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33 - Developmental origins of health and disease: implications for primary intervention for cardiovascular and metabolic disease

Published online by Cambridge University Press:  08 August 2009

By
Terrence Forrester
Edited by
Peter Gluckman  and
Mark Hanson
Terrence Forrester
Affiliation:
University of the West Indies
Peter Gluckman
Affiliation:
University of Auckland
Mark Hanson
Affiliation:
University of Southampton
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Summary

Introduction

The impact of the environment on our lives over the aeons has been a dominant force helping to shape our genome, and within it the encrypted forms and functions that characterise our species. Throughout most of our evolutionary history, the environment has posed its nutritional challenges within the rubric of malnutrition and infection, and the drive to establish and retain food security has so dominated our activities over these millennia that survival advantage has accrued to thrifty genomes and thrifty ‘phenomes’ (Neel 1999, Hales and Barker 2001). That we should now be threatened by agricultural surplus is perhaps poetic justice. Regardless, in establishing our mastery over nature, and extracting three square meals per day, every day, as well as essentially relieving ourselves of the requirement for muscular work to secure food or defend life, we have fallen prey to the asynchronous kinetics of biological adaptation and environmental change (Gluckman and Hanson 2004). We have simply not had enough evolutionary time to adapt successfully to the increasing availability of food and reduction in physical activity required for daily life that have taken place at an increasingly rapid pace over the past 300 years.

The invention of agriculture some 10,000 years ago enabled the emergence of modern civilisations by ensuring surplus, fostering labour specialisation and thus the eventual rise of the capitalist approach to economic growth (Diamond 1998). Consistent food supply for populations enabled escape from malnutrition and infection.

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Developmental Origins of Health and Disease , pp. 436 - 445
Publisher: Cambridge University Press
Print publication year: 2006

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References

American Heart Association (2003). Hypertension Primer: the Essentials of High Blood Pressure, 3rd edn. Baltimore, MD: Lippincott Williams and Wilkins.
Barker, D. J. P. (1995). Fetal origins of coronary heart disease. BMJ, 311, 51–7.CrossRefGoogle ScholarPubMed
Barker, D. J. P. (1998). Mothers, Babies and Health in Later Life, London: Churchill Livingstone.Google Scholar
Barker, D. J. P., Eriksson, J. G., Forsen, T. and Osmond, C. (2002). Fetal origins of adult disease: strength of effects and biological basis. Int. J. Epidemiol., 31, 1235–9.CrossRefGoogle ScholarPubMed
Benediktsson, R., Lindsay, R. M., Noble, J., Seckl, J. R. and Edwards, C. R. (1993). Glucocorticoid exposure in utero: a new model for adult hypertension. Lancet, 41, 339–41.CrossRefGoogle Scholar
Bertram, C. E. and Hanson, M. A. (2002). Prenatal programming of postnatal endocrine glucocorticoids. Reproduction, 124, 459–67.CrossRefGoogle ScholarPubMed
Bjorntorp, P. (1992). Abdominal obesity and the metabolic syndrome. Ann. Med., 24, 465–8.CrossRefGoogle ScholarPubMed
Bjorntorp, P. and Rosmond, R. (2000). The metabolic syndrome: a neuroendocrine disorder?Br. J. Nutr., 83 (Suppl. 1), S49–57.CrossRefGoogle ScholarPubMed
Braunwald, E. (1997). Heart Disease: a Texbook of Cardiovascular Medicine, 5th edn. Philadelphia, PA: Saunders.Google Scholar
Brenner, B. M. and Chertow, G. M. (1994). Congenital oligonephropathy and the etiology of adult hypertension and progressive injury. Am. J. Kidney Dis., 23, 171–5.CrossRefGoogle Scholar
Diamond, J. (1998). Guns, Germs and Steel: a Short History of Everybody for the Last 13,000 Years. London: Vintage.Google Scholar
Dodic, M., May, C. N., Wintour, E. M. and Coughlan, J. P. (1998). An early prenatal exposure to excess glucocorticoid leads to hypertensive offspring in sheep. Clin. Sci., 94, 149–55.CrossRefGoogle Scholar
Doris, P. A. (2002). Hypertension genetics, single nucleotide polymorphisms, and the common disease:common variant hypothesis. Hypertension, 39, 323–33.CrossRefGoogle ScholarPubMed
Drake, A. J. and Walker, B. R. (2004). The intergenerational effects of fetal programming: non-genomic mechanisms for the inheritance of low birth weight and cardiovascular risk. J. Epidemiol., 180, 1–16.Google ScholarPubMed
Eriksson, J. G., Forsen, T., Tuomelhito, J., Osmond, C. and Barker, D. J. P. (2003). Early adiposity rebound in childhood and risk of type 2 diabetes in adult life. Diabetologia, 46, 190–4.CrossRefGoogle ScholarPubMed
Evans, R. M., Barish, G. D. and Wang, Y. (2004). PPARS and the complex journey to obesity. Nat. Med., 10, 1–7.CrossRefGoogle ScholarPubMed
Forrester, T. E. (2003). Research into policy: hypertension and diabetes mellitus in the Caribbean. West Indian Med. J., 52, 164–9.Google ScholarPubMed
Fowden, A. L., Li, J. and Forhead, A. J. (1998). Glucocorticoids and the preparation for life after birth: are there long term consequences of the life insurance?Proc. Nutr. Soc., 57, 113–22.CrossRefGoogle ScholarPubMed
Francois, P. J. and James, W. P. T. (1994). An assessment of nutritional factors affecting the BMI of a population. Eur. J. Clin. Nutr., 48 (Suppl. 3) S90–7.Google ScholarPubMed
Freeman, V., Fraser, H., Forrester, T. E.et al. (1996). A comparative study of hypertension prevalence, awareness, treatment and control rates in St. Lucia, Jamaica and Barbados. J. Hypertens., 14, 495–502.CrossRefGoogle Scholar
Frumkin, H. (2002). Urban sprawl and public health. Public Health Rep., 117, 201–17.CrossRefGoogle ScholarPubMed
Gluckman, P. D. and Hanson, M. A. (2004). The developmental origins of the metabolic syndrome. Trends Endocrinol. Metab., 15, 183–7.CrossRefGoogle ScholarPubMed
Haffner, S. M. (1998). Epidemiology of type 2 diabetes: risk factors. Diabetes Care, 21 (Suppl. 3) C3–6.CrossRefGoogle ScholarPubMed
Hales, C. N. and Barker, D. J. P. (2001). The thrifty phenotype hypothesis. Br. Med. Bull., 60, 5–20.CrossRefGoogle ScholarPubMed
Hales, C. N. and Ozanne, S. E. (2003a). The dangerous road of catch-up growth. J. Physiol., 547, 5–10.CrossRefGoogle Scholar
Hales, C. N. and Ozanne, S. E. (2003b). For debate: fetal and early postnatal growth restriction lead to diabetes, the metabolic syndrome and renal failure. Diabetologia, 46, 1013–19.Google Scholar
Handy, S. C., Boarnet, M. G., Ewing, R. and Killingsworth, R. E. (2002). How the built environment affects physical activity: views from urban planning. Am. J. Prev. Med., 23, 64–73.CrossRefGoogle ScholarPubMed
Hill, D. J. and Duville, B. (2000). Pancreatic development and adult diabetes. Pediatr. Res., 48, 269–74.CrossRefGoogle ScholarPubMed
Hu, F. B. and Wilett, W. C. (2002). Optimal diets for prevention of coronary heart disease. JAMA, 288, 2569–78.CrossRefGoogle ScholarPubMed
Huxley, R. R., Shiell, A. W. and Law, C. M. (2000). The role of size at birth and postnatal catch-up growth in determining systolic blood pressure: a systematic review of the literature. J. Hypertens., 18, 815–31.CrossRefGoogle ScholarPubMed
Knowler, W. C., Saad, M. F., Pettitt, D. J., Nelson, R. G. and Bennett, P. H. (1993). Determinants of Diabetes mellitus in Pima Indians. Diabetes Care, 16, 216–27.CrossRefGoogle ScholarPubMed
Langley, S. C. and Jackson, A. A. (1994). Increased systolic pressure in adult rats induced by fetal exposure to maternal low protein diets. Clin. Sci., 86, 217–22.CrossRefGoogle ScholarPubMed
Langley-Evans, S. C. (2001). Fetal programming of cardiovascular function through exposure to maternal undernutrition. Proc. Nutr. Soc., 60, 505–13.CrossRefGoogle ScholarPubMed
Langley-Evans, S. C., Sherman, R. C., Welham, S. J., Nwagwu, M. O., Gardner, D. S. and Jackson, A. A. (1999). Intrauterine programming of hypertension: the role of the renin angiotensin system. Biochem. Soc. Trans., 27, 88–93.CrossRefGoogle ScholarPubMed
Law, C. M. and Shiell, A. W. (1996). Is blood pressure inversely related to birth weight? The strength of evidence from a systematic review of the literature. J. Hypertens., 14, 935–41.CrossRefGoogle ScholarPubMed
Law, C. M., Barker, D. J. P., Osmond, C., Fall, C. H. and Simmonds, S. J. (1992). Early growth and abdominal fatness in adult life. J. Epidemiol. Comm. Health, 46, 184–6.CrossRefGoogle ScholarPubMed
Lindsay, R. S., Lindsay, R. M., Waddell, B. J. and Seckl, J. R. (1996). Programming of glucose tolerance in the rat: role of placental 11 beta-hydroxysteroid dehydrogenase. Diabetologia, 39, 1299–305.CrossRefGoogle Scholar
Lucas, A. (1991). The childhood environment and adult disease. In Programming by Early Nutrition in Man (ed. Bock, G. R.. and Whelan, J.). Chichester: Wiley, pp. 38–55.Google Scholar
Luke, A., Durazo-Arvisu, R., Rotimi, C.et al. (1997). Relation between body mass index and body fat in black population samples from Nigeria, Jamaica and the United States. Am. J. Epidemiol., 145, 620–8.CrossRefGoogle ScholarPubMed
Martorell, R., Stein, A. D. and Schroeder, D. G. (2001). Early nutrition and later adiposity. J. Nutr., 13, 874–80s.CrossRefGoogle Scholar
McMullen, S., Gardner, D. S. and Langley-Evans, S. C. (2004). Prenatal programming of angiotensin 11 type 2 receptor expression in the rat. Br. J. Nutr., 91, 133–40.CrossRefGoogle Scholar
Murray, C. J., Lauer, J. A., Hutubessy, R. C.et al. (2003). Effectiveness and costs of interventions to lower blood pressure and cholesterol: a global and regional analysis on reduction of cardiovascular-disease risk. Lancet, 361, 717–25.CrossRefGoogle ScholarPubMed
Neel, J. V. (1999). The thrifty genotype in 1998. Nutr. Rev., 57, 52–9.Google ScholarPubMed
Newsome, C. A., Shiell, A. W., Fall, C. H., Phillips, D. I., Shier, R. and Law, C. M. (2003). Is birth weight related to later glucose and insulin metabolism? A systematic review. Diabet. Med., 20, 339–48.CrossRefGoogle ScholarPubMed
Norgan, N. G. (1994). Population differences in body composition in relation to body mass index. Eur. J. Clin. Nutr., 48 (Suppl. 3), S10–27.Google ScholarPubMed
Nwagau, M. D., Cook, A. and Langley-Evans, S. C. (2000). Evidence of progressive deterioration of renal function in rats exposed to a maternal low protein diet in utero. Br. J. Nutr., 83, 79–85.Google Scholar
Osmond, C. and Barker, D. J. P. (2000). Fetal, infant and childhood growth are predictors of coronary heart disease, diabetes, and hypertension in adult men and women. Environ. Health Perspect., 108 (Suppl. 3), 545–53.CrossRefGoogle ScholarPubMed
Ozanne, S. E. (1999). Programming of hepatic and peripheral insulin sensitivity by maternal protein restriction. Biochem. Soc. Trans., 27, 94–7.CrossRefGoogle ScholarPubMed
Ozanne, S. E. and Hales, C. N. (1999). The long term consequences of intrauterine protein malnutriton for glucose metabolism. Proc. Nutr. Soc., 58, 615–19.CrossRefGoogle Scholar
Petrik, J., Reusens, B., Arany, E.et al. (1999). A low protein diet alters the balance of islet cell replication and apoptosis in the fetal and neonatal rat and is associated with a reduced pancreatic expression of insulin-like growth factor 11. Endocrinology, 140, 4861–73.CrossRefGoogle Scholar
Rolland-Cachera, M. F., Deheeger, M., Bellisle, F., Sempe, M., Guillaud-Bataille, M. and Patois, E. (1984). Adiposity rebound in children: a simple marker for predicting obesity. Am. J. Clin. Nutr., 39, 129–35.CrossRefGoogle Scholar
Seckl, J. R. (1998). Physiological programming of the fetus. Clin. Perinatol., 25, 939–62.CrossRefGoogle ScholarPubMed
Shirai, K. (2004). Obesity as the core of the metabolic syndrome and the management of coronary disease. Curr. Med. Res. Opin., 20, 295–304.CrossRefGoogle Scholar
Wintour, E. M., Moritz, K. M., Johnson, K., Ricardo, S., Samuel, C. S. and Dodic, M. (2003). Reduced nephron number in adult sheep hypertensive as a result of prenatal glucocorticoid treatment. J. Physiol., 549, 929–35.CrossRefGoogle ScholarPubMed
World Health Organization (2000). Obesity: Preventing and Managing the Global Epidemic. WHO Technical Report Series, 894. Geneva: World Health Organization.
World Health Organization (2002). Programming of Chronic Disease by Impaired Fetal Nutrition: Evidence and Implications for Policy and Intervention Strategies. WHO/NHD/02.3; WHO/NPH/02.1. Geneva: World Health Organization.
World Health Organization (2003). Diet, Nutrition and Prevention of Chronic Diseases: Report of the Joint WHO/FAO Expert Consultation. WHO Technical Report Series, 916. Geneva: World Health Organization.

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