Papers

Birth weight and non-insulin dependent diabetes: thrifty genotype, thrifty phenotype, or surviving small baby genotype?

^a Diabetes and Arthritis Epidemiology Section, Phoenix Epidemiology and Clinical Research Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Phoenix, Arizona 85014, United States Correspondence to: Dr

Abstract

Objective : To determine the prevalence of diabetes in relation to birth weight in Pima Indians.
Design : Follow up study of infants born during 1940-72 who had undergone a glucose tolerance test at ages 20-39 years.
Setting : Gila River Indian community, Arizona.
Subjects : 1179 American Indians.
Main outcome measure : Prevalence of non-insulin dependent diabetes mellitus (plasma glucose concentration >=11.1 mmol/l two hours after ingestion of carbohydrate).
Results : The prevalence was greatest in those with the lowest and highest birth weights. The age adjusted prevalences for birth weights <2500 g, 2500-4499 g, and >=4500 g were 30%, 17%, and 32%, respectively. When age, sex, body mass index, maternal diabetes during pregnancy, and birth year were controlled for, subjects with birth weights <2500 g had a higher rate than those with weights 2500-4499 g (odds ratio 3.81; 95% confidence interval 1.70 to 8.52). The risk for subsequent diabetes among higher birthweight infants (>=4500 g) was associated with maternal diabetes during pregnancy. Most diabetes, however, occurred in subjects with intermediate birth weights (2500-4500 g).
Conclusions : The relation of the prevalence of diabetes to birth weight in the Pima Indians is U shaped and is related to parental diabetes. Low birth weight is associated with non-insulin dependent diabetes. Given the high mortality of low birthweight infants selective survival in infancy of those genetically predisposed to insulin resistance and diabetes provides an explanation for the observed relation between low birth weight and diabetes and the high prevalence of diabetes in many populations.

Introduction

Recent findings have suggested that low birth weight and weight at 1 year are related to the development of glucose intolerance.*RF 1-3* In men aged 64 years in Hertfordshire, England, the prevalence of non- insulin dependent diabetes or impaired glucose tolerance fell progressively from 40% in those subjects who weighed 2500 g or less at birth to 14% in those whose birth weight was 4310 g or above.¹ Subsequently a similar inverse association between birth weight and plasma glucose concentration 30 minutes after carbohydrate ingestion was reported for men aged 18-25 years,² and between birth weight and either impaired glucose tolerance or diabetes in subjects of both sexes aged 50 years.³ The trends seemed to be independent of current body mass index and social class. These findings have been interpreted as long term effects of nutritional factors which reduce fetal and infant growth and impair the development of the endocrine pancreas and other tissues.⁴

The Pima Indian residents of the Gila River Indian community in Arizona have the highest reported prevalence of non-insulin dependent diabetes, which often has its onset at an early age.*RF 5-7* The importance of maternal glucose intolerance on the intrauterine environment, in addition to the effects of genetic factors, for increased birth weight and subsequent diabetes in this population has been shown previously.*RF 8-10* We examined the relation between birth weight and subsequent glucose tolerance, how this is influenced by parental diabetes, and whether low birth weight is predictive of non-insulin dependent diabetes in this population.

Subjects and methods

A longitudinal study of diabetes and its complications has been conducted among the American Indian population of the Gila River Indian community in Arizona.¹¹ This analysis includes 1179 subjects born between 1940 and 1972 with recorded birth weight, whose heritage was at least half Pima or Tohono O'odham (Papago) or a mixture of these two closely related tribes, who were singleton births, and whose glucose tolerance was evaluated at ages 20-39 years.

For those born before 1965 birth weights were obtained from the medical records of the babies of all women aged 25-44 years who had participated in a population based epidemiological study between 1 March 1965 and 1 March 1967.¹² From 1965-72 birth weights were collected prospectively as part of an ongoing population based study of pregnancy.

About every two years all residents of the community aged 5 years and over are asked to participate in a standardised medical examination which includes the determination of venous plasma glucose concentration two hours after ingesting 75 g carbohydrate. Diabetes was diagnosed according to World Health Organisation criteria if the plasma glucose concentration two hours after ingestion was at least 11.1 mmol/l¹³ at a survey examination or if a casual plasma glucose concentration >=11.1 mmol/l was observed in the course of routine medical care. Blood pressure was measured in supine subjects with a large adult cuff and a mercury sphygmomanometer (W A Baum, Copiaque, New York). Korotkoff sounds phase I and IV were used for systolic and diastolic pressures, respectively. Plasma glucose concentration was estimated by an Autoanalyzer using the potassium ferricyanide method (Technicon Instruments Corporation, Tarrytown, New York).

As parental diabetes is known to be associated with the development of diabetes in young adults and diabetes or glucose intolerance in pregnancy is a risk factor for both high birth weight and diabetes in this population,*RF 8,10-14* the association of birth weight and diabetes was also examined in relation to the presence or absence of parental diabetes and among subjects whose mothers were known not to have diabetes during the pregnancy. Parental diabetes at the latest examination was defined as absent (neither parent diabetic) or present in at least one parent.

The significance of differences in prevalence of diabetes and abnormal glucose tolerance according to age and birth weight was analysed by a Mantel-Haenszel X² test and logistic regression analysis. Age adjustment was made either by the direct method using the age distribution of the 1179 subjects at the time of their glucose tolerance assessment as the reference population (see table II) or by logistic regression using a series of indicator variables for the various categories of birth weight and body mass index for offspring aged 30 years (see table III). As the results did not vary by sex of the offspring the sexes were combined. There were no significant interactions (product terms) in the model. For comparability with previous studies the results presented are confined to singleton pregnancies, and eight sets of twins and one set of triplets were excluded. Inclusion of these multiple births in the analysis, however, did not alter the findings.

Results

Of 2512 singleton births recorded in 1940-72 birth weight was known in 2028, 1179 of whom subsequently had at least one glucose tolerance test when aged 20-39 years. Table I shows the prevalences of abnormal glucose tolerance (plasma glucose concentration at two hours >=7.8 mmol/l) and diabetes according to age group and birth weight. Table II shows the age adjusted prevalence of diabetes. The prevalence of diabetes showed a U shaped relation with birth weight, with the highest rates in those with the highest and those with the lowest birth weights. The age adjusted prevalences of diabetes for birth weights <2500 g, 2500-2999 g, 3000-3499 g, 3500-3999 g, 4000-4499 g, and >=4500 g were 30%, 18%, 16%, 17%, 18%, and 32%, respectively. When examined as a continuous variable in a logistic regression model, age, concurrent body mass index, birth weight, and the quadratic term of birth weight (to allow for a parabolic or U shaped relation) contributed significantly to the prediction of the prevalence of diabetes (P<0.05).

TABLE I - Prevalences of diabetes and abnormal glucose tolerance according to
age group and category of birth weight in 1179 Pima Indians at last biennial
examination
---------------------------------------------------------------------------
                         No (%) within birth weight groups (g)
Age group  ----------------------------------------------------------------
(years)        <2500          2500-3499         3500-4499         >=4500
---------------------------------------------------------------------------
           Plasma glucose concentration at two hours >=11.1 mmol/l
20-24       3/25 (12.0)     18/272 (6.6)      10/173 (5.8)     3/12 (25.0)
25-29       3/10 (30.0)     27/162 (16.7)     20/129 (15.5)    3/11 (27.3)
30-34       3/6 (50.0)      35/145 (24.1)     26/95 (27.4)     3/7 (42.9)
35-39       3/5 (60.0)      32/82 (39.0)      20/43 (46.5)     1/2 (50.0)
---------------------------------------------------------------------------
Total      12/46 (26.1)    112/661 (16.9)     76/440 (17.3)   10/32 (31.3)
---------------------------------------------------------------------------
          Plasma glucose concentration at two hours >=7.8 mmol/l
20-24       7/25 (28.5)     45/272 (16.5)     24/173 (13.9)    5/12 (41.7)
25-29       3/10 (30.0)     56/162 (34.6)     34/129 (26.4)    3/11 (27.3)
30-34       5/6 (83.3)      58/145 (40.0)     46/95 (48.4)     3/7 (42.9)
35-39       4/5 (80.0)      46/82 (56.1)      29/43 (67.4)     1/2 (50.0)
---------------------------------------------------------------------------
Total      19/46 (41.3)    205/661 (31.0)    133/440 (30.2)   12/32 (37.5)

TABLE II - Age adjusted prevalences (68% confidence intervals) of diabetes
according to birth weight among 1179 Pima20Indians aged 20-39 years. Age
adjusted by direct method with age distribution of all subjects as
reference population
---------------------------------------------
                         Age adjusted
                        prevalence (68%
                          confidence
Birth weight (g)           interval)
---------------------------------------------
<2500                30.2 (23.4 to 37.0)
2500-2999            18.4 (15.6 to 21.2)
3000-3499            16.3 (14.6 to 17.9)
3500-3999            17.1 (15.3 to 19.0)
4000-4499            18.2 (13.9 to 22.5)
>=4500               32.2 (23.8 to 40.6)

As the prevalence of diabetes is related to concurrent obesity, the association with low birth weight was examined according to obesity. Within each third of body mass index (weight (kg)/(height (m))²) the highest age adjusted prevalences in general occurred in subjects with the lowest and in those with the highest birth weights. The effect of birth weight on the subsequent prevalence, however, was most evident in the lower third of body mass index (<29.8; table III).

TABLE III - Age-adjusted prevalences (68% confidence intervals) of diabetes
according to birth weight and category of current body mass index among 1179
Pima Indians. Age adjusted to a mean age of 30 years by using logistic
regression
------------------------------------------------------------------
                                               Age adjusted
                                                prevalence
Body mass index                              (68% confidence
(kg/m2)        Birth weight (g)           interval)
------------------------------------------------------------------
Lowest third            <2500              35.4 (23.2 to 49.9)
                        2500-3499          13.0 (10.7 to 15.7)
                        3500-4499          12.2 (9.3 to 15.8)
                        >=4500             52.4 (36.1 to 68.2)
Middle third            <2500              35.6 (23.0 to 50.6)
                        2500-3499          18.6 (16.0 to 21.5)
                        3500-4499          21.4 (17.8 to 25.6)
                        <4500              22.7 (8.8 to 47.0)
Upper third             <2500              32.6 (19.5 to 49.5)
                        2500-3499          25.8 (22.5 to 29.3)
                        3500-4499          23.4 (20.1 to 27.1)
                        >=4500             36.0 (23.8 to 50.2)

Among subjects with at least one diabetic parent, the age adjusted prevalences for birth weights <2500 g, 2500-4499 g, and >=4500 g were 38%, 20%, and 35%, respectively. By contrast, diabetes was present in only four of the 155 subjects with two non-diabetic parents, and thus the effect of birth weight on the prevalence in this group could not be assessed. Nevertheless, this illustrates that the relation of low birth weight and subsequent diabetes is seen primarily in subjects with a parental history of diabetes.

As diabetes in pregnancy is an established risk factor for both high birth weight and diabetes in this population,*RF 8,10-14* the relation between prevalence and birth weight was examined in offspring of women who did not have diabetes during pregnancy. The age adjusted prevalence in this group of 903 subjects according to birth weights <2500 g, 2500- 4499 g, and >=4500 g was 34%, 15%, and 20%, respectively. A birth weight of <2500 g was significantly associated with a higher prevalence (age adjusted Mantel-Haenszel odds ratio 3.37%; 95% confidence interval 1.58 to 7.14; P=0.002) than a birth weight of 2500-4499 g. Exclusion of subjects whose mothers may have had diabetes in pregnancy clearly reduced the proportion with diabetes in the highest birthweight category (>=4500 g).

The independent association of birth weight and diabetes was also examined in all 1179 subjects by using logistic regression analysis. When age, sex, body mass index, maternal diabetes during pregnancy, and birth year were controlled for by logistic regression analysis, subjects with low birth weights (<2500 g) were significantly more likely to have diabetes than those with birth weights of 2500-4499 g (3.81; 1.70 to 8.52; table IV). The risk of diabetes in subjects with high birth weights (>=4500 g) seems to be attributable primarily to maternal diabetes during pregnancy because after we included diabetes in pregnancy in the model the association of high birth weight with diabetes was no longer significant, but the strong significant relation between low birth weight and subsequent diabetes remained.

TABLE IV - Multiple logistic regression analysis for diabetes in 1179 Pima
Indians controlled for birth weight, age, body mass index, maternal diabetes
during pregnancy, and birth year
----------------------------------------------------------------------------------
                                                   Odds ratio
                                                (95% confidence
Variable                                           interval)            P value
----------------------------------------------------------------------------------
Age (per 10 years)                            3.08 (1.96 to 4.86)        0.0001
Body mass index                               1.06 (1.04 to 1.09)        0.0001
Low birth weight* (low/normal)                3.81 (1.70 to 8.52)        0.001
High birth weight* (high/normal)              1.80 (0.63 to 5.10)        0.269
Maternal diabetes during pregnancy (yes/no)  10.73 (4.76 to 24.17)       0.0001
Birth year (per year)                         0.94 (0.90 to 0.97)        0.001
----------------------------------------------------------------------------------
 *Low birthweight and high birthweight variables compared weights below
2500 g and above 4500 g, respectively, with those 2500-4499 g. Sex was not
significant and therefore was not included as a covariate.

Mean systolic and diastolic blood pressure did not differ significantly among any of the birthweight categories.

Discussion

In Pima Indian adults, as in British populations,*RF 1-3* low birth weight is associated with an increased prevalence of non-insulin dependent diabetes. In the Pima this relation is evident in subjects as young as 20- 30 years of age. In contrast with the reports of Hales and Barker and their colleagues, which showed much higher rates of diabetes in low than in high birthweight subjects,*RF 1-3* the overall relation of glucose tolerance with birth weight in Pima Indians is U shaped, with higher rates of diabetes in those with high as well as in those with low birth weights.

The increased risk of diabetes among Pima Indians with high birth weight can largely be explained by the presence of maternal diabetes during pregnancy,^8,9 perhaps mediated by metabolic fuel abnormalities in utero.¹⁵ We have shown previously how this effect may give rise to an increasing prevalence of diabetes in successive generations.⁸ Exclusion of offspring of mothers who developed diabetes during pregnancy or controlling for maternal diabetes in pregnancy reduced the prevalence of diabetes in subjects with birth weights of >=4500 g to levels similar to those seen in subjects with normal birth weights. The lack of an association between high birth weight and glucose intolerance in British studies probably reflects a lower prevalence of diabetes during pregnancy.

Although our study is a longitudinal population based study, birth weights were known for only 81% of the subjects born between 1940 and 1972, and only 58% of these had had glucose tolerance tests at ages 20-39 years. Most of the others had received glucose tolerance tests but had not been examined at 20-39 years of age and were therefore not considered in the present analysis. Unless the birth weights of low birthweight infants destined to develop diabetes 20 or more years later were selectively recorded, it seems unlikely that incomplete ascertainment would influence our results. Other possible sources of bias are temporal trends of socioeconomic status, health care, and an increasing prevalence of diabetes, but when we controlled for year of birth with logistic regression low birth weight was still independently associated with a higher prevalence of diabetes. Furthermore, the relation of birth weight to prevalence of diabetes remains after current body mass index was controlled for and are seen primarily among subjects with at least one parent with diabetes.

Thrifty genotype, thrifty phenotype

In 1962, as an explanation for the high prevalence of diabetes, Neel hypothesised the evolution of a "thrifty genotype" which resulted in selective survival advantage in times of fluctuating feast and famine by allowing storage of calories in times of plenty.¹⁶ He argued that such a thrifty genotype became detrimental when food supplies were constant and abundant and led to an increased prevalence of obesity and non-insulin dependent diabetes in certain populations such as the Pima.^17,18 Recently Hales and Barker have hypothesised that low birth weight, which is a reflection of nutritional deprivation in utero¹⁹ and which impairs the development of the fetal pancreas,*RF 20-23* predisposes to diabetes in later life.⁴ They have suggested that non-insulin dependent diabetes is mainly the result of environmental factors and that genetic factors play little or no role in its development and called this the "thrifty phenotype" hypothesis.⁴ In their studies of birth weight, as in ours, follow up into adulthood is of necessity limited to survivors, and their hypothesis takes no account of the high mortality associated with low birth weight.

In spite of the excess of diabetes associated with low and high birth weight in the Pima, only 6% who developed diabetes by 20-39 years of age had a birth weight <2500 g; a similar proportion had birth weights >=4500 g. Consequently, most Pimas who develop diabetes have birth weights that fall within the usual range. Thus, the high prevalence of diabetes in this population cannot reasonably be attributed to nutritional deficiencies in utero of the type that led to low birth weight, and other explanations for the relation of diabetes to birth weight and the high prevalence of the disease in the Pima and other populations must be sought.

Surviving small baby genotype

As an alternative we propose that the increase in prevalence of diabetes among subjects with low birth weight, now shown in several studies, could reflect the selective survival of low birthweight infants genetically susceptible to developing diabetes. As insulin resistance seems to be an important abnormality preceding non-insulin dependent diabetes in the Pima Indians^24,25 and in other populations²⁶ low (and high) birth weight might be expected to be associated with insulin resistance. We propose therefore that genetic predisposition to insulin resistance may represent the mechanism which facilitates such selective survival advantage and over many generations ultimately leads to high prevalences of diabetes and other manifestations of insulin resistance in contemporary populations.

There are several studies consistent with this hypothesis. Recently Barker et al have shown a high prevalence of the insulin resistance syndrome in adults who had been low birthweight infants.²⁷ In addition, highly significant inverse relations between birth weight and insulin concentrations after fasting and two hours after carbohydrate ingestion, blood pressure, truncal obesity, and an index of the insulin resistance syndrome have been reported in Mexican-Americans and non-Hispanic white people from San Antonio.²⁸ Thus, several characteristics related to insulin resistance, besides diabetes and glucose intolerance, are found more often in subjects with low birth weights.

Conclusion

s

The present study in Pima Indians provides further evidence for an association between low birth weight and glucose tolerance. Unlike the findings of previous British studies, however, the association of birth weight and diabetes is U shaped, with a higher prevalence of diabetes occurring in subjects with both low and high birth weights. Given the high mortality among low birthweight infants and that most diabetes occurs in Pima Indians with birth weights in the usual range, we propose that the excess of diabetes seen in subjects with low birth weight in the Pima and other populations may reflect the selective survival of infants genetically susceptible to insulin resistance and subsequently to developing non-insulin dependent diabetes.

We thank the members of the Gila River Indian community for taking part in the study and the staff of the diabetes and arthritis epidemiology section for performing the clinical examinations and laboratory tests.

1. Hales CN, Barker DJP, Clark PMS, Cox LJ, Fall C, Osmond C, et al. Fetal growth and impaired glucose tolerance at age 64. BMJ 1991;303:1019-22.
2. Robinson S, Walton RJ, Clark PM, Barker DJP, Hales CN, Osmond C. The relation of fetal growth to plasma glucose in young men. Diabetologia 1992;35:444-6. [Medline]
3. Phipps K, Barker DJP, Hales CN, Fall CHD, Osmond C, Clark PMS. Fetal20growth and impaired glucose tolerance in men and women. Diabetologia 1993;36:225-8. [Medline]
4. Hales CN, Barker DJP. Type 2 (non-insulin-dependent) diabetes mellitus: the thrifty phenotype hypothesis. Diabetologia 1992;35:595- 601. [Medline]
5. Knowler WC, Bennett PH, Hamman RF, Miller M. Diabetes incidence and prevalence in Pima Indians: a 19-fold greater incidence than in Rochester, Minnesota. Am J Epidemiol 1978;108:497-505. [Abstract/Free Full Text]
6. Knowler WC, Pettitt DJ, Saad MF, Bennett PH. Diabetes mellitus in the20Pima Indians: incidence, risk factors and pathogenesis. Diabetes Metab Rev 1990;6:1-27. [Medline]
7. Savage PJ, Bennett PH, Senter RG, Miller M. High prevalence of diabetes in young Pima Indians: evidence of phenotypic variation in a genetically isolated population. Diabetes 1979;28:939-42.
8. Pettitt DJ, Aleck KA, Baird HR, Carraher MJ, Bennett PH, Knowler WC. Congenital susceptibility to NIDDM: role of intrauterine environment. Diabetes 1988;37:622-8. [Abstract]
9. Pettitt DJ, Bennett PH, Saad MF, Charles MA, Nelson RJ, Knowler WC. Abnormal glucose tolerance during pregnancy in Pima Indian women: longterm effects on offspring. Diabetes 1991;40:126-30.
10. Pettitt DJ, Baird HR, Aleck KA, Bennett PH, Knowler WC. Excessive obesity in offspring of Pima Indian women with diabetes during pregnancy. N Engl J Med 1983;308:242-5. [Abstract]
11. Bennett PH, Burch TA, Miller M. Diabetes mellitus in American (Pima) Indians. Lancet 1971;ii:125-8.
12. Comess LJ, Bennett PH, Burch TA, Miller M. Congenital anomalies and diabetes in Pima Indians of Arizona. Diabetes 1969;18:471-7. [Medline]
13. WHO Study Group on Diabetes Mellitus. Second report. World Health Organ Tech Rep Ser 1985;727:9-17.
14. 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;3:458-64. [Abstract]
15. Frienkel N. Of pregnancy and progeny. Diabetes 1980;29:1023-9. [Abstract]
16. Neel JV. Diabetes mellitus; a thrifty genotype rendered detrimental by `progress'? Am J Hum Genet 1962;14:353-62.
17. Neel JV. The thrifty genotype revisited. In: Kobberling J, Tattersall20R, eds. The genetics of diabetes mellitus. Proceedings of the Serono symposium. London: Academic Press, 1982;283-93.
18. Thrifty genotype rendered detrimental by progress? [editorial].20Lancet 1989;ii:839-40.
19. McCance RA, Widdowson EM. The determinants of fetal growth and form. Proc R Soc Lond 1974;185:1-17. [Medline]
20. Sweene I, Bone AJ, Howell SL, Hellerstrom C. Effects of glucose and amino acids on the biosynthesis of DNA and insulin in fetal rats maintained in tissue culture. Diabetes 1981;29:686-92. [Medline]
21. Sweene I, Crace CJ, Milner RDG. Persistent impairment of insulin20secretory response to glucose in adult rats after limited period of protein-calorie malnutrition early in life. Diabetes 1987;36:454-8. [Abstract]
22. Van Assche FA, Aerts L. The fetal endocrine pancreas. Contrib Gynecol Obstet 1979;5:44-57. [Medline]
23. Wilkin TJ. Early nutrition and diabetes mellitus (editorial). BMJ 1993;306:283-4.
24. Lillioja S, Mott DM, Howard BV, Bennett PH, Yki-Jarvinen H, Freymond D, et al. Impaired glucose tolerance as a disorder of insulin action: longitudinal and cross-sectional studies in Pima Indians. N Engl J Med 1988;318:1217-25. [Abstract]
25. Lillioja S, Mott DM, Spraul M, Ferraro R, Foley JE, Ravussin E, et al. Insulin20resistance and insulin secretory dysfunction as precursors of non -insulin dependent diabetes mellitus: prospective studies in Pima Indians. N Engl20J Med 1993;329:1988-92.
26. Martin BC, Warram JH, Krolewski AS, Bergman RN, Soeldner JS, Kahn CR. Role of glucose and insulin resistance in development of Type 2 diabetes mellitus: results of a 25-year follow-up study. Lancet 1992;340:925-9. [Medline]
27. Barker DJP, Hales CN, Fall CHD, Osmond C, Phipps K, Clark PMS. Type 2 (non-insulin-dependent) diabetes mellitus, hypertension and hyperlipidaemia (syndrome X): relation to fetal growth. Diabetologia 1993;36:62-7. [Medline]
28. Athens M, Valdez R, Stern M. Effect of birth weight on future development of "Syndrome X" in adult life. Diabetes 1993;42:(suppl 1):61A.

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    StumbleUpon    Technorati    What's this?

This article has been cited by other articles:

• Rajaleid, K., Hallqvist, J., Koupil, I. (2009). The effect of early life factors on 28 day case fatality after acute myocardial infarction. Scand J Public Health 37: 720-727 [Abstract]  
• Muhlhausler, B. S., Duffield, J. A., Ozanne, S. E., Pilgrim, C., Turner, N., Morrison, J. L., McMillen, I. C. (2009). The transition from fetal growth restriction to accelerated postnatal growth: a potential role for insulin signalling in skeletal muscle. J. Physiol. 587: 4199-4211 [Abstract] [Full text]  
• Chiavaroli, V., Giannini, C., D'Adamo, E., de Giorgis, T., Chiarelli, F., Mohn, A. (2009). Insulin Resistance and Oxidative Stress in Children Born Small and Large for Gestational Age. Pediatrics 124: 695-702 [Abstract] [Full text]  
• Plagemann, A., Harder, T. (2009). Birth Weight and Type 2 Diabetes in Adults. JAMA 301: 1540-1540 [Full text]  
• Mandl, L A, Costenbader, K H, Simard, J F, Karlson, E W (2009). Is birthweight associated with risk of rheumatoid arthritis? Data from a large cohort study. Ann Rheum Dis 68: 514-518 [Abstract] [Full text]  
• Kaijser, M., Edstedt Bonamy, A.-K., Akre, O., Cnattingius, S., Granath, F., Norman, M., Ekbom, A. (2009). Perinatal Risk Factors for Diabetes in Later Life. Diabetes 58: 523-526 [Abstract] [Full text]  
• Chen, W., Srinivasan, S. R., Berenson, G. S. (2009). Influence of Birth Weight on White Blood Cell Count in Biracial (Black-White) Children, Adolescents, and Young Adults: The Bogalusa Heart Study. Am J Epidemiol 169: 214-218 [Abstract] [Full text]  
• Whincup, P. H., Kaye, S. J., Owen, C. G., Huxley, R., Cook, D. G., Anazawa, S., Barrett-Connor, E., Bhargava, S. K., Birgisdottir, B. E., Carlsson, S., de Rooij, S. R., Dyck, R. F., Eriksson, J. G., Falkner, B., Fall, C., Forsen, T., Grill, V., Gudnason, V., Hulman, S., Hypponen, E., Jeffreys, M., Lawlor, D. A., Leon, D. A., Minami, J., Mishra, G., Osmond, C., Power, C., Rich-Edwards, J. W., Roseboom, T. J., Sachdev, H. S., Syddall, H., Thorsdottir, I., Vanhala, M., Wadsworth, M., Yarbrough, D. E. (2008). Birth Weight and Risk of Type 2 Diabetes: A Systematic Review. JAMA 300: 2886-2897 [Abstract] [Full text]  
• Rotteveel, J., van Weissenbruch, M. M., Twisk, J. W. R., Delemarre-Van de Waal, H. A. (2008). Infant and Childhood Growth Patterns, Insulin Sensitivity, and Blood Pressure in Prematurely Born Young Adults. Pediatrics 122: 313-321 [Abstract] [Full text]  
• Duffield, J. A., Vuocolo, T., Tellam, R., Yuen, B. S., Muhlhausler, B. S., McMillen, I. C. (2008). Placental restriction of fetal growth decreases IGF1 and leptin mRNA expression in the perirenal adipose tissue of late gestation fetal sheep. Am. J. Physiol. Regul. Integr. Comp. Physiol. 294: R1413-R1419 [Abstract] [Full text]  
• Xiao, X., Zhang, Z.-X., Cohen, H. J., Wang, H., Li, W., Wang, T., Xu, T., Liu, A., Gai, M.-Y., Ying, S., Schmitz, O., Yi, Z. (2008). Evidence of a Relationship Between Infant Birth Weight and Later Diabetes and Impaired Glucose Regulation in a Chinese Population. Diabetes Care 31: 483-487 [Abstract] [Full text]  
• O'Regan, D., Kenyon, C. J, Seckl, J. R, Holmes, M. C (2008). Prenatal dexamethasone 'programmes' hypotension, but stress-induced hypertension in adult offspring. J Endocrinol 196: 343-352 [Abstract] [Full text]  
• Pettitt, D. J., Jovanovic, L. (2007). Low Birth Weight as a Risk Factor for Gestational Diabetes, Diabetes, and Impaired Glucose Tolerance During Pregnancy. Diabetes Care 30: S147-S149 [Full text]  
• Kelishadi, R. (2007). Childhood Overweight, Obesity, and the Metabolic Syndrome in Developing Countries. Epidemiol Rev 0: mxm003v1-26 [Abstract] [Full text]  
• Huxley, R., Owen, C. G, Whincup, P. H, Cook, D. G, Rich-Edwards, J., Smith, G. D., Collins, R. (2007). Is birth weight a risk factor for ischemic heart disease in later life?. Am. J. Clin. Nutr. 85: 1244-1250 [Abstract] [Full text]  
• Arfa, I., Abid, A., Malouche, D., Ben Alaya, N., Roland Azegue, T., Mannai, I., Majdi Zorgati, M., Chiheb Ben Rayana, M., Ben Ammar, S., Blousa-Chabchoub, S., Ben Romdhane, H., Zouari, B., Koussay Dellagi, M., Abdelhak, S. (2007). Familial aggregation and excess maternal transmission of type 2 diabetes in Tunisia. Postgrad. Med. J. 83: 348-351 [Abstract] [Full text]  
• Harder, T., Rodekamp, E., Schellong, K., Dudenhausen, J. W., Plagemann, A. (2007). Birth Weight and Subsequent Risk of Type 2 Diabetes: A Meta-Analysis. Am J Epidemiol 165: 849-857 [Abstract] [Full text]  
• Jovanovic, L. (2007). . Diabetes Spectr. 20: 82-83 [Full text]  
• Ozaki, R., Qiao, Q., Wong, G. W K, Chan, M. H M, So, W.-Y., Tong, P. C Y, Ho, C S, Tin-Choi Ko, G., Kong, A. P S, Lam, C. W K, Tuomilehto, J., Chan, J. C N (2007). Overweight, family history of diabetes and attending schools of lower academic grading are independent predictors for metabolic syndrome in Hong Kong Chinese adolescents. Arch. Dis. Child. 92: 224-228 [Abstract] [Full text]  
• Thomas, G N., Schooling, C M., McGhee, S. M, Ho, S.-Y., Cheung, B. M Y, Wat, N. M, Janus, E. D, Lam, T. H., for the Hong Kong Cardiovascular Risk Factor Preva, (2006). Identification of factors differentially associated with isolated impaired fasting glucose and isolated post-load impaired glucose tolerance: the Hong Kong Cardiovascular Risk Factor Study.. Eur J Endocrinol 155: 623-632 [Abstract] [Full text]  
• de Rooij, S. R., Painter, R. C., Phillips, D. I.W., Osmond, C., Michels, R. P.J., Godsland, I. F., Bossuyt, P. M.M., Bleker, O. P., Roseboom, T. J. (2006). Impaired Insulin Secretion After Prenatal Exposure to the Dutch Famine. Diabetes Care 29: 1897-1901 [Abstract] [Full text]  
• Arya, R., Demerath, E., Jenkinson, C. P., Goring, H. H.H., Puppala, S., Farook, V., Fowler, S., Schneider, J., Granato, R., Resendez, R. G., Dyer, T. D., Cole, S. A., Almasy, L., Comuzzie, A. G., Siervogel, R. M., Bradshaw, B., DeFronzo, R. A., MacCluer, J., Stern, M. P., Towne, B., Blangero, J., Duggirala, R. (2006). A quantitative trait locus (QTL) on chromosome 6q influences birth weight in two independent family studies. Hum Mol Genet 15: 1569-1579 [Abstract] [Full text]  
• Franks, P. W., Looker, H. C., Kobes, S., Touger, L., Tataranni, P. A., Hanson, R. L., Knowler, W. C. (2006). Gestational Glucose Tolerance and Risk of Type 2 Diabetes in Young Pima Indian Offspring. Diabetes 55: 460-465 [Abstract] [Full text]  
• Sloboda, D. M., Moss, T. J. M., Li, S., Doherty, D. A., Nitsos, I., Challis, J. R. G., Newnham, J. P. (2005). Hepatic glucose regulation and metabolism in adult sheep: effects of prenatal betamethasone. Am. J. Physiol. Endocrinol. Metab. 289: E721-E728 [Abstract] [Full text]  
• Barker, D. J.P., Bagby, S. P. (2005). Developmental Antecedents of Cardiovascular Disease: A Historical Perspective. J. Am. Soc. Nephrol. 16: 2537-2544 [Abstract] [Full text]  
• Sachdev, H. S, Fall, C. H., Osmond, C., Lakshmy, R., Dey Biswas, S. K, Leary, S. D, Reddy, K. S., Barker, D. J., Bhargava, S. K (2005). Anthropometric indicators of body composition in young adults: relation to size at birth and serial measurements of body mass index in childhood in the New Delhi birth cohort. Am. J. Clin. Nutr. 82: 456-466 [Abstract] [Full text]  
• Syddall, H. E., Sayer, A. A., Simmonds, S. J., Osmond, C., Cox, V., Dennison, E. M., Barker, D. J. P., Cooper, C. (2005). Birth Weight, Infant Weight Gain, and Cause-specific Mortality: The Hertfordshire Cohort Study. Am J Epidemiol 161: 1074-1080 [Abstract] [Full text]  
• Meyre, D., Boutin, P., Tounian, A., Deweirder, M., Aout, M., Jouret, B., Heude, B., Weill, J., Tauber, M., Tounian, P., Froguel, P. (2005). Is Glutamate Decarboxylase 2 (GAD2) a Genetic Link between Low Birth Weight and Subsequent Development of Obesity in Children?. J. Clin. Endocrinol. Metab. 90: 2384-2390 [Abstract] [Full text]  
• Prentice, A M, Moore, S E (2005). Early programming of adult diseases in resource poor countries. Arch. Dis. Child. 90: 429-432 [Abstract] [Full text]  
• Touger, L., Looker, H. C., Krakoff, J., Lindsay, R. S., Cook, V., Knowler, W. C. (2005). Early Growth in Offspring of Diabetic Mothers. Diabetes Care 28: 585-589 [Abstract] [Full text]  
• Jimenez-Chillaron, J. C., Hernandez-Valencia, M., Reamer, C., Fisher, S., Joszi, A., Hirshman, M., Oge, A., Walrond, S., Przybyla, R., Boozer, C., Goodyear, L. J., Patti, M.-E. (2005). {beta}-Cell Secretory Dysfunction in the Pathogenesis of Low Birth Weight-Associated Diabetes: A Murine Model. Diabetes 54: 702-711 [Abstract] [Full text]  
• Boney, C. M., Verma, A., Tucker, R., Vohr, B. R. (2005). Metabolic Syndrome in Childhood: Association With Birth Weight, Maternal Obesity, and Gestational Diabetes Mellitus. Pediatrics 115: e290-e296 [Abstract] [Full text]  
• Simmons, R. (2004). Fetal Origins of Adult Disease: Concepts and Controversies. NeoReviews 5: e511-e515 [Full text]  
• Barker, D.J.P. (2004). The Developmental Origins of Adult Disease. J. Am. Coll. Nutr. 23: 588S-595S [Abstract] [Full text]  
• O'Regan, D., Kenyon, C. J., Seckl, J. R., Holmes, M. C. (2004). Glucocorticoid exposure in late gestation in the rat permanently programs gender-specific differences in adult cardiovascular and metabolic physiology. Am. J. Physiol. Endocrinol. Metab. 287: E863-E870 [Abstract] [Full text]  
• Alberti, G., Zimmet, P., Shaw, J., Bloomgarden, Z., Kaufman, F., Silink, M. (2004). Type 2 Diabetes in the Young: The Evolving Epidemic: The International Diabetes Federation Consensus Workshop. Diabetes Care 27: 1798-1811 [Full text]  
• McCarron, P, Davey Smith, G, Hattersley, A T (2004). Type 2 diabetes in grandparents and birth weight in offspring and grandchildren in the ALSPAC study. J. Epidemiol. Community Health 58: 517-522 [Abstract] [Full text]  
• Bloomgarden, Z. T. (2004). Type 2 Diabetes in the Young: The evolving epidemic. Diabetes Care 27: 998-1010 [Full text]  
• Saw, S-M, Tong, L, Chia, K-S, Koh, D, Lee, Y-S, Katz, J, Tan, D T H (2004). The relation between birth size and the results of refractive error and biometry measurements in children. Br J Ophthalmol 88: 538-542 [Abstract] [Full text]  
• Cianfarani, S., Martinez, C., Maiorana, A., Scire, G., Spadoni, G. L., Boemi, S. (2004). Adiponectin Levels Are Reduced in Children Born Small for Gestational Age and Are Inversely Related to Postnatal Catch-Up Growth. J. Clin. Endocrinol. Metab. 89: 1346-1351 [Abstract] [Full text]  
• Jovanovic, L. (2004). Never Say Never in Medicine: Confessions of an old dog. Diabetes Care 27: 610-612 [Full text]  
• Eriksson, J. G., Forsen, T. J., Osmond, C., Barker, D. J.P. (2003). Pathways of Infant and Childhood Growth That Lead to Type 2 Diabetes. Diabetes Care 26: 3006-3010 [Abstract] [Full text]  
• Lauren, L., Jarvelin, M.-R., Elliott, P., Sovio, U., Spellman, A., McCarthy, M., Emmett, P., Rogers, I., Hartikainen, A.-L., Pouta, A., Hardy, R., Wadsworth, M., Helmsdal, G., Olsen, S., Bakoula, C., Lekea, V., Millwood, I. (2003). Relationship between birthweight and blood lipid concentrations in later life: evidence from the existing literature. Int J Epidemiol 32: 862-876 [Abstract] [Full text]  
• Hypponen, E., Power, C., Smith, G. D. (2003). Prenatal Growth, BMI, and Risk of Type 2 Diabetes by Early Midlife. Diabetes Care 26: 2512-2517 [Abstract] [Full text]  
• Yajnik, C. S., Joglekar, C. V., Pandit, A. N., Bavdekar, A. R., Bapat, S. A., Bhave, S. A., Leary, S. D., Fall, C. H.D. (2003). Higher Offspring Birth Weight Predicts the Metabolic Syndrome in Mothers but Not Fathers 8 Years After Delivery: The Pune Children's Study. Diabetes 52: 2090-2096 [Abstract] [Full text]  
• Anazawa, S., Atsumi, Y., Matsuoka, K. (2003). Low Birth Weight and Development of Type 2 Diabetes in a Japanese Population. Diabetes Care 26: 2210-2211 [Full text]  
• Veening, M. A., van Weissenbruch, M. M., Heine, R. J., Delemarre-van de Waal, H. A. (2003). {beta}-Cell Capacity and Insulin Sensitivity in Prepubertal Children Born Small for Gestational Age: Influence of Body Size During Childhood. Diabetes 52: 1756-1760 [Abstract] [Full text]  
• Birgisdottir, B. E, Gunnarsdottir, I., Thorsdottir, I., Gudnason, V., Benediktsson, R. (2003). Reply to ND Willows and K Gray-Donald. Am. J. Clin. Nutr. 77: 1529-1530 [Full text]  
• Goran, M. I., Ball, G. D. C., Cruz, M. L. (2003). Obesity and Risk of Type 2 Diabetes and Cardiovascular Disease in Children and Adolescents. J. Clin. Endocrinol. Metab. 88: 1417-1427 [Abstract] [Full text]  
• Sothern, M. S., Gordon, S. T. (2003). Prevention of Obesity in Young Children: A Critical Challenge for Medical Professionals. CLIN PEDIATR 42: 101-111  
• Wei, J.-N., Sung, F.-C., Li, C.-Y., Chang, C.-H., Lin, R.-S., Lin, C.-C., Chiang, C.-C., Chuang, L.-M. (2003). Low Birth Weight and High Birth Weight Infants Are Both at an Increased Risk to Have Type 2 Diabetes Among Schoolchildren in Taiwan. Diabetes Care 26: 343-348 [Abstract] [Full text]  
• Murtaugh, M. A., Jacobs, D. R. Jr., Moran, A., Steinberger, J., Sinaiko, A. R. (2003). Relation of Birth Weight to Fasting Insulin, Insulin Resistance, and Body Size in Adolescence. Diabetes Care 26: 187-192 [Abstract] [Full text]  
• Lindsay, R. S., Hanson, R. L., Wiedrich, C., Knowler, W. C., Bennett, P. H., Baier, L. J. (2003). The Insulin Gene Variable Number Tandem Repeat Class I/III Polymorphism Is in Linkage Disequilibrium With Birth Weight but Not Type 2 Diabetes in the Pima Population. Diabetes 52: 187-193 [Abstract] [Full text]  
• Laakso, M., Kuusisto, J. (2003). Diabetology for cardiologists. Eur Heart J Suppl 5: B5-B13 [Abstract]  
• Gunnarsdottir, I., Birgisdottir, B. E, Thorsdottir, I., Gudnason, V., Benediktsson, R. (2002). Size at birth and coronary artery disease in a population with high birth weight. Am. J. Clin. Nutr. 76: 1290-1294 [Abstract] [Full text]  
• Jaquet, D., Tregouet, D. A., Godefroy, T., Nicaud, V., Chevenne, D., Tiret, L., Czernichow, P., Levy-Marchal, C. (2002). Combined Effects of Genetic and Environmental Factors on Insulin Resistance Associated With Reduced Fetal Growth. Diabetes 51: 3473-3478 [Abstract] [Full text]  
• Veening, M. A., van Weissenbruch, M. M., Delemarre-van de Waal, H. A. (2002). Glucose Tolerance, Insulin Sensitivity, and Insulin Secretion in Children Born Small for Gestational Age. J. Clin. Endocrinol. Metab. 87: 4657-4661 [Abstract] [Full text]  
• Seghieri, G., Anichini, R., De Bellis, A., Alviggi, L., Franconi, F., Breschi, M. C. (2002). Relationship Between Gestational Diabetes Mellitus and Low Maternal Birth Weight. Diabetes Care 25: 1761-1765 [Abstract] [Full text]  
• Sandhu, M. S., Luben, R., Day, N. E., Khaw, K.-T. (2002). Self-Reported Birth Weight and Subsequent Risk of Colorectal Cancer. Cancer Epidemiol. Biomarkers Prev. 11: 935-938 [Abstract] [Full text]  
• Grant, P. J (2002). Diabetes and cardiovascular disease: the Gordian Knot. British Journal of Diabetes & Vascular Disease 2: 347-348  
• Simmons, D., Breier, B. H. (2002). Fetal Overnutrition in Polynesian Pregnancies and in Gestational Diabetes May Lead to Dysregulation of the Adipoinsular Axis in Offspring. Diabetes Care 25: 1539-1544 [Abstract] [Full text]  
• Bertin, E., Gangnerau, M.-N., Bellon, G., Bailbe, D., Arbelot De Vacqueur, A., Portha, B. (2002). Development of beta -cell mass in fetuses of rats deprived of protein and/or energy in last trimester of pregnancy. Am. J. Physiol. Regul. Integr. Comp. Physiol. 283: R623-R630 [Abstract] [Full text]  
• La Batide-Alanore, A., Tregouet, D.-A., Jaquet, D., Bouyer, J., Tiret, L. (2002). Familial Aggregation of Fetal Growth Restriction in a French Cohort of 7,822 Term Births between 1971 and 1985. Am J Epidemiol 156: 180-187 [Abstract] [Full text]  
• Innes, K. E., Byers, T. E., Marshall, J. A., Baron, A., Orleans, M., Hamman, R. F. (2002). Association of a Woman's Own Birth Weight With Subsequent Risk for Gestational Diabetes. JAMA 287: 2534-2541 [Abstract] [Full text]  
• Jensen, C. B., Storgaard, H., Dela, F., Holst, J. J., Madsbad, S., Vaag, A. A. (2002). Early Differential Defects of Insulin Secretion and Action in 19-Year-Old Caucasian Men Who Had Low Birth Weight. Diabetes 51: 1271-1280 [Abstract] [Full text]  
• Dyck, R., Klomp, H., Tan, L. K., Turnell, R. W., Boctor, M. A. (2002). A Comparison of Rates, Risk Factors, and Outcomes of Gestational Diabetes Between Aboriginal and Non-Aboriginal Women in the Saskatoon Health District. Diabetes Care 25: 487-493 [Abstract] [Full text]  
• Araneta, M. R. G., Wingard, D. L., Barrett-Connor, E. (2002). Type 2 Diabetes and Metabolic Syndrome in Filipina-American Women : A high-risk nonobese population. Diabetes Care 25: 494-499 [Abstract] [Full text]  
• Li, C., Johnson, M. S., Goran, M. I. (2001). Effects of Low Birth Weight on Insulin Resistance Syndrome in Caucasian and African-American Children. Diabetes Care 24: 2035-2042 [Abstract] [Full text]  
• Lindsay, R. S., Kobes, S., Knowler, W. C., Bennett, P. H., Hanson, R. L. (2001). Genome-Wide Linkage Analysis Assessing Parent-of-Origin Effects in the Inheritance of Type 2 Diabetes and BMI in Pima Indians. Diabetes 50: 2850-2857 [Abstract] [Full text]  
• Hales, C N., Barker, D. J P (2001). The thrifty phenotype hypothesis: Type 2 diabetes. Br Med Bull 60: 5-20 [Abstract] [Full text]  
• Lindsay, R. S, Bennett, P. H (2001). Type 2 diabetes, the thrifty phenotype - an overview. Br Med Bull 60: 21-32 [Full text]  
• Frayling, T. M, Hattersley, A. T (2001). The role of genetic susceptibility in the association of low birth weight with type 2 diabetes. Br Med Bull 60: 89-101 [Abstract] [Full text]  
• Bertram, C. E, Hanson, M. A (2001). Animal models and programming of the metabolic syndrome: Type 2 diabetes. Br Med Bull 60: 103-121 [Abstract] [Full text]  
• Eriksson, J., Lindstrom, J., Tuomilehto, J. (2001). Potential for the prevention of type 2 diabetes. Br Med Bull 60: 183-199 [Full text]  
• IJzerman, R. G., Stehouwer, C. D. A., van Weissenbruch, M. M., de Geus, E. J., Boomsma, D. I. (2001). Evidence for Genetic Factors Explaining the Association Between Birth Weight and Low-Density Lipoprotein Cholesterol and Possible Intrauterine Factors Influencing the Association Between Birth Weight and High-Density Lipoprotein Cholesterol: Analysis in Twins. J. Clin. Endocrinol. Metab. 86: 5479-5484 [Abstract] [Full text]  
• Jaquet, D., Vidal, H., Hankard, R., Czernichow, P., Levy-Marchal, C. (2001). Impaired Regulation of Glucose Transporter 4 Gene Expression in Insulin Resistance Associated with in UteroUndernutrition. J. Clin. Endocrinol. Metab. 86: 3266-3271 [Abstract] [Full text]  
• Hall, N. F., Gale, C. R., Syddall, H., Martyn, C. N., Phillips, D. I. W. (2001). Relation between Size at Birth and Age-Related Cataract. IOVS 42: 614-619 [Abstract] [Full text]  
• Yajnik, C. (2001). Commentary: Fetal origins of cardiovascular risk--nutritional and non-nutritional. Int J Epidemiol 30: 57-59 [Full text]  
• IJzerman, R. G., Stehouwer, C. D. A., Boomsma, D. I. (2000). Evidence for Genetic Factors Explaining the Birth Weight-Blood Pressure Relation : Analysis in Twins. Hypertension 36: 1008-1012 [Abstract] [Full text]  
• Byrne, C D, Phillips, D I (2000). Fetal origins of adult disease: epidemiology and mechanisms. J. Clin. Pathol. 53: 822-828 [Abstract] [Full text]  
• Jarvelin, M.-R. (2000). CONGENITAL HEART DISEASE: Fetal and infant markers of adult heart diseases. Heart 84: 219-226 [Full text]  
• Godfrey, K. M, Barker, D. J. (2000). Fetal nutrition and adult disease. Am. J. Clin. Nutr. 71: 1344S-1352 [Abstract] [Full text]  
• Jaquet, D., Gaboriau, A., Czernichow, P., Levy-Marchal, C. (2000). Insulin Resistance Early in Adulthood in Subjects Born with Intrauterine Growth Retardation. J. Clin. Endocrinol. Metab. 85: 1401-1406 [Abstract] [Full text]  
• Rasmussen, S. K., Lautier, C., Hansen, L., Echwald, S. M., Hansen, T., Ekstrøm, C. T., Urhammer, S. A., Borch-Johnsen, K., Grigorescu, F., Smith, R. J., Pedersen, O. (2000). Studies of the Variability of the Genes Encoding the Insulin-Like Growth Factor I Receptor and Its Ligand in Relation to Type 2 Diabetes Mellitus. J. Clin. Endocrinol. Metab. 85: 1606-1610 [Abstract] [Full text]  
• Flanagan, D. E., Moore, V. M., Godsland, I. F., Cockington, R. A., Robinson, J. S., Phillips, D. I. W. (2000). Fetal growth and the physiological control of glucose tolerance in adults: a minimal model analysis. Am. J. Physiol. Endocrinol. Metab. 278: E700-E706 [Abstract] [Full text]  
• Bertin, E., Gangnerau, M.-N., Bailbe, D., Portha, B. (1999). Glucose metabolism and beta -cell mass in adult offspring of rats protein and/or energy restricted during the last week of pregnancy. Am. J. Physiol. Endocrinol. Metab. 277: E11-E17 [Abstract] [Full text]  
• BARKER, D. J P (1999). Early growth and cardiovascular disease. Arch. Dis. Child. 80: 305-307 [Full text]  
• Rich-Edwards, J. W., Colditz, G. A., Stampfer, M. J., Willett, W. C., Gillman, M. W., Hennekens, C. H., Speizer, F. E., Manson, J. E. (1999). Birthweight and the Risk for Type 2 Diabetes Mellitus in Adult Women. ANN INTERN MED 130: 278-284 [Abstract] [Full text]  
• Barker, D. J.P. (1999). The Fetal Origins of Type 2 Diabetes Mellitus. ANN INTERN MED 130: 322-324 [Full text]  
• Waterland, R. A, Garza, C. (1999). Potential mechanisms of metabolic imprinting that lead to chronic disease. Am. J. Clin. Nutr. 69: 179-197 [Abstract] [Full text]  
• Orchard, T. (1998). Diabetes: a time for excitement---and concern. BMJ 317: 691-692 [Full text]  
• Rosenbloom, A. L., House, D. V., Winter, W. E. (1998). Non-Insulin Dependent Diabetes Mellitus (NIDDM) in Minority Youth: Research Priorities and Needs. CLIN PEDIATR 37: 143-152 [Abstract]  
• Soares, J. d. A C, Dornhorstt, A., Beard, R. W (1997). Should we screen for gestational diabetes? The case for screening for gestational diabetes. BMJ 315: 737-739 [Full text]  
• Rich-Edwards, J. W, Stampfer, M. J, Manson, J. E, Rosner, B., Hankinson, S. E, Colditz, G. A, Hennekens, C. H, Willet, W. C (1997). Birth weight and risk of cardiovascular disease in a cohort of women followed up since 1976. BMJ 315: 396-400 [Abstract] [Full text]  
• Curhan, G. C., Willett, W. C., Rimm, E. B., Spiegelman, D., Ascherio, A. L., Stampfer, M. J. (1996). Birth Weight and Adult Hypertension, Diabetes Mellitus, and Obesity in US Men. Circulation 94: 3246-3250 [Abstract] [Full text]  
• Lindsay, R. S., Lindsay, R. M., Edwards, C. R.W., Seckl, J. R. (1996). Inhibition of 11ß-Hydroxysteroid Dehydrogenase in Pregnant Rats and the Programming of Blood Pressure in the Offspring. Hypertension 27: 1200-1204 [Abstract] [Full text]