Number of Children and Telomere Length in Women: A Prospective, Longitudinal Evaluation

Abstract

Life history theory (LHT) predicts a trade-off between reproductive effort and the pace of biological aging. Energy invested in reproduction is not available for tissue maintenance, thus having more offspring is expected to lead to accelerated senescence. Studies conducted in a variety of non-human species are consistent with this LHT prediction. Here we investigate the relationship between the number of surviving children born to a woman and telomere length (TL, a marker of cellular aging) over 13 years in a group of 75 Kaqchikel Mayan women. Contrary to LHT’s prediction, women who had fewer children exhibited shorter TLs than those who had more children (p = 0.045) after controlling for TL at the onset of the 13-year study period. An “ultimate” explanation for this apparently protective effect of having more children may lay with human’s cooperative-breeding strategy. In a number of socio-economic and cultural contexts, having more chilren appears to be linked to an increase in social support for mothers (e.g., allomaternal care). Higher social support, has been argued to reduce the costs of further reproduction. Lower reproductive costs may make more metabolic energy available for tissue maintenance, resulting in a slower pace of cellular aging. At a “proximate” level, mechanisms involved may include the actions of the gonadal steroid estradiol, which increases dramatically during pregnancy. Estradiol is known to protect TL from the effects of oxidative stress as well as increase telomerase activity, an enzyme that maintains TL. Future research should explore the potential role of social support as well as that of estradiol and other potential biological pathways in the trade-offs between reproductive effort and the pace of cellular aging within and among human as well as in non-human populations.

Early-life stress and reproductive cost: A two-hit developmental model of accelerated aging?

“…The following empirical observations would seem consistent with this claim: (1) perinatal and childhood adversity plays an etiological role in the programming of late-life disease, resulting in increased morbidity and reduced longevity [2,12]; (2) increased fertility coincides with reduced longevity in birds and mammals [13], as well as in primates [14], although this association has not gone unchallenged in the human case [15][16][17]. From an evolutionary life-history perspective, organisms facing risks that could reduce their chances of surviving to reproductive age should, if possible, accelerate their development and thereby increase their prospects of passing on genes to future generations before becoming unable to do so due to an early death [7,18].…”

“…Thus, even though accelerated development may prove detrimental to health and even longevity in the longer term, such costs are regarded as ones which natural selection would discount, according to lifehistory theory, given the primacy placed on reproductive success [55,[58][59][60]. Consistent with such a life-history perspective is long-standing evidence that earlier timing of reproduction and shorter lifespans are related across taxa [61], including birds and mammals [13], as well as primates [14] and humans [62,63], although, as noted earlier, inconsistencies exist in the latter case [15][16][17]. Such data become especially noteworthy if the biological processes involved in linking reproduction and lifespan play a role in regulating developmental rate, reproduction and aging, which is exactly what we are predicting.…”

Leukocyte Telomere Length in Postmenopausal Women

“…There may be a protective effect from female hormones during pregnancy, or a higher level of social support in larger families. At least one study found longer LTL associated with having more children, and the authors suggested that levels of estradiol experienced during pregnancy might counter the adverse physiological effects anticipated to occur from multiple pregnancies (Barha et al, 2016). Recent research also proposes that social support may have a protective effect on LTL such that higher levels of social and spousal support are associated with longer LTL (Barger & Cribbet, 2016; Barha et al, 2016).…”

Child mortality, hypothalamic-pituitary-adrenal axis activity and cellular aging in mothers

“…Of the 94 women, 19 were excluded from our sample because critical demographic information was missing for 2013 (e.g., no information on parity or child mortality) [40]. These exclusions resulted in a sample size of 75 women.…”

“…Previously we showed that increased parity is associated with reduced telomere shortening in women in our study population [40]. To account for this effect of parity, we included total number of children born to a woman as a covariate in our model.…”