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United States Department of Agriculture

Agricultural Research Service

Title: Letter to Editor: Reply to Dr. Exley comments on: Jugdaohsingh R et al, Increased Longitudinal Growth in Rats on a Silicon Depleted Diet. Bone. 2008; 43:596-606

item Jugdaohsingh, Ravin -
item Powell, Jonathan -
item Anderson, Simon -
item Thompson, Richard -
item Calomme, Mario -
item Robinson, Karen -
item Nielsen, Forrest
item D'Haese, Patrick -
item Geusens, Piet -
item Loveridge, Nigel -

Submitted to: Bone
Publication Type: Other
Publication Acceptance Date: March 20, 2009
Publication Date: April 20, 2009
Repository URL:
Citation: Jugdaohsingh, R., Powell, J.J., Anderson, S.H., Thompson, R.P., Calomme, M.R., Robinson, K., Nielsen, F.H., D'Haese, P., Geusens, P., Loveridge, N. 2009. Letter to Editor: Reply to Dr. Exley comments on: Jugdaohsingh R et al, Increased Longitudinal Growth in Rats on a Silicon Depleted Diet. Bone. 2008; 43:596-606.

Technical Abstract: We thank Dr Exley for his unremitting interest in our work and the opportunity for us to clarify several points. If, as is commonly believed, absorbed dietary silicon (orthosilicic acid, Si(OH)4)is a molecule readily distributed in the extracellular fluid, and is readily filtered by the kidney with no re-absorption, and no tissue homeostasis, then following a 12 hour fast, one would expect the serum silicon concentrations of our animals to drop to very low levels, since they were previously maintained on a diet containing a very low level of silicon. We refer interested readers to the body of work examining whole body water and markers thereof (e.g. [1]). However, for silicon, this turns out not to be the case (Fig. 1; [2]). We used individual (means±SD) and steady-state silicon concentrations of urine:serum, following respectively, a 6 and 12 hour fast, at weeks 25 and 26–27, as an illustration of this finding [2]. We acknowledge that, ideally, these serum and urine collections would have been collected at the same time but practically this was not possible. Animals from the three groups underwent the same treatment at the same time to allow valid between-group comparisons. Serum silicon concentrations were not from a series of times but at necropsy. For a more comprehensive discussion of silicon (orthosilicic acid) metabolism, we refer interested readers to Refs. [3–9]. Taken together we conclude that in fasted rats, on a very low silicon diet, it is noteworthy that their serum silicon levels drop to only ~50% of those of animals on a silicon-supplemented diet or even on standard laboratory chow. We surmise that renal conservation is the most likely operative mechanism although we cannot preclude a large tissue pool. Either case deserves scrutiny. We furthermore disagree with Dr Exley's further assumptions. First, while oral supplementation (drinking water) with orthosilicic acid, given to otherwise silicon-deprived animals, failed to increase bone silicon concentrations over and above those of silicon-deprived animals without the supplemented water, this is not the case for animals on normal laboratory chow (Fig. 1, Pb0.0001, [2]). Thus we cannot conclude that silicon will not enter bone above and beyond that seen for silicon-deprived animals but, rather, that it is ‘environment specific’: for example, some dietary co-factor may be present in the standard chow but considerably less so in the formulated silicon-depleted diet (please see our Discussion on page 604, 2nd paragraph [2]). Part of Dr Exley's misunderstanding may be that he thinks our animals on a silicon-deprived diet were ingesting laboratory chow (paragraph 3, Letter to the Editor, C Exley). Please see Table 1 and pages 598, 604 and 605 of our recent paper [2], which discusses in detail the nature of the formulated diet. Although not reported, the aluminium content of the formulated diet is very low (0.5±0.2 µg/g). We are, of course, well aware of the work showing that aquated aluminium and silicon can interact such that toxicity for lower animals to aluminium is reduced. Indeed, the first and senior authors were part of the team recently reporting that silicon undergoes Al-induced homeostasis in the water snail, Lymnaea stagnalis [10], supporting our previous findings in this model [11], and again we were in correspondence with Dr Exley over this work [12]. However, such findings [10,11,13] are yet to be translated to higher animals, especially mammals, and even if silicon and aluminium were shown to interact in this way in mammals, by no means would this imply that this is the only biological role of silicon. Our findings, published in Bone [2] exemplify this point. Silicon-deprived animals showed greater body lengths, greater long-bone lengths, significant correlations between long-bone lengths and fasting serum silicon levels and, reduced phosphorus levels in bone. Bone toxicity due to chronic aluminium exposure in animals is hallmarked by decreased calcium content of bone (not found in our work) and increased phosphorus content(opposite to our findings) [14,15]. Bone weight, is also decreased [15]; which againwas not found in our study. In chicks aluminium causes a decrease in long bone length [16], again, opposite to our findings. Effects of aluminium on bone density may be related to concomitant dietary silicon levels [17], but whether this is an interaction or independent activities remains to be determined. In an era of increasing interest on the potential biochemistry of silicon [18] and the description of silicon transporters[19,20,21], Dr Exley continues to make clear his view that silicon undergoes no biological homeostasis and has no other role than to ‘neutralise’ toxic aluminium. On the latter point he may be correct, as the mechanisms of action of silicon remain elusive, but data such as those presented by us recently in Bone [2], and elsewhere, make it increasingly difficult to reconcile observations between silicon and connective tissue health with prevention of aluminium toxicity. We acknowledge Dr Exley's committed views but caution against over-reaching to fit data to a belief system. We have discussed, in detail, our interpretations for the observed effects of silicon deprivation on rat bone (pages 604–605, [2]) and we would now welcome quality peer-reviewed data that could support the hypothesis that the biological role of silicon in higher animals is solely to prevent aluminium toxicity.

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