The circadian pacemaker imposes stereotypic patterns of daily variatio
n on the activity of human neuroendocrine systems. In a number of case
s, these patterns exhibit waveforms that are characterized by distinct
diurnal and nocturnal periods with relatively discrete transitions be
tween them (corresponding to a biological day, a biological dusk, a bi
ological night, and a biological dawn). In humans, for example, diurna
l periods of absence of melatonin secretion, low prolactin secretion,
and falling levels of cortisol alternate with nocturnal periods of act
ive melatonin secretion, high prolactin secretion and rising levels of
cortisol. In response to light, the circadian pacemaker synchronizes
the timing of the biological day and night so that their timing and du
ration are appropriately matched with the timing and duration of the s
olar day and night. As the pacemaker carries out this function, it is
able to adjust the duration of the biological day and night to match s
easonal variation in the duration of the solar day and night. Thus, af
ter humans have been chronically exposed to long nights (scotoperiods)
, the duration of nocturnal periods of active melatonin secretion, hig
h prolactin secretion and rising levels of cortisol is longer than it
is after they have been chronically exposed to short nights. Furthermo
re, the sleep-related peak of growth hormone secretion is half as high
after exposure to long nights as it is after exposure to short nights
. These responses to seasonal changes in duration of the natural scoto
period are suppressed in most individuals - especially men - who live
in modern urban environments in which they are exposed to artificial l
ight after dark and artificial darkness during the daytime.