The benefits were even greater when strength training was combined with aerobic exercise. However, researchers found no additional advantage from doing more than 120 minutes of strength training per week. That level of exercise was linked to a 19% lower risk of death from cardiovascular disease and a 27% lower risk of death from neurological disease.

Strength Training and Long-Term Health

While the life-extending benefits of aerobic exercise are well established, the impact of muscle-strengthening activities on overall mortality and specific causes of death has been less clear. Researchers wanted to determine whether strength training alone, or combined with aerobic exercise, could influence those risks.

To investigate, they analyzed data collected over three decades from three major studies: the Health Professionals Follow-up Study (1992-2022), the Nurses’ Health Study (2002-21), and the Nurses’ Health Study II (2003-21). Together, the studies included 147,374 participants (31,540 men and 115,834 women).

Every two years, participants reported how much time they spent each week doing strength training and aerobic exercise. Aerobic activities included brisk walking, running, jogging, swimming, cycling, tennis, squash, strenuous outdoor work, and stair climbing. Strength training included exercises using weights or body weight, such as press ups, squats, and lunges.

At the start of the study, participants were an average of 54 years old. Those who reported higher levels of strength training were generally younger, weighed less, followed healthier lifestyles, and engaged in more aerobic activity than those who did no strength training.

What the Researchers Found

About three quarters (74%) of participants exceeded the recommended 150 minutes of moderate intensity aerobic exercise per week, equivalent to 7.5 MET hours over the long term. METs measure how many calories are burned during physical activity compared with resting.

Nearly half (46%) of participants reported doing some form of strength training.

Over the 30-year follow-up period, 35,798 participants died. Researchers found that higher long-term levels of weekly strength training were associated with a lower risk of death.

After accounting for other factors that could affect the results, participants who performed 90-119 minutes of strength training per week had a 13% lower risk of death from any cause. No additional reduction in risk was observed above 120 minutes per week.

That same 90-119 minute range was also associated with a 19% lower risk of death from cardiovascular disease and a 27% lower risk of death from neurological disease.

Cancer-related benefits appeared at lower amounts of strength training. Participants who performed 1-29 minutes per week had a 21% lower risk of cancer death, while those doing 30-59 minutes per week had an 18% lower risk.

The Power of Combining Cardio and Strength Training

Compared with people who did less than 7.5 MET hours of aerobic activity per week and no strength training, participants who performed strength training alone for 1-59 minutes or 60-119 minutes per week had a 7-11% lower risk of death.

Aerobic exercise on its own also showed strong benefits. Any amount above 7.5 MET hours per week was associated with a 26-43% lower risk of death.

The lowest mortality risk was seen among people who combined high levels of aerobic exercise with strength training. Those who accumulated 30-44 MET hours of aerobic activity per week and 60-119 minutes of strength training had a 45% lower risk of death.

Even greater reductions were observed among participants who performed 45+ MET hours of aerobic activity per week. In that group, the risk of death was 53% to 58% lower regardless of how much strength training they did.

Important Limitations

The researchers emphasized that this was an observational study, meaning it cannot prove that strength training directly caused the reductions in mortality risk.

They also noted several limitations. Exercise habits were self reported, which can introduce inaccuracies. The analysis did not include certain forms of strength training, such as calisthenics and Pilates. In addition, information was not available on the duration of individual workouts or the intensity of strength training sessions, factors that could have influenced the results.

Despite those limitations, the researchers concluded:

“Our findings on different dose-response relationships between long-term resistance training with all-cause and cause-specific mortality suggest that different amounts of resistance training may be needed to optimize benefits across outcomes.

“The observed pattern that adding resistance training further reduced mortality risk across all levels of aerobic activity up to 45 MET hours/week supports current recommendations encouraging both types of activity to maximize mortality benefits.”

The parasite commonly infects coyotes, foxes, and other canids. While these animals often show no signs of illness, the tapeworm can cause severe disease in domestic dogs and humans if transmission occurs.

For decades, E. multilocularis has been recognized as a significant public health concern across parts of Europe and Asia. In North America, however, it was once considered exceptionally rare. That changed roughly 15 years ago when infections began appearing in dogs and people in Canada and the Midwest, signaling that the parasite was expanding its range.

Tapeworm Found in Pacific Northwest Coyotes

Researchers from the University of Washington surveyed 100 coyotes in the Puget Sound region and discovered that 37 carried the parasite. Their findings were published in PLOS Neglected Tropical Diseases.

“This parasite is concerning because it has been spreading across North America. There have been numerous cases of dogs getting sick, and a handful of people have also picked up the tapeworm,” said lead author Yasmine Hentati, who recently graduated from the UW with a doctorate in environmental and forest science. “The fact that we found it here in one-third of our coyotes was surprising, because it wasn’t found anywhere in the Pacific Northwest until earlier this year.”

When E. multilocularis infects a person or animal, it can produce cancer-like cysts in the liver and, in some cases, other organs. Without treatment, the infection can be fatal.

How the Parasite Spreads

Despite the danger it poses, many infected animals never become ill. The parasite relies on a complex life cycle involving several different hosts.

Coyotes and other canids serve as the primary hosts for adult tapeworms. These animals can carry thousands of worms in their intestines without becoming sick. The worms release eggs that pass into the environment through feces.

Rodents are another key part of the cycle. After consuming food contaminated with coyote feces, they can become infected. The parasite eggs migrate to the rodents’ livers and develop into cysts, eventually weakening or killing the animals. Coyotes then become infected when they eat those rodents, continuing the cycle.

Humans and domestic dogs are considered accidental hosts. People can become infected by swallowing tapeworm eggs, such as through food contaminated with coyote or dog feces. Infection can lead to alveolar echinococcosis, a disease marked by slow-growing metastatic cysts. Symptoms may not appear until five to 15 years after exposure, making diagnosis and treatment particularly challenging.

Alveolar echinococcosis is considered the third most important food-borne illness globally and is listed by the World Health Organization among the top 20 neglected tropical diseases. Many countries have established extensive monitoring programs to track the disease.

Risks for Dogs and People

Dogs exposed to E. multilocularis do not always become sick. The outcome depends largely on which stage of the parasite they encounter. In many cases, dogs carry the parasite and shed eggs without developing symptoms. However, dogs exposed to parasite eggs can develop the same cancer-like cysts seen in other infected animals.

“To minimize the risk of dogs getting infected with E. multilocularis, owners should not let them prey on rodents or scavenge their carcasses,” said co-author Guilherme Verocai, an associate professor and director of the Parasitology Diagnostic Laboratory at the Texas A&M University College of Veterinary Medicine and Biomedical Sciences.

Verocai also recommends routine veterinary care, including parasite testing, as well as preventative medications for worms and ticks.

Although more than one-third of the coyotes examined in the study carried the parasite, researchers found little evidence that it has become widespread in other hosts. One study documented seven canine cases in Washington, Oregon, and Idaho since 2023, including five in Washington. Human infections remain rare in the United States, and no cases have been reported on the West Coast.

“The reason that it’s so high in coyotes is because they are regularly eating raw rodents, and that is the primary way for them to get infected. Most domestic dogs are not eating the raw livers of wild rodents,” Hentati said.

A More Infectious Variant

Reports of E. multilocularis have surfaced before in North America. Prior to the rise in cases seen during the 2010s, the parasite had been documented on remote islands in northwestern Alaska.

Researchers say those earlier cases involved a different strain than the one driving the current spread. Genetic analyses indicate the older infections were linked to a tundra variant, while today’s outbreak is associated with a more infectious strain of European origin. The coyotes examined in this study carried the newer variant, which is now believed to be the dominant form circulating in both the United States and Canada.

Scientists are still unsure how the parasite became established in North America. One possibility is that infected dogs entering the U.S. and Canada were not required to undergo deworming treatment. Another theory, proposed in earlier studies, suggests the parasite may have arrived in red foxes imported for hunting about a century ago.

“The main takeaway is that Echinococcus multilocularis is here, it’s pretty prevalent in the local coyote population and people should be aware of potential risks,” Hentati said.

Co-authors include Ellie Reese, lab manager at UW; Samantha Kreling, UW doctoral graduate in environmental and forest science; Laura Prugh, a UW professor of environmental and forest science; Chelsea Wood, a UW associate professor of aquatic and fishery science; Claire Curran of the College of William and Mary; Erika Miller of Sound Data Management; Dakeishla M. Díaz-Morales of DePaul University; and Christopher J. Schell of UC Berkeley.

The study was funded by the National Science Foundation and the University of Washington Hall Conservation Genetics Fund.

Researchers discovered that packed rice grains behave in an unusual way under pressure. When compressed slowly, the grains remain relatively strong. But when squeezed quickly, they actually become weaker. This surprising behavior has allowed scientists to create a new material that could one day be used in soft robots that automatically adjust their stiffness and protective equipment that responds differently depending on the force of an impact.

The international research team, led by the University of Birmingham, reported its findings in the journal Matter.

Rice’s Unusual Response to Pressure

Experiments showed that tightly packed rice grains respond very differently depending on how quickly a load is applied. At higher loading speeds, the material weakens significantly.

This phenomenon, known as “rate softening,” is uncommon in most materials. Researchers found that it happens because friction between individual rice grains drops sharply when forces are applied rapidly. As a result, the internal networks of forces that normally help support the load become weaker.

The team used this unusual property to develop a new metamaterial, an engineered composite structure designed to exhibit behaviors not found in naturally occurring materials.

Creating a Self-Adapting Metamaterial

To build the new material, researchers combined rice-based granular units with materials such as sand, which become stronger when subjected to rapid loading. The result was a granular metamaterial capable of responding differently to slow movements and sudden impacts.

Depending on the situation, the material can bend, buckle, or stiffen in different ways, all without electronics, sensors, or active control systems.

Dr. Mingchao Liu, from the University of Birmingham, said: “Rice might be best known as a staple food globally, but it’s rarely associated with advanced engineering. Our research shows that it can form the basis of a new class of functional materials.

“Rather than treating this phenomenon as curiosity, we turned it into a design principle. This approach enabled us to create a material that can bend, buckle, or stiffen differently under slow movements versus sudden impacts — without electronics, sensors, or active control. Instead of telling a structure how to respond, we let physics decide: fast loads trigger one behavior, slow loads another.”

The researchers say the work highlights how common granular materials can be transformed into engineered systems that respond intelligently through their own mechanical properties.

Potential Applications in Robotics and Safety Gear

The speed-sensitive metamaterial could open new possibilities in soft robotics. Unlike traditional metal robots, future systems built with these materials could be lighter, safer, and more adaptable.

Such robots could be especially useful for working alongside people, operating in challenging environments, and performing delicate tasks, including assisting with surgery.

The material may also have applications in protective equipment. Because it can respond differently depending on the speed of an impact, it could absorb energy or deform in a controlled way during a collision, helping reduce the risk of injury.

Importantly, these responses occur without the need for electronics, external power, or sensors, allowing the material itself to automatically adapt to changing conditions.

Their findings show that lower levels of phosphatidylcholine reduce the flexibility of mitochondria, accelerating age-related deterioration. The researchers also found that supplying phosphatidylcholine through diet helped restore mitochondrial function in aging laboratory organisms. The results suggest that some aspects of biological aging may be more adjustable than previously believed.

Why Mitochondria Matter in Aging

One of the biggest questions in aging research is why people tend to lose energy and vitality over time.

Mitochondria are best known for generating the energy cells need to function, but scientists now understand that they do much more. These structures also help coordinate communication within cells, support adaptation to changing conditions, and regulate many processes essential for life. They provide the energy needed for movement, growth, and tissue repair.

Although mitochondrial performance is known to decline with age, the reasons behind this gradual deterioration have remained unclear.

A Key Role for Membrane Lipids

For many years, researchers suspected that genetic damage inside mitochondria was the primary cause of their decline. However, a new study published in Nature Communications points to another important factor.

The international research team, led by Dr. Maria Ermolaeva of FLI, found that disruptions in the mitochondrial network are linked to changes in membrane composition. At the center of the discovery is phosphatidylcholine, one of the most abundant lipids found in biological membranes.

Phosphatidylcholine helps membranes remain flexible and able to reorganize when needed. This flexibility is especially important for mitochondrial fusion, a process in which individual mitochondria join together to form interconnected networks.

These networks allow cells to share and distribute vital components, including energy molecules, metabolic products, DNA, and signaling compounds. By remaining connected, mitochondria can balance resources and replace damaged parts more effectively.

The researchers discovered that phosphatidylcholine production naturally decreases with age. As levels fall, mitochondrial membranes become increasingly fragmented and dysfunctional.

When the team disabled genes involved in phosphatidylcholine production in young worms, the mitochondria quickly began to resemble those typically seen in much older animals. Even more striking, feeding the worms phosphatidylcholine or its precursor, choline, restored a more youthful mitochondrial structure within just two days.

“We were surprised ourselves by how strongly this molecule influences the structure, connectivity, and function of mitochondria,” explains Dr. Tetiana Poliezhaieva, the study’s first author.

How Aging Disrupts Cellular Energy Networks

What may seem like a small biochemical change can have widespread effects throughout the cell.

Under healthy conditions, mitochondria form a highly dynamic network that adjusts continuously to changing energy needs. As aging progresses, that network becomes less stable and less efficient.

“You can imagine the whole system as a finely branched power grid that becomes increasingly damaged with age: connections break down and currents stall,” explains Dr. Maria Ermolaeva, the study’s lead author.

“Although energy production continues, it becomes less efficient and sustainable, and energy can no longer be distributed flexibly.”

As a result, cells lose what scientists call metabolic plasticity, their ability to rapidly adapt to shifting energy demands. This adaptability is important not only for individual cells but also for tissues and entire organ systems. Reduced metabolic flexibility has increasingly been recognized as a hallmark of aging and is also associated with diseases such as diabetes.

From Worms to Human Data

To investigate the mechanisms involved, the researchers combined several different approaches.

The study included experiments in the nematode Caenorhabditis elegans, investigations using human cell cultures, and analysis of extensive clinical datasets. The team examined proteomic and lipidomic profiles, genetic variation, gene activity, and metabolic function across different stages of human aging.

By integrating these datasets, the researchers were able to connect molecular changes observed in laboratory models with patterns found in humans. Experimental validation and whole-body analyses in worms helped reveal a direct link between gradual molecular alterations and broader aging processes.

New Clues About How Aging Unfolds

The results suggest that mitochondrial aging is driven not only by accumulated genetic damage but also by age-related changes in lipid production.

This expands current understanding of why mitochondria become less effective over time and highlights membrane lipid dynamics as another important factor in the aging process.

The study also revealed that aging may occur in distinct stages rather than as one continuous process. According to the data, cells first experience a decline in stress resistance and disruptions in protein homeostasis, the system responsible for maintaining protein stability. Metabolic changes follow, with epigenetic alterations appearing later.

Researchers also observed sex-specific differences in lipid metabolism. Human metabolomic data showed the most pronounced relative decline in phosphatidylcholine levels among women around the time of menopause.

“This observation is particularly noteworthy, as it coincides with a time when many women report a significant decline in energy levels and the onset of persistent fatigue,” adds Dr. Ermolaeva.

Can Diet Help Slow Cellular Aging?

Perhaps the most significant finding was that some age-related mitochondrial changes appeared reversible.

When phosphatidylcholine levels were increased in older C. elegans, mitochondrial networks became more stable and energy production improved. The results indicate that targeted metabolic interventions may help preserve cellular function and extend the period of healthy aging.

“Our work shows that both mitochondrial aging and broader systemic aging are, at least in part, modifiable. If we understand the underlying processes, we may be able to take targeted countermeasures,” summarizes Dr. Ermolaeva.

Additional research will be needed to determine whether these findings can lead to therapies for humans. However, the role of nutrition is particularly intriguing, as certain dietary supplements may help support cellular health later in life.

The researchers note that phosphatidylcholine supplementation remained effective even when introduced during middle or advanced age. Overall, the findings shift attention away from the idea that aging is solely an irreversible decline and toward the possibility that some aspects of the process can be influenced, opening new avenues for promoting healthy aging.