History of previous work: Most people --especially clinicians and healthcare students-- who are familiar with my work know that most of my teaching originated from the work that I did when I started teaching Orthopedics and Rheumatology for the Naturopathic Medicine Program at Bastyr University in 2000 and 2001; from those seedling course notes blossomed the books initially published as Integrative Orthopedics (2004, 2007, 2011), Integrative Rheumatology (2006, 2007, 2014 and now published as Inflammation Mastery, 4th Edition in 2016) and also Musculoskeletal Pain: Expanded Clinical Strategies, commissioned by the Institute for Functional Medicine in 2008. During all these years, I have published more than 110 professional articles and letters on the topics of nutrition and pain and inflammation, and I have given innumerable post-graduate presentations internationally. Many of my articles such as on vitamin D (2004) and mitochondrial nutrition (2014) have been potent "paradigm shifts" in the way clinicians view specific problems and solutions in clinical practice. Likewise, my most recent major article is titled "Neuroinflammation in fibromyalgia and CRPS is multifactorial" published in Nature Reviews Rheumatology (March 2016).
The way we previously viewed pain and inflammation: Previously, we were aware of local inflammation (such as occurs following an acute injury or trauma), and then later we became aware of systemic inflammation in the absence of trauma (such as occurs with obesity, diabetes, and cardiovascular disease). From a medical standpoint, we have used anti-inflammatory drugs such as NSAIDs (non-steroidal antiinflammatory drugs, such as aspirin and naproxin) and DMARDs (disease-modifying antiinflammatory drugs, such as prednisone and methotrexate and later the "biologics" which target TNF). From a nutritional standpoint, we used and have continued to use natural and nutritional antiinflammatory interventions such as diet (review part 1, 2004), n3 fatty acids (review part 2, 2005), ginger and other nutrients (review part 3, 2005), targeted inhibition of NFkB (review part 4, 2005) and correction of dysbiosis (review part 6, 2006).
With the development of my "functional inflammology protocol" (first presented and published in 2012; see video introduction from our 2013 International Conference on Human Nutrition and Functional Medicine) we have progressively appreciated that we can change immunocyte phenotype via nutritional interventions, what I have called "nutritional immunomodulation" most recently detailed in Chapter 5 of Inflammation Mastery, 4th Edition and identically in the two-volume set Textbook of Clinical Nutrition and Functional Medicine, Volume 2 (2016).
The way we must currently view pain and inflammation: What is becoming clear --both from the science as well as the pharmaceutical industry's attempt to exploit that science-- is that pain and inflammation are inextricably intertwined. Simplistically yet accurately, we can state that inflammation promotes (amplifies) pain, and also that pain promotes (neuro)inflammation.
I diagrammed this relationship in the updated version (2016) of my work on migraine (originally published in 2004) and fibromyalgia (originally published in 2008); this is available in Chapter 5 of my 4th Edition work (op cit) and also in a separate monograph Pain Revolution (full color) and Brain Inflammation (grayscale). I underscored this concept in a recent press release; with more thought and reflection and reading, I have progressively understood this concept at a deeper level.
As I have shown on the book covers of Pain Revolution and Brain Inflammation, these are vicious cycles. Pain triggers neuroinflammation which promotes neurogenic inflammation for additional pain and inflammation. Beyond that and within that, mitochondrial dysfunction is triggered by inflammation while also promoting neuronal hypersensitivity, promoting neuroexcitation and additional depolarization, additional pain reception, and additional inflammation.
Thus, pain and inflammation are not simply associated; they are unified, united, identical. One creates the other so that they (can and often do) become one continuum. Thus, we may one day use a cojoined term such as painflammation to connect and express our understanding of the connection between pain and inflammation and how chronic pain is dependent on brainflammation while pain (sensory reception of nociceptive signals) also leads to inflammation of nerves, brain regions.
*Although the word "paradigm" is commonly overused and implies a subconscious view of something, it is a stronger term than is "model" (a consciously held view) and will be used here. Here the term emphasizes 1) a complete model that 2) defines the corresponding behavior.
The complete work is Inflammation Mastery 4th Edition; the color excerpt is Pain Revolution in Migraine and Fibromyalgia (digital ebook available); the cheaper grayscale excerpt is Brain Inflammation in Chronic Pain (same digital ebook).
Original source for this article, "Brain Inflammation Blog #1": http://www.ichnfm.org/#!BRAIN-INFLAMMATION-BLOG-1-The-New-Paradigm/c7a5/571e1b630cf26b6d6841f772