question: There are many 'faces' of early life adversity (ELA), such as childhood trauma, institutionalisation, 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 immunosenescence, 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 immunosenescence and systemic inflammation. We conclude that ELA might act 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 ELA 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.