Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Is Early Life Adversity a Trigger towards Inflammageing?

Version 1 : Received: 7 March 2021 / Approved: 9 March 2021 / Online: 9 March 2021 (09:26:00 CET)

A peer-reviewed article of this Preprint also exists.

Seal, S.V.; Turner, J.D. The ‘Jekyll and Hyde’ of Gluconeogenesis: Early Life Adversity, Later Life Stress, and Metabolic Disturbances. Int. J. Mol. Sci. 2021, 22, 3344. https://doi.org/10.3390/ijms22073344 Seal, S.V.; Turner, J.D. The ‘Jekyll and Hyde’ of Gluconeogenesis: Early Life Adversity, Later Life Stress, and Metabolic Disturbances. Int. J. Mol. Sci. 2021, 22, 3344. https://doi.org/10.3390/ijms22073344

Journal reference: International Journal of Molecular Sciences 2021, 22, 334
DOI: 10.3390/ijms22073344

Abstract

There are many ‘faces’ of early life adversity (ELA), such as childhood trauma, institutionalization, abuse or exposure to environmental toxins. These have been implicated in the onset and severity of a wide range of chronic non-communicable diseases later in life. The later-life disease risk has a well-established immunological component. This raises the question as to whether accelerated immune-ageing mechanistically links early-life adversity to the lifelong health trajectory resulting in either ‘poor’ or ‘healthy’ ageing. Here we examine observational and mechanistic studies of ELA and inflammageing, highlighting common and distinct features in these two life stages. Many biological processes appear in common including reduction in telomere length, increased immuno-senescence, metabolic distortions and chronic (viral) infections. We propose that ELA shapes the developing immune, endocrine and nervous system in a non-reversible way, creating a distinct phenotype with accelerated immuno-senescence and systemic inflammation. We believe that ELA acts as an accelerator for inflammageing and age-related diseases. Furthermore, we now have the tools and cohorts to be able to dissect the interaction between early life adversity and later life phenotype. This should, in the near future, allow us to identify the ecological and mechanistic processes that are involved in ‘healthy’ or accelerated immune-ageing.

Subject Areas

early life adversity; stress; psychosocial stress; hypothalamus-pituitary-adrenal axis; ageing; immuno-senescence; inflammageing; Developmental origins of health and disease

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