Parasites, Pathogens, and Progress: Diseases and Economic Development

July 5, 2017 | Autor: Robert A. McGuire | Categoria: Environmental History, Applied Economics, Multidisciplinary, Historical Studies
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The Social Science Journal 50 (2013) 135–137

Contents lists available at SciVerse ScienceDirect

The Social Science Journal journal homepage: www.elsevier.com/locate/soscij

Book review Parasites, Pathogens, and Progress: Diseases and Economic Development By Robert A. McGuire and Philip R.P. Coelho; MIT Press, 2011, 343 pp. History requires perspective on the importance of population change and how it relates to larger social transformations. For example, the rise of the western world and its transformation from feudalism to capitalism was related, at least in part, to the population change associated with the Black Death. The European bubonic plague of 1346–1347 was related to sanitation conditions, and lower socioeconomic groups were more vulnerable to poor sanitation conditions than individuals in higher socioeconomic groups. As a result, the plague disproportionately affected the working class, and higher mortality rates among lower socioeconomic groups made unskilled labor relatively scarce, allowing unskilled labor to command higher wages. Higher socioeconomic groups, therefore, had to pay higher wages to the working poor, which disrupted the reciprocal relationships between social classes that existed for generations under feudalism. Therefore, population change is frequently integral in larger social and economic movements that change history. A key to understanding population dynamics is the demographic transition, where primitive societies start with high birth and high death rates. The corresponding net population increase is low. With economic development, death rates decline, followed by declining birth rates; as birth rates lag death rates, populations transition from low net fertility, through high net fertility, and converge on low birth, low death, and low net fertility. Associated with this demographic transition is Omran’s epidemiological transition, which accounts for how mortalities change over the course of the demographic transition. Mortality in early developing economies is high and fluctuates widely because of pestilence and famine. Mortality steadily declines, and pandemics recede; life expectancy increases. Finally, longer life expectancy is associated with increased degenerative and man-made diseases, such as Alzheimer’s and obesity. To bridge this population gap, McGuire and Coelho start with a comprehensive discussion on how population change is associated with human evolution and trace larger forces shaping society. Therefore, Parasites, Pathogens, and Progress contributes to developing a greater 0362-3319/$ – see front matter http://dx.doi.org/10.1016/j.soscij.2012.12.011

appreciation for how population change is related to history. As 18th and 19th century Northern Europeans immigrated to North America, passage costs were high and typically beyond an average field hands annual salary, creating a conundrum. Cash starved but labor abundant European workers were unable to afford the early costs of trans-Atlantic ship fares to migrate to North America. Labor starved but land abundant New World planters sought to fill their labor demands with working class Europeans in exchange for assuming transportation costs. As a result, New World planters developed a complex credit allocation system to populate North America with Europeans. However, North American planters did not have to choose only between employing indentured servants and going without. Planters also used African slaves who were brutally coerced into migration by slave traders. To compare the profitability of servants and slaves, slave owners had to know crop prices, slave relative to servant price, the net revenues each produced, and the length of time each was bound. Planters then used the mode of labor that produced the greatest expected net present value and profits. All this assumes a degree of perfect foresight, where slave masters knew agricultural output, prices, revenues, interest rates, and length of service. Moreover, colonial planters had to integrate knowledge about the likelihood that workers survived in various climates and disease environments. This was complicated because blacks and whites respond differently to given disease environments, and blacks do better in Southern climates due to subtle biological differences; whites do better in Northern climates. Over generations in the New World, Africans and Europeans alike adapted to life in North America, and planters had to maximize the net present value on their servant–slave investments, including health and biological welfare. The distribution of planter choices between servants and slaves was related to disease environments and the biological endowments laborers carried with them to different US regions. For example, vitamin D deficiency is related with several diseases, and the primary source of vitamin D is not milk and dairy products but exposure to the sun when cholesterol and sunlight are synthesized into vitamin D in the epidermis. Vitamin D is produced in the skin’s lower epidermis’ stratum granuloseum. The upper epidermis, the stratum corneum, shields the lower epidermis, and individuals with greater melanin in the stratum

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Book review

corneum – darker skin pigmentation – are less efficient at vitamin D production than individuals with less melanin in the stratum corneum. The result is that fairer complexioned Europeans produce more vitamin D than darker complexioned Africans, especially at low sunlight latitudes. Therefore, the 17th and 18th century forced migration of Africans to North American latitudes placed Africans into areas where they were not biologically suited; northern latitudes receive less sunlight, and Africans already produce less vitamin D because they have greater amounts of melanin in their epidermis, with the disastrous result that modern US black populations are afflicted more with Vitamin D related diseases, such as prostate cancer for men and breast and ovarian cancer for women. Colon cancer is also related to vitamin D, and blacks are more prone to colon cancer than fairer complexioned whites. Furthermore, these evolutionary patterns interact with hemoglobin, and blacks are less vulnerable to insect-vector related diseases, such as malaria. As a result, any theory for the 17th and 18th century’s population of North America with Africans and Europeans must account for the biological differences between them. Therefore, because Southern states received more sunlight with greater amounts of standing waters that are host to mosquitoes and disease carrying insects, blacks concentrated in the American South. Whites, who are biologically less protected against hookworm and malaria suffered greater disease rates in the South. Hookworm and malaria are two parasitic diseases that were endemic in the 19th century American South. Hookworm attaches its larvae to the host’s intestines and devours significant quantities of its nutrition. The result is anorexia, abdominal pains, nausea, headaches, rashes, weakness, vomiting, diarrhea, dysentery, and intestinal bleeding. In other cases, hookworm is associated with dementia, and if children infected with hookworm are exposed to it for extended periods during formative ages, results can include permanent stunting, mental retardation, and failure to develop cognitively. While hookworm is typically not fatal, it is debilitating, and hookworm symptoms are consistent with many Southern ailments. Hookworm spreads rapidly among populations that do not have proper human waste treatment facilities because its larvae are spread through infected hosts’ waste. The South was especially vulnerable to hookworm because most of the 19th century South was rural, and rural locations are not sufficiently populated to justify large-scale waste treatment facilities. For example, before 1900, only one of the US’s top ten populated cities – New Orleans – was in the South, and without proper waste treatment facilities, rural residents were frequently exposed to areas where hookworm was spread. Malaria is a mosquito-borne infectious disease that was prominent in the 19th century American South. Malaria results from the multiplication of plasmodium parasites within red blood cells, and sickle cell is a blood disorder where the circulatory system produces an abnormal type of oxygen carrying hemoglobin in red blood cells. Sickling and sickle cell provides carriers with some natural immunity to malaria, and 19th century slaves from West Africa had greater incidence of sickling and were less likely

than white Europeans to die from malaria. Therefore, blacks have some degree of biological resistance to hookworm and malaria. Genetics determine, in part, a person’s predisposition to contracting and dying from disease. For example, tropical West Africans have the sickle cell trait and blood abnormalities that provide protection against malaria. Whites are genetically less equipped to fight malaria, yellow fever, and hookworm, three diseases that affected 17th through 19th century southern white workers in greater numbers than darker complexioned blacks. Moreover, hookworm’s spread after the Civil War reduced Southern productivity and may be responsible for the decrease in Southern agricultural productivity. The result was that while Southern colonies initially used white European indentured servitude, their high mortality and morbidity rates reduced their profitability and increased the relative value of African slaves. Blacks in northern climates were more likely than whites to die from cold weather diseases, such as measles, whooping cough, pleurisy, influenza, and other lung diseases. McGuire and Coelho rely heavily on this innate response to hookworm and malaria to explain how black chattel slavery came to dominate Southern labor markets. Given the choice between northern white Europeans and African slaves, Southern planters selected the labor force that maximized their expected profits and chose Africans who had innate resistance to the Southern diseases of hookworm and malaria. Faced with considerable data constraints, modern economic historians use diverse sources to support various theories. A population’s average stature reflects its net cumulative nutrition. When a population’s nutrition relative to calories required for work and to fend off disease increases, average stature increases and decreases when it deteriorates. In a pattern known as the antebellum paradox, average 19th century statures declined during the 2nd and 3rd quarters, while average wages monotonically increased. Various plausible explanations are offered, and nutrition is typically regarded as the primary factor associated with the mid-19th century US stature variation. McGuire and Coelho’s thesis is that 18th and 19th century disease was the major factor associated with stature variation. However, Rick Steckel and John Komlos, two leaders in the development of anthropometric history, maintain that the majority of this stature diminution is the result of changes in nutrition. In a frequently cited interaction in the 2000 Journal of Economic History, McGuire and Coelho challenge Steckel’s interpretation of diminished statures in Coastline manifest records and maintain that rather than deteriorating nutrition, it was increased disease among slaves that was responsible for the 2nd and 3rd quarter slump. Nonetheless, Steckel aptly responds that it is the interaction between diets and disease that leads to stature variation; after all, stature is related with the interaction of diets and disease. The interplay ends with a respect for the interaction between diets and disease, but subsequent evidence supports the nutrition hypothesis. For example, on the eve of the Civil War, there was an increase in Black and White Texas statures with the 1850s cotton boom. Moreover, US female statures declined before the 1820s, and if males and females shared the same disease environments,

Book review

female statures should have declined later if their stature diminution was related only to disease. McGuire and Coelho offer possible economic demography and epidemiological explanations for choices made by profit maximizing slave masters. However, Parasites, Pathogens, and Progress may not be well supported by current economic historians’ explanation for why indentured servants and African slaves were substituted as determined only by the US disease environment. Moreover, McGuire and Coelho’s disease-only explanation for the substitution of slaves for servants suggests disease was responsible for the substitution. Slave efficiency or human capital is not mentioned as possible explanations for why slavery became localized in the South. Surely, a generation of slavery scholars disagrees over such an assertion. This is not to say that disease was not important, but there are a plethora of explanations for why slavery came to dominate in the South and servitude dominate in the North. Finally, the 1850 through 1900 federal census mortality schedules are used to consider 19th century mortality and how they were related by region and by age group. If the disease hypothesis is true, the reader wants to know if white malaria and hookworm mortality rates were greater for blacks. Setting aside the problems with the census mortality schedules that are well known among economic

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historians – they are discussed in an appendix – Parasites, Pathogens, and Progress only addresses mortality by upper respiratory, warm weather diseases, intestinal parasites/worms, and gastrointestinal tract diseases. To isolate mortality differentials, hookworm and malaria mortalities should be reported. Economists, epidemiologists, and historians have long known that disease rates were key in the development in 19th century US labor markets. Robert McGuire and Phil Coelho add to our understanding of proprietor labor market choices by race. The book is one of many articles and volumes that illuminate the importance of disease and health during economic development, and it is a useful contribution to social science graduate students, historians and interested epidemiologists. Scott Alan Carson ∗ School of Business, University of Texas, Permian Basin, 4901 East University, Odessa, TX 79762, USA ∗ Tel.:

+1 432 552 2195; fax: +1 432 552 2174. E-mail address: Carson [email protected]

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