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inflammation and fascia: what does inflammation do to connective tissues?


In order to understand today’s post, you must understand two simple concepts; inflammation and connective tissue.  Connective Tissues are just that — tissues that physically connect various parts of you to other parts of you (FASCIA is a great example of this).  Besides fascia, which is the most abundant connective tissue, the others include LIGAMENTS, TENDONS, CARTILAGE, and BONE.  And as crazy as it sounds, blood is actually a connective tissue that certain individuals are claiming has a fascial component (HERE).  But what about inflammation?

Inflammation is the name given to the group of chemical compounds made by your body for the express purpose of allowing cells and tissues to communicate with each other during the body’s response to tissue damage.  Thus, while a certain amount of local inflammation is vital for healing injured or damaged tissues (connective tissues included), any amount of inflammation over and above what is necessary is problematic, leading to a myriad of health-related problems (MINIMAL EFFECTIVE DOSE). 

So, when inflammation becomes “SYSTEMIC,” it will adversely affect every cell, tissue, and organ in your body, as well as becoming a frequent contributor to CHRONIC PAIN.  If you want to know more about inflammation (scratch that, you need to really understand inflammation), simply CLICK THIS LINK.

If you don’t want to read this post in its entirety, all you really need in order to understand that inflammation always leads to fibrosis (thickened tissue that microscopically looks and acts more like a hair tangle than combed hair), and that fibrosis always leads to degeneration, is THIS POST.  For the rest of you, allow me to show you some of the finer details of the many ways that inflammation wreaks havoc on your connective tissues, causing mechanical dysfunctions that not only lead to NEUROLOGICAL ISSUES, but are believed by increasing numbers of scientists to be the root of all sickness and disease (HERE).

For years there has been a raging debate over whether run-of-the-mill connective tissue injuries (PARTICULARLY OVERUSE INJURIES) are inflammatory, or purely degenerative.  The best example of this phenomenon is found in the Tendinosis / Tendinitis debate.  Starting about 35 years ago, researchers began publishing a wave of studies claiming that most tendon problems were not the result of inflammation (itis is the Latin word for inflammation, so Tendinitis would indicate an inflammation of the tendon), but are instead the result of an overuse-induced degeneration known as TENDINOSIS (osis means a derangement of).  

This debate came to the forefront in a 2009 issue of Arthritis Research & Therapy (Pathogenesis of Tendinopathies: Inflammation or Degeneration?) in which the authors concluded, “It is conceivable that inflammation and degeneration are not mutually exclusive, but work together in the pathogenesis of tendinopathies.”   Below are some cherry-picked conclusions that helped solidify what I wrote earlier this year about a 2017 showing that yes, there is indeed an inflammatory component to Tendinosis (HERE).

“Historically, the term tendinitis was used to describe chronic pain referring to a symptomatic tendon, thus implying inflammation as a central pathological process. However, traditional treatment modalities aimed at modulating inflammation have limited success and histological studies of surgical specimens consistently show the presence of degenerative lesions, with either absent or minimal inflammation. 

Experimental findings suggest that acute inflammation may be involved from the start and that a degenerative process soon supersedes it.  Observations in human tendinopathies further support the entangled roles of inflammation and subsequent degeneration within tendons.  Inflammation and degeneration are not mutually exclusive, but work together in the pathogenetic cascade of tendinopathy.”

We see something similar with fascia.  If you are not familiar with FASCIA, just click the link and start reading.  As many of you are already aware, fascia is an extremely important tissue, and thanks to increasing amounts of research on the topic, it’s no longer the red-headed stepchild of anatomy and physiology, ignored at every turn.  And although few seem to be aware of the fact, the very same debate seen with tendonopathies (inflammation -vs- degeneration) is going on with fascia. 

Nowhere is this seen more clearly than with PLANTAR FASCIITIS.  Case in point, an article in Runners Connect by John Davis (Is Reducing Inflammation Really the Best Way to Treat Running Injuries?)

“What is the role of inflammation in running injuries?  For a long time, inflammation has been identified as the main culprit for pain resulting from running injuries. But is this inflammatory model valid?   By definition, inflammation has features that are observable both on the macroscopic level of sensations in your body (like pain, redness, swelling—things a doctor would call “clinical features”), and on the microscopic level of the inner workings of your cells—this consists mainly of special inflammatory cells which flood an inflamed area and mediate your body’s response to the injury.

Using tissue samples taken from patients with chronic tendon or plantar fascia injuries who undergo surgery (and are hence being sliced open anyhow), recent studies have demonstrated a lack of inflammatory markers at the cellular level.  Instead, what they observe in injured tissue under a microscope is profound damage and degeneration in the microscopic structure of the tissue.”

The Merck Manual is the “Physician’s Bible” — historically the most common reference book used by doctors (I have a copy from my school days).  Listen to what Dr. Kendrick Alan Whitney says in an online article for the Merck Manual called Plantar Fasciosis. “Plantar fasciosis is sometimes referred to as plantar fasciitis. However, the term plantar fasciitis is not correct. The term fasciitis means inflammation of the fascia, but plantar fasciosis is a disorder where the fascia is repeatedly stressed rather than inflamed.” 

In a similar article written for the site Evidence for Exercise (Plantar Fasciitis – Inflammatory or Degenerative Condition?), author David Evans quotes peer-review, revealing that, “studies report a predominance of degenerative changes at the plantar fascia.  Direct evidence of inflammation has rarely been detected histologically in chronic plantar fasciitis.

What’s my opinion?  We know that under certain conditions (we’ll get to those momentarily) fascia undergoes physical changes consistent with a scar.  But does fascia get inflamed or does it not get inflamed?  I think that it’s hard to argue that it doesn’t.  Before we discuss the common ways that inflamed fascia causes pain and dysfunction, let me show you the uncommon ways (these are fascia-related inflammatory problems that few of you will ever have to worry about).

  • NECROTIZING FASCIITIS:  Necrosis means dead or dying, thus Necrotizing Fasciitis pertains to dead or dying fascia.  More common in the geriatric population and found more often in folks who have unhealthy lifestyles and bad habits (the same ones that tend to cause most other diseases), this rare but deadly bacterial fascial infection affects between 1,500 and 2,000 Americans annually.
  • PROLIFERATIVE FASCIITIS:  Although benign, Proliferative Fasciitis is a ‘proliferation’ of unknown origin of the part of fascia that makes collagen (fibroblasts).  Although it’s not CANCEROUS, it does require surgical removal of the proliferative area.  It is frequently called Nodular Fasciitis.
  • EOSINOPHILIC FASCIITIS:  Also known as Shulman’s Syndrome (not to be confused with Schurmann’s Syndrome), EF is similar to SCLERODERMA, but is quite rare.

For the record, after almost three decades of experience, my opinion is that yes, fascia commonly becomes inflamed for a wide variety of reasons.  These reasons include various forms of trauma (WHIPLASH INJURIES are a common one), repetitive injuries which we spoke of earlier, and even POSTURAL DISTORTIONS — all of which can not only be caused by inflammation, but can actually generate inflammation as well. In this next section I want to show you how inflammation affects fascia, and in the final section show you what you can do about it.


“The hyperactivity of the hypothalamic-pituitary-adrenal axis, which is highly active during the stress response, leads to a decrease in growth hormone.  Furthermore, a state of sympathetic dominance, which goes hand-in-hand with chronic stress, leads to increased fascial tension via a tensioning / constriction of the outer layer of connective tissue surrounding structures in the body, and the endothelium, the inner layer of blood vessels. 

From a physical perspective, stress in the form of tissue strain or injury causes fascia to respond by increasing pro-inflammatory cytokines to begin the healing process.  This processes is coordinated by fibroblasts, the cells of fascia which also play a key role in producing, repairing, and maintaining homeostatis of the extracellular matrix.  In response to strain, fibroblasts alter the shape and alignment of the the fascial matrix and secrete inflammatory cytokines. 

If mechanical stress continues, without allowing time for proper recovery, fascia becomes disorganized as excess amounts of collagen and extracellular maxtrix are deposited as a means of coping with the high amount of stress, leading to increased fibrosis and fascial adhesions.” From elite strength and conditioning coach, Patrick Ward, of Optimum Sports Performance (Fascia: Its Relationship to Stress, Growth Hormone, and Pain)

“The clinician needs to recognize that fascia, rather than muscle, is an important source of pain and that pathological change within the fascia, such as inflammation, can stimulate additional nociceptive neurons and the spread of pain receptive fields. Moreover, recognize that changes in fascia density and sliding do not have clear pathological changes, but may be sufficient to cause pain.

Cells within the ECM are demonstrably influenced by external mechanical factors resulting in an ECM protein milieu that is modulated by exercise, inflammation and disease processes….  In Fascia it was shown that in scar, chronically inflamed tissue, and cancer-associated tissues, fibroblasts have the ability to transform into contractile cells, or myofibroblasts, which can increase ECM stiffness by generating sustained and continued tension on the ECM.

This increase in ECM stiffness is accompanied by greater interstitial pressure and lymphatic flow, which may predispose an individual to fibrosis, cancer invasion and metastasis. The mechanical and biochemical factors in the ECM may well be found at a larger scale in fascial tissues throughout the body. 

Finally, nutrition plays a role in reducing inflammation. The anti-inflammatory diet is presented… with application to musculoskeletal disorders. The same diet is also useful for cardiac conditions, and for cancer.” Cherry-picked from the Fascia Congress’s article, Fascia Research 2015 – State of the Art

As I mentioned earlier, there are times and conditions where fascia should be inflamed, as inflammation is part of a normal healing process.  If you want to see what these phases of healing entail as well as their respective time-frames, take a look at my COLLAGEN SUPER-PAGE.  As injured cells rupture and die, they spill their contents into circulating fluids, which attract INFLAMMATORY MEDIATORS

In a nutshell, when soft tissues are compromised in any manner, there is a dilation of blood vessels and increased permeability that brings more nutrients and blood / fluid to the area (swelling), in an attempt to get rid of the metabolic waste products created by the injury and repair process (this phase only lasts a few days). 

These inflammatory mediators start the process of repair, which forms clots at these often-times “microscopic” injuries.  As I said earlier in the post, inflammation always leads to the SCAR TISSUE that the medical community refers to as FIBROSIS (this phase lasts about three weeks). 

And while a certain amount of fibrosis is exactly how your body is designed to heal connective tissues, by its very nature it leads to restricted motion and subsequent dysfunction and pain (which is why you had better not ignore the final phase of tissue healing — the remodeling phase — which can last as long as two years or more, and is where the scar can become stronger and more elastic). 

Elasticity is critical because the end result of joints that don’t work correctly over time is multi-tissue DEGENERATION.  This is why starting to deal with inflammation immediately after an acute injury is critical (as is keeping your body out of a state of chronic inflammation).  As far as dealing with acute inflammation goes, I am always shocked at how many people come from the ER, told to use heat instead of ice (HERE) — especially true for LOW BACK PAIN

Furthermore, ANTI-INFLAMMATION MEDICATIONS and CORTICOSTEROIDS, while being undeniably powerfully anti-inflammatory, seriously compromise the healing of all connective tissues, fascia included.  This means that drugs from the “BIG FIVE” actually increase your chances of winding up on the MEDICAL MERRY-GO-ROUND.

One thing you must also be aware of is the way that inflammation “THICKENS” tissues, including connective tissues (HERE also).  This is how fibrosis works and helps explain why, as bizarre or outlandish as it may sound initially, fibrosis / scar tissue is the leading cause of death and disability in America (HERE). World famous PT, John Barnes, talks about this thickening and tension in an article titled What is Fascia?

“The most interesting aspect of the fascial system is that it… is actually one continuous structure that exists from head to toe without interruption. In this way you can begin to see that each part of the entire body is connected to every other part by the fascia, like the yarn in a sweater. 

Trauma, inflammatory responses, and/or surgical procedures create Myofascial restrictions that can produce tensile pressures of approximately 2,000 pounds per square inch on pain sensitive structures that do not show up in many of the standard tests.  When one experiences physical trauma, emotional trauma, scarring, or inflammation, however, the fascia loses its pliability. It becomes tight, restricted, and a source of tension to the rest of the body.”

Note that when Barnes talks about restriction or tension here, he’s not simply saying “gee, my muscles are a bit tight today.”  Fascial tension has serious consequences, one of which is that resultant FASCIAL ADHESIONS cause problems in areas that are often far-removed from where the pain is or vice versa.  Some of this is due to irritation of the nervous system, and some of it is due to inflammation.  

In her interview for the Liberated Body Podcast, DR HELENE LANGEVIN said of this inflammation, “How does fascia generate pain? The soft tissues of the back can be the source of pain if they have a source of persistent inflammation in the tissues.”  And while this is certainly true, it’s not just true of the back.  She could just as easily be talking about SHOULDERS, RIBS, ELBOWS, NECKS, etc, etc, etc.  However, let’s stick with the back for a moment because what’s true for fascia in the back (IT’S CALLED THE THORACOLUMBAR FASCIA), will likewise be true for fascia in the rest of the body as well.

A study from earlier this year — the May issue of BioMed Research International (The Lumbodorsal Fascia as a Potential Source of Low Back Pain: A Narrative Review) — stated, “The lumbodorsal fascia (LF) has been proposed to represent a possible source of low back pain.  the density of nociceptive fibers was found to be increased in the inner layer of the rat LF, following chronic inflammation.  Remember that firing off nociceptors can cause pain. As microinjuries and inflammation are suspected to be a major cause of pain… the observations indicate a high nociceptive susceptibility of fascia to these processes.” 

What processes?  How about the fact that “chronic inflammation in the local musculature induces a threefold increase of dorsal horn [sensory] neurons.”  The relationship between nociception and inflammation (HERE) might help explain why renowned neurologist, DR. CHAN GUNN, has repeatedly said that adhesed or scarred fascia can be over 1000X more pain-sensitive than normal tissue.

And it’s not like this is new information.  Five years prior, the Journal of Anatomy (The Thoracolumbar Fascia: Anatomy, Function and Clinical Considerations) revealed of inflamed thoracolumbar / lumbodorsal fascia…..

“The question arises as to which factors could influence the proliferation and activity of lumbar myofibroblasts? Increased mechanical strain, such as hypertonicity, as well as biochemical changes have been described as stimulatory conditions. One of the strongest physiological agents for stimulating myofibroblast activity is the cytokine tumor growth factor (TGF)-B1. Because high sympathetic activity tends to go along with increased TGF-B1 expression, it is possible that it might also be a contributing factor for stiffening and loss of elasticity in the thoracolumbar fascia. Other contributory factors could be… inflammatory cytokines.”

In other words, while FIBROBLASTIC ACTIVITY is a sign of healing and something that on some level we try and promote via treatment, hyper-stimulation of fascia (mechanical strain and hypertonicity) causes the thickening or “DENSIFICATION” so commonly seen in the presence of inflammation as well as the fibrosis (in this case caused by TGF-β1 and other inflammatory cytokines) that always follows.  Oh; and guess what’s associated with this fascia-thickening inflammatory process?  Can anyone say “sympathetic activity” (SYMPATHETIC DOMINANCE)?  Speaking of densification and thickening…

I found a crazy fascinating article on this topic pertaining to hair loss (The Ultimate Hair Loss Flowchart: Why We Lose Our Hair).  The flowchart shows how fibrosis leads to decreased blood flow, which leads to decreased O2, which leads to a buildup of ROS (REACTIVE OXYGEN SPECIES), which eventually leads to hair loss.  After showing why current theories about hair loss cannot explain what’s really going on, the author (Rob of Perfect Hair Health) stated that the problem is essentially a fibrotic or densified scalp caused by; you guessed it — inflammation.  This is super intriguing in light of my posts on SKULL PAIN showing that the scalp is mostly made up of fascia.

“Using your hands, feel the thinning areas of your scalp. Then feel your non-thinning areas. Notice anything? In balding sites, our skin feels thicker, less pliable, and significantly less elastic. Balding regions have thicker, tighter skin.  Why do balding parts of the scalp feel tighter, thicker, and look shinier and more swollen?  Your balding scalp is tighter, thicker, and shinier because of an overproduction of something called collagen.  Interestingly, men with pattern hair loss have four times the amount of collagen fibers at the temples and vertex than men with no hair loss at all. What does that indicate?

Balding skin is ridden with scar tissue. There’s another word to describe the over-accumulation of collagen: fibrosis. Cause #1: Chronic Inflammation.  Chronic inflammation is not healthy. This is when inflammation never resolves – like a virus that won’t go away, or an ulcer that won’t heal. In these cases, inflammation is always present, so our tissues never fully repair. This is the type of inflammation associated with autoimmunity and cancer – and often leads to scarring (read: fibrosis).”

Speaking of the link between autoimmunity, fascia, and inflammation; besides the article I wrote for you a few months ago (HERE), a study from the journal American Academy of Rheumatology: Meeting Abstracts (Fascia Is a Target Organ of Inflammation in Autoimmune Diseases) helps solidify this relationship a bit more. 

Sixty-three patients presented with myalgia [muscle pain], muscle weakness, and elevated levels of muscle enzymes.  26 with dermatomyositis, 19 with polymyositis, 9 with amyopathic dermatomyositis, 7 with lupus, and 2 with adult-onset Still’s disease. MRI was performed in all sixty-three patients. Fascia involvement was observed in 45 or 71.43%) of patients.  Conclusion: Fasciitis occurred in patients with various autoimmune diseases. Patients with myalgia may have fasciitis in autoimmune diseases.” 

Speaking of autoimmunity….. With 30,000,000+ cases of THYROID DISEASE in the US alone (90% of it being autoimmune), let me show you a mind-bending real life example of this in action.

The classic sign of Graves Disease, otherwise known as autoimmune hyperthyroidism, is eyes that literally bulge from the sockets (the best examples are Don Knotts or Marty Feldman). This bulging is known as Thyroid Associated Ophthalmopathy or TAO.  Enter the husband and wife team of Roy and Helga Moncayo of WOMED (a women’s medical faculty in Innsbruck Austria). 

Roy is an MD (Internist, Endocrinologist, and heads up the local university’s department of Nuclear Medicine).  He is also into all sorts of alternative medicine, including Chinese Medicine, acupuncture, and a form of chiropractic called Applied Kinesiology.  His research specialty is Thyroid Disease.  His wife, Dr. Helga, is an OB/GYN who specializes in female endocrine disorders. 

Together they authored a study in BMC Musculoskeletal Disorders called A Musculoskeletal Model of Low Grade Connective Tissue Inflammation in Patients with Thyroid Associated Ophthalmopathy (TAO): The WOMED Concept of Lateral Tension and its General Implications in Disease.

The Moncayo’s team took a group of 30 thyroid patients and divided them into two groups, those with TAO and those without.  They then looked not only at blood levels of several minerals and electrolytes, but evaluated these individuals posturally and functionally (ranges of motion and proprioception — one of the tests they used was called the Functional Proprioceptive Test).  The cherry-picked results were as follows.

“TAO patients presented facial asymmetry with displaced eye fissure inclination (mean 9.1°) as well as tilted head-on-neck position (mean 5.7°). A further asymmetry feature was external rotation of the legs and feet (mean 27°). Both foot inversion as well as foot rotation induced a condition of neuromuscular deficit. 

In 5 patients, foot rotation produced a phenomenon of moving toes in the contra lateral foot. In addition foot rotation was accompanied by an audible tendon snapping. Lower erythrocyte Zn levels and altered correlations between Ca2+, Mg, and Fe were found in TAO.  The most common finding was an arch-like displacement of the body, i.e. eccentric position, with foot inversion and head tilt to the contra lateral side and tendon snapping. 

Based on the close relation between vision and posture control we hypothesized that elements related to biomechanical features of posture and gait could be present in TAO patients and that such changes could be related to a low grade systemic inflammation.  On clinical grounds, thyroid disease can be found to be associated with musculoskeletal components such as with polymyositis, eosinophilic fasciitis, as well as with myalgia and swelling of the calves and fasciitis.”

The study went on to talk extensively about the relationship between PROPRIOCEPTIVE FUNCTION and inflammatory markers such as IL-6.  This is yet another reason that there is a growing number of brilliant scientists, physicians, and researchers, who are saying that issues in the fascia could potentially be the root of all sickness and disease (HERE).  And lest anyone think this was not a well researched study, the bibliography had a whopping 370 citations.

Bottom line, the various experts and authors that tout “Fasciosis” to the exclusion of “Fasciitis” are on some level missing the boat.  We know this because in many cases, albeit temporarily, doctors can relieve patient’s symptoms of THESE PROBLEMS pharmaceutically. 

If there was no inflammation present, anti-inflammation drugs would have no effect.  The problem, however, is that I have shown you how this class of drugs has numerous and potentially serious SIDE EFFECTS, including soft tissue degradation, BONY DEGENERATION, and herniation / total rupture of any and all connective tissues (HERE).  All of which begs the question; what the heck are suffering people supposed to do?


“We’re finding that the health of nerves can be greatly influenced by their mechanical relationship to the body’s fasciae.   Blood supply, axoplasmic flow, nerve conduction, and inflammation are all modified when a nerve is stretched or compressed.   Conditions like carpal tunnel syndrome, sciatica, tension headaches, trigger points, and radicular pain are common ailments seen in our treatment rooms, and each is caused or helped along by nerve entrapment.  

Even in patients where no nerve involvement is suspected, we find that our musculoskeletal models are missing something important about the function and feel of nerve tissue.  When we exclude fascia from our conception of the nervous system, we’re left with overly simplistic models for nerve pathology.  Likewise, fascial release techniques can be aimless or even harmful if fascia is conceived without its neural axis.  Movement disciplines that gloss over the body’s nerve mechanics are robbed of key insights into proprioception, alignment, and chronic restriction.” From Michael Hamm of Neurofascia (What is a Neurofascial Approach?)

“Mechanically based techniques, such as… deep tissue work, rely on the  mechanics of fascia, aiming to ‘break up’ adhesions leading to a speedy return to normal function and  tissue quality. These therapies intend to create a permanent alteration of tissue structure. This is  achieved, at least partially, by fibers of collagen slowly sliding past one another in a response to stretch  (know  as creep), creating a loosening of cross-links between collagen fibers. This changes the character of the tissue (making it softer) and may cause the release of inflammatory mediators to apparently speed healing.”  Cherry-picked from the Academy of Physical Medicine Research Paper Review (A Theoretical Framework for the Role of Fascia in Manual Therapy)

Dealing with connective tissue-based problems requires a three pronged approach.  It is my firm belief, however, that in the world’s increasingly Westernized cultures; while techniques and procedures for addressing musculoskeletal problems have certainly improved, the first step of the process is frequently being ignored / skipped in lieu of prescribing drugs.  Unfortunately this ignorance seems to occur just as commonly within practitioners (maybe more so) as it does patients. 

  • ADDRESSING / REDUCING INFLAMMATION:  I get some CRAZY AMAZING RESULTS with many of the people who come to see me.  However, if patients are not willing to address the root sources of systemic inflammation in their lives, these changes are less likely to be permanent, and at the very least, will require more treatment than would otherwise be needed (HERE).  Because inflammation always results in fibrosis and scar tissue (HERE), these folks are less likely to find permanent resolution.  In fact, I would argue that our own medical profession is creating significant amounts of inflammation by helping destroy our collective microbiomes (HERE and HERE).  If people don’t get on board and address their systemic inflammation, they will not be able to successfully deal with the CRAZY NUMBER OF INFLAMMATION-BASED DISEASES (not to mention the AUTOIMMUNITY) that’s taking over the Westernized world, let alone their inflamed connective tissues (HERE). 
  • DEALING WITH ADHESED FASCIA:  There are about a jillion ways of dealing with STUCK AND THICKENED CONNECTIVE TISSUES, some of them more effective than others (HERE is what this process looks like in my clinic).  And like I’ve said many times, if you don’t tackle these issues like you would play THIS CARNIVAL GAME, results are frequently compromised (OR SHORT-LIVED).  The cool thing about being a chiro and doing this sort of work is that once the adhesions are broken up, people tend to hold adjustments much better / longer (HERE).  Once you begin to understand the relationship between PROPRIOCEPTION, restricted fascia, and SUBLUXATION, this point may make you question what you have been doing previously. 
  • CORRECTING ABERRANT POSTURE / PULLING ADHESED FASCIA APART:  Here’s the deal; if you fail to pull the adhesed connective tissues apart after they’ve been broken (see previous bullet), the tissue is going to re-heal in a TANGLED WAD — just like it was previously.  The cool thing is that I have lots and lots of ways to address this for those who have undergone Tissue Remodeling Treatment (HERE, HERE, HERE, and HERE are starting points).  This is why, while stretching can certainly be a good thing, for those who are “TETHERED” by restricted connective tissues, it can actually be a significant aggravator (HERE).

I have actually covered most of this in the free protocol I offer my patients and readers (HERE).  As you should be starting to notice, a failure to address any one of these points above, dramatically decreases your chances of solving whatever musculoskeletal problems you happen to be dealing with (not to mention many non-musculoskeletal problems as well).  If you appreciate the information found on our site, be sure to like, share, follow on FACEBOOK.


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