this makes me think that telomeres are not the main cause of aging-related death. My mental model is: if you run out of telomere before you get old, you start to get disease - and that’s maladaptive. So there’s evolutionary pressure to slow down your shortening rate, up to a point. Once it becomes unlikely that you’ll outlive your telomeres, there’s no more pressure. So your telomere length + rate becomes a measurement of your species lifespan.
> this makes me think that telomeres are not the main cause of aging-related death
That's an interesting argument, but couldn't you use the same reasoning to argue that telomeres are the main cause of aging-related death? The mental model I'm thinking is: As you run out of telomeres, you get diseases and you can't reproduce - and that’s maladaptive. So there’s evolutionary pressure to slow down the shortening rate, up to the point where you have children (plus grandchildren in the case of humans). When you're living long enough to have one or two generations of offspring, there’s no more pressure to correct the telomere problem.
Wouldn't your argument and mine be equally consistent with the featured article (that shortening rate predicts life span)?
Yes, but because of increased risk of disease and lower physical ability, you would also be a larger strain on your group/family. I think we should see this more as a survival of offspring and less as fathering more offspring.
There's probably pressure for species to not have longer lifespans. Youthful thinking and fresh perspectives are important. Wise old perspectives can get deeply ingrained and can't be changed easily. The free market for example experiences similar phenomenon where a new startup will outcompete a big old corporation. An industry that moves quicker (tech) evolves faster than one that doesn't (healthcare).
The evidence doesn't support what you imply: that older people can't learn or come up with novel ideas. Fresh perspectives are important, but there are more ways than ignorance (e.g. youth) to find them. For example, cross domain work often yields amazing new results; it's a great way to bring in fresh perspectives.
Humans are double-viviparous species, meaning average grandparent lives past its grandchild's puberty. Humans are also atricial. These traits are shared by elephants, whales and dolphins too. However, humans are the only animal species those are triple-viviparous in occasions, meaning great-grandparent lives past its great-grandchild's puberty.
Historical average is relevant. I have an 18 year old cat. It's an aberration. We evolved under specific pressures. Only recently, have we removed specific age gates.
And infectious disease was probably a much smaller problem for hunter gatherers living in small groups, which has been the case for the vast majority of our evolutionary history.
Should be context dependent. New parents benefit a lot from their own elder family members giving them advice on the basics; in an environment with less information (i.e. no internet), the advantage vs. people with no parents or family to help would have been substantial. So unless we expand the definition of “child-rearing years”, I think it could go either way.
If you do end up with telomeres that shorten very slowly, could there also be pressure to shorten them more quickly, so it really is just a measurement? Hypothesis: telomerase, which fights the shortening, also promotes cancer. I think I've even seen that before.
"Some experiments have raised questions on whether telomerase can be used as an anti-aging therapy, namely, the fact that mice with elevated levels of telomerase have higher cancer incidence and hence do not live longer. Telomerase also favors tumorogenesis, which leads to questions about its potential as an anti-aging therapy.[36] On the other hand, one study showed that activating telomerase in cancer-resistant mice by overexpressing its catalytic subunit extended lifespan.[37]
A study that focused on Ashkenazi Jews found that long-lived subjects inherited a hyperactive version of telomerase.[38] " https://en.wikipedia.org/wiki/Telomerase
One of the biggest challenges for studying telomere biology in the context of human aging, is that mice are quite different from humans in terms of their telomere structure.
The shortes mouse telomere is longer than the longest human one
http://link.springer.com/10.1007/s00114-014-1152-8 Stindl, Reinhard - The telomeric sync model of speciation: species-wide telomere erosion triggers cycles of transposon-mediated genomic rearrangements, which underlie the saltatory appearance of nonadaptive characters (2014)
oh and, a letter where Stindl outlines the problem in detail: https://www.researchgate.net/profile/Reinhard_Stindl/publica... Stindl, Reinhard - The reanalysis of three large datasets uncovers progressive telomere erosion between healthy human generations and supports an 11-year-old model of telomere-driven macroevolution (2015)
I find it EXTREMELY strange that the OP paper cites NONE of these papers. Like, what the hell?
The total number of heartbeats also predicts lifespan, although apparently not as accurately. So is the heartbeat total just a coincident or still a factor somehow?
I've seen this before and get the gist, but at face value, it's ridiculous. A human who runs every day may expend twice the heartbeats of a sedentary person. He or she will not live half as long, or anything close to it.
I think the idea is that a frequent runner will have a much lower resting pulse rate, and the “extra” beats they use while exercising will be more than offset by the fewer beats that accumulate during rest?
When I was a runner, I had a resting heart rate in the low 50s. While running I would hover at 180bpm. Now that I’m sedentary (knee accident) I have a heart rate in the 70s.
There are about 10k minutes per week and I ran for about 300 of them. That means my active lifestyle had about 588k beats per week and my sedentary lifestyle has about 750k beats per week. Sedentary life added about 27% total heart rate.
That's the assumption, but I have never seen or done the math either, which is ridiculous because it shouldn't take more than 5 minutes to get some estimates.
Thanks. I actually confused myself when I was writing it. I should have taken that as a sign to change the names. (I was going for a reference[1], but that shouldn't muddle things!)
No wonder I dread going to the gym, I find it really strenuous. I'm 37, unfit, and try to hit 180 while running on a treadmill. I was using the same target BPM that I used in college.
Thanks! I'll try 160 BPM next time. Running 45 mins should be more doable.
It depends on your goals. If you just want to do the 5K as fast as possible, you'll be close to your max heart rate (180). If you're just "leisure" running (aka. you can talk while running) I suppose 140 is reasonable.
I belive the comparison of heartbeats isn't meant to compare within a species. It works to predict lifespan comparisons between species from total heartbeats.
It's true, and the microscopic theory was done by the same physicist who found the macroscopic relationship, Geoffrey West (one of my personal heroes an current director of the Santa Fe Institute). The theory also explains the upper and lower bounds for the possible size of an animal. If you want to read about it he wrote an amazing book called Scale. I _highly_ recommend it.
OK, I'll add a bit to my previous comment. Is there a limit to how small a mammal can be? If so, what sets the scale?
TL;DR – effective pumping of blood requires precise allowable branching network of capillaries in the circulatory system. At a certain size this network goes from AC to DC and sets the scale for metabolic rate and lifespan in all animals with a circulatory system.
The scale is set by impendance matching of the circulatory system. The heart pumps blood. It is AC. To prevent the AC wave of blood from reflecting back when the capillaries branch out and get smaller, the branching network of the capillaries requires the cross-sectional area of the mother branch to be equal to the sum of the cross-sectional areas of the daughter branches. But when capillaries get too small the heart loses this AC advantage and goes from AC blood wave to purely DC.
So the smallest mammal a shrew has 2 capillary branches, 1 AC, 1 DC. Humans have 8 branches 6 AC then 2 like the shrew 1AC, 1 DC. A blue whale has 15 branches 7 AC then 8 like a human (6 AC then 2 like the shrew 1AC, 1 DC). This branching network sets the smallest length scale of a mammal (actually for any animal that uses blood and mitochondria as its metabolic energy source).
Going back, a shrew has 2 branches 1AC, 1DC. A shrew is 4cm in length and its heart must beat 20 times a second, as nearly all the hearts energy for all animals is expended to push blood through the last small DC branch portion of the capillaries. The shrew must be only 4cm and pump blood with the same pressure and speed as a human (which is the same speed and pressure as a blue whale) through the shrew’s tiny little heart. That is, smaller the animal the larger the metabolic rate. The larger the metabolic rate, the more wear and tear and repair on cells, the shorter the life span.
How are early capillary branches (think of liver network in mammals) and metabolic rate irregularities accounted in this scheme (e.g. average human lives thrice as long and has a metabolism which works twice as fast as in an animal of comparable size)?
The idea is that when you're doing strenuous exercise your heart rate is significantly elevated—more than double resting rate. So if you spend hours each day in strenuous exercise (like elite athletes do) your average heart rate could be close to double your resting heart rate. You'd have to exercise a LOT though, and even then it would be difficult to get to double that of a sedentary person, which will be higher than the resting rate of an athlete.
A very fit person will have a resting heart rate of around 50-55BPM, and could have a rate as high as 160BPM or even higher during strenuous exercise. Say they maintain that rate for four hours per day, that brings the average up to around 70. (Actually more since it will be elevated for a while after exercising as well.) Still won't be double though.
For humans, about 15 kbp telomere can be reduced to 50% in about 107 years at the rate of about 70 bp per year. That number goes well with the max life spans we observe in humans.
The life span of a species can mean at least two things. The lifespan of individuals that belong to the species or how long the entire species can survive without mutating. I believe extinction, species lifespan and the theory of recapitulation (ontogeny recapitulates phylogeny) are intertwined https://en.wikipedia.org/wiki/Recapitulation_theory
I had read somewhere that telomere length reduces each time a cell divides. Assuming that, telomere shortening rate is directly indicative of the number of times cells have gone through division. Could that not mean that telomere shortening rate is just estimating cell division rates and the latter relate to life span for an entirely different reason? Is this or some other study show that shortening rate is a better predictor of life span than cell division rate?
If telomere's ending were of significance, then their lengths would be a good predictor of life span. The OP is saying that it's not the length but the shorting rate that counts.
Other than being born with the right genes? Moderate exercise, like 30 min. of cardio 3 times a week, may help increase telomere length just as much as marathon running. Omega 3 and most things associated with a good diet also correlate with longer telomeres. A study showed that processed meat (like bologna with nitrate) has a negative effect on telomeres. Go figure.
There is a very strong negative association between chronic stress and telomeres. The worse the stress is and the longer the episode, the more your telomeres are impaired. If a woman is chronically stressed or had low emotional support in childhood, her kids may get shorter telomeres in utero. Social isolation also seems to be terrible for telomere length.
Disclaimer: Telomeres are a relatively new area of interest. Studies showing the above haven’t been replicated enough to be comfortably stated as fact. Of course, telling correlation from causation is difficult.
Yes there are several companies that do this. TeloYears is one. They use a blood sample to index your telomere length (actual length) against other people your age (expected length). One of the outputs is a percentile rank for cellular age. While this can be useful information, there are a couple issues. One is that you can’t reliably predict expected lifespan simply using telomere length. The other is that it is over $100. You already know if you’re healthy and have good genes. I guess it could be used for benchmarking to see whether your telomeres are on the right track.
