Studies of the fetal and infant origins of obesity are part of a wider field of research on the early origins of adult diseases (33) It is now known that people who had low birth weight, or who were thin or stunted at birth, are at increased risk of type 2 diabetes, coronary heart disease, and hypertension (34-40). These diseases, especially type 2 diabetes, are associated with obesity (41). Their association with small body size at birth has led to the conclusion that they originate in persisting changes in the body's structure, physiology, and metabolism that result from fetal undernutrition and are associated with slow growth in utero (15,33).
Figure 2 shows the path of growth of boys who as adults were either admitted to hospital with coronary heart disease or died from the disease. They belong to a cohort of 4630 boys born in Helsinki (40). Their body size is expressed as mean standard deviation or Z scores. The Z score for the cohort is set at zero, and a boy maintaining a steady position as large or small in relation to other boys would follow a horizontal path on the figure. Boys who later developed coronary heart disease, however, having been small at birth and during infancy, had accelerated gain in weight and body mass index thereafter. A 1-unit increase in standard deviation score for body mass index between 1 and 12 years was associated with a hazard ratio of 1.20 (95% CI 1.08-1.33). The effect of increase in body mass index, however, was conditioned by birthweight and, more strongly, by ponderal index at birth (birth weight/length3), a measure of fatness.
Table 2 shows that at any body mass index at 12 years, the latest age for which there are data, the risk of coronary heart disease was greater in boys who were thin at birth. Findings at younger ages in childhood were similar. In animals accelerated or ''compensatory'' growth after a period of undernutrition during development can have long-term costs, including reduced life span (42). Whether this general biological phenomenon is related to the association between rapid childhood weight gain and human disease is not known.
The same general pattern of growth, small size at birth and during infancy followed by compensatory growth in childhood, is associated with type 2 diabetes and hypertension (38,39). There are differences in detail
Figure 2 Growth of 357 boys who later developed coronary heart disease in a cohort of 4630 boys born in Helsinki.
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