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In case anyone was curious like me: the standard deviation of lifespan is ~12-15 years in developed countries.
So environmental effects, sleep, diet, lifestyle, etc (I.e. modifiable factors) maybe account for half of that, so like 6-7.5 years of variance. Which… sounds about right to me.
Lifespan is not even half the story though, health span is much more important. Your life is completely different if you can ski or split your own wood at 80+ vs being barely able to use stairs at 50. Both might die at 90 but one "lived" 30 years more
It is almost never reasonable to assume normality and make calculations like this. This is particularly the case when you are dealing with lifespan, which isn't normally-distributed even in the slightest. The actual ranges are likely smaller than you are stating here, and variance is just not a very practical or interpretable metric to use when dealing with such a skewed distribution.
We should be stating something like a probability density interval (i.e. what is the actual range / interval that 95% of age-related deaths occur within), and then re-framing how much genetic variation can explain within that range, or something like it. As it is presented in the headline / takeaway, the heritability estimate is almost impossible to translate into anything properly interpretable.
https://biology.stackexchange.com/questions/87850/why-isnt-l...
One note: the standard deviation of the remaining effects would be sqrt(1/2) as large, not 1/2 as large. So more like 8.5-10.5 years.
This is a nice example/re-stating of what the heritability % "means" here.
I'm curious, with something like smoking/drinking, how you can be confident that you've untangled genetic predispositions to addiction or overconsumption from those "modifiable factors". I guess that's just captured within the 50% heritability? And if you could confidently untangle them, you might find heritability is higher than 50%?
Lifespan isn't as important as healthy lifespan. Lifestyle can mean the difference between being able to complete an Ironman triathlon at age 80 vs being bedbound.
> the standard deviation of lifespan is ~12-15 years in developed countries.
That seems rather higher than I would have expected, at least if one corrects for preventable accidents and other such things (that I would expect to shift the results away from a normal distribution).
Environmental effects are not necessarily modifiable. It includes randomness, background radiation, unknown risk factors, anything which is not genetic.
>By contrast, intrinsic mortality stems from processes originating within the body, including genetic mutations, age-related diseases, and the decline of physiological function with age
So we put genetic diseases in the bucket of intrinsic mortality and then found that intrinsic mortality has a heritable component?
Yeah this paper came across to me basically as "if you ignore environmental causes of death, the heritability of death goes up"... which seems kind of circular.
Keep in mind this research is based on correcting twin study heritability estimates for confounding effects. However, new research shows that heritability estimates derived from twin studies are themselves dramatically inflated: https://open.substack.com/pub/theinfinitesimal/p/the-missing...
For a counterpoint to Sasha’s view, you should probably check out https://open.substack.com/pub/astralcodexten/p/the-good-news...
The 50% number is a bit mysterious, but if I understand the text of the article correctly, it essentially means that if we do not account for the noise added by accidents and such, we get a Pearson correlation of life expectancies of monozygotic twins of ~0.23. If we correct for accidents, the correlation rises to 0.5, hence 50% (with some further analysis they go up to 0.55, hence "above 50%" in the abstract). Now, in practical terms, this means that, given a MZ twin who died recently of natural causes, we could obtain an estimate for ourselves, but only if we make additional assumptions. A correlation coefficient alone is not very informative.
>Now, in practical terms, this means that, given a MZ twin who died recently of natural causes, we could obtain an estimate for ourselves,
Uh... am I misreading your comment, or are you suggesting that when your identical twin dies of non-accidental death, you can be pretty sure you're about to croak in the next wee days or weeks yourself? Very difficult to engineer that alarm bell (you either have a twin, or not), and too damned late to matter.
There's a lot of genes that impact lifespan, both good and bad. For example my father has hereditary hemochromatosis due to 2 copies of the HFE C282Y mutation. He was diagnosed in his 50's, so I'd expect the damage it did to his body to impact lifespan.
In my case I don't have it (I'm just a genetic carrier). If I did have the genotype and took the necessary dietary measures to avoid the phenotype, then it likely wouldn't impact lifespan.
On one hand you can argue a heritable disease like HHC has an impact on lifespan, but with genetic testing and treatment you can argue it doesn't impact lifespan (or it's impact is significantly mitigated).
Wait. They studied twins, removed accidents etc. But wouldn’t this lead to overestimation of heritability due to shared environment?
FTA: “We use mathematical modeling and analyses of twin cohorts raised together and apart”
So, take one cohort of twins raised together and see how well their life spans correlate.
Take another cohort of twins separated at or near birth and do the same.
Then, do some math magic with both to estimate heritability.
Yeah I’d take this study with a spoon of salt. As with many human studies, it’s hard to control for all factors.
If you look at dog breeds the difference between longest living (~15 years) and shortest (~10 years) is ~5years or 50% of the lifetime.
However we still struggle to appoint the very same to humans. In popular sciences and general understanding we still give so much attention to food and exercise and lifestyle and etc.
As if somehow changing the diet and exercise plan of Chihuahua you could make it into Doberman.
Of course, you play with the cards you get. Diet and exercise help. However you should still be aware about the game you play.
But dog breeds are much more diverse than humans. For example, a chihuahua weights about 2kg, a St. Bernard about 70kg. That's a 35x size difference.
Western individualistic thinking struggles with the concept of biological limits. Our genes influence nearly everything we do or are, and there's nothing we can do about it.
Years ago, I read the book "The Sports Gene" by David Epstein. I was particularly struck by how sled racing dogs are now bred for motivation to train, rather than just their physical running ability. That is, breeders select for genes that make it so fun for the dogs to run that they keep going, while the dogs not bred this way just give up when they feel a little tired.
The story made me really think to what extent is my motivation to exercise, or do anything for that matter, affected by my genes? And if this sort of stuff is genetic, is there any more point to punishing myself for laziness than to feeling bad for being too short?
This finding rectified my mental model of longevity after a long, perplexing period where longevity was estimated to be much less heritable than expected when comparing to other studied traits.
How is heritabiltity of life span useful if by the time the lifespan becomes known (eg at 80yrs old) the inheritance is not possible anymore (eg menopause)?
Heritability acts on lineages, not individuals (in general, not always) - a good rule of thumb is that traits that benefit 3 or more generations of a family have a good shot at being propagated. In this case, the advantage (of both menopause and longevity) is increased well-being of the tribe, ampliyfing the positive effects of culture and stability. Wisdom of the elders is implicit to the genetics. This is a tradeoff with the cost in resources; at some point the cost to keep someone around might exceed the benefit, but from an evolutionary standpoint, the accounting is over a lifetime; in a relatively stable environment, genes that improve longevity and healthspan will be reinforced by the positive feedback loops of culture and nurture and civilization and technology. Menopause is also prevalent in orcas and a handful of other mammals - and older females help rearing and protecting babies, and so forth, with a protoculture providing that feedback loop.
It's not useful. Indeed that's likely why we die of old age - there is no selective pressure to remove harmful mutations that don't reduce your ability to pass on your genes so such harmful mutations just accumulate over many generations. You might have a mutation that will cause your heart to rupture at age 150, but you'll never know it because you'll die of something else first.
It is possible though to selectively breed animals like flies for long lifespan. You wait to see how long one generation lives and cull the descendants of those that died early. It's inefficient but lifespan extensions of 50-60% have been demonstrated. One could imagine through gene editing that a species might be able to reap the benefits without the culling.
Note that evolution isn't about individuals, it's about genes (which we should further note is more than just DNA, but that's a different discussion). If it weren't valuable for humans to live at all without being fertile, then the average age of menopause and the average age of death would likely be much closer together. As it turns out, the human genes that were best able to pass themselves along were those that kept old people around despite being infertile, presumably to the benefit of helping to raise grandchildren, among other things.
Explanation I've heard in popscience books:
Healthy grandparents that are around to support their children and take care of grandchildren increase the fitness of the entire lineage by helping their children have more children and those grandchildren to be healthier/safer.
We're social animals. Anything that benefits the extended tribal unit is advantageous. Adults beyond child-bearing age contribute significantly to child raising, education, leadership etc of the entire tribe.
Similar effects are seen in other species
What is the question you are asking? What does "useful" mean, in other words? How does it contribute to the reproductive success of the offspring?
In (quantitative) genetics literature, heritability is usually defined (simplifying a bit) as the proportion of variance of a trait (lifespan, height, etc), in a population, that can be explained by genetics. The rest, by environmental factors, or error.
If height were a 100% heritability means that all differences in height between individuals would be explainable by genetics.
the more little old ladies around, the easier it is to raise kids.
It's probably not that useful (evolutionarily) beyond some age. Old people consuming resources without adding anything or holding back societies.
I know enough about heritability to know that the science people use words differently than I expected, but not enough to explain that so here's someone's article about it:
Heritability IMO falls into the same bin as "standardized/relative effect sizes" (e.g. correlation coefficients, Cohen's d, odds-ratios, "explained variance", relative risk, etc), in that a division / re-scaling is introduced to supposedly increase interpretability, but, in reality, this has precisely the opposite effect.
Heritability is a bit worse though because the variance is partitioned into three giant piles of mush, at least two of which piles are very poorly measured / controlled at all.
The problem with twin studies:
1. There are genetic mutations that make you immune to HIV.
2. Monozygotic twins will both be immune, or not immune, while dizygotic twins may be either, one can be immune, while the other one could get AIDS.
3. Thus, a twin study would likely show that AIDS is a genetic defect.
There's serious issues with heritability research in general, it's observability stuff -- not experimentation, so imv, its at best proto-science, and in many cases plainly pseudoscience. "Heritability" itself has little to do with whether something is inherited, and speaks only to correlation with genes. Since we have a vast amount of genes which are shared for all sorts of reasons (ie., mating is based on shared culture, wealth, geography, etc.) -- the metric is mostly useless.
Accents are highly heritable, since they always correlated with location which is always correlated with genes.
Even if you do these twin studies, you have to assume a model of how genes and the environment interact, and all such models are obviously false.
Thus even if you grant that heritability measures on high quality twin studies are 'sign correct', in the sense that they show P(genetic effect) > P(no genetic effect) -- any magnitude of this effect, or any theory of is, is more or less pseudoscience (unless there are experimental studies showing gene-trait mechanism).
For example, it is "obvious" that P(genetic effect) > P(none) for intelligence, since genes control the structure of the brain and body. But there is no evidence (I'm aware of...) that beyond provision of a functioning brain, our genetics play any role in intelligence stratification. ie., all correlation with task performance and IQ can be explained by correlations in the metal retardation / mental deficiency range.
This doesn't mean intelligence is very malleable beyond a certain age. My own views is that genes are basically providing functioning hardware to the womb, and after that point its early development (both pre-birth and probs up to at most 3yo) which locks in a lot of the observed intelligence stratification. This is a very different story than popularisers of IQ research communicate though, but be aware, none are very good scientists and most of this research is methodologically unfit
Geneticist would say it's intended design of twin studies. Your example doesn't show AIDS is a genetic defect, but that genetics may predispose/protect against it.
It's interesting on my mother's side of the family, most everyone lived well into their 80's and 90's. The execution being for my Mom and her sisters who smoked heavily. Her brothers both died in their 60's but were in the Vietnam war and were definitely exposed to Agent Orange and both had brain cancer. My dad lived until nearly 80 after smoking since he was 12 years old and 2-3 packs per day.
Genetics may predispose for nicotine addiction, obesity, alcoholism, etc. This is intended design of genetic studies which look at multiple genes, like twin studies, GWAS studies, etc.
I think the studies which find a single gene variant which would have large impact on lifespan would be interesting. Not sure if variants like that exist though.
Rats. I have ancestors that died at 97, others at 81. Some even younger. So, no telling.
In the absence of other evidence, isn't it the case that any given trait is 50% heritable and 50% environmental?
tangentially, readers may be interested in this paper: https://stateofutopia.com/papers/1/evolving-brains-cull-long...
(you can reproduce its results yourself in a few minutes).
There's also some wisdom in that if you make kids later in life, you pass them the genes to survive (with 50% probability it seems) up to that age.
So if you're in the kind of family that dies of cancer at 30, and make kids at 25, perspectives don't look great.
Now, not to these people shouldn't make kids but perhaps, choose a spouse whose family dies on average at 60+?
Marry "up", not "down" :)
Seemingly due to reduction in extrinsic factors affecting lifespan.
whats the impact of epigenetics on this, given we're looking at a cohort of Boomers whose parents in many cases underwent extreme dietary restriction across the years of puberty or close?
the post ww2 children are the ones I'm talking about: their parents have in large part had cataclysm events in their fertile windows. my parents were 192x babies and their parents in turn were 1890/1900 window, and so dodged a lot of things because of a peace bonus. But my parents began a family in the 1950s after stress, and since neither fought nor were in the ETO or Asia, I suspect impact on me is minor but for dutch, or german, or french, or polish or chinese ...