Lifestyle and environmental factors affect health and ageing more than our genes
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ox.ac.uk
Dogs (and many other animals) begin reproducing at a much younger age. Their genetics and genetic development evolved to support releasing a number of offspring to continue the species, but beyond that, the biological system had no longer value for the animal, and therefore genetics which enhanced longevity did not promote into the next generation.
People rear children later, and when those children are growing, the human still plays a very active role in the development and maturity of those children. The genes which promoted longer life where therefore selected out as the children who were not reared with parents in reaching late 30s had a lower chance of survival.
In addition, humans have a strong drive to live. Dogs, as they reach the end of their life, seem to be quite happy to find a nice place to lie down and die. They have no concept of "not dying". Not that they won't protect themselves, but they have no idea of medicine, of health, these are not concepts many other species can understand, and even if they could, there is not much they could do for them.
With royalty and family, younger generations cared for the older, which increased lifespan beyond the generally accepted declining years.
For example (I work in sleep), sleep begins degrading in our 30s, and this degradation is linked to all markers of aging and health. Our immune system weakens, our metabolic and cardiovascular systems decline, etc etc. Potentially there was/is some evolutionary selection here as well where the children who cared for their elderly were also more likely to survive longer, but I think that is a weak link.
I'm not refuting the OP, but at one point genetics got us so far, and then lifestyle and environmental factors are now taking over.
(edit) I originally posted this as a response the question about dog lifespan, but then realized it probably stands on it's own as a comment.
The article is a based on a over generalisation from study results that are not applicable in the way that the article claims.
*The dog metaphor is sort of a joke, but it is true for the human case to, due to the fact that you cant factor out the genetic "effect" on behaviour.... ie. behaviour and genes are too intertwined to separate from each other. Smokers smoke in part cause they have the genes that make them more likely to smoke (or exercise, or overeat, or do whatever; just pick any example that is unhealthy).
https://www.sciencedirect.com/science/article/pii/S221112471...
That's all there is to it, some people smoke and live long, some people don't smoke and die young, but statistically no one smokes a lot and live longer as a result.
Just look at the leading causes of mortality, they're mostly behavior or environment related
I would note, however, that this result is going to be extremely influenced by the society being studied. If famine is widespread, then many genetic factors won't matter. Similar for war, etc. (And this is probably partially why socioeconomic factors have a big influence.)
The estimate of the magnitude of genetics effects in this study is “silly low”, roughly by an order of magnitude. (Notice the hedging in the PR piece.)
The heritability of a trait is a function of environmental stability and quality. In a stable environment—Sweden or Iceland from 1900 to 2000—-heritability of lifespan is still low; about 15 to 25%. But that is way different than 2%. Claiming 2% is more of a socio-political statement: to focus on what we can influence ourselves.
Re telomere length. I wish it were that simple. Telomere length is not the main cause of aging in mammals. Read the title if the paper that you cite: “correlates with”! My presbyopia correlates beautifully with my age but did not cause me to age.
I would not even rank telomere length among the top ten (the putative “Hallmarks of Aging”). But it is a great story which makes good headline fodder.
I think the comment about dogs is really just highlighting the wide range of differences in maximum lifespan among species.
This indicates that DNA variants indirectly or directly modulate the baseline tempo of aging between a short lived mammal (less than a year) to species like us that live 100 years. There is really no doubt about this.
And of course DNA variants do the same thing but over a much more modest range within a sexually reproducing species. Some mice make it to 500 days, some make it to 1000 days in exactly the same environment. Reduce environmental variance sufficiently and heritability begins to get up to 40%. Out in the wild here almost no mouse dies of natural cause heritability should approach zero.
Aging is highly polygenic. There will be 100s of DNA variants and de novo mutations contributing to aging per se and to disease risks. And many processes.
There are some surprising notes in https://en.wikipedia.org/wiki/Jeanne_Calment#Health_and_life... such as:
Calment continued smoking in her elderly years until she was 117
And https://en.wikipedia.org/wiki/Christian_Mortensen :
Mortensen enjoyed cigars in moderation and drank lots of water
Also some stats on the countries represented in the above list:
US 38F 27M 65T
Japan 23F 19M 42T
France 7F 4M 11T
UK 5F 5M 10T
Canada 3F 2M 5TIt is completely unproven despite a thorough investigation, but reaching the age of 122 is so unlikely that some people think that fraud is still the most likely explanation.
Also, I understand why they tested multi-vitamins and fish oil, but I wonder why they asked about glucosamine?
I don’t see that in the linked article or in the paper. The words vitamin and fish don’t appear anywhere in the paper either. I didn’t see supplement use in the tables.
Where are you seeing this?
Fig. 2: Environmental architecture of mortality in the UKB.
https://www.nature.com/articles/s41591-024-03483-9/figures/2
Like, we should not repeatedly go to the shoe store to play with their new x-ray foot measuring device, or use those new glow-in-the-dark radium cosmetics.
Say it isn't so . . .
How relevant this study actually is?