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Effect of body composition on vitamin D response to supplementation in healthy adults

Published online by Cambridge University Press:  30 November 2009

L. K. Forsythe
Affiliation:
Northern Ireland Centre for Food and Health, University of Ulster, Coleraine BT52 1SA, UK
J. M. W. Wallace
Affiliation:
Northern Ireland Centre for Food and Health, University of Ulster, Coleraine BT52 1SA, UK
M. S. Barnes
Affiliation:
Northern Ireland Centre for Food and Health, University of Ulster, Coleraine BT52 1SA, UK
G. Horigan
Affiliation:
Northern Ireland Centre for Food and Health, University of Ulster, Coleraine BT52 1SA, UK
K. D. Cashman
Affiliation:
Department of Food and Nutritional Sciences, University College Cork, Cork, Republic of Ireland
M. Kiely
Affiliation:
Department of Food and Nutritional Sciences, University College Cork, Cork, Republic of Ireland
A. J. Lucey
Affiliation:
Department of Food and Nutritional Sciences, University College Cork, Cork, Republic of Ireland
T. R. Hill
Affiliation:
Department of Food and Nutritional Sciences, University College Cork, Cork, Republic of Ireland
M. B. E. Livingstone
Affiliation:
Northern Ireland Centre for Food and Health, University of Ulster, Coleraine BT52 1SA, UK
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Abstract

Type
Abstract
Copyright
Copyright © The Author 2009

Alterations in the vitamin D endocrine system may occur in the obese state(Reference Compston, Vedi and Ledger1, Reference Bell, Epstein and Greene2). Some studies have observed an inverse relationship between BMI and vitamin D status(Reference Barger-Lux, Heaney and Dowell3) and reported that vitamin D (as a fat-soluble vitamin) may get ‘locked’ in the adipose tissue(Reference Wortsman, Matsuoka and Chen4). More recent research suggests that BMI may also influence the response to vitamin D supplementation(Reference Blum, Dallal and Dawson-Hughes5). The aim of the present study was to investigate the effect of body composition on serum 25-hydroxycholecalciferol (S-25(OH)D3) response to supplementation in young adults. Healthy volunteers aged 20–40 years (n 237) were randomised to receive 5, 10 or 15 μg cholecalciferol or placebo daily for 22 weeks during the winter months (October–March). A fasting blood sample, obtained at baseline and post intervention, was used to measure S-25(OH)D3 concentration. Anthropometric measurements included height, weight, waist circumference, and percentage body fat (calculated from four-site skinfold thickness measurements). Fat and fat-free mass (kg) were then calculated and adjusted for height to give fat mass index (kg fat mass/m2) and fat-free mass index (kg fat-free mass/m2) respectively. At baseline S-25(OH)D3 was not significantly different between males and females (77.7 nmol/l v. 74.6 nmol/l; P=0.27); however, as a result of gender differences in body composition, data for men and women were analysed separately.

* Negatively associated with post-intervention S-25(OH)D3 (analysis of covariance (ANCOVA), P<0.05), including baseline S-25(OH)D3, age and treatment group as covariates in each model.

In men ANCOVA showed that fat mass (kg or %), fat mass index and percentage fat:fat-free mass were inversely associated with post-intervention S-25(OH)D3, after controlling for baseline S-25(OH)D3, age and treatment group. Weight, BMI, waist circumference or fat-free mass were not associated with the S-25(OH)D3 response to supplementation in men. Body composition did not significantly influence the S-25(OH)D3 response to supplementation in women.

In conclusion, adiposity appears to impair S-25(OH)D3 response to supplementation in healthy young men (20–40 years). These results also highlight the importance of measuring body fatness, rather than using BMI or waist circumference alone, and appropriately adjusting for body size when examining the associations between vitamin D status and adiposity.

We would like to acknowledge the Department of Education & Learning and the Food Standards Agency for their support.

References

1. Compston, JE, Vedi, S, Ledger, JE et al. (1981) Am J Clin Nutr 34, 23592363.Google Scholar
2. Bell, NH, Epstein, S, Greene, A et al. (1985) J Clin Invest 76, 370373.CrossRefGoogle Scholar
3. Barger-Lux, MJ, Heaney, RP, Dowell, S et al. (1998) Osteoporos Int 8, 222230.Google Scholar
4. Wortsman, J, Matsuoka, LY, Chen, TC et al. (2000) Am J Clin Nutr 72, 690693.Google Scholar
5. Blum, M, Dallal, GE & Dawson-Hughes, B (2008) J Am College Nutr 27, 274279.Google Scholar
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