The enemy of these telomeres is age: damage occurs to them during cell division, hence the part of the DNA which watches after the DNA is no longer to fulfill its duty: and that is an open door to all types of cancer.
In other words, if nothing kills you at old age, cancer will do it.
That cancer cell lines are often immortal is interesting circumstantial evidence for this.
Telomere shortening for example is hypothesized as one stop mechanism for runaway cell division.
My bet would be that this is part of the answer but not the whole answer. Biological systems rarely have one part match one function. Biology is not “designed” the way humans design things.
So one hypothesis is that telomeres shrink with age which causes runaway growth (i.e. cancer) to burn up all it's telomeres early and start crunching through sequences responsible for building proteins essential to life, therefore causing some of the cancer cells to die out. Whether that hypothesis holds is a different matter but the referenced paper points towards various other mechanisms which are seemingly caused by cell age as well.
My inclination is that this could still just be a selection effect. For people who are prone to cancer, you are probably dead by 80.
https://www.cancer.gov/about-cancer/causes-prevention/risk/a...
tl;dr low iron causes less cell cycle activity. which means less errors including deregulation which is what cancer is.
its not that ground breaking.
but the iron contribution is. its actually a bit clickbait because they focus more on increasing iron in old people to prompt better recovery of everything else.
Hardly a consolation.
The other thing to consider is that once you get to 85, you're likely to die from just about everything else, not just heart disease and cancer.
> The enemy of these telomeres is age: damage occurs to them during cell division, hence the part of the DNA which watches after the DNA is no longer to fulfill its duty: and that is an open door to all types of cancer.
This sounds a little off. Telomeres aren't known to be the mechanics of anything. They fulfill their role by existing.
Imagine if, whenever you copied a file, the copy was missing the first and last 40 bytes of the original. (And, for completeness, those 80 bytes are also removed from the original.) That's how DNA copying works - a little bit of the beginning of the strand, and a little bit of the end, aren't copied and don't exist in the new copies.
Telomeres address this problem by existing in large numbers at the beginning and end of DNA strands (telos being Greek for "end"), providing padding that can be omitted from copies without hurting the organism. The creation of gametes involves refilling the worn-out telomeres of the parent organism so that the infant who eventually develops will have a full complement. But you don't do the same thing for your own cells, so eventually your cells try to divide, eat into their own DNA, and die.
Because cancer cells divide quickly, this mechanism will quickly kill them. So cancers also need to be able to refill their own telomeres. That's one of the mutations necessary for a cancer to originate.
But you'll note that a loss of function in the telomeres doesn't leave the door open for cancer. For cancer, you need to restore the telomeres.
Translating that to normalspeak: Lower metabolism leads to lower incidence of cancer.
It sounds like common sense to me; cancers form from damage and mutations to DNA during cell replication (kind of like uncaught bitflips during file copy operations), so the less replication there is (lower metabolism) the lower the risk of cancer and vice versa.
Also for some sort of related anecdata: My mother passed from stomach cancer, she had a lifelong chronic iron deficiency due to underperformant hemoglobins which she compensated for by taking iron supplements. Towards the end she ended up getting some iron infusions because her blood iron levels were so abysmally low.
as we age we eat less, move less which slows down MTOR
Doctor: Oh no, and in fact even a slight breeze could k…
Mr Burns: Innndestructibllllle.
More honest title : "The risk of Cancer Fades Over 80 Years Old, and We May Know Why."
I am not saying you are wrong, I don’t know, but I know that hair becomes grey due to decreased melanin production in your hair follicles as people age.
So the natural conclusion based on what you are saying (assuming it is true) is that the decrease of melanin production in hair follicles reduces the risk of cancer. How so?
I read a paper about the depth of the tree of division of stem cells that also backs up the aging-is-side-effect-of-fighting-cancer. Sorry, I don't remember paper title or better keywords.
Cancer at a later age, like at 85, is "less risky", because you'll be likely to die of something else than the cancer before you're 90 anyway.
Cancer at a later age, like 60, is "less risky" because your body have had plenty of time to grow indolent and lazy cancers by then, and your immune system is winding down, letting them bloom up a bit.
Cancer at like 30, while many are treatable nowadays, is usually bad news as why are you having cancer at 30 of your genes aren't massively prone to spawn cancer or you had some environmental exposure to serious mutagens.
But even in the older age categories there's plenty of really nasty cancers that lead to ugly deaths, which is why I don't like generalizations like this.
And then always researchers try to find a clue in the patient and see like oh hey they have more iron, iron must be the solution, but maybe the person just didn't get cancer because (s)he had a healthy lifestyle and relatively little stress.
I'm not saying that these are the cause, but there are ton of similar, simple statistical arguments you'd have to rule out before arriving at a relatively complex conclusion about human biology.
Those who died would still have been at risk into their 80s; many of them didn't make it though.
As a pure thought experiment using made up numbers, let's suppose that people are divided into two equal-sized groups: group A has a 75% chance of developing cancer after age 60, whereas group A has zero risk. We have no idea who is in what group. So it looks like people have a 37% chance of getting cancer after 60. Now suppose many of those who get cancer after 60 due to this risk end up passing away. They are of course from group A, and so more of the group B is represented among the survivors going past 80. Since in the 80+ group, the mix of A:B is no longer 50%, but has fewer A people, the risk of cancer is lower.
Prostate cancer is surprisingly prevalent but (commonly) slow-proliferating, and is often “beaten to the punch” by other causes of mortality.
https://pmc.ncbi.nlm.nih.gov/articles/PMC2825758/
There's some suggestion that P. gingivalis is implicated in system wide effects: https://www.nature.com/articles/s41368-022-00215-y
I've read various other things about it's pro-inflammatory effect.
I'm somewhat wary of dental hygienists given how much trauma they seem to impart and the consequential risk of getting oral bacteria into the bloodstream.