Starting a series related to causation and aging, this being part 1. Don’t expect super-systematic explication, more like inter-linked fragments.
My October, 2019 Philosophy PhD Seminar talk at Eötvös Loránd University in Budapest had a twin-focus, one on a recursive definition of biological aging, the second on causation in aging. The two questions are conceptually interconnected at a level of figuring out whether the hallmark processes used to define biological aging can be considered necessary or sufficient causes of the overall biological aging process. My understanding of causation has been profoundly influenced by Judea Pearl & Dana Mackenzie’s The Book of Why and in general by Pearl’s causal inference handling technique, one source being Bayesian networks, another source being counterfactual probabilities amongst others. As a biologist am already indebted to a different Bayesian analysis method and as an analytically trained I’ve been using counterfactual type of analysis all the time, being at the core of thought experimentation. To my surprise, I’ve also managed to attract the attention of Judea Pearl himself on Twitter to the problematics and need for a proper causal analysis related to biological aging. Let’s see whether we can turn the attention into concentration.
The first several posts in the series is going to be a quick write-up of my slides I presented. The slides are available here.
Please see below how I consider at first the different, yet fundamental causation layers in the context of aging. I dubbed this figure as The ladder of causation in aging as an obvious paraphrase/allusion of Pearl’s Ladder of causation, and while there’s a lot of connection between the 2 ladders, there’s no strict mapping between the different shelves. Basically, all 3 ladders of Pearl’s causation ladder – association, intervention, counterfactuals – are aspects that can be examined, considered, excluded, applied in the context of the different layers in aging.
The bottom step of the ladder is also the most mysterious level that seems to be so intimately linked with all things aging that many people cannot think further: time. Or the problem is that they might stop thinking further and equating aging with time, so basically aging is exhausted by being chronological aging, but by saying this, or acknowledging time’s determining and definitive role in all things aging they use it as explanation of all aging processes occurring. Indeed, the question that can be asked in the light of this overwhelming role time seems to be playing in all things aging is this: How can time play a causal role in bringing about different forms of aging, and in our case, more specifically: can time be a cause in any conceptual or empirical sense in the diverse processes of biological aging? I try to elaborate on this idea a bit further in a subsequent post.
The second level is by far the most important one in order to understand and modulate biological aging to achieve healthy longevity. There’s finally an emerging scientific consensus about our understanding of the major molecular and cellular hallmark processes driving biological aging. In my recursive definition of aging I’m using these processes to as components of the recursion. But the big question is what kind of causative role exactly can be attributed to these processes? More on this later.
The third, topmost level goes back to the chronological level, but not from the depth of the physical time concept but from the phenotypic, human sized, organismal, well-known and familiar, expected level of increasing morbidity, co-morbidity and mortality rates occurring with increasing chronological age.
From physical time to molecules and cells and then further up to whole organisms, these 3 levels form our initial steps of the rudimentary ladder of causation in aging, I’d like to focus on in this series of posts.
Please see next post: The rabbit hole of temporal causation and biological aging