supplemented with fatty acids alone in a larger number of patients, both chronic as well as never medicated, and for a longer duration of treatment while the dietary intake is monitored. This may establish the EPUFA supplementation a very effective treatment to improve the outcome for an extended period of time.

Topics: Adult; Antioxidants; Ascorbic Acid; Brief Psychiatric Rating Scale; Drug Therapy, Combination; Fatty Acids, Omega-6; Female; Humans; Male; Quality of Life; Schizophrenia; Schizophrenic Psychology; Severity of Illness Index; Vitamin E

Topics: Ascorbic Acid; Brain; Glutamates; Humans; Parkinson Disease; Schizophrenia

This report concerns a 37-year-old chronic schizophrenic patient who derived substantial benefit from the addition of ascorbic acid (vitamin C) to his neuroleptic treatment. The case highlights the potential usefulness of vitamin C as an adjunctive agent in the treatment of chronic schizophrenia.

Topics: Adult; Ascorbic Acid; Chronic Disease; Drug Therapy, Combination; Haloperidol; Humans; Male; Schizophrenia; Treatment Outcome

Topics: Adult; Antioxidants; Ascorbic Acid; Brain; Drug Synergism; Drug Therapy, Combination; Free Radicals; Humans; Lorazepam; Male; Schizophrenia; Schizophrenic Psychology; Vitamin E

Topics: Adult; Ascorbic Acid; Clozapine; Drug Eruptions; Drug Interactions; Humans; Male; Niacin; Schizophrenia; Schizophrenic Psychology; Tryptophan

Concentrations of HVA, 5-HIAA, ascorbic acid, and uric acid in the lumbar and cisternal cerebrospinal fluid (CSF) were measured in psychiatric and neurologically impaired patients. The concentration of HVA is 6.1 times and of 5-HIAA 2.7 times higher in cisternal than in lumbar samples, the cisternal level of uric acid is half that of the lumbar region, but no significant differences were found in ascorbic acid concentrations. Correlation between lumbar and cisternal metabolite concentrations is high for 5-HIAA and ascorbic acid, and is less for HVA and uric acid. In cisternal CSF there is a significant correlation between levels of HVA-5-HIAA, 5-HIAA-ascorbic acid, and 5-HIAA-uric acid. These correlations disappear in lumbar CSF. These findings indicate that extrapolations to cisternal neurotransmitter metabolite concentration from lumbar measures are unwarranted for HVA, but not for 5-HIAA.

Topics: Adult; Aged; Alcohol Amnestic Disorder; Ascorbic Acid; Brain; Dementia; Female; Homovanillic Acid; Humans; Hydroxyindoleacetic Acid; Male; Middle Aged; Neurocognitive Disorders; Schizophrenia; Uric Acid

Schizophrenic patients on the same hospital diet as control group subjects had significantly lower levels of fasting plasma vitamin C (p less than 0.05) and 6-hr urinary vitamin C excretion after an ascorbic acid load test (p less than 0.01). After administration of 70 mg of ascorbic acid for 4 weeks there was no longer any difference in plasma vitamin C levels between schizophrenics and control group subjects, but the urinary vitamin C excretion after the vitamin C loading test remained significantly lower in schizophrenics (p less than 0.05). The administration of 1 g ascorbic acid for 4 weeks, in addition to eliminating differences in the plasma vitamin C level, also increased the urinary vitamin C excretion of schizophrenic patients to the level of the control group subjects. The results of this study are in agreement with the hypothesis that schizophrenic patients require higher levels of vitamin C than the suggested optimal ascorbic acid requirement for healthy humans.

Topics: Adult; Anxiety Disorders; Ascorbic Acid; Ascorbic Acid Deficiency; Dose-Response Relationship, Drug; Female; Humans; Male; Nutritional Requirements; Schizophrenia; Schizophrenic Psychology; Somatoform Disorders

Topics: Adult; Aged; Aging; Alcoholism; Antioxidants; Ascorbic Acid; DNA Repair; Female; Free Radicals; Genes; Humans; Lipid Peroxidation; Male; Middle Aged; Oxygen; Schizophrenia; Vitamin E

Recent reports have suggested an augmentation by ascorbic acid of haloperidol treatment of schizophrenic patients. This study was designed to examine whether pharmacokinetic interactions between ascorbic acid and haloperidol occur in this population. Eight male inpatients diagnosed as having chronic schizophrenia by DSM-III-R criteria and stabilized on a fixed dose of haloperidol were given oral doses of ascorbic acid, 4.5 grams daily, for 2 weeks in an open trial. Serum concentrations of haloperidol and is metabolite, reduced haloperidol, were measured by high performance liquid chromatography. Psychiatric symptoms were monitored using the Psychiatric Symptom Assessment Scale performed by nursing staff blind to the haloperidol status but not to the ascorbic acid dosage. The addition of ascorbic acid was not associated with any change in psychopathology in this group of patients, nor was there any apparent pharmacokinetic interaction with haloperidol.

Topics: Ascorbic Acid; Haloperidol; Humans; Male; Neurotransmitter Agents; Oxidation-Reduction; Psychiatric Status Rating Scales; Schizophrenia

Topics: Amenorrhea; Antipsychotic Agents; Ascorbic Acid; Drug Therapy, Combination; Female; Humans; Middle Aged; Schizophrenia

Topics: Adult; Ascorbic Acid; Humans; Middle Aged; Psychiatric Status Rating Scales; Schizophrenia; Schizophrenic Psychology

Vitamin C status was determined in schizophrenic subjects using fasting plasma levels and the urinary dose response after an oral load of 1.0 g ascorbic acid. The study was carried out in 20 schizophrenic patients and 15 controls with the diagnosis of neurosis who were on the same hospital diet for at least 2 months. The schizophrenic subjects had significantly lower fasting plasma vitamin C levels (P less than 0.05) and 6-h urinary vitamin C excretion after an ascorbic acid load test (P less than 0.01). Since urinary vitamin C excretion in both groups was significantly associated with differences in fasting vitamin C plasma levels (P less than 0.001), a new group of 15 schizophrenics and 15 controls was supplemented with 70 mg of ascorbic acid daily for 4 weeks in order to optimize and standardize their vitamin C plasma levels before the ascorbic acid loading test. The results showed that after 4 weeks of supplementation the average fasting plasma vitamin C levels were almost identical in both examined groups, but the urinary vitamin C excretion was again significantly lower in schizophrenic patients (P less than 0.05). These results are in agreement with the hypothesis that schizophrenia may be associated with impaired ascorbic acid metabolism.

Topics: Adult; Ascorbic Acid; Female; Humans; Male; Schizophrenia

Topics: Ascorbic Acid; Female; Humans; Male; Schizophrenia

Topics: Animals; Ascorbic Acid; Brain; Ceruloplasmin; Guinea Pigs; Humans; Male; Schizophrenia; Scurvy

Plasma vitamin C was measured in 885 patients in a psychiatric hospital and in 110 healthy controls. The average value was lower in the patients (0.51 mg/100 ml) than in the controls (0.87 mg/100 ml). Length of stay in hospital had little effect on plasma vitamin C in the patients, but the values were marginally lower in males, females on iron therapy and in those with senile dementia. In the patients, many of whom had been offered a similar diet for several years, age was not associated with a change in plasma vitamin C and this suggests that changes in vitamin C with age that have been reported reflect differences in intake. Few patients had values as low as those found in clinical scurvy (less than 0.1 mg/100 ml), but many (32 per cent) had concentrations below the threshold (0.35 mg/100 ml) at which some detrimental effects on health have been reported.

Topics: Affective Disorders, Psychotic; Age Factors; Aged; Ascorbic Acid; Chlorpromazine; Dementia; Female; Hospitals, Psychiatric; Humans; Iron; Length of Stay; Male; Middle Aged; Psychotic Disorders; Schizophrenia; Sex Factors

The recent upsurge in megavitamin therapy raises questions about the role of vitamin deficiencies and dependencies in mental health. With this in mind, the plasma levels of folic acid, ascorbic acid, pyridoxine, and riboflavin were studied in approximately 125 children admitted to a child psychiatric unit. There were no apparent decreased levels of vitamins in these children in terms of their age, race, or psychiatric diagnosis. It is postulated that vitamin deficiencies per se cannot be proposed as etiological factors in any of the psychiatric deficits represented. Megavitamin therapy, if successful, is not effective due to crrection of vitamin deficiencies as opposed to vitamin dependencies and may be due to the metabolic onus and consequent effects of such heavy doses of vitamins.

Topics: Adolescent; Affective Symptoms; Ascorbic Acid; Autistic Disorder; Child; Child Behavior Disorders; Child, Preschool; Folic Acid; Humans; Intellectual Disability; Male; Orthomolecular Therapy; Psychotic Disorders; Pyridoxine; Riboflavin; Schizophrenia

Topics: Animals; Ascorbic Acid; Brain Chemistry; Homeostasis; Humans; Orthomolecular Therapy; Rabbits; Schizophrenia

Topics: Ascorbic Acid; Humans; Schizophrenia

Topics: Aged; Alcoholism; Ascorbic Acid; Avitaminosis; Child; Dose-Response Relationship, Drug; Evaluation Studies as Topic; Folic Acid; Humans; Mental Disorders; NAD; Nicotinic Acids; Psychiatry; Pyridoxine; Schizophrenia; Substance-Related Disorders; Vitamin B 12; Vitamins

Topics: Ascorbic Acid; Common Cold; Humans; Schizophrenia; Vitamins

Topics: Adult; Aged; Ascorbic Acid; Chlorpromazine; Diuresis; Drinking; Evaluation Studies as Topic; Female; Hospitalization; Humans; Male; Middle Aged; Nicotiana; Nutritional Requirements; Phenylhydrazines; Plants, Toxic; Schizophrenia; Smoking; Water-Electrolyte Balance

Topics: Ascorbic Acid; Ceruloplasmin; Copper; Female; Hemoglobins; Humans; Male; Schizophrenia

Topics: Animals; Ascorbic Acid; Brain Chemistry; Dopamine; Dopamine beta-Hydroxylase; Guinea Pigs; Humans; Hydroxydopamines; Hydroxylation; Hypothalamus; Models, Biological; Norepinephrine; Oxidation-Reduction; Quinones; Rats; Receptors, Drug; Schizophrenia

Topics: Acute Disease; Adolescent; Adult; Analysis of Variance; Ascorbic Acid; Catatonia; Ceruloplasmin; Female; Humans; Male; Middle Aged; Schizophrenia; Sex Factors

Topics: Adolescent; Adult; Aftercare; Aged; Ascorbic Acid; Female; Health Education; Humans; Male; Middle Aged; Nicotinic Acids; Physician-Patient Relations; Schizophrenia; Voluntary Health Agencies

Topics: Ascorbic Acid; Chronic Disease; Colorimetry; Dementia; Female; Humans; Male; Schizophrenia

Topics: Ascorbic Acid; Chronic Disease; Dopamine; Humans; Metabolism, Inborn Errors; Methyldopa; Schizophrenia; Thalamus; Tyrosine

Topics: Adult; Ascorbic Acid; Autoimmune Diseases; Ceruloplasmin; Chronic Disease; Copper; Diet; Humans; Male; Mathematics; Metabolism, Inborn Errors; Middle Aged; Schizophrenia; Time Factors

Topics: Adolescent; Adult; Alpha-Globulins; Ascorbic Acid; Beta-Globulins; Blood Protein Disorders; Blood Protein Electrophoresis; Ceruloplasmin; Copper; Female; gamma-Globulins; Humans; Male; Middle Aged; Schizophrenia; Serum Albumin

Topics: Acute Disease; Adolescent; Adult; Amobarbital; Anti-Bacterial Agents; Antimalarials; Ascorbic Acid; Chlortetracycline; Convulsive Therapy; Electroconvulsive Therapy; Female; gamma-Globulins; Humans; Male; Penicillins; Phenobarbital; Schizophrenia; Streptomycin; Thiamine; Triazines; Vitamins

Topics: 5-Hydroxytryptophan; Alkylation; Animals; Ascorbic Acid; Behavior, Animal; Exploratory Behavior; Hallucinogens; Humans; Injections, Intraperitoneal; Male; Rats; Schizophrenia; Serotonin

Topics: Ascorbic Acid; Chlorpromazine; Female; Humans; Penicillamine; Pigmentation Disorders; Schizophrenia

Topics: Ascorbic Acid; Ascorbic Acid Deficiency; Humans; Male; Schizophrenia

Topics: Ascorbic Acid; Brain; Brain Damage, Chronic; Carcinoma, Bronchogenic; Dementia; Diagnosis, Differential; Drug Therapy; Geriatrics; Humans; Niacin; Psychotic Disorders; Schizophrenia; Urine

Topics: Adult; Ascorbic Acid; Humans; In Vitro Techniques; Schizophrenia

Topics: Ascorbic Acid; Biological Transport; Blood-Brain Barrier; Cerebrospinal Fluid Proteins; Humans; Intellectual Disability; Nucleosides; Nucleotides; Schizophrenia; Spectrophotometry

Topics: Ascorbic Acid; Ceruloplasmin; Humans; Schizophrenia; Serum Globulins

Topics: Ascorbic Acid; Female; Humans; Pregnancy; Schizophrenia

Topics: Aniline Compounds; Anxiety; Anxiety Disorders; Ascorbic Acid; Copper; Humans; Phenylenediamines; Schizophrenia

Topics: Ascorbic Acid; Electricity; Exercise; Humans; Mental Disorders; Oxidoreductases; Psychotic Disorders; Schizophrenia; Vitamins

Topics: Aniline Compounds; Ascorbic Acid; Coloring Agents; Phenylenediamines; Psychotic Disorders; Schizophrenia

Topics: Ascorbic Acid; Humans; Neurotic Disorders; Psychiatry; Reserpine; Schizophrenia

Topics: Ascorbic Acid; Convulsive Therapy; Humans; Insulin; Schizophrenia; Vitamins

Topics: Ascorbic Acid; Basal Metabolism; Blood Proteins; Blood Sedimentation; C-Reactive Protein; Copper; Hematologic Tests; Humans; Liver Function Tests; Oxidoreductases; Schizophrenia; Sulfobromophthalein

Topics: Ascorbic Acid; Ascorbic Acid Deficiency; Brain; Humans; Schizophrenia; Vitamins

Topics: Ascorbic Acid; Female; Humans; Mental Disorders; Pregnancy; Pregnancy Complications; Schizophrenia; Scurvy; Vitamins

Topics: Antisocial Personality Disorder; Ascorbic Acid; Female; Humans; Mental Disorders; Pregnancy; Schizophrenia; Scurvy; Vitamins

Topics: Ascorbic Acid; Blood; Child; Female; Humans; Infant; Pregnancy; Schizophrenia; Syndrome; Vitamins

Topics: Ascorbic Acid; Humans; Schizophrenia; Vitamins

Topics: Ascorbic Acid; Breast Feeding; Exploratory Behavior; Female; Humans; Lactation; Pregnancy; Schizophrenia; Vitamins

Topics: Adrenal Cortex Hormones; Ascorbic Acid; Desoxycorticosterone Acetate; Schizophrenia; Vitamins

Topics: Ascorbic Acid; Humans; Iron; Minerals; Schizophrenia; Vitamins