Re: Re: Back to AGEs

[Guest guest]

Hi Rodney

The study conclusions do not accurately represent the results of the

study.

The higher levels of AGEs in the so called vegetarian group in the

study came from the high use of Honey and of Dried Fruit. The only

fruit that showed a somewhat increase was the Apple due to its higher

fructose content.

From the study you are referencing

typical difference of alternative

nutrition in

comparison to traditional nutrition besides a higher consumption of

whole grain products, sprouts, seeds and plant fats also concerns the

significantly higher intake of fruit and vegetables . Many species of vegetables and fruit have

higher proportion of fructose

in comparison to glucose. Intake

of fruit and vegetables with higher content of fructose vs. glucose and intake

of apples and honey evaluated from the dietary questionnaires indicated

that fructose consumption is

significantly higher in vegetarians as compared to subjects on a

traditional diet (Table 1). Fresh

and dried apples have almost a twofold content of fructose

vs. glucose and their consumption is higher in vegetarians. Furthermore

the intake of honey is three times higher in vegetarians.

This was not a

healthy vegetarian diet.

Also, to put this and these numbers in better perspective, here is some

more info. As you will see, in the great context of things, fruit, and

even apples are fairly low in relationship to many other common and

regularly consumed foods

Regards

Jeff

Clin J Am Soc Nephrol 1: 1293-1299, 2006. Advanced Glycation End

Products and Nephrotoxicity of High-Protein Diets

AGE in the Diet

Recent work indicates that food,

particularly protein of animal origin, is a major source of AGE (45,46).

A portion of these preformed AGE is absorbed from the gastrointestinal

tract as glycated amino acids and peptides. A database listing the

content of CML in more than 200 food items has been compiled (45). AGE

content in food is influenced by the distribution of macronutrients

(proteins and fats more than carbohydrates) and by cooking conditions,

including temperature, time, and moisture (45). In

particular, cooking at high temperature generates a large amount of AGE

because the reactions that produce these compounds are accelerated by

increased heat. Culinary methods that are water based (steaming,

poaching, boiling, and stewing) instead of fat based and/or

browning methods (frying, broiling, and grilling) could greatly reduce

AGE ingestion despite the same macronutrient content of foods. For

example, a skinless chicken breast contains 692 AGE kilounits raw, 1011

AGE kilounits boiled, 5245 AGE kilounits broiled, and 6651 AGE

kilounits fried (45).

Journal of the American Dietetic Association

April 2005 (Vol. 105, Issue 4, Page 647)

Advanced glycoxidation end products (AGEs), the derivatives of

glucose-protein or glucose-lipid interactions, are implicated in the

complications of diabetes and aging. The objective of this article was

to determine the AGE content of commonly consumed foods and to evaluate

the effects of various methods of food preparation on AGE production.

Design

Two-hundred fifty foods were tested for their content in a common

AGE marker ϵN-carboxymethyllysine (CML), using an enzyme-linked

immunosorbent assay based on an anti-CML monoclonal antibody. Lipid and

protein AGEs were represented in units of AGEs per gram of food.

Results

Foods of the fat group showed the highest amount of AGE content

with a mean of 100±19 kU/g. High values were also observed for the meat

and meat-substitute group, 43±7 kU/g. The

carbohydrate group contained the lowest values of AGEs, 3.4±1.8 kU/g. The

amount of AGEs present in all food categories was related to cooking

temperature, length of cooking time, and presence of moisture. Broiling

(225°C) and frying (177°C) resulted in the highest levels of AGEs,

followed by roasting (177°C) and boiling (100°C).

Conclusions

The results indicate that diet can be a significant environmental

source of AGEs, which may constitute a chronic risk factor for

cardiovascular and kidney damage.

From the above study

AGE Amounts In Food (per serving)

(As you can see, it is not the potato, the sweet potato, or the

slice of bread that is contributing to the AGE load of most people.)

Starchy vegetables

Corn, 20

Sweet potato, roasted, 72

White potato, boiled, 17

White potato, french fries, homemade 694

White potato, french fries, fast food 1,522

White potato, roasted, 45 min, prepared with 5 mL oil 218

Grains/legumes

Bean, red kidney, raw 116

Bean, red kidney, canned 191

Bean, red kidney, cooked 1 h 298

Pasta, cooked 8 min 112

Pasta, spiral, cooked 12 245

Bran Flakes 10

Corn Flakes 70

Frosted Flakes 128

Oatmeal instant, 4

Oatmeal,h instant 25

Bread

Whole wheat, center 16

Whole wheat, center toasted 25

Whole wheat, crust 22

Whole wheat, crust, toasted 36

Pita pocket 16

Fruits

Apple 13

Apple, baked 45

Banana 9

Cantaloupe 20

Raisin 36

Even good fats and/or good fats that are heated produce high levels of

AGEs

Almonds, roasted 1,995

Avocado 473

Cashews, roasted 2,942

Olive, ripe 501

Peanut butter, smooth 2,255

Walnuts, roasted 2,366

From the above numbers, if I switch from a sweet potato to an avocado,

I RAISE my levels of AGEs over 600%

The REAL Culprits

Cream cheese, 3,265

Mayonnaise 9470

Butter 1,324

Beef

furter, boiled 7 min 6,736

furter, broiled 5 min 10,143

Hamburger, fried 6 min 2,375

Hamburger, fast food 4,876

Meatball, boiled in sauce 2,567

Shoulder cut, broiled 5,367

Bacon, microwave 1,173

Deli ham, smoked 2,114

Pork chop, pan fried 4,277

Chicken breast, skinless cubes

Steamed 10 min and broiled 12 min 5,071

Pan fried 10 min and boiled 12 min 5,706

Chicken breast, skinless cutlet

Raw 692

Boiled 1 h 1,011

Broiled 15 min 5,245

Fried 8 min 6,651

Roasted, barbecue sauce 4,291

Roasted, breaded 4,102

Roasted, breaded, microwave, 1 min 55,157

Fish

Salmon, raw 502

Salmon, smoked 515

Trout, raw 705

Trout, roasted 25 min 1,924

Cheese

American, processed 2,603

American, processed,e low fat 1,425

Brie 1,679

Cottage cheese, 1,744

Feta 2,527

Mozzarella,e part skim 503

Parmesan,e grated 2,535

[Guest guest]

Hi Rodney,

A bit of a pain it was, but, I am pleased to help.

Cheers, Al

From: Rodney <perspect1111@...>Subject: [ ] Re: Back to AGEs Date: Saturday, August 2, 2008, 7:06 AM

Hi folks:

This is a very interesting, and extraordinarily well organized, study. Among its findings are that CR mice consuming an AGE-enhanced diet live less long than fully fed mice eating regular mouse chow. This seems to indicate the overwhelming importance of avoiding dietary AGEs, something that had gone somewhat over my head until I saw this paper. It might be argued that the benefit of a CR diet is derived from the fact that, when eating 40% less food one is consuming 40% fewer AGEs.

While investigating this I came across the following quote:

"... the plasma AGE content of healthy vegetarians has been reported to be higher than that of omnivores - suggesting that something about vegetarian diets may promote endogenous AGE production. Some researchers have proposed that the relatively high fructose content of vegetarian diets may explain this phenomenon ........ ", from PMID: 15607576.

Uh oh. Fructose again. Fruits! Low methionine but high fructose!

And while talking about AGEs, the AGE content of various foods has been discussed in PMID: 15281050. It found fats generally contain very high AGE levels. About thirty times more as a group than carbohydrates as a group.

Possibly the problem with a high fat diet is not the fat, but rather the AGEs that, it seems, inevitably accompany the fat?

Of course, cooking time and temperature are also critical to AGE formation, as noted in that paper. And AGEs are created 'endogenously' as well as being consumed in food.

In one paper the expression "antioxidant homeostasis" was used, which was a new perspective to me. One needs, it seems, to make sure one's body's capacity to handle (eradicate) these things is not overwhelmed by excessive amounts of them.

Rodney.

>> Recent news on significant difference made by heat treatment of CR > diet on various health parameters.> > > Oral glycotoxins determine the effects of calorie restriction on > oxidant stress, age-related diseases, and lifespan.Cai W, He JC, Zhu > L, Chen X, Zheng F, Striker GE, Vlassara H.> Department of Geriatrics,Mount Sinai School of Medicine, One Gustave > Levy Place, New York, NY 10029, USA.> > We previously showed that the content of advanced glycation end > products (AGEs) in the diet correlates with serum AGE levels, oxidant > stress (OS), organ dysfunction, and lifespan. We now show that the > addition of a chemically defined AGE (methyl-glyoxal- BSA) to low-AGE > mouse chow increased serum levels of AGEs and OS, demonstrating that

> dietary AGEs are oxidants that can induce systemic OS. OS predisposes > to the development of cardiovascular and chronic kidney diseases; > calorie restriction (CR) is the most studied means to decrease OS, > increase longevity, and reduce OS-related organ damage in mammals. > Because reduction of food intake also decreases oxidant AGE s intake, > we asked whether the beneficial effects of CR in mammals are related > to the restriction of oxidants or energy. Pair-fed mice were provided > either a CR diet or a high-AGE CR diet in which AGEs were elevated by > brief heat treatment (CR-high). Old CR-high mice developed high > levels of 8-isoprostanes, AGEs, RAGE, and p66(shc), coupled with low > AGER1 and GSH/GSSG levels, insulin resistance, marked myocardial and > renal fibrosis, and shortened lifespan. In contrast, old CR mice had > low OS, p66(shc), RAGE, and

AGE levels, but high AGER1 levels, > coupled with longer lifespan. Therefore, the beneficial effects of a > CR diet may be partly related to reduced oxidant intake, a principal > determinant of oxidant status in aging mice, rather than decreased > energy intake.> > PMID: 18599606 [PubMed - in process]> PMCID: PMC2475771 [Available on 02/01/09]>

[Guest guest]

Glycolysis is a big subject.

Perhaps:

http://en.wikipedia.org/wiki/Advanced_glycation_endproduct"AGE formationAGEs may be formed external to the body (exogenously) by heating (e.g. cooking) sugars with fats or proteins[2]; or, inside the body (endogenously) through normal metabolism and aging. Under certain pathologic conditions (e.g. oxidative stress due to hyperglycemia in patients with diabetes), AGE formation can be increased beyond normal levels"

In http://www.biomed.cas.cz/physiolres/pdf/51/51_313.pdf

I wonder the level of exercise in test subjects, and how much ethanol?

My HbA1c was 5.0. in 2005.

Fruit consumption is at least 15 oz. That's what one of my pears weighs.

Regards

[ ] Re: Back to AGEsHi folks:This study finding posted by raises an interesting point:"Blood fructose, cholesterol, fructosamine and ***glycated hemoglobin*** levels, and urine lipid peroxidation productswere significantly higher in fructose-fed rats compared with theother sugar-fed and control rats."How many people here know their glycated hemoglobin (HbA1C) level? And among them how many would be prepared to make an off-the-cuff guess as to their normal fruit intake? (Rating, perhaps, from zero to 10). If we had a couple of dozen, or more, data points for these two variables we might be able to take a VERY approximate stab at determining whether, among us, it appears that high fruit intake is associated with higher HbA1C.Of course this would be nowhere even remotely close to being definitive. But it might be helpful if we cannot find any published source of this information in humans. If high fruit intake is accelerating aging it is certainly something we would want to know about. And the supposed problems with HFCS would be explained as well.I would rate my fruit intake at 3·5 on that scale (relatively low) and my most recent HbA1C was 4·7 (OK but not remarkable). Especially interesting would be the HbA1Cs of people who never eat fruit. Any takers? Please!Rodney.