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Seafood Mercury Concerns Subside Amid New Research

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Fish and other marine life have been integral to human diets since the Paleolithic era. Some researchers even speculate that these foods “made us human” by enabling the rapid expansion of grey matter in the cerebral cortex. For three million years of evolution during the time of Australopithecus, brain capacity remained constant, but then curiously doubled during a one-million-year period between Homo erectus and Homo sapiens.1 The reasons for this great expansion are not entirely known, but increased dietary omega-3 from fish and shellfish was likely involved.

Fish consumption remains critically important today, but comes with complications unimaginable to our distant ancestors. Industrial pollution has greatly increased environmental mercury, much of which ends up in oceans and lakes, and finally, in small amounts, in the bodies of fish. In higher amounts, mercury is toxic and is especially problematic for developing babies. For years, the FDA was advising pregnant women to limit their fish consumption during pregnancy, but last year, they issued a draft revision encouraging prenatal fish consumption.2 This draft, which will eventually replace their previous recommendations, reflects a growing awareness, seen in the scientific literature, that fish is essential for developing babies and contains nutrients that limit, or even counter, the potentially harmful effects of mercury.

Recently published in the American Journal of Clinical Nutrition, a new study, representing 30 years of research in the Seychelles, is one of the longest and largest population studies regarding seafood and mercury.3 The Seychelles is a nation of islands clustered together in the Indian Ocean, where residents consume 10 times as much seafood as do Europeans and Americans, making it an ideal place to study the long-term impact of mercury exposure via seafood. The researchers concluded that high fish consumption by pregnant mothers, as much as 12 meals per week (the FDA recommends three), does not cause developmental problems in children.

To the contrary, fish is extremely beneficial for development, and contains special nutrients that protect against mercury. Lead author Dr. Sean Strain explained, “This research provided us the opportunity to study the role of polyunsaturated fatty acids [PUFAs] on development and their potential to augment or counteract the toxic properties of mercury.”4 Mercury is thought to damage the brain through oxidation and corresponding inflammation. Fish are rich in omega-3 PUFAs, which prevent inflammation, as opposed to omega-6 PUFAs, which promote inflammation. This was reflected in the study whereby children of mothers who had higher omega-6 blood levels performed worse on tests designed to measure motor skills.

This study builds upon an impressive body of research conducted by Dr. Nicholas Ralston and colleagues at the University of North Dakota. Ralston has demonstrated that selenium also protects against mercury toxicity and that foods with relatively higher amounts of selenium with respect to mercury, pose neither developmental nor neurological risks based on mercury toxicity.5 “This may explain,” Ralston says, “why studies of maternal populations exposed to foods that contain Hg [mercury] in molar excess of Se [selenium], such as shark or pilot whale meats, have found adverse child outcomes, but studies of populations exposed to MeHg [methylmercury] by eating Se-rich ocean fish observe improved child IQs instead of harm.”6

The vast majority of commonly consumed fish and shellfish contain far more selenium relative to mercury and many have significant amounts of omega-3 PUFAs. This means that fish and shellfish, two important components of the Paleo diet, should not be limited nor discontinued based on mercury concerns. Whether for pregnant women, babies, children, or adults, we encourage you to keep seafood on the menu.

Christopher James Clark, B.B.A.

@nutrigrail
Nutritional Grail
www.ChristopherJamesClark.com

Christopher James Clark | The Paleo Diet TeamChristopher James Clark, B.B.A. is an award-winning writer, consultant, and chef with specialized knowledge in nutritional science and healing cuisine. He has a Business Administration degree from the University of Michigan and formerly worked as a revenue management analyst for a Fortune 100 company. For the past decade-plus, he has been designing menus, recipes, and food concepts for restaurants and spas, coaching private clients, teaching cooking workshops worldwide, and managing the kitchen for a renowned Greek yoga resort. Clark is the author of the critically acclaimed, award-winning book, Nutritional Grail.

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REFERENCES

[1] Bradbury, J. (May 2011). Docosahexaenoic Acid (DHA): An Ancient Nutrient for the Modern Human Brain. Nutrients, 3(5). Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3257695/

[2] U.S. Food and Drug Administration. (June 2014). Fish: What Pregnant Women and Parents Should Know. Draft Updated Advice by FDA and EPA. Retrieved from http://www.fda.gov/Food/FoodborneIllnessContaminants/Metals/ucm393070.htm

[3] Strain, JJ, et al. (January 2015). Prenatal exposure to methyl mercury from fish consumption and polyunsaturated fatty acids: associations with child development at 20 mo of age in an observational study in the Republic of Seychelles. American Journal of Clinical Nutrition, 101(1). Retrieved from http://ajcn.nutrition.org/content/early/2015/01/21/ajcn.114.100503

[4] University of Rochester Medical Center. (January 21, 2015). Fatty acids in fish may shield brain from mercury damage. ScienceDaily. Retrieved from www.sciencedaily.com/releases/2015/01/150121144835.htm

[5] Ralston, NV and Raymond, NJ. (November 2010). Dietary selenium’s protective effects against methylmercury toxicity. Toxicology, 278(1). Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/20561558

[6] Ibid, Ralston.

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Best Keto & Paleo Tortillas, Taco Shells & Nachos

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When I first made my keto tortillas I found the dough hard to roll as it kept tearing apart. I don’t give up and I kept adjusting the recipe. Using whole psyllium husks and ground chia seeds and leaving the dough to rest for at least half an hour helped making it very flexible. You can roll the dough out until paper thin without it tearing apart.

This dough is versatile: you can make tortillas, tortilla bowls, taco shells and nachos – all from the same dough! The only difference is the cooking style – some are made in the oven, some on a pan. You can cook them until lightly browned but still flexible (tortillas) or until crispy (nachos).

Here are the meals you can create using the same dough:

Tortillas: I always have some of my keto tortillas at hand. They are great when you’re busy and have little time to cook. Simply add any filling you like and wrap it up. Try smoked salmon & cream cheese, pulled pork with avocado, shredded chicken, tuna & home-made mayo with freshly cut vegetables. With tortillas you can also make burritos, enchiladas or quesadillas. Those of you who have my iPad or iPhone apps: Make sure you try Best Keto Enchiladas using my Essential Keto Crepes! or these keto tortillas.

Tortilla Bowls: Great with Guacamole (easy avocado salad, recipe is in the KetoDiet apps) or any of your favourite salads.

Taco Shells: Great when filled with meat, avocado & freshly chopped vegetables and topped with soured cream or grated cheddar cheese (recipe coming soon!). If you can do dairy, check out these amazingly simple and delicious Cheddar Taco Shells from DJ Foodie!

Nachos: Nachos are perfect snacks for the upcoming Super Bowl! I like them with Guacamole, soured cream dip (soured cream, finely chopped chives or spring onion), cheese & jalapeño dip (cream cheese, grated Manchego cheese, finely chopped jalapeño peppers and hot sauce) or green salsa.

Preparation time:

Hands-on: 20 minutes
Overall: 1 hour

Nutritional values (per tortilla):

Total Carbs7.3grams
Fiber5.7grams
Net Carbs1.5grams

Protein5.1grams
Fat14grams
of which Saturated3.1grams

Energy165kcal

Magnesium74mg (19%)
Potassium194mg (10%)

Macronutrient ratio: Calories from carbs (4%), protein (13.3%), fat (82.7%)

Ingredients (makes 10 tortillas):

Dry ingredients:

1 cup almond flour (100 g / 3.5 oz)
¾ cup flaxmeal (110 g / 4 oz)
¼ cup coconut flour (30 g / 1.1 oz)
2 tbsp whole psyllium husks (8 g / 0.3 oz)
2 tbsp chia seeds, ground (15 g / 0.5 oz)
1 tsp salt (I like pink Himalayan)

Wet ingredients:

1 cup water, lukewarm (240 ml / 8 fl oz)
2 tbsp lard or ghee (you can make your own) (30 g / 1.1 oz)

Optional seasonings:

1 tsp paprika + ¼ tsp chili powder (+ 0.1 g net carbs per serving) OR
½ tsp onion powder + ½ tsp garlic powder (+ 0.2 g net carbs per serving, my favourite!!!) OR
½ tsp curry powder + ¼ tsp ground cumin + ¼ tsp turmeric powder (+ 0.1 g net carbs) OR
½ tsp dried oregano + ½ tsp dried basil + ½ tsp dried thyme + ¼ tsp dried lemon zest or 1 tsp fresh lemon zest (+ 0.1 g net carbs per serving) OR
¼ cup pesto (only use ¾ cup water). You can try my Red Pesto (+ 0.3 g net carbs per serving) or green Paleo Avocado Pesto (+ 0.6 g net carbs per serving)

You can make 10 regular tortillas (8 inch / 20 cm), or 5 large tortillas (12 inch / 30 cm). If you roll them out really thin, you can make up to 12 regular tortillas.

Instructions

Place the flaxmeal, coconut flour, almond flour and psyllium husks into a bowl. Make sure you use whole psyllium husks. Using whole husks makes the tortillas more compact and flexible. This is different from my Ultimate Keto Buns where you need to use psyllium husk powder.

Add any of your favourite seasonings.

Add the ground chia seeds. To grind them, use a blender and pulse until powdered. I prefer using my Bamix immersion blender with the dry mill because it’s easy to clean. Pour in the water and process until well combined using your hands. Let the dough rest in the fridge or on the kitchen counter for up to an hour.

Remove from the fridge and cut the dough into 6 equal pieces. You will use the cut-offs to make the remaining 4 tortillas. Place a piece of the dough between two pieces of baking paper and roll out until the dough is very thin. Alternatively, use a nonstick silicon covered roller and a silicon mat like I did.

Use a 20 cm / 8 inch lid or bowl to cut out the tortilla.

Repeat with the remaining dough and the cut-offs. If you have any dough left, use it for making nachos.

To make Tortillas:

Preheat a heavy-bottom pan greased with ~ 1 tsp ghee or lard. Place the tortilla on top of the hot pan and cook over a medium heat on each side for ~ 2 minutes until lightly browned. Don’t overcook or the tortillas will become too crispy and will lose their flexibility. Grease more when needed and repeat for the rest of the tortillas. When done, leave them to cool down. To avoid the tortillas from getting too dry and hard, place in an airtight container and store for up to a week.

To make Tortilla Bowls:

Preheat the oven to 400 F / 200 C. Place the raw tortilla over a small heat-resistant bowl lined with baking paper and fold the edges round it to create a bowl shape. Lining the bowl is very important to prevent the dough from sticking. Place in the oven and bake for about 10 minutes until the top is lightly browned.

To make Taco Shells:

Cut small pieces of baking paper and place the tortillas on top. Place over a grid in the oven and turn the oven on. Make sure you make them wide enough so you can fit the filling. Cook until it reaches 400 F / 200 C and then cook for further 5-8 minutes or until crispy.

First time I made them, they were quite narrow (see below) so I now use one more grid to fit more filling in without breaking the shell.

To make Nachos:

Roll out the dough and use a knife to cut triangular shaped nachos. Place on a pan greased with ghee or lard and cook on a medium heat for ~ 3 minutes on each side or until golden. Unlike tortillas, nachos should be crispy.

When done, enjoy!

Comments

KellyR (reply)
I love you!!!!! Thanks so much for this recipe OMG!
Anne (reply)
Great post!!!
celine (reply)
I can't thank you enough Martina!!! This is what what my son has been missing (epilepsy) and I couldn't find anything he liked. Now here is your recipe :-) We love your keto buns and I'm sure these will be amazing too :-)

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Wheat: Opening the Barrier to Poor Gut Health

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It was a comment I’ve heard too many times. I was watching tennis with a friend who knew me as a cyclist, not as someone who researches nutrition. The commentators were discussing world No. 1 ranked tennis player Novak Djokovic’s newfound success since going on a gluten-free diet. My friend got noticeably irritated and finally blurted “I’m tired of this gluten-free fad! There’s not a scrap of evidence it makes a difference unless you have celiac disease.” As much as I wanted to, I chose not to respond, but thought to myself, “The bottom drawer of my research cabinet is awfully heavy for not having a scrap of anything in it.

This viewpoint that the health benefits of a gluten-free diet are more fad than science is a pervasive one. But what has led so many, including doctors and scientists, to say the research doesn’t exist?

Certainly the science is extensive for celiac disease where the role of gluten is indisputable. Gliadin, a protein in gluten, binds to a molecule in our bodies called tissue transglutaminase. In celiac patients it’s this new, combined molecule that sets off the inappropriate immune response.1, 2, 3

Without gluten, celiac disease couldn’t exist.

Recently other gluten-related disorders like gluten allergies and gluten ataxia have been identified.4, 5  But admittedly, these conditions affect only about 2% – 10% of the population. Outside of these diseases my friend has a point; research showing gluten having a direct pathogenic role, as it does in celiac disease, isn’t there.

But perhaps this is where the disconnect exists.

While a great deal of published research is showing that wheat and gluten can promote a large range of chronic conditions4, 6, 7, 8, gluten’s role is not so direct. Instead, gluten may breakdown the body’s natural defenses, setting up an inflammatory environment. This environment is highly conducive to a variety of chronic diseases in those of us who are unfortunate enough to have the wrong genetics.9, 10 Gluten sets the stage.

Looking at gluten this way, the bottom drawer of my cabinet suddenly gets a lot heavier. I hope to share a few posts on the ways in which wheat can set the stage for unwanted inflammation and disease. Let’s start with a surprising function that came out of celiac research.

LOOSENING OUR BORDERS

One of the most important roles of our gut, beside processing nutrients and hosting a rich microflora, is to provide a barrier blocking the entry of unwanted particles. Fortunately tight junctions (TJ) between the epithelial cells of our intestine carefully regulate entry of all but a few small molecules and essential nutrients.

Over the last 20 years, Dr. Alessio Fasano at the University of Maryland has researched breakdowns in this barrier, ultimately identifying a molecule produced in our guts called zonulin.14 Zonulin has the unique ability to dissolve the occludins, claudins, zonular occluden, and ZO-1 proteins that make up the structural cytoskeletons of our tight junctions.6, 15, 16, 17, 18

Put simply, zonulin can breakdown our barrier and increase intestinal permeability. An effect that’s often referred to around the web as “leaky gut.” It is rapid, reproducible, and fortunately, reversible.16

To date, two powerful triggers for zonulin have been identified.

The first trigger is exposure to bacteria in the intestine. Interestingly, infection by both pathogenic and “healthy” bacteria can have a triggering effect. However, it’s amplified with the “bad guys” as we can see from the chart below on the left.19

Wheat: Opening the Barrier to Poor Gut Health | The Paleo Diet

Wheat: Opening the Barrier to Poor Gut Health | The Paleo Diet

It is believed that zonulin evolved to protect us against bacterial colonization in the gut.6, 17, 19 When there’s an overload of bacteria in an otherwise healthy digestive tract, zonulin opens up the tight junctions allowing fluid to rush into the gut and flush out microorganisms.

The second powerful activator of the zonulin system is gliadin.

Gliadin fragments bind to the CXCR3 receptor on the epithelial cells of the gut. Then through a MyD88 signaling process, these epithelial cells release zonulin and cause an opening of tight junctions.6, 15, 17, 20, 21

It’s a complex process, but all you need to know is that gliadin can do this from inside the gut. It doesn’t have to get into our systems. More importantly, gluten is inappropriately high jacking a powerful defense mechanism designed to handle bacterial contamination.17

In the above right figure, we can see from Dr. Fasano’s research how gliadin’s ability to stimulate zonulin can be as powerful as bacterial triggers.6

Finally, while gliadin’s effect is much stronger in individuals with celiac disease, gliadin does not discriminate, and it happens in all peoples guts.6, 17

PERMEABLE CONSEQUENCES

With a healthy gut barrier, large molecules are degraded before entering the body and are well tolerated by the immune system.12 Intestinal permeability caused by gluten and bacteria allows these large molecules to get into circulation and act as antigens (activators) for the immune system.15, 17, 22

This becomes a real concern considering gluten is normally consumed with a meal. Its rapid effect on gut permeability happens at the same time that the gut is being hit by a large number of foreign antigens.

 

Wheat: Opening the Barrier to Poor Gut Health | The Paleo Diet

Dr. Fasano and his group proposed that once these antigens gain entry, they can be misinterpreted by the immune system in genetically susceptible individuals. The result is an inappropriate immune response that ultimately leads to chronic illness.6, 12, 15, 23, 24, 25In a healthy gut, these antigens would never gain access to the immune system.

The image above provides a nice representation of how gluten can open tight junctions and lead to diseases such as celiac disease and type 1 diabetes.6

LOSING THE BARRIER TO DISEASE

So, what does this all amount to? Intestinal permeability caused by either bacterial overgrowth or gluten (both of which are heavily influenced by diet) may be a key early step to set the body up for many chronic illness.

But is there any research? Fortunately, this is where I have to start using more drawers in my research cabinet.

Higher zonulin levels and intestinal permeability have been associated with and often precede many autoimmune conditions including type 1 diabetes,16, 30, 31, 32, 33celiac disease,17, 28, 34 multiple sclerosis,35, 36 rheumatoid arthritis,37, 38ankylosing spondylitis,37, 39 and Crohn’s disease.40, 41Eating wheat has been directly linked to diabetes.31, 42, 43, 44

A popular theory of autoimmune disease – called the molecular mimicry theory – proposed that autoimmune disease is initiated by viruses that mimic our bodies.26, 27 Dr. Fasano and his group suggested instead that dietary antigens passing through a leaky gut may be the environmental trigger. To test their theory, they were able to use a zonulin inhibitor to reduce the severity of celiac disease symptoms in humans 28 and the incidence of type 1 diabetes in mice.29

Intestinal permeability isn’t just associated with autoimmune conditions. Permeability may affect asthmatics by increasing their exposure to allergens.45, 46 Elevated zonulin levels have been found in irritable bowel disease 47, 48 and cancer.49, 50Even schizophrenia has recently been linked to gluten consumption and zonulin levels.51, 52

But a final question remains.

In a world where most people reach for a bagel and toast as soon as they get out of bed, intestinal permeability may just be a part of western life that gets an unfair rap by association. In other words, is it too easy to just link permeability with chronic disease? Does it really play a role?

In his 2011 review of zonulin and disease, Dr. Fasano addressed this question pointing out a number of studies where symptoms and incidence rates were reduced when gluten was removed from the diet or when zonulin’s effects were blocked.6

Wheat, a no-no for any good Paleo dieter, was clearly opening doors.

Regards,

Trevor Connor

Trevor Connor | The Paleo DietTrevor Connor is Dr. Cordain’s last mentored graduate student and will complete his M.S. in HES and Nutrition from the Colorado State University this year and later enter the Ph.D. program. Connor was the Principle Investigator in a large case study, approximately 100 subjects, in which he and Dr. Cordain examined autoimmune patients following The Paleo Diet or Paleo-like diets.

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REFERENCES

[1]Dieterich, W., et al., Identification of tissue transglutaminase as the autoantigen of celiac disease. Nature Medicine, 1997. 3(7): p. 797-801.

[2]Molberg, O., et al., Tissue transglutaminase selectively modifies gliadin peptides that are recognized by gut-derived T cells in celiac disease. Nature Medicine, 1998. 4(6): p. 713-717.

[3]Plenge, R.M., Unlocking the pathogenesis of celiac disease. Nat Genet, 2010. 42(4): p. 281-2.

[4]Sapone, A., et al., Spectrum of gluten-related disorders: consensus on new nomenclature and classification. BMC Med, 2012. 10: p. 13.

[5]Hadjivassiliou, M., et al., Gluten ataxia in perspective: epidemiology, genetic susceptibility and clinical characteristics. Brain, 2003. 126(Pt 3): p. 685-91.

[6]Fasano, A., Zonulin and its regulation of intestinal barrier function: the biological door to inflammation, autoimmunity, and cancer. Physiol Rev, 2011. 91(1): p. 151-75.

[7]Biesiekierski, J.R., et al., Gluten causes gastrointestinal symptoms in subjects without celiac disease: a double-blind randomized placebo-controlled trial. Am J Gastroenterol, 2011. 106(3): p. 508-14; quiz 515.

[8]Bernardo, D., et al., Is gliadin really safe for non-coeliac individuals? Production of interleukin 15 in biopsy culture from non-coeliac individuals challenged with gliadin peptides. Gut, 2007. 56(6): p. 889-890.

[9]Palova-Jelinkova, L., et al., Gliadin fragments induce phenotypic and functional maturation of human dendritic cells. J Immunol, 2005. 175(10): p. 7038-45.

[10]De Palma, G., et al., Effects of a gluten-free diet on gut microbiota and immune function in healthy adult human subjects. Br J Nutr, 2009. 102(8): p. 1154-60.

[11]Yu, Q.H. and Q. Yang, Diversity of tight junctions (TJs) between gastrointestinal epithelial cells and their function in maintaining the mucosal barrier. Cell Biol Int, 2009. 33(1): p. 78-82.

[12]Fasano, A., Physiological, Pathological, and Therapeutic Implications of Zonulin-Mediated Intestinal Barrier Modulation Living Life on the Edge of the Wall. American Journal of Pathology, 2008. 173(5): p. 1243-1252.

[13]Shen, L. and J.R. Turner, Role of epithelial cells in initiation and propagation of intestinal inflammation. Eliminating the static: tight junction dynamics exposed. Am J Physiol Gastrointest Liver Physiol, 2006. 290(4): p. G577-82.

[14]Di Pierro, M., et al., Zonula occludens toxin structure-function analysis. Identification of the fragment biologically active on tight junctions and of the zonulin receptor binding domain. J Biol Chem, 2001. 276(22): p. 19160-5.

[15]Sander, G.R., et al., Rapid disruption of intestinal barrier function by gliadin involves altered expression of apical junctional proteins. FEBS Lett, 2005. 579(21): p. 4851-5.

[16]Visser, J., et al., Tight junctions, intestinal permeability, and autoimmunity: celiac disease and type 1 diabetes paradigms. Ann N Y Acad Sci, 2009. 1165: p. 195-205.

[17]Drago, S., et al., Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac intestinal mucosa and intestinal cell lines. Scand J Gastroenterol, 2006. 41(4): p. 408-19.

[18]Fasano, A., et al., Zonula occludens toxin modulates tight junctions through protein kinase C-dependent actin reorganization, in vitro. J Clin Invest, 1995. 96(2): p. 710-20.

[19]El Asmar, R., et al., Host-dependent zonulin secretion causes the impairment of the small intestine barrier function after bacterial exposure. Gastroenterology, 2002. 123(5): p. 1607-15.

[20]Lammers, K.M., et al., Gliadin induces an increase in intestinal permeability and zonulin release by binding to the chemokine receptor CXCR3. Gastroenterology, 2008. 135(1): p. 194-204 e3.

[21]Clemente, M.G., et al., Early effects of gliadin on enterocyte intracellular signalling involved in intestinal barrier function. Gut, 2003. 52(2): p. 218-23.

[22]Fasano, A., Intestinal zonulin: open sesame! Gut, 2001. 49(2): p. 159-62.

[23]Cereijido, M., et al., New diseases derived or associated with the tight junction. Arch Med Res, 2007. 38(5): p. 465-78.

[23]Fasano, A., Surprises from celiac disease. Sci Am, 2009. 301(2): p. 54-61.

[24]Mowat, A.M., Anatomical basis of tolerance and immunity to intestinal antigens. Nat Rev Immunol, 2003. 3(4): p. 331-41.

[25]Oldstone, M.B.A., MOLECULAR MIMICRY AND AUTOIMMUNE-DISEASE. Cell, 1987. 50(6): p. 819-820.

[26]Wucherpfennig, K.W. and J.L. Strominger, MOLECULAR MIMICRY IN T-CELL-MEDIATED AUTOIMMUNITY – VIRAL PEPTIDES ACTIVATE HUMAN T-CELL CLONES SPECIFIC FOR MYELIN BASIC-PROTEIN. Cell, 1995. 80(5): p. 695-705.

[27]Paterson, B.M., et al., The safety, tolerance, pharmacokinetic and pharmacodynamic effects of single doses of AT-1001 in coeliac disease subjects: a proof of concept study. Aliment Pharmacol Ther, 2007. 26(5): p. 757-66.

[28]Watts, T., et al., Role of the intestinal tight junction modulator zonulin in the pathogenesis of type I diabetes in BB diabetic-prone rats. Proc Natl Acad Sci U S A, 2005. 102(8): p. 2916-21.

[29]Bosi, E., et al., Increased intestinal permeability precedes clinical onset of type 1 diabetes. Diabetologia, 2006. 49(12): p. 2824-7.

[30]Mojibian, M., et al., Diabetes-specific HLA-DR-restricted proinflammatory T-cell response to wheat polypeptides in tissue transglutaminase antibody-negative patients with type 1 diabetes. Diabetes, 2009. 58(8): p. 1789-96.

[31]Sapone, A., et al., Zonulin upregulation is associated with increased gut permeability in subjects with type 1 diabetes and their relatives. Diabetes, 2006. 55(5): p. 1443-1449.

[32]De Magistris, L., et al., Altered mannitol absorption in diabetic children. Ital J Gastroenterol, 1996. 28(6): p. 367.

[33]De Palma, G., et al., Intestinal dysbiosis and reduced immunoglobulin-coated bacteria associated with coeliac disease in children. BMC Microbiol, 2010. 10: p. 63.

[34]Westall, F.C., Abnormal hormonal control of gut hydrolytic enzymes causes autoimmune attack on the CNS by production of immune-mimic and adjuvant molecules: A comprehensive explanation for the induction of multiple sclerosis. Med Hypotheses, 2007. 68(2): p. 364-9.

[35]Yacyshyn, B., et al., Multiple sclerosis patients have peripheral blood CD45RO+ B cells and increased intestinal permeability. Dig Dis Sci, 1996. 41(12): p. 2493-8.

[36]Smith, M.D., R.A. Gibson, and P.M. Brooks, Abnormal bowel permeability in ankylosing spondylitis and rheumatoid arthritis. J Rheumatol, 1985. 12(2): p. 299-305.

[37]Edwards, C.J., Commensal gut bacteria and the etiopathogenesis of rheumatoid arthritis. J Rheumatol, 2008. 35(8): p. 1477-14797.

[38]Liu, J., et al., Identification of disease-associated proteins by proteomic approach in ankylosing spondylitis. Biochem Biophys Res Commun, 2007. 357(2): p. 531-6.

[39]D’Inca, R., et al., Increased intestinal permeability and NOD2 variants in familial and sporadic Crohn’s disease. Aliment Pharmacol Ther, 2006. 23(10): p. 1455-61.

[40]Irvine, E.J. and J.K. Marshall, Increased intestinal permeability precedes the onset of Crohn’s disease in a subject with familial risk. Gastroenterology, 2000. 119(6): p. 1740-4.

[41]Maurano, F., et al., Small intestinal enteropathy in non-obese diabetic mice fed a diet containing wheat. Diabetologia, 2005. 48(5): p. 931-7.

[42]Ziegler, A.G., et al., Early infant feeding and risk of developing type 1 diabetes-associated autoantibodies. JAMA, 2003. 290(13): p. 1721-8.

[43]Funda, D.P., et al., Gluten-free but also gluten-enriched (gluten+) diet prevent diabetes in NOD mice; the gluten enigma in type 1 diabetes. Diabetes-Metabolism Research and Reviews, 2008. 24(1): p. 59-63.

[44]Knutson, T.W., et al., Effects of luminal antigen on intestinal albumin and hyaluronan permeability and ion transport in atopic patients. J Allergy Clin Immunol, 1996. 97(6): p. 1225-32.

[45]Hijazi, Z., et al., Intestinal permeability is increased in bronchial asthma. Arch Dis Child, 2004. 89(3): p. 227-9.

[46]Arrieta, M.C., et al., Reducing small intestinal permeability attenuates colitis in the IL10 gene-deficient mouse. Gut, 2009. 58(1): p. 41-8.

[47]Weber, C.R. and J.R. Turner, Inflammatory bowel disease: is it really just another break in the wall? Gut, 2007. 56(1): p. 6-8.

[48]Lai, C.H., et al., Proteomics-based identification of haptoglobin as a novel plasma biomarker in oral squamous cell carcinoma. Clin Chim Acta, 2010. 411(13-14): p. 984-91.

[50]Dowling, P., et al., 2-D difference gel electrophoresis of the lung squamous cell carcinoma versus normal sera demonstrates consistent alterations in the levels of ten specific proteins. Electrophoresis, 2007. 28(23): p. 4302-10.

[51]Wan, C., et al., Abnormal changes of plasma acute phase proteins in schizophrenia and the relation between schizophrenia and haptoglobin (Hp) gene. Amino Acids, 2007. 32(1): p. 101-8.

[52]Kalaydjian, A.E., et al., The gluten connection: the association between schizophrenia and celiac disease. Acta Psychiatr Scand, 2006. 113(2): p. 82-90.

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