Article Text

Download PDFPDF
Are housing circumstances associated with faster epigenetic ageing? A commentary on Clair et al
  1. Faye Sanders1,
  2. Alexandre A Lussier2,3,4,
  3. Esther Walton1
  1. 1Department of Psychology, University of Bath, Bath, UK
  2. 2Center for Genomic Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA
  3. 3Department of Psychiatry, Harvard Medical School, Boston, Massachusetts, USA
  4. 4The Broad Institute of Harvard and, Boston, Massachusetts, USA
  1. Correspondence to Dr Esther Walton, Department of Psychology, University of Bath, Bath, UK; ew685{at}bath.ac.uk

Statistics from Altmetric.com

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

We read the article by Clair et al reporting an association between housing and biological ageing with great interest.1 This publication built on preliminary work on how the physically built environment associates with DNA methylation (DNAm)2 by focusing on DNAm age (also known as epigenetic age or epigenetic clock).

However, we note the authors investigated only one DNAm age measure: DunedinPACE. The authors argued that DunedinPACE was selected due to its greater association with mortality and morbidity than other measures of epigenetic age. While the paper they cited did indeed show that DunedinPACE predicted mortality better than the Hannum, Horvath and Levine clocks,3 it did not compare the performance of DunedinPACE to GrimAge, a more recently developed epigenetic clock for mortality.

Associations between exposures and DNAm age vary widely according to which clocks are used. Hence, we sought to …

View Full Text

Footnotes

  • X @sandersfaye_

  • Contributors FS generated the idea for the paper and conducted the analysis. FS, AAL and EW drafted the text, contributed to the interpretation of the results and critical revisions of the paper.

  • Funding The UK Medical Research Council and Wellcome (Grant ref: 217065/Z/19/Z) and the University of Bristol provide core support for ALSPAC. This publication is the work of the authors and they will serve as guarantors for the contents of this paper. A comprehensive list of grants funding is available on the ALSPAC website (http://www.bristol.ac.uk/alspac/external/documents/grant-acknowledgements.pdf); This research was specifically funded by the BBSRC (Grant ref: BBI025751/1 and BB/I025263/1). EW received funding from the European Union’s Horizon 2020 research and innovation programme (grant references: 848158, EarlyCause), from UK Research and Innovation (UKRI) under the UK government’s Horizon Europe/ERC Frontier Research Guarantee (BrainHealth, grant number EP/Y015037/1) and from the National Institute of Mental Health of the National Institutes of Health (award number R01MH113930). AAL is supported by a postdoctoral fellowship from the Canadian Institutes of Health Research and an MQ Fellows Award from the MQ Foundation.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; internally peer reviewed.