Inflammatory Exposure and Historical Changes in Human Life-Spans

By C. Finch, E. Crimmins. Science, 2004

756 citations recorded by the source corpus.

Subfields: Demography, Pediatrics, Perinatology and Child Health, Sociology and Political Science

View Paper: https://www.semanticscholar.org/paper/417478ebcb4f2419857d882b4cc9e04d08c1010a

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Citations in the corpus

Aging and cumulative inequality: how does inequality get under the skin? (2009, background): “A review by Finch and Crimmins (2004) reveals that infections during the early years of life increase the likelihood that the person will develop diseases as an adult, including cancer, diabetes, and cardiovascular disease (see also Blackwell, Hayward, & Crimmins, 2001 ).”
Leukocyte telomere length and cardiovascular disease in the cardiovascular health study. (2006, neutral): “Inflammation is considered a major player in human aging (24–26) and longevity (27), and leukocyte telomere dynamics may capture in part the effect of this process.”
Early life origins of chronic obstructive pulmonary disease (2009, background): “and FVC. Early life environment might further influence physiological factors directly related to lung function throughout life (ie, by causing persistent inflammation).”
Adverse Childhood Experiences and Adult Risk Factors for Age-Related Disease (2009, neutral): “Because of the increasing recognition that preventable risk exposures in early life may contribute to pathophysiological processes leading to agerelated disease,(5,6) the science of aging has turned to a life-course perspective.(7,8) Capitalizing on this perspective, this study tested the contributi”
Population Policies, Fertility, Women's Human Capital, and Child Quality (2007, neutral): “…to improved adult health status, reduced chronic health problems after a individual reaches age 50, and increased years of disability-free life in old age, controlling in some cases for later socioeconomic status ( Kannisto, et al. 1994; Finch and Crimmins, 2004; Gluckman and Hanson, 2006).”
Trade‐offs between longevity and pathogen resistance in Drosophila melanogaster are mediated by NFκB signaling (2006, background): “This work establishes a precedent for effective modulation of the activity of immunity-related pathways and suggests a mechanistic basis for a link between immunity, inflammation, and longevity (DeVeale et al., 2004; Finch & Crimmins, 2004; Pletcher et al., 2005).”
Evolutionary Causes and Consequences of Immunopathology (2005, background): “Immunopathology may also have delayed fitness consequences, reducing lifespan in people prone to strong immune responses (Finch & Crimmins 2004).”
Psychological Stress in Childhood and Susceptibility to the Chronic Diseases of Aging: Moving Towards a Model of Behavioral and Biological Mechanisms (2011, background): “These findings have fueled interest in whether the psychosocial environment might also have a role in calibrating the immune system’s response tendencies (Bilbo & Schwarz, 2009; Coe & Lubach, 2005, 2007; Finch & Crimmins, 2004; McDade, 2005; Prescott, 2006; Wright, 2007).”
Longevity Among Hunter‐ Gatherers: A Cross‐Cultural Examination (2007, background): “Finch and Crimmins (2004) show that the level of child mortality explains 85 percent of the variance in old-age mortality in cohorts in Sweden and the United States, and that early mortality has a threefold greater predictive effect on old-age mortality for those cohorts than”
Functionally Defective High-Density Lipoprotein: A New Therapeutic Target at the Crossroads of Dyslipidemia, Inflammation, and Atherosclerosis (2006, background): “This mechanism is consistent with a recent hypothesis that accelerated development of atherosclerosis in old age is related to increased inflammation and concomitant endothelial dysfunction during early life (Finch and Crimmins, 2004; Charakida et al., 2005; Napoli et al., 2005).”
The evolution of senescence from a comparative perspective (2008, background): “Processes that are widely believed to cause senescence, particularly the accumulation of oxidative damage (Harman 1956) or damage caused by inflammation (Finch & Crimmins 2004), also have received close scrutiny (Finch 2007; Vleck, Haussmann & Vleck 2007).”