Maternal Depletion Research Articles

Changes in body fat distribution in relation to parity in American women: A covert form of maternal depletion

Using data from the Third National Health and Nutrition Examination Survey (NHANES III), conducted from 1988-1994, we investigated the effect of reproduction on the distribution of body fat in well-nourished American women. While women tend to gain weight and fat with succeeding pregnancies, if age and body mass index are controlled, increasing parity is associated with a decrease in hip and thigh circumferences, suprailiac and thigh skinfolds, and body fat estimated from skinfolds, while waist circumference increases, resulting in a relative decrease in lower-body fat. The mobilization of fat stores in the lower body during late pregnancy and lactation may help to meet the special needs of the developing brain for essential fatty acids and energy during the time of peak growth. When fat is regained after the postpartum period, relatively more is stored in central vs. peripheral depots, resulting in a patterned change in body shape with parity.

Effects of a reduction in maternal renal mass on pregnancy and cardiovascular and renal function of the pregnant ewe

Maternal renal disease is associated with high maternal and fetal morbidity. To establish an animal model to study renal dysfunction in pregnancy and its potential role in programming for renal disease and hypertension in adult life, a kidney was removed from each of 16 nonpregnant ewes, and a branch of the renal artery of the remaining kidney was ligated (STNx ewes). The 16 STNx and 15 intact ewes were time mated 2.5-17 mo later and studied at 119-132 days of gestation. STNx ewes demonstrated renal hypertrophy and glomerular hyperfiltration. They had higher diastolic arterial pressures (P < 0.05) and larger left ventricles (P < 0.0005), drank more water (P < 0.01), were hypochloremic (P < 0.01) and hyperglycemic (P < 0.0005), and had higher plasma creatinine levels (P < 0.0005) than intact ewes. Effective renal plasma flows and glomerular filtration rates were lower (P < 0.01) and protein excretion was greater (P < 0.05) in STNx than in intact ewes. Glomerulotubular balance was impaired in STNx ewes. Proximal tubular Na(+) reabsorption was reduced (P < 0.05), so Na(+) excretion was increased (P < 0.05). In STNx ewes, filtered K(+) loads were reduced (P < 0.005), but K(+) excretion was the same as in intact ewes. There was net K(+) secretion in STNx ewes; in intact ewes, there was net reabsorption. Plasma renin and angiotensinogen concentrations in STNx and intact ewes were similar, so the hypertension in STNx ewes was not renin dependent. STNx fetuses grew normally, and their blood gases, blood pressure, and heart rates were normal. These alterations in maternal fluid and electrolyte balance and the potential risk of maternal salt depletion or hyperkalemia may adversely affect the fetus.

SOX7 is an immediate-early target of VegT and regulates Nodal-related gene expression in Xenopus

In zebrafish, the divergent F-type SOX casanova acts downstream of Nodal signaling to specify endoderm. While no casanova orthologs have been identified in tetrapods, the F-type SOX, SOX7, is supplied maternally in Xenopus (Fawcett and Klymkowsky, 2004. GER 4, 29). Subsequent RT-PCR and section-based in situ hybridization analyses indicate that SOX7 mRNA is localized to the vegetal region of the blastula-stage embryo. Overexpression and maternal depletion studies reveal that the T-box transcription factor VegT, which initiates mesoendodermal differentiation, directly regulates SOX7 expression. SOX7, but not SOX17 (another F-type SOX), binds to sites within the Xnr5 promoter and SOX7, but not SOX17, induces expression of the Nodal-related genes Xnr1, Xnr2, Xnr4, Xnr5, and Xnr6, the homeodomain transcription factor Mixer, and the endodermal marker SOX17β; both SOX7 and SOX17 induce expression of the pan-endodermal marker endodermin. SOX7's induction of Xnr expression in animal caps is independent of Mixer and Nodal signaling. In animal caps, VegT's ability to induce Mixer and Edd appears to depend upon SOX7 activity. Whole embryo experiments suggests that vegetal factors partially compensate for the absence of SOX7. Based on the antagonistic effects of SOX7 and SOX3 (Zhang et al., 2004. Dev. Biol. 273, 23) and their common binding sites in the Xnr5 promoter, we propose a model in which competitive interactions between these two proteins are involved in refining the domain of endodermal differentiation.

Association between short birth intervals and schizophrenia in the offspring

Pregnancy burdens maternal folate reserves. Postpartum restoration to normal folate values may take up to 1 year. Maternal folate deficiency during early pregnancy has been hypothesized as a cause of schizophrenia in the offspring. We investigated whether the risk of schizophrenia is increased in persons conceived shortly after another birth. A population-based cohort was established of 1.43 million persons born in Denmark between 1950 and 1983, yielding 17.6 million person-years of follow-up. Schizophrenia in cohort members (5095 cases) and their siblings and parents was identified by linkage with the Danish Psychiatric Case Register. Relative risks of schizophrenia were estimated by use of log-linear Poisson regression. As compared to intervals of 45 months and longer, the schizophrenia risk ratio was 1.14 (95% confidence interval [CI], 0.97 to 1.35) for interbirth intervals of up to 15 months, 1.32 (95% CI, 1.12 to 1.56) for intervals of 15 to 17 months, 1.38 (95% CI, 1.18 to 1.61), for intervals of 18 to 20 months and 1.13 (95% CI, 1.00 to 1.29) for intervals of 21 to 26 months. Relative risks did not essentially change after adjustment for age, sex, calendar year of diagnosis, maternal and paternal age, history of mental illness in a parent or sibling, sibship size, place of birth, and distance to younger sibling. These results show an association between short birth intervals and schizophrenia in the offspring. Although maternal folate depletion may play a role in this association, we cannot rule out other explanations such as maternal stress during pregnancy and childhood infections.

The maternal depletion transition in northern Kenya: the effects of settlement, development and disparity

Maternal depletion syndrome, defined as a broad pattern of maternal malnutrition resulting from the combined effects of dietary inadequacy, heavy workloads, and energetic costs of repeated rounds of reproduction, has been determined to be an important predictor of maternal and child health. Debates regarding the existence of maternal depletion syndrome have centred on the inability to identify a single universal pattern of parity-related depletion. However, it is becoming increasingly apparent that patterns of depletion may be linked to overall dietary adequacy and conditioned by socioeconomic development. Therefore, variable patterns of maternal depletion are useful for examining changing patterns of women's nutrition in the process of development. This study examines the nutritional status and dietary intakes of 912 Rendille women in one nomadic and four settled communities in northern Kenya, and tests the assertion that settlement of former nomadic pastoralists results in improved diet and nutrition. Both long-term and short-term reproduction-related changes in BMI, triceps skin fold and upper arm muscle area are examined in relation to parity, age, and socioeconomic factors. Overall community comparisons reveal improvements in dietary adequacy and nutritional status only among women residing in the District capitol, Marsabit. Women in small settlements and the nomadic community, by contrast, display patterns of long-term chronic energy deficiency that obscure short-term reproduction-related energy costs. In addition, data reveal that economic disparity increases in the process of settlement and development and that low socioeconomic status negatively influences dietary intake and nutritional well being. The findings highlight the importance of examining variation within and between communities for understanding the complex nature of the maternal depletion transition.

The Risk of Maternal Nutritional Depletion and Poor Outcomes Increases in Early or Closely Spaced Pregnancies

An adequate supply of nutrients is probably the single most important environmental factor affecting pregnancy outcome. Women with early or closely spaced pregnancies are at increased risk of entering a reproductive cycle with reduced reserves. Maternal nutrient depletion may contribute to the increased incidence of preterm births and fetal growth retardation among these women as well as the increased risk of maternal mortality and morbidity. In the past, it was assumed that the fetus functioned as a parasite and withdrew its nutritional needs from maternal tissues. Studies in both animals and humans demonstrate, however, that if the maternal nutrient supply is inadequate, the delicate balance between maternal and fetal needs is disturbed and a state of biological competition exists. Furthermore, maternal nutritional status at conception influences how nutrients are partitioned between the mother and fetal dyad. In severe deficiencies maternal nutrition is given preference; in a marginal state the fetal compartment is favored. Although the studies of nutrient partitioning have focused on energy and protein, the partitioning of micronutrients may also be influenced by the maternal nutritional status. Marginal intakes of iron and folic acid during the reproductive period induce a poor maternal status for these nutrients during the interpregnancy interval. Poor iron and folic acid status has also been linked to preterm births and fetal growth retardation. Supplementation with food and micronutrients during the interpregnancy period may improve pregnancy outcomes and maternal health among women with early or closely spaced pregnancies.

Protective effect of N-acetylcysteine against fetal death and preterm labor induced by maternal inflammation

Objective: Intrauterine and maternal systemic infections are proposed causes of preterm labor. The resulting prematurity is associated with 75% of infant mortality and 50% of long-term neurologic handicaps. We hypothesize that free radicals generated in large quantities during an inflammatory response shift the fetomaternal redox balance to an oxidative state, compromising the fetus. Thus, if our working hypothesis is correct, selective inactivation of free radicals with N-acetylcysteine (NAC), an antioxidant and glutathione (GSH) precursor, would improve the outcome of preterm deliveries associated with inflammation. We tested aspects of this hypothesis in an animal model of preterm labor and fetal damage (death). Study Design: NAC (1 g/kg) was administered orally to C57Bl/6 mice injected intraperitoneally with either 10 μg lipopolysaccharide (LPS) or saline solution (CRL) on day 16 of gestation. The latency period (time from injection to delivery of the first pup) and fetal viability were recorded. To discriminate between an effect of prematurity from an effect of inflammation, and to document any improvement in survival, mice were killed at 3, 6, and 16 hours after injection. Maternal and fetal redox states were approximated by measuring hepatic GSH. Results: Each C57Bl/6 LPS-treated mouse delivered prematurely after a significantly shorter latency period (LPS: 16.8 hours [95% CI 15.9-17.6] vs CRL: 54.7 hours [95% CI 43.8-65.5]). NAC doubled the latency interval of LPS-treated animals to 35.2 hours (95% CI 21.0-49.2). LPS alone resulted in a 100% rate of stillbirth. Fifty-eight percent of fetuses were already dead 16 hours after LPS. In contrast, only 33% of fetuses were dead 16 hours after LPS (P = .001) when NAC was given. LPS was followed by a reduction in maternal (LPS: 26.3 nmol/mg [95% CI 19.9-32.8] vs CRL: 41.3 nmol/mg [95% CI 34.7-47.9, P < .01]) and fetal GSH (LPS: 19.7 nmol/mg [95% CI 11.7-27.8] vs CRL: 34.5 nmol/mg [95% CI 32.0-37.0, P < .001]). This decline was reversed by NAC (NAC/LPS maternal GSH: 37.0 nmol/mg [95% CI 22.5-51.5] and fetal GSH: 28.4 nmol/mg [95% CI 22.8-33.9]). Importantly, maternal liver GSH impacted on fetal survival. NAC/LPS mothers with living pups 16 hours after LPS had significantly higher liver GSH compared with NAC/LPS mothers whose pups died in utero. In fact, all NAC-treated mice whose hepatic GSH exceeded 20 nmol/mg had living fetuses at 16 hours. Conclusion: Maternal inflammation in C57Bl/6 mice results in oxidative stress associated with maternal and fetal GSH depletion. Oxidative stress damages the fetus independent of prematurity. Restoration of maternal and fetal oxidative balance by NAC protects the fetus and reduces the rate of preterm birth. (Am J Obstet Gynecol 2003;188:·203-8.)

Somatic versus reproductive energy allocation in Papua New Guinea: life history theory and public health policy.

A fundamental evolutionary problem faced by organisms is how to allocate energy to somatic and reproductive functions in ways that optimize fitness. Given that energy is limited in all environments, energy allocation necessarily involves physiological tradeoffs between such factors as growth and reproduction, reproduction and condition, and current reproduction and future survival. Ultimately, the "decisions" that are made about energy allocation among growth, survival, and reproduction determine life history patterns and trajectories of organisms. For humans, knowing how energy allocation to reproduction will likely impact other aspects of the somatic well-being of individuals may also have practical implications for public health policy. This article reviews the evidence for energy tradeoffs between somatic and reproductive functioning in a range of human societies. It also seeks to corroborate the results of earlier work in Papua New Guinea on lactation-related maternal energy depletion using an independent measure of maternal energy reserves, tetrapolar bioelectrical impedance analysis. The current analysis shows that maternal energy reserves decline over the course of lactation and that a cumulative parity-specific decline in maternal energy reserves also exists. A longitudinal follow-up of five women over 11 years shows the decline to amount to about 3 mm of subcutaneous fat per round of pregnancy and lactation. The results corroborate predictions from life history theory and have applied public health implications. In particular, It is suggested that policies such as lactation advocacy that encourage enhanced energy allocation to reproduction in order to promote child health may have the unintended result of compromising maternal well-being, particularly in nations of the developing world. Consequently, it is recommended that nutritional support of mothers be implemented in concert with lactation promotion.

Non-Invasive Fetal Sex Determination on Fetal Erythroblasts from the Maternal Circulation Using Fluorescence in situ Hybridisation

Objective: The main purpose of this study was to evaluate the potential of a non-invasive method for fetal sex determination in clinical practice using dual-colour fluorescence in situ hybridisation (FISH) analysis. We evaluated the differences in nucleated red blood cell (NRBC) recovery from the maternal circulation using various slide preparation procedures following high-gradient magnetic cell separation (double MACS). Methods: NRBCs were enriched from peripheral blood mononuclear cells of 63 pregnant women between 12 and 37 weeks of gestation by double MACS involving simultaneous CD14+ and CD45+ maternal cell depletion and CD71+ fetal cell enrichment. Isolated cells were analysed by dual-colour FISH with X- and Y-specific probes. Before applying the FISH technique, cells were treated using three different protocols. Cells were either fixed in methanol:acetic acid (3:1) and dropped immediately onto glass slides (protocol 1) or treated with 75 mM KCl before resuspension in fixative (protocol 2). Alternatively, isolated cells were transferred onto glass slides and then treated using a method described in the literature (protocol 3). Results: Using various slide preparation procedures, fixed cell numbers as well as the quality of slides differed significantly. Using protocol 1, fetal sex was well determined in 30 cases, in 15 out of 17 male fetuses (1–13, mean 3 fetal cells were found among 5–164, mean 50 maternal cells) and in 15 female fetuses (7–178, mean 56 fixed cells). On the other hand, interpretation difficulties occurred in 7 out of 8 studied cases using protocol 2 due to a lack of cells or damage to the isolated cells. The highest recovery of fixed cells was achieved using protocol 3 (27–411, mean 186); fetal cells positive for the Y signal (2–12, mean 6) were detectable in all studied cases (n = 16). In 7 of the samples from women carrying female fetuses, we could only detect cells with two X signals (51–182, mean 103). All of the experiments were interpretable due to the presence of compact cells with well-visible red and green signals. Conclusion: Our study revealed that using protocol 3 as the post-MACS treatment results in improved NRBC recovery and enables a reliable prospective non-invasive fetal sex determination.

Demographic consequences of unpredictability in fertility outcomes

Child survival is probabilistic, but the unpredictability in family formation and completed family size has been neglected in the fertility literature. In many societies, ending the family cycle with too few or too many surviving offspring entails serious social, economic, or fitness consequences. A model of risk- (or variance-) sensitive adaptive behavior that addresses long-term fertility outcomes is presented. The model shows that under conditions likely to be common, optimal, risk-sensitive reproductive strategies deviate systematically from the completed family size that would be expected if reproductive outcome is were predictable. This is termed the "variance compensation hypothesis." Variance compensation may be either positive or negative, resulting in augmented or diminished fertility. Which outcome obtained is a function of identifiable social, economic, and environmental factors. Through its effect on fertility behavior, variance compensation has a direct bearing on birth spacing and completed fertility, and thereby on problems in demography and human population biology ranging from demographic transitions to maternal depletion and child health. Risk-sensitive models will be a necessary component of a general theory of fertility.

Study of maternal influences on fetal iron status at term using cord blood transferrin receptors

AIMSTo determine effects of maternal iron depletion and smoking on iron status of term babies using serum transferrin receptors (STfR) and their ratio to ferritin (TfR-F index) in cord blood.METHODSIron,...

Birth intervals and early childhood mortality in a migrating Mennonite community

This study explores the significance of birth spacing with regard to neonatal postneonatal and early childhood mortality among rural Mennonites belonging to one congregation in Russia and one in Kansas. Analysis is based on the two causal mechanisms: maternal depletion and sibling competition. Respondents comprised a total of 930 and 1484 births in Russia and Kansas respectively by 381 mothers obtained from the vital events of families reconstructed from church records. In general the multivariate analyses are consistent with the bivariate analyses and further clarify the interrelationships that 1) the subsequent interval seems to explain more of the variance than the previous interval at least in most settings; 2) maternal age is the statistically significant covariate rather than birth order or parity. These and other observations may provide at least tentative support for the action of both mechanisms: maternal depletion and sibling competition (and disease). Other evidences were discussed extensively.

Interacting effects of nutrition and social class differentials on fertility and infant mortality in a pre-industrial population

Inadequate nutrition of both the mother and her offspring at each stage of its development - before pregnancy, in the womb, in infancy and during early childhood - played an important role in the patterns of subfertility and infant mortality in a saturated, marginal, preindustrial community. It is suggested that the three social classes had different diets but all were deficient in some essential constituents. Differences in nursing practices in the social groups contributed to differential exogenous mortality and to malnourishment and maternal depletion in the subsistence and (paradoxically) in the elite classes, producing an interacting web of effects and generating a vicious circle from which they could not escape for 150 years. Although the population apparently preferred daughters, the persistent generation effect of low birthweight girls bearing low birthweight daughters probably contributed to the steady-state conditions in this compromised community.

When Nomads Settle: The Effects of Commoditization, Nutritional Change, and Formal Education on Ariaal and Rendille Pastoralists

When Nomads Settle: The Effects of Commoditization, Nutritional Change, and Formal Education on Ariaal and Rendille Pastoralists

Maternal and Fetal Insulin-Like Growth Factor System and Embryonic Survival During Pregnancy in Rats: Interaction between Dietary Chromium and Diabetes

Chromium (Cr) depletion may exacerbate hyperglycemia and negative outcomes of pregnancy in the streptozotocin (STZ) diabetic pregnant rat model through the regulation of the insulin-like growth factor (IGF) system. To test this hypothesis, 40 female rats, all fed a low Cr diet (i.e., 70 μg Cr/kg diet ) from 21 d of age, were randomly assigned one of four treatments, applied on Day 1 of pregnancy, in a 2 × 2 factorial design: 1) very low Cr diet (40 μg Cr/kg diet) + citrate buffer injection, 2) very low Cr diet + STZ injection (30 mg STZ/kg body wt in citrate buffer), 3) adequate Cr diet (2 mg Cr [from added CrK(SO4)2]/kg diet) + citrate buffer injectionand 4) adequate Cr diet + STZ injection. Blood and tissues were collected on Day 20 of pregnancy. Chromium depletion increased (P < 0.05) urinary hydroxyproline excretion, 22-kDa IGF binding protein (IGFBP) concentration and litter size but decreased (P < 0.05) placental wt, percentage of protein per fetus, and fetal IGF-I and -II concentrations. Chromium had no effect (P > 0.10) on maternal hormones, 32-kDa IGFBP, glucose, or placental and fetal hydroxyproline concentrations. Diabetes decreased (P < 0.05) maternal wt gain, embryonic survival, litter size, mean pup wt and maternal insulin concentrations, increased (P < 0.05) maternal blood glucose, IGF-I concentrations and maternal hydroxyproline excretion but did not affect fetal concentrations of hormones, IGFBP, glucose or hydroxyproline. Interaction between chromium and diabetes tended (P < 0.10) to affect maternal IGF-II concentrations, but had no effect on other maternal or fetal variables. In conclusion, maternal chromium depletion did not exacerbate hyperglycemia or pregnancy outcome in STZ-induced diabetic rats, but may negatively affect fetal protein content by decreasing fetal IGF-II concentrations. Diabetes may negatively affect fetal growth through its effect on maternal glucose, insulin and IGF-I.

Linking maternal and infant benefits of a nutritional supplement during pregnancy and lactation

To evaluate the effect of a nutritional supplement on change in women’s weight during a reproductive cycle and on the difference in birth weight between one infant and the previous one, we analyzed data on 176 complete reproductive cycles from an experiment that was conducted in rural Guatemala. Women with an initial weight <50 kg were classified as marginally nourished or malnourished. Women whose intake of the supplement was in the top 2 tertiles were distinguished from those whose intake was in the lowest tertile. Linear regression modeling was used to estimate the effect of supplementation on these outcomes and to control for confounding factors. Malnourished women gained weight during the reproductive cycle, but their second (study) infant tended to weigh less at birth than their prior-born infant. Higher intakes of supplement were associated with a less negative difference in birth weight. Marginally nourished women lost weight during the reproductive cycle and their second (study) infant tended to weigh more at birth than their prior-born infant. Higher intakes of supplement were associated with a less negative weight [corrected] trend for the women themselves. Well-nourished women and their infants did not show any of these benefits from supplementation. These findings help explain past contradictory findings on maternal depletion as well as on the benefits of nutritional supplementation for mothers and their infants. Am J Clin Nutr 1998;68:656–61.

Effects of Breastfeeding on Maternal Health and Well-Being

Lactation occurs as part of a reproductive and may have different effects on maternal nutritional status, depending on its duration and intensity. Thus, its effect on maternal health will differ with cultural setting and level of development. Lactation helps women to maintain a healthy body weight. Among well-nour-shed women, it may help to prevent obesity. Among poorly pour/shed women, breastfeeding also leads to weight loss, but with adequate birth spacing brought about by lactational anovulation, maternal depletion can be avoided. Lactation is probably not responsible for osteoporosis. Current evidence suggests that breastfeeding helps to prevent pre-menopausal breast cancer and is not associated with post-menopausal disease Furthermore, breastfeeding may also help reduce ovarian cancer. Positive effects of breastfeeding occur at all levels of development and are most likely when biological, political, and sociocultural conditions interact to support its initiation and continuation.

Vitamin B-12 deficiency and malabsorption are highly prevalent in rural Mexican communities

Vitamin B-12 status of rural Mexicans was evaluated in two studies, 6 y apart. In the first, a single blood sample was collected from children and adults, including pregnant and lactating women. Prevalence of deficient plasma vitamin B-12 values ranged from 19% to 41% among groups, but plasma folate status was normal in all individuals. Breast milk vitamin B-12 concentration was low in 62% of samples. The second study was conducted in 219 children aged 18-36 mo in five communities, whose prevalence of deficient and low plasma vitamin B-12 concentrations, respectively, was 8% and 33% on entry, 3% and 22% 6 mo later, and 7% and 29% 12 mo later. Prevalence of low holotranscobalamin II concentrations, indicating malabsorption of the vitamin, averaged 18-40% across the three same periods. Both vitamin B-12 status indicators differed significantly between communities. The widespread vitamin B-12 deficiency was probably caused by malabsorption, perhaps exacerbated by low dietary intake and, for young children, maternal depletion of the vitamin.

A Hypothesis for the Origin and Evolution of Menopause

Menopause is widely believed by biological anthropologists and life history theorists to have arisen early in human evolution. In this paper, I suggest that female reproductive senescence was the result of the escalating energetic cost of gestation, lactation and childcare that accompanied the continuing encephalization of early hominid offspring and the ensuing increase in infant altriciality, or helplessness, and the concomitant prolongation of juvenile dependence. Natural selection favored females who became prematurely infertile, as the escalating cost of raising each offspring led to maternal depletion and made it more profitable in terms of lifetime reproductive success to continue investing in existing offspring rather than attempting late pregnancies. Results of a mathematical model are presented which show that reproductive senescence can be advantageous even when maximum potential lifespan is only 50 years, if the premature cessation of reproduction allows females to moderately increase the survival and fertility of their existing subadult offspring. These findings suggest that menopause could have originated as much as 1.5 million years ago, and that if menopause is indeed such an old trait, it was more likely the result of selective pressure on females to invest more in their own children, as opposed to their grandchildren.

A hypothesis for the origin and evolution of menopause.

Menopause is widely believed by biological anthropologists and life history theorists to have arisen early in human evolution. In this paper, I suggest that female reproductive senescence was the result of the escalating energetic cost of gestation, lactation and childcare that accompanied the continuing encephalization of early hominid offspring and the ensuing increase in infant altriciality, or helplessness, and the concomitant prolongation of juvenile dependence. Natural selection favored females who became prematurely infertile, as the escalating cost of raising each offspring led to maternal depletion and made it more profitable in terms of lifetime reproductive success to continue investing in existing offspring rather than attempting late pregnancies. Results of a mathematical model are presented which show that reproductive senescence can be advantageous even when maximum potential lifespan is only 50 years, if the premature cessation of reproduction allows females to moderately increase the survival and fertility of their existing subadult offspring. These findings suggest that menopause could have originated as much as 1.5 million years ago, and that if menopause is indeed such an old trait, it was more likely the result of selective pressure on females to invest more in their own children, as opposed to their grandchildren.