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Stress Management – The Bright Side

As we come closer to the end of this semester, we reflect on what we have learned throughout it. We know that stress affects our health negatively in a variety of ways and we know that many of us are experience stressors on a daily basis.  What we learn from the readings assigned this week is that we can always find healthy ways to cope with the stress we face in our everyday lives and reveres the negative effects of stress.

In his chapter, Sapolsky begins by telling us there is hope. Sapolsky discusses many stress reduction techniques, including exercise. Exercising is, of course, great for your body, through a variety of ways. We know that it decreases our chance of getting cardiovascular diseases, on top of that it generally makes us feel good about ourselves, putting us in a positive mood. I can definitely speak to this statement. During my first year of graduate school, I would much rather be working for an hour than go to the gym for an hour.  By the end of the year, I had gained a weight and also just felt horrible about myself. Sure I did great in my classes and learned so much in a year, but I begin to realize I shouldn’t just be improving my mind, but my body as well.  I had been doing my body an injustice by ignoring it for so long. So starting this semester, I decided to begin working out 3-5 times a week for one hour. Now, after two months of following this routine (not perfectly, I’ll admit, but I do workout every week!), I can say I feel much better about myself. Additionally, I feel less stressed than last year and can’t imagine skipping a whole week of working out. Not only does Sapolsky suggest exercise decreases stress and increases our mood, but there are many studies to back up his claim. For example, a study conducted by Von Haaren and colleagues (2015) examined if a 20-week aerobic exercise intervention (AET) can be used as a preventative measure to improve emotional stress reactivity during finals for previously inactive students. The study was designed to have inactive students assigned to either a waitlist or AET group. Pre-intervention baseline was taken at the beginning of the semester and every two days students reported their perceived stress. Lastly, a post-intervention assessment was tested during final exam period. The researchers found AET was beneficial on emotional stress reactivity, thus AET could be a strategy used to prevent the negative health outcomes of extreme stress for students (Von Haaren, et al., 2015).

On top of working out, another popular way of reducing stress is through mindfulness. Something that I personally have never done, mindfulness is meant to have the individual pay attention to themselves in a way that allows them to be in the present moment, without judgment. While therapists have used mindfulness-based cognitive behavioral therapy and stress reduction (MBCT/MBSR), little research has been focused on understanding whether mindfulness can be used for individuals with comorbid physical and psychological disorders. A recent review conducted by Alsubaie and colleagues (2017) sought to answer this question. Their review revealed that not enough research has been conducted to understand the mechanisms of change with MCBT/MBSR in those with physical conditions, such as chronic pain, compared to psychological conditions such as anxiety or depression. However, in regard to psychological conditions, MBCT/MBSR seem to have a mediating effect. This study highlights the need for more research on the topic of physical conditions (Alsubaie, et al., 2017).

Additionally, we learn that a change in behavior can help us cope with stressors. A study conducted by Evers and colleagues (2006) found that individualized transtheoretical model (TTM) – tailored interventions that were meant to increase stress management skills worked such that those in the treatment group who completed the study had significantly increased their stress-management skills and were able to significantly reduce stress more than the control group (Evers et al., 2006). Thus, we see that TTM-tailored interventions have been shown to be successful.

Thankfully, all this research has been conducted for us and has provided us some idea of how to successfully manage stress, or prevent the negative health outcomes from it. I’ve taken one step in reducing my stress by using exercise, but I am becoming more and more intrigued by mindfulness training and hope to learn the practice one day.


Stress Management I – The Bad

After a long week of being a graduate student, there is nothing I like doing more than grabbing some drinks with a group of friends. While most Americans do this every so often there comes a point where this behavior begins to spiral out of control. Some individuals might no longer go out once a month, but it may escalate to once a week, escalating even further to grabbing a drink every day. Also, in most cases, the amount of drinks consumed do not stop at one but can increase to five or even ten drinks. An even scarier idea is that graduate students are not the only ones that could be using substances to cope with stress. Adolescents and college students are turning to the bottle, more so than individuals their same age that are not attending college (Substance Abuse and Mental Health Services Administration, 2015).  So why is it that those who tend to be under more stress turn to substances such as alcohol?

In order to answer this question, we first need to understand the underlying neurological mechanisms that guide the pleasure we receive when using such substances. Sapolsky (2004) does a great job taking us through the neurochemistry of pleasure. To no surprise, we learn that the pleasure pathway is really guided by the neurotransmitter dopamine. The ventral tegmentum area (VTA) and nucleus accumbens (NaCC)  are important brain regions in dopaminergic projection. From the VTA and NaCC, dopamine will then project to the frontal cortex, anterior cingulate cortex, and amygdala, which will ultimately affect our behaviors. It is this pleasure pathway, in particular, that is affected by substance abuse. For example, when an individual becomes addicted to a substance, they will develop tolerance to that substance. This happens because when the substance is inside the body, dopamine (depending on which drug) begins pouring out of cells a thousand times more than normal. The neurons receiving the dopamine are not used to receiving so much of the neurotransmitter at once so they begin to become less sensitive to dopamine. So, in order for an individual to feel that same high that they did when they first tried the drug, they need more of it. Thus, an endless cycle of desensitizing your neurons every time you use, happens. Throughout Sapolsky’s chapter, there are many references to studies using rats that show stress increases the likelihood of self-administering a drug. Not only does stress increase the odds of abusing a drug, it can also make withdrawal worse, and relapse a lot more likely if an individual were to quite (Sapolsky, 2004). So now that we have a general idea of the pathways responsible for addiction, we can come back to contemplate why substance use happens more often in certain populations than others.

Hoffmann (2016) sought to understand the theoretical pathway that guides the increase or decrease of substance use across one of the most important stages of life, adolescence to early adulthood. A key theory Hoffmann had regarding why adolescence may be more prone to taking substances is the idea that many stressful life events happen over this already stressful time period that may drive an adolescent to use substances in order to cope with such stressful events. In other words, the cumulation of stressful events can increase the likelihood of substance use in the future. There are theoretical frameworks that bolster Hoffman’s hypothesis, such that adolescents may be more sensitive to what they perceive as stressful situations (Agnew, 1997). While the author provides clear reasoning behind his hypothesis, the results presented in the article showed that for some adolescent users, it was not the cumulative stress itself that drove these individuals to use, but the combination of stress and peer substance use (Hoffmann, 2016).

Another important group that has been shown to be more prone to using substances to cope with experiencing an extremely stressful event are those with posttraumatic stress disorder (PTSD). Unfortunately, we are seeing that close to half of the men and women who meet the criteria for lifetime PTSD will have a substance use disorder. While those with PTSD think using substances will help them “cope” with their PTSD, using substances does the exact opposite. Substance use increases symptoms of PTSD and is a predictor of poorer treatment response (Ouimette, Finney, & Moos, 1999). Bowen, De Boer, and Bergman (2017) focused on understanding if mindfulness played a mediating role in the relationship between PTSD symptoms and how dependent individuals were on substances. The authors found that those who showed greater PTSD symptom severity had lower levels of mindfulness which increased the severity of substance dependence (Bowen, De Boer, & Bergman, 2017).

So while we are all stressed out, there are always better ways to cope with the stress. For example, while I like drinking with my friends to release stress, it may be better that instead of drinking we could play sports together or play video games together. By improving the way we manage our stress, we lower our chances of developing unhealthy coping habits (Lipschitz, Paiva, Redding, Butterworth, a& Prochaska, 2015).


Agnew, R. (1997). Stability and change over the life course: A strain theory explanation.In T. P. Thornberry (Ed.), Developmental theories of crime and delinquency (pp. 101-132). New Brunswick, NJ: Transaction Publishers.

Bowen, S., De Boer, D., & Bergman, A.L. (2017). The role of mindfulness as approach-based coping the the PTSD-substance abuse cycle. Addictive Behaviors, 64, 212-216.

Hoffman, J.P. (2016). Cumulative stress and substance use from early adolescence to emerging adulthood. Journal of Drug Issues, 46(3), 267-288.

Lipschitz, J.M., Paiva, A.I., Redding, C.A., Butterworth, S., and Prochaska, J.O. (2015). Co-occurrence and coaction of stress management with other health risk behaviors. Journal of Health Psychology. 20(7), 1002-1012.

Ouimette, P.C., Finney, J. W., & Moos, R.H. (1999). Two-year posttreatment functioning and coping of substance abuse patients with posttraumatic stress disorder. Psychology of Addictive Behaviors, 13(2), 105-114.

Sapolsky, R.M. (2004) Why zebras don’t get ulcers: A guide to stress, stress related diseases, and coping. New York: W.H. Freeman.

Substance Abuse and Mental Health Services Administration (SAMHSA). 2015 National Survey on Drug Use and Health (NSDUH). Table 6.84B—Tobacco Product and Alcohol Use in Past Month among Persons Aged 18 to 22, by College Enrollment Status: Percentages, 2014 and 2015. Available at:

Geopolitical World

Personally, when the presidential election was unfolding last year, I had no desire to watch any debates or to listen to any candidates stance on anything. In fact, I did not even vote in this past election. I mostly use the excuse that I never received my out of state voting slip from Texas and since I am not a Massachusetts resident I could not vote here. But honestly, I did not care to vote. I did not care that my slip never arrived, and my vote probably would not have made a difference. I do not really care about politics at all, for many reasons. The most important reason for me is the stress that comes with worrying about how our country is being run. I am stressed out already by so many things, if I can prevent more stress, I will. There was a time that I used to think of changing my ways and maybe giving more of my attention to learning about the individuals who run our country and what their values are. However, after living with my roommate for a year, I saw how this knowledge could be detrimental. For example, my roommate is a hardcore democrat, feminist, social rights activist, etc. She has hardcore beliefs that define the person she is. While this does not bother me at all, it does bother me how this past presidential election drove her crazy. When she found out Trump was our next President she literally could not go to work for days after. Me, on the other hand, was shocked with the outcome but did not let it hinder my ability to get my work done.

Our readings this week really sought to understand how politics can affect our stress levels for the group of people that lose. Specifically, one study by Trawalter and colleagues (2011) examined physiological stress responses to the 2008 presidential election and wanted to measure if this physiological stress responses change in part by individuals levels of social dominance orientation (SDO). SDO is the measurement of how much an individual supports the hierarchical arrangement in the US, were racial minority groups are at the bottom, while Whites are at the top. Their results showed that individuals with higher SDO exhibited higher cortisol values post-election, amongst other findings (Trawalter, Chung, DeSantis, Simon, & Adam, 2011). This study is just one that shows how politics can affect our cortisol levels for the worse. While this study was conducted on the election Obama won, one study was conducted on the past election. Majumder and colleagues (2017) used surveys to better understand the risk factors associated with pre and post-election stress in the US. While a majority of Republicans were devastated with Obama’s win, I doubt they were as upset as Democrats were this past election. The authors’ results found women were more likely to score higher on stress related to the election than men. Additionally, the authors found many other factors that could contribute to election-related stressors (Majumder, Nguyen, Sacco, Mahan, & Brownstein, 2017).  While these studies provide evidence of the detriments politics can have on our health, terrorism can also have a great effect on both our mental and physical health.

There is no doubt that both domestic and foreign terrorism affect the US in many ways. A review conducted by Garfin & Holman (2016), presented evidence of both indirect and direct consequences of experiencing a traumatic event on our both mental and physical health. These consequences include developing posttraumatic stress disorder (PTSD) as well as posttraumatic symptoms (PTS). Additionally, a number of negative life events that occur before a terrorist attack, may influence how we respond to the attack (Garfin & Holman, 2016). Lastly, a study conducted by Strand and colleagues (2016) showed that there was a greater increase of health outcomes during the first four weeks after a terrorist attack in Norway (Strand et al., 2016). Taken together, this information can help guide how we can improve our mental and physical health in order to prevent the detrimental effects of terrorism.



This week we discuss some downfalls of being in a society where technology now rules everything. While this might be exciting, it also presents downfalls. I remember when I started working in my social/cognitive lab back at UTEP the graduate student I was working with told me that every time I get an email from him, I had to respond to him within 24-hours. Of course, I took him too seriously and responded to him right away every time he emailed me. A habit that I still have. Every time my advisor emails me (or anyone for that matter, even the students I TA) I always have to respond to them as soon as I see their email, even if that means responding at 2 in the morning. There are many reasons for this. For one thing, I get a feeling of guilt if I read an email and do not respond because I feel as though somehow they know that I’ve read the email. Secondly, if I don’t respond to an email I have anxiety and start to just think about the email until I respond to it. Same thing happens if my advisor gives me a task to do. Even if I am running errands or shopping, if Lisa emails me to do something I drop everything I am doing to do it because if I put it off I feel anxiety.

This very thing is discussed in an article by Ayyagari, Grover, and Purvis (2011) where their aim was to develop a model of technostress – the inability to cope or deal with information and communication technologies in a healthy way, a term created by a clinical psychologist named Craig Brod – that would allow us to understand the relationship between technology and stressors that arise from it. In their article, they outline many characteristics that could make technology stressful to use.  One such characteristic is usability. Is the technology being used at a company easy to manage? Is it easy to use by anyone or do you need extra training to learn how to use the software? The authors state that because of some constraints that are placed on businesses, employees have to use the software they are given making them unable to use a software they are used to or that makes their lives easier. Secondly, there are intrusive characteristics, were work-home conflict arises. Since we have email at our fingertips, we may now no longer be able to keep our work in the office, putting a burden not just on ourselves, but our families as well. Lastly, we have dynamic characteristics which present problems such as job insecurity. With growing technology, many people’s jobs might be in danger because it might be cheaper using technology. This study was important in detangling which of these characteristics lead to stress in one’s life. Their results found that pretty much all characteristics described in the paper were significant besides the perception of technology as being an invasion of privacy (Ayyagri, Grover, & Purvis, 2011).

Furthermore, given that social media outlets are so popular, many studies have sought to understand if outlets, such as Facebook, leads to negative mental health outcomes such as depression and anxiety. Many studies have already been conducted on this issue, but there have been many inconsistencies in the literature. Therefore, Frost and Rickwood (2017) conducted a meta-analysis to try and find a clear-cut answer to how Facebook affects mental health. Overall, their results showed that Facebook did, in varying degrees, affect anxiety, depression, body image and disordered eating, drinking cognitions, and alcohol use. Additionally, this meta-analysis discusses how Facebook addiction can have detrimental outcomes for individual’s mental health (Frost & Rickwood, 2017). This meta-analysis really opened my eyes to the potential detrimental effects that are associated with Facebook use and really made me analyze the reasons that make me open the app on my phone. While I do not think I am addicted to Facebook, I do have it at my fingertips and anytime I need a break from work I open up the app, it passes the time more than anything for me.

Lastly, while we review some detriments that could be attributed to technology, there are also some useful ways in which technology can help us with research collection. An article by Kirchner & Shiffman (2016) discusses how ecological momentary assessment methodologies can be used to study individuals’ experience and how their environmental surroundings contribute to their experiences. By combining both geographically momentary assessment with ecological momentary assessment, researchers are able to use multi-level sources of information form neighborhood conditions to understand subjective experiences. This is beneficial, in order to learn how to protect neighborhoods against substance misuse and other mental health problems (Kirchner & Shiffman, 2016).

Intergroup Contexts

This week we seek to understand the stress response in individuals who are faced with prejudices, interracial contact, and health disparities. We learn that interracial interaction can produce an increased stress response in white individuals with high external motivation (Trawalter, 2011). Additionally, there are many health disparities associated with being a stigmatized group. Furthermore, we learn that individuals who are at the lower SES have much more problems than individuals on the higher end of the SES spectrum. Sadly to say, it was not until I moved from my world in El Paso that I noticed these disparities around me.

Growing up in a city that is 80% Hispanic and 96% Spanish speaking, I never really experienced or witnessed prejudice. Additionally, El Paso is one of the cheapest cities to live in with the average income being $45,000, so while there were some individuals that were rich in our city, a majority of the people I interacted with were on the low end of the SES. Living in El Paso is kinda like living with a huge family where everyone knows the struggle of making money or being Hispanic (although there really was no stress associated with being Hispanic since we all were!). It was not until I interned at UT Austin when I noticed the differences in interracial interactions and SES. I made an observation one day when eating at a restaurant called Odd Duck. It was a tapas restaurant where small portions were served with a very large bill attached to them (I would have never chosen this restaurant to eat at, but I had no choice). While eating at the restaurant I noticed a majority of the people there were white and old. We left and passed a McDonalds where I saw many African Americans going in and out of. This was the first time I noticed what everyone else in the US talked about, White privilege. It saddens me that it took me so long to acknowledge such a problem was actually in the US because I was shielded by it all in my little piece of heaven where it normally doesn’t happen. So reading the articles this week that sought to understand how these disadvantages stigmatized groups face could lead to health disparities/problems made me look back at that experience.

In the Sapolsky chapter, there is a section that discusses socioeconomic status, stress, and disease where he describes how being on the lower end of the SES have increased health disparities such as increased glucocorticoids, increased stress-related diseases and lack of options to make your life better. While we weren’t dirt poor, my dad was the only one that worked in my family. Even though we lived in one of the cheapest cities in the US, having three kids and a wife to be financially responsible for still made money very tight. My parents also never attended college, so the job my dad had didn’t pay well at all and was actually very dangerous. I remember the constant stress my dad was under when he constantly wondered how he was going to pay the mortgage while also getting things my brothers and I wanted on top of having to work in a career he hated but didn’t have a choice but to stay in. We were never able to take family vacations to exotic places every year and we never had savings – ever. So when one of us got sick we never wanted to go to the doctor because we didn’t want to have another bill my dad had to find a way to pay. Reading this chapter really made me analyze how it was like growing up because of our situation and how that made me the person I am today.

In the event that my family or I needed to go to the doctors, I noticed how difficult it would be for the doctors to treat the patients who only spoke Spanish.  This doctor-patient interaction is discussed in the article by Major, Mendes, & Dovidio (2013). Specifically, the paper goes on to say that medical care professionals who treat patients from a disadvantaged group tend to be less effective and less helpful for that member in the disadvantaged group (Major, Mendes, & Dovidio, 2013). I can see how this is true when the doctor who is treating patients that only speak Spanish would have a hard time talking to patients in depth about their diagnoses when the doctor doesn’t know how to even explain the patient’s symptoms in another language, upon other things. Additionally, I can see how it can be hard for doctors to have concerns about appearing prejudice when speaking to Mexican individuals. They might try to talk slowly or in simple terms, making them seem prejudiced. This phenomenon is talked about extensively in the Trawalter and colleagues (2011) article where they conducted two experiments to determine whether individual’s concerns about appearing prejudiced would lead to an increased stress response during interracial contact. The first study showed that there was an increase stress response during these interactions in individuals with high external motivation (a high motivation to respond without prejudiced) as measured by cortisol. Study 2 sought to understand if this interaction was a chronic stressor and would change the cortisol response days after the interracial interaction. Studying cortisol awakening response, the authors found the psychological stress that was brought on by interracial interaction was still present days later for high external motivation individuals (Trawalter, Adam, Chase-Lansdale, & Richeson, 2011).

Besides looking at cortisol, studies are currently examining Telomere length as well to evaluate Worldview Verification Theory that is the inconsistency in a preexisting expectation of justice and a personal experience of injustice can the stress response in racial minorities (Lucas et al., 2017). The use of biological measures of stress response will hopefully help the general population understand the struggles individuals from diverse populations face.


Lucas, T., Pierce, J., Lumley, M.A., Granger, D.A., Lin, J., & Epel, E.S. (2017). Telomere length and procedural justice predict stress reactivity responses to unfair outcomes in African Americans. Psychoneuroendocrinology, 86, 104-109.

Major, B., Mendes, W.B., & Dovidio, J.F. (2013). Intergroup relations and health disparities: A social psychological perspective. Health Psychology, 32(5), 514-524.

Sapolsky, R.M. (2004) Why zebras don’t get ulcers: A guide to stress, stress related diseases, and coping. New York: W.H. Freeman.

Trawalter, S., Adam, E.K., Chase-Lansdale, L.P., & Richeson, J.A. (2012). Concerns about appearing prejudiced get under the skin: Stress responses to interracial contact int he moment and across time. Journal of Experimental Social Psychology, 48, 682-693.

Traumatic Stress

This week we discuss my favorite topic and personal passion: traumatic stress. There is no way we can discuss traumatic stress without discussing the disorder that may develop after experiencing such stress – Post-Traumatic Stress Disorder (PTSD). PTSD is now listed under the Trauma and Stress-related disorders in the DSM-5. In order for an individual to meet DSM-5 criteria for PTSD, they need to have experienced a traumatic event in which they were exposed to death, threatened death, natural disasters, and other events. Additionally, an individual needs to have experienced a certain amount of symptoms in each of the four symptom clusters. These symptoms clusters include intrusion symptoms, avoidance symptoms, negative alterations in cognitions and mood, and alterations in arousal and reactivity. Lastly, all symptoms must be present for at least one month and cause significant distress or functional impairment (APA, 2013).

Close to 75% of the general population will experience a traumatic event at least once in their lifetime (Breslau and Kessler, 2001). However, only 8% of the general population will go on to develop PTSD after experiencing a traumatic event (Kessler et al., 2005). Much research has been conducted to understand why some people are more susceptible to developing the disorder than others. A review conducted by Yehuda and LeDoux (2007) examined risk factors for developing PTSD, brain structures that are important in the disorder, altered fear processing and regulation, and genetics. In this review, we learn that interpersonal violence as compared to other traumatic events is more potent stressors. Additionally, we learn the neurological mechanisms that underlie the disorder. The hippocampus plays a role in memory processes and contextual fear conditioning (Shin, 2006) and is smaller in individuals with PTSD. Additionally, the amygdala is important in the acquisition and expression of conditioned fear, while the prefrontal cortex is important in inhibiting the amygdala’s response to conditioned fear when appropriate too. In PTSD, it seems there is an inability for the prefrontal cortical structures to inhibit the amygdala from responding to conditioned associations, leading to many of the symptoms associated with the disorder.

While having the disorder alone can be debilitating, many impairments also stem from having the disorder. The general public and veterans with PTSD are more prone to developing health problems such as obesity, hypertension, and heart disease (Kibler et al. 2008; Cohen et al. 2009b). We delve more into this topic in two readings this week. The first, a review (meta-analysis-ish) that discusses physical activity and eating disorders in relation to the disorder written by Hall and colleagues (2014). In this review, we learn that in regard to physical activity, some studies state that there is a decrease of activity in PTSD, while other studies report no differences. Furthermore, there is also mixed findings for inactivity in PTSD. Some studies have found that an increase in PTSD symptoms leads to a decrease in physical activity.  This review also examines PTSD and eating behaviors, specifically if PTSD was a predictor of eating disorders. Some studies have shown a higher prevalence of PTSD symptoms in women who engaged in binge eating, those with PTSD are more likely to eat fast food and drink soda and eat fewer servings of fruit in a day. In all, this review provides a large amount of information on the relationship between PTSD and physical activity/eating habits. However, the studies presented show much inconsistency and mixed findings that it is hard to make a conclusion with such data.

A study conducted by Kubzansky and colleagues in 2014 examined if PTSD alters the trajectory of weight gain in a sample of women. To do this, the authors had women who were originally a part of an ongoing prospective study of female registered nurses, complete the Trauma and PTSD Screening Questionnaire (a retrospective measure) was used to determine which women would be eligible to take part in the study and when trauma exposure/PTSD occurred. In order to assess trauma and PTSD, the authors used a variety of retrospective measures. Additionally, they asked women to report their weight biennially. Ultimately, the author’s results showed that symptoms of PTSD were associated with faster weight gain and increased risk of obesity in women.

The way I would like to end this post is with some implications. Schnurr (2015) brings up many important implications in her article that discuss how traumatic exposure can lead to physical health decline. When speaking to research, she stresses the importance of integrating efforts to reduce health risk behaviors with treatment. For example, we can start using exercise in addition to cognitive behavioral treatment in order to reduce obesity rate and PTSD symptoms in the disorder. Additionally, many clinicians need to read the research that is out there on physical health and PTSD in order to shape treatment to the individual patient. Lastly, as a whole, we need to be aware of how traumatic exposure can affect individuals differently. For example, the current events in Las Vegas have left many people in attendance traumatized. We as a society should do everything we can to make sure the individuals who experienced the event are mentally well taken care of. Most people experience a traumatic event and do not talk about the event for months, increasing their likelihood of developing symptoms of the disorder. Clinicians and others should make sure to make themselves available for such publicised traumatic events.


American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders : DSM-5(5th ed.). Arlington, VA: American Psychiatric Association.

Bresleu, N., and Kessler, R.C. (2001). The stressor criterion in DSM-IV posttraumatic stress disorder: an empirical investigation. Biol. Psychiatry, 50, 699-704.

Cohen, B.E., Marmar, C., Ren, L., Bertenthal, D., and Seal, K.H. (2009b). Association of cardiovascular risk factors with mental health diagnoses in Iraq and Afghanistan war veterans using VA health care. JAMA, 302, 489-491.

Hall, K.S., Hoerster, K.D., and Yancy, W.S. (2015). Post-traumatic stress disorder, physical activity, and eating behaviors. Epidemiologic Reviews, 37, 103-115.

Kessler, R.C., Chiu, W.T., Demier, O., and Walters, E.E. (2005). Prevalence, severity, and comorbidity of twelve-month DSM-IV disorders in the National Comorbidity Survey Replication (NCS-R). Arch. Gen. Psychiatry, 62, 617-627.

Kibler, J.L., Joshi, K., and Ma, M. (2008). Hypertension in relation to posttraumatic stress disorder and depression in the US National Comorbidity SurBehavioralioral Medicine, 34, 125-131.

Kubzansky, L.D., Bordelois, P., Jin Jun, H., Roberts, A.L., Cerda, M., Bluestone, N., Koenen, K.C. (2014). The weight of traumatic stress a prospective study of posttraumtic stress disorder symptoms and weight status in women. JAMA Psychiatry, 71(1), 44-51.

Schnurr, P.P. (2015). Understanding pathways from traumatic exposure to physical health. Evidence Based Treatments for Trauma-Related Psychological Diosrders: A Practical Guide for Clinicians. U. Schnyder, M. Cloitre (eds.).

Shin, L.M., Rauch, S.L., and Pitman, R.K. (2006). Amygdala, medial prefrontal cortex, and hippocampal function in PTSD. Ann. N.Y. Acad. Sci., 1071, 67-79.

Yehuda, R., and Ledoux, J. (2007). Response variation following trauma: A translational neuroscience approach to understanding PTSD. Neuron, 56, 19-32.

Immunity, Stress, and Disease

Many of us are stressed in our everyday lives and while we know stress can take a toll on our bodies, it is surprising how much stress can affect our ability to fight off diseases. This week we are focusing on how stress can affect our immunity and ultimately increase our susceptibility to disease. While much research has been conducted on the topic, it is quite surprising that definitive answers have yet to be found. We discuss how stress can affect our immune system thus leading to susceptibility to developing the common cold, as well as how other diseases may or may not be easier to develop because of stress.

In Chapter 8 of Sapolsky’s book: Why Zebras Don’t Get Ulcers (2004) we are given an introduction to how our immune system works. We know through our middle school science courses that our immune system is supposed to attack things that are foreign to our body while ignoring the cells our bodies produce. While this sounds easy, our immune system is actually quite complicated. From this chapter we learn that are immune defenses are lead by cells that circulate throughout our bodies called lymphocytes and monocytes (white blood cells). Specifically, there are T and B cells that work together in different ways to fight off infectious diseases. In some cases, T cells especially will fail to extinguish foreign invaders from our own healthy cells leading to autoimmune diseases or they may fight against objects that are ingested or touched such as allergens. From this chapter, we begin to understand the details of how our immune system works, but now we want to focus on how stress can affect our immune system and lead to the potential development of diseases. When an individual is stressed they will fail to form new lymphocytes and the lymphocytes that are currently circulating in their bodies will have a short life. They will be unable to create new antibodies when they get in contact with something infectious and there will no longer be communication among lymphocytes causing havoc, all caused by the increase of glucocorticoids in our system. So while we know how stress can affect the immune response, questions that spark our interests currently are whether or not stress makes us more susceptible to developing illnesses such as cancer, the common cold, and depression.

There has been a great number of studies that have sought to answer the question proposed above. One such study was conducted by Cohen and Colleagues (2012) to determine how chronic stress may make an individual susceptible to developing the common cold.  They answered this question in two separate studies. The first study assessed stressful life events and glucocorticoid receptor resistance (GCR). GCR refers to the lack of sensitivity immune cells have to glucocorticoid hormones that are designed to stop inflammatory response. The results of their first study found that stressed individuals had a greater risk for developing a common cold. This is caused by the interference by GCR with the HPA down-regulation of pro-inflammatory cytokine is released in response to an infectious agent. Study 2 sought to use the measurement of GCR as a predictor for how much local pro-inflammatory cytokine was produced in response to an infection. Their results showed that greater GCR predicted production of more local pro-inflammatory cytokines in individuals with the common cold. This data suggests that dealing with prolonged stress can result in GCR which interferes with the regulation of inflammation which makes individuals susceptible to developing the common cold (Cohen et al., 2012). Additionally, a review paper by Hodes and colleagues (2015) discuss how elevated pro-inflammatory cytokines circulating throughout our bodies that increase leukocytes can contribute to development and maintenance of depression (Hodes, Kana, Menard, Merad, and Russo, 2015).

Lastly, there is a false concept that increased stress can lead to the development of cancer. While there are many animal studies that show stress can, in fact, increase tumor sizes, there are many studies that find no association between stress and cancer. One of those studies was conducted by Shoemaker and colleagues (2016) that sought to understand whether the frequency of stress and adverse life events had anything to do with the risk of developing breast cancer. This study is unique in that they used a cohort of 106,000 women from the United Kingdom. From these women, they gathered breast cancer diagnoses every 3 years as well as any stressful or adverse life events. Their results showed there to be no association of breast cancer risk with the overall frequency of stress. To many, these results may seem surprising which is understandable. In his chapter, Sapolsky explains many ways stress can attribute to tumor growth and development and he discusses why some studies that do show associations between stressful life events and cancer could be false because of their retrospective aspect. However, even in the discussion, Shoemaker and colleagues (2016) do not provide a concrete reason for their results (Shoemaker et al., 2016).

Together these articles and book chapter help us understand how stress can affect our bodies in more ways than one. One question I have been contemplating that has yet to be answered is how other stressors such as working out can impact our susceptibility to developing diseases? Is the stress we put our bodies through while working out the same physiologically to losing a loved one?


Cohen, S., Janicki-Deverts, D., Doyle, W.J., Miller, G.E., Frank, E., Rabin, B.S., & Turner, R.B. (2012) Chronic stress, glucocorticoid receptor resistance inflammation, and disease risk. PNAS, 109(16), 5995-5999.

Hodes, G.E., Kana, V., Menard, C., Merad, M., & Russo, S.J. (2015). Neuroimmune mechanisms of depression. Nature Neuroscience, 18(10), 1386-1393.

Sapolsky, R.M. (2004) Why zebras don’t get ulcers: A guide to stress, stress related diseases, and coping. New York: W.H. Freeman.

Shoemaker, M.J., Jones, M.E., Wright, L.B., Griffin, J., McFadden, E., Ashworth, A., & Swerdlow, A.J. (2016). Psychological stress, adverse lfie events and breast cancer incidence: a cohort investigation in 106,000 women in the United Kingdom. Breast Cancer Research, 18(72).

Metabolism, Nutrition, & Health Decision Making

In Chapter 4, Sapolsky (2004) yet again explains a complicated process in the simplest way. Specifically, he uses an analogy to describe how our bodies work throughout the chapter, but what I liked most from this read was his discussion of both juvenile and adult diabetes. As an undergraduate, I worked in a behavioral neuroscience laboratory where we focused on understanding the neural mechanisms that mediate addiction to drugs of abuse, such as nicotine. We wanted to uncover why close to 20% of diabetic individuals continue to smoke and have a harder time staying smoke-free when trying to stop. To answer this question, we injected rats with a drug called Streptozotocin (STZ). In humans, this drug is used to treat pancreatic cancer, but in rats, can destroy the insulin-producing beta cells in the pancreas to stop the production of insulin altogether. While I was reading the chapter, it reminded me that when we would explain our research in posters/publications we would always state that using STZ to induce diabetes was modeling Type 1 diabetes or an advanced form of Type 2 diabetes. As an undergrad, I just nodded my head in agreement, but it was not until reading Sapolsky’s article (sadly, I guess) that I understood what this phrase meant. Type 1 insulin-dependent diabetes is pretty easy to understand. Your body attacks the insulin-producing cells in the pancreas, which is pretty much what STZ does, but what I did not know was that in an individual with type 2 diabetes can go on to develop Type 1 diabetes because of all the damage they put their pancreas through. In the end, our study found that diabetic rats showed enhanced rewarding effects from nicotine and enhanced withdrawal effects from the drug. Thus, it may be that humans who are diabetic and who smoke are finding cigarettes more rewarding and when trying to quit smoking, have enhanced withdrawal effects to the drug as well. While this information was rewarding because we may have found the underlying mechanisms mediating diabetic smokers behaviors, we still need to find a way to encourage these individuals to quit smoking. The review article by Magnan, Shorey Fennell, and Brady (2017) may help us in doing so. In their article, they describe different social cognitive models of health behaviors and introduce cognitive-based models that describe how different individuals would react in certain situations. I wonder whether one of these models would be better than the other in deterring diabetic smokers to change their smoking behavior. My gut is leaning me towards the Social Cognitive Theory proposed by Bandura because it emphasizes an interaction between the individual and the environment (Magnan, Shorey Fennell, & Brady, 2017). Back in the 1950’s everyone smoked. They smoked in buildings including schools, offices, you name it. Today, because of the damaging effects of smoking cigarettes, no one smokes. I’ve heard some people say even smelling smoke is revolting to them. Additionally, many places do not let you smoke even close to their building. Because of these perceived personal, social, and environmental obstacles, I feel as though this model would push such individuals to change their smoking habits.

Additionally, continuing with the theme of addiction, Finch & Tomiyama (2014) make the point to emphasize how stress-induced eating can activate the neural reward circuitry just as other addictions such as smoking can. Unfortunately, as outlined in their paper, repeatedly indulging in stress-induced eating leads to the accumulation of visceral fat brought on by the increase in glucocorticoids and insulin (Finch & Tomiyama, 2014). I would definitely say that I experienced this during my first year of graduate school when I put on close to 20 lbs. of fat because, without noticing, I would eat when not hungry and eat when stressfully preparing for my stats quizzes/finals. Furthermore, the meals that I decided to indulge in during these stressful times were high in fats. Kecolt-Glaser et al. (2015) sought to understand the impact daily stressors and previous history of depression had on the metabolic responses to different high-fat diets. They found that individuals who experience a greater amount of stressors the day before eating a high-fat meal had decreased energy after consuming the meal. Furthermore, greater stressors were also associated with lower fat oxidation and higher insulin production which enhances fat storage (Kecolt-Glaser et al., 2015). Thus, there should be many things we think about before we make the decision to eat a high-fat meal. Sure, eating some high-fat diet meals aren’t going to kill us (immediately), but it is definitely all about variety.

Finch, L.E., & Tomiyama, A.J. (2014). Stress-induced eating dampens physiological and behavioral stress responses. Nutrition in the Prevention and Treatment of Abdominal Obesity. Elsevier Inc.

Kiecolt-Glaser, J.K., Habash, D.L., Fagundes, C.., Andridge, R., Peng, J., Malarkey, W.B., and Belury, M.A. (2015). Daily stressors, past depression, and metabolic responses to high-fat meals: a novel path to obesity. Biological Psychiatry, 77, 653-660.

Magnan, R.E., Shorey Fennell, B.R., Brady, J.M. (2017). Health decision making and behavior: the role of affect-laden constructs. Soc Personal Psychol Compass, 11, e12333.

Sapolsky, R.M. (2004) Why zebras don’t get ulcers: A guide to stress, stress related diseases, and coping. New York: W.H. Freeman.

CVD and Stess

In chapter three of Why Zebras Don’t Get Ulcers (2004), Sapolsky does a great job in describing how stress affects our cardiovascular system. We learn that when stressed, our cardiovascular system changes to allow us to function during unexpected emergencies. For example, our heart rate increases, the force with which our heart beats increases, and there is less blood flow to parts of our bodies that are not important during emergencies (such as our bladder and gut). While all these cardiovascular changes are important during extremely stressful events that require an individual to take action (e.g., running away from a mountain lion), these cardiovascular changes can happen even when thinking of an upcoming stressful event. In my case, October will be one of the most stressful months this year since I will be proposing my masters, presenting a talk in front of 80 undergrads, and preparing various assignments for classes. When I think about these upcoming events I feel a wave of dread pass through my body. Unfortunately, if I continue to stress over events like these, I can cause serious damage to my body. There is a chance I could develop hypertension, damaging my blood vessels and causing plaque build-up, making it more difficult for blood to pass through them. While I can tell myself to stop stressing over these things because, in the end, everything will be okay, the problem is that because of the distress my blood vessels are going through, every new stressor that occurs will be even more damaging to my body because my arteries have been clogged by the plaque build-up so bad that my heart itself may not be receiving sufficient blood flow. On top of all of this, being a woman does not help. The diagnosis of cardiovascular disease in women is rising, while they are decreasing in men. Moreover, women who suffer heart attacks are more likely to be disabled after the episode because we usually experience them later in life. While Sapolsky’s (2004) chapter is highly informative and is important to read, it is also a bit depressing. I am in a field where stressing is the norm. A prospective study conducted by Chandola and colleagues found that employees with chronic work stress were twice as likely to develop a metabolic syndrome such as cardiovascular disease (Chandola, Brunner, Marmot, 2006). While being a professor is rewarding, it is also extremely stressful especially when trying to obtain tenure. As researchers we stress over publications, funding, running participants, ensuring there are enough participants to run, etc. On top of that, at times we may work in hostile environments because we are so stressed and because we want to succeed in our careers, perhaps burning bridges along the way.

On the positive side, there are things we can do to keep us from getting to a position that is hard to bounce back from. A study conducted by Tuck and colleagues (2017) sought to understand whether the ability to make oneself express positive emotion predicted cardiovascular disease risk scores. Participants performed a test of expressive skill and biological, demographic, and behavioral data were collected to determine cardiovascular disease risk for participants. The authors found that individuals who were able to express positive emotion had a lower cardiovascular risk score (Tuck, Adams, Pressman, & Consedine, 2017). Furthermore, a study done by Newman and colleagues (2011) wanted to determine the relationship between hostility and cardiovascular disease. The authors found that participants who were hostile did, in fact, have a 2-fold greater risk of developing cardiovascular disease (Newman et al., 2011). An editorial comment was made by Whooley and Wong (2011) in response to the Newman and colleagues (2011) article stating that the real message from this study should be the absence of hostility is protective against cardiovascular disease (Whooley & Wong, 2011). These two studies illustrate some easy adjustments we can make to ensure we do not develop cardiovascular disease. While conducting research can be a battle with ourselves, our colleagues, and undergrads, we have to remember why we conduct research and have undergrads in the first place. We do not conduct research for the accolades, the money, or fame nor do we have undergrads for free labor. We conduct the research we love because we want to make an impact on society and we have undergrads work alongside us in order to teach them all we know so they can create their own scientific breakthroughs. So, we should take these studies to heart (ha) and when we feel hostile towards undergrads that may have no idea what they’re doing, take a second, think back to when we were undergrads and remember we all start somewhere. This will put us in a positive mood and maybe even put a smile on our faces, ultimately decreasing our risk for cardiovascular disease.


Chandola, T., Brunner, E., & Marmot, M. (2006). Chronic stress at work and the metabolic syndrome: prospective study. BMJ, 332:521.

Newman, J.D., Davidson, K.W., Shaffer, J.A., Schwartz, J.E., Chaplin, W., Kirkland, S., & Shimbo, D. (2011). Observed hostility and the risk of incident ischemic heart disease. Journal of the American College of Cardiology, 58(12), 1222-8.

Sapolsky, R.M. (2004) Why zebras don’t get ulcers: A guide to stress, stress related diseases, and coping. New York: W.H. Freeman.

Tuck, N.L., Adams, K.S., Pressman, S.D., & Consedine, N.S. (2017) Greater ability to express positive emotion is associated with lower projected cardiovascular disease risk. J Behav Med.

Whooley, M.A., & Wong, J. (2011). Hostility and cardiovascular disease. Journal of the American College of Cardiology, 58(12), 1229-30.

Stress & Emotion

I am a researcher who believes that in order to be a great scientist you need to know your topic in all aspects. For example, in the summer I sat in on a psychiatric genomic consortium workshop that had the main goal of understanding the best practices in traumatic stress genomics. I do not have a genetics background, I do not know anything about genes besides what I learned in high school, but thought this would be a rewarding experience to learn about the genetic research being conducted on PTSD. When I arrived, I was surprised to see that I was the only non-geneticist (give or take two others) that was present at the event. Of course, while it is important for geneticists to be there, how beneficial is it for only geneticists to know what research is being conducted in their own field? This experience came to my mind again while I was reading the book chapters written by Lazarus (1999). Specifically, Lazarus discusses how absurd the idea of studying stress without also studying emotions and coping, is. To him, the idea is absurd because when something stressful happens or is about to happen as humans we are going to display emotions that will help others understand the situation. Likewise, coping is equally important to discuss when discussing stress and emotions. Understanding the emotion one feels after a stressful situation will determine how an individual will cope with that situation. If an individual has negative emotions for the stressful situation, chances are they will not cope well. Furthermore, Lazarus goes on to say that individuals who work in the social sciences in general often have a narrow-minded outlook on their topic. While I might lose my head trying, I am so passionate about PTSD research that I wish to know all the research that has been done on the disorder. Whether it be basic or applied research, the more I know about the disorder in all aspects the better a researcher I will become. So I very much appreciate Lazarus’ statement.

Another piece of information my attention was drawn to while reading these chapters was the discussion of habituation. Habituation happens when we are repeatedly exposed to a stimulus and get used to the stimulus so that we no longer elicit a response to it. As an undergraduate, I was in a behavioral neuroscience laboratory where we would test rats using multiple testing paradigms such as light/dark box, elevated plus maze, and a forced swim paradigm. Days before the rats would complete these tests we would habituate them to the testing room so they were not stressed out about the new environment they were in. I bring up this experience because I can understand how rats in a laboratory can habituate to a given situation. However, Romero and Wingfield (2016) discuss the stress model of habituation in the context of free-living animals. I am having a hard time understanding how habituation would be beneficial, besides what was already discussed in the chapter about habituating to weather, to something that is stressful in free-living animals. As discussed in the Sapolsky (2004) our bodies adapt to acute stressors in order to focus on surviving. Specifically, when faced with an emergency, such as getting eaten, long-term things such as sexual desire can wait. I can see where habituation would be especially important because if our bodies were always in a stressed mode we would be unable to procreate or feel pain or our immune system would be down all the time. However, a question I have is in what other situations would free-living animals be able to habituate since they would certainly be unable to habituate to predators?


Lazarus, R. S. (1999). Stress and emotion: A new synthesis. New York: Springer.

Romero, L.M., & Wingfield, J.C. (2016). Tempests, poxes, predators, and people: Stress in wild animals and how they cope. New York: Oxford University Press.

Sapolsky, R.M. (2004). Why zebras don’t get ulcers. New York: Owl Book/Henry Holt and Co.,