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Environmental Health Perspectives Supplements 101 (SuppL 2): 39-44 (1993)
Environmental Factors Influencing Growth and
Pubertal Development
by Henriette A. Delemarre-van de Waal
Postnatal growth is based on hereditary signals and environmental factors in a complex regulatory network. Each factor must be in an optimal state for normal growth of the child. Fetal conditions may also have consequences on postnatal height. Intrauterine growth retardation can be recovered postnatally, although postnatal growth remains depressed in about one-third of cases. After birth, the environment may exert either a positive or negative effect on growth. In underdeveloped countries, malnutrition plays a major role in inhibiting the growth process. Children from families of higher socioeconomic classes are taller than their coevals in the lower socioeconomic groups. Urbanization also has a positive effect on growth. Better child care is supported by sufficient food supply, appropriate health and sanitation services, and a higher level of education. Over the last century, these factors have induced a taller stature and a more rapid maturity in Europe, North America, and Australia; a phenomenon which has been referred to as "the secular trend" in growth. Recently, a secular trend has also been reported in some developing countries. Although urbanization in general appears to be associated with better conditions of living, this is not the case in the slums of South America or in Africa where rural children are better off than children living in the poor cities. This paper describes in more detail the different hereditary and environmental factors that act duringthe fetal period and postnatally, and which play a role in human growth and pubertal development.
Introduction
Growth is the result of the concerted effect of a (^) complex network of many regulatory factors with varying interac- tions. Each individual has a genetic base with a definite growth potential, which may be modulated by these fac- tors both in the prenatal period and in postnatal life (1). Optimal growth can only be achieved when all these factors operate in harmony. Postnatal growth is determined by hereditary factors, the length of^ the newborn baby which^ was^ achieved^ pre- natally, and environmental factors^ to^ which the^ child^ is exposed during the^ growth period postnatally (Fig. 1). During puberty, the pubertal growth spurt produces an extra increase in (^) height, but thereafter (^) growth soon ends (2). There is a close relationship between pubertal develop- ment and the growth process, and the onset of puberty is more correlated with skeletal age than with chronological age (3). Therefore, when growth is retarded, there will usually be an associated retardation of skeletal matura- tion, and this^ will result^ in^ delayed puberty as an^ additional complication. In^ many countries, the^ environmental^ condi- tions are such that there is incomplete expression of
Department of Pediatrics, Free University Hospital, P. 0. Box 7057, 1007 MB Amsterdam, The Netherlands. This manuscript was presented at^ the^ Conference on^ the^ Impact of the Environment on (^) Reproductive Health that was held 30 (^) September October 1991 in (^) Copenhagen, Denmark.
hereditary components, and this may have consequences on prenatal and postnatal growth.
Genetic Factors
It is well known that the parents' height has an influence on the stature of their children. However, the relationship between the height of the baby and that of the parents is
not appareilt at birth but becomes more evident toward the
age of 2 years, and thereafter the correlation becomes greater with increasing age (4). The Louisville Twin^ Study examined height data longitudinally from birth^ to matu- rity in^ twin families, and from this^ it^ was^ estimated^ that heredity accounted for 90% or more of the factors that de- termined (^) height from the (^) age of (^6) years and after (5). These investigators observed a substantial and constant correlation between the height of the children and their parents from the age of 3 years and onwards. Monozygotic twins, with identical genetic composition, had a greater difference in final height when reared apart than when reared together. However, this^ difference^ was^ less^ than the difference between (^) dizygotic twins (^) (6). The difference in height ofmonozygotic twins is probably caused by environ- mental factors. Body proportions are probably also under the influence of genetic control. In relative terms, the Australian Abori- gines and the Africans in Ibadan have the longest legs (1). During the growth phase, the gain of leg length in^ com- parison to^ gain in^ total^ length can^ be^ proportionally
H. A. DELEMARRE-VAN DE WAAL
psychosocial
genetics season/climate
prenatal growth postnatal growth physical activity
nutrition urbanization
disease socioeconomics
FIGURE 1.^ Factors influencing postnatal growth.
different in different populations. As an example, Chinese children at a young age have relatively long legs, but as they become taller they gain less leg length per unit length of sitting height than London children. The mixing of races produces children with stature and body proportions intermediate between the parental populations (1). Hereditary diseases and (^) chromosomal aberrations may affect (^) the growth process, usually exerting a suppressive influence. Thrner's syndrome (karyotype 45,XO), other X chromosomal (^) abnormalities, and (^) Klinefelter's syndrome are well-known diseases associated with either short or long stature. In (^) spite of (^) many new developments in (^) endo- crine therapy such as growth hormone treatment for Thrner's syndrome, it is difficult to manipulate genetically defined (^) growth characteristics (^) (7).
Environmental Factors
Prenatal Growth
The fetus does not develop optimally in poor environ- mental conditions. Weight gain is the first parameter to be inhibited, but after prolonged inadequacy height is also negatively affected (8). Environmental conditions account for about (^) 60% of (^) the variability of birth (^) weight and genetic factors for (^) the remaining 40% (^) (9). Such environmental factors, among others, include^ maternal^ age, order of birth, and (^) crowding within the uterus (^) (10). Primiparous mothers either older than 38 or younger than 20 years of age have an increased risk of giving birth to small-for-date babies (11). First-born babies have a birth weight of about 100 g less than second or third babies, and in multiple pregnancies the weight gain of each fetus after the 30th week of gestation is less than that of single-pregnancy fetuses (12). An^ inhibiting effect on fetal growth is also exerted (^) by illness in the (^) mother, malnutrition, therapeutic drug treatment, alcohol and other^ social^ drug addiction, and cigarette smoking. Offspring of mothers with insulin-dependent diabetes are known to be at greater risk of developing congenital malformations, and the incidence of abnormalities is rela- ted to poor control of blood sugar levels in^ the first trimes- ter. It is (^) important to (^) ensure precise diabetic control (^) early in (^) gestation so that a more normal environment of (^) glucose, insulin, and ketone levels is maintained in order to dimin- ish congenital anomalies (13). Antihypertensive and anti- convulsant drugs in particular are therapeutic agents that
have a disturbing effect on fetal growth and morpho- genesis (14). Alcohol, drug addiction, and smoking may have a severe effect on the height and weight of babies (15-17), and smoking is known to increase the risk of prematurity (18). The underlying mechanisms appear to be maternal mal- nutrition with a deficiency of trace elements and placental dysfunction in addition to a direct toxic effect on the fetus. Alcohol addiction also increases the incidence of congeni- tal malformations (19). Malnutrition is still a worldwide problem. Fetal growth is inhibited by maternal malnutrition whether it is a defi- ciency ofprotein, calories, or trace elements. Furthermore, malnutrition may reduce fetal brain development (20). There are three phases of cellular growth and organ development, the first being a phase of cell proliferation, followed by a phase of proliferation with concomitant hypertrophy, and a third phase of hypertrophy alone. Disturbances of the proliferation phase of brain tissue, for example, results in a lower DNA and protein content, which is irreversible and from which the brain does not recover. Therefore, the earlier the phase during which malnutrition occurs, the more serious is the lack of brain growth. This^ explains why fetal malnutrition may induce long-term damage to the child. Since brain development continues postpartum into infancy it is clear that postnatal malnutrition (^) may also (^) affect the brain (21). Climate also has a (^) regulatory effect on birth (^) weight. Babies born in the mountains of Peru on average weigh 1500 g less than the-newborns of Lima (22).- The socioeconomic environment in even the well-devel- oped countries is still undergoing changes, and modern women have the opportunity of working in male-oriented industries. Over the next decade, information will be gathered about possible factors such as toxins and work- load, which may interfere with providing a safe internal environment for the developing fetus (23). The prenatal effects on weight and height may disappear postnatally. Catch-up growth with respect to height occurs during infancy, but this may be incomplete (24), and the final height may be severely compromised by prenatal factors.
Postnatal Growth
Postnatal environmental factors affecting growth include nutrition, disease, socioeconomic status, urbanization, physi- cal activity, climate, and psychosocial deprivation. Nutrition. Malnutrition results in^ failure to grow, involving both weight and (^) height. Increased (^) growth hor- mone secretion occurs in protein malnutrition, presumably inducing mobilization of the remaining fat tissue (25). On the other hand, growth hormone levels are decreased in calorie malnutrition. When malnutrition is corrected, the affected children soon recover, and when this reversal occurs at (^) a young age, most children will attain a complete remission in (^) height and (^) weight to (^) equal their (^) siblings before (^) puberty (26,27). However, this is not (^) always the case, probably because^ of^ long-term deficits, and^ the home diet following hospital admission may play a role in such an
40
H. A. DELEMARRE-VAN DE WAAL
dency toward early maturation among swimmers. How- ever, self-selection may be the basis of this difference. If the sport itself does have an effect on body development, it may be limited to those who indulge in intensive training.
Puberty
The onset of puberty, in addition to the rate of matura- tion, appears to^ be dependent on^ heredity and the environ- ment. The age at menarche of identical twin sisters is within 1-2 months of each other, whereas in dizygotic twins there is about a years difference (51). In general, girls in poor countries have later menarche than in coun- tries with better socioeconomic conditions (^) (1). The secular trend over the last century includes a change in^ the^ timing of^ puberty and also^ a^ change in^ the rate of maturation during puberty. Environmental factors have an important bearing on this trend, and the secular changes affecting height and puberty are not always associated. For example, in the period from 1965 to 1980, women in the Netherlands became taller, whereas the age at menarche remained almost constant (52). In the last 20 years, the secular trend is slowing down in Europe (53). The earlier age at menarche in Southern Europe may be due either to genetic factors or to the climate. There is more and more evidence suggesting that age at menarche is under the influence of genetic control. Australian girls in Sydney born to immigrant parents fron Northwest and Central Europe have a menarcheal age of 13.1 years, whereas those born to immigrant parents from Southern Europe have menarche at 12.5 (^) years, and both these ages are close to the menarcheal (^) age of the (^) parts of (^) Europe from where the parents emigrated (42). The menarcheal age ofAmerican girls living in the hot and humid climate of Rio de Janeiro is not different from the girls living in the temperate United States. Overall, the assumption that climate has a major role in the timing of the onset of puberty appears to be erroneous (54). Liestol (55) suggested that there is an important influ- ence of social factors at a young age on the timing of puberty. He observed a clear relationship between social conditions during infancy and age ofmenarche in^ Norway, however, social conditions became less important later in childhood.
Precocious (^) Puberty
In general, prematurepubertal development is defined as
the onset of sex characteristics at an age more than two standard deviations below the mean for that population. This corresponds to an^ age of^ younger than about^ 8 in^ girls and younger than^ about^ 9 in^ boys. When^ pubertal development is caused by premature activation of the hypothalamic- pituitary-gonadal axis, this is called central precocious puberty (56). Development of sex characteristics may also
be stimulated by gonadotropin-independent sex steroid
production or by intake of exogenous sex steroids, and this
is pseudoprecocious puberty. Recently, Pasquino et al. (57) described a transient form of central (^) precocious puberty in which (^) regression of (^) pubertal signs and (^) suppression of
hormone secretion occurs after a period of months of central endocrine stimulation. A slowly progressive vari- ant of central precocious puberty has also been reported (58). Other forms of pubertal development are isolated breast development (premature thelarche) and isolated appearance of pubic hair (premature pubarche). The exact incidence of central precocious puberty and the other forms of premature maturation is unknown. Kaplan and Grumbach (59) reported the age distribution of central precocious puberty in 96 girls using the age of onset (younger than 8 years) as the diagnostic criterion. Physical signs became apparent between the ages of 6 and 7 years in 54% of cases, between 2 and 6 years in 28%, and before 2 years of age in 18%. The age distribution for 10 boys with central precocious puberty (onset before the age of 9 years) showed 40% with pubertal signs before the age of 6 years. These authors consider that the high incidence in (^) girls between the ages of 6 and 7 years is a reflection of the physiological variability in the normal age of puberty. Boneh et al. (60) reported an increase in the incidence (^) of isolated (^) premature thelarche and also of (^) central preco- cious puberty over the last 10 years in girls in Jerusalem. There was a significantly higher incidence in spring than in the other seasons. There have also been reports of premature thelarche in Italy and Puerto Rico with a suggestion that this has been caused by the ingestion of estrogens (61,62). These conclusions have not been sub- stantiated. Over the last 20 years, European families have been increasingly adopting children from developing coun- tries, and these children have been exposed to poor socio- economic conditions at a young age before adoption. They
should be expected to show catch-up growth and should
therefore attain a taller final stature compared to the children of their native country. However, there is evidence that adopted children achieved premature puberty, which had negative influence on final height (63,64). A group of 107 Indian girls adopted by Swedes had a significantly earlier menarcheal (^) age (mean 11.5 (^) years) compared to (^) girls in India (mean 12.8 years), although the final height was the same (63). Oostdijk et al. (64) investigated 465 girls and 394 boys from South Korea, Colombia, India, and Indonesia adop- ted by Dutch families. The mean age at adoption was 2.9 + 2.1 years. The mean age of the girls at menarche was significantly lower than the girls in^ their country of^ origin. A taller stature was (^) expected because of (^) catch-up growth, but the mean final (^) height for both (^) boys and (^) girls was similar to the height of adults in their own countries.
It is concluded that adopted children are exposed to better
conditions, which result in greater growth and an earlier
puberty. These two effects counteract each other, with the
earlier puberty preventing the more rapid growth from
producing a^ greater final^ height. The^ regulatory mecha- nisms, which are probably central in origin, underlying the interactions between growth and maturation are unknown.
Conclusion
The final (^) height of an individual (^) depends on (^) genetic
factors and environmental factors and is influenced by
42
ENVIRONMENT GROWTH, AND PUBERTY 43
prenatal as well as postnatal growth. Before the age of 2 years, there is no correlation between the height of the parents and the height of the offspring, but there is a direct correlation after the age of 2. Prenatal growth factors include maternal age, parity, alcohol consumption, drug addiction, smoking, therapeutic medication, climate, altitude, and malnutrition. Prenatal malnutrition has an effect on the developing brain, and the final effects produced depend on the age at which the malnutrition occurs. Postnatal growth is affected by nutrition, socioeconomic factors, disease, urbanization, psychosocial stress, and physical activity. There is a complex interaction among these different factors, and periods of retardation can be compensated by ensuing catch-up growth if the adverse factors are remedied. Final height is determined by an interaction of growth rate and age at puberty, (^) however, optimal conditions that stimulate growth may also advance the age of puberty with a negligible net effect on adult height.
REFERENCES
- Eveleth, P. B., and (^) Tanner, J. M. Worldwide Variation in Human Growth. (^) Cambridge Univer-sity Press, Cambridge, 1990.
- Bourguignon, J. P. Linear growth as a function of age at onset of puberty and sex steroid dosage, therapeutic implications. Endocrinol. Rev. 9: 467-488 (1988).
- Marshall, W. A., and de Limongy, Y. Skeletal maturity and prediction of age at menarche. Ann. Hum. Biol. 3: 235-245 (1976).
- Smith, D. W., Truog, W., and Rogers, J. E. Shifting linear growth during infancy: illustration of genetic factors in growth from fetal life through infancy. J. Pediatr. 89: 225-230 (1976).
- Philips, K., and Matheny, A. P. Quantitative genetic analysis of longitudinal trends in height: preliminary results from the Louisville Twin Study. Acta Genet. Med. Gemellol. 39: 143-163 (1990).
- Shields, J. Monozygotic T\wins. Oxford University Press, London,
- Ranke, M.^ B., and Rosenfeld, R.^ Thrner's Syndrome and Growth Promoting Therapies. Excerpta Medica, Amsterdam,^ 1991.
- Usher, R. H., and McLean, F. H. Normal fetal growth and the significance of fetal growth retardation. In: Scientific Foundations of Paediatrics (J. A. Davis, J. Dobbing, and W. Heinemunn, Eds.), Medical Books Ltd., London, 1974, pp. 69-79.
- Polani, P. E. Size of Birth. Ciba Foundation Symposium, Exerpta Medica, Amsterdam, 1974.
- Giovannelli, G., Bernasconi, S., and Ghizzoni, L. Environmentai fac- tors and growth. In: Growth Abnormalities (J. R. Bierich, E.^ Cac- ciarci, and S. Raiti, Eds.), (Serono Symposia Publications, Vol. 56) Raven Press, New York, 1989.
- (^) Lobl, M., Welcher, D. (^) W., and (^) Mellits, E. D. Maternal age and intellectual functioning of offspring. Johns Hopkins Med. J. 128: 347- (^361) (1971).
- Underwood, L. E. In: Textbook of Endocrinology (J. P. Wilson and D. W. Foster, Eds.), Saunders Co., Philadelphia, 1985.
- Miodovnik, M., Mimouni, (^) F, Dignan, P. S. J., Berk, M. A., Ballard, J. L., Siddiqi, T. A., Khoury, J., and Tsang, R. C. Major malformations in infants of IDDM women. Diabetes Care 11:^ 713-718^ (1988).
- Hill, R. M., and Tennyson, L. M.^ Maternal^ drug therapy: effect^ on^ fetal and neonatal (^) growth and neurobehavior. (^) Neurotoxicology 7: 121- (1986).
- Jones, K. L., Smith, D. W., Ulleland, C. N., and Streissguth, A. P. Pattern of malformation of chronic alcoholic mothers. Lancet i: 1267- 1268 (1973).
- Fulroth, R. Philips, B., and Durand, D. J. Perinatal outcome of infants exposed to cocaine and/or heroin in utero. Am. J. Dis. Child. 143: 905- 910 (1989).
- Hoff, C., Wertelecki, W., Blackburn, W. R, Mendenhall, H., Wiseman, H., and Stumpe, A. Trend associations of smoking with maternal, fetal and neonatal morbidity. Obstet. Gynecol. 68: 317-321 (1986).
- Fedrick, J., and Adelstein, P. Factors associated with low birth weight of infants delivered at term. Br. J. Obstet. Gynecol. 85: 1-7 (1978).
- Streissguth, A. (^) P, Heiman, C. (^) S, and Smith, D. W. Intelligence, behaviour and dysmorphogenesis in the fetal alcohol syndrome: a report on 20 patients. J. Pediatr. 92: 363-367 (1978).
- Winick, M. Cellular growth during early malnutrition. Pediatrics 47: 969-978 (1971).
- Winick, M., and Rosso, P. The effect of severe early malnutrition on cellular growth of human brain. Pediatr. Res. 3: 181-184 (1969).
- Krugher, H, and Arias-Stella, J. The placenta and the newborn infant at high altitudes. Am. J. Obstet. Gynecol. 106: 586-591 (1970).
- (^) McCloy, E. C. Work, environment and the fetus. Midwifery 5: 53- (1989).
- Fitzhardinge, P. M., Inwood, S. Long-term growth in small-for-date children. Acta Paediatr. Scand. (suppl.) 349: 27-33 (1989).
- Primestone, B. L, Barbezat, G, Hansen, J. D. L., and Muriay, P. Studies on growth hormone secretion in protein-calorie malnutrition. Am. J. Clin. Nutr. 21: 482 (1968).
- Garrow, J. S., and Pike, M. C. The long-term prognosis of severe infantile malnutrition. Lancet i: 1-4 (1967).
- Hansen, J. D. L., Freesemann, C, Moodie, A. D, and Evans, D. E. What does nutritional growth retardation imply? Pediatrics 47:^ 299- 313 (1971).
- MacWilliam, K. M., and Dean, R. F. A. The^ growth^ of^ malnourished children after hospital treatment.^ East^ African Med.^ J.^ 42: 297- (1965).
- Graham, G. G. The later growth of malnourished infants: effects of age, severity and^ subsequent diet.^ In:^ Calorie Deficiencies and^ Pro- tein Deficiencies (^) (R. A. McCance and E. M. Widdowson, Ed.), Church- ill, London, 1968, pp. 301-316.
- Brown, G. M., Seggie, J. A., Chambers, J. W., and Ettigi, P. G. Psycho- neuro-endocrinology and growth hormone: a review. Psychoneuroen- docrinology 3: 131-153 (1978).
- Eisenberg, E. Toward an understanding of reproduction function in anorexia nervosa. Fertil. Steril. 36: 543-550 (1981).
- Blanco, R. A., Acheson, R. M., Canosa, C., and Salomon, J. B. Height, weight and lines of arrested growth in young Guatemalan children. Am. J. Physical. Anthropol. 40: 39-48 (1974).
- Groll, A., Candy, D., Preece, M., Tanner, J., and Harries, J. Short stature as the primary manifestation of coeliac disease. Lancet ii: 1097-1099 (1980).
- Prader, A., Tanner, J. M, and von^ Harnack,^ G.^ A.^ Catch-up^ growth following illness or^ starvation. J.^ Pediatrics 62: 646-659^ (1963).
- Tanner, J. M.^ Catch-up growth in man. Br.^ Med.^ Bull.^ 37: 233- (1981).
- Goldstein, H. Factors influencing the height of seven-year-old chil- dren. Results from the National Child Development Study. Hum. Biol. 43: 92-111 (1971).
- Douglas, J. W. B., and Simpson, H. R. Height in relation to puberty, family size and social class. Millbank Mem. Fund Q. 42: 20-35 (1964).
- Brindtland, G., Liestol, K., and Walloe, L. W. Height, weight and men- archeal age of Oslo school children during the last 60 years. Ann. Hum. Biol. 7: 307-322 (1980),
- Cook, J., Altman, D.^ G, Morre, D. M.^ C., (^) TopA S. G., Holland, W. W., and (^) Elliot, A. A (^) survey of the nutritional status of schoolchildren. Re- lation between nutrient intake and socio-economic factors. Br. J. Prevent. Soc. Med. 27: 91-99 (1973).
- Tanner, J. M., and Eveleth, P. B. Urbanisation and growth. In: Man in Urban Environments (G. A. Harrison and J. B. Gibson, Eds.), Claren- don Press, Oxford, 1976, pp. 144-166.
- Hamill, P. V. V., Johnston, F. E., and Lereshow, S. Height and Weight of Children: Socio-Economic Status. Department of^ Health, Educa- tion and Welfare (^) Publication, No. (^) 73-1606, Vital Health Statistics Series 11, No.^ 119.^ U.S. Goverment^ Printing^ Office,^ Washington,^ DC,^ 1972.
- Jones, D. L., Hemphill, W., and Meyers E. S. A. Height, weight and other physical characteristics of New South Wales children. Part 1. Children aged five years and over. New South Wales Department of Health, G.96543-a K5705, Sydney, Australia, 1973.
- Villarejos, V. M., Osborne, J. A., Payne, F. J., and Arguedes, J. A. Heights and weights of children in urban and rural Costa Rica.
