Pacific cities much older than previously thought

New evidence of one of the first cities in the Pacific shows they were established much earlier than previously thought, according to new research from The Australian National University (ANU).

The study used aerial laser scanning to map archaeological sites on the island of Tongatapu in Tonga.

Lead author, PhD scholar Phillip Parton, said the new timeline also indicates that urbanisation in the Pacific was an indigenous innovation that developed before Western influence.

"Earth structures were being constructed in Tongatapu around AD 300. This is 700 years earlier than previously thought," Mr Parton said.

"As settlements grew, they had to come up with new ways of supporting that growing population. This kind of set-up -- what we call low density urbanisation -- sets in motion huge social and economic change. People are interacting more and doing different kinds of work."

Mr Parton said traditionally, studying urbanisation in the Pacific has been tricky due to challenges collecting data, but new technology has changed that.

"We were able to combine high-tech mapping and archaeological fieldwork to understand what was happening in Tongatapu," he said.

"Having this type of information really adds to our understanding of early Pacific societies.

"Urbanisation is not an area that had been investigated much until now. When people think of early cities they usually think of traditional old European cities with compact housing and windy cobblestone streets. This is a very different kind of city.

"But it shows the contribution of the Pacific to urban science. We can see clues that Tongatapu's influence spread across the southwest Pacific Ocean between the 13th and 19th centuries."

According to Mr Parton, the collapse of this kind of low-density urbanisation in Tonga was largely due to the arrival of Europeans.

"It didn't collapse because the system was flawed; it was more to do with the arrival of Europeans and introduced diseases," he said.

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The Moon is 40 million years older than previously thought

Led by researchers at the Field Museum and the University of Glasgow, the study was made possible by Northwestern University's atom-probe tomography facility, which "nailed down" the age of the oldest crystal in the sample. By revealing the age of these telltale zircon crystals -- found hidden within dust collected from the Moon -- researchers were able to piece together the timeline of the Moon's formation.

The study was published today (Oct. 23) in the journal Geochemical Perspectives Letters.

"This study is a testament to immense technological progress we have made since 1972 when the last manned Moon mission returned to Earth," said Northwestern's Dieter Isheim, who co-authored the study. "These samples were brought to Earth half-a-century ago, but only today do we have the necessary tools to perform microanalysis at the requisite level, including atom-probe tomography."

The atom-by-atom analysis enabled researchers to count how many atoms in the zircon crystals have undergone radioactive decay. When an atom undergoes decay, it sheds protons and neutrons to transform into different elements. Uranium, for example, decays into lead. Because scientists have established how long it takes for this process to unfold, they can assess the age of a sample by looking at the proportion of uranium and lead atoms.

"Radiometric dating works a little bit like an hourglass," said the Field Museum's Philipp Heck, the study's senior author. "In an hourglass, sand flows from one glass bulb to another, with the passage of time indicated by the accumulation of sand in the lower bulb. Radiometric dating works similarly by counting the number of parent atoms and the number of daughter atoms they have transformed to. The passage of time can then be calculated because the transformation rate is known."

Isheim is a research associate professor of materials science and engineering at Northwestern's McCormick School of Engineering and manager of Northwestern's Center for Atom-Probe Tomography (NUCAPT). David Seidman, the Walter P. Murphy Professor Emeritus of Materials Science and Engineering at McCormick and founding director of NUCAPT, also co-authored the study. Heck is the Field Museum's Robert A. Pritzker Curator for Meteorites and Polar Studies, senior director of the Negaunee Interactive Research Center and professor at the University of Chicago. Jennika Greer, a research associate professor at the University of Glasgow, is the study's lead author. When the research began, she was a Ph.D. candidate in Heck's laboratory.

More than 4 billion years ago, when the solar system was still young and the Earth was still growing, a giant Mars-sized object crashed into the Earth. A colossal hunk broke off Earth to form the Moon, and the energy of the impact melted the rock that eventually became the Moon's surface.

"When the surface was molten like that, zircon crystals couldn't form and survive," Heck said. "So, any crystals on the Moon's surface must have formed after this lunar magma ocean cooled. Otherwise, they would have been melted and their chemical signatures would be erased."

Because the crystals must have formed after the magma ocean cooled, determining the age of the zircon crystals would reveal the minimum possible age of the Moon. But, to pinpoint the maximum possible age of the Moon, researchers turned to Northwestern's atom-probe tomography instruments.

"In atom-probe tomography, we start by sharpening a piece of the lunar sample into a very sharp tip, using a focused ion beam microscope, almost like a very fancy pencil sharpener," Greer said. "Then, we use UV lasers to evaporate atoms from the surface of that tip. The atoms travel through a mass spectrometer, and how fast they move tells us how heavy they are, which in turn tells us what they're made of."

After determining the materials in the sample and performing radiometric dating, the researchers concluded that the oldest crystals are about 4.46 billion years old. That means the Moon must be at least that old.

It's important to know when the Moon formed, Heck said, because "the Moon is an important partner in our planetary system. It stabilizes the Earth's rotational axis. It's the reason there are 24 hours in a day. It's the reason we have tides. Without the Moon, life on Earth would look different. It's a part of our natural system that we want to better understand, and our study provides a tiny puzzle piece in that whole picture."

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Evidence from the remains of 1918 flu pandemic victims contradicts long-held belief that healthy young adults were particularly vulnerable

New analysis of the remains of victims of the 1918 influenza pandemic, which killed an estimated 50 million people worldwide, contradicts the widespread belief the flu disproportionately impacted healthy young adults.

Because so many people fell ill so quickly, physicians at the time believed the healthy were as likely to die from the flu as those who had already been sick or frail. Despite numerous historical accounts, though, it turns out there is no concrete scientific evidence to support that belief.

Researchers at McMaster University and the University of Colorado Boulder who analyzed victims' age of death and studied lesions on victims' bones report that the most susceptible to dying of the flu had exhibited signs of previous environmental, social and nutritional stress.

"Our circumstances -- social, cultural and immunological -- are all intertwined and have always shaped the life and death of people, even in the distant past," explains Amanda Wissler, an assistant professor in the Department of Anthropology at McMaster and lead author on the study, published today in the journal PNAS.

"We saw this during COVID-19, where our social backgrounds and our cultural backgrounds influenced who was more likely to die, and who was likely to survive," she says.

Much of the research on the 1918 pandemic relies on historical documentation such as vital statistics, census data and life insurance records, none of which include information on pre-existing conditions, or general environmental, dietary or other chronic stressors which can impact one's overall health over the course of a lifetime.

For the study, researchers examined the skeletal remains of 369 individuals from the Hamman-Todd Documented skeletal collection, which is housed at the Cleveland Museum of Natural History. All had died between 1910 and 1938. The sample was divided into two groups: a control group who had died before the pandemic, and those who died during the pandemic.

A living person's skeletal structure may undergo lasting changes due to poor health, resulting in diminished height, irregular growth, developmental tooth defects and other indicators.

The team searched for lesions, or indicators of stress, on the shinbones of the pandemic victims. New bone formation occurs in response to inflammation caused by physical trauma or infection, for example. Researchers can determine if a lesion had been active, in the midst of healing or had completely healed, all of which provide evidence of underlying conditions.

"By comparing who had lesions, and whether these lesions were active or healing at the time of death, we get a picture of what we call frailty, or who is more likely to die. Our study shows that people with these active lesions are the most frail," says Sharon DeWitte, a biological anthropologist at the University Colorado Boulder and co-author on the study.

Preexisting medical conditions such as asthma or congestive heart failure are common risk factors which can contribute to poor outcomes from infectious diseases such as influenza.

Racism and institutional discrimination can amplify these effects, as evidenced in the COVID-19 pandemic, say researchers. During the Black Death in London, for example, individuals who had previously suffered environmental, nutritional and disease stressors were more likely to die from the plague than their healthier peers.

"The results of our work counter the narrative and the anecdotal accounts of the time," says Wissler. "This paints a very complicated picture of life and death during the 1918 pandemic."

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Reinventing cosmology: New research puts age of universe at 26.7 -- not 13.7 -- billion years

Our universe could be twice as old as current estimates, according to a new study that challenges the dominant cosmological model and sheds new light on the so-called "impossible early galaxy problem."

"Our newly-devised model stretches the galaxy formation time by a several billion years, making the universe 26.7 billion years old, and not 13.7 as previously estimated," says author Rajendra Gupta, adjunct professor of physics in the Faculty of Science at the University of Ottawa.

For years, astronomers and physicists have calculated the age of our universe by measuring the time elapsed since the Big Bang and by studying the oldest stars based on the redshift of light coming from distant galaxies. In 2021, thanks to new techniques and advances in technology, the age of our universe was thus estimated at 13.797 billion years using the Lambda-CDM concordance model.

However, many scientists have been puzzled by the existence of stars like the Methuselah that appear to be older than the estimated age of our universe and by the discovery of early galaxies in an advanced state of evolution made possible by the James Webb Space Telescope. These galaxies, existing a mere 300 million years or so after the Big Bang, appear to have a level of maturity and mass typically associated with billions of years of cosmic evolution. Furthermore, they're surprisingly small in size, adding another layer of mystery to the equation.

Zwicky's tired light theory proposes that the redshift of light from distant galaxies is due to the gradual loss of energy by photons over vast cosmic distances. However, it was seen to conflict with observations. Yet Gupta found that "by allowing this theory to coexist with the expanding universe, it becomes possible to reinterpret the redshift as a hybrid phenomenon, rather than purely due to expansion."

In addition to Zwicky's tired light theory, Gupta introduces the idea of evolving "coupling constants," as hypothesized by Paul Dirac. Coupling constants are fundamental physical constants that govern the interactions between particles. According to Dirac, these constants might have varied over time. By allowing them to evolve, the timeframe for the formation of early galaxies observed by the Webb telescope at high redshifts can be extended from a few hundred million years to several billion years. This provides a more feasible explanation for the advanced level of development and mass observed in these ancient galaxies.

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Multivitamin improves memory in older adults, study finds

Taking a daily multivitamin supplement can slow age-related memory decline, finds a large study led by researchers at Columbia University and Brigham and Women's Hospital/Harvard.

"Cognitive aging is a top health concern for older adults, and this study suggests that there may be a simple, inexpensive way to help older adults slow down memory decline," says study leader Adam M. Brickman, PhD, professor of neuropsychology at Columbia University Vagelos College of Physicians and Surgeons.

Many older people take vitamins or dietary supplements under the assumption that they will help maintain general health. But studies that have tested whether they improve memory and brain function have been mixed, and very few large-scale, randomized trials have been done.

Study methods

In the current study, more than 3,500 adults (mostly non-Hispanic white) over age 60 were randomly assigned to take a daily multivitamin supplement or placebo for three years. At the end of each year, participants performed a series of online cognitive assessments at home designed to test memory function of the hippocampus, an area of the brain that is affected by normal aging. The COSMOS-Web study is part of a large clinical trial led by Brigham & Women's Hospital and Harvard called the COcoa Supplement and Multivitamin Outcomes Study (COSMOS).

By the end of the first year, memory improved for people taking a daily multivitamin, compared with those taking a placebo. The researchers estimate the improvement, which was sustained over the three-year study period, was equivalent to about three years of age-related memory decline. The effect was more pronounced in participants with underlying cardiovascular disease.

The results of the new study are consistent with another recent COSMOS study of more than 2,200 older adults that found that taking a daily multivitamin improved overall cognition, memory recall, and attention, effects that were also more pronounced in those with underlying cardiovascular disease.

"There is evidence that people with cardiovascular disease may have lower micronutrient levels that multivitamins may correct, but we don't really know right now why the effect is stronger in this group," says Brickman.

Good nutrition important for aging brain

Though the researchers did not look at whether any specific component of the multivitamin supplement was linked to the improvement in memory, the findings support growing evidence that nutrition is important for optimizing brain health as we age.

"Our study shows that the aging brain may be more sensitive to nutrition than we realized, though it may not be so important to find out which specific nutrient helps slow age-related cognitive decline," says Lok-Kin Yeung, PhD, a postdoctoral researcher in Columbia's Taub Institute for Research on Alzheimer's Disease and the Aging Brain and first author of the study.

"The finding that a daily multivitamin improved memory in two separate cognition studies in the COSMOS randomized trial is remarkable, suggesting that multivitamin supplementation holds promise as a safe, accessible, and affordable approach to protecting cognitive health in older adults," says co-author JoAnn Manson, MD, chief of the Division of Preventive Medicine at Brigham and Women's Hospital.

"Supplementation of any kind shouldn't take the place of more holistic ways of getting the same micronutrients," adds Brickman. "Though multivitamins are generally safe, people should always consult a physician before taking them."

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Agriculture linked to changes in age-independent mortality in North America

The transition to agriculture from hunting and gathering in pre-colonial North America led to changes in age-independent mortality, or mortality caused by factors that are not associated with age, according to a new study by a Penn State-led research team. The team found that the intensification of crop use occurred in two phases, the first of which led to a decline in human age-independent mortality, while the second is associated with a rise in it. The study is the first to tie patterns of age-independent mortality to food production.

"This study tells the story of our shared human experience," said George Milner, distinguished professor of anthropology at Penn State and lead author. "We have several examples around the world where we see a move toward crop domestication as an independent event -- eastern North America, particularly the midcontinent, being one of them, but so too the Fertile Crescent in the Middle East. Also, there are demographic changes happening. This paper addresses the relationship between the move toward agriculture and demographic change."

The researchers examined previously published data to identify general trends in archaeobotanical samples, or the remains of plants in the archaeological record, and skeletal samples from sites across eight states stretching from Illinois to northern Alabama. They wanted to study the relationship between the domestication of crops and an index that uses skeletal data to capture the frequency of juveniles aged five to 19 years old relative to all individuals aged five or more. Anthropologists normally use the index to measure fertility rates and population growth, but the new work shows it is more responsive to age-independent mortality.

Mortality models, including those for pre-industrial societies, contain three components: juvenile mortality, which declines as children get older; adult mortality, where the probability of dying increases with advancing age; and age-independent mortality, an equal probability of dying for members of all age groups, which might occur in extreme events like food shortages, epidemics or warfare.

The researchers studied the archaeobotanical data to identify where the record showed an increase in the consumption of domesticated crops compared to foraged foods like nuts. They also examined skeletal data to identify decreases or increases in the indicator of age-independent mortality. The index focuses on individuals between five and 19 years old because in human populations that age range is characterized by low mortality relative to other age groups. Increases in mortality for this age group would indicate the occurrence of events like famines or conflict.

The researchers identified a strong correlation between crop domestication and changing age-independent mortality rates. Crop domestication happened in two stages in pre-colonial North America, with a decrease in age-independent mortality noted during the first stage of crop domestication and a rise during the second stage. The researchers reported their findings in the Proceedings of the National Academy of Sciences.

"What we've found is the index that has traditionally been interpreted as a fertility and population growth indicator is more tightly correlated to age-independent mortality, which reflects the number of deaths in the part of the age distribution where very few people die," said Milner. "This means that the pattern of first adoption of agriculture, seen elsewhere in the world and observed in eastern North America as well, coincides with lower age-independent mortality. Basically, it's good times, and that's what we see culturally."

The first stage of agricultural intensification in North America, which includes the cultivation of plants such as squash, sunflower and other native plants, occurred approximately 2,000 years ago during the Middle Woodland period up to about A.D. 500, said Milner. Indigenous societies flourished during this time. They established long-distance exchange networks, had an incredibly rich ceremonial life, and constructed big mounds and earthwork complexes.

The archaeological record shows that in the centuries just before A.D. 1000, and from that time onward, there was an increase in warfare. During this time Indigenous societies began cultivating maize and beans, and a number of new cultural changes occurred, including the initial development of powerful chiefdom societies. Age-independent mortality increased during this period, presumably due to conflict and the spread of diseases from higher numbers of individuals living near one another.

"The overall pattern seen in the demographic picture of North American pre-European contact is similar to other datasets from around the world," Milner said. "The entire story makes perfect sense in terms of agricultural productivity, demographic change and cultural developments, including change over time in conflict and sociopolitical systems."

The study links, for the first time, a worldwide pattern to age-independent mortality and agricultural developments, according to Milner.

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Study reveals average age at conception for men versus women over past 250,000 years

The length of a specific generation can tell us a lot about the biology and social organization of humans. Now, researchers at Indiana University can determine the average age that women and men had children throughout human evolutionary history with a new method they developed using DNA mutations.

The researchers said this work can help us understand the environmental challenges experienced by our ancestors and may also help us in predicting the effects of future environmental change on human societies.

"Through our research on modern humans, we noticed that we could predict the age at which people had children from the types of DNA mutations they left to their children," said study co-author Matthew Hahn, Distinguished Professor of biology in the College of Arts and Sciences and of computer science in the Luddy School of Informatics, Computing and Engineering at IU Bloomington. "We then applied this model to our human ancestors to determine what age our ancestors procreated."

According to the study, published today in Science Advances and co-authored by IU post-doctoral researcher Richard Wang, the average age that humans had children throughout the past 250,000 years is 26.9. Furthermore, fathers were consistently older, at 30.7 years on average, than mothers, at 23.2 years on average, but the age gap has shrunk in the past 5,000 years, with the study's most recent estimates of maternal age averaging 26.4 years. The shrinking gap seems to largely be due to mothers having children at older ages.

Other than the recent uptick in maternal age at childbirth, the researchers found that parental age has not increased steadily from the past and may have dipped around 10,000 years ago because of population growth coinciding with the rise of civilization.

"These mutations from the past accumulate with every generation and exist in humans today," Wang said. "We can now identify these mutations, see how they differ between male and female parents, and how they change as a function of parental age."

Children's DNA inherited from their parents contains roughly 25 to 75 new mutations, which allows scientists to compare the parents and offspring, and then to classify the kind of mutation that occurred. When looking at mutations in thousands of children, IU researchers noticed a pattern: The kinds of mutations that children get depend on the ages of the mother and the father.

Previous genetic approaches to determining historical generation times relied on the compounding effects of either recombination or mutation of modern human DNA sequence divergence from ancient samples. But the results were averaged across both males and females and across the past 40,000 to 45,000 years.

Hahn, Wang and their co-authors built a model that uses de novo mutations -- a genetic alteration that is present for the first time in one family member as a result of a variant or mutation in a germ cell of one of the parents or that arises in the fertilized egg during early embryogenesis -- to separately estimate the male and female generation times at many different points throughout the past 250,000 years.

The researchers were not originally seeking to understand the relationship of gender and age at conception over time; they were conducting a broader investigation about the number of mutations passed from parents to children. They only noticed the age-based mutation patterns while seeking to understand differences and similarities between these pattens in humans versus other mammals, such as cats, bears and macaques.

"The story of human history is pieced together from a diverse set of sources: written records, archaeological findings, fossils, etc.," Wang said. "Our genomes, the DNA found in every one of our cells, offer a kind of manuscript of human evolutionary history. The findings from our genetic analysis confirm some things we knew from other sources (such as the recent rise in parental age), but also offer a richer understanding of the demography of ancient humans. These findings contribute to a better understanding of our shared history."

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Age vs. genetics: Which is more important for determining how we age?

Amid much speculation and research about how our genetics affect the way we age, a University of California, Berkeley, study now shows that individual differences in our DNA matter less as we get older and become prone to diseases of aging, such as diabetes and cancer.

In a study of the relative effects of genetics, aging and the environment on how some 20,000 human genes are expressed, the researchers found that aging and environment are far more important than genetic variation in affecting the expression profiles of many of our genes as we get older. The level at which genes are expressed -- that is, ratcheted up or down in activity -- determines everything from our hormone levels and metabolism to the mobilization of enzymes that repair the body.

"How do your genetics -- what you got from your sperm donor and your egg donor and your evolutionary history -- influence who you are, your phenotype, such as your height, your weight, whether or not you have heart disease?" said Peter Sudmant, UC Berkeley assistant professor of integrative biology and a member of the campus's Center for Computational Biology. "There's been a huge amount of work done in human genetics to understand how genes are turned on and off by human genetic variation. Our project came about by asking, 'How is that influenced by an individual's age?' And the first result we found was that your genetics actually matter less the older you get."

In other words, while our individual genetic makeup can help predict gene expression when we are younger, it is less useful in predicting which genes are ramped up or down when we're older -- in this study, older than 55 years. Identical twins, for example, have the same set of genes, but as they age, their gene expression profiles diverge, meaning that twins can age much differently from each other.

The findings have implications for efforts to correlate diseases of aging with genetic variation in humans, Sudmant said. Such studies should perhaps focus less on genetic variants that impact gene expression when pursuing drug targets.

"Almost all human common diseases are diseases of aging: Alzheimer's, cancers, heart disease, diabetes. All of these diseases increase their prevalence with age," he said. "Massive amounts of public resources have gone into identifying genetic variants that predispose you to these diseases. What our study is showing is that, well, actually, as you get older, genes kind of matter less for your gene expression. And so, perhaps, we need to be mindful of that when we're trying to identify the causes of these diseases of aging."

Sudmant and his colleagues reported their results this week in the journal Nature Communications.

Medawar's hypothesis

The findings are in line with Medawar's hypothesis: Genes that are turned on when we are young are more constrained by evolution because they are critical to making sure we survive to reproduce, while genes expressed after we reach reproductive age are under less evolutionary pressure. So, one would expect a lot more variation in how genes are expressed later in life.

"We're all aging in different ways," Sudmant said. "While young individuals are closer together in terms of gene expression patterns, older individuals are further apart. It's like a drift through time as gene expression patterns become more and more erratic."

This study is the first to look at both aging and gene expression across such a wide variety of tissues and individuals, Sudmant said. He and his colleagues built a statistical model to assess the relative roles of genetics and aging in 27 different human tissues from nearly 1,000 individuals and found that the impact of aging varies widely -- more than twentyfold -- among tissues.

"Across all the tissues in your body, genetics matters about the same amount. It doesn't seem like it plays more of a role in one tissue or another tissue," he said. "But aging is vastly different between different tissues. In your blood, colon, arteries, esophagus, fat tissue, age plays a much stronger role than your genetics in driving your gene expression patterns."

Sudmant and colleagues also found that Medawar's hypothesis does not hold true for all tissues. Surprisingly, in five types of tissues, evolutionary important genes were expressed at higher levels in older individuals.

"From an evolutionary perspective, it is counterintuitive that these genes should be getting turned on, until you take a close look at these tissues," Sudmant said. These five tissues happen to be the ones that constantly turn over throughout our lifespan and also produce the most cancers. Every time these tissues replace themselves, they risk creating a genetic mutation that can lead to disease.

"I guess this tells us a little bit about the limits of evolution," he said. "Your blood, for instance, always has to proliferate for you to live, and so these super-conserved, very important genes have to be turned on late in life. This is problematic because it means that those genes are going to be susceptible to getting somatic mutations and getting turned on forever in a bad, cancerous way. So, it kind of gives us a little bit of a perspective on what the limitations of living are like. It puts bounds on our ability to keep living."

Sudmant noted that the study indirectly indicates the effect on aging of one's environment, which is the impact of everything other than age and genetics: the air we breathe, the water we drink, the food we eat, but also our levels of physical exercise. Environment amounts to up to a third of gene expression changes with age.

Sudmant is conducting similar analyses of the expressed genes in several other organisms -- bats and mice -- to see how they differ and whether the differences are related to these animals' different lifespans.

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Astronomers map distances to 56,000 galaxies, largest-ever catalog

How old is our universe, and what is its size? A team of researchers led by University of Hawaii at Manoa astronomers Brent Tully and Ehsan Kourkchi from the Institute for Astronomy have assembled the largest-ever compilation of high-precision galaxy distances, called Cosmicflows-4. Using eight different methods, they measured the distances to a whopping 56,000 galaxies. The study has been published in the Astrophysical Journal.

Galaxies, such as the Milky Way, are the building blocks of the universe, each comprised of up to several hundred billion stars. Galaxies beyond our immediate neighborhood are rushing away, faster if they are more distant, which is a consequence of the expansion of the universe that began at the moment of the Big Bang. Measurements of the distances of galaxies, coupled with information about their velocities away from us, determine the scale of the universe and the time that has elapsed since its birth.

"Since galaxies were identified as separate from the Milky Way a hundred years ago, astronomers have been trying to measure their distances," said Tully. "Now by combining our more accurate and abundant tools, we are able to measure distances of galaxies, and the related expansion rate of the universe and the time since the universe was born with a precision of a few percent."

From the newly published measurements, the researchers derived the expansion rate of the universe, called the Hubble Constant, or H0. The team's study gives a value of H0=75 kilometers per second per megaparsec or Mpc (1 megaparsec = 3.26 million light years), with very small statistical uncertainty of about 1.5%.

There are a number of ways to measure galaxy distances. Generally, individual researchers focus on an individual method. The Cosmicflows program spearheaded by Tully and Kourkchiincludes their own original material from two methods, and additionally

incorporates information from many previous studies. Because Cosmicflows-4 includes distances derived from a variety of independent, distinct distance estimators, intercomparisons should mitigate against a large systematic error.

Cosmic dilemma

Astronomers have assembled a framework that shows the universe's age to be a little more than 13 billion years old, however a dilemma of great significance has arisen in the details.

Physics of the evolution of the universe based on the standard model of cosmology predicts H0=67.5 km/s/Mpc, with an uncertainty of 1 km/s/Mpc. The difference between the measured and predicted values for the Hubble Constant is 7.5 km/s/Mpc -- much more than can be expected given the statistical uncertainties. Either there is a fundamental problem with our understanding of the physics of the cosmos, or there is a hidden systematic error in the measurements of galaxy distances.

Additional studies

Cosmicflows-4 is also being used to study how galaxies move individually, in addition to flowing with the overall expansion of the universe. Deviations from this smooth expansion arise due to the gravitational influences of clumps of matter, on scales ranging from our Earth and Sun up to congregations of galaxies on scales of a half billion light years. The mysterious dark matter is the dominant component on larger scales. With knowledge of the motions of galaxies in response to the mass around them, we can recreate the orbits that galaxies have followed since they were formed, giving us a better understanding of how the universe's vast, dark-matter dominated structures have formed over the eons of time.

From Science Daily

How a single protein could unlock age-related vision loss

Research led by Sanford Burnham Prebys professor Francesca Marassi, Ph.D., is helping to reveal the molecular secrets of macular degeneration, which causes almost 90% of all age-related vision loss. The study, published recently in the Biophysical Journal, describes the flexible structure of a key blood protein involved in macular degeneration and other age-related diseases, such as Alzheimer's and atherosclerosis.

"Proteins in the blood are under constant and changing pressure because of the different ways blood flows throughout the body," says Marassi. "For example, blood flows more slowly through small blood vessels in the eyes compared to larger arteries around the heart. Blood proteins need to be able to respond to these changes, and this study gives us fundamental truths about how they adapt to their environment, which is critical to targeting those proteins for future treatments."

There are hundreds of proteins in our blood, but the researchers focused on vitronectin, one of the most abundant. In addition to circulating in high concentrations in the blood, vitronectin is found in the scaffolding between cells and is also an important component of cholesterol.

Vitronectin is a key player in many age-related diseases, but for Marassi's team, the most promising target is macular degeneration, which affects as many as 11 million people in the United States. This number is expected to double by 2050.

"This protein is an important target for macular degeneration because it accumulates in the back of the eye, causing vision loss. Similar deposits appear in the brain in Alzheimer's disease and in the arteries in atherosclerosis," says Marassi. "We want to understand why this happens and leverage this knowledge to develop new treatments."

To approach this question, the researchers were interested in learning how the protein changes its structure at different temperatures and under different levels of pressure, approximating what happens in the human body.

"Determining the structure of a protein is the most important part of determining its function," adds Marassi. Through detailed biochemical analysis, the researchers found that the protein can subtly change its shape under pressure. These changes cause it to bond more easily to calcium ions in the blood, which the researchers suggest leads to the buildup of calcified plaque deposits characteristic of macular degeneration and other age-related diseases.

"It's a very subtle rearrangement of the molecular structure, but it has a big impact on how the protein functions," says Marassi. "The more we learn about the protein on a structural and mechanistic level, the better chance we have of successfully targeting it with treatments."

These structural insights will streamline the development of treatments for macular degeneration because it will allow researchers and their partners in the biotech industry to custom-design antibodies that selectively block the protein's calcium binding without disrupting its other important functions in the body.

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Your liver is just under three years old

The liver has a unique ability to regenerate after damage. However, it was unknown whether this ability decreases as we age. International scientists led by Dr. Olaf Bergmann at the Center for Regenerative Therapies Dresden (CRTD) at TU Dresden used a technique known as retrospective radiocarbon birth dating to determine the age of the human liver. They showed that no matter the person's age, the liver is always on average less than three years old. The results demonstrate that aging does not influence liver renewal, making the liver an organ that replaces its cells equally well in young and old people.

The liver is an essential organ that takes care of clearing toxins in our bodies. Because it constantly deals with toxic substances, it is likely to be regularly injured. To overcome this, the liver has a unique capacity among organs to regenerate itself after damage. Because a lot of the body's ability to heal itself and regenerate decreases as we age, scientists were wondering if the liver's capacity to renew also diminishes with age.

The nature of liver renewal in humans also remained a mystery. The animal models provided contradictory answers. "Some studies pointed to the possibility that liver cells are long-lived while others showed a constant turnover. It was clear to us that if we want to know what happens in humans, we need to find a way to directly assess the age of human liver cells," says Dr. Olaf Bergmann, research group leader at the Center for Regenerative Therapies Dresden (CRTD) at TU Dresden.

The Human Liver Remains a Young Organ

The interdisciplinary team of biologists, physicists, mathematicians, and clinicians led by Dr. Bergmann analyzed the livers of multiple individuals who died at ages between 20 and 84 years old. Surprisingly, the team showed that the liver cells of all subjects were more or less the same age.

"No matter if you are 20 or 84, your liver stays on average just under three years old," explains Dr. Bergmann. The results show that the adjustment of liver mass to the needs of the body is tightly regulated through the constant replacement of liver cells and that this process is maintained even in older people. This ongoing liver cell replacement is important for various aspects of liver regeneration and cancer formation.

Liver Cells with More DNA Renew Less

However, not all the cells in our liver are that young. A fraction of cells can live up to 10 years before renewing itself. This subpopulation of liver cells carries more DNA than the typical cells. "Most of our cells have two sets of chromosomes, but some cells accumulate more DNA as they age. In the end, such cells can carry four, eight, or even more sets of chromosomes," explains Dr. Bergmann.

"When we compared typical liver cells with the cells richer in DNA, we found fundamental differences in their renewal. Typical cells renew approximately once a year, while the cells richer in DNA can reside in the liver for up to a decade," says Dr. Bergmann. "As this fraction gradually increases with age, this could be a protective mechanism that safeguards us from accumulating harmful mutations. We need to find out if there are similar mechanisms in chronic liver disease, which in some cases can turn into cancer."

Lessons from the Nuclear Fallout

Determining the biological age of human cells is a massive technical challenge, as methods commonly used in animal models cannot be applied to humans.

Dr. Bergmann's group specializes in retrospective radiocarbon birth dating and uses the technique to assess the biological age of human tissues. Carbon is a chemical element that is ubiquitous and forms the backbone of life on Earth. Radiocarbon is one of a variety of types of carbon. It appears naturally in the atmosphere. Plants incorporate it through photosynthesis, in the same way as typical carbon, and pass it on to animals and humans. Radiocarbon is weakly radioactive and unstable. These characteristics are taken advantage of in archeology to determine the age of ancient samples.

"Archeologists have used the decay of radiocarbon successfully for many years to assess the age of specimens, one example being dating of the shroud of Turin," says Dr. Bergmann. "The radioactive decay of radiocarbon is very slow. It provides enough resolution for archeologists but it is not useful for determining the age of human cells. Nevertheless, we can still take advantage of the radiocarbon in our research."

The aboveground nuclear tests carried out in the 1950s introduced massive amounts of radiocarbon into the atmosphere, into the plants, and into the animals. As a result, cells formed in this period have higher amounts of radiocarbon in their DNA.

Following the official ban of aboveground nuclear testing in 1963, the amounts of atmospheric radiocarbon started to drop and so did the amounts of radiocarbon incorporated into the animal DNA. The values of atmospheric and cellular radiocarbon correspond to each other very well.

"Even though these are negligible amounts that are not harmful, we can detect and measure them in tissue samples. By comparing the values to the levels of atmospheric radiocarbon, we can retrospectively establish the age of the cells," explains Dr. Bergmann.

Unparalleled Insights Directly From the Source

The Bergmann group also explores the mechanisms that drive the regeneration of other tissues considered as static, such as the brain or the heart. The team has previously used their expertise in retrospective radiocarbon birth dating to show that the formation of new brain and heart cells is not limited to prenatal time but continues throughout life. Currently, the group is investigating whether new human heart muscle cells can still be generated in people with chronic heart disease.

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New target may help protect bones as we age

Drugs we take like prednisone can weaken our bones and so can aging, and scientists working to prevent both have some of the first evidence that the best target may not be the logical one.

They are finding that in aging bone, the mineralocorticoid receptor, better known for its role in blood pressure regulation, is a key factor in bone health, says Dr. Meghan E. McGee-Lawrence, biomedical engineer in the Department of Cellular Biology and Anatomy at the Medical College of Georgia.

And drugs that block the receptor, like the hypertension medications spironolactone and eplerenone, may help protect bone cells, says McGee-Lawrence, corresponding author of the study in the Journal of Bone and Mineral Research.

Drugs like prednisone are glucocorticoids, which are better known for their roles in reducing inflammation and suppressing the immune response, which is why they work so well for problems like irritable bowel syndrome and arthritis. But, like aging, they can also disrupt the healthy, ongoing dynamic of bone being made and being destroyed.

Our natural glucocorticoid levels increase with age, and bone, at least when we are young, has more glucocorticoid receptors than mineralocorticoid receptors. Glucocorticoids can actually coax stem cells to make bone-forming osteoblasts, but it also causes those osteoblasts to store more fat, and too much fat in the bone, like anywhere on our body, is probably not good and typically correlates with bone loss, McGee-Lawrence says.

So reducing the impact of glucocorticoid receptors seemed like a logical way to protect bone.

The MCG scientists had already been surprised to find that the loss of functioning glucocorticoid receptors did not protect against bone loss in younger mice on calorie-restricted diets. In fact, there was increased fat accumulation in the bone marrow and worsened osteoporosis.

This time they were looking at the impact of endogenous glucocorticoids in an aging model, and found again that when the glucocorticoid receptor was blocked, older mice also experienced more fat accumulation in the bone marrow and worsening bone disease.

They also found that the mice had a smaller muscle mass, chose to move around less than mice typically do and had higher blood pressure.

Another surprise was that when they used drugs to inhibit the mineralocorticoid receptor, many of the problems were reversed.

"The only way we have found to get rid of that lipid storage by osteoblasts was to inhibit the mineralocorticoid receptor with drugs," she says, and fortunately because of the receptors' clear role in blood pressure there are already drugs that do that.

"I think what it means is if we want to understand what these stress hormones, these endogenous glucocorticoids, are doing we cannot just think about signaling through one receptor," McGee-Lawrence says. For older bone, she thinks mineralocorticoid receptors may be a better target.

"We thought that knocking out the glucocorticoid receptor would make things better, but it made them worse," McGee-Lawrence says. "We think the mineralocorticoid receptor may explain a lot of what is going wrong in aging bone."

Both receptors are members of the steroid receptor family and mineralocorticoid receptors are thought to have equal affinity for mineralocorticoids and glucocorticoids. It may be the signaling paths are different in young and older individuals, she notes.

McGee-Lawrence and her colleagues already have some evidence that bone's expression of mineralocorticoid receptors goes up, potentially significantly, as you age. They have early mixed results on whether glucocorticoid receptors go down with age and are exploring more about what happens with both receptor levels as well as learning more about the role of mineralocorticoid receptors in bone, particularly aging bone.

"We want to know what would cause bone cells to change which receptors they are expressing and how they are responding to these," she says. "But there are a lot of things that happen with aging. We know inflammation changes with aging, so there are a lot of different cues that could cause these things to change."

The whole body impact they saw from their manipulation of receptors, like a higher blood pressure from deleting the glucocorticoid receptor, also is evidence of bone's importance as an endocrine organ, she says.

"By changing glucocorticoid signaling in the bone, not only are we seeing changes in the bone, but we are seeing changes in the fat, muscle, adrenal glands, in physical activity," she says which means something from the bone is communicating with all these other body systems, an emerging role of research in her field.

In fact, the increased fat presence in the bone marrow found in osteoporosis has resulted in it also being considered a metabolic disease of the bone, much as obesity, particularly excess weight around the middle, is considered a metabolic disease. Increased fat in the bone marrow is associated with disuse, like following a spinal cord injury, a high-fat diet, taking glucocorticoids, like steroids, and aging.

While the fat is a ready energy source for bone cells, too much can hinder bone cell formation. The scientists don't yet know whether the cells are no longer using fat well or they are pulling more in, or both; they do know fat accumulating in the bone cells coincides with less bone being made, she reiterates.

"We are trying to figure out exactly why these things are going wrong so that we can pick the right avenue to pursue for a treatment strategy," she says.

There is a lot of evidence in people that the synthetic glucocorticoids we take via pill or injection, can impact bone, creating an unhealthy imbalance between the amount of bone made and the amount broken down.

A focus of the research at MCG has been examining the bone impact from our endogenous glucocorticoids, the ones we make, a less-explored area. For years, McGee-Lawrence and her colleagues have been studying bone-forming osteoblasts which, like most cells, don't function optimally as we age.

But it may be that even synthetic glucocorticoids also work through these alternative receptors to damage the bone, which means trying to prevent their damage may also mean a different target, she says, noting again that the pathway may change as the person ages.

Interestingly some other tissues that are known to have a lot of mineralocorticoid receptors inactivate glucocorticoids, which bone cannot do, but perhaps it compensates by not having a lot of mineralocorticoid receptors, at least in youth, she says.

Read more at Science Daily

Chang'e-5 samples reveal key age of moon rocks

A lunar probe launched by the Chinese space agency recently brought back the first fresh samples of rock and debris from the moon in more than 40 years. Now an international team of scientists -- including an expert from Washington University in St. Louis -- has determined the age of these moon rocks at close to 1.97 billion years old.

"It is the perfect sample to close a 2-billion-year gap," said Brad Jolliff, the Scott Rudolph Professor of Earth and Planetary Sciences in Arts & Sciences and director of the university's McDonnell Center for the Space Sciences. Jolliff is a U.S.-based co-author of an analysis of the new moon rocks led by the Chinese Academy of Geological Sciences, published Oct. 7 in the journal Science.

The age determination is among the first scientific results reported from the successful Chang'e-5 mission, which was designed to collect and return to Earth rocks from some of the youngest volcanic surfaces on the moon.

"Of course, 'young' is relative," Jolliff said. "All of the volcanic rocks collected by Apollo were older than 3 billion years. And all of the young impact craters whose ages have been determined from the analysis of samples are younger than 1 billion years. So the Chang'e-5 samples fill a critical gap."

The gap that Jolliff references is important not only for studying the moon, but also for studying other rocky planets in the solar system.

As a planetary body, the moon itself is about 4.5 billion years old, almost as old as the Earth. But unlike the Earth, the moon doesn't have the erosive or mountain-building processes that tend to erase craters over the years. Scientists have taken advantage of the moon's enduring craters to develop methods of estimating the ages of different regions on its surface, based in part on how pocked by craters the area appears to be.

This study shows that the moon rocks returned by Chang'e-5 are only about 2 billion years old. Knowing the age of these rocks with certainty, scientists are now able to more accurately calibrate their important chronology tools, Jolliff said.

"Planetary scientists know that the more craters on a surface, the older it is; the fewer craters, the younger the surface. That's a nice relative determination," Jolliff said. "But to put absolute age dates on that, one has to have samples from those surfaces."

"The Apollo samples gave us a number of surfaces that we were able to date and correlate with crater densities," Jolliff explained. "This cratering chronology has been extended to other planets -- for example, for Mercury and Mars -- to say that surfaces with a certain density of craters have a certain age."

"In this study, we got a very precise age right around 2 billion years, plus or minus 50 million years," Jolliff said. "It's a phenomenal result. In terms of planetary time, that's a very precise determination. And that's good enough to distinguish between the different formulations of the chronology."

Other interesting findings from the study relate to the composition of basalts in the returned samples and what that means for the moon's volcanic history, Jolliff noted.

The results presented in the Science paper are just the tip of the iceberg, so to speak. Jolliff and colleagues are now sifting through the regolith samples for keys to other significant lunar science issues, such as finding bits and pieces tossed into the Chang'e 5 collection site from distant, young impact craters such as Aristarchus, to possibly determining the ages of these small rocks and the nature of the materials at those other impact sites.

Jolliff has worked with the scientists at the Sensitive High Resolution Ion MicroProbe (SHRIMP) Center in Beijing that led this study, including study co-author Dunyi Liu, for over 15 years. This long-term relationship is possible through a special collaboration agreement that includes Washington University and its Department of Earth and Planetary Sciences, and Shandong University in Weihai, China, with support from Washington University's McDonnell Center for the Space Sciences.

"The lab in Beijing where the new analyses were done is among the best in the world, and they did a phenomenal job in characterizing and analyzing the volcanic rock samples," Jolliff said.

"The consortium includes members from China, Australia, the U.S., the U.K. and Sweden," Jolliff continued. "This is science done in the ideal way: an international collaboration, with free sharing of data and knowledge -- and all done in the most collegial way possible. This is diplomacy by science."

Jolliff is a specialist in mineralogy and provided his expertise for this study of the Chang'e-5 samples. His personal research background is focused on the moon and Mars, the materials that make up their surfaces and what they tell about the planets' history.

Read more at Science Daily

Age and aging have critical effects on the gut microbiome

Researchers at Cedars-Sinai have found that aging produces significant changes in the microbiome of the human small intestine distinct from those caused by medications or illness burden. The findings have been published in the journal Cell Reports.

"By teasing out the microbial changes that occur in the small bowel with age, medication use and diseases, we hope to identify unique components of the microbial community to target for therapeutics and interventions that could promote healthy aging," said Ruchi Mathur, MD, the study's principal investigator.

Research exploring the gut microbiome, and its impact on health, has relied predominantly on fecal samples, which do not represent the entire gut, according to Mathur. In their study, investigators from Cedars-Sinai's Medically Associated Science and Technology (MAST) Program analyzed samples from the small intestine-which is over 20 feet in length and has the surface area of a tennis court-for examination of the microbiome and its relationship with aging.

"This study is the first of its kind to examine the microbial composition of the small intestine of subjects 18 years of age to 80. We now know that certain microbial populations are influenced more by medications, while others are more affected by certain diseases. We have identified specific microbes that appear to be only influenced by the chronological age of the person," said Mathur, an endocrinologist and director of the Diabetes Outpatient Treatment & Education Center.

The 21st century has been referred to as the "era of the gut microbiome" as scientists turn considerable attention to the role trillions of gut bacteria, fungi and viruses may play in human health and disease. The microbiome is the name given to the genes that live in these cells. Studies have suggested that disturbances in the constellations of the microbial universe may lead to critical illnesses, including gastroenterological diseases, diabetes, obesity, and some neurological disorders.

While researchers know that microbial diversity in stool decreases with age, Cedars-Sinai investigators identified bacteria in the small bowel they refer to as "disruptors" that increase and could be troublesome.

"Coliforms are normal residents of the intestine. We found that when these rod-shaped microbes become too abundant in the small bowel-as they do as we get older-they exert a negative influence on the rest of the microbial population. They are like weeds in a garden," said study co-author Gabriela Leite, PhD.

Investigators also found that as people age, the bacteria in the small intestine change from microbes that prefer oxygen to those that can survive with less oxygen, something they hope to understand as the research continues.

Read more at Science Daily

There’s a bright side to being a ‘Debbie Downer’

New research shows that keeping busy with a variety of activities can elicit both positive and negative emotions, and some of the relationship could depend on your age. A new study published in the Journal of Gerontology finds that engaging in diverse daily activities is associated with a diverse set of emotions.

"Experiencing a broad spectrum of emotions is adaptive and beneficial to health because it means having a more balanced and nuanced appraisal of daily life," said Soomi Lee, assistant professor of aging studies in the University of South Florida College of Behavioral and Community Sciences. "For example, even for negative emotions, feeling intense anger across situations may mean that the individual has a narrow appraisal of situations, whereas feeling a mix of anger, sadness and shame may indicate a broader and more nuanced appraisal."

Lee reviewed data collected on nearly 3,000 middle-aged participants enrolled in the Midlife in the United States Study who are considered relatively healthy and well-educated. She found individuals who regularly participated in a broad range of daily activities experienced diverse emotional experiences -- both positive and negative -- with those between ages 33-44 experiencing more diverse positive emotions compared to those between ages 68-84.

The study looked at the amount of time individuals spent participating in seven activities: paid work, spending time with children, chores, leisure, physical activities, formal volunteering and helping someone outside of their household, such as a neighbor. Participants recorded their activities for eight consecutive days, as well as their positive and negative emotions, which were used to calculate emodiversity scores.

Emodiversity is a term used to describe rich and balanced emotions. Emodiversity was broken into 13 positive emotions: cheerful, in good spirits, extremely happy, calm and peaceful, satisfied, full of life, enthusiastic, attentive, proud, active, close to others, belonging and confident, as well as 14 negative emotions: worthlessness, nervous, restless or fidgety, hopeless, afraid, jittery, irritable, ashamed, upset, lonely, angry, frustrated, that everything is an effort and so sad that nothing could cheer you up.

Lee says the younger demographic may have stronger emotions than older adults since their activities are more diverse. Many spend more time at work and with children, which tends to decrease with age. Also, older adults may have more muted or monotonic emotions as a result of wisdom or their strategy to reduce the range of novel social interactions to avoid potentially negative situations. Interestingly, the overall amount of time spent participating in activities was not associated with neither positive nor negative emodiversity, suggesting that total activity time is not what matters, but rather that an even amount of time is spent participating in a broad range of activities.

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Metabolism changes with age, just not when you might think

Most of us remember a time when we could eat anything we wanted and not gain weight. But a new study suggests your metabolism, the rate at which you burn calories, actually peaks much earlier and starts its inevitable decline later than you might think.

The findings appear in the journal Science.

"As we age, there are a lot of physiological changes that occur in the phases of our life such as during puberty and in menopause. . What's odd is that the timing of our 'metabolic life stages' doesn't appear to match the markers we associate with growing up and getting older," said study co-author Jennifer Rood, PhD, Associate Executive Director for Cores and Resources at Pennington Biomedical Research Center.

Four Pennington Biomedical researchers were part of an international team of scientists who analyzed the average calories burned by more than 6,600 people as they went about their daily lives. The participants' ages ranged from one week old to 95 years, and they lived in 29 different countries. The other Pennington Biomedical scientists are Peter Katzmarzyk, PhD, Associate Executive Director for Population and Public Health Sciences; Corby Martin, PhD, Professor and Director, Ingestive Behavior Laboratory; and Eric Ravussin, PhD, Associate Executive Director for Clinical Science.

Most previous large-scale studies measured how much energy the body uses for basic vital functions -- breathing, digesting, and pumping blood -- the calories you need just to stay alive. But basic functions account for just 50 percent to 70 percent of the calories we burn each day. They don't include the energy we spend doing everything else: washing the dishes, walking the dog, breaking a sweat at the gym, even just thinking or fidgeting.

To come up with a number for total daily energy expenditure, the researchers turned to the "doubly labeled water" method. It's a urine test that involves having a person drink water in which the hydrogen and oxygen in the water molecules have been replaced with naturally occurring "heavy" forms, and then measures how quickly they're flushed out.

Scientists have used the technique -- considered the gold standard for measuring daily energy expenditure during normal daily life outside of the lab -- to measure energy expenditure in humans since the 1980s. But previous studies were limited in size and scope due to cost. To get around that limitation, multiple labs shared their data in a single database, to see if they could tease out truths hidden or only hinted at in previous studies.

Pooling and analyzing energy expenditures across the entire lifespan revealed some surprises.

"Some people think of their teens and 20s as the age when their calorie-burning potential hits its peak," Dr. Katzmarzyk said. "But the study shows that, pound for pound, infants had the highest metabolic rates of all."

Energy needs shoot up during the first 12 months of life. By their first birthdays, babies burn calories 50 percent faster for their body size than adults.

And that's not just because infants are busy tripling their birth weight in their first year.

"The babies grow rapidly, which accounts for much of the effect. However, after you control for this, their energy expenditures tend to be higher than what you would expect for their body size," Dr. Martin said.

An infant's explosive metabolism may help explain why children who don't get enough to eat during this developmental stage are less likely to survive and grow up to be healthy adults.

"More research is needed to better understand the metabolism of babies. We need to know what is driving higher energy expenditures," Dr. Martin said.

After the initial surge in infancy, a person's metabolism slows by about 3 percent each year until our 20s, when it levels off into a new normal.

Surprisingly, the growth spurts of adolescence didn't generate an increase in daily calorie needs after researchers took body size into account. Another surprise? People's metabolisms were most stable from their 20s through their 50s. Calorie needs during pregnancy grew no more than expected.

The findings suggest that other factors lie behind the so-called "middle-age spread."

The data suggest that our metabolisms don't really start to decline again until after age 60. The slowdown is gradual, only 0.7 percent a year. But a person in their 90s needs 26 percent fewer calories each day than someone in midlife.

Lost muscle mass as we get older may be partly to blame, the researchers say, since muscle burns more calories than fat. But it's not the whole picture.

"We took dwindling muscle mass into account. After 60, a person's cells slow down," Dr. Ravussin said.

The patterns held even when differing activity levels were taken into account.

Aging goes hand in hand with so many other physiological changes that it has been difficult to parse what drives the shifts in energy expenditure. But the new research supports the idea that it's more than age-related changes in lifestyle or body composition.

Read more at Science Daily

New insights into the relationship between how we feel and our views on aging

A new study finds that the disconnect between how old we feel and how old we want to be can offer insights into the relationship between our views on aging and our health.

Subjective age discordance (SAD) -- the difference between how old you feel and how old you would like to be -- is a fairly new concept in the psychology of aging. However, the work to this point has used SAD to look at longitudinal data and how people's views on aging evolve over months or years.

"We wanted to see whether SAD could help us assess day-to-day changes in our views on aging, and how that may relate to our physical health and well-being," says Shevaun Neupert, co-author of the study and a professor of psychology at North Carolina State University.

SAD is determined by taking how old you feel, subtracting how old you would like to be and then dividing it by your actual age. The higher the score, the more you feel older than you want to be.

For this study, researchers enrolled 116 adults aged 60-90 and 107 adults aged 18-36. Study participants filled out an online survey every day for eight days. The survey was designed to assess how old participants felt each day, their ideal age, their positive and negative mood over the course of the day, any stresses they experienced, and any physical complaints, such as backaches or cold symptoms.

"We found that both older adults and younger adults experienced SAD," Neupert says. "It was more pronounced in older adults, which makes sense. However, it fluctuated more from day to day in younger adults, which was interesting."

"We think younger adults are getting pushed and pulled more," says Jennifer Bellingtier, first author of the paper, and a researcher at Friedrich Schiller University Jena. "Younger adults are concerned about negative stereotypes associated with aging, but may also be dealing with negative stereotypes associated with younger generations and wishing they had some of the privileges and status associated with being older."

Two additional findings stood out.

"On days when the age you feel is closer to your ideal age, people tend to have a more positive mood," Bellingtier says. "And, on average, people who have more health complaints also had higher SAD scores."

Neither finding was surprising, but both show the value of the SAD concept as a tool for understanding people's views on age and aging. It may also offer a new approach for the way we think about aging and its impacts on health.

"Previous research has found that how old you feel can affect your physical and mental well-being, and interventions to address that have focused on trying to make people feel younger," Neupert says.

Read more at Science Daily

Feeling younger buffers older adults from stress, protects against health decline

People who feel younger have a greater sense of well-being, better cognitive functioning, less inflammation, lower risk of hospitalization and even live longer than their older-feeling peers. A study published by the American Psychological Association suggests one potential reason for the link between subjective age and health: Feeling younger could help buffer middle-aged and older adults against the damaging effects of stress.

In the study, published in Psychology and Aging, researchers from the German Centre of Gerontology analyzed three years of data from 5,039 participants in the German Ageing Survey, a longitudinal survey of residents of Germany age 40 and older. The survey included questions about the amount of perceived stress in peoples' lives and their functional health -- how much they were limited in daily activities such as walking, dressing and bathing. Participants also indicated their subjective age by answering the question, "How old do you feel?"

The researchers found, on average, participants who reported more stress in their lives experienced a steeper decline in functional health over three years, and that link between stress and functional health decline was stronger for chronologically older participants.

However, subjective age seemed to provide a protective buffer. Among people who felt younger than their chronological age, the link between stress and declines in functional health was weaker. That protective effect was strongest among the oldest participants.

"Generally, we know that functional health declines with advancing age, but we also know that these age-related functional health trajectories are remarkably varied. As a result, some individuals enter old age and very old age with quite good and intact health resources, whereas others experience a pronounced decline in functional health, which might even result in need for long-term care," said study lead author Markus Wettstein, PhD, who is now at University of Heidelberg. "Our findings support the role of stress as a risk factor for functional health decline, particularly among older individuals, as well as the health-supporting and stress-buffering role of a younger subjective age."

The results suggest that interventions that aim to help people feel younger could reduce the harm caused by stress and improve health among older adults, according to the researchers -- though further study is needed to help determine what kind of interventions would work best. For example, Wettstein said, messaging campaigns to counteract ageism and negative age stereotypes and to promote positive views on aging could help people feel younger. In addition, more general stress-reduction interventions and stress management training could prevent functional health loss among older adults, according to Wettstein.

 Read more at Science Daily

Study reveals roadmap of muscle decline with age

 Scientists have produced a comprehensive roadmap of muscle aging in mice that could be used to find treatments that prevent decline in muscle mobility and function, according to a report published today in eLife.

The study reveals which molecules in the muscle are most significantly altered at different life stages, and shows that a molecule called Klotho, when administered to mice in old, but not very old, age, was able to improve muscle strength.

Age-related loss of skeletal muscle mass and function -- called sarcopenia -- is associated with loss of mobility and increased risk of falls. Yet, although scientists know how sarcopenia affects the appearance and behaviour of muscle tissues, the underlying molecular mechanisms for sarcopenia remain poorly understood. Current treatments for sarcopenia largely involve prescribing physical activity or dietary modifications, and these have shown moderate success.

"Although there are no proven treatments for sarcopenia yet, there are some pharmaceutical treatments entering clinical trials. Interestingly, many of these act on mechanisms that also involve a protein called Klotho," says co-first author Zachary Clemens, Doctoral Student at the Department of Environmental and Occupational Health, University of Pittsburgh, Pennsylvania, US. "Evidence suggests that Klotho levels gradually decline with age, and so we wanted to test whether supplementation with Klotho may attenuate the development of sarcopenia."

The team first characterised and compared changes in the structure, function and gene activity in skeletal muscle across the lifespan in mice. They grouped mice into four age categories -- young, middle-aged, old and oldest-old -- and looked at muscle weight, type of muscle fibers, whether the muscles had accumulated fat, and skeletal muscle function. Although old mice displayed mild sarcopenia, the common clinical features of sarcopenia were only present in the oldest-old mice.

Next, they looked at changes in muscle gene activity and found a progressive disruption in genes known to be associated with the hallmarks of aging from the young to the oldest-old mice.

"To date, most studies in skeletal muscle have focused on the identification of specific pathways that are associated with sarcopenia to identify a molecular mechanism linked to the condition," explains co-first author Sruthi Sivakumar, Doctoral Student at the Department of Bioengineering, University of Pittsburgh. "We employed an integrative approach, where we created a network by converting gene expression levels to protein-protein interactions, and then we studied how this interaction network changed over time."

From this network, the team determined the 'network entropy' of the muscle cells as a means to estimate the loss of molecular order within the system over time. They found the greatest difference in order between the young and old age groups (at which point it reached maximal entropy), with little difference between the old and oldest-old mice. Additionally, when they looked at human muscle gene data from different age groups, they saw that entropy reached its lowest level in the fourth decade of life, after which time entropy escalated. This was of interest to the team as the fourth decade of life is the time point when sarcopenia often starts to develop.

Next, they looked at whether administering Klotho to mice would have beneficial effects on the muscle healing after injury. They found that applying Klotho after muscle injury reduced scarring and increased structures associated with force production in the animals. Injured mice that received Klotho also had better muscle function -- such as muscle twitch and force production -- and their whole-body endurance improved two-fold.

Finally, the team looked at whether giving the mice Klotho could reverse age-related declines in muscle quality and function. They found that Klotho administration led to some improvements in the old mice: force production was improved by 17% and endurance when supporting whole body weight was 60% greater compared to mice without treatment. But this was only seen in the old mice, and not in the oldest-old animals. Further investigation showed that Klotho affected genes associated with the hallmarks of aging in all age groups, but that the oldest-old mice showed a dysregulated gene response.

Read more at Science Daily

Memories of past events retain remarkable fidelity even as we age

 Scientists studying the complex relationship between aging and memory have found that in a controlled experiment, people can remember the details about past events with a surprising 94% accuracy, even accounting for age. These results, published in the journal Psychological Science, suggest that the stories we tell about past events are accurate, although details tend to fade with time.

"These results are surprising to many, given the general pessimism about memory accuracy among scientists and the prevalent idea that memory for one-time events is not to be trusted," said Nicholas Diamond, the study's lead researcher, a former graduate student at Baycrest's Rotman Research Institute (RRI), and currently a postdoctoral researcher at the University of Pennsylvania.

About 400 academics, including memory scientists, surveyed as part of this study estimated memory accuracy to be around 40% at best, expecting this score to be even lower for older participants or when greater amounts of time had elapsed since the events.

"This study shows us that memory accuracy is actually quite good under normal circumstances, and it remains stable as we age," said Brian Levine, a senior scientist at RRI and a professor of psychology and neurology at the University of Toronto and co-author on the study. "These results will be helpful for understanding memory in healthy aging."

For their study, the researchers created an immersive, scientifically controlled event for their participants: a 30-minute audio-guided tour of art and other items displayed at Baycrest. Two days later, participants were asked to tell the researcher everything they could remember about the tour. The responses were recorded and then verified against the facts.

The researchers also tested Baycrest employees on their recall of a standardized, scripted procedure that they had experienced one month to three years prior. This allowed the researchers to examine the effect of delay between the event and memory recall, while the standardized nature of the procedure made it possible to verify accuracy.

Using standardized, verifiable events to test memory is an innovative approach, the researchers said, as scientists typically use artificial laboratory stimuli, such as random word lists, rather than real-life experiences, or they test participants' memory for personal past experiences, which cannot be verified.

"This pessimism originates from earlier studies showing that memory can be manipulated using certain testing methods," said Levine. "While those studies were important in showing the ways in which memory can fail, we wanted to know what happens when people freely recall events without such manipulation. We found that they are overwhelmingly accurate."

The results showed that participants' accuracy was high in both cases, though, as expected, the number of details they remembered decreased with age and time. At best, they recalled about 25% of their experience. "This suggests that we forget the majority of details from everyday events, but the details we do recall correspond to the reality of the past," Diamond said.

In a related study also published in Psychological Science, Diamond and Levine examined the degree to which people's memories matched the true order of events. In this case, younger adults tended to perform better than older adults, suggesting that while accuracy of details remains high with age, older adults are less likely to correctly remember the true sequence of past events. That is, the order of our memories becomes disorganized as we age.

"The results of these studies can contribute to identifying differences in memory among those who develop dementia," said Dr. Levine.

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