LongeCityNews Last Updated: 02 April 2026 - 03:21 AM

A recent study suggests that the transition of king penguins from the wild to a zoo environment, which resembles a sedentary, well-fed Western lifestyle, results in accelerated aging and changes in metabolic pathways [1].

A unique model system

A sedentary lifestyle and obesity are linked to accelerated aging in humans and, at the molecular level, negatively impact the hallmarks of aging [2, 3]. On the other hand, such interventions as increasing physical activity [4], caloric restriction [5], and manipulation of nutrient-sensing pathways [6] are reported to have a positive impact on the rate of aging. However, much of the data on this topic comes from mouse models, which have limitations, and whether these findings will translate to humans and provide lifelong improvements remains debated [7], creating the need for alternative model systems.

A team of researchers based in Europe decided to explore this research area using king penguins. King penguins, when living in the wild, show a unique behavior among model systems studied to date: voluntary fasting. Specifically, during their breeding cycle, king penguins undergo prolonged fasting periods (up to 8 weeks) that have been shown to involve physiological traits similar to those observed in human fasting [8]. These fasting periods are followed by periods of extreme physical activity.

While penguins are not the kind of animals routinely kept in labs, they are frequent inhabitants of zoos around the world, where researchers can study them. When penguins are moved from the wild to the zoo, the transition resembles a shift to a Western lifestyle in humans: their physical activity levels decline, and animals frequently become overweight. [9] This kind of lifestyle change creates a unique opportunity for experimentation, in which the wild environment, with high levels of physical activity and voluntary caloric restriction, serves as the control state, while the zoo environment, with continuous feeding and sedentary behavior resembling the Western lifestyle, is treated as the experimental manipulation. The researchers hypothesized that such a Western-style environment would accelerate aging in zoo-housed king penguins.

“We wanted to investigate whether turning these penguins into nonchalant, well-fed, and well-cared-for individuals would alter their aging trajectory. Since this lifestyle already occurs in zoos, the setup was ideal,” said Robin Cristofari from the University of Helsinki, first author of the study.

Faster aging but longer lives

To estimate penguins’ biological age, the researchers relied on a penguin genome-adapted methylation-based epigenetic clock, as is commonly done in other species and humans. The results showed that zoo-housed king penguins exhibit accelerated epigenetic aging compared with age-matched penguins living in the wild. The numerical value of the acceleration varied between different modeling approaches but was estimated to be between around 2.5 and 6.5 years. Such age acceleration is comparable (when adjusted for the penguin’s lifespan) to the differences seen between smokers and non-smokers in humans.

This accelerated epigenetic aging didn’t translate to faster death. The researchers reported that the median survival age was almost 21 years for zoo-housed penguins and 13.5 years for those in the wild. Those differences are caused by high mortality among young penguins in the wild and zoo animals being protected from predators and having an abundance of food and medical care that allows them to live longer.

“A 15-year-old penguin in the zoo has the body of a 20-year-old penguin in the wild. However, the interesting part is that zoo penguins also live longer, overall. They may be less physically fit, but with no natural predators or Antarctic storms to contend with and with access to veterinary care, they can survive long past the age at which they would typically die in the Southern Ocean,” explains co-researcher Céline Le Bohec, from the French CNRS. This data suggests that the Western lifestyle might increase lifespan but not healthspan, which is in line with observations in humans.

Metabolic changes

To understand age acceleration in the zoo environment, the researchers searched for differences in methylation patterns between the two groups, identifying nearly 300 genes clustered into 11 different molecular pathways. Those pathways were involved in cell growth and in linking nutrient sensing to aging and age acceleration, all supporting the hypothesis that a Western-like sedentary, well-fed lifestyle influences core metabolic processes in king penguins.

Further analysis of the specific genes identified in this study emphasizes their impact on metabolism. For example, a few identified genes are known to play a role in coping with excessive nutrient intake, while others were linked to heart function and physical activity.

The researchers report that their results suggest that zoo-housed penguins need to make significant changes in their gene expression and metabolism to compensate for shifts in diet, especially in lipid composition and food abundance, compared with their wild diet. Additional epigenetic changes are also caused by the substantial decrease in physical activity

Finding a balance

This study adds additional data supporting the detrimental role of a sedentary lifestyle combined with abundant food in age acceleration, a phenomenon that appears to be conserved across various animal species. What’s more, the conclusions drawn from these observations suggest that age acceleration results from the suppression of physical activity and periodic caloric restriction, rather than from being overweight, as the penguins in this study were not clinically obese.

The researchers plan to continue this research in the hope of identifying a lifestyle that can extend both lifespan and healthspan. “We are currently conducting a study in which we induce penguins to eat less and exercise more. It is important to find a moderate lifestyle in a world of abundance—for us humans as well,” concluded research curator Leyla Davis from Zoo Zurich.

Literature

[1] Cristofari, R., Davis, L. R., Bardon, G., Nitta Fernandes, F. A., Figueroa, M. E., Franzenburg, S., Gauthier-Clerc, M., Grande, F., Heidrich, R., Hukkanen, M., Le Maho, Y., Ollikainen, M., Paciello, E., Rampal, P., Stenseth, N. C., Trucchi, E., Zahn, S., Le Bohec, C., & Meyer, B. S. (2026). Lifestyle change accelerates epigenetic ageing in King penguins. Nature communications, 10.1038/s41467-026-70527-8. Advance online publication.

[2] de Rezende, L. F., Rey-López, J. P., Matsudo, V. K., & do Carmo Luiz, O. (2014). Sedentary behavior and health outcomes among older adults: a systematic review. BMC public health, 14, 333.

[3] Tam, B. T., Morais, J. A., & Santosa, S. (2020). Obesity and ageing: Two sides of the same coin. Obesity reviews : an official journal of the International Association for the Study of Obesity, 21(4), e12991.

[4] Ekelund, U., Steene-Johannessen, J., Brown, W. J., Fagerland, M. W., Owen, N., Powell, K. E., Bauman, A., Lee, I. M., Lancet Physical Activity Series 2 Executive Committe, & Lancet Sedentary Behaviour Working Group (2016). Does physical activity attenuate, or even eliminate, the detrimental association of sitting time with mortality? A harmonised meta-analysis of data from more than 1 million men and women. Lancet (London, England), 388(10051), 1302–1310.

[5] Maegawa, S., Lu, Y., Tahara, T., Lee, J. T., Madzo, J., Liang, S., Jelinek, J., Colman, R. J., & Issa, J. J. (2017). Caloric restriction delays age-related methylation drift. Nature communications, 8(1), 539.

[6] Madeo, F., Pietrocola, F., Eisenberg, T., & Kroemer, G. (2014). Caloric restriction mimetics: towards a molecular definition. Nature reviews. Drug discovery, 13(10), 727–740.

[7] Phelan, J. P., & Rose, M. R. (2005). Why dietary restriction substantially increases longevity in animal models but won’t in humans. Ageing research reviews, 4(3), 339–350.

[8] Groscolas, R., & Robin, J. P. (2001). Long-term fasting and re-feeding in penguins. Comparative biochemistry and physiology. Part A, Molecular & integrative physiology, 128(3), 645–655.

[9] Fens, A., & Clauss, M. (2024). Nutrition as an integral part of behavioural management of zoo animals. Journal of Zoo and Aquarium Research, 12(4), Epub ahead of print.

Animal studies show that ascending doses of nanoplastic particle infiltration into tissues eventually rise to the level of inducing dysfunction. Evidently harmful nanoplastic exposure doses are considerably higher than what are thought to be environmental exposure doses in the wild at the present time, but equally it is challenging, costly, and takes a long time to build a body of literature focused on subtle effects that may only emerge over the long term to affect the pace of aging. This is a work in progress.

The difference between nanoplastics and particulate air pollution is that there is a very large body of evidence to quantify the harms done by exposure to air pollution in human populations, alongside convincing mechanistic studies to show how long-term health and pace of aging can be negatively impacted. That body of evidence has yet to be constructed for nanoplastic exposure in human populations, so while there is a great deal of concern around this topic, it is unclear as to how much of that concern is justified. The level of interest in the topic means that the necessary epidemiological and supporting mechanistic data, analogous to the existing body of work covering air pollution, will almost certainly be produced in the years ahead, however.

Micro- and Nanoplastics Exposure Across the Lifespan: One Health Implications for Aging and Longevity

Microplastics and nanoplastics (MNPs) are pervasive environmental contaminants with growing relevance for human health across the lifespan. Older adults may be especially vulnerable to their effects due to cumulative lifetime exposure, age-related physiological changes, and a higher burden of chronic disease. Adopting a One Health perspective, this review synthesizes current evidence on the sources, exposure pathways, and biological effects of MNPs, integrating findings from environmental, animal, and human studies with a specific focus on aging populations.

Experimental studies consistently show that MNP exposure triggers oxidative stress, inflammation, mitochondrial dysfunction, and cellular senescence, mechanisms central to biological aging. These processes are linked to dysfunction of the cardiovascular, nervous, gastrointestinal, and immune systems, suggesting that MNPs may contribute to the development or progression of age-related diseases. Within the One Health framework, MNPs also act as carriers of chemical additives and environmental pollutants, potentially amplifying health risks through combined and cumulative exposures along food chains and ecosystems.

Despite increasing mechanistic evidence, direct epidemiological data in older adults remain limited. This review highlights key knowledge gaps and emphasizes the need for integrative, longitudinal research to clarify the role of MNPs in aging and to inform public health and environmental policy.

For many hundreds of years, Easter has been associated with rebirth and rejuvenation. Let’s see what’s been done last month to rejuvenate animals and people.

Team and Activities

Support the Human Ageing Genomic Resources: João Pedro de Magalhães has launched a fundraiser to help maintain this database, which has supported thousands of scientists worldwide in aging and longevity research. With over 200,000 visitors per year and 1,000+ citations, it has become the benchmark platform in the biology of aging.

Advocacy and Analysis

When Doctors Prescribe Horoscopes: The Trouble With Biological Age Tests: In this op-ed, Dr. Matt Kaeberlein takes the stance that most common biological aging tests do not actually measure aging.

Cellular Senescence and Senotherapeutics: The Expert Roundup: We asked four leaders of senescence-focused biotech companies to discuss what drew them to the field, what makes their approaches unique, the obstacles they face on the path to the clinic, and what senotherapeutics might ultimately achieve for human health.

Research Roundup

Novel Mechanism for Parkinson’s Is Linked to ATP Deficiency: Scientists have discovered that ATP deficiency disrupts dopamine processing in synapses, leading to the accumulation of the harmful protein species that characterize Parkinson’s disease.

Resistance Exercise Training Slows Down Brain Aging: Using models that analyzed MRI images of the brains of elderly people, researchers concluded that both heavy and moderate resistance training slow brain aging.

How Inflammaging Makes Pneumonia Worse in Mice: Researchers publishing in Aging Cell have discovered how older organisms’ susceptibility to pneumonia is related to inflammatory factors.

Fat Composition Affects T Cell-Mediated Immunity: Scientists have found that the ratio between poly- and monounsaturated fatty acids affects the viability of T cells as well as both humoral and anti-tumor immunity.

A Review of How the Heart Ages: The European Heart Journal has published a review of what happens to the human heart as it ages, noting the cellular effects of mitochondrial dysfunction and cellular senescence along with more visible changes such as hypertrophy and fibrosis.

Scientists Successfully Freeze and Rewarm Mouse Brain Slices: Researchers have vitrified mouse brain slices and then a complete brain with encouraging results: upon rewarming, much of the neuronal function was preserved.

People With Positive Outlooks Have Better Aging Outcomes: These researchers reported that a significant number of older adults who participated in the study experienced an improvement in cognitive and/or physical functioning.

The Many Dangers of 7-Ketocholesterol: A group of researchers, including Matthew O’Connor of Cyclarity Therapeutics, has published a review detailing what effects 7-ketocholesterol (7KC) has in the human body.

Gut Bacteria Might Affect Cognition via the Vagus Nerve: A new study suggests that microbiome remodeling is a mechanism behind age-related cognitive decline, with one particular bacterial species identified as the likely culprit. In mice, antibiotics seem to reverse this effect.

How Zinc Protects Injured Arteries From Accelerated Aging: Researchers publishing in Aging Cell have discovered that the nuclei of the cells that line injured arteries quickly become misshapen. Delivering zinc to these cells partially alleviates this dysmorphism.

Study Links a Gut Bacterium to Increased Muscle Strength: Scientists have found a positive correlation between the abundance of the bacterium Roseburia inulinivorans in the gut and muscle strength in mice and humans, although the mechanism behind it is still unclear.

Negative Interactions Are Associated With Faster Aging: A new study reported an association between having more problematic people in close networks and increased biological aging.

Using mRNA to Fight Tau Aggregation in Alzheimer’s: Researchers publishing in Cell Reports Medicine have described the development of a lipid nanoparticle that delivers mRNA to neurons in order to stop the formation of tau aggregates and fight Alzheimer’s disease.

Meat Consumption May Benefit APOE4 Carriers: A new study has found a negative association between unprocessed meat consumption and cognitive decline in carriers of the “pro-Alzheimer’s” APOE ε4 allele.

In Vivo Created CAR T Cells Eliminate Tumors in Mice: An ingenious CRISPR-based tool was used to create CAR T cells in vivo instead of the usual in vitro approach. It showed higher efficacy across three cancer types, including a solid tumor.

Two Polyunsaturated Lipids Demonstrate Senolytic Activity: A new study identified two polyunsaturated fatty acids, α-eleostearic acid (α-ESA) and α-ESA methyl ester (α-ESA-me), that showed senolytic activity in cell cultures and a mouse model.

Mitochondria Delivery Method Rescues Parkinson’s in Mice: Scientists used red blood cells as membrane donors to encapsulate healthy mitochondria and send them into diseased cells, achieving improvements across multiple models and conditions.

How a Growth Factor and SIRT1 Might Combat Disc Degeneration: Researchers publishing in Aging Cell have discovered that using FGF21 to upregulate the sirtuin SIRT1 delays spinal disc degeneration in a rat model.

Modified Immune Cells Target Cancer’s Metabolic Signature: Arming NK and T cells with metabolite-sensing receptors enhances their ability to infiltrate tumors and improves cancer outcomes in mice.

Human microphysiological systems of aging recreate the in vivo process expediting evaluation of anti-geronic strategies: This chip recapitulates, in 4 days, aging-associated hallmarks that occur after decades of aging in people, including gene expression shifts and oxidative DNA damage.

Ultrasonic exposure enhances the body’s antioxidant capacity: This study is the first in the world to demonstrate enhanced antioxidant capacity in vivo through non-invasive intervention using ultrasound.

Lifelong behavioral screen reveals an architecture of vertebrate aging: These researchers suggest that aging involves discrete life stages rather than a gradual, continuous decline.

A hierarchy of causes of death in senescent C. elegans: Late-life pathologies can compete in a hierarchical fashion to cause death, such that removal of one cause of death can unmask another.

The glycolytic metabolite phosphoenolpyruvate restricts cGAS-driven inflammation to promote healthy aging: Here, the researchers show that phosphoenolpyruvate (PEP), a glycolytic metabolite, acts as a protective factor against age-related chronic inflammation.

A global metagenomic atlas of aging identifies a microbiota phase transition associated with disease risk: Overall, the global gut microbiome atlas uncovers a critical age transition phase, highlighting opportunities for microbiota-based therapies and offering novel insights into evolutionary dynamics during aging.

Astaxanthin, meclizine, mitoglitazone, pioglitazone, alpha-ketoglutarate, mifepristone, methotrexate, and atorvastatin-telmisartan do not increase lifespan in UM-HET3 mice: Despite prior evidence suggesting lifespan benefits, none of these tested compounds significantly increased lifespan in male or female mice.

Restoring circadian rhythms in the hypothalamic paraventricular nucleus reverses aging biomarkers and extends lifespan in male mice: Age-related circadian disruptions accelerate physiological decline and shorten lifespan. Enhancing circadian amplitude has emerged as a promising strategy for ameliorating age-associated disorders.

Metabolomic signatures of extreme old age: findings from the New England Centenarian Study: These results highlight metabolic pathways that may be targeted to promote metabolic resilience and healthy aging.

Comparing fourteen consensus biomarkers of aging: epigenetic pace of aging as the strongest predictor of mortality in BASE-II: In adjusted models of all-cause mortality, HGS, IL-6, standing balance, cognitive health, and the epigenetic clock (DunedinPACE) statistically significantly predicted mortality, with DunedinPACE emerging as the strongest predictor.

Biologically Younger Individuals, as Identified by MARK-AGE Biological Age Scores, Display a Distinct Favourable Blood Chemistry Profile Regardless of Age: These researchers discovered a dichotomy of correlations that may point to different roles of such markers: drivers versus bystanders of aging.

Longitudinal changes in epigenetic clocks predict survival in the InCHIANTI cohort: These findings suggest that dynamic changes in epigenetic aging reflect evolving health status and may serve as sensitive indicators for interventions aimed at extending healthspan and longevity.

Effects of daily multivitamin–multimineral and cocoa extract supplementation on epigenetic aging clocks in the COSMOS randomized clinical trial: Although the statistically significant but small effects of daily MVM supplementation on slowing biological aging are encouraging, additional studies are needed.

Inosine promotes erythrocyte metabolic reprogramming and restores oxygen release for rejuvenation via 2,3-BPG-PNP axis: Impaired glucose metabolic reprogramming resulting from decreased BPGM activity underlies red blood cell bioenergetic decline and is a novel hallmark of aging.

Vitamin C inhibits ACSL4 to alleviate ferro-aging in primates: This work establishes iron-related aging (ferro-aging) as a core, targetable mechanism of primate aging and positions vitamin C as a translatable geroprotective strategy.

Dietary rhythms and biological aging risk across multiple organs: This study revealed optimal meal timing and duration differ for biological aging across different organs, ages, genders, disease status, energy intake, and dietary quality.

Biological evidence of the life expectancy limit in human aging: The life expectancies of many countries are expected to reach the Japanese life expectancy of 87.5.

Avoidance of rejuvenation: a stress test for evolutionary theories of aging: With data from eusocial insects that can rejuvenate, the researchers present the idea that the avoidance of such rejuvenation is poorly explained by classic theories of aging in their standard formulations.

Aging is not a disease: an evolutionary and comparative biological reappraisal: Maintaining a clear conceptual distinction between time-dependent biological remodeling and pathological dysfunction may provide a more coherent basis for both scientific inquiry and therapeutic development.

News Nuggets

Buck Institute Launches Healthspan Horizons: Healthspan Horizons is a new initiative designed to address one of the most urgent challenges in modern medicine: how to measure, understand, and extend healthspan.

BioAge Labs Provides Business Updates: BioAge provided financial results for the full year ended December 31, 2025 and business updates for the fourth quarter ended December 31, 2025.

Rubedo Announces Positive Preliminary Results for RLS-1496: Rubedo announced preliminary results from a single-center, ascending-dose, randomized, double-blind, vehicle-controlled trial in patients with plaque psoriasis, atopic dermatitis, and skin aging.

Coming Up

Vitalist Bay 2026 Returns to Berkeley May 14–17: The Vitalism Foundation announces Vitalist Bay 2026, the world’s largest longevity festival, returning to the Lighthaven Campus in Berkeley, California from May 14–17, 2026.

Xplore Program 2026: A Remote Summer Fellowship in Longevity: For the third summer in a row, Longevity Xplorer (LongX) is opening applications for the Xplore Program, a fully remote summer fellowship designed to help students and early-career professionals translate interest in longevity into practical experience.

Neuroscience of Vitality and Aging Conference in Boston: The Neuroscience of Vitality and Aging (NOVA) Conference is bringing together leaders from across neuroscience, biotechnology, policy, and investment to examine one of the most urgent questions in medicine today: how to preserve brain health across the lifespan and accelerate progress against neurodegenerative disease.

Partial reprogramming involves exposure of cells to one or more of the Yamanaka factors, (OCT4, SOX2, KLF4, and MYC, collectively OSKM) in order to induce a shift in epigenetic management of nuclear DNA structure to a more youthful state, while avoiding any dedifferentiation of target cell populations into induced pluripotent stem cells. This strategy has been demonstrated to produce some degree of rejuvenation in mice, but comes with the risk of cancer and tissue dysfunction if not carefully managed, particularly in the liver and intestines. Most of the funding presently devoted to development of rejuvenation therapies is focused on partial reprogramming, concentrated in a small number of well funded organizations, primarily Altos Labs. The first clinical trial of partial reprogramming has commenced, conducted by Life Biosciences. It is narrowly focused on the eye, where exposure can be limited and controlled. Significant challenges remain to be overcome before reprogramming can be reasonably safely applied to more of the body, however.

Despite its therapeutic promise, in vivo partial reprogramming remains far from clinical readiness. The primary obstacle is the risk that cells may inadvertently revert to pluripotency. Even brief or low-level induction of pluripotency factors can, in some cells, cross the threshold into dedifferentiation, producing teratomas and tissue dysfunction in animal models. The tissue microenvironment further complicates this dedicate balance, as certain proinflammatory signals can sensitize cells to reprogramming, which makes it difficult to limit OSKM activity to the desired level or location.

Heterogeneous expression and delivery of reprogramming factors is another concern. Systemic delivery of doxycycline-inducible OSKM often yields unequal induction: some tissues receive too much, while others receive too little. Organs with naturally high plasticity, such as the liver and the intestine, are especially vulnerable, given their rapid uptake of doxycycline, plus their intrinsic epigenetic flexibility, which means they reprogram first and most strongly, leading to malabsorption and toxicity long before other tissues benefit. Achieving precise spatial and temporal control remains technically demanding.

Chemical partial reprogramming avoids genomic integration but introduces new challenges. A deeper molecular understanding of each small-molecule cocktail is needed to minimize off-target effects, as many compounds affect multiple pathways. On top of all this, reprogramming itself is stochastic and inefficient; only a fraction of cells respond as expected, making outcomes unpredictable and raising dosing concerns.

In vivo reprogramming, therefore, reflects an intrinsic trade-off between regenerative plasticity and pathological risk. Transient relaxation of cell identity and proliferative constraints can enhance tissue repair in permissive contexts, yet the same plasticity may drive teratoma formation, tumorigenesis, or organ dysfunction when genetic safeguards are compromised or tissue context is unfavorable. Accordingly, the outcome of OSKM induction is dictated by dosage, duration, tissue context, and genetic background, underscoring the need for precise spatiotemporal control.

Progress will depend on tools that can quantitatively define and monitor the 'safe window' of rejuvenation temporally and spatially, including real-time biomarkers of epigenetic reset, tissue-specific or stress-responsive promoters, and nonintegrating delivery systems. Integrating these advances with single-cell profiling and longitudinal functional assays will be essential to establish whether partial reprogramming can be applied safely and predictably in humans.

Link: https://doi.org/10.1016/j.molmed.2026.01.007