Ge – Germanium is found in igneous rocks at 5.4 ppm; shales at 1.6 ppm; sandstones at 0.8 ppm; limestones at 0.2 ppm; sea water at 0.00007 ppm; soil at 1 ppm in humus, especially in alkaline soils marine animals at 0.3 ppm.
Mendeleev had predicted the existence of the element germanium in his periodic table, but it was not until 1886, that a German scientist, Clemens Winkler isolated this element and named it germanium. Radio do-it-yourself kits from the 40’s and 50’s utilized the germanium diode crystal to attract the radio signal to your radio. The germanium atom is structured so it accepts and transmits electrons, thus acting as a semiconductor – it is therefore not too surprising that germanium is closely related to silica and carbon.
Biologically, germanium is a highly efficient electrical impulse initiator intracellularly and acts as a metallic cofactor for oxygen utilization.
In 1950, Dr. Kazuhiko Asai, a Japanese chemist, found traces of germanium in fossilized plant life. Russian researchers quickly attributed anti-cancer activity to germanium. Dr. Asai was able to connect the healing properties of certain herbs to relatively high levels of germanium -many of these herbs are accumulator plants for germanium. Germanium is known to enhance the immune system by stimulating production of natural killer cells, lymphokines such as IFN (Y), interferon, macrophages and T-suppressor cells.
Asai synthesized GE-132-carboxyethyl germanium sesquioxide in 1967 by a hydrolysis method. This organic germanium structure forms a cubic structure with three negative oxygen ions at the base of a cubic triangle.
As an organic or chelate form of germanium GE-132 is absorbed at the rate of 30 percent efficiency and the total intake is excreted in one week.
Food plants and animals contain small amounts of germanium (Le, beans-4.67 ppm; tuna-2.3 ppm). Healing herbs such as garlic, aloe, comfrey, chlorella, ginseng, watercress, Shfitake mushroom, pearl barley, sanzukon, sushi, waternut, boxthorn seed and wisteria knob contain germanium in amounts ranging from 100 to 2,000 ppm.
The “holy waters” at Lourdes, known world wide for their healing properties contains large amounts of germanium.
Severely reduced immune status, arthritis, osteoporosis, low energy and cancer typify deficiencies of germanium.
Twenty to 30 mg per day is the recommended maintenance dose for germanium; 50 to 100 mg per day are commonly used when an individual has a serious illness that requires an increased oxygen level in the body.
1.Goodman, S.: Therapeutic Effects of Germanium. Med.Hypoth.26: 207.1988.
2.Suzuki, F., et al.: Ability of Sera from Mice Treated with Ge-132, an Organic Germanium Compound, to Inhibit Experimental Murine Ascites Tumours. Br.J.Cancer-52: 75 7.1985.
Biol Trace Elem Res 1994 Aug;42(2):151-164
Effects of germanium and silicon on bone mineralization.
Seaborn CD, Nielsen FH
United States Department of Agriculture, Grand Forks Human Nutrition
Research Center, ND 58202.
The chemical properties of Ge are similar to Si. This study investigated whether Ge can substitute for, or is antagonistic to, Si in bone formation. Sixty male weanling Sprague-Dawley rats were randomly assigned to treatment groups of 12 and 6 in a 2 x 4 factorially arranged experiment. The independent variables were, per gram fresh diet, Si (as sodium metasilicate) at 0 or 25 micrograms and Ge (as sodium germanate) at 0, 5, 30, or 60 micrograms. Results confirmed that Ge does not enhance Si deprivation and provided evidence that Ge apparently can replace Si in functions that influence bone composition. When Si was lacking in the diet, calcium and magnesium concentrations of the femur were decreased; this was reversed by feeding either Ge and/or Si. Similar effects were found for zinc, sodium, iron, manganese, and potassium of vertebra. There were some responses to Si deprivation that Ge could not reverse; Ge did not increase femur copper, sodium, or phosphorus or decrease molybdenum of vertebra, effects that were evoked by Si supplementation. Additionally, some findings suggested that 60 micrograms Ge/g diet could be a toxic intake for the rat. On the other hand, some responses induced by Ge indicate that this element may be acting physiologically other than as a substitute for Si. Germanium itself affected bone composition. Germanium supplementation decreased Si and molybdenum in the femur and increased DNA in tibia. Regardless of the amount of Si fed, animals fed 30 micrograms Ge/g diet had increased tibial DNA compared to animals fed 0 or 60 micrograms Ge; however, tibial DNA of animals fed 30 micrograms Ge was not statistically different from those animals fed 5 micrograms Ge. Thus, Ge may be of nutritional importance.
Effect of organic germanium compound (Ge-132) on experimental osteoporosis in rats.
Fujii A, Kuboyama N, Yamane J, Nakao S, Furukawa Y
Department of Pharmacology, Nihon University School of Dentistry, Chiba,
1. The therapeutic effect of organic germanium compound, 2-carboxyethyl germanium sesquioxide (Ge-132), for experimental osteoporosis was studied using ovariectomized rats maintained on a low calcium containing diet. 2. Serum calcitonin (sCT) level was decreased and serum parathyroid hormone (sPTH) level was increased by ovariectomy and the decrement and increment rates, respectively, were reduced by administration of Ge-132. Thus, the sCT/sPTH ratio was greater in the groups given Ge-132, indicating that the resorption was somehow inhibited by Ge-132. 3. The transverse strength of femur bone was significantly enhanced by Ge-132. 4. A trend was found in the group given Ge-132 for a larger femur cortical bone index. 5. The relative femur bone wet weight was greater in the group given Ge-132. 6. These results indicate that Ge-132 prevents decreased bone strength, and affects the femur cortical bone index, and bone mineral mass caused by osteoporosis.
Inhibitory effect of Germanium (IV) sodium ascorbate on the in vitro reverse transcriptase of Human immunodeficiency virus
A.M. Badawi, in Metal Ions in Biology and Medicine. Eds. Ph. Collery, LA. Poirier, M. Manfait, J.C. Etienne. John Libbey Eurotext, Paris 0 1990, pp. 517-519
Department of Application, Petroleum Research Institute, Nasr City, Cairo, Egypt
Many factors involved in host resistance to acquired immune deficiency syndrome (AIDS) might be significantly dependent upon the availability of ascorbate. Ascorbic acid was investigated for its inactivation of bacterial viruses (Murata, 1974; Murata et al., 1975). The mechanism of in vitro viral inactivation is still unclear. It was postulated that free-radical intermediates produced during ascorbate oxidation are the active agents in viral inactivation (Murata, 1975).
Carboxyethyl germanium sesquioxide (Ge-132) was recently disclosed as an oral interferon inducer with antiviral activity (Ishida et al., 1984).
To investigate the possibility that the antiviral activity of ascorbic acid can be potentiated with germanium, it occurred to us to react ascorbic acid with sodium germanate to give the corresponding germanium and sodium ascorbate derivative (GeNaA).
The resulting compound was submitted to U.S. Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, Maryland, U.S.A., for reverse transcriptase (RT) assay for human immunodeficiency virus (HIV). GeNaA was found to significantly inhibit in vitro RT suggesting AIDS-retarding activity.
The HlV-RT result summery shows that GeNaA inhibited HlV-RT by 50% at approximately 99 mcg/ml, 50 mcg/ml and 20 mcg/ml during three different experiments. The first LD50 value 99 mcg/ml appears to be too high and may be dropped, thus the LD50 will be average of the other two values: 50 and 20 mcg/ml. The investigation presented here demonstrates that GeNaA has a significant inhibitory effect on HIV replication in vitro and might be related to an unclear mechanism of action targeted at RT. Although organic germanium’s properties of oxygen modulation are not yet precisely elucidated (Goodman, 1988), the possible oxygenating effect of germanium and/or dehydroascorbic radical might be responsible for the inhibition of HIV RT enzyme.