September 14, 2013

Spermidine induces autophagy in multiple species and mimics calorie restriction and increases longevity in mice by 10%

Spermidine induced autophagy was presented at SENS6.

Spermidine is a natural occurring polyamine that declines continuously during aging of organisms. They found that external administration of spermidine triggers autophagy across species and prolongs lifespan of yeasts, flies and worms in a autophagy dependent manner. Moreover, spermidine extends healthsspan of mice.

They propose that the anti-aging potential of spermidine roots in epigenetic transformation of the cell and indicate its therapeutic potential for the avoidance of age associated diseases.

Josh Mitteldorf information

Fed to yeast cells, it increases life span dramatically, with smaller but still significant effects in flies and worms. Life span of mice can be increased by about 10% with spermidine in the diet. The mechanism seems to be stimulation of the process called autophagy, by which each cell cleans up its waste products, digesting them in organelles called lysosomes. Spermidine is part of the body’s metabolism, but its concentration declines with age. The best dietary source is a Japanese fermented soy product called natto, which is famous for its vile flavor. Other dietary sources include soy products and wheat germ. And yes, it is found at high concentrations in semen.

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 (Saccharomyces cerevisiae), nematodes (Caenorhabditis elegans) and flies (Drosophila melanogaster) and significantly reduces age-related 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.

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