Lim and Dinges have written a very nice comprehensive overview of the effects of sleep loss on human physiology, cognitive functioning and mood states. They describe the long standing two process model of state regulation and then present a synopsis of the more recent state stability/instability hypothesis and its accompanying biological basis. Finally, they turn to a discussion of individual differences in the vulnerability to sleep loss and conclude with a statement of the societal costs associated with the sleep loss.
As the authors point out, individual differences in the cognitive vulnerability to sleep loss are large and much greater than test-re-test differences within individuals. Sleep loss probably exerts its effects in a selective manner, varying between individuals dependent on individual system vulnerabilities. Comparatively little work has been devoted to the study of individual differences in vulnerability to sleep loss, and it is reasonable to expect that predisposing genetics, age, and environment will influence the relative risks to health and well-being associated with sleep loss. The importance of sleep loss for human functioning, well-being and long-term health will be borne out in the individual differences.
Hormones, such as cortisol, generally vary on a diurnal basis and are also influenced by sleep, so interpreting the effects of sleep loss is best done with a view to the full day-night cycle. The changes in the diurnal pattern of cortisol seen in some studies following a night without sleep is not usually described as a "rebound" but as an elevation of the circadian nadir of cortisol.
IL-6 is a potent stimulator of CRP production in the liver, and the finding of increased CRP in peripheral circulation of sleep deprived individuals (Meier-Ewert et al., 2004) is consistent with findings of increased IL-6 (Shearer et al., 2001), and it is possible that sleep loss is a factor mediating the relationship between short sleep and risk for developing diabetes and cardiovascular disease (Ayas et al., 2003a; Ayas et al., 2003b).
Orexin and hypocretin are not "two related neuropeptides", they are synonomous. Orexin A is also known as hypocretin 1 and orexin B also as hypocretin 2.
It is very true that fatigue and loss of vigor are increased during sleep deprivation and even when there is only minor elevation in negative mood states, optimism and sociability show a linear decline (Haack and Mullington, 2005). Related to this and of particular interest, is the finding that vigilance sensitive performance increases in a dose dependent manner whereas there is an apparent asymptote in the subjective assessment of fatigue (Van Dongen et al, 2003). This important mismatch may contribute to performance impairment because it suggests that our ability to self-monitor is also impaired by sleep loss, with consequent influence on decision making and judgment.