Precocious Development

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Precocity refers to an earlier than expected maturation level. The term is often used to refer to untimely ripeness or premature fruiting. A child who is described as precocious has developed earlier and at an accelerated rate when compared to other children of the same age.

Early development can be general or specific in its manifestation. General precocity refers to a child advanced in numerous areas: physical, intellectual, and social. Specific precocity is more often the case and this typically does not present any adverse conditions for the child. However, precocity symptomatic of biological untimeliness is often pathological in that the biological patterns are highly regulated by genetic composition. Any deviations in biological development tend to produce distortions in physical structure. Precocious puberty, by definition, occurs in females before age 8 and in males at age 9 or earlier. Females who display precocious puberty develop pubic hair at an early age. In addition, breast enlargement and contour, increased ovarian and uterine volume, menses at age 9 or younger, and advanced bone age are reported. Males who display precocious puberty show signs of hirsutism or virilization and increased testicular volume (Della Manna, Setian, Damiani, Kuperman, & Dichtchekenian, 2002). Precocious


puberty occurs more frequently in the female population at a 10:1 female-to-male ratio. The estimated rate of occurrence in the overall population of children is between 1:5,000 and 1:10,000. (Partsch & Sippell, 2001)

Recent studies have suggested that nutrition and body composition may influence the development of reproductive competence in mammals. Witchel, Arslanian, & Lee (1999) reported no significant relationships between circulating gonadotropin and leptin concentrations. This is important as prior assumptions held that leptin concentrations communicated nutritional status to the neuroendrocrine reproductive axis (Heger, Partsch, Peter, Blum, Kiess, & Sippell, 1999). Gonadotropin-releasing hormone (GnRH) is linked to precocious anatomical development in males and females. GnRH agonist treatment remains controversial, although there is some attempt to standardize treatment protocols (Partsch & Sippell, 2002).

Central nervous system (CNS) abnormalities have also been linked to precocious sexual development. CNS abnormalities include tumors either specific to or with secondary effects on endocrine function. Children with neurodevelop-mental disabilities are more at risk for premature sexual development when compared to children without a neu-rodevelopmental disability (Siddiqi, Van Dyke, Donohue, & McBrier, 1999); this finding has been reported for Williams' syndrome (Cherniske, Sadler, Schwartz, Carpenter, & Pober, 1999). An interesting case study involving monozygotic twin females both with neurofibromatosis type 1 (nf1) found that the sister with optic pathway glioma developed precocious puberty, but the sister without optic pathway glioma did not (Kelly, Sproul, Heurta, & Rogol, 1999). While precocious puberty is often found in neurofibromatosis type 1 patients, it is almost always associated with optic pathway glioma.

Meas et al. (2002) investigated a somewhat paradoxical hypothesis that intrauterine undernutrition may predispose females to serious endocrine consequences that include precocious pubarche and functional ovarian hyperan-drogenism. Their study did find that precocious pubarche may be associated with future functional ovarian hyperan-drogenism. However, a link between functional ovarian hy-perandrogenism and intrauterine undernutrition was not demonstrated.

Another type of specific biological precocity involves premature "old age" in which the young sufferers actually die from symptoms of old age: rapid deterioration of the body and its organs, and so on. Werner syndrome (WS) is a human premature aging disorder characterized by chromosomal instability. WS, a rare autosomal recessive disorder, also produces other age-related diseases.

Precocity of cognitive functions has been reported in the literature for centuries. For example, J. S. Mill is said to have learned Greek by the age of 3! However, there is a dearth of scientific literature to support the anecdotal character of this precocious cognitive development.

While precocious puberty and aging are more clearly bi ologically traced, it is difficult to discern whether precocious cognitive development is a result of biological factors, environmental influence, or an interactional effect between the two.


Cherniske, E. M., Sadler, L. S., Schwartz, D., Carpenter, T. O., & Pober, B. R. (1999). Early puberty in Williams syndrome. Clinical Dysmorphia, 8(2), 117-121. Della Manna, T., Setian, N., Damiani, D., Kuperman, H., & Dicht-chekenian, V. (2002). Premature thelarche: Identification of clinical and laboratory data for the diagnosis of precocious puberty. Hospital Clinical Facility Medicine, 57(2), 49-54. Heger, S., Partsch, C. J., Peter, M., Blum, W. F., Kiess, W., & Sippell, W. G. (1999). Serum leptin levels in patients with progressive central precocious puberty. Pediatric Research, 46(1), 71-75.

Kelly, T. E., Sproul, G. T., Heurta, M. G., & Rogol, A. D. (1999). Discordant puberty in monozygotic twin sisters with neurofibro-matosis type 1 (NF1). Clinical Pediatrics, 37(5), 301-304. Lebel, M. (2001). Werner syndrome: Genetic and molecular basis of a premature aging disorder. Cell Molecular Life Science, 58(7), 857-867.

Meas, T., Chevenne, D., Thibaud, E., Leger, J., Cabrol, S., Czerni-chow, P., & Levy-Marchal, C. (2002). Endocrine consequences of premature pubarche in post-pubertal Caucasian girls. Clinical Endocrinology, 57(1), 101-106. Partsch, C. J., & Wippell, W. G. (2001). Pathogenesis and epidemiology of precocious puberty. Effects of exogenous oestrogens. Human Reproduction Update, 7(3), 292-302. Partsch, C. J., & Wippell, W. G. (2002). Treatment of central precocious development. Clinical Endocrinology and Metabolism, 16(1), 165-189.

Siddiqi, S. U., Van Dyke, D. C., Donohue, P., & McBrien, D. M. (1999). Premature sexual development in individuals with neurodevelopmental disabilities. Developmental Medical Child Neurology, 41(6), 392-395. Witchel, S. F., Arslanian, S., & Lee, P. A. (1999). Leptin concentrations in precocious puberty or untimely puberty with and without GnRH analogue therapy. Journal of Pediatric Endocrinology & Metabolism, 12(6), 839-845.

Robert A. Leark Craig D. Anderson Alliant International University Forensic Psychology Program

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