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While there is strong evidence that maternal smallpox infection can cause foetal loss, it is not clear whether smallpox infections were a demographically important cause of stillbirths historically. In this paper, we use parish-level data from the Swedish Tabellverket data set for 1780–1839 to test the effect of smallpox on stillbirths quantitatively, analysing periods before and after the introduction of vaccination in 1802. We find that smallpox infection was not a major cause of stillbirths before 1820, because most women contracted smallpox as children and were therefore not susceptible during pregnancy. We do find a small, statistically significant effect of smallpox on stillbirths from 1820 to 1839, when waning immunity from vaccination put a greater share of pregnant women at risk of contracting smallpox. However, the reduced prevalence of smallpox in this period limited its impact on stillbirths. Thus, smallpox was not an important driver of historical stillbirth trends.

While there is strong evidence that maternal smallpox infection can cause foetal loss, it is not clear whether smallpox infections were a demographically important cause of stillbirths historically. In this paper, we use parish-level data from the Swedish Tabellverket data set for 1780–1839 to test the effect of smallpox on stillbirths quantitatively, analysing periods before and after the introduction of vaccination in 1802. We find that smallpox infection was not a major cause of stillbirths before 1820, because most women contracted smallpox as children and were therefore not susceptible during pregnancy. We do find a small, statistically significant effect of smallpox on stillbirths from 1820 to 1839, when waning immunity from vaccination put a greater share of pregnant women at risk of contracting smallpox. However, the reduced prevalence of smallpox in this period limited its impact on stillbirths. Thus, smallpox was not an important driver of historical stillbirth trends.

While there is strong evidence that maternal smallpox infection can cause foetal loss, it is not clear whether smallpox infections were a demographically important cause of stillbirths historically. In this paper, we use parish-level data from the Swedish Tabellverket data set for 1780–1839 to test the effect of smallpox on stillbirths quantitatively, analysing periods before and after the introduction of vaccination in 1802. We find that smallpox infection was not a major cause of stillbirths before 1820, because most women contracted smallpox as children and were therefore not susceptible during pregnancy. We do find a small, statistically significant effect of smallpox on stillbirths from 1820 to 1839, when waning immunity from vaccination put a greater share of pregnant women at risk of contracting smallpox. However, the reduced prevalence of smallpox in this period limited its impact on stillbirths. Thus, smallpox was not an important driver of historical stillbirth trends.

While there is strong evidence that maternal smallpox infection can cause foetal loss, it is not clear whether smallpox infections were a demographically important cause of stillbirths historically. In this paper, we use parish-level data from the Swedish Tabellverket data set for 1780–1839 to test the effect of smallpox on stillbirths quantitatively, analysing periods before and after the introduction of vaccination in 1802. We find that smallpox infection was not a major cause of stillbirths before 1820, because most women contracted smallpox as children and were therefore not susceptible during pregnancy. We do find a small, statistically significant effect of smallpox on stillbirths from 1820 to 1839, when waning immunity from vaccination put a greater share of pregnant women at risk of contracting smallpox. However, the reduced prevalence of smallpox in this period limited its impact on stillbirths. Thus, smallpox was not an important driver of historical stillbirth trends.

While there is strong evidence that maternal smallpox infection can cause foetal loss, it is not clear whether smallpox infections were a demographically important cause of stillbirths historically. In this paper, we use parish-level data from the Swedish Tabellverket data set for 1780–1839 to test the effect of smallpox on stillbirths quantitatively, analysing periods before and after the introduction of vaccination in 1802. We find that smallpox infection was not a major cause of stillbirths before 1820, because most women contracted smallpox as children and were therefore not susceptible during pregnancy. We do find a small, statistically significant effect of smallpox on stillbirths from 1820 to 1839, when waning immunity from vaccination put a greater share of pregnant women at risk of contracting smallpox. However, the reduced prevalence of smallpox in this period limited its impact on stillbirths. Thus, smallpox was not an important driver of historical stillbirth trends.

Previous work has shown that England's pre-industrial elites had more surviving off-spring than their lower-class counterparts. This evidence was used to argue that the spread of upper-class values via downward social mobility helped England grow rich. We contest this view, showing that the lower classes outperformed the rich in terms of reproduction once singleness and childlessness are accounted for. Indeed, Merchants, Professionals and Gentry married less, and their marriages were more often childless. Many died without descendants (decessit sine prole). We also establish that the most prosperous socio-economic group in terms of reproduction was the middle class, which we argue was instrumental to England's economic success because most of its new industrialists originated from middle-class families.

IntroductionInjury is a significant and increasingly common cause of morbidity and mortality in sub-Saharan Africa; however, the social and economic factors underlying these trends are not well understood. We evaluated the relationship between socioeconomic status (SES) and trauma outcomes using a prospective registry of patients presenting to the largest trauma hospital in Yaoundé, Cameroon.MethodsTrauma patients (n=2855) presenting to the emergency ward at Central Hospital, Yaoundé between April 15 and October 15, 2009 were surveyed regarding demographic and socioeconomic background, nature and severity of injuries, treatment, and disposition. A wealth score was estimated for each patient, corresponding to an SES index constructed using principle components analysis of the urban Cameroonian Demographic and Health Survey. Logistic regression was used to evaluate the effects of SES on care-seeking behaviour, injury severity, and treatment outcome.Main outcome measuresSES wealth score, care-seeking prior to visiting hospital, injury severity, treatment outcome.ResultsPatients aged 1-89 presented with road traffic injuries (59.83%), falls (7.76%), and penetrating trauma (6.16%), and had higher SES than the broader urban Cameroonian population. Within the Yaoundé sample, being in the lowest SES quintile was associated with an increased likelihood of having sought care elsewhere before presenting to the hospital (aOR=3.28, p<0.001), after controlling for background and injury characteristics. Patients in the lowest SES quintile were also more likely to present with moderate/severe injuries (aOR=4.93, p<0.001), and were more likely to be transferred to the operating room.ConclusionsPatients presenting to this trauma centre were wealthier than the broader community, suggesting the possibility of barriers to accessing care. Poorer patients were more likely to have severe injuries and more likely to need surgery, but were less likely to seek care from a major trauma c

IntroductionInjury is a significant and increasingly common cause of morbidity and mortality in sub-Saharan Africa; however, the social and economic factors underlying these trends are not well understood. We evaluated the relationship between socioeconomic status (SES) and trauma outcomes using a prospective registry of patients presenting to the largest trauma hospital in Yaoundé, Cameroon.MethodsTrauma patients (n=2855) presenting to the emergency ward at Central Hospital, Yaoundé between April 15 and October 15, 2009 were surveyed regarding demographic and socioeconomic background, nature and severity of injuries, treatment, and disposition. A wealth score was estimated for each patient, corresponding to an SES index constructed using principle components analysis of the urban Cameroonian Demographic and Health Survey. Logistic regression was used to evaluate the effects of SES on care-seeking behaviour, injury severity, and treatment outcome.Main outcome measuresSES wealth score, care-seeking prior to visiting hospital, injury severity, treatment outcome.ResultsPatients aged 1-89 presented with road traffic injuries (59.83%), falls (7.76%), and penetrating trauma (6.16%), and had higher SES than the broader urban Cameroonian population. Within the Yaoundé sample, being in the lowest SES quintile was associated with an increased likelihood of having sought care elsewhere before presenting to the hospital (aOR=3.28, p<0.001), after controlling for background and injury characteristics. Patients in the lowest SES quintile were also more likely to present with moderate/severe injuries (aOR=4.93, p<0.001), and were more likely to be transferred to the operating room.ConclusionsPatients presenting to this trauma centre were wealthier than the broader community, suggesting the possibility of barriers to accessing care. Poorer patients were more likely to have severe injuries and more likely to need surgery, but were less likely to seek care from a major trauma c

Shilpa Bhardwaj,1,2 Shalini Selvarajah,3 Eric B Schneider31Griffin Hospital, Derby, CT, USA; 2Yale University, New Haven, CT, USA; 3Center for Surgical Trials and Outcomes Research, Johns Hopkins School of Medicine, Baltimore, MD, USAAbstract: Statins have demonstrated substantial benefits in supporting cardiovascular health. Older individuals are more likely to experience the well-known muscle-related side effects of statins compared with younger individuals. Elderly females may be especially vulnerable to statin-related muscle disorder. This review will collate and discuss statin-related muscular effects, examine their molecular and genetic basis, and how these apply specifically to elderly women. Developing strategies to reduce the incidence of statin-induced myopathy in older adult women could contribute to a significant reduction in the overall incidence of statin-induced muscle disorder in this vulnerable group of patients. Reducing statin-related muscle disorder would likely improve overall patient compliance, thereby leading to an increase in improved short- and long-term outcomes associated with appropriate use of statins.Keywords: statins, older adults, elderly, females, epidemiology

US combat operations in Iraq and Afghanistan have resulted in a greater proportion of service members with head and neck wounds caused by explosions compared with that of previous wars. Although penetrating traumatic brain injury (TBI) is frequently associated with these wounds, the epidemiology of penetrating TBI from these conflicts has not been well described. The Joint Theater Trauma Registry was queried for January 2003 through December 2010 to identify all patients with moderate-to-- severe brain injury with a maximum Abbreviated Injury Scale (AIS) score of the head of 3 or greater and a diagnosis of penetrating or closed TBI in accordance with the Department of Defense Traumatic Brain Injury Surveillance definition. The epidemiology of these injuries was examined, including demographics, TBI severity, overall injury severity, and surgical interventions provided. A total of 1,255 TBI patients (774 penetrating, 481 closed) meeting criteria were identified. Penetrating brain injuries were more severe, more likely to be battle related, and less likely to be isolated injuries than a group of moderate-to-severe closed TBIs within the same range of anatomic injury severity. During the 5-year period of the Iraq war with the largest numbers of TBIs (2004 2008), the numbers of penetrating TBIs exceeded closed TBIs by a ratio of 2:1. During the 3-year period of the Afghanistan war with the greatest numbers of TBIs (2008 2010), the ratio of penetrating to closed TBIs was substantially lower, approximately 1.3:1. This study represents the first comprehensive report on the epidemiology of moderate-to-severe penetrating and closed TBIs resulting from the wars in Iraq and Afghanistan using Joint Theater Trauma Registry data. With the maturing theater of conflicts, penetrating TBIs were substantially less predominant compared with closed TBIs., Published in Journal of Trauma and Acute Care Surgery v73 n6 Suuplement 5 pS496-S502, 2012.

This article explores how child growth has changed over the past 150 years and links changes in child growth to the recent decline in child stunting in low- and middle-income countries (LMICs). The article begins by defining the four characteristics of the growth pattern in height: size at birth, size at adulthood, the timing of the pubertal growth spurt, and the speed of maturation. It then shows how these characteristics have changed over time and links these characteristics to child stunting. Stunted children are too short for their age relative to healthy standards, and their share in the population is used as an indicator of malnutrition in LMICs today. The article then surveys the literature on the causes of changes in the growth pattern and reductions in child stunting, comparing research on current LMICs with historical research on current high-income countries (HICs) in the past. To limit the scope of the contemporary literature, I focus on explanations of the so-called “Indian enigma:” why Indian children are shorter than sub-Saharan African children despite India's lead in many indicators of economic development. The article closes with ideas for what historical and contemporary researchers can learn from one another.

Evidence on the post-weaning benefits of early-life breastfeeding is mixed, and highly context-dependent. Moreover, this evidence is drawn almost exclusively from modern settings, limiting our understanding of the relationship between breastfeeding and subsequent health in the past. We provide novel evidence on the nature and reach of these post-weaning benefits in a historical setting, drawing on a rich new longitudinal dataset covering nearly 1000 children from the Foundling Hospital, an orphanage in turn-of-the-century London. We find that even after the cessation of breastfeeding, ever-breastfed status reduced mortality risk and raised weight-for-age in infancy, that exclusive breastfeeding conferred additional benefits, and that breastfeeding duration had little impact. We also find a U-shaped pattern in weight-for-age by time since weaning, indicating a deterioration in health shortly after weaning, followed by a recovery. The early post-weaning advantages associated with breastfeeding, however, did not persist into mid-childhood. This indicates that any protective effects of earlier breastfeeding attenuated with age, and suggests a strong role for catch-up growth. This study contributes to the data and empirical settings available to explore the relationship between infant feeding and post-weaning health, and helps shed light on the contribution of changing breastfeeding norms to trends in health in twentieth-century Britain.

This article uses the health shock on Japanese civilians of the Second World War to understand the effects of health shocks at different developmental stages on children's long-run growth pattern and to test whether recovery is possible after an early-life health shock. We construct a prefecture-level dataset of mean heights of boys and girls aged 6–19 from 1929 to 2015. Linking the heights recorded at different ages for the same birth cohort, we measure a counterfactual causal effect of the health shocks during the Second World War on the cohort growth pattern of children. We find that the war effect was greatest for cohorts exposed to the war in late childhood and adolescence: these cohorts were 1.7–3.0 cm shorter at adulthood and had delayed pubertal growth and slower maturation than they would have had if the war had never occurred. However, there were no persistent health penalties for children exposed to the war in early life, suggesting that catch-up growth was possible as health conditions improved after the war. These findings challenge the thousand-days consensus that children cannot recover from nutritional shocks in early life and indicate that adolescence is a sensitive period for health shocks.

While there is strong evidence that maternal smallpox infection can cause foetal loss, it is not clear whether smallpox infections were a demographically important cause of stillbirths historically. In this paper, we use parish-level data from the Swedish Tabellverket data set for 1780–1839 to test the effect of smallpox on stillbirths quantitatively, analysing periods before and after the introduction of vaccination in 1802. We find that smallpox infection was not a major cause of stillbirths before 1820, because most women contracted smallpox as children and were therefore not susceptible during pregnancy. We do find a small, statistically significant effect of smallpox on stillbirths from 1820 to 1839, when waning immunity from vaccination put a greater share of pregnant women at risk of contracting smallpox. However, the reduced prevalence of smallpox in this period limited its impact on stillbirths. Thus, smallpox was not an important driver of historical stillbirth trends.

Woods (2009) argued that smallpox was an important cause of stillbirths in the past. While there is strong evidence that maternal smallpox infection could lead to fetal loss, it is not clear whether smallpox infections were a demographically important source of stillbirths. In this paper, we use parish-level data from the Swedish Tabellverket dataset from 1780 to 1839 to test the effect of smallpox on stillbirths quantitatively. We use two empirical strategies: dynamic panel regressions that test the instantaneous effect of smallpox epidemics on stillbirths; and a continuous treatment difference-in-difference strategy to test whether the reduction in smallpox prevalence following vaccination led to a larger decrease in the stillbirth rate in parishes where smallpox was more prevalent before vaccination. We find very little evidence that smallpox infection was a major cause of stillbirths in history. Our coefficients are largely insignificant and close to zero. This is because the vast majority of women contracted smallpox as children and therefore were no longer susceptible during pregnancy. We do find a small, statistically significant effect of smallpox on stillbirths from 1820-39 when waning immunity from vaccination put a greater share of pregnant women at risk of contracting smallpox. However, the reduced prevalence of smallpox limited the demographic impact. Thus, smallpox was not an important driver in historical stillbirth trends and did not contribute to in utero scarring effects for cohorts born when smallpox prevalence was high.

There is a complex inter-relationship between nutrition and morbidity in human health. Many diseases reduce nutritional status, but on the other hand, having low nutritional status is also known to make individuals more susceptible to certain diseases and to more serious illness. Modern evidence on these relationships, determined after the introduction of antibiotics and vaccines, may not be applicable to historical settings before these medical technologies were available. This paper uses a historical cohort study based on records from the London Foundling Hospital to determine the causal effect of nutritional status of children, proxied by weight- and height-for-age Z-scores, on the odds of contracting five infectious diseases of childhood (measles, mumps, rubella, chicken pox and whooping cough) and on sickness duration from these diseases. I identify a causal effect by exploiting the randomisation of environmental conditions as foundling children were removed from their original homes, then fostered with families in counties nearby London and later returned to the Foundling Hospital’s main site in London. I find no effect of nutritional status on the odds of contracting the five diseases, but I do find a historically important and statistically significant effect of nutritional status on sickness duration for measles and mumps. These findings have three implications. First, historical incidence of these diseases was unrelated to nutritional status, meaning that poor nutritional status during famines or during the Colombian Exchange did not affect the spread of epidemics. However, undernutrition in these events may have exacerbated measles severity. Second, improving nutritional status in the past 150 years would have reduced the severity of measles and mumps infections but not affect the decline in whooping cough mortality. Finally, selective culling effects from measles would be larger than those from whooping cough since whooping cough severity was not correla

There is a complex inter-relationship between nutrition and morbidity in human health. Many diseases reduce nutritional status, but on the other hand, having low nutritional status is also known to make individuals more susceptible to certain diseases and to more serious illness. Modern evidence on these relationships, determined after the introduction of antibiotics and vaccines, may not be applicable to historical settings before these medical technologies were available. This paper uses a historical cohort study based on records from the London Foundling Hospital to determine the causal effect of nutritional status of children, proxied by weight- and height-for-age Z-scores, on the odds of contracting five infectious diseases of childhood (measles, mumps, rubella, chicken pox and whooping cough) and on sickness duration from these diseases. I identify a causal effect by exploiting the randomisation of environmental conditions as foundling children were removed from their original homes, then fostered with families in counties nearby London and later returned to the Foundling Hospital’s main site in London. I find no effect of nutritional status on the odds of contracting the five diseases, but I do find a historically important and statistically significant effect of nutritional status on sickness duration for measles and mumps. These findings have three implications. First, historical incidence of these diseases was unrelated to nutritional status, meaning that poor nutritional status during famines or during the Colombian Exchange did not affect the spread of epidemics. However, undernutrition in these events may have exacerbated measles severity. Second, improving nutritional status in the past 150 years would have reduced the severity of measles and mumps infections but not affect the decline in whooping cough mortality. Finally, selective culling effects from measles would be larger than those from whooping cough since whooping cough severity was not correla

Economic historians have long been aware of many forms of bias that could lead to spurious causal inferences. However, our approach to these biases has been muddled at times by dealing with each bias separately and by confusion about the sources of bias and how to mitigate them. This paper shows how the methodology of directed acyclical graphs (DAGs) formulated by Pearl (2009) and particularly the concept of collider bias can provide economic historians with a unified approach to managing a wide range of biases that can distort causal inference. I present ten examples of collider bias drawn from economic history research, focussing mainly on examples where the authors were able to overcome or mitigate the bias. Thus, the paper addresses how to diagnose collider bias and also strategies for managing it. The paper also shows that quasi-random experimental designs are rarely able to overcome collider bias. Although all of these biases were understood by economic historians before, conceptualising them as collider bias will improve economic historians’ understanding of the limitations of particular sources and help us develop better research designs in the future.

This article employs a household survey of low-income working-class households conducted in Tokyo in 1930 to investigate nutritional attainment levels and the relationship between calorie intake and morbidity. We find that the daily calorie intake was 2,118 kcal per adult male equivalent, high enough to satisfy the energy requirements for moderate physical activity. Richer households purchased more expensive calories mainly by substituting meat and vegetables for rice. We find negative associations between morbidity and income and crowding, but no significant associations for nutrition, tentatively suggesting that income and crowding were more important for morbidity in 1930 Tokyo than nutrition.

Bodenhorn et al. (2017) have sparked considerable controversy by arguing that the fall in adult stature observed in military samples in the United States and Britain during industrialization was a figment of selection on unobservables in the samples. While subsequent papers have questioned the extent of the bias (Komlos and A'Hearn 2019; Zimran 2019), there is renewed concern about selection bias in historical anthropometric datasets. Therefore, this article extends Bodenhorn et al.'s discussion of selection bias on unobservables to sources of children's growth, specifically focusing on biases that could distort the age pattern of growth. Understanding how the growth pattern of children has changed is important because these changes underpinned the secular increase in adult stature and are related to child stunting observed in developing countries today. However, there are significant sources of unobserved selection in historical datasets containing children's and adolescents' height and weight. This article highlights, among others, three common sources of bias: (1) positive selection of children into secondary school in the late nineteenth and early twentieth centuries; (2) distorted height by age profiles created by age thresholds for enlistment in the military; and (3) changing institutional ecology that determines to which institutions children are sent. Accounting for these biases adjusts the literature in two ways: evidence of a strong pubertal growth spurt in the nineteenth century is weaker than formerly acknowledged and some long-run analyses of changes in children's growth are too biased to be informative, especially for Japan.

This paper reconsiders the fertility of historical social groups by accounting for singleness and childlessness. We find that the middle class had the highest reproductive success during England's early industrial development. In light of the greater propensity of the middle class to invest in human capital, the rise in the prevalence of these traits in the population could have been instrumental to England's economic success. Unlike earlier results about the survival of the richest, the paper shows that the reproductive success of the rich (and also the poor) were lower than that of the middle class, once accounting for singleness and childlessness. Hence, the prosperity of England over this period can be attributed to the increase in the prevalence of middle-class traits rather than those of the upper (or lower) class.

This paper is the first to use individual-level, longitudinal measures of child growth to document changes in the growth pattern in Britain between the 1850s and 1970s. Based on a unique dataset gathered from the records of the training ship Indefatigable, we analyse the mean heights of boys at admission and their longitudinal growth using regressions that control for observable characteristics. We find a secular increase in boys’ mean height over time, and the height gain was most rapid during the interwar period. In addition, longitudinal growth velocity was low and similar at different ages for boys born before the 1910s, suggesting that there was no marked pubertal growth spurt like that which occurs in modern populations. However, for boys born in the 1910s and later, higher growth velocities associated with pubertal growth appeared for boys in a narrow range of ages, 14 to 16. Thus, it appears that there was a substantial change in the growth pattern beginning in the 1910s with the emergence of a strong pubertal growth spurt. The timing of this shift implies that declines in child morbidity and improved hygiene mattered more for the changing growth pattern than improvements in nutrition that occurred before the 1910s.

This article challenges the growing consensus in the literature that medieval manorial managers were price responsive in their production decisions. Using prices of and acreages planted with wheat, barley, and oats on manors held by the bishop of Winchester from 1325 to 1370, price elasticities of supply are estimated for each grain in aggregate and on each particular manor. Aggregate price elasticities of supply for wheat, barley, and oats were rarely statistically significant and when significant were very low compared with elasticities estimated for developing and developed countries in the nineteenth and twentieth centuries. The low levels of agricultural supply response in fourteenth‐century England suggest that commercialization was not as dominant in the medieval economy as has been argued. Thus, structural changes in the economy, such as the leasing of demesnes, the growth of wage labour, and the end of villeinage, may have been more important than price fluctuations in driving long‐run economic change after the Black Death. Likewise, a shift from low price responsiveness to higher price responsiveness could have been an important part of the capitalist transformation of agriculture in the early modern period.

This paper assesses how the disease environment, proxied by infant mortality rates, influenced children’s growth in interwar Japan. We use data drawn from government records from 1929 to 1939 which report the mean heights of boys and girls in school at each age (6-18) for each of Japan’s 47 prefectures. We focus on two key questions: 1) how important was the disease environment in infancy in shaping the growth pattern of children? and 2) were shocks to child health more salient in the first thousand days of life, often held as a critical window to prevent stunting, or at later ages? We quantify the characteristics of growth pattern of birth cohorts using the SITAR growth model and then relate the predicted SITAR parameters to infant mortality in the year of birth. In addition, we test for instantaneous effects of morbidity, proxied by infant mortality, on growth at ages 6-11. We find that infant mortality in early life did not have a strong influence on the growth pattern of children, but there were statistically significant and economically meaningful instantaneous effects of infant mortality on child height at ages 6-11 for both boys and girls. This suggests that interventions outside of the thousand-day critical window can be effective and that the secular increase in height in interwar Japan was more strongly influenced by cumulative responses to the health environment across child development rather than simply improvements in early life health.

Child malnutrition is a very important global health challenge. 155 million children globally suffer from malnutrition and are consequently stunted, much shorter than healthy children at the same age. Reducing stunting was an important target in the Millenium Development Goals and is also a target under Goal 2 of the Sustainable Development Goals. This report summarises recent research on child stunting that was presented and discussed at a conference, STUNTING: PAST, PRESENT AND FUTURE, at the London School of Economics and Political Science in September 2017. The conference brought together academics across a wide range of disciplines with policy experts and influencers from the third sector. There were four key lessons that participants took away from the conference. First, stunting was present in currently developed countries at the beginning of the twentieth century, which suggests that reductions in stunting were a corollary to the secular increase in mean adult height across the twentieth century. Second, there needs to be more research on catchup growth in adolescence to determine whether catch-up growth in height is also associated with improvements in other dimensions of health and human capital that are affected by malnutrition, for instance cognitive deficiencies. If interventions in adolescence can be effective, then it may be possible to mitigate some of the consequences of stunting for already stunted children. Third, researchers need to be aware of the large degree of spatial variation in stunting within countries and the distinct age pattern of stunting between ages 0 and 5 when trying to understand why children become stunted. Fourth, participants agreed that more interdisciplinary collaboration is necessary to design experiments and models to capture the multi-dimensional nature of child stunting.

Bodenhorn et al. (2017) have recently sparked considerable controversy by arguing that the fall in adult stature observed in military samples in the United States and Britain during industrialisation was a figment of sample selection bias. While subsequent papers have questioned the extent of the bias (Komlos and A’Hearn 2016; Zimran 2017), there is renewed concern about selection bias in historical anthropometric datasets. This paper extends Bodenhorn et al.’s discussion of selection bias on unobservables to sources of children’s growth, specifically focussing on biases that could distort the age pattern of growth. Understanding how the growth pattern of children has changed is important since these changes underpinned the secular increase in adult stature and are related to child stunting observed in developing countries today. However, there is potential for selection on unobservables in historical datasets containing children’s and adolescents’ height, so scholars must be aware of these biases before analysing these sources. This paper highlights, among others, three common sources of bias: 1) positive selection of children into secondary school in the late nineteenth and early twentieth centuries; 2) distorted height by age profiles created by age thresholds for enlistment in the military; and 3) changing institutional ecology which determines to which institutions children are sent. Accounting for these biases weakens the evidence of a strong pubertal growth spurt in the nineteenth century and raises doubts on some long run analyses of changes in children’s growth, especially for Japan.

In explaining England's early industrial development, previous research has highlighted that wealthy pre-industrial elites had more surviving offspring than their poorer counter- parts. Thus, entrepreneurial traits spread and helped England grow rich. We contest this view, showing that lowerclass reproduction rates were no different from the elites when accounting for singleness and childlessness. Elites married less and were more often childless. Many died without descendants (decessit sine prole). We find that the middle classes had the highest reproduction and argue that this advantage was instrumental to England's economic success because the middle class invested most strongly in human capital.

This paper assesses how the disease environment in interwar Japan influenced children’s growth and health. The data is drawn from government records from 1929 to 1939 which report the average heights of boys and girls in school at each age (6-21) for each of Japan’s 47 prefectures. We test the influence of disease in two ways. First, we test the influence of the disease environment at birth, proxied by the infant mortality rate, on the cohort growth pattern of children using the SITAR model to parameterise the growth pattern. In addition, we use a bilateral-specific fixed effects model to understand how disease instantaneously influenced growth controlling for prefecture-birth cohort effects. Our results suggest that health conditions in early life did not have a strong influence on the growth pattern of children in Japan. However, we do find a significant and economically meaningful instantaneous effect of the infant mortality rate on child height at ages 6-11 for both boys and girls. This suggests that child morbidity was very important to the increase in stature during interwar Japan, but it also suggests that the emphasis placed on preventing child stunting in the first thousand days in the modern development literature may be misplaced. The secular increase in height in interwar Japan was more strongly influenced by cumulative responses to the health environment across child development rather than being simply the outcome of improving cohort health.

Social class gradients in children’s health and development are ubiquitous across time and geography. The authors develop a conceptual framework relating three actions of class—material allocation, salient group identity, and inter-group conflict—to the reproduction of class-based disparities in child health. A core proposition is that the actions of class stratification create variation in children’s mesosystems and microsystems in distinct locations in the ecology of everyday life. Variation in mesosystems (e.g., health care, neighborhoods) and microsystems (e.g., family structure, housing) become manifest in a wide variety of specific experiences and environments that produce the behavioral and biological antecedents to health and disease among children. The framework is explored via a review of theoretical and empirical contributions from multiple disciplines and high-priority areas for future research are highlighted.

Many empirical studies have shown that health conditions in utero can have long lasting consequences for health across the life course. However, despite this evidence, there is no clear consensus about how fetal health has changed in the very long run. This paper analyses historical birth weights and perinatal mortality rates to construct a coherent picture of how health conditions in utero have changed over the past 150 years. In short, the evidence suggests that fetal health has been relatively stagnant. Limited evidence on birth weights shows that they had already reached their current levels in North America and Northern and Western Europe by the late nineteenth century, and they have changed very little in between. Perinatal mortality rates have fallen dramatically since the late 1930s, but this decline was mainly caused by improvements in intrapartum treatments after the introduction of Sulfa drugs and antibiotics. Thus, the health benefits associated with the perinatal mortality decline were concentrated among those at risk and did not influence the population at large. Finding stagnant fetal health during a period when many other indicators of health improved dramatically is provocative and suggests two conclusions: either fetal health did not improve or the indicators used to measure fetal health, indicators still widely used today, may not accurately capture all aspects of health in utero. If fetal health has been stagnant, then better conditions in utero cannot explain cohort improvements in life expectancy over the twentieth century. If the indicators of fetal health are problematic, then researchers must move beyond birth weight and perinatal mortality to understand how developmental plasticity based on the prenatal environment influences later life health.

This article presents a new adaptive framework for understanding children's growth in the past. Drawing upon the recent work on adaptive responses in relation to growth, it presents prenatal and postnatal adaptive mechanisms that affect the growth patterns of children. The most novel adaptive response to the historical literature is the prenatal predictive adaptive response where the metabolism and growth trajectory of a child is programmed to match predicted conditions later in life. Having discussed the framework in detail, a reinterpretation of the growth pattern of American slaves is then suggested. It seems likely that a mismatch between relatively good conditions in utero and absolutely appalling conditions in infancy and early childhood led slave children to become extremely stunted by the age of three or four. However, after this age, slave children experienced catch‐up growth because their immune systems had become more developed and because their diet improved tremendously and hookworm exposure was reduced. Thus, it seems that American slave children may have experienced substantial catch‐up growth because they were prenatally programmed for a higher metabolism and growth trajectory. The article concludes by setting out some stylized facts about children's growth in the past and pointing toward areas of future research.

This paper is the first to use the individual level, longitudinal catch-up growth of boys and girls in a historical population to measure their relative deprivation. The data is drawn from two government schools, the Marcella Street Home (MSH) in Boston, MA (1889-1898) and the Ashford School of the West London School District (1908- 1917). The paper provides an extensive discussion of the two schools including the characteristics of the children, their representativeness, selection bias and the conditions in each school. It also provides a methodological introduction to measuring children’s longitudinal catch-up growth. After analysing the catch-up growth of boys and girls in the schools, it finds that there were no substantial differences between the catch-up growth by gender. Thus, these data suggest that there were not major health disparities between boys and girls in late nineteenth century America and early twentieth century Britain.