Every once and a while a piece of research blows up in the blog-o-sphere and mainstream media. Almost invariably, these research pieces are misrepresented by catchy one-liners that make for great sound bites but have little truth behind them.
A couple of weeks ago, this article from IFLScience! called “Does Non Celiac Gluten Intolerance Actually Exist” was posted. The blog post, which became hugely popular (picked up by the likes of Forbes and Business Insider as well as countless bloggers), was based on this research that came out of Monash University in Australia called “No Effects of Gluten in Patients With Self-Reported Non-Celiac Gluten Sensitivity After Dietary Reduction of Fermentable, Poorly Absorbed, Short-Chain Carbohydrates.”
We have had a few people in our community question the validity of this study, since we often talk about the toxic and harmful effects of grains, especially gluten containing grains, on the body. So naturally, I am going to write this blog about it, to help bring some clarity to the issue.
First, lets quickly go over a couple of technical terms:
Gluten
Gluten is a protein component of wheat and other grains (rye, barley, spelt). Gluten has two components gliadin and glutenin. Gliadin is more abundant than glutenin and is the component linked to the negative impact of gluten on the gut.
FODMAP (Fermentable Oligo-Di-Monosaccharides and Polyols)
FODMAPs are certain types of carbohydrates (sugars) found in a number of different foods. These include:
- Fructose: fruit, honey, high fructose corn syrup
- Lactose: dairy
- Fructans (inulin fiber): wheat, onion, garlic
- Galactans: beans, lentils, legumes, soy
- Polyols: sweeteners containing sorbitol, mannitol, xylitol, maltitol, and stone fruits such as avocado, apricots, cherries, nectarines, peaches, plums
FODMAPs pull water into the intestinal tract, the technical term for this is osmotic. They are often not digested or absorbed well. As a result, bacteria in the intestinal tract ferment them. This is especially problematic when eating large quantities of FODMAP containing foods.
Due to the osmotic properties and fermentation of FODMAPs, symptoms of gas, bloating, cramping and diarrhea may occur in those who are sensitive to the effects of FODMAPs.
A low FODMAP diet is often used by people with irritable bowel syndrome (IBS). It has been shown in multiple research studies to improve the symptoms of people with IBS.
Okay, now lets get back to the article. The research that they did was complicated. The test subjects were a group of people who had irritable bowl syndrome but not celiac disease, who self reported gluten sensitivity prior to the study.
First, everybody was given a two-week diet of reduced FODMAPs.
Then they were split randomly into three groups.
- One group was placed on a high-gluten diet, with sixteen grams of gluten per day.
- One group was given no gluten. They had sixteen grams of whey per day instead.
- One group was placed on a low-gluten diet, with two grams of gluten per day and fourteen grams of whey.
They did this for a week and they tracked their symptoms on a visual scale.
After that, the real fun began.
They took two weeks off from the test diets to go back on the low FODMAP diet until their symptoms went away.
Then, finally, came a three-day ‘challenge’ where the people were again put into one of three groups:
- High Gluten (16g/day)
- High Whey (16g/day)
- No whey or gluten
Their symptoms were reported on a visual scale.
The researchers also took blood and stool samples and this is what they found.
- Everyone felt better on the low FODMAP diet.
- The ‘challenge’ diets made people feel worse, whether they had gluten or whey.
- They did not find any changes in the markers that they measured in the blood and stool samples.
From this, they concluded that gluten does not make a difference in symptoms for people and that it is FODMAPs that make a difference.
“We found no evidence of specific or dose-dependent effects of gluten in patients with NCGS (non-celiac gluten sensitivity) placed on diets low in FODMAPs.”
Okay. That was a lot, I know. This study is complicated.
Now, I will tell you my take on this.
- Of course they felt better on a low FODMAP diet. A low FODMAP diet eliminates wheat, legumes, fructose and dairy. All of which are irritating to the gut for most people. Not to mention, as we already discussed, a low FODMAP diet has been shown in many studies to effectively reduce symptoms in people with IBS.
- They felt worse when given gluten. Yes, they also felt worse when given whey, but that does not negate the fact that they felt worse when given gluten. Many people have problems digesting dairy and are sensitive to whey, especially people who have preexisting digestive and autoimmune conditions, such as IBS. The researchers should not discount the change in symptoms because both test groups felt worse.
- The tests they did on the blood and stool samples do not make sense.
The researchers took blood and stool samples of the subjects and analyzed them for markers of intestinal inflammation and immune activation.
Specifically, what they tested for in the blood was antibodies to whole gliadin (IgA and IgG) and deamidated gliadin (IgA and IgG), also for IgE antibodies to wheat.
To explain what that means briefly, IgA, IgG and IgE are types of immune cells that react to things like infections and allergens. In this case, they were looking for ones that react to gliadin and wheat.
I found this odd since these tests are conducted to diagnose Celiac disease, which they had previously determined the test subjects did no have. So these blood tests do not offer relevant information when they are investigating non-celiac gluten sensitivity.
In the stool samples they checked for β-defensin-2. This 2013 article discusses that the role of β-defensin-2 is still not well known.
They also checked for fecal calprotectin. Calprotectin is a calcium and zinc binding protein found in certain immune cells. It is released from the cells in times of cell stress or damage and can be detected within feces.
Both β-defensin-2 and calprotectin are typically high in people with irritable bowl syndrome, which the subjects are already known to have. So again, I am not sure why they are investigating these when looking for gluten sensitivity.
In all of the studies that I have read looking at the effect of gluten (or gliadin) causing gut dysfunction, the mechanism was an increase in gut permeability (leakiness) caused by an increase in a compound called zonulin.
In this study, they did not do any tests looking for zonulin or other gut permeability testing. So, they did not actually look for indications of the known mechanism of damage caused by wheat in the body.
For these reasons, I am having trouble seeing how they came to the conclusion that gluten had no effect on these people. A better conclusion would be that the few things they checked did not change when the people added gluten to their diets. But the people did still feel worse.
My conclusion
This study does not make sense to me. They did not test for the right things to determine whether or not wheat was ruining the subjects’ guts without causing an autoimmune response. The difference between celiac and non-celiac is the autoimmune response. In both cases, the gut gets destroyed. But in celiac disease, there is an autoimmune response causing major symptoms in the intestines.
This is another classic example of people trying to make a causative argument where one does not exist.
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If you want to find out about what gluten does in the body, here are a bunch of studies that actually look at what gluten does in the body.
I hope you enjoy them! And if you have any questions, please ask away!
The Dietary Intake of Wheat and other Cereal Grains and Their Role in Inflammation (2013)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3705319/
Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac (2006)
http://www.ncbi.nlm.nih.gov/pubmed/16635908
Gluten causes gastrointestinal symptoms in subjects without celiac disease: a double blind randomized placebo-controlled trial
http://www.ncbi.nlm.nih.gov/pubmed/21224837
Early effects of gliadin on enterocyte intracellular signaling involved in intestinal barrier function (2003)
http://www.ncbi.nlm.nih.gov/pubmed/12524403
Zonulin and its regulation of intestinal barrier function: the biological door to inflammation, autoimmunity, and cancer (2011)
http://www.ncbi.nlm.nih.gov/pubmed/21248165
Gliadin induces an increase in intestinal permeability and zonulin release by binding to the chemokine receptor CXCR3 (2008)
http://www.ncbi.nlm.nih.gov/pubmed/18485912
Gliadin stimulation of murine macrophage inflammatory gene expression and intestinal permeability are MyD88-dependent: role of the innate immune response in Celiac disease (2006)
http://www.ncbi.nlm.nih.gov/pubmed/16456012
Interactions among secretory immunoglobulin A, CD71, and transglutaminase-2 affect permeability of intestinal epithelial cells to gliadin peptides (2012)
http://www.ncbi.nlm.nih.gov/pubmed/22750506
Intestinal permeability in coeliac disease: insight into mechanisms and relevance to pathogenesis (2012)
http://www.ncbi.nlm.nih.gov/pubmed/21890812
Morphology of the mucosal lesion in gluten sensitivity
http://www.sciencedirect.com/science/article/pii/0950352895900322
Demonstration of high opioid-like activity in isolated peptides from wheat gluten hydrolysates
http://www.ncbi.nlm.nih.gov/pubmed/6099562
These are articles specifically on FODMAPs and IBS:
Extending our knowledge of fermentable, short-chain carbohydrates for managing gastrointestinal symptoms
http://www.ncbi.nlm.nih.gov/pubmed/23614962
Manipulation of dietary short chain carbohydrates alters the pattern of gas production and genesis of symptoms in irritable bowel syndrome (2010)
http://www.ncbi.nlm.nih.gov/pubmed/20659225
A diet low in FODMAPs reduces symptoms of irritable bowel syndrome (2014)