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Kazuhiko Asai, a Japanese researcher, helped establish the Coal Research Foundation in 1945, from which came most of the early work on germanium. Research and painstaking analysis, in those days without sophisticated equipment, established the existence of germanium in Japanese coal, predominantly in the woody section, or vitrit.
Dr. Asai, intuited that germanium in coal was from the plant matter not from the surrounding soil, which led to a whole series of experiments investigating the germanium content in plants known to be therapeutic in Chinese medicine, such as shelf fungus, ginseng, Wisteria gall, and other health promoting foods, including aloe, comfrey and garlic. Asai found a high germanium content in these plants and hypothesized that germanium plays important roles in the photo-electrochemical process of photosynthesis, the metabolism and self defense process of these plants.
Inorganic forms had been extracted from coal for use by the electronics industry, and now Asai's group set out to do the reverse: to convert the extracted inorganic germanium into an organic form. This was finally achieved in November 1967, by which time Asai himself was suffering from severe rheumatoid arthritis. He tested the organic germanium on his condition, which, within ten days, had disappeared.
Organic germanium is a naturally occurring substance and is non-toxic, though one strain of manufactured germanium has been shown to cause some transient nervous side effects.
It is easily absorbed and eliminated from the body without undergoing metabolic alteration, and administered orally, has also been shown to be ubiquitously distributed in all organs - there are no specific target organs, and no differences in distribution patterns between the sexes. It leaves no residual concentration after 12 hours in the body, and is excreted, unchanged metabolically, in the urine in 24 hours.
The only report of a death occurred in a woman who had been taking a germanium compound of 600mg per day over 18 months and died of renal failure. Analysis of the compound revealed mainly germanium dioxide, with some organic germanium and an autopsy revealed gross cellular abnormalities of kidney tissues and an increased accumulation of germanium in several organs. However, it was not possible to determine whether germanium caused the renal failure, or whether the renal failure caused the accumulation of germanium, since it is eliminated mainly by the kidneys.
Germanium occurs in trace amounts in most foods, but in higher concentrations only in clams, canned tuna, and baked beans. Analysis has revealed only trace amounts in plants used for Chinese medicine.
Il Germanio ha una struttura chimica ordinatissima, molto simile alla Grafite e al Silicio.
In elettronica veniva usato prima della Silice, poi abbandonato per la sua antieconomicità, ora é tornato in uso.
L’altro uso é in medicina, nella terapia dei tumori allo stomaco. Anche se in realtà non é così miracoloso.
Chimicamente ha qualità intermedie fra il Silicio e lo Stagno.
Ha molte indicazioni per patologie molto distruttive.
Alimenti che contengono molto GERMANIO SONO I PESCI, IN MODO PARTICOLARE IL TONNO.
J Gastroenterol. 2003;38(6):525-32.
Propagermanium: a nonspecific immune modulator for chronic hepatitis B.
Hirayama C, Suzuki H, Ito M, Okumura M, Oda T.
Second Department of Medicine, Faculty of Medicine, Tottori University, Yonago, Japan.
Although antiviral agents have been adopted for the management of chronic hepatitis B, they have only limited efficacy because of the underlying impaired immune status. Propagermanium, a hydrophilic polymer of 3-oxygermyl propionate, has been reported to have potent immune modulatory activity associated with antiinflammatory and antineoplastic properties. For example, propagermanium augments lymphocyte functions in CD4 and CD8 cells, and in natural killer (NK) cells, and induces the production of several cytokines. A controlled pilot study of 16-week treatment with propagermanium for chronic hepatitis B (of moderate and mild grades on hepatic histology) revealed a sustained clearance of hepatitis B e (HBe) antigen and a favorable biochemical response at week 16 of treatment and at week 48 post-treatment. An open study also supported the clearance of hepatitis B virus from the blood and the possible improvement of histologic grading in the liver. There were few adverse events. A postmarketing survey, however, revealed the occurrence of moderate to severe liver damage after the treatment in about 4% of patients. Despite the exact nature of the liver damage being unclear, a putative cause is the swift removal of virus-infected hepatocytes by an immune reaction through the treatment. A subtle balance between host and viral conditions is the factor which most determines hepatitis B virus persistence. The rationale for a nonspecific immune modulator for the treatment of chronic hepatitis B will be the restoration of cellular immune responsiveness to viral infection. Although the cellular immunity for hepatitis B virus prior to the treatment should be studied, adequate observation of hepatic functions and viral markers in the recipients is clinically useful to predict liver failure during the treatment. In summary, the propagermanium regimen offers a potent and safe approach that is cost-effective for appropriate chronic hepatitis B patients with reserve hepatic capacity, and will provide new perspectives for immune therapy in chronic hepatitis B.
Mutat Res. 1997 Dec;387(3):141-6.
Mutagenicity, carcinogenicity and teratogenicity of germanium compounds.
Gerber GB, Leonard A.
Teratogenicity and Mutagenicity Unit, Catholic University of Louvain, Brussels, Belgium.
The metalloid germanium has found widespread application in electronics, nuclear sciences and in medicine. General toxicity of germanium is low, except for the tetrahydride germane, and few observations on toxicity of germanium in man exist. Germanium is not carcinogenic and even appears to inhibit cancer development and, in the form of the organic germanium compound, spirogermanium, to destroy cancer cells. Germanium compounds have no mutagenic activity and may, under certain conditions, inhibit the mutagenic activity of other substances. High doses of germanium may result in an increased embryonic resorption, but possible malformations have been reported only after administration of dimethyl germanium oxide to pregnant animals. Germanium may thus be considered an element of rather low risk to man.
Regul Toxicol Pharmacol. 1997 Jun;25(3):211-9.
Hazard assessment of germanium supplements.
Tao SH, Bolger PM.
Center for Food Safety and Applied Nutrition, Food and Drug Administration, Washington, DC 20204, USA.
Germanium-containing dietary supplements became popular in the 1970s in Japan and later in other countries, as elixirs for certain diseases (e.g., cancer and AIDS). Germanium is not an essential element. Its acute toxicity is low. However, at least 31 reported human cases linked prolonged intake of germanium products with renal failure and even death. Signs of kidney dysfunction, kidney tubular degeneration, and germanium accumulation were observed. Other adverse effects were anemia, muscle weakness, and peripheral neuropathy. Recovery of renal function is slow and incomplete even long after germanium intake was stopped. The total dose of ingested germanium (as dioxide, carboxyethyl germanium sesquioxide, germanium-lactate-citrate, or unspecified forms) varied from 15 to over 300 g; the exposure duration varied from 2 to 36 months. In laboratory animals, elevated germanium in tissues and impaired kidney and liver function were observed in a life-time drinking water (5 ppm germanium) study. Other toxicities associated with ingested germanium products in human cases were also demonstrated in animal studies with germanium dioxide and sometimes other germanium compounds. Based on the evidence of persistent renal toxicity associated with germanium dioxide, the lack of conclusive findings of differential nephrotoxicity of organic germanium compounds, and the possibility of contamination of the organic germanium products with inorganic germanium, it is clear that germanium products present a potential human health hazard.
Biol Trace Elem Res. 1991 Jun;29(3):267-80.
Nephrotoxicity and neurotoxicity in humans from organogermanium compounds and germanium dioxide.
Life Sciences Division, American Institute for Biosocial Research, Inc., Tacoma, WA 98401.
There is no known biological requirement for germanium (Ge), germanates, or any organogermanium compound. Ge deficiency has not been demonstrated in any animal. The estimated average dietary intake of Ge in humans is 1.5 mg/d. Ge is widely distributed in edible foods, all of which, with few exceptions, contain less than 5 ppm Ge, since higher levels are toxic to most plants. Ingestion of Ge compounds has been shown to produce toxic effects in experimental animals. In recent years inorganic germanium salts and novel organogermanium compounds, such as carboxyethyl germanium sesquioxide (Ge-132) and lactate-citrate-germanate (Ge lactate citrate) have been sold as "nutritional supplements" in some countries for their purported immunomodulatory effects or as health-producing elixirs, resulting in intakes of Ge significantly exceeding the estimated average dietary intake. Since 1982, there have been 18 reported cases of acute renal dysfunction or failure, including two deaths, linked to oral intake of Ge elixirs containing germanium dioxide (GeO2) or Ge-132. In these cases, biopsies show vacuolar degeneration in renal tubular epithelial cells, without proteinuria or hematuria, in the absence of glomerular changes. Serum creatinine levels have been well above 400 mumol/L in such patients. In 17 of 18 cases, accumulated elemental Ge intakes reportedly ranged between 16 to 328 g over a 4-36 mo period, or between 100 to 2000 times the average estimated dietary intake for human. In surviving patients, renal function improved after discontinuation of Ge supplementation. However, in no case was recovery complete. One organogermanium compound, an azaspiran organogermanium compound, 2-aza-8-germanspiro[4,5] decane-2-propamine-8,8-diethyl-N,N-dimethyl dichloride (spirogermanium), has been found to cause both neurotoxicity and pulmonary toxicity in phase I and II studies examining its chemotherapeutic potential as an antitumor drug in the treatment of various malignancies. In cancer patients given the drug spirogermanium, 40% experienced marked, yet transient neurotoxicity. Two patients suffered from pulmonary toxicity. Results of phases I and II human cancer trials for spirogermanium have not been favorable, with the exception of moderate benefits for three types of malignancies. It is recommended that patients exposed to long-term (greater than 3 mo) Ge supplementation at levels well above the estimated daily intake be medically supervised and monitored for potential renal-, pulmonary- or neurotoxicity. Further study regarding the mechanism of Ge-induced nephrotoxicity in human is warranted.
No To Shinkei. 1990 Sep;42(9):851-6.
[A case of inorganic germanium poisoning with peripheral and cranial neuropathy, myopathy and autonomic dysfunction]
Iijima M, Mugishima M, Takeuchi M, Uchiyama S, Kobayashi I, Maruyama S.
Department of Neurology, Tokyo Women's Medical College, Japan.
A 51-year-old man, taking beverage containing inorganic germanium (Ge), (90-100 mg/day, total 70 g) for two years, developed body weight loss, anemia, renal dysfunction, peripheral neuropathy, myopathy, autonomic dysfunctions and multiple cranial nerve palsies. Serum CK, GOT, LDH, BUN, and creatinine levels were elevated. The cerebrospinal fluid showed albumino-cytologic dissociation. Sural nerve biopsy showed axonal degeneration, and peroneal muscle biopsy showed neurogenic changes including type 2 fiber atrophy and ragged red fibers. High level of Ge content was detected from the hair and nail by inductively coupled plasma atomic emission spectrometry. Despite discontinuation of Ge taking, the peripheral neuropathy and autonomic dysfunction progressed. The symptoms remained unchanged even in the treatment with prednisolone. These findings suggest that inorganic Ge has a serious irreversible multiple system toxicity.