"Raw food also answers the call to "go green," since it supports sustainable organic farming; and as a vegetarian diet, it's cruelty-free lifestyle."
AGEs (ADVANCED GLYCOXIDATION END PRODUCTS)
Victoria Boutenko in her book, 12 Steps to Raw Foods writes:
"Besides acrylamide, HCAs, PAHs, and other mutagens and carcinogens, scientists have discovered yet another large group of particularly harmful substances in common foods, resulting from heating. In the process of cooking, glucose binds to proteins and forms abnormally tight (glycated) complexes. They are called advanced glycoxidation end products (AGEs). These processes are also known as the Maillard reaction. AGEs have a pathological structure, in which sugars and amino acids are strongly bound together in an irreversible connection. It has been suggested that no other molecule has the versatility of structure and the potential toxic effects on proteins as AGEs. AGEs cause cross-linking reactions in blood vessels, in heart muscle, and in the lens of the eye and thus progressively damage tissue elasticity."
It has been proven that all the muscles become stiffer, with the formation of AGEs and AGE-crosslinks are non-enzymatic processes. AGEs are irreversible by enzymes that are able to disrupt other protein bonds, destroying healthy protein structures, inhibiting protein physiologic function and causing irreversible disease conditions to vital organs while triggering inflammation especially in patients with cardiovascular disease, kidney failure, neurodegeneration and diabetes. Age-related disorders linked to AGEs include cardiovascular disease, arteriosclerosis, hypertension, stroke and decreased resilience and flexibility in tendons and ligaments.
AGE FORMATION IN DISEASES
The formation and accumulation of advanced glycation endproducts (AGEs) has been implicated in the progression of age-related diseases. AGEs have been implicated in Alzheimer's Disease, cardiovascular disease, and stroke. The mechanism by which AGEs induce damage is through a process called cross-linking that causes intracellular damage and apoptosis. They form photosensitizers in the crystalline lens,which has implications for cataract development. Reduced muscle function is also associated with AGEs.
Many cells in the body (for example, endothelial cells, smooth muscle, and cells of the immune system) from tissue such as lung, liver, kidney, and peripheral blood bear the Receptor for Advanced Glycation End-products (RAGE) that, when binding AGEs, contributes to age- and diabetes-related chronic inflammatory diseases such as atherosclerosis, asthma, arthritis, myocardial infarction, nephropathy, retinopathy, peridontitis and neuropathy. There may be some chemicals, such as aminoguanidine, that limit the formation of AGEs by reacting with 3-deoxyglucosone.
The total state of oxidative and peroxidative stress on the healthy body, and the accumulation of AGE-related damage is proportional to the dietary intake of exogenous (preformed) AGEs, the consumption of sugars with a propensity towards glycation such as fructose and galactose.
AGEs affect nearly every type of cell and molecule in the body, and are thought to be one factor in aging and some age-related chronic diseases. They are also believed to play a causative role in the vascular complications of diabetes mellitus.
They have a range of pathological effects, including increasing vascular permeability, inhibition of vascular dilation by interfering with nitric oxide, oxidising LDL, binding cells including macrophage, endothelial, and mesangial cells to induce the secretion of a variety of cytokines and enhancing oxidative stress.
From Wikipedia, the free encyclopediais
Named for the chemist Louis-Camille Maillard, who first described it in the 1910s while attempting to reproduce biological protein synthesis.
Receptor systems in the body have been suggested to have evolved to remove glycation-modified molecules, such as AGEs, to eliminate their effects. The adverse effects of AGE accumulation appear to be mediated by numerous different AGE receptors. Examples include AGE-R1, galectin-3, CD36, and, most noted, RAGE, the receptor for AGEs.
Advanced glycation in numerous different locations within the eye can prove detrimental. In the cornea, whose endothelial cells have been known to express RAGE and galectin-3, the accumulation of AGEs is associated with thickened corneal stroma, corneal edema, and morphological changes within patients with diabetes. Within the lens, Maillard chemistry has been studied extensively in the context of cataract formation. Advanced glycation is known to alter fiber membrane integrity in the lens, and dicarbonyl compounds are known to cause increased aggregate formation within the lens. This effect is exacerbated by both diabetes and aging. Furthermore, it is thought that AGE-inhibiting compounds are effective in preventing cataract formation in diabetics.
Glycation in Maillard reactions may lead to destabilization of the vitreous gel structure within the eye via unnecessary cross-linking between collagen fibrils. Again, this process is more strongly observed within diabetic patients. Within the retina, the accumulation of AGEs in the Drusen and Bruch’s membrane has been associated with age, and has also been observed at a higher level among patients with age-related macular degeneration (AMD). This is manifested by the thickening of the Bruch’s membrane. Furthermore, it has been observed that AGE levels increase with age within the lamina cribosa, and the products of the Maillard reaction have been observed there, as well.