I never forgot reading those words by Norman Walker:
"We eat ourselves to death", by eating mucous-forming cooked foods void of enzymes, and not following the proper food combining rules.
Now, a study published at US National Library of Medicine, confirms this.
From personal experience of eating raw living foods according to Ann Wigmore for 1 week, I never felt better and younger.
To Your Health,
Health Essentials LLC.
Published on http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3704564/
Modern diets are largely heat-processed and as a result contain high levels of advanced glycation end products (AGEs). Dietary advanced glycation end products (dAGEs) are known to contribute to increased oxidant stress and inflammation, which are linked to the recent epidemics of diabetes and cardiovascular disease. This report significantly expands the available dAGE database, validates the dAGE testing methodology, compares cooking procedures and inhibitory agents on new dAGE formation, and introduces practical approaches for reducing dAGE consumption in daily life. Based on the findings, dry heat promotes new dAGE formation by >10- to 100-fold above the uncooked state across food categories. Animal-derived foods that are high in fat and protein are generally AGE-rich and prone to new AGE formation during cooking. In contrast, carbohydrate-rich foods such as vegetables, fruits, whole grains, and milk contain relatively few AGEs, even after cooking. The formation of new dAGEs during cooking was prevented by the AGE inhibitory compound aminoguanidine and significantly reduced by cooking with moist heat, using shorter cooking times, cooking at lower temperatures, and by use of acidic ingredients such as lemon juice or vinegar. The new dAGE database provides a valuable instrument for estimating dAGE intake and for guiding food choices to reduce dAGE intake.
Advanced glycation end products (AGEs), also known as glycotoxins, are a diverse group of highly oxidant compounds with pathogenic significance in diabetes and in several other chronic diseases (1–6). AGEs are created through a nonenzymatic reaction between reducing sugars and free amino groups of proteins, lipids, or nucleic acids. This reaction is also known as the Maillard or browning reaction (7). The formation of AGEs is a part of normal metabolism, but if excessively high levels of AGEs are reached in tissues and the circulation they can become pathogenic (2). The pathologic effects of AGEs are related to their ability to promote oxidative stress and inflammation by binding with cell surface receptors or cross-linking with body proteins, altering their structure and function (8–10). Among the better-studied AGEs are the stable and relatively inert Nε-carboxymethyllysine (CML) and the highly reactive derivatives of methyl-glyoxal (MG). Both these AGEs can be derived from protein and lipid glycoxidation (11,12).
In addition to AGEs that form within the body, AGEs also exist in foods. AGEs are naturally present in uncooked animal-derived foods, and cooking results in the formation of new AGEs within these foods. In particular, grilling, broiling, roasting, searing, and frying propagate and accelerate new AGE formation (7,13). A wide variety of foods in modern diets are exposed to cooking or thermal processing for reasons of safety and convenience as well as to enhance flavor, color, and appearance. The fact that the modern diet is a large source of AGEs is now well-documented (3,7,13). Because it had previously been assumed that dietary AGEs (dAGEs) are poorly absorbed, their potential role in human health and disease was largely ignored. However, recent studies with the oral administration of a single AGE-rich meal to human beings as well as labeled single protein-AGEs or diets enriched with specific AGEs such as MG to mice clearly show that dAGEs are absorbed and contribute significantly to the body’s AGE pool (14–16).
And here is more http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3583887/
Glycation-associated skin autofluorescence was shown to correlate with chronological aging in a large number of healthy subjects.65
Consequences of AGE deposition in skin
AGEs can be formed intracellularly and extracellularly. Their presence in biological molecules modifies their biomechanical and functional properties. Proteins, lipids and nucleic acids can be targets of advanced glycation, modifying enzyme-substrate interactions, protein-DNA interactions, protein-protein interactions, DNA regulation and epigenetic modulation, thus interfering with numerous physiological functions of the organism. Moreover, AGEs are themselves reactive molecules which through interaction with their receptors activate various molecular pathways in vivo, thus becoming involved in inflammation, immune response, cell proliferation and gene expression
Intermediate filaments such as vimentin in fibroblasts and CK10 in keratinocytes have been found to be modified by AGEs.18,22 Cytoskeletal proteins are important in providing stability of the cytoskeleton and are crucially involved in numerous cellular functions such as migration and cellular division. Various other intracellular proteins including enzymes and growth factors may be targets of non-enzymatic modification by sugars. Glycated basic fibroblast growth factor (bFGF) displays impaired mitogenic activity in endothelial cells.80 Glycation of enzymes of the ubiquitin-proteasome system and of the lysosomal proteolytic system has been shown to inhibit their action.81Antioxidant and other protective enzymes such as Cu-Zn-SOD can be inactivated.82 Other intracellular components, such as DNA and lipids can be glycated with detrimental effects on their function.13,83
3. Receptors for AGEs: RAGE
AGEs do not only act by altering the physicochemical properties of glycated proteins. Interestingly, AGEs may bind to their cell surface receptor, RAGE, initiating a cascade of signals influencing cell cycle and proliferation, gene expression, inflammation and extracellular matrix synthesis (reviewed in Bierhaus et al.).41 As mentioned above, RAGE is broadly expressed in human skin and in epidermal keratinocytes, dermal fibroblasts and endothelial cells in vitro. It is highly found in sites of solar elastosis, and its expression is induced by advanced glycation end products and proinflammatory cytokines like TNFα.45 In skin cells RAGE has been shown to decrease cell proliferation, induce apoptosis and increase MMPs production.47 Many of these effects involve NFκB signaling.47
4. Effects of AGEs on resident skin cells
AGEs have been shown to affect various functions of skin cells in vitro (Table 3). They decrease proliferation and enhance apoptosis of human dermal fibroblasts, an effect which is at least partly RAGE-dependent and correlates with the activation of NFκB and caspases.87 In keratinocytes, AGEs decrease cell viability and migration and induce the expression of proinflammatory mediators.84 Moreover, AGEs are able to induce premature senescence in human dermal fibroblasts and in normal human keratinocytes in vitro.86,89,90 Collagen and ECM protein synthesis have been also found to be decreased, while the expression of MMPs is induced.47 Dicarbonyls such as glyoxal and methylglyoxal impair the signaling of epidermal growth factor receptor (EGFR), a receptor controlling various cellular functions such as proliferation, differentiation, motility and survival, by formation of EGFR crosslinks, blocking of phosphorylation and impaired activation of ERKs and phospholipase C.92 Various other growth factors or proteins significant for cellular functions, like bFGF, may be glycated inhibiting their functions.80 In the context of extrinsic aging, AGEs seem to render cells more sensitive to external stimuli, as UVA irradiated fibroblasts and keratinocytes exhibit decreased viability after exposure to AGEs.