Re: Re: Back to AGEs /a plea for sanity

[Guest guest]

Let’s have some sanity here. We have studies which point to berries and other fruits as being beneficial for disease prevention; studies which directly point to moderate red wine drinking as being correlated with longer lifespan (and the grapes seem to be implicated, not the alcohol, noting that beer and other drinkers don’t get the benefit).

We also have a long, long list of suspects for shortening life; the latest before this having been methionine. Shall we now switch to fruit :-)))

I’m not saying we shouldn’t explore this. I’m just saying that it sounds flaky to me personally and joins a long list of yet to be proven suspects.

If one is confused, you can always follow the diets of the long-lived peoples of the world (Okinawans for example – or the Mediterranean diet).

Moderation and caution is my mantra.

From: Rodney <perspect1111@...>

Reply-< >

Date: Mon, 04 Aug 2008 11:31:19 -0000

< >

Subject: [ ] Re: Back to AGEs

Hi folks:

This study finding posted by raises an interesting point:

" Blood fructose, cholesterol, fructosamine and ***glycated hemoglobin*** levels, and urine lipid peroxidation products

were significantly higher in fructose-fed rats compared with the

other 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.

>

> Useful low AGE meal plan with some cooking instructions

>

> http://www.mendosa.com/Low%20AGE%20Meal%20Plan%20Instructions.pdf

>

> On fructose consumption and its effects relative to endogenous AGE

> formation, this 10 year old(!) study:

>

> Long-Term Fructose Consumption Accelerates Glycation and Several Age-

> Related Variables in Male Rats1,2,3

> Boaz Levi and Moshe J. Werman4

>

> Department of Food Engineering and Biotechnology, TechnionIsrael

> Institute of Technology, Haifa, Israel

>

> Fructose intake has increased steadily during the past two decades.

> Fructose, like other reducing sugars, can react with proteins through

> the Maillard reaction (glycation), which may account for several

> complications of diabetes mellitus and accelerating aging. In this

> study, we evaluated the effect of fructose intake on some age-related

> variables. Rats were fed for 1 y a commercial nonpurified diet, and

> had free access to water or 250 g/L solutions of fructose, glucose or

> sucrose. Early glycation products were evaluated by blood glycated

> hemoglobin and fructosamine concentrations. Lipid peroxidation was

> estimated by urine thiobarbituric reactive substances. Skin collagen

> crosslinking was evaluated by solubilization in natural salt or

> diluted acetic acid solutions, and by the ratio between - and -

> collagen chains. Advanced glycation end products were evaluated by

> collagen-linked fluorescence in bones. The ratio between type-III and

> type-I collagens served as an aging variable and was measured in

> denatured skin collagen. The tested sugars had no effect on plasma

> glucose concentrations. Blood fructose, cholesterol, fructosamine and

> glycated hemoglobin levels, and urine lipid peroxidation products

> were significantly higher in fructose-fed rats compared with the

> other sugar-fed and control rats. Acid-soluble collagen and the type-

> III to type-I ratio were significantly lower, whereas insoluble

> collagen, the to ratio and collagen-bound fluorescence at 335/385

> nm (excitation/emission) were significantly higher in fructose-fed

> rats than in the other groups. The data suggest that long-term

> fructose consumption induces adverse effects on aging; further

> studies are required to clarify the precise role of fructose in the

> aging process.

>

> http://jn.nutrition.org/cgi/content/full/128/9/1442

>

> This study strogly suggests the significant implication of AGEs in

> diabetes pathology. It was a kind of milestone for the authors, for

> after it they became bolder in their assertions when discussing the

> results of an impressive series of follow up studies and papers,

> claiming to have established a CAUSAl relationship between high AGE

> consumption and various pathologies :

>

> http://diabetes.diabetesjournals.org/cgi/content/full/51/7/2082?

> ijkey=fcfaf2a6e8dd95606ff89944cec527f43b03dc05

>

> Taken from the write up this very interesting and novel bit:

>

> Islet morphology.

> Histological examination and insulin immunostaining were performed in

> pancreatic sections from each group at the end of the study. Islets

> of HAD-fed db/db mice exhibited hyperplasia and hypertrophy combined

> with loss of islet structure and cellular homogeneity, changes seen

> only infrequently in islets from LAD-fed db/db mice. In addition,

> islet degeneration and insulin degranulation, including glucagon-

> producing cell displacement from the periphery to the center of the

> islets, were more evident in HAD-fed db/db mice than in LAD-fed db/db

> mice. Overall, LAD-fed db/ db mice presented better preserved,

> compact islets with intensely positive staining for insulin (Fig. 5).

> Comparing 10 consecutive pancreatic sections per mouse from the LAD-

> (n = 5) and HAD-fed (n = 5) control mice, we could not observe a

> discernible difference in islet structure and insulin immunostaining.

>

> Regards,

>