HealthAnxiety May Cancel Out The Benefits Of Healthy Eating

Anxiety May Cancel Out The Benefits Of Healthy Eating

For most people when they hear the word “inflammation,” they probably imagine the typical symptoms associated with the condition: redness and swelling accompanied by a warm sensation and pain. Though perhaps irritating to those individuals experiencing it, inflammation plays a critical role in the human immune response to injury. Specifically, inflammation increases blood flow to the site of an injury, increases cellular metabolism in the affected area, and also leads to increased permeability of cells1. These changes enable the necessary nutrients and immune system cells to reach the affected areas as quickly as possible, speeding up recovery time.

Increasing evidence suggests that the body produces an inflammatory response to life stressors as well2-3. For instance, your body might experience inflammation on a cellular level after a very difficult test or presentation4. In addition, a growing number of studies have found that the foods you eat can also lead to an inflammatory response. For instance, when a person eats a meal high in saturated fats (e.g., animal fats), they experience an increased inflammatory response in the hours following the meal relative to when they consume a meal high in unsaturated fats (e.g., olive oil)5-7. Thus, the human inflammatory response is much more complicated than one might initially think.

Though acute inflammation can help the body heal, chronic inflammation is associated with bad health outcomes. For instance, chronic inflammation has been associated with diseases such as chronic obstructive pulmonary disease (COPD)8, coronary heart disease9, and Type 1 diabetes10. Furthermore, these findings are not limited to the physical domain. Researchers have reported strong relationships between chronic inflammation and psychological disorders such as depression11-12, anxiety13 and PTSD14. Though it is unclear whether the increased inflammatory response actually plays a causal role in these disorders, such findings have spurred researchers to further investigate what factors lead to chronic inflammation so as to better prevent its development.

One important question is whether and how certain factors might combine to increase your chances of developing chronic inflammation. For example, given that both acute life stressors and foods high in saturated fat can cause inflammation, could life stressors also affect the amount of inflammation experienced when consuming certain foods? Recently, in a study soon to be published in Molecular Psychiatry, Dr. Kiecolt-Glaser of The Ohio State University and her colleagues investigated this very question15. To this end, the researchers recruited 58 healthy women.

During the course of the study, participants visited the lab twice. During one visit, they consumed a meal high in saturated fats, and during the other visit, they consumed a meal high in unsaturated fats. After these meals, researchers took blood samples from the women to examine their inflammatory responses. The day before each visit, all participants ate nutritionally equivalent meals, provided by the experimenters, to ensure that they all had consistent baseline measurements. Finally, participants filled out a questionnaire where they reported whether they had experienced significant life stressors the previous day.

As had been found in previous studies, women who had not experienced a major life stressor the day before the study produced a reduced inflammatory response to the meal high in unsaturated fats relative to when they consumed the meal high in saturated fats. Thus, once again, saturated fats were found to produce an increased inflammatory response as compared to unsaturated fats. However, women who reported at least one life stressor the day before testing displayed a completely different pattern of results. They demonstrated equal inflammation for both types of meals. In other words, life stressors seemed to have the same effect on the body as eating a meal high in unsaturated fat.

At first glance, these findings are particularly alarming. However, these results actually provide a crucial step forward in research on mental disorders such as depression and anxiety. In particular, this study highlights that the inflammation caused by life stressors has a lasting effect on the immune system and can affect body chemistry at least 24 hours later. This knowledge is crucial in understanding how individual life stressors can accumulate over time to increase the likelihood of developing a mental disorder and how disorders such as depression, which magnifies the effects of life stressors16, are related to physical ailments such as heart disease17. Thus, though these findings don’t immediately point in the direction of a new treatment, they will aid researchers as they work to develop more targeted medicines and treatments to help individuals suffering from chronic mental disorders.


1. Ferrero‐Miliani, L., Nielsen, O. H., Andersen, P. S., & Girardin, S. E. (2007). Chronic inflammation: importance of NOD2 and NALP3 in interleukin‐1β generation. Clinical & Experimental Immunology, 147(2), 227-235.

2. Bierhaus, A., Wolf, J., Andrassy, M., Rohleder, N., Humpert, P. M., Petrov, D., … & Joswig, M. (2003). A mechanism converting psychosocial stress into mononuclear cell activation. Proceedings of the National Academy of Sciences, 100(4), 1920-1925.

3. Pace, T. W., Mletzko, T. C., Alagbe, O., Musselman, D. L., Nemeroff, C. B., Miller, A. H., & Heim, C. M. (2006). Increased stress-induced inflammatory responses in male patients with major depression and increased early life stress. American Journal of Psychiatry.

4. Heinz, A., Hermann, D., Smolka, M. N., Rieks, M., Gräf, K. J., Pöhlau, D., … & Bauer, M. (2003). Effects of acute psychological stress on adhesion molecules, interleukins and sex hormones: implications for coronary heart disease. Psychopharmacology, 165(2), 111-117.

5. Bellido, C., López-Miranda, J., Blanco-Colio, L. M., Pérez-Martínez, P., Muriana, F. J., Martín-Ventura, J. L., … & Pérez-Jiménez, F. (2004). Butter and walnuts, but not olive oil, elicit postprandial activation of nuclear transcription factor κB in peripheral blood mononuclear cells from healthy men. The American journal of clinical nutrition, 80(6), 1487-1491.

6. Peairs, A. D., Rankin, J. W., & Lee, Y. W. (2011). Effects of acute ingestion of different fats on oxidative stress and inflammation in overweight and obese adults. Nutrition journal, 10(1), 1.

7. Pillon, N. J., Azizi, P. M., Li, Y. E., Liu, J., Wang, C., Chan, K. L., … & Lee, W. L. (2015). Palmitate-induced inflammatory pathways in human adipose microvascular endothelial cells promote monocyte adhesion and impair insulin transcytosis. American Journal of Physiology-Endocrinology and Metabolism, 309(1), E35-E44.

8. Gan, W. Q., Man, S. F. P., Senthilselvan, A., & Sin, D. D. (2004). Association between chronic obstructive pulmonary disease and systemic inflammation: a systematic review and a meta-analysis. Thorax, 59(7), 574-580.

9. Danesh, J., Whincup, P., Walker, M., Lennon, L., Thomson, A., Appleby, P., … & Pepys, M. B. (2000). Low grade inflammation and coronary heart disease: prospective study and updated meta-analyses. Bmj, 321(7255), 199-204.

10. Schalkwijk, C. G., Poland, D. C. W., Van Dijk, W., Kok, A., Emeis, J. J., Dräger, A. M., … & Stehouwer, C. D. A. (1999). Plasma concentration of C-reactive protein is increased in type I diabetic patients without clinical macroangiopathy and correlates with markers of endothelial dysfunction: evidence for chronic inflammation. Diabetologia, 42(3), 351-357.

11. Dantzer, R., O’Connor, J. C., Freund, G. G., Johnson, R. W., & Kelley, K. W. (2008). From inflammation to sickness and depression: when the immune system subjugates the brain. Nature reviews neuroscience, 9(1), 46-56.

12. Miller, A. H., Maletic, V., & Raison, C. L. (2009). Inflammation and its discontents: the role of cytokines in the pathophysiology of major depression. Biological psychiatry, 65(9), 732-741.

13. Vogelzangs, N., Beekman, A. T. F., De Jonge, P., & Penninx, B. W. J. H. (2013). Anxiety disorders and inflammation in a large adult cohort.Translational psychiatry, 3(4), e249.

14. Gill, J. M., Saligan, L., Woods, S., & Page, G. (2009). PTSD is associated with an excess of inflammatory immune activities. Perspectives in psychiatric care, 45(4), 262-277.

15. Kiecolt-Glaser, J. K., Fagundes, C. P., Andridge, R., Peng, J., Malarkey, W. B., Habash, D., & Belury, M. A. (2016). Depression, daily stressors and inflammatory responses to high-fat meals: when stress overrides healthier food choices. Molecular Psychiatry.

16. Husky, M. M., Mazure, C. M., Maciejewski, P. K., & Swendsen, J. D. (2009). Past depression and gender interact to influence emotional reactivity to daily life stress. Cognitive Therapy and Research, 33(3), 264-271.

17. Rugulies, R. (2002). Depression as a predictor for coronary heart disease: a review and meta-analysis1 1The full text of this article is available via AJPM Online at www. ajpm-online. net. American journal of preventive medicine,23(1), 51-61.

Program Analyst, U.S. Department of Agriculture at Emory University

Sam Hunley holds a doctorate in cognitive psychology from Emory University. He pursued his Bachelor's degree in psychology from Furman University and a master's from Emory. Sam's research, alongside Dr. Stella Lourenco, focuses on human perception of the space surrounding the body, exploring the impact of anxiety and phobias on this perception. Together, they contribute to articles. Post-graduation, Sam became a Presidential Management Fellow.


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