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Obstet Gynecol Clin North Am. Author manuscript; available in PMC Jun 1, 2008.
Published in final edited form as:
PMCID: PMC2043158
NIHMSID: NIHMS26882

The Increasing Prevalence of Diabetes in Pregnancy

SYNOPSIS

We review studies published in the past 10 years that examine the prevalence and trends in the prevalence of gestational diabetes mellitus (GDM). The prevalence of GDM in a population is reflective of the prevalence of type 2 diabetes in that population. In low-risk populations, such as those found in Sweden, the prevalence in population-based studies is lower than 2% even when universal testing is offered, while studies in high-risk populations, such as the Native American Cree, Northern Californian Hispanics and Northern Californian Asians, reported prevalence rates ranging from 4.9% to 12.8%. Prevalence rates for GDM obtained from hospital-based studies similarly reflect the risk of type 2 diabetes in a population with a single hospital-based study in Australia reporting prevalences ranging from 3.0% in Anglo-Celtic women to 17.0% in Indian women. Finally, of the eight studies published that report on trends in the prevalence of GDM, 6 studies report an increase in the prevalence of GDM across most racial/ethnic groups studied. In summary, diabetes during pregnancy is a common and increasing complication of pregnancy.

Keywords: gestational diabetes mellitus, prevalence, trends, diagnostic criteria

INTRODUCTION

As the incidence of diabetes continues to rise and increasingly affects individuals of all ages, including young adults and children, women of childbearing age are at increased risk of diabetes during pregnancy(17). The lifetime risk of diabetes among the cohort of individuals born in the United States in 2000 was estimated to be 33% in males and 39% in females based on information obtained from the National Health and Nutrition Examination Surveys (NHANES) conducted 1984–2000(8). Moreover, the estimated lifetime risk of diabetes was higher at birth and throughout life for ethnic and racial minority groups than for non-Hispanic whites and for women when compared to men(8). The estimated lifetime diabetes risk at birth ranged from 31.2% in non-Hispanic white women to 52.5% in Hispanic women and from 26.7% in non-Hispanic white men to 45.4% in Hispanic men(8).

The epidemic of diabetes is not limited to western countries, but reaches worldwide affecting individuals in countries such as India and China(911). A recent study estimates the global prevalence of diabetes in 2000 at 2.8%, translating into 171 million individuals with diabetes, and projects that in 2030 the prevalence will be 4.4%, translating into 366 million individuals with diabetes worldwide(9). The increased prevalence is attributed to the aging population structure, urbanization, the obesity epidemic and physical inactivity.

At first glance, the obesity epidemic driven by changes in lifestyle appears to be the driving force behind the increased prevalence of diabetes. The current epidemic of obesity and overweight is widespread, affecting both children and adults of many ethnic backgrounds in North America and internationally(12,13). In each consecutive NHANES survey starting with NHANES I, conducted from 1971 to 1974, through completion of the most recent NHANES survey cycle, conducted from 1999 to 2002, there has been a marked increase in the prevalence of obesity in both children and adults across all ethnic, gender, and age strata(1418). In contrast to diabetes where both men and women of minority populations are affected disproportionately, minority women but not men tend to be disproportionately obese. The prevalence of obesity ranged from 50% in non-Hispanic black women to 30% in non-Hispanic white women in NHANES conducted 1999–2000(16). In contrast, in men the prevalence was 27% in non-Hispanic white men, 29% in Mexican American men and 28% in non-Hispanic black men(16).

Traditionally, epidemiologic studies of risk factors associated with type 2 diabetes have focused on adults and characteristics of adult study participants. However, early life exposures are emerging as potentially important risk factors. The “fetal origin of disease” hypothesis proposes that gestational programming may critically influence adult health and disease(19). Gestational programming is a process whereby stimuli or stresses that occur at critical or sensitive periods of development permanently change structure, physiology and metabolism, which predispose individuals to disease in adult life(20). Many animal studies provide support for gestational programming, as do epidemiologic studies of the Dutch Hunger Winter and the “thrifty phenotype” hypothesis which proposes that low birth weight, indicative of poor prenatal nutrition, has an effect on development that manifests itself later in life as an increased risk for a number of chronic diseases(2137).

In contrast to times of famine, today the intrauterine environment is more likely to expose the fetus to hyperglycemia or excess energy. Obesity prior to pregnancy, and high weight gain during pregnancy, predispose women to gestational diabetes mellitus (GDM) and early onset type 2 diabetes(3841). Maternal diabetes during gestation exposes the fetus to hyperglycemia, resulting in increased fetal insulin levels that both promote the storage of excess energy as fat and act as a growth factor. Exposure to maternal diabetes early in pregnancy is associated with birth defects, and later in pregnancy is associated with high birth weight, increased childhood and adult obesity and increased risk of type 2 diabetes(4250). Children exposed in utero to maternal diabetes are at higher risk of obesity and diabetes than their unexposed siblings, suggesting that the increased risk to the exposed offspring is not exclusively genetic(51,52). In the Pima Indians, the population with the highest known rate of diabetes, a study found that the increased exposure to diabetes in utero and increased weight in children accounted for most of the increased prevalence of diabetes over the past 30 years in Pima Indian children(53).

If the diabetic intrauterine environment is substantially contributing to the obesity and diabetes epidemics, not only will the prevalence continue to increase across all populations, but populations with a high prevalence of diabetes, such as non-Hispanic blacks and Mexican Americans, will continue to be disproportionately affected by these epidemics, resulting in a perpetual widening of health disparities between racial and ethnic groups. For these reasons, it is imperative to understand the trans-generational epidemiology and etiology of diabetes and develop simple, economical, and effective prevention strategies. Because the prevalence of diagnosed diabetes (either type 1 or type 2) prior to pregnancy is addressed in studies of the increasing prevalence of diabetes, the current review is focused on GDM defined as glucose intolerance with onset or first recognition during pregnancy. GDM is a common complication of pregnancy and often a precursor of type 2 diabetes. Therefore, our objectives were to review studies examining the prevalence of GDM as well as studies examining trends in the prevalence of GDM. In this context, we also review the diagnostic criteria for diabetes and GDM and their changes over time.

METHODS

Literature Search

A literature search was conducted in MEDLINE using the following search criteria: “gestational diabetes” as a MeSH term or text word, combined with “epidemiology” as a subheading or MeSH term, “prevalence” as a MeSH term, or “trend” or “screening” as a text word. In addition the search was limited to English language articles published in the last 10 years (July 1st, 1996 through October 1st, 2006). Using these search criteria yielded 1025 articles. The lead author (KJH) reviewed either the abstract or title of these articles to determine if they were suitable to asses either the current prevalence of GDM or trends in the prevalence of GDM. The review was limited to population-based studies that included at least 500 pregnant women or hospital-based studies that included at least 1000 pregnant women with at least 70% of the population being screened for GDM. In addition, articles that assessed GDM trends were required to span at least 3 years. When multiple articles were published on a single population the article containing the most recent information was retained. In addition to conducting the literature search in MEDLINE, reference lists of review articles obtained from the MEDLINE search were reviewed for additional pertinent studies.

Diabetes and GDM, screening and definitions

The definition of diabetes has changed over the past 10 years. Table 1 summarizes the definitions of diabetes commonly employed in recent epidemiologic literature. While the 1985 and 1999 World Health Organization (WHO) criteria require a 2-hour 75g oral glucose tolerance test (OGTT), the 1997 American Diabetes Association (ADA) criteria are focused on fasting glucose, but also recognize a casual or 2-hour 75g OGTT glucose level greater than or equal to 200 mg/dL as diagnostic of diabetes. Therefore, epidemiologic studies based on the ADA criteria may be based exclusively on fasting glucose levels or include information from an OGTT.

Table 1
Definitions of diabetes commonly employed in recent epidemiologic literature.

The recommended definition of GDM and criteria identifying who should be screened for GDM has varied widely across populations and over time; therefore, we review both screening criteria and diagnostic criteria for GDM employed in recent epidemiologic literature. Table 2 summarizes screening criteria, while Table 3 summarizes widely accepted GDM diagnostic criteria. In summary, recommended screening ranges from selective screening of average and high risk individuals to universal diagnostic testing of the entire population dependent on the risk of diabetes in the population.

Table 2
Gestational diabetes mellitus screening criteria.
Table 3
Gestational diabetes mellitus diagnostic criteria.

The diagnostic criteria for GDM have evolved over time and are not agreed upon internationally; therefore, definitions of GDM utilized in the epidemiologic literature vary considerably. Notably, at the 4th International Workshop Conference on GDM it was agreed that the Carpenter and Coustan(54) (C & C) criteria should replace the National Diabetes Data Group(55) (NDDG) criteria, resulting in a significant lowering of the thresholds and an increase in the prevalence of GDM. Because a number of organizations currently endorse the C & C criteria(5658), for consistency throughout the review we refer to the C & C criteria or to the NDDG criteria when they are utilized in different references.

RESULTS

Population-based studies

For purposes of this review, population-based studies were defined as studies which attempted to include a representative sample of the general population in a defined geographical area. Moreover, because the focus for population-based studies was having a representative study population, universal screening or testing for GDM was not required for inclusion in the review. Population-based studies of more than 500 individuals are summarized in Table 4. The prevalence of GDM varied depending upon the diagnostic criteria employed in the study, whether the study was retrospective or prospective, the source of the study data, as well as the country of residence, ethnicity and racial group of the study participants. In general, we observed lower prevalence rates in retrospective studies utilizing preexisting databases or routinely collected health statistics where a clear screening policy for GDM was not in place(5964), compared to retrospective or prospective studies which report universal screening for GDM.

Table 4
Prevalence of GDM in Population-based studies.

In studies conducted in North America, the observed prevalence was higher in Asians, African Americans, Native North Americans from Canada, and Hispanics than in non-Hispanic whites(39,60,61,6569). In a retrospective cohort study of the Kaiser Permanente Medical Care Group of Northern California, where 93.5% of the population was screened for GDM, the prevalence ranged from 2.5% in white women to 5.7% in Asian women using the NDDG criteria and from 3.9% in white women to 8.3% in Asian women using the C & C criteria(65). In the Nurses Health Study II, which relied on self-reported diagnosis, the observed prevalence was over 10% in African Americans (10.6%) and Asians (10.5%), and around 5% in whites (4.8%) (39). Finally, in retrospective studies conducted in Native North Americans in Canada, the prevalence based on NDDG criteria ranged from 8.4% to 12.8%(61,6769). The single study conducted in South America was a prospective study conducted in Brazil in a diverse population and reported a prevalence of 2.4% based on ADA(56) criteria using the 2-hour 75g OGTT diagnostic criteria and 7.2% based on WHO criteria(70).

Population-based studies conducted in northern Europe used a 2-hour 75g OGGT to diagnose GDM; however, varying diagnostic cutpoints were employed. Using the 2-hour 75g OGTT, observed prevalence rates in the United Kingdom, Holland, Sweden and Denmark ranged from 0.6% in Dutch women to 3.6% using local criteria in a Danish population(62,63,7175). In two studies conducted in Italy, a 3-hour 100g OGTT using the C & C criteria following universal screening was employed to diagnose GDM. In the earlier study conducted in north-west Tuscany the prevalence was 6.3%(76), while in the later study conducted in a volunteer population in Sardinia the prevalence was 22.3%(77).

Reported prevalence rates in population-based studies in Turkey, Iran, Bahrain, Ethiopia and India ranged from 1.2% in Turkey (NDDG criteria following universal screening) to 15.5% in Bahraini women (C & C with a 3-hour 75g OGTT following universal screening) (7883). In a retrospective study in Australia, which included all singleton deliveries in Victoria in 1996 and utilized routinely collected information in two databases, the prevalence was 3.6% in non-Aboriginal women and 4.3% in Aboriginal women(64). In a study conducted in 6 urban districts in Tianjin, China, using 1999 WHO diagnostic criteria and universal screening, the prevalence was 2.3%(84). Finally, in a study conducted in Japan, using the Japanese Society of Obstetrics and Gynecology (JSOG) criteria for GDM and universal screening, the prevalence was 2.9%(85).

Hospital-based studies

Hospital-based studies of more than 1000 unselected individuals, where universal screening or testing was employed and at least 70% of the population was screened for GDM, are summarized in Table 5. Similar to the population-based studies, in the hospital-based studies the prevalence of GDM varied depending upon the diagnostic criteria employed in the study, whether the study was retrospective or prospective as well as the country of residence, ethnicity and racial group of the study participants. Three of the hospital-based studies directly compare GDM prevalence rates based on NDDG and C & C criteria(8688). In these three studies, NDDG rates range from 3.2% in a study conducted in Mexico(86) to 8.8% in a study conducted in Spain(87) with corresponding C & C rates ranging from 4.1% to 11.6%(8688).

Table 5
Prevalence of GDM in hospital-based studies.

The hospital-based studies conducted in the United States diagnosed GDM based on a 3-hour OGTT and report prevalence rates ranging from 2.7% using the NDDG criteria to 6.8% in a largely Mexican American population using the C & C criteria(8991). In a Canadian study at the Saskatoon Royal University Hospital, using the NDDG criteria, the prevalence was 11.5% in the Aboriginal population and 3.5% in the non-Aboriginal population(92). In a study conducted at the University Hospital in Monterrey, Mexico which compared a number of diagnostic criteria the prevalence was 3.2%, 4.1%, and 8.7% based on NDDG, C & C and 1999 WHO diagnostic criteria, respectively(86). In Europe, hospital-based studies were conducted in Spain and Italy. Three studies in Spain reported prevalence rates ranging from 3.3% to 8.8% using NDDG criteria(87,93,94). The two Italian studies report prevalence rates of 4.6% and 8.7% based on C & C criteria(88,95).

Reported prevalence rates in hospital-based studies in Turkey, Iran, Pakistan, India and Sri Lanka are between 4.1% and 4.7%, with the exception of the study conducted in India, which used the 1999 WHO diagnostic criteria and reports a prevalence of 18.9%, as well as the study conducted in Turkey, which reports a prevalence of 6.6% using the C & C criteria(96100). Both hospital-based studies conducted in Australia employed the Australasian Diabetes in Pregnancy Society (ADIPS) criteria, with one reporting an overall prevalence of 5.2%(101) and the second reporting prevalence rates as low as 3.0% in Anglo-Celtic participants and as high as 10.0, 15.0 and 17.0% in Aboriginal, Chinese and Indian participants, respectively(102). A single hospital-based study conducted in Japan reported a prevalence of 1.8% based on the JSOG diagnostic criteria(103).

Trends in the prevalence of GDM

Eight retrospective studies conducted in the past 10 years in the United States, Canada and Australia examine trends in the prevalence of GDM (Table 6) (104111). Three of the four studies conducted in the United States report either universal screening criteria in place and/or evidence of consistent screening in the population, with a screening rate of 96 to 98% in the Kaiser Permanente of Colorado study and 86.8% in the Northern California Kaiser Permanente study(104106). Each of the four studies conducted in the United States reports a statistically significant increase in the prevalence of GDM or diabetes during pregnancy during the study period(104107). The Kaiser Permanente study conducted in a population representative of the Denver metropolitan area reports a prevalence increase from 2.1% in 1994 to 4.1% in 2002, based on the NDDG diagnostic criteria throughout the study(104). In addition, they report a greater increase for minorities than whites(104). Similarly, the Kaiser Permanente study conducted in a population representative of Northern California reports a prevalence increase from 5.1% in 1991 to 7.4% in 1997, which leveled off through 2000 at 6.9% based on the C & C diagnostic criteria(105). A study conducted on all women with singleton deliveries in New York city, where universal screening criteria have been practiced since the 1980s, reports a prevalence of 2.6% in 1990 increasing to 3.8% in 2001, with significantly increasing rates of GDM in all major racial/ethnic groups except non-Hispanic whites(106). The final study conducted in the United States utilized birth records of American Indian and white mothers in Montana and North Dakota for the years 1989 through 2000(107). In both states a statistically significant increase in prevalence of GDM was identified in whites, from 1.8 to 2.6% in Montana and from 1.6 to 3.2% in North Dakota(107). In contrast, in the smaller population of American Indians within each state, a statistically significant increase in prevalence of GDM was reported for Montana (from 3.1 to 4.1%), but not North Dakota (from 3.8 to 4.8%)(107).

Table 6
Trends in the prevalence of GDM

The study conducted in Canada included over 100,000 perinatal records from 39 hospitals in Northern and Central Alberta and used NDDG criteria and universal screening throughout the study period(108). The study reports a prevalence ranging between 2.2 and 2.8% between 1991 and 1997 with a non-significant test for linear trend for the duration of the study(108). One of the three studies conducted in Australia is the only study to report a decrease in the prevalence of GDM over time(110). The study was conducted in far North Queensland using a hospital database with 7,567 entries(110). Using ADIPS diagnostic criteria and universal screening, with 78 to 85% of the population being screened throughout the study period, prevalence was 14.4% in 1992 and had dropped to 5.3% by 1996(110). Improvement in medical care and a dietary intervention were given as potential explanations for the decline in GDM during the study period(110). A second study conducted in Australia included all deliveries in South Australia between 1988 and 1999 and reports an annual rate increase of 4.7% in the non-Aboriginal population, but not in the Aboriginal population (non-statistically significant annual rate increase of 0.5%)(109). Finally, using information on over 40,000 women attending Mercy Hospital for Women in Melbourne, Australia, a statistically significant increasing prevalence from 2.9% (1971–1980) to 8.8% (1991–1994) is reported(111).

DISCUSSION

In this study, we review studies published in the past 10 years that examine the prevalence and trends in the prevalence of GDM. In summary, the prevalence of GDM in a population is reflective of the prevalence of type 2 diabetes in that population; therefore, ethnic and racial populations with a high prevalence of type 2 diabetes are at higher risk of GDM. In low-risk populations such as those found in Sweden the prevalence in population-based studies is lower than 2% even when universal testing is offered (7173), while studies in high-risk populations such as the Native American Cree, Northern Californian Hispanics and Northern Californian Asians reported prevalence rates based on NDDG diagnostic criteria following universal screening ranging from 4.9% to 12.8%(61,65,6769). Prevalence rates for GDM obtained from hospital-based studies similarly reflect the risk of type 2 diabetes in a population. A single hospital-based study in Australia using ADIPS diagnostic criteria and universal screening reports prevalences ranging from 3.0% in Anglo-Celtic women to 17.0% in Indian women(102). Finally, of the eight studies published in the past 10 years that report on trends in the prevalence of GDM(104111), one study reports a significant decline in the prevalence of GDM(110), one study reports no significant change in the prevalence of GDM(108), and 6 studies report an increase in the prevalence of GDM across most racial/ethnic groups studied(104107,109,111).

A number of factors influence the prevalence of GDM identified in a population and make it difficult to compare prevalences across populations. In the United States the definition of GDM and screening policies concerning GDM have changed considerably in the past 20 years and still vary substantially. Despite four international conferences aimed at developing a consensus definition for GDM worldwide, the definition and screening criteria for GDM continue to vary, making it difficult to compare prevalences between countries. A critical change in the definition of GDM occurred at the 4th International Workshop conference on GDM in 1997, endorsed by the ADA, when it was largely agreed that the C & C criteria should replace the NDDG criteria, significantly lowering the accepted cutpoints and therefore raising the prevalence of GDM(58). Finally, because GDM encompasses undiagnosed type 2 diabetes prior to pregnancy, the definition, screening strategies and awareness of type 2 diabetes in a population ultimately influences the observed prevalence of GDM in a population. This is of particular importance during the past decade because the diagnostic criteria for diabetes and recommended screening practices have changed in the United States and internationally, namely the threshold for a fasting glucose level diagnostic of diabetes was lowered from 140 mg/dL to 126 mg/dL(112,113).

In addition to the varied definitions and screening policies for GDM and diabetes there are a number of factors which make it difficult to compare GDM prevalence rates across populations and over time. Increased maternal age at delivery is a strong risk factor for GDM. Hence, a contributing factor to increased prevalence rates of GDM in a given population over time, or differences observed between populations, is increased maternal age at delivery. Because we are unable to age standardize our prevalence rates across studies, we are unable to determine the impact of maternal age at delivery on prevalence rates across studies. However, increasing maternal age at delivery is one factor likely influencing the increasing prevalence of GDM in developed countries. Maternal age at delivery is also likely to vary and affect prevalence differences when comparing developed and undeveloped countries. Because the prevalence of GDM in a population reflects the prevalence of type 2 diabetes in a population, and certain racial and ethnic groups are at increased risk of type 2 diabetes, a second factor which may influence changes in prevalence overtime in a given population is a change in the racial/ethnic composition of that population. While racial/ethnic group specific prevalences of GDM reflect the prevalence within a specific segment of the population, they may fail to reflect the broader public health impact of GDM as the overall population prevalence increases.

Changes in lifestyle including decreased physical activity and increased caloric consumption continue to fuel the obesity epidemic. Obesity, often accompanied by insulin resistance, is a strong risk factor for GDM and likely contributes to the increasing prevalence of GDM. The National Longitudinal Survey of Youth, a prospective cohort study of children aged 4 to 12 years carried out between 1986 and 1998 in the United States, indicated that the prevalence of overweight children increased significantly and steadily throughout the study(114). By the end of the study in 1998, obesity affected an estimated 21.5% of African American children, 21.8% of Hispanic children and 12.3% of non-Hispanic white children(114). In the 2003–2004 NHANES, 17.1% of individuals ages 2 to 19 years were overweight; more than triple the percent in 1980(115). In adults of childbearing age the prevalence of obesity also continues to rise; in 18- to 29-year olds the prevalence of obesity rose from 7.1% in 1991 to 12.1% in 1998 in the Behavioral Risk Factor Surveillance System survey (116).

As obesity and diabetes increasingly affect young adults and women of childbearing age, understanding the public health impact of diabetes during pregnancy and its affect on infant health becomes important. Exposure to maternal diabetes later in pregnancy is associated with high birth weight, increased childhood and adult obesity and increased risk of type 2 diabetes (42,44,45,48,117121); therefore, the diabetic intrauterine environment may not only be a result of the obesity and diabetes epidemics, it may be partially responsible and currently fueling the epidemics. Moreover, because both obesity and diabetes disproportionately affect minority women including minority women of childbearing age(8,16), if the intrauterine environment is contributing to the epidemics, it perpetuates and widens health disparities between racial and ethnic groups.

The population health impact of GDM is not limited to exposed offspring, but affects maternal health as well. Once diagnosed with GDM, a woman has a substantial chance of developing type 2 diabetes following delivery, with some studies reporting a 5 year cumulative incidence rate of over 50%(122). Moreover, because childbearing women are relatively young, women with GDM who develop overt diabetes acquire it at a young age, substantially increasing their lifetime risk of developing complications from diabetes. The Diabetes Prevention Program was one of several clinical trials which indicates that either through diet and exercise, or with the aid of a pharmacological agent, it is possible to lower the incidence or delay the onset of diabetes among individuals at high risk of the disease(123126). Women with GDM, because of their high diabetes risk and young age, are ideally suited to be targeted for lifestyle or pharmacological interventions to delay or prevent the onset of overt diabetes(123126). Moreover, because women with GDM are of childbearing age, preventing or delaying the onset of overt diabetes not only improves the woman’s health, but protects future offspring from the harmful effects of elevated glucose levels in pregnancy(127,128).

In summary, diabetes during pregnancy is a common and increasing complication of pregnancy that differentially affects racial and ethnic minority populations dependent upon their underlying risk of diabetes. Hence, an important public health priority, consistent with reducing health disparities between racial and ethnic groups, is prevention of diabetes, starting with maternal health pre- and post-conception.

Footnotes

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References

1. Burke JP, Williams K, Gaskill SP, Hazuda HP, Haffner SM, Stern MP. Rapid rise in the incidence of type 2 diabetes from 1987 to 1996: results from the San Antonio Heart Study. Arch Intern Med. 1999;159:1450–1456. [PubMed]
2. Dabelea D, Pettitt DJ, Jones KL, Arslanian SA. Type 2 diabetes mellitus in minority children and adolescents. An emerging problem. Endocrinol Metab Clin North Am. 1999;28:709–29. viii. [PubMed]
3. Fagot-Campagna A, Pettitt DJ, Engelgau MM, Burrows NR, Geiss LS, Valdez R, Beckles GL, Saaddine J, Gregg EW, Williamson DF, Narayan KM. Type 2 diabetes among North American children and adolescents: an epidemiologic review and a public health perspective. J Pediatr. 2000;136:664–672. [PubMed]
4. Fagot-Campagna A, Saaddine JB, Flegal KM, Beckles GL. Diabetes, impaired fasting glucose, and elevated HbA1c in U.S. adolescents: the Third National Health and Nutrition Examination Survey. Diabetes Care. 2001;24:834–837. [PubMed]
5. Harris MI, Flegal KM, Cowie CC, Eberhardt MS, Goldstein DE, Little RR, Wiedmeyer HM, Byrd-Holt DD. Prevalence of diabetes, impaired fasting glucose, and impaired glucose tolerance in U.S. adults. The Third National Health and Nutrition Examination Survey, 1988–1994. Diabetes Care. 1998;21:518–524. [PubMed]
6. Rosenbloom AL, Joe JR, Young RS, Winter WE. Emerging epidemic of type 2 diabetes in youth. Diabetes Care. 1999;22:345–354. [PubMed]
7. Cowie CC, Rust KF, Byrd-Holt DD, Eberhardt MS, Flegal KM, Engelgau MM, Saydah SH, Williams DE, Geiss LS, Gregg EW. Prevalence of diabetes and impaired fasting glucose in adults in the U.S. population: National Health And Nutrition Examination Survey 1999–2002. Diabetes Care. 2006;29:1263–1268. [PubMed]
8. Narayan KM, Boyle JP, Thompson TJ, Sorensen SW, Williamson DF. Lifetime risk for diabetes mellitus in the United States. JAMA. 2003;290:1884–1890. [PubMed]
9. Wild S, Roglic G, Green A, Sicree R, King H. Global prevalence of diabetes: estimates for the year 2000 and projections for 2030. Diabetes Care. 2004;27:1047–1053. [PubMed]
10. Pan XR, Yang WY, Li GW, Liu J. Prevalence of diabetes and its risk factors in China, 1994. National Diabetes Prevention and Control Cooperative Group. Diabetes Care. 1997;20:1664–1669. [PubMed]
11. Ramachandran A, Snehalatha C, Kapur A, Vijay V, Mohan V, Das AK, Rao PV, Yajnik CS, Prasanna Kumar KM, Nair JD. High prevalence of diabetes and impaired glucose tolerance in India: National Urban Diabetes Survey. Diabetologia. 2001;44:1094–1101. [PubMed]
12. World Health Organization. World Health Organization Technical Support Series No. 894. Geneva, Switzerland: World Health Organization; 2000. Obesity: Preventing and Manageing the Global Epidemic.
13. Wang Y. Cross-national comparison of childhood obesity: the epidemic and the relationship between obesity and socioeconomic status. Int J Epidemiol. 2001;30:1129–1136. [PubMed]
14. Update prevalence of overweight among children, adolescents, and adults--United States, 1988–1994. MMWR Morb Mortal Wkly Rep. 1997;46:198–202. [PubMed]
15. Troiano RP, Flegal KM, Kuczmarski RJ, Campbell SM, Johnson CL. Overweight prevalence and trends for children and adolescents. The National Health and Nutrition Examination Surveys, 1963 to 1991. Arch Pediatr Adolesc Med. 1995;149:1085–1091. [PubMed]
16. Flegal KM, Carroll MD, Ogden CL, Johnson CL. Prevalence and trends in obesity among US adults, 1999–2000. JAMA. 2002;288:1723–1727. [PubMed]
17. Ogden CL, Flegal KM, Carroll MD, Johnson CL. Prevalence and trends in overweight among US children and adolescents, 1999–2000. JAMA. 2002;288:1728–1732. [PubMed]
18. Hedley AA, Ogden CL, Johnson CL, Carroll MD, Curtin LR, Flegal KM. Prevalence of overweight and obesity among US children, adolescents, and adults, 1999–2002. JAMA. 2004;291:2847–2850. [PubMed]
19. Barker DJ. Fetal origins of coronary heart disease. BMJ. 1995;311:171–174. [PMC free article] [PubMed]
20. Lucas A. Programming by early nutrition in man. In: Bock GR, Whelan J, editors. The childhood environment and adult disease. Chichester, United Kingdom: John Wiley and Sons; 1991. pp. 38–55.
21. Ravelli AC, van der Meulen JH, Osmond C, Barker DJ, Bleker OP. Obesity at the age of 50 y in men and women exposed to famine prenatally. Am J Clin Nutr. 1999;70:811–816. [PubMed]
22. Ravelli GP, Stein ZA, Susser MW. Obesity in young men after famine exposure in utero and early infancy. N Engl J Med. 1976;295:349–353. [PubMed]
23. Hales CN, Barker DJ, Clark PM, Cox LJ, Fall C, Osmond C, Winter PD. Fetal and infant growth and impaired glucose tolerance at age 64. BMJ. 1991;303:1019–1022. [PMC free article] [PubMed]
24. Hales CN, Barker DJ. Type 2 (non-insulin-dependent) diabetes mellitus: the thrifty phenotype hypothesis. Diabetologia. 1992;35:595–601. [PubMed]
25. Valdez R, Athens MA, Thompson GH, Bradshaw BS, Stern MP. Birthweight and adult health outcomes in a biethnic population in the USA. Diabetologia. 1994;37:624–631. [PubMed]
26. McCance DR, Pettitt DJ, Hanson RL, Jacobsson LT, Knowler WC, Bennett PH. Birth weight and non-insulin dependent diabetes: thrifty genotype, thrifty phenotype, or surviving small baby genotype? BMJ. 1994;308:942–945. [PMC free article] [PubMed]
27. Rich-Edwards JW, Colditz GA, Stampfer MJ, Willett WC, Gillman MW, Hennekens CH, Speizer FE, Manson JE. Birthweight and the risk for type 2 diabetes mellitus in adult women. Ann Intern Med. 1999;130:278–284. [PubMed]
28. Robinson S, Walton RJ, Clark PM, Barker DJ, Hales CN, Osmond C. The relation of fetal growth to plasma glucose in young men. Diabetologia. 1992;35:444–446. [PubMed]
29. Robinson S, Walton RJ, Clark PM, Barker DJ, Hales CN, Osmond C. The relation of fetal growth to plasma glucose in young men. Diabetologia. 1992;35:444–446. [PubMed]
30. Curhan GC, Chertow GM, Willett WC, Spiegelman D, Colditz GA, Manson JE, Speizer FE, Stampfer MJ. Birth weight and adult hypertension and obesity in women. Circulation. 1996;94:1310–1315. [PubMed]
31. Curhan GC, Willett WC, Rimm EB, Spiegelman D, Ascherio AL, Stampfer MJ. Birth weight and adult hypertension, diabetes mellitus, and obesity in US men. Circulation. 1996;94:3246–3250. [PubMed]
32. Barker DJ, Osmond C, Golding J, Kuh D, Wadsworth ME. Growth in utero, blood pressure in childhood and adult life, and mortality from cardiovascular disease. BMJ. 1989;298:564–567. [PMC free article] [PubMed]
33. Barker DJ, Bull AR, Osmond C, Simmonds SJ. Fetal and placental size and risk of hypertension in adult life. BMJ. 1990;301:259–262. [PMC free article] [PubMed]
34. Law CM, de Swiet M, Osmond C, Fayers PM, Barker DJ, Cruddas AM, Fall CH. Initiation of hypertension in utero and its amplification throughout life. BMJ. 1993;306:24–27. [PMC free article] [PubMed]
35. Rich-Edwards JW, Stampfer MJ, Manson JE, Rosner B, Hankinson SE, Colditz GA, Willett WC, Hennekens CH. Birth weight and risk of cardiovascular disease in a cohort of women followed up since 1976. BMJ. 1997;315:396–400. [PMC free article] [PubMed]
36. Osmond C, Barker DJ, Winter PD, Fall CH, Simmonds SJ. Early growth and death from cardiovascular disease in women. BMJ. 1993;307:1519–1524. [PMC free article] [PubMed]
37. Fall CH, Vijayakumar M, Barker DJ, Osmond C, Duggleby S. Weight in infancy and prevalence of coronary heart disease in adult life. BMJ. 1995;310:17–19. [PMC free article] [PubMed]
38. Berkowitz GS, Lapinski RH, Wein R, Lee D. Race/ethnicity and other risk factors for gestational diabetes. Am J Epidemiol. 1992;135:965–973. [PubMed]
39. Solomon CG, Willett WC, Carey VJ, Rich-Edwards J, Hunter DJ, Colditz GA, Stampfer MJ, Speizer FE, Spiegelman D, Manson JE. A prospective study of pregravid determinants of gestational diabetes mellitus. JAMA. 1997;278:1078–1083. [PubMed]
40. Dornhorst A, Paterson CM, Nicholls JS, Wadsworth J, Chiu DC, Elkeles RS, Johnston DG, Beard RW. High prevalence of gestational diabetes in women from ethnic minority groups. Diabet Med. 1992;9:820–825. [PubMed]
41. Zhang S, Folsom AR, Flack JM, Liu K. Body fat distribution before pregnancy and gestational diabetes: findings from coronary artery risk development in young adults (CARDIA) study. BMJ. 1995;311:1139–1140. [PMC free article] [PubMed]
42. Freinkel N. Banting Lecture 1980. Of pregnancy and progeny. Diabetes. 1980;29:1023–1035. [PubMed]
43. Dabelea D, Hanson RL, Bennett PH, Roumain J, Knowler WC, Pettitt DJ. Increasing prevalence of Type II diabetes in American Indian children. Diabetologia. 1998;41:904–910. [PubMed]
44. Silverman BL, Rizzo T, Green OC, Cho NH, Winter RJ, Ogata ES, Richards GE, Metzger BE. Long-term prospective evaluation of offspring of diabetic mothers. Diabetes. 1991;40 (Suppl 2):121–125. [PubMed]
45. O’Sullivan JB, Gellis SS, Dandrow RV, Tenney BO. The potential diabetic and her treatment in pregnancy. Obstet Gynecol. 1966;27:683–689. [PubMed]
46. Dabelea D, Hanson RL, Bennett PH, Roumain J, Knowler WC, Pettitt DJ. Increasing prevalence of Type II diabetes in American Indian children. Diabetologia. 1998;41:904–910. [PubMed]
47. Dabelea D, Hanson RL, Lindsay RS, Pettitt DJ, Imperatore G, Gabir MM, Roumain J, Bennett PH, Knowler WC. Intrauterine exposure to diabetes conveys risks for type 2 diabetes and obesity: a study of discordant sibships. Diabetes. 2000;49:2208–2211. [PubMed]
48. Pettitt DJ, Knowler WC, Baird HR, Bennett PH. Gestational diabetes: infant and maternal complications of pregnancy in relation to third-trimester glucose tolerance in the Pima Indians. Diabetes Care. 1980;3:458–464. [PubMed]
49. Pettitt DJ, Knowler WC, Bennett PH, Aleck KA, Baird HR. Obesity in offspring of diabetic Pima Indian women despite normal birth weight. Diabetes Care. 1987;10:76–80. [PubMed]
50. Pettitt DJ, Knowler WC. Long-term effects of the intrauterine environment, birth weight, and breast-feeding in Pima Indians. Diabetes Care. 1998;21 (Suppl 2):B138–B141. [PubMed]
51. Pettitt DJ, Aleck KA, Baird HR, Carraher MJ, Bennett PH, Knowler WC. Congenital susceptibility to NIDDM. Role of intrauterine environment. Diabetes. 1988;37:622–628. [PubMed]
52. Hanson RL, Elston RC, Pettitt DJ, Bennett PH, Knowler WC. Segregation analysis of non-insulin-dependent diabetes mellitus in Pima Indians: evidence for a major-gene effect. Am J Hum Genet. 1995;57:160–170. [PMC free article] [PubMed]
53. Dabelea D, Hanson RL, Bennett PH, Roumain J, Knowler WC, Pettitt DJ. Increasing prevalence of Type II diabetes in American Indian children. Diabetologia. 1998;41:904–910. [PubMed]
54. Carpenter MW, Coustan DR. Criteria for screening tests for gestational diabetes. Am J Obstet Gynecol. 1982;144:768–773. [PubMed]
55. National Diabetes Data Group. Classification and diagnosis of diabetes mellitus and other categories of glucose intolerance. Diabetes. 1979;28:1039–1057. [PubMed]
56. American Diabetes Association Clinical Practice Recommendations 2001. Diabetes Care. 2001;24(Suppl 1):S1–133. [PubMed]
57. ACOG Practice Bulletin. Clinical management guidelines for obstetrician-gynecologists. Number 30, September 2001 (replaces Technical Bulletin Number 200, December 1994). Gestational diabetes. Obstet Gynecol. 2001;98:525–538. [PubMed]
58. Metzger BE, Coustan DR. Summary and recommendations of the Fourth International Workshop-Conference on Gestational Diabetes Mellitus. The Organizing Committee. Diabetes Care. 1998;21 (Suppl 2):B161–B167. [PubMed]
59. Rosenberg TJ, Garbers S, Lipkind H, Chiasson MA. Maternal obesity and diabetes as risk factors for adverse pregnancy outcomes: differences among 4 racial/ethnic groups. Am J Public Health. 2005;95:1545–1551. [PMC free article] [PubMed]
60. Williams MA, Emanuel I, Kimpo C, Leisenring WM, Hale CB. A population-based cohort study of the relation between maternal birthweight and risk of gestational diabetes mellitus in four racial/ethnic groups. Paediatr Perinat Epidemiol. 1999;13:452–465. [PubMed]
61. Godwin M, Muirhead M, Huynh J, Helt B, Grimmer J. Prevalence of gestational diabetes mellitus among Swampy Cree women in Moose Factory, James Bay. CMAJ. 1999;160:1299–1302. [PMC free article] [PubMed]
62. Janghorbani M, Stenhouse E, Jones RB, Millward A. Gestational diabetes mellitus in Plymouth, U.K.: prevalence, seasonal variation and associated factors. J Reprod Med. 2006;51:128–134. [PubMed]
63. Weijers RN, Bekedam DJ, Oosting H. The prevalence of type 2 diabetes and gestational diabetes mellitus in an inner city multi-ethnic population. Eur J Epidemiol. 1998;14:693–699. [PubMed]
64. Stone CA, McLachlan KA, Halliday JL, Wein P, Tippett C. Gestational diabetes in Victoria in 1996: incidence, risk factors and outcomes. Med J Aust. 2002;177:486–491. [PubMed]
65. Ferrara A, Hedderson MM, Quesenberry CP, Selby JV. Prevalence of gestational diabetes mellitus detected by the national diabetes data group or the carpenter and coustan plasma glucose thresholds. Diabetes Care. 2002;25:1625–1630. [PubMed]
66. Kieffer EC, Carman WJ, Gillespie BW, Nolan GH, Worley SE, Guzman JR. Obesity and gestational diabetes among African-American women and Latinas in Detroit: implications for disparities in women’s health. J Am Med Womens Assoc. 2001;56:181–7. 196. [PubMed]
67. Rodrigues S, Robinson E, Gray-Donald K. Prevalence of gestational diabetes mellitus among James Bay Cree women in northern Quebec. CMAJ. 1999;160:1293–1297. [PMC free article] [PubMed]
68. Rodrigues S, Robinson EJ, Ghezzo H, Gray-Donald K. Interaction of body weight and ethnicity on risk of gestational diabetes mellitus. Am J Clin Nutr. 1999;70:1083–1089. [PubMed]
69. Harris SB, Caulfield LE, Sugamori ME, Whalen EA, Henning B. The epidemiology of diabetes in pregnant Native Canadians. A risk profile. Diabetes Care. 1997;20:1422–1425. [PubMed]
70. Schmidt MI, Duncan BB, Reichelt AJ, Branchtein L, Matos MC, e Forti Costa, Spichler ER, Pousada JM, Teixeira MM, Yamashita T. Gestational diabetes mellitus diagnosed with a 2-h 75-g oral glucose tolerance test and adverse pregnancy outcomes. Diabetes Care. 2001;24:1151–1155. [PubMed]
71. Ostlund I, Hanson U. Occurrence of gestational diabetes mellitus and the value of different screening indicators for the oral glucose tolerance test. Acta Obstet Gynecol Scand. 2003;82:103–108. [PubMed]
72. Ostlund I, Hanson U. Repeated random blood glucose measurements as universal screening test for gestational diabetes mellitus. Acta Obstet Gynecol Scand. 2004;83:46–51. [PubMed]
73. Aberg AE, Jonsson EK, Eskilsson I, Landin-Olsson M, Frid AH. Predictive factors of developing diabetes mellitus in women with gestational diabetes. Acta Obstet Gynecol Scand. 2002;81:11–16. [PubMed]
74. Jensen DM, Molsted-Pedersen L, Beck-Nielsen H, Westergaard JG, Ovesen P, Damm P. Screening for gestational diabetes mellitus by a model based on risk indicators: a prospective study. Am J Obstet Gynecol. 2003;189:1383–1388. [PubMed]
75. Kvetny J, Poulsen HF, Damgaard DW. Results from screening for gestational diabetes mellitus in a Danish county. Dan Med Bull. 1999;46:57–59. [PubMed]
76. Di CG, Benzi L, Casadidio I, Orsini P, Rossi L, Fontana G, Malara N, Villani G, Di CA, Trifiro R, Bottone P, Luchi C, Fantoni M, Teti G, Marselli L, Volpe L, Navalesi R. Screening of gestational diabetes in Tuscany: results in 2000 cases. Ann Ist Super Sanita. 1997;33:389–391. [PubMed]
77. Murgia C, Berria R, Minerba L, Malloci B, Daniele C, Zedda P, Ciccotto MG, Sulis S, Murenu M, Tiddia F, Manai M, Melis GB. Gestational diabetes mellitus in Sardinia: results from an early, universal screening procedure. Diabetes Care. 2006;29:1713–1714. [PubMed]
78. Erem C, Cihanyurdu N, Deger O, Karahan C, Can G, Telatar M. Screening for gestational diabetes mellitus in northeastern Turkey (Trabzon City) Eur J Epidemiol. 2003;18:39–43. [PubMed]
79. Keshavarz M, Cheung NW, Babaee GR, Moghadam HK, Ajami ME, Shariati M. Gestational diabetes in Iran: incidence, risk factors and pregnancy outcomes. Diabetes Res Clin Pract. 2005;69:279–286. [PubMed]
80. Hadaegh F, Tohidi M, Harati H, Kheirandish M, Rahimi S. Prevalence of gestational diabetes mellitus in southern Iran (Bandar Abbas City) Endocr Pract. 2005;11:313–318. [PubMed]
81. Al Mahroos S, Nagalla DS, Yousif W, Sanad H. A population-based screening for gestational diabetes mellitus in non-diabetic women in Bahrain. Ann Saudi Med. 2005;25:129–133. [PubMed]
82. Seyoum B, Kiros K, Haileselase T, Leole A. Prevalence of gestational diabetes mellitus in rural pregnant mothers in northern Ethiopia. Diabetes Res Clin Pract. 1999;46:247–251. [PubMed]
83. Zargar AH, Sheikh MI, Bashir MI, Masoodi SR, Laway BA, Wani AI, Bhat MH, Dar FA. Prevalence of gestational diabetes mellitus in Kashmiri women from the Indian subcontinent. Diabetes Res Clin Pract. 2004;66:139–145. [PubMed]
84. Yang X, Hsu-Hage B, Zhang H, Yu L, Dong L, Li J, Shao P, Zhang C. Gestational diabetes mellitus in women of single gravidity in Tianjin City, China. Diabetes Care. 2002;25:847–851. [PubMed]
85. Maegawa Y, Sugiyama T, Kusaka H, Mitao M, Toyoda N. Screening tests for gestational diabetes in Japan in the 1st and 2nd trimester of pregnancy. Diabetes Res Clin Pract. 2003;62:47–53. [PubMed]
86. Santos-Ayarzagoitia M, Salinas-Martinez AM, Villarreal-Perez JZ. Gestational diabetes: Validity of ADA and WHO diagnostic criteria using NDDG as the reference test. Diabetes Res Clin Pract. 2006 [PubMed]
87. Ricart W, Lopez J, Mozas J, Pericot A, Sancho MA, Gonzalez N, Balsells M, Luna R, Cortazar A, Navarro P, Ramirez O, Flandez B, Pallardo LF, Hernandez A, Ampudia J, Fernandez-Real JM, Corcoy R. Potential impact of American Diabetes Association (2000) criteria for diagnosis of gestational diabetes mellitus in Spain. Diabetologia. 2005;48:1135–1141. [PubMed]
88. Corrado F, Stella NC, Mancuso A, Triolo O, Bruno L, Artenisio AC. Screening for gestational diabetes in Sicily. J Reprod Med. 1999;44:875–878. [PubMed]
89. Yogev Y, Langer O, Xenakis EM, Rosenn B. Glucose screening in Mexican-American women. Obstet Gynecol. 2004;103:1241–1245. [PubMed]
90. Stamilio DM, Olsen T, Ratcliffe S, Sehdev HM, Macones GA. False-positive 1-hour glucose challenge test and adverse perinatal outcomes. Obstet Gynecol. 2004;103:148–156. [PubMed]
91. Danilenko-Dixon DR, Van Winter JT, Nelson RL, Ogburn PL., Jr Universal versus selective gestational diabetes screening: application of 1997 American Diabetes Association recommendations. Am J Obstet Gynecol. 1999;181:798–802. [PubMed]
92. Dyck R, Klomp H, Tan LK, Turnell RW, Boctor MA. A comparison of rates, risk factors, and outcomes of gestational diabetes between aboriginal and non-aboriginal women in the Saskatoon health district. Diabetes Care. 2002;25:487–493. [PubMed]
93. Jimenez-Moleon JJ, Bueno-Cavanillas A, Luna-Del-Castillo JD, Garcia-Martin M, Lardelli-Claret P, Galvez-Vargas R. Prevalence of gestational diabetes mellitus: variations related to screening strategy used. Eur J Endocrinol. 2002;146:831–837. [PubMed]
94. Bartha JL, Martinez-Del-Fresno P, Comino-Delgado R. Gestational diabetes mellitus diagnosed during early pregnancy. Am J Obstet Gynecol. 2000;182:346–350. [PubMed]
95. Di Cianni G, Volpe L, Lencioni C, Miccoli R, Cuccuru I, Ghio A, Chatzianagnostou K, Bottone P, Teti G, Del PS, Benzi L. Prevalence and risk factors for gestational diabetes assessed by universal screening. Diabetes Res Clin Pract. 2003;62:131–137. [PubMed]
96. Yalcin HR, Zorlu CG. Threshold value of glucose screening tests in pregnancy: could it be standardized for every population? Am J Perinatol. 1996;13:317–320. [PubMed]
97. Larijani B, Hossein-nezhad A, Rizvi SW, Munir S, Vassigh AR. Cost analysis of different screening strategies for gestational diabetes mellitus. Endocr Pract. 2003;9:504–509. [PubMed]
98. Hassan A. Screening of pregnant women for gestational diabetes mellitus. J Ayub Med Coll Abbottabad. 2005;17:54–58. [PubMed]
99. Seshiah V, Balaji V, Balaji MS, Sanjeevi CB, Green A. Gestational diabetes mellitus in India. J Assoc Physicians India. 2004;52:707–711. [PubMed]
100. Wagaarachchi PT, Fernando L, Premachadra P, Fernando DJ. Screening based on risk factors for gestational diabetes in an Asian population. J Obstet Gynaecol. 2001;21:32–34. [PubMed]
101. Davey RX, Hamblin PS. Selective versus universal screening for gestational diabetes mellitus: an evaluation of predictive risk factors. Med J Aust. 2001;174:118–121. [PubMed]
102. Yue DK, Molyneaux LM, Ross GP, Constantino MI, Child AG, Turtle JR. Why does ethnicity affect prevalence of gestational diabetes? The underwater volcano theory. Diabet Med. 1996;13:748–752. [PubMed]
103. Miyakoshi K, Tanaka M, Ueno K, Uehara K, Ishimoto H, Yoshimura Y. Cutoff value of 1 h, 50 g glucose challenge test for screening of gestational diabetes mellitus in a Japanese population. Diabetes Res Clin Pract. 2003;60:63–67. [PubMed]
104. Dabelea D, Snell-Bergeon JK, Hartsfield CL, Bischoff KJ, Hamman RF, McDuffie RS. Increasing prevalence of gestational diabetes mellitus (GDM) over time and by birth cohort: Kaiser Permanente of Colorado GDM Screening Program. Diabetes Care. 2005;28:579–584. [PubMed]
105. Thorpe LE, Berger D, Ellis JA, Bettegowda VR, Brown G, Matte T, Bassett M, Frieden TR. Trends and racial/ethnic disparities in gestational diabetes among pregnant women in New York City, 1990–2001. Am J Public Health. 2005;95:1536–1539. [PMC free article] [PubMed]
106. Ferrara A, Kahn HS, Quesenberry CP, Riley C, Hedderson MM. An increase in the incidence of gestational diabetes mellitus: Northern California, 1991–2000. Obstet Gynecol. 2004;103:526–533. [PubMed]
107. Moum KR, Holzman GS, Harwell TS, Parsons SL, Adams SD, Oser CS, Spence MR, Helgerson SD, Gohdes D. Increasing rate of diabetes in pregnancy among American Indian and white mothers in Montana and North Dakota, 1989–2000. Matern Child Health J. 2004;8:71–76. [PubMed]
108. Xiong X, Saunders LD, Wang FL, Demianczuk NN. Gestational diabetes mellitus: prevalence, risk factors, maternal and infant outcomes. Int J Gynaecol Obstet. 2001;75:221–228. [PubMed]
109. Ishak M, Petocz P. Gestational diabetes among Aboriginal Australians: prevalence, time trend, and comparisons with non-Aboriginal Australians. Ethn Dis. 2003;13:55–60. [PubMed]
110. Kim S, Humphrey MD. Decrease in incidence of gestational diabetes mellitus in Far North Queensland between 1992 and 1996. Aust N Z J Obstet Gynaecol. 1999;39:40–43. [PubMed]
111. Beischer NA, Wein P, Sheedy MT, Steffen B. Identification and treatment of women with hyperglycaemia diagnosed during pregnancy can significantly reduce perinatal mortality rates. Aust N Z J Obstet Gynaecol. 1996;36:239–247. [PubMed]
112. Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Diabetes Care. 1997;20:1183–1197. [PubMed]
113. Report of a WHO Consultation. Definition, Diagnosis and Classification of Diabetes Mellitus and its Complications. In: Alwan A, King H, editors. Part 1: Diagnosis and Classification of Diabetes Mellitus. Geneva: World Health Organization. Department of Noncommunicable Disease Surveillance; 1999. pp. 1–59.
114. Strauss RS, Pollack HA. Epidemic increase in childhood overweight, 1986–1998. JAMA. 2001;286:2845–2848. [PubMed]
115. Ogden CL, Carroll MD, Curtin LR, McDowell MA, Tabak CJ, Flegal KM. Prevalence of overweight and obesity in the United States, 1999–2004. JAMA. 2006;295:1549–1555. [PubMed]
116. Mokdad AH, Serdula MK, Dietz WH, Bowman BA, Marks JS, Koplan JP. The spread of the obesity epidemic in the United States, 1991–1998. JAMA. 1999;282:1519–1522. [PubMed]
117. Dabelea D, Hanson RL, Bennett PH, Roumain J, Knowler WC, Pettitt DJ. Increasing prevalence of Type II diabetes in American Indian children. Diabetologia. 1998;41:904–910. [PubMed]
118. Dabelea D, Hanson RL, Bennett PH, Roumain J, Knowler WC, Pettitt DJ. Increasing prevalence of Type II diabetes in American Indian children. Diabetologia. 1998;41:904–910. [PubMed]
119. Dabelea D, Hanson RL, Lindsay RS, Pettitt DJ, Imperatore G, Gabir MM, Roumain J, Bennett PH, Knowler WC. Intrauterine exposure to diabetes conveys risks for type 2 diabetes and obesity: a study of discordant sibships. Diabetes. 2000;49:2208–2211. [PubMed]
120. Pettitt DJ, Knowler WC, Bennett PH, Aleck KA, Baird HR. Obesity in offspring of diabetic Pima Indian women despite normal birth weight. Diabetes Care. 1987;10:76–80. [PubMed]
121. Pettitt DJ, Knowler WC. Long-term effects of the intrauterine environment, birth weight, and breast-feeding in Pima Indians. Diabetes Care. 1998;21 (Suppl 2):B138–B141. [PubMed]
122. Kim C, Newton KM, Knopp RH. Gestational diabetes and the incidence of type 2 diabetes: a systematic review. Diabetes Care. 2002;25:1862–1868. [PubMed]
123. Chiasson JL, Josse RG, Gomis R, Hanefeld M, Karasik A, Laakso M. Acarbose for prevention of type 2 diabetes mellitus: the STOP-NIDDM randomised trial. Lancet. 2002;359:2072–2077. [PubMed]
124. Knowler WC, Barrett-Connor E, Fowler SE, Hamman RF, Lachin JM, Walker EA, Nathan DM. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med. 2002;346:393–403. [PMC free article] [PubMed]
125. Pan XR, Li GW, Hu YH, Wang JX, Yang WY, An ZX, Hu ZX, Lin J, Xiao JZ, Cao HB, Liu PA, Jiang XG, Jiang YY, Wang JP, Zheng H, Zhang H, Bennett PH, Howard BV. Effects of diet and exercise in preventing NIDDM in people with impaired glucose tolerance. The Da Qing IGT and Diabetes Study. Diabetes Care. 1997;20:537–544. [PubMed]
126. Tuomilehto J, Lindstrom J, Eriksson JG, Valle TT, Hamalainen H, Ilanne-Parikka P, Keinanen-Kiukaanniemi S, Laakso M, Louheranta A, Rastas M, Salminen V, Uusitupa M. Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. N Engl J Med. 2001;344:1343–1350. [PubMed]
127. Dabelea D, Knowler WC, Pettitt DJ. Effect of diabetes in pregnancy on offspring: follow-up research in the Pima Indians. J Matern Fetal Med. 2000;9:83–88. [PubMed]
128. Dabelea D, Pettitt DJ. Intrauterine diabetic environment confers risks for type 2 diabetes mellitus and obesity in the offspring, in addition to genetic susceptibility. J Pediatr Endocrinol Metab. 2001;14:1085–1091. [PubMed]
129. Report of a WHO Study Group. Technical Report Series 727. Vol. 727. Geneva, Switzerland: World Health Organization; 1985. Diabetes mellitus: Report of a WHO Study Group; pp. 1–113. [PubMed]
130. Lind T, Phillips PR. Influence of pregnancy on the 75-g OGTT. A prospective multicenter study The Diabetic Pregnancy Study Group of the European Association for the Study of Diabetes. Diabetes. 1991;40 (Suppl 2):8–13. [PubMed]
131. ACOG technical bulletin. Diabetes and pregnancy. Number 200--December 1994 (replaces No. 92, May 1986). Committee on Technical Bulletins of the American College of Obstetricians and Gynecologists. Int J Gynaecol Obstet. 1995;48:331–339. [PubMed]
132. Hoffman L, Nolan C, Wilson JD, Oats JJ, Simmons D. Gestational diabetes mellitus--management guidelines. The Australasian Diabetes in Pregnancy Society. Med J Aust. 1998;169:93–97. [PubMed]
133. O’Sullivan JB, Charles D, Mahan CM, Dandrow RV. Gestational diabetes and perinatal mortality rate. Am J Obstet Gynecol. 1973;116:901–904. [PubMed]
134. Sugawa T. Report from a committee on nutritional and metabolic problems. Nippon Sanka Fujinka Gakkai Zasshi. 1984;36:2055–2058. [PubMed]
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