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.

"There are many unifying systems within the body. The circulatory system supplies blood to every tissue and organ. The nervous system connects and integrates all of the body’s functions. A third unifying system is comprised of a connective tissue matrix called fascia, is a continuous sheath of living tissue that connects the body front to back, head to toe. It surrounds every muscle, organ, nerve and blood vessel. A primary function of this fascial system is to support and lubricate. Thus, the circulatory system, the nervous system and the fascia all help to organize the body into a unified continuous whole. The human body is always working to maintain a state of balanced function. For example, blood pressure, blood sugar and the heart rate are actively kept within a normal range."  From Tervuren Osteopathic Clinic, Belgium (History & Principles of Osteopathy)

But what happens when the blood sugar is not kept in normal range? I've attended numerous seminars on NEUROLOGY, ENDOCRINOLOGY, FUNCTIONAL MEDICINE, and GUT HEALTH, and the consensus by the brilliant instructors is that most of the health-related problems physicians see on a day-to day-basis are the result of BLOOD SUGAR.  In other words, way too many of us are caught up in living the HIGH CARB LIFESTYLE.  It's why one in ten Americans has full-blown DIABETES, and over half of our adult population has pre-diabetes (otherwise known as CARDIOMETABOLIC SYNDROME).  The problem is so big and widespread that calling it an epidemic would be a massive understatement.

All blood sugar dysregulation issues (including HYPOGLYCEMIA, which is an early step on the path to diabetes) share a common denominator --- INFLAMMATION.  The harsh truth is that SUGAR IS ONE OF THE MOST INFLAMMATORY THINGS (I can't bring myself to call it a food) that you can put in your mouth.  Furthermore, diabetes and the issues leading up to it (including INSULIN RESISTANCE) are themselves considered to be inflammatory (they are not only caused by inflammation, but they cause inflammation as well).  You already know what blood sugar does to the nerves of those with diabetes (NEUROPATHY), but today I want to look at what current research says sugar does to connective tissues, including FASCIA, LIGAMENTS, and TENDONS (and even bone --- yes, bone is a connective tissue as well).

"In the skin: With the glycosylation of collagen, the collagen in your skin becomes less elastic and stiffer than a happy-hour martini. In your connective tissues: When glucose attaches to collagen in your connective tissues, you end up with less elasticity. You need collagen for the smooth functioning of joints. High blood sugar magnifies all aches and pains and can lead to impaired joint movement—and eventually arthritis.  In your lungs: The glycosylation of collagen results in abnormal recoil of the elastic tissue, so you have trouble getting the air out as well as in. This occurs slowly in lung connective tissue, but 40 years of high glucose levels often lead to respiratory failure—the inability to get enough oxygen into your blood without the use of an oxygen tank."  DR. OZ talking about the effects of sugar on SKIN and lungs (COPD) in a short article called What Does Glycosylation Do to Your Body?

"At least 9% of Americans are living with diabetes.  A foot ulcer is the initial event in more than 85% of major amputations that are performed on people with diabetes.  In the United States, every year about 73,000 amputations of the lower limb not related to trauma are performed on people with diabetes.  Of non-traumatic amputations in the United States, 60% are performed on people with diabetes."  From 25 Must Know Statistics About Amputation Due to Diabetes on the Azura Vascular Care website

"Diabetes is characterized by chronic hyperglycemia and an altered cellular homeostasis, which lead to diffuse vascular damage and multi-organ dysfunction. Diabetic patients risk both micro- and macro-vascular complications: the former result from damage to retinal, renal, and neural tissues, which is the cause of blindness, end-stage renal failure, and non-traumatic lower limb amputation.  Reactive oxygen species (ROS) are the unifying mechanism behind the main pathological pathways triggered by hyperglycemia, one of which leads to the formation of advanced glycation end products (AGEs)."  From the October 2016 issue of Intech (A Potential Mechanism for Diabetic Wound Healing: Cutaneous Environmental Disorders)

There are many of you out there saying to yourself, "Hey; I DON'T HAVE DIABETES so I don't have to worry about posts like this."  Wrong. If you are eating the wrong foods, something called Glycosolation / Glycation is creating large numbers of ADVANCED GLYCATION ENDPRODUCTS or AGES, and is already working overtime to kick your butt.  Glycosolation is the process of chemically attaching to a sugar to a protein or fat molecule via specific enzymes.  When this system runs without enzymes (which it often does --- especially when sugars are being attached to Red Blood Cells), it's called glycation and leads to an overproduction of AGES.  The more sugar or high glycemic index carbs a person consumes, the more AGES they make.

This creates a situation I've spoken of numerous times in regards to a whole host of tissues --- THE LEAKIES.  Only in this case, the AGES attack the tight cellular junctions in the walls of your arteries, causing the vessels to leak.  The body cannot tolerate excess fluid leaking out of its blood vascular system so it patches it with --- you guessed it --- CHOLESTEROL.  This process also leads to an inability to clear HOMOCYSTEINE, a molecule associated with HYPERTENSION and HEART DISEASE, from an increasingly toxic body.  On top of everything else, the process leads to the formation of FREE RADICALS / OXIDATIVE STRESS.

Lots of sugar, lots of inflammation, lots of AGES, lots of homocysteine and ROS formation, and you'll have lots of cholesterol building up in your arteries (which is why 99% of you who were told that your cholesterol issue is due to "BAD GENES" were lied to).  This buildup of arterial plaques not only leads to all the things we typically think of (heart attacks, strokes, a lifetime of STATIN DRUGS), it leads to problems with vision (Diabetic Retinopathy) as well as an array of Diabetic Wounds and Ulcers, which tend to get worse in body parts that are farther away from the heart.  AGES in your blood can actually be measured by a simple blood test known as the A1C (the HbA1C measures glycosylated hemoglobin).  While a fasting blood sugar test measures what you blood sugar is here and now, the A1C provides a longer-term view because it measures the amount of glucose that has attached to the oxygen-carrying protein hemoglobin, over the lifespan of the RBC --- about 90 days.

Blood vessels are made up of many layers of both connective tissues and smooth muscles.  Attack the connective tissues in arteries and as you will see throughout this post, the arteries will become stiff and inelastic --- not a good property for arteries as, among other issues, it always results in high BP.   Furthermore, because these AGES block angiogenisis (the production of new blood vessels), your body will have a tough time healing wounds.  Take a look at some of the cherry-picked conclusions from a 2006 issue of Diabetes (Receptor for Advanced Glycation End Products Is Involved in Impaired Angiogenic Response in Diabetes).

"One consequence of long-term hyperglycemia is the formation of advanced glycation end products (AGEs); the accumulation of AGEs in the vessel wall has been implicated in the pathogenesis of diabetes complications. Among a variety of AGE receptor or AGE-binding proteins that have been described, the receptor for AGEs (RAGE) is probably the best-characterized molecule. RAGE belongs to the immunoglobulin superfamily of cell surface molecules to which AGEs bind.  Recently, RAGE has been shown to be involved in both microdiabetic and macrodiabetic vascular complications.   In this study, we showed for the first time that RAGE is involved in impaired angiogenic response in diabetes. Moreover, our results implicate esRAGE as a therapeutic factor to protect impaired angiogenic response in diabetes. In addition to the vaso-degenerative changes, several observations indicated that angiogenic response or development of new vessels in response to local ischemia/inflammation is significantly reduced in diabetic patients and animals." 

Here is how this scenario plays out.  Not only does jacked blood sugar cause major issues with the RBC's themselves, it stiffens the connective tissue in arteries, while causing them to be filled with thick, waxy, plaques that eventually harden to the consistency of stone.  When I was doing cadaver dissections at both Kansas State University and Logan College of Chiropractic, it was easy to tell which arteries had "hardened".  Tap them with your scalpel and many would not only feel like you were tapping on a rock, it would actually sound like it as well.   The obvious result is a starvation of blood / oxygen / nutrients to all cells and tissues, but particularly those farthest from the heart.  It's not hard to see why this is such an important issue.

According to the American Podiatric Medical Association (Diabetic Wound Care) as many as a quarter, "of patients with diabetes who develop foot ulcers will require an amputation."  A decade old issue of the Journal of Clinical Investigation (Cellular and Molecular Basis of Wound Healing in Diabetes) has a list of, "Over 100 known physiologic factors that contribute to wound healing deficiencies in individuals with diabetes."   I'm going to leave you with a few of them that affect connective tissues.

• DECREASED OR IMPAIRED GROWTH FACTOR PRODUCTION:  Many of these are similar to HGH (human growth hormone), and when they are not present, connective tissue cannot grow / repair properly.

 

• DECREASED ANGIOGENIC RESPONSE:  Although this was previously mentioned, it goes along with the previous point.  Any tissue or wound healing requires a blood supply in the form of new capillary beds.  So not only is blood sugar screwing up the vessels that are already there, it's preventing new ones from forming.

 

• DECREASED MACROPHAGE FORMATION:  Macrophages are like mini Pac Man units running around and eating cellular debris.  As you might imagine, there is an abundance of cellular debris in degenerative diseases like diabetes.  A failure to clean this garbage up leaves you both TOXIC and prone to CHRONIC INFECTIONS (macrophages also present antigens such as germs to the T-CELLS so they can be destroyed).

 

• DECREASED COLLAGEN ACCUMULATION:  Without COLLAGEN --- nature's protein building block --- how would you ever hope to heal a wound?
  

 

• DECREASED EPIDERMAL BARRIER FUNCTION:  This is a no-brainer. Diminished quality of the tissues that make up the skin, and it won't be the barrier is was meant to be. 

 

• DECREASED QUANTITY OF GRANULATION TISSUE:  Granulation Tissue is simply the name for new connective tissue and it's capillary bed that forms on wound surfaces during the healing process.  You could have deduced this from what we've already seen.

 

• DECREASED KERATINOCYTE AND FIBROBLAST MIGRATION & PROLIFERATION:  FIBROBLASTS are the cells that create Collagen.  Keratinocytes are the cells that create keratin --- a fibrous structural protein that not only makes up hair and fingernails, but is the tougher outermost layer of the skin. 

 

• DECREASED NUMBER OF EPIDERMAL NERVES:  This is a hallmark of NEUROPATHY.  Just today I talked to a patient who had a relative who dropped a huge chunk of wood on their foot, and never felt it or knew it had been broken because they can no longer feel their feet.  This person was under forty.
  

 

• DECREASED BONE HEALING: For those not in the know, bone is a connective tissue.

 

• FOULED UP BALANCE BETWEEN ECM COMPONENTS AND THEIR REMODELING:  Although in some connective tissues the process is slow, while in others it's very rapid, they are always being remodeled (broken down and built back up) by the body.  Higher blood sugar skews this process towards the catabolic (breaking down) side of the equation, while moving it away from the anabolic side (building up).  ECM is an important part of all connective tissues, including fascia.
  

"Fascia is essentially our second skin, covering muscle, nerve, joints and organs.  It’s located beneath our skin layer, acting as a deeper inner skin layer that weaves throughout the body.   Fascia acts as a communicator transmitting input from one area to the body to another.  Your entire body is connected by this fibrous collagen filled inner or “second skin”.  As I mentioned in my newest book, The Fascia Fix Food Plan, the number one fascia buster is sugar!  Excess dietary sugar binds to collagen and goes through a process called glycation where these new sugar linked proteins, appropriately called AGE’s (advanced glycation endproducts) cause inflammation and collagen degradation.  Internally, unhealthy fascia will cause muscle stiffness, aching joints, headaches and anxiety. Externally, you will see cellulite and sagging skin.  AGE’s literally cause you to age too fast!  For youthful collagen (or perhaps… to not AGE it too fast) a dietary approach is essential.  You need to protect and nourish.  Protect collagen by avoiding sugar and high carbohydrate foods....."   From Dr. Sherri Jacob's site, Health E-Coaching (AGEs and Your Second Skin: Fascia)

Knowing what we know about diabetes and wound healing, it's not a leap --- especially after what we learned of the relationship between CANCER AND POLARITY just a few days ago --- that diabetes affects the polarity / electrical fields of connective tissues like fascia as seen by the name of the study Glucose Suppresses Biological Ferroelectricity in Aortic Elastin.  An article in Science Daily said of this study, "When researchers treated elastin with sugar, they found that glucose suppressed ferroelectric switching by up to 50 percent. This interaction between sugar and protein mimics a natural process called glycation, in which sugar molecules attach to proteins, degrading their structure and function."  This is a huge deal because elastin is the elastic protein that is found in fascia, which gives it its ability to stretch.

One of the things I talk about at length to my patients is the importance of full and unrestricted Ranges of Motion (ROM).  Lose ROM and it not only tends to cause pain, but is a huge factor in developing DEGENERATIVE ARTHRITIC CONDITIONS.  We see this occurring in something known as Diabetes Induced Limited Joint Mobility (LJM).  In fact, a 2011 study from the Journal of Musculoskeletal Medicine talked about this in regards to it's ability to mimic several common issues associated with adhesed fascia (DUPUYTREN'S & PALMAR FASCIITIS were discussed).  "Limited joint mobility (LJM) is a common complication of diabetes mellitus (DM). LJM often is characterized by hand stiffness, but other joints may be involved. The prayer and tabletop signs is a condition characterized by hand stiffness resulting from flexion contractures of the fingers and by thickened, tight, waxy skin. “LJM” is the newer, preferred term used in describing the condition because joints other than those in the hands (eg, in the wrists and elbows, feet, and spine) also may be involved."

The problem with diabetes attacking connective tissues is so large that Dr. Frits Holleman (MD / Ph.D), Professor of Medicine at the Academic Medical Center in Amsterdam, wrote an article for Diapedia called Connective Tissue Disorders, noting how AGES particularly attack collagen. "In the pathogenesis of diabetes complications various processes play a part. One of these is the formation of Advanced Glycation Endproducts (AGEs) in blood and tissues by irreversible binding of glucose degradation products to proteins such as albumin, myelin and collagen."  Some of the problems he associated with diabetes included, "Limited Joint Mobility (LJM), Dupuytren´s disease, Flexor tenosynovitis (Trigger finger), Carpal Tunnel Syndrome, Shoulder capsulitis (Frozen shoulder), Stiff hand syndrome, Scleredema diabeticorum (also known as Scleroderma diabeticorum), and Necrobiosis lipoidica (diabeticorum."  None of this is new information as Holleman's statement was virtually identical to the conclusions of a 1996 issue of Endocrinology & Metabolism Clinics of North America (Connective Tissue and Joint Disease in Diabetes Mellitus).

In 2006, The Journal of the CCA (The Musculoskeletal Effects of Diabetes Mellitus) contained a list of the various side effects seen when diabetes attacks various collagen-based connective tissues (although muscles are not officially a connective tissue, I'll include them here).

• MUSCLE CRAMPS:  These authors gave many metabolic pathways that this occurs, including loss of electrolytes.  After concluding that, "electrolyte imbalances are common in people with Type II diabetes," the authors of a 2015 New England Journal of Medicine study (Electrolyte and Acid–Base Disturbances in Patients with Diabetes Mellitus) discussed the ways that this disease adversely affects your body's intricate ACID / ALKALI balance.  Why?  Because all of these electrolytes are ions that have either a positive or negative charge.  Too much positive charge (H+) and you'll be acidic.  Not enough negative charges (OH-) and you'll be acidic as well.  It's why uncontrolled diabetes leads to ketoacidosis (not to be confused with KETOSIS that occurs purposefully as the result of a Ketogenic Diet).
  

 

• DIABETIC MUSCLE INFARCTION:  Also known as Spontaneous Diabetic Myonecrosis, this is when a muscle, due to a non-blood clot related occlusion, dies because it can't get enough oxygen.  Not super common, but admittedly "under-diagnosed" by numerous studies.
  

 

• CRPS:  Although it used to be called Reflex Sympathetic Dystrophy (RSD), Complex Regional Pain Syndrome (CRPS) is what happens when the nervous system gets tipped way beyond standard, run-of-the-mill SYMPATHETIC DOMINANCE that is so common in today's pedal-to-the-metal society.  A study from one of last year's issues of the Annals of Rehabilitation Medicine (Relationship Between HbA1c and Complex Regional Pain Syndrome in Stroke Patients With Type 2 Diabetes Mellitus) concluded plainly that, "Diabetes is considered highly related to CRPS occurrence."  BTW, one of the visible manifestations of CRPS is that the skin and fascia of the affected areas thickens.
  

 

• HYDROXYAPATITE DEPOSITION DISEASE (HADD):  A year ago in September, the journal Radiology Research and Practice (Calcium Apatite Deposition Disease: Diagnosis and Treatment) concluded that, "Calcium apatite deposition disease (CADD) is a common entity characterized by deposition of calcium crystals within and around connective tissues.  An association has also been found between adult onset diabetes and calcific tendinitis."  That association is that diabetics are about 300% more likely to have this issue than non-diabetics.

 

• LIMITED JOINT MOBILTY (LJM):  We discussed this earlier.

 

• DIABETIC STIFF HANDS SYNDROME (DSHS) / CHEIROARTHROPATHY:  This is the part of LMJ above that affects the hands and wrists.  How common is it?  A study from a 2013 issue of the Annals of Medical and Health Sciences Research (Prevalence of Hand Disorders in Type 2 Diabetes Mellitus and its Correlation with Microvascular Complications) concluded that, "Physicians have long recognized the association between diabetes mellitus and several pathologic conditions of the hand.  Diabetic foot has always been a point of worry for treating physicians but complications like diabetic hand syndrome might not have gained enough recognition. Diabetes is complicated by musculoskeletal problems of upper extremity and particularly the hand, collectively referred as “the diabetic hand.” This study found that the hand disorders were present in two third of the patients of type 2 diabetes." Re-read that last sentence if you didn't quite grasp (no pun intended) its implications.
  

 

• NEUROPATHIC JOINTS:  We already know that the neurology of diabetics is affected severely.  We also know that many, maybe most, neurological diseases have their origins in blood sugar dysregulation.  Thus, it can't be a surprise to see that joints are affected neurologically as well.  And if joints are affected, we see that not only is bone affected, but cartilage also --- yes, cartilage is the last of the main connective tissues we had not yet mentioned.  Also called Charcot Arthropathy or Diabetic Osteoarthrothapy, Medscape says, "Charcot arthropathy results in progressive destruction of bone and soft tissues at weightbearing joints; in its most severe form, it may cause significant disruption of the bony architecture. Charcot arthropathy can occur at any joint; however, it occurs most commonly in the lower extremity, at the foot and ankle."  Just last year the journal Diabetes Research shed even more light (Charcot Neuropathic Arthropathy of the Foot: A Literature Review and Single-Center Experience) by concluding that, "Charcot neuropathic osteoarthropathy of the foot is a relatively common complication of diabetic neuropathy. Incorrect diagnosis and improper treatment often result in the extremity having to be amputated."  This happens because when DIABETIC NEUROPATHY is present, people can't feel their joints (particularly their feet) due to a massive loss of PROPRIOCEPTION (abnormal joint function always causes joint degeneration).
  

 

• CARPAL TUNNEL SYNDROME:  Once you realize that this diabetes-induced thickening or "DENSIFICATION" of the tissues of the hand and wrist occurs at the FLEXOR RETINACULUM (a cross between a fascia and a ligament), it's easy to see why diabetes would be associated with CARPAL TUNNEL SYNDROME.
  

 

• ADHESIVE CAPSULITIS / FROZEN SHOULDER SYNDROME:  There are dozens upon dozens of articles linking Frozen Shoulder to type II diabetes.  Just last month, an article in Very Well called Adhesive Capsulitis and Diabetes: Diabetes and Frozen Shoulder stated, "The shoulder joint capsule actually adheres (or sticks) to the head of the humerus bone. The humerus is the long bone that extends from your shoulder to your elbow. The joint capsule is a protective sleeve of connective tissue that surrounds the joint."  Last year, researchers from England published a study in the journal MLTJ called Adhesive Capsulitis of the Shoulder and Diabetes: A Meta-Analysis of Prevalence, that looked at over 5,400 studies and determined that "A high prevalence of adhesive capsulitis exists in diabetes, and an equally high prevalence of diabetes is present in adhesive capsulitis."  How high?  Depending on the study, incidence was anywhere from 3 to 8 times higher than the non-diabetic population.
  

 

• TENOSYNOVITIS:  Tenosynovitis is an inflammation of the fluid-filled membrane that surrounds certain tendons --- particular those in the hands --- usually manifesting in the form of trigger fingers or a thumb issue known as DeQUERVAIN'S SYNDROME.  In a study from Diabetes Care (HbA1c Values Determine the Outcome of Intrasheath Injection of Triamcinolone for Diabetic Flexor Tenosynovitis), the worse the blood sugar values, the greater the chance that treatment would not be effective.  Furthermore, "Tenosynovitis has a reported incidence ranging from 1.7 to 2.6% in the general population. However, the incidence of tenosynovitis in diabetes is reported to be between 10 and 20%."
  

 

• DUPUYTREN'S CONTRACTURE:  This is a thickening of the palmar surface of the hand (see earlier link).
  

 

• OSTEOPOROSIS:  Both OSTEOPOROSIS and diabetes are in the "inflammatory" family of diseases.  Our government's own NIH talks about this link in an article called What People With Diabetes Need to Know About Osteoporosis.  As far as peer-review, the studies are numerous.  One of the best can be found in a 2014 issue of the International Journal of Endocrinology (Osteoporosis, Fractures, and Diabetes).  "It is well established that osteoporosis and diabetes are prevalent diseases with significant associated morbidity and mortality. Patients with diabetes have an increased risk of bone fractures. In type 1 diabetes, the risk is increased by 6 times and is due to low bone mass.  Diabetes itself is associated with increased risk of fracture, although T2DM is often characterized by normal or high bone mineral density (BMD). Thus, diabetes may be associated with a reduction of bone strength, that is, not reflected in the measurement of BMD."  In other words, a bone density examination (DEXA Scan) not likely to give you anything helpful as far as osteoporosis is concerned.
  

 

• OSTEOMYELITIS / SEPTIC ARTHRITIS:  These pertain to infections of the bone.  And while not particularly common, diabetics are at far greater risk simply because they are at far greater risk of infections period.  Why?  Because in the same way that SUGAR FEEDS CANCER, sugar also happens to be ROCKET FUEL FOR INFECTIONS (this included DYSBIOSIS).
  

 

• DIFFUSE IDIOPATHIC SKELETAL HYPEROSTOSIS (DISH):  I've seen plenty of DISH in my day, and I cannot recall one that was in a person that was not either diabetic, or functionally a diabetic (obese, sedentary, poor diet, etc).  On x-ray, DISH looks like someone poured wax down the spine (huge amounts of calcification).  The authors of this list trotted out twenty year old research showing that possibly over a quarter of diabetics will develop DISH.
  

 

• OSSIFICATION OF THE POSTERIOR LONGITUDINAL LIGAMENT:  The PLL is a long ligament that runs the length of the back of the vertebral body (which puts it inside the spinal canal acting almost like a lining for the spinal cord).  As I have written before pertaining to SPINAL STENOSIS, when this ligament thickens or calcifies (ossifies), it crowds the spinal cord.  The result is spinal stenosis or a shrinking of the spinal canal.  It's a miserable problem that can affect either the neck or the low back, and is often accompanied by RADICULOPATHY or SCIATICA.
  

Much of what you see on this list this boils down to what are known as crosslinks.  Connective Tissues --- particularly fascia --- look somewhat like netting under a microscope.  There are, of course, the main fibers that run parallel to each other, but there are the cross-links that keep these main fibers in line.  While having more cross-links tends to make tissue stronger and more stable, it also makes it stiff and inelastic.  Listen to what renowned podiatrist, Dr. Emily Splichal, says in her book called Barefoot Strong: Unlock the Secrets to Movement Longevity. 

"Although crosslinks provide strength and stability, excessive or what are called non-specific crosslinks create stiffness and a lack of elastic recoil in the connective tissue.  It is these non-specific crosslinks we call fascial adhesions.  These non-specific crosslinks are formed through a process of glycation, which occurs in the presence of excess glucose.  These AGES are responsible for forming non-specific crosslinks in collagen, resulting in stiffer and non-elastic fascia and tendons.  The stiffer the connective tissue, the increased risk of tearing during dynamic movement."

this is why there are others that could be added to the list above.  For starters an article in Everyday Health (The Role of Fascia in Rheumatoid Arthritis) talked about the link between RHEUMATOID ARTHRITIS and problems in the fascia.  WebMD upped the ante earlier this year in an article called Rheumatoid Arthritis and Diabetes: Are They Linked?  In it they said, "research shows that RA raises your risk for diabetes by about 50%. And diabetes raises your risk of having arthritis, including RA and arthritis-related issues, by about 20%. Nearly half of American adults who have diabetes also have arthritis."  And how about PF.

PLANTAR FASCIITIS (PF) affects millions of Americans each year, and if not dealt with properly can be debilitating.  In a study led by Dr. Maria Craig of Sydney's Institute of Endocrinology and Diabetes in Australia (Plantar Fascia Thickness, a Measure of Tissue Glycation, Predicts the Development of Complications in Adolescents With Type 1 Diabetes) her team concluded exactly what the title said, that the thickness of the PF is an "alternative index of tissue glycation and a marker of microvascular disease."  Granted, this was for Type 1 diabetics, but I'll bet you a dime to a dollar that the same would be true for Type 2's.  By the way, you see the same thing for something known as plantar fibromatosis, which is essentially Dypyertyns of the bottom of the foot instead of the palm of the hand.

Before we cover our last topic of the day (tendons), I want to take a moment to discuss the relationship between diabetes and the odds of developing POST-SURGICAL ADHESIONS.  Not only is it easy to find studies discussing the increased risk of diabetics developing post-surgical SCAR TISSUE, but having this disease dramatically increases their chances of the incision site not holding (HERE).  An August study published in the journal Hernia (Advanced Glycation End Products as a Biomarker for Incisional Hernia) concluded...

"Incisional hernia is one of the most frequent complications after abdominal surgery, with incidences up to 30%.  Advanced glycosylation end products (AGEs), also known as non-enzymatic collagen crosslinks, are correlated with aging, smoking, hyperglycemia, hyperlipidemia and oxidative stress.  Due to the auto-fluorescent properties of AGEs, measurements can be carried out on the skin using auto-fluorescent readers (AF readers). The levels of accumulated AGEs measured in the skin correlate with systemic AGE levels.  A preoperative screening tool or biomarker for postoperative surgical complications may be helpful to select patients who are fit for surgery. This could lead to prevention of major complications like wound complications or anastomotic leakage.  AGE accumulation measured in the skin indirectly with autofluorescence might be associated with incisional hernia."

I do want to briefly mention one more problem before we move on; something called Necrotizing Fasciitis.  Although NF is not common, it's an increasingly bigger issue thanks in part to diabetes.  Less than two weeks ago, Medscape said of this problem:  "The frequency of necrotizing fasciitis has been on the rise because of an increase in immuno-compromised patients with diabetes....  Necrotizing fasciitis is a rapidly progressive inflammatory infection of the fascia, with secondary necrosis of the subcutaneous tissues. The speed of spread is directly proportional to the thickness of the subcutaneous layer. Necrotizing fasciitis moves along the fascial plane."

Last year, the journal Advances in Experimental Medicine and Biology published a paper called Does Diabetes Mellitus Affect Tendon Healing?  Describing pathophysiological processes we have already discussed, these authors, from the Department of Clinical Neuroscience of Karolinska Institute in Stockholm, Sweden showed that it does in a big way.  Another study from last year, this one from the journal Diabetes Complications showed that ACHILLES RUPTURE in women was linked to diabetes as well.  Yet another article from last year, this one from the Diabetes Council (Is Tendon Pain Linked to Diabetes?) concluded that....

"The tendons connect muscle to bone or to specific structures or organs—for example, the eye. Tendons are flexible but non-elastic cords made up of a specific type of protein, collagen.  In Type 2 Diabetes, there are a number of tendon conditions that can be relatively common.  These conditions are usually associated with poor blood sugar control as well as by how long someone has been diagnosed.  Diabetic patients are at higher risk for these tendon conditions, likely because of the inflammation that is consistent with high blood sugar levels.  Poor glycemic control— chronic high levels of blood sugar—cause the formation of advanced glycation end products or AGEs. The critical characteristic of AGEs that can cause tendon (and other) damage is that they can form chemical cross-links between proteins.  Think of it as ropes that are tangled with each other and all knotted up—these ropes aren’t useful anymore.  When proteins and other molecules become cross-linked—they lose their function.  The risk of tendon disorders also increases in diabetic patients who also have diabetic neuropathy."

This last sentence is a huge deal because I am not only seeing tons of younger Type II diabetics in my clinic (it's no longer uncommon to see teens with Type II), but increasingly younger patients with Diabetic Neuropathy.  In fact, I've previously shown you that as many as half of those with neuropathy don't know it because even though it would be detected on a test, they have not had major loss of sensory or motor function (OR SEXUAL FUNCTION) ---- yet.  This is why there are studies showing that by the time people are actually diagnosed with T2D, half will have some degree of neuropathy.  And if you have neuropathy, you will have tendon issues (HERE).  Much of this has to do with the fact that tendinosis is both an inflammatory and a degenerative problem (HERE).

What's my best advice to you?  The first point would be to realize that while sugar is heavily associated with Type II diabetes, T2D is not so much a sugar issue as it is an inflammation issue.  In other words, there are a myriad of drivers of inflammation other than sugar that could be the chief culprit in diabetes.  It's is why reading THIS POST is important, and helps explain why some people go on strict low carb diets but cannot control their blood sugar.  I not only show you what diets typically work to combat diabetes, but how to potentially rid your body of diabetes-inducing inflammation as well.

For more than three decades, the peer-reviewed scientific literature has said that most tendinopathies (TENDINOSIS included) are not inflammatory --- in other words, when the tendons were biopsied, there were no inflammatory cells present.   I reported this but always said that even though these tendinopathies might not contain inflammation, inflammation undoubtedly helps drive the process.  It seems the science is changing in this area and that tendinosis is inflammatory after all.   What's the evidence for this assertion and what difference does it make as far as your issues are concerned? Follow along.

• Last year's book, Metabolic Influences on Risks for Tendon Disorders, carried a chapter called Inflammation in Tendon Disorders which described the criteria for inflammation to be an issue in tendon disorders.  "The role of inflammation in tendon disorders has long been a subject of considerable debate. Developments in our understanding of the basic science of inflammation have provided further insight into its potential role in specific forms of tendon disease, and the circumstances that may potentiate this. Such circumstances include excessive mechanical stresses on tendon and the presence of systemic inflammation associated with chronic diseases."  The last half of the last sentence is paramount.  Not sure what SYSTEMIC INFLAMMATION is or what causes it?  Just click the link. Remember this concept because we will briefly revisit it at the end of the post.

 

• Remember the famous tendon researcher and orthopedic surgeon Dr. GA Murrell that I have quoted many times (see "tendinosis" link above)?  Here is one of his more recent studies.  This January's issue of the journal Nature Reviews: Rheumatology (Inflammatory Mechanisms in Tendinopathy – Towards Translation) concluded, "These disorders are common, account for a high proportion (30%) of referrals to musculoskeletal practitioners, and confer a large socioeconomic burden of disease.  The advent of modern molecular techniques has highlighted the presence of immune cells and inflammatory mechanisms throughout the spectrum of tendinopathy in both animal and human models of disease. Key inflammatory mediators — such as cytokines, nitric oxide, prostaglandins and lipoxins — play crucial parts in modulating changes in the extracellular matrix within tendinopathy."  In other words, the ECM is "scarred" and there are inflammatory markers in the tendons.   Thanks to METABOLOMICS we can now see this. 

 

• April's issue of the inflammation journal Cytokine (The Influence of Chronic IL-6 Exposure, in Vivo, on Rat Achilles Tendon Extracellular Matrix) simply stated in its abstract that, "Elevated levels of IL-6 are associated with tendinopathy."  IL-6 (interleukin six) is probably the most common and well known of the numerous biomarkers of inflammation.

 

• March's Frontier in Aging Neuroscience (Commentary: Role of VEGF, Nitric Oxide, and Sympathetic Neurotransmitters in the Pathogenesis of Tendinopathy: A Review of the Current Evidences) provided a comment by a researcher, arguing by listing numerous other studies, that yes, tendinosis is indeed inflammatory.

 

• March's issue of PLoS One (The Effects of Substance P and Acetylcholine on Human Tenocyte Proliferation Converge Mechanistically Via TGF-β1) showed how certain inflammatory mediators caused a thickening of the tendons via "proliferation" of the cells that make tendon material (tenocytes).  While a degree of this is needed, when the process gets out of kilter the tendons get too thick, which makes them less functional and weaker.

 

• Last July's issue of Scientific Reports (A Possible Link Between Loading, Inflammation and Healing: Immune Cell Populations During Tendon Healing....) revealed that the link discussed in the study's title is present. "Loading influences tendon healing, and so does inflammation. We hypothesized that the two are connected....  Mechanical loading has a profound influence on tendon healing. Reduced loading has been shown in numerous models to impair healing.  Recently, we have noticed that anti-inflammatory drugs impair tendon healing mainly by impairing the response to loading or microdamage, and also that the expression of inflammation-related genes was involved. This points to a possible connection between loading, inflammation and healing.  By analyzing the cell populations from healing tissue by flow cytometry with markers for several inflammatory and regulatory cell types, we can describe the composition of the population and use it as an “inflammatory signature”. Changes in the signature over time can then show how the inflammatory reaction is influenced under varying conditions."  BTW, the idea that anti-inflammation drugs impair healing is not new and will be discussed at the end of the post.
  

 

• The term "apoptosis" refers to a cell's propensity to die in a pre-programed fashion, and is controlled by a part of the immune system known as the TH-17 SYSTEM, which, by the way, is heavily associated with AUTOIMMUNE DISEASES.  In fact, the Polish journal Archivum Immunologiae et Therapiae Experimentalis (The Role of IL-17 and Th17 Lymphocytes in Autoimmune Diseases) concluded that, "The identification of the new subpopulation of T helper cells producing IL-17 modified our model of the Th1–Th2 paradigm and it was named Th17. High abilities to stimulate acute and chronic inflammation made these cells an ideal candidate to be the crucial player in the development of autoimmune disorders."  Last June's issue of Scientific Reports (IL-17A Mediates Inflammatory and Tissue Remodeling Events in Early Human Tendinopathy) talked about the heavy-hitters of the inflammatory modulator community, saying that, "Increasingly, inflammatory mediators are considered crucial to the onset and perpetuation of tendinopathy.  Endogenous expression of TNFα, IL-1β, IL-6, IL-10, VEGF and TGFβ has been demonstrated in tenocytes.  Increased expression of IL-17A was detected in ‘early tendinopathy’ compared to both matched samples and non-matched control samples. Double immunofluoresence staining revealed IL-17A expression in leukocyte subsets including mast cells, macrophages and T cells. IL-17A treated tenocytes exhibited increased production of proinflammatory cytokines, altered matrix regulation with increased Collagen type III, and increased expression of several apoptosis related factors."  I have said forever that Systemic Tendinosis, which we will discuss shortly, is almost always autoimmune ---even though it does not have an official name because the specific auto-antigen remains unknown.
  

 

• As I have shown you many times, inflammation always leads to fibrosis --- the medical word for Scar Tissue (HERE).  Thus, when last November's issue of Arthritis Research and Therapy (Profibrotic Mediators in Tendon Disease: A Systematic Review) started talking about fibrosis in tendinopathies, I was interested.  Their conclusions; "Tendon disease is characterized by the development of fibrosis," were not surprising as we were already aware of this.  The fact that the authors linked any number of inflammatory mediators to the process was, however, interesting.  Especially considering that for decades this was believed not to be the case.  Be aware that the progression of virtually all disease, tendinopathies included, is Inflammation, Fibrosis, Degeneration (REPEAT).
  

Again, the questions we'll answer at the end of the post; does it matter, and what can we do about this other than simply prescribe more drugs to MOP UP the inflammation rather than shutting off the Systemic Inflammation at its source?

Further evidence that inflammation is involved in tendinopathies comes in the form of just how many studies are talking not only about inflammatory markers, but about the numerous inflammatory comorbidites (concurrent diseases caused by inflammation --- HERE is a list of some of them) that are commonly found in folks struggling with tendinosis.  In other words, if you are fighting tendinosis, your chances of having some serious health issues, CANCER INCLUDED, go up dramatically.

• SHOULDER ARTHRITIS AND TENDINOSIS:  The suffix "itis" lets you know that something is inflammatory as it is the Latin term for inflammation.  A recent study from PLoS One (TREM-1, HMGB1 and RAGE in the Shoulder Tendon: Dual Mechanisms for Inflammation Based on the Coincidence of Glenohumeral Arthritis) revealed that, "Rotator cuff injury is a major disorder in the adult population where inflammation and pain are contributing factors. Coincidence of other clinical conditions like glenohumeral arthritis aggravates inflammation and delays the healing response.  The principal findings in this study reveal significant expression of TREM-1, RAGE and HMGB1 in the shoulder tendon tissue with respect to severity of glenohumeral arthritis."  As you might suspect, these substances are yet other inflammatory biomarkers / mediators that we have not discussed previously.

 

• DIABETES AND TENDINOSIS:  March's issue of Scientific Reports stated that, "People with diabetes are susceptible to tendinopathy and tendon rupture. Diabetic tendons are characterized by weaker mechanical properties than non-diabetic tendons, including lower stiffness, maximum load, Young’s modulus, and strain at break point. Tendons are mainly composed of highly organized collagen fibers as well as various minor structural molecules, such as proteoglycans and glycoproteins. In tendons, tenocyte is the fundamental cell population responsible for maintaining tissue homeostasis, and loss of its genetic traits can cause tendon dysfunction."  The same month the cancer journal Oncotarget concluded, "Patients with diabetes are at great risk to suffer many musculoskeletal disorders, such as tendinopathy, tendon rupture and impaired tendon healing.  In this study, we found that high glucose could inhibit cell proliferation and induce cell apoptosis of TDSCs (tendon-derived stem cells) in vitro. The tenogenic differentiation ability of TDSCs was decreased in the initial stage in vitro. All these findings proved our hypothesis and accounted for the potential pathogenesis of diabetic tendon disorders including diabetic tendinopathy, tendon rupture and impaired tendon healing." By the way, most of this is not really new information.

 

• NEUROPATHY AND TENDINOSIS:  While certainly not the only reason for neuropathic pain, DIABETES is by far the most common.  February's British Journal of Pain concluded that, "This study suggests that neuropathic pain as identified by the painDETECT questionnaire may be common in patients with chronic lower limb tendinopathy conditions.  28% of respondents scored 19 or higher with painDETECT (neuropathic component to pain likely), 29% scored 13-18 (equivocal result)." 

 

• HEART DISEASE AND TENDINOPATHY:   February's issue of the Journal of Occupational and Environmental Medicine (Association Between Cardiovascular Disease Risk Factors and Rotator Cuff Tendinopathy: A Cross-Sectional Study) revealed that, "Recent evidence has found potential associations between cardiovascular disease (CVD) risk factors and common musculoskeletal disorders.  A strong association was observed between CVD risk scores and both glenohumeral joint pain and rotator cuff tendinopathy. The results show a dose-response trend of increasing risk.  Individual risk factors were associated with both outcomes. Combined, CVD risk factors demonstrated a strong correlation with glenohumeral joint pain and an even stronger correlation with rotator cuff tendinopathy. Results suggest a potentially modifiable disease mechanism."  I've talked about this particular link before HERE).

 

• DYSBIOSIS AND/OR INFECTIONS CAUSE TENDON RUPTURE?  We know that virtually all forms of DYSBIOSIS and INFECTION are inflammatory.  March's copy of The American Journal of Sports Medicine (Presence of Bacteria in Spontaneous Achilles Tendon Ruptures) showed that, "The structural pathology of Achilles tendon (AT) ruptures resembles tendinopathy.  Recently, a number of diseases were found to be attributed to bacterial infections, resulting in low-grade inflammation and progressive matrix disturbance [fibrosis / scar tissue].  AT rupture samples exhibited histopathological features characteristic of tendinopathy, and most healthy hamstring tendon samples displayed normal tendon features.  The authors have demonstrated the presence of bacterial DNA in ruptured AT samples."  You need to be aware that not only is sugar one of the most inflammatory things you can consume (HERE), but that it actually feeds both dysbiosis and infection (HERE).
  

 

• OBESITY AND TENDINOSIS:  What do we know about OBESITY?  Only that it is one of the chief of the myriad of inflammatory conditions.  One of last year's copies of Advances in Experimental Medicine and Biology (How Obesity Affects Tendons?) had this to say on the subject.  "Several epidemiological and clinical observations have definitely demonstrated that obesity has harmful effects on tendons."  Notice, however, that this is not simply a "weight" issue. "In addition to overload, attributable to the increased body weight, which significantly affects load-bearing tendons, systemic factors play a relevant role. Several bioactive peptides (chemerin, leptin, adiponectin and others) are released by adipocytes, and influence tendon structure by means of negative activities on mesenchymal cells."  This is very similar to what we saw in THIS POST where I showed you how adipose tissue becomes it's own endocrine gland. "The ensuing systemic state of chronic, sub-clinicical, low-grade inflammation can damage tendon structure. Metabolic disorders (diabetes, impaired glucose tolerance, and dislipidemia), frequently associated with visceral adiposity [BELLY FAT], are concurrent pathogenetic factors. Indeed, high glucose levels increase the formation of Advanced Glycation End-products, which in turn form stable covalent cross-links within collagen fibers, modifying their structure and functionality."  We are warned all the time about AGES from grilled foods, when the biggest form of AGES comes from inflammatory sugar.
  

Here are a few of the tidbits gleaned from recent peer-review (mainstream journals, one and all), showing what's being studied and contemplated as far as solving tendon issues are concerned.

• PRP IS A MICROBIOME THING:  There are lots of studies on PRP INJECTIONS for tendinosis, some saying it works, just as many saying not so much.  Interestingly, a new study from March's issue of Acta Orthopedica (Effect of Platelet-Rich Plasma on Rat Achilles Tendon Healing is Related to Microbiota) concluded --- as might be imagined from the study's title --- that, "In 3 papers in Acta Orthopaedica 10 years ago, we described that platelet-rich plasma (PRP) improves tendon healing in a rat Achilles transection model. Later, we found that microtrauma has similar effects, probably acting via inflammation."  This is exactly why potentially "HARSH" methods such as TISSUE REMODELING have merit, and why GUT HEALTH is so blamed critical to truly solve your issue.  BTW, the authors concluded that rats with Staph (not an active infection but as part of their normal MICROBIOME) actually healed better than those without.

• LOW LEVEL LASER THERAPY IS HELPFUL FOR TENDINOSIS: This month's issue of the Dutch / German journal Zeitschrift für Rheumatologie (Low Level Laser Therapy : A Narrative Literature Review on the Efficacy in the Treatment of Rheumatic Orthopaedic Conditions) concluded that, "While earlier studies often failed to demonstrate the efficacy of LLLT, several recent studies of increasing quality proved the efficacy of LLLT in the treatment of multiple musculoskeletal pain syndromes like neck or lower back pain, tendinopathies (especially of the Achilles tendon) and epicondylolpathies, chronic inflammatory joint disorders like rheumatoid arthritis or chronic degenerative osteoarthritis of the large and small joints. In addition, there is recent evidence that LLLT can have a preventive capacity and can enhance muscle strength and accelerate muscle regeneration.  LLLT shows potential as an effective, noninvasive, safe and cost-efficient means to treat and prevent a variety of acute and chronic musculoskeletal conditions."  Interested in my LOW LEVEL LASER THERAPY posts?  Just click the link.

• TREATING TENDINOPATHIES WITH SUPPLEMENTS:  A group of six Italian orthopedists published a study in a 2016 copy of Muscles, Ligaments, and Tendons called Nutraceutical Supplement in the Management of Tendinopathies: A Systematic Review, in which they looked at 46 studies concerning the popular joint supplements glucosamine and chondroitin sulphate, vitamin C, hydrolazed type 1 collagen, arginine alpha-keto-glutarate, bromelain, curcumin, boswellic acid, and methil-sulfonil-methane.  The authors concluded that, "In the last years, the increase of sport activities, life expectancy, and other factors such as environment, diet, systemic diseases and some drug therapies have led to a rise in the incidence of tendinopathies.  Nutraceuticals are not only used in the general population, but also in athletes.  Preclinical results are very encouraging..."  As noted in this paper, certain drugs (THESE ANTIBIOTICS ARE THE MOST DANGEROUS AND BRUTAL) actually cause inflammation.  And once again we see that Systemic Inflammation / Systemic Disease is a big deal.

 

• INJECTING TENDONS WITH VARIOUS HORMONES CAUSES?  There are tons of studies on DRY NEEDLING techniques, with most of them showing promise for tendinopathies and similar musculoskeletal issues.  A study from the February issue of Muscles, Ligaments, and Tendons (Therapeutic Use of Hormones on Tendinopathies: A Narrative Review) looked at the efficacy of injecting various hormones (ESTROGEN, TESTOSTERONE, THYROID, etc, etc) directly into tendons.  Conclusions?  "At present, experimental studies and preliminary observations in humans suggest that parathyroid and growth hormones, locally administered, are promising therapeutic tools in specific tendon disorders. Local injections of glucocorticoids are useful in several tendinopathies, exploiting their anti-inflammatory and anti-proliferative properties, but carry the risk of further tendon degeneration and ruptures, due to the detrimental direct effect of glucocorticoids on the tendon structure."  Speaking of glucocorticoid (corticosteriods and cortisone) risks...........

We've repeatedly seen that tendinopathy accounts for about 1/3 of the visits to the doctor's office in people going in with musculoskeletal issues.  And while there are a few cutting-edge doctors and clinics out there that are using these and other not-quite-mainstream treatment methods, the standard medical fare for tendinosis is still anti-inflammation medication ---- CORTICOSTEROIDS and NSAIDS.  I have shown you study after study and textbook after MEDICAL TEXTBOOK that say in various ways just how bad these drugs are as far as fouling the healing process is concerned.  Here are a couple more (I could have given you dozens, if not hundreds).

• NSAIDS EFFECTS ON TENDON HEALING:  Two medical doctors (one a Ph.D as well) wrote a well-bibbed article (48 sources) for Rhematology Network called Do NSAIDs Impair Healing of Musculoskeletal Injuries? "NSAIDs are among the most frequently used and prescribed medications in the management of musculoskeletal pain and injury. Many physicians consider them to be the medication of choice.  However, a number of studies have questioned the value of NSAIDs in the healing process of bone, muscle, tendon, and ligament injuries. Studies have demonstrated that prostaglandins and leukotrienes are produced during the acute phase of a tendon injury... In the first few days after acute tendon injury, there is an initial inflammatory phase and entry of inflammatory cells into the injury site.  There appears to be little role for NSAIDs outside of the initial symptomatic pain relief during the first few days after injury."  This is an interesting paper because while actually acknowledging PGE2, LEKOTRIENES, and other inflammatory mediators, the authors are not high on the long-term effects of blocking these mediators we refer to as "inflammation".
  

 

• INJECTING TENDONS / JOINTS WITH STEROIDS: Listen folks; I've only shown you about a hundred times how bad this stuff is over the long haul.  Here's one more for those who may have missed the rest.  December's Expert Opinion on Drug Safety (Clinical Benefits and Drawbacks of Local Corticosteroid Injections in Tendinopathies) showed us yet again that the short-term relief sometimes provided by corticosteroids is not worth the long term grief.  "Local glucocorticoids injections are widely administered for the treatment of tendinopathies. positive results have been observed in some tendinopathies but not in others. moreover, worsening of symptoms, and even spontaneous tendon ruptures has been reported. Several experimental studies suggest that the direct action of glucocorticoids on tendons is detrimental. Loss of collagen organization, impaired viability of fibroblasts, depletion of stem cells pool, and reduced mechanical properties have been observed."   How about boosting COLLAGEN production and FIBROBLASTIC ACTIVITY instead of suppressing it!  This bullet helps explain why I've repeatedly argued that that IMMUNE SYSTEM SUPPRESSION is America's number one form of medical treatment.
  

Have you ever been so far behind you thought you were in the lead?  For decades, the research side of the medical community told us that TENDINOSIS is not an inflammatory condition --- it's purely mechanical (fibrosis).  Since most docs never got that memo --- continuing to treat with their usual array of drugs --- the fact that the science has changed yet again didn't affect them one iota.  But what does this information mean to you, the individual struggling with tendinosis, who does not want the drugs? 

It means that as I just showed you, the "alternatives" are every bit as effective as mainstream care (drugs, chiefly steroids and NSAIDS).  And while inflammation is certain a factor in tendinosis, addressing the inflammation (the "itis") without addressing the fibrotic changes (the "osis") is just as ineffective today as it was yesterday, last week, last year, or back in the 20th century.  Sure, I want you to deal with the inflammation.  What you have to remember, however, is that the local inflammation is a critical part of the healing process (HERE).  It's the SYSTEMIC INFLAMMATION that must be addressed, and unfortunately, you can't take care of this kind of inflammation with a pill, potion, or lotion.  Remember the last part of the last sentence of the very first bullet point of this post that I said I would come back to? Local inflammation is probably not your problem ---- it's the presence of systemic inflammation associated with chronic diseases that is making your tendon train go off the rails in so many different ways.

What you need to do is deal with underlying systemic inflammation like you would for any other inflammatory problem (HERE) --- after all, study after study (as I showed you again today) reveals just how inter-related these disease processes really are.  That's why they refer to these as "comorbidites" (Co = "along with or beside; concurrent" and Morbidity = "illness or sickness").  A failure to address the systemic inflammation means that you will probably be repeating the whole tendinopathy thing over and over again along with at least some of THESE DISEASES.  However, address the systemic inflammation successfully and you end up taking care of any number of "comorbidites".  HERE'S a really cool example of someone who addressed a handful at the same time.

As for treating tendinosis in my clinic, this information doesn't really change anything I'll be doing other than warning people about the relationship between diet / lifestyle and their chronic pain by handing out more copies of my CLINIC'S "ONLINE" WEB CHECKLIST.  In other words, it's not like this information completely snuck up on me --- I've been increasingly talking about the role of inflammation in tendinopathy for awhile now (HERE and HERE).  And for those of you struggling with SYSTEMIC TENDINOSIS (not the stuff caused by fluoroquinolone antibiotics such as Cipro), I have plenty of info for you as well.  Not surprisingly, I have always maintained that it's largely an autoimmune issue driven by --- you guessed it --- inflammation.  And truthfully, if you swapped out the word FASCIA for tendon in this post, it would probably all still be true.

There are mountains of evidence showing that tendinopathies such as tendinosis are not inflammatory (HERE).  In fact, clicking the link will take you to a number of posts that address the debate over whether tendinitis (tendon inflammation) even exists at all.  So how is it we now have studies linking an obviously inflammatory problem (HEART DISEASE) with a non-inflammatory problem such as tendinosis?  According to this month's issue of the Journal of Occupational and Environmental Medicine (Association Between Cardiovascular Disease Risk Factors and Rotator Cuff Tendinopathy: Cross-Sectional Study)....

"Recent evidence has found potential associations between cardiovascular disease (CVD) risk factors and common musculoskeletal disorders.  A strong association was observed between CVD risk scores and both glenohumeral joint pain and rotator cuff tendinopathy.  The results show a dose-response trend of increasing risk [i.e. the more of one you found, the more likely you were to find the other along with it].  CVD risk factors demonstrated a strong correlation with glenohumeral joint pain and an even stronger correlation with rotator cuff tendinopathy.  Results suggest a potentially modifiable disease mechanism."

The last sentence is particularly interesting.  It is suggesting that, in similar fashion to the myriad of CHRONIC INFLAMMATORY DEGENERATIVE DISEASES (which include virtually everything on THIS LIST of autoimmune diseases), TENDINOSIS can be controlled by "modification" --- which is the code word for diet and lifestyle.  Let me break this down and give you my thoughts.

While it's true that tendinosis itself is not inflammatory (it does not contain inflammatory markers when biopsied), it is likely that inflammation --- SYSTEMIC INFLAMMATION --- can affect the mechanical qualities of the tendon.  In other words, tendinosis is not throwing off inflammation, but is certainly affected by it.  Because inflammation is caused by damaged tissues, there are a couple of things that come immediately to mind. 

Not knowing exactly how they diagnosed the tendinopathy, It would not surprise me to learn that much of what the authors are referring to as tendinopathy is actually FASCIAL ADHESION.  And as I've told you before, it doesn't really matter as far as treating it is concerned (HERE).  The other thing is that at least in America, the number one cause of tissue damage-causing inflammation is arguable our collectively poor diets.  Although the authors have nothing to say about diet in this study (they didn't even measure blood markers of inflammtion due to lack of funding), I've yet to see any health issue (even many of the "GENETIC DISEASES") that cannot be helped / modified / aided / changed / improved by cleaning up one's diet.

Writing for Practical Pain Management (Rotator Cuff Tendinopathy Found Associated with Cardiovascular Disesase Risk), Thomas Ciccone, interviewing Dr, Kurt Hegmann, the study's co-author and  professor and director at the Rocky Mountain Center for Occupational & Environmental Health at the University of Utah stated (I'm cherry-picking), "Over the years, doctors have explored the theory that inflammation could be a risk factor for cardiovascular disease. Now, some new epidemiological evidence could provide credence to this theory.  The study, adds yet another angle to the growing body of research exploring the possibility that common musculoskeletal disorders, such as carpal tunnel syndrome, Achilles tendinopathy, and lateral epicondylitis, are associated with cardiovascular disease risk factors."

Dr. Hegmann went on to say, "Physical activity level at work was not associated with glenohumeral joint pain or rotator cuff tendinopathy, despite the fact the cohort consisted of a diverse range of employment types, from sedentary, office-based jobs to highly physically demanding jobs requiring frequent exertion. We would think that ultimately people would show that there is some risk of rotator cuff tendinitis from job factors, but the fact that this was negative was unexpected.  Oftentimes, low grade inflammation is one such explanation behind this, whereby the body’s immunological response through circulating inflammatory markers could be indicative of an increased risk for compromised cardiovascular health."

In other words, according to Dr. H's research, the physicality of your job doesn't matter a fraction as much as whether you are systemically "inflamed" or not, with some of the problems mentioned being ACHILLES TENDINOPATHY, LATERAL EPICONDYLITIS (Tennis Elbow), and CARPAL TUNNEL SYNDROME.  What have I shown you to be true of inflammation according to the most current research?  

• INFLAMMATION IS THE ROOT OF ALMOST ALL HEALTH PROBLEMS:  This is not only true of physical problems (see the earlier lists) but mental / emotional problems as well (for instance, both ANXIETY and DEPRESSION are considered "inflammatory").
• INFLAMMATION ALWAYS LEADS TO SCAR TISSUE:  Who cares that the medical community refers to this Scar Tissue as "FIBROSIS".  I have shown you over and over again via at least a dozen posts that inflammation always leads to Scar Tissue (HERE and HERE). 
• INFLAMMATION INDUCED FIBROSIS IS AMERICA'S #1 CAUSE OF DEATH:  Now we're talking real money!  For those who were not aware, America's #1 cause of death is Fibrosis (HERE) --- just ahead of medical errors (HERE).
• INFLAMMATION IS A MIGHTY BEAST, BUT A BEAST THAT CAN LARGELY BE TAMED: This, folks, is where the rubber meets the road.  As Arnold said in his hit movie Predator, 'If it bleeds we can kill it'.  In this case, all we have to do is figure out what's driving the inflammation.  While it's true that there are any number of potentials, looking at diet first is simply going after the low-hanging fruit. 

For those of you looking to get off the MEDICAL MERRY-GO-ROUND and get your lives back, I've created a generic protocol for doing so that will help you figure out what's driving inflammation and allow you to start taking charge of your health (HERE).

"Today (5-12-16), the FDA is requiring labeling changes for antibacterial drugs called fluoroquinolones, including an updated boxed warning, stating that the serious side effects associated with fluoroquinolones generally outweigh the benefits for patients with sinusitis, bronchitis and uncomplicated urinary tract infections who have other treatment options.   An FDA safety review has shown that fluoroquinolones are associated with disabling and potentially permanent, serious side effects that can occur together.  These side effects can involve the tendons, muscles, joints, nerves and central nervous system."   Cherry picked from Thursday's FDA warning concerning Fluoroquinolone Antibiotics (FDA Announces Safety Labeling Changes for Fluoroquinolones)

Back in November of last year, the FDA's Antimicrobial Drugs Advisory Committee (ADMAC) got together with the Drug Safety and Risk Management Advisory Committee (DSRMAC) to have a sit down about the dangers of FLUOROQUINOLONE ANTIBIOTICS.  Although they did not really do anything substantial (they did talk about this class of antibiotic causing NEUROPATHY, DEMENTIA, and hallucinations, as well as the fact they are associated with C. DIFF INFECTIONS), the committee members voted (nearly unanimously) that something should be done.  Because heel dragging is par-for-the-course inside the FDA, we should not be surprised that America is way behind the curve on this issue.

One of the earliest "official" warnings by the FDA that Fluoroquinolone Antibiotics can cause joint pain and TENDINOSIS / Tendon Rupture came out eight years ago.  Look at what Todd Zwillich wrote clear back in July of 2008 for that bastion of truth, WebMD (FDA Warning: Cipro May Rupture Tendons ---- Agency Issues 'Black Box' Warning for Antibiotics Known as Fluoroquinolones).

"The new warnings apply to fluoroquinolones, a class of antibiotics that includes the popular drug Cipro. The FDA has told companies that the drugs must now carry "black box" warnings alerting doctors and patients that the drugs can increase risk of tendinitis and tendon rupture in some patients. Fluoroquinolones have carried similar warnings for years, but officials say they continue to receive reports of safety problems. A "black box" warning is the FDA's sternest warning.   Most of the tendinitis and tendon ruptures affect the Achilles tendon, behind the ankle. But the agency has also received reports of tendinitis and ruptures in the shoulder and hand.  Researchers don't know exactly what fluoroquinolones do that promotes tendon rupturing. Theories suggest the drug may impede collagen formation or interrupt blood supply in joints.  FDA officials would not confirm the number of reports of ruptures it has received, citing the ongoing litigation."

Unfortunately for the general public, this class of antibiotic is no different than other drugs or VACCINES when it comes to "Underreporting".   Scores of studies reveal that only 1% to 10% of drug reactions are ever reported --- HERE).  Although the government tells us that Fluoroquinolone Antibiotics only affect about 1 in 25,000 people, I will assure you that this number is low --- way too low.  In 25 years of busy rural practice, I have probably, give or take, seen 25,000 unique individuals.  According to the FDA, this means I should have seen one case of tendon problem caused by Flouroquinolones.   The problem is, have seen dozens of such people who have been messed up by varying degrees by these drugs (and like STATIN DRUGS or CORTICOSTEROIDS; who knows how many others who not put two and two together concerning what messed them up).  In fact, this problem is so common that there is actually a term used to describe it --- being "Floxed" (the name comes from the fact that there are about a hundred different Fluoroquinolones whose names end with "floxacin").

I see this problem as having two different layers.  Firstly, is the underreporting mentioned above.  It's virtually impossible to argue that the vast majority of physicians have totally ignored this phenomenon.  They continue to prescribe drugs like Cipro (Ciprofloxacin) at the same rate they always have.  Secondly, what do we know about doctor's prescription habits for ANTIBIOTICS IN GENERAL?  Only that study after study continues to say that half or more are completely unnecessary or improperly prescribed (HERE).  Cipro achieved rock star status shortly after the towers fell in 2001.  If you don't remember, just Google "anthrax scare cipro".  Because so many people now ask for it by name, it is frequently prescribed for things it has no business being prescribed for such as SINUS INFECTIONS and UPPER-RESPIRATORY INFECTIONS (colds and bronchitis) -- almost all of which are viral.  Or THE FLU, which is always viral.

What does the federal government actually say about Fluoroquinolone Antibiotics on their website?  Glad you asked.  In light of the dozens upon dozens of citizen websites and message boards warning of the dangers of this particular class of antibiotic, we shouldn't surprised that the FDA has chimed in as well (other than the brand new warning at the top of this post).

"CIPRO belongs to a class of antibiotics called fluoroquinolones. CIPRO can cause side effects that may be serious or even cause death. If you get any of the following serious side effects, get medical help right away.  Tendon rupture or swelling of the tendon (tendinitis). Pain, swelling, tears and inflammation of tendons including the back of the ankle (Achilles), shoulder, hand, or other tendon sites can happen in people of all ages who take fluoroquinolone antibiotics, including CIPRO.....    Sometimes infections are caused by viruses rather than by bacteria. Examples include viral infections in the sinuses and lungs, such as the common cold or flu. Antibiotics, including CIPRO, do not kill viruses."

In that November meeting from last year, it was reported that since 2010, approximately 23 million Americans are taking these drugs --- each and every year.  No matter how you slice it folks, that's a lot of people.  Furthermore, the largest group taking this class of drug are those with UTI's (Urinary Tract Infections).  Although this problem can affect folks (usually women) of any age, it's typically found in the elderly ---- those who are already at greater risk for tendon rupture. 

If you are finding yourself struggling with chronic health issues of any sort, there's almost always a natural solution.  But it depends on whether or not you are willing to study, learn, and make some changes in the way you live your life.  To see what I'm talking about, take a quick peek at THIS POST.

"Confusion between Tendonitis versus Tendinosis:  Tendonitis is a very common, but misleading term. Corticosteroids are drugs that reduce inflammation. They are typically injected into tendinosis along with a small amount of the numbing drug lidocaine.  By definition, anything that ends in "itis" means "inflammation of."  Research shows that tendons are weaker following corticosteroid injections. Tendinitis is still a very common diagnosis, though research increasingly documents that what is thought to be tendinitis is usually tendinosis."   From Wikipedia's listing for Tendinitis

"Tendinosis, is damage to a tendon at a cellular level (the suffix "osis" implies a pathology of chronic degeneration without inflammation).  It is thought to be caused by microtears in the connective tissue in and around the tendon, leading to an increase in tendon repair cells. This may lead to reduced tensile strength, thus increasing the chance of tendon rupture. Tendinosis is often misdiagnosed as tendinitis due to the limited understanding of tendinopathies by the medical community. The term tendinitis should be reserved for tendon injuries that involve larger-scale acute injuries accompanied by inflammation."  From Wikipedia's listing for Tendinosis

I just finished putting a bunch of custom diagnoses into my tablet computer for the switch from ICD-9 to ICD-10 that occurs today.  We went from 13,000 potential diagnosis to nearly 70,000.  Although the government has any number of reasons for this switch, some definitely more sinister than others, one that we have heard repeatedly is that it gives those treating patients the ability to be extremely specific with the diagnostic codes that describe what is wrong. 

For instance, there is a code (V97.29) for your local airport's luggage cart driver being sucked into a jet engine -- without any damage to the aircraft.  And if the driver happens to be a male under 5'5", slightly balding, and wearing a tank top, who got sucked into said engine during a full moon, we can code for that too (V97.29&A#gE).   It's not all bad, as there are actually a few good codes to describe FASCIAL ADHESIONS.  However, there is a major problem with the codes that describe Tendinosis.

Despite huge amounts of research showing that Tendinitis is either rare or does not exist at all (HERE), it is the only diagnosis I find when searching for the proper ICD-10 codes.  I can find hundreds of diagnosis for all kinds of Tendinitis, but none --- not a single solitary one ---- for any form of Tendinosis.  Is this a big deal, or am I making a mountain out of a mole hill?  Let's answer that by creating a chart concerning three things we know about Tendinitis, Tendinosis, and the treatment thereof.

• A.)     If you read the quotes from the top of the page, or take a quick glance at the link above (or THIS ONE), you quickly realize that not only is Tendinitis rare, there is actually some debate about whether or not it even exists at all (in other words, some experts believe that everything we are diagnosing as Tendinitis is actually Tendinosis).
• B.)     After looking on any number of websites (my favorite was ICD-10 Data), the ICD-10 Chirocode Book, as well as notes / materials from Drs. Ron Short, Gary Street, and Evan Gwilliam, I can't find any diagnosis information on Tendinopathy, let alone Tendinosis.  However, I can find hundreds upon hundreds of listings for Tendinitis and Tenosynovitis (an inflammation of the sheath surrounding the tendon).
• C.)     The suffix 'itis' means that the problem is based on INFLAMMATION, while the suffix 'osis' indicates that the tendon has become frayed, weakened, and microscopically deranged.  In order to fix a Tendinosis, you had better be about the business of doing something to INCREASE FIBROBLASTIC ACTIVITY.  In order to effectively treat true Tendinitis, you need to diminish Inflammation (HERE is how I suggest to do that).  How do medical doctors typically accomplish this?  Although they commonly go all-in by prescribing the "BIG FIVE" ---- especially for people with SYSTEMIC TENDON ISSUES they don't really understand --- they are almost surely going to prescribe CORTICOSTEROIDS and NSAIDS.  If you click the links, you'll see that not only are these drugs well known for their brutal side effects, but the 'Standards of Care' that are supposed to guide their use actually recommend against using them for tendon problems (see link on corticosteroids directly above).  This is unfortunate for patients who wind up being treated 180 opposite the most current EVIDENCE-BASED guidelines.

So, while I can put down a code that says you were struck by a turtle (W5922XA), are having problems with your in-laws (Z63.1), fell into a bucket of water and drowned (W16.221), have a bizarre personal appearance (R46.1) and were injured while doing arts and crafts (Y93.D), were seriously burned when your water skis caught fire (V91.07XD), had an injurious collision with a spacecraft (W22.02XD: V95.43XS), or suffered a non-venomous insect bite on your anus (S30.867) while attending the opera (Y92.253), I am forced to use Tendinitis codes that were outdated two decades ago to describe my patient's Tendinosis.

A couple of days ago, I got this email from an individual from Alaska.  Because I thought it was relative to any number of conditions, I wanted to share it with you in the form of a blog post.

Firstly, let me first say that I feel for your situation.  CHRONIC PAIN and Chronic Dysfunction are a set of twins that no one should have to deal with.  The August 29 issue of The Lancet (Pain in the USA: States of Suffering)  says that, "In the USA, the estimated financial cost of treatment and loss of productivity as a consequence of chronic pain is US $560–635 billion per year... According to the findings of the 2012 National Health Interview Survey, an estimated 126.1 million (55.7%) adults had some pain in the 3 months before the survey, and an estimated 14.4 million (6.3%) had the highest severity of pain [Category IV]."  Secondly, although I have said it before, I promise that there is someone out there who has a solution for your particular problem.  It's just a matter of finding that person.  In the meantime, you're stuck with me.

Systemic Tendinosis, while not super common, is far from unheard of.  In fact, there is a website devoted to helping those who suffer with Chronic Tendinosis (Tendinosis dot org).   My experience with SYSTEMIC TENDINOSIS (this link is to an article I wrote for that site ----- HERE, HERE, and HERE are some other similar articles) is that there are two chief causes.  The first is ANTIBIOTICS --- all of them, but most specifically the Fluoroquinolones (HERE, HERE, HERE, and HERE).  I do not consider myself an expert on this topic, and do not know how to solve it.

It is my opinion that the second type of Systemic Tendinosis is, as you mentioned, a form of AUTOIMMUNITY.  Although there are hundreds of named Autoimmune Diseases (HERE are some of the more common), there are many times more that have no name because no one has figured out yet what the auto-antigen is (in other words, the experts are not even sure what tissue, enzyme, chemical, molecule, is being attacked).   Regardless, we ultimately need to figure out what is driving Inflammation.  Even though TENDINOSIS itself is not considered "INFLAMMATORY" because it does not contain inflammatory cells, Inflammation is ultimately what causes the Autoimmune reaction that can cause the body to attack some aspect or another of the tendons.  Below is a list of some of the more common drivers of Inflammation.

• FOOD SENSITIVITIES:  This category includes things like GLUTEN or GLUTEN CROSS-REACTORS, DAIRY, FODMAPS, NIGHTSHADES, additives such as MSG or ASPARTAME, or any number of others.   Gluten is an especially big deal because of its known NEURO-TOXICITY.  However, because Autoimmunity is intimately related to Gluten (HERE), I would stay away from it as a matter of course if you are dealing with a chronic health issue --- or they run in your family (HERE).  And to answer your question, I am not convinced that testing is nearly as sensitive as a good ELIMINATION DIET.  If a person's Immune System is weakened enough, they will not produce enough antibodies to test positive for Gluten, even though they are massively sensitive.   Also, here is my post on ANTI-INFLAMMATORY DIET.

• BLACK MOLD:  When it comes to BLACK MOLD, all bets are off.  This stuff is nasty, and the more you study its potential effects, the scarier it is. 

• HEAD INJURIES:  HEAD INJURIES (HERE, HERE, or HERE) are a huge component in developing Autoimmunity.  Click the first link to understand why.  I have a long-distance patient that I was able to solve several years ago after she had a bike wreck in a cemetery and hit her head on a gravestone.  Unfortunately, she just reignited her problem.  She was at a nice resort pulling a towel out of a wall-mounted rack.  When the towel stuck, she gave it a sharp jerk that pulled the rack (a steel cage) off the wall and into her face.  Her all-over pain is back with a vengeance.

• PARASITES:  Parasites are one of those things we don't think much about, but have a huge potential to drive Inflammation and Autoimmunity (HERE). 

• HEAVY METAL TOXICITY:  MERCURY & ALUMINUM (yes, I realize that Aluminum is not a "heavy" metal) and any number of others, have the potential to wreak havoc on the Immune System, as do the VACCINES that so often contain them.

• INCREASED INTESTINAL PERMEABILITY:   Also called "LEAKY GUT SYNDROME," not only is this problem caused by Inflammation, it drives it as well, creating a vicious cycle.

• STRESS:  When I talk about stress, I could be talking about physical stress, emotional stress, DIETARY STRESS, etc.  The bottom line is that stress causes the Adrenal Glands to kick into overdrive, often times burning them out and leading to something called ADRENAL STRESS / FATIGUE. 

• CHRONIC INFECTIONS / DYSBIOSIS / POOR GUT HEALTH:  Each and every passing day leads to new discoveries in this field (tick-borne infections are a particularly hot topic right now).  Antibiotics destroy the MICROBIOME, leading to poor GUT HEALTH and DYSBIOSIS.  Because 80% of the Immune System resides in the Gut (HERE), anything that affects the Gut has the ability to cause serious amounts of Inflammation and Immune System Dysfunction.

• OTHERS:  I could go on (EMF's, DRUG REACTIONS, OXIDATIVE STRESS, abnormal Methylation, etc, etc) but hopefully you are getting the point.

You are correct in your assertion that there is no "cure" for Autoimmunity.  However, the Immune System can be modulated up or down via ---- you guessed it ---- INFLAMMATION.  Everything you do is either driving Inflammation or squelching it.  HERE is my blog category for pointing people in a direction that will help them solve (or at the very least, address) these types of issues.

"Inflammation is the primary process through which the body repairs tissue damage and defends itself against infection.  Most immune responses in healthy individuals are of limited duration and resolve completely, and normal tissue integrity is re-established.  We associate acute inflammation with resolution, whereas chronic inflammation tends to persist.  In persistent inflammation, the resolution phase becomes disordered, and results in the long-term survival of the inflammatory infiltrate, tissue hyperplasia and, ultimately, tissue destruction and scarring.   This type of scar tissue can interfere with normal tissue function."  From the Textbook of Orthopaedics, Trauma and Rheumatology by Drs. Raashid Luqmani, James Robb, Daniel Porter, and Benjamin Joseph .  Bear in mind that I refer to "fasciosis" as Fascial Adhesions.

"The concept is that there is a loss of inflammatory response and chronic scar formation with fascia and tendon injuries. The proper terms for such injuries are fasciosis and tendinosis rather than the more commonly used terms of fasciitis and tendonitis. In fasciitis and tendonitis cases, there is good blood supply to the problematic region but there is an inflammatory response that is painful. In fasciosis and tendinosis issues, the fascia and ligament have a decrease in inflammatory response, a reduction in the growth/healing factors and a chronic scar formation that prevents the healing process."  Dr. Babak Baravarian from the May 2009 issue of Podiatry Today

Cristiano Ronaldo (age 29) will be playing in the World Cup Soccer Tournament in Rio de Janerio, Brazil for the Portuguese national team.  Because he is widely considered the world's best soccer player (many would argue that Argentina's Lionel Messi is the greatest), any injury is big news.  And because he has played for two of the world's most famous soccer clubs (Manchester United and Real Madrid, his current team), the world is dying to know more about his injury. Cristiano has TENDINOSIS --- more specifically PATELLAR TENDINOSIS --- of the left knee.  Although you have likely heard of Tendinitis, this news begs the question of what exactly is Tendinosis?  Rather than me explain it to you (follow the links if you wish) listen to some of these definitions from recent sports articles.

A two-day-old article from Yahoo says that, "tendinosis is a non-inflammatory condition involving a previously injured tendon that heals with weak collagenous fibers, low weight-bearing resistance and has a high risk of future injury".  BreakingNews.com describes Tendinosis as, "a degeneration of tendon's collagen due to chronic overuse".  And in a June 4 article by Andi Thomas (Cristiano Ronaldo has Tendinosis. What the Hell is Tendinosis?) we learn even more.  Listen to what Thomas writes......  "According to tendinosis.org, it's a "chronic injury of failed healing". Basically, it's when a lot of tiny tears to the connective tissue around the tendon start to have a cumulative effect on the strength of the tendon. Think pain, think stiffness, think mild swelling around the left knee. It's not to be confused with the more common tendonitis, which involves inflammation of the tendon itself."

Having written a couple of articles for Tendinosis.org (HERE is one of them), I can assure you that Tendinitis is not more common.  In fact, there are researchers and specialists in the field that say Tendinitis does not even exist, or if it does exist, it is extremely uncommon.  This is why ANTI-INFLAMMATORY MEDICATIONS and more specifically CORTICOSTEROID INJECTIONS have no place in helping athletes deal with these sorts of injuries.   I would assume that as the world's greatest soccer player, Cristiano's doctors are throwing everything but the kitchen sink at his knee  ---- TISSUE REMODELING, PRP, COLD LASER, Massage, Stretches / Exercises, etc, etc, etc. The problem is, what he probably needs most, is a few weeks of rest.  We will all get to see how his knee is when Team Portugal takes the pitch against the German Nationals on Monday, June 16 --- one week from yesterday.  You can read numerous articles about TENDINOSIS by following the link.