From the social science point of view, a life course approach concentrates on age-related transitions that are socially created, socially recognized, and shared [ 7 ]. Sociologists have investigated how the individual's life course is structured by institutions and culture, social and historical change, and changes in individual aging processes.
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The life course approach to ageing suggests that the rate of decline in function for a particular organ or system is not only dependent on contemporary influences but on the level of peak function attained earlier in life, which in turn depends partly on developmental processes and early environmental influences (Dodds et al.
Therefore the life course perspective promotes analyses that take into account both social and biological opportunities at a specific historical time. Both structure and agency contribute to an understanding of health inequalities (Abel and Frohlich 2012 ).
Turning to potential interventions, the life course approach indicates that a shift in trajectory may need to be produced at a time when an individual or population group is fundamentally healthy and not accessing health services voluntarily (Hanson & Gluckman, 2011 b ).
Health disparities are the result of population-level life trajectories formed as a result of life experiences and exposures within a dynamic multilevel system. Life course perspectives provide important concepts to understand and address the origins, persistence, and transmission across generations of health disparities.
This means that the notion of a family comes from an ideological need or want to reproduce, to develop community, or at the very least from the culture which dictates what a "family" means to them, particularly. Life theory, though, relies on the intersection of these social factors of influence with the historical factor of moving through time, paired against personal development as an ...
I n limning the etymology of the concept of the life course, Alwin makes a number of prime points and paves the way toward further conceptual development. For me, one of the more prominent takeaway messages is that there is no standard model—to borrow a phrase from particle physics. He makes clear that life course analysis is not an exact science, and, sticking with the same analogy for a ...
Article citations More>>. Giele, J. and Elder, G. (1998) Life Course Research: Development of a Field. In: Giele, J. and Elder, G., Eds., Methods of Life Course ...
Life course theory (LCT) is an emerging interdisciplinary theory that seeks to understand the multiple factors that shape people’s lives from birth to death, placing individual and family development in cultural and historical contexts.
Elder has recently stated that the idea of developmental risk and protection as a major theme of the life course perspective. Other life course scholars have suggested that it is not simply the timing and sequencing of hardships but also their duration and spacing that provide risk for youth as they make the transition into adulthood.
Growing out of widely shared images and social values, an ideal old age legitimates norms and roles appropriate to the last stage of life. This article discusses the "late Calvinist" and "civilized" models of old age that flourished in Protestant, middle-class America between 1800 and 1920. It argues that the growing cultural dominance of science and the accelerating pace of capitalist productivity undercut the essential vision underlying these models: the view of life as a spiritual journey. The result has been a serious weakening of social meaning in aging and old age.
E. Michael Brady. Autobiography is an important means of facilitating adult learning and development. The process which is most associated with autobiography is memory. Memory is more than the recollection of past events; it is a critical element in the search for and construction of meaning in human experience in that it provides ...
Policies and programmes need to recognise the accumulated consequences of Analyn's disadvantage throughout life in order to better address her rights in older age.
A social pension was introduced by the government. This went some way to mitigate against the negative consequences of Analyn's lack of education as a young girl , and her lifetime of insecure informal work. However, the high cost of medicine and food in the local market means her pension did not go far.
From the moment we are born, we all begin ageing. This is the start of a complex and varied lifecourse. Each of us live through different events, we make choices, we face the consequences of policies and systems, and intersecting forms of discrimination that influence our lives. As we grow older, the impact on us of these different experiences accumulates.
Analyn. As a girl, Analyn did not have the opportunity to go to school. This had consequences throughout the lifecourse. She worked at a market, but her income was low and insecure. She wanted to make sure she could pay for her children to go to school and enjoy the education she never had.
The life course trajectory can also be used to show when an individual's health declines to a critical stage of dependence on medical care or, conversely how great their resilience to challenges such as infection or injury will be. It also relates to their likely longevity, and animal studies show that developmental influences such as nutrition in prenatal and early postnatal life can have dramatic effects on lifespan (Jennings et al. 1999 ). This concept can be extrapolated to different socio‐economic or resource settings (see Abstract figure) showing not only how potential longevity is influenced but also how resilience is affected. Intervention at early stages in the life course can have a dramatic effect on the entire trajectory, but some plasticity is manifest even in later life.
The life course model of ageing is also relevant to clinical practice as it may provide an opportunity to identify individuals at risk of accelerated ageing early in the life course, using early biomarkers of such risk (Martin‐Ruiz et al. 2011 ). It also suggests that the window for instituting beneficial interventions should be widened to include early life, when adverse environments may have long‐term effects on ageing (Drury et al. 2012 ). Furthermore, knowledge of underlying mechanisms may lead to the development of new interventions to regulate the rate of ageing or to minimize its detrimental effects.
There is increased awareness that the process of human ageing commences as early as conception with the inheritance of a specific genome, and it does not cease until death. Epidemiological studies have demonstrated that environmental influences during intrauterine and early postnatal life are associated with alterations in form and function across a range of systems, which establish predisposition to age‐related system decline (Sayer et al. 1998 ). The biological process through which these changes in gene expression are established is known as ‘developmental plasticity’. This process is ubiquitous throughout the animal world, and in some plants, and it provides the mechanism whereby a given genotype can develop into a range of phenotypes which are best adapted to the environment that they are likely to meet once development is completed, a concept formalized as a predictive adaptive response (Gluckman & Hanson, 2004 ). Such adaptive responses are usually thought to operate on Darwinian fitness, i.e. survival to the time of successful reproduction, rather than on ageing per se. New concepts challenge this view, and this paper reviews these using musculoskeletal and cardiovascular ageing as examples, and discusses some common underlying mechanisms. It concludes by noting the potential for translational public health strategies to promote healthy ageing by adopting a developmental perspective.
2013 ), biomarkers (or hallmarks) of ageing can be grouped into primary (gene and protein stability, telomere length, epigenetic processes ), secondary (regulation of nutrient sensing, mitochondrial function, cellular senescence) and integrative (stem cell provision and intercellular communication) mechanisms. The primary markers are believed to represent the underlying causes of ageing, while the secondary markers represent potential compensatory responses. The integrative markers are believed to contribute directly to ageing‐related phenotypes of health and disease (López‐Otín et al. 2013 ). López‐Otín and co‐workers provide an elegant model of temporal events, which may contribute either directly or indirectly to physiological disturbances related to ageing. Such temporal events interact at multiple levels of biological organization, which may involve several feed‐forward and feedback mechanisms. Disturbances in homeostatic mechanisms which regulate these markers of ageing are likely to play an important role in the development of ageing‐related disorders.
1994 ), or alteration in gene expression associated with errors in transcription (Kirkwood & Austad 2000 ). Human somatic cells are believed to possess the ability to undergo a finite number of possible mitoses (the Hayflick limit), although this may not be the basis for ageing (Williams, 1957 ). In cell lines, accumulation of errors in protein transcription (Miller, 1999 ), and of cross‐links in macromolecules, may cause structural and functional changes associated with ageing. A number of theories have focused on the role of exposure to metabolic or waste products, for example reducing sugars or free radicals, as the cause of such deteriorative changes (Rattan, 2008 ). At a more holistic level, homeostatic systems such as the hypothalamic–pituitary axis or the immune system may play a fundamental role (see below) and a link has been proposed between psychosocial factors such as stress and ageing (Nilsson, 1996 ).
Organ systems are most susceptible to such effects during periods in which they are growing rapidly. During the embryonic period (the first 2 months of gestation in the human), progenitor cells undergo extensive differentiation without rapid cell replication. The highest growth rates are observed during the subsequent fetal period, and thus some organs are most susceptible to environmental cues at this point (Gluckman & Hanson, 2004 ). Relative growth slows in late gestation and continues to slow in childhood. This plasticity is lost later in life when the organism has a relatively fixed functional capacity, although there is a limited capacity for renewal through stem cells in some tissues and it is possible that developmental processes can influence the degree to which stem cell lineages can provide such renewal later on (Obernier et al. 2014 ). Developmental plasticity provides a fitness benefit through the ability to adapt to environmental changes over a relatively short time span, i.e. one generation (Gluckman & Hanson, 2004 ). In some circumstances, usually following potent disruptive exposures such as environmental chemicals, this benefit can be passed to several subsequent generations without the need for re‐exposure to the stimulus (Skinner et al. 2010 ), although this is not necessarily true of milder, nutritional stimuli.
Theories of ageing can be grouped using several criteria. One distinction views ageing as either genetically predetermined (‘the biological clock’ concept) or as a response to accumulated detrimental but otherwise random events over time (Medvedev, 1990 ). Another contrasts ageing which evolved as an adaptive process or as a non‐adaptive by‐product of other processes. These groups are not mutually exclusive. This paper starts from the premise that ageing is one aspect of a life course strategy initiated in early life in each individual as part of a cassette of evolved adaptive responses (Gluckman et al. 2007 ). In this sense, ageing can be considered as a normal process: this in turn raises the question of whether abnormal ageing can occur. Clearly it can in unusual conditions such as progeria (Gabr et al. 1960 ). However, in the population as a whole there are wide variations in the rate of ageing in terms of declining functional capacity, which may be regarded in part either as normal responses to common challenges or as pathological processes. Distinguishing between these processes may have important consequences for the identification of individuals or groups at risk of accelerated ageing, and for interventions. In this paper we discuss these issues with specific reference to musculoskeletal and cardiovascular disorders, using a life course model of functional capacity.
Thus, because many of the developmental life stages also have socially constructed parameters, life stages should be examined for whether they are expected to have universal or unique within-population characteristics and whether health outcomes are best explained by using a developmental perspective, a structural perspective, or a combination of both.
Life course perspectives on health disparities propose that socially patterned environmental exposures influence the development of biological, physiological, and psychosocial systems, including structural and functional changes in the brain. Developmental and structural perspectives on the life course arise from distinct theories that warrant closer integration into research on how biological mechanisms result in health disparities (see the boxon page S52). Developmental approaches emphasize the timing of adversity relative to critical and sensitive periods of development. Each life stage has unique biological, physiological, and psychosocial developmental properties that confer differential susceptibility (either elevated or suppressed) to stressors and buffers. Thus, research is needed to consider life stage timing in addition to the intensity and valence of exposures that result in health disparities.
We conclude that the science of health disparities will be advanced by integrating life course approaches into etiologic and intervention research on health disparities. The following 4 strategies are offered to guide in this process: (1) advance the understanding of multiple exposures and their interactions, (2) integrate life course approaches into the understanding of biological mechanisms, (3) explore transgenerational transmission of health disparities, and (4) integrate life course approaches into health disparities interventions.
Developmental perspectives on health disparities emphasize the biological and behavioral mechanisms by which structurally patterned exposures during critical and sensitive periods of the life course result in sustained shifts in health trajectories that may endure despite later intervention.1,7Understanding the mechanisms underlying these periods is of primary importance, as is establishing the timing of critical or sensitive periods for a broad range of social and environmental exposures. Differential exposure to social and environmental factors during sensitive periods is therefore viewed as a primary driver of population-level health disparities.
Altered development of one system can create lasting effects across multiple systems because these systems are interconnected. Moreover, exposures during early life stages can affect the maximum capacity for health through the direct alteration of the developing physiological and psychological systems . Exposure to additional adversity later in development would be expected to potentiate these earlier biological deviations and compound health risks. These processes may be synergistically accelerated through the adoption of negative health behaviors, including substance use, inadequate exercise, and poor nutrition and sleep habits.19
Structural perspectives focus on how biopsychosocial mechanisms translate “fundamental social causes” into different population distributions of health, disease, and longevity.12Struct ural perspectives acknowledge the importance of the timing of exposures across developmental windows, yet emphasize that exposures in young through middle adulthood outside of developmental windows are particularly important for understanding population health inequity.4Mechanistically, the structural perspective focuses on physiological processes that are repeatedly or chronically activated across the life course in disadvantaged groups because of high-effort coping with stressors. For example, the scientific premise of the weathering hypothesis is that cumulative and stress-mediated wear and tear on cellular integrity leads to accelerated biological aging, the dysregulation or exhaustion of important body systems by midlife, and the early onset of chronic diseases of aging, health-induced disability, and excess mortality among marginalized groups.13
Individual and population health risks arise from multiple sources across the life course. Risk factors and adverse exposures are found in multiple domains and often cluster in socially patterned ways that synergistically influence short- and long-term consequences. Most research designs characterize effects on health outcomes of single exposures and rarely assess the importance of the timing of exposures or influences over time. Although some composite measures of biomarkers assess the cumulative effect of undetermined exposures, direct links between cumulative exposures and specific outcomes need to be clarified.16Thus, a gap exists in the ability to examine and measure how exposures are socially patterned, interact, and dynamically change; how timing influences effects; and how exposures cumulatively increase or diminish the magnitude of health disparities. Measures are needed to assess the composite effect of exposures across multiple levels (e.g., individual, interpersonal, community, and societal) and life stages (e.g., gestation, childhood, adolescence, young adulthood, midlife, and old age). Beyond the assessment of the interactive effects of exposures, a need exists to identify protective factors at these same levels that may mitigate or buffer against adverse consequences.
Growing out of widely shared images and social values, an ideal old age legitimates norms and roles appropriate to the last stage of life. This article discusses the "late Calvinist" and "civilized" models of old age that flourished in Protestant, middle-class America between 1800 and 1920. It argues that the growing cultural dominance of science and the accelerating pace of capitalist productivity undercut the essential vision underlying these models: the view of life as a spiritual journey. The result has been a serious weakening of social meaning in aging and old age.
E. Michael Brady. Autobiography is an important means of facilitating adult learning and development. The process which is most associated with autobiography is memory. Memory is more than the recollection of past events; it is a critical element in the search for and construction of meaning in human experience in that it provides ...