Pubic Hair Tanner

Age, years figure 1-3 The growth of De Montbeillard's son 1759-1777: Velocity. (Redrawn from Tanner JM. Growth at Adolescence, 2nd ed. Oxford: Blackwell Scientific Publications, 1962.)

growth is smooth and rapid during the first half of pregnancy. Indeed, it is so smooth between 11 and 14 postmenstrual weeks, when the growth velocity is 10-12 mm/week-1, gestational age can be calculated from a single measurement to within ±4.7 days. The 95% error band when three consecutive measurements are taken is ±2.7 days. Intrauterine growth charts for weight demonstrate that growth over the last trimester of pregnancy follows a sigmoid pattern and, like the sigmoid pattern reflected in height distance at adolescence, demonstrates a growth spurt when velocity is derived. The spurt should reach a peak at about 34-36 weeks. Why should the fetus be growing so quickly in terms of weight at this time? Results from an analysis of 36 fetuses in the mid-1970s demonstrated that, between 30 and 40 post-menstrual weeks, fat increases from an average of 30 g to 430 g. This dramatic accumulation of fat is directly related to the fact that fat is a better source of energy per unit volume than either protein or carbohydrate. Therefore, a significant store of energy is available to the fetus for the immediate postnatal period.

While the prenatal spurt and juvenile growth spurt may vary in magnitude, they seem to occur at roughly the same age, both within and between the sexes. The adolescent growth spurt, however, varies in both magnitude and timing within and between the sexes: Males enter their adolescent growth spurt almost 2 years later than females and have a slightly greater magnitude of height gain. The result is increased adult height for males, mainly resulting from their 2 years of extra growth prior to adolescence. At the same time, other skeletal changes are occurring that result in wider shoulders in males and, in relative terms, wider hips in females. Males demonstrate rapid increases in muscle mass and females accumulate greater amounts of fat. Their fat is distributed in a "gynoid" pattern, mainly in the glu-teofemoral region, rather than in the "android" pattern, with more centralized distribution characteristics of males (see Chapter 13). Physiologically, males develop greater strength and lung capacity. Thus, by the end of adolescence, a degree of morphological difference exists between the sexes: Men are larger and stronger and more capable of hard physical work. Such sexual dimorphism is found to a greater or lesser extent in all primates and reminds us that these physical devices had, and perhaps still have, important sexual signaling roles (see Chapter 14).

In addition to dramatic growth during adolescence, increased adult size in men is also achieved because of the extended period of childhood growth. This period of childhood is peculiar to the human child, and its existence raises important questions about the evolution of the pattern of human growth. Theoretical work on this evolution has been done recently by Barry Bogin at the University of Michigan. He argues (see Chapter 14) that humans have a childhood because it creates a reproductive advantage over other species through the mechanism of reduced birth spacing and greater lifetime fertility. In addition, slow growth during childhood allows for "developmental plasticity" in sympathy with the environment, with the result that a greater percentage of human young survive than the young of any other mammalian species.

other patterns of growth

The pattern of growth in height, as demonstrated by De Montbeillard's son, is only one of several patterns of growth found within the body. Figure 1-4 illustrates the major differences in pattern as exemplified by neural tissue (brain and head), lymphoid tissue (thymus, lymph nodes, intestinal lymph masses), and reproductive tissue (testes, ovaries, epididymis, prostate, seminal vesicles, Fallopian tubes) in addition to the general growth curve of height or weight and some major organ systems (respiratory, digestive, urinary). The data on which this figure is based are old, having originally been reported by R. E. Scammon in 1930,11 but they are sufficient to allow us to appreciate that lymphoid, neural, and reproductive tissue have patterns of growth very different from the general growth curve we initially observed. Neural tissue exhibits strong early growth and is almost complete by 8 years of age, while reproductive tissue does not really start to increase in size until 13 or 14 years of age. The lymphatic system, which acts as a circulatory system for tissue fluid and includes the thymus, tonsils, and spleen in addition to the lymph nodes, demonstrates a remarkable increase in size until the early adolescent years, then declines, perhaps as a result of the activities of sex hormones during puberty (see Chapters 4 and 5). The majority of our interest in this and other issues on growth concerns the pattern of growth as exhibited by height and weight; that is, the "general" pattern in Figure 1-4. It is clear, however, that research on the growth of neural tissue must be targeted at fetal and infant ages and research on the growth of reproductive tissue on adolescent or teenage years when growth is at a maximum.

Pubis Tanner

figure 1-4 Growth curves of different parts and tissues of the body, showing the four main types: lymphoid (thymus, lymph nodes, intestinal lymph masses); brain, neural tissue, and head (brain and its parts, dura, spinal cord, optic system, cranial dimensions); general tissue (whole body linear dimensions, respiratory and digestive organs, kidneys, aortic and pulmonary trunks, musculature, blood volume); reproductive tissue (testes, ovary, epididymis, prostate, seminal vesicles, Fallopian tubes). (From Tanner JM. Growth at Adolescence. Oxford: Blackwell Scientific Publications, 1955.)

figure 1-4 Growth curves of different parts and tissues of the body, showing the four main types: lymphoid (thymus, lymph nodes, intestinal lymph masses); brain, neural tissue, and head (brain and its parts, dura, spinal cord, optic system, cranial dimensions); general tissue (whole body linear dimensions, respiratory and digestive organs, kidneys, aortic and pulmonary trunks, musculature, blood volume); reproductive tissue (testes, ovary, epididymis, prostate, seminal vesicles, Fallopian tubes). (From Tanner JM. Growth at Adolescence. Oxford: Blackwell Scientific Publications, 1955.)

growth versus maturity

Although we have concentrated on the growth of one boy in eighteenth century France, De Montbeillard's son, it is now evident that his curves of growth (i.e., distance and velocity) reflect patterns found in all children who live in normal environmental circumstances. We may differ in the magnitude of growth that occurs as is evident from our varying adult statures, but to reach our final height, we all experience a similar pattern of human growth to a greater or lesser degree. It is evident that growth in height is not the only form of somatic growth that occurs in the human body. We already discussed that, as we experience the process of growth in linear dimensions (i.e., as we get taller), we also experience other forms of growth. We get heavier, fatter, and more muscular; and we experience changes in our body proportions. In addition, we become more "mature" in that we experience an increase in our functional capacity with advancing age, which may be evidenced in our increasing ability to undertake physical exercise in terms of both magnitude and duration (see Chapter 15). Although we tend to think of "growth and development" as a single biological phenomenon, both aspects have distinct and important differences. Growth is defined as an increase in size, while maturity or development is an increase in functional ability. The end point of growth is the size we attain by adulthood, roughly corresponding to growth rates of less than 1 cm/yr-1, and the end point of maturity is when we are functionally able to successfully procreate. This involves not simply to be able to produce viable sperm in the case of men and viable ova in the case of women. Successful procreation in a biological sense requires that the offspring survive so that they may also procreate. Therefore, successful maturation requires not just biological maturity but also behavioral and perhaps social maturity.

The relationship between somatic growth and maturity is perhaps best illustrated by Figure 1-5. The figure shows three boys and three girls who are of the same ages within gender: The boys are exactly 14.75 years old and the girls 12.75 years old. The most striking feature of this illustration is that, even though they are the same age, they demonstrate vastly different degrees of maturity. The boy and girl on the left are relatively immature compared to those on the right. To be able to make these distinctions in levels of maturity, we must use some assessments of maturation, "maturity indicators" (see Chapter 17). These may well include the obvious development of secondary sexual characteristics (breast and pubic hair in girls and genitalia and pubic hair in boys), in addition to dramatic changes in body shape, increases in muscularity in boys and increases in body fat in girls. If we look carefully, we see that distinct changes in the shape of the face also occur, particularly in boys, which result in "stronger" features compared to the rather soft outline of the preadolescent face. However, the maturity indicators we use to assess maturation for clinical and research purposes are constrained by the need to demonstrate "universality"—they must appear in the same sequence within both sexes— and similarity in both beginning and end stages. Because human size is governed by factors other than the process of maturation, we cannot use an absolute size to determine maturation. Even though, in very general terms, someone who is large is likely to be older and more mature than someone who is small, it is apparent from Figure 1-4 that, as the two individuals approach each other in terms of age, this distinction becomes blurred. We therefore use the appearance and relative size of structures rather than their absolute size to reflect maturity. The most common

Adolescent Pubic Hair

figure 1-5 Three boys and three girls photographed at the same chronological ages within sex: 12.75 years for girls and 14.75 years for boys. (From Tanner JM. Growth and endocrinology of the adolescent. In: Gardner L (ed). Endocrine and Genetic Diseases of Childhood, 2nd ed. Philadelphia: W. B. Saunders, 1975.)

figure 1-5 Three boys and three girls photographed at the same chronological ages within sex: 12.75 years for girls and 14.75 years for boys. (From Tanner JM. Growth and endocrinology of the adolescent. In: Gardner L (ed). Endocrine and Genetic Diseases of Childhood, 2nd ed. Philadelphia: W. B. Saunders, 1975.)

maturity indicators are secondary sexual development, skeletal maturity, and dental maturity (see Chapter 17).

the control of growth

Clearly, the process of human growth and development, which takes almost 20 years to complete, is a complex phenomenon. It is under the control of both genetic and environmental influences, which operate in such a way that, at specific times during the period of growth, one or the other may be the dominant influence. At conception, we obtain a genetic blueprint that includes our potential for achieving a particular adult size and shape. The environment alters this potential. Clearly, when the environment is neutral, when it is not exerting a negative influence on the process of growth, the genetic potential can be fully realized. However, the ability of environmental influences to alter genetic potential depends on a number of factors, including the time at which they occur; the strength, duration, and frequency of their occurrence; and the age and gender of the child (see Chapter 9).

The control mechanism that environmental insult affects is the endocrine system. The hypothalamus or "floor" of the diencephalon, situated at the superior end of the brain stem, coordinates the activities of the neural and endocrine systems. In terms of human growth and development, its most important association is with the pituitary gland, which is situated beneath and slightly anterior to the hypothalamus. The rich blood supply in the infundibulum, which connects the two glands, carries regulatory hormones from the hypothalamus to the pituitary gland. The pituitary gland has both anterior and posterior lobes. The anterior lobe, or adenohy-pophysis, releases the major hormones controlling human growth and development: growth hormone, thyroid-stimulating hormone, prolactin, the gonadotrophins (luteinizing and follicle-stimulating hormones), and adrenocorticotrophic hormone (see Chapters 4 and 5). Normal growth does not depend simply on an adequate supply of growth hormone but is the result of a complex and at times exquisite relationship between the nervous and endocrine systems. Hormones rarely act alone but require the collaboration or intervention of other hormones to achieve their full effect. Therefore, growth hormone causes the release of insulin-like growth factor 1 (IGF-1) from the liver. IGF-1 directly affects skeletal muscle fibers and cartilage cells in the long bones to increase the rate of uptake of amino acids and incorporate them into new proteins, thus it contributes to growth in length during infancy and childhood. At adolescence, however, the adolescent growth spurt will not occur without the collaboration of the gonadal hormones: testosterone in boys, estrogen in girls.

There is ample evidence from research on children with abnormally short stature that a variety of environmental insults disturb the endocrine system, causing a reduction in the release of growth hormone. However, other hormones are also affected by such insults, making the diagnosis of growth disorders a complex and engrossing series of investigations that increasingly requires an appreciation of both genetic and endocrine mechanisms (see Chapters 5, 10, and 11).

growth reference charts

The growth of De Montbeillard's son is interesting, not only because he depicts a normal pattern of growth but also because he achieved an adult height that was over 180 cm, or about 6 feet. He was quite tall for a French man in the eighteenth century. How do we know that someone is "tall" or "short"? What criteria do we use to allow us to make such a judgment? Those not involved in the study of human growth make such a judgment based on their exposure to other people. If, for instance, they have lived only among the pygmies of Zaire, then anyone over 165 cm (5 ft, 5 in.) would be very tall. If, on the other hand, they had lived only among the tall Nilotic tribesmen of North Africa, anyone less than 175 cm (5 ft, 9 in.) would be unusually small. Most of us live in regions of the world in which the majority of people have adult heights that lie between these extremes and view average adult heights at about 178 cm (5 ft, 10 in.) for men and 170 cm (5 ft, 7 in.) for women as "normal." Of course, adult heights range about these average values and that range gives us an estimate of the normal variation in adult stature. Beyond certain points in that range, we begin to think of an individual's height as either "too tall" or "too short." This is also true of the heights of children during the process of growth. Each age from birth to adulthood has a range of heights that reflects the sizes of normal children; that is, children who have no known disease or disorder that adversely affects height (e.g., bone dysplasias, Turner syndrome). To assess the normality or otherwise of the growth of children, we use growth reference charts. These charts depict both the average height to be expected throughout the growing years (typically from birth to 18 years) and the range of normal heights, in the form of percentile (centile) distributions.

Figure 1-6 is such a reference chart. It depicts the normal range of heights for British boys from 4 to 18 years old. The normal range is bound by outer centile limits of the 0.4th and 99.6th centiles. Therefore, "normal" heights are thought of as heights that fall between these limits; although, of course, 0.8% of normal children will have heights below the 0.4th or above the 99.6th centile (see Chapter 18). The illustrated centiles have been chosen because they each equate roughly to 0.67 Z-scores or standard deviation (SD) scores from the 50th centile or average values. Hence, the 25th centile is 0.675 Z-scores below the mean, the 10th centile is 1.228, and the 2nd centile is 1.97. Their importance is that, not only do they provide a reasonable point at which to investigate possible abnormalities of growth, but they also provide reasonable guidelines for how we expect growth to proceed within the normal range. It has recently been suggested, for instance, that a child whose growth exhibits a movement of 0.67 Z-scores is exhibiting a clinically significant response to the alleviation of some constraining factor (see "catch-up"

Score Tanner
figure 1-6 Growth reference chart for U.K. boys from 4 to 18 years old (© Child Growth Foundation).

growth, later).12 So, the movement of a child's height or weight upward through the centiles from the 10th to the 25th or downward from the 98th to the 75th can be viewed by clinicians as more than simply a chance occurrence.

Children who have no constraints on their growth exhibit patterns of growth that fall steadily and continuously parallel to the centile lines prior to adolescence. However, as the adolescent growth spurt takes place, they depart from this parallel pattern, and all adolescents demonstrate "centile crossing." In "early developers," the height-for-age curve rises through the centiles before their peers and levels off early, as they achieve their adult stature. "Late developers," on the other hand, initially appear to fall away from their peers as the latter enter their growth spurts, and then accelerate into adolescence rising through the centile lines when their peers have ceased or nearly ceased growing. Even the child who enters their growth spurt at the average age for the population crosses centile lines. This is because the source data for these reference charts were collected in cross-sectional studies: studies in which children of different ages were measured on a single occasion. They thus reflect the average heights, weights, and the like of the population rather than the growth of an individual child. If one were able to undertake a growth study of the same children over many years (a longitudinal study), one could theoretically adjust the data so that it illustrated the adolescent growth spurt of the average child; that is, the child experiencing the adolescent growth spurt at the average age. In such a hypothetical situation, the growth curve of the average child would fall exactly on the 50th centile line. But that is not the case with growth reference charts based on cross-sectional data. The average child initially falls away from the 50th centile line as he or she enters the growth spurt and then crosses it at the time of maximum velocity (peak velocity) before settling back onto the 50th centile as he or she reaches adult height.

Figure 1-7 illustrates the typical growth patterns exhibited by early, average, and late developers. The early developing girl (E) accelerates into adolescence at about 8 years old, some 2 years prior to the average, and rapidly crosses centile lines to move from just above the 50th to the 90th centile. However, her growth slows at about 13 years and her height centile status falls back to the 50th centile. Conversely, the late developer (L) is almost 13 years old before she starts to accelerate, and that delay causes her height centile status to fall from the 50th to below the 10th centile before rising to the 50th centile as she approaches adulthood. Finally, the average girl initially falls away from the 50th centile but then accelerates through it at the average age of peak velocity before following the 50th centile as adulthood is reached.

canalization

Figure 1-7 demonstrates more than simply the crossing of centiles by early and late developers. It also tells us something about the control of human growth. These are not hypothetical curves. They are the growth curves of real children who were measured on a 6- or 3-month basis throughout childhood and adolescence.13 Note that, during childhood, they were growing on or near to the 50th centile, and after the deviations brought about by their adolescent growth spurts, they returned to that same centile position in adulthood. Such adherence to particular centile positions

figure 1-7 Growth curves of average (A), early (E), and late (L) developers. (Data from numbers 35, 38, 45 in Tanner JM, Whitehouse RH. Atlas of Human Growth. London: Academic Press, 1980.)

is found time and again when one studies the growth of children. Indeed, it is true to say that all children, when in an environment that does not constrain their growth, exhibit a pattern of growth that is more or less parallel to a particular centile or within some imaginary "canal." This phenomenon was described by a British geneticist, C. H. Waddington, in 1957,14 and has been termed canalization or homeor-rhesis. It is most likely that this pattern is genetically determined and that growth is target seeking, in that we have a genetic potential for adult stature and the process of growth, in an unconstrained environment, takes us inexorably toward that target.

catch-up growth

However, none of us has lived or been brought up in a completely unconstrained environment. Toward the end of our intrauterine life, our growth was constrained by the size of the uterus. During infancy and childhood, we succumbed to a variety of childhood diseases that caused us to lose our appetite and at those times our growth would have reflected the insult by appearing to slow down or, in a more severe case, to actually cease.

Waddington14 likens growth to the movement of a ball rolling down a valley floor. The sides of the valley keep the ball rolling steadily down the central course (point A in Figure 1-8). If an insult occurs, it tends to push the ball out of its groove or canal and force it up the side of the valley (point B). The amount of deviation from the predetermined pathway depends on the severity and duration of the insult. However, every insult causes a loss of position and a reduction in growth velocity, as the ball is confronted by the more severe slope of the valley wall. The magnitude of the loss of velocity also depends on the severity and duration of the insult. Thus, a small insult of short duration causes a slight shift onto the valley sides, which entails a minor change in velocity. The alleviation of the insult results in a rapid return to the valley floor at an increased velocity (point C). Having reached the floor normal growth velocity is resumed (point D).

This analogy may be seen to apply appropriately to the process of human growth. Figure 1-9 shows the growth chart of a girl who has suffered from celiac syndrome.13 In this condition, an abnormality of the lining of the gut impedes absorption of food, resulting in the child being starved. The result in terms of growth is that the height velocity is gradually reduced as the malnutrition becomes more and more severe. The reduction in height velocity means that the height distance curve leaves the normal range of centiles and the child becomes abnormally short for her age. So, at the age of almost 12 years, she is the average height of a 5-year-old. On diagnosis the child is switched to a gluten-free diet, which alleviates the malabsorption. Recovery of height velocity is rapid and jumps from 1 cm/yr-1 to 14 cm/yr-1, returning the child to the normal range of centiles within 3 years. Indeed, this girl ends up within the range of heights one would expect given the heights of her parents. So she demonstrates "complete" catch-up growth, in that she returns to the centile position from which she most probably started.

Catch-up growth is not always complete, however, and appears to depend on the timing, severity, and duration of the insult. This appears to be particularly true in the treatment of hormone deficiencies. Initial diagnosis is often delayed until the child is seen in relation to other children and the deficiency in stature becomes obvious. Usually a hormone deficiency, such as growth hormone deficiency, is accompanied by a delay in maturation. Response to treatment appears to depend

figure 1-8 A pictorial illustration of the phenomenon of canalization. A = normal canalized growth; B = the point at which an impact causes the ball to deviate up the side of the valley; C = the alleviation of the impact and a return to the valley floor; D = the resumption of normal canalized growth.

figure 1-8 A pictorial illustration of the phenomenon of canalization. A = normal canalized growth; B = the point at which an impact causes the ball to deviate up the side of the valley; C = the alleviation of the impact and a return to the valley floor; D = the resumption of normal canalized growth.

on pretreatment factors, such as chronological age, height, weight, and skeletal maturity; that is, on how long the child has been deficient, how severe the deficiency in height and weight are, and by how much the maturity has been affected.

conclusion

This chapter forms an introduction to the study of human growth and development. The curve of human growth has been a characteristic of Homo sapiens for as long as we have been walking on this earth. It has changed in duration and

figure 1-9 Catch-up growth exhibited by a child with celiac syndrome. (Data from number 102 in Tanner JM, Whitehouse RH. Atlas of Human Growth. London: Academic Press, 1980.)

magnitude as we have been freed of the environmental constraints that affected us throughout our evolution, but its major characteristics have remained unaltered. That curve reflects two major stages during which adjustment to final size and shape are the direct consequences. Infancy and adolescence are times of adjustment and assortment. More than 50% of infants exhibit either catch-up or catch-down growth during the first 2 years of life.12 These adjustments have long-term consequences in terms of final size, shape, morbidity, and perhaps mortality. The timing of the adolescent growth spurt, its magnitude, and its duration are fundamentally important in terms of healthy and successful survival. The biological phenomena of canalization and catch-up growth dictate the magnitude, duration, and ultimate success of these alterations and adjustments.

No one would argue that environmental constraints on growth through the processes of famine and disease have been constant influences, not only on our survival but also on our size and shape at any age. Past millennia of environmental insult have resulted in the survival of representatives of the species Homo sapiens who are adapted and adaptable to their environment. We are the survivors and as such we use survival strategies to ensure that we continue the species. One of the most powerful of these strategies is the plasticity of our growth and development. Throughout the following chapters you will learn how that plasticity is inherited, controlled, and expressed—it is a fascinating story and one of the most fundamental biological phenomena of our species.

references

1. http://www.ucmp.berkeley.edu/history/evolution.

2. Bloomsbury Guide to Human Thought. London: Bloomsbury Press, 1993.

3. Bourdier F. Principaux aspects de la vie et de l'oevre de Buffon. In: Heim R (ed). Buffon. Paris: Publications Françaises, 1952:15-86.

4. Tanner JM. History of the Study of Human Growth. New York: Academic Press, 1988.

5. Scammon RE. The first seriatim study of human growth. Am J Phys Anthrop. 1927;10:329-336.

6. Lampl M, Veldhuis JD, Johnson ML. Saltation and stasis: A model of human growth. Science. 1992;158:801-803.

7. Preece MA, Baines MK. A new family of mathematical models describing the human growth curve. Ann Hum Biol. 1978;5:1-24.

8. Tanner JM. Some notes on the reporting of growth data. Hum Biol. 1951;23:93-159.

9. Thompson D'AW. On Growth and Form. Cambridge: Cambridge University Press, 1917.

10. Thompson D'AW. On Growth and Form, rev. ed. Cambridge: Cambridge University Press, 1942.

11. Scammon RE. The measurement of the body in childhood. In: Harris JA, Jackson CM, Patterson DG, Scammon RE (eds). The Measurement of Man. Minneapolis: University of Minnesota Press, 1930:171-215.

12. Ong KL, Ahmed ML, Emmett PM, Preece MA, Dunger DB, Avon Longitudinal Study of Pregnancy and Childhood Study Team. Association between postnatal catch-up growth and obesity in childhood: Prospective cohort study. Brit Med J. 2000;320:967-971.

13. Tanner JM, Whitehouse RH. Human Growth and Development. London: Academic Press, 1980.

14. Waddington CH. The Strategy of the Genes. London: Allen and Unwin, 1957.

+2 -2

Responses

Post a comment