I'll note that the authors here favor programmed aging, a vocal minority in the research community at the moment. This has a number of varieties, but essentiall

I'll note that the authors here favor programmed aging, a vocal minority in the research community at the moment. This has a number of varieties, but essentially boils down to the root cause of aging is considered to be epigenetic changes. So epigenetic changes -> damage. The majority view in the research community is vice versa, that damage -> epigenetic changes. Aging is an accumulation of cell and tissue damage, something that spirals down ever faster as the damage starts to cause damage repair systems to fail. The forms of fundamental damage that cause aging are actually well agreed upon, but there is a lot of argumentation over which are more important and how exactly they cause specific age-related conditions. How can a field sustain two such diametrically opposed sets of theory? Because while we know the differences between old and young tissue, we still don't have a full accounting of cellular metabolism, and certainly don't have a full map of how a->b->c for all molecular biology at any given time, let alone over the entire course of aging sufficent to explain from start to finish any specific age-related condition. This is why SENS ("repair the damage, don't try to understand why it causes age-related disease, just fix it and things will become clear one way or another") is so important. We can repair the damage. That is much, much easier and cheaper than trying to understand the full chain of cause and effect. The next five to ten years should see one or other side proven conclusively wrong. The challenge is that addressing secondary effects in aging can still produce benefits. The water is muddy. On the damage viewpoint, we have things like senescent cell clearance now under development in companies like Oisin Biotechnologies and UNITY Biotechnology. Clearance extends life in mice. Senescent cells are known to contribute to many age-related diseases. On the epigenetic alteration side we have things like restoration of youthful GDF11 levels, which improves health in mice by signaling stem cells to go back to work. From the damage viewpoint, those stem cells are in decline as a reaction to damage, and the signaling therapy is an override. From the programmed aging point of view the signaling change is the primary cause. I think that the most compelling argument against programmed aging and for damage is that some forms of damage cannot be repaired by our biochemistry. Specifically persistent glucosepane cross-links in the extracellular matrix, for example, causing loss of structural properties such as elasticity. Also some of the constituents of liposfusin that builds up in long-lived cells and causes their lysosomes to malfunction. It doesn't matter how youthful your epigenetic patters are, you cannot break them down.