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Average life span and 95% confidence intervals for Old Order Amish mothers who lived to at least age 50 years and were born between 1749 and 1912 by the number of children, Lancaster County, Pennsylvania. Average age of death and 95 percent confidence interval by number of children. Trend lines represent piecewise linear regression with one knot and smooth polynomial model as described in text. Secondary axis gives sample size. 

Average life span and 95% confidence intervals for Old Order Amish mothers who lived to at least age 50 years and were born between 1749 and 1912 by the number of children, Lancaster County, Pennsylvania. Average age of death and 95 percent confidence interval by number of children. Trend lines represent piecewise linear regression with one knot and smooth polynomial model as described in text. Secondary axis gives sample size. 

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The relationship between parity and life span is uncertain, with evidence of both positive and negative relationships being reported previously. We evaluated this issue by using genealogical data from an Old Order Amish community in Lancaster, Pennsylvania, a population characterized by large nuclear families, homogeneous lifestyle, and extensive g...

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Context 1
... (14,20–23), we anticipated that the simple linear regression approach would provide us with unbiased estimates of effect measures, but inflated variances of these parameters. We therefore repeated all analyses using a variance component modeling framework that allowed us to account for the residual correlations in age at death potentially existing among related individuals (24). Briefly, the variance component approach models the correlations between the independent and dependent variables conditional on the residual correlations among individuals implied by the pedigree structure. Specifically, the covariance between each pair of individuals within the pedigree is estimated as a function of their degree of relationship, the trait heritability, and the phenotypic variance of the trait. The model is thus defined as: Y 1⁄4 x b þ g þ e ; where Y is a vector of values correlating to each individual’s age at death, x is a matrix of fixed covariates, and b are the effects of interest. The g term is a covariance component that is distributed multivariate normally with a mean of zero and a covariance equal to two times the kinship matrix times the expected variance due to the additive effect of genes. The e term is a normally distributed error component. The likelihood of the pedigree data was then computed under the assumption of multivariate normality. As expected, the point estimates obtained under the simple linear regression and variance component frameworks were similar, although a larger variance for the regression coefficients (and hence wider confidence intervals [CI]) was estimated under variance components. All parameter estimates and significance testing presented in this report are based on the more con- servative variance component modeling. Polynomial regression models were constructed to iden- tify nonlinear relationships between variables (25). The results of the polynomial models were used to determine inflection points for piecewise linear regression models using the above framework. These piecewise linear models were created to aid in the interpretation of the results. Analyses were conducted for men and women separately and were performed using the SOLAR software package (24). All p values reported are two sided. The study included 2015 individuals (937 mothers and 1078 fathers) born between 1749 and 1912. Summary characteristics of these individuals are shown in Table 1 according to birth cohort and sex. Women had on average (standard deviation) 7.2 (3.5) offspring during this time period, and men 7.4 (3.6). Among women, mean age at last birth was 38.6 (5.2) years, and mean age at death was 76.4 (11.0) years. The corresponding estimates for men were 41.1 (6.3) years and 75.2 (10.6) years for mean age at last birth and age at death. Year of birth was not correlated with number of offspring in either men or women but was positively correlated with life span, with this correlation achieving statistical significance in men only. Results of subsequent analyses were essentially unchanged when the analyses were repeated with year of birth as an additional covariate. Of the 937 women in our study, 88 (9.4%) had hus- bands who died prior to their (the wife’s) 50th birthday. Because these women might have had limited reproductive capability, as only seven of the women went on to have children with other men, analyses were performed again with those 88 women removed from the sample. Results of analyses based on exclusion of these women were essentially unchanged. We have previously reported in the OOA that there is significant familial aggregation for both age at death (14) and number of offspring (26). The familial correlations for age at death recalculated in these data correspond to heritability estimates of 31% in men and 25% in women; for number of offspring, the heritability estimates are 22% and 27% in men and women, respectively ( p , .0001 for all). These estimates represent the proportion of variance in life span (or number of offspring) due to the additive effect of genes, i.e., narrow sense heritability. We then re- estimated the heritability of life span both with and without covariates. The heritability was not appreciably changed for either men or women upon controlling for number of children, age at last birth, or both, suggesting that genes influencing longevity are largely independent of those that influence parity and the ability to reproduce later in life. Figure 1 shows the distribution of age at death among the 1078 fathers surviving until age 50 or older according to number of children. Longevity increased in linear fashion with the number of children; there was an average 0.23-year increase (95% CI, 0.05–0.40; p 1⁄4 .01) in life span with each additional child. Among the 937 women with children, an association was also observed between number of children and life span, with life span increasing with increasing number of children up to 14 children and then decreasing thereafter. Figure 2 shows results from both a smooth polynomial model and piecewise linear regression. Both the positive association between life span and higher parity prior to the 14th child and the negative association seen afterward were statistically significant. The piecewise regression predicts an increase in life span of 0.32 years (95% CI, 0.10–0.54 years; p .004) for each additional offspring until child number 14. For each additional child after the 14th, a woman’s life span was predicted to decrease by 4.01 years (95% CI, 1.81–6.20 years; p 1⁄4 .0004). Thirty-nine women in the cohort gave birth to 14 or more children. Older ages of both the mother and father at birth of the last child were significantly associated with increased life span, with the association particularly strong for the mothers. In men, the effect of age at last birth was completely obliterated after accounting for the number of children fathered, with each additional year of age at last birth associated with an average increase in life span of only 0.0007 years ( p 1⁄4 .91). This result suggests that the number of children fathered, rather than the timing of the births, is the better predictor of life span. The reverse was seen among women. After adjusting for the number of children, the age at last birth remained strongly associated with life span, with each additional year of age at last birth associated with an average increase in life span of 0.29 years ( p 1⁄4 .001). Moreover, after accounting for age at last birth, the correlation observed in women between number of children and life span was eliminated. Figure 3 shows the association between number of children and postreproductive life span after accounting for age at last birth. Age at last birth accounts for the positive association seen in Figure 2 between the birth of a woman’s first child and to her 14th. Over a large range of parity values, 1–14 children, parity has little or no association with life span in the presence of a strong positive association between life span and later age childbirth. Of the 6711 children born to women in our cohort, 3455 (51.5%) were sons and 3254 (48.5%) were daughters. Two children were of unknown sex. Table 2 shows the effects of sons and daughters on life span when modeled separately. We assessed the hypothesis that sons and daughters have differential effects on the life span of their parents by including separate variables for the number of sons and number of daughters into a single model. We then performed a log likelihood ratio test constraining the two effects to be equal (e.g., effect associated with birth of a son equals that associated with birth of a daughter). For neither fathers nor mothers was there significant evidence for a differential effect between birth of a son and birth of a daughter. The OOA provide an excellent opportunity to study the relationship between parity and longevity. Amish families continue to be characterized by large family sizes, with average family sizes remaining relatively constant over the 163-year duration of our study period. Moreover, the very high parity characteristic of some of these families allows us to evaluate the impact of ultrahigh parity on life span. The egalitarian nature of Amish culture offers a further advantage as it reduces or eliminates much of the variation among social lines, such as that attributable to differences in income or access to health care, which could confound the relationship between longevity and family size. Our analyses revealed a correlation between increasing parity and increasing life span in both women (among those with less than ultrahigh parity) and men. Notably, the correlation observed in women, but not men, was largely due to a later age at last birth, as the parity–life span correlation was essentially eliminated when differences in this variable were taken into account. The correlation observed among women in our study between older age at last birth and longer life span has been reported by others (7,10,27–30). What are some possible explanations for the parity–life span correlation observed in this population? One likely possibility is that highly parous parents may represent a healthy subset of the population, whose favorable genetic constitutions and/or healthy lifestyles lead them to be both more fertile and to live longer lives. According to this spe- culation, parity itself may have no direct relationship to life span, but rather high parity may be merely a reflection of men and women who are destined to live long lives. Notably, the correlation of life span with parity disappears after accounting for age at last birth among women but not men. Possibly, late childbirth in OOA women may be a marker for delayed menopause, which, in turn, could reflect a slower rate of biological aging. In this context, the delayed reproductive aging of these women may be associated with reduced risk or delay of cardiovascular and other diseases in later life. ...
Context 2
... models were constructed to iden- tify nonlinear relationships between variables (25). The results of the polynomial models were used to determine inflection points for piecewise linear regression models using the above framework. These piecewise linear models were created to aid in the interpretation of the results. Analyses were conducted for men and women separately and were performed using the SOLAR software package (24). All p values reported are two sided. The study included 2015 individuals (937 mothers and 1078 fathers) born between 1749 and 1912. Summary characteristics of these individuals are shown in Table 1 according to birth cohort and sex. Women had on average (standard deviation) 7.2 (3.5) offspring during this time period, and men 7.4 (3.6). Among women, mean age at last birth was 38.6 (5.2) years, and mean age at death was 76.4 (11.0) years. The corresponding estimates for men were 41.1 (6.3) years and 75.2 (10.6) years for mean age at last birth and age at death. Year of birth was not correlated with number of offspring in either men or women but was positively correlated with life span, with this correlation achieving statistical significance in men only. Results of subsequent analyses were essentially unchanged when the analyses were repeated with year of birth as an additional covariate. Of the 937 women in our study, 88 (9.4%) had hus- bands who died prior to their (the wife’s) 50th birthday. Because these women might have had limited reproductive capability, as only seven of the women went on to have children with other men, analyses were performed again with those 88 women removed from the sample. Results of analyses based on exclusion of these women were essentially unchanged. We have previously reported in the OOA that there is significant familial aggregation for both age at death (14) and number of offspring (26). The familial correlations for age at death recalculated in these data correspond to heritability estimates of 31% in men and 25% in women; for number of offspring, the heritability estimates are 22% and 27% in men and women, respectively ( p , .0001 for all). These estimates represent the proportion of variance in life span (or number of offspring) due to the additive effect of genes, i.e., narrow sense heritability. We then re- estimated the heritability of life span both with and without covariates. The heritability was not appreciably changed for either men or women upon controlling for number of children, age at last birth, or both, suggesting that genes influencing longevity are largely independent of those that influence parity and the ability to reproduce later in life. Figure 1 shows the distribution of age at death among the 1078 fathers surviving until age 50 or older according to number of children. Longevity increased in linear fashion with the number of children; there was an average 0.23-year increase (95% CI, 0.05–0.40; p 1⁄4 .01) in life span with each additional child. Among the 937 women with children, an association was also observed between number of children and life span, with life span increasing with increasing number of children up to 14 children and then decreasing thereafter. Figure 2 shows results from both a smooth polynomial model and piecewise linear regression. Both the positive association between life span and higher parity prior to the 14th child and the negative association seen afterward were statistically significant. The piecewise regression predicts an increase in life span of 0.32 years (95% CI, 0.10–0.54 years; p .004) for each additional offspring until child number 14. For each additional child after the 14th, a woman’s life span was predicted to decrease by 4.01 years (95% CI, 1.81–6.20 years; p 1⁄4 .0004). Thirty-nine women in the cohort gave birth to 14 or more children. Older ages of both the mother and father at birth of the last child were significantly associated with increased life span, with the association particularly strong for the mothers. In men, the effect of age at last birth was completely obliterated after accounting for the number of children fathered, with each additional year of age at last birth associated with an average increase in life span of only 0.0007 years ( p 1⁄4 .91). This result suggests that the number of children fathered, rather than the timing of the births, is the better predictor of life span. The reverse was seen among women. After adjusting for the number of children, the age at last birth remained strongly associated with life span, with each additional year of age at last birth associated with an average increase in life span of 0.29 years ( p 1⁄4 .001). Moreover, after accounting for age at last birth, the correlation observed in women between number of children and life span was eliminated. Figure 3 shows the association between number of children and postreproductive life span after accounting for age at last birth. Age at last birth accounts for the positive association seen in Figure 2 between the birth of a woman’s first child and to her 14th. Over a large range of parity values, 1–14 children, parity has little or no association with life span in the presence of a strong positive association between life span and later age childbirth. Of the 6711 children born to women in our cohort, 3455 (51.5%) were sons and 3254 (48.5%) were daughters. Two children were of unknown sex. Table 2 shows the effects of sons and daughters on life span when modeled separately. We assessed the hypothesis that sons and daughters have differential effects on the life span of their parents by including separate variables for the number of sons and number of daughters into a single model. We then performed a log likelihood ratio test constraining the two effects to be equal (e.g., effect associated with birth of a son equals that associated with birth of a daughter). For neither fathers nor mothers was there significant evidence for a differential effect between birth of a son and birth of a daughter. The OOA provide an excellent opportunity to study the relationship between parity and longevity. Amish families continue to be characterized by large family sizes, with average family sizes remaining relatively constant over the 163-year duration of our study period. Moreover, the very high parity characteristic of some of these families allows us to evaluate the impact of ultrahigh parity on life span. The egalitarian nature of Amish culture offers a further advantage as it reduces or eliminates much of the variation among social lines, such as that attributable to differences in income or access to health care, which could confound the relationship between longevity and family size. Our analyses revealed a correlation between increasing parity and increasing life span in both women (among those with less than ultrahigh parity) and men. Notably, the correlation observed in women, but not men, was largely due to a later age at last birth, as the parity–life span correlation was essentially eliminated when differences in this variable were taken into account. The correlation observed among women in our study between older age at last birth and longer life span has been reported by others (7,10,27–30). What are some possible explanations for the parity–life span correlation observed in this population? One likely possibility is that highly parous parents may represent a healthy subset of the population, whose favorable genetic constitutions and/or healthy lifestyles lead them to be both more fertile and to live longer lives. According to this spe- culation, parity itself may have no direct relationship to life span, but rather high parity may be merely a reflection of men and women who are destined to live long lives. Notably, the correlation of life span with parity disappears after accounting for age at last birth among women but not men. Possibly, late childbirth in OOA women may be a marker for delayed menopause, which, in turn, could reflect a slower rate of biological aging. In this context, the delayed reproductive aging of these women may be associated with reduced risk or delay of cardiovascular and other diseases in later life. Although attractive, this hypothesis must be viewed as speculative because historical measures of meno- pausal status are unavailable from women in our study. Social factors may also influence the parity–life span relationship. One possibility, for example, is that large family sizes may simply reflect happier marriages, which may in turn be associated with extended life span. Alter- natively, large offspring sizes might directly lead to extended parental life span insofar as an increased number of offspring may provide stronger social networks for the parents in their older ages. Thus, the correlation between parity and increased life span might be mediated through social factors that act indirectly by increasing both parity and life span or directly by strengthening familial networks that are valuable for survival into old age. Our data suggest that life span is reduced among women of ultrahigh parity ( . 14 children). The reason for this is not evident. Possibly, any social and/or biological benefits associated with multiparity and/or late childbirth are over- whelmed by detrimental effects incurred by repeated pregnancies and childbirths. Several studies [recently reviewed in (31)], have highlighted the risk of adverse maternal and fetal outcomes associated with very high parity, and have concluded that there was ‘‘possible evidence’’ of increased maternal risk (e.g., diabetes, essential hypertension) in these women. However, few studies appear to have directly assessed the long-term survival of ultrahigh parous women. There are significant heritable components to both fertility and life span, and it is therefore intriguing to speculate whether genes favoring increased parity might also favor increased life span. In our data, we observed no appreciable change in the ...

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... However, to date, there is no reliable biomarker of oocyte quality that can aid in the assessment and treatment of age-related infertility. Demographic studies among different ethnic groups and different epochs positively correlated late female reproduction with signs of general health and longevity [6][7][8][9][10]. These studies suggest that extended fertility and delayed aging have a common genetic background. 2 of 11 Telomeres are highly conserved nucleoprotein complexes composed of tandem six nucleotide DNA repeats and associated proteins [11]. ...
... According to one, telomeres shorten with the accumulating number of pregnancies and deliveries or period of caregiving, hindering the initially longer telomere length set point in the EF women having nine or more children. Indeed, some demographic studies reported a possible trade-off between fertility and longevity, suggesting that increased parity is correlated with shorter telomeres and a shorter lifespan [6,18,19]. However, other reports suggest otherwise [8]. ...
Article
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Current social trends of delayed reproduction to the fourth and fifth decade of life call for a better understanding of reproductive aging. Demographic studies correlated late reproduction with general health and longevity. Telomeres, the protective ends of eukaryotic chromosomes, were implicated in various aging-associated pathologies and longevity. To examine whether telomeres are also associated with reproductive aging, we measured by Southern analysis the terminal restriction fragments (TRF) in leukocytes of women delivering a healthy infant following a spontaneous pregnancy at 43–48 years of age. We compared them to age-matched previously fertile women who failed to conceive above age 41. The average TRF length in the extended fertility group (9350 bp) was significantly longer than in the normal fertility group (8850 bp; p-value = 0.03). Strikingly, excluding women with nine or more children increased the difference between the groups to over 1000 bp (9920 and 8880 bp; p-value = 0.0009). Nevertheless, we observed no apparent effects of pregnancy, delivery, or parity on telomere length. We propose that longer leukocyte telomere length reflects higher oocyte quality, which can compensate for other limiting physiological and behavioral factors and enable successful reproduction. Leukocyte telomere length should be further explored as a novel biomarker of oocyte quality for assessing reproductive potential and integrating family planning with demanding women’s careers.
... The evolutionary theories of aging have suggested that delaying reproductive time can prolong life span. Previous studies have identified that late fertility had positive effects on post-reproductive survival (35)(36)(37)(38)(39)(40). This study indicated that ICA and LCA were significantly higher in centenarian women than in women aged 80-99 years. ...
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Background Despite research efforts in this field for more than a century, the relationship between female fertility and longevity is unclear. This study was designed to investigate this relationship in Chinese oldest-old population. Methods The China Hainan Centenarian Cohort Study was performed in 18 cities and counties of Hainan. A total of 1,226 females, including 758 centenarian women and 468 women aged 80–99 years, were enrolled in this study. Using a standardized protocol, in-person interviews and blood analyses were conducted by a well-trained research team through home visits. Results Centenarian women had significantly lower number of children (NOC) and higher initial childbearing age (ICA) and last childbearing age (LCA) than women aged 80–99 years (p < 0.05 for all). Multivariate logistic regression analysis showed that NOC and testosterone (T) levels were positively associated with women aged 80–99 years, when centenarian women was considered as reference (p < 0.05 for all). ICA, LCA, and estradiol (E2) levels were negatively associated with women aged 80–99 years, when centenarian women was considered as reference (p < 0.05 for all). Conclusions The centenarians had crucial characteristics of less and delayed childbearing, indicating a negative relationship between female fertility and longevity in Chinese oldest-old population. Serum E2 levels were positively associated and serum T levels were negatively associated with longevity. The less and late childbearing might be a significant factor of longevity, and successful aging might be promoted by reducing and delaying female childbearing.
... women with an older ALB tend to be long-lived 17 . Women who deliver higher numbers of live births have longer lifespans [18][19][20][21] . Finally, older ages at natural menopause are associated with longer lifespans 22 . ...
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Ageing may be due to mutation accumulation across the lifespan, leading to tissue dysfunction, disease, and death. We tested whether germline autosomal mutation rates in young adults predict their remaining survival, and, for women, their reproductive lifespans. Age-adjusted mutation rates (AAMRs) in 61 women and 61 men from the Utah CEPH (Centre d’Etude du Polymorphisme Humain) families were determined. Age at death, cause of death, all-site cancer incidence, and reproductive histories were provided by the Utah Population Database, Utah Cancer Registry, and Utah Genetic Reference Project. Higher AAMRs were significantly associated with higher all-cause mortality in both sexes combined. Subjects in the top quartile of AAMRs experienced more than twice the mortality of bottom quartile subjects (hazard ratio [HR], 2.07; 95% confidence interval [CI], 1.21–3.56; p = 0.008; median survival difference = 4.7 years). Fertility analyses were restricted to women whose age at last birth (ALB) was ≥ 30 years, the age when fertility begins to decline. Women with higher AAMRs had significantly fewer live births and a younger ALB. Adult germline mutation accumulation rates are established in adolescence, and later menarche in women is associated with delayed mutation accumulation. We conclude that germline mutation rates in healthy young adults may provide a measure of both reproductive and systemic ageing. Puberty may induce the establishment of adult mutation accumulation rates, just when DNA repair systems begin their lifelong decline.
... Strikingly, one study estimated the difference in telomere length between parous and non-parous women to be equivalent to 11 years of cellular agingan effect observed to be larger than the effect smoking or obesity had on telomere length (Pollack et al., 2018). Conversely, longer telomere lengths have been observed in women who had their last child at a later age (Fagan et al., 2017) which has been linked to greater longevity (Perls et al., 1997;McArdle et al., 2006;Sun et al., 2015) and a resistance to dementia later in life (Gilsanz et al., 2018). Interestingly, longer telomeres have also been associated with greater breastfeeding duration (Kresovich et al., 2018) as well as greater endogenous estrogens which is typically associated with lower parity (Lin et al., 2011). ...
Article
Risk and resilience in brain health and disease can be influenced by a variety of factors. While there is a growing appreciation to consider sex as one of these factors, far less attention has been paid to sex-specific variables that may differentially impact females such as pregnancy and reproductive history. In this review, we focus on nervous system disorders which show a female bias and for which there is data from basic research and clinical studies pointing to modification in disease risk and progression during pregnancy, postpartum and/or as a result of parity: multiple sclerosis (MS), depression, stroke, and Alzheimer's disease (AD). In doing so, we join others (Shors, 2016; Galea et al., 2018) in aiming to illustrate the importance of looking beyond sex in neuroscience research.
... These findings are consistent with previous evidence on subjective survival probabilities as well as on actual mortality. Respondents who live with young or adult children report higher survival expectations (Liu, Tsou, and Hammitt 2007;Mirowsky 1999;Ross and Mirowsky 2002) and the lifespan of parents increases in line with the number of children (McArdle et al. 2006). Higher SES is associated with higher subjective life expectancy (Rappange, Brouwer, and Exel 2016;Liu, Tsou, and Hammitt 2007;Hurd and McGarry 1995;Kutlu-Koc and Kalwij 2017) as well as lower mortality (Nandi, Glymour, and Subramanian 2014). ...
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... Career achievements have also shown beneficial effects on health [7]. Other psychosocial factors affecting lifespan include education [8], prosocial behavior [9], extreme lifestyle [10], optimism and positive emotions [11 -12], stress resistance [13], family socioeconomic status [14], having a family [15], and the number of children in a family [16]. However, the positive effects of different psychosocial factors on lifespan and health are still unclear. ...
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In this study we examined 100 pairs of monozygotic (MZ) twins to determine if lifestyle differences between control and experimental twins affected lifespan and health. We used the twin database of the Russian Humanitarian Scientific Foundation. The dependent variables were the difference in lifespan and the number of socially significant diseases between control and experimental twins. The independent variables were the differences within different psychosocial factors (education, family, children, career, prosocial behavior, religiousness, residence, relocations) between control and experimental twins. Using the ANOVA test, we obtained that career (F=11.12, p=0.000), education (F=3.272, p=0.042), living in a large city (F=6.674, p=0.008), having family (F=3.926, p=0.023) and relocations (F=3.757, p=0.046) increased lifespan. For women, one of the most significant positive factors that increased lifespan was education (F=5.992, p=0.005). For men, relocation (F=7.835, p=0.027) was one of the most significant factors that increased lifespan. Having family significantly reduced the number of socially significant diseases (F=3.477, p=0.035). Although this study represents statistically significant data showing that distinct lifestyles have different effects on lifespan and health, future studies with a database of a larger amount of MZ twin pairs are needed to confirm this data.
... Extensive studies have been performed in order to investigate the effect of reproduction on longevity both in humans and lower life forms (Doblhammer, 2000), but varying results have been reported. Many clinical studies have shown a positive relationship between longevity and reproduction (Doblhammer, 2000;Muller et al., 2002;McArdle et al., 2006), while others have suggested a trade-off or no association between these two factors (Voland and Engel, 1986;Kirkwood and Rose, 1991;Le Bourg et al., 1993;Korpelainen, 2000;Smith et al., 2009;Tabatabaie et al., 2011). The depletion of resources necessary for self-maintenance in an attempt to be used for reproductive purposes has been associated with decreased longevity. ...
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Mutations of a single gene can lead to a major increase in longevity in organisms ranging from yeast and worms to insects and mammals. Discovering these mutations (sometimes referred to as “longevity genes”) led to identification of evolutionarily conserved molecular, cellular, and organismal mechanisms of aging. Studies in mice provided evidence for the important role of growth hormone (GH) signaling in mammalian aging. Mice with mutations or gene deletions leading to GH deficiency or GH resistance have reduced body size and delayed maturation, but are healthier and more resistant to stress, age slower, and live longer than their normal (wild type) siblings. Mutations of the same genes in people can provide remarkable protection from age-related disease, but have no consistent impact on lifespan. Ongoing research indicates that genetic defects in GH signaling are linked to extension of healthspan and lifespan via a variety of interlocking mechanism, including improvements in genome and stem cell maintenance, stress resistance, glucose homeostasis, and thermogenesis, along with reductions in the mechanistic target of rapamycin (mTOR) C1 complex signaling and in chronic low grade inflammation.
... All methods were performed in accordance with the relevant guidelines and regulations. Details of these studies design, recruitment, and phenotyping had been described previously [33][34][35][36] . Briefly, the AFOS was started in March 1997 to study genes that are important for bone health. ...
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Wnt1-inducible signaling pathway protein-1 (WISP1) is a novel target of the Wnt pathway for modulating osteogenesis and improving bone strength. However, it is not clear if genetic variants in the WISP1 region are associated with bone mineral density (BMD) in human. The aim of this study is to investigate the role of genetic variation in WISP1 gene as a determinant of BMD in 1,510 Old Order Amish (OOA). We performed regional association analysis of 58 tag variants within 5 kb upstream and downstream to WISP1 with BMD and found 5 variants that were associated with BMD at multiple skeletal sites (P values from 2.89 × 10-6 to 1.62 × 10-2), with some significant associations even after adjustment for multiple comparisons. To replicate these results in an independent dataset, we performed a look-up of BMD associations with these variants in European ancestry subjects from the large GEFOS Consortium and observed the nominal associations of two of these variants with BMD (P values: 0.031 to 0.048). In conclusion, we have demonstrated that genetic variants surrounding WISP1 are associated with BMD at multiple skeletal sites in the OOA, thus influencing osteoporosis risk. These results support a role for the WISP1 gene on influencing variation in BMD.
... Health and medical research has considered Amish women's lives from childhood through menopause and beyond (Documét, et al. 2008;Hairston, et al. 2013;Hewner 2001;McArdle, et al. 2006;Miller, et al. 2007;Thomas, et al. 2002;Von Gruenigen, et al. 2000). ...
... In particular, health research has relied on cursory descriptions of Amish life, characterized in one cancer study as simply a "lifestyle which does not include watching television, using computers, using automated farm equipment or automobiles" (Katz, et al. 2012, 435). Alternatively, authors point to the "strong social structure" (Rogers et al. 2013, 918) of their Amish patients, their "close knit familial units" (McArdle, et al. 2006), with little in the way of what that actually means. One such study wonders if "changes observed in the nature of farm work accompanying mechanization may further complicate the relationship between [farming] occupation and physical activity." ...
Article
In this article, I explore the connections between Amish gender socialization and Amish birth practices to suggest that an Amish construction of femininity shapes the ways that Amish women experience childbirth. This study is framed by Amish women’s health research and takes as a point of departure two observations often made about Amish childbirth practices: (1) medical research has found that Amish women have shorter labors than their non-Amish (English) counterparts, and (2) doctors, midwives, and birth attendants have argued that Amish women’s expression of pain during labor and delivery differs substantially from their English counterparts. I draw on my two years of ethnographic work on Amish midwifery and homebirth to argue that there is deep sociological richness in medical findings that often dismiss Amish life as merely culturally anomalous. I argue that Amish birth is shaped by the norms of Amish society, particularly those that govern gender. I conclude that many of the features of Amish birth that have so interested health researchers cannot be fully understood without a sociological investigation of Amish life, and plain Anabaptist scholarship seems well positioned to foreground the social and cultural features of Amish society that likely remain invisible to health researchers. Reciprocally, comparative health studies on the Amish may illuminate areas of inquiry that were previously understudied and offer new possibilities for future social and cultural research within plain Anabaptist studies.
... The importance of this investigation is underscored by numerous studies which have found that that parity and the exposure to various pregnancy outcomes has significant effects on life expectancy. [23][24][25] Record linkage studies examining pregnancy associated life expectancy are needed to help to identify how the number of pregnancies, number of deliveries, and types of pregnancy outcomes may affect the health and longevity of women. These findings, in turn, may then contribute to better screening to identify the subsets of women who may most benefit from interventions to ameliorate any harmful effects and/or to enhance any beneficial effects associated with pregnancy and pregnancy management. ...
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Objectives Measures of pregnancy associated deaths provide important guidance for public health initiatives. Record linkage studies have significantly improved identification of deaths associated with childbirth but relatively few have also examined deaths associated with pregnancy loss even though higher rates of maternal death have been associated with the latter. Following PRISMA guidelines we undertook a systematic review of record linkage studies examining the relative mortality risks associated with pregnancy loss to develop a narrative synthesis, a meta-analysis, and to identify research opportunities. Methods MEDLINE and SCOPUS were searched in July 2015 using combinations of: mortality, maternal death, record linkage, linked records, pregnancy associated mortality, and pregnancy associated death to identify papers using linkage of death certificates to independent records identifying pregnancy outcomes. Additional studies were identified by examining all citations for relevant studies. Results Of 989 studies, 11 studies from three countries reported mortality rates associated with termination of pregnancy, miscarriage or failed pregnancy. Within a year of their pregnancy outcomes, women experiencing a pregnancy loss are over twice as likely to die compared to women giving birth. The heightened risk is apparent within 180 days and remains elevated for many years. There is a dose effect, with exposure to each pregnancy loss associated with increasing risk of death. Higher rates of death from suicide, accidents, homicide and some natural causes, such as circulatory diseases, may be from elevated stress and risk taking behaviors. Conclusions Both miscarriage and termination of pregnancy are markers for reduced life expectancy. This association should inform research and new public health initiatives including screening and interventions for patients exhibiting known risk factors.