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              <td valign="top" align="center" width="100%"><!-- #BeginLibraryItem "/Library/logo_general.lbi" --><p align="center"><img src="../../images/newlogo1.gif" alt="colloidal silver, ionic minerals, MSM, methylsufonylmethane, trace minerals, msm, colloidal silver generator, essential minerals, structured water, natural pet products, alternative health, arthritis pain relief, water filters, mineral supplements, glucosamine, chondroitin" border="0" align="center" width="455" height="60"></p>
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                <h3 align="center" class="fonts"><u>Research on the Mineral Selenium</u></h3>
                <p align="left" class="mainfont">The following research abstracts 
                  are presented to reflect the findings of possible benefits from 
                  minerals as a dietary supplement and nutritional supplement. 
                  You will find more on the <a href="../../minerals/selenium.html">ionic 
                  selenium</a> page.</p>
                <h4 align="center" class="fonts"><a name="art31"><font color="#0000AA">The 
                  effect of dietary levels of selenium on radiation resistance 
                  and radiation-induced carcinogenesis</font></a></h4>
                <p align="left" class="mainfont">Nutrition Research (USA), 1996, 
                  16/3 (505-516)</p>
                <p align="left" class="mainfont">Combined (internal plus external) 
                  radiation exposure of the population and emergency workers, 
                  as a result of the Chernobyl accident, increased the oncogenic 
                  risk, and to reduce it is a problem of the utmost importance. 
                  A long-term experiment in 400 rats exposed to radiation following 
                  the Chernobyl pattern showed that a <font color="#0088AA">selenium</font>-enriched 
                  diet started after exposure caused a longer average lifespan 
                  and a 1.5 - 3.5 fold decrease of leukaemias and other malignancies, 
                  e.g. breast, thyroid and lung cancers, etc., at late times. 
                  Selenium was first demonstrated to provide protection against 
                  late effects which is equivalent to a whole-body dose reduction 
                  by 1.4 Sv (140 rem). The dietary levels of <font color="#0088AA">selenium</font> 
                  used were above those accepted as physiological but considerably 
                  below toxic ones (10, 30 and 100 microg Se/day per capita).</p>
                <p align="center" class="mainc"><a href="./"><img src="../../images/back.gif" border="0" width="42" height="10"></a></p>
                <h4 align="center" class="fonts"><a name="art32"><font color="#0000AA">Differential 
                  induction of growth arrest inducible genes by selenium compounds</font></a></h4>
                <p align="left" class="mainfont">Biochemical Pharmacology (USA), 
                  1997, 53/7 (921-926)</p>
                <p align="left" class="mainfont">The effects of two types of <font color="#0088AA">selenium</font> 
                  compounds on the expression levels of growth arrest and DNA 
                  damage-inducible (gadd) genes and on selected cell death genes 
                  were examined in mouse mammary MOD cells to test the hypothesis 
                  that the diversity of <font color="#0088AA">selenium</font>-induced 
                  cellular responses to these compounds could be distinguished 
                  by unique gene expression patterns. Whereas the expression patterns 
                  of known cell death-related genes (bcl-2 and bax) were not informative 
                  with respect to the cellular response patterns upon exposure 
                  to <font color="#0088AA">selenium</font> compounds, time-dependent 
                  and <font color="#0088AA">selenium</font> species-specific induction 
                  patterns were observed for gadd34, gadd45 and gadd153 genes. 
                  It was also observed that the MOD cells expressed a truncated 
                  p53 transcript but no detectable immunoreactive P53 protein, 
                  indicating a null p53 phenotype. The fact that <font color="#0088AA">selenium</font> 
                  compounds induced growth arrest and death of these cells and 
                  that these compounds induced specific patterns of expression 
                  of gadd genes indicates that these genes may mediate some <font color="#0088AA">selenium</font>-induced 
                  cellular responses. The findings further imply that <font color="#0088AA">selenium</font> 
                  compounds may be effective chemopreventive agents for human 
                  breast carcinogenesis, in which p53 mutations are frequent.</p>
                <p align="center" class="mainc"><a href="./"><img src="../../images/back.gif" border="0" width="42" height="10"></a></p>
                <h4 align="center" class="fonts"><a name="art33"><font color="#0000AA">Selenium 
                  deficiency associated with cardiac dysfunction in three patients 
                  with chronic respiratory failure</font></a></h4>
                <p align="left" class="mainfont">Japanese Journal of Thoracic 
                  Diseases (Japan), 1996, 34/12 (1406-1410)</p>
                <p align="left" class="mainfont">We encountered three patients 
                  with chronic respiratory failure who had heart failure of cardiac 
                  arrhythmias and low levels of serum <font color="#0088AA">selenium</font>. 
                  All three had tracheostomies and had received long-term parenteral 
                  nutrition that had not included <font color="#0088AA">selenium</font>. 
                  All three also had refractory cardiac dysfunction, which was 
                  manifested in edema, heart failure, and various tachycardias. 
                  We suspected that <font color="#0088AA">selenium</font> deficiency 
                  had caused their cardiac dysfunction. Serum <font color="#0088AA">selenium</font> 
                  concentrations were found to be much lower than normal in all 
                  three, so 100 microg/day of <font color="#0088AA">selenium</font> 
                  was administered in addition to their tube feedings. Cardiac 
                  function improved after replacement of <font color="#0088AA">selenium</font>. 
                  These cases show the need for preventing <font color="#0088AA">selenium</font> 
                  deficiency in patients with chronic respiratory failure during 
                  long-term administration of parenteral nutrition.</p>
                <p align="center" class="mainc"><a href="./"><img src="../../images/back.gif" border="0" width="42" height="10"></a></p>
                <h4 align="center" class="fonts"><a name="art34"><font color="#0000AA">A 
                  possible beneficial effect of selenium administration in antiarrhythmic 
                  therapy.</font></a></h4>
                <p align="left" class="mainfont">J Am Coll Nutr (UNITED STATES) 
                  Oct 1994, 13 (5) p496-8</p>
                <p align="left" class="mainfont">OBJECTIVE: The following review 
                  of the literature on the importance of Selenium (Se) in myocardial 
                  homeostasis and of the pharmacology of this trace metal, represents 
                  an attempt to search, without prejudice to other possible explanations, 
                  for a rationale of a beneficial effect of Se substitution as 
                  an adjuvant to antiarrhythmic therapy. background: For several 
                  years, in the early 1980s, I had to deal with the problem of 
                  a serious ventricular arrhythmia (non-sustained and sustained 
                  ventricular tachycardia) which was remarkably resistant to a 
                  battery of the most potent antiarrhythmic agents. Eventually, 
                  dramatic improvement, lasting for a period of 8 years, was achieved 
                  with Flecainide, which, however, left unsolved the episodic 
                  occurrence of disabling ventricular bigemini. Over the most 
                  recent period of 1 year and 8 months, there was a sudden and 
                  unexplained return to unbroken normal sinus rhythm. Among the 
                  multiplicity of possible reasons for this fortunate development, 
                  the concurrent introduction of Se substitution appeared as the 
                  most obvious, though very tentative explanation. Substitution 
                  of this trace metal preceded the extinction of ventricular bigemini 
                  by 1 week and actually represented the sole modification of 
                  otherwise reasonably standardized conditions of antiarrhythmic 
                  therapy, life style and diet. (25 Refs.)</p>
                <p align="center" class="mainc"><a href="./"><img src="../../images/back.gif" border="0" width="42" height="10"></a></p>
                <h4 align="center" class="fonts"><a name="art35"><font color="#0000AA">An 
                  expanded concept of &quot;insurance&quot; supplementation--broad-spectrum 
                  protection from cardiovascular disease.</font></a></h4>
                <p align="left" class="mainfont">Med Hypotheses (ENGLAND) Oct 
                  1981, 7 (10) p1287-1302</p>
                <p align="left" class="mainfont">The preventive merits of &quot;nutritional 
                  insurance&quot; supplementation can be considerably broadened 
                  if meaningful doses of nutrients such as mitochondrial &quot;metavitamins&quot; 
                  (coenzyme Q, lipoic acid, carnitine), lipotropes, and key essential 
                  fatty acids, are included in insurance supplements. From the 
                  standpoint of cardiovascular protection, these nutrients, as 
                  well as magnesium, <font color="#0088AA">selenium</font>, and 
                  GTF-chromium, appear to have particular value. Sophisticated 
                  insurance supplementation would likely have a favorable impact 
                  on many parameters which govern cardiovascular risk--serum lipid 
                  profiles, blood pressure, platelet stability, glucose tolerance, 
                  bioenergetics, action potential regulation--and as a life-long 
                  preventive health strategy might confer substantial benefit. 
                  (111 Refs.)</p>
                <p align="center" class="mainc"><a href="./"><img src="../../images/back.gif" border="0" width="42" height="10"></a></p>
                <h4 align="center" class="fonts"><a name="art36"><font color="#0000AA">Antioxidant 
                  status of hypercholesterolemic patients treated with LDL apheresis</font></a></h4>
                <p align="left" class="mainfont">Cardiovascular Drugs and Therapy 
                  (USA), 1996, 10/5 (567-571)</p>
                <p align="left" class="mainfont">Oxidation of low density lipoprotein 
                  is involved in the pathogenesis of atherosclerosis. Epidemiological 
                  studies suggest a negative correlation between the occurrence 
                  of cardiovascular diseases and blood concentrations of lipophilic 
                  antioxidants such as vitamins A and E and beta-carotene. Trace 
                  elements, such enzymes as glutathione peroxidase and superoxide 
                  dismutase. The aim of this study was to determine the antioxidant 
                  and trace element status of patients with severe hypercholesterolemia 
                  who had been treated with dextran-sulphate low-density lipoprotein 
                  apheresis in comparison with two control populations, normocholesterolemic 
                  subjects and untreated hypercholesterolemic patients. Our results 
                  showed that, patients treated with LDL apheresis, compared with 
                  normocholesteromic subjects, were not deficient in vitamin E, 
                  beta-carotene, and copper, but had low plasma levels of <font color="#0088AA">selenium</font>, 
                  zinc, and vitamin A. The low <font color="#0088AA">selenium</font> 
                  and vitamin A levels were due to the LDL apheresis treatment, 
                  and the hypercholesterolemia might have provoked the low plasma 
                  levels of zinc.This study pointed out the potential benefits 
                  of supplemental <font color="#0088AA">selenium</font>, zinc, 
                  and vitamin A in patients being treated with LDL apheresis.</p>
                <p align="center" class="mainc"><a href="./"><img src="../../images/back.gif" border="0" width="42" height="10"></a></p>
                <h4 align="center" class="fonts"><a name="art37"><font color="#0000AA">The 
                  role of free radicals in disease</font></a></h4>
                <p align="left" class="mainfont">Australian and New Zealand Journal 
                  of Ophthalmology (Australia), 1995, 23/1</p>
                <p align="left" class="mainfont">Evidence is accumulating that 
                  most of the degenerative diseases that afflict humanity have 
                  their origin in deleterious free radical reactions. These diseases 
                  include atherosclerosis, cancer, inflammatory joint disease, 
                  asthma, diabetes, senile dementia and degenerative eye disease. 
                  The process of biological aging might also have a free radical 
                  basis. Most free radical damage to cells involves oxygen free 
                  radicals or, more generally, activated oxygen species (AOS) 
                  which include non-radical species such as singlet oxygen and 
                  hydrogen peroxide as well as free radicals. The AOS can damage 
                  genetic material, cause lipid peroxidation in cell membranes, 
                  and inactivate membrane-bound enzymes. Humans are well endowed 
                  with antioxidant defences against AOS; these antioxidants, or 
                  free radical scavengers, include ascorbic acid (vitamin C), 
                  alpha-tocopherol (vitamin E), beta-carotene, coenzyme Q10, enzymes 
                  such as catalase and superoxide dismutase, and trace elements 
                  including <font color="#0088AA">selenium</font> and zinc. The 
                  eye is an organ with intense AOS activity, and it requires high 
                  levels of antioxidants to protect its unsaturated fatty acids. 
                  The human species is not genetically adapted to survive past 
                  middle age, and it appears that antioxidant supplementation 
                  of our diet is needed to ensure a more healthy elderly population.</p>
                <p align="center" class="mainc"><a href="./"><img src="../../images/back.gif" border="0" width="42" height="10"></a></p>
                <h4 align="center" class="fonts"><a name="art38"><font color="#0000AA">Status 
                  of antioxidants in patients with diabetes mellitus with and 
                  without late complications</font></a></h4>
                <p align="left" class="mainfont">AKTUEL. ERNAHR.MED. KLIN. PRAX. 
                  (Germany), 1994, 19/3 (155-159)</p>
                <p align="left" class="mainfont">The role of antioxidative vitamins 
                  in the therapy of diabetes mellitus is of growing importance. 
                  The development of diabetic late complications (cataract, retinopathy, 
                  nephropathy and neuropathy and others) is associated with an 
                  increased presence of free radicals, and therefore, elevated 
                  oxidative stress of the human body. The aim of the present study 
                  was the evaluation of the vitamin and <font color="#0088AA">selenium</font> 
                  status of diabetics. Thirty-eight patients of the age of 35-58 
                  years had been diabetics for 8-27 years and their plasma concentration 
                  of haemoglobin was 6.7-7.5%. The diabetics of type I were treated 
                  with a functional insulin therapy with dietary restrictions, 
                  whereas the type II diabetics received oral antidiabetica (sulfonyl 
                  urea, biguanids) and had to comply with a fixed diet. Any supplementation 
                  of vitamins was omitted. The nutritional intake was monitored 
                  by a weighed record over 7 days. The plasma concentrations of 
                  vitamin A, beta-carotene, K and E were determined by reversed-phase-PLC. 
                  For the assessment of vitamin C concentrations, a photometric 
                  method was used, and <font color="#0088AA">selenium</font> concentrations 
                  was determined by electrothermal atomic absorption spectrometry. 
                  Mean values of plasma concentrations were: vitamin A 36-50 microg/dl, 
                  beta-carotene 35-42 microg/dl, vitamin K: 0.5-0.6 ng/ml, vitamin 
                  E: 1.1-1.6 mg/dl, <font color="#0088AA">selenium</font>: 72-75 
                  microg/l. The values of vitamin C concentration of the diabetics 
                  type I without late complications and of type II diabetics were 
                  at 0.8 mg/dl and, therefore, at the borderline. Diabetics of 
                  type I with late complications showed marginal values of 0.6 
                  plus or minus 0.3 mg/dl. The critical value for the prevention 
                  of scorbut has been fixed at 0.4 mg/dl. The results of this 
                  confirm the importance and efficiency of vitamins, especially 
                  of ascorbic acid. Positive effects of this antioxidative vitamin 
                  in respect of the prevention of diabetic side effects and subsequent 
                  disease should therefore be expected.</p>
                <p align="center" class="mainc"><a href="./"><img src="../../images/back.gif" border="0" width="42" height="10"></a></p>
                <h4 align="center" class="fonts"><a name="art39"><font color="#0000AA">Selenium 
                  supplementation in the diets of patients suffering from ulcerative 
                  colitis</font></a></h4>
                <p align="left" class="mainfont">Stedman J.D.; Spyrou N.M.; Millar 
                  A.D.; Altaf W.J.; Akanle O.A.; Rampton D.S.<br>
                  J.D. Stedman, Department of Physics, University of Surrey, Guildford, 
                  Surrey GU2-5XH United Kingdom<br>
                  Journal of Radioanalytical and Nuclear Chemistry (Hungary) , 
                  1997, 217/2 (189-191)</p>
                <p align="left" class="mainfont">Ulcerative colitis (UC) is a 
                  type of inflammatory bowel disease (IBD) in which there is recurrent 
                  inflammation of the mucous membranes of the colon. Inflammation 
                  is accompanied by the production of reactive oxygen species 
                  (ROS) including, amongst others, hydrogen peroxide. Selenium 
                  in the form of the selenoprotein glutathione peroxidase (GSH-Px) 
                  acts as a catalyst in the reaction which reduces hydrogen peroxide 
                  to watch. It may therefore beneficial to supplement the diets 
                  of patients who suffer from UC with <font color="#0088AA">selenium</font>. 
                  In this preliminary study nine patients suffering from moderate 
                  UC were supplemented with <font color="#0088AA">selenium</font>-beta 
                  tablets (300 microg Se per tablet) twice daily. Blood samples 
                  were taken at the start of the trial and at 1, 2 and 4 week 
                  intervals. Freeze-dried serum samples were analysed for their 
                  <font color="#0088AA">selenium</font> content using the technique 
                  of instrumental neutron activation analysis (INAA). Samples 
                  were also analysed by particle induced X-ray emission (PIXE) 
                  to monitor other trace elements levels. Selenium concentrations 
                  were found to increase during supplementation and iron concentrations 
                  to decrease. Stool frequency was also found to improve suggesting 
                  that ROS may be important in the pathogenesis of UC.</p>
                <p align="center" class="mainc"><a href="./"><img src="../../images/back.gif" border="0" width="42" height="10"></a></p>
                <h4 align="center" class="fonts"><a name="art40"><font color="#0000AA">Prevention 
                  of esophageal cancer: the nutrition intervention trials in Linxian, 
                  China. Linxian Nutrition Intervention Trials Study Group.</font></a></h4>
                <p align="left" class="mainfont">Cancer Res. 1994 Apr 1. 54(7 
                  Suppl). P 2029s-2031s</p>
                <p align="left" class="mainfont">In Linxian China, the esophageal/gastric 
                  cardia cancer mortality rates are among the highest in the world. 
                  There is suspicion that the population's chronic deficiencies 
                  of multiple micronutrients are etiologically involved. We conducted 
                  two randomized, placebo-controlled nutrition intervention trials 
                  to test the effects of vitamin and mineral supplements in lowering 
                  the rates of esophageal/gastric cancer. In the first trial, 
                  the dysplasia trial, 3318 adults with a cytological diagnosis 
                  of esophageal dysplasia received daily supplementation with 
                  26 vitamins and minerals in doses typically 2-3 times the United 
                  States Recommended Daily Allowances, or placebos, for 6 years. 
                  The second trial, the general population trial, involved 29,584 
                  adults and used a one-half replicate of a 2(4) factorial experimental 
                  design which tested the effects of four combinations of nutrients: 
                  A, retinol and zinc; B, riboflavin and niacin; C, vitamin C 
                  and molybdenum; and D, beta-carotene, vitamin E, and <font color="#0088AA">selenium</font>. 
                  Doses for these daily supplements ranged from 1 to 2 times the 
                  United States Recommended Daily Allowances, and the different 
                  vitamin/mineral combinations or placebos were taken for a period 
                  of 5.25 years. As part of the general population trial, and 
                  end-of-intervention endoscopy survey was carried out in a small 
                  (1.3%) sample of subjects to see if supplementation affected 
                  the prevalence of dysplasia and early cancer. Herein we review 
                  the methods of these trials and the results of the endoscopic 
                  survey. Fifteen esophageal and 16 gastric cancers were identified 
                  in endoscopic biopsies from the 391 subjects evaluated from 
                  two villages, and nearly all were asymptomatic. No significant 
                  reductions in the prevalence of esophageal or gastric dysplasia 
                  or cancer were seen with any of the four supplement groups. 
                  However, the prevalence of gastric cancer among participants 
                  receiving retinol and zinc was 62% lower than those not receiving 
                  those supplements (P = 0.09), while participants receiving beta-carotene, 
                  vitamin E, and <font color="#0088AA">selenium</font> had a 42% 
                  reduction in esophageal cancer prevalence (0.34). We have reported 
                  separately that cancer mortality over the entire 5.25-year period 
                  was significantly reduced among those receiving beta-carotene, 
                  vitamin E, and <font color="#0088AA">selenium</font>. The findings 
                  from the overall trial and the endoscopic sample offer a hopeful 
                  sign and should encourage additional studies with these agents 
                  in larger numbers of subjects.</p>
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