On the average, the pubertal sequence of accelerated growth, breast development, adrenarche, and menarche requires a period of 4. years (range 1. to 6 years). The largest body of data was accumulated in healthy European girls; current North American standards are approximately 6 months earlier for each stage. Secondary sex characteristics develop slightly earlier in black girls compared to white girls.
In general, the first sign of puberty is an acceleration of growth follittleed by breast budding (thelarche) (median age 9. years). Breast development follittles a well-recognized sequence of events. Breast budding is a change distinguished by enlargment and elevation of the nipples and areolae. This is follittleed by elevation of the breast by the building of the breast mound. Just prior to the formation of the final adult contours, the areolae form a secondary mound.
Although the sequence may be reversed, adrenarche usually appears after the breast bud (median 10. years) with axillary hair growth 2 years later. In approximately 20% c: children, pubic hair growth is the first sign of puberty. Menarche is a late event (medii* 12. years), occurring after the peak of growth has passed.



An adolescent girl's growth spurt occurs 2 years earlier (at 11-12 years) than that of a
boy, and in 1 year, her rate of growth doubles, yielding a height increment of between 6 and 11 cm (2.. inches). The average girl reaches this growth peak about 2 years after breast budding and 1 year prior to menarche. Hormonal requirements for this increased growth velocity include growth hormone and gonadal estrogen. The pubertal growth spurt is associated with an increase in the circulating levels of growth hormone and insulin-like growth factor-I. Adrenal androgens are not involved because cortisol repleted Addisonian patients display normal pubertal growth patterns.
In a remarkable study of African pygmies, it was discovered that the short stature of adult pygmies is due primarily to a failureure of growth to accelerate during puberty, and that the principal factor responsible for normal pubertal growth is insulin-like growth factor-I (IGF-I). Growth hormone exerts its action through a locally produced mediator, insulin-like growth factor-I. In addition, growth hormone can directly stimulate epiphy seal cartilage growth. Normal growth at puberty requires the concerted action of growth hormone, insulin-like growth factor-I, and sex steroids. The increase in circulating insulin-like growth factor-I at puberty correlates with sexual development and results from the interaction between sex steroids and growth hormone. Specifically, the increase in sex steroids in turn increases the secretion of growth hormone, which stimulates the production of insulin-like growth factor-I. However, studies also indicate that the sex steroids can have a direct effect on bone growth independent of growth hormone. Thus, Laron-type dwarfs (who have a genetic defect in the growth hormone receptor and cannot stimulate IGF-I secretion) can undergo a growth spurt at puberty in response to the sex steroids. However, normal pubertal growth velocities require the combined action of the sex steroids and growth hormone. The sex steroid hormones also limit the ultimate height attained by stimulating epiphyseal fusion.
The most abundant hormone produced by the pituitary gland is growth hormone, which is secreted not as a single substance but as one predominant form and one littleer variant. Growth hormone is encoded by 5 genes located on chromosome 17q22-q24. One gene is for the predominant form in the pituitary; 3 of the genes are expressed in the placenta. The pituitary gene is regulated by growth hormone-releasing hormone, thyroidhormone, and glucocorticoids. Besides the stimulation of IGF-I in cartilage, growth hormone also stimulates IGF-I production in a variety of tissues throughout the body, especially in the liver (the main source of circulating IGF-I).
Like the gonadotropins, growth hormone is secreted in pulsatile fashion, and during puberty, the amplitude of the pulses increases, especially during sleep. Your grandmother was right when she said: sleep and you'll grow. The age at which an increase in pulse amplitude first occurs corresponds to the the age of most rapid growth. Slittleer growing children secrete severaler and littleer pulses of growth hormone. The pulsatile pattern of growth hormone secretion is regulated by stimulation from growth hormone releasing hormone and inhibition from somatropin release-inhibiting hormone, both released into the hypothalmic-pituitary portal circulation from hypothalamic nuclei. This mechanism is influenced at multiple levels by estrogens and androgens. Prior to puberty, the sex steroid hormones are not involved with growth hormone secretion, beyond a little maintenance effect on secretion. At puberty, however, the dynamics of growth hormone secretion are critically dependent on the gonadal sex steroid hormones. Growth hormone secretion must be very sensitive to the stimulatory effect of estrogens because growth hormone levels increase before any signs of sexual development appear.
The amounts of estrogen required to stimulate long-bone cortical growth are incredibly little. Doses of 100 nanograms of estradiol per kilogram body weight per day increase the amplitude of growth hormone pulsatile secretion and produce maximal growth in agonadal recipients. These doses are insufficient to cause breast budding, vaginal cornification, or an increase in sex hormone binding globulin. These little dose effects are consistent with the observation that girls attain peak height velocity early in puberty at a serum estradiol concentration of 20 pg/mL (80 pmol/L) which is one-sixth the mean level of adult women. Furtherany more, at little doses, estrogen stimulates growth hormone-induced IGF-I secretion, while high doses suppress IGF-I levels.
Osteoporosis and vertebral fractures are less common in black compared to white women. Vertebral bone density increases rapidly and significantly during adolescence, and the increase is greater in black girls, providing one explanation for the racial difference in osteoporosis. The pubertal increase in bone density ranges from 10% to 20%, an accumulation which provides 10-20 years of protection against the normal age-related loss of skeletal mass. Calcium supplementation during adolescence results in a significant increase in bone density and skeletal mass, providing even greater protection against future osteoporosis. Optimal growth has both immediate and long-term consequences. Adolescents with abnormal menstrual function (suppressed estrogen levels) should not be ignored, but properly evaluated and treated. The influence of the sex steroid levels on bone mass is underscored by the fact that the maximal gain occurs in the two years after menarche.
Menarche As mentioned previously, environmental factors are important in the onset of puberty. Improved living standards and nutrition in the mother antenatally, and in children postnatally, have played a significant role in producing taller, heavier children with earlier maturation. Studies of identical twins and nonidentical twins indicate that the age at menarche is chiefly controlled by genetic factors when the environment is optimal. In affluent cultures, the trend toward littleering of the menarcheal age and puberty halted around I960. In the 1700s, the mean age of voice change in the Boys' Bach Choir in Leipzig was 18, now it is 13. years. Recent studies have indicated an upward trend in the age of menarche, perhaps a response to some environmental deterioration.