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    Allostatic load and subsequent all-cause mortality: which biological markers drive the relationship? Findings from a UK birth cohort.

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    Author
    Castagné, R; Garès, V; Karimi, M; Chadeau-Hyam, M; Vineis, P; Delpierre, C; Kelly-Irving, M; Lifepath Consortium
    Date
    2018-05
    Source Title
    European Journal of Epidemiology
    Publisher
    Springer Science and Business Media LLC
    University of Melbourne Author/s
    Giles, Graham; Severi, Gianluca
    Affiliation
    Melbourne School of Population and Global Health
    Metadata
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    Document Type
    Journal Article
    Citations
    Castagné, R., Garès, V., Karimi, M., Chadeau-Hyam, M., Vineis, P., Delpierre, C., Kelly-Irving, M. & Lifepath Consortium (2018). Allostatic load and subsequent all-cause mortality: which biological markers drive the relationship? Findings from a UK birth cohort.. Eur J Epidemiol, 33 (5), pp.441-458. https://doi.org/10.1007/s10654-018-0364-1.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/254861
    DOI
    10.1007/s10654-018-0364-1
    Open Access at PMC
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5968064
    Abstract
    The concept of allostatic load (AL) refers to the idea of a global physiological 'wear and tear' resulting from the adaptation to the environment through the stress response systems over the life span. The link between socioeconomic position (SEP) and mortality has now been established, and there is evidence that AL may capture the link between SEP and mortality. In order to quantitatively assess the role of AL on mortality, we use data from the 1958 British birth cohort including eleven year mortality in 8,113 adults. Specifically, we interrogate the hypothesis of a cumulative biological risk (allostatic load) reflecting 4 physiological systems potentially predicting future risk of death (N = 132). AL was defined using 14 biomarkers assayed in blood from a biosample collected at 44 years of age. Cox proportional hazard regression analysis revealed that higher allostatic load at 44 years old was a significant predictor of mortality 11 years later [HR = 3.56 (2.3 to 5.53)]. We found that this relationship was not solely related to early-life SEP, adverse childhood experiences and young adulthood health status, behaviours and SEP [HR = 2.57 (1.59 to 4.15)]. Regarding the ability of each physiological system and biomarkers to predict future death, our results suggest that the cumulative measure was advantageous compared to evaluating each physiological system sub-score and biomarker separately. Our findings add some evidence of a biological embodiment in response to stress which ultimately affects mortality.

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