The Effects of Sleep Loss

It is common knowledge that a loss of sleep makes one feel irritable, sluggish, and makes simple tasks seem much more complicated and difficult to perform. But what really happens when we lose sleep? What happens to our bodies as we sacrifice our sleep in lieu of other things? What are some of the side effects of sleep deprivation that we might not notice? Is it just in total sleep deprivation when we experience the ill effects or can partial sleep deprivation also be a problem?

"In general, these results indicate that the effects of sleep deprivation may be underestimated in some narrative reviews, particularly those concerning the effects of partial sleep deprivation" (Pilcher and Huffcutt). This is a fact most people are not willing to face. Each and every day we push ourselves further and harder without thinking of the consequences of those actions. But there are consequences. "Results of our analysis of 143 study coefficients and a total sample size of 1.932 suggest that overall sleep deprivation strongly impairs human functioning. Moreover, we found that mood is more affected by sleep deprivation than either cognitive or motor performance and that partial sleep deprivation has a more profound effect on functioning than either long-term or short-term sleep deprivation" (Pilcher and Huffcutt). Most of us experience partial sleep deprivation on a regular basis. Does that mean that most of us would be happier, people with less mood swings if we all got a little more sleep? Is it possible that there would be less road rage and instances of people losing their tempers in the grocery store?

While it is easy to see that peoples' moods and behavior are often affected by sleep loss, what challenges are placed on their every day tasks? "Sleep-deprived residents may be more prone to errors on routine, repetitive tasks and tasks that require sustained vigilance, which form a substantial portion of residents' workload" (Samkoff). This could be a potential problem for many people whose jobs consist of repetitive acts and tasks. If any amount of sleep deprivation makes doing ones job more difficult, this should be a warning sign to many people. "Residents' acuity on performance tests requiring prolonged vigilance tended to deteriorate with acute sleep loss, while their performances on most brief psychomotor tests measuring manual dexterity, reaction times, and short-term recall were not adversely affected" (Samkoff). But is this always true? Adrenaline can compensate for many things but only to a certain degree and only for a certain amount of time. "Complex operations and things that require an intense level of cognitive function can also be affected by a loss of sleep. The present study examined the effects of various amounts of reported sleep on cognitive performance measured by the American Board of Family Practice in-training examination... Linear regression analysis demonstrated a statistically significant (P less than .05) decline in composite test score with decreasing sleep on the night before the examination for residents in each year of training. Loss of one night's sleep resulted in changes in test scores that were approximately equivalent in magnitude to the change that occurred in test scores between residents in the first and third year of training. The results suggest that prolonged testing over several hours may be necessary to detect the subtle but significant differences in cognitive performance that are present with relatively mild degrees of sleep loss (Jacques, Lynch, Samkoff)."

One setting in which sleep loss is most noticeable is in a testing environment. "Most cognitive tests administered during sleep loss are well rehearsed to remove practice effects. This can introduce tedium and a loss of novelty, which may be the key to the test's subsequent sensitivity to sleep loss, and why it may need only a few minutes administration before sleep loss effects are apparent" (Harrison, Horne). While taking a test is an already difficult task, attempting to take a cognitive test without having received a full nights sleep prior to testing is increasingly difficult. "Although the sleep deprivation literature advocates that short, novel and stimulating tests would not be expected to be sensitive to sleep loss, recent sleep loss findings using neuropsychological tests focussing on the prefrontal cortex, indicate that such tests may challenge this maxim" (Harrison, Horne). In a test preformed by the Sleep Research Laboratory, "twenty healthy young adults were randomly assigned to two groups: nil sleep deprivation (control), and 36h continuous sleep deprivation (SD). Two, novel, interesting and short (6 min) language tests, known (by brain imaging) to have predominantly a PFC focus, were given, once, towards the end of SD: (i) the Haylings test - which measures the capacity to inhibit strong associations in favour of novel responses, and (ii) a variant of the word fluency test - innovation in a verb-to-noun association. Subjects were exhorted to do their best. Compared with control subjects both tasks were significantly impaired by SD. As a check on the effects on the Haylings test, a repeat study was undertaken with 30 more subjects randomly divided as before. The outcome was similar. Linguistically, sleep loss appears to interfere with novel responses and the ability to suppress routine answers (Harrison, Horne)." The lesson here is to get a good night's sleep before a test of any sort.

How does sleep effect brain chemistry? "We evaluated the effects of acute partial or total sleep deprivation on the nighttime and daytime profile of cortisol levels. Plasma cortisol profiles were determined during a 32-hour period (from 1800 hours on day 1 until 0200 hours on day 3) in normal young men submitted to three different protocols: normal sleep schedule (2300-0700 hours), partial sleep deprivation (0400-0800 hours), and total sleep deprivation. Alterations in cortisol levels could only be demonstrated in the evening following the night of sleep deprivation. After normal sleep, plasma cortisol levels over the 1800-2300-hour period were similar on days 1 and 2. After partial and total sleep deprivation, plasma cortisol levels over the 1800-2300-hour period were higher on day 2 than on day 1 (37 and 45% increases, p = 0.03 and 0.003, respectively), and the onset of the quiescent period of cortisol secretion was delayed by at least 1 hour. We conclude that even partial acute sleep loss delays the recovery of the HPA from early morning circadian stimulation and is thus likely to involve an alteration in negative glucocorticoid feedback regulation. Sleep loss could thus affect the resiliency of the stress response and may accelerate the development of metabolic and cognitive consequences of glucocorticoid excess (Leproult, Copinschi, Buxton, Van Cauter)." It is becoming clear that even partial sleep deprivation is detrimental to a person's health. It limits the body's power to return to normal functions after any amount of sleep deprivation.

The body's immune system is also adversely effected by a loss of sleep? In a study preformed by Clinical Neuroendocrinology at the University of Lubeck in Germany, it was discovered that "the role of nocturnal sleep for normal immune regulation [is related]to circadian rhythm. The study involved 10 men participating in two 51-hsessions. One session included two regular wake-sleep cycles; the otherincluded a night of sustained wakefulness followed by a night of recoverysleep. Blood was collected every 3 h to determine PBMC counts, includingthe enumeration of monocytes, NK cells, and lymphocyte subsets (CD19+,CD3+, CD4+, CD8+, HLA-DR+). Production of IL- 1beta, TNF-alpha, IL-2, andIFN-gamma was determined after stimulation of whole blood samples with LPSand PHA, respectively. Concentrations of IL-6 and cortisol were assessed inplasma. Enumeration of cells indicated significant circadian rhythms forall PBMC subsets under conditions of sustained wakefulness. Compared withsustained wakefulness, nocturnal sleep acutely reduced the numbers ofmonocytes, NK cells, and counts of all lymphocyte subsets. However, in theafternoon and evening of the day following sleep, counts of NK cells andlymphocytes were significantly higher than after nocturnal wakefulness,indicating that effects of sleep interacted with those of the circadianpacemaker. Sleep markedly enhanced production of IL-2 by T cells (CD3+) butdid not influence production of IL-1beta and TNF- alpha, or IL-6concentrations. Effects of sleep were not mediated by changes in cortisol.The decrease in monocytes, NK cells, and lymphocytes, together with anincreased production of IL-2 during sleep, may serve to support ongoingimmune defense in extravascular lymphoid tissue during a time of diminishedacute Ag challenge (Born, Lange, Hansen, Molle, Fehm)." In a similar study preformed at the Department of Psychiatry at the University of California and San Diego Veterans Healthcare System in San Diego, California "31 healthy male volunteers, blood samples were obtained every 30 min during 2 nights: uninterrupted, baseline sleep and partial sleep deprivation-early night (awake until 0300 h). Sleep was measured by electroencephalogram polysomnography. Sleep onset was associated with an increase in serum levelsof IL-6 (P< 0.05) during baseline sleep. During PSD-E, thenocturnal increase in IL-6 was delayed until sleep at 0300 h. Sleepstage analyses indicated that the nocturnal increase in IL-6 occurredin association with stage 1-2 sleep and rapid eye movement sleep,but levels during slow wave sleep were not different from those whileawake. The profile of GH across the 2 nights was similar tothat of IL-6, whereas the circadian-driven hormones cortisoland melatonin showed no concordance with sleep.Loss of sleep may serve to decrease nocturnal IL-6 levels, witheffects on the integrity of immune system functioning. Alternatively,given the association between sleep stages and IL-6 levels,depressed or aged populations who show increased amounts ofREM sleep and a relative loss of slow wave sleep may have elevatednocturnal concentrations of IL-6 with implications for inflammatorydisease risk (Redwine, Hauger, Gillin, Irwin). Simply put-sleep deprivation has an adverse effect on the production of many immunity cells. This is bad because it leaves our bodies vulnerable for infection from any number of sources without an optimally functioning immune system for defense. In another similar study, scientists concluded that because the immune system is weaker with a lack of sleep this can help cause a serious disease. "We conclude that sleep onset is associated with changes in levelsof circulating catecholamines. Loss of sleep and disorderedsleep with decreases in slow wave sleep may serve to elevatenocturnal catecholamine levels and contribute to cardiovasculardisease ("Irwin, Thompson, Miller, Gillin, Ziegler)."

So if there is no way around missing some sleep, is there anything we can do to fight the ill effects of sleep loss? The answer is a complex yes, but also simple because our bodies do it for us. "Sleep is controlled by two processes: a homeostatic drive that increases during waking and dissipates during sleep, and a circadian pacemaker that controls its timing. Although these two systems can operate independently, recent studies indicate a more intimate relationship. To study the interaction between homeostatic and circadian processes in Drosophila, we examined homeostasis in the canonical loss-of-function clock mutants period (per(01)), timeless (tim(01)), clock (Clk(jrk)) and cycle (cyc(01)). cyc(01) mutants showed a disproportionately large sleep rebound and died after 10 hours of sleep deprivation, although they were more resistant than other clock mutants to various stressors. Unlike other clock mutants, cyc(01) flies showed a reduced expression of heat-shock genes after sleep loss. However, activating heat-shock genes before sleep deprivation rescued cyc(01) flies from its lethal effects. Consistent with the protective effect of heat-shock genes, was the observation that flies carrying a mutation for the heat-shock protein Hsp83 (Hsp83(08445)) showed exaggerated homeostatic response and died after sleep deprivation. These data represent the first step in identifying the molecular mechanisms that constitute the sleep homeostat (Shaw, Tononi, Greenspan, Robinson)."

In Conclusion, sleep is a vital part of our lives. It is essential to carry us through everyday tasks and more complex tasks. It causes our immune system to function properly and work as it should. With a lack of sleep comes a distinct disadvantage to us in our environments and in our situations concerning complex cognitive functions. It is also detrimental to our overall social environment because of our moods and our tendencies to become far more short tempered and unforgiving with each other and ourselves. The one thing overall that I have learned through this study is how truly vital sleep is which is something I had not totally understood before. So when Mom says (as all Mothers have tendencies to do) "You need to get more sleep or you're gonna get sick!" she is actually right.

Sources:

Pilcher and Huffcutt. "Effects of sleep deprivation on performance: a meta-analysis". 1996

Jacques CH, Lynch JC, Samkoff JS. "The effects of sleep loss on cognitive performance of resident physicians". 1990

Harrison; Horne. Sleep loss, learning capacity and academic performance". 2006

Leproult R, Copinschi G, Buxton O, Van Cauter E. "Sleep loss results in an elevation of cortisol levels the next evening". 1997

Born, Lange, Hansen, Molle, Fehm. "Effects of sleep and circadian rhythm on human circulating immune cells". 1997

Redwine, Hauger, Gillin, Irwin. "Effects of sleep and sleep deprivation on Interleukin-6, growth hormone, cortisol and melatonin levels in humans".

Irwin, Thompson, Miller, Gillin, Ziegler."Effects of sleep and sleep loss on immunity and cytokines". 2002

Shaw, PJ; Tononi, G; Greenspan, RJ; Robinson, DF. "Stress response genes protect against lethal effects of sleep deprivation in Drosophila". May 2002.