John F. Martin
Professor Emeritus
Ph.D., University of Chicago
SHESC Themes: Culture, Heritage and Identity; Biological, Social and Cultural Dimensions of Human Health
Field Specializations: Hunter-Gatherers, Kinship, Medical Anthropology, Population Dynamics, Social Organization, Sociocultural Anthropology
Regional Focus: North America (Southwest)
Contact: John F. Martin, SHESC 274
Research:
John F. Martin's research focuses on the interrelations between biology and the economic and political dimensions of social life. He has published on the effects of economic variables and population structure on the sizes and compositions of local groups among hunter-gathers, the effects of population variables on kin marriage systems and on systems of inheritance and succession.
More recently, this focus on the interrelations of power and economics with biology has led him to analyses of the epidemiology of type 2 diabetes (AKA non-insulin dependent diabetes mellitus) and to experimental studies exploring its physiological bases. The experimental work confirms previous research that indicates that, while fetal protein malnutrition permanently impairs insulin secretory capacity, it does not induce insulin resistance. Hence, the pathway to diabetes that involves insulin resistance and impaired insulin secretory capacity does not begin in the diabetic's fetal life unless post natal over-nutrition induces insulin resistance. However, fetal malnutrition induced impaired insulin secretory capacity does predispose fetally malnourished females to hyperglycemic pregnancies which in turn predispose their offspring to insulin resistance and chronic hyperinsulinemia.
His preliminary findings suggest that the chronic hyperinsulinemia through its effects on free fatty acid and glucocorticoid concentrations eventually reduce insulin secretory capacity and leads to diabetes. Since high diabetes prevalence rate populations are uniformly populations that have recently suffered widespread, severe malnutrition due to political and economic factors, the suggestion is that their diabetes epidemics are rooted in the fetal malnutrition of women who were conceived during those famines because the offspring of those women were insulin resistant and prone to both diabetic pregnancies and diabetes.
Presently, Martin, along with colleagues in anthropology and nutrition, are exploring the possibility suggested by the cited research, that control of maternal metabolism during pregnancy may break the cycle in which insulin resistance and a predisposition to diabetes is transmitted from mother to offspring through the mother's gestational hyperglycemia.
Research Projects:
Pathways to Insulin Resistance And Type II Diabetes
Select Publications:
Benyshek, D., Johnston, C. & Martin, J. F. (2006). Glucose metabolism is altered in the adequately nourished grand-offspring (F3 generation) of rats malnourished in utero. Diabetologia, 49(5), 1117-1119.
Benyshek, D., Johnston, C. & Martin, J. (2004). Post-natal diet determines insulin resistance in fetally malnourished low birthweight rats (F1) but does not modify the insulin resistance of their offspring (F2). Life Sciences, 74(24), 3033-3041.
Benyshek, D., Martin, J. & Johnston, C. (2001). A reconsideration of the origins of the type 2 diabetes epidemic among Native Americans and the implications for intervention policy. Medical Anthropology, 20, 25-64.
Martin, J., Johnston, C., Han, C-T. & Benyshek, D. (2000). Nutritional origins of insulin resistance: A rat model for diabetes-prone human populations. Journal of Nutrition, 1130, 741-744.