Unlocking Longevity: Delving into the 12 Hallmarks of Aging (Part 1)

If you’ve witnessed your loved ones aging poorly saddled with illness or injury, getting older is probably not something you’re particularly eager to do. But age you will, so the question is: how will it go down? The good news is that you have more control over how well and quickly you age than you may realize.

Most of us were raised to think about aging as this mysterious thing that just happens to us. But over the past decade or so, scientists have made great strides in figuring out what’s going in our bodies at a cellular and even molecular level to explain the differences between a 30-year-old and a 70-year-old, and why it is the older we get, the more vulnerable we become to the dreaded “diseases of aging.” Sounds like a bummer, right? Well, this is actually good news, for a few different reasons.

First up, the better we understand what researchers call the “hallmarks” of aging, the more we appreciate that our lifestyle choices affect all of them. Your “healthspan,” the number of active years you get to enjoy on the planet, is more determined by you than by the genes you inherited. Next up, when a “hallmark” is identified, it can be measured, either now or in the very near future, so you should be able to get a personalized read-out on your particular weak spots — more incentive to shore them up for the healthy long haul. Last but not least, the more you know about what’s going on “under the hood” right now, the better positioned you’ll be to take advantage of new therapies being developed to counteract the damage done by these “hallmarks,” in essence, to slow down aging.

I feel so strongly about the importance of this research, and its power to impact our lives right now and in years to come, I’m devoting four posts to the 12 key aging hallmarks. In this first post of the series, I’ll tackle the first three hallmarks to put on your radar: 1) genomic instability; 2) telomere attrition and 3) epigenetic alterations. Here’s a topline on these hallmarks and what you need to know:

What is a “hallmark of aging” and how many are there?

For much of the last half of the past century, scientists were hunting for a “grand unified theory” of aging, a single process that sets in motion all the changes that, in total, we think of as “getting old.” They failed. So, researchers took a new tack, producing a list of what they believe are the nine most important drivers, or hallmarks, of aging, a list that recently some have expanded to include twelve hallmarks or more. All these hallmarks operate on distinct parts of our physiology – whether it’s at the micro level, for instance the DNA in our cells, or a more macro level, for instance, specific proteins or cells. But they all link up.  You could think of the hallmarks as dominoes. It doesn’t matter which domino tips over, in the front or the middle or the back of the line, the effect will ripple through the whole bunch, setting in motion familiar and unwelcome aging changes.

• Genomic instability – when the code gets hard to read

Your DNA contains your genetic code, a blueprint if you like, for the entire body, responsible for everything from the production of enzymes and hormones to the creation of new cells that keep us from running out of spare parts. It’s valuable cargo which is why evolution has tucked it into the protected center of almost every cell, the nucleus. But our DNA is under constant attack, by some estimates, a million “hits” a day. It comes from outside the body – for instance, exposure to the sun’s UV rays and environmental toxic chemicals – as well as from inside. Our cells produce energy, necessary for life, but in the process, they spin off “free radical” molecules that bombard the DNA. Eating a high-sugar, high-starch diet just compounds the punishment. Fortunately for us, nature has provided us with our own antioxidant defenses but over time, the bad guys gain the upper hand. The damage the DNA sustains, “genomic instability” in the scientific lingo, causes harmful mutations that age us, and more dramatically, gives rise to cancers and other degenerative diseases that can kill us, the risk going up in lockstep with the years.  We can slow aging down and keep our cancer risk as low as possible by getting plenty of physical activity and keeping a lid on the sugars and starches we eat. Intermittent fasting strategies may help as well, as may supplements like pterostilbene and olive leaf extract.

• Telomere attrition – the body’s aging clock winding down?

The second hallmark, telomere attrition, takes us back inside the DNA in the cell nucleus, specifically the tips of our chromosomes. Every time a chromosome divides, to create new cells, a little bit of genetic material is lost. That’s why they’re outfitted with protective caps – think of the caps at the end of your shoelaces – that can be progressively snipped off (the “attrition”) without doing us any harm. That is, until cells that frequently divide – skin, gut, immune cells – run out of telomeres and die. When the role of telomeres in cellular aging was first unraveled some decades ago, there was huge excitement. Maybe this was the aging clock inside the body? Now the consensus is that telomeres are one such clock, working in tandem with others. But they can still provide us with a useful barometer to measure aging, more broadly considered. Studies have found that people who live stressful lives, caregivers for example, have shorter than average telomeres; those who are physical active, eat a healthy diet and manage stress effectively have longer than average ones. Another study, published in Nature, found that meditation was associated with longer telomeres.

And a bonus — we do have the technology to measure telomere length. If you’re interested, you can work with an integrative health practitioner to get a handful of read-outs over a period time. It should provide you with a handy barometer to measure the effectiveness of any lifestyle changes you make. You can be pretty well be assured that what’s good for your telomeres is good for you. Exercise and higher, healthy levels of omega 3 fatty acids have tested out as being associated with longer telomeres, and supplements like astaxanthin and astragalus root may be helpful as well.

• Epigenetic alterations – those sticky on/off switches

With the third hallmark, epigenetic alterations, we’re still inside the cell nucleus, looking at aging at the deepest molecular level. But here, we’re focusing our attention not on the genes themselves, the DNA blueprints, but rather the epigenome, the chemical compounds that tell the genes when to turn on and off. Think of it this way. Our cells all contain the same package of DNA but it’s the epigenome, by controlling the on/off switches, that determines whether a given cell is, say, a liver cell or bone cell. Like the rest of us, these chemical switches work less and less well with age. But unlike our DNA, our epigenome is directly affected by our lifestyle choices – how we eat, move, sleep, deal with stress. The worse our choices, the more mistakes creep into the program. In fact, researchers now believe that it is these epigenetic alterations that account for much of the “genetic instability” that drives cancer, and likely many other diseases of aging. (As you can see, the hallmarks are all connected.) It’s possible that the medicine of the future will be able to reprogram our epigenome when it goes awry. For now, you should know what to do and not do: no smoking, limit or lose the alcohol, ditch the junk food, move the body, prioritize good sleep and stress management. And know that polyphenols, the family of chemical compounds found in vegetables, fruits and green tea, can also do their part to keep your epigenome in good working order. Supplements like spermidine, pterostilbene and olive leaf extract may be helpful too.

So where do we go from here? What’s next after genomic instability, telomere attrition and epigenetic alterations? See my post next week when I cover the next three hallmarks of aging, including:  proteostatis, deregulated nutrient sensing and mitochondrial dysfunction

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