Isn't it simply because these people won't ever get cancer, and so they die of something else. So if you reach a certain age you outlive most people that would die from cancer.
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.
Could this be an artifact of how we measure cancer? My own grandfather probably had cancer when he died, but so much else wasn’t working that I think the docs just didn’t bother testing for cancer or diagnosing it. Treatment would not improve his prognosis at that point.
I’ve heard from medical student, that at later age cancer is less risky due to slower overall metabolism. Not a fertile environment for cancer to grow.
Medical students often miss the fine nuances, I would know, I used to be one.
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.
The risk of getting diagnosed with cancer fades over 80 years old. Tumor cells might take many years, or decades to develop into a diagnosable form of cancer, so much of the story relates to things that happen well before the 80+ years detection date.
This is an explicit hypothesis I have heard: that aging arises in part from a compromise between longevity and not getting cancer. Obviously an immortal who gets a bunch of tumors is not immortal.
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.
There's also some details about how stem cell divide. Stem cells exist just so that they can be clean copies.
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.
There’s cellular senescence that helps control the malignancies. Then we have an increase in senescent cell burden with age. Of course, you can put two and two together and say that aging protects from cancer. But that’s a wild jump. For one thing, we can’t prove there’s any kind of (evolutionary) benefit in controlling tumors in older age.
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?
This is super interesting. I've been wondering for a while about the role of iron in health, with consideration of things like the influence of the iron scavenger P. gingivalis. I do wonder if iron is the real reason for red meat being associated with worse health outcomes.
I'm happy to accept I'm talking complete nonsense if I know my error, so presuming those that downvote this response have some insight I don't, I'd really appreciate them sharing.
Which to my straw man's understanding is also why cancer in young people is more likely to go out of control and seems to be more lethal than on older people.
>What emerged was higher levels of a protein called NUPR1 in the older mice. This caused cells to act as if they were deficient in iron, which in turn limited their regeneration rates – putting restrictions on both healthy growth and cancerous tumors. ... "Aging cells lose their capacity for renewal and therefore for the runaway growth that happens in cancer."
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.
This is against any established biological common sense I heard of: telomeres are known to be the mechanics of the DNA.
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's not entirely accurate. Telomeres shorten with age but cancers generally are triggered by mutations or defects much further in the DNA away from the telomeres.
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.
Telomeres are anti-cancer. Cells can only divide a limited number of times before the telomeres run out. The cost is a loss of vitality (senescence) as the individual cells end up being older since they aren't able to divide and renew.
> telomeres are known to be the mechanics of the DNA.
> 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.
Well thats why I read the article instead of just the headline.
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.
I haven't heard this before - the change isn't that large but but it really does drop after 80
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...
Isn't it simply because these people won't ever get cancer, and so they die of something else. So if you reach a certain age you outlive most people that would die from cancer.
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.
85 year olds die from cancer like 70 year olds but still over twice the rate of a 55 year old.
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.
Mr Burns: so what you’re saying is, I’m indestructible!
Doctor: Oh no, and in fact even a slight breeze could k…
Mr Burns: Innndestructibllllle.
Could this be an artifact of how we measure cancer? My own grandfather probably had cancer when he died, but so much else wasn’t working that I think the docs just didn’t bother testing for cancer or diagnosing it. Treatment would not improve his prognosis at that point.
I’ve heard from medical student, that at later age cancer is less risky due to slower overall metabolism. Not a fertile environment for cancer to grow.
Medical students often miss the fine nuances, I would know, I used to be one.
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.
Fwiw this is a graph of being diagnosed with cancer, not dying.
science reporting is pretty bad. unsubstantiated, weak, or wrong claims are hyped up .
Misleading title. This is true about 5-10% of the human life. For 90-95% of the human life, the exact opposite is happening.
More honest title : "The risk of Cancer Fades Over 80 Years Old, and We May Know Why."
The risk of getting diagnosed with cancer fades over 80 years old. Tumor cells might take many years, or decades to develop into a diagnosable form of cancer, so much of the story relates to things that happen well before the 80+ years detection date.
For everyone in disbelief like I was: “… past the age of 80
Ageing itself is a anti-cancer strategy...
Like the old joke - growing old sucks but it beats the alternative.
This is an explicit hypothesis I have heard: that aging arises in part from a compromise between longevity and not getting cancer. Obviously an immortal who gets a bunch of tumors is not immortal.
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.
There's also some details about how stem cell divide. Stem cells exist just so that they can be clean copies.
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.
There’s cellular senescence that helps control the malignancies. Then we have an increase in senescent cell burden with age. Of course, you can put two and two together and say that aging protects from cancer. But that’s a wild jump. For one thing, we can’t prove there’s any kind of (evolutionary) benefit in controlling tumors in older age.
I’ve heard that hair going grey is a cancer mitigation strategy.
Do you have any additional info on this?
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?
This is super interesting. I've been wondering for a while about the role of iron in health, with consideration of things like the influence of the iron scavenger P. gingivalis. I do wonder if iron is the real reason for red meat being associated with worse health outcomes.
I believe Dr Greger (well known vegan doctor who provides research support for his claims) has some videos on this.
I'm happy to accept I'm talking complete nonsense if I know my error, so presuming those that downvote this response have some insight I don't, I'd really appreciate them sharing.
isn't it just lower MTOR activity = lower risk of cancer?
as we age we eat less, move less which slows down MTOR
Our cells also probably just don't divide as fast anymore. The entire metabolism slows down.
Which to my straw man's understanding is also why cancer in young people is more likely to go out of control and seems to be more lethal than on older people.
>What emerged was higher levels of a protein called NUPR1 in the older mice. This caused cells to act as if they were deficient in iron, which in turn limited their regeneration rates – putting restrictions on both healthy growth and cancerous tumors. ... "Aging cells lose their capacity for renewal and therefore for the runaway growth that happens in cancer."
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.
This is against any established biological common sense I heard of: telomeres are known to be the mechanics of the DNA.
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's not entirely accurate. Telomeres shorten with age but cancers generally are triggered by mutations or defects much further in the DNA away from the telomeres.
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.
Telomeres are anti-cancer. Cells can only divide a limited number of times before the telomeres run out. The cost is a loss of vitality (senescence) as the individual cells end up being older since they aren't able to divide and renew.
When you read the article, did this argument occur to you in light of what they found with NUPR1?
> telomeres are known to be the mechanics of the DNA.
> 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.
Well thats why I read the article instead of just the headline.
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.