Do You Try To Avoid Advanced Glycation End-product?

barbwirehouse

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https://en.wikipedia.org/wiki/Advanced_ ... nd-product

In human nutrition and biology, advanced glycation end products, known as AGEs, are substances that can be a factor in the development or worsening of many degenerative diseases, such as diabetes, atherosclerosis, chronic renal failure, and Alzheimer's disease.

Dietary AGEs (dAGEs) can be present in some foods (particularly meat, also butter and some vegetable products), and can form in food during cooking, particularly in dry cooking such as frying, roasting and baking, far less so in boiling, stewing, steaming and microwaving.

http://www.sciencedaily.com/releases/20 ... 094144.htm

They cooked 549 foods by different methods and measured the AGE content of the cooked food. They found that the higher the cooking temperature, the higher the AGE content. For example, 100 grams of raw beef had 707 kU of AGEs, but 100 grams of roast beef had 6071 kU.

http://anti-inflammatoryremarks.blogspo ... s.html?m=1[3]

An example would be a raw chicken breast, if you boil it, you will increase the AGEs about 50%, microwaving increases AGEs two-fold, broiling increases AGEs eight-fold, and frying will multiply AGEs ten-fold.

http://inhumanexperiment.blogspot.com.a ... foods.html
 

jyb

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Yet another concern for the typical restaurant meat menu.
 

jyb

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http://www.google.com/patents/US20130040812 same as activated charcoal?

Other sources of AGEs according to Wikipedia...

In diabetes[edit]
In diabetes, in cells unable to reduce glucose intake (e.g., endothelial cells), hyperglycemia results in higher intracellular glucose levels.[8] [9][10] Higher intracellular glucose levels result in increased levels of NADH and FADH, increasing the proton gradient beyond a particular threshold at which the complex III prevents further increase by stopping the electron transport chain.[11] This results in mitochondrial production of reactive oxygen species, activating PARP1 by damaging DNA. PARP1, in turn, induces ADP-ribosylation of GAPDH, a protein involved in glucose metabolism, leading to its inactivation and an accumulation of metabolites earlier in the metabolism pathway. These metabolites activate multiple pathogenic mechanisms,[which?] one of which includes increased production of AGEs.[citation needed]

In diabetics who have an increased production of an AGE, kidney damage reduces the subsequent urinary removal of AGEs, forming a positive feedback loop that increases the rate of damage. A 1997 study concluded that adding sugar to egg whites causes diabetics to be 200 times more AGE immunoreactive
 
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barbwirehouse

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What paleo dieters think about them - http://robbwolf.com/2010/10/26/the-pale ... pisode-51/


"The medical and nutrition community have the bad habit of always looking toward exogenous sources when they identify something bad. In this case, it has been shown that AGEs within the body, as a result of insulin resistance and hyperglycemia, increases the rate of aging and the risk of diseases such as heart disease. The medical community then identifies food sources of AGEs and recommends that we do not consume them. Interestingly the consumption of foods containing AGEs has not been shown to be all that problematic (maybe a little bit of arterial dysfunction but even that study is questionable).



The real problem is often endogenous production, as opposed to exogenous sources. AGEs result when blood sugars are elevated. AGE formation is rampant when blood sugar levels reach 180 mg/dL or higher. But high blood sugar levels are the result of insulin resistance, which is the result of excess carbohydrate, specifically fructose, consumption. AGEs are problematic when they result from excess blood sugar levels, not so much when they are consumed from food. That being said, it is wise to try to minimize AGE consumption and slow cooking at low temperatures is one way to do that.


I slow cook everything at low temperatures in a crock pot or the oven. Boiling meat does not appeal to me in any way."
 
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AGEs within the body, as a result of insulin resistance PUFA and hyperglycemia PUFA (according to Ray Peat)
 

Kasper

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AGEs within the body, as a result of insulin resistance PUFA and hyperglycemia PUFA (according to Ray Peat)

I doubt that he says that, would be quite off if he did.
 
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Kasper said:
AGEs within the body, as a result of insulin resistance PUFA and hyperglycemia PUFA (according to Ray Peat)

I doubt that he says that, would be quite off if he did.

I think Ray Peat said polyunsaturated fats create them five times better than sugar.
 

schultz

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From Rays article on unsaturated fat

The fragments of deteriorating PUFA combine with proteins and other cell materials, producing immunogenic substances. The so-called "advanced glycation end products," that have been blamed on glucose excess, are mostly derived from the peroxidation of the "essential fatty acids." The name, “glycation,” indicates the addition of sugar groups to proteins, such as occurs in diabetes and old age, but when tested in a controlled experiment, lipid peroxidation of polyunsaturated fatty acids produces the protein damage about 23 times faster than the simple sugars do (Fu, et al., 1996).

From Rays article on Glycemia, starch, and sugar in context

The bulk of the age-related tissue damage classified as “glycation end-products” (or “advanced glycation end-products,” AGE) is produced by decomposition of the polyunsaturated fats, rather than by sugars, and this would be minimized by the protective oxidation of glucose to carbon dioxide.
 

Kasper

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The bulk of the age-related tissue damage classified as “glycation end-products” (or “advanced glycation end-products,” AGE) is produced by decomposition of the polyunsaturated fats...

Wow... I guess biochemistry is not Ray Peat's strongest point. :roll:

Fact is, without protein you can't produce any AGE, without PUFA's you can. You can produce ALE's from PUFA, I think he means that, or maybe when he wrote this when ALE's where classified as a subset of AGE 's?

Otherwise this is just nonsense. This is better information about AGE/ALE: http://www.waiwiki.org/index.php?title= ... d_reaction
 

BingDing

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Kasper said:
The bulk of the age-related tissue damage classified as “glycation end-products” (or “advanced glycation end-products,” AGE) is produced by decomposition of the polyunsaturated fats...

Wow... I guess biochemistry is not Ray Peat's strongest point. :roll:

Fact is, without protein you can't produce any AGE, without PUFA's you can. You can produce ALE's from PUFA, I think he means that, or maybe when he wrote this when ALE's where classified as a subset of AGE 's?

Otherwise this is just nonsense. This is better information about AGE/ALE: http://www.waiwiki.org/index.php?title= ... d_reaction

From the link you cited:

Alpha-Lipoic acid inhibits AGEs formation [76] by inhibiting lipid peroxidation...

Taurine (from cysteine, fish or meat) inhibits AGE formation by inhibiting lipid peroxidation...

IMHO, Ray knows as much about biochemistry as anyone on earth.

Edit: To answer the question, I don't worry about, though my diet doesn't expose me to much of the common ways of forming it. Minimizing PUFA and keeping systemic antioxidants up is enough, I think.

From the interesting factoid department, when you slice open an apple and leave in on the counter for a few days, the brown skin that develops on the flesh is an AGE. As is the film on the surface of a cup of coffee with cream. The longer either is left out the thicker the AGE gets.
 
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LOL Ray Peat's problem is that he knows too much about it, not too little. There is not necessarily an immediate link between what he says, or remembers, is involved in what reaction. This is what makes his articles necessary and not a waste of internet like other "gurus" or textbook copy-paste blogs.
 

jyb

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A lot of discussions on AGEs over the internet, past and present. PUFA related harmful products have been described by Ray but others too. Three interesting claims that I've come across at least once are that exogenous products (e.g., barbecue) are not important compared to endogenously produced ones, that hyperglycaemic diabetic people tend to produce more AGEs and that the combination the PUFA and high glycaemia might be the most harmful combination.
 

stargazer1111

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I think the discrepancy here is that ALE and AGE result in the same end byproducts, if I'm remembering correctly. ALEs produce the damage much faster than AGEs, I think.
 

YourUniverse

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As for removal of AGEs, I have not asked Ray and have not found a solid answer online. It may be like lipofuscin, where Ray has said "once [lipofuscin] stops forming, it will slowly remove".

Vitamin E and aspirin to blunt PUFA, b1, b3 and sugar to increase CO2, but for removal of existing AGEs? Alcohol, proteolytic enzymes (Serra, bromelain)?

Alcohol is very interesting, because it can be made by fermenting fruit, which can occur within our intestines.
 

mimmo123

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Glucose and sucrose for diabetes.

Increasing the rate of respiration by replacing the fats with glucose reduces the availability of electrons that can trigger lipid peroxidation and produce toxic free radicals, and the shift of fuel also increases the amount of carbon dioxide produced, which can protect the protein amino groups such as lysine from glycation and lipoxidation.

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Carbon dioxide protects nerves and muscles against excessive excitation. It inhibits lactic acid formation, and lipid peroxidation (measured in the blood) can be completely suppressed by a pC02 of about 90 mm, which isn't high enough to produce acidosis.
 

cs3000

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D-ribose increases this a lot apparently. and lowers blood glucose at ~14g human dose but not ~7g.
But both doses increased AGE , increased inflammation & i think both induced kidney damage

I was gonna try ribose for speeding up bowel transit time but this looks like a bad idea
 
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Motorneuron

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Any natural inhibitors about it? so milk, yogurt and cheese have less impact?
 
EMF Mitigation - Flush Niacin - Big 5 Minerals

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