Perhaps, but it was rocket fuel for human population.
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That’s called the Hayflick limit and there is a growing understanding of why that limit exists (hint: telomeres). There is also a growing number of methods to overcome that limit to create immortalized cells for use in regenerative medicine. Practical Use of Immortalized Cells in Medicine: Current Advances and Future Perspectives - PMC
In other words, your “awareness” is woefully out of date.
Yeah, whatever. This is highly simplified because the details would take too long. There are two broad theories about aging. The first is that aging occurs because of the accumulation of mutations, damage, wear/tear etc. In this view 120 years is the max limit and there is not much one can do about it. The second is that aging is genetically programmed. This would occur if there is an optimal age limit for the survival of the population. It is easy to imagine why this would be. During periods of scarcity it may be in the best interests of the species to skew younger so that limited resources go to individuals that reproduce.
If there is a genetic program for aging, then understanding how that program works could allow its manipulation and a quantum leap in longevity.
You guys keep ignoring this, but I think the observation that bursts of aging occur at set times (age 44 and 60) is suggestive of a genetic program. The same is true of mutations that accelerate aging. If that is the case, then aging is like a genetic disease. We are rapidly learning how to treat genetic diseases.
For the first time in human history, we have the technological tools/resources needed to manipulate aging. These include the DNA sequence of the human genome, whole genome methods to detect what, when, and where genes are expressed, methods to manipulate genes, methods to deliver artificial RNAs and proteins to specific tissues at specific times, methods to reprogram cells, the list goes on.
The number of companies studying aging is only now booming.
Most notably it has only been in the last couple of years that funding on aging research has taken off, particularly in the private sector. Aging has only very recently become a hot topic of research. Expect to see a lot of advances in the coming years. Follow the money.
A sometimes-slow flow of federal and philanthropic funding over 50 years is now becoming sufficient to understand how the processes of aging drive disease. The amount has not yet been enough to push the benefits of geroscience into new therapeutics, but that is poised to change. Prominent billionaires, venture capitalists, and new foundations are investing billions in researching approaches for preventing, delaying, or curing the chronic diseases of older people; major pharmaceutical companies are poised to join them once the Food and Drug Administration qualifies aging as a treatable condition. The coming decade could see considerable progress, not only in the science but also in the creation of fresh nonprofit and for-profit funding streams. The Funding Channels of Geroscience - PMC
I am pretty sure our kids will on average live a good 50 years longer than us. As long as they have money that is and are able to find success in a climate change impacted future. What I am less certain is whether the growing collection of anti-aging therapeutics will be affordable to the general public.
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Sometimes … sometimes for a while.
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….and if the craptaculous lifestyle choices are totally responsible for any maladies….and the time spent indulging in improper lifestyle choices hasn’t caused irreversible damage.
Yeah, I just let that one slide. People say it all the time, but it doesn’t mean what they think it means.
Hypothetically, if longevity could be increased by a multiple (2x, 3x, etc), that would be a disaster. Imagine…babies keep being born, and no one dies for a loooong time. That would exacerbate the overpopulation problems we already have.
I’m just hoping that the tech btresist was mentioning will alleviate the suffering associated with old age. Resolve dementia, resolve osteoporosis, etc. I’m OK with dying some day, I just don’t want the gradual deterioration of the mind, or the loss of bodily controls. Healthy right up until the clock runs out is what I want.
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Is there a sex difference here? Women’s reproduction ends around 40-45 and child care becomes less important by age 60.
DB2
We’re not ignoring it. It just doesn’t mean what you think it means. Of course aging is the result of, and caused by, human genetics - just like puberty, menopause, and other biological functions that occur at (generally) specific times in an organ|sm’s lifespan. That doesn’t mean it’s “like a genetic disease,” in the way you mean.
Some attributes of your biology are indeed the result of a single gene, and certain genetic diseases result from the disordering or expression of a single gene. I’ve mentioned sickle-cell anemia, which is like that. If the characteristic is due to a single gene existing, being damaged, or expressing/not expressing, then you can have a therapy that treats that characteristic that’s likely to be achievable in the next few decades given where the cutting edge of science is. We already have such a therapy for sickle-cell.
But a lot of characteristics of the human body aren’t like that. They’re determined by genetics, but not by just one (or a few) genes. They’re polygenic traits, the result of countless genes - which means they are not capable of being addressed or altered by just targeting a small number of genes and changing them or turning them on or off.
So consider a human being’s height. You don’t have a single gene in your body that determines your height. There’s not a spot in the genetic code that if it’s on (or off or changed) you might be able to be eight feet tall - your height is determined by countless genes. And you have tons of attributes that are like that. You have two arms and one stomach entirely because of your genetics, but it’s not like there’s a single gene that if you tweaked it you could have four arms or two stomachs. It’s written into much more of your genetic code than a single gene. And even though there exist animals that have more than two arms and more than one stomach, you couldn’t change human biology by just replacing a humans “one stomach gene” with a cow’s “four stomach gene,” or suppressing (or activating) the single thing in human biology that gives us one stomach and not four. It’s not set up that way. It’s entirely genetic, but having one stomach instead of four isn’t the sort of outcome that can be altered by targeting a small number of genes or processes.
In the fullness of centuries, it might be possible for humans to change that. But it’s utterly implausible that the tools we’ve recently developed (CRISPR and mapping the genome and advanced protein folding) are going to be able to change fundamental polygenic traits in a material way in so short a time frame as a few decades. So if aging is like that - a product of our genetic biology like us having two eyes or a particular range of heights or not being able to regenerate severed limbs - then we’re probably out of luck over the time frame you’re describing.
And unfortunately, “aging” is something that has all of the hallmarks of a polygenic trait, rather than one like the genetic diseases that I think you’re thinking of. Aging is ubiquitous (every single human ages, and indeed virtually every animal on earth ages). It’s not a single trait, but a complex collection of changes that occurs over nearly every human system, organ, and biological function. It’s not a binary condition (like, say, having sickle-cell anemia or not), but more like height - everyone has a height (just as everyone ages), but people will exhibit different attributes of aging across a spectrum of outcomes. People have some attributes of aging early, some very late - and most people have them at around the “normal” time, just like we have tall people and short people and most people are clustered around the “normal” average. And aging involves and affects every part of the body, not a single organ or function.
All of that taken together makes it far more likely that “aging” is going to be a polygenic trait, one that stems from many many parts of our genetic code and can’t possibly be “switched off” the way a monogenic disorder like cystic fibrosis or sickle-cell anemia could be. There’s probably not a single gene or genes that cause you to age, so the cutting edge tools that might create radically new treatments in the near future are not plausibly going to be able to generate the kind of radical change in aging you’re thinking. They’re capable, with time, of perhaps completely eliminating certain outcomes of our genetic code. But just like CRISPR and gene mapping aren’t going to be capable of altering the number of eyes we have or change the speed at which our brains process visual information or make us eight feet tall, they aren’t going to be usable to materially stop or delay aging unless it turns out that aging is more like a monogenic disorder. But again, that seems incredibly unlikely.
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Nope. Gender differences were the first thing looked at. PhDs aren’t as dumb as they look.
Note that different species age at different rates and have vastly different life spans. In fact, in some species males die shortly after mating. These observations are much more consistent with species-specific genetic programs for aging than non-program theories based on the accumulation of mutations or cell damage over time.
And yet a mutation in single genes can cause premature human aging. Mutations Involved in Premature-Ageing Syndromes - PMC
Many genes might influence how one ages, but that doesn’t mean that manipulating a single gene or gene product cannot dramatically impact aging. Many genes are involved in weight regulation, include those that control hunger, digestion, and absorption. Yet Ozempic has proven to be pretty effective at inducing weight loss.
Your post pretty much summarizes how most thought about aging about 20 years ago. Much has happened since then in aging research that is shifting support to the programmed aging model. That’s not my opinion. It is rather an observation of where the field is heading.
Aging research is moving in multiple directions with a lot of promising results. One interesting idea comes from David Sinclair’s lab at Harvard who promotes the information theory of aging. The idea is that aging occurs not because of changes to DNA due to the accumulation of mutations, but rather through epigenetic factors that bind to DNA and affect its structure and thereby its function. Turns out that manipulating these epigenetic factors is relatively easy to do, allowing Sinclair’s lab to demonstrate the ability to reverse or advance the aging process in mice.
“We hope these results are seen as a turning point in our ability to control aging,” said Sinclair. “This is the first study showing that we can have precise control of the biological age of a complex animal; that we can drive it forwards and backwards at will.” https://hms.harvard.edu/news/loss-epigenetic-information-can-drive-aging-restoration-can-reverse
From Merriam-Webster: Quantum leap: an abrupt change, sudden increase, or dramatic advance
Words and phrases can have multiple meanings or do you believe having a “magnetic personality” means being attractive to iron?
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Now that’s an interesting dichotomy! Humans not fully using technology that is readily available to save the planet, while at the same time pursuing a technology that will allow them to live longer on the planet they’re destroying.
I suppose there will always be those who want to live longer, even as we turn Earth into an inhospitable hellscape.
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Again, not really the issue we’re talking about. I’m fully on board that aging is determined by genetic programming, which can vary between species the same way that size can vary from tiny to elephantine or number of legs can vary from two to more than a thousand. All determined by genetics. That’s not the relevant question, since obviously things like the number of stomachs you have (also a genetically determined characteristic) isn’t a monogenic trait that can be increased by switching a single gene (either removing/altering a gene or suppressing/activating a gene).
The fact that aging might be programmed doesn’t change that, either. The issue isn’t whether aging is genetic or caused by events in life (assume it’s genetic) or whether aging is programmed or inadvertent (assume it’s programmed). It’s whether the polygenic nature of aging allows it to be susceptible to fundamental changes based on where the cutting edge tools are today vs. not.
Sure - Ozempic can change how one’s body reacts to food (or lack thereof) to somewhere within the normal range of human appetite. We know we can develop treatments that can bring people that are outside of the extant distribution of human traits (or in a to-them undesirable place within that extant distribution) to somewhere else in the extant distribution. What we can’t do with any tools we have now is take people very far outside of the extant distribution.
So things like HGH can take a child that is unusually short and give them a few inches more of height, because there’s one thing that can move them within the extent distribution. But we can’t create 8 foot tall humans, because there’s countless aspects of the human genetic code that dictate the range of human height.
That’s what I think you’re missing about the unlikelihood of changing the range of human biology. Within the range of distribution of polygenic traits, a single genetic defect or condition can occur; but a single genetic defect or condition generally won’t change the range of distribution. For example, you can have a monogenic disorder that causes you to be blind and have zero functioning eyes instead of two; but there won’t exist a disorder that causes you to have four functioning eyes instead of two.
Aging might very well be programmed into your genes, but it is likely programmed into your genes the way having two eyes instead of five is programmed into your genes. While we can envision a lot of treatments using existing cutting-edge tools to correct defects and bring people back into the “normal” distribution of traits, none of those tools are plausible mechanisms for changing polygenic traits to take us outside the “normal” distribution of traits.
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Actually, there was a “grandmother” effect during human evolution where the grandmothers took care of the grandchildren, enabling the mothers to forage for food and have more children, thus enhancing family increase. This hypothesis explains why women live past menopause.
Wendy
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You might want to research the genetics of “super-agers.”
Wendy
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When i was in residency there was this big push to NOT deny surgery to people in their 80s, and in fact most of them did really well. The thinking was well if they lived to 80 and were functionally fit (completely independent, driving, living without assistance, often golfing, traveling etc), they did so because they were healthy and had led pretty healthy lives. Most dont make it to 80 with any major diseases/comorbidites/addictions. Had good protoplasm we would say. Chronologically they were 83 but biologically equivalent to most 50 or 60 year olds
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My dentist used to take my blood pressure before certain interventions. I have no clue about his reasons.
The Captain
I am (or was) a physicist. It’s a misuse of the term. I know the colloquial meaning, but it’s still wrong.
They also included “ain’t” in the dictionary many years ago, but it’s still not a valid contraction.
Just because a lot of people do it doesn’t mean it is correct. A lot of people believe evolution is bogus, but that doesn’t mean they are right. (They aren’t, as you well know.)
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No offense, but your knowledge of genetics is fairly rudimentary and so I think you should be a bit more circumspect about the claims you make. With respect to the above, Google “homeotic genes”. Mutations in a single gene can create duplicate body parts in a number of species. That’s how genetic programs often work.
Your argument is irrelevant anyway. Attempts to delay aging are not trying create something new or additional, like an extra stomach or additional eyes. It is simply trying to maintain the status quo. That’s a much simpler objective.
You are thinking of aging as the body wearing down, like the erosion of a cliff face. The other way of thinking about aging is that it is evolution’s way of culling the herd. In that scenario, at about age 44 a genetic signal is sent telling cells to slow their metabolism. This affects the entire body but with particular relevance to aging it makes DNA repair and chromosome maintenance less efficient. At age 60 another signal is sent to slow things down even more.
Interrupt or delay one or both signals and one can see how aging can be significantly delayed
You are missing the argument. Our current understanding is that aging occurs because of degradation in the maintenance of chromosomes. Stuff like telomeres shortening and changes in in chromatin structure. We are reaching the point where it will be possible to protect and maintain chromosomes through artificial means. This is analogous to Ozempic. Ozempic artificially counters the body’s natural hunger response. Analogously, anti-aging tech artificially counters the body’s natural degradation of chromosome maintenance over time.
Again, proposed anti-aging tech isn’t trying to protect chromosomes beyond what is naturally observed. It is simply trying to protect chromosomes at the same efficiency as occurs before 40 years have gone by.
This statement makes no sense and probably indicates a profound misunderstanding of polygenic, but don’t really want to pursue it. Instead I just want to respond to the phrase “outside the “normal” distribution of traits.” Note that I am not talking about immortality. My claim is that my kids will likely have the opportunity to live 50 years longer than the average today. That is something like a 60% increase in the average lifespan (approx. 90) or about a 40% increase in the projected maximum “natural” life span (120 years). This is roughly in the same ball park that scientists have extended the lifespan in other species through experimental manipulations (30%-100% increase).
It is an expansion of the term with the relevant meaning being a discontinuous change. Seriously, do you also object to the term “nuclear family” if the parents are not a proton and neutron? Your life must be very stressful.
People use the term evolution in all kinds of contexts that have nothing to do with the biological theory. The evolution of the cell phone or how online shopping evolved. Doesn’t bother me, but then I’ve learned to consider context.
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Yea same. They did this for the first time recently. Thought maybe it was bc i was in my 30s now? Who knows. Maybe a defensive medicine legal thing, dont want ppl fainting in thier chairs, or maybe if they have really high blood pressure the gums won’t stop bleeding. Beats me
@WendyBG Neil Tyson DeGrasse recently commented not good nutrition. The people before 1840 had free-range meat, organic food, purer water, and healthier air. Made little difference in 1840; half the people were dead by age 35.
If anything people were also overactive.
I started doing it routinely years ago. A"value added” item that was useful for medico legal reasons. Seems a reasonable thing to do since there are so many folk walking around with undiagnosed high blood pressure….even when they’re not in the sort of shape where the index of suspicion is high.
I’ve dodged a couple of bullets too…..sent patients home when blood pressure was sky high without doing the planned procedure and found out later that they’d had a stroke. I would no doubt have heard from some ambulance chasing shyster lawyer if they’d have had a local anaesthetic with epinephrine prior to the event.
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Could you please provide a link or two to examples of this 40% increase in the maximum life span of other species, as distinct from a 40% increase in life expectancy? That’s something I’d be curious to see.
Also, do you think that you could allow a human being to have four arms instead of two by interrupting or changing a specific signal that was sent to the body? I’m aware of homoeotic genes generally, and specifically how they affect polydactylism (love those Hemingway cats). But for systems that don’t depend on homeotic genes to regulate the number of a body part (like eyes or stomachs, as opposed to fingers or toes), there’s no mechanism to interrupt or signal in order to create “extra” fully functioning eyes or stomachs.
It’s not trying to maintain the status quo, It’s changing the status quo. Isn’t that the whole point of the argument you’ve been making - that aging is the natural result of genetic programming inside the body, and not the accumulation of external environmental factors? The status quo is that you age, just like the status quo is that humans only get two working arms or will be less than eight feet in height. If you want to change that, you have to make a change to the body - and that change is probably going to have to be pretty radical.
You used Ozempic as an illustrative example, but it’s not a very strong one - because it was very well established prior to Ozempic that humans can have more moderate appetite. There are countless individuals who naturally have that trait, and there are countless conditions and medications that cause humans to lose their appetite (or moderate it). It was entirely foreseeable that there could be a substance (or range of substances) that could cause humans to have reduced appetite, because there already existed lots of things that caused humans to have reduced appetite.
Nothing like that exists for pushing humans to a longer-than-extant lifespan. Unlike reduced appetite, we’ve never encountered anything on earth that can cause a human to live 150 years - no substance, no disease, no mutation. We’ve had the opportunity to observe billions of humans in the more-or-less modern era, where even pretty rare mutations or abnormalities or weird outcomes can get disseminated. No 150-year-olds, though - which really reduces the likelihood that there’s some feasibly interruptible signal that can simply be stopped to prevent aging. Doesn’t preclude it, of course - but it makes it more likely that the current outliers of “normal” agers (between 110 and 120) are the outer limit until we develop tools that can more radically change human biology than a mix of CRISPR and AI is going to be able to do in a few decades.
I’m not thinking about aging that way at all. I totally agree with you that aging could very well be the result of a genetic signal telling cells to slow down their metabolism - that’s why I used the examples of puberty and menopause above. If that “signal” is coming from a particular “place” or gene or small set of genes, we would potentially have the tools to interrupt it one day as a foreseeable extension of the cutting edge tools we have now. But if it’s not, if it’s more akin to the genetic framework that establishes how tall you’ll be and isn’t the result of a singular or discrete thing that can be interrupted, then those tools probably won’t be adequate to the task.
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