AGE

, Volume 35, Issue 4, pp 1401–1409 | Cite as

Persistence of the effect of birth size on dysglycaemia and type 2 diabetes in old age: AGES-Reykjavik Study

  • Mikaela B. von Bonsdorff
  • Majon Muller
  • Thor Aspelund
  • Melissa Garcia
  • Gudny Eiriksdottir
  • Taina Rantanen
  • Ingibjörg Gunnarsdottir
  • Bryndis Eva Birgisdottir
  • Inga Thorsdottir
  • Gunnar Sigurdsson
  • Vilmundur Gudnason
  • Lenore Launer
  • Tamara B. Harris
  • for the Age, Gene/Environment Susceptibility-Reykjavik Study Investigators
Article

Abstract

We studied the effect of birth size on glucose and insulin metabolism among old non-diabetic individuals. We also explored the combined effect of birth size and midlife body mass index (BMI) on type 2 diabetes in old age. Our study comprised 1,682 Icelanders whose birth records included anthropometrical data. The same individuals had participated in the prospective population-based Reykjavik Study, where BMI was assessed at a mean age of 47 years, and in the AGES-Reykjavik Study during 2002 to 2006, where fasting glucose, insulin and HbA1c were measured and homeostasis model assessment for the degree of insulin resistance (HOMA-IR) calculated at a mean age of 75.5 years. Type 2 diabetes was determined as having a history of diabetes, using glucose-modifying medication or fasting glucose of >7.0 mmol/l. Of the participants, 249 had prevalent type 2 diabetes in old age. Lower birth weight and body length were associated with higher fasting glucose, insulin, HOMA-IR and HbA1c among old non-diabetic individuals. Higher birth weight and ponderal index at birth decreased the risk for type 2 diabetes in old age, odds ratio (OR), 0.61 [95 % confidence interval (CI), 0.48–0.79] and 0.96 (95 % CI, 0.92–1.00), respectively. Compared with those with high birth weight and low BMI in midlife, the odds of diabetes was almost five-fold for individuals with low birth weight and high BMI (OR, 4.93; 95 % CI, 2.14–11.37). Excessive weight gain in adulthood might be particularly detrimental to the health of old individuals with low birth weight.

Keywords

Aging Birth size Type 2 diabetes Dysglycaemia Birth weight AGES-Reykjavik Study 

Notes

Acknowledgements

The AGES-Reykjavik Study was supported by a grant from the National Institutes of Health (N01-AG-1-2100), National Institute on Aging Intramural Research Program, Hjartavernd (the Icelandic Heart Association) and the Althingi (the Icelandic Parliament). The Reyjavik Study was funded by the Icelandic Heart Association. M.B.vB. was supported by grants from the Academy of Finland; University of Jyväskylä; Yrjö Jahnsson Foundation and Fulbright Center, the Finland–US Educational Exchange Commission. I.T. was supported by grants from The Icelandic Research Council and Research Fund of the University of Iceland. The Gerontology Research Center is a joint effort between the University of Jyväskylä and the University of Tampere, Finland.

References

  1. Atladottir H, Thorsdottir I (2000) Energy intake and growth of infants in Iceland—a population with high frequency of breast-feeding and high birth weight. Eur J Clin Nutr 54:695–701PubMedCrossRefGoogle Scholar
  2. Barker DJ (1995) Fetal origins of coronary heart disease. BMJ 311:171–174PubMedCrossRefGoogle Scholar
  3. Bateson P, Barker DJ, Clutton-Brock T, Deb D, D'Udine B, Foley RA et al (2004) Developmental plasticity and human health. Nature 430:419–421PubMedCrossRefGoogle Scholar
  4. Bhargava SK, Sachdev HS, Fall CH, Osmond C, Lakshmy R, Barker DJ et al (2004) Relation of serial changes in childhood body-mass index to impaired glucose tolerance in young adulthood. N Engl J Med 350:865–875PubMedCrossRefGoogle Scholar
  5. Birgisdottir BE, Gunnarsdottir I, Thorsdottir I, Gudnason V, Benediktsson R (2002) Size at birth and glucose intolerance in a relatively genetically homogeneous, high-birth weight population. Am J Clin Nutr 76:399–403PubMedGoogle Scholar
  6. Chan JCN, Malik V, Jia W, Kadowaki T, Yajnik CS, Yoon KH et al (2009) Diabetes in Asia. Epidemiology, risk factors, and pathophysiology. JAMA 301:2129–2140PubMedCrossRefGoogle Scholar
  7. Danaei G, Singh GM, Cowan MJ, Cowan MJ, Paciorek CJ, Lin JK et al (2011) National, regional, and global trends in fasting plasma glucose and diabetes prevalence since 1980: systematic analysis of health examination surveys and epidemiological studies with 370 country-years and 2.7 million participants. Lancet 378:31–40PubMedCrossRefGoogle Scholar
  8. Eriksson JG, Forsen TJ, Osmond C, Barker DJP (2003) Pathways of infant and childhood growth that lead to type 2 diabetes. Diabetes Care 26:3006–3010PubMedCrossRefGoogle Scholar
  9. Eriksson M, Wallander MA, Krakau I, Wedel H, Svärdsudd K (2004) Birth weight and cardiovascular risk factors in a cohort followed until 80 years of age: the study of men born in 1913. J Intern Med 255:236–246PubMedCrossRefGoogle Scholar
  10. Forsen T, Eriksson JG, Tuomilehti J, Reunanen A, Osmond C, Barker D (2000) The fetal and childhood growth of persons who develop type 2 diabetes. Ann Intern Med 133:176–182PubMedCrossRefGoogle Scholar
  11. Garofano A, Czernichow P, Breat B (1997) Beta-cell mass and proliferation following late fetal and early postnatal malnutrition in the rat. Diabetologia 40:1231–1234PubMedCrossRefGoogle Scholar
  12. Gunnarsdottir I, Birgisdottir BE, Benediktsson R, Gudnason V, Thorsdottir I (2002) Relationship between size at birth and hypertension in a genetically homogeneous population of high birth weight. J Hypertens 20:623–628PubMedCrossRefGoogle Scholar
  13. Hales CN, Barker DJ (1992) Type 2 (non-insulin-dependent) diabetes mellitus: the thrifty phenotype hypothesis. Diabetologia 35:595–601PubMedCrossRefGoogle Scholar
  14. Hales CN, Barker DJP, Clark PMS, Cox LJ, Fall C, Osmond C et al (1991) Fetal and infant growth and impaired glucose tolerance at age 64. BMJ 303:1019–1022PubMedCrossRefGoogle Scholar
  15. Harding JE (2001) The nutritional basis of the fetal origins of adult disease. Int J Epidemiol 30:15–23PubMedCrossRefGoogle Scholar
  16. Harris TB, Launer LJ, Eiriksdottir G, Kjartansson O, Jonasson PV, Sigurdsson G et al (2007) Age, Gene/Environment Susceptibility-Reykjavik Study: multidisciplinary applied phenomics. Am J Epidemiol 165:1076–1087PubMedCrossRefGoogle Scholar
  17. Hattersley AT, Tooke JE (1999) The fetal insulin hypothesis: an alternative explanation of the association of low birthweight with diabetes and vascular disease. Lancet 353:1789–1792PubMedCrossRefGoogle Scholar
  18. Imbault P, Prins JB, Stolic M, Russell AW, O'Moore-Sullivan T, Despres JP et al (2003) Aging per se does not influence glucose homeostasis. Diabetes Care 26:480–484CrossRefGoogle Scholar
  19. Kajantie E, Osmond C, Barker DJ, Forsen T, Phillips DI, Eriksson JG (2005) Size at birth as a predictor of mortality in adulthood: a follow-up of 350 000 person-years. Int J Epidemiol 34:655–663PubMedCrossRefGoogle Scholar
  20. Lapidus L, Andersson SW, Bengtsson C, Björkelund C, Rossander-Hulthen L, Lissner L (2008) Weight and length at birth and their relationship to diabetes incidence and all-cause mortality—a 32-year follow-up of the population study of women in Gothenburg, Sweden. Prim Care Diabetes 2:127–133PubMedCrossRefGoogle Scholar
  21. Lawlor DA, Davey Smith G, Clark H, Leon DA (2006) The associations of birthweight, gestational age and childhood BMI with type 2 diabetes: findings from the Aberdeen Children of the 1950s cohort. Diabetologia 49:2614–2617PubMedCrossRefGoogle Scholar
  22. Lindström J, Ilanne-Parikka P, Peltonen M, Aunola S, Eriksson JG, Hemiö K et al (2006) Sustained reduction in the incidence of type 2 diabetes by lifestyle intervention: follow-up of the Finnish Diabetes Prevention Study. Lancet 368:1673–1679PubMedCrossRefGoogle Scholar
  23. Lithell HO, McKeigue PM, Berglund L, Mohsen R, Lithell UB, Leon DA (1996) Relation of size at birth to non-insulin dependent diabetes and insulin concentrations in men aged 50–60 years. BMJ 312:406–410PubMedCrossRefGoogle Scholar
  24. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC (1985) Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 28:412–419PubMedCrossRefGoogle Scholar
  25. Olafsdottir E, Aspelund T, Sigudsson G, Thorsson B, Benediktsson R, Harris TB et al (2009) Unfavorable risk factors for type 2 diabetes mellitus are already apparent more than a decade before onset in a population-based study of older persons: from the Age, Gene/Environment Susceptibility-Reykjavik Study (AGES-Reykjavik). Eur J Epidemiol 24:307–314PubMedCrossRefGoogle Scholar
  26. Ozanne SE, Olsen GS, Hansen LL, Tingey KJ, Nave BT, Wang CL et al (2003) Early growth restriction leads to down regulation of protein kinase C zeta and insulin resistance in skeletal muscle. J Endocrinol 177:235–241PubMedCrossRefGoogle Scholar
  27. Poulsen P, Vaag AA, Kyvik KO, Moller-Jensen D, Beck-Nielsen H (1997) Low birth weight is associated with NIDDM in discordant monozygotic and dizygotic twin pairs. Diabetologia 40:439–446PubMedCrossRefGoogle Scholar
  28. Preis SR, Hwang SJ, Coady S (2009) Trends in all-cause and cardiovascular disease mortality among women and men with and without diabetes mellitus in the Framingham Heart Study, 1950 to 2005. Circulation 119:1728–1735PubMedCrossRefGoogle Scholar
  29. Ravelli ACJ, van der Meulen JHP, Michels RPJ, Osmond C, Barker DJP, Hales CN et al (1998) Glucose tolerance in adults after prenatal exposure to famine. Lancet 351:173–177PubMedCrossRefGoogle Scholar
  30. Sigurdsson E, Thorgeirsson G, Sigvaldason H, Sigfusson N (1995) Unrecognized myocardial infarction: epidemiology, clinical characteristics, and the prognostic role of angina pectoris. The Reykjavik Study. Ann Intern Med 122:96–122PubMedCrossRefGoogle Scholar
  31. Szoke E, Shrayyef MZ, Messing S, Woerle HJ, van Haeften TW, Meyer C et al (2008) Effect of aging on glucose homeostasis. Diabetes Care 31:539–543PubMedCrossRefGoogle Scholar
  32. Tian JY, Cheng Q, Song XM, Li G, Jiang GX, Gu YY et al (2006) Birth weight and risk of type 2 diabetes, abdominal obesity and hypertension among Chinese adults. Eur J Endocrinol 155:601–607PubMedCrossRefGoogle Scholar
  33. Vilbergsson S, Sigurdsson G, Sigvaldsson H, Hreidarsson AB, Sigfusson N (1997) Prevalence and incidence of NIDDM in Iceland: evidence for stable incidence among males and females 1967–1991—the Reykjavik Study. Diabet Med 14:491–498PubMedCrossRefGoogle Scholar
  34. Whincup PH, Kaye SJ, Owen CG, Huxley R, Cook DG, Anazawa S et al (2008) Birth weight and risk of type 2 diabetes. A systematic review. JAMA 300:2886–2897PubMedCrossRefGoogle Scholar

Copyright information

© American Aging Association 2012

Authors and Affiliations

  • Mikaela B. von Bonsdorff
    • 1
    • 2
  • Majon Muller
    • 1
    • 3
  • Thor Aspelund
    • 4
    • 5
  • Melissa Garcia
    • 1
  • Gudny Eiriksdottir
    • 4
  • Taina Rantanen
    • 2
  • Ingibjörg Gunnarsdottir
    • 6
  • Bryndis Eva Birgisdottir
    • 6
  • Inga Thorsdottir
    • 6
  • Gunnar Sigurdsson
    • 5
  • Vilmundur Gudnason
    • 4
    • 5
  • Lenore Launer
    • 1
  • Tamara B. Harris
    • 1
  • for the Age, Gene/Environment Susceptibility-Reykjavik Study Investigators
  1. 1.Laboratory of Epidemiology, Demography and Biometry, Intramural Research ProgramNational Institute on AgingBethesdaUSA
  2. 2.Gerontology Research Center and Department of Health SciencesUniversity of JyväskyläJyväskyläFinland
  3. 3.Department of Internal MedicineVU University Medical Center AmsterdamAmsterdamThe Netherlands
  4. 4.Icelandic Heart AssociationKopavogurIceland
  5. 5.Faculty of MedicineUniversity of IcelandReykjavikIceland
  6. 6.Unit for Nutrition ResearchUniversity of Iceland and Landspitali, National University Hospital of IcelandReykjavikIceland

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