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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.
Source publication
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...
Contexts in source publication
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 ...
Citations
... In plants, a review by Obeso (2002) concluded that most case studies generally support the predictions of the costof-reproduction hypothesis. In humans, there is some evidence in Amish people that increasing parity is correlated with a number of adverse health outcomes for women, such as obesity, diabetes, and cardiovascular disease (McArdle et al., 2006), while it probably lowers the risk of breast and ovarian cancer (Smith et al., 2002). A study conducted by Doblhammer (2000) also supports the proposition that reproduction comes at a cost. ...
... If it is assumed that coital inability is associated with a serious disease, there is a reduction in longevity for women with few children (Smith et al., 2002). This healthy-pregnant-woman effect is also supported by the results of Perls et al. (1997) and McArdle et al. (2006). Doblhammer (2000), Smith et al. (2002), Mirowsky (2005), and McArdle et al. (2006) found that women who give birth to a child at later ages will experience higher postreproductive survival. ...
... This healthy-pregnant-woman effect is also supported by the results of Perls et al. (1997) and McArdle et al. (2006). Doblhammer (2000), Smith et al. (2002), Mirowsky (2005), and McArdle et al. (2006) found that women who give birth to a child at later ages will experience higher postreproductive survival. These results are also supported by historical data (Mueller, 2004), and are consistent with evolutionary theories proposed by Rose et al. (1997). ...
Previous research has investigated several different aspects of the relationship between having a child and parental mortality. One aspect of research that has been neglected until now is the age of the child. If children have an effect on parental mortality, this is likely to change as they grow up. We apply hazard regression models to longitudinal Swedish register data of the total population for men and women separately. Adjusting for a variety of control variables, we find that parents with younger children experience a substantive mortality advantage compared to parents—of the same age—who have older children. The mortality advantage decreases gradually as the age of the youngest child increases. Robustness checks confirm that this result cannot be explained by differences in the parent’s age and parental age at first birth. Childless women and men of the same age experience the highest mortality. Additional models for different causes of death suggest that selection, behavioral changes, and unobserved protective effects contribute to this pattern.
... While our analysis focused on mutational pleiotropy between reproduction and lifespan, the relationship between reproduction and lifespan at the phenotypic level is debated. For example, a negative relationship between female fertility and longevity was reported in Chinese oldest-old individuals 40 , while an opposite trend was found in the Amish 41 . In our data, given polygenic scores for reproduction, individuals with two children have a higher probability of survival to 76 than those with 0, 1, or 3 children. ...
The antagonistic pleiotropy hypothesis posits that natural selection for pleiotropic mutations that confer earlier or more reproduction but impair the post-reproductive life causes aging. This hypothesis of the evolutionary origin of aging is supported by case studies but lacks unambiguous genomic evidence. Here we genomically test this hypothesis using the genotypes, reproductive phenotypes, and death registry of 276,406 UK Biobank participants. We observe a strong, negative genetic correlation between reproductive traits and lifespan. Individuals with higher polygenetic scores for reproduction ( PGS R ) have lower survivorships to age 76 ( SV 76 ), and PGS R increased over birth cohorts from 1940 to 1969. Similar trends are found from individual genetic variants examined. PGS R and SV 76 remain negatively correlated upon the control of the offspring number, revealing horizontal pleiotropy between reproduction and lifespan. Intriguingly, regardless of PGS R , having two children maximizes SV 76 . These and other findings strongly support the antagonistic pleiotropy hypothesis of aging in humans.
... It is therefore difficult to see why longevity would not also increase male fitness equally, given that longer life would provide opportunities for additional mating. Data exist to support a correlation between parity (i.e., reproductive fitness) and longevity in both sexes (Barclay & Kolk, 2019;McArdle et al., 2006). Within this naive evolutionary framework for human reproduction, which disregards culture, family, and parental collaboration, longevity thus appears to be an advantage for both sexes. ...
The target article presented a plausible argument that females' susceptibility to threats might be self-protection for staying alive, but some evidence requires scrutiny. We need to consider (1) the biases of narrative reviews, (2) subjective life quality, and (3) the shadow side of extreme reactions to threats before concluding that females' threat-based response is a self-protection mechanism that promotes survival.
... It is therefore difficult to see why longevity would not also increase male fitness equally, given that longer life would provide opportunities for additional mating. Data exist to support a correlation between parity (i.e., reproductive fitness) and longevity in both sexes (Barclay & Kolk, 2019;McArdle et al., 2006). Within this naive evolutionary framework for human reproduction, which disregards culture, family, and parental collaboration, longevity thus appears to be an advantage for both sexes. ...
Extending Campbell's (1999) staying alive theory (SAT) beyond aggression, we reviewed evidence that females are more self-protective than males. Many commentators provided additional supporting data. Sex differences in life-history adaptations, in the optimal relation between survival and reproduction, and in the mechanisms underlying trade-offs involved with self-protection remain important topics with numerous opportunities for improved understanding.
... It is therefore difficult to see why longevity would not also increase male fitness equally, given that longer life would provide opportunities for additional mating. Data exist to support a correlation between parity (i.e., reproductive fitness) and longevity in both sexes (Barclay & Kolk, 2019;McArdle et al., 2006). Within this naive evolutionary framework for human reproduction, which disregards culture, family, and parental collaboration, longevity thus appears to be an advantage for both sexes. ...
We extend Benenson et al.'s hypothesis from the individual level to the societal level. Because women have highly limited reproductive rates, societies have generally prioritized female survival and regarded males as expendable. We describe various lines of evidence that are consistent with this hypothesis, and we offer additional predictions about differential attitudes toward male versus female endangerment.
... Hank (2010), based on the data of the German Socio-Economic Panel, found that in West Germany, early motherhood was accompanied by poor physical health, while in East Germany, late motherhood was accompanied by poor mental health. In terms of gender differences, early motherhood reduced the survival time of elderly women (Li and Zhang, 2017), and late motherhood was only related to women's longevity, but not for men (McArdle et al., 2006). The Hypothesis 3 was formulated accordingly: ...
... This was why rural women tended to have a higher 'true level of health' than their urban counterparts, so that their own level of health moderates the impact of the number of births on their mortality risk, while urban women faced a higher mortality risk from having more children (six or more). Secondly, in terms of differences in mortality risk between male and the elderly women, on the one hand, foreign studies had shown that maternal longevity increased linearly with the number of children, with each additional child increasing life expectancy by 0.32 years, and this linear relationship was maintained up to 14 children (Mcardle et al., 2006). Similarly, contemporary Chinese women with a higher number of previous or current children also bene tted from a longer and healthier longevity in old age (Li and Zhang, 2017), and the available ndings seemed to support women were better able to cope with the negative effects of childbearing. ...
Background
The trade-off between fertility and longevity stands or falls in China, concerning the realization of the welfare of the parents in later life. With healthy ageing and the implementation of the three-child policy, the policies will always aim to safeguard the welfare of the elderly and increase the level of fertility. Based on Chinese households, whether this trade-off relationship is established or not is of great significance to family fertility orientation and the welfare in later life.
Methods
Based on data from the Chinese Longitudinal Healthy Longevity Survey (CLHLS) from 2008 to 2018, a Cox proportional risk model and an accelerated failure time model were used to examine the impact of the number of children, the number of sons and the number of daughters on longevity.
Results
The study found that the trade-off between childbearing and longevity only existed for those with five or more children, and that for those with fewer than five children, their longevity was not associated with having more children. We further found that having five or more children significantly increased the risk of death for both rural male older adults and urban older adults; and that having a son had a greater negative impact on parental longevity than having a daughter. The timing of childbearing, both too early and late childbearing, adversely affects the longevity of older people.
Conclusions
Based on current policy fertility levels and desire of fertility in family, the negative impact of current fertility patterns on older people's longevity is not present, and promoting fertility and ensuring well-being in later life can be achieved simultaneously. The implications are as follows, firstly, for families, having three children does not affect later life welfare under the three-child policy. Secondly, in terms of fertility support policies, improving fertility services for women while increasing attention to the role of men and fertility services for urban residents; and promoting scientific fertility to avoid the negative effects of unreasonable childbearing behavior.
... 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]. ...
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.
... It is therefore difficult to see why longevity would not also increase male fitness equally, given that longer life would provide opportunities for additional mating. Data exist to support a correlation between parity (i.e., reproductive fitness) and longevity in both sexes (Barclay & Kolk, 2019;McArdle et al., 2006). Within this naive evolutionary framework for human reproduction, which disregards culture, family, and parental collaboration, longevity thus appears to be an advantage for both sexes. ...
Many male traits are well explained by sexual selection theory as adaptations to mating competition and mate choice, whereas no unifying theory explains traits expressed more in females. Anne Campbell's “staying alive” theory proposed that human females produce stronger self-protective reactions than males to aggressive threats because self-protection tends to have higher fitness value for females than males. We examined whether Campbell's theory has more general applicability by considering whether human females respond with greater self-protectiveness than males to other threats beyond aggression. We searched the literature for physiological, behavioral, and emotional responses to major physical and social threats, and found consistent support for females’ responding with greater self-protectiveness than males. Females mount stronger immune responses to many pathogens; experience a lower threshold to detect, and lesser tolerance of, pain; awaken more frequently at night; express greater concern about physically dangerous stimuli; exert more effort to avoid social conflicts; exhibit a personality style more focused on life's dangers; react to threats with greater fear, disgust and sadness; and develop more threat-based clinical conditions than males. Our findings suggest that in relation to threat human females have relatively heightened protective reactions compared to males. The pervasiveness of this result across multiple domains suggests that general mechanisms might exist underlying females’ unique adaptations. An understanding of such processes would enhance knowledge of female health and well-being.
... 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. ...
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 . ...
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.
