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• Early life social conditions and adult cancers: a fundamental research question
  Michelle Kelly-Irving
  Published on: 24 May 2016

• Published on: 24 May 2016

  Early life social conditions and adult cancers: a fundamental research question

  • Michelle Kelly-Irving, Senior researcher
  • Other Contributors:
    • Thierry Lang, Cyrille Delpierre

  We commend the authors for taking the hypothesis that cancer may have its roots in early life social conditions seriously [1]. Social inequalities exist for many cancer types and are usually attributed to differences in lifestyles and behaviours. Thus, attempts at primary prevention are often confined to relatively proximal disease risk factors at the individual level.

  Cancer development has mainly been conside...

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  We commend the authors for taking the hypothesis that cancer may have its roots in early life social conditions seriously [1]. Social inequalities exist for many cancer types and are usually attributed to differences in lifestyles and behaviours. Thus, attempts at primary prevention are often confined to relatively proximal disease risk factors at the individual level.

  Cancer development has mainly been considered as a consequence of DNA mutations and consequently tends to be viewed through the lens of molecular biology. However, cancer may be a disease model particularly relevant to investigate how the social becomes biological, via a lifecourse approach. Many socially stratified biological mechanisms have been identified as being part of the causal chain of risk for cancers: material exposures (including inert ones such as asbestos, or living ones such as the Helicobacter pylori virus) and behavioural mechanisms (including tobacco consumption and fatty food intake). Furthermore, the lifecourse approach is of particular interest when studying cancer because of the long latent time period during which exposures occur, before the onset of disease. There is increasing evidence for the role of chronic stress from early life in cancer development and progression.

  Upstream, cancer aetiologies differ, some being exogenous in origin (viruses, smoking) and others endogenous (hormonal cancers). However all cancers are at some point rooted in the immune and inflammatory system, and thereby their initiation is susceptible to factors affecting biological mechanisms at some point along this aetiological pathway. If the immune system is impaired from killing-off damaged cells, the risk of developing tumour cells is heightened [2]. A damaged immune system is also an important accelerator of cancer progression [3]. This root in the immune system is currently the source of the most promising immune-therapy treatment for many cancers [4]. In fact, there is increasing evidence that chronic stress may influence immune and inflammatory systems, implicating socially driven epigenetic mechanisms, which may represent an overall set of early life social determinants of cancer development over the lifecourse [5]

  Evidence on the link between early life stress and cancer in epidemiology remains sparse and inconclusive, and presents difficult methodological issues. Measuring early life physiological stress remains a challenge, but one worth investing in since acute versus chronic stress, and the timing of stress in early life may be important for subsequent stress responses. Stressful events are likely to be experienced differently depending on an individual's hierarchical position on the social gradient. Individuals lower on the social gradient may be more vulnerable to the physiological or behavioural effects of stressful environmental exposures with fewer resources and buffering strategies at their disposal compared to individuals with a higher social position [6]. Social gradients may also confer stress to individuals via status anxiety, which has also been shown in non-human primates [7]. Intra-familial conditions occurring from conception into adolescence may program physiological responses during sensitive periods of development, altering an individual's biology, rendering them susceptible when faced with exposures later in life [8]. We hypothesize that taking into account socially driven early life exposures to chronic stress is important to understanding the aetiology of cancers, which have a common root in the immune and inflammatory systems. These systems form part of the overall physiological stress response.

  We have inadequately attempted to examine this hypothesis, showing that early life adversity and social position is associated with adult cancers before the age of 50 [9]. However, due to a gaping hole in the available lifecourse data combined with good quality cancer incidence data in adulthood, the hypothesis remains to be fully investigated. As well as having mortality data, cancer incidence data provided by registries would allow for a better understanding of cancer aetiological pathways from early life social conditions onwards, and potentially highlight new areas for the primary prevention of cancers. We agree with the authors' point about investing resources into data, and we would emphasise the need for quality data on cancer incidence specifically. To truly get to grips with the aetiology of cancers, concerted investment in the birth cohort studies, and their linkage with registries is paramount.

  1 Vohra J, Marmot MG, Bauld L, et al. Socioeconomic position in childhood and cancer in adulthood: a rapid-review. J Epidemiol Community Health 2016;70:629-34. 2 Stewart TJ, Abrams SI. How tumours escape mass destruction. Oncogene 2008;27:5894-903. 3 Kim R, Emi M, Tanabe K. Cancer immunoediting from immune surveillance to immune escape. Immunology 2007;121:1-14. 4 Dustin ML. Cancer immunotherapy: Killers on sterols. Nature 2016;531:583 -4. 5 Kelly-Irving M, Mabile L, Grosclaude P, et al. The embodiment of adverse childhood experiences and cancer development: potential biological mechanisms and pathways across the life course. International Journal of Public Health 2013;58:3-11. 6 Baum A, Garofalo JP, Yali AM. Socioeconomic Status and Chronic Stress: Does Stress Account for SES Effects on Health? Ann N Y Acad Sci 1999;896:131-44. 7 Sapolsky RM. The Influence of Social Hierarchy on Primate Health. Science 2005;308:648-52. 8 Bailey DBJ, Bruer JT, Symons FJ, et al., eds. Critical thinling about critical periods. Baltimore: Paul H. Brookes publishing co. 2001. 9 Kelly-Irving M, Lepage B, Dedieu D, et al. Childhood adversity as a risk for cancer: findings from the 1958 British birth cohort study. BMC Public Health 2013;13:767.

  Conflict of Interest:

  None declared

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  Conflict of Interest:
  None declared.

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