Note: The following abstracts are written in extremely technical language and include technical research and case studies. References are provided. For 'user-friendly' informative reading, check out the health topics presented by Dr. Martin and Dr. Davenport. Feel free to contact us for more information or if you have any questions.
Grace A. Goldsmith Award lecture. Trace element regulation of immunity and infection
Protein-calorie malnutrition is associated with impaired immunocompetence and increased susceptibility to infection. Clinically evident nutritional deficiency syndromes, however, are composite of deficits of many essential nutrients, each of which may exert an important regulating effect on immunity. Among other nutrients, several trace elements have been shown to regulate immune responses, particularly cell-mediated immunity. Zinc undernutrition results in lymphoid atrophy and reduced capacity to respond to many T-cell-dependent antigens. Plaque forming cell response to heterologous erythrocytes is decreased, as is the function of B cells. In zinc deficient rodents, the generation of cytotoxic lymphocytes in the spleen is reduced. Antibody-dependent cell-mediated cytotoxicity is largely unchanged. In acrodermatitis enteropathica, lymphocyte proliferation response to mitogens is decreased and there are significant changes in delayed hypersensitivity responses and in the proportion of various T cell subsets. Neutrophil function is not changed by zinc deficiency. Iron deficiency results in a slight decrease in the number of rosette-forming T cells and a significant impairment of lymphocyte response to mitogens and antigens. Polymorphonuclear leukocytes are unable to kill ingested bacteria and fungi in an efficient manner. Copper deficiency impairs cell-mediated immunity, as does selenium deficiency when it is associated with vitamin E lack. Several pathogenetic mechanisms may underlie such alterations in immunity. Many heavy metals impair immune responses. These effects of trace elements on immunity may have important fundamental and practical implications.
J-Am-Coll-Nutr. 1985; 4(1): 5-16
Minerals: exercise performance and supplementation in athletes
This paper examines whether mineral supplements are necessary for athletes, and whether these supplements will enhance performance. Macrominerals (calcium, magnesium, and phosphorus) and trace minerals (zinc, copper, selenium, chromium, and iron) are described. Calcium supplements are important for the health of bones. Athletes tend to have enhanced calcium status as assessed by bone mineral density, with the notable exception of female amenorrhoeic athletes. Magnesium status is adequate for most athletes, and there is no evidence that magnesium supplements can enhance performance. Phosphorus status is adequate for athletes. Phosphorus supplementation over an extended period of time can result in lowered blood calcium, however, some studies have shown that acute 'phosphate loading' will enhance performance. Athletes may have a zinc deficiency induced by poor diet and loss of zinc in sweat and urine. Limited data exist on the relationship of performance and zinc status. Widespread deficiencies in copper have not been documented, and there are no data to suggest that copper supplementation will enhance performance. There is no reason to suspect a selenium deficiency in athletes. The relationship between selenium status and performance has not been established, but selenium may play a role as an antioxidant. Because of the low intakes of chromium for the general population, there is a possibility that athletes may be deficient. Exercise may create a loss in chromium because of increased excretion into the urine. Many athletes, particularly female, are iron depleted, but true iron deficiencies are rare. Iron depletion does not affect exercise performance but iron deficiency anaemia does. Iron supplements have not been shown to enhance performance except where iron deficiency anaemia exists. In conclusion, poor diets are perhaps the main reason for any mineral deficiencies found in athletes, although in certain cases exercise could contribute to the deficiency. Mineral supplementation may be important to ensure good health, but few studies have definitively documented any beneficial effect of mineral supplementation on performance.
J-Sports-Sci. 1991 Summer; 9 Spec No: 91-116
Selenium supplementation suppresses tumor necrosis factor alpha-induced human immunodeficiency virus type 1 replication in vitro
Selenium is a nutritionally essential trace element that is important for optimal function of the immune system, It is incorporated into selenoproteins as the amino acid selenocysteine and it is known to inhibit the expression of some viruses, In this study, we show that selenium supplementation for 3 days prior to exposure to tumor necrosis factor alpha (TNF-alpha) partially suppresses the induction of human immunodeficiency virus type 1 (HIV-1) replication in both chronically infected T lymphocytic and monocytic cell lines, In acute HIV-1 infection of T lymphocytes and monocytes in the absence of exogenous TNF-alpha, the suppressive effect of selenium supplementation was not observed, However, selenium supplementation did suppress the enhancing effect of TNF-alpha on HIV-1 replication in vitro in acutely infected human monocytes, but not in T lymphocytes, Selenium supplementation also increased the activities of the selenoproteins, glutathione peroxidase (GPx) and thioredoxin reductase (TR), which serve as cellular antioxidants, Taken together, these results suggest that selenium supplementation may prove beneficial as an adjuvant therapy for AIDS through reinforcement of endogenous antioxidative systems.
Author(s): Hori K (REPRINT) ; Hatfield D; Maldarelli F; Lee BJ; Clouse KA
Journal: AIDS RESEARCH AND HUMAN RETROVIRUSES, 1997, V13, N15 (OCT 10), P
Viral isolation from cases of epidemic neuropathy in Cuba
Objective.--To investigate the possibility of a viral agent in the central nervous system of patients with epidemic neuropathy. Design.--Virus isolation attempts, in cell cultures and suckling mice, from cerebrospinal fluid (CSF) of neuropathy patients and
controls undergoing lumbar puncture for unrelated reasons. Serologic studies in patients, contacts, and controls.
Setting.--An epidemic of optic and peripheral neuropathy affected more than 50,000 people in Cuba in 1991 through 1993. Illness was associated with dietary limitations and increased physical demands accompanying the shortages of food and fuel experienced in Cuba since 1989. Most patients responded to parenteral vitamin therapy, and the epidemic began to subside when oral vitamin supplementation was begun for the entire Cuban population.
Results.--Coxsackievirus A9 (five isolates) and a similar, less cytopathic virus (100 isolates) were recovered from 105 (84%) of 125 CSF specimens from neuropathy patients. The strains with light cytopathic effect were antigenically related to Coxsackieviruses A9 and B4 by cross-neutralization and immunoblotting assays. Virus persisted in CSF of some patients for 1 to 12 months. Cerebrospinal fluid from patients and both types of virus from cell culture produced illness, including complete posterior flaccid paralysis, in newborn mice, and virus was reisolated from the mice. Mouse tissues and sural nerve biopsy specimens from patients were stained by immunoperoxidase and colloidal gold techniques using hyperimmune rabbit antisera against the virus with light cytopathic effect.
Conclusions.-Coxsackievirus A9 or an antigenically related agent with a light cytopathic effect was present in CSF of 84% of 125 patients with epidemic neuropathy. The role of these agents, probably in combination with nutritional factors, in the pathophysiology of the disease requires further investigation.
Author(s): Mas P; Pelegrino JL; Guzman MG; Comellas MM; Resik S; Alvarez M; Rodriguez R; Mune M; Capo V; Balmaseda A; Rodriguez L; Rodriguez MP; Handy J (REPRINT) ; Kouri G; Llop A
Journal: ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE, 1997, V121, N8 (AUG), P825-833