The Psychoneuroimmunology of Chronic Disease: The Role of ...



The Psychoneuroimmunology of Chronic Disease: The Role of Inflammation in Disease. And How Mental State Affects Them Both

Kathleen Kendall-Tackett

In the summer of 2006, I was tasked with two apparently separate assignments. The first was to prepare a presentation for a research meeting on the health effects of violence against women, specifically focusing on the impact of violence on the development of heart disease and diabetes. My second task was to prepare for a plenary presentation at the International Lactation Consultant Association on new research in postpartum depression. As a health psychologist, I generally split my time between these two topics. I have written or edited several books on each, and was well-aware of what the psychoneuroimmunology (PNI) literature had to say about both. I’ve found PNI research to be a useful framework for conceptualizing the impact of traumatic events on health, and for understanding depression in pregnant and postpartum women (Kendall-Tackett, 2007a, 2007b). What I had not appreciated until that summer, however, was the continuity between these topics. That realization astonished me, and has some fantastic implication for how we understand and treat disease. The idea for this book came about shortly after.

Inflammation and Disease

One important component of PNI research is the role of inflammation in disease. Researchers have discovered that a wide range of illnesses—heart disease, diabetes, MS, Alzheimer’s, and autoimmune disorders—have an inflammatory etiology (Kiecolt-Glaser et al., 2007; Pace et al., 2007; Roble et al., 2007). The first three chapters in this book describe the inflammation-disease connection in more detail. But PNI research does not stop at simply assessing the link between inflammation and disease. Psychological or mental states can trigger this same inflammatory process, and therefore have an important role in the etiology of a wide range of chronic illnesses. In other words, negative mental states can trigger inflammation, thereby increasing the risk of disease.

The research literature is full of examples where researchers have observed an association between, say, depression and heart disease, without necessarily understanding why it occurs (Surtees et al., 2008). PNI research allows us to understand the potential mechanisms that underlie the association between negative mental states and poor health. For example, inflammation is elevated in depressed people. Chronic inflammation damages endothelium and increases coaguability, thereby increasing depressed people’s risk of heart attack and stroke (Kop & Gottdiener, 2005; Robles et al., 2005).

In perinatal health, the findings are equally intriguing. Take, for example, preterm birth. A number of recent studies have found that mothers who are depressed or anxious while pregnant have an increased risk of preterm birth, even while controlling for other risk factors (e.g., Dayan et al., 2006; Orr et al., 2007). Preterm birth is substantially more common among ethnic minority mothers, particularly among African Americans, and accounts for a significant portion of ethnic-group disparities in infant mortality. It is interesting to note that the same ethnic groups with high rates of heart disease, metabolic syndrome, and diabetes—inflammatory illnesses all—also have high rates of preterm birth. This suggests a possible inflammatory link. And indeed, this is what researchers have found (Coussons-Read et al., 2005; Groër et al., this volume). The proinflammatory cytokines involved in inflammation (IL-6 and TNF-alpha) also ripen the cervix. Depression increases levels of these proinflammatory cytokines, and this increased inflammation tells the body that it’s time to have the baby—even if early.

Book Overview

This book is divided into two major sections. In Section I, the chapter authors address is the role of inflammation in disease. Inflammation is part of the immune response, which is designed to protect us from pathogens and to heal wounds. However, when it is chronically elevated, inflammation increases the risk of disease by damaging the very system it was meant to protect (McEwen, 2003). Inflammation is generally measured in the plasma, by measuring levels of proinflammatory cytokines—messenger molecules of the immune system that increase inflammation. If you are new to this field, more information about this process is found in our introductory chapter.

Chapters in Section II describe the role of psychosocial stress in relation to inflammation and disease. Do negative mental states increase inflammation, thereby increasing the risk of disease? The negative mental states researchers have examined most often include depression, hostility, and traumatic stress. But other negative states appear to also have a role.

The final chapter of Section II discusses depression, but considers it from the angle of treatment. There are a wide range of treatments with known efficacy for depression, and yet, they all differ from each other. Recently, researchers have begun to document that effective treatments for depression are also anti-inflammatory, suggesting a possible underlying similarity between treatment types. This research is another line of evidence that supports an inflammatory etiology of depression, and why it increases the risk of disease.

Throughout this volume, the authors synthesize cutting-edge research examining various aspects of the relationship between negative mental states, inflammation and chronic disease. This new research also allows us to address some important questions about treatments for both depression and chronic illness. Some of the more innovative work has examined the role of anti-inflammatory omega-3 fatty acids in the prevention and treatment of both depression and disease. For example, in a recent study of patients with acute coronary syndrome (N=795), depression was higher in patients with low levels of the long-chain omega-3 fatty acids, EPA and DHA (Amin et al., 2008). For every 4.54% rise in the omega-3 index, there was a one point decline in depressive symptoms. Chapters 3 and 8 will specifically address the impact of omega-3s on physical and mental health.

Most of the chapters in this book are quite technical. Studies in psychoneuroimmunology tend to be both technical and cross-disciplinary, as is the authorship of this book. To aid you as a reader, we have included a short glossary and a summary of key findings for each chapter. These will allow you to understand the main points before tackling the more detailed text. We have also provided a basic overview of inflammation and its role in the stress response in the introduction.

Summary

The authors of this book are an elite group of researchers who explore the interaction between stress, inflammation, and chronic disease. We hope to disseminate this information to researchers as well as the wider medical and psychological community, as competent treatment of chronic disease will require a truly interdisciplinary focus. The findings presented in this book provide evidence of a substantial mind-body connection in health, demonstrating that treating medical conditions while ignoring mental state is, at best, incomplete. Finally, there are important implications for how we advise patients. Patients have more control over their health than they often realize, and may be able to take some relatively simple steps that can lower their risk of life-threatening illness. For patients at-risk for chronic disease, this knowledge can literally save their lives. We hope these findings are useful in your work.

References

Amin, A.A., Menon, R.A., Reid, K.J., Harris, W.S., & Spertus, J.A. (2008). Acute coronary syndrome patients with depression have low blood cell membrane omega-3 fatty acid levels. Psychosomatic Medicine, 70, 856-862.

Coussons-Read, M.E., Okun, M.L., Schmitt, M.P., & Giese, S. (2005). Prenatal stress alters cytokine levels in a manner that may endanger human pregnancy. Psychosomatic Medicine, 67, 625-631.

Dayan, J., Creveuil, C., Marks, M.N., Conroy, S., Herlicoviez, M.A., Dreyfus, M., & Tordjman, S. (2006). Prenatal depression, prenatal anxiety, and spontaneous preterm birth: A prospective cohort study among women with early and regular prenatal care. Psychosomatic Medicine, 68, 938-946.

Kendall-Tackett, K.A. (2007). A new paradigm for postpartum depression: The central role of inflammation and how breastfeeding and anti-inflammatory treatments decrease risk. International Breastfeeding Journal, 2, 6,

Kendall-Tackett, K.A. (2007). Cardiovascular disease and metabolic syndrome as sequelae of violence against women: A psychoneuroimmunology approach. Trauma, Violence and Abuse, 8, 117-126.

Kiecolt-Glaser, J. K., Belury, M.A., Porter, K., Beversdoft, D., Lemeshow, S., & Glaser, R. (2007). Depressive symptoms, omega-6: omega-3 fatty acids, and inflammation in older adults. Psychosomatic Medicine, 69, 217-224.

Kop, W.J., & Gottdiener, J.S. (2005). The role of immune system parameters in the relationship between depression and coronary artery disease. Psychosomatic Medicine, 67, S37-S41.

McEwen, B. S. (2003). Mood disorders and allostatic load. Biological Psychiatry, 54, 200-207.

Orr, S.T., Reiter, J.P., Blazer, D.G., & James, S.A. (2007). Maternal prenatal pregnancy-related anxiety and spontaneous preterm birth in Baltimore, Maryland. Psychosomatic Medicine, 69, 566-570.

Pace, T. W., Hu, F., & Miller, A. H. (2007). Cytokine-effects on glucocorticoid receptor function: relevance to glucocorticoid resistance and the pathophysiology and treatment of major depression. Brain, Behavior and Immunity, 21(1), 9-19.

Robles, T. F., Glaser, R., & Kiecolt-Glaser, J. K. (2005). Out of balance: A new look at chronic stress, depression, and immunity. Current Directions in Psychological Science, 14, 111-115.

Surtees, P.G., Wainwright, N.W.J., Bockholdt, S.M., Luben, R.N., Warcham, N.J., & Khaw, K-T. (2008). Major depression, C-reactive protein, and incident ischemic heart disease in health men and women. Psychosomatic Medicine, 70, 850-855.

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