Menopause explains why some female whales live so long

Females of some whale species have evolved to live drastically longer lives so they can care for their families, new research shows.

The study focussed on five whale species that -- along with humans -- are the only mammals known to go through menopause.

The findings show that females of these whale species that experience menopause live around 40 years longer than other female whales of a similar size.

By living longer without extending their "reproductive lifespan" (the years in which they breed), these females have more years to help their children and grandchildren, without increasing the "overlap" period when they compete with their daughters by breeding and raising calves at the same time.

This new research shows that -- despite being separated by 90 million years of evolution -- whales and humans show remarkably similar life histories, which have evolved independently.

The study was carried out by the universities of Exeter and York, and the Center for Whale Research.

"The process of evolution favours traits and behaviours by which an animal passes its genes to future generations," said lead author Dr Sam Ellis, from the University of Exeter.

"The most obvious way for a female to do this is to breed for the entire lifespan -- and this is what happens in almost all animal species. There are more than 5,000 mammal species, and only six are known to go through menopause.

"So the question is: how and why did menopause evolve? Our study provides some of the answers to this fascinating puzzle."

Menopause is known to exist in five species of toothed whale: short-finned pilot whales, false killer whales, killer whales, narwhals and beluga whales.

As well as outliving females of other similar-sized species, females in these five species outlive the males of their own species. For example, female killer whales can live into their 80s, while males are typically dead by 40.

"The evolution of menopause and a long post-reproductive life could only happen in very specific circumstances," said Professor Darren Croft, of the University of Exeter and Executive Director at the Center for Whale Research

"Firstly, a species must have a social structure in which females spend their lives in close contact with their offspring and grand-offspring.

"Secondly, the females must have an opportunity to help in ways that improve the survival chances of their family. For example, female toothed whales are known to share food and use their knowledge to guide the group to find food when it is in short supply."

Professor Dan Franks, from the University of York, said: "Previous research on menopause evolution has tended to focus on single species, typically humans or killer whales.

"This study is the first to cross several species, enabled by the recent discovery of menopause in multiple species of toothed whales.

"Our study provides evidence that menopause evolved by expanding female lifespan beyond their reproductive years, rather than from reduced reproductive lifespan.

"This is a question that has long been asked in anthropology, but can only be directly answered with a comparative study."

Commenting on parallels with the evolution of menopause in humans, Professor Croft added: "It's fascinating that we share this life history with a taxonomic group we're so different from.

"Despite these differences, our results show that humans and toothed whales show convergent life history -- just like in humans, menopause in toothed whales evolved by selection to increase the total lifespan without also extending their reproductive lifespan."

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Longevity gene from naked mole rats extends lifespan of mice

In a groundbreaking endeavor, researchers at the University of Rochester have successfully transferred a longevity gene from naked mole rats to mice, resulting in improved health and an extension of the mouse's lifespan.

Naked mole rats, known for their long lifespans and exceptional resistance to age-related diseases, have long captured the attention of the scientific community. By introducing a specific gene responsible for enhanced cellular repair and protection into mice, the Rochester researchers have opened exciting possibilities for unlocking the secrets of aging and extending human lifespan.

"Our study provides a proof of principle that unique longevity mechanisms that evolved in long-lived mammalian species can be exported to improve the lifespans of other mammals," says Vera Gorbunova, the Doris Johns Cherry Professor of biology and medicine at Rochester. Gorbunova, along with Andrei Seluanov, a professor of biology, and their colleagues, report in a study published in Nature that they successfully transferred a gene responsible for making high molecular weight hyaluronic acid (HMW-HA) from a naked mole rat to mice. This led to improved health and an approximate 4.4 percent increase in median lifespan for the mice.

A unique mechanism for cancer resistance

Naked mole rats are mouse-sized rodents that have exceptional longevity for rodents of their size; they can live up to 41 years, nearly ten times as long as similar-size rodents. Unlike many other species, naked mole rats do not often contract diseases -- including neurodegeneration, cardiovascular disease, arthritis, and cancer -- as they age. Gorbunova and Seluanov have devoted decades of research to understanding the unique mechanisms that naked mole rats use to protect themselves against aging and diseases.

The researchers previously discovered that HMW-HA is one mechanism responsible for naked mole rats' unusual resistance to cancer. Compared to mice and humans, naked mole rats have about ten times more HMW-HA in their bodies. When the researchers removed HMW-HA from naked mole rat cells, the cells were more likely to form tumors.

Gorbunova, Seluanov, and their colleagues wanted to see if the positive effects of HMW-HA could also be reproduced in other animals.

Transferring a gene that produces HMW-HA

The team genetically modified a mouse model to produce the naked mole rat version of the hyaluronan synthase 2 gene, which is the gene responsible for making a protein that produces HMW-HA. While all mammals have the hyaluronan synthase 2 gene, the naked mole rat version seems to be enhanced to drive stronger gene expression.

The researchers found that the mice that had the naked mole rat version of the gene had better protection against both spontaneous tumors and chemically induced skin cancer. The mice also had improved overall health and lived longer compared to regular mice. As the mice with the naked mole rat version of the gene aged, they had less inflammation in different parts of their bodies -- inflammation being a hallmark of aging -- and maintained a healthier gut.

While more research is needed on exactly why HMW-HA has such beneficial effects, the researchers believe it is due to HMW-HA's ability to directly regulate the immune system.

A fountain of youth for humans?

The findings open new possibilities for exploring how HMW-HA could also be used to improve lifespan and reduce inflammation-related diseases in humans.

"It took us 10 years from the discovery of HMW-HA in the naked mole rat to showing that HMW-HA improves health in mice," Gorbunova says. "Our next goal is to transfer this benefit to humans."

They believe they can accomplish this through two routes: either by slowing down degradation of HMW-HA or by enhancing HMW-HA synthesis.

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Why do some people live to be 100? Intestinal bacteria may hold the answer

We are pursuing the dream of eternal life. We fast to stay healthy. And each year, we spend billions of kroner on treatment to make sure we stay alive. But some people turn 100 years old all by themselves. Why is that?

Researchers from the Novo Nordisk Foundation Center for Protein Research at the University of Copenhagen have set out to find the answer.

Studying 176 healthy Japanese centenarians, the researchers learned that the combination of intestinal bacteria and bacterial viruses of these people is quite unique.

"We are always eager to find out why some people live extremely long lives. Previous research has shown that the intestinal bacteria of old Japanese citizens produce brand new molecules that make them resistant to pathogenic -- that is, disease-promoting -- microorganisms. And if their intestines are better protected against infection, well, then that is probably one of the things that cause them to live longer than others," says Postdoc Joachim Johansen, who is first author of the new study.

Among other things, the new study shows that specific viruses in the intestines can have a beneficial effect on the intestinal flora and thus on our health.

"Our intestines contain billions of viruses living of and inside bacteria, and they could not care less about human cells; instead, they infect the bacterial cells. And seeing as there are hundreds of different types of bacteria in our intestines, there are also lots of bacterial viruses," says Associate Professor Simon Rasmussen, last author of the new study.

Joachim Johansen adds that aside from the important, new, protective bacterial viruses, the researchers also found that the intestinal flora of the Japanese centenarians is extremely interesting.

"We found great biological diversity in both bacteria and bacterial viruses in the centenarians. High microbial diversity is usually associated with a healthy gut microbiome. And we expect people with a healthy gut microbiome to be better protected against aging related diseases," says Joachim Johansen.

Once we know what the intestinal flora of centenarians looks like, we can get closer to understanding how we can increase the life expectancy of other people. Using an algorithm designed by the researchers, they managed to map the intestinal bacteria and bacterial viruses of the centenarians.

"We want to understand the dynamics of the intestinal flora. How do the different kinds of bacteria and viruses interact? How can we engineer a microbiome that can help us live healthy, long lives? Are some bacteria better than others? Using the algorithm, we are able to describe the balance between viruses and bacteria," says Simon Rasmussen.

And if the researchers are able to understand the connection between viruses and bacteria in the Japanese centenarians, they may be able to tell what the optimal balance of viruses and bacteria looks like.

Optimising intestinal bacteria

More specifically, the new knowledge on intestinal bacteria may help us understand how we should optimise the bacteria found in the human body to protect it against disease.

"We have learned that if a virus pays a bacterium a visit, it may actually strengthen the bacterium. The viruses we found in the healthy Japanese centenarians contained extra genes that could boost the bacteria. We learned that they were able to boost the transformation of specific molecules in the intestines, which might serve to stabilise the intestinal flora and counteract inflammation," says Joachim Johansen, and Simon Rasmussen adds:

"If you discover bacteria and viruses that have a positive effect on the human intestinal flora, the obvious next step is to find out whether only some or all of us have them. If we are able to get these bacteria and their viruses to move in with the people who do not have them, more people could benefit from them."

Even though this requires more research, the new insight is significant, because we are able to modify the intestinal flora.

Read more at Science Daily

Early life experiences can have long-lasting impact on genes

Early life experiences can impact the activity of our genes much later on and even affect longevity, finds a new study in fruit flies led by UCL researchers.

In the study published in Nature Aging, the scientists report that gene expression 'memory' can persist across the lifespan, and may present a novel target for improving late-life health.

Lead author Dr Nazif Alic (UCL Institute of Healthy Ageing, UCL Biosciences) said: "Health in old age partially depends on what a person experienced in their youth or even in the womb. Here, we have identified one way in which this happens, as changes in gene expression in youth can form a 'memory' that impacts health more than half a lifetime later."

The scientists were building on their previous research in which they found that fruit flies fed a high-sugar diet early in life lived shorter lives, even after their diets were improved in adulthood. Here, they uncover the mechanism likely explaining the finding.

In their previous study, the researchers found that a high-sugar diet inhibited a transcription factor called dFOXO, which is involved in glucose metabolism and is known from multiple studies to affect longevity, so they now sought to enact the opposite effect by directly increasing the activity of dFOXO. Transcription factors are proteins that regulate transcription, or copying, of information from DNA into messenger RNA, which is the first and key step in gene expression. For this study, the researchers activated dFOXO by increasing its levels in female fruit flies during the first three weeks of the fly's adulthood.

They found that these early-life experiences caused changes to chromatin -- a mixture of DNA and proteins that can be seen as the 'packaging' of DNA -- that persisted and resulted in genes being expressed differently late in life. This counteracted some changes that would be expected as part of the normal ageing process, eventually improving health in late life and impacting the fruit flies' lifespan more than a month (half a fruit fly lifetime) later.

The researchers say their findings could lead to ways to impact late-life health in people as well.

Dr Alic said: "What happens early on in an animal or person's life can affect what their genes do late in life, for better or for worse. It may be that a poor diet early in life, for example, could impact our metabolism later in life by tweaking how our genes are expressed, even after substantial dietary changes over the years -- but fortunately, it may well be possible to reverse this.

"Now that we know how gene expression memory can persist across the lifespan to affect gene activity, we may be able to develop ways to counteract these changes later in life to preserve health and enable people to stay healthy for longer."

Read more at Science Daily

Honey bee life spans are 50% shorter today than they were 50 years ago

A new study by University of Maryland entomologists shows that the lifespan for individual honey bees kept in a controlled, laboratory environment is 50% shorter than it was in the 1970s. When scientists modeled the effect of today's shorter lifespans, the results corresponded with the increased colony loss and reduced honey production trends seen by U.S. beekeepers in recent decades.

Colony turnover is an accepted factor in the beekeeping business, as bee colonies naturally age and die off. But over the past decade, U.S. beekeepers have reported high loss rates, which has meant having to replace more colonies to keep operations viable. In an effort to understand why, researchers have focused on environmental stressors, diseases, parasites, pesticide exposure and nutrition.

This is the first study to show an overall decline in honey bee lifespan potentially independent of environmental stressors, hinting that genetics may be influencing the broader trends seen in the beekeeping industry. The study was published November 14, 2022, in the journal Scientific Reports.

"We're isolating bees from the colony life just before they emerge as adults, so whatever is reducing their lifespan is happening before that point," said Anthony Nearman, a Ph.D. student in the Department of Entomology and lead author of the study. "This introduces the idea of a genetic component. If this hypothesis is right, it also points to a possible solution. If we can isolate some genetic factors, then maybe we can breed for longer-lived honey bees."

Nearman first noticed the decline in lifespan while conducting a study with entomology associate professor Dennis van Engelsdorp on standardized protocols for rearing adult bees in the laboratory. Replicating earlier studies, the researchers collected bee pupae from honey bee hives when the pupae were within 24 hours of emerging from the wax cells they are reared in. The collected bees finished growing in an incubator and were then kept as adults in special cages.

Nearman was evaluating the effect of supplementing the caged bees' sugar water diet with plain water to better mimic natural conditions when he noticed that, regardless of diet, the median lifespan of his caged bees was half that of caged bees in similar experiments in the 1970s. (17.7 days today versus 34.3 days in the 1970s.) This prompted a deeper review of published laboratory studies over the past 50 years.

"When I plotted the lifespans over time, I realized, wow, there's actually this huge time effect going on," Nearman said. "Standardized protocols for rearing honey bees in the lab weren't really formalized until the 2000s, so you would think that lifespans would be longer or unchanged, because we're getting better at this, right? Instead, we saw a doubling of mortality rate."

Although a laboratory environment is very different from a colony, historical records of lab-kept bees suggest a similar lifespan to colony bees, and scientists generally assume that isolated factors that reduce lifespan in one environment will also reduce it in another. Previous studies had also shown that in the real world, shorter honey bee lifespans corresponded to less foraging time and lower honey production. This is the first study to connect those factors to colony turnover rates.

When the team modeled the effect of a 50% reduction in lifespan on a beekeeping operation, where lost colonies are replaced annually, the resulting loss rates were around 33%. This is very similar to the average overwinter and annual loss rates of 30% and 40% reported by beekeepers over the past 14 years.

Nearman and vanEngelsdorp noted that their lab-kept bees could be experiencing some sort of low-level viral contamination or pesticide exposure during their larval stage, when they're brooding in the hive and worker bees are feeding them. But the bees have not shown overt symptoms of those exposures and a genetic component to longevity has been shown in other insects such as fruit flies.

Read more at Science Daily

Clusters of genes help mice live longer

Researchers from the National Institute on Aging (NIA)-funded Interventions Testing Program recently reported the discovery of multiple candidate genes that influence longevity. The three Interventions Testing Program sites -- The University of Texas Health Science Center at San Antonio, The University of Michigan at Ann Arbor and The Jackson Laboratory at Bar Harbor, Maine -- collaborated on the study with the labs of Robert W. Williams, PhD, of the University of Tennessee Health Science Center at Memphis and Johan Auwerx, MD, PhD, of the École Polytechnique Fédérale de Lausanne in Lausanne, Switzerland.

"Some candidate genes impacted female life span while others affected the male life span," said Randy Strong, PhD, of the Sam and Ann Barshop Institute for Longevity and Aging Studies at UT Health San Antonio. "One cluster of genes increased longevity of both sexes. In a rarity for these types of studies, the findings were made in a population of mice with genetic diversity comparable to human populations."

The high-impact journal Science published the findings Sept. 30. Strong directs the Interventions Testing Program site at the Barshop Institute, which first attracted National Institute on Aging (NIA) grant funding for the Interventions Testing Program in 2003 and is in its 19th year of the NIA funding.

Genetic smorgasbord

"The study models what happens in people," said research coauthor James Nelson, PhD, of the Barshop Institute. "Unlike mice in many other studies, mice in this newly reported research are not all the same. Each has different genetic variants, resulting in slightly different proteins that do slightly different things, which together can impact aging."

Even subtle differences can lead to different health outcomes as we age. Slight variations in the hemoglobin gene, for example, can cause the hemoglobin protein in red blood cells to be less effective at binding to oxygen and transferring it from the lungs to the body's tissues, Nelson noted. Anemia is one effect.

Female longevity

The discovery of genetic loci that influence longevity only in females is interesting and important, Strong said. Genetic loci are clusters of between 10 and 100 genes.

"Females and males differ in almost every aspect of aging you can explore," Strong said. "They each must be studied, both to understand aging in the two sexes and to develop effective treatments. If we offer the same drug therapies to females that we offer to males, and females' aging is caused by different genes, we are not going to be as effective in our treatments."

Confirmation in roundworms

The next steps are scrutinizing these candidate genes to find ones that are responsible for increased longevity. In the final part of the Science article, the team reported doing this. The researchers tested candidate genes in roundworms, which are often used in aging research because of their short life span. "A number of the candidate genes did affect longevity in the worms," Nelson said.

That doesn't prove that those same genes in humans are going to affect human life span, the researchers said. But it's another part of the case for continuing to study the genetic basis of longevity.

Powerful study design

As envisioned when the Interventions Testing Program began, having three sites where studies are conducted ensures statistical power and rigor and reproducibility of findings, Strong said.

The study is unique in that it is based on a large sample size of animals numbering several thousand, the authors said. "It is among the largest number of mice of any study that has attempted to identify genes that influence life span," Nelson said.

Barshop Institute excellence

The Interventions Testing Program is one of several NIA-funded centers at the Sam and Ann Barshop Institute. Among them, the Nathan Shock Center of Excellence in the Basic Biology of Aging provides core services to enhance research of the fundamental biological questions of aging. The Claude D. Pepper Older Americans Independence Center, named for the late U.S. representative, is a center of excellence aimed at increasing scientific knowledge to develop better ways of maintaining or restoring independence in senior adults. The Barshop Institute is the only institute or university in the nation to have these three centers.

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Hibernation slows biological aging in bats

The most common bat in the United States, the big brown bat, boasts an unusually long lifespan of up to 19 years. A new study led by University of Maryland researchers identifies one of the secrets to this bat's exceptional longevity: hibernation.

"Hibernation has allowed bats, and presumably other animals, to stay in northerly or very southerly regions where there's no food in the winter," said the study's senior author, UMD Biology Professor Gerald Wilkinson. "Hibernators tend to live much longer than migrators. We knew that, but we didn't know if we would detect changes in epigenetic age due to hibernation."

The researchers determined that hibernating over one winter extends a big brown bat's epigenetic clock -- a biological marker of aging -- by three-quarters of a year. The study, published in the journal Proceedings of the Royal Society BonAugust 10, 2022, also included scientists from McMaster University and the University of Waterloo, both in Ontario, Canada.

They analyzed small tissue samples taken from the wings of 20 big brown bats (Eptesicus fuscus) during two periods: in the winter when they hibernated and in the summer when they were active. The bats, kept in a research colony at McMaster University, ranged in age from less than 1 year old to a little over 10 years old.

Once the samples were collected, the researchers measured changes in DNA methylation -- a biological process associated with gene regulation -- between samples taken from the same animal during active and hibernating periods. They discovered that changes in DNA methylation occurred at certain sites in the bat's genome, and these sites appeared to be affecting metabolism during hibernation.

"It's pretty clear that the sites that decrease methylation in the winter are the ones that appear to be having an active effect," Wilkinson said. "Many of the genes that are nearest to them are known to be involved in regulating metabolism, so they presumably keep metabolism down."

Some of these genes are the same ones that Wilkinson and fellow researchers identified as "longevity genes" in a previous study. Wilkinson said that there is significant overlap between the hibernation genes and the longevity genes, further highlighting the link between hibernation and longer lifespans.

The earlier study also established the first epigenetic clock for bats, capable of accurately predicting the age of any bat in the wild. That clock was applied to this latest study, enabling the researchers to demonstrate that hibernation reduces a bat's epigenetic age in comparison to a non-hibernating animal of the same age.

Studies like this help explain why bats have longer lifespans than expected for a small mammal about the size of a mouse. However, they also raise new questions.

"We still don't have a very good understanding of why some bats can live a really long time and other ones don't," Wilkinson said. "We've shown that the ones that live a really long time all share the ability to hibernate, or to go into torpor frequently. That seems to be a corollary, but it's not sufficient because hibernating rodents don't live 20 years."

Read more at Science Daily

High optimism linked with longer life and living past 90 in women across racial, ethnic groups

Higher levels of optimism were associated with longer lifespan and living beyond age 90 in women across racial and ethnic groups in a study led by researchers at Harvard T.H. Chan School of Public Health.

"Although optimism itself may be affected by social structural factors, such as race and ethnicity, our research suggests that the benefits of optimism may hold across diverse groups," said Hayami Koga, a PhD candidate in the Department of Social and Behavioral Sciences at Harvard Chan School and lead author of the study. "A lot of previous work has focused on deficits or risk factors that increase the risks for diseases and premature death. Our findings suggest that there's value to focusing on positive psychological factors, like optimism, as possible new ways of promoting longevity and healthy aging across diverse groups."

The study will be published online on June 8, 2022, in the Journal of the American Geriatrics Society.

In a previous study, the research group determined that optimism was linked to a longer lifespan and exceptional longevity, which was defined as living beyond 85 years of age. Because they had looked at mostly white populations in that previous study, Koga and her colleagues broadened the participant pool in the current study to include women from across racial and ethnic groups. According to Koga, including diverse populations in research is important to public health because these groups have higher mortality rates than white populations, and there is limited research about them to help inform health policy decisions.

For this study, the researchers analyzed data and survey responses from 159,255 participants in the Women's Health Initiative, which included postmenopausal women in the U.S. The women enrolled at ages 50-79 from 1993 to 1998 and were followed for up to 26 years.

Of the participants, the 25% who were the most optimistic were likely to have a 5.4% longer lifespan and a 10% greater likelihood of living beyond 90 years than the 25% who were the least optimistic. The researchers also found no interaction between optimism and any categories of race and ethnicity, and these trends held true after taking into account demographics, chronic conditions, and depression. Lifestyle factors, such as regular exercise and healthy eating, accounted for less than a quarter of the optimism-lifespan association, indicating that other factors may be at play.

Koga said that the study's results could reframe how people view the decisions that affect their health.

"We tend to focus on the negative risk factors that affect our health," said Koga. "It is also important to think about the positive resources such as optimism that may be beneficial to our health, especially if we see that these benefits are seen across racial and ethnic groups."

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Key protein identified for brain stem cell longevity

A receptor that was first identified as necessary for insulin action, that also is located on the neural stem cells found deep in the brains of mice, is pivotal for brain stem cell longevity, according to a Rutgers study, a finding that has important implications for brain health and future therapies for brain disorders.

The study, appearing in the journal Stem Cell Reports, pinpoints a specific protein known as the insulin receptor (INSR), which is abundant on the neural stem cells that reside in the brain's subventricular zone. During development, neural stem cells give rise to the entire nervous system, and they persist into adulthood. Over the lifespan these neural stem cells produce new neurons and non-neuronal cells that maintain the infrastructure and functioning of the brain.

Separately, the scientists made another finding when examining brain tumors: INSR plays a crucial role in sustaining and maintaining a population of specialized brain cancer cells known as glioblastoma (GBM) stem cells. When they inactivated the INSR in the GBM stem cells they inhibited the growth of those primitive tumor forming cells.

"It's important to understand the molecular mechanisms that are critical for the growth and sustenance of the brain's stem cells under normal and abnormal growth states," said study author Steven Levison, a professor of neuroscience in the Department of Pharmacology, Physiology and Neuroscience and director of the Laboratory for Regenerative Neurobiology at Rutgers New Jersey Medical School. "Comprehending the signals that regulate these primitive cells could one day lead to new therapeutics for brain disorders."

Many neurodegenerative disorders, such as multiple sclerosis, Parkinson disease and Alzheimer's disease, are connected with the destruction of brain cells, said co-author Teresa Wood, a Distinguished Professor and Rena Warshow Endowed Chair in Multiple Sclerosis in the Department of Pharmacology, Physiology and Neuroscience at Rutgers New Jersey Medical School.

"If we could influence how brain stem cells function then we can use this knowledge to replace diseased or dead brain cells with living ones, which would advance the treatment of neurological diseases and brain injuries," said Wood, who also teaches and conducts research at the Cancer Institute of New Jersey.

Cell receptors such as INSR are protein molecules that reside on the surfaces of cells. Substances, either natural or human-made, that open the "lock" of a receptor can spur a cell to divide, differentiate or die. By identifying which receptors perform these functions on specific cell types, and by understanding their structures and functions, scientists can design substances that act as keys to receptors, to turn them "on" or "off."

Previous studies by this research team had shown that a certain "key," the signaling protein known as the insulin-like growth factor-II (IGF-II), was necessary to maintain the neural stem cells in the two places of the adult brain that harbor these primitive cells. In the current experiment, scientists were looking to identify the receptor. To do so, they used genetic tools that allowed them to both delete the INSR and introduce a fluorescent protein so they could track the neural stem cells and the cells they generate. They found that the numbers of neural stem cells in the subventricular zone in the brains of mice lacking the INSR collapsed.

Adult neurogenesis -- the idea that new cells are produced in the adult brain -- has been a burgeoning field of scientific inquiry since the late 1990s, when researchers confirmed what had only been a theory in lab studies of human, primate and bird brains. Neural stem cells in the adult are stem cells that can self-renew and produce new neurons and the supporting cells of the brain, oligodendrocytes and astrocytes.

"Given the widespread interest in stem cells as well as interest in whether alterations to adult stem cells might contribute to cancer, our research findings should be of interest," Levison said.

Read more at Science Daily

Bioengineers visualize fat storage in fruit flies

For the first time, researchers have visually monitored, in high resolution, the timing and location of fat storage within the intact cells of fruit flies. The new optical imaging tool from the lab of bioengineering professor Lingyan Shi at the University of California San Diego is already being used to untangle often discussed, yet mysterious, links between diet and things like obesity, diabetes and aging.The work from bioengineers at the UC San Diego Jacobs School of Engineering is published in the journal Aging Cell.

The optical microscopy platform developed by the UC San Diego bioengineers is unique. It allows the researchers to visually track, in high resolution within fat cells, how specific dietary changes affect the way flies turn the energy from their food into fat. The tool also allows the researchers to monitor the reverse process of changing fat back into energy. In addition, the researchers can now visually monitor changes in size in individual fat-storage "containers" within the class of fruit fly cells that is analogous to mammalian fat (adipose) cells.

In the new paper in Aging Cell, the researchers demonstrated the ability to visually track changes in fat (lipid) metabolism in flies after they were put on a wide range of different diets. The diets included calorie-restricted diets, high protein diets, and diets with twice, four-times, and ten-times the sugar of a standard diet.

"With our new optical microscopy system, we can see both where and when fats are being put into storage and taken out of storage," said Shi, the bioengineering professor at UC San Diego who is the corresponding senior author on the new paper. "This is the first imaging technology that can visualize fat metabolism at high resolution in both space and time within individual fat cells. We have demonstrated that we can see both where and when lipid metabolism changes within individual fruit fly fat body cells in response to dietary changes."

"Interest in optimizing the human diet is intense," Shi continued. "People want answers to questions like, 'What are the best diets to slow aging? What are the best diets for losing weight? What are the best diets for extending health span?' I don't yet have answers to these questions, but in my lab, we develop new technologies that are getting us closer to answering some of the big dietary questions out there."

In the new work in Aging Cell, for example, the researchers report a new way to answer questions like:

How much does a specific diet, such as a high-protein diet, or a high-sugar diet, or a calorie-restricted diet, alter a fruit fly's process of turning energy from food into fat? And how much do these same diets affect a fruit fly's process of turning fat back into energy?

"We developed this tool to help us untangle the relationships between diet and phenomena like obesity, diabetes, aging, and longevity," said Shi.

Tracking the size of fat droplets within intact fruit fly cells is one example of what's possible with the new visualization platform.

"Droplet size is a way to track how much of the stored fat is 'turning over' or getting converted back into energy. This is an important aspect of lipid metabolism, and we now have a tool that allows us to track changes in the size of specific lipid droplets within individual cells of fruit flies," said Yajuan Li, MD. PhD, who is a postdoctoral researcher in the Shi lab at UC San Diego and the first author on the paper in Aging Cell.

Heavy water

The new visualization platform builds on some of Shi's earlier work using a variation on regular water, called heavy water or (D2O). Heavy water is, literally, heavier than regular water. Heavy water molecules contain one oxygen atom like regular water. But in place of the pair of hydrogen atoms -- the "H2" in "H20" -- heavy water contains a pair of heavier deuterium atoms.

Like "regular" water, heavy water is freely incorporated into cells in living organisms. So when the researchers provide heavy water to a fruit fly, and then that fruit fly begins to convert energy from its food into fat molecules to be stored, some of those fat molecules contain deuterium. In this way, the prevalence of deuterium atoms in lipids stored within the fat cells of fruit flies provides a way to measure how much fat that fly has stored.

By changing a fly's diet at the same time that you introduce heavy water, you have a way to monitor how the diet changes lipid turnover. More details on how the system works are in this 2021 profile, in which Shi said, "When we are developing a new technology, a new tool, it will definitely inspire us to ask new biological questions."

Read more at Science Daily

Unravelling the mystery of parrot longevity

Parrots are famous for their remarkable cognitive abilities and exceptionally long lifespans. Now, a study led by Max Planck researchers has shown that one of these traits has likely been caused by the other. By examining 217 parrot species, the researchers revealed that species such as the scarlet macaw and sulphur-crested cockatoo have extremely long average lifespans, of up to 30 years, which are usually seen only in large birds. Further, they demonstrated a possible cause for these long lifespans: large relative brain size. The study is the first to show a link between brain size and lifespan in parrots, suggesting that increased cognitive ability may have helped parrots to navigate threats in their environment and to enjoy longer lives.

Despite the fact that parrots are well known for their long lives and complex cognition, with lifespans and relative brain size on par with primates, it remains unknown whether the two traits have influenced each other.

"The problem has been sourcing good quality data," says Simeon Smeele, a doctoral student at the Max Planck Institute of Animal Behavior (MPI-AB) and lead author on the study, published in Proceedings of the Royal Society B. Understanding what has driven parrot longevity is only possible by comparing living parrots. "Comparative life-history studies require large sample sizes to provide certainty, because many processes are a play at once and this creates a lot of variation," says Smeele.

To generate an adequate sample size, scientists from the MPI-AB and the Max Planck Institute for Evolutionary Anthropology (MPI-EvA) teamed up with Species360, which draws on animal records from zoos and aquaria. Together, they compiled data from over 130,000 individual parrots sourced from over 1000 zoos. This database allowed the team to gain the first reliable estimates of average life span of 217 parrot species -- representing over half of all known species.

The analysis revealed an astonishing diversity in life expectancy, ranging from an average of two years for the fig parrot up to an average of 30 years for the scarlet macaw. Other long-lived species include the sulphur crested cockatoo from Australia, which lives on average 25 years.

"Living an average of 30 years is extremely rare in birds of this size," says Smeele who worked closely with Lucy Aplin from MPI-AB and Mary Brooke McElreath from MPI-EvA on the study. "Some individuals have a maximum lifespan of over 80 years, which is a respectable age even for humans. These values are really spectacular if you consider that a human male weights about 100 times more."

Next, the team employed a large-scale comparative analysis to determine whether or not parrots' renowned cognitive abilities had any influence on their longevity. They examined two hypotheses: First, that having relatively larger brains enable longer lifespans. In other words, smarter birds can better solve problems in the wild, thus enjoying longer lives. Second, that relatively larger brains take longer to grow, and therefore require longer lifespans. For each species, they collected data on relative brain size, as well as average body weight and developmental variables.

They then combined the data and ran models for each hypothesis, looking at which model best explained the data. Their results provide the first support that increased brain size has enabled longer lifespans in parrots. Because brain size relative to body size can be an indicator for intelligence, the findings suggest that the parrots with relatively large brains had cognitive capabilities that allowed them to solve problems in the wild that could otherwise kill them, and this intelligence enabled them to live longer lives.

"This supports the idea that in general larger brains make species more flexible and allow them to live longer," says Smeele. "For example, if they run out of their favourite food, they could learn to find something new and thus survive."

The scientists are surprised that factors such as diet, or the greater developmental time required to develop larger brains, did not lead to longer average lifespans. "We would have expected the developmental path to play a more important role because in primates it is this developmental cost that explains the link between brain size and longevity," says Smeele.

In the future, the team plan to explore if sociality and cultural learning in parrots might have also contributed to long lifespans. Says Smeele: "Large-brained birds might spend more time socially learning foraging techniques that have been around for multiple generations. This increased learning period could potentially also explain the longer life spans, as it takes more time but also makes the foraging repertoire more adaptive."

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How long can a person live? The 21st century may see a record-breaker

The number of people who live past the age of 100 has been on the rise for decades, up to nearly half a million people worldwide.

There are, however, far fewer "supercentenarians," people who live to age 110 or even longer. The oldest living person, Jeanne Calment of France, was 122 when she died in 1997; currently, the world's oldest person is 118-year-old Kane Tanaka of Japan.

Such extreme longevity, according to new research by the University of Washington, likely will continue to rise slowly by the end of this century, and estimates show that a lifespan of 125 years, or even 130 years, is possible.

"People are fascinated by the extremes of humanity, whether it's going to the moon, how fast someone can run in the Olympics, or even how long someone can live," said lead author Michael Pearce, a UW doctoral student in statistics. "With this work, we quantify how likely we believe it is that some individual will reach various extreme ages this century."

Longevity has ramifications for government and economic policies, as well as individuals' own health care and lifestyle decisions, rendering what's probable, or even possible, relevant at all levels of society.

The new study, published June 30 in Demographic Research, uses statistical modeling to examine the extremes of human life. With ongoing research into aging, the prospects of future medical and scientific discoveries and the relatively small number of people to have verifiably reached age 110 or older, experts have debated the possible limits to what is referred to as the maximum reported age at death. While some scientists argue that disease and basic cell deterioration lead to a natural limit on human lifespan, others maintain there is no cap, as evidenced by record-breaking supercentenarians.

Pearce and Adrian Raftery, a professor of sociology and of statistics at the UW, took a different approach. They asked what the longest individual human lifespan could be anywhere in the world by the year 2100. Using Bayesian statistics, a common tool in modern statistics, the researchers estimated that the world record of 122 years almost certainly will be broken, with a strong likelihood of at least one person living to anywhere between 125 and 132 years.

To calculate the probability of living past 110 -- and to what age -- Raftery and Pearce turned to the most recent iteration of the International Database on Longevity, created by the Max Planck Institute for Demographic Research. That database tracks supercentenarians from 10 European countries, plus Canada, Japan and the United States.

Using a Bayesian approach to estimate probability, the UW team created projections for the maximum reported age at death in all 13 countries from 2020 through 2100.

Among their findings:
 

• Researchers estimated near 100% probability that the current record of maximum reported age at death -- Calment's 122 years, 164 days -- will be broken;
• The probability remains strong of a person living longer, to 124 years old (99% probability) and even to 127 years old (68% probability);
• An even longer lifespan is possible but much less likely, with a 13% probability of someone living to age 130;
• It is "extremely unlikely" that someone would live to 135 in this century.

As it is, supercentenarians are outliers, and the likelihood of breaking the current age record increases only if the number of supercentenarians grows significantly. With a continually expanding global population, that's not impossible, researchers say.

People who achieve extreme longevity are still rare enough that they represent a select population, Raftery said. Even with population growth and advances in health care, there is a flattening of the mortality rate after a certain age. In other words, someone who lives to be 110 has about the same probability of living another year as, say, someone who lives to 114, which is about one-half.

"It doesn't matter how old they are, once they reach 110, they still die at the same rate," Raftery said. "They've gotten past all the various things life throws at you, such as disease. They die for reasons that are somewhat independent of what affects younger people.

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Daily exposure to blue light may accelerate aging, even if it doesn't reach your eyes

Woman looking at blue light from at computer screen.

Prolonged exposure to blue light, such as that which emanates from your phone, computer and household fixtures, could be affecting your longevity, even if it's not shining in your eyes.

New research at Oregon State University suggests that the blue wavelengths produced by light-emitting diodes damage cells in the brain as well as retinas.

The study, published today in Aging and Mechanisms of Disease, involved a widely used organism, Drosophila melanogaster, the common fruit fly, an important model organism because of the cellular and developmental mechanisms it shares with other animals and humans.

Jaga Giebultowicz, a researcher in the OSU College of Science who studies biological clocks, led a research collaboration that examined how flies responded to daily 12-hour exposures to blue LED light -- similar to the prevalent blue wavelength in devices like phones and tablets -- and found that the light accelerated aging.

Flies subjected to daily cycles of 12 hours in light and 12 hours in darkness had shorter lives compared to flies kept in total darkness or those kept in light with the blue wavelengths filtered out. The flies exposed to blue light showed damage to their retinal cells and brain neurons and had impaired locomotion -- the flies' ability to climb the walls of their enclosures, a common behavior, was diminished.

Some of the flies in the experiment were mutants that do not develop eyes, and even those eyeless flies displayed brain damage and locomotion impairments, suggesting flies didn't have to see the light to be harmed by it.

"The fact that the light was accelerating aging in the flies was very surprising to us at first," said Giebultowicz, a professor of integrative biology. "We'd measured expression of some genes in old flies, and found that stress-response, protective genes were expressed if flies were kept in light. We hypothesized that light was regulating those genes. Then we started asking, what is it in the light that is harmful to them, and we looked at the spectrum of light. It was very clear cut that although light without blue slightly shortened their lifespan, just blue light alone shortened their lifespan very dramatically."

Natural light, Giebultowicz notes, is crucial for the body's circadian rhythm -- the 24-hour cycle of physiological processes such as brain wave activity, hormone production and cell regeneration that are important factors in feeding and sleeping patterns.

"But there is evidence suggesting that increased exposure to artificial light is a risk factor for sleep and circadian disorders," she said. "And with the prevalent use of LED lighting and device displays, humans are subjected to increasing amounts of light in the blue spectrum since commonly used LEDs emit a high fraction of blue light. But this technology, LED lighting, even in most developed countries, has not been used long enough to know its effects across the human lifespan."

Giebultowicz says that the flies, if given a choice, avoid blue light.

"We're going to test if the same signaling that causes them to escape blue light is involved in longevity," she said.

Eileen Chow, faculty research assistant in Giebultowicz's lab and co-first author of the study, notes that advances in technology and medicine could work together to address the damaging effects of light if this research eventually proves applicable to humans.

"Human lifespan has increased dramatically over the past century as we've found ways to treat diseases, and at the same time we have been spending more and more time with artificial light," she said. "As science looks for ways to help people be healthier as they live longer, designing a healthier spectrum of light might be a possibility, not just in terms of sleeping better but in terms of overall health."

In the meantime, there are a few things people can do to help themselves that don't involve sitting for hours in darkness, the researchers say. Eyeglasses with amber lenses will filter out the blue light and protect your retinas. And phones, laptops and other devices can be set to block blue emissions.

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