scholarly journals Intergenerational transmission of longevity is not affected by other familial factors: Evidence from 16,905 Dutch families from Zeeland, 1812-1962

2019 ◽  
Author(s):  
R.J. Mourits ◽  
N.M.A. van den Berg ◽  
M. Rodríguez-Girondo ◽  
K. Mandemakers ◽  
P.E. Slagboom ◽  
...  

AbstractStudies have shown that long-lived individuals seem to pass their survival advantage on to their offspring. Offspring of long-lived parents had a lifelong survival advantage over individuals without long-lived parents, making them more likely to become long-lived themselves. We test whether the survival advantage enjoyed by offspring of long-lived individuals is explained by environmental factors. 101,577 individuals from 16,905 families in the 1812-1886 Zeeland cohort were followed over time. To prevent that certain families were overrepresented in our data, disjoint family trees were selected. Offspring was included if the age at death of both parents was known. Our analyses show that multiple familial resources are associated with survival within the first 5 years of life, with stronger maternal than paternal effects. However, between ages 5 and 100 both parents contribute equally to offspring’s survival chances. After age 5, offspring of long-lived fathers and long-lived mothers had a 16-19% lower chance of dying at any given point in time than individuals without long-lived parents. This survival advantage is most likely genetic in nature, as it could not be explained by other, tested familial resources and is transmitted equally by fathers and mothers.

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yisong Huang ◽  
Shaoyong Su ◽  
Harold Snieder ◽  
Frank Treiber ◽  
Gaston Kapuku ◽  
...  

AbstractIncreased arterial stiffness measured by pulse wave velocity (PWV) is an important parameter in the assessment of cardiovascular risk. Our previous longitudinal study has demonstrated that carotid-distal PWV showed reasonable stability throughout youth and young adulthood. This stability might be driven by genetic factors that are expressed consistently over time. We aimed to illustrate the relative contributions of genetic and environmental factors to the stability of carotid-distal PWV from youth to young adulthood. We also examined potential ethnic differences. For this purpose, carotid-distal PWV was measured twice in 497 European American (EA) and African American (AA) twins, with an average interval time of 3 years. Twin modelling on PWV showed that heritability decreased over time (62–35%), with the nonshared environmental influences becoming larger. There was no correlation between the nonshared environmental factors on PWV measured at visit 1 and visit 2, with the phenotypic tracking correlation (r = 0.32) completely explained by shared genetic factors over time. Novel genetic influences were identified accounting for a significant part of the variance (19%) at the second measurement occasion. There was no evidence for ethnic differences. In summary, novel genetic effects appear during development into young adulthood and account for a considerable part of the variation in PWV. Environmental influences become larger with age for PWV.


1995 ◽  
Vol 25 (2) ◽  
pp. 6A-7A ◽  
Author(s):  
Allan M. Ross ◽  
Shyuan Cho ◽  
Conor Lundergan ◽  
Jonathan Reiner ◽  
Maarten Simoons ◽  
...  

2020 ◽  
Author(s):  
Tatyana Dobreva ◽  
David Brown ◽  
Jong Hwee Park ◽  
Matt Thomson

AbstractAn individual’s immune system is driven by both genetic and environmental factors that vary over time. To better understand the temporal and inter-individual variability of gene expression within distinct immune cell types, we developed a platform that leverages multiplexed single-cell sequencing and out-of-clinic capillary blood extraction to enable simplified, cost-effective profiling of the human immune system across people and time at single-cell resolution. Using the platform, we detect widespread differences in cell type-specific gene expression between subjects that are stable over multiple days.SummaryIncreasing evidence implicates the immune system in an overwhelming number of diseases, and distinct cell types play specific roles in their pathogenesis.1,2 Studies of peripheral blood have uncovered a wealth of associations between gene expression, environmental factors, disease risk, and therapeutic efficacy.4 For example, in rheumatoid arthritis, multiple mechanistic paths have been found that lead to disease, and gene expression of specific immune cell types can be used as a predictor of therapeutic non-response.12 Furthermore, vaccines, drugs, and chemotherapy have been shown to yield different efficacy based on time of administration, and such findings have been linked to the time-dependence of gene expression in downstream pathways.21,22,23 However, human immune studies of gene expression between individuals and across time remain limited to a few cell types or time points per subject, constraining our understanding of how networks of heterogeneous cells making up each individual’s immune system respond to adverse events and change over time.


2019 ◽  
Vol 9 (6) ◽  
pp. 146 ◽  
Author(s):  
Sheerin ◽  
Kovalchick ◽  
Overstreet ◽  
Rappaport ◽  
Williamson ◽  
...  

: Genes, environmental factors, and their interplay affect posttrauma symptoms. Although environmental predictors of the longitudinal course of posttraumatic stress disorder (PTSD) symptoms are documented, there remains a need to incorporate genetic risk into these models, especially in youth who are underrepresented in genetic studies. In an epidemiologic sample tornado-exposed adolescents (n = 707, 51% female, Mage = 14.54 years), trajectories of PTSD symptoms were examined at baseline and at 4-months and 12-months following baseline. This study aimed to determine if rare genetic variation in genes previously found in the sample to be related to PTSD diagnosis at baseline (MPHOSPH9, LGALS13, SLC2A2), environmental factors (disaster severity, social support), or their interplay were associated with symptom trajectories. A series of mixed effects models were conducted. Symptoms decreased over the three time points. Elevated tornado severity was associated with elevated baseline symptoms. Elevated recreational support was associated with lower baseline symptoms and attenuated improvement over time. Greater LGLAS13 variants attenuated symptom improvement over time. An interaction between MPHOSPH9 variants and tornado severity was associated with elevated baseline symptoms, but not change over time. Findings suggest the importance of rare genetic variation and environmental factors on the longitudinal course of PTSD symptoms following natural disaster trauma exposure.


1984 ◽  
Vol 33 (1) ◽  
pp. 130-143 ◽  
Author(s):  
Greta Robertson ◽  
Michael D. Lebowitz

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 461-461
Author(s):  
Carlton Haywood ◽  
Sophie Lanzkron

Abstract Background: The purpose of this study was to use the NIS to describe hospital utilization and in-hospital mortality among adults with SCA in the US between 1993-2003. Methods: The NIS is designed to approximate a 20% stratified sample of U.S. community hospitals. We restricted our analyses to discharge records with ICD-9-CM diagnosis codes 28261 or 28262 (SCA without/with crisis), and where the age was listed as 18 or older. Analyses were conducted using tests of linear combinations of coefficients, χ2, and linear and logistic regression. Results: There were an estimated 705,080 hospitalizations over the time period (mean of 64,098 hospitalizations/year). 54% of all hospitalizations were for females. 50% of the hospitalizations were expected to be paid for by Medicaid. The mean patient age over the time period was 31.3 yrs. The mean patient age increased from 30.3 in 1993 to 32.1 in 2003 (p < 0.001). Mean age over time increased even after adjusting for the gender makeup and hospital region (β=0.162, p < 0.001). There were no gender differences in the median age (30) of patients. Mean length of stay (LOS) was 6.5 days for the time period. LOS decreased from 7.5 days in 1993 to 6.4 days in 2003 (p=0.001). Adult women experienced longer LOS than adult men (6.8 days vs. 6.3 days, p <0.001). This difference remained significant even after controlling for age, time, insurance status, and hospital region (β = 0.49, p<0.001). Mean charges/discharge increased from $16,799 in 1993 to $22,281 in 2003, even after adjusting for inflation (p < 0.001). There were an estimated 4497 in-hospital deaths during the time period (0.64% of hospitalizations). The median age at death was 38. The median age at death increased from 35 in 1993 to 42 in 2003 (p = 0.0061). This was due to an increase in age of death (39) for women (p=0.0052). In men the median age of death (37) did not change over time(p=0.4352). In bivariate analyses of median age at death, women were older than men (39 vs. 37 p=0.0056). A simple logistic regression of deaths over time found no significant trends in the odds of an in-hospital death over the time period. In a multivariate model of death over time patients in the South and the West experienced higher odds of an in-hospital death than patients in the Northeast and Midwest. Conclusions: Our analysis shows that women with SCA have longer in-hospital LOS than men, and are older in age at death than men. While the median age at death among persons hospitalized with SCA has been increasing since 1993, this increase is seen exclusively in women. There has been no change in longevity in men hospitalized with SCA over the time period studied.


2014 ◽  
Vol 17 (6) ◽  
pp. 535-544 ◽  
Author(s):  
Lisa Mather ◽  
Gunnar Bergström ◽  
Victoria Blom ◽  
Pia Svedberg

Background: This study aims to assess whether the associations between burnout and sick leave due to stress-related mental disorders, other mental disorders, and somatic conditions are influenced by familial (genetic and shared environmental) factors.Methods: In this prospective cohort study, 23,611 Swedish twins born between 1959 and 1985, who answered a web-based questionnaire, including the Pines Burnout Measure 2004–2006, were included. Registry data on sick leave spells from the response date until December 31, 2010 were obtained from the Swedish Social Insurance Agency. Logistic regression analysis was performed to assess odds ratios with 95% confidence intervals for the association between burnout and sick leave for the whole sample, while conditional logistic regression of the same-sex discordant twin pairs was used to estimate the association between burnout and sick leave, adjusting for familial confounding. The Bivariate Cholesky models were used to assess whether the covariation between burnout and sick leave was explained by common genetic and/or shared environmental factors.Results: Burnout was a risk factor for sick leave due to stress-related and other mental disorders, and these associations were explained by familial factors. The phenotypic correlation between burnout and sick leave due to somatic conditions was 0.07 and the association was not influenced by familial factors. The phenotypic correlations between burnout and sick leave due to stress-related (0.26) and other mental disorders (0.30) were completely explained by common genetic factors.Conclusions: The association between burnout and sick leave due to stress-related and other mental disorders seems to be a reflection of a shared genetic liability.


2020 ◽  
Author(s):  
Christopher Beam ◽  
Patrizia Pezzoli ◽  
Jane Mendle ◽  
S. Alexandra Burt ◽  
Michael C. Neale ◽  
...  

Conventional longitudinal behavioral genetic models estimate the relative contribution of genetic and environmental factors to stability and change of traits and behaviors. Longitudinal models rarely explain the processes that generate observed differences between genetically and socially related individuals. We propose that exchanges between people and their environments (i.e., phenotype-environment effects) can explain the emergence of observed differences over time. Such models, however, require violation of the independence assumption of standard behavioral genetic models, that is, uncorrelated genetic and environmental factors (Beam & Turkheimer, 2013; de Kort, Dolan, & Boomsma, 2012; Dolan, De Kort, Van Beijsterveldt, Bartels, & Boomsma, 2014). We review how specification of phenotype-environment effects contributes to understanding observed changes in genetic variability over time and longitudinal correlations among nonshared environmental factors. We then provide an example using 30 days of positive and negative affect scores from an all-female sample of twins. Results demonstrate that the phenotype-environment effects explain how heritability estimates fluctuate as well as how nonshared environmental factors persist over time. We discuss possible mechanisms underlying change in gene-environment correlation over time, the advantages and challenges of including gene-environment correlation in longitudinal twin models, and recommendations for future research.


2019 ◽  
Vol 95 (1) ◽  
pp. 94-96 ◽  
Author(s):  
Dmitry V. Lanin ◽  
T. M. Lebedeva

In children under aerotechnogenic impact of phenol, methanol and formaldehyde, these substances are identified in the blood in significantly higher concentrations than in the unexposed group. There was found the activation of the mechanisms of the innate immunity (phagocytic activity) and inhibition of markers of the acquired immunity (reduction of relative indices of the content of T-lymphocytes (CD3+) and their subsets (CD4+- and CD8+-lymphocytes). Out of the markers of neuroendocrine regulation there was proved the significant decline of cortisol. Under the impact of anthropogenic chemical environmental factors there are occurred rearrangement and the transformation of interactions within the neuroendocrine and immune systems, as well as “early”, not manifested yet in the nature of specific nosological forms, but over time having the possibility to lead to the shaping of various pathology changes in the neuroendocrine regulation of the immune system.


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