The hypothesis is that babies who are small at birth and during first year of life may have been undernourished and this increases risk of chronic disease later in life. However, this hypothesised programming requires later-life additional risk to push into crisis.
Here are two examples of studies done on biological programming.
Forsdahl (1970s) suspected that adverse environmental conditions in infancy and early childhood could increase the risk of CHD in adult life. Forsdahl speculated that permanent damage may be caused by nutritional deficits in early life that rendered individuals less able to tolerate particular forms of at in their adult diet So early life social disadvantage might interact with affluence in later life to increase CHS risk.
Barker et al (1990s) revisited the foetal origins hypothesis. There had been problems in earlier studies regarding inadequate measuring/controlling of early-life exposures. Their study focuses on the long-term effects of in utero biological programming associated with maternal and foetal under-nutrition. For CHD, growth weight in utero not birth size per se is important.
These refer to the primary, secondary and tertiary prevention to reduce smoking, improve diets and increase physical activity.
The life course approach combines the previous two theories, i.e the polarisation of well-known adult risk factors and biological programming in utero. Life course approach bridges the perinatal and adult period by studying the contribution of early-life factors with later-life factors to identify risk and protective processes across the life course. E.g. Age at smoking cessation is important in determining the extent to which disease risk declined over time. In terms of early life influences, studies have suggested that low birth weight babies have increase risk of respiratory disease in later life, which could be owing to poor lung development in utero. Maternal smoking has also been associated.
1. Life course approach takes into account the complex ways that various biological and social, economic and psychological factors independently, cumulatively and interactively influence health and disease in adult life over time.
2. Health and quality of life in old and middle age depends as much on past circumstances as on present ones. Adopting a life course approach should not be construed as suggesting that the recognition of important early-life influences on chronic disease implies deterministic process that negate the possibility of later-life intervention.
3. A life course approach to chronic disease epidemiology explicitly recognizes the importance of time and timing in understanding casual links between exposures and outcomes within an individual life course, across generations and on population level disease trends. The importance of time is illustrated by the fact that chronic conditions (cancers, cardiovascular diseases, stroke, diabetes choric obstructive pulmonary disease) have long latency period, i.e. they develop over time. Time lags between exposure, disease initiation and clinical recognition (latency period) suggest that exposures early in life are involved in initiating disease process prior to clinical manifestations. Many important adult risk factors for chronic disease (poverty, smoking, diet, physical activity, atmosphere pollution) cause their damage slowly and over time - e.g. what people eat or do not eat in adulthood may be sensitive to the dietary habits they established in childhood.
4. Emphasis in policies is on enabling individuals to make more appropriate choices. Partnership approaches are also used.
Models
(1) Critical period model emphasises the timing of exposure - i.e. exposure at a specific period in the life course has long-lasting effects. For example, very early postnatal infection with Heapatitis B is associated with risk of adult liver cancer. Additionally there may be sensitive periods, where the effect of an exposure is magnified more than the effect of the same exposure in another time period. For example, poverty during periods of important childhood social transitions such as school entry.
(2) Risk models - these look at how effects accumulate over the life course
Applications
(1) Life course approach also offers a way to conceptualize how underlying socio-environmental determinants of health, experience at different life course stages can differentially influence the development of chronic diseases, as mediated through proximal specific biological processes. Individual's biological development takes place within a social context which structures their life chances so that advantage and disadvantages tend to cluster cross-sectionally and accumulate longitudinally. Risk factors for cardiovascular disease in adult life have been found to be linked in varying strengths to both childhood and adulthood socioeconomic positions.
(2) An ambitious application of life course approach to chronic disease epidemiology is to integrate knowledge from individual level studies to explain population level trends in different diseases. This means understanding how the arrays of life course risk factors are configured across successive birth cohorts and their long-term trends.
Methodological Challenges
1. Investigating life course processes for chronic disease requires measuring data at multiple time points from birth (or before) to middle and older ages and potentially across generation. The timing of these data collections is informed by some knowledge of the relevant latency periods between particular life course exposures and outcomes. That is why much of the current knowledge in the life course epidemiology of chronic disease has been derived from reconstructed cohorts where information about early-life conditions and events was gathered form cohorts born in the late 19th and early 20th centuries. This means that the life course processes studied in these cohorts are reflections of the past and may not in some cases be as applicable to current generations.
2. Reconstructing early-life exposure from adult recall is limited because it introduces possibilities of bias and measurement error so objective data collected at the relevant life course stage are most desirable.
3. Life course exposures may operate through the timing of their action and/or through their accumulation. Testing critical and sensitive-period exposure requires that the exposure is measured at multiple points spanning the hypothesised time period. (as does measuring the accumulation of risk) Such repeatedly measured exposure data are rare and expensive to collect.
4. Long term life course studies of chronic diseases will make the problems of missing data even more acute than they are now. Advances in multiple imputation techniques are likely to be important.