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In this chapter, I review recent evidence on the developmental origins of health inequality. I discuss the origins of the education-health gradient, the long-term costs caused by early life adversity, and how early life experiences affect the biology of the body. Additionally, I provide complementary evidence on enrichment interventions which can at least partially compensate for these gaps. I highlight emerging lines of scientific inquiry which are likely to have a significant impact on the field. I argue that, while the evidence that early life conditions have long-term effects is now uncontroversial, the literature needs to be expanded both in a theoretical and empirical direction. On the one hand, a model linking early life origins to ageing needs to be developed; on the other hand, a better understanding of the mechanisms – both biological and socioeconomic – is required, in order to design more effective interventions.

This study aims to empirically examine how the Khmer Rouge regime (1975–1979) in Cambodia continues to affect the health of the second generation.

The 2000 and 2005 Cambodia Demographic and Health Surveys were used in the analysis. The study sample were women with a child/children in 2000/2005. The sample population was identified according to whether the person was in utero “91 months or earlier before the Khmer Rouge regime,” “46–90 months before the Khmer Rouge regime” and “1–45 months before the Khmer Rouge regime” and during the Khmer Rouge regime. The authors then regressed the size of babies of the targeted population on the timing of the mothers being in utero.

Mothers who were in utero during the regime had a higher likelihood of giving birth to smaller-than-average babies. Additionally, mothers born in the areas that had a higher probability of death of children aged five or under during the regime were at risk of giving birth to smaller-than-average babies if they were in utero during that time.

This is the first paper to assess the impact of the Khmer Rouge regime on the health of the second generation.

We estimate the parental investment response to the child endowment at birth, by analysing the effect of child birth weight on the hours worked by the mother two years after birth. Mother’s working hours soon after child birth are a measure of investments in their children as a decrease (increase) in hours raises (lowers) her time investment in the child. The child birth endowment is endogenously determined in part by unobserved traits of parents, such as investments during pregnancy. We adopt an instrumental variables estimation. Our instrumental variables are measures of the father’s health endowment at birth, which drive child birth weight through genetic transmission but does not affect directly the mother’s postnatal investments, conditional on maternal and paternal human capital and prenatal investments. We find an inverted U-shape relationship between mothers worked hours and birth weight, suggesting that both low and extremely high child birth weight are associated with child health issues for which mothers compensate by reducing their labour supply. The mother’s compensating response to child birth weight seems slightly attenuated for second and later born children. Our study contributes to the literature on the response of parental investments to child’s health at birth by proposing new and more credible instrumental variables for the child health endowment at birth and allowing for a heterogeneous response of the mother’s investment for first born and later born children.

This study aims to examine the effect of maternal food intake before and during pregnancy on birth weight.

As a prospective cohort study, a total of 585 pregnant women of first trimester, visiting Tehran Metropolitan Area public health centers and private sectors (clinics and hospitals), were interviewed at first phase, and pregestational dietary intake was obtained by a 168-item semiquantitative food frequency questionnaire. At the third trimester, dietary recalls were collected via interview. Finally, birth weight information was extracted from health records. Univariate and multivariate analysis was used to explore the effect of maternal and nutritional factors on birth weight.

The results of the analysis show that direct measures of nutrition, measured as food group consumption at first and third trimester of pregnancy, had no significant effect on birth weight once the confounding factors were controlled (p > 0.05). Of control variables included in the analysis, twin pregnancy outcome (p = 0.000), pregnancy number (p = 0.04), prepregnancy weight (p = 0.004) (marginally significant) and gestational age (p = 0.000) (marginally significant) were associated with birth weight.

The results of this study show no significant role of mother’s nutrition during pregnancy on birth weight, while long-term nutrition outcomes such as prepregnancy weight had significant role. It seems the main reasons behind less important role of pregnancy nutrition on birth weight in this study include the following: food intake deficiency is not a major problem for participants, and cross-sectional data on food intake are less important on outcome of pregnancy weight than long-term nutritional status outcome variables such as mother’s weight and height. This finding should be addressed in public health planning for women at childbearing age.

Since World War II, rates of type 2 diabetes (henceforth diabetes) have skyrocketed, leading to talk of an “epidemic,” believed to result from formerly “adaptive” genotypes colliding with “affluent” postindustrial societies – largely their food excesses and physically undemanding jobs. Hence, experts describe diabetes as a struggle between biology and behaviors – “genes-as-destiny” and “lifestyles-as-choice” – said to have spared no social group. However, racial and ethnic minorities and the poor are affected disproportionately.

In this paper I challenge the “genes–lifestyle” framework and argue that the epidemic, particularly its distribution, is produced not by affluence but by poverty. The cumulative effect of malnutrition or hyperglycemia during pregnancy, of stunting in young children, of structural constraints over healthy lifestyles, and of the lack of a right to adequate medical care, which are all the results of poverty, leads to diabetes and its complications, and to disparities in their distribution among social groups. Hence, diabetes disparities are not mere differences but differences that are avoidable, unnecessary, and unjust. I also highlight selected conceptual problems of the genes–lifestyle framework that mislead about the potential contributions of genetics to human health.

I conclude that because the roots of the diabetes epidemic lie in inequities in social power, the solutions required are not medical but political, and ought to concern a sociologically informed bioethics. I also conclude that insofar as dominant accounts of the diabetes epidemic ignore or downplay these roots, they will legitimize research and policies that reproduce or even increase diabetes disparities. The paper is part of a larger project on the political ecology of diabetes.

Prenatal exposure to adverse conditions is known to affect health throughout the life span. It has also been shown that health is unevenly distributed at advanced ages. This chapter investigates whether health inequalities at old age may be partially caused by prenatal circumstances. We use a sample of people aged 71–91 from eight European countries and assess how shocks in GDP that occurred while the respondents were still in utero affect four important dimensions of later-life health: cognition, depression, functional limitations, and grip strength. We find that early-life macro-economic circumstances do not affect health at advanced ages, nor do they affect inequalities in health. In additional analyses, we show that the least healthy people may not enter our sample as the probability of dying before reaching age 71 is high, and mortality rates among those who were prenatally exposed to adverse GDP shocks are higher. We conclude that selective mortality may mask effects of early-life circumstances on health and health inequality at old age.

Recurrent pregnancy losses (RPL), a major contributor of reproductive wastage, affect maternal health both physically and mentally. Folate and B12 (Vitamin B12) deficiency anemia is common in the reproductive age group women in developing countries like India. And due to proven role of folate in various maternal and fetal anomalies, women are routinely prescribed folic acid under various national policies. However, B12 supplementation is rare, despite known deleterious effects of its deficiency. The purpose of this paper is to understand RPL through anemia with special reference to folate and B12 imbalance.

Multiparous women with normal obstetric outcomes (n=135) and women with Idiopathic RPL (n=105) were recruited in the study. All women were non-pregnant and belonged to North Indian population. Hb, serum folate and B12 and plasma homocysteine were measured in all the women. Anemia was classified according to WHO guidelines (Hemoglobin (Hb)<12g/dL).

The incidence of Anemia was more among normal multiparous women (73 percent) as compared to women with RPL (60 percent). However, unlike folate deficiency anemia among controls, B12 deficiency anemia was observed in women with RPL. Moreover, these women, despite being less anemic, with high B12 deficiency and folate sufficiency (presumably due to folate supplementation) had more imbalanced vitamin metabolism, as evident from homocysteine levels. The study suggests that anemic or non-anemic deficiencies of B12 and folate among women with RPL may be combated by screening for both vitamins, rather than supplementing folate indiscriminately to all.

One of the limitations is that ferritin levels for iron deficiency anemia could not be measured in this study.

The present study is the first study, to the best of our knowledge, where we looked for the role of imbalance of folate and B12 in women with RPL.

We explore what health-capital theory has to offer in terms of informing and directing research into health inequality. We argue that economic theory can help in identifying mechanisms through which specific socioeconomic indicators and health interact. Our reading of the literature, and our own work, leads us to conclude that non-degenerate versions of the Grossman (1972a, 1972b) model and its extensions can explain many salient stylized facts on health inequalities. Yet, further development is required in at least two directions. First, a childhood phase needs to be incorporated, in recognition of the importance of childhood endowments and investments in the determination of later-life socioeconomic and health outcomes. Second, a unified theory of joint investment in skill (or human) capital and in health capital could provide a basis for a theory of the relationship between education and health.