Death-Rates in Great Britain and Sweden Some General Regularities and Their Significance

Kermack, W. O.; McKendrick, A. G.; Mckinlay, P. L.

doi:10.1016/s0140-6736(00)92530-3

Cited by 299 publications

(171 citation statements)

References 2 publications

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“…1), there was no statistical support for an association between early-life disease exposure and mortality risk after age 15 (Table 1 and SI Appendix, Table S4). Previous studies have found evidence for links between early-life cohort mortality rate and later survival (4,5,8), but without considering that such a measure of disease exposure could be confounded by spatial variation, social status, other intrinsic and extrinsic conditions as well as disease exposure, and improvements in living conditions and hygiene across time. Demographic studies have applied statistical techniques such as Hodrick-Prescott decomposition to trending environmental data and found generally weak associations between early and later cohort mortality (37)(38)(39)(40), although some of these studies have still detected significant correlations (19,41).…”

Section: Discussionmentioning

confidence: 99%

“…Longer adult life expectancy has been accompanied by increased incidence of previously rare chronic health problems, and thus identifying the drivers of enhanced life span is an important question for global health. Declines in adult mortality rate since the 18th century in Europe were more closely linked to year of birth than to the year in which mortality was assessed, leading to the hypothesis that "the expectation of life was determined by the conditions which existed during the child's earlier years" (4). The "cohort morbidity phenotype" hypothesis suggests that the link between declining birth year mortality rate and increasing adult survival is due to reduced exposure to infectious diseases in early life and reduced lifelong burden of chronic inflammation (5)(6)(7)(8).…”

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confidence: 99%

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Early-life disease exposure and associations with adult survival, cause of death, and reproductive success in preindustrial humans

Hayward

Rigby

Lummaa

2016

Proc. Natl. Acad. Sci. U.S.A.

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A leading hypothesis proposes that increased human life span since 1850 has resulted from decreased exposure to childhood infections, which has reduced chronic inflammation and later-life mortality rates, particularly from cardiovascular disease, stroke, and cancer. Early-life cohort mortality rate often predicts later-life survival in humans, but such associations could arise from factors other than disease exposure. Additionally, the impact of early-life disease exposure on reproduction remains unknown, and thus previous work ignores a major component of fitness through which selection acts upon life-history strategy. We collected data from seven 18th-and 19th-century Finnish populations experiencing naturally varying mortality and fertility levels. We quantified early-life disease exposure as the detrended child mortality rate from infectious diseases during an individual's first 5 y, controlling for important social factors. We found no support for an association between early-life disease exposure and all-cause mortality risk after age 15 or 50. We also found no link between early-life disease exposure and probability of death specifically from cardiovascular disease, stroke, or cancer. Independent of survival, there was no evidence to support associations between early-life disease exposure and any of several aspects of reproductive performance, including lifetime reproductive success and age at first birth, in either males or females. Our results do not support the prevailing assertion that exposure to infectious diseases in early life has long-lasting associations with later-life all-cause mortality risk or mortality putatively linked to chronic inflammation. Variation in adulthood conditions could therefore be the most likely source of recent increases in adult life span.inflammation | stress | infection | life history | fitness

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Early-life disease exposure and associations with adult survival, cause of death, and reproductive success in preindustrial humans

Hayward

Rigby

Lummaa

2016

Proc. Natl. Acad. Sci. U.S.A.

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“…Kermack et al (1934) argued that the correlation between infant mortality and cohortspecific adult mortality is less clear-cut than the correlation between child mortality and cohort-specific adult mortality. But Crimmins and Finch (2006) and Floud et al (2011, p. 257) observed that this depends on the country.…”

Section: Exposure To Infectious Diseasementioning

confidence: 99%

Early-life conditions and adult mortality decline in Dutch cohorts born 1812–1921

Schellekens

Poppel

2016

Population Studies

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“…The idea that environmental exposures early in life condition risk for disease in adulthood first emerged from group-level analyses of vital statistics showing that community death rates in infancy and childhood predict life expectancy within birth cohorts, independently of current living conditions (Kermack et al 1934;Forsdahl 1977). Pre-natal under nutrition-as indicated most commonly by lower birth weight-has since been the focus of efforts to explain these cohort effects (Barker & Osmond 1986), while more recent research including a wider range of human populations and experimental animal models has demonstrated that pre-natal and early post-natal nutritional stressors increase risk for cardiovascular and metabolic diseases later in life through developmental modifications to physiological systems, organ growth and metabolism (Barker 1994;Gluckman et al 2008).…”

Section: Introductionmentioning

confidence: 99%

Early origins of inflammation: microbial exposures in infancy predict lower levels of C-reactive protein in adulthood

et al. 2009

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Ecological factors are important determinants of the development and function of anti-pathogen defences. Inflammation is a central part of innate immunity, but the developmental factors that shape the regulation of inflammation are not known. We test the hypothesis that microbial exposures in infancy are associated with high sensitivity C-reactive protein (CRP) in adulthood using prospective data from a birth cohort in the Philippines (n ¼ 1461). Lower birth weight was associated with increased CRP, consistent with a role for inflammation in the widely documented inverse relationship between birth weight and adult cardiovascular diseases. In addition, higher levels of microbial exposure in infancy were associated with lower CRP. These associations were independent of socioeconomic status, measures of current body fat and other health behaviours. We conclude that measures of microbial exposure and nutrition during the pre-natal and early post-natal periods are important predictors of CRP concentration in young adulthood. We speculate that the development of anti-inflammatory regulatory networks in response to early microbial exposure represents plasticity in the development of anti-pathogen defences, and that this process may help explain the low CRP concentrations in this population.

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Death-Rates in Great Britain and Sweden Some General Regularities and Their Significance

Cited by 299 publications

References 2 publications

Early-life disease exposure and associations with adult survival, cause of death, and reproductive success in preindustrial humans

Early-life disease exposure and associations with adult survival, cause of death, and reproductive success in preindustrial humans

Early-life conditions and adult mortality decline in Dutch cohorts born 1812–1921

Early origins of inflammation: microbial exposures in infancy predict lower levels of C-reactive protein in adulthood

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