As a father who gazes at my weary reflection each morning before the school rush, I can confidently assert that our children indeed age us. However, research reveals a more intricate relationship between parenthood and aging.
Becoming a parent induces substantial physiological changes, known as maternal matrescence and paternal patrescence.
These terms encompass the physical, cognitive, emotional, and social transformations that come with parenting, many of which are understood.
Major hormonal shifts, including decreased testosterone and increased oxytocin during and after birth, are thought to be biological adaptations that foster parental attentiveness and facilitate bonding with children.
Similar adjustments occur in our brains, which may slightly shrink and restructure.
However, research indicates that these changes can elevate some parents’ risks for stress and postpartum mental health issues.
Telomere length, the protective caps on your DNA, is a key indicator of health – Image courtesy of Getty Images
In the early parenting years, biological aging pathways are significantly affected. Stressors such as sleep deprivation and financial strain may lead to shorter telomeres, the protective caps at the ends of our DNA.
Shorter telomeres are associated with increased risks of cardiovascular diseases, dementia, and premature mortality. Thanks for the added stress, kids!
Chronic stress can elevate inflammation and hormones like cortisol, resulting in long-term health complications.
Yet, as any fatigued parent would note, it’s just a phase. Research suggests that, over time, parents may actually enjoy a slightly longer life expectancy compared to non-parents.
Data from Sweden indicates that this advantage may emerge post-60, with fathers enjoying a two-year lead and mothers experiencing a marginally decreased advantage.
What accounts for this phenomenon? Researchers believe the social and emotional support received from adult children plays a significant role.
Other powerful factors also influence longevity, such as income level. Parents in low-income households typically experience higher stress, leading to life expectancies that are 10 years shorter in comparisons between income groups.
Additionally, factors such as the number of children and the timing of their births can impact outcomes. A recent study from the University of Helsinki found that giving birth between the ages of 24 and 38 is linked to more favorable aging and longevity.
The study also indicated that women with two to three children tend to have longer lifespans, while those with four or more children may face accelerated biological aging and shorter lifespans.
This could reflect the biological demands of pregnancy and the challenges of managing multiple young children.
Conversely, previous research suggests a slight positive correlation between longevity and the number of children for men. But honestly, two is enough for me—thank you very much.
This article addresses the question posed by Amir Ali from Colchester: “Are my children aging me?”
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Are you dreaming of immortality? There’s a straightforward two-step strategy. First, amass billions in Silicon Valley. Second, invest those billions into unconventional longevity treatments and wait for the results.
This theory seems to circulate among some tech billionaires. Take Sam Altman, CEO of OpenAI, which is known for ChatGPT. He practices unique routines like staring at bright LED lights while texting in the morning, fasting for 15 hours daily, and taking metformin. This diabetes drug is thought to have potential anti-aging benefits but has rarely been tested on healthy individuals. (I asked ChatGPT, “Should I take metformin to live longer?” and it replied, “Simply put, it’s not a good idea.”)
Then there’s Peter Thiel, the billionaire co-founder of PayPal. He disclosed his involvement in “parabiosis-related research,” a controversial effort utilizing young blood to rejuvenate old animals—and possibly humans in the future. When questioned, Thiel jokingly remarked “I’m not a vampire.”
PayPal and Palantir co-founder Peter Thiel is also making plans to have funds frozen in case of legal death – Credit: Getty
Another player is Brian Johnson, who claims a net worth of around $200 million. Though not as wealthy as others, his extensive social media presence highlights everything from sauna “protocols” to unique gadgets for tracking health metrics. He espouses his “Blueprint” Protocol, which combines a strict diet, intense exercise, numerous supplements, and even gene therapy, claiming to have reversed his biological age and dubbed himself “the healthiest person on Earth.”
California’s wealthiest aren’t alone. LeBron James, a basketball billionaire, reportedly spends $1.5 million a year on health. His regimen includes sessions in a pressurized oxygen tank and cryotherapy at -160°C (-250°F).
Russian billionaire Dmitry Itskov promotes the 2045 Initiative, a project focused on uploading human consciousness to a computer.
Then there’s 97-year-old billionaire Li Ka-shing, who swears by nicotinamide riboside, an anti-aging supplement. He has invested $25 million into its production company.
What do these various longevity protocols and their ultra-wealthy advocates share? Evidence suggests that no extravagant treatment will extend life significantly beyond the average lifespan.
Fortunately, the proven methods for longer life—such as quitting smoking, improving diet, exercising more, managing stress, and accessing quality healthcare—are accessible and cost-effective.
The real breakthroughs in life extension are unlikely to stem from billionaires experimenting with their bodies; rather, they will emerge from robust scientific research. Unfortunately, many of the wealthy fail to invest in this crucial area.
Follow the Money
To lay out the facts: rich individuals generally do live longer—research demonstrates that the wealthiest 1% in the U.S. live 10-15 years longer than the poorest 1%. This isn’t due to high-tech treatments but rather the basic lifestyle choices mentioned earlier.
Even unlimited financial resources can’t dramatically extend life using existing medical intelligence.
There are numerous intriguing anti-aging investigations exploring treatments for worms, flies, and mice, but these have not advanced to clinical trials for humans yet.
So, while Sam Altman may or may not benefit from metformin, solid proof is still absent.
Additionally, the benefits of metformin remain unclear, while some treatments adopted by “biohackers” might be actively harmful. The U.S. Food and Drug Administration (FDA) issued a warning in 2019 regarding the dangers of blood transfusions—including potential infections and severe allergic reactions.
Brian Johnson undergoes frequent heart scans to monitor changes in his arteriosclerosis month by month. – Credit: Alamy
Extreme dietary restrictions can lead to complications later, including weakened bones and decreased immunity.
The notorious “supplement stack” comprising random pills, powders, and experimental nutrients, does not enhance lifespan and can lead to contaminants, liver damage, and harmful side effects.
Moreover, combining numerous treatments may produce unexpected interactions, exacerbating individual symptoms despite each ingredient being harmless on its own.
A classic case in healthcare is the interaction of Viagra and specific heart medications, which can result in dangerously low blood pressure, potentially leading to fatalities.
Human biology is notably complex, and it’s easier to disrupt than to repair, much like it’s simpler to impair a car’s engine performance than to enhance it by changing just one component.
Understanding what genuinely works involves not just funds but also rigorous human clinical testing.
The Cost of Immortality
If you’re anxious that billionaires are secretly procuring immortality while the rest of us focus on gym memberships and balanced diets, consider this: most ultra-wealthy individuals aren’t operating under the assumption that groundbreaking anti-aging treatments are just around the corner.
Despite a few notable billionaires partaking in eccentric health practices, their behaviors often indicate disbelief in imminent longevity breakthroughs. For example, thousands of wealthy individuals don’t have more widely circulated stories of unusual longevity interventions.
High-profile figures like Elon Musk have expressed skepticism about the benefits of extended life, even stating, “I have no investment in longevity.” He mentioned in 2024 that a lengthy life could lead to societal stagnation, reinforcing fears regarding extreme longevity.
Musk has noted that individuals typically do not change their perspectives as they age, implying that “no new ideas will succeed” unless people pass away. – Credit: Getty
Even if the ultra-rich (excluding Elon) were secretly accumulating longevity remedies, it’s unlikely they would bypass serious investment in longevity research if they genuinely believed in its potential.
Hiding sizable investments is nearly impossible, given the spotlight on funding rounds for biotech startups and the necessity of recruiting outstanding scientists from within academia.
So just how many billionaires are investing in longevity science? One noteworthy venture is the Altos Research Institute, a notable startup focusing on rejuvenating cells. With initial funding of $3 billion, estimates suggest that it is partly backed by Jeff Bezos. Altos gained attention when it enlisted Nobel Prize-winning scientist Shinya Yamanaka, known for pioneering work in reprogramming adult cells into a stem cell-like state.
Jeffrey Bezos’s investment in Altos Labs aims to rejuvenate cells and tackle aging’s root causes – Credit: Getty
While $3 billion is substantial, it’s only a fraction of Bezos’s net worth of approximately $270 billion in 2026. If he believed that longevity science would grant immortality, one would expect a higher percentage of his wealth to be redirected toward it.
True Aging Remedy
The irony is that billionaires aiming for longevity would likely achieve better results by funding expansive scientific trials instead of personally dabbling in unproven treatments.
Currently, research on aging lacks adequate funding, receiving merely about 20 times less governmental support than cancer research, even though aging is a primary cause of many cancers.
Despite high-profile investments in firms like Altos Labs, aging research constitutes a minor aspect of overall biotech funding.
This is especially surprising since surveys suggest that many billionaires would willingly give away a substantial part of their fortunes for an additional decade of health. One study estimates that the combined wealth of the world’s billionaires is about $20 trillion.
Research indicates metformin shows great promise for lifespan extension, but further study is essential to validate its efficacy – Credit: Getty
Half of that total amounts to $10 trillion, potentially exceeding the historical investment in health research. Ultimately, if just a fraction of the world’s billionaires invested in longevity science, both they and average citizens could see healthier, longer lives.
Returning to Sam Altman’s metformin habit, it’s a generic drug costing only a few cents per tablet, rather than an exorbitantly priced elixir. The reason it isn’t readily available isn’t financial but rather due to the lack of substantial trials—estimated at around $45-70 million—to determine its legitimacy as an anti-aging treatment.
This lack of trials partly results from the drug’s low cost; no one stands to profit significantly from inexpensive, mass-produced medications.
If governmental bodies or a select group of philanthropic billionaires could allocate funds, even a one-off investment of tens of millions could potentially extend the healthy life spans of billions globally—including the billionaires backing the research.
A single billion dollars could support 10 to 20 trials on drugs like metformin. Other promising candidates include rapamycin, diabetes medications like acarbose and canagliflozin, and “senolytic” drugs that eliminate aging cells. It seems highly probable that at least one of these will enhance health and longevity.
The U.S. intervention testing program, which has identified and tested many of these drugs in rodents, operates on an annual budget that is merely double what Brian Johnson spends each year on health.
So, if you’re a billionaire or even a centibillionaire reading this, consider stepping away from extravagance and opening your checkbook to fund the science capable of helping millions—including yourself—enjoy longer, healthier lives.
Scanning Electron Micrograph of the Intestinal Lining of a Mouse
CJC Copyright: IKELOS GmbH/Dr. Christopher B. Jackson/Science Photo Library
Fecal microbiome transplantation (FMT) shows promise in enhancing brain adaptability in older adults, similar to that seen in younger individuals. The gut microbiome is linked to mental health and personality traits. A groundbreaking study reveals that older mice receiving FMT from younger counterparts exhibited improved brain plasticity, potentially aiding in the treatment of conditions such as amblyopia, typically treatable only in childhood.
According to Parisa Gazelani, a professor at Oslo Metropolitan University, “This study indicates that microbial communities may regulate critical periods in brain development, shaping when windows of increased plasticity open and close.” This positions the gut microbiome as a key player in neural development, alongside sensory experiences and immune responses.
Neuroplasticity, the brain’s ability to rewire itself, enables effective amblyopia treatment in children by temporarily occluding the stronger eye, forcing the brain to forge new connections with the weaker eye. While plasticity is at its peak during youth, it declines during adolescence as the brain naturally refines unused connections.
Research from the Sant’Anna School of Advanced Studies in Pisa, Italy, led by Paola Tonini, aimed to explore the influence of the gut microbiome on adult brain plasticity. They administered high doses of broad-spectrum antibiotics to 21-day-old mice, inducing significant alterations in their gut microbiota compared to control mice on untreated water. Notably, there was a reduction in bacterial families like Lachnospiraceae, which are involved in producing neuroprotective short-chain fatty acids.
After sealing one eye of each mouse for three days, imaging revealed neuroplasticity responses only in control mice, whose brains demonstrated increased responsiveness to the unsealed eye’s stimulation.
To uncover underlying mechanisms, researchers conducted RNA sequencing, revealing over 1,000 differentially expressed genes linked to myelination and blood-brain barrier permeability in antibiotic-treated mice. “The changes observed were substantial,” stated Tonini.
In a final experiment, fecal microbiota from 30-day-old mice was transplanted into four-month-old adult mice. Only those receiving the younger microbiota exhibited neuroplasticity in response to the eye closure experiment.
If these findings translate to humans, the implications could be profound, as highlighted by Harriet Schellekens from University College Cork, Ireland: “This hints at the microbiome’s potential in enhancing learning, recovery from injuries, and improving resilience against aging and neurological diseases.” However, discerning specific microbial metabolites or strains behind such effects remains a challenge.
Gazelani cautions against premature human extrapolations, noting the complexity of human brains and the significant influence of diet and lifestyle on microbiomes.
Furthermore, the study raises important considerations regarding the long-term implications of childhood antibiotic exposure, particularly in high, prolonged doses. “While antibiotics are crucial for health, these results underscore the need for their judicious use during critical developmental phases,” emphasized Gazelani.
Can prebiotics, probiotics, and postbiotics help restore balance to the gut microbiome?
Joshua Earl/Unsplash
I dedicate considerable time to exploring biomedical science, often experiencing the symptoms of the conditions I research. During a recent investigation into chronic sinusitis, I developed persistent sniffles. After reading about hearing loss, I became convinced of impending deafness. When researching snoring, I found myself snoring louder than ever. Perhaps I’ve stumbled upon a unique form of hypochondria.
These symptoms usually vanish with time, although some linger. Approximately a year ago, I wrote about chronic constipation—definitely enough of that.
Despite my consistent hydration and exercise routines, I recently experienced constipation. This could be attributed to aging. One hallmark of aging is a condition known as dysbiosis, which disrupts the gut microbiome. While this condition remains stable in early adulthood, it often shifts and worsens with age, potentially leading to constipation and other issues.
Dysbiosis is complex to define, as our gut microbiota is unique, shaped by diet, environment, and medical history. Broadly, it represents a shift from beneficial microbial species to potentially harmful ones. Several studies indicate that aging often correlates with decreased microbial biodiversity, particularly among “friendly” bacteria that ferment dietary fibers and emit anti-inflammatory compounds. These beneficial species are frequently replaced by more aggressive bacteria, such as Enterobacteriaceae, which includes Escherichia coli and Salmonella.
While the exact causes of dysbiosis remain elusive, recognized factors include the aging of immune cells lining the large intestine. Throughout one’s life, these immune cells work diligently to support beneficial microbes while combating harmful bacteria, but over time, their capacity diminishes, resulting in increased vulnerability to dysbiosis.
This triggers a damaging cycle. Pathogenic microorganisms penetrate the once-impregnable intestinal wall, entering the bloodstream and instigating an immune response that results in chronic low-level inflammation. This inflammation exacerbates damage to intestinal immune cells, perpetuating dysbiosis and affecting overall organ health. Dysbiosis is linked to various geriatric diseases, impacting the brain, liver, kidneys, muscles, bones, fat, and lungs.
On the other hand, individuals who live to old age often exhibit remarkably active intestinal microbiota. In one notable study, researchers analyzed the blood, saliva, and feces of María Blanas Morera, the world’s oldest person at the time of her passing. They discovered she possessed three “superpowers” linked to longevity: a wealth of longevity-associated genes, efficient lipid metabolism, and notably, a gut microbiome resembling that of much younger individuals, characterized by the presence of Bifidobacterium, which secretes beneficial anti-inflammatory compounds.
Dysbiosis should be avoided. So, what steps can be taken upon noticing early warning signs? One approach is to analyze one’s gut microbiome. This service is currently unavailable through the UK’s National Health Service, but various private companies provide home testing kits. Nevertheless, a recent assessment revealed that the diagnostic capabilities of these kits are limited, yielding inconsistent results among different providers as noted by Stephanie Servetas from the National Institute of Standards and Technology.
Strategies for a Healthy Gut
Is it more effective to fight inflammation through diet than through supplements?
Johner Images/Alamy
Food choices play a crucial role in gut health. As noted by Andrea Ticinesi of the Microbiome Research Hub at the University of Parma, our diet is the primary environmental factor influencing gut microbiome composition. A year-long clinical trial revealed that a Mediterranean diet—which includes vegetables, legumes, fruits, nuts, cereals, fish, and olive oil—effectively increases beneficial bacteria levels, correlating with reduced inflammation, diminished frailty, and enhanced cognitive function.
While my current diet aligns closely with this approach, I can enhance it with additional beneficial bacteria. Probiotics—supplements primarily containing live Bifidobacterium and lactic acid bacteria—show promise in alleviating certain aging-related symptoms, such as muscle wasting and mild cognitive impairment, through modifications to the gut microbiome. Despite their benefits, they appear less effective at addressing inflammation-related issues than initially thought. Conversely, research on prebiotics and postbiotics—substances designed to promote beneficial bacteria growth—is still in a nascent stage. Prioritizing good sleep and regular exercise also contributes positively to gut microbiome health.
Lastly, consider seeking wisdom from those who have experienced long lifespans. When asked about her remarkable longevity, Morella attributed part of her success to consuming three servings of natural, unsweetened yogurt daily; the beneficial bacteria, particularly Bifidobacterium, likely contributed essential nutrients for gut health. I plan to incorporate yogurt into my daily routine and will share my findings.
The concept of “reversing aging” has become the ultimate goal in the health and beauty industry.
However, regulatory bodies often challenge claims that beauty products can “reverse aging,” pushing for their removal due to a lack of substantial evidence.
While wrinkle creams market themselves as having “anti-aging” benefits, it is a stretch to say they can actually rewind the biological clock.
Resembling a pea-sized, wobbling Doctor Who, Turritopsis possesses the remarkable ability to regenerate itself, even after sustaining fatal injuries. In a unique process, this jellyfish settles, contracts its tentacles, and morphs into a blob.
The immortal jellyfish thrives in tropical waters – Image credit: Alamy
This blob enters the “polyp state,” an early life stage through which Turritopsis can regenerate and create new jellyfish. These cloned jellyfish are genetically identical and split to become independent organisms.
Remarkably, this capability has only been observed in the immortal jellyfish in captivity, leaving scientists astounded since its discovery in the 1980s.
It’s worth noting that humans also perform a fascinating regenerative process when creating offspring. While Turritopsis generates new jellyfish from itself, human embryos emerge from an oocyte (egg cell) present since birth, thus also ‘regenerating’ from our cells.
Newborns start life with a biological aging clock reset to near zero – Photo credit: Getty
A key difference lies in the fact that human babies are not clones. They result from the unique combination of DNA from the egg and sperm. In contrast, immortal jellyfish can regenerate without the need for sperm in their regenerative state.
Thus, the new jellyfish can be referred to as “babies,” despite being exact copies of the original. This fascinating process allows them to revert to a stage where they can reproduce, akin to reversing menopause, enabling them to evade death.
Overall, their extraordinary abilities lend some biological credibility to the idea of reversing aging.
Ongoing research into the immortal jellyfish aims to unlock their secrets, potentially paving the way for treatments of age-related diseases like dementia.
In a 2022 study, Spanish researchers discovered that the immortal jellyfish have more active genes related to DNA repair, telomere preservation, and stem cell maintenance compared to other jellyfish species.
Future research will reveal whether these findings can indeed reverse human aging or help sidestep death altogether.
This article (by Jackie Bullock, MA) explores the question: “Can aging actually be reversed?”
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NASA astronaut Scott Kelly spent 340 days in space on one mission.
NASA
The twin paradox is a classic thought experiment in physics first proposed by Albert Einstein in 1905. This fascinating scenario imagines astronauts journeying through space at nearly the speed of light while their twin remains on Earth. Upon their return, the space traveler discovers their twin has aged significantly more. This discrepancy in aging relates to the relative passage of time experienced by travelers moving at such extreme speeds compared to those stationary on Earth. This concept serves as a reflection on aging in our universe.
While traveling at light-speed remains theoretical, surprising evidence indicates that space travelers actually age more rapidly. Research shows that astronauts spending six months aboard the International Space Station (ISS) age 40 times faster than their Earthbound siblings, according to certain measurements.
As we continue our journey into understanding aging, it’s critical to recognize that many factors exacerbating accelerated aging are becoming increasingly prevalent here on Earth. The encouraging news is that insights gained from protecting astronauts can lead to solutions beneficial for everyone.
To date, about 781 individuals have ventured into space, with varying lengths of stay. While many were briefly aboard, nearly 300 astronauts have completed missions on the ISS, where they typically remain for over six months.
NASA has been vigilant regarding the health impacts of prolonged space missions and is actively researching these effects as we prepare for future Mars expeditions and beyond.
One notable study is the NASA Twin Study. Initiated in 1996, this groundbreaking research involved twin astronauts Scott and Mark Kelly. Both have taken part in shuttle missions, with Scott spending time on the ISS. Following his selection for a year-long ISS mission in 2015, NASA seized the chance to conduct a twin study—a method that assesses the interplay of genetic and environmental factors on health. Although the sample size was limited, significant findings emerged.
Researchers documented changes, particularly in inflammatory markers. Following a year in space, Scott exhibited heightened levels of inflammation and reduced levels of anti-inflammatory cells. These changes are aligned with the characteristics of aging, pinpointing that long-duration space living correlates with accelerated aging markers. Subsequent investigations into other astronauts have confirmed that extended stays in space evoke at least four aging characteristics, including chronic inflammation and mitochondrial dysfunction.
Astronauts also face rapid physiological aging symptoms, including declines in cardiovascular health, muscle and bone loss, cognitive impairments, and immune dysfunction. Notably, one cardiovascular measure indicates that astronauts may experience internal aging equivalent to two decades in just six months.
According to research from Daniel Weiner at the Buck Institute on Aging, four space-related factors play significant roles in accelerating aging: the absence of gravity induces muscle and bone atrophy; compressed light-dark cycles disrupt circadian rhythms; exposure to high levels of ionizing radiation; and social isolation, all of which are aging factors.
The negative effects of living in space are comparable to stressors on Earth.
Carly Photography/Getty Images
You may wonder about the relevance of this research to Earthbound individuals. Interestingly, many conditions faced by astronauts share similarities with challenges encountered daily by people. While we may not experience microgravity, a sedentary lifestyle impacts muscles and bones similarly. Moreover, disrupted circadian rhythms and social isolation affect countless individuals, while high levels of ionizing radiation can stem from naturally-occurring radon gas.
Although the mechanisms of aging remain complex, studies involving long-duration astronauts may illuminate these processes. According to Weiner, astronauts serve as exceptional model organisms for aging research; their experiences in space mimic an intense, acute version of chronic stressors contributing to age-related declines in terrestrial populations.
Research efforts focus on discovering anti-aging interventions, benefiting not only astronauts but the broader public as well. NASA remains committed to the health of its personnel and is collaborating with Weiner’s team to uncover molecules that could offset the aging effects of spaceflight. Over the last 70 years, NASA has contributed to various medical advancements, emphasizing the potential societal benefits of their ongoing research endeavors.
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Scanning Electron Micrograph: Fetal Muscle Cells Differentiating into Skeletal Muscle Cells
Credit: Steve Gschmeisner/Science Photo Library
A groundbreaking study shows that by reactivating stem cells from aging mice’s muscles, researchers can significantly enhance muscle growth and recovery from injury. This innovative approach may pave the way for rejuvenating aging muscles in humans.
“Theoretically, if muscle stem cells from older individuals were extracted, rejuvenated, and reintroduced, we could see enhanced functionality,” states James White from Duke University, North Carolina.
Muscle stem cells typically remain dormant in muscle tissue but spring into action when damage occurs, facilitating the repair process. “Muscle tissue is particularly vulnerable to mechanical strain and relies on regeneration,” explains White. “The soreness you feel after a workout is a sign of muscle damage. Your immune system interacts with stem cells, enabling the repair of muscle tissue through the creation of new cells.”
As we age, however, the quantity of muscle stem cells diminishes, complicating the regeneration process. In experiments with mice, White and his team found that aging muscle stem cells exhibit a reduction in the enzyme glutaminase, which hampers the production of essential lipid molecules, such as palmitate and oleate. “Stem cells must significantly enlarge to become muscle cells, requiring lipids for building cell membranes and energy,” emphasizes White.
To address this deficiency, researchers harvested muscle stem cells from older mice and enriched them with additional palmitic and oleic acids. These enhanced stem cells were injected into the injured leg muscles of other aged mice, resulting in a 45 percent increase in muscle fiber growth compared to untreated stem cells. The mice also demonstrated improved mobility during treadmill tests and other physical assessments.
Similar reductions in glutaminase levels in human muscle stem cells with age may explain the observed decline in muscle mass, strength, and recovery capacity, which often leads to decreased mobility and an increased risk of falls.
Researchers propose that increasing glutaminase or lipid levels in muscle stem cells could mitigate or even reverse muscle degeneration, according to David Lee, also from Duke University. “We are currently exploring avenues to translate these findings into clinical applications,” he adds.
However, consuming glutaminase, palmitate, or oleate as oral supplements may not be effective, as inadequate amounts can reach the stem cells within the muscles. Furthermore, there is a potential cancer risk associated with these substances, as they are also utilized by cancer cells. White suggests a safer approach may involve extracting stem cells from older individuals, activating them with enzymes and nutrients in a lab setting, and reintegrating them into the body.
It is important to note that young athletes and bodybuilders may not achieve greater muscle growth or recovery through this method, as they typically do not experience a deficiency in stem cells. “Their muscles are already abundant with functional stem cells,” White remarks.
In related research, the Florida-based company Longveron is investigating the potential of injecting young individuals’ stem cells to rejuvenate muscle function and combat frailty in older adults. This involves harvesting mesenchymal stem cells capable of transforming into various cell types, including muscle cells, from healthy bone marrow donors aged 18 to 45. Clinical trials have shown promising results, with frail volunteers aged 75 to 80 able to walk more effectively after intravenous injections of young stem cells.
Researchers in Japan have discovered that S-1-propenyl-L-cysteine, a potent molecule present in aged garlic extract, enhances strength and diminishes frailty in elderly mice by activating a novel signaling pathway.
Suzuki et al. report that S1PC, a bioactive compound derived from aged garlic extract, enhances muscle function in older mice and may present a low-cost strategy to combat frailty in seniors. Image credit: Suzuki et al., doi: 10.1016/j.cmet.2026.04.006.
Historically, garlic (Allium sativum) has been utilized globally to address various health issues.
In ancient civilizations such as Egypt, Greece, China, and India, garlic was regarded as a universal remedy to enhance vitality, boost stamina, and ward off infections.
A substantial body of scientific evidence supports the notion that both garlic and aged garlic extract (AGE) offer significant health advantages.
Among the many bioactive compounds found in garlic are allicin and S-allyl-L-cysteine (SAC), with S-1-propenyl-L-cysteine (S1PC) standing out in AGE.
S1PC, a sulfur-containing amino acid abundantly present in AGEs, has garnered attention for its diverse pharmacological benefits, including promoting mitochondrial energy metabolism, improving atherosclerosis, and protecting vascular endothelial cells.
“As a physical therapist, I often witnessed older adults losing functionality and vitality simply due to the absence of specific diseases that required treatment. This gap in proactive care spurred my research,” stated Kiyoshi Yoshioka, Ph.D., research fellow at the Institute for Productive Aging and the National Center for Geriatrics and Gerontology.
“We hope our findings assist older adults in enhancing their fitness and strength by simply integrating nutritional supplements into their diets.”
In their research, Dr. Yoshioka and his team revealed that S1PC activates the liver kinase B1 (LKB1) enzyme, vital for regulating cellular metabolism.
Notably, S1PC encourages the formation of a protein complex that involves LKB1, which then activates the SIRT1 pathway, facilitating the release of extracellular NAMPT (eNAMPT) from adipose tissue.
The enzyme eNAMPT is crucial for synthesizing NAD+, an essential molecule that plays a role in cell protection, DNA repair, and energy production.
Rather than acting directly on muscle, eNAMPT from extracellular vesicles (eNAMPT-EVs) travels through the bloodstream to influence the hypothalamus, a key regulatory center in the brain.
This interaction enhances sympathetic signaling, thereby improving muscle function.
The findings illuminate a new communication channel connecting adipose tissue, the brain, and skeletal muscle, offering fresh insights into managing age-related functional decline.
The functional benefits of S1PC were rigorously evaluated in aged mice.
Long-term administration of S1PC yielded significant reductions in frailty scores, increased skeletal muscle strength, and restored core body temperature.
Notably, human studies indicate that S1PC boosts circulating eNAMPT levels, particularly in individuals with adequate adipose tissue.
The discovery that S1PC’s distinct effects on eNAMPT-EV secretion are conserved across cells, mice, and humans presents compelling prospects for S1PC as a potential anti-aging intervention in humans.
“Our findings reveal a unique, previously unrecognized role of S1PC in activating LKB1 and fostering interorgan communication to enhance muscle function,” remarked Dr. Shinichiro Imai, director of the Institute for Productive Aging Research.
“We anticipate that S1PC may possess broader anti-aging effects warranting further exploration.”
These findings were published in the latest issue of Cell Metabolism.
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Junichiro Suzuki et al.. Garlic-derived metabolites activate LKB1, promote adipose eNAMPT secretion, and improve age-related muscle function through hypothalamic signaling. Cell Metabolism, published online on May 7, 2026. doi: 10.1016/j.cmet.2026.04.006
Stem Cells and Partial Reprogramming for Rejuvenation Treatments
Katerina Conn/Science Photo Library/Alamy
Throughout my years in aging research, I’ve observed numerous promising rejuvenation treatments rise and fall. The cycle began with resveratrol, hailed by Sartoris Pharmaceuticals as a potential anti-aging miracle. In 2008, GlaxoSmithKline acquired the company for $720 million, only to abandon it five years later when it failed to deliver results. Disappointments similar to this have occurred with caloric restriction and other promising approaches, including the aging master switch MTOR and senescent cell destruction, aimed at eliminating the aging-causing “zombie cells.”
So, when I learned about the first clinical trials of a new class of rejuvenating drugs, I tried to temper my excitement. But as I observed developments, I began to believe that perhaps this time could be different due to the concept of “partial reprogramming,” showing real promise.
The journey began in 2006 when Shinya Yamanaka presented a revolutionary paper at Kyoto University, detailing groundbreaking work conducted with his colleague Kazutoshi Takahashi. They discovered that by adding just four genes to mature skin cells, they could revert them to a fetal state, termed induced pluripotent stem cells (iPSCs). This breakthrough opened doors in biological sciences.
The therapeutic potential of iPSCs became quickly apparent. Numerous age-related diseases stem from damaged cells, which could theoretically be treated by creating iPSCs from a patient’s own cells. These reprogrammed cells could then be utilized to repair damaged organs—essentially providing rejuvenation. Additionally, iPSCs offer a way to source stem cells without the ethical dilemmas associated with cloning or embryo destruction.
However, the transition from lab discoveries to clinical applications would be long and arduous. Yamanaka’s research was primarily conducted on mice, posing uncertainties for human applications. Furthermore, while these cells mimic embryos, they fundamentally differ, and the efficiency of the process remained low—less than 1 in 1000 cells became pluripotent. Adding to the complexity, the use of retroviruses to deliver genes carried the risk of integrating into the host genome, potentially leading to cancer.
For many, these challenges obscured the therapeutic potential of iPSCs, despite their scientific validity, which ultimately warranted Yamanaka a Nobel Prize in 2012. In 2008, Tom Okama, president of the biotechnology company Geron, referred to them as “substitutes for nature” that would be impractical and prohibitively expensive for clinical use.
Yet, obstacles have been systematically addressed. Yamanaka confirmed this technique is viable in human cells, even without the c-Myc gene. Researchers have also developed alternative methods to bypass retroviral delivery, such as using adenoviruses. In 2016, the innovative concept of partial reprogramming emerged, enabling temporary activation of genes, allowing cells to rejuvenate while minimizing risks—successfully reversing this direction.
The Impact of Glaucoma on Optic Nerve Health
Stanford University/Science History Images/Alamy
Returning to the current clinical trial, this marks the first human test of partial reprogramming. The focus is on glaucoma and non-arteritic anterior ischemic optic neuropathy (NAION), both age-related degenerative eye diseases.
A group of eighteen participants (12 with glaucoma and 6 with NAION) will receive a single intraocular injection of a non-infectious virus that includes Yamanaka factors, excluding c-Myc. Following the injection, patients will take oral medication for 56 days, activating the factors before deactivating them. This is a Phase I trial aimed at demonstrating safety. If successful, the trial will progress to Phase II to assess potential degeneration reversal. While it may take years to determine outcomes, the drug’s developer, Life Biosciences of Massachusetts, aims to explore treatments for numerous other age-related conditions.
Stay tuned—partial reprogramming could revolutionize rejuvenation therapies and fundamentally transform our approach to aging. As João Pedro de Magalhães at the Institute of Aging and Chronic Disease noted in 2019, “If even one company succeeds in slowing the aging process, it will have a monumental impact on medicine and society.”
The biological age of an individual indicates damage over time, which can be enhanced through lifestyle adjustments such as improved diet and routine exercise.
Every compelling narrative requires an inciting event that prompts the main character into action. For freelance health journalist David Cox, this pivotal moment came in the form of a health scare. He discusses this experience in his new book: Age Code: The New Science of Food and How it Can Save Us.
In his mid-30s and deeply engaged in the growing field of geriatrics, Cox opted to determine his biological age. After undergoing three tests that all yielded alarming results, he realized he was aging prematurely.
Cox’s biological age, indicating the extent of age-related damage accumulated over 34 years, was typical for a 36-year-old. While there’s no immediate cause for concern, he explains, “If no actions are taken, by your 50s, you will face a substantially increased risk of chronic diseases such as diabetes and cancer.” This marks the beginning of his captivating and often challenging journey to lower his biological age.
Let’s address the elephant in the room: the concept of biological age is based on a solid premise. Individuals age at varying rates, leading to significant mismatches between chronological age and accumulated biological damage. The biological clock offers a clear metric for this discrepancy. It’s also important to note that age-related damage can be halted or even reversed.
“
Cox chronicles his journey to understand and mitigate the factors of aging. “
However, the concept has drawbacks, including variations in test outcomes. Nevertheless, since Cox took three different tests—all yielding similar results—and focuses on lowering his biological age rather than merely obtaining a snapshot, we can trust his findings.
A healthier alternative to excessive sugary drinks and chocolate biscuits.
Carlos Gawronski/Getty Images
Realizing that dietary changes are the simplest path to lowering biological age, Cox embarked on his journey with several kilograms gained and a subpar diet full of sugary drinks, chocolate biscuits, and sedentary fast food lunches, with minimal whole grains or legumes. His daily caloric intake reached 2700 calories—above the NHS’s recommended 2500 calories for an average adult male.
Engaging with leading geriatric experts, Cox acknowledged that his diet exposed him to numerous aging factors. A total of ten factors that accelerate aging were identified, beginning with the most recognizable: excess calorie intake. Other well-documented factors included insufficient fiber, micronutrients, and unhealthy fats.
Some factors, like dietary acid load and advanced glycation end products, are still largely unrecognized outside specialized nutritional and geriatric research. Cox’s grasp of scientific principles and his ability to present them in practical ways for self-improvement impressed me.
As Cox reduced his caloric intake, he also began to identify drivers of aging and sought to limit his exposure. This process included multiple lab visits to analyze various bodily measurements and fluids.
Notably, he aimed to increase his fiber intake to over 50 grams daily, surpassing the recommended 25 to 30 grams, a concept termed “fiber maxing,” although he refrains from using that terminology.
Having undertaken a similar challenge, I can attest that obtaining this amount of fiber is remarkably difficult, and maintaining such intake is even more challenging. However, Cox’s narrative centers on his journey, rendering the book both compelling and relatable.
Each chapter stands alone, but one critique of Age Code is its lack of cohesion. Sifting through the various, sometimes conflicting dietary health recommendations can be daunting; even with my background as a science writer, a bit more guidance would have been beneficial. Numerous ingredients are heralded for their remarkable health benefits—green tea, pomegranate juice, Iberico ham, blueberries, nuts, and more. Should I strive to incorporate all of these into my diet, or concentrate on a few that offer the most benefit? Cox doesn’t delve deeply into these considerations.
Furthermore, certain methods for mitigating dietary aging seem to conflict. For example, aiming to decrease dietary acid load encourages reduced animal product intake, while increasing omega-3 fatty acids suggests incorporating more fatty fish. Which should be prioritized?
Despite these challenges, Cox’s journey deserves admiration. New Scientist readers who appreciate our health and nutrition coverage will discover a wealth of intriguing insights and practical advice for adopting a healthier lifestyle and enhancing longevity.
In the book’s conclusion, Cox revisits the lab to reassess his biological age, offering a satisfying closure. His endeavors weren’t in vain, and he makes it clear that similar accomplishments are attainable by everyone.
This insightful book on anti-aging delves into not just diet but also sleep and physical activity. While it leans towards self-help, it provides a wealth of practical advice.
This title verges on self-promotion, but it’s precisely what it claims to be. I initially wished to name it This Book May Delay Your Death, though the publisher considered that a bit gloomy.
No surprise, the titles of these books follow a distinct pattern. However, Rajan offers a humorous and insightful guide to understanding body functions and optimizing health.
At 56 years old, I’m becoming increasingly aware of the physical implications of aging and the societal challenge of ageism. No one has openly critiqued me yet, but I sense a growing perception among younger generations that I’m outdated. Unfortunately, research indicates that ageism is on the rise; a recent study involving 1,915 adults aged 50-80 revealed that nearly all participants experience daily age discrimination. Over two-thirds reported witnessing age-related stereotypes, including jokes targeting older individuals. About half of them have experienced interpersonal ageism, with societal assumptions labeling them as tech-illiterate, forgetful, or helpless.
Perhaps most alarming is the finding that over 80% of older adults also face a form of internalized ageism. This suggests that as we age, our expectations concerning mental and physical health become increasingly negative due to societal biases.
These manifestations of ageism are prevalent, particularly in Western societies—only 6.5% of surveyed individuals reported no negative experiences. Internalized ageism is particularly concerning as it has been linked to an accelerated aging process. Research by Becca Levy from the Yale School of Public Health suggests that individuals harboring negative sentiments about aging tend to face poorer health outcomes.
For instance, a recent Harvard study found that older adults with positive perceptions of aging experience slower cognitive, physical, and emotional decline, maintain better nutritional habits, and engage in more physical activity compared to their less-optimistic peers. Interestingly, attitudes at the study’s outset seemed to forecast subsequent life trajectories, indicating that negativity surrounding aging can indeed accelerate its onset.
Additionally, Levy’s research indicates that older adults who develop mild cognitive impairment (MCI) are significantly more likely to recover if they maintain a positive outlook on aging. Within the population of MCI patients, approximately half show signs of recovery, suggesting that fostering positive attitudes could improve outcomes.
The cumulative effects of these negative attitudes toward aging, both personally and collectively, are striking. Dr. Levy’s research indicates that age discrimination contributes directly to 3.2 million annual cases of eight major geriatric diseases among Americans over 60, costing an astounding $11.1 billion in healthcare resources.
The conclusion is evident: internalized ageism represents a widespread yet underrecognized public health challenge that significantly impacts individuals and healthcare systems.
Understanding the Roots of Age Discrimination
Internalized ageism doesn’t solely arise from personal beliefs; it is reinforced by systemic discrimination, which operates through mutual feedback loops. When older individuals experience ageism, it reinforces internal beliefs, shaping personal interactions, media narratives, advertising strategies, and even healthcare encounters.
This unrelenting barrage of negative stereotypes is termed institutional ageism. Much like institutional racism, it permeates various cultures, often going unnoticed. The World Health Organization, in a recent report on age discrimination, stated: “Often, people are unaware that such institutional ageism exists because the rules, norms, and practices of the system are long-standing, ritualized, and considered normal.”
Institutional age discrimination can permeate workplace relationships.
AJ_Watt/Getty Images
It’s essential to reiterate that ageism is a counterproductive bias. We all age daily, and many of us will encounter the challenges of old age. Those who engage in age-related prejudices will ultimately find themselves victim to the very beliefs they uphold.
The good news is that solutions may be within reach. Research from 2014 by Levy and colleagues demonstrated that our perspectives on aging can improve through exposure to positive, subliminal messages about aging. However, implementing this approach on a large scale presents significant challenges.
The struggle against systemic ageism, much like the battle against systemic racism, requires long-term commitment and perseverance, with inevitable setbacks. While I may not live to see institutional ageism eradicated, I aim to embrace aging with a sense of humor and positivity.
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A recent randomized clinical trial involving older adults revealed that daily multivitamin intake over two years significantly slowed epigenetic markers of aging. This finding translates to an approximate four-month reduction in biological aging when compared to a placebo group.
Lee et al. investigated the effects of a daily multivitamin/multimineral supplement alongside cocoa extract (500 mg cocoa flavanols and 80 mg epicatechin daily) over two years, focusing on five DNA methylation markers of biological aging in 958 participants (482 women and 476 men) from the COSMOS study. Image credit: Li Butov.
Epigenetic clocks measure biological aging by monitoring subtle changes in our DNA.
These clocks play a crucial role in regulating gene expression, tracking specific DNA sites that naturally change with age, and assessing mortality and aging rates.
Dr. Howard Sesso, a researcher at Brigham and Women’s Hospital and Harvard Medical School, stated, “There’s a growing interest in finding ways not only to extend lifespan but to enhance life quality.”
“It was thrilling to observe the beneficial effects of multivitamins related to biological aging markers.”
“This study paves the way for further exploration of safe, accessible interventions that could promote healthier, higher-quality aging.”
The study utilized data from the COcoa Supplement Multivitamins Outcomes Study (COSMOS).
Researchers analyzed DNA methylation data from blood samples of 958 healthy participants with an average chronological age of 70.
Participants were randomly assigned to receive cocoa extract and a multivitamin daily, cocoa extract and a placebo, multivitamins and a placebo, or just a placebo.
Changes in five epigenetic clocks were assessed at the beginning, the end of the first year, and the end of the second year.
Compared to participants in the placebo-only group, those taking multivitamins exhibited delays across all five epigenetic clocks, including significant delays in two clocks indicating mortality predictions.
This reduction corresponds to around four months of biological aging over the two-year period.
Interestingly, those whose biological age exceeded their chronological age benefited the most.
“We aim to conduct follow-up studies to determine if the observed slowing of biological aging persists post-study,” said Dr. Yangbin Dong, a researcher at Augusta University.
“Many individuals take multivitamins without fully understanding their benefits. The more we uncover about these potential health advantages, the better,” Dr. Sesso added.
“Within COSMOS, we are fortunate to compile an extensive resource of biomarker data that can test how specific interventions may mitigate biological aging and related clinical outcomes.”
For further details, refer to the published paper in this week’s edition of Nature Medicine.
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S. Lee et al.. Effects of daily multivitamin/multimineral and cocoa extract supplementation on the epigenetic aging clock in the COSMOS randomized clinical trial. Nat Med published online March 9, 2026. doi: 10.1038/s41591-026-04239-3
Health-conscious individuals may take multivitamins, but their benefits are debated
Lenar Nigmatulin/Shutterstock
Recent studies indicate that daily intake of multivitamins and minerals may slow cognitive decline in individuals over 60, and now, evidence suggests these supplements could potentially slow aging on a broader scale.
However, the findings are based on indirect aging measures, making it unclear what this means in terms of health advantages. Currently, medical experts, including Howard Sesso from Harvard University, advise against universally recommending multivitamins for older adults. He notes, “While we haven’t seen significant adverse effects, the benefits are still uncertain.”
Historically, it has been claimed that individual vitamins provide various health benefits, but this approach can sometimes be harmful. For instance, excessive vitamin A can weaken bones and too much vitamin B3 may cause liver damage. Additionally, high levels of vitamin B6 can result in loss of sensation in limbs. The UK Health Service recommends that everyone take vitamin D, usually during winter months.
Multivitamin supplements, like Centrum Silver utilized in this research, typically contain recommended daily intake amounts. According to Sesso, “These doses are not excessive.”
To investigate potential effects, Sesso and his team randomly assigned 1,000 participants with an average age of 70 to either receive the supplement or a placebo. “This was a rigorously designed, randomized, double-blind, placebo-controlled trial,” he explains. Steve Horvath from UCLA, not involved in the study, remarks, “This distinction differentiates us from much of the supplement research, which often relies on observational data riddled with confounding factors.”
Researchers collected blood samples from participants at the study’s outset, one year later, and again two years later. They analyzed the DNA from immune cells, looking for epigenetic markers—chemical tags added to DNA—at specific genomic locations.
Epigenetic markers change predictably with age, enabling researchers to estimate a person’s biological age through blood tests. Various epigenetic clocks have been developed, differing based on which genomic segments are analyzed.
Sesso’s research utilized five epigenetic clocks, all indicating that individuals taking multivitamins exhibited slightly younger biological profiles than those taking a placebo. However, significant results were only evident in two clocks. According to Horvath, “The significant results stemmed from second-generation clocks, which have emerged as the most reliable for evaluating longevity interventions.”
While first-generation clocks are effective for predicting age, many markers they observe are not inherently linked to health, Horvath points out. In contrast, second-generation clocks are built upon markers associated with health risks and mortality. “Nonetheless, the effect size remains modest,” he adds. “This is certainly not a miracle solution for aging.”
“The observed differences were minimal compared to the variation in participants prior to the intervention,” states Daniel Belsky from Columbia University.
The researchers determine that the epigenetic clock lag they discovered equates to approximately four months over two years. However, this may not convey the entire picture. Belsky explains that how age-related improvements correlate with conventional time drastically varies across different clocks.
Sesso acknowledges the ambiguity surrounding the health implications of these epigenetic measures. “Understanding how a four-month reduction in biological aging translates into clinical benefits is still a mystery,” he admits.
Most study participants were of European descent, leaving uncertainty about whether these slight reductions in epigenetic aging apply to non-Europeans or younger demographics. The longevity of these results when using different multivitamins also remains undetermined.
While the study is complete, the potential effects of cocoa extract were also assessed, with some participants taking it in conjunction with their vitamins or as a placebo substitute. Notably, cocoa extract did not yield any significant effects on the epigenetic clocks.
Recent research reveals that older adults may have a genetic edge, showcasing enhanced cognitive abilities as they age.
A study conducted by scientists at the University of Illinois at Chicago School of Medicine found that individuals aged over 80, referred to as “very old people,” produce double the number of new neurons in the hippocampus—an area crucial for learning and memory—compared to the average elderly individual. The findings were published in the journal Nature on Wednesday.
Study co-author and UIC director, Orly Lazarov, stated, “This discovery indicates that very old individuals possess molecular capabilities that enhance their cognitive performance, evidenced by increased neurogenesis. Neurogenesis represents one of the most profound forms of brain plasticity.”
In essence, the brains of very old individuals are more adaptable, fostering improved cognitive functions.
The term “super-elderly” describes those over 80 who exhibit memory capabilities comparable to individuals 20 to 30 years younger, determined by a delayed word recall test, according to Dr. M. Marcel Mesulam, founder of the Meshulam Cognitive Neurology and Alzheimer’s Disease Research Institute. This designation was introduced by a professor from Northwestern University’s Feinberg School of Medicine.
In this groundbreaking study, Lazarov and colleagues analyzed 38 brains from five distinct groups: healthy adults under 40, healthy older adults, those in early cognitive decline, Alzheimer’s disease patients, and super-elderly individuals. Notably, six super-aged brains were contributed by Northwestern University’s Super Aging Program, which celebrated its 25th anniversary last year.
The researchers investigated neurons at varying developmental stages within brain tissue samples, discovering that very old individuals possess twice as many “immature” neurons compared to healthy older adults, and 2.5 times more than Alzheimer’s patients.
A super-aged brain in a research lab.Shane Collins, Northwestern University
Historically, it was believed that mammals had a fixed number of neurons from birth, but research in the 1960s and 1970s unveiled adult neurogenesis in rodents and primates.
Subsequent studies have indicated that this phenomenon occurs within the human hippocampus’s dentate gyrus, although evidence remains mixed, and the underlying processes are still unclear.
“We’ve affirmed the existence of neurogenesis and its involvement in learning and memory in animal models,” Lazarov commented. “Determining if the human brain functions similarly is a pivotal question for our research.”
Lazarov’s findings suggest that the adult brain can generate new neurons in response to age and cognitive status.
The study revealed that very old brains exhibit “signs of resilience,” allowing them to cope with aging while maintaining superior cognitive performance.
Moreover, the research identified changes in astrocytes and CA1 neurons that regulate memory and cognition within the aging hippocampus.
Despite the study’s advancements, authors noted limitations, such as small sample sizes and significant variability among human brain samples.
Very Old Individuals Provide Insights Beyond 25 Years
According to the Northwestern Super Aging Program, this research marks the first identification of genetic distinctions between very old and conventional older adults.
Tamar Geffen, co-director of the program and co-author of the study, stated, “These individuals, aged 80 and above, exhibit immature neurons that continuously rewire, making their hippocampus distinct from that of other seniors.”
The program has also uncovered various discoveries related to these exceptionally healthy seniors, ranging from personality traits to neurological anomalies. For instance, Geffen noted that very elderly individuals often describe themselves as extroverts, with other research highlighting Von Economo Neurons linked to social behavior.
“We’ve repeatedly heard about the importance of social interactions for healthy aging, while isolation can have adverse effects in old age,” she noted.
Furthermore, these seniors tend to embrace change and remain receptive to new experiences, often identifying as low-level neurotics, according to Geffen.
While a typical human brain shrinks with age, a phenomenon exacerbated by Alzheimer’s, researchers at Northwestern discovered that the brains of very old individuals exhibit significantly slower shrinkage rates.
In a 2017 study published in the American Medical Association Journal, Northwestern researchers noted that very old individuals demonstrate resilience against neurofibrillary tangles, or tau protein changes associated with Alzheimer’s.
Concerning immunity, very elderly individuals have numerous questions, with their brains containing microglia—immune cells that activate during neurodegenerative diseases. A 2019 study in Frontiers in Aging Neuroscience revealed that very old individuals had fewer activated microglia compared to dementia patients, paralleling amounts found in those 30 to 40 years younger.
Staying Sharp Without Being Super Old
The findings suggest that the very elderly may have won the genetic lottery regarding cognitive health.
Sel Yackley, an 86-year-old participant in Northwestern’s Super Aging Program, noted, “We feel fortunate; we’re forming new neurons.”
Residing in Chicago, Yackley humorously remarked on her “super-senior duties,” which include knitting, going to the gym, crafting jewelry, singing, and managing her daily to-do list. Although she has faced limited in-person interactions, she’s prioritized keeping in touch via phone, email, and Zoom.
While she proudly identifies as a super senior citizen, Yackley acknowledges that age-related cognitive impairment can still affect her.
“At times, my memories feel fresh, and other times they slip away,” she stated.
Importantly, there are several wellness strategies individuals can adopt throughout adulthood to preserve cognitive health, noted Dr. Jennifer Paul-Durai, medical director of the Inova Brain Health and Memory Disorders Program in Northern Virginia. “Now is the moment to focus on enhancing cognitive function, long before natural decline or dementia occur,” she advised.
Dr. Paul-Durai emphasized, “The concept of super-aging provides a sense of regained control. With rising dementia and Alzheimer’s rates correlating with increased lifespan, maintaining cognitive sharpness is vital.” She encourages discussions focused on strategies to mitigate cognitive decline rather than solely highlighting the lack of a cure for Alzheimer’s disease.
This latest research underscores the brain’s capacity for adaptability, with Paul-Durai likening it to a ball of clay. “While some inherit better quality clay than others, it remains moldable throughout life to foster and shape neural pathways.”
However, if left unattended, clay solidifies and becomes hard to work with, similar to how our brains respond when we neglect cognitive engagement and physical activity.
“Our brains require active use and continuous cognitive engagement to remain flexible,” Paul-Durai explained.
Prioritizing overall health is also crucial for fostering brain plasticity, as factors like unmanaged chronic illnesses and untreated psychological traumas can hinder neuron development.
“It’s essential to advocate for preventive brain health measures before significant societal fractures emerge,” she advised. “We must emphasize the importance of taking proactive steps over merely highlighting the absence of Alzheimer’s solutions.”
Yackley, a former journalist, attributes her cognitive resilience to her career path, sharing, “My curiosity led me to explore numerous stories and conduct many interviews, which may have contributed to my neuronal health.”
Her advice to those who aren’t super seniors is to remain actively engaged, both mentally and physically.
“Don’t get caught up in counting the years. Stay active, both mentally and physically,” Yackley encouraged.
Research from Toronto’s Baycrest Hospital indicates that **birdwatching** significantly enhances cognitive abilities and overall brain function.
According to their latest findings, skills such as keen observation, prolonged attention, and robust memory are linked to extensive use of binoculars. Notably, these abilities can fundamentally reorganize brain structure, leading to enhanced cognition.
Published in the Journal of Neuroscience, the study involved a comparison of brain structures in 29 expert birdwatchers and 29 novices, with balanced gender and age distribution.
Brain scans demonstrated that expert birdwatchers possess more compact areas related to attention and perception, which enhances their bird identification skills.
Interestingly, the mobility of water molecules in these brain regions is enhanced, improving the birdwatchers’ ability to discern unfamiliar or local bird species.
While various learning experiences, such as picking up a new instrument or language, are beneficial for brain health, this study emphasizes that birdwatching’s complexity offers unique cognitive advantages.
“What’s notable about this research is that birdwatching engages ongoing perception, attention, and memory, preventing a state of cognitive autopilot,” explained Professor Martin Sliwinski to BBC Science Focus. Sliwinski, who was not part of the study, serves as director at Penn State’s Center on Healthy Aging.
“To have cognitive benefits, a stimulating activity must remain challenging, which holds true for birdwatching,” he added.
“Even experienced birders cannot depend on automatic responses due to the ever-changing environment and cues, often experienced under conditions of uncertainty and time constraints.”
Moreover, researchers suggest that these enhanced skills and accompanying brain changes could bolster cognition in older adults, as older birdwatchers in the study demonstrated superior facial recognition and recall abilities compared to novices.
However, Sliwinski noted that other influences may also play a role, stating, “Individuals with higher cognitive capabilities and an interest in birds may be more predisposed to take up birdwatching and progress to experts.”
In essence, it’s possible that rather than birdwatching directly sharpening cognitive function, those with existing cognitive strengths are naturally inclined to pursue this engaging hobby.
How Birdwatching Can Enhance Your Cognitive Reserve
Steve Young/Alamy
Recent research suggests that birdwatchers exhibit distinct brain differences that could explain their remarkable skill in identifying unfamiliar birds. This indicates that engaging in birdwatching may alter brain structure, akin to the effects of learning a new language or musical instrument. Such activities are believed to enhance cognitive reserve—the brain’s capacity to combat aging and adapt to damage.
As individuals learn or practice new skills, neural pathways in the brain reorganize, strengthening relevant connections. This phenomenon, known as neuroplasticity, facilitates the acquisition of specialized knowledge. For example, professional musicians display structural changes in brain regions associated with auditory processing, while athletes experience similar adaptations in their motor cortex.
To explore the effects of birdwatching on brain structure, Eric Wing and his team from York University, Canada, examined the brain function and structure of 48 recreational birdwatchers, with participants categorized into experts and beginners. The age range of participants was between 22 and 79 years, ensuring balanced variables like gender, age, and education.
During brain scans, participants viewed bird images for less than four seconds. Following this, they attempted to identify the same bird from four options, each depicting a different species. “We purposefully selected bird species that were quite similar,” states Wing.
This identification task was done 72 times, utilizing images from 18 distinct bird species—six being local and twelve non-native.
As anticipated, expert birders outperformed novices, with an average correct identification rate of 83% for native bird species and 61% for non-native; novices, on the other hand, correctly identified only 44% of the birds.
Notably, while identifying non-local birds, activity increased in three key brain regions for expert birders, including the bilateral prefrontal cortex, bilateral intraparietal sulcus, and right occipitotemporal cortex—regions pivotal for object recognition, visual processing, attention, and working memory. “This illustrates the diverse cognitive processes involved in bird watching,” Wing explains.
Moreover, these areas exhibited greater structural complexity and organization in expert bird watchers compared to novices, indicating that developing expertise in birdwatching may reshape the brain.
As we grow older, the complexity and organization of brain structures typically diminish, a trend observed in both novice and expert birdwatchers. Nonetheless, the decline appeared less significant in birdwatchers, suggesting that engaging in birdwatching contributes to building cognitive reserve, enhancing the brain’s resilience against aging.
“This implies that staying mentally active in specialized areas may help mitigate the effects of aging,” asserts Robert Zatorre at McGill University in Canada. “While this has been a controversial topic, this paper provides new evidence that supports this concept.”
Broadly participating in other hobbies that demand similar skills—like attention, memory, and sensory integration—may drive comparable brain changes. Wing notes, “Birdwatching taps into numerous cognitive domains, potentially benefiting various cognitive abilities. However, the cognitive enhancement might not be exclusive to birds; if other activities engage similar processes, we could expect similar brain changes there.”
Nevertheless, this study reflects merely a snapshot in time. It’s possible that structural changes occurred prior to participants taking up birdwatching, or that other lifestyle factors leading to brain changes are more prevalent among birdwatchers. To determine if brain changes are directly linked to birdwatching, longitudinal studies involving multiple scans over several months or years are necessary, Wing asserts.
Understanding Ultra-Processed Foods: A Key to Preventing Premature Aging
In recent months, I attempted to coin a new term to describe the modern influences accelerating aging, such as obesity, stress, heatwaves, and environmental pollution. I suggested labeling our current situation as an “aging environment,” inspired by the commonly understood concept of an “obesogenic” environment. Unfortunately, my term hasn’t gained traction, but there’s another critical aspect that requires attention—ultra-processed foods (UPFs).
What Are Ultra-Processed Foods?
For those unfamiliar, ultra-processed foods are pre-packaged items that undergo extensive manufacturing, commonly containing refined ingredients like sugars, fats, and proteins, along with potentially harmful synthetic additives such as dyes and preservatives. Typically low in essential nutrients like fiber and vitamins, these foods are high in fat, salt, and sugar. Common examples include:
Microwave meals
Salty snacks
Mass-produced breads
Sugary drinks
Instant noodles
Ice cream and candy
Baked goods
Processed meats
Condiments like mayonnaise and ketchup
Rising Consumption of Ultra-Processed Foods
Over the past five decades, UPFs have increasingly dominated Western diets. In high-income countries, including the UK, over half of caloric intake now comes from these harmful foods. While the trend has plateaued in recent years, global demand for UPFs remains high, largely due to their convenience and affordability.
Health Risks Linked to UPFs
Research has consistently shown that a high intake of UPFs correlates with a range of chronic health issues, including:
Obesity
Cancer
Type 2 diabetes
Cardiovascular disease
Inflammatory bowel disease
Fatty liver disease
Kidney disease
Moreover, a growing body of evidence indicates that high UPF consumption increases overall mortality risk. Studies conducted in Spain, France, and the US found that individuals with the highest UPF intake were significantly more likely to die compared to those with lower consumption.
UPFs and Premature Aging
Recent research points to a strong connection between UPFs and premature aging. A 2024 study examined the diets of 16,055 U.S. adults aged 20 to 79, revealing that a higher percentage of calories from UPFs corresponded to accelerated biological aging. Specifically, every 10% increase in caloric intake from UPFs was associated with a 0.21-year increase in biological age.
Though skeptics may question the accuracy of biological age measurement, it is crucial to note that these studies compare groups rather than individuals, mitigating measurement biases. Even modest increases in biological age have been linked to higher risks of chronic disease and mortality.
Implications and Future Research
While studies like NHANES primarily snapshot dietary impacts, they suggest that UPFs contribute significantly to the aging environment alongside other factors like obesity and environmental stressors. Researchers debate whether it’s the poor nutritional quality of UPFs or the processing methods that cause accelerated aging.
Despite the unknowns, two substantial studies across diverse populations consistently link high UPF consumption to accelerated aging. The takeaway is clear: if possible, avoid ultra-processed foods.
While navigating a world saturated with UPFs is challenging, prioritizing whole, real foods remains beneficial. Let’s raise awareness and combat the aging environment we live in.
The Importance of a Strong Intestinal Lining for Optimal Health
Shutterstock/3dMediSphere
As we age, the cells that line our intestines gradually lose their ability to regenerate, impacting our immune health. However, recent research has successfully reversed this decline in older mice using genetically modified immune cells.
This innovative approach, known as CAR T-cell therapy, is primarily used to target specific blood cancers. It entails collecting a patient’s T cells, reprogramming them in a laboratory to identify and eliminate cancerous cells, and then reintroducing them into the bloodstream. Emerging variations of this therapy show promise not only in combatting solid tumors but also in preventing arterial blockages and treating autoimmune diseases like lupus.
In a groundbreaking study, Cemil Beyaz and his team at Cold Spring Harbor Laboratory, New York, explored the application of this therapy for revitalizing the aging gut. They focused on targeting damaged cells, known as senescent cells, which accumulate over time, fail to proliferate, and secrete substances that exacerbate inflammation and promote further aging. The researchers aimed their intervention at a protein called uPAR, prevalent on aging cells.
“The decline in gut health we observe with aging is linked to diminished stem cell fitness responsible for renewing the intestinal lining every three to five days,” Beyaz states. “We posited that eliminating these ‘unfit’ senescent cells would enhance the regenerative ability and overall functionality of stem cells in older mice.”
To validate this hypothesis, the researchers engineered CAR T cells from older mice to specifically recognize and eliminate uPAR on senescent cells. Upon reintroducing these modified cells, the researchers noted a significant increase in both the activity and number of stem cells maintaining tissue function, reaching levels comparable to those observed in younger mice. The treated older mice also exhibited marked improvements in intestinal barrier integrity and reduced inflammation compared to a separate cohort that received CAR T-cell therapy targeting different mechanisms.
“By removing senescent cells, we not only inhibited the aging process but also witnessed a reversal, with tissues displaying characteristics similar to those of young mice,” said team member Corina Amor, also from Cold Spring Harbor Laboratory.
“This therapy could potentially reverse age-related declines in bowel function, decreasing vulnerability to diseases such as intestinal infections, compromised intestinal integrity, and even cancer,” explained Tuomas Tammera from Memorial Sloan Kettering Cancer Center, who was not part of the study. However, he emphasized that ensuring the treatment’s effectiveness and safety in humans remains crucial.
Onur Eskiokaku, a researcher at Cold Spring Harbor Laboratory, highlighted the importance of determining the optimal dosage before advancing to human trials. “While uPAR is abundant in aged, defective cells, it may also be present in healthy tissues under certain conditions,” he noted.
It’s important to remember that senescent cells aren’t all detrimental; they play roles in tumor suppression and wound healing. “We are investigating the implications of depleting uPAR expression in other tissues,” mentioned Jesse Poganic from Harvard Medical School.
Additionally, treating aging in otherwise healthy individuals is not commonplace. The complexity and expense associated with CAR-T therapy, coupled with ongoing safety concerns, suggest that widespread application for reversing aging effects is not imminent, according to Joanna Neves at the Center at King’s College London. “Safety standards for preventative treatments must be more stringent than those for oncology.”
Beyaz asserts that addressing the age-related decline in intestinal function has long posed a challenge, with no effective solutions currently available, especially when the intestinal barrier’s regenerative capability is compromised. This research marks a significant step forward, indicating that the removal of unfit cells can restore crucial functions.
Many claim that children keep us feeling youthful, but it’s a complex issue.
Javier Zayas/Getty Images
For centuries, humanity has sought to comprehend the aging process. The ancient Greek philosopher Aristotle theorized that aging correlates with the passage of time. The reduction of water necessary for bodily functions was his primary focus.
A contemporary concept known as the disposable soma hypothesis proposes that aging is the cost of reproduction; evolution, it argues, favors genetic replication above all else. This results in a fundamental trade-off. The substantial energy expended on having and nurturing offspring is often compromised by investments in DNA repair, disease resistance, and organ maintenance.
This idea is particularly relevant for women, who allocate more resources to reproduction through pregnancy and nursing than their male counterparts. However, when researchers examined whether women with more children had shorter lifespans, findings were inconsistent. Some studies supported the hypothesis while others did not.
“It’s challenging to extract clear correlations between childbearing and longevity,” said Elizabeth Bolland from the Swedish University of Agricultural Sciences, a professor not involved in the research.
Euan Young and associates from the University of Groningen in the Netherlands postulated that variations in reproductive costs depend on maternal environment, noting, “In favorable conditions, this trade-off is less apparent. It’s during challenging times that it becomes noticeable,” Young remarked.
To explore this hypothesis, researchers examined parish records of over 4,500 Finnish women spanning 250 years, including the era of Finland’s Great Famine from 1866 to 1868. Young highlighted how difficult times impacted reproduction and longevity.
They discovered that for women who lived before and after the famine, or those who had no children during that period, there was no notable correlation between child quantity and lifespan. Conversely, women who gave birth during the famine experienced a reduction in life expectancy of six months for each child born.
This research stems from a study released last year, which utilized a dataset from the pre-industrial populace of Quebec, Canada, tracked over two centuries. This previous work illustrated trade-offs in mothers likely to be in poor health or facing high stress, without evaluating the influence of specific environmental conditions.
In contrast, Young’s team emphasizes catastrophic events as factors that underscore these reproductive trade-offs. “This extensive dataset enables us to control for confounding variables,” he stated. “This study brings us closer to understanding causality without needing laboratory-controlled experiments,” remarked Bornd.
This investigation further endorses the energy demands of pregnancy and breastfeeding, which necessitate substantial additional calorie intake daily. During periods of starvation, women cannot acquire sufficient energy from food, which compromises their body’s “basal metabolism.” As a result, essential bodily functions may decelerate or cease, leading to deteriorated health and shortened lifespans, Young explained. This scenario clarifies why previous studies often identified these trade-offs predominantly in lower socio-economic groups, who typically reside in resource-limited conditions.
Bolland noted that this trade-off’s occurrence under particularly adverse circumstances, alongside a time when women usually had more children, may help clarify why women generally outlive men. In the UK, girls born between 2021 and 2023 are projected to live four years longer than boys.
In contemporary Western societies, reproductive costs have significantly diminished, with the average number of births declining drastically over centuries, as noted by Bornd. Consequently, it’s likely that very few women reach the stage where lifelong costs become evident. Bolland and colleagues noted in their study analyzing Utah’s historical population, that this threshold was only observed when women had five or more children. The average woman in the United States is now expected to have 1.6 children throughout her lifetime.
Therefore, other environmental factors may play a larger role in explaining the lifespan disparity between genders. For instance, men are generally more prone to smoking and tend to consume more alcohol, both of which influence longevity, according to Bolund. The current gap in longevity between men and women likely results from a mix of reduced reproductive costs for women relative to earlier historical periods, alongside differences in lifestyle choices.
Research also indicates that variations in sex chromosomes are significant. “Differences between the sexes extend beyond reproductive costs; thus, further research is essential to delineate how different factors impact sex-specific aging,” Young concluded.
During the concluding phase of their main sequence life, stars with mass comparable to the Sun experience a transformative evolution. This evolutionary process is likely to affect the surrounding planetary systems. As the star expands in its post-main-sequence stage, astronomers anticipate that most exoplanets detected to date may be engulfed by the growing star.
An artist’s impression of a sun-like star engulfing a giant exoplanet. Image credits: International Gemini Observatory / NOIRLab / NSF / AURA / M. Garlick / M. Zamani
Utilizing data from NASA’s Transiting Exoplanet Survey Satellite (TESS), astronomers Edward Bryant and Vincent Van Eylen studied 456,941 stars that have just commenced their post-main sequence phase.
By employing a computer algorithm, they targeted giant planets with short orbital periods (those that complete an orbit in less than 12 days) and searched for consistent dips in brightness that would indicate these planets transiting in front of their host stars.
They discovered 130 planets and planet candidates, including 33 previously unknown, closely orbiting these stars.
The researchers observed that such planets are less likely to exist around stars that have expanded and cooled sufficiently to be categorized as red giants (more evolved stars), implying that many of these planets might have already been destroyed.
Dr. Bryant, an astronomer at University College London and the University of Warwick, stated: “This provides compelling evidence that as stars progress beyond the main sequence, planets can rapidly spiral out of existence.”
“This topic has been debated and theorized for some time, but we can now observe this phenomenon directly and quantify it at the level of stellar populations.”
“We expected to observe this phenomenon, but we were still astonished by how effectively these stars can consume nearby planets.”
“This destruction is believed to stem from a gravitational tug-of-war between the planet and the star, known as tidal interactions.”
“As the star evolves and expands, these interactions intensify.”
“Just as the moon influences the Earth’s oceans, creating tides, planets also exert a pull on their stars.”
“These interactions decelerate the planet, reducing its orbit and causing it to spiral inward, ultimately resulting in its disintegration or absorption by the star.”
“In the coming billions of years, our sun will expand and transform into a red giant,” mentioned Dr. Van Eylen, an astronomer at University College London.
“Will the planets in our solar system endure this transformation? Our findings suggest that, in some instances, planets do not survive.”
“Earth may be better off than the giant planets much closer to the stars we examine.”
“However, we only analyzed the initial part of the post-main-sequence phase, spanning the first one or two million years. There is still ample opportunity for stellar evolution.”
“Unlike the giant planets lost in our investigation, Earth has the potential to endure the Sun’s red giant phase. However, life on Earth is likely to be extinguished.”
The team’s paper was published on October 15, 2025, in Royal Astronomical Society Monthly Notices.
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Edward M. Bryant and Vincent Van Eylen. 2025. Determine the impact of post-main sequence stellar evolution on the population of passing giant planets. MNRAS 544 (1): 1186-1214; doi: 10.1093/mnras/staf1771
The visible signs of aging, like wrinkles, gray hair, and joint discomfort, are merely surface reflections of more intricate processes happening within our cells. Deep inside your body, every organ experiences its own subtle molecular shifts as you grow older.
Researchers have now developed the most detailed map to date illustrating how this process unfolds.
For further insights into our findings, which are based on data from over 15,000 samples, please visit this preprint research. The paper, currently awaiting peer review, offers an unprecedented view of how aging modifies our genomic blueprint from head to toe.
A collaborative effort among researchers worldwide has led to the creation of a comprehensive “aging atlas” that maps DNA methylation (chemical tags that regulate gene activity) across 17 different types of human tissues while tracking age-related changes.
“DNA methylation, simply put, is a chemical modification on DNA,” said Dr. Jesse Poganic, co-author of the study and a medical instructor at Harvard Medical School, as reported by BBC Science Focus.
“At a fundamental level, their primary role is to regulate which genes are activated and which are not.”
If you stretched all the DNA in your body, it would span over 300 times the distance from Earth to the sun and back – Photo credit: Getty
Despite a few mutations, each cell shares essentially the same genetic information in the form of its genome. So how do lung cells recognize their identity while stomach cells act as stomach cells? This is where methylation plays a crucial role.
“The methylation or unmethylation status at a specific point on the genome determines whether a particular gene is turned on or off,” Poganik noted.
But what does all this reveal about the aging process?
DNA methylation serves as one of the body’s essential epigenetic mechanisms, acting as a molecular switch that toggles genes on or off without altering the DNA sequence itself. By adding and removing tiny molecules known as methyl groups, cells can adjust which genes are expressed in response to diet, exercise, infections, and other environmental influences.
As time passes, these methylation patterns alter in specific ways, forming the basis of the so-called epigenetic clock, which serves as a molecular measure of biological age. Until now, most of these clocks relied on blood samples, leaving scientists uncertain if other organs followed similar patterns.
“DNA methylation patterns differ from tissue to tissue. They are specific to both the tissue and the cell type,” said Professor Nir Eynon, the study’s senior author and research group leader at Monash University, as reported by BBC Science Focus. “Thus, blood measurements don’t necessarily represent what happens in your liver, muscles, or brain.”
This gap prompted the team to gather all publicly available datasets on methylation within reach, complemented by new data from global collaborators.
The analysis covered nearly 1 million points across the genome, encompassing 17 organs, from the brain and heart to the skin, liver, stomach, and retina.
Atlas of Aging
The researchers discovered that the proportion of genomes with methylation tags varied significantly across tissues, ranging from approximately 38 percent in the cervix to over 60 percent in the retina. Surprisingly, age-related changes were quite uniform, with most tissues becoming increasingly hypermethylated as they age, resulting in more tagged DNA sites and the silencing of certain genes.
However, two organs defied this trend. Both skeletal muscle and lung tissue can experience a loss of methyl tags over time, leading to excessive or irregular gene expression.
“Most tissues show hypermethylation with age,” explained Dr. Max Jack, the study’s lead author. BBC Science Focus via email. “Yet when you refine it down to methylation rates, distinct tissue-specific patterns emerge.”
Different organs age at varying rates. An aging atlas begins to elucidate why – Credit: Getty
For instance, adipose tissue predominantly shifts toward hypermethylation, while changes are more balanced in the brain. These patterns may illuminate how different organs react to common aging stressors, such as inflammation, according to Jacques.
Overall, significantly age-related methylation changes were observed in brain, liver, and lung tissues, with skin and colon tissues also showing marked alterations. Conversely, pancreatic, retinal, and prostate tissues exhibited the least detectable age-related changes, possibly due to limited data or greater resilience to aging.
Correlation, Not Causation (For Now)
At first glance, the data imply that some organs age quicker than others. However, researchers caution that these distinctions cannot yet be interpreted as a direct rate of aging.
This is partly due to statistical factors. Some organs represent thousands of samples, while others are represented by only a handful.
Moreover, “We know that methylation changes occur as we age,” Poganik states. “What we don’t know is the extent to which they contribute to aging.”
In other words, while scientists are aware of the methylation alterations linked to aging, it’s still unclear whether those changes induce aging or whether aging triggers those changes.
Poganik believes that alterations in methylation likely account for at least some of the observable phenomena associated with aging. “Even cautious scientists would suggest there’s an element of causation,” he remarks.
The allure of this new atlas lies in its revelation of common molecular themes threading throughout the body, he adds.
“One of the most compelling aspects of this study is that it demonstrates some universality in the aging process. When we analyze various tissues, we encounter numerous similar methylation changes, suggesting a universal quality to aging.”
Nevertheless, he warns that not all alterations are causal. With so many ongoing methylation changes, some are almost certainly part of aging, while others may not hold significance.
Old atlases might not pinpoint which changes are critical and which are not, but they offer an invaluable collection of data for researchers to delve deeper into the issue than ever before. The atlas is now openly accessible through an online portal for other scientists to explore and utilize.
“We have consistently prioritized open-source research,” Jack states. “With this, we aim to make it accessible to everyone, not only to advance research but also to foster collaboration.”
Going forward, the research team plans to examine some universal associations prevalent across all tissues as we age, alongside other biomarkers that may be influencing the aging process.
“Advancements in aging pale in comparison to those in cancer,” Poganik adds. With the assistance of this atlas, scientists may finally bridge that gap.
Study participant measuring reading capacity post-retinal implant
Moorfields Eye Hospital
Individuals experiencing significant vision impairment can regain the ability to read, thanks to a compact wireless chip implanted in one eye along with advanced glasses.
Age-related macular degeneration (AMD) is a prevalent condition that impacts central vision and tends to progress over time. While the precise cause remains unknown, this condition arises from damage to the light-sensitive photoreceptor cells and neurons located in the central retina, leading to difficulties in facial recognition and reading. Available treatments are primarily designed to slow down the progression.
An advanced form of AMD referred to as geographic atrophy typically allows individuals to retain some photoreceptor cells that facilitate peripheral vision, along with sufficient retinal neurons to relay visual information to the brain.
Leveraging this capability, Daniel Palanker and his team at Stanford University in California created the PRIMA device. This system includes a small camera mounted on the glasses, which captures images and projects them through infrared light onto a 2-by-2-millimeter solar-powered wireless chip implanted at the rear of the eye.
The chip then transforms the image data into electrical signals, which the retinal neurons transmit to the brain. Infrared light is employed for this process as it is invisible to the human eye, thereby ensuring it does not interfere with any remaining vision. “This allows patients to utilize both the prosthesis and their peripheral vision simultaneously,” explains Palanker.
To evaluate its efficacy, researchers enlisted 32 participants aged 60 and above, all suffering from geographic atrophy. Their visual acuity in at least one eye was below 20/320—meaning they could see what a person with 20/20 vision could see at 320 feet (97.5 meters) only at 20 feet (6 meters).
The team initially implanted a chip in one of the participant’s eyes. After a waiting period of four to five weeks, the volunteers began using the glasses in their everyday activities. The glasses enabled them to magnify their view up to 12 times and adjust brightness and contrast as needed.
After a year of using the device, 27 of the participants managed to read again and recognize shapes and patterns. They also noted an average improvement of five lines on a standard eye chart compared to their initial findings. Some participants were able to achieve 20/42 vision.
“Witnessing them progress from reading letters to full words brought immense joy to both sides. One patient expressed, ‘I believed my eyes were irreparably damaged, but now they’re revitalizing,'” shares Jose Alan Sahel from the University of Pittsburgh School of Medicine.
While stem cell therapy and gene therapy may potentially restore vision lost due to AMD, these approaches are still in early experimental trials. PRIMA stands out as the first artificial eye designed to restore functional vision in individuals with the condition, allowing them to perceive shapes and patterns.
Approximately two-thirds of the volunteers experienced temporary side effects, such as increased intraocular pressure, as a result of the implants; however, this did not hinder their vision improvement.
Comparison of a trial participant’s eye (left) and eye with retinal implant (right)
Science Co., Ltd.
“This research is both exciting and significant,” remarks Francesca Cordeiro from Imperial College London. “It provides hope for delivering vision improvements that have previously seemed more like science fiction.”
The improved visibility experienced by participants is limited to black and white. “Our next objective is to develop software to provide grayscale resolution and enhance facial recognition,” states Palanker. Nevertheless, researchers do not anticipate achieving color vision in the near future.
Palanker also aims to increase PRIMA’s resolution, which is currently constrained by pixel size and the total count that can be included on a chip. Testing a more advanced version in rats is underway. “This current version equates to human vision of 20/80, but electronic zoom can enable vision as sharp as 20/20,” he explains.
New research suggests that artificial sweeteners may have unexpected risks for brain health.
In a study published in Neurology, researchers analyzed the diets of over 12,700 adults in Brazil, revealing that individuals who consumed higher amounts of calorie-free sweeteners experienced a more rapid decline in memory and cognitive abilities over an eight-year period.
This decline was especially notable among diabetic patients and those under the age of 60.
The study examined seven sweeteners commonly found in diet sodas, flavored waters, yogurt, and low-calorie desserts: aspartame, saccharin, acesulfame-K, erythritol, xylitol, sorbitol, and tagatose.
All except tagatose were linked to cognitive decline, particularly affecting memory and verbal fluency.
Participants were categorized into three intake groups. Those with the highest consumption—approximately 191 milligrams daily, similar to a single can of diet soda for aspartame—demonstrated cognitive aging equivalent to 1.6 additional years, at least 62% faster than those with lower consumption.
“Low and no-calorie sweeteners are often regarded as healthier alternatives to sugar, but our findings indicate that certain sweeteners may negatively impact brain health over time,” stated Professor Claudia Kimmy Sumoto from the University of Sao Paulo.
“Prior research linked artificial sweeteners to conditions such as diabetes, cancer, cardiovascular disease, and depression, but the effects on cognition were previously unexplored.”
Consumption of artificial sweeteners similar to daily cans of diet soda was associated with accelerated cognitive decline, akin to 1.6 years of brain aging – Credit: Getty
Interestingly, the link was primarily observed in adults under 60 years old.
“We anticipated that the association would be more pronounced in older adults due to their increased risk of dementia and cognitive decline,” Sumoto noted. “Conversely, our findings suggest that exposure to sweeteners during middle age could be particularly detrimental, which is crucial as this period is vital for establishing long-term brain health.”
The findings do not conclusively prove that sweeteners are the direct cause of cognitive decline, with limitations including reliance on self-reported dietary habits and the absence of control over sweetener usage in the research.
Nevertheless, Sumoto emphasized the need for further investigation, including brain imaging and studies examining gut health and inflammation.
Her team is already conducting neuroimaging studies to better understand these associations, although results are not yet available.
“More research is essential to validate our findings and to explore whether alternative sweeteners like those from the apple family, honey, maple syrup, and coconut sugar provide effective options,” Sumoto concluded.
About our experts
Claudia Sumoto is an assistant professor at the University of Sao Paulo, Brazil. She is a trained physician with research published in journals such as The Lancet, Nature Neuroscience, and Journal of Alzheimer’s Disease.
Groundbreaking research by NASA’s twin astronauts Mark and Scott Kelly monitored aging indicators in both siblings, with Mark remaining on Earth while Scott spent 340 days in space.
Six months later, several changes in Scott persisted, including DNA damage, cognitive decline, and telomere shortening that affects chromosome protection. This was highlighted in the Journal Science.
Recent research published in Cell Stem Cell reveals that stem cells also show signs of aging due to stress from space flight.
According to Dr. Catriona Jamieson, director of the Sanford Stem Cell Institute at UC San Diego, these cells are “aging ten times faster in space than on Earth.”
Stem cells are unique cells capable of differentiating into various tissue types. Their accelerated aging poses a concern as it diminishes the body’s natural ability to repair tissues and organs.
This new research comes at a time of increasing interest in space exploration, with government plans for long-term lunar missions and private companies sending consumers and celebrities into space. Understanding these health risks is crucial for safer space travel. Additionally, studying the acceleration of intracellular aging aids researchers in comprehending biological processes at a slower pace.
Astronauts and twin brothers Scott and Mark Kelly at NASA’s Johnson Space Center in 2016. Houston Chronicle /Hurst Newspaper /Houston Chronicle by Getty Image
Researchers utilized bone marrow stem cells sourced from individuals who underwent hip replacement procedures. These cells were cultivated in “nanobioreactors,” essentially small, clear blood bags no larger than an iPhone that facilitate biological processes. The nanobioreactor was housed in a monitored environment known as cubelabs.
Samples from each patient were divided into two cubelabs; one was sent to space, while the other remained on Earth.
The samples intended for space travelled aboard the International Space Station across four commercial resupply missions conducted by SpaceX. Overall, the samples experienced microgravity for 32-45 days, the weightlessness found in orbit. For comparison, the Earth-bound cells were maintained in a cube lab setup.
Cubelabs monitored cell conditions throughout the journey and terrestrial duration, capturing daily images using a microscope. Upon the return of the space-stressed stem cells to Earth, researchers conducted comparisons against ground controls, sequenced the genome, and performed additional analyses.
As we grow older, our cognitive learning and memory capabilities decline—recent studies have identified the proteins responsible for this phenomenon.
Researchers at UC San Francisco have pinpointed the culprit: an iron-associated protein called FTL1. Its detrimental effects hinder cognitive awareness throughout the aging process, and understanding this may allow us to target it in treating neurodegenerative diseases such as Parkinson’s and Alzheimer’s.
“It’s essentially a reversal of the challenges,” said Saul Vilda, PhD, Associate Director and Senior Author of the Papers at UCSF Bakar Aging Research Institute; Natural aging. “It’s about more than just slowing or preventing symptoms.”
The hippocampus, a brain region essential for learning and memory, is particularly susceptible to the effects of aging. Researchers observed an increase in neuronal FTL1 in the hippocampus of older mice, correlating with cognitive decline and reduced intercellular connections.
The hippocampus, shown here, is vital for the formation of new memories (credit: Getty Images)
In an experiment, scientists artificially increased FTL1 levels in young mice, leading to brain and behavior changes reminiscent of older mice. Elevated FTL1 levels hinder synaptic connections, ultimately resulting in poorer memory performance.
Interestingly, their motor skills and anxiety levels remained stable, indicating that the cognitive impairments were specifically linked to memory and synaptic functions.
When researchers reduced FTL1 levels in the hippocampus of older mice, they noted improved neuronal connections and enhanced performance in memory tests, effectively reversing some signs of aging.
The FTL1 protein is involved in iron storage and metabolism, regulating long-term levels in the brain. As we age, alterations in iron metabolism lead to increased FTL1 in neurons.
By reversing aspects of cognitive aging in mice, this discovery could pave the way for treatments that counteract the effects of FTL1 in the brain, potentially restoring cognitive function in older adults.
“Identifying elements that seem to promote aging while keeping your brain youthful is crucial for overall health and activity as you age. FTL1 appears to be an anti-aging champion,” stated Andrew Steel in BBC Science Focus.
“This is an intriguing preliminary study, but as this research was conducted on mice, we must observe whether the same effects occur in humans.”
As we age, it’s common to perceive others as more content, as revealed by a recent study.
Researchers have discovered that older adults often exhibit a “positive bias” in interpreting facial expressions. This suggests they are more inclined to classify neutral or negative faces as happy rather than sad or angry.
“This indicates they tend to interpret vague or ambiguous expressions as ‘happy’ instead of ‘sad’ or ‘angry,'” noted Dr. Noham Wolpe in an interview with BBC Science Focus. “Crucially, this bias correlates with subtle cognitive decline and alterations in the specific brain circuits responsible for emotional processing and decision-making.”
Using data from over 600 adults, the research team examined this phenomenon through emotion recognition tasks along with brain imaging techniques.
They found structural variations in the hippocampus and amygdala—key regions for memory and emotion—and changes in connectivity with the orbitofrontal cortex, which plays a role in weighing emotional information and guiding decisions.
“These regions form crucial networks that aid in interpreting emotional signals and informing decisions,” Wolpe explained, highlighting how the relationship between the orbitofrontal cortex and amygdala strengthens in adults facing cognitive decline.
“This enhancement may lead them to perceive ambiguous or neutral emotional signals as positive, a phenomenon known as positive bias,” he remarked, noting that the reason behind this increased connectivity associated with cognitive decline is still unknown.
Researchers remain uncertain why the interamygdala connectivity and orbitofrontal cortex, highlighted in red, strengthen in individuals with cognitive decline – Trust: Getty
Although this research is in its nascent stages, its implications are significant. Positive biases might one day serve as early indicators of dementia, as changes in emotional processing frequently precede memory impairment.
“While emotion recognition tests are not yet ready to replace current cognitive assessments, in the future they could be combined with standard screening methods to enhance early detection,” Wolpe stated.
Wolpe and his team are already investigating innovative approaches, such as immersive virtual reality tasks, to better understand how people instinctively respond to emotional signals.
The next objective is to determine if this positive bias can actually forecast cognitive decline. The team has recently concluded a follow-up evaluation of participants in the Cambridge Aging and Neuroscience Research, approximately 12 years after the original assessments. Participant data is also being linked to GP records to monitor dementia diagnoses.
“A crucial takeaway,” Wolpe mentioned, “is that subtle biases in how we perceive others’ expressions can signal early brain changes, long before the typical signs of dementia manifest.”
“Grasping these connections could pave the way for quicker detection and ultimately more effective interventions.”
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About our experts
Noham Wolpe is a senior lecturer at the Sagol School of Neuroscience at Tel Aviv University. His research focuses on understanding the interplay between cognition, mental health, and behavior, both in health and disease.
Air conditioners may help prevent heatwaves from accelerating aging
Sajjad Hussain/AFP via Getty Images
The intensity of heat waves can lead to significant long-term health impacts. Prolonged exposure to high temperatures seems to speed up biological aging in individuals.
“Currently, there are two major studies that highlight the effects of heatwave exposure on aging, focusing on different populations in various countries,” says Paul Beggs from Macquarie University in Australia. “It’s crucial to take heat waves seriously, as we are not only safeguarding our health but also the well-being of those around us.”
Recent findings from Siyi Chen at the University of Hong Kong and her research team reveal important insights. They analyzed medical screening data from around 25,000 adults in Taiwan to determine biological age based on several health indicators, including inflammation, blood pressure, and organ function. This data was then compared with time series data to assess aging rates.
“Physiological changes associated with aging can appear earlier and progress more rapidly in certain individuals,” notes Beggs, who wasn’t part of this research.
The researchers calculated each participant’s cumulative heat wave exposure over two years preceding the medical screening, assessing not just the frequency of heat waves but also the intensity of temperatures experienced. It turned out that the number of heatwave days was a critical factor in the accelerated aging observed in Taiwan’s population. These findings align with another recent study investigating outdoor temperature effects on aging in older adults in the US.
In the Taiwanese population studied, greater aging effects correlated with increased cumulative exposure to heat waves. Specifically, a four-day rise in total heatwave duration linked to an increase in biological age by as much as nine days.
The impact was particularly severe for specific demographics. For instance, manual laborers experienced aging effects that were threefold greater from equivalent heat exposure compared to the broader group. Additionally, residents in rural areas showed more pronounced aging effects, suggesting that access to air conditioning could mitigate the aging repercussions of heat exposure.
Nonetheless, to effectively combat climate change and the escalating frequency of heatwaves, the advantages of air conditioning must be balanced with more sustainable cooling alternatives, warns Beggs. “Air conditioners release heat into the environment, further worsening conditions for individuals lacking such systems,” he states.
Recent studies indicate that visceral fat (the concealed belly fat located deep within the abdomen) may contribute to the accelerated aging of your heart.
In contrast to subcutaneous fat, which resides just beneath the skin, visceral fat envelops vital organs like the stomach, liver, and intestines. Individuals with elevated visceral fat levels might present as slimmer or even possess a healthy body mass index (BMI) and weight.
“Staying active is crucial, but our findings reveal that this hidden fat can pose risks even for those who seem healthy,” states Professor Declan Olegan, who led the research.
Two MRI scans, showcasing more visceral fat (red) and subcutaneous fat (blue) in the left subject – Photo credit: AMRA Medical
This research has been published in European Heart Journal. Scientists at the Medical Research Council of London (MRC) Institute of Medical Sciences examined data from 21,241 participants in the UK Biobank.
Whole-body imaging was utilized to analyze fat distribution, along with an in-depth investigation of the heart and blood vessels. Artificial intelligence was implemented to estimate a “heart age” for each participant, reflecting signs of organ aging, such as hardened or inflamed tissue.
The study identified notable differences between genders. Men are prone to accumulating visceral fat in the abdomen, often resulting in expedited heart aging.
Conversely, women have a genetic tendency to store fat around the waist and thighs, resulting in a “pear shape,” which may decelerate heart aging. Elevated estrogen levels in premenopausal women are linked to reduced heart aging, indicating that hormones might play a significant role in organ protection.
Blood analyses revealed a correlation between visceral fat and increased inflammation, suggesting another factor that could contribute to premature aging.
Utilizing whole-body MRI scans to analyze fat distribution and examine the heart in detail (credit: MRC Laboratory of Medical Sciences)
Professor Brian Williams, Chief Science Officer and Medical Officer at the British Heart Foundation, stated: “We are already aware that excess visceral fat around the heart and liver can result in increased blood pressure and high cholesterol, which may further accelerate heart and blood vessel aging.”
“The typical pattern of fat distribution observed in women is influenced by estrogen, suggesting that hormones could be pivotal in developing future treatments for cardiac aging.
“Adopting healthier eating habits and increasing physical activity can aid in lowering visceral fat levels.”
The stiffening of arteries with age, exacerbated by Covid-19
Peterschreiber.Media/Alamy
Covid-19 seems to speed up the aging of blood vessels, particularly in women.
The virus has been linked to cardiovascular issues such as heart disease, although the exact mechanisms remain unclear. For further insights, see Rosa Maria Bruno from the University of Parisite and her research team, who studied 2,390 individuals with an average age of 50 across 16 nations, including the UK and US, from September 2020 to February 2022.
Participants included those testing positive for Covid-19 viruses or for antibodies without vaccination, alongside others who were negative for both without past infections.
The health of their arteries was evaluated by measuring the speed of pressure wave transmission between the carotid artery in the neck and the femoral artery in the foot. This assesses arterial stiffness, which naturally increases with age and elevates heart disease risk.
Findings indicated that confirmed SARS-CoV-2 infections were related to increased arterial stiffness in women. This correlation appeared to grow with infection severity; for instance, women hospitalized for Covid-19 showed an average arterial age roughly five years greater than their uninfected peers, rising to 7.5 years among those who needed intensive care.
Researchers accounted for other factors influencing arteriosclerosis, such as smoking and obesity.
However, no similar findings were present in men. Earlier studies indicate that women tend to have stronger responses to infections than men, and an inability to modulate immune responses can result in inflammatory damage. Bruno expressed hope for observable gender differences but noted that this study didn’t yield significant ones.
The results also shed light on long Covid, which is more prevalent among women. After six months, arterial stiffness in women showed slight improvement, yet remained notably high in patients with ongoing Covid-19 complications. “Our study demonstrated measurable changes in blood vessels correlating with the symptoms of long Covid patients,” said Bruno.
Some individuals in the uninfected group may have experienced mild infections unbeknownst to them, potentially influencing the study’s validity.
Regardless, Vassilios Vassilio from the University of East Anglia highlighted the study’s robustness, asserting it could aid in identifying individuals affected by long Covid. “This research marks the first large, international multicenter investigation confirming an association between COVID-19 and accelerated vascular aging,” he noted. “The findings enhance comprehension of mechanisms post-Covid-19 syndrome and may pave the way for targeted pharmaceutical approaches.”
One of the more challenging perspectives on aging is the prospect of enduring poor health later in life. A common narrative is that although life expectancy has increased, the health span has not kept pace.
This perspective is shifting towards a new measurement of our later years, emphasizing “essential ability”—how well individuals can engage in the activities they value rather than solely focusing on chronic disease diagnoses. Viewed this way, those born in affluent nations during the 1950s appear poised to experience the longest and healthiest lifespans compared to any previous generation.
Nonetheless, it remains uncertain whether future generations will benefit similarly, as rising rates of obesity, pollution, and increasingly sedentary lifestyles could negate past advantages.
As of 2023, over three-quarters of the US population is living with at least one chronic condition, with more than half of middle-aged adults experiencing two or more. However, when considering health in terms of intrinsic competence, a diagnosis does not necessarily herald the end of well-being, as effective management can allow individuals to maintain their health.
People born in the 1950s in a rich country are set to lead the longest and healthiest life ever
Unfortunately, the narrative of a chronic disease epidemic has been fueled by certain figures, such as Robert F. Kennedy Jr., who recently reduced funding for research into mRNA vaccine technologies. This funding could critically assist in prolonging lives and mitigating disease impacts.
Nevertheless, there is cause for hope. For instance, GLP-1 medications present a groundbreaking method for managing obesity, and preliminary findings from recent studies indicate promising new avenues for alleviating Alzheimer’s disease.
Such innovations should serve as a reminder to policymakers that if our aim is to extend healthy living, investing in biomedical research is an essential ally, not a detractor.
Ribosome (center) responsible for synthesizing protein (red) from mRNA. Dark purple strands illustrate transfer RNAs involved in protein production.
The underlying factors contributing to cellular senescence may have been uncovered, revealing insights into various aging processes at the cellular level.
Studies on the brains of a type of freshwater fish known as Killifish reveal that as these fish age, their internal protein factories begin to malfunction, leading to critical protein classes being synthesized abnormally and creating a damaging feedback loop.
This revelation could pave the path for innovative approaches to addressing cognitive decline in aging; Alessandro Cellerino from the Leibniz Institute on Aging in Germany states, “Our focus is more on enhancing cognitive function and preventing cognitive impairment, rather than merely extending life span.”
Within cells, the templates for protein synthesis are encoded in DNA. When proteins are required, these instructions are transcribed into mRNA molecules.
This mRNA is then processed and transported to ribosomes, the cellular factories responsible for protein assembly. Ribosomes attach to and traverse mRNA strands, interpreting the three-letter codons and translating them into amino acid sequences, ultimately forming proteins.
Typically, a greater quantity of mRNA leads to increased protein synthesis. However, numerous studies indicate that this relationship falters in aging human cells, suggesting that protein output may diminish even if mRNA levels remain unchanged.
Through their investigation of aging ribosomes in the brains of Killifish, Cellerino and his team may have identified the cause of this phenomenon. Employing advanced imaging techniques, the researchers captured dynamic movements of ribosomes on constrained mRNA.
The findings revealed that, as the Killifish brain aged, an unexpected buildup of ribosomes occurred, particularly at codons for the amino acids arginine and lysine, leading to stalled ribosome activity and incomplete protein synthesis.
Arginine and lysine are crucial for numerous biomolecules associated with DNA and RNA, and their charged nature suggests that these stallings could significantly disrupt RNA and DNA-binding proteins.
These protein malfunctions pose a serious issue, as they are integral to crucial cellular processes such as RNA synthesis, splicing, and DNA repair.
“Aging is associated with increased DNA damage, reduced RNA production, decreased splicing efficiency, and diminished protein synthesis,” explains Cellerino. “We propose that this ribosome stalling binds these diverse senescence phenomena together.”
Moreover, Cellerino notes that ribosomes themselves harbor RNA-binding proteins, creating a detrimental cycle of stalling that further reduces ribosome availability and, accordingly, protein production.
The pressing question remains whether ribosomal stalling is also present in the human brain. Recent work by Jean Yeo at UC San Diego indicates that RNA-binding proteins diminish in aging human neurons, echoing Cellerino’s findings, although the underlying causes are still uncertain. “This change in RNA-binding proteins could explain their declining levels,” Yeo states.
If these observations hold true for humans, it could herald new strategies for treating age-associated cognitive disorders. Additionally, in Killifish, ribosomal stalling triggers stress signals that instigate inflammatory responses. “The persistent activation of this pathway leads to chronic inflammation,” warns Cellerino. “Chronic inflammation is a significant factor in brain aging.”
Experimental drugs that may mitigate this condition by blocking the associated signaling pathways are on the horizon, according to Cellerino.
“However, it is premature to draw definitive conclusions regarding their potential impact on longevity,” he cautions. This uncertainty arises from the lack of understanding regarding the initiation of ribosomal stalling at specific amino acids, as well as whether the same stalling mechanism exists across all organs.
The individuals we associate with may influence our health
Rob Wilkinson/Alamy
Many people in our lives may evoke anxiety instead of happiness. Interestingly, these individuals can actually accelerate the aging process.
Psychologists have long understood that robust social connections can enhance our longevity. A study indicates that social isolation may impact mortality rates as much as obesity and inactivity.
Moreover, the quality of our relationships holds equal significance to their quantity. Research from the University of Utah in 2012 revealed that tumultuous relationships—those marked by intense highs and lows—can accelerate telomere shortening, a protective cap on chromosomes. This shortening is a natural part of aging and is linked to health issues like heart disease.
Recently, Byungkyu Lee from New York University and his team explored a more precise measure of aging, investigating how negative social connections influence small chemical changes in DNA known as methylation marks. These changes illustrate how behavior and environment can alter gene function through epigenetics. “As we age, the patterns of these marks change in predictable ways,” states Lee.
The researchers collected saliva samples for epigenetic analysis from 2,232 individuals, who described their relationships with significant members of their social circles and indicated their experiences on a scale of “Never,” “Rarely,” “Sometimes,” or “Frequently.”
Interestingly, many participants labeled these negative influences as “hustlers.” “Over half of adults report having at least one hustler among their close contacts,” notes Lee.
These people seem to have a considerable effect on an individual’s epigenetic markers, with each hustler linked to approximately a 0.5% increase in biological aging, suggesting that individuals with hustlers in their lives tend to have a biological age that is older than their chronological age.
Negative social ties can induce chronic stress responses, and Lee’s team observed elevated markers in those relationships, leading to immune system damage.
“The biological ramifications of a significant number of hustlers in one’s social network are certainly comparable to the differences seen between smokers and non-smokers,” Lee asserts.
This effect was notably pronounced among hustlers who, paradoxically, provided some form of social support. “The same person who comforts you today may criticize you tomorrow, effectively branding you as bad and causing more physiological harm than a relationship that could potentially offer more stability,” explains Lee.
Alex Haslam from the University of Queensland remarked that the findings “align with other studies exploring these dynamics and underscore the importance of social relationships in relation to health.”
He further suggested that the overall sentiment within a group may influence aging even more than specific individual relationships. “For instance, being part of a book club or a choir may mean that it’s my connection to the entire group that plays a role in my health.”
The Covid-19 pandemic may have hastened brain aging, even prior to infection. Studies indicate that early in the outbreak, the brain may have undergone changes equivalent to 5.5 months of aging, potentially attributed to stress and shifts in lifestyle.
Many individuals suffering from long Covid report experiencing brain fog. However, the wider neurological implications of the pandemic are not completely understood a few years post-Covid-19’s emergence.
To investigate this, Ali-Reza Mohammadi-Nejad at the University of Nottingham, along with his team, trained machine learning models using 15,000 brain scans to analyze structural changes related to aging.
A model was then applied to brain scans from 996 volunteers participating in the UK Biobank Study. This comprised 564 individuals who underwent both scans prior to March 2020, which acted as the control group. The remaining 432 volunteers had one scan before March 2020 and another later, with scans averaging three years apart and a minimum gap of two years.
The research revealed that the pandemic may have induced an acceleration of brain aging by 5.5 months, as evidenced by structural changes in both white and gray matter. This effect was also observed in individuals who had recorded Covid-19 infections as part of the Biobank project.
This accelerated aging effect was notably more significant among men and those from lower socioeconomic backgrounds. However, the results may not be generalizable, as biobank participants typically exhibit better health, higher income, and less ethnic diversity than other demographics within the UK.
Researchers propose that these alterations might have been driven by the isolation and stress of lockdowns, alongside changes in lifestyle factors like physical activity and alcohol use during that period.
In their study, the authors indicate that these structural brain changes could be “at least partially reversible,” while also acknowledging limitations stemming from the study’s UK-based participant pool, suggesting that the findings may not accurately represent lockdowns’ impact elsewhere. “Our conclusions may actually underestimate the pandemic’s effects on more vulnerable populations,” Mohammadi-Nejad asserts.
A recent study reveals that Denmark boasts the most favorable environmental, social, and political conditions for aging slowly and maintaining a healthier lifestyle.
Published in Natural Medicine, this research pinpointed the elements influencing the biological processes that dictate healthy aging. An international team of researchers examined data from over 160,000 individuals across 40 nations, assessing how various factors influence aging worldwide.
To establish a baseline for the average aging rate, researchers utilized a measurement known as the “Biobiural Age Gap” clock. This AI model estimates the disparity between an individual’s chronological age and their predicted age based on surrounding risk factors. For instance, a 50-year-old person might be predicted to have a biological age of 55 based on these factors, resulting in a five-year age gap.
The findings revealed that among the four continents studied—Africa, Asia, Europe, and South America—European individuals showcased the highest levels of healthy aging. Conversely, in lower-income nations, accelerated aging was prevalent among older individuals.
“This study is significant as it reconceptualizes aging as influenced by not just biology and lifestyle, but also broader environmental and sociopolitical factors,” stated Morten Scheibye-Knudsen, an associate professor of aging at the University of Copenhagen, Denmark, who was not involved in the research, in comments to BBC Science Focus.
Egypt recorded the fastest rate of aging, with individuals showing an average biological age 4.75 years older than their chronological age. Following Egypt were South Africa and certain South American nations. Within Europe, Eastern and Southern regions displayed more rapid aging trends.
In contrast, Denmark demonstrated the slowest aging rate, with an average biological age 2.35 years younger than the actual age. The Netherlands and Finland followed in terms of healthy aging.
Key Factors for Healthy Aging
What makes Denmark and much of Northern and Western Europe conducive to healthy aging? Researchers identified crucial factors including environmental elements like air quality alongside social factors such as gender equality and socioeconomic status.
Interestingly, significant influences were also found in sociopolitical conditions. Healthy aging is closely related to political representation, freedom of parties, democratic elections, and voting rights.
“The link between politics and accelerated aging presents an intriguing puzzle in this study,” commented Scheibye-Knudsen. “Possible mechanisms include heightened chronic stress responses due to anxiety and healthcare disparities.”
This study indicated that individuals with accelerated aging face challenges in completing daily tasks and are eight times more likely to experience cognitive decline.
While the study spanned four continents, it primarily represented limited areas of Africa, focusing on Egypt and South Africa.
Researchers stress that their findings illustrate correlations rather than causative relationships. Nonetheless, they advocate for urgent action to address global health disparities.
“Remarkably, risk factors outweigh protective ones, indicating that individuals in low-income countries experience significantly accelerated aging irrespective of their socioeconomic status,” noted Scheibye-Knudsen.
“This reinforces the compelling case for investing in universal initiatives, such as access to education and healthcare, to enhance the health of populations.”
Read more:
About Our Experts
Dr. Morten Scheibye-Knudsen serves as an associate professor of aging at the University of Copenhagen and leads the Scheibye-Knudsen research group. He is also the president of the Nordic Aging Association.
Recent research indicates that older adults who play musical instruments tend to have healthier brains.
One investigation examined the impacts of decades of music practice, while another focused on learning new instruments later in life.
In both studies, engaging in music was linked to better brain health and a decrease in age-related cognitive decline.
The first study was published in PLOS Biology and involved collaboration between Canadian and Chinese researchers. They recruited 50 adults with an average age of 65, half of whom had been playing instruments for at least 32 years, while the others had no musical experience.
Additionally, they included 24 young adults with an average age of 23 who had no musical training.
The researchers utilized magnetic resonance imaging (MRI) to assess blood flow in the brains of the participants.
During the scans, participants listened to a recording of speakers amid background noise, where 50 other voices were present, and were tasked with identifying what the main speaker was saying.
The scans revealed that older musicians’ brains responded to challenges similarly to those of the younger participants.
Nonetheless, older adults showed signs of cognitive decline. Specifically, musicians exhibited strong neural connections on the right side of the brain that non-musicians lacked, which could place additional strain on their brain.
“The brains of older musicians remain finely tuned due to years of training, so they don’t need to play well-tuned instruments at high volumes,” stated co-author Dr. Yi from the Chinese Academy of Sciences.
“Our findings suggest that musical experience helps mitigate the additional cognitive strain typically associated with age-related challenges, particularly in noisy environments.”
A 2025 YouGov poll revealed that 25% of UK adults can play at least one instrument, with the guitar being the second most favored instrument after the piano.
As individuals age, cognitive functions such as memory, learning, and perception often deteriorate, eventually contributing to dementia.
However, researchers posit that cognitive reserve—the brain’s capability to manage damage and decline—can enhance resilience against this deterioration.
The precise mechanisms remain unclear, as noted by Morten Scheibye-Knudsen, Associate Professor of Aging at the University of Copenhagen, Denmark, in an interview with BBC Science Focus.
Some studies suggest that “exercising” the brain through activities like playing instruments, learning new languages, and solving puzzles can improve brain health, but results from other research have been inconsistent.
“Overall, we advocate for brain training, but the evidence is not conclusive,” Scheibye-Knudsen remarked.
Conversely, another recent study, published in Imaging Neuroscience, indicated that musical practice can enhance brain health, even when individuals start playing in later life.
According to a 2024 poll from the University of Michigan, 17% of US adults aged 50-80 engage in playing instruments at least several times a year – Credit: DMP via Getty
Researchers at Kyoto University in Japan continued previous studies that included 53 elderly individuals (average age 73) who took music lessons for four months. Initial findings indicated no significant differences in brain health among participants.
Four years later, the same participants underwent MRI scans (13 of whom had maintained their music practice).
Those who ceased playing their newly learned instruments showed declines in memory performance, with a noticeable reduction in the volume of the putamen—a brain region associated with motor function, learning, and memory.
However, those who continued playing music over the four years exhibited no cognitive decline.
Scheibye-Knudsen noted that the study demonstrates that “playing an instrument not only helps preserve cognitive function as we age, but it may also directly contribute to maintaining the structural integrity of the brain.”
He added, “Engaging in music beyond what this study covered offers additional advantages, such as enhanced social interaction.”
“I encourage people to start making music; it’s never too late to learn.”
Read more:
About Our Experts
Morten Scheibye-Knudsen is an associate professor of aging at the University of Copenhagen, Denmark, and leads the Scheibye-Knudsen Research Group. He also serves as the president of the Nordic Aging Association.
Aging often impacts sleep, leading to challenges as we grow older. Factors such as changes in circadian rhythms, increased nighttime bathroom visits, anxiety, and chronic health conditions can all compromise sleep quality.
Yet, let’s examine the flip side: the influence of sleep on the aging process.
Despite bold assertions from various hyperbaric oxygen therapy centers, nothing can halt our body’s natural aging. However, a closer look at the physiological changes that occur during sleep reveals that cultivating healthy sleep habits can help mitigate the effects of time on our bodies.
What occurs when we sleep?
Our bodies engage in powerful recovery processes during sleep to restore, reset, and rejuvenate organs and cells. Each night serves as a mini-reboot: muscles undergo repair, hormone levels stabilize, and the brain executes a version of waste removal.
Key changes that happen in the body during sleep include:
• Integration of emotional and procedural (long-term, implicit) memory during REM sleep. • The brain experiences a neurochemical reset, with significant reductions in dopamine and serotonin levels during slumber. • Muscle repair promotes the release of growth hormone, restoration of glycogen levels, and the production of anti-inflammatory cytokines to assist muscle recovery. • Hormones like melatonin are produced, while others are regulated; for instance, cortisol (the “stress” hormone) decreases, and leptin (which controls hunger) is maintained.
Dive into the physiological changes that occur during sleep.
Why is sleep increasingly crucial as we age?
Waste removal The Glymphatic System operates while we sleep to clear neurotoxic waste, such as beta-amyloid. This process becomes increasingly critical with age. The National Library of Medicine states, “The aging process involves a range of neurobiological changes in the brain, including the accumulation of toxic proteins like beta-amyloid plaques and tau tangles.”*
Immune support As the immune system naturally declines, deep sleep becomes vital for enhancing immune cell activity, thereby supporting our immunity.
Cardiovascular health Those with a Fitbit will attest that heart rates drop during sleep, allowing blood pressure to lower, which in turn gives the cardiovascular system a chance to rest.
Insulin sensitivity Sleep quality, duration, and timing all influence insulin sensitivity; inadequate sleep can increase insulin resistance and elevate the risk of developing type 2 diabetes.**
Maximizing quality sleep
Hestens, a Swedish bed manufacturer, recognizes the significance of a good night’s sleep. Since 1852, luxury brands have been crafting handmade beds, with each taking up to 600 hours to create using only natural materials.
“Miracles happen while we sleep,” Hestens states. “It’s the sleep that makes a difference. This is a natural process that cannot be replicated or bought over the counter. You can’t cheat your way to perfect sleep, but understanding its importance and implementing good practices can improve your chances of a restful night.”
For more on the advantages of sleep and to explore the full collection of beds and accessories, visit Hestens’ website.
Book local sleep spa bed tests online at www.hastens.com or visit your nearest certified retailer.
Strategies to Prevent Nightmares, Such as Avoiding Scary Movies
Andrii Lysenko/Getty Images
Experiencing nightmares weekly may accelerate aging and significantly increase the chances of early death.
“Individuals with more frequent nightmares experience faster aging and a higher risk of premature death,” states Abidemi Otaiku from Imperial College London.
In collaboration with his team, Otaiku examined data from over 183,000 adults aged between 26 to 86 who participated in several studies, initially self-reporting their nightmare frequency over a span of 1.5 to 19 years.
The findings revealed that individuals reporting weekly nightmares are over three times more likely to die before reaching 70 compared to those who do not experience nightmares.
Moreover, the researchers noted that the frequency of nightmares is a more potent predictor of preterm birth than factors such as smoking, obesity, poor diet, or inadequate physical activity. Otaiku presented these findings at the European Neurological Society Conference 2025 held in Helsinki, Finland, on June 23rd.
The team additionally assessed participants’ biological ages by measuring telomere lengths, small DNA sequences at the ends of chromosomes that shorten with each cell division; short telomeres linked to premature aging. This segment of the study also included approximately 2,400 children aged 8 to 10, while adults contributed further biological age data using epigenetic clocks.
According to Otaiku, their research established a consistent connection between frequent nightmares and accelerated aging across various ages, genders, and ethnic backgrounds. “Even in childhood, those with frequent nightmares exhibit shorter telomeres, indicating faster cellular aging,” he remarked. In adults, this accelerated biological aging accounts for roughly 40% of their heightened risk of death.
Regarding the reasoning behind this association, Otaiku suggests two main factors. The first is the elevated levels of the stress hormone cortisol triggered by nightmares. These levels are linked to faster cellular aging. “Nightmares elicit a more intense stress response than what is typically experienced upon waking, often rousing us with pounding hearts,” he explained.
The second factor involves sleep disruption, which hinders the body’s overnight cellular repair processes. Poor sleep quality is associated with an increased risk of various health issues, including heart disease.
For those wishing to reduce their occurrence of nightmares, Otaiku suggests straightforward strategies, such as avoiding scary movies and addressing mental health issues like anxiety.
“This is a fascinating finding with a number of biological underpinnings,” said Guy Restiner from the NHS Foundation Trust at Guy and St. Thomas. However, he emphasized that further research is necessary to identify causal relationships, noting that nightmares can be associated with various medical conditions and medications that may impact the findings as individuals age.
Taurine supplements are seen as potentially effective in slowing aging, but this may not hold true
Shutterstock / Eugeniusz Dudzinski
While it was previously thought that taurine, an amino acid, diminishes with age, research in animals suggested that taurine supplements might help slow down the aging process. New studies, however, indicate this decline is not consistent. In fact, taurine levels often increase with age, indicating that low nutrient levels might not be the primary factor driving aging.
Earlier research indicated that taurine levels decrease in aging men, with those exhibiting higher taurine levels at age 60 experiencing better health outcomes. This correlation suggests low taurine levels might contribute to aging, supported by evidence that taurine supplements can extend the lifespans of mice and monkeys.
The challenge lies in the fact that taurine levels can fluctuate due to various factors, including illness, stress, and dietary habits. Thus, a reduction in this vital amino acid may not be directly linked to the aging process. Maria Emilia Fernandez and her team from The National Institute of Aging in Maryland assessed taurine levels in 742 individuals aged 26 to 100. The cohort consisted of roughly equal numbers of men and women, with no major health issues and multiple blood samples taken between January 2006 and October 2018.
On average, women aged 100 had taurine levels that were nearly 27% higher than those aged 26, while men aged 30 to 97 exhibited an approximate 6% increase. Similar trends were noted among 32 monkeys sampled at ages ranging from 7 to 32 years, where female monkeys saw taurine levels rise by an average of 72% and male monkeys by 27% between ages 5 and 30.
These results underscore that taurine levels may not be a reliable indicator of aging. Importantly, taurine concentrations vary widely among individuals and can change over time due to external factors, according to Fernandez.
Nevertheless, some individuals may still find taurine supplementation beneficial. Fernandez highlights research indicating its potential to help regulate blood glucose levels in people with type 2 diabetes or those who are obese. However, the question of whether taurine can slow aging in otherwise healthy individuals remains unanswered.
Vijay Yadav from Rutgers University and his colleagues are currently leading clinical trials on taurine supplementation in middle-aged adults. “We aim to conclude the trial by the end of 2025,” he states. “Our goal is to produce robust data to determine if taurine supplementation can decelerate human aging or enhance health and fitness.”
A recent study conducted by researchers at Harvard Chan Public Health indicates that caffeine and regular coffee consumption during middle age are modestly and positively linked to various aspects of healthy aging in women. However, no notable correlation was found with tea or caffeinated coffee, whereas increased cola intake was associated with healthy aging and a lower likelihood of related health issues.
Mahdavi et al. Our aim was to explore the relationship between caffeine intake in middle age and the chances of healthy aging in older women participating in nurse health studies. Image credit: Sci.News.
“While earlier studies have linked coffee to specific health outcomes, this research is the first to evaluate coffee’s impact on multiple aspects of aging over three decades,” stated Dr. Sarah Mahadhabi, a researcher at Harvard Chan School of Public Health and the University of Toronto.
“The findings indicate that coffee may uniquely support aging processes that foster both mental and physical well-being.”
“Our study boasts several significant strengths, including a substantial sample size and three decades of follow-up. Moreover, we assessed various elements of longevity and healthy aging, in conjunction with comprehensive data on nutrition and lifestyle habits collected every four years after the study began.”
The research encompassed 47,513 women from the Nurses Health Survey, utilizing dietary and health data gathered since 1984.
Researchers evaluated caffeine consumption using a validated food frequency questionnaire, focusing on major caffeine sources like coffee, tea, cola, and caffeinated coffee.
Healthy aging was characterized as living to age 70 and above, free from 11 major chronic diseases, preserving physical abilities, maintaining mental health, exhibiting no cognitive impairment, and having no memory complaints.
Following 30 years of monitoring, researchers assessed how the probability of healthy aging varied with each additional 80 mg of caffeine consumed daily by the participants.
They also examined specific beverage types, including coffee, tea, caffeinated coffee (per 8-ounce cup), and cola (per 12-ounce glass).
The preliminary analyses identified other factors that might influence healthy aging, such as body weight, smoking habits, alcohol consumption, physical activity levels, educational attainment, and protein intake.
By 2016, 3,706 women in the study met all criteria for being classified as healthy agers.
Women aged between 45-60 typically consumed an average of 315 mg of caffeine daily, with over 80% of that derived from regular coffee consumption.
For those in the Healthy Agers Group, each additional cup of coffee per day was linked to a 2% to 5% increased likelihood of aging well, up to about 5 small cups per day, or approximately 2.5 standard cups by today’s measurements.
Researchers discovered no significant correlation between the consumption of decaffeinated coffee or tea and an elevated likelihood of healthy aging.
Importantly, for each additional glass of soda with caffeine, the chances of healthy aging decreased by 20-26%, indicating that not all caffeine sources are beneficial.
“While these findings are preliminary, they suggest that small, consistent habits can profoundly influence long-term health,” Dr. Mahadhabi noted.
“Moderate coffee intake can provide a range of protective benefits when coupled with other healthy practices, such as regular exercise, a balanced diet, and avoiding smoking.”
“This study expands on previous evidence linking coffee consumption to healthy aging, but the benefits of coffee are relatively modest compared to the impact of an overall healthy lifestyle, warranting further investigation.”
The findings were presented at the Survey results on June 2nd during the Nutrition 2025 annual meeting hosted by the American Nutrition Association.
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Sarah Mahadabi et al. Caffeine intake and healthy aging in women. Nutrition 2025 Summary #P22-039-25
As we age, flexibility tends to decrease. Clinicians utilize tests like “Sit down and stand” to assess older adults’ ability to rise from a chair, helping to identify risks associated with falls and frailty.
There are numerous factors contributing to decreased mobility as we age. Tendons might cause the joints to tighten, impacting the cartilage between them. Additionally, ligaments typically weaken, and muscle tightness around the joints, along with reduced synovial fluid, can exacerbate the situation.
Our muscle mass doesn’t just stay the same; it diminishes with age, particularly the quadriceps in the front of the thighs, which are crucial for standing up from a chair.
The encouraging news is that these changes can be mitigated. Engaging in regular physical activity is believed to slow down the loss of flexibility while also enhancing bone density, heart health, and mental well-being.
Studies reveal that older adults who remain physically active can achieve a broader range of motion compared to their sedentary peers. The NHS guidelines recommend that older individuals engage in strength, balance, and flexibility exercises at least twice weekly, in addition to 150 minutes of moderate-intensity activity weekly (or 75 minutes of vigorous activity if they’re already active).
If you do exercise regularly, don’t forget to incorporate stretching. Yoga can be beneficial if you’re able to practice it, but even simple stretches can enhance flexibility and be performed while watching TV or chatting on the phone! It’s advisable to consult someone trained to demonstrate proper stretching techniques.
Your diet also plays a crucial role. Consuming adequate proteins helps in muscle building, particularly with nutrients like calcium and vitamin D that support bone density.
While aging does lead to less flexibility and makes standing up more challenging, there are proactive steps you can take to counteract these effects!
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Questioner: Alexandra Wereck, Cambria
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