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Dangers of cesium chloride for cancer
Hveragerthi Views: 8,565
Published: 11 years ago

Dangers of cesium chloride for cancer

There has been a lot of talk about cesium chloride for the treatment of cancer.  I have not seen any proof of effectiveness, and no talk about the dangers, including death.  So I am going to address these here.  As for effectiveness it has been claimed to be highly effective against all cancers.  So how do they explain this study?

Zero efficacy with cesium chloride self-treatment for brain cancer

Samadani U, Marcotte P. Mayo Clin Proc. 2004 Dec;79(12):1588


Safety is also a big concern as the side effects can not only be very dangerous, but deaths have been reported as well.

Cesium-induced QT-interval prolongation in an adolescent.

Pharmacotherapy. 2008 Aug;28(8):1059-65.

Acquired long QT syndrome and monomorphic ventricular tachycardia after alternative treatment with cesium chloride for brain cancer.

Mayo Clin Proc. 2004 Aug;79(8):1065-9.

Blood and tissue concentration of cesium after exposure to cesium chloride: a report of two cases.

Biol Trace Elem Res... 2003 Aug;94(2):97-104

RESULTS: High levels of cesium were found in brain, liver, kidney, bile, gastric content, and whole blood collected at autopsy as compared to reference levels. The administration of cesium chloride resulted in blood levels a factor of 1100 higher than normal. The highest Cs concentrations were found in the liver (1029 microg/g, dry wt), followed by the kidney (815 microg/g, dry wt) and brain (219 microg/g, dry wt). CONCLUSION: The high accumulation in the liver suggests that hepatotoxicity from Cs might be an initial presenting symptom in Cs-poisoning cases. This is the first report describing two cases with high Cs levels in human tissues.

Cesium toxicity: a case of self-treatment by alternate therapy gone awry.

Cesium salts have been used in animal models to induce cardiac arrhythmias for several decades, but the sequelae of human cesium toxicity have seldom been described. The authors describe a case of cesium toxicity manifested by syncope, polymorphic ventricular tachycardia, hypokalemia, and a QT interval prolonged to 650 milliseconds that resolved over 4 days following withdrawal of cesium. The patient had a 2-year history of colon cancer and had self-treated with cesium chloride, 3 g/d, for several weeks, using cesium as a form of alternate therapy for cancer. The authors describe the pathophysiologic correlates and risks of cesium consumption and conclude that cesium toxicity should be considered among the differential diagnoses of prolonged QT interval.

Acquired long QT syndrome secondary to cesium chloride supplement.

“The use of complementary medication is on the rise worldwide. More often than not, the treating physicians are unaware of this and also unfamiliar with the potential benefit or toxicity of the agents. Here, we present the case of a 39-year-old woman who presented with new onset of syncope as a result of acquired long QT syndrome secondary to taking a cesium chloride supplement. A brief discussion of the pathophysiology of this agent follows the case presentation.

Cesium chloride induced ventricular arrhythmias in dogs: three dimensional activation patters and their relation to the cesium dose applied.

Cesium-induced atrial tachycardia degenerating into atrial fibrillation in dogs: atrial torsades de pointes?

Three-dimensional activation sequence of cesium-induced ventricular arrhythmias.

Relative protection given by extract of Phyllanthus emblica fruit and an equivelant amount of vitamin C against known clastogen—caesium chloride

Aqueous extracts of Phyllanthus emblica L. fruit and an equivalent amount of vitamin C were administered orally by gavage to laboratory-bred Swiss albino mice for 7 days in order to evaluate the protection afforded by the two extracts against clastogenic effects of different doses of caesium chloride (CsCl) on bone marrow cells of Mus musculus in vivo. Both pretreatments significantly reduced the frequency of chromosome aberrations induced by CsCl given at three different doses, indicating that vitamin C, an essential component of P. emblica extract, was the effective agent in protecting against the clastogenicity of the metal salt.


The reason that they have to prevent clastogenicity of cesium chloride is because clastogencity refers to breakage of chromosomes. This is one of the contributing factors to the formation or cell damage and cancer.

Inhibition of clastogenic effects of cesium chloride in mice in vivo by chlorophyllin.

The antagonistic effect of chlorophyllin was tested in reducing the clastogenic action of cesium chloride (CsCl) in vivo on mice bone marrow cells. CsCl induced chromosomal aberration in frequencies directly proportional to the dose administered. Chlorophyllin, when given alone, was not clastogenic even at a concentration of 1.5 mg/kg body wt. of the animal. Simultaneous administration of chlorophyllin and CsCl reduced chromosomal aberrations significantly at 24 h. Exposure to the same dose of chlorophyllin 2 h before exposure to CsCl also decreased clastogenic effects but to a lesser extent. These findings are of importance in view of the uptake of radioactive Cs by green plants after nuclear fallout.

Comparative efficacy of chlorophyllin in reducing cytotoxicity of some heavy metals.

The potential of chlorophyllin in reducing clastogenicity was studied against two concentrations of each of three potent metallic clastogens (cesium chloride, mercuric chloride and cobalt chloride) in bone marrow cells of mice in vivo. The respective salts and chlorophyllin were administered orally to mice by gavaging in different combinations. Simultaneous administration of chlorophyllin with both concentrations of each salt reduced the clastogenic effects in the order Cs greater than Hg greater than Co. Chlorophyllin could not decrease the clastogenic effects when administered 2 h before the salts.

Modification of cesium toxicity by calcium in mammalian system.

The interaction between cesium chloride CsCl and calcium chloride CaCl2 was observed in bone marrow chromosomes of mice. The two salts were administered orally to laboratory bred Swiss albino mice in vivo singly or one followed by the other, or both simultaneously. CsCl induced chromosomal aberrations in frequencies directly proportional to the dose administered. The frequency of aberrations was reduced significantly when the two chemicals were administered simultaneously or when CaCl2 was given 2 h before CsCl. Thus, CaCl2 is able to protect against the cytotoxicity of CsCl.

Cytogenetic damage induced in vivo to mice by single exposure to cesium chloride.

Female laboratory bred albino mice (2n = 40) were orally administered cesium chloride (CsCl) in aqueous solution as a single dose and the damage induced at the chromosomal level was observed in bone marrow cells after 6, 12, 18, and 24 hours of exposure. The concentrations of the chemical given were calculated as fractions of the LD50, namely 1/5, 1/10, and 1/20. The cytogenetic endpoints screened for were chromosomal aberrations (CA) and divisional frequency or mitotic index (MI). The frequency of chromosomal aberrations induced was directly proportional to the concentration of the chemical administered. The highest dose was the most toxic and was considered to be the maximum tolerance level. Effects on divisional frequency were variable, the highest concentration being significantly mitostatic, the middle one ineffective, and the lowest slightly mitogenic. In general, the observations indicate that CsCl is clastogenic when administered orally to mice in vivo and the effects are dose-dependent.

Clastogenic effects of cesium chloride on mouse bone marrow cells in vivo.

Clastogenic effects of cesium chloride (CsCl) on mouse bone marrow cells in vivo following oral administration were studied after 24 h. The incidence of chromosome aberrations increased linearly with increasing concentrations of the chemical from 1/20th to 1/5th of the LD50. The frequency of cell division was also enhanced by the lower doses but higher doses were mitostatic. This report is the first on the clastogenicity of cesium on animals.

Note the quote “The frequency of cell division was also enhanced by the lower doses”. Last thing you should do with cancer is enhance cellular division, which is what cancer basically is. Cells dividing at an abnormally fast rate. Higher doses stop this division, but as we have seen from the other studies the toxicity of cesium increases with dose. Toxic reactions from cesium chloride use can include heart rhythm abnormalities and death.

Early and delayed afterdepolarizations associated with cesium chloride-induced arrhythmias in the dog.

Cardiovascular and metabolic effects of caesium chloride injection in dogs—limitations as a model for the long QT syndrome.

The morphological features of these caesium induced ventricular tachyarrhythmias, their response to overdrive pacing, and their occurrence despite substantial hyperkalaemia are quite different from the properties of the clinical long QT syndrome, which is overdrive suppressible, favoured by hypokalaemia, and rarely degenerates to ventricular fibrillation.”

A toxicology evaluation of postnatal maternal exposure to cesium.

The effect of postnatal maternal exposure to CsCl on the newborn was studied in the mouse. Maternal ingestion of 1 mEq CsCl solution as the only drinking fluid began immediately after birth and the offspring were breast-fed until weaning. They were then separated from the nursing dams and remained Cs free for a subsequent 2 weeks prior to sacrifice. Maternal Cs exposure decreased the weanling body weight from controls and they attained normal body weight after 2 weeks of Cs-free period during development. Maternal Cs ingestion caused a reduction in offspring brain weight of both sexes compared to controls. The kidney weight of the developing female, but not male, offspring was also decreased from controls as a consequence of maternal Cs exposure. The offspring's hepatic alcohol and aldehyde dehydrogenase were not altered from controls as a function of maternal exposure to Cs salt. Little changes occurred in offspring heart lactate dehydrogenase by the maternal Cs treatment. The results suggest that maternal Cs exposure during breast-feeding affected body weight and the CNS of the offspring. The change noted in weanling kidney weight was sex dependent. These gross pathological changes in weanling organ weight were not apparent when maternal breast-feeding was eliminated. The data indicates that Cs adversely affected the newborn which was eliminated after cessation of the Cs exposure.

Magnesium suppression of early afterdepolarizations and ventricular tachyarrhythmias induced by cesium in dogs.

Cesium induced sustained monomorphic ventricular tachycardia, torsades de pointes, or ventricular fibrillation in 12 of 13 dogs before magnesium infusion, and in eight of 11 dogs 1 to 2 hr after stopping infusion, but in only three of 13 dogs during magnesium infusion.


For those not familiar with ventricular tachycardia, torsades de pointes, and ventricular fibrillation, these are VERY dangerous heart rhythm abnormalities.

Effect of cesium and potassium salts on survival of rats bearing Novikoff hepatoma.

Rats treated with CsCl for 12 consecutive days prior to or immediately after inoculation with 1.0 ml of viable hepatoma cell suspension showed an increase in mortality score from corresponding controls.

Effect of cesium and ethanol on tumor bearing rats.


The results indicate potentiation of the hepatoma toxicity by CsCl which may be minimized by ethanol.



Bottom line is that cesium chloride has not been demonstrated to have anti-cancer activity against all cancers as is being claimed.  But study after study has shown a high potential for toxicity, especially on the heart, and possibly even death.  There are so many safe treatments for cancer out there that I personally would avoid getting anywhere near this dangerous therapy.


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