Sunday, 9 February 2020

The New Science Of Aging + How To Biohack Your Way To A Longer, Healthier Life

Everyone gets older...and death, of course, is one of the few things we know to be inevitable. But what many of us also seem to think is inevitable is that with age comes exhaustion, aches and pains, a general lack of vitality, and eventually some type of chronic disease like cancer or Alzheimer's. I can't tell you how many times I've half-joked that my crunching knees and occasionally crippling fatigue exist because I'm now in my 30s.
Slowly but surely, however, the whole idea of aging is being flipped on its head. Given breakthroughs in research that have led to new understandings of what drives the aging process on a molecular and cellular level, more scientists than ever are saying, hey, maybe we don't actually have to age—at least not nearly as quickly or painfully as we do now. Maybe we can strategically target the underlying mechanisms of aging in a way that adds years to our lives (we're talking beyond 100) and makes those years truly worth living.
That's the goal, at least, of Harvard geneticist David Sinclair, Ph.D., who is perhaps the most outspoken proponent of this emerging idea that aging itself should be classified as a disease that can, in fact, be treated. 
"What if I told you that you could be just as happy, healthy, and satisfied as you are today at age 120?" Sinclair asked a group of Google employees in September of 2019 while giving a talk about his research and new book Lifespan: Why We Age—and Why We Don't Have To. "We have the technologies to be able to be healthy much, much longer until later in life. The hope is that our generations will be able to expect to live until 90 and play tennis, or even make it to 100 and have a career—a second, third, or fourth career."
Pretty enticing stuff, right? And while part of what Sinclair is referring to when he speaks of these "technologies" is medications and genetic therapies that are being tested for their life-extending, disease-preventing (and possibly disease-reversing) potential, his research—and that of other experts in the field—has also uncovered key lifestyle practices and nutrients that target these same longevity pathways in the body. Things that all of us, right now, can tap into. 
So let's unpack some of this, shall we? Here, we dive into the latest research on what actually drives aging on the micro-level, the innovations we may be seeing in the near future, and what functional docs, and Sinclair, believe to be the best habits to adopt for a long, healthy life.

So what is aging & what drives it on a cellular level?

Right now you might find yourself asking, what exactly is aging? Sure, you may associate it with disease and frailty, but what exactly is it that makes someone more likely to lose muscle mass, experience significant declines in energy, and get cancer at age 70 rather than at age 25? It seems like it should be a simple explanation, but it's pretty darn complex—and experts' views on what drives aging have changed quite a bit over the years. 
"In simplest terms, aging is wear and tear—you do something over and over again and the parts break down," says Robert Rountree, M.D., renowned integrative medicine physician who makes a point to stay on top of new aging research. "Additionally, there are a lot of bad proteins being made in our cells all the time; there's a lot of debris generated—but when we're younger, we have the ability to compensate for the 'mistakes.' So basically, there are mistakes and there is damage, and as we get older, the factories in our cells make more mistakes and are less able to recover from damage."
But what's causing these mistakes and this damage? Back in the day—we're talking from the 1950s up until the 1980s—the free radical theory of aging dominated. Originally described by Denham Harman, the theory states that organisms age because they accumulate oxidative damage caused by reactive oxygen species, or free radicals. These free radicals would supposedly damage DNA, damage proteins, and basically wreak havoc throughout the body. "So if you follow that theory, you'd think that you'd want to take as many antioxidants like vitamins C and E, zinc, and selenium as possible and that would keep you from aging," says Rountree. "Except when [researchers] did that in animal studies, it didn't work." 
So, what do we think now? In the past decade or so, scientists have settled on nine "hallmarks," or causes, of aging, says Sinclair, although this list will likely evolve in the future. And the idea is that if we can address these issues, we can slow aging, prevent disease, and add healthy years to a person's life. These hallmarks include:
  • Genomic instability caused by DNA damage
  • Wearing away of the protective chromosomal end caps, or telomeres
  • Alterations to the epigenome that controls which genes are turned on and off
  • Loss of healthy protein maintenance, known as proteostasis
  • Deregulated nutrient sensing caused by metabolic changes
  • Mitochondrial dysfunction
  • Accumulation of senescent zombielike cells that inflame healthy cells
  • Exhaustion of stem cells
  • Altered intercellular communication and the production of inflammatory molecules
We're not going to dive into all of these, but let's cover a couple that have been getting some extra attention lately: senescent cells, for example. Turns out, there's a limit to the number of times a cell can reproduce, called the Hayflick limit. When cells reach this limit, they're called senescent. "We used to think, well, they're old and in the way, but they're harmless," says Rountree. "But it turns out, they're releasing harmful signals and inflammation to the body." 
Another topic you've likely read about right here on mbg is mitochondrial dysfunction. Think back to high school biology class—mitochondria are the powerhouses of our cells, which produce ATP or energy. "When we get older, we tend to lose mitochondria because mitochondria don't have the same kind of repair mechanisms as our DNA," says Rountree. "So over time, we get more tired and we don't have the energy to fuel our cellular mechanisms."
But—and here's where things get a little crazy—Sinclair believes there could be one common driver of all nine of these processes, which he sums up with his information theory of aging. "The theory proposes that all of the causes of aging that people are working on—from loss of mitochondria to senescent cells to telomere shortening—are manifestations of a very simple principle, which is a loss of epigenetic information in the cell rather than genetic information. Meaning that cells lose their ability to read the right genes at the right time, in the same ways that scratches on a CD would mess up the ability to play a beautiful album," he says. (The epigenome, if you're unfamiliar, essentially tells the genome what to do.) 
"What I'm proposing," he says, "is that if we can stop the epigenome from degrading, all of these other things go away." But if Sinclair's new theory is true, it raises the question: How the heck do you prevent these scratches (aka epigenome degradation) so cells continue to read the right genes at the right time, and so you can avoid things like fatigue, frailty, and cancer? And can we "clean up" damage that's already there and essentially turn back the clock? 
According to Sinclair, there are sort of two levels to that answer. One, there seems to be quite a bit we can do that may effectively slow the aging process (i.e., prevent these scratches) via targeted dietary and lifestyle changes and a few promising supplements, which we'll dive into in the section below.* As for the second part of the question, to truly turn back the clock, lifestyle changes won't cut it. But future therapies and drugs could make that possible. 

"We think we've figured out how to reset the age of cells," says Sinclair. "We've figured out that there's essentially a backup hard drive with this epigenetic information that we can access and tell the cells to be young again and reset their clock." Sinclair admits that this work is still quite preliminary, but they've just had some very promising results in animal studies with gene therapy treatments (right now they're injections, but they could eventually be pills). In a study from July 2019, they were able to reprogram damaged optic nerve cells in mice with glaucoma and restore vision. 
"That's another level of science that's coming, and we're still in the early stages, but if we can restore vision, what else might we be able to reset?" he asks. Which, to be honest, is equal parts freaky and fascinating.

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