Chronic Neck Pain : Postural Causes and A Unique Fix
Unbelievably, for some unlucky few there doesn't seem to be any food safe to eat.
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— Gluten Grains and Nightshades
— Other specificities of lectins such as those in beans
— Sulfites and sulfates
— Other Lectins as in Beans
— Processed oils
— Sulfite* and sulfate* containing foods (and drugs)
— Methods of cooking: roasted, fried, grilled, baked
RECAP—Avoid Personal Food Intolerances: If foods cause heartburn, abdominal distress or other reactions; which might include headaches, redness of the eyes, and/or swelling of eyelids or the delicate tissues beneath, leg spasms or cramps at night, high or very low blood pressure, postural orthostatic tachycardia (POTS); your gastric mast cells may be sensitive to these particular foods and are releasing inflammatory mediators. Not everyone has the same problem foods. But problematic foods may include:
—Foods you are allergic to by skin prick or RAST testing
—Spicy Foods, depends on the spice. Some directly degranulate mast cells.
—Foods with higher levels of histamine; includes aged cheeses and smoked meats, pickled and marinated foods, fermented foods, alcohol, food left too long at room temperature or stored too lone in the refrigerator (Bacteria and fungi break down protein into amino acids (like histidine) to form histamine and other bio-active amines), Also gene polymorphisms are common in human histamine diamine oxidase-DAO, which breaks down histamine in the gut. These variants effect the function of DAO and can make a person more or less sensitive to food sources of histamine. See the abstracts: Genetic variability of human diamine oxidase: occurrence of three nonsynonymous polymorphisms and study of their effect on serum enzyme activity by Avuso et al. and Association of single nucleotide polymorphisms in the diamine oxidase gene with diamine oxidase serum activities. by Laura Maintz et al., and Maintz and Novak's important article, "Histamine and histamine intolerance"
—Foods that release histamine from mast cells; includes citrus fruit, tomato, wheat germ, coffee, cocoa, alcohol, salicylate–containing foods such as some fruits and mint flavoring (see the Salicylate Sensitivity Food Guide), certain food additives (benzoates, food dyes like tartrazine, nitrites, sulfites, sulfates).
—Foods that block DAO the enzyme that breaks down histamine in the gut; includes alcohol, tea, and cocoa. (Some medicines can block DAO and also another enzyme present within cells, Histamine N-Methyl Transferase, See the List)
If you have a large number of food allergies or intolerances, a registered dietician may be able to help. (note: Nutritionists are not registered or certified, virtually anyone can call themselves a nutritionist per a dietitian friend of mine). Research beforehand on the web: Histamine-Restricted Diet at the International Chronic Urticaria Society website. See also the U.K. Histamine Intolerance Website Food List. (Problems with access to this website? Click here for the Histamine Intolerance Food list)
Also see the RPAH (Royal Prince Albert Hospital) Elimination Diet (Also known as the Failsafe diet) which eliminates additives, salicylates, amines (including histamine) and glutamates.
The Controversy Over Gluten Grains and Nightshade Plants: Do They worsen Arthritic and/or Intestinal Inflammation? I am intolerant to these and don't eat them, but then I have intolerances to many foods and eat a very restricted diet. I can't say for sure if avoiding gluten grains and nightshades is what has improved my spinal or toe joint inflammation. But I am convinced that by avoiding all the foods I am intolerant of, joints that had been sore have improved over and above the improvement in my posture.
— The gluten grains are wheat, barley, rye. The nightshade plants include tomato, potato, eggplant, chili and bell pepper. These contain lectins (specific sugar–binding proteins, see The Lectin Report, and Gyco Forum for details) that bind to chitin, a polymer/chain of N-acetylglucosamine units, which make up the tough outer layer of insects and crustaceans (shrimp, lobsters etc.). But as well, N-acetylglucosamine is found bonded to many proteins in our bodies. This wouldn't matter if lectins were easily inactivated by cooking or by our digestive tracts like many proteins are, but depending on the specific lectin, they can be resistant to ordinary cooking temperatures and digestion. Now it happens that the nutrient absorptive surfaces of the small intestine—the microvilli of the brush border—are lined with proteins studded with N-acetylglucosamine and acetylneuraminic acid. Lectins specific for these two carbohydrates cause microvilli to lengthen, distort, and vesiculate, while lectins specific for other carbohydrates such as galactose, glucose, mannose, and N-acetylgalactosamine have no effect (shown in rabbits but would apply to us). See the abstract: Hart et al. Lectin induced damage to the enterocyte brush border. An electron-microscopic study in rabbits. The inference is that lectins binding the enterocyte brush border interfere with absorption of nutrients by damaging the microvilli.
— "Potato lectin activates basophils and mast cells..."
— Plant Lectins, Cornell University college of Agriculture and Life Sciences.
— Opening Pandora's Bread Box: The Critical Role of Wheat Lectin in Human Disease by Sayer Ji. (Very informative essay and references)
— Antinutritive effects of wheat-germ agglutinin and other N-acetylglucosamine-specific lectins. Pusztai et al. Abstract: Incorporation of N-acetylglucosamine-specific lectins from wheat germ, thorn apple or nettle in the diet at the level of 7 g/kg reduced the digestibility and utilization of dietary proteins and the growth of rats, with wheat germ lectin being the most damaging. All three lectins bound to and were endocytosed (taken into the cell) by the epithelial cells of the small intestine, and all three served as growth factors for the gut and interfered with its metabolism and function to varying degrees. WGA was particularly effective; it induced extensive hyperplastic and hypertrophic growth of the small bowel. "Furthermore, an appreciable portion of the endocytosed WGA was transported across the gut wall into the systemic circulation, where it was deposited in the walls of the blood and lymphatic vessels. WGA also induced the hypertrophic growth of the pancreas and caused thymus atrophy."
— "The gluten-lectin theory: celiac lesions represent a response to a toxic lectin, putatively wheat germ agglutinin (WGA)." "Elevated levels of serum antibodies to the lectin wheat germ agglutinin in celiac children lend support to the gluten-lectin theory of celiac disease." Fälth-Magnusson K., Magnusson KE.
— Blocking of chitin specific lectins may be a possible reason why acetylglucosamine supplements sometimes help arthritic pain. See *Do Dietary Lectins cause Disease?—"In diet responsive rheumatoid arthritis one of the commonest trigger foods is wheat, and wheat lectin is specific for N-acetyl glucosamine—the sugar that is normally hidden but exposed in rheumatoid arthritis. This suggests that N-acetyl glucosamine ...might be an effective treatment for diet associated rheumatoid arthritis ....Wheat lectin is blocked by the sugar N-acetyl glucosamine and its polymers ....Interestingly, the health food trade has already seized on N-acetyl glucosamine as an antiarthritic supplement." Also see Fibromyalgia: The Diet Connection, an article at WebMD.
–Also gluten has been found by researchers in Australia to cause digestive symptoms and fatigue in people without Celiac disease (Non-celiac gluten intolerance). Abstract: Biersiekierski et al, 2011."Gluten causes gastrointestinal symptoms in subjects without celiac disease: a double-blind randomized placebo-controlled trial."
— Celiac Disease: Approximately 25% of the general caucasian population is genetically predisposed to developing celiac disease (those with HLA-DQ2 and/or HLA-DQ8 genetic markers) but only 4% go on to develop it. A combination of genetic and environmental factors is involved. (see "Celiac disease: how complicated can it get?" by Tjon, Bergen and Koning.) Key factors include: Type and gene dose of HLA-DQ, version "2' binds more types of gluten peptides than version "8"; factors that affect T cell reactivity; amount of gluten in the diet (widespread in the modern diet, and up to 100 different gluten proteins found in modern wheat varieties); and activity of the tissue enzyme that modifies gluten into peptides that bind HLA-DQ2.
— Gluten increases intestinal permeability through zonulin signaling. Those with celiac disease showed greater releases of zonulin with exposure to gluten, but non-celiac individuals still showed some release of zonulin with a correspondingly smallerbut significant increase in permeability. See the article: Gliadin Induces an Increase in Intestinal Permeability and Zonulin Release by Binding to the Chemokine Receptor CXCR3 by Lammers et al, 2008. and abstracts: Rapid disruption of intestinal barrier function by gliadin involves altered expression of apical junctional proteins. byi Sander et al, 2005. and Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac intestinal mucosa and intestinal cell lines. by Drago et al, 2006. "Based on our results, we concluded that gliadin activates zonulin signaling irrespective of the genetic expression of autoimmunity (coeliac disease), leading to increased intestinal permeability to macromolecules." Effect of Gliadin on Permeability of Intestinal Biopsy Explants from Celiac Disease Patients and Patients with Non-Celiac Gluten Sensitivity, Hollon et al (2015) "...gliadin exposure induces an increase in intestinal permeability in all individuals, regardless of whether or not they have celiac disease. The results of this study suggest that gluten exposure leads to altered barrier function in both Active Celiac Disease and Gluten Sensitivity, resulting in an exaggerated increase in intestinal permeability when compared to Recovered Celiac Disease [on gluten-free diet]."
Emulsifiers and additives such as carboxymethyl cellulose (CMC), carrageenan, pectin, xanthan gum and modified starches such as maltodextrin
Crohn's Disease-Associated Adherent-Invasive Escherichia coli Adhesion Is Enhanced by Exposure to the Ubiquitous Dietary Polysaccharide Maltodextrin Nickerson and McDonald (2012)
Beal et al (2012)Late onset necrotizing enterocolitis in infants following use of a xanthan gum-containing thickening agent.
Some beans are known degranulators of mast cells (kidney and pinto beans) But when prepared correctly** are generally not a problem. See Lectins in Foods (Individual listings below the table of blood type specificities of lectins) at the Owen Foundation Website.(** must be soaked overnight, the soak water disposed of, and then cooked in fresh water for a good long while or pressure cooked.)
The relatively high lectin content of peanut oil may contribute to artherosclerosis. See "Lectin may contribute to the atherogenicity of peanut oil." by Kritchevsky et al. "The biologically active lectin of peanut oil has an affinity for glycoproteins found specifically on arterial smooth muscle cells. Peanut lectin has been shown to stimulate growth of smooth muscle and pulmonary arterial cells. Vigorous washing of peanut oil reduces its lectin content by 46%. ....rabbits fed cholesterol and washed peanut oil exhibited less severe atherosclerosis in the aortic arch (by 9%) and in the thoracic aorta (by 31%). The data suggest that peanut oil's endogenous lectin may contribute significantly to its atherogenic properties."
Includes sulfur dioxide*used to preserve dry fruit. (These seem to be my personal "allergy" rather than a general mast cell degranulator, but many people have intolerances to sulfites, sulfates and sulfa meds) See Sulfite Allergy on About.com for symptoms, incidence and a list of high and low sulfite foods, and medications with sulfites. Many sulfite sensitivites do not appear to be true IgE allergies but intolerance to their toxic properties. Sulfites are toxic to microbes and are added as food preservatives and also they inhibit the enzyme that causes oxidative browning of foods (see Enzymatic Browning of Apples). Also common are intolerances/allergies to the sulfa (sulfonamide) drugs such as the antibiotic, Septra; thiazide diuretics prescribed for high blood pressure; and sulfonylureas for type 2 diabetes.
* sulfur dioxide = 1 sulfur + 2 oxygens; sulfite=1 sulfur + 3 oxygens; sulfate=1 sulfur + 4 oxygens, sulfa/sulfonamides, within a larger molecule: a group with 1 sulfur + 2 oxygens, (also potassium metabisulfite (K2S205) sodium metabisulfite (Na2S205) used as an antioxidant or antimicrobial in foods and beverages. see Wikipedia)
(An unfinished story.) We've mostly replaced the stable saturated fats with polyunsaturated fats that are easily damaged by oxidation and heating, yet are widely regarded as healthier. But are we really healthier? There must be a reason I can't tolerate any of them. See "The questionable role of saturated and polyunsaturated fatty acids in cardiovascular disease." Ravnskov, and Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease, by Siri-Tarino et al, who conclude "that there is no significant evidence ...that dietary saturated fat is associated with an increased risk of CHD (coronary heart disease) or CVD (cardiovascular disease including stroke)". They call for studies to discover if CVD risks are influenced by replacements for saturated fat. There is no doubt that partially hydrogenated trans fatty acids are strongly implicated in CVD.
—Polyunsaturated fats oxidize easily and produce lipid peroxides and secondary products such as toxic alkenals. Highly unsaturated Omega-3 fish and krill oil supplements are found to have greater concentrations of peroxides and alkenals than fresh vegetable oils. But after heating to simulate typical food preparation conditions such as sauteing and frying, peroxide and alkenal levels of vegetable oils greatly increased. Monounsaturated olive oils in general yielded the least increase in toxic oxidized byproducts than more unsaturated oils such as canola and corn oil. See "Determination of lipid oxidation products in vegetable oils and marine omega-3 supplements" by Halmorsen and Blomhoff. Surprisingly, rat feeding experiments show that oxidized polyunsaturated oils reduce triacylglycerols, cholesterol and very low density lipoproteins, however it is widely believed that consuming high levels of oxidized vegetable oils does present a health risk. See — A high oxidised frying oil content diet is less adipogenic, but induces glucose intolerance in rodents. Chao et al.; Ingestion of native and thermally oxidized polyunsaturated fats acutely increases circulating numbers of endothelial microparticles. (an index of endothelial injury) Sutherland et al.; Oxidized fat induces oxidative stress but has no effect on NF-κB-mediated proinflammatory gene transcription in porcine intestinal epithelial cells. Ringseis et al.; and see Frying Oils-Nutritional Aspects at the AOCS Lipid Library.
— olive oil and especially butter have high levels of AGEs—Advanced Glycation End Products, which form from any protein present. See Methods of Cooking, next
(chicken or turkey simmered in water is fine, but I react to Thanksgiving slow–roasted turkey, and grilled or fried chicken. Why? I found numerous articles about how cooking methods change the structure of proteins in foods. Advanced Glycation End Products (AGEs) form when protein, fat and carbohydrate, heated together at high temperatures, and especially without moisture, accelerate the chemical reaction of glucose and other monosaccharides such as fructose with proteins—no enzymes involved. The "browning reaction" of meat is an example. So is glycated hemoglobin (HbA1c) that is much increased in diabetics whose blood glucose is too high over an extended time. Results of several studies show that diet can be a significant source of AGEs, and high dietary AGEs may be a risk factor for cardiovascular and kidney damage. For references including levels of AGEs in common foods see References and Links for AGEs.