What is sleep and do we really need it?

The restoration theory of sleep (Oswald, 1980) suggests that its function is to restore the body, including the replenishment of neurotransmitters, and the repair of tissue cells and muscles. It suggests that Slow Wave Sleep (SWS) is responsible for aiding physical recovery; support for this suggestion comes from findings that runners slept for 1.5 hours longer than average the two nights following an ultra-marathon. Significantly, the increase of SWS observed in these two consecutive nights was large, suggesting that it may in fact play a part in recovery of the body after physical stress (Shapiro et al, 1981). Indeed, it has been found that the production of growth hormone from the pituitary gland is strongly associated with SWS; such production may stimulate protein synthesis, thus contributing to the repair of bodily tissues (Moruzzi, 1972). Sassin and colleagues (1969) support this theory with evidence that when the sleep-wake cycle is reversed by 12 hours, so is the release of growth hormone. This manipulation clearly demonstrates a strong correlation between the release of growth hormone and sleep; however we must consider that it is a correlation, therefore meaning that we cannot confidently establish causality. Potentially, sleep could be brought on as a response to growth hormone release, rather than vice versa. Nonetheless, further research suggesting that a lack of SWS leads to reduced functioning of the immune system again provides support that, whichever way the cause and effect functions, there is evidence of a strong correlation between sleep and growth hormone release. Because antibodies are proteins, they must be regenerated during protein synthesis; this requires growth hormone, and thus without SWS during which it is released, the body cannot effectively replenish antibody stocks (Krueger, Walter & Levin, 1985). A second approach to the theory of sleep takes an evolutionary standpoint. Meddis (1975) suggests that sleep is an adaption evolved for the purpose of predator avoidance, and sleep patterns are dictated by environmental, predatory threats. The theory is that prey species must sleep less as they are under constant threat and must remain vigilant to avoid predators, whereas predator species can ‘afford’ to sleep more. Support for this suggestion can be found in findings from Allison and Cicchetti (1976) that species at a higher risk of predation do in fact sleep less. However, they also found some exceptions to this; for example, rabbits have high predatory risk and yet sleep as long as moles, which have low risk. An explanation for the exception could be the species habitat; rabbits sleep in underground burrows, potentially reducing their predation risk due to physical barriers and protection. This therefore sparks the question of whether the presence of a safe sleeping place may also dictate sleeping patterns in different species. Further support that risk in the individual’s environment dictates sleep is found in observations of dolphins in the river Indus, who are at constant risk of falling debris. Because of this, the dolphins only sleep for seconds at a time, demonstrating that (although not a high-risk prey species) their sleep-wake cycle has adapted to threats in their environment (Pilleri, 1979). Although Meddis’ suggestion does have support, it can be criticised on the grounds that it does not explain why animals sleep at all; according to this theory, if sleep is adaptive then species at the highest risk would benefit most from not sleeping at all. Therefore, sleep must have another function not explored by this theory for it to be present.