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Developmental origins of osteoporotic fracture: the role of maternal vitamin d insufficiency

Developmental origins of osteoporotic fracture: the role of maternal vitamin d insufficiency
Developmental origins of osteoporotic fracture: the role of maternal vitamin d insufficiency
Osteoporosis is a major cause of morbidity and mortality through its association with age-related fractures. Although most efforts in fracture prevention have been directed at retarding the rate of age-related bone loss and reducing the frequency and the severity of trauma among elderly people, evidence is growing that peak bone mass is an important contributor to bone strength during later life. The normal patterns of skeletal growth have been well characterized in cross-sectional and longitudinal studies. It has been confirmed that boys have higher bone-mineral content, but not volumetric bone density, than girls. Furthermore, there is a disassociation between the peak velocities for height gain and bone mineral accrual in both genders. Puberty is the period during which volumetric density appears to increase in both axial and appendicular sites. Many factors influence the accumulation of bone mineral during childhood and adolescence, including heredity, gender, diet, physical activity, endocrine status, and sporadic risk factors (e.g., cigarette smoking). In addition to these modifiable factors during childhood, evidence has also accrued that fracture risk might be programmed during intrauterine life. Epidemiological studies have demonstrated a relationship between birthweight, weight in infancy, and adult bone mass. This appears to be mediated through modulation of the set-point for basal activity of endocrine systems such as the GH/IGF-1 and parathyroid hormone/vitamin D axes. Maternal vitamin D insufficiency is associated with reduced bone mineral acquisition during intrauterine and early postnatal life. Furthermore, both low birth size and poor childhood growth are directly linked to the later risk of hip fracture. The optimization of maternal nutrition and intrauterine growth should also be included within preventive strategies against osteoporotic fracture, albeit for future generations.
osteoporosis, epidemiology, growth, programming
0022-3166
2728S-2734S
Cooper, Cyrus
e05f5612-b493-4273-9b71-9e0ce32bdad6
Javaid, Kassim
69bf78c2-9bb1-48b8-8c26-157a823b3421
Westlake, Sarah
91d63b6c-1af8-45d1-a7e1-302407b78e3d
Harvey, Nicholas
6a655234-2597-4d42-8dba-0ffd7e6bfa39
Dennison, Elaine
ee647287-edb4-4392-8361-e59fd505b1d1
Cooper, Cyrus
e05f5612-b493-4273-9b71-9e0ce32bdad6
Javaid, Kassim
69bf78c2-9bb1-48b8-8c26-157a823b3421
Westlake, Sarah
91d63b6c-1af8-45d1-a7e1-302407b78e3d
Harvey, Nicholas
6a655234-2597-4d42-8dba-0ffd7e6bfa39
Dennison, Elaine
ee647287-edb4-4392-8361-e59fd505b1d1

Cooper, Cyrus, Javaid, Kassim, Westlake, Sarah, Harvey, Nicholas and Dennison, Elaine (2005) Developmental origins of osteoporotic fracture: the role of maternal vitamin d insufficiency. Journal of Nutrition, 135 (11), 2728S-2734S.

Record type: Article

Abstract

Osteoporosis is a major cause of morbidity and mortality through its association with age-related fractures. Although most efforts in fracture prevention have been directed at retarding the rate of age-related bone loss and reducing the frequency and the severity of trauma among elderly people, evidence is growing that peak bone mass is an important contributor to bone strength during later life. The normal patterns of skeletal growth have been well characterized in cross-sectional and longitudinal studies. It has been confirmed that boys have higher bone-mineral content, but not volumetric bone density, than girls. Furthermore, there is a disassociation between the peak velocities for height gain and bone mineral accrual in both genders. Puberty is the period during which volumetric density appears to increase in both axial and appendicular sites. Many factors influence the accumulation of bone mineral during childhood and adolescence, including heredity, gender, diet, physical activity, endocrine status, and sporadic risk factors (e.g., cigarette smoking). In addition to these modifiable factors during childhood, evidence has also accrued that fracture risk might be programmed during intrauterine life. Epidemiological studies have demonstrated a relationship between birthweight, weight in infancy, and adult bone mass. This appears to be mediated through modulation of the set-point for basal activity of endocrine systems such as the GH/IGF-1 and parathyroid hormone/vitamin D axes. Maternal vitamin D insufficiency is associated with reduced bone mineral acquisition during intrauterine and early postnatal life. Furthermore, both low birth size and poor childhood growth are directly linked to the later risk of hip fracture. The optimization of maternal nutrition and intrauterine growth should also be included within preventive strategies against osteoporotic fracture, albeit for future generations.

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More information

Published date: 2005
Additional Information: Supplement: the influence of vitamin D on bone health across the life cycle
Keywords: osteoporosis, epidemiology, growth, programming

Identifiers

Local EPrints ID: 25383
URI: https://eprints.soton.ac.uk/id/eprint/25383
ISSN: 0022-3166
PURE UUID: eef11744-adb7-4f4a-a930-d1fddbe7cf2a
ORCID for Cyrus Cooper: ORCID iD orcid.org/0000-0003-3510-0709
ORCID for Elaine Dennison: ORCID iD orcid.org/0000-0002-3048-4961

Catalogue record

Date deposited: 07 Apr 2006
Last modified: 10 Jan 2019 01:37

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