ERROR LOADING HTML FROM SOURCE (http://ncf.sobek.ufl.edu//design/skins/UFDC/html/header_item.html)

An Exploratory Investigation of Sleep Disturbance in the Pathogenesis of Depression

Permanent Link: http://ncf.sobek.ufl.edu/NCFE004305/00001

Material Information

Title: An Exploratory Investigation of Sleep Disturbance in the Pathogenesis of Depression
Physical Description: Book
Language: English
Creator: Ponte, Kristen Linnae
Publisher: New College of Florida
Place of Publication: Sarasota, Fla.
Creation Date: 2010
Publication Date: 2010

Subjects

Subjects / Keywords: Sleep
Depression
Stress
Genre: bibliography   ( marcgt )
theses   ( marcgt )
government publication (state, provincial, terriorial, dependent)   ( marcgt )
born-digital   ( sobekcm )
Electronic Thesis or Dissertation

Notes

Abstract: The relationships among stress, sleep, and depression were examined to understand the role of sleep in the etiology of depression. A sample of 335 participants, age range 18-29 years, completed the Pittsburgh Sleep Quality Index (PSQI), the Perceived Stress Scale (PSS), and the Depression Anxiety Stress Scale (DASS-21). Perceived stress, sleep quality, and sleep duration predicted levels of depression. Sleep quality and duration interacted with perceived stress and levels of depression. As sleep quality worsened or duration decreased, levels of depression increased much more rapidly. Sleep disruption should no longer be considered a stress-related outcome, but rather a biological stressor in itself that can lead to the development and maintenance of depression.
Statement of Responsibility: by Kristen Linnae Ponte
Thesis: Thesis (B.A.) -- New College of Florida, 2010
Electronic Access: RESTRICTED TO NCF STUDENTS, STAFF, FACULTY, AND ON-CAMPUS USE
Bibliography: Includes bibliographical references.
Source of Description: This bibliographic record is available under the Creative Commons CC0 public domain dedication. The New College of Florida, as creator of this bibliographic record, has waived all rights to it worldwide under copyright law, including all related and neighboring rights, to the extent allowed by law.
Local: Faculty Sponsor: Bauer, Gordon

Record Information

Source Institution: New College of Florida
Holding Location: New College of Florida
Rights Management: Applicable rights reserved.
Classification: local - S.T. 2010 P8
System ID: NCFE004305:00001

Permanent Link: http://ncf.sobek.ufl.edu/NCFE004305/00001

Material Information

Title: An Exploratory Investigation of Sleep Disturbance in the Pathogenesis of Depression
Physical Description: Book
Language: English
Creator: Ponte, Kristen Linnae
Publisher: New College of Florida
Place of Publication: Sarasota, Fla.
Creation Date: 2010
Publication Date: 2010

Subjects

Subjects / Keywords: Sleep
Depression
Stress
Genre: bibliography   ( marcgt )
theses   ( marcgt )
government publication (state, provincial, terriorial, dependent)   ( marcgt )
born-digital   ( sobekcm )
Electronic Thesis or Dissertation

Notes

Abstract: The relationships among stress, sleep, and depression were examined to understand the role of sleep in the etiology of depression. A sample of 335 participants, age range 18-29 years, completed the Pittsburgh Sleep Quality Index (PSQI), the Perceived Stress Scale (PSS), and the Depression Anxiety Stress Scale (DASS-21). Perceived stress, sleep quality, and sleep duration predicted levels of depression. Sleep quality and duration interacted with perceived stress and levels of depression. As sleep quality worsened or duration decreased, levels of depression increased much more rapidly. Sleep disruption should no longer be considered a stress-related outcome, but rather a biological stressor in itself that can lead to the development and maintenance of depression.
Statement of Responsibility: by Kristen Linnae Ponte
Thesis: Thesis (B.A.) -- New College of Florida, 2010
Electronic Access: RESTRICTED TO NCF STUDENTS, STAFF, FACULTY, AND ON-CAMPUS USE
Bibliography: Includes bibliographical references.
Source of Description: This bibliographic record is available under the Creative Commons CC0 public domain dedication. The New College of Florida, as creator of this bibliographic record, has waived all rights to it worldwide under copyright law, including all related and neighboring rights, to the extent allowed by law.
Local: Faculty Sponsor: Bauer, Gordon

Record Information

Source Institution: New College of Florida
Holding Location: New College of Florida
Rights Management: Applicable rights reserved.
Classification: local - S.T. 2010 P8
System ID: NCFE004305:00001


This item is only available as the following downloads:


Full Text

PAGE 1

The Science of Sleep: An Exploratory Investigation of Sleep Disturbance in the Pathogenesis of Depression By Kristen Linnae Pont A Thesis Submitted to the Division of Social Sciences New College of Florida in partial fulfillment of the requirements for the degree Bachelor of Arts Under the sponsorship of Dr. Gordon Bauer Sarasota, Florida May 2010

PAGE 2

i

PAGE 3

ii This thesis is dedicated to my grandfather, mentor, and friend, Dr. Donald Ferguson, for his everlasting curiosity that in spired my passion for learning.

PAGE 4

iii Acknowledgements I acknowledge my thesis sponsor, Dr. Gordon Bauer, for his knowledge, enthusiasm, and guidance; Dr. Al Beulig, for introducing me to the field psychoneuroimmunology; and Heidi Harley, for serving on my thesis committee. I thank my mother for her unconditional love and support and my family for always believing in me. I would also like to thank a ll of my friends and peers who made my undergraduate years so fulfilling. A special thanks to Helen Kesl er, my mentor and friend; and Christian, my partner in crime.

PAGE 5

iv Table of Contents Dedication……………………………………..…………………………………………..ii Acknowledgements………………………..……………………………………………..iii Table of Contents……………………………..…………………………………………..iv Abstract…………………………………..………………………………………………..v Introduction……………………………………………...…….………………………….1 Sleep: Theoretical Perspectives …………………………………………………..2 Psychological Consequences of Sleep Impairments………………………………6 Stress: Theoretical & Bi ological Correlates……………………………………..12 Neuroendocrine Regulation of the Sleep/Wake Cycle…………………….…….17 Depression: Epidemiology, Etiology, & A ssociations with Sleep Impairments...21 Method…………………………………………...………………………………………27 Results…………………………………………...……………………………………….31 Discussion…………………………………………...…………………………………...33 References…………………………………………...…………………………………..39 Table 1…………………………………………...……........……………………………47 Figures…………………………………………...………….........………………………48 Appendix A: Pittsburgh Sleep Quality Index………………….………………………...50 Appendix B: Perceive d Stress Scale……………………………...……………...………55 Appendix C: Depression Anxiety Stress Scale………………………………………….57

PAGE 6

v THE SCIENCE OF SLEEP: AN EXPLORATORY INVESTIGATION OF SLEEP DISTURB ANCE IN THE PATHOGENESIS OF DEPRESSION Kristen Linnae Pont New College of Florida, 2010 ABSTRACT The relationships among stress, sleep, and depression were examin ed to understand the role of sleep in the etiology of depression. A sample of 335 participants, age range 18-29 years, completed the Pittsburgh Sleep Quality Index (PSQI), the Perceived Stress Scale (PSS), and the Depression Anxiety Stress Sc ale (DASS-21). Perceived stress, sleep quality, and sleep duration predicted levels of depression. Sleep quality and duration interacted with perceived stress and levels of depression. As sleep quality worsened or duration decreased, levels of depression incr eased much more rapi dly. Sleep disruption should no longer be considered a stress-related outcome, but rather a biological stressor in itself that can lead to the develo pment and maintenance of depression. Dr. Gordon Bauer Division of Social Sciences

PAGE 7

Sleep 1 Sleep disorders have been considered for a long time as a cardinal symptom of depression (Adrien, 2002) and while it has long been established that poor sleep quality has adverse effects on mood, motivation, a nd cognitive functioning (Harvey, 2008), only recently have researchers begun to delineate the relationships among stress, sleep, and mood in both healthy and vulnerable populations Past research has focused primarily on sleep disruption as a stress-related outcome (Hamilton et al., 2007), but recent findings suggest that sleep disruption may modulate the stress response and should be considered a biological stress or in itself. Many depressed individual s report that sleep problems are the single most debilitating feature of their disorder (Benca et al., 1997) and more than 65% of individuals diagnosed with depr ession report at least one co mplaint related to difficulty falling asleep, frequent awaken ings, and/or early morning awakenings (Sbara & Allen, 2009). Sleep disturbance can potentially expl ain many of the cognitive impairments associated with depression in cluding a negative or threaten ing interpretive bias towards ambiguous stimuli (Ree & Harvey, 2006) and an overabundance of negatively encoded declarative memories (Walker & van der Helm 2009). Chronic sleep deprivation has also been shown to enhance dysregulation of the stress response system (S piegel et al., 1999), which is one of the most robust and relia ble findings in depression. Together, this evidence suggests that sleep im pairments should be considered a risk factor in the development of depression. There are converging data to suggest that the American population is not only sleeping less, but that sleep disturbance is becoming exponentially more prominent in all age groups (Steptoe et al., 2008), with nearly a quarter of the U.S. population affected by

PAGE 8

Sleep 2 sleep disturbance (Opp et al., 2009). Considerin g that sleep is not the only biological rhythm, it is not surprising that poor sleep quality, associated with chronic sleep debt and/or chronic shifting of the sleep/wake cycle has been shown to have adverse endocrine, immunologic, and metabolic consequences (Harvey, 2008). Before introducing the current study, a re view of literature will be presented to establish sleep, stress, and depression as they have come to be understood through empirical research. The functions of sleep as well as the psyc hological and biological consequences of sleep impairments will first be discussed, followed by theoretical perspectives of the stress response an d biological correlates involved. Next, neuroendocrine correlates of the daily rhyt hms involved in regulat ion of the sleep/wake cycle will be presented. Lastly, the concep tual framework surrounding depression will be laid, followed by a comparison of the biol ogical alterations observed in sleep impairments and the etiology of depression. Sleep: Theoretical Perspectives Sleep is essential for most organisms, without which life cannot continue for more than a few days, (Bryant et al., 2004) a nd humans spend approximately one third of a lifetime asleep (Walker & Van der Helm, 2009) Despite the ostensible need we have for its restitution, exhibited by the sometimes impairing homeostatic drive for sleep, it was not until the twentieth century with the developmen t of technology to record electrical activity of the br ain, that the underlying neural correlates of sleep were uncovered. This first technology, called the electr oencephalogram (EEG) is attributed to the work of Hans Berger who discovered th at neural activity in animals could be measured through the electrical changes that reliably reflected such brain activity. By

PAGE 9

Sleep 3 1938, thirteen years after his initial discove ry, Berger had published 23 papers outlining the EEG responses evoked by various stim uli as well as the EEG rhythms that accompany sleep and wakefulness in mammals (Siegel, 2002). Today, sleep is typically measur ed using polysomnography (PSG) which combines EEG with electroocculogram (EOG) to measure eye movements, and electromyogram (EMG) to measure muscle tension (Akerstedt, 2006). Through the frequency and amplitude recorded by EEG, sleep can be divided into five stages, with stage five characterized by rapid eye movements (REM), which have been thought to occur during dreaming. Rapid eye movements are absent in stages one through four, which is why sleep is usually categorized into REM or non-REM (NREM) sleep (Siegel, 2002). A typical night’s sleep involves four to si x cycles of the five stages of sleep, with stages 3 and 4, referred to as slow-wave slee p (SWS), dominating the first half and REM dominating the second half (Walker & Van der Helm, 2009). NREM sleep constitutes approximately 80% of total sleep time a nd its restorative effects include: energy conservation, CNS restoration, and promotion of immune function. While researchers have made si gnificant headway in discovering how we sleep since the pioneering discovery by Hans Berger, the question why we sleep remains “one of the most persistent and perplexing mysteries in bi ology” (Frank, 2006). All mammals sleep (Siegel, 2005) and so do fish, birds, and even fruit flies. Rats have been shown to die from sleep deprivation before they die from starvation (Siegel, 2005). But why ? Evolutionary theorists have mapped out so me possible adaptive functions of sleep: energy conservation, decreased ri sk of injury, decreased re source consumption, decreased risk of detection by pred ators (Siegel, 2005).

PAGE 10

Sleep 4 Yet for a trait to be adaptive, in genera l, the benefits should outweigh the costs. While inactivity and energy conservation may be helpful for survival, sleep can also be perceived as largely negative for survival co nsidering that sleeping animals are not only vulnerable to predation, but also that sleep is incompatible with behaviors that ensure survival: eating, procreating, caring for proge ny, monitoring the environment for danger, and scouting for prey (Siegel, 2005). Jerome Siegel (2009), a prominent sleep researcher from University of California Los Angeles, has proposed the theory that sleep is a state of adaptive inactivity, whose primary function is to “increase animals’ efficiency and minimize their risk by regulating the duration and timing of their behavior.” As such, Siegel posits that sleep can be understood as a state of dormancy that is common throughout the plant and animal kingdoms. This statement is qualified with evidence showing that many species have evolved “daily or seasonal dormancy patterns that allow them to anticipate periods that are not op timal for survival and propagation” (Siegel, 2009). According to this hypothesis, if humans are dormant for a third of their lifetime, it is because humans would not benefit from being awake for more than two-thirds. Evolutionary theorists typically have perc eived sleep as a stat e of inactivity, as sleep has usually been consid ered throughout history. The ap pearance of brain imaging techniques has led research toward investig ating the functional components of sleep as a restorative process that is vital for survival (Siegel, 2005). Such theorists hold that, because there are so many risks involved for an individual during a dormant, less responsive state, sleep must serve some physiological or ne ural function that cannot be accomplished during wakefulness (Cirelli & Giuloi, 2008).

PAGE 11

Sleep 5 Robert Stickgold, a neuros cientist and prominent sleep researcher from Harvard University has proposed the critical func tion of sleep to be the organization and consolidation of memory (S tickgold et al., 2001). Stickgol d’s contemporary theory of “offline memory processing” is evidenced by EEG studies displaying neural activity between the hippocampus, the prominent memo ry center of the brai n, and the neocortex, such that experiences accumulated throughout waking life are reprocessed and integrated into other neural structures (Stickgold et al., 2001). A similar hypothesis was first proposed in 1983 when pioneering researchers Crick and Mitchison (1983) proposed the function of dream sleep (REM) to be a re verse learning mechanism such that during REM sleep, undesirable “modes” of interaction in neural networks within the cerebral cortex are eliminated. Crick and Mitchison’s theory, thus, suggests that we “sleep to forget.” Additionally, sleep has been proposed to play a vital role in affect regulation and may be of considerable importance in the development and maintenance of mood disorders (Walker & Van der Helm, 2009; Harvey, 2008). The latter proposed function is of pr imary concern for the current discussion. Perhaps the integral role of sleep in humans that has allo wed it to pers ist throughout our phylogeny involves psychological re storation rather than phys iological restoration. In accordance with University of Pennsylvania neuroscientist Marcos Frank’s statement (2006), “sleep is for the brain rather than th e body,” most everyone can attest to the fact that “grumpiness” can result from an inadequate night’s sleep. But why ? What occurs during a somnolent state that leaves us f eeling refreshed and rejuvenated? While the entire body undoubtedly benefits from the period of restitution (Cirelli & Giuloi, 2008), interestingly, the most immediate consequence of sleep deprivation is cognitive

PAGE 12

Sleep 6 impairment (Cirelli & Tononi, 2008). Are the mo od alterations associated with poor sleep quality merely secondary to the well-validat ed cognitive impairments (irritability due to memory inhibition, loss of focus, etc), or is there a restorativ e function at the neural level that plays a vital role in mood regulation? While no solitary, vital role for the purpose of sleep will probably ever be revealed, its importance is lucidly illustra ted from studies on acute and chronic sleep deprivation as well as from indi viduals with sleep disorders. Disordered sleep occurs in association with many psychiatric disorders, such as depression, and has been correlated with many medical conditions including cardi ovascular, infectious, and inflammatory diseases (Irwin et al., 2002). Psychological Consequences of Sleep Impairments Returning to the idea that “sleep is for the brain,” several line s of research have shown that sleep is necessary to recover fr om stress and that the lack of its proper restoration can lead to myriad health consequences, one of which includes the development of depression. It was once common ly believed that individuals who were depressed experienced sleep disturbance as a secondary symptom of depression. Researchers are uncovering evidence to suggest an opposite direction of causation: that sleep disturbance may lead to depression (Per lis et al., 1997). Recovery from acute stress is usually followed by a reparative sleep re bound characterized by an increase in REM sleep and SWS, suggesting the restorativ e function sleep plays in maintaining homeostasis. Exposure to chronic stress leads to fragmented sleep, probably driven by a stress-induced increase in corticoste roids (Van Reeth et al., 2000).

PAGE 13

Sleep 7 Johnson and colleagues (2006) explored the direction of association between sleep impairments and major depression in a commun ity-based sample. Structured interviews were conducted to assess sleep impairment s and depression in 1,014 participants. Prior depression was not associated with later sleep impairments, however, prior sleep impairments were associated with onset of depression in 69% of comorbid cases after adjusting for gender, race/ethnicity, and a ny prior anxiety disorder. Similarly, a metaanalysis conducted by Perlis et al. (1997) found that patien ts who suffer from recurrence of depressive episodes exhibit increased levels of sleep dist urbance several weeks prior to the recurrence. Studies on acute sleep deprivation suggest that the cognitive impairments involved in the lack of sleep may lead individuals to perceive next day stimu li as more threatening (Ree & Harvey, 2006) and emotionally valenced (Walker & Van der Helm, 2009). While ethical restrictions limit humans from par ticipating in prolonge d sleep deprivation experiments, studies suggest additive effects over time may lead to health problems, including depression. Researchers have found salient associa tions between depression and cognitive impairments as well as alterations in the en coding of declarative me mories. Increasingly, research findings are gaining support for a bidirectional relations hip between affect regulation and circuits involve d in sleep (Harvey, 2008). Indivi duals have been shown to become increasingly irritable and affectivel y volatile with increas ing sleep deprivation (Harvey, 2008). Research into the role of sleep in regulating psychophysiological reactivity and emotional brain networks, a once commonly overl ooked topic in the pathophysiology of depression, is now rapidly emerging.

PAGE 14

Sleep 8 An investigation by Ree & Harvey (2006) examined the presence of an interpretive bias in sleepy i ndividuals compared with cont rols. Sleepiness was assessed using the Stanford Sleepiness Scale with slee py participants scori ng 3 or above and notsleepy participants scoring 2 or below with a final sample of 55 sleepy participants and 23 not-sleepy participants. Pa rticipants completed a lexical decision task in which ambiguous sentences were paired with one word that corresponded to each possible meaning of the sentence. For example, a sentence such as “ Rosemary tried to disguise the size of her bags” was presented and participants we re requested to choose whether the word “shopping” or “ eyes ” best fit the interpretation of the sentence. The open-ended responses were coded by two judges, according to whether the alternate choice represented a generally threatening interpre tation compared to the neutral choice. A significant interaction was found between the sl eepiness group and target word type, such that those in the sleepy group res ponded more quickly (measured in ms ) to the general threat-consistent target word ( eyes ) than to the general threat-inconsistent target word ( shopping ). The option “ eyes” may be considered more threatening to a sleepy participant who fears exhibiti ng noticeable sleep deprivation symptoms such as having bags under the eyes. Individual differences in reaction times are t hought to reflect the extent to which a word is congruent with a person’s own concerns and cognitions (Ree & Harvey, 2006). The authors have suggested th at a sleepiness-linked bias may serve to increase arousal levels in sleepy individuals, which may contribute to the cognitive impairments that are characteristic of sleep disturbance. There is growing evidence in line with cognitive theories of depression to suggest that depressed individuals have a tendency to interpret ambiguous information in a

PAGE 15

Sleep 9 negative manner (Beck, 1976), and that such an interpretive bias may play an important role in the development and maintenance of depressed mood. An experiment conducted by Mogg et al. (2005) examined interpretive bias for ambiguous material in clinically depressed individuals using a homophone tas k. Forty-eight participants (24 depressed without co-morbid anxiety dia gnosis and 24 non-depressed) liste ned to a list of 14 orally presented homophones that had either a nega tive or a non-negative meaning (e.g. die/dye, weak/week) and were asked to record the wo rd on paper. A significant difference was found in homophone bias scores between the de pressed and control groups, such that depressed patients recorded significantly more negative meaning versions of the homophone. It should be noted that a homophone task is susceptible to response bias effects, but the results nonetheless support c onverging evidence for an interpretive bias of ambiguous stimuli in depressed individuals. Memory impairments have been observed in depression (Burt et al., 1995) and the relationship between sleep and memory consol idation is well documented (Walker & van der Helm, 2009). A recent investigation by Walk er & Tharani (2009) tested the effects of acute sleep deprivation prior to a learning session of emotionally valenced words. Participants who were sleep deprived dem onstrated a 40% deficit in memory encoding relative to participants who ha d slept normally prior to lear ning. In participants who had slept (control group), both positive and negative stumuli were associated with superior retention levels relative to th e neutral condition, consistent with the notion that emotion facilitates memory encoding (Phelps, 2004) In the sleep-deprived group, a severe encoding impairment was evident for neutral and especially positive emotional

PAGE 16

Sleep 10 memories, with sleep-deprived participants e xhibiting a significant, 59% retention deficit relative to participants in the control condition (Walker & Tharani, 2009). Most interesting was the relative resi stance of negative emotional memory to sleep deprivation, for which markedly sm aller and nonsignificant impairment was evident. Thus, the encoding of negative memo ry appears to be more resistant to the effects of prior sleep loss offering novel me mory insights into a ffective mood disorders that express co-occurring sleep abnorma lities (Buysse, 2004). The findings by Walker & Tharani (2009) can be seen to support Crick & Mitchison’s “s leep to forget” theory such that without sleeping, relativel y more, non-salient information was available. However, if one considers that sleep loss represents a vulnerable state, having greater access to negative memories could function to keep a sl eep-deprived organism away from potential danger. Although based on findings from acute sleep deprivation, it is noteworthy that chronic accumulated sleep debt associated with depression may impair the ability to form and retain memories of positive (and neutral) affective valence, yet leave preserved the formation and hence long-term dominance of negative experiences (Walker & van der Helm, 2009). Such an encoding bias would resu lt in a perceived autobiographical history dominated by negative life events, despite being potentially filled with both positive and negative daily experiences. Indeed, this im balance may provide a converse explanation for the higher incidence of depression in populations expressing impairments in sleep. The experiment conducted by Walker and Tharan i (2009) thus gives ev idence that sleep deprivation is associated with an enhanced bias toward negative encoding of memories that may contribute to the development of depression.

PAGE 17

Sleep 11 In addition to the damaging effects sleep disruption may have on learning, cognitive, and memory processes, res earchers have observed alterations in neuroendocrine systems that may result from acute and chronic sleep disturbance, with salient implications for stre ss-related mood disorders, namely depression. The stress response and circuits involved in sleep re gulation, both adaptive biological systems, function to react and restore an organism with in its environment (Van Reeth et al., 2000). In the past there has been a paucity of resear ch to delineate the interactions between the stress response system and sleep regulation. W ith the spawn of inter-d isciplinary research fields that strive to integrat e the neural, endocrine, and immu ne functions of an organism such as psychoneuroimmunology, research ers are uncovering the pathways of communication between the stre ss response system and sleep regulation that may have therapeutic implications. Add itionally, a greater understandi ng of the feedback between stress and sleep systems could shed li ght on the high comorbidity between sleep disturbances and mood disorders, both posited to be preceded and maintained by stress (Harvey, 2008). Stress: Theoretical Perspect ives & Biological Correlates In 1935, Hans Selye published "A Syndrome Produced by Diverse and Nocuous Agents" which outlined the concept of "stress" as the "nonspecific result of any demand upon the body" that can be produced fr om a variety of dissimilar situationsemotional arousal, effort, fatigue, pain, f ear, concentration, humiliation, loss of blood, and even great and unexpected success, (Selye, 1936). Selye further developed the concept of stress by outlining the "general adaptation syndrome," the stages of physiological response to stress that is still commonly referred to today.

PAGE 18

Sleep 12 The general adaptation syndrome (GAS) can be organized into three stages beginning with (1) the alarm reaction, dur ing which numerous biological systems including the neuroendo crine axis are engaged. The state of alarm cannot be maintained very long, and if the organism survives it will transition into (2) the stage of resistance. The stage of resistance is characterized by th e activated biological systems returning to normal. If the noxious stimulus persists, the ac quired adaptation is lost and the organism enters into (3) the stage of exhaustion that ca n lead to illness or death of the organism (Selye, 1936). Selye's "alarm" stage of the stress res ponse is known to elic it activation of the sympathetic nervous system (SNS). The SNS in itiates a "flight or fight" response within seconds of a threat, allowing an organism to be aroused and to generate energy in order to escape ("flight") or confront (" fight") the stressor. Activation of the SNS results in a great energy expenditure including mobilization of energy (free fatty acids, glycerol, glucose, amino acids) from storage units (triglycer ides, glycogen, proteins) and stopping all further energy storage until the stressor subsid es. Activation of the SNS is concurrently characterized by release of catecholamines such as epinephrine, increase in cardiovascular activity, as well as suppre ssion of digestion, gr owth, reproduction, inflammatory responses, and immunity (Van Reeth, 2000). The "resistance" stage of Selye's GAS concerns the "rest and digest" phase elicited by the parasympathetic nervous system (PNS). Functionally complementary to the SNS, the PNS acts to reinstate homeos tasis in the organism by release of acetylcholine to resume normal cardiac activit y, increase intestinal and gland activity, and decrease blood pressure to normal functioning (Vedhara & Irwin, 2005).

PAGE 19

Sleep 13 If the noxious stimulus persists, the organi sm enters into the third and final stage of the GAS, the stage of “exhaustion.” The onset of exhaustion has been proposed to occur upon depletion of adaptation energy stor es, characterized by enhanced activity of the hypothalamic-pituitary-adrenal axis and pathophysiological changes in the immune system and gastrointestinal tract. Such change s increase the organism’s susceptibility to infectious agents and gastrointestinal ulcers resulting ultimately in i llness or death of the organism (Selye, 1936). Though the stress response system has e volved in such a way to be capable of recognizing and responding to pot ential threats and enabling an organism to return to homeostasis, dysregulation is known to occu r when stressors are prolonged beyond what is adaptive for an organism and feedback mechanisms fail in restoring equilibrium which can lead to myriad health consequences (Ve dhara & Irwin, 2005). Sleep can be seen as a paramount restoring mechanism of an organi sm. Some of the restorative functions of sleep include the elimination of oxidative st ress that is accumulated throughout a waking period as well as an increased secretion of hormones such as growth hormone and an increase of immune secretions. While Selye’s GAS theory contributed greatly to the unders tanding of “stress,” more recent research has begun to illuminate th e variability present in the stress response cascade such that activation of the stress HPA axis does not follow a generalizable, uniform model. Kemeny (2003) has outlined th e integrated specificity model to suggest that the biological response of an organi sm is highly dependent upon the organism’s cognitive appraisal. Factors su ch as perceived control, soci al status, and perceptions of threat versus challenge have shown to significantly impact an organism’s

PAGE 20

Sleep 14 psychobiological response to stress For exampl e, humans who are exposed to stressors in a laboratory setting demons trate increased HPA activation if the stressors are uncontrollable than if they are controllable. Similarly, it has been demonstrated that demanding performance tasks elic it greater HPA activation when one’s social status or social self-esteem is threatened by performance failures (Kemeny, 2003). Additionally, McEwen (2006) uses the term “allostasis” to describe the activation of neural, neuroendocrine and neuroendocri ne-immune mechanisms in the face of potentially stressful challenges th at allows an organism to adapt. This “stability through change,” as allostasis has been described, is an essential component of maintaining homeostasis. Accordingly, McEwen (2006) has proposed that individual differences in response to challenge depend not only on the 1) appraisal of the situa tion, but also on 2) the condition of the body and its ability to withstand repeat ed adjustive demands. When allostatic systems are overworked or fail to shut off after the stre ssful event is over, “allostatic load” is seen to o ccur. Allostatic load can be altered via health-damaging and health-promoting behaviors such as smoking, dr inking, choice of diet, exercise and most importantly for the current discussion, adequate sleep. Sleep, which functions to restore an organi sm within its environment, appears to be an important determinant in the health and resilience, as a biobehavioral resource that minimizes allostatic load (Hamilton et al., 2007). With a robust and well-documented association between stress and the devel opment of depression (Rooij et al., 2009), behavioral contributions that may functi on to decrease allostat ic load should be considered of paramount importance for homeostasis of an organism, especially during periods of repeated adjustive demands. While Selye’s GAS may not be as “general” as

PAGE 21

Sleep 15 once believed, there is evid ence to suggest that endogenous stressors including sleep deprivation and infection ar e considered similarly by bi ological resources, as are exogenous stressors originating from “out side” an organism (McEwen, 2006). Sleep, therefore, may be considered to play a moderating role in the stress/depression relationship. Conversely, the most salient ev idence for this relationship is seen when sleep disturbance occurs, leaving an organism vulnerable to a stress related disorder such as depression. Among the responses elicited by stress are activation of the h ypothalamic-pituitaryadrenal (HPA) and the sympathetic-adren al-medullary (SAM) axes. The hallmark sympathetic “flight or fight” response is characterized by global activation of the SAM axis and features typical physiological and be havioral activation incl uding increased heart rate, increased blood pressure, and rapid breathing, along with release of catecholamines including epinephrine from the adrenal medu lla. The SAM axis is characterized by its speed of onset which occurs within seconds of a stessful stimulus, its ability to begin in anticipation of an event being stressful, and its interaction w ith the HPA axis (Van Reeth, 2000). Within minutes of response to stressful stimuli, the hypothalamic-derived releasing hormones corticotrophin-releasing hormone (CRH), growth-hormone-releasing hormone (GHRH), thyrotropin-releasing hormone (T RH), and gonadotropin-releasing hormone (GnRH) stimulate the synthesis and release of anterior pituitary adrenocorticotrophic hormone (ACTH), growth hormone (GH), thyroid-stimulating hormone (TSH), leutinizing hormone (LH), and folliclestim ulating hormone (FSH), respectively. These hormones are then released into the circulatory system where they act on specific tissues.

PAGE 22

Sleep 16 ACTH specifically stimulates the production of cortisol from the cortex of the adrenal gland. Cortisol has been identified as th e "main effector hormone of the HPA axis, gaining access to every cell in the body a nd influencing many essential stress-related cellular processes" (Vedhara & Irwin, 2005). The cortisol re sponse is much slower than activation of the SAM axis, with peak levels not seen for 1520 minutes after the onset of the stress. Early actions of the HPA system provide additional energy resources for the stress response, while slower gene-related effects over the next few minutes to hours serve to restrain ongoing actions of the st ress response which, if left unchecked, may prove to be unsustainable for the organi sm. Additionally, corticotrophin-releasing hormone (CRH) has been shown to activate re lease of norepinehprin e, inducing increased levels of arousal, which may have salie nt implications for stress-related sleep disturbances. Increased levels of cortisol provide negative feedback to inhibit further release of CRH and ACTH. The hippocampus, which is endo wed with high levels of receptors for adrenal steroids, is also a regulator of the stress response (McEwen, 2006) and exerts a large inhibitory effect to promote shut-off of the HPA axis. Ac ute stress that elevates adrenal steroids has been shown to suppress neuronal mechanisms that subserve short-term memory involving the hippocampus, though the effects are reversib le and relatively s hort-lived. Prolonged stress coupled with chronic increased leve ls of glucocorticoids, however, can cause atrophy of hippocampal dendrites and subse quent death of neurons (McEwen, 2006). The effects of glucocorticoid excess on the hippoc ampus are two-fold. Considering that the hippocampus is the primary brain region involve d in the consolidation of memories and

PAGE 23

Sleep 17 is also involved in the appr aisal of stressors, hippocampa l damage can result in both memory impairments along with impairme nts in responding to stressors (McEwen, 2006). Neuroendocrine Regulation of the Sleep/Wake Cycle Several hormones of the HPA axis show a daily rhythm. For example, the daily rhythm of cortisol secretion is referred to as the ultradian rhythm, a biological rhythm that is repeated throughout a 24-hour circadian day. Other ultradian rhythms include heart rate, thermoregulation, urinati on, bowel activity, and appetite, but the cortisol ultradian rhythm, specifically, is marked by a morning ze nith and an evening nadir (Bryant et al., 2004). Cortisol can be seen as a “wakefulness” or “arousal” hormone that prepares us for the day, receding during the night when sleep oc curs. The nadir for cortisol occurs around midnight (Buckley & Schatzbeg, 2005) and cor tisol levels begin to rise about 2-3 hours after sleep onset and continue to rise into the early waking hours. Slow wave sleep (SWS), which dominat es the first part of the night, is characterized by a pulsatile release of growth hormone. Growth hormone has been proposed as a putative inhibitor of the HPA axis, as CRH releas e is seen to be inhibited during SWS when circulating stress hormones reach diurnal a minimum. Elevated CRH levels have been shown to increase sleep EEG frequency, possibly by activation of epinephrine, thereby decreasing SWS and increasing light sleep and wakefulness (Buckley & Schatzberg, 2005). Nocturnal awak enings are associated with pulsatile releases of cortisol (Buckley & Schatzberg, 2005). The peak of cortisol has been shown to occur around 9:00 AM and is marked by a rapid rise in cortisol and ACTH that continues for approximately 60 minutes.

PAGE 24

Sleep 18 The ultradian rhythm of cort isol is susceptible to altera tions if hyperarousal of the HPA axis occurs, most likely from stress or sleep deprivation. In a study by Rosmond and colleagues (2002), it was shown that th e HPA-axis in healthy individuals is characterized by a wide ultradia n rhythm, a discrete but small response to an acute stress, and an appropriate suppression of cortisol levels following stress. Chronically stressed individuals displayed a decr eased ultradian variability and inadequate cortisol suppression after acute stress, indicating an altered pattern of secretion and impaired negative feedback with result ant cortisol hypersecretion. Th e effects of hypercortisolism in the brain can lead to cognitive dysfunc tion (Bhagwagar, 2003), depression, anxiety, along with a cascade of the metabolic syndr ome characterized by bone loss, obesity, hypertension, and insulin resist ance (Vedhara & Irwin, 2005). The term “circadian” means “about one day” (Harvey, 2008) and refers to the biological rhythm that has evol ved in response to the 24-hour cy cle of the sun. Sunlight is the primary zeitgeber, or “timegiver” of the circadian rhythm that enables mammals to be synchronized with the outside world. The bi ological “time clock” that entrains an organism to its environment is located in the suprachiasmatic nucleus (SCN) in the anterior hypothalamus (Harvey, 2008). Cells in the SCN stimulate the pineal gland to modulate body temperature and production of melatonin, the primary sleep inducing hormone (Harvey, 2008). Melatonin follows a 24hour rhythm with the highest point at night and lowest in the morn ing, functionally and temporally opposite to the rhythm of cortisol secretion. This active process of en trainment allows mammals the flexibility to change environments, such as different time z ones, and to adapt to new light/dark phases.

PAGE 25

Sleep 19 Sleep is under the dual c ontrol of circadian rhythmicity as well as a homeostatic process relating to the dept h of sleep and the duration of prior wakefulness. The homeostatic process is proposed to involve a putative sleep factor that increases during waking and decays exponentially during slee p (Van Cauter et al., 2000). While the circadian timing of sleep is less often shifted, with the exception of time zone changes during travel, and the bi-yearly daylight savi ngs, the homeostatic drive for sleep is more easily amenable to being shif ted (Wirz-Justice, 2006). Most everyone can attest to becoming mo re aware of their homeostatic drive for sleep after having slept for an extended period during the da y with subsequent wakefulness during the quiescent period. Chr onic shifting of the homeostatic drive for sleep can lead to adverse metabolic, endocri ne, and immune functio ning (Wirz-Justice, 2006) as the onset of sleep is seen to initia te the release of growth hormone as well as inhibit the HPA axis (Van Cauter et al., 2000) In both animals and humans, the HPA axis plays an important role in sleep-wake regula tion and in alterations of the sleep-wake cycle after acute or chronic stress including sleep deprivation. There is a clear and robust temporal association between sleep-wake states and activity of the HPA axis (Van Reeth, 2000) such that increases in melatonin secr etion promote feelings of sleepiness and increases in secretion of co rtisol promote wakefulness. Depression: Epidemiology, Etiology, & A ssociations with Sleep Impairments Depression can be described as a conditi on that primarily involves a disturbance of mood, and this affective disturbance is characterized by a mood that is sad, hopeless, discouraged, or simply depressed (American Psychiatric Association, 2000). According to the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) (APA, 2000),

PAGE 26

Sleep 20 major depressive disorder (MDD) is characteri zed by one or more episodes with five or more of the following symptoms most of the da y, nearly every day for at least two weeks: 1) depressed mood; 2) markedly diminished interest or pleasure in most activities; 3) significant weight loss or wei ght gain; 4) insomnia or hypersomnia; 5) psychomotor agitation or retardation; 6) fati gue or loss of energy, feelings of worthlessness, diminished ability to think or concentrate; and 7) recurrent thoughts of death (APA, 2000). With regard to epidemiology, the lifetime prevalence of the depression is 6% to 10% and begins most commonly in the 20’s a nd 30’s. Risk factors for depression include prior episodes of the il lness, family history of depressi on, prior suicide attempts, lack of social support, medical comorb idity, stressful life events a nd current substance abuse. Additionally, women are at twice the lifetim e risk as men, and the postpartum period increases the risk of first onset of the illness and a r ecurrence in those already ill (Shaffrey et al., 2003). Research has suggested that sleep problems should be classified as a biological stressor and not just a conse quence of stressful events. When rats have been induced to sleep deprivation there was an observable act ivation of the HPA axis (Bryant et al., 2004). Shift work and disruption of the norma l circadian clock have been linked with breast cancer and cardiovascular abnormalities as well as the development and maintenance of mood disorders (Harvey, 2008). Sleep deprivation repr esents a stressful experience that, via activation of the major st ress hormonal systems, is likely to alter health function. The absence of sleep onset has been shown to associate with hi gher cortisol levels at the quiescent period. Given that the day-l ong decrease of cortis ol levels partially

PAGE 27

Sleep 21 reflects the recovery of the HPA axis from the early morning circadian stimulation that occurs in response to increased CRH drive dur ing the second part of the night, elevation of evening cortisol levels might thus reflect an alteration of the rate of recovery of the HPA axis from the endogenous challenge that is likely to involve impairment of the feedback regulation of the HPA axis (Van Reeth et al., 2002). Spiegel et al. (1999) assessed activity of the HPA axis in 11 young men after time in bed had been restricted to 4 hours per ni ght for 6 nights. Sleep-debt measures were compared with the sleep-recovery period when participants were allowed 12 hours in bed per night for 6 nights. Both salivary cortisol and total plasma concentration of cortisol were measured. Along with decreased glucos e tolerance and increas ed activity of the SNS, the sleep debt conditi on was characterized by increased levels of cortisol concentrations in the afternoon and evening. The rate of decrease of free cortisol concentrations between 4 PM and 9 PM was a pproximately six times slower in the sleepdebt condition than in the sleep reco very condition (Spieg el et al., 1999). That sleep disruption mirrors hypercor tisolism associated with chronic stress suggests that the ability of th e HPA axis to recover from exogenous stimulation would be affected by sleep loss. Due to the deteri orating effects of hypercortisolism on the hippocampus, and that the hippocampus is the primary feedback regulator of cortisol, sleep deprivation coupled with stress may promote further alterations in the feedback mechanisms of the HPA axis. Chronic sleep loss may therefore accelerate the development of metabolic and cognitive conseq uences of glucocorticoid excess, such as cognitive deficits and decreased carb ohydrate tolerance (Van Reeth, 2000).

PAGE 28

Sleep 22 Interestingly, in addition to being a para mount structure in feedback regulation of cortisol, the hippocampus is responsible for memory organization and consolidation. As sleep is known to play a considerable role in the consolidation of declarative memories (Born et al., 2000), sleep depr ivation could affect the hi ppocampus two-fold, modulating both cognitive resources and receptor func tion. Hippocampal volume reduction has also been observed in major depression. Bremner ( 2000) demonstrated that participants with depression had a statistically significant 19% smaller left hippocampal volume than control subjects, implying the learning and memory impairments that may be involved in depression. Similarly, depression is marked by alterati ons in the HPA axis that are similar to chronic exposure to stress. Overactivity of the HPA axis within individuals with major depressive disorder has been documented since the late 1950s (McKay et al., 2010). Cortisol hypersecretion is regarded as important in the pathophysiology of major depression and the underlying dysregulations of the HPA axis in depression and chronic stress seem to follow a similar pattern. Both conditions are characterized by increases in cortisol secretion which is proposed to reflect altered capac ity or function of glucocortocoid receptors (Pruessner et al ., 2003). More refined analyses of the HPA system have revealed that impairments in glucocorticoid receptors result among other changes, in increased production and secre tion of CRH (Holsboer, 2000). Findings such as these have led to the hypothesis that impa ired glucocorticoid rece ptor signalling is a key mechanism in the pathogenesis of depression (Holsboer, 2000). Increased sleep latency, decreased sl eep continuity (increased time awake between sleep onset and final awakening), early morning awakeni ngs, and nonrestorative

PAGE 29

Sleep 23 or poor quality sleep represent the most commonly encountered subjective sleep complaints in depressed individuals (Wi nokur et al., 2001). Polysomnographic studies have found reliable objective a lterations in sleep architect ure in depressed patients (Winokur et al., 2001). In addition to corr oborating the subjective sleep complaints including increased latency, increased awak enings, and early morn ing awakenings, PSG measures have observed decreased SWS, reduced REM latency, increased REM during the first half of the night (when SWS us ually dominates) and overall increased REM density. Both objective and subjective sleep measures can be seen to reflect alterations in the HPA axis in depressed patients. Effects of stress hormones on sleep architecture have been demonstrated through exogenous administ ration of each of the major mediators of the HPA axis. Pulsatile administration of CRH has been shown to produce reduced SWS and reduced REM latency along with increases in the amount of shallow sleep (stages I and II) (Holsboer, 1999;Van Reeth, 2000). In line with the hypothesis that increased CRH levels are present in depressed patients and this may play a causal role in observed sleep disruption, clinical studies investigating a CRH-receptor-antagonist in patients with depression have shown an improvement in sl eep quality and increased SWS shortly after initiation of treatment (Schmind et al., 2008). A meta-analysis conducted by Burke et al. (2005) showed that depressed patients, compared to non-depressed controls, exhibited a blunted cortisol res ponse to acute stress and impaired stress recovery. During the “r ecovery” period, depressed patients’ cortisol levels remained higher when compared to controls. This evidence further implicates impaired feedback of the HPA axis in depression (Burke et al., 2005).

PAGE 30

Sleep 24 The rise in salivary-free cortisol that follows waking is a simple and reliable means of assessing the dynamic activity of the HPA axis activity and may therefore offer advantages of the HPA axis activity over isolated measures of basal salivary cortisol. Pruessner et al. (2003) examined the rela tionship between depressive symptomatology, measures of stress, and the cortisol res ponse to awakening in healthy male college students. A positive association between elevated cortisol levels after awakening and the self-reported severity of depressi ve symptoms was demonstrated. Similarly, Bhagwagar and colleagues (2005) investig ated the pattern of waking salivary cortisol in 20 unmedicated acutely depressed subj ects and 40 healthy controls. It was found that patients with acute depression secreted approximately 25% more cortisol than controls. It was concluded that depr essed patients have increased early morning cortisol secretion. If depresse d patients have higher levels of cortisol, potentially throughout the night and in the early morning, th is may explain the sleep disturbance that is commonly seen in conjunction with depression. Bhagwagar (2003) found similarly increas ed cortisol levels after waking in medication-free euthymic, or not depressed, su bjects with a past history of recurrent depression. This suggests that hypersecretion of salivary cort isol in relation to waking may represent a trait marker of depression be cause it appeared to persist when patients were clinically recovered. Authors present data supporting the hypothe sis that HPA axis hyperactivity is not a simple consequence or epiphenomenon of depression, but on the contrary that it is a risk factor to the development of depression. Consistent with the notion that impair ed glucocorticoid receptor function is crucial for HPA axis hyperactivity in depr ession, anti-depressant treatment has been

PAGE 31

Sleep 25 shown to increase glucocorticoid receptor expression, glucocorticoid receptor function and glucocorticoid receptor-mediated HPA axis feedback inhibition in laboratory animals as well as in humans, thereby reducing resting and stimulated HPA axis activity (Pariante, 2008). Finally, normalization of glucocorticoid receptor function by antidepressant treatment has been found to be a significant predictor of long-term clinical outcome (Pariante, 2008). Research findings are burgeoning that corroborate a bidirect ional relationship between sleep impairments and daytime sy mptoms of depression. Harvey (2008) has proposed an escalating “vicious” cycle, such that disturbance in mood during the day interferes with nighttime sleep and conversely, the effects of sleep disturbance contribute to mood-regulation difficulty along with cogni tive and memory impairments. In this light, sleep can be seen as the common denominator: increases in sleep quality improve daytime functioning and mitigate depressive symptoms, whereas sleep impairments decrease daytime functioning and ex acerbate symptoms of depression. Considering the comparable cognitive memory, and biological impairments associated with sleep disturbance and depr ession, the current exploratory study attempted to bolster previous findings by investigati ng the relationships among stress, sleep, and depression. It was expected th at stress, sleep quality, and sleep duration would predict levels of depression, with increases in stre ss and decreases in sl eep quality and duration predicting increased symptoms of depressi on. Additionally, sleep quality and duration were analyzed for their contributing role in the stress/depression re lationship. If increases in sleep predict lower levels of depression, a nd decreases in sleep pr edict higher levels of

PAGE 32

Sleep 26 depression, then the current study will provide fu rther evidence for the ro le of sleep in the development and maintenance of depression. Method Participants A total of 426 participants from a small liberal arts college in southwest Florida responded to a survey. Ninety-one participan ts were omitted on the basis of incomplete answers. The final sample c onsisted of 335 participants, of which 213 were female and 122 were male. Participants we re recruited by convenience a nd did not receive incentive for participation. Materials PSQI The Pittsburgh Sleep Quality Index is a well-validated, widely used 19-item self-report measure developed in 1989 to examine sleep quality over the previous month. It contains seven sub-scales measuring domains such as subjective sleep quality, sleep latency, sleep duration, and sleep disturbance, which combine to yield a global score of sleep quality. Global sleep quali ty scores are continuous (rang e 0-21) with higher scores reflecting poorer sleep quality, and scor es less than 5 indicating good sleep (see Appendix A). The PSQI has been demonstrat ed to have high internal consistency (Cronbach’s alpha = 0.83), te st-retest reliability (0.85-0.87) (Backhaus et al., 2002) as well as a diagnostic sensitivity of 89.6% a nd specificity of 86.5% (kappa = 0.75, p < 0.001) in distinguishing good and poor sleepers. (Buysse et al., 1989) PSS The Perceived Stress Scale is a 10-it em self-report questionnaire designed to measure perceptions of stress over the past month. Responses are given on a 5-point Likert scale (see Appendix B) with half of responses reverse scored to yield a single

PAGE 33

Sleep 27 score. Scores range from 0-40 with higher sc ores reflecting higher levels of perceived stress. Because levels of appraised stress ar e influenced by alterati ons in daily hassles, major stressful events, and coping resources the predictive validity of the scale is expected to decrease after a period of four to eight weeks. Because the PSS was not designed as a diagnostic tool, no clinical cut-off points are available. A large sample ( N = 2,387) collected by Cohen & Williamson (1988) found that the mean score for participants between the age of 18 and 29 was 14.2 ( SD = 6.2). Higher PSS scores are associated with failure to quit smoking, failure among diabetics to control blood suga r levels, and greater vulnerabi lity to stressful-life-eventelicited depressive symptoms (Cohen, 1994). A dditionally, an investigation by Cohen et al. (1983) showed that scores on the PSS were moderately correlate d with number of stressful life events in a college sample a nd a community sample. In the same sample, Cronbach’s alpha for the PSS was .85 in the college sample and .86 in the community sample. An investigation by Cohen et al. (1993) assessed perceived stress levels in 394 healthy participants before participants were exposed to a common cold virus. Participants were quarantined for two days prior to and 7 days following the viral challenge in a large apartment and monitored for the development of biologica lly verified clinical illness. Consistent with the notion that psychologi cal stress increases an individual’s susceptibility to infection, higher scores on the PSS were associ ated with greater risk of developing a cold. In short, the PSS has been shown to re liably measure perceptions of stress over the past two weeks.

PAGE 34

Sleep 28 DASS-21 The Depression Anxiety Stre ss Scale is a shortened version of Lovibond & Lovibond’s (1995) original 42-item questionnaire of depression, anxiety, and stress (DASS). Composed of 21 Likert-sca le questions with seven questions for each subscale, the DASS-21 examines the affec tive components of stress, anxiety, and depression over the past week. Higher scores signify increased severity of symptoms with scores ranging between 0-14 (see Appendix C). An investigation by Henry & Crawford ( 2005) tested the psychometric properties of the DASS-21 subscales with 1,794 non-clinical participan ts. Using Cronbach’s alpha, the Depression subscale was shown to have an internal reliability of .88. Henry & Crawford (2003) also investigat ed the convergent validity of the DASS-21 by calculating Pearson product moment co rrelations between each of the DASS-21 subscales with two independent measures of anxiety and depressi on, the Hospital Anxiety and Depression Scale (HADS) (Zigmond & Snai th, 1983), and the Personal Disturbance Scale (sAD) (Bedford & Foulds, 1978). With a non-clinical sample of 1,771 participants, the depression subscale correla ted with the sAD depression scale (.78). Th e correlation between the depression subs cale of the DASS-21 and the HADS depression scale was .66. The correlations between the DASS-21 and the sAD and HADS both exceeded the correlation found between the sAD depressi on scale and the HADS depression scale ( p < .001) suggesting that the converg ent validity of the DASS-21 is superior to other scales examined. Procedure Participants were provided a link via E-mail to access an online survey using SurveyMonkey, which they were told was design ed to assess their sl eep habits and stress

PAGE 35

Sleep 29 over specified periods of time. The survey included the PSQI, followed by the PSS and DASS-21. After providing informed consent, pa rticipants were requested to read each statement and to indicate the best answer by clicking on the response. Upon completion, participants were debriefed and thanked for their participation. Statistical Analyses Pearson r correlations were performed to examine the correlation coefficients between each of the pr edictor variables and depression. A multiple regression correlation was conducted on two models (1) Depression = Perceived Stress + Sleep Quality (2) Depression = Perceived Stress + Duration to ascertain the predictive validity of the each. Semi-partial correlations were also perfor med on each model to determine the unique contribution of each predictor variable on depression. Significant interactions were analyzed using ITALASSI a downloadable statistical analysis program that allows the graph to be rotated and viewed from all angles to further elucidate the relationships between the thre e variables. A visibl e plane distortion is indicative of an interaction (see Figure 1 and Figure 2). Results The mean score obtained for the Pitt sburgh Sleep Quality Index (PSQI) was 8.29 ( SD = 3.02, range = 2-21) which is markedly high when considering a PSQI score greater than 5 is thought to indicate clinical sleep impairments (Buysse et al.,1989). The sample mean score was significantly higher than the c linical cutoff for low qua lity sleep, t(337) = 20.06, p < .0001. The mean score obtained for th e Perceived Stress Scale (PSS) was 19.0 ( SD = 6.76, range = 3-38) which is significantly great er than the population average of 14.2, t(376) = 13.68, p < .0001, for individuals between the age of 18 and 29, (Cohen &

PAGE 36

Sleep 30 Williamson, 1988). Higher scores indicating high er levels of Perceived Stress in the sample population may be somewhat reflectiv e of the rigorous academic experience at New College of Florida during finals when da ta were collected. While some authors have chosen to group subjects into categories based on scores on the PSS and PSQI (e.g. Low Perceived Stress/High Perceived Stress; Poor Sleep Quality/Good Sleep Quality), this procedure reduces information. For this reas on, all variables were kept continuous. The mean score for the Depression subscale of the DASS (DASS_D) was 5.8 ( SD = 4.22), with females ( M = 5.85, SD = 4.19) scoring similarly to males ( M = 5.77, SD = 4.28) in the mild depression range (5-6.5) re ported by Lovibond & Lovibond (1995). Table 1 shows all Pearson r correlations among the PSQI, PSS, and the DASS_D. Poor Sleep Quality was associated with higher levels of Perceived Stress r (334) = .506, p < .0001 and higher levels of Depression r (328) = .500 p < .0001. Additionally, increases in Perceived Stress were associated with higher levels of Depression r (367) = .658, p < .0001, supporting the well-documented relati onship between stress and depression (Shaffrey et al., 2003). Poor Sleep Continuity was associated with higher levels of Depression r (365) = .229, p < .0001. Sleep Continuity refers to time awake between sleep onset and final awakening. The lower the score on the Sleep Continuity meas ure, the fewer awakenings after sleep onset, accounting for the positive (rather than negative) correlation between Sleep Continuity and Depression. Decreases in Duration were associated with higher levels of Perceived Stress r (358) = -0.302, p < .0001. Additionally, decreases in Duration were associated with

PAGE 37

Sleep 31 higher levels of Depression, though the st rength of the rela tionship was weak r (348) = 0.184, p = .0006. Relationship of Depression with Perceived Stress and Sleep Quality Perceived Stress and Sleep Quality had moderately strong predictive validity for Depression (R = .487, p < .0001). Semi-partial correlations were used to evaluate the unique contribution that Perceived Stress a nd Sleep Quality had on Depression. Perceived Stress had a strong uni que contribution ( b = .166, p < .017, sr = .435, p < .0001) followed by Sleep Quality ( b = -0.146, p = .419, sr = 0.039, p < .0001). Lower Sleep Quality scores indicate better sleep quality, accounting for th e negative contribution that Sleep Quality has on depression. There was a significant interaction betw een Perceived Stress and Sleep Quality ( b = 0.021, p = .0055) (see Figure 1). Increases in Pe rceived Stress and decreases in Sleep Quality (higher scores) predicted higher levels of Depression, but Depression levels increased much more rapidly as Sleep Quality decreased (scores became greater). Relationship of Depression with Perceived Stress and Sleep Duration Perceived Stress and Sleep Duration had mode rately strong predictive validity for Depression (R = .424, p < .0001). Semi-partial correlations were used to evaluate the unique contribution that Pe rceived Stress and Sleep Duration had on Depression. Perceived Stress had a st rong unique contribution ( b = 0.738, p < .0001,sr = .416, p < .0001). Sleep Duration did not yiel d a significant contribution. There was a significant interaction be tween Perceived Stress and Duration ( b = .048 p = .035). Increases in Perceived Stress a nd decreases in Duration predicted higher

PAGE 38

Sleep 32 levels of Depression, but Depr ession levels increased more rapidly as Duration decreased (Figure 2). Discussion The goal of the present study was to ex amine the relationships among perceived stress, sleep quality and durat ion, and depression in a sample of college students. The results supported the hypothese s that perceived stress, sleep quality, and sleep duration would predict levels of depression. Additi onally, the results supported the hypothesized moderating role that sleep would play in the stress/depression relationship. Participants who reported worse sleep quality or shorter sleep duration were found to exhibit more symptoms of depression than participants with equal amounts of stress who reported better sleep quality and highe r average sleep duration. While all data were correl ational, obscuring the dire ction of causation, previous research has found sleep impairments to prec ede the development of depression (Johnson et al., 2004). In line w ith evidence that sleep impairment s represent a biological stressor evidenced by increased activation of the HPA axis (Van Reeth et al., 2002) that may be involved in the pathophysiology of depression, the current study found decrements in sleep quality correlate d with increased symptoms of depression. Additionally, sleep continuity, a measur e of time awake between initial sleep onset and final awakening correlated with sy mptoms of depression. Decreases in sleep continuity were associated with increases in depression. Nocturnal awakenings have been observed to cause a pulsatile release of the cort isol (Buckley & Schatzberg, 2005). An increase in sleep fragmentation may thereby increase nocturnal levels of cortisol, the wakefulness promoting hormone, when cortisol is supposed to be at a diurnal minimum.

PAGE 39

Sleep 33 Decreases in sleep continuity have been obser ved in depressed indivi duals with elevated levels of CRH. Levels of CRH are at thei r lowest during slow wa ve sleep (SWS), and elevated levels have been shown to be asso ciated with decreased SWS and increased light sleep (stages 1 and 2), possibly by activation of epinephrine. Considering that light sleep, compared to SWS, is characterized by a decr eased arousal threshold, elevated levels of nocturnal CRH could be a mechanism through which depressed individuals experience increased sleep fragmentation (Buckley & Schatzberg, 2005). The present findings corroborate the role of perceived stress in the development and maintenance of depression. While stressful life events have been shown to precede the onset and relapse of depression (Shaffrey et al., 2003), objective measures of stress are limited in that they cannot account for va riability among individuals in appraising and reacting to stressful experien ces (Cohen, 1994). For example, an employment promotion may be considered a positive life event on an objective measure of stress, but perhaps the employee had to move to a new city to work in a position that was fa r less predictable or rewarding. In this case, while an objective stress measure would deem the promotion to be a positive event, a subjective measure w ould more accurately tap into how the event was appraised by the individual. Stress theorist s have emphasized the ro le of appraisal in responding to events since the concept of st ress was first outlined by Hans Seyle (1936). An individual who perceives an event as th reatening, uncontrollable, and unpredictable is likely to elicit a greater physiological stress response than someone who perceives the event as challenging, contro llable, and predictable, t hough the events are similar (Kemeny, 2003, Cohen, 1994).

PAGE 40

Sleep 34 While Perceived Stress was seen to have a greater unique contribution to Depression than either Sleep Quality or Duration, evidenced by larger semi-partial correlations, both models yielded significant interactions between Perceived Stress and Sleep, supporting the moderati ng role of sleep in the st ress/depression relationship. Because perceptions of stress may increase fo llowing sleep impairments, future research in this area should measure objective and s ubjective stress to determine how sleep may mediate the two. Sleep has been proposed to function as a biobehavioral resource that minimizes allostatic load (Hamilton, 2007). If th is is true, then restorative sleep should allow an individual to experience objective st ress with less increase in perceived stress. On the other hand, as sleep impairments are seen to increase allostatic load (McEwen, 2006), an individual with impaired sleep would be more likely to report greater perceived stress to a similar objective stressor. In accordance with McEwen’s theory of stress, individual differences in response to challenge depend not only on appraisal of the stressor, but also on the condition of the body and its ability to withsta nd repeated adjustive demands Sleep impairments activate the stress response system, increasing allostat ic load and decreasing resiliency, limiting the ability of an individual to experience increases in stress before illness occurs (McEwen, 2006). Stress-related disorders including depressi on can be compared with Selye’s final stage of the GAS, the stage of “exhaustion.” The biological systems that maintain homeostasis, notably the HPA axis, are no l onger functioning to allow an organism to adapt within its environment.

PAGE 41

Sleep 35 Rather, allostatic systems have become overworked and fail to shut off properly (McEwen, 2006), evidenced by impaired glucoc orticoid feedback with concomitant hyperarousal of the HPA axis. The current study has important implicat ions for the role of sleep in the development and maintenance of depression. Sleep impairments should be considered a “red-flag” for the development of depression. Individuals with a past history or family history of depression should be especially conscientious to get re storative sleep, since sleep disruptions represent a salient risk factor for dysregulation of the HPA axis, a hallmark biological marker observed in depr ession. Additionally, treatment of sleep disturbance could prevent the development of depression, and re duce the likelihood for relapse among vulnerable populations. Lastl y, because comorbid conditions are more difficult to treat and indicate a poorer prognosis than a prim ary disorder alone (Johnson et al., 2007), health practicioners s hould pay particular attention to altera tions in patients’ sleep quality to avoid developm ent of a comorbid condition that could have been avoided with treatment of the sleep impairment. A greater emphasis on maintaining a st able sleep/wake cy cle and practicing adequate sleep hygiene would be beneficial for student populations, especially during times of increased stress such as mid-terms a nd finals. Sleep hygiene refers to behaviors that are believed to promote improved quantit y and quality of sleep (Stepanski & Wyatt, 2003). Some common recommendations for impr oving sleep hygiene include maintaining consistent sleep and wake times, avoiding ca ffeine and other stimulants 4-6 hours before bedtime, avoiding naps, avoiding exercise before bed, along with creating a sleep environment that is quiet, dark, comfortable and absent of distra ctions (Stepanski &

PAGE 42

Sleep 36 Wyatt, 2003). Additionally, following an established pre-sleep ritual coupled with activities that promote relaxation have been shown to improve sleep quality (Stepanski & Wyatt, 2003). Considering that one cannot influence a genetic or developmental predisposition to depression, attention to da ily behavioral patterns that can decrease vulnerability should be perceived as vital for maintaining homeostasis. Future research in this area should inve stigate the role of sleep in longitudinal investigations which will elucidate the rela tionships among stress, sleep, and depression and allow for causal relationships to be infe rred. While retrospective measures allow for analysis of large amounts of data often with little investment, pr ospective studies are important for research into the etiology of di sease and would be helpful in this field of research (Clark & Doughty, 2008). Additionally considering the data showing direct effects of clinically effec tive antidepressants on HPA axis function (Pariante, 2008), this area should be furthe r investigated. In closing, the current study supports the hypothesis that sleep plays a role in the relationship between stress and depression. Restorative sleep plays a moderating role in the stress/depression relationship, allowing an organism to adapt and decrease allostatic load. On the other hand, sleep impairments can be seen to exacerbate the relationship between stress and depression, increasing al lostatic load, decreasing resiliency, and leaving the organism vulnerable to the develo pment of a stress-related disorder such as depression. Lastly, sleep disr uption should no longer be considered a stress-related outcome, but rather a biological stressor in it self that can lead to the development and maintenance of depression.

PAGE 43

Sleep 37 References Adrien, J. (2002). Neurobiological bases for the relation between sl eep and depression. Sleep Medicine Reviews 6 341-351. Akerstedt, T. (2006). Stress, sleep, and rest itution: In B. Bengt & R. Ekman (Eds.), Stress in Health and Disease Wiley-VHC. American Psychiatry Association (2000). Diagnostic and Statistical Manual of Mental Disorders (4th edn revised) Washington, DC: American Psychiatric Association. Backhaus, J., Junghanns, K., Broocks, A., Ri emann, D., Hohagen, F. (2002). Test-retest reliability and validity of the Pittsburgh Sleep Quality Index in primary insomnia. Journal of Psychosomatic Research 53 737-740. Bedford, A., & Foulds, G. (1978). Delusions-Sym ptoms-States Inventory state of anxiety and depression. Windsor: NFER-Nelson. Benca, R. M., Okawa, M., Uchiyama, M, Ozaki, S., Nakajima, T., Shibui, K., & Obermeyer, W. H. (1997). Sleep and mood disorders. Sleep Medicine Reviews 1 45-56. Bhagwagar, Z., Hafizi, S., Cowen, P. J. (2003). Increased concentration of waking salivary cortisol in recove red patients with depression. American Journal of Psychiatry 160 18901891. Bhagwagar, Z., Hafizi, S., Cower, P. J. (2005) Increased salivary cortisol after waking in depression. Psychopharmacology 182 54-57.

PAGE 44

Sleep 38 Bremner, J. D., Narayan, M., Anderson, E. R., Staib, L. H., Miller, H. L., & Charney, D. S. (2000). Hippocampal volume reduction in major depression. American Journal of Psychiatry 157 115-117. Bryant, P. A., Trinder, J., & Curtis, N. (2004). Sick and tired: Does sl eep have a vital role in the immune system? Nature Reviews 4 457-467. Buckley, T. M. & Schatzberg, A. F. (2005). On the interactions of the hypothalamicpituitary-adrenal (HPA) axis and sleeo: Normal HPA axis activity and circadian rhythm, exemplary sleep disorders. The Journal of Clinical Endocrinology & Metabolism 90 3106-3114. Burke, H. M., Davis, M. C., Otte, C., & Mohr, D. C. (2005). Depression and cortisol responses to psychological stress: A meta-analysis. Psychoneuroendocrinology 30 846-856. Burt, D. B., Zembar, M. J., Niederehe, G. (1995). Depression and memory impairment: A meta-analysis of the association, its pattern, and specificity. Psychological Bulletin 117 285-305. Buysse, D. J., Reynolds, C. F., Monk, T. H., Berman, S. R., & Kupfer, D. J. (1989). Pittsburgh Sleep Quality Index. Psychiatry Research 28 193-213. Cirelli, C. & Tononi, G. (2008). Is sleep essential? PLoS Biology 6 1605-1611. Clark, M. & Doughty, D. (2008). Retrosp ective versus prospective cohort study designs for evaluating treatment of pre ssure ulcers: A comparison of 2 studies. Journal of Wound, Ostomy and Continence Nursing 35 391-394.

PAGE 45

Sleep 39 Cohen, S., Davie, A. J., & Smith, A. P. ( 1994). Psychological stress and susceptibility to the common cold. In Steptoe, A., Ward le, J., eds. Psychosocial Processes and Health. New York, NY: Cambridge University Press, 171-187. Cohen, S., Tyrrell, D. A., Andrew, S. P. ( 1993). Negative life events perceived stress, negative affect, and susceptibility to the common cold. Journal of Personality and Social Psychology 64 131-140. Cohen, S., Kamarack, T., & Mermelstein, R. (1983). A global measure of perceived stress. Journal of Health of Social Behavior 24 386-396. Cohen, S. & Williamson, G. (1988). Perceived stress in a probability sample of the United States. In: Spacapan S, Oskamp S, eds. The social psychology of health. Newbury Park, Cali: Sage, 31-67. Crick, F. & Mitchison, G. (1983) The function of dream sleep. Nature 304 111-114. Frank, M. G. (2006). The mystery of sleep f unction: Current perspectives and future directions. Reviews in the Neurosciences 375-392. Hamilton, N. A., Catley, D., & Karlson, C. ( 2007). Sleep and the affective response to stress and pain. Health Psychology 3 288-295. Harvey, A. G. (2008). Sleep and circadia n rhythms in bipolar disorder: Seeking synchrony, harmony, and regulation. American Journal of Psychiatry 165 820-829. Harvey, A. G. (2008). Insomnia, psychiat ric disorders, and the transdiagnostic perspective. Current Directions in Psychological Science 17 299-303.

PAGE 46

Sleep 40 Henry, J. D. & Crawford, J. R. (2005). The s hort-form version of the Depression Anxiety Stress Scales (DASS-21): Construct validity and normative data in a large non-clinical sample. British Journal of Clinical Psychology 44 227-239. Holsboer, F. (2000). The corticosteri od receptor hypothesis of depression. Neuropsychopharmacology 23 477-501. Irwin, M. (2002). Effects of sleep loss on immunity and cytokines. Brain Behavior and Immunity 16 503-512. Jensen, D. R. (2003). Understanding sleep di sorders in a college student population. Journal of College Counseling 6 25-34. Johnson, E. O., Roth, T., & Breslau, N. (2006). The association of insomnia with anxiety disorders and depression: Explor ation of the direction of risk. Journal of Psychiatric Research 40 700-708. Kemeny, M. E. (2003). The psychobiology of stress. Current Discussions in Psychological Science 12 124-129. Lovibond, P. F. & Lovibond, S. H. (1995). The structure of negativ e emotional states: Comparison of the Depression Anxiety Stress Scales (DASS) with the Beck Depression and Anxi ety Inventories. Behavior Research and Therapy 33 335343. McEwen, B. S. (2006). Stress, adaptation, and disease. Annals New York Academy of Sciences 33-44. McKay, M. S. & Zakzanis, K. (2010). The imp act of treatment on HPA axis activity in unipolar major depression. Journal of Psychiatric Research, 44 183-192.

PAGE 47

Sleep 41 Mogg, K., Bradbury, K. E., & Bradley, B. P. (2006). Interpretation of ambiguous information in clinical depression. Behaviour Research and Therapy 44 11411419. Opp, M. R. (2009). Sleeping to fuel the imm une system: Mammalian sleep and resistance to parasites. BMC Evolutionary Biology 9 1-3. Pariante, C. M. & Lightman, S. L. (2008). Th e HPA axis in major depression: Classical theories and new developments. Trends in Neuroscience 31 464-468. Perlis, M. L., Giles, D. E., Buysse, D. J., Tu, X., Kupfer, D. J. (1997). Self-reported sleep disturbance as a prodromal sy mptom in recurrent depression. Journal of Affective Disorders 42 209-212. Phelps, E. A. (2004). Emotion and cognitio n: Insights from studies of the human amygdala. Annual Review of Psychology 57 27-53. Pruessner et al. (2003). Self-repo rted depressive symptoms a nd stress levels in healthy young men: associations with cortisol response to awakening. Psychosomatic Medicine, 65 92-99. Ree, M. J. & Harvey, A. G. (2006). Interp retive biases in chronic insomnia: An investigation using a priming paradigm. Behavior Therapy 248-258. Rooij, S. R., Schene, A. H., Phillips, D. I., & Roseboom, T. J. (2009). Depression and anxiety: Association wi th biological and perceive d stress reactivity to a psychological stress protocol in a middle-aged population. Psychoneuroendocrinology (in press).

PAGE 48

Sleep 42 Rosmond, R. (2005). Role of stress in the pa thogenesis of the metabolic syndrome. Psychoneuroendocrinology 30 1-10. Sbarra, D. A. & Allen, J. J. B. (2009). Deco mposing depression: On the prospective and reciprocal dynamics of mood and sleep disturbances. Journal of Abnormal Psychology 118 171-182. Schmid, D. A., Brunner, H., Lauer, C. J., Uhr, M., Yassouridis, A., Holsboer, F., & Friess, E. (2008). Acute cortisol admini stration increases sleep depth and growth hormone release in patients with major depression. Journal of Psychiatric Research 42 991-999. Selye, H. (1956). The stress of life. New York: McGraw-Hill Book Company. Selye, H. (1936). History of the stress res ponse. In L. Goldberger & S. Breznitz (2ndEd.), Handbook of Stress: Theoretical and Clinical Aspects (pp. 7-17). New York: The Free Press. Shaffrey, J., Horrmann, R., & Armitage, R. (2003). The neurobiology of depression: Perspectives from animal and human sleep studies. Neuroscientist 9 82-98. Siegel, J. H. (2002). The neural control of sleep and waking. New York, NY: Springer -Verlag. Siegel, J. M. (2005). Clues to the functions of mammalian sleep. Nature, 437 1264-1271. Siegel, J. M. (2009). Sleep viewed as a state of adaptive inactivity. Nature Reviews 747-753. Spiegel, K., Leproult, R., & Van Cauter, E. ( 1999). Impact of sleep de bt on metabolic and endocrine function. The Lancet 354 1435-1439.

PAGE 49

Sleep 43 Stepanski, E. J. & Wyatt, J. K. (2003). Use of sleep hygiene in the treatment of insomnia. Sleep Medicine Reviews 7 215-225. Steptoe, A., O’Donnel, K., Marmot, M., & Wardle, J. (2008). Positive affect, psychological well-being, and good sleep. Journal of Psychosomatic Research 64 409-415. Stickgold, R., Hobson, J. A., Fosse, R., Fosse, M. (2001). Sleep, learning, and dreams: Off-line memory reprocessing. Science 294, 1052-1057. Van Cauter, E., Leproult, R., & Plat, L. (2000). Age-related changes in slow wave sleep and REM sleep and relationship with gr owth hormone and cortisol levels in healthy men. JAMA 284 861-868. Van Reeth, O., Weibel, L., Spiegel., K., Lepr oult, R., Dugovic, C., & Maccari, S. (2000). Interactions between stress and sleep: From basic resear ch to clinical situations. Sleep Medicine Reviews 4 201-219. Vedhara, K. & Irwin, M. (2005). Human psychoneuroimmunology. New York: Oxford University Press. Walker, M. P. & Tharani, A. (2009). The im pact of pre-training sleep deprivation on emotional and neutral memory formation. In press. Walker, M. P. & Van der Helm, E. (2009). Ov ernight therapy? The role of sleep in emotional brain processing. Psychological Bulletin 5 731-748. Winokur, A., Gary, K. A., Rodner, S., RaeRed, C., Fernando, A. T., & Szuba, M. P. (2001) Depression, sleep physiol ogy, and antidepressant drugs. Depression and Anxiety 14, 19-28.

PAGE 50

Sleep 44 Wirz-Justice, A. (2006). Biological rhyt hm disturbances in mood disorders. International Clinical Psychopharmacology 21 S11-S15. Zigmond, A. S., & Snaith, R. P. (1983). Th e hospital anxiety and depression scale. Acta Psychiatrica Scandinavica 67 361-370.

PAGE 51

Sleep 45 Table 1 Bivariate Correlations (p Value and Number of Observations Below) between All Factors Measured: Perceived Stress, DASS_D, Sleep Quality, Duration, and Continuity PSS DASS_D PSQI DURAT DASS_D 0.65789 <.0001 367 PSQI 0.50627 0.50095 <.0001 <.0001 334 328 DURATION -0.30204 -0.18354 -0.47426 <.0001 0.0006 <.0001 358 348 320 CONT 0.18462 0.22853 0.41574 -0.17152 0.0003 <.0001 <.0001 0.0011 375 365 338 359

PAGE 52

Sleep 46 Figure 1 Three-Dimensional Depiction of the Two -Way Interaction between Sleep Quality and Perceived Stress on Depression, from ITALASSI

PAGE 53

Sleep 47 Figure 2 Three-Dimensional Depiction of the Two-Way Interaction between Sleep Duration and Perceived Stress on Depression, from ITALASSI

PAGE 54

Sleep 48 Appendix A PITTSBURGH SLEEP QUALITY INDEX INSTRUCTIONS: The following questions relate to your usual sleep habits during the past month only. Your answers should indicate the mo st accurate reply fo r the majority of days and nights in the past month. Please answer all questions. 1. During the past month, what time have you usually gone to bed at night? BED TIME ___________ 2. During the past month, how long (in mi nutes) has it usually taken you to fall asleep each night? NUMBER OF MINUTES ___________ 3. During the past month, what time have you usually gotten up in the morning? GETTING UP TIME ___________ 4. During the past month, how many hours of actual sleep did you get at night? (This may be different than the number of hours you spent in bed.) HOURS OF SLEEP PER NIGHT ___________ For each of the remaining questions, ch eck the one best response. Please answer all questions. 5. During the past month, how often hav e you had trouble sleeping because you a) Cannot get to sleep within 30 minutes Not during the Less than Once or twice Three or more past month_____ once a week_____ a week_____ times a week_____

PAGE 55

Sleep 49 b) Wake up in the middle of the night or early morning Not during the Less than Once or twice Three or more past month_____ once a week_____ a week_____ times a week_____ c) Have to get up to use the bathroom Not during the Less than Once or twice Three or more past month_____ once a week_____ a week_____ times a week_____ d) Cannot breathe comfortably Not during the Less than Once or twice Three or more past month_____ once a week_____ a week_____ times a week_____ e) Cough or snore loudly Not during the Less than Once or twice Three or more past month_____ once a week_____ a week_____ times a week_____ f) Feel too cold Not during the Less than Once or twice Three or more past month_____ once a week_____ a week_____ times a week_____ g) Feel too hot Not during the Less than Once or twice Three or more past month_____ once a week_____ a week_____ times a week_____ h) Had bad dreams Not during the Less than Once or twice Three or more past month_____ once a week_____ a week_____ times a week_____ i) Have pain Not during the Less than Once or twice Three or more past month_____ once a week _____ a week_____ times a week_____ j) Other reason(s), please describe_________________ __________________ ______________________ ________________________ ___________________________ _____________

PAGE 56

Sleep 50 How often during the past month have you had trouble sleeping because of this? Not during the Less than Once or twice Three or more past month_____ once a week_____ a week_____ times a week_____ 6. During the past month, how would y ou rate your sleep quality overall? Very good ____________ Fairly good ____________ Fairly bad ____________ Very bad ____________ 7. During the past month, how often hav e you taken medicine to help you sleep (prescribed or "over the counter")? Not during the Less than Once or twice Three or more past month_____ once a week_____ a week_____ times a week_____ 8. During the past month, how often have you had trouble st aying awake while driving, eating meals, or engaging in social activity? Not during the Less than Once or twice Three or more past month_____ once a week_____ a week_____ times a week_____ 9. During the past month, how much of a problem has it been for you to keep up enough enthusiasm to get things done? No problem at all __________ Only a very slight problem __________ Somewhat of a problem __________ A very big problem __________

PAGE 57

Sleep 51 10. Do you have a bed par tner or room mate? No bed partner or room mate __________ Partner/room mate in other room __________ Partner in same room, but not same bed __________ Partner in same bed __________ If you have a room mate or bed partner, as k him/her how often in the past month you have had a) Loud snoring Not during the Less than Once or twice Three or more past month_____ once a week_____ a week_____ times a week_____ b) Long pauses between breaths while asleep Not during the Less than Once or twice Three or more past month_____ once a week_____ a week_____ times a week_____ c) Legs twitching or jerking while you sleep Not during the Less than Once or twice Three or more past month_____ once a week_____ a week_____ times a week_____ d) Episodes of disorientation or confusion during sleep Not during the Less than Once or twice Three or more past month_____ once a week_____ a week_____ times a week_____ e) Other restlessness while you sleep; please describe_________________ __________________ ______________________ ________________________ _____________________ ___________________ Not during the Less than Once or twice Three or more past month_____ once a week_____ a week_____ times a week_____

PAGE 58

Sleep 52 Appendix B Perceived Stress Scale The questions in this scale ask you about your feelings and thoughts during the last month In each case, you will be asked to indicate by circling how often you felt or thought a certain way. 0 = Never 1 = Almost Never 2 = Someti mes 3 = Fairly Often 4 = Very Often 1. In the last month, ho w often have you been upset because of something that happened unex pectedly? ............ ................. 0 1 2 3 4 2. In the last month, how often have you felt that you were unable to control the important things in your life? .................... ...........….. .......... 0 1 2 3 4 3. In the last month, how often have you felt nervous and “stressed”? .... 0 1 2 3 4 4. In the last month, ho w often have you felt conf ident about your ability to handle your personal problems? ........... ................ ................ .............. 0 1 2 3 4 5. In the last month, how oft en have you felt that things were going your way?........... .................. .................. ................ ............. 0 1 2 3 4 6. In the last month, how often have you found that you could not cope with all the things that you had to do? ...... ............... ................ ...........….. 0 1 2 3 4 7. In the last month, how often have you been able to control irritations in your life? .......... .................. ............... ......……....... 0 1 2 3 4 8. In the last month, how often have you felt that you were on top of 9. things?……………………………………………………………………… 0 1 2 3 4 9. In the last month, ho w often have you been angered because of things that were outside of y our control? ....... ...............…..... 0 1 2 3 4 10. In the last month, how o ften have you felt difficulties were piling up so high that you could not overcome them? .......…. ......... 0 1 2 3 4

PAGE 59

Sleep 53 Appendix C DASS 21 Please read each statement and circle a numbe r 0, 1, 2 or 3 which indicates how much the statement applied to you over the past week There are no right or wrong answers. Do not spend too much time on any statement. The rating scale is as follows: 0 Did not apply to me at all 1 Applied to me to some degree, or some of the time 2 Applied to me to a considerable degree, or a good part of time 3 Applied to me very much, or most of the time 1 I found it hard to wind down 0 1 2 3 2 I was aware of dryness of my mouth 0 1 2 3 3 I couldn't seem to experience any positive feeling at 0 1 2 3 4 I experienced breathing difficulty (eg, excessively rapid breathing, breathlessness in the absence of phys ical exertion) 0 1 2 3 5 I found it difficult to work up the initiative to do things 0 1 2 3 6 I tended to over-react to situations 0 1 2 3 7 I experienced trembling (eg, in the hands) 0 1 2 3 8 I felt that I was using a lot of nervous energy 0 1 2 3 9 I was worried about situations in which I might panic and make a fool of myself 0 1 2 3 10 I felt that I had nothing to look forward to 0 1 2 3 11 I found myself getting agitated 0 1 2 3 12 I found it difficult to relax 0 1 2 3 13 I felt down-hearted and blue 0 1 2 3 14 I was intolerant of anything that kept me from getting on with what I was doing 0 1 2 3 15 I felt I was close to panic 0 1 2 3 16 I was unable to become enthusiastic about anything 0 1 2 3 17 I felt I wasn't worth much as a person 0 1 2 3 18 I felt that I was rather touchy 0 1 2 3 19 I was aware of the action of my heart in the absence of physical exertion (eg, sense of heart rate increase, heart missing a beat) 0 1 2 3 20 I felt scared without any good reason 0 1 2 3 21 I felt that life was meaningless 0 1 2 3


ERROR LOADING HTML FROM SOURCE (http://ncf.sobek.ufl.edu//design/skins/UFDC/html/footer_item.html)