Abstract
Blood pressure and bone metabolism appear to share commonalities in their physiologic regulation. Specific antihypertensive drug classes may also influence bone mineral density. However, current evidence from existing observational studies and randomised trials is insufficient to establish causal associations for blood pressure and use of blood pressure–lowering drugs with bone health outcomes, particularly with the risks of osteoporosis and fractures. The availability and access to relevant large-scale biomedical data sources as well as developments in study designs and analytical approaches provide opportunities to examine the nature of the association between blood pressure and bone health more reliably and in greater detail than has ever been possible. It is unlikely that a single source of data or study design can provide a definitive answer. However, with appropriate considerations of the strengths and limitations of the different data sources and analytical techniques, we should be able to advance our understanding of the role of raised blood pressure and its drug treatment on the risks of low bone mineral density and fractures. As elevated blood pressure is highly prevalent and blood pressure–lowering drugs are widely prescribed, even small effects of these exposures on bone health outcomes could be important at a population level.
| Original language | English |
|---|---|
| Pages (from-to) | 315-326 |
| Number of pages | 12 |
| Journal | Osteoporosis International |
| Volume | 33 |
| Issue number | 2 |
| Early online date | 13 Oct 2021 |
| DOIs | |
| Publication status | Published - Feb 2022 |
Bibliographical note
Preprint version appears in the SSRN: https://papers.ssrn.com/sol3/papers.cfm?abstract_ id= 3825832.Funding Information:
Dexter Canoy received support from the National Institute of Health Research (NIHR) Oxford Biomedical Research Centre (BRC) and the British Heart Foundation outside the submitted work. Nicholas C Harvey reports consultancy/lecture fees/honoraria/grant funding from Alliance for Better Bone Health, Amgen, MSD, Eli Lilly, Radius Health, Servier, Shire, UCB, Consilient Healthcare and Internis Pharma outside the submitted work. Daniel Prieto-Alhambra’s department reports grants and other from AMGEN; grants, non-financial support and other from UCB Biopharma; grants from Les Laboratoires Servier; consultancy service fee from Astra Zeneca; and grants from EMA, all outside the submitted work; Janssen, on behalf of IMI-funded EHDEN and EMIF consortiums, and Synapse Management Partners have supported training programmes organised by Daniel Prieto-Alhambra’s department and open for external participants. Professor Cyrus Cooper has received lecture fees and honoraria from Amgen, Danone, Eli Lilly, GSK, Kyowa Kirin, Medtronic, Merck, Nestlé, Novartis, Pfizer, Roche, Servier, Shire, Takeda and UCB outside of the submitted work. Haakon E. Meyer and Bjørn Olav Åsvold declare no conflict of interest. MN has received studentship from the British Heart Foundation for a project outside of this submitted work. KR received support from the NIHR Oxford BRC, British Heart Foundation and Oxford Martin School at University of Oxford outside of this submitted work. Funding organisations had no role in the conception, manuscript preparation, interpretation, review or approval to submit for publication.
Publisher Copyright:
© 2021, The Author(s).
