revisiting the inflammation / fibrosis (scar tissue) connection as the solution to chronic pain and chronic disease

FOR THOSE STRUGGLING WITH CHRONIC PAIN AND / OR CHRONIC DISEASE
PAY ATTENTION!

Inflammation Fibrosis

INFLAMMATION & FIBROSIS
THE FORMER ALWAYS LEADS TO THE LATER

“When you see smoke (inflammation), you had better start looking for fire (fibrosis).”  – Dr. Russell Schierling

“Nearly 45% of all deaths in the developed world are attributed to some type of chronic fibroproliferative disease [fibrosis].  Fibroproliferative diseases, including pulmonary fibrosis, systemic sclerosis, liver cirrhosis, cardiovascular disease, progressive kidney disease, and macular degeneration, are a leading cause of morbidity and mortality and can affect all tissues and organ systems. Despite its enormous impact on human health, there are currently no approved treatments that directly target the mechanism(s) of fibrosis.  Damage to tissues can result from various acute or chronic stimuli, including infections, autoimmune reactions, and mechanical injury. Although initially beneficial, the healing process becomes pathogenic if it continues unchecked, resulting in substantial formation of permanent scar tissue. Pathogenic fibrosis typically results from chronic inflammatory reactions — defined as responses that persist for several weeks or months and in which inflammation, tissue destruction, and repair processes occur simultaneously.  Dr. Thomas Wynn from The Journal of Clinical Investigation (Common and Unique Mechanisms Regulate Fibrosis in Various Fibroproliferative Diseases).  The good news for those of you struggling with chronic pain or chronic illness is that the author goes on to say that there is an, emerging paradigm that fibrosis is a reversible process.”

As you may have noticed from the quote above, there are any number of factors that drive tissue damage in the body (note that overlap is not only a possibility, but in most cases, a probability).

Inflammation is the name given to the hundreds of chemical mediators that act as the body’s cellular messengers for the purpose of healing damaged tissue.  The body doesn’t really care how the tissue injury occurred (or in many chronic cases, is ongoing), but will do what it takes to heal it by manufacturing and releasing the chemicals (inflammation) to do so.  The thing to remember here is that while a certain amount of inflammation is needed, anything over that amount causes a wide variety of problems.  Although the list of potential problems caused by unbridled inflammation are virtually limitless, one sticks out above the rest due to it’s penchant for causing pain, sickness, disability, and death, all on a grand scale (the quote at the top shows that it causes almost half of all deaths).  We are talking about Fibrosis.

I have shown you any number of times (HERE is the best example), that too much or too many of the chemical mediators needed to heal damaged tissue (INFLAMMATION) always leads to formation of the Scar Tissue that the medical community refers to as “FIBROSIS“.  Thus, it should be fairly clear that we are not only talking here about the SCAR TISSUE that I deal with all day long in my clinic as far as solving CHRONIC PAIN SYNDROMES is concerned.  We are talking about the microscopic adhesions that form the foundation of virtually every single disease process you can name (and hundreds more you can’t). 

Bottom line, inflammation kills via a process of your body weaving microscopic webs that ensnare and entangle cells, tissues, and organs, preventing them from moving, gliding, or functioning biochemically as they should.  For those of you who think I’m “whistlin Dixie,” this post is for you.  Follow along as I prove this to you this from the peer-reviewed literature of the past two or three months (all quotes are cherry-picked due to restraints on time and space).  Which is exactly why you should be living an ANTI-INFLAMMATORY LIFESTYLE — even if you are healthy.  Especially if you are healthy!  Taking your health for granted because you are free of symptoms today, can inhibit your body’s ability to fight off or heal whatever life decides to throw at it tomorrow.

INFLAMMATION ALWAYS LEADS TO FIBROSIS
THE PEER-REVIEWED RESEARCH FROM THE PAST COUPLE OF MONTHS

SKIN OR WOUND INJURIES (CAN ANYONE SAY FASCIA?):  I’ve talked previously about the way that SKIN is linked to FASCIA, including those things we refer to as “STRETCHMARKS“.  The link is much deeper than that, and inflammation is a huge factor.  The October issue of the Journal of Investigative Dermatology (Targeted Disruption….. Is Sufficient to Induce Skin Inflammation and Fibrosis) revealed that a specific gene can contribute to, “inflammation and development of skin fibrosis with extensive accumulation of interstitial and microfibrillar collagens.”   A different study from the same journal talked about one of the many chemical mediators that makes up what we refer to as inflammation (TGF-β), showing how when levels are suppressed, “the epidermis displays decreased scarring.”  Research from last month’s issue of the Journal of Neuromuscular Diseases (…Inflammation and Fibrosis of Skeletal Muscles) was based on, “the interplay between cytokines / chemokines, growth factors [“mediators of inflammation] and permanent low-grade inflammation favoring cellular and molecular modifications resulting in fibrosis.”   And finally, last month’s issue of Frontiers in Physiology summed it all up with a study called Wound Healing Problems in the Mouth.  Under the header, Normal Wound Healing Process, the authors said that, “Wound healing requires multiple finely tuned processes that occur in a specific sequence.  Intact inflammatory mechanisms are needed….together with collagen synthesis. Further wound healing involves regeneration (the substitution of damaged tissues with the same cell type) and fibrosis (replacement of damaged tissues with connective tissue).”  COLLAGEN is great — until the healing process goes off the rails due to rampant inflammation.

WEED, INFLAMMATION, & FIBROSIS:  The November issue of the Journal of the Federation of American Societies for Experimental Biology carried a fascinating study called Cannabinoids, Inflammation, and Fibrosis, which compared the anti-inflammatory abilities of NSAIDS to WEED.  The study revealed that, “Cannabinoids apparently act on inflammation through mechanisms different from those of agents such as nonsteroidal anti-inflammatory drugs (NSAIDs). As a class, the cannabinoids are generally free from the adverse effects associated with NSAIDs. Their clinical development thus provides a new approach to treatment of diseases characterized by acute and chronic inflammation and fibrosis. Several cannabinoids may be considered candidates for development as anti-inflammatory and antifibrotic agents. Of special interest is their possible use for treatment of chronic inflammation, a major unmet medical need.”   As you wind your way through today’s post, pay close attention to how many mainstream journals are running trials on various herbs, plants, and botanicals as alternates to pharmaceuticals.

GENERALIZED INFLAMMATION, FIBROSIS AND DISEASE:         Less than a month ago, Fundamental & Clinical Pharmacology published a study called Purinergic Receptors: New Targets for the Treatment of Gout and Fibrosis.  This study showed that, “Extracellular ATP [energy] release by activated or necrotic [dead or dying] cells may activate various purigenic receptors and especially P2X7R.  P2X7R is known to regulate the activation of the NLRP3 inflammasome, which permit the release of IL-1β, a potent pro-inflammatory cytokine. The P2X7R/NLRP3 pathway is involved in many inflammatory diseases, such as gout, and in fibrosis diseases associated with inflammatory process, liver or lung fibrosis.”  Bottom line, researchers are looking for various compounds to be patented as blockers of this pathway that could be sold for huge profit at drugstores.

INFLAMMATORY BOWEL DISEASE:        The October issue of Gastroenterology (Mechanisms, Management, and Treatment of Fibrosis in Patients with Inflammatory Bowel Diseases) concluded that, “In the last 10 years, we have learned much about the pathogenesis, diagnosis, and management of intestinal fibrosis in patients with inflammatory bowel diseases (IBD). Just a decade ago, intestinal strictures were considered to be an inevitable consequence of long-term inflammation… IBD-associated fibrosis was seen as an irreversible process that frequently led to intestinal obstructions requiring surgical intervention.”  Unfortunately, even though things are improving, this sort of fibrosis is still largely irreversible via medications (HERE).  Case in point, a study from October’s issue of the American Journal of Physiology Gastroenterology & Liver Physiology (Hydroxylases Regulate Intestinal Fibrosis.) which concluded, “Fibrosis is a complication of chronic inflammatory disorders such as inflammatory bowel disease (IBD), a condition which has limited therapeutic options.”  There were also several studies discussing various compounds to block the body’s inflammatory pathways.  Last month’s issue of Crohn’s & Colitis (Genetic Deletion of Tissue Inhibitor of TIMP-1 Alters Inflammation and Attenuates Fibrosis) revealed that, “Increased levels of tissue inhibitor (TIMP-1) have been detected in both inflammatory and fibrotic lesions in Crohn’s disease….  Chronic inflammation and fibrosis were associated with an increase in TIMP-1.

ABDOMINAL ADHESIONS:  Pirfenidone is an anti-fibrotic drug that works by down-regulating the production of growth factors and pro-collagen substances.  In a study from August’s issue of the Journal of Investigative Surgery (Effect of Pirfenidone on Vascular Proliferation, Inflammation and Fibrosis in an Abdominal Adhesion Rat Model), the authors started out by subjecting three groups of female rats to a model that is known to create abdominal adhesions.  The rats were treated in various ways by the drug Pirfenidone.  Not that I’m really interested in this drug, but we learned that, “Intraperitoneal administration of pirfenidone compared to oral administration was more effective in reducing tissue levels of inflammatory markers.”  Why did this matter to the authors?  Because Inflammation always leads to Fibrosis!  “Pirfenidone is an effective agent on the prevention of postoperative vascular proliferation, inflammation and fibrosis in scarred tissue.”  By the way, I get lots of questions about POST-SURGICAL SCAR TISSUE.  The real question that needs to be answered as related to this particular bullet is whether it’s in the ABDOMINAL WALL OR ABDOMINAL CAVITY.

SYSTEMIC SCLEROSIS A.K.A SCLERODERMA:  Scleroderma is one of the Autoimmune Diseases my sister cured herself of (along with Rheumatoid Arthritis, something similar to Lupus, and two others — HERE).  It is an all over fibrosis, that causes a wide variety of pain syndromes and organ problems.  Last month’s issue of the American Journal of Physiology (Transforming Growth Factor β… Inflammation and Pulmonary Fibrosis) concluded that, “TGF-β signaling [“inflammation”] affects pulmonary abnormalities… that manifests three important lung pathological features: fibrosis, inflammation, and vascular remodeling.”  A study from the October issue of the Journal of Clinical and Experimental Rheumatology (Th17 Cells and IL-17 Promote the Skin and Lung Inflammation and Fibrosis….) concluded that the TH-17 SYSTEM, “participates in the pathogenesis of skin and lung fibrosis by enhancing fibroblast proliferation and cytokine [inflammation] production.”  HERE is information about fibroblasts (scar tissue / collagen forming cells) as related to this subject.  Not surprisingly, two weeks ago the journal Arthritis Research & Therapy (Intestinal Dysbiosis is Common in Systemic Sclerosis….) related it all to GUT HEALTH and something called DYSBIOSIS.  “Recent evidence suggests altered microbiota composition, commonly referred to as dysbiosis, has been shown to induce and modulate systemic inflammation in rheumatic diseases and immune-mediated inflammatory diseases. In the field of rheumatology, intestinal dysbiosis has been associated with rheumatoid arthritis, systemic lupus erythematosus, Sjögren’s syndrome and ankylosing spondylitis.  In Scleroderma, small intestinal bacterial overgrowth [SIBO] is a well-described complication associated with GI dysmotility, GI discomfort, and malnutrition. Dysbiosis was more severe in patients with elevated serum markers of inflammation. We suggest that an aberration of the intestinal microbiota may contribute to the development of systemic inflammation and fibrosis.”  October’s issue of the Journal of Investigative Dermatology (Glycyrrhizin Ameliorates Fibrosis, Vasculopathy, and Inflammation…) looked at the effects of licorice root as a solution to this problem.  “Systemic sclerosis is a multisystem inflammatory and vascular disease resulting in extensive tissue fibrosis. Glycyrrhizin, clinically used for chronic hepatic diseases and itching dermatitis, modulates the pathological processes of inflammation, vasculopathy, and fibrosis in human diseases.  These results indicate that glycyrrhizin ameliorates dermal fibrosis through the inhibition of fibroblast activation [fibrosis].” 

METABOLIC SYNDROME:  Metabolic Syndrome, more commonly referred to as Cardiometabolic Syndrome or Pre-Diabetes, is absurdly out of control here in America (HERE).  Characterized by having two of seven distinct entities (HERE), this problem potentially affects all organ systems.  The September issue of Obesity Science & Practice (Highly Purified Eicosapentaenoic Acid Ameliorates Cardiac Injury and Adipose Tissue Inflammation…) showed how PFGO (my clinic’s number one selling product) can prevent both inflammation and fibrosis. “The present study has here shown that EPA attenuated adipocyte hypertrophy [fat cell growth] and inflammation in visceral fat [fat around organs] as well as fibrosis, diastolic dysfunction, oxidative stress and inflammation in obese rats. The beneficial effects of EPA on the heart are likely due to reduced cardiac oxidative stress and inflammation.”  The September issue of the Canadian Journal of Physiology and Pharmacology dealt with the DIABETES DRUG Gemigliptin, saying that it, “ameliorated inflammation and fibrosis through suppression of oxidative stress.”  In a similar study from October’s issue of Medical Hypothesis, a drug originally made from flowers (Colchicine) specifically for people who don’t tolerate NSAIDS, was tested on people with Metabolic Syndrome.  Authors concluded that, “it appears to exert an anti-inflammatory, anti-fibrotic, and immuno-modulatory effect“.  How effective are these and similar drugs at actually solving Metabolic Syndrome?  Despite what these last two studies are saying, unfortunately not too (see previous link). 

FULL-BLOWN DIABETES:  Truth be known, for all intents and purposes, if you have pre-diabetes you are a functional diabetic.  So it’s no surprise to see that this month’s issue of Pharmacology and Therapeutics dealt with the issue in a study called Cardiac Oxidative Stress in Diabetes: Mechanisms….  What is the mechanism for developing diabetes?   In a study that addresses AGES, Vascular Complications of Diabetes….., we saw yet again that, “cardiac oxidative stress is associated with increased cardiac fibrosis and hypertrophy, and reduced cardiac performance and contractility, leading to severe cardiac dysfunction and potentially fatal cardiac events. It occurs under conditions of excessive synthesis of reactive oxygen species [FREE RADICALS].  The ensuing activation produces inflammation, fibrosis, and further oxidative stress, which itself causes DNA and membrane damage.”  The October issue of Biomedicine & Pharmacotherapy published as study showing that one way to halt this damage was via a Chinese herb known as Dendrobium Officinale Kimura.  The authors concluded that this herb, “possesses cardioprotective potential against diabetic cardiomyopathy, which may be due to the inhibition of oxidative stress, cardiac lipid accumulation, pro-inflammatory cytokines and cardiac fibrosis.”  Needless to say, there were several similar studies talking about inflammation and fibrosis the liver, lungs, and other organs as related to diabetes (HERE is my article on Fascia as related to Diabetes).

HEART:  Bear in mind that a myocardial infarction (MI) is the medical way of saying “Heart Attack”. Last month’s issue of Arthritis Care and Research (Magnetic Resonance-Detected Myocardial Inflammation and Fibrosis in Rheumatoid Arthritis….) concluded that, “Myocardial dysfunction and heart failure are increased in rheumatoid arthritis (RA).  These data suggest that MR findings indicating myocardial inflammation/fibrosis are correlated with RA disease activity and alterations in myocardial structure known to associate with precede clinical heart failure.” The November issue of Inflammation published a study on inflammation and fibrosis as it relates to heart attacks, saying that, “Inflammation has been implicated in myocardial infarction. MDM2 associates with nuclear factor-κB (NF-κB)-mediated inflammation.  MDM2 inhibition reduced cardiac dysfunction and fibrosis after MI.” Just a couple of weeks ago, the British Journal of Pharmacology published a similar study called SITA Reduces Inflammation, Fibrosis and Preserves Diastolic Function……  In this study we saw that, “SITA positively interferes with inflammatory-related endothelial dysfunction and fibrosis…   Myocardial levels of pro-inflammatory TNF-α, IL-6 and MCP-1 were reduced. The markers of oxidative and nitrosative stress were decreased. Moreover, increase of collagen deposition and activation of pro-fibrotic signaling, that lead to elevated myocardial stiffness, were attenuated by SITA.”  Last month’s issue of the Journal of Biochemical and Molecular Toxicology carried research that dealt with a substance called Galectin (a group of proteins characterized by the way they bind to sugar) as it relates to monocrotaline (a toxic plant constituent that poisons livestock and humans through the ingestion of contaminated grains and other foods, which causes an array of heart problems).  “Galectin-3 (Gal-3) plays a critical role in vascular inflammation and fibrosis. The role of TGF-β1 in mediating pulmonary vascular fibrosis is well documented; thus, we suspected that Gal-3 could be an important factor in TGF-β1-induced fibrosis in pulmonary fibroblasts.”  What are FIBROBLASTS?  Click for the answer (blasts are “builders,” thus fibroblasts build fibrous tissue.  This is fine and is necessary for healing as long as there is not too much inflammation in the system, which always ends up causing fibrosis.

LUNGS / ASTHMA:  This month’s issue of the American Journal of Respiratory, Cell, and Molecular Biology published a study about the way that inflammation causes fibrosis after chronic UPPER RESPIRATORY INFECTIONS.  “NFkB is a major controller of pulmonary fibrosis, a finding that has potentially important relevance to airway remodeling produced by repetitive viral infections”  This is a huge deal once you understand how important NFkB really is.  According to Wikipedia it’s, “a protein complex that controls transcription of DNA, cytokine production and cell survival. NF-κB is found in almost all animal cell types and is involved in cellular responses to stimuli such as stress, cytokines, free radicals, heavy metals, ultraviolet irradiation, oxidized LDL, and bacterial or viral antigens. NF-κB plays a key role in regulating the immune response to infection.”  Another study from the same issue of the same journal looked at similar compounds concluding, “that the redistribution of SOD3 as a result of the R213G SNP protects mice from bleomycin-induced fibrosis and secondary pulmonary hypertension by improved resolution of alveolar inflammation.”   Interestingly enough, when researching this post I found numerous studies on the anti-inflammatory herb curcumin.  Last month’s issue of Inflammation carried a study which concluded, “Pulmonary fibrosis is associated with irreversible, or partially reversible, airflow obstruction and ultimately unresponsiveness to asthma therapies such as corticosteroids. Intranasal curcumin, an anti-inflammatory molecule, has been found effective in allergic asthma.”  Wow! Why has it been effective?  “Curcumin significantly inhibited airway inflammation and pulmonary fibrosis. These results suggest that intranasal curcumin regulates airway inflammation and remodeling in chronic asthma.”  Another study with curcumin, this one from the November issue of Pharmacological Research (Curcumin Use in Pulmonary Diseases) revealed that, “Over the last several decades, the therapeutic properties of curcumin have slowly been elucidated. It has been shown that curcumin regulates transcription factors (NF-kB), cytokines (IL6, TNF-alpha), adhesion molecules (ICAM-1), and enzymes (MMPs) that play a major role in inflammation and cancerogenesis. These effects may be relevant for several pulmonary diseases that are characterized by abnormal inflammatory responses, such as asthma or chronic obstructive pulmonary disease, acute respiratory distress syndrome, pulmonary fibrosis, and acute lung injury. Furthermore, some preliminary evidence suggests that curcumin may have a role in the treatment of lung cancer.” speaking of Cancer as related to fibrosis (we already know Cancer is considered an “INFLAMMATORY DISEASE“)……..

CANCER:  Because CANCER is running rampant in the United States, it pays to understand its link to inflammation and fibrosis. The November issue of Cancer Letters revealed how intimate the relationship via its title, G Protein-Coupled Estrogen Receptor Deficiency Accelerates Liver Tumorigenesis by Enhancing Inflammation and Fibrosis.  Earlier this year, the Soviet journal Molekuliarnaia Biologiia (S100A4, A Link Between Metastasis and Inflammation) concluded that, “Chronic inflammation is acknowledged to be a hallmark of neoplasia – both in cancer initiation and metastasis progression [spreading to other areas within the body]. Here we summarise data suggesting that S100A4 is а trigger of the cascade events that establish an inflammatory milieu and provide a potent flame for primary tumour growth and especially for its metastatic dissemination.  This protein is also involved in the pathogenesis of autoimmune diseases, fibrosis, and other disorders. Therefore, we suggest that S100A4 is a common pro-inflammatory factor involved in the pathogenesis of diverse diseases including cancer.”   This next study looks at the whole inflammation / fibrosis / cancer link as it pertains to a tropical flowering plant called Plumbago Genus.  October’s issue of Oncotarget revealed that, “Results shown that plumbagin increased survival rate, reduced liver congestion and inflammation, and remarkably diminished liver fibrosis and inflammation in the chronic liver injury model.  Plumbagin may be a powerful drug candidate to protect the liver from acute and chronic damage by inhibiting inflammation and collagen production [fibrosis].

OBESITY:  OBESITY is yet another of those common health issues that falls under the category of “Inflammatory”.  Last month’s issue of Scientific Reports (A High-Fat High-Sucrose Diet Rapidly Alters Muscle Integrity, Inflammation and Gut Microbiota…) concluded something we are already largely (no pun intended) aware of (HERE), “Abnormal muscle repair is defined by sustained muscle fibrosis, which interferes with the appropriate healing of muscle tissue.  We show that intramuscular fat, fibrosis, and the number of pro-inflammatory cells increased by day three and was sustained across twenty eight days of high-fat high-sugar feeding compared to control-diet animals.  This muscle wasting includes both intramuscular adipose [fat] accumulation and muscle fibrosis, and moreover, intramuscular fat and inflammatory cell accumulation is associated with the onset of insulin resistance.  Adipose tissue lipid storage is altered with obesity, and adipose tissue fibrosis is considered a hallmark of metabolic alterations.  Moreover, insulin resistance is reported to be a consequence of human adipose tissue fibrosis.”  Did you catch that?  Read it again carefully if you didn’t.  Although intimately related to each other, Insulin Resistance occurs long before diabetes or even pre-diabetes (HERE).   The important point to remember here is that not all fat is created equal (HERE).  Because dietary fat can either drive inflammation or squelch inflammation, it would be interesting to see this study repeated with a wide variety of dietary fats.  DO NOT BE AFRAID OF DIETARY FAT — make fat your friend!

POST-SURGICAL DISC PROBLEMS:  Earlier this year, an issue of the Annals of Neuroscience published a study called Experimental Model of Intervertebral Disk Mediated Postoperative Epidural Fibrosis.  In this study, we learned that, “It is known that scar tissue is always formed as a physiological reaction to any surgical intervention in response to the surgical trauma. However, the intensity and duration of this process may be different and depends on many factors.  Postoperative epidural fibrosis after lumbar discectomy is its most common and at the same time controversial issue.  Epidural fibrosis has been described in 24-38% of patients with failed back surgery syndrome. Re-operations, aimed at scar resection are difficult and ineffective and have higher risk of complications.  Data analysis shows that there are different inflammatory substances involved in formation of scar adhesions after spinal surgery, and various degrees of peridural fibrosis are detected.  In addition, it is known that the tissue of degenerated nucleus pulposus can maintain a state of chronic inflammation in spinal canal and nerve roots, membranes of spinal cord and epidural adipose tissue, and it causes reactive changes therein which leads to development of scar adhesions [fibrosis]. Intervertebral disk tissue is avascular; it is formed separately from the immune system and possesses antigenic properties. The destruction of intervertebral cartilage triggers the cascade mechanism of cellular immunity, which leads to formation of anti-disk antibodies. Antigen-antibody complexes stimulate the production of pro-inflammatory substances (cytokines, prostaglandin) and proteolytic enzymes (proteases, collagenases) that induces progressive degeneration of the intervertebral disk and adhesions development with other structures of the spinal canal.” Pay attention because in the same way that tissue from INJURED BRAIN is attacked as “foreign” once it’s displaced into the bloodstream, so can the disc’s inner jelly (NUCLEUS) be likewise attacked.  In either case, the result is an AUTOIMMUNE REACTION.  This is why the protocol I will show you at the end of the post can dramatically and often times rapidly help many of you struggling with disc issues.

SPINAL CORD INJURY:  You need to know a bit about GLIAL CELLS for this bullet.  A month ago today, Brain Research carried a study called Curcumin Inhibits Glial Scar Formation by Suppressing… Inflammation and Fibrosis.  The authors concluded, “Spinal cord injury leads to glial scar formation by astrocytes, which severely hinders neural regeneration. Curcumin can inhibit glial scar formation. We found that curcumin and… could inhibit astrocyte activation through suppressing NF-κb signaling pathway, which led to down-regulate the expression of chemokines MCP-1, RANTES and CXCL10 [inflammation], thus reducing the inflammation in the glial scar.  Curcumin reduced α-SMA (an important symbol of fibrosis) and inhibited glial scar formation by regulating fibrosis. This study confirmed that curcumin could reduce the expression of intracellular and extracellular glial scar components through dual-target regulating of both inflammation and fibrosis.”  Looks to me like you should be thinking about adding “The Yellows” (circumin, boswellia, tumeric, etc) to your nutritional regimen.

SCOLIOSIS:  This amazing study done on fish (Unilateral Perivertebral Fibrosis Associated with Lordosis, Kyphosis and Scoliosis (LKS) in Farmed Chinook Salmon…) was carried in the October issue of Diseases of Aquatic Organisms.  “Radiography and histology were used to quantify lordosis, kyphosis and scoliosis (LKS) and perivertebral fibrosis… The most frequent histological finding was unilateral perivertebral fibrosis that often resulted in separation or loss of myocytes [muscle cells]. Histology of other tissues revealed multifocal inflammation within muscle, peripheral connective tissues and myocardium. In this study, LKS was consistently and significantly associated with perivertebral fibrosis, suggesting that perivertebral fibrosis is an important process in the development of LKS.”  This is not surprising considering that farmed salmon is raised in warm waters and fed grain (both skew the fatty acid profile away from OMEGA THREE), while wild cold-water salmon are loaded with naturally occurring (anti-inflammatory) Omega-3 fatty acids.  Cold water is what causes high Ω-3 fatty acid profiles.  Could something similar be occurring in humans? Probably on some level.  Considering that the average American is consuming about 1/30th the amount of Ω-3’s they should be, it makes sense.

SHOULDER INJURIES:  Less than two weeks ago, the Journal of Orthopedic Surgery and Research carried a study on shoulder problems.  In it they concluded, “We hypothesized that a rat shoulder contracture model using immobilization would be capable of producing effects on the glenohumeral joint similar to those seen in patients with frozen shoulder.  Infiltration of inflammatory cells was found in the synovial tissue until 2 weeks after immobilization. However, inflammatory cells were diminished and fibrosis was dominantly observed in the synovium and subsynovial tissue 3 weeks after immobilization. Our study demonstrated that a rat frozen shoulder model using immobilization generates the pathophysiologic process of inflammation leading to fibrosis on the glenohumeral joint similar to that seen in patients with frozen shoulder.”  Although I treat tons of SHOULDER PROBLEMS very successfully, I don’t have the rapid (often times instant) results with frozen shoulders.  By the way, the “official” name of Frozen Shoulder Syndrome is Adhesive (adhesion = fibrosis) Capsulitis (itis = inflammation).  Thus, it’s fibrotic change occurring deep down in the joint’s ligamentous capsule.

MICROBIOME MODULATES BOTH INFLAMMATION AND FIBROSIS:  On Pearl Harbor Day, the official journal of the American Heart Association (Circulation) carried a study called High Fibre Diet and Acetate Supplementation Change the Gut Microbiota and Prevent the Development of Hypertension and Heart Failure.  The authors concluded that, “Dietary intake of fruit and vegetables is associated with lower incidence of hypertension, but the mechanisms involved have not been elucidated.  We found that high consumption of fibre modified the gut microbiota populations and increased the abundance of acetate-producing bacteria.  Acetate had similar effects and also markedly reduced renal fibrosis. Transcriptome analyses showed that the protective effects of high fibre and acetate were accompanied by the down-regulation of cardiac and renal Egr1, a master cardiovascular regulator involved in cardiac hypertrophy, cardiorenal fibrosis and inflammation.”  If you are interested in the relationship of one’s MICROBIOME to inflammatory and autoimmune illnesses, as well as chronic pain, just follow the link.

BPA CAUSES BOTH INFLAMMATION AND FIBROSIS:  BPA is a highly toxic chemical found in plastics, similar synthetics, the lining of food cans (huh?), and any number of other sources.  Trust me when I tell you it’s bad news (among other things, it’s a hardcore XENOESTROGEN).  This month’s International Journal of Experimental Pathology confirmed this with a study called Inflammation, Oxidative Stress and Apoptosis Cascade Implication in Bisphenol A-induced Liver Fibrosis….  Authors concluded that, “Bisphenol A (BPA) is a key monomer in the production of plastics. Inflammation and oxidative stress are closely linked with liver fibrosis…  In addition, there was inflammation, oxidative stress, reduction in glutathione [a powerful antioxidant] and apoptosis [cell death].  Thus, the mechanism by which BPA induced liver fibrosis seems to be related to stimulation of the inflammatory response”  This, folks, is downright freaky!

SLEEP APNEA:  Most commonly the result of obesity, SLEEP APNEA is in the news again; this time in a study published in the November issue of the Journal of Biomedical Research (Chronic Intermittent Hypoxia Induces Cardiac Inflammation and Dysfunction…).  The authors determined that, “Chronic intermittent hypoxia is considered to play an important role in cardiovascular pathogenesis during the development of sleep apnea. Chronic intermittent hypoxia disrupted normal arrangement of cardiac fibers and increased Sirius stained collagen fibers [fibrosis]. The expression levels of hypoxia induced factor (HIF)-1α, NF-kB, IL-6, and matrix metallopeptidase 2 (MMP-2) [inflammation] were significantly increased in the hearts exposed to chronic intermittent hypoxia. In conclusion, the left ventricular function was adversely affected by chronic intermittent hypoxia, which is associated with increased expression of HIF-1α and NF-kB signaling molecules and development of cardiac inflammation, apoptosis and fibrosis.

KIDNEY INJURY AND / OR KIDNEY DISEASE: A few months ago, the journal Mediators of Inflammation published a study called TGF-β1/Smads and miR-21 in Renal Fibrosis and Inflammation.  For the record, both the substances in the title would be classified as “inflammation”.  This study did as good a job as I’ve seen of showing that fibrosis is always the end-product of inflammation, and that it can be deadly.  “A link between renal inflammation and fibrosis is well established.  Renal fibrosis, irrespective of its etiology, is a final common stage of almost all chronic kidney diseases. Increased apoptosis [cell death] and inflammatory cell infiltration characterize the injured kidney.  The importance of fibrotic diseases rises in a global awareness, as approximately 45% of all deaths in the Western world are related to various forms of fibrosis. Fibrosis develops in response to injury, when the normal wound-healing process is dysregulated and pathologically sustained. Excessive deposition of extracellular matrix (ECM) is a hallmark of all fibrotic diseases as ECM accumulation replaces functional tissue with a scar and this process alters organ physiological function and leads to its failure.”  I could have come up with dozens of other studies in this area of the kidneys, but we’ll call it good with this one.

LIVER:  Honestly, there were so many (hundreds) of studies linking Inflammation to Fibrosis in the liver, I am barely touching on this bullet considering I could have written volumes from what came out in the past weeks alone.  Last month, the World Journal of Gastroenterology published a study that said, “Non-alcoholic fatty liver disease (NAFLD) is one of the most common comorbidities associated with overweight and metabolic syndrome. Importantly, NAFLD is one of its most dangerous complications because it can lead to severe liver pathologies, including fibrosis.  The major risk factor that defines the prognosis of all chronic liver disease, including NAFLD, is fibrosis.  It is becoming increasingly clear that these diseases are the result of the same underlying pathophysiological processes associated with metabolic syndrome, such as insulin resistance, chronic systemic inflammation and dyslipidemia.”  The February 2017 issue of Mathematical Biosciences and Engineering (yes, it’s already out) stated in the first sentence of its abstract that, “Fibrosis is the formation of excessive fibrous connective tissue in an organ or tissue, which occurs in reparative process or in response to inflammation. Fibrotic diseases are characterized by abnormal excessive deposition of fibrous proteins, such as collagen, and the disease is most commonly progressive, leading to organ disfunction and failure”  The September issue of the Journal of the Science of Food Agriculture looked at pomegranate juice’s ability to stop or at least slow down both inflammation and fibrosis.  “The high-fat, high sugar diet plus pomegranate juice group had significantly lower hepatic steatosis, ballooning, lobular inflammation and portal inflammation; lower hepatic pro-inflammatory and pro-fibrotic gene expression.

What does all of this mean to you, the patient who is struggling with CHRONIC PAIN or Chronic Illnesses, including autoimmune diseases or funky neurological problems?  It means that you can’t go another day without addressing your inflammation / fibrosis.  Which raises the question of how best to go about accomplishing this.  My suggestion is to start with the short, simple post I created for this very purpose.  Consider it my Christmas gift to you since I’m providing it to you free of charge.  It’s easy to follow and cheap to implement (HERE IT IS).

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