AGEs / ALEs

[Aytundra]

The problem with potatoes from a Wai perspective is that they have to be heated to nearly 100°C. But it's only 7.5-10 g of protein. Acrylamide does not form at this low temperature. HCAs also are not an issue (low temperature and not muscle meat). I don't see a problem with it.

Maybe it is not Acrylamide or HCAs.

[dime]

The consensus is that acrylamide forms at temps above 120C.
HCAs and PAHS are very much meat and fish-specific.
In any case, I'm sure boiling at 100C produces some substances, no clue how harmful are they though.
You could slow cook potatoes for a few hours at 70-80C? Potato starch gelatinizes at ~60C, so 70-80C would be enough to cook potatoes I guess, especially if you cut them in small pieces.

[RRM]

HCAs and PAHS are very much meat and fish-specific.

Yes, indeed. But not totally.
And there are many substances formed from fatty or protein with carb or other molecules that fall outside the category of HCA,
but in the more wider category of AGEs/ALEs.
And they are associated with ageing.
http://www.waiwiki.org/index.php?title= ... d_reaction

Maybe it is not Acrylamide or HCAs.

Exactly. They are just a small group of compounds and a single compound within a very divers group of compounds: AGEs / ALEs.
i could have mentioned AGEs/ALEs, but that also includes harmless stuff.

[dime]

This provides a good overview of AGEs: http://www.ncbi.nlm.nih.gov/pmc/article ... po=20.8333

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.

Potatoes have a really low amount after boiling (17 kU/100g), whereas french fries are loaded with 1000+ kU/100g.
For reference, raw beef has 707 kU/100g.

I couldn't find information on ALEs but I have a feeling it's probably a similar case as the AGEs?

[RRM]

This provides a good overview of AGEs: http://www.ncbi.nlm.nih.gov/pmc/article ... po=20.8333

"AGE Content of Foods as Determined by CML Levels"
CML is just one end product.
This is justified by largely similar MG content patterns.
But MG and CML are related, as MG may result in CML.
This results in attributing high AGE levels to high CML/MG foods,
and low AGE contents to foods low in CML/MG.
I think we need a more profound approach than that.

MG (or MGO; methylglyoxal) is a Maillard intermediate; its both a a metabolite of glucose (aldehyde) and a ketone (from lipidoxidation)
CML is a Maillard end-product (both an AGE and ALE).

I couldn't find information on ALEs but I have a feeling it's probably a similar case as the AGEs?

Though AGE and ALES share intermediates and end-products, they also have different pathways and precursors.
I think its premature to make a list of AGEs / ALEs in food if you investigate the levels of only 1 (or 2) end products.

For reference, raw beef has 707 kU/100g.

That will depend on what the cow ate.
As in humans, AGEs/ALEs accumulate in animals. (not in fruits etc)
CML is a good example of a AGE/ALE that accumulates endogenously, particular in certain conditions.
If the cow grazes raw grasses, its meat will contain less AGEs/ALEs than cows fed processed feeds.

[RRM]

Potatoes may be very high in reducing sugars Wójcik-Stopczyńska B, which are precursors for various AGEs.

[JeffC]

I consider boiled potatoes the most desirable option available.
-By removing the skin and boiling, I avoid most glycoalkaloid antinutrients.
-We agree that there is no acrylamide at this temperature.
-We agree that HCAs and PAHs are mainly in meats.
-We agree that the AGE (CML) content after boiling is 17 kU/100g (less than raw cantaloupe).
-I don't have the AGE (AG) number, but generally there's a 0.8 correlation between CML and AG content.
I still don't see why boiled potatoes are so terrible, especially for someone avoiding fructose.

Meanwhile, I found this study... "Long-Term Fructose Consumption Accelerates Glycation and Several Age-Related Variables in Male Rats."

[Oscar]

It's not that fructose is bad per se, but that it becomes problematic when too much of free fructose is consumed. Fructose follows a different pathway than glucose, and is processed in the liver, which means it does not induce insulin secretion. It also does not induce leptin secretion, which gives the feeling of having had enough. This can easily lead to overeating, especially in case of fructose only diets. Glucose does not have this issue, so as long as either a combination of fructose with glucose and/or both molecules combined in sucrose is consumed, this problem can be avoided. As far as I know there aren't any fruits that contain only fructose, so no worries there.

As for the Maillard reaction, that can happen between fructose and amino acids. To get those amino acids, you'd have to denaturate the protein first. Granted, the Maillard reaction can happen at room temperature, if you wait long enough. The question is how long you'd normally wait and how much HCA's would have formed by then.

Another consideration might be how detrimental the consuming of less optimal foods is compared to the consumption of fructose.

[RRM]

-We agree that the AGE (CML) content after boiling is 17 kU/100g

No, we do not agree on that at all.
That is the CML level established in a sample of boiled potatoes.
That does not say anything about hundreds of other AGEs.
The level of AGEs in boiled potatoes very much depends on how high the level of reducing sugars (and was in the original raw potato.
(and the level of ALE formation depends on the levels of lipid derived aldehydes)
This co-depends on the variety, the length of storage, storage temperature, etc.

I don't have the AGE (AG) number, but generally there's a 0.8 correlation between CML and AG content.

No, that correlation has never been established.
That so called correlation between CML and AGEs is actually the correlation between CML and MGO (and these 2 are related compounds).
The proper method to establish a correlation between CML and total AGEs, would be to actually establish the levels of all AGEs in at least a few products.
They did not do that.

Meanwhile, I found this study... "Long-Term Fructose Consumption Accelerates Glycation and Several Age-Related Variables in Male Rats."

True.
Fructose is one of the precursors of AGEs,
but so are amino acids and other sugars (particularly reducing sugars that may be very high in potatoes).
Lipid derived aldehydes are potent precurors for ALEs. http://www.waiwiki.org/index.php?title= ... d_reaction
Levels of lipid-derived aldehydes in potatoes increase by boiling.Ruiz del Castillo ML et al

[JeffC]

The level of AGEs in boiled potatoes very much depends on how high the level of reducing sugars (and was in the original raw potato.
(and the level of ALE formation depends on the levels of lipid derived aldehydes)

Potatoes, boiled, cooked in skin, flesh, without salt
Total Carbohydrate 27.4 g
Sugars 1.2 g
Sucrose 258 mg
Glucose 503 mg
Fructose 408 mg
Total Fat 0.1g

So there is only 0.9 g of reducing sugars (for potential AGE formation) and 0.1 g of total fat (for potential ALE formation)? Why assume that 'other AGE' content is high when CML wasn't?

Why not worry much more about AGEs forming inside the body because of high fruit/fructose consumption?

[dime]

I find this recent study very interesting: http://ajph.aphapublications.org/doi/ab ... lCode=ajph

Results. After adjustment for sociodemographic and health-related characteristics, sugar-sweetened soda consumption was associated with shorter telomeres (b = –0.010; 95% confidence interval [CI] = −0.020, −0.001; P = .04). Consumption of 100% fruit juice was marginally associated with longer telomeres (b = 0.016; 95% CI = −0.000, 0.033; P = .05). No significant associations were observed between consumption of diet sodas or noncarbonated SSBs and telomere length.

I don't have the whole article so can't tell if this means that fruit juice is associated with lengthening of telomeres, or just smaller shortening than with sugar-sweetened soda. I'm quite sure it actually means small but measurable lengthening of telomeres. Longer telomeres - slower aging. Which would be a good answer to your question.

[RRM]

Why not worry much more about AGEs forming inside the body because of high fruit/fructose consumption?

Both sugars (particularly reducing sugars, including those from complex sugars) and amino acids promote the formation of AGES,
and fatty acids the formation of ALEs (particularly omega-3 fatty acids, as they are very susceptible to lipoxidation.).
So, yes, you can opt for a diet of mainly fats instead, but that would increase endogenous lipoxidation and ALEs formation.

Regarding the endogenous formation of both AGEs and ALEs, i rely on autophagy.

So there is only 0.9 g of reducing sugars

You mean in that study in those potatoes.
It may also be 1.69% Wójcik-Stopczyńska B
or more.
"The content of reducing sugars exceeded the recommended highest level (0.5%) in the majority of the tested samples"

[RRM]

Consumption of 100% fruit juice was marginally associated with longer telomeres

That must be because of all the substances in fruit juices that inhibit AGE/ALE formation:
http://www.waiwiki.org/index.php?title= ... Inhibitors

[Aytundra]

I'm quite sure it actually means small but measurable lengthening of telomeres.

or you could reread their sentence:

Consumption of 100% fruit juice was marginally associated with longer telomeres

and reinterpret it as:
In this study, telomeres of 100% fruit juice consumers had longer telomeres relative to sugar-sweetened soda consumers =
In this study, telomeres of sugar-sweetened soda consumers had shorter telomeres relative to 100% fruit juice consumers.
Meaning that 100% fruit juice consumers did not have lengthened telomeres, instead the sugar-sweetened soda consumers had reduced telomeres.
{imo, I think telomeres can only be preserved from reduction in length. Each time the cell divides, telomeres of that cell reduces in telomere length.}

[JeffC]

Study: Advanced glycation end products and nutrition.

Comparison of nutrition and plasma AGEs in vegetarian and omnivorous groups shows that the higher intake of fructose in alternative nutrition of healthy subjects may cause an increase of AGE levels.

This study compared a 'traditional omnivorous' group with an 'alternative vegetarian' group (lower protein, higher fruit). CML and fluorescent AGE values were significantly higher in the high fruit group, and fructose is attributed as the cause.

Both sugars (particularly reducing sugars, including those from complex sugars) and amino acids promote the formation of AGES,
and fatty acids the formation of ALEs (particularly omega-3 fatty acids, as they are very susceptible to lipoxidation.).
So, yes, you can opt for a diet of mainly fats instead, but that would increase endogenous lipoxidation and ALEs formation.

Yes, from what I've read, excessive polyunsaturated fats are even more damaging than fructose. Thus, vegetable oils/margarine have a deserved terrible reputation, and nuts/seeds/legumes should be avoided. But we can opt for a diet high in coconut oil and animal fats (more of what I'd call Weston Price foods).

Wai philosophy: Goal is optimal health with minimal aging as found through science
Weston Price philosophy: Goal is optimal health as indicated by oral/dental health
Wai foods: Very high fruit, some fat, low protein, avoiding excess heat and antinutrients.
Weston Price foods: Very high non-polyunsaturated fats (mostly animal-origin), some protein, low carbs, avoiding excess heat and antinutrients.

I've done Weston Price foods since 2013, in a way that I feel doesn't violate Wai philosophy. I aim to minimize both fructose and polyunsaturated fats (beyond necessary omega3/6s).