And what do you plan to do about it? (was:]Methionine and Brain Function)

February 27, 2008

Here’s what I would like to throw out to the group. Let us suppose that methionine restriction (and some other amino acid (glycine?) are the reasons that CR works (through eating less of them and also eating mainly a low calorie, plant rich diet).

If one assumes the above to be true, does this now mean that one can eat as many calories of non-methionine (non-glycine) rich foods one wants to eat?

2) And does that mean that some foods are no longer demonized? Such as sugar. I’ve been using sucralose for 8 years now and limiting all desserts – is dessert off the “bad” List? Most serious CRONIES do something similar.

3) We’ve had on on-going argument about extreme CRON and moderate CRON and this group has taken the moderate stance (BMI between 18.5 and 22 or so - see our files for studies citing these numbers for longest life). If the above amino acids prove to be the reasons that CRON works, would that prove that extreme CRON has lost the argument? IOW, it’s unnecessary, and potentially dangerous?

4) Some high methionine foods (legumes) are contradictorily associated with greater longevity. What are we do to with this contradictory information?

Right now I’m not changing anything in my diet and hedging all my bets. That includes moderate red wine (for longevity insurance), low sugar, and CRON. But I’d be interested in hearing what if anything the others are planning to do with this information, if anything.

From: Rodney <perspect1111@...>

Reply-< >

Date: Tue, 26 Feb 2008 21:46:58 -0000

< >

Subject: [ ] Methionine and Brain Function

Hi folks:

I do not remember seeing this one previously:

" These beneficial [Methionine restriction] induced changes .......... can play a key role in the protection against aging-associated neurodegenerative disorders. "

Rejuvenation Res. 2007 Dec;10(4):473-84

Methionine restriction decreases endogenous oxidative molecular damage and increases mitochondrial biogenesis and uncoupling protein 4 in rat brain.

Department of Experimental Medicine, Faculty of Medicine, University of Lleida-IRBLLEIDA, c/Montserrat Roig 2, Lleida, Spain.

Aging plays a central role in the occurrence of neurodegenerative diseases. Caloric restriction (CR) mitigates oxidative stress by decreasing the rate of generation of endogenous damage, a mechanism that can contribute to the slowing of the aging rate induced by this intervention. Various reports have recently linked methionine to aging, and methionine restriction (MetR) without energy restriction also increases life span. We have thus hypothesized that MetR can be responsible, at least in part, for the decrease in endogenous oxidative damage in CR. In this investigation we subjected male rats to exactly the same dietary protocol of MetR that is known to increase their life span. We have found that MetR: (1) decreases the mitochondrial complex I content and activity, as well as complex III content, while the complex II and IV, the mitochondrial flavoprotein apoptosis-inducing factor (AIF) and ATP content are unchanged; (2) increases the mitochondrial biogenesis factor PGC-1alpha; (3) increases the resistance of brain to metabolic and oxidative stress by increasing mitochondrial uncoupling protein 4 uncoupling protein 4 (UCP4); and (4) decreases mitochondrial oxidative DNA damage and all five different markers of protein oxidation measured and lowers membrane unsaturation in rat brain. No changes were detected for protein amino acid composition. These beneficial MetR-induced changes likely derived from metabolic reprogramming at the cellular and tissue level can play a key role in the protection against aging-associated neurodegenerative disorders.

PMID: 17716000

Rodney.

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