I didn't know why you said 'itia-itia', so I had to google it. "ouch ouch sickness", a case of mass cadmium poisoning in Toyama Prefecture, Japan, starting around 1912. The cadmium poisoning caused softening of the bones and kidney failure.
I'm very interested in health issues, so I couln't resist looking this up. Some of the stuff further down is a bit beyond me at this stage, but It looks like there's no definite proof about how bone softening happens.
Quote:
Epidemiological and clinical studies in Japan since 1962 have shown that the bone effects develop only at very high cadmium exposures and that persons with low intakes of calcium or vitamin D are particularly at risk.
Six possible mechanisms may explain the cadmium-induced bone effects: (1) interference with parathyroid hormone (PTH) stimulation of vitamin D production in kidney cells; (2) reduced activity of kidney enzymes activating vitamin D; (3) increased excretion of calcium in urine; (4) reduced absorption of calcium from intestines; (5) direct interference with calcium incorporation into bone cells; and (6) direct interference with collagen production in bone cells. The high cadmium exposures needed to produce bone effects may still occur in developing countries, where many people have poor nutritional status and could be vulnerable to such effects.
http://www.ncbi.nlm.nih.gov/pubmed/1303956
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Quote:
Extensive epidemiological studies have recently demonstrated increased cadmium exposure correlating significantly with decreased bone mineral density and increased fracture incidence in humans at lower exposure levels than ever before evaluated. Studies in experimental animals have addressed whether very low concentrations of dietary cadmium can negatively impact the skeleton. This overview evaluates results in experimental animals regarding mechanisms of action on bone and the application of these results to humans. Results demonstrate that long-term dietary exposures in rats, at levels corresponding to environmental exposures in humans, result in increased skeletal fragility and decreased mineral density. Cadmium-induced demineralization begins soon after exposure, within 24 h of an oral dose to mice. In bone culture systems, cadmium at low concentrations acts directly on bone cells to cause both decreases in bone formation and increases in bone resorption, independent of its effects on kidney, intestine, or circulating hormone concentrations. Results from gene expression microarray and gene knock-out mouse models provide insight into mechanisms by which cadmium may affect bone. Application of the results to humans is considered with respect to cigarette smoke exposure pathways and direct vs. indirect effects of cadmium. Clearly, understanding the mechanism(s) by which cadmium causes bone loss in experimental animals will provide insight into its diverse effects in humans. Preventing bone loss is critical to maintaining an active, independent lifestyle, particularly among elderly persons. Identifying environmental factors such as cadmium that contribute to increased fractures in humans is an important undertaking and a first step to prevention.
http://www.ncbi.nlm.nih.gov/pubmed/19463839
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