Sleep deprivation (SD) has been shown to be an effective treatment for the immediate relief of depressive symptoms (Schwartzhaupt et al., 2009; Danilenko & Putilov, 2005; Evan et al., 2005). Several studies have concluded that sleep deprivation or total sleep deprivation has successfully elevated the moods of patients diagnosed with depression. Voderholzer et al. (2004) conducted a study on depressed patients by measuring the cortisol secretions before, during, and after SD; since sleep deprivation is associated with abnormalities of the hypothalamic-pituitary-adrenal (HPA) axis. The patients in their study were not medicated; cortisol levels were tested by sampling blood at 30-minute intervals for three consecutive nights prior to the night of SD. Saliva samples were also collected during the day in 30-minute intervals as well. The results of the study indicated that during the night of SD cortisol levels were significantly higher. During the daytime cortisol levels were higher to the individuals that responded to SD. Voderholzer et al. concluded that higher cortisol levels after SD “might transiently improve negative feedback to the hypothalamus or interact with other neurotransmitters.”
Other studies that have looked into sleep deprivation have focused on the interaction between medication with SD in order to promote faster remedial effects of core depressive symptoms. Wu et al. (1999) conducted a study on thirty-six patients with unipolar depression and 26 non depressed patients with PET scans before and after SD. According to the Hamilton Depression Rating Scale about 40% of the patients had a significant reduction of symptoms of depression after SD. The patients that responded to SD had higher metabolic rates in the medial prefrontal cortex, ventral anterior cingulate, and posterior subcallosal. After sleep deprivation there was a significant decrease in metabolic rates in the medial prefrontal cortex and the frontal pole. Wu et al. concluded that metabolic rates “after treatment in the medial prefrontal cortex may characterize a subgroup of depressed patients who improve following SD.”
Two studies that combined sleep deprivation and medications had inconclusive results. Reynolds et al. (2005) looked at the effects of sleep deprivation and the drug Modafinil. Modanfil is an alertness drug. Participants in his study were patients diagnosed with depression. Half of the participants were given the medication the other half was given a placebo, both groups went through SD therapy. Reynolds study concluded that the participants that were sleep deprived and on the medication did not experience any less symptoms than the patients who were only submitted to SD. His data suggest that the two interventions might have counteracted each other.
Another intriguing look into why sleep deprivation therapy has its immediate success can be due to neuroendocrine research on ghrelin. Ghrelin is an endogenous neurotransmitter that is hypothesized to play a key role in energy balance, stimulating food intake, and body weight also appears to be involved in sleep regulation. Ghrelin promotes slow wave sleep and the nocturnal release of GH, cortisol and prolactin in humans. Steiger (2007) demonstrated this through his rat experiment of systematic administration of ghrelin to rats. Ghrelin administered in the early morning increases secretion of cortisol and growth hormone without affecting sleep, and sleep deprivation results in ghrelin elevation. Ghrelin also enters the hippocampus formation and forms synapses that have been shown to enhance special learning and memory. This leads to two conclusions 1) ghrelin impacts the brain by cognitively enhancing the effects of receptors and 2) indirectly with food intake through appetite and energy utilization. Both can lead to the immediate relief of core depressive symptoms.
Another interesting study on sleep deprivation has been conducted in relation to caffeine and its stimulating effects. Participants in this study were given caffeine and SD therapy. However the results weren’t significant enough to determine whether caffeine was the reason for the depressive symptom changes. Though caffeine did stimulate less depressive symptoms for a few individuals. This idea is something that should be further looked into.
Sleep deprivation has been proven to work, though no data show how it works. All in all, SD is effective for short relief of core depressive symptoms.