Type II Diabetes, the Modern Epidemic of American Indians in the United States

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Gail King


Hill (1997) stated that in 1940 the occurrence of diabetes among Native Americans was almost unknown. Diabetes began appearing in 1950, until during the 1960s, it became a common condition. The incidence of diabetes exploded in the 1970s, becoming an epidemic. Presently, in the 1990s, nearly every Native American is involved either personally with diabetes, or with family and friends with diabetes. It has been called the new smallpox. The difference is that smallpox killed swiftly, but diabetes "kills softly, one fry bread at a time" (Hill, 1997:27). During the past ten years increasing concern about the epidemic of diabetes has caused the American and international medical community, the Indian Health Service, and American Indian communities to hold many conferences in an effort to identify the underlying factors and propose a solution. Bill Burke (Umatilla Tribe of Pendleton, Oregon), who attended one such conference, stated that diabetes has become a normalized condition among American Indians and that he does not want to lose another relative or friend. For him it was not a question as to whether or not you are going to become diabetic, but when. His opinion reflected the intense concerns of members of the Native American community (Gohdes and Bennett, 1993; Nashville Area Indian Health Service Diabetes Program, 1996; Hill, 1997).

My hypothesis is that the lifestyle and social conditions of particular tribes along with underlying genetic susceptibility are factors, which contribute to the prevalence of Type II Diabetes among Native Americans of the United States. This paper is an endeavor to gather information concerning the adaptive mechanism involved in the cause of Type II Diabetes among the Native American population, about how it differs from the rest of the population of the United States, how economic and social aspects of people living in areas served by the Indian Health Service influence the prevalence of diabetes, and the prognosis for delaying or stopping the onset of diabetes.

Type II Diabetes Mellitus

Type II Diabetes is also referred to as non-insulin dependent diabetes (NIDDM) or adult-onset diabetes. Individuals with NIDDM may have insulin concentrations that appear to be normal or high. This characteristic of Type II Diabetes sets it apart from Type I Diabetes (Insulin Dependent Diabetes, IDDM, or juvenile-onset diabetes), because in IDDM the pancreas no longer produces insulin. IDDM is the autoimmune form and results from the destruction of the pancreatic beta cells (Davidson, 1998). IDDM is associated with genetic mutations in the human leukocyte blood group (HLA) system (Shapiro, 1997). Approximately 75% of patients, who are diagnosed with this form of diabetes, are below 30 years of age (Davidson, 1998).

In 1962 it was proposed that there are certain individuals who respond to the ingestion of food, by producing insulin at a "greater-than-normal availability" (Neel, 1962:355). It was not known at this time that this was a specific type of diabetes, which would later be known as Type II Diabetes. As research continued it became evident that in this form of diabetes insulin is produced, but fails to perform its metabolic function normally. When carbohydrates are ingested beta cells of the pancreas release insulin in response to elevated levels of glucose circulating in the blood (Bindon, 1988). (Knowler et al (1993) stated that overt diabetes (NIDDM) with worsening hyperglycemia may then occur as a result of beta cell defects or exhaustion. Insulin resistance may occur if insulin receptor sites on cell walls (peripheral muscle mass) are continually bombarded with elevated levels of insulin in the bloodstream (DeFronzo, 1982). McGarry (1991) reviewed several studies about the development of NIDDM and concluded that diabetes is caused by abnormal fat metabolism rather than sugar metabolism. The pathophysiology of NIDDM involves both genetic and environmental variables (MCGarry, 1991; Shapiro, 1997).

Complications can be peripheral vascular disease (leads to disruption of blood circulation in extremities, causing lower leg amputations) and diabetic neuropathy (leads to loss of feeling in limbs), proliferative diabetic retinopathy (lesions in the retina of the eye, bleeding, which leads to blindness), kidney disease (leads to kidney failure), coronary artery disease (leads to heart attack), stroke, periodontal disease, infection, ketoacidosis (leads to the build up of ketone or acetone bodies in the blood), and hypertension (Nashville Area Indian Health Service Diabetes Program, 1996).

Etiology of Non-insulin Dependent Diabetes

The "Thrifty" Genotype

Extensive research has been conducted to explain why a serious condition such as NIDDM has increased to epidemic proportions among American Indians, especially during modernization. Neel (1962) proposed the "thrifty"genotype model to explain why diabetes mellitus occurs at such high rates in some populations. He used this model to explain why excessive caloric intake, and rapid as well as elevated insulin secretion had enabled these populations of hunter-gatherers to survive sporadic food availability under feast or famine conditions. Since 1962 an updated model has been developed because of increasing information about the metabolism of diabetes mellitus (Cahill, 1979; Neel, 1982; Bindon, 1983; Baker, 1984; Zimmet, 1989; Bindon and Baker, 1997).

One such revision was by Neel (1976) himself, who stated that the "thrifty" genotype model involved a distinct type of diabetes mellitus, NIDDM, which was separate in etiology from IDDM. He stated that heterogeneity of diabetes had finally been recognized. In 1962 he had focused on the acute symptoms of IDDM. He revised his hypothesis, because of the evidence showing that civilized man had a relatively high frequency of diabetes mellitus. Since diabetes occurred at a low frequency in primitive man, Neel felt that further research must be undertaken. He speculated that the "thrifty genotype" could be needed in the future, considering the problems facing the world with overpopulation and decreasing food supplies (Neel, 1976).

The etiology of NIDDM is extremely complex and the "thrifty" genotype model was not intended to account for NIDDM in all populations. It is used to explain why populations, such as Polynesians and American Indians, have substantial rates of NIDDM (Bindon and Baker, 1997).

Wendorf (1989) hypothesized that the Amerindian "thrifty" genotype arose from selective pressures during the Paleoindian migration into the Americas south of the continental glaciers. These populations moved quite rapidly from a harsh tundra environment into a new environment at lower latitudes, south of continental glaciers. He stated that these Paleoindian hunter-gatherers did not have the opportunity to gradually adapt to lower latitude environments and prey species as they moved south from eastern Beringia. The "thrifty" genotype would have benefited them during this period of adjustment to new food resources.

Wendorf (1989) compared these Paleoindians to the hunter-gatherers ancestral to Athapaskan peoples who migrated south from Beringia somewhat later through a widened corridor containing environments more typical of the sub-Arctic. The Athapaskans had a longer time to adapt to their environment. The "thrifty" genotype in these people would not have been as necessary for survival. Wendorf cited studies that showed that among Amerindians only the Eskimo and certain Athapaskans, such as the Navajo and Apache in the Southwest United States and Alaska and Canada, have NIDDM rates which compared to Caucasians (Weiss et al., 1984; Szathmary, 1986) He pointed to other studies on descendants of the Paleoindians (Clovis and Folsom), such as the Pima and Papago (Wendorf, 1989). The Pima of Arizona have the highest reported rate of NIDDM reported in the world literature (Knowler et al, 1978). Wendorf cited another study, reported by West (1974), in which obesity in several Indian tribes in Oklahoma was thought to be linked to NIDDM. Knowler et al (1981) found that although obesity was strongly related to NIDDM in the Pima and Papago, that a study conducted by Nagules-paran et al (1980), showed that the level of insulin resistance was great enough to point to other causes for NIDDM than could be explained by obesity.

The "thrifty" genotype is based on the biochemical responses an individual has when glucose is taken in as part of the diet (Neel, 1962). Bindon and Baker (1997) stated that when insulin is released by the beta cells of the pancreas because of the presence of circulating glucose, an intricate biochemical response begins. The response is different for individuals with the "thrifty" genotype. In the periods of feast, hypersecretion of insulin by the beta cells allows a more efficient storage of the caloric excess. This exaggerated secretion of insulin, when carbohydrates are ingested, is known as hyperinsulinemia (Zimmet, 1989). This stored excess is there when there is a deficit in available food caloric intake (Bindon and Baker, 1997).

Bindon (1988) stated that this was the primary force for selection in Neel's model (1962), which he based on the hypothesis that hunter/gatherer bands underwent periods of feast and famine. The individuals who were genetically endowed with the "thrifty" genotype had a selective advantage, because of their increased ability to store energy for use during times of famine (Bindon, 1988). Theses genes would have been the most likely to have been passed on in certain groups, who survived the feast or famine conditions, and could explain the prevalence of high NIDDM rates and high obesity rates (Zimmet, 1982).

The "Non-thrifty" Genotype

Allen and Cheer (1996) stated that although the "thrifty" genotype concept presupposes the existence of a "non-thrifty" genotype, there has been very little discussion of this in the literature. They suggest the reason for this neglect may be that the "thrifty" genotype was originally defined in contrast to an Euro-American norm. Euro-American anthropologists are more concerned with the anthropological "other" than with themselves (Allen and Cheer, 1996:831). Anthropologists have been willing to accept the standard and rather facile explanations for why the "thrifty" genotype does not exist in all human populations (Allen and Cheer, 1996). Allen and Cheer (1996) believe, though, that the interest in the "thrifty" genotype has also been driven by an attempt to understand and treat health problems associated with diabetes and obesity, which are very common in recently Westernized populations.

The explanation for the "non-thrifty" genotype is currently inadequate. Abundant food in Europe has not long been a feature of the diet. An explanation for this genotype might be the following: The European populations living at high latitudes were hunter-gatherers, who had limited access to simple sugars. After Indo-European agriculturalists and pastoralists migrated into these areas, the hunter-gatherers bioculturally adapted to milk in their diet. A strong selection for lactose absorption ability could have occurred at these high latitudes to compensate for the loss of vitamin D in calcium uptake. Diabetes could have resulted when populations with low simple-sugar intake were introduced to lactose. The simple sugar, lactose, promotes high-insulin secretion(Allen and Cheer, 1996). It was proposed that diabetes became the "price" not of civilization, but of the use of lactose(Allen and Cheer, 1996:838). Until the use of lactose became established, both culturally and genetically, selection was for "non-thrifty" genotype individuals. In order to study the "non-thrifty" genotype further, observing other populations as they adopt the Western diet provide an answer. Studying populations with high NIDDM rates and those who are exhibiting increasing NIDDM rates could prove relevant to the "non-thrifty" genotype hypothesis. Lactose consumption causes a high insulin response. Susceptibility to NIDDM in certain populations could be enhanced by lactose consumption (Allen and Cheer, 1996).


One of the truisms of human biological studies of modernization is that mean adult weight and prevalence of obesity usually increase with modernization (McGarvey et al., 1989; Shapiro, 1939; Reed et al., 1970; Bindon and Baker, 1985).

A "thrifty" genotype model was proposed by Zimmet et al (1989) to provide an answer as to why high frequencies of NIDDM and obesity among modernizing Oceanic populations. Figure 1 below is a modification of this model and was proposed by Bindon and Baker (1997).

Figure 1  from Bindon and Baker, 1997:204.

When modernization occurs, traditional diets and physical activities based on local subsistence practices change to a diet of purchased foods and wage-employment occupations, with reduced physical activities. According to researchers the change to more modern or Western diets and to sedentary activities have resulted in a positive energy balance with increased body weight and adiposity (McGarvey et al., 1989; Ringrose and Zimmet, 1979; Trowell, 1981; Coyne et al., 1984; Koike et al., 1984).

The modern diet of the United States has evolved in content. Protein content has decreased and fat content has increased. Vitamin and mineral content have changed because of unavailability of fresh produce grown locally (Hill, 1997). Beginning in 1910 until 1980, one of the major changes in the American diet was from the consumption of more complex carbohydrates to low molecular weight, simple, refined sugars. Not only have there been changes in the types of carbohydrates consumed, but the recent trend in replacing sugar by nonnutritive sweeteners has grown tremendously. Saccharin was discovered in 1879 and for the past 20 years, it has been the most widely used, at the rate of about 5,000 tons per year. During the past ten years, several nonnutritive sweeteners have become available in various parts of the world. These include: cyclamates, aspartame, acesulfame-K, alitame, sucralose, stevioside, and theumatin. These so-called dietetic foods are marketed toward people who want to lose weight. Carbohydrates are often 70% to 80% of the mass and two-thirds of the calories. When they are replaced with a nonnutritive sweetener, the caloric content decreases, caloric density will increase, and fat content will increase (Gracey et al., 1991).

Modernization tends to decreases physical activity, therefore lack of exercise appears to be a major contributory factor in onset of diabetes. As modernization has progressed in the United States, our daily lives require very little physical activity. Riding in a car, watching television and movies, playing video games, and sitting at computers require very little muscle movement. Many Native Americans probably have at least one of these. Minuk et al (l981); DeFronzo and Ferrannini (1982); Krotkiewski et al (1985); Bindon and Baker (1997) reported that insulin receptors on the peripheral muscle cells of NIDDM patients become more sensitive to binding with circulating insulin with increasing activity. The amount of insulin secreted by the pancreas in response to glucose in the blood decreases with physical activity. This reduces hyperinsulinemia and its accompanying metabolic effects.

Other Underlying Factors

The usefulness of the clinal analysis was proposed by Birdsell (1972) to analyze simple genetic traits. Ritenbaugh (1981) used clinal analysis to show the distribution of NIDDM prevalence rates. Clinal maps of diabetes prevalence rates were created for female and for male members of Native American tribes living in Arizona plus Zuni (living on the border of eastern Arizona). These maps were compared to a simplified isothermal map of the January mean-minimum temperature, and the male NIDDM rates showed "striking" similarities (Ritenbaugh, 1981:185). Further statistical analysis also showed a significant correlation between the male NIDDM rate and the January isothermal map (Ritenbaugh, 1981).

In Arizona, vegetation at different altitudes varies directly with moisture and temperature. If there is an environmental component involved in Type II diabetes, its distribution may be similar to the distribution of an environmental factor, such as moisture and temperature, which may also be related to altitude. It was concluded that while there is in some sense a genetic predisposition to every condition that occurs in the human body, the environmental factors in diabetes seem likely to be highly significant and our understanding of them would provide the most promising route to prevention (Ritenbaugh, 1981).

Trowell et al (1973) proposed that dietary fiber-starchy foods are conducive to the development of diabetes mellitus in susceptible human genotypes. A fiber-depleted starchy food is defined as one in which processing has removed a considerable amount of the fiber.

Experiments using sand rats, which were fed a very-low-natural fiber synthetic diet, exhibited decreased carbohydrate tolerance, increased plasma insulin levels, and increased body weight (Hackel et al, 1967). Trowell et al (1975) stated it would appear that fiber-reduced food promoted obesity and diabetes. They also pointed out that certain rodent mutants develop diabetes mellitus, and usually obesity, if fed various cereal foods and that health in both of these diseases improved if dietary intake is reduced. (Trowell et at (1975) suggested that a very high prevalence of diabetes, such as that found in the Pima Indians, may reflect sudden change from high-fiber carbohydrates of food-gatherer huntsmen to low-fiber cereal products of Westernized diets.

Medical Care for Native Americans

Indian Health Service

Since 1955, the Indian Health Service (IHS) has had the responsibility for providing comprehensive health services to American Indian and Alaska Native people in order to elevate their health status to the highest possible level. It is the principle federal health care provider and health advocate. The mission of the IHS is to provide a comprehensive health services delivery system for federally recognized American Indians and Alaska Natives with opportunity for maximum Tribal involvement in developing and managing programs to meet their health needs. It exists as an agency within the Department of Health and Human Services.

The Indian Health Service responsibilities extend to all or part of 35 states known as Reservation States. It operates thirty-seven hospitals, sixty-one health centers, four school health centers, and forty-eight health stations.

The Indian Health Service responsibilities extend to all or part of 35 states known as Reservation States. It operates thirty-seven hospitals, sixty-one health centers, four school health centers, and forty-eight health stations. The Indian Health Service is comprised of 12 regional administrative units called Area Offices. They are as follows: Aberdeen, Alaska, Albuquerque, Bemidji, Billings, California, Nashville, Navajo, Oklahoma City, Phoenix, Portland, and Tucson (U.S. Department of Health and Human Services, 1997) Chart 1 (click here)  shows a map of the regional Areas.

Source of Chart 1: U.S. Department of Health and Human Services. Regional Differences in Indian Health, 1997: 17.

Prevalence Rates of NIDDM in Native Americans

Comparison to U.S. Rate

The rates of NIDDM ranged from 1% among adult Alaskan Athabaskans (Mouratoff, 1969) to approximately 50% among adult Pima of Arizona and neighboring states (Bennett, 1971). During the same period the prevalence rate was 6% among U. S. whites (Rittenbaugh, 1981).

The National Center for Chronic Disease Prevention and Health Promotion reported in 1996 the age-adjusted prevalence of Type II diabetes among all American Indian/Alaska Natives (AI/AN) was 7.5%, which was 2.5 times the prevalence in the U.S. population (3%).

Among AI/AN males <45 years, the age-adjusted prevalence of diabetes was 1.9 times the prevalence in the U.S. males in the same age group; among AI/AN males 45-64 years, the prevalence was 2.7 times the prevalence in the U.S.; and among AI/AN males >65 years, the prevalence was 1.8 times the prevalence in the U.S.

Among AI/AN females <45 years, the age-adjusted prevalence of diabetes was 2.1 times the prevalence in the U.S. females in the same age group; among AI/AN females 45-64 years, the prevalence was 3.5 times the prevalence in the U.S.; and among AI/AN females >65 years, the prevalence was 2.3 times the prevalence in the U.S. The prevalence of diabetes in all Indian Health Service Areas, except Alaska, was 1.4-3.7 times the prevalence in the U.S (Center for Disease Control and Prevention, 1998).

Prevalence Rates of IHS population, U.S. Whites, U.S. Blacks

Chart 2

Chart 2 shows the age-adjusted prevalence of diabetes (percent) by gender in the Indian Health Service population for 1996. Age adjustment was computed by using the 1980 U.S. population. The prevalence rates were obtained from statistical information compiled by the U.S. Centers for Disease Control and Prevention, February 14, 1998. On both charts the U.S. White and U.S. Black rates are male and female rates added together.

Chart 2 displays noticeable differences between male and female prevalence rates in Native American rates, with female rates always being higher than male rates, except in the U.S. Blacks and the U.S. Whites rates. There are averaged female/male rates. Rates of Native Americans, except in Alaska are significantly higher than U.S. Whites. U.S. Black rates are higher than Alaska and California Native Americans only and significantly higher than U.S. Whites.

Pima Indian Studies

Knowler et al (1993) stated that the ancestors of the Pima Indians of the Gila River Indian Community of central Arizona are thought to have lived near that area for about 2,000 years. According to Haury (1976) the Pimas descended from the Hohokam, who moved into the Gila River Valley from Mexico around 300 B.C. Their successful adaptation to desert life continued until settlement of the area by European-derived people, which led to the diversion of the water supply and a disruption of their traditional agricultural lifestyle. It is believed that the Pimas were adapted to a feast-famine situation, where there were sporadic disruptions in their food supplies. Knowler et al (1993) believe that the recent increase in diabetes incidence following the availability of an abundant food supply points out that the efficient storage of energy during periods of feast and famine probably has led to obesity, insulin resistance, and diabetes.

Kuller (1993) stated that studies of diabetes risk among the Pima Indians are some of the best examples of the interplay between epidemiology, genetics, clinical research, and basic metabolic studies. This research has yielded more information about the etiology and natural history of NIDDM than any other research.

Bogardus (1993) reported that the Pima Indians of Arizona have the highest reported prevalence of diabetes mellitus of any population in the world and it is exclusively NIDDM. Knowler et al (1993) reported that the highest rates were found in 45+ years. For males the diabetes prevalence rate was 67% and for females it was 73%. See Table 1 below for complete analysis of age groups and length of study from 1965-1990. Bogardus (1993) stated that NIDDM in the Pima Indians is characterized by four major metabolic abnormalities, which include obesity, abnormal insulin secretion, insulin resistance, and excess hepatic glucose output. Cross-sectional studies as well as ongoing longitudinal studies suggest that the natural history of the disease begins with insulin resistance, after which insulin secretion fails. Increase in hepatic glucose output then occurs resulting in increasing fasting hyperglycemia. Obesity is not the sole cause for the insulin resistance that precedes the development of fasting hyperglycemia. Insulin resistance tends to be family related and genetic determinants are suggested from the trimodel frequency distribution of insulin action in vivo (Bogardus, 1993).

Table 1 below shows the prevalence (%) of diabetes in Pima Indians by age, sex, and time periods ranging from 1965 to 1990.

Table 1.













































































Knowler et al., 1993:218

For each period, data from each subject obtained at the biennial examination closest to the midpoint of the period are used.

Data from Table 1 clearly show a significant increase in diabetes prevalence rate after the age of 25 for both males and females, and females in the majority prevalence rates shown have a higher prevalence rate of diabetes, when compared to males.

NIDDM Rates and Indian Blood Degree

In 1988 the Strong Heart Study was conducted in central Arizona, southern Oklahoma, and North and South Dakota on cardiovascular disease. Participants in the study were enrolled members of one of the 13 Indian tribes or communities living in the survey areas: the Pima/Maricopa/Papago of the Gila River, Salt River, and Ak-Chin Indian Communities near Phoenix, Arizona; the Apache, Caddo, Comanche, Delaware, Fort Sill Apache, Kiowa, and Wichita in southwestern Oklahoma; and the Oglala Sioux and Cheyenne River Sioux in South Dakota and the Devils Lake Sioux in the Fort Totten area of North Dakota. Each individual provided information as to amount of American Indian heritage. Medical records, physical examinations, and personal interviews were conducted on each participant. NIDDM prevalence rates were compiled from this information.

Chart 3 below was compiled from this information to show how the degree of Native American ancestry, gender, and obesity affects NIDDM rates. (Lee et al., 1995).

Chart 3 Source of Chart 3:  Lee et al., 1995: 606.

The rate of diabetes increased consistently in all three centers with amount of Indian ancestry. The prevalence in individuals with 50% or more Indian ancestry was significantly (P<0.0001) higher than that in those with <50% Indian ancestry. In South and North Dakota, diabetes rates in the full-blood Indians were more than four and nine times higher in men and women, respectively, than in the Indians with <25% Indians ancestry. The full-blood Indians in Oklahoma had more than three times higher diabetes rates, than those reporting 25-49% Indian ancestry. The differences in diabetes rates among the groups defined by degrees of Indian ancestry are highly significant (P<0.01) in both the Dakotas and Oklahoma groups, even after controlling for the effect of obesity (Lee et al, 1995).

NIDDM Rates, Educational Level, and Economic Conditions

Using NIDDM rates from each Indian Health Service area and U.S. population (percentages) to compare with statistical information, also from each Indian Health Service area and U.S. population (percentages), compiled by the United States Department of Health and Human Services, five graphs were created. The points on the graphs are from left to right as follows: Aberdeen, Alaska, Albuquerque, Bemidji, Billings, California, Nashville, Navajo, OK City, Phoenix, Portland, Tucson, and United States population. Below Graphs four and five show female and male NIDDM rates compared to female and male unemployment rates respectively. Graph six shows NIDDM rates compared to <poverty level rates. Graph seven shows NIDDM rates compared to rates of high school graduates. Chart eight shows NIDDM rates compared to rates of college graduates.

Chart 4

Chart 5

Chart 6

Chart 7

Chart 8

The following is an explanation of the categories used in Charts 4, 5, 6, 7, and 8:  High School Graduate - age 25 and older, 1990 census state-level Indian data, Bachelor's Degree - age 25 and older, 1990 census state-level Indian data, Females Unemployment - age 16 and older, 1990 census state-level Indian data, Poverty Level - includes data for 35 Reservation States (South Carolina and Indiana were added as Reservation States in 1994 and 1995, respectively, 1990 census state-level Indian date.

Correlation of NIDDM Prevalence rates and Socioeconomic Indicators




Female Unemployment Rates

.443 .013

Male Unemployment Rates

.141 .206

Percent Below poverty level

.397 .021

Percent High school graduates

.317 .045

Percent College graduates

.208 .117

Female unemployment rates and below poverty level rates show the most correlation with NIDDM rates. High school graduate rates show a slight correlation. Male unemployment rates and college graduate rates show no correlation

Prognosis and Conclusion

The risk of developing diabetes in the American Indian/Alaska Native population is high. It is extremely high in the age groups of 45 years and older in tribes residing in several Indian Health Service Areas (Prevalence of Diabetes in American Indians and Alaska Natives, 1996). The U.S. Department of Health and Human Services (1997) compared the Native American population and the U.S. (all races) population. It was found that 33% of the Native American population and that 22% U.S. All Races are under 15 years. Considering the present rate of increase in NIDDM prevalence rates, and that one-third of the Native American population is under 15 years, the prevalence of NIDDM will increase significantly as this younger population ages.

The Indian Health Service Diabetes Program believes that Type II Diabetes can be effectively treated and possibly even prevented by appropriate lifestyle modifications. The Program lists the four causes for diabetes as follows: genetic tendency, inactivity, obesity, and a diet high in sugar. NIDDM is associated with factors that are modifiable, such as obesity and physical inactivity and with factors that are non-modifiable such as heredity and older age (Prevalence of Diabetes in American Indians and Alaskan Natives, 1996).

This paper has attempted to show the in-depth research that has been carried out in order to establish the underlying causes of NIDDM. I feel that the data collected from this research has conclusively identified a genetic basis for NIDDM among American Indians. When Neel (1962) proposed the "thrifty" genotype, he was indeed summing up a unique characteristic of the American Indian. He did not understand, at that time, that this was associated with a different type of diabetes, separate from Type I Diabetes. He did not realize several underlying factors: that the migratory patterns of the Americans Indians into the American continents could have affected this genotype; that the higher the Indian Blood degree, the higher the risk for developing NIDDM; that there would be a higher prevalence of NIDDM among females; that the onset of NIDDM would be age related, with a significant increase in NIDDM rates at approximately the age of 25 and with a dramatic increase in NIDDM rates at the age of 45 years and older. In 1962 Neel could not predict how profound the effects of modernization on the American Indian would be when Western diets and more sedentary patterns as wage earners were gradually transforming their way of life. He could not predict that social conditions, such as unemployment, poverty level, and level of education would also have an effect. NIDDM is a very complex modern epidemic for the American Indian and will continue to be, until it is fully understood by those who are at risk for NIDDM.



Allen JS and SM Cheer (1996) The non-thrifty genotype. Current anthropology, 37(5):831:842.

Baker PT (1984) Migration , genetics, and the degenerative diseases of South Pacific Islanders. In AJ Boyce (ed): Migration and Mobility. pp. 209-239, Taylor & Francis, Ltd., London. Ltd., pp 209-239.

Bennett PH, TA Burch and M Miller (1971) Diabetes Mellitus in American (Pima) Lancet, II:125-128.

Bindon JR (1983) The role of modernization in changing patterns of human adaptation: A case study among Samoans. Southern Anthropological Society Meeting Abstracts:8.

Bindon JR (1988) The natural history of diabetes in Samoa. Collegium Athropologicum, 12 (suppl): 85.

Bindon JR and PT Baker (1985) Modernization, migration and obesity among Samoan adults. Annals of Human Biology, 12:67-76.

Bindon JR and PT Baker (1997) Bergmann’s rule and the thrifty genotype. American Journal of Physical Anthropology, 104:201-210.

Birdsell JB (1972) The problem of the evolution of human races: classification or clines? Social Biology, 19:136-162.

Bogardus C (l993) Insulin resistance in the pathogenesis of NIDDM in Pima Indians. Diabetes Care, 16(1):228-231.

Burrows NR (1998) Prevalence of diabetes in American Indians and Alaskan Native, 1996. Centers for Disease Control and Prevention, Atlanta, Georgia.

Cahill GF (1979) Human evolution and insulin dependent (IDD) and non-insulin dependent diabetes (NIDDM). Metabolism, 28(suppl. 1):389-393.

Coyne T, J Badcock and R Taylor (1984) The effect of urbanization and western diet on the health of Pacific Island population. South Pacific Commission Technical Paper No. 186, Noumea, New Caledonia.

Davidson, Mayer B. (1998) Diabetes Mellitus, Diagnosis and Treatment, 4th Edition. W.B. Saunders Company, Philadelphia.

DeFronzo RA and E Ferrannini (l982) The pathogenesis of non-insulin dependent diabetes: an update. Medicine, 61:125-140.

Gohdes D and PH. Bennett (1993) Diabetes in American Indians and Alaska Native. Diabetes Care, 16(1):214-215.

Gracey M, N Kretchmer, and E Rossi (1991) Sugars in Nutrition, Raven Press, New York.

Hacket DB, HE Lebovitz, LA Frohman, E Mikat, and K Schmidt-Nielsen (1967) Effect of calorie restriction on the glucose tolerance and plasma insulin of the sand rat. Metabolism, 16:1133-1139.

Haury EM (1976) The Hohokam: Desert Farmers and Craftsmen, Excavation at Snaketown, 1964-1965. University of Arizona Press, Tucson.

Hill MA (1997) The diabetes epidemic in Indian country. Winds of Change, American Indian Science and Engineering Quarterly, Summer:26-31.

Koike G, O Yokono, S Lino, M Adachi, T Yamamoto, T Puloka, and M Suzuki (1984) Medical and nutritional surveys in the Kingdom of Tonga: Comparison of physiological and nutritional status of adult Tongans in urbanized (Kolofo-ou) and rural (Uiha) areas. Journal of Nutritional Science and Vitamins, 30:341-356.

Knowler WC, Bennet PH, Hamman RF, and Miller M (1978) Diabetes incidence and prevalence in Pima Indians: A 19-fold greater incidence than in Rochester, Minnesota. American Journal Epidemiology, 108: 497-505.

Knowler WC, Pettit DJ, Savage PJ, and Bennett PH (1981) Diabetes incidence in Pima Indians: Contribution of obesity and parental diabetes. American Journal of Epidemiology, 113:144-156.

Knowler WC, MF Saad, DJ Pittitt, RG Nelson, and PH Bennett (1993) Determinants of diabetes mellitus in the Pima Indians. Diabetes Care, 16(1):216-227.

Kuller LH. (1993) Diabetes Care, 16(1):380-382

Lee ET, BV Howard, PJ Savage, LD Cowan, RR Fabsitz, AJ Oopik, J Yeh, O Go, DC Robbins, and TK Welty (1995) Diabetes and impaired glucose tolerance in three Indian populations age 45-74 years. Diabetes Care, 18(5):599-610.

McGarry J (1991) What if Minowski had been Ageustic? An alternative angle on diabetes. Science, 258:766-770.

McGarvey ST, JR Bindon, DE Crews, and DE Schendel (1989) Modernization and adiposity: causes and consequences. Human Population Biology, 263-279, Oxford University Press, London.

Mouratoff, GJ (1969) Diabetes Mellitus in Athabaskan Indians. Diabetes, 18:29-35.

Nagulsparan M, Savage PJ, Mott DM, Johnson GC, Unger RH, and Bennett PH (1980) Increased insulin resistance in obese glucose-intolerant Southwestern American Indians: Evidence for a defect not explained by obesity. Journal Clinical Endocrinology Metab. 51:739-743.

Nashville Area Indian Health Service Diabetes Program (1996) Introduction to Type II Diabetes. Albuquerque, New Mexico: Indian Health Service Diabetes Program.

Neel JV (1962) Diabetes mellitus: A ‘thrifty genotype rendered detrimental by "progress?" American Journal of Human Genetics, 14:353-362.

Neel JV (1982) The thrifty genotype revisited. In: J. Kobberling and J Tattersall (eds): The Genetics of Diabetes Mellitus. Academic Press, New York.

Reed D, D Labarthe, and R Stallones (l970) Health effects of westernization and migration among Chamorros. American Journal of Epidemiology, 92:96-112.

Ringrose H and P Zimmet ((1979) Nutrient intakes in an urbanized Micronesian population with a high diabetes prevalence. American Journal of Clinical Nutrition, 32:1334-1341.

Ritenbaugh C (1981) A clinal view of diabetes. In: The Perception of Evolution. Anthropology UCLA, 7(1,2):183-188.

Shapiro HL (1939) Migration and Environment. Oxford University Press, New York.

Shapiro JS (1997) Non-Insulin Dependent Diabetes Mellitus among American Indians: a problem in human ecology. American Indian Culture and Research Journal, 21 (2):197-227.

Szathmary EJE (1986) Diabetes in Arctic and Subarctic populations undergoing acculturation. Collegium Anthropologicum, 10(2):145-158.

Trowell HC (1973) Tropical malabsorption and fiber-depleted starchy carbohydrates. American Journal of Clinical Nutrition, 26:477-478.

Trowell et al (1975) Dietary-fiber hypothesis of the etiology of diabetes mellitus. Diabetes, 24(8):762-765.

Trowell H (1981) Hypertension, obesity, diabetes mellitus and coronary heart disease. In Western Disease: Their Emergence and Prevention (ed. H. Trowell and D. P. Burkitt), pp.3-32. Harvard University Press, Cambridge.

United States Department of Health and Human Services (1997) Regional Differences in Indian Health. Rockville, Maryland: Public Health Service and Indian Health Service.

Weiss KM, Ferrell RE, and Hanis CL (1984) A New World syndrome of metabolic diseases with a genetic and evolutionary basis. Yearbook of Physical Anthropology. 27:153-178.

Wendorf M (1989) Diabetes, the ice free corridor, and the Paleoindian settlement of North America. American Journal of Physical Anthropology, 79(4):503-520.

West KM (1974) Diabetes in American Indians and other Native populations of the New World. Diabetes 23:841-855.

Zimmet P (1982) Type 2 (non-insulin-dependent) diabetes: an epidemiological overview. Diabetologia, 22:399-419.

Zimmet P (1989) Non insulin-dependent (type 2) diabetes mellitus-does it really exist? Diabetic Med. 6:728-735.