Researchers sound alarm after recording sudden drop in species used to help fight diseases: 'That is really, really dangerous'
However, that lizard's population is dwindling, leaving increasing mosquito populations to feed on other animals and people instead.
As WLRN and The Miami Herald jointly reported, brown anole lizards have been declining in numbers due to reptile collectors releasing their unwanted pets in the wild — primarily, the outlet said, the larger Peter's rock agamas were out-competing the brown anoles for food, dwindling the local population. In the past, brown anoles were prime targets for local mosquitoes.
The report noted that an agama "hides in cracks and crevices as soon as the sun begins to set," generally making it less susceptible to mosquito bites than brown anole lizards. Researchers studied whether fewer brown anoles means more birds will get bitten by mosquitoes. Birds are dangerous hosts because of their propensity to spread mosquito-borne diseases.
To test their theory about mosquitoes' shifting behaviors, the researchers captured and studied mosquitoes and studied the DNA to identify forensic evidence of what they were biting when they had anoles in their area and when the researchers had caught many anoles and subtracted them from the area. The hypothesis was that when there are not many anoles in the area, the rates of bird bites rise.
This WLRN and Miami Herald report came in the middle of these efforts, so it's a "to be continued" for now. But when the results are available, they hope to better understand how humans' introduction of non-native species damages ecosystems and has unintended consequences that risk human health.
A University of Florida invasion ecologist, Melissa Miller, said, "Brown anoles seem like such a small component of the ecosystem, but even removing that can have impacts that are felt much higher up the food chain, all the way to humans."
This research is significant because of the disease risks mosquitoes carry and because mosquito activity is becoming more common in places like Florida. Our planet's steady overheating is creating ideal conditions for mosquitoes to thrive and multiply.
With this population boost comes the increased spread of vector-borne illnesses that cause people to become very sick and even die. Mosquitoes are evolving and adapting to rising global temperatures, making diseases like dengue, malaria, and Zika more common in places they've never existed.
It is expected that within the next 25 years, mosquito season in the U.S. will last two months longer than it does now.
Do you worry about getting diseases from bug bites?
Absolutely
Only when I'm camping or hiking
Not really
Never
Click your choice to see results and speak your mind.
"That is really, really dangerous, because toward the end of the transmission period, that is when most of these mosquitoes are infected," said Miami-Dade's Mosquito Control's division chief, Dr. John-Paul Mutebi. "They keep on picking up the pathogens as the season goes."
Studies like this one contribute to our greater comprehension of how healthy ecosystems work and the impacts of eliminating any species.
Fortunately, research teams are working to find solutions. For example, one group found that disease threats can be curbed by restricting mosquitoes' preferred plant food sources. Other scientists have been working to disable mosquitoes' ability to spread diseases through gene editing and DNA modification.
As an individual, you can help prevent mosquito-spread diseases by limiting your impact on the environment.
Never release invasive species into the wild because the widespread ecosystem impacts could be devastating. You can also protect yourself from mosquitoes by paying attention to public health alerts, limiting outdoor activity during prime mosquito times, and eliminating standing water sources in your yard.
Join our free newsletter for good news and useful tips, and don't miss this cool list of easy ways to help yourself while helping the planet.
Try Our AI Features
Explore what Daily8 AI can do for you:
Comments
No comments yet...
Related Articles
Yahoo
27-06-2025
- Yahoo
Caffeine Flips a Cellular Switch That May Slow Aging, Scientists Discover
We know caffeine is good for an alertness boost first thing in the morning or during an afternoon lull, but researchers have also linked the compound to healthy aging – and a new study takes a close look at some of the cellular mechanisms responsible for that link. Scientists from Queen Mary University of London (QMUL) and the Francis Crick Institute in the UK used fission yeast as stand-ins for human cells, analyzing how doses of caffeine affected the lifespan of the cells and their ability to withstand damage. "These findings help explain why caffeine might be beneficial for health and longevity," says biochemist John-Patrick Alao, from QMUL. "And they open up exciting possibilities for future research into how we might trigger these effects more directly – with diet, lifestyle, or new medicines." Previous research found that caffeine could operate a biological switch called TOR (target of rapamycin), which helps regulate the growth of cells in response to food and energy availability. With the latest experiments, the researchers determined that caffeine doesn't interact directly with TOR. Instead, it controls it through the AMPK pathway, which works kind of like a fuel gauge for cells. We already know that AMPK takes care of some vital jobs in terms of keeping cells running and helping them resist wear and tear more effectively. Now we also know that caffeine has an effect on it. "When your cells are low on energy, AMPK kicks in to help them cope, and our results show that caffeine helps flip that switch," says geneticist and biologist Charalampos Rallis, from QMUL. With caffeine operating the TOR lever through the AMPK enzyme, cells are affected in three different ways, the researchers found: in how they grow, in how they repair their DNA, and in how they respond to stress. That all adds up to cells that stay healthier for longer. When the researchers interrupted the genetic chain reaction that caffeine triggers, the cells didn't get all of the same health benefits – confirmation of how the compound is working, and perhaps, how we might be able to utilize it in the future. The diabetes drug metformin is currently being looked at as a way of keeping us in better shape for a longer period of time, and it too operates through AMPK – suggesting caffeine-based drugs may have a similar effect. Any kind of medication or treatment is still a long way off however, not least because these findings are from yeast cells rather than human cells. The researchers are still keen to learn more about the precise way caffeine interacts with AMPK and TOR. What we can certainly say for now is that more and more studies are showing positive effects from caffeine consumption, whether that's losing body fat, protecting against cardiovascular disease, or keeping dementia at bay. "Direct pharmacological targeting of AMPK may serve towards healthspan and lifespan benefits beyond yeasts, given the highly conserved nature of this key regulatory cellular energy sensor," write the researchers in their published paper. The research has been published in Microbial Cell. People Are Trying Nicotine Gum For Long Covid – Could It Treat Brain Fog? Your Cell's Powerhouses Are Secretly Helping Fight Bacteria, Study Finds Heavy Drinkers Face Higher Risk of Brain Lesions And Alzheimer's Markers
Yahoo
26-06-2025
- Yahoo
Your morning coffee could help you stay young — but there's a catch
Could coffee be the liquid key to longevity? A new study reports that the world's most widely used stimulant can extend lifespan and affect how cells respond to genetic damage — though there's a potential complication. A team of researchers at Queen Mary University of London confirms that caffeine interacts with the systems that influence aging, DNA response and cellular stress. The team studied fission yeast, a single-celled organism that is analogous to human cells and uses similar pathways to manage energy, DNA repair and stress. Researchers measured the response of fission yeast to different forms of cellular stress, including DNA damage, toxic exposure and nutrient deprivation. Then they added caffeine to gauge how cells would respond. They found that while caffeine extended the lifespan of yeast, it also affected how cells responded to stress, particularly when the molecular systems that regulate stress were already activated. The findings were published this week in the journal Microbial Cell. The research team previously established that caffeine supports the longevity of cells by activating TOR (target of rapamycin), a biological switch that determines when cells should grow based on the availability of food and energy. According to the team, the TOR switch has been actively controlling energy and stress responses in living things for over 500 million years. In this latest study, the team learned that caffeine doesn't directly activate TOR, but rather influences it by activating AMPK, a cellular fuel reserve in yeast and humans. 'When your cells are low on energy, AMPK kicks in to help them cope,' said study senior author Charalampos (Babis) Rallis. 'And our results show that caffeine helps flip that switch.' The yeast model demonstrated that caffeine's influence on flipping that switch directly impacts how cells grow, repair their DNA and respond to stress — all of which relate to aging. Quite surprisingly, the team found that rather than protecting damaged DNA, caffeine amplified the damage. Typically, when a cell detects DNA damage, it stops dividing to repair it. However, researchers found that caffeine overrides this stop, allowing unhealed cells to continue dividing and making them more vulnerable to future damage. The team assured that this doesn't make your morning cup inherently dangerous. Caffeine's ability to alter how cells respond to problems can be positive or negative, depending on the situation. The team noted that the benefits of caffeine depend on the presence of specific proteins and pathways. The fact that caffeine's effects are neither universal nor automatic may help explain why previous studies exploring the link between caffeine and improved health have been inconsistent. 'These findings help explain why caffeine might be beneficial for health and longevity,' said John-Patrick Alao, the postdoctoral research scientist leading this study. 'And they open up exciting possibilities for future research into how we might trigger these effects more directly — with diet, lifestyle or new medicines.' The team acknowledged that because the study relied only on fission yeast, the findings may not directly translate to human cells. Coffee has long been lauded for its health benefits. Rich in antioxidants, it may enhance brain function. It's also been shown to increase alertness, aid in weight management, boost mood and potentially lower the risk of Type 2 diabetes and heart disease. A 2018 study of nearly half a million British adults found that coffee drinkers had a slightly lower risk of death over 10 years than abstainers. Other research, encompassing more than 170,000 adults in the UK, proposed that those who drink between two and four daily cups of coffee, regardless of whether they have added sugar, live longer than those who don't drink coffee. A 2025 study led by researchers at Tulane University tied a morning brew to lower mortality rates than espresso later in the day. And three to five cups a day at midlife was associated with a decreased risk of Alzheimer's disease later in life, research determined. In addition to Alzheimer's, some studies found that java junkies have up to a 60% lower risk of Parkinson's disease. The more coffee they drank, the lower the risk.
Yahoo
19-06-2025
- Yahoo
Previously unknown 76M-year-old, raccoon-sized monstersaur species discovered in Utah
Hank Woolley was visiting the Natural History Museum of Utah one day when he stumbled across a jar labeled 'lizard.' Inside was a 76-million-year-old fossil that paleontologists had uncovered from Grand Staircase-Escalante National Monument in 2005. It was eventually transported to the Natural History Museum of Utah in Salt Lake City, where it ended up being stored in a jar. Woolley, a postdoctoral research fellow at the Natural History Museum of Los Angeles County's Dinosaur Institute, opened the jar to find a fragmentary skeleton, which inspired him to dig deeper. 'We know very little about large-bodied lizards from the Kaiparowits Formation in Grand Staircase-Escalante National Monument in Utah, so I knew this was significant right away,' he explained in a statement. That decision a few years ago is now helping researchers gain a better understanding of the fossil's importance, as it gives them an improved glimpse of what Utah's ecosystem looked like 76 million years ago. Woolley is the lead author of a new study identifying a prehistoric ancestor of the Gila monsters that roam southern Utah and the Southwest U.S. today. His team's findings were published in the journal Royal Society Open Science on Tuesday. 'Discovering a new species of lizard that is an ancestor of modern Gila monsters is pretty cool in and of itself, but what's particularly exciting is what it tells us about the unique 76-million-year-old ecosystem it lived in,' said co-author Randy Irmis, an associate professor at the University of Utah and curator of paleontology at the Natural History Museum of Utah, and one of the study's co-authors. Paleontologists knew the fossil was 'significant' when they first uncovered it two decades ago, Irmis explains. They brought it back to Salt Lake City, where it sat and waited for the right expert to know its gravity. Woolley, who specializes in lizard evolution, happened to be that guy. He quickly got to work assembling the team that pieced together the fossils and then analyzed its skull, vertebrae and limbs, as well as other features. The team discovered that the lizard was much more intact than many lizard species of its time, and that they had uncovered a species previously unknown to experts. The species would have been about the size of a raccoon, making it one of the smaller creatures of its time, which is when southern Utah was more of a subtropical floodplain, researchers point out. The team decided to name the species Bolg amondol, or 'Bolg' for short. It's a nod to the goblin prince from J.R.R. Tolkien's 'The Hobbit,' largely for the lizard's goblin-like skull. 'The fact that Bolg coexisted with several other large lizard species indicates that this was a stable and productive ecosystem where these animals were taking advantage of a wide variety of prey and different microhabitats,' Irmis said. The team says the discovery could help piece together the evolution of lizards, especially since it was a precursor to modern-day species like the Gila monster. Irmis co-authored another study published earlier this year that explored how crocodiles and alligators may have survived extinction, which included species that would have existed at the same time as Bolg. Meanwhile, the researchers also believe there were probably other species like it that existed during the Late Cretaceous Period, which is a more probable theory thanks to Bolg. The next discovery could be waiting to be uncovered in Utah's public lands, or stored safely away in a jar like Borg.
