Nevner det meste om hvordan hvete og korn påvirke vår helse, med mye fokus på lekk-tarm syndrom. Nevner også Paleo Diet. Den viser til at betennelsesmarkører ikke er så forskjellige før eller etter korn-diett, muligens fordi målemetodene ikke er sensitive nok. I studier som sammenligner grovkorn og finkorn på helse er kontrollgruppen vanlig finkorn og man ser derfor ingen endring i betennelser fra eller til.
http://www.mdpi.com/2072-6643/5/3/771
Helle Studien i dropbox.
«cereal grains contain ―anti-nutrients,‖ such as wheat gluten and wheat lectin, that in humans can elicit dysfunction and disease.»
«Inflammation is the response of the innate immune system triggered by noxious stimuli, microbial pathogens and injury. When a trigger remains, or when immune cells are continuously activated, an inflammatory response may become self-sustainable and chronic. Chronic inflammation has been associated with many medical and psychiatric disorders, including cardiovascular disease, metabolic syndrome, cancer, autoimmune diseases, schizophrenia and depression [1–3]. Furthermore, it is usually associated with elevated levels of pro-inflammatory cytokines and acute phase proteins, such as interferons (IFNs), interleukin (Il)-1, Il-6, tumor necrosis factor-α (TNF-α), and C-reactive protein (CRP).»
«Stimulation of immune cells by gliadin is not only restricted to CD patients; the incubation of peripheral blood mononuclear cells (PBMC) from healthy HLA-DQ2-positive controls and CD patients with gliadin peptides stimulated the production of IL-23, IL-1β and TNF-α in all donors tested. Nevertheless, the production of cytokines was significantly higher in PBMC derived from CD patients [14]. Similar results were obtained by Lammers et al. [15], who demonstrated that gliadin induced an inflammatory immune response in both CD patients and healthy controls, though IL-6, Il-13 and IFN-γ were expressed at significantly higher levels in CD patients. »
«Human data showing the influence of WGA intake on inflammatory markers are lacking, however, antibodies to WGA have been detected in the serum of healthy individuals [56]. Significantly higher antibody levels to WGA were measured in patients with CD compared to patients with other intestinal disorders. These antibodies did not cross-react with gluten antigens and could therefore play an important role in the pathogenesis of this disease [57].»
«Refined wheat products contain less WGA, but still contain a substantial amount of gluten. It should be noted that whole grains contain phytochemicals, like polyphenols, that can exert anti-inflammatory effects which could possibly offset any potentially pro-inflammatory effects of gluten and lectins [73]. »
«The substitution of refined cereal grains and white bread with three portions of whole wheat food or one portion of whole wheat food combined with two servings of oats significantly decreased the systolic blood pressure and pulse pressure in middle-aged, healthy, overweight men and women, yet none of the interventions significantly affected systemic markers of inflammation [70]».
«Most of the intervention studies mentioned above attempted to increase whole grain intake and were using refined grain diets as controls, thereby making it very difficult to draw any conclusions on the independent role of cereal grains in disease and inflammation.»
«In healthy sedentary humans, the short-term consumption of a paleolithic type diet improved blood pressure and glucose tolerance, decreased insulin secretion, increased insulin sensitivity and improved lipid profiles [75].»
«The patients receiving gluten reported significantly more symptoms compared to the placebo group. The most striking outcome of this study was that for all the endpoints measured, there were no differences in individuals with or without HLA-DQ2/DQ8, indicating that the intake of gluten can cause symptoms also in individuals without this specific HLA-profile. No differences in biomarkers for inflammation and intestinal permeability were found between both groups, however, inflammatory mediators have been implicated in the development of symptoms in patients with irritable bowel syndrome [78]. It could therefore be inferred that the markers used to measure inflammation and intestinal permeability were not sensitive enough to detect subtle changes on the tissue level.»
] do not consistently increase in proportion to PCO 2. 
] decrease to near resting values as maximalV˙O 2 is approached, despite increasing Pv̄CO2. 
], whereas less than one-fourth is due to the combination of venoarterial differences in [CO2] and [NH-CO2] at rest to Max.»
] plays the dominant role in CO2 exchange at the lung, whereas [CO2] and [NH-CO2] play smaller roles in total CO2 exchange. Although PCO 2differences account for the transfer of CO2 out of blood, >75% of the quantity transferred comes from the dissociation of mixed venous [HCO 
].»
concentrations increase without an increase in 
. Thus CO2 from aerobic metabolism is converted to
rather than being eliminated by the lungs.»
generated as phosphocreatine is converted to creatine.»
relative to pulmonary O2 uptake (
) can be used to quantify θL validly if aerobic and hyperventilatory sources can be ruled out, i.e. θL is then attributable to the decrease in muscle and blood [HCO3−
Verkstedet Bodywork & Breathing System 