Psyc 395 Research Paper

THE EFFECTS OF CHRONIC STRESS ON RECOGNITION MEMORY IN YOUNG ADULTS 1
The Effects of Chronic Stress on Recognition Memory in Young Adults
Alexandra Brenza
Student #260410758
McGill University
Course: PSYC 395
Supervisor: Dr. Jens Pruessner
Date Submitted: December 3rd, 2013

Introduction
The term “chronic stress” is frequently used in our busy population, but what it
means is not always easy to articulate. Chronic stress can be experienced and interpreted
in a myriad of different ways, and is harmful to our physical and psychological function
(Smyth, Zawadzki, & Gerin, 2013). Exposure to chronic stress has been consistently
associated with an increased susceptibility to harmful physical and psychological
outcomes. For example, people’s exposure to chronic stress has higher levels of clinical
depression, increased upper respiratory infection, more flare-ups of allergic or
autoimmune conditions, and increased progression of chronic diseases (Miller & Cohen,
2005; Monroe & Hadjiyannakis, 2002; Pereira & Penedo, 2005; Rozanski, Blumenthal,
& Kaplan, 1999; Wright, Rodriguez, & Cohen, 1998). These chronic stress effects exist
across one’s lifespan, and are often quite large in effect. (Miller, Chen, & Zhou, 2007)
Better understanding chronic stress is particularly relevant to psychology, as it can help
clarify the development and pathology of psychological disorders, and help develop
treatments to alleviate the negative effects of chronic stress.
In research, chronic stress is often defined as stimulus-based, in which a specific
population is enduring circumstances that most would view as troubling and persistent
(Miller, Chen, & Zhou, 2007). Stress can be defined as a consequence of the interaction
between the person in the environment characterized by use and/or consumption of
personal or environmental resources (Schlotz & Schulz, 2004). Schlotz and Schulz
propose that this interaction creates stress if personal control over the interaction is lost or
threatened, such as if the interaction lasts too long, is characterized by a high degree of
responsibility, is unsuccessful, is aversive, conflict-laden, is under occupational and

social success pressure, is missing or too short, or if the person is overextended. These 9
categories result in 9 different chronic, or prolonged, stress types: work overload, social
overload, lack of social recognition, work discontent, social tension, performance
pressure at work, performance pressure in social interactions, social isolation, and
overextended at work (Schlotz & Schulz, 2004). These 9 categories represent a way to
measure chronic stress experiences for a variety of populations, including the sample of
university students observed in this study.
It is well established that the hypothalamic-pituitary-adrenocortical (HPA) axis is
essential in mediating stress. The stress response of the HPA axis starts with the release
of corticotrophin-releasing factor (CRF) from the anterior hypothalamus (Seaward,
2013). CRF activates the pituitary gland, which releases adrenocorticotropic hormone
(ACTH) (Seaward, 2013). ACTH is released into the bloodstream to activate the adrenal
cortex, which then releases corticosteroids, such as the glucocorticoid cortisol and the
mineralocorticoid aldosterone (Seaward, 2013). These corticosteroids increase metabolic
function and alter body fluids and blood pressure (Seaward, 2013). The effects of these
hormones, released by the adrenal cortex, are prolonged because these corticosteroids
activate functions that last from minutes to hours (Seaward, 2013). These adrenal stress
hormones also act upon regions of the brain associated with memory, and differentially
impact various memory phases (Smeets, Otgaar, Candel, & Wolf, 2008) The HPA axis
releases neurotransmitters called catecholamines, such as dopamine, norepinephrine, and
epinephrine, that activate areas of the brain such as the amygdala, responsible for
emotional memory (Smeets et al., 2008). Further corticosteroids bind to receptors in the
medial prefrontal cortex and hippocampus, and these areas have proven to be a target site

for the negative feedback effects for glucocorticoids (Diorio, Viau, & Meaney, 1993;
Jacobson & Sapolsky, 1991). Evidence over the past 50 years has linked prolonged
activation of HPA axis, cortisol, and stressors to an increased vulnerability to disease
(Miller et al., 2007). However, there is some contradictory evidence explaining the link
between chronic stress, cortisol, and disease. Some studies indicate increased activation
of the HPA axis, resulting in increased cortisol output, leads to increased disease
susceptibility, while other models postulate that stress-induced declines in cortisol are
responsible for such adverse outcomes (Miller et al., 2007; Sternberg, 1991; Yehuda,
Golier, & Kaufman, 2005). Miller, Chen, and Zhou’s meta-analysis of chronic stress and
the HPA axis in humans shows that variability in the HPA axis response is mediated by
stressor and person features. Therefore, HPA activity is mediated by a person’s subjective
response to stress, and cortisol release increases with the extent to which the person
subjectively experiences distress. Hence, it seems that the subjective experience is a key
feature in understanding and predicting the biological consequences of chronic stress.
In addition to physical repercussions, past research have found that stress affects
cognition. Stress hormones are known to act upon regions of the brain that are critical for
memory, such as medial temporal lobe regions such as hippocampus, and amygdala, and
the prefrontal cortex (Bowman, Beck, & Luine, 2003; De Leon et al., 1997; De Quervain
et al., 2003; De Quervain, Roozendaal, & McGaugh, 1998; De Quervain, Roozendaal,
Nitsch, McGaugh, & Hock, 2000; Kuhlmann & Wolf, 2006; Lupien et al., 1997; Oei et
al., 2007; Smeets et al., 2008). Furthermore, stress hormones lead to neurochemical,
behavioral/functional, and structural changes in these brain regions (Smeets et al., 2008;
Bowman, Beck, & Luine, 2002). These hormones differentially impact memory,

depending on the memory phase. More specifically, evidence show that stress negatively
affects memory retrieval for items learned before stress exposure due to increasing the
levels of stress-induced cortisol (De Quervain et al., 1998; De Quervain et al., 2000;
Lupien et al., 1997). Tests reveal that cortisol impairs memory retrieval by reducing
blood flow to the memory-critical hippocampus and medial temporal lobe, and
decreasing activation in memory centers such as the hippocampus and prefrontal cortex,
during memory retrieval (De Leon et al., 1997; De Quervain et al., 2003; Oei et al.,
2007). On the other hand, glucocorticoids have also been shown to enhance memory
consolidation, especially, particularly when released in response to an acutely stressful
learning experience (Kuhlmann & Wolf, 2006). The beneficial effects of cortisol on
consolidation are enhanced when encoding emotionally arousing stimuli, by facilitating a
stronger amygdala response in related brain centers (Kuhlmann & Wolf, 2006; van
Stegeren et al., 2007). Taken together, this plethora of evidence supports the association
between stress and memory.
Long term exposure to increased levels of corticosteroids, resulting from chronic
stress, seems to have harmful effects on brain structure and function, such as decreased
neural plasticity and neural atrophy in the hippocampus and prefrontal cortex, and
decreased hippocampal volume in humans. Studies have also shown that increased
exposure chronic stress leads to neuronal loss in the hippocampus. For example, adult
male rats who were injected with corticosterone (CORT) for 21 days show decreased
numbers of apical dendritic branch points and decreased total apical dendritic length in
CA3 pyramidal cells in the hippocampus (Watanabe, Gould, & McEwen, 1992; Woolley,
Gould, & McEwen, 1990). These changes in CA3 pyramidal cells suggest early stages of

hippocampal degeneration, resulting in neuronal loss (Watanabe et al., 1992; Woolley et
al., 1990). Furthermore, prolonged exposure to CORT accelerates the process of cell loss
in the hippocampus (Sapolsky, Krey, & McEwen, 1985). Animals treated with CORT for
three months were similar to aged rats: both revealed depletions of CORT receptors in the
hippocampus, due in part to the loss of CORT-concentrating cells, especially in the CA3
region, and both groups lost neurons the same size in the hippocampus (Sapolsky et al.,
1985). Chronic stress also suppresses neurogenesis of dentate gyrus granule neurons
various lab animals, leading to decreased dentate gyrus volume of up to 30% in animals
such as tree shrews (McEwen, 1999). Together, these structural changes in the
hippocampus inhibit neural firing and decrease plasticity, as well as accelerate the aging
process (McEwen, 1999; Sapolsky et al., 1985; Sauro, Jorgensen, & Pedlow, 2003).
Furthermore, glucocorticoid-induced damage in the hippocampus causes a decline in its
ability to inhibit pituitary adrenal activity by impairing the “turn off” for glucocorticoid
secretion in the brain’s feedback mechanisms, leading to higher amounts of
glucocorticoids, and increased amounts of damage, through a “cascade” effect (McEwen,
1992). Finally, research has shown that stress-induced atrophy and cell death from stress-
vulnerable neurons in the prefrontal cortex compromised neural plasticity by
destabilizing proteins involved in organizing the neuronal skeleton and translating
neurotropic signals in the prefrontal cortex (Cook & Wellman, 2004; Kuipers, Trentani,
Den Boer, & Ter Horst, 2003). This abundance of research illustrates the deleterious
effects of long term exposure to corticosteroids, induced by chronic stress, on the brain’s
structures and functions.

Research exploring cognitive performances following long-term exposure to
glucocorticoids, or chronic stress, also indicates an effect on memory. Chronically
stressed rodents have repeatedly demonstrated impairments in visual and spatial memory
tasks as a result of chronic exposure to glucocorticoids (Beck & Luine, 1999; Bowman et
al., 2003; Luine, Villegas, Martinez, & McEwen, 1994). Furthermore, these animal
studies demonstrated that chronic exposure to stress hormones impairs memory by
facilitating neural atrophy and neural loss, as well as by decreasing dendritic branches
and length and decreasing neural plasticity in the hippocampus and prefrontal cortex
(Beck & Luine, 1999; Bowman et al., 2003; Cook & Wellman, 2004; Kuipers et al.,
2003; Luine et al., 1994; Pavlides, Nivón, & McEwen, 2002) These changes mirror
alterations that occur in the brain during aging, and can be reversed when chronic stress is
alleviated (Luine et al., 1994). Similarly, human literature, which has primarily examined
conditions with cortisol deregulation, such as depression, post-traumatic stress disorder,
and Cushing’s syndrome, associate chronic stress with declines in memory performance.
An association with reduced hippocampal volume, memory dysfunction, and increased
levels of cortisol has been observed among patients with hypercortisolemia, due to
Cushing syndrome (Starkman, Gebarski, Berent, & Schteingart, 1992) These patients
showed reduced hippocampal volume and lower scores on verbal paired learning
associate and verbal recall memory tests from the Wechsler Memory Scale (Starkman et
al., 1992). Additional studies have shown that, and cortisol levels declined to normal
concentrations, the hippocampus increased in volume and participants showed a
functional improvement in memory performance (van Stegeren, 2009). Furthermore,
multiple studies observed the effects chronic stress related to psychopathology, such as

patients with major depressive disorder or PTSD, on memory, because both disorders are
characterized by disturbances in the HPA-axis, and thus cortisol deregulation ((van
Stegeren, 2009; Vythilingam et al., 2004). A recent study by Yehuda and colleagues
revealed that Veterans with PTSD indicated poorer performance on the Wechsler Logical
Memory test and Digit Span test compared to veterans without PTSD. Another study
investigating memory performance among patients with major depressive disorder found
that patients had significantly greater deficits in delayed memory and percent retention on
the verbal section of the Wechsler Memory scale, and that these impairments improved
significantly with successful treatment of antidepressants, hence normal regulation of
cortisol and the HPA-axis. (Yehuda et al., 2007) Finally, a few studies have shown that
chronic stress is associated with memory deficits in nonclinical populations, through
disturbances in the HPA-axis and glucocorticoid regulation (Sauro et al., 2003) Despite
the plethora of research on chronic stress and memory, relevant studies with humans are
extremely rare, especially among healthy populations. Furthermore, There is yet to be
research assessing human’s performance recognition memory performance in relation to
their chronic stress levels.
In this project, I will explore effects of chronic stress on recognition memory
performance of university students, a population that is both cognitively fit and. Because
of the academic environment, this population is prone to be exposed to regular and
chronic stress. In accordance with previous research, I hypothesize that students with
higher levels chronic stress will perform more poorly on memory tasks.

Materials and Methods
Subjects
University students aged 18 to 23 years were recruited through posting on a
university psychology participants’ website. There were no exclusion criteria. The study
was reviewed and approved by Douglas Mental Health Institute Ethic Board and
informed written consent was obtained from each subject before participation.
Procedure
The subject was introduced to the testing room and provided with information
regarding the study. After providing informed written consent for their participation in
the study, they were placed in front of a 17” Macintosh Laptop to began the first half
(encoding) of a two parts computerized task assessing recognition memory. In a five
minutes break between the two parts of the task, the participant completed the Montreal
Cognitive Assessment (MoCA), a chronic stress assessment, and an acute stress
assessment. Then, the participant completed the second half (recognition) of the
computer task. Before leaving the laboratory, the participant was given a debriefing form
to provide more information on the study.
Chronic and present stress assessment
Chronic Stress levels were assessed with an English translation of the short version of the
Trier Inventory for the Assessment of Chronic stress (TIC-S). This questionnaire has
been shown to have a good reliability and validity coefficients. The TIC-S is a 30 item
self-report scale for the assessment of chronic stress. Subjects were requested to assess on
a 5 point rating scale how frequently they experienced specific stressful situations during
the past three months. It consists of 10 scales: work overload, social overload,

overextension at work, lack of social recognition, work discontent, social tension,
performance pressure at work, performance pressure in social interactions, social
isolation, and worry propensity. Worry propensity was added to the most recent version
of the TIC-S to control for the accuracy of retrospective self-report, as the creators of the
TIC-S have observed people who are more worry-prone as a reaction to events are more
likely perceive past events as more aversive, intense, and lasting a longer period of time
(Schlotz & Schulz, 2004). Finally, a composite score of chronic stress was computed for
each participating by adding the scores from all 10 scales. To look at the influence of
performance anxiety on recognition memory, we also assessed subjects’ subjective level
of stress during the assessment. More specifically, subjects were asked to indicate their
current stress level on a 10- point visual analogue scale with 1 being very low and 10
being extremely high.
Memory assessment
Stimuli. 68 neutral black-and-white neutral faces were taken from Kennedy, Hope
and Raz et al. (2009) were used in this experiment. These were divided into 3 lists of 22
items and the remaining stimuli were used as practice items. 2 of these lists were used in
the encoding phase while the other one was used as a distractor list in the recognition
procedure. Each list was equalized for picture quality, ethnicity, familiarity, age, sex and
memorability.
Encoding. Participants were instructed to memorize faces presented on a
Macintosh laptop using the software program SuperCard 4.7 (copyright 2012 by
Solutions Etcetera, CA, USA). The encoding was performed in 2 blocks of 22 faces each.
The order of blocks was counterbalanced between subjects. For each of the 2 blocks

participants were instructed to answer a question to favor a deep encoding of the stimuli.
During the first block, participants were asked to indicate whether they found the face
friendly or not by pressing on a “Yes” or “No” button on the screen, using a computer
mouse. During the second block, participants were prompt to indicate if the faces look
upset or not, again by pressing on a “Yes” or “No” button on the screen. Faces were
shown for 4 seconds and followed by an inter-stimulus interval of 500-milliseconds.
Recognition. The recognition took place 5 minutes after the encoding phase.
During the interval, participants were asked to complete the MoCA, a simple
questionnaire assessing general cognitive abilities (orientation, verbal fluency,
naming…). At the time of the recognition, subjects were first presented with standard
instructions related to the forthcoming recognition procedure. The recognition was self-
paced. Stimuli were presented one at a time on the center of the screen. Subjects were
then instructed to indicate whether the stimulus was new or old, by pressing a “Yes” or
“No” button on the screen. Each trial was followed by a 500-millisecond interval. To
ensure participants’ comprehension of the recognition procedure, they were asked to
complete 4 practice trials. 2 of the trials consisted of items presented in the encoding, and
the two others were distractors.

Figure 1: Recognition Memory Task Design
Statistical Analysis
Recognition memory was characterized by measuring the recognition accuracy of
participants during the recognition memory assessment. The recognition accuracy was
computed by subtracting the proportion of false alarms from the proportion of hits.
Finally, Pearson correlations were calculated to describe possible associations between
stress and recognition memory performance.
Results
1. Demographic Statistics
The sample population included 30 university students. The age range of the
sample was 18-23, with a median of 20. The mean age of the sample was 20.19 and a
standard deviation of 1.50. There were 26 females and 4 males in the sample.
2. Recognition memory task performance
The participants’ average for hits on the memory task was 32.10 (standard deviation,
4.35), and the participants had an average of 2.87 (standard deviation 2.06) for false
alarms on the recognition memory task. The participants had a recognition accuracy of
design
Standard encoding trial:
ISI: 500msec
4000msec
4000msec
1st
Encoding
Block
2nd
Encoding
Block
ISI: 500msec
5 mins interval
Ques onnaires
Recogni on
Procedure:
OLD/NEW?
ISI: 500msec
Standard recogni on trial:

0.60 on the recognition memory performance task, with a standard deviation of 0.14.
Refer to Figure 2 for recognition memory task performance
Figure 2: Recognition Memory Performance
3. Stress assessment
For stress scores, the participants rated their present stress levels to be 5.36 on
average (standard deviation, 2.36)) and their cumulative chronic stress scores to be an
average of 47 (standard deviation 10.99). For the Trier Inventory of Chronic Stress
subscales, participants scored an average of 6.97 (standard deviation, 1.73) for work
overload, an average of 4.00 (standard deviation 1.68) for social overload, an average of
3.8 (standard deviation 1.97) for overextended at work, an average of 3.93 (standard
deviation, 1.98) for work discontent, an average of 3.10 (standard deviation, 1.68) for
social tension, an average of 5.89 (standard deviation, 2.01) for performance pressure at
work, an average of 5.23 (standard deviation, 2.04) for performance pressure in social
interactions, an average of 4.60 (standard deviation, 2.40) for social isolation, and an
average of 6.77 (standard deviation 2.40) for worry propensity. Figure 3 illustrates the
chronic stress ratings for the nine subscales on the Trier Inventory for Chronic Stress.

Figure 3. Chronic Stress ratings for the 9 TIC-S Subscales.
3. Correlation analysis
Overall, correlational analyses revealed no significant association between stress and
recognition memory. There was no significant correlation between recognition accuracy
and total chronic stress score (r = -.023, p≥.05, see figure 4), and recognition accuracy
and present stress level (r=.125, p ≥ .05, see figure 5). Further assessment on correlations
between accuracy and subscales of chronic stress also did not lead to significant
correlations (accuracy vs. social overload (r=.16, p ≥.05), accuracy vs. lack of social
recognition (r = -.144, p ≥.05), accuracy vs. work discontent (r=-.155, p ≥.05), accuracy
vs. social tension (r= -.012, p ≥ .05), accuracy vs. work performance pressure (r= .055, p
≥.78), accuracy vs. social performance pressure (r = -.09, p ≥ 05), accuracy vs. worry
propensity (r= -.120, p ≥ .05).

Figure 4: Correlation Between Cumulative Chronic Stress Scores and Recognition Accuracy
Figure 5: Correlation Between Current Stress Level and Recognition Memory
Conclusion
The present study examined the relationship between chronic stress and
recognition memory performance in healthy university students. It was hypothesized that
higher levels of chronic stress among university students would result in lower
0
0.1
0.2
0.3
0.4
0.5
0.6
0.7
0.8
0.9
0 20 40 60 80 100
RecognitionAccuracy
Cumulative Chronic Stress Scores
Correlation Between Cumulative Chronic Stress Scores
and Recognition Accuracy
0
0.1
0.2
0.3
0.4
0.5
0.6
0.7
0.8
0.9
0 2 4 6 8 10
RecognitionAccuracy
Current Stress Level
CorrelationBetweenCurrent Stress Level and
RecogntionAccuracy

performance ratings on a recognition memory task. This hypothesis is in line with
previous literature that has illustrated the negative of chronic stress on hippocampal and
prefrontal areas of the brain associated memory, subsequently hindering individual
memory performance. However, this study revealed no significant correlations between
chronic stress and recognition memory performance, which differs from previous
research on the topic.
This lack of significant results might have occurred for several reasons. First,
most studies showing that chronic stress exposure leads to negative effects on memory
have been done on clinical populations (McEwen, 1999; van Stegeren, 2009;
Vythilingam et al., 2004; Wolf, 2009; Yehuda et al., 2007). These populations include
patients with Post-Traumatic Stress Syndrome, major depressive disorder, and Cushing
Syndrome. They are unique in that they are under severe chronic stress, with serious and
prolonged disturbance in HPA-axis activity and cortisol deregulation, creating
abnormalities in brain volume, structure, and function, including decreased memory
performance (van Stegeren, 2009; Vythilingam et al., 2004; Wolf, 2009; Yehuda et al.,
2007). This population of young university students, however, was not characterized by
psychopathology or severe HPA disturbance, and therefore might not have been stressed
enough to have the hormonal deregulation that leads to brain dysfunction, and consequent
memory disturbance. These findings reveal that it might be important to distinguish the
neurological effects daily chronic stress from more severe forms of chronic stress seem in
psychopathologies, or even lifetime stress resulting from traumatic life events. The
insignificant correlation between daily chronic stress and recognition memory
performance might imply that the daily chronic stress felt by a healthy, subclinical

population might not be enough to cause brain abnormalities leading to memory
impairment.
Furthermore, this study might not have yielded significant results because the
population might have been too young to show stress-related memory impairments.
Another population proven to have chronic stress-related memory impairment is elderly
individuals. Chronic stress exacerbates age-related declines in cognitive structure and
function, decreasing memory performance in later adulthood - even among healthy
populations. The age range of this test sample was 18-23, with a mean age of 20.19, and a
standard deviation of 1.49. An example of a healthy, elderly population whose memory
was affected by chronic stress had an age range between 71-74 (Head, Singh, & Bugg,
2012). Thus, the results of this study further implicate age as a significant factor in the
negative effect of chronic stress on brain and memory, as the effects of aging on the brain
confound the negative affects of chronic stress. To summarize, it is possible that chronic
stress only leads to memory impairment in vulnerable populations.
There are several limitations to this experiment, with one such limitation being
the small sample number. A greater number of participants would have provided a more
concise assessment on the effects of chronic stress on recognition memory. Further, a
larger sample would be more representative of the population being tested: young,
healthy university students. Because of the recruitment process, we were limited to a
small portion of this population: psychology students who were motivated to participate
in the study to receive course credit. The time allotted for testing, and the singular
method of recruitment thus yielded a biased, limited sample that posed as a limitation to
this study.

Another factor limiting the results of this study is associated with the lack of
motivation and carelessness found in some subject’s performance of the tasks. The scores
of the recognition memory tasks were sometimes lower than expected scores for young,
healthy individuals. Further, some subjects did not respond to all of the questions in their
tasks, such as not always indicating if a face looked friendly or upset in the first part of
the memory assessment, or neglecting to rate their present stress level. Therefore, it can
be inferred that lack of motivation and negligence during participation might have
hindered test scores, and further negatively impacted the results of the study.
Another limitation is the extremely high representation of women in the study.
Testing a mostly female sample might explain the non-significant association between
chronic stress and memory. Studies with both humans and animals have shown that
chronic stress effects on memory are mediated by sex differences (Bowman et al., 2003;
Buchanan & Tranel, 2008; Luine, 2002; Wolf, Schommer, Hellhammer, McEwen, &
Kirschbaum, 2001). These differences include increased memory impairment among
chronically stressed men, but no effect and/or enhancement on memory tasks among
females chronically exposed to stress. In studies with rodents, males stressed for a period
of 21 days were impaired on object recognition and spatial memory performance tasks,
while females stressed for 21 days showed enhanced spatial memory and showed no
effects on object recognition tasks (Bowman et al., 2003; Luine, 2002). Further, human
studies have shown that brain function in response to chronic stress, and consequent
effects on memory are similarly sexually dimorphic. (Buchanan & Tranel, 2008; Wolf et
al., 2001) In a recent experiment, Buchanan and Tranel found that men in the stressed
condition responded worse to neutral stimuli than women in the stress condition. Further,

it was found that stressed women’s recognition performance was enhanced, compared to
women in the control condition (Buchanan & Tranel, 2008). Further, in 2001, a study by
Wolf et al. found that exposure to psychosocial stress did not significantly impair recall
memory, but found a negative association between cortisol increase and memory
performance among men. This finding, however, was not replicated with women. Wolf et
al., and the later studies might provide an explanation for the non-significant results of
this study. Because stress did not seem to affect females in recognition and other memory
tasks in previous studies, it might not be surprising that chronic stress was not associated
memory performance in this primarily-female experiment. Furthermore, having a more
equal number of men and women would have provided a more representative sample of
the effects of stress on recognition memory on a healthy, young adult population. Finally,
having a greater amount of male participants would have allowed for a better assessment
of the mediating effects of sex on chronic stress and memory
Another explanation for the insignificant test results might be due to the method
chosen for measuring chronic stress in this study. Several studies yielding a significant
correlation between chronic stress and memory impairment in animals and humans
induce stress in participants as a method of stress assessment. Methods of inducing stress
in participants include causing participants to think about stressful situations before
memory testing, injecting subjects with a stress hormone for several days, or placing rats
in a stressful environment for several days to several weeks. These methods assure the
subject is stressed either before the memory assessment. Studies using these methods
have revealed heighted cortical response was associated with impaired memory,
especially in hippocampus mediated memory function (Kirschbaum, Pirke, &

Hellhammer, 1993; Kirschbaum, Wolf, May, Wippich, & Hellhammer, 1996; John W.
Newcomer, Craft, Hershey, Askins, & Bardgett, 1994; J. W. Newcomer, Selke, Melson,
& et al., 1999). These methods differ greatly from the present study’s method of
assessing chronic stress, in which a chronic stress questionnaire is administered in
between the encoding of stimuli and the recognition memory task. One might argue the
methodology of this study is similar studies done by de Quervain et al., 2001 and Wolf et
al., 2001, in which stress was measured in between encoding and retrieval, and yielded
significant associations between higher levels of stress and poorer memory retrieval.
However, these studies allowed for delayed retrieval of items of at least an hour. In
contrast, this study did not follow a delayed retrieval paradigm, and thus any stress that
might have been induced by the questionnaire might not have influenced the retrieval of
stimuli. Finally, either the encoding, consolidation, or retrieval process can mediate
recognition memory performance. Thus, it is not possible to identity the process
responsible for the performance. This further indicates that placing the chronic stress
questionnaire before retrieval would affect this specific type of memory.
Finally, another factor contributing to the insignificant results of the study are
problems with self-report bias in the TIC-S. One of the major limitations of the study was
that we relied on subject self-reporting for the assessment of chronic stress. A self
reporting bias, has been shown in the assessment and treatment of psychopathologies like
depression, where individuals often underreport their symptoms on self-report scales such
as the Beck Depression Inventory (BDI) ((Hunt, Auriemma, & Cashaw, 2003). Findings
indicate that due to the self-report bias and underreporting of symptoms, community
samples of depression might not be representative of true rates of depression ((Hunt et al.,

2003). Further, Hunt, Aureimma, and Cashaw found increases in reporting core
symptoms of depression when the BDI-II was disguised in the experiment. The impact of
the self-report bias might be applicable to the present study, where participants were well
aware of the nature and function of the TIC-S and present stress questionnaire. Thus,
participants might have followed previous trends in underreporting of symptoms,
decreasing and confounding true scores of chronic and present stress.
There are several directions one might take in future research on chronic stress
and its impact on recognition memory. These future directions would indeed tackle some
of the weaknesses of the present study, such as the methodology of chronic stress
assessment and the limited sample population. For example, future studies might assess
the effect of self-report bias and underreporting on the Trier Inventory of Chronic Stress.
Further, future experiments might look at other methods of assessing chronic stress in
relation to recognition memory, such as the use of cortisol injection for a prolonged
period before the recognition memory task. In addition, there are future studies that could
assess the relationship between chronic stress and recognition memory with a modified
sample of participants. For example, one might want to replicate the study, but with an
increased number of participants, with an equal male to female ratio. This would not only
paint a clearer picture on the effects of chronic stress on recognition memory, but would
allow one to assess potential sex differences in the effects of chronic stress on recognition
memory. Finally, one might want to perform a similar experiment, but assess a sample of
a chronically stressed population consistently facing circumstances that most would
consider troubling, in comparison to a control population. This experiment would utilize
a different working definition of chronic stress, in which stress can be defined as

circumstances that one considers threatening or exceeding his or her ability to cope
(Lazarus & Folkman, 1984). In this experimental context, one can define chronic as an
eliciting stimulus maintained in the environment for sustained period of time (such as
caring for a sick family member indefinitely), or the extended threat the stimulus poses
on the person if the stimulus itself does not (such as sadness from losing a job) (Baum,
Cohen, & Hall, 1993; Miller et al., 2007). The sample of chronically stressed individuals
might include victims of sexual assault, people who have lost their partners or job,
caregivers of the chronically ill, and soldiers in combat can all be viewed as populations
experiencing chronic forms of stress (Miller, Chen, & Zhou, 2007). This assessment of
chronic stress, and sample population differs from those of the present experiment in that
it is observing a more targeted population undergoing chronic stress, and might provide
further insight into the effects of severe chronic stress on recognition memory when
compared to a control sample that has not had such experience.
In sum, this study proves that there is much more that needs to be investigated
about the relationship between chronic stress and recognition memory. While the present
study showed no significant results between chronic stress and recognition memory
impairment, there are many possible reasons for insignificant results that have been
addressed above. These reasons and limitations show that there is still much that needs to
be researched to further refine and shed more insight on the relationship between chronic
stress and recognition memory.

REFERENCES
Baum, A., Cohen, L., & Hall, M. (1993). Control and intrusive memories as possible
determinants of chronic stress. Psychosomatic Medicine, 55(3), 274-286.
Beck, K. D., & Luine, V. N. (1999). Food deprivation modulates chronic stress effects on
object recognition in male rats: Role of monoamines and amino acids. Brain
Research, 830(1), 56-71.
Bowman, R. E., Beck, K. D., & Luine, V. N. (2003). Chronic stress effects on memory:
sex differences in performance and monoaminergic activity. Hormones and
Behavior, 43(1), 48-59. doi: http://dx.doi.org/10.1016/S0018-506X(02)00022-3
Buchanan, T. W., & Tranel, D. (2008). Stress and emotional memory retrieval: Effects of
sex and cortisol response. Neurobiology of Learning and Memory, 89(2), 134-
141. doi: http://dx.doi.org/10.1016/j.nlm.2007.07.003
Cook, S. C., & Wellman, C. L. (2004). Chronic stress alters dendritic morphology in rat
medial prefrontal cortex. Journal of neurobiology, 60(2), 236-248.
De Leon, M. J., McRae, T., Rusinek, H., Convit, A., De Santi, S., Tarshish, C., . . .
McEwen, B. (1997). Cortisol reduces hippocampal glucose metabolism in normal
elderly, but not in Alzheimer's disease. Journal of Clinical Endocrinology and
Metabolism, 82(10), 3251-3259.
De Quervain, D. J. F., Henke, K., Aerni, A., Treyer, V., McGaugh, J. L., Berthold, T., . . .
Hock, C. (2003). Glucocorticoid-induced impairment of declarative memory
retrieval is associated with reduced blood flow in the medial temporal lobe.
European Journal of Neuroscience, 17(6), 1296-1302.
De Quervain, D. J. F., Roozendaal, B., & McGaugh, J. L. (1998). Stress and
glucocorticoids impair retrieval of long-term spatial memory. Nature, 394(6695),
787-790.
De Quervain, D. J. F., Roozendaal, B., Nitsch, R. M., McGaugh, J. L., & Hock, C.
(2000). Acute cortisone administration impairs retrieval of long-term declarative
memory in humans. Nature Neuroscience, 3(4), 313-314.
Diorio, D., Viau, V., & Meaney, M. J. (1993). The role of the medial prefrontal cortex
(cingulate gyrus) in the regulation of hypothalamic-pituitary-adrenal responses to
stress. The Journal of Neuroscience, 13(9), 3839-3847.
Head, D., Singh, T., & Bugg, J. M. (2012). The moderating role of exercise on stress-
related effects on the hippocampus and memory in later adulthood.
Neuropsychology, 26(2), 133.
Hunt, M., Auriemma, J., & Cashaw, A. C. A. (2003). Self-Report Bias and
Underreporting of Depression on the BDI-II. Journal of Personality Assessment,
80(1), 26-30. doi: 10.1207/S15327752JPA8001_10
Jacobson, L., & Sapolsky, R. (1991). The Role of the Hippocampus in Feedback
Regulation of the Hypothalamic-Pituitary-Adrenocortical Axis. Endocrine
Reviews, 12(2), 118-134. doi: 10.1210/edrv-12-2-118
Kirschbaum, C., Pirke, K. M., & Hellhammer, D. H. (1993). The 'Trier social stress test' -
A tool for investigating psychobiological stress responses in a laboratory setting.
Neuropsychobiology, 28(1-2), 76-81.

Kirschbaum, C., Wolf, O. T., May, M., Wippich, W., & Hellhammer, D. H. (1996).
Stress- and treatment-induced elevations of cortisol levels associated with
impaired declarative memory in healthy adults. Life Sciences, 58(17), 1475-1483.
Kuhlmann, S., & Wolf, O. T. (2006). Arousal and cortisol interact in modulating memory
consolidation in healthy young men. Behavioral Neuroscience, 120(1), 217-223.
doi: 10.1037/0735-7044.120.1.217
Kuipers, S. D., Trentani, A., Den Boer, J. A., & Ter Horst, G. J. (2003). Molecular
correlates of impaired prefrontal plasticity in response to chronic stress. Journal
of Neurochemistry, 85(5), 1312-1323. doi: 10.1046/j.1471-4159.2003.01770.x
Lazarus, R. S., & Folkman, S. (1984). Stress, appraisal, and coping: Springer Publishing
Company.
Luine, V. (2002). Sex Differences in Chronic Stress Effects on Memory in Rats. Stress,
5(3), 205-216. doi: doi:10.1080/1025389021000010549
Luine, V., Villegas, M., Martinez, C., & McEwen, B. S. (1994). Repeated stress causes
reversible impairments of spatial memory performance. Brain Research, 639(1),
167-170. doi: http://dx.doi.org/10.1016/0006-8993(94)91778-7
Lupien, S. J., Gaudreau, S., Tchiteya, B. M., Maheu, F., Sharma, S., Nair, N. P. V., . . .
Meaney, M. J. (1997). Stress-induced declarative memory impairment in healthy
elderly subjects: Relationship to cortisol reactivity. Journal of Clinical
Endocrinology and Metabolism, 82(7), 2070-2075.
McEwen, B. S. (1999). Stress and hippocampal plasticity. Annual Review of
Neuroscience, 22(1), 105-122.
Miller, G. E., Chen, E., & Zhou, E. S. (2007). If it goes up, must it come down? Chronic
stress and the hypothalamic-pituitary-adrenocortical axis in humans.
Psychological Bulletin, 133(1), 25-45. doi: 10.1037/0033-2909.133.1.25
Miller, G. E., & Cohen, S. (2005). Infectious disease and psychoneuroimmunology.
Human psychoneuroimmunology, 219-242.
Monroe, S. M., & Hadjiyannakis, K. (2002). The social environment and depression:
Focusing on severe life stress.
Newcomer, J. W., Craft, S., Hershey, T., Askins, K., & Bardgett, M. E. (1994).
Glucocorticoid-induced impairment in declarative memory performance in adult
humans. The Journal of Neuroscience, 14(4), 2047-2053.
Newcomer, J. W., Selke, G., Melson, A. K., & et al. (1999). DEcreased memory
performance in healthy humans induced by stress-level cortisol treatment.
Archives of General Psychiatry, 56(6), 527-533. doi: 10-1001/pubs.Arch Gen
Psychiatry-ISSN-0003-990x-56-6-yoa8291
Oei, N. Y. L., Elzinga, B. M., Wolf, O. T., de Ruiter, M. B., Damoiseaux, J. S., Kuijer, J.
P. A., . . . Rombouts, S. A. R. B. (2007). Glucocorticoids decrease hippocampal
and prefrontal activation during declarative memory retrieval in young men.
Brain Imaging and Behavior, 1(1-2), 31-41.
Pavlides, C., Nivón, L. G., & McEwen, B. S. (2002). Effects of chronic stress on
hippocampal long-term potentiation. Hippocampus, 12(2), 245-257. doi:
10.1002/hipo.1116
Pereira, D. B., & Penedo, F. J. (2005). Psychoneuroimmunology and chronic viral
infection: HIV infection. Human psychoneuroimmunology, 165-194.

Rozanski, A., Blumenthal, J. A., & Kaplan, J. (1999). Impact of psychological factors on
the pathogenesis of cardiovascular disease and implications for therapy.
Circulation, 99(16), 2192-2217.
Sapolsky, R. M., Krey, L. C., & McEwen, B. S. (1985). Prolonged glucocorticoid
exposure reduces hippocampal neuron number: Implications for aging. Journal of
Neuroscience, 5(5), 1222-1227.
Sauro, M. D., Jorgensen, R. S., & Pedlow, T. (2003). Stress, Glucocorticoids, and
Memory: A Meta-analytic Review. Stress: The International Journal on the
Biology of Stress, 6(4), 235-245. doi: 10.1080/10253890310001616482
Seaward, Brian L. (2013). Physiology of Stress Managing Stress: Principles and
Strategies for Health and Well-Being (Eighth ed., pp. 34-48): John & Bartlett
Publishers.
Smeets, T., Otgaar, H., Candel, I., & Wolf, O. T. (2008). True or false? Memory is
differentially affected by stress-induced cortisol elevations and sympathetic
activity at consolidation and retrieval. Psychoneuroendocrinology, 33(10), 1378-
1386. doi: http://dx.doi.org/10.1016/j.psyneuen.2008.07.009
Smyth, J., Zawadzki, M., & Gerin, W. (2013). Stress and Disease: A Structural and
Functional Analysis. Social and Personality Psychology Compass, 7(4), 217-227.
doi: 10.1111/spc3.12020
Starkman, M. N., Gebarski, S. S., Berent, S., & Schteingart, D. E. (1992). Hippocampal
formation volume, memory dysfunction, and cortisol levels in patients with
Cushing's syndrome. Biological Psychiatry, 32(9), 756-765. doi:
http://dx.doi.org/10.1016/0006-3223(92)90079-F
Sternberg, E. M., Chrousos, G. P., Wilder, R. L., & Gold, P. W. (1992). The stress
response and the regulation of inflammatory disease. Archives of Internal
Medicine, 117, 854–866. (1991). The stress response and the regulation of
inflammatory disease. Archives of Internal Medicine, 117, 13.
van Stegeren, A. H. (2009). Imaging stress effects on memory: A review of neuroimaging
studies. The Canadian Journal of Psychiatry / La Revue canadienne de
psychiatrie, 54(1), 16-27.
van Stegeren, A. H., Wolf, O. T., Everaerd, W., Scheltens, P., Barkhof, F., & Rombouts,
S. A. R. B. (2007). Endogenous cortisol level interacts with noradrenergic
activation in the human amygdala. Neurobiology of Learning and Memory, 87(1),
57-66.
Vythilingam, M., Vermetten, E., Anderson, G. M., Luckenbaugh, D., Anderson, E. R.,
Snow, J., . . . Bremner, J. D. (2004). Hippocampal volume, memory, and cortisol
status in major depressive disorder: effects of treatment. Biological Psychiatry,
56(2), 101-112. doi: http://dx.doi.org/10.1016/j.biopsych.2004.04.002
Watanabe, Y., Gould, E., & McEwen, B. S. (1992). Stress induces atrophy of apical
dendrites of hippocampal CA3 pyramidal neurons. Brain Research, 588(2), 341-
345.
Wolf, O. T. (2009). Stress and memory in humans: Twelve years of progress? Brain
Research, 1293(0), 142-154. doi: http://dx.doi.org/10.1016/j.brainres.2009.04.013
Wolf, O. T., Schommer, N. C., Hellhammer, D. H., McEwen, B. S., & Kirschbaum, C.
(2001). The relationship between stress induced cortisol levels and memory

differs between men and women. Psychoneuroendocrinology, 26(7), 711-720.
doi: http://dx.doi.org/10.1016/S0306-4530(01)00025-7
Woolley, C. S., Gould, E., & McEwen, B. S. (1990). Exposure to excess glucocorticoids
alters dendritic morphology of adult hippocampal pyramidal neurons. Brain
Research, 531(1–2), 225-231. doi: http://dx.doi.org/10.1016/0006-
8993(90)90778-A
Wright, R. J., Rodriguez, M., & Cohen, S. (1998). Review of psychosocial stress and
asthma: an integrated biopsychosocial approach. Thorax, 53(12), 1066-1074.
Yehuda, R., Golier, J. A., & Kaufman, S. (2005). Circadian Rhythm of Salivary Cortisol
in Holocaust Survivors With and Without PTSD. The American Journal of
Psychiatry, 162(5), 998-1000. doi: 10.1176/appi.ajp.162.5.998
Yehuda, R., Golier, J. A., Tischler, L., Harvey, P. D., Newmark, R., Yang, R. K., &
Buchsbaum, M. S. (2007). Hippocampal volume in aging combat veterans with
and without post-traumatic stress disorder: Relation to risk and resilience factors.
Journal of Psychiatric Research, 41(5), 435-445. doi:
http://dx.doi.org/10.1016/j.jpsychires.2005.12.002

Psyc 395 Research Paper

Recommended

Recommended

More Related Content

Viewers also liked

Viewers also liked (15)

Similar to Psyc 395 Research Paper

Similar to Psyc 395 Research Paper (20)

Psyc 395 Research Paper