Emotional Awareness Therapy for Chronic Musculoskeletal Pain

Chronic pain conditions appear to fall into two categories: those that accompany identifiable illnesses like rheumatoid arthritis, neuropathy, and tumors, and those viewed as central sensitization or augmentation syndromes such as fibromyalgia and some other musculoskeletal pain conditions, pelvic pain, and some headaches. Neurons that conduct pain impulses to the central nervous system (peripheral nociceptive afferent processes) play a major role in the identifiable conditions. For fibromyalgia and other puzzling types of chronic pain, the central nervous system (CNS) appears to be the primary player: “Psychological stress or trauma, emotion dysregulation, interpersonal conflict, and learning processes such as conditioning, expectations, and attributions appear to play a primary role in predisposing, precipitating, and perpetuating pain.” Unlike patients with an identifiable pain-causing pathology, these patients do not response to cognitive behavior therapy that teaches people how to manage pain with relaxation training, goal setting, activity pacing, and other tactics.

Amanda J. Burger and colleagues at Wayne State University (Detroit, Michigan) decided to test whether an emotional processing approach could help patients with chronic musculoskeletal pain not tied to structural pathology. In their 2016 study, they cite earlier research involving patients with central sensitization-type pain in which patients were taught to see pain as a learned response, often tied to emotional processes: “Emotionally difficult experiences during development as well as other learning processes (eg, classical conditioning, modeling) create CNS pathways that are directly linked to pain pathways. Later in life, stress, exposure to eliciting stimuli, and fearful beliefs that the pain implies bodily damage then generate or amplify pain.” Burger et al hypothesized that an emotional processing approach would reduce pain intensity (primary outcome), interference in daily activity, depression, and distress. They conducted an uncontrolled trial involving 72 patients with central sensitization-based chronic musculoskeletal pain (primarily back pain), 13 of whom had a diagnosis of fibromyalgia.

At baseline, the participants took the Brief Pain Inventory (BPI), the 20-item Center for Epidemiologic Studies Depression Scale, the McGill Pain Questionnaire Short-form, and the 53-item Brief Symptom Inventory. Each person, then, had a physical exam with the physician who also explained the difference between peripheral pain, due to pathology, and learned, CNS-based pain. When a group of six to ten patients had been recruited, the group took part in weekly two-hour group sessions for four weeks with homework exercises. The book Unlearn Your Pain by H. Schubiner, MD, (2010) provided the curriculum, which included 1) information about the mind-body neural pathway model of chronic pain; 2) emotional awareness techniques such as awareness of emotions, body responses, breath, and positive affirmations; 3) daily emotion-based writing exercises concerning past and current life stressors; and d) re-engagement in activities that were avoided due to pain.

Pain intensity reduced significantly with this treatment: “…only four patients (5.6%) had a BPI pain rating of 2.0 or less at baseline (pre-consultation), but at post-treatment, 30 patients (41.7%) had pain of 2.0 or less, and at 6-month follow-up, 36 patients (50%) reached this level.” Pain interference and depression also declined significantly after treatment and at the six-month follow-up. Interestingly, the authors report: “…we found that patients with greater depressive symptoms at baseline actually had more improvement in pain and other outcomes and were more likely to complete the study (6-month follow-up) than patients with lesser depressive symptoms.”

Burger et al note several limitations in this uncontrolled study and would like to see a randomized controlled study comparing this approach against usual treatment and alternative treatment such as cognitive behavior therapy, tracking changes in pain-relieving medication. Also, they note that patients in this study were self-selected and well educated. The authors don’t know how well the therapy would work for less educated folk or for those who are tied to pharmaceutical pain management.

Burger and colleagues have developed a 16-to-20-hour course for training therapists to conduct the group sessions used in this study.

Burger AJ, et al. The effects of a novel psychological attribution and emotional awareness and expression therapy for chronic musculoskeletal pain: A preliminary, uncontrolled trial. Journal of Psychosomatic Research. 2016;81:1-8.

The Neglected Field of Environmental Medicine

How much of the upsurge in chronic disease in the US is due to or exacerbated by the deluge of environmental chemicals and EMF pollution in the environment? The observation that environmental chemicals contribute to diagnosable medical conditions first arose in the early 1950s, as William J. Meggs, MD, explains in his June 2017 article on the history of US environmental medicine. Dr. Theron Randolph and other Midwestern allergists reported that food and chemical sensitivities, unrelated to IgE antibody-mediated allergy reactions, caused diverse conditions such as asthma, dermatitis, sinusitis, chronic fatigue, colitis, depression, and joint and muscle pains, in some patients. These symptoms lessened or resolved when patients avoided offending foods during elimination diets. In some cases, patients made a distinction between unsprayed fruit from abandoned orchards and store-bought fruit exposed to pesticide and preservatives; the store-bought fruit caused problems while fruit from the abandoned orchard did not. Also, some patients reported that chemical inhalants such as cigarette smoke, wood smoke, diesel fuel, natural gas, ozone, perfumes, and formaldehyde worsened their symptoms. Thus, the concept of chemical sensitivity was born.

To identify and treat food and chemical sensitivity, Dr. Randolph housed patients in an environmental control unit (ECU) in a hospital ward, constructed of materials that released minimal volatile chemicals. Patients drank glass-bottled spring water, breathed filtered air, and ate organic foods on a rotation basis. Patients who improved in this environment were then challenged with specific foods and chemical exposures.

Dr. Randolph noticed symptom patterns. When regularly consumed trigger foods were removed from the diet, the patient would develop withdrawal symptoms that would resolve within five to seven days, symptoms such as dermatitis, colitis, asthma, head/neck/back ache, joint pain, brain fog, depression, irregular pulse, hypertension, anemia, and/or phlebitis. Then, chronic symptoms tied to the trigger would lessen or go into remission. Reintroducing the food or chemical trigger typically produced a severe reaction, including hyperactivity, anxiety, twitching, aggression, and seizures. If patients continued to be exposed to sub-lethal toxicant exposures long-term, inflammation and, eventually, tissue damage occurred.

Environmental control units are still used to identify and treat chemical sensitivity. In a 2016 article, William J. Rea, MD, at the Environmental Health Center (Dallas, TX), outlines the principles of diagnosis and treatment of chemical sensitivity. In addition to food and chemical exposures, electromagnetic fields (EMF), mold, pollen, and dust are known to be possible toxicants. Sub-lethal exposures to a toxic substance can cause gastrointestinal and genitourinary malfunction, kidney disease, cardiovascular and brain dysfunction, fatigue, and fibromyalgia. In addition to avoiding triggers, nutrient supplementation supports the body’s detoxification of toxicants; people with chemical sensitivity display biochemical markers indicating abnormal detoxification.

The importance of environmental medicine has largely been suppressed, according to Dr. Meggs. Medical conditions whose treatment consists of chemical removing rather than adding pharmaceutical chemicals threaten many corporate interests, including the food industry, chemical industry, pharmaceutical industry, and, now, the mobile phone and computer industries. Workers’ compensation insurance companies have also fought against chemical sensitivity diagnoses. Dr. Meggs says those suppressing environmental medicine and the idea of chemical sensitivity use the same tactics that the cigarette industry used to hide the disease-causing effects of smoking: hiring “experts” to attack the research and discredit researchers; smear campaigns against researchers and physicians; and proposing alternative explanations such as symptoms are due to psychological not physiological dysfunction (i.e., patients are crazy).

But opposition has also come from those who should be vanguards of health. Around three decades ago, the American Academy of Allergy and Immunology, California Medical Association, and American Medical Association all published position statements belittling the concept of chemical sensitivity—statements that have not been rescinded. Researchers are denied funding for chemical sensitivity studies, and medical journals refuse to publish chemical sensitivity articles. Furthermore, medical doctors who treat patients with chemical sensitivity have been called before state medical boards, facing huge legal defense fees and possible loss of their medical license.

Dr. Meggs says, “The development of environmental medicine in the United States should have been one of the greatest achievements of 20^th-century medicine….The suffering from diseases ranging from depression to obesity and type 2 diabetes could have been greatly reduced by environmental medicine instead of soaring out of control.” And the vast majority of practitioners know nothing about it.

Meggs WJ. History of the Rise and Fall of Environmental Medicine in the United States. Ecopsychology. June 2017; 9(2):72-79.

Rea WJ. History of chemical sensitivity and diagnosis. Rev Environ Health. 2016;31(3):353-361.

Neuroimages for Fibromyalgia

In January 2017, Marina López-Solà and colleagues reported finding a characteristic brain signature, identified with fMRI during painful pressure and non-painful multisensory (visual-auditory-tactile) stimulation, which allowed them to identify people with fibromyalgia with 92% sensitivity and 94% specificity when compared to healthy controls. “If replicated, these brain features may constitute objective neural targets for therapeutic interventions,” according to the study abstract. “The results establish a framework for assessing therapeutic mechanisms and predicting treatment response at the individual level.”

Michael E. Robinson, PhD, and colleagues at the University of Florida value neuroimaging studies, such as the one above, for “providing useful insights for understanding neural mechanisms underlying pain processing,” but they question their clinical use. The Florida researchers used machine learning techniques to compare the effectiveness of neuroimaging vs. self-report of pain intensity and mood to classify individuals with and without pain: “Overall, models derived from self-report data outperformed neuroimaging models by an average of 22%.” Mood data, specifically anger, was a more accurate predictor of pain intensity than brain data. (Self-report has the additional advantage of being much less expensive than brain imaging.)

In a 2016 editorial, Robinson and another group of colleagues argue that brain-derived biomarkers for pain cannot differentiate various chronic pain conditions: “The clinical values of a biomarker for chronic pain (or indeed, the diagnosis of any condition) is more nuanced than simply considering the sensitivity and specificity. It is also imperative to consider base rates of the condition, in the particular context or setting in which the biomarker is intended for use.” Patient self-report provides valuable information, to a practitioner who listens, that biomarkers cannot.

López- Solà M et al. Towards a neurophysiological signature for fibromyalgia (abstract). Pain. Jan. 2017;158(1):34-47.

Robinson M, Boissoneault J, et al. The Effect of Base rate on the Predictive Value of Brain Biomarkers. J Pain. 2016;17(6):637-641.

Robinson ME, et al. Comparison of machine classification algorithms for fibromyalgia: Neuroimages versus self-report. J Pain. 2015:16(5):472-477.

Candida Overgrowth Prevention

Preventing Candida overgrowth is easier than treating it, say Natália Martins and her Portuguese colleagues. Candida, a genus of yeast, is a normal part of human microbiota. Its presence, most commonly the species C. albicans, limits the growth of other fungi and promotes immune function. Normally, immune cells and probiotic bacteria prevent Candida from becoming invasive. When the microbial balance is disrupted, Candida species can invade the gastrointestinal system, genitourinary system, cardiovascular system, and respiratory tract, causing multiple symptoms. Candida readily forms biofilms with other microbes. Factors that contribute to Candida overgrowth include decreased digestive secretions, diets with a high-sugar and/or high fungi-yeast content, nutritional deficiencies, impaired immune function, and some medications such as antacids, corticosteroids, and antibiotics.

Recognizing that antibiotics disrupt microbial balance, an Indian research team, led by Suresh Kumar, MD, tested the use of a probiotic combination to prevent Candida overgrowth in 144 critically-ill children, age three months to 12 years, as an alternative to pharmaceutical anti-fungal drug treatment. Pharmaceuticals promote resistant strains, have adverse effects, and cost more. Children enrolled in this 2013 double-blind, placebo-controlled study were being treated with broad spectrum antibiotics for at least 48 hours. The probiotic preparation, which was given twice daily for one week, included Lactobacillus rhamnosum, Bifidobacterium longum, Bifodobacterium bifidum, Saccharamyces boulardi, Saccharomyces thermophilus, and fructo-oligosaccharides.

The authors report a statistically significant increase in Candida colonization (from rectal swabs) at day 7 and day 14 in children receiving the lactose placebo, but not in the probiotic group: “…concurrent administration of probiotics for 1 wk in critically ill children receiving broad spectrum antibiotic therapy decreased the prevalence of Candida colonization by 34.5% on day 7 and 37.2% on day 14.” Also, prevalence of candiduria, a marker for systemic candidiasis, was 50 percent less in the probiotic group compared to control. The authors say, “Concurrent use of probiotics with antibiotics should be evaluated as a strategy to reduce the Candida colonization and prevalence of candidemia in critically ill children, in a multicentric study.”

Kumar S, et al. Evaluation of Efficacy of Probiotics in Prevention of Candida colonization in a PICU-A Randomized Controlled Trial. Critical Care Medicine. February 2013; 41(2): 565-572.

Martins N, et al. Candidiasis: predisposing factors, prevention, diagnosis and alternative treatment. Mycopathologia. 2014;177(5-6):223-240.