Imperial College London

Professor Duncan Bassett

Faculty of MedicineDepartment of Metabolism, Digestion and Reproduction

Professor of Endocrinology
 
 
 
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Contact

 

+44 (0)20 3313 4613d.bassett Website

 
 
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Location

 

10N6 Commomwealth BuildingHammersmith HospitalHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Van:2018:10.1002/jbmr.3426,
author = {Van, Vliet NA and Noordam, R and Van, Klinken JB and Westendorp, RGJ and Bassett, JHD and Williams, GR and Van, Heemst D},
doi = {10.1002/jbmr.3426},
journal = {Journal of Bone and Mineral Research},
pages = {1318--1325},
title = {Thyroid stimulating hormone and bone mineral density: evidence from a two-sample Mendelian randomization study and a candidate gene association study},
url = {http://dx.doi.org/10.1002/jbmr.3426},
volume = {33},
year = {2018}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - With population aging, prevalence of low bone mineral density (BMD) and associated fracture risk are increased. To determine whether low circulating thyroid stimulating hormone (TSH) levels within the normal range are causally related to BMD, we conducted a two-sample Mendelian randomization (MR) study. Furthermore, we tested whether common genetic variants in the TSH receptor (TSHR) gene and genetic variants influencing expression of TSHR (eQTLs) are associated with BMD. For both analyses, we used summary-level data of genome-wide association studies (GWAS) investigating BMD of the femoral neck (N = 32,735) and the lumbar spine (N = 28,498) in cohorts of European ancestry from the Genetic Factors of Osteoporosis (GEFOS) Consortium. For the MR study, we selected 20 genetic variants that were previously identified for circulating TSH levels in a GWAS meta-analysis (N = 26,420). All independent genetic instruments for TSH were combined in analyses for both femoral neck and lumbar spine BMD. In these studies, we found no evidence that a genetically determined 1 standard deviation (SD) decrease in circulating TSH concentration was associated with femoral neck BMD (0.003 SD decrease in BMD per SD decrease of TSH, 95% C.I. -0.053; 0.048, P = 0.92) or lumbar spine BMD (0.010 SD decrease in BMD per SD decrease of TSH, 95% C.I. -0.069; 0.049, P = 0.73). A total of 706 common genetic variants have been mapped to the TSHR locus and expression loci for TSHR. However, none of these genetic variants were associated with BMD at the femoral neck or lumbar spine. In conclusion, we found no evidence for a causal effect of circulating TSH on BMD, nor did we find any association between genetic variation at the TSHR locus or expression thereof and BMD. This article is protected by copyright. All rights reserved.
AU - Van,Vliet NA
AU - Noordam,R
AU - Van,Klinken JB
AU - Westendorp,RGJ
AU - Bassett,JHD
AU - Williams,GR
AU - Van,Heemst D
DO - 10.1002/jbmr.3426
EP - 1325
PY - 2018///
SN - 1523-4681
SP - 1318
TI - Thyroid stimulating hormone and bone mineral density: evidence from a two-sample Mendelian randomization study and a candidate gene association study
T2 - Journal of Bone and Mineral Research
UR - http://dx.doi.org/10.1002/jbmr.3426
UR - https://www.ncbi.nlm.nih.gov/pubmed/29544020
UR - http://hdl.handle.net/10044/1/58399
VL - 33
ER -