There are some more studies:
Review - Advanced Glycation End Products
Review - Nonenzymatic Glycation of Collagen in Aging and Diabetes
Advanced glycoxidation end products in commonly consumed foods
Orally absorbed reactive glycation products (glycotoxins): An environmental risk factor in diabetic nephropathy
The AGE-diet, but not the CL-diet, produced distinct elevations in serum AGE levels in direct proportion to amount ingested
There is also Masterjohn post about how ketones are even worst....
Where Do Most AGEs Come From
He seem to think that endogenous AGE serve for signaling purpose apart from causing harm:
All this said, does the endogenous production of AGEs cause harm? In future posts, I will make a case that AGEs and their dicarbonyl precursors may emerge as key signaling molecules, but that in many situations they do indeed cause harm.
This may be true, but as far as I know, AGEs are made trough glycation, and endogenous production is made enzymaticaly, via glycosilation and indeed has many functions. From "Glycosylation in Cellular Mechanisms of Health and Disease"
Glycosylation modulates interactions of receptors and ligands with themselves, coregulatory molecules, and distinct membrane domains of intact cells, thereby altering signal transduction
The authors of review think that dietary carbohydrate input has little to do with it. I was reading this to see if Paul Jaminets hypothesis of "safe starches" and glycosylation deficiency does make sense.
Except in cases of rare genetic defects, dietary intake of monosaccharides or mammalian glycans has not been rigorously established to have a beneficial effect on human health or in the treatment of disease
Fructose is definitely much worst then glucose. From the above mentioned review:
The rate of AGE formation on intracellular proteins is slowest in the presence of glucose and more rapid with intracellular natural sugars, like fructose, glyceraldehyde-3-phopshate, and glucose-6-phosphate.5,67 Ten times more fructose-derived AGEs form after 5 days than glucose-derived AGEs in vivo.68 Intracellular AGE formation significantly increases in endothelial cells after 1 week in a hyperglycemic environment.
All in all, it looks like it could be a problem. Furthermore, although Kurt Harris recently said (in Rosedale safe starch thread) that there are de-glycation pathways, I read around that glycation is irreversible:
In contrast to glycosylation, glycation refers to the covalent linkage of saccharides such as glucose to proteins by a nonenzymatic and irreversible process that is elevated in various diseases and may be a factor in the pathology of aging
What troubles me the most is that DHA/EPA seem to be the worst. From here:
Note that this equation makes the omega-3 fatty acids DHA and EPA (with their 6 and 5 double bonds, respectively) the worst offenders.
This is also conclusion of study: "Plasma levels of antioxidant vitamins in relation to ischemic heart disease and cancer"
In conclusion, the presently available data
suggest that in order to achieve the potentially
maximum prophylactic effect of the essential
antioxidants against important health hazards
a minimum daily intake can be recommended
for fl-carotene of 15 mg, vitamin C of 100 mg,
and vitamin E of 60 IU. Even higher intakes
may be necessary for optimum health and
during PUFA-enriched diets.
Thats when I decided to supplement it either on empty stomach, with vitamin C which prevents glycation (is there anything in the world that vitamin C doesn't do ?), or with low carb meal:
The inhibitors included ascorbic acid, tocopherol, pyridoxal, niacinamide, sodium selenite, selenium yeast, and carnosine. A significant correlation was found between the inhibition of glycation and the inhibition of AGE formation (P < 0.001). One of the nutrients, ascorbic acid, was used in a pilot study. Eighteen normal subjects, 7 college age and 10 middle age, were supplemented with 1,000 mg of ascorbic acid in the form of Re-Natured Vitamin C® for a period of 4 weeks. Serum protein glycation was decreased an average of 46.8% (P < 0.01).
To be honest, there are some in-vitro studies claiming vitamin C is glycation agent, most are realted to eye lenses and this one is not. However, those are ALL in-vitro and in-vivo studies never found such thing to my knowledge and eyes are naturally very high in vitamin C, probably to protect it from pathogen exposure as they are in direct contact with the world. There are even protocols to help with glaucoma where you sip vitamin C in eyes and some people do it as prevention. Furthermore, animals would glycate at fantastic speed if that was the case. So I don't think those studies are relevant. On the other hand, apart from mentioned one there are several in-vivo studies. See here, here or here