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At least 667 records · Page 37Linked to original sources
PubMed1995

Vitamin status of eating disorder patients: relationship to clinical indices and effect of treatment.

Vitamin abnormalities in eating disorder patients may contribute to altered neuropsychological status and the development of sequelae such as cognitive dysfunction. We examined the relationship between vitamin status and clinical indices in 13 low-weight patients with anorexia or bulimia nervosa at admission to a treatment program. Vitamin status was evaluated again at discharge (2-6 weeks later) in nine of these patients. Four patients (31%) initially had erythrocyte enzyme activity indices suggesting deficiency for riboflavin and for vitamin B-6. Patients with biochemical evidence for riboflavin deficiency had lower relative body weight than those with normal riboflavin status (p < .02). Three patients (23%) had elevated plasma cholesterol concentrations (> 5.69 mmol/L). Plasma retinol concentrations were within the normal range. Plasma alpha-tocopherol concentrations were positively associated with serum albumin (p < .04), cholesterol (p < .0003), and total lipids (p < .0003), and were inversely associated with body mass index (p < .04). At discharge, thiamin, riboflavin and vitamin B-6 status indicators were normal in all cases examined. Suboptimal vitamin status is common in eating disorder patients but is normalized with dietary intervention and nutritional rehabilitation.

Adult↗
PubMed1987

Nutrition and sickle cell disease.

The role of protein and calorie deficiency in sickle cell disease remains poorly defined. While such features as growth retardation, impaired immune function, and delayed menarche do suggest a relationship between sickle cell disease and undernutrition, measurement of more direct nutritional parameters in these patients have yielded mixed results. Anthropometric measurements such as skinfold thickness are subnormal in many but not all reports. Serum protein levels are normal, but low values for serum lipids have been reported. Finally, one small study shows an improvement in both growth parameters and clinical course following caloric supplementation. A variety of micronutrient deficiencies have been suggested in sickle cell disease. Numerous case reports describing an exacerbation of the chronic anemia that was reversed by folic acid therapy led to routine folate supplementation. More recent studies have shown, however, that clinically significant folic acid deficiency occurs only in a small minority of sickle cell patients. Clearly, more work is necessary to define the cost/benefit ratio of routine folic acid supplementation. Pharmacological amounts of vitamin B6 and certain of its derivatives possess in vitro antisickling activities. Nevertheless, a small clinical trial failed to demonstrate any consistent hematologic effects of B6 supplementation. Several reports indicate that vitamin E levels are low in sickle erythrocytes. Since these abnormal red cells both generate excessive oxidation products and are more sensitive to oxidant stress, and because oxidants appear to play a role in ISC formation, vitamin E deficiency could well be linked to ISC formation and hemolysis. Small clinical trials, however, have again failed to produce a clear hematological response in sickle cell anemia. The role of zinc in sickle cell disease has received considerable attention. Though studies are generally small, most do support a relationship between sickle cell disease and zinc deficiency. Etiologic associations between zinc deficiency and such complications of sickle cell disease as poor ulcer healing, growth retardation, delays in sexual development, immune deficiencies, and high ISC counts have all been suggested. Most of these studies need further corroboration. Iron deficiency is now known to be a relatively common occurrence in sickle cell anemia, especially in children and pregnant women. The theoretical benefits of concomitant iron deficiency and sickle cell anemia remain to be proven in a controlled clinical trial.(ABSTRACT TRUNCATED AT 400 WORDS)

Anemia, Sickle Cell↗
PubMed1985

Epidemiology of neural tube defects in South America.

We present data from the Latin American Collaborative Study of Congenital Malformations (ECLAMC) on prevalence rates and etiologic factor associations in neural tube defects. Two series of data are analyzed: the A series, including 740,139 consecutive infants born in the 1967-1979 period suitable for secular trend analysis and case-control study of risk factors; and the B series, including 255,834 consecutive stillborn and liveborn infants of the 1980-1982 period suitable for prevalence rate analysis. Anencephaly was registered in 6.0/10,000 births, A spina bifida aperta in 6.2/10,000 births, and cephalocele in 2.4/10,000 births. A stable secular trend was observed for the frequency of all three neural tube defect types. Spina bifida was more frequent in Chile than in the rest of South America. No differences in prevalence rates were seen between tropical and non tropical areas. Parental consanguinity and environmental prenatal factors including maternal illnesses, drug intake, and radiation exposure were found in association with anencephaly and spina bifida.

Anencephaly↗
PubMed2002

Neuromuscular diseases and disorders of the alimentary system.

This review outlines the relationship and interaction between neuromuscular diseases and disorders of the alimentary system. Neuromuscular manifestations of gastrointestinal and hepatobiliary diseases are first considered. Such diseases may cause neuromuscular disorders by leading to nutritional deficiency or by more direct mechanisms. The pathogenesis, clinical features, and treatment of these various neuromuscular manifestations are discussed. The impact of disorders of nerve, neuromuscular transmission, and muscle on the alimentary system is then reviewed. The main sequelae are impaired deglutition and gastrointestinal dysmotility. The management of these complications is considered.

Avitaminosis↗
PubMed2005

Nutritional inadequacy in adults with muscular dystrophy.

Patients with muscular dystrophy may be prone to nutrient deficiency due to mobility limitations or oropharyngeal weakness. Patients with myotonic muscular dystrophy (DM1) may be particularly prone to nutritional deficiencies from associated dysmotility of the entire gastrointestinal tract. We prospectively evaluated nutritional intake, body composition, and muscle strength in adult patients with DM1 (n = 29) and other muscular dystrophies (n = 22) on two occasions separated by approximately 6 months. Handgrip was significantly lower and knee extension higher for DM1 compared to other dystrophies, with no between-group differences in nutritional intakes. Many patients in both groups demonstrated inadequate nutrient intake of protein, energy, vitamins (water and fat soluble), and minerals (calcium and magnesium). Significant correlations were found between measures of strength and certain individual nutrients (e.g., copper and water-soluble vitamins). These data indicate that a substantial number of adults with muscular dystrophy do not meet current dietary intake recommendations. The potential clinical implications of these findings are discussed.

Adult↗
PubMed1985

Cognitive effects of nutritional deficiency.

Deficiencies of various nutrients, primarily vitamins, impair cognition. The link is strongest for vitamin B12, thiamine, and niacin. Yet even for these, the role of mild "subclinical" or multiple deficiencies in the genesis of mental dysfunction is unclear. Most information in this field is based on animal studies often poorly applicable to the human condition or on clinical pathology complicated by advanced age, alcoholism, and intercurrent disease. There is a need for well controlled, double-blind, prospective trials to elucidate the cognitive effects of malnutrition.

Adult↗
PubMed1983

Vitamin deficiencies in rice-eating populations. Effects of B-vitamin supplements.

Rice is the staple food in many countries of Asia. Recent nutrition surveys in eight states, conducted by the National Nutrition Monitoring Bureau of India, show that though the average energy intake is adequate, more than 50% of the households surveyed consumed less than the Recommended Dietary Allowance (RDA) of energy. These households generally had per capita incomes of less than Rupees 2/- (US+ 0.25) per day. The average intake of vitamin A was only 42% of the RDA and that of riboflavin, 70% of the RDA. The average intake of other nutrients such as thiamin, niacin, ascorbic acid, iron and calcium was adequate, although thiamin deficiency was present in populations where rice was the main cereal, but not in populations where rice was the main cereal, but not in populations that consumed mixed cereal or cereal-millet diets. The magnitude of the riboflavin deficiency (after correction or energy) was also more marked in the former. Vitamin A intake was not related to the type of cereal, but had some relationship to the quantity of vegetables consumed. Nutrition surveys from Japan also reveal deficiencies in intake of energy, vitamin A, thiamin and riboflavin. The Japanese diet tends to be deficient by 20% in vitamin A and riboflavin, but not thiamin. Thus, vitamin A, riboflavin and energy (in that order) are the major nutritional constraints in rice-eating populations. Clear-cut correlations between the magnitude of dietary deficiency and the prevalence of signs and symptoms of vitamin deficiency were not apparent in the comparisons between populations, suggesting that as well as dietary deficiency other environmental factors play a role in the development of clinical deficiency. Attempts to correlate clinical deficiency with the magnitude of biochemical deficiency have also failed. Recent studies aimed at examining the effects of food supplements (rural Gambian women) or vitamin supplements (rural Indian boys) on vitamin status suggest that in some communities, vitamin intakes close to the RDA fail to saturate the tissues, as judged by biochemical tests. In the Indian boys, there was a marked rise in urinary excretion of riboflavin during winter when the incidence of respiratory infections was high. Metabolic losses of vitamins due to infections may preclude tissue saturation despite adequate dietary intake. Administration for 1 year of B-vitamins at levels close to the RDA failed to reduce the prevalence of clinical deficiency signs, but did produce some improvement in hand steadiness - a psychomotor test.(ABSTRACT TRUNCATED AT 400 WORDS)

Asia↗
PubMed1976

Vitamin E concentrations in term and preterm newborns and their clinical course.

Vitamin E deficiency in premature infants has been described as being associated with low hemoglobin levels in the 2nd month of life. Recently, low vitamin E concentrations were suspected as being associated with sudden death in infancy. As vitamin E is absorbed incompletely from the premature's intestine, vitamin E levels in the serum were determined in 80 prematures on the 10th day of life. The result was correlated to the clinical course of the infants and to the hemoglobin levels up to the 30th day. Low concentrations of vitamin E and lower hemoglobin levels were found more frequently in new borns, whose clinical course was characterized by additional complications and who received parenteral nutrition. A group of uncomplicated newborns showed no correlation of vitamin E to hemoglobin values. Thus early diagnosis of vitamin E-dependent anemia is not possible and the usefulness of vitamin E should be investigated only in newborns with an uneventful clinical course.

Anemia↗