Introduction
Parenthood leads to major changes in activities, lifestyles, and allocation of resources; and pregnancy, parturition, and lactation involve considerable physiological changes for women. Long-established evolutionary theories of aging posit a negative relationship between fertility and longevity, reflecting trade-offs in investment in younger-age reproductive fitness and somatic maintenance in the post-reproductive period (Kirkwood and Rose
1991), and a growing literature has indicated linkages between fertility history and later-life health and mortality. In general, previous studies have indicated a J-shaped association between overall parity and mortality, with higher risks for childless and high-parity parents than for parents of two or three children (for reviews, see Högnäs et al.
2017; Hurt et al.
2006; Zeng et al.
2016). Although many studies have considered only women, those that have included men have tended to report similar albeit less strong associations suggesting underlying biosocial processes, as well as specific physiological effects that apply only to women. Timing of parenthood has been shown to be important, with many studies showing increased later-life mortality and poorer health outcomes among those entering parenthood at a young age, although with some contextual variations (Grundy and Foverskov
2016). Mechanisms underlying these associations are hypothesized to include a range of partly offsetting factors (Grundy and Tomassini
2005). On the positive side, children provide an incentive for healthier behaviors and a source of social interaction and support during both child-rearing and subsequent phases of life. Less positively, parenthood involves stresses, including the stress involved in pregnancy and childbearing for women, and substantial economic costs. For women, biological mechanisms include lowered estrogen exposure and harmful changes to lipid and glucose metabolism during pregnancy (Hardy et al.
2007). Additionally, studies have shown that women who give birth in their teens have higher risks of developing eclampsia, pregnancy-related hypertension, lasting insulin resistance, and altered cholesterol profiles (Lacey et al.
2017). Moreover, complications of pregnancy—including hypertension, gestational diabetes, preterm birth, and low birth weight—are associated with cardiometabolic risk (Hardy et al.
2007). In addition to these biological challenges for women, more general stresses related to child-rearing may also affect fathers. Cumulative effects of these stresses may outweigh salutogenic effects of parenthood, especially for young parents, who may be less resilient to stress and have fewer social and economic resources (Falci et al.
2010), and for those with closely spaced births (Grundy and Kravdal
2010) and large family sizes (D’Elio et al.
1997). Moreover, early parenthood may lead to disruption of educational and career progression and is associated with increased risk of partnership breakdown, all of which may increase risks of socioeconomic and social disadvantage (Grundy and Read
2015). Additionally, despite evidence that parenthood may be associated with less risky behaviors arising from social control exerted by partners and children and the motivation that parenthood brings to set a good example, some studies have suggested a positive association with obesity (Sowers
2003).
An important complicating factor is the need to account for selection to particular fertility pathways. Epigenetic and hormonal influences prompted by unstable environments in childhood may lead to earlier sexual maturation, sexual debut, and poorer choice of partners (Waynforth
2012), and numerous studies have shown that early parenthood is associated with childhood disadvantage (Kiernan
1997; Sigle-Rushton
2005) as well as with disadvantageous health behaviors and health outcomes across the life course (Henretta
2007; Nyström Peck
1994). The complexity of these associations means that our understanding of underlying processes and mechanisms is still limited.
The aim of this study is to contribute to our understanding of these processes by examining associations between aspects of fertility histories and midlife biomarkers indicative of health status, which may mediate progression to later disability and mortality. On the one hand, positive effects of parenthood (such as the social control of health-related behaviors) may imply, for example, less smoking among parents. Parents, and parents with more children, may also receive greater social support than childless or low-parity individuals (Grundy and Read
2015), which may buffer health-damaging effects of stress. These mechanisms imply lower cardiometabolic risks and better respiratory function among parents than among childless individuals as well as possibly increased benefits of having a larger family size. On the other hand, the negative effects of some patterns of childbearing and child-rearing (such as greater stress associated with early parenthood and high parity) may have negative implications for these indictors of health. For example, as noted earlier, higher parity has been found to be associated with higher risks of obesity, a well-established cardiometabolic risk factor (Smith
2003; Sowers
2003).
One of the main problems besetting efforts at unravelling these associations is that early-life socioeconomic and health factors are known to be strongly associated both with fertility trajectories and with later-life health. Many previous studies have either not been able to take account of these selection processes or had to rely on rather limited accounts of childhood circumstances reported retrospectively by older adults (Grundy and Foverskov
2016; Grundy and Read
2015). We use high-quality prospective data from the 1958 National Child Development Study (NCDS), combining information from Sweeps 0 (1958) to 7 (2004; age 46) and from a biomedical survey collected in 2002 (age 44). We examine aspects of parenthood trajectories, including parity and age at first and at last birth, and their associations with midlife biomarkers indicative of cardiometabolic risk and respiratory function. Our aim is to investigate the extent to which associations between fertility history indicators and these related outcomes show a consistent pattern, suggestive of a common underlying mechanism of action.
Previous Research
The literature on associations between fertility and later-life health has focused partly on the association between the number of children and all-cause or cause-specific mortality (Dior et al.
2013; Doblhammer
2000; Grundy and Kravdal
2007,
2010; Grundy and Tomassini
2006; Hinkula et al.
2005; Hurt et al.
2006; Jaffe et al.
2009,
2011; Tamakoshi et al.
2010) and has generally shown a J-shaped relationship between parity and mortality. Individuals who have two or three children have a lower mortality risk than those who are childless, have one child, or have four to five or more children. Many studies are restricted to women, but results from those also including men suggest that although associations are weaker, the J-shaped association is still observed. The similarity of findings for men and women suggests underlying biosocial pathways (Grundy and Kravdal
2007). Cause-specific mortality analyses provide some insights into possible underlying mechanisms. For example, results from Norway and Sweden showed inverse associations between parity and deaths from lung cancer, alcohol-related causes, and accidents and violence, with the highest mortality rates among childless individuals (Barclay et al.
2016; Grundy and Kravdal
2010). Mortality from these causes is strongly related to smoking, heavy alcohol use, and other risky behaviors, which would suggest that a lack of social control (from children) of health behaviors is one possible underlying mechanism. However, selection may be as or more important given that those who have experienced early disadvantage and/or developed poor health behaviors in adolescence may include groups less likely to find a partner and form a family.
Early disadvantage is also associated with a higher risk of early parenthood, as shown in other studies investigating the association later-life health and fertility history (Grundy and Kravdal
2014) or combined effects of fertility and partnership histories (Kravdal et al.
2012). Many studies that investigated associations between timing of fertility and later-life health indicated that early parenthood is associated with a higher risk of later-life mortality. This relationship is partially explained by socioeconomic background, health-related factors, and (in some settings) ethnicity (Grundy
2009; Kravdal et al.
2012; Spence and Eberstein
2009). However, analyses controlling for these influences, including sibling comparison studies (Barclay et al.
2016; Einiö et al.
2015), have also found an adverse association between early parenthood and later mortality risks, especially risks associated with poor health behaviors (e.g., lung cancer, accidents and violence), as for the childless (Barclay et al.
2016; Grundy and Kravdal
2010).
Other research has focused on associations between fertility and health outcomes, rather than mortality, both in midlife and at older ages (Buber and Engelhardt
2008; Grundy and Holt
2000; Grundy and Tomassini
2005; Gunes
2016; Hank
2010; Hanson et al.
2015; Henretta
2007; O’Flaherty et al.
2016; Pirkle et al.
2014; Read et al.
2011; Williams et al.
2011). Outcomes investigated include self-reported health, disability, presence of limiting long-term illness, chronic diseases, allostatic load, grip strength, psychological well-being, and mental health (Grundy and Read
2015; Henretta et al.
2008; Keenan and Grundy
2018; Spence
2008). Findings are similar to those reported for mortality, with early parenthood, childlessness, and high parity associated with poorer health outcomes. Also, some studies have indicated that later age at first parenthood is associated with better health later in life (Grundy and Tomassini
2005; Read and Grundy
2011). As for mortality, studies have indicated that the relationship between fertility and health is partially confounded or mediated by life course socioeconomic factors and partnership status, with some evidence of contextual influences (Grundy and Foverskov
2016; Grundy and Read
2015).
Most of these studies of associations between fertility histories and health have relied on self-reported indicators. These measures have some limitations: for example, they may be influenced by health expectations, which are also correlated with socioeconomic status (Daltroy et al.
1999; Jürges
2007; Quesnel-Vallee
2007). Recently, other measures have become available thanks to the collection of blood samples and observer-measured indicators collected in nurse-administered survey modules. However, relatively few studies to date have looked specifically at the association between fertility history and biomarkers. Lawlor et al. (
2003), in analyses of data for men and women aged 60–79 included in the British Regional Heart Study and the British Women’s Health and Heart Study, examined associations between parity and a range of coronary heart disease (CHD) risk factors, including systolic and diastolic blood pressure, obesity, lipid profiles, and diabetes. Results showed an association between increasing number of children and increasing obesity among both women and men, although this was attenuated among men after the researchers controlled for adult lifestyle and socioeconomic indicators. Among women, higher parity was also associated with metabolic risk factors. These investigators concluded that lifestyle factors associated with having large families may be associated with obesity and CHD risk in both women and men and that women may suffer additional influences arising from biological changes associated with pregnancy, such as lipid and glucose metabolism and adverse coagulation. Hardy et al. (
2007) used data from the 1946 British birth cohort to investigate the association between number of children and CHD risk factors, using blood pressure, body mass index (BMI), waist-to-hip ratio (WHR), total cholesterol, high-density lipoprotein and low-density lipoprotein cholesterol and triglyceride levels, and glycated hemoglobin at age 53. They found that BMI, WHR, and type 2 diabetes in women, and glycated hemoglobin in men showed a linearly increasing trend with increasing number of children; however, the authors found no associations with other outcomes investigated and concluded that the associations observed were mostly explained by behavior and lifestyle. Grundy and Read (
2015) looked at the link between retrospectively collected fertility histories and allostatic load (and long-term illness) among people born before 1952 in England. The measure of allostatic load was derived using nine biomarkers: systolic and diastolic blood pressure, WHR, peak expiratory flow, HDL/total cholesterol ratio (mg/dL), triglycerides, glycated hemoglobin, fibrinogen, and C-reactive protein. They found that earlier ages at first birth were associated with worse allostatic load, with the relationship mediated in part by wealth, physical activity, and smoking. No association between childlessness and allostatic load was found. Lacey et al. (
2017) used data from the 1958 NCDS to look specifically at the association between age at first birth and biomarkers representing cardiovascular risk factors and found that experiencing a teenage birth was associated with an adverse cardiovascular profile in midlife.
Thus, results of research focusing on biomarkers and observer-measured health indictors are not always consistent with findings from studies using self-reported health outcomes; generally, studies using self-reported measures have reported a stronger association between parity and health than studies using biomarkers. We build on this past research and analyze associations between fertility histories and several biomarkers of cardiometabolic and respiratory function. These markers are related to health behaviors and experiences of cumulated stress (Dariotis et al.
2011; Umberson et al.
2010) and thus are plausibly linked to social control of behaviors and provision of social support mechanisms hypothesized to underlie linkages between fertility history and health. We thus aim to contribute to elucidating the mechanisms underlying associations between fertility histories and later health.
Discussion
Previous studies have reported that both nulliparous and high-parity women (and in some studies, men) have higher risks of mortality and morbidity than parents of two or three children. In our study, indicators of cardiometabolic risk among high-parity women tended to be raised, but associations were attenuated once we controlled for a wide range of variables relating to early-life socioeconomic background, childhood physical and mental health and cognitive ability, and adult socioeconomic characteristics. However, even in the fully adjusted model, high-parity was significantly associated with high WHR and metabolic syndrome among women and with raised glycated hemoglobin among both men and women with four or more children (and remained so in analyses applying the Bonferroni correction). These findings are consistent with studies that reported an association between higher parity and obesity and glycated hemoglobin and stronger associations between higher parity and these cardiometabolic risk factors among women compared with men (Lawlor et al.
2003). We were not able, however, to formally test whether sex differences in the strength of these associations were statistically significant. Possible reasons for a differential effect on women and men might be related to changes experienced in pregnancy and also greater effects of child-rearing on the eating and physical activity patterns of mothers compared with fathers. However, this would need to be examined in a different study. Perhaps, gender differences in associations between family-building and obesity become more evident in later middle age. Hardy et al. (
2007), in a study that extended to age 53, found that the difference in BMI between men without children and men with at least one child changed with increasing age with a faster increase in BMI among fathers. We included a much wider range of controls for earlier life circumstances than previous studies, thus reducing the chance that these results reflect confounding by circumstances prior to family building. Even so, some caution is needed in interpreting these results because in our robustness check analyses using negative controls, we also found an association between high parity and arm from which the blood sample was taken among women. Given that there is no conceivable mechanism that could link these variables, there may be some underlying source of bias. We found no indicators of adverse biomarker measures for the nulliparous other than some suggestion of a worse FEV1/FVC score for childless men (significant only at 10% level), which is consistent with previous studies showing worse health from smoking-related diseases in this group.
Our finding that associations between parity and the biomarkers considered were rather weaker than might have been expected from some other studies may have resulted from our controlling for a much wider range of contemporaneously collected childhood factors, including some (e.g., cognitive ability and mental health) that cannot be reliably assessed retrospectively (Jivraj et al.
2017), in addition to educational level, experience of unemployment, reported teenage smoking, and indicators of adult partnership history. However, results (reported in the
online appendix) from analyses using a reduced set of covariates, similar to those included in other studies with more limited information, were very close to those from the fully adjusted models. This does not mean that the additional covariates we included are unimportant. Several, such as birth weight and physical coordination problems at age 11, were consistently associated with the biomarker outcomes considered (
online appendix, Table A
5). However, in other studies lacking such information, the effect of these factors may be indirectly captured via intermediary or associated covariates included.
Contextual influences may also be important. Those born in the United Kingdom in 1958 have had access to modern methods of birth control throughout their reproductive life: oral contraceptives became available in 1961, and abortion was legalized in 1967. Results from the 1976 Family Formation Survey (Dunnell
1979) showed a large increase between the mid-1960s and the mid-1970s in the proportion of higher-order births reported as planned, and it seems reasonable to assume that this proportion has subsequently increased further. Other studies that focused on earlier-born cohorts may have included a larger proportion of high-parity parents who had not made an active choice to have a large family. These parents might have experienced greater stress than the small group of high-parity parents considered here as suggested by evidence of long-term effects of unintended births on mental health (Herd et al.
2016). Age at point of observation may in itself be relevant when comparing our findings with those of other studies. Possibly some health-related sequelae of parity become evident only in later-middle or older age.
Our findings on associations between age at childbearing and biomarkers indicative of respiratory and cardiometabolic risk are more consistent with previous research. Overall results suggest an inverse relationship between age at first birth and biomarkers indicative of poorer health, including those associated with inflammation and obesity; outcomes were worse for those who had become parents at an early age compared with those who postponed entry to parenthood. Among women with two or more children, having had the last one before age 25 was also associated with some negative health indicators. In general, associations appear greater for women than for men, which is consistent with the general impact of parenthood on women’s activities and roles, although as we already noted, we were not able to formally test for gender difference. A small adverse association between late age at last motherhood (40 or older) and WHR was also observed; however, this may reflect the short interval between the last birth and the collection of the biomarker data, which may not have given some women sufficient time to return to their prepregnancy body weight.
Given the wide range of controls included in the analyses, these results are supportive of the hypothesis that stressors associated with early parenthood may have long-term health consequences. Results are partly consistent with the small literature on fertility history and biomarkers. For example, Grundy and Read (
2015) found a negative association between age at first birth and higher (worse) allostatic load, with the relationship being mediated in part by wealth, physical activity, and smoking; Lacey et al. (
2017) found that becoming a parent before age 20 was associated with an adverse cardiovascular profile by midlife for both men and women.
Strengths of this study include the availability of a large population-based and representative prospective study, the wealth of information on potential confounders gathered contemporaneously rather than retrospectively, and the availability of midlife biomarker data enabling us to use observer-measured indicators of health rather than relying on self-reported measures that may be influenced by health expectations and morale. Additionally, biomarker data provide some information on possible underlying mechanisms that may lead to poor health.
To explore differences that may arise using biomarkers rather than self-reported measures, we estimated models using self-rated health at the time of biomedical sweep as the outcome (see the
online appendix for results). For women, associations among number of children, age at first/last birth, and poor or fair self-rated health were broadly consistent with those observed using biomarkers. Among men, however, there were some differences. For example, age at entry to fatherhood was associated with hemoglobin, obesity, and metabolic syndrome but not with fair/poor self-rated health. This may indicate that some men are not aware of, or are unwilling to report, conditions associated with poorer health outcomes and perhaps do not consider being overweight or obese as indicative of health status. This is something that merits further investigation.
We can identify five limitations of this study. First, a large proportion of data were missing because of attrition. We took account of this by using multiple imputation with chained equations (see the
online appendix). We additionally performed the same set of analyses on the complete case sample (reported in the
online appendix). These models produced broadly similar results in terms of point estimates, but fewer reached conventional levels of statistical significance, reflecting the much smaller sample size. Aside from the lack of power, some differences in the value of point estimates from models based on multiply imputed data and those from complete case analysis are expected because in this instance missing data can be found in the independent control variables as well as the outcome. In such instances, complete case analysis is biased (Hughes et al.
2019). Second, selection into fertility pathways is an important factor to consider, and even though we were able to include in the analysis many confounders related to childhood health and early-life conditions, it is still possible that some unobserved variables might explain the associations we found. To address this issue, we used negative controls, a technique designed to detect possible sources of spurious causal inference. We found no association between fertility histories and negative controls as expected except that (as mentioned earlier) women who had four or more children were less likely to have their blood taken from their left arm, possibly suggesting that the relationship between parity and biomarkers is partly due to confounding and/or measurement error. Third, we could not fully tackle issues of reverse causation. Particular fertility patterns may be the outcome of health problems; for example, poor health may delay fertility or decrease chances of parity progression. We included a large range of control variables capturing health in childhood and adolescence but had no specific information on fecundity. Because we did not include measures of health in adulthood, measures in this design would be mediators and not proper confounders. A fourth limitation is that although we hypothesized that earlier parenthood may have adverse implications for later-health because of the effects of cumulated stress, we do not have any measures of this collected at the time. This would be a fruitful area for further research using data from younger cohorts. Finally, the respondents in our sample were only 45 years old when the NCDS biomedical sweep was conducted. Thus, some of them (especially men) might not have yet completed their fertility, and associations between fertility history and health indicators may vary by age.
Our aim in this study was to investigate associations between fertility patterns and biomarkers indicative of cardiometabolic health in midlife, controlling for a wide range of potential confounders from earlier in life. Unlike several previous studies (e.g., Henretta
2007), we deliberately did not include in our analysis variables from later in the life course—such as other health indicators in midlife—that might be either confounders or mediators of associations with biomarkers. Examining these later pathways more thoroughly would be a fruitful line for further enquiry.
We conducted multiple tests and from a conventional null hypothesis significance testing perspective, this increases the probability of type I error. Therefore, we further evaluated our findings with the conservative Bonferroni correction, setting the significance cutoff at α /
n = .05 / 9 = .0055, also reported in the
online appendix. Even with this conservative correction, we found associations among age at first birth, cholesterol, obesity, and WHR in women. Going beyond conventional levels of statistical significance, evaluation of the pattern of associations, the magnitude of the point estimates, and pattern of
p values points to an association between age at first birth and various biomarkers.
Results from this analysis help shed some light on the association between fertility and health and identify groups in the population that are more at-risk of health issues later in life. In particular, our findings support previous findings suggesting potential negative consequences of very early ages at first birth, which emphasizes the need for continuing policy attention to the sexual and reproductive health of young adults and the support of young parents.
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