In many older detective stories, the punch line famously
is, "the butler did it." In the minds of many contemporary
Americans, gluten is the "butler." Increasingly, when
individuals experience symptoms such as fatigue,
headaches and gastrointestinal distress, including gas,
bloating and diarrhea, gluten is called out as the culprit.
The passage of partially digested or undigested gluten
through the intestines and the gut barrier may also contribute
to additional symptoms not limited to those involving the
development of food sensitivities and intolerances. The answer
in this paradigm is to avoid all gluten-containing foods, such
as wheat, oats, rye, barley and spelt. The problem with this
paradigm is that other than for a quite small percentage of the
populace, there is little evidence that gluten per se is the culprit
or that gluten avoidance will solve all or even most gluten-associated
issues. This topic often leads to heated debates.
Readers should be aware that the gluten-as-villain story has
quite serious skeptics.1,2
Who Reacts to Gluten?
Gluten, a protein, is a large, complex molecule that contains
thousands of folded amino acid sequences composed of
globulans, albumins, glutenin and gliadin, with the gliadin
fraction believed to cause most of the symptoms associated
with gluten sensitivity. Gluten's exceptionally rich proline
content contributes to resistance to digestion. When this big
ball of peptides is insufficiently broken down, amino acid bonds
within each molecule remain resulting in a partially-degraded
protein that can lead to an array of symptoms. Some authorities
suggest that if gluten is a sufficiently rich component of the
diet (a rare situation), it will lead to reactions even in those
otherwise tolerant as a result of these difficulties in digestion.
There is a spectrum of gluten-related disorders, including
celiac disease, gluten sensitivity, and wheat allergy, the latter
affecting only on the order of 0.1 percent of individuals in
Westernized countries.3,4 Non-celiac gluten intolerance involves
heightened immunologic reaction to gluten in genetically
susceptible people whereas celiac disease involves a complex
autoimmune response in the small intestine to gluten
ingestion.5,6 The estimated prevalence of celiac disease is
approximately one percent of the populace.7
This is where things start to become very interesting in
ways that suggest that the "gluten did it" scenario may be a
bit misleading. As summarized in a fine article a few years
back in the New York Times, "roughly 30 percent of people with
European ancestry carry predisposing genes, for example. Yet
more than 95 percent of the carriers tolerate gluten just fine. So
while these genes (plus gluten) are necessary to produce the
disease, they're evidently insufficient to cause it."8
This observation becomes more intriguing in light of
recent blood serum studies. In one, an examination of 9,133
frozen blood samples taken from US Air Force recruits between
1948 and 1954 for the antibody that people with celiac disease
produce in reaction to gluten found that only about one in seven
hundred tested positive, or 0.2 percent. This was compared to
rates of celiac disease among 12,768 people who either had
similar years of birth (i.e. were born around 1930) or who were
of a similar age to the original donors at the time of sampling
(i.e. young adults today). The rates of celiac disease were 0.8
percent and 0.9 percent respectively, or a 4 to 4.5-fold increase.
In other words, in populations that genetically were virtually
identical, celiac rates had increased more than 400 percent
in a mere 50 years.9 Another study that analyzed blood serum
from more than 3,500 Americans who had been followed since
1974 found that by 1989 the prevalence of celiac disease in this
cohort had doubled.10
More recent studies have confirmed the rising risk of
developing celiac among otherwise similar groups in the past.
So have cross-national comparative studies. The populations
in adjacent Russian Karelia and Finland are equally exposed
to grain products and share partly the same ancestry, but live
in completely different socioeconomic environments. The two
study populations are culturally, linguistically and genetically
related with predisposing gene variants are similarly prevalent in
both groups. Examination of 5,500 subjects yielded a prevalence
of roughly one in 100 among Finnish children whereas the same
diagnostic methods indicated only one in 500 among their
In line with a number of studies looking at the prevalence of
asthma and other forms of autoimmune disease, the Finnish/
Russian data suggest modern sanitary and dietary practices are
leading to poorer health in unexpected ways. For instance, three
of four Russian Karelian children harbored Helicobacter pylori in
comparison with one in 20 Finnish children. H. pylori can cause
ulcers and stomach cancer, but mounting evidence suggests
that exposure also reduces the incidence of asthma. The author
of the New York Times article mentioned above notes that one
author of the Finnish study suspects that Russian Karelians'
microbial wealth (exposure to a much larger variety of microbes
compared to more Westernized and metropolitan populations)
protects them from autoimmune and allergic diseases by
strengthening the arm of the immune system that guards
against such illnesses. Similarly, Yolanda Sanz, a researcher at
the Institute of Agrochemistry and Food Technology in Valencia,
Spain, makes a compelling case for the importance of intestinal
microbes. "Years ago, Dr. Sanz noted that a group of bacteria
native to the intestine known as bifidobacteria were relatively
depleted in children with celiac disease compared with healthy
controls. Other microbes, including native E. coli strains, were
overly abundant and oddly virulent."
Quite a number of authors have noted a possible role for
longer breast-feeding of infants in helping to confirm bifidobacteria in a more dominant role in the large intestine in
children and later life as well as controlling E. coli growth. Other
changes in Western practices similarly may influence the role of
foodstuffs. For example, a study published in 2011 found that
a specially fermented wheat flour-derived product did not lead
to any sort of toxic reaction after being given to celiac patients
for 60 days. This is in line with research indicating that the
manufacture of wheat and rye breads or pasta with durum flours
by using selected sourdough lactobacilli markedly decreases
the toxicity of gluten. In Western countries, cereal baked goods
typically are manufactured by fast processes. As noted by
researchers, this avoids the traditional long fermentation by
sourdough—a cocktail of acidifying and proteolytic lactic acid
bacteria—and has replaced fermentation with chemical and
baker's yeast leavening agents. Under these conditions, cereal
components are not degraded during manufacture.12
Again, a number of researchers have uncovered evidence
that keeping bifidobacteria and lactobacilli at sufficiently high
levels in the appropriate areas of the intestines strongly
influences tendencies toward autoimmune diseases.
Other Contributors to the Modern Gluten Intolerance
Gluten has been in the human food chain for thousands of
years, yet gluten intolerance has become widespread in recent
decades. Along with some items already mentioned, here is an
extended list of possible culprits:
- Changes in baking techniques; to speed processing and reduce costs, modern breads almost never are fully yeast-raised as in the past, a process that makes gluten more digestible; similarly, the long steaming of wheat and rye breads typical of Central and Eastern Europe makes breads more digestible
- Changes in the gluten content of wheat—since the 1950s the USDA, without public notice, has been involved in wheat breeding to increase gluten content
- Novel processing techniques when using gluten-derived compounds in foodstuffs, such as deamidation involving removing an amino group (NH2); this makes the peptides more soluble and smaller, but also increases their chances of breaching the gut lumen and activating immune responses
- Changes in refrigeration and storage, which, in turn, change our gut bacteria and lead to novel intolerance reactions to foods
- Reduced breast-feeding and altered feeding and weaning practices; changes in infant formulas; suspected changes in mother's milk itself at the populace at large becomes more prone to overweight and obesity plus the foods consumed by mothers change
- C-sections becoming more common, which tends to alter the bacteria babies inherit (or do not inherit) from the mother via the birth canal
- Reduced exposure to various dusts and other challenges from the natural world that help train the developing immune system and reduce autoimmune overreactions
- GMOs and the chemicals linked to these are ubiquitous in the food supply
Although, as indicated above, heightened sensitivity to gluten
extends back several decades, GMOs may be true game-changers
for future generations. According to Jeffrey Smith
and the Institute for Responsible Technology (IRT), a "possible
environmental trigger [for gluten intolerance] may be the
introduction of genetically modified organisms (GMOs) to the
American food supply, which occurred in the mid-1990s," describing
the nine GM crops currently on the market. In soy, corn, cotton
(oil), canola (oil), sugar from sugar beets, zucchini, yellow
squash, Hawaiian papaya, and alfalfa, "Bt-toxin, glyphosate,
and other components of GMOs, are linked to five conditions that
may either initiate or exacerbate gluten-related disorders." It's
the Bt-toxin in genetically modified foods that kills insects by
"puncturing holes in their cells." The toxin is present in ‘every
kernel' of Bt-corn and survives human digestion, with a 2012
study confirming that it punctures holes in human cells as well.
According to an IRT report, GMO-related damage is linked
to five different areas: intestinal permeability, imbalanced gut
bacteria, immune activation and allergic response, impaired
digestion, and damage to the intestinal wall. The IRT release
also indicated that glyphosate, a weed killer sold under the
brand name 'Roundup,' was found to have a negative effect
on intestinal bacteria. GMO crops contain high levels of this
toxin at harvest. "Even with minimal exposure, glyphosate can
significantly reduce the population of beneficial gut bacteria and
promote the overgrowth of harmful strains."13,14
Sometimes the Villains Aren't Bad Guys and How To Promote the Good Guys
A word of caution is in order regarding gut bacteria. Just as
gluten may not be the primary actor in its own drama, so, too,
are some "bad" bacteria not so bad after all. Above, the case of H. pylori was presented as perhaps not quite as black-and-white
as normally argued. Another example is E. coli. Which E. coli?
Recent research has uncovered that small molecules produced
by the microbiota and related to indole extend healthspan in
geriatric worms, flies, and mice.15 According to the authors of
this research, the term "healthspan" describes the length of
time a human or animal, while aging, can stay active and resist
stress. In this research, the focus is on whether the animals
live healthier, but not necessarily longer. The study identified
indole and related molecules as compounds released by E. coli
bacteria. Indoles may be keeping the intestinal barrier intact
and/or limiting systemic inflammatory effects. Moreover, there
are specialty E. coli strains that are well-researched as excellent
probiotics useful in treating a number of gastro-intestinal
disorders and even helping to maintain remission in patients
with ulcerative colitis.16,17 The trick is to encourage the presence
of the right E. coli to limit the growth of the wrong E. coli.
What about daily foods that boost good gut
microbiome, including diversity in the gut? It is
important to be able to promote gut health via
daily food habits rather than relying on prebiotic
supplements alone. Here are some everyday choices
according to a 2016 survey conducted in Europe:18
Good foods for boosting the gut microbiome
Bad habits that hurt the microbial ecosystem
- Fruit and vegetables
- Red wine
- A high-calorie diet
- A high-carbohydrate diet
- Sugar-sweetened beverages
- Frequent snacks
Medications have the biggest influence on gut
microbiome diversity. Antibiotics, proton-pump
inhibitors and metformin (a common diabetes drug)
all are linked to lower microbiome diversity.
Blaming gluten for GI-tract issues, allergies and even weight
gain is akin to the pharmaceutical world's "magic bullet"
approach once encapsulated as "one disease, one drug." In
reality, in the modern Western world a host of changes have
taken place in food growing and processing along with changes
in personal habits and some of these changes have led to an
otherwise and previously relatively innocuous protein, gluten,
becoming a source of health issues. Eliminating gluten from
the diet (along with wheat, oats, rye, barley and spelt) is not
the answer to environmental mistakes, such as the growing
prevalence of poor bread-making practices and the use of
GMOs. A better approach is to learn the nature of the non-health-
promoting practices and then to find alternatives.
- Gaesser GA, Angadi SS. Gluten-free diet: imprudent dietary advice for the general population. J Acad Nutr Diet. 2012 Sep;112(9):1330–3.
- Shewry PR, Hey SJ. Do we need to worry about eating wheat? Nutr Bull. 2016 Mar;41(1):6–13.
- Piezak M. Celiac disease, wheat allergy, and gluten sensitivity: When gluten free is not a fad. JPEN J Parental Enterol Nutr. 2012;36(suppl 1):68S–75S.
- Sapone A, Bai JC, Ciacci C, et al. Spectrum of gluten-related disorders: Consensus on new nomenclature and classification. BMC Med. 2012; 10:13.
- Hadjivassiliou M, Grunewald RA, Davies-Jones GAB. Gluten sensitivity as a neurological illness. J Neurol Neurosurg Psychiatry. 2002;72(5): 560–3.
- Briani C, Samaroo D, Alardini A. Celiac disease: From gluten to autoimmunity. Autoimmunity Rev. 2008;7(8):644–50.
- Catassi C, Fassano A. Celiac disease. Curr Opin Gastroenterol. 2008;24(6):687–91.
- Moises Velasquez-Manoff. Who Has the Guts for Gluten? New York Times. February 23, 2013.
- Rubio-Tapia A, Kyle RA, Kaplan EL, Johnson DR, Page W, Erdtmann F, Brantner TL, Kim WR, Phelps TK,
- Lahr BD, Zinsmeister AR, Melton LJ 3rd, Murray JA. Increased prevalence and mortality in undiagnosed celiac disease. Gastroenterology. 2009 Jul;137(1):88–93.
- Catassi C, Kryszak D, Bhatti B, Sturgeon C, Helzlsouer K, Clipp SL, Gelfond D, Puppa E, Sferruzza A, Fasano A. Natural history of celiac disease autoimmunity in a USA cohort followed since 1974. Ann Med. 2010 Oct;42(7):530–8.
- Kondrashova A, Mustalahti K, Kaukinen K, Viskari H, Volodicheva V, Haapala AM, Ilonen J, Knip M, Mäki M, Hyöty H; Epivir Study Group. Lower economic status and inferior hygienic environment may protect against celiac disease. Ann Med. 2008;40(3):223–31.
- Francavilla R, De Angelis M, Rizzello CG, Cavallo N, Dal Bello F, Gobbetti M. Selected Probiotic Lactobacilli Have the Capacity To Hydrolyze Gluten Peptides during Simulated Gastrointestinal Digestion. Appl Environ Microbiol. 2017 Jun 30;83(14).
- GMOs linked to gluten disorders plaguing 18 million Americans https://www.rt.com/usa/gmo-gluten-sensitivitytrigger-343/
- Are Genetically Modified Foods a Gut-Wrenching Combination? http://responsibletechnology.org/glutenintroduction/
- "Chemicals from gut bacteria maintain vitality in aging animals: Indoles help worms/flies/mice live stronger for longer." ScienceDaily. ScienceDaily, 21 August 2017. www.sciencedaily.com/releases/2017/08/170821151052.htm.
- Fuchssteiner H, Nigl K, Mayer A, Kristensen B, Platzer R, Brunner B, Weiß I, Haas T, Benedikt M, Gröchenig HP, Eisenberger A, Hillebrand P, Reinisch W, Vogelsang H. [Nutrition and IBD-Consensus of the Austrian Working Group of IBD (Inflammatory Bowel Diseases) of the ÖGGH]. Z Gastroenterol. 2014 Apr;52(4):376–86. 17. Enck P, Zimmermann K, Menke G, Klosterhalfen S. Randomized controlled treatment trial of irritable bowel syndrome with a probiotic E.-coli preparation (DSM17252) compared to placebo. Z Gastroenterol. 2009 Feb;47(2):209–14.
- Zhernakova A, Kurilshikov A, Bonder MJ, Tigchelaar EF, Schirmer M, Vatanen T, Mujagic Z, Vila AV, Falony G, Vieira-Silva S, Wang J, Imhann F, Brandsma E, Jankipersadsing SA, Joossens M, Cenit MC, Deelen P, Swertz MA; LifeLines cohort study, Weersma RK, Feskens EJ, Netea MG, Gevers D, Jonkers D, Franke L, Aulchenko YS, Huttenhower C, Raes J, Hofker MH, Xavier RJ, Wijmenga C, Fu J. Population-based metagenomics analysis reveals markers for gut microbiome composition and diversity. - Science. 2016 Apr 29;352(6285):565–9.