The normal linear growth of a child is an expression of adequate nutrition and freedom from major illness; however, there is a remarkable range of what is considered normal. At each growth period-infancy, childhood, and adolescence–the growth rate results from the dynamic interplay of nutrition, physical activity, and hormonal processes upon the genetically determined template. Linear growth velocity decelerates rapidly from 30 cm/year during the first few months of life to approximately 9 cm/year at age 2 to 7 cm/year at age 5. Linear growth then continues at approximately 5.5 cm/year before slowing slightly just before puberty (preadolescent “dip”). For an average girl, the growth velocity increases sharply at approximately age 10, reaches a peak of approximately 10.5 cm/year at age 12, and decelerates toward zero as epiphyseal fusion occurs around age 15. For males, who follow a typical growth curve, the pubertal spurt begins around age 12, reaches a peak velocity of 12 cm/year at age 14, and then decelerates toward zero around age 17. The total growth at puberty is approximately 25 cm for girls and 28 cm for boys. If one adds the 2 extra years of prepubertal growth for boys, one has the 13 cm (5+5+3) difference in the mean height between men and women.
The overall contribution of heredity to adult size and body configuration varies with environmental circumstances, and the two continuously interact throughout the entire period of growth. The genetic control of the tempo of growth is apparently independent of that for size and configuration.
There has been a secular trend toward additional height and earlier sexual development documented at least over the past 150 years, with children of average economic status increasing their height by 1 to 2 cm per decade. During the 20th century, the age of menarche in Western Europe and the United States has decreased 2 to 3 months per decade, now averaging 12.8 years in middle class communities.1
Size at birth is determined more by intrauterine and placental factors and maternal nutrition than by genetic growth potential. Although length at age 2 and adult height have a correlation coefficient of 0.80, the correlation is but 0.25 at birth, reflecting those factors noted above.2 Growth during the first 2 years is characterized by gradual deceleration in both linear growth velocity and rate of weight gain. Most infants will cross growth percentile lines as they “catch-up” or “lag-down” toward their genetically determined target.3 In addition, body shape changes toward a more linear one as fat accumulation wanes and the child becomes more muscular.
Growth during childhood is a relatively stable process as the infancy shifts in growth channel are complete and the child follows the trajectory previously attained and grows at an average rate of 5 to 6 cm/year.” 1,4 During this stage, growth primarily depends on the thyroid hormones, those of the GH/IGF-I axis and insulin.
The onset of puberty corresponds to a skeletal (biological) age of approximately 11 years in girls and 13 years in boys.5 Most methods for detecting skeletal age use a single radiograph of the left hand and wrist. On average girls enter and complete each stage of puberty earlier than boys, but there is significant intra- and interindividual variation in the timing and tempo of puberty. One of the hallmarks of puberty is the adolescent growth spurt, often preceded by slowing of prepubertal growth, also known as the “pre-adolescent dip.” Girls gain an average of 25 cm and boys 28 cm during pubertal growth.6,7 Boys enter puberty 2 years later than girls; the longer duration of prepubertal growth in combination with greater ~ of 13 cm between men and women.
Marked changes in body composition occur during puberty and result in the android and gynoid patterns of fat distribution in the adult. The hormonal regulation of growth and alterations in body composition increasingly become dependent on gonadal steroid hormones (driven by central gonadotropin secretion) and a dramatic activation of the GH/IGF-I axis, especially the interaction between them.8 Estrogens either secreted directly or converted peripherally from androgen precursors affect hormonal secretion of the GH/IGF-I axis and are responsible for skeletal maturation and the ultimate fusion of the epiphyseal plates.9
Variations of Normal Growth
There is wide variation in the timing and tempo of puberty, even among healthy children. When one determines the appropriateness of a particular growth velocity, the child’s degree of biological maturation must be considered. Skeletal or pubertal maturation may be used to determine the child’s degree of biological development. The bone age is determined as the “mean” of the skeletal ages of a number of the small bones of the hand and wrist. Pubertal maturation status is based on development of breasts and pubic hair in girls and pubic hair and genitals in boys. This range of normal variability is expanded to an even greater degree by alterations in energy intake and expenditure. Although moderate activity is associated with cardiovascular benefits and favorable changes in body composition, excessive physical activity during childhood and adolescence may negatively impact growth and adolescent development.
Sports that emphasize strict weight control in the setting of high energy output
are of particular concern especially among scholastic wrestlers and female
gymnasts and dancers, although selection criteria for certain body types make
selection bias a confounding variable in the assessment of the impact of
training on growth and adolescent development.10,11 One must consider that
some of these changes are transient, at least in the wrestlers. The same
markers of growth and body composition that were slowed during training
(in season) were accelerated after the season, permitting “catch-up” to
control children and left no permanent growth reductions.10
Perhaps it is important to establish an active lifestyle that may carry over to
adult life during the childhood years because of the later health benefits
(lessened coronary artery disease, hypertension, obesity) rather than for
the immediate childhood-adolescent time frame. There are, however, data from
a properly controlled study that indicate that moderate activity does not
negatively impact growth and adolescent maturation in boys.12
1. Tanner JM. Fetus into man: physical growth from conception to maturity. Cambridge, MA: Harvard Univ Press, 1989.
2. Tanner JM, Healy MJR, Lockhart RD, et al. Aberdeen growth study I. The prediction of adult body measurement from measurements taken each year from birth to five years. Arch Dis Child 1956;31:372.
3. Smith DW, Truog W. Rogers JE, Greitzer, Skinner AL, McCann JJ, Harvey MA. Shifting linear growth during infancy: illustration of genetic factors from fetal life through infancy. J Pediatr 1976;89:225-30.
4. Roche AF, Himes JH. Incremental growth charts. Am J Clin Nutr 1980;33:2042-52.
5. Tanner JM, Whitehouse RH, Marshall WA, Carter BS. Prediction of adult height, bone age and occurrence of menarche, at ages 4 to 16 with allowance for mid-parental height. Arch Dis Child 1975;50:14-26.
6. Marshall WA, Tanner JM. Variations in patterns of pubertal changes in girls. Arch Dis Child 1969;44:291-303.
7. Marshall WA, Tanner JM. Variations in patterns of pubertal changes in boys. Arch Dis Child 1970;45: 13-23.
8. Martha PM Jr, Rogol AD, Veldhuis JD, et al. Alterations in the pulsatile properties of circulating GH concentrations during puberty in boys. J Clin Endocrinol Metab 1989;69:563-70.
9. Smith EP, Boyd J. Frank GR, et al. Estrogen resistance caused by a mutation in the estrogen-receptor gene in man. N Engl J Med 1994;331:1056.
10. Roemmich JN, Sinning WE. Sport-seasonal changes in body composition, growth, power and strength in adolescent wrestlers. Int J Sports Med 1996;17:92-9.
11. Malina RM. Physical growth and biological maturation of young athletes. Exerc Sport Sci Rev 1994;22:389 434.
12. Beunen GP, Malina RM, Renson R. Wimons J. Ostyn M, LeFeure J. Physical activity and growth maturation and performance: a longitudinal study. Med Sci Sports Exerc 1992;324:576-85.
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