You're lying awake in bed at 4 am. - it's another sleepless night. Your legs are twitching and pulsating, your mind is racing aimlessly with blurred abstract nonsense and the giant purple bags under your eyes continue to darken and grow larger.
Yes, we've all been there.
The last thing you need to hear is that your STRESS and LACK OF SLEEP are actually making the problem WORSE!
But, it's the truth.
And now that you know this, you can do something about it.
As the powerful influence of inflammation continues to move to the forefront of the media, more and more studies are being done to find out just how widespread its effects are. This includes studies I'll present to you on this website showing that both stress and insomnia increase inflammation levels.
This page provides scientific evidence that stress increases inflammation levels.
For information on how insomnia increases inflammation levels, please visit the page
Studies Showing How Insomnia Increases Inflammation Levels .
from "Chronic Stress Changes Immune Cell Genes, Leading To Inflammation" Huffington Post, 11/07/2013
A new study provides a better understanding of why chronic stress leads to high levels of inflammation in the body.
Researchers found that chronic stress changes gene activity of immune cells before they enter the bloodstream so that they're ready to fight infection or trauma -- even when there is no infection or trauma to fight. This then leads to increased inflammation.
"There is a stress-induced alteration in the bone marrow in both our mouse model and in chronically stressed humans that selects for a cell that's going to be pro-inflammatory," study researcher John Sheridan, a professor at Ohio State University and associate director of the university's Institute for Behavioral Medicine Research, said in a statement. "So what this suggests is that if you're working for a really bad boss over a long period of time, that experience may play out at the level of gene expression in your immune system."
Similar results were found in humans. The University of California, Los Angeles researchers looked at blood samples from both the stressed mice, as well as humans who came from differing socioeconomic statuses. Just like in the mouse part of the experiment, 387 genes were identified that had differences in activity between the people who came from low socioeconomic backgrounds and those who came from high socioeconomic backgrounds. And just like in the mice, the up-regulated genes in those who came from low socioeconomic backgrounds were pro-inflammatory.
In addition, a third of the genes that seemed to be affected by chronic stress were the same in both the humans and mice.
"This study provides a nice mechanism for how psychology impacts biology," study researcher Nicole Powell, a research scientist in oral biology at Ohio State University, said in a statement. "Other studies have indicated that these cells are more inflammatory; our work shows that these cells are primed at the level of the gene, and it's directly due to the sympathetic nervous system."
"Social stress up-regulates inflammatory gene expression in the leukocyte transcriptome via B-adrenergic induction of myelopoiesis."
Nicole D. Powell,
Erica K. Sloan,
Michael T. Baileya,
Jesusa M. G. Arevalo,
Gregory E. Miller,
Michael S. Kobor,
Brenda F. Reader,
John F. Sheridana and Steven W. Cole. Proceedings of the National Academy of Sciences (PNAS). October 8, 2013. vol. 110 no. 41. 16574–16579, doi: 10.1073/pnas.1310655110
You can read the full study here:
from "Dwelling on stressful events can increase inflammation in the body, study finds." Ohio University Office of Research Communications. March 13, 2013.
Dwelling on negative events can increase levels of inflammation in the body, a new Ohio University study finds.
Researchers discovered that when study participants were asked to ruminate on a stressful incident, their levels of C-reactive protein, a marker of tissue inflammation, rose. The study is the first to directly measure this effect in the body.
The research team recruited 34 healthy young women to participate in the project. Each woman was asked to give a speech about her candidacy for a job to two interviewers in white laboratory coats, who listened with stone-faced expressions, Zoccola said.
Half of the group was asked to contemplate their performance in the public speaking task, while the other half was asked to think about neutral images and activities, such as sailing ships or grocery store trips.
The researchers drew blood samples that showed that the levels of C-reactive protein were significantly higher in the subjects who were asked to dwell on the speech, Zoccola reported.
For these participants, the levels of the inflammatory marker continued to rise for at least one hour after the speech. During the same time period, the marker returned to starting levels in the subjects who had been asked to focus on other thoughts.
The C-reactive protein is primarily produced by the liver as part of the immune system’s initial inflammatory response. It rises in response to traumas, injuries or infections in the body, Zoccola explained.
C-reactive protein is widely used as a clinical marker to determine if a patient has an infection, but also if he or she may be at risk for disease later in life.
“More and more, chronic inflammation is being associated with various disorders and conditions,” Zoccola said. “The immune system plays an important role in various cardiovascular disorders such as heart disease, as well as cancer, dementia and autoimmune diseases.”
"Differential effects of poststressor rumination and distraction on cortisol and C-reactive protein."
Zoccola, P. M., Figueroa, W. S., Rabideau, E. M., Woody, A. & Benencia, F. Health Psychol. 2017 Jan 27.
You can read the full study here:
from "How Stress Influences Disease: Carnegie Mellon Study Reveals Inflammation as the Culprit." Carnegie Mellon News (April 2012).
A research team led by Carnegie Mellon University's Sheldon Cohen has found that chronic psychological stress is associated with the body losing its ability to regulate the inflammatory response. Published in the Proceedings of the National Academy of Sciences, the research shows for the first time that the effects of psychological stress on the body's ability to regulate inflammation can promote the development and progression of disease.
"Inflammation is partly regulated by the hormone cortisol and when cortisol is not allowed to serve this function, inflammation can get out of control," said Cohen, the Robert E. Doherty Professor of Psychology within CMU's Dietrich College of Humanities and Social Sciences.
Cohen argued that prolonged stress alters the effectiveness of cortisol to regulate the inflammatory response because it decreases tissue sensitivity to the hormone. Specifically, immune cells become insensitive to cortisol's regulatory effect. In turn, runaway inflammation is thought to promote the development and progression of many diseases.
Cohen, whose groundbreaking early work showed that people suffering from psychological stress are more susceptible to developing common colds, used the common cold as the model for testing his theory. With the common cold, symptoms are not caused by the virus — they are instead a "side effect" of the inflammatory response that is triggered as part of the body's effort to fight infection. The greater the body's inflammatory response to the virus, the greater is the likelihood of experiencing the symptoms of a cold.
"When under stress, cells of the immune system are unable to respond to hormonal control, and consequently, produce levels of inflammation that promote disease. Because inflammation plays a role in many diseases such as cardiovascular, asthma and autoimmune disorders, this model suggests why stress impacts them as well."
He added, "Knowing this is important for identifying which diseases may be influenced by stress and for preventing disease in chronically stressed people."
"Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk."
Sheldon Cohena, Denise Janicki-Deverts, William J. Doyle, Gregory E. Miller, Ellen Frank, Bruce S. Rabin and Ronald B. Turner. Proceedings of the National Academy of Sciences (PNAS). March 26, 2012.
You can read the full study here:
from "Brain pathways linking social stress and inflammation identified." from Science Daily. (2010, August 9)
Lead author George Slavich, a postdoctoral fellow at the UCLA Cousins Center for Psychoneuroimmunology, and senior author Shelley Taylor, a UCLA professor of psychology, show that individuals who exhibit greater neural sensitivity to social rejection also exhibit greater increases in inflammatory activity to social stress.
And although such increases can be adaptive, chronic inflammation can increase the risk of a variety of disorders, including asthma, rheumatoid arthritis, cardiovascular disease, certain types of cancer, and depression.
The study appears in the current online edition of the journal Proceedings of the National Academy of Sciences.
Their results showed that individuals who exhibited greater neural activity in the dorsal anterior cingulate cortex and anterior insula during social rejection in the brain scanner also exhibited greater increases in inflammatory activity when exposed to acute social stress in the lab.
"This is further evidence of how closely our mind and body are connected," Slavich said. "We have known for a long time that social stress can 'get under the skin' to increase risk for disease, but it's been unclear exactly how these effects occur. To our knowledge, this study is the first to identify the neurocognitive pathways that might be involved in inflammatory responses to acute social stress."
Although increases in inflammatory activity are part of our immune system's natural response to potentially harmful situations, Slavich noted, "frequent or chronic activation of the system may increase risk for a variety of disorders, including asthma, rheumatoid arthritis, cardiovascular disease, and even depression."
One critical question raised by the present findings is why neural sensitivity to social rejection would cause an increase in inflammation. There are several possible reasons, the authors note. For one, since physical threats have historically gone hand in hand with social threat or rejection, inflammation may be triggered in anticipation of a physical injury. Inflammatory cytokines -- proteins that regulate the immune system -- are released in response to impending (or actual) physical assault because they accelerate wound-healing and reduce the risk of infection.
While short-term inflammation is useful in battling an injury, chronic inflammation arising from the mere perception of social rejection is not.
"Neural sensitivity to social rejection is associated with inflammatory responses to social stress"
George M. Slavich, Baldwin M. Way, Naomi I. Eisenberger and Shelley E. Taylorb. Proc Natl Acad Sci U S A. Aug 17, 2010; 107(33): 14817–14822. doi: 10.1073/pnas.1009164107.
You can read the full study here: