Susan A. New
University of Surrey
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Featured researches published by Susan A. New.
Journal of Bone and Mineral Research | 2003
Jaana Nurmi-Lawton; Adam Baxter-Jones; Robert L. Mirwald; Jacki A Bishop; Patricia Taylor; C Cooper; Susan A. New
The skeletal effects from intensive exercise throughout puberty are undefined. Forty‐five female gymnasts and 52 controls were studied over 3 years, including a heredity aspect. The effects of size, maturity, exercise, and diet were identified using a multilevel regression model. Results demonstrated sustained skeletal benefits resulting from exercise throughout all stages of pubertal development.
Journal of Bone and Mineral Research | 2001
Helen M. Macdonald; Fiona A. McGuigan; Susan A. New; Marion K Campbell; Michael H. N Golden; Stuart H. Ralston; David M. Reid
Genetic factors play an important role in the pathogenesis of osteoporosis but the genes that determine susceptibility to poor bone health are defined incompletely. Previous work has shown that a polymorphism that affects an Sp1 binding site in the COL1A1 gene is associated with reduced bone mineral density (BMD) and an increased risk of osteoporotic fracture in several populations. Data from cross‐sectional studies have indicated that COL1A1 Sp1 alleles also may be associated with increased rates of bone loss with age, but longitudinal studies, which have examined bone loss in relation to COL1A1> genotype, have yielded conflicting results. In this study, we examined the relationship between COL1A1 Sp1 alleles and early postmenopausal bone loss measured by dual‐energy X‐ray absorptiometry (DXA) in a population‐based cohort of 734 Scottish women who were followed up over a 5‐ to 7‐year period. The distribution of genotypes was as expected in a white population with 484 “SS” homozygotes (65.9%); 225 “Ss” heterozygotes (30.7%), and 25 “ss” homozygotes (3.4%). Women taking hormone‐replacement therapy (HRT; n = 239) had considerably reduced rates of bone loss at the spine (−0.40 ± 0.06%/year) and hip (−0.56 ± 0.06%/year) when compared with non‐HRT users (n = 352; spine, −1.36 ± 0.06%/year; hip, −1.21 ± 0.05%/year; p < 0.001 for both sites). There was no significant difference in baseline BMD values at the lumbar spine (LS) or femoral neck (FN) between genotypes or in the rates of bone loss between genotypes in HRT users. However, in non‐HRT users (n = 352), we found that ss homozygotes (n = 12) lost significantly more bone at the lumbar site than the other genotype groups in which ss = −2.26 ± 0.31%/year compared with SS = −1.38 ± 0.07%/year and Ss = −1.22 ± 0.10%/year (p = 0.004; analysis of variance [ANOVA]) and a similar trend was observed at the FN in which ss = −1.78 ± 0.19%/year compared with SS = −1.21 ± 0.06%/year and Ss = −1.16 ± 0.08%/year (p = 0.06; ANOVA). The differences in spine BMD loss remained significant after correcting for confounding factors. Stepwise multiple regression analysis showed that COL1A1 genotype independently accounted for a further 3.0% of the variation in spine BMD change after age (4.0%), weight (5.0%), and baseline BMD (2.8%). We conclude that women homozygous for the Sp1 polymorphism are at significantly increased risk of excess rates of bone loss at the spine, but this effect may be nullified by the use of HRT.
Proceedings of the Nutrition Society | 1997
Simon P. Robins; Susan A. New
In recent years, there has been both an increasing awareness of, and interest in, bone health which has been combined with a recognition that nutritional factors may have an influential role in developing and maintaining bone status. In contrast to the situation approximately 15 years ago, when only 5 % of general practitioners acknowledged the occurrence of osteoporosis, this disorder of bone metabolism is now much more widely recognized. With 60 000 hip fractures resulting from osteoporosis each year in the UK alone, this debilitating disease has dramatic effects on society in both social and economic terms. It is important, therefore, that research defines more closely the mechanisms of bone loss that give rise to osteoporosis and the nutritional influences on these processes. The aim of the present paper is, first, to summarize the biochemical techniques currently available for assessing bone metabolism and, second, to review the current knowledge of nutritional influences on bone turnover using these markers.
Archive | 2003
Susan A. New; Jean-Philippe Banjour; Velimir Matkovic; Zelijka Crncevic-Orlic; John D. Landoll
Calcium intake below requirement level during bone modeling and skeletal consolidation could lower peak bone mass in the population
Archive | 2003
Susan A. New; Jean-Philippe Banjour; David Reid
Summary This article explains the pathogenesis and diagnosis of osteoporosis and treatment options for patients with the condition. It also discusses service provision and focuses on the nurse’s role in treating patients with osteoporosis. Author
The American Journal of Clinical Nutrition | 2000
Susan A. New; Simon P. Robins; Marion K Campbell; James C. Martin; Mark Garton; Caroline Bolton-Smith; David A Grubb; Sue J Lee; David M. Reid
The American Journal of Clinical Nutrition | 2005
Helen M. Macdonald; Susan A. New; William D. Fraser; Marion K Campbell; David M. Reid
The American Journal of Clinical Nutrition | 2004
Susan A. New; Helen M. Macdonald; Marion K Campbell; James C. Martin; Mark Garton; Simon P. Robins; David M. Reid
Bone | 2004
Helen M. Macdonald; Fiona McGuigan; William D. Fraser; Susan A. New; Stuart H. Ralston; David M. Reid
Osteoporosis International | 2005
Helen M. Macdonald; Susan A. New; Marion K Campbell; David M. Reid