SCIENTIFIC STUDIES SHOW THAT ANY NUMBER OF CHRONIC HEALTH PROBLEMS CAN BE HELPED OR PREVENTED
- Three months ago, the Journal of Bodywork and Movement Therapies (Evidence for the Existence of Nociceptors in Rat Thoracolumbar Fascia) showed a mechanism for CHRONIC LOW BACK PAIN. We already know that it is almost impossible to correlate both arthritis and disc problems found on x-rays or MRI, to the amount or area of pain a person is having (HERE). This study revealed at least part of the reason why. As per the title of the study, nociceptors (pain receptors) have been found in the connective tissue that covers the low back and ‘hips’ — the THORACOLUMBAR FASCIA. Click the link to see 10 second videos side by side of the Thoracolumbar Facia in people with low back pain, versus the Thoracolumbar Fascia in people without low back pain. Astounding!
- Speaking of arthritis, last month’s issue of Rheumatic & Musculoskeletal Diseases Open published a study about post-traumatic arthritis (Post-Traumatic Arthritis: Overview on Pathogenic Mechanisms and Role of Inflammation). I went through school being taught that this was essentially the mechanism for most arthritis (HERE). However, we now know that most “degenerative” arthritis (osteoarthritis) is caused by the group of immune system chemicals released by our tissues in order to heal said tissues when they are injured or compromised —- INFLAMMATION. The most interesting aspect of this study (besides the fact that the medical community continues to use CORTICOSTEROIDS, which were deemed unfit for tissue injury decades ago) is that, “Evidence in human and animal articular cartilage suggested the activation of the remaining viable chondrocytes [cartilage cells] through the enhanced cell metabolism and the generation of oxygen radicals [they cause cancer and tissue degradation], matrix-degrading enzymes and inflammatory mediators. The exacerbation of the tissue biomechanical and physicochemical properties results in significant changes in chondrocytes, altering their ability to express proteins involved in metabolic pathways and leading to cell death [aka cellular apoptosis]. Since chondrocytes are responsible for maintenance of articular cartilage function, their death through apoptotic mechanisms is central in the development of post-traumatic osteoarthritis.” The authors go on to conclude that, “Since activation of inflammatory mechanisms is considered to be critical to development of chronic disease, anti-inflammatory interventions may represent the best available opportunity to intervene early in the acute post-traumatic period.” Great, but I just showed you the problems associated with corticosteroids and the rest of the “BIG FIVE” when used for soft tissue injuries (HERE is another crazy example). Stick with me because we will talk about non-pharmaceutical interventions for inflammation at the end of the post
- This month’s issue of Neuroscientist (The Effects of Extended Pain on Behavior…) dealt with the way that CHRONIC PAIN affects your brain as well as the way you think and act. “Chronic pain is frequently associated with anxiety, depression, and cognitive dysfunction.” If you’ve ever been around people with Chronic Pain, you already know this. “Functional changes, including increases in the activity within specific neuronal pathways and in the levels of specific synaptic components, that are associated with the behavior changes, have recently been identified. Broadly projecting modulatory systems and widely expressed factors such as cytokines and growth factors also contribute to pain-associated behavior.” Plainly stated, they are saying that with Chronic Pain comes very specific brain dysfunctions and inflammation. This is why some of you will need to see a FUNCTIONAL NEUROLOGIST to have any prayer at solving a BRAIN-BASED problem.
- MICROGLIA are amazing. They are one of the GLIAL CELLS make up as much as 15% of the mass of your brain and act as its first defense against anything foreign (they engulf it and digest it like “The Blob”). Because the blood brain barrier prevents most antibodies from passing into the brain (they are too large), microglia must be Johnny-on-the-spot; recognizing, eating, and digesting / destroying invaders, while INITIATING THE BODY’S T-CELL RESPONSE. A failure to act quickly can result in damage to both brain and cord. Mast Cells are a type of white blood cells (immune system cells) that release two of the chemicals we that make up the spectrum of chemicals we call inflammation — histamine & heparin. A couple of weeks ago, CNS Neurological Disorders Drug Targets (Mast Cell – Glia Dialogue in Chronic Pain and Neuropathic Pain: Blood-Brain Barrier Implications) said that, “Mast cells and microglia, working singly and in partnership, elaborate pro-inflammatory molecules which play key roles in a wide array of nervous system disorders. Such neuroinflammatory settings may compromise integrity of both the blood-nerve barrier, blood-brain barrier and blood-spinal cord barrier. Mast cells and glia possess endogenous homeostatic mechanisms/molecules which are up-regulated following tissue damage. Such molecules include the N-acylethanolamine family. In particular, N-palmitoylethanolamine is proposed to have a key role in maintaining cellular homeostasis against external stressors provoking, for example, inflammation.” In the same manner that chronic inflammation can lead to something called LEAKY GUT SYNDROME (Increased Intestinal Permeability) it can likewise lead to other “leakies” — in this study, Leaky Brain / Cord / Nerve Syndrome. Although this study was searching for drug-like compounds to target specific chemical entities, it provides more evidence that you had better control inflammation as though your life depends on it. Stick around and I’ll show you how to at least get started without drugs.
- Adiponectin, leptin, and resistin are chemicals that are made and released by fat (adipose tissue) and known as adipokines. It’s important to recall that many of the substances that end in “kine” are classified as inflammation — chemokines, cytokines, kinnins). Last months issue of Cephalalgia (Investigating the Role of Adipokines in Chronic Migraine) said that, “Adiponectin, leptin, and resistin are adipocyte-derived secretory factors involved in endothelial function [Leakies], weight, inflammation, and insulin resistance. Recent studies suggested a role for adipokines in episodic migraine as mediators of inflammatory processes. Serum levels of adiponectin and resistin were significantly increased in chronic migraineurs in comparison with controls. After correction for BMI, sex and age, leptin levels were significantly increased in chronic migraineurs. A positive correlation between leptin concentrations and both indices of insulin resistance and markers of inflammation was found. Our data suggest that adiponectin and resistin are altered in non-obese chronic migraineurs.” It’s important to understand that every single health problem listed in this bullet (HEADACHES & MIGRAINES INCLUDED) is inflammatory (HERE is a list). Although it may not be relevant, also remember that while only about one third of our population is actually OBESE, more than that many again are overweight. What makes things even more interesting is that a large segment of the “normal weight” population are actually considered to be metabolically obese (MONW), which is sometimes referred to as “Skinny Fat”.
- Your Sympathetic Nervous System is the part of your nervous system associated with “fight or flight”. It dumps epinephrine (adrenaline) in your system, causing everything up in your musculoskeletal system and heart to ramp up, while decreasing blood flow and function to your organs of digestion. On the other hand, the Parasympathetic Nervous System is all about rest, relaxation, and digestive function. Unfortunately, huge numbers of Americans live in a perpetual state of SYMPATHETIC DOMINANCE. Not only does this set people up for Chronic Pain, but it usually means that even though they live in a state of exhaustion, they can’t really sleep. Most have a wide variety of health problems as well. The August issue of the Journal of Neuroscience (Localized Sympathectomy Reduces Mechanical Hypersensitivity by Restoring Normal Immune Homeostasis in Rat Models of Inflammatory Pain) had some fascinating things to say about this phenomenon. The researchers essentially “cut out” (oversimplified) the Sympathetic Nervous System of rats that had been chemically induced with Chronic Pain resulting in, “profound sustained reductions in pain behaviors induced by local dorsal root ganglia inflammation (a rat model of low back pain). Effects of microsympathectomy were evident within one day. Microsympathectomy reduced local inflammation and macrophage density in the affected tissues (as indicated by paw swelling and histochemical staining). Cytokine profiling in locally inflamed DRG showed increases in pro-inflammatory Type 1 cytokines and decreases in the Type 2 cytokines present at baseline, changes that were mitigated by microsympathectomy.” The point here is not that I am suggesting anyone try and find a surgeon that will cut out your Sympathetic Nervous System. What I am suggesting is that there are any number of things you can do to potentially reduce the inflammatory load on this part of your nervous system, thereby diminishing (or maybe even solving) Sympathetic Dominance.
- Anytime you see the word “itis” you must realize the topic is inflammation. Adhesive Capsulitis (aka “Frozen Shoulder Syndrome”) is an inflammation of the ligaments that make up the capsule that surround the shoulder joint and contain the synovial fluid. Also understand that inflammation always leads to the SCAR TISSUE that the medical community refers to as fibrosis (HERE). The March issue of Medical Hypotheses (Adhesive Capsulitis: An Age Related Symptom of Metabolic Syndrome and Chronic Low-Grade Inflammation?) revealed that, “Obesity and metabolic syndrome, which are strongly associated with chronic low grade inflammation, are becoming increasingly understood to underlie a raft of morbid states including upper limb pain syndromes, diabetes, cardiovascular disease, cancer and central nervous system dysfunction and degeneration. Notwithstanding age, two of the strongest established risk factors for adhesive capsulitis are diabetes and cardiovascular disease. The hypothesis argues that similar to diabetes and cardiovascular disease, the inflammation and capsular fibrosis seen in adhesive capsulitis is precipitated by metabolic syndrome and chronic low grade inflammation. These pathophysiological mechanisms are highly likely to be perpetuated by upregulation of pro-inflammatory cytokine production, sympathetic dominance, and neuro-immune activation.” Here’s the deal folks; forget adhesive capsulitis for a second. We could insert almost any sort of chronic illness / Chronic Pain into the equation and these conclusions would still be true. This reminds me of a patient whose severe low back pain was being driven by a combination of GLUTEN SENSITIVITY and OVER-CONSUMPTION OF PROCESSED CARBS. What does this study really mean for you, the struggling person who’s reading this right now?
It means that the more time you spend on my site, the more you realize that when it comes to chronic illness and chronic pain, everything is really one big thing — different manifestations of out-of-control inflammation. In other words, as long as your problem is not totally genetic (most are actually EPIGENETIC) or LARGELY BIOMECHANICAL, figuring out what’s driving the inflammation in your body is the key to helping you get better. The really cool thing is that much of it can be done yourself, although some of you might require a Functional Neurologist or a specialist in Functional Medicine. For the rest of you (the majority of you), HERE is a basic protocol. Does it work? For most of you reading this, if you do it correctly it will work like magic (HERE).