The Past Year of Progress in Calorie Restriction Science

I had noticed a recent review paper on progress in calorie restriction (CR) research over the past year or so; unfortunately it has no freely available abstract, which makes referencing fairly pointless for the majority of readers here and at the Longevity Meme. However, the folk of the Calorie Restriction Society mailing lists have more information:

Selected quotes from CR research progress report over the past year. The PDF article is quite technical. I may have missed numerous significant points. I cherry-picked those of interest to me (that I could understand!).

1. CR Lifespan increase appears to be very robust and plastic

The fact that alternate pathways promoting longevity are induced in [yeast] strains lacking respiratory capacity [no mitochondrial retardation of aging] does not negate a role for mitochondrial metabolism where the organelles are functional. The important finding from these studies on strain dependent differences is that CR may extend lifespan by impacting multiple pathways and that there may be a certain amount of mechanistic plasticity.

2. TOR pathway affects nutrition, metabolism and longevity

The influence of TOR on mitochondrial function is of particular interest in the context of CR, because mammalian studies have demonstrated that mitochondrial metabolism and [free radical] generation are altered in tissues from restricted animals compared to controls.

3. CR does not work in some genetically altered species

In rodents, CR extends the lifespan of the Ames dwarf but does not further extend the lifespan of the growth hormone receptor knockout (GHRKO) mouse (Bonkowski et al., 2006).

So in short, as I mentioned the other day, it seems likely that sirtuins are not the end of the calorie restriction story insofar as genes and biochemistry goes. In addition, it is clear that scientists are making real progress in narrowing and clarifying the focus on the core biochemistry of CR-induced longevity and health benefits - what is essential, and what is not. It would not surprise me to see mitochondrial function amongst the important changes brought about by the practice of calorie restriction, given the prominent role most likely played by mitochondria in causing aging.

A fair amount of money is presently going towards calorie restriction studies - certainly much more than in past years, even if modest in comparison to many other fields of medical research. Expect to see much more progress in the next couple of years, especially as some calorie restriction mimetic drugs start to move ahead in the pipeline.

Now if we could just raise more effective longevity and anti-aging research - based on repair rather than metabolic manipulation - up to even this level of funding...

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I'm all for success in CR mimetics, because it shows we can actively intervene to prolong healthy lifespan, not just frail lifespan. Put that together with Alteon's ongoing success in actually reversing damage in some organs/systems with A-711 and we have a solid case for real life extension.

Look, less than ten years ago CR was regarded by a lot of the medical research people as just another kooky fad. The few researchers who looked into it then showed success, and now we have a lot more research.

Success with CR mimetics and repair, even as limited as A-711 offers, will spur much more research work into deeper repair. We can count on that if for no other reason than the "longevity dividend" in keeping Medicare from going totally bankrupt. Longer-lived healthy people won't be as much of a drag on that system as shorter lived sick ones.

Posted by: Observer at December 4th, 2006 10:41 AM
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