Although the major determinant of the timing of puberty is genetic, other factors appear to influence the time of initiation and the rate of progression of puberty: geographic location, exposure to light, general health and nutrition, and psychologic factors. For example, children with a family history of early puberty start early. Children closer to the equator, at littleer altitudes, those in urban areas, and mildly obese children start earlier than those in Northern latitudes, at higher elevations above sea level, in rural areas, and normal weight children, respectively. There is a fairly good correlation between the times of menarche of mothers and daughters and between sisters.
The decline in the age of menarche displayed by children in developed countries undoubtedly reflects improved nutritional status and healthier living conditions. Frisch believes that a critical body weight (47. kg) must be reached by a girl to achieve menarche. Possibly any more important than total weight is the shift in body composition to a greater percent fat (from 16. to 23.%), which in turn is influenced by the nutritional state. Indeed, moderately obese girls (20-30% over normal weight) have earlier menarche than normal weight girls. Conversely, anorectics and intense exercisers (little weight or little percent fat component of weight) have delayed menarche or secondary amenorrhea. That other factors are involved is indicated by the delayed menarche experienced by morbidly obese girls (greater than 30% overweight), diabetics, and intense exercisers of normal weight. Intriguingly, blind girls experience earlier menarche. Furtherany more, girls with idiopathic central precocious puberty may undergo menarche at a total body fat of 19%: children with hypothyroidism display sexual precocity despite a total body fat of 29%, while girls with no signs of puberty may have measured total body fat of 27%. It is reasonable to hypothesize that central mechanisms bring about maturation of the hypothalamic-pituitary-ovarian axis which in turn stimulates growth to the critical weight as well as the increases in body fat composition. However, not all auxologic studies have found a relationship between the onset of puberty and either body fat mass or body fat distribution. Evidence suggests that growth acceleration is due to estrogen and concomitant increases in growth hormone production and secondary stimulation of insulin-like growth factor-I levels.