Estado nutricional, ingesta alimentaria y riesgo de enfermedad cardiovascular en individuos con esquizofrenia en el sur de Brasil: estudio de casos-controles / Nutritional status, food intake and cardiovascular disease risk in individuals with schizophrenia in southern Brazil: A case-control study

Objetivos: Verificar los patrones de ingesta alimentaria y la presencia de parámetros antropométricos de riesgo en pacientes esquizofrénicos, al mismo tiempo que tratamos de valorar algunos factores de riesgo cardiovascular modificables. Métodos: Se incluyeron 25 pacientes ambulatorios esquizofrénicos, atendidos en el Hospital de Clínicas de Porto Alegre, Brasil, y a 25 individuos de control, sanos, emparejados por sexo, edad e índice de masa corporal (IMC). Se obtuvieron las características demográficas (edad, sexo y posición socioeconómica), antropométricas (peso, estatura y perímetro de la cintura), clínicas (antipsicóticos) y datos del consumo de alimentos (cuestionario de frecuencia de alimentos). Resultados: Hubo una frecuencia de sobrepeso del 40% y de obesidad del 40%, según lo verificado por el IMC, y un aumento del riesgo de complicaciones metabólicas del 80%, según lo determinado por el perímetro de la cintura. La mayoría de pacientes (68%) utilizaban antipsicóticos atípicos y no se encontró una asociación entre la distribución del estado nutricional de acuerdo con el IMC y el tipo de antipsicótico usado. Entre los casos se identificó una mayor ingesta de calorías totales, calorías y proteínas por kilogramo de peso corporal, porcentaje de hidratos de carbono y una menor ingesta de ácidos grasos omega 6, fitoesteroles, vitamina A y _-tocoferol. La ingesta de colesterol y de sodio no difirió entre el grupo de casos (365±152 mg de colesterol en los casos y 313±146 mg en los individuos de control; 3.499±1.695 mg de sodio entre los casos y 2.874±800 entre los individuos de control). Conclusión: En la muestra de pacientes esquizofrénicos del presente estudio se observó un mayor consumo de calorías y un menor consumo de _-tocoferol y fitoesteroles, comparado con individuos de control. También fue evidente una ingesta elevada de sodio y colesterol y una alta frecuencia de sobrepeso y obesidad centrípeta (AU)

Objectives: To verify food consumption patterns and presence of risk anthropometric parameters in schizophrenic patients, trying to assess some modifiable cardiovascular risk. Method: Twenty-five schizophrenic outpatients, attended at the Hospital de Clínicas de Porto Alegre, Brazil, and 25 healthy controls matched by sex, age and body mass index (BMI) were included. Demographic (age, sex and socioeconomic status), anthropometric (weight, height and waist circumference), clinical (antipsychotics) and dietary consumption data (food frequency questionnaire) were obtained. Results: There was a 40% frequency of overweight and 40% of obesity as verified by BMI, and 80% of increased risk of metabolic complications as measured by waist circumference. Most of the patients (68%) used atypical antipsychotics and no association was found between the distribution of the nutritional status according to BMI and type of antipsychotic used. There was a higher intake of total calories, calories and protein per kilogram of body weight, percentage of carbohydrates, and lower intake of omega-6, phytosterols, vitamin A and _-tocopherol by cases. Cholesterol and sodium intake did not differ between groups (365±152 mg of cholesterol in cases and 313±146 mg in controls; (3499±1695 mg sodium by cases and 2874±800 by controls). Conclusion: In this sample of schizophrenic patients there was a higher intake of calories and lower consumption of _-tocoferol and phitosterols, compared to controls. There was also elevated sodium, and cholesterol intake, and high frequency of overweight and central obesity (AU)

Gestational and postnatal low protein diet alters insulin sensitivity in female rats.

Nutrition during pregnancy and lactation can program an offspring's metabolism with regard to glucose and lipid homeostasis. A suboptimal environment during fetal, neonatal and infant development is associated with impaired glucose tolerance, type 2 diabetes and insulin resistance in later adult life. However, studies on the effects of a low protein diet imposed from the beginning of gestation until adulthood are scarce. This study's objective was to investigate the effects of a low protein diet imposed from the gestational period until 4 months of age on the parameters of glucose tolerance and insulin responsiveness in Wistar rats. The rats were divided into a low protein diet group and a control group and received a diet with either 7% or 25% protein, respectively. After birth, the rats received the same diet as their mothers, until 4 months of age. In the low protein diet group it was observed that: (i) the hepatic glycogen concentration and hepatic glycogen synthesis from glycerol were significantly greater than in the control group; (ii) the disposal of 2-deoxyglucose in soleum skeletal muscle slices was 29.8% higher than in the control group; (iii) there was both a higher glucose tolerance in the glucose tolerance test; and (iv) a higher insulin responsiveness in than in the control group. The results suggest that the low protein diet animals show higher glucose tolerance and insulin responsiveness relative to normally nourished rats. These findings were supported by the higher hepatic glycogen synthesis and the higher disposal of 2-deoxyglucose in soleum skeletal muscle found in the low protein diet rats.

Desnutrição, maturação do sistema nervoso central e doenças neuropsiquiátricas / Malnutrition, central nervous system maturation and neuropsychiatric diseases

A nutrição exerce profundo impacto no desenvolvimento das estruturas e funções cerebrais. Além da programação metabólica induzida pela desnutrição fetal com o propósito de aumentar as chances de sobrevivência do feto e na vida pós-natal, estudos apontam a deficiência nutricional pré-natal como fator de risco para o desenvolvimento de doenças neuropsiquiátricas. Este artigo propõe-se a considerar aspectos da desnutrição relacionados ao desenvolvimento cerebral, à extensão temporal e funcional do impacto que a mesma acarreta, assim como estabelecer correlações com doenças neuropsiquiátricas, considerando artigos disponíveis na base de dados Medline de 1962 a 2005. Fatos derivados da desnutrição precoce apontam, em sua maioria, caráter permanente em algum grau, se não imediato, prospectivo e comprometedor da performance bioquímica, fisiológica e comportamental. Apesar dos denominados atrasos no desenvolvimento de parâmetros neurológicos, estes não constituem apenas erros funcionais isolados, uma vez que as inter-relações e conexões ideais são influenciadas, ampliando os erros temporais de ocorrência de eventos. A impressão da marca da desnutrição no código genético, ao aumentar os horizontes dos efeitos da desnutrição em uma perspectiva multigeneracional, amplifica os seus efeitos. Aspectos caracterizados como mecanismos compensatórios se, por um lado, apontam para uma habilidade em se adaptar ao estresse, por outro poderiam ser comprometidos na contingência de estresse adicional de ordem ambiental ou emocional. Considerações a respeito dos efeitos subliminares ou expressivos das doenças neuropsiquiátricas sobre a qualidade de vida consolidam a importância do desenvolvimento de pesquisas que se dirijam à compreensão dos impactos e mecanismos que modulam os efeitos da desnutrição sobre o neurodesenvolvimento.

Nutrition has a profound impact on the development of cerebral structures and functions. Over and above the metabolic programming induced by fetal malnutrition in order to increase the chances of survival of the fetus in post-natal life, studies point to pre-natal nutritional deficiency as a risk factor for the development of neuropsychiatric diseases. The present review aims to consider aspects of malnutrition in relation to cerebral development, the temporal and functional extension of its impact, as well as establishing correlations with neuropsychiatric diseases, considering articles of periodicals enlisted by Medline from 1962 to 2005. Events arising from early malnutrition display, for the most part, a permanent character to some degree, if not immediate, prospective and compromising of biochemical, physiological and behavioral performance. Despite the apparent delays in the development of neurological parameters, these do not represent mere isolated functional errors, as the ideal inter-relations and connections are influenced, extending the temporal errors of the occurrence of events. The impression of the mark of malnutrition at the level of the genetic code, in extending the horizon of the effects of malnutrition to a multigenerational level, amplifies its effects. Aspects characterized as compensatory mechanisms, while, on the one hand they display an ability to adapt to severe early stress, on the other they may be compromised in the eventuality of additional environmental or emotional stress. Concern with regard to the subliminal or expressive effects of neuropsychiatric diseases on the quality of life consolidate the importance of the development of research aimed at understanding and elucidating the impacts and mechanisms that modulate the effects of malnutrition on neurodevelopment.

Avaliação nutricional em pacientes graves: [revisão] / Nutritional assessment of the severely ill patient: [review]

Considerando a importância e as dificuldades inerentes à avaliação do estado nutricional, assim como da interpretação dos resultados, além da inexistência de diretrizes específicas e validadas quanto aos métodos aplicados ao paciente crítico, o objetivo deste estudo foi contribuir para a análise e recomendação de métodos eficazes, passíveis de utilização e fidedignos do ponto de vista da interpretação no contexto do paciente grave. A presença de edema e alterações inespecíficas nas concentrações plasmáticas de proteínas; variáveis antropométricas alteradas, refletindo muito mais o rearranjo da água corporal total do que modificações do estado nutricional; estudos pouco conclusivos com a bioimpedância elétrica; ausência de dados relativos à aplicação da avaliação subjetiva global; indicadores bioquímicos alterados como conseqüência das mudanças metabólicas, entre outros, indicam as várias limitações dos métodos a esses pacientes. Na ausência de estudos que os validem, existem recomendações baseadas em evidências clínicas, observação e fundamentação nas alterações fisiopatológicas. Independentemente dos métodos, a observação clínica pela equipe de saúde é imprescindível em todas as etapas. Há necessidade de maiores estudos que identifiquem claramente os métodos e sua especificidade para a detecção, avaliação de risco ou monitorização.

Considering the importance and the difficulties inherent to nutritional state assessment, as well as the results interpretation and the inexistence of specific and validated guidelines related to applied methods to the severely ill patient, the present revision aims to contribute to the analysis and recommendation of efficient methods, which are suitable to use and reliable in terms of interpretation in the context of the severely ill patient. The presence of edema and unspecific alterations in the plasmatic concentrations of proteins; altered anthropometrics variables reflecting more the rearrangement of the total body water than the nutritional state changes; inconclusive studies with electric bioimpedance; absence of data related to the application of the global subjective assessment to severely ill patients; altered biochemical markers as a consequence of the metabolic changes that, among others, indicate several method limitations to these patients. Notwithstanding the lack of studies to validate the various methods, recommendations based on clinical evidences, observation and physiopathology alterations are available. Independent from the methods, clinical observation by the health staff at all stages is mandatory. It is crucial to dedicate more efforts to identify methods and their specificity to detection, risk assessment or monitoring.

Interação medicamento-nutriente na prática clínica / Drug-nutrient interaction in clinical practice / Interacción fármaco-nutrientes en la práctica clínica

Embora a importância das interações medicamento-nutriente seja reconhecida, a abordagem sistemática para prevenção e monitorização destas interações como parte integrante da terapêutica, permitindo uma melhor predição das respostas clínicas, ainda é deficitária. O manejo inapropriado de algumas interações pode desencadear falha na terapêutica ou severos efeitos adversos ao paciente. A maior parte das interações envolve mudanças na biodisponibilidade oral e absorção, embora outros mecanismos também sejam sugeridos. Fatores que influenciam a interação medicamento-nutriente podem estar ligados ao hospedeiro, ao medicamento ou ao próprio nutriente. A maior parte das interações do tipo 1 podem ser evitadas, evitando-se a mistura do nutriente e o fármaco na mesma infusão. Enquanto algumas interações do tipo 2 podem ser evitadas separando-se o tempo de administração do medicamento e o nutriente, a maior parte das interações do tipo 2, envolvendo metabolismo e transporte, não pode ser evitada pela separação temporal da administração da alimentação e do medicamento. As interações relacionadas à nutrição enteral, indicam a recomendação de não administração de medicamentos diretamente na formulação enteral; não administração via sonda para nutrição, durante a nutrição enteral e a interrupção da mesma por duas horas antes e depois da administração de medicamentos. Princípios gerais para o manejo clínico e prevenção das interações medicamento-nutriente que poderão contribuir para implementar e facilitar a prática clínica, envolvem a identificação das consequências clínicas no curto e longo prazo, tais como sintomas clínicos e modificações de valores laboratoriais como resultado da interação, a consideração da necessidade de ajustes para doses de medicamentos ou suplementação nutricional e, considerações sobre a viabilidade de tratamento alternativo.

Although the importance of drug-nutrient interactions is recognized, a systematic approach to prevention and monitoring of these interactions as part of therapy, allowing better prediction of clinical response is poor. The inappropriate management of some interactions may trigger therapeutic failure or severe adverse effects to the patient. Most interactions involve changes in oral bioavailability and absorption, although other mechanisms are also suggested. Factors that influence drug-nutrient interaction may be linked to the host, the drug itself or the nutrient. Most of the interactions of type 1 can be prevented by avoiding the mixture of the same nutrient and drug infusion. While some interactions of type 2 can be avoided by separating the time of drug administration and the nutrient, most of the interactions of type 2, involving metabolism and transport, can not be avoided by temporal separation of the administration of food and medicine. The interactions related to enteral nutrition, indicate the recommendation of no drug administration directly into the enteral formula, not via the administration tube for nutrition, enteral feeding and during the same interrupt for two hours before and after drug administration. General principles for clinical management and prevention of drug-nutrient interactions that may contribute to implement and facilitate clinical practice, involving the identification of clinical consequences in the short and long term, such as clinical symptoms and changes in laboratory values as a result of the interaction, consideration of the need for adjustments to doses of medication or nutritional supplementation, and considerations about the feasibility of alternative treatment.

A pesar de la importancia de las interacciones fármaco-nutriente se reconoce, un enfoque sistemático para la prevención y el control de estas interacciones como parte del tratamiento, lo que permite una mejor predicción de la respuesta clínica es pobre. El manejo inadecuado de algunas interacciones pueden provocar fracaso terapéutico o efectos adversos graves para el paciente. La mayoría de las interacciones implican cambios en la biodisponibilidad oral y la absorción, aunque otros mecanismos también se sugirió. Factores que influyen en la interacción fármaco-nutrientes pueden ser vinculados a la acogida, la propia droga o de nutrientes. La mayoría de las interacciones de tipo 1 puede prevenirse si se evita la mezcla de los mismos nutrientes y la infusión de drogas. Mientras que algunas interacciones de tipo 2 se pueden evitar mediante la separación de la época de la administración de fármacos y nutrientes, la mayoría de las interacciones de tipo 2, del metabolismo y el transporte, no se puede evitar mediante una separación temporal de la administración de alimentos y medicinas. Las interacciones relacionadas con la nutrición enteral, indica la recomendación de no administración de la droga directamente en la fórmula de nutrición enteral, no a través del tubo de la administración de la nutrición, la alimentación enteral y durante la misma interrupción durante dos horas antes y después de la administración de drogas. Principios generales para la gestión clínica y la prevención de las interacciones entre medicamentos y nutrientes que pueden contribuir a poner en práctica y facilitar la práctica clínica, que incluirá la identificación de las consecuencias clínicas a corto y largo plazo, tales como los síntomas clínicos y los cambios en...

Nutritional assessment of the severely ill patient. / Avaliação nutricional em pacientes graves.

Considering the importance and the difficulties inherent to nutritional state assessment, as well as the results interpretation and the inexistence of specific and validated guidelines related to applied methods to the severely ill patient, the present revision aims to contribute to the analysis and recommendation of efficient methods, which are suitable to use and reliable in terms of interpretation in the context of the severely ill patient. The presence of edema and unspecific alterations in the plasmatic concentrations of proteins; altered anthropometrics variables reflecting more the rearrangement of the total body water than the nutritional state changes; inconclusive studies with electric bioimpedance; absence of data related to the application of the global subjective assessment to severely ill patients; altered biochemical markers as a consequence of the metabolic changes that, among others, indicate several method limitations to these patients. Notwithstanding the lack of studies to validate the various methods, recommendations based on clinical evidences, observation and physiopathology alterations are available. Independent from the methods, clinical observation by the health staff at all stages is mandatory. It is crucial to dedicate more efforts to identify methods and their specificity to detection, risk assessment or monitoring.

Effect of 2-deoxy-D-glucose on aminoacids metabolism in rats' cerebral cortex slices.

We studied the effect of different concentrations of 2-deoxy-D-glucose on the L-[U-14C]leucine, L-[1-14C]leucine and [1-14C]glycine metabolism in slices of cerebral cortex of 10-day-old rats. 2-deoxy-D-glucose since 0.5 mM concentration has inhibited significantly the protein synthesis from L-[U-14C]leucine and from [1-14C]glycine in relation to the medium containing only Krebs Ringer bicarbonate. Potassium 8.0 mM in incubation medium did not stimulate the protein synthesis compared to the medium containing 2.7 mM, and at 50 mM diminishes more than 2.5 times the protein synthesis compared to the other concentration. Only at the concentration of 5.0 mM, 2-deoxy-D-glucose inhibited the CO2 production and lipid synthesis from L-[U-14C] leucine. This compound did not inhibit either CO2 production, or lipid synthesis from [1-14C]glycine. Lactate at 10 mM and glucose 5.0 mM did not revert the inhibitory effect of 2-deoxy-D-glucose on the protein synthesis from L-[U-14C]leucine. 2-deoxy-D-glucose at 2.0 mM did not show any effect either on CO2 production, or on lipid synthesis from L-[U-14C]lactate 10 mM and glucose 5.0 mM.

Effects of protein malnutrition on oxidative status in rat brain.

OBJECTIVES: This study evaluated the effects of protein malnutrition on oxidative status in rat brain areas. METHODS: We investigated various parameters of oxidative status, free radical content (dichlorofluorescein formation), indexes of damage to lipid (thiobarbituric acid-reactive substances assay), and protein damage (tryptophan and tyrosine content) in addition to total antioxidant reactivity levels and antioxidant enzyme activities of superoxide dismutase, glutathione peroxidase, and catalase in different cerebral regions (cortex, hippocampus, and cerebellum) from rats subjected to prenatal and postnatal protein malnutrition (control 25% casein and protein malnutrition 7% casein). RESULTS: Protein malnutrition altered various parameters of oxidative stress, especially damage to macromolecules. Free radical content was unchanged by protein malnutrition. There was an increase in levels of thiobarbituric acid-reactive substances, the index of lipid peroxidation, in the cerebellum and cerebral cortex (P < 0.05) from protein-malnourished rats. Moreover, significant decreases in tryptophan and tyrosine in all tested brain structures (P < 0.05) were observed. Catalase activity was significantly decreased in the cerebellum (P < 0.05). In addition, a significant decrease in total antioxidant reactivity levels (P < 0.05) was observed in the cerebral cortex from protein-malnourished rats. CONCLUSIONS: The present data indicated that protein malnutrition increased oxidative damage to lipids and proteins from the studied brain areas. These results may be an indication of an important mechanism for changes in brain development that are caused by protein malnutrition.

Gestational and postnatal malnutrition affects sensitivity of young rats to picrotoxin and quinolinic acid and uptake of GABA by cortical and hippocampal slices.

It is widely known that a complex interaction between excitatory and inhibitory systems is required to support the adequate functioning of the brain and that significant alterations induced by early protein restriction are complex, involving many systems. Based on such assumptions, we investigated the effects of maternal protein restriction during pregnancy and lactation followed by offspring protein restriction on some GABAergic and glutamatergic parameters, which mediate inhibitory and excitatory transmission, respectively. The sensitivity of young malnourished rats to convulsant actions of the GABA(A) receptor antagonist picrotoxin (PCT; s.c.) and to N-methyl-d-aspartate (NMDA) receptor agonist quinolinic acid (QA; i.c.v) and also gamma-amino-n-butyric acid (GABA) and glutamate uptake by cortical and hippocampal slices were evaluated in P25 old rats. Early protein malnutrition induced higher sensitivity to picrotoxin, which could be associated with the observed higher GABA uptake by cortical, and hippocampal slices in malnourished rats. In contrast, we observed lower sensitivity to quinolinic acid in spite of unaltered glutamate uptake by the same cerebral structures. Picrotoxin enhanced GABA uptake in hippocampus in well- and malnourished rats; however, it did not affect cortical GABA uptake. Our data corroborate our previous report, showing that malnutrition depresses the glutamatergic activity, and point to altered modulation of GABAergic neurotransmission. Such findings allow us to speculate that malnutrition may affect the excitatory and inhibitory interaction.

High extracellular K+ levels stimulate acetate oxidation in brain slices from well and malnourished rats.

We investigated the effect of high (12, 20, and 50 mM) extracellular K+ concentrations ([K+]0) on [U-14C] acetate oxidation to CO2 in cerebral cortex slices of control and perinatal malnourished rats. High [K+]o increased the acetate oxidation, compared with a medium containing 2.7 mM [K+]0. By investigating the mechanisms involved in this stimulation, it was shown that (i) ouabain (1 mM) and monensin (10 microM) prevented this increase; (ii) in a medium with physiological [K+]0 (2.7 mM), the decreasing of [Na+]0 stimulated acetate oxidation. These results suggest that the stimulatory effect of [K+]0 on acetate oxidation was due to the decreasing of Na1 levels. Considering that malnutrition could alter the activity of Na+,K(+)-ATPase and/or other pertinent proteins, its effect on acetate oxidation was investigated. The malnutrition, which altered the body and cerebral weight of rats, did not modify the acetate oxidation in any protocol.

Utilization of energy nutrients by cerebellar slices.

We performed an ontogenetic study about the utilization of glycine, glutamine, beta-hydroxybutyrate and glycerol as energy nutrients by rat cerebellum slices. Production of CO2 from glycerol and glutamine increased with the animals' age and glutamine was the most used nutrient for CO2 production. In adult age, glutamine oxidation to CO2 was 15 to 35 times higher than all other nutrients studied. CO2 production from glycine decreased markedly with age and 10 day-old rats showed an oxidation 7.5 times higher than that of adult rats. At fetal age and at 10 postnatal days, glycine oxidation to CO2 was only 2 times lower than glutamine oxidation to CO2. Lipid synthesis from beta-hydroxybutyrate was highest in adult rats. We did not observe any difference in the utilization of beta-hydroxybutyrate between slices of cerebral cortex and cerebellum at the ages of 10 days and adult. The main nutrients used for lipid synthesis were glycerol and beta-hydroxybutyrate.