the sympathetic nervous system and/or hypothalamic hormones (Spiegel et al., 2004), which also influence appetite.
Obesity also contributes to obstructive sleep apnea (OSA). This most likely occurs through fat deposition in airways, causing them to narrow. This point is inferred from studies finding that large neck size is a better predictor of OSA than is BMI (Katz et al., 1990) and the finding that central obesity (obesity around the waist) is a better predictor of OSA than total obesity (Grunstein, 2005b). The relationship has been found in well-designed epidemiological studies of young children (Locard et al., 1992; Sekine et al., 2002; von Kries et al., 2002) and adults (Vioque et al., 2000; Kripke et al., 2002; Gupta et al., 2002; Taheri et al., 2004; Hasler et al., 2004).
Taken as a whole, the body of evidence suggests that the serious public health problem of obesity may continue to grow as sleep loss trends continue to worsen. It also suggests that addressing obesity will likely benefit sleep disorders, and treating sleep deprivation and sleep disorders may benefit individuals with obesity (Taheri et al., 2004).
Two large epidemiological studies and one experimental study found an association between sleep loss and diabetes, or impaired glucose tolerance. Impaired glucose tolerance, which is a precursor to diabetes, is manifested by glucose levels rising higher than normal and for a longer period after an intravenous dose of glucose. In the Sleep Heart Health Study, which is a community-based cohort, adults (middle-aged and older) who reported 5 hours of sleep or less were 2.5 times more likely to have diabetes, compared with those who slept 7 to 8 hours per night (Figure 3-3, [Gottlieb et al., 2005]). Those reporting 6 hours per night were about 1.7 times more likely to have diabetes. Both groups were also more likely to display impaired glucose tolerance. Adults with sleep times of 9 hours or more also showed these effects, a finding consistent with the Nurses Health Study. Adjustment for waist girth, a measure of obesity, did not alter the significance of the findings, suggesting that the diabetes effect was independent of obesity.
The relationship between shorter sleep times and impaired glucose tolerance is also supported by an experimental study in which 11 healthy male volunteers were restricted to 4 hours of sleep for a total of six nights (Spiegel et al., 1999). Even after this relatively short period of time, the study found that sleep loss, compared with a fully rested state, led to impaired glucose tolerance. The effect resolved after restoring sleep to normal. Glucose clearance was 40 percent slower with sleep loss than with sleep recovery. Further, mice that have a mutation in a gene that regulates