Unusual Links to Stress – Sahaja Online Unusual Links to Stress – Sahaja Online

Stress Management

Unusual Links to Stress

Research from the past few decades has provided overwhelming evidence that negative stress  can trigger, accelerate and increase risk for a host of serious illnesses, including:

  • cardiovascular disease (e.g., heart attacks, hypertension)
  • immune system deficiencies
  • diabetes
  • depression
  • anxiety
  • some cancers
  • inflammatory disorders (e.g., arthritis)
  • autoimmune disorders
  • accelerating aging and osteoporosis
  • HIV/AIDS and other infectious diseases (including colds and flu viruses)
  • ulcers
  • migraine syndrome

These are the links we often hear about, but the reach of stress extends to many other aspects of our health and well-being, including its stealth role as an “unknown trigger factor” in many health problems. Following are some links to stress that you may not know about along with studies that reveal the (sometimes odd) ways we respond to stress and what those responses can teach us about mitigating the effects of negative stress…

Stress and Reward

Empathy – ‘Tis better to give than to receive

The mental health benefits of social support, it turns out, are not just about what we receive from others; they’re also about what we give to others.

One fMRI study at UCLA showed that when their boyfriends were experiencing stressful events (such as receiving painful electric shocks), women who provided emotional support to their boyfriends (e.g., by holding their arms) showed increased activity in reward-related regions of the brain, such as the ventral striatum and septal area. Activity in the ventral striatum and septal region has often been associated with receiving pleasure and reward (e.g., chocolate, money etc.), suggesting that the brain processes support-giving as a rewarding experience. The septal region also plays a role in stress reduction by inhibiting other regions of the brain that process threats, such as the amygdala. Women who showed greater activity in the septal area showed less activity in the amygdala, suggesting that support-giving may have stress-reducing effects for the person who’s doing the giving (Inagaki, Eisenberger, 2011). And the greater the reward-related neural activity, the more connected these women reported feeling with their boyfriends while providing support.




Dark chocolate may ease emotional stress.

Good news for the “chocolate cure!” Several studies have found that chocolate may ease emotional stress and that antioxidants and other beneficial substances in dark chocolate may reduce risk factors for heart disease and other physical health problems. But a recent clinical trial suggests the mechanism by which chocolate may exert its stress-relief effects: it may modify our metabolism. The study found that people with high stress levels who ate about an ounce-and-a-half (1.4 ounces, to be precise) of dark chocolate each day for two weeks reduced stress hormone levels and partially corrected other stress-related biochemical imbalances (Martin et al, 2009).


Pleasurable behaviors reduce stress.


Pleasurable activities provide more than just pleasure; they may actually reduce stress by inhibiting anxiety responses in the brain, which may help explain the powerful motivation to consume comfort food during times of stress.

One study found that even small amounts of pleasurable foods can reduce the effects of stress and that the pleasurable properties of tasty foods, excluding the caloric properties, are enough to offer stress relief. Rats who were given a sugar solution twice daily for two weeks exhibited reduced heart rate and lower stress hormone levels. They also became more sociable and open to new experiences: they were more willing to explore unfamiliar environments and socially interact with other rats. The reduced-stress effects continued for at least seven days, suggesting possible long-term benefit. The key neural circuitry underlying this comfort food effect appeared to revolve around a weakened response to stress by the hypothalamic-pituitary-adrenocortical (HPA) axis, which is regulated by an area in the amygdala (Ulrich-Lai et al, 2010).

Link between stress, appetite and obesity.

The unavailability of food can bring about dramatic changes in the way our neurons communicate with each other. Researchers have uncovered a mechanism by which stress may increase our food drive. The brain produces neurotransmitters called endocannabinoids that send signals to control appetite, but the lack of food activates the stress response (e.g., release of stress hormones in the hypothalamus), which triggers a temporary re-wiring of neural pathways in the brain that impairs the endocannabinoids’ ability to regulate food intake. The result? We get hungrier, and not necessarily from the lack of nutrients, but from the stress caused by absence of food, a mechanism that might help explain the relationship between stress and obesity. So you might want to think twice about skipping a meal. The stress will only increase your appetite (Crosby et al, 2011)!




When making decisions, stress causes us to focus on the upside.

Feeling stressed changes how we weigh risk and reward. One study shows that, surprisingly, stress makes us focus on the way things could go right, which is counterintuitive, since stress is usually associated with negative thinking, experiences and outcomes. But researchers found that when people were put under stress by, for example, giving a speech or submerging their hands in ice water for a few minutes, they paid more attention to positive information and discounted negative information. One explanation may be that stress helps us learn from positive feedback and impairs our ability to learn from negative feedback. The practical implication is that, for better or worse, if we’re making a difficult decision under stress, we may pay more attention to the upsides of the choices we’re weighing and less to the downsides. For example, someone who’s stressing about whether to accept a new job offer might pay more attention to the salary increase than the new, longer commute. This blind focus on the positive sheds light on why stressed individuals have a harder time controlling urges and are more vulnerable to addiction. The compulsion to get that reward becomes more powerful and they’re less able to resist because they may only be thinking of the pleasurable feelings they’ll experience from drugs or alcohol, while the downsides fade into the distance (Mather, Lighthall, 2012).

The “reflection effect” — from stress to financial mess.

Making financial decisions under stress can make financial woes worse and you may have a phenomenon known as the reflection effect to blame.

One study found that stress exacerbates the reflection effect, which is a tendency to make more conservative choices when choosing between two potentially positive outcomes, but riskier choices when choosing between two gambles that could result in a loss. Under stress, we fall back on automatic, lower-level thought processes and are less capable of using rational, deliberative thinking to make financial decisions, especially if we’re making decisions in stressful environments (Porcelli et al, 2009).

Stress, Gender, Race & Social Behavior

Who’s most stressed in the U.S.?

I am! you may be thinking. In fact, a 2012 Carnegie Mellon University study of changes in perceived stress from 1983 to 2009 found a 10 to 30 percent increase in reported stress across all demographics. While that doesn’t necessarily mean that Americans are “more stressed” today than they were a couple of decades ago, the study does indicate populations that are at greater risk for health problems.

In a nutshell: more women than men say they’re stressed; stress decreases with age (and retirement); and individuals with lower income and less education are have higher levels of stress.

The 2008-2009 economic downturn most significantly impacted white, middle-aged men with college educations and full-time jobs, perhaps because they may have had the most to lose, with both their jobs and savings at risk (Cohen, Janicki-Deverts, 2012).

Emotional distress is harder on the female heart.

While some studies have shown that men’s hearts become more constricted (decreased blood flow) than women’s under stress (e.g., during exercise), women have been found to be more likely than men to experience cardiac problems after emotional upsets, such as losing a spouse. A study that may shed new light on this phenomenon found that emotional stress actually increases coronary blood flow in men, but not in women, suggesting that women may be more susceptible — even predisposed — to adverse cardiac events when under stress (American Physiological Society, 2012).

Stressed men are more social.

Psychology of the 1990s established that women often adopt a “tend-and-befriend” response to stress, becoming protective (“tending”) and friendship-offering (“befriending”), while stress always triggers aggressive, fight-or-flight behavior in men. But a new German study found that men under stress showed significantly more positive social behavior than control subjects not in stressful situations. Sociable behavior and positive social contact with a trusted person was found to be a coping strategy that men used to reduce their stress response before, during and after experiencing a stressor, suggesting that they may be more befriending than previous research had given them credit for (von Dawans et al, 2012).

In stressful situations, “men check out,” women engage and empathize.

Perhaps the silent, stoic response to stress is “a guy thing,” after all. A USC study examining the effects of stress on social behavior found key gender differences in how men and women process one of the most basic social transactions — processing facial expressions. In response to viewing fearful or angry facial expressions, men under acute stress showed decreased brain activity in the fusiform gyrus (the “face recognition area”), as well as in areas of the brain responsible for empathy and social understanding (neural circuitry involving the insula, inferior frontal region and amygdala). Women under stress, however, showed increased activity in the fusiform face area and increased coordination among areas of the brain that interpret the facial emotions of others. Under acute stress, men tend to withdraw socially, while women are more apt to understand others’ feelings and seek emotional support (Mather et al, 2010). Perhaps “checking out” helps explain why men might find it easier to be more social under stress?

Under stress, men are more likely to gamble and takes risks.

Several studies have found that men are more likely than women to respond to stress by taking risks and engaging in risky behavior, as gambling, smoking, unsafe sex and illegal drug use. One study found that stressed women, in contrast, tend to moderate their behavior and become less likely to make risky choices. Researchers speculated that, evolutionarily speaking, it may have been more beneficial for men to be aggressive in stressful, high-arousal situations when risk and reward are involved. Applied to financial risk-taking, this tendency might be similar to competition for territory or other valuable resources. But while it’s often assumed that men are more likely to enter more risky financial situations than women, this study found that there was no significant statistical difference in risky behavior between men and women who were not under stress (Lighthall et al, 2009).

When stressed, men charge ahead, but women are more cautious.

A new study shows that stress causes men and women to respond differently to risky decision-making. Under stress, men were more likely to act quickly, charge ahead — even for small rewards. Women, on the other hand, were more likely to take their time and didn’t feel driven to get a reward. In the study, participants played a risk-taking game in which they could earn $4 – $45 for their performance under stress. Men showed heightened brain activity in brain areas associated with receiving a reward or satisfying an addiction, while women showed decreased activity in these same brain areas. Perhaps one takeaway is that important decisions made under stress can benefit from gender diversity (Lighthall et al, 2011).

Racial discrimination linked to oxidative stress and stress-related illnesses.

Several studies have found that psychological stress increases oxidative stress, the process by which free radicals or reactive oxygen molecules damage the components of cells (e.g., DNA, proteins or fats). The emotional stress associated with racial discrimination is thought to be one of the factors involved in racial disparities for health conditions such as high blood pressure, obesity, cardiovascular problems and premature disease-related disability. A recent study uncovered the potential cellular pathways by which racial discrimination may amplify cardiovascular disease and other stress-related health problems. African-Americans who reported suffering from racial discrimination had higher levels of oxidative stress originating from their red blood cells than whites and other blacks who did not report suffering from racial discrimination. Racial discrimination may help partially explain why African-Americans have a higher prevalence of age-associated chronic diseases associated with oxidative stress (Szanton, 2011).

Stress, Memory and Aging

Stress impairs our ability to recall positive words.

Under stress, the body amps up secretion of the stress hormone cortisol. One study of 60 healthy men found that exposing them to a standard lab stressor (the Trier Social Stress Test) triggered the expected acute, stress-induced cortisol secretion, which compromised their ability to retrieve (recall) positive, pleasant words from memory and caused more recall errors. The results suggest that acute stress impairs our memory for positive stimuli, and that stress-induced cortisol secretion may also interfere with the accuracy of memory retrieval; that is, our ability to discriminate true memories from false ones (Domes et al, 2004).

Chronic stress, bad memory.

Stress takes a toll on our ability to remember and think clearly. We’ve long known that repeated stress (via stress hormones) influences the workings of the prefrontal cortex (PFC), a brain region that controls high level, executive functions such as attention, working memory and decision making. But new research shows that chronic, long-term stress also decreases glutamate receptors in the brain, which results in impaired memory (Eunice, Yuen et al, 2012). Glutamate is an excitatory transmitter that’s involved in learning, memory and brain plasticity.

Memory decline linked to distractions.

Even in healthy older adults, a decline in memory performance has been linked to an inability to ignore distracting, irrelevant information when forming memories. Our brains should be able to suppress a response to distractions, but distraction has been found to actually increase brain activity in older adults, and quickly (within 200 milliseconds after the distraction appears). Even when we’re warned in advance that a distraction is coming, we find it difficult to ignore (Zanto, 2010).

Getting forgetful in your old age?

Stress can be hard on the brain at any age, but new research shows that stress may be linked to increasing forgetfulness in older brains through two neural receptors that react to the stress hormone cortisol. One receptor is activated by low levels of cortisol, which aids memory, but when cortisol levels become too high, they spill over onto a second receptor, which activates brain processes that contribute to memory impairment. The may help explain why too chronic, prolonged stress interferes with the normal process of storing everyday memories. While a little bit of stress might help us better remember emotional memories, lower overall cortisol levels can prevent us from tripping that second receptor in the brain that makes us forgetful (Yau et al, 2011).

Aging stereotypes can trigger false memories.

Many older adults tend to assume that age has impaired their memory, and this negative aging stereotype itself may actually influence memory performance. One study found that when presented with a list of words associated with “sleep,” (such as “bed,” “rest,” “awake,” “tired” and “night”), older adults were more likely than younger adults to falsely recall that the word “sleep” was included in the list (Thomas et al, 2011). But older adults who were primed before testing — i.e., they were told that they were expected to perform as well as younger adults — were less susceptible to reconstructing false memories than those who were told to expect age differences in memory performance.

If you think memory worsens with age, yours probably will.

Another study showing that older adults’ ability to remember suffers in the face of negative stereotypes found that believing your memory will get worse as you age can be a self-fulfilling prophecy. Interestingly, the study found that the negative effects were greatest for older adults with the highest levels of education, perhaps because people who most value their ability to remember are the most likely to be sensitive to the negative implications of stereotypes, thus are more likely to be impacted by the stereotype (Hess et al, 2009).

Spring-clean your cluttered brain to improve your memory.

Keeping a clutter-free mind can become harder as we age, especially when our attention is focused on stressors. One study found that one reason older individuals have learning and memory deficits (e.g., reduced working memory) is that they don’t purge irrelevant information, so their minds tend to be cluttered when they’re attempting to learn or remember something. In a sequential memory task where participants responded to random images, older adults were found to have more of a tendency than younger adults to repeatedly respond to previously relevant images, exhibiting what’s known as poor inhibition deletion — the ability to delete irrelevant information. The researchers found that relaxation exercises help de-clutter the brain (Blair et al, 2010).

Stress and Disease

Seeking immunity — how long are your telomeres?

Every human cell contains a tiny clock called a telomere, a protective cap on the end of our chromosomes that shorten each time the cell divides. An enzyme within the cell called telomerase keeps immune cells young by preserving their telomere length and their ability to continue dividing. Oxidative stress and inflammation accelerate this shortening, thus telomere length is effectively a measure of biological aging. In fact, telomere length has been directly linked to age-related diseases, unhealthy lifestyles, and longevity. The cells of people under chronic stress have shorter telomeres, which may be explained by the fact that the stress hormone cortisol suppresses our immune cells’ ability to activate their telomerase. Under stress, the body boosts production of cortisol to support its fight-flight response. But if cortisol levels remain elevated in the bloodstream for prolonged periods, our immune system is compromised, cell by cell (Effros, 2008).

Depression and chronic stress accelerate aging.

People who have recurrent depression and higher cortisol levels (indicative of exposure to chronic stress) have been found to have shorter telomeres in their white blood cells, which suggests compromised immunity.  Depressed people typically have disturbed cortisol regulation, which underscores how cortisol regulation and stress play a major role in depressive disorders (Wikgren, 2011).

Caregiver stress and anticipatory stress accelerates cellular aging.

For those of us who tend to have higher anticipatory threat perception (a tendency to anticipate greater threat), our major stressors may influence how we respond to minor stressors, such as traffic jams, making presentations at work or losing the car keys. A study of 50 women, about half of whom were caring for relatives with dementia, found that those most threatened by the anticipation of stressful events (e.g., public speaking, solving math problems, lab stress tests), had shorter telomeres — i.e., they were biologically older at the cellular level. The caregivers’ tendency to anticipate greater threat put them at increased risk for shortened telomeres, which increases risk for a host of chronic, age-related diseases, including cancer, heart disease and stroke (O’Donovan, 2012).

Stress increases breast cancer tumor aggressiveness.

Psychosocial stress (e.g., fear, anxiety and feeling isolated) has been found to contribute to tumor aggressiveness in breast cancer patients, particularly within minority populations such as blacks and Hispanics. More research is needed to determine whether stress directly triggers tumor aggressiveness, whether it results from receiving a more worrisome diagnosis and more stressful treatments, or both (American Association for Cancer Research, 2011).

Stress receptor stimulates growth and migration of breast cancer cells.

Stress activates the sympathetic nervous system, which communicates with receptors on cells through the release of the neurotransmitters norepinephrine and neuropeptide Y (NPY), which are part of our normal fight-or-flight stress response. But breast cancer cells express the receptors for NPY, and NPY has been found to greatly accelerate cell growth, as well as cell migration — two critical steps in primary tumor growth, as well as in metastasis. Women with a family history of breast cancer have been shown to exhibit greater physiological stress responses to normal everyday stressors. And since the female breast contains a dense supply of sympathetic nerves, NPY may be released in greater amounts in the breasts of those at risk for breast cancer (Medeiros et al, 2011).

Early childhood stress may predict cardiovascular disease in adulthood.

In times of stress, we have higher levels of stress hormones, which can even affect how our genes express themselves. A 2010 study at the Medical College of Georgia found that early life stress increases sensitivity to angiotensin II, a hormone known to increase blood pressure, which ultimately increases cardiovascular risk in adult life. Stress activates the renin-angiotensin system, which produces angiotensin II and is a major regulator of blood vessel growth and inflammation — both of which are heavily implicated in heart disease. This mechanism that translates early life stress into cardiovascular risk may result in genetic alterations at a vulnerable time in development that prevents the individual from adapting to stress as well as those who don’t experience early life stress.

Chronic stress linked to Alzheimer’s.

We don’t think of Alzheimer’s disease as a product of stress, but a 2012 study found that repeated emotional stress triggers the production and accumulation of insoluble tau protein aggregates in the brain cells of mice that are similar to human neurofibrillary tangles (NFTs) or modified protein structures that are a hallmark of Alzheimer’s disease (AD) in humans. The effect was most notable in the hippocampus, a brain region involved in the formation, organization and storage of memories. In AD patients, the hippocampus is typically the first brain region affected by tau pathology and the hardest-hit by cell death and shrinkage. This discovery may partly explain the strong link between people with chronic stress and sporadic Alzheimer’s disease (AD), which accounts for up to 95 percent of AD cases. The study found that acute, single-episode, stress-induced modifications to cells did not produce debilitating long-lasting changes and were possibly even beneficial in that they can be useful for brain plasticity and facilitating learning. But chronic stress and continuous activation of stress pathways was found to cause pathological changes in stress circuitry — perhaps an example of “too much of a good thing.” And as our neuronal circuits age, they become less plastic and robust, and less able to fully rebound from the effects of stress (Rissman et al, 2012).

Stress linked to autoimmune diseases.

Not only does stress cause disease, the disease itself also causes significant stress, creating a vicious cycle. Autoimmune disorders (e.g, rheumatoid arthritis, Addison’s disease or lupus) have historically been linked to genetic, environmental, hormonal, and immunological factors, but at least half of all autoimmune disorders are attributed to “unknown trigger factors.” A recent study shows that emotional stress just may be one of those unknown factors.Numerous studies have demonstrated the impact of negative stress on immune function, finding that up to 80 percent of patients were experiencing extreme emotional distress before disease onset. Stress-triggered neuroendocrine hormones led to immune dysregulation, which can trigger autoimmune disease by altering or amplifying cytokine production. (Cytokines are regulatory proteins, such as the interleukins and lymphokines, that are released by immune cells and help generate our immune response.) The authors suggested that treatment of autoimmune disease should include stress management and behavioral intervention to prevent stress-related immune imbalance (Stojanovich, Marisavljevich, 2008).


American Association for Cancer Research (2011, September 19).

American Physiological Society (APS) (2012, April 24). Mental stress may be harder on women’s hearts.

Blair, Mervin, Kiran Vadaga, Joni Shuchat, Karen Li. The role of age and inhibitory efficiency in working memory processing and storage components. The Quarterly Journal of Experimental Psychology, 2010; 99999 (1): 1.

Cohen, Sheldon, Denise Janicki-Deverts. Who’s Stressed? Distributions of Psychological Stress in the United States in Probability Samples from 1983, 2006, and 20091. Journal of Applied Social Psychology, 2012; 42 (6): 1320.

Crosby, Karen M., Wataru Inoue, Quentin J. Pittman, Jaideep S. Bains. Endocannabinoids Gate State-Dependent Plasticity of Synaptic Inhibition in Feeding Circuits. Neuron, Volume 71, Issue 3, 529-541, 11 August 2011

Domes, G, Heinrichs M, Rimmele U, Reichwald U, Hautzinger M.. Acute stress impairs recognition for positive words — association with stress-induced cortisol secretion. Stress. 2004 Sep;7(3):173-81.

Effros, Rita. Mechanism Behind Mind-body Connection Discovered. Brain, Behavior and Immunity, May, 2008.

Eunice, Y. Yuen, Jing Wei, Wenhua Liu, Ping Zhong, Xiangning Li, Zhen Yan. Repeated Stress Causes Cognitive Impairment by Suppressing Glutamate Receptor Expression and Function in Prefrontal Cortex. Neuron, 2012.

Hart, A.C., Sims, S., and Kaplan, J.M. (1995). Synaptic code for sensory modalities revealed by C. elegans GLR-1 glutamate receptor. Nature 378, 82–84.

Hess et al. Moderators of and Mechanisms Underlying Stereotype Threat Effects on Older Adults’ Memory Performance. Experimental Aging Research, 2009; 35 (2): 153

Inagaki, Tristen K., Eisenberger, Naomi I.. Neural Correlates of Giving Support to a Loved One. Psychosomatic Medicine, 2011;

Liat Amir-Zilberstein, Janna Blechman, Yehezkel Sztainberg, William H.J. Norton, Adriana Reuveny, Nataliya Borodovsky, Maayan Tahor, Joshua L. Bonkowsky, Laure Bally-Cuif, Alon Chen, Gil Levkowitz. Homeodomain Protein Otp and Activity-Dependent Splicing Modulate Neuronal Adaptation to Stress. Neuron, 2012; 73 (2): 279-291

Lighthall, N. R.,  M. Sakaki, S. Vasunilashorn, L. Nga, S. Somayajula, E. Y. Chen, N. Samii, M. Mather. Gender differences in reward-related decision processing under stress. Social Cognitive and Affective Neuroscience, 2011.

Lighthall, Nichole. Risky Business: Stressed Men, But Not Stressed Women, More Likely To Gamble And Takes Risks. University of Southern California (2009, July 1).

Martin et al. Metabolic Effects of Dark Chocolate Consumption on Energy, Gut Microbiota, and Stress-Related Metabolism in Free-Living Subjects. Journal of Proteome Research, 2009

Mather, M., N. R. Lighthall. Risk and Reward Are Processed Differently in Decisions Made Under Stress. Current Directions in Psychological Science, 2012; 21 (1): 36.

Mather, Mara, Nichole R. Lighthall, Lin Nga, Marissa A. Gorlick. Sex differences in how stress affects brain activity during face viewing. NeuroReport, 2010; 21 (14): 933.

Medeiros, Philip J., Baraa K. Al-Khazraji, Nicole M. Novielli, Lynne M. Postovit, Ann F. Chambers, Dwayne N. Jackson. Neuropeptide Y stimulates proliferation and migration in the 4T1 breast cancer cell line. International Journal of Cancer, 2011

Medical College of Georgia (2010, February 10). Early life stress may predict cardiovascular disease.

O’Donovan, Aoife. Janet Tomiyama, Jue Lin, Eli Puterman, Nancy E. Adler, Margaret Kemeny, Owen M. Wolkowitz, Elizabeth H. Blackburn, Elissa S. Epel. Stress appraisals and cellular aging: A key role for anticipatory threat in the relationship between psychological stress and telomere length. Brain, Behavior, and Immunity, 2012

Porcelli et al. Acute Stress Modulates Risk Taking in Financial Decision Making. Psychological Science, 2009; 20 (3): 278.

Robert A. Rissman,  Michael A. Staup,  Allyson Roe Lee, Nicholas J. Justice,  Kenner C. Rice,  Wylie Vale,  and Paul E. Sawchenko. Corticotropin-releasing factor receptor-dependent effects of repeated stress on tau phosphorylation, solubility, and aggregation. Proceedings of the National Academy of Sciences, 2012

Stojanovich L, Marisavljevich, D.. Stress as a trigger of autoimmune disease. Autoimmun Rev. 2008 Jan;7(3):209-13. Epub 2007 Nov 29.

Thomas, Ayanna T, Dubois,  Stacey J.. Reducing the Burden of Stereotype Threat Eliminates Age Differences in Memory Distortion. Psychological Science, 2011.

Ulrich-Lai, Y. M., A. M. Christiansen, M. M. Ostrander, A. A. Jones, K. R. Jones, D. C. Choi, E. G. Krause, N. K. Evanson, A. R. Furay, J. F. Davis, M. B. Solomon, A. D. de Kloet, K. L. Tamashiro, R. R. Sakai, R. J. Seeley, S. C. Woods, J. P. Herman. Pleasurable behaviors reduce stress via brain reward pathways. Proceedings of the National Academy of Sciences, 2010

von Dawans, B., Fischbacher, U., Kirschbaum, C., Fehr, E., & Heinrichs, M. The social dimension of stress reactivity: Acute stress increases prosocial behavior in humans. Psychological Science, 2012.

Wikgren, Mikael,  Martin Maripuu, Thomas Karlsson, Katarina Nordfjäll, Jan Bergdahl, Johan Hultdin, Jurgen Del-Favero, Göran Roos, Lars-Göran Nilsson, Rolf Adolfsson, Karl-Fredrik Norrback. Short Telomeres in Depression and the General Population Are Associated with a Hypocortisolemic State. Biological Psychiatry, 2011

Yau, J. L. W., Noble, J.,  Seckl, J. R.. 11 -Hydroxysteroid Dehydrogenase Type 1 Deficiency Prevents Memory Deficits with Aging by Switching from Glucocorticoid Receptor to Mineralocorticoid Receptor-Mediated Cognitive Control. Journal of Neuroscience, 2011; 31 (11): 4188.

Zanto et al. Predictive knowledge of stimulus relevance does not influence top-down suppression of irrelevant information in older adults. Cortex, 2010; 46 (4): 564.