Humans spend a lot of their time in life sleeping. Sleep is necessary for people to live a healthy and useful existence. Nevertheless, several people suffer from sleeping problems and complications. For instance, students and busy employees have higher chances of practicing deprived sleep behaviors (Callaway & Bodenhamer-Davis, 2008). Because of this, many of them suffer from sleep-related disorders. Some research specifies that sleep difficulties frequently co-occur with numerous psychological health conditions.
Both scholars and medics have many times investigated the connection between sleep and mood (Morin, 2007). Morin (2007) notes that persons with insomnia symptoms have higher levels of despair and nervousness compared with individuals with normal sleep habits. As such, they are nine times more likely to exhibit signs of clinical depression. Similarly, they are sixteen times more likely to develop clinical anxiety compared with people who have normal sleep. The study indicates that the more an individual experiences sleeplessness, the higher chances for him or her to suffer from depression.
Disruptive sleep, apnea, has also been associated with despair. Apnea is a disorder in which somebody wakes up recurrently and very temporarily all through the night (Backhaus, Junghanns, & Broocks, 2002). One research conducted on over 18, 000 participants indicated that individuals with apnea four times more likely to agonize from medical depression (Ancoli-Israel & Kripke, 1991). The researchers suggested that when sleep is repeatedly interrupted it could modify mind activity and neurochemicals, which influence our temper and thinking.
Carpenter & Andrykowski (1998) suggested that the link between sleep and mood is multifaceted. They highlighted that disturbed sleep may cause emotional imbalances, clinical despair, or nervousness. Notably, the study noted that the above disorders could also interrupt sleep (Carpenter & Andrykowski, 1998). They asserted that irregular sleep habits are the leading cause of many psychological health issues.
In one study, partakers were administered with antidepressant prescriptions, cognitive behavioral therapy, and a control treatment (Gunklman & Johnstone, 2005). The results showed that participants who received cognitive behavioral therapy together with the antidepressant medicine progressed well compared with those who were treated with control treatment and antidepressants. The percentage of reduction of despair for those administered with control and antidepressant was 33.0%. While, the declining rate for persons treated with cognitive behavioral therapy alongside antidepressants was 62.0%.
The proportion of cutback of sleeplessness was 8.0% for those who were treated with both control and antidepressants. The above figures illustrate that cognitive behavioral therapy has an affirmative result in this test. The treatment had increased reduction for sleeplessness and depression. It implied that when the sleep inhibitor was treated other signs of unhappiness were enhanced. In this regard, it is apparent that managing the sleep disrupter may aid the general depression.
Hammond (2005) established that patients exhibiting depression symptoms and suicidal thoughts could be linked apnea and insomnia. The unhappy clients with sleeplessness recorded higher points on the Beck Scale for Suicidal Ideation. According to the research, the focal clinical effect of the suicidal thoughts or sleep disorders correlation is that sleep evaluation can enhance the assessment of suicidal threat in clients with critical key depressive illnesses. Therefore, when treating depression disorder, sleep inhibitors should be accounted.
Numerous biological concepts explain the relationship between sleep and depression (Baehr & Rosenfeld, 2004). The theories offer some explanation about the relations of the above conditions. For instance, SCN, hypothalamus pituitary adrenal axis, cortisol stages, and circadian beat procedures are associated related to both levels of despair and sleeplessness. The SCN controls circadian processes. The variations in activity in the SCN are analogous to the sleep/wake sequence. As such, an electrical action is advanced in the day when people are attentive and exposed to light. The activity is reduced during the night persons are less energetic and have little contact with natural light. Instabilities in the SCN are positive among individuals with depression and anxiety issues.
Many researchers have been undertaken to understand the above connections (Kerson, Sherman, & Kozlowski, 2009). However, the relationship among sleep, despair, and nervousness has not been fully comprehended. Astonishingly, little investigation has explicitly investigated the extent that anxiety affects the relationship between depressive symptomology and reduced sleep disturbances among non-clinical populations. The above imply that many questions are still unanswered with respect to the kinds of sleep complaints affecting undergraduates and the impact on their psychological health. The article below seeks to investigate the issue among students from Monash University. Before relating the precise particulars of the current study, a brief literature review is offered to describe former explorations that have investigated the phenomenon. Through the study, the relationships between sleep disturbance, depression, and anxiety will be established. Indicated below are the papers hypotheses:
- The positive correlation between sleep and depression will become insignificant after anxiety is controlled.
- Depression measured by DASS will be positively correlated to sleep measured by PSQI. The stress was measured by DASS will be interrelated with sleep and depression will be associated with anxiety.
The above study was intended to inspect the relationship among people’s sleep behaviors, depression, and nervousness. The findings support former results that suggested that depression is linked with apprehension and sleeplessness (Daley & Savard, 2009). Nevertheless, contrasting past studies, the above research aimed to identify the extent that anxiety affects the relationship between depressive symptomology and reduced sleep disturbances among non-clinical populations (Sateia, 2009). As hypothesized, there was a noteworthy affiliation amid depressive symptomology and sleep disorder among non-clinical populations. As such, depression evaluated by DASS was found to be positively linked with sleep appraised by PSQI.
Similarly, the hypothesis that a relation existed between depressive symptomology and sleep disorders when nervousness is controlled was supported. For instance, the results showed the existence of a positive correlation between sleep and depression because the link became trivial when nervousness was regulated. Notably, depression and anxiety are usually diagnosed in patients exhibiting sleeping disorders. Both scholars and medics have many times investigated the connection between sleep and mood. For instance, one study examining relations between depression and insomnia noted that the leading cause of sleeplessness is depressive symptoms and unhappiness. During the study, the researchers identified that there was a link between both insomnia and despair.
During the analysis process, the results were analyzed using an SPSS program. A bivariate Pearson’s correlation factor (r) was computed to evaluate the connection among unhappiness, sleep, and nervousness. The bivariate factor among hopelessness and sleep was positive and modest, r (258) =.386, p<.001. The bivariate link between anxiety and sleep was positive and robust, r (258) =.441, p<.001. The association between nervousness and unhappiness was positive and strong, r (258) =.596, p<.001. The fractional relationship was used to evaluate the linear relationship amid depression and sleep, after regulating nervousness. The parietal link was statistically noteworthy but with no connection, r (258) =.171, p<.001.
Based on the above findings, it is apparent that variations in mental state achieved by regulating anxiety led to disparities in the quality of sleep. A motivating reflection was that all results examined in this research resembled the justifications for distressed sleep as backed by the hyper-arousal concept of insomnia (Arns, Gunkelman & Breteler, 2008). As formerly deliberated, the theory presents a bio-psychosocial procedure whereby usual sleep is considered an involuntary process (Gunkelman, 2006). The sleep system and the CNS are imbalanced in insomnia incidents. Severe sleep disorders are thought to be activated by situational stressing agents that lead to enhanced cognitive activity.
The activities include a strong emphasis on symptoms, contemplation, anxiety, and autonomic stimulation. The above issues combined with poor sleep habits result in prolonged sleep difficulties. According to Moore (2000), the hyper-arousal concept of insomnia and trans-diagnostic models of insomnia also forecast the existence of unhappiness in people with deprived sleep. The above theories were supported in the study as demonstrated by the clinical elevations on manifold acts of depression (Cortoos & Cluydts, 2010). However, the linear relationship amid unhappiness and sleep after regulating nervousness suggested that medics should first emphasize their managements on addressing signs of nervousness when sleep is a central presenting issue.
The study also supported the findings by other investigations (Agnihotri, Paul & Singh, 2007). The results showed that participants who received cognitive behavioral therapy together with the antidepressant medicine progressed well compared with those who were treated with control treatment and antidepressants. The treatment had increased reduction for sleeplessness and depression. It implied that when the sleep inhibitor was treated other signs of unhappiness were enhanced (Allen, Harmon-Jones & Cavender, 2001). In this regard, it is apparent that managing the sleep disrupter may aid the general depression as indicated by the current study.
The current study experienced some limitations. One major problem was that there were no considerable measurements to evaluate some of the psychological health glitches. Even though structured interviews are inexistent, the absence of a self-report tool that precisely evaluates nonconforming depression factors was a limitation to the contemporary study (Masterpasqua & Healey, 2003). An additional challenge of the current research is the generalizability of the conclusions. The non-clinical sample was drawn from a university population. Thus, the results may not extend to all non-clinical populaces.
There are many possibilities for upcoming research. As showed above, new tools for assessing of uncharacteristic signs of unhappiness, insomnia, and anxiety are required to explore the links among downheartedness, sleep difficulties, and nervousness. Besides, the research should examine the despair subtypes and sleep complications in diverse populations.
With respect to implications, it was noted that the link between sleep and mood was intricate. As such, disturbed sleep may cause emotional imbalances, clinical despair, or nervousness. Notably, the study noted that the above disorders could also interrupt sleep. As such, sleep is necessary for people to live a healthy and useful existence (Masterpasqua & Healey, 2003). In general, the study indicated that the more individual experiences sleeplessness, the higher chances for him or her to suffer from depression or anxiety complications.
Agnihotri, H., Paul, M., & Singh Sandhu, J. (2007). Biofeedback approach to the treatment of generalized anxiety disorder. Iranian Journal of Psychiatry, 2(3), 90 95.
Allen, J., Harmon-Jones, E., & Cavender, J. (2001). Manipulation of frontal EEG asymmetry through biofeedback alters self-reported emotional responses and facial EMG. Psychophysiology, 38(6), 685-693.
Ancoli-Israel, S., & Kripke, K. (1991). Prevalent sleep problems in the aged. Applied Psychophysiology and Biofeedback, 16(4), 349-359.
Arns, M., Gunkelman, J., & Breteler, M (2008). EEG phenotypes predict treatment outcome to stimulants in children with ADHD. Journal of Integrative Neuroscience, 7(3), 421-438.