Tag Archives: Biological

“Biological Annihilation” – Stanford Scientists Discover Human-Driven Mass Extinction Is “Mutilating” the Tree of Life – SciTechDaily

  1. “Biological Annihilation” – Stanford Scientists Discover Human-Driven Mass Extinction Is “Mutilating” the Tree of Life SciTechDaily
  2. Scientists warn entire branches of the ‘Tree of Life’ are going extinct Yahoo News
  3. Three-million-year-old lineage of the Yarrow’s spiny lizard is nearly extinct Earth.com
  4. Experts warn of a “biological holocaust” as human-caused extinction “mutilates” the tree of life Salon
  5. Humans are driving loss of entire branches of ‘Tree of Life,’ warn scientists WION
  6. View Full Coverage on Google News

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Overactive Cell Metabolism Linked to Biological Aging

Summary: Human cells with impaired mitochondria expend more energy. While this hypermetabolism enhances a cell’s short-term survival, it also dramatically increases the rate at which the cell ages.

Source: Columbia University

Why do cells, and by extension humans, age? The answer may have a lot to do with mitochondria, the organelles that supply cells with energy. Though that idea is not new, direct evidence in human cells had been lacking. Until now.

In a study published Jan. 12 in Communications Biology, a team led by Columbia University researchers has discovered that human cells with impaired mitochondria respond by kicking into higher gear and expending more energy.

While this adaptation—called hypermetabolism—enhances the cells’ short-term survival, it comes at a high cost: a dramatic increase in the rate at which the cells age.

“The findings were made in cells from patients with rare mitochondrial diseases, yet they may also have relevance for other conditions that affect mitochondria, including neurodegenerative diseases, inflammatory conditions, and infections,” says principal investigator Martin Picard, PhD, associate professor of behavioral medicine (in psychiatry and neurology) at Columbia University Vagelos College of Physicians and Surgeons.

“In addition, hypermetabolism may be a key reason why most cells deteriorate as we get older.”

Hypermetabolic cells age faster

It was generally assumed that mitochondrial defects (which impair the conversion of food sources into usable energy) would force cells to slow their metabolic rate in an effort to conserve energy.

However, by analyzing metabolic activity and energy consumption in cells from patients with mitochondrial diseases, the researchers found that cells with impaired mitochondria double their energy expenditure.

Moreover, re-analyzing data from hundreds of patients with different mitochondrial diseases showed that mitochondrial defects also increase the energetic cost of living at the whole-body level.

Although this energy boost keeps cells running, it also degrades the cell’s telomeres (caps that protect the ends of our chromosomes) and activates stress responses and inflammation. The net effect accelerates biological aging.

“When cells expend more energy to make proteins and other substances essential for short-term survival, they’re likely stealing resources from processes that ensure long-term survival, like maintaining telomeres,” says Gabriel Sturm, a graduate student and lead author on this study.

Hypermetabolism, fatigue, and aging

This hypermetabolic state could explain why people with mitochondrial diseases experience fatigue and exercise intolerance, among other symptoms.

“To make up for the extra energy use in your cells, your body ‘tells’ you not to overexert yourself, to conserve energy. We likely see the same dynamic as people age and their vitality diminishes,” Picard says.

Mitochondrial defects caused by rare genetic mutations cause human cells to increase their metabolism. Though that helps short-term survival, it comes at a high cost: a dramatic increase in the rate at which the cells age. Hypermetabolism also may be a key reason why most cells deteriorate as everyone gets older. Credit: Martin Picard

The study doesn’t point to any new remedies for patients with mitochondrial diseases, which are currently not treatable, but it does reinforce the current recommendations for patients to move more.

“That may seem counterintuitive, since if you’re more active, you’re going to expend more energy and possibly make your symptoms worse,” Sturm says. 

“But exercise is known to increase the efficiency of an organism. An individual who runs, for example, uses less energy to sustain basic bodily processes than someone who is not physically active.”

Improving organismal efficiency, which would lower energy use in the cells and improve fatigue and other symptoms, may partially explain the health benefits of exercise in patients with mitochondrial diseases and otherwise healthy people.

In their search for new treatments for mitochondrial diseases, researchers should focus on hypermetabolism, Picard says. “Although mitochondrial defects do impair the ability of cells to produce energy, energy deficiency may not be the primary disease initiator. Our study shows these defects increase energy consumption. To move the needle therapeutically, we may need to target hypermetabolism. We need more research to know if that would work.”

Hypermetabolism is also common to other diseases. If increased cellular energy expenditure plays a causal role in driving the aging process, targeting hypermetabolism may be a way to improve fatigue, improve people’s quality of life, or even to slow biological aging.

Funding:

The research was supported by grants from the National Institutes of Health (R01AG066828), the Baszucki Brain Research Fund, the J. Willard and Alice S. Marriott Foundation, Muscular Dystrophy Association, Nicholas Nunno Foundation, the JDF Fund for Mitochondrial Research, and the Shuman Mitochondrial Disease Fund.

The authors declare no competing interests.

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About this aging and cell metabolism research news

Author: Helen Garey
Source: Columbia University
Contact: Helen Garey – Columbia University
Image: The image is credited to Martin Picard/Columbia University

Original Research: Open access.
“OxPhos defects cause hypermetabolism and reduce lifespan in cells and in patients with mitochondrial diseases” by Martin Picard et al. Communications Biology


Abstract

OxPhos defects cause hypermetabolism and reduce lifespan in cells and in patients with mitochondrial diseases

Patients with primary mitochondrial oxidative phosphorylation (OxPhos) defects present with fatigue and multi-system disorders, are often lean, and die prematurely, but the mechanistic basis for this clinical picture remains unclear.

By integrating data from 17 cohorts of patients with mitochondrial diseases (n = 690) we find evidence that these disorders increase resting energy expenditure, a state termed hypermetabolism.

We examine this phenomenon longitudinally in patient-derived fibroblasts from multiple donors. Genetically or pharmacologically disrupting OxPhos approximately doubles cellular energy expenditure.

This cell-autonomous state of hypermetabolism occurs despite near-normal OxPhos coupling efficiency, excluding uncoupling as a general mechanism. Instead, hypermetabolism is associated with mitochondrial DNA instability, activation of the integrated stress response (ISR), and increased extracellular secretion of age-related cytokines and metabokines including GDF15.

In parallel, OxPhos defects accelerate telomere erosion and epigenetic aging per cell division, consistent with evidence that excess energy expenditure accelerates biological aging.

To explore potential mechanisms for these effects, we generate a longitudinal RNASeq and DNA methylation resource dataset, which reveals conserved, energetically demanding, genome-wide recalibrations.

Taken together, these findings highlight the need to understand how OxPhos defects influence the energetic cost of living, and the link between hypermetabolism and aging in cells and patients with mitochondrial diseases.

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Is Muscle Weakness the New Smoking? Grip Strength Tied to Accelerated Biological Age

Summary: Muscle weakness marked by grip strength was associated with accelerated biological aging, a new study reports.

Source: University of Michigan

Everyone ages at a different pace. That’s why two 50-year-olds, despite living the same number of years, may have different biological ages—meaning that a host of intrinsic and extrinsic factors have caused them to age at varying paces with different levels of risk for disease and early death.

Lifestyle choices, such as diet, and smoking, and illness all contribute to accelerating biological age beyond one’s chronological age. In other words, your body is aging faster than expected.

And for the first time, researchers have found that muscle weakness marked by grip strength, a proxy for overall strength capacity, is associated with accelerated biological age.

Specifically, the weaker your grip strength, the older your biological age, according to results published in the Journal of Cachexia, Sarcopenia and Muscle.

Researchers at Michigan Medicine modeled the relationship between biological age and grip strength of 1,274 middle aged and older adults using three “age acceleration clocks” based on DNA methylation, a process that provides a molecular biomarker and estimator of the pace of aging. The clocks were originally modeled from various studies examining diabetes, cardiovascular disease, cancer, physical disability, Alzheimer’s disease, inflammation and early mortality.

Results reveal that both older men and women showed an association between lower grip strength and biological age acceleration across the DNA methylation clocks.

“We’ve known that muscular strength is a predictor of longevity, and that weakness is a powerful indicator of disease and mortality, but for the first time, we have found strong evidence of a biological link between muscle weakness and actual acceleration in biological age,” said Mark Peterson, Ph.D., M.S., lead author of the study and associate professor of physical medicine and rehabilitation at University of Michigan.

“This suggests that if you maintain your muscle strength across the lifespan, you may be able to protect against many common age-related diseases. We know that smoking, for example, can be a powerful predictor of disease and mortality, but now we know that muscle weakness could be the new smoking.”

The real strength of this study was in the 8 to 10 years of observation, in which lower grip strength predicted faster biological aging measured up to a decade later, said Jessica Faul, Ph.D., M.P.H., a co-author of the study and research associate professor at the U-M Institute for Social Research.

Past studies have shown that low grip strength is an extremely strong predictor of adverse health events. One study even found that it is a better predictor of cardiovascular events, such as myocardial infarction, than systolic blood pressure—the clinical hallmark for detecting heart disorders. Peterson and his team have previously shown a robust association between weakness and chronic disease and mortality across populations.

This evidence coupled with their study’s recent findings, Peterson says, shows potential for clinicians to adopt the use of grip strength as a way to screen individuals for future risk of functional decline, chronic disease and even early mortality.

“Screening for grip strength would allow for the opportunity to design interventions to delay or prevent the onset or progression of these adverse ‘age-related’ health events,” he said.

Lifestyle choices, such as diet, and smoking, and illness all contribute to accelerating biological age beyond one’s chronological age. Credit: Justine Ross, Michigan Medicine

“We have been pushing for clinicians to start using grip strength in their clinics and only in geriatrics has this sort of been incorporated. However, not many people are using this, even though we’ve seen hundreds of publications showing that grip strength is a really good measure of health.”

Investigators say future research is needed to understand the connection between grip strength and age acceleration, including how inflammatory conditions contribute to age-related weakness and mortality.

Previous studies have shown that chronic inflammation in aging—known as “inflammaging”—is a significant risk factor for mortality among older adults. This inflammation is also associated with lower grip strength and may be a significant predictor on the pathway between lower grip strength and both disability and chronic disease multimorbidity.

Additionally, Peterson says, studies must focus on how lifestyle and behavioral factors, such as physical activity and diet, can affect grip strength and age acceleration.

“Healthy dietary habits are very important, but I think regular exercise is the most critical thing that somebody can do to preserve health across the lifespan,” he said. “We can show it with a biomarker like DNA methylation age, and we can also test it with a clinical feature like grip strength.”

See also

Additional authors include Stacey Collins, M.A., Helen C.S. Meier, Ph.D., M.P.H., Alexander Brahmsteadt, M.D., all of University of Michigan.

About this aging and muscle strength research news

Author: Noah Fromson
Source: University of Michigan
Contact: Noah Fromson – University of Michigan
Image: The image is credited to Justine Ross, Michigan Medicine

Original Research: Open access.
“Grip strength is inversely associated with DNA methylation age acceleration” by Mark D. Peterson et al. Journal of Cachexia, Sarcopenia and Muscle


Abstract

Grip strength is inversely associated with DNA methylation age acceleration

Background

There is a large body of evidence linking muscular weakness, as determined by low grip strength, to a host of negative ageing-related health outcomes. Given these links, grip strength has been labelled a ‘biomarker of aging’; and yet, the pathways connecting grip strength to negative health consequences are unclear. The objective of this study was to determine whether grip strength was associated with measures of DNA methylation (DNAm) age acceleration.

Methods

Middle age and older adults from the 2006 to 2008 waves of the Health and Retirement Study with 8–10 years of follow-up were included. Cross-sectional and longitudinal regression modelling was performed to examine the association between normalized grip strength (NGS) and three measures of DNAm age acceleration, adjusting for cell composition, sociodemographic variables and smoking. Longitudinal modelling was also completed to examine the association between change in absolute grip strength and DNAm age acceleration. The three DNAm clocks used for estimating age acceleration include the established DunedinPoAm, PhenoAge and GrimAge clocks.

Results

There was a robust and independent cross-sectional association between NGS and DNAm age acceleration for men using the DunedinPoAm (β: −0.36; P < 0.001), PhenoAge (β: −8.27; P = 0.01) and GrimAge (β: −4.56; P = 0.01) clocks and for women using the DunedinPoAm (β: −0.36; P < 0.001) and GrimAge (β: −4.46; P = 0.01) clocks. There was also an independent longitudinal association between baseline NGS and DNAm age acceleration for men (β: −0.26; P < 0.001) and women (β: −0.36; P < 0.001) using the DunedinPoAm clock and for women only using the PhenoAge (β: −8.20; P < 0.001) and GrimAge (β: −5.91; P < 0.001) clocks. Longitudinal modelling revealed a robust association between change in grip strength from wave 1 to wave 3 was independently associated with PhenoAgeAA (β: −0.13; 95% CI: −0.23, −0.03) and GrimAgeAA (β: −0.07; 95% CI: −0.14, −0.01) in men only (both P < 0.05).

Conclusions

Our findings provide some initial evidence of age acceleration among men and women with lower NGS and loss of strength over time. Future research is needed to understand the extent to which DNAm age mediates the association between grip strength and chronic disease, disability and mortality.

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Genetics May Explain Link Between Unhealthy Teen Lifestyles and Accelerated Biological Aging

Summary: The epigenetic clocks of those who indulged in unhealthy behaviors as teens were 1.7 to 3.3 years older than individuals who reported more healthy lifestyles as teens.

Source: eLife

Biological aging results from damage to cells and tissues in the body that accumulates over time. The results of the study could lead to new ways of identifying young people at risk of developing unhealthy habits that are associated with accelerated biological aging and suggest interventions to prevent poor health outcomes later on. 

“Unhealthy lifestyles during adolescence when cells are rapidly dividing may have lasting harmful effects,” says lead author Anna Kankaanpää, a doctoral researcher at the Gerontology Research Center and Faculty of Sport and Health Sciences at the University of Jyväskylä, Finland.

“Activities like drinking or smoking, for example, may contribute to increased biological aging and related health conditions like heart or lung disease and premature death.” 

To measure the effects of unhealthy teen behavior on aging at the cellular level, Kankaanpää and colleagues analyzed the link between behavior and cellular aging in 824 twins who participated in the Finn Twin12 Study.

Participants were 21 to 25 years of age and had completed surveys about their behaviors at ages 12, 14 and 17. Most of the teens reported overall healthy, active lifestyles, but the researchers classified two groups as having unhealthy lifestyles.

One group had high body mass index scores – an approximate measure of whether a person is at a healthy weight, based on their height and body mass. The other group regularly smoked, binge-drank alcohol, and did not exercise regularly. 

The team measured DNA methylation, the addition of chemical tags on DNA that can turn on or off gene expression, in blood samples taken from the participants. They used several algorithms or “epigenetic clocks” – biochemical tests based on DNA methylation levels – to determine if the individuals were experiencing accelerated biological aging, and looked to see if there was any connection between unhealthy behaviors and more rapid aging. 

Overall, the clocks suggested that individuals in the two groups classified as having unhealthy behaviors were, on average, 1.7 to 3.3 years older than individuals who reported more healthy lifestyles during their adolescence. This is equivalent to aging about 2 to 3 weeks faster each calendar year.

The results varied depending on which epigenetic clock they used, but the link between lifestyle and accelerated aging was primarily due to shared genetics. 

“Previous studies in twins have shown that lifestyle and biological aging are largely inherited,” Kankaanpää says. “Our study suggests that genetics may underlie the link between unhealthy behaviors and accelerated aging.” 

Overall, the clocks suggested that individuals in the two groups classified as having unhealthy behaviours were, on average, 1.7 to 3.3 years older than individuals who reported more healthy lifestyles during their adolescence. Image is in the public domain

The study benefits from having a large sample size, extended follow-up on participants, and the inclusion of individuals with shared genetic backgrounds. However, because the teens reported their activities themselves, the authors say that some falsely reported having healthy behaviors to appear more virtuous, which may have skewed some of the results. 

More studies are needed to fully disentangle the role that genetics play in lifestyle habits and how these habits in turn affect biological aging in adolescents. Genes that contribute to obesity or substance use may directly cause accelerated biological aging, or the genes may indirectly accelerate aging by contributing to harmful behaviors that cause cell damage. 

“Learning more about the aging process and the role of genetics in it may help us identify individuals early in life who may be at risk of unhealthy behaviors during adolescence or who may be prone to faster aging and related diseases later in life,” concludes senior author Elina Sillanpää, Associate Professor at the Gerontology Research Center, University of Jyväskylä.

“Early identification of at-risk individuals may allow earlier intervention to change behaviors and prevent poor health outcomes later in life.” 

About this epigenetics and neurodevelopment research news

Author: Emily Packer
Source: eLife
Contact: Emily Packer – eLife
Image: The image is in the public domain

See also

Original Research: Open access.
“The role of adolescent lifestyle habits in biological aging: A prospective twin study” by Anna Kankaanpää et al. eLife


Abstract

The role of adolescent lifestyle habits in biological aging: A prospective twin study

Background:

Adolescence is a stage of fast growth and development. Exposures during puberty can have long-term effects on health in later life. This study aims to investigate the role of adolescent lifestyle in biological aging.

Methods:

The study participants originated from the longitudinal FinnTwin12 study (n = 5114). Adolescent lifestyle-related factors, including body mass index (BMI), leisure-time physical activity, smoking, and alcohol use, were based on self-reports and measured at ages 12, 14, and 17 years. For a subsample, blood-based DNA methylation (DNAm) was used to assess biological aging with six epigenetic aging measures in young adulthood (21–25 years, n = 824). A latent class analysis was conducted to identify patterns of lifestyle behaviors in adolescence, and differences between the subgroups in later biological aging were studied. Genetic and environmental influences on biological aging shared with lifestyle behavior patterns were estimated using quantitative genetic modeling.

Results:

We identified five subgroups of participants with different adolescent lifestyle behavior patterns. When DNAm GrimAge, DunedinPoAm, and DunedinPACE estimators were used, the class with the unhealthiest lifestyle and the class of participants with high BMI were biologically older than the classes with healthier lifestyle habits. The differences in lifestyle-related factors were maintained into young adulthood. Most of the variation in biological aging shared with adolescent lifestyle was explained by common genetic factors.

Conclusions:

These findings suggest that an unhealthy lifestyle during pubertal years is associated with accelerated biological aging in young adulthood. Genetic pleiotropy may largely explain the observed associations.

Funding:

This work was supported by the Academy of Finland (213506, 265240, 263278, 312073 to J.K., 297908 to M.O. and 341750, 346509 to E.S.), EC FP5 GenomEUtwin (J.K.), National Institutes of Health/National Heart, Lung, and Blood Institute (grant HL104125), EC MC ITN Project EPITRAIN (J.K. and M.O.), the University of Helsinki Research Funds (M.O.), Sigrid Juselius Foundation (J.K. and M.O.), Yrjö Jahnsson Foundation (6868), Juho Vainio Foundation (E.S.) and Päivikki and Sakari Sohlberg foundation (E.S.).

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The ovarian “biological clock” and other reproductive health metaphors science got wrong

There is a lot scientists still don’t know about the female reproductive system. They don’t know enough about how to treat the most common vaginal infection, bacterial vaginosis. They don’t have good solutions for many people suffering from endometriosis, a common and sometimes incredibly painful condition where tissue similar to what grows inside the uterus grows elsewhere in the body. They still have a lot of questions about what menopause does to a body.

So a few years ago, Rachel Gross, a science reporter who focuses on reproductive health, set out to write a book about the mysteries of the female reproductive system. But as she dove into the research, she started to wonder about the phrase she was using — the phrase “female reproductive system.”

First, not everyone with the organs she was researching was female. She was speaking to nonbinary people, intersex people, trans people; all people for whom this anatomy was relevant and intimate.

Also, the idea that these organs — the clitoris, the vagina, even the ovaries — were only playing a role in reproduction started to feel reductive. Of course, these organs are involved in baby-making, but, she says, “I was finding that they were doing so much else, not just sexual stuff, which is huge and often overlooked, but they were participating in immunity and protection and regeneration.”

On Unexplainable — Vox’s podcast that explores big mysteries, unanswered questions, and all the things we learn by diving into the unknown — Gross talks about one of these organs: the ovaries. She tells us a familiar story: that the ovaries are “biological clocks” that only lose eggs, without ever gaining any back. But then, she walks us through new research that questions that idea, suggesting that the ovaries may be able to generate new eggs using stem cells.

And, as Gross explains, this new way of understanding and imagining the ovaries might lead to new fertility treatments — but also, potentially, new ways to treat some of the health effects associated with menopause, like loss of bone density.

In her book, Vagina Obscura: An Anatomical Voyage, Gross finds many examples of metaphors like the ovarian “ticking clock,” or even whole stories about various pelvic organs, that have stymied science and maybe even kept scientists from solving some of the big questions about these organs.

“When you study the human body, even though the human body is not changing, you really see what you expect to see … and you kind of just blur out the rest,” she says.

I asked Gross to walk me through some more examples from her book. What follows is our conversation, edited for clarity and length.

Byrd Pinkerton

What’s an example of an organ we’ve told an incorrect story about and how it misguided science?

Rachel Gross

So one big example is the clitoris. It has been called a minuscule phallus or an underdeveloped penis or a tiny nub for hundreds and hundreds of years. And science has sort of minimized it in many ways, from literally omitting it in anatomical textbooks to just not studying 90 percent of it, which is under the surface.

It took a female urologist to say, “Wait, the research on the female side is a lot less rigorous than the male side. We haven’t looked at all the nerves, the erectile bodies.”

She found out that the clitoris has these roots and these bulbs that actually hug the vagina and swell with blood and become erectile just like the penis. So you have the exact same erectile tissues, you have the head — or the glans clitoris — which is the part you can see and touch. But then you also have a shaft that goes back into the body and you have bulbs and kind of arms that flow back into the pelvis. And all of these are made up with the same erectile tissues as the penis.

These things are super important for women undergoing surgery in this area who don’t want their nerves cut off.

If you look at it [the clitoris] as a homologous organ [to the penis], you come to such a different conclusion than it’s a tiny phallus or a little nub that’s hard to find.


This video digs into another misleading story scientists told for decades — this one about the role the sperm and egg play in fertilization.

Byrd Pinkerton

[At the beginning of her book, Rachel Gross describes a personal experience. She got a persistent vaginal infection, and her gynecologist recommended that she put boric acid in her vagina. The poison would kill a lot of the organisms in her vagina, including, hopefully, the one causing her problems.

Boric acid is also used as a rat poison, however, so the harshness of the treatment surprised Gross. And as she dived into the research, she realized that a new way of imagining the vagina might lead to more effective, less poisonous treatments.]

You talked about putting this boric acid pill into your vagina. Is that treatment based on any outdated story or a metaphor around the vagina that people are reconsidering?

Rachel Gross

So I think there’s been a strong attitude toward the vagina of like … it should be pure, it should be clean, it should be sterile. And from that you get all of these vaginal cleansing products. What blew my mind was looking at the vaginal microbiome as this teeming ecosystem of protection instead.

Byrd Pinkerton

What is the vaginal microbiome?

Rachel Gross

So, you’ve heard of the gut microbiome, the specific bacteria that help maintain digestive health.

Byrd Pinkerton

Yep.

Rachel Gross

Well, your vagina also has a microbiome, and it’s actually really unique to humans. It’s a mildly acidic environment created by mostly bacteria called lactobacilli, but also other bacteria, some viruses, and fungi. And they all live in harmony and protect you from invaders and kind of keep this liminal space between you and not-you healthy. It’s up against whatever gets up there, whether that is tampons, semen, birth control, jade eggs, other stuff you put in there … like your vagina is responding, protecting you and reaching a new equilibrium.

Byrd Pinkerton

Interesting. So if you’re thinking of that space as like a garden that fends off invaders, it does feel like you would reimagine putting rat poison in the middle of your garden.

Rachel Gross

Exactly. If you reimagine it as a garden and it’s fine to have weeds and different species in a garden, then it’s not about stripping it of life, which is what the rat poison does. It’s about cultivating the right mix. And that has led to innovations in vaginal microbiome transplants or probiotics that could kind of terraform the vagina. All these different ideas, it’s not clear that all of them will work, but there’s just so many smarter and more imaginative ways to think of having a healthy vagina.

Byrd Pinkerton

So, do we know anything about our bodies? Or is it all just sort of stories we’re telling ourselves that are shaping the directions that we’re taking?

Rachel Gross

I do think that we know a lot about bodies and we use that knowledge very practically in medicine to heal them and make things better. But there’s a lens of language that just directs the questions we’re asking and what we consider interesting and worthwhile. So could you swing that lens a little to the left, to the part that’s all blurred out, and focus on that? And what would you see?

Byrd Pinkerton

How do you swing the lens and reshape what we know about the reproductive system?

Rachel Gross

By introducing new people with new backgrounds into science and having them ask their questions and be interested in what they’re interested in. And for a long time, we’ve had a very similar lens.

You had people that were centering the male body as representing something and looking at the female body as an afterthought or as something that was mainly involved in reproduction. That’s mainly the interesting difference between types of bodies. So yeah, my whole book is about how once you get new voices and people in science, the whole lens changes in really exciting ways.

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Alzheimer’s Disease Affects Most Known Biological Pathways in the Brain

Summary: Out of 341 known biological pathways, 91% are linked to Alzheimer’s disease.

Source: Beth Israel Deaconess Medical Center

Nearly 6 million older adults have Alzheimer’s disease in the United States, a number expected to double by 2050.

Already the sixth leading cause of death, Alzheimer’s disease is a complex neurodegenerative disease that causes memory loss, confusion, poor judgment, depression, delusions and agitation that robs people of their ability to live independently.

Currently, the biological mechanisms underlying Alzheimer’s disease are poorly understood; as a result, there are few effective treatments and no cure for the disease.

In a recent study, a research team led by scientists at Beth Israel Deaconess Medical Center (BIDMC) conducted a systematic assessment of more than 200,000 scientific publications to understand the breadth and diversity of biological pathways—key molecular chain reactions that drive changes in cells—that contribute to Alzheimer’s disease by research over the last 30 years.

The team found that, while nearly all known pathways have been linked to the disease, the most frequently associated biological mechanisms—including those related to the immune system, metabolism and long-term depression—have not significantly changed in 30 years, despite major technological advances.

The scientists’ work, published in Frontiers in Aging Neuroscience, will advance research into the mechanisms of neurodegeneration.

“The burden of Alzheimer’s disease is steadily increasing, driving us towards a neurological epidemic,” said Winston A. Hide, Ph.D., director of the Precision RNA medicine Core Facility at BIDMC and an associate professor of medicine at Harvard Medical School.

“Our findings suggest that not only is this disorder incredibly complex, but that its pathology includes most known biological pathways. This means that the disease’s effects are far broader in the body than we realized.”

The team performed an exhaustive text search of 206,324 pathway-specific dementia publication abstracts published since 1990. Next, they looked at 341 known biological pathways and determined how many publications linked a given pathway to the disease.

The researchers found that 91 percent of pathways—all but seven—were linked to Alzheimer’s disease. Nearly half of the pathways were linked to Alzheimer’s disease in more than 100 scientific papers.

The team found that, while nearly all known pathways have been linked to the disease, the most frequently associated biological mechanisms—including those related to the immune system, metabolism and long-term depression—have not significantly changed in 30 years, despite major technological advances. Image is in the public domain

They also found that the top-ranked 30 pathways most frequently referred to in literature remained relatively consistent over the last 30 years suggesting that most studies of the disease have focused on a small subset of all the known disease-associated pathways.

“Clinical trials aiming to either delay the onset or slow the progression of Alzheimer’s disease have largely failed,” said study first author Sarah Morgan, a postdoctoral researcher at BIDMC during the extent of this research and now a lecturer at Queen Mary University of London.

“Given that an unexpected diversity of pathways is associated with Alzheimer’s disease, a wide range of disease processes are not being successfully targeted in clinical trials. We hypothesize that comprehensively targeting more of the associated underlying mechanisms in Alzheimer’s disease will increase the chances of success in future drug trials.”

About this Alzheimer’s disease research news

Author: Press Office
Source: Beth Israel Deaconess Medical Center
Contact: Press Office – Beth Israel Deaconess Medical Center
Image: The image is in the public domain

Original Research: Open access.
“Most Pathways Can Be Related to the Pathogenesis of Alzheimer’s Disease” by Sarah L. Morgan et al. Frontiers in Neuroscience


Abstract

See also

Most Pathways Can Be Related to the Pathogenesis of Alzheimer’s Disease

Alzheimer’s disease (AD) is a complex neurodegenerative disorder. The relative contribution of the numerous underlying functional mechanisms is poorly understood.

To comprehensively understand the context and distribution of pathways that contribute to AD, we performed text-mining to generate an exhaustive, systematic assessment of the breadth and diversity of biological pathways within a corpus of 206,324 dementia publication abstracts.

A total of 91% (325/335) of Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways have publications containing an association via at least 5 studies, while 63% of pathway terms have at least 50 studies providing a clear association with AD.

Despite major technological advances, the same set of top-ranked pathways have been consistently related to AD for 30 years, including ADimmune systemmetabolic pathwayscholinergic synapselong-term depressionproteasomediabetescancer, and chemokine signaling. AD pathways studied appear biased: animal model and human subject studies prioritize different AD pathways.

Surprisingly, human genetic discoveries and drug targeting are not enriched in the most frequently studied pathways.

Our findings suggest that not only is this disorder incredibly complex, but that its functional reach is also nearly global. As a consequence of our study, research results can now be assessed in the context of the wider AD literature, supporting the design of drug therapies that target a broader range of mechanisms.

The results of this study can be explored at www.adpathways.org.

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Finding the Biological Roots for the Pathological Social Withdrawal Known as ‘Hikikomori’

Summary: Hikikomori is a mental health disorder identified as a pathological social withdrawal. Researchers have discovered a number of biomarkers in the blood associated with hikikomori.

Source: Kyushu University

Researchers at Kyushu University have identified a number of key blood biomarkers for pathological social withdrawal, known as hikikomori.

Based on their findings, the team was able to distinguish between healthy individuals and hikikomori patients as well as determine the severity of the condition.

According to Japan’s Ministry of Health, Labour, and Welfare, hikikomori is a condition in which individuals do not leave their dwelling and isolate themselves away from society and family for a period exceeding six months.

Also identified as “pathological social withdrawal,” hikikomori is estimated to afflict more than one million people in Japan today.

While it has been historically identified as a Japanese culture-bound syndrome, evidence over the last few decades has shown that it is becoming a global phenomenon, with some fearing the COVID-19 pandemic catalyzing a global wave of hikikomori patients.

In 2013, the Kyushu University Hospital established the world’s first outpatient clinic for hikikomori research in hopes of developing support systems for patients through biological, psychological, and social understanding of the condition.

In a report published in Dialogues in Clinical Neuroscience, lead researcher Takahiro A. Kato of Kyushu University’s Faculty of Medical Sciences explains that while the sociological underpinnings of the condition are carefully studied, major gaps remain in the understanding of the biological aspects of hikikomori.

“Mental illnesses such as depression, schizophrenia, and social anxiety disorder are occasionally observed in hikikomori individuals. However, our past research shows that it is not that simple, and that it is a complex condition with overlaps of different psychiatric and non-psychiatric elements,” explains Kato.

“Understanding what happens biologically will help us greatly in identifying and treating hikikomori.”

The team conducted blood biochemical tests and collected data on the plasma metabolome—small molecules found in blood such as sugars, amino acids, and proteins—from 42 unmedicated hikikomori individuals and compared it with data from 41 healthy volunteers. In total, data for 127 molecules were analyzed.

“Some of our key findings showed that, in the blood of men with hikikomori, ornithine levels and serum arginase activity were higher while bilirubin and arginine levels were lower,” states first author of the paper Daiki Setoyama.

“In both men and women patients, long-chain acylcarnitine levels were higher. Moreover, when this data was further analyzed and categorized, we were able to distinguish between healthy and hikikomori individuals, and even predict its severity.”

Ornithine is an amino acid produced from the amino acid arginine with the help of the enzyme arginase. These molecules are vital in many bodily functions, including blood pressure regulation and the urea cycle.

Bilirubin is made when the liver breaks down red blood cells and is often used as a marker for proper liver function. Patients with major depression and seasonal affective disorder have been reported to have lower blood bilirubin levels.

While it has been historically identified as a Japanese culture-bound syndrome, evidence over the last few decades has shown that it is becoming a global phenomenon, with some fearing the COVID-19 pandemic catalyzing a global wave of hikikomori patients. Image is in the public domain

Finally, acylcarnitines play an important role in supplying energy to the brain. Its levels decrease when patients with depression take selective serotonin reuptake inhibitors.

However, patients with hikikomori differ from patients with depression in that only the long-chain acylcarnitines are elevated in hikikomori whereas short-chain acylcarnitines remain the same.

Says Kato, “Identifying the biomarkers of hikikomori is the first step in uncovering the biological roots of the condition and connecting them to its severity. We hope these findings will lead to better specialized treatments and support for hikikomori.”

See also

“Many questions remain, including understanding the root causes behind these biomarkers. Today, hikikomori is spreading worldwide, thus, we must conduct international investigations to understand the similarities and differences between patients with hikikomori globally,” he concludes.

About this psychology research news

Author: Press Office
Source: Kyushu University
Contact: Press Office – Kyushu University
Image: The image is in the public domain

Original Research: Open access.
“Blood metabolic signatures of hikikomori, pathological social withdrawal” by Daiki Setoyama et al. Dialogues in Clinical Neuroscience


Abstract

Blood metabolic signatures of hikikomori, pathological social withdrawal

Background

A severe form of pathological social withdrawal, ‘hikikomori,’ has been acknowledged in Japan, spreading worldwide, and becoming a global health issue. The pathophysiology of hikikomori has not been clarified, and its biological traits remain unexplored.

Methods

Drug-free patients with hikikomori (n = 42) and healthy controls (n = 41) were recruited. Psychological assessments for the severity of hikikomori and depression were conducted. Blood biochemical tests and plasma metabolome analysis were performed. Based on the integrated information, machine-learning models were created to discriminate cases of hikikomori from healthy controls, predict hikikomori severity, stratify the cases, and identify metabolic signatures that contribute to each model.

Results

Long-chain acylcarnitine levels were remarkably higher in patients with hikikomori; bilirubin, arginine, ornithine, and serum arginase were significantly different in male patients with hikikomori. The discriminative random forest model was highly performant, exhibiting an area under the ROC curve of 0.854 (confidential interval = 0.648–1.000). To predict hikikomori severity, a partial least squares PLS-regression model was successfully created with high linearity and practical accuracy. In addition, blood serum uric acid and plasma cholesterol esters contributed to the stratification of cases.

Conclusions

These findings reveal the blood metabolic signatures of hikikomori, which are key to elucidating the pathophysiology of hikikomori and also useful as an index for monitoring the treatment course for rehabilitation.

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A Reliable and Renewable Biological Photovoltaic Cell

This system, containing blue-green algae, powered a microprocessor continuously for a year using nothing but ambient light and water. Credit: Paolo Bombelli

Algae-Powered Computing

Scientists used a widespread species of blue-green algae to power a microprocessor continuously for a year — and counting — using nothing but ambient light and water. Their system has the potential as a reliable and renewable way to power small electronic devices.

The system, comparable in size to an AA battery, contains a type of non-toxic algae called Synechocystis that harvests energy naturally from the sun through photosynthesis. The tiny electrical current this generates then interacts with an aluminum electrode and is used to power a microprocessor.

“Our photosynthetic device doesn’t run down the way a battery does because it’s continually using light as the energy source.” — Chris Howe

The system is made of ordinary, inexpensive, and mostly recyclable materials. This means it could easily be replicated hundreds of thousands of times to power large numbers of small devices as part of the Internet of Things. The researchers say it is likely to be most useful in off-grid situations or remote locations, where small amounts of electrical power can be very beneficial.

“The growing Internet of Things needs an increasing amount of power, and we think this will have to come from systems that can generate energy, rather than simply store it like batteries,” said Professor Christopher Howe in the University of Cambridge’s Department of Biochemistry, joint senior author of the paper.

He added: “Our photosynthetic device doesn’t run down the way a battery does because it’s continually using light as the energy source.”

In the experiment, the device was used to power an Arm Cortex M0+, which is a microprocessor used widely in Internet of Things devices. It operated in a domestic environment and semi-outdoor conditions under natural light and associated temperature fluctuations, and after six months of continuous power production the results were submitted for publication.

The study is published on May 12, 2022, in the journal Energy & Environmental Science.

“We were impressed by how consistently the system worked over a long period of time – we thought it might stop after a few weeks but it just kept going,” said Dr. Paolo Bombelli in the University of Cambridge’s Department of Biochemistry, first author of the paper.

The algae does not need feeding, because it creates its own food as it photosynthesizes. And despite the fact that photosynthesis requires light, the device can even continue producing power during periods of darkness. The researchers think this is because the algae processes some of its food when there’s no light, and this continues to generate an electrical current.

The Internet of Things is a vast and growing network of electronic devices — each using only a small amount of power — that collect and share real-time data via the internet. Using low-cost computer chips and wireless networks, many billions of devices are part of this network — from smartwatches to temperature sensors in power stations. This figure is expected to grow to one trillion devices by 2035, requiring a vast number of portable energy sources.

The researchers say that powering trillions of Internet of Things devices using lithium-ion batteries would be impractical: it would need three times more lithium than is produced across the world annually. And traditional photovoltaic devices are made using hazardous materials that have adverse environmental effects.

The work was a collaboration between the University of Cambridge and Arm, a company leading the design of microprocessors. Arm Research developed the ultra-efficient Arm Cortex M0+ testchip, built the board, and set up the data-collection cloud interface presented in the experiments.

Reference: “Powering a microprocessor by photosynthesis” by P. Bombelli, A. Savanth, A. Scarampi, S. J. L. Rowden, D. H. Green, A. Erbe, E. Årstøl, I. Jevremovic, M. F. Hohmann-Marriott, S. P. Trasatti, E. Ozer and C. J. Howe, 12 May 2022, Energy & Environmental Science.
DOI: 10.1039/D2EE00233G

The research was funded by the National Biofilms Innovation Center.



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Stop the Clocks: Brisk Walking May Slow Biological Aging Process

Summary: A new study found a causal link between brisk walking and telomere length. Researchers found that 10 minutes of brisk walking per day was associated with longer life expectancy, and brisk walkers have up to 20 years’ greater life expectancy than those who walk slowly.

Source: University of Leicester

A new study of genetic data published today (Wednesday) of more than 400,000 UK adults has revealed a clear link between walking pace and a genetic marker of biological age.

Confirming a causal link between walking pace and leucocyte telomere length (LTL) – an indicator of biological age – the Leicester-based team of researchers estimate that a lifetime of brisk walking could lead to the equivalent of 16 years younger biological age by midlife.

Researchers from the University of Leicester at the National Institute for Health Research (NIHR) Leicester Biomedical Research Centre studied genetic data from 405,981 middle-aged UK Biobank participants and found that a faster walking pace, independent of the amount of physical activity, was associated with longer telomere.

Telomeres are the ‘caps’ at the end of each chromosome, and hold repetitive sequences of non-coding DNA that protect the chromosome from damage, similar to the way the cap at the end of a shoelace stops it from unravelling.

Each time a cell divides, these telomeres become shorter – until a point where they become so short that the cell can no longer divide, known as ‘replicative senescence’. Therefore, scientists consider LTL a strong marker for ‘biological age’, independent from when an individual was born.

Although the relationship between telomere length and disease is not fully understood, the build-up of these senescent cells is believed to contribute to a range of symptoms we associate with aging, such as frailty and age-related diseases.

While the physical, mental, social and health benefits of walking are well-documented, this study is one of the first of its kind to compare genetic data with both self-reported walking speeds, as well as actual measurements of movement intensity from wearable activity tracking devices worn by participants.

Dr Paddy Dempsey is a Lecturer and Research Fellow at the University of Leicester and within the NIHR Leicester Biomedical Research Centre, part of the University Hospitals of Leicester (UHL) NHS Trust, and lead author on the study published in Communications Biology. He said:

“Previous research on associations between walking pace, physical activity and telomere length has been limited by inconsistent findings and a lack of high-quality data.

“This research uses genetic data to provide stronger evidence for a causal link between faster walking pace and longer telomere length. Data from wrist-worn wearable activity tracking devices used to measure habitual physical activity also supported a stronger role of habitual activity intensity (e.g. faster walking) in relation to telomere length.

“This suggests measures such as a habitually slower walking speed are a simple way of identifying people at greater risk of chronic disease or unhealthy ageing, and that activity intensity may play an important role in optimising interventions.

For example, in addition to increasing overall walking, those who are able could aim to increase the number of steps completed in a given time (e.g. by walking faster to the bus stop). However, this requires further investigation.”

Although the relationship between telomere length and disease is not fully understood, the build-up of these senescent cells is believed to contribute to a range of symptoms we associate with aging, such as frailty and age-related diseases. Image is in the public domain

Researchers from the University of Leicester have previously shown using UK Biobank that as little as 10 minutes of brisk walking a day is associated with longer life expectancy, and that brisk walkers have up to 20 years’ greater life expectancy compared to slow walkers.

This new study demonstrates a causal link between brisk walking and telomere length and, significantly, not the other way round.

Tom Yates, senior author and Professor of Physical Activity, Sedentary Behaviour and Health at the University of Leicester and NIHR Leicester Biomedical Research Centre, added:

“Whilst we have previously shown that walking pace is a very strong predictor of health status, we have not been able to confirm that adopting a brisk walking pace actually causes better health. In this study we used information contained in people’s genetic profile to show that a faster walking pace is indeed likely to lead to a younger biological age as measured by telomeres.”

Funding: The study was funded by the UK Medical Research Council, Biotechnology and Biological Sciences Research Council, British Heart Foundation, and supported by the NIHR Leicester BRC – a partnership between Leicester’s Hospitals, the University of Leicester and Loughborough University.

About this aging research news

Author: Jonathan Whitney
Source: University of Leicester
Contact: Jonathan Whitney – University of Leicester
Image: The image is in the public domain

Original Research: Open access.
“Investigation of a UK biobank cohort reveals causal associations of self-reported walking pace with telomere length” by Paddy Dempsey et al. Communications Biology


Abstract

See also

Investigation of a UK biobank cohort reveals causal associations of self-reported walking pace with telomere length

Walking pace is a simple and functional form of movement and a strong predictor of health status, but the nature of its association with leucocyte telomere length (LTL) is unclear.

Here we investigate whether walking pace is associated with LTL, which is causally associated with several chronic diseases and has been proposed as a marker of biological age. Analyses were conducted in 405,981 UK Biobank participants.

We show that steady/average and brisk walkers had significantly longer LTL compared with slow walkers, with accelerometer-assessed measures of physical activity further supporting this through an association between LTL and habitual activity intensity, but not with total amount of activity. Bi-directional mendelian randomisation analyses suggest a causal link between walking pace and LTL, but not the other way around.

A faster walking pace may be causally associated with longer LTL, which could help explain some of the beneficial effects of brisk walking on health status.

Given its simple measurement and low heritability, self-reported walking pace may be a pragmatic target for interventions.

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Russia calls U.N. meeting alleging U.S. “military biological activities” in Ukraine — U.S. calls it “false flag effort”

United Nations – Russia hastily called a Friday morning U.N. Security Council meeting late on Thursday evening to discuss in open debate what it called “the military biological activities of the US on the territory of Ukraine” — leading the Biden administration to immediately denounce it as a “false flag effort.”

In a comment sent to CBS News, Olivia Dalton, spokesperson for the U.S. Mission to the United Nations, said, “We’re not going to let Russia gaslight the world or use the UN Security Council as a venue for promoting their disinformation.”

“Russia has a well-documented history of using chemical weapons and has long maintained a biological weapons program in violation of international law,” Dalton said, adding, “Russia also has a track record of falsely accusing the West of the very violations that Russia itself is perpetrating.”

“This is exactly the kind of false flag effort we have warned Russia might initiate to justify a biological or chemical weapons attack,” she said.

The Friday meeting was announced by Russia’s Deputy U.N. Ambassador Dmitry Polyansky in a tweet linking to the Russian Ministry of Defense, claiming analysis of documents about U.S. “military biological activities” in Ukraine, with a half-dozen documents attached with graphs and charts.

Washington had warned earlier this week that Russia could escalate the violence in its war in Ukraine with the use of biological or chemical weapons, or by claiming Ukrainian forces used them as a pretext.

White House press secretary Jen Psaki on Wednesday dismissed Russia’s claims as “preposterous” and suggested Russia may be laying the groundwork for using such weapons itself. “This is all an obvious ploy by Russia to try to try to justify its further premeditated, unprovoked, and unjustified attack on Ukraine.”

Pentagon spokesman John Kirby also refuted the claims as “absurd” and “classic Russian propaganda.”

“They’re laughable,” Kirby said Wednesday. “We are not, not developing biological or chemical weapons inside Ukraine. It’s not happening.”

The Friday meeting will hear briefings from U.N. disarmament chief Izumi Nakamitsu and Under Secretary General Rosemary DiCarlo, a former U.S. Mission to the U.N. Ambassador-rank official.



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