No offense Edouard but the fact that the quercetin-consuming mice lived 10% shorter lives is helpful information. Of course you’ve got to analyze this in terms of the dose and what the dose equivalent in people would be – but I don’t think that’s a good thing to decrease lifespan. At the least if means there’s a limit beyond which more harm than good is done – like most ‘medicines’. Again, we’re tilting at windmill’s each statistical increase in lifespan in mice may have nothing to do with increasing human lifespan. The most important think I think is to realize the a living thing is not just a collection of genes. Yes, there are something like twenty-something thousand proteins, and then with alternate reading frames and differential splicing we might double that number, but there are hundreds of thousands of enhancer regions, and dozens (at least estimates range into the millions) of histone codons, there is the heirarchical organization of the interphase nucleus influencing gene regulation, There is a four dimensional structure to a life – you are not given a collection of genes – those genes are exposed in a partcular order as development proceeds – you become an embryo, a fetus, a neonate, a baby, a todler – and ending with, late middle age, early old age, middle old age, old old age – death) the entire scenario that you are born with – that you act out throughout your lives.
I think the bacterial virus T4 most influenced me – it played out its life like a lighted fuse – transcription starting at the 5′ end of the organism and traveling towards the 3′ end. At the 5′ end are all the “early” genes (early early, middle early and late early) that chew apart the host DNA substitute their own sigma factors to direct the host RNA polymerase to viral DNA- and at the 3′-end is the lysozyme gene whose product will lyse the bacterial cell wall (all of this has been taking place in a bacterium), releasing all the progeny. Now our lives have many more choices – (T4 has none, bacteriophage lambda can choose to be lytic or become a dormant part of the host DNA) – but I think the basic plan is the same – a four dimensional progression. Even when we look at the progression of hemoglobins during development we see the different hemoglobin genes are linearly arrange in the order they appear in the embryo/fetus/newborn.