I guess this goes back to the issue of defining things and what you mean by hallmarks. If you define your hallmarks broadly enough they may include almost anything while being so vague that they are only useful for posters and ads. In the case of vague hallmarks you’d be right, if you fix them you’re all good. But even in this extreme case I do expect the number of vague hallmarks to grow a little bit over time as we learn more. In fact, to me they feel incomplete and ill-defined already.
Looking at the classic “The Hallmarks of Aging” paper (first published as López-Otín et al. 2013 I think) or Aubrey’s seven causes of aging I do feel like they are way too vague. Let’s take genomic instability as an example. Fix it and you make progress against aging. However, that is just an empty phrase like “repair the engine of the car”; that’s usually the reason why it stops in the middle of the highway. Which genome, mitochondria, nuclear? Which pathway do you target? Hundreds of genes involved in repair, hundreds of genes involved in prevention of DNA damage via the intricate ROS- and stress-sensing pathways. Which type of lesion to prevent? Damaged bases or strand breaks? Which type of existing damage to repair and remedy post facto? Actual mutations (not just temporary damage), small indels, aneuploidies, large deletions, inversions, translocations or more complex chromosomal rearrangements and clonally expanded cell populations? Don’t forget to fix chromatin organisation and epigenetic marks and all the inter-related extra-nuclear factors that promote genomic instability (could be inflammation, could be reduced autophagy, let’s speculate). Want to use nanobots instead? Be my guest, then you are solving advanced physics, engineering and AI problems.
Regarding incompleteness and definitions: Why did they choose to define telomere attrition as its own hallmark? First of all, this is an incredibily specific problem and secondly telomeres are part of the nuclear genome, i.e. they fit entirely within the scope of genomic instability. On the other hand, extracellular matrix aging is not part of The Hallmarks even though it has been suggested to be a life-limiting pathology since the early 20th century with good supporting evidence (think vascular aging).
As you can see these Hallmarks are a political, strategic and scientific compromise. (One can guess telomeres are on there because of the Nobel prize, public perception that they matter or some telomere researcher on the paper.)
However, I do see the appeal of these words, hallmarks, causes, even if their use in practise is limited.
Aubrey’s case for trying to focus on the hallmark is that there are a lot less of them then illnesses and it’s thus easier to focus on hallmarks then on illnesses.
It seems that this thesis is basically wrong if they are two vague to be individually targeted.