Fight Aging!

A wealth of long-lived mammals can be found in the laboratories of aging researchers. The healthy life spans of these animals are extended by comparatively minor genetic alterations, drugs such as rapamycin, or environmental changes like calorie restriction that are used to identify targets for future genetic engineering. This is the domain of the metabolic engineers, who see no better way forward than to gently slow aging by tweaking the operation of human metabolism. It will be a long and expensive road, and at the end will not produce results that can help people who are already old. Metabolic engineering cannot produce rejuvenation, the reversal of aging - yet it is the dominant body of longevity science in this day and age.

Thus most of the new research you'll see or read about is directly only towards either understanding or at best slowing aging, with significant results not really expected for a couple of decades. Here is a review of the sort of foundational work taking place in this field:

Studies of the effects of single-gene mutations on longevity in Caenorhabditis elegans, Drosophila melanogaster and Mus musculus identified homologous, highly conserved signalling pathways that influence ageing. In each of these very distantly related species, single mutations which lead-directly or indirectly-to reduced insulin, insulin-like growth factor (IGF) or insulin/IGF-like signalling (IIS) can produce significant increases in both average and maximal lifespan. In mice, most of the life-extending mutations described to date reduce somatotropic (growth hormone (GH) and IGF-1) signalling.

The reported extensions of longevity are most robust in GH-deficient and GH-resistant mice, while suppression of somatotropic signalling 'downstream' of the GH receptor produces effects that are generally smaller and often limited to female animals. This could be due to GH influencing ageing by both IGF-1-mediated and IGF-1-independent mechanisms.

In mutants that have been examined in some detail, increased longevity is associated with various indices of delayed ageing and extended 'healthspan'. The mechanisms that probably underlie the extension of both lifespan and healthspan of these animals include increased stress resistance, improved antioxidant defences, alterations in insulin signalling (e.g. hypoinsulinaemia combined with improved insulin sensitivity in some mutants and insulin resistance in others), a shift from pro- to anti-inflammatory profile of circulating adipokines, reduced mammalian target of rapamycin-mediated translation and altered mitochondrial function including greater utilization of lipids when compared with carbohydrates.

None of this is useless knowledge: the more that is known about aging and biology in mammals, the easier it will be to strike off and build working rejuvenation technology that can repair and revert the biochemical differences between a young person and an old person. But we are already well past the point at which it is practical to do this: time spent acquiring further knowledge of aging biology is now nowhere near as valuable as time spent on building the known forms of repair-based rejuvenation biotechnology. The different in time taken to produce results and the difference between slowing aging and reversing aging is counted in hundreds of millions of lives.

While you were reading this sentence, a dozen people just died, worldwide. There. Another dozen people have perished.

And this will continue until we build the means to treat aging as a disease and cure the old by repairing the accumulated cellular and biochemical damage that is killing them.