Learning Objectives
By the end of this section, you should be able to
- 12.3.1 Describe the factors that influence interindividual variability in the stress response
- 12.3.2 Explain the concept of resilience and describe some of the beneficial effects of stress
- 12.3.3 Describe some useful strategies to optimize the stress response
Not surprisingly, individuals vary greatly in their response to stress due to factors like genetics, epigenetics, biological sex, developmental and later life history, and even preconceptional and transgenerational influences. Additionally, factors like how a stressor is perceived, whether it’s predictable or controllable and the social milieu can dramatically alter an individual’s response. The good news is that not all stress is bad—moderate stressors have beneficial effects. In addition, multiple interventions including physical exercise, breathing exercises, meditation, and mindfulness-based stress reduction are proven techniques that can help not just mitigate but optimize one’s response to stress.
Factors that influence interindividual variability in response to stress
So far, we have described the generic response that is activated by stress—a response that is similar between many different manifestations of stress (physical, social or psychological) and evolutionarily conserved across taxa. This response involves the stereotypical neural and endocrine axis activation, but it can vary greatly between individuals. Biological, life history and psychological factors all contribute to this interindividual variability. For example, an individual’s genetic and epigenetic makeup, biological sex, and stress exposure during critical periods (e.g., in utero, neonatal and early life, adolescence, and exposure during aging later in life) all impact their response to stress. Recent evidence suggests that preconceptional and transgenerational mechanisms are also involved in setting up or shaping this interindividual variability. Finally, factors like an individual’s physiological and emotional state (are they hungry, tired), psychological differences in how a person perceives/appraises a stressor, whether the stressor is deemed as predictable or controllable, the availability of social resources, and specific characteristics of the encountered stressor can all lead to a more heterogeneous and fine-tuned response.
Genetic factors
Genetic factors that influence the stress response include polymorphisms in genes involved in glucocorticoid signaling and HPA axis regulation, monoamine neurotransmitter function, and regulation of brain plasticity. For example, the gene encoding FK506-binding protein 51 (FKBP5/FKBP51) is an important modulator of stress responses. FKBP5 acts as a co-chaperone for the glucocorticoid receptor. Specific alleles of the FKBP5 gene (e.g. T allele) are associated with blunted GR-dependent feedback inhibition of the HPA axis, resulting in dysregulated axis function (e.g. prolonged cortisol responses). In other words, people with certain genetic forms of the FKBP5 protein will take longer to turn off the HPA axis (and get their circulating cortisol levels back to normal) after a stressor because of impaired GR function compared to people with more typical forms of FKBP5.
These mutations in FKBP5 (and the chronically impaired shutdown of stress responses) have clinically relevant effects on behavior. For example, the T allele is associated with increased anxiety, attentional bias towards threat, hippocampal activation after fear/threat induction, and changes in amygdala volume which can predispose to development of stress-related pathology. In fact, alleles associated with greater FKBP5 induction and longer cortisol responses are associated with higher risk for Major Depressive Disorder, Posttraumatic Stress Disorder, suicidality, psychosis, aggression and violent behavior (for review see Zannas et al., 2016).
Developmental Perspective: Critical periods for stress exposure
Just like there are critical periods for learning and development, there are critical periods for stress exposure (see Chapter 5 Neurodevelopment). During periods of our development, the brain is especially plastic, allowing for changes that can translate to risk or resilience in the face of stress later in life. During these periods, factors in the environment combine with those of our genetics to influence neurodevelopment. These effects can persist into adulthood, influence the trajectory of our lives, and manifest as vulnerabilities to mental health.
In utero
Before birth, our neurodevelopment is already being influenced by the world around us. Many studies of prenatal stress come from retrospective studies where a mother has experienced a disaster, for example war, malnutrition, hardship in personal relationships, or tensions in their everyday environment. Many of these retrospective studies have focused on historical events, for example, a year of extreme food shortage in the Netherlands during World War II, known as the Dutch famine, or more recently the events in New York City on September 11, 2001, also known as the 9/11 attacks, which affected women at different stages of pregnancy.
As we know, stress exposure elicits an HPA axis and neural response. Although the placenta acts as a selective barrier, some stress hormones produced by the mother can cross through the placenta and reach the fetus, triggering release of additional stress hormones (Weinstock, 2005). Evidence suggests that maternal stress exposure is associated with shorter gestational age, increase in preterm births, low birthweight, and small size for gestational age (Class et al., 2011). This exposure to maternal stress and high cortisol levels can also lead to deficits in mental development scores and cognitive ability once a fetus matures into childhood (Brouwers et al., 2001; Bergman et al., 2010). It is also associated with autistic traits and ADHD behaviors (Ronald et al., 2011), emotional problems (O'Connor et al., 2002), and higher cortisol response to a stressor (Davis et al., 2011). Animal models show that maternal stress alters HPA axis function, cortisol, and CRH levels throughout the lifetime of the offspring (Weinstock, 2008). Thus, the effects of maternal stress hormones can alter neurodevelopment in the fetus and contribute to adverse consequences throughout life.
Early life stress
Exposure to stress that occurs in the timeframe from infancy to adolescence, can also have a major impact on the trajectory of development. During this period, stress can come from maltreatment, neglect, or exposure to trauma or stressful life events (see Chapter 5 Neurodevelopment). Early life stress can increase the risk of developing psychiatric disorders in adulthood (Carr et al., 2013), for example depression and anxiety (Heim and Nemeroff, 2001). It can also increase the likelihood of developing alcohol or drug dependence (Enoch, 2011). In rodents and primates, early life stress can evoke depression-like behaviors and altered HPA axis responsiveness that lasts into adulthood (Pryce et al., 2005).
Epigenetics, the chemical modification of DNA without a change in nucleotide sequence, can account for a major part of the developmental trajectory following stress. To understand this idea of epigenetic modification, we first need to appreciate how DNA is packed into the nucleus. The DNA contained in each cell’s nucleus is not lying about like loose spaghetti. It is actually packed together quite purposefully, folded and wrapped around on itself and around proteins called histones so that the ~3 billion nucleotide base pairs that make up the human genome can fit into the cramped quarters of the nucleus. Epigenetic changes are chemical modifications attached to the DNA itself or to the histones that the DNA wraps around. These modifications change how loosely or tightly the DNA is packed. Genes that are in stretches of DNA that are packed up especially tightly are less readily expressed (transcribed into RNA) while genes in segments of DNA that are packed more loosely are accessible and more easily transcribed.
Early life stress has been shown to induce changes in the epigenome, specifically in genes that regulate the HPA axis, which persist throughout life and can modulate HPA axis and stress reactivity. For example, the quality of maternal care during the neonatal period—modeled in rodents as increased pup licking and grooming by rat mothers—results in epigenetic modifications that enhance feedback sensitivity and efficient HPA axis shutdown following stress. See Feature Box on the persistent effect of maternal care on stress vulnerability and resilience. Similarly, early life stress (duration of maternal separation, for example) has been shown to induce changes in the epigenome that persist throughout life and can confer either vulnerability or resilience to stress. Additionally, recent research is beginning to uncover how transgenerational effects (i.e., events experienced by previous generations) can modulate individual variability in stress responses. See Feature Box on preconceptional, historical and transgenerational effects of stress.
Adolescence
The transition from childhood to adolescence represents another vulnerable period to stress exposure. Internally, dramatic physiological and hormonal changes occur (see Chapter 11 Sexual Behavior and Development). At the same time, the development of complex behaviors, including a notable dependence on peer relationships, as opposed to parental ones, emerges. These intense changes combined with high brain plasticity makes adolescence a crucial period in development where vulnerability is heightened. Exposure to stress during this period has been shown to increase the risk for depression and is associated with social and educational impairments (Fletcher, 2010).
Aging
In aging populations, changes in the brain and in the endocrine system occur in some, but not all individuals. A particularly vulnerable part of the brain to the aging process is the hippocampus. During aging, a decrease in hippocampal function and reactivity to cortisol leads to a decrease in the efficient shut down of HPA axis activation. This is seen in some aged individuals as hyper-reactivity to stress, resulting in higher levels of baseline and stress-related cortisol, and a deficient shutdown of activation. This is a vicious cycle for the aging hippocampus, as the increased levels of cortisol lead to increased neurodegeneration, cellular vulnerability and memory decline, which contributes to greater effects from stressors and could be at least partially responsible for aging the hippocampus (Miller and O’callaghan, 2005).
People behind the science: The persistent effect of maternal care on stress vulnerability and resilience
How a mother cares for their child can vary widely. There are variations in social, emotional, and socio-economic contexts. If these variations result in neglect or abuse towards a child, they can lead to persistent negative effects on stress reactivity (vulnerability to stress). Drs. Darlene Francis, Frances Champagne, Michael Meany, and Moshe Szyf have made significant contributions to our understanding of the long- term effects of maternal care on stress reactivity. Through their work with rodents, initiated primarily at McGill University and subsequently pursued at other institutions, they showed that early experiences can translate into later life behaviors via epigenetic mechanisms. They studied this phenomenon using rats as a model. Rats, it turns out, can be very caring mothers and one of the main ways they care for their pups is by regularly licking and grooming them. Through observations of rat maternal behaviors like pup licking, grooming, and nursing, this team of researchers found that a greater frequency of these behaviors resulted in increased numbers of hippocampal GRs, enhanced glucocorticoid feedback sensitivity and more modest HPA axis responses to stress in the adult offspring of high maternal care mothers. Furthermore, their work showed that GR gene expression is controlled by epigenetic modifications (altered chromatin structure and DNA methylation of a promoter region for the GR gene) which can persist into adulthood (Liu et al., 1997; Weaver et al., 2004). Ultimately, their work provided valuable insight into the epigenetic processes behind transmission of individual variabilities in stress reactivity.
Preconceptional, historical and transgenerational effects of stress
Stress has obvious effects on one’s own body and offspring, but there can be detrimental effects on subsequent generations as well. Ancestral environments and behaviors can create lasting beneficial or detrimental effects. One way in which the effects of stress can be transferred to a future generation is through biological inheritance. For example, when a mother conceives a female embryo, that offspring creates all the eggs she will have throughout her lifetime before she even leaves the womb. Any experiences of the grandmother then could have some effect on the granddaughter. Another mechanism of transmission is social inheritance. Maternal care is an excellent example of this: here a mother’s care for their child can affect emotional outcomes later in life. Lastly, ecological inheritance or the shared experience of trauma at a community level can also be a mechanism of transmission. Survivors of the Holocaust and Native American experiences of genocide and oppression provide evidence that effects of trauma and stress can extend beyond the generation directly exposed and contribute to the development of depression, anxiety and PTSD in offspring that themselves were not exposed. These transgenerational effects most likely also rely on epigenetic modification of DNA. Evidence suggesting this ecological inheritance is seen in the offspring of trauma survivors, where low cortisol levels are associated with parental PTSD (Yehuda & Bierer., 2007; Perroud et al., 2014). Epigenetic modifications in the FKBP5 gene, a co-chaperone for the glucocorticoid receptor (discussed above under genetic factors affecting interindividual variability), have also been observed in both Holocaust survivors (mothers) and their offspring (Yehuda et al., 2016).
Transgenerational transmission is not only seen in humans, it applies to other species as well. Caenorhabditis elegans (nematode worms), for example, show altered gene expression in response to temperature changes for at least 14 generations (Klosin et al., 2017). They also show changes in small RNAs (regulators of gene expression) if ancestors were starved for extended periods (Rechavi et al., 2014). Drosophila melanogaster (fruit flies) also show an obesity phenotype for two generations if an ancestor was placed on a high-calorie diet (Buescher et al., 2013). In rodents, work by Dr. Brian Dias is revealing the epigenetic mechanisms involved in transgenerational inheritance of fear learning. You can learn more about Dr. Dias’ innovative work and his path in research in the talk “Great Scientists, Great Failures”.
Biological sex differences
Sex differences in stress responses have garnered significant attention within the field of neuroscience and psychology. Numerous studies have demonstrated that males and females exhibit distinct patterns of physiological and behavioral responses when faced with stressful situations. These differences extend to both acute and chronic stressors, with variations in stress hormone secretion, neural activation, and coping strategies. For example, rodent studies have shown that females exhibit unique patterns in the number, distribution, membrane trafficking, and signaling of CRH receptors (Bangasser and Wiersielis, 2018) - patterns which are affected by estrogen. Similarly, female rats are known to release higher levels of glucocorticoids after acute restraint stress (Goel et al., 2014). These differences point to nuanced, sex-specific HPA axis function in response to stress.
At the behavioral level, studies have shown, for example, that female rodents generalize fear responses more than males (see Chapter 18 Learning and Memory). Fear generalization occurs when conditioned fear responses ‘spread’ (or generalize) to new stimuli. This effect is dependent upon estrous cycle phase and thus has been linked to sex hormone, specifically estrogen signaling. Although stress is thought to affect fear learning-related brain regions similarly in males and females, distinct molecular and gene expression profiles at the synaptic level are sex-specific. Understanding these types of differences will allow us to develop more tailored and effective interventions. Women, for example, have higher prevalence of PTSD which involves aberrant fear conditioning, fear generalization and a lack of proper fear-extinction. For review, see Fleischer and Frick, 2023.
A main challenge in the field is the difficulty of setting up experimental designs that represent true sex differences using animal models. For example, some rodent models like social defeat stress are based on behaviors mainly exhibited by males. Thus, it has been challenging to examine stress responses using the same set of stressors and behavioral assays in animals of different sexes.
Stress perception, appraisal, and reappraisal
Appraisal of a stressor, whether a person perceives it as harmful or a positive, challenging experience, can dramatically change the stress response. Interestingly, an individual’s response to stress seems to have a strong inherent or innate component. In humans, for example, an individual’s genetic and environmental/epigenetic makeup affects their processing and perception of stress (i.e., positive or negative valence attributed to a stressor) such that individuals respond differently to the same stressor. A study by Forkosh et al., 2019 identified four stable ‘personality types’ in mice (termed identity domains) based on unbiased behavioral tracking which persisted through time, developmental stages and stressful changes in their social environment. These ‘personality types’ corresponded to specific patterns of gene expression in the insular cortex, mPFC and amygdala.
Numerous studies have found that individuals who perceive stress as having a negative impact on their health suffer more serious health problems, including premature death (Keller et al., 2012; Nabi et al., 2013). Not surprisingly, abnormal patterns of appraisal are seen in various stress-related psychopathologies. The good news is that the stress response can be changed by reframing it as helpful. As mentioned in 12.1 What Is Stress?, a study by Jamieson et al. (Jamieson et al., 2012) tested whether reappraisal of stress-induced arousal (for example, a ‘racing’ heart) as helpful and adaptive, as opposed to harmful, could improve physiological and cognitive outcomes. The results showed that participants in the reappraisal group displayed a more adaptive physiological response (improved cardiovascular functioning), reported higher levels of perceived resources and showed decreased attentional bias for emotionally negative information. That is, they dealt much better with the stressful situation even when the reappraisal training consisted of brief instructional materials. Notice that the reappraisal intervention did not change the actual increased physiological arousal caused by the stressor; it is not an intervention aimed at decreasing or dampening arousal. What changed was the ‘rethinking’ of what that arousal means (whether it’s positive versus negative) and that is what ultimately influenced the measured outcomes. Neuroimaging studies have shown that reappraisal is associated with activation of frontal cortical areas (i.e., regions regulating executive functions) like the dorsal anterior cingulate cortex and medial PFC (Kalisch, 2009).
Stress predictability and controllability in animal models
To understand the molecular mechanisms underlying appraisal, we must turn to animal models. However, animals cannot report if they are ‘reappraising’ a stressful situation, thus, we must examine whether things like predictability or controllability over the stressor can change their response. Experiments have shown that rodents exposed to stressors that were not predictable had significantly higher and longer glucocorticoid responses than those presented with a regularly scheduled stressor. Similarly, the work of Steven Maier’s group at the University of Colorado Boulder has shown that controllability (a rat controls the cessation of a presented stressor by turning a wheel, for example) alters the neural and behavioral response, but doesn’t change the HPA axis output. Animals receiving the exact same stressor (i.e., amount, intensity, and duration of an electrical shock) but who differed on whether they could terminate the shock or not, displayed similar HPA axis activation but dramatically different behavioral responses. Animals that could not stop the shock (uncontrollable stress) later failed to learn to escape in a different context, were afraid of new things, were less dominant, showed less social interactions, and had exaggerated responses to drugs of abuse (see Figure 12.21).
A large amount of work has gone into understanding the neural circuitry of this behavioral difference. Studies have found that uncontrollable stress produces robust activity in the dorsal raphe nucleus which increases release of serotonin, amygdala activation, and development of learned helplessness. Exposure to controllable stress, however, activates the medial PFC which inhibits dorsal raphe nucleus activation and blocks the negative behavioral outcomes (Amat et al., 2005; Amat et al., 2006).
Social support and buffering of the stress response
Many social animals display an interesting characteristic: when together with a conspecific they show dampened stress responses and better recovery from stressful experiences. This phenomenon is called social buffering and it has been observed in numerous species including rodents, felines, birds, nonhuman primates and humans.
Candidate molecular mediators of social buffering
Not much is known about the molecular mechanisms or neural pathways mediating the effects of social buffering. A candidate molecular mediator is the neuropeptide oxytocin—which is known for its role in social affiliative behaviors in many mammalian species.
Although no direct mechanism has been established, evidence suggests that oxytocin is released in response to stress, is associated with social/affiliative interactions after stress and can decrease HPA axis activation (via inhibition of CRH activation and ACTH and corticosteroid release), as well as SNS responses (Taylor, 2002). Additional mediators involved in stimulating and regulating the effects of social support include norepinephrine/noradrenaline, prolactin, vasopressin, serotonin and endogenous opioids.
Brain regions involved in social buffering
In humans, a study by Eisenberger et al., (Eisenberger et al., 2007) found that greater social support and decreased cortisol responses to a social stressor were associated with decreased activity in the dorsal anterior cingulate cortex (dACC) and prefrontal cortex (PFC)—brain regions that have been linked to social distress. A recent study in adolescent mice also points to a role for the PFC. In this study, social support (the presence of a mouse attempting to free a restrained mouse) blocked the negative effects of restraint stress on working memory, memory consolidation and retrieval. These stress-alleviating effects were dependent upon inhibition of stress-induced signaling cascades and normalization of stress-induced gene expression changes in the PFC (Kim et al., 2018).
Stress drives social affiliation
Social buffering is encouraged by the fact that, in many social species, stress directly promotes behaviors that will increase social interaction. Thus, stress and social buffering can form a loop, where stress drives affiliative behaviors, which in turn reduce the experience of stress (see Figure 12.22). For example, moderate stress is associated with increased affiliative behaviors in rats. A study by Muroy et al (Muroy et al., 2016) found that moderate stress exposure increased affiliative behaviors (huddling/affiliative contact, better sharing of a water resource, improved homecage stability (dominance rank) and oxytocin signaling). When the stress was made more severe by addition of predator odor, however, oxytocin signaling was reduced and the positive social effects were eliminated. These findings suggest that even the drive for affiliation by stress may follow an inverted-U pattern.
In humans, acute stress has also been shown to increase affiliative interactions and prosocial behavior. For example, increased time interacting and higher group cohesion were observed in study participants awaiting an electrical shock versus groups awaiting a mildly embarrassing or ambiguous stimulus (Morris et al., 1976). In terms of prosocial behavior, participants exposed to a socioevaluative stressor (the TSST) showed greater trust and sharing in interactive games with monetary stakes (von Dawans et al., 2012). Importantly, affiliative social interactions, for example, contact with a friend or other supportive person during times of stress can decrease sympathetic reactivity and cortisol levels, facilitating recovery. This, in turn, can positively influence health and life expectancy (for review see House et al., 1988; Taylor, 2011). Lack of social connection (e.g. social isolation), on the other hand, can increase HPA axis and SNS activity and is a major risk factor for stress-related psychiatric conditions like depression and anxiety.
Summary of factors affecting interindividual variability in the stress response
Figure 12.23 shows a summary of the factors discussed in this section. Factors and their associated brain regions are displayed at the top. Some brain regions are attuned to various factors. For example, the reward system is sensitive to predictability (i.e., novelty), controllability and duration of a stressor. The frontal cortex is similarly attuned to duration, controllability and stressor predictability, and additionally mediates stressor appraisal; the stress dampening effects of social support are integrated here as well. Brainstem regions, the circumventricular organs and the limbic system are attuned to stressor type and the physiological state of the organism (metabolic, inflammatory state, for example), which can influence an individual’s perception of stress.
The brain assimilates both external and internal inputs and constructs a ‘grid’ of brain activity specific for each stressor. This pattern of brain activity varies 1) between individuals (due to individual differences based on genetics, epigenetics, life history events, biological sex, emotional and physiological state, etc.) and 2) between different stressors. The response is then integrated at the level of the hypothalamus and specific brainstem nuclei to produce fine-tuned neural and endocrine outputs that are designed to deal with the specific challenge. For example, stressors that exert metabolic pressure (hypoglycemia) induce secretion of growth hormone from the pituitary gland (Jezova et al., 2007) while stressors that elicit pain activate pain relief pathways. The severity of the painful stressor further fine-tunes which type of pain relief pathway is activated: opioid versus non-opioid. Exposure to heat or cold stress requires activation of brown fat to restore internal body temperature, while encountering a mountain lion requires priming of the immune system in case of injury. For the latter two examples, specificity is mediated by differential activation of sympathetic fibers in adipose tissue and the spleen (an immune organ) respectively, in response to different types of physical stressors (Iriki and Simon, 2012). SNS peripheral nerve terminals can also co-secrete various neuropeptides that further fine tune the generic stress response.
Thus, the type of neural activation (e.g., which SNS fibers), variety of secreted factors, their concentration and different combinations diversify the stereotypical neural and endocrine stress response. Moreover, even secretion of the canonical stress hormones ACTH and corticosterone depend on the stressor context. For example, lactating female rats caring for a litter generally show blunted ACTH and glucocorticoid responses to common laboratory stressors. However, if the stressor involves danger to the pups (inclusion of predator odor or a male intruder in the home cage), then plasma levels of ACTH and glucocorticoids rise significantly (Deschamps et al., 2003). In this example, the organism’s physiological state is also an important factor. For in depth review, see Haykin and Rolls, 2021.
Resilience
Resilience is the capacity to adapt following adversity. It is not a fixed trait—it can change throughout life and is multidimensional: for example, a person can be resilient to injury but not to psychological stress. The inverted-U curve can be used to understand how stress responsivity (vulnerability or resilience) varies between individuals (Sapolsky, 2015). For example, the curve can be right- or left-shifted along the x-axis (see the blue and orange curves in Figure 12.24).
The ‘right’ amount of stress (eustress) that yields optimum function for the person with the blue curve is much higher than that for the person with the orange curve. This optimal level will also vary in different domains for the same person and for the same person at different points in time (intraindividual variability). Curves could also be flattened (wider; see green curve). The individual with the green curve would require really low or really high HPA axis activation for it to be detrimental to their function.
Little is known about the mechanisms that shift inverted-U curves to the right, that is, towards resilience. Most resilience studies have been done at the group level and few have focused on individuals, i.e., those who respond (are vulnerable) versus those that don’t respond (are resilient) to stress. Additionally, does resilience mean that there was no change or a lack of molecular response? Or was there a protective response that helped resilient individuals bounce back? The answer seems to point to the latter, but the mechanisms are yet mostly unknown.
How to optimize the stress response
How can we optimize our response to stress? That is, modulate it towards eustress versus distress? As mentioned before, reappraisal of a (mild-moderate) stressor as an adaptive challenge can improve physiological and cognitive stress outcomes. We can also engage in exercise—a physical stressor—which can enhance our adaptive capacity and has been shown to have numerous beneficial effects on stress responses. Exercise produces in the short-term feelings of calmness and reduced anxiety and can lead to long-lasting adaptations in neuroendocrine/HPA axis function after chronic training. It has reported antidepressant effects and has been shown to increase overall resilience, well-being and healthspan. Acute vigorous exercise increases levels of endogenous cannabinoids in the bloodstream (see Chapter 3 Basic Neurochemistry). These neurotransmitters are similar to compounds found in cannabis (marijuana) and may mediate post-exercise feelings of calm, reduced anxiety and sometimes euphoria, colloquially referred to as a ‘runner’s high’ (Raichlen et al., 2013; Volkow et al., 2017). Training over several weeks attenuates resting/basal levels of stress hormones (Hackney, 2006). Furthermore, the stress-attenuating effects of chronic exercise training seem to carry over into reduced stress responses to other life stressors (Traustadóttir et al., 2005).
Meditation is an Eastern spiritual-associated practice that has been adapted for stress reduction and is currently a very active area of study. Research into meditation seems to point to enhanced executive control of attention (Tang et al., 2007), reduced cortisol levels (Tang et al., 2007; Fan et al., 2014) and improvements in mood (Basso et al., 2019). Note that research is limited to human subjects and correlational studies. Please see the demonstration video for an example of a short, guided meditation. To learn more about meditation research, see the work of Richard Davidson (University of Wisconsin-Madison; current leader in the field) and the Mind & Life Institute.
Finally, there are interventions like Mindfulness-based stress reduction (MBSR) (Kabat-Zinn, 2013) - an evidence-based program that combines mindfulness meditation, body awareness and examination of patterns of thought, emotion, behavior/action as tools for effectively coping with stress. MBSR has been shown to enhance attention skills, increase emotional regulation and significantly reduce rumination and worry. It has been very successfully utilized as an intervention for ameliorating anxiety, depression, and pain.