This Common Blood Pressure Drug Extends Lifespan And Slows Aging in Animals
The hypertension drug rilmenidine has been shown to slow down aging in worms, an effect that in humans could hypothetically help us live longer and keep us healthier in our latter years.
Previous research has shown rilmenidine mimics the effects of caloric restriction on a cellular level. Reducing available energy while maintaining nutrition within the body has been shown to extend lifespans in several animal models.
Whether this translates to human biology, or is a potential risk to our health, is a topic of ongoing debate. Finding ways to achieve the same benefits without the costs of extreme calorie cutting could lead to new ways to improve health in old age.
In a study published in 2023, young and old Caenorhabditis elegans worms treated with the drug – which is normally used to treat high blood pressure – lived longer and presented higher measures in a variety of health markers in the same way as restricting calories, as the scientists had hoped.
"For the first time, we have been able to show in animals that rilmenidine can increase lifespan," said molecular biogerontologist João Pedro Magalhães, from the University of Birmingham in the UK.
"We are now keen to explore if rilmenidine may have other clinical applications."
The C. elegans worm is a favorite for studies, because many of its genes have similarities to counterparts in our genome. Yet in spite of these similarities, it is still a rather distant relation to humans.
Further tests showed that gene activity associated with caloric restriction could be seen in the kidney and liver tissues of mice treated with rilmenidine.
In other words, some of the changes that caloric restriction gives in animals and thought to confer certain health benefits also appear with a hypertension drug that many people already take.
Another discovery was that a biological signaling receptor called nish-1 was crucial in the effectiveness of rilmenidine. This particular chemical structure could be targeted in future attempts to improve lifespan and slow down aging.
"We found that the lifespan-extending effects of rilmenidine were abolished when nish-1 was deleted," the researchers explained in their paper.
"Critically, rescuing the nish-1 receptor reinstated the increase in lifespan upon treatment with rilmenidine."
Low-calorie diets are hard to follow and come with a variety of side effects, such as hair thinning, dizziness, and brittle bones.
It's early days still, but the thinking is that this hypertension drug could confer the same benefits as a low-calorie diet while being easier on the body.
What makes rilmenidine a promising candidate as an anti-aging drug is that it can be taken orally, it's already widely prescribed, and its side effects are rare and relatively mild (they include palpitations, insomnia, and drowsiness in a few cases).
There's a long way to go yet in figuring out if rilmenidine would work as an anti-aging drug for actual humans, but the early signs in these worm and mice tests are promising. We now know much more about what rilmenidine can do, and how it operates.
"With a global aging population, the benefits of delaying aging, even if slightly, are immense," said Magalhães.
The research was published in Aging Cell.
An earlier version of this article was published in January 2023.
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Scientific American
5 days ago
- Scientific American
Animal Lifespans Offer Clues about the Science of Aging
Could the spectrum of animal lifespans hold clues about the science of aging? By , Fonda Mwangi & Alex Sugiura Rachel Feltman: For Scientific American 's Science Quickly, I'm Rachel Feltman. In the animal kingdom lifespans can stretch from mere hours to entire centuries, but that's just the start. Some creatures deteriorate so slowly that we've never actually caught them dying of old age. Others don't seem to age at all. And some can apparently reset their biological clocks and bounce back to infancy to start all over again. Plenty of humans would like to figure out how that works—and potentially harness the ability for our own use. But science has a long way to go. The truth is that we barely understand why or how we age in the first place—let alone how we might stop it. On supporting science journalism If you're enjoying this article, consider supporting our award-winning journalism by subscribing. By purchasing a subscription you are helping to ensure the future of impactful stories about the discoveries and ideas shaping our world today. My guest today is João Pedro de Magalhães. He's the chair of molecular biogerontology at the University of Birmingham in England, and he's here to tell us all about the nascent science of aging. Thank you so much for coming on to chat today. João Pedro de Magalhães: My pleasure. Thank you for the invitation. Feltman: So I'm sure that all of our listeners know that different species have different lifespans, but could you start by giving us a sense of some of the extremes that are out there? Magalhães: Absolutely. It's been a mystery of biology for a very long time, ever since Aristotle noticed [these] differences in lifespan across species. And we know that some animals have very short lifespans; others have very long lifespans. And this happens even amongst closely related species like mammals. For example, hamsters live about two years; mice and rats can live up to three or four years; and, you know, of course, humans, we can live over 100 years. And then at the other end of the spectrum we have certain species of whales that have been estimated to live over 200 years ... Feltman: Mm. Magalhães: So it is quite remarkable how much of a variation in longevity there is. Feltman: Yeah, and then, besides mammals, I would assume that things get even more extreme when you're talking about less closely related species. Magalhães: Well, there's some very unusual animals. There's this type of jellyfish which appears to be immortal, or it appears to have the ability to rejuvenate, to go back in biological time, so adults can go back to earlier stages of development and start again their own lives. So it's not that they're immortal [in] that you can't kill them, but they are biologically immortal in the sense that biological time, for them, doesn't roll in one direction, like it happens for us. Feltman: Mm. Magalhães: So there's very unusual animals—again, we're talking invertebrates like rotifers or very simple animals—whose adults don't have mouths. Feltman: Mm. Magalhães: They don't have a way of feeding. So they're very clear examples of mechanical limitations that will result in the demise of organisms. So you have a very big variety in terms of not just longevity and paces of aging but even in aging phenotypes and how species degenerate and die. Feltman: And fundamentally, what is aging? Magalhães: So aging, we are all familiar with it—I tend to have a very broad definition of aging as a, a progressive and inevitable physiological degeneration, an increase in vulnerability and decrease in viability. Now, of course, there's many facets to aging. I mean, it involves physiological degeneration. I mean, our bodies get weaker. We become frailer with age. But there's also, of course, many cellular, molecular changes that occur as well. And then, of course, there's increased incidence of diseases: cancer, cardiovascular diseases, neurological diseases, and so on. So one of the hallmarks of aging is that once you reach about age 30 your chance of dying [doubles] roughly every eight years, and that's very consistent across populations. And that happens as well in animals, only in animals like mice, it varies a bit between strains, but it'll be something like every few months the chance of dying doubles. Feltman: Hmm, and what do we know about what causes aging? You know, why is it inevitable for most species, but then, you know, for some, like those jellyfish, it doesn't seem to be? Magalhães: Well, that's a big question, and we don't have a good answer yet. We don't have a good understanding why some species age very fast. So for example, mice and rats, as I mentioned, they only live up to three or four years, but they also age much faster than human beings. No matter how you take care of them, a mouse will age about 20, 25, 30 times faster than a human being. So we know there's a very big diversity, also, in rates of aging, but what's behind it is not well-understood. We know there must be genetic differences, again, because no matter how well you take care of your mouse or hamster or rat, it will age a lot faster than a human being. So, you know, you can let it watch Netflix all it wants, it will still age much faster than human beings, right? So there has to be genetic differences. It's not environment, it's not the diet; it has to be genetically determined—it has to be encoded in our genomes how fast we age. But then, of course, the question is, 'Okay, but what [are] the biochemical, molecular, cellular determinants?' That's something we don't understand well yet. Having said that, there are some hypotheses. For example, one idea that's been around for decades is the idea that damage to the DNA and mutations in the DNA accumulate gradually with age and then cause aging. And the hypothesis being that in mice, for example, [this] accumulation of mutations occurs much faster—for which there is some experimental evidence. So that is one hypothesis. And at the moment, however, it's still unproven or unknown, really, why human beings age. Feltman: Hmm, and are there any factors that long-living organisms have in common? Magalhães: There are multiple factors associated with long lifespans. I mean, the important point is that we are a product of our evolutionary history. Of course, we now have technology, and we have medicine, but we didn't evolve in these conditions; we evolved as, as [cavemen], you know, hundreds of thousands or millions of years ago. And the same for every other species. And so the major determinant of whether a species evolves a short lifespan or a long lifespan is extrinsic mortality, so how much they die of—in particular, predation. So if you have animals like—short-lived animals like mice, I mean, mice in the wild very rarely live more than one year, not just because of diseases but primarily because of predators ... Feltman: Mm-hmm. Magalhães: And because they have very short lifespans, even in the wild, then, you know, they have to grow very quickly, they have to develop very quickly, and they have to reproduce very quickly, and so everything happens very quickly. So it's a very fast life history, a very fast life that they live. On the other hand, humans or the Galápagos tortoise would be an example or big whales or underground, subterranean animals like mole rats, they're protected from predators. I mean, we are protected from predators, one, because we're relatively big for primates and, of course, because of our intelligence, which [allowed] us to escape predators when we were, of course, in the time of cavemen and when we were evolving. And that means that because we have fewer predators, we are top of the food chain, that means that we have more time to grow, to develop, and then, of course, that leads to a longer lifespan as well. So across species there's this pattern, of course, of, you know, we are a product of our evolution, and we have the life history and the longevity that fits our evolutionary history. Feltman: What kinds of tools are researchers using to try to answer all of these questions we have about aging and lifespan? Magalhães: So there's different types of tools we can use. I mean, one big technological breakthrough was DNA sequencing. We can sequence DNA relatively cheaply and relatively rapidly nowadays. I mean, the human genome sequencing cost billions of dollars, but nowadays you can sequence your own genome, anyone can sequence their genomes for [a] few hundred dollars. So it's relatively cheap to sequence genomes, which means we can also sequence the genomes of different species, species with different lifespans. So for example, our lab, we sequenced the genome of the bowhead whale, which is the longest-lived mammal, [which has] been estimated to live over 200 years, as well as naked mole rats and other long-lived, disease-resistant species. And there's now hundreds of genome [sequences] from many different species with different lifespans. And so what you can do with that trove of information is analyze it for patterns associated with the evolution of longevity. You can ask questions—so for example, you know, 'Do species that live a longer lifespan, do they have more DNA repair genes?' So you can use that information on the DNA to study the evolution of longevity, then try to find specific genes and pathways associated with it. Feltman: Mm. Magalhães: Now, the other approach we use to study aging, of course, is in model systems. I mean, unfortunately we cannot really study aging in human beings—or we can, but it's very difficult and time-consuming—and so we tend to use short-lived model systems like mice or fruit flies or worms. [Some] worms live a few weeks. We tend to use fruit flies, Drosophila, that live a few months. Mice can live up to three, four years. So we can study these animals to try to gather insights into the mechanisms of aging, hoping that some of these will be applicable to humans. I mean, there's some rationale for it because we know the basic biochemistry of life in a mouse is quite similar to humans. We can also manipulate aging to some degree in animal models, particularly at the genetic level. We can tweak genes in animals, including in mice, and extend their lifespan. In mice [it's] up to about 50 percent. But for example, in worms we can tweak a single gene in worms and extend by about 10 times ... Feltman: Mm. Magalhães: Which is quite remarkable. So we can do a lot of studies in animal models: we can manipulate aging to some degree in animals, and then we can do mechanistic studies. We can look at their molecules, we can look at their cells, we can look at their hormones and try to test mechanistic [hypotheses] of aging. Feltman: What do you think are the biggest questions that we should be tackling about human aging and human lifespans? Magalhães: Well, I suppose the big question is still why we age. I mean, why do human beings age? As I said, there's hypotheses like DNA damage and mutations, like oxidative damage, like loss of protein, homeostasis. There's different hypothesis, but we still don't know why we age, and I think that remains the big question in the field. There's other questions, of course: Can we manipulate human aging? Because although we can manipulate, to some degree, aging in animal models, we don't know if that's possible or not in human beings. We can manipulate, to some degree, our longevity by exercise, eating healthy, not smoking, not drinking too much alcohol, and so on. But whether, for example, can we develop a longevity drug? And there's a number of companies and labs trying to develop longevity pills, and—but whether they're gonna be effective in humans, that's still something that's up to discussion and will require, for example, clinical trials. Feltman: Mm. Magalhães: So one aspect that's quite fundamental and important in, in aging is that there are complex species—like some species of reptiles like the Galápagos tortoise; some species of fishes, like rockfishes; some species in salamanders, like the olm—that appear not to age at all. There's no mammals in this category, but there are complex vertebrates that, in studies spanning decades, do not exhibit increased mortality, do not exhibit increased physiological degeneration. So that is quite a fascinating observation, that some species—I mean, maybe they do age after a very long time, but at the very least they age much, much, much slower than human beings ... Feltman: Hmm. Magalhães: Which I think is a great inspiration as well. Because, so, for example, just like the Wright brothers took inspiration from birds: they saw birds—'Well, birds are heavier than air, and yet they can fly, so there's no reason to think we cannot build a machine that's heavier than air and can make us fly.' We can take inspiration [from] these animals. There's no physical limit that [holds] that every organism has to age. And so we can take [inspiration] from the species that appear not to age and think, 'Well, maybe with technology and, and therapeutics we can, at the very least, slow our aging process.' Feltman: Thank you so much for coming on to talk today. This has been great. Magalhães: Well, thank you. My pleasure. Feltman: That's all for today's episode. We'll be back on Friday. Science Quickly is produced by me, Rachel Feltman, along with Fonda Mwangi, Kelso Harper, Naeem Amarsy and Jeff DelViscio. This episode was edited by Alex Sugiura. Shayna Posses and Aaron Shattuck fact-check our show. Our theme music was composed by Dominic Smith. Subscribe to Scientific American for more up-to-date and in-depth science news.
Yahoo
07-06-2025
- Yahoo
‘Superorganisms' were just seen in the wild for the first time ever
If you purchase an independently reviewed product or service through a link on our website, BGR may receive an affiliate commission. For years, scientists have watched nematodes build massive superorganisms in the form of writhing towers. But, they've only seen it happen in the lab. Now, though, researchers write that they've observed these massive, disturbing towers writhing in the wild for the first time ever. Previously, researchers believed that the behavior was meant to be an attempt to escape from the rest of the group. However, new images of the writhing towers appear to suggest they're actually used cooperatively, to benefit many worms instead of just one. Today's Top Deals Best deals: Tech, laptops, TVs, and more sales Best Ring Video Doorbell deals Memorial Day security camera deals: Reolink's unbeatable sale has prices from $29.98 The researchers reported their findings in a report published in Current Biology, writing that these towering superorganisms only existed naturally in their imaginations for the longest of times. Observing the towers also taught researchers quite a bit about how different species of nematode work together. While watching the towers, the scientists note that while many different species crawled through the worm towers, only one species, a tough larval stage known as a dauer, actually participated in building up the writing masses. This specificity in the construction of the tower points to something more than just random cooperation. These towers are truly superorganisms, then, and not just piles of writing worm bodies. This discovery also got researchers thinking: could other worms form writhing towers like this, too? To test that hypothesis, they stuck a toothbrush bristle into a food-free agar plate, then unleashed a bunch of roundworms from the species Caenorhabditis elegans into the structure. Immediately, the worms began to work together and build up a tower. Within two hours, the researchers say the C. elegans had formed a tower using the bristle as its spine. The researchers watched as some worms along the superorganism writhed and acted as exploratory arms. Others acted as bridges between gaps. To see how the superorganism would respond, the researchers tapped the top of the tower with a glass pick. Almost immediately, the worms began to wriggle and move toward the area. This, they say, shows that these towers are always growing and moving toward stimulus. It's an intriguing show of cooperation between the worms, and just one more way that worms continue to astound scientists. It also raises more questions about why these superorganisms form in the first place. Even more interesting, though, is that the roundworms didn't appear to hold any kind of class system in place. Where the nematodes only relied on the larval stage worms to create the tower, all the roundworms chimed in to help build up the mass. Researchers will need to dig deeper to see exactly why worms form these writhing superorganisms. Hopefully other species, like the parasitic hairworm, aren't capable of this same kind of behavior. More Top Deals Amazon gift card deals, offers & coupons 2025: Get $2,000+ free See the
Yahoo
06-06-2025
- Yahoo
This ‘Tower of Worms' Is a Squirming Superorganism
When food runs out, certain tiny roundworms, barely visible to the naked eye, crawl toward one another and build living, wriggling towers that move as one superorganism. For the first time, we've caught them doing that in nature on video. Scientists spent months pointing their digital microscope at rotting apples and pears to finally catch a glimpse of these living towers formed by Caenorhabditis roundworms in an orchard that is just downhill from the Max Planck Institute of Animal Behavior's location in Konstanz, Germany. 'It wasn't that hard to find. It's just the people didn't have the interest or time or funding for this kind of research,' says biologist Daniela Perez, lead author of the study. Perez and her team at the Max Planck Institute of Animal Behavior then studied this behavior in a laboratory to learn more. To spur the towering, they placed groups of Caenorhabditis elegans in a dish without food, alongside a toothbrush bristle that could work as a scaffold. Dozens of worms quickly climbed on top of the bristle and one another to form a structure that moved in an eerily coordinated manner. The tower responded to the touch of a glass pipe by attempting to latch onto it; it stretched to bridge the gap between the bottom of the dish and its lid; and it even waved its tip around to probe the surrounding environment. The results were published Thursday in Current Biology. [Sign up for Today in Science, a free daily newsletter] Researchers had previously observed this towering in the lab but didn't know that it was an actual survival strategy in the wild. 'Discovering [this behavior] in wild populations is really important as it shows this is a part of how these animals live and not just a lab artifact,' says William Schafer, a geneticist at the University of Cambridge, who studies C. elegans and was not involved in the study. Why do the worms do this? The researchers think towering helps worms set out to find richer food sources. When resources are limited, 'it probably makes sense for microscopic organisms to cooperate for dispersing by forming something bigger,' says the study's senior author Serena Ding. The towers could allow some of their members to reach new places or to hitchhike on other organisms such as fruit flies. The bigger question is how the worms communicate within the towers. If the worms on top latch onto a fly, how do those at the bottom know to detach from where they're anchored? They could communicate chemically through pheromones and mechanically through movement patterns, Schafer suggests. Perez says her team plans to test this next. 'Every time we have a meeting, we end up with 10 new project ideas,' she says. 'There are so many directions we can take this.'
