Exposures during the prepuberty period and future offspring's health: Evidence from human cohort studies

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  • Cecilie Svanes, Centre for International Health, Department of Global Public Health and Primary Care, University of Bergen, Bergen, Department of Occupational Medicine, Haukeland University Hospital, Bergen, Norge
  • Randi J Bertelsen, Department of Clinical Science, University of Bergen, Oral Health Centre of Expertise in Western Norway, Bergen, Norge
  • Simone Accordini, University Hospital of Verona, Verona, Italien
  • John W Holloway, Faculty of Medicine, University of Southampton, University Hospital Southampton, Southampton, Hampshire SO16 6YD, UK., NIHR Southampton Biomedical Research Centre, University Hospital Southampton NHS Foundation Trust, University of Southampton, Southampton, United Kingdom., Storbritannien
  • Pétur Juliusson, Department of Clinical Science, University of Bergen, Department of Health Register Research and Development, National Institute of Public Health, Bergen, Norge
  • Eistine Boateng, Research Center Borstel - Leibniz Lung Center, Tyskland
  • Susanne Krauss-Eschmann, Research Center Borstel - Leibniz Lung Center, Institute of Experimental Medicine, Christian-Albrechts-Universität zu Kiel, Tyskland
  • Vivi Schlünssen
  • Francisco Gomez-Real, Department of Clinical Science, University of Bergen, Department of Gynaecology and Obstetrics, Haukeland University Hospital, Bergen, Norge
  • Svein Magne Skulstad, Department of Occupational Medicine, Haukeland University Hospital, Bergen, Norge

Emerging evidence suggests that exposures in prepuberty, particularly in fathers-to-be, may impact the phenotype of future offspring. Analyses of the RHINESSA cohort find that offspring of father's exposed to tobacco smoking or overweight that started in prepuberty demonstrate poorer respiratory health in terms of more asthma and lower lung function. A role of prepuberty onset smoking for offspring fat mass is suggested in the RHINESSA and ALSPAC cohorts, and historic studies suggest that ancestral nutrition during prepuberty plays a role for grand-offspring's health and morbidity. Support for causal relationships between ancestral exposures and (grand-)offspring's health in humans has been enhanced by advancements in statistical analyses that optimize the gain while accounting for the many complexities and deficiencies in human multigeneration data. The biological mechanisms underlying such observations have been explored in experimental models. A role of sperm small RNA in the transmission of paternal exposures to offspring phenotypes has been established, and chemical exposures and overweight have been shown to influence epigenetic programming in germ cells. For example, exposure of adolescent male mice to smoking led to differences in offspring weight and alterations in small RNAs in the spermatozoa of the exposed fathers. It is plausible that male prepuberty may be a time window of particular susceptibility, given the extensive epigenetic reprogramming taking place in the spermatocyte precursors at this age. In conclusion, epidemiological studies in humans, mechanistic research, and biological plausibility, all support the notion that exposures in the prepuberty of males may influence the phenotype of future offspring.

OriginalsprogEngelsk
TidsskriftBiology of Reproduction
Vol/bind105
Nummer3
Sider (fra-til)667–680
ISSN0006-3363
DOI
StatusUdgivet - sep. 2021

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© The Author(s) 2021. Published by Oxford University Press on behalf of Society for the Study of Reproduction.

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