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Child spacing effects on infant and child mortality

2 Literature Review

2.3. Child spacing effects on infant and child mortality

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Also, by 2015, the global partnership goals evolved into the Sustainable Development Goals (SDGs), where child mortality became an indicator instead of a goal on itself. The now renewed target plans to reduce neonatal mortality to 12 per 1,000 live births and under-5 mortality to 25 per 1,000 live births by 2030 (United Nations, 2015b).

In 2017, children 0 to 5 years old died in the same proportions –5.4 million– as older age groups did: 5 million of the 65-69 years old group, 5.3 million from the 70-74 years old group or the 85-89 years old group with 5.3 million deaths (Institute for Health Metrics and Evaluation, 2018). These facts along with the failure to reduce the original millennium goal, the new multiple goals reflected on the SDGs and the downgrading of child mortality from a pressing issue to yet another indicator, places more uncertainty on the effective achievement of this target in the foreseeable future.

2.3. Child spacing effects on infant and child mortality

The spacing of births has a long-documented association with infant and child mortality outcomes, in fact, the earliest studies date of almost a century ago and already present the notions of the deleterious effect of shorter birth spacing and optimal interbirth intervals (Stevenson (1923) and Hughes (1923) as cited in Hobcraft, McDonald &

Rutstein (1983)). The research on this effect has been approached from different disciplines, such as population studies, medicine, sociology and economics, to name a few. Nonetheless, it has moved to mainstream knowledge as a result of international organizations endorsing this proposal as a policy recommendation.

Particularly, the World Health Organization (WHO) has expressly suggested waiting at least 24 months after a live birth to attempt another pregnancy, that is, an interbirth interval of 33 months or roughly 3 years. The recommendation pursues the objective of reducing the risk of adverse maternal, perinatal and infant outcomes (World Health Organization, 2007). Experts that participated on that 2005’s technical consultation agreed on the notion of an the deleterious effect of short intervals, and concluded the following: (1) birth-to-pregnancy intervals of six months or shorter had a higher associated risk of maternal mortality; and (2) birth-to-pregnancy intervals shorter than 18 months had a greater risk of infant, neonatal and perinatal mortality, lower weight at birth, being smaller for gestational age, and pre-term delivery (World Health Organization, 2007).

Multidisciplinary studies have attempted, for almost a century, to provide evidence on this long-running seemingly strong negative relationship. Although, the

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exploration of formal channels or mechanism by which child spacing can have deleterious effect on maternal and child health and survival started in the mid-1960s. In spite of the multiple causal mechanism assessed over the years, the literature usually coincides in three main mechanism for the “short intervals-infant mortality” relationship: a) maternal depletion syndrome, b) sibling competition and c) insufficient breastfeeding (Conde-Agudelo, et al., 2012). Most of the studies also include confounding factors, that if controlled, can isolate the effect of child spacing. Some of these factors include socioeconomic conditions and previous birth outcomes, to name a few.

2.3.1. Causal mechanism of effects of spacing in infant mortality a) Maternal depletion syndrome

This mechanism was first discussed by Jelliffe and Maddocks in 1964, although, their early proposal did not include child spacing. The authors introduced the notion that women who are in a continuous cycle of reproduction, synthesizing fetal and placental protein and producing breast milk non-stop, might affect the weight of their children and her health status (Jelliffe & Maddocks, 1964). When including child spacing, a mother with constant pregnancies and short birth intervals does not get the chance to recover and replenish her nutritional values, therefore increasing the odds of pregnancy losses and having low birth weight children (Hobcraft, et al., 1983).

Among some of the representations of maternal depletion that affect mother’s and child health outcomes are the exhaustion of energy and protein resulting from short interpregnancy intervals (King, 2003) and the risk of folate insufficiency, which parallelly, impacts their children’s hazard of neural tube defects, retarded intrauterine growth, and preterm birth (Smits & Esseds, 2001). DaVanzo, et al. (2008) found that the survival outcome of the pregnancy amplifies the maternal depletion syndrome, that is, live births or stillbirths are more depleting than miscarriages or abortions. Additionally, live births are usually followed by periods of breastfeeding which further depletes maternal physiological and nutritional stores.

Children with low weight at birth have a greater risk of mortality than those with an average normal weight and the group differences are accentuated for those with socioeconomic disadvantages (McCormick, 1985). Regardless of technological improvements and increased use of modern medical methods, the change in survival for very low birth weight –those who weighed less than 1500g at birth– had barely improved between 1990 and 2002 (Fanaroff, et al., 2007). The situation worsens for developing

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countries. Children severely growth-restricted and those who were born preterm are at higher risk of perinatal death, primarily of complications that in are not fatal in developed countries, but which care access is limited and difficult for developing countries (Kramer

& Victora, 2001). Since women that already have inadequate food intake and are unable to adjust their energy expenditure to lower levels are the most likely to suffer from maternal depletion (Conde-Agudelo, et al., 2012), low-income mothers are more vulnerable to be affected by this mechanism.

b) Sibling competition

Another potential mechanism whereby a short or long interval may decrease the odds of survival is for the children in the family is sibling competition. This occurs in two instances: on one hand, when two or more children, are closely spaced, they will grow up close in ages which may lead them to compete for family scarce economic resources and parental care (Conde-Agudelo, et al., 2012); on the other hand, when children are spaced longer, older siblings may take precedence in taking the limited available food supplies or resources of the family (Hobcraft, et al., 1983).

This mechanism is usually tested by including the survival status of the preceding child or the index child and the preceding or subsequent interval. Nevertheless, caution is advised when assessing the survival of the preceding sibling and its impact on the length of the interpregnancy interval. If the precedent child dies in infancy, the interval to the next birth could be shortened by an involuntary cessation of breastfeeding and temporal infertility associated with lactational amenorrhea and/or the mother’s grief (Sweemer, 1984) and desire to replace the deceased child (Conde-Agudelo, et al., 2012). Thus, providing evidence on this effect has been a challenge, both theoretically and empirically, since arguably this effect is prompt to be harsher in poor families in developing countries in contrast with middle- and high- income households.

c) Breastfeeding-pregnancy overlap

This effect is also depicted as a type of competition among the precedent child and the new shortly spaced pregnancy. The new pregnancy induces earlier weaning on the precedent child, with consequent deleterious effects on his survival (Hobcraft, et al., 1983). Additionally, when breastfeeding–pregnancy overlap, the intakes per feeding are lower and the weight gain associated with breastfeeding nurture decreases in the corresponding for one month (Marquis, et al., 2002). Another possible effect of the overlapping breastfeeding and pregnancy is change in the composition of breast milk,

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particularly affecting immunity nutrients on it, such as lysozyme concentration, lactoferrin concentration and Immunoglobulin A (Marquis, et al., 2003).

Interestingly, the breastfeeding-pregnancy overlap and the short interval can be related in two ways that lead to the detrimental effect on the survival of children. For instance, the short interval can lead to early weaning and lower quality breast milk, which affects the survival odds of the preceding child; and on the other hand, the maternal decision on the length of breastfeeding also affects the birth interval through lactational amenorrhea inducing effects on mortality of both the preceding and subsequent child.

d) Alternative mechanisms

The mechanisms described above are among the most commonly used to support the detrimental effects of child spacing and child mortality. Nonetheless, these are far from being the only possible channels of impact in the odds of survival. Many studies opt for controlling for socioeconomic variables or confounding factors, such as income, which is a determinant of nutritional intake for the family; parents’ education, particularly mother’s, as it represents maternal use of contraception, awareness of child care, and so forth (Sweemer, 1984; Hobcraft, et al., 1983; Boerma & Bicego, 1992; Forste, 1994;

DaVanzo, et al., 2008).

There’s a gap in the literature that should be addressed more, which is interpregnancy intervals and whether they change according to the outcome of the preceding pregnancy, i.e. whether it resulted on live birth, stillbirth, miscarriage, or induced abortion (DaVanzo, et al., 2008). These outcomes are key to properly identifying the dimension of the mechanism described above. For instance, non-live outcomes should be less depleting that a full-term live pregnancy that is followed by breastfeeding, also if the pregnancy outcome is not a live birth, there’s no immediate sibling to compete or to overlap breastfeeding and pregnancy with.

Lastly, there are some more difficult to measure the mechanism of impact such as the psychological and emotional drain of mothers responsible for caring of a large family with scarce resources. These mental and emotional health effects or quality-of-life effects caused by larger families and shorter intervals are not measured nor included but maybe impacting maternal physical and psychological reserves (Winikoff, 1987).

2.3.2. Empirical evidence of the mechanisms in the literature

Previously it’s been indicated research that has pioneered hypothesizing and/or proving the causal mechanism that leads short or very long intervals to result in child

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mortality. In this subsection, research that provides evidence or questions the existence of such mechanisms is summarized.

In regards to the maternal depletion syndrome mechanism, the effects of intervals in child mortality are greater for the shortest intervals, which are the ones that give the littlest time for mother’s recovery (DaVanzo, et al., 2008; Rutstein, 2005; Sweemer, 1984); while King (2003) confirms that depletion syndrome through the analysis of deficiencies in micronutrients, iron and folate in closely spaced pregnancies, which are at high risk of mortality, lastly, Boerma and Bicego (1992) provide evidence of both, maternal depletion and breastfeeding-pregnancy overlap causal mechanism, of how shortly spaced births affect mother's physiology and nutritional status, which in turn impacts the odds of child survival.

Regardless, other empirical studies have not found evidence for maternal depletion syndrome or inconsistent proof. For instance, Dewey (2007) found that longer birth intervals are associated with lower child malnutrition in some populations analyzed, but not all of them. She also found little evidence of the inverse relationship, shorter intervals with higher child nutrition, which remarks about the lack of statistical significance of this relationship. Winkvist, et al. (1994) propose that how the nutrients get assigned to mothers or children is affected primarily by the mother’s nutritional status rather than the child spacing. In this case, the authors suggest than endorsing longer intervals is not effective enough, and that a better approach is to support nutrition for women at all stages of her reproductive cycle.

As for the sibling competition hypothesis, DaVanzo, et al. (2008) and Sweemer (1984) found supporting evidence of this effect. Particularly the former found for the post-neonatal period and childhood, the detrimental effects of close spacing are greater if the preceding child is still alive at the time of the subsequent child’s birth –giving them room to compete for family resources– than if the preceding had died.

On the contrary, Boerma and Bicego (1992) controlled for survival status of the preceding child and found that it does not reflect on increasing the effects of close spacing on mortality when the previous child is still alive, i.e. a supposed ‘competition’

environment. Therefore, they conclude that the sibling competition mechanism is not evidenced nor operative at all, but rather that the effects of familiar mortality risks are stronger than the competition mechanism. Thus, prenatal mechanisms are more relevant than postnatal ones, when explaining the causal nature of the child spacing effects on child mortality.

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For the breastfeeding-pregnancy overlap, most studies argue for an effect of early cessation of breastfeeding, weaning, as a result of a closely spaced conception (Hobcraft, et al.,1983, Sweemer, 1984; Forste, 1994; DaVanzo, et al., 2008). Despite medical literature assessing the impact in breast milk nutrients and child weight, there’s little direct evidence of these quality effects affecting child mortality through a shorter birth interval (Marquis, et al., 2002; Marquis, et al., 2003).

Research that aims to untangle the relationship between child spacing and child mortality is very broad, expands through disciplines and deals with complex multilateral relationships between variables and mechanisms. Experts fail to agree on the existence of certain effects and channels, as the discussion grows into different realities. In fact, human fertility is subject to many unmeasurable variables –culture, religiousness– and fundamental differences –developed and developing countries, health care systems– than unanimity upon the subject is not expected.

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