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RESEARCH ARTICLE
Contents Vol 19(8)

Altering systemic acid–base balance through nutrition failed to change secondary sex ratio

John R. Roche A B C and Julia M. Lee A
+ Author Affiliations
- Author Affiliations

A Dexcel, Hamilton, New Zealand.

B University of Tasmania, PO Box 3523, Burnie, Tasmania 7320, Australia.

C Corresponding author. Email: john.roche@utas.edu.au

Reproduction, Fertility and Development 19(8) 887-890 https://doi.org/10.1071/RD06053
Submitted: 10 June 2006  Accepted: 9 August 2007   Published: 11 September 2007

Abstract

There is evidence that differences in either maternal blood pH or dietary mineral content can result in alterations in secondary sex ratio in mammals. Altering the proportions of certain dietary minerals is known to influence blood pH, offering a possible explanation for this effect of diet on secondary sex ratio. The present study was performed to investigate whether altering blood pH by manipulating the dietary cation–anion difference (DCAD) would alter secondary sex ratio. The DCAD is calculated (in mEq per 100 g dry matter) as the difference between metabolically strong cations (Na + K) and metabolically strong anions (Cl + S) in the diet. Three hundred female mice were randomly allocated to either a low or high DCAD ration for 3 weeks before coitus. Urine pH was monitored before beginning the experiment, as well as before and after the breeding period, as a proxy for blood pH. Mice on the low DCAD diet had a lower urine pH (mean (± s.d.) 6.0 ± 0.1) than mice on the high DCAD diet (8.2 ± 0.6), but DCAD did not affect the percentage of mice that became pregnant, the number of offspring per pregnant mouse or the sex ratio of the neonate group. These results suggest that blood pH alone does not alter sex ratio and that an altered systemic pH is not the reason for reported mineral-related variations in sex ratio.

Additional keywords: blood pH, dietary cation–anion difference, minerals, urine pH.


Acknowledgements

The authors acknowledge the technical assistance of R. Broadhurst, G. Smith and B. Smith, and the statistical expertise of B. Dow. The hypotheses tested and presented here benefited greatly from discussions with Mr P. Moate and T. Clarke. Encouragement and advice from Drs J. Parsons, C. Grainger, D. Dalley and E. Kolver are also gratefully acknowledged. This work was joint-funded by Dexcel Ltd., New Zealand and the Department of Primary Industries, Victoria, Australia.


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