Exploring Gluten Related Disorders and the Gut-Brain Axis

I myself, am gluten intolerant, which means that I present with some of the signs and symptoms, but do not test positive for the specific markers of the disease. Finding this information out and taking it seriously changed my life. I was sick for years, overweight, tired and swollen. I spent so much time seeing specialists that all told me I was fine. I wasn’t fine and even now if I get exposed to gluten I have pretty severe swelling in my feet (especially on my right side), along with abdominal distention and fatigue. I’m not complaining, just sharing my story! My health issues have been such a blessing in disguise because of how much I have learned and the empowerment I feel by taking charge of my health and my life. I love Science and research and I had a lot of fun making this infographic because I find joy in creating content that can help other people along their health journey.

 

Some other noteworthy non-gastrointestinal manifestations not mentioned in the graphic:

  • nutrient deficiencies (commonly folate, B6 and/or B12)
  • dental issues, including dental enamel hypoplasia (permanent teeth)
  • delayed puberty
  • osteoporosis/osteopenia
  • arthritis
  • epilepsy
  • hair thinning and/or loss

*When food allergies are unknown and not treated, it can manifest chronic disease.

If you feel like you can strongly relate to these signs and symptoms. I encourage you to read the rest of this post. Feel free to read on simply for the insight and information. Maybe you can help someone else! Enjoy. (and if you just want to know what to do, skip to the bottom paragraphs)


Introduction

Wheat is the most consumed cereal grain worldwide, after maize. “Gluten” refers to specific proteins from wheat, barley and rye. Consumption of these cereal grains causes chronic inflammation and/or intestinal villous atrophy, as seen in a growing population of affected individuals.Gluten-related disorders have become more common today than ever before, especially in Europe and the United States where the industrialization of food production is most highly developed. Gluten-related disorders present a wide variety of symptoms onset at any age, making it difficult to diagnose. Inflammatory response to gluten is present in both immediate and long term exposure, with strict adherence to a gluten free diet being the only successful treatment to date. Growing studies in the past few decades support a gluten-free diet as a successful treatment for various neurological diseases in children and adults. A gluten free diet has also shown health benefits in individuals without diagnostic criteria for a gluten related disorder. The biochemical mechanisms of these benefits are not yet fully understood on a holistic level. This review will discuss the nature of  gluten-related disorders, the role of the gut-brain axis and explain how these disorders may present neurological manifestations.

A Little History

Humans were not always consuming grains. Cultivation of grain is estimated to have started between 10,000 and 11,000 years ago and is believed to have originated in southwestern Asia (Lev-Yadun et al, 2000). This development is a product of evolutionary growth within the dawn of advancing civilization, a time in which humans began settling and growing food, during the Mesolithic-to-Neolithic transition.This period is marked by profound changes in diet and other lifestyle conditions along with the birth of substantial agriculture and animal husbandry (Cordain et al., 2005). Grain agriculture spread from Ancient Anatolia to the Mediterranean and central Europe; reaching Britain about 6,000 years ago (Schiermeier, 2015).  Centuries of drought lead to the cultivation of rye, then to einkorn, emmer and kamut; grain ancestors of wheat. Ancient Anatolia or modern day Turkey, is the area where wild einkorn grass contains the identical genetic fingerprint of today’s domesticated wheat (The Economist, 2005). Wheat is one of the most widely grown crops of the modern day world with over 25,000 different plant varieties (Sapone et al., 2012).

However, the wheat today is criticized by nutrition buffs as being a harmful mutant, far different from ancient grains. With the transition from stone mills to steel mills in the 1870s, the most nutritive portions of wheat were lost, the bran and germ. In the early 1900s, Italian plant breeder Nazareno Strampelli was the first to hybridize wheat species and bred some of the rust resistant, parent plants used in wheat breeding after WWII (Salvi et al, 2012). Strampelli’s model also included interspecific hybridization with wild wheat species of the Triticeae subtribe based on phenotypic selection for several morphological and physiological factors including elasticity, stiffness, and resistance to stress (Scarascia Mugnozza, G.T., 1998).

In the mid-twentieth century Dr. Norman Borlaug (dude in the photo above) led the Mexican Wheat Research and Production Program, which created high-yielding, rust resistant dwarf (as well as, double and triple dwarf) bread-wheat varieties in efforts to impact the world food supply (Borlaug, 1968). This was the foundation of the Green Revolution (initiative to increase agricultural production worldwide). Borlaug’s resistant dwarf bread-wheat seeds were used to start high input farming of this genetically modified grain worldwide, in massive amounts, and at low cost.

WHY IS THE HISTORY IMPORTANT?

The wheat today is far different from the ancient grains of Anatolia. The weight of grain over the course of crop evolution has increased either due to deliberate selection of desired phenotypes or the unintended consequences of the crop-cultivation processes (Golan et al, 2015). Increased applications of nitrogen fertilizer to wheat, results in increased gliadin and increased dough extensibility (Godfrey et al, 2010). We do not truly know the specific ways in which breeding, crop cultivation practices and industrial processing have affected human interaction with gluten containing grains. What further muddles this mystery is the usage of food additives. For example, the usage of potassium bromate to bleach dough and enhance elasticity. Potassium bromate is a cancer causing agent and can be found in food products that are not fully baked. This food additive is illegal is several countries outside of the US. From the birth of industrial food development to today’s heavy dependence on the food business industry, there has been little consideration for affects on nutrition and health. In the past decade, it is now more widely accepted that food processing does indeed have a significant impact on the health of the world population. The nutritional characteristics of food are being altered in food processing and this is a key contributor to the rise of chronic disease (Cordain et al., 2005).

Dietary guidelines in Europe and the United States encourage consumption of whole cereal grains containing “anti-nutrients”, such as wheat gluten and wheat lectin, eliciting dysfunction and disease in humans (Punder & Pruimboom, 2013). There is a large handful of food additives that are legal in the United States and banned from other countries. Increasing reports of food allergies and sensitivities were first observed in the US, Europe, and UK, but are now increasing worldwide. This is because the human genome has not adequately adjusted to the nutritional habits of the Western diet. There is evolutionary discordance of the ancient human genome and the consumption of modern day foods and food-products. Adverse reactions to gluten present as allergic, autoimmune and immune- mediated response; wheat allergy (WA), celiac disease (CD) and non-celiac gluten sensitivity (NCGS).

 

GLUTEN GRAIN PROTEINS: What Are They?

 

OVERVIEW

Gluten is a viscoelastic protein complex found in wheat, barley, rye and related cereal grains. The grain proteins of gluten are what determine the viscoelastic properties of bread dough, that make it chewy and flexible for desired results in food processing (Tatham et al., 2002). The main storage proteins of gluten prolamin (gliadin) and glutelin (glutenin).  Wheat, barley and rye are wild grasses of the tribe Triticeae and have genetic similarities making their storage proteins of similar constitution. In 1981 Lawrence and Shepherd presented genetic evidence confirming that the characteristic amino acid composition for the high molecular weight (HMW) components for wheat, barely, and rye are indeed homologous proteins. The prolamin fractions of wheat, barley and rye are found in the grain’s seed endosperm and contain the gluten protein complex. Gliadin is the primary focus in studies concerning Celiac Disease pathogenesis. There are other grain constituents that contribute to inflammation, but they are not nearly as well studied and understood. These other components include the prolamin gluteomorphin and the lectin wheat germ agglutinin (WGA).

There is still so much to learn about gluten protein fractions and how they effect our system. This is important when considering other grains that are not considered “gluten grains”. It would be smart to be weary of gluten-free snack substitutes (as processed foods are never as good for us as fresh foods). To help understand the breakdown of these grain storage proteins, look at the chart below. 

Screen Shot 2017-03-18 at 4.29.43 PM.png
sourced from Mark J Donohue “The Great Grain Conundrum”
As you can seen, there are many protein fractions that make up the grains we eat, which is why there is so much more research to be done.

PROLAMINS

Prolamines function primarily as storage proteins. “Prolamin” is the term used for gliadin and glutenin because of their high content of proline and glutamine. They differ in their primary, secondary, tertiary and quaternary structure (Waga, 2004). Gluten proteins are divided into two main fractions according to their solubility in aqueous alcohols, insoluble glutenins and soluble gliadins (Wieser, 2007).

(Related grains, barley and rye, have their own prolamin fractions that can trigger inflammation in susceptible individuals. )

Glutenin

Glutenin is a type of glutelin (acts as the glue holding prolamins together). Glutenin molecules have high molecular weight (HMW) subunits stabilized by covalent intermolecular disulfide bonds, forming the elastic backbone of gluten, hence responsible for strong dough elasticity (Shewry, 2002a). Glutamine, glycine and proline represent 70% of these HMW subunits’ total residues (Biagi et al., 2001). Glutenin proteins in their native state form large polymeric structures in which polypeptide chains are connected with intra- and inter-chain disulfide linkages (Rasheed et al., 2015). Glutenin contributes most of the viscoelastic solid properties to gluten behavior (Xu et al., 2001).

Gliadin

Gliadins are monomeric polypeptides in their native state with weak hydrogen bonds (Waga, J., 2004) Gliadin proteins are held together with low energy van der Waals forces and electrostatic interactions and are primarily intra-molecular disulfide bonded. Gliadins are classified according to their different primary structures into the alpha/beta, gamma and omega type (Wieser, 2007). Gliadin is responsible for modifying gluten’s viscoelastic behavior by shifting from viscous to more viscoelastic (Xu et al., 2001, 2002, 2006; Hou et al., 1996; Hussain & Lukow, 1997). There are at least 50 epitopes of gliadin that have immunomodulatory, cytotoxic and gut-permeating activities (Punder, 2013). Gliadin is one of the environmental triggers contributing to intestinal damage upon exposure to gluten (Drago, 2006). Gliadin interacts with the intestinal gatekeeper molecule zonulin in a cascade of events leading to immune response and villous atrophy. The affects gliadin on gut permeability will be further discussed in later section.

Glutenin and Gliadin

Both gliadin and glutenin interact and form polymers of various size and shape through molecular interactions occurring during processing or when hydrated (Johansson et al., 2013). Non-covalent bonds such as hydrogen bonds, ionic bonds and hydrophobic bonds are important for the aggregation of gliadins and glutenins (Wieser, H).  Glutenins and gliadins undergo partial digestion in the upper gastro-intestinal tract, resulting in the formation of peptides that are resistant to digestion by proteases (Salhy et al, 2015).

Gluteomorphin

Gluteomorphin is also known as gliadorphin. This wheat derived peptide had been of particular focus in autism research, but there is evidence to support that it could also play a role in gluten-related disorders by activating opioid receptors (Trivedi, 2014). Dr. Aristo Vojdani asserts that about 50% of persons with celiac disease are not diagnosed because the laboratory testing does not include the antigens or peptides such as omega-gliadin, gamma-gliadin, glutenin, gluteomorphin, prodynorphin or wheat germ agglutinin (Vojdani, 2013). In is noteworthy to mention, that in autism spectrum disorders, positive antibodies to opioid peptides such as gluteomorphin are present in this patient population (Vojdani, 2013).

IIc. LECTINS

Lectins are carbohydrate-binding proteins abundant in raw legumes and grains. Plant lectins can function as a defense against pests and insects. Lectins are resistant to human digestion and thus have been widely labeled as ‘anti-nutrients’ in food. The gut-lining of individuals with irritable bowl syndrome is more sensitive to food lectins.

Wheat Germ Agglutinin (WGA)-WGA is a lectin with the capacity to bind to cells and tissue antigens of the intestinal brush border and when bound, can induce toxic damage, inflammation, and autoimmunity (Vojdani, 2011).

Gut Permeability: Zonulin and the Gut-Brain Axis

 “Circulating antibodies to common foodstuffs, such as gliadin and bovine milk protein, are of frequent occurrence in man” (Mascord et al., 1978).

 

Search result for "gluten gut permeability zonulin"
tight junctions are the tinsy tiny spaces between the cells lining your intestinal wall. When there is an issue with your absorption due to the presence of a gluten protein of anti-nutrient, prolonged exposure can induced the phenomena seen on the left hand side on this digram “faulty tight junctions”. So when those undigested particles enter the blood, this stimulates the body’s immune system to combat the foreign invader. This is why food allergies and digestion of food toxins can cause chronic inflammation leading to autoimmune disease.  aka “Immunoexcitotoxicity”

Zonulin is a “gate-keeper molecule”, a key physiological modulator of intercellular tight junctions (TJ). Gluten increases the production of zonulin , which compromises the competence of the intestinal wall’s function in limiting the passage of macromolecules across the intestinal epithelial barrier (Lammers, 2008). This mechanism is made possible through the binding of gliadin to CXCR3 (a chemokine receptor).

Zonulin is also referred to as Zonula occludens toxin (Zot), the enterotoxin that affects the tight junction competency (PAR2 protein activation, binding and activation of intracellular signaling) and Zot may mimic the effect of a functionally and immunologically related endogenous modulator of epithelial tight junctions (Fasano, 2011).

Overexpression of zonulin could be involved in the blood brain barrier disruption similarly to the role that zonulin plays in increasing intestinal permeability (Lionetti et al., 2015). The relationship between gut microbiota, chronic inflammation and the central nervous system indicate that microbial dysbiosis can alter brain function and contribute to cognitive impairment (Cryan & Dinan, 2012).

The book “Cereal Killers:Celiac Disease and Gluten -Free A to Z”, written by Dr. Ron Hoggan, states that during the development of the cholera vaccine, zonulin was discovered as a protein that disrupts the protective tight junctions in the small intestine and in the blood brain barrier and is excessively produce, by some people, in response to ingestion of wheat and other analogous grains.

What is interesting is that not only are these claims supported by books written by reputable doctors, evidence in scientific research is growing that supports this phenomena.

The Gut-Brain Axis 

The bidirectional communication between the central and enteric nervous system (Carabotti, 2016). This is basically cross talking between intestinal functions and the emotional & cognitive centers of the brain.

Every person has distinct gut microbiota. Your gut microbiota ( gut flora – the microbe population living in your intestine) is so important! This because in interacts with your intestinal cells and the with your central nervous system (brain and spinal cord) through neuroendocrine and metabolic pathways. The collection of beneficial bacteria performs many functions necessary for a healthy body.

 

Screen Shot 2017-03-18 at 6.50.14 PM.png
sourced from Nature.com
This relationship is the foundation supporting the wild popularity of prebiotic and probiotic supplements! (ex. Kombucha & Kevita drinks…my personal favorite)

 

So what does this have to do with gluten?

Diet is a major environmental factor influencing gut microbiota. What you eat dictates the diversity and the functionality of your gut microbiome. For gluten sensitive individuals, the gluten proteins cause microbial dysbiosis (a disruption in the balance between you and your intestinal bacteria). This imbalance leaves you more vulnerable to potentially pathogenic bacteria.

The use of probiotics with strict adherence to a gluten free diet can restore a normal proportion of of beneficial bacteria in the gastrointestinal tract (Marasco, 2016).

 

Gluten Related Disorders & Testing

The term ‘koiliakos’ was coined about 2,000 years ago by the Greek physician Aretaeus to describe “suffering in the bowels”; the word that eventually became the word “celiac” (Rostami et al, 2004).

Current testing for for reactivity to wheat protein fractions is only for specific gluten fractions like alpha-gliadin. This leaves many people consuming substances that are toxic to their biochemistry, which leads to autoimmunity (Vojdani, 2013).

Celiac disease – intestinal symptoms are most prevalent. Classic celiac disease is a chronic inflammatory condition affecting particularly the small intestine and the jejunum; this pathology results in atrophy of intestinal microvilli and subsequent malabsorption of nutrients (Gasbarrini, G.B., Mangiola, F., 2014). Coeliac disease is diagnosed under primary circumstances; testing for the presence of gluten autoantibodies and intestinal biopsy revealing villous atrophy. Anti-tissue transglutaminase (anti-tTG) is a specific marker for CD. Not all CD patients present with these antibodies, but have the microvilli atrophy, which is the most definitive maker of the disease. About 95% of genetically susceptible individuals carry the major histocompatibility complex class II human leukocyte antigen (HLA) DQ2 or DQ8 haplotype (Farrell and Kelly, 2002).

villi damage in small intestine due to celiac disease image by Mayo Fdn
diagram of villous atrophy due to long term gluten exposure. The intestinal microvilli can regenerate back to a healthy brush border when adhering to a strict gluten free diet

Non-celiac gluten sensitivity (NCGS) : characterized by gastrointestinal symptoms that respond to gluten withdrawal without underlying circumstances of celiac disease (Nijeboer, P., Bontkes, H.J., Mulder, C.J.J., Bouma, G., 2013). Non-celiac gluten sensitivity has been related to neuro-psychiatric disorders, such as autism, schizophrenia and depression (Lionetti, 2015).

Wheat Allergy and Intolerance The ingestion of wheat products elicits IgE-mediated allergic reactions.(leading cause is is glutenin)

Silent Celiac Disease: no apparent intestinal symptoms or atypical symptoms. (Dr. Alesio Fasano, ‘What is Gluten’)

Gluten Free Diet Treatment

Lifelong adherence to a strict gluten-free diet (GFD) leads to clinical and histological improvement in celiac disease, gluten sensitivity, and wheat allergy (Nijeboer, P., Bontkes, H.J., Mulder, C.J.J., Bouma, G., 2013). GFD is also is used as treatment for neurodegenerative and neuropsychiatric disorders. GFD shows improvement for conditions of ASD and attention deficit disorder, without the use of medication (Vojdani, 2013).

What does this information tell you?

Test yourself! If you feel that you may be gluten intolerant, you might be. I welcome everyone to try a gluten-free diet (even my hypochondriacs). Two months of strict adherence is advised, although some people feel improvement of symptoms after a couple of weeks.

The diagnostic testing for gluten sensitivity only looks for a  few specific markers out of many possible inflammatory triggers. So, your doctor can order the tests and everything can come back reporting that you are just fine. But you don’t feel fine? It’s very likely they could have missed it. Not because your doctor isn’t great, but because the diagnostic criteria is not efficient in accurately diagnosing gluten sensitivity. The test is most specifically designed to diagnose Celiac Disease which is still not even close to being 100% reliable.

 

SO WHAT IS A STRICT DIET?

This means absolutely NO gluten exposure. It’s harder than you think (I’ve been gluten free since 2014 and I still fall prey to accidental exposure).  Remember that your body operates on a microscopic level. According to Dr. Perlmutter’s book,”Grain Brain” it only takes 1/300th fraction of a piece of bread to illicit an immune response to gluten, that means inflammation!

 

Here is a helpful list to identify gluten on nutrition label ingredients

The Obvious

  • Wheat (Triticum vulgare)
  • Barley (Hordeum vulgare)
  • Rye (secale cereale)

The Not- So-Obvious

  • glutamine peptides (protein powders use this name instead of hydrolyzed wheat protein)
  • Spelt (Triticum spelta)
  • Triticale (wheat-rye hybrid)
  • Bulgur
  • Couscous
  • Farina
  • Seitan
  • modified food starch or just starch if not labeled gluten free can be derived from wheat (ex.vegetable starch)
  • malt
  • dextrin and maltodextrin (watch out for chips & seasonings)
  • whey
  • oats (while oats are not a wheat grain, unless labeled gluten free, there is a high possibility of cross-contamination due to share food machinery. Yes, it’s that serious)
  • Brewer’s yeast
  • hydrolyzed vegetable protein
  •  natural flavor/artificial flavor/seasoning/flavoring/

 

Good Luck!

-Tavia Rahki

Sourced from ortoday.com

References

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Borlaug, N. Wheat Breeding and its Impact on World Food Supply. 3rd. Int. Wheat Genet. Symp. Canberra 1968.

Carabotti, M., et al. (2016). The gut-brain axis: interactions between enteric microbiota, central and enteric nervous systems. Annals of Gastroenterology.Vol 28(2). 203-209. 

Collin, P.,Pirttila, T., Nurmikko, T. Celiac Disease, brain atrophy, and dementia. The Official Journal of the American Academy of Neurology. 1991. Vol.41 no. 3 372

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Cryan, J.F., Dinan, T.G. Mind- altering microorganisms: the impact of the gut microbiota on brain and behavior. Nat Rev Neurosci 2012; 13(10):701-712.

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Elli, L., Dolfini, E., Bardella, M.T. Gliadin cytotoxicity and in vitro cell cultures. Toxicology Letters. 146: 1-8.  2003.

Farrell, R.J., Kelly, C.P., (2002). Celiac sprue. N. Engl. J. Med. 346, 180–188.

Fasano, A. (2011). Zonulin and Its Regulation of Intestinal Barrier Function: The Biological Door to Inflammation, Autoimmunity, and Cancer. Physiological Reviews. Vol. 91 (10, 151-175. 

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Golan, G., Oksensberg, A., Peleg, Z. Genetic Evidence for differential selection of grain and embryo weight during wheat evolution under domestication. Journal of Experimental Botany. 2015.

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Litchtwark, I.T., Newnham, E.D., Robinson, S.R., Shepherd, S.J., Hosking, P., Gibson, P.R., Yelland, G.W. (2014). Cognitive impairment in coeliac disease improves on a gluten free diet and correlates with histological and serological indices of disease severity. Alimentary Pharmacology and Therapeutics. 40(2), 160-170.

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