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Lifetime Stress Exposure and Health: A Review of Contemporary Assessment Methods and Biological Mechanisms


Abstract and Figures

Life stress is a central construct in health research because it is associated with increased risk for a variety of serious mental and physical health problems, including anxiety disorders, depression, cardiovascular disease, autoimmune disorders, Alzheimer's disease, certain cancers, and other diseases of aging. In this review, we examine how lifetime stress exposure contributes to elevated disease risk and explore ongoing measurement and scientific issues related to this topic. To accomplish these goals, we first review existing instruments that have been developed for assessing perceived stress, self-reported life events, interviewer-assessed life stressors, and lifetime stress exposure. Next, we describe laboratory-based tasks that have been used for characterizing individual differences in psychological and biological stress reactivity. These methods have yielded an enormous amount of data showing how life stress influences the activity of the hypothalamic–pituitary–adrenal axis, hypothalamic–pituitary–gonadal axis, sympathetic–adrenal–medullary axis, and immune system, and how such processes can in turn cause allostatic load and biological embedding of the stress effect at the level of the human brain and genome. At the same time, many critical measurement and scientific issues remain unresolved, and we discuss these topics last while describing some pressing issues and opportunities for future research on stress and health.
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Lifetime stress exposure and health:
A review of contemporary assessment methods
and biological mechanisms
Grant S. Shields
|George M. Slavich
Department of Psychology, University of
California, Davis, CA, USA
Cousins Center for Psychoneuroimmunology
and Department of Psychiatry and
Biobehavioral Sciences, University of
California, Los Angeles, CA, USA
George M. Slavich, Cousins Center for
Psychoneuroimmunology, University of
California, Los Angeles, UCLA Medical Plaza
300, Room 3156, Los Angeles,
CA 900957076, USA.
Funding information
Society in ScienceBranco Weiss Fellowship;
Brain and Behavior Research Foundation,
Grant/Award Number: 23958; National
Institutes of Health, Grant/Award Number:
K08 MH103443
Life stress is a central construct in health research because it is
associated with increased risk for a variety of serious mental and
physical health problems, including anxiety disorders, depression,
cardiovascular disease, autoimmune disorders, Alzheimer's disease,
certain cancers, and other diseases of aging. In this review, we
examine how lifetime stress exposure contributes to elevated
disease risk and explore ongoing measurement and scientific issues
related to this topic. To accomplish these goals, we first review
existing instruments that have been developed for assessing
perceived stress, selfreported life events, interviewerassessed life
stressors, and lifetime stress exposure. Next, we describe laboratory
based tasks that have been used for characterizing individual
differences in psychological and biological stress reactivity. These
methods have yielded an enormous amount of data showing how
life stress influences the activity of the hypothalamicpituitary
adrenal axis, hypothalamicpituitarygonadal axis, sympathetic
adrenalmedullary axis, and immune system, and how such
processes can in turn cause allostatic load and biological embedding
of the stress effect at the level of the human brain and genome. At
the same time, many critical measurement and scientific issues
remain unresolved, and we discuss these topics last while describing
some pressing issues and opportunities for future research on stress
and health.
disease, health, life stress, measurement, risk, STRAIN
The concept of stressis ubiquitous in daily life, which is both a blessing and a curse for stress researchers. On the
one hand, stress has long been readily understood as something that negatively affects health (e.g., Rosengren,
DOI: 10.1111/spc3.12335
Soc Personal Psychol Compass. 2017;11:e12335.
© 2017 John Wiley & Sons 1of17
OrthGomér, Wedel, & Wilhelmsen, 1993). On the other hand, the term stresshas been associated with many
different processesincluding both life stress exposure and the psychological and biological consequences of such
exposuresmaking the literature on stress imprecise and complicated. Improving how scientists conceptualize
and assess stress exposure and reactivity has the potential to refine thinking and research on this important topic,
but critical definitional and measurement issues are often overlooked, thus impeding progress.
The goal of this review is to provide an overview of conceptual and measurement issues in contemporary
life stress research, and a summary of the presentday understanding of how stress exposure occurring over
the life course affects health. First, we define stress and its various forms. Second, we describe selfreport
and interviewbased instruments for assessing stress, with an eye toward newer technologies that have enabled
investigators to assess lifetime stress exposure in a more lowcost, nuanced manner. Third, we describe
experimental paradigms that have been developed for characterizing individual differences in acute stress
reactivity in the laboratory. Fourth, we survey the present literature linking stress to poor health outcomes.
Finally, we highlight some pressing measurement and scientific issues, and suggest possible avenues for
future research.
Researchers have proposed that there are several different forms of life stress exposure, with each form having
potentially different consequences for health. In this context, a stressor has been defined as any situation, or set
of external demands, that requires an organism to expend resources to adapt or cope with its circumstances
(Monroe, 2008). Situations that are most likely to be categorized as stressful,in turn, are those that threaten
the self and violate personal expectations, coupled with a perceived lack of coping ability (Lebois, Hertzog,
Slavich, Barrett, & Barsalou, 2016; Slavich & Cole, 2013). Stressors can either be acute life events that occur
and cease relatively quickly, such as a lifethreatening accident or learning of impending companywide layoffs,
or they can occur as chronic difficulties that persist over time, such as caretaking for a terminally ill spouse or
lacking a stable place to live (Brown & Harris, 1978; Slavich, 2016). Although conceptually separate, these forms
of stress are often related. For example, an acute life event, such as the termination of employment, can
sometimes (but not always) initiate a chronic difficulty, such as persistent unemployment or an ensuing financial
difficulty; likewise, a chronic difficulty, such as living in a lowincome neighborhood, can sometimes (but not
always) give rise to specific acute life events, such as witnessing a major crime. Finally, lifetime stress exposure
refers to the total sum of the acute life events and chronic difficulties that a person has experienced over his
or her lifespan.
Intuition tells us that greater lifetime stress exposure is associated with poorer health, and research generally
supports this idea. For example, greater stress exposure has been found to predict the onset or exacerbation of
several mental health problems, such as depression, schizophrenia, and bipolar disorder, as well as several physical
health conditions including cardiovascular disease, autoimmune disorders, and Alzheimer's disease (Bangasser &
Valentino, 2014; Juster, McEwen, & Lupien, 2010; G. E. Miller, Chen, & Parker, 2011; MyinGermeys,
Krabbendam, Delespaul, & Van Os, 2003; Silverman & Sternberg, 2012; Slavich & Irwin, 2014). Greater stress
exposure can also impair cognitive function (Shields, Sazma, & Yonelinas, 2016; Shields, Trainor, Lam, & Yonelinas,
2016)presumably degrading quality of life (Diamond, 2013)and is a strong predictor of earlier mortality
(Rosengren et al., 1993). Multiple models have been proposed to account for these findings, and these models
have been discussed in several excellent reviews (e.g., Doom & Gunnar, 2013; Heim & Binder, 2012; Hostinar
& Gunnar, 2013; Koenig, Walker, Romeo, & Lupien, 2011; McEwen, 1998; Nederhof & Schmidt, 2012). At the
same time, not all individuals are at equal risk for poor health following stress (e.g., due to individual differences
in stress responsivity), making it important to assess both lifetime stress exposure and stress reactivity (Boyce &
Ellis, 2005; Slavich, 2015).
Exposure to life stress has been measured in numerous ways over the years and has included assessing individuals'
overall perceived stress burden, as well as their experience of specific life stressors. Commonly used methods have
included selfreport perceived stress scales (e.g., Cohen, Kamarck, & Mermelstein, 1983; Levenstein et al., 1993),
selfreport life event checklists (e.g., Brugha & Cragg, 1990; Gray, Litz, Hsu, & Lombardo, 2004; Holmes & Rahe,
1967), and investigatorbased life stress interviews (e.g., Brown & Harris, 1978; Hammen et al., 1987). The advantages
and disadvantages of these approaches have been extensively reviewed elsewhere (Cohen, Kessler, & Gordon, 1997;
Dohrenwend, 2006; Monroe, 2008). Therefore, we provide only a summary of the main issues here and in Table 1,
followed by a discussion of the newest methods for assessing lifetime stress exposure.
3.1 |Selfreport measures of perceived stress
Questionnaires assessing perceived life stress, such as the Perceived Stress Scale (Cohen et al., 1983), are among the
most frequently used instruments in stress research because they are very inexpensive and easy to administer. These
questionnaires ask participants a number of different questions that assess perceived stress levels over a given period
of time, such as Over the last month, how often have you felt difficulties were piling up so high that you could not
overcome them?, and the results can be automatically scored if the questionnaire is completed on a computer.
Because of their low cost and ease of use, these scales have been extensively validated against many different
healthrelated outcomes, including physical and mental health complaints, brain structure and function, and biological
aging (Cohen et al., 1983; Epel et al., 2004; Gianaros et al., 2007).
TABLE 1 Comparison of existing instruments for assessing life stress
Instrument Advantages Disadvantages
SelfReport Perceived
Stress Scales
Quick and easy to use
Only moderate correspondence with
actual stress exposure
Correlate strongly with personality
One main outcome variable
Very limited stress assessment timeframe
(e.g., past month)
SelfReport Life Event
Checklist Measures
Inexpensive Suffer from intracategory variability problem
Quick and easy to use Only one to two outcome variables
Scalable Very limited stress assessment timeframe
(e.g., past month)
Interviewing Systems
Extensively validated; considered the
gold standard of stress assessment
Very expensive
Extremely resource intensive
Require extensive training for interviewer(s)
and rater(s)
Not scalable
Limited stress assessment timeframe
(e.g., past 12 years)
Thorough stress assessment with
numerous outcome variables
Independent, investigatorbased
stress exposure ratings
Ability to examine stress exposure by
different life domains and stressor
Automated Lifetime Stress
Assessment Systems
Inexpensive Limited validation data to date
Current absence of independent stress
exposure ratings
Quick and easy to use
Thorough stress assessment with
numerous outcome variables
Ability to examine stress exposure
by different life domains and
stressor characteristics
Assesses stress exposure across the
entire life course
Ironically, the main purpose of these measures (i.e., to assess perceived stress) is also frequently described as one
of their main limitations (Monroe, 2008). The primary concern here is that if peoples' perceptions of stress are entirely
selfgenerated, then these perceptions may lack objectivity or be only weakly related to the actual stressors that have
occurred in peoples' lives. Consistent with this critique is the finding that certain personality traits, such as neuroticism
and selfefficacy, are strongly correlated with perceived stress levels (Ebstrup, Eplov, Pisinger, & Jørgensen, 2011),
meaning that these scores may reflect aspects of personality as much as stress levels. A second limitation of these
measures is that they assess stress over only a relatively short timeframe (e.g., preceding month), even though many
contemporary models of stress and health hypothesize that stressors occurring across the entire life course are rele-
vant for health (Graham, Christian, & KiecoltGlaser, 2006; Lupien, McEwen, Gunnar, & Heim, 2009; Malat, Jacquez, &
Slavich, in press; McEwen, 1998).
3.2 |Selfreport life event checklist measures
Researchers who aim to catalogue the specific life stressors that individuals have experienced, rather than their overall
perceived stress levels, have most often used selfreport life event checklist measures of stress (Brugha, Bebbington,
Tennant, & Hurry, 1985; Crandall, Preisler, & Aussprung, 1992; Gray et al., 2004; Holmes & Rahe, 1967), given that
these instruments are also inexpensive, are easy to administer, and can be automatically scored. Selfreport
measures of this type ask each participant if a variety of different life events have happened during a given timeframe
(e.g., within the preceding year). Given their ability to detect such life events, these instruments have been found to
predict a wide variety of healthrelated outcomes, including mental health problems and psychiatric diagnoses,
immune system function, diagnosis of autoimmune disorders such as psoriasis, and early mortality (Naldi et al.,
2005; Peng et al., 2012; Risch et al., 2009; Rosengren et al., 1993; Schlesinger & Yodfat, 1991).
As summarized in Table 1, however, selfreport checklist measures also have several limitations. First, similar to
perceived stress scales, selfreport checklist measures of stress typically assess life stress exposure over only a short
timeframe, such as during early childhood or over the previous week or year (cf. Gray et al., 2004). Second, although
individuals are arguably expertson the types of life events they have experienced, individuals differ greatly in how
they interpret life event questions. When asked if someone close to the participant has recently died, for example,
some participants may consider an estranged but once close high school friend as someone close,whereas other
participants may not consider anyone except an immediate family member as close.This issue, which has been called
the intracategory variability problem (Dohrenwend, 2006), can cause substantial measurement error and lead to poor
concurrent validity of these instruments with more probing, investigatorbased measures of life stress exposure
(Monroe, 2008).
3.3 |Investigatorbased life stress interviews
To address these limitations, some researchers have utilized a third method for assessing life stressnamely, investi-
gatorbased life stress interviews, such as the Life Events and Difficulties Schedule (LEDS; Brown & Harris, 1978) and
UCLA Life Stress Interview (Hammen et al., 1987). These systems employ a life stress interviewer, who is trained to
focus on the unique biographical details of the respondent and the objective characteristics of each life stressor that is
reported. In addition, these systems typically employ an independent team of life stress raters, who are trained in the
expert assessment of stress and who consult elaborate rating manuals when categorizing different life stressors and
judging their objective severity.
Because of these features, investigatorbased life stress interviewing systems are presently heralded as the gold
standardmethod for assessing stress exposure (Monroe & Slavich, 2016; Monroe, Slavich, & Georgiades, 2014).
Nevertheless, these systems also have some limitations that are not frequently discussed. First, they require highly
trained interviewers and raters, who must follow relatively complicated rules for obtaining and rating life stressor
information. Investigatorbased systems are thus very costly in terms of both money and time. Administering the
LEDS, for example, can take up to 6 hr per participant (i.e., 2 hr to complete the interview, 1 hr to create the summary
report, 2 hr to rate the case, and 1 hr to enter and crosscheck the data), meaning that these systems are used only by
the few investigators worldwide who have the time and resources that are needed to employ such an elaborate
instrument. Second, although these systems yield veryhighresolution stress data, the timeframe covered is
extremely short (i.e., 12 years maximum). Therefore, the life stressors captured may be relevant for understanding
the development of some specific health outcomes, such as onset of a major depressive episode, but these data
are generally not useful for predicting the development of disease states that evolve more slowly over the life course,
such as the metabolic syndrome, cardiovascular disease, cancer, and Alzheimer's disease.
3.4 |Automated systems for assessing lifetime stress exposure
Most recently, the limitations associated with each of the methods described above have provided the impetus for
developing new methods for assessing life stress exposure that combine the depth and sophistication of a life stress
interview with the simplicity of a selfreport instrument. These automated life stress interviews are internetor com-
puterbased instruments that utilize branching logic to prompt the same types of followup questions that an expert
life stress interviewer would typically ask in order to ascertain exactly what happened to the respondent (e.g., When
did the stressor occur? How many times did you experience that stressor? How long did the stressor last? How much
did the stressor interfere with your goals, plans, or aspirations for the future?). Similar to investigatorbased systems,
therefore, these automated systems provide information that is critical for fully characterizing an individual's lifetime
stress exposure, but they do so in a much more costeffective and scalable manner. Likewise, these systems have the
benefit of being easy to administer and score, just like selfreport checklist measures of life stress, but they yield
information that is much more nuanced and informative than what selfreport checklists can produce.
To date, the only automated system that easily assesses stress exposure occurring across the entire life course is
the Stress and Adversity Inventory (STRAIN). The current version of the STRAIN enquires about 55 different
stressors, including 26 acute life events and 29 chronic difficulties, that are known to impact health (see http:// These stressors cover all of the major life domains that are important for functioning, including
health, intimate relationships, friendships, education, work, finances, housing, living conditions, and crime. They
also cover several core socialpsychological characteristics that may have differential effects on lifespan health
specifically, interpersonal loss, physical danger, humiliation, entrapment, and role change or disruption. The STRAIN
is available in English, Spanish, Italian, German, Swiss (High) German, and Brazilian Portuguese, and investigators
can choose between two different interviewing platforms depending on whether they need to assess lifetime stress
exposure in adolescents (i.e., Adolescent STRAIN) or adults (i.e., Adult STRAIN).
One important feature of the STRAIN is its ability to predict not just selfreported health outcomes that could be
influenced by reporting biases, such as selfreported anxietyor depressive symptoms, but a wide varietyof psychological,
biological, and clinical outcomes. To date, these outcomes include memory (Goldfarb, Shields, Daw, Slavich, & Phelps,
2017), diurnal cortisol levels (Cuneo et al., in press), biological reactivity to acute stress (Lam, Shields, Trainor, Slavich, &
Yonelinas, 2017), metabolic function (Kurtzman et al., 2012), cancerrelated depression and fatigue (Bower, Crosswell,
& Slavich, 2014; Dooley, Slavich, Moreno, & Bower, 2017), physical and mental health problems (Shields, Moons, &
Slavich, 2017; Toussaint, Shields, Dorn, & Slavich, 2016), and likelihood of being diagnosed with a stressrelated illness
or autoimmune disorder (Slavich & Shields, in press; see also Slavich & Toussaint, 2014). Moreover, when compared to
other stress assessment instruments that are commonly used, such as selfreport measures of perceivedstress and stress-
ful life events, the STRAIN has emerged as a stronger predictor of respondent health (Slavich & Shields, in press).
As these technologies continue to improve and investigators come to appreciate the power of automated
interviewing platforms, we believe that use of simple paperandpencil selfreport measures of life stress and more
timeconsuming investigatorbased systems will give way to sophisticated online interviewing platforms like the
STRAIN, which enable investigators to acquire lifetime stress exposure information in a more costefficient, reliable,
and scalable manner. Ultimately, these platforms are not a substitute for intensive investigatorbased systems like
the LEDS, but they do cover the entire life course, which is something that even the prevailing gold standard systems
cannot accomplish. Looking forward, then, the adoption of such systems will be important for conducting empirical
tests of existing theoretical models that aim to explain how stressors occurring across the entire life course
accumulate to impact human health and wellbeing.
The foregoing review summarizes methods that have been employed for assessing life stress exposure as a means of
better understanding who is at risk for poor health. It is well known, however, that stress does not impact everyone
equally (Boyce & Ellis, 2005; Monroe et al., 2014; Slavich & Cole, 2013), which means that it is also important to
characterize individual differences in stress reactivity that could explain why some individuals become ill following
stress while others do not. To accomplish this, investigators have utilized different methods for inducing acute stress
in the laboratory, where environmental conditions can be carefully controlled and psychological and biological
outcomes can be closely measured. The characteristics of the three most commonly used methods for inducing stress
in the laboratory (Shields, Sazma, McCullough, & Yonelinas, 2017) are summarized in Table 2.
4.1 |Trier Social Stress Test
The gold standard task for inducing acute stress in the laboratory is the Trier Social Stress Test (TSST), which was
developed in the early 1990s (Kirschbaum, Pirke, & Hellhammer, 1993). In the stress portion of this task, a participant
is taken to a laboratory room and told that he or she will give an upcoming speech in front of a panel of evaluators and
a video camera. He or she is then given a brief period of time (usually 510 min) to prepare a speech on his or her
qualifications for an important job (e.g., administrative assistant at his or her school). The participant is further told that
the evaluators are trained in monitoring nonverbal behavior and that a video analysis of their speech will be conducted
after the session. In reality, the evaluators are research assistants who are trained to say only scripted lines and give no
verbal or nonverbal signs of approval.
After the brief preparation phase, the participant is brought into the testing room for the speech task. The speech
task lasts 5 min, and if a participant stops talking prior to the end of the 5 min, the evaluators prompt the participant to
continue. After this task is finished, participants are given a difficult mental arithmetic task in front of the evaluators. In
the arithmetic task, participants are told to verbally subtract 13 from 1,022 as quickly and accurately as possible. The
evaluators are further instructed to tell the participant to restart at 1,022 every time he or she makes a mistake. After
5 min, the arithmetic task is finished and the participant is brought back to the preparation room.
This version of the TSST has been used in numerous studies and produces a relatively reliable and robust psycho-
logical and biological response that varies in magnitude across people (Allen, Kennedy, Cryan, Dinan, & Clarke, 2014;
Dickerson & Kemeny, 2004; Kirschbaum et al., 1993; Shields, Sazma, et al., 2017). In addition, a group version of the
TSST has also been developed (von Dawans, Kirschbaum, & Heinrichs, 2011). The reliably strong effect that the TSST
has on markers of stress reactivity is arguably its biggest advantage. Its biggest limitation, in contrast, involves the fact
that the TSST is very resource intensive. For example, it requires three trained evaluators and an experimenter to be
present for every participant, which means either that data collection proceeds slowly or that several people in the
laboratory must be devoted to running multiple TSST sessions every day or week.
TABLE 2 Comparison of existing laboratorybased psychosocial stress tasks
Construct validity Ease of use Ecological validity
Trier Social Stress Test High Low High
Cold pressor test High High Low
Socially evaluated cold pressor test High Moderate Moderate
4.2 |Cold pressor test
Another very common acute stress manipulation is the cold pressor test (CPT), which has been used in laboratory
settings for nearly 100 years (Hines & Brown, 1932). However, only recently has it gained traction as a way to induce
acute stress (e.g., Cahill, Gorski, & Le, 2003; Felmingham, Tran, Fong, & Bryant, 2012; Gluck, Geliebter, Hung, & Yahav,
2004). In this task, a participant is told to submerse his or her nondominant hand up to the wrist joint in either nearly
freezing water (usually 03 °C) for the stress condition or in lukewarm water for the control condition, both for up to
13 min. Afterward, the participant is instructed to withdraw his or her arm from the water and is then given a towel
to dry off.
The CPT has been validated in numerous stress studies and is the task of choice in certain areas of stress research,
such as examining postencoding stress effects on memory (Shields, Sazma, et al., 2017). The CPT thus has the advan-
tage of being relatively quick, well validated, and easy on resources (e.g., it requires only one experimenter, a bucket of
cold or lukewarm water, and less than 5 min to complete). However, the CPT induces a weaker cortisol response than
theTSST (Shields, Sazma, et al., 2017), and this reduced stress response is a limitation compared to other tasks like the
TSST. Another limitation of the CPT is that it does not include a socioevaluative component, which has been found to
be an important feature of laboratory stressors that reliably induce strong cortisol and inflammatory reactivity
(Dickerson & Kemeny, 2004; Slavich, Way, Eisenberger, & Taylor, 2010).
4.3 |Socially evaluated CPT
To address these limitations of the CPT, some researchers have developed hybrid stressor tasks that incorporate
elements of both the TSST and CPT. One such task, the socially evaluated cold pressor test, incorporates a stern
evaluator and video camera (similar to theTSST), and thus produces a larger biological stress response than the classic
CPT (Schwabe, Haddad, & Schachinger, 2008). Another task called the Maastricht Acute Stress Test requires
participants to alternate between immersing their hand in ice water and performing a TSSTlike arithmetic task while
they are being watched by an evaluator and filmed by a video camera (Smeets et al., 2012). This task thus evokes a
greater stress response than the CPT and one that is on par with the TSST. Considered together, these hybrid tasks
are slightly more resource intensive than the CPT, but they have the advantage of being able to induce a greater stress
response, making them worth the additional resources. In terms of limitations, hybrid stressors are regarded as less
ecologically valid than the TSST because they combine physical and social challenges that are not encountered in
everyday life (e.g., immersing your hand in ice water while being socially evaluated).
Together, methods like those described above for assessing life stress exposure and reactivity have yielded a
tremendous amount of data on biological processes linking stress and health. These pathways have been described
in great detail elsewhere (e.g., Graham et al., 2006; Irwin & Cole, 2011; Lupien et al., 2009; McEwen, 1998; G. Miller,
Chen, & Cole, 2009; Slavich & Cole, 2013; Slavich & Irwin, 2014). In this section, therefore, we summarize only the
most important details presently known about how stress gets represented by the brain and how the brain in turn
regulates peripheral physiologic and immune system processes that affect health.
5.1 |Neural and peripheral mechanisms of the stress response
In response to a stressor, the brain is thought to initiate a complex cascade of events that culminate in what is generally
referred to as the biological stress response. As described below, at least four major systems are often involved: the
hypothalamicpituitaryadrenal (HPA) axis, hypothalamicpituitarygonadal axis, sympatheticadrenalmedullary
(SAM) axis, and immune system (Allen et al., 2014; Lennartsson, Kushnir, Bergquist, Billig, & Jonsdottir, 2012;
Segerstrom & Miller, 2004).
The HPA axis regulates secretion of hormones, such as the glucocorticoid cortisol (Dedovic, Duchesne,
Andrews, Engert, & Pruessner, 2009; Sapolsky, Rivier, Yamamoto, Plotsky, & Vale, 1987; Sapolsky, Romero, &
Munck, 2000). Under stress, activity within parts of the brain that are involved in processing socialenvironmental
experiences, such as the dorsal anterior cingulate cortex and amygdala, signal to the hypothalamus (Dedovic et al.,
2009), and activity in the paraventricular nucleus of the hypothalamus in turn results in the secretion of a
corticotropinreleasing hormone (Lovallo & Thomas, 2000; Sawchenko, Li, & Ericsson, 2000). The corticotropin
releasing hormone then stimulates the pituitary to release an adrenocorticotropic hormone (Lovallo & Thomas,
2000; Sawchenko et al., 2000). Once released, the adrenocorticotropic hormone enters the bloodstream and travels
to the adrenal glands, where it stimulates the adrenals to produce and release cortisol into the bloodstream
(Sapolsky et al., 2000).
Activation of the hypothalamicpituitarygonadal axis is similar to that of the HPA axis in that it starts with the
hypothalamus, which secretes a gonadotropinreleasing hormone (Millar et al., 2004). The gonadotropinreleasing
hormone then triggers the pituitary gland to produce a luteinizing hormone and folliclestimulating hormone (Meethal
& Atwood, 2005; Millar et al., 2004). These hormones then act on the gonads to upregulate production of sex
hormones such as testosterone and estrogen, which are released into the bloodstream (Meethal & Atwood, 2005).
Activation of the SAM axis, in turn, begins with neural activity in the locus coeruleus and other regions of the
brainstem stimulating the sympathetic nervous system, which innervates the adrenal medulla (Allen et al., 2014;
Sabban & Kvetňanský, 2001). The adrenal medulla then upregulates production of norepinephrine and epinephrine,
and releases them into the bloodstream.
Finally, the immune system is believed to be activated during stress largely by the SAM axis. An end product of
SAM axis activation, norepinephrine, circulates in the body and acts on immune cell receptors to upregulate the
activity of transcription factor nuclear factorκB (Bierhaus et al., 2003). Through a complex series of intracellular
events, nuclear factorκB activation in turn promotes the synthesis of proinflammatory cytokines, which are then
released into circulation. This is not the only way that stress influences the immune system (Silverman & Sternberg,
2012), since cortisol is also a strong regulator of inflammatory activity (Slavich & Irwin, 2014), but it represents a
primary pathway through which stress affects immunity and health.
The systems described above are not the only ones affected by stress. For example, stress also influences, and
may be modulated by, the opioid system, and may impair some cognitive functions through these effects (Laredo
et al., 2015; Slavich, Tartter, Brennan, & Hammen, 2014). Glucocorticoids, sex hormones, sympathetic nervous system
activation, and the immune system all have welldocumented implications for health, though, which is why we focused
on them here.
5.2 |Allostatic load
These stressresponsive systems are intended to promote biological stability during environmental change. For
example, upregulation of norepinephrine and cortisol primes the body to fight or fleefrom a stressor (McEwen &
Sapolsky, 1995), while activation of the immune system facilitates healing should an injury or infection occur as a
result of the stressor or associated threat (Dhabhar, 2002). This process of stability through changehas been labeled
allostasis (McEwen, 1998; Sterling & Eyer, 1988), and it is a wellestablished mechanism through which the body deals
with an everchanging, and sometimes threatening, environment.
Over time and with repeated activation, however, the functionality of these stressresponsive systems can
change and produce biological wear and tear,or allostatic load, that affects health (Juster et al., 2010; McEwen,
1998, 2005, 2007). For example, greater life stress exposure has been associated with reduced HPA axis responses
to acute stress (Carpenter et al., 2007), chronic lowgrade inflammatory activity (Slavich & Irwin, 2014), and an
inability for cortisol to properly regulate inflammatory activity (Cohen et al., 2012; Silverman & Sternberg, 2012).
Moreover, these changes have been directly implicated in the development of disease (Cohen et al., 2012; Silverman
& Sternberg, 2012; Slavich & Irwin, 2014).
One interpretation of the above data suggests that these physiological changes are adaptive for dealing with a
chronically unstable environment. This interpretation is similar to the matchmismatch hypothesis, which argues that
stress leads to negative health outcomes when an early environment is either more or less stressful than a later
environment (Nederhof & Schmidt, 2012; Santarelli et al., 2014; Zalosnik, Pollano, Trujillo, Suárez, & Durando,
2014). Consistent with this formulation, both the brain and the immune system calibrate to the environment and
are predictive systems that attempt to anticipate future challenges and threats (Chiel & Beer, 1997; Dhabhar,
2002; Schultz, Dayan, & Montague, 1997). As a result of these dynamics, the immune system can respond to bodily
damage or infection relatively quickly, and sometimes before actual physical or biological damage has occurred
(Dhabhar, 2002).
5.3 |Consequences of lifetime stress exposure and allostatic load
Adapting to conditions of environmental uncertainty is biologically beneficial but also has physiological costs that can
degrade health over the long term. In particular, by adapting to repeated elevations of glucocorticoids, certain cells in
the body, such as immune system cells, become insensitive to glucocorticoids, which has been called glucocorticoid
resistance (Cohen et al., 2012; A. H. Miller, Pariante, & Pearce, 1999; Pariante, 1999; Silverman & Sternberg, 2012;
Wang, Wu, & Miller, 2004). Because glucocorticoids are primary regulators of inflammatory activity (Auphan,
DiDonato, Rosette, Helmberg, & Karin, 1995; Silverman & Sternberg, 2012), glucocorticoid resistance disinhibits
the release of inflammatory proteins from immune cells, leading to chronic, lowgrade inflammation (Cohen et al.,
2012; A. H. Miller et al., 1999; Silverman & Sternberg, 2012; Slavich & Irwin, 2014). This chronic, lowgrade inflamma-
tory state is in turn believed to promote the development or exacerbation of multiple diseases, including autoimmune
disorders (such as rheumatoid arthritis), Alzheimer's disease, cardiovascular disease, and depression (Akiyama et al.,
2000; CouzinFrankel, 2010; Feigenson, Kusnecov, & Silverstein, 2014; Libby, 2002; Ridker, Cushman, Stampfer,
Tracy, & Hennekens, 1997; Silverman & Sternberg, 2012; Slavich & Irwin, 2014).
5.4 |Biological embedding of life stress
The above consequences of greater lifetime stress exposure and allostatic load are due in part to the fact that lifetime
stress exposure can become embedded on a neural and genomic level. For example, stress can induce lasting changes
in catecholaminergic and cholinergic function in the brain (Sabban & Kvetňanský, 2001; Soreq, Kaufer, Friedman, &
Seidman, 1998). Stress occurring over the lifespan can also promote lasting structural changes in the brain, especially
in regions such as the prefrontal cortex (DiasFerreira et al., 2009; Hinwood, Morandini, Day, & Walker, 2012;
Hinwood et al., 2013) and hippocampus (McEwen, 2007; McEwen & Sapolsky, 1995; Zalosnik et al., 2014), which
underpin cognitive processes that are important for everyday life. Together, these stressrelated neural changes
can alter the functioning of the physiologic stress systems described above, as well as how subsequent life stressors
are perceived and managed.
Lifetime stress exposure can also have sustained effects on health by becoming embedded at the level of the
human genome (Slavich & Cole, 2013). For example, stress is known to upregulate the expression of genes that code
for proinflammatory cytokines and downregulate the expression of genes that code for antiviral cytokines. These
alterations can promote a state of persistently elevated inflammation coupled with an inability to properly fight viral
infections, thus increasing a person's risk for both inflammationrelated disease and viral infection (Slavich & Cole,
2013). Chronic or repeated stress exposure can also lead to persistent alterations in glucocorticoid receptor gene
expression in the brain, including reductions in the expression of hippocampal and cerebellar glucocorticoid receptors
(Kitraki, Karandrea, & Kittas, 1999; Liu et al., 1997). These changes reduce the ability of glucocorticoids to initiate the
negative feedback loop in the hippocampus that reduces the production of glucocorticoids, ultimately leading to a less
controlled glucocorticoid response to stress that can promote inflammation and cause disease (Liu et al., 1997).
Despite the abundance of studies that have been conducted on stress and health, and the continued importance and
public health relevance of this work, a majority of stress studies still employ assessment methods that have critical
limitations. As a result, many important questions remain unanswered. We highlight some of these issues below,
focusing first on existing measurement challenges and then on lingering scientific questions.
6.1 |Measurement issues
One of the greatest ongoing challenges in stress measurement involves the lack of tools for assessing life stress
exposure that are inexpensive, easily scalable, and valid. Most instruments that presently exist for assessing life stress
have inherent tradeoffs between cost and validity. For example, although paperandpencil measures are cheap, their
validity is limited; in contrast, investigatorbased interviewing systems are well validated, but very expensive. Online
systems like the STRAIN have made substantial progress in combining the sophistication of investigatorbased
interviewing systems with the ease of selfreport instruments, but more methodological advancement is needed along
these lines to improve how researchers assess stress.
Second, stress can occur on several different timescales, from momenttomoment stress, to daily, to weekly, to
lifetime stress exposure. However, no measurement system presently exists for assessing stress across multiple time-
scales. As a result, studies frequently assess stress at one timescale (e.g., daily hassles or major life events) but do not
combine this information with other timescales, making an individual's stress profile arguably incomplete. This need
could be addressed by developing tools that assess stress reactivity or exposure on an ongoing basis, but the challenge
here is to create instruments that individuals are willing to use and find noninvasive.
Third, assessing both life stress exposure and stress reactivity is important for characterizing resilience to stress
and for identifying persons at highest risk for poor health. However, current research and measurement strategies
do not typically take both aspects of the stress process into account. Incorporating this measurement goal into future
studies would be an important development methodologically, but this advancement could also yield important new
discoveries on stress, coping, and resilience.
Finally, there is a need to further validate existing computerbased instruments for assessing life stress and to
develop new applications for helping individuals manage stress. With respect to the first goal, it is possible that
automated systems will eclipse paperandpencilbased systems for assessing stress, but to be useful, these systems
need to be validated across all major levels of analysis (e.g., psychological, neural, physiologic, molecular, and genomic)
and across different population groups and cultures. With respect to the second goal, automated systems are
presently being developed to help individuals cope with stresssuch as the acceptance and commitmentbased
smartphone app (Ly, Asplund, & Andersson, 2014) and BeWell smartphone app (Lane et al., 2014)but development
of these tools is still in its infancy, and additional research is needed to examine which tools provide the greatest
stressreducing benefit.
6.2 |Scientific issues
Partly because of these ongoing measurement issues, stress research has yet to address many important scientific
questions that are relevant for public health. For example, why does major life stress precipitate illness in some
individuals and not others? Moreover, what factors determine the type of stressrelated disorder that develops?
These questions have been answered in part (e.g., Elliott, EzraNevo, Regev, NeufeldCohen, & Chen, 2010; Santarelli
et al., 2014; Shansky, 2015; Slavich & Irwin, 2014). Unfortunately, however, this work has not yet produced
translational models that would enable healthcare providers to make predictions in the clinic, which is what would be
most useful for preventing and mitigating stressrelated disease burden.
In addition, there is a pressing need to better understand mechanisms that underlie specific mental and
physical disorders, as well as the cooccurrence of such disorders. Some biological processes, such as inflammation,
that may underlie the development of certain diseases and also represent a common mechanism that increases
risk for poor health in general have recently been described (CouzinFrankel, 2010; Slavich, 2015). However,
inflammation itself does not sufficiently explain why individuals develop certain inflammationrelated health problems
(e.g., cardiovascular disease) versus others (e.g., cancer).
Several other scientific issues are also ripe for investigation. For example, it has been proposed that humans have
sensitive periods during which time stress is particularly impactful (Andersen & Teicher, 2008). However, it remains
unclear when those sensitive periods are and what exact processes would be responsible for enhancing the effects
of stress on health. Second, resilience to stress has been the subject of a great deal of research (Baratta, Rozeske,
& Maier, 2013; Charney, 2004; Dooley et al., 2017; Elliott et al., 2010; Shansky, 2015; van der Werff, van den Berg,
Pannekoek, Elzinga, & van der Wee, 2013), but a complete understanding of the psychological and biological factors
that confer resilience to stress is still unavailable. Finally, psychological and psychopharmacological interventions have
been heralded as having great potential for reducing stress and enhancing human health, but we still do not have
interventions that are costeffective and scalable, and that have been shown to reduce the negative effects that stress
has on healthrelevant psychological, biological, and clinical outcomes.
In summary, lifetime stress exposure refers to the total sum of the acute stressful life events and chronic difficulties
that a person has experienced over his or her lifespan. Theorists have proposed that lifetime stress exposure increases
risk for a variety of mental and physical health problems, including depression, cancer, schizophrenia, Alzheimer's dis-
ease, and autoimmune disorders (Juster et al., 2010; McEwen, 1998; G. E. Miller et al., 2011; Silverman & Sternberg,
2012; Slavich & Cole, 2013; Slavich & Irwin, 2014; Slavich, O'Donovan, Epel, & Kemeny, 2010; Slavich, 2015). To date,
however, only a few studies have actually measured lifetime stress exposure. Indeed, the rest of the vast literature on
stress and health has assessed stress exposure using selfreport checklist measures or investigatorbased interviewing
methods that assess stress over only short periods of time (e.g., past week or year), which is not sufficient for testing
existing theories of lifetime stress exposure and health.
Looking forward, researchers have developed new online systems for assessing stress exposure that combine the
thoroughness of a life stress interview with the ease of administration of a selfreport checklist measure. The only
online system that presently assesses lifetime stress exposure, though, is the STRAIN, and although this system
performs well, it needs to be tested in additional populations and in relation to other psychological, biological, and
clinical outcomes. These methodological advancements will ultimately combine with innovative new tools for reducing
stress to have a substantial impact on human health. However, much more research is needed to develop these
instruments to address the enormous disease burden that is caused by stressrelated health problems worldwide.
Preparation of this article was supported by a Society in ScienceBranco Weiss Fellowship, NARSAD Young
Investigator Grant #23958 from the Brain and Behavior Research Foundation, and National Institutes of Health grant
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Grant S. Shields, M.A., is a Ph.D. candidate in the Department of Psychology at the University of California, Davis.
His research is broadly aimed at understanding the effects of stress on cognition and health, with an interest in
elucidating mechanisms underlying these effects. His work on these topics has been published in Psychological
Bulletin,Perspectives on Psychological Science,Neuroscience & Biobehavioral Reviews,Psychoneuroendocrinology,
and Stress, among others.
George M. Slavich, Ph.D., is a leading expert in the conceptualization, assessment, and management of life stress,
and in psychological and biological mechanisms linking stress with disease. He developed the first online system
for assessing lifetime stress exposure; formulated the first fully integrated, multilevel theory of depression; eluci-
dated the neural mechanisms underlying inflammatory reactivity to social stress; and is helping pioneer a new field
of research, called human social genomics. In addition to these basic research efforts, he is deeply devoted to
teaching and mentoring and to developing groups that promote student development. He has received 17 awards
for these contributions since 2009, the most recent of which include the American Psychosomatic Society
Herbert Weiner Early Career Award, Academy of Behavioral Medicine Research Neal E. Miller New Investigator
Award, and Society for a Science of Clinical Psychology Susan NolenHoeksema Early Career Research Award.
Dr. Slavich completed undergraduate and graduate coursework in psychology and communication at Stanford
University and received his Ph.D. in clinical psychology from the University of Oregon. After graduate school,
he was a clinical psychology intern at McLean Hospital in Boston, Massachusetts, and a clinical fellow in the
Department of Psychiatry at Harvard Medical School. He subsequently completed 3 years of postdoctoral training
in health psychology and psychoneuroimmunology at the University of California, San Francisco, and University of
California, Los Angeles (UCLA). He is presently an associate professor in the Department of Psychiatry and Bio-
behavioral Sciences at UCLA, a Research Scientist at the Cousins Center for Psychoneuroimmunology, Associate
Director of the National Institute on Agingsupported Stress Measurement Network, and Director of the UCLA
Laboratory for Stress Assessment and Research (
How to cite this article: Shields GS, Slavich GM. Lifetime stress exposure and health: A review of contempo-
rary assessment methods and biological mechanisms. Soc Personal Psychol Compass. 2017;11:e12335. https://
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A number of studies have associated financial wealth changes with health‐related outcomes arguing that the effect is due to psychological distress and is immediate. In this paper, I examine this relationship for cumulative shocks to the financial wealth of American retirees using the allostatic load model of pathways from stress to poor health. Wealth shocks are identified from Health and Retirement Study reports of stock ownership along with significant negative discontinuities in high‐frequency S&P500 index data. I find that a one standard deviation increase in cumulative shocks over two years increases the probability of elevated blood pressure by 9.5%, increases waist circumference by 1.2% and the cholesterol ratio by 6.1% for those whose wealth is all in shares. My findings suggest that the combined effect of random shocks to financial wealth over time is salient for health outcomes. This is consistent with the allostatic load model in which repeated activation of stress responses leads to cumulative wear and tear on the body.
... The link between perceived stressors, chronic stress exposure, inflammation, and disease, is widely supported [59,60]. We refer to the common mechanism of inflammation as an underlying component of most disease development/expression, since what critical mass is required for adaptive to maladaptive transition, or why some individuals develop particular inflammationassociated disorders remains a complex dynamic interaction between specific genetic, transcriptional, proteomic, metabolomic, psychosocial, and environmental factors. ...
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... One of the most popular neuropsychological instruments of cognitive flexibility is the Wisconsin card sorting test-WCST (Lange et al., 2017), which assesses executive function (Miles et al., 2021;Sherman, Tan & Hrabok, 2020). The WCST measures a sub-component of the executive function, the ability of set-shifting (Kopp et al., 2020;Lange et al., 2017). ...
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Cognitive flexibility plays a crucial role in psychological health and this research aimed to investigate its assessment. We developed a novel Reversal learning task (RLT) paradigm adding pure reward (+ 100 points, 0) and punishment (− 100 points, 0) conditions to the classic reward–punishment condition (+ 100, − 100); we also analyzed the RLT convergent validity with approach-avoidance questionnaires (BIS-BAS and Approach-Avoidance Temperament questionnaire) and the Wisconsin card sorting test (WCST) scores through a Principal component analysis. In a sample of 374 participants, we found that these three conditions differently assess flexibility and that high RLT reward sensitivity in the punishment condition (0; − 100) is related with high BAS reward responsiveness. Moreover, we found that RLT and WCST flexibility scores, although associated, detect different facets of cognitive flexibility. Finally, in a second sample (N = 172), we explored the impact of stress, moderated by gender, on RLT and WCST. Whereas, WCST was not impacted by these variables, in RLT stressed women showed increased perseverative errors in punishment condition (− 100, 0) and reduced punishment sensitivity in reward condition (+ 100, 0). Overall, our newly developed RLT paradigm and the WCST seem to provide different ways to assess cognitive flexibility and to be differently affected by moderators, such as gender and stress.
Although exposure to acute stress undoubtedly contributes to psychopathology, most individuals do not develop psychopathology following stress exposure. To explain this, scholars have implicated biological, emotional, and cognitive responses to stress, but individual differences in executive control (i.e., top-down control of cognition and behavior) measured in response to stress has only recently emerged as a potential factor contributing to psychopathology. In this review, we introduce a model—the integrated model of stress, executive control, and psychopathology—positing that the impairing effects of acute stress on executive control can contribute to psychopathology. We link to research on biological, emotional, and cognitive processes, all of which can be impacted by executive control, to propose a framework for how poorer executive control under conditions of acute stress can contribute to psychopathology. This integrated model is intended to further our understanding of who is more susceptible to the negative consequences of stress.
The aim was to examine the mental and physical health trajectories of mothers, fathers, and children before and after union dissolution. Register data covering the entire Norwegian population, and including information on consultations with general practitioners in 2006–2018, were used. Constant unobserved characteristics were controlled for with individual fixed effects. As judged by the number of consultations, mothers’ and fathers’ mental health deteriorates before the dissolution but improves immediately afterwards. In contrast, a worsening mental health among children before the dissolution is followed by an even more adverse development afterwards. There is only modest evidence of predissolution increases in noninfectious physical diseases, but more clearly rising numbers afterwards especially for mothers and daughters. Less adverse trends are seen for infections, although mothers experience a sharp temporary increase at the breakup time. On the whole, mothers’ health is more adversely affected by dissolution than that of fathers. Daughters may have a disadvantage compared to sons, but results vary across model specifications. The results suggest that effects on children's health do not operate through parents’ health. With respect to union type, the health changes before and after dissolution of a consensual union are not very different from those before and after marital separation.
Background: Research has shown that sexual minority people of color experience pervasive and sometimes severe life stressors that increase their risk of experiencing mental health problems, and that can contribute to lifelong health disparities. However, no studies in this population have investigated stressor exposure occurring over the entire lifespan. Moreover, it remains unknown whether these stressor-health effects differ based on the timing or types of stressors experienced. Purpose: The purpose of this study is to examine how cumulative lifetime stressor exposure is associated with mental health among Black, Latinx, and biracial Black-Latinx sexual minority persons. Method: Participants were 285 ethnic/racial minority young adults (Mage = 25.18 years old, SD = 1.94, age range = 19-29 years), who completed the Stress and Adversity Inventory for Adults to assess for retrospective reports of lifetime stressor count and severity. The Brief Symptom Inventory was used to assess participants' symptoms of anxiety, depression, and somatization, which were the main outcomes. Most participants identified as cisgender male (94.7%) and gay (74.2%), with the remaining participants identifying as transgender or genderqueer/nonbinary for gender and bisexual/pansexual, queer, or another sexual orientation. Results: Multiple regression analyses indicated that experiencing more-and more severe-stressors across the lifespan was related to greater anxiety, depressive, and somatization symptoms. These effects were robust while controlling for race/ethnicity, sexual orientation, education, and employment status, and they differed based on stressor exposure timing, type, primary life domain, and core social-psychological characteristic. Conclusion: Greater cumulative lifetime stressor exposure is related to poorer mental health among sexual minority people of color. Screening for lifetime stressors may thus help identify at-risk persons and provide an opportunity to intervene to help mitigate or prevent mental health disparities in multiply stigmatized adults.
Context : Cognitive and physical fatigue are common symptoms experienced by oncology patients. Exposure to stressful life events (SLE), cancer-related stressors, coping styles, and levels of resilience may influence the severity of both dimensions of fatigue. Objectives : Evaluate for differences in global, cancer-specific, and cumulative life stress, as well as resilience and coping in oncology patients (n=1332) with distinct cognitive fatigue AND evening physical fatigue profiles. Methods : Latent profile analysis, which combined the two symptom scores, identified three subgroups of patients with distinct cognitive fatigue AND evening physical fatigue profiles (i.e., Low, Moderate, High). Patients completed measures of global, cancer-specific, and cumulative life stress as well measures of resilience and coping. Differences among the latent classes in the various measures were evaluated using parametric and nonparametric tests. Results : Compared to Low class, the other two classes reported higher global and cancer-specific stress. In addition, they reported higher occurrence rates for sexual harassment and being forced to touch prior to 16 years of age. Compared to the other two classes, High class reported lower resilience scores and higher use of denial, substance use, and behavioral disengagement. Conclusion : To decrease both cognitive and evening physical fatigue, clinicians need to assess for relevant stressors and initiate interventions to increase resilience and the use of engagement coping strategies. Additional research is warranted on the relative contribution of various social determinants of health to both cognitive and physical fatigue in oncology patients receiving chemotherapy.
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The number of infertility treatment cycles in Japan is the highest worldwide. Studies have shown that stigma is a predictor of stress-related symptoms including anxiety and depression in women undergoing infertility treatment. Stress management to prevent stress-related symptoms may be crucial; however, few studies have examined the model of stigma and stress responses. Based on the stress-coping model, we hypothesized that stigma threatens the identity of such women and that coping failure increases stress responses. We aimed to explore the role of cognitive appraisals and coping strategies as mediators of the association between the stigma of infertility and stress responses. In December 2021, we conducted a cross-sectional study in Japan, in which 254 women undergoing infertility treatment completed a web-based survey. Hierarchical multiple regression analysis was conducted to analyze the associations between stigma, cognitive appraisals, coping strategies, and stress responses. The results showed that explanatory power increased with each additional variable in the following order: stigma, cognitive appraisals, and coping. Participants with a high level of stigma evaluated it as threatening, and used self-blame and venting coping strategies, and showed higher stress responses. Conversely, participants who used positive reframing coping strategies exhibited lower stress responses. Based on this, effective strategies to address stigma and stress responses are necessitated.
BACKGROUND: Evidence suggests that diets rich in flavonoids affect human health. Among flavonoids, anthocyanins have been demonstrated to exert beneficial effects toward brain through modulation of neuroinflammation, neurogenesis, neuronal signaling and by modulating gut microbiota. OBJECTIVE: This study aimed to investigate the association between consumption of anthocyanin-rich fruits (strawberries, berries, cherries, prickly pears, grapes, blood oranges) and mental health in an Italian cohort study. METHODS: Dietary information was collected using a validated food frequency questionnaire. Mental health outcomes were assessed using the Pittsburgh Sleep Quality Index (PSQI), the Perceived Stress Scale (PSS), the 10-item Center for the Epidemiological Studies of Depression Short Form (CES-D-10) as a screening tool for sleep quality, perceived stress and depressive symptoms, respectively. RESULTS: A significant inverse association between higher anthocyanin-rich fruits intake and occurrence of poor sleep quality, high perceived stress, and depressive symptoms was found. In the most adjusted model, individuals in the highest tertile of anthocyanin-rich fruits were less likely to have poor sleep quality (OR = 0.63, 95% CI: 0.47–0.86), high perceived stress (OR = 0.68, 95% CI: 0.51–0.92), and depressive symptoms (OR = 0.67, 95% CI: 0.49–0.90). CONCLUSIONS: Diets including fruits rich in anthocyanins may result in positive mental health outcomes.
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Although prior research has examined how early adversity and chronic stress exposure relate to hypothalamic‐pituitary‐adrenal (HPA) axis responses to acute stress, to date, no studies have examined how stressors occurring over the entire lifespan predict such responses. To address this issue, we recruited 61 healthy young adults and measured their exposure to 55 different types of acute life events and chronic difficulty occurring over the lifespan. In addition, we characterized differences in participants’ HPA axis responses to acute stress by measuring their salivary cortisol and DHEA responses to the Trier Social Stress Test for Groups. Greater cumulative stress exposure was associated with a blunted cortisol response, but a heightened DHEA response, to the acute stressor. Moreover, it was participants’ exposure to these stressors (i.e., lifetime count), not their perceived severity, which predicted their cortisol and DHEA responses to acute stress. Furthermore, differential effects were observed by stress exposure domain. Notably, only adulthood and marital/partner stressors significantly predicted cortisol responses to acute stress, whereas stress was more uniformly associated with DHEA responses to the acute stressor. These results thus reveal how cumulative stress exposure is associated with HPA axis responsivity to acute stress, while highlighting the fact that different stressors may have substantially different associations with these biological outcomes.
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Objective: Numerous theories have proposed that acute and chronic stressors may exert a cumulative effect on lifespan health by causing biological "wear and tear", or allostatic load, which in turn promotes disease. Very few studies have directly tested such models, though, partly because of the challenges associated with efficiently assessing stress exposure over the entire life course. To address this issue, we developed the first online system for systematically assessing lifetime stress exposure, called the Stress and Adversity Inventory (STRAIN), and describe its initial validation here. Methods: Adults recruited from the community (n=205) were administered the STRAIN, CTQ-SF, and PSS, as well as measures of socioeconomic status, personality, social desirability, negative affect, mental and physical health complaints, sleep quality, computer-assessed executive function, and doctor-diagnosed general health problems and autoimmune disorders. Results: The STRAIN achieved high acceptability and was completed relatively quickly (Mean=18 minutes, 39 seconds; IQR=12-23 minutes). The structure of the lifetime stress data best fit two latent classes overall and five distinct trajectories over time. Concurrent associations with the CTQ-SF and PSS were good (rs=.147-.552). Moreover, the STRAIN was not significantly related to personality traits or social desirability characteristics and, in adjusted analyses, emerged as the measure most strongly associated with all six of the health and cognitive outcomes assessed except current mental health complaints (βs=.16-41; RRs=1.02-1.04). Finally, test-retest reliability for the main stress exposure indices over 2-4 weeks was excellent (rs=.904-.919). Conclusions: The STRAIN demonstrated good usability and acceptability; very good concurrent, discriminant, and predictive validity; and excellent test-retest reliability.This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.
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Stress: Concepts, Cognition, Emotion, and Behavior: Handbook in Stress Series, Volume 1, examines stress and its management in the workplace and is targeted at scientific and clinical researchers in biomedicine, psychology, and some aspects of the social sciences. The audience is appropriate faculty and graduate and undergraduate students interested in stress and its consequences. The format allows access to specific self-contained stress subsections without the need to purchase the whole nine volume Stress handbook series. This makes the publication much more affordable than the previously published four volume Encyclopedia of Stress (Elsevier 2007) in which stress subsections were arranged alphabetically and therefore required purchase of the whole work. This feature will be of special significance for individual scientists and clinicians, as well as laboratories. In this first volume of the series, the primary focus will be on general stress concepts as well as the areas of cognition, emotion, and behavior. Offers chapters with impressive scope, covering topics including the interactions between stress, cognition, emotion and behaviour Features articles carefully selected by eminent stress researchers and prepared by contributors representing outstanding scholarship in the field Includes rich illustrations with explanatory figures and tables Includes boxed call out sections that serve to explain key concepts and methods Allows access to specific self-contained stress subsections without the need to purchase the whole nine volume Stress handbook series.
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A growing body of research has indicated that acute stress can critically impact memory. However, there are a number of inconsistencies in the literature, and important questions remain regarding the conditions under which stress effects emerge as well as basic questions about how stress impacts different phases of memory. In this meta-analysis, we examined 113 independent studies in humans with 6,216 participants that explored effects of stress on encoding, postencoding, retrieval, or postreactivation phases of episodic memory. The results indicated that when stress occurred prior to or during encoding it impaired memory, unless both the delay between the stressor and encoding was very short and the study materials were directly related to the stressor, in which case stress improved encoding. In contrast, postencoding stress improved memory unless the stressor occurred in a different physical context than the study materials. When stress occurred just prior to or during retrieval, memory was impaired, and these effects were larger for emotionally valenced materials than neutral materials. Although stress consistently increased cortisol, the magnitude of the cortisol response was not related to the effects of stress on memory. Nonetheless, the effects of stress on memory were generally reduced in magnitude for women taking hormonal contraceptives. These analyses indicate that stress disrupts some episodic memory processes while enhancing others, and that the effects of stress are modulated by a number of critical factors. These results provide important constraints on current theories of stress and memory, and point to new questions for future research. (PsycINFO Database Record
The Life Events Checklist (LEC), a measure of exposure to potentially traumatic events, was developed at the National Center for Posttraumatic Stress Disorder (PTSD) concurrently with the Clinician Administered PTSD Scale (CAPS) to facilitate the diagnosis of PTSD. Although the CAPS is recognized as the gold standard in PTSD symptom assessment, the psychometric soundness of the LEC has never been formally evaluated. The studies reported here describe the performance of the LEC in two samples: college undergraduates and combat veterans. The LEC exhibited adequate temporal stability, good convergence with an established measure of trauma history—the Traumatic Life Events Questionnaire (TLEQ)— and was comparable to the TLEQ in associations with variables known to be correlated with traumatic exposure in a sample of undergraduates. In a clinical sample of combat veterans, the LEC was significantly correlated, in the predicted directions, with measures of psychological distress and was strongly associated with PTSD symptoms.
There has been a long-standing interest in better understanding how social factors, contribute to racial disparities in health, including birth outcomes. A recent emphasis in this context has been on identifying the effects of stress exposure and protective factors experienced over the entire lifetime. Yet despite repeated calls for a life course approach to research on this topic, very few studies have actually assessed how stressors and protective factors occurring over women’s lives relate to birth outcomes. We discuss this issue here by describing how challenges in the measurement of lifetime stress exposure and protective factors have prevented researchers from developing an empirically-based life course perspective on health. First, we summarize prevailing views on racial inequality and birth outcomes; second, we discuss measurement challenges that exist in this context; and finally, we describe both new tools and needed tools for assessing lifetime stress exposure and suggest opportunities for integrating information on stress exposure and psychosocial protective factors. We conclude that more studies are needed that integrate information about lifetime stress exposures and the protective factors that promote resilience against such exposures to inform policy and practice recommendations to reduce racial disparities in birth outcomes.
Exposure to stress throughout life can cumulatively influence later health, even among young adults. The negative effects of high cumulative stress exposure are well-known, and a shift from episodic to stimulus–response memory has been proposed to underlie forms of psychopathology that are related to high lifetime stress. At the other extreme, effects of very low stress exposure are mixed, with some studies reporting that low stress leads to better outcomes, while others demonstrate that low stress is associated with diminished resilience and negative outcomes. However, the influence of very low lifetime stress exposure on episodic and stimulus–response memory is unknown. Here we use a lifetime stress assessment system (STRAIN) to assess cumulative lifetime stress exposure and measure memory performance in young adults reporting very low and moderate levels of lifetime stress exposure. Relative to moderate levels of stress, very low levels of lifetime stress were associated with reduced use and retention (24 h later) of stimulus–response (SR) associations, and a higher likelihood of using context memory. Further, computational modeling revealed that participants with low levels of stress exhibited worse expression of memory for SR associations than those with moderate stress. These results demonstrate that very low levels of stress exposure can have negative effects on cognition.