A lot of paleo/primal recipes and cooking methods seem to overlook the issue of heat damage to fats and protein, making liberal use of frying or sauteing, in other words cooking things in fat (paleo fats like butter and coconut oil, but still) at a very high temperature. Supposedly, this is a major source of Advanced Glycation End-products, or AGEs, which arise from fat and protein being glycated. These seem to have numerous detrimental health effects, such as increasing endothelial damage (i.e. to the lining of the blood vessels) and accelerating the aging process.
In addition, there is the question of oxidative changes to fats when they are heated, particularly the more unstable (i.e. unsaturated) fats, which is also thought to be detrimental.
So... how important is it to avoid this? And what are the best strategies to do so without resorting to a raw-food diet?
(personally I try to never cook things in fat, but rather add any fat at the end of the cooking process to add calories and/or flavour)
asked byarchaea (2254)
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on February 22, 2010
at 04:09 PM
It seems that AGEs and ALEs produced inside the body are more harmful than those produced during cooking. The data on the negative health effects of exogenous AGEs/ALEs is somewhat unclear.
A couple of observations from the literature:
- The amount of AGEs eaten isn't necessarily reflected in plasma levels of AGEs
- Fructose is much more prone to form AGEs than glucose
- PUFAs are even worse than fructose
Fructation, glycation and lipid peroxidation can all happen within the body as well as outside the body, so simply avoiding heating isn't enough if you want to avoid AGEs and ALEs.
The accumulation of AGEs/ALEs is recognized as one of the seven types of aging damage, but as far as I know, it's still unclear how dangerous they are in the grand scheme of things.
Some ways to avoid AGEs/ALEs:
- Avoid cooking with high heat for long periods
- Avoid cooking with PUFAs
- Avoid an excess intake of PUFAs
- Avoid an excess intake of fructose
- Eat foods that inhibit AGEs/ALEs (carotenoids, green tea, etc)
- Supplement with AGE breakers (pyridoxamine, aminoguanidine, etc)
See the link on PUFAs for more information.
on February 21, 2010
at 07:55 AM
Dietary AGEs don't really have anything to do with endogenous glycation in the body. Glycated amino acids, even if they were absorbed in the gut, would not end up causing damage because they are no longer reactive, and would not get incorporated into your body's proteins.
on October 19, 2011
at 09:09 AM
Masterjohn made a new post recently about glycation showing a ketogenic/atkins diet is the most glycating diet. And insulin is protective against glycation. So you could make the argument high carb insulin spiking diets are the best for anti-glycation and longevity, which happens to fit nicely with epidemiological evidence.
on October 19, 2011
at 07:25 AM
There are some more studies:
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
on September 04, 2011
at 10:55 PM
I think evidence suggests AGEs can meaningfully affect health.
What I'm less certain about is whether amounts of AGE normally encountered with say, McDonald's fried potatoes, are an important factor in health/disease (and if so, how important). I also wonder if the type of oil used in frying has a significant effect (i.e. unstable PUFAs vs stable saturated fats).
Can someone clarify if the amounts of AGE in everyday foods should be of concern?