AGEs / ALEs

About specific vitamines, minerals or fiber, for example
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RRM
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Re: AGEs / ALEs

Post by RRM »

Aytundra wrote:What if fructose enters liver but fails to become glucogen?
Fructose is readily converted into glycogen if glycogen depots are not completely repleted.
Aytundra wrote:
RRM wrote:If we consume more fructose than required for liver glycogen synthesis (about 400 kcal), and it is not used for muscle activity, and this extra fructose is also not used for triglyceride production (bodyfat), then it may be available for AGEs formation.
that's what I based my heist metaphor on.
"it" Is "it" a fructose or a glucose?
Fructose.
I was under the impression that temporarily was a referral to fructose temporarily being stored as glycogen prior to utilisation for energy.
If not, what did you have in mind when you wrote "temporarily" in the following quote?
aytundra wrote:Yes, more thieves in a city might lower crime rates temporarily, as most criminals in this imaginary city are too busy plotting a heist.
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Re: AGEs / ALEs

Post by Aytundra »

Aytundra wrote: Yes, more thieves in a city might lower crime rates temporarily, as most criminals in this imaginary city are too busy plotting a heist.
Temporarily, in that short moment of time everything is perfect, fructose is where it should be being turned into glucose or glycogen.
As the glucose and glycogen stores build up and more and more fructose is added, eventually the glycogen stores will fill-up, glycogen to triglycerides form, and excess fructose awaits processing.Without the capacity to meet excess fructose, excess fructose wanders and then we might have a problem.

Let's pretend fructose systems' maximum capacity = 100 fructose molecules:
- If we have liver and sucrase system at full capacity [100],
and we put in some fructose (5 fructose),
then there will be some fructose (like 3 fructose, while the other 2 fructose trickle into the system as the system outputs 1 glycogen) wandering endogenously, a probability that endogenous AGEs might form from these (three) fructose.

- If we have liver and sucrase system at vacant capacity [0],
and we put in a lot of fructose (102 fructose),
then there will be a lower probability (relative to other liver, sucrase system scenarios) that endogenous AGEs might form.

- If we have liver and sucrase system at half capacity [50], and we put in a lot of fructose (75 fructose),
then there will be some left over fructose (25 fructose),
then there will be some probability that endogenous AGEs might form from the (20) extra fructose wandering.

- If we have liver and sucrase system at full capacity again [100],
and we put in a lot of fructose (60 fructose),
there will be a lot of fructose not processed yet (~50), and these might wander and form endogenous AGEs if the climate is right.

- If liver capacity are full, and the liver stores glycogen as fats, the fats now has a chance to become ALEs if given the right circumstances.
-- Hence the heist, not only potential of AGEs from fructose, but also potential for ALEs from fructose after the liver processing.
-- But we don't have to be scared, just use up glycogen and use up liver fat accordingly. They may plot but we may empty.
--- But what if the systems are damaged?
--- What if we don't empty at the right times accordingly?


AGEs ALEs bad?
- If we have a lot of fructose in the body not converted into glucose, glycogen or stored as glycogen depots, then they are free to wander around.
Like an elevator, if we have lots of people waiting for an elevator these people wander the hallway.
- Wandering reducing sugars are not bad, and things they do are not necessarily bad.
- As you have pointed out not all AGEs or ALEs formed are bad, they don't necessarily correlate to bad health, like your opinion on CML and veggie/fruit eaters.
But it matters who is waiting at the elevators.
If I have adults (glucose) versus toddlers (fructose) at the elevator doors, toddlers will be more prone to activity, and some activities make a mess, some a bad mess (bad AGEs).
I don't have to worry much for sucrose (adults minding a toddler), in a sucrase pathway.
Only when sucrase capacity is full, then do I have to worry about sucrose and perhaps with attention to the fructose that sucrose contains.

- Glucose is readily used in the body, but fructose must be converted before it can be used.
- Glucose is a reducing sugar, it may form endogenous AGEs if given the right circumstances.
- Fructose is a reducing sugar, it may form endogenous AGEs if given the right circumstances.
- But because glucose has a higher probability of being used by the body,
since, a glucose molecule floating freely might meet a muscle cell that needs some energy,
while, a fructose molecule floating freely might meet a muscle cell and cannot be used for energy immediately,
then a fructose is a more inert reducing sugar to have floating around, ("inert" relative to the ease of usage for energy).
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Re: AGEs / ALEs

Post by dime »

Here's a review of a nice study, on how fruit consumption correlates proportionally to reduced risk for Alzheimer's.
It's even better than exercise/running. Check the diagram at the end.
http://www.runnersworld.com/health/exer ... -and-fruit
Original study: http://www.ncbi.nlm.nih.gov/pubmed/25408208
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Re: AGEs / ALEs

Post by Aytundra »

Pretty molecular sketch of AGE receptor and glycated hemoglobin (sugar lysine).
http://www.rcsb.org/pdb/101/motm.do?momID=186
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Re: AGEs / ALEs

Post by Aytundra »

Today, Emeira brought my attention to reread the Uribarri et al.'s article again.
Uribarri, J., Woodruff, S., Goodman, S., Cai, W., Chen, X., Pyzik, R., Yong, A., Striker, G.E., & Vlassara H. (2010). Advanced Glycation End Products in Foods and a Practical Guide to Their Reduction in the Diet. J Am Diet Assoc. 2010 Jun; 110(6): 911–16.e12. doi: 10.1016/j.jada.2010.03.018
Retrieved from: http://www.ncbi.nlm.nih.gov/pmc/article ... po=18.7500


This time I took a closer look at the Uribarri et al's table 1:
Uribarri et al. 2010 wrote:"Table 1 - The advanced glycation end product (AGE) content of 549 foods, based on carboxymethyllysine content." (Uribarri et al. 2010).
I took the time to sift through over 500 food entries, and found these items that might be of interest to Wai dieters.

AGE kU/100g Food Item
0/100g sugar
0/100 g orange juice from fresh fruit
2/100g --- apple juice
3 or 6/100g --- orange juice with calcium or orange juice
7/100g honey
9/100 g apple Macintosh
9/100g banana
20/100g cantaloupe
23/100g tomato
31/100g cucumber
43 or 63/100g ------ egg whites 10 min or 12 min
60/100g --- Dates, Sun-Maid California chopped (Sun-Maid, Kingsburg, CA)
90/100g ------ egg poached 5 min simmer {Because Uribarri et al, did not measure raw egg yolks, I placed this here in place of egg yolks.}
120/100g --- Raisin, from Post Raisin Bran (Kellogg Co)
167/100g --- plums, Sun-Maid dried pitted prunes
307/100g --- Coconut milk, leche de coco, (Goya)
517 or 528/100g salmon raw previously frozen, salmon raw
590/100g --- Coconut, Baker’s Angel Flake, sweetened (Kraft)
707/100g ------ beef raw
769/100 g ------ chicken breast raw
783/100g ------ trout raw
826/100g ------ lamb leg raw
933/100g --- Coconut cream, Coco Goya cream of coconut (Goya, Secaucus, NJ)
1193 or 1680/100g --------- egg yolks cooked 10 min or 12 min
1577/100g avocado
1670/100g --- olive ripe large 5 g
2633/100g --- fig dried
5473/100g --------- Almonds, blanched slivered (Bazzini’s Nut Club, Bronx, NY)
7877/100g --------- walnuts roasted
10040/100g --- Oil, olive, extra virgin, first cold pressed (Colavita, Linden, NJ)
11900/100g------ olive oil

LEGEND:
If I marked with a line, it means some thinking required to decide if it could be a Wai item to eat.
--- = not really Wai because it is containerized (container coating) or not fresh or was canned or was dried.
------ = some people might eat these items on this forum like for consideration in slow cooking.
--------- = I included these cooked items for reference, because no raw items were listed in Uribarri et al.'s article for these items
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Re: AGEs / ALEs

Post by RRM »

There are thousands of specific AGEs.
Some are harmless.
Some are carcinogenic.
Some are natural.
Some only originate due to extreme heating.

Why do you pay attention to the levels of just one of those thousands AGE/ALE, and more particularly one that is naturally formed inside the human body and other organisms?
Instead, should you not pay attention to the level of all AGEs/ALEs combined?
or better, to the level of the most harmful ones?
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Re: AGEs / ALEs

Post by Aytundra »

RRM wrote:There are thousands of specific AGEs...or better, to the level of the most harmful ones?
"thousands?"
awesome!
I did 1000 -1.
Where are the other n -1 links to articles with tables?
RRM wrote:Why do you pay attention to the levels of just one of those thousands AGE/ALE, and more particularly one that is naturally formed inside the human body and other organisms?
No, specific reason.
Emeira asked me if I read that article this past Monday.
If she gave me 10 articles with 10 new AGE/ALE and 10 interesting tables + if I have the spare time (I was on vacation this past Monday) + if I think of something interesting to do with it, I would have scrutinized all of it.

I reranked that table with the question:
Do Wai items land at the bottom of each category?
I was much amused by the answers.

Most categories, Wai (like) items did appear at the top, because these items had the lowest not-likely-that-harmful AGE of carboxymethyllysine content.
For example, Salmon (first 3 and last 3 items of 15 salmon items on Uribarri et al (2010)'s table 1.):
Salmon, raw, previously frozen 517 kU AGE carboxymethyllysine/100g
Salmon, raw 528
Salmon, smoked 572
...
Salmon, pan fried in olive oil 3,083
Salmon, fillet, broiled 3,347
Salmon, broiled with olive oil 4,334

Chicken was similar, raw chicken at the top vs, cooked chicken.
Trout was similar, raw trout at the top vs, cooked trout.
Beef however was interesting, salami 628 kU and corned brisket deli 199 kU had less AGE than raw Beef 707 kU, however, I think it might be because these food items are processed and contained very little beef content.
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Re: AGEs / ALEs

Post by RRM »

Aytundra wrote:Where are the other n -1 links to articles with tables?
Food tables?
I have no idea, because with regards to health it is totally uninteresting, as health is not about a few dozen (or just one) of AGEs/ALEs (in food stuffs) that are formed endogenously.
If you are interested about the health impacts of foods, knowing the contents of this one AGE/ALE tells you absolutely nothing (other than these contents).
That is because with regards to health you need to know (at least) about the combined impact of all known hazardous AGEs/ALEs.

The only way that knowing the level of just one specific AGE/ALE in various foods could be somewhat interesting (regarding health), is if that one AGE/ALE is the most toxic / hazardous one currently known. But even that would totally pale in comparison to knowing the combined occurrence of a large group (dozens, at least) of the most hazardous AGEs/ALEs.
With your health in mind, looking at the contents of naturally endogenously formed AGEs/ALEs in food stuffs is utterly misleading. Even if you combine data of hundreds of such endogenously formed AGEs/ALEs.
From taking such a look, one might conclude that consuming olive oil has adverse health. (scientific studies show the opposite)
Beef however was interesting, salami 628 kU and corned brisket deli 199 kU had less AGE than raw Beef 707 kU, however, I think it might be because these food items are processed and contained very little beef content.
Please do not say "had less AGE"...
But yes, i do agree it is interesting to see that processed meat may contain fewer CML than raw meat,
probably due to lower meat content (it is naturally formed in any 'live meat').
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Re: AGEs / ALEs

Post by Aytundra »

That would be ideal, to know every hazardous AGEs/ALEs.
But is that do-able counting/considering every factor?
RRM wrote:From taking such a look, one might conclude that consuming olive oil has adverse health. (scientific studies show the opposite)
Which, you guessed right, I was skeptical of olive oil for a brief moment in time.
Also, roasted nuts too after reranking Uribarri. But to be fair, olive oil is heat sensitive, not ideal for cooking compared to other oils. Uribarri et al (2010)'s article did take a closer look at olive oil with different heat treatments in Table 2, which Uribarri et al measured measured " methylyglyoxal (MG) and carboxymetyllysine (CML) content of selected foods" [sic].
Is MG a hazardous AGE?
But yes, i do agree it is interesting to see that processed meat may contain fewer CML than raw meat, probably due to lower meat content (it is naturally formed in any 'live meat').
Please do not say "it"...
"it" assuming "it" = CML, "CML is naturally formed in any 'live meat'." ?.
Does that mean CML formation stops in dead meat?
But olives are not meat.

----------
Hypothetical example:
f = filler
c = cooked (other AGEs/ALEs hiding inside this portion)
j = beef
t = CML
25 letters = 100 g sample

jjjjj jjjjj cccct fffff fffff = corned beef
jjjjj jjjjj jjjjj jjjjj jjjtt = raw beef

The beef meat content per 100g sampled product, could be less than the raw beef meat content per 100 g sampled product, because of fillers (spices, starch...) in the processed beef item, but the processed-beef-meat-sans-filler proportion "j" + "c" + "t" could contain an overall more AGEs/ALEs per processed beef meat per gram, than raw beef meat per gram.
---

In your quote "it is naturally formed in any 'live meat'.", that is interesting.
How do you know CML forms endogenously in live meat?
As in "j" becomes "t", endogenously.
If we cook and kill the meat, making it dead, "j" to "c".
Than "c" can't become "t"?; Because "j" is used up to make "c"?.
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Re: AGEs / ALEs

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Aytundra wrote:That would be ideal, to know every hazardous AGEs/ALEs.
But is that do-able counting/considering every factor?
No, but we know many very hazardous AGEs/ALEs (eg HCAs).
The least we should do, is restrict ourselves to the ones that have clearly (in numerous studies) been shown to have substantial toxic / carcinogenic properties.
CML does not represent that group.
CML represents the AGEs/ALEs that are naturally formed inside the body (and may also originate due to specific food processing), and which may be potentially hazardous.
RRM wrote:Is MG a hazardous AGE?
No, methylglyoxal is a (very reactive) intermediate, not an advanced glycation / lipoxidation end product.
MG may lead to the formation of hazardous or harmless (AG/AL) end products.
CML is an end product.
Please do not say "it"...
"it" assuming "it" = CML, "CML is naturally formed in any 'live meat'." ?.
Does that mean CML formation stops in dead meat?
But olives are not meat.
Yes. Yes.
No, not at all.
No, they are not meat.
How do you know CML forms endogenously in live meat?
Most of our understanding of CML is based on scientific studies studying the endogenous formation of CML.
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Re: AGEs / ALEs

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"Recently, diet has been recognized as a major environmental source of AGEs that could cause proinflammatory reactions and organ damage in vivo"
Yamagishi S et al
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