Commentary: The course of life and life, of course: a commentary on Ben-Shlomo, Cooper and Kuh

The review by Ben-Shlomo, Cooper and Kuh in this current special issue offers, with the authors’ usual acuity and attentiveness to detail, a comprehensive summary of the conception, gestation, early life and developmental maturation of the life course epidemiology field. Beginning in the early 1990s and propelled in particular by the 1997 publication of the seminal first edition of A Life Course Approach to Chronic Disease Epidemiology,1 there has been a sustained amassing of studies addressing ‘long-term biological, behavioural and psychosocial processes that link adult health and disease risk to physical or social exposures [in early life]’. This should come as no great surprise, given enduring cultural convictions—crossing geography and time—that the special sensibilities of young children, when exposed to psychological and physical adversities, can produce forms of morbidity extending well beyond the exposure itself and into the domains of adult life. Biologist René Dubos invoked ‘biological Freudianism’ to argue that adverse exposures in childhood can produce lasting neurobiological risks that persist even when such exposures are later abated or gone.2 A multidisciplinary working group of the Canadian Institute for Advanced Research (CIFAR) showed how population health and developmental science coincide to reveal powerful societal effects on child development and health and how such effects are transcribed into lifetimes of socially partitioned differences in risk for adult disease.3 The American Academy of Pediatrics recently called public attention to the issues of significant adversity and ‘toxic stress’ in the lives of young children and asserted that many of the chronic disorders of adult life should now be regarded as ‘developmental disorders’, stemming as they do from adverse childhood experiences and events.4 Further, three major reports—in the USA,5 the UK6 and Canada7—have catalyzed strong consensus that the experiences of early life, dramatically partitioned by aspects of socioeconomic status (SES) and social position, result in societies with widely divergent developmental and health outcomes. Although the course of life reflects a massive abundance of potential linkages between early exposures and later morbidities, the long and abiding uncertainties of life, of course, remain mysteries largely untouched by the eruditions of contemporary science. Nonetheless, among the scientific developments and frontiers addressed in the Ben-Shlomo et al. review, we would highlight the following territories of research as those most likely to yield fundamental, and relatively immediate, new insights with significant potential for expanding the perimeter of life course epidemiology. First is the indispensability of longitudinal observation spanning important developmental transitions and epochs. Although cross-sectional studies have produced immense stockpiles of suggestive and sometimes informative associations, reliable, new knowledge of development can emanate only from prospective, longitudinal studies of change over time.8 Second, main effects can tell us much about the most powerful, pervasive drivers of risk and morbidity within human populations; but equally, or sometimes more revealing, are carefully recorded individual differences in the effects of environmental exposures and interventions.9 Variation in life course trajectories of risk has the potential for both deepening understanding of the true nature of environmental exposures and refocusing intervention goals. Third, the advent of massive arrays of continuously recorded, digital data, captured from environmental sensors, health records and high-throughput molecular genomics, is introducing transformative change in both how we will do future life course research and the analytical approaches we will take to producing credible findings.10 Fourth, molecular-level descriptions of the processes governing onset and offset of critical and sensitive periods are redefining the role of developmental time in the genesis of human afflictions. Indeed, we are poised on the brink of pharmacological and other molecular interventions capable of opening and closing windows of developmental opportunity.11 Finally, life course epidemiology offers magnificent, new opportunities for studying and understanding the molecular events underpinning gene-environment interaction and the shifting, epigenetic processes that likely guide the formation of longitudinal trajectories of health and disease. Notwithstanding the availability of a rich, relevant and rapidly growing knowledge base in this field, however, significant reductions in population-level disparities in health and longevity associated with adversity have been exceedingly difficult to achieve. That said, the challenge of moving from a deeper level of analysis to a more effective action strategy demands fresh approaches and new ideas. For policy makers, the challenge is to overcome the widespread belief that social class differences in health and the linkages between adversity and disease over the life course are impossible to change beyond small incremental gains. For practitioners across a broad range of health and human services, the dramatic mismatch between the magnitude of burdens facing the most disadvantaged people and the limited effectiveness of most conventional interventions have produced a parallel sense of modest expectations about how much life prospects can be altered. Raising the bar for both policy makers and practitioners—and achieving far greater impacts across the life course—will require creative thinking, a rigorous approach to the design and testing of new strategies and greater attention to learning from interventions that don’t work. Central to the success of this effort is the need to leverage converging insights from both life course epidemiology and the biology of adversity to address three critical issues identified by Ben-Shlomo et al. The first is the need to further elucidate the pathogenic mechanisms that lead to the social partitioning of health outcomes across the life span. The second is the critical importance of understanding variation in susceptibility to adverse experiences. The third is the need for measures of biological and bio-behavioural indicators of toxic stress effects that are valid and reliable short-term markers of increased risk for long-term impairments. Together, these three areas of investigation offer a wealth of evolving knowledge that could be used to close the gap between what we know about the predictors of health trajectories and what we do to enhance well-being over the life course. Converging advances in the biological, behavioural and social sciences offer a remarkable opportunity to deepen our knowledge about how the process of healthy development unfolds (from conception to ageing), how it can be derailed by adversity and how to get it back on track or (even better) prevent it from getting derailed in the first place. Testable hypotheses based on identified causal mechanisms should be guiding the development and evaluation of new strategies that target specified environmental variables or individual behaviours to achieve explicit, pre-defined outcomes. Although dramatic progress at a societal level will require a broad-based commitment to reducing poverty, violence, racism and other sources of social exclusion, the impacts of specific policies and programmes targeted toward disadvantaged groups could be augmented considerably by a science-informed approach to determining ‘what works’ and which specific components of a successful strategy are its active ingredients. Understanding why and how adversity affects different people in different ways at different points in the life cycle is also essential for developing and prioritizing more effective policies for both prevention and treatment. New discoveries from investigations in both life course epidemiology and the biological sciences could inform the development of a suite of strategies matched to differences in how children and adults respond to different hardships and alternative services. The subsequent transition from successful demonstration projects to population-level impacts will require an approach to measurement, evaluation and replication that moves beyond the question of whether a policy or programme is effective, to address the more important questions of who benefits most from a specific intervention strategy and why (which should trigger targeted scaling) and who benefits least or not at all and why (which should galvanize the search for new or complementary approaches). Drawing on lessons learned from dramatic gains that have been made in the management of infectious disease, comparable progress could be achieved in reducing the lifelong consequences of adversity through multiple strategies. These could range from policies focused explicitly on the primary prevention or reduction of precipitants of toxic stress in children (e.g. parental substance misuse, child maltreatment) to focused efforts on strengthening defences against adversity, matching different interventions to different causal agents, and overcoming resistance to available treatments by developing new strategies across the life course. Rigorous measures of biological (e.g. stress hormones and inflammatory markers) and bio-behavioural (e.g., assessments of attention and self-regulation) indicators of toxic stress effects will become increasingly used over the next several years. These measures will provide important information above and beyond global predictors of risk, that are helpful for screening purposes [e.g. socioeconomic status (SES), inventories of adverse childhood experiences] but have no diagnostic significance for individuals. The value of new assessment batteries will be determined by their sensitivity to short-term changes in potential mediators of long-term health outcomes and their acceptability and affordability in community-based settings. Egregious historical examples of the misuse of biology to stigmatize racial or ethnic minority groups underscores the necessity of community co-ownership of the use of these measures, to prevent inappropriate labelling and the medicalization of socioeconomic adversity. Finally, above and beyond developing new intervention programmes, science-informed innovation must be incorporated within multidimensional systems that cross sectors and are more than simply an amalgamation of services. These systems are complex entities that set priorities, formulate policies and facilitate the implementation of a variety of practices. Considerable effort will be needed to incorporate scientific knowledge in a way that drives fresh thinking and innovative action within highly entrenched structures and practices. As the frontiers of life course epidemiology and the biology of adversity continue to converge, a deeper understanding of causal mechanisms that are amenable to targeted intervention will produce a powerful resource for change agents focused on reducing disparities across the life span. Past experience, however, indicates that the translation of that knowledge into significant impacts will be exceedingly difficult. The achievement of true population-level change will depend upon the collective contributions of scientists, policy makers, practitioners and community leaders—and breakthrough outcomes will require a strategic blend of scientific rigour, public will and effective political leadership. The work of W. Thomas Boyce is supported in part by the Lisa and John Pritzker Distinguished Professorship in Developmental and Behavioral Health and that of Jack P. Shonkoff by the Julius B. Richmond FAMRI Professorship of Child Health and Development. Conflict of interest: The authors have had no involvements that might raise questions of bias in the conclusions, implications, or opinions stated.

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