50 Shades Re-written

« | »

50 Shades of Gluten (Intolerance)

by Chris Kresser, Huffington Post

S-CELIAC-DISEASE-154x114Celiac disease (CD) was initially described in the first century A.D. by a Greek physician named Aretaeus of Cappadocia.
But neither Aretaeus nor anyone else knew that CD is caused by an
autoimmune reaction to gluten, a protein in wheat. That didn't become
clear until 1950 — several centuries later — when Dr. Willem Dicke,
a Dutch pediatrician, conclusively proved that gluten was the culprit.
Dicke's discovery saved millions of children and adults from the perils
of untreated celiac disease, including malnutrition, stunted growth,
cancer, severe neurological and psychiatric illness and even death.

Since then, the mainstream view of gluten intolerance has been
relatively black or white: Either you have celiac disease, in which case
even a small amount of gluten will send you running to the bathroom in
three seconds flat, or you don't, and you can chug down beer and bagels
without fear. This "all-or-nothing" view has led to some doctors telling
patients that suspect they're sensitive to gluten but test negative for
CD that they're simply imagining an affliction that doesn't exist.

It turns out those doctors are wrong.

The Many Shades of Gluten Intolerance

In order to explain why, I have to give you a quick lesson in the biochemistry of wheat and wheat digestion.

Wheat contains several different classes of proteins. Gliadins and
glutenins are the two main components of the gluten fraction of the
wheat seed. (They're essential for giving bread the ability to rise
properly during baking.) Within the gliadin class, there are four
different epitopes (i.e. types): alpha-, beta-, gamma- and
omega-gliadin. Wheat also contains agglutinins (proteins that bind to
sugar) and prodynorphins (proteins involved with cellular
communication). Once wheat is consumed, enzymes in the digestive tract
called tissue transglutaminases (tTG) help to break down the wheat
compound. In this process, additional proteins are formed, including
deamidated gliadin and gliadorphins (aka gluteomorphins).

Here's the crucial thing to understand: Celiac disease is
characterized by an immune response to a specific epitope of gliadin
(alpha-gliadin) and a specific type of transglutaminase (tTG-2). But we
now know that people can (and do) react to several other components of
wheat and gluten — including other epitopes of gliadin (beta, gamma, omega), glutenin, WGA and deamidated gliadin — as well as other types of transglutaminase, including type 3 (primarily found in the skin) and type 6 (primarily found in the brain).

This is a huge problem because conventional lab testing for CD and of
gluten intolerance only screens for antibodies to alpha-gliadin and
transglutaminase-2. If you're reacting to any other fractions of the
wheat protein (e.g., beta-gliadin, gamma-gliadin or omega-gliadin), or
any other types of transglutaminase (e.g., type 3 or type 6), you'll
test negative for CD and gluten intolerance no matter how severely
you're reacting to wheat.

Beyond Celiac: Why CD Is Just the Tip of the Iceberg

Official statistics suggest that Celiac disease affects
between 0.7 percent and 1 percent of the U.S. population. But
considering the limited scope of the testing, it's possible that the
actual incidence might be much higher.

In addition, CD is only the tip of the iceberg when it comes to
gluten intolerance. Celiac disease is caused by a distinct autoimmune
response to wheat proteins and transglutaminase enzymes in the gut. But
CD is just one possible expression of gluten intolerance; there are many
other ways that sensitivity to gluten can manifest in the body. These
are collectively referred to as "Non-Celiac Gluten Sensitivity," or

There's no consensus definition of NCGS yet, but the most common
understanding is that it's a reaction to gluten that is not autoimmune
(like CD) or allergic (like wheat allergy). Another definition
I've seen is, "a reaction to gluten that resolves when gluten is
removed from the diet and CD and allergy have been ruled out."

It's difficult to estimate the prevalence of NCGS because there is no
definitive diagnostic test for it. As I mentioned above, the currently
available tests for gluten sensitivity are primitive and only screen for
a small fraction of the components of wheat that people react to.
Another issue is the variety of symptoms caused by CD and NCGS. While
most people assume that gluten intolerance always causes digestive
distress, this is not the case. Almost 50 percent of new patients
diagnosed with CD do not have gastrointestinal symptoms. Moreover, for every one case of CD that is diagnosed, there are 6.4 cases that remain undiagnosed — the majority of which are atypical or silent forms without gastrointestinal symptoms.

Gluten intolerance can affect nearly every tissue in the body,
including the brain, skin, endocrine system, stomach, liver, blood
vessels, smooth muscles and even the nucleus of cells. CD and NCGS are
associated with an astonishing variety of diseases,
from schizophrenia and epilepsy, to Type 1 diabetes and osteoporosis,
to dermatitis and psoriasis, to Hashimoto's hypothyroidism to peripheral
neuropathy. Because the range of symptoms associated with gluten
intolerance is so broad and nonspecific (e.g., can be attributed to any
number of conditions), many patients and doctors don't suspect gluten
may be the cause.

Even with these limitations, some estimates suggest NCGS may occur in as many as 1 in 20 Americans.
And while some mainstream medical professionals continue to insist that
NCGS doesn't exist, several studies have validated it as a distinct
clinical condition — including gold-standard, double-blind, placebo-controlled trials.

The Gluten-Free Challenge: Still the Best Test for Gluten Intolerance

With all of this in mind, the obvious question that arises is,
"What's the best way to test for gluten intolerance?" Because of the
limitations of current laboratory testing I described above, most
experts on gluten sensitivity agree that the only reliable test is a
"gluten challenge." This involves removing gluten from the diet
completely for a period of at least 30 days, and then adding it back in
after that. If symptoms improve during the elimination period, and
return when gluten is reintroduced, a diagnosis of NCGS can be made.

However, for many people a gluten-free diet isn't enough. Some grains
that don't contain gluten, such as corn, oats and rice, contain
proteins that are similar enough in structure to gluten to elicit an
immune response in people with CD or NCGS. In addition, about 50 percent
of patients with CD show signs of intolerance to casein, the protein in milk. This may explain why up to 30 percent of CD patients continue to have symptoms
or clinical signs after adopting a gluten-free diet. For this reason, I
recommend a completely grain- and dairy-free diet during the gluten
challenge period. (A Paleo diet is an excellent choice. Visit my website to learn more.)

Finally, though the gluten challenge is still the gold standard test for gluten intolerance, there is a relatively new lab (Cyrex Laboratories)
offering a comprehensive blood test which screens for all of the wheat
and gluten proteins and transglutaminase enzymes I mentioned above. This
can be a helpful diagnostic tool, but it should never replace a
gluten/Paleo challenge. (Note: It must be ordered by a physician or
health care practitioner.)

Now I'd like to hear from you. Do you suspect you may have gluten
intolerance? If so, has removing gluten resolved your symptoms — or
have you found it necessary to remove grains and dairy as well? If you
haven't tried a gluten challenge, what's holding you back?

Speak Your Mind