1,144 g/day) at 6 months (N = 56), 637 g/day (range, 205 to 1,185 g/day) at 9 months (N = 46), and 445 g/day (range, 27 to 1,154 g/day) at 12 months (N = 40) (Dewey et al., in press).

Several studies indicate that potential milk production in humans is considerably higher than the average intake by single infants. Kaucher and colleagues (1945) measured maximum milk output with intrusive and tedious mechanical methods to extract all the mother's milk and reported that production averaged almost 1,200 g/day at 6 to 10 days post partum. This level is much higher than the 500 to 700 g/day consumed by breastfed infants at the same age (Casey et al., 1986; Saint et al., 1984). In two separate studies, milk production increased by 15 to 40% when a breast pump was used to remove additional milk after feedings (Dewey and Lönnerdal, 1986; Neville and Oliva-Rasbach, 1987). Mothers who exclusively breastfeed twins or triplets can produce 2,000 to 3,000 g/day, although this involves nursing an average of 15 or more times per day (Saint et al., 1986). Women who express surplus milk for a milk bank have been shown to produce as much as 3,000 g/day (Macy et al., 1930).

BREAST DEVELOPMENT AND PHYSIOLOGY

The data discussed above illustrate that lactation is a physiologic process with a great deal of plasticity—that is, milk production can be regulated up or down, depending on the degree of stimulation to the mammary gland. The processes leading to a woman's ability to secrete milk start long before lactation commences.

Mammary development begins in early fetal life and extends through puberty; it resumes early in pregnancy. The process is influenced by several hormones, including estrogens, progesterone, and lactogenic hormones (Neville and Neifert, 1983). Mammary gland enlargement is especially pronounced during the first half of pregnancy, when lobuloalveolar growth is accompanied by differentiation of the epithelial cells. Both prolactin and placental lactogen may initiate this enlargement, although either one alone may provide sufficient stimulus for mammary development. Insufficient development before or during pregnancy may contribute to lactation failure (Neifert and Seacat, 1986). The prevalence of this problem has not been studied but is likely to be very low.

Lactogenesis, defined as ''the onset of copious milk secretion around parturition" (Neville and Neifert, 1983, p. 108), is believed to be triggered by the decrease in progesterone following parturition. Incomplete delivery of the placenta has been shown to delay lactogenesis, presumably because it is accompanied by continued high levels of progesterone (Neifert et al., 1981). Prolactin is believed to be essential for normal lactogenesis, but the mechanism or mechanisms for its influence are not clearly understood. Once milk production has begun, the hormonal mechanisms maintaining milk secretion are believed to depend primarily on the actions of prolactin and oxytocin.



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