As Peter Attia, Canadian-born physician whose medical practice focuses on the science of longevity, asks in his lectures:

What is the greatest risk factor for atherosclerosis (deposition of plaques of fatty materials on arteries inner walls?“) …

… the answers from students and laypersons alike rebound back at him in rapid fire: smoking!… high blood pressure!… apoB!… LDL!… inflammation!…

These are all good logical answers.

And then he responds, “… the number one cause of atherosclerosis is age, hands down.

Yup, aging kills.

Welcome to Part 3 (Parts 1 and 2 are here and here) of my occasional dive into the science and maybe… science-fiction-like discussion of AGING, LIFESPAN, and HEALTHSPAN.

Yes, aging, and what we can do to slow it down. Or heaven forbid and glory be… reverse it!

We’re in the opening innings of a long game versus the profound effects of aging that could go well past the 9th inning before we declare something resembling a winner.

But this doesn’t mean we shouldn’t take a few swings of the bat when some tempting pitches come floating across our plate that auger well for a single or a double, ie. a potentially longer lifespan and healthspan.

So, this week, I’m cherry-picking another one of the 9 Hallmarks of Aging that I find particularly interesting.

Please remember, this is written in very simplistic terms. This topic is a very deep hole with exhausting complexity.

But first, as always… the fine print.

(I spent my professional life working in the sciences, but I am not a scientific expert. I am an interpreter with an interest in this stuff, so I’ll share with you what I’ve found and provide some links for you to follow if you have a deeper interest too. Also, science by its nature is incomplete and evolving, meaning that what I share today may be replaced tomorrow by newer research that sounds different. It’s science but it’s not omnipotent… )

Part 3, let’s go…

Senescence… my name is Cellular Senescence

It’s like we live in the world of The Walking Dead except internally, in our guts and cells, we have The Floating Dead… yes, Zombie cells…

Cellular senescence … way back in 1961, a couple of researchers by the names of Hayflick and Moorhead tried an experiment (here) to see if human cells could multiply over and over indefinitely in a lab dish.

The answer? Nope, these cultured human cells do not replicate forever but start to slow their divisions and just kind of nod off into a Zombie Zone. This is called cell senescence (the term senescence comes from the Latin “Senex”, which means “old man” in Latin).

But these cells don’t actually die.

In fact, they have an increased resistance to cell death by finding pathways that allow them to escape our immune system clearance and survive. They also begin to do some weird things, like changing their shape and size as well as secreting inflammatory molecules, which, in turn, can cause other cells to become senescent.

Scientists suggest that one of the main reasons that our cells have gained the ability to cause cells to stop dividing and doing their “job” is that senescence prevents the replication of cells that contain damaged DNA. This serves a critical function in preventing cancer and limits tissue damage by stopping the multiplication of faulty cells.

The link between aging and senescence has been well established. Simply, as we get older, our cells continue to be exposed to a cumulative stress (of many internal and external forms), which, ultimately, leads to an increase in the number of cells that become senescent.

On the bright side, Cellular senescence may play an important role in tumour suppression, wound healing, and protection against tissue fibrosis…

… but, there’s increasing evidence that the accumulation of senescent cells as we age may produce harmful effects and can contribute to tissue changes, biological aging, and many age-related diseases.

Senescent cells secrete hundreds of factors that include pro-inflammatory cytokines, chemokines, growth factors, and proteases (Kuilman and Peeper, 2009), some helpful, while others are nasty.

So, do senescent cells actually cause us problems as we grow older? It would seem, yes, according to this summary in December 2020 from the journal, Aging Cell.

Senescence is likely a double-edged sword.

Can we do something about this to increase our lifespan and healthspan? Anything?

There is really only a little we can actively do right now… but… we also have a lot to look forward to as research lifts the cover off some of these aging mysteries.

Strategies against cell senescence that can be used as “therapy” in humans can be classified into the following 3 groups:

  • non-drug interventions that prevent the accumulation of senescent cells, such as avoiding excessive UV radiation, and healthy dietary habits that include foods with anti-oxidation activity. Also, calorie restriction would appear to be beneficial as restricting calories is known to suppress oxidative stress (here), a major cause of DNA damage and cancers.
  • pharmacological therapies aimed at reducing the amount of inflammatory molecules secreted by already existing senescent cells.
  • pharmacological therapies aimed at reducing the number of senescent cells (or what researchers call senolytics). In early studies, senolytics appear to delay, prevent or alleviate frailty, cancers and cardiovascular, neuropsychiatric, liver, kidney, musculoskeletal, lung, eye, haematological, metabolic and skin disorders, as well as complications of organ transplantation, radiation and cancer treatment (Journal of Internal Medicine, 2020.)

LAST WORD: If you intend to participate in the Centenarian Olympics, your and my chances should be significantly increased if the quandaries of cellular senescence can be better understood and alleviated.

While you’re waiting for this to happen, maybe try working on your handstands!

Jagmeet Singh (Canadian NDP Party Leader) can walk on his hands at 42… will he still be able to do this at 100??