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DOES FASCIA MATTER?

Paul Ingraham, Vancouver Canada

TABLE OF CONTENTS

1. Introduction

2. 1.1Barely known to science!


3. 1.2En garde! The fascia science challenge
4. 1.3Why fascia matters medically (get ready to cringe)

5. Sloppy fascia reasoning

6. 2.1Electrified by piezoelectricity
7. 2.2Fuzzy logic: Gil Hedley’s “fuzz” speech
8. 2.3Ida’s idea about thixotropy
9. 2.4The acupuncture connection: is fascia actually magic?
10. 2.5Not so exotic after all
11. 2.6Extreme “fascial release” therapy injures a patient, maybe permanently

12. Real fascia science that supposedly matters

13. 3.1Fascia is much too tough to “release”


14. 3.2“Release” may not even be real
15. 3.3Does stimulating fascia reduce post-exercise muscle soreness?
16. 3.4Does it matter that fascia contains muscle cells?
17. 3.5Fascia strong like bull! Or … mouse?
18. 3.6Do weak fascial contractions matter?
19. •3.7 No clinical relevance at all? Not even a teensy bit?
20. 3.8Is fascial contraction even interesting?
21. 3.9What does Dr. Schleip think?
22. •3.10 Thicker, stiffer thoracolumbar fascia in back pain: what does it mean?
23. Conclusions
Results of the Fascia Science Challenge so far…

24. 4.1To be continued…


25. 4.2The “Father of Fascia” is so over it

26. Appendices

27. 5.1Further Reading


28. 5.2What’s new in this article?
29. 5.3Notes

• • • • • dots before headings indicate updated sections ?

Barely known to science!

There is a lot of fascia research going on these days. None of that research
is clearly relevant to therapy. Some of it might be, but it’s all quite debatable. There are no
slam dunks. In place of firm theories based on hard data, there’s a lot of speculating
about why fascia is important, which leads to some claims that it has (clinically relevant)
properties and functions that are still barely known to science. For instance, perhaps fascia
can actively cinch up like a corset around muscles, or maybe it is the medium of a liquid
crystal communication system, or even maybe it melts like butter when you move. Who
knows! Anything’s possible!

In the history of science and medicine, knowledge gaps get filled with guesses, and the
guesses usually turn out to be wrong.4 Exotic biology is rarely useful biology. Interesting,
but not useful. No one can get safe, effective, reliable treatment protocols out of barely
understood biology. If you could, the biology wouldn’t be poorly understood anymore —
and you’d be famous for pushing back the frontiers of human knowledge and reducing
human suffering.
Some fascia research is truly intriguing. What many researchers are saying about fascia is
reasonable. Many are not reaching awkwardly beyond the data. Unfortunately, many
therapists fascinated by fascia are reaching beyond — way beyond — what the science
can actually support, or probably ever will. In some cases, in fact, we already know
enough to know that an interesting property of fascia is only interesting, and irrelevant to
working with patients.

Please beware the implication of therapeutic significance from scraps of basic biology. It is
easy to sound cool talking about new biology, because biology is cool. It is hard to make
biology useful. Few basic biology facts ever become the basis for any kind of treatment.
Certainly a lot of fascia science is “right,” but I question whether or not it mattersthat it is
right.

In fact, on one occasion, a rather pedantic experimental psychologist was telling him
about a long, complicated experiment he had done, incorporating all the proper
controls and using considerable technical virtuosity. When he saw Crick’s
exasperated expression he said, “but Dr. Crick, we have got it right — we know it’s
right,” Crick’s response was, “The point is not whether it’s right. The point is:
does it even matter whether its right or wrong?

The fascia science challenge

Fascia is biologically interesting! All biology is. But clinical relevance is the central
question of this article: if fascia science cannot actually improve treatment, then it makes
no sense to be fascinated by it in a therapeutic context. You might as well get excited
about the biology of the immune system, or olfaction, or epigenetics, for all they have to
do with hands-on healing.

Reader suggestions and feedback are welcome, both critical and supportive. However,
hate mail will be ignored. I receive a quite a bit of hate mail on this topic,which
reflects poorly on the community of “fascia therapists” and their beliefs. Good ideas
stand on their own just fine without rude defenders. So please think twice before you hit
send.
Fascia enthusiasts routinely denounce this article, accusing me of ignorance of the current
Science of Fascia. However, you should know that I am pretty up on massage-related
research — it’s basically my full-time job — so I feel confident challenging critics to cite
even one example of fascia research with clear, direct relevance to what happens in
treatment. If such a thing exists, I will be happy to publicly discuss it, and acknowledge my
oversight. I could be wrong about fascia. I even hope that I am. Maybe it is important to
manipulate fascia specifically.

This article covers:

 For context, some fascia basics from mainstream medicine, which sounds boring, but
get ready to cringe: it involves amputation!

 For more context, several of the stranger and sloppier examples fascia “science”:
piezoelectricity, fuzz, thixotropy, and the acupuncture connection.

 And the main event: three key examples of allegedly clinically relevant fascia
research below.

Three key examples may not sound like much, but the article is already several thousand
words long, so be careful what you wish for. And all three are excellent examples of fascia
science with low clinical relevance or worse. We do not have a winner yet.

Why fascia matters medically (get ready to cringe)

All theories and controversies aside, what is the actualclinical significance of fascia in
medicine? Why would it come up for a family doctor or surgeon?

It’s boring but critical: fascia functions as an important infection barrier. Much like skin
prevents pathogens from getting into the bottom in the first place, layers of fascia limit their
spread.5

But there’s a dark side to this vital function — one of the most unpleasant phenomena in
all of medicine (which is saying something). If fascia stops the spread of disease, what
happens behind the barrier? Well, it can get grim: a blocked infection is also
a trapped infection, which can destroy a compartment, with dire consequences. Journalist
Miles O’Brien lost a forearm to “compartment syndrome,” a raging infection that came out
of nowhere and inflated his forearm like a high-pressure sausage.Journalist Miles O’Brien
lost a forearm to compartment syndrome,6 a raging infection that came out of nowhere
and inflated his forearm like a high-pressure sausage. Since fascia is so tough and will not
yield, circulation gets cut off and all the flesh in the compartment begins to die. The
compartment must be sliced wide open to bleed off the pressure — a huge, grisly wound
and a slow, difficult recovery even if all goes well. And it didn’t all go well for O’Brien:

Things tanked even further once I was on the table. And when I lost blood pressure during
the surgery due to the complications of compartment syndrome, the doctor made a real-
time call and amputated my arm just above the elbow. He later told me it all boiled down to
a choice…between a life and a limb.

Now that is clinical relevance. That’s how the properties of fascia medically matter — its
toughness as a wrapping, primarily.

Some people will leap from here to the idea that people who get compartment syndrome
must have something wrong with their fascia — too tough, too tight, needs release to
prevent further compartment syndromes. And that might sound like extremely reasonable
clinical reasoning to some people, and indeed it’s a reasonable enough hypothesis on its
face. But you have to check these things, and someone did, and it’s just not true.7 (And if
it’s not true of something like compartment syndrome, it’s probably not true of subtler
problems either.)

Perhaps there are subtler fascial properties that also matter. But keep this life-or-death
example in mind as we look at why massage therapists and chiropractors think fascia
might medically matter, starting with the most dubious ideas…

There is a crack in everything


That’s how the light gets in.

Leonard Cohen, Anthem


PART 2

SLOPPY FASCIA REASONING

Electrified by piezoelectricity

The piezoelectric effect is an electric charge generated by flexing crystals. It’s a popular
notion that this fascinating property of crystals is at work in fascia, and that it’s the
mechanism for fascial “release.” These ideas have never been more than speculation. The
first is possible but unproven. The second goes much too far and is demonstrably false
and clearly contradicted by modern researchers.

Crystalline properties are a firm pre-requisite for peizoelectricity. To get a piezoelectric


“spark,” you have to have crystals. In the famous 1987 book Job’s Body — which I read
three times, back in the day — Juhan proposes that connective tissue may behave like a
“liquid crystal.”8 A strong emphasis on may: this has never actually been shown to be the
case. Juhan was speculating. This doesn’t mean that there is no piezoelectric effect in
fascia, and there are plenty of problems with the idea, but it’s not totally out to lunch.
We do know that piezoelectricity “sparks” fly when bone is flexed and stressed, and this
guides the slow remodelling of bone,9 which is super cool. It’s a terribly clever system!

It’s also a great example of a clinically irrelevant biological property. It has nothing to do
with anything a manual therapist could ever do to a bone. It is beautifully evolved to
change bone extremely slowly in response to extremely specific stimuli which, presumably,
cannot remotely be simulated by manual therapy. Trying to affect that system with your
hands is quite futile. That’s going to be the case for the great majority of physiological
systems, known and unknown — even if you understand them, it doesn’t mean you
can use them, or affect them with your hands.

Maybe fascia does something similar to bone with piezeoelectric effect. It wouldn’t “shock”
me. But no one has ever demonstrated that it actually does. Indeed, no one has
even tried to find that property of fascia, as far as I can tell.
Some people have run with the idea like it’s a proven fact, though. For instance, James
Oschman states unequivocally and overconfidently that “connective tissue is
piezoelectric,” a fact that can be used as a firm foundation for the further speculation that it
accounts for the fascial “releases.”10

Is this a “straw man”? Nope. A “straw man” would be an idea that no one actually
believes or takes seriously — and therefore meaningless to criticize. Certainly not
everyone interested in fascia thinks that fascial piezeoelectricity is real or important.
However, enough do that it’s no straw man! It may not represent the best thinking in the
field, but it is certainly out there.

And it’s simply inconsistent with the reality of fascial plasticity, which we doknow quite a lot
about. There’s no point in speculating about how fascia responds quickly to manipulation,
because it can’t and doesn’t: it’s too tough and slow-changing.11 In contrast to the total
absence of research into fascial piezeoelectricity, the properties of fascial plasticity are
well studied, and there simply is no short term change in fascia to explain! It can’t respond
to the pressures of massage therapy any more than bone can. In addition to the footnote,
this will be substantiated in various ways throughout the rest of the article.

Could piezoelectricity be at work in some other way in fascia? Anything’s possible. But
now we’re cruising into pure guess work. Do we know anything at all about it, let alone the
physiological intricacies of such a phenomenon? Do we know why it evolved? What it
does, how it does it? Can we affect it? And, if we don’t know these things, how can we
possibly use it to devise a reliable therapy? Obviously we cannot.

Another fine example of imprecise scientific enthusiasm is Gil Hedley’s extremely popular
“fuzz” speech. In this video with a bazillon views, Hedley plays fast and loose with a
dissection observation: there are cobwebby layers of fine, loose connective tissue between
thicker sheets of fascia. The anatomy is interesting — anatomy is always interesting — but
Gil Hedley’s interpretations are dubious. His leaps of logic are charismatic, but also large
and precarious.

“That stiff feeling you have is the solidifying of the fuzz,” Hedley confidently explains. He
thoroughly makes the case that fuzz explains the sensation of stiffness.
At best, that is an unsafe assumption, and one that ignores many other highly relevant
factors — like neurology, say, or the fact that he’s looking at a dead person. He does not
know what happens to that tissue in a living body. In fact, that fuzzy texture only
manifests post mortem — according to biotensegrity expert, Dr. Steven Levin.12 This is a
very interesting passage, worth reading carefully, but note the emphasized phrase
particularly:

In Guimberteau’s video, ‘Strolling Under The Skin’, what you see there is that the
‘fuzzy’ stuff is really dynamic tissue that is under constant change. Tissues don’t
‘slide’, there is no shear, they reconfigure with each movement. The dynamics of a
cell ceases with death. Ca++ [calcium ions] flood into the cell and it stiffens — that’s
rigor mortis. It starts within minutes of death, as soon as the circulating ATP [energy
molecule] runs out. The ‘fuzz’ is connective tissue that is stiffened during rigor mortis,
and it doesn’t happen unless you die. It occurs within minutes of death, and you
can almost watch it happen. It is like snot hardening. The mucus booger that comes
out of your nose quickly hardens and becomes quite stiff; at death, the mucus that
connects all our tissues, does the same.

All that ‘melting the fuzz’ is conjecture based on misinterpreted observations on dead
tissue. Even so called “fresh” cadavers are but poor players in the game of life.

Almost any amount of normal movement is sufficient to sustain a normal range of motion.
“Fuzz solidification” either isn’t happening or doesn’t matter, because it’s effortless to move
through. Also, there are other explanations for the sensation of stiffness: better, evidence-
based, and un-fuzzy explanations.

Ida’s idea about thixotropy

A shabby, decades-old idea is still often seriously cited as the explanation for how fascial
therapy works: because it softens fascia with “thixotropic effect.” The idea came from Ida
Rolf (founder of “Rolfing”). Fascia researcher Robert Schleip:13

Many of the current training schools which focus on myofascial treatment have been
profoundly influenced by Rolf (1977). In her own work Rolf applied considerable manual or
elbow pressure to fascial sheets in order to change their density and arrangement. Rolf’s
own explanation was that connective tissue is a colloidal substance in which the ground
substance can be influenced by the application of energy (heat or mechanical pressure) to
change its aggregate form from a more dense ‘gel’ state to a more fluid ‘sol’ state.

A quick look at how thixotropy works in human physiology shows that this just doesn’t add
up. The thixotropic effect is nifty physiology, but it’s not a therapeutic effect in itself, nor is it
the mechanism of one. Ida’s idea was wrong. And, in Ida’s defense, she knew it was! In
fact, she called it nonsense herself!14

Thixotropy is an obscure physical property of certain slimy body fluids that get thinner
when agitated or stressed. You can easily observe thixotropic effect in beach sand, near
the water’s edge: stamp your feet in the sand, and it starts to liquify.

What makes these substances gooey and slimy? Why, a family of carbohydrate
molecules, of course: the glycosaminoglycans. Also known as the snot molecule. Think of
any movie monster with tons of ropy saliva — that’s glycosaminoglycans!

Thixotropic fluids in the human body include synovial fluid in joints, mucus, semen, and the
gelatinous and poorly-named goo called “ground substance” — the stuff that gristly
connective tissue fibres are embedded in like bits of coconut in Jello. Ground substance is
the most plentiful thixotropic substance in the body.

But thixotropy is minor, slow, and temporary, and fascia is too tough to change.

Fascial sheets are incredibly tough, and you can’t “change their density and arrangement”
quickly or easily. And thixotropy just isn’t fast enough to explain the relatively speedy,
dramatic effects on tissues that therapists claim to achieve. Dr. Schleip: “either much
longer amounts of time or significantly more force are required for permanent deformation
of dense connective tissues.”15 Thixotropy might slowly make fascia more pliable, but
not stretchier. If thixotropy had the power to increase the extensibility of connective tissue,
then we would become obviously more flexible just from sitting in a sauna — I’ve tested
this repeatedly and never observed any increase in flexibility just from being hot.16

Even if it works in some small way, thixotropic effect is going to be temporary, fading within
seconds or minutes after hands are removed. When the stimulation stops, so does the
thixotropy, and a therapy can’t work if the affected tissue immediately reverts to its
previous state.Thixotropy will stop when the stimulation stops … but a therapy can’t work if
the affected tissue immediately reverts to its previous state. Dr. Schleip calls this the
“reversibility problem” and “definitely not an attractive implication of this model for the
practitioner.”

Last but not least, thixotropic effect is simply a minor effect. It’s occurring a little bit all the
time, with or without massage. Massage surely does induce it a little, but just as surely
much less than ordinary physical activity — like with circulation. Massage therapists are
very fond of claiming that massage “increases circulation,” but if it does so at all, the effect
is much smaller than what exercise does! Perspective matters. Another similar thought
experiment: if sustained pressures or sheering could significantly change connective
tissue, then working a chair all day long — or any long-duration posture — would also
deform your fascia.

The idea of thixotropy is hardly state-of-the-art thinking about fascia, but it is certainly still
prevalent among therapists practicing fascially-focussed therapy, and trying to explain
what they do. Unfortunately, it was never even a good idea in the first place, even decades
ago.

The acupuncture connection: is fascia actually magic?

Another disconcertingly popular notion about why fascia matters is that the meridians of
Chinese medicine correspond directly to fascial anatomy and function. If you polled
therapists doing fascial manipulation, I think you would find that a great many believe that
they are doing the same thing that an acupuncturist is doing — just in a different way.
They believe that fascial therapy works for the same reasons acupuncture works.

Indeed, most fascial therapists probably believe that acupuncture works. And therein lies
the problem. Unfortunately for fascial release therapy, acupuncture is not a good ally: it
has been failing many fair, good quality scientific tests for years now, and is simply not
what it seems to be.

Acupuncture as we know it today is not so ancient after all: its current form is
a modern (not ancient) invention of the pediatrician Cheng Dan’an (承淡安, 1899-1957) in
the early 1930s1718 For most of history, acupuncture existed primarily as a method of
bloodletting — exactly like the prescientific medieval European practice.Before that, for
most of history, it existed primarily as a method of bloodletting — much like the
prescientific medieval European practice. And then there’s the myth of acupuncture’s
popularity.19Even its alleged popularity and widespread use in China is trumped up — it
is, for instance, not actually used for anaesthesia,20 despite widespread belief in this
phenomenon.

These are embarrassing facts for acupuncture. All of this and more is discussed in more
detail (and heavily referenced) in my main acupuncture article:

Does Acupuncture Work for Pain? A review of modern acupuncture evidence and myths,
particularly with regards to treating low back pain and other common pain problems~ 7,500
words

I was not a skeptic about acupuncture originally. I came to this position only after a long,
uncomfortable period of eduation and gradually eroding faith. But I now accept that
acupuncture is obsolete Eastern folk medicine propped up by Western hype and wishful
thinking.

Therefore, the proposed association between “fascial meridians” and the “chi meridians” of
traditional Chinese medicine is meaningless. Even if meridians and all the other rubric of
acupuncture were real, acupuncturists are unable to demonstrate their power clearly: their
needles are consistently no more helpful than placebos.21 Even pro-acupuncture
researchers have repeatedly admitted that the effect of the needles is small at best. And if
the acupuncturists can’t manipulate these meridians effectively enough to achieve clearly
measurable effects, why would pulling on fascia be able to do it?

Acupuncture lore has no business in a serious discussion about fascia and its possible
importance in therapy.
Not so exotic after all

Piezoelectricity, fuzz, and fascial meridians are three good examples of popular but poor
reasons why fascia supposedly matters. There are other reasons, both better and worse,
and discussion of genuine fascia science is still coming. But first I want to make it clear
that common fascia talk often fails to even reach the level of being “science-y.” Despite all
the talk of exotic properties of fascia, fascia’s clinical importance is usually expressed only
in terms of a couple extremely simplistic rationales, which don’t seem exotic at all:

1. it’s everywhere and connects everything (well, yeah),

2. and it gets tight (not clear, see below).

A strong theme in fascial therapy is the emphasis on the interconnectedness of anatomy


via fascia, always making the point that pulling on any one part of fascia affects the whole
body, like pulling on the corner of a sweater affects all the threads. (That sweater analogy
appears virtually everywhere online that fascia is mentioned. It gets really tiresome,
actually. Didn’t think it mattered much ten years ago. Still don’t.)

The main idea of fascial therapy is that the stuff can get tight and restrictive, like clothing a
size too small, and needs to be “released,” and that therapists can achieve this by various
methods of yanking on it. The yanking may be extremely intense, too — some flavours of
fascial therapy are among the most painful of all hands-on techniques.22

And that’s what fascial therapy boils down to most of the time, in the wild. I have
personally encountered lots of talking about fascia that is exactly this rudimentary … and
even worse, like the example I quoted in the introduction — “The fascia will make
everything better!” Many therapists are perfectly capable of discussing the topic more
intelligently, of course, but low quality reasoning and communication about fascia is
distressingly common (and my exposure is quite extensive, due to the large volume of
email I receive).

Consider this gem of simplistic rationalization:


Restricted fascia is full of pockets. When the tissue starts to release, these pockets
are opened up. When these pockets open, the sensations that were trapped in them
are released.

Such overconfident, poor quality clinical reasoning isn’t universal — just excessively
common within the culture of fascia enthusiasts.

Now, let’s get to some real fascia science.

The greatest enemy of knowledge is not ignorance, it is the


illusion of knowledge.

Stephen
Hawking

Extreme “fascial release” therapy injures


a patient, maybe permanently

This is one of the most striking stories of incompetent and harmful manual therapy that I
have ever received from a reader. (And I get a lot.) It is notable not only for the
seriousness of the outcome, but also for the glaring excess of the treatment: so
unnecessary! If condemnation and negativity isn’t justified here, I don’t know where it is:
the degree of fascia-o-centric incompetence and poor clinical judgement is just appalling.
What happened to this patient needs to be discussed openly. Although this is an unusually
nasty example, negative outcomes like this are shockingly common, and almost
never reported to the therapist who perpetrated them — or, if it is, the therapist rationalizes
it away as a “healing crisis” or any one of a list of other intellectually dishonest evasions.
Funny drawing for a most unfunny story. (Drawing by Claude Serre.)

The story

I have re-written the story a little to anonymize and condense it, but it is otherwise
presented as it was received:

I visited a massage therapist a month ago for treatment for soreness/achiness in the
balls of both feet and in the toes. Claiming that tight calf muscles and hamstrings
were causing my heel to lift too far (thus placing pressure on the balls of my feet), she
proceeded with a half hour fascial release therapy on my calves, using her full
weight and her elbows.

It was extremely painful, but I gritted my teeth, thinking it necessary "to break up the
knotty muscles." She moved from point to point up and down my calves, twice. A
week later I had another such treatment, and she also also persuaded me to buy a
rubber roll so that I could do the "therapy" at home. She told me I should try to
reproduce the same pain level, on calves and hamstrings. I did this every day for
one hour for five days. I did the same with a wooden roller under my feet, using my
own weight.

During that time, I started getting stabbing and burning pains in my feet, the backs of
my legs, and then later my hands and armpits. The stabbing pains varied from a
pinprick feeling to electric-shock/lance-like, and they varied in their frequency rate.
The burning was either tingly or felt like bad sunburn. The pain seemed to be
aggravated by walking, and was always worse by afternoon/evening. I had trouble
sleeping, because I could not have heavy bedclothes on my feet, and nor could I
put one leg on top of the other, without pain.

I returned to my GP, had blood tests, x-rays, a CT scan. Because my symptoms


seemed neuropathic in nature, I was referred to a neurologist. After eliminating a
number of other diagnoses, the neurologist thinks the problem is biomechanical or
related to muscles, and that the MFR may have caused an oversensitivity to pain.

I then searched the Internet for information about myofascial release being damaging
or making pain worse. It was very difficult to find, because of all the "positive" hype
around MFR. Fortunately, I found your website …

The implications

What happened here? Aggressive and intense manual therapy with no regard for the state
of the patient’s nervous system or the potential to provoke an extremely serious chronic
pain state, probably via the mechanism of “central sensitization.” This patient’s prognosis
is impossible to call: it could last another week, or this patient could suffer excessively for
the rest of her life.

For the duration of my decade as a massage therapist, I had a reputation as a gentle


therapist, and many of my patients were “refugees” from excessively intense treatment,
many of whom vented angrily to me about the abuse they had received from other
therapists. Vancouver is a “fascial release” mecca, with many therapists who believe that
there is no gain without pain, and many or all painful problems are caused by fascial
“restrictions” that must be painfully “released.” As a therapist who defined himself in
opposition to this obvious trend, I was treated to many, many outraged patient anecdotes
about the brutality of other therapists.

Having also personally experienced that intense style of fascial release many times, I
knew all too well what these patients were talking about. Almost none had found the
courage to discuss their concerns with the confident (overbearing?) therapists who had
mistreated them. Almost all had even earnestly tried to like it, at first. Sometimes, rather
sadly, they were even still trying to rationalize it as positive, i.e. “I’m sure it was probably
what I needed, but I just couldn’t take it anymore!”

Of course some people enjoy intense therapy — and hey, if your nervous system is okay
with it, that’s fine. Most of those therapists have many devoted patients who, for various
reasons biological and psychological, are more willing and able to tolerate extreme
therapy. However, they are also leaving behind them a trail of angry, injured patients …
patients who never raised a word of objection.

That’s why stories like this are important. There are bound be therapists reading this who
have actually done this to patients, who do it every day. Many will react defensively. Many
will delude themselves into believing that they are the more judicious exception to the rule.
But some, perhaps a few who are already questioning their own methods, will probably be
moved further in that direction. I hope.

Better still if patients feel emboldened to reject such treatment more quickly.

The conceptual cancers at the heart of this incident are structuralism and the for-profit
trademarking and packaging of treatment methods, what I call modality empires — and
“fascia” is a defining, central feature of several of the most famous modality empires.
Fascia sells. It’s prevalence in the marketplace has much more to do with marketing than
sound clinical reasoning.

Now, back to the science.

PART 3
REAL FASCIA SCIENCE THAT SUPPOSEDLY MATTERS

Fascia is much too tough to “release”

“Manual therapists need not feel threatened by the news that we


cannot stretch fascia.”

If We Cannot Stretch Fascia, What Are We


Doing? Alice Sanvito, Massage Therapist

My original challenge to readers (in the fall of 2011) to suggest fascia science that
supports fascial therapy was kicked off with a fine example: one that is just about the exact
opposite of what I asked for, underminding the clinical relevance of fascia rather than
supporting it. Despite the extraordinary number of comments I received on early versions
of this article, few readers answered my challenge directly. Of the handful of scientific
papers that were suggested to me, this was the most “interesting”:

“Three-dimensional mathematical model for deformation of human fasciae in manual


therapy”
Chaudhry et al. Journal of the American Osteopathic Association. Volume 108,
Number 8, 379–90. Aug 2008.

The Chaudhry et al article is indeed “clinically relevant” to fascial therapy … but not in a
supportive way. This fascia science actually contradicts the big idea of fascial therapy.

The main point of manipulating fascia23 is to physically change it in some way — to


achieve what is usually described as a “release.” Although the concept of release may
correspond to some other physiological phenomenon — another discussion — it certainly
cannot be explained in general by physically changing the fascia.

What Chaudhry and colleagues showed is that fascia is much too tough to “release"
(mechanical deformation24) by stretching it. Although they oddly imply in their summary
that it might be possible to do so with the superficial nasal fascia, the main text of the
paper makes it clear that even that thin tissue is extremely tough, and would only
mechanically deform if subjected to surprisingly intense forces. This is consistent with well-
established properties of fascia, namely that it’s extremelytough stuff. Collagen is like that.

If I could write my own conclusion to this paper, it would go more like this:

CONCLUSION: You cannot change the structure of fascia, because it is tougher than
Kevlar. If the stuff were thicker, people would be bulletproof.25

CLINICAL IMPLICATIONS: If you want to physically change someone's fascia by


force, you're going to have to get medieval. This directly contradicts a major popular
rationale for fascial manipulation.

This paper is only clinically relevant to fascial therapy insofar as it presents evidence that
discourages and undermines existing common practices and beliefs. Therefore, perhaps it
was a poor choice to cite it in this context.

It’s also just old news that fascia is too tough to change. For instance, Dr. Robert Schleip
debunked the idea in his 2003 paper about fascial plasticity, and if you don’t take his word
for it — a well-respected fascia researcher — then whose opinion would be credible
enough? He dismisses the traditional explanations of thixotropy and peizoelectric-effect-
mediated adaptation, and thoroughly describes fascial toughness. He concludes that
plastic fascial change in response to moderate loading is “impossible to conceive.”26

As strongly stated as that may be, I’ll go even further. Dr. Schleip (and virtually everyone
else) assumes that “release” is a real thing that needs explaining. I’m not so sure…

.
“Release” may not even be real

In the context of fascial therapy, a “release” is:

 a palpable, relatively quick change in tissue texture

 clinically meaningful (makes some kind of real difference to the patient)

 somewhat lasting (if it didn’t last, what would be the point?)

 somewhat predictable (that is, it’s happening because of treatment)

And fascial therapists more or less unanimously assume that it’s fascia, specifically, that is
doing the releasing.

No doubt the first thing — a quick change in texture — happens in the course of manual
therapy. It is not safe to assume the rest, though. And what’s left of the concept of a
release if you take away the clinically meaningful, lasting, and predictable parts? What if
it’s just a change in texture, a bit of movement under the skin?

Yes, I do have experience.Many readers accuse me of having no practical experience


with patients, when in many cases I clearly have more (and better) than they do. Not that
it’s a contest, but it’s just so deeply ironic and amusing when people assume that the only
possible explanation for my opinions is that I must not have any work experience as a
massage therapist. I have a decade of it, and this fact is readily available in my bio.

In my many years working as a massage therapist, I felt various and sundry ripplings,
twitchings, and shifts under the skin. But in order to qualify as “releases,” those
movements should have correlated strongly with my intentions and with the patient’s
experience. Sometimes they did, but often they did not. So I always thought they were
really quite random, occurring with great variety pretty much no matter what I did, or what
patients reported.27 So while I certainly felt something change, I rarely thought of those
changes as a meaningful “release.”

Dr. Schleip’s 2003 paper about fascial plasticity basically just said that fascia is too tough
to change, but muscle may react to touch and pressures, and that this is probably
mediated by sensory nerve endings in all soft tissues. This is hardly surprising — it
basically just means that people react when poked and prodded — and it doesn’t really
have anything to do with fascia in particular, except insofar as fascia has nerves in it, just
like everything else. We have no idea whether or not any of that actually constitutes a
meaningful mechanism for a “therapy.” I can also make someone twitch their quadriceps
by bonking their patellar tendon: does it matter, other than as a test of the reflex itself?

Releases are probably mostly just trivial tissue “noise” in the hands-on experience, not a
pivotal event in therapy. Or, if they are more meaningful, they are nearly impossible to
interpret. It’s not that nothing’s going on … it’s that nothing in particular and knowable is
going on. But we have trouble grappling with that, so we round it off to something more
specific and definite and meaningful, an oversimplification that is more poetic than biologic.
I have no objection to using “release” as a description of an experience, but I think it is
quite misleading to pretend that it describes a particular biological event with clinical
meaning and value — which is exactly how most therapists imagine it, which is the only
thing that really needs explaining. (And that’s not difficult: it boils down to a thick stew of
good intentions, ego, and the human habit of imposing simplistic explanations on chaotic
systems.)

Does stimulating fascia reduce post-exercise muscle soreness?

Perhaps … but the clinical relevance of this data is tenuous at best — so low that I would
never normally be interested in this paper. In fact, I would never have chosen to read it
myself, because I don’t think it’s good enough science. I spent some time on it only as an
gesture of good faith to a critic, who supplied the paper as an example of basic fascia
science that matters. It was probably not a good choice for that purpose.

“In vitro modeling of repetitive motion injury and myofascial release”


Meltzer et al. Journal of Bodywork & Movement Therapies.Volume 14, Number 2,
162–71. Apr 2010.

This is a test tube study showing that naked cells handled stress better (fewer signs of
harm) if they were treated with “simulated myofascial release” (MFR). A meaningful,
accurate simulation of manual therapy on naked cells is an amusing notion, and it’s clear
that what happened to those cells differs dramatically from what would happen in a real
living body.

Even if true and reproducible, this data would mainly support the rationale for MFR
specifically for post-exercise soreness — something of a dead end for clinical relevance,
because exercise-induced soreness has little to do with the main claims of fascial release
therapy, which primarily concerns correcting postural asymmetries, eliminating alleged
restrictions, and treating chronic pain.

Post-exercise soreness is comparatively trivial, and patients usually don’t seek therapy for
it.28 There’s a lot of research showing that exercise-induced soreness is basically
invincible anyway.29 A meaningful, accurate simulation of manual therapy on naked cells
is an amusing notion.For this property of fascia to be clinically relevant, it would have to
imply that MFR might be able to treat chronic pain from other causes … not the transient
annoyance of soreness after a game of soccer.

This isn’t a rejection of all possible clinical relevance of the data. My point is that there are
so many problems that its relevance is watered down to quite a thin sauce — way too thin.

I do concede that the paper shows some evidence that fibroblasts have interesting and
perhaps positive responses to mechanical forces. That is inherently interesting biology,
and perhaps well worth investigating further — but it’s a long reach to postulate any clinical
relevance to what most therapists do, most of the time, with patient’s fascia.

“Reach” is what the authors do, however. I suspect they are deeply interested in validating
the notion that “fascia is important,” because they seem to be seeking evidence to support
their pre-conceptions — typical of The National Center for Complementary and Alternative
Medicine-funded research, and a hallmark of low quality science. It’s quite likely that if
neutral researchers — with no interest in fascial therapy — did this experiment they would
not get or report the same results.
Does it matter that fascia contains muscle cells?

The next example of fascia science was suggested to me by Gil Hedley. Since he clearly
believed me to be ignorant of fascia science and in dire need of educating, I asked him to
recommend some reading to me — a favourite paper showing something interesting and
clinically relevant about fascia. As expected, he recommended a paper I was already
familiar with, because it is something of a classic of fascia science: Robert Schleip’s 2006
dissertation on the contractile properties of fascia. Much more interesting stuff than the
previous two examples. I will get into much more detail about this paper than the first two.

“Fascia is able to contract in a smooth muscle-like manner and thereby influence


musculoskeletal mechanics”
Schleip et al. Proceedings of the 5th World Congress of Biomechanics,
Munich. Volume , Number , 51–54. 2006.

Schleip and colleagues convincingly showed that fascia contains muscle cells and that
they can contract — slowly and weakly. That is undeniably interesting biology! But the
point of this analysis is to ask: Does it even matter whether its right or wrong? Is it clinically
relevant? Does it improve how we do therapy? Can we use the knowledge to affect the
body with hands? That is the question.

It is also a question that Dr. Schleip and his colleagues have addressed themelves on their
website, FasciaResearch.de. What follows is my own analysis, which is generally
consistent with theirs. However, interested readers should definitely have a look
at their article: it is readable and chock full of useful perspective, answering questions like
“Does fascia contract in response to emotional stress?” and “Can fascia contract on its
own?”

“Fascia Contractility FAQ,” a webpage on FasciaResearch.de.

Important update: Dr. Schleip has read this article and corresponded with me about it
amiably, and expressed clear agreement with my main point. Although he also had some
thoughtful criticisms, we agree on what matters, and he shares my frustration with clinical
overconfidence in fascia. I invited him to make a statement for my readers about this: look
for it at the end of this part of the discussion.

Fascia strong like bull! Or … mouse?

Before we get to clinical relevance, I’ll quickly explain what Schleip et al. found: a kind of
muscle cell in rat fascia, which they described as “rather unexpected.”30 They also tried
out various methods of stimulating them in vitro (test tube) and found that, by golly, those
muscle cells did what muscle cells do: they contracted! Slow, weak contractions. But they
contracted.

Perspective

By any measure, fascial contractions are dramatically less powerful than muscular
contractions. If anything, this diagram gives far too much credit to the power of fascia,
which would barely register at all if depicted more accurately.
It’s certainly not difficult research to understand.

Some important context that fascia fans will appreciate: for a long time, fascia was and
often still is incorrectly thought of as a fairly lifeless, inert substance, the Saran Wrap of
biology. I still hear various educated people referring to it in this way. However, massage
therapists and chiropractors (in particular) are prone to swinging to the opposite extreme
and talking about fascia as though it is more interesting than a lifetime subscription
to National Geographic. The truth is somewhere in the middle.31 Dr. Schleip’s research
demonstrates this. Fascia is not inert.

But neither is it all that lively — at least not in terms of contractility. We are not talking
about a lot of muscle cells here. If you had blueberries with your cereal in the same
proportion, you’d be disappointed — not enough blueberries! It’s just a few muscle cells
scattered throughout the fascia. There’s so few that they are visible only when you
look very closely and in just the right way.

Nor are we talking about particularly strong contractions. Fascia isn’t going to be ripping
apart any chains with its bare hands. The maximum force generated by a small bundle of
contractile rat fascia was around 35mN.32 In plain English that’s “not very dang much” or
the somewhat more precise “about what it takes to set an AA battery rolling on a nice
smooth surface.” (It took me a long time to work that out. I have a weird job.) That’s not
bad for a bundle of rat fascia, perhaps, but it doesn’t really hold a candle to middle-of-the-
night charlie horses either.

Compared to the power of muscle contraction, fascia power barely even registers.

The “bull versus mouse” comparison is a little unfair though, because it’s not just a matter
of strong versus weak. Although fascial contractions may be weak compared to muscles,
they could nevertheless be powerful in another way — their effects might, for instance,
accumulate over time to produce contractures (permanent “seizing up” of tissues). So it’s
still worth considering how these contractions might be clinically relevant.
Do weak fascial contractions matter?

Schleip et al.’s basic finding seems sound enough, and I see no reason at this time to
dispute the observation that fascia can contract. If there’s anything wrong with their
research methods, I don’t know what it is. But for the property they described to matter to
therapists who are choosing to focus their therapeutic attention on fascia —
for any biological property to be clinically relevant — it must be significant enough to have
an effect on health. (It then must also be something that we can do something about, but
let’s start with it mattering in the first place.)

Schleip et al. characterized the raw power of fascial contraction quite differently than I just
did. I deliberately made it sound trivial, within the bounds of their numbers.33 In their
words, however, in the large sheets of fascia in the low back, the contraction could be
“strong enough to influence low back stability and other aspects of human
biomechanics.”

Stability? Even if you exaggerate their numbers, they would still only account for a small
fraction of the postural muscle power involved in dynamic spinal stabilization, never mind
the generally astounding structural toughness and resilience of the human spine. The idea
that low back stability could be affected in any way by such a small, slow-motion force is a
bit much for me to swallow.3435

And that’s based on an estimate of the theoretical maximumforce generated by the


biggest, thickest blankets of fascia in human anatomy. In most places in the body, fascia is
much less substantial — tough for its weight, but mostly quite thin and wispy, and a lot of it
even microscopic.36 The forces generated must be dwarfed by that of muscle itself — in
rough proportion to the number and size of contractile cells involved.

That fascial contractions might influence “other aspects of human biomechanics” is a bit
vague. A general example of such “aspects” might be that contracting fascia could be
involved in biomechanical asymmetries — tighter on one side than the other. The validity
of such a concern depends on just how sensitive you think human biomechanics are to
forces so subtle that no one really had any idea that fascia contraction was even
happening before this study. As regular readers here will know, I think biomechanics are
over-rated as a factor in all kinds of pain problems, and there’s extensive evidence that
human beings are wonderfully adaptable and cope surprisingly well even with gross
deformities, never mind subtle asymmetries and “imbalances.” I make that case in great
detail in another article.37

The wording of the conclusions of Schleip et al.’s paper is synonymous with saying that
fascial contraction is relevant only if structuralism is a useful mode for doing and thinking
about therapy. Also, their phrasing shows a strong bias in favour of the “importance” of
fascia. And the study was funded by the International Society of Biomechanics, the Rolf
Institute of Structural Integration, and the European Rolfing Association.38

Weak, slow fascial contractions strike me as being scientifically valid and interesting, but
clinically minor. Once again, far from making me interested in fascia as a target for
therapy, fascia science is convincing me of just the opposite.

No clinical relevance at all? Not even a teensy bit?

If it makes anyone feel better about all this, I’m happy to concede that fascial contractility
might be a little bit clinically relevant. Other evidence might even reveal something
important — although that would surprise me. It doesn’t hurt my main point to make these
concessions. To make my point, all I have to establish is that the clinical relevance is
debatable and probably minor at best, rather than the slam dunk it would have to be to
support even half of the “excitement” about fascia you see in the therapy industry today.39

What about fascia and trigger points? Schleip et al. don’t bring trigger points (muscle
knots) into this discussion, but a lot of other people certainly have. The notion is that a
trigger point is being squeezed and sustained by clenching fascia, but this clinical concept
suffers even more than other examples from the relative weakness of fascial contractions.
I explore this specific claim of clinical relevance in detail in my trigger points tutorial.

In his original dissertation, Schleip limited his speculation about clinical implications to the
broad generalization that it can “influence musculoskeletal mechanics,” such as spinal
stability. In a follow-up paper for Medical Hypotheses,40 he and several colleagues
generally suggest that fascial contractility is a factor in muscle stiffness. The high water
mark for potential clinical relevance is spelled out in this passage:

This offers the possibility of a new understanding for many pathologies that involve a
chronically increased myofascial tonus. Examples include conditions such as
torticollis, low back pain associated with paraspinal compartment syndrome, tension
headaches, and others. Similarly a decreased fascial tone could be a contributing
factor in conditions that are often associated with decreased myofascial tension, such
as in back pain due to segmental spinal instability, peripartum pelvic pain, or
fibromyalgia. While usually other factors play a major role as wellin these
pathologies, it is possible that their progress could be influenced additionally by the
regulation of fascial tissue tone …

The emphasized phrase is key — it’s an understatement. For instance, other factors don’t
“usually” play a major role in those conditions, they always do. And the role of those
factors isn’t just “major,” but probably nearly total — relative to the presumably minor (and
still unconfirmed) contribution of a little fascial tension. Some of the items listed are
particularly implausible to me. I’ve already mentioned how hyperbolic it is to suggest that
fascia could have any serious impact on spinal stability.

Another peculiar item here is fibromyalgia, a fascinating condition that might conceivably
be affected in some small way by fascial contraction, but which is overwhelmingly a nasty
disease of the nervous system. Suggesting it as a main example41 of how fascial
contraction might matter makes about as much sense to me as saying that people with
cancer might have some contracted fascia — would it matter if they did?

The most interesting item listed is “compartment syndrome,” which is decidedly not a
common complication or cause of back pain, but certainly is a problem (especially in the
shins).42 Compartment syndrome is excessive pressure in a fascial compartment, like a
sausage swollen in its wrapping. If fascia were to start squeezing a compartment for some
reason, it might be a problem. It is the one item listed where there is a clear, direct and
logical connection between “fascia can contract” and a way that it could contribute
significantly to a health problem. That is clinical relevance. And yet there is still a clear
problem with the scale of the forces here. Compartment syndrome is by definition only a
problem when the pressure is significant, probably dramatically exceeding the maximum
force with which fascia could squeeze the compartment.Visualize a hot water heater that
isn’t venting pressure — the valve is busted, and it’s in danger of blowing. The pressure
inside is immense, and it would make no practical difference if the hot water heater itself
was a little larger or smaller. Again, fascial contraction is probably not nearly strong
enough to matter. Still, at least it’s easy to see how it could matter in principle, and the
numbers might favour fascial contraction as factor.

And then there’s the fact that we know from Dahl et al that “structural and mechanical
properties are unlikely to explain chronic compartment syndrome. To prevent chronic
exertional compartment syndrome, it is necessary to address aspects other than the
muscle fascia.”

So you see how this goes: for one candidate example after another, the clinical relevance
of fascial contraction is dubious or minor.

Is fascial contraction even interesting?

One of the lower moments in biology history was the labelling of non-coding DNA as “junk
DNA” in 1972. The first time anyone with a scrap of imagination heard that, they thought,
“Yeah, right.” As biologists slowly figured out what all that “junk” is for,43 there was a lot of
“Well, yeah, okay, that’s more like it. Of course.” It’s interesting science, but in some ways
those discoveries are still overshadowed by the way we’re all not so very surprised.

Similarly, the presence of muscle cells in fascia is no shocker. I never believed fascia was
entirely inert any more than I believed in the junkiness of any DNA. If you spend much time
studying biology, it quickly becomes apparent that there are no sharp lines or divisions,
and that we consist of an incomprehensibly diverse and interconnected community of
cells. That connective tissue has a small population of muscle cells strikes me as
blindingly unsurprising.Muscle blends exquisitely into tendon, with no clear demarcation at
the cellular level: at the microscopic level, it’s like walking through the overlapping zone of
two heavily integrated adjacent neighbourhoods, and the further you go away from the
muscle, the fewer muscle cells you see, and the more fibroblasts and their fibres. That
connective tissue has a small population of muscle cells strikes me as
blindingly unsurprising. Fascia surrounds and fractally wraps every muscle inside and out,
for crying out loud — how could it not have a few muscle cells and overlapping properties?

I didn’t know that before it was confirmed, but I certainly don’t find it particularly surprising.
I suspect that the slightly contractile properties of fascia are simply at one end of a
continuum of motor function. Our muscular system is overwhelmingly our primary means
of reacting to stimuli — the major output of our nervous systems — and in general terms
the slight contractility of fascia is probably just the fringes of that functionality, a little bit
more of the same. There are probably some subtle differences, but they are subtle and
arcane and ultimately just a slight variation on the biological theme of muscularity. I’m not
saying it’s completely uninteresting, but it’s overshadowed by the much more interesting
muscular system as a whole, about which fascia is simply a mildly intriguing subtopic. And,
in terms of clinical relevance, the muscular system itself is in turn overshadowed by
neurology.

What does Dr. Schleip think?

Recently Dr. Schleip read my article and wrote to express his basic agreement with my
key point about his research: “Your comments on the small size of fascial contractions are
right on, at least when viewing these within the periods of seconds to minutes, as is
usually applicable for bodywork techniques.” He also wanted me to know that he shares
my annoyance with the “over-zealous claims and projections” of therapists doing fascial
work. He is not thrilled with the way his research is being used to justify premature
overconfidence in fascial therapy.

He also offered some thoughtful criticism on some specific points (and I made some
changes, and will probably make more). Nevertheless, he had no major objections, and
was generally pleased with what he read here: “You have my respect for your detailed and
critical analysis of the present work on fascia. Most of the people who criticize you have
not done a portion of your reading work and could certainly learn a lot from the debate you
started.”
I invited him to make a statement for my readers about this. Here is it in full, with some
emphasized highlights:

I share your emotional frustration with the current trend among bodyworkers of
attributing anything wonderful or astonishing to the properties of fascia.In fact,
our Fascia Research Group at Ulm University has been receiving an almost
exponentially increasing number of inquiries from enthusiastic healers (and martial art
teachers) worldwide who wish that we would sanctify their claims that fascial
contraction provides the explanation for their observed miracle powers. While I do
tend to believe that the fascial net plays much larger roles in human functioning than
previously assumed in orthopedic medicine, I am afraid that such over-zealous
claims and projections are undermining the seriousness of the
investigation and academic rigor that characterizes the work of the current leaders in
fascia research, such as P. Huijing, H. Langevin, T. Findley, P. Standley and A.
Vleeming.

As a bodywork clinician myself, I have learned that there is hardly a more


dangerous attitude among therapists than the hero healer/manipulator who is
damn sure about his diagnosis and supposed treatment effects . This of course
applies as much to fascia-oriented therapists as it does to those who base their work
on supposed neuromuscular or other physiological effects, most of which are still
unproven. “There is hardly a more dangerous attitude among therapists than the hero
healer who is damn sure about his diagnosis & supposed treatment effects.”While
scientists can learn a whole lot from the intuitive and experiential wisdom of
complementary therapists, particularly about the non-fragmented and connecting
properties of the fascial net, we bodyworkers can learn at least as much from the
careful, questioning approach of good scientists, who are willing to doubt their own
assumptions and to refrain from premature confidence and over interpretation
of their findings. It is this mutual learning and interdisciplinary enrichment which in
my opinion characterizes the best qualities of the current fascia research field, as
expressed in the international Fascia Congress series and associated activities.

Again, Dr. Schleip and I do not agree about everything — but that is unimportant
compared to our shared values and commitment to cautiously reserving judgement. We
have each placed our bets on this topic, but not closed our minds. I fully support and
endorse his enthusiasm to explore the biology … and he supports and endorses the value
of my critical analysis.

Thicker, stiffer thoracolumbar fascia in back pain: what does it mean?

Over the last couple years, by far the most common answer to my fascia science
challenge has been: Langevin, Langevin, Langevin. Specifically Langevin et al.’s 2009 and
2011 papers presenting evidence that the thoracolumbar fascia is thicker and stiffer in
people with chronic low back pain.4445

This is interesting evidence that comes as close to being a good answer to the challenge
as anything I’ve seen yet. But I still don’t think it actually achieves clinical significance.

I’m not going to question the findings at all for now (though of course one always can and
probably should do that46). I’m going to take their results at face value and write only
about what they mean to us as thoughtful therapists and patients, keen on biology but
wishing to avoid false hope.

The thoracolumbar fascia is the shield-shaped sheet of thick fascia that more or less
completely covers the low back.

Exactly what Langevin et al. found

In people with chronic low back pain:

 The thoracolumbar fascia was about 25% thicker in people with back pain, which is
quite a bit, and a surprising finding with potentially major — but unknown — clinical
significance. The authors suggest that it could be related to “genetic factors, abnormal
movement patterns and chronic inflammation.”
 The thoracolumbar fascia had about 20% reduced “shear strain,” measurement of the
deformation of a structure. In other words, it was 20% stiffer than in people without
back pain. Again, that’s quite a bit.

What’s it all mean?

Chronic back pain is a notoriously inexplicable and invisible condition. Things that turn up
on MRI that seem like they might explain the pain are often irrelevant. A clear, consistent,
measurable biological sign of cLBP like thickened fascia would be inherently interesting —
downright cool, even!

But that thickened, stiffened fascia is probably not the cause of back pain. At best, it’s
probably a clue about the nature of back pain — inflammatory, perhaps?47 But it might be
even less meaningful: it could be a trivial, transient consequence of pain and limited
mobility, something that happens because you’re in pain for a long time, and which fades
away as steadily as it came. It couldbe as boring as “use it or lose it” — we stiffen up a bit
when you’re in pain for a long time. mind blown

Indeed that is the most likely explanation. And if that’s all there is to it, it’s really a big
whoopty-doo.

But no one knows. The research didn’t explain a phenomenon, it just identified one.
Maybe.

Clinical relevance

The purpose of this article is to challenge hype about fascia. The point of the fascia
science challenge is that most science does not at this time inform diagnosis or treatment,
and therefore there is no scientific justification at this time for “fascial therapy” to be a
popular phenomenon.

Langevin et al.’s research clearing comes closer to influencing diagnosis or treatment than
anything else I’ve seen, but I think it’s a case of so-close-yet-so-far.
Does knowing that the thoracolumbar fascia is thicker and stiffer inform diagnosis? Not
really. Because no clinician can (a) know whether or not it’s actually the case, or (b) has
any idea whether it’s a cause of back pain or a trivial consequence of it.

Does knowing this inform treatment? Not really. There’s no point in trying to treat it unless
(a) you know it’s actually a significant cause, or a consequence that complicates, and (b)
no one has the slightest idea (and it’s rather unlikely) that anyone can make it thinner or
more flexible with their bare hands.

It’s conceivable that follow-up research could fill in some of these blanks, but, until then,
this research isn’t good for much beyond raising eyebrows. It’s only clinically relevant
insofar as it could lead somewhere clinically relevant. If the findings can reproduced. If
they can be explained. If the explanation does in fact turn out to be clinically relevant.

That’s a lot of ifs.

A contrasting example: frozen shoulder

Frozen shoulder is one of the few common musculoskeletal problems that can be blamed
on misbehaving fascia. It’s technical name (adhesive capsulitis) suggests that it is a
disease of “stickyness” of the joint capsule, but in fact the best available evidence to date
suggest that it is more a disease of shrinkage — connective tissue contracture. Maybe this
contracture has something in common with what Langevin et al. observed in the low back.

In the case of the shoulder, joint capsule contracture is quite clearly an etiologic factor:
it’s freezing shoulders and causing much woe.

In the case of the back, it’s technically conceivable but extremely unlikely that fascial
contracture is the cause of low back pain. But, just for the sake of argument, let’s say it is.
Let’s imagine that people get back pain because their thoracolumbar fascia seizes up for
mysterious biological reasons, much like frozen shoulder. This is not a completely absurd
notion, but I don’t actually believe it for a moment: it would be the biggest discovery in the
history of musculoskeletal medicine. This is just a thought experiment!

No one has the foggiest notion how to “melt” a frozen shoulder. That joint capsule is
exceedingly tough. When it contractures, that’s it: it yields only to intense, traumatic forces.
Frozen shoulder defies manual therapists all the time (despite cocky claims to the
contrary). And so, even if back pain is like frozen shoulder and caused by fascial
contracture, I don’t think there’s a snowball’s chance in hell that it could be treated with
any kind of hands-on manipulation. Both shoulder capsules and the thoracolumbar fascia
are super tough human gristle, and are unlikely to change much or for long — if at all — in
response to any non-traumatic external stimulus.

So even in the most spectacular hypothetical scenario where the thoracolumbar fascia is
actually a major cause of back pain… even then it’s still not going to translate into a
good treatment option. And so Lanvegin et al. cannot and should not be used as
justification for a clinical obsession with fascia.

PART 4

CONCLUSIONS

Results of the Fascia Science Challenge so far…

 Piezeoelectricity may occur in fascia, but its clinical relevance is nil — not enough is
known about it to even speculate about how it could be exploited in manual therapy.

 Gil Hedley’s theory that congealing fascial “fuzz” causes stiffness is simplistic and
wrong. It is not a plausible explanation for the sensation of stiffness, or a mechanism
of action for fascial therapy or stretching.

 Fascial “meridians” relate fascial therapy to the “meridians” of acupuncture, which


don’t exist or — even if they do — can’t actually be exploited for any therapeutic
effect even by acupuncturists.

 Chaudhry et al showed that fascia is too tough to “release.” Indeed, even thin
fascia is so tough that it is basically inconceivable that it could be physically changed
(stretched, loosened) without vice grips. This directly contradicts a major popular
rationale for fascial manipulation, and is only clinically relevant to fascial therapy
insofar as it presents evidence that discourages and undermines existing common
practices and beliefs.
 Meltzer et al concluded that stimulated fibroblasts might be happier fibroblasts —
specifically, they might be more resistant to post-exercise soreness. The results of
this test tube study are questionable, but even if you take the data and interpretation
at face value, it is a long reach from a test tube study to clinical reality. Treating post-
exercise muscle soreness is not even a common goal for manual therapy.

 Schleip et al established that fascia is contractile, but this isn’t biologically


surprising, and it’s clinically trivial. It is definitely not a factor in any of the common
problems most manual therapists work with — maybe none at all — and, even if it
was, it is somewhat unlikely that hands-on therapy could make a difference.

To be continued…

There is more fascia science, and I will extend this article with more analysis in the future. I
honestly hope that there is clinically relevant fascia science — that would be terrific. So far,
however, I see no good reason for therapists to be fascinated by fascia and to make it a
target tissue.

Other alleged fascial properties and clinical relevance issues I intend to address eventually
(definitely not a complete list):

 The claim that connective tissue is a colloidal substance in which the ground
substance can be “melted” by heat or mechanical deformation (thixotropy), and that
this is the basis of a therapeutic “release.” Done February 2013.

 The claim that fascia is a “liquid crystal.” While it certainly has some elements of truth
in it, the relevance to therapy is extremely dubious. This is closely related to the
piezeoelectricity claim already covered by the article, but there is more to say about
the liquid crystal idea specifically. Done February 2013.

 The claim that fascial therapy is justified by the finding that the thoracolumbar fascia
is thicker and stiffer in back pain patients. Done March 2017.
 The claim that fascia contains “memories” in some sense. I will likely dispute both the
property and its relevance.

 The claim that fascia is structurally important and tensegrity is interesting (agree), and
that this is clinically relevant (disagree). Much of my rebuttal on this score already
exists in my article about structuralism. For another sneak preview, see also this
amusingly vague bit of junk science about “tensegrity-based” massage.

 The claim that the phenomenon of “force-transmission” means that much “muscle”
tightness is actually attributable to fascial restriction. Although there is little doubt that
fascia transmits and distributes force in interesting and probably counter-inuititive
ways, I will probably dispute that the phenomenon is clinically relevant, because I
doubt that it is either abnormal or treatable.

 The claim that there are fascial adhesions that matter and can be released/treated
with the right manipulation.

The “Father of Fascia” is so over it

What better way to end this article than with the momentous news that Tom Myers is
“pulling back from that old ‘fascia’ buzzword” … but cells are still neat, therefore therapy!

I’m genuinely pleased to see Myers write this (and he must have known when he wrote it
that it would be enthusiastically quoted by his critics):

I am so over the word ‘fascia’. I have touted it for 40 years — I was even called the
‘Father of Fascia’ the other day in New York (it was meant kindly, but…) — now that
‘fascia’ has become a buzzword and is being used for everything and anything, I am
pulling back from it in top-speed reverse. Fascia is important, of course, and folks
need to understand its implications for biomechanics, but it is not a panacea, the
answer to all questions, and it doesn’t do half the things even some of my friends say
it does.
I don’t think it has important implications for biomechanics, and I don’t think it does a tenth
as much. But this is still progress!

Cells are neat, therefore therapy

After pulling back from that old “fascia” buzzword in top-speed reverse, Myers goes on to
tell us about some science about how cells sense the texture of their surroundings:

Organismic movement and stretching — yoga, pilates, training, manual therapy —


can help cells to their proper tension environment by relieving pressure or strain, and
this results in better functioning all over. Why should yoga help digestive problems, or
some of my bodywork clients report increased regularity of their periods? This points
the way.

No, there is no way-pointing here: it’s nifty cellular biology, but it’s about as relevant to our
macroscopic activities as knowing how oxygen binds to hemoglobin. We’re talking about
molecular scale structures that are the functional equivalent of nerve endings, “feelers”
that tell cells “whether they are on a rigid or a soft surface,” cell proprioception. I’m glad for
the cells, and I’m glad someone maybe identified how they do this. That’s great, truly it is,
go Team Science!
But it’s also about as surprising in principle as a tree in a forest. Such a mechanism more
or less had to be there. Cells are marvellous little critters, so of course they must know all
about what’s going on around them, and doubtless they do it in many clever ways.

Connecting that to yoga and manual therapy is an odd but inevitable spin. Read that
again: he goes from cells have cool molecules that detect tension to bodywork makes
periods more regular. That’s quite a leap — over a thousand other variables and
mechanisms of vitality!

And this is a perfect example of what has always been the problem with the fascia
hype: torturing basic biology until it confesses to being relevant to $1+/minute manual
therapy.That is really what this article is about.

PART 5

APPENDICES

Further Reading

 PS Your Back Is Not Out of Alignment — Debunking the obsession with alignment,
posture, and other biomechanical bogeymen as major causes of pain.

 PS Pain is Weird — Pain science reveals a volatile, misleading sensation that is often
more than just a symptom, and sometimes worse than whatever started it. The role of
the nervous system in chronic pain is the major alternative to focussing on fascia. It
has much clearer clinical relevance.

 PS Does Massage Therapy Work? — A review of the science of massage therapy …


such as it is.
 PS Trigger Points & Myofascial Pain Syndrome — A guide to the unfinished science
of muscle pain, with reviews of every theory and self-treatment and therapy option.
Includes a section on the relationship between fascia and trigger points (e-book
customers only).

 Greg Lehman, a chiropractor and physiotherapisthas a thoughtful new fascia article,


“Fascia Science: Stretching the power of manual therapy.”

 Todd Hargrove, a Rolfer and writer (BetterMovement.org), has a good post on fascia
and foam rolling and fascia under the microscope.

 “If We Cannot Stretch Fascia, What Are We Doing?,” a webpage on Massage-


StLouis.com. Massage therapist Alice Sanvito’s clear summary of Dr. Robert
Schleip’s theory that fascial “release” may be attributable to changes in muscle tone
stimulated by mechanoreceptors in fascia and other soft tissues, and not by plastic
deformation of fascia.

What’s new in this article?

March — New section: In which I finally explore one of the most interesting findings in
fascia science. [Section: Thicker, stiffer thoracolumbar fascia in back pain: what does it
mean?]

February — Science update: Cited an unusually on-point study of fascial thickness and
stiffness in patients with and without compartment syndrome. [Section: No clinical
relevance at all? Not even a teensy bit?]

2016 — New conclusion: [Section: The “Father of Fascia” is so over it.]

2015 — Minor update: Small addendum regarding physical


therapy. [Section: Introduction.]

2014 — Minor update: More introduction editing for readability.


2013 — New section: Well, sort of new. I blogged about this in the summer of 2011, and
I’m just now getting around to transplanting it here. But “here” was always its ultimate
destination. [Section: Real fascia science that supposedly matters.]

2013 — Minor update: Edited introduction for clarity, and added a couple new “to-do”
topics.

2013 — Minor update: Interesting new information about what Ida Rolf believed about the
relationship beween thixotropy and the idea of fascial release (hint:
“nonsense”). [Section: Ida’s idea about thixotropy.]

2013 — Rewritten: A major editing job, particularly to include the much more specific idea
that piezoelectricity accounts for releases. [Section: Electrified by piezoelectricity.]

2013 — New section: No notes. Just a new section. [Section: Ida’s idea about thixotropy.]

2013 — New section: No notes. Just a new section. [Section: “Release” may not even be
real.]

2013 — Minor update: Several minor additions and edits.

2012 — Minor update: Added some acknowledgement that fascia contractility may still
have some slow-motion “power” even if it is quite weak. I’ll probably expand on this
soon. [Section: Fascia strong like bull! Or … mouse?]

2012 — Minor update: Added a very useful link to FasciaResearch.de. [Section: Does it
matter that fascia contains muscle cells?]

2012 — New section: No notes. Just a new section. [Section: The acupuncture
connection: is fascia actually magic?]

2012 — Major update: Article launched as a compilation of about four previous articles on
this topic, with revisions and some new information.
Notes

1. Physical therapists are less likely to be excited about fascia than their colleagues in
alternative medicine, but they are certainly not immune to it, or other dubious
treatment ideas. One of the largest fascia-centric modality empires was founded by a
physical therapist. BACK TO TEXT

2. This article is quite “negative” — in the sense that critical analysis is always negative.
But I have fun taking therapy seriously. Criticism and deconstruction of ideas is
normal and healthy and necessary for therapy professions to grow and change.
See Why So “Negative”? BACK TO TEXT

3. I hadn’t presented her with any musculoskeletal problem. She was pathologizing at
random. It was supposed to be a relaxation massage, in a spa. And yet she was a
Registered Massage Therapist — unusually well-trained in this neck of the woods.
And that’s probably exactly why she felt compelled to strut her stuff and “troubleshoot”
my case and talk about fascia. BACK TO TEXT

4. The poor track record people have guessing about how things really work is a well-
known principle. It is enshrined in a scientific concept: the “null hypothesis,” the
assumption that ideas are probably wrong until proven right. BACK TO TEXT

5. Gray’s Anatomy for Students:

Clinically fascias are extremely important because they often limit the spread of
infection and malignant disease. When infection or malignant diseases cross a
fascial plain, a primary surgical clearance may require a far more extensive
dissection to render the area free of tumor or infection.
A typical example of a fascial layer would be that overlying the psoas muscle.
Infection within an intervertebral body secondary to tuberculosis can pass
laterally into the psoas muscle. Pus fills the psoas muscle but is limited from
further spread by the psoas fascia, which surrounds the muscle and extends
inferiorly into the groin pointing below the inguinal ligament.

BACK TO TEXT

6. Milesobrien.com [Internet]. O'Brien M. “Just a Flesh Wound”; 2014 Jun 22 [cited 14


Nov 27]. BACK TO TEXT

7. Dahl M, Hansen P, Stål P, Edmundsson D, Magnusson SP. Stiffness and thickness of


fascia do not explain chronic exertional compartment syndrome. Clin Orthop Relat
Res. 2011 Dec;469(12):3495–500. PubMed #21948310. PainSci #53566.

Biopsies of the fascial comaprtment of the anterior tibialis muscle were taken from
several patients with compartment syndrome, with compartment syndrome and
diabetes, and some healthy individuals for comparison. Although there was a lot of
variability between individuals, on average there were no important differences, and
in fact stiffness was 70% greater in the healthy patients — exactly the opposite of
what one would expect to see if compartment syndrome was caused by stiff, thick
fascia. The authors concluded that “structural and mechanical properties are unlikely
to explain chronic compartment syndrome. To prevent chronic exertional
compartment syndrome, it is necessary to address aspects other than the muscle
fascia.”

BACK TO TEXT

8. Juhan D. Job’s body: a handbook for bodywork.expanded ed. Barrytown; 1998. If you
can manage the density of the language, Job’s Body is thick with creative insights into
physiology and healing. Perhaps too many of them, and perhaps too creative — but
very stimulating! Juhan tries to explain why bodyworkers often seem so uncannily
effective. This is a job that certainly needed doing. In trying to explain
bodywork, Job’s Body is a philosophical introduction to the science of the human
body — a physiology textbook with a heart. Many chapters are devoted to pure
science — just barely accessible to the hard-reading layperson, and mainly offering
perspective for the health care professional. Still more chapters are devoted to pure
philosophy. Juhan frequently dares to ask (and answer) the hardest questions in the
health sciences: why and so what? I took a workshop with Juhan many years later.
I’m sorry to say that he seemed cocky and jaded. My main impression was that he
was bored and had drunk to much of his own Kool-Aid. BACK TO TEXT

9. The full details of how bone responds to stress are spelled out in Dr. Harold
Frost’s Mechanostat model. For more information, see Tissue Provocation
Therapies. BACK TO TEXT

10. This kind of (wild) speculation is hardly unusual for Oschman: his writings are laced
with much stranger ideas. BACK TO TEXT

11. Dr. Robert Schleip, from his 2003 article, “Fascial plasticity: a new neurobiological
explanation”:

The half-life span of non-traumatized collagen has been shown to be 300–500


days, and the half-life of ground substance 1.7–7 days (Cantu & Grodin 1992).
While it is definitely conceivable that the production of both materials could be
influenced by piezoelectricity, both life cycles appear too slow to account for
immediate tissue changes that are significant enough to be palpated by the
working practitioner.

BACK TO TEXT
12. The quoted passage is from my personal correspondence with Dr. Levin, and is used
with his permission and endorsement. For information about Dr. Levin’s work,
see Biotensegrity: A new way of modeling biologic forms. BACK TO TEXT

13. Schleip R. Fascial plasticity: a new neurobiological explanation. Journal of Bodywork


& Movement Therapies. 2003 Jan;7(1):11–19. PainSci #54759. BACK TO TEXT

14. Reader Jeff Linn, “something of an apostate Rolfer and instructor at one of the major
structural integration schools,” offers a nifty clarification for me on this point. He has
done extensive research in the Rolf Institute and Guild for Structural Integration
archives and has listened to quite a bit of Rolf’s lectures. He has an audio clip of Rolf
saying that the sol/gel idea is a “nonsense teaching.” Transcript:

…under your hands you feel the change. Now this is going to call for some
smart researching sometime. And who’s going to do this I don’t know. I hope
somebody is going to come out of the blue who is going to be peculiarly well-
fitted for this kind of a job. And I haven’t the foggiest idea what it
means. Possibly it means a general change in pH of the tissue locally. Possibly it
means, this is the simplest way to express it, the greater energy that goes in
there and makes the sol, the gel a sol. Possibly this is what it means. This is
what I’ve taught that it means. But this is a nonsense teaching really! What
does it make into ‘sol’? Does it make the wall of the blood vessel sol? This is
absurd!

Mr. Linn: “My impression from listening to somewhere around 100 hours of Rolf’s
lectures is that many of her ideas regarding her theory were preliminary and/or
provisional and that she expected research to be done (which never really was). Her
provisional ideas were simply assumed to be gospel and elevated to dogma and
transmitted accordingly.” The transcript is from Tape A5 1970, Side 1, available to
members only on www.rolfguild.org.

BACK TO TEXT
15. Here’s Dr. Schleip’s full reasoning from his article, “Fascial plasticity: a new
neurobiological explanation”:

In most systems of myofascial manipulation, the duration of an individual ‘stroke’


or technique on a particular spot of tissue is between a few seconds and 1½
minute. Rarely is a practitioner seen — or is it taught — to apply uninterrupted
manual pressure for more than 2 minutes. Yet often the practitioners report
feeling a palpable tissue release within a particular ‘stroke’. Such rapid — i.e.
below 2 minutes — tissue transformation appears to be more difficult to explain
with the thixotropy model. As will be shown later, studies on the subject of ‘time
and force dependency’ of connective tissue plasticity (in terms of creep and
stress relaxation) have shown that either much longer amounts of time or
significantly more force are required for permanent deformation of dense
connective tissues (Currier & Nelson 1992).

BACK TO TEXT

16. Some people will undoubtedly protest this, claiming that they certainly get more
flexible in a sauna. Heat alone, without stretching, will definitely make us feel less
stiff (a change in sensation), but does not actually increase flexibility. I’ve tested this
very carefully myself: see A Stretching Experiment. BACK TO TEXT

17. ScienceBasedMedicine.org [Internet]. Kavoussi B. The Acupuncture and Fasciae


Fallacy; 2011 Jan 13 [cited 14 Sep 24]. BACK TO TEXT

18. ScienceBasedMedicine.org [Internet]. Ramey D. Acupuncture and history: The


“ancient” therapy that’s been around for several decades; 2010 Oct 18 [cited 14 Nov
27]. BACK TO TEXT

19. ScienceBasedMedicine.org [Internet]. McKenzie B. How popular is acupuncture?;


2011 Mar 28 [cited 12 Feb 19].) BACK TO TEXT
20. ScienceBasedMedicine.org [Internet]. Atwood KC. Acupuncture Anesthesia: A
proclamation from Chairman Mao; 2009 May 15 [cited 12 Feb 19]. BACK TO TEXT

21. Berman BM, Langevin HH, Witt CM, Dubner R. Acupuncture for Chronic Low Back
Pain. N Engl J Med. 2010 Jul 29;(363):454–461. PubMed #20818865. PainSci
#54942.

A bizarre and already infamous paper: bizarre because the authors clearly
acknowledge that acupuncture is no better than a placebo, and bizarre because they
conclude that it should be recommended, and most bizarre of all because it is
published in The New England Journal of Medicine. Truly, one of the lowest moments
in the history of that famous journal!

The best criticisms of the NEJM’s editorial choices here can both be found
on Science-Based Medicine, by Drs. Crislip (NEJM and Acupuncture: Even the best
can publish nonsense) and Novella (Acupuncture Pseudoscience in the New England
Journal of Medicine). Dr. Crislip’s post is really quite funny.

BACK TO TEXT

22. Some fascial therapy is gentle, but I have personally encountered intense fascial
therapy in the wild on numerous occasions. I prefer gentler therapy and usually
request it. Despite being a confident and assertive communicator about my
preferences, I have still had many unpleasantly intense fascial therapy
experiences. BACK TO TEXT

23. According to a great many therapists. Not all, but probably most. It’s spelled out
clearly by a prominent fascial therapy pioneer, Luigi “Inventor of Fascial Manipulation”
Stecco. This is someone who has the respect of large numbers of fascial therapists;
his thinking about how fascial therapy works can be considered strongly
representative not only of common thinking about fascial therapy, but also of its
bleeding edge. In a review of the rationale for a workshop, he repeats the basic idea
of tissue stuckness in need of releasing in an impressive array of fancier terms. This
is just a small sample:

Once a limited or painful movement is identified, then a specific point on the


fascia is implicated and, through the appropriate manipulation … movement can
be restored.

BACK TO TEXT

24. “Mechanical deformation” is lasting change in the shape of the tissue, like working
clay. This is in contrast to elastic deformation, where the tissue snaps back to its pre-
manipulation state. To “deform” in this context is not a bad thing (as in deformity), but
a change in form — the goal that therapists generally have, in fact. BACK TO TEXT

25. People are not bullet proof thanks to their fascia, alas — wouldn’t that be handy! And
yet the hyperbole is definitely true in a sense. Fascia is mostly much too thin to
actually be bulletproof. If fascia was just as thick as a Kevlar vest, it might well be just
as bulletproof (or a little more, or a little less). This is just like how spider silk is
“stronger than steel cable” — pound for pound, it is. The catch in the comparison is
that fascia most likely doesn’t have the same “puncture resistance” property that
Kevlar does. There are many kinds of toughness (i.e. bones resist compression
exceedingly well, but are quite vulnerable to torsion). The point was simply that the
research showed quite clearly that the forces required for plastic deformation of fascia
significantly exceed what can be applied to it with hands. Whatever therapists are
feeling when they claim to detect a “release,” it’s not that. BACK TO TEXT

26. Schleip R. Fascial plasticity: a new neurobiological explanation. Journal of Bodywork


& Movement Therapies. 2003 Jan;7(1):11–19. PainSci #54759.
While high-velocity thrust techniques might create forces within that range, it
seems clear that the slower soft tissue manipulation techniques are hardly strong
enough to create the described tissue response [plastic deformation of fascia].
This research leads to a simple thought experiment. In everyday life the body is
often exposed to pressure similar to the application of manual pressure in a
myofascial treatment session. While the body naturally adapts structurally to
long-term furniture use, it is impossible to conceive that adaptations could occur
so rapidly that any uneven load distribution in sitting (e.g. while reading this
article) would permanently alter the shape of your pelvis within a minute.

BACK TO TEXT

27. Sometimes I felt things that seemed “big” that the patient seemed not to notice at all.
Sometimes the patient had a profound sensory experience when I had noticed no
change in the tissue whatsoever. I could not consistently elicit anything clearly. I am
not a dumb guy, but I found it all quite uninterpretable and mostly unpredictable. I got
tired of trying to find meaning in my sensations, and by my last three years in practice
I abandoned all conceit that I could induce specific changes in tissue, and focussed
pretty much exclusively on my patients’ sensations — not mine. BACK TO TEXT

28. If it’s bad enough to think that you need help, you’re also too sore to want anyone to
touch you (let alone push on you). In any case, post-exercise muscle sorness is
usually all wrapped up before patients can get to an appointment. BACK TO TEXT

29. PS Ingraham. Delayed Onset Muscle Soreness (DOMS): The biological mysteries of
“muscle fever,” nature’s little tax on exercise. PainScience.com. 9685 words. BACK
TO TEXT

30. Is it really surprising? I’ll return to that question below. That phrasing doesn’t actually
come from the paper, so you won’t find it there, but from a poster they made to
summarize the paper. BACK TO TEXT
31. Or perhaps somewhat to one side of the middle… BACK TO TEXT

32. A millinewton is 1000th of Newton, which is a measurement of force. A full Newton is


not a lot: enough to accelerate a mass of one kilogram at a rate of one meter per
second squared, without friction. Imagine what it would take to get a small weight
moving a little bit … in space. Now divide by a thousand. BACK TO TEXT

33. I’d like to think I made it sound “accurate,” and the result just happens to be
trivial. BACK TO TEXT

34. A little personal perspective: my lovely wife has titanium in her back, installed to
stabilize a massive fracture of her T12 vertebra in 2010. Such is the toughness of
spines that the titanium fixations installed to protect her actually broke on both sides
— came loose from the brackets screwed into her bones. Similarly, severe scoliosis
can twist titanium fixations like pretzels as it advances. Those are the kinds of forces
involved in the back. Fascial contractions are a miniscule part of such impressive
equations. BACK TO TEXT

35. It is also noteworthy that the contractions they described were slow motion
contractions, taking many seconds to develop at their fastest. BACK TO TEXT

36. Analogy: in the circulatory system, there are only a few gigantic blood vessels, but
countless fine and microscopic ones. The fascial system is similar: a few large,
obvious sheets of fascia, a bunch of more modest and delicate structures, and then a
nearly infinite network of extremely thin and microscopic structures. This is why I say
that we are wrapped in fascia “fractally.” BACK TO TEXT
37. PS Ingraham. Your Back Is Not Out of Alignment: Debunking the obsession with
alignment, posture, and other biomechanical bogeymen as major causes of
pain. PainScience.com. 15634 words. BACK TO TEXT

38. Despite what it seems like, I am not actually accusing Schleip et al. of having any
overt or serious conflicts of interest. In general, COIs are more common and less of a
big deal in science than people think: where there is science there is funding, such is
life, and funding sources affect science in muddy, complicated degrees ranging
from not really at all to truly, madly, deeply. This seems like a borderline case to me,
somewhere on the edge of being a problem. It’s safe to say that these organizations
probably would not fund — or continue to fund — research that came to
the opposite conclusion, i.e. not “strong enough to influence low back stability and
other aspects of human biomechanics.” BACK TO TEXT

39. This is another form of what I call failing “the impress me test.” Usually I bring that up
to make the point that there needs to be strong evidence that treatments works before
they can be considered “proven” — small and temporary treatment effects should not
impress anyone. In this case, though, it’s the clinical relevance of fascial contractility
that is failing to impress. BACK TO TEXT

40. Schleip R, Naylor IL, Ursu D, et al. Passive muscle stiffness may be influenced by
active contractility of intramuscular connective tissue. Med Hypotheses.
2006;66(1):66–71. PubMed #16209907. BACK TO TEXT

41. If you’re not going to list really good, relevant examples here, where are you going to
do it? BACK TO TEXT

42. I have written quite a lot about compartment syndrome with regards to their role in
shin splints (see Save Yourself from Shin Splints!). The lower leg is by far the most
common place in the body for compartment syndromes, both in the shins and the calf.
They are more or less unheard of elsewhere in the body — rare and generally minor
and self-limiting. If fascial compartments were prone to problematic contraction, we’d
constantly be getting “compartment syndromes” all over the body. BACK TO TEXT

43. Basically, only a fraction of the genome is for coding proteins, but that important
minority is regulated and tweaked by the rest of the non-coding DNA. So a (very
rough) analogy is that the coding DNA is like software that makes you who you are,
but the “junk” DNA is the operating system that it needs to run on. Not so
junky. BACK TO TEXT

44. Langevin HM, Stevens-Tuttle D, Fox JR, et al. Ultrasound evidence of altered lumbar
connective tissue structure in human subjects with chronic low back pain. BMC
Musculoskelet Disord. 2009 Dec;10:151. PubMed #19958536. PainSci #53554.
BACK TO TEXT

45. Langevin HM, Fox JR, Koptiuch C, et al. Reduced thoracolumbar fascia shear strain
in human chronic low back pain. BMC Musculoskelet Disord. 2011
Sep;12:203. PubMed #21929806. PainSci #53517. BACK TO TEXT

46. Back pain is an extremely complex phenomenon, and these findings may not be
consistently measurable: no other researchers have even tried yet (2017). It’s par for
the course for findings like this to be elusive. As ever in science and life, what you
“see” in depends on how you “look.” BACK TO TEXT

47. Langevin et al. speculate about the cause: “genetic factors, abnormal movement
patterns and chronic inflammation.” Willard et al. write:

The reduction in shear-strain could be due to tissue adhesions induced by


previous injury or inflammation, and could then be consistent with the proposed
etiology suggested by Dittrich (1963) and Bednar et al. (1995). However, as the
authors of this recent study emphasize themselves, it is also possible that the
observed tissue changes are merely the result of a reduction (immobility) in
everyday lumbar movements related to low back pain. In this case, the fascial
changes would be the effect of low back pain rather than a cause.

BACK TO TEXT

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