S A Tanumihardjo1, B M Gannon2,3, C Kaliwile4, J Chileshe5, N C Binkley6. 1. Department of Nutritional Sciences, University of Wisconsin-Madison, 1415 Linden Dr., Madison, WI, 53706, USA. sherry@nutrisci.wisc.edu. 2. Department of Nutritional Sciences, University of Wisconsin-Madison, 1415 Linden Dr., Madison, WI, 53706, USA. 3. Cornell University, Ithaca, NY, USA. 4. National Food and Nutrition Commission of Zambia, P.O. Box 32669, Lusaka, Zambia. 5. Tropical Diseases Research Center, Ndola, Zambia. 6. Osteoporosis Clinical Research Program, University of Wisconsin-Madison, Madison, WI, USA.
Abstract
This analysis was performed in Zambian children who had a high prevalence of hypervitaminosis A, defined as > 1.0 μmol retinol/g liver. Bone parameters included markers of bone formation (P1NP), bone resorption (CTX), parathyroid hormone, calcium, vitamin A, and vitamin D. Low dietary vitamin A intake increased P1NP. PURPOSE: Vitamin A (VA) interacts with bone health, but mechanisms require clarification. In countries where multiple interventions exist to eradicate VA deficiency, some groups are consuming excessive VA. Bone metabolism and inflammatory parameters were measured in Zambian children who had high prevalence of hypervitaminosis A determined by 13C-retinol isotope dilution. METHODS:Children (n = 143), 5 to 7 years, were recruited into a placebo-controlled biofortified orange maize feeding study for 90 days. Bone turnover (P1NP and CTX) and inflammatory (C-reactive protein (CRP) and alpha-1-acid glycoprotein) biomarkers were measured in fasting blood samples before and/or after intervention with the following: (1) VA at the recommended dietary allowance (400 μg retinol activity equivalents/day (as retinyl palmitate)), (2) maize enhanced with the provitamin A carotenoid β-carotene (2.86 mg/day), or (3) a placebo. Parathyroid hormone, calcium, and 25(OH)-vitamin D were measured at end line. RESULTS:Bone formation, as measured by P1NP, increased (P < 0.0001) in the placebo group who consumed low preformed VA during the intervention. Bone resorption, measured by CTX, was not affected. P1NP and CTX were negatively associated with inflammation, most strongly with CRP. Serum calcium did not differ among groups and was low (7.29 ± 0.87 μg/dL). Serum 25(OH) D did not differ among groups (54.5 ± 15 nmol/L), with 91% < 75 nmol/L and 38% < 50 nmol/L. CONCLUSIONS: Reduction of dietary preformed VA in Zambian children for 4 months improved bone formation. Chronic consumption of preformed VA caused hypervitaminosis A and may impair bone formation. In children, this could be associated with failure to accrue optimal peak bone mass. TRIAL REGISTRATION: The NIH Clinical Trial registry number is NCT01814891; https://clinicaltrials.gov/ct2/show/NCT01814891 .
RCT Entities:
This analysis was performed in Zambian children who had a high prevalence of hypervitaminosis A, defined as > 1.0 μmol retinol/g liver. Bone parameters included markers of bone formation (P1NP), bone resorption (CTX), parathyroid hormone, calcium, vitamin A, and vitamin D. Low dietary vitamin A intake increased P1NP. PURPOSE:Vitamin A (VA) interacts with bone health, but mechanisms require clarification. In countries where multiple interventions exist to eradicate VA deficiency, some groups are consuming excessive VA. Bone metabolism and inflammatory parameters were measured in Zambian children who had high prevalence of hypervitaminosis A determined by 13C-retinol isotope dilution. METHODS:Children (n = 143), 5 to 7 years, were recruited into a placebo-controlled biofortified orange maize feeding study for 90 days. Bone turnover (P1NP and CTX) and inflammatory (C-reactive protein (CRP) and alpha-1-acid glycoprotein) biomarkers were measured in fasting blood samples before and/or after intervention with the following: (1) VA at the recommended dietary allowance (400 μg retinol activity equivalents/day (as retinyl palmitate)), (2) maize enhanced with the provitamin A carotenoid β-carotene (2.86 mg/day), or (3) a placebo. Parathyroid hormone, calcium, and 25(OH)-vitamin D were measured at end line. RESULTS: Bone formation, as measured by P1NP, increased (P < 0.0001) in the placebo group who consumed low preformed VA during the intervention. Bone resorption, measured by CTX, was not affected. P1NP and CTX were negatively associated with inflammation, most strongly with CRP. Serum calcium did not differ among groups and was low (7.29 ± 0.87 μg/dL). Serum 25(OH) D did not differ among groups (54.5 ± 15 nmol/L), with 91% < 75 nmol/L and 38% < 50 nmol/L. CONCLUSIONS: Reduction of dietary preformed VA in Zambian children for 4 months improved bone formation. Chronic consumption of preformed VA caused hypervitaminosis A and may impair bone formation. In children, this could be associated with failure to accrue optimal peak bone mass. TRIAL REGISTRATION: The NIH Clinical Trial registry number is NCT01814891; https://clinicaltrials.gov/ct2/show/NCT01814891 .
Authors: A Prats-Puig; T Puig; C Sitjar; M Mas-Parareda; P Grau-Cabrera; P Soriano-Rodríguez; M Montesinos-Costa; M Diaz; F de Zegher; L Ibáñez; J Bassols; A López-Bermejo Journal: Osteoporos Int Date: 2011-08-30 Impact factor: 4.507
Authors: Paige K Berger; Norman K Pollock; Emma M Laing; Valerie Chertin; Paul J Bernard; Arthur Grider; Sue A Shapses; Ke-Hong Ding; Carlos M Isales; Richard D Lewis Journal: J Nutr Date: 2015-10-21 Impact factor: 4.798
Authors: Sherry A Tanumihardjo; Robert M Russell; Charles B Stephensen; Bryan M Gannon; Neal E Craft; Marjorie J Haskell; Georg Lietz; Kerry Schulze; Daniel J Raiten Journal: J Nutr Date: 2016-08-10 Impact factor: 4.798
Authors: Martha E van Stuijvenberg; Serina E Schoeman; Jana Nel; Maretha le Roux; Muhammad A Dhansay Journal: Matern Child Nutr Date: 2019-12-17 Impact factor: 3.092