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A substantial challenge to longevity

November 8, 2020

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A substantial challenge to longevity

We at Fortinberry Murray are enthusiastic members of the University of Queensland-led CRC on Longevity. Personally, I am interested in research into extending our active physical and mental life well into our 90s and even 100s.  

A few recent studies in this area are truly revolutionary. This is one of them.

We know that all humans share similar changes during aging, such as grey hair, wrinkles, and a general, though uneven, decline in function. Aging is, by most researchers, considered to be the result of a cellular wear-and-tear process due to accumulated random damage, such as genetic mutations or DNA structural damage.

So, how is it that random, disorganized damage, which accumulates differently among different humans, and moreover, among different cells of the same individual eventually leads to the same outcomes? Several theories try to address this paradox, and they have great implications for our ability to affect the aging process, making elderly life better and longer. The potential to develop treatments for aging depends on understanding the fundamental process of growing old.

Conventional wisdom among researchers has been that most cells in the human body are barely damaged during aging, while just a few “rotten apples” – a small fraction of non-functioning cells—are significantly damaged. Accordingly, a potential treatment for aging could involve removing these few highly-damaged cells.

Approximately 15 years ago, a maverick researcher Prof. Jan Vijg of the Albert Einstein College of Medicine in NY proposed a different approach. He suggested that the proper function of biological tissues may decline during aging because many cells lose their ability to tightly regulate their genes. According to Vijg’s theory, there are no single non-functioning cells—or rotten apples—on the one hand, but none of the apples is “fresh” on the other. Evidence for Vijg’s theory has never been fully presented, until now.

In a study published in the journal Nature Metabolism, researchers report evidence that supports Vijg’s theory for the first time. Using a novel approach from physics, they developed a computational method that quantifies the coordination level between different genes. With this approach, they measured the gene activity of individual cells and compared cells from old and young subjects, discovering phenomena never before observed: old cells lost significant coordination levels compared to young cells.

To test the consistency of this phenomenon, they analyzed data collected from more than twenty experiments from six different labs around the world. In all cases they found reduced levels of coordination during aging among different cell types: brain cells, Hematopoietic stem cells, pancreatic cells and more.

What the researchers say: “In biology it is very difficult to achieve consistent results for different types of cells, tissues, experiments and organisms due to the high sensitivity of equipment and experimental setup,” said the study’s lead author. “Our method found the same pattern in more than 20 datasets. Finding evidence for coordination of genes was amazing, but even more outstanding was finding that this property of coordination dramatically declines with age.”

The researchers also observed coordination reduction in tissues with an increased level of damage, suggesting a direct link between increased damage level and coordination breakdown. The findings support the theory that during aging, accumulated random damage affects regulation mechanisms and disrupts the ability of genes to coordinate (resulting in a general decrease in tissue function), just like an orchestra without proper coordination between musicians ruins a symphony.

This study conclusively demonstrates the long-speculated relationship between aging, gene regulation and somatic damage. The results open up new avenues of research with practical implications. If the same level of coordination reduction between genes is indeed a leading cause for aging phenomena, there may be a need to change of course in current efforts to develop aging treatments.

So, what? Almost everything that the conventional wisdom thought about aging has proven to be misplaced over the last few years. Even the concept of aging itself. For one thing, it has been known for some time that we don’t all age at the same speed and that chronological age is the least reliable indicator of a person’s ability to function.

Biological age is far more important. An eighty-year-old may have the functioning ability of a person of sixty.

Then there’s cognitive age. We now know that dementia begins its awful journey at a very young age, largely in response to childhood experience. We also know that continuous learning—keeping brain cells exercised—is a powerful tool to delay the onset of Alzheimer’s and other dementia.

Finally, there’s perceptual age. We functionally age more slowly if we are surrounded by younger people and faster if we’re just surrounded by older folks. Our perception of ourselves ages according to our environment. If we’re another person’s carer we age more slowly—being valued or useful makes us see ourselves as younger and our bodies react accordingly.

There’s some very interesting material on the whole concept of aging coming out of a really left-field area—that of quantum mechanics and sub-atomic physics. Some researchers I have spoken to are questioning the whole idea of the linear nature of time. The past, the present and the future may all be “happening” at the same time they say. We’re aging, we’re being born and we’re living our past and future simultaneously.

So, our cells are decaying, but in another sense, they’re renewing. Fascinating stuff.

Dr Bob Murray

Bob Murray, MBA, PhD (Clinical Psychology), is an internationally recognised expert in strategy, leadership, influencing, human motivation and behavioural change.

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