The dominant topic for this past week of posts was the beneficial biochemistry of eating less; changes to gene expression and metabolism, enhanced health and extended longevity. That wasn't an intentional choice - it just worked out that way as various items caught my eye. All the same, why not round it off with an paper on intermittent fasting research, noticed by the folk who keep sci.life-extension stocked.

Intermittent fasting and calorie restriction are two ways of reducing your calorie intake to obtain health benefits. Intermittant fasting might be accomplished by eating every other day, for example, while calorie restriction means eating every day, but eating less. In both cases, you have to make sure your intake of micronutrients is optimal, and your physician agrees, as for any sane dietary choice.

The paper is a demonstration that intermittent fasting quickly hits one of the same biochemical triggers as calorie restriction: TOR, or target of rapamycin, which in turn boosts the process of autophagy:

In many organisms, dietary restriction appears to extend lifespan, at least in part, by down-regulating the nutrient-sensor TOR (Target Of Rapamycin). TOR inhibition elicits autophagy, the large-scale recycling of cytoplasmic macromolecules and organelles.

More autophagy is a good thing; more aggressively cleaning out damaged cellular components should extend functional life span by lowering the rate at which further damage accumulates, and there is a fair weight of scientific evidence behind that viewpoint. In any case, here is the intermittent fasting study; notice that some changes in metabolic operation show up very quickly in response to changing dietary intake:

Intermittent fasting (IF) was shown to increase whole-body insulin sensitivity, but it is uncertain whether IF selectively influences intermediary metabolism. ... Glucose, glycerol, and valine fluxes were measured after 2 wk of IF and a standard diet (SD) in 8 lean healthy volunteers ... Phosphorylation of mTOR was significantly lower after IF than after the SD.

The cost of running small, quick studies of this sort in humans is fairly low - certainly far lower than your average study of metabolism and aging in mice and rats. This cost will only fall as the tools of biotechnology become better and cheaper. Given that, I'd expect to see many more studies over the next few years that carefully compare the initial metabolic response of various mammals - humans included - to a lower calorie intake. In theory that should lead to a better handle on how the long-term effects of calorie restriction or intermittent fasting will play out in humans.