"This means that the production of nucleotides is essential to keep cells young," Delfarah said. "It also means that if we could prevent cells from losing nucleotide synthesis, the cells might age more slowly."
Am I the only one wondering if this person is confusing cause and effect?
> Am I the only one wondering if this person is confusing cause and effect?
No you are not. I work in this field and confusions of cause and effect are a daily occurrence. It is as dumfoundedd said, the reality is that aging is a complex causal network. I think everyone knows that but can't resist the temptation to pretend like the one edge they are working on in the network is the end-all.
It can get very ridiculous. At this year's aging meeting someone was actually proposing DNN predictions of age based on people's faces as a gold standard for biomarkers of aging. That is, they were suggesting people's faces were a better indicator of their internal biological state of aging than both their actual age and any internal biological marker.
Metagenomics is another one, although more debatable. I personally find it much more plausible that changes in the aging gut cause changes in the microbiome than the reverse (in general).
Horvath's epigenetic clock is another one, he presented a elastic net model that could predict age based on DNA methylation using a few hundred loci. For several years and even now, way too many investigators thought those loci were actually causal in aging because they don't understand how statistics work.
It annoys me. I have long considered writing a review to remind people what causality means. It is far too common for people to observe correlations and just straight to predicting causality without any additional evidence besides the correlation.
The interesting finding of this paper is that inhibition of nucleotide synthesis can induce senescence. But the (simplistic) definition of senescence is inability to replicate. You can't replicate without nucleotides, but this doesn't at all mean that the ordinary cause of senescence is lack of nucleotides. The common understanding is that it is G1 or G2 arrest due to DNA damage of one sort or another. Furthermore, the observation that senescent cells don't produce many nucleotides is kind of a duh. It is useful and important that they quantified it, but still it is hardly surprising.
But there is still hope. I just saw my chair in the hall, told him about this paper, and asked his opinion of the idea that "fixing nucleotide synthesis may help reduce cell senescence or help cells age more slowly". His response was to laugh, pat me on the shoulder, and walk away, if that says anything.
That'd be like giving CPR to dead squirrels. It seems more promising to introduce a mechanism to gradually kill off cells that aren't producing nucleotides. Though there must be easier symptoms of senescence to key off of.
It probably isn't the root cause but it probably isn't the final symptom either. Solving aging seems to resemble working up a complicated tree of causality with multiple roots. Fixing nucleotide synthesis won't make us immortal but it may prevent significant downstream impacts.
I think they probably are, but they could also be right (maybe without realizing the nuances).
It may be true that slowing down loss of nucleotide synthesis, while not fixing the root cause, may still slow down the aging process. Just like giving Parkinson's patients L-DOPA doesn't resolve the root cause of the disease; it's treating the effect and not the cause. But there isn't really anything better out there (AFAIK), and it slows down the brain degeneration process by replenishing one of the important things that gets destroyed in the degeneration, just as fixing nucleotide production may slow down cell degeneration. It's a very imperfect solution, but it still provides some relief for many people. We've got to work with what we've got.
Am I the only one wondering if this person is confusing cause and effect?