One of the nice things about writing online is that if you procrastinate on a topic for long enough, someone else will write that post for you. Often it will be far better than the one you would have turned out, had you been more motivated. The topic for today, and one I've been meaning to discuss for a while, is what happens to science when it passes through the mangler of journalism; in particular, what happens to aging and longevity science. Let me point you to a well-written reminder that professional journalists are known to write spectacularly dumb, inaccurate, and misleading articles on aging research:
Recent work in Newcastle, UK and at the University of Ulm, Germany has been toted as discovering the "secrets to aging" but is really just another small step in understanding why our bodies wear down. The research was published in the journal Molecular Systems Biology, picked up by the Telegraph and then redistributed by the usual lot of copy and paste news feeds. Using human cells, mouse cells and computer simulations, the British-German team explored the mechanism that produces cell senescence - the state in which a cell stops dividing and eventually dies. They found a certain protein pathway was responsible for cells with damaged DNA becoming senescent. That’s a cool bit of science, but it’s not the “secret to aging” and its lightyears from a cure for aging. Unfortunately, journalists can’t sell “scientists take another steady step in large complex problem that may not be solved for decades”, so we’re left with an over-hyped, misunderstood development. Which is a shame, because the Newcastle-Ulm group actually made some interesting discoveries.
Reading mainstream or popular science coverage is a skill, much like reading the scientific journals, though possibly a little easier. You really have to learn how to sift the nonsense from the responsible coverage, and then how to use that responsible coverage to determine what the latest news actually means.
But let us look at the actual paper. You might recall that increasing numbers of senescent cells are one cause of aging; they don't behave well, and secrete biochemicals that cause further disruption in surrounding tissues. The paper's authors suggest that senescence may be largely the result of mitochondrial DNA damage and resulting mitochondrial dysfunction - which would be good, if that is indeed the case. Collapsing two root causes of aging down into one would improve the odds of attaining rejuvenation technologies within our lifetimes, though old people would still no doubt need their existing senescent cell populations cleared out.
The bottom line here is this:
Importantly, our results show that interventions against individual components of the senescent phenotype (e.g. ROS production) are possible in deep senescence. Even if these interventions do not rescue the growth arrest phenotype, they can ameliorate the phenotypic impact of senescent cells onto their microenvironment (the 'bystander effect'). There is a preliminary evidence that ‘anti-senescence’ interventions have potential to delay aging. However, interventions upstream of the cell cycle checkpoint machinery may significantly increase cancer risk.
That last point is important, as senescence is the evolutionary counterbalance to the rising risk of cancer with age. But it will become much less important with time, as cancer therapies become very powerful, safe, and efficient - and very cheap, shortly thereafter.
Passos, J., Nelson, G., Wang, C., Richter, T., Simillion, C., Proctor, C., Miwa, S., Olijslagers, S., Hallinan, J., Wipat, A., Saretzki, G., Rudolph, K., Kirkwood, T., & von Zglinicki, T. (2010). Feedback between p21 and reactive oxygen production is necessary for cell senescence Molecular Systems Biology, 6 DOI: 10.1038/msb.2010.5