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Original research
Height, social position and coronary heart disease incidence: the contribution of genetic and environmental factors
  1. Karri Silventoinen1,2,
  2. Hannu Lahtinen1,
  3. George Davey Smith3,4,
  4. Tim T Morris3,4,
  5. Pekka Martikainen1,5,6
  1. 1 Population Research Unit, Faculty of Social Sciences, University of Helsinki, Helsinki, Finland
  2. 2 Department of Public Health, Faculty of Medicine, University of Helsinki, Helsinki, Finland
  3. 3 Bristol Medical School, Population Health Sciences, University of Bristol, Bristol, UK
  4. 4 MRC Integrative Epidemiology Unit at the University of Bristol, Bristol, UK
  5. 5 Centre for Health Equity Studies, Stockholm University, Stockholm, Sweden
  6. 6 Max-Planck-Institute for Demographic Research, Rostock, Germany
  1. Correspondence to Dr Karri Silventoinen, Population Research Unit, Faculty of Social Sciences, University of Helsinki, Helsinki, Finland; karri.silventoinen{at}helsinki.fi

Abstract

Background The associations between height, socioeconomic position (SEP) and coronary heart disease (CHD) incidence are well established, but the contribution of genetic factors to these associations is still poorly understood. We used a polygenic score (PGS) for height to shed light on these associations.

Methods Finnish population-based health surveys in 1992–2011 (response rates 65–93%) were linked to population registers providing information on SEP and CHD incidence up to 2019. The participants (N=29 996; 54% women) were aged 25–75 at baseline, and there were 1767 CHD incident cases (32% in women) during 472 973 person years of follow-up. PGS-height was calculated based on 33 938 single-nucleotide polymorphisms, and residual height was defined as the residual of height after adjusting for PGS-height in a linear regression model. HRs of CHD incidence were calculated using Cox regression.

Results PGS-height and residual height showed clear gradients for education, social class and income, with a larger association for residual height. Residual height also showed larger associations with CHD incidence (HRs per 1 SD 0.94 in men and 0.87 in women) than PGS-height (HRs per 1 SD 0.99 and 0.97, respectively). Only a small proportion of the associations between SEP and CHD incidence was statistically explained by the height indicators (6% or less).

Conclusions Residual height associations with SEP and CHD incidence were larger than for PGS-height. This supports the role of material and social living conditions in childhood as contributing factors to the association of height with both SEP and CHD risk.

  • SOCIAL CLASS
  • CARDIOVASCULAR DISEASES
  • GENETICS

Data availability statement

Data may be obtained from a third party and are not publicly available. The data underlying this article were provided by third party by permission. Data will be shared on request to the corresponding author with permission of third party.

https://doi.org/10.1136/jech-2022-219907

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    Data availability statement

    Data may be obtained from a third party and are not publicly available. The data underlying this article were provided by third party by permission. Data will be shared on request to the corresponding author with permission of third party.

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    Footnotes

    • Contributors All authors contributed to the study conception and design. HL performed the analyses. KS prepared the first draft of the manuscript. HL, GDS, TTM and PM revised the manuscript critically for important intellectual content. All authors approved the final version of the manuscript and agree to be accountable for all aspects of the work thereby ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. KS is responsible for the overall content as the guarantor.

    • Funding This work was supported by the Academy of Finland grant (#345219) for Hannu Lahtinen. Pekka Martikainen was supported by the Academy of Finland (#308247, # 345219), the European Research Council under the European Union’s Horizon 2020 research and innovation programme (grant agreement No 101019329) and the Max Planck—University of Helsinki Center for Social Inequalities in Population Health. George Davey Smith and Tim Morris work within the MRC Integrative Epidemiology Unit at the University of Bristol, which is supported by the Medical Research Council (MC_UU_00011/1).

    • Competing interests None declared.

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

    • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.