76 replies to this topic

[wydell]

A few question to those with a better understanding of chemistry than mine:

Why is butter so high in AGEs (or ALEs)?

Butter is mostly saturated and monounsaturated, so it should not oxidise easily, right? Yet, since butter is almost entirely fat, isn't lipid peroxidation the only way butter would have AGEs/ALEs?

What about other highly saturated fats, like coconut oil or palm oil - would they be low in AGEs? A lot of the studies on AGEs warn against using saturated fat, but it seems that polyunsaturated fats would be a much bigger problem. Maybe I'm missing something.

One guess: butter is pasteurized, though I don't know if the age content would be different from a butter made from raw cream

[CobaltThoriumG]

A few question to those with a better understanding of chemistry than mine:

Why is butter so high in AGEs (or ALEs)?

Butter is mostly saturated and monounsaturated, so it should not oxidise easily, right? Yet, since butter is almost entirely fat, isn't lipid peroxidation the only way butter would have AGEs/ALEs?

What about other highly saturated fats, like coconut oil or palm oil - would they be low in AGEs? A lot of the studies on AGEs warn against using saturated fat, but it seems that polyunsaturated fats would be a much bigger problem. Maybe I'm missing something.

One guess: butter is pasteurized, though I don't know if the age content would be different from a butter made from raw cream

I think it's something other than pasteurization because the AGE data for milk is low and I assume they tested pasteurized milk. Same question for cheese, why so high? Yogurt, like milk, is low.

[Michael]

All:

I've been meaning to post on this for a while. As already discussed, and put in spreadsheet format by Edward last year, per the previous report,(2) using an assay of just ONE AGE (CML -- an important caveat, as glycotoxins are a highly complex and heterogeneous mix, with different underlying substrates and reaction chemistries), cooking fats and proteins together appeared to generate much higher levels of nasties than simply cooking carb, tho' one expects that mixing simpler carbs PLUS protein and fat (say, in a sugary- or even fruit-juice-sauced stirfry) is the worst of all.

One striking oddity in this list was a relaively high content of CML in olive oil, which should be chemically impossible, due to its lack of substrate (lysine). (1) in fact reports that "We could not detect CML in olive oil above the level present in the blank" and chalks the earlier report (2) down to experimental error. Moreover, after following a much more painstaking protocol to test a much more limited range of foods, white bread crust came out several times HIGHER in CML per gram than does fried, minced beef, contrary to Vlassara's earlier findings. Here is their Table 5, where all the goods are:



While of course most people eat a whole slice of bread (if one eats the junk at all, of course), of which most of the mass is lower in CML, I speculate that the crust may not be too much higher than much of the mass of a piece of toast.

Again, there are all kinds of other glycotoxins, and we don't know either how this compares to any other specific glycotoxins, nor WHICH glycotoxins are most injurious to health.

An easy rule is, of course, to avoid foods cooked at high temperatures and/or for extneded periods, rather than focussing on any ONE possible offender. Note that cooking WITH fats and sugars is both silly and largely unnecessary: eg, one can "stirfry" protein sources in water with spices, and then add sugary stuff and fats after turning off the heat and stirring up.

-Michael

1: Assar SH, Moloney C, Lima M, Magee R, Ames JM. Determination of
Nepsilon-(carboxymethyl)lysine in food systems by ultra performance liquid chromatography-mass spectrometry. Amino Acids. 2009 Feb;36(2):317-26. Epub 2008 Apr 4. PubMed PMID: 18389168.

2. J Am Diet Assoc. 2004 Aug;104(8):1287-91.
Advanced glycoxidation end products in commonly consumed foods.
Goldberg T, Cai W, Peppa M, Dardaine V, Baliga BS, Uribarri J, Vlassara H.
PMID: 15281050 [PubMed - indexed for MEDLINE]

[JLL]

Nice find, thanks for posting that.

I also wondered about the AGEs in olive oil. My understanding of chemistry is very limited, but why wouldn't it be possible for some CML to be formed in olive oil from the peroxidation of unsaturated fatty acids?

[aikikai]

Vegetables AGEs (U/g) Serving (g) AGEs/serving (kU)
Broccoli, carrots, celery, grilled 2,260 100 226
Carrots, canned 103 100 10
Green beans, canned 179 100 18
Onion, raw 358 100 36
Tomato, raw 234 100 23

How can vegetables like onion have serveral times more AGE's than fired bief??

[Michael]

I also wondered about the AGEs in olive oil. My understanding of chemistry is very limited, but why wouldn't it be possible for some CML to be formed in olive oil from the peroxidation of unsaturated fatty acids?

Again, CML is "carboxymethyllysine": no lysine, no CML. Indeed, no protein, no AGE per se -- tho' there are Maillard toxins formed from cooking without them, such as anything caramelized. And of course, lipid peroxidation products aren't good for one, either ...

Vegetables AGEs (U/g) Serving (g) AGEs/serving (kU)
Broccoli, carrots, celery, grilled 2,260 100 226
Carrots, canned 103 100 10
Green beans, canned 179 100 18
Onion, raw 358 100 36
Tomato, raw 234 100 23

How can vegetables like onion have serveral times more AGE's than fired bief??

They can't, of course: it looks like you're directly comparing Vlassara's study, in arbitrary units (U), to Assar et al, who report in mg. (And, again, you probably couldn't directly compare anyway, as Vlassara's data are from a much rougher and apparently sometimes inaccurate method). Look instead at the numbers from Vlassara for :

Beef, Hamburger, fried, 6 min 26,000 90 2,300,000

-Michael

Edited by Michael, 17 December 2009 - 08:41 PM.

[JLL]

I also wondered about the AGEs in olive oil. My understanding of chemistry is very limited, but why wouldn't it be possible for some CML to be formed in olive oil from the peroxidation of unsaturated fatty acids?

Again, CML is "carboxymethyllysine": no lysine, no CML. Indeed, no protein, no AGE per se -- tho' there are Maillard toxins formed from cooking without them, such as anything caramelized. And of course, lipid peroxidation products aren't good for one, either ...

Right, thanks for the clarification. Looks like I incorrectly remembered what this paper said: http://www.jbc.org/c...71/17/9982.full

N-(Carboxymethyl)lysine (CML) is an advanced glycation end product formed on protein by combined nonenzymatic glycation and oxidation (glycoxidation) reactions. We now report that CML is also formed during metal-catalyzed oxidation of polyunsaturated fatty acids in the presence of protein.

[niner]

Thanks for that, Michael. A couple things pop out at me: Pasteurization of milk is not that bad after all, at least as measured by CML, which does seem like a good AGE marker for milk. Butter looks much nicer here than in other reports, but again, it's CML, and how much lysine is really there? So butter is still a question mark I suppose. Finally, this validates my crusade to make cutting crusts off of bread socially acceptable (based on rat data and earlier measurements). Just say no to crusts! I never liked the taste of them anyway. The AGE level of the inside of the bread is quite low.

[kismet]

Thanks for that, Michael. A couple things pop out at me: Pasteurization of milk is not that bad after all, at least as measured by CML, which does seem like a good AGE marker for milk.

Well, there's no reason it should be high in AGEs. Pasteurisation - contrary to "health" propaganda - is a very quick and painless procedure. The stuff's basically raw. I haven't seen any evidence suggesting the contrary (mechanistic speculation *presupposing/assuming* that pasteurisation is responsible for high AGE levels is not really evidence).

Good that I've already gotten used to cutting off any crusts.

As to the lysine & olive oil. I think I've argued along those lines elsewhere (there's no darn lysine in there!), although, I speculated that it may've been contaminated by protein somehow..

Edited by kismet, 17 December 2009 - 10:16 PM.

[JLL]

Another blog post related to the subject of glycation & lipid peroxidation:

Carotenoids and Lipid Peroxidation: Can Vegetables & Fruit Reduce ALEs?

Carotenoids may be effective in reducing lipid peroxidation and thus the accumulation of ALEs. Lutein in particular seems useful: at doses of 5-10 mg per day, it has been shown to increase plasma levels of lutein and reduce some of the markers of lipid peroxidation. Other carotenoids, such as astaxanthin and bixin, may be beneficial as well.

It should be noted that some of the evidence is contradictory. Some studies have found no benefit, and one study even found a slight increase in lipid peroxidation from various carotenoids. A certain balance of carotenoids may be necessary for inhibiting the formation ALEs; lycopene in particular may be important.

[Skötkonung]

Another blog post related to the subject of glycation & lipid peroxidation:

Carotenoids and Lipid Peroxidation: Can Vegetables & Fruit Reduce ALEs?

Carotenoids may be effective in reducing lipid peroxidation and thus the accumulation of ALEs. Lutein in particular seems useful: at doses of 5-10 mg per day, it has been shown to increase plasma levels of lutein and reduce some of the markers of lipid peroxidation. Other carotenoids, such as astaxanthin and bixin, may be beneficial as well.

It should be noted that some of the evidence is contradictory. Some studies have found no benefit, and one study even found a slight increase in lipid peroxidation from various carotenoids. A certain balance of carotenoids may be necessary for inhibiting the formation ALEs; lycopene in particular may be important.

As always JLL, another great post.

[TheFountain]

'It should be noted that some of the evidence is contradictory. Some studies have found no benefit, and one study even found a slight increase in lipid peroxidation from various carotenoids.'

It's shit like this that makes me question some of the ethics of people conducting these studies. Who knows who is being honest in the end?

[Skötkonung]

'It should be noted that some of the evidence is contradictory. Some studies have found no benefit, and one study even found a slight increase in lipid peroxidation from various carotenoids.'

It's shit like this that makes me question some of the ethics of people conducting these studies. Who knows who is being honest in the end?

Carotenoids can be structurally different, hence the multiple derivatives. In some of the studies, some types of carotenoids provide more benefit than others. Sometimes the quantity of benefit is so small that it is with the margin of error. Other times a unique synergy exists between multiple nutrient groups.

If you are looking for definitive, black and white, answers you will find very little of them in Nutrition. The field is relatively new and is still evolving. Right now we only have varying degrees of probability.

[InquilineKea]

Hmm, a lot foods with low AGEs on this table have very high acrylamide content (on acrylamide tables). A lot of the cereals and baked products, for example, have low AGEs on this table, but some of them have really high acrylamide levels (even when they dont have that much fat or protein)

Also, are the cashews I get from Costco roasted ones? Or are they raw ones, and relatively AGE-free?

Microwaving doesn't seem to increase AGE-content as much as other types of cooking do. It irritates me that my parents (who are asian) keep on thinking that "microwaves are bad" and "cooked foods are good" when in reality, it's far from the case.

[JLL]

Also, are the cashews I get from Costco roasted ones? Or are they raw ones, and relatively AGE-free?

What, you can't tell by the color?

[Sillewater]

Just thought I would post some studies I came upon (sorry again for the lack of explanation).

Food Chemistry Volume 121, Issue 4, 15 August 2010, Pages 1039-1045
Inhibitory effect of fermentation byproducts on formation of advanced glycation end-products
Xiu-Juan Yea, T.B. Nga, , and Ryoji Nagaib

Pharmacol Res. 2010 Jun;61(6):482-8. Epub 2010 Feb 25.
The multifaceted therapeutic potential of benfotiamine.
Balakumar P, Rohilla A, Krishan P, Solairaj P, Thangathirupathi A.

Food Chemistry Volume 120, Issue 1, 1 May 2010, Pages 261-267
Inhibitory effects of microalgal extracts on the formation of advanced glycation endproducts (AGEs)
Zheng Suna, Xiaofang Penga, Jin Liua, King-Wai Fana, Mingfu Wang, a, and Feng Chen, a,

Food Chemistry Volume 122, Issue 3, 1 October 2010, Pages 768-774
Comparison of anti-glycation capacities of several herbal infusions with that of green tea
Su-Chen Hoa, , , Szu-Pei Wub, Shyh-Mirn Linc and Ya-Li Tangc

Biol Pharm Bull. 2010 Feb;33(2):329-33.
3,5-Di-O-caffeoyl-epi-quinic acid from the leaves and stems of Erigeron annuus inhibits protein glycation, aldose reductase, and cataractogenesis.
Jang DS, Yoo NH, Kim NH, Lee YM, Kim CS, Kim J, Kim JH, Kim JS.

Anti-glycation Effect of Spices and Chilies Uses in Traditional Mexican Cuisine

Some interseting journal articles by Wang M.
http://www.hku.hk/bi...wmf/wmfpub.html

Edited by Sillewater, 12 May 2010 - 10:38 AM.

[Jay]

Interesting articles. I am reading through some of them now. Thanks.

Can anyone PM me the full text of this study? I want to see if there is any commentary on why butter is so high in AGEs, a fact that still perturbs me.

Edited by Jay, 12 May 2010 - 03:35 PM.

[Michael]

Can anyone PM me the full text of this study? I want to see if there is any commentary on why butter is so high in AGEs, a fact that still perturbs me.

Ahem. Please see post 33 in this thread .

[stephen_b]

Michael, you comment in post 33 refers to olive oil. Any thoughts on whether the butter numbers reflect heated butter?

[Lucas]

The kind of oil used to fry interferes with the content of AGE of the fried food? For example, I usually cook for only 3-4 minutes my meat in coconut oil/grass-fed butter. Can I expect to be eating less AGEs than for example, the same time of cooking but with safflower oil?

[JLL]

Depends on which kind of AGE you mean; or rather, whether you mean ALEs (a result of lipid peroxidation) or AGEs or both.

Coconut oil is less prone to lipid peroxidation, but I'm not sure whether it causes less glycation than safflower oil when it reacts with sugar -- anybody?

[Sillewater]

found over at sci.life.extension

Advanced Glycation End Products in Foods and a Practical Guide to Their Reduction in the Diet.

J Am Diet Assoc. 2010 Jun;110(6):911-916.e12.
Advanced Glycation End Products in Foods and a Practical Guide to
Their Reduction in the Diet.
Uribarri J, Woodruff S, Goodman S, Cai W, Chen X, Pyzik R, Yong A,
Striker GE, Vlassara H.
Abstract
Modern diets are largely heat-processed and as a result contain high
levels of advanced glycation end products (AGEs). Dietary advanced
glycation end products (dAGEs) are known to contribute to increased
oxidant stress and inflammation, which are linked to the recent
epidemics of diabetes and cardiovascular disease. This report
significantly expands the available dAGE database, validates the dAGE
testing methodology, compares cooking procedures and inhibitory agents
on new dAGE formation, and introduces practical approaches for
reducing dAGE consumption in daily life. Based on the findings, dry
heat promotes new dAGE formation by >10- to 100-fold above the
uncooked state across food categories. Animal-derived foods that are
high in fat and protein are generally AGE-rich and prone to new AGE
formation during cooking. In contrast, carbohydrate-rich foods such as
vegetables, fruits, whole grains, and milk contain relatively few
AGEs, even after cooking. The formation of new dAGEs during cooking
was prevented by the AGE inhibitory compound aminoguanidine and
significantly reduced by cooking with moist heat, using shorter
cooking times, cooking at lower temperatures, and by use of acidic
ingredients such as lemon juice or vinegar. The new dAGE database
provides a valuable instrument for estimating dAGE intake and for
guiding food choices to reduce dAGE intake. Copyright © 2010 American

Edited by Sillewater, 28 May 2010 - 06:25 AM.

[Sillewater]

Just some food choices:

Total MG nmol/100 mL Total CML kU/100 mL
Liquids (per 100 mL food)
Milk, whole 620 4.9
Olive oil, fresh (Colavita, Linden, NJ) 7,700 5,852

Food item AGEa kU/100g
Bacon, fried 5 min no added oil 91,577
Butter, whipped 26,480
Avocado 1,577
Beef, ground, boiled, marinated 10 min w/lemon juice 1,538
Egg, fried, one large 2,749
Bagel, toasted 167
Rice, white, quick cooking, 10 min 9
Pasta, cooked 12 min 242
Potato, sweet, roasted 1 h 72
Coconut milk, leche de coco, (Goya) 307
Vegetables, grilled (broccoli, carrots, celery) 226

Summary:

AGE determined by CML Levels
Fats contain more dAGE (dietary AGE per gram of weight)
However since meat is eaten in greater amounts they are the biggest contributor
In meat its possibly due to intracellular components lean muscle containing highly reactive amino-lipids and reducing sugars.

High fat spreads are highest.
Carbohydrate group contained lowest, possibly due to antioxidants and vitamins.
Grains, legumes, breads, vegetables, fruits, and milk are lowest in dAGE

AGE determined by MG Levels
Correlation between MG levels and CML levels, so basically the same.

As we all know, lower heat and moist is better than high heat and dry.

~50% reduction in cooked meat due to acidic marinades.

Average dAGE intake in New York is 14,700+-680 AGE kU/day

(Based on my rough calculation from the data tables my daily dAGE intake is around ~3000kU/day if you exclude butter. (which is considerably less on my fasting days)). I'm sure others on this forum has lower daily dAGE intake than this. Now the only problem is how to balance endogenous and exogenous intake.

[Sillewater]

A very good review on the subject (short and sweet):

Physiol Res. 2010;59(2):147-56. Epub 2009 Jun 19.
Glycotoxines, carbonyl stress and relevance to diabetes and its complications.
Turk Z.

Whereas glucose is involved in glycation
reactions exclusively in its aliphatic form, accounting for only 0.001% of total glucose
concentration, α-oxoaldehydes are characterized by extremely high chemical activity. They
are up to 20,000-fold as reactive as glucose, thus being able to form AGE-structures even at
very low concentrations. Physiologically, α-oxoaldehydes react directly with protein terminal
amino acid residues.

The author got the number from this study which I don't have access too:
Ann N Y Acad Sci. 2005 Jun;1043:111-7.
Dicarbonyl intermediates in the maillard reaction.
Thornalley PJ.

Also from the review:

Some 10% of AGEs ingested are absorbed into the body's
circulation, and over 65% of those absorbed are retained

I also posted this study over here:
J Lipid Res. 2002 Mar;43(3):523-9.
UV analysis of Amadori-glycated phosphatidylethanolamine in foods and biological samples.
Oak JH, Nakagawa K, Miyazawa T.

Where they tried to measuring glycated phosphatidylethanolamine and found none in butter (at least not determinable). But I don't quite have a grasp on whether their method is applicable.

Here's also a very good study on the effects of dAGEs on various physiological measurements:
European Journal of Nutrition
Association of dietary AGEs with circulating AGEs, glycated LDL, IL-1α and MCP-1 levels in type 2 diabetic patients
Pei-chun Chao1, 2, Chien-ning Huang3, Cheng-chin Hsu1, Mei-chin Yin4, 5 and Yu-ru Guo4

When I read over many of the Kitavan studies the subjects had very low HbA1c measurements. Also when I was super gun-ho about paleo and eating very low-carb and lots of meat and veggies, my HbA1c was around 4.8. Based on the study by Pei-chun et al, maybe for all those paleo go-ers its the intermediaries that are causing the higher HbA1c, unlike the high-carb kitavans which consume the much more stable glucose.

[Sillewater]

Are AGEs fat soluble?

Minerva Endocrinol. 2009 Jun;34(2):97-104.
The acute effect of Orlistat on dietary glycotoxins in diabetics and healthy women.
Diamanti-Kandarakis E, Piperi C, Alexandraki KI, Papailiou J, Ekonomou F, Koulouri E, Kandarakis H, Creatsas G.

Endocrine Section, First Department of Medicine, Laiko Hospital, Medical School, University of Athens, Athens, Greece. akandara@otenet.gr
Abstract
AIM: Advanced glycation end products (AGEs) formation is implicated in diabetic complications. Exogenous AGEs, namely glycotoxins, are present in certain foods and are absorbed from the gastrointestinal tract. Experimental data suggest that lifestyle interventions reducing their content in diet have beneficial effect. METHODS: Fourteen healthy (age: 42.14 +/- 12.38 years; body mass index [BMI]: 27.85 +/- 7.06 kg/m2) and ten women with type 2 diabetes (T2DM) (age: 48.70 +/- 9.31 years; BMI: 32.55 +/- 7.14 kg/m2) were enrolled in the study. A meal rich in AGEs was provided in a two-day protocol and on day 2, 240 mg of Orlistat were administered post-meal. RESULTS: On day 1, serum AGEs levels showed a rise at 3 hours post-meal compared to baseline values in both groups (controls: 12.2%; P<0.001), T2DM: 2.6%; P=0.013), but at 5 hours post-meal only in the controls (control: 12.2%; P<0.001); T2DM: 1.9%; P=0.075). On day 2 at 3 hours post-meal control values showed a rise of 3.1% (P=0.003); T2DM of 1.9% (P=0.013); at 5 hours post-meal rise for controls was 4.6% (P=0.012); and for T2DM was 1.8% (P=0.009). The corresponding rise was significantly lower on day 2 only in controls at 3 and 5 hours post-meal (P=0.003; P=0.05, respectively). CONCLUSIONS: Orlistat reduced the absorption of glycotoxins acutely and improved the metabolic profile in the control group, without an apparent beneficial effect in the diabetic group. The clinical significance of this observation should be further investigated in normal population, while in diabetics long-term studies may be required to demonstrate possible clinically significant effects.

PMID: 19471234 [PubMed - indexed for MEDLINE]

[Sillewater]

Is Butter High in AGEs? by Chris Masterjohn.

I was going to look at the issue but Chris Masterjohn beat me to it. The article definitely sounds biased but it makes sense. The low specificity of the test would also explain the high AGE content in olive oil (which has no amino acids). In his post he refers to a chromatography test of butter and milk:

Amino Acids. 2009 Feb;36(2):317-26. Epub 2008 Apr 4.


Determination of Nepsilon-(carboxymethyl)lysine in food systems by ultra performance liquid chromatography-mass spectrometry.
Assar SH, Moloney C, Lima M, Magee R, Ames JM.

Which shows butter isn't as high as what the immunoassay shows us it is. I still don't know what to think considering that if you read the process by which butter is created it is passed through some pretty high temperatures (but the book I read about butter making was from like the 1940s), is there something more recent?

[Skötkonung]

Is Butter High in AGEs? by Chris Masterjohn.

I was going to look at the issue but Chris Masterjohn beat me to it. The article definitely sounds biased but it makes sense. The low specificity of the test would also explain the high AGE content in olive oil (which has no amino acids). In his post he refers to a chromatography test of butter and milk:

Amino Acids. 2009 Feb;36(2):317-26. Epub 2008 Apr 4.


Determination of Nepsilon-(carboxymethyl)lysine in food systems by ultra performance liquid chromatography-mass spectrometry.
Assar SH, Moloney C, Lima M, Magee R, Ames JM.

Which shows butter isn't as high as what the immunoassay shows us it is. I still don't know what to think considering that if you read the process by which butter is created it is passed through some pretty high temperatures (but the book I read about butter making was from like the 1940s), is there something more recent?

I made a separate thread about this but...

One of the primary AGE components of milk products is pyrraline:

Glycation in food and metabolic transit of dietary AGEs

"Given the data for pyrraline excretion, it can be concluded that dietary pyrraline is nearly completely released and resorbed during digestion, followed by rapid elimination via the kidneys, thus leading to nearly complete recovery of dietary pyrraline in the urine. This indicates that, in contrast with Amadori products, of which only up to 5% are recovered in the urine [24,25], pyrraline obviously is not metabolized within the body."

And..

"Above all, however, it has to be realized that the term 'AGE' comprises a large number of individual amino acid derivatives, of which only a minority have been identified and quantified either in foods or in vivo."

Are we distinguishing the types of AGEs when we measure them? (Or are we lumping them all together like what was done with cholesterol?) Are food derived AGEs eaten as part of a meal less harmful then analogues produced in a lab and fed in isolation? (Like most AGE studies I've read?) Again, if butter is as bad as these measurements indicate, why hasn't it been identified epidemiologically as such a bad food? Those with the highest butter consumption tend to be the healthiest (although I suppose because it displaces margarine). I can understand why all AGEs might be harmful to someone with compromised kidneys.

Exogenous AGEs are disparate. Some are easily cleared from the body and others are not. And then there is the rather complicated structure of AGEs, which makes it seem unlikely that many could survive digestion (discounting that many might suffer a leaky gut as the result of certain plant foods or artificial chemicals). We don't know enough about exogenous AGEs to state that we should avoid all cooked or high fat foods.

Edited by Skötkonung, 28 October 2010 - 08:10 PM.

[Sillewater]

....
Exogenous AGEs are disparate. Some are easily cleared from the body and others are not. And then there is the rather complicated structure of AGEs, which makes it seem unlikely that many could survive digestion (discounting that many might suffer a leaky gut as the result of certain plant foods or artificial chemicals). We don't know enough about exogenous AGEs to state that we should avoid all cooked or high fat foods.

I agree that our understanding is far from complete. However based on all the research showing how AGE affects lifespan and metabolism (studies done by Vlassara) and studies done on humans showing the effects of dietary AGEs (promoting inflammation and etc...) I would think it is best to be cautious with dietary sources of AGEs (dAGEs).

While based on hormetic arguments a bit of AGE could be beneficial:

Exp Gerontol. 2010 Oct;45(10):752-62. Epub 2010 Aug 10.


Preconditioning with Maillard reaction products improves antioxidant defence leading to increased stress tolerance in cardiac cells.
Ruhs S, Nass N, Bartling B, Brömme HJ, Leuner B, Somoza V, Friess U, Silber RE, Simm A.

i still think considering all the data lowering our overall AGE intake is best. I love the taste of butter and would love to get to the bottom of this.

[JLL]

Is there really data on AGEs in otherwise healthy humans causing problems? All I've seen is studies on AGEs in diabetics -- and we know diabetics can't handle AGEs like Tom Cruise couldn't handle the truth in A Few Good Men.

[Skötkonung]

Is there really data on AGEs in otherwise healthy humans causing problems? All I've seen is studies on AGEs in diabetics -- and we know diabetics can't handle AGEs like Tom Cruise couldn't handle the truth in A Few Good Men.

Exactly, the majority of Helen Vlassara's research has been in the context of diabetes, An impaired metabolism is obviously going to have implications on the metabolic transit of AGEs. Admittedly I haven't done much research on this... but if you look at the constitute AGEs in various foods (like butter), it often appears that many types of AGEs are excreted from the body. The example I used earlier was pyrralines, the dominant AGE in dairy products (like butter). When ingested, 95% can be collected in the urine suggesting they aren't metabolized.

From the study I posted earlier:
"In contrast with previously published reports, we therefore conclude that urinary pyrraline is almost exclusively of dietary origin and is affected to only a minor extent by in vivo catabolic pathways for AGEs. Recently published findings, in which close correlations between urinary pyrraline as well as other endogenously formed AGEs and oxidative stress [22] or glycaemic control [21] were postulated without taking dietary influence into consideration, are therefore questionable."