Finger on the Pulse of Longevity

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To maximize our lifespan, the target resting heart rate may be one beat a second or less.

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Immanuel Kant, the 18th century philosopher, described the chemistry of his day as a science, but not really science, because it wasn’t grounded in mathematics – at least not until a century later. The same could be said for biology, the study of life.

In math, physics, quantum physics, etc., there are constants: physical quantities thought to be both universal and unchanging. Biology, though, was considered too complex, too messy to be governed by simple, natural laws. But in 1997, a theoretical high energy physicist from Los Alamos joined up with two biologists to describe universal scaling laws that appear to apply across the board. Are there any clinical implications of these types of theories?

Well, a fascinating observation was published. The number of heartbeats per lifetime is remarkably similar, whether you’re a hamster, all the way up to a whale. So, even though mice only live less than two years, their heart rate is like 500 to 600 beats a minute—up to ten beats a second, whereas the heart of a Galapagos tortoise beats 100 times slower, but they live about 100 times longer.

There’s such a remarkable consistency in the number of heartbeats animals get in their lifetimes that a provocative question was asked: “Can human life be extended by cardiac slowing?” In other words, if humans are predetermined to have about three billion heartbeats, period, in a lifetime, then would a reduction in average heart rate extend life? This is not just some academic question. If that’s how it works, then one might estimate that a reduction in heart rate from an average of more than 70 beats per minute, down to what many athletes have, 60 beats per minute, could theoretically increase lifespan by over a decade.

Seems a bit off the wall, but that’s how the scientific method works: you start out with an observation, like these striking heartbeat data, and then you make an educated guess, or hypothesis, that you can then put to the test. How might one demonstrate a life-prolonging effect of cardiac slowing in humans?

Well, perhaps a first attempt in this direction would be to see if people with slower hearts live longer lives, lamenting the fact that there is no drug that just lowers heart rate that researchers can give to people, since drugs like beta blockers lower heart rate, but also lower blood pressure. So, these drugs aren’t ideal for testing the question at hand, but we can do that first part.

And indeed, from the evidence accumulated so far, we know that a high resting heart rate, meaning how fast our heart beats when we’re just sitting at rest, is associated with an increase in mortality in the general population, as well as those with chronic disease. A faster heart rate may lead to a faster death rate. Faster resting heart rates (RHRs) are associated with shorter life expectancies, and are considered a strong independent risk factor for heart disease and heart failure. You can see how those with the higher heart rates were about twice as likely over the next 15 years to experience heart failure, in middle-aged people, older people, men, and women. And what’s critical is that this link between how fast your heart goes, and how fast your life goes, is independent of physical activity.

At first, I was like, duh, of course, lower resting heart rates are associated with a longer lifespan. Who has a really slow pulse? Athletes. As you can see, the more physically fit we are, the lower our resting pulse. But no, they found that, irrespective of level of physical fitness, people with higher resting heart rates fare worse than people with lower heart rates; so, it appears it’s not just a marker of risk, but a bona fide risk factor, independent of how fit we are, or how much we exercise.

Why? Well, when our heart rate is up 24 hours a day, even when we’re sleeping, all that pulsatile stress may break some of elastic fibers within the arterial wall, causing our arteries to become stiff. It doesn’t allow enough time for our arteries to relax between beats. And so, the faster our heart, the stiffer our arteries. But there are all sorts of theories about how an increased resting heart rate can decrease our time on Earth. Regardless, this relationship is now well recognized.

It’s not just a marker of an underlying pathology. It’s not merely a marker of inflammation.

The reason it’s important to distinguish a risk factor from a risk marker is that if you control the risk factor, you control the risk. But if it was just a risk marker, it wouldn’t matter if we brought our heart rate down. But now, we even have evidence from drug trials (now that there are actually medications that just affect heart rate) that lowering our heart rate lowers our death rate.

It’s now been shown in at least a dozen trials so far, basically, we don’t want our heart to be beating more than about one beat per second at rest—you can measure your pulse right now! For the maximum lifespan, the target is like one beat a second, to beat the clock. But don’t worry if you’re too fast; heart rate is a modifiable risk factor. Yes, there are drugs, but there are also lifestyle regimens that can bring our resting pulse down. And, this video is already too long; so, I’ll cover what we can do about it next.

To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video. This is just an approximation of the audio contributed by Katie Schloer.

Please consider volunteering to help out on the site.

Images thanks to odolphie, Public Domain, and HerPhotographer via Flickr and MG via Wikimedia Commons.

Immanuel Kant, the 18th century philosopher, described the chemistry of his day as a science, but not really science, because it wasn’t grounded in mathematics – at least not until a century later. The same could be said for biology, the study of life.

In math, physics, quantum physics, etc., there are constants: physical quantities thought to be both universal and unchanging. Biology, though, was considered too complex, too messy to be governed by simple, natural laws. But in 1997, a theoretical high energy physicist from Los Alamos joined up with two biologists to describe universal scaling laws that appear to apply across the board. Are there any clinical implications of these types of theories?

Well, a fascinating observation was published. The number of heartbeats per lifetime is remarkably similar, whether you’re a hamster, all the way up to a whale. So, even though mice only live less than two years, their heart rate is like 500 to 600 beats a minute—up to ten beats a second, whereas the heart of a Galapagos tortoise beats 100 times slower, but they live about 100 times longer.

There’s such a remarkable consistency in the number of heartbeats animals get in their lifetimes that a provocative question was asked: “Can human life be extended by cardiac slowing?” In other words, if humans are predetermined to have about three billion heartbeats, period, in a lifetime, then would a reduction in average heart rate extend life? This is not just some academic question. If that’s how it works, then one might estimate that a reduction in heart rate from an average of more than 70 beats per minute, down to what many athletes have, 60 beats per minute, could theoretically increase lifespan by over a decade.

Seems a bit off the wall, but that’s how the scientific method works: you start out with an observation, like these striking heartbeat data, and then you make an educated guess, or hypothesis, that you can then put to the test. How might one demonstrate a life-prolonging effect of cardiac slowing in humans?

Well, perhaps a first attempt in this direction would be to see if people with slower hearts live longer lives, lamenting the fact that there is no drug that just lowers heart rate that researchers can give to people, since drugs like beta blockers lower heart rate, but also lower blood pressure. So, these drugs aren’t ideal for testing the question at hand, but we can do that first part.

And indeed, from the evidence accumulated so far, we know that a high resting heart rate, meaning how fast our heart beats when we’re just sitting at rest, is associated with an increase in mortality in the general population, as well as those with chronic disease. A faster heart rate may lead to a faster death rate. Faster resting heart rates (RHRs) are associated with shorter life expectancies, and are considered a strong independent risk factor for heart disease and heart failure. You can see how those with the higher heart rates were about twice as likely over the next 15 years to experience heart failure, in middle-aged people, older people, men, and women. And what’s critical is that this link between how fast your heart goes, and how fast your life goes, is independent of physical activity.

At first, I was like, duh, of course, lower resting heart rates are associated with a longer lifespan. Who has a really slow pulse? Athletes. As you can see, the more physically fit we are, the lower our resting pulse. But no, they found that, irrespective of level of physical fitness, people with higher resting heart rates fare worse than people with lower heart rates; so, it appears it’s not just a marker of risk, but a bona fide risk factor, independent of how fit we are, or how much we exercise.

Why? Well, when our heart rate is up 24 hours a day, even when we’re sleeping, all that pulsatile stress may break some of elastic fibers within the arterial wall, causing our arteries to become stiff. It doesn’t allow enough time for our arteries to relax between beats. And so, the faster our heart, the stiffer our arteries. But there are all sorts of theories about how an increased resting heart rate can decrease our time on Earth. Regardless, this relationship is now well recognized.

It’s not just a marker of an underlying pathology. It’s not merely a marker of inflammation.

The reason it’s important to distinguish a risk factor from a risk marker is that if you control the risk factor, you control the risk. But if it was just a risk marker, it wouldn’t matter if we brought our heart rate down. But now, we even have evidence from drug trials (now that there are actually medications that just affect heart rate) that lowering our heart rate lowers our death rate.

It’s now been shown in at least a dozen trials so far, basically, we don’t want our heart to be beating more than about one beat per second at rest—you can measure your pulse right now! For the maximum lifespan, the target is like one beat a second, to beat the clock. But don’t worry if you’re too fast; heart rate is a modifiable risk factor. Yes, there are drugs, but there are also lifestyle regimens that can bring our resting pulse down. And, this video is already too long; so, I’ll cover what we can do about it next.

To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video. This is just an approximation of the audio contributed by Katie Schloer.

Please consider volunteering to help out on the site.

Images thanks to odolphie, Public Domain, and HerPhotographer via Flickr and MG via Wikimedia Commons.

Doctor's Note

How might we slow our resting heart rate? Watch Slow Your Beating Heart: Beans vs. Exercise for one way.

Other lifespan-expanding strategies are detailed in:

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