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Cooking and AGE prevention


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#1 stephen_b

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Posted 30 March 2008 - 07:54 PM


I was reading in the April 2008 issue of LEF magazine (p. 37) an article about the impact of AGE content in prepared foods. I knew about AGE (advanced glycation endproduct) formation and the importance of supplements like benfotiamine that break their bonds down, but I was unaware of how important preparation method is to the AGE content of the foods you eat.

Actually, I was under the false impression that AGEs form only in the body. It turns out that certain methods of preparing foods, high temperature cooking methods like searing, grilling, and frying, can have a big impact on the level of AGEs the food will have when it's eaten.

In the "What your doctor may not tell you about diabetes" book summarized by the article, the case is made that 1) that AGE ingestion is particularly bad for diabetics, 2) that diabetes is in certain ways an accelerated form of aging, and that 3) those interested in slowing aging should pay attention to how much AGEs they eat.

Maybe blackened fish, bar-b-que, and wok cooking are not the way to go, or does benfotiamine supplementation by itself solve the problem? Has anyone changed the way they eat and cook out of concern for AGE formation?

Stephen

#2 balance

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Posted 30 March 2008 - 10:30 PM

Benfotiamine cannot solve this problem entirely, not even if taken in conjunction with other nutrients, you can however minimize the damage significantly. Obviously, if you really are into longevity, avoiding those cooking methods/foods is the way to go. Having a high dose benfotiamine, high dose carnosine, carnitine, lipoic acid, B6, green tea, and some DMAE would be very beneficial against glycation.

You are referring to April 2003 issue, not 2008, that's not released yet.

Edited by piet3r, 30 March 2008 - 10:31 PM.


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#3 stephen_b

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Posted 30 March 2008 - 11:42 PM

This being LEF, the article is of course followed by an add for their mitochondrial optimizer product, which has many of the things in your list. Funny how they do that. :) The article is actually from the April 2008 issue; it came in the mail a few weeks ago. I didn't know that green tea or DMAE help, but that's good to hear.

Wikipedia seems to have a nice article on AGEs, but they neglect to mention benfotiamine. Apparently there's a drug alagebrium in trials as an AGE breaker.

Stephen

#4 Gerald W. Gaston

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Posted 31 March 2008 - 12:20 AM

This being LEF, the article is of course followed by an add for their mitochondrial optimizer product, which has many of the things in your list. Funny how they do that. :) The article is actually from the April 2008 issue; it came in the mail a few weeks ago. I didn't know that green tea or DMAE help, but that's good to hear.

Wikipedia seems to have a nice article on AGEs, but they neglect to mention benfotiamine. Apparently there's a drug alagebrium in trials as an AGE breaker.

Stephen


Yep the 7 page article by Dr. Steve Joyal (he's the guy on the cover with better hair than most 15yrs olds). I take 150mg benfotiamine per meal and also Carnosine and BA, drink green tea etc... but this article was the final nudge to move most of my few remaining fried foods to poached, steamed, boiled, low heat crock pot, etc. We all know we should but its not always easy to do with todays fast-paced lifestyles.

Search the forum and you will find a few folks here are taking alagebrium (ALT-711).

#5 s123

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Posted 31 March 2008 - 10:49 PM

Green tea against AGEs: http://www.jstage.js.../30/8/1369/_pdf

Good info about AGE's:
http://www2.warwick....age/imars_chem/
http://www.andersonc...n_top/ages.html

Most recently, evidence from animal studies points to AGE restriction as an effective means for extending median life span, similar to that previously shown by marked caloric restriction.

Source: http://www.annalsnya...ract/1043/1/452

I have read about sorbitol and AGEs. The polyol pathway (sorbitol pathway) causes the formation of AGEs. This is because sorbitol is converted to fructose which can cause AGEs (maybe worse than glucose) but can sorbitol form AGEs directly without fist being converted to fructose. I have read that sorbitol can’t because it lacks the reactive ‘site’. Glucose for example has an aldehyde group and it’s this group that causes the formation of AGEs. But maybe sorbitol can cause AGEs (without first being converted into fructose) under certain conditions? Does anyone knows the answer?

#6 health_nutty

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Posted 31 March 2008 - 10:58 PM

I've been more aware and tried to do more boiling or at least use lower heat to grill or "pan fry" (or wrap in aluminum foil when bbqing).

#7 yoyo

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Posted 31 March 2008 - 11:28 PM

are consumed AGEs a problem? i would have thought digestion would take care of them.

#8 s123

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Posted 31 March 2008 - 11:38 PM

are consumed AGEs a problem? i would have thought digestion would take care of them.


It seems to be a problem. Like I stated above:

Most recently, evidence from animal studies points to AGE restriction as an effective means for extending median life span, similar to that previously shown by marked caloric restriction.


You cannot consider AGEs as just proteins with sugar molecules added to them. When a sugar molecule is added to the protein it undergoes a whole range of chemical changes (schiff base reaction, amadori reaction,...). Probably these changes will prevent the breakdown of these molecules.

#9 lynx

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Posted 01 April 2008 - 02:25 PM

My understanding is that AGE molecules activate the RAGE receptor, which is proinflammatory. Certainly functional AGE molecules in the body are detrimental, but provided that inflammatory processes are held in check, dietary AGE might not be that bad.

#10 stephen_b

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Posted 04 April 2008 - 03:58 AM

I found this study's abstract interesting:

Diet-Derived Advanced Glycation End Products Are Major Contributors to the Body's AGE Pool and Induce Inflammation in Healthy Subjects
Advanced glycation end products (AGEs) are a heterogeneous group of compounds that form continuously in the body. Their rate of endogenous formation is markedly increased in diabetes mellitus, a condition in which AGEs play a major pathological role. It is also known, however, that AGEs form during the cooking of foods, primarily as the result of the application of heat. This review focuses on the generation of AGEs during the cooking of food, the gastrointestinal absorption of these compounds, and their biological effects in vitro and in vivo. We also present preliminary evidence of a direct association between dietary AGE intake and markers of systemic inflammation such as C-reactive protein in a large group of healthy subjects. Together with previous evidence from diabetics and renal failure patients, these data suggest that dietary AGEs may play an important role in the causation of chronic diseases associated with underlying inflammation.

s123, thanks for the links. I'm a little flabbergasted after reading this:

Bread crusts are a convenient source of high AGE content food. An experimental group of rats were fed chow with bread crusts replacing 25% of the wheat flour in the control group. Both groups were pair-fed resulting in each pair of animals having identical calorie intake. The rats fed bread crusts for six weeks weighed ~25% more and had higher internal organ weight than the control group fed regular rat chow. The rats fed bread crust also had a 3 times higher level of a tumor causing agent and had approximately 70% kidney function loss (proteinuria) (link).

Ouch.

Stephen

#11 niner

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Posted 04 April 2008 - 04:31 AM

I found this study's abstract interesting:

Diet-Derived Advanced Glycation End Products Are Major Contributors to the Body's AGE Pool and Induce Inflammation in Healthy Subjects
Advanced glycation end products (AGEs) are a heterogeneous group of compounds that form continuously in the body. Their rate of endogenous formation is markedly increased in diabetes mellitus, a condition in which AGEs play a major pathological role. It is also known, however, that AGEs form during the cooking of foods, primarily as the result of the application of heat. This review focuses on the generation of AGEs during the cooking of food, the gastrointestinal absorption of these compounds, and their biological effects in vitro and in vivo. We also present preliminary evidence of a direct association between dietary AGE intake and markers of systemic inflammation such as C-reactive protein in a large group of healthy subjects. Together with previous evidence from diabetics and renal failure patients, these data suggest that dietary AGEs may play an important role in the causation of chronic diseases associated with underlying inflammation.

I'm not sure what "contributors to the body's AGE pool" means. If the AGE pool refers to circulating AGEs, then that would make sense. Although I don't want circulating AGEs which would be pro-inflammatory, at least they are quickly excreted. I'm more concerned about extracellular AGEs, which are hard to get rid of and cause all sorts of problems. I don't see how consuming AGEs in foods could cause those.

s123, thanks for the links. I'm a little flabbergasted after reading this:

Bread crusts are a convenient source of high AGE content food. An experimental group of rats were fed chow with bread crusts replacing 25% of the wheat flour in the control group. Both groups were pair-fed resulting in each pair of animals having identical calorie intake. The rats fed bread crusts for six weeks weighed ~25% more and had higher internal organ weight than the control group fed regular rat chow. The rats fed bread crust also had a 3 times higher level of a tumor causing agent and had approximately 70% kidney function loss (proteinuria) (link).

Ouch.

Wow. That's pretty amazing, if true. 25% weight increase?! Holy crap, I mean how can that even be? Were these rats eating the same number of calories? Did the bread crusts taste better to the rats? This totally vindicates my six year old, who wants me to cut the crusts off his toast.

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#12 s123

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Posted 04 April 2008 - 03:42 PM

Bread crusts are a convenient source of high AGE content food. An experimental group of rats were fed chow with bread crusts replacing 25% of the wheat flour in the control group. Both groups were pair-fed resulting in each pair of animals having identical calorie intake. The rats fed bread crusts for six weeks weighed ~25% more and had higher internal organ weight than the control group fed regular rat chow. The rats fed bread crust also had a 3 times higher level of a tumor causing agent and had approximately 70% kidney function loss (proteinuria) (link).



And some people are suggesting that we should consume more bread crusts because they contain an AGE that works as an antioxidant.

Aroma and colouring compounds in food form under the influence of heat in the course of non-enzymatic browning reactions. Different chemical reactions result in many browning products, among others the so-called melanoidines. Due to the complex and frequently high-molecular structures of the melanoidines, only a few physiologically active compounds have so far been identified and quantified in foods. Among these are pronyl lysine, first detected in bread crust, and N-methylpyridinium, whose formation is associated with the roasting degree of coffee beans. Both compounds have been found to be chemopreventively active in isolated intestinal cells, and N-methylpyridinium also in animal experiments. Pronyl lysine, furthermore, is the most effective antioxidant in bread crust. Antioxidative action of melanoidines has been shown in in-vitro-studies on roasted coffee and after consumption of espresso coffee in healthy test persons. Furthermore, it is assumed that melanoidines are capable of forming intestinal complexes of compounds detrimental to health and, thus, may reduce the exposition of the organism to potentially mutagenic or cancerogenic compounds. A prebiotic action of melanoidines is also discussed; after incubation with samples of human faeces, the growth of lactobacilli and of bifidobacteria increased. These antimutagenic, anticancerogenic and prebiotic effects could so far not be related to certain structures, however. This also applies to an anticariogenic action now discussed, which so far has only been shown for melanoidines in roasted coffee. Future research should be concerned with relating the effects of chemically defined melanoidines to certain structures. Concentrations of health-promoting melanoidines in heat-treated foods could then be optimized by selection and composition of the initial products and by specific processing technologies.


Source: http://www.cababstra...cNo=20053133664

Edited by s123, 04 April 2008 - 03:44 PM.





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