Farmerchick, you can have my share of the hfcs. And my sons', my husband's, the cats'.......
Some people are "genetically blessed" and do have the ability to absorb a great deal of damage. Others get damage and don't see it, so as long as they are skinny, they don't worry about it until it bites them in the but.
Research GLYCATION sometime when you are in a nerdy mood. Fructose plays a big role. One of the effects of glycation (besides wrinkles) is joint damage.
"This study demonstrates that long-term fructose feeding accelerates aging as expressed by changes in various age-related markers measured in collagen from skin and bones. The focus on collagen is warranted because collagen is present ubiquitously, accounts for as much as 30% of body proteins, mainly in the extracellular matrix, and provides the basic functional properties of most vulnerable tissues such as renal basement membrane, the cardiovascular system and retinal capillaries. "
http://jn.nutrition.org/content/128/9/1442.full
"The term glycation refers only to this initial step, a sugar molecule attaching to a protein, and this part of the process is reversibleif blood-sugar levels are low enough, the sugar and protein will disengage, and no damage will be done. If blood sugar is elevated, however, then the process of forming an advanced glycation end-product will move forward. The protein and its accompanying glycated sugars will undergo a series of reactions and rearrangements until the process culminates in the convoluted form of an advanced glycation end-product. These AGEs will then bind easily to other AGEs and to still more proteins through a process known as cross-linkingthe sugars hooked to one protein will bridge to another protein and lock them together. Now proteins that should ideally have nothing to do with each other will be inexorably joined.
In the mid-1970s, Rockefeller University biochemist Anthony Cerami and Frank Bunn independently recognized that AGEs and glycation play a major role in diabetes.*56 Both Cerami and Bunn were initially motivated by the observation that diabetics have high levels of an unusual form of hemoglobin the oxygen-carrying protein of red blood cellsknown as hemoglobin A1c, a glycated hemoglobin. The higher the blood sugar, the more hemoglobin molecules undergo glycation, and so the more hemoglobin A1c can be found in the circulation. Ceramis laboratory then developed an assay to measure hemoglobin A1c, speculating correctly that it might be an accurate reflection of the diabetic state. Diabetics have two to three times as much hemoglobin A1c in their blood as nondiabetics, a ratio that apparently holds true for nearly all glycated proteins in the body. (The best determination of whether diabetics are successfully controlling their blood sugar comes from measuring hemoglobin A1c, because it reflects the average blood sugar over a month or more.)
Since 1980, AGEs have been linked directly to both diabetic complications and aging itself (hence the acronym). AGEs accumulate in the lens, cornea, and retina of the eye, where they appear to cause the browning and opacity of the lens characteristic of senile cataracts. AGEs accumulate in the membranes of the kidney, in nerve endings, and in the lining of arteries, all tissues typically damaged in diabetic complications. Because AGE accumulation appears to be a naturally occurring process, although it is exacerbated and accelerated by high blood sugar, we have evolved sophisticated defense mechanisms to recognize, capture, and dispose of AGEs. But AGEs still manage to accumulate in tissues with the passing years, and especially so in diabetics, in whom AGE accumulation correlates with the severity of complications.
One protein that seems particularly susceptible to glycation and cross-linking is collagen, which is a fundamental component of bones, cartilage, tendons, and skin. The collagen version of an AGE accumulates in the skin with age and, again, does so excessively in diabetics. This is why the skin of young diabetics will appear prematurely old, and why, as the Case Western University pathologist Robert Kohn first suggested, diabetes can be thought of as a form of accelerated aging, a notion that is slowly gaining acceptance. Its the accumulation and cross-linking of this collagen version of AGEs that causes the loss of elasticity in the skin with age, as well as in joints, arteries, and the heart and lungs.
The process can be compared to the toughening of leather. Both the meat and hide of an old animal are tougher and stiffer than those of a young animal, because of the AGE-related cross-linking that occurs inevitably with age. As Cerami explains, the aorta, the main artery running out of the heart, is an example of this stiffening effect of accumulated and cross-linked AGEs. If you remove the aorta from someone who died young, says Cerami, you can blow it up like a balloon. It just expands. Let the air out, it goes back down. If you do that to the aorta from an old person, its like trying to inflate a pipe. It cant be expanded. If you keep adding more pressure, it will just burst. That is part of the problem with diabetes, and aging in general.
You end up with stiff tissue: stiffness of hearts, lungs, lenses, joints.... Thats all caused by sugars reacting with proteins.
AGEs and the glycation process also appear to play at least one critical role directly in heart disease, by causing the oxidation of LDL particles and so causing the LDL and its accompanying cholesterol to become trapped in the artery wall, which is an early step in the atherosclerotic process. Oxidized LDL also appears to be resistant to removal from the circulation by the normal mechanisms, which would also serve to increase the LDL levels in the blood. As it turns out, LDL is particularly susceptible to oxidation by reactive oxygen species and to glycation.*57 In this case, both the protein portion and the lipid portion (the cholesterol and the fats) of the lipoprotein are susceptible. These oxidized LDL particles appear to be markedly elevated in both diabetics and in nondiabetics with atherosclerosis, and are particularly likely to be found in the atherosclerotic lesions themselves.
That glycation and AGEs are critical factors in diabetic complications and in heart disease has recently been demonstrated by experiments with compounds known as anti-AGE compounds or AGE breakers. These will reverse arterial stiffness, at least in laboratory animals, and, as one recent report put it, ameliorate the adverse cardiovascular and [kidney-related] changes associated with aging, diabetes and hypertension. Whether these or similar compounds will work in humans remains to be seen.
When biochemists discuss oxidative stress, glycation, and the formation of advanced glycation end-products, they often compare whats happening to a fire simmering away in our circulation. The longer the fire burns and the hotter the flame, the more damage is done. Blood sugar is the fuel. Current evidence points to glucose not only as the bodys main short-term energy source, as the American Diabetes Association recently put it, but also as the long-term fuel of diabetes complications.
But there is no reason to believe that glucose-induced damage is limited only to diabetics, or to those with metabolic syndrome, in whom blood sugar is also chronically elevated. Glycation and oxidation accompany every fundamental process of cellular metabolism. They proceed continuously in all of us. Anything that raises blood sugarin particular, the consumption of refined and easily digestible carbohydrateswill increase the generation of oxidants and free radicals; it will increase the rate of oxidative stress and glycation, and the formation and accumulation of advanced glycation end-products. This means that anything that raises blood sugar, by the logic of the carbohydrate hypothesis, will lead to more atherosclerosis and heart disease, more vascular disorders, and an accelerated pace of physical degeneration, even in those of us who never become diabetic." - Gary Taubes, Good Calories Bad Calories
