Clinical Effects of Cesium Intake

Abstract

The knowledge about cesium metabolism and toxicity is sparse. Oral intake of cesium chloride has been widely promoted on the basis of the hypothesis referred to as "high pH cancer therapy", a complimentary alternative medicine method for cancer treatment. However, no properly confirmed tumor regression was reported so far in all probability because of neither theoretical nor experimental grounds for this proposal. The aim of the present review was to resume and discuss the material currently available on cesium salts and their applications in medicine. The presence of cesium in the cell does not guarantee high pH of its content, and there is no clinical evidence to support the claims that cancer cells are vulnerable to cesium. Cesium is relatively safe; signs of its mild toxicity are gastrointestinal distress, hypotension, syncope, numbness, or tingling of the lips. Nevertheless, total cesium intakes of 6 g/day have been found to produce severe hypokalemia, hypomagnesemia, prolonged QTc interval, episodes of polymorphic ventricular tachycardia, with or without torsade de pointes, and even acute heart arrest. However, full information on its acute and chronic toxicity is not sufficiently known. Health care providers should be aware of the cardiac complications, as a result of careless cesium usage as alternative medicine.

Full text

Clinical Effects of Cesium Intake
Petr Melnikov &Lourdes Zélia Zanoni
Received: 2 July 2009 /Accepted: 23 July 2009
#Humana Press Inc. 2009
Abstract The knowledge about cesium metabolism and toxicity is sparse. Oral intake of
cesium chloride has been widely promoted on the basis of the hypothesis referred to as
“high pH cancer therapy”, a complimentary alternative medicine method for cancer
treatment. However, no properly confirmed tumor regression was reported so far in all
probability because of neither theoretical nor experimental grounds for this proposal. The
aim of the present review was to resume and discuss the material currently available on
cesium salts and their applications in medicine. The presence of cesium in the cell does not
guarantee high pH of its content, and there is no clinical evidence to support the claims that
cancer cells are vulnerable to cesium. Cesium is relatively safe; signs of its mild toxicity are
gastrointestinal distress, hypotension, syncope, numbness, or tingling of the lips.
Nevertheless, total cesium intakes of 6 g/day have been found to produce severe
hypokalemia, hypomagnesemia, prolonged QTc interval, episodes of polymorphic
ventricular tachycardia, with or without torsade de pointes, and even acute heart arrest.
However, full information on its acute and chronic toxicity is not sufficiently known.
Health care providers should be aware of the cardiac complications, as a result of careless
cesium usage as alternative medicine.
Keywords Cesium .Cardiac effects .Arrhythmias
Introduction
Cesium (Cs) is by no means a novel topic in mineral metabolism. More than 120 years ago,
Sidney Ringer, the scientist who is well known for his isotonic solution resembling with blood
Biol Trace Elem Res
DOI 10.1007/s12011-009-8486-7
Sources of support—FUNDECT (Brazilian agency).
P. Melnikov
Federal University of Mato Grosso do Sul, Campo Grande, Mato Grosso do Sul, Brazil
L. Z. Zanoni (*)
Department of Pediatrics, Campus Universitário, Campo Grande CEP 79070-900 Mato Grosso do Sul,
Brazil
e-mail: lzzanoni@yahoo.com.br

serum in its salt constituents, engaged in a study of this rare alkaline element. For the first time,
he postulated that cesium (as well as rubidium, another heavy element) was supposed to behave
partly as physiological analog for potassium [1]. Lately, this hypothesis has been corroborated
to the full extent.
After the Chernobyl nuclear accident, cesium has been recommended as preventive
therapy for radiation poisoning by the isotope
137
Cs. The principle of this treatment is quite
clear: to saturate the body with the stable cesium enhancing the clearance of radionuclide
and effectively replacing it with a safer ion. Actually, the data suggest that there is a
threshold of maximum Cs saturation in the red blood cells and any additional exposure will
stimulate
137
Cs excretion [2]. Oral intake of cesium chloride has been widely promoted on
the basis of the hypothesis referred to as “high pH cancer therapy”advanced in 1984 by Ph.D. in
physics K.A. Brewer [3].
Cesium chloride therapy named as “complementary alternative method”has never been
approved neither by the US Food and Drug Administration (FDA) nor by the European
Agency for the Evaluation of Medicinal Products. It is no surprise as this proposal plainly
assumes that the usage of alkaline ions and, in particular, cesium might (or should) provoke
substantial increase in pH within malignant cells. It assumes also that only tumor cells tend
to incorporate cesium ions. This alone is enough to establish that the therapy is not based on
good information. Nevertheless, the problem is not as simple as that.
The alkalinity is no more than a measure of the ability of a solution to neutralize acids to
the equivalence point of carbonate or bicarbonate. Alkalinity and pH are distinctly different
from each other, although their definitions are frequently confused. It is easy to believe that
solutions with high pH are likely to be high in alkalinity. However, this is not necessarily
true [4]. A salt formed between a weak acid and a strong base is a basic salt, for example
cesium acetate, CsCH
3
COO, or cesium carbonate, Cs
2
CO
3
. On the other hand, salts of
strong acids and strong bases, for example cesium chloride, CsCl, would completely ionize,
so one would not expect that the solution containing this salt can provoke an increase in pH
value. In this sense, CsCl is not different from KCl, as dissociation degrees of their
respective hydroxides are very close. Like caustic soda, cesium hydroxide, CsOH, cannot
be used in medicine because of extremely corrosive properties. Hence, the presence of
cesium ions in the cell can not guarantee pH. Moreover, at present, no tests can accurately
evaluate intracellular pH in human body. So, there are neither theoretical nor experimental
grounds for the idea of CsCl application in cancer treatment.
Meanwhile, average Internet users and desperate patients looking for an immediate
miraculous relief from cancer would not go into these subtleties, conceiving what is happening
just outside their range of limited medical knowledge. The fact that this method is not currently
officially endorsed led to adverse reaction that is blaming the “medical establishment”for their
conservative and unsupportive standpoint. Internet and e-mail ads stimulated self-treatment
without bearing in mind that it could lead to serious problems. Ordinary people and individuals
with discovery delusions started to take and recommend large amounts of cesium chloride with
no clinical evaluation of its possible hazardous consequences.
In EC, there are no specific regulations as to the usage of cesium in medicine. Cesium
chloride is sold as a dietary supplement in the USA. Unlike companies that produce drugs,
the providers do not have to show evidence of safety or health benefits to the FDA before
selling their products. The companies selling them do not claim that the supplements can
prevent, treat, or cure any specific disease. Anyway, advices are provided on the Net as how
to purchase large quantities of cesium chloride outwitting standard rules, if supply houses
would be reticent to sell chemicals because of liability concerns. An average price of the
treatment is US $3.000, with no health insurance providing compensation for expenses.
Melnikov and Zanoni

Finally, a paper has recently been published, bluntly stating that two patients suffering
from terminal malignancies “were administered intravenous doses of an unapproved
therapy”, consisting of a solution containing cesium chloride [5]. Both patients have died.
As the cases are unrelated, it seems that the procedures were carried out with experimental
purposes. No “informed consent”has been issued. No data as to the dosage applied, clinical
circumstances, or results of postmortem examination of these ethically inappropriate events
were supplied. The aim of the present review is to resume and discuss the material currently
available on cesium salts and their applications in medicine.
Basic Information on Cesium
It is important to note that all the above considerations are applied to the biochemical properties
of natural stable cesium 133 and not to its radioactive analog cesium 137 or other radionuclides.
The latter are generally associated with the operation of fuel reprocessing plants, accidents in
nuclear reactors like it was in Chernobyl (Russia), and as an unpredicted result of nuclear tests.
It can also be accidentally released into environment from lead containers like it happened in
Goiania (Brazil) in 1987, launching the second largest accident after Chernobyl [6,7].
Radiocesium 137 is extremely dangerous due to the beta and gamma radiations emitted
during its decay and isomeric transition into
137
Ba-m. These isotopes as well as the above-
mentioned metastable radioactive barium are external hazards that are hazards without being
taken into the body [8,9] and have nothing to do with stable cesium. Knowledge of the
biochemistry and toxicology of cesium thus became necessary for better understanding of its
metabolism and reducing the damaging effects of arbitrary unauthorized usages.
Cesium is a soft silvery rose metal with the relatively low melting point (28°C). It belongs in
the group of alkaline metals, which also includes lithium, sodium, potassium, rubidium, and
francium, a short-lived radioactive element. Cesium metal can cause serious burns when it
comes into contact with the skin. This most alkaline of all elements reacts explosively with the
halogens to produce a fluoride, chloride, bromide, and iodide. It reacts with water and even with
ice at low temperatures [10]. Cesium is naturally present as the stable
133
Cs in various ores
and to a lesser extent in soil. It occurs in useful amounts in some varieties of beryl, but
pollucite, an aluminosilicate of cesium [11], is still the only rich source. The concentration of
cesium in the earth’s crust is 1.9 mg/kg, and the concentration in the seawater is about 0.5μg/
kg [8]. Cesium enters easily into the plant and animal systems and is deposited in soft tissues
[12]. The total content of this intracellular form is very low, no more than 0.00131 g [13].
Metallic cesium is used in photoelectric cells, hot-cathode arcs, various optical instruments,
and in atomic clocks, as well as for removing traces of ozone and oxygen from vacuum tubes.
Cesium salts are used as catalysts and for the production of special glasses and ceramics.
Recently, a method for the isolation of plasmid DNA was developed using cesium chloride
concentrated solution as medium for gradient centrifugation [14]. Radioactive cesium isotopes
are used to treat prostate and other cancers, but this field belongs to radiation therapy and is
not considered herein. World production of cesium compounds is around 20 tons per year
coming mainly from Canada, Russia, and partly from South Africa [10,11].
Cesium Distribution in the Body
An extensive literature including vast reviews arose concerning the distribution and
residence times of cesium in the body and means of enhancing its excretion. Descriptions of
Clinical Effects of Cesium Intake

accumulation and excretion by the human body often are related to potassium due to the
physical and chemical similarities of these two elements. Biokinetic model presented in
Fig. 1suggests that once cesium (stable or radioactive) enters the body, it is distributed
through the system, with higher concentrations in the kidneys, skeletal muscle, liver, and
red blood cells [15]. Naturally, it binds preferably to anionic intracellular components of
erythrocytes and decreases their ability to give up oxygen in tissues [16]. Absorption of
cesium from the stomach to blood is assumed to be negligible, the same as for potassium.
On the contrary, fractional absorption from the small intestine appears to be nearly complete
under most conditions, but may be reduced substantially by the presence of certain
substances in the contents. When cesium is ingested in the form of chloride (and, probably,
other halides like bromide and iodide), the absorption represents nearly 100% [17]. The
sizable reduction in the residence time in the body that occurs during oral administration of
Prussian Blue, insoluble ferric (III) hexacyanoferrate (II), which bonds cesium and prevents
reabsorption, provides evidence of a large amount of cesium recycling between
gastrointestinal contents and systemic circulation [18,19].
Cesium is eliminated in humans primarily through the kidneys. Biokinetic model
provides the following percentages: urine 85%, feces 13%, and sweat 2%. These calculated
data are consistent with experimental results. The renal mechanisms for excretion of Cs
appear to be quantitatively similar to those of potassium [15]. For reasons unknown,
clearance from the body is somewhat quicker for children and adolescents. In persons with
renal insufficiency during the first stages of the disease, the cesium content is increased in
blood plasma and erythrocytes (+73% and +51%, respectively) [20]. The mean long-term
biological half-life depends on the place of the research and number of individuals study.
Fig. 1 Cesium flow in accordance to biokinetic model, from [15] with modifications
Melnikov and Zanoni

However, average values are rather close. They do not exceed 100 days for men and
75 days for women [21–23].
Clinical Manifestation After Cesium Intake
Herein, only representative clinical examples will be discussed. In a report released in April
2004, US Agency for Toxic Substances and Disease Registry stated that no communica-
tions had been located in literature regarding death in humans following acute,
intermediate, or chronic duration exposure to stable cesium [24]. However, yet in 2003, a
paper has been published describing two deaths following acute exposure to this element
[5]. Case 1 was a 41-year-old male with kidney cancer, and case 2 was an 82-year-old male
with lung cancer. As mentioned before, both patients were administrated a solution
containing cesium chloride and additionally aloe vera. Forensic records collected on these
two cases indicated that on one patient (case 1), two therapies were administrated on two
consecutive days. Information from these records described the formation of uncontrolled
chills and seizures following the first intravenous therapy. During his second therapy, the
patient went into cardiac arrest while in the doctor’s office. Case 2 apparently collapsed
while he was receiving the intravenous injection containing the cesium chloride and aloe
vera preparation. According to comparison of cesium levels in exposed and nonexposed
tissues, in case 1, cesium content in liver tissue was 100,000 times higher than in control
samples, and it was 10,000 times higher in brain than in controls. In case 2, cesium levels
were substantially lower—10,000 and 1,000 times, respectively. In both instances, cesium
in whole blood was relatively lower, indicating its immediate migration from arterial
plasma and saliva into tissues in accordance to the model previously discussed [15]. So,
these cases should be qualified as acute poisoning with cesium chloride. It is worth
reminding that even more innocuous potassium chloride is lethal, when injected
intravenously in the form of concentrated solution [25].
In order to illustrate the safety of high pH therapy, single case report has described the
effects of oral intake of cesium chloride [26]. The author volunteered to experience on
himself the effect of short-term, i.e., 36 consecutive days, oral administration of cesium
chloride. It was taken 6 g per day in two equally divided doses. The drug was dissolved in
8 oz fluid and consumed immediately after the morning and evening meals which were
diet-restricted, to attain approximately 1% potassium intake. There was an initial general
feeling of well-being and heightened sense perception. A gradual decrease in appetite was
noted initially before it was stabilized at a later date. Discontinuation of rich bread meals
resulted in prenausea sensation which was followed by diarrhea 48 h later. A tingling
sensation in the lip and cheek regions was experienced 15 min subsequent the cesium
chloride dosage. No harmful effects were noted in intellectual capacities or in driving skill.
Another self-treatment by alternate therapy [27] is related to a 52-year-old woman
presented to the emergence department following an episode of hypotension syncope. The
patient was thirsty, disoriented, and hypotensive (blood pressure 95/58 mmHg on arrival).
An electrocardiogram indicated a sinus rhythm with a long QTc interval (580 ms), with
episodes of polymorphic ventricular tachycardia. The patient has a 2-year history of colon
cancer with liver metastases and had received chemotherapy. At the same time, she had
been self-treating with an alternative therapy of 3 g/day of oral cesium salts for several
weeks and a vegetarian diet. The patient experienced diarrhea repetitively, but this
gastrointestinal side effect was disregarded. As in the previous case, the patient experienced
numbness or tingling of the lips. She developed hypokalemia (3.2–2.8 mmol/L), but
Clinical Effects of Cesium Intake

magnesium and calcium levels were unchanged. She was treated with saline solution
supplemented with potassium, discharged herself 3 h late, but return the next day following
a second episode of syncope or possible seizure and still was hypokalemic.
Electrocardiogram depicted sinus bradycardia, premature ventricular, and a more prolonged
QTc interval (560 ms). During the next 3 days, following discontinuance of cesium, the QTc
interval gradually shortened to 390 ms, and potassium levels remained in the reference levels.
This observation confirmed the history of cesium consumption but could not be directly related
to the dose of cesium in the animal’s models, because those models involved intravenous
administration and acute response rather than chronic exposure to oral cesium salts.
Another case of cesium chloride therapy [28] was reported describing a 62-year-old man
presented with recurrent syncope, who underwent a naturopathic treatment consisting of 2 g
of cesium chloride four times a day intravenously for 2 weeks for prostate cancer. During
treatment, he had his first episode of syncope. He continued to take 1 g tablets of cesium
chloride three times a day. Two months later, he was hospitalized because of recurrent
syncope. The electrocardiogram showed a prolonged QTc interval (approximately 700 ms)
and ventricular ectopic beats arising from the terminal part of the T wave. Runs of torsade
de pointes tachycardia were recorded on telemetry. The serum potassium level was
2.8 mEq/L. Analysis of a blood sample revealed a plasma cesium level of 830 μmol/L that
is approximately 276,000 times higher than reference data and comparable to the values
found in the case of acute poisoning discussed early [5] but without a lethal outcome. The
patient was treated with intravenous potassium and magnesium. The QTc interval remained
prolonged and ventricular premature beats persisted after normalization of the serum
potassium level. The patient agreed to stop taking cesium chloride. After 6 months of
follow-up, he had not had any further episode of syncope and the corrected QTc interval
had returned to normal.
Another case presentation, in this case with no cancer involvement [29], concerns a
previous well 39-year-old woman presented to a local hospital after experiencing three
episodes of syncope during the past week. Prior to this, she had never had either syncope or
near syncope. Her latest syncopal episode required cardiopulmonary resuscitation including
two chest compressions. She had no prior history of cardiovascular or neurological disease
and was taking no prescription medications. However, she was taking an array of dietary
supplements and natural products including cesium salt. She described this as part of a
“detoxification program”for menorrhagia that entailed drinking 1 to 2 gal of water a day
along with cesium salt. She had been doing this for the last 2 weeks. An electrocardiogram
revealed normal sinus rhythm and profound QTc prolongation with QTc interval of 616 ms.
Besides the severely prolonged QTc interval, there were prominent U waves as well. She
had only mild hypokalemia and mild hypomagnesemia.
These were corrected with no significant change in the QTc. Although there was never
electrocardiographic documentation of torsade de points, her physician recognized that cesium
might have prolonged the QTc interval and induced arrhythmia. Hence, she was treated by
prompt cessation of her “detoxification regimen”and correction of electrolyte abnormalities. A
urine assay for cesium revealed a level of 750 mg/L, which is 65,000 times higher than the data
for general population. Daily electrocardiograms showed gradual normalization of her resting
QTc. At discharge, the QTc had decreased to 466 ms, and at 2 months follow-up, the QTc was
413 ms, which is approximately the 50th percentile QTc for women. This correlated with a
reduction in her urine cesium levels over the same time period. The patient did well and has
returned to her previously asymptomatic syncope-free state.
Recently, a life-threatening torsade de pointes resulting from “nature”cancer treatment was
described in a case report of a 65-year-old lady with recurrent syncope attacks. One of her
Melnikov and Zanoni

naturopathic drugs was subsequently confirmed containing 89% CsCl by weight. Besides
conventional treatment of QT prolongation and torsade de pointes, the patient was given a 4-
week course of oral Prussian blue to enhance gastrointestinal elimination of cesium. This is the
first published case of a nonradioactive cesium poisoning treated with Prussian blue [30].
Practically no data are available for children, but recently, a case was described [31]in
an adolescent 16-year-old girl with metastatic hepatocellular carcinoma. She had received
courses of chemotherapy that resulted in minimal tumor regression. Against the advice of
her oncologist, an alternative regimen was started that included cesium chloride supple-
ments. Two weeks later, two brief syncopal episodes were observed. An electrocardiogram
revealed occasional premature ventricular contractions, a QTc interval of 683 ms, and an “R
on T”phenomenon. After admitting to the hospital, she experienced monomorphic
ventricular tachycardia. Her plasma cesium level was 2,400 mg/L. Two days later, the QTc
interval on electrocardiogram had decreased to 546 ms.
It is worth reminding that cardiac K
+
channels are membrane-spanning proteins that
allow the passive movement of K
+
ions across the cell membrane along its electrochemical
gradient. They regulate the resting membrane potential, the frequency of pacemaker cells,
and the shape and duration of the cardiac action potential. In mammalian cardiac cells, K
+
channels include among other rapid (I
Kr
) and slow (I
Ks
) components of the delayed rectifier
current, as well as the inward rectifier current (I
K1
). Changes in the expression of K
+
channels explain the regional variations in the morphology and duration of the cardiac
action potential among different cardiac regions and are influenced by heart rate,
intracellular signaling pathways, drugs, and cardiovascular disorders. A progressive number
of cardiac and noncardiac drugs block cardiac K
+
channels and can cause a marked
prolongation of the action potential duration (i.e., an acquired long QTc syndrome) and
torsade de pointes. In cases of extreme gravity, the arrhythmias can deteriorate to
ventricular fibrillation and cardiac arrest.
Thus, the pathophysiological mechanisms of the immediate Cs
+
effects on cardiac
tissues consist in replacing K
+
, leading to the blockade of inwardly rectifying K
+
current at
ventricular level [32], and nodal hyperpolarization-activated cation current [33,34], both of
which primarily affect the resting membrane potential. Furthermore, Cs
+
block of I
K1
involves interactions between cations at binding sites within the channel pore [35,36], and
the inhibition of inward I
K1
is likely to be explained by Cs
+
entry into I
K1
channels, favored
by hyperpolarization.
In an animal models, the acquired long QTc syndrome observed in man was also
reproduced but others arrhythmias are observed as ventricular tachycardia and torsade de
pointes. These arrhythmogenic effects of Cs
+
ions have been linked to the inhibition of
hyperpolarization-activated current and a reduction in cardiac K
+
currents [37–39], which
may be blocked by Cs
+
ions from the intracellular or extracellular side.
Experimentally, results have been obtained in previous investigations in dogs and
rabbits, when intravenous CsCl provoked an instant ventricular tachycardia [40,41]
associated with monophasic early after-depolarizations. At tissue level, it was also shown
that Cs
+
causes a voltage-dependent block of inward K
+
currents in resting skeletal muscle
fibers [42]. It is to suggest that the mechanisms involved are basically the same.
Conclusions
1. The toxicity of cesium depends on dose, but full knowledge on its acute and chronic toxicity
is not available.
Clinical Effects of Cesium Intake

2. The presence of cesium in the cell does not guarantee high pH of its content.
3. There is no either theoretical or clinical evidence to support the claims that cancer cells
are vulnerable to cesium.
4. Relying on this type of treatment and avoiding conventional medical care may have
serious health consequences.
5. Health care providers should be aware of the cardiac complications and even acute
heart arrest as a result of cesium usage.
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Clinical Effects of Cesium Intake