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Barium is a trace element which can apparently affect thyroid function and which may be especially toxic for persons with thyroid disease, especially hyperthyroidism.

Barium sulfate (BaSO4) is commonly used as a contrast medium in radiography of the intestinal tract.  For these purposes a quite large amount is given orally to the person. 

Barium carbonate (BaCO4) is rat poison.  This works by interfering with the sodium-potassium pump and causing a paralysis of the muscles, including the heart muscles and respiratory muscles, causing death.

Because barium interferes with the sodium-potassium pump, which seems already disturbed in hyperthyroidism, any ingestion of barium may be very toxic to someone with hyperthyroidism (or anyone for that matter).

Some hyperthyroids get periodic hypokalemic (potassium deficiency) paralysis from a deficiency of potassium or a reduced permeability of the muscles to potassium entry.  Barium seems to cause the same reduced permeability to potassium and this may be its mode of toxicity.

Here are some pertinent studies:


Periodic paralysis and the sodium-potassium pump.
Layzer RB
Ann Neurol, 11(6):547-52 1982 Jun

Analysis of the pathophysiology of hypokalemic paralysis, as it occurs in barium poisoning, chronic potassium deficiency, and thyrotoxicosis, suggests that these disorders may have a similar mechanism. An increased ratio of muscle sodium permeability to potassium permeability reduces the ionic diffusion potential, while the resting membrane potential is sustained by an increase of Na-K pump electrogenesis. The result is that potassium entry (the sum of active and passive influx) exceeds potassium efflux; this causes a large shift of extracellular potassium into muscle until the Na-K pump turns off, leading to depolarization and paralysis. The primary defect in familial hypokalemic periodic paralysis, as in the example of barium poisoning, may be a marked reduction of muscle permeability to potassium.


Hypokalemic paralyses: a review of the etiologies, pathophysiology, presentation, and therapy.
Stedwell RE; Allen KM; Binder LS
Department of Emergency Medicine, Texas Tech University Health Sciences Center, El Paso 79905.
Am J Emerg Med, 10(2):143-8 1992 Mar

Acute hypokalemic paralysis is an uncommon cause of acute weakness. Morbidity and mortality associated with unrecognized disease include respiratory failure and death. Hence, it is imperative for physicians to be knowledgeable about the causes of hypokalemic paralysis, and consider them diagnostically. The hypokalemic paralyses represent a heterogeneous group of disorders with a final common pathway presenting as acute weakness and hypokalemia. Most cases are due to familial hypokalemic paralysis; however, sporadic cases are associated with diverse underlying etiologies including thyrotoxic periodic paralysis, barium poisoning, renal tubular acidosis, primary hyperaldosteronism, licorice ingestion, and gastrointestinal potassium losses. The approach to the patient with hypokalemic paralysis includes a vigorous search for the underlying etiology and potassium replacement therapy. Further therapy depends on the etiology of the hypokalemia. Disposition depends on severity of symptoms, degree of hypokalemia, and chronicity of disease.

Study 3:

Food Addit Contam 1997 Jul;14(5):483-90

Preliminary assessment of potential health hazards associated with barium leached from glazed ceramicware.

Assimon SA, Adams MA, Jacobs RM, Bolger PM

Center for Food Safety and Applied Nutrition, US Food and Drug Administration, Washington, DC 20204, USA.

Ceramic glazes contain several elements which have the potential to leach into food or beverages that are held or stored in ceramicware. Recently, barium salts have been investigated as one of the alternatives to lead in frit formulations for glazes. This preliminary evaluation addresses the potential health hazards associated with barium at levels that might leach from glazed ceramicware. A set of specialty ceramicware, consisting of five teacups and a pitcher, was examined for extractable barium. Exposure to barium that adults (18-44 years) might encounter using the vessels for coffee, tea, or orange juice was estimated. The exposure estimate was derived from values for intakes of the beverages and for the barium migration from glazed ceramicware test samples. An established reference dose (RfD) for barium exposure for the critical effect of hypertension was identified. The potential hazard associated with the leaching of barium from glazed ceramicware varied with the level of use. Consuming beverages in amounts up to the 95th percentile would not result in total barium intake in amounts that exceed the RfD; consuming large quantities (> 95th percentile) of beverages such as tea or coffee from glazed vessels might. This suggests that for a small portion of the population of users, intake of barium may be in quantities that warrant further consideration as a potential health hazard. Analyses of a broad sample of ceramicware and study of barium leaching behavior under actual use conditions are needed to assess further the significance of these findings.

PMID: 9328533, UI: 97469061