Journal List > Korean J Obstet Gynecol > v.53(6) > 1006422

Choi: Fetal origins of adult disease

Abstract

Human epidemiological and animal studies show that many chronic adult disease have their antecedents in compromised fetal and early postnatal development. Developmental programming is defined as the response by the developing mammalian organism to a specific challenge during a critical time window that alters the trajectory of development with resulting persistent effects on phenotype. Each individual's phenotype is influenced by the developmental environment as much as their genes. Also, the term 'fetal origins of adult disease' was coined on the basis of the inverse association between low birth weight and blood pressure, adult-onset diabetes, coronary heart disease, and stroke seen in numerous epidemiological studies. However, it seems unlikely that birth weight is involved in causal pathways underlying theses observations, and if it were then the significance to public health of these findings is very limited because of our inability to modify birth weight to a relevant extent in humans. There has been a major focus on maternal nutrition. Important targets for future research include distinction between the effects of different pregnancy conditions, such as maternal malnutrition, preeclampsia, and maternal infection, which may have dissimilar late-life consequences. This will be a crucial step when the associations that are currently emerging will be translated into disease prevention.

Figures and Tables

Figure 1
Left panel: the traditional etiologic view of diseases. Right panel: events in utero and during the preimplantation period can shape future health (From Rinaudo PF, et al. Semin Reprod Med 2008; 26: 436-45, with permission from Thieme Medical Publishers).9
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Figure 2
Incidence of death from cardiovascular disease and incidence of diabetes increase in individuals with smaller birth weight but are lower in individuals with higher birth weight. Each column represent weight in pounds (From Rinaudo PF, et al. Semin Reprod Med 2008; 26: 436-45, with permission from Thieme Medical Publishers).9
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Table 1
Responses of the growing organism in utero to an external environment (From Gluckman PD, et al. J Intern Med 2007; 261: 461-71, with permission from Blackwell Publishing Ltd.)11
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GH: growth hormone, IGF: insulin growth factor.

Table 2
Hazard ratios (95% confidence interval) for death from coronary heart disease according to birth weight and weight at one year in 10,636 men in Herfordshire (From Barker DJ. J Am Coll Nutr 2004; 23: 588S-95S, with permission American College of Nutrition.)46
kjog-53-475-i002
Table 3
Percentage of men aged 64 with impaired glucose tolerance or diabetes according to birth weight and weight at age one year in 370 men (From Barker DJ. J Am Coll Nutr 2004; 23: 588S-95S, with permission American College of Nutrition.)46
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*Adjusted for body mass index.

Table 4
Ten principles of developmental programming (From Nijland MJ et al. Curr Opin Obstet Gynecol 2008; 20: 132-8, with permission Lippincott Williams.)5
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Table 5
Odds ratios (95% confidence interval) for type 2 diabetes and hypertension according to birth weight and body mass index at 11 years among 13,517 men and women (From Barker DJ. J Am Coll Nutr 2004; 23: 588S-95S, with permission American College of Nutrition.)46
kjog-53-475-i005

Odds ratios adjusted for sex and year of birth.

Table 6
Hazard Ratios (95% confidence interval) for Coronary heart disease in 3,676 men according to ponderal index at birth (birth weight/length) and taxable income in adult life (From Barker DJ. J Am Coll Nutr 2004; 23: 588S-95S, with permission American College of Nutrition.)46
kjog-53-475-i006
Table 7
Cumulative incidence (%) of hypertension according to birth weight and father's social class in 8,760 men and women (From Barker DJ. J Am Coll Nutr 2004; 23: 588S-95S, with permission American College of Nutrition.)46
kjog-53-475-i007
Table 8
Types of developmental response to environmental influences (From Gluckman et al. Proc Biol Sci 2005; 272: 671-7, with permission the Royal Society's licence to publish.)52
kjog-53-475-i008

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