Anticopper Strategies

Although copper-chelating compounds could be useful in lowering copper availability, the safest and most effective natural compounds known to do so are molybdenum and its relatives. Diets deficient in copper may also be of some use.

In the human study mentioned in Chapter 8, administration of the molybdenum compound tetrathiomoly-bdate appeared to stop the growth of advanced cancers in five of six patients, apparently by inhibiting angio-genesis. Tumor growth inhibition occurred when plasma ceruloplasmin concentrations were reduced to about 20 percent of baseline for 90 days or more. Side effects of the treatment were minimal as long as anemia was prevented by maintaining the hematocrit above 80 percent of baseline.129 The dose of tetrathiomolybdate used was 120 milligrams per day in six divided doses.

(The findings in this phase I study must be verified by controlled studies.)

Tetrathiomolybdate, (NH4)2MoS4, is an experimental drug used to treat Wilson's disease, which is marked by high concentrations of unbound copper and low plasma copper-binding proteins (ceruloplasmin).130 The use of tetrathiomolybdate was pioneered by Dr. George Brewer. The idea for its use came from reports that copper deficiency symptoms appeared in livestock grazing on molybdenum-rich soils. Of the molybdenum compounds, tetrathiomolybdate is probably the most effective at lowering copper concentrations; because it is experimental, however, it is not yet available commercially.

Conceivably, it may be possible to use molybdenum compounds already available. The anticopper effect of molybdenum is greatly increased if sulfur is co-administered (sulfur occurs in tetrathiomolybdate). Thus sodium molybdate, Na2MoO4, could be combined with calcium sulfide, CaS, as an anticopper therapy. The dose of tetrathiomolybdate used in the human trials contained 44 milligrams of molybdenum per day. In animal experiments, the combination of sodium molybdate and calcium sulfide was roughly 10-fold less potent than tetrathiomolybdate in reducing copper lev-els.131 Accordingly, doses as high as 440 milligrams of molybdenum in sodium molybdenum may be required when used in conjunction with calcium sulfide. This is an excessive molybdenum dose, however. Still, based on the ability of various molybdenum compounds to produce toxic effects in animals (via copper depletion), it may be possible that doses closer to 44 milligrams could still be effective. Clearly, many uncertainties remain about the required dose and effectiveness of sodium molybdate and calcium sulfide combinations. The use of such combinations is only mentioned here as an interesting possibility that requires further study.

The toxic molybdenum dose in humans is uncertain, but it appears that the LOAEL dose is about 1.6 mg/kg and the NOAEL dose about 0.9 mg/kg in rats. The human equivalent of these is about 26 and 15 milligrams per day, respectively. A dose of 26 milligrams per day is much higher than the 0.2 to 0.5 milligram per day dose commonly prescribed in noncancerous conditions. At high doses, side effects of molybdenum can include aching joints resembling gout, headache, anemia, and adverse effects on fetal development. Anemia and fetal impacts, which were seen in rodents, may be largely caused by low plasma copper concentrations: low copper concentrations can produce iron deficiency and inhibit the angiogenesis needed for fetal development.

The risks of adverse effects of long-term copper depletion remain to be fully characterized. Based on the hu man anticancer study mentioned above, copper depletion therapies do, however, promise few adverse effects. Copper does play crucial roles in the body, and a minimal amount is required to maintain normal functions. For example, since copper is a component of the anti-oxidant enzyme copper/zinc superoxide dismutase, copper deficiency can reduce antioxidant capability. Therefore, caution must be used in anticopper therapies, especially if they part of long-term treatment. It may be prudent to monitor iron, hematocrit, and ceruloplasmin in patients receiving high-dose molybdenum treatment.

We end by noting that although zinc is commonly used as an anticopper agent in the treatment of Wilson's disease, it may not be the best choice for lowering copper levels in cancer patients. Zinc, like copper, plays a role in many enzymes required for cell function, including immune cell function. The effects of zinc are thus complex, and studies on the metal have produced mixed results. On one hand, cancer patients are commonly deficient in zinc, zinc supplementation may improve immune response, zinc deficiency is associated with increased tumor load and stage of some cancers, and zinc supplementation may improve the efficacy of some chemotherapy drugs.132-137 On the other, zinc chelators reduce cancer invasion in vitro, zinc enhances telo-merase activity in vitro, zinc administration can promote metastasis and tumor growth in animals, high zinc levels are associated with increased metastasis of some cancers in humans, zinc deficiency inhibits tumor growth in animals, and animal tumors sequester zinc under zinc-deficient conditions.138-148 Therefore, until the effects of zinc administration in human cancer patients become clear, anticopper therapies other than zinc administration may be preferable.

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