Category Archives: malnutrition

Disease and Discrimination in Colonial Atlantic America


Reviewed by Michelle Ziegler

Dale Hutchinson. Disease and Discrimination: Poverty and Pestilence in Colonial Atlantic America. University of Florida Press, 2016. $85

Dale Hutchinson’s latest book fits into a recent trend of a more critical analysis of the role disease played in the demographic collapse of Native Americans in the Colonial period. After spending most of his career working on the Spanish Colonial system in Florida,  in Disease and Discrimination, he discusses the English and French colonies along the Atlantic seaboard.

By his own description, “this book is a series of narratives about changing landscapes of America — not only the natural landscapes, but the social, political and economic landscapes — and how they all contributed to the nutrition and health of natives and newcomers in the Atlantic coastal colonies” (p. 10) He goes on to warn the reader that landscapes he intends to paint are “neither exhaustive nor completely factual representations”; he has “chosen what to accentuate” (p.11).   In painting his landscapes he chose to use an informal, conversational tone that should make it the science easier to understand but also leads to a somewhat rambling style that sometimes lacks structure and yields uneven coverage. Disease and Discrimination is divided into four sections: ‘Of Apples and Edens’,  ‘Natives and Newcomers’, and Planters and Pestilence, and ‘Measuring the Lands’.

In the first section, he discusses landscapes and disease processes.  He opens the second chapter with a nice introduction to disease ecology and terminology but then moves on build off of McNeill’s “civilized disease pools”, which is now quite outdated. This would have been an ideal place to discuss syndemics, but he does not apply syndemic theory anywhere in the book. From here he moves into a rather free flowing discussion of plague pandemics. To be honest, I felt this discussion was out of place in a book that does not otherwise discuss bubonic plague. If he wanted to discuss the Old World origins of New World epidemics, then wouldn’t it have been better to discuss the disease ecology of an organism that made the ‘Columbian exchange’?

Opening with a discussion of syphilis, the next chapter discusses historical epidemiology and then the virgin soil epidemic hypothesis. As he notes, attenuation (weakening over time) is a core principle of the virgin soil hypothesis that lacks pervasive scientific evidence. It is not always in the best interest of a pathogen to become less virulent. Indeed, some times it’s quite the opposite.  Hutchison correctly points out that many of the examples of virgin soil epidemics were more likely to be caused by environmental contingencies like over crowding and poor sanitation on Indian reservations. Consulting David Jones (2003) work on refuting the virgin soil hypothesis would have been helpful here.

In the second section, Hutchinson reviews the European settlement, resource extraction and interactions with the Native tribes. He pays particular attention to the interactions between the French, Dutch and English colonists with the tribes, providing a handy table of seventeenth-century epidemics (table 4.1). It is interesting that all but one of these epidemics are credited to viruses (smallpox, measles, and influenza). Just over half of these epidemics were recorded by the Jesuits working in the French colonies. The 1630s were a particularly bad time for the colonies with measles, smallpox and other poorly recognized diseases impacted both the colonists and the Native American tribes in the Northeast. Hutchinson spends some valuable time discussing the differential impacts of the French and English interests in resource extraction, how that affected the landscape, and how the tribes moved, mixed and formed new entities due to attrition. Despite the reputation of epidemics among native tribes, the Europeans and Africans were ravaged by smallpox and measles as well.  Children born to both Europeans and Africans would have been as immunologically naive as the Native Americans (although variolation would have protected the few who received it from smallpox). Malnutrition affected all three groups but in different circumstances and to different degrees, as did the effects of war. A key difference between natives and newcomers is that more Europeans and Africans could immigrate to bolster their numbers, while Native Americans were still being enslaved or facing hostile encounters.

As the English began to attempt to transform the landscape, to ‘improve’ it, they began to build plantations, essentially recreating English manors in the New World. The New World landscapes did not yield easily and it dragged out long enough to spawn its own pestilence, known by contemporaries as ‘the seasoning’.  Hutchinson discusses the ecological causes including rice farming, deforestation, and diseases clusters (primarily typhoid and malaria).  The ‘seasoning’ is discussed in terms of immunology but it would have been helpful to consider the seasoning as a type of syndemic. In addition to gaining some immunological protection, the mortality rate was often very high in the first few years after arriving on the frontier.  In the Carolinas, rice farming learned from West African slaves quickly went from sustenance to export along with indigo and timber, taken for lumber and pine tar. The radical changes to the Carolina landscape primed it for its own blend of ‘seasoning’ microbes led by malaria.  The production environment of the Carolinas stimulated the import of African slaves who brought more malaria and were vulnerable to infections primed by enslavement conditions.

As the plantation landscape developed beyond the coast the stratification of society became extreme enough to be detected in osteological assessments of their health. Indentured servants and slaves both show evidence of a very hard life with overdeveloped muscle attachments on their bone indicating hard labor and evidence of malnutrition including signs of rickets, scurvy, and protein malnutrition. Corn (maize) replaced European grains, especially for servants and slaves. The caloric intake may be similar but the nutritional value is not. The typical diet of cornmeal, fatback, molasses, and an assortment of vegetables given to slaves is not a balanced diet. Fatback is a slice of pork under the back skin with hard fat with little or no muscle. It was often left to slaves and indentured servants to hunt or fish for most of their protein. Protein malnutrition is particularly evident in the remains of children who got the proportionally worst diet.  Through at least the early seventeenth century Native Americans continued to be a significant percentage of slaves, 20% in one Carolina census, and when census are compared, proportionally more Native American slaves were added than African. It was not until the end of the seventeenth century that the birth rate exceeded the death rate in Chesapeake, and even then, parents “were about as likely to die before their children reached their teens as their children were to reach maturity” (p. 137). Many children would be forced into early hard labor to survive. Although Hutchison does not discuss infection and nutrition as a syndemic, he does recognize the “synergistic relationship between nutrition and infectious disease” (p. 139). He notes that slave owners treated infectious disease but tended to ignore chronic or nutritional disorders that made the slaves more prone to serious infectious disease. I do wonder if this was not the attitude of most people except the richest families. It is unclear if they understood the nature of their malnutrition.

In the last section, Hutchinson turns more toward the first cities and urban life. In the last full chapter, he discusses the rapid development of New York City from the original Dutch colony to New York City on the verge of the Civil War. Early New York did not have a sanitary infrastructure so that it quickly became an extremely contaminated environment that was unhealthy for all of its inhabitants. Poverty was an issue for the inhabitants of New York from its earliest days. A constant stream of new poor immigrants meant that the labor market always had access to laborers for less than a living wage. Crowd diseases like smallpox and measles and filth diseases like dysentery always had a constant supply of vulnerable people to prey upon. The city streets were a zoo of animals that contributed to its disease ecology: hogs roamed the street eating refuse, mice and rats multiplied along with stray dogs and constant horse traffic. The city buzzed with urban mosquitoes and New York fell victim to Yellow fever 19 times between 1702 and 1822, but it still did not suffer as much or as often as Philadelphia or Charlestown (p. 166). By 1760 Beloe Island in New York Bay hosted a pesthouse for smallpox and yellow fever; fifty years later the island was ceded to the federal government for the construction of Fort Wood, now the foundation for the base of the Statue of Liberty. A sewage and water system was not installed in New York City until 1850.  As with other large cities in the more distant past, New York’s high mortality rate was offset by an even higher immigration rate into the city.

Hutchinson accomplished his goal of painting a very complex landscape of disease in Colonial America. To gain a more complete picture of the causes and effects of malnutrition and disease, social, cultural and economic factors have to be brought into play along with biological and ecological conditions.

It seems that this book overlapped in the publication process with the collected study Beyond Germs: Native Depopulation in North America, published in 2015. These two books complement each other even though there does not seem to be any contact between the authors. It seems we are on the verge of a new era of Native American studies that will be very welcome.


Jones, D. S. (2003). Virgin soils revisited. The William and Mary Quarterly, 60(4), 703–742.

Catherine Cameron, Paul Kelton, Alan Swedlund, Eds. Beyond Germs: Native Depopulation in North America. University of Arizona Press, 2015.


Leptin: Linking Malnutrition and Vulnerability to Infection

The correlation between malnutrition and vulnerability to infection has been well established (discussed previously here). While the immune dysfunction could be characterized it was not until the last 10-15 years that an exact mechanism began to resolve.

It all began with the discovery of a new hormone called leptin from an unexpected place, adipose tissue (fat cells). Leptin, a product of the obese (ob) gene, was discovered while looking for factors that regulate body fat. As a consequence of manipulating this gene in an attempt to regulate body fat, it was discovered that mice deficient in leptin had profound immune deficiencies.

The amount of leptin produced by adipose cells (fat cells) is directly proportional to the amount of fat in the cells. (The number of fat cells in adults does not change,  their size just shrinks or swells.) Leptin levels drop as body fat decreases or during fasting. Once leptin levels fall below a threshold, the lack of leptin puts the mammalian body into a starvation response. Areas of leptin activity are signaled by the production of the leptin receptor (OBR gene). Tissues producing the leptin receptor include areas of the hypothalamus that regulate body weight, bone mass, and appetite; ovarian cells, beta-cells of the pancreas, endothelial cells, and bone marrow stem cells, macrophages, and lymphocytes (1). Leptin influences cellular function by directly interacting with peripheral tissues including immune cells in lymph nodes, bone marrow, pancreatic function and bone homeostasis, but also by triggering hormonal changes in the brain, specifically in the hypothalamus. Study of leptin levels has opened previously unsuspected linked between central nervous system control and the development of the immune system.

The Hormonal Trigger of the Starvation Response

Leptin’s control of metabolism and the  immune system. (Ref. 2)

As long as leptin levels stay within normal levels, all of the functions displayed above function normally. As the leptin levels drop, many of these functions are adversely effected. It is a wide-spread trigger for a starvation response.  Why cripple the immune response during starvation? My best guess would be because of the huge energy expenditure required to keep the immune response running normally, especially in cellular proliferation.

When leptin levels drop too low, physiological dysfunction occurs in haematopoiesis (blood cell production), bone metabolism, glucose metabolism and angiogenesis (blood vessel production and maintenance) and immune suppression involving both the innate (non-specific) and adaptive immune system. During malnutrition, the size of the thymus gland shrinks with diminished T cell development. This may be one of the long-term consequences of childhood malnutrition. Children with congenitally low leptin levels have a higher mortality rate due to childhood infections (2).

Leptin modulates immune function (ref. 1)

With all the functions illustrated above, it’s not very surprising that malnutrition is the second most common cause of secondary immune suppression today (2). Alternatively, high leptin levels in obese people have also been linked with increased vulnerability to infection possibly through the development of leptin resistance due to prolonged exposure to excessively high levels of leptin (2). Food for thought considering that obesity was one of the only risk factors for a poor outcome during the recent H1N1 influenza pandemic. We have come to expect malnutrition induced immune suppression, but we may also have to consider over-nutrition induced immune suppression and/or autoimmunity as outcomes of immune dysregulation due to leptin resistance.


[1] La Cava, A., & Matarese, G. (2004). The weight of leptin in immunity Nature Reviews Immunology, 4 (5), 371-379 DOI: 10.1038/nri1350

[2] Procaccini C, Jirillo E, & Matarese G (2012). Leptin as an immunomodulator. Molecular aspects of medicine, 33 (1), 35-45 PMID: 22040697

Health and Healing Sessions at Kalamazoo 2012

Regular readers might remember that last fall I was regularly posting and tweeting a call for papers for a session on health and healing in early medieval Europe for the International Congress on Medieval Studies at Kalamazoo in 2012. The schedule for the Congress is now out so I can tell everyone all about it. As you can see I got a great response to my CFP and the Congress committee let me put together two sessions. So without further ado, here are the sessions co-sponsored by The Heroic Age and Medica: The Society for the Study of Healing in the Middle Ages.

Session 264 (Friday 1:30)
Schneider 1255

Health and Healing in Early Medieval Britain and Ireland
Presider: Deanna Forsman, North Hennepin Community College

  • Famine and Pestilence in the Irish Sea Region, 500–800 AD: Michelle Ziegler
  • Regional Patterns of Health in Early Medieval Ireland: Distributions of Non-specific Stress Indicators: Mara Tesorieri, Univ. College Cork
  • The Experience and Practice of Medicine by the Laity in Anglo-Saxon England: Julia Bolotina, Univ. of Cambridge
  • By Rome, or By Spain? Possible Mediterranean Origins of Irish Holy Well Veneration: Silas J. Mallery, North Hennepin Community College

Session 319 (Friday 3:30)
Schneider 1255

Medical Texts of the Early Medieval Mediterranean
Presider: Michelle Ziegler

  • Animal-Derived Medicines in Early Medieval Pharmacy: Jayna Brett, Centre for Medieval Studies, Univ. of Toronto
  • A Medieval Hippocrates? The construction of the Articella during the eleventh century.: Marco A. Viniegra, Harvard Univ.
  • Book-Learning and Medicine in Medieval Byzantium: Theory and Practice in the Alexiad of Anna Comnena: Glen M. Cooper, Brigham Young Univ.