Early-Life Conditions and Old-Age Mortality in a Comparative Perspective: Nineteenth Century Sweden and Belgium
Bengtsson, Tommy, and George C. Alter. 2019. "Early-Life Conditions and Old-Age Mortality in a Comparative Perspective: Nineteenth Century Sweden and Belgium." In Old and New Perspectives on Mortality Forecasting edited by Bengtsson, Tommy, Keilman, Nico. Cham: Springer International Publishing.
Kermack et al. (1934) proposed the cohort explanation in their analysis of the aggregated mortality decline in England, Wales, Scotland, and Sweden. Their conclusion was that reductions in the death rates of the various age groups attained at any particular time depended primarily on the individuals' date of birth, and only indirectly on the particular year under consideration. The essential effects on health and survival of adults and older persons were mainly caused by improvements and beneficial effects on their respective birth cohorts during childhood several decades earlier. Jones (1956) brought up the cohort approach anew and recently it has gained focus again through works in medicine but also in historical demography (Barker 1994; Elo and Preston 1992; Fogel 1994; Fridlizius 1989; Kuh and Ben-Shlomo 1997; Preston et al. 1998; Finch and Crimmins 2004). The plausible causal relationships between early-life experiences and old-age mortality have been discussed, with special attention to intrauterine cellular development and cellular development during early childhood. Robert Fogel (1994) has proposed several plausible causal mechanisms that connect malnutrition in utero and during early life to chronic diseases in later life. These propositions are also supported by the work of Barker (1994, 1995) who suggested that the preconditions for coronary heart disease, hypertension, stroke, diabetes, and chronic thyroiditis are initiated in utero without becoming clinically manifest until much later in life. In contrast, Jones (1956), and later Fridlizius (1989), in his analysis of the aggregated mortality decline in Sweden, proposed that the genesis of disease in later life could be due to exposure to certain infectious diseases in the first years of life. Fridlizius argued that this was caused by life-long reduced immunity, which consequently gave higher general risk of other infectious diseases in later life. The knowledge of the medical mechanisms today seems to be more in favour of permanent retardation of organs due to infections rather than immunological mechanisms (Finch and Crimmins 2004). Either way, it implies that factors other than nutrition are important early-life determinants of mortality in later life, because the outcome of some other important infectious diseases, like smallpox, is almost completely unrelated to the nutritional status of the infected individual (Rotberg and Rabb 1985).