Life course epidemiology
Idea: How do we identify and disentangle the biological and social factors that build on each other over the life course from gestation through to old age?
Guidelines for annotations
Notes and annotations from 2007 course
Initial notes from PT
The readings mostly relate to "life course epidemiology," that is, Fetal & developmental origins of diseases in late life (Barker being generalized by Ben-Shlomo=common reading 1), in some tension with development over the life course (incl. Berney reviewing lifetime accumulation of hazards in relation to health in old age). In contrast to this approach, we have Brown on life course influences on depression (not necessarily in old age)=common reading 2. In what ways could either side usefully draw methods, data, results from the other?
From DBJ: Class exercise: Take the topic for your portfolio and think of some examples of the life events according to the critical period vs. the accumulated risk model. Look at Figure 1 in Ben-Shlomo on page 286. In class we can all try to draw similar diagrams to represent some (not all) biological and psychosocial life course exposures on the diseases studied for the final portfolio.
Annotations on common readings
Common reading – A life course approach to chronic disease epidemiology: conceptual models, empirical challenges and interdisciplinary perspectives (Ben-Shlomo and Kuh, 2002)
As indicated in the title, authors discuss the life course approach from a threefold perspective. One distinctive quality of the life course approach to chronic disease epidemiology is that it bridges the gap between biological, psychological and social perspective when trying to explain causes of different diseases, chronic diseases in particular. This model works though different (potential) pathways: biological pathway (e.g. adverse event during fetal development), social pathway (e.g. adverse exposures during childhood or adulthood, like smoking), socio-biological pathway (e.g. likelihood of exposure to infections), and bio-social pathway (e.g. frequent infections during childhood may lead to obtaining lower education and lower SES). Therefore, the life course approach not only bridges the gap but also has another quality – to go beyond early life exposures, to look into complex inter-relationships, and to identify other potential intermediary and confounding factors causing chronic diseases.
Ben-Shlomo and Kuh identify two main conceptual models – critical period model and accumulation of risks model, as well as some sub models. They define critical period as a period “when an exposure acting during a specific period has lasting or lifelong effects on the structure or function of organs” (p.286). However, while critical period model was often associated with fetal origins and assumed its permanent effect or damage, they emphasize the importance of later life effects as also being part of the critical period model. The second conceptual model is the accumulation of risk, defined as risks accumulating gradually over the life course. These accumulated risks can be independent and uncorrelated exposures (e.g. earthquake, death of a sibling, divorce), or they can be correlated, even clustered (poor living conditions, exposure to domestic violence, low job satisfaction). They also identify what they call “chains of risk”, which accumulate over time and may have additive effect. For example, lower education may lead to unemployment, which can further lead to financial insecurity and marital conflicts even abuse, and finally lead to divorce. Divorce may be a result of the additive effect of these events, or a result of the trigger effect of the domestic abuse. The authors also distinguish between critical and sensitive periods, which are often used in epidemiology interchangeably. While a critical period is defined as a limited time window in which exposure can have adverse effects on diseases, a sensitive period assumes a time period when an exposure has a stronger effect on the disease than it would have at other times.
Finally, the authors also point to the limitations of the life course approach, from its limited scope within a single cohort, to limitations due to missing data for biological mechanisms, for succeeding populations or for different time periods. They also emphasize that the life course approach, while being intuitively obvious, is also empirically complex and lacks the empirical evidence (DBJ 09).
Annotated additions by students
