Many homeopaths recently suggest VANADIUM 30 as a remedy for oxygen deficiency in blood during the current Covid 19 pandemic. This suggestion is based on the statements in some homeopathic materia Medica works regarding the “oxygen carrier” capacity of vanadium.
First of all, let us see what is said in Boericke Materia Medica about Vanadium:
“Its action is that of an oxygen carrier and a catalyzer, hence its use in wasting diseases. Increases amount of hemoglobin, also combines its oxygen with toxines and destroys their virulence. Also increases and stimulates phagocytes. A remedy in degenerative conditions of the liver and arteries.
Anorexia and symptoms of gastro intestinal irritation; albumen, casts and blood in urine. Tremors; vertigo; hysteria and melancholia; neuro-retinitis and blindness. Anaemia, emaciation. Cough dry, irritating and paroxysmal, sometimes with haemorrhages. Irritation of nose, eyes and throat. Tuberculosis, chronic rheumatism, diabetes.
Acts as a tonic to digestive function and in early tuberculosis. Arterio-sclerosis, sensation as if heart was compressed, as if blood had no room in the aorta. Anxious pressure on whole chest. Fatty heart. Degenerative states, has brain softening. Atheroma of arteries of brain and liver.
Dose: 6-12 potency. The best form is Vanadiate of Soda, 2 mg daily, by mouth.”
Clarke’s Dictionary of Materia Medica says about Vanadium as follows :
“Addison’s disease. Atheroma. Fatty degeneration. Innutrition.
Burnett tells how he came to use Vanadium through reading the result of some experiments on animals in which the Salts of Vanadium produced “true cell destruction, the pigment escaping, the liver being hit hardest.” Burnett had at the time a case of “fatty liver, atheroma of the arteries, much pain corresponding to the course of the basilar artery, large, deeply pigmented patches on forehead, profound adynamia.” Vanadium restored the patient, who was seventy, and at eighty he was “hale and hearty.” Marc Jousset tells of experiments with salts of Vanadium, chiefly the meta-vanadate of sodium, by Lyonnet and others. Animals poisoned by intravenous injections rapidly develop Cheyne-Stokes respiration; with little or no action on circulation or blood. These observers gave Vanadates to two hundred patients suffering from tuberculosis, chlorosis, chronic rheumatism, neurasthenia etc, and produced in nearly all cases increased appetite, strength, and weight. The amount of urea was also increased. They regard Vanadium as “an energetic excitant of nutrition,” and probably an oxydent stimulating organic combustion. The dose was 2-5 mgr. in twenty-four hours, and only on three separate days in the week.”
Obviously, Boericke and Clarke were saying about the use of “2-5 mg of Sodium Vanadate daily”. Not Vanadium 30! It makes a big difference.
Sodium vanadate is the inorganic compound with the chemical formula Na3VO4·2H2O (sodium orthovanadate dihydrate). It is a colorless, water-soluble solid.
Vanadates exhibit a variety of biological activities, in part because they serve as structural mimics of PHOSPHATES. By this mimicking, it acts as a COMPETITIVE INHIBITOR of ATPases, alkaline and acid phosphatases, and protein-phosphotyrosine phosphatases. By this competitive relationship VANADIUM acts as a SIMILIMUM for many disease conditions involving inhibitions of ATPases by various endogenous or exogenous pathogenic molecules having phosphate functional groups or moieties.
ATPases adenylpyrophosphatase, ATP monophosphatase, triphosphatase, SV40 T-antigen, adenosine 5′-triphosphatase, ATP hydrolase, complex V (mitochondrial electron transport), (Ca2+ + Mg2+)-ATPase, HCO3−-ATPase, adenosine triphosphatase) etc are a class of enzymes that catalyze the decomposition of ATP into ADP and a free phosphate ion or the inverse reaction. This dephosphorylation reaction releases energy, which the enzyme (in most cases) harnesses to drive other chemical reactions that would not otherwise occur. This process is widely used in all known forms of life
Transmembrane ATPases import many of the metabolites necessary for cell metabolism and export toxins, wastes, and solutes that can hinder cellular processes.
All the symptoms described by Boericke and Clarke are actually due to this inhibitory actions of vanadites upon the various enzymes listed above, which lead to blocking of all biological pathways associated with involvement of PHOSPHATES.
Please understand, Vanadium potentized above 12c used in homeopathy will not contain even a single molecule or atom of Vanadium. It contains only MOLECULAR IMPRINTS of vanadium, and hence, will act just opposite to the actions of Molecular or crude forms of Vanadium. These Molecular imprints actually act by removing the molecular inhibitions caused in the various enzymes by Vanadium or any other pathogenic molecules having functional groups similar to vanadites or phosphates.
Obviously, Vanadium 30 will not supply oxygen to the tissues as some homeopaths wrongly believe, but may be useful in deactivating harmful reactive oxygen species or ROS generated in the body during the disease processes.
Even though Boericke and Clarke talks about use of “Vanadium Vanadate 2-5 mg daily” for therapeutic purposes, as per advanced scientific knowledge, vanadium is not a safe substance for human consumption.
Vanadium excess can be toxic and detrimental to human health like any other metal. For instance, occupational inhalation exposure to vanadium was found to induce acute respiratory symptoms, DNA damage in blood cells of workers from a vanadium pentoxide factory, and altered neurobehavioral functions. In turn, environmental overexposures to vanadium oxides attached to fine particulate matter were associated with increased risk of respiratory symptoms in children, and a higher risk of cardiovascular and respiratory hospitalizations of older people. ilRecently, urinary vanadium concentrations during pregnancy were positively associated with impaired fetal growth and preterm or early-term delivery. Association between the high level of trace elements including vanadium in the drinking water and the increased thyroid cancer incidence was suggested. A suicidal death after ingestion of an undetermined amount of ammonium vanadate has also been reported. In addition, laboratory-based studies conducted in animal models or cell cultures found that vanadium exposure can induce a variety of toxic effects such as cardiovascular effects, vascular endothelial dysfunction and arterial hypertension, immune toxicity, damage to the spleen and thymus, neurotoxicity, hippocampal alterations and memory loss, developmental disturbances, increased embryolethality and skeletal defects, and pulmonary toxicity. It should be added that, besides the dose of vanadium and the route of vanadium exposure, many other factors such as the form of vanadium (inorganic versus organic forms) and interactions with other elements such as selenium or magnesium can also influence vanadium toxicity.
Along with the studies of the toxic effects of vanadium, many investigators have been focused on the examination of potential medical applications of this mineral. These include antidiabetic or insulin-mimetic actions, antiviral effects, and anticarcinogenic activity. Among these effects, the antidiabetic action of vanadium complexes with organic ligands has been very intensively studied, which entered into stage II clinical trials. However, due to kidney problems in some patients, this study as an antidiabetic agent could not progress to the next phase of research. Indeed, the risks associated with vanadium intoxication such as vanadium-induced reactive oxygen species generation, adverse effects on the immune system, and a risk of mutagenesis are listed among the arguments against the antidiabetic application of vanadium. Reviews of the results of past and recent human studies on vanadium in diabetes have concluded that the use of vanadium compounds in oral diabetes therapy is misplaced.
Vanadium occurs as a natural component of the earth crust in various minerals, coal, and crude oil, and is released to the environment mainly due to human activities. The unique chemical and physical features of vanadium compounds make it an indispensable material in many industries. Its compounds are frequently used in the production of steel and titanium-aluminum alloys, as catalysts in the sulfuric acid manufacture, and in the production of pigments, inks, and varnishes. The latest use of vanadium involves green technologies and the production of vanadium-based redox flow batteries, which can store electricity produced from renewable sources such as wind or sun. The industrial use of vanadium is on the increase and so is the release of vanadium to the environment. Vanadium is one of the elements listed on the second drinking water contaminant candidate list that was announced by the United States Environmental Protection Agency in 2005. This is a list of contaminants that are known or anticipated to occur in public water systems and may require future regulations. Vanadium was reported to contribute to soil pollution. Heavy oil combustion contributes to the release of vanadium as a component adhering to fine particulate matter observed in large urban and industrial agglomerations. High groundwater concentrations of vanadium of natural geological sources have been noted in volcanic areas. Vanadium excess can be toxic and detrimental to human health like any other metal. For instance, occupational inhalation exposure to vanadium was found to induce acute respiratory symptoms, DNA damage in blood cells of workers from a vanadium pentoxide factory, and altered neurobehavioral functions. In turn, environmental overexposures to vanadium oxides attached to fine particulate matter were associated with increased risk of respiratory symptoms in children, and a higher risk of cardiovascular and respiratory hospitalizations of older people. Recently, urinary vanadium concentrations during pregnancy were positively associated with impaired fetal growth and preterm or early-term delivery. Association between the high level of trace elements including vanadium in the drinking water and the increased thyroid cancer incidence was suggested. A suicidal death after ingestion of an undetermined amount of ammonium vanadate has also been reported. In addition, laboratory-based studies conducted in animal models or cell cultures found that vanadium exposure can induce a variety of toxic effects such as cardiovascular effects, vascular endothelial dysfunction and arterial hypertension, immune toxicity, damage to the spleen and thymus, neurotoxicity, hippocampal alterations and memory loss, developmental disturbances, increased embryolethality and skeletal defects, and pulmonary toxicity. It should be added that, besides the dose of vanadium and the route of vanadium exposure, many other factors such as the form of vanadium (inorganic versus organic forms) and interactions with other elements such as selenium or magnesium can also influence vanadium toxicity.
Along with the studies of the toxic effects of vanadium, many investigators have been focused on the examination of potential medical applications of this mineral. These include antidiabetic or insulin-mimetic actions, antiviral effects, and anticarcinogenic activity. Among these effects, the antidiabetic action of vanadium complexes with organic ligands has been very intensively studied, which entered into stage II clinical trials. However, due to kidney problems in some patients, this study as an antidiabetic agent could not progress to the next phase of research. Indeed, the risks associated with vanadium intoxication such as vanadium-induced reactive oxygen species generation, adverse effects on the immune system, and a risk of mutagenesis are listed among the arguments against the antidiabetic application of vanadium. Reviews of the results of past and recent human studies on vanadium in diabetes have concluded that the use of vanadium compounds in oral diabetes therapy is misplaced. Vanadium compounds have attracted interest of researchers as potential antitumor agents. Vanadium as vanadyl sulfate has been used by weight training athletes as a nutritional supplement that can increase muscle mass. The role of vanadium in muscle development has been emphasized to be associated with its insulin-mimetic properties and anabolic effects. So far, however, human studies have failed to demonstrate significant effects of vanadium on the body composition and performance enhancement, and the use of vanadium as a sport nutrition supplement is not recommended. Vanadium is also a well-known constituent of the most commercialized titanium alloy named Ti-6Al-4V, which has been widely used in the manufacture of biomedical implants such as artificial hip joints, knee joints, and dental implants due to its excellent physical and mechanical properties. Again, however, the potential cytotoxicity of vanadium limits the medical value of the Ti-6Al-4V alloy. Recently, for example, a case of systemic allergic dermatitis to vanadium has been reported in a patient following placement of a titanium alloy plate in the left foot. Summing up, due to the intensive use of vanadium in industry and the vanadium environmental pollution often related with it as well as the popularity of vanadium-based dietary supplements and medicinal applications of vanadium compounds, increasing numbers of humans are likely to experience the exposure to vanadium compounds in the near future.
Vanadium enters the human body via the gastrointestinal tract or respiratory system. In the bloodstream, transferrin is the major serum protein of vanadium transport from blood into tissues. Other serum proteins, i.e., albumin, hemoglobin, and immunoglobulin, and low-molecular ligands, e.g., lactate and citrate, can be involved in the blood transport of vanadium as well. From the blood, vanadium is transferred to different tissues such as the liver, kidney, heart, spleen, brain, and bones. Final excretion of absorbed vanadium occurs through urine. In the human body, vanadium can exist in oxidation state +5 (vanadate ions) or +4 (vanadyl cations). Cellular uptake of vanadium species proceeds via receptor-mediated endocytosis of vanadium-laden proteins (transferrin, albumin), phosphate or sulfate ion channels, or membrane citrate transporters. Reductants, e.g., glutathione, ascorbic acid, or NADH, convert pentavalent vanadium to a tetravalent state, the latter being regarded as a predominant oxidation state of vanadium within the cell. Simultaneously, oxidants such as NAD+, O2, and O22- can oxidize vanadyl back to vanadate.
Metabolic detoxification of vanadium possibly involves reduction of vanadate to vanadyl by cellular reductants, and complexation reactions during which vanadyl interacts with cellular agents such as reduced glutathione (GSH), an oxidized form of glutathione (GSSG), L-cysteine, and cystine forming stable, nonharmful complexes. In addition, vanadium accumulates in bones by replacing bone phosphate in apatite Ca5(PO4)OH with vanadate. The storage of vanadium in bones is also recognized as a potent detoxification mechanism of vanadium in animals.
In contrast to the aforementioned chelating compounds, ascorbic acid was suggested to be a very effective and safe pharmacologic agent for the treatment of vanadium toxicity in humans. Detoxification of vanadium by ascorbic acid mainly relies on ascorbic acid-mediated reduction of vanadate to vanadyl and its high capacity to scavenge reactive oxygen species. Furthermore, vanadyl was found to interact with oxidation products of ascorbic acid forming stable complexes, which may allow excretion of vanadium from the organism. In addition, the results of studies have shown that pyruvic acid could be another potential antidote for the treatment of vanadium toxicity. The studies showed that this alpha-keto acid protected against vanadium-induced oxidative stress and cytotoxicity in a cell culture model. The mechanism of protection probably involves antioxidative effects of pyruvate, especially its ability to neutralize hydrogen peroxide, but still more research is required to elucidate this issue.
It is well known that many edible plants are the main source of natural compounds acting as exogenous antioxidants. Exogenous antioxidants cannot be produced in the body and therefore must be provided through daily nutrition. They reinforce our intrinsic antioxidant system in the protection of the organism against reactive oxygen species-mediated injuries. As shown below in this review, research studies indicate that vanadium toxicity, which is strongly associated with prooxidant mechanisms, can be efficiently reduced or alleviated by dietary and plant-derived antioxidants.
Very early studies already explored the efficiency of vitamin C (ascorbic acid, ascorbate) in the prevention and treatment of vanadm toxicity, and found that vitamin C was effective against acute vanadate and vanadyl intoxication.
Some studies focused on the role of vitamin E (α-tocopherol) in the treatment of vanadium toxicity, which provided in vivo evidence that vitamin E acetate decreased sodium metavanadate-induced oxidative stress and histopathological changes in the testes of rats. Furthermore, vitamin E was demonstrated to exhibit protective activity against sodium metavanadate-mediated neurotoxicity in rat pups. In this study, vitamin E increased performance in neurobehavioral tests, and decreased reactive astrogliosis in brain tissue of vanadium-treated animals. Both vitamins C and E exhibited protective activity against vanadium pentoxide-induced genotoxicity measured using a micronucleus assay in mouse polychromatic erythrocytes.
In addition, polyphenolic compounds (and other phytochemicals) may prove beneficial for the treatment of vanadium toxicity.
In conclusion, although the investigations cited in this review show that supplementation with dietary antioxidants has beneficial effects on vanadium poisoning.
First of all, let us see what is said in Boericke Materia Medica about Vanadium:
“Its action is that of an oxygen carrier and a catalyzer, hence its use in wasting diseases.
Increases amount of hemoglobin, also combines its oxygen with toxines and destroys their virulence. Also increases and stimulates phagocytes. A remedy in degenerative conditions of the liver and arteries.
Anorexia and symptoms of gastro intestinal irritation; albumen, casts and blood in urine. Tremors; vertigo; hysteria and melancholia; neuro-retinitis and blindness. Anaemia, emaciation. Cough dry, irritating and paroxysmal, sometimes with haemorrhages. Irritation of nose, eyes and throat. Tuberculosis, chronic rheumatism, diabetes.
Acts as a tonic to digestive function and in early tuberculosis. Arterio-sclerosis, sensation as if heart was compressed, as if blood had no room in the aorta. Anxious pressure on whole chest. Fatty heart. Degenerative states, has brain softening. Atheroma of arteries of brain and liver.
Dose: 6-12 potency. The best form is Vanadiate of Soda, 2 mg daily, by mouth.”
Clarke’s Dictionary of Materia Medica says about Vanadium as follows :
“Addison’s disease. Atheroma. Fatty degeneration.
Innutrition.Burnett tells how he came to use Vanadium through reading the result of some experiments on animals in which the Salts of Vanadium produced “true cell destruction, the pigment escaping, the liver being hit hardest.” Burnett had at the time a case of “fatty liver, atheroma of the arteries, much pain corresponding to the course of the basilar artery, large, deeply pigmented patches on forehead, profound adynamia.” Vanadium restored the patient, who was seventy, and at eighty he was “hale and hearty.” Marc Jousset tells of experiments with salts of Vanadium, chiefly the meta-vanadate of sodium, by Lyonnet and others. Animals poisoned by intravenous injections rapidly develop Cheyne-Stokes respiration; with little or no action on circulation or blood. These observers gave Vanadates to two hundred patients suffering from tuberculosis, chlorosis, chronic rheumatism, neurasthenia etc, and produced in nearly all cases increased appetite, strength, and weight. The amount of urea was also increased. They regard Vanadium as “an energetic excitant of nutrition,” and probably an oxydent stimulating organic combustion. The dose was 2-5 mgr. in twenty-four hours, and only on three separate days in the week.”
Obviously, Boericke and Clarke were saying about the use of “2-5 mg of Sodium Vanadate daily”. Not Vanadium 30! It makes a big difference.
Sodium vanadate is the inorganic compound with the chemical formula Na3VO4·2H2O (sodium orthovanadate dihydrate). It is a colorless, water-soluble solid.
Vanadates exhibit a variety of biological activities, in part because they serve as structural mimics of PHOSPHATES. By this mimicking, it acts as a COMPETITIVE INHIBITOR of ATPases, alkaline and acid phosphatases, and protein-phosphotyrosine phosphatases.
All the disease conditions described by Boericke and Clarke are actually due to this inhibitory actions of vanadites upon the various enzymes listed above, which lead to blocking of all biological pathways associated with PHOSPHATES.
Please understand, Vanadium potentized above 12c used in homeopathy will not contain even a single molecule or atom of Vanadium. It contains only MOLECULAR IMPRINTS of vanadium, and hence, will act just opposite to the actions of Molecular or crude forms of Vanadium. These Molecular imprints actually act by removing the molecular inhibitions caused in the various enzymes by Vanadium or any other pathogenic molecules having functional groups similar to vanadites or phosphates. Obviously, Vanadium 30 will not supply oxygen to the tissues as some homeopaths wrongly believe, but may be useful in deactivating harmful reactive oxygen species or ROS generated in the body during the disease processes.
Even though Boericke and Clarke talks about use of “Vanadium Vanadate 2-5 mg daily” for therapeutic purposes, as per advanced scientific knowledge, vanadium is not a safe substance for human consumption.
Vanadium excess can be toxic and detrimental to human health like any other metal. For instance, occupational inhalation exposure to vanadium was found to induce acute respiratory symptoms, DNA damage in blood cells of workers from a vanadium pentoxide factory, and altered neurobehavioral functions. In turn, environmental overexposures to vanadium oxides attached to fine particulate matter were associated with increased risk of respiratory symptoms in children, and a higher risk of cardiovascular and respiratory hospitalizations of older people. ilRecently, urinary vanadium concentrations during pregnancy were positively associated with impaired fetal growth and preterm or early-term delivery.
Association between the high level of trace elements including vanadium in the drinking water and the increased thyroid cancer incidence was suggested. A suicidal death after ingestion of an undetermined amount of ammonium vanadate has also been reported. In addition, laboratory-based studies conducted in animal models or cell cultures found that vanadium exposure can induce a variety of toxic effects such as cardiovascular effects, vascular endothelial dysfunction and arterial hypertension, immune toxicity, damage to the spleen and thymus, neurotoxicity, hippocampal alterations and memory loss, developmental disturbances, increased embryolethality and skeletal defects, and pulmonary toxicity. It should be added that, besides the dose of vanadium and the route of vanadium exposure, many other factors such as the form of vanadium (inorganic versus organic forms) and interactions with other elements such as selenium or magnesium can also influence vanadium toxicity.
Along with the studies of the toxic effects of vanadium, many investigators have been focused on the examination of potential medical applications of this mineral. These include antidiabetic or insulin-mimetic actions, antiviral effects, and anticarcinogenic activity. Among these effects, the antidiabetic action of vanadium complexes with organic ligands has been very intensively studied, which entered into stage II clinical trials. However, due to kidney problems in some patients, this study as an antidiabetic agent could not progress to the next phase of research. Indeed, the risks associated with vanadium intoxication such as vanadium-induced reactive oxygen species generation, adverse effects on the immune system, and a risk of mutagenesis are listed among the arguments against the antidiabetic application of vanadium. Reviews of the results of past and recent human studies on vanadium in diabetes have concluded that the use of vanadium compounds in oral diabetes therapy is misplaced.
REDEFINING HOMEOPATHY 