Proof that Food causes Infammation?

I haven't used this yet but I got this info through the post so I thought I would share. The physiological process of digestion converts food into a form that is usable by cells, primarily glucose and free fatty acids. Glucose liberated from dietary carbohydrate enters cells where it is metabolised via glycolysis and Krebs cycle. Dietary fatty acids are also an important respiratory fuel for many tissues, especially muscles, and are metabolised via β-oxidation, with the products (acetyl CoA) entering Krebs cycle for further processing. Most of the time, digestion alters food from ‘foreign’ to ‘self’. However, partially digested food particles are sometimes identified as ‘non-self’ by the immune system, stimulating an inflammatory immune response that has dramatic consequences for cellular metabolism, as it interferes with the mechanism by which glucose enters cells.When glucose cannot enter cells for combustion, some of the excess is converted to glycogen in the liver, but most is diverted, along with free fatty acids, for conversion into body fat stores as triacylglycerol. The production of fat from glucose occurs mainly in liver and fat (adipose) cells. The aforementioned immune response which promotes fat storage revolves around small, undigested particles of food, which evade complete digestion and are absorbed into the body through three mechanisms • across the gut wall mucosa • across the plasma membrane of the gut epithelial cells or enterocytes (transcellular route) • across tight junctions between enterocytes (the paracellular route) Once in the circulation, these molecular aggregates can become antigenic and instigate an immune response. These immune responses start in Peyer’s patches in the mucosa of the small intestine, but soon spread as the aggregates are drawn into the circulation. It is these immune responses and resulting inflammation that are at the centre of the science behind the product. Inflammatory responses in the intestine and bloodstream As it is frequently exposed to pathogens, the gut wall is equipped to allow nutrients to pass through into the blood system, while preventing access to harmful pathogens, such as bacteria. To protect against pathogens, the gut wall contains a variety of immune cells including T and B lymphocytes, and phagocytic leucocytes such as macrophages, MAST cells, eosinophils and neutrophils. Undigested food particles (macromolecular aggregates), reaching the lumen of the small intestine, sometimes interact with mucosal MAST cells and cause an immune response similar to that of a pathogen. The NOVO programme is able to detect which aggregates cause such responses, and thus the patient is able to avoid them. When aggregates do cause an immune response, the MAST cells, via the release of chemoattractant cytokines such as tumour necrosis factor-alpha (TNFalpha), recruit neutrophils from the bloodstream into the gut lumen. The primed neutrophils then release pro-inflammatory mediators including more TNFalpha and interferon gamma (IFN gamma). In some cases, MAST cell degranulation occurs, releasing even more cytokines, which attracts even more neutrophils to the region and releases other inflammatory enzymes and oxygen radicals. Paradoxically, this mechanism for attracting neutrophils to the gut increases the permeability of the gut epithelium, which in turn allows the now antigenic food macromolecules to enter the bloodstream, taking the inflammatory response one step further. The presence of macromolecules in the blood stream also allows for the phenomenon of ‘frustrated phagocytosis’ in which a phagocytic cell that is unable to engulf food-complexes (due to their size or overwhelming quantity), releases enzymes from its phagosomes directly into its environment. This release of enzymes and inflammatory mediators further exacerbates the situation. Such immune responses disturb both glucose and fatty acid metabolism. Glucose and fatty acid metabolism in the presence of an immune response GLUCOSE Muscle and fat cells can only take up glucose when insulin is present. Insulin causes glucose transporters, known as GLUT4, to come to the surface of muscle and fat cells, where they transport glucose into the cell for metabolism to energy. Another hormone, insulin-like growth factor-I (IGF-I), can also activate GLUT4 and promote glucose uptake into cells. The muscle and fat cells interact with insulin and IGF-1 through the tyrosine kinase receptor. This interaction causes the GLUT4 receptors to move from the cytoplasmic vesicles, in the centre of muscle cells, to the cell surface; here GLUT4 receptors are able to transport glucose. However, immune responses caused by food aggregates, specifically TNFalpha, severely disturb this glucose transport. IGF-1 also binds to another surface receptor, the integrine receptor. Integrine and tyrosine kinase receptors are normally found in equal numbers on cell surfaces. TNFalpha causes the upregulation of integrine receptors, which compete for IGF-1 binding with the tyrosine kinase receptors. When IGF-1 has bound to more integrine than tyrosine kinase receptors, the GLUT4 receptors retreat back into the cell cytoplasm, halting any glucose metabolism (even in the presence of insulin). FATTY ACIDS This phenomenon, where TNFalpha prevents glucose metabolism, even in the presence of insulin is called ‘insulin resistance’. Excess glucose is then taken up by liver cells (a process that is not insulin dependent) and converted into triacylglycerols, which are redirected to muscle cells for fuel, and to adipocytes for storage. So, although less glucose enters fat cells (adipocytes), more ready-made fat arrives for storage from the liver and is accumulated. The altered metabolism of the adipose cell also results in shunting of what little glucose there is into a metabolic pathway known as the hexosamine biosynthesis pathway, the products of which are now also thought to promote inflammation and insulin resistance. Indeed, TNFalpha is also produced by adipocytes and its expression is increased in obesity. To add to the problem, TNFalpha activates hormone–sensitive lipase, thereby mobilising Free Fatty Acids (FFAs), which leak into the circulation. FFAs can result in significant yperlipidaemia, which is an important risk factor for cardiovascular disease. Another important cytokine produced by fat cells is interleukin-6 (IL-6) and, like TNFalpha, circulating levels of IL-6 are also elevated in obesity. Both TNF-alpha and IL-6 inhibit lipoprotein lipase (found on capillary endothelial walls) so clearance of circulating FFAs is reduced. As adipocytes themselves produce TNFalpha, this exacerbates the local inflammatory responses initiated by primed leucocytes. In fact, it is only relatively recently that obesity was recognised as a chronic, inflammatory disorder. Glucose and fatty acid metabolism…how it should be, and the NOVO solution GLUCOSE The NOVO programme is able to avoid food aggregate-associated immune responses. When food is digested without immune responses, muscle and fat cells are able to metabolise both glucose and fatty acids correctly. On consumption and digestion of carbohydrates, insulin levels rise and it binds to tyrosine kinase receptors on the muscle and fat cell surfaces. This causes autophosphorylation of tyrosine residues in the ß-subunits, initiating insulin signal transduction, and the cytoplasmic vesicles fuse with the cell membrane. The GLUT4 glucose transporters are then inserted into the plasmalemma, allowing glucose to enter the cell. The release of insulin after a meal produces a 30-fold increase in the rate at which a fat cell takes up glucose. Once in the cell, glucose either enters glycolysis pathways to produce energy, or is converted into triacylglycerols and stored as fat for future use. When blood levels of insulin fall again, the tyrosine kinase receptors are no longer occupied, and tyrosine dephosphorylation terminates the insulin signal. As a result, the glucose transporters are recycled back into the cytoplasm and glucose can no longer enter the cell. FAT Two main enzymes are involved in the mobilisation of fatty acids from fat cells: hormone sensitive lipase (HSL) and lipoprotein lipase (LPL). Fat is primarily stored in the form of triacylglycerols in the adipocytes, with some free fatty acids present in circulation. When blood glucose levels are low, free fatty acids act as an important, alternative fuel source, especially for muscle cells. In this situation, the pancreas stops making insulin and, instead, secretes the fat burning hormone, glucagon. Glucagon switches off fat storage and switches on the mobilisation of free fatty acids from adipose stores by indirectly activating the hormone- sensitive lipase found within fat cells. HSL hydrolyses triacylglycerides (also known as triglycerides) into their glycerol and free fatty acid components. Glycerol is then processed via glycolysis, while the free fatty acids leave the cell and bind to albumin in the circulation. The FFAs are then transported to tissues needing energy such as skeletal and heart muscle cells. FFAs can enter cells via simple diffusion, or via a fatty acid transport protein 1 (FATP1 - an acyl-CoA synthetase) that is expressed by certain tissues, especially skeletal muscle cells and adipocytes. Interestingly, muscle cells prefer using FFAs as a fuel as it is biologically more efficient than using glucose. The second fat-processing enzyme, lipoprotein lipase (LPL), is also produced by adipocytes, but a proportion enters the circulation to sit on the capillary endothelium. LPL helps to control the balance between the levels of triacylglycerols stored in adipose tissue, the FFAs transported to cells and the amount of FFAs released from serum triacylglycerols that remain in the circulation. IGF-1 is secreted in finite levels from the liver and other tissues in response to growth hormone. What happens when we react to the foods that we eat? Both the integrine (immune pathway) receptor and the tyrosine kinase (glucose metabolism) receptor are regulated by insulin-like growth factor 1(IGF-1). Levels of IGF-1 in the body are finite and, if more IGF-1 is required or used by one of the receptors, less is available for the other. When the body produces an immune response to a particular food a number of things occur. As the body identifies the foreign food substance it sends signals to the cells to launch an immune response. This uses much of the free IGF-1 to bind to the integrine receptors (immune system activators, whose expression is increased) in order to command the cells to fight the intruder. This leaves less IGF-1 to bind to the tyrosine kinase receptor (metabolism) the key that promotes cell glucose uptake. As a result, less glucose enters the cell, and is instead processed via the liver to produce triacylglycerols that are stored as fat. A further consequence is that the muscles of the body get less energy and therefore will send a signal to the brain telling it to eat more in order to get more energy. NOVO identifies the foods to which a person mounts an immune response. Eliminating these foods from the diet reduces the inflammatory response, and allows a more balanced interaction between IGF-1, tyrosine kinase and integrine receptors. When foods trigger an immune response, white blood cells including neutrophils become activated. This activation involves the release of pro-inflammatory cytokines such as TNF alpha, but also phagocytosis, degranulation, or cell death. These phenomenons are accompanied by morphological changes, which can be identified using advanced laser screening technology. NOVO is a new and scientific approach to personalised patient nutrition. The NOVO programme is a well-researched and highly effective route to weight loss, increased energy and general well-being. The programme is based on principles within immunology and human metabolism. The rationale is that partially digested food components provoke an immune response. For healthy metabolism, the products of digestion - glucose and fatty acids - are absorbed into body cells where they are metabolised for energy. However, over a certain threshold of immune response, cell membranes change, reducing the uptake of glucose. In this scenario, the excess glucose is diverted from cell metabolism for energy, and is frequently stored as fat. In addition, these immune responses can cause fluctuations in insulin levels, and the production of free radicals; both of which have their own health issues.