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Found 8 results

  1. To All, No more doughnuts brought up the topic of Lectins today so I thought I would start a topic on it. Here is the research I am aware of ...20 years ago...it was controversial enough then to get a doctor fired over discussing this theory... https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1115436/ It doesn't mean he was right...but it was concerning enough people felt unsettled/threatened over this topic....I would like to hear the forum members opinions...about whether he was right or not??? it would explain the cross contamination issues of eating things other than gluten that might be causing/mimicking a gluten reaction like someone who can't tolerate corn for example...celiac.com has done articles on this topic but some people might feel like commenting on an article ...that might more at ease discussing it as part of thread on related disorders/or further/other celiac research.... Posterboy,
  2. Celiac.com 11/02/2019 - Now that celiac disease has been allowed official entry into the pantheon of established medical conditions, and gluten intolerance is no longer entirely a fringe medical concept, the time has come to draw attention to the powerful little chemical in wheat known as ‘wheat germ agglutinin’ (WGA) which is largely responsible for many of wheat’s pervasive, and difficult to diagnose, ill effects. Not only does WGA throw a monkey wrench into our assumptions about the primary causes of wheat intolerance, but due to the fact that WGA is found in highest concentrations in “whole wheat,” including its supposedly superior sprouted form, it also pulls the rug out from under one of the health food industry’s favorite poster children. Below the radar of conventional serological testing for antibodies against the various gluten proteins and genetic testing for disease susceptibility, the WGA “lectin problem” remains almost entirely obscured. Lectins, though found in all grains, seeds, legumes, dairy and our beloved nightshades: the tomato and potato, are rarely discussed in connection with health or illness, even when their presence in our diet may greatly reduce both the quality and length of our lives. Although significant progress has been made in exposing the dark side of wheat over the past decade, gluten receives a disproportionate share of the attention. Given that modern bread wheat (Triticum Aestivum) is a hexaploid species containing three distinct sets of chromosomes capable of producing well over 23,000 unique proteins, it is not surprising that we are only now beginning to unravel the complexities of this plant’s many secrets. [1] What is unique about the WGA glycoprotein is that it can do direct damage to the majority of tissues in the human body without requiring a specific set of genetic susceptibilities and/or immune-mediated articulations. This may explain why chronic inflammatory and degenerative conditions are endemic to wheat-consuming populations even when overt allergies or intolerances to wheat gluten appear to be exceedingly rare. The future fate of wheat consumption, and by implication our health, may depend largely on whether or not the toxic qualities of WGA come to light in the general population. Nature engineers, within all species, a set of defenses against predation, though not all are as obvious as the thorns on a rose or the horns on a rhinoceros. Plants do not have the cell-mediated immunity of higher life forms, like ants, nor do they have the antibody driven, secondary immune systems of vertebrates with jaws. They must rely on a much simpler, innate immunity. It is for this reason that seeds of the grass family, e.g. rice, wheat, spelt, rye, have exceptionally high levels of defensive glycoproteins known as lectins. Cooking, sprouting, fermentation and digestion are the traditional ways in which man, for instance, deals with the various anti-nutrients found within this family of plants, but lectins are, by design, particularly resistant to degradation through a wide range of pH and temperatures. WGA lectin is an exceptionally tough adversary as it is formed by the same disulfide bonds that make vulcanized rubber and human hair so strong, flexible and durable. Like man-made pesticides, lectins are extremely small, resistant to break-down by living systems, and tend to accumulate and become incorporated into tissues where they interfere with normal biological processes. Indeed, WGA lectin is so powerful as an insecticide that biotech firms have used recombinant DNA technology to create genetically modified WGA-enhanced plants. We can only hope that these virtually unregulated biotech companies, who are in the business of playing God with the genetic infrastructure of Life, will realize the potential harm to humans that such genetic modifications can cause. Lectins are glycoproteins, and through thousands of years of selectively breeding wheat for increasingly larger quantities of protein, the concentration of WGA lectin has increased proportionately. This, no doubt, has contributed to wheat’s global dominance as one of the world’s favored monocultures, offering additional “built-in” pest resistance. The word lectin comes from the same etymological root as the word select, and literally means “to choose.” Lectins are designed “to choose” specific carbohydrates that project off the surface of cells and upon which they attach. In the case of WGA the two glycoproteins it selects for, in order of greatest affinity, are N-Acetyl Glucosamine and N-Acetylneuraminic acid (sialic acid). WGA is Nature’s ingenious solution for protecting the wheat plant from the entire gamut of its natural enemies. Fungi have cell walls composed of a polymer of N-Acetylglucosamine. The cellular walls of bacteria are made from a layered structure called the peptidoglycan, a biopolymer of N-Acetylglucosamine. N-acetylglucosamine is the basic unit of the biopolymer chitin, which forms the outer coverings of insects and crustaceans (shrimp, crab, etc.). All animals, including worms, fish, birds and humans, use N-Acetyglucosamine as a foundational substance for building the various tissues in their bodies, including the bones. The production of cartilage, tendons, and joints depend on the structural integrity of N-Acetylglucosamine. The mucous known as the glycocalyx, or literally, “sugar coat” is secreted in humans by the epithelial cells which line all the mucous membranes, from nasal cavities to the top to the bottom of the alimentary tube, as well as the protective and slippery lining of our blood vessels. The glycocalyx is composed largely of N-Acetylglucosamine and N-Acetylneuraminic acid (also known as sialic acid), with carbohydrate end of N-Acetylneuraminic acid of this protective glycoprotein forming the terminal sugar that is exposed to the contents of both the gut and the arterial lumen (opening). WGA’s unique binding specificity to these exact two glycoproteins is not accidental. Nature has designed WGA perfectly to attach to, disrupt, and gain entry through these mucosal surfaces. It may strike some readers as highly suspect that wheat—the “staff of life”—which has garnered a reputation for “wholesome goodness” the world over, could contain a powerful health-disrupting anti-nutrient, which is only now coming to public attention. WGA has been overshadowed by the other proteins in wheat. Humans—not Nature—have spent thousands of years cultivating and selecting for larger and larger quantities of these proteins. These pharmacologically active, opiate-like proteins in gluten are known as gluten exorphins (A5, B4, B5, C) and gliadorphins. They may effectively anesthetize us, in the short term, to the long term, adverse effects of WGA. Gluten also contains exceptionally high levels of the excitotoxic l-aspartic and l-glutamic amino acids, which can also be highly addictive, not unlike their synthetic shadow molecules aspartame and monosodium glutamate.[1] In a previous article on the topic, The Dark Side of Wheat: New Perspectives on Celiac Disease and Wheat Intolerance[2], we explored the role that these psychotropic qualities in grains played in ushering in civilization at the advent of the Neolithic transition 10,000 BC. No doubt the narcotic properties of wheat are the primary reason why suspicions about its toxicity have remained merely speculation for thousands upon thousands of years. WGA is most concentrated in the seed of the wheat plant, likely due to the fact that the seeds are the “babies” of these plants and are invested with the entire hope for continuance of their species. Protecting the seed against predation is necessarily a first priority. WGA is an exceedingly small glycoprotein (36 kilodaltons) and is concentrated deep within the embryo of the wheat berry (approximately 1 microgram per grain). WGA migrates during germination to the roots and tips of leaves, as the developing plant begins to project itself into the world and outside the safety of its seed. In its quest for nourishment from the soil, its roots are challenged with fungi and bacteria that seek to invade the plant. In its quest for sunlight and other nourishment from the heavens the plant’s leaves become prey to insects, birds, mammals, etc. Even after the plant has developed beyond the germination and sprouting stages it contains almost 50% of the levels of lectin found in the dry seeds. Approximately one third of this WGA is in the roots and two thirds is in the shoot, for at least 34 days [3] Each grain contains about 1 microgram of WGA. That seems hardly enough to do any harm to animals our size. Lectins, however, are notoriously dangerous even in minute doses and can be fatal when inhaled or injected directly into the bloodstream. According to the U.S. Centers for Disease Control it takes only 500 micrograms (about half a grain of sand) of ricin (a lectin extracted from castor bean casings) to kill a human. A single, one ounce slice of wheat bread contains approximately 500 micrograms of WGA, which if it were refined to its pure form and injected directly into the blood, could, in theory, have platelet aggregating and erythrocyte agglutinizing effects strong enough to create an obstructive clot such as occurs in myocardial infarction and stroke. This, however, is not a likely route of exposure and in reality the immediate pathologies associated with lectins like ricin and WGA are largely restricted to the gastrointestinal tract where they cause mucosal injuries. The point is that WGA, even in small quantities, could have profoundly adverse effects, given suitable conditions. Ironically, WGA is exceptionally small, at 36 kilodaltons (approximately the mass of 36,000 hydrogen atoms) and it can pass through the cell membranes of the intestine with ease. The intestines will allow passage of molecules up to 1,000 kilodaltons in size. Moreover, one wheat kernel contains 16.7 trillion individual molecules of WGA, with each molecule of WGA having four N-Acetylglucosamine binding sites. The disruptive and damaging effects of whole wheat bread consumption are formidable in someone whose protective mucosal barrier has been compromised by something as simple as Non-Steroidal Anti-Inflammatory Drug (NSAID) use, or a recent viral or bacterial infection. The common consumption of both wheat and NSAIDs may suggest the frequency of the WGA vicious cycle. Anti-inflammatory medications, such as ibuprofen and aspirin, increase intestinal permeabilty and may cause absorption of even larger than normal quantities of pro-inflammatory WGA. Conversely, the inflammation caused by the absorption of WGA lectin is the very reason there is a great need for the inflammation-reducing effects of NSAIDs. One way to gauge just how pervasive the adverse effects of WGA are among wheat-consuming populations is the popularity of the dietary supplement glucosamine. In the USA, a quarter billion dollars’ worth of the glucosamine is sold annually. The main source of glucosamine on the market is from the N-Acetylglucosamine rich chitin exoskelotons of crustaceans, like shrimp and crab. Glucosamine is used for reducing pain and inflammation. We do not have a dietary deficiency of the pulverized shells of dead sea critters, just as our use of NSAIDs is not caused by a deficiency of these synthetic chemicals in our diet. When we consume glucosamine supplements, the WGA, instead of binding to our tissues, binds to the pulverized chitin in the glucosamine supplements, sparing us from the full impact of WGA. Many millions of Americans who have greatly reduced their pain and suffering by ingesting glucosamine and NSAIDs may be better served by removing wheat, the underlying cause of their malaise, from their diets. This would result in even greater relief from pain and inflammation along with far less dependency on palliative supplements and medicines alike. To further underscore this point, the following are several ways that WGA depletes our health while glucosamine works against it: WGA may be Pro-inflammatory At exceedingly small concentrations (nanomolar) WGA stimulates the synthesis of pro-inflammatory chemical messengers (cytokines) including Interleukin 1, Interleukin 6 and Interleukin 8 in intestinal and immune cells.[4] WGA has been shown to induce NADPH-Oxidase in human neutrophils associated with the “respiratory burst” that results in the release of inflammatory free radicals called reactive oxygen species[5] WGA has been shown to play a causative role in patients with chronic thin gut inflammation.[6] WGA may be Immunotoxic WGA induces thymus atrophy in rats [7] and may directly bind to, and activate, leukocytes [8]. Anti-WGA antibodies in human sera have been shown to cross-react with other proteins, indicating that they may contribute to autoimmunity [9]. Indeed, WGA appears to play a role in the pathogenesis of celiac disease (CD) that is entirely distinct from that of gluten, due to significantly higher levels of IgG and IgA antibodies against WGA found in patients with CD, when compared with patients with other intestinal disorders. These antibodies have also shown not to cross-react with gluten antigens [10] [11] WGA may be Neurotoxic WGA can pass through the blood brain barrier (BBB) through a process called “adsorptive endocytosis”[12] and is able to travel freely among the tissues of the brain which is why it is used as a marker for tracing neural circuits [13]. WGA’s ability to pass through the BBB, pulling bound substances with it, has piqued the interest of pharmaceutical developers who are looking to find ways of delivering drugs to the brain. WGA has a unique binding affinity for N-Acetylneuraminic acid, a crucial component of neuronal membranes found in the brain, such as gangliosides which have diverse roles such as cell-to-cell contact, ion conductance, as receptors, and whose dysfunction has been implicated in neurodegenerative disorders. WGA may attach to the protective coating on the nerves known as the myelin sheath [14] and is capable of inhibiting nerve growth factor [15] which is important for the growth, maintenance, and survival of certain target neurons. WGA binds to N-Acetylglucosamine which is believed to function as an atypical neurotransmitter functioning in nocioceptive (pain) pathways. WGA may be Cytotoxic WGA has been demonstrated to be cytotoxic to both normal and cancerous cell lines, capable of inducing either cell cycle arrest or programmed cell death (apoptosis). [16] WGA may interfere with Gene Expression WGA demonstrates both mitogenic and anti-mitogenic [17] activities. WGA may prevent DNA replication[18] WGA binds to polysialic acid (involved in posttranslational modifications) and blocks chick tail bud development in embryogenesis, indicating that it may influence both genetic and epigenetic factors. WGA may disrupt Endocrine Function WGA has also been shown to have an insulin-mimetic action, potentially contributing to weight gain and insulin resistance [19]. WGA has been implicated in obesity and “leptin resistance” by blocking the receptor in the hypothalamus for the appetite satiating hormone leptin. WGA stimulates epidermal growth factor which when upregulated is associated with increased risk of cancer. WGA has a particular affinity for thyroid tissue and has been shown to bind to both benign and malignant thyroid nodules [20] WGA interferes with the production of secretin from the pancreas, which can interfere with digestion and can cause pancreatic hypertrophy. WGA attaches to sperm and ovary cells, indicating it may adversely influence fertility. WGA may be Cardiotoxic WGA induces platelet activation and aggregration [21]. WGA has a potent, disruptive effect on platelet endothelial cell adhesion molecule-1, which plays a key role in tissue regeneration and safely removing neutrophils from our blood vessels [22]. WGA may adversely effect Gastrointestinal Function WGA causes increased shedding of the intestinal brush border membrane, reduction in surface area, acceleration of cell losses and shortening of villi, via binding to the surface of the villi. WGA can mimic the effects of epidermal growth factor (EGF) at the cellular level, indicating that the crypt hyperplasia seen in celiac disease may be due to the growth-promoting effects of WGA. WGA causes cytoskeleton degradation in intestinal cells, contributing to cell death and increased turnover. WGA decreases levels of heat shock proteins in gut epithelial cells leaving these cells less well protected against the potentially harmful content of the gut lumen.[23] WGA may share pathogenic similarities with certain Viruses There are a number of interesting similarities between WGA lectin and viruses. Both viral particles and WGA lectin are several orders of magnitude smaller than the cells they enter, and subsequent to their attachment to the cell membrane, are taken into the cell through a process of endocytosis. Both influenza and WGA gain entry through the sialic acid coatings of our mucous membranes (glycocalyx) each with a sialic acid specific substance, the neuriminidase enzyme for viruses and the sialic acid binding sites on the WGA lectin. Once the influenza virus and WGA lectin have made their way into wider circulation in the host body they are both capable of blurring the line in the host between self-and non-self. Influenza accomplishes this by incorporating itself into the genetic material of our cells and taking over the protein production machinery to make copies of itself, with the result that our immune system must attack its own virally transformed cell, in order to clear the infection. Studies done with herpes simplex virus have shown that WGA has the capacity to block viral infectivity through competitively binding to the same cell surface receptors, indicating that they may affect cells through very similar pathways. WGA has the capability of influencing the gene expression of certain cells, e.g. mitogenic/anti-mitogenic action, and like other lectins associated with autoimmunity, e.g. soy lectin, and viruses like Epstein-Barr Virus, WGA may be capable of causing certain cells to exhibit class 2 human leukocyte antigens (HLA-II), which mark them for autoimmune destruction by white blood cells. Since human antibodies to WGA have been shown to cross react with other proteins, even if WGA does not directly transform the phenotype of our cells into “other,” the resulting cross-reactivity of antibodies to WGA with our own cells would result in autoimmunity nonetheless. Given the multitude of ways in which WGA may disrupt our health, gain easy entry through our intestinal mucosa into systemic circulation, and remain refractory to traditional antibody-based clinical diagnoses, it is altogether possible that the consumption of wheat is detracting from the general health of the wheat-consuming world and that we have been, for all these years, “digging our graves with our teeth.” This perspective may come as a great surprise to the health food industry whose particular love affair for whole wheat products has begun to go mass market. The increasingly hyped-up marketing of “whole wheat,” “sprouted grain,” and “wheat germ” enriched products, all of which may have considerably higher levels of WGA than their processed, fractionized, non-germinated and supposedly “less healthy” equivalents, may contribute to making us all significantly less healthy. It is my belief that a careful study of the wheat plant will reveal that, despite claims to the contrary, man does not have dominion over nature. All that he deems fit for his consumption may not be his inborn right. Though the wheat plant’s apparently defenseless disposition would seem to make it suitable for mass human consumption, it has been imbued with a multitude of invisible “thorns,” with WGA being its smallest and perhaps most potent defense against predation. While WGA may be an uninvited guest at our table, wheat is equally inhospitable to us. Perhaps the courteous thing to do, having realized our mistaken intrusion, is to lick our wounds and simply go our separate ways. Perhaps as the distance between man and his infatuation with wheat grows, he will grow closer to himself and will discover far more suitable forms of nourishment that Nature has not impregnated with such high levels of addictive and potentially debilitating proteins. Sources: Desmond S. T. Nicholl, An Introduction to Genetic Engineering, 3rd Edition ISBN-13: 9780521615211 Ji, Sayer “The Dark Side of Wheat—New Perspectives on Celiac Disease & Wheat Intolerance.” Winter, 08’, Journal of Gluten Sensitivity Distribution of Wheat Germ Agglutinin in Young Wheat Plants. Plant Physiol. 1980 Nov;66(5):950-955. PMID: 16661559 Effects of wheat germ agglutinin on human gastrointestinal epithelium: insights from an experimental model of immune/epithelial cell interaction. Toxicol and Applied Pharmacology 2009 Jun 1;237(2):146-53. Epub 2009 Mar 28. PMID 19332085 Wheat germ agglutinin induces NADPH-oxidase activity in human neutrophils by interaction with mobilizable receptors. Infection and Immunity. 1999 Jul;67(7):3461-8. PMID 10377127 Lectin glycosylation as a marker of thin gut inflammation. The FASEB Journal. 2008;22:898.3 Antinutritive effects of wheat-germ agglutinin and other N-acetylglucosamine-specific lectins.The British Journal of Nutrition 1993 Jul;70(1):313-21. PMID: 8399111 Lectinlike properties of pertussis toxin. . Infection and Immunity 1989 Jun;57(6):1854-7. PMID: 2722243 Natural human antibodies to dietary lectins. FEBS Lett. 1996 Nov 18;397(2-3):139-42. PMID: 8955334 Antibodies to wheat germ agglutinin in coeliac disease. Clin Exp Immunol. 1986 January; 63(1): 95–100. PMID: 3754186 Elevated levels of serum antibodies to the lectin wheat germ agglutinin in celiac children lend support to the gluten-lectin theory of celiac disease. Pediatr Allergy Immunol. 1995 May;6(2):98-102. PMID: 7581728 Transcytotic pathway for blood-borne protein through the blood-brain barrier. Proceedings from the National Academy of Sciences U S A. 1988 Jan;85(2):632-6. PMID: 2448779 Transsynaptic transport of wheat germ agglutinin expressed in a subset of type II taste cells of transgenic mice. BMC Neuroscience. 2008 Oct 2;9:96. PMID: 18831764 Distribution of concanavalin A and wheat germ agglutinin binding sites in the rat peripheral nerve fibres revealed by lectin/glycoprotein-gold histochemistry. The Histochem Journal. 1996 Jan;28(1):7-12. PMID: 8866643 Wheat germ agglutinin, concanavalin A, and lens culinalis agglutinin block the inhibitory effect of nerve growth factor on cell-free phosphorylation of Nsp100 in PC12h cells. Cell Struct and Function 1989 Feb;14(1):87-93. PMID:2720800 Wheat germ lectin induces G2/M arrest in mouse L929 fibroblasts. J Cell Biochem. 2004 Apr 15;91(6):1159-73. PMID: 15048871 Wheat germ agglutinin and concanavalin A inhibit the response of human fibroblasts to peptide growth factors by a post-receptor mechanism. J Cell Physiol. 1985 Sep;124(3):474-80. PMID: 2995421 DNA replication in cell-free extracts from Xenopus eggs is prevented by disrupting nuclear envelope function. J Cell Sci. 1992 Jan;101 ( Pt 1):43-53. PMID: 1569128 Effects of wheat germ agglutinin and concanavalin A on the accumulation of glycosaminoglycans in pericellular matrix of human dermal fibroblasts. A comparison with insulin. Acta Biochim Pol. 2001;48(2):563-72. PMID: 11732625 Analysis of lectin binding in benign and malignant thyroid nodules. Arch Pathol Lab Med. 1989 Feb;113(2):186-9. PMID: 2916907 Further characterization of wheat germ agglutinin interaction with human platelets: exposure of fibrinogen receptors. Thromb Haemost. 1986 Dec 15;56(3):323-7. PMID: 3105108 Wheat germ agglutinin-induced platelet activation via platelet endothelial cell adhesion molecule-1: involvement of rapid phospholipase C gamma 2 activation by Src family kinases. Biochemistry. 2001 Oct 30;40(43):12992-3001. PMID: 11669637 Decreased levels of heat shock proteins in gut epithelial cells after exposure to plant lectins. Gut. 2000 May;46(5):679-87. PMID: 10764712
  3. Celiac.com 12/01/2015 - Lectins are carbohydrate binding proteins which promote inflammatory responses like Crohn's disease, systemic lupus, asthma, and rheumatoid arthritis. They were discovered over 100 years ago and cause leaky gut and gastrointestinal dysbiosis yet the push for a plant-based diet focusing on legumes as meat alternatives has overlooked the damage lectins cause to the gut. Legumes offer inferior nutrition compared to animal proteins so toxicity needs to be considered when recommending food choices. As carbohydrate binding proteins, lectins are difficult to digest and irritate the brush border of the small intestine. Consequently, the tight junctions of the microvilli are damaged by prolamin and agglutinins which can lead to numerous disorders of the gastrointestinal tract and autoimmune diseases. Lectins are also a major contributor to leptin resistance which contributes to obesity. As described in The Handbook of Plant Lectins: Properties and Biomedical Applications (John Wiley, 1998), foods that contain these toxic lectins are members of the pea family and include peanuts, pigeon peas, soybeans, kidney beans, mung beans, lima beans, lentils, fava beans, chickpeas, carob, green and yellow peas. Green beans, snow peas and snap peas are usually well tolerated once the gut has been healed since they are immature protein sources with minor amounts of lectins. Lectins are found in other foods including grains and pseudo-grains. Grains are seeds from grasses—barley, oats, rice, rye, millet, wheat, teff, corn, kamut, spelt and possibly wild rice. Many gastroenterologists believe that the detrimental affects of lectins in grains are a factor in the development of celiac disease. Genetics and frequent consumption possibly play a critical role in the severity of sensitivities to these foods. Pseudo-grains are seeds from broadleafed plants—amaranth, buckwheat, chia, and quinoa. These seed products were geographically limited to specific populations and only available on a limited basis seasonally. But modern agriculture has greatly increased the consumption of these pseudo-grains because they can be labeled “gluten-free” because US standards allow any grain with less than 20 ppm gluten to be called gluten-free. Omitting toxic lectins—prolamins and agglutinins—from the diet is critical for gut health. Prolamins are predominately found in the seeds of plants. Gluten is the most widely known source of prolamins. They get their name from the high content of the amino acid proline. Research studies have shown that the prolamins in quinoa, corn and oats can cause damage to the digestive tract in people with celiac disease, yet these grains are frequently included in a gluten-free diet. Aggltinins are named for their ability to cause clumping of red blood cells. The most recent example of how this toxic lectin works is the bioterrorism threat caused from ricin. Ricin is the compound in castor beans that is so toxic that only tiny amounts are needed to cause death. Agglutinins are found on the seed coatings of grains and pseudo-grains and serve to protect the seed from fungus growth. Genetically modified crops—wheat, corn, soybeans—have higher amounts of agglutinins to insure higher yields. A leaky gut is harmful to the innate and adaptive immune systems. Toxic lectins cause inflammation and induce cytokine production. As few as five soaked, uncooked kidney beans can lead to gut distress for the raw foodies while 1 tablespoon of peanut butter leads to peanut agglutinins entering the bloodstream soon after consumption. Paolo Zatto and Pamela Zambenedetti from Padova, Italy studied lectins, microglia and Alzheimer's Disease (AD) as reported in Lectins and Pathology, 2000. The microglia of 10 AD brains stained intensely for agglutinins. Their research concluded that the glycation reaction seen in AD from lectins may serve as a significant factor in amyloid plaque development and disease progression. Bacteria overgrowth in the gut is associated with a wide variety of diseases- septicemia, pulmonary infections, enteropathies. Adhesion of pathogenic bacteria to epithelial cells in the gut can be a critical first stage in the infectious disease process. Michele Mouricout and Bruno Vedrine of Limoges, France described how lectins cause adhesion of numerous bacterial strains to intestines, brain tissues, urinary tract, lung and corneal cells. Their research is reported in Lectins and Pathology, 2000 illustrates the mosiac effect of how agglutinins cause tissue damage. Even though lectins have been identified for decades, little interest has been shown by biological and medical science. Since they are so widely distributed in foods consumed daily, lectins may finally become recognized as partners in the pathogenesis of diseases like cancer. Galectin-3 (gal 3) galactoside-binding lectin is found on the surface of most cancer cells and has been reported to promote angiogenesis. Lectins are not oncogenes but they help in cancer progression once initiated. Some are implicated in adhesion while others cause metatasis. Isn't it about time that nutrition science took a closer look at the lectin levels in foods consumed daily and customize the diet for lectin sensitivity to better manage inflammation and auto immune diseases? The higher intact of GMO food in the diet, the more lectins are consumed. Without food labeling of GMOs, consumers will continue to be misled and many will remain sick.
  4. To All, I came across this research recently on Lectins in beans and grains though it would be worth sharing. https://www.sciencedaily.com/releases/2007/08/070801091240.htm There was an article on Celiac.com on Lectins once I thought but I couldn't find the article again. I thought it was interesting how the GI tract is always rebuilding itself. Posterboy,
  5. Celiac.com 09/21/2019 (Originally published 04/05/2010) - I am a veterinarian who is doing research on the origins of disease. This came about after my miraculous recovery from multiple ailments following my diagnosis of food intolerance, particularly celiac disease. I have chronicled my recovery and findings on my website, www.dogtorj.com. I’ve come to the conclusion that most of what we call “diseases” are long-term symptoms arising from the “civil war” taking place in our bodies, between its residents—our cells and those entities designed to help and protect those residents (e.g. viruses and bacteria) and the constant barrage of immune challenges that we throw at them (e.g. food lectins, carcinogens, chemicals/preservatives, trans fats, fluoride (an “antibiotic” and carcinogen) air pollution, etc., etc. These, coupled with our horrific fast-food diets, inadequate sleep/exercise/sunlight, and self-induced misery through alcohol/drug abuse and our penchant for sugar have brought all of the plagues of Pandora’s Box on humankind. Yet we keep pointing the finger at microorganisms like viruses and bacteria, including L-forms and mollicutes, as the enemy. Granted, most don’t know or fully understand the true nature of viruses and bacteria - that they are crucial for our survival, being important instruments in our adaptation to this ever-changing environment in which we live. But shouldn’t intelligent people be asking why these guys are so ubiquitous yet a relative few people are suffering from the “diseases” caused by these “culprits? The fact is that viruses and L forms do what they do because they need to survive because they are crucial to our survival. Would you disagree that if we could snap our fingers and make all viruses and bacteria disappear from the planet that the entire ecosystem would collapse? Certainly, we know that the vast majority of these bacteria are not pathogenic? What really distinguishes a pathogen from a saprophyte—or a helper? When huge numbers of the population are infected with various “pathogenic” bacteria and yet remain asymptomatic, shouldn’t it give us pause? Why do they become such culprits of disease in the “unfortunate” few? Are they just unfortunate or have they done something—or lived somewhere, in the case of pollution—that has brought this plague on themselves? We know that the number one risk of developing legionnaire’s disease was/is cigarette smoking. Now there’s a surprise. I believe down to my core that viruses and bacteria work in concert to help us all, especially when it comes to adaptation and survival. Bacteria form L-forms and viruses mutate because they need to survive - they are critical to our survival and only become pathogens when we have forced them into doing so with the laundry list of abuses given above. Cancer is little more than a virus (and/or an intracellular bacteria) forcing that cell to duplicate out of control in a desperate attempt to protect itself, and the cell it was designed to protect, as well as escaping those noxious elements (we call them “carcinogens”) that have forced them into this final phase of adaptation. Our immune systems tried valiantly to deal with this during the preceding “autoimmune” phase, a term I no longer use because the thought of our immune system attacking itself for no reason is preposterous, especially in light of research on L-forms. And, we can’t say we weren’t warned by the broad array of symptoms we were given: the heartburn; IBS; allergies; hives; cough; migraines; seizures; fatigue/depression; etc.; etc. Certainly, there are those who have become so afflicted and immune challenged that they need some pharmaceutical aid to deal with these helper-turned-“culprit” bacteria but to become dependent upon antibiotics for any significant length of time is both potentially dangerous and unnecessary. If we stop the assault we are visiting on these misunderstood and reactionary residents, we can come off the drugs (like I did) and re-establish the status quo, and long before the two or three year mark in most cases, I believe. People simply need to know that we are the culprit, not these microorganisms at which we keep pointing our scientific fingers. Why? Because these organisms—the viruses, bacteria, L-forms and mollicutes—are here to stay! It is we who are the transient visitors. And if we want to enjoy our stay, we’re going to have to learn how to treat ourselves, and those who reside within us, a whole lot better.
  6. Celiac.com 05/31/2019 (originally published 10/08/2010) - Hello. My name is Gerald Cooper. My wife was diagnosed with sickle cell anemia at the age of three. She’s 38 now and we are seeking the cure for this disease. I get on website after website and find cures for cancers and just about everything else. I am so thankful that people are getting cured from their problems, for I hate all diseases. I just get frustrated now and then because I have not found ANYONE saying that they have the cure for sickle cell anemia. I am seeking to find right now and we are desperate. We are desperate. My wife had a hip replacement due to the sickle cell anemia causing a vascular necrosis. She was also scheduled to have both shoulders replaced and her other hip. The doctors are also saying that the sickle cell anemia is eating at her spine as well. We need help now. We need help right now. WE NEED HELP RIGHT NOW. PLEASE **************************************** Hi Mr. Cooper, I am so sorry that you wife is having this problem and that more help has not been afforded her. You are experiencing the frustration that many, including myself, have experienced when it comes to getting REAL answers to their medical woes. I hope that I can be of some help in getting you and your wife headed in the right direction. As I state in my welcome message, I am NOT an MD (“just a veterinarian”) BUT I can point you to some of the right rocks to look under. When it comes to sickle cell disease, the texts imply that they really don’t understand the syndrome very well. And, I guess that statement is true if they are stating that. However, there are some very critical observations to be made that I believe shed abundant light on the disease process. First of all, the sickle cell gene is/was ESSENTIAL to have in those living in Africa and along the Mediterranean where malaria is an issue. Without the sickle cell gene, people would die from malaria. If the sickle cell gene was present, when the malaria organism infected a blood cell, the cell would form a sickle cell, which would not support the malaria organism, thus protecting the individual from the disease. Again, it was ESSENTIAL that this gene be present to PROTECT that individual. SO, what happened??? What in the world would turn an essential trait into a lethal one? You need look no further than the diets of those individuals and the catastrophic change that took place when they came to America and started eating the standard American diet. In Africa, they ate NO gluten grains, consumed NO cow milk products, NO soy and NO corn...the four damaging foods that I write so much about. These “Big 4” (or the “four horsemen of the apocalypse” as I now call them) are doing so much harm to susceptible individuals. And who are they doing the most harm to? Those who have had the least amount of time to adapt to those foods, namely Black Americans, American Indians, Hispanic Americans and Asian Americans. This should be no surprise whatsoever when viewed through the eyes of food intolerance, supported by a little stroll through history, which I do in my main paper The Answer. What you and your wife need to fully understand is the concept of food intolerance and how the “big 4” damage the gut and block absorption of essential nutrients such as calcium, iron, iodine, B complex vitamins, vitamin C, and trace minerals and how these proteins (lectins) are capable of doing phenomenal amounts of harm to all tissues, including the walls of arteries, blood cells themselves, and every other tissue including the brain. I’m sure that your wife’s medical history will make perfect sense to you when viewed through these eyes, including concurrent and pre-existing symptoms like headaches/migraines, heartburn/IBS, allergies, etc etc. that may have been occurring for years before the serious things started occurring. One huge piece of the puzzle lies in the work of Dr. Adamo who has written a number of books concerning eating for your blood type, based on lectins and how individuals with certain blood types are more susceptible to these food issues than others. If sickle cell disease were my medical problem, the very first thing I would do would be to begin the elimination diet that I already eat right now...it requires strict avoidance of all gluten (wheat, barley, rye), cow milk products, soy, and corn. This is easier than you may think. I would also avoid all trans fats/hydrogenated oils, which is also getting easier as they are being taken out of prepared foods right and left. I would also consider avoiding the entire legume family (soy, beans except green beans, and peas) as these lectins are problematic for many people, as Dr. D’Adamo and that lectin link above point out. The other thing to consider is having her blood tested, which will show secondary foods to which she may now be intolerant. You simply need to see how these dietary proteins are wreaking havoc on our bodies and how they can cause ALL of the symptoms seen in sickle cell disease. As I wrote in The Answer, I called my brother up one night after reading about Sickle Cell in the human Merck manual, a sort of medical encyclopedia of disease. I said “What does this sound like to you?” He said “That sounds like celiac disease”, the wheat/gluten intolerance that he and I suffer from. And it did sound just like it. Why? Because the common link is these dietary proteins and the damage they can do to our bodies. Ultimately, I am convinced that the sickle cell gene is a viral adaptation, just as most of our adaptations are. That is what viruses do for us in our bodies... they allow for adaptation. And, the presence of the malaria organism stimulates the cell to become a sickle cell, as we stated above. And it is the protein in that organism that the cells (and our immune systems) respond to. However, when this same cell is challenged by other proteins (e.g. lectins in sensitized individuals) long enough and in high enough doses, a multitude of other responses by the viruses in our cells can take place, including the development of cancers. The process that is supposed to be governing/over-seeing this whole dynamic is the (healthy) immune system. But, as the process of food intolerance continues, the immune system fails. As I have stated many times in my writing, the immune system becomes over-worked and under-paid. And when the immune system weakens and ultimately fails, that is when the serious things occur. That is why one could carry the sickle cell gene for years and not be afflicted until later in life. I would also expect post-menopausal women with sickle cell disease to get much worse. I hope this helps and at least gives you some insight into this horrible condition. I think you will find plenty of supportive evidence if you start looking for answers along these lines. Again, understanding lectins and Dr. D’Adamo’s work should really help. You may even attempt to contact him through the site mentioned above. Please keep in touch. I will try to help as much as I can.
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