AGEs / ALEs
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Re: AGEs / ALEs
What will you do when you will find that high intake of saturat fat is not good at all for your health ?
(By the Way, Weston Price never advocates a diet high in saturat fat, as he wrote a letter to his nieces and nephews, instructing them in the diet he hoped they would eat. "The basic foods should be the entire grains such as whole wheat, rye or oats, whole wheat and rye breads, wheat and oat cereals, oat-cake, dairy products, including milk and cheese, which should be used liberally, and marine foods.")
Weston Price died of a heart attack at age 68, Stephen Byrnes died of a stroke at age 41, Mary Enig died of a stroke at 82 and Sally fallon is now fat...
Hum, saturat fat...
(By the Way, Weston Price never advocates a diet high in saturat fat, as he wrote a letter to his nieces and nephews, instructing them in the diet he hoped they would eat. "The basic foods should be the entire grains such as whole wheat, rye or oats, whole wheat and rye breads, wheat and oat cereals, oat-cake, dairy products, including milk and cheese, which should be used liberally, and marine foods.")
Weston Price died of a heart attack at age 68, Stephen Byrnes died of a stroke at age 41, Mary Enig died of a stroke at 82 and Sally fallon is now fat...
Hum, saturat fat...
Re: AGEs / ALEs
i think, when high temperature is involved, only then saturated fats are bad choice. Coconut contains even more saturated fat than butter does, but that doesn't make it unhealthy (as long as it's raw).fred wrote: saturat fat is not good at all for your health
AGEs / ALEs
JeffC, you are now focussing on one sub-group of AGEs, and ignoring all the other sub-groups of AGEs.
If you focus on AGEs that are readily formed from fructose,
you will find that fructose is most correlated with AGEs.
You could also focus on some other sub-group.
For example, you could focus on AGEs readily formed from creatine.
Then you will find that creatine is most correlated with AGEs.
That is called a "tunnel-vision".
Let me explain (again).
AGEs are a extremely diverse group of all kinds of sub-groups of compounds originating from the interaction of proteins / nucleic acids and carbs.
CML is just one AGE.
It is one of a sub-group of AGES that readily form endogenously under the influence of oxidative radicals (eg from omega-3 fats) specifically from reducing sugars and lysine,
Fluorescent AGEs are a specific sub-group of AGEs.
Their level (as a group) can easily be measured, which makes them a popular subject for representing AGEs.
The downside of that approach is that they only represent a sub-group of AGEs.
In specific conditions, levels of fluorescent AGEs may be low, and that of specific other AGEs very high,
or the other way around.
Let me give you an example.
HCAs are another sub-group of AGEs and generally not fluorescent.
Unlike CML, which particularly originates in the presence of reducing sugars and lysine,
HCAs particularly originate in the presence of creatine and tryptophan, glutamine or tyrosine.
Creatine is found in high levels in meat and fish.
So that if you let HCAs represent AGEs, you will find that vegetarians have higher levels of HCAs than omnivores.
PhIP is an example of an AGE of the sub-group of HCAs.
The level of damage caused by PhIP is much higher in meat consumers than in vegetarians. Magagnotti C et al
And to a much greater extend (6.7 : 0.7) than the fluorescent AGEs (190 : 130) or CML (525 : 427) in the study you quoted (traditional vs high-fructose diet).
You are generalizing.
Generalizing does not get you closer to the truth.
Let me give you an example.
Olive oil is a plant oil.
It contains only 1% PUFAs, but 72% oleic acid.
In contrast to PUFAs, oleic acid is remarkably resistant to lipoxidation.
Hazelnuts are also very high in oleic acid (77%).
Coconut oil contains 7% oleic acid.
Palmitoleic acid is also a lipoxidation inhibitor.
Olive oil contains 1% palmitoleic acid.
That is why animal oils have a short shelf life.
So, you are trying to minimize AGEs (from fructose), resulting in more ALEs (and AGEs from other sugars).
AGEs and ALEs are equally damaging. (they may even be exactly the same compounds)
If you really want to try to limit the uptake and endogenous origination of both AGEs and ALEs,
you should take a look at the list of compounds that inhibit lipoxidation: http://www.waiwiki.org/index.php?title= ... Inhibitors
and the list of compounds that inhibit the formation of AGEs / ALEs: http://www.waiwiki.org/index.php?title= ... Inhibitors
If you focus on AGEs that are readily formed from fructose,
you will find that fructose is most correlated with AGEs.
You could also focus on some other sub-group.
For example, you could focus on AGEs readily formed from creatine.
Then you will find that creatine is most correlated with AGEs.
That is called a "tunnel-vision".
Yes, this is (again) about CML and fluorescent AGEs specifically.JeffC wrote:Study: Advanced glycation end products and nutrition.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.Kudlácková wrote: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.
Let me explain (again).
AGEs are a extremely diverse group of all kinds of sub-groups of compounds originating from the interaction of proteins / nucleic acids and carbs.
CML is just one AGE.
It is one of a sub-group of AGES that readily form endogenously under the influence of oxidative radicals (eg from omega-3 fats) specifically from reducing sugars and lysine,
Fluorescent AGEs are a specific sub-group of AGEs.
Their level (as a group) can easily be measured, which makes them a popular subject for representing AGEs.
The downside of that approach is that they only represent a sub-group of AGEs.
In specific conditions, levels of fluorescent AGEs may be low, and that of specific other AGEs very high,
or the other way around.
Let me give you an example.
HCAs are another sub-group of AGEs and generally not fluorescent.
Unlike CML, which particularly originates in the presence of reducing sugars and lysine,
HCAs particularly originate in the presence of creatine and tryptophan, glutamine or tyrosine.
Creatine is found in high levels in meat and fish.
So that if you let HCAs represent AGEs, you will find that vegetarians have higher levels of HCAs than omnivores.
PhIP is an example of an AGE of the sub-group of HCAs.
The level of damage caused by PhIP is much higher in meat consumers than in vegetarians. Magagnotti C et al
And to a much greater extend (6.7 : 0.7) than the fluorescent AGEs (190 : 130) or CML (525 : 427) in the study you quoted (traditional vs high-fructose diet).
No, its not that simple at all.Yes, from what I've read, excessive polyunsaturated fats are even more damaging than fructose. Thus, vegetable oils/margarine have a deserved terrible reputation,
You are generalizing.
Generalizing does not get you closer to the truth.
Let me give you an example.
Olive oil is a plant oil.
It contains only 1% PUFAs, but 72% oleic acid.
In contrast to PUFAs, oleic acid is remarkably resistant to lipoxidation.
Hazelnuts are also very high in oleic acid (77%).
Coconut oil contains 7% oleic acid.
Palmitoleic acid is also a lipoxidation inhibitor.
Olive oil contains 1% palmitoleic acid.
Actually, animal fats may be highly susceptible to lipoxidation (rancidity).But we can opt for a diet high in coconut oil and animal fats (more of what I'd call Weston Price foods).
That is why animal oils have a short shelf life.
Fats originate ALEs.Weston Price foods: Very high non-polyunsaturated fats (mostly animal-origin)
So, you are trying to minimize AGEs (from fructose), resulting in more ALEs (and AGEs from other sugars).
AGEs and ALEs are equally damaging. (they may even be exactly the same compounds)
If you really want to try to limit the uptake and endogenous origination of both AGEs and ALEs,
you should take a look at the list of compounds that inhibit lipoxidation: http://www.waiwiki.org/index.php?title= ... Inhibitors
and the list of compounds that inhibit the formation of AGEs / ALEs: http://www.waiwiki.org/index.php?title= ... Inhibitors
Re: AGEs / ALEs
Your reasoning is a little bit off.(By the Way, Weston Price never advocates a diet high in saturat fat, as he wrote a letter to his nieces and nephews, instructing them in the diet he hoped they would eat. "The basic foods should be the entire grains such as whole wheat, rye or oats, whole wheat and rye breads, wheat and oat cereals, oat-cake, dairy products, including milk and cheese, which should be used liberally, and marine foods.")
Weston Price died of a heart attack at age 68, Stephen Byrnes died of a stroke at age 41, Mary Enig died of a stroke at 82 and Sally fallon is now fat...
Hum, saturat fat...
First you say that the Weston Price diet is not high in saturated fat, then you claim that people that followed the weston price diet, died (early) because of strokes, and then you blame saturated fat for that !
According to wikipedia, Weston Price died at age 77 years old btw.
But sorry for hijacking the thread, it is very interesting to read!
Re: AGEs / ALEs
@Kasper : Weston Price died at 78 years old and not at 68 as I wrote. I apology for this error.
However, I never said that the Weston Price diet as recommended by the foundation was not high in saturat fat!
@Emeira : It seems that food choice is as important as the way it is eaten (raw/cooked). Saturat fat happends to be the most resistant to heat treatment, and WAPF recommends raw dairy. Yet they suffer from poor health.
However, I never said that the Weston Price diet as recommended by the foundation was not high in saturat fat!
@Emeira : It seems that food choice is as important as the way it is eaten (raw/cooked). Saturat fat happends to be the most resistant to heat treatment, and WAPF recommends raw dairy. Yet they suffer from poor health.
Re: AGEs / ALEs
I just want the specific reason that the potatoes I'm eating are excluded from the Wai diet. I've been talking about CML because in food analyses, CML has been the most widely used marker for AGEs. Boiled potato tested extremely low in CML. RRM's response is that there are many other kinds of AGEs, with the implication that high levels of other AGEs might be found in boiled potatoes? I am not seeing anywhere an actual study with numbers that says, "yes, we found high levels of [some other AGE] in boiled potatoes."RRM wrote:JeffC, you are now focusing on one sub-group of AGEs, and ignoring all the other sub-groups of AGEs.
Does Accumulation of Advanced Glycation End Products Contribute to the Aging Phenotype?:
Semba does not say "relatively low in CML." Semba purposefully says "relatively low in AGEs."Semba wrote:Foods that are either eaten raw or cooked at lower temperatures are relatively low in AGEs, and such foods include raw fruits and vegetables, raw fish, raw nuts, yoghurt, tofu, pasta, boiled rice, boiled potatoes, and other boiled or simmered foods.
Vitamins B1, B3, B6, C just happen to be what potatoes are fairly high in.RRM wrote:If you really want to try to limit the uptake and endogenous origination of both AGEs and ALEs,
you should take a look at the list of compounds that inhibit lipoxidation: http://www.waiwiki.org/index.php?title= ... Inhibitors
and the list of compounds that inhibit the formation of AGEs / ALEs: http://www.waiwiki.org/index.php?title= ... Inhibitors
Cooked potatoes ranked #17 overall on foods highest in total antioxidant capacity.
Re: AGEs / ALEs
Boiled potatoes
-High in AGE inhibitors
-Low in exogenous AGEs
-Low fructose = low endogenous AGEs
Fruit
-High in AGE inhibitors
-Low in exogenous AGEs
-High fructose = high endogenous AGEs
Conclusion: boiled potatoes are healthier than raw fruit.
What is incorrect about this reasoning?
-High in AGE inhibitors
-Low in exogenous AGEs
-Low fructose = low endogenous AGEs
Fruit
-High in AGE inhibitors
-Low in exogenous AGEs
-High fructose = high endogenous AGEs
Conclusion: boiled potatoes are healthier than raw fruit.
What is incorrect about this reasoning?
Re: AGEs / ALEs
You can't make that conclusion because we can't quantify "High in AGE inhibitors". Maybe fruits are 1000x higher in AGE inhibitors, which would completely compensate for the High in fructose.
Re: AGEs / ALEs
No, not that "fast", one "=" sign?JeffC wrote:-High fructose = high endogenous AGEs, What is incorrect about this reasoning?
Aytundra Thinks ---> High fructose = High fructose on plate = High fructose in mouth = High fructose in gut = High fructose in blood stream = Maybe leftover unprocessed fructose = Some free endogenous fructose = High potential to be endogenous AGEs, if free fructose meets with amino acid under the right temperatures and maybe create endogenous AGEs.
Aytundra Thinks ---> High reducing sugars = High reducing sugars on plate = High reducing sugars in mouth = High reducing sugars in gut = High reducing sugars in blood stream = Maybe leftover unprocessed reducing sugars = Some free endogenous reducing sugars = High potential to be endogenous AGEs, if free reducing sugars meets with amino acid under the right temperatures and maybe create endogenous AGEs.RRM wrote:but so are amino acids and other sugars (particularly reducing sugars that may be very high in potatoes).
A tundra where will we be without trees? Thannnks!
Re: AGEs / ALEs
Let's take a look at this "high reducing sugars in potatoes" comment that started with RRM.Aytundra wrote:Aytundra Thinks ---> High reducing sugars = High reducing sugars on plate = High reducing sugars in mouth = High reducing sugars in gut = High reducing sugars in blood stream = Maybe leftover unprocessed reducing sugars = Some free endogenous reducing sugars = High potential to be endogenous AGEs, if free reducing sugars meets with amino acid under the right temperatures and maybe create endogenous AGEs.
What that study says is that potatoes bought in Szczecin, Poland in spring had more reducing sugars than autumn potatoes. Probably because they were stored at a cold temperature all winter. Potatoes have to be stored at a very cold temperature (1ºC) for months to increase the reducing sugar amount. PintoRRM wrote:Potatoes may be very high in reducing sugars Wójcik-Stopczyńska B, which are precursors for various AGEs.
And let's put it in perspective. The nutrition data on 1 boiled potato (118 calories) says it has 0.9 g of pure reducing sugars (glucose + fructose).
1 cup of orange juice (112 calories) has 12.2 g of pure glucose + fructose. Plus 8.7 g of sucrose.
(Fructose- and sucrose-fed rats excreted significantly higher amounts (74 and 34%, respectively) of lipid peroxidation products in urine. Levi)
Re: AGEs / ALEs
I find this discussion very interesting. I'm always very interested in second-best options. And you have convinced me that potatoes may be one of those second best options. But you haven't convinced me that it stand on equal footing with fruit.
I understand that you don't tolerate fructose well @jeffc, but I think you are overestimating the negative effects of fructose on people that tolerate fructose well.
Personally I think that fructose is essential on a healthy diet, and I think your best option is to try to fix your fructose intolerance.
One other reason to include fructose in a diet, is that it stabilizes blood sugar. If I remember correctly, high blood sugar levels also increase AGE formation, so therefore one could doubt if fructose is really that bad for AGE.
I understand that you don't tolerate fructose well @jeffc, but I think you are overestimating the negative effects of fructose on people that tolerate fructose well.
Personally I think that fructose is essential on a healthy diet, and I think your best option is to try to fix your fructose intolerance.
http://www.ncbi.nlm.nih.gov/pubmed/2729168A balance study was conducted to assess the effects of consuming low-copper diets, high in fructose or cornstarch. The study involved 19 apparently healthy males, aged 21-57 y. The two experimental diets averaged 0.35 mg Cu/1000 kcal and provided 20% of the calories from fructose or cornstarch. Cu, zinc, calcium, magnesium, and iron balances were determined 1 wk before the study (pretest) when the subjects consumed self-selected diets and after consuming the experimental diets for 6 wk. No major differences in mineral balances were evident between the two groups during the pretest study when the subjects ate self-selected diets. In contrast, when fed the test diets, the group consuming the low-Cu fructose diet had significantly more positive balances for all minerals studied than the group fed the low-Cu cornstarch diet. The results indicate that dietary fructose enhances mineral balance.
One other reason to include fructose in a diet, is that it stabilizes blood sugar. If I remember correctly, high blood sugar levels also increase AGE formation, so therefore one could doubt if fructose is really that bad for AGE.
http://www.ncbi.nlm.nih.gov/pubmed/8678268The benefits of fructose-specific metabolic effects reported in the literature and corroborated by the results of out own study suggest that fructose is an important nutrient that contributes to metabolic stabilization, especially in the post-aggression phase and in septic patients. Hyperglycaemic states are largely prevented and fewer patients require ex
http://m.advances.nutrition.org/content/4/2/246.fullThe field of sugar metabolism, and fructose metabolism in particular, has experienced a resurgence of interest in the past decade. The “fructose hypothesis” alleges that the fructose component common to all major caloric sweeteners (sucrose, high-fructose corn syrup, honey, and fruit juice concentrates) plays a unique and causative role in the increasing rates of cardiovascular disease, hypertension, diabetes, cancer, and nonalcoholic fatty liver disease. This review challenges the fructose hypothesis by comparing normal U.S. levels and patterns of fructose intake with contemporary experimental models and looking for substantive cause-and-effect evidence from real-world diets. It is concluded that 1) fructose intake at normal population levels and patterns does not cause biochemical outcomes substantially different from other dietary sugars and 2) extreme experimental models that feature hyperdosing or significantly alter the usual dietary glucose-to-fructose ratio are not predictive of typical human outcomes or useful to public health policymakers. It is recommended that granting agencies and journal editors require more physiologically relevant experimental designs and clinically important outcomes for fructose research.
Re: AGEs / ALEs
You cook potatoes but not fruits, I think that's where those sugars make a difference.JeffC wrote:What that study says is that potatoes bought in Szczecin, Poland in spring had more reducing sugars than autumn potatoes. Probably because they were stored at a cold temperature all winter. Potatoes have to be stored at a very cold temperature (1ºC) for months to increase the reducing sugar amount. PintoRRM wrote:Potatoes may be very high in reducing sugars Wójcik-Stopczyńska B, which are precursors for various AGEs.
And let's put it in perspective. The nutrition data on 1 boiled potato (118 calories) says it has 0.9 g of pure reducing sugars (glucose + fructose).
1 cup of orange juice (112 calories) has 12.2 g of pure glucose + fructose. Plus 8.7 g of sucrose.
(Fructose- and sucrose-fed rats excreted significantly higher amounts (74 and 34%, respectively) of lipid peroxidation products in urine. Levi)
Re: AGEs / ALEs
We know potatoes have high vitamins and antioxidants...dime wrote:we can't quantify "High in AGE inhibitors". Maybe fruits are 1000x higher in AGE inhibitors
You cook potatoes but not fruits, I think that's where those sugars make a difference.
We know boiled potatoes measured CML at only 17 kU (raw fruit level)...
I was on a very low carb diet for over a year (02-2013 to 04-2014). As soon as I reintroduced a small amount of orange juice, digestive problems returned. To me it is like trying to tell someone who developed a reduced ability to metabolize alcohol because of many years of hard drinking that they need to "fix it."Kasper wrote:I think your best option is to try to fix your fructose intolerance.
Likewise there are studies justifying alcohol consumption.The results indicate that dietary fructose enhances mineral balance.
Fructose is an important nutrient that contributes to metabolic stabilization.
Long-term light alcohol intake lowered cardiovascular and all-cause mortality risk and increased life expectancy.
Ethanol protects neurons.
Alcohol consumption raises HDL cholesterol levels.
But it is also oxidative and health damaging.
Fructose: it's "alcohol without the buzz".
Lustig wrote:In the hypercaloric glycogen-replete state, intermediary metabolites from fructose metabolism overwhelm hepatic mitochondrial capacity, which promotes de novo lipogenesis and leads to hepatic insulin resistance, which drives chronic metabolic disease. Fructose also promotes reactive oxygen species formation, which leads to cellular dysfunction and aging, and promotes changes in the brain's reward system, which drives excessive consumption. Thus, fructose can exert detrimental health effects beyond its calories and in ways that mimic those of ethanol, its metabolic cousin. Indeed, the only distinction is that because fructose is not metabolized in the central nervous system, it does not exert the acute neuronal depression experienced by those imbibing ethanol. These metabolic and hedonic analogies argue that fructose should be thought of as "alcohol without the buzz."
Re: AGEs / ALEs
Ah, you are reading Lustig.
He seems to be on some queest to blame fructose for all health issues.
And maybe if you react badly on fructose, then that sounds very convincing.
But remember, most people don't react bad on fructose at all, and I find this report quite convincing in showing why Lustig claims just don't hold for humans:
http://m.advances.nutrition.org/content/4/2/246.full
Even, this weston price inspired paleo guru warns against the fructose is poison hype that Lustig started:
http://chriskresser.com/ask-chris-is-fr ... y-that-bad
He seems to be on some queest to blame fructose for all health issues.
And maybe if you react badly on fructose, then that sounds very convincing.
But remember, most people don't react bad on fructose at all, and I find this report quite convincing in showing why Lustig claims just don't hold for humans:
http://m.advances.nutrition.org/content/4/2/246.full
Even, this weston price inspired paleo guru warns against the fructose is poison hype that Lustig started:
http://chriskresser.com/ask-chris-is-fr ... y-that-bad
Re: AGEs / ALEs
I don't disagree with these articles, but it doesn't change my view.
'Fructose doesn't cause obesity.' I concur.
They essentially say that fructose isn't all that bad unless you take an extreme amount.
Like the lab rats. Like JeffC.
Alcohol is also 'not that bad' if you don't abuse it.
Lustig even says so.
But I would rather abstain from alcohol and fructose because they are unnecessary and damaging.Studies of ethanol use show that small doses are healthy because ethanol increases HDL and improves insulin sensitivity and longevity. Like alcohol, a small dose of fructose has been shown in some studies to have a beneficial effect on insulin secretion. The negative effects of fructose, just like alcohol, are dose dependent.