P Vi

Low Middle High

BMI at birth (thirds of distribution)

Figure 4 Synergistic effect of BMI at birth and age 16 on systolic blood pressure of Cebu (Philippines) boys: ■ high; ■ middle; and □ low BMI. Data from the Cebu Longitudinal Health and Nutrition Survey.

Women

Weight

Figure 5 Z-scores for height, weight, and BMI from 7 to 15years in 975 boys and 983 girls who later developed hypertension. Mean values for all 7086 subjects in cohort are zero. (Reproduced with permission from Eriksson J, Forsen T, Tuomilehto J, Osmond C, and Barker D (2000) Fetal and childhood growth and hypertension in adult life. Hypertension 36(5): 790-794.)

as adults). The degree to which rapid infant growth represents risk may depend on whether it occurs in the context of recovery from fetal growth restriction and results in normalization of body weight versus excess growth leading to infant obesity.

There is more consistent evidence of increased risk associated with rapid weight gain in later childhood. In a Philippines cohort, larger weight increments from age 8 to 15 years increased risk of high blood pressure in boys who were relatively thin at birth. However, higher childhood weight gain in the absence of fetal growth restriction was not a risk factor in this population.

Fetal undernutrition may result in a reduced number of nephrons. Such deficits may not increase disease risk in individuals who remain small, but excess growth may challenge the ability of the kidneys to effectively regulate blood pressure. Catch-up linear growth has not been consistently implicated as a risk factor for later elevated blood pressure. In fact, continued poor linear growth, particularly in association with more rapid weight gain, increases risk of later elevated blood pressure.

Insulin Resistance and Diabetes

Most evidence relates to type 2 diabetes, but one large, population-based case-control study of type 1 diabetes in European populations found that height and weight were higher in cases starting at 1 month after birth, with maximum differences in cases and controls between 1 and 2 years of age. In the case of type 2 diabetes, both continued growth faltering in infancy and more rapid growth are associated with increased risk. Postnatal faltering in length is associated with impaired insulin metabolism.

As was the case for blood pressure, highest risk is associated with the combination of small size at birth and rapid postnatal growth gain. In a well-studied cohort in Finland, men and women who developed type 2 diabetes had lower birth weight, length, and ponderal index, and accelerated growth in weight and height from age 7 to 15 years. Precursors of diabetes such as insulin resistance have been studied. For example, in a follow-up study of British children who were born preterm, fasting split proinsulin and glucose concentration 30min after a glucose load were highest in children with the greatest increase in weight centile between birth and time of measurement, regardless of early size.

Extensive studies of early origins of type 2 diabetes have been conducted in India, where rates are rising very rapidly. Indian babies who are small at birth have a deficit in skeletal muscle, but not body fat compared to normal size infants. These infants tend to grow into adults that retain a lower skeletal muscle mass, but have increased abdominal obesity. This body composition is strongly related to increased risk of type 2 diabetes. Prospective studies of Indian children show an interaction between birth weight and subsequent growth. For example, children who were born small but were relatively large at age 4 had higher plasma glucose and insulin concentrations 30 min after an oral glucose load, and greater insulin resistance at age 8.

Higher growth rates in previously growth-restricted individuals may pose excessive demands on systems initially adapted to function in the face of limited resources, leading to increased risk of diseases, particularly those associated with the metabolic syndrome. Rapid growth in weight during infancy and childhood, and in particular, rapid growth following prenatal growth restriction, increases risk of developing obesity, especially abdominal obesity. Factors that contribute to early onset of obesity are therefore important to control, since obesity tracks from early life to adulthood, and is a well-recognized risk factor for diseases such as type 2 diabetes, hypertension, and coronary heart disease.

In sum, the continued vulnerability and responsiv-ity of the developing infant and child suggest the importance of a life course perspective on the development of diseases that are typically thought of as 'adult onset.'

See also: Breast Feeding. Cancer: Epidemiology and Associations Between Diet and Cancer. Coronary Heart Disease: Hemostatic Factors; Lipid Theory. Diabetes Mellitus: Etiology and Epidemiology. Hyperlipidemia: Overview; Nutritional Management. Hypertension: Dietary Factors. Infants: Nutritional Requirements. Lipids: Chemistry and Classification.

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