In the last 4 posts of this study I’ve built up an argument showing the need for a definition of biological aging that consolidates existing consensus knowledge in the field but also flexible enough to incorporate new knowledge within that current paradigm.
This is still not the final formulation, but this is what I have right now:
‘Biological aging is agings underneath, the result of multiple, separate, diverse, interconnected, but malleable processes, eventually compromising normal functions of the organism at different rates and at all (organisational, spatiotemporal) levels.’
What are some open problems left with this definition?
This is part 2 of my series on causation and aging. Last time I introduced the ladder of causation in aging where the bottom step of the ladder was also the most mysterious one that seems to be so intimately linked with all things aging that many people cannot think further: time. Our guiding questions were: How can time play a causal role in bringing about different forms of aging, and in our case, more specifically: can time be factored in as a cause in any conceptual or empirical sense of the diverse processes of biological aging? Here’s the edited slide I presented on this during my PhD seminar talk in Budapest.
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.