Sunday, June 4, 2017

Depression and Chronic and Autoimmune Disease

Depression and Chronic and Autoimmune Diseases  
Depression has a powerful affect on the immune and inflammatory response systems. It increases cortisol and other inflammatory cytokines such as IL-6, and an enzyme called IDO (Müller & Schwarz, 2007). These substances decrease the body's ability to heal, which can increase vulnerability to autoimmune diseases such as systemic lupus erythematosus (SLE). The goal of this paper is to describe the association between depression and SLE, explain the factors of the disease that account for its high co-occurrence with depression, and discuss the role of stress hormones and inflammation in SLE. Further, it will explain three teaching strategies that might reduce the effects of SLE and effective methods to encourage the adoption of strategies to reduce the effects of SLE.
Depression and Systemic Lupus Erythematosus

 High levels of inflammatory factors and depression are characteristic of many autoimmune diseases (Laureate Education, Inc., 2012). For example, depression is highly comorbid with systemic lupus erythematosus (SLE). More than 65% of patients with chronic rheumatological disorders, such as SLE suffer from depression (Maes et al., 2011). Patients with SLE have several comorbidities including hypertension, gall bladder disorders, cataracts, cardiovascular disease, and neurologic and endocrine disorders (Wolfe et al., 2010). Almost 40% of patients with SLE are diagnosed with depression, which, has been linked to a lower life quality (Wolfe et al., 2010). Palagini et al., (2013) claimed SLE is co-occuring with depression in 14% to 89% of patients. Women with SLE have at least a 47% chance of being diagnosed with depression. Further, anxiety and depression have been associated to permanent deformation of the joints and active inflammation in SLE patients (Waheed, Hameed, Khan, Syed, & Mirza, 2006). Depression is, however, the most prevalent comorbidity associated with SLE (Wekking, 1993).

The Role of Stress Hormones and Inflammation in SLE

Depression associated with SLE may be mediated by an autoimmune mechanism (Palagini et al., 2013). Bachen, Chesney, and Criswell (2009) hypothesized proinflammatory cytokines play a role in SLE's inflammatory response. The body's cytokine immune response has been implicated in depression as well as in some autoimmune diseases (Wilson & Warise, 2008). Cytokines are immune proteins that regulate the immune system, especially during a stress response (Wilson & Warise, 2008). Cytokines, have an inflammatory effect on the neurotransmission of serotonin, a neurotransmitter that has been known to have a profound effect on psychological health and well-being (Dabhar, 2011; Salih & Feyza, 2012; Wilson & Warise, 2008).

SLE and other chronic inflammatory diseases are associated with depression (Wilson & Warise, 2008). It is well known that stress exacerbates symptoms of SLE (Peralta-Ramirez, Jimenez-Alonso, Godoy-Garcia, & Perez-Garcia, 2004). Further, cytokine imbalances are characteristic of autoimmune diseases, such as SLE, especially during its beginning stages as well as during disease progression (Freiri, 2003). When an excess of cytokines are flushed into the blood stream during stress, an enzyme called IDO is activated, and this enzyme degrades serotonin (Müller & Schwarz, 2007). This inflammatory process degrades the body's serotonergic system, which decreases the body's ability to manufacture serotonin. The lowered level of serotonin leaves the individual more susceptible to depression.

Maes (2010) found depression shares the same inflammatory pathways with other diseases, and rather than the existence of two separate degenerative processes, for example, one for SLE, and one for depression, these comorbidities may be symptoms of one degenerative process. Inflammatory processes may have a variety of causes, such as diet, lifestyle, and genetic predispositions, but the biological process may be singular (Maes, 2010). In addition, Maes (2010) found that this shared biological process is bidirectional, and cyclical, in that inflammation provoked degeneration and vice versa.

Teaching Strategies to Reduce Anxiety
Cognitive-Behavioral Stress Management
Cognitive-behavioral stress management (CBSM) has been proven effective in ameliorating stress that accompanies chronic illness and has been shown to help individuals cope effectively with disease-related treatment and manage social resources (Nezu, Nezu, & Xanthopoulos, 2011). CBSM increased individuals' ability to find benefit in their illness as well as their ability to remain optimistic amid the challenge of chronic disease (Nezu et al., 2011). Stress and anxiety are common in SLE patients, and in general, they are not as aware of effective coping strategies as the general population, and the strategies they tend to use are inadequate and less effective than other strategies such as CBSM (Peralta-Ramirez et al., 2004). Patients who implemented CBSM perceived themselves less likely to have a flare of symptoms, felt confident about their future, experienced significant improvement in their psychological health and well-being, felt more vital, and experienced significantly less pain (Peralta-Ramirez et al., 2004).


Exercise has been shown to be a possible antidepressant and it exercise also generates neurons in adults (National Institute on Mental Health, 2010). Home-based exercise made a significant difference in a group of sedentary women with SLE (Yuen et al., 2013). Physical exercise was proven useful and successful in improving symptoms of SLE without provoking disease activity (Reis-Neto, Silva, Monteiro, Camargo, & Sato, 2013). Similarly, Ayán and Martín (2007) concluded SLE patients can benefit from exercise.

Relaxation Techniques

Smith and Balaban (1983) found behavioral therapy that included deep relaxation, hypnosis and psychodynamic psychotherapy was effective for pain management, coping, and negative emotions associated with the stress of SLE. Torem (2007) postulated the immune system interacts with the central nervous system, and believed hypnosis and imagery could affect the immune system. Torem found this treatment effective in patients with autoimmune diseases. Zhang, Wei, and Wang (2013) discovered psychological interventions had the potential to help patients with SLE manage negative emotions and reduce stress.

Encouraging Health Behavior Change

Changing health behaviors is a complex undertaking, and effective interventions must consider the individual (Glanz, Rimer, & Viswanath, 2008). The Transtheoretical Model (TTM) of behavior change is concerned with individually tailored interventions (Brug, 2004). When encouraging behavior change, it seems important to account for various individual factors in patients, especially their stage of understanding and their readiness for education. The TTM takes into account patients' attitudes and beliefs, which will have an effect on whether they can make changes in their health behavior (Glanz et al., 2008). Because this model of behavior change accommodates individual needs, it may be a salient component in developing effective interventions (Velicer, Redding, Sun, & Prochaska, 2007). This may be especially true in patients with SLE because this population has fewer effective stress management strategies than the general population (Peralta-Ramirez et al., 2004). Lack of awareness, education, and experience, may contribute to this deficiency, and understanding their personal experience and readiness may be important in establishing durable behavior change.
Depression is commonly found in a significant number of individuals diagnosed with SLE. The body's inflammatory immune response to stress has been implicated in depression and autoimmune diseases, such as SLE (Wilson & Warise, 2008). In particular, proinflammatory cytokines play a role in depression as well as in SLE's inflammatory response (Bachen, Chesney, & Criswell, 2009). Maes (2010) hypothesized that depression and illnesses such as SLE may share inflammatory pathways and a foundational cause. Since lifestyle and stress have the potential to cause inflammation, exercise, CBSM, and relaxation techniques may provide relief and decrease symptoms of depression and SLE (Zhang, Wei, & Wang, 2012). Utilizing the TTM, effective coping and stress management strategies that account for personal readiness can be developed for positive health outcomes and to instigate durable behavior change (Glanz et al., 2008).


Ayán, C., & Martín, V. (2007). Systemic lupus erythematosus and exercise. Lupus, 16(1), 5-9. Bachen, E., Chesney, M., & Criswell, L. (2009). Prevalence of mood and anxiety disorders in women with systemic lupus erythematosus. Arthritis & Rheumatism: Arthritis Care & Research, 61(6), 822-829. doi:10.1002/art.24519

Brug, J. (2004). The Transtheoretical Model and stages of change: A critique: Observations by five Commentators on the paper by Adams, J. and White, M. (2004) Why don't stage- based activity promotion interventions work? Health Education Research, 20(2), 244- 258. doi: 10.1093/her/cyh005

Dhabhar, F. S. (2011). Effects of stress on immune function: Implications for immunoprotection and immunopathology. In R. J. Contrada & A. Baum (Eds.), The handbook of stress science: Biology, psychology, and health (pp. 47–63). New York, NY: Springer Publishing Company.

Frieri, M. (2003). Neuroimmunology and inflammation: Implications for therapy of allergic and autoimmune diseases. Annals of Allergy, Asthma, & Immunology, 90(6, Suppl. 3), 34-40.

Glanz, K., Rimer, B. K., & Viswanath, K. (Eds.). (2008). Health behavior and health education: Theory, research, and practice (4th ed.). San Francisco, CA: Jossey-Bass.

Laureate Education, Inc. (2012). Stress, the immune system, chronic illness, and your body. [Handout].

Maes, M. (2010). An intriguing and hitherto unexplained co-occurrence: Depression and chronic fatigue syndrome are manifestations of shared inflammatory, oxidative and nitrosative (IO&NS) pathways. Progress in Neuro-Psychopharmacology and Biological Psychiatry. doi: 10.1016/j.pnpbp.2010.06.023

Maes, M. M., Kubera, M. M., Obuchowiczwa, E. E., Goehler, L. L., & Brzeszcz, J. J. (2011). Depression's multiple comorbidities explained by (neuro) inflammatory and oxidative & nitrosative stress pathways. Neuroendocrinology Letters, 32(1), 7-24.

Müller, N., & Schwarz, M. J. (2007). The immune-mediated alteration of serotonin and glutamate: Towards an integrated view of depression. Molecular Psychiatry, 12(11), 988- 1000. doi: 10.1038/

National Institute of Mental Health. (Producer). (2010, November 23). NIMH investigators talk about new evidence that suggests exercise and positive environment can help hedge against stress related depression [Audio podcast]. NIH Radio. Retrieved from evidence-that-suggests-exercise-and-positive-environment-can-help-hedge-against-stress- related-depression.shtml

Nezu, A. M., Nezu, C. M., & Xanthopoulos, M. S. (2011). Stress reduction in chronically ill patients. In R. J. Contrada & A. Baum (Eds.), The handbook of stress science: Biology, psychology, and health (p. 475-500). New York, NY: Springer Publishing Company.

Palagini, L., Mosca, M., Tani, C., Gemignani, A., Mauri, M., & Bombardieri, S. (2013). Depression and systemic lupus erythematosus: a systematic review. Lupus, 22(5), 409- 416. doi:10.1177/0961203313477227

Peralta-Ramírez, M., Jiménez-Alonso, J., Godoy-García, J., & Perez-García, M. (2004). The effects of daily stress and stressful life events on the clinical symptomatology of patients with lupus erythematosus. Psychosomatic Medicine, 66(5), 788-794.

Reis-Neto, E., Silva, A., Monteiro, C., Camargo, L., & Sato, E. (2013). Supervised physical exercise improves endothelial function in patients with systemic lupus erythematosus. Rheumatology (Oxford, England), [serial online].

Salih, G., & Feyza, A. (2012). Inflammation in depression: the role of cytokines. Journal Of Marmara University Institute Of Health Sciences, 2(3), 103-107.

Smith, S. J., & Balaban, A. B. (1983). A multidimensional approach to pain relief: Case report of a patient with Systemic Lupus Erythematosus. International Journal Of Clinical And Experimental Hypnosis, 31(2), 72-81. doi:10.1080/00207148308406594

Torem, M. S. (2007). Mind-Body Hypnotic Imagery in the Treatment of Auto-Immune Disorders. American Journal of Clinical Hypnosis, 50(2), 157-170. doi: 10.1080/00029157.2007.10401612

Velicer, W. F., Redding, C. A., Sun, X., & Prochaska, J. O. (2007). Demographic variables, smoking variables, and outcome across five studies. Health Psychology, 26, 278-287.

Wilson, D. R., & Warise, L. (2008). Cytokines and their role in depression. Perspectives in Psychiatric Care, 44(4), 285–289.

Waheed, A., Hameed, K., Khan, A., Syed, J., & Mirza, A. (2006). The burden of anxiety and depression among patients with chronic rheumatologic disorders at a tertiary care hospital clinic in Karachi, Pakistan. JPMA. The Journal Of The Pakistan Medical Association, 56(5), 243-247.

Wolfe, F., Michaud, K., Li, T., & Katz, R. (2010). Chronic conditions and health problems in rheumatic diseases: comparisons with rheumatoid arthritis, noninflammatory rheumatic disorders, systemic lupus erythematosus, and fibromyalgia. Journal Of Rheumatology, 37(2), 305-315. doi:10.3899/jrheum.090781

Wekking, E. (1993). Psychiatric symptoms in systemic lupus erythematosus: an update. Psychosomatic Medicine, 55(2), 219-228.

Yuen, H., Breland, H., Vogtle, L., Holthaus, K., Kamen, D., & Sword, D. (2013). The process associated with motivation of a home-based Wii Fit exercise program among sedentary African American women with systemic lupus erythematosus. Disability And Health Journal, 6(1), 63-68. doi:10.1016/j.dhjo.2012.08.003

Zhang, J., Wei, W., & Wang, C. (2012). Effects of psychological interventions for patients with systemic lupus erythematosus: a systematic review and meta-analysis. Lupus, 21(10), 1077-1087. doi:10.1177/0961203312447667

Sunday, July 13, 2014

Critical Thinking and Objectivity

The scientific method and critical thinking offer some level of objectivity, and as Browne and Keeley (2013) described, the systematic evaluation that is critical thinking, has the potential to produce applicable and useable results.  Researchers may be no more aware of the gate keeping provided by critical thinking than they are of their own biases.  Critical thinking can potentially help individuals question their own thoughts and understand personal biases, which may be an important step in becoming more aware of when these biases intrude and how to more effectively curtail their ability to skew information (Innes & Fraser, 1971).

Browne, M. N., & Keeley, S. M. (2013). Asking the right questions: A guide to critical thinking 9/e (Custom Edition). Upper Saddle River, NJ: Pearson Prentice Hall.

Innes, J. M., & Fraser, C. (1971). Experimenter bias and other possible biases in psychological research. European Journal Of Social Psychology, 1(3), 297-310.

The Importance of Critical Thinking

Critical thinking is crucial to the evolution of knowledge; it raises vital questions that contribute to the ongoing transformation and expansion of the knowledge base. Without the ability to react with systematic evaluation, the psychological sciences, and all sciences, for that matter, would not be able to produce accurate and reliable information, and would be subject to common conjecture and radically varying opinion (Brown & Keeley, 2013). Critical thinking minimizes the shortcomings of human thinking, such as egocentrism and sociocentrism. It requires thinkers to remain open-minded and skeptical simultaneously, and enables the development of lucid strategies for questioning, observing, and resolving ambiguities. It is a self-corrective thinking process, in which the thinker has the capacity to question his or her own thoughts. Critical thinking limits biased, simplistic, and rigid thinking.

It is important to consider the limitations of information, even that which is scientifically gained; whether it is the diversity or number of participants, the length and location of the study, as well as the manner in which comparisons were made. Even the most conscientiously derived information is gained, at least in part, through processes supported by human nature, which has its inherent limitations. For example, when faced with ambiguities, humans naturally impose their personal perspectives to resolve to the ambiguity ( Brown & Keeley, 2013; Stewart & Bennett, 2006). For scientists, this process of imposition may be so deeply held that it becomes an unconscious bias and an inaccuracy that is difficult to recognize.

In the psychological sciences, as well as for any final or capstone project, utilizing a critical thought process helps ensure a quality standard and objectivity, and prevents bias. Asking the most appropriate questions can act as a grounding force in psychological research, and encourages researchers to make accurate and intelligent statements and realistic and reasonable predictions (Browne & Keeley, 2013). Since research from the psychological professions serves humanity in a variety of ways, and is often the basis of care, treatments, and interventions, the standards and quality of that research must be the most accurate and reliable possible. If a researcher does not question the information itself, and the sources from which it comes, it is likely the final product may be flimsy, illusory, or merely superficial, and without merit where it is needed.

Browne, M. N., & Keeley, S. M. (2013). Asking the right questions: A guide to critical thinking 9/e (Custom Edition). Upper Saddle River, NJ: Pearson Prentice Hall.

Stewart, E. C., & Bennett, M. J. (2006). American cultural patterns: a cross-cultural perspective. Yarmouth, ME: Intercultural Press.

The Chicken and the Egg

I was thinking about the chicken and egg conundrum, and how it relates to the discussion of whether illness comes before depression or vice versa, and I wondered if possibly inflammation comes first.  Medical science tells us that inflammation is the root of most, perhaps all disease.  To add to this idea, I reviewed Filakovic, Bijan, and Petek (2008), which found similar elevated levels of pro inflammatory cytokines in depression and psoriasis.  These authors believed the basis of both disorders was shared inflammatory pathways mediated by the immune system. 

Similarly, Potter and Steffans (2007) found depression was commonly diagnosed in individuals with mild cognitive impairment, which may lead to Alzheimer's Disease (AD).  Maes et al., (2010) found depression was an antecedent to AD.  The similarity is in the Maes et al. explanation that depression and neurodegenerative diseases, such as AD are the result of inflammation that is basically part of the same biological process, along the same inflammatory pathways.  Maes et al. believed the degeneration of inflammatory pathways created a cycle in which neuroinflammation provoked neurodegeneration and created a process by which depression exacerbated the comorbidity, and vice versa.   

This idea of disease-sharing pathways was fascinating to me.  I wonder if comorbidities are not independent occurrences, but rather are two symptoms of the same process, it seems we will have to rethink the idea of comorbidities, such as anxiety and depression (Hirschfeld, 2001).  Rather than treating two diseases or comorbidities, perhaps they will be treated as one degenerative process.

Filakovic, P., Bijan, D., & Petek, A. (2008). Depression in dermatology: An integrative perspective. Psychiatria Danubina, 20(3), 419-425.

Hirschfeld, R. (2001). The comorbidity of major depression and anxiety disorders: recognition and management in primary care. Primary Care Companion To The Journal Of Clinical Psychiatry, 3(6), 244-254.

Maes, M. (2010). An intriguing and hitherto unexplained co-occurrence: Depression and chronic fatigue syndrome are manifestations of shared inflammatory, oxidative and nitrosative (IO&NS) pathways. Progress in Neuro-Psychopharmacology and Biological Psychiatry. doi: 10.1016/j.pnpbp.2010.06.023

Potter, G. G., & Steffens, D. C. (2007). Contribution of Depression to Cognitive Impairment and Dementia in Older Adults. The Neurologist, 13(3), 105-117. doi: 10.1097/01.nrl.0000252947.15389.a9