What is aging? The question has always been hard to answer, making it difficult to change the process, let alone to reverse its clinical progress. Unfortunately, much of the problem derives from the way we look at aging in the first place. Making the wrong assumptions, we arrive at the wrong conclusions. While human beings […]
What is Aging?
What is aging?
The question has always been hard to answer, making it difficult to change the process, let alone to reverse its clinical progress. Unfortunately, much of the problem derives from the way we look at aging in the first place. Making the wrong assumptions, we arrive at the wrong conclusions.
While human beings have the unique ability to routinely employ metaphor and analogy as cognitive tools, using the wrong analogy is – to use an analogy – like trying to saw wood with a hammer. Use the wrong tool and we produce completely useless furniture. In aging, not only do we usually choose the wrong analogy and naively assume we have an understanding of aging, but the outcome is seldom useful. While “theories” of aging abound, many are not only at variance with available biological and medical data, but they are sadly untestable to boot. Theory may be an aid to understanding, but when it can’t be falsified, it isn’t theory, it’s illusion.
As a physician, my goal is not simply theory, but intervention. If we can’t test it and we can’t use it in a clinical trial, then it may be entertaining philosophy, but it’s neither good science nor useful medicine.
One of the most pernicious analogies found among scientists and lay people alike is the notion that aging is like rusting. After all, I age and my car rusts, so what can you expect? Things get old and there’s nothing anyone can do about it, is there? You’re going to rust.
Wrong analogy: people aren’t cars and aging isn’t rusting.
As a slightly better analogy, consider your cell phone – a common piece of technology that we all use on a daily basis. Does your cell phone get old and fall apart – does it “rust”? Most of us have no idea, because – unless we break them – we almost always trade them in long before they actually fall apart. In fact, the way our cell phones “age” is a good analogy to the way our bodies age. Most cell phones get traded every few years, regardless of whether they’re working or not. Our bodies do almost exactly the same thing: most of our molecules get “traded in” every few days, regardless of whether they’re working or not. Your body is continually “trading in” molecules – recycling if you will – and the result is that most of your molecules are “new” and they work quite well.
At least, that’s true when you’re young.
But as you get older, the rate of recycling – like cell phones being traded in every 10 years instead of every year or two – gets slower and slower. The reason your body ages is not that the molecules “go bad”, but that the trade-in period gets longer and longer, with the result that it gets harder and harder to find molecules that work. So if you have a thousand molecules, almost all of them work when you’re ten years old, but perhaps only half of them still work when you’re one hundred. Imagine a thousand people with one year old cell phones: almost all of them work fine. But if they all have ten year old cell phones, most of them are worthless.
The problem is not that molecules – or cell phones – get damaged, but that the rate of recycling gets slower and slower as we get older. It’s not the rust, it’s not the free radicals, it’s not the day-to-day damage, it’s the steadily decreasing rate of repair and recycling that makes you old. The rate of repair is set by telomere lengths, which are in turn controlled by a number of things, but mostly be cell division. Every time your cells divide, the telomeres shorten, and every time your telomeres shorten, the rate of repair and recycling goes down another notch.
But what if we re-extend the telomeres? When we do exactly that – in the laboratory – human cells act young again. The cells repair the damage, the recycling rate climbs, and the cells reset the aging process. Moreover, when we try the same thing with human tissues – in the laboratory – we end up with tissue that looks and acts like younger tissue. Can we do the same thing, not in the laboratory, but in people? Can we reverse aging and prevent the diseases of aging?
Until recently, the problem has been to find a way to relengthen telomeres in all of those billions of cells that trigger age-related diseases, including the cells in your brain, your heart, and your joints. For the past seven years, there has been an informal human trial of several relatively weak oral compounds – astragalosides – that work indirectly to lengthen telomeres. The results suggest that we can not only lengthen telomeres, but we can show that parts of the body – the immune system – begin to act younger and more effectively. What we need, however, is a way to directly lengthen telomeres in all the cells that trigger diseases such as Alzheimer’s dementia, heart disease, strokes, osteoarthritis, and others.
Our role – at Double Helix – is to cure and prevent disease. Over the past twenty years, we have identified the tools we need to reset telomere lengths, reset the cellular aging process, and intervene in human disease. Now it’s time to come out of the lab and into the clinics. It’s time we use compassion and hard work to create healthy lives.