Spermidine and Another Vote For Autophagy
For many years, up until fairly recently, life science researchers who talked in public about altering or reversing the course of aging found that this was a quick and effective way to destroy fundraising prospects. The mainstream institutions involved in grants are conservative indeed. So next to nobody said anything - in public at least. But times are changing. It has to be said that scientists involved in aging research are now becoming noticeably more comfortable about talking in public on the topic of extending life span. Perhaps a little too comfortable here in the choice of title, but the science is sound:
Spermidine: A novel autophagy inducer and longevity elixir:
Spermidine is a ubiquitous polycation that is synthesized from putrescine and serves as a precursor of spermine. Putrescine, spermidine and spermine all are polyamines that participate in multiple known and unknown biological processes. Exogenous supply of spermidine prolongs the life span of several model organisms including [yeast, nematodes, and flies] and significantly reduces agerelated oxidative protein damage in mice, indicating that this agent may act as a universal anti-aging drug.Spermidine induces autophagy in cultured yeast and mammalian cells, as well as in nematodes and flies. Genetic inactivation of genes essential for autophagy abolishes the life span-prolonging effect of spermidine in yeast, nematodes and flies. These findings complement expanding evidence that autophagy mediates cytoprotection against a variety of noxious agents and can confer longevity when induced at the whole-organism level.
We hypothesize that increased autophagic turnover of cytoplasmic organelles or long-lived proteins is involved in most if not all life span-prolonging therapies.
I've mentioned spermadine in the context of longevity and autophagy in the past, and the authors of the paper quoted above are far from the only folk who think that all roads lead to autophagy when it comes to altering metabolism to increase life span.
The better known life extension mechanisms in lesser animals are all driven by changes in autophagy - or so say the autophagy specialists. It's true that the various hyperspecialized communities of modern biology are overly cloistered and ignorant of one another's research, but the autophagy researchers are assembling compelling evidence for this position.
You might notice the similarity between the longevity-enhancing effects of calorie restriction and those of spermadine: both stop working if researchers eliminate autophagy in lower animals.
Madeo F, Eisenberg T, Büttner S, Ruckenstuhl C, & Kroemer G (2010). Spermidine: A novel autophagy inducer and longevity elixir. Autophagy, 6 (1) PMID: 20110777
I agree about the importance of autophagy and intracellular turnover (recycling) to longevity. I would add that the lysosomes in nondividing cells become clogged with lipofuscin, so that eventually there is no space for new autophagosomes to unload their cargos. So, while upregulation of autophagy is an important piece of the whole therapy, work is also needed to eliminate or prevent lipofuscin accumulation, especially in nondividing cells.