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SUPEROXIDE DISMUTASES (SOD) AND NUTRITIONAL MODULATION AGAINST OXYGEN FREE RADICALS - Pt. 1

Mar. 23rd, 2006 | 02:29 am
mood: accomplished

SUPEROXIDE DISMUTASES (SOD) AND NUTRITIONAL MODULATION AGAINST OXYGEN FREE RADICALS

Hildegarde Staninger, Ph.D., RIET-1 & Doctor of Integrative Medicine 1,2,3

1 Assistant Professor & Research Coordinator, Capital University of Integrative Medicine, 4820 MacArthur Blvd., N.W., Washington, D.C.  20007 Phone: 202-338-4646  Direct phone: 213-382-2786  E-mail:  venusia55@aol.com

2 Chief Scientist, MPS Global, Inc. USA Division, 2801 Towne Ave. # C-1, Pomona, CA  91767 Phone: 909-445-9366

3 Chief Toxicologist, D-Tek, Inc. A Division of Page One Science, Inc., 1321 Powhathan St., Alexandria, VA 2231401342

 

ABSTRACT:  Superoxide dismutases are critical enzymes responsible for the elimination of superoxide radicals and are considered to be a key antioxidant in aerobic cells.  Cellular consumption of oxygen is essential for oxidative phosphorylation during ATP generation in the mitochondria, yet this cellular metabolism also leads to the production of oxygen free radicals such as the reactive oxygen species (ROS), the superoxide radicals (O2 * -) and hydrogen peroxide (H2O2).  Accumulation of ROS results in cellular oxidative stress and cellular malnutrition, if not corrected, can lead to the damage of important biomolecular structures such as membranes lipids, proteins and DNA.  Prolonged accumulation of high levels of free radicals in cells may cause irreversible cellular injury and cell death, and have been implicated in diseases such as cancer, Alzheimer’s, Down Syndrome, cancer and premature aging.  Nutritional modulation with foods that contain superoxide dismutases or aid in the covalent conjugation of superoxide dismutase have been found to increase the circulatory half-life and provide prolonged protection from partially reduced oxygen species known as oxygen free radicals.

 

 SUPEROXIDE DISMUTASES AND NUTRITIONAL MODULATION AGAINST OXYGEN  FREE RADICALS

 

Enzymes and Toxicity

 

The ultimate regulators of metabolism are enzymes and their associated factors of trace elements, vitamins, hormones, and antimetabolites.  Substances that act chemically to produce injury to organs and tissues of the body usually do so by two basic means:  either by depressing or by stimulating the activity of the enzyme systems.  Severe, acute effects such as destruction of cell membrane integrity by corrosive agents or protein coagulants, etc., are obvious exceptions.  A single substance may have more than one pathway and site of action.  Multiple pathways of action may be invoked simply by differing doses of the toxic agents which create oxidative stress or covalent bonding and oxygen radicals functioning as mediators of cell injury are the result of the following: (1) low doses may stimulate enzyme action; (2) high doses depress and inhibit the same or different enzyme systems.  This is a characteristic action of most, if not all, toxic substances, including arsenic, benzene, chloroform, cobalt, fluoride, x-rays, vanadium, snake venoms, biofilms, and marine toxins and cellular toxins known as the “Maverick Compounds.”  A number of aspects of toxicity are shown in Figure 1.1,2,3

 

Systemic toxicity is, by and large, a matter of the activity of enzyme systems, either by inhibition or over stimulation (removal of a natural inhibitor system), all accomplished at the free-radical and oxygen radical level.

 

Substances display differing toxicities and have selective sites of action because different substances affect, to differing degrees, the various metabolic compartments and, thus, raise or lower the level of “observed toxicity.”  Different substances have differing chemical affinities for tissue sites and cellular organelles as shown in Figure 2.4

 

Potentiation and synergism, the enhanced toxicity of two or more simultaneously acting substances, can be explained by the action of one preventing the elimination or the metabolism of the other, wholly or in part, thus maintaining elevated systemic levels of the toxic agent, resulting in an observed toxicity greater than the additive toxicity of the combined components (Figure I).

 

Antagonistic action is explained by one component preventing, wholly or in part, the toxic action of another.  This occurs when one component induces or supplies additional amounts of a critical enzyme system or factor that is being attacked by another component, the net result being to greatly reduce or even completely eliminate cellular toxicity.  A similar mechanism appears to explain the antagonism of ethyl alcohol for methyl alcohol toxicity.  In this case the liver alcohol dehydrogenase preferentially attacks ethyl alcohol, thus slowing down or preventing the oxidation of methyl alcohol to neurotoxic metabolites (Figure 1).

 

It is important to realize that most of the metabolic activity of the body is a result of the activity of enzymes, which are biological catalysts formed by living cells throughout the body.  Consequently, it is reasonable that the bulk of all toxic mechanisms should involve interference in some way with normal enzyme activity.

 

All enzymes have a basic protein structure composed of 20 or more amino acids grouped in various chain arrangements in a three-dimensional structure.  To perform, the myriad of metabolic reactions of the body requires an estimated million diverse enzymes.  This diversity of structure and function makes any simple classification inadequate.  However, just as the major types of metabolism and detoxication were classified (Figure 3), so can the major metabolic reactions catalyzed by enzymes be classified.

 

Various Classes of Enzymes

 

The enzymes that perform oxidation-reduction reactions constitute one of the larger groups. The oxidases, which reduce the inhaled oxygen carried throughout the body by hemoglobin and myoglobin, reduce oxygen directly.  One of the most important of these is cytochrome oxidase.  Other important oxides are xanthine oxidase with riboflavin as a prosthetic group, the polyphenol oxidases, with copper as prosthetic group, and tyrosinase responsible for the oxidation of tyrosine to the dark melanin pigment.

 

Closely related in action are the dehydrogenases, which catalyze the removal of hydrogen, and thus “oxidize” organic molecules.  As body oxidations generally (respiration) proceed in this manner, there are several highly specific dehydrogenases.  All cellular respiration involves three major classes of dehydrogenases:  1) pyridine-linked dehydrogenases, which require a dinucleotide as coenzyme, 2) flavin-linked dehydrogenase, which contain flavin nucleotide, and 3) the cytochromes, which contain an iron-porphyrin ring system.  More than 150 of the pyridine-linked dehydrogenases are known.  One of these, glucose -6-phosphated dehdyrogenase (G-6-PD), features prominently as the key system in rendering an individual hypersusceptible to hemolytic hazardous materials.5  A genetic deficiency in G-6-PD can make a person susceptible to incurring a hemolytic crisis from exposure to such hazardous materials by either blocking the action of certain components of the G-6-PD system in the red cells or by the chemical’s utilizing the hydrogen critically needed for cell respiration, resulting in loss of red cell integrity, and consequent cell lysis.

 

Another large and diversely acting group is the hydrolytic enzymes, chief among which are the phosphatases, which hydrolyze esters of phosphoric acid.  These enzymes are involved in all catabolic (destructive) and anabolic (synthetic) reactions of the cells.  Other representative hydrolytic enzymes are the esterases, such as liver esterases and pancreatic esterases.  Others in this group are those that hydrolyze protein structures, proteolytic enzymes that break the common peptide bond of these structures.  This group is further comprised of more specialized enzymes, the peptidases, the carboxyl- and aminopeptidases, so named because of action on peptides with adjacent carboxyl (COOH) or amino (NH2) groups; those that hydrolyze glycosidic linkages, the carbohydrases, which act on polysaccharides and glycosides.

 

The decarboxylases are a widespread group composed of keto-acid decarboxylase, which is responsible for the liberation of the end product of metabolism, carbon dioxide.  Amino acid decarboxylases are responsible for the formation of amines by carbon dioxide liberation from amino acids.  In the chain of metabolic end reactions, oxidative delaminating enzymes remove the amino group from these toxic amines, be they endogenous or of foreign origin, resulting in reduced toxicity, liberation of the end product, ammonia, and its excretion of the urine.  Some of the ammonia, however, is transferred to other substances by transferases.  These transferases can also transfer other groups such as methyl, phosphate, and amino groups.

 

The above classes of enzymes, with other enzymes such as superoxide dismutases and other enzymes not classified, represent all the metabolic catalysts the body can muster to handle foreign chemical structures.  As these structures may vary from closely similar to remotely related to the natural substrates of these enzymes, it is not difficult to see that destruction of a foreign toxic substance can range from nearly complete to scarcely perceptible.

Enzymatic Action

 

Enzymatic actions occur throughout the body without restriction to any particular organ site, although the liver cells perform a major portion of the metabolic activity of the body.  Similarly active, however, but less diversified, are the enzymes in the lung, kidney, intestine, brain and nervous tissue, and bone.  For this, it may be inferred that enzymatic mechanisms may occur with the enzyme situated at cell surfaces or within the cell itself.  Although the activity of enzymes, in normal circumstances, occurs within or on cells which are inaccessible for measurement (except as biopsied tissue), toxic injury to cells may result in enzyme release in proportion to the injury into the blood and body fluids where they can be measured and serve as biologic indictors of exposure and/or response. 6,7

 

In “metabolizing” a foreign substance, it is important to observe that the enzyme is merely performing a function that it normally performs in metabolizing natural foodstuffs; no special enzymes exist to metabolize toxic substances.  Although “drug-metabolizing” enzymes are commonly mentioned, this does not mean that the body develops a new class of enzymes in response to the administration of a drug, genetic material/drug, herbal remedy, nanofood, far infrared, fungal therapy or any other technology, however, these technologies, may act to induce larger amounts of enzyme activity within the individual body. 8,9,10

 

Enzyme Characteristics

 

It is now recognized that certain enzymes, heretofore considered homogenous in composition and in action, may consist of several distinct components, each still acting, however, on the same substrate; these components are called isoenzymes, or isozymes.  Superoxide dismutases are of this category of enzymes and will be discussed in more detail later in this paper.  Isozyme components can differ in number and activity, depending on the tissue of origin, e.g. lactic acid dehydrogenase has as many as five different isozymes, depending upon whether originating from the heart, kidney, liver, or lung.

 

Many enzymes have additional specificity requirements, in that they require a metal or a vitamin, or both, as cofactor(s) or activator(s).  For example, the enzyme cacaroxylase that splits carbon dioxide from certain organic acids, requires vitamin B1 and magnesium ions as necessary constituents before it can function.  It these subcomponents were not present in one or more area of the enzyme the enzyme would not function and be observed by the clinician as inactive, inhibited, or depleted.

 

Because enzymes are proteins, they exhibit the physical and chemical properties of proteins.  They undergo denaturation 1) by heat, as in burns (a photon type source); 2) by marked changes in acidity or alkalinity as affected, for example, by contact with corrosive agents, biofilms, cigarette smoke, illegal drugs, chemotherapeutic agents or mycotoxins 8; or 3) by chemical denaturing agents, such as urea in high concentrations.  These agents alike cause structural, configurational changes, and crystallization in tissues/cells in the protein, and the characteristic specificity is lost, and with it the catalystic activity of the enzyme.

 

Enzyme activity can be inhibited in a number of ways.  For example, among the enzymes requiring a specific metal as activator, any agent that will displace or render inactive the metal will render the enzyme inactive to the degree that the metal was rendered inert or removed from the enzyme. Certain metals with similar spatial requirements for the specific metal required by the enzyme may do this.  Certain poisonous metals such as beryllium are believed to act in this way.  Cyanide may combine with the iron of an iron-dependent enzyme (i.e. Fe-SOD) and inactivate or inhibit the enzyme.

 

A third way by which enzyme activity is inhibited is by accumulation of the product of the enzyme’s activity.  This is one of the natural ways by which body enzyme activity is regulated and is known as metabolite inhibition.  A prime example of this is exposure to MSG and aspartame where the cellular connective glue of the outer membrane of the mitochondria becomes unglued from the cytoplasm of a cell, thus causing increased obesity.11

 

The fundamental aspects of enzyme activity with respect to toxicity may be summarized as follows.  Enzymes combine with the toxicity substance.  This combination may result in partial or complete inhibition of enzyme activity or the enzyme may act on the toxic substance more or less incompletely, possibly with the production of even more toxic substances, but generally with production of degraded, less toxic substances.  If the enzyme whose activity is blocked is a critical one; there may be slowing down of some vital function, resulting in alteration of cellular constituents in amount or type, even in cell death.

Superoxide Dismutases and Oxygen Radicals as Mediators of Toxic Cell Injury

 

Superoxide dismutase (SOD) is a critical enzyme responsible for the elimination of superoxide radicals and is considered to be a key anti-oxidant in aerobic cells, Cellular consumption of oxygen is essential for oxidative phosphorylation during ATP generation in the mitochondria, yet this cellular metabolism also leads to the production of reactive oxygen species (ROS, including the superoxide radical (O2*-) and hydrogen peroxide (H2O2).  SOD is made up of isoenzymes that have functional metal groups for its catalytic action within the cell and externally.  Many pictures taken with GRASP software show that there is an electrostatic field around an active site of the enzyme superoxide dismutase, which controls oxygen toxicity by converting the superoxide radical to less dangerous forms.  These electrostatic fields may be a combination of Brownian dynamics, covalent bonding with valence charges, and super-radiant states as associated with cooper pairs in quantum biophysics. 12,13,14

 

Superoxide dismutase (SOD) may be in the form of copper/zinc superoxide dismutase (Cu/Zn-SOD), manganese superoxide dismutase (Mn-SOD), and iron superoxide dismutase (Fe-SOD)15.  Recent genome applications in enzymonics and proteinomics has shown that their may be additional isoenzymes in the form of selenium superoxide dismutase (Se-SOD) and nickel superoxide dismutase (Ni-SOD), even cadmium superoxide dismutase (Cd-SOD) has been associated with this enzyme.  The latter having a high valence charge (cadmium) that may play a negative role in the destruction of the free oxygen radical mechanisms within the cell. 16

 

Molecular oxygen, necessary for the survival of aerobic organisms, is a diradical in its ground state.  Despite oxygen’s radical nature, its reactivity is surprisingly low.  The tow unpaired electrons of molecular oxygen possess the same spin.  Thus, the reaction of oxygen with electron donors to form covalent bonds is kinetically unfavored and very slow; however, oxygen can readily participate in one-electron reductions.2 This is very important in cellular metabolism because approximately 90% of the oxygen consumed by humans is used by the cell’s mitochondria.  Mitochondrial oxidative stress, caused by oxygen free radicals that are produced when faulty electron transfer occurs at any point of the electron transport chain, has been linked to conditions such as Alzheimer’s, heart disease, and cancer.  Cells immobilize oxygen free radicals in the mitochondria by using the metabolic enzyme, superoxide dismutase (SOD), which simultaneously reduces and oxidizes (dismutation) superoxide free radical to form hydrogen peroxide and oxygen.  Hydrogen peroxide is then converted into water and oxygen by catalase enzymes.17

 

The stepwise reduction of oxygen to water produces a variety of potentially toxic intermediates.  The addition of a single electron produces the superoxide anion.  In turn, a second electron reduces superoxide to the peroxide ion.  At physiciological pH, the peroxide ion exists primarily as hydrogen peroxide.  Addition of the third electron splits the oxygen-oxygen bond to form the hydroxyl radical (and a hydroxide anion that is essentially water).  Addition of the final electron to the hydroxyl radical yields another molecule of water.2

 

These partially reduced, and thereby activated, forms of oxygen are continuously generated in all aerobic cells as a result of oxidative processes, both autocatalytic and enzymatic.  Superoxide anion and hydrogen peroxide are produced by various oxidases (e.g. xanthine oxidase and cytochrome P-450) as well as by the redox cycling of electron transport carriers, thiols, and catecholamines.  Activated phagocytes also generate superoxide anions and hydrogen peroxide.  The formation of these activated oxygen species is, in turn, related to the bactericidal activity of these cells and probably also contributes to the development of inflammation in tissues where these cells accumulate as seen in Syndrome X and morbid obesity.18  By contrast, cytochrome C oxidase mediates the complete reduction of oxygen to water.  It is a well coupled system and does not represent a source of activated oxygen under normal conditions, especially since the pH of water is 7.0 and any other significant increase between 7.1 – 7.9 would result in a balancing affect upon cellular acidosis as when exposed to organophosphates, carbamates and later stages of cancer as seen in early experiments with eccelerated water and Genie Spa Spheres.19

 

Aerobic organisms have developed numerous mechanisms which protect the cell from the physiological generation of activated oxygen.  However, when the generation of such species over whelms the cell’s ability to detoxify them, cell injury can result.  The superoxide dismutases dispose of superoxide anions.  As illustrated in Equation 1, these metal-containing enzymes catalyze the dismutation of two molecules of the superoxide anion to give hydrogen peroxide and dioxygen.

 

         O2-  +  O2-  +  2H+ ----->  H2O2  +  O2        (1)

 

In eukaryotic cells, there are two distinct superoxide dismutase (SOD) enzymes, a copper-zing containing enzyme found in the cytosol and in manganese-containing enzyme found in the mitochondria.   The SODs present in prokaryotic cells contain either iron or manganese at the active site.  Obligatory anaerobes have no SOD activity.  SOD activity can be induced under conditions of excess oxygen radical formation.  For example, pulmonary SOD can be induced by hyperbaric oxygen or far infrared administration.20,21  This induction has been related to a protection of the organism from the deleterious effects of oxidative stress, which untreated will cause diseases such as cancer, Alzheimer’s, chronic fatigue, fibramyalgia, and multiple sclerosis.18,22 In turn, inhibition of SOD with, for example disulfiram, is known to sensitize a cell to oxidative stress.  Disulfiram is used not only as a drug but a weed killer, too.  (Proceed to Pt. 2)

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SUPEROXIDE DISMUTASES (SOD) AND NUTRITIONAL MODULATION AGAINST OXYGEN FREE RADICALS - Pt. 2

Mar. 23rd, 2006 | 02:20 am
mood: accomplished

 

The hydrogen peroxide produced by the action of superoxide dismutses and other oxidative processes can be detoxified by two different systems.  The enzyme catalase converts hydrogen peroxide to water.

 

             2H2O2  --> 2H2O  +  O2           (2)

 

This reduction of hydrogen peroxide by catalase occurs without the intermediate formation of the hydroxyl radical.  Catalase is a homoprotein that is found almost exclusively within peroxisomes.  Similar to the inhibition of superoxide dismutase, inhibition of catalase with aminotriazole potentiates oxidative stress cell injury.

 

The enzyme glutathione peroxidase also catalyzes the reduction of hydrogen peroxide to water.  Reduced glutathione is used as the source of reducing equivalents necessary to drive this reaction.  In this process, two molecules of glutathione are oxidized to yield one molecule of glutathione disulfide (GSSG).  Glutathione disulfide is efficiently reduced to glutathione by glutathione reductase.  NADPH serves as the source of the reducing equivalents.  The glutathione peroxidase-reductase system seems to be the first line of defense against hydrogen peroxide, and catalyse is a secondary system.  Catalase is also a specific defense against hydrogen peroxide formed within the peroxisomes.

 

Glutathione peroxidase is found in the cytosol of most cells as well as within the mitochondria.  Glutathione peroxidase also shows considerable activity toward organic hydroperoxides, converting them to their corresponding alcohols.  By contrast, catalase will only catabolize hydrogen peroxide.  The cytosolic and mitochondrial forms of glutathione peroxidase are dependent upon the metal selenium for activity.  It is not surprising that selenium deficiency has been demonstrated to exacerbate oxidant-stress injury 23 and when selenium and vitamin E are depleted in a tumor cell the cell is carcinogenic.24  It is very important to note that SODs within the cell may be found to be interdependent upon the fat soluble vitamin such as vitamin E vs. the water soluble vitamin C as found on the outer cell membrane.  Their common link being the phospholipidation of the cell, especially the skin cells where compounds may be absorbed within 25 seconds into the circulatory system vs. 10 seconds for dimethylsulfoxide (DMSO) and olive oil.25

 

The importance of glutathione reductase is emphasized by the observation that inhibition of this enzyme also potentiates the cytotoxicity of oxidative stress.  With the inhibition of glutathione reductse, oxidized glutathione is not converted to reduced glutathione, a result that limits the effectiveness of the peroxidase by limiting the supply of glutathione.  The chemotherapeutic alkylating agent, 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) inhibits glutathione reductase without effect on glutathione peroxidase and catalase.  This compound sensitizes a number of cell types to the toxicity of hydrogen peroxide and other organic hydroperoxides.  It should also be noted that, during severe oxidative stress, NADPH levels are markedly depleted, and effect related to the consumption of NADPH by glutathione reductase.  Such a depletion may exert a substrate \-level inhibition of the reductase.  Thus, the NADPH depletion that results from oxidative stress may actually sensitize the cell to the oxidative stress.  Superoxide dimutase and catalase provide antioxidant protection by inhibiting the formation of the hydroxyl radical as found in free oxygen radicals.

 

The Future of Superoxid Dismutases and Nutritional Modulation

 

NASA principal investigator, Dr. Gloria Borgstahl, formerly of the University of Toledo, and now of the University of Nebaraska, has successfully crystallized E. coli manganese superoxide dismutase (MnSOD), antioxidant enzymes that are homologous to those found in cellular mitochondria, on the International Space Station during the period of December 2001 to April 2002.  Several of the MnSOD crystals grown on ISS were 80 times greater in crystal volume than earth-grown crystals.  Di spots to 1.26 resolutions were observed  providing significantly improved data obtained from crystals grown in earth laboratories.  An exciting result was that the MnSOD crystals grown on ISS were suitable for neutron studies and time-Laue studies-methods that require large, perfect crystals. With the neutron examples the researchers hope to be able to obtain the, never-before-seen, three-dimensional structure of the hydrogen’s on each amino acid of the protein and thereby be able to answer the unsolved questions concerning the source of these hydrogens in this reaction mechanism.  With the time-resolved Laue experiments, the team will be able to generate the superoxide substrate within the crystals with a laser pulse and thus film the “movie” of the enzyme converting it to the products peroxide and water.  The  enzyme MnSODs in the body is important, and in-depth study of their structure is not to the ability to understand their true function, but these experiments may lead to new therapeutics for the treatment of various degenerative diseases.18

 

Superoxide dismutases (SODs) are antioxidant metalloenzymes catalyzing the redox disproportion in the (dismutation) of superoxide radical, O2*- as previously discussed in Equation (1).

 

It is generally accepted that in all SODs the metal ion (M) catalyzes dismutation of the superoxide radical through a cyclic oxidation reduction mechanism:

 

           M3+  +  O2*-  -->  M2+  +  O2       (1.1)

 

          M2+  +  O2*-  +  2H+  --->  M3+  +  H2O2    (1.2)

 

The four classes of SODs are known, distinguished by the metal prosthetic groups:  Cu/Zn, FE, Mn and Ni.   Fe- and Mn- SODs constitute a structural family.26,27  Fe- and Mn- SODs are unequally distributed throughout the kingdoms of living organisms and are located in different cellular compartments.28,29,30,31  In particular, Fe-SOD is found in obligate anaerobes and aerobic diazotrophs (exclusively), facultative aerobes (exclusively or together with Mn-SOD).  In the cytosol of cyanobacteria, in the chloroplast stroma of higher plants, in the protozoa, kelp, Yamatoshinjo and Oaky Smoky (Cu/Zn-SOD, Fe-SOD, Mn-SOD)TM 32,33,34  Fe-SOD and Mn-SOD form some organisms (e.g. Escherichia coli ) exhibit almost absolute metal specificity ,35 while other enzymes, such as “cambialistic” SOD form Propionibacterium shermanii, are captive with either metal.36  Fe- and Mn-SODs occur as homodimers or homotetramiers. 

 

The 3-D structures of several Fe-SODs have been determined. 36,37,38,39,40  The monomers fold into two domains.  The N-terminal domain consists of two long antiparallel helices.  The C-terminal domain contains a central beta-sheet formed by three antiparallel beta strands with 4-6 surrounding helices.  The iron atom is lignaded by two residues from each of the N-terminal helices and two residues from the loops in the C-terminal domain.

 

The active site iron is pentacoordinate, with the metal lignands (N x epsilon) of three conserved His residues, O x delta of the conserved Asp residue of a water molecule) arranged in distorted trigonal bipyramidal geometry, which opposite of the tetrahydronal molecule of water.  The first His residue and a solvent molecule fill the two axial positions.  In the azide-FeIII –SOD complex, the iron becomes hexacoodinate with distorted octahedral geometry (similar to the fat soluble Vitamin E), with azide coordinated trans to ASP ligand.41 Table 1 lists the mononuclear iron environment residues in known 3D structures with their PDB Code and Reference.

 

Superoxide dismutases (SODs) have been found in various nutritional sources such as Jerusalem artichoke powder and Bifidobacterium. 42,43 Juice Plus + Vineyard Blend, foods grown in red clay soils, Yamatoshinjo and hemp oil. 44, 34,45  The use of these nutritional modulators have shown significant risk to oxidative stress via the superoxide radical as they have maintained cellular integrity and reduced cellular sensitization as individual whole foods with an individual’s meals.

 

Summary

 

Cells are continuously exposed to a variety of oxidative process which could potentially lead to cellular injury or death.  As a result, aerobic organisms possess effective defense mechanisms against oxidative stress as associated with the superoxide radical and improper nutritional modulation that would reduce superoxide dismutases (SODs) in the cell and thereby circumvent toxic cell injury.  These protective mechanisms fall into two broad categories:  (1) those which prevent the initiation of lipid peroxidation and (2) those which prevent its propagation.

 

Superoxide dismutase and catalase provide antioxidant protection by inhibiting the formation of the hydroxyl radical.  Chelation of the ferric iron necessary for the formation of the hydroxyl radical and direct removal of this species by radical scavengers (e.g., mannital) are also protective.  The generation of species capable of initiating peroxidation may exceed the capacity of effectively remove them.  Thus, there are other defenses to prevent the uncontrolled propagation of lipid peroxidation and oxidative stress as associated with free oxygen radicals/hydroxyl radicals.  These include water-soluble antioxidants, such as ascorbic acid (vitamin C) and reduced glutathione, and fat-soluble antioxidants, most notably alpha-tocopherol (vitamin E).  It appears that vitamins E and C and glutathione combine in some as yet poorly defined cycle to donate hydrogen atoms to lipid and/or peroxy radicals, thereby preventing further propagation of the lipid peroxidation, which was initiated by free oxygen radicals. 

 

The metabolism of toxic substances as associated with hazardous materials by mixed function oxidation or other mechanisms leads to irreversible cell injury thorough mechanisms that have been related either to the covalent binding of reactive metabolites, to changes in protein thiols, to alterations in intracellular calcium homeostasis, or to the formation of partially reduced oxygen species.  The relative roles that each of these mechanisms plays in any particular example of toxic cell injury remains controversial and a subject of continuing investigation through the advancement of new analytical technologies/equipment.  In the case of the various forms of superoxide dismutases, “quickened” advances in science, chemistry and wave genetics 46 will show that these metalloenzymes will play a major character role in the explanation of “creation” through the variable of true far infrared sources, superluminal radiance, the effects of Cooper pairs upon EcceleratedTM intelligent water and the role of the white worm hole found in black holes as recently found in the DNA molecule.  These future researchers will be the Indigo and Crystal children – our grand children with their little pet black rabbit with pink ears and a white spot  named Ben as it hops down a white worm hole in the quantum biophysics of the human cell.  Time and Eternity will show all of us the wonders that will amaze the original Creator of us all through the marvels of science, spirituality, art and medicine.

 

References

 

1  U.S. Department of Health, Education, and Welfare.  Occupational Diseases:  A Guide to Their Recognition.  U.S. Government Printing Office, Washington, D.C. Revised Edition June 1977 pgs. 31-41.

2 Kyle, Marlene E. and John L. Farber.  Handbook of Toxicologic Pathology.  Chapter 6:  Biochemical Mechanisms of Toxic Cell Injury.  Academic Press, Inc. New York © 1991.

3  Goldberg, Burton.  Alternative Medicine Guide to Cancer.  Future Medicine, Inc., Tiberon, CA.

   pgs, 731-736 Maverick Test by Dr. Hildegarde Staninger.  © 1996

4  Staninger, Hildegarde.  Maverick Compounds and Their Relationship to Target Organ Injury.

   World Life Research Institute.  Colton, California © 1995

5  Sacarello, Hildegarde L.  The Comprehensive Handbook of Hazardous Materials:  Regulations,

   Handling, Monitoring, and Safety.  Lewis Publishers/CRC Press.  Boca Raton, FL © 1994

6  Goldberg, Burton. The Definitive Guide to Alternative Medicine.  Future Medicine, Inc., Tiberon, CA  © 1995 page 561.

7  IBID.  Kyle, Marlene E. and John L. Farber. Pgs 81 & 82.

8  Staninger, Hildegarde.  Mycotoxins and Their Effect on the Human Body.  World Safety Organization.  17th International Environmental Heath and Safety Conference & Expo 2003 Proceedings.  WSO, Warrensburg, MO © 2003

9  Park, Sang-Hwoi.  Yamatoshinjo Research. University of Tokyo. Tokyo, Japan. © 2005

10  Staninger, Hildegarde.  “What is Far Infrared?”  Korean Health Magazine. Los Angeles, CA

  Volume 1 © 2004

11  Staninger, Hildegarde.  “MSG and Other Glutamates” Korean Health Magazine. Los Angeles, CA. Volume 4 © 2004

12  Potter, Michael.  UC San Diego.  Image of the Week – Superoxide Dismutase © 2005

   www.imageoftheweek.com

13  Infrared Science.  www.infraredscience.com  © 2005

14  Staninger, Hildegarde.  “How Do Genie Spa Spheres Work?” www.geniespaspheres.com

    © 2005

15  Staninger, Hildegarde.  Superoxide Dismutase 1, 2 and 3. www.pandleylab.com

    SOD enzyme genome  © 2003 John Hopkins University College of Medicine.

16  www.downsyndromefoundation.com (Oxidative Stress on Down Syndrome Individuals)

17  Hileman, E.A., Achanta, G. and P. Huang.  “Superoxide Dismutase:  An Emerging Target for Cancer Therapeutics.” Expert Opinion on Therapeutic Targets. 1 December 1002, vol. 5, no. 6 pp. 697-719 (14).  Ashley Publications

18  NASA. Biological Crystal Growth in Space – Image of the Week.  “Manganese Superoxide Dismutase (MnSOD) Crystal Grown on the International Space Station. Cape Kennedy, Fl © 2005 (www.nasa.com)

19  Kaylor, Mark and Ken Babal.  Syndrome X and SX-Fraction.  Woodland Publishing. Pleasant Grove, Utah. © 2003

20  Parsons, James Monroe.  Hyperbaric Medicine.  World Center for Anti-Aging Medicine.  Porta Plata, Dominican Republic. © 1995

21  Jung, S., Staninger, H., and D. Farrier.  The Definition of True Far Infrared.  Research Department.  MPS Global, Inc. Pomona, CA  © 2004

22  Morgan, Donald P.  Recognition and Management of Pesticide Poisonings, 4th Edition. US

    EPA, US Government Printing Office, Washington, D.C.  © 1989

23  IBID.  Handbook of Toxicolgic Pathology.  Chapter 19:  Cardiovascular and Skeletal Muscular Systems.  Academic Press, Inc. New York © 1991

24  Evans, Scott J. and H. Sacarello.  Symposium on Short-Term Genetic Bioassays in the Evaluation of Complex Environmental Mixtures.  “Genetic Cancer Risk Assessment of Electrophilic Hydrocarbon Mixtures in Subsurface Water Supplies.”  Genetic Toxicology Division, Health Effects Research Laboratory, US Environmental Protection Agency, Research Park, North Carolina  March 27-29, 1984 (recipient of President Walter Lowrie award Martin Marietta Aerospace, Orlando, FL 1984)

25  Staninger, Hildegarde.  “Olive Oil: It’s Medicinal Uses for a Healthier You.” Dragon Environmental Corporation.  Sanford, FL © 1998

26  Parker, M.W., Blake. C.C., Barra, D., Bossa, F. , Schinina, M.E., Bannister, W.H. and Bannister, J.V. (1987) Structure identity between the iron and manganese-containing superoxide dismutases.  Protein Engineering 1, 393-397.

27  Parker, M.W. and Blake, C.C.  (1988)  Iron and manganese-containing superoxide dismutases can be distingusished by analysis of their primary structures.  FEBS Lett. 229, 377-382.

28  Grace, S.C. (1990)  Phylogenic distribution of superoxide dismutase supports an endosymbiotic origin of chloroplasts and mitochondria.  Life Sci. 47, 1875-1886.

29   Staninger, Hildegarde.  Oaky SmokyTM Analyses Report.  US Copyright Office, Washington, D.C. © 2004

30  Staninger, Hildegarde.  Kelp and Radiation.  Korean Health Magazine. Vol. 5 © 2004

31  Liberman, Shari and ken Babal.  Maitake Mushroom and D-fraction.  Woodland Publishing.

   Orem, Utah. © 2004

32  Staninger, Hildegarde.  Bio Clear with Kelp.  Why the Earthworm Does Not Get Cancer!  Work in progress.  © 2005

33  Staninger, Hildegarde.  Registeration of Oaky SmokyT nano level superoxide dismutase with Pandey Lab/John Hopkins University College of Medicine and oxybenzone with Small chemical molecules, Harvard University.  Research Dept. Capital University of Integrative Medicine, Washington, D.C. and IBHM, Inc., Los Angeles, CA  © 2003

34  Beyer, W.F., Jr., Reynolds, J.A., and Fridovich, I.  (1980)  Differences between the manganese and the iron containing superoxide dismutases of Escherichia coli detected through sedimentation equilibrium, hydrodynamic, and spectroscopic studies.  Biochemistry 28, 4403-4409.

35  Sehn, A.P. and Meier, B. (1994)  Regulation of an in vivo metalexchangeable superoxide dismutase from Propionibacterium shermanii exhibiting activity with different metal cofactors.  Biochem. J. 304, 803-808.

36   Lim, J.H., Yu, Y.G., Han, Y.S., Cho, S. , Ahn, B.Y., Kim, S.H. and Cho. Y. (1997)  The crystal structure of an Fe-superoxide dismutase from the hyperthermophile Aquifex pyrophilus at 1.9 A resolution:  Structural basis for thermostability.  J. Mol. Biol.  270, 259-274.

37   Lah, M.S., Dixon, M.M., Pattridge, K.A., Stallings, W.C., Fee, J.A., and Ludwig, M.L. (1995)  Structure – function in Escherichia coli iron superoxide dismutase: Comparisons with the manganese enzyme from Thermus thermophilus.  Biochemistry 34, 1646-1660.

38   Cooper, J.B., McIntyre, K., Badasso, M.O., Wood, S.P., Garbe, T.R. and Young, D. (1995)  Xray structure analysis of the iron dependent superoxide dismutase form Mycobacterium tuberculosis at 2.0 A resolution reveals novel dimer-dimer interactions.  J. Mol. Biol.  246, 531-544.

39   Stoddard, B.L., Howell, P.L., Ringe, D. and Petsko, G.A. (1990a) The 2.1 A resolution structure of iron superoxide dismutase from Pseudomonas ovalis.  Biochemistry 29, 8885-8893.

40  Schmidt, M. Meier, B., and Parak, F.  (1996)  Xray structure of the cambialistic superoxide dismutse from Propionibacterium shermanii active with Fe or Mn.  J. Biol. Inorg. Chem. 1, 532-541.

41  Borgstahl, G.E.O., M. Pokross, R. Chehab, A. Sekher, and E.H. Snell. (2000) Cryotrapping the sixcoordinate, distored-octahedral active site of manganese superoxide dismutase.  J. Mol. Biol. 296:951-959.

42  Loes, Michael.  The Healing Power of Jerusalem Artichoke Fiber.  Freedom Press, Topanga, CA © 2000. 

43  Mjolsness, Alton and H. Staninger.  PSP, Inc. largest producer of Jerusalem Artichoke in North America. (Patented seed stock for high FOS yields).  Reseach in the nutritional modulation factors of Jerusalem Artichoke powder.  Premium Sweetner and Products, Inc., Fargo, North Dakota.  1998 – 2005

44  Wise, John A. Morin, Robert J. , Sanderson, Roger, and Kenneth Blum.  Changes in Plasma Carotenoid, Alpha-tocopherol, and Lipid Peroxide Levels in Response to Supplemtnaiton with Concentrated Fruit and Vegetable extracts:  A Pilot Study.  Current Therapeutic Research. Vol. 57, No. 6, Excerpta Medica, Inc. March 1996

45   Staninger, Hildegarde.  The Earthworm:  A Microcosmos of “No Disease” as Compared to the Human Being, A Macrocosmos of Chaos and the Disease, Cancer.  A Comparative Research Thesis.  Capital University of Integrative Medicine.  Washington, D.C., Nov. 4, 2001

46   Staninger, Hildegarde.  Acoustical Wave Genetics.  Page One Science, Inc. Alexandria, VA

     © 2005.

 

 

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MYCOTOXINS & THEIR EFFECT ON THE HUMAN BODY - Part 2 TABLES

Nov. 3rd, 2005 | 01:25 am
mood: accomplished


TABLES:

TABLE 1-1: A partial list of known extrinsic mutagenic agents. Taken from Levitan, Max and Ashley Montagu. Textbook of Human Genetics. Oxford University Press. New York. (c) 1971, pgs. 671 & 672.

  1. Radiations

A. Ionizing, X-rays, alpha particles, beta particles, gamma rays, Neutrons (various speeds), cosmic rays.

B. Non-ionizing, ultraviolet light (0.014-0.315 u), near-visible light (0.320-0.400 u)

  1. Temperature changes

Heat, heat shocks, cold shock.

  1. Chemicals

A. Compounds related to DNA or RNA bases adenine (purine), 2-amino purine (purine analogue), 5-bromouracil (pyrimidine analogue), caffeine (purine), 2,6-diamino purine (purine analogue), theobromide (purine analogue), formaldehyde (known to react with purines and pyrimidines), nitrous oxide (known to react with purines and pyrimidines) deoxyribonuclease (DNA metabolic enzymes).

B. Alkylating agents (mustard gases and related compounds), nitrogen mustards, sulfur mustards, ethylene oxide, ethyl methyl sulfates, halogenated and not, diethyl and dimethyl sulfate, diepoxybutane.

C. Acridine dyes, acridine orange, acriflavine, proflavine.

D. Carcinogens, 1,2,5,6 dibenzanthracene, methyl cholanthene, benzpyrene, beta-naphthylamine.

E. Inorganic salts, copper sulfate, ferrous chloride, manganous chloride.

F. Organic acids, acetic acid, carbolic acid (phenol) and related compounds, formic acid, and lactic acid.

G. Inorganic acids, boric acid.

H. Others, ammonia, colchicines, hydrogen peroxide, necrosine, neutral red (in the presence of light), sodium desoxycholate, triazine, urethane and certain other carbamates.


TABLE 2-2: Fungal Mycotoxin Postulated Diseases. Taken from http://www.mold-help.org/definition_of_fungalbionics.htm and http://www.doctorfungus.com (c) July 15, 2002.

COLCHICINE-RESPONSIVEM

Acute Gouty Arthritis

Alcoholic Cirrhosis

Familial Mediterranean Fever

Mollaret's Meningitis

Belchet's Syndrome

Psoriasis

Thrombocytopenic Purpura

Chronic Lymphocytic Leukemia

Amyloidosis North African

Leukocytoclastic Vasculitis

Sarcoid Arthritis

 

GRISEOFULVIN-RESPONSIVE

Atherosclerosis (Angina)

Systemic Sclerosis

Raynaud's Syndrome/Disease

Shoulder-Hand Syndrome

ALLOPURINOL-RESPONSIVE

Sarcoidosis

Oxalate Nephrolithopathy

Idiopathic Respiratory

Distress Syndrome/Newborns

Rheumatoid Arthritis (some)

Calcium Pyrophosphatopathy

Hyperlipidemia

Inflammatory Bowel Disease

COLCHICINE PREVENTS IN EXPERIMENTAL ANIMALS

Atherosclerosis

Casein Indusce Amyloidosis

Cushing's Disease

 

NYSTATIN-RESPONSIVE

Psoriasis

Inflammatory Bowel Disease

Hyperactivity Syndrome

Multiple Sclerosis

Duchenne's Muscular Dystrophy

 

KETOCONAZOLE-RESPONSIVE

Inflammatory Bowel Disease

Disseminated Vascular

Coagulation

Idiopathic Female Infertility

Precocious Puberty in Boys

Hyper-Low Density

L poproteinemia

Hyperaldosteronism aldosteronism

Prostrate Carcinoma

 

Note: The anti-fungal nature of colchicines and allopurinol has been fully documented.


TABLE 3-3: Food from farmers, middlemen, and retail outlets in Bangkok, Thailand. Note: Surface was sterilized prior to fungal study. Taken from Pilt JL, Hocking AD, Bhudhasamai K, Miscamble BF, Wheeler EKP: The Normal Mycoflora of Commodities from Thailand, part 1 Nuts and Oilseeds. International Journal Food Microbiology 20:211-226, 1993.

CORN

PEANUTS

Acremonium siricium
Aspergillus flavus
Aspergillus niger
Aspergillus tamarii
Aspergillus wentii
Bipolaris maydis
Chaetomium globosum
Chaetomium funicola
Chaetomium spp.
Curvularia lunata
Eurotium amstelodami
Eurotium chevalieri
Eurotium rubrum
Fusarium moniliforme
Fusarium proliferatum
Fusarium semitectum
Nigrospora oryzae
Penicillium citrinum
Penicillium pinophilum
Penicillium raistrickii
Phoma spp.
Rhizoctonia solani
Rhizopus oryzae
Rhisopus arrhizus
Trichoderma harzianum

Aspergillus candir
Aspergillus flavus
Aspergillus niger
Aspergillus tamarii
Aspergillus wentii
Chaetomium globosum
Chaetomium funicola
Chaetomium spp.
Eurotium amstelodami
Eurotium chevalien
Eurotium repens
Eurotium rubrum
Fusarium equiseti
Fusarium semitectum
Fusarium solani
Lasiodiplodia theobromae
Macrophomina phaseolina
Nigrospora oryzae
Penicillium aethiopicum
Penicillium citrinum
Penicillium funiculosum
Penicillium glabrum
Penicillium janthinellum
Penicillium olsonii
Rhizopus oryzae


TABLE 4-4: Mycotoxicoses in which Experimental and Epidemiological Data Suggesting Human Involvement, http://www.mold-help.org/definition of_fungalbionics.htm and http://www.doctorfungus.com

<td style="BORDER-RIGHT: #d4d0c8; PADDING-RIGHT: 3.75pt; BORDER-TOP: #d4d0c8; PADDING-LEFT: 3.75pt; PADDING-BOTTOM: 3.75pt; BORDER-LEFT: #d4d0c8; PADDING-TOP: 3.75pt; BORDER-BOTTOM: #d4d0c8

DISEASE

SPECIES

FOOD/FEED

MYCOTOXIN

Gout/Hyper-uricema

Fowl

Moldy Corn

Oosporein

 

Fowl

Barley

Ochratoxin

 

Chicks

 

Kojic acid

 

Chickens

 

Oxalic acid

 

Pigeons

 

Alloxan

 

Rats

 

Yeast

 

Primate

 

Aflatoxin

 

Man

 

Cyclosporin

 

Man

 

Penicillin

 

Man

Beer/Wine/Bread

Multiple

 

Man

Meat Products

Multiple

 

Man

Rye

Ergotamine

Atherososclerosis/

Sheep

 

Sporidesmin

Hyperlipidemia

Man

 

Cyclosporin

 

Primates

 

Fumonisin

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MYCOTOXINS & THEIR EFFECT ON THE HUMAN BODY - Part 1

Nov. 3rd, 2005 | 01:17 am
mood: accomplished

REPRINTED WITH PERMISSION

MYCOTOXINS AND THEIR EFFECT ON THE HUMAN BODY

Presented to

World Safety Organization
17th International Environmental Safety & Health Conference& Exposition
November 3 - 5, 2003

Conference Theme: "Safety & Health In the Changing Environment."


ABSTRACT

A mycotoxin is a highly toxic principle produced by molds or fungi. One type, the aflatoxins, is a member of the tricothecene group produced by the fusarium fungus. This has been identified in samples of the so-called "yellow rain" in Southeast Asia, where it is said to have been the cause of many deaths among war refugees. Its presence there is subject to some conjecture, since the Fusarium fungus cannot germinate in the humid environment of that area. There is substantial evidence (blood tests, autopsies, and contaminated gas masks) that the former U.S.S.R. have used such lethal agents in Afghanistan, just as many other countries have used these lethal agents throughout the dawn of history. The human body once exposed to a mycotoxin runs a triple risk to its toxic effects. The triple risk factors are direct toxic effect of the mycotoxin, acquisition of mutated RNAi from the mycotoxin's parent fungus and creation of an internal biofilm, which will harbor a toxic soup of disease.

INTRODUCTION

Mycotoxins represent an important class of xenobiotics (in terms of morbidity), which cause renal injury in humans and food animals.1 They are not the indigenous microorganisms of man. The flora and fauna indigenous to man are often referred to simply as normal flora. In this context, "flora" denotes all microscopic life forms and "normal" becomes a statistical term. One must not equate normal with nonpathogenic, for many organisms found on and in the body can pose problems under conditions such as the following:

  1. Deterioration of the host's defense mechanisms.
  2. Relocation of microorganisms, when an organism finds its way to another area of the body previously uninhabited by it.
  3. A disturbance of the "normal flora."

Normal floras are commonly referred to as amphibionts, ranging from commensals to pathogens. The amphibionts are obligately parasitic on man and other animals but are not obligately pathogenic. They are encountered at least as often in the absence of disease as in its presence. The indigenous microorganisms may flourish in the general region of tissue damage and contribute to the disease state as opportunists, rather than primary etiological agents. Thus, these organisms may be implicated although Koch's postulates would not necessarily hold true.2

Amphibiont Sites

As a rule, few or no microorganisms are found in the following anatomical locations: blood, larynx, trachea, nasal sinuses, bronchi, esophagus, stomach, upper intestinal tract, upper urinary tract (including the posterior urethra), and posterior genital tract (passage above cervix included). However, in studies with animals, notably dogs and rabbits, microorganisms from the mouth and throat regions and from the lower intestine were found in the blood and other tissues after these animals were subjected to various types of physical or mental stress and trauma. In particular, Clostridium perfringes (one of the causative agents of gas gangrene) has been isolated from the "healthy" tissues of these animals.

The regions of the body that constitute the major habitats for indigenous microorganisms include the skin and contiguous mucous membranes, conjunctivae, upper respiratory tract (oral-pharynx included), mouth, lower intestine, external genitalia, anterior urethra, and vagina. It will become apparent that each habitat has certain characteristics, which allow a different overall range of microorganisms to thrive. These differences can be categorized into the following three types of environment:

  1. Extremely high levels of both moisture and nutrients, as in the lower intestines and the mouth.
  2. A high level of moisture and a low level of nutrients, as with mucous membranes.
  3. A low level of moisture and a moderate level of nutrients, as on the skin.

Other variables include availability of oxygen, pH, temperature, and relative exposures to contaminants and ventilation.

Numbers of total aerobic and anaerobic bacteria in certain anatomical regions:

Lower intestine - approximately 100 billion microorganisms per gram of fecal matter.

Mouth - approximately 1 billion microorganisms per ml of saliva.

Nose - approximately 20,000 microorganisms per ml of nasal washing.

Skin - approximately 1 million microorganisms per cm2; this value is dependent upon the skin surface tested.

Development of the indigenous flora begins with the normal birth process, since the infant has been bathed during the ingestion period in a sterile amniotic fluid. As the baby passes through the birth canal it begins to pick up organisms, many of which may remain with it for its lifetime. Additional microorganisms are acquired by the infant as a consequence of coming into contact with the air of the environment and with hospital personnel. Such organisms may be transient in nature, or may become permanent members of the flora.

Appreciable numbers of bacteria have been cultured from the mouths of infants within 6 to 10 hours of birth and in the feces within 10 to 20 hours.

The human body has various anatomical organ areas, each anatomical area varies in relation to pH, oxygen content, nutrients, and moisture as well as bactericidal factors, thus different organisms will predominate. While the amphibionts persist in their respective locations, saprophytic as well as many parasitic microorganisms are destroyed or excreted. These locations can change as a consequence of changes brought about by the maturation process of the individual, e.g., hormonal regulation, alteration in dietary habits, chemical exposure, IAQ buildings, AIDS and chemotherapy.

The indigenous fungi are primarily saprophytes of soil, which show preference for a parasitic habitat. Because of their primary saprophytic role, it may appear questionable to call them amphibionts. However, according to Rosenbury, an amphibiont may be considered to be any organism, which is ". . . encountered in one or more typical indigenous locations frequently, and distinctly more frequently, than in the adjacent environment." On this basis, and according to the propositions that an organism routinely isolated from the body in the absence of disease may be indigenous, fungi are included, even though they rarely are indigenous to the human body.2, 3

WHAT ARE FUNGI?

Fungi are single cell living forms of life, which inhabit the land, air, and waters of our planet, earth. They are everywhere in our environment, soil and home.

They are more highly developed than bacteria and viruses. They are composed of many more species than are found in other microorganisms. It is estimated that there are over 500,000 different species.

Fungi have been on earth several billion years and, quite remarkably, have had little genetic change over that period of time. They are survivalists. They can change their form from rapidly growing to no growth for thousands of years, such as seen in their living spores which have been found in Egyptian tombs. They secrete and make a poisonous toxin called a mycotoxin.

Single fungi cells can only be seen under the microscope but a colony of these cells makes a visible presence in the form of mushrooms, toadstools and molds on food and other habitats.

While plants, animals and humans are alive and well, the fungi around us are unable to overcome the natural defense mechanisms which higher forms of life possess. But once death overtakes the living, the fungi are the principle undertakers and managers: they reduce all that have ever lived into the molecules from which they were assembled. Biologists call this the carbon cycle while theologist call it "from dust to dust."4, 5

However, there is one exception to this simple balanced equation of life and death and that is that the fungi can attack the living while they are alive.

At its most simplistic perspective, one has many fungi entering the intestinal tract, the nose and lungs, and organs exposed to the world at large. We generally do not develop an infection from these intruders. However, a person might contract a fungal infection such as "athlete's foot" or a "ring worm" on the skin.

At the opposite extreme is the patient with AIDS who faces death-threatening major fungal infections because that person's immune system has lost its effectiveness against fungi. In between the extremes are fungal infections associated with diseases such as diabetes, cancer and other conditions including cross infections amongst humans.

Forturnately, the average person does not succumb to a serious fungal infection such as Candida albicans (yeast) and average life into the 70's.

All humans are colonized by Candida albicans and normal healthy persons do not die from this organism. This organism plays a very little role in causing human diseases. It has been known to have tremendous elevated growth patterns in individuals who have been diagnosed as being multichemical sensitive or acutely poisoned from exposure to hazardous materials, such as urethane, carbamates, nitrogen mustards and other compounds. It is interesting to note that these same chemicals are known to be extrinsic mutagenic agents in both fungi and human genes.6 This type of extrinsic mutagenic activity by chemicals is also known as a "directed mutation."7 (See Table 1-1.)

Mycotoxins may be friends or foe. There are as many as 1,000 compounds, classifiable as mycotoxins, where studied by the pharmaceutical industry as potential antibiotics in the 1930's and 1940's only to be discarded as being too toxic for higher life forms to be of value in treating bacterial diseases in humans. Little, if any of the discarded data was published. Yet, what these toxicity studies actually documented was the existence of a large number of fungal-derived toxins, which caused serious, target organ injury in various animal models.

Obviously, in retrospect, what was being seen was the pathology produced by the mycotoxins, in order to understand this toxicity, one only has to look at what some of these mycotoxins, used as medications, causes in humans:

The mycotoxin cyclosporin used for transplantation causes cancer and atherosclerosis, complete with hyperlipidemia in ALL humans who have received it. Many others develop gout and other diseases.

As a friend, the study of such fungal metabolites gave us penicillin at the beginning, which was replaced by a chemical cyanamide man made compound from 1945 to present day. Quite later on cyclosporin, the most potent immuno-suppressant transplantation drug, lovastatin, and the other "statins", which have revolutionized the treatment of hyperlipidemia and atherosclerosis. The latter group is quite interesting in that they were initially developed as anti-fungal agents which just happened to have an effect in lowering blood levels of low density lipoproteins (commonly refereed to as "bad cholesterol").

The members of this group of drugs are joined by another anti-fungal antibiotic, griseofulvin, which is also a remarkably efficient anti-atherosclerosis drug. All of this goes a long way to confirm the fungal etiology of atherosclerosis. This appears to be a quite valid conclusion since all of the other effective anti-cholesterol and/or anti-atherosclerotic therapeutic modalities share nothing in common except that they possess anti-fungal and/or anti-mycotoxin activity. Diseases of unknown etiology, which respond to anti-fungal-effective drugs, suggest the probability that they have a fungal origin, particularly when there is no other proven explanation as to how the drug is working. Table 2-2 provides a number of human diseases, which so respond and suggest a fungal or mycotoxin origin.

ENVIRONMENT, FOOD CHAIN and STORED FOOD

Fungi grow all over this planet. They are found in the soil, on trees and in water. Their spores travel throughout the lands by the winds from the four corners of our world. Biosensor testing conducted by the U.S. military has resulted in an increase population of Aspergillus niger on homes, trees and other materials in various areas of the United States of America.8

Over the last decade, starting in the 1990's, research has implicated many toxin-producing fungi, such as Stachybotrys, Penicillim, Aspergillus and Fusarium species, to indoor air quality problems and building related illnesses. Inhalation of mycotoxin producing fungi in contaminated buildings is the most significant exposure, however, dermal contact form handling contaminated materials and the chance of ingesting toxin containing spores through eating, drinking and smoking is likely to increase exposure in a contaminated environment. Recent advances in technology have given laboratories the ability to test for specific mycotoxins without employing cost-prohibitive gas chromatography or high performance liquid chromatography techniques. Currently, surface, bulk, food and feeds, and air samples can be analyzed relatively inexpensively for mycotoxins.

Homes that have been damaged by water or have had improper construction of ventilations systems have become infected with fungal overgrowth and biofilms, which resulted in bacteria, algae and fungi growing together as a communal colony with microtubules connecting to each other to exchange nutrients. Thus, creating the most toxic forms of mycotoxins, endotoxins, and exotoxins with the potential of forming DNA plasmids in mycoplasma, with mutated RNAi sub-mutated forms of fungi genes.9, 10

The most toxic forms of fungi, mycotoxin is coming from our food itself, which is characteristically present in stored and fermented food. Pesticides used on cereals as a fungicide, such as benomyl have potentated the mycotoxin in selective genes. In 1987 at Yale University, Karl Hager and Mike Plamann performed a very important study, which was based on the plasmid pH303 and its derivatives integrated at his-3 by a single crossover. When introduced to benomyl, the mutant allele of his-3(1-234-723) was present in the genome, and its mutation was mapped to be somewhere downstream of the Sall restriction site. A cloning will occur at a higher transformation frequency using linear than using circular DNA, and the transformation frequencies are independent of the mating type of the host.11

If food is loaded with fungi, then the myctoxin concept is fully operative and the disease-producing potential is more than obvious.

This important question of how much fungal colonization of food exists is answered by the most recent reported mycological study of some quite representative foods; corn kernels, peanuts, cashew nuts and copra (dried coconut). Table 3-3 demonstrates the remarkable degree of fungal colonization of the interior of corn kernels and peanuts.12

Humans who eat these foods are ingesting both the toxicogenic fungi and their mycotoxins. These fungi are capable of surviving in the intestinal stream where they may continue to produce their toxins.

Similarly, animals fed fungal colonized/mycotoxic feed are not only at risk of developing mycotoxicoses, their meat and their fat, constitute another vehicle for human exposure to excessive mycotoxin intake. Animal fat is increasingly being documented to be a major risk factor for a number of human cancers and atherosclerosis. It must be noted that fat, stores polycyclic organic xenobiotics and they are highly lipid soluble. They concentrate in fat depots, which results in low plasma levels and extended half-lives. These same compounds are known to cause distinct mutations. When cattle were accidentally fed contaminated feed in Michigan by PBB's in 1973, these compounds became stored first in fat deposits of the cows and then, via milk fat, bioaccumulated in fat stores of the people of Michigan, where PBB's can still be detected. While there is no known effect of PBB's at the storage site, this store is a potential hazard since mobilization during starvation or other stress could lead to efflux into the bloodstream with subsequent redistribution and toxicity. Similarly, patients treated for acute exposure to organophosporous pesticides may be released from the hospital and later suffer a relapse due to mobilization of the insecticide from fat stores.13

Mycotoxins have been documented to cause a number of specific types of diseases and very specific organ lesions both in animals and in humans. Table 4-4 provides a summary of some of this documentation.

DISEASES ASSOCIATED WITH VARIOUS MYCOTOXINS

Aflatoxin

Aflatoxin is one of the most potent carcinogens known to man and has been linked to a wide variety of human health problems. The FDA has established maximum allowable levels of total aflatoxin in food commodities at 20 parts per billion. The maximum level for milk products is even lower at 0.5 parts per billion. Primarily Aspergillus species fungi produce aflatoxin.

Ochratoxin

Ochratoxin is primarily produced by species of Penicillim and Aspergillus. Ochratoxin is damaging to the kidneys and liver and is also a suspected carcinogen. There is also evidence that it impairs the immune system.

T-2 Toxin

T-2 Toxin is trichothecene produced by species of Fusarium and is one of the more deadly toxins. If ingested in sufficient quantity, T-2 toxin can severely damage the entire digestive tract and cause rapid death due to internal hemorrhage. T-2 has been implicated in the human diseases alimentary toxi aleukia and pulmonary hemosiderosis. Damage caused by T-2 toxin is often permanent.

Fumonisin

Fumonisin is a toxin associated with species of Fusarium. Fumonisisn is commonly found in corn and corn-based products, with recent outbreaks of veterinary mycotoxicosis occurring in Arizona, Indiana, Kentucky, North Carolina, South Carolina, Texas and Virginia. The animals most affected were horses and swine, resulting in dozens of deaths. Fumonisin toxin causes "crazy horse disease", or leukoencephalomalcia, a liquefaction of the brain. Symptoms include blindness, head butting and pressing, constant circling and ataxia, followed by death. Chronic low-level exposure in humans has been linked to esophageal cancer. The American Association of Veterinary Laboratory Diagnosticians (AAVLD) advisory levels for fumonisin is horse feed is 5 ppm.

Vomitoxin or Deoxynivalenol (DON)

Vomitoxin, chemically known as Deoxynivalenol, a tricothecene mycotoxin, is produced by several species of Fusarium. Vomitoxin has been associated with outbreaks of acute gastrointestinal illness in humans. The FDA advisory level for vomitoxin for human consumption is 1 ppm.

Zearalenone

Zearalenone is also a mycotoxin produced by Fusarium molds. Zearalenone toxin is similar in chemical structure to the female sex hormone estrogen and targets the reproductive organs.

Citrinin

Citrinin is a nephrotoxin produced by Penicillium and Aspergillus species. Renal damage, vasodilatation, and bronchial constriction are some of the health effects associated with this toxin.

Alternariol

Alternariol cytotoxic compound derived from Alternia alternata.

Satratoxin H

Satratoxin H is a macrocyclic tricothecene produced by Stachybotrys chartaru, Trichoderma viridi and other fungi. High doses or chronic low doses are lethal. This toxin is abortogenic in animals and is believed to alter immune system function and makes affected individuals more susceptible to opportunistic infection.

Gliotoxin

Gliotoxin is an immunosuppressive toxin produced by species of Alternaria, Penicillium and Aspergillus.

Patulin

Patulin is a mycotoxin produced by Penicillium, Aspergillus and a number of other genera of fungi. It is believed to cause hemorrhaging in the brain and lungs and is usually associated with apple and grape spoilage.

Sterigmatocystin

Sterigmatocystin is a nephrotoxin and a hepatotoxin produced by Aspergillus versicolor. This toxin is also considered to be carcinogenic. Other mycotoxins include - Penicillic acid, roquefortine, cyclopiazonic acid, verrucosidin, rubratoxins A and B, PR toxin, luteoskyrin, cychlochlorotine, rugulosin, erythroskyrine, secalonic acid D, viridicatumtoxin, kojic acid, xanthomegnin, viomellein, chaetroglobosin C, echinulin, flavoglaucin, versicolorin A, austamid, maltayzine, aspergillic acid, paspaline, aflatrem, fumagillin nigragilin, chlamydosporol, iscotrichodermin and many more. As previously discussed there are many mycotoxins that can cause adverse health effects and even death in humans. These synergistic effects of exposure to multiple mycotoxins simultaneously are very poorly understood. Even more poorly understood are the by-products of mycotoxin degradation, particularly under the influence of strong oxidizing agents such as sodium hypochlorite and/or ozone, agents frequently used or misused by hazardous materials personnel or remediation remediators in industry. More research is required in this field to better understand the relationship of fungal contamination, relative humidity, temperature and ventilation in fungal growth in buildings and on building substrates as they relate to disease.14

VOLATILE FUNGAL METABOLITES

During exponential growth, many fungi release low molecular weight, volatile organic compounds (VOCs) as products of secondary metabolism. These compounds comprise a great diversity of chemical structure, including ketones, aldehydes, and alcohols as well as moderately to highly modified aromatics and aliphatics. Cultural studies of some common household molds suggest that the composition of VOCs remains qualitatively stable over a range of growth media and conditions. Furthermore, the presence of certain marker compounds common to multiple species, such as 3-methylfuran, may be monitored as a proxy for the presence of a fungal amplifier.14 This method has been suggested as a means of monitoring fungal contamination in grain storage facilities. Limited evidence suggests that exposure to low concentrations of VOCs may induce respiratory irritation independent of exposure to allergenic particulate. Volatile organic compounds may also arise through indirect metabolic effects. A well-known example of this is the fungal degradtion of urea formaldehyde foam insulation. Fungal colonization of this material results in the cleavage of urea from the polymer, presumably to serve as a carbon or nitrogen source for primary metabolism. During this process formaldehyde is evolved as a derivative, contributing to a decline in Indoor Air Quality.12

INTEGRATIVE HEALTH CARE TREATMENT

Many fungi, mycotoxins, and their VOC's are at a level of detection within the human body that is very hard to determine at relatively low costs. Tissue samples of blood, urine and even direct organ/tissue biopsy will determine the presence of a fungi, mycotoxin and/or their VOC's. To kill fungi and remove other substances it is necessary to look at a variety of treatment modalities. Current, anti-fungal formulations have been developed to address specific fungal infections. In many cases it is very hard for the healthcare provider and physician to determine what species of fungi was present that created what specific mycotoxin, which is a billion dollar revenue to the pharmaceutical industry.

In AIDS patient's fungal infections have been observed in tissue biopsy reports to be growing within the tissue and this causes great health risks to the patient. The use of far infrared as a treating modality can address the electromagnetic spectrum in micron and micrometers (nano level), which would be an ideal choice, in treating fungal infected patients. The far infrared segment of the electromagnetic spectrum occurs just below, or "infra" to, red light as the next lowest energy band. This band of light is as the next lowest energy band. This band of light is not visible to human eyes but can be seen by special cameras that translate infrared into visible colors. We can, however, feel this type of light, which we perceive as heat. The sun produces most of its energy in the infrared segment of the spectrum. Our atmosphere has a "window" in it that allows infrared rays-in the 7 to 14 micron bands, with peak output at 10 microns.

Our tissues normally produce infrared energy for warmth and tissue repair. Tissue production of infrared energy is associated with a variety of healing responses. At times the infrared energy in our tissues may require a boost to higher level to ensure the fullest healing possible for tissue repair. Body tissues that need an infrared boost selectively absorb infrared rays, after boosting a tissue's infrared energy; the remaining rays pass onward harmlessly. This phenomenon is called "resonant absorption." Our bodies radiate infrared energy through the skin at 3 to 50 microns, with most output at 9.4 microns. Our palms emit infrared energy too, from 8 to 14 microns. Palm healing, an ancient tradition in China, has used the healing properties of infrared rays for 3,000 years. Yogis in India also employ palm healing and recommended it especially for relieving eyestrain.

An MPS Capsule from MPS, Inc. Seoul, Korea, which generates far infrared energy from special carbon fibers manufactured by Daiugin and high gem graded jade balls with far infrared proprietary technology; may be a future solution for individuals suffering from fungal infections. Its dome generates temperatures as high as 1650F and the spinal column area as high as 1480F. These temperatures are known to kill fungi and release VOCs that have a lower melting point, like benzene at 810F.15, 16

The use of activated charcoal has been recognized by the U.S. Environmental Protection Agency in their text, Recognition and Management of Pesticide Poisonings, 4th Edition, in absorbing volatile organic compounds (VOCs), which are the same type of compounds found in fungal metabolites.17 Activated charcoal is made from burnt coconut husk. It is able to absorb at a minimum 35 % of the VOCs found in the intestinal tract from reabsorbing into the blood stream. It does not absorb in other areas of the body were VOC's may accumulate, such as in the lungs, brain, liver and fat. Research conducted at the Korean Atomic Institute have shown that Kuh Sung YLS-95 (Trade Marks Bio-Oaky & Oaky Smoky) a liquid yielding high plant infrared, which is made from oak wood charcoal vinegar is highly effective in significantly reducing carbon tetrachloride in rats and ethanol in humans within one hour after exposure.18

CONCLUSION:

One could test the validity of how poisonous mycotoxins are by eating a handful of poison mushrooms, a species of fungus. However, it would be less fatal to realize that many forms of fungus produce mycotoxins, which are chemical substances that are toxic to man and other life forms. In addition, fungi produce volatile organic compounds (VOCs), which may bind to fat within in your body and cause internal re-exposure to the toxic effects of these compounds. Current, integrative technologies in the health care area have produced far infrared MPS Capsules and Kuh Sung YLS-95 (Trade Mark Bio-Oaky & Oaky Smoky) that will kill fungus and neutralize VOC's in other tissue organs within the human body respectfully. These technologies may be the answer to current biological weapons of mass destruction and the risk of exposure to biological pesticides by killing these microorganisms at micron (0.000,001) and nano (0.000,000,001) levels within our human body. Cellular detoxification and its remediation are on the break of a new horizon through terahertz, far infrared and subnano technologies.  
PART 2 - SEE TABLES

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JERUSALEM ARTICHOKE POWDER (JAP) FOS/INULIN

Aug. 17th, 2005 | 01:53 am
mood: accomplished

Jerusalem Artichoke Powder (JAP)

by Hildegarde Staninger, Ph.D,,RIET-1

Industrial Toxicologist/IH & Doctor of Integrative Medicine

   © August 17, 2005

 

Jerusalem Artichoke Powder (JAP) comes from Helianthus tuberosus, the Sunflower family.  It has rough branching stems bearing large golden-yellow flower heads (up to 3 inches).  Its tubers have been cultivated and prepared as food by Native Americans and was even dined by Lewis and Clark in 1805.

 

Whole Tuber Jerusalem Artichoke Powder, with natural Probiotic Factors (F. Bifidum, B. Breve, B. Infantis, B. Adolescentis, B. Longum,  L. Salivarius and L. Rhamnosus) that act as immune-boosters and fertilizers to the natural intestinal flora. JAP is a concentrated source of Fructo-oligosaccharides and Inulin that helps Bifidobacterium literally recolonize in the colon.  This product contains over 6 million Bifidobacterium per serving. Leading Canadian bacteriologist 

Dr. Edward Brochu, of the Institute Rosell of Montreal, reports that Lactobacilli Rhamnosus has been shown to have very exciting immune-boosting properties including the following:

 

l        Activation of natural killer cells to reduce cancer risk.

l        Improved resistance to listeria monocytogenes which can cause encephalitis.

l        Improved phagocytic activity by the body’s white blood cells called macrophages.

l        Increased levels of infection-fighting immunoglobulins.

l        And Inulin helps to boost the body’s levels of all resident beneficial bacteria.

 

Our product is not regular Jerusalem Artichoke Powder (JAP), but the whole Jerusalem Artichoke tuber is dehydrated and made into a micro-powder in a special proprietary process to provide a concentrated source of Fructo-oligosaccharides, natural Inulin and cellular Biolumninescense that helps the friendly Bifido Bacterium literally re-colonize in the colon as it maintains cellular photonic life within the cell.

 

JAP is EXCELLENT for people with CANDIDA (yeast) and other fungal or bacterial infections.  It also works as a blood sugar stabilize4r for people with DIABETES by creating a natural insulin effect in the body.  JAP contains 8 million Bifido Bacterium per serving.  The bifido change the pH factor which KILLS the Candida which cannot survive in the more acidic environment.

 

What is 100% Natural FOS? 

Jerusalem Artichoke Powder contains 100% NATURAL FOS.  FOS stands for a unique carbohydrate known as fructooligosaccharides, which are composed of natural sugars that travel directly into our lower intestinal track and colon and are consumed by specific beneficial bacteria.  These beneficial bacterial grow and multiply by 500% to 1500% with each daily dose of JAP.  This

‘fertilizing or feeding of our good bacteria” has tremendous influence over our health and well being.

 

Taking 100% NATURAL FOS as found in JAP increases the number of friendly Bifidobacteria and Lactobacillus bacteria in our colon and intestine.  These good bacterial competitively eliminate unfriendly bacteria like E. Coli, Salmonella, and the fungus Candida.  Eventually these beneficial bacterial protect us from a wide range of health problems by lining our gastrointestinal system.  This protective lining helps reduce the level of harmful bacteria and disease causing toxins within our bodies.

 

Some Noted Health Benefits from 100% NATURAL FOS as found in Jerusalem Artichoke Powder are the following:

 

l        Assists the Immune System

l        Eliminates Toxins

l        Fees and Multiplies Critical Beneficial Bacteria

l        Reduces Cholesterol, Blood Pressure and Blood Sugar Levels

l        Reduces Problem Diarrhea and Constipation

l        Reduces the Detoxifying Load of the Liver

l        Reduces the Risk of Degenerative Diseases

l        Produces Short Chain Fatty Acids for additional energy and colon health.

l        Produces Vitamins B1, B2, B6, B12, Niacin and Folic Acid

l        Produces Natural Antibiotics

l        Protects from exposure to Pathogenic Bacteria

l        Improves the Digestive Process

l        Increases Vitamin and Mineral Absorption

l        Restores the Colon Flora, Especially Important After a Course of Antibiotics

l        Reduces Diaper Rash

l        Reduces Vaginitis

l        Reduces Fishy Odor Syndrome

 

What is Inulin?  Inulin is a natural occurring complex sugar molecule found in Jerusalem Artichoke Powder (JAP) and has beneficial effects as a food ingredient.  Inulin is considered to be a health-enhancing food ingredient.  Inulin is also known as a prebiotic-since it promotes growth of beneficial bacteria such as acidophilus, bifidus and faecium.  Inulin is among the most powerful and beneficial prebiotics known at this time. And inulin derived from JAP has greater biological activity.  Inulin offers the following benefits to human gastrointestinal ecology:

l        Stimulates growth of acidophilus, bifidus and faecium.

l        Normalizes fecal pH.

l        Enhances elimination of toxic metabolites.

l        Reduces serum cholesterol and triglyceride levels.

l        Reduces blood pressure among the elderly with high blood lipids.

l        Reduces carbohydrate absorption, thereby normalizing blood glucose.

l        Offers alternative sweeteners for diabetics and dieters.

l        It is nontoxic and free of side effects that are commonly associated with artificial sweeteners.

 

Dr. Michael Loes stated in his book, The Healing Power of Jerusalem Artichoke Fiber, “toxins exist internally and externally and as chemicals and environmental emotional intelligence.  Our physical and energetic body must shield and actively defend itself.  Here, inulin is very helpful.  An arsenal of defenders must be present, trained and ready to act.  Any threat to the physical and energetic body must be met with active forces.  A healthy immune system is essential, as in the belief of God.  Vitamins, minerals, herbs, antioxidants, enzymes and fiber are key defenders- especially inulin.” Maintain supernutrient status as you accept your healthy blessings from Jerusalem Artichoke Powder.

 

References

1.  Loes, M.D., M.D.(N), Michael.  The Healing Power of Jerusalem Artichoke Fiber.  Freedom Press.  Topanga, CA. © 2000.

2.  Cohen, M. “Epidemiology of drug resistance:  implications for a post-antibiotic era.”  Science. 1992: 257: 1050.

3.  Moshfegh, A.J., et al.  Presence of inulin and oligofructos in the diets of Americans.”  Journal of Nutrition, 1999; 129(7 Suppl):  14075-14115.

4.  Fukata, T. et al.  “ Inhibitory effects of competitive exclusion and fructooligosaccaharide, singly and in combination, on Salmonella colonization of chicks. “  J. Food Prot. 1999:  62(3):  229-233.

5.  Bouhnik, Y., et al.  “Effects of bifidobacterium sp fermented milk ingested with or without insulin on colonic bifidobacteria and enzymatic activities in healthy humans. “  Eur J Clin Nutr. 1996:  50(4): 269-273.

 

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MSG & OTHER GLUTAMATES

May. 6th, 2005 | 02:01 am
mood: accomplished

MSG & OTHER GLUTAMATES

 

Dr. Hildegarde Staninger

May 6, 2004


It was in 1907 that Professor Kikunae Ikeda of Tokyo Imperial University was thinking about the taste of food: "There is a taste which is common to asparagus, tomatoes, cheese and meat but which is not one of the four well-known tastes of sweet, sour, bitter and salty." He knew that it was present in the "broth" made from Kombu (a type of seaweed) found in traditional Japanese cuisine. Starting with a tremendous quantity of kombu broth, he succeeded in extracting crystals of glutamic acid (or glutamate). Glutamate is an amino acid, and is a building block of protein. Professor Ikeda found that glutamate had a distinctive taste, different form sweet, sour, bitter, and salty, and he named it "umani", 100 grams of dried kombu contain about 1 gram of glutamate. A new seasoning was born called glutamate, but it would cake up by absorbing humidity, so he modified it by adding sodium to create monosodiumglutamate commonly known as MSG.

John Erb, a research assistant at the University of Waterloo, while conducting research for his book entitled The Slow Poisoning of America made a discovery that scientists were creating obese mice and rats to use in diet or diabetes test studies.

No strain of rat or mice is naturally obese, so the scientists have to create them. They make these morbidly obese creatures by injecting them with MSG when they are first born. The MSG triples the amount of insulin the pancreas creates, causing rats (and humans?) to become obese. They even have a title for the race of fat rodents they create: "MSG-Treated Rats".

Glutamate is produced in the human body and plays an essential role in metabolism. It is found in mother's milk (humans 21.6 mg/100G; chimpanzees 38.9 mg/100G; cows 1.9 mg/100G and mice 2.2 mg/100G).

Studies have shown that the body uses glutamate, an amino acid, as a nerve impulse transmitter in the brain and that there are glutamate-responsive tissues in other parts of the body as well. Abnormal function of glutamate receptors has been linked with certain neurological diseases, such as Alzheimer's disease and Huntington's chorea.

Kirk R. Anders and David Botstein, Department of Genetics, Stanford University have found the wild type of yeast Saccharomyces cerevisiae, if exposed to benomyl create a gene defect for the microtubules within its cell are increased if glutamate or aspartate to alanine results in the loss of potential binding of the microtubles, which means the cell can not absorb its nutrients. This same effect may occur in our own bodies if we had the wild phenotype of Saccharomyces cerevisiae in our body and we were ingesting large amounts of monosodiumglutamate (MSG) and aspartame (NutraSweetTM). Further complications could occur if we had a mutated common ring worm infection, which could create a severe skin rashes as described in MSG-sensitivity reactions.

Toxoplasmosis (a protozoan), psittacosis (virus) and ringworm (fungus) are organisms called Zoonoses. They create diseases that can be passed from different species of animals to man. International experts addressed this concern at a joint WHO, UN's Food and Agriculture Organization (FAO) and World Organization Health (OIE) issued a joint message, which warned that the emergence of new diseases that are passed from animals to humans such as avian flu, Ebola, SARS and leishmaniasis, was accelerating and they were ill-equipped to counter the trend. Zoonoses break the species barrier, but do they break it because of the species or from the aide of a mutated wild type of fungus, bacteria, or virus that utilizes compounds like MSG and aspartame to accomplish internal cellular dysfunction, injury and disease.


Hildegarde Staninger, Ph.D., RIET-1
Health Life
3130 Wilshire Blvd., Suite 408
Los Angeles, CA 90010
Telephone: 213-383-9120
Fax: 213-383-9780

 

 

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KELP & RADIATION POISONING

May. 9th, 2004 | 02:06 am
mood: accomplished

Flowers of the Sea

By Dr. Hildegarde Staninger

May 9, 2004



"Call us not weeds, we are flowers of the sea." E.L. Aveline 

Kelp a/k/a brown seaweed, no doubt, outdates man by a considerable period of time. Man has been using seaweed for food and in the growth of plants since his very beginning. Early man, perhaps, cared less why seaweed influenced plant growth. He found them, used them and was happy. Man of necessity is concerned about the environment in which he lives. This environment is living and active and is the home of many living things in the air, the soil and the water. The bacteria, fungi, nematodes represent lower forms of life, whereas many kinds of plants on land in the oceans represent the higher forms of living things. It is estimated that more than half the food we eat contains applied chemicals, many of them are residues from the 2.3 billion pounds of pesticides farmers apply to their crops each year. Some pesticides are suspected carcinogens; others are highly toxic and the affects of biological pesticides (genetically engineered pesticides from bacteria, viruses, fungi and other life forms DNA) are being seen as the genocide cocktails for the genocide of non-native species of plants in the United States.

Two-thirds of the earth's surface is covered with water, and marine algae constitute most of the whole vegetation, which exists in this area. And there are many varieties of seaweed - blue-green, grass green, olive-green, brown, and red.

Kelp specifically refers to various flat brown seaweeds, includes species of Laminaria and Macrocystis that grow on rocks mainly in cold oceanic water of the Northern Hemisphere. Kelps have been used as human and animal food, medicines, and fertilizers for thousands of years by coastal peoples of Greece, China, Korea, Japan, Europe and North America. The seaweeds have been most commonly used to counter goiter (enlargement of the thyroid gland, which is located on the neck) and under active thyroid (hypothyroidism). The scientific rationale for these uses began in 1812 with the discovery in kelp of iodine, a mineral necessary for the body to produce thyroid hormones.

A number of countries, since the 1920's have added iodine to salt. This can effectively reduce goiter and other diseases associated with iodine deficiencies, but in some parts of the world these conditions remain serious public health problems that could be alleviated by consumption of kelp or other seaweeds.

Kelp is a natural antidote to radiation poisoning as seen with plutonium, uranium, radon, I-131 and I-125. It was used as the primary antidote for the effects of radiation poisoning after the U.S. bombing of Hiroshima, Japan. Lots and lots of misu soup were consumed by the Japanese to counter radiation poisoning.

As Chernobyl proved, and health experts now agree, the greatest health concerns affecting the largest number of people form a nuclear accident or explosion are likely to be form radioactive iodine readily carried by the winds many miles downwind from the site of a nuclear event.

Radio active Iodine (I-131 & I-125) is a major radioisotope constituent of both nuclear power plant accidents, nuclear bombs, contaminated milk in Panama and used as a ground water monitoring agent for oil wells right at Beverly Hills High School grounds (http://www.beverlyhillswater.com). Thyroid cancer attributable to Chernobyl has been documented up to 500 km from the accident site. Even very small amounts of inhaled or ingested radioiodine can do grave damage as it will always concentrate, and be retained, in the small space of the thyroid gland. And pregnant women breath 7 times more oxygen than a non-pregnant woman from the time of conception, thus allowing them to be at 7 times more risk than other people.

Animal studies performed by Hong Kong researchers have shown that kelps and other seaweeds rich in iodine and other nutrients were able to suppress the thyroid's ability to absorb radioactive iodine, thus preventing the organ from being injured by the harmful effects of radiation. All individuals should be wise and stock their kitchens with misu soup, roasted seaweed or make their favorite dishes using kelp as an ingredient, because the use of radio active I-131, I-125 and NORMs are being used in every oil well in the USA as a testing agent for cracks in the pipes, but who is collecting the radiation that leaks from the none lead pipes. And we all have read that the lead plumbing in Rome is what drove Nero mad as he burned his own city. And know one knows what cascading effect radiation combined with petroleum compounds will have on our bodies.


Hildegarde Staninger, Ph.D., RIET-1
Health Life
3130 Wilshire Blvd., Suite 408
Los Angeles, CA 90010
Telephone: 213-383-9120
Fax: 213-383-9780

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