Understanding The Odd Science Of Aging – A supporter asks if the Hallmarks of Aging can be effectively replaced by the seven categories of cellular and molecular damage in the platform. The answer is ‘no’, because the Hallmarks include both too much and too little, and most importantly because the Hallmarks fail as a road map to the biomedical postponement of aging.
Ible Question: The Hallmarks of Aging has become an extremely widely used framework for categorizing aging changes. For the purpose of having a shared language, would it make e simply adopt the Hallmarks instead of the seven strands of , while still attacking the damage of aging with the help of the “damage-repair” heuristic?
Understanding The Odd Science Of Aging
That’s a great question. By the end of September 2023, the original Hallmarks of Aging paper had been cited 12,801 times in the scientific literature according to Google Scholar, while the paper in which a version of Seven Strands first appeared had been “only” cited. 270 times, despite the fact that she published a decade earlier and with equally prominent coauthors.
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At the time when Dr. First proposed by Aubrey de Gray and colleagues, all the aging interventions scientists have successfully used in laboratory animals — calorie restriction, mutations in the insulin/IGF-1 pathway, and (a few years later) the drug rapamycin — were
. Scientists had learned that they could pull one of these levers and slow down many aspects of aging at the same time, resulting in an extension of healthy lifespan.
An important innovation with which Dr. de Gray introduced the idea that instead of trying to tackle all aging at once, aging could be slowed down or even reversed with a piece of “
” approach. The paper identified discrete categories of cellular and molecular aging damage whose particular members were common enough that scientists could deploy common strategies to remove, repair or replace the constituent lesions. And if that categorization system was comprehensive enough, then attacks from all its components
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At the time, this strategic insight was new and largely untested, and it drew some pushback from otherwise right-minded biogerontologists: “de Gray does not mention that any of these approaches have ever been shown to extend the lifespan of any organism, let alone humans. ” Like Dr.
– has ever been shown to extend the lifespan of any organism. I don’t recall Henry Ford warning potential customers that the components of a car
The Hallmarks paper came a few short years after that heated exchange, and now—a decade later—the Hallmarks categorization system has become a science.
To talk about different types of changes in the aging organism. And because scientists have become accustomed to thinking and talking about aging in this segmented way, it has become completely mainstream to think about tackling aging by focusing on individual Hallmarks rather than master regulatory switches for the process as a whole. With this significant shift in scientific thinking achieved and with the Hallmarks so widely used and understood, is it now time for the Seven to “fade into glorious obscurity” in their favor?
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The short answer is “no.” While the Hallmarks paper used rational criteria for identifying features of aging that are causally related
To the increasing risk of death and disease, those criteria are not strategically organized to bring the goal of identifying a suite of goals aging under full medical control. In the absence of an overarching strategic framework such as the “damage-repair” strategy, they tended to focus on “Hallmarks” in the literal sense of “characteristic features” rather than in the biomedically useful sense of “critical targets .” As a result, they won with a mixture of causes and effects of aging, and with things that are “causes” in different es. And as we shall see, the Hallmarks paper also lacks other critical objectives, while others include others that are mutually redundant.
Both the Hallmarks and the Seven start from the cone position that (as the Hallmarks paper put it) “The time-dependent
Is widely regarded as the general cause of aging (Gems and Partridge, 2013; Kirkwood, 2005; Vijg and Campisi, 2008). … Therefore, cancer and aging can be considered as two different manifestations of the same underlying process – namely the accumulation of cellular damage. The Hallmarks paper then sets out its criteria for identifying potential Hallmarks: “Each hallmark should ideally meet the following criteria: (1) it must manifest during normal aging; (2) its experimental deterioration must accelerate aging; and (3 )’s experimental improvement is supposed to slow down the normal aging process and thereby increase a healthy life span. However, they give themselves a lot of latitude on the latter criterion:
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The last criterion is the most difficult to achieve, even if limited to only one aspect of aging. For this reason, not all characteristics are yet fully supported by interventions that succeed in improving aging. This caveat is tempered by the extensive interconnectedness among the aging traits, which implies that experimental improvement of one particular trait can affect others.
With those criteria in hand, the authors have “nine characteristics of aging [that] are grouped into three categories”: primary Hallmarks, compensatory (or antagonistic) Hallmarks, and integral Hallmarks.
Of aging-induced damage.” Note the phrasing carefully, as this is the first and critical divergence between the Hallmarks and the Seven. The authors did not develop the Hallmarks as a system to organize the cellular and molecular
. This is because such damage is the exclusive target of the “damage repair” strategy, and the Seven are organized around platform technologies that scientists can tweak to attack multiple particular molecular lesions within each category.
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This blog post is not the place to rehash the matter, but Dr. de Gray in developing the heuristic was to “let the physiological sources of aging-causing damage” operate without interference and instead attack aging damage
Is a superior strategy for the medical conquest of aging. The damage-repair approach sidesteps competing risks tradeoffs; reduces the risk of side effects; and
Accumulated when he or she begins therapy rather than simply the rate at which a person accumulates
Aging damage ahead. And because it is amenable to iterative cycles of improvement, the strategy opens up the potential for longevity escape velocity if scientists have developed and deployed a sufficiently comprehensive initial panel of rejuvenation biotechnologies. (Some of these points are the subject of a previous blog post, and we made the case for the approach in detail with all the science you need to understand the overall plan in Ending Aging).
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Another thing that is problematic about focusing on the “sources of harm” rather than the harm itself as the basis for a catalog of adaptive age changes is that it does not actually
Of damages that change with age. You can imagine that our bodies are free of aging-damaging processes when we are young and that a switch is flipped sometime in mid-life, after which our bodies begin to wreck themselves. For the most part, this is not true: as far as we can track, our bodies produce most of the aging damage in our lifetime, and even the rate at which it is generated does not consistently increase with age. The burden of beta-amyloid plaque in the brain gradually increases until a person reaches the point of substantial cognitive impairment, at which point it plateaus; Some populations of mitochondria produce more free radicals later in life, but other populations seem to produce them at a constant rate—and production decreases next to nothing in the small number of cells overtaken by mitochondria with large deletions.
Of that damage. And again, it is this damage—its accumulation, and its removal or repair—that is the sole focus of the Seven, and not where the damage comes from.
An additional difference between the Hallmarks and the Seven at this basic level (and a limitation of the former) is that the original Hallmarks focus myopically on
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Damage, which ignores other types of aging damage that occur inside and outside the cells — damage that is included in the scheme.
We will return later in this post to go over the specific Hallmarks in each of these subcategories; for now, let’s look at the next subgroup of Hallmarks.
. These reactions initially reduce the damage, but eventually, if chronic or aggravated, they become harmful themselves. This is one of the characteristics of degenerative aging that make treating the particular “diseases of aging” so difficult. The body responds to cellular and molecular damage by trying to counteract the effects of that damage, such as by sending in the immune system to remove damaged cells or molecules; or by pushing harder on the biochemical gas pedals to increase a function that is declining due to damage to its cellular and molecular engine; or by turning
A process that is essential for normal function but that generates too many problems because of such damaged cellular and molecular parts (like the co-operation of a faulty engine spewing pollution).
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Such maladaptive responses to cellular and molecular damage are certainly characteristic features of aging, so they fit well into the original design plan for the Hallmarks. And we will return later in this post to evaluate the specific aging changes that they assigned to this subcategory. Mar
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