Skip to main content

Archived Comments for: Is there a positive association between mammographic density and bone mineral density? Authors' response

Back to article

  1. Alcohol verses mitigating folic acid intake in mineral density verse BC risk profiles, confounding geological environment.

    Bernhard Hochwimmer, B. Hochwimmer & Associates Pty Ltd, Consulting Geologists in Mineral Exploration, Mining and Environmental Geology.

    25 May 2006

    It is possible alcohol (in moderation) adds mineral density through stimulating growth hormone, yet alcohol by itself increases breast cancer (BC) risk. Then mitigating circumstances would be folic acid against alcohol induced BC risk, while still enhancing bone mineral density.

    One assumes naturally breast density may not dictate BC risk, if at all. So it’s worth speculating on mineral density and BC risk directly, rather than focusing only on breast density. While this response dose not address breast and bone mineral density association directly, it highlights potential utility of a multidisciplinary approach in BC risk that may under some circumstances include bone mineral density and interplay of non anthropogenic factors, including the geological environment.

    Moderate exercise may show less mineral density than intensive or extreme sports. These may require antioxidants, to be on an equal oxidant risk profile to those engaged in moderate exercise, in which case antioxidants appear to have minimal impact general. Most suggestions have been that moderate exercise slightly reduces BC and some other cancer risk. Adding alcohol, perhaps worse, hormone supplementation or other stimulants in sport may yield synergistic BC risk yet add mineral density.

    Thus a simple bone density-BC risk association under normal circumstances may not follow, particularly as these people may be expected to have a higher osteoprotegerin and lower bone IL6 profile, osteoblast promoting, to the general lower exercising population of developed countries. In this sense it would be interesting to look further, mineral density and tumorigenesis, particularly metastasis in bone, if all caveats of methodology can be met.

    While experimental methodology can be queried or improved in future studies in terms of addressing variability, so can dietary aspects not considered, not least bioflavonoid intake such as lycopene, but synergistic combinations, particularly photoestrogens, in terms of mineral density and BC risks. A generally lower epigenetic defect profile resulting from these diets has obvious implications. Adverse risks are likely confined to tumorigenesis in treatment only, rather than carcinogenesis, and specifically if genistein competes with tamoxifin (less or more so with raloxifene?) reducing its effectiveness. In other aspects reducing bone microhabitat by increasing mineral density and simultaneously mitigating turnover. In this regard they may mitigate adverse effects of bisphosphonates in which recent evidence suggest while mineral density is favourable bone metastasis is enhanced by turnover in bisphosphonate use. The general interplay between bone mineral density, phytoestrogen and bisphosphonate use in osteoporosis and subsequent BC risk needs evaluation.

    In specific geological and anthropogenic environments compounding factors may include metal movement, including lead and phosphorous between bone and kidney and this could be an area of fertile future research in conjunction with phosphorylation, signaling modulators such as through inorganic arsenic and osteoblast function involving the geological domain, particularly through competing arsenic and fluorine. Anthropogenic and anthropogenic geological associations may compound anthropogenic risk factors including lifestyle and particularly agricultural practice. A possible scenario may present arsenic in ground water consumption and irrigation in the presence of simultaneous selenium deficiency in skeletal soils, imparted by regional scale dredging in otherwise agriculturally fertile graben environments. Selenium is essential in abrogating BC risk in the form of the selenoprotein glutathione peroxidase (GPx-1 ) in which polymorphism for its gene may require more selenium in at risk individuals who show low activity of the enzyme (Ya Jun Hu., Diamond, A.M., Diamond., 2003. Polymorphism lowers selenium response, which may increase breast cancer risk Cancer Research 2003;63:3347-3351 in Gale K., Reuters Health, June 20, 2003).

    Furthermore selenium may compensate for the deleterious effects of arsenic.

    A possible environmental match is the Ovens grabben of Australia purported to include the highest BC incidence in Australia according to Melbourne’s Monash University work that considers potential anthropogenic agricultural practice as the main risk factors. We contend possible compounding geological factors (Hochwimmer, B., Cruz L. R., 2005. Polygonal Vortex Mineralisation Model: A predictive tool of health indices, First Cuban Geological Convention April, 2005, Havana, Cuba). Initially this large alluvial graben valley was populated by Italian immigrants, a dominant agricultural force in this large food bowl. Viticulture is prominent and the first gold leaf tobacco was grown here in Australia. Irrigation is fortified with groundwater. We consider high alcohol consumption and speculate mineral density in an environment that facilitates metal mobility with simultaneous selenium deficiency conspire with anthropogenic sprays, some arsenical, may play a role in BC within the Ovens graben. On top is the use of high mineral waters ground waters and implication for fluorine. induced mitogenic activity for osteoblasts. One study (Riggs, B., and Melton, L.J., III (1995). Osteoporosis: Etiology, Diagnosisi and Management. Raven Press, New York.) suggested fluorine is mitogenic for osteoblasts leading to increases in bone mineral density.

    It is worth mentioning natural apatite is a mineralogical ligand for cerium phosphate minerals monazite and yttrium phosphate mineral xenotime, in turn ligands for thorium, generally around 4% and potentially other radio nuclei. Should replication in human bio apatite occur the geological background environment may require investigation; some geological domains have high background monazite over large regions. Potential is much wider on top of the normal substitution of calcium by sodium, lead and strontium in varied geological domains. For instance there are arsenates and vanadates that form virtually identical apatite like crystal structures, and these usually contain lead rather than calcium. Another yttrium containing natural apatite, Britholite-Y, one of a series of phosphate apatite’s contain silicon substitutes for phosphorus with a second cation in addition to calcium, yttrium, with fluorine in the channelways (Catherin. H., Skinner W., in Selinus, Essentials of Medical Geology, 2005, Elsevier). Mineralised environments with passive bone mineral promoting fluorine may have less benign associates, of which arsenic may be widespread and ingested in similar mode, irrigated foods products by mineralised waters, in drinking waters, and particularly ground waters.

    A known past practice in the Ovens Valley is use of mine waters to fortify water supply that at times is sparse, even as human drinking water. There are still instances of this practice. Anoxic mine waters impart labile arsenic. A plethora of gold veins in the Ovens graben have arsenical and minor lead associations, but the main risk will be natural arsenic accumulation in graben groundwaters. Arsenic is more often thought to be involved in skin, liver, intestinal, kidney, bladder, lung and leukaemia cancers, rather than BC, but there is still much to be learned about arsenic carcinogenesis in general. Arsenic suppresses the hTERT gene coding for one of the building blocks of telomerase. Arsenic carcinogenesis often involves oncogenes evaluated, including p53. The effect of speciation such as environmental ribose and methyl arsenates may be of particularly active forms as toxins and carcinogens. As for inorganic arsenic, this dose not appears to operate in ‘normal’ genotoxic and mutagenic form, but rather as a promoter through signal transduction. (Simonov, P.P., et al., 2000. Mechanisms of arsenic Carcinogenicity: Genetic or Epigenetic Mechanisms, J. Environ. Pathol. Toxicol. Oncol., 19, 281-286.). Gene expression modulation or DNA binding activities of key transcription factors are involved including NFkB, tumour suppressor protein P53. AP-1 (by trivalent arsenic) is involved including MAPK cascade leading to increased expression and or phosphorylation of two major AP-1 constituents, c-jun and c-fos (Simonov, P.P., et al., 2000).

    Ethnic or lifestyle, and environmental difference, as both anthropogenic and non anthropogenic geological factors, may yield initial clues in bone mineral density, metal mobility, BC risk and treatment outcomes. Mineral density and BC risk may be tenuous conjecture for the population as a whole, but future research in specific environments may yield fertile research in known problem areas. In such environments one can reasonably expect a confounding involvement including the geological domain.

    Competing interests

    I declare no competing interests. The only possible overlap in my geological profession is in Medical Geology, of personal interest only.