International journal for vitamin and nutrition research. Supplement = Internationale Zeitschrift fur Vitamin- und Ernahrungsforschung. Supplement最新文献

A number of various mechanisms are prone to develop pain symptomatology. Among them infection, inflammation, degeneration, metabolic deviations, and traumas may be at the origin of complex reactions currently gathered under the terminology "rheumatism." For some time now, practitioners have introduced vitamins in the array of their antalgic supply; these were mainly vitamins of the B-group. Meanwhile research has enlarged knowledge about the oxidative mechanisms that are at the origin of inflammation, and has suggested the use of antioxidant substances, among them 9 vitamins. Finally, most of the antalgic drugs used for relief of pains have prooxidative effects, which in turn should be controlled by antioxidant substances. These different interrelations are discussed within the limits of the field of vitamins.

Vitamins serve primarily as regulators of metabolic functions, many of which are critical to exercise performance. Depending upon the nature of their sport, e.g., strength, speed, power, endurance, or fine motor control, athletes may use megadoses of various vitamins in attempts to increase specific metabolic processes important to improved performance. Surveys have indicated that most elite athletes do take vitamin supplements, often in dosages greater than 50-100 times the United States Recommended Dietary Allowances. The theoretical basis underlying the use of each vitamin depends upon its specific metabolic function in relation to sport. Vitamin A functions to maintain night vision; thiamin, riboflavin, niacin, and pantothenic acid are all involved in muscle cell energy metabolism; niacin may also block free fatty acid release; pyridoxine is involved in the synthesis of hemoglobin and other oxygen transfer protein; folic acid and vitamin B12 are integrally involved in red blood cell (RBC) development; vitamins C and E are antioxidants, possibly preventing the destruction of the red blood cell membrane during exercise; vitamin D may be involved in muscle cell energetics through its influence on calcium. These are but a few of the possible metabolic functions of vitamins which have been suggested to have ergogenic applications to sport. Research has shown that a vitamin deficiency impairs physical performance. If this deficiency is corrected, performance usually improves. In general, vitamin supplementation to an athlete on a well-balanced diet has not been shown to improve performance. However, additional research with certain vitamins appears to be warranted, such as with the vitamin B complex and fine motor control, and with vitamin E and endurance at high altitudes. Moreover, research with megadose supplementation may also be necessary.

The clinical use of nicotinic acid, nicotinamide, and pyridylcarbinol as drugs against hypercholesterolemia is critically reviewed. Though several questions remain open as to the mode of action of these compounds, it is concluded that they indeed belong to the most useful drugs for the treatment of hypercholesterolemia and for the prevention of coronary disease.

According to animal experiments, deficiency in vitamin E may be related to arterial lesions. In current cross-cultural epidemiology of middle-aged men representing 11 European populations with different mortality from ischemic heart disease (IHD) all principal antioxidant vitamins and selenium were compared in plasma. The vitamin E concentration within lipoproteins (alpha-tocopherol/cholesterol ratio) showed the most prominent correlation with IHD. This highly significant correlation seemed to be independent of the risk of coronary mortality attributable to hypercholesterolemia. The levels of lipid-standardized vitamin E associated with a relatively higher IHD risk were still in a range which has hitherto been considered "normal." The differences between individuals of lipid-standardized plasma vitamin E were reflected by corresponding changes of vitamin E in the erythrocyte and buccal mucosa. On the other hand, membrane vitamin E varied independently from the level of polyunsaturated fatty acids (PUFAs) in the membrane. The present data suggest that the plasma level of lipid-standardized vitamin E is a hitherto underrated risk factor of IHD which may substantially complement previously known risk factors, such as hypercholesterolemia and a critical state of PUFAs. A conceivable preventive effect of (an enlarged RDA of) vitamin E remains to be elucidated by an intervention trial.

In comparison with drugs, the postabsorptive curves of nutrients must be interpreted differently concerning their pharmacokinetic behavior: (1) Most nutrients do not behave as "nonreactives" in a strict sense. (2) For nutrients, the calculation of the retained quantity is important and not the calculation of the attainable concentration as in the case with drugs. These principles are shown for a lipid and a water soluble substance by calculated and observed cumulation curves: (1) The carotenoid canthaxanthin shows limited absorption. The primary invasion occurs via lymphatics as chylomicra. After absorption, the carotenoid shifts in part into other lipoprotein fractions with very low elimination constants, thus forming typical cumulation curves of very high plasma concentrations. (2) Vitamin B6, in contrast, is absorbed in an unlimited way up to very high doses. Nevertheless, rapid excretion prevents longlasting cumulation effects. However, chronical ingestion causes higher concentrations of binding proteins in different tissues. In this way, another type of long-lasting cumulation effect is induced.

The use of elevated dosages of vitamin E in humans has led to the discovery of vitamin E deficiency syndromes in neurological areas. This evidence comes from careful clinical studies in which elevated vitamin E dosages were applied. In long-term studies it has now been established that retinal and neurological abnormalities are due to vitamin E deficiency and can be ameliorated by therapy with a large amount of the vitamin enterally or parenterally, which can possibly completely prevent the development of clinical manifestations if adequate treatment is given from an early age. It has also become clear that similar neurological and ocular lesions occur in other chronic fat malabsorptive states such as cholestatic liver diseases, cystic fibrosis, and extensive resection of the gut, with respect to an elevated dosage of vitamin E therapy. More recently, several patients with spinocerebellar degeneration from vitamin E deficiency without other evidence of malabsorption have been reported on in whom the progression of the diseases is cessated by the vitamin E therapy. Whether or not the use of elevated dosages of vitamin E should be recommended for certain diseases in premature infants is controversial. Previously, it has been thought that newborn infants, especially premature infants, suffer from vitamin E deficiency, because of their low plasma vitamin E concentrations and high susceptibility of erythrocytes to hydrogen peroxide hemolysis test. Furthermore, tocopherol deficiency has been implicated in four neonatal conditions: anemia of prematurity, retrolental fibroplasia (RLF), bronchopulmonary dysplasia (BPD), and intraventricular hemorrhage (IVH). A hemolytic anemia, associated with thrombocytosis and edema, which is responsive to vitamin E therapy, is not well recognized and occurs in a minority of preterm infants, who were given high amounts of polyunsaturated fatty acids in their formula. However, prophylactic use of an elevated dosage of vitamin E to prevent anemia in the majority of premature infants is controversial. There is no evidence for beneficial effects in BPD. In addition, the prophylactic use of pharmacological dosages of vitamin E for prevention of RLF and IVH has also had conflicting results. In the course of therapy with elevated dosages of vitamin E, administered either orally, intramuscularly, or intravenously, many problems arose in the infants, such as unexpected death, increased frequency of necrotizing enterocolitis (NEC) and sepsis, and the development of unusual symptoms including hepatic injuries.(ABSTRACT TRUNCATED AT 400 WORDS)

Scientific theories allow definition of the requirements of vitamins for humans, and reasonable judgements lead to recommendations for the daily dietary allowance. However, the scarceness of the available experimental data allows only for rough estimates of the requirements, and the lack of consensus between the various national and international bodies in making reasonable and normative judgments has led to a plurality of recommendations.

There are few documented reports in humans that link teratogenic consequences to high intakes of supplemental R or RE, taken either acutely or chronically. This is in contrast to the well-documented teratogenicity in humans of RA and some of its synthetic derivatives. Both R and RE are documented teratogens in animals. Therefore, until more is known about the mechanisms of placental transfer and control as well as about the dose-related teratogenicity of vitamin A at different stages of gestation, there are few justifications for routine ingestion by fertile women of supplemental vitamin A in excess of 8-10,000 IU. Exceptions are when clinical signs are evident and habitual diets are unusually deficient. Even then, however, high dosages should be restricted to single administrations followed by frequent or daily dosages not exceeding 10,000 IU. Available evidence indicates that high-dosage supplements of beta-carotene can be safely taken; the dosages probably should be of a level to sustain blood concentrations below 300 micrograms/dl.

There are two sources of vitamin D available to man: The more important source is the cholecalciferol (vitamin D3), which is produced photochemically in the skin from the provitamin, 7-dehydrocholesterol; vitamin D ingested with food is of secondary importance, but assumes a critical role when an individual is deprived of solar exposure. Vitamin D therefore is not strictly a vitamin. A deficiency of vitamin D ultimately results in osteomalacia in adults and rickets in children, and provision of sunlight or small oral doses of the vitamin can cure this bone condition. There are, however, many less common conditions in which small doses of the vitamin are ineffective, whereas larger doses of vitamin D can achieve healing of the bone disease. These conditions are collectively called vitamin D-resistant diseases and include hypoparathyroidism, genetic and acquired hypophosphataemic osteomalacias, renal osteodystrophy, vitamin D-dependent rickets, and the osteomalacia associated with liver disease and intestinal malabsorption. Unfortunately, large doses of vitamin D continue to be prescribed for a wide variety of diseases in which there is little scientific evidence of their efficacy. The benefits and dangers of high doses of vitamin D are discussed and the problems arising from inappropriate or poorly supervised treatment with vitamin D presented. The serum concentration of the active metabolite of vitamin D, 1,25 dihydroxyvitamin D is increased in certain disease states, and the pathophysiology of some these diseases are presented. The exciting developments in tumour differentiation and the role of high doses of 1,25 dihydroxyvitamin D for the control of leukaemia and other blood and skin diseases are discussed.

Subjects with a variety of enteropathies, hemolytic anemias, acute respiratory distress syndrome, hepatitis, Gaucher's disease as well as those on TPN and hemodialysis, often have low ("deficient") blood levels of vitamin E. A deficiency of vitamin E can be manifested by accelerated red blood cell destruction and neuromuscular deficit. Supplementation of these patients may be advisable. Neurological dysfunction has been observed in adults with prolonged vitamin E deficiency resulting from lipid malabsorption. Long-term treatment with high doses of vitamin E results in improvement. Administration of 800 IU/day of vitamin E to subjects with G6PD deficiency, sickle-cell anemia and beta-thalassemia has resulted in improvement of hematological parameters. Supplementation with 300 IU/day for 3-6 months has resulted in improved walking distances and improved blood flow in patients with intermittent claudication. In a limited number of controlled studies, 300-600 IU/day resulted in improvement in premenstrual syndrome, tardive dyskinesia and also arthritis. Epidemiological studies suggest that high levels of serum vitamin E are associated with lower risk of certain cancers, cardiovascular disease and infections. In some cases the high levels are difficult to obtain by diet alone. High levels of vitamin E are contraindicated in subjects who are receiving vitamin K antagonists as anticoagulant therapy. Except for this interaction with vitamin K, there are no specific side effects associated with high doses of vitamin E. Thus, there are various reasons for supplementations with vitamin E and, with the exception noted, the risk of such supplementation is very low.