1.4 Adolescent Nutrition
Adolescence is a transition phase when children become adults. During adolescence hormonal changes accelerate growth in height. Growth is faster than at any other time in the individual’s postnatal life except the first year.62
TABLE 1.7: Prevalence of stunting among first-grade schoolchildren in Latin America and the Caribbean by area of residence
Sources: 49, 50, 53, 54, 60,
Research has shown that better-nourished girls have higher premenarcheal growth velocities and reach menarche earlier than undernourished girls, who grow more slowly but for longer, as menarche is delayed.63 Ultimately, these two factors tend to balance out, and total height achieved during adolescence may be similar for well-nourished and undernourished adolescents.64, 65 The adult height finally attained, however, may still differ as a result of pre-existing childhood stunting.
Because underweight adolescent girls are growing for longer, they may not finish growing before their first pregnancy In India, for example, up to 67% of girls were classified as at obstetric risk (by weight and height criteria) in their 15th year compared with about 20% in their 19th year.66 The mean age of first conception was 15.3 years in six large north Indian states.67 In general, at least 25% of adolescent girls in the developing world have had their first child by age 19 and a great many more shortly thereafter.68
Adolescents who are still growing are likely to give birth to smaller infants than mature women of the same nutritional status2 because of the competition for nutrients between the growing adolescent and the growing foetus69 and poorer placental function.70 Calcium status is a particular concern, as the bones of adolescents still require calcium for growth at a time when foetal needs for bone growth are also high.
Adolescent pregnancies also confer a higher risk of maternal and infant mortality and preterm delivery. Maternal mortality ratios for 15 - to 19-year-olds in Bangladesh are twice as high as those for 20 - to 24-year-olds.71 These grave risks are further heightened by the fact that pregnant adolescent girls are less likely to use antenatal and obstetric services.
Adolescent growth varies significantly worldwide with many of the differences observed according to chronological age attributable to variation in timing of the growth spurt.65 There is a dearth of detailed methodological work on the specific cutoffs, predictive values, and attributable risks of adolescent anthropometric indices.2 More applied research is urgently required in these areas.
Data on adolescent nutritional status are also scarce. The most complete set of studies to date on adolescent nutritional status was carried out by the International Center for Research on Women (ICRW), which compared adolescent stunting rates as part of a multicountry study.72 Stunting was recorded in 9 of the 11 studies (with prevalences ranging between 27 and 65%). The stunting process occurred in earlier childhood, for these children were stunted as they came into adolescence. Height-for-age did not improve across the eight years of adolescence.
Can undernourished children catch up on incomplete childhood growth during adolescence? There is little evidence to suggest that the growth retardation suffered in early childhood can be significantly compensated for in adolescence. Several types of studies have addressed this question. Some measure the effects of adoption (sudden environmental improvement), and some track changes over time in longitudinal studies.44 These studies show that some catch-up growth may be possible. Very little work has been completed to determine whether nutritional and health interventions targetted to adolescents will bring about significant improvements. Stunted children are thus more likely than non-stunted children to become stunted adults as long as they continue to reside in the same environment that gave rise to the stunting.
Moreover, even if adolescent catch-up growth could be brought about by an intervention and stunting thus reduced, this would not necessarily rectify all of the problems for which stunting is merely a marker. For example, while a reduction in stunting would probably reduce obstetric risk due to small maternal size, it would not necessarily reverse the effects of early childhood stunting on cognitive function.46 Both stunting and its functional correlates could, however, be addressed if the environment in which the young child grows is improved within the first two years of life.44
The INCAP follow-up study in Guatemala found that nearly 67% of severely stunted and 34% of moderately stunted three-year-old girls later became stunted adult women.73 In addition, the prevalence of low birthweight was nearly twice as high in infants of women who suffered severe stunting at three years of age compared with those who were not stunted at the same age. Women with greater growth retardation during childhood also had smaller body frames and were thus at greater risk of obstructed labour. In another study in India, early childhood stunting among young girls was found, a generation later, to be significantly related to the birthweights and infant mortality risk of their children.74
Examining national anthropometric data in the Second Report, the ACC/SCN found a strong correlation between prevalence of underweight among preschool children in the 1970s and the prevalence of underweight in adult women in the 1980s.75 Furthermore, strong associations existed between prevalence of underweight in adult women and low birth-weight prevalence, and between low birthweight (1988) and preschool child underweight (1990) prevalence. These correlations are again broadly indicative of the tendency for smallness to be transmitted from one generation to another.
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