Lussekatter
TASTES JUST LIKE CHRISTMAS! SOFT, SWEET AND ABSOLUTELY GLUTENFREE. Lussekatter is another staple of the Swedish Christmas season, and we've made this first version of a recipe that makes great...
For a small part of the population, eating gluten-free is not a choice. IT'S A MUST. For a larger part, eating gluten-free should be an essential health choice. BUT IT ISN'T!
The following is a comprehensive, sourced article from our friends at Holistic Health - the big GlutenGuide - that better explains why any of us really shouldn’t be eating gluten. If you want to read it in Swedish, you can find the original text here.
Gluten is a protein found in the grains rye, wheat and barley. In Latin, gluten means glue and gluten creates a sticky network when kneading dough, which gives airy and stable breads and pastries. From an evolutionary point of view, humans have been eating gluten-free for 99.9% of their existence and our intestines do not have the enzymes required to break down gluten. In addition, in the last 50 years, we have been exposed to gluten to a much greater degree than before.
Gluten consists of the proteins gliadin and glutenin and is found in wheat, rye and barley (1). Spelt, rye wheat, emmer wheat, kamut, bulgur and couscous also contain gluten.
Most gluten is found in wheat where gluten makes up 80-85% of the total protein content (2). When baking bread and pastries, gluten creates a network of sticky threads during kneading that is important for the properties of the dough (1). Gluten is like a glue that holds the bread together and gluten means glue in Latin (3).
The gluten network gives the dough a structure that means that the carbon dioxide formed during fermentation is retained in the dough, which results in an airy bread (4). Today's refined wheat contains more gluten and extra gluten is added to bread, baked goods and other foods to give desired properties. This has led to a twenty-fold increase in the amount of gluten in bread since bread was made from the original grains (5).
In the last 50 years, we have been exposed to gluten to a much greater degree than before. Today's wheat contains more gluten and more gluten is added to bread, baked goods and other foods. Perhaps it is not so surprising that many people do not feel well from eating gluten. In addition to celiac disease (gluten intolerance), wheat allergy and gluten sensitivity have increased in recent years.
People started eating gluten in connection with the introduction of agriculture about 10,000 years ago. This is relatively recent from an evolutionary perspective as humans have existed for about 2.5 million years. In other words, we have eaten gluten-free for 99.9 percent of our existence. The introduction of agriculture meant a major change in lifestyle, not least in terms of diet.
At the same time, our genes have been basically the same since modern humans evolved about 200,000 years ago and have therefore not been adapted to the diet that most people eat today. Some believe that we feel best on a hunter-gatherer diet, also called a Stone Age diet, the diet that humans ate before agriculture and that dominated during our evolution.
In fact, archaeological studies show that humans got more infections, started to get caries and poorer skeletal growth in connection with the introduction of agriculture (6). In addition, welfare diseases such as diabetes and cardiovascular diseases have increased after the introduction of agriculture and especially after the industrialization that contributed to our eating more wheat and gluten today (7). Modern research also shows that a Stone Age diet, which is naturally gluten-free, provides health benefits in welfare diseases such as type 2 diabetes (8).
Celiac disease or gluten intolerance means that you cannot tolerate gluten. In a person with celiac disease, the immune system in the intestines is activated upon exposure to gluten, which leads to an inflammation that damages the intestinal mucosa. Nutritional deficiencies are common in celiac disease because the intestinal lining absorbs the nutrients from the food we eat (9).
Celiac disease is classified as an autoimmune disease as not only gluten is attacked by the immune system, but also transglutaminase, which is a substance of the body's own. Transglutaminase is an enzyme found in the intestine that partially breaks down gluten into gliadin and other proteins. Celiac disease is characterized by an immune response against a specific part of gliadin (alpha-gliadin) and a specific type of transglutaminase (transglutaminase-2).
But some people react to several other parts of wheat and gluten. It can be, for example, other parts of gliadin and other types of transglutaminase. This is a problem because school medical tests for celiac disease only analyze antibodies to alpha-gliadin and transglutaminase-2.
A person who reacts to other fractions of gluten (for example beta-gliadin, gamma-gliadin or omega-gliadin), or any other type of transglutaminase (for example type 3 or type 6), will test negative for celiac disease even though the person may react strongly to gluten (10,11,12,13,14).
Celiac disease affects at least 1–1.5% of the population in the Western world (15) and at least 3% of Swedish youth (16). The prevalence of celiac disease is highest in Sweden and Finland, but is increasing worldwide (17). The unknown number is probably large because some with celiac disease do not have clear symptoms and diagnostics are inadequate (18).
The prevalence of celiac disease is greater in people with other autoimmune diseases (19). The longer a person with celiac disease is exposed to gluten, the greater the risk that the person will develop more autoimmune diseases (20). Therefore, it is important to get tested for celiac disease if you have an autoimmune disease. Children who have a genetic predisposition to celiac disease are at greater risk of developing the disease the greater the amount of gluten they eat during their first five years of life (21).
You can be sensitive to gluten without having celiac disease or a classic allergy to wheat. It is called Non-celiac gluten sensitivity (NCGS). The occurrence of NCGS is not fully understood, but it is known that NCGS is much more common than celiac disease and wheat allergy (22). Symptoms of NCGS are similar to those of celiac disease and can range from fatigue, depression, joint pain, skin problems and IBS to autoimmune disorders. Unlike celiac disease, the intestinal lining is not broken down in NCGS (23), however, it is known that the immune system in the intestine is activated by gluten in NCGS with increased inflammation as a result. Research shows that NCGS patients have elevated IgG antibodies to gluten (24). If celiac disease and wheat allergy have been ruled out, you can therefore test yourself for NCGS via tests that measure IgG antibodies against gluten in the blood, for example via Holistic's Food Intolerance Test.
In both celiac disease and NCGS, an increased permeability of the intestine is seen, which means that, among other things, bacteria and partially digested food can pass from the intestine to the bloodstream, which activates the immune system. Even gliadin from gluten can cross the intestinal mucosa and irritate the immune system (22). There is a relationship between increased intestinal permeability and autoimmunity, and approximately 25% of all NCGS patients have an autoimmune disease (25). There is also a connection between NCGS and IBS.
In a study on IBS patients where celiac disease was ruled out, a gluten-free diet reduced symptoms compared to a gluten-containing diet. The patients who ate gluten-free also had reduced intestinal permeability (26).
Regardless of whether you have celiac disease, wheat allergy or NCGS, it is important to remove gluten from the diet and support the healing of the intestinal mucosa with substances such as vitamin D, zinc, L-glutamine and butyric acid. (27,28,29,30).
Gluten-containing foods such as bread and pasta are generally not healthy as these foods often contain fast carbohydrates with a high glycemic index (GI). Some types of bread even have a higher GI than sugar. Our intestinal flora is negatively affected by gluten (31) and our intestines cannot break down gluten properly and thus assimilate it as nutrition (5). Studies show connections between gluten intake and diseases such as arthritis, allergy, autoimmune diseases, rheumatic disease, dementia, depression, diabetes, obesity, toxic goiter, IBS, IBD, psoriasis, osteoporosis and schizophrenia. Intake of gluten is also associated with lethargy, fatigue and low energy, while a gluten-free diet is associated with increased energy (32,33).
Intake of gluten leads to more or less increased intestinal permeability in all people. This is because the gluten protein gliadin causes the intestinal cells, which build up the intestinal wall, to secrete a substance called zonulin (34,35). Zonulin is a protein that affects the permeability of the small intestinal mucosa by stimulating the opening of so-called Tight Junctions (TJ). The TJ acts as a kind of floodgate to open and close the passage from the small intestine to the blood. When zonulin increases, TJ is negatively affected and this means that larger molecules can pass from the small intestine to the blood, which contributes to a harmful permeability in the intestine, so-called leaky gut. In addition to gliadin, zonulin release is stimulated by some bacteria and bacterial toxins such as lipopolysaccharides (36).
An increased permeability in the intestine leads to the activation of the immune system, which can lead to inflammatory processes, not only in the intestine but in various places in the body. Health problems often show up where we have our weakest genetic link. Increased zonulin levels and increased intestinal permeability are associated with autoimmune diseases, cardiovascular problems, diabetes and other welfare diseases. A study shows that healthy centenarians have significantly lower levels of zonulin and lipopolysaccharides (bacterial toxin) in their blood compared to young patients with cardiovascular disease. Zonulin release in the intestine leads to increased intestinal permeability, which in turn can lead to lipopolysaccharides leaking into the blood and causing low-grade chronic inflammation that in turn sets the stage for welfare diseases (37).
In conclusion, we humans are not evolutionarily adapted for a gluten-rich diet and our intestines cannot break down gluten properly. Gluten also increases the formation of zonulin in the intestine, which leads to increased intestinal permeability (leaky gut) which in turn creates the basis for increased inflammation with everything from psychological problems to welfare diseases and autoimmune diseases as a result.
References
1. Furugren (2018) Vegetabilier - livsmedel och matkunskap s. 228–339 Lund KFS i Lund.
2. Biesiekierski, J.R. What Is Gluten? J. Gastroenterol. Hepatol. 2017, 32, 78–81.
3. Akhondi H, Ross AB. Gluten Associated Medical Problems. 2022 Oct 31. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan.
4. Wieser H. Chemistry of gluten proteins. Food Microbiol. 2007 Apr;24(2):115-9.
5. Bengmark S. (2018) Välj hälsa! - mina samlade råd för ett friskare liv - hela berättelsen om antiinflammatorisk kost, god tarmflora och hur du ändrar din livsstil. Volante.
6. Spencer Larsen C., Biological Changes in Human Populations with Agriculture. Annual Review of Anthropology. 1995, 24:185-213.
7. Cordain L., et al. Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr. 2005 Feb;81(2):341-54.
8. Jönsson T., et al. Beneficial effects of a Paleolithic diet on cardiovascular risk factors in type 2 diabetes: a randomized cross-over pilot study. Cardiovasc Diabetol. 2009 Jul 16;8:35.
9. Tarar ZI., et al. The Progression of Celiac Disease, Diagnostic Modalities, and Treatment Options. J Investig Med High Impact Case Rep. 2021 Jan-Dec;9:23247096211053702.
10. Vader W., et al. The gluten response in children with celiac disease is directed toward multiple gliadin and glutenin peptides. Gastroenterology. 2002 Jun;122(7):1729-37.
11. Van de Wal Y., et al. Glutenin is involved in the gluten-driven mucosal T cell response. Eur J Immunol. 1999 Oct;29(10):3133-9.
12. Hadjivassiliou M., et al. Autoantibodies in gluten ataxia recognize a novel neuronal transglutaminase. Ann Neurol. 2008 Sep;64(3):332-43.
13. Kim SY, Jeitner TM, Steinert PM. Transglutaminases in disease. Neurochem Int. 2002 Jan;40(1):85-103.
14. Aleanzi M., et al. Celiac disease: antibody recognition against native and selectively deamidated gliadin peptides. Clin Chem. 2001 Nov;47(11):2023-8.)
15. Lerner A, O'Bryan T, Matthias T. Navigating the Gluten-Free Boom: The Dark Side of Gluten Free Diet. Front Pediatr. 2019 Oct 15;7:414.
16. Celiaki, hos vuxna - Internetmedicin
17. Lerner A, Jeremias P, Matthias T. The world incidence of celiac disease is increasing: a review. Int J Recent Sci Res. (2015) 6:5491–6.
18. Tarar ZI., et al. The Progression of Celiac Disease, Diagnostic Modalities, and Treatment Options. J Investig Med High Impact Case Rep. 2021 Jan-Dec;9:23247096211053702.
19. Fasano A, Berti I, Gerarduzzi T, et al. Prevalence of celiac disease in at-risk and not-at-risk groups in the United States: a large multicenter study. Arch Intern Med. 2003;163(3):286–292.
20. Ventura A, Magazzù G, Greco L. Duration of exposure to gluten and risk for autoimmune disorders in patients with celiac disease. SIGEP Study Group for Autoimmune Disorders in Celiac Disease. Gastroenterology. 1999 Aug;117(2):297-303.
21. Agardh, D et al. Association of Gluten Intake During the First 5 Years of Life With Incidence of Celiac Disease Autoimmunity and Celiac Disease Among Children at Increased Risk. JAMA. 2019;322(6):514-523.
22. Cárdenas-Torres FI., et al. Non-Celiac Gluten Sensitivity: An Update. Medicina (Kaunas). 2021 May 24;57(6):526.
23. Umberto Volta U, Bardella MT, Calabrò A, Troncone R, Corazza GR. and The Study Group for Non-Celiac Gluten Sensitivity. An Italian prospective multicenter survey on patients suspected of having non-celiac gluten sensitivity. BMC Med. (2014) 12:85.
24. Uhde M., et al. Subclass Profile of IgG Antibody Response to Gluten Differentiates Nonceliac Gluten Sensitivity From Celiac Disease. Gastroenterology. 2020 Nov;159(5):1965-1967.e2.
25. Mansueto, P., et al. Autoimmunity Features in Patients With Non-Celiac Wheat Sensitivity. Am. J. Gastroenterol. 2021, 116, 1015–1023.
26. Khoshbin K, Camilleri M. Effects of dietary components on intestinal permeability in health and disease. Am J Physiol Gastrointest Liver Physiol. 2020 Nov 1;319(5):G589-G608.
27. Al-Toma A., et al. European Society for the Study of Coeliac Disease (ESsCD) guideline for coeliac disease and other gluten-related disorders. United European Gastroenterol J. 2019 Jun;7(5):583-613.
28. Achamrah N., et al. Glutamine and the regulation of intestinal permeability: from bench to bedside. Curr Opin Clin Nutr Metab Care. 2017 Jan;20(1):86-91.
29. Assa A, Vong L, Pinnell LJ, Avitzur N, Johnson-Henry KC, Sherman PM. Vitamin D deficiency promotes epithelial barrier dysfunction and intestinal inflammation. J Infect Dis. 2014 Oct 15;210(8):1296-305.
30. Chen P., et al. Association of vitamin A and zinc status with altered intestinal permeability: analyses of cohort data from northeastern Brazil. J Health Popul Nutr 21: 309–315, 2003.
31. Turnbaugh PJ., et al. The effect of diet on the human gut microbiome: a metagenomic analysis in humanized gnotobiotic mice. Sci Transl Med. 2009 Nov 11;1(6):6ra14.
32. Ruuskanen A., et al. Positive serum antigliadin antibodies without celiac disease in the elderly population: does it matter? Scand J Gastroenterol. 2010 Oct;45(10):1197-202.
33. Sapone A., et al. Divergence of gut permeability and mucosal immune gene expression in two gluten-associated conditions: celiac disease and gluten sensitivity. BMC Med. 2011 Mar 9;9:23.
34. 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): 1607–15.
35. Drago S, El Asmar R, Di Pierro M, 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): 408–19.
36. Fasano A. All disease begins in the (leaky) gut: role of zonulin-mediated gut permeability in the pathogenesis of some chronic inflammatory diseases. F1000Res. 2020 Jan 31;9:F1000 Faculty Rev-69.
37. Carrera-Bastos P., et al. Serum Zonulin and Endotoxin Levels in Exceptional Longevity versus Precocious Myocardial Infarction. Aging Dis. 2018 Apr 1;9(2):317-321.
TASTES JUST LIKE CHRISTMAS! SOFT, SWEET AND ABSOLUTELY GLUTENFREE. Lussekatter is another staple of the Swedish Christmas season, and we've made this first version of a recipe that makes great...
A crispy, spicy Christmas! Pepparkakor, or gingerbread cookies / ginger biscuits / gingersnaps, are synonymous with the Swedish Christmas season..... from the 1st of advent these crispy, spicy biscuits are...
CRUNCHY, CHEWY FRENCH BAGUETTE - PACKED WITH FLAVOUR. OHAH - AND IT'S GLUTEN-FREE. This recipe is still under development - but it's good enough to make most "glutisar" (what we...