I think what you mean here is "glycosylation". And yes, lots of things get glycosylated when there is a ton of glucose floating around unused in the body. Actually, one of the worst effects of glycosylation is the thickening of basement membrane in the capillary beds of various organs such as the kidney. This is one of the pathways by which diabetes causes kidney damage. Many physicians have drawn the erroneous conclusion that ketones (which are high in diabetics) are the cause of kidney failure, when really its glucose. I too have not seen any studies to indicate that a ketogenic diet has any deliterious effects on kidney function. This doesn't mean that it doesn't have bad effects, but since this diet has been around since the 70's, you would have thought something would have shown up by now. Right? And it's not like people haven't been trying to discredit Adkins. Heck, most dieticians would like his head on a platter. Thus, if there were any indication that this diet were at all a health risk, it would have been jumped on and researched to death years ago.
Thus, I am not sure if Edziu's "cat" analogy is entirely correct. Certainly they have to deal with lots of ketones, but you are literally comparing apples and celery. One has to be very careful drawing correlations between animals and humans. For instance, dogs are omnivores, yet have a very low tolerance for ibuprofen--far below that of humans. So, can you say that ibuprofen is toxic to all omnivors? Certainly not. Rats which are omnivorous, can also drink alcohol at 10-20% in their drinking water for 50% of their lifespan with no liver problems--whereas humans can't. I have to admit, I am not a cat physiologist, but cats may have very large kidneys for many and quite different reasons than merely handling lots of ketones.
Also, speaking of radicals, Edziu mentioned that most radicals are from lipid peroxidation. This is not true. Some sort of radical (oxygen, toxin, etc.) has to be formed first, which then abstracts a hydrogen from a polyunsaturated lipid molecule, resulting in lipid peroxidation. If you believe Bruce Ames (a famous toxicologist) the ultimate source of >99.9% of the oxidative stress that our body is exposed to comes from the oxygen that we breathe. His theories go that oxygen radicals are produced at enormous levels by mitochondria all the time, just merely as a consequence of producing energy. As was stated before in this thread, we have antioxidant systems to take care of this, and it is only a problem when these radicals are produced in excess of what your system can handle. Calorie restiction may, as stated earlier, reduce oxidative stress, but it has also been shown to increase the expression of antioxidant systems, and enzymes like manganese superoxide dismutase (MnSOD).
What I find interesting about calorie restriction research, at least from Hansen et al's work, is that in non-human primates they find these longevity effects by maintaining bodyfat percentages (to between 10-20%) and not really by "classical" calorie restriction. If this is true, then a BB lifestyle may very well increase lifespan. But, then again these animals don't spend much time at a squat rack either. Incidentally, these researchers also believe that most of the early deaths seen in the ad lib fed group in their primate studies are caused by type II diabetes, again pointing toward excess glucose as the culprit.
Thus, I am not sure if Edziu's "cat" analogy is entirely correct. Certainly they have to deal with lots of ketones, but you are literally comparing apples and celery. One has to be very careful drawing correlations between animals and humans. For instance, dogs are omnivores, yet have a very low tolerance for ibuprofen--far below that of humans. So, can you say that ibuprofen is toxic to all omnivors? Certainly not. Rats which are omnivorous, can also drink alcohol at 10-20% in their drinking water for 50% of their lifespan with no liver problems--whereas humans can't. I have to admit, I am not a cat physiologist, but cats may have very large kidneys for many and quite different reasons than merely handling lots of ketones.
Also, speaking of radicals, Edziu mentioned that most radicals are from lipid peroxidation. This is not true. Some sort of radical (oxygen, toxin, etc.) has to be formed first, which then abstracts a hydrogen from a polyunsaturated lipid molecule, resulting in lipid peroxidation. If you believe Bruce Ames (a famous toxicologist) the ultimate source of >99.9% of the oxidative stress that our body is exposed to comes from the oxygen that we breathe. His theories go that oxygen radicals are produced at enormous levels by mitochondria all the time, just merely as a consequence of producing energy. As was stated before in this thread, we have antioxidant systems to take care of this, and it is only a problem when these radicals are produced in excess of what your system can handle. Calorie restiction may, as stated earlier, reduce oxidative stress, but it has also been shown to increase the expression of antioxidant systems, and enzymes like manganese superoxide dismutase (MnSOD).
What I find interesting about calorie restriction research, at least from Hansen et al's work, is that in non-human primates they find these longevity effects by maintaining bodyfat percentages (to between 10-20%) and not really by "classical" calorie restriction. If this is true, then a BB lifestyle may very well increase lifespan. But, then again these animals don't spend much time at a squat rack either. Incidentally, these researchers also believe that most of the early deaths seen in the ad lib fed group in their primate studies are caused by type II diabetes, again pointing toward excess glucose as the culprit.
. He also goes on to say that it is not the glycation that is the problem, but the repair enzymes (fidelity) that determine any subsequent detrimental effects such as mutations (you'll note that this supports what I posted earlier).